It is currently believed that the cause of superior mesenteric artery syndrome (SMAS) is compression of the duodenum in the angle between the aorta and superior mesenteric artery (SMA). It is recognized that a decrease in aortomesenteric angle (AMA) <25° and intervascular distance < 8 mm, caused by fat loss, is characteristic of SMAS. Based on these statements, surgeons operate on patients with symptoms of dyspepsia only based on a reduction of AMA. This study is devoted to the analysis of the literature, including four own studies on this issue. Results: Measurement of the length of the constriction in the third part of the duodenum on radiograms from available sources showed that its true length ranged from 2.5 to 4.2 (3.30±0.15) cm and began a few centimeters cranial to the AMA. Therefore, it could not have been caused by compression in the AMA. In terms of length (3.20±0.15 cm) and location, this constriction corresponded to Ochsner’s sphincter, which normally short-term contracts to prevent the penetration of an acid bolus into the jejunum. Conscientious studies have shown that AMA is proportional to BMI, i.e., a decrease in AMA is observed in all thin people. An analysis of 211 cases of SMAS made it possible to differentiate two types of diseases. In 101 patients, the disease occurred acutely 1–53 (8.2 ± 1.9) days after stressful situations, accompanied by a catabolic reaction and hypersecretion of hydrochloric acid. In 110 patients, SMAS developed 3-72 (17.2±3.2) months after the diagnosis of acid-dependent diseases. Conclusion: The analysis of the literature led to the conclusion that hypersecretion of hydrochloric acid causes damage to the upper level of the digestive system, including duodenal dyskinesia. One of the manifestations of duodenal dyskinesia is an increase in tone and hypertrophy of the Ochsner’s sphincter. The clinic of the disease depends on the varying degree of Ochsner’s sphincter dyskinesia. In severe cases, partial or complete intestinal obstruction. New ideas about the etiology and pathogenesis of the so-called SMAS have made it possible to propose a tactic for the diagnosis and treatment of Ochsner’s sphincter dyskinesia, where there is no place for surgical treatment.
Objective. Congenital anal stenosis (CAS) is a rare form (2%) of anorectal malformations (ARM). All authors acknowledge the presence of the anal canal, but there are different ideas about the pathological anatomy and physiology of the CAS. Some believe that stenosis occupies a short distance between the wall of the anal canal and the anus. Others claim a long taper up to the dentate line. The volume of the operation depends on this. In the first case, the stenosis is dissected, and in the second, a pull-through operation is performed that destroys the anal canal. Methods. To detail the anatomy of the CAS, we analyzed X-ray studies of the CAS from our own experience and from literature sources to determine the length and location of the narrowed segment, as well as the width of the rectum, using our radiometric method. Results. A total of 7 X-ray studies of patients with CAS were analyzed, as well as 82 X-ray studies of different types of ARM. It has been shown that all forms of ARM, except for the true cloaca, develop in the embryological period in the same way with the formation of the anal canal because of the advancement of the internal anal sphincter (IAS) in the craniocaudal direction. The absence of the anus indicates that the exogenous rudiment of the anal canal does not move upward to meet the endogenous one. Therefore, penetration of the IAS beyond the anal canal leads to the formation of a narrow, rigid ring. If IAS penetrates through the subcutaneous tissue and skin, then CAS is formed. In other cases, the anus moves forward and upward, emerging outward or into any cavity, forming an ectopic anus onto the perineum, vestibule, urethra, or into the vagina. Conclusion. Congenital anal stenosis is one of the forms of ARM, characterized by the presence of a normal anal canal, where the stenosis of the normally located anus has a length of 2 to 5 mm. X-ray examination provides an accurate anatomical and physiological characteristic of the defect. Treatment should be carried out as early as possible to prevent the development of megacolons. Dissection of the rigid ring and insertion of a tube into the anal canal can lead to complete recovery. A hypothesis of the embryological development of ARA is described.
Modern gastroenterology, which occupies the pages of scientific journals without alternative, began as an initiative of manufacturers of diagnostic equipment. For widespread advertising, they selected practical doctors who were not familiar with the methodology of science and superficial knowledge of physiology. This is how a group led by DeMeester arose, which in 1976 published the DeMeester score, i.e., the normal limit for esophageal pH monitoring. pH <4, less than 4% of the time per day was considered normal, i.e., it was unreasonably claimed that such reflux is physiological. This article proves that this study was carried out with numerous methodological errors, which led to an erroneous conclusion. For a long time, pH monitoring was considered the gold standard and with its help hypotheses were proposed that form the basis of modern gastroenterology. The article proves the fallacy of 13 hypotheses, which are presented as theories. Numerous articles using pH monitoring have publicized this method. Practitioners became "great scientists", equipment manufacturers became successful businessmen. Over time, they found other groups of practitioners to promote devices for impedance ph monitoring, high-resolution manometry, and many others. At the same time, a network of reviewers who believe in the infallibility of the luminaries do not allow studies that contradict their faith to be published. Thus, fundamental science was destroyed, which alone could assess the harm of false research both for science and for patients. Conclusion This study provides a list of hypotheses, that were previously considered theories, but since scientific evidence has proven these assumptions to be false, they should be excluded from subsequent use and citation.
Continence and defecation are two essential functions of the human body. Continence is the ability to retain feces until an acceptable time for defecation. Defecation is the evacuation of fecal material from the colon. Both functions involve complex physiologic processes that are not completely understood. The normal anatomy of the gastrointestinal tract is well documented in the literature. The data on the physiology of these processes are controversial and sketchy. For example, muscular contraction is accompanied by energy expenditure and resource depletion. All the known muscles, including the heart, relax after the contraction. During the relaxation, their contractile capacity is recovered. It is still not clear how the anal canal is in the continuous contraction, and which muscles are involved in the act of defecation. It is known that the external anal sphincter (EAS) is responsible for the emergency continence during the increase of abdominal pressure. However, the intensity of contraction promptly decreases after 8-15 seconds. It is hard to ascribe the continence to continuous contraction of the internal anal sphincter (IAS). A clear understanding of the normal physiology of the anorectal zone could significantly improve our approach to such pathological conditions like chronic constipation, fecal incontinence, anorectal malformations, etc. This work presents a new hypothesis of the continence and defecation, based on analysis of the literature and our own studies.
Hirschsprung’s Disease (HD) is relatively common in children. Surgical treatment is aimed at removing the aganglionic section of the gut and repairing the intestinal tract. Despite some achievements of recent years, the diagnosis of the disease is not always timely. After surgical correction, functional problems may arise. The final diagnosis of HD is based on rectal biopsy. Nevertheless, the diagnostic process may involve a contrast barium enema, which in some cases allows to reject the putative diagnosis of HD, and in 70%–90% of cases establish the location of the transition zone. Some authors recommended the use a manometric study to exclude HD, but its use is recently decreasing. During normal early embryonic development, the nerve cells invade the primary intestine in a craniocaudal direction. The enteric ganglia are interconnected to form two plexuses that extend along the length of the bowel: an outer myenteric (Auerbach) plexus running through the full length of the gut, and an inner submucosal (Meissner) plexus, found only in the small and large intestine. The myenteric plexus develops first and
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 Oclisner 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.
