Sphincter of Oddi function and dysfunction
Nearly 400 hundred years ago, Frances Gliesson first described a sphincter structure at the distal end of the common bile duct where it enters the duodenum, but it was not until 1889, when Rugero Oddi described its anatomy and physiology in detail, that the function of this structure and its role in the control of flow of bile and pancreatic juices were appreciated. Oddi also postulated that patients would experience symptoms when this sphincter, which now bears his name, malfunctions. Since these initial observations, numerous studies have been conducted with the aim of understanding the way that the sphincter of Oddi (SO) functions and how its dysfunction produces a variety of clinical syndromes. As we enter into the 21st century, our knowledge of the normal function of the sphincter has been considerably enhanced by these studies, and patients with dysfunctioning sphincters that produce symptoms can be identified. Furthermore, for a number of patients, therapies exist that produce good long term results. However, there are still large gaps in our understanding of the mechanism of dysfunction, and successful therapies for a significant number of individuals with SO dysfunction are lacking.
The SO has been shown to be predominantly made up of circular and longitudinally orientated smooth muscle fibres that are embryologically distinct from the duodenum.
The muscular connections with the duodenum are thought to act as anchoring points and not to be functionally important. The SO shows similarities to duodenal activity in that its phase 3 activity of the migrating myoelectrical complex always precedes the duodenal phase 3 activity, but for the rest of the time the SO functions independently from the duodenum with regular phasic activity and no quiescent phase.
The function of the SO in humans has been characterized by manometric techniques that allow direct measurement of pressure changes using a small catheter directed into either the common bile duct or pancreatic duct (Figure 1). Intraluminal perfusion manometry has been able to characterize the human SO as having a modest basal tone with superimposed high pressure phasic waves (Figure 2). The predominant function of the human SO appears to be to act as a resistor to the flow of bile and pancreatic secretions because most flow occurs between phasic waves. In humans, SO phasic waves may serve to keep the sphincter segment empty. There is considerable species variation. The SO in the American opossum has been show to act as a pump using cineradiography. This finding has drawn an analogy with the systolic and diastolic cycles of the heart, with flow occurring during systolic contraction and sphincter filling occurring during diastole. Tachycardia of the heart can lead to pump failure, and tachyoddia (high frequency SO phasic activity) can lead to a decrease in flow across the sphincter. The common factor across species with respect to SO function is that post- prandially, flow across the sphincter is enhanced, regardless of whether the SO acts as a resistor or pump.
Figure 1) Endoscopic sphincter of Oddi manometry. The triple lumen catheter is passed through the biopsy channel of a duodenoscope and inserted into either the common bile duct (CBD) or pancreatic duct (PD) so that the three ports record from the sphincter. Reproduced with permission from reference 3
In humans, both postprandially and following duodenal infusion of fats, SO tonic activity has been shown to be reduced. These SO changes that lead to the delivery of bile and pancreatic secretions into the duodenum are under neurohormonal control. Neural connections of the SO to the duodenum and gallbladder have been identified using immunohistochemical techniques. Functional studies have demonstrated adrenergic, cholinergic and nonadrener- gic noncholinergic (NANC) innervation. The adrenergic innervations are inhibitory and the cholinergic innervations are excitatory. NANC innervation appears to be inhibitory and mediated by nitric oxide. Local reflexes involving the SO have been demonstrated between the duodenum, and gallbladder and bile ducts. The predominant hormonal agent affecting SO motility is cholecys- tokinin (CCK). CCK is released by the duodenal mucosa into the circulation in response to duodenal luminal acid and nutrients, especially fats and amino acids. In humans, CCK has been shown to decrease the basal pressure and the amplitude of phasic waves of the SO. CCK re-lease is inhibited by pancreatic enzymes and bile salts in the duodenum.
Get the medication you need. Buy online
Figure 2) Normal sphincter of Oddi (SO) manometry