Where is the sphincter?

Fundamental misconceptions about the lower esophageal sphincter (LES) pervade the literature of manometry.

It is widely believed there is a subphrenic esophageal segment that contains the sphincter.

It is also believed that intraabdominal pressure "backs up" the physiologic sphincter rendering it competent(1) Such statements imply that their authors believe the sphincter is in this subphrenic segment.

It is believed to be 2.5 cm or more in length.

Click for larger image
Click image for larger version
Unfortunately, these beliefs provide the rationale for antireflux surgical procedures. It is equally unfortunate that the actual sphincter described and named by Lerche(2), that is plainly visible radiologically, has been misinterpreted(3) and even described as an obstructive lesion similar to the LER.(4) Radiologically, there is no difficulty in locating the normal sphincter: it is at the end of the peristaltic wave. The peristaltic wave does not pass through the diaphragm. Hence there could hardly be a subphrenic segment of esophagus.

As the PEL in inserted at the sphincter, the sphincter will be above the diaphragm in a patient with normal LM tone. In a sense the sphincter is the stationary end of the peristaltic wave. There is no peristalsis in the fundus of the stomach or distal to the sphincter in the .3-3 cm aperistaltic esophageal segment interposed between the sphincter and the fundus.

The manometric data are detailed, pervasive and hazardous to challenge as they are backed by immense authority. It has been done, however, although the work has been successfully ignored. In 1985 Clark(5) resected the sphincter area and replaced it with a tube of jejunum or colon in 12 Rhesus monkeys. Remarkably, a high pressure zone (HPZ) was recorded on 89.6% of the manometer tracings after jejunal interposition! Even the pattern of "receptive relaxation" during the pharyngeal phase of swallowing was recorded in many. Moreover, some of the reported pharmacological effects on the sphincter were reproduced in these animals. Clark concluded that ". . . the HPZ resulted mainly from compression of the bulky jejunum as it passed through the oblique right crus of the diaphragm."

Click for larger image
Click image for larger version
Clark's criticism of the HPZ location of the LES is well taken and may explain the belief in a subphrenic sphincter. The manometer must be recording a squeeze of the fundus in the hiatus. This was demonstrated unintentionally by a study in which the GE junction area was simultaneously recorded by both cineradiography and manometry in 13 patients with lower esophageal rings (LER).(6) The HPZ was found to lie below the LER. In rigid conformity with manometric doctrine, the authors were forced to conclude that, "The lower esophageal ring was found at the proximal margin of the lower esophageal sphincter in all [13] patients."

As the number of pathological examinations of LER's increases, it becomes impossible to maintain that the LER is not exactly at the junction of squamous and glandular mucosa. The above finding can only have one interpretation: the HPZ the manometer was recording was in the stomach! Examination of the reproduced cine frames shows this to be the case. Metal tipped catheters are 2.5-3 cm into a hiatus hernia and hence subject to a hiatal squeeze.

If manometry places the HPZ about 2.5 cm distal to the true GE junction, i.e. in the stomach, 100% of the time in 13 patients, we have an explanation for the manometric inference of a subdiaphragmatic esophagus: the low resolving power of the manometer could easily misplace it.

It is interesting to note in Clark's report that all of the familiar "sphincter" phenomena - reduced pressure with deglutition, pharmacologic effect of propantheline, etc. - were present at the HPZ after extirpation of the sphincter! Clark advances this as evidence that there is no LES, but it also demonstrates that something will lessen the "squeeze" pressure being measured at the HPZ whether or not it is acting on a sphincter. That something, it will be shown, is the LM. The pharmacological effects, etc. could be equally well be due to action of the drug on the LM.

Click for larger image
Click image for larger version
The lower esophageal sphincter: Here the bulb-sryringe action of mesentery crowding into the tented PEL is powerful enough to override the sphincter, forcing the captive bolus back into the body of the esphagus. At this instant, the true length of the sphincter is seen to be only 7-8 mm - far shorter than has been supposed from the evidence of manometry. The sphincter remains closed against this considerable force from below, but when it does yield (after 3 seconds) it then relaxes completely within a second. Gastric mesentery crowded into the PEL tent by the Valsalva maneuver is the driving force.
Another splendid piece of evidence that manometers are not measuring the sphincter is provided by manometry itself. Using multiple catheters - as many as 8 - it has been shown that the "sphincter" pressure is asymmetrical about the radius of the lumen.(7) ,(8) It is mechanically impossible, however, for a contracting ring of muscle to exert anything but radially invariant pressure on the lumen. The multiple catheters must be measuring extrinsic pressure on the lumen, i.e., hiatal squeeze which can vary depending on proximity to the hiatus.

If , for example, one were to loop a cord around the a hollow organ as an external constraint, traction on the cord would press on only one side of the lumen. The organ would move laterally until constrained by equal pressure from the opposite side. On the other two sides the pressure would be intermediate. Intraluminal readings would vary depending on where pressure was being measured. What is this external constraint? It could only be the hiatal ring.

Click for larger image
Click image for larger version
Synthesis. The site of muscular thickness, muscle fiber arrangement. PEM, and Z-line are related to each other.

Figure 12 from Liebermann-Meffert, D. et al., Muscular equivalent of the lower esophageal sphincter, Gastroenterology 76:32-8, 1979 Used with permission.
These conclusions introduce a perplexing question: if the HPZ is not the LES, why isn't the true sphincter being demonstrated on manometric tracings? We can see from the captive bolus phenomenon that it is a very effective sphincter and undoubtedly is capable of preventing reflux. Yet there seems to have been no manometric evidence of it! It is quite possible, however, that mere introduction of a foreign object is enough to obliterate evidence of the true sphincter. A barium tablet arrested in the distal esophagus, for example, will provoke repeated LM contractions. Like air contrast esophograms, manometry is unphysiologic.

Liebermann-Meffert and her collaborators,(9),(10) perhaps because of their exacting technical methods, have had the last word as far as anatomical sphincters in the region. They described a gastroesophageal ring (GER) of circular smooth muscle 16.4 mm' below the descending limb of the PEL. The ring was 4.2 mm thick on the greater curvature side and a mm less on the lesser curvature side. It tapered up into the normal esophageal CM thickness of 2.1 mm over a distance of about 5 cm but tapered more abruptly distally. It was asymmetrically higher on the greater curvature side. [See their Figure 12]

As can be seen from their figure, the fibers do not run circularly but consist of short clasp-like fibers on the lesser curvature side and oblique, almost longitudinal, fibers on the greater curvature side. The axial length of the thickening was determined to be 2.3 cm on the lesser curvature side and 3.1 cm on the greater curvature, but because of the tapering, it is difficult to define the end points.

It is difficult to see what significance should be attached to this GER but the suggestion that it represents the physiologic LES must be refuted. It is 9-21 mm below the ora serrata. [We must recall that the mucosal LER is here.] It is even farther below the PEL. If all of its fibers were to contract simultaneously, they would produce a distortion of the GE junction, but not the annular constriction required for sphincter function.

Click for larger image
Click image for larger version
It has, nevertheless, been widely accepted as the anatomical counterpart of the physiologic sphincter as defined by manometry. The acceptance derives from the fact that manometry also assigns a 3-5 cm length to the physiologic sphincter and locates it below the diaphragm, well below the PEL. This places it below the aperistaltic segment that can be demonstrated radiologically between the sphincter and the ora serrata. As this has a length of .3 to 2.5 cm, the Libermann-Meffert muscle thickening is 1.4 to 4.6 cm below the lower edge of the radiological LES - that is, well below the endpoint of the peristaltic wave and clearly in the stomach.

I cannot find any justification for supposing that the physiologic sphincter of the esophagus is in the stomach and in a region quite devoid of peristaltic activity. It is in an area that, if above the diaphragm, would be a HH!

The Libermann-Meffert GER does not make sense in physiological terms. It is physiologically and logically imperative that the p-wave pass uninterruptedly to the sphincter - passing the baton, so to speak. If there were a gap, the bolus would be lost and reflux would occur back into the body of the esophagus as soon as the advancing ring of circular muscle contraction stopped and died out.

The p-wave does stop. It then either dies out or it does not. If it dies out, it loses control of the bolus. If it does not, then it is, by definition - a stationary ring of contracted CM - a sphincter. The point where the p-wave stops is where we have to look for the sphincter. Yet Ott(11) probably expresses the consensus of current opinion when he states that the sphincter ". . . . is not a distinct muscular entity."

Actually, it has been found, accurately described, located and illustrated as a "muscular ring" in several articles and texts but misidentified as ". . . . a distinct radiologic and clinical entity." although "relatively rare." and mostly occurring in children.(12) It is Wolf's(13) "A ring." It is listed as a cause of dysphagia for which bougienage and even surgery may be appropriate therapy.(14) One shudders to think that it may even have been resected!

No one recognizes it as the sphincter(15),(16),(17) because innumerable manometric reports have conditioned even radiologists to be looking for a 3 to 5 cm constriction below the diaphragm, not the actual 9-11 mm sphincter above the diaphragm. Wu states that ". . . . some authors even dispute their [muscular rings] existence."

The captive bolus phenomenon reveals the sphincter: its location relative to the mucosal junction (.2-3 cm above), its length (8-11 mm) and its competency. It becomes apparent at the point where the p-wave stops. There it resists the considerable back-pressure from the bulb- syringe effect of the Valsalva effort. When it is forced from below by that pressure, its proximal margin is displayed in sharp contrast to the relaxed CM of the esophageal body. It then disappears as the esophagus is dilated by refluxing fluid.






References

Last Updated July 26, 2007 by David PJ Stiennon

1. 1. Johnson, Lawrence F., Overview: physiology of the lower esophageal sphincter. In: Esophageal Disorders, Eds. DeMeester, Tom R. and Skinner, David B., Raven Press, New York, 1985.

2. 2.Lerche, W., The esophagus and pharynx in action. Charles C. Thomas, Springfield, Illinois, 1950.

3. 3.Wolf, B.S., The inferior esophageal sphincter - roentgenologic and manometric correlation, contradictions and terminology. AJR 110: 260-77, 1970.

4. 4. Ott, David J., Gelfand, David W., Wu, Wallace C., et al., Esophagogastric region and its rings. AJR :142, 281-7, 1984.

5. 5. Clark, John, A critical look at reproducibility of distal esophageal manometry. In: Esophageal Disorders, Eds. DeMeester, Tom R. and Skinner, David B., Raven Press, New York, 1985.

6. 6. Cauthorne, R.T., Vanhoutte, John J., Donner, Martin W. and Hendrix, Thomas R., Study of patients with lower esophageal ring by simultaneous cineradiography and manometry. Gastroenterology 49: 632-40, 1965.

7. 7. Wynans, C.S., Manometric asymetry of the lower esophageal sphincter. Am. J. Dig. Dis. 22:348-52, 1977.

8. 8. Soffer, Edy E, Ambulatory recording of lower esophageal sphincter pressure: adding the missing link. Editorial, Gastroenterology 108:289-91, 1995.

9. 9.Liebermann, D., Allgower, M., Schmid, P., and Blum, A.L., Muscular equivalent of the lower esophageal sphincter. Gastroenterology 76: 31-8, 1979.

10. 10.Liebermann-Meffert, D., Heberer, M. and Allgower, The muscular counterpart of the lower esophageal sphincter. In: Esophageal Disorders, Eds. DeMeester, Tom R. and Skinner, David B., Raven Press, New York, 1985.

11. 11. tt, David J. ,In: Gastrointestinal Radiology, Eds, Gore, Richard M., Levin, Mark S. & Laufer, Igor, Eds., W.B. Saunders, Philadelphia, 1994.

12. 12. u, W.C., Esophageal rings and webs. In Castell, D.O., The Esophagus, Little Brown, Boston, 1992.

13. 13.Wolf, B.S., Roentgen features of the normal and herniated esophagogastric region, Am. J. Dig. Dis. 5:751-69, 1960.

14. 14. Ott, D.J., Gelfand, D.W., Wu, W.C. and Castell, D.O., Esophagogastric region and its rings, AJR 142:281-7, 1984.

15. 15. Ott, David J, Radiology of the oropharynx and esophagus. In Castell, D.O., The Esophagus, Little Brown, Boston, 1992.

16. 16. Goyal, R.K., Clancey, J.J. and Spiro, H.M., Lower esophageal ring, NEJM 282:1355-64, 1970.

17. 17.Gastrointestinal Radiology, Gore, Richard M., Levine, Mark S. & Laufer, Igor, Eds., W.B. Saunders, Philadelphia, 1994.