What is the role of a cricopharyngeus spasm in functional obstruction of the proximal esophagus?
T. Lerut (Leuven)
The so-called spontaneous rupture of the esophagus or Boerhaave's syndrome in its typical clinical presentation is preceded by an episode of vomiting.
During the normal vomiting reflex there is coordination between the increased intra-abdominal pressure caused by rapid diaphragmatic descent and abdominal wall contraction and relaxation of the esophageal sphincter. Failure of relaxation of the upper-esophageal sphincter results in increase in intra-esophageal pressure and rupture of the esophagus.
This seems to be a well accepted explanation for the pathophysiology of the so-called spontaneous perforation or Boerhaave syndrome [1].
However very little is documented about the role of a cricopharyngeus dysfunction and subsequent functional obstruction of the proximal esophagus as a cause of spontaneous perforation.
For obvious reasons functional investigation of the pharyngo-esophageal behavior during vomiting in man are scarce, and most available knowledge is based on animal studies.
On the basis of radiocinematographic studies in cats four phases are distinguished: esophageal dilatation, expulsion of gastric contents, return in to the stomach and esophageal collapse [2].
The pharyngeal and esophageal responses associated with vomiting have been extensively studied in awake chronically instrumented dogs by Lang et al. [3].
To induce vomiting episodes, apomorphine was administered.
Four distinct motor events of the pharynx associated with vomiting were described:
1) increased swallowing frequency;
2) increased tonus of pharynx and esophagus;
3) phasic relaxation and contraction of the pharyngo-esophageal region during retching and vomiting;
4) retrograde contraction of the pharyngo-esophageal region preceded by contraction of the geniohyoideus muscle during vomitus expulsion.
No specific motor responses of the thoracic esophagus associated with vomiting were found except for the increased frequency of swallow-initiated peristaltic contractions. The lower esophageal sphincter (LES) and gastric fundus, tone relaxed before, during and after vomiting.
The vomit occurs when the dome fibers of the diaphragm contract but hiatal fibers relax.
The physiologic function of the tonic longitudinal contraction of the pharyngo-esophageal junction may be to facilitate gastroesophageal reflux by pulling orally the relaxed LES and proximal stomach thereby:
1) eleminating the abdominal portion of the esophagus;
2) deforming the stomach in the shape of a funnel and removing the acute angle of Hiss.
The esophagopharyngeal retrograde contraction may prevent the return of esophageal contents to the stomach and propel the vomit to the pharynx.
One can hypothesize that incoordination or dysfunction of the upper esophageal segment may result in a functional obstruction of the proximal esophagus during retching and vomiting resulting in an esophageal trauma, e.g. tear by increased intraluminal pressure.
However, contraction of the geniohyoideus muscle has been recorded during vomiting and several studies have shown that contraction of the geniohyoideus can significantly lower pressure within the upper esophageal sphincter, even when the sphincter is not relaxed [4].
In conclusion, whether cricopharyngeal spasm is a contributing factor in the "spontaneous rupture" or Boerhaave's syndrome is, although an attractive hypothesis, difficult to prove.
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