Zenker's diverticulum pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Pathophysiology
The pathophysiology of the Zenker's diverticulum is as follows
- Zenker's diverticula (ZD) is thought to be due to the result of motor abnormalities of the esophagus.
- ZD is a defect over the Killian's triangle, a point of weakness in the muscular wall of the hypopharynx.
- Killian's triangle is surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle.
- ZD should be considered a pseudodiverticulum as it includes only mucosa and submucosa.
- Chronic strain on the Killian's triangle leads to an evagination of the sphincter, which may be because of the following
- High pressures in the food bolus in the course of swallowing.
- Difficulty in swallowing because of abnormalities of the upper esophageal sphincter (UES).
- This failure to achieve adequate diameter for effective bolus clearance leads to a subsequent increase in the hypopharyngeal pressure gradient.
- Increased intrabolus pressures found in patients with ZD can be secondary to impaired bolus passage in combination with or as a result of gastroesophageal reflux disease.
- As the diverticulum enlarges, it may compress the pharyngoesophageal segment as well as increased stiffness and the intrabolus pressure.
- Increased intrabolus pressure is also increased in older patients who perform multiple swallows to achieve bolus clearance.
- Various hypothesis involved in the pathogenesis of the Zenker's diverticulum are as follows[1][2][3][4][5][6][7]
- Zenker's diverticulum is a disorder of diminished upper esophageal sphincter, incomplete sphincter opening is probably the cause of dysphagia. Increased hypopharyngeal pressures throughout swallowing are probably important in the pathogenesis of the diverticulum.
- The nemaline bodies and red ragged fibers are usually the normal cricopharyngeous findings. whereas the Zenker's diverticulum is characterized by adipose tissue deposition and degeneration of the fiber these structural modifications can impair the UES opening and dysphagia ensues.
- Nineteen patients in the sample were found to have reflux and 20 had dysmotility. These findings suggest that pharyngeal pouches are not a purely localized incoordination of the cricopharyngeal sphincter but are associated with a generalized oesophageal muscle dysfunction.
- Acid reflux induces longitudinal esophageal shortening, which in turn increases the chance for the development of herniation between 2 spatially associated structures, the pharyngeal constrictors and cricopharyngeus muscles, leading to the development of Zenker diverticulum
- Zenker's diverticulum is thought to result from disordered coordination among the pharynx and upper esophageal sphincter.
- Manometric studies of the upper esophagus were used in testing the hypothesis of dysmotility in the formation and growth of a Zenker's diverticulum; however, the data have provided conflicting evidence.
- Manometric studies show that resting upper esophageal sphincter strain is normal in some patients with Zenker's diverticulum and decreased in others. abnormal premature relaxation and contraction of the upper esophageal sphincter seen in some patients with Zenker's diverticulum may be accompanied with the aid of pharyngeal contractions against a closed sphincter.
- This abnormality is thought by a few investigators to be the cause of Zenker's diverticulum, but not by others who have found normal upper sphincter relaxation.
- In summary, in-coordination of pharyngeal contraction and UES opening has also been variably demonstrated by some investigator.
- All the above-mentioned hypotheses lead to herniation within the Killian's triangle, inclusive of disorders associated with altered UES function, unusual esophageal motility, esophageal shortening.
- Impaired bolus passage leads to increases intrabolus pressure which leads to herniation in the Killians triangle.
- Acid reflux is thought to lead to increased spasm of the UES which in turn increases the intrabolus pressures during swallowing, given that swallowing is frequently distinct from episodes of acid reflux disease.
Histopathological Findings: Zenker's diverticulum
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References
- ↑ Cook IJ, Gabb M, Panagopoulos V, Jamieson GG, Dodds WJ, Dent J, Shearman DJ (1992). "Pharyngeal (Zenker's) diverticulum is a disorder of upper esophageal sphincter opening". Gastroenterology. 103 (4): 1229–35. PMID 1397879.
- ↑ Cook IJ, Blumbergs P, Cash K, Jamieson GG, Shearman DJ (1992). "Structural abnormalities of the cricopharyngeus muscle in patients with pharyngeal (Zenker's) diverticulum". J. Gastroenterol. Hepatol. 7 (6): 556–62. PMID 1283083.
- ↑ Fulp SR, Castell DO (1992). "Manometric aspects of Zenker's diverticulum". Hepatogastroenterology. 39 (2): 123–6. PMID 1634178.
- ↑ Sasaki CT, Ross DA, Hundal J (2003). "Association between Zenker diverticulum and gastroesophageal reflux disease: development of a working hypothesis". Am. J. Med. 115 Suppl 3A: 169S–171S. PMID 12928096.
- ↑ Resouly A, Braat J, Jackson A, Evans H (1994). "Pharyngeal pouch: link with reflux and oesophageal dysmotility". Clin Otolaryngol Allied Sci. 19 (3): 241–2. PMID 7923848.
- ↑ Mulder CJ, Costamagna G, Sakai P (2001). "Zenker's diverticulum: treatment using a flexible endoscope". Endoscopy. 33 (11): 991–7. doi:10.1055/s-2004-826106. PMID 11715923.
- ↑ Hunt PS, Connell AM, Smiley TB (1970). "The cricopharyngeal sphincter in gastric reflux". Gut. 11 (4): 303–6. PMC 1411416. PMID 5428852.