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Comparative Study
. 1994 May;37(5):424-9.
doi: 10.1007/BF02076185.

Sustained internal sphincter hypertonia in patients with chronic anal fissure

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Comparative Study

Sustained internal sphincter hypertonia in patients with chronic anal fissure

R Farouk et al. Dis Colon Rectum. 1994 May.

Abstract

Purpose: This study was designed to determine whether functional variations of internal sphincter activity occur in order to differentiate between patients with anal fissures from those with hemorrhoids.

Methods: Thirty patients with chronic anal fissure (median age, 28 years; 12 females), 22 patients with hemorrhoids (median age, 37 years; 7 females), and 33 control volunteers (median age, 48.5 years; 21 females) underwent ambulatory anal sphincter fine-needle electromyography and anorectal manometry.

Results: The median internal sphincter electromyography frequency was similar: fissure group, 0.49 Hz; hemorrhoid group, 0.46 Hz (P > 0.05), and control group, 0.44 Hz (P > 0.05). Median anal resting pressures were similar in the fissure group (132 cm. H2O) and the hemorrhoids group (116 cm of H2O) (P > 0.05), but significantly greater than those in the control group (94 cm. H2O) (P < 0.05). The median number of transient relaxations of the internal and sphincter with an associated rise in rectal pressure and fall in anal pressure was 1 (range, 0-4) per hour in the fissure group, 6 (range, 4-7) per hour in the hemorrhoid group, and 4 range, 3-6) per hour in the control group. Six patients with fissures were reassessed following lateral internal sphincterotomy. Median and pressure was 102 cm of H2O (P > 0.1 vs. controls) and the number of internal sphincter relaxations increased to 4 per hour (P < 0.01 vs. preoperative number).

Conclusions: Internal anal sphincter relaxation occurs on fewer occasions in patients with chronic anal fissures that have failed to heal in comparison to patients with hemorrhoids and normal controls. This evidence further supports the hypothesis that internal sphincter hypertonia may be relevant to the pathogenesis of this disorder.

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