Pudendal neuropathy is the only parameter differentiating leakage from solid stool incontinence

Fecal incontinence may occur in several forms. Although some patients are grossly incontinent, other patients experience only leakage. In patients with gross incontinence, severity can range from the mildest forms (limited to loss of control of flatus) to the most severe forms (involving loss of solid stool). This study was undertaken to determine which physiologic parameters differentiate female patients with incontinence of solid stool from patients with control of formed stool and incontinence limited to seepage.

Thirty-eight consecutive female patients with a primary complaint of seepage or solid stool incontinence were evaluated using water perfusion manometry, balloon inflation assessment of rectal sensitivity, and pudendal nerve terminal motor latency. A prospectively maintained database was used for collection of data. The findings in the two patient groups were compared with patients in a group of normal control individuals. Ages of the women in the three groups were similar.

Both groups of patients demonstrated statistically significant (P < 0.05) decreases in rest and squeeze sphincter lengths, pressures, and pressure volumes compared with normal volunteers. The patients also had significantly more asymmetric high-pressure zones and hypersensitive rectums. No significant difference between the two groups of incontinent patients could be identified using any of these parameters. Significant differences between the groups were found in pudendal nerve function. The distal rectoanal excitatory reflex was abnormal in 58.1 percent of grossly incontinent women compared with 28.6 percent of patients with leakage (P < 0.05). The majority of patients with leakage alone (65 percent) had normal pudendal nerve terminal motor latency, whereas only 22.6 percent of women with gross fecal incontinence had normal pudendal nerve terminal motor latency bilaterally (P = 0.01).

Normal bilateral pudendal nerve function can partially compensate for abnormal sphincter symmetry and function, permitting women with grossly abnormal parameters to maintain control of bowel movements. It remains to be seen whether, with advancing age, patients with leakage will have development of slowed pudendal nerve conduction and, if so, whether their condition will progress to gross incontinence.