Combined ischemic and neuropathic insult to the anal canal in an animal model of obstetric-related trauma.

BACKGROUND

Childbirth, in particular, when it involves instrumental vaginal delivery, can result in direct trauma to the external anal sphincter muscle. In addition, a global injury to the pelvic floor, including neurovascular injury to the anal sphincter complex, may occur.

OBJECTIVE

The aims of this study were to determine whether sensory drive from the anal canal and oxygenation of the external anal sphincter were compromised during simulated labor in a validated animal model of obstetric trauma.

DESIGN

Fifteen female Wister rats were operated on. Group 1 (n = 5) underwent pelvic balloon compression for 1 hour to simulate increased pelvic pressure during childbirth. Somatosensory cortical potentials, evoked by electrically stimulating the anal canal, were tracked. In group 2 (sham), the balloons were not inflated. In group 3, tissue PO2 values of the external anal sphincter and femoral arterial blood flow were measured simultaneously during the period of balloon inflation.

RESULTS

The peak amplitude of cortical evoked potentials was reduced (from 11.8 ± 1.5 μV to 3.1 ± 1.1 μV) during pelvic compression (p = 0.002, ANOVA). During this period, arterial blood flow to the hindlimb and the external anal sphincter tissue PO2 decreased by 20% (p < 0.001) and 60% (p < 0.001).

CONCLUSION

Pelvic compression that mimics obstetric trauma is associated with diminished anocortical drive. This neural insult may be compounded by concomitant ischemia of the external anal sphincter.