BACKGROUND: Persistent defects after primary sphincter repair and occult sphincter tears are common after vaginal deliveries. Anal incontinence may be associated with these morphological defects. MATERIAL AND METHODS: Forty-six primiparous women were evaluated with ultrasonography, manometry and electrophysiology. Twenty-four women had undergone primary repair of obstetric sphincter tears (sphincter group), 16 women had no clinical sphincter tear but developed anal incontinence postpartum (symptom group), and six were delivered by elective cesarean section (cesarean group). RESULTS: In the sphincter group, 50% had anal incontinence at follow-up. At ultrasonography, 70% had injuries anteriorly in the midanal canal. At manometry, 4% had decreased resting pressure and 50% decreased squeeze pressure. At electrophysiology, 19% had pathologic pudendal latency and 25% pathologic fiber density. In the symptom group, 44% had injuries anteriorly in the midanal canal at ultrasonography. At manometry, all women had normal resting pressure and 19% had a decreased squeeze pressure. At electrophysiology, 46% had pathologic pudendal latency and 29% pathologic fiber density. In the cesarean group, 33% had mild anal incontinence at follow-up. Ultrasonography and manometry were normal in all women. At electrophysiology, 33% had pathologic pudendal latency and 17% pathologic fiber density. CONCLUSION: Anal sphincter injuries at childbirth are often inadequately diagnosed and primary repair frequently results in persisting defects in the anal sphincter. Anatomic injuries to the anal sphincter play an important role in the development of anal incontinence after delivery, but a significant proportion of symptomatic women also demonstrate neurologic impairment at electrophysiologic testing.
BACKGROUND: Persistent defects after primary sphincter repair and occult sphincter tears are common after vaginal deliveries. Anal incontinence may be associated with these morphological defects. MATERIAL AND METHODS: Forty-six primiparous women were evaluated with ultrasonography, manometry and electrophysiology. Twenty-four women had undergone primary repair of obstetric sphincter tears (sphincter group), 16 women had no clinical sphincter tear but developed anal incontinence postpartum (symptom group), and six were delivered by elective cesarean section (cesarean group). RESULTS: In the sphincter group, 50% had anal incontinence at follow-up. At ultrasonography, 70% had injuries anteriorly in the midanal canal. At manometry, 4% had decreased resting pressure and 50% decreased squeeze pressure. At electrophysiology, 19% had pathologic pudendal latency and 25% pathologic fiber density. In the symptom group, 44% had injuries anteriorly in the midanal canal at ultrasonography. At manometry, all women had normal resting pressure and 19% had a decreased squeeze pressure. At electrophysiology, 46% had pathologic pudendal latency and 29% pathologic fiber density. In the cesarean group, 33% had mild anal incontinence at follow-up. Ultrasonography and manometry were normal in all women. At electrophysiology, 33% had pathologic pudendal latency and 17% pathologic fiber density. CONCLUSION:Anal sphincter injuries at childbirth are often inadequately diagnosed and primary repair frequently results in persisting defects in the anal sphincter. Anatomic injuries to the anal sphincter play an important role in the development of anal incontinence after delivery, but a significant proportion of symptomatic women also demonstrate neurologic impairment at electrophysiologic testing.
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