Hypothesis / aims of study
Injury to the external and internal anal sphincter (EAS and IAS) can occur during vaginal delivery. Involuntary loss of flatus or faeces occurs in 20% of women one year after childbirth (1). The risk of developing anal incontinence increases in women who suffer an obstetric anal sphincter injury (OASI). The IAS is vital in the maintenance of anal continence.
The aim of this study was to investigate to relationship between IAS muscle thickness and function, with anal incontinence symptoms in postpartum women who have suffered a perineal tear. It was hypothesised that thinning to the anal sphincter would result in reduced continence function and hence increased symptoms of anal incontinence.
Study design, materials and methods
Women referred to Pelvic Floor Clinic postnatally following OASI were investigated. These women had suffered an OASI during their most recent childbirth. Women were excluded if they were pregnant at the time of appointment. Anal Manometry and Endoanal Ultrasound were performed by a trained healthcare professional. Symptoms were assessed with clinical history and completion of the validated Birmingham Bowel and Urinary Symptoms Questionnaire (BBUSQ-22).
IAS measurements were carried out by an operator blinded from patient’s symptoms and degree of perineal tear. The patient’s average IAS thickness was correlated with anal maximal resting a squeeze pressures, and total score from questions 3-6 of the BBUSQ-22 assessing incontinence.
Eighty-nine women were investigated. They were aged 17-44 years (mean =30.5, SD=5.4).
Women were seen between 6-108 weeks postpartum (mean=23 weeks, SD=15). Women seen later reported more symptoms (Spearmans corr = 0.313, p=0.03). Of the 89 women, 67 reported symptoms of faecal incontinence (75%) and 20 reported only flatal incontinence (22%).
There was a significant positive correlation between resting and squeeze pressures (Spearman corr =0.619, p=<0.001).
Spearmans correlation analysis was used to assess the relationship between IAS thickness, anal pressures and symptoms. There was no correlation between patients resting or squeeze pressures and IAS average thickness. Also, no correlation was found between resting pressure and symptoms of anal incontinence. However as squeeze pressure increased, BBSUQ-22 scores decreased (corr=-0.274, p=0.009) and so did the incidence of flatal incontinence. There was no correlation between IAS thickness and patient symptoms. Parity and the time from birth to appointment had no effect of IAS thickness. There was an association between IAS injury on ultrasound and symptoms (Chi Sq 4.55, p=0.038) but surprisingly no association between symptoms and EAS injury (Chi Sq 9.53, p-0.994).
Patients with an OASI involving the IAS had a significantly lower resting pressure than those who did not (3a: mean=49.5, SD= 13.9 | 3b: mean=46.1, SD=15.0 | 3c: mean=41.3, SD=16.3 | 4: mean=38.3, SD = 5.2) (Mann-Whitney U injury mean rank=31.5, no injury mean rank=47.97, p=0.019).
Pearsons correlation showed older women had greater IAS thickness than the younger women (corr=0.396, p=<0.001). There was however no significant difference in the ages of women with each OASI grade or reported symptoms meaning age was not a confounder.
Ethnicity had no relationship to IAS thickness, reported symptoms, resting and squeeze pressure.
Interpretation of results
There was a relationship between the squeeze pressure and anal continence status. There was an association between IAS injury and faecal or flatal incontinence but not symptom severity. When comparing women with and without injury to the IAS, only 16 patients had an injury resulting in low power of only 42%. There does not appear to a relationship between IAS thickness and anal continence status.