Aetiology
The aetiology of faecal incontinence is often complex and multifactorial. There are essentially seven aetiological subgroups, with patients falling into one or more groups.[8][9]
Structural anorectal abnormalities (e.g., sphincter trauma [including third- and fourth-degree obstetric injury], rectal prolapse). This also includes congenital abnormalities, as symptoms may recur in adult life despite previous surgical repair.
Neurological conditions (e.g., multiple sclerosis, stroke, pudendal neuropathy).[10]
Alterations in stool consistency (e.g., infectious diarrhoea, inflammatory bowel disease).
Overflow (e.g., impaction, reduced reservoir function due to bowel surgery).
Cognitive/behavioural dysfunction (e.g., dementia, learning difficulties).
General disability (e.g., may be caused by ageing or acute illness).
Idiopathic.
There is a weak association with diabetes mellitus; autonomic neuropathy may result in internal sphincter dysfunction and passive incontinence.[11] Neurological diseases can affect continence by interfering with the relevant sensory and/or motor pathways.
Obstetric sphincter damage is the most common cause of incontinence in young women, and sphincter damage has been estimated to occur in 11% of women who give birth vaginally.[12] It occurs more commonly with forceps delivery, larger babies, delayed second stage of labour, midline episiotomy, and occipitoposterior presentation.[12][13] Iatrogenic injury is a rare cause, but some procedures such as lateral sphincterotomy involve incision of the sphincter muscle and can result in faecal incontinence if too much is divided.
Operations to reduce the length of bowel can reduce reservoir function, especially if involving the rectum.
Pathophysiology
The complex mechanism of continence depends on an interaction with sphincter function, stool consistency, transit of colonic contents, rectal reservoir function and compliance, anorectal sensation, and pelvic floor anatomy.[14] Normally, passage of stool or flatus into the rectum allows distension and temporary relaxation of the internal sphincter so that the contents can be sampled by the richly innervated anal transition zone. Higher centre perception allows further relaxation of the sphincter complex in order to evacuate if socially acceptable. If unacceptable, the external sphincter complex is contracted and the urge to defecate is resisted until later. Any disruption, dysfunction, or overwhelming of this pathway may result in incontinence. Incontinence is rarely attributable to a single pathogenic mechanism, with local, anatomical, or systemic factors all potentially contributing.[15]
Use of this content is subject to our disclaimer