FI is a sign or a symptom, not a diagnosis, Deficits of individual functional components of the continence mechanism can be partially compensated for a certain period, until the compensating components themselves fail. For example,
obstetric injury may precede onset by decades, but
postmenopausal changes in the tissue strength reduce in turn the competence of the compensatory mechanisms.
Diabetes mellitus is also known to be a cause, but the mechanism of this relationship is not well understood.
Childbirth Vaginal delivery causes stretching of the pelvic muscles and the pudendal nerve. Obstetric injury is a leading cause of fecal incontinence. Obstetric injury may tear the anal sphincters, and some of these injuries may be occult (undetected). The risk of injury is greatest when labor has been especially difficult or prolonged, when
forceps are used, with higher
birth weights, or when a midline
episiotomy is performed. Only when there is post-operative investigation of FI such as
endoanal ultrasound is the injury discovered. The nerve is especially vulnerable to stretch damage during childbirth because of the course of the nerve, as it runs in close proximity to pelvic muscles (piriformis and coccygeus) and ligaments, before exiting and then re-entering the pelvic cavity. The damage is likely to occur at the exit from the pudendal canal, because the course of the nerve is relatively fixed at this point. Stretching occurs during delivery, especially from the child's head. 60% of females who sustained
obstetric tears were demonstrated to also have pudendal nerve damage. Any damage to the pudendal nerve occurring during childbirth may not become fully apparent until years later, for example at the onset of
menopause.
Anal sphincter weakness The anal canal presents the final barrier to continence. The resting tone of the anal canal is not the only important factor; both the length of the high-pressure zone and its radial translation of force are required for continence. This means that even with normal anal canal pressure, focal defects such as the
keyhole deformity can be the cause of substantial symptoms.
External anal sphincter (EAS) dysfunction is associated with impaired voluntary control, whereas
internal anal sphincter (IAS) dysfunction is associated with impaired fine-tuning of fecal control. The external anal sphincter is supplied by the pudendal nerve. Damage to the nerve supply of the external anal sphincter on one side may not result in severe symptoms because there is substantial overlap in innervation by the nerves on the other side. Disruption of the function of the internal anal sphincter results in reduced resting pressure in the anal canal. This is associated with passive leakage.
Obstructed defecation (incomplete evacuation of stool) Normal evacuation of rectal contents is 90100%. Obstructed defecation is often due to
anismus (paradoxical contraction or relaxation failure of the puborectalis). Rectal storage capacity (i.e. rectal volume + rectal compliance) may be affected in the following ways. Surgery involving the rectum (e.g.
lower anterior resection, often performed for colorectal cancer), radiotherapy directed at the rectum, and inflammatory bowel disease can cause scarring, which may result in the walls of the rectum becoming stiff and inelastic, reducing compliance. Reduced rectal storage capacity may lead to urge incontinence, Pudendal neuropathy is one cause of rectal hyposensitivity and may lead to fecal loading or impaction,
megarectum and overflow FI (see
overflow incontinence).
Overflow incontinence This may occur when there is a large mass of feces in the rectum (fecal loading), which may become hardened (
fecal impaction). Liquid stool elements can pass around the obstruction, leading to incontinence. Megarectum (enlarged rectal volume) and rectal hyposensitivity are associated with overflow incontinence. Hospitalized patients and care home residents may develop FI via this mechanism,
Central nervous system Continence requires conscious and subconscious networking of information from and to the anorectum. Defects or brain damage may affect the
central nervous system focally (e.g. stroke, tumor, spinal cord lesions, trauma, multiple sclerosis) or diffusely (e.g. dementia, multiple sclerosis, infection,
Parkinson's disease or drug-induced). FI (and
urinary incontinence) may also occur during
epileptic seizures.
Dural ectasia is an example of a spinal cord lesion that may affect continence.
Diarrhea Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea. Orlistat is an
anti-obesity (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea, and steatorrhea.
Radiation Irradiation may occur during
radiotherapy, e.g. for
prostate cancer. Radiation-induced FI may involve the anal canal as well as the rectum, when
proctitis, anal fistula formation, and diminished function of internal and external sphincter occur. Most people casually engaging in anal sex do not experience subsequent fecal incontinence. However, some practices are more strongly associated with incontinence; including anal
fisting, high frequency of anal sex, psychoactive drug use and
BDSM. Females have lower anal canal pressures and less robust sphincters than males, which may make them more susceptible to incontinence, particularly if coercion is involved.
Congenital defects Anorectal anomalies and spinal cord defects may be a cause in children. These are usually picked up and operated upon during early life, but continence is often imperfect thereafter. == Pathophysiology ==