Fecal incontinence occurs when one or more mechanisms that maintain continence are disrupted

to an extent that other mechanisms are unable to compensate. Fecal incontinence is often
multifactorial and the pathophysiological mechanism often overlap. The pathophysiological
mechanism can be divided into anal sphincter weakness, anatomical disturbance of pelvic floor,
anorectal inflammation, and central nervous system disease.1,2
1. Anal sphincter weakness
Anal sphincter weakness occurs because of several possible causes, such as injury (e.g.
obstetric trauma, hemorrhoidectomy internal sphincterotomy, fistulotomy), non-traumatic
(e.g. scleroderma, internal sphincter thinning of unknown etiology), and neuropathy (e.g.
stretch injury, obstetric trauma, diabetes mellitus), with obstetric trauma as the most common
cause. In anal sphincter weakness, disruption or weakness of external anal sphincter (EAS)
causes urge-related or diarrhea-associated fecal incontinence, and damage to the internal anal
sphincter (IAS) muscle or the anal endovascular cushions may lead to a poor seal and an
impaired sampling reflex. The injury may involve the EAS, the IAS, the pudendal nerves, or
a combination of these structures, which may cause passive incontinence or fecal seepage,
often under resting conditions. Anorectal surgery for hemorrhoids, fistula, and fissures may
cause anatomic disruption, which can cause incontinence by inadvertently damaging the IAS
or through the loss of endovascular cushions. Anal dilation or lateral sphincterotomy may
result in permanent incontinence due to fragmentation of the anal sphincter apparatus.
Accidental perineal trauma or a pelvic fracture may also cause direct sphincter trauma
leading to fecal incontinence. The mechanism leading to fecal incontinence caused by
neuropathy is due to prolonged Pudendal Nerve Terminal Motor Latency (PNTML),
resulting in progressive damage to the striated anal sphincter muscle due to repeated stretch
injury during straining. This excessive straining may cause increased perineal descent that
can stretch and thereby damage the pudendal nerve and also make the anorectal angle more
obtuse. Sphincter degeneration secondary to pudendal neuropathy and obstetric trauma is
often sustained during childbirth, probably due to stretching of the nerves during elongation
of the birth canal or through direct trauma during the passage of the fetal head. Damage to
the pelvic nerves may lead to impaired accommodation and rapid transit through the
rectosigmoid region, overwhelming the continence barrier mechanisms.
2. Anatomical disturbance of pelvic floor
One example of anatomical disturbance of pelvic floor is descending perineum syndrome.
This is caused by long-standing constipation and history of excessive straining for many
years, leading to progressive denervation of the pelvic floor, excessive perineal descent, and
sphincter weakness, which may lead to rectal prolapse. Rectal prolapse may develop to fecal
incontinence depending on the state of the pelvic floor and the strength of the sphincter
muscles.
3. Anorectal inflammation
Anorectal inflammation, which is caused by Crohns disease, ulcerative colitis, anorectal
infection, etc., will affect the consistency, volume, and frequency of stool. Prolonged
retention of stool in the rectum can lead to fecal impaction. Fecal impaction may also cause
 prolonged relaxation of IAS tone, which allows liquid stool to flow around impacted stool
and to escape through the anal canal. If rectal wall compliance is impaired, a small volume of
stool material can generate high intrarectal pressure that can overwhelm anal resistance and
cause incontinence. In the presence of large-volume liquid stools, which often transit the
hind-gut rapidly, continence can only be maintained through intact sensation and a strong
sphincteric barrier. Similarly, in patients with bile salt malabsorption, or lactose or fructose
intolerance or rapid dumping of osmotic material into the colon, the colonic transit is too
rapid for both gaseous and stool contents and can overwhelm the continence mechanisms.
4. Central Nervous System (CNS) disease
Pelvic nerves may play a role in accommodating and storing feces and gas. Damage to the
pelvic nerves may lead to impaired accommodation and rapid transit through the
rectosigmoid region, overwhelming the continence barrier mechanisms. Damage to the motor
cortex from (CNS) lesions may lead to incontinence due to damage to both the sensory and
motor nerve fibers, resulting in sensory impairment. This damage can impair conscious
awareness of rectal filling as well as the associated reflex responses in the striated pelvic
floor sphincter muscles. Impaired rectal sensation may lead to excessive accumulation of
stool, causing fecal impaction, mega-rectum (extreme dilation of the rectum), and fecal
overflow. Causes of impaired sensation include neurological damage such as multiple
sclerosis, diabetes mellitus, or spinal cord injury.

REFERENCE
1. Rao S. Pathophysiology of adult fecal incontinence. Gastroenterology. 2004;126:S14-S22.
2. Bharucha A, Dunivan G, Goode P, Lukacz E, Markland A, Matthews C et al. Epidemiology,
Pathophysiology, and Classification of Fecal Incontinence: State of the Science Summary for the
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Workshop. The
American Journal of Gastroenterology. 2014;110(1):127-136.