What is anal incontinence all about?
Anal incontinence refers to anorectal restraint and defecation dysfunction, inability to discharge and control stool and gas at will, inability to sense the volume and nature of rectal contents, and inability to control nighttime defecation.
It is called “fecal incontinence”, which refers to the involuntary discharge of solid and liquid feces, and is a more serious form of anal incontinence. The inability to control the gas and liquid in the intestine at will is also anal incontinence, but to a lesser extent.
Clinical classification according to the degree of incontinence is as follows.
1.Complete anal incontinence: loss of anal control of stool, mucus and gas.
2.Incomplete anal incontinence: the anus can control solid stool, but not liquid stool and gas.
3.Sensory anal incontinence: local loss of sensation of intestinal contents in the rectum and anus, and frequent involuntary discharge of small amounts of liquid stool, mucus or gas.
4.Poo urgency: When the feces accumulates to a certain amount in the rectal cavity, or when diarrhea produces a strong need for defecation, and the surrounding environment does not have defecation conditions at that time, artificial control of defecation is needed, and if defecation cannot be inhibited and delayed for at least 5 minutes even by contracting the anus, it is called a stool urgency.
Mechanism of anal control of defecation
Before exploring the reasons why anal incontinence occurs, let’s look at how the anus functions as a closure.
The anus is the exit of the human digestive tract and is responsible for defecating and closing the digestive tract to prevent the leakage of intestinal contents. The bowel control role of the anus is divided into two states: resting and emergency.
1.The mechanism of anal stool control in the resting state
The resting state means that the anus is in a state of rest and stillness, which means that the anus maintains a continuous and tireless unconscious closing state during the time other than defecation and bowel movement.
So what factors are at play in this closure? There are four major factors: nerve, muscle, angle (the angle between the anal canal and rectum) and anal cushion, and if one or more of these factors has a problem, it can lead to anal closure dysfunction and incontinence.
Nerve factors: These include nerves and nerve centers, which control and direct the activities of anorectal muscles and local sensory system to open and close the anus and to complete defecation and bowel control actions.
There are two nerve centers related to the anorectum: the higher center is located in the cerebral cortex and the lower center is located in the sacral spinal cord, and the two are connected by spinal nerves. The anorectum is connected to the lower center via nerves in the pelvis. Therefore, the nerves in the brain, the spinal cord and the pelvic cavity constitute the nervous system that controls the anorectum, and if we use a tree as an analogy, the root of the tree is the brain center, the trunk is the spinal cord and the branches are the local nerves of the anus.
If the center is damaged, the anal muscles will be paralyzed and the anus will be relaxed and incontinent. If the local anorectal nerve is damaged it affects the function of the specific innervated tissue.
The anus is innervated by the anal nerve from sacral 2 to sacral 4 in addition to the internal sphincter. The anal nerve reaches the anus from both sides through the colorectal fossa and innervates the external anal sphincter, anal levator muscle, and anal margin skin. This nerve is under subjective control, and it is through this nerve that we act when doing anal lift exercises. It is important to avoid damage to it during clinical procedures for abscesses of the sciatic rectal fossa.
The rectal and internal anal sphincter is innervated by a vegetative nerve that originates from the presacral plexus and is divided into sympathetic and parasympathetic nerves. It is through this nerve that we perceive the onset of bowel movements. The defecation receptors located near the anorectal junction belong to this group of nerves, and damage to them can lead to sensory anal incontinence.
Muscular factors: These include the internal and external sphincters around the anus and the anal levator muscle from the pelvic floor, which is the most rigid and dominant factor in anal closure.
The muscles involved in anal closure at rest are mainly the internal anal sphincter, the type I muscle fibers of the external anal sphincter and the puborectalis muscle, of which the role of the internal sphincter accounts for 75% to 85% of them and is the most dominant muscle for anal closure. If surgically injured or congenitally lacking, the anus is in a flaccid state and gas, fluid or fecal incontinence occurs.
The type II muscle fibers of the external anal sphincter are only able to contract quickly and autonomously to control defecation when abdominal pressure suddenly rises. The puborectalis muscle starts from both sides of the posterior pubic bone and penetrates laterally in the vagina and anal canal, mainly controlling the excretion of solid feces, and its continuous resting tension keeps the anal canal and rectum at an angle.
Angle factor: It is the angle formed at the junction of the anal canal and rectum, clinically called the anal canal-rectal angle or rectal perineal curve, and is now considered an important factor in anal autonomy.
Why does the angle have a closing effect? A water pipe has the maximum flow in a straight state, when bent from the middle the flow decreases, and if bent to 90 degrees or less than 90 degrees, it blocks the flow. The rectal angle of the anal canal closes the anus for this reason. The force that maintains this angle is the puborectalis muscle, which is usually at about 90 degrees in the usual state and about 130 degrees during defecation, and nearly 180 degrees in patients with rectal prolapse, so patients with rectal prolapse are mostly accompanied by anal incontinence.
If the puborectal muscle is cut it will increase the rectal angle and lead to a decrease in closure function. The angle is destroyed by anal (rectal) cancer surgery, and an artificial method is usually used to recreate an angle to prevent incontinence.
Anal cushion factor: It is a mild mucosal bulge at the lower end of the rectum, which used to be considered as internal hemorrhoids, but since it is found in many normal human bodies, it is considered to be a physiological need of the human body rather than hemorrhoids, and plays a “cushion-like” role when the anus is closed, and is named anal cushion.
The size of the anal cushion is governed by a number of factors, and if the cushion is completely removed during surgery, mild leakage of stool may occur. The anal cushion surface is rich in defecation receptors, and sensory anal incontinence may occur if the anal cushion is severely damaged.
2.The mechanism of anal stool control in the emergency state
The emergency state refers to the state in which the physiological need to defecate and the surrounding environment does not allow defecation and requires artificial control to close the anus. When stool accumulates to a certain amount in the rectal cavity or when there is loose stool, it will stimulate the rectal wall and cause contraction of the rectum, and at the same time the internal anal sphincter will expand involuntarily, at which time the stool will be expelled if not controlled artificially. We usually contract the anus to stop the bowel movement. How is this process accomplished, and why is it sometimes controlled and sometimes not (fecal urgency)?
When the anus is contracted, the transverse pelvic floor muscles, including the external anal sphincter and the anal levator, which are governed by the consciousness, are contracted first, and the internal sphincter is compressed by the external sphincter, causing the anus to close forcibly, while the rectal wall muscles relax and a bowel movement is terminated. The successful completion of this process is based on a normal nerve reflex arc, normal volume and compliance of the rectum, and a sound internal and external sphincter.
If the internal sphincter is deficient or damaged, the contraction of the external sphincter alone is difficult to sustain and leads to incontinence due to loss of anal control. The external sphincter is a skeletal muscle that is easily fatigued, and generally the continuous contraction to close the anal canal can only last for about one minute, beyond which the canal is out of control.
Therefore, the internal and external sphincter factors are crucial to the effective control of defecation in emergency situations, especially the internal sphincter.
Causes of fecal incontinence
Through the above analysis, we conclude that where injury and affect the nerve, anal muscle, angle and anal pad four elements are the cause of anal incontinence, for these causes of morbidity, we can effectively carry out prevention.
1, central and neurological factors: central nervous system diseases, such as brain tumors, trauma, cerebrovascular accidents, etc. Spinal cord and sacrococcygeal nerve damage, such as spinal cord tumor, spina bifida, spinal cord spinal membrane bulge, spinal cord surgery and trauma, etc. Damage to the pelvic nerves, such as degeneration of the pubic nerves caused by excessive stretching of the pelvic floor during long-term constipation, damage to the anal nerves during anorectal surgery, and damage to the pelvic floor muscle nerves during maternal delivery.
2, anal canal and pelvic floor muscle factors: congenital anal atresia and rectal prolapse, absence or incomplete absence of the anal sphincter. Maternal injuries lead to mechanical rupture of the anal sphincter, and some studies say that the incidence of maternal fecal incontinence can reach 9.6% in the 3 months after childbirth. In a study with 62 cases of fecal incontinence related to obstetric operations, endorectal ultrasonography revealed external sphincter injury in 90% of patients and internal sphincter injury in 65% of patients.
Damage to the anal canal muscles from anorectal surgery is also a major factor in anal incontinence and will be specifically addressed in the next section. Postoperative perianal scarring, anal canal malformation, and mucosal ectasia are also common causes of incomplete anal incontinence. In addition, long-term diarrhea, tumor, radiotherapy, and Crohn’s disease may destroy the function of the sphincter and develop.
3, anal canal rectal angle factors: puborectalis muscle is the main factor to maintain the anal canal rectal angle, if damaged will increase this angle, the emergence of anal closure dysfunction. High abscess and anal fistula surgery may damage the puborectalis muscle. In addition, if the anus is displaced forward, it will also increase the anorectal angle, and the posterior fixation tissue of the anal caudal ligament should be protected during surgery.
4.Anal cushion factor: some unreasonable surgery for the treatment of internal hemorrhoids.
5, rectal factors: rectal volume is too small and compliance is reduced so that a very small amount of feces will stimulate defecation resulting in anal incontinence. Proctitis, prolapse of the rectum, rectal resection, ileal storage pouch is too small, resulting in small rectal volume. Colonic dysmotility in patients with diabetes mellitus and generalized sclerosis can lead to constipation, diarrhea, bacterial overgrowth and acquired megacolon, and if accompanied by internal sphincter atrophy leads to difficulty with anal autonomy.
Can anorectal surgery cause anal incontinence?
Anal incontinence after anorectal surgery occurs frequently, both domestically and abroad, so what clinical conditions and procedures are associated with this risk?
The traditional loop hemorrhoidectomy and high fistulotomy (ligature) are considered the procedures most likely to cause anal incontinence in anorectal surgery.
Pioneered by Whitehead, hemorrhoidectomy involves complete removal of the growing area of the hemorrhoid nucleus, followed by docking and suturing of the mucosa of the intestinal cavity to the skin of the anal verge. The advantage is that the nucleus is completely removed, but the disadvantage is that the anal cushion and skin of the anal canal are destroyed, resulting in incomplete anal closure and sensory anal incontinence. This procedure is still used by some general surgeons.
High anal fistulas and abscesses are recognized as difficult conditions, and because the lesion exceeds the anorectal ring, the traditional surgical approach cuts the anorectal ring at the same time as the lesion is incised. The anorectal ring is a collection of muscles in the wall of the anal canal. In 1934, the British scholar Millgan-Mongang proposed the concept of the anorectal ring and believed that it would not cause anal incontinence as long as the anorectal ring was not cut.
The current domestic surgical methods, including the hanging wire method, inevitably cut the anorectal ring. Therefore, high anal fistulotomy (hanging wire) is the most serious surgery for anal canal muscle damage in anorectal disease, and if the surgical method is not improved, postoperative anal incontinence of different degrees will occur.
In women, the anterolateral muscles are weak, and anal incontinence can occur with a little carelessness during surgery. Therefore, anterolateral fistulas, even if they are low, should be incised with caution. For anterolateral anal fissures, it is better to avoid the anterior side when performing sphincter release and choose the lateral or posterior position.
Ligation surgery for cricoid mixed hemorrhoids often results in excessive destruction of the anal cushion, dentate line and anal canal skin, resulting in postoperative stricture, mucosal ectasia and sensory anal incontinence. Therefore, care should be taken to preserve the skin and mucosal bridges in this type of surgery.
Some topical medications for hemorrhoids and anal fistulas and fissures cause extensive damage to the skin of the anal canal and anal margin due to the strong corrosive nature of these medications, which can also result in excessive postoperative scarring, poor anal closure, incomplete incontinence and sensory incontinence.
Temporary fluid incontinence can occur after some anorectal diseases, causing postoperative anal itching, which can usually recover on its own after 3 months to 6 months.
There is no doubt that anal surgery leads to anal incontinence, but it is not an equal relationship. Understanding the principle of anal closure, scientific design of surgical plan, reasonable avoidance of high-risk factors and protection of anal canal tissues are completely possible to avoid the occurrence of anal incontinence while treating the disease.