Anal sphincters are muscular structures that assist in controlling the flow of body wastes (feces and flatus) from the colon. The internal anal sphincter (IAS) and the external anal sphincter (EAS) encircle the anal canal and comprise the anorectal ring. The IAS is a thickening of the gastrointestinal smooth muscle; it maintains continence at rest. The EAS is composed of striated, voluntary muscle. The EAS, the puborectalis, and the levator ani muscles work in concert to prevent leakage of flatus and feces when there is an increase in abdominal pressure or when the internal anal sphincter relaxes after rectal distention.
When one or both sphincters become defective or incompetent, the control of feces and/or flatus is impaired. Incontinence of the feces and flatus is socially and psychologically disabling for the afflicted patient. It is a major factor prejudicing the rehabilitation and placement prospects of the elderly and disabled, preventing many of them from being cared for at home.
The normal mechanisms of anorectal continence include the motor function of the anal sphincters and pelvic floor muscles, the role of the rectum and sigmoid colon as a fecal reservoir with capacitance and compliance and as a propulsive force with intrinsic motor activity, the effects of stool consistency, volume and delivery rate, the anorectal angle, and anorectal sensation. It is the coordinated integration of these factors that confers continence.
There are two distinct etiologies for anorectal incontinence. The most common cause of anorectal incontinence is a structural deformity due to anatomic disruption of the sphincter mechanism, which may be caused by obstetric injuries (perineal laceration and improperly performed median episiotomies), complications of fistula or fissure surgery (keyhole deformities), traumatic injuries (e.g., impalement injuries), or cancer. Alternatively, anorectal incontinence may result from deterioration of the sphincter muscles due to age, congenital disorders, systemic and metabolic diseases, acquired neurological defects, and diseases of the colon and rectum.
Present treatment modalities for anorectal incontinence include nonsurgical and surgical therapy. Nonsurgical therapy for incontinence must be tailored to each individual: patients suffering from urgency incontinence may benefit from the use of bulk-forming agents and laxatives or enemas; individuals with minor degrees of incontinence may find biofeedback and perineal strengthening exercises beneficial in alleviating symptoms of seepage and occasional loss of control.
Current nonsurgical treatments for anorectal incontinence include the use of electrical stimulation to improve contraction of the sphincter muscles and the use of anorectal plugs which are designed to expand post-insertion.
U.S. Pat. Nos. 3,650,275 and 3,749,100 describe an electrostimulation device to maintain contraction of the sphincter muscle. A magnetic artificial anus closing device is described in U.S. Pat. No. 3,952,726. U.S. Pat. No. 4,209,009 discloses an anus closure tampon with nonhomogeneous sections having differential diametrical compressibility to provide a plug effect. U.S. Pat. No. 4,401,107 describes an intestinal control valve arranged to surround the anal-terminating descending intestine, thereby functioning as an artificial sphincter. A device comprising three inflatable chambers (the first, positioned outside the rectum; the second, within the anal sphincter muscle; the third, outside the body between the buttocks) to maintain anal continence is disclosed in U.S. Pat. No. 4,686,985. U.S. Pat. Nos. 4,781,176 and 4,969,902 teach an artificial anus comprising a hollow tubular support member and a releasable plug for sealing closed the support member. A pressure transducer or electrical contact is provided on the support member and connected to an electrode in contact with the patient's skin, so that when the colon becomes pressurized the patient is signalled that the plug should be released. U.S. Pat. No. 4,904,256 describes a magnetic artificial anus assembly, having a sphincter function similar to the natural anus, which comprises an annular bag structure filled with a magnetic fluid and a plug structure having a magnet member.
Surgical therapy must also be individualized, and is directed either at (i) repair of the disrupted sphincter or (ii) augmentation (with autogenic transplanted muscle or commercially available Silastic sheet prostheses) of existing structures to improve physiologic function. Diverting colostomy is rarely necessary.
Unfortunately, there are inherent difficulties and risks in these corrective methods. For example, anorectal plugs will often cause infection, fibrosis of the mucosa, or muscularis of the bowel near the plug. Also, patients complain about the discomfort and inconvenience of temporary plugs that function similar to absorbent pads. An artificial sphincter may extrude or malfunction, necessitating additional surgery or corrective action. Surgery also can result in infection or other complications, such as host-graft rejection, and is a significant expense. Therefore, it is desirable to treat anal sphincter deficiencies on a cost-effective, outpatient basis, such that the inherent difficulties presented by the current methods are avoided.
Injectable biomaterials, e.g., Polytef.RTM. paste (polytetrafluoride, Mentor), injectable liquid silicone, and collagen, have been used to augment incompetent lower esophageal sphincters and urinary sphincters over the past ten years. These so-called sphincters, however, are not true sphincteric muscles because they are controlled by pressure changes, rather than neurological stimulation from the brain. Furthermore, the use of injectable biomaterials for treating lower esophageal and urinary sphincters is simply to bulk up the surrounding tissue by injecting the biomaterial to close the respective orifice.