Fecal incontinence is defined as the inability to control defecation and retain feces until voluntary, conscious defecation is initiated. Animals with fecal incontinence pass feces involuntarily and are often euthanized because of the difficult social issues that result. Fecal incontinence can be caused by neurologic disorders that affect function of the anal sphincter, primary disorders of the external anal sphincter (e. g., non-neurogenic sphincter disorders), or diseases that affect the normal reservoir function of the colon or rectum (e. g., reservoir incontinence) (Box Causes of Fecal Incontinence). In general, animals with sphincter incontinence have more severe signs (e. g., lack of conscious posture to defecate, uncontrolled passage of feces) and are likely to be irreversibly affected. Animals with severe inflammatory disease may also have loss of voluntary control of defecation as a result of urgency to defecate, tenesmus, or hematochezia, but the problem may resolve with appropriate treatment of the disease.
Causes of Fecal Incontinence
Sacral spinal cord
Congenital vertebral malformation
Sacrococcygeaf hypoplasia of Manx cats
Repair of perineal hernia
Surgery (anal sac, perineal hernia, rectal resection)
Irritable bowel syndrome
History and Physical Examination
Determination of the cause of fecal incontinence requires a careful, complete history. In particular, it is important to distinguish fecal incontinence from urgency to defecate. Furthermore, the mere presence of fecal material accumulating around the anus must be distinguished from lack of ability to control the anal sphincter and fecal dribbling. Examples of diseases or circumstances that may damage nerves or muscles and lead to fecal incontinence include previous spinal cord disease, pelvic trauma, dystocia, chronic constipation, and anorectal surgery. Animals with frequent, conscious defecation associated with normal posturing usually have normal anal sphincter and nerve function but may have incontinence as a result of loss of reservoir function. The most common causes of reservoir dysfunction are inflammatory, infectious, and neoplastic diseases of the colon, rectum, or anus that cause decreased compliance and abnormal motility. Severe large bowel diarrhea secondary to colonic inflammation can cause fecal incontinence for the same reason. In most animals with neurogenic or non-neurogenic sphincter incontinence, the fecal stream is normal. Furthermore, in animals with neurogenic sphincter incontinence, abnormal micturition often occurs concurrently because of the common neural pathways. The urinary abnormalities may include dribbling urine, incomplete voiding, or inability to void, and when these occur in conjunction with fecal incontinence, neurologic dysfunction should be strongly considered.
The physical examination should include careful inspection of the perineum for evidence of abscesses, fistulas, hernias, masses, or other abnormalities. After the visual inspection, a digital rectal examination is performed to assess for normal anal sphincter tone, fecal impaction, strictures, or masses. Abdominal palpation is necessary to determine the presence of colonic impaction, as well as bladder size and expressibility. A distended, flaccid bladder from which urine is easily expressed is consistent with a lesion of the sacral spinal cord, the sacral nerves, or the pudendal nerve. A complete neurologic examination, including observation of gait and posture, evaluation of myotactic and postural responses, and assessment of lumbosacral pain, is required in any animal suspected of having fecal incontinence. The neurologic deficits that may be present in dogs with neurogenic sphincter incontinence are abnormal posture, hindlimb gait abnormalities, decreased myotactic reflexes, or an abnormal pudendal (anal) reflex. The anal reflex, which is a measure of perianal sensation and sacral spinal cord function (via the pudendal nerve), is tested by pinching the perianal skin, which results in an immediate contraction of the anal sphincter. This reflex should be present on both the right and left sides of the anus. The pudendal-anal reflex (bulbocavemosus reflex) is tested by squeezing the penis or vulva while observing for normal anal contraction. Lesions of the perineal afferent nerves, the sacral spinal cord, or the pudendal efferent nerves can decrease or abolish these reflexes and cause a dilated anus, loss of perineal sensation, and a loss of micturition control.
When loss of colorectal reservoir function is suspected, the diagnostic plan should include an examination of the fecal stream (e. g., fecal floatation, cytology) and proctoscopy or colonoscopy with biopsy to identify the primary disease. If signs of systemic disease are also detected, further evaluation (e. g., hematology, serum chemistries, radiographs, ultrasonography) is warranted as indicated. Sphincter incontinence (either neurogenic or non-neurogenic) is usually apparent from the history and physical examination. Neurogenic and non-neurogenic dysfunction are differentiated by neurologic examination. If further confirmation is necessary, anal sphincter electromyography or monometry is used to prove sphincter incompetence; however, this is rarely necessary and not universally available. When lesions of the lumbar spinal cord or the cauda equina are suspected, vertebral radiographs, myelography, computed tomography, magnetic resonance imaging, or cerebral spinal fluid analysis may be indicated. The causes of fecal incontinence are listed in Box Causes of Fecal Incontinence.
Control of fecal continence is maintained by the muscles of internal and external anal sphincters, the rectum, and the coccygeus and levator ani muscles of the pelvis, which are innervated by the pelvic, hypogastric, pudendal, and sacral nerves. Both motor and sensory impulses are integrated into the sacral spinal cord to coordinate normal fecal continence. The non-neurogenic causes of sphincter incontinence are usually due to reservoir incontinence (e. g., colitis, neoplasia) or to trauma to the anorectal muscles (e. g., surgery, hernia, fistula, neoplasia) (see Box Causes of Fecal Incontinence).
Therapy and Prognosis
The treatment of fecal incontinence depends entirely on the primary cause; for example, loss of reservoir function due to colitis often resolves completely with appropriate treatment, whereas loss of neurologic function is permanent and rarely treatable. Some forms of non-neurogenic incontinence are transient (e. g., postoperative complication, trauma), and some forms of neurogenic incontinence may improve after specific treatment (e. g., spinal surgery to reduce compression or subluxation). However, in these cases no specific drugs or diets are particularly effective. Highly digestible diets may be beneficial, because they reduce the volume of fecal material. Enemas and exercise may stimulate defecation at desired times and can be used to help control the social unacceptability of the problem. A surgical technique using an implanted Silastic sling, and placement of an autogenous muscle graft to augment the muscles of continence, have been described, but the success rates for these procedures are not satisfactory. Recently, a technique to create a new sphincter using muscle transplants has shown promise for providing a functional stomal sphincter in dogs with chronic fecal incontinence. Nevertheless, in many pets euthanasia is chosen because in most cases the prognosis is poor for return to normal or acceptable sphincter function.