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E - Bowel Continence

Effects of SCI on Bowel Function SCI or disease results in many unique consequences and complications in bowel evacuation, due to the effect of varying levels and degrees in paralysis of voluntary muscle, impairment of sensory afferent nerves and autonomic function. NBD is experienced by individuals, with any injury or disease to the nervous system responsible for bowel function, especially those with SCI or disease, multiple sclerosis and spina bifida (see Figure 1.0 on previous page). The main functions of the colon are storage, propulsion and defecation of feces/stool. The colon also supports the growth of symbiotic bacteria, and resorbs fluid and electrolytes, short-chain fatty acids and bacterial metabolites. Colonic motility is regulated by systemic factors including neural inputs, hormonal, metabolic and drug effects; and local factors such as diet, laxatives, bacterial endotoxins and bile acids. Colonic motility refers to local mixing peristaltic and propulsive movements and superimposed gastrocolic, rectocolic and rectoanal reflexes. Neural influences are from the intrinsic (Auerbach’s and Meissner’s plexuses) or extrinsic neural plexuses (parasympathetic, sympathetic and somatic nervous system). The intrinsic plexus influences gut wall contraction and secretion of digestive juices. The parasympathetic nervous system stimulates the gut wall, and the sympathetic nervous system relaxes the gut wall, the ileocecal valve and the internal anal sphincter. The somatic nervous system influences the external anal sphincter, pelvic floor and abdominal wall muscles. Several investigators have studied bowel activity following SCI,5-11 with varying results in heterogeneous populations, with evolving clinical assessment tools to determine the level and extent of NBD. In general, these studies showed delayed colonic transit, especially in the left and sigmoid colon and impaired anorectal function. Recent studies of gastrointestinal transit times (GITT) report poor reproducibility for segmental studies, but overall colonic transit studies had reasonable reproducibility. With this limited reproducibility in mind, Faaborg et al.12 found that GITT did not change significantly in two groups studied, at one and 19 years post injury, and again, twelve years later. This is particularly interesting and somewhat controversial, given that 30% of symptoms of NBD are reported to increase with duration of injury.13 Notwithstanding the above, some general statements can be made about common patterns of NBD, given the level of SCI. Injury above the sacral segments produces an upper motor neuron (UMN) bowel, with preserved intrinsic motility and reflex function, but lack of ability to influence the voluntary external anal sphincter, pelvic floor and abdominal muscles to assist with defecation. These individuals have a higher incidence of problems with constipation. Injury to the sacral segments results in a lower motor neuron (LMN) bowel with preserved intrinsic function, preserved gastrocolic reflex, but absent rectocolic and rectoanal reflexes; and lack of volitional anal sphincter or pelvic floor activity, but preserved abdominal wall muscles. Individuals with LMN injury have a higher incidence of problems with incontinence due to pelvic floor and anal sphincter weakness. Patients, with both upper and lower motor neuron bowel dysfunction, commonly experience bloating, abdominal pain and bleeding from hemorrhoids. Figure 2.0 Schematic drawing of upper and lower motor neuron bowel dysfunction 62 CAPTURING CAPACITY IN CANADIAN SCI REHABILITATION


E - Bowel Continence
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