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Colorectal motility and defecation after spinal cord injury in humans
L.C. Weaver and C. Polosa (Eds.) Progress in Brain Research, Vol. 152 ISSN 0079-6123 Copyright r 2006 Elsevier B.V. All rights reserved
CHAPTER 22
Colorectal motility and defecation after spinal cord injury in humans A.C. Lynch and F.A. Frizelle Colorectal Unit, Department of Surgery, Christchurch Hospital and Burwood Spinal Unit, Christchurch, New Zealand
Abstract: Following spinal cord injury, colorectal problems are a significant cause of morbidity, and chronic gastrointestinal problems remain common with increasing time after injury. Although many cordinjured patients achieve an adequate bowel frequency with drugs and manual stimulation, the risk and occurrence of fecal incontinence, difficulties with evacuation, and need for assistance remain significant problems. The underlying physiology of colorectal motility and defecation is reviewed, and consequences of spinal cord injury on defecation are reported. A discussion of present management techniques is undertaken and new directions in management and research are suggested. There is need for more intervention in regard to bowel function that could improve quality of life, but there is also a need for more research in this area.
with increasing time after injury (Stone et al., 1990a). The inability to defecate normally means that bowel care often occupies a significant part of the day, and, although many cord-injured people achieve an adequate bowel frequency with drugs and manual stimulation, the risk and occurrence of fecal incontinence, difficulties with evacuation, and need for assistance remain significant life-limiting problems (Stone et al., 1990a, b; Levi et al., 1995; Glickman and Kamm, 1996; Han et al., 1998; Lynch et al., 2001). Long-term gastrointestinal complications can develop in cord-injured people. Fecal impaction is common. Diverticular disease and volvulus are more frequent and are perhaps related to higher intracolonic pressures in those with upper motor neuron lesions. The occurrence of hemorrhoids and mucosal prolapse was also identified by Lynch et al. (2000c) as occurring more frequently after spinal cord injury by an incidence of hemorrhoidectomy of 9% compared with a control group incidence of 1.5% (po0.001). This may be
Introduction Bowel dysfunction is a problem following spinal cord injury Bowel dysfunction following spinal cord injury is increasingly recognized as an area of major physical and psychological difficulty. Surveys of spinal cord-injured people show that bowel function is as much of a problem as loss of mobility or sexual function. The problem is twofold as, not only does spinal cord injury result in changes to bowel motility and sphincter control, but also the concurrent loss of mobility and gross motor dexterity makes bowel management a major life-limiting problem. Immediately after spinal cord injury, colorectal problems are a significant cause of morbidity, and chronic gastrointestinal problems remain common Corresponding author. Tel.: +64-3-3640-640; Fax: +64-3-3640-352; E-mail: [email protected] DOI: 10.1016/S0079-6123(05)52022-3
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multifactorial due to altered anorectal tone or trauma with manual evacuation, and is a frequent source of bleeding or autonomic dysreflexia. Impact on lifestyle Spinal cord-injured people rate difficulties with bowel management as similar to problems associated with loss of mobility and sexual function. Hanson and Franklin (1976) reported that 80% of male paraplegics and 46% of male tetraplegics would rank bladder and bowel as their greatest functional loss after loss of mobility. It was interesting that when they asked the same question to spinal unit staff, only 39% ranked bladder and bowel problems as high. Toileting Survey data shows that 61% of cord-injured people would spend more than 15 min per day toileting, compared with only 9% of controls (Lynch et al., 2001). Those doing manual evacuations spend the longest time. Half of all cord-injured people need assistance with toileting. The need for assistance with toileting relates very closely with level of injury and has implications for provision of carers and dependence on family members. It is recognised that having family members perform such intimate tasks can be emotionally charged and negatively affect family interrelationships. This was significantly associated with the reported perception that bowel function was a source of distress. Colonic function following spinal cord injury Questionnaires exploring bowel function in spinal injured people have found that over half of those with an injury above the second lumbar segment (L2) suffer from constipation (DeLooze et al., 1998). People with higher injuries defecate less frequently compared to those with lower injuries and the general population. It is apparent that even with medications and other methods, spinal cord-injured people do not achieve a bowel motion
frequency similar to a control population. Changes to the extrinsic autonomic innervation of the bowel are presumed to decrease the normal postprandial increase in motility and to decrease colonic compliance. Laxative use among the cord-injured population is common as a means of regulating bowel habit. Two-thirds of those with high injuries report using laxatives either occasionally or regularly, compared to the 4% in a control group drawn from the general population (po0.0001, Fisher’s exact test, Lynch et al., 2000c). However, the diarrhea produced by laxatives and the resultant risk of incontinence may limit their use for some. Patterns of gut dysmotility have been described for different levels and degrees of spinal cord injury with the level of the spinal cord lesion determining the effect on colonic motility. Marker transit studies show that lesions above the first thoracic segment (T1) result in delayed mouth-tocaecum time, but lesions below this level result in normal transit times to the caecum. Beyond the ileocaecal valve, transit times are markedly delayed (Menardo et al., 1987). For people with an upper motor neuron lesion, transit studies and scintigraphy have demonstrated variable changes in colonic transit. If the spinal cord lesion is above the lumbar region, transit is slowed throughout the whole colon. The velocity of the median position of bowel contents throughout the colon was significantly slower in cord-injured people (0.637 0.33 cm/h in cord-injured; 2.5871.2 cm/h in controls, po0.001). One study by Nino-Murcia et al. (1990), involving 28 cord-injured subjects, also demonstrated distal small bowel dilatation in 10 people, all of whom had abdominal symptoms and 9 of whom had a spinal cord lesion above T5. A lower motor neuron injury from a lesion affecting the conus, cauda equina or pelvic nerves results in interruption of the parasympathetic supply to the colon and reduced spinal cord-mediated reflex peristalsis. Stool propulsion is by segmental colonic peristalsis only. The mechanism for colonic dysmotility following a spinal cord injury may be a loss of descending inhibitory modulation from the sympathetic nervous system. This theory is supported by studies in the cat by Gillis et al. (1987) in which
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a2-adrenergic receptor activation resulted in profound inhibition of colonic motility, and sectioning of splanchnic nerves (containing preganglionic sympathetic innervation of the intestine) produced an increase in colonic contraction. In cord-injured people, colonic transit delays are more profound in higher injuries, where the sympathetic injury should be more pronounced. The delay may in part be due to loss of colonic compliance. With a spinal cord lesion above L1, the left colon has an abnormal response to increasing volume. Distension with water produces a pressure–volume curve (colometrogram) showing a steep increase in intracolonic pressure with increasing volume. This is similar to the hyperreflexic response described by Meshkinpour et al. (1983) during bladder cystometry for injuries at a similar level. For injuries above T5, the right colon is also affected. The lack of compliance leads to functional obstruction, increased transit times, abdominal distension, bloating and discomfort. It suggests that the central nervous system (CNS) is necessary to modulate colonic motility. Colonic myoelectric activity has been recorded in a group of spinal injury subjects with injuries at varying levels and controls. This demonstrated a significantly higher level of basal colonic activity in cord-injured subjects (12.6 vs. 3.3 spikes per 10 min), and no demonstrable gastrocolic reflex. This would support the assumption that the CNS exerts a tonic inhibitory influence on basal colonic activity and is consistent with the hypertonicity seen on colometrograms.
Colonic neurotransmitters following spinal cord injury The intramural distribution of regulatory neuropeptides within the bowel wall is distinct. Substance P is exclusively localized in nerves (Ferri et al., 1983). Large numbers of vasoactive intestinal polypeptide- and substance P-containing enteric nerves supply the ganglionated plexuses and are especially numerous in the circular muscle layer. They have a role in colon motility while those supplying the mucosa are involved with electrolyte and fluid transport. Substance P has been shown
to accelerate the transit of a charcoal meal in rats. It increases intraluminal pressure mainly by circular muscle contraction by direct action on the muscle as well as by simultaneous activation of excitatory cholinergic pathways and of inhibitory vasoactive intestinal polypeptide-independent, nitric oxide-regulated pathways. Substance P is reduced in the colonic mucosa of patients with chronic constipation, and mucosal substance P levels correlate significantly with disease state (Goldin et al., 1989). A similar scenario exists with diabetic constipation where substance P in the rectal mucosa of diabetics with constipation is significantly lower than in diabetics with normal bowel function (Lysy et al., 1993). The fact that mucosal substance P levels are associated with two disorders of colonic transit suggests a role in the pathogenesis of intestinal transit disorders. Whereas mucosal substance P may be decreased with chronic constipation, concentrations in the muscle layers may be increased. Sjolund et al. (1997) examined tissue from the colon of 18 subjects with slow-transit constipation. Tissue concentrations of vasoactive intestinal polypeptide and substance P were measured by radioimmunoassay. Significantly increased concentrations of both peptides were found in the ascending colon, and in the descending colon, substance P was increased in the myenteric plexus. Recovery of bladder and bowel function following traumatic spinal cord injury is dependent on reorganisation of reflex pathways in the periphery and CNS. Part of this reorganisation may be influenced by spinal cord–target organ interactions mediated by neurotrophic factors released by the peripheral organs. Interrupting the descending modulation from the CNS may lead to changes in the autonomic and somatic outflow reaching target organs from the spinal cord caudal to the lesion and alter target organ function. In rats, spinal cord injury leads to hypertrophy of the bladder as well as electrophysiological and morphological changes in bladder afferent neurons (de Groat et al., 1993; Yoshimura et al., 1993). In the colon, however, the intrinsic enteric nervous system appears intact. Nerve fibres containing the intrinsic neurotransmitters substance P and vasoactive intestinal polypeptide appear to be present in
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approximately similar amounts in specimens from cord-injured and control subjects (Lynch et al., 2000b). The colon may therefore continue to function independently of CNS modulation after spinal cord injury.
Anorectal function Continence The incidence of fecal incontinence in people with spinal cord injury is more common than in the general population. When compared to matched controls by using standardized scoring systems, the mean fecal incontinence score was higher for cord-injured people than controls (po0.0001), and for complete spinal cord injury compared with incomplete injury ðp ¼ 0:0023Þ: Having fecal incontinence also impacts on the quality of life of those with a spinal cord injury more frequently than of neurologically intact persons [62% of cord-injured people report that fecal incontinence impacts upon their everyday life, compared to 8% of control subjects, po0.0001 (Lynch et al., 2000c)]. Fecal continence requires the ability to maintain internal anal sphincter resting tone and to contract the external anal sphincter in response to increased intra-abdominal pressure, rectal distension and rectal contraction. These are spinal reflexes that are intact following spinal cord injury, but no longer modulated by cortical input. Basal sphincter tone is mainly an activity of the internal anal sphincter, the maintenance of which seems to be due to a tonic excitatory sympathetic discharge. Frenckner and Ihre (1976) observed that anorectal manometry performed on cord injury subjects shows a persistent anal tone that is reduced compared to control subjects. They described changes in anal tone in eight healthy subjects following spinal anesthesia. High spinal anesthesia resulted in a significantly lower resting anal pressure than either low spinal or pudendal block. Of note, people with lumbosacral injuries, who have external anal sphincter paralysis but persistent internal anal sphincter activity, still appear to maintain a degree of anorectal tone, higher than rectal pressure, but lower than normal. The external anal sphincter
also continues to show tonic activity, but again generates a lower than normal pressure. Manometric studies on cord-injured subjects show a maximal mean basal sphincter pressure (which probably reflects external anal sphincter pressure) significantly lower than control group pressures. Spinal cord-injured subjects can produce a small rise in sphincter pressure with voluntary squeeze (p40.05). This is, however, much less than the increase in pressure generated by control subjects performing a similar maneuver who can generate a four-fold increase in external anal sphincter pressure. People with incomplete injuries can produce a greater increase in sphincter pressure with a Valsalva maneuver than those with complete injuries. The Valsalva maneuver is expiration against a closed glottis. This may reflect the greater increase in intra-abdominal pressure, as measured by rectal pressure, that people with incomplete or low injuries are able to generate due to incomplete paralysis of their abdominal musculature. For those with a complete injury, attempts at squeezing result in a straining response rather than a true squeeze. People with lesions above T5 will be unable to use abdominal muscles and rely on intercostal and diaphragmatic muscle contraction to increase intra-abdominal pressure. Those with cervical injuries can only use the diaphragm. These observations fit the concept that external anal sphincter contraction is mediated by a spinal reflex, triggered by tension receptors in the pelvic floor that respond to an increase in intra-abdominal pressure. This is supported by another study by MacDonagh et al. (1992) that found the rise in sphincter pressure with the Valsalva maneuver to be directly proportional to the rise in intraabdominal pressure.
Rectal sensation All normal subjects experiencing rectal distension as part of anorectal manometry studies report a range of sensation starting at a rectal volume of about 10 ml, and ranging from sensations of ‘wind’ to pain. This is compared to 78% of cord-injured subjects with complete injuries, and 43% of those with incomplete injuries, who report no sensation
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on rectal distension (Lynch et al., 2000a). Those that did report sensation described non-specific abdominal sensation that did not prevent further rectal distension. A previous study by MacDonagh et al. (1992), examining similar sensations, proposed that sympathetic nerves entering the thoracic spinal cord above the level of the injury conveyed this dull pelvic sensation. However, such sensations have also been identified in five people with complete cervical injuries, making the origin of this sensation unclear. Rectal compliance A normally compliant rectum accommodates an increase in volume with little change in pressure. As rectal volume increases, a normal sphincter response is the relaxation of the internal anal sphincter with continence being maintained by continued external anal sphincter contraction. The ability of the rectum to distend to store bowel volume is an important component of normal bowel function, as it means defecation can be delayed until an appropriate time. People with complete cervical injuries can have increased rectal tone with low compliance, i.e., a sharp rise in rectal pressure occurs with rectal distension, as the rectum does not expand to accommodate the increase in volume. Sphincter tone can also increase with rectal distension, because internal anal sphincter contraction is an enteric reflex, normally suppressed by descending inhibitory pathways. The loss of inhibitive sympathetic tone has also been proposed as a mechanism for the absent rectal relaxation and linear pressure/volume relationship during rectal distension (MacDonagh et al., 1992). Most people with low lumbosacral injuries have an areflexic rectum with an attenuated sphincter response to rectal distension (Shafik, 1995). The rectum is flaccid and capacious producing no rise in rectal pressure with increasing volume. Urgency Fecal urgency, or an inability to delay defecation, is more often a problem following spinal cord
injury. It becomes even more significant as a quality of life issue when reduced mobility and poor hand dexterity are compounded by the difficulties associated with finding a wheelchair-able toilet. Fecal urgency can be assessed by asking respondents how long defecation can be delayed. Overall 81% of controls can delay defecation, compared with only 41% of cord-injured people. There is also an approximately ten-fold increase in the proportion of cord-injured people, compared to controls, who have to defecate immediately. Of note, many people with complete injuries have no sensation, and thus never sense the need to defecate. The incidence of fecal incontinence is often higher for cord-injured people who are unable to delay defecation. Defecation Many defecatory problems seen after spinal cord injury are the result of altered anorectal function. Defecation requires the complex integration of reflex and voluntary muscular control. Cortical inhibition of the external anal sphincter occurs in a coordinated fashion on straining as the rectal smooth muscle contracts. This modulation of the intrinsic nervous system by the extrinsic system is disrupted following a complete supra-conal spinal cord injury. This means that straining by increasing intra-abdominal pressure does not improve evacuation by the usual external anal sphincter relaxation in response to the rectal and intra-abdominal pressure increase. Rather, external anal sphincter tone increases. Thus, coordinated reflex defecation is difficult for cord-injured people. It is often inefficient and incomplete, resulting in incontinence and/or constipation. Therefore, defecation is planned on regular basis to avoid constipation or an increased chance of fecal incontinence. High spinal cord injuries The difficulties with defecation following high spinal cord injury result from discoordinate anal sphincter function. The normal synergistic activity of colonic smooth muscle and pelvic striated muscle
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is lost. There is a loss of conscious sphincter control and, due to abdominal muscle paralysis, an inability to significantly increase intra-abdominal pressure. Loss of rectal sensation and a spastic external anal sphincter require defecation to be anticipated. The conus-mediated increase in external anal sphincter tone with increasing intra-abdominal pressure acts against straining to defecate. However, reflex relaxation of the internal and external anal sphincters by mucosal stimulation, either digitally or with a suppository, can be exploited in order to defecate. Insertion of a gloved finger into the rectum with gentle sustained pressure towards the sacrum relaxes the spastic external anal sphincter and pelvic muscles. Rapid or excessive stretching can precipitate sphincter spasm. Rotation of the finger continues the stimulation until a reflex peristaltic wave is generated in the rectum, flatus is passed and stool comes down. The recto-anal inhibitory reflex is initiated, the internal anal sphincter relaxes, and the recto-colic reflex stimulates pelvic nerve-mediated peristalsis. If there is no reflex relaxation of the external anal sphincter complex, evacuation will not occur or be incomplete. Manual evacuation or enemata are often required in this situation. This reflex relaxation can also lead to fecal incontinence by two means. The anal sphincter may relax at relatively low rectal volume in response to a small increase in intra-abdominal pressure, or as people with high-level injuries often have no sensation of rectal fullness, reflex defecation in response to a full rectum can result in fecal incontinence that is unpredictable and episodic.
Low spinal cord injuries Complete or partial injuries to the cauda equina result in a lower motor neuron pattern of injury. A person with a lower motor neuron lesion following spinal cord injury will have absent external anal sphincter tone, flaccid pelvic muscles and decreased reflex peristalsis. Rectal compliance is increased in response to rectal distension. The loss of parasympathetic control of the internal anal sphincter means that resting anal tone is low and unresponsive
to changes in intra-abdominal pressure. Thus, a Valsalva maneuver can result in fecal leakage, and the rectum has to be kept empty to avoid fecal incontinence. Reflex-mediated defecation does not occur with spinal cord lesions below the conus, so stool has to be removed digitally, assisted by a Valsalva maneuver and abdominal massage. Change in bowel function with time from injury Studies do not demonstrate a change in fecal incontinence with either duration of injury or increasing age for cord-injured people. One survey of bowel dysfunction in cord-injured people by Stone et al. (1990a) found that chronic gastrointestinal problems were rare in the first 5 years following injury, but problems with defecation became more common with increasing time. The incidence of abdominal pain and distension was increased in long-term cord-injured people (more than 18 years since injury) whose bowel regimen was less frequent than once a day (Stone et al., 1990a). Another study of chronic gastrointestinal problems in cord-injured subjects by Han et al. (1998) concluded that bowel habit appeared to settle by about 6 months after injury, and that subsequent bowel dysfunction was not related to age, duration or level of injury. Current management strategies The approach to bowel management after spinal cord injury should address specific issues such as fecal incontinence, constipation and functional mobility. This must be within the context of the patient as a whole person and consider his/her cultural, social, sexual and vocational roles. A bowel care regimen needs to be generated that fits the person’s long-term routine. The aim should be effective colonic evacuation without fecal incontinence or other complications. Regularity of evacuation prevents excessive build-up of feces and impaction. Appropriate equipment, such as commode chairs and wheelchair-able toilets, needs to be supplied for an adequate long-term bowel program. Dietary manipulation is important. Adequate water intake promotes transit by keeping the stool
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soft. Fibre is promoted to give the stool bulk and plasticity. This is thought to assist colonic transit in neurologically intact patients, probably by promoting propulsive activity secondary to increased colonic wall distension. The effects of increased fibre on colonic function after spinal cord injury are not yet fully understood, and may be counterproductive. A study carried out by Cameron et al. (1996) at the Spinal Injury Unit, Austin Hospital, Heidelberg, Australia demonstrated that significantly increasing dietary fibre in a group of cordinjured subjects with a range of injuries resulted in an increase in mean colonic transit time from 28.2 to 42.2 h (po0.05), and in mean recto-sigmoid transit time from 7.9 to 23.3 h (po0.02). However, an increase in stool bulk may mean more time spent with bowel care. Stool softeners other than fibre, such as docusate sodium increase the amount of water in stool without increasing volume and have no effect on bowel motility. They can also affect the intestinal absorption of other drugs, resulting in higher plasma levels. The stool is more likely to be liquid, so continence will not be improved. They are most useful when fecal incontinence is not a risk and straining is to be avoided, such as for patients with hemorrhoids or autonomic dysreflexia. Stimulant laxatives act by increasing intestinal motility, resulting in less time for water reabsorption. Senna has a direct stimulant effect on the myenteric plexus and also increases intraluminal fluid. Bisacodyl has a similar mode of action and is often used as a suppository to initiate bowel evacuation. Dose-dependent side effects can occur. These include abdominal cramping, diarrhea and electrolyte imbalance. Chronic use of stimulant laxatives, especially senna, can result in a progressive unresponsiveness. Osmotic laxatives such as lactulose draw fluid into the colon. They can result in more liquid stool and cause cramping. Prokinetic agents such as cisapride have been employed to reduce constipation in cord-injured people. Transit times are improved, but cardiac arrhythmias have been noted with long-term use. Enemata are often employed when suppositories or digital stimulation fail. Long-term use can result in enema dependences and side effects such as rectal trauma and autonomic dysreflexia can occur.
Spinal cord-injured people with upper motor neuron lesions can exploit the recto-colic reflex to effect defecation. Digital stimulation can result in a reflex wave of conus-mediated rectal peristalsis. The recto-anal inhibitory reflex is intact, so this causes internal anal sphincter relaxation and defecation. Rectal sensation is reduced, however, so defecation has to be anticipated on a regular basis. These people require a bowel management program that keeps the rectum empty to reduce the incidence of incontinence. If people with upper motor neuron lesions are unable to defecate using the recto-colic reflex, then a management plan needs to minimize anorectal trauma but still allow adequate rectal evacuation to avoid constipation. Cord-injured people with lower motor neuron lesions have a rectum that is areflexic, reduced sphincter tone and an attenuated sphincter response to rectal distension or a Valsalva maneuver. These dysfunctions lead to an increased risk of incontinence, especially with liquid stool. The aim, therefore, is to keep stool consistency firm. Local anorectal reflexes are often insufficient to result in defecation, and a compliant rectum acts as a large reservoir, so stool is digitally removed. Arnold et al. (1986) noted that a Brindley sacral anterior nerve root stimulator (S2–S4) can be used for electromicturition to achieve regular, complete bladder emptying. Often deafferentiation of the sacral posterior nerve roots is performed before the stimulator is implanted to produce detrusor areflexia and interim urinary continence. The deafferentiation also results in loss of the sacral reflexes necessary for defecation. The stimulator can then be used to initiate defecation. This does not occur during stimulation due to the simultaneous rectal and sphincter contraction, but when stimulation stops the external anal sphincter relaxes instantaneously and the rectum relaxes slowly, resulting in spontaneous defecation. This method has been shown to result in quicker, more controllable defecation than the reflex method.
Does a colostomy improve bowel function? Colostomy has been reported to result in improved quality of life for people after spinal cord injury
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(Frisbie et al., 1986; Saltzstein and Romano, 1990; Stone et al., 1990b; Randell et al., 2001). It can not only reduce fecal incontinence, but also simplify bowel care in those for whom bowel evacuation is difficult, reducing the amount of time spent on bowel care from 99 to 18 min per day (Stone et al., 1990b). The only long-term management problem reported has been occasional appliance leakage and mucoid discharge per rectum. All subjects involved in a study by Craven and Etchells (1998) found the stoma had impacted significantly on their lifestyle with increased feelings of independence, freedom and raised self-esteem. Sacral pressure ulcers are a common reason for stoma formation in people who had no bowel function problems previously. Deshmukh et al. (1996) examined the use of colostomy as an adjunct measure in the healing of pressure sores in cordinjured people. Their findings similarly showed that a colostomy improved bowel management and was well accepted. However, they noted that the primary goal of pressure sore healing was accomplished in only 6 out of 27 cord-injured people, and stoma formation resulted in significant morbidity with stomal prolapse and difficulties with wound healing. Of the 19 subjects reviewed in this study, none wanted their stoma reversed, and all felt that their quality of life was improved. A colostomy can improve bowel management for some people after cord injury. Dependence on assistance with toileting is decreased as even tetraplegics with limited dexterity are able to manage suitable stoma appliances. Enthusiasm for bowel diversion procedures should be tempered with an acknowledgment that the risks associated with any surgical procedure may not make it acceptable to all cord-injured people.
Future objectives for the investigation and management of bowel dysfunction Bowel dysfunction has a major impact on the quality of life for many people with spinal cord injury. This difficulty has been shown to improve with appropriate early identification and management of their problems. Interview and clinical examination can generate an impression of their
general bowel function and identify problems such as constipation, fecal impaction, anal fissures and hemorrhoids. Simple tests of anorectal function are available that can be performed on all cordinjured people in the same manner that bladder dysfunction is investigated. Anorectal manometry will identify those with dyssynergic sphincter function. For those with abdominal bloating and constipation, abdominal X-ray and colonic motility studies can be helpful. Although improving colonic motility and appropriate bowel management may help, some cordinjured people will have ongoing bowel problems. Colostomy formation has been used to provide the patient with relief from constipation and anorectal dysfunction and with an independent means of managing their own bowel function. Further research needs to be done to examine the differences in quality of life and bowel function following colostomy formation in cord-injured people.
References Arnold, E.P., Gowland, S.P., MacFarlane, M.R., Bean, A.R. and Utley, W.L.F. (1986) Sacral anterior root stimulation of the bladder in paraplegics. Aust. N.Z. J. Surg., 56: 319–324. Cameron, K.J., Nyulasi, I.B., Collier, G.R. and Brown, D.J. (1996) Assessment of the effect of increased dietary fibre intake on bowel function in patients with spinal cord injury. Spinal Cord, 34(5): 277–283. Craven, M.L. and Etchells, J. (1998) A review of the outcome of stoma surgery on spinal cord injured patients. J. Adv. Nurs., 27: 922–926. de Groat, W.C. (1993) Anatomy and physiology of the lower urinary tract. Urol. Clin. North Am., 20(3): 383–401. DeLooze, D., Van Laere, M., De Muynck, M., Beke, R. and Elewault, A. (1998) Constipation and other chronic gastrointestinal problems in spinal cord injury patients. Spinal Cord, 36: 63–66. Deshmukh, G.R., Barkel, D.C., Sevo, D. and Hergenroeder, P. (1996) Use or misuse of colostomy to heal pressure ulcers. Dis. Colon Rectum, 39: 737–738. Ferri, G.-L., Adrian, T.E., Ghatei, M.A., O’Shaughnessy, D.J., Probert, L., Lee, Y.C., Buchan, A.M., Polak, J.M. and Bloom, S.R. (1983) Tissue localisation and relative distribution of regulatory peptides in separated layers from the human bowel. Gastroenterology, 84: 777–786. Frenckner, B. and Ihre, T. (1976) Influence of autonomic nerves on the internal anal sphincter in man. Gut, 17: 306–312. Frisbie, J.H., Tun, C.G. and Nguyen, C.H. (1986) Effect of enterostomy on quality of life in spinal cord injury patients. J. Am. Paraplegia Soc., 9(1–2): 3–5.
343 Gillis, R.A., Dias Souza, J., Hicks, K.A., Mangel, A.W., Pagani, F.D., Hamilton, B.L., Garvey III, T.Q., Pace, D.G., Browne, R.K. and Norman, W.P. (1987) Inhibitory control of proximal colonic motility by the sympathetic nervous system. Am. J. Physiol., 253(4, Pt 1): G531–G539. Glickman, S. and Kamm, M.A. (1996) Bowel dysfunction in spinal-cord-injury patients. Lancet, 347: 1651–1653. Goldin, E., Karmeli, F., Selinger, Z. and Rachmilewitz, D. (1989) Colonic substance P levels are increased in ulcerative colitis and decreased in chronic severe constipation. Dig. Dis. Sci., 34(5): 754–757. Han, T.R., Kim, J.H. and Kwon, B.S. (1998) Chronic gastrointestinal problems and bowel dysfunction in patients with spinal cord injury. Spinal Cord, 36: 485–490. Hanson, R.W. and Franklin, M.R. (1976) Sexual loss in relation to other functional losses for spinal cord injured males. Arch. Phys. Med. Rehabil., 57: 291–293. Levi, R., Hultling, C., Nash, M.S. and Seiger, A˚. (1995) The Stockholm spinal cord injury study: 1. medical problems in a regional SCI population. Paraplegia, 33: 308–315. Lynch, A., Anthony, A., Dobbs, B. and Frizelle, F. (2000a) Anorectal physiology following spinal cord injury. Spinal Cord, 38: 73–80. Lynch, A., Anthony, A., Dobbs, B. and Frizelle, F. (2000b) Colonic neurotransmitters following spinal cord injury. Tech. Coloproct., 4: 93–97. Lynch, A., Anthony, A., Dobbs, B. and Frizelle, F. (2001) Bowel dysfunction following spinal cord injury; a review. Spinal Cord, 39: 193–203. Lynch, A., Wong, C., Anthony, A., Dobbs, B. and Frizelle, F. (2000c) Bowel dysfunction following spinal cord injury: a description of bowel function in a spinal cord-injured population and comparison with age and gender matched controls. Spinal Cord, 38: 717–723. Lysy, J., Karmeli, F. and Goldin, E. (1993) Substance P levels in the rectal mucosa of diabetic patients with normal bowel function and constipation. Scand. J. Gastroenterology, 28: 49–52.
MacDonagh, R., Sun, W.M., Thomas, D.G., Smallwood, R. and Read, N.W. (1992) Anorectal function in patients with complete supraconal spinal cord lesions. Gut, 33: 1532–1538. Menardo, G., Bausano, G., Corazziari, E., Fazio, A., Marangi, A., Genta, V. and Marenco, G.L. (1987) Large bowel transit in paraplegic patients. Dis. Colon Rectum, 30(12): 924–928. Meshkinpour, H., Nowroozi, F. and Glick, M.E. (1983) Colonic compliance in patients with spinal cord injury. Arch. Phys. Med. Rehabil., 64: 111–112. Nino-Murcia, M., Stone, J.M., Chang, P.J. and Perkash, I. (1990) Colonic transit in spinal cord-injured patients. Invest. Radiol., 25(2): 109–112. Randell, N., Lynch, A., Anthony, A., Dobbs, B., Roake, J. and Frizelle, F. (2001) Does a colostomy alter quality of life in patients with spinal cord injury? A controlled study. Spinal Cord, 39(5): 279–282. Saltzstein, R.J. and Romano, J. (1990) The efficacy of colostomy as a bowel management alternative is selected spinal cord injury patients. J. Am. Paraplegia Soc., 13(2): 9–13. Shafik, A. (1995) Electrorectogram study of the neuropathic rectum. Paraplegia, 33: 346–349. Sjolund, K., Fasth, S., Ekman, R., Hulten, L., Jiborn, H., Nordgren, S. and Sundler, F. (1997) Neuropeptides in idiopathic chronic constipation (slow transit constipation). Neurogastroenterol. Motil., 9(3): 143–150. Stone, J.M., Nino-Murcia, M., Wolfe, V.A. and Perkash, I. (1990a) Chronic gastrointestinal problems in spinal cord injury patients: a prospective analysis. Am. J. Gastroenterol., 85(9): 1114–1119. Stone, J.M., Wolfe, V.A., Nino-Murcia, M. and Perkash, I. (1990b) Colostomy as treatment for complications of spinal cord injury. Arch. Phys. Med. Rehabil., 71: 514–518. Yoshimura, N. and de Groat, W.C. (1993) Changes in electrophysiological and pharmacological properties of rat bladder afferent neurons following spinal cord injury. J. Urol., 149: 340A.
CHAPTER 22
Colorectal motility and defecation after spinal cord injury in humans A.C. Lynch and F.A. Frizelle Colorectal Unit, Department of Surgery, Christchurch Hospital and Burwood Spinal Unit, Christchurch, New Zealand
Abstract: Following spinal cord injury, colorectal problems are a significant cause of morbidity, and chronic gastrointestinal problems remain common with increasing time after injury. Although many cordinjured patients achieve an adequate bowel frequency with drugs and manual stimulation, the risk and occurrence of fecal incontinence, difficulties with evacuation, and need for assistance remain significant problems. The underlying physiology of colorectal motility and defecation is reviewed, and consequences of spinal cord injury on defecation are reported. A discussion of present management techniques is undertaken and new directions in management and research are suggested. There is need for more intervention in regard to bowel function that could improve quality of life, but there is also a need for more research in this area.
with increasing time after injury (Stone et al., 1990a). The inability to defecate normally means that bowel care often occupies a significant part of the day, and, although many cord-injured people achieve an adequate bowel frequency with drugs and manual stimulation, the risk and occurrence of fecal incontinence, difficulties with evacuation, and need for assistance remain significant life-limiting problems (Stone et al., 1990a, b; Levi et al., 1995; Glickman and Kamm, 1996; Han et al., 1998; Lynch et al., 2001). Long-term gastrointestinal complications can develop in cord-injured people. Fecal impaction is common. Diverticular disease and volvulus are more frequent and are perhaps related to higher intracolonic pressures in those with upper motor neuron lesions. The occurrence of hemorrhoids and mucosal prolapse was also identified by Lynch et al. (2000c) as occurring more frequently after spinal cord injury by an incidence of hemorrhoidectomy of 9% compared with a control group incidence of 1.5% (po0.001). This may be
Introduction Bowel dysfunction is a problem following spinal cord injury Bowel dysfunction following spinal cord injury is increasingly recognized as an area of major physical and psychological difficulty. Surveys of spinal cord-injured people show that bowel function is as much of a problem as loss of mobility or sexual function. The problem is twofold as, not only does spinal cord injury result in changes to bowel motility and sphincter control, but also the concurrent loss of mobility and gross motor dexterity makes bowel management a major life-limiting problem. Immediately after spinal cord injury, colorectal problems are a significant cause of morbidity, and chronic gastrointestinal problems remain common Corresponding author. Tel.: +64-3-3640-640; Fax: +64-3-3640-352; E-mail: [email protected] DOI: 10.1016/S0079-6123(05)52022-3
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multifactorial due to altered anorectal tone or trauma with manual evacuation, and is a frequent source of bleeding or autonomic dysreflexia. Impact on lifestyle Spinal cord-injured people rate difficulties with bowel management as similar to problems associated with loss of mobility and sexual function. Hanson and Franklin (1976) reported that 80% of male paraplegics and 46% of male tetraplegics would rank bladder and bowel as their greatest functional loss after loss of mobility. It was interesting that when they asked the same question to spinal unit staff, only 39% ranked bladder and bowel problems as high. Toileting Survey data shows that 61% of cord-injured people would spend more than 15 min per day toileting, compared with only 9% of controls (Lynch et al., 2001). Those doing manual evacuations spend the longest time. Half of all cord-injured people need assistance with toileting. The need for assistance with toileting relates very closely with level of injury and has implications for provision of carers and dependence on family members. It is recognised that having family members perform such intimate tasks can be emotionally charged and negatively affect family interrelationships. This was significantly associated with the reported perception that bowel function was a source of distress. Colonic function following spinal cord injury Questionnaires exploring bowel function in spinal injured people have found that over half of those with an injury above the second lumbar segment (L2) suffer from constipation (DeLooze et al., 1998). People with higher injuries defecate less frequently compared to those with lower injuries and the general population. It is apparent that even with medications and other methods, spinal cord-injured people do not achieve a bowel motion
frequency similar to a control population. Changes to the extrinsic autonomic innervation of the bowel are presumed to decrease the normal postprandial increase in motility and to decrease colonic compliance. Laxative use among the cord-injured population is common as a means of regulating bowel habit. Two-thirds of those with high injuries report using laxatives either occasionally or regularly, compared to the 4% in a control group drawn from the general population (po0.0001, Fisher’s exact test, Lynch et al., 2000c). However, the diarrhea produced by laxatives and the resultant risk of incontinence may limit their use for some. Patterns of gut dysmotility have been described for different levels and degrees of spinal cord injury with the level of the spinal cord lesion determining the effect on colonic motility. Marker transit studies show that lesions above the first thoracic segment (T1) result in delayed mouth-tocaecum time, but lesions below this level result in normal transit times to the caecum. Beyond the ileocaecal valve, transit times are markedly delayed (Menardo et al., 1987). For people with an upper motor neuron lesion, transit studies and scintigraphy have demonstrated variable changes in colonic transit. If the spinal cord lesion is above the lumbar region, transit is slowed throughout the whole colon. The velocity of the median position of bowel contents throughout the colon was significantly slower in cord-injured people (0.637 0.33 cm/h in cord-injured; 2.5871.2 cm/h in controls, po0.001). One study by Nino-Murcia et al. (1990), involving 28 cord-injured subjects, also demonstrated distal small bowel dilatation in 10 people, all of whom had abdominal symptoms and 9 of whom had a spinal cord lesion above T5. A lower motor neuron injury from a lesion affecting the conus, cauda equina or pelvic nerves results in interruption of the parasympathetic supply to the colon and reduced spinal cord-mediated reflex peristalsis. Stool propulsion is by segmental colonic peristalsis only. The mechanism for colonic dysmotility following a spinal cord injury may be a loss of descending inhibitory modulation from the sympathetic nervous system. This theory is supported by studies in the cat by Gillis et al. (1987) in which
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a2-adrenergic receptor activation resulted in profound inhibition of colonic motility, and sectioning of splanchnic nerves (containing preganglionic sympathetic innervation of the intestine) produced an increase in colonic contraction. In cord-injured people, colonic transit delays are more profound in higher injuries, where the sympathetic injury should be more pronounced. The delay may in part be due to loss of colonic compliance. With a spinal cord lesion above L1, the left colon has an abnormal response to increasing volume. Distension with water produces a pressure–volume curve (colometrogram) showing a steep increase in intracolonic pressure with increasing volume. This is similar to the hyperreflexic response described by Meshkinpour et al. (1983) during bladder cystometry for injuries at a similar level. For injuries above T5, the right colon is also affected. The lack of compliance leads to functional obstruction, increased transit times, abdominal distension, bloating and discomfort. It suggests that the central nervous system (CNS) is necessary to modulate colonic motility. Colonic myoelectric activity has been recorded in a group of spinal injury subjects with injuries at varying levels and controls. This demonstrated a significantly higher level of basal colonic activity in cord-injured subjects (12.6 vs. 3.3 spikes per 10 min), and no demonstrable gastrocolic reflex. This would support the assumption that the CNS exerts a tonic inhibitory influence on basal colonic activity and is consistent with the hypertonicity seen on colometrograms.
Colonic neurotransmitters following spinal cord injury The intramural distribution of regulatory neuropeptides within the bowel wall is distinct. Substance P is exclusively localized in nerves (Ferri et al., 1983). Large numbers of vasoactive intestinal polypeptide- and substance P-containing enteric nerves supply the ganglionated plexuses and are especially numerous in the circular muscle layer. They have a role in colon motility while those supplying the mucosa are involved with electrolyte and fluid transport. Substance P has been shown
to accelerate the transit of a charcoal meal in rats. It increases intraluminal pressure mainly by circular muscle contraction by direct action on the muscle as well as by simultaneous activation of excitatory cholinergic pathways and of inhibitory vasoactive intestinal polypeptide-independent, nitric oxide-regulated pathways. Substance P is reduced in the colonic mucosa of patients with chronic constipation, and mucosal substance P levels correlate significantly with disease state (Goldin et al., 1989). A similar scenario exists with diabetic constipation where substance P in the rectal mucosa of diabetics with constipation is significantly lower than in diabetics with normal bowel function (Lysy et al., 1993). The fact that mucosal substance P levels are associated with two disorders of colonic transit suggests a role in the pathogenesis of intestinal transit disorders. Whereas mucosal substance P may be decreased with chronic constipation, concentrations in the muscle layers may be increased. Sjolund et al. (1997) examined tissue from the colon of 18 subjects with slow-transit constipation. Tissue concentrations of vasoactive intestinal polypeptide and substance P were measured by radioimmunoassay. Significantly increased concentrations of both peptides were found in the ascending colon, and in the descending colon, substance P was increased in the myenteric plexus. Recovery of bladder and bowel function following traumatic spinal cord injury is dependent on reorganisation of reflex pathways in the periphery and CNS. Part of this reorganisation may be influenced by spinal cord–target organ interactions mediated by neurotrophic factors released by the peripheral organs. Interrupting the descending modulation from the CNS may lead to changes in the autonomic and somatic outflow reaching target organs from the spinal cord caudal to the lesion and alter target organ function. In rats, spinal cord injury leads to hypertrophy of the bladder as well as electrophysiological and morphological changes in bladder afferent neurons (de Groat et al., 1993; Yoshimura et al., 1993). In the colon, however, the intrinsic enteric nervous system appears intact. Nerve fibres containing the intrinsic neurotransmitters substance P and vasoactive intestinal polypeptide appear to be present in
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approximately similar amounts in specimens from cord-injured and control subjects (Lynch et al., 2000b). The colon may therefore continue to function independently of CNS modulation after spinal cord injury.
Anorectal function Continence The incidence of fecal incontinence in people with spinal cord injury is more common than in the general population. When compared to matched controls by using standardized scoring systems, the mean fecal incontinence score was higher for cord-injured people than controls (po0.0001), and for complete spinal cord injury compared with incomplete injury ðp ¼ 0:0023Þ: Having fecal incontinence also impacts on the quality of life of those with a spinal cord injury more frequently than of neurologically intact persons [62% of cord-injured people report that fecal incontinence impacts upon their everyday life, compared to 8% of control subjects, po0.0001 (Lynch et al., 2000c)]. Fecal continence requires the ability to maintain internal anal sphincter resting tone and to contract the external anal sphincter in response to increased intra-abdominal pressure, rectal distension and rectal contraction. These are spinal reflexes that are intact following spinal cord injury, but no longer modulated by cortical input. Basal sphincter tone is mainly an activity of the internal anal sphincter, the maintenance of which seems to be due to a tonic excitatory sympathetic discharge. Frenckner and Ihre (1976) observed that anorectal manometry performed on cord injury subjects shows a persistent anal tone that is reduced compared to control subjects. They described changes in anal tone in eight healthy subjects following spinal anesthesia. High spinal anesthesia resulted in a significantly lower resting anal pressure than either low spinal or pudendal block. Of note, people with lumbosacral injuries, who have external anal sphincter paralysis but persistent internal anal sphincter activity, still appear to maintain a degree of anorectal tone, higher than rectal pressure, but lower than normal. The external anal sphincter
also continues to show tonic activity, but again generates a lower than normal pressure. Manometric studies on cord-injured subjects show a maximal mean basal sphincter pressure (which probably reflects external anal sphincter pressure) significantly lower than control group pressures. Spinal cord-injured subjects can produce a small rise in sphincter pressure with voluntary squeeze (p40.05). This is, however, much less than the increase in pressure generated by control subjects performing a similar maneuver who can generate a four-fold increase in external anal sphincter pressure. People with incomplete injuries can produce a greater increase in sphincter pressure with a Valsalva maneuver than those with complete injuries. The Valsalva maneuver is expiration against a closed glottis. This may reflect the greater increase in intra-abdominal pressure, as measured by rectal pressure, that people with incomplete or low injuries are able to generate due to incomplete paralysis of their abdominal musculature. For those with a complete injury, attempts at squeezing result in a straining response rather than a true squeeze. People with lesions above T5 will be unable to use abdominal muscles and rely on intercostal and diaphragmatic muscle contraction to increase intra-abdominal pressure. Those with cervical injuries can only use the diaphragm. These observations fit the concept that external anal sphincter contraction is mediated by a spinal reflex, triggered by tension receptors in the pelvic floor that respond to an increase in intra-abdominal pressure. This is supported by another study by MacDonagh et al. (1992) that found the rise in sphincter pressure with the Valsalva maneuver to be directly proportional to the rise in intraabdominal pressure.
Rectal sensation All normal subjects experiencing rectal distension as part of anorectal manometry studies report a range of sensation starting at a rectal volume of about 10 ml, and ranging from sensations of ‘wind’ to pain. This is compared to 78% of cord-injured subjects with complete injuries, and 43% of those with incomplete injuries, who report no sensation
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on rectal distension (Lynch et al., 2000a). Those that did report sensation described non-specific abdominal sensation that did not prevent further rectal distension. A previous study by MacDonagh et al. (1992), examining similar sensations, proposed that sympathetic nerves entering the thoracic spinal cord above the level of the injury conveyed this dull pelvic sensation. However, such sensations have also been identified in five people with complete cervical injuries, making the origin of this sensation unclear. Rectal compliance A normally compliant rectum accommodates an increase in volume with little change in pressure. As rectal volume increases, a normal sphincter response is the relaxation of the internal anal sphincter with continence being maintained by continued external anal sphincter contraction. The ability of the rectum to distend to store bowel volume is an important component of normal bowel function, as it means defecation can be delayed until an appropriate time. People with complete cervical injuries can have increased rectal tone with low compliance, i.e., a sharp rise in rectal pressure occurs with rectal distension, as the rectum does not expand to accommodate the increase in volume. Sphincter tone can also increase with rectal distension, because internal anal sphincter contraction is an enteric reflex, normally suppressed by descending inhibitory pathways. The loss of inhibitive sympathetic tone has also been proposed as a mechanism for the absent rectal relaxation and linear pressure/volume relationship during rectal distension (MacDonagh et al., 1992). Most people with low lumbosacral injuries have an areflexic rectum with an attenuated sphincter response to rectal distension (Shafik, 1995). The rectum is flaccid and capacious producing no rise in rectal pressure with increasing volume. Urgency Fecal urgency, or an inability to delay defecation, is more often a problem following spinal cord
injury. It becomes even more significant as a quality of life issue when reduced mobility and poor hand dexterity are compounded by the difficulties associated with finding a wheelchair-able toilet. Fecal urgency can be assessed by asking respondents how long defecation can be delayed. Overall 81% of controls can delay defecation, compared with only 41% of cord-injured people. There is also an approximately ten-fold increase in the proportion of cord-injured people, compared to controls, who have to defecate immediately. Of note, many people with complete injuries have no sensation, and thus never sense the need to defecate. The incidence of fecal incontinence is often higher for cord-injured people who are unable to delay defecation. Defecation Many defecatory problems seen after spinal cord injury are the result of altered anorectal function. Defecation requires the complex integration of reflex and voluntary muscular control. Cortical inhibition of the external anal sphincter occurs in a coordinated fashion on straining as the rectal smooth muscle contracts. This modulation of the intrinsic nervous system by the extrinsic system is disrupted following a complete supra-conal spinal cord injury. This means that straining by increasing intra-abdominal pressure does not improve evacuation by the usual external anal sphincter relaxation in response to the rectal and intra-abdominal pressure increase. Rather, external anal sphincter tone increases. Thus, coordinated reflex defecation is difficult for cord-injured people. It is often inefficient and incomplete, resulting in incontinence and/or constipation. Therefore, defecation is planned on regular basis to avoid constipation or an increased chance of fecal incontinence. High spinal cord injuries The difficulties with defecation following high spinal cord injury result from discoordinate anal sphincter function. The normal synergistic activity of colonic smooth muscle and pelvic striated muscle
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is lost. There is a loss of conscious sphincter control and, due to abdominal muscle paralysis, an inability to significantly increase intra-abdominal pressure. Loss of rectal sensation and a spastic external anal sphincter require defecation to be anticipated. The conus-mediated increase in external anal sphincter tone with increasing intra-abdominal pressure acts against straining to defecate. However, reflex relaxation of the internal and external anal sphincters by mucosal stimulation, either digitally or with a suppository, can be exploited in order to defecate. Insertion of a gloved finger into the rectum with gentle sustained pressure towards the sacrum relaxes the spastic external anal sphincter and pelvic muscles. Rapid or excessive stretching can precipitate sphincter spasm. Rotation of the finger continues the stimulation until a reflex peristaltic wave is generated in the rectum, flatus is passed and stool comes down. The recto-anal inhibitory reflex is initiated, the internal anal sphincter relaxes, and the recto-colic reflex stimulates pelvic nerve-mediated peristalsis. If there is no reflex relaxation of the external anal sphincter complex, evacuation will not occur or be incomplete. Manual evacuation or enemata are often required in this situation. This reflex relaxation can also lead to fecal incontinence by two means. The anal sphincter may relax at relatively low rectal volume in response to a small increase in intra-abdominal pressure, or as people with high-level injuries often have no sensation of rectal fullness, reflex defecation in response to a full rectum can result in fecal incontinence that is unpredictable and episodic.
Low spinal cord injuries Complete or partial injuries to the cauda equina result in a lower motor neuron pattern of injury. A person with a lower motor neuron lesion following spinal cord injury will have absent external anal sphincter tone, flaccid pelvic muscles and decreased reflex peristalsis. Rectal compliance is increased in response to rectal distension. The loss of parasympathetic control of the internal anal sphincter means that resting anal tone is low and unresponsive
to changes in intra-abdominal pressure. Thus, a Valsalva maneuver can result in fecal leakage, and the rectum has to be kept empty to avoid fecal incontinence. Reflex-mediated defecation does not occur with spinal cord lesions below the conus, so stool has to be removed digitally, assisted by a Valsalva maneuver and abdominal massage. Change in bowel function with time from injury Studies do not demonstrate a change in fecal incontinence with either duration of injury or increasing age for cord-injured people. One survey of bowel dysfunction in cord-injured people by Stone et al. (1990a) found that chronic gastrointestinal problems were rare in the first 5 years following injury, but problems with defecation became more common with increasing time. The incidence of abdominal pain and distension was increased in long-term cord-injured people (more than 18 years since injury) whose bowel regimen was less frequent than once a day (Stone et al., 1990a). Another study of chronic gastrointestinal problems in cord-injured subjects by Han et al. (1998) concluded that bowel habit appeared to settle by about 6 months after injury, and that subsequent bowel dysfunction was not related to age, duration or level of injury. Current management strategies The approach to bowel management after spinal cord injury should address specific issues such as fecal incontinence, constipation and functional mobility. This must be within the context of the patient as a whole person and consider his/her cultural, social, sexual and vocational roles. A bowel care regimen needs to be generated that fits the person’s long-term routine. The aim should be effective colonic evacuation without fecal incontinence or other complications. Regularity of evacuation prevents excessive build-up of feces and impaction. Appropriate equipment, such as commode chairs and wheelchair-able toilets, needs to be supplied for an adequate long-term bowel program. Dietary manipulation is important. Adequate water intake promotes transit by keeping the stool
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soft. Fibre is promoted to give the stool bulk and plasticity. This is thought to assist colonic transit in neurologically intact patients, probably by promoting propulsive activity secondary to increased colonic wall distension. The effects of increased fibre on colonic function after spinal cord injury are not yet fully understood, and may be counterproductive. A study carried out by Cameron et al. (1996) at the Spinal Injury Unit, Austin Hospital, Heidelberg, Australia demonstrated that significantly increasing dietary fibre in a group of cordinjured subjects with a range of injuries resulted in an increase in mean colonic transit time from 28.2 to 42.2 h (po0.05), and in mean recto-sigmoid transit time from 7.9 to 23.3 h (po0.02). However, an increase in stool bulk may mean more time spent with bowel care. Stool softeners other than fibre, such as docusate sodium increase the amount of water in stool without increasing volume and have no effect on bowel motility. They can also affect the intestinal absorption of other drugs, resulting in higher plasma levels. The stool is more likely to be liquid, so continence will not be improved. They are most useful when fecal incontinence is not a risk and straining is to be avoided, such as for patients with hemorrhoids or autonomic dysreflexia. Stimulant laxatives act by increasing intestinal motility, resulting in less time for water reabsorption. Senna has a direct stimulant effect on the myenteric plexus and also increases intraluminal fluid. Bisacodyl has a similar mode of action and is often used as a suppository to initiate bowel evacuation. Dose-dependent side effects can occur. These include abdominal cramping, diarrhea and electrolyte imbalance. Chronic use of stimulant laxatives, especially senna, can result in a progressive unresponsiveness. Osmotic laxatives such as lactulose draw fluid into the colon. They can result in more liquid stool and cause cramping. Prokinetic agents such as cisapride have been employed to reduce constipation in cord-injured people. Transit times are improved, but cardiac arrhythmias have been noted with long-term use. Enemata are often employed when suppositories or digital stimulation fail. Long-term use can result in enema dependences and side effects such as rectal trauma and autonomic dysreflexia can occur.
Spinal cord-injured people with upper motor neuron lesions can exploit the recto-colic reflex to effect defecation. Digital stimulation can result in a reflex wave of conus-mediated rectal peristalsis. The recto-anal inhibitory reflex is intact, so this causes internal anal sphincter relaxation and defecation. Rectal sensation is reduced, however, so defecation has to be anticipated on a regular basis. These people require a bowel management program that keeps the rectum empty to reduce the incidence of incontinence. If people with upper motor neuron lesions are unable to defecate using the recto-colic reflex, then a management plan needs to minimize anorectal trauma but still allow adequate rectal evacuation to avoid constipation. Cord-injured people with lower motor neuron lesions have a rectum that is areflexic, reduced sphincter tone and an attenuated sphincter response to rectal distension or a Valsalva maneuver. These dysfunctions lead to an increased risk of incontinence, especially with liquid stool. The aim, therefore, is to keep stool consistency firm. Local anorectal reflexes are often insufficient to result in defecation, and a compliant rectum acts as a large reservoir, so stool is digitally removed. Arnold et al. (1986) noted that a Brindley sacral anterior nerve root stimulator (S2–S4) can be used for electromicturition to achieve regular, complete bladder emptying. Often deafferentiation of the sacral posterior nerve roots is performed before the stimulator is implanted to produce detrusor areflexia and interim urinary continence. The deafferentiation also results in loss of the sacral reflexes necessary for defecation. The stimulator can then be used to initiate defecation. This does not occur during stimulation due to the simultaneous rectal and sphincter contraction, but when stimulation stops the external anal sphincter relaxes instantaneously and the rectum relaxes slowly, resulting in spontaneous defecation. This method has been shown to result in quicker, more controllable defecation than the reflex method.
Does a colostomy improve bowel function? Colostomy has been reported to result in improved quality of life for people after spinal cord injury
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(Frisbie et al., 1986; Saltzstein and Romano, 1990; Stone et al., 1990b; Randell et al., 2001). It can not only reduce fecal incontinence, but also simplify bowel care in those for whom bowel evacuation is difficult, reducing the amount of time spent on bowel care from 99 to 18 min per day (Stone et al., 1990b). The only long-term management problem reported has been occasional appliance leakage and mucoid discharge per rectum. All subjects involved in a study by Craven and Etchells (1998) found the stoma had impacted significantly on their lifestyle with increased feelings of independence, freedom and raised self-esteem. Sacral pressure ulcers are a common reason for stoma formation in people who had no bowel function problems previously. Deshmukh et al. (1996) examined the use of colostomy as an adjunct measure in the healing of pressure sores in cordinjured people. Their findings similarly showed that a colostomy improved bowel management and was well accepted. However, they noted that the primary goal of pressure sore healing was accomplished in only 6 out of 27 cord-injured people, and stoma formation resulted in significant morbidity with stomal prolapse and difficulties with wound healing. Of the 19 subjects reviewed in this study, none wanted their stoma reversed, and all felt that their quality of life was improved. A colostomy can improve bowel management for some people after cord injury. Dependence on assistance with toileting is decreased as even tetraplegics with limited dexterity are able to manage suitable stoma appliances. Enthusiasm for bowel diversion procedures should be tempered with an acknowledgment that the risks associated with any surgical procedure may not make it acceptable to all cord-injured people.
Future objectives for the investigation and management of bowel dysfunction Bowel dysfunction has a major impact on the quality of life for many people with spinal cord injury. This difficulty has been shown to improve with appropriate early identification and management of their problems. Interview and clinical examination can generate an impression of their
general bowel function and identify problems such as constipation, fecal impaction, anal fissures and hemorrhoids. Simple tests of anorectal function are available that can be performed on all cordinjured people in the same manner that bladder dysfunction is investigated. Anorectal manometry will identify those with dyssynergic sphincter function. For those with abdominal bloating and constipation, abdominal X-ray and colonic motility studies can be helpful. Although improving colonic motility and appropriate bowel management may help, some cordinjured people will have ongoing bowel problems. Colostomy formation has been used to provide the patient with relief from constipation and anorectal dysfunction and with an independent means of managing their own bowel function. Further research needs to be done to examine the differences in quality of life and bowel function following colostomy formation in cord-injured people.
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