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The bladder and bowel dysfunction that may follow a spinal cord injury (SCI) can have a major impact on quality of life. Bowel dysfunction results from a complex interplay between intrinsic nerve supply of the gut, its external autonomic innervation and the somatic innervation involving the sphincters. While symptoms of bladder dysfunction can be broadly defined by the level and severity of the injury, this relationship is less predictable in the case of bowel dysfunction. Symptoms vary between individuals, resulting in variable strategies for bowel management and their outcomes.

This study aimed to describe the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the American Spinal Injury Association Impairment Scale (AIS).

A secondary outcome measure was to seek any correlation between bowel dysfunction and urodynamic dysfunction over the course of time.

Method

Patients selection

Participants were identified from discharge data documented at the Burwood Spinal Unit. Those injured 1–3 years earlier, and those injured over a two-year period 20 years ago, were identified. Those aged under 16, those who had non-traumatic lesions, those who had a colostomy or a Brindley sacral anterior root stimulation plus deafferentation, were excluded.

An information sheet was sent to each potential participant, followed by a phone call from the spinal research nurse, to answer any questions and to encourage participation. Each were then asked to provide informed consent. The most recent urodynamic reports were checked from Unit records. The study design was a non-randomised non-controlled cross-sectional analysis.

Participants were grouped according to level of injury into cervical and upper thoracic (T1–5), lower thoracic (T6–11) and conus/cauda (T12 and below). Complete lesions were AIS A, while AIS B-D were grouped together because of small numbers.

Survey

A symptoms questionnaire was developed in consultation with colorectal surgeons, spinal rehabilitation physicians, nurses and urologists; it was pre-tested on five patients. It included questions on bowel sensation, constipation, incontinence and the details of its management including the need for a carer to assist. SurveyMonkey was used to collect the data which was then entered into a spreadsheet for further analysis. Data from the latest urodynamic tests were also entered.

Analysis

Because of the small numbers of participants and the large number of variables, statistical analysis was not possible.

Approvals

The study and questionnaire was approved by the cultural advisor at Burwood Hospital.

Ethics approval was provided the University of Otago Human Ethics Committee (Reference HD15/038).

Results

There were 127 potential participants, 19 had died and 52 were either non-contactable or declined. Patients with non-traumatic lesions were excluded. Finally, 52 were included. Data was incomplete in five.

Table 1 outlines the levels of injury and AIS of patients included in the study.

Table 1:Demographics.

Because of small numbers, AIS categories were grouped together and all patients were analysed according to the level of injury.

Table 2 reports the bowel symptoms, according to level of injury, and faecal continence rates.

Table 2: Bowel symptoms.

‘Autonomic’ symptoms included bloating, nausea, abdominal pain, goose bumps, sweating and headaches when the bowel needed to be emptied. Autonomic dysreflexia was noted in 14/52 (27%) and all these were cervical or thoracic levels. All were T7 or above, with only one at T10.

Those who had faecal incontinence were not further stratified according to frequency of these accidents.

Table 3 outlines bowel management according to level of injury, the use of manual evacuation, suppositories and enemas. Carer assistance with bowels, frequency of this, time taken for bowel cares and bother from bowels is included in this table. Change in bowel function, since the end of the first-year post injury, is provided.

Table 3: Bowel management.

Table 4: Bowel control and urodynamics.

Discussion

We have described the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the AIS. What is most noticeable is the variable nature of symptoms to level of spinal injury and the high number suffering from faecal incontinence. Our study did not show any correlation between bowel dysfunction and bladder dysfunction. This was the conclusion reached by others too, where none of the urodynamic parameters including cystometric capacity, presence of detrusor overactivity, poor bladder compliance, nor detrusor-sphincter-dyssynergia, correlated with any of the bowel symptom scores.1

According to Liu et al, factors which impact on the severity of the Neurogenic Bowel Dysfunction Score included high level of cord injury, its completeness on the AIS score and length of time since injury (>10 years).2

Specific symptoms such as constipation are more difficult to evaluate since there is reduced physical activity and some use laxatives too without always stating this. In our study, about 75% of patients with a SCI use manual evacuation methods to empty the bowels and half of these used suppositories in addition. Hence symptoms such as length of time for bowel cares, use of laxatives, manual evacuation or suppositories, may be more helpful that the Bristol Stool Scores in these patients. Suppositories were more commonly used in high lesions than in those with conus/cauda lesions. Where suppositories are effective, this suggests the possibility of reflex stimulation, which might be somatic or autonomic, involving colo-rectal and recto-anal reflexes.3

Emmanuel et al found that constipation was more prominent in patients with a lesion above T5 compared to 55% in patients with lesions below T5, 20 years after injury.4 These authors also showed that constipation correlated with a slower gut transit time, which was pan-colonic. The delay was greater in high spinal lesions, where loss of sympathetic inhibition resulted in greater mucosal blood flow than in those with lower lesions. Another group observed that upper gastrointestinal transit was prolonged in subjects with SCI suffering from bowel problems, not only in subjects with cervical or high thoracic lesions but also in subjects with conus/cauda equina lesions.5 This group speculated that the prolonged transit was secondary to colonic dysfunction and constipation.

In a study from a US VA medical centre, megacolon (bowel diameter > 6cm on plain x-ray), was reported in 94/128 (73%) and was shown to increase with time from SCI.6 Evidence is conflicting however, and other researchers have shown no increase in megacolon.7 In our study with increasing time since injury, 15/52 (29%) indicated it look longer to empty the bowels. This is in agreement with an earlier study, which found in addition that faecal incontinence did not change with time.8 Little change was noted with time in another cross-sectional study but the authors drew attention to the need for longitudinal studies.9

Nausea, distension, bloating and vague discomfort are presumably related to the autonomic innervation. About 50% of all patients had some of these symptoms. For those with conus and cauda lesions, the sensation might be mediated by somatic sensation. To these can be added symptoms of autonomic dysreflexia like headache, sweating and reflex hypertension. In our study, autonomic dysreflexia was noted in 27% and all these were cervical or thoracic levels; all except one were T7 or above.

Bowel symptoms and their management caused moderate or severe bother for 21/52 (40%) and seemed to affect those with conus/cauda level lesions as much as the cervical ones. However, more of the cervical lesion patients had carer assistance and this reduced the level of bother.

Lynch et al demonstrated that ano-rectal manometry did not show a consistent relation to bowel dysfunction after SCI.8 The lack of a predictable bowel dysfunction after SCI probably relates to the complex innervation of the bowel with extensive intrinsic autonomic innervation and interaction with the somatic system in the rectum, anus and sphincters. The presence of intrinsic and extrinsic autonomic nerve supply to the bowel and their interactions are complex.

There are multiple clinical examples of surgical bowel denervation that do not lead to reproducible bowel dysfunction. For example:

Parasympathetic denervation: Truncal vagotomy formerly used in the treatment of peptic ulcers causes parasympathetic denervation of the bowel from the stomach to the splenic flexure. After an initial period of flaccidity, peristalsis returned, indeed often with increased activity associated with diarrhoea, as might be predicted as the parasympathetic system is motor to the gut. Disordered small bowel motility with absence of cyclical activity was seen in some.10

Sympathetic denervation: Damage to the lumbar sympathetic nerves can occur during surgery in the formerly used operation of surgery for hypertension, in a pre-sacral neurectomy formerly done for dysmenorrhoea, as part of a retroperitoneal lymph node dissection for testis tumours, in aortic aneurysm repair and with colectomy including extended lymph node dissection. However, there was no definable effect on subsequent bowel function after these procedures.11,12

Somatic sacral denervation: Where the conus or the cauda equina are damaged, the somatic nerve supply to the pelvic floor and sphincters of bladder and anus is interrupted, resulting in abolition of reflex activity and flaccidity. The pelvic floor weakness can lead to stress urinary and bowel incontinence. Such incontinence can develop after surgical deafferentation to achieve continence by abolishing reflex detrusor contractions as part of the Brindley sacral anterior root stimulation procedure.

Reflexes between the anal margin, anal sphincter and bowel contraction are important in both defecation and bowel control. These reflexes involve both somatic and autonomic nervous systems. Further there is evidence that the urethral sphincter is subject to similar reflex actions as the anal sphincter. Chronic constipation with a distended rectum can activate the recto-anal inhibitory reflex causing bowel incontinence.

This is a small study, with a relatively low return rate of the electronic questionnaire and as such may be subject to bias, for example those who replied may be patients who are more likely to be having trouble with their bowels. Both groups, being those injured 1–3 years earlier, and those injured over a two-year period twenty years ago, were analysed as a single cohort. This was not the original intention of the study but due to small numbers, no meaningful interpretations were able to be drawn from the two groups which otherwise appeared to show very similar patterns. A larger study with more complete follow-up is recommended.

This study does give valuable insight into the variable bowel habit experienced by the SCI patients and draws attention to the fact that symptoms are not as predictable as previously thought. Hence, bespoke bowel management plans are often required irrespective of the level of the spinal lesion.

Summary

Abstract

Aim

To document the symptoms of bowel dysfunction, and how the bowels are managed, in a cohort of patients following a spinal cord injury. To relate these to the level of the spinal injury and to examine the relationship between bowel symptoms and bladder dysfunction.

Method

Participants were identified from the discharge data from the Burwood Spinal Unit, one of two national Spinal Units in New Zealand, in two two-year sets from 1-3 years post-injury and from 20-21 years post-injury. With informed consent, they completed a survey developed for symptoms and management using Survey Monkey. This was cross-related to the level of cord injury and the AIS Scale, and then to the latest urodynamic analysis.

Results

A total of 54 patients were included; data was incomplete in five patients. No specific relation was found between bowel sensation, bowel continence, bowel management, nor with bladder function.

Conclusion

Lack of correlation of patterns of bowel function with the level and severity of the cord lesion indicates the need to continue to individualise advice on bowel care according to symptoms.

Author Information

- Edwin P Arnold, Clinical Professor of Urology, Department of Surgery, University of Otago, Christchurch; Giovanni Losco, Consultant Urologist, Department of Urology, Canterbury District Health Board, Christchurch; Sharon English, Consultant Urologist,

Acknowledgements

The authors wish to acknowledge the assistance of: Dr Raj Singhal, Clinical Director, Burwood Spinal Unit; Professor Chris Frampton for statistical advice; Marian Lippiatt, Registered Nurse, Burwood Spinal Unit; Lucy Eames, Research Assistant, the patients for their participation and the Burwood Academy of Independent Living for oversight of the project. Funding was received from the Burwood Spinal Unit Education and Research Trust and the Urological Research Foundation.

Correspondence

Mr Giovanni Losco, Department of Urology, Canterbury District Health Board, Christchurch Hospital, Private Bag 4710, Christchurch 8140.

Correspondence Email

giovanni@urology.co.nz

Competing Interests

Nil.

  1. Cameron AP, Rodriguez GM, Gursky A, et al. The severity of bowel dysfunction in patients with neurogenic bladder. Neurourol Urodyn. 2014; 33:993–4.
  2. Liu C-W, Huang C-C, Chen C-H, et al. Prediction of severe neurogenic bowel dysfunction in persons with spinal cord injury. Spinal Cord. 2010; 48:554–9.
  3. Pan Y, Liu B, Li R, et al. Bowel dysfunction in spinal cord injury: current perspectives. Cell Biochem Biophys. 2014; 69:385–8.
  4. Emmanuel AV, Chung EAL, Kamm MA, Middleton F. Relationship between gut-specific autonomic testing and bowel dysfunction in spinal cord injured patients. Spinal Cord. 2009; 47:623–7.
  5. Fynne L, Worsoe J, Gregersen T, et al. Gastric and small intestinal dysfunction in spinal cord injury patients. Acta Neurol Scand. 2012; 125:123–8.
  6. Harari D, Minaker KL. Megacolon in patients with chronic spinal cord injury. Spinal Cord. 2000; 38:331–9.
  7. Faaborg PM, Christensen P, Finnerup N, et al. The pattern of colorectal dysfunction changes with time since spinal cord injury. Spinal Cord. 2008; 46:234–8.
  8. Lynch AC, Anthony A, Dobbs BR, Frizelle FA. Anorectal physiology following spinal cord injury. Spinal Cord. 2000; 38:573–80.
  9. Adriaansen JJE, van Asbeck FWA, Tepper M, et al. Bladder-emptying methods, neurogenic lower urinary tract dysfunction and impact on quality of life in people with long-term spinal cord injury. J Spinal Cord Med. 2017; 40:43–53.
  10. Madrid AML, Ledesma S, Landskron G, et al. Small bowel motility disorders in vagotomized patients. Neurogastroenterol Motil. 2012; 173 Suppl 24(2):173.
  11. Dobrowolski S, Wojciechowski J, Dobosz M, et al. Prospective evaluation of the defecatory functional results in patients following aorto-aortic reconstruction surgery for an abdominal aortic aneurysm. Surg Today. 2007; 37:831–6.
  12. Thorsen YS, Stimec B, Andersen SN, et al. Bowel function and quality of life after superior mesenteric nerve plexus transection in right colectomy with D3 extended mesenterectomy. Tech Coloproctol. 2016; 20:445–53.

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

The bladder and bowel dysfunction that may follow a spinal cord injury (SCI) can have a major impact on quality of life. Bowel dysfunction results from a complex interplay between intrinsic nerve supply of the gut, its external autonomic innervation and the somatic innervation involving the sphincters. While symptoms of bladder dysfunction can be broadly defined by the level and severity of the injury, this relationship is less predictable in the case of bowel dysfunction. Symptoms vary between individuals, resulting in variable strategies for bowel management and their outcomes.

This study aimed to describe the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the American Spinal Injury Association Impairment Scale (AIS).

A secondary outcome measure was to seek any correlation between bowel dysfunction and urodynamic dysfunction over the course of time.

Method

Patients selection

Participants were identified from discharge data documented at the Burwood Spinal Unit. Those injured 1–3 years earlier, and those injured over a two-year period 20 years ago, were identified. Those aged under 16, those who had non-traumatic lesions, those who had a colostomy or a Brindley sacral anterior root stimulation plus deafferentation, were excluded.

An information sheet was sent to each potential participant, followed by a phone call from the spinal research nurse, to answer any questions and to encourage participation. Each were then asked to provide informed consent. The most recent urodynamic reports were checked from Unit records. The study design was a non-randomised non-controlled cross-sectional analysis.

Participants were grouped according to level of injury into cervical and upper thoracic (T1–5), lower thoracic (T6–11) and conus/cauda (T12 and below). Complete lesions were AIS A, while AIS B-D were grouped together because of small numbers.

Survey

A symptoms questionnaire was developed in consultation with colorectal surgeons, spinal rehabilitation physicians, nurses and urologists; it was pre-tested on five patients. It included questions on bowel sensation, constipation, incontinence and the details of its management including the need for a carer to assist. SurveyMonkey was used to collect the data which was then entered into a spreadsheet for further analysis. Data from the latest urodynamic tests were also entered.

Analysis

Because of the small numbers of participants and the large number of variables, statistical analysis was not possible.

Approvals

The study and questionnaire was approved by the cultural advisor at Burwood Hospital.

Ethics approval was provided the University of Otago Human Ethics Committee (Reference HD15/038).

Results

There were 127 potential participants, 19 had died and 52 were either non-contactable or declined. Patients with non-traumatic lesions were excluded. Finally, 52 were included. Data was incomplete in five.

Table 1 outlines the levels of injury and AIS of patients included in the study.

Table 1:Demographics.

Because of small numbers, AIS categories were grouped together and all patients were analysed according to the level of injury.

Table 2 reports the bowel symptoms, according to level of injury, and faecal continence rates.

Table 2: Bowel symptoms.

‘Autonomic’ symptoms included bloating, nausea, abdominal pain, goose bumps, sweating and headaches when the bowel needed to be emptied. Autonomic dysreflexia was noted in 14/52 (27%) and all these were cervical or thoracic levels. All were T7 or above, with only one at T10.

Those who had faecal incontinence were not further stratified according to frequency of these accidents.

Table 3 outlines bowel management according to level of injury, the use of manual evacuation, suppositories and enemas. Carer assistance with bowels, frequency of this, time taken for bowel cares and bother from bowels is included in this table. Change in bowel function, since the end of the first-year post injury, is provided.

Table 3: Bowel management.

Table 4: Bowel control and urodynamics.

Discussion

We have described the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the AIS. What is most noticeable is the variable nature of symptoms to level of spinal injury and the high number suffering from faecal incontinence. Our study did not show any correlation between bowel dysfunction and bladder dysfunction. This was the conclusion reached by others too, where none of the urodynamic parameters including cystometric capacity, presence of detrusor overactivity, poor bladder compliance, nor detrusor-sphincter-dyssynergia, correlated with any of the bowel symptom scores.1

According to Liu et al, factors which impact on the severity of the Neurogenic Bowel Dysfunction Score included high level of cord injury, its completeness on the AIS score and length of time since injury (>10 years).2

Specific symptoms such as constipation are more difficult to evaluate since there is reduced physical activity and some use laxatives too without always stating this. In our study, about 75% of patients with a SCI use manual evacuation methods to empty the bowels and half of these used suppositories in addition. Hence symptoms such as length of time for bowel cares, use of laxatives, manual evacuation or suppositories, may be more helpful that the Bristol Stool Scores in these patients. Suppositories were more commonly used in high lesions than in those with conus/cauda lesions. Where suppositories are effective, this suggests the possibility of reflex stimulation, which might be somatic or autonomic, involving colo-rectal and recto-anal reflexes.3

Emmanuel et al found that constipation was more prominent in patients with a lesion above T5 compared to 55% in patients with lesions below T5, 20 years after injury.4 These authors also showed that constipation correlated with a slower gut transit time, which was pan-colonic. The delay was greater in high spinal lesions, where loss of sympathetic inhibition resulted in greater mucosal blood flow than in those with lower lesions. Another group observed that upper gastrointestinal transit was prolonged in subjects with SCI suffering from bowel problems, not only in subjects with cervical or high thoracic lesions but also in subjects with conus/cauda equina lesions.5 This group speculated that the prolonged transit was secondary to colonic dysfunction and constipation.

In a study from a US VA medical centre, megacolon (bowel diameter > 6cm on plain x-ray), was reported in 94/128 (73%) and was shown to increase with time from SCI.6 Evidence is conflicting however, and other researchers have shown no increase in megacolon.7 In our study with increasing time since injury, 15/52 (29%) indicated it look longer to empty the bowels. This is in agreement with an earlier study, which found in addition that faecal incontinence did not change with time.8 Little change was noted with time in another cross-sectional study but the authors drew attention to the need for longitudinal studies.9

Nausea, distension, bloating and vague discomfort are presumably related to the autonomic innervation. About 50% of all patients had some of these symptoms. For those with conus and cauda lesions, the sensation might be mediated by somatic sensation. To these can be added symptoms of autonomic dysreflexia like headache, sweating and reflex hypertension. In our study, autonomic dysreflexia was noted in 27% and all these were cervical or thoracic levels; all except one were T7 or above.

Bowel symptoms and their management caused moderate or severe bother for 21/52 (40%) and seemed to affect those with conus/cauda level lesions as much as the cervical ones. However, more of the cervical lesion patients had carer assistance and this reduced the level of bother.

Lynch et al demonstrated that ano-rectal manometry did not show a consistent relation to bowel dysfunction after SCI.8 The lack of a predictable bowel dysfunction after SCI probably relates to the complex innervation of the bowel with extensive intrinsic autonomic innervation and interaction with the somatic system in the rectum, anus and sphincters. The presence of intrinsic and extrinsic autonomic nerve supply to the bowel and their interactions are complex.

There are multiple clinical examples of surgical bowel denervation that do not lead to reproducible bowel dysfunction. For example:

Parasympathetic denervation: Truncal vagotomy formerly used in the treatment of peptic ulcers causes parasympathetic denervation of the bowel from the stomach to the splenic flexure. After an initial period of flaccidity, peristalsis returned, indeed often with increased activity associated with diarrhoea, as might be predicted as the parasympathetic system is motor to the gut. Disordered small bowel motility with absence of cyclical activity was seen in some.10

Sympathetic denervation: Damage to the lumbar sympathetic nerves can occur during surgery in the formerly used operation of surgery for hypertension, in a pre-sacral neurectomy formerly done for dysmenorrhoea, as part of a retroperitoneal lymph node dissection for testis tumours, in aortic aneurysm repair and with colectomy including extended lymph node dissection. However, there was no definable effect on subsequent bowel function after these procedures.11,12

Somatic sacral denervation: Where the conus or the cauda equina are damaged, the somatic nerve supply to the pelvic floor and sphincters of bladder and anus is interrupted, resulting in abolition of reflex activity and flaccidity. The pelvic floor weakness can lead to stress urinary and bowel incontinence. Such incontinence can develop after surgical deafferentation to achieve continence by abolishing reflex detrusor contractions as part of the Brindley sacral anterior root stimulation procedure.

Reflexes between the anal margin, anal sphincter and bowel contraction are important in both defecation and bowel control. These reflexes involve both somatic and autonomic nervous systems. Further there is evidence that the urethral sphincter is subject to similar reflex actions as the anal sphincter. Chronic constipation with a distended rectum can activate the recto-anal inhibitory reflex causing bowel incontinence.

This is a small study, with a relatively low return rate of the electronic questionnaire and as such may be subject to bias, for example those who replied may be patients who are more likely to be having trouble with their bowels. Both groups, being those injured 1–3 years earlier, and those injured over a two-year period twenty years ago, were analysed as a single cohort. This was not the original intention of the study but due to small numbers, no meaningful interpretations were able to be drawn from the two groups which otherwise appeared to show very similar patterns. A larger study with more complete follow-up is recommended.

This study does give valuable insight into the variable bowel habit experienced by the SCI patients and draws attention to the fact that symptoms are not as predictable as previously thought. Hence, bespoke bowel management plans are often required irrespective of the level of the spinal lesion.

Summary

Abstract

Aim

To document the symptoms of bowel dysfunction, and how the bowels are managed, in a cohort of patients following a spinal cord injury. To relate these to the level of the spinal injury and to examine the relationship between bowel symptoms and bladder dysfunction.

Method

Participants were identified from the discharge data from the Burwood Spinal Unit, one of two national Spinal Units in New Zealand, in two two-year sets from 1-3 years post-injury and from 20-21 years post-injury. With informed consent, they completed a survey developed for symptoms and management using Survey Monkey. This was cross-related to the level of cord injury and the AIS Scale, and then to the latest urodynamic analysis.

Results

A total of 54 patients were included; data was incomplete in five patients. No specific relation was found between bowel sensation, bowel continence, bowel management, nor with bladder function.

Conclusion

Lack of correlation of patterns of bowel function with the level and severity of the cord lesion indicates the need to continue to individualise advice on bowel care according to symptoms.

Author Information

- Edwin P Arnold, Clinical Professor of Urology, Department of Surgery, University of Otago, Christchurch; Giovanni Losco, Consultant Urologist, Department of Urology, Canterbury District Health Board, Christchurch; Sharon English, Consultant Urologist,

Acknowledgements

The authors wish to acknowledge the assistance of: Dr Raj Singhal, Clinical Director, Burwood Spinal Unit; Professor Chris Frampton for statistical advice; Marian Lippiatt, Registered Nurse, Burwood Spinal Unit; Lucy Eames, Research Assistant, the patients for their participation and the Burwood Academy of Independent Living for oversight of the project. Funding was received from the Burwood Spinal Unit Education and Research Trust and the Urological Research Foundation.

Correspondence

Mr Giovanni Losco, Department of Urology, Canterbury District Health Board, Christchurch Hospital, Private Bag 4710, Christchurch 8140.

Correspondence Email

giovanni@urology.co.nz

Competing Interests

Nil.

  1. Cameron AP, Rodriguez GM, Gursky A, et al. The severity of bowel dysfunction in patients with neurogenic bladder. Neurourol Urodyn. 2014; 33:993–4.
  2. Liu C-W, Huang C-C, Chen C-H, et al. Prediction of severe neurogenic bowel dysfunction in persons with spinal cord injury. Spinal Cord. 2010; 48:554–9.
  3. Pan Y, Liu B, Li R, et al. Bowel dysfunction in spinal cord injury: current perspectives. Cell Biochem Biophys. 2014; 69:385–8.
  4. Emmanuel AV, Chung EAL, Kamm MA, Middleton F. Relationship between gut-specific autonomic testing and bowel dysfunction in spinal cord injured patients. Spinal Cord. 2009; 47:623–7.
  5. Fynne L, Worsoe J, Gregersen T, et al. Gastric and small intestinal dysfunction in spinal cord injury patients. Acta Neurol Scand. 2012; 125:123–8.
  6. Harari D, Minaker KL. Megacolon in patients with chronic spinal cord injury. Spinal Cord. 2000; 38:331–9.
  7. Faaborg PM, Christensen P, Finnerup N, et al. The pattern of colorectal dysfunction changes with time since spinal cord injury. Spinal Cord. 2008; 46:234–8.
  8. Lynch AC, Anthony A, Dobbs BR, Frizelle FA. Anorectal physiology following spinal cord injury. Spinal Cord. 2000; 38:573–80.
  9. Adriaansen JJE, van Asbeck FWA, Tepper M, et al. Bladder-emptying methods, neurogenic lower urinary tract dysfunction and impact on quality of life in people with long-term spinal cord injury. J Spinal Cord Med. 2017; 40:43–53.
  10. Madrid AML, Ledesma S, Landskron G, et al. Small bowel motility disorders in vagotomized patients. Neurogastroenterol Motil. 2012; 173 Suppl 24(2):173.
  11. Dobrowolski S, Wojciechowski J, Dobosz M, et al. Prospective evaluation of the defecatory functional results in patients following aorto-aortic reconstruction surgery for an abdominal aortic aneurysm. Surg Today. 2007; 37:831–6.
  12. Thorsen YS, Stimec B, Andersen SN, et al. Bowel function and quality of life after superior mesenteric nerve plexus transection in right colectomy with D3 extended mesenterectomy. Tech Coloproctol. 2016; 20:445–53.

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

The bladder and bowel dysfunction that may follow a spinal cord injury (SCI) can have a major impact on quality of life. Bowel dysfunction results from a complex interplay between intrinsic nerve supply of the gut, its external autonomic innervation and the somatic innervation involving the sphincters. While symptoms of bladder dysfunction can be broadly defined by the level and severity of the injury, this relationship is less predictable in the case of bowel dysfunction. Symptoms vary between individuals, resulting in variable strategies for bowel management and their outcomes.

This study aimed to describe the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the American Spinal Injury Association Impairment Scale (AIS).

A secondary outcome measure was to seek any correlation between bowel dysfunction and urodynamic dysfunction over the course of time.

Method

Patients selection

Participants were identified from discharge data documented at the Burwood Spinal Unit. Those injured 1–3 years earlier, and those injured over a two-year period 20 years ago, were identified. Those aged under 16, those who had non-traumatic lesions, those who had a colostomy or a Brindley sacral anterior root stimulation plus deafferentation, were excluded.

An information sheet was sent to each potential participant, followed by a phone call from the spinal research nurse, to answer any questions and to encourage participation. Each were then asked to provide informed consent. The most recent urodynamic reports were checked from Unit records. The study design was a non-randomised non-controlled cross-sectional analysis.

Participants were grouped according to level of injury into cervical and upper thoracic (T1–5), lower thoracic (T6–11) and conus/cauda (T12 and below). Complete lesions were AIS A, while AIS B-D were grouped together because of small numbers.

Survey

A symptoms questionnaire was developed in consultation with colorectal surgeons, spinal rehabilitation physicians, nurses and urologists; it was pre-tested on five patients. It included questions on bowel sensation, constipation, incontinence and the details of its management including the need for a carer to assist. SurveyMonkey was used to collect the data which was then entered into a spreadsheet for further analysis. Data from the latest urodynamic tests were also entered.

Analysis

Because of the small numbers of participants and the large number of variables, statistical analysis was not possible.

Approvals

The study and questionnaire was approved by the cultural advisor at Burwood Hospital.

Ethics approval was provided the University of Otago Human Ethics Committee (Reference HD15/038).

Results

There were 127 potential participants, 19 had died and 52 were either non-contactable or declined. Patients with non-traumatic lesions were excluded. Finally, 52 were included. Data was incomplete in five.

Table 1 outlines the levels of injury and AIS of patients included in the study.

Table 1:Demographics.

Because of small numbers, AIS categories were grouped together and all patients were analysed according to the level of injury.

Table 2 reports the bowel symptoms, according to level of injury, and faecal continence rates.

Table 2: Bowel symptoms.

‘Autonomic’ symptoms included bloating, nausea, abdominal pain, goose bumps, sweating and headaches when the bowel needed to be emptied. Autonomic dysreflexia was noted in 14/52 (27%) and all these were cervical or thoracic levels. All were T7 or above, with only one at T10.

Those who had faecal incontinence were not further stratified according to frequency of these accidents.

Table 3 outlines bowel management according to level of injury, the use of manual evacuation, suppositories and enemas. Carer assistance with bowels, frequency of this, time taken for bowel cares and bother from bowels is included in this table. Change in bowel function, since the end of the first-year post injury, is provided.

Table 3: Bowel management.

Table 4: Bowel control and urodynamics.

Discussion

We have described the bowel function and bowel management strategies used by a group of SCI patients with injuries at various levels and degrees of completeness according to the AIS. What is most noticeable is the variable nature of symptoms to level of spinal injury and the high number suffering from faecal incontinence. Our study did not show any correlation between bowel dysfunction and bladder dysfunction. This was the conclusion reached by others too, where none of the urodynamic parameters including cystometric capacity, presence of detrusor overactivity, poor bladder compliance, nor detrusor-sphincter-dyssynergia, correlated with any of the bowel symptom scores.1

According to Liu et al, factors which impact on the severity of the Neurogenic Bowel Dysfunction Score included high level of cord injury, its completeness on the AIS score and length of time since injury (>10 years).2

Specific symptoms such as constipation are more difficult to evaluate since there is reduced physical activity and some use laxatives too without always stating this. In our study, about 75% of patients with a SCI use manual evacuation methods to empty the bowels and half of these used suppositories in addition. Hence symptoms such as length of time for bowel cares, use of laxatives, manual evacuation or suppositories, may be more helpful that the Bristol Stool Scores in these patients. Suppositories were more commonly used in high lesions than in those with conus/cauda lesions. Where suppositories are effective, this suggests the possibility of reflex stimulation, which might be somatic or autonomic, involving colo-rectal and recto-anal reflexes.3

Emmanuel et al found that constipation was more prominent in patients with a lesion above T5 compared to 55% in patients with lesions below T5, 20 years after injury.4 These authors also showed that constipation correlated with a slower gut transit time, which was pan-colonic. The delay was greater in high spinal lesions, where loss of sympathetic inhibition resulted in greater mucosal blood flow than in those with lower lesions. Another group observed that upper gastrointestinal transit was prolonged in subjects with SCI suffering from bowel problems, not only in subjects with cervical or high thoracic lesions but also in subjects with conus/cauda equina lesions.5 This group speculated that the prolonged transit was secondary to colonic dysfunction and constipation.

In a study from a US VA medical centre, megacolon (bowel diameter > 6cm on plain x-ray), was reported in 94/128 (73%) and was shown to increase with time from SCI.6 Evidence is conflicting however, and other researchers have shown no increase in megacolon.7 In our study with increasing time since injury, 15/52 (29%) indicated it look longer to empty the bowels. This is in agreement with an earlier study, which found in addition that faecal incontinence did not change with time.8 Little change was noted with time in another cross-sectional study but the authors drew attention to the need for longitudinal studies.9

Nausea, distension, bloating and vague discomfort are presumably related to the autonomic innervation. About 50% of all patients had some of these symptoms. For those with conus and cauda lesions, the sensation might be mediated by somatic sensation. To these can be added symptoms of autonomic dysreflexia like headache, sweating and reflex hypertension. In our study, autonomic dysreflexia was noted in 27% and all these were cervical or thoracic levels; all except one were T7 or above.

Bowel symptoms and their management caused moderate or severe bother for 21/52 (40%) and seemed to affect those with conus/cauda level lesions as much as the cervical ones. However, more of the cervical lesion patients had carer assistance and this reduced the level of bother.

Lynch et al demonstrated that ano-rectal manometry did not show a consistent relation to bowel dysfunction after SCI.8 The lack of a predictable bowel dysfunction after SCI probably relates to the complex innervation of the bowel with extensive intrinsic autonomic innervation and interaction with the somatic system in the rectum, anus and sphincters. The presence of intrinsic and extrinsic autonomic nerve supply to the bowel and their interactions are complex.

There are multiple clinical examples of surgical bowel denervation that do not lead to reproducible bowel dysfunction. For example:

Parasympathetic denervation: Truncal vagotomy formerly used in the treatment of peptic ulcers causes parasympathetic denervation of the bowel from the stomach to the splenic flexure. After an initial period of flaccidity, peristalsis returned, indeed often with increased activity associated with diarrhoea, as might be predicted as the parasympathetic system is motor to the gut. Disordered small bowel motility with absence of cyclical activity was seen in some.10

Sympathetic denervation: Damage to the lumbar sympathetic nerves can occur during surgery in the formerly used operation of surgery for hypertension, in a pre-sacral neurectomy formerly done for dysmenorrhoea, as part of a retroperitoneal lymph node dissection for testis tumours, in aortic aneurysm repair and with colectomy including extended lymph node dissection. However, there was no definable effect on subsequent bowel function after these procedures.11,12

Somatic sacral denervation: Where the conus or the cauda equina are damaged, the somatic nerve supply to the pelvic floor and sphincters of bladder and anus is interrupted, resulting in abolition of reflex activity and flaccidity. The pelvic floor weakness can lead to stress urinary and bowel incontinence. Such incontinence can develop after surgical deafferentation to achieve continence by abolishing reflex detrusor contractions as part of the Brindley sacral anterior root stimulation procedure.

Reflexes between the anal margin, anal sphincter and bowel contraction are important in both defecation and bowel control. These reflexes involve both somatic and autonomic nervous systems. Further there is evidence that the urethral sphincter is subject to similar reflex actions as the anal sphincter. Chronic constipation with a distended rectum can activate the recto-anal inhibitory reflex causing bowel incontinence.

This is a small study, with a relatively low return rate of the electronic questionnaire and as such may be subject to bias, for example those who replied may be patients who are more likely to be having trouble with their bowels. Both groups, being those injured 1–3 years earlier, and those injured over a two-year period twenty years ago, were analysed as a single cohort. This was not the original intention of the study but due to small numbers, no meaningful interpretations were able to be drawn from the two groups which otherwise appeared to show very similar patterns. A larger study with more complete follow-up is recommended.

This study does give valuable insight into the variable bowel habit experienced by the SCI patients and draws attention to the fact that symptoms are not as predictable as previously thought. Hence, bespoke bowel management plans are often required irrespective of the level of the spinal lesion.

Summary

Abstract

Aim

To document the symptoms of bowel dysfunction, and how the bowels are managed, in a cohort of patients following a spinal cord injury. To relate these to the level of the spinal injury and to examine the relationship between bowel symptoms and bladder dysfunction.

Method

Participants were identified from the discharge data from the Burwood Spinal Unit, one of two national Spinal Units in New Zealand, in two two-year sets from 1-3 years post-injury and from 20-21 years post-injury. With informed consent, they completed a survey developed for symptoms and management using Survey Monkey. This was cross-related to the level of cord injury and the AIS Scale, and then to the latest urodynamic analysis.

Results

A total of 54 patients were included; data was incomplete in five patients. No specific relation was found between bowel sensation, bowel continence, bowel management, nor with bladder function.

Conclusion

Lack of correlation of patterns of bowel function with the level and severity of the cord lesion indicates the need to continue to individualise advice on bowel care according to symptoms.

Author Information

- Edwin P Arnold, Clinical Professor of Urology, Department of Surgery, University of Otago, Christchurch; Giovanni Losco, Consultant Urologist, Department of Urology, Canterbury District Health Board, Christchurch; Sharon English, Consultant Urologist,

Acknowledgements

The authors wish to acknowledge the assistance of: Dr Raj Singhal, Clinical Director, Burwood Spinal Unit; Professor Chris Frampton for statistical advice; Marian Lippiatt, Registered Nurse, Burwood Spinal Unit; Lucy Eames, Research Assistant, the patients for their participation and the Burwood Academy of Independent Living for oversight of the project. Funding was received from the Burwood Spinal Unit Education and Research Trust and the Urological Research Foundation.

Correspondence

Mr Giovanni Losco, Department of Urology, Canterbury District Health Board, Christchurch Hospital, Private Bag 4710, Christchurch 8140.

Correspondence Email

giovanni@urology.co.nz

Competing Interests

Nil.

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