Cell Biochem Biophys DOI 10.1007/s12013-014-9842-6
REVIEW PAPER
Bowel Dysfunction in Spinal Cord Injury: Current Perspectives Yuehai Pan • Bin Liu • Ruijun Li • Zhixin Zhang Laijin Lu
•
Ó Springer Science+Business Media New York 2014
Abstract Permanent disruptions of gastrointestinal function are very common sequel of spinal cord injury (SCI). When motor and sensory nervous integrity are severely affected, neurogenic gastrointestinal dysfunction is an inevitable consequence. Autonomic nervous system miss function has significantly diminished or lost sensory sensations followed with incomplete evacuation of stool from the rectal vault, immobility, and reduced anal sphincter tone all of those predisposing to increased risk of fecal incontinence (FI). The FI is, beside paralysis of extremities, one of the symptoms most profoundly affecting quality of life (QOL) in patients with SCI. We are reviewing current perspectives in management of SCI, discussing some pathophysiology mechanisms which could be addressed and pointing toward actual practical concepts in use for evaluation and improvements necessary to sustain SCI patients QOL. Keywords Spinal cord injury Bowel dysfunction Gastrointestinal dysfunction Fecal incontinence
Introduction Spinal cord-injured (SCI) patients have delayed colonic motility and severely impaired anorectal dysfunction resulting in functional obstruction, constipation, and fecal incontinence (FI) or a combination of all above mentioned [1]. We are here exploring pathogenesis, functional and
Y. Pan B. Liu (&) R. Li Z. Zhang L. Lu Department of Hand Surgery, The First Hospital of Jilin University, 1 Xinmin Street, Changchun 130021, People’s Republic of China e-mail: [email protected]
morphological pathology, and several approaches currently used in management of SCI. Traumatic SCI (TSCI) cases have standard definition as those involving any primary or secondary diagnosis of an acute traumatic lesion of the spinal cord or cauda equina using ICD-9-CM18 diagnosis codes 806.0–806.9 and 952.0–952.9, fulfilling the requirements of case definition for TSCI provided by the Centers for Disease Control and Prevention (CDC) [2]. Since it is not yet possible to treat initial cause in the SCI condition, all the treatments are of palliative nature, which are traditionally considered by different authors’ ‘‘time and resource consuming.’’ SCI Epidemiology By February 2013, data estimated annual incidence of SCI with exclusion those who die at the scene of accident are *40 cases per million persons in the U.S., which are in absolute number 12,000 new cases each year [3]. Approximately 250,000 Americans are living with the typically devastating neurological deficits and debilitating somatic and autonomic reflexes that develop in chronic SCI [2]. Regarding the overall prevalence, the number of people who are alive in 2013 and have SCI has been estimated to be *273,000 persons (range 238–332,000 persons) [1, 3]. These are incidence, and estimates obtained from different studies. The data from the National SCI Database are actively in surveillance from 1973, and in their estimate, 13 % of new SCI cases are in the U.S. being in database 29,096 persons who sustained SCI. Currently majority of SCI has trauma origin. The SCI has as chronic complications, and it is usually associated with additionally debilitating conditions presumed to be of the similar prevalence as in the general population. But current investigations found that it is highly probable that subclinical stages of
123
Cell Biochem Biophys
these chronic diseases may become overt with the onset of the SCI due to the stress associated with the trauma [4]. It has been reported that cardiovascular disease often remains undiagnosed in SCI patients due to their physical inactivity and impaired sensations, which increase the risk of disease progression and shorten overall survival [5–7]. Gastrointestinal symptoms usually present in SCI patients are constipation, fecal incontinence, and fecal impaction, later being one of the most common complications reported in 39 % of the patients [8]. Colorectal Physiology and Pathophysiology in SCI Spinal cord injury causes anorectal problems, whose pathophysiology still remains poorly characterized. A comprehensive method in evaluation of spino-anorectal function is still lacking. The neuropathophysiology of bowel dysfunction in SCI has been evaluated in different studies by motor-evoked potentials (MEP) of anus and rectum, trans-spinal magnetic stimulation, and anorectal physiology [8, 9]. Some previous studies of colorectal pathophysiology demonstrated that distension of the descending colon can be associated with an increase in rectal tone known as the ‘‘colorectal’’ reflex [10, 11]. Rectal distension provokes an opposite effect, and it reduces colonic tone and phase motor activity, being termed the ‘‘rectocolic’’ reflex. There are opposite findings on reflex reproducibility. While Law et al. [10] have shown that the rectocolic response is clear and reproducible, while colorectal response being more subtle, studies from Suttor et al. [11] demonstrated a clear and definitive colorectal response and a more variable rectocolic response. The exact neural pathways involved are unknown. Neither these reflexes in humans nor the role of the spinal cord is clear. Patients with complete SCI can be observed as human model of SCI and its neural pathways because of preserved local intrinsic pathways. It is important to emphasis necessity for additional studies of enteric motor reflexes in patients with SCI because of their clinical importance. Intestinal motor response to food ingestion has been well documented. Nevertheless, controversy remains regarding neural mechanisms involved. Several manometric studies explored colonic meal response in healthy subjects and SCI patients indicating a cephalic or central nervous system (CNS) response [12, 13]. Some of them failed to demonstrate a gastrocolonic response to sham feeding which is in favor of response independent of CNS involvement [14]. Findings of impaired colonic tonic response which correlates to the colonic motor response to meal ingestion have opposite tendency leaning toward perception of the CNS participation in the normal gastrocolonic response [15]. The gastrorectal response has been explored in relatively less number of studies, which when
123
summarized predominately explored healthy subjects [16] and only in small number SCI patients [17]. Evaluation Methods of Bowel Dysfunction in SCI Patients Prior to the management of bowel dysfunction, it is important to accurately evaluate it. There are a few methods known for such purpose. The colon transit time is known as an objective method for evaluating the motility of the colon [18]. The most widely used method in assessment of the bowel pattern is taking the clinical history. However, this can be highly variable since being dependable on patients’ subjective symptoms. It has been reported in the literature that people’s memory of their bowel habit is inaccurate in certain number of cases and has low index of correlation with the colon transit time, a proved objective method for its evaluation [19]. Since every method has its limitations, the inspectors must be aware of this possible miss interpretation in order to attain accuracy. Another simple and less time consuming method is plain abdominal radiography used for evaluating the distribution of faces in the colon and the visualization of the presence of megacolon. Its also has its limitation, and the colon transit time is for the moment the most objective method for evaluating the motility of the colon. Perhaps the main advantage of colon transit time is that it can evaluate total colon motility as well as segmental colon motility which is important in patients with SCI. In addition to the bowel patterns, the constipation score has to be evaluated according to the Rome II Diagnostic Criteria which includes projection of the bowel frequency (during one week period), the presence of straining, lumpy, or hard stools, the presence of incomplete evacuation sensation and sensation of anorectal obstruction, and the need for additional manual maneuvers to facilitate defecation. Morphological stool characteristics are also recorded as well [20]. Management of Fecal Incontinence in Spinal Cord Injury Initial management of FI includes, prior to clinical assessment, the evaluation of level of lesion. By these criteria, lesions can be divided into few groups: the first comprising cauda equina lesion (this occurs in settings of lumbar disk prolaps) or peripheral nerve lesion (in radical pelvic surgery), suprasacral spinal cord lesion occurring most frequently in trauma and group of suprapontine lesions characteristic for Parkinson disease [3, 21]. Clinical assessment commonly includes patients’ history (pre-morbid bowel function algorithm), physical and neurological examination, functional assessment, and basic
Cell Biochem Biophys
exam (stool exam and plain film abdomen if indicated). Finally thorough assessment also has to evaluate environmental factors which comprise toilet accessibility, assistive device, carrier’s support, and attitude-distance. Bowel function is usually assessed at baseline and at termination of analysis period using some of the current scoring systems such as the Cleveland Clinic Constipation Scoring System (CCCSS; 0–30, 30 severe symptoms), St. Mark’s Fecal Incontinence Grading System (FIGS; 0–24, 24 severe symptoms), and the Neurogenic Bowel Dysfunction score (NBD; 0–47, 47 severe symptoms) [22–25]. There are different modalities for treating FI in patients with SCI. Conservative treatments can include diet adjustments, medications, biofeedback, massage, transanal irrigation, electro-stimulation, and anal plug. But there has been established progressive nature of FI symptoms, finally needing different therapeutic options [26–30]. Clinical therapeutic options are colostomies, graciloplasties, artificial bowel sphincters, Malone anterograde continence enemas, and sacral anterior root implantation stimulators [31–34]. Based on presumed diagnosis, further treatment is applied. Though bowel dysfunction in overall population is not rare event and can be labeled as common complication of SCI, the number of studies addressing this issue is scarce. The importance of gas-trointestinal (GI) problems has been relatively ignored; perhaps, this can be explained by nonlife threatening nature of gastrointestinal motility symptoms and bowel dysfunction, since SCI patients have symptoms of the neurogenic bladder, common urinary complication, and respiratory problems too [35–38]. Anorectal dyssynergy demonstrates similarities in symptomatic phase to those seen in the bladder following SCI. Why is important to deal with this issue? In long-term management of patients with SCI, one of the most important problems that reduce the quality of life (QOL) and delays social adjustment is bowel dysfunction [39–42]. Furthermore, GI symptoms are more often associated with depression, anxiety, and significant impairments in QOL in a significant portion of persons with SCI [43, 44]. In conclusion, the long-term follow-up of patients’ postSCI needs the specialized management which includes patient education, an adequate fiber diet-oriented dietary adjustments, concomitant use of oral laxatives, suppositories, and other conservative treatment modalities [45]. Further studies with clear management protocols are needed to evaluate their utility. In periods of symptom progression and more severe symptoms, the trans-anal irrigation, the Malone appendicostomy, or a colostomy could be recommended [46]. To sustain patients QOL, an individually tailored approach modified from current-validated protocols should be applied taking into consideration whenever possible patient’s personal differences.
References 1. Chiu, W. T., Lin, H. C., Lam, C., et al. (2010). Review paper: epidemiology of traumatic spinal cord injury: comparisons between developed and developing countries. Asia-Pacific Journal of Public Health, 22, 9–18. 2. Hagen, E. M., Eide, G. E., Rekand, T., et al. (2010). A 50-year follow-up of the incidence of traumatic spinal cord injuries in Western Norway. Spinal Cord, 48, 313–318. 3. Selassie, A., Snipe, L., Focht, K. L., & Welldaregay, W. (2013). Baseline prevalence of heart diseases, hypertension, diabetes, and obesity in persons with acute traumatic spinal cord injury: potential threats in the recovery trajectory. Topics in Spinal Cord Injury Rehabilitation, 19(3), 172–182. doi:10.1310/sci1903-172. 4. ICD-9-CM. International Classification of Diseases, 9th rev. Clinical Modification. 3d edition, volumes 1, 2 and 3. (1990) Official authorized addendum effective October 1, 1990–HCFA. J Am Med Rec Assoc.61(8):suppl 1–35. 5. The University of Alabama at Birmingham Spinal Cord Injury Model System (UAB-SCIMS). http://www.spinalcord.uab.edu. Accessed 14 Oct 2013. 6. Thurman, D. J., Sniezek, J. E., et al. (1995). Guidelines for surveillance of central nervous system injury. Atlanta: Centers for Disease Control and Prevention. 7. Orakzai, S. H., Orakzai, R. H., Ahmadi, N., et al. (2007). Measurement of coronary artery calcification by electron beam computerized tomography in persons with chronic spinal cord injury: evidence for increased atherosclerotic burden. Spinal Cord, 45(12), 775–779. 8. Lee, C. S., Lu, Y. H., Lee, S. T., Lin, C. C., & Ding, H. J. (2006). Evaluating the prevalence of silent coronary artery disease in asymptomatic patients with spinal cord injury. International Heart Journal, 47(3), 325–330. 9. Christensen, P., Bazzocchi, G., Coggrave, M., Abel, R., Hultling, C., Krogh, K., et al. (2006). A randomized, controlled trial of transanal irrigation versus conservative bowel management in spinal cord-injured patients. Gastroenterology, 131(3), 738–747. 10. Law, N. M., Bharucha, A. E., & Zinsmeister, A. R. (2002). Rectal and colonic distension elicit viscerovisceral reflexes in humans. American Journal of Physiology-Gastrointestinal and Liver Physiology, 283, G384–G389. 11. Suttor, V. P., Ng, C., Rutkowski, S., Hansen, R. D., Kellow, J. E., & Malcolm, A. (2009). Colorectal responses to distension and feeding in patients with spinal cord injury. American Journal of PhysiologyGastrointestinal and Liver Physiology, 296(6), G1344–G1349. 12. Brading, A. F., & Ramalingam, T. (2006). Mechanisms controlling normal defecation and the potential effects of spinal cord injury. Progress in Brain Research, 152, 345–358. 13. Marino, R. J., Barros, T., Biering-Sorensen, F., et al. (2003). International standards for neurological classification of spinal cord injury. Journal of Spinal Cord Medicine, 26(suppl 1), S50–S56. 14. Sun, E. A., Snape, W. J, Jr, Cohen, S., & Renny, A. (1982). The role of opiate receptors and cholinergic neurons in the gastrocolonic response. Gastroenterology, 82, 689–693. 15. Bruninga, K., & Camilleri, M. (1997). Colonic motility and tone after spinal cord and cauda equina injury. American Journal of Gastroenterology, 92, 891–894. 16. Sloots, C. E., Felt-Bersma, R. J., Meuwissen, S. G., & Kuipers, E. J. (2003). Influence of gender, parity, and caloric load on gastrorectal response in healthy subjects: a barostat study. Digestive Diseases and Sciences, 48, 516–521. 17. Aaronson, M. J., Freed, M. M., & Burakoff, R. (1985). Colonic myoelectric activity in persons with spinal cord injury. Digestive Diseases and Sciences, 30, 295–300.
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Cell Biochem Biophys 18. Faaborg, P. M., Christensen, P., Rosenkilde, M., et al. (2011). Do gastrointestinal transit times and colonic dimensions change with time since spinal cord injury? Spinal Cord, 49, 549–553. 19. Krogh, K., Mosdal, C., & Laurberg, S. (2000). Gastrointestinal and segmental colonic transit times in patients with acute and chronic spinal cord lesions. Spinal Cord, 38, 615–621. 20. Krogh, K., & Christensen, P. (2009). Neurogenic colorectal and pelvic floor dysfunction. Best Practice & Research Clinical Gastroenterology, 23, 531–543. 21. Enck, P., Greving, I., Klosterhalfen, S., et al. (2006). Upper and lower gastrointestinal motor and sensory dysfunction after human spinal cord injury. Progress in Brain Research, 152, 373–384. 22. Lynch, A. C., Wong, C., Anthony, A., et al. (2000). 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. 23. Krogh, K., Christensen, P., Sabroe, S., et al. (2006). Neurogenic bowel dysfunction score. Spinal Cord, 44, 625–631. 24. Krogh, K., Perkash, I., Stiens, S. A., et al. (2009). International bowel function extended spinal cord injury data set. Spinal Cord, 47, 235–241. 25. Lin, V. W., & Cardenas, D. D. (2003). Spinal cord medicine: Principles and practice. New York: Demos. 26. Anderson, K. D. (2004). Targeting recovery: priorities of the spinal cord-injured population. Journal of Neurotrauma, 21, 1371–1383. 27. Krogh, K., Nielsen, J., Djurhuus, J. C., et al. (1997). Colorectal function in patients with spinal cord lesions. Diseases of the Colon and Rectum, 40, 1233–1239. 28. Glickman, S., & Kamm, M. A. (1996). Bowel dysfunction in spinal cord-injury patients. Lancet, 347, 1651–1653. 29. Krogh, K., Olsen, N., Christensen, P., et al. (2003). Colorectal transport during defecation in patients with lesions of the sacral spinal cord. Neurogastroenterology and Motility, 15, 25–31. 30. Christensen, P., Bazzocchi, G., Coggrave, M., et al. (2006). A randomized, controlled trial of transanal irrigation versus conservative bowel management in spinal cord-injured patients. Gastroenterology, 131, 738–747. 31. Krogh, K., Perkash, I., Stiens, S. A., et al. (2009). International bowel function basic spinal cord injury data set. Spinal Cord, 47, 230–234. 32. Juul, T., Bazzocchi, G., Coggrave, M., et al. (2011). Reliability of the international spinal cord injury bowel function basic and extended data sets. Spinal Cord, 49, 886–891.
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33. Spinal Cord Medicine Consortium. (1998). Clinical practice guidelines: neurogenic bowel management in adults with spinal cord injury. Journal of Spinal Cord Medicine, 21, 248–293. 34. Malone, P. S., Ransley, P. G., & Kiely, E. M. (1990). Preliminary report: the antegrade continence enema. Lancet, 336, 1217–1218. 35. Preziosi, G., & Emmanuel, A. (2009). Neurogenic bowel dysfunction: pathophysiology, clinical manifestations and treatment. Expert Review of Gastroenterology and Hepatology, 3, 417–423. 36. Worsøe, J., Christensen, P., Krogh, K., et al. (2008). Long-term results of antegrade colonic enema in adult patients: assessment of functional results. Diseases of the Colon and Rectum, 51, 1523–1528. 37. Coggrave, M., Wiesel, P. H., & Norton, C. (2006). Management of faecal incontinence and constipation in adults with central neurological diseases. Cochrane Database of Systematic Review, 19(2), CD002115. 38. Christensen, P., Andreasen, J., & Ehlers, L. (2009). Cost-effectiveness of transanal irrigation versus conservative bowel management for spinal cord injury patients. Spinal Cord, 47, 138–143. 39. Faaborg, P. M., Christensen, P., Kvitsau, B., et al. (2009). Long term outcome and safety of transanal colonic irrigation for neurogenic bowel dysfunction. Spinal Cord, 47, 545–549. 40. Christensen, P., Kvitzau, B., Krogh, K., et al. (2000). Neurogenic colorectal dysfunction—use of new antegrade and retrograde colonic wash-out methods. Spinal Cord, 38, 255–261. 41. Furlan, J. C., Urbach, D. R., & Fehlings, M. G. (2007). Optimal treatment for severe neurogenic bowel dysfunction after chronic spinal cord injury: a decision analysis. British Journal of Surgery, 94, 1139–1150. 42. Mowatt, G., Glazener, C., & Jarrett, M. (2008). Sacral nerve stimulation for fecal incontinence and constipation in adults: a short version Cochrane review. Neurourology and Urodynamics, 27, 155–161. 43. Branagan, G., Tromans, A., & Finnis, D. (2003). Effect of stoma formation on bowel care and quality of life in patients with spinal cord injury. Spinal Cord, 41, 680–683. 44. Randell, N., Lynch, A. C., Anthony, A., et al. (2001). Does a colostomy alter quality of life in patients with spinal cord injury? A controlled study. Spinal Cord, 39, 279–282. 45. Safadi, B. Y., Rosito, O., Nino-Murcia, M., et al. (2003). Which stoma works better for colonic dysmotility in the spinal cord injured patient? American Journal of Surgery, 186, 437–442. 46. Stone, J. M., Wolfe, V. A., Nino-Murcia, M., et al. (1990). Colostomy as treatment for complications of spinal cord injury. Archives of Physical Medicine and Rehabilitation, 71, 514–518.
REVIEW PAPER
Bowel Dysfunction in Spinal Cord Injury: Current Perspectives Yuehai Pan • Bin Liu • Ruijun Li • Zhixin Zhang Laijin Lu
•
Ó Springer Science+Business Media New York 2014
Abstract Permanent disruptions of gastrointestinal function are very common sequel of spinal cord injury (SCI). When motor and sensory nervous integrity are severely affected, neurogenic gastrointestinal dysfunction is an inevitable consequence. Autonomic nervous system miss function has significantly diminished or lost sensory sensations followed with incomplete evacuation of stool from the rectal vault, immobility, and reduced anal sphincter tone all of those predisposing to increased risk of fecal incontinence (FI). The FI is, beside paralysis of extremities, one of the symptoms most profoundly affecting quality of life (QOL) in patients with SCI. We are reviewing current perspectives in management of SCI, discussing some pathophysiology mechanisms which could be addressed and pointing toward actual practical concepts in use for evaluation and improvements necessary to sustain SCI patients QOL. Keywords Spinal cord injury Bowel dysfunction Gastrointestinal dysfunction Fecal incontinence
Introduction Spinal cord-injured (SCI) patients have delayed colonic motility and severely impaired anorectal dysfunction resulting in functional obstruction, constipation, and fecal incontinence (FI) or a combination of all above mentioned [1]. We are here exploring pathogenesis, functional and
Y. Pan B. Liu (&) R. Li Z. Zhang L. Lu Department of Hand Surgery, The First Hospital of Jilin University, 1 Xinmin Street, Changchun 130021, People’s Republic of China e-mail: [email protected]
morphological pathology, and several approaches currently used in management of SCI. Traumatic SCI (TSCI) cases have standard definition as those involving any primary or secondary diagnosis of an acute traumatic lesion of the spinal cord or cauda equina using ICD-9-CM18 diagnosis codes 806.0–806.9 and 952.0–952.9, fulfilling the requirements of case definition for TSCI provided by the Centers for Disease Control and Prevention (CDC) [2]. Since it is not yet possible to treat initial cause in the SCI condition, all the treatments are of palliative nature, which are traditionally considered by different authors’ ‘‘time and resource consuming.’’ SCI Epidemiology By February 2013, data estimated annual incidence of SCI with exclusion those who die at the scene of accident are *40 cases per million persons in the U.S., which are in absolute number 12,000 new cases each year [3]. Approximately 250,000 Americans are living with the typically devastating neurological deficits and debilitating somatic and autonomic reflexes that develop in chronic SCI [2]. Regarding the overall prevalence, the number of people who are alive in 2013 and have SCI has been estimated to be *273,000 persons (range 238–332,000 persons) [1, 3]. These are incidence, and estimates obtained from different studies. The data from the National SCI Database are actively in surveillance from 1973, and in their estimate, 13 % of new SCI cases are in the U.S. being in database 29,096 persons who sustained SCI. Currently majority of SCI has trauma origin. The SCI has as chronic complications, and it is usually associated with additionally debilitating conditions presumed to be of the similar prevalence as in the general population. But current investigations found that it is highly probable that subclinical stages of
123
Cell Biochem Biophys
these chronic diseases may become overt with the onset of the SCI due to the stress associated with the trauma [4]. It has been reported that cardiovascular disease often remains undiagnosed in SCI patients due to their physical inactivity and impaired sensations, which increase the risk of disease progression and shorten overall survival [5–7]. Gastrointestinal symptoms usually present in SCI patients are constipation, fecal incontinence, and fecal impaction, later being one of the most common complications reported in 39 % of the patients [8]. Colorectal Physiology and Pathophysiology in SCI Spinal cord injury causes anorectal problems, whose pathophysiology still remains poorly characterized. A comprehensive method in evaluation of spino-anorectal function is still lacking. The neuropathophysiology of bowel dysfunction in SCI has been evaluated in different studies by motor-evoked potentials (MEP) of anus and rectum, trans-spinal magnetic stimulation, and anorectal physiology [8, 9]. Some previous studies of colorectal pathophysiology demonstrated that distension of the descending colon can be associated with an increase in rectal tone known as the ‘‘colorectal’’ reflex [10, 11]. Rectal distension provokes an opposite effect, and it reduces colonic tone and phase motor activity, being termed the ‘‘rectocolic’’ reflex. There are opposite findings on reflex reproducibility. While Law et al. [10] have shown that the rectocolic response is clear and reproducible, while colorectal response being more subtle, studies from Suttor et al. [11] demonstrated a clear and definitive colorectal response and a more variable rectocolic response. The exact neural pathways involved are unknown. Neither these reflexes in humans nor the role of the spinal cord is clear. Patients with complete SCI can be observed as human model of SCI and its neural pathways because of preserved local intrinsic pathways. It is important to emphasis necessity for additional studies of enteric motor reflexes in patients with SCI because of their clinical importance. Intestinal motor response to food ingestion has been well documented. Nevertheless, controversy remains regarding neural mechanisms involved. Several manometric studies explored colonic meal response in healthy subjects and SCI patients indicating a cephalic or central nervous system (CNS) response [12, 13]. Some of them failed to demonstrate a gastrocolonic response to sham feeding which is in favor of response independent of CNS involvement [14]. Findings of impaired colonic tonic response which correlates to the colonic motor response to meal ingestion have opposite tendency leaning toward perception of the CNS participation in the normal gastrocolonic response [15]. The gastrorectal response has been explored in relatively less number of studies, which when
123
summarized predominately explored healthy subjects [16] and only in small number SCI patients [17]. Evaluation Methods of Bowel Dysfunction in SCI Patients Prior to the management of bowel dysfunction, it is important to accurately evaluate it. There are a few methods known for such purpose. The colon transit time is known as an objective method for evaluating the motility of the colon [18]. The most widely used method in assessment of the bowel pattern is taking the clinical history. However, this can be highly variable since being dependable on patients’ subjective symptoms. It has been reported in the literature that people’s memory of their bowel habit is inaccurate in certain number of cases and has low index of correlation with the colon transit time, a proved objective method for its evaluation [19]. Since every method has its limitations, the inspectors must be aware of this possible miss interpretation in order to attain accuracy. Another simple and less time consuming method is plain abdominal radiography used for evaluating the distribution of faces in the colon and the visualization of the presence of megacolon. Its also has its limitation, and the colon transit time is for the moment the most objective method for evaluating the motility of the colon. Perhaps the main advantage of colon transit time is that it can evaluate total colon motility as well as segmental colon motility which is important in patients with SCI. In addition to the bowel patterns, the constipation score has to be evaluated according to the Rome II Diagnostic Criteria which includes projection of the bowel frequency (during one week period), the presence of straining, lumpy, or hard stools, the presence of incomplete evacuation sensation and sensation of anorectal obstruction, and the need for additional manual maneuvers to facilitate defecation. Morphological stool characteristics are also recorded as well [20]. Management of Fecal Incontinence in Spinal Cord Injury Initial management of FI includes, prior to clinical assessment, the evaluation of level of lesion. By these criteria, lesions can be divided into few groups: the first comprising cauda equina lesion (this occurs in settings of lumbar disk prolaps) or peripheral nerve lesion (in radical pelvic surgery), suprasacral spinal cord lesion occurring most frequently in trauma and group of suprapontine lesions characteristic for Parkinson disease [3, 21]. Clinical assessment commonly includes patients’ history (pre-morbid bowel function algorithm), physical and neurological examination, functional assessment, and basic
Cell Biochem Biophys
exam (stool exam and plain film abdomen if indicated). Finally thorough assessment also has to evaluate environmental factors which comprise toilet accessibility, assistive device, carrier’s support, and attitude-distance. Bowel function is usually assessed at baseline and at termination of analysis period using some of the current scoring systems such as the Cleveland Clinic Constipation Scoring System (CCCSS; 0–30, 30 severe symptoms), St. Mark’s Fecal Incontinence Grading System (FIGS; 0–24, 24 severe symptoms), and the Neurogenic Bowel Dysfunction score (NBD; 0–47, 47 severe symptoms) [22–25]. There are different modalities for treating FI in patients with SCI. Conservative treatments can include diet adjustments, medications, biofeedback, massage, transanal irrigation, electro-stimulation, and anal plug. But there has been established progressive nature of FI symptoms, finally needing different therapeutic options [26–30]. Clinical therapeutic options are colostomies, graciloplasties, artificial bowel sphincters, Malone anterograde continence enemas, and sacral anterior root implantation stimulators [31–34]. Based on presumed diagnosis, further treatment is applied. Though bowel dysfunction in overall population is not rare event and can be labeled as common complication of SCI, the number of studies addressing this issue is scarce. The importance of gas-trointestinal (GI) problems has been relatively ignored; perhaps, this can be explained by nonlife threatening nature of gastrointestinal motility symptoms and bowel dysfunction, since SCI patients have symptoms of the neurogenic bladder, common urinary complication, and respiratory problems too [35–38]. Anorectal dyssynergy demonstrates similarities in symptomatic phase to those seen in the bladder following SCI. Why is important to deal with this issue? In long-term management of patients with SCI, one of the most important problems that reduce the quality of life (QOL) and delays social adjustment is bowel dysfunction [39–42]. Furthermore, GI symptoms are more often associated with depression, anxiety, and significant impairments in QOL in a significant portion of persons with SCI [43, 44]. In conclusion, the long-term follow-up of patients’ postSCI needs the specialized management which includes patient education, an adequate fiber diet-oriented dietary adjustments, concomitant use of oral laxatives, suppositories, and other conservative treatment modalities [45]. Further studies with clear management protocols are needed to evaluate their utility. In periods of symptom progression and more severe symptoms, the trans-anal irrigation, the Malone appendicostomy, or a colostomy could be recommended [46]. To sustain patients QOL, an individually tailored approach modified from current-validated protocols should be applied taking into consideration whenever possible patient’s personal differences.
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