Abbreviations
AD
autonomic dysreflexia
BC
bowel care
CTT
colonic transit time
NBD
neurogenic bowel dysfunction
DRF
digital removal of feces
DRS
digital rectal stimulation
EAS
external anal sphincter
ENS
enteric nervous system
LMN
lower motor neuron
NB
neurogenic bowel
SARS
sacral anterior root stimulation
SC
spinal cord
SCI
spinal cord injury
UMN
upper motor neuron
Introduction
Spinal cord injury (SCI) results in loss of motor, sensory and autonomic functions, causing dysfunction of practically all body systems leading to long-term complications ( Table 1 ). Neurogenic bowel (NB) is one of these main impairments after spinal cord injury. It occurs because of changes in innervation of the colon and rectum, as well as the loss of voluntary control of the anal sphincter, affecting colonic motility and defecation maneuvers. Between 80% and 97% of people with SCI suffer at least one NB-related symptom ( ; ), mostly constipation and/or fecal incontinence, but also a prolonged and difficult defecation, sense of incomplete emptying, abdominal pain and distension, autonomic dysreflexia (AD), hemorrhoids, and rectal prolapse. Twenty-seven percent of the subjects considers that bowel dysfunction is a greater problem than bladder or sexual dysfunction, and 38% perceive it limits their quality of life (QoL) or social activities ( ).
| Respiratory complications a Atelectasis, pneumonia and respiratory failure |
| Cardiovascular complications b Orthostatic hypotension, autonomic dysreflexia, bradycardia |
| Neurogenic bladder |
| Neurogenic bowel |
| Sexual and fertility dysfunction |
| Spasticity c |
| Chronic pain Nociceptive pain Neuropathic pain: Above the level, at the level or below the level of injury |
| Secondary immunodeficiency d Increased susceptibility to infections |
| Osteoporosis Increased risk of low impact fractures |
| Neurogenic heterotopic ossification e |
| Pressure sores |
a Due to paralysis of the phrenic nerve, intercostal muscles and/or abdominal muscles leaving to reduced lung capacity and ineffective cough.
b Due to loss of supraspinal sympathetic control in patients with injury at T6 and above.
c Velocity-dependent increase in muscle tone with exaggerated deep tendon reflexes that results from injury to upper motor neurons.
d Systemic dysfunction of macrophages, T cells, B cells, and natural killer cells due to disruption of central nervous system input to immune organs.
e Ectopic bone formation in the connective tissue around joints.
The level of injury, severity, and presence or absence of sacral reflexes influences NB clinical manifestations and its management. Constipation and incontinence tend to become chronic and are stubborn toward currently available treatments, being a relevant source of complications. This, and the amount of time people with spinal injury spend on their bowel care, causes neurogenic bowel dysfunction (NBD) to have a very negative effect on QoL.
Characteristics of neurogenic bowel in spinal cord injury
Nervous control of the colon is done through the enteric, autonomic, and central nervous systems ( ; ). The enteric nervous system (ENS) is key for generating colonic propulsive activity. It functions independently, but is modulated by the spinal cord (SC) through the sympathetic fibers arising in the intermediolateral column of T5 to L3 and parasympathetic fibers that originate in segments S2 to S4. Sympathetic fibers inhibit colon motility, while parasympathetic fibers enable the contraction of the left colon, sigmoid, and rectum. The motor neurons in S2–S4 innervate the external anal sphincter (EAS), the puborectalis muscle, and the muscles of the pelvic floor; they receive voluntary control from motor neurons of the cerebral cortex and sensitive information from mechanoreceptors of the pelvic floor. SCI causes disturbances in autonomic and central innervation, and consequently loss of voluntary control of defecation, and changes in intestinal motility and sphincter tone. Various studies report a slowing of total and/or segmental colonic transit ( ; ), increased colonic wall tone, changes in rectal compliance ( ) and in sphincter tone and sensitivity, as well as lack of relaxation of the anal sphincter in response to rectal distension ( ). Although the function of the ENS remains, it has been shown there is loss of neurons and decrease of nerve fiber density in the myenteric plexus ( ) after SCI. The inflammatory process and changes of extrinsic innervation may alter neuromuscular structures of the colon and contribute to decrease bowel function ( ). Not much research has been carried out on the changes of gut microbiota; however, it may well be a contributing factor and thus a target of study for the development of new treatments ( ).
Based on the level of SCI, two bowel dysfunction patterns may be distinguished. Lesions over the medullary cone cause upper motor neuron NB syndrome or hyperreflexic bowel , in which case there is loss of supraspinal control, but reflex coordination and stool propulsion are preserved. This syndrome is characterized by the increase in the tone of colonic and anal wall, the sphincter remains its tone or it becomes hypertonic, and spasticity of pelvic floor muscles may occur. It associates with constipation and fecal retention; incontinence due to overflow or reflex relaxation of the anal sphincter may also develop. Lesions in the medullary cone and cauda equina cause lower motor neuron NB syndrome or areflexic bowel , in which case there is loss of supraspinal control, reflex activity mediated by the spinal cord, and the sphincter is hypotonic. Colonic peristalsis occurs only because of the activity of the ENS, which results in an increase of colonic transit time (CTT). The areflexic bowel is associated to constipation, less difficulty during defecation, and high risk of incontinence due to EAS atony.
Clinical manifestations
Constipation, fecal incontinence, pain, and abdominal distension are the main symptoms of NB in people with SCI. Constipation is associated with slowing colonic transit, failure to increase intra-abdominal pressure during defecation, absence of anal relaxation during the defecation, and increase of rectal and sigmoid compliance ( ; ). Immobility and use of drugs such as opioids or anti-cholinergics, also favor constipation ( ). Mean time for stool evacuation is longer, with 35% of SCI patients requiring more than an hour ( ; ). Fecal incontinence is associated with the loss of voluntary control of the anal sphincter, atonic or hypotonic sphincter, low rectal compliance, low anal pressure at rest, and uninhibited rectal contractions ( ; ; ). It has been more frequently reported in subjects with lower motor neuron NB than in upper motor neuron NB ( ). Inadequate bowel management and use of laxatives also favor incontinence.
Abdominal pain is a frequent symptom, emerging later than neuropathic pain (in average 4.2 years after the injury) ( ). Its prevalence is over 30% in chronic SCIs ( ). It characterizes for being diffuse; some patients describe it as a prick, itch, warmth, or burning. It is closely associated with constipation, it worsens or improves with bowel movement.
Abdominal distension and flatulence are symptoms linked with constipation and fecal impaction. Pathologies of the rectum and anus , such as hemorrhoids, prolapse, anal fissures, rectal ulcers, and rectal bleeding, are favored by digital rectal stimulation (DRS), manual rectal evacuation (MRE), and the use of suppositories and enemas. Fecal impaction, anal fissures, and defecation routine per se are stimuli that trigger autonomic dysreflexia ( ). Arterial hypertension may occur without accompanying symptoms that alert of AD (silent AD) ( ). The relevance of this lies on the fact that recurrent AD episodes associate with immunosuppression, involvement of cardiac mechanics, cerebrovascular changes, and cognitive impairment after SCI ( ).
It is easy to understand that NBD due to its clinical manifestations and complications, negatively affect physical and psychological well-being, with a significant association between NBD severity and impact on QoL ( ).
Diagnosis
The medical history is key to know the symptoms and their severity, patients’ pathological background, and the medication being received. It must include the presence of sensation of defecation, diet, physical activity, frequency of bowel movements, stool consistency, and tested strategies for bowel management. The Bristol scale is a useful instrument to assess stool consistency in a fast and simple way ( ). The time spent in bowel toileting is particularly relevant; reducing this time is one of the aims of treatment. Recording a diary of defecation by de patient will allow knowing the response to therapeutic measures. Uniformity in data collection is important when comparing results. The International SCI Bowel Function Basic Data Set ( ) gathers the basic data on bowel function following SCI that may be used in clinical practice.
Physical examination includes general, neurological, and abdominal inspection, as well as of the anorectal area. Other aspects to assess are the functional ability, balance in sitting position, and presence of spasticity. Examination of the anorectal area allows assessing the sensitivity, anal sphincter tone, and voluntary contraction. The presence of anal and bulbocavernosus sacral reflexes are indicative of anorectal reflex activity.
General blood tests are very useful to assess patients’ general condition, detect warning signs, or endocrine and metabolic disorders that may contribute to bowel dysfunction.
Plain abdominal X-ray is useful to assess the amount and distribution of stools in the colon and detect megacolon, fecal impaction, and volvulus.
Colonoscopy has the same indication as for the general population, although it requires a more intensive gut preparation than in subjects who are neurologically intact ( ).
Other tests not used routinely are the measurement of CTT (total and segmental) and anorectal manometry , which may help identify the primary physiopathological mechanism of the symptoms.
Assessment scales
Multiple scales allow measuring the symptoms in bowel dysfunction, primarily constipation and incontinence, as well as the impact it has on QoL, although few have been validated for the SCI population. The Cleveland Clinic Constipation Scoring System ( ) and the Wexner Continence Grading Scale ( ), are frequently used in studies with SCI patients. The 36-Item Short Form Survey ( ) and the Fecal Incontinence Quality of Life questionnaire ( ) are widely used instruments in QoL studies.
The Neurogenic Bowel Dysfunction Score ( Table 2 ) is a scale developed and validated specifically for adult SCI patients ( ). It allows scoring the clinical symptoms of colorectal and anal dysfunction; the importance of each item was established based on the strength of its association with self-perceived QoL. The greater the scoring, the greater the impact on QoL ( ).
| Items | Points |
|---|---|
| (1) Frequency of defecation | |
| Daily (0) Two to six times every week (1) Less than once a week (6) | |
| (2) Time used for each defecation | |
| 0–30 min (0) 31–60 min (3) More than 1 h (7) | |
| (3) Uneasiness, headache, or perspiration during defecation | |
| No (0) Yes (2) | |
| (4) Regular use of tablets against constipation | |
| No (0) Yes (2) | |
| (5) Regular use of drops against constipation | |
| No (0) Yes (2) | |
| (6) Digital stimulation or evacuation of the anorectum | |
| Less than once every week (0) Once or more every week (6) | |
| (7) Frequency of fecal incontinence | |
| Less than once every month (0) One to four times every month (6) One to six times every week (7) Daily (13) | |
| (8) Medication against fecal incontinence | |
| No (0) Yes (4) | |
| (9) Flatus incontinence | |
| No (0) Yes (2) | |
| (10) Perianal skin problems | |
| No (0) Yes (3) | |
| Total NBD score (range 0–47) | |
| NBD score | Bowel dysfunction |
|---|---|
| 0–6 | Very minor |
| 7–9 | Minor |
| 10–13 | Moderate |
| 14 or more | Severe |
Conservative treatment of the neurogenic bowel
General recommendations
First, it is convenient to check the medications the patient is taking and make adjustments on those that might be contributing to the symptoms. Analgesics, anti-cholinergics, anti-depressants, and anti-psychotics, as well as iron supplements and aluminum compounds, which favor constipation. Excessive use of laxatives favors fecal incontinence, abdominal pain, and flatulence. Assessing the eating habits of the patient is also important.
Diet
Stool volume and consistency can be regulated through diet. Low fluid intake increases the probability of suffering constipation. On the other hand, high intake (> 2 L/day), may be associated with prolonged bowel care ( ). Recommendation on fluid intake should be tailored and balanced with the type of bladder management.
Fiber helps increase fecal mass and its capacity to retain water. Consequently, colonic transit is accelerated and feces become softer. Although there are no accepted recommendations for SCI, an initial daily intake of 15 g of dietary fiber is suggested, monitoring the effect, and if necessary, increase the amount of fiber slowly and gradually, taking into account that high-fiber diets (30 g/day) may increase CTT in these patients ( ).
Physical exercise
Regular physical exercise may improve constipation symptoms, as it affects bowel motility, speeding up the colonic and gut transit time, and stimulates abdominal muscles helping move fecal matter toward the rectum ( ). In people with SCI, standing seems to improve bowel function, although this has not been demonstrated in clinical trials ( ).
Abdominal massage
The mechanisms suggested to explain the effect of abdominal massage on the bowel are the increase of abdominal pressure and improvement of peristalsis. It may be performed during bowel routine to help pass stool. Fifteen minutes of abdominal massage following digital stimulation, decreases CTT, abdominal distension and fecal incontinence, and increases the frequency of defecation ( ). Similarly, electrical stimulation of the abdominal muscles during the bowel care program shortens the time until the feces come out and total time of bowel care ( ).
Mechanical techniques to ease bowel movements
Digital rectal stimulation (DRS) dilates the anal canal relaxing the puborectalis muscle, which reduces the resistance of stool to come out, triggers rectal contraction, and increases contractile activity of the descending and sigmoid colon ( ). Manual rectal evacuation (MRE) of feces is the most frequent form of bowel evacuation in some series ( ; ). It is often the only effective way to empty the bowel in patients with areflexic bowel. In subjects with reflex function, MRE may be necessary to complete the emptying process ( ) ( Table 3 ).
| Mechanical interventions |
|---|
| Digital rectal stimulation |
| Manual evacuation (digital removal of feces) |
| Pharmacological interventions | |||
|---|---|---|---|
| Presentation | Mechanism of action | Characteristics | |
| Glycerine | Suppositories, microenemas (5–10 mL) | Stimulant and osmotic laxative | Effective in 15–30 min Side effects: Irritation, stinging, anal itching |
| Bisacodyl (with a polyethylene glycol base or a hydrogenated vegetable oil base) | Suppositories | Stimulant laxative | Effective in 10–30 min Side effects: Abdominal pain and diarrhea |
| Docusate sodium or calcium | Microenemas (5–10 mL) | Stool softener | Effective in 2–15 min |
| Sodium citrate, sodium lauryl sulfoacetate, sorbitol | Microenemas (5–10 mL) | Osmotic laxative | Effective in 5–15 min Side effects: Abdominal pain and diarrhea |
| Sodium phosphate | Enemas (80, 140, 250 mL) | Saline laxative | Effective in 1–5 min Side effects: Abdominal bloating and pain, vomiting, renal impairment |
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