Bowel dysfunction in spinal cord injury

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 ( ).

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.

Conservative treatment of the neurogenic bowel