The colon, anorectum, and spinal cord patient. A review of the functional alterations of the denervated hindgut.

As humans have become more mechanized, the number of persons sustaining spinal cord injuries resulting in quadriplegia or paraplegia has increased. Because colorectal function is modulated by a combination of neural, hormonal, and luminal influences, many of the normal regulatory mechanisms remain intact in patients with spinal cord injuries. Management of these patients, however, requires an understanding of altered function in the denervated hindgut. The foregut and midgut are innervated by parasympathetic fibers in the vagus and sympathetic fibers from the lower six thoracic vertebra. In contrast, the hindgut is innervated by parasympathetic fibers arising from the sacral plexus and sympathetic fibers from the lumbar spinal column. Consequently, in most spinal cord injuries, the foregut and midgut remain normally innervated whereas the hindgut looses input from cerebral and spinal cord sources. In high cord lesions this results in decreased colonic motility. In low cord injuries there is loss of inhibitory influences that normally down-regulate left colonic and rectosigmoid sphincter activity. This increased motility causes a loss of left colonic compliance and increases left colonic transit, thus leading to chronic constipation. At the same time in both high and low cord injuries, reflex activity of the anorectum is left unregulated by cerebral input. Once stimulated by distention, the rectum spontaneously evacuates its contents. Thus, fecal impaction and incontinence in these patients principally results from loss of inhibitory influences on rectosigmoid sphincter activity and on rectal reflex activity.