Fecal Incontinence Anal continence depends on a complex interaction of cognitive, anatomic, neurologic, and physiologic mechanisms. The continence mechanism can often compensate for a deficiency in one of these processes, but it can be overwhelmed with increased severity or decreased function over time. Systemic etiologies of fecal incontinence often are due to disease states that cause diarrhea. The rapid transport of large volumes of liquid stool to the rectum can produce urgency and incontinence even in healthy individuals (28). Fecal incontinence frequently results from infectious diarrhea caused by bacteria (e.g., Clostridium, Escherichia coli, Salmonella, Shigella, Yersinia, Campylobacter), viruses (e.g., Rotavirus, Norwalk, HIV), and parasites (e.g., Entamoeba, Giardia, Cryptosporidium, Ascaris). Numerous medications and dietary items cause diarrhea and fecal incontinence (Table 28.3). Endocrine factors that can lead to fecal incontinence include diabetes mellitus and hyperthyroidism. With diabetes, diarrhea can develop from autonomic dysfunction, bacterial overgrowth, osmotic diarrhea with sugar substitutes, and pancreatic insufficiency. Inﬂammatory bowel disease is considered an idiopathic or autoimmune systemic factor. Ulcerative colitis and Crohn disease cause fecal incontinence during exacerbations with bouts of bloody diarrhea. Inﬂammatory bowel disease can also result in structural abnormalities, such as anal fissures, fistulas, abscesses, and operative complications that lead to fecal incontinence.
As with defecatory dysfunction, neurologic causes of fecal incontinence can be divided into central and peripheral disorders. Among the central nervous system disorders, upper motor neuron lesions above the level of the defecation center (located in the sacral cord) cause spastic bowel dysfunction. Cortical communication is disrupted, resulting in impaired cognitive control and sensory deficit. The anal sphincter is under spastic contraction, but digital stimulation can be performed to initiate reﬂex evacuation. Head trauma, neoplasms, and cerebral vascular accidents that damage portions of the frontal lobe result in loss of control of both micturition and defecation. Greater loss of inhibition is present when the lesion is located more anteriorly in the frontal lobe. Spinal cord trauma and lower motor neuron lesions above the defecation center tend to cause permanent loss of cortical control. For 2 to 4 weeks following spinal cord injury, “spinal shock” occurs, resulting in a temporary loss of reﬂexes below the level of the lesion, ﬂaccid bowel function, constipation, and fecal impaction. After the
Table 28.3 Drugs and Dietary Items Associated with Diarrhea
Dietetic foods, candy or chewing gum, and elixirs with sorbitol, mannitol, or xylitol initial shock, spastic paralysis ensues with hyperactive bowel function. The gastrocolic reﬂex, along with digital stimulation, initiates reﬂex evacuation in the absence of cortical inhibition. Fortunately, IAS tone is maintained despite the loss of EAS control for stress and urge situations. Both constipation and fecal incontinence can occur in these patients.