New concepts in the pathophysiology of fecal incontinence

The pathophysiology of fecal incontinence (FI) is often considered to primarily depend on disturbed mechanisms of faecal containment. Barrier mechanisms such as the anal sphincters and puborectalis muscle provide an easily comprehensible model for FI that satisfies some clinical observations in relation to risk, e.g., obstetric trauma, iatrogenic injury during anal surgery and diagnostic findings, e.g., anal contractile pressures and integrity on ultrasound evaluation. However, this barrier-centric containment model is insufficient to explain many lived observations of FI, including the origin of the symptom of urgency and continence development over the life course. It also fails to explain several other major risk factors such as rectal inflammation and irritable bowel syndrome, epidemiological (e.g., roughly equal prevalence in men) and treatment observations, i.e., the general failure of barrier augmentation vs. success of a treatment that does not overtly alter barrier closure [sacral neuromodulation (SNM)]. This review presents a revisionist view where reflex control of rectal contractility is considered central to FI pathogenesis and the anorectum is considered a single functional unit that cooperates with the colon and central nervous system (CNS) to maintain continence. This revised understanding implicates the barrier not only as a means of containment but also as a reflex controller of rectal function. Together, this serves as a much more adequate theory to explain human observations of the condition and a better starting point for the development of new treatments.