![]() The majority of patients present in their late 50s when combined exposures to risks, e.g., serial pregnancy, childbirth, and age are sufficient to compromise normal function. Risk factors for FIįI can result from a single catastrophic event such as major anorectal injury, but more commonly develops from accumulated risks ( Table 1). This review questions current dogma and proposes a new approach. While most new developments in medicine now arise from targeting defined disease mechanisms, progress for FI has been limited by poor understanding of pathophysiology and a dependence on looking for, and trying to treat, the obvious ( 2). It is not necessarily accompanied by urinary leakage, although the two disorders often occur together. FI may consist of feces of normal consistency, only liquid form, or mostly of flatus. ![]() Received: 10 November 2021 Accepted: 29 April 2022 Published: 30 April 2022.įecal incontinence (FI) defined as the recurrent uncontrolled passage of feces ( 1) is a relatively common condition with considerable unmet needs in terms of effective treatments. Keywords: Anal sphincter disease pathophysiology fecal incontinence (FI) incontinence pudendal nerve 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. This revised understanding implicates the barrier not only as a means of containment but also as a reflex controller of rectal function. 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. success of a treatment that does not overtly alter barrier closure. 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. 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. 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. Policy of Dealing with Allegations of Research MisconductĪbstract: The pathophysiology of fecal incontinence (FI) is often considered to primarily depend on disturbed mechanisms of faecal containment.Policy of Screening for Plagiarism Process.
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