Pathy's Principles and Practice of Geriatric Medicine. Группа авторов

internal anal sphincter is a circular muscle layer that starts from the rectum. The internal anal sphincter is contracted at rest, preventing the involuntary loss of stool and gas. The pressure at the anus is increased by the presence of anal cushions, along with the muscular tone of the internal and external anal sphincters and puborectalis. The internal anal sphincter contributes 50–85% of the resting tone of the sphincter complex, with the external anal sphincter contributing 25–30% and the remaining 15% coming from the anal cushions.¹¹ The puborectalis forms a sling around the rectum and, when contracted, causes the anorectal angle to form. The external sphincter comprises striated muscle and is under voluntary control; the internal sphincter is formed from smooth muscle and is under the control of the autonomic system. At rest, the anus forms an angle of approximately 90° to the rectum. In the normal state, the rectum is empty¹²; it is an organ of expulsion, not of storage.

      Defecation

As stool is passed into the rectum by peristalsis, the rectal pressure increases, and the internal anal sphincter pressure constricts and then relaxes. A small quantity of rectal contents is passed into the anal canal, where the composition of the stool – solid, liquid, or gaseous – is assessed by sensory receptors in the anal epithelium.¹³ If convenient and socially appropriate, once the individual has reached appropriate facilities and disrobed, the process of defecation begins. A seated or squatting position straightens the anorectal angle to ease the passage of stool.¹⁴ The pelvic floor is relaxed, and there is an involuntary increase in colorectal motor activity combined with a voluntary Valsalva manoeuvre, which leads to rectal pressure being higher than anal pressure, allowing stool to pass. The differential in pressure required to allow the stool to pass is a function of stool consistency, with higher pressure needed to pass hard type 1 stool compared to softer or liquid stool¹⁵; by extension, liquid stool is more difficult to contain.

Changes relating to ageing

      Healthy ageing is associated with a linear reduction in strength of voluntary anal squeeze from the seventh decade in women and the ninth in men,¹⁶ and rectal sensation may also decrease with age with a rise in anorectal sensitivity thresholds.¹⁷ Imaging studies suggest that the anal sphincter decreases in thickness with age,¹⁸ but the functional significance of this change is unknown. Rectal sensory thresholds may also decrease with ageing in healthy older adults without associated changes in compliance or tone,¹⁹ with 30% fewer enteric neurons and greater fatty tissue deposition in those over 65 compared to those under 30.²⁰ These changes may impair the ability to distinguish stool from flatus. Although not measured in clinical practice, there is an increase in pudendal nerve latency in older women,¹⁹ and it is unclear if rectal motility is affected by normal ageing.²¹ Studies in older people suggest that both antibiotic use and diet affect the microbiome and metabolome²² and that the frail and those living in institutions have less diverse microbiota than community‐dwelling older people.²³ The extent to which these changes influence faecal incontinence or can guide therapeutic interventions is unknown and represents a significant gap and opportunity in the research base.

Epidemiology of faecal incontinence

      Prevalence

      Faecal incontinence is under‐reported by sufferers, and as such, it is challenging to collect accurate prevalence data. In a US representative sample of 2229 women and 2079 men, Whitehead and colleges reported a prevalence of faecal incontinence (defined as any involuntary loss of mucous, liquid, or solid stool in the preceding month) of 15.3% in the over‐75 age group.²⁴ In New Zealand, Sharma et al. surveyed 2000 adults by post, with an average age of 51.6: 14.7% of participants ‘felt they had a problem with bowel control’, and 12.4% had faecal incontinence when defined using the Faecal Incontinence Severity Index table as ‘leakage of liquid or solid stool ≥ 1/month’.²⁵ A systematic review in 2016 synthesized 30 trials, reporting a prevalence of monthly FI of 8.3–8.4% in face‐to‐face or telephone interviews and 11.2–12.4% for postal surveys. Age‐stratified data were not reported.²⁶ The prevalence among those living in long‐term care is unsurprisingly higher, with a recent systematic review reporting rates between 10 and 70% using a wide variety of data‐collection tools and case definitions. The median prevalence in all studies was 42%.²⁷ In younger people, the prevalence of faecal incontinence is higher in women, largely driven by obstetric anal sphincter injury (OASIS), but this differential disappears in older age.²⁸ Faecal and urinary incontinence frequently co‐exist, and those presenting with urinary incontinence should be asked specifically about bowel control and faecal incontinence.

Correlates and risk factors

      Gastrointestinal disorders

      Stool consistency is one of the primary contributors to faecal continence. As seen earlier, loose or liquid stool is more difficult to retain than formed stool, and an acute diarrhoeal illness can induce faecal incontinence in even healthy individuals; one study reported an odds ratio for faecal incontinence of 53 with diarrhoea.²⁹ Both loose and hard stool can contribute to faecal incontinence in older people, with faecal impaction with associated diarrhoea being strongly associated with faecal incontinence in hospitalized older people³⁰. Irritable bowel syndrome has also been associated with faecal urgency and incontinence, with diarrhoea, loose stool, increased colonic transit time, and increased rectal sensitivity all potential mechanisms.

      Injury to the anal sphincter complex itself or its pudendal nerve supply through childbirth (OASIS),³¹ sexual activity,³² or surgery, including haemorrhoidectomy, anal fissure repair, or anal dilatation³³ may disrupt the functioning of the sphincter and lead to faecal incontinence, often many years from the event. Rectal prolapse, the protrusion of rectal mucosa through the anus, is also associated with FI, with up to two‐thirds of those with complete rectal prolapse experiencing some leakage.³⁴ Other GI conditions, including inflammatory bowel disease, coeliac disease, and bile salt malabsorption, should also be considered.

      Non‐GI risk factors

      Numerous illnesses not directly involving the GI tract have been shown to be associated with the development of faecal incontinence.

      Neurological

Parkinson’s disease is associated with significant bowel dysfunction. More people with Parkinson’s complain of infrequent passage of stool (<3/week), difficulty passing stool, and loose stool than in the general population,³⁵ but without a greater prevalence of faecal incontinence than people of a similar age without Parkinson’s disease.³⁶ Similarly, multiple sclerosis is associated with a high prevalence of constipation and dysfunctional voiding, and half of those in a study in 1990 reported faecal incontinence in the preceding three months.³⁷ Treatments for muscle spasticity in MS, such as baclofen, are also associated with faecal incontinence and should be taken into account.³⁸ Only one in three young people with spina bifida report normal bowel function,³⁹ and with the passage of time, this group will become of interest to geriatricians.

      Spinal cord injury, be it traumatic or (more commonly in older adults) metastatic, can commonly lead to faecal incontinence. A cord injury below T12 leads to a lower motor neuron syndrome or areflexic bowel due to impaired parasympathetic function and reduced peristalsis. By contrast, a cord lesion below T12 leads to increased anal tone and the inability to relax the external sphincter, resulting in faecal impaction.⁴⁰ A patient presenting with acute faecal incontinence should always raise the possibility of spinal cord injury. The impact of dementia and cognitive impairment is discussed in the section ‘Geriatric Syndromes’.

      Endocrine, diabetes, and metabolic

      Obesity has been shown to be associated with faecal incontinence in women in some studies,^41,42 and weight loss through bariatric