Jump to content
Main menu
Main menu
move to sidebar
hide
Navigation
Main page
Recent changes
Random page
Help about MediaWiki
Special pages
Niidae Wiki
Search
Search
Appearance
Create account
Log in
Personal tools
Create account
Log in
Pages for logged out editors
learn more
Contributions
Talk
Editing
Fecal incontinence
(section)
Page
Discussion
English
Read
Edit
View history
Tools
Tools
move to sidebar
hide
Actions
Read
Edit
View history
General
What links here
Related changes
Page information
Appearance
move to sidebar
hide
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
== Causes == FI is a sign or a symptom, not a diagnosis,<ref name="NICE guidelines" /> and represents an extensive list of causes. Usually, it is the result of a complex interplay of several coexisting factors, many of which may be simple to correct.<ref name="NICE guidelines"/> Up to 80% of people may have more than one abnormality that is contributing.<ref>{{cite book| veditors = Abrams P |display-editors=etal |title=Incontinence : 4th International Consultation on Incontinence, Paris, July 5-8, 2008|year=2009|publisher=Health Publications|location=[Paris]|isbn=978-0-9546956-8-2|edition=4th|page=255|chapter=Pathophysiology of Urinary Incontinence, Faecal Incontinence and Pelvic Organ Prolapse}}</ref> Deficits of individual functional components of the continence mechanism can be partially compensated for a certain period, until the compensating components themselves fail. For example, [[obstetric]] injury may precede onset by decades, but [[menopause|postmenopausal]] changes in the tissue strength reduce in turn the competence of the compensatory mechanisms.<ref name="ASCRS core subjects FI" /><ref name="Coloproctology textbook" /> The most common factors in the development are thought to be obstetric injury and after-effects of anorectal surgery, especially those involving the anal sphincters and hemorrhoidal vascular cushions.<ref name="ASCRS core subjects FI" /> The majority of incontinent persons over the age of 18 fall into one of several groups: those with structural anorectal abnormalities (sphincter [[Trauma (medicine)|trauma]], sphincter degeneration, [[Anal fistula|perianal fistula]], rectal prolapse), [[neurological disorder]]s ([[multiple sclerosis]], [[spinal cord]] injury, [[spina bifida]], [[stroke]], etc.), constipation or [[fecal loading]] (presence of a large amount of feces in the rectum with stool of any consistency), cognitive or behavioral dysfunction ([[dementia]], [[learning disability|learning disabilities]]), diarrhea, [[inflammatory bowel disease]]s (e.g. ulcerative colitis, Crohn's disease), irritable bowel syndrome, [[disability]] related (people who are frail, acutely unwell, or have [[Chronic (medicine)|chronic]] or [[Acute (medicine)|acute]] disabilities), and those cases which are [[idiopathic]] (of unknown cause).<ref name="NICE guidelines">{{cite book|last=(UK)|first=National Collaborating Centre for Acute Care|title=Faecal incontinence the management of faecal incontinence in adults|year=2007|publisher=National Collaborating Centre for Acute Care (UK)|location=London|isbn=978-0-9549760-4-0|url=https://www.ncbi.nlm.nih.gov/books/NBK50665/|series=National Institute for Health and Clinical Excellence: Guidance}}</ref><ref name="Nusrat 2012">{{cite journal | vauthors = Nusrat S, Gulick E, Levinthal D, Bielefeldt K | title = Anorectal dysfunction in multiple sclerosis: a systematic review | journal = ISRN Neurology | volume = 2012 | pages = 376023 | year = 2012 | pmid = 22900202 | pmc = 3414061 | doi = 10.5402/2012/376023 | doi-access = free }}</ref> [[Diabetes mellitus]] is also known to be a cause, but the mechanism of this relationship is not well understood.<ref name="Rodrigues 2012">{{cite journal | vauthors = Rodrigues ML, Motta ME | title = Mechanisms and factors associated with gastrointestinal symptoms in patients with diabetes mellitus | journal = Jornal de Pediatria | volume = 88 | issue = 1 | pages = 17β24 | date = JanβFeb 2012 | pmid = 22344626 | doi = 10.2223/jped.2153 | doi-broken-date = 18 January 2025 | doi-access = free }}</ref> === Childbirth === Vaginal delivery causes stretching of the pelvic muscles<ref name="Leslie2024">{{cite book | vauthors = Leslie SW, Antolak S, Feloney MP, Soon-Sutton TL | chapter =Pudendal Neuralgia |date=2024 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK562246/ | title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=32965917}}</ref> and the pudendal nerve. Obstetric injury is a leading cause of fecal incontinence.<ref name="Kumar2017">{{cite journal |last1=Kumar |first1=L |last2=Emmanuel |first2=A |date=August 2017 |title=Internal anal sphincter: Clinical perspective. |journal=The Surgeon: Journal of the Royal Colleges of Surgeons of Edinburgh and Ireland |volume=15 |issue=4 |pages=211β226 |doi=10.1016/j.surge.2016.10.003 |pmid=27881288}}</ref> Obstetric injury may tear the anal sphincters, and some of these injuries may be occult (undetected). The risk of injury is greatest when labor has been especially difficult or prolonged, when [[Forceps in childbirth|forceps]] are used, with higher [[birth weight]]s, or when a midline [[episiotomy]] is performed. Only when there is post-operative investigation of FI such as [[endoanal ultrasound]] is the injury discovered.<ref name="ASCRS textbook" /> Vaginal birth may lead to pudendal nerve damage. The pudendal nerve may sustain irreversible injury if it is stretched more than 12% of its original length.<ref name="Steele2021">{{cite book | vauthors = Steele SR, Hull TL, Hyman N, Maykel JA, Read TE, Whitlow CB |title=The ASCRS Textbook of Colon and Rectal Surgery |date=20 November 2021 |publisher=Springer Nature |location=Cham, Switzerland |isbn=978-3-030-66049-9 |edition=4th |language=en}}</ref><ref name="Clark2023">{{cite book |editor1-last=Clark |editor1-first=S |title=Colorectal Surgery: A Companion to Specialist Surgical Practice |date=31 October 2023 |publisher=Elsevier |isbn=978-0-7020-8501-7 |page=6 |language=en}}</ref> The nerve is especially vulnerable to stretch damage during childbirth because of the course of the nerve,<ref name="Kinter2023" >{{cite book | vauthors = Kinter KJ, Newton BW | chapter = Anatomy, Abdomen and Pelvis, Pudendal Nerve |date=2023 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK554736/|title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=32134612|access-date=2021-07-30}}</ref> as it runs in close proximity to pelvic muscles (piriformis and coccygeus) and ligaments, before exiting and then re-entering the pelvic cavity.<ref name="Kaur_2021" >{{cite book | vauthors = Kaur J, Singh P | chapter = Pudendal Nerve Entrapment Syndrome|date=2023| chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK544272/| title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=31334992|access-date=2021-07-29}}</ref> The damage is likely to occur at the exit from the pudendal canal, because the course of the nerve is relatively fixed at this point.<ref name="Docimo2022">{{cite book |editor1-last=Docimo |editor1-first=L |editor2-last=Brusciano |editor2-first=L |title=Anal Incontinence: Clinical Management and Surgical Techniques |series=Updates in Surgery |date=2023 |publisher=Springer International Publishing |isbn=978-3-031-08391-4 |pages=14,192 |doi=10.1007/978-3-031-08392-1 |url=https://link.springer.com/book/10.1007/978-3-031-08392-1 |language=en}}</ref> Stretching occurs during delivery, especially from the child's head.<ref name="Leslie2024" /> The risk increases when delivering larger-than-average babies or with [[prolonged labour|prolonged]] (especially [[Childbirth#Second stage: fetal expulsion|second stage]]) or [[Obstructed labour|difficult labour]].<ref name="Leslie2024" /> The risk of damage to the pudendal nerve is also higher if [[obstetrical forceps]] are used.<ref name="Rao2015">{{cite book |editor1-last=Rao |editor1-first=SSC |editor2-last=Parkman |editor2-first=HP |editor3-last=McCallum |editor3-first=RW |title=Handbook of gastrointestinal motility and functional disorders |date=2015 |publisher=SLACK Incorporated |location=Thorofare, NJ |isbn=978-1-61711-818-0 |page=285 |language=en}}</ref> 60% of females who sustained [[Perineal tear|obstetric tear]]s were demonstrated to also have pudendal nerve damage.<ref name="Steele2020">{{cite book |last1=Steele |first1=SR |last2=Maykel |first2=JA |last3=Wexner |first3=SD |title=Clinical Decision Making in Colorectal Surgery |date=11 August 2020 |publisher=Springer International Publishing |isbn=978-3-319-65941-1 |page=256 |language=en}}</ref> Any damage to the pudendal nerve occurring during childbirth may not become fully apparent until years later, for example at the onset of [[menopause]].<ref name="Clark2023" /> ===Surgery=== FI is a much under-reported complication of surgery. The IAS is easily damaged with an anal [[surgical retractor|retractor]] (especially the [[Park's anal retractor]]), leading to reduced resting pressure postoperatively. Since the hemorrhoidal vascular cushions contribute 15% of the resting anal tone, surgeries involving these structures may affect continence status.<ref name="ASCRS textbook" /> Partial internal [[sphincterotomy]], [[fistulotomy]], anal stretch ([[Lord's operation]]), [[hemorrhoidectomy]] or transanal advancement flaps may all lead to FI postoperatively, with soiling being far more common than solid FI. The "keyhole deformity" refers to scarring within the anal canal and is another cause of mucus leakage and minor incontinence. This defect is also described as a groove in the anal canal wall and may occur after posterior midline [[fissurectomy]] or fistulotomy, or with lateral IAS defects.<ref name="ASCRS textbook" /> There is increased risk of FI after [[radical prostatectomy]] for [[prostate cancer]].<ref>{{Cite journal |last1=Shamliyan |first1=Tatyana A. |last2=Bliss |first2=Donna Z. |last3=Du |first3=Jing |last4=Ping |first4=Ryan |last5=Wilt |first5=Timothy J. |last6=Kane |first6=Robert L. |date=2009 |title=Prevalence and risk factors of fecal incontinence in community-dwelling men |url=https://pubmed.ncbi.nlm.nih.gov/20065920/ |journal=Reviews in Gastroenterological Disorders |volume=9 |issue=4 |pages=E97β110 |issn=1949-4386 |pmid=20065920}}</ref> === Anal sphincter weakness === The anal canal presents the final barrier to continence. The resting tone of the anal canal is not the only important factor; both the length of the high-pressure zone and its radial translation of force are required for continence. This means that even with normal anal canal pressure, focal defects such as the [[Keyhole defect|keyhole deformity]] can be the cause of substantial symptoms. [[External anal sphincter]] (EAS) dysfunction is associated with impaired voluntary control, whereas [[internal anal sphincter]] (IAS) dysfunction is associated with impaired fine-tuning of fecal control.<ref name="ASCRS core subjects FI" /> Defects of the external anal sphincter are associated with urge incontinence.<ref name="Desprez2021">{{cite journal |last1=Desprez |first1=C |last2=Turmel |first2=N |last3=Chesnel |first3=C |last4=Mistry |first4=P |last5=Tamiatto |first5=M |last6=Haddad |first6=R |last7=Le Breton |first7=F |last8=Leroi |first8=AM |last9=Hentzen |first9=C |last10=Amarenco |first10=G |title=Comparison of clinical and paraclinical characteristics of patients with urge, mixed, and passive fecal incontinence: a systematic literature review. |journal=International Journal of Colorectal Disease |date=April 2021 |volume=36 |issue=4 |pages=633β644 |doi=10.1007/s00384-020-03803-8 |pmid=33210162}}</ref> The external anal sphincter is supplied by the pudendal nerve. Damage to the nerve supply of the external anal sphincter on one side may not result in severe symptoms because there is substantial overlap in innervation by the nerves on the other side.<ref name="ASCRS textbook" /><!-- page 5 --> The internal anal sphincter receives extrinsic autonomic innervation via the [[inferior hypogastric plexus]], with sympathetic innervation derived from spinal levels L1-L2, and parasympathetic innervation derived from S2-S4.<ref name=":224" >{{Cite book |last=Standring |first=Susan |url=https://www.worldcat.org/oclc/1201341621 |title=Gray's Anatomy: The Anatomical Basis of Clinical Practice |year=1201 |isbn=978-0-7020-7707-4 |edition=42th |location=New York |pages=683 |oclc=1201341621}}</ref> Disruption of the function of the internal anal sphincter results in reduced resting pressure in the anal canal. This is associated with passive leakage.<ref name="Desprez2021" /> [[Lesion]]s which mechanically interfere with, or prevent the complete closure of the anal canal can cause a liquid stool or mucous [[rectal discharge]]. Such lesions include [[Hemorrhoid|piles]] (inflamed hemorrhoids), [[anal fissure]]s, [[anal cancer]], or fistulae.<ref name="ASCRS textbook" /> Nontraumatic conditions causing anal sphincter weakness include [[scleroderma]], damage to the [[pudendal nerve]]s, and IAS degeneration of unknown cause.<ref name="Yamada textbook" /> === Pelvic floor weakness and pudendal neuropathy=== Many people with FI have a generalized weakness of the [[pelvic floor]], especially [[puborectalis]].<ref name="Yamada textbook" /> A weakened puborectalis leads to widening of the anorectal angle and impaired barrier to the stool in the rectum entering the anal canal, and this is associated with incontinence to solids. Abnormal descent of the pelvic floor can also be a sign of pelvic floor weakness. Abnormal descent manifests as [[descending perineum syndrome]] (>4 cm perineal descent).<ref name="Yamada textbook" /> This syndrome initially gives constipation, and later FI. The pelvic floor is innervated by the [[pudendal nerve]] and the [[Sacral spinal nerve 3|S3]] and [[Sacral spinal nerve 4|S4]] branches of the [[pelvic plexus]]. With recurrent straining, e.g. during difficult labour or long-term constipation, then stretch injury can damage the nerves supplying [[levator ani]]. If the pelvic floor muscles lose their innervation, they cease to contract and their muscle fibres are in time replaced by fibrous tissue, which is associated with pelvic floor weakness and incontinence. Increased pudendal nerve terminal motor latency may indicate pelvic floor weakness.<ref name="Clark2023" /> Pudendal neuropathy (nerve damage) is detectable in up to 70% of people with FI.<ref name="Schlachta2018">{{cite book |editor1-last=Schlachta |editor1-first=CM |editor2-last=Sylla |editor2-first=P |title=Current Common Dilemmas in Colorectal Surgery |date=22 December 2018 |publisher=Springer International Publishing |isbn=978-3-030-09934-3 |page=160 |url=https://books.google.com/books?id=TvrmwQEACAAJ |language=en}}</ref> ===Obstructed defecation (incomplete evacuation of stool)=== Normal evacuation of rectal contents is 90{{ndash}}100%.<ref name="ASCRS textbook" /> If there is incomplete evacuation during defecation, residual stool will be left in the rectum and threaten continence once defecation is finished. This is a feature of people with soiling secondary to [[obstructed defecation]].<ref>{{cite journal | vauthors = Rao SS, Ozturk R, Stessman M | title = Investigation of the pathophysiology of fecal seepage | journal = The American Journal of Gastroenterology | volume = 99 | issue = 11 | pages = 2204β2209 | date = November 2004 | pmid = 15555003 | doi = 10.1111/j.1572-0241.2004.40387.x | s2cid = 27454746 }}</ref> Obstructed defecation is often due to [[anismus]] (paradoxical contraction or relaxation failure of the puborectalis).<ref name="ASCRS textbook" />{{rp|38}} Whilst anismus is largely a [[functional disorder]], [[organic disease|organic]] pathologic lesions may mechanically interfere with rectal evacuation. Other causes of incomplete evacuation include non-emptying defects like a [[rectocele]].<!-- <ref name="ASCRS textbook" /> p.37 --> Straining to defecate pushes stool into the rectocele, which acts like a [[diverticulum]] and causes stool sequestration. Once the voluntary attempt to defecate, albeit dysfunctional, is finished, the voluntary muscles relax, and residual rectal contents are then able to descend into the anal canal and cause leaking.<ref name="ASCRS textbook" />{{rp|37}} The various types of prolapse of the posterior compartment (e.g. [[Rectal prolapse#Complete rectal prolapse|external rectal prolapse]], [[Rectal prolapse#Mucosal prolapse|mucosal prolapse]] and [[Rectal prolapse#Internal rectal intussusception|internal rectal intussusception]] & [[Rectal prolapse#Solitary rectal ulcer syndrome and colitis cystica profunda|solitary rectal ulcer syndrome]]) may also cause coexisting [[obstructed defecation]].{{citation needed|date=August 2020}} === Reduced rectal storage capacity === The [[rectum]] needs to be of a sufficient volume to store stool until defecation. The rectal walls need to be "compliant" i.e. able to distend to an extent to accommodate stool.<ref name="hoffmann 1995">{{cite journal | vauthors = Hoffmann BA, Timmcke AE, Gathright JB, Hicks TC, Opelka FG, Beck DE | title = Fecal seepage and soiling: a problem of rectal sensation | journal = Diseases of the Colon and Rectum | volume = 38 | issue = 7 | pages = 746β748 | date = July 1995 | pmid = 7607037 | doi = 10.1007/bf02048034 | s2cid = 38351811 }}</ref> Rectal storage capacity (i.e. rectal volume + rectal compliance) may be affected in the following ways. Surgery involving the rectum (e.g. [[lower anterior resection]], often performed for colorectal cancer), radiotherapy directed at the rectum, and inflammatory bowel disease can cause scarring, which may result in the walls of the rectum becoming stiff and inelastic, reducing compliance. Reduced rectal storage capacity may lead to urge incontinence,<ref name="Desprez2021" /> where there is an urgent need to defecate as soon as stool enters the rectum, where normally stool would be stored until there was enough to distend the rectal walls and initiate the defecation cycle. Tumors and [[rectal stricture]]s also may impair reservoir function. ===Rectal hyposensitivity=== Rectal sensation is required to detect the presence, nature, and amount of rectal contents.<ref name="hoffmann 1995" /> Reduced rectal sensation may be a contributory factor. If the sensory nerves are damaged, the detection of stool in the rectum is dulled or absent, and the person will not feel the need to defecate until too late. Rectal hyposensitivity may manifest as constipation, FI, or both. Rectal hyposensitivity was reported to be present in 10% of people with FI.<ref name="Burgell 2012">{{cite journal | vauthors = Burgell RE, Scott SM | title = Rectal hyposensitivity | journal = Journal of Neurogastroenterology and Motility | volume = 18 | issue = 4 | pages = 373β384 | date = October 2012 | pmid = 23105997 | pmc = 3479250 | doi = 10.5056/jnm.2012.18.4.373 }}</ref> Pudendal neuropathy is one cause of rectal hyposensitivity and may lead to fecal loading or impaction, [[megarectum]] and overflow FI (see [[#Overflow_incontinence|overflow incontinence]]).<ref name="Rao 2004">{{cite journal | vauthors = Rao SS | title = Pathophysiology of adult fecal incontinence | journal = Gastroenterology | volume = 126 | issue = 1 Suppl 1 | pages = S14βS22 | date = January 2004 | pmid = 14978634 | doi = 10.1053/j.gastro.2003.10.013 | doi-access = free }}</ref> === Overflow incontinence === This may occur when there is a large mass of feces in the rectum (fecal loading), which may become hardened ([[fecal impaction]]). Liquid stool elements can pass around the obstruction, leading to incontinence. Megarectum (enlarged rectal volume) and rectal hyposensitivity are associated with overflow incontinence. Hospitalized patients and care home residents may develop FI via this mechanism,<ref name="NICE guidelines" /> possibly a result of lack of mobility, reduced alertness, the constipating effect of medication, or dehydration. In overflow incontinence, the rectum is constantly distended because of the presence of retained feces in the rectum.<ref name="Gray's2021" /> Therefore, the recto-anal inhibitory reflex (RAIR) is persistently activated, meaning the internal anal sphincter relaxes, which is not under voluntary control.<ref name="Gray's2021">{{cite book |editor1-last=Standring |editor1-first=S |title=Gray's Anatomy: the anatomical basis of clinical practice |date=2021 |publisher=Elsevier |location=Amsterdam |isbn=978-0-7020-7707-4 |page=1203 |edition=42nd |language=en}}</ref> {| class="wikitable" style="float: right; width:400px;" |+ Drugs that may exacerbate FI and diarrhea<ref name="NICE guidelines Appendix J">{{cite book|last=(UK)|first=National Collaborating Centre for Acute Care|title=Faecal incontinence the management of faecal incontinence in adults|chapter=Appendix J|year=2007|publisher=National Collaborating Centre for Acute Care (UK)|location=London|isbn=978-0-9549760-4-0|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK50674/}}</ref> |- ! Drug or mechanism of action !! Common examples |- | Drugs altering sphincter tone || [[Nitrates]], [[calcium channel antagonist]]s, [[beta-adrenoceptor antagonist]]s ([[beta-blocker]]s), [[sildenafil]], [[selective serotonin reuptake inhibitor]]s |- | [[Broad-spectrum antibiotic]]s || [[Cephalosporin]]s, [[penicillin]]s, [[macrolide]]s |- | Topical drugs applied to the anus (reducing pressure) || [[Glyceryl trinitrate (pharmacology)|Glyceryl trinitrate]] ointment, [[diltiazem]] gel, [[bethanechol]] cream, [[botulinum toxin]] A injection |- | Drugs causing profuse diarrhea || [[Laxative]]s, [[metformin]], [[orlistat]], selective serotonin reuptake inhibitors, magnesium-containing [[antacid]]s, [[digoxin]] |- | Constipating drugs || [[Loperamide]], [[opioid]]s, [[tricyclic antidepressant]]s, aluminium-containing antacids, [[codeine]] |- | [[Tranquiliser]]s or [[hypnotic]]s (reducing alertness) || [[Benzodiazepine]]s, tricyclic antidepressants, selective serotonin reuptake inhibitors, [[anti-psychotic]]s |} === Central nervous system === Continence requires conscious and subconscious networking of information from and to the anorectum. Defects or brain damage may affect the [[central nervous system]] focally (e.g. stroke, tumor, spinal cord lesions, trauma, multiple sclerosis) or diffusely (e.g. dementia, multiple sclerosis, infection, [[Parkinson's disease]] or drug-induced).<ref name="ASCRS core subjects FI" /><ref name="Salat-Foix 2012">{{cite journal | vauthors = Salat-Foix D, Suchowersky O | title = The management of gastrointestinal symptoms in Parkinson's disease | journal = Expert Review of Neurotherapeutics | volume = 12 | issue = 2 | pages = 239β248 | date = February 2012 | pmid = 22288679 | doi = 10.1586/ern.11.192 | s2cid = 220783 }}</ref> FI (and [[urinary incontinence]]) may also occur during [[epileptic seizures]].<ref>{{cite book | veditors = Bromfield EB, Cavazos JE, Sirven JI |chapter=Clinical Epilepsy |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK2511/ |title=An Introduction to Epilepsy |date=2006 |publisher=American Epilepsy Society |id={{NCBIBook2|NBK2508}} |pmid=20821849 | vauthors = Bromfield EB, Cavazos JE, Sirven JI }}</ref> [[Dural ectasia]] is an example of a spinal cord lesion that may affect continence.<ref name="Nallamshetty 2002">{{cite journal | vauthors = Nallamshetty L, Ahn NU, Ahn UM, Nallamshetty HS, Rose PS, Buchowski JM, Sponseller PD | title = Dural ectasia and back pain: review of the literature and case report | journal = Journal of Spinal Disorders & Techniques | volume = 15 | issue = 4 | pages = 326β329 | date = August 2002 | pmid = 12177551 | doi = 10.1097/00024720-200208000-00012 }}</ref> === Diarrhea === Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea.<ref name="NICE guidelines" /> Some consider diarrhea to be the most common aggravating factor.<ref name="ASCRS textbook" /> Where diarrhea is caused by temporary problems such as mild infections or food reactions, incontinence tends to be short-lived. Chronic conditions, such as irritable bowel syndrome or [[Crohn's disease]], can cause severe diarrhea lasting for weeks or months. Diseases, drugs, and indigestible dietary fats that interfere with the [[intestine]]al absorption may cause [[steatorrhea]] (oily rectal discharge & fatty diarrhea) and degrees of FI. Respective examples include [[cystic fibrosis]], [[orlistat]], and [[olestra]]. [[Postcholecystectomy syndrome|Postcholecystectomy diarrhea]] is diarrhea that occurs following gall bladder removal, due to excess [[bile acid]].<ref>{{cite journal | vauthors = Sadowski DC, Camilleri M, Chey WD, Leontiadis GI, Marshall JK, Shaffer EA, Tse F, Walters JR | display-authors = 6 | title = Canadian Association of Gastroenterology Clinical Practice Guideline on the Management of Bile Acid Diarrhea | journal = Clinical Gastroenterology and Hepatology | volume = 18 | issue = 1 | pages = 24β41.e1 | date = January 2020 | pmid = 31526844 | doi = 10.1016/j.cgh.2019.08.062 | doi-access = free | hdl = 10044/1/76745 | hdl-access = free }}</ref> Orlistat is an [[anti-obesity]] (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea, and steatorrhea.<ref>{{cite journal | vauthors = Kang JG, Park CY | title = Anti-Obesity Drugs: A Review about Their Effects and Safety | journal = Diabetes & Metabolism Journal | volume = 36 | issue = 1 | pages = 13β25 | date = February 2012 | pmid = 22363917 | pmc = 3283822 | doi = 10.4093/dmj.2012.36.1.13 }}</ref> ===Radiation=== Irradiation may occur during [[radiotherapy]], e.g. for [[prostate cancer]]. Radiation-induced FI may involve the anal canal as well as the rectum, when [[proctitis]], anal fistula formation, and diminished function of internal and external sphincter occur.<ref name="ASCRS textbook" /> === Trauma=== Fecal incontinence caused by trauma is uncommon.<ref name="ASCRS textbook" /> Rare causes of traumatic injury to the anal sphincters include military or traffic accidents complicated by [[pelvic fracture]]s, spine injuries or [[perineum|perineal]] [[lacerations]], insertion of [[foreign bodies]] in the rectum, and anal [[Anal sex#Health risks|sexual abuse]].<ref name="ASCRS textbook" /> ===Anal penetration=== Most people engaging in anal sex do not experience subsequent fecal incontinence. However, some cases of anal sex have been associated with an increased risk. Factors include high frequency, and practices such as anal [[fisting]], psychoactive drug use and [[BDSM]].<ref>{{Cite journal |last1=Chen |first1=Avital Bar |last2=Kalichman |first2=Leonid |date=2024-11-01 |title=Pelvic Floor Disorders Due to Anal Sexual Activity in Men and Women: A Narrative Review |journal=Archives of Sexual Behavior |language=en |volume=53 |issue=10 |pages=4089β4098 |doi=10.1007/s10508-024-02995-2 |issn=1573-2800 |pmc=11588838 |doi-access=free|pmid=39287780 }}</ref> Females have lower anal canal pressures and less robust sphincters than males, which may make them more susceptible to incontinence, particularly if coercion is involved.<ref>{{Cite journal |last1=Gana |first1=Tabitha |last2=Hunt |first2=Lesley M |date=2022-08-11 |title=Young women and anal sex |url=https://doi.org/10.1136/bmj.o1975 |journal=BMJ |volume=378 |pages=o1975 |doi=10.1136/bmj.o1975 |pmid=35953092 |issn=1756-1833 |url-access=subscription}}</ref> === Congenital defects=== [[Anorectal anomalies]] and spinal cord defects may be a cause in children. These are usually picked up and operated upon during early life, but continence is often imperfect thereafter.<ref name="ASCRS textbook" />
Summary:
Please note that all contributions to Niidae Wiki may be edited, altered, or removed by other contributors. If you do not want your writing to be edited mercilessly, then do not submit it here.
You are also promising us that you wrote this yourself, or copied it from a public domain or similar free resource (see
Encyclopedia:Copyrights
for details).
Do not submit copyrighted work without permission!
Cancel
Editing help
(opens in new window)
Search
Search
Editing
Fecal incontinence
(section)
Add topic