Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5256_Библиотеки_им_академика_М_И_Перельмана.pdf
63
Fig. 4.2 Anorectal angle during contraction and relaxation of puborectal and pelvic oor muscles.
(Source: Created by the authors)
rectum, reaching 2–5mm of thickening, and extends until about 1.5cm below the
pectine line, where it ends in a rounded edge. Being a smooth muscle, its involun-
tary permanent tonus accounts for 50–85% of the resting pressure of the anal canal
(basal anal pressure) [7, 20] (see Fig.4.3).
In resting conditions, the internal anal sphincter is the main occluder of the anal
canal and exerts function in continence by performing transient periods of conti-
nence. In addition, its sensitive epithelium gets an analysis of rectal contents. This
phenomenon, described as the anal sampling mechanism or rectoanal inhibitory
reex, contributes to the individual having the necessary discrimination, for exam-
ple, for the release of gases without loss of fecal material [20, 21]. Weakness or
disruption of the internal anal sphincter results in the passive leakage of fecal con-
tents and incontinence of atus [22, 23].
4.3.3 External Anal Sphincter Muscle
The external anal sphincter is an expansion of the levator ani muscles and measures
0.6–1cm in thickness. It surrounds the anal canal, internal anal sphincter, and con-
joined longitudinal muscle in a cylindrical conformation, being composed of stri-
ated muscles (see Fig.4.3).
Although with different innervations, the two sphincters act integrally on anal
continence, both at rest and in situations where there is an increase in intrarectal
pressure. The external anal sphincter complements the pressure exerted by the inter-
nal anal sphincter by means of a characteristic that distinguishes it from the rest of
the striated muscles, which is the existence of a basal tonus. The external anal
sphincter contains slow-twitch muscle bers that can maintain contraction for long
4 Normal Defecation andMechanisms forContinence
64
Fig. 4.3 Pelvic oor and the sphincterian apparatus. (Source: Created by Mr. Marcos Retzer (in
memoriam); use authorized by Dr. Afonso Henrique da Silva e Sousa Jr. and Dr. Ilario
Froehner Junior)
periods of time. These bers generate 25–30% of the resting anal sphincter tone
[7, 17].
When there is a distension of the rectum, it is up to the external anal sphincter to
perform the contraction necessary to raise the pressure at the level of the anal canal,
to avoid escape of the rectal contents, even in the event of reex relaxation of the
internal anal sphincter [24]. External injury or dysfunction results in urge fecal
incontinence [22].
4.3.4 Longitudinal Anal Muscle
The longitudinal anal muscle is a vertical layer of muscular tissue interposed
between the circular layers of the internal and external anal sphincters. From the
anorectal junction, it extends along the anal canal, receives bers from the inner-
most part of the puborectalis and the puboanalis muscles, and terminates with seven
to nine bro-elastic septa. The septa traverse the subcutaneous part of the external
anal sphincter, reaching the perianal dermis. The longitudinal anal muscle measures
about 1.5–2mm of thickness [25].
The longitudinal muscle fuses with striated bers of the levator ani and puborec-
talis muscles at the level of the anorectal ring to form the conjoined longitudinal
muscle [25] (see Fig.4.3). The bers descend between the internal and external anal
sphincters and continue through the lower portion of the external sphincter compos-
ing the corrugator cutis ani, which inserts in the perianal skin [25]. Longitudinal
anal muscle represents a strong muscular structure that connects the visceral and
M. M. de la Quintana et al.
65
somatic parts of the anal sphincter complex contributing to the occlusion and short-
ening of the anal canal and exerting an important function in continence [24].
4.4 Neural Control
4.4.1 Central Nervous System
The brain and spinal cord coordinate and integrate afferent signals from the anorectum
and maintain continence until socially appropriate to defecate. The characterization of
specic pathways involved in the central regulation of defecation is limited. In brain
magnetic resonance imaging studies of healthy individuals subject to rectal distention,
areas of the brain associated with sensation of rectal lling and urge to defecate include
the anterior cingulate gyrus, insula, thalamus, and secondary somatosensory cortex
[26]. Anal and rectal responses were observed at Brodmann area 4, part of the primary
motor cortex, when cortical mapping with transcranial magnetic stimulation was per-
formed [27]. The parasagittal motor cortex houses the upper motor neurons for the
external anal sphincter muscles, which communicate with Onuf’s nucleus, located in
the ventral horn gray matter of S2–S4 levels of the sacral spinal cord [28].
The conscious recognition of the need to defecate and the coordination of the
proper social response are regulated by the frontal cortex [29]. A defecation center in
the lumbosacral spinal cord, located in the second to fourth sacral segments, has also
been described, through which the central nervous system can exert control over
defecation by interacting with the enteric nervous system [30]. If an interruption in
the spinal-cortical pathway to the defecation center occurs, such as in spinal cord
injury, voluntary control of defecation is lost [30]. This results in fecal incontinence
due to decreased anal sphincter resting tone, loss of voluntary control, and loss of
anorectal reexes [31]. Central control does not contribute signicantly to baseline
colonic tone, but is important in affecting the voluntary relaxation of the external
anal sphincter and contraction of abdominal muscles to facilitate defecation [32].
4.4.2 Peripheral Nervous System
Motor neurons in the Onuf nucleus innervate external anal sphincter and levator
ani muscle through the inferior rectal branches of right and left pudendal nerves
[22]. The levator ani muscle is innervated by the sacral roots (S2, S3, and S4) on
its pelvic surface, and by the perineal branch of the pudendal nerve on its under-
side. The puborectal muscle receives additional innervation by the lower rectal
nerves [33].
The external anal sphincter is innervated on each side by the lower rectal branch
(S2 and S3) of the pudendal nerve and the perineal branch of S4. Despite some dif-
ference in innervation, the puborectal muscles and the external sphincter seem to act
as a unit [34].
4 Normal Defecation andMechanisms forContinence
66
4.4.2.1 Autonomic Nervous System
Sympathetic and parasympathetic neural pathways, which are modulated by inputs
from the central nervous system, modulate colonic motility according to the broader
needs of the organism.
The sympathetic supply originates at the level of the rst lumbar vertebrae—L1,
L2, and L3. The preganglionic bers through the sympathetic lumbar nerves make
synapses in the preaortic plexus. The postganglionic bers follow the branches of
the mesenteric and upper rectal mesenteric arteries to the left and the upper rectus
colon. The lower rectum is innervated by the pre-sacral plexuses, which are formed
by fusion of the aortic plexus and lumbar splanchnic nerves. Below the promontory,
the pre-sacral nerves branch to form the right and left hypogastric nerves, which
originate near the lateral wings of the rectum, the right and left pelvic plexus or
lower hypogastric [17].
Sympathetic nerves mediate internal anal sphincter contraction through the stim-
ulation of alpha-adrenergic receptors and colon relaxation through beta 1, beta 2
and beta 3 adrenergic receptors [22].
The parasympathetic supply originates from the second to the fourth sacral ver-
tebrae—S2, S3, and S4, and constitutes the pelvic nerves. Its bers emerge from the
sacral foramen, pass laterally forward and upward, to join the sympathetic hypogas-
tric nerves in the pelvic plexus. Postganglionic parasympathetic bers are distrib-
uted to the left colon and upper rectum via the inferior mesenteric plexus, and
directly to the distal portion of the rectum [17].
Parasympathetic stimulation causes relaxation of the internal anal sphincter
through nitric oxide-containing neurons located in the myenteric plexus of the rec-
tum [22]. Parasympathetic pathways to the colon synapse onto myenteric neurons,
via excitatory nicotinic cholinergic synapses, leading to increased activity in enteric
pathways and colon excitatory or inhibitory effects. The excitatory effect is impor-
tant for colonic propulsive activity, especially during defecation [21].
4.5 Influence ofColonic Transit, Volume, andConsistency
ofStool
Coordinated colonic motor activity drives transit, and hence the rate at which
colonic contents are delivered to the rectum, as well as the physical and chemical
nature of feces itself. Stool volume and consistency are directly related to gastroin-
testinal transit time [34] and may also play a role in the pathogenesis of inconti-
nence, besides the presence or absence of irritants in stool. As a general rule (though
not absolute), loose stools are associated with more rapid gastrointestinal/colonic
transit [35, 36], whereas constipation may be associated with slow gastrointestinal
transit and reduced motility [37].
M. M. de la Quintana et al.
67
4.6 Continence andDefecation
Fecal continence is a complex function, sustained by the interaction of multiple
mechanisms, including feces consistency, colonic motility, rectal capacity and com-
pliance, rectal and anal canal sensitivity, sphincter function and muscle and nerves
of the pelvic oor.
At rest, the anus remains occluded due to the tonic contraction of the internal
anal sphincter, with reinforcement of the external anal sphincter and the puborectal
handle, constituting the postural reex [15]. Abrupt increases in intra-abdominal
pressure, such as those caused by coughing or laughing, are associated with
increases in anal sphincter pressure. The cough reex is achieved through contrac-
tion of the puborectalis [24].
Rectoanal contractile reex or rectal anal excitatory reex is the contraction of
the external anal sphincter in response to rectal distension [24].
Defecation involves the function of several integrated and complex mechanisms
under the control of the Central Nervous System. The anal canal must open, and the
intrarectal pressure must exceed that of the anal canal pressure. Inhibition of tonic
pelvic oor activity allows relaxation of the puborectalis and straightening of the
anorectal angle [7].
The lling of the rectum by the contents of the sigmoid triggers defecation. The
distension of the rectum is consciously perceived as the desire to defecate by means
of stretch receptors. Rectal distension also activates the rectoanal inhibitory reex.
Relaxation of the internal anal sphincter, by opening the superior anal canal, exposes
the rectal contents to the highly sensitive mucosa of the anal canal, and then the dif-
ferentiation between gases and feces can be made. This sampling mechanism deter-
mines the urgency of evacuation. Meanwhile, the simultaneous reex contraction of
the external sphincter of the anus maintains continence. If defecation is delayed, the
conscious contraction of external anal sphincter allows the recovery of internal
sphincter function [38].
If the urge to defecate is answered, the sitting or squatting position is assumed,
and with this, the anorectal angle tends to widen. Elevation of intrarectal and intra-
abdominal pressures results in reex relaxation of external anal sphincter, internal
anal sphincter and puborectal muscles and, at this point, defecation can occur effort-
lessly. However, some effort is usually needed to start the evacuation of the rectum.
The effort leads to an even greater relaxation of the sphincters and puborectal mus-
cle, and the anorectal angle is even more obtuse. Consequently, the descent and
tapering of the pelvic oor occur, and rectal contents are expelled by direct trans-
mission of increased intra-abdominal pressure to the relaxed pelvic oor [38].
A combination of reex and voluntary relaxation of the external anal sphincter
with increasing rectal distension, prolonged relaxation of the internal anal sphincter,
and “attening” of the anal cushions due to the action of the conjoined muscle
causes the anal pressure to fall [38].
After the evacuation of the rectum is completed, the transient contraction of the
external anal sphincter and puborectal, the so-called “closing reex,” restores the
tonus of the internal anal sphincter and closes the anal canal [7, 15].
4 Normal Defecation andMechanisms forContinence
68
Table 4.1 Anatomical structures and reexes involved in defecation and respective contribution
to fecal continence
Structure, reex, or
function Contribution toward continence
Anal canal Stores feces until an acceptable place for defecation is found
Longitudinal anal
muscle
Occludes the anal canal
Internal anal
sphincter
Accounts for 50–85% of the resting sphincter pressure
External anal
sphincter
Accounts for 25–30% of the resting anal sphincter pressure
Anal vascular
cushions
Accounts for 15% of resting anal pressure
Cough reex Increased abdominal pressure causes reex puborectalis contraction
Rectoanal
inhibitory reex
Sampling mechanism that allows atus to be expelled without feces
Rectal distension Signals the central nervous system that defecation is needed and
accommodates the accumulation of feces until defecation
Postural reex Contraction of the puborectalis when the sampling reex occurs and
when defecation nishes
Rectoanal
contractile reex
External anal sphincter contraction in response to rectal distension
contributing to solid and liquid stool continence
Puborectal
continence reex
Puborectal contraction in response to rectal distension contributing to
solid stool continence
Closing reex Puborectal and external sphincter contraction to restore the anorectal
angle upon completion of defecation
The puborectalis and external anal sphincter temporarily contract and restore the
anorectal angle, and the internal anal sphincter recovers its tone, which along with
passive distension of the anal vascular cushions closes the anal canal [16].
The postural reex is reinstated as a result of the decrease in intra-abdominal
pressure, and the puborectalis sling returns to its contracted state to form an acute
angle at the anorectal junction [15]. Table4.1 shows a summary of the main ana-
tomical structures and reexes involved in defecation and their respective contribu-
tion to fecal continence.
4.7 Fecal Incontinence
The maintenance of continence and defecation is determined by innumerable com-
plex and multifactorial mechanisms, involving the integration of several functions
and dependent on important factors [39]. There are a number of potential areas of
injury or dysfunction in the complex mechanisms required for continence that might
result in incontinence. Fecal incontinence occurs when one or more mechanisms
that maintain continence are disrupted to an extent that other mechanisms are unable
to compensate [40].
M. M. de la Quintana et al.
69
The major factors necessary for fecal continence are an enteric content that is
substantially rm and bulky, a passively distensible, capacious, and evacuable res-
ervoir, and an effective barrier to outow. Therefore, changes in the quantity and/or
quality of stool presented to the sphincter, the inability of the rectum to accommo-
date its contents, damage to or interference with the anal sphincter mechanism, and/
or an impaired sensation can result in fecal incontinence. As a result, common
causes of fecal incontinence include diarrhea, fecal impaction with overow,
impaired rectal storage, loss of rectal sensation to distension, rectal prolapse, and
isolated or combined weakness/impairment of the internal anal sphincter, external
anal sphincter, and puborectalis muscle. Frequently, it is a combination of more than
one of these mechanisms [41].
Fecal continence involves a complex interplay of sphincter and levator tone with
pudendal nerve function. Risk factors for postpartum fecal incontinence include a
history of operative delivery (forceps or vacuum) and an anal sphincter laceration.
Third and fourth-degree lacerations occur more frequently with macrosomic infants
and the use of midline episiotomy. A prolonged second stage of labor may lead to
an operative delivery and subsequent fecal incontinence [39]. Obstetric trauma is
the most common cause of fecal incontinence in women, and this symptom of
incontinence that persists for more than 6months after delivery is reported by a
quarter of women [42]. Perineal tears, even when carefully repaired, can be associ-
ated with incontinence, and patients may either present immediately or several
years following delivery [43].
Longer duration of defecation or incomplete emptying indicates constipation, as
patients have to spend more time on the toilet. Constipation is also one of the signi-
cant risk factors related to fecal incontinence [44].
Fecal incontinence also may appear even after the simplest anal surgery. It may
occur after hemorrhoidectomy as well as surgeries for anal ssures or stulae. This
procedure may result in the inability to discriminate between the contents of the
rectum with resulting incontinence [45]. Hemorrhoidal vascular cushions and the
anal canal mucosa support fecal continence, with the capacity of expansion to keep
the anal canal closed and to prevent fecal incontinence when the anal pressure
decreases. The importance of cushions becomes obvious when patients present with
fecal soiling after hemorrhoidectomy, even with normal sphincter pressure [39].
Fecal incontinence following anorectal surgery can result from several issues. In
cases such as stulotomy, the sphincter muscle may have been intentionally divided
with an underestimation of the functional consequence. At other times, damage to
the anal sphincter or associated nerves occurs unintentionally. This has also been
seen with intact sphincters, as the hemorrhoidal cushions are known to provide 15%
of the patient’s resting anal tone, and removal can unmask issues with incontinence
that were being aided by these cushions [41].
Similar to obstetrical injuries, anorectal surgeries (hemorrhoidectomy, sphincter-
otomy, stula surgeries) are frequently identied in patients with symptoms of
incontinence. This is at variance with low percentages of incontinence when out-
comes of such surgical series are reported. The explanation for this discrepancy may
be found in the fact that such observational cohort studies frequently lack long-term
4 Normal Defecation andMechanisms forContinence
70
follow-up of more than 10years and hence fail to capture the delayed onset of
symptoms to determine the true incidence of this long-term complication [4].
Pelvic radiotherapy may lead to changes in anorectal function, resulting in
incontinence-related complaints. Low to moderate quality evidence indicates that
radiotherapy reduces anal resting pressure, decreases rectal distensibility, and fre-
quently induces telangiectasias of rectal mucosa. These changes may be associated
with fecal incontinence, defecation urgency, and frequent bowel movements [46].
Further details regarding the evaluation and treatment of people with fecal incon-
tinence will be covered in the following chapters.
Acknowledgments To Dr. Afonso Henrique da Silva e Sousa Júnior and Dr. Ilario Froehner
Junior, for making available the gures used in this chapter, and to Mr. Marcos Retzer (in memo-
riam), the artist who created the gures. We also acknowledge Dr. Tania das Graças de Souza Lima
for her participation in the last edition of the chapter construction.
References
1. Trzpis-Bremer M, Sun G, Chen J, Huizinga J, Broens PM. Physiological mechanisms underly-
ing fecal continence. Am J Physiol-Gastrointest Liver Physiol. 2023;324(1):G1–9.
2. O’Donnell MT, Bleier JI. Pelvic oor conditions: fecal incontinence. In: Steele SR, Maykel
JA, Wexner SD, editors. Clinical decision making in colorectal surgery. Switzerland AG:
Springer Cham; 2020. p. 255–63.
3. Kim M, Oh B-Y, Lee J-S, Yoon D, Chun W, Son IT.A systematic review of translation and
experimental studies on internal anal sphincter for fecal incontinence. Ann Coloproctol.
2022;38(3):183.
4. Ruiz NS, Kaiser AM.Fecal incontinence- challenges and solutions. World J Gastroenterol.
2017;23(1):11–24.
5. Sagar PM, Pemberton JH. Anorectal and pelvic oor function. Gastroenterol Clin.
1996;25(1):163–82.
6. Sun W, Donnelly T, Read N.Utility of a combined test of anorectal manometry, electromyog-
raphy, and sensation in determining the mechanism of ‘idiopathic’ faecal incontinence. Gut.
1992;33(6):807–13.
7. Kadam-Halani PK, Arya LA, Andy UU.Clinical anatomy of fecal incontinence in women.
Clin Anat. 2017;30(7):901–11.
8. Salvioli B, Bharucha AE, Rath-Harvey D, Pemberton JH, Phillips SF.Rectal compliance, capac-
ity, and rectoanal sensation in fecal incontinence. Am J Gastroenterol. 2001;96(7):2158–68.
9. Siproudhis L, Bellissant E, Juguet F, Allain H, Bretagne J, Gosselin M. Perception of
and adaptation to rectal isobaric distension in patients with faecal incontinence. Gut.
1999;44(5):687–92.
10. Siproudhis L, El Abkari M, El Alaoui M, Juguet F, Bretagne JF.Low rectal volumes in
patients suffering from fecal incontinence: what does it mean? Aliment Pharmacol Ther.
2005;22(10):989–96.
11. Speakman C, Kamm M.Abnormal visceral autonomic innervation in neurogenic faecal incon-
tinence. Gut. 1993;34(2):215–21.
12. Read N, Haynes W, Bartolo D, Hall J, Read M, Donnelly T, etal. Use of anorectal manom-
etry during rectal infusion of saline to investigate sphincter function in incontinent patients.
Gastroenterology. 1983;85(1):105–13.
13. Rao SS.Pathophysiology of adult fecal incontinence. Gastroenterology. 2004;126:S14–22.
14. Campos F, Regadas F, Pinho M. Tratado de Coloproctologia. São Paulo: Atheneu; 2012.
M. M. de la Quintana et al.
71
15. Palit S, Lunniss PJ, Scott SM. The physiology of human defecation. Dig Dis Sci.
2012;57(6):1445–64.
16. Thomson H. The anal cushions—a fresh concept in diagnosis. Postgrad Med
J. 1979;55(644):403–5.
17. Kaiser AM, Ortega AE.Anorectal anatomy. Surg Clin. 2002;82(6):1125–38.
18. Ashton-Miller JA, DeLancey JO.Functional anatomy of the female pelvic oor. Ann N Y
Acad Sci. 2007;1101(1):266–96.
19. Brookes S, Dinning P, Gladman M. Neuroanatomy and physiology of colorectal function
and defaecation: from basic science to human clinical studies. Neurogastroenterol Motil.
2009;21(s2):9–19.
20. Frenckner B, Ihre T.Inuence of autonomic nerves on the internal and sphincter in man. Gut.
1976;17(4):306–12.
21. Wald A. Neuromuscular physiology of the pelvic oor. In: Said HM, editor. Physiology of the
gastrointestinal tract. London, UK: Elsevier; 2018. p. 565–84.
22. Bharucha AE, Brookes SJ. Neurophysiologic mechanisms of human large intestinal motility.
In: Said HM, editor. Physiology of the gastrointestinal tract. London, UK: Elsevier; 2018.
p. 517–64.
23. Penninckx F, Lestar B, Kerremans R.The internal anal sphincter: mechanisms of control and
its role in maintaining anal continence. Baillieres Clin Gastroenterol. 1992;6(1):193–214.
24. Finazzi AE, Salvatore S, Braga A, DeLancey J, Fernando J, Iacovelli V, et al. Pathophysiology
of urinary incontinence, pelvic organ prolapse and fecal incontinence. In: Cardozo L, Rovner
E, Wagg A, Wein A, Abrams P, editors. Incontinência. 15. 7th ed. Bristol: International
Continence Society; 2023. p. 247–397.
25. Lunniss P, Phillips R. Anatomy and function of the anal longitudinal muscle. Br J Surg.
1992;79(9):882–4.
26. Bittorf B, Ringler R, Forster C, Hohenberger W, Matzel K.Cerebral representation of the ano-
rectum using functional magnetic resonance imaging. Br J Surg. 2006;93(10):1251–7.
27. Turnbull GK, Hamdy S, Aziz Q, Singh KD, Thompson DG.The cortical topography of human
anorectal musculature. Gastroenterology. 1999;117(1):32–9.
28. Bharucha AE. Pelvic oor: anatomy and function. Neurogastroenterol Motil.
2006;18(7):507–19.
29. Sultan AH, Nugent K.Pathophysiology and nonsurgical treatment of anal incontinence. BJOG
Int J Obstet Gynaecol. 2004;111(s1):84–90.
30. Furness JB, Callaghan BP, Rivera LR, Cho H-J.The enteric nervous system and gastrointesti-
nal innervation: integrated local and central control. In: Lyte M, Cryan JF, editors. Microbial
endocrinology: the microbiota-gut-brain axis in health and disease, Advances in experimental
medicine and biology. NewYork: Springer; 2014. p.39–71.
31. Coggrave M, Norton C.Neurogenic bowel. Handb Clin Neurol. 2013;110:221–8.
32. Steele SR, Hull TL, Read TE, Saclarides TJ, Senagore AJ, Whitlow CB.The ASCRS textbook
of colon and rectal surgery. 3rd ed. NewYork: Springer; 2016.
33. Tagliaco A, Perez MM, Martinoli C.High-resolution ultrasound of the pudendal nerve: nor-
mal anatomy. Muscle Nerve. 2013;47(3):403–8.
34. Shak A.A concept of the anatomy of the anal sphincter mechanism and the physiology of
defecation. Dis Colon Rectum. 1987;30(12):970–82.
35. Degen L, Phillips S.How well does stool form reect colonic transit? Gut. 1996;39(1):109–13.
36. Davies G, Crowder M, Reid B, Dickerson J.Bowel function measurements of individuals with
different eating patterns. Gut. 1986;27(2):164–9.
37. O’Donnell LJ, Virjee J, Heaton KW.Detection of pseudodiarrhoea by simple clinical assess-
ment of intestinal transit rate. BMJ. 1990;300(6722):439–40.
38. Bharucha AE. Lower gastrointestinal functions. Neurogastroenterol Motil.
2008;20(s1):103–13.
39. Barleben A, Mills S.Anorectal anatomy and physiology. Surg Clin N Am. 2010;90(1):1–15.
40. Oliveira C.Fisiologia anorretal. 2nd ed. Rio de Janeiro: Editora Rubio; 2017.
4 Normal Defecation andMechanisms forContinence
72
41. Kunitake H, Poylin V. Complications following anorectal surgery. Clin Colon Rect Surg.
2016;29(1):14–21.
42. Chin K.Obstetrics and fecal incontinence. Clin Colon Rectal Surg. 2014;27(3):110–2.
43. Rao SSC, American College of Gastroenterology Practice Parameters Committee. Diagnosis
and management of fecal incontinence. Am J Gastroenterol. 2004;99(8):1585–604.
44. Fitzpatrick M, Herlihy C.The effects of labour and delivery on the pelvic oor. Best Pract Res
Clin Obstet Gynaecol. 2001;15(1):63–79.
45. Roslani AC, Ramakrishnan R, Azmi S, Arapoc DJ, Goh A.Prevalence of faecal incontinence
and its related factors among patients in a Malaysian academic setting. BMC Gastroenterol.
2014;14(1):95.
46. Krol R, Smeenk RJ, Van Lin ENJT, Yeoh EEK, Hopman WPM.Systematic review: anal and
rectal changes after radiotherapy for prostate cancer. Int J Color Dis. 2014;29(3):273–83.
M. M. de la Quintana et al.