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_1408_Библиотеки_им_академика_М_И_Перельмана
.pdf
At week 7 of gestation the urogenital system and the anorectum are supposed to sep-
arate, but in recent studies
10
the mechanism of separation by the urorectal septum has
been a subject of debate. Changes in the previously described position of the dorsal cloaca, the process of cloacal membrane rotation, and the transformation of the cloacal configuration have been reported.
11
In their studies, Kluth et al.12evaluated rat embryos through electron microscopy,
which allowed them to study the embryologic structures in three dimensions during
the development of the hindgut. They concentrated on the following points: (1) the development of the cloacal shape, (2) signs of lateral cloacal wall component fusion, (3) signs of
cloacal membrane disintegration, and (4) signs of anal opening migration. They found
noticeable ventral growth of the cloaca and a shift of the cloacal membrane from a vertical
to a horizontal position that had a fixed point in the fold of the distal portion. The changes
in cloacal shape were produced by the outgrowth of the genital tubercles. They found no
signs of fusion of the lateral components of the cloacal wall, with respect to the urorectal
fold and the cloacal membrane in the normal development of the cloaca. They also stated
that the urethral area was larger than the anorectal area. The authors concluded that the
microscopic study of rat embryos demonstrated that the subdivision of the cloaca was not
the result of lateral cloacal ridges or the fusion of wall components of the lateral cloaca and
that their importance had been overestimated in the past. According to the results of the
study, hindgut development depends on the normal formation of the cloacal membrane,
thus refuting the migration theory. They found that the future anal opening was observed
in the dorsal part of the cloacal membrane, near the distal tail groove, in all the embryos.
Embryonic cell differentiation, proliferation, and apopt osis have also been reported,
specifically in murine models, to play an essential role in the configuration of the embryonic anorectum.
13,14
Zhang et al.15studied 108 human embryos from week 3 to 8 and
described the morphologic development of the anorectum in three phases:
1. The cloacal period from week 3 to 5;
2. The development of the urogenital and the anorectum systems from week 5 to 7; and
3. The formation of the anus and perineum from week 8.
During week 8, the urogenital system progressively grows ventrally and its epithelium
fuses with the ventral part of the endodermal layer of the cloacal membrane, with persistent epithelium between the mesenchyme of the two structures. The mesenchyme of the
urogenital tubercle is inserted into the two layers of the cloacal membrane to form the
urethra. The urogenital system confluence with the endoderm and ectoderm of the cloacal membrane forms the perineal body.
Regarding the space-time distribution of apoptosis and the proliferation of the embryonic anorectum, Zhang et al. described the presence of apoptotic cells in the epithelium of
the anorectum, urogenital system, and urorectal septum at week 6 that specifically began
to appear inside the anal opening. Those cells were observed in the mesenchyme of the
terminal rectum and dorsal rectum at week 7 and were not detected in those epithelia at
week 8, whereas the fusion of the urogenital system and cloacal membrane remained
Chapter 1 • Embryology of the Anorectum 5
permanent and strong. The proliferative cells were scarce in the epithelia of the zone at
week 6 but were more numerous in the mesenchyme of the urogenital system at week
7 and in the epithelium of the urethra and the anorectum at week 8; especially in the zone
of the fused tissue between the urogenital system and the ventral part of the cloacal membrane. The authors described how the urogenital system was not fused with the dorsal cloacal membrane. They therefore concluded that the normal development of the anorectum
depends on the dorsal cloaca and the dorsal part of the cloacal membrane, and that the
distribution of apoptosis and proliferation in the anorectum and the ventral cloacal mesenchyme plays an essential role in the formation of the anorectum.
In another recent study Hashimoto
16
depicted new forms of development through the
analysis of human embryos. He evaluated the embryos from the perspective of the distal
portion (tail) and the splanchnic mesenchyme from Carnegie stages 11 to 23, corresponding to day 23 to 60 or, in other words, from week 3 to 9 (the Carnegie stages are used for the
study of embryonic development from fertilization to 60 days/8 weeks, because after that
date the embryo is called a fetus). Hashimoto carried out the histologic study of
17 embryos, finding that the cloaca that extended caudally to the hindgut enlarged dramatically, particularly in its dorsal portion and its membrane, that is to say the cloacal
membrane. The splanchnic mesenchyme that surrounds the hindgut extended ventrally
toward the urorectal septum, suggesting its participation in the formation of the septum.
No fusion of the urorectal septum with the cloacal membrane was found. The splanchnic
mesenchyme proliferated and developed into smooth muscle layers (circular and longitudinal) in a cranial-to-caudal direction along the hindgut. The distal portion (tail)
appears to cause both adequate dorsal cloaca dilation and cloacal membrane lengthening. Its dorsal portion in particular is necessary for normal anorectal development. The
splanchnic mesenchyme developed and descended toward the pectinate line and formed
the internal sphincter muscle at the terminal intestine.
The union between the endodermal and ectodermal portions of the anal canal is represented by the pectinate line that is found immediately under the anal columns. The cylindric epithelium is transformed into stratified epithelium at the level of that line, as
previously reported.
In general parts of the traditional theories continue to be adopted, but the advances in
the study of embryology have unfolded novel aspects of anorectal embryogenesis. More
studies will certainly be conducted, supporting new research and providing a greater
understanding of embryology in humans.
References
1.
Sadler TW, Leland J, Susan L, et al. Digestive system. In: Langman’s Medical Embryology. 10th ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2006:204–227.
2. Kluth D. Embryology of anorectal malformations. Semin Pediatr Surg. 2010;19:201–208.
3. Sadler TW. Aparato digestivo. In: Sadler TW, ed. Embriologı´a M!edica Con Orientacio´n Clı´nica. 8th ed.
Espan˜a: Panamericana; 2002:262–293.
6 ANORECTAL DISORDERS
4. Tourneux F. Sur le premiers developments due cloaque du tubercle genitale et de 1 Anus chez
1’embryon mouton s, avec quelques remarques concernant le development des glandes prostatiques.
J Anat Physiol. 1888;24:503–517.
5. Retterer E. Sur 1’origin et de 1’evolution de la region ano-genitale des mammiferes. J Anat Physiol.
1890;26:126–210.
6. Stephens FD. Congenital Malformations of the Rectum, Anus, and Genitourinary Tract. Edinburgh:
Livingstone; 1963.
7. van der Putte SC. Normal and abnormal development of the anorectum. J Pediatr Surg.
1986;21:434–440.
8. Bill AH, Johnson RJ. Failure of migration of the rectal opening as the cause for most cases of imper-
forate anus. Surg Gynecol Obstet. 1958;106:643–651.
9. Gans SL, Friedman NB. Some new concepts in the embryology, anatomy, physiology, and surgical
correction of imperforate anus. West J Surg Obstet Gynecol. 1961;63:34–37.
10. Penington EC, Hutson JM. The absence of lateral fusion in cloacal partition. J Pediatr Surg.
2003;38:1287–1295.
11. Paidas CN, Morreale RF, Hutchins GM, et al. Normal and abnormal embr yonic development of the
anorectum in human embryos. Teratology. 1998;57:70–78.
12. Kluth D, Fiegel HC, Metzger R. Embryology of the hindgut. Semin Pediatr Surg. 2011;20:152–160.
13. Sasaki C, Yamaguchi K, Akita K. Spatiotemporal distribution of apoptosis during normal cloacal devel-
opment in mice. Anat Rec A Discov Mol Cell Evol Biol. 2004;279:761–767.
14. Qi BQ, Williams A, Beasley S, et al. Clarification of the process of separation of the cloaca into rectum
and urogenital sinus in the rat embryo. J Pediatr Surg. 2000;35:1810–1816.
15. Zhang T, Zhang HL, Wang DJ, Tang XB, Jia HM, Bai YZ. Normal development of hindgut and anorec-
tum in human embryo. Int J Colorectal Dis. 2011;26:109–116.
16. Hashimoto R. Development of the human tail bud and splanchnic mesenchyme. Congenit Anom.
2013;53(1):27–33.
Chapter 1 • Embryology of the Anorectum 7
2
Anorectal Anatomy and Function
Ravinder K. Mittal
DEP A R T M ENT O F MEDI C I N E/G A S T ROE N T E R OLO G Y , UNI V E R S ITY O F CAL I F O R NIA ,
SAN D I EGO , C A, U N I T ED S T ATE S
Abbreviations
EAS external anal sphincter
IAS internal anal sphincter
PRM puborectalis muscle
2.1 Introduction
Fecal incontinence (FI) is defined as the recurrent uncontrolled passage of fecal material
for at least 3 months or more. According to a recent study
1
that determined the prevalence
and severity of FI in a large sample of United States residents using a mobile app called
MyGiHealth, 14% (one in seven) of the subjects reported FI in the past, and 33% within the
past 7 days. FI was found to be age-related and more prevalent among individuals with
inflammatory bowel disease, celiac disease, irritable bowel syndrome, or diabetes. The etiology of FI is clearly multifactorial: stool consistency, rectal reservoir function, and anal
sphincter function play important roles in its genesis.
2,3
There is general consensus
though that anal sphincter function is the most important factor in the development of
FI.
4,5
Recent studies that utilized a functional luminal imaging probe (FLIP) to assess
the anal-closure function revealed that in majority of subjects referred to the tertiary care
center, anal canal distensibility was higher in FI patients as compared to controls.
6,7
Severe
FI symptoms are most often observed in women as compared to man, which is most likely
due to the fact that women are susceptible to childbirth-related injury to the anal sphincter and pelvic-floor muscles. From 20% to 35% of women develop damage to the EAS and
PRM following vaginal child birth.
8,9
One finds that more than 80% of patients in clinical
trials for the treatment of FI are women.
10–12
What is not clear though is why there is a
delay of 2–3 decades between the obstetrical injury that occurs during the childbearing
years (typically 20s and 30s) and the patients becoming symptomatic. All of the above
observations prove that the anal sphincter or anal-closure mechanism is the major continence mechanism. The aim of this chapter is to provide the reader with information on
the recent advances in our understanding of the anal sphincter anatomy and of the imaging and functional assessment tools. There are three distinct anatomical structures, the
internal anal sphincter (IAS), external anal sphincter (EAS), and puborectalis muscle
Anorectal Disorders.
https://doi.org/10.1016/B978-0-12-815346-8.00002-3
© 2019 Elsevier Inc. All rights reserved.
9
(PRM), the last one being a part of the pelvic-floor or levator-ani muscle that contributes
to the anal-closure/sphincter mechanism.
2.2 Internal Anal Sphincter
The circular muscle layer of the rectum expands caudally into the anal canal to become
the IAS (Fig. 2.1). The circular muscles in the sphincter region are thicker than those of the
rectum with discrete septa in between the muscle bundles.
13,14
The longitudinal muscles
of the rectum extend into the anal canal and end up as thin septa that penetrate into the
circular muscle layer, PRM, EAS, and perianal fat.
15
The longitudinal muscle of the anal
canal is also known as the conjoined tendon (muscle) because it was felt that the skeletal
muscles of the pelvic floor contribute to its formation. A recent study, however, indicates
that the longitudinal muscles of the rectum are the major contributors to the longitudinal
muscles of the anal canal, even though their function in the anal sphincter and dysfunction is not clear.
14
There is general consensus that the IAS is a major contributor to the
resting or baseline anal sphincter pressure (>70%). Many investigators have attempted
to identi fy what is responsible for the resting IAS tone. The IAS tone is myogenic in
origin, i.e., it is due to the unique property of the sphincter smooth muscle cells because
isolated muscle strips of the IAS in the muscle bath, devoid of endocrine and neural
influence, maintain tonic contraction.
16
Studies show that the source of calcium, which
Levator ani
Anal columns (of Morgagni)
Anal sinus
Anorectal (pectinate,
or dentate) line
Internal rectal venous plexus
in submucous space
Conjoined longitudinal muscle
Anal valve
Anal crypt
Anal glands
Transverse fibrous septum
Musculus submucosae ani
Perianal space
Corrugator cutis ani muscle
External rectal venous plexus in perianal space
Intermuscular groove (white line of Hilton)
Deep ext anal sphincter
Int. anal sphincter
Subcutaneous ext anal sphincter
Superficial ext anal
sphincter
5–6 cm
4–5 cm
2.5–3 cm
0.5–1 cm
Sweat glands and
hairs in perianal skin
Anal verge
Pecten
Anoderm
Surgical anal canal
Anatomical
anal canal
Muscularis mucosae
F Netter. Atlas of Human Anatom
y
FIG. 2.1 This schematic shows that the external anal sphincter is made up of subcutaneous, superficial, and deep parts.
It is believed that deep external anal sphincter is actually the puborectalis muscle. Modified from Netter Anatomy
Illustration Collection, Elsevier Inc.
10 ANORECTAL DISORDERS
is crucial for muscle contraction, is extracelular in the phasic (such as rectal muscle) but
intracelular in the tonic muscle (such as IAS).
17
Studies show differences in the intracel-
lular messengers, RhoA/Rho-kinase (ROCK) pathway in the phasic versus tonic muscles.
18
The critical intracellular step in the contraction of smooth muscle is the phosphorylation
of myosin light chain through a kinase (MLCK), which induces muscle contraction. The
MLCK is dephosphorylated by myosin light chain phosphatase (MLCP) resulting in muscle relaxation. The critical difference between a phasic and tonic muscle is that the RhoA/
ROCK machinery is more active in tonic muscles like IAS. The activation of RhoA/ROCK by
intracellular calcium (also known as calcium sensitization) leads to inhibition of MLC
phosphatase resulting in sustained elevation of phosphorylated MLC, which induces sustained tonic contraction. Known extracellular signals that activate RhoA/ROCK are products of the renin angiotensin system (angiotensin 2) and arachidonic acid pathway
(thromboxane A
2
and prostaglandin F2α).19Platelet activating factor (PAF), a product of
inflammation, is also a major inducer of low lower esophageal sphincter (LES) tone.
17
There is evidence that the interstitial cells of Cajal (ICC) present in the IAS and other
smooth muscle sphincters, play a significant role in IAS tone generation.
20
2.3 Neural Control of the Internal Anal Sphincter
The autonomic nerves, sympathetic (spinal nerves), and parasympathetic nerves (pelvic
nerves) supply the IAS.
21,22
Sympathetic fibers originate from the lower thoracic ganglia to
form the superior hypogastric plexus. Parasympathetic fibers originate from the second,
third, and fourth sacral nerves to form the inferior hypogastric plexus, which in turn gives
rise to superior, middle, and inferior rectal nerves that ultimately supply the rectum and
anal canal. These nerves synapse with the myenteric plexus of the rectum. Interestingly,
there are no myenteric neurons in the IAS, the latter only receives processes of neurons
located in the rectum. Sympathetic nerves mediate IAS contraction through the stimulation of α receptors,
23
and relaxation through β1, β2, and β3 adrenergic receptors.
24,25
Studies show a predominance of low-affinity β3 receptors in the IAS. Stimulation of parasympathetic or pelvic nerves causes IAS relaxation through nitric oxide-containing neurons located in the myenteric plexus of the rectum.
16,26
There are no myenteric neurons in
the anal sphincter itself; however, it is richly innervated by the processes of myenteric
inhibitory neurons located in the rectum. Besides, nitric oxide, vasoactive intestinal peptide (VIP), carbon monoxide (CO), and ATP are the other potential inhibitory neurotransmitters that likely play some, although limited, roles in IAS relaxation.
27
Degeneration of
myenteric neurons results in impaired IAS relaxation, which is a hallmark of Hirschsprung’s disease.
2.4 External Anal Sphincter
The anatomy of EAS has been a subject of significant debate. The original description by
Santorini (1769) is of EAS being made of three separate muscles bundles: subcutaneous,
superficial, and deep.
28
In most of the schematics published in the literature, including the
Chapter 2 • Anorectal Anatomy and Function 11
one by Netter (Fig. 2.1), the EAS is also made of three components. A close inspection of
these schematics reveals that the PRM is entirely missing from these drawing, or it is possible that even though it is not labeled as such, the PRM is considered to be a part of the
levator ani muscle. Shafik described the EAS as consisting of three loops with PRM being
located cranial to them.
29
The subcutaneous portion of the EAS sits caudal to the IAS and
the superficial portion surrounds the distal IAS. Several investigators have argued that
only the subcutaneous and superficial muscle bundles constitute the EAS.
A histological study by Fritsch
30
and the MR imaging of Hussain31are quite convincing
in demonstrating that the EAS muscle is composed of only the subcutaneous and superficial portion. Based on our 3D-ultrasound (US) imaging, it is clear that the deep part of the
EAS is actually the PRM, because it is shaped like a “U”; it does not surround the anal canal
in a circumferential fashion.
32
Another intriguing aspect of the EAS anatomy is that it is thought to be attached to the
perineal body at the ventral end or, in other words, it is not a circular muscle in its configuration.
33,34
The perineal body is a midline fibro-tendinous structure to which, besides
the EAS, other muscles of the perineum, i.e., transverse perinea and bulbospongiosus are
attached. These muscles along with the EAS are also referred to as the superficial muscles
of the perineum. A recent study found that the perineal body is not the site of insertion of
the superficial muscles of the perineum, instead it is the crossing site of the superficial
muscle of the perineum. In other words, the EAS muscles pass from the right and left sides,
crossing in the midline perineal body, to the opposite sides, and continue on as transverse
perinea and bulbospongiosus muscles (Fig. 2.2).
35
The two transverse perinea mus cles
may not have definitive attachments to the bone (they traverse and merge into the septa
of ischiorectal fat), the bulbospongiosus muscles on the other hand are attached to the
pubic rami close to the symphysis pubis. At the posterior end, the muscles of the EAS continue as anococcygeal raphe. Micro CT imaging and histological study show that the muscle fibers of the EAS from the right and left sides decussate at the posterior end and then
continue as anococcygeal raphe, which is attached to the tip of coccyx (anococcygeal
raphe) (
Fig. 2.3). Putting the entire anatomy together, the EAS is neither a donut-shaped
structure, nor made up of a ring of circular muscles fibers. The EAS is configured
FIG. 2.2 External anal sphincter: true morphology: a purse string—not a donut. From Mittal RK, Bhargava V, Sheean G,
Ledgerwood M, Sinha S. Am J Physiol 2014;306 (6):G505–14.
12 ANORECTAL DISORDERS
approximately in a figure of eight with a perineal body in the center with crossing mus cle
fibers in the midline at the ventral and dorsal ends of the anal canal that attach to the
pubic rami at the ventral end and the coccyx at the dorsal end. The EAS is no different
from other skeletal muscles in the body that have origin from and insertion into the bone.
In the case of EAS the origin is from the pubic rami (fixed end) and the insertion is into the
coccyx (mobile end). Dynamic magnetic resonance (MR) imaging studies show that the
coccyx moves approximately 10 mm, ventrally and cranially with contraction of the
EAS and pelvic-floor muscles.
36
Magnetic resonance diffusion tensor imaging (MRDTI)
is a novel technique used to determine the myoarchitecture at a mesoscale level (in
between histology or microscopic and macroscopic)
37,38
and using the above technique
we observed that the entire figure of eight configuration of the EAS can be visualized
by MRDTI (
Fig. 2.4).
35
Future studies may reveal that MRDTI is a better imaging technique
than the current “gold standard” US imaging method used to assess the anatomical integrity of the EAS muscle.
The unique morphology of the EAS has many clinical implications
1
: endoanal US
imaging is gold-standard to assess damage to the pelvic-floor muscle and because it
assumes an annular morphology of the EAS, which is not accurate, it cannot provide complete information on the structural integrity of the EAS in patients with FI
2
; lateral episiotomy that sections through the bulbospongiosus and transverse perinea muscle is not a
sphincter-sparing operation; and
3
sphincteroplasty for the surgical repair of the EAS muscle restores a circular shape of the EAS, but if it is not an annular muscle to begin with,
sphincteroplasty cannot be an effective surgical procedure for the treatment of FI.
Long-term studies indeed show that sphincteroplasty is not an effective operation for
the treatment of FI.
The muscle fibers of EAS are composed of fast- and slow-twitch types, which allow it to
maintain sustained tonic contraction at rest and also allow it to contract rapidly with voluntary squeeze. Motor neurons in the Onuf nucleus (located in the sacral spinal cord)
innervate the EAS muscles through the inferior rectal branches of the right and left pudendal nerves.
FIG. 2.3 Frontal and side view of the EAS and other muscle attached to the bony pelvis.
Chapter 2 • Anorectal Anatomy and Function 13
2.5 Puborectalis and Deep Pelvic Floor Muscles (Levator Ani)
According to Sappey (1869), “the levator-ani is one of those muscle which has been studied the most, and at the same time one about which we know the least.”
33,39
Sappey also
mentioned that the “The doctrine of continuity of fibers between two or more muscles of
independent actions has been applied to the levator-ani at various scientific epochs, and
this ancient error, renewed without ceasing, has singularly contributed to complicate
its study.” It is interesting that even in the year 2018 the nomenclature of the various
pelvic-floor muscles, precise anatomy, neural innervation, and functions of the levator
ani/pelvic diaphragm are still veiled in deep mystery. Holl (1897) was the first to suggest
that some of the pubococcyg eus muscle fibers, instead of inserting into the coccyx, looped
around the rectum and he named these fibers “puborectalis” or “sphincter recti.”
40
Prior
depictions only show pubococcygeus, ileococcygeus, and ischiococcygeus as being the
deep pelvic-floor or levator-ani muscles (
Fig. 2.5). Whether puborectalis and pubococcy-
geus are two separate muscles is not clear, but what is clear is that they are, or it is, located
inferior/caudal to the ileococcygeus muscle. In the OB/GYN and urogynecology literature
many authors use the term pubovisceral muscle
41
for what is referred to as puborectalis by
others. Irrespective of the above inconsistencies, puborectalis is a U-shaped muscle with
MR diffusion tensor based muscle fiber tracking external anal sphincte
r
FIG. 2.4 Magnetic resonance diffusion tensor image of the external anal sphincter.
14 ANORECTAL DISORDERS
FIG. 2.5 (A) Pelvic-floor muscles seen in the sagittal section of pelvis. (B) Pelvic-floor muscles as seen from the perineal
surface.
Chapter 2 • Anorectal Anatomy and Function 15
Соседние файлы в папке Библиотека им академика М.И. Перельмана