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Anorectal Disorders: Diagnosis and Non-Surgical Treatments
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Commencer à lireLongueur: 616 pages5 heures
- Éditeur:
- Academic Press
- Sortie:
- Mar 6, 2019
- ISBN:
- 9780128153475
- Format:
- Livre
Description
Anorectal Disorders: Diagnosis and Nonsurgical Treatments incorporates the most recent major advances in the understanding of anal and rectal anatomy to provide clinical evidence of care for those suffering from anorectal disorders. By condensing basic and practical aspects in the knowledge of anorectal disorders, this book provides a comprehensive review of the anatomy and physiology of the anorectal region. It includes new technology that expands and modifies current perceptions about the functional anatomy of the anorectal region and ultimately impacts how we conceive muscle and nerve structures functioning together to maintain fecal continence and properly execute the process of defecation.
Perfect for medical researchers, gastroenterologists, general practitioners, internal medicine doctors and general surgeons, this title will provide diagnosis and treatment options for all patients suffering from anorectal disorders.
Identifies frequent, but not well understood, anorectal disorders, including ulcers, constipation, dyssynergic defecation, tumors and malformations Condenses the basic and practical aspects of anorectal disorders for better treatment of patients Includes clinical cases that summarize chapter content in a clinical contextInformations sur le livre
Anorectal Disorders: Diagnosis and Non-Surgical Treatments
Longueur: 616 pages5 heures
Description
Anorectal Disorders: Diagnosis and Nonsurgical Treatments incorporates the most recent major advances in the understanding of anal and rectal anatomy to provide clinical evidence of care for those suffering from anorectal disorders. By condensing basic and practical aspects in the knowledge of anorectal disorders, this book provides a comprehensive review of the anatomy and physiology of the anorectal region. It includes new technology that expands and modifies current perceptions about the functional anatomy of the anorectal region and ultimately impacts how we conceive muscle and nerve structures functioning together to maintain fecal continence and properly execute the process of defecation.
Perfect for medical researchers, gastroenterologists, general practitioners, internal medicine doctors and general surgeons, this title will provide diagnosis and treatment options for all patients suffering from anorectal disorders.
Identifies frequent, but not well understood, anorectal disorders, including ulcers, constipation, dyssynergic defecation, tumors and malformations Condenses the basic and practical aspects of anorectal disorders for better treatment of patients Includes clinical cases that summarize chapter content in a clinical context- Éditeur:
- Academic Press
- Sortie:
- Mar 6, 2019
- ISBN:
- 9780128153475
- Format:
- Livre
En rapport avec Anorectal Disorders
Aperçu du livre
Anorectal Disorders
Mexico
1
Embryology of the Anorectum
Mercedes Amieva-Balmori⁎,†; José María Remes-Troche⁎ ⁎ Digestive Physiology and Gastrointestinal Motility Laboratory, Institute of Medical and Biological Research, University of Veracruzana, Veracruz, Mexico
† Mexican Institute of Social Security, Regional General Hospital, Orizaba, Mexico
Abstract
The epithelium of the digestive tract and the parenchyma of its derivatives arise from the endoderm, whereas the components of the connective tissue, muscle, and peritoneal tissues originate in the mesoderm. The differentiation of the gut and its derivatives depends on the reciprocal interaction between the endoderm of the gut tube and its surrounding mesoderm and begins at the third week of gestation. The digestive system extends from the buccopharyngeal membrane to the cloacal membrane and is divided into four parts: pharyngeal gut, foregut, midgut, and hindgut. The hindgut gives rise to the structures extending from the distal third of the transverse colon to the upper portion of the anal canal. The lower portion of the anal canal derives from the ectoderm. Normal development is dependent on the cloacal membrane. In recent years, new processes involved in anorectal embryogenesis have been described, which we shall review in the following section.
Keywords
Endoderm; Mesoderm; Cloaca; Anorectum
1.1 Introduction
Despite a long history of embryologic research, the mechanisms involved in the development of the hindgut, which gives rise to the anorectum, are not completely understood.¹ That limitation of knowledge is related to numerous factors that include: a scarcity of material for appropriate study; technical problems, such as the difficulty in interpreting serial sections; and a lack of experience in performing three-dimensional reconstructions.²
In general, four steps are considered in the development of the primitive gut and its derivatives (Fig. 1.1):
1.Pharyngeal gut or pharynx, which extends from the buccopharyngeal membrane to the tracheobronchial diverticulum;
2.Foregut, situated caudal to the pharyngeal tube and arriving caudally at the origin of the liver bud;
3.Midgut, begins caudal to the liver bud and extends to the site, in the adult, of the right two-thirds and the left third of the transverse colon; and
4.Hindgut, which extends from the left third of the transverse colon to the cloacal membrane.
Fig. 1.1 Development of digestive system.
The formation of the digestive tract begins at week 3 of gestation. It is created from the cranio-caudal and lateral folding of the embryo, resulting in the incorporation of one portion of the endoderm-lined yolk sac into the embryo to form the primitive gut. The other two portions of the endoderm-lined cavity, the yolk sac and the allantois, remain outside of the embryo. The primitive gut forms a blind-ending tube in the cephalic and caudal parts of the embryo, corresponding to the foregut and hindgut, respectively. The middle portion, or midgut, transitorily maintains its communication with the yolk sac through the omphalomesenteric duct, or vitelline pedicle.
The endoderm forms the epithelial lining of the gastrointestinal tract and gives rise to the parenchyma of glands, such as the liver and pancreas. Muscle and peritoneal components of the gut wall, as well as its connective tissue, derive from the splanchnic leaf of the mesoderm. The differentiation of various regions of the gut and its derivatives depends on a reciprocal interaction between the endoderm of the gut tube and the surrounding splanchnic mesoderm. The mesoderm determines the type of structure that can be formed (i.e., the colon).
1.2 Embryology of the Hindgut
The hindgut gives rise to the distal third of the transverse colon, the descending colon, the sigmoid colon, the rectum, and the upper portion of the anal canal. The hindgut endoderm also lines the bladder and the urethra.
The primitive cloaca
is traditionally considered to be divided by the urorectal septum (which appears at week 4) into an anterior urogenital system (ventral) and a posterior anorectal system (dorsal). The division of the cloaca is completed at week 6, when the urogenital system is fused with the cloacal membrane.
The term cloaca
has different uses, one of which describes a transitional organ system in human embryos, another refers to a congenital abnormality, and a third describes a normal organ in birds. The terminal portion of the hindgut is continuous with the posterior region of the cloaca, which is the primitive anorectal canal, and the allantois is continuous with the anterior portion of the cloaca, which is the primitive urogenital sinus. The cloaca is an endoderm-lined cavity, whose ventral end is also lined with surface ectoderm. The boundary between the endoderm and ectoderm forms the cloacal membrane. A layer of mesoderm, the urorectal septum, separates the region between the allantois and the hindgut. That septum derives from the fusion of the mesoderm covering the yolk sac with the mesoderm that surrounds the allantois. As the embryo grows and the caudal folding continues, the urorectal septum moves closer to the cloacal membrane, but the two structures never make contact with one another.
At the end of week 7, the cloacal membrane ruptures, creating the opening for the hindgut and a ventral orifice for the urogenital sinus. The tip of the urorectal septum forms the perineal body between the two openings. At that time, ectoderm proliferation closes the region most caudal to the anal canal. During week 9, that region is recanalized, signifying that the caudal portion of the anal canal is of ectodermal origin and is irrigated by the inferior rectal arteries, which are branches of the internal pudendal arteries.
The cranial portion of the anal canal arises from the endoderm and is vascularized by the superior rectal artery, which is the continuation of the inferior mesenteric artery that supplies the hindgut (Fig. 1.2).³
Fig. 1.2 Embryology from 4 to 7 weeks. (A, B) The fusion of the hindgut with the allantois and mesonephric ducts is partitioned by the urorectal septum, creating the urogenital sinus anteriorly and the anorectum posteriorly. The once common chamber terminates blindly at the cloacal membrane, which similarly is divided into the anterior urogenital membrane and posterior anal membrane. (C) The ectodermal layer of the anal membrane gives rise to the surrounding protuberances, the anal folds and creates a central depression, the proctodeum, which develops into the distal anal canal.
1.3 Theories on the Development of the Hindgut
Since the 19th century work of Tourneux and Retterer, it has been accepted that normal development of the primitive hindgut depends on the subdivision of the cloaca by the so-called urorectal septum.⁴,⁵ According to that theory, abnormal septation development would always result in abnormal cloacal development. However, there is no agreement on the nature and formation of that septum and recent studies have presented another form of development. Tourneux thought that the septum moved downwards in a cranial-to-caudal manner like a French curtain
and Retterer speculated that the lateral folds or ridges appeared in the lumen of the cloaca. Those ridges would become fused at the midline to form the septum, beginning cranially and ending caudally at the level of the cloacal membrane. These theories were supported by numerous researchers. Stephens described a combination of the two theories, which he thought could better explain the different types of anorectal malformations. He stated that the cranial part of the septum would grow downward, as explained by Tourneux, whereas in the caudal portion of the septum, the lateral ridges would fuse to form the septum.⁶
Nevertheless, in 1986, van der Putte rejected the idea that the urorectal septum played the main role in the process of cloacal differentiation.⁷ Studying the morphology of rectal malformations in newborns, Bill and Johnson⁸ and Gans and Friedman⁹ concluded that, in the majority of cases, the fistula could be an ectopic anal opening. They posited that the rectum, situated at a high level, in fact migrates toward the anal opening during normal development, and if that process were to be altered the resulting ectopic anal canal would open creating the fistula. However, there is no embryologic evidence of that migration.
At week 7 of gestation the urogenital system and the anorectum are supposed to separate, but in recent studies¹⁰ 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.¹² evaluated 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 apoptosis 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.¹⁵ studied 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 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 Hashimoto¹⁶ 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 T.W., 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 T.W. Aparato digestivo. In: Sadler T.W., ed. Embriología Médica Con Orientación Clínica. 8th ed. España: Panamericana; 2002:262–293.
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 F.D. Congenital Malformations of the Rectum, Anus, and Genitourinary Tract. Edinburgh: Livingstone; 1963.
7 van der Putte S.C. Normal and abnormal development of the anorectum. J Pediatr Surg. 1986;21:434–440.
8 Bill A.H., Johnson R.J. Failure of migration of the rectal opening as the cause for most cases of imperforate anus. Surg Gynecol Obstet. 1958;106:643–651.
9 Gans S.L., Friedman N.B. 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 E.C., Hutson J.M. The absence of lateral fusion in cloacal partition. J Pediatr Surg. 2003;38:1287–1295.
11 Paidas C.N., Morreale R.F., Hutchins G.M., et al. Normal and abnormal embryonic development of the anorectum in human embryos. Teratology. 1998;57:70–78.
12 Kluth D., Fiegel H.C., 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 development in mice. Anat Rec A Discov Mol Cell Evol Biol. 2004;279:761–767.
14 Qi B.Q., 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 H.L., Wang D.J., Tang X.B., Jia H.M., Bai Y.Z. Normal development of hindgut and anorectum 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.
2
Anorectal Anatomy and Function
Ravinder K. Mittal Department of Medicine/Gastroenterology, University of California, San Diego, CA, United States
Abstract
The aim of this chapter is to provide the reader with information on the recent advances in our understanding of anal sphincter anatomy and of imaging and functional assessment tools. There are three distinct anatomical structures, the internal anal sphincter (IAS), external anal sphincter (EAS), and puborectalis muscle (PRM), the last one being a part of the pelvic-floor or levator-ani muscle that contributes to the anal-closure/sphincter mechanism.
Keywords
External anal sphincter; Morphology; Pelvic floor; Anal incontinence; Fecal continence
Abbreviations
EAS
external anal sphincter
IAS
internal anal sphincter
PRM
puborectalis muscle
Disclosures
Author has no conflict of interest.
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 study¹ 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 (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 identify 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 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 intracellular 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 A2 and prostaglandin F2α).¹⁹ Platelet 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
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