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Home , Anal valves, Annular pancreas, Ascending colon, Cloaca (embryology), Hepatic diverticulum, Hepatogastric ligament

Development of 11

Learning Objectives

At the end of this chapter, students would be able to define and understand the following: •• Development of the and •• Rotation of the loop •• Development of the •• Formation and fate of the •• Anorectal anomalies

Keywords: Tracheoesophageal , annular pancreas, imperforate , .

part of the is incorporated into the Introduction to form the primitive gut. Primitive gut is divisible into , Gastrointestinal tract (GIT) extends from midgut, and (Fig. 11.1). We will now the (an ectodermal depression discuss the parts of GIT under each one of at cranial end) to the (an ecto­ them. dermal depression at caudal end) of the embryo. Thus, lining of terminal parts is ecto­ dermal in origin, while rest of it is formed by Foregut the of the yolk sac. The surrounding splanchnic forms the connec­ The derivatives of foregut are , tive tissue and muscular elements of the wall esophagus, stomach, (proximal to of the gut. The development of , tooth, the opening of ), , biliary appa­ and is dealt in Chapter 10. ratus, and pancreas. These derivatives of the foregut except the pharynx, lower respira­ tory tract, and most of the esophagus are supplied by celiac , which is the artery Formation of the of the foregut. Primitive Gut Midgut During the fourth week, the embryo under­ goes folding both cephalocaudally as well as The derivatives of the midgut are duodenum laterally. Because of this folding, the dorsal distal to the opening of the bile duct, , 106 Chapter 11

Pharynx

Stomodeum Gastric and duodenal region

Yolk stalk Coeliac trunk (foregut A.)

Allantois Superior mesenteric artery (midgut A.)

Cloacal membrane

Cloaca Inferior mesenteric artery (hindgut A.)

Fig. 11.1 Section of the early embryo after folding showing the three parts of GIT: foregut, midgut, and hindgut along with their blood supply. , and , , Table 11.1 lists the parts of the GIT and and right two-thirds of the . the associated transcription factors. These derivatives are supplied by the supe­ There seems to be reciprocal interac­ rior mesenteric artery, which is the artery of tion between the endoderm and splanchnic the midgut. . This is initiated by sonic hedgehog (SHH) expression. This then causes Hindgut Table 11.1 Transcription factors associated The derivatives of the hindgut are left one- with the development of various parts of the third of transverse colon, , GIT , , and upper two-thirds Transcription of the above the pectinate line. Part of the gut tube factor These derivatives of the hindgut are supplied by the inferior mesenteric artery, which is Esophagus and stomach SOX2 the artery of the hindgut. Duodenum PDX1 The development of different parts of CDXC the gut is governed by various transcription factors. and rectum CDXA Development of Gastrointestinal Tract 107 expression of Hox genes in the mesoderm septum and communication of lumens which brings in the differentiation of the of the two tubes: the trachea and endoderm in different regions such as small esophagus (Fig. 11.3). intestine, colon, cecum, etc. 2. Short esophagus: It results from the We will now consider the fate of each failure of the esophagus to elongate. part of the primitive gut sequentially starting This draws a part of the stomach into from the foregut. the thorax through esophageal hiatus The foregut starts with the pharynx, in the diaphragm causing congenital which has been dealt with pharyngeal appa­ hiatal . ratus in Chapter 10. The subsequent parts, that is, esophagus, stomach, and duodenum shall now be considered. Development of the Stomach Development of the It appears as a fusiform dilatation along the Esophagus caudal part of the foregut around the fourth week. It is initially oriented in the median The primitive pharynx shows appearance of plane. It presents two ends: the proximal and folds called tracheoesophageal folds from the distal; two borders: the ventral and the its lateral walls. They fuse to form tracheo­ dorsal; two folds: the ventral mesogastrium esophageal septum which divides pharyn­ and the dorsal mesogastrium, anchoring the geal gut into ventrally placed trachea and borders of the stomach to the respective dorsally placed esophagus. In the beginning, abdominal walls; and two surfaces: right and the esophagus is short. It elongates due to left (Fig. 11.4). growth of the body, development and descent of heart and lungs, and reaches its definitive Rotation of the Stomach relative length by about the seventh week. Its and the glands are derived The stomach undergoes 90-degree rotation from the endoderm while connective tissue around its own longitudinal axis, and with and the muscular elements of its wall are this the following occurs: derived from the surrounding splanchnic 1. Its ventral border goes to the right mesenchyme. However, the striated muscle side, grows less, and forms the lesser in the wall of the upper third of the esoph­ curvature. agus is contributed by the branchial meso­ 2. Its dorsal border goes to the left side, derm. During the course of development, grows more, and forms the greater the epithelium proliferates to obliterate the curvature. lumen. This is then followed by vacuolization 3. Its right surface becomes posterior and recanalization (Fig. 11.2). Its failure can surface and is innervated predomi­ cause esophageal stenosis or atresia. nantly by the right vagus . 4. Its left surface becomes anterior Anomalies surface and is innervated mainly by the left . 1. : It occurs due After the rotation, the stomach assumes to the failure of recanalization. It is its final position. Its proximal end sinks usually associated with tracheoesoph­ downward and to the left and forms the ageal fistula. The malformation results cardiac end, while the distal end goes toward from deviation of tracheoesophageal right and forms the pyloric end. 108 Chapter 11

Level of section b Primitive pharynx

Laryngotracheal diverticulum Tracheo-oesophageal fold

Pharynx Primordium of laryngo-tracheal tube a b

Level of section d

Lung bud

Tracheo-oesophageal Folds fused fold Oesophagus

d

c

Level of section f Oesophagus Laryngotracheal tube

Laryngotracheal tube

f

e Fig. 11.2 (a–f) Illustrations showing development of oesophagus.Note how tracheo- esophageal septum develops at 4 to 5-weeks separating esophagus and the laryngotracheal tube. Development of Gastrointestinal Tract 109

Esophageal Trachea atresia Fistula

Esophagus

abcd Fig. 11.3 (a–d) Illustrations showing schematic representation of various types of tracheoesophageal fistula.

Longitudinal axis

Lesser curvature

Stomach Greater curvature

Duodenum

abc

Fundus

Anteroposterior axis Duodenum Body

Pylorus

d e Fig. 11.4 (a–e) Illustrations showing the development and rotation of the stomach. 110 Chapter 11

Fate of the Mesogastrium 2. The part between the liver and the stomach forms lesser omentum. In the ventral mesogastrium, liver develops. Likewise, the spleen develops in the With this, the following changes occur: dorsal mesogastrium. This splits the dorsal 1. The part of the ventral mesogas­ mesogastrium into (1) gastrosplenic trium between the ventral abdominal between the stomach and the spleen and wall and the liver forms falciform (2) lienorenal ligament between the spleen ligament. and the (Fig. 11.5).

Stomach Ventral Dorsal mesentery

Level of section b Liver Level of section c Spleen Celiac artery Dorsal Ventral pancreatic bud

a

Kidney Stomach Spleen Liver Aorta Dorsal mesentery

Liver Kidney

b Falciform Lienorenal ligament lgament Hepatogastric ligament

Gastrosplenic ligament c Fig. 11.5 Illustration showing the fate of ventral and dorsal mesogastrium. (a) Sagittal section. (b, c) Transverse sections. Development of Gastrointestinal Tract 111

Anomaly embedded in the tail of the pancreas or in the . Congenital Hypertrophic : It occurs with the frequency of 1 in 150 male infants and 1 in 750 female infants, that is, Development of the the condition is five times more frequent in males. It presents with marked thickening at Duodenum pyloric end of the stomach. It is due to the hypertrophy of circular musculature and to It is of dual origin, that is, it is derived from some extent even longitudinal muscle. This both the foregut and the midgut. In the fourth causes marked stenosis (narrowing) of the week, duodenum begins to develop from the pyloric canal leading to obstruction to the caudal part of the foregut and the cranial part passage of food. Infants with this condition of the midgut. This gives rise to the lining have projectile vomiting. There is a possi­ epithelium and the glands. The connective bility of some genetic factor responsible for tissue and the musculature develop from the it, since it is seen with high frequency in both splanchnic mesenchyme surrounding the members of the monozygotic twin pair. The primitive gut. number of the autonomic ganglion cells in The junction of the two (developmen­ pyloric region in this condition is remarkably tally different) parts of the duodenum is reduced. marked by the opening of the bile duct. As these parts grow rapidly, the duodenum forms a “C-shaped” loop projecting ventrally Development of the (Fig. 11.6). Spleen Rotation of the Duodenum The spleen is derived from the differentia­ tion of the mesenchymal cells between the With the rotation of the stomach through 90 two layers of the dorsal mesogastrium. These degrees, the duodenal loop rotates onto the mesenchymal cells form the capsule, the right side. It soon becomes retroperitoneal­ connective tissue, and the parenchyma of the ized by fusion and subsequent disappearance spleen. Its development begins around the of the (visceral and parietal) fifth week and is nearly complete during the on the back of the duodenum. During the fetal period. In the fetus, the spleen is lobu­ fifth and the sixth week, the lumen of the lated. It serves the hemopoietic function till developing duodenum is obliterated due to the late fetal period (Fig. 11.5). the proliferation of the lining epithelium. Subsequently, vacuolization occurs, thus, Anomaly the duodenum gets recanalized. Because the duodenum is derived from both the foregut Accessory Spleen: It is met with the as well as the midgut, it is supplied by frequency of nearly 10% in the general popu­ branches from celiac trunk, the artery of the lation. It consists of splenic tissue and may foregut, as well as from superior mesenteric appear at the hilum of the spleen or may be artery, the artery of the midgut. 112 Chapter 11

Ventral Dorsal Mesentry mesentery Stomach region Foregut Hepatic Midgut diverticulum Yolk stalk Duodenum

a Dorsal mesentery Ventral mesentery Dorsal pancreatic bud Developing liver Foregut Midgut

Gall bladder b

Septum transversum

Bile duct Stomach

Liver Dorsal pancreatic Cystic bud duct

Gall bladder Duodenal loop Ventral pancreatic bud c

Diaphragm

Stomach

Cystic duct

Falciform ligament Pancreas Gall bladder

Bile duct

d Fig. 11.6 Illustrations showing stages of development of duodenum, pancreas, liver, and extrahepatic biliary apparatus. (a) 4 weeks, (b, c) 5 weeks, and (d) 6 weeks. Development of Gastrointestinal Tract 113

Anomalies Development of the 1. Duodenal stenosis: In duodenal stenosis, there is narrowing of the Pancreas duodenal lumen. This could be due to either of the following two causes: It develops from the ventral pancreatic bud (a) Incomplete recanalization. (VPB) and the dorsal pancreatic bud (DPB). (b) Pressure exerted by the annular They are endodermal in origin and arise pancreas. from the caudal part of the foregut (future This results in duodenal obstruc­ duodenal part). The VPB develops close tion associated with bilious vomiting to the future site of entry of the bile duct (Fig. 11.7). into the duodenum and is smaller than the 2. : Blockage of the dorsal bud. The DPB is larger of the two and duodenal lumen due to the failure develops into the dorsal mesentery. of recanalization results in duodenal As the duodenal loop (C-shaped) rotates atresia. Mostly it involves the second to the right, the VPB along with the bile duct or the third part of the duodenum. migrates to the dorsal side. It then fuses with Bile-contained vomitus occurs in few the DPB and forms the lower part of the head hours after the birth (Fig. 11.7). and the uncinate process of the pancreas.

Narrow lumen

Dilated Stomach duodenum Level of section a1 Duodenal stenosis

Stenosis a a1 a2

Dilated duodenum Septum

Duodenal atresia Level of section b2

Duodenum Atresia (decreased in size) b1 b2 b Fig. 11.7 Illustrations showing duodenal anomalies. (a) Duodenal stenosis, (b) duodenal atresia. 114 Chapter 11

Rest of the pancreas, that is, upper part of the the , located head, , body, and the tail of the pancreas about 2 cm proximal to the major is formed by the DPB (Fig. 11.8). duodenal papilla.

Pancreatic Ducts Histogenesis

1. Main : Its juxtaduo­ The pancreatic acini (exocrine part) develop denal part is formed by the duct of from the endoderm of the pancreatic buds. VPB, while the distal part of the duct They form meshwork of tubules. The acini is formed by the duct of DPB. It opens develop from the cell clusters at the ends of at the summit of the major duodenal the tubules. The islets of Langerhans develop papilla. from the group of cells which separate from 2. Accessory pancreatic duct: It is the tubules. The hormones, insulin, and formed by the proximal part of the glucagon are secreted from the 20th week duct of DPB. It opens at the summit of onward.

Developing liver

Dorsal pancreatic bud

Gall bladder Ventral pancreatic bud a

Dorsal pancreatic duct

Ventral pancreatic duct Accessory pancreatic duct b

Minor duodenal papilla

Main pancreatic duct c Fig. 11.8 (a–c) Illustrations showing the development of the pancreas. Development of Gastrointestinal Tract 115

Anomalies 2. Heterotophic/accessory pancreatic tissue: It may be located in the wall of 1. Annular pancreas: It results from the the stomach, duodenum, or in Meckel’s bifurcation of the VPB. Because of this, diverticulum and this may cause pancreatic tissue surrounds the second ulcerations. part of duodenum causing duodenal obstruction. Men are affected more frequently than women (Fig. 11.9).

Dorsal pancreatic bud Stomach

Bile duct

Bifid ventral pancreatic bud

a

Dorsal pancreatic bud

Bile duct

b

Bile duet

Duodenum

Annular pancreas

Site of duodenal obstruction c Fig. 11.9 (a–c) Illustrations showing development of annular pancreas leading to duodenal obstruction. 116 Chapter 11

lesser omentum stretches from the liver to Development of the Liver stomach forming hepatogastric ligament and and Biliary Apparatus to the duodenum forming . In the early fourth week, a ventral outgrowth appears along the caudal part of the foregut. Anomalies This is called /bud. It grows into the septum transversum. It 1. Accessory hepatic ducts: Usually, they shows two parts: the larger cranial part and run from the right lobe of the liver to the smaller caudal part. The larger cranial the . part is the primordium of the liver. The cells 2. : Though it is rare, it is of this part proliferate giving rise to inter­ a serious anomaly. It occurs due to the lacing cords of the liver cells (hepatocytes). failure of recanalization of biliary duct. These cords anastomose around endotheli­ It warrants liver transplant or else it ally lined spaces which develop into hepatic is fatal. sinusoids. The mesenchyme of the septum 3. Phrygian cap: In this, the gallbladder transversum gives rise to the fibrous tissue, has folded fundus (Fig. 11.10). hemopoietic cells, and the Kupffer cells. 4. Hartman’s pouch: In this, the neck of The rapidly growing liver occupies most of the gallbladder shows outpouching. the space in the and has the right It is called Hartman’s pouch. It may and left lobes almost equal in size initially. harbor (silent) gall stones (Fig. 11.10). However, with the ductus venosus, shunting the blood from left to the right side, left lobe of liver undergoes relative regression in size. Development of the Soon caudate and quadrate lobes develop as Midgut part of the right lobe. By about the twelfth week, the hepatocytes start bile formation. The midgut has the following derivatives: Hemopoiesis occurs in the liver starting from 1. Small intestine starting from the the sixth week (Fig. 11.6). second part of the duodenum distal to The smaller caudal part of the hepatic the opening of the bile duct followed diverticulum is the cystic bud. It develops by jejunum and ileum. into the gallbladder. Its stalk forms the cystic 2. Cecum and appendix. duct. It then joins the hepatic duct to form 3. Ascending colon. the bile duct that reaches the ventral part of 4. Right two-third of the transverse colon. the developing duodenal loop. Subsequently They all are supplied by the superior with the rotation of the duodenal loop, the mesenteric artery (artery of midgut). bile duct attains its definitive position, that Initially, the midgut forms a loop, which is, dorsal (posteromedial) aspect of the undergoes rotation. duodenum. By the 13th week, bile secreted by the liver Rotation of the Midgut Loop and concentrated by the gallbladder reaches duodenum via bile duct making meconium With elongation, the midgut forms a “U- (intestinal contents), which is dark green shaped” midgut loop, directed ventrally. It in color. has the midgut artery (superior mesenteric With the development of the liver, the artery) within the “U” of the loop. The loop, ventral mesentery forms two : the thus presents the following: falciform ligament ventral to the liver and 1. Cranial/prearterial limb. lesser omentum dorsal to the liver. Later, the 2. Caudal/postarterial limb. Development of Gastrointestinal Tract 117

Phrygian cap Hartmann’s pouch (folded fundus) (site of gall stones) Fig. 11.10 Illustrations showing anomalies of gall bladder.

Midgut loop projecting out into the con- left saccules (on either side of anterior teniae necting stalk, and it is called umbilical hernia. coli) are equal in size; however, subsequently This occurs between the sixth and the tenth the right saccule grows more than the left. week. This is due to the following factors: This pushes the base of the appendix closer 1. Rapid growth of the midgut loop. to the ileocecal junction (Fig. 11.11). 2. Relatively large size of the hepar (developing liver). Return of the Midgut Loop to the 3. Relatively large size of the meso­ Abdomen nephroi (developing kidneys). This occurs during/around the 10th week. 4. Relatively smaller size of the abdom­ The following factors are responsible for this: inal cavity. 1. Increment in the size of abdomen. The midgut loop undergoes total 270 2. Relative regression in the size of the degrees of rotation in anticlockwise direc­ hepar (liver). tion. Out of this, the initial 90 degrees rota­ 3. Relative regression in the size of the tion occurs when the midgut loop is within mesonephroi (kidneys). the . With this, the cranial During return, the cranial limb returns limb comes to lie on the right side and the first and to the left because most of the caudal limb comes to lie on the left side. The right side is occupied by the developing rotation occurs around an axis provided by liver. The caudal limb returns later and to the superior mesenteric artery. The cranial the right. With this, further 180 degrees of limb forms the intestinal loop and the caudal rotation is accomplished, thus completing limb shows cecal diverticulum. This forms total 270 degrees of rotation. On return, the primordium of the cecum and vermi­ the caudal limb derivatives come to lie on form appendix. With further development, the right side; with this, the cecum lies in the the apical portion of the cecal diverticulum subhepatic position (till ascending colon is does not grow to the same extent and forms formed). Subsequently, with the formation of appendix. The cecum also undergoes a differ­ ascending colon, cecum occupies its defini­ ential growth. Initially, both of its right and tive position in the right iliac fossa. 118 Chapter 11

Superior Prearterial mesenteric Limb artery

Caecal diverticulum Postarterial Limb After 900 rotation Initial position b a

Caecum (subhepatic)

Small intestine

d After 1800 rotation c

Transverse colon

Ascending colon

After 2700 rotation e Fig. 11.11 (a–e) Illustrations showing rotation of the midgut loop umbilical hernia (6–10 weeks) and then return of the intestine into the abdomen and fixation of the gut. Total of 270 degrees of anticlockwise rotation occurs. Development of Gastrointestinal Tract 119

Fixation of the Gut 5. Reverse rotation: In this, the midgut loop rotates in clockwise direction On return of intestines to the abdomen, the instead of anticlockwise direction. attachment of the dorsal mesentery to the Therefore, the duodenum lies in front posterior is in midline. Some and the transverse colon lies behind parts of the intestines, that is, duodenum, the superior mesenteric artery. ascending and descending colon pass behind 6. Subhepatic cecum: It is due to the peritoneum or become retroperitoneal. failure of elongation of the colon. Mesentery of jejunum and ileum is It may be asymptomatic. It poses initially in midline, however, with rotation of problem in the diagnosis of appendi­ the gut, it twists around the superior mesen­ citis which needs to be differentiated teric artery and finally gets attachment, from acute cholecystitis. passing down from duodenojejunal (to the left of L2 vertebra) to the ileocecal junction (right sacroiliac joint) (Fig. 11.12). Meckel’s Diverticulum

Anomalies It is also called ileal diverticulum (Fig. 11.13). It is one of the most frequent anomalies of 1. : In this, the intestines the gastrointestinal tract. It occurs in about 2 fail to return to the abdomen due to 4% individuals. It is about three times more to incomplete lateral folding during frequent in men as compared to women.

the fourth week. This may produce Embryologically, it represents the remn­ larger defect with most of the viscera ant of the proximal part of the yolk stalk. It remaining outside the abdomen, appears to be arising from the antimesenteric covered by transparent amnion. border of the ileum. It is 3 to 6 cm long and 2. Umbilical hernia: In this condition, about 40 to 50 cm proximal to the ileocecal

the intestines return during the 10th junction. It may be connected to the umbil­ week and then herniate. It differs from icus by a fibrous cord or a fistula. Structurally, the omphalocele, being covered by the the wall of the diverticulum contains all the subcutaneous tissue and the skin. layers of the ileum and may possess pieces of 3. Nonrotation of the midgut: It is often the gastric or pancreatic tissues. The secre­ called left-sided colon. It may present tion of acid and enzymes from this can cause with . In this condition, the ulceration. midgut loop does not rotate during return to the abdomen. The caudal limb returns first and to the left (large Clinical Aspects intestine lies on left) and the small 1. Sometimes the diverticulum becomes intestine to the right. inflamed and clinically it mimics 4. Mixed rotation: In this, the cecum lies appendicitis. below the and is fixed to the 2. Presence of gastric or pancreatic tissue posterior abdominal wall by peritoneal in its wall may lead to ulceration and bands passing over the duodenum. It is even bleeding. due to the failure of last 90 degrees of rotation of the midgut loop. 120 Chapter 11

Dorsal abdominal wall

Ascending colon Jejunum Descending colon

a

Stomach

Inferior recess Duodenum of lesser sac

Greater omentum Dorsal abdominal Descending colon wall b

Jejunum Ascending colon Left paracolic gutters c

Stomach

Pancreas

Duodenum Transverse colon

Mesentery

d Fig. 11.12 Fixation of the gut and formation of . (a, b) Before fixation, and (c, d) After fixation. Development of Gastrointestinal Tract 121

Meckel’s diverticulum

Meckel’s diverticulum Fibrous cord

Ileum

ab

Meckel’s diverticulum

Umbilicoileal Vitelline fistula cyst

c d Fig. 11.13 (a–d) Illustrations showing Meckel’s diverticulum (ideal diverticulum) and various anomalies associated with it.

Anomalies Development of the 1. Umbilical sinus: Persistence of the Hindgut yolk stalk close to the umbilicus results in the formation of the umbil­ The derivatives of the hindgut are as follows: ical sinus. 1. Left third of the transverse colon. 2. Umbilicoileal fistula: It results from 2. Descending colon. the persistence of the intra-abdominal 3. Pelvic/sigmoid colon. portion of the yolk stalk (maintaining 4. Rectum. its lumen). 5. Upper part of the anal canal. 3. Vitelline cyst: It results from the 6. Lining epithelium of the urinary persistence of the part of the yolk stalk. bladder and most of the . 122 Chapter 11

The inferior mesenteric artery supplies and ventral parts by . There these hindgut derivatives. The terminal part are two views regarding the development of of the hindgut is dilated to form the cloaca. urorectal septum (Fig. 11.14). Let us now consider the formation and fate 1. It develops from the fusion of the supe­ of the cloaca. rior Tourneux’s fold with paired infer­ olateral Rathke’s folds. Cloaca 2. It develops as a coronal sheet or a wedge of mesenchyme from the junc­ Cloaca is the terminal part of the hindgut tion of with the hindgut beyond allantois. It is divided into dorsal (Tourneux’s fold). It grows caudally

Yolk stalk Midgut Allantois Hindgut

Proctodeum Urorectal septum Cloaca

a

Phallus

Urorectal Cloacal septum membrane b

Developing

Urogenital membrane Urorectal Anal membrane septum Anal canal Rectum

c Fig. 11.14 (a–c) Illustrations showing partitioning of the cloaca by development of the urorectal septum into dorsal rectum and the anal canal and ventral part the . Development of Gastrointestinal Tract 123

toward the . It has Anal Canal fork-like extensions which produce infoldings of the lateral walls (Rathke’s It is the terminal part of the gastrointestinal folds) of the cloaca. These folds meet tract having dual origin. Its cranial two- each other, thus dividing the cloaca thirds are derived from the hindgut (endo­ into the following parts: derm), while caudal one-third is derived (a) Dorsal—rectum and upper part of from the proctodeum (). The junc­ the anal canal. tion being marked by the pectinate line. The (b) Ventral—urogenital sinus. line represents the site of the anal membrane Around the seventh week, the urorectal (Fig. 11.15). septum fuses with the cloacal membrane. The part of the anal canal above the pecti­ This divides the cloacal membrane into the nate line is: following two parts: 1. Supplied by the superior rectal artery. 1. Dorsal: Anal membrane. 2. Supplied by the autonomic . 2. Ventral: Urogenital membrane. 3. Drained by the superior rectal The mesenchyme surrounding the cloaca (portal tributary). forms the cloacal . It also divides 4. Drained into the inferior mesenteric into dorsal and ventral components. Its nodes. dorsal part forms anal sphincter and ventral The part below the pectinate line is: part forms perineal muscles. Perineal body 1. Supplied by the inferior rectal artery. represents the site of fusion of the urorectal 2. Supplied by the somatic nerves— septum with the cloacal membrane. It forms inferior rectal nerve and hence this a fibromuscular node located in the center of part is sensitive to pain, touch, temper­ the . ature, and pressure.

Rectum

Anal column Endodermal origin (hindgut)

Anal valves Pectinate line (landmark)

Anal canal White line of Hilton

Ectodermal origin (proctodeum)

Fig. 11.15 Illustration showing development of the rectum and the anal canal from different germ layers. Upper two third of the anal canal is endodermal (hindgut) while lower one third is ectodermal (proctodeum) in origin. The blood supply, venous and lymphatic drainage and innervations is therefore different. 124 Chapter 11

3. Drained by the inferior rectal vein 3. Tumors of the upper part arise from (systemic tributary). the columnar epithelium, while those 4. Drained into the superficial inguinal of the lower part arise from the squa­ group of lymph nodes. mous epithelium. Clinical Aspects Anomalies 1. The above difference in the blood, nerve Most of the anorectal malformations result supply, venous and the lymphatic from abnormal development of the urorectal drainage becomes significant consid­ septum. This leads to incomplete separa­ ering the spread of tumors involving tion of the cloaca into urogenital sinus and anal canal. anorectal portion. 2. The lesions of the upper part are pain­ Anorectal malformations can be classi­ less, while those of the lower part are fied into low and high types (Fig. 11.16). painful. Low-type malformations are as under:

Uterus

Urinary bladder

Rectocloacal fistula

Persistent anal Persistent membrane cloaca

a b

Rectourethral Rectovaginal fistula fistula

Anal pit c d Rectum

Anal stenosis e Fig. 11.16 (a–e) Illustrations showing various anorectal anomalies. Development of Gastrointestinal Tract 125

1. : The anal membrane High type of anorectal malformations are fails to perforate at the end of the as under: eighth week. This separates the cavity 1. Anorectal agenesis: It may be with of the anal canal from the exterior. or without fistula. This is the most 2. Anal stenosis: The anus is in the common anorectal malformation normal position. The anal canal is, accounting for about two-thirds of however, narrow permitting insertion the anomalies involving anorectal of probe only. region. Rectum ends well above the 3. Anal agenesis: This may or may not be anal canal. It may be connected to associated with fistula. The anal canal (a) urinary bladder—rectovesical fistula, ends blindly. There may be an ectopic (b) urethra—rectourethral fistula, and anus (anoperineal fistula). The fistula (c) —rectovaginal fistula. may open into the vulva. 2. Rectal atresia: Rectum ends blindly 4. : Failure of urorectal and is widely separated from the anal septum to develop resulting in persis­ canal. The cause being failure of recan­ tent cloaca. alization or defective blood supply.