11 Development of

Gastrointestinal Tract
Learning Objectives
At the end of this chapter, students would be able to define and understand the
following:
•• Development of the esophagus and stomach
•• Rotation of the midgut loop
•• Development of the pancreas
•• Formation and fate of the cloaca
•• Anorectal anomalies

Keywords: Tracheoesophageal fistula, annular pancreas, imperforate anus, pectinate line.

Introduction part of the yolk sac is incorporated into the

embryo to form the primitive gut.
Primitive gut is divisible into foregut,
Gastrointestinal tract (GIT) extends from
midgut, and hindgut (Fig. 11.1). We will now
the stomodeum (an ectodermal depression
discuss the parts of GIT under each one of
at cranial end) to the proctodeum (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 endoderm of the yolk sac. The surrounding
splanchnic mesenchyme forms the connec­ The derivatives of foregut are pharynx,
tive tissue and muscular elements of the wall esophagus, stomach, duodenum (proximal to
of the gut. The development of tongue, tooth, the opening of bile duct), liver, biliary appa­
and palate 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

Formation of the supplied by celiac artery, which is the artery

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, jejunum,
106 Chapter 11

Pharynx

Stomodeum Gastric and

duodenal region
Septum transversum Heart

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.

ileum, cecum and appendix, ascending colon, Table 11.1 lists the parts of the GIT and
and right two-thirds of the transverse colon. 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. mesoderm. 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, descending colon, GIT
sigmoid colon, rectum, and upper two-thirds
of the anal canal above the pectinate line. Transcription
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 Small intestine CDXC
the gut is governed by various transcription
factors. Large intestine 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 hernia.
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
relative length by about the seventh week.
Rotation of the Stomach
Its epithelium 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 nerve.
4. Its left surface becomes anterior
Anomalies surface and is innervated mainly by
the left vagus nerve.
1. Esophageal atresia: 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

Level of section f
Oesophagus
Laryngotracheal
tube

Laryngotracheal
tube

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

a b c d

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

tracheoesophageal fistula.

Longitudinal
axis

Lesser
curvature

Stomach Greater
curvature

Duodenum

a b c

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 ligament
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 kidney (Fig. 11.5).

Stomach
Aorta
Ventral
mesentery Dorsal mesentery

Level of section b
Liver Level of section c

Spleen
Falciform
ligament Celiac artery
Dorsal pancreatic
bud
Ventral pancreatic
bud

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

gastrosplenic ligament.
Congenital Hypertrophic Pyloric Stenosis:
It occurs with the frequency of 1 in 150 male
infants and 1 in 750 female infants, that is,
the condition is five times more frequent in
Development of the
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 peritoneum (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,
the duodenum gets recanalized. Because the
Anomaly 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
Peritoneal cavity

Duodenum
Foregut
Hepatic
Midgut
diverticulum
Yolk stalk

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. Duodenal atresia: 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 minor duodenal papilla, located
head, neck, 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 pancreatic duct: 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
Major
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

Dorsal pancreatic bud

Bile
duct

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

Development of the Liver lesser omentum stretches from the liver to

stomach forming hepatogastric ligament and
and Biliary Apparatus to the duodenum forming hepatoduodenal
ligament.
In the early fourth week, a ventral outgrowth
appears along the caudal part of the foregut. Anomalies
This is called hepatic diverticulum/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 gallbladder.
part is the primordium of the liver. The cells 2. Biliary atresia: 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 abdomen 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
and concentrated by the gallbladder reaches
Rotation of the Midgut Loop
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 ligaments: 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 connecting stalk. 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 abdominal wall 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 flexure
(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. Omphalocele: 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 volvulus. 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 pylorus 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

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 mesenteries. (a, b) Before fixation, and
(c, d) After fixation.
 Development of Gastrointestinal Tract 121

Meckel’s
diverticulum

Meckel’s
diverticulum Fibrous
cord

Ileum

a b

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 urethra.
122 Chapter 11

The inferior mesenteric artery supplies and ventral parts by urorectal septum. 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.
2. It develops as a coronal sheet or a
Cloaca
wedge of mesenchyme from the junc­
Cloaca is the terminal part of the hindgut tion of allantois 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

Phallus

Urorectal
Cloacal
septum
membrane
b

Developing
urinary bladder

Urogenital membrane Urorectal

Anal membrane septum
Anal canal Rectum

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 urogenital sinus.
 Development of Gastrointestinal Tract 123

toward the cloacal membrane. 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 (ectoderm). 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 nerves.
2. Ventral: Urogenital membrane. 3. Drained by the superior rectal vein
The mesenchyme surrounding the cloaca (portal tributary).
forms the cloacal sphincter. It also divides 4. Drained into the inferior mesenteric
into dorsal and ventral components. Its lymph 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 perineum. 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. Imperforate anus: 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) vagina—rectovaginal fistula.
may open into the vulva. 2. Rectal atresia: Rectum ends blindly
4. Persistent cloaca: 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.