1. The midgut forms a U-shaped loop that herniates through the umbilical ring and undergoes two rotations to return to the abdominal cavity, positioning the appendix on the right. 2. Failure of the midgut to return or complete rotation can result in defects like omphalocele, malrotation, intestinal atresia or stenosis. 3. Common midgut defects include Meckel's diverticulum from persistence of the vitelline duct and intestinal malrotation from incomplete rotation.

1. Midgut
• Lower duodenum
• Jejunum
• Ileum
• Caecum
• Appendix
• Ascending colon
• Proximal transverse 2/3 colon

2. DISTAL DUODENUM
• Distal or lower duodenum arises from the cranial most portion of the
midgut and is served by anterior and posterior branches of the
inferior pancreaticoduodenal artery, which is a branch of the superior
mesentery artery.
• As with the rest of the duodenum, becomes secondarily
retroperitoneal as with the rest of the entire gi tract, the lumen is
obliterated transiently during development and then recanalizes.
• Failure to recanalize the duodenum can result in stenosis (narrowing)
or atresia (complete blockage)

3. Development of the midgut and colon
Herniation and rotation:
• Growth of the GI tract exceeds volume of abdominal
cavity so the tube herniates through umbilicus
• While herniated, gut undergoes a primary rotation
(fig B) of 90° “counterclockwise” (when looking at
the embryo); this corresponds with the rotation of
the stomach, and positions the appendix on the left.
The primary rotation also brings the right vagus n. to
the FRONT (hence the change in its name to
ANTERIOR vagus n.
• With the growth of the embryo, the abdominal
cavity expands thus drawing the gut tube back
within the abdominal cavity and causing an
additional, secondary rotation (fig C) of 180° CCW
(positioning the appendix on the RIGHT)
• Once in the abdominal cavity, the colon continues to
grow in length, pushing the appendix to its final
position in the lower right quadrant.
• Note the attachment of the vitelline duct to the gut
at the region of the ileum. The duct normally
regresses during development, but not always….

4. • 1. Development. The midgut forms a U-shaped loop (midgut loop)
that herniates through the primitive umbilical ring into the
extraembryonic coelom (i.e., physiological umbilical herniation)
beginning at week 6. The midgut loop consists of a cranial limb and a
caudal limb. The cranial limb forms the jejunum and upper part of
the ileum. The caudal limb forms the cecal diverticulum, from which
the cecum and appendix develop; the rest of the caudal limb forms
the lower part of the ileum, ascending colon, and proximal two
thirds of the transverse colon. The midgut loop rotates a total of
270_ counterclockwise around the superior mesenteric artery as it
returns to the abdominal cavity, thus reducing the physiological
herniation, around week 12.

6. • 2. Sources. Simple columnar absorptive cells lining midgut
derivatives, goblet cells, Paneth cells, and enteroendocrine cells
comprising the intestinal glands are derived from endoderm.
• The lamina propria, muscularis mucosae, submucosa, and inner
circular and outer longitudinal smooth muscle of the muscularis
externa and serosa are derived from visceral mesoderm.

7. • 3. Clinical considerations
• a. Omphalocele: occurs when abdominal contents herniates through
the umbilical ring and persists outside the body, covered variably by a
translucent peritoneal membrane sac (a light gray, shiny sac)
protruding from the base of the umbilical cord.
• Large omphaloceles may contain stomach, liver, and intestines. Small
omphaloceles contain only intestines. Omphaloceles are
• usually associated with other congenital anomalies (e.g., trisomy 13,
trisomy 18, or Beckwith-Wiedemann syndrome) and with
• increased levels of alfa-fetoprotein.

9. • b. Gastroschisis: occurs when there is a defect in the ventral
abdominal wall, usually to the right of the umbilical ring, through
which there is a massive evisceration of intestines (other organs may
also be involved). The intestines are not covered by a peritoneal
membrane, are directly exposed to amniotic fluid, are thickened, and
are covered with adhesions.

11. • c. Ileal diverticulum (Meckel’s diverticulum): occurs when a remnant
of the vitelline duct persists, thereby forming an outpouching located
on the antimesenteric border of the ileum. The outpouching may
connect to the umbilicus via a fibrous cord or fistula. A Meckel’s
diverticulum is usually located about 30 cm proximal to the ileocecal
valve in infants and varies in length from 2 to 15 cm. Heterotopic
gastric mucosa may be present, which leads to ulceration,
perforation, or gastrointestinal bleeding, especially if a large number
of parietal cells are present. It is associated clinically with symptoms
resembling appendicitis and bright-red or dark-red stools (bloody).

12. • d. Nonrotation of the midgut loop: occurs when the midgut loop rotates only
90_ counterclockwise, thereby positioning the small intestine entirely on the right
side and the large intestine entirely on the left side, with the cecum located
either in the left upper quadrant or the left iliac fossa.
• Note the small intestines (SI) on the right side and the large intestines (LI) on the
left side.
• e. Malrotation of the midgut loop: occurs when the midgut loop undergoes only
partial counterclockwise rotation.
• This results in the cecum and appendix lying in a subpyloric or subhepatic
location and the small intestine being suspended by only a vascular pedicle (i.e.,
not a broad mesentery). A major clinical complication of malrotation is volvulus
(twisting of the small intestines around the vascular pedicle), which may cause
necrosis due to compromised blood supply. (Note: The abnormal position of the
appendix due to malrotation of the midgut should be considered when
diagnosing appendicitis).

13. • g. Intestinal atresia and stenosis: Atresia occurs when the lumen of
the intestines is completely occluded, whereas stenosis occurs when
the lumen of the intestines is narrowed.
• The causes of these conditions seem to be both failed recanalization
and/or an ischemic intrauterine event (“vascular accident”).

14. • i. Intussusception: occurs when a segment of bowel invaginates or
telescopes into an adjacent bowel segment, leading to obstruction or
ischemia. This is one of the most common causes of obstruction in
children younger than 2 years of age, is most often idiopathic, and is
most commonly involves the ileum and colon (i.e., ileocolic). It is
associated clinically with acute onset of intermittent abdominal pain,
vomiting, bloody stools, diarrhea, and somnolence.

16. • j. Retrocecal and retrocolic appendix occurs when the appendix is located
on the posterior side of the cecum or colon, respectively. These anomalies
are very common and important to remember during appendectomies.
Note: The appendix is normally found on the medial side of the cecum.
• Derivatives of the hindgut are supplied by the inferior mesenteric artery.
• A. Distal one third of the transverse colon, descending colon, sigmoid
colon.
• 1. Development. The cranial end of the hindgut develops into the distal
one third of the transverse colon, descending colon, and sigmoid colon.
The terminal end of the hindgut is an endoderm-lined pouch called the
cloaca, which contacts the surface ectoderm of the proctodeum to form
the cloacal membrane.

17. Defects associated with gut herniation and
rotation: vitelline duct abnormalities
Vitelline duct abnormalities of some sort occur in ~2% of all live
births. Note that these aberrant structures are almost always
found along the ileal portion of the GI tract.
Langman’s fig 14-32

18. Defects associated with gut herniation
and rotation: oomphalocoele
Langman’s fig 14-31

19. Midgut Anomalies
• Clinical correlation –
• Duodenal atresia is due to failed canalization.
• Omphalocele results from failure of the midgut loop to return to the
abdomen.
• Meckel’s diverticulum occurs when a remnant of the yolk sac (Vitelline duct)
persists.
• Malrotation occurs if the midgut does not complete the rotation prior to
returning to the abdomen.

20. Malrotation
Slide from S Baker, MD

21. Defects associated with gut herniation
and rotation: abnormal rotation
Absent or incomplete
secondary rotation
Reversed secondary rotation
(90 CCW primary rotation occurs as usual
but followed by abnormal 180 CW rotation.
Net rotation is 90° CW; viscera are in their
normal location, but note that the duodenum
is anterior to the transverse colon)
Langman’s fig 14-33

22. Defects associated with gut herniation
and rotation: volvulus
Fixation of a portion of the gut tube to the body wall;
subsequent rotation causes twisting of the tube, possibly
resulting in stenosis and/or ischemia.
Carlson fig 15-13