ESA 3 - GI

Development of the midgut begins with rapid elongation of the gut and its mesentery resulting in the primary intestinal loop. The loop has a cephalic limb, which will become the distal part of the duodenum, the jejunum and part of the ileum, and a caudal limb which will become the rest of the ileum, cecum, appendix, ascending colon and proximal 2/3 of transverse process. Between the 2 limbs lies the superior mesenteric artery as the axis, around which the midgut will rotate. The primary intestinal loop remains in contact with the yolk sac via the vitelline duct.

During the 6th week of development the rapid elongation, particularly of the cephalic limb, and the expansion of the liver result in the abdominal cavity not being big enough to contain all the intestinal loops. Therefore the loops enter the extraembyonic cavity in the umbilical cord. Omphaleocoele is persistance of physiological herniation, where the gut stays in the amniotic sac surrounded by amnion. It is associated with chromosomal defects and neural tube defects.

During physiological herniation, the primary intestinal loop rotates 90 degrees around the superior mesenteric artery in counterclockwise direction so that the caudal limb is on the left and the cranial limb is on the right. Elongation of the loop continues and the cephalic limb forms a number of loops and the caudal limb lengthens but does not coil. On returning back the abdominal cavity, the intestinal loops rotate 180 in the counterclockwise direction so that the cephalic limb is on the left and the caudal limb is on the right. If rotation does not occur properly then the retraction of herniated loops into the abdominal cavity will be abnormal.

During the 10th week of development the loops start to move back into the abdominal cavity. The proximal part of the jejunum is the first part to re-enter the abdominal cavity and lies on the left side. The other intestinal loops come to lie next to the jejunum and the last part to enter is the caecal bud. The cecal bud develops on the caudal limb in the 6th week. Temporarily the cecal bud lies in the right upper quadrant directly below the right lobe of the liver but eventually it descends into the right iliac fossa. The ascending limb and hepatic flexure then lie on the right hand side. The distal end of the cecal bud forms the narrow diverticulum called the appendix. It is a retrocecal structure.

The mesentry proper is the mesentry of the primary intestinal loop. When the caudal limb moves to the right side of the abdominal cavity the dorsal mesentery twists around the origin of the superior mesenteric artery. When the cecum descends into the right iliac fossa, the ascending limb and descending limb take their definitive positions (right and left). Their mesocolons fuse with the posterior peritoneum so that the ascending and descending limb become secondary retroperitoneal structures. The transverse colon mesoderm fuses with the posterior wall of the greater omentum but remains present so the transverse colon is mobile from hepatic flexure to splenic flexure. The appendix, lower end of caecum and sigmoid colon retain their mesenteries. The jejunum and ileum maintain their mesentery proper from the intraperitoneal duodenum to the ileocecal junction. ( it is no longer attached to the mesentery of the ascending colon).

In the ascending limb the mesocolon completely fuses with posterior peritoneum, except for at the hepatic flexure. If the mesocolon fails to fuse, this will make the ascending limb and caecum mobile. This mobility can lead to abnormal movements and potentially volvulus of the caecum which can lead to strangulation. Incomplete fusion of the mesocolon could give rise to retrocolic pocket formation behind the ascending mesocolon. A retrocolic hernia is entrapment of portions of the small intestine behind the mesocolon.

Omphalocele is persistence of physiological herniation due to the failure of the bowel to re-enter the abdominal cavity in week 10. Instead the viscera remain outside of the abdominal cavity, surrounded by amnion. It is associated with many other congenital defects eg neural tube defects and chromosome abnormalities. It is different from umbilical hernias as these are covered by skin and subcutaneosu tissue where as in omphalocele, the viscera are surrounded by amnion.

Gastroschisis literally means split stomach. It is the protrusion of abdominal contents through the body wall directly into the amniotic fluid. The protrusion occurs on the right lateral side of the umbilicus usually. The viscera are not covered by peritoneum or amnion and so may be damaged by exposure to amniotic fluid. It is increasing in frequency amongst young mothers with frequent recreational drug use. Unlike omphalaocele it is not associated with other severe defects and is caused by failure of the anterior abdominal wall to close.

Mekels diverticulum
- When the vitelline duct persists as the fibrous vitelline ligament forming an outpocketing of the ileum, mekel’s diverticulum
- It is usually asymptomatic except when gastric or pancreatic tissue is present in the diverticulum and this can cause ulceration, bleeding and perforation
- 2% population, usually detected in under 2s, found 2 feet from ileocecal valve, 2 inches long, 2:1 male to female ratio
Vitelline cyst
- Both ends of the vitelline duct become fibrous cords and the middle part becomes a large cyst
- Intestinal loops may twist around the vitelline ligaments and become obstructed causing strangulation or volvulus.
Vitelline fistula
- The vitelline duct remains patent so that the ileum is in direct contact with the opening of the umbiclus and fecal discharge may empty at the umbilicus.

Abnormal rotation – gut loop only rotates 90 degrees counterclockwise instead of 270. Therefore the colon and cecum re-enters the abdominal cavity first instead of the jejunum. This results in left sided colon, with the small intestinal loops on the right hand side.
Reversed rotation of the intestinal loop – the primary intestinal loop rotates 90 degrees clockwise resulting in the transverse colon lying posterior to the duodenum and the superior mesenteric artery.

Most atresias and stenoses occur in the duodenum, equal amounts occur in the jejunum and ileum and very few occur in the colon.

Atresias in the upper duodenum are probably due to lack of recanalisation. Otherwise they are most likely caused by vascular accidents such as malrotation, volvulus, gastroshisis and omphalocele. As a result blood supply to that region is compromised and ischaemia of the tissue occurs.

During development of the primitive gut tube, the cells multiply at such a high rate that they occlude the lumen. This mainly happens in the oesophagus, bile duct and small intestine. Later on the lumen is reformed by recanalisation. However sometimes there is a failure of recanalisation eg duodenum atresia.

Pyloric stenosis is common in children from birth -1month old. It is caused by hypertrophy of the circular smooth muscle in the pylorus of the stomach. This happens after birth so it is not a recanalisation failure. The children will projectile vomit non bilous vomit.

The hindgut forms the distal third of the transverse colon, the descending colon, sigmoid colon, the rectum and the upper part of the anal canal. The endoderm of the hindgut also forms the internal lining of the bladder and urethra. The urorectal septum, a layer of mesoderm, divides the cloaca into the urogenital sinus which leads on to an anterior opening via the alantosis at the umbilicus, and the anorectal canal. The urorectal septum meets the clocal membrane in the anal pit at the perineal body. The anal pit is formed by the ectoderm on the surface of the cloaca proliferating and invaginating. The clocal membrane degenerates and this forms the opening the urogenital sinus opening and the anal canal opening. Due to the invaginationg of cloacal ectoderm, the caudal anal canal originates from ectoderm and the cranial anal canal originates from endoderm. The junction between ectoderm and endoderm is separated by the pectinate line.

The pectinate line divides the superior and inferior anal canal.
The superior anal canal
- Originates from endoderm
- Splanchnic – only stretch sensation
- Columnar epithelium
- Superior rectal artery ( a continuation of the inferior mesenteric artery)
The inferior anal canal
- Originates from ectoderm
- Somatic – pain, temperature and touch sensation
- Stratified squamous epithelium
- Inferior rectal arteries ( branches of the internal pudendal arteries – enters the greater sciatic foramen and returns to the pelvis via the lesser sciatic foramen)

As only stretch receptors are found in the superior anal canal, but pain, temp and touch receptors are found in the inferior anal canal, tumours below the pectinate line will be discovered sooner.

If the urorectal septum does that extend far enough caudally or the cloaca is too small, then the opening of the hindgut shifts anteriorly into the urethra or vagina.

Imperforate anus occurs when the anal membrane fails to break down.

Midgut:
- SMA, SMV
- Parasympathetic innervations via vagus nerve
- Sympathetic innervations – superior mesenteric ganglion and plexus
Hindgut
- IMA, IMV
- Parasympathetic innervations via pelvic nerve (s2,s3,s4)
- Sympathetic innervations - inferior mesenteric ganglion and plexus.
Anal canal receives dual blood supply and innervation
Superior anal canal:
- superior rectal artery –continuation of IMA
- s2,s3,s4 pelvic parasympathetic
Inferior anal canal:
- inferior rectal artery – branch from internal pudendal artery
- S2,s3,s4 pudendal nerve