Normal Midgut Development
Midgut = small intestine distal to bile duct + cecum + appendix + ascending colon + right 2/3 of colon.
Blood supply = superior mesenteric artery
rotates counterclockwise 270 degrees, then reenters abdominal cavity.
- Midgut loops
- Midgut herniates into umbilical cord because there isn’t room for it (“physiological umbilical herniation”)
- The loop twists counterclockwise 270 degrees
- The small intestine reenters the abdominal cavity
- The large intestine reenters the abdominal cavity and undergoes a 180 degree counterclockwise rotation
The physiologic umbilical hernia happens at ~6 weeks.
The midgut gets nutrients from yolk sac through omphaloenteric duct.
The midgut loops is suspended from the dorsal abdominal wall by the dorsal mesogastrium.
Top layer of the loop eventually becomes the super convoluted small intestine and bottom layer is minimally changed and becomes part of colon.
Notable caudal loop modifications: cecal swelling/diverticulum, primordium of the cecum, and appendix.
Reduction of the midgut hernia occurs at ~10 weeks.
After reduction of the midgut loop, the enlarged colon pushes the duodenum and pancreas posteriorly. As a result, most of the duodenal mesentery gets absorbed into the peritoneum. This is why the proximal duodenum and head of the pancreas are considered retroperitoneal.
The cecal diverticulum forms anti to the dorsal mesentery.
The appendix may be retrocecal (~64% of people), retrocolic, or pelvic.
Developmental Anomalies of the Midgut
Omphalocele
- persistence of umbilical hernia
- small abdominal cavity
- intestines covered by peritoneum and amnion
- results from impaired mesoderm (muscle) or ectoderm (skin)
Umbilical hernia
- intestines originally return around 10th week like they are supposed to, but they later re-herniate
- defect occurs through linea alba
Gastroschisis
- defect in abdominal wall
- name is a misnomer because wall is split, not stomach
- like umbilical hernia, but without umbilical involvement
Malrotation of the gut
- improper rotation
- makes you prone to volvulus and bilious emesis
Nonrotation of the gut
- no rotation of the gut when it reenters the abdomen
- caudal limb of midgut loop (colon) reenters first
- R:L :: small intestine:large intestine
- subhepatic cecum and appendix
Volvulus
- twisting of intestines
- can cause atresia/blockage
- can cause blockage of superior mesenteric artery and subsequent intestinal infarction and gangrene
Reversed rotation of the gut
- goes the wrong way
Subhepatic cecum and appendix
- cecum can adhere to inferior liver
- clinical relevance: appendectomy
Mobile cecum
- incomplete fixation of ascending colon
- may lead to volvulus
- could herniate into right inguinal canal (rare)
Internal hernia
- sac forms from small intestine passing through the mesentery as midgut loop reduces around week 10
- usually without symptoms
Stenosis and atresia of the intestine
- 1/3 of intestinal occlusion cases
- 1/4 in duodenum
- 2/4 in ileum
- results from insufficient vacuolation during recanalization (restoration of the lumen)
- could results from fetal vascular accident from volvulus, fetal distress, or drug exposure
Ileal diverticulum and omphaloenteric remnants
- congenital/Meckel diverticulum in 2-4% of people
- clinical relevance: inflamed ileal diverticulum can mimic appendicitis
- wall of diverticulum contains all layers of the ileum with potential gastric mucosa and pancreatic tissues, which can lead to acid secretion and ulceration
- may be connected to the umbilicus
- may form omphaloenteric fistula
Duplication of intestine
- usually cystic, but could be tubular
- tubular duplication usually continuous with intestinal lumen
- results from bad recanalization
- could contain ectopic gastric mucosa, which may lead to ulceration and bleeding
Normal Hindgut Development
Hindgut = left 1/3 of transverse colon + descending colon + sigmoid colon + rectum + superior 2/3 of anal canal + epithelium of urinary bladder + most of urethra
Blood supply = inferior mesenteric artery
Cloaca = where the hindgut and allantois empty
Cloacal partitioning
Urorectal septum
- divides cloaca into dorsal and ventral parts
- promotes infolding of cloacal wall
- causes separation into urogenital sinus and rectum
- does not fuse with cloacal membrane, meaning no anal membrane exists
- cloacal membrane ruptures via apoptosis
- anorectal lumen is clogged with an epithelial plug
- apoptosis of plug leads to anal pit (proctodeum) formation
Anal Canal Development
Superior 2/3 from hindgut + pectinate line + inferior 1/3 from anal pit
Anocutaneous (white) line = columnar –> stratified squatmous epithelium
Blood supply = superior 2/3 from IMA –> superior rectal a./v.; inferior 1/3 from pudendal a. –> inferior rectal a./v.
Lymphatic drainage = superior 2/3 to inferior mesenteric lymph nodes; inferior 1/3 to superficial inguinal lymph nodes
Nerve supply = superior 2/3 from ANS; inferior 1/3 from inferior rectal n., sensitive to pain, temperature, touch, and pressure
Clinical relevance = metastasis; carcinoma (cancer in epithelium) – superior part are painless, inferior painful