Mesenteries Of The Intestinal Loops

The mesentery of the primary intestinal loop, the mesentery proper, undergoes profound changes with rotation and coiling of the bowel. When the caudal limb of the loop moves to the right side of the abdominal cavity, the dorsal mesentery twists around the origin of the superior mesenteric artery (Fig. 13.24). Later, when the ascending and descending portions of the colon obtain their definitive positions, their mesenteries press against the peritoneum of the posterior abdominal wall (Fig. 13.30). After fusion of these layers, the ascending and descending colons are permanently anchored in a retroperi-toneal position. The appendix, lower end of the cecum, and sigmoid colon, however, retain their free mesenteries (Fig. 13.30B).

The fate of the transverse mesocolon is different. It fuses with the posterior wall of the greater omentum (Fig. 13.13) but maintains its mobility. Its line of attachment finally extends from the hepatic flexure of the ascending colon to the splenic flexure of the descending colon (Fig. 13.30B).

The mesentery of the jejunoileal loops is at first continuous with that of the ascending colon (Fig. 13.12A). When the mesentery of the ascending mesocolon fuses with the posterior abdominal wall, the mesentery of the jejunoileal loops obtains a new line of attachment that extends from the area where the duodenum becomes intraperitoneal to the ileocecal junction (Fig. 13.30B).

CLINICAL CORRELATES Abnormalities of the Mesenteries

Normally the ascending colon, except for its most caudal part (approximately 1 inch), fuses to the posterior abdominal wall and is covered by peritoneum on its anterior surface and sides. Persistence of a portion of the mesocolon gives rise to a mobile cecum. In the most extreme form, the mesentery of the ascending colon fails to fuse with the posterior body wall. Such a long mesentery allows abnormal movements of the gut or even volvulus of the cecum and colon. Similarly, incomplete fusion of the mesentery with the posterior body wall may give rise to retrocolic pockets behind the ascending mesocolon. A retrocolic hernia is entrapment of portions of the small intestine behind the mesocolon.

Body Wall Defects

Omphalocele (Fig. 13.31, A and B) involves herniation of abdominal viscera through an enlarged umbilical ring. The viscera, which may include liver, small and large intestines, stomach, spleen, or gallbladder, are covered by amnion. The origin of the defect is a failure of the bowel to return to the body cavity from its physiological herniation during the 6th to 10th weeks. Omphalocele occurs in 2.5/10,000 births and is associated with a high rate of mortality (25%) and severe malformations, such as cardiac anomalies (50%) and neural tube defects (40%). Approximately half of live-born infants with omphalocele have chromosomal abnormalities.

Gastroschisis (Fig. 13.31 C) is a herniation of abdominal contents through the body wall directly into the amniotic cavity. It occurs lateral to the umbilicus usually on the right, through a region weakened by regression of the right umbilical vein, which normally disappears. Viscera are not covered by peritoneum or amnion, and the bowel may be damaged by exposure to amni-otic fluid. Gastroschisis occurs in 1 /10,000 births but is increasing in frequency, especially among young women; this increase may be related to cocaine use.

Lum 110000Gastroschisis Pictures

Figure 13.31 A. Omphalocele showing failure of the intestinal loops to return to the body cavity after physiological herniation. The herniated loops are covered by amnion. B. Omphalocele in a newborn. C. Newborn with gastroschisis. Loops of bowel return to the body cavity but herniate again through the body wall, usually to the right of the umbilicus in the region of the regressing right umbilical vein. Unlike omphalocele, the defect is not covered by amnion.

Figure 13.31 A. Omphalocele showing failure of the intestinal loops to return to the body cavity after physiological herniation. The herniated loops are covered by amnion. B. Omphalocele in a newborn. C. Newborn with gastroschisis. Loops of bowel return to the body cavity but herniate again through the body wall, usually to the right of the umbilicus in the region of the regressing right umbilical vein. Unlike omphalocele, the defect is not covered by amnion.

Unlike omphalocele, gastroschisis is not associated with chromosome abnormalities or other severe defects, so the survival rate is excellent. Volvulus (rotation of the bowel) resulting in a compromised blood supply may, however, kill large regions of the intestine and lead to fetal death.

Vitelline Duct Abnormalities

In 2 to 4% of people, a small portion of the vitelline duct persists, forming an outpocketing of the ileum, Meckel's diverticulum or ileal diverticulum (Fig. 13.32A). In the adult, this diverticulum, approximately 40 to 60 cm from the ileocecal valve on the antimesenteric border of the ileum, does not usually

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Figure 13.32 Remnants of the vitelline duct. A. Meckel's, or ileal, diverticulum combined with fibrous cord (vitelline ligament). B. Vitelline cyst attached to the umbilicus and wall of the ileum by vitelline ligaments. C. Vitelline fistula connecting the lumen of the ileum with the umbilicus.

cause any symptoms. However, when it contains heterotopic pancreatic tissue or gastric mucosa, it may cause ulceration, bleeding, or even perforation. Sometimes both ends of the vitelline duct transform into fibrous cords, and the middle portion forms a large cyst, an enterocystoma, or vitelline cyst (Fig. 13.32B). Since the fibrous cords traverse the peritoneal cavity, intestinal loops may twist around the fibrous strands and become obstructed, causing strangulation or volvulus. In another variation the vitelline duct remains patent over its entire length, forming a direct communication between the umbilicus and the intestinal tract. This abnormality is known as an umbilical fistula, or vitelline fistula (Fig. 13.32C). A fecal discharge may then be found at the umbilicus.

Gut Rotation Defects

Abnormal rotation of the intestinal loop may result in twisting of the intestine (volvulus) and a compromise of the blood supply. Normally the primary intestinal loop rotates 270° counterclockwise. Occasionally, however, rotation amounts to 90° only. When this occurs, the colon and cecum are the first portions of the gut to return from the umbilical cord, and they settle on the left side of the abdominal cavity (Fig. 13.33 A). The later returning loops then move more and more to the right, resulting in left-sided colon.

Reversed rotation of the intestinal loop occurs when the primary loop rotates 90° clockwise. In this abnormality the transverse colon passes behind the duodenum (Fig. 13.33B) and lies behind the superior mesenteric artery.

Duplications of intestinal loops and cysts may occur anywhere along the length of the gut tube. They are most frequently found in the region of the ileum, where they may vary from a long segment to a small diverticu-lum. Symptoms usually occur early in life, and 33% are associated with other defects, such as intestinal atresias, imperforate anus, gastroschisis, and omphalocele. Their origin is unknown, although they may result from abnormal proliferations of gut parenchyma.

Omphalocele

Transverse colon

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Descending colon

Figure 13.33 A. Abnormal rotation of the primary intestinal loop. The colon is on the left side of the abdomen, and the small intestinal loops are on the right. The ileum enters the cecum from the right. B. The primary intestinal loop is rotated 90° clockwise (reversed rotation). The transverse colon passes behind the duodenum.

Transverse colon

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Descending colon

Figure 13.33 A. Abnormal rotation of the primary intestinal loop. The colon is on the left side of the abdomen, and the small intestinal loops are on the right. The ileum enters the cecum from the right. B. The primary intestinal loop is rotated 90° clockwise (reversed rotation). The transverse colon passes behind the duodenum.

Gut Atresias and Stenoses

Atresias and stenoses may occur anywhere along the intestine. Most occur in the duodenum, fewest occur in the colon, and equal numbers occur in the jejunum and ileum (1/1500 births). Atresias in the upper duodenum are probably due to a lack of recanalization (Fig. 13.18). From the distal portion of the duodenum caudally, however, stenoses and atresias are most likely caused by vascular "accidents." These accidents may be caused by malrotation, volvulus, gastroschisis, omphalocele, and other factors. As a result, blood supply to a region of the bowel is compromised and a segment dies, resulting in narrowing or complete loss of that region. In 50% of cases a region of the bowel is lost, and in 20% a fibrous cord remains (Fig. 13.34, A and B). In another 20% there is narrowing, with a thin diaphragm separating the larger and smaller pieces of bowel (Fig. 13.34C). Stenoses and multiple atresias account for the remaining 10% of these defects, with a frequency of 5% each (Fig. 13.34D). Apple peel atresia accounts for 10% of atresias. The atresia is in the proximal jejunum, and the intestine is short, with the portion distal to the lesion coiled around a mesenteric remnant (Fig. 13.35). Babies with this defect have low birth weight and other abnormalities.

Hindgut

The hindgut gives rise to the distal third of the transverse colon, the descending colon, the sigmoid, 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 (see Chapter 14).

Atresia Intestinal

Figure 13.34 The most commonly occurring bowel atresias and stenoses. A, the most common, occurs in 50% of cases; B and C occur in 20% each of cases, and D occurs in 5% of cases. Most are caused by vascular accidents; those in the upper duodenum may be caused by a lack of recanalization. Atresias (A,B, and C) occur in 95 % of cases, and stenoses (D), in only 5%.

Figure 13.34 The most commonly occurring bowel atresias and stenoses. A, the most common, occurs in 50% of cases; B and C occur in 20% each of cases, and D occurs in 5% of cases. Most are caused by vascular accidents; those in the upper duodenum may be caused by a lack of recanalization. Atresias (A,B, and C) occur in 95 % of cases, and stenoses (D), in only 5%.

Apple Peel Mesnetery
Figure 13.35 Apple peel atresia, which occurs in the jejunum and accounts for 10% of bowel atresias. The affected portion of the bowel is coiled around a remnant of mesentery.

The terminal portion of the hindgut enters into the posterior region of the cloaca, the primitive anorectal canal; the allantois enters into the anterior portion, the primitive urogenital sinus (Fig 13.36A). The cloaca itself is an endoderm-lined cavity covered at its ventral boundary by surface ectoderm. This boundary between the endoderm and the ectoderm forms the cloacal membrane (Fig. 13.36). A layer of mesoderm, the urorectal septum, separates

Allantois

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Cloaca

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Cloaca

Cloacal Septum

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Urogenital membrane

Urinary bladder

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Figure 13.36 Cloacal region in embryos at successive stages of development. A. The hindgut enters the posterior portion of the cloaca, the future anorectal canal; the al-lantois enters the anterior portion, the future urogenital sinus. The urorectal septum is formed by merging of the mesoderm covering the allantois and the yolk sac (Fig. 13.1 D). The cloacal membrane, which forms the ventral boundary of the cloaca, is composed of ectoderm and endoderm. B. As caudal folding of the embryo continues, the urorectal septum moves closer to the cloacal membrane, although it never contacts this structure. C. Lengthening of the genital tubercle pulls the urogenital portion of the cloaca anteriorly; breakdown of the cloacal membrane creates an opening for the hindgut and one for the urogenital sinus. The tip of the urorectal septum forms the perineal body. D. Histological section through the cloacal region of a 6-week human embryo similar to that depicted in B. The cloaca (cl) has a smaller posterior region at the opening of the hindgut (hg) and a larger anterior region, the urogenital sinus (us). The urorectal septum (urs) partially divides the two regions, and the cloacal membrane (cm) forms a boundary at the caudal limit of the cloacal cavity; gt, genital tubercle. E. Histological section though the cloacal region of a 7-week human embryo similar to C. The urorectal septum (urs) lies close to the cloacal membrane (cm), which is just beginning to break down, leaving the anal opening (ao) for the hindgut (hg) and a separate opening for the urogenital sinus (us). The tip of the urorectal septum will form the perineal body. Growth of the genital tubercle (gt) will change the shape of the urogenital sinus, which will eventually be closed by fusion of the urethral folds in the male. In the female the opening will remain as the vestibule to the vagina and urethra (see Chapter 14).

the region between the allantois and hindgut. This septum is derived from the merging of mesoderm covering the yolk sac and surrounding the allantois (Figs. 13.1 and 13.36). As the embryo grows and caudal folding continues, the tip of the urorectal septum comes to lie close to the cloacal membrane, although the two structures never make contact (Figs. 13.36, B and D). At the end of the seventh week, the cloacal membrane ruptures, creating the anal opening for the hindgut and a ventral opening for the urogenital sinus. Between the two, the tip of the urorectal septum forms the perineal body (13.36C and E). At this time, proliferation of ectoderm closes the caudalmost region of the anal canal. During the ninth week, this region recanalizes. Thus, the caudal part of the anal canal originates in the ectoderm, and it is supplied by the inferior rectal arteries, branches of the internal pudendal arteries. The cranial part of the anal canal originates in the endoderm and is supplied by the superior rectal artery, a continuation of the inferior mesenteric artery, the artery of the hindgut. The junction between the endodermal and ectodermal regions of the anal canal is delineated by the pectinate line, just below the anal columns. At this line, the epithelium changes from columnar to stratified squamous epithelium.

CLINICAL CORRELATES Hindgut Abnormalities

Rectoanal atresias, and fistulas, which occur in 1/5000 live births, are caused by abnormalities in formation of the cloaca. Thus, if the posterior portion of the cloaca is too small and consequently the posterior cloacal membrane is short, the opening of the hindgut shifts anteriorly. If the defect in the cloaca is small, the shift is small, causing a low opening of the hindgut into the vagina or urethra (Figs. 13.37, A and B). If the posterior region of the cloaca is very small, the location of the hindgut opening shifts more anteriorly to a higher location (Fig. 13.37C). Thus, rectoanal atresias and fistulas are due to ectopic positioning of the anal opening and not to defects in the urorectal septum. Low lesions are twice as common as high ones, with the intermediate variety being the least common. Approximately 50% of children with rectoanal atresias have other birth defects.

With imperforate anus, there is no anal opening. This defect occurs because of a lack of recanalization of the lower portion of the anal canal (Fig. 13.37 D).

Congenital megacolon is due to an absence of parasympathetic ganglia in the bowel wall (aganglionic megacolon or Hirschsprung disease). These ganglia are derived from neural crest cells that migrate from the neural folds to the wall of the bowel. Mutations in the RET gene, a tyrosine kinase receptor involved in crest cell migration (see Chapter 19), can result in congenital megacolon. In most cases the rectum is involved, and in 80% the defect extends to the midpoint of the sigmoid. In only 10 to 20% are the transverse and right-side colonic segments involved, and in 3% the entire colon is affected.

Transverse Colon Abnormalities

Figure 13.37 A. Normal development of the cloacal region at 7 weeks. The anterior portion of the cloaca (cl) forms the urogenital sinus (us); the posterior portion extends to the opening of the hindgut (hg). The cloacal membrane (cm) closes the cloaca and extends posteriorly beneath the end of the hindgut. Urs, urorectal septum; nt, neural tube; gt, genital tubercle. B. The cloacal region of a 7-week embryo showing a decrease in the size of the posterior portion of the cloaca and shortening of the cloacal membrane (arrow). Such a defect causes ectopic placement of the anal opening into the urogenital sinus (arrowhead) and a low urorectal fistula. C. High urorectal fistula resulting from a large decrease in size of the posterior portion of the cloaca and cloacal membrane that shifts the opening of the hindgut further anteriorly. D. Imperforate anus. The anal canal fails to recanalize, leaving a diaphragm between the upper and lower portions of the anal canal.

Figure 13.37 A. Normal development of the cloacal region at 7 weeks. The anterior portion of the cloaca (cl) forms the urogenital sinus (us); the posterior portion extends to the opening of the hindgut (hg). The cloacal membrane (cm) closes the cloaca and extends posteriorly beneath the end of the hindgut. Urs, urorectal septum; nt, neural tube; gt, genital tubercle. B. The cloacal region of a 7-week embryo showing a decrease in the size of the posterior portion of the cloaca and shortening of the cloacal membrane (arrow). Such a defect causes ectopic placement of the anal opening into the urogenital sinus (arrowhead) and a low urorectal fistula. C. High urorectal fistula resulting from a large decrease in size of the posterior portion of the cloaca and cloacal membrane that shifts the opening of the hindgut further anteriorly. D. Imperforate anus. The anal canal fails to recanalize, leaving a diaphragm between the upper and lower portions of the anal canal.

Summary

The epithelium of the digestive system and the parenchyma of its derivatives originate in the endoderm; connective tissue, muscular components, and peritoneal components originate in the mesoderm. Differentiation of the gut and its derivatives depends upon reciprocal interactions between the gut endoderm (epithelium) and its surrounding mesoderm. HOX genes in the mesoderm are induced by sonic hedgehog (SHH) secreted by gut endoderm and regulate the craniocaudal organization of the gut and its derivatives. The gut system extends from the buccopharyngeal membrane to the cloacal membrane (Fig. 13.1) and is divided into the pharyngeal gut, foregut, midgut, and hindgut. The pharyngeal gut gives rise to the pharynx and related glands (see Chapter 15).

The foregut gives rise to the esophagus, the trachea and lung buds, the stomach, and the duodenum proximal to the entrance of the bile duct. In addition, the liver, pancreas, and biliary apparatus develop as outgrowths of the endodermal epithelium of the upper part of the duodenum (Fig. 13.15). Since the upper part of the foregut is divided by a septum (the tracheoesophageal septum) into the esophagus posteriorly and the trachea and lung buds anteriorly, deviation of the septum may result in abnormal openings between the trachea and esophagus. The epithelial liver cords and biliary system growing out into the septum transversum (Fig. 13.15) differentiate into parenchyma. Hematopoietic cells (present in the liver in greater numbers before birth than afterward), the Kupffer cells, and connective tissue cells originate in mesoderm. The pancreas develops from a ventral bud and a dorsal bud that later fuse to form the definitive pancreas (Figs. 13.21 and 13.22). Sometimes, the two parts surround the duodenum (annular pancreas), causing constriction of the gut (Fig. 13.23).

The midgut forms the primary intestinal loop (Fig. 13.24), gives rise to the duodenum distal to the entrance of the bile duct, and continues to the junction of the proximal two-thirds of the transverse colon with the distal third. At its apex the primary loop remains temporarily in open connection with the yolk sac through the vitelline duct. During the sixth week, the loop grows so rapidly that it protrudes into the umbilical cord (physiological herniation) (Fig. 13.26). During the 10th week, it returns into the abdominal cavity. While these processes are occurring, the midgut loop rotates 270° counterclockwise (Fig. 13.25). Remnants of the vitelline duct, failure of the midgut to return to the abdominal cavity, malrotation, stenosis, and duplications of parts of the gut are common abnormalities.

The hindgut gives rise to the region from the distal third of the transverse colon to the upper part of the anal canal; the distal part of the anal canal originates from ectoderm. The hindgut enters the posterior region of the cloaca (future anorectal canal), and the allantois enters the anterior region (future urogenital sinus). Breakdown of the cloacal membrane covering this area provides communication to the exterior for the anus and urogenital sinus. Abnormalities in the size of the posterior region of the cloaca shift the entrance of the anus r anteriorly, causing rectovaginal and rectourethral fistulas and atresias (Figs. 13.36 and 13.37).

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