Chapter 7: The Gut Tube and the Body Cavities

Intro

A Tube on Top of a Tube

During the third and fourth weeks the top layer (ectoderm) of the trilaminar embryonic disc forms the neural plate that rolls up into a tube to form the brain and spinal cord by the process called neurulation (see Chapter 6). Almost simultaneously, the ventral layer (endoderm) rolls down to form the gut tube, such that the embryo consists of a tube on top of a tube: the neural tube dorsally and the gut tube ventrally (Fig. 7.1). The middle layer (mesoderm) holds the two tubes together and the lateral plate component of this mesoderm layer also splits into visceral (splanchnic) and parietal (somatic) layers. The visceral layer rolls ventrally and is intimately connected to the gut tube; the parietal layer, together with the overlying ectoderm, forms the lateral body wall folds (one on each side of the embryo), which move ventrally and meet in the midline to close the ventral body wall (Fig. 7.1). The space between visceral and parietal layers of lateral plate mesoderm is the primitive body cavity, which at this early stage is a continuous cavity, since it has not yet been subdivided into the pericardial, pleural, and abdominopelvic regions.

Figure 7.1.Transverse sections through embryos at various stages of closure of the gut tube and ventral body wall.

Transverse sections through embryos at various stages of closure of the gut tube and ventral body wall

A. At approximately 19 days, intercellular clefts are visible in the lateral plate mesoderm. B. At 20 days, the lateral plate is divided into somatic and visceral mesoderm layers that line the primitive body cavity (intraembryonic cavity). C. By 21 days, the primitive body cavity (intraembryonic cavity) is still in open communication with the extraembryonic cavity. D. By 24 days, the lateral body wall folds, consisting of the parietal layer of lateral plate mesoderm and overlying ectoderm are approaching each other in the midline. E. At the end of the fourth week, visceral mesoderm layers are continuous with parietal layers as a double-layered membrane, the dorsal mesentery. Dorsal mesentery extends from the caudal limit of the foregut to the end of the hindgut.

Formation of the Body Cavity

At the end of the third week, intraembryonic mesoderm differentiates into paraxial mesoderm, which forms somitomeres and somites that play a major role in forming the skull and vertebrae; intermediate mesoderm, which contributes to the urogenital system; and lateral plate mesoderm, which is involved in forming the body cavity (Fig. 7.1). Soon after it forms as a solid mesodermal layer, clefts appear in the lateral plate mesoderm that coalesce to split the solid layer into two (Fig. 7.1B): (1) the parietal (somatic) layer adjacent to the surface ectoderm and continuous with the extraembryonic parietal mesoderm layer over the amnion. Together, the parietal (somatic) layer of lateral plate mesoderm and overlying ectoderm are called the somatopleure; (2) the visceral (splanchnic) layer adjacent to endoderm forming the gut tube and continuous with the visceral layer of extraembryonic mesoderm covering the yolk sac (Figs. 7.1B). Together, the visceral (splanchnic) layer of lateral plate mesoderm and underlying endoderm are called the splanchnopleure. The space created between the two layers of lateral plate mesoderm constitutes the primitive body cavity. During the fourth week, the sides of the embryo begin to grow ventrally forming two lateral body wall folds (Fig. 7.1B and C). These folds consist of the parietal layer of lateral plate mesoderm, overlying ectoderm, and cells from adjacent somites that migrate into the mesoderm layer across the lateral somitic frontier (see Chapter 11). As these folds progress, the endoderm layer also folds ventrally and closes to form the gut tube (Fig. 7.1D and E). By the end of the fourth week, the lateral body wall folds meet in the midline and fuse to close the ventral body wall (Fig. 7.1C,D–E). This closure is aided by growth of the head and tail regions (folds) that cause the embryo to curve into the fetal position (Fig. 7.2). Closure of the ventral body wall is complete except in the region of the connecting stalk (future umbilical cord). Similarly, closure of the gut tube is complete except for a connection from the midgut region to the yolk sac called the vitelline (yolk sac)duct (Fig. 7.2D). This duct is incorporated into the umbilical cord, becomes very narrow (Fig. 8.16), and degenerates with the yolk sac between the second and third months of gestation. (Note that throughout the process of body cavity and gut tube development, the parietal and visceral layers of lateral plate mesoderm are continuous with each other at the junction of the gut tube with the posterior body wall [Fig. 7.1D,E]).

Figure 7.2.Midsagittal sections of embryos at various stages of development showing cephalocaudal folding and its effects upon position of the heart, septum transversum, yolk sac, and amnion.

Figure 7.2

Note that, as folding progresses, the opening of the gut tube into the yolk sac narrows until it forms a thin connection, the vitelline (yolk sac) duct, between the midgut and the yolk sac D. Simultaneously, the amnion is pulled ventrally until the amniotic cavity nearly surrounds the embryo. A.17 days. B. 22 days. C. 24 days. D. 28 days. Arrows: head and tail folds.

Serous Membranes

Some cells of the parietal layer of lateral plate mesoderm lining the body wall of the primitive embryonic cavity become mesothelial and form the parietal layer of the serous membranes lining the outside of the peritoneal, pleural, and pericardial cavities. In a similar manner, some cells of the visceral layer of lateral plate mesoderm form the visceral layer of the serous membranes covering the abdominal organs, lungs, and heart (Fig. 7.1E). Visceral and parietal layers are continuous with each other as the dorsal mesentery (Fig. 7.1E), which suspends the gut tube from the posterior body wall into the peritoneal cavity. Dorsal mesentery extends continuously from the caudal limit of the foregut to the end of the hindgut. Ventral mesentery exists only from the caudal foregut to the upper portion of the duodenum and results from thinning of mesoderm of the septum transversum, a block of mesoderm that forms connective tissue in the liver and the central tendon of the diaphragm (see Figs. 7.2D and 7.5). These mesenteries are double layers of peritoneum that provide a pathway for blood vessels, nerves, and lymphatics to the organs.


Clinical Correlates

Ventral Body Wall Defects

Ventral body wall defects occur in the thorax, abdomen, and pelvis and involve the heart (ectopia cordis), abdominal viscera (gastroschisis), and/or urogenital organs (bladder or cloacal exstrophy), depending upon the location and size of the abnormality. The malformations are due to a failure of the ventral body wall to close and probably involve the lateral body wall folds to a greater extent than the head and tail folds. Thus, one or both of the lateral body wall folds fail to progress ventrally or there are abnormalities in the fusion process once they meet in the midline. An omphalocele also represents a ventral body wall defect; however, its primary cause is not due to inhibition of body wall closure. Instead, this abnormality occurs when a portion of the gut tube fails to return to the abdominal cavity following its normal herniation into the umbilical cord (see p. 220).

Ectopia cordis occurs when lateral body wall folds fail to close the midline in the thoracic region causing the heart to lie outside the body cavity (Fig. 7.3A). Sometimes, the closure defect begins at the caudal end of the sternum and extends into the upper abdomen resulting in a spectrum of abnormalities called Cantrell pentalogy. This spectrum includes ectopia cordis, defects in the anterior region of the diaphragm, absence of the pericardium, defects in the sternum, and abdominal wall defects including omphalocele and gastroschisis. (Note, omphaloceles that may occur in Cantrell pentalogy are secondary to the body wall closure defect, not primary. The closure defect reduces the size of the abdominal cavity and prevents the return of the intestinal loops from the umbilical cord; see p. 220).

Figure 7.3.Examples of ventral body wall defects due to failure of the ventral body wall to close.

Examples of ventral body wall defects due to failure of the ventral body wall to close

A. Ectopia cordis. The heart lies outside the thorax, and there is a cleft in the thoracic wall. B. Gastroschisis. Intestines have herniated through the abdominal wall to the right of the umbilicus, the most common location for this defect. C. Bladder exstrophy. Closure in the pelvic region has failed. In males, the defect usually includes a split in the dorsum of the penis, a defect called epispadius. D. Cloacal exstrophy. A larger closure defect in which most of the pelvic region has failed to close, leaving the bladder, part of the rectum, and the anal canal exposed.

Gastroschisis occurs when body wall closure fails in the abdominal region (Fig. 7.3B). As a result, intestinal loops herniate into the amniotic cavity through the defect, which usually lies to the right of the umbilicus. The incidence of gastroschisis is increasing (3.5/10,000), and it is most common in infants from thin women younger than 20 years of age. The defect can be detected by fetal ultrasound and by elevated ?-fetoprotein (AFP) concentrations in maternal serum and the amniotic fluid. The malformation is not associated with chromosome abnormalities, but other defects occur in 15% of cases. Affected loops of bowel may be damaged by exposure to amniotic fluid, which has a corrosive effect, or by twisting around each other (volvulus) and compromising their blood supply.

Bladder and cloacal exstrophy results from abnormal body wall closure in the pelvic region. Bladder exstrophy represents a less severe closure defect in this region and only the bladder is exposed (Fig. 7.3C); in males, the penis may be involved and epispadius [a split in the dorsum of the penis; see Chapter 16] is common). Cloacal exstrophy results from a more severe failure of body wall closure in the pelvis such that the bladder and rectum, which are derived from the cloaca (see Chapter 16), are exposed (Fig. 7.3D).

Omphalocele represents another ventral body wall defect (Fig. 7.4), but it does not arise from a failure in body wall closure. Instead, it originates when portions of the gut tube (the midgut) that normally herniates into the umbilical cord during the sixth to the tenth weeks (physiological umbilical herniation) fails to return to the abdominal cavity (see Chapter 15). Subsequently, loops of bowel, and other viscera, including the liver, may herniate into the defect. Since the umbilical cord is covered by a reflection of the amnion, the defect is covered by this epithelial layer. (In contrast, loops of bowel in gastroschisis are not covered by amnion because they herniate through the abdominal wall directly into the amniotic cavity.) Omphalocele, which occurs in 2.5/10,000 births, is associated with high mortality rates and severe malformations, including cardiac abnormalities and neural tube defects. Furthermore, chromosome abnormalities are present in 15% of cases. Like gastroschisis, omphaloceles are associated with elevated AFP concentrations.

Figure 7.4.Examples of omphaloceles, a defect that occurs when loops of bowel, that normally herniate into the umbilical cord during the sixth to the tenth weeks of gestation (physiological umbilical herniation), fail to return to the body cavity.

 Figure 7.4

A. Drawing showing loops of herniated bowel within the umbilical cord that have failed to return to the abdominal cavity. The bowel is covered by amnion because this membrane normally reflects onto the umbilical cord. B. Infant with an omphalocele. The defect is associated with other major malformations and chromosome abnormalities.