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Skandalakis’ Surgical Anatomy > Chapter 16. Small Intestine >


The anatomic and surgical history of the small intestine is found in Table 16-1.

Table 16-1. Anatomic and Surgical History of the Small Intestine

Sushruta 6th century B.C. Wrote oldest known descriptions of bowel surgery. Described using a cautery over the swelling of strangulated hernias. Used the mandibles of black ants to clamp the edges of bowel wounds together.
Hippocrates (460-370 B.C.)   Argued against surgical treatment of the abdomen. Provided a detailed description of intestinal obstruction: “In ileus, the belly becomes hard, there are no motions; the whole abdomen is painful, there are fever and thirst and sometimes the patient is so tormented that he vomits bile.”
Praxagoras 350 B.C. Advocated opening the abdomen as a last resort to relieve “iliac passion” making an incision over the swelling of a strangulated hernia, freeing the intestine and establishing an artificial anus
Herophilus (334-280 B.C.)   Referred to the “beginning of the intestines, prior to the beginning of the loops” as the “dodekadactilon”
Rufus of Ephesus (98-117 A.D.)   Noted that a sphincter regulated the flow of gastric contents into the duodenum
Aretaeus the Cappadocian (81-138 A.D.)   Described in detail ileus secondary to incarcerated hernia
Galen (131-201)   In performing several abdominal procedures as surgeon to the Roman gladiators, he observed and described the anatomy of the small intestine
Fabricius d’Aquapendente 12th century As reported by Duverger, he described a procedure of intestinal repair involving end-to-end anastomosis
Roger of Palermo Early 13th century Wrote, “. . .if a part of the tender intestine is wounded, it is better to leave the treatment to God than to man, since Death will follow it very soon.” Used the entrails of animals to protect eviscerated bowel until it could be replaced within the abdominal cavity.
Lanfranc 13th century Used animal tracheas to connect divided segments of bowel
Rolandus ca. 1400 Wrote a surgical text in which a picture depicts a physician preparing a patient with an eviscerated intestine using the open abdomen of a cat
Benedetti 1497 Claimed that the duodenum served as a “gate” controlling stomach-to- jejunal passage
Paracelsus (1491-1541) and Fabricius Hildanus (1560-1624)   Each observed spontaneous fistulas due to penetrating bowel injury
Sanctus 16th century Treated intestinal obstructions by giving patients metallic mercury (up to three pounds) and using the weight of the mercury to try to open the intestines
Vesalius 1543 Studied the relationship between the duodenum and the extrahepatic biliary tract
Franco 1556 Described his experience in surgically treating strangulated inguinal hernia. He made an incision over the swelling, divided the constricting band, inserted a goose-quill-sized cannula, and returned the bowel to the peritoneum.
Sydenham (1624-1689)   Managed intestinal obstruction using opium. He also recommended rest and horseback rides as therapy.
Kerckring 1670 Described the intestinal valvulae conniventes
Peyer 1677 Noted the presence of lymphoid follicles in the small intestine
Bidloo 1685 Provided a description of the duodenal papillae, the hepatopancreatic ampulla, and the junction of the pancreatic and common bile ducts
Nuck 1692 Reported his experiences helping a young surgeon treat volvulus, using his finger to draw out and treat a strangulated hernia
Mery 1701 Removed several feet of gangrenous bowel and established an artificial anus in a woman suffering from a strangulated hernia
Vater 1720 Described the duodenal papilla now commonly called the papilla of Vater
Le Peyronie 1723 Removed gangrenous bowel from a man with intestinal obstruction. Brought two loops out into the wound to serve as an artificial anus, placing traction on a suture placed in the mesentery between the two loops to quickly heal the fistula.
Ramdohr 1727 Removed two feet of gangrenous small bowel and invaginated the proximal end of the bowel into the lumen of the distal segment, securing the connection with a few sutures
Duverger 1747 Excised several inches of gangrenous bowel while suturing the two ends together over a piece of dog trachea that was passed 21 days later
Velse 1751 According to von Haller, he repaired an intestinal intussusception by removing the bowel, placing it in tepid milk until it returned to normal, and replacing it inside the abdomen
Mensching 1756 Used repeated intestinal puncture to treat obstructed bowels
Pott 1771 Inverted his patients to treat intestinal strangulation, arguing, “The nearer the posture approaches to what is commonly called standing on the head, the better, as it causes the whole packet of small intestines to hang, as it were, but the strangulated portion, and may thereby disengage it”
Meckel 1781-1833 Described diverticulum iliei verum, also known as Meckel’s diverticulum
Cooper 1804 Inverted patients, suspending them over the shoulders of a strong attendant, to treat strangulated hernias. Also used isinglass (ichthyocolla) and suture in experiments connecting divided canine intestines.
Travers 1812 While experimenting with suture techniques, he noted that wounds closed with sutures that passed through all layers of the bowel wall healed well
Jobert 1824 Performed end-to-side anastomoses in dogs and cats using continuous wax suture
Lembert 1826 Developed a suture technique employing interrupted sutures that passed through the entire bowel wall except for the mucous membrane
d’Etiolles 1826 Used electrical stimulation of the abdominal wall to treat intestinal obstructions
Amussat 1839 Presented an autointoxication theory of intestinal obstruction, based on the assumption that it was caused by enteric toxin. Essentially the theory was used as a means for justifying the continued usage of emetics, laxatives, and bloodletting to treat obstructions. 
Nélaton 1839-1840 Fixed a distended loop of bowel, proximal to the obstruction, in the wound using sutures penetrating the lumen and incising the exposed bowel (enterostomy). Although his first patient died, he was successful in 1849 and in 1852.
Duchenne 1855 Reported several successful instances where he treated intestinal obstruction with faradic current (electrodes placed in the rectum, abdomen, and sometimes the stomach)
Pfluger 1857 Observed that splanchnic nerve stimulation inhibited small intestinal movement
Ludwig 1861 Observed what he called “Pendelbwegungan” or the motion made by the bowel between peristaltic contractions
Auerbach and Meissner 1862 Published a study describing the intrinsic nerve plexus of the small intestine
Kussmaul 1869 Used gastric lavage to treat intestinal obstructions
Hutchinson 1871 Performed a successful operation for the reduction of intussusception in an infant. He published a review on the subject in 1874.
H.O. Thomas 1879 Enthusiastically followed Sydenham’s opium recommendations, adding more to the recommended dosages. He thought that abdominal operations were not only unsuccessful but dangerous.
Billroth 1881 Anastomosed parts of the small bowel to circumvent intestinal obstructions
1885 Invented the Billroth II procedure
Halsted 1887 Altered Lembert’s suture technique, passing the needle through the submucosa but not into the bowel lumen
Witzel 1891 Published a description of an oblique enterostomy over a catheter
J.B. Murphy 1892 Used a button he devised to simplify intestinal anastomosis (Murphy’s button)
Jourdain 1895 Performed what may have been the first mobilization of the duodenum
Mall 1896 Caused an acute intestinal obstruction by reversing a piece of bowel in order to prove that intestinal anatomy ensured that peristalsis moves only in the aboral direction
Schlatter 1897 Anastomosed the lower esophagus to the upper small intestine after performing a total gastrectomy
Bayliss and Starling 1899 Discovered that peristalsis was due to a reflex of the intrinsic nerve plexus
Treves 1899 After winning the 1883 Jacksonian Prize of the Royal College of Surgeons for a thesis regarding the benefits of operative management of intestinal obstruction, he wrote in 1899: “It is less dangerous to leap from the Clifton Suspension Bridge than to suffer from acute intestinal obstruction and decline operation.” His work stimulated a movement toward the modern era of surgical management of intestinal obstruction.
MacCormac 1899-1902 As consulting surgeon during the Boer War he claimed, “. . . in this war, a man wounded in the abdomen dies if he is operated upon and remains alive if he is left in peace.” This “MacCormac’s Aphorism” was widely adopted.
Kocher 1903 Developed his classical method of duodenal mobilization (Kocher’s maneuver)
Schwartz 1911 Used x-ray films to determine areas of intestinal distention
Hartwell and Hoguet 1912 Proved that subcutaneous injections of saline prolonged the life of dogs with (artificially produced) bowel obstruction. Their findings helped debunk the theory of autointoxication.
Richards 1915 Recorded his World War I experience with five cases of laparotomy. Two of his patients survived resections of 2-4 feet of bowel.
Dragstedt 1918 Proved that experimental animals could survive a total duodenectomy
Kloiber 1919 Published a paper emphasizing the usefulness of x-rays in discerning the level of intestinal obstruction
Ryle 1920s Introduced methods of passing tubes into the stomach for decompression
Gamble 1925 Used prolific fluid resuscitation in patients undergoing abdominal surgery
Monrad 1926 Treated intussusception using manipulative taxis through the abdominal wall after anesthetizing his patients
Hipsley 1926 Recommended using hydrostatic pressure from water in a rectal tube to treat intussusception
Olsson and Pallin 1926-1927 Used a column of barium passed through a rectal tube to treat intussusception
Wangensteen 1932 Advanced methods of intestinal decompression to treat intestinal obstruction (reducing mortality from 60-80% to 20%) while advocating excessive saline infusion for patients with a high obstruction. He changed the initial stage of a three-stage decompression from a proximal cutaneous jejunostomy to a more distal cutaneous jejunostomy; the other two stages (enterolysis and stoma closure) went unchanged.
Miller and Abbot 1934 Invented a tube to be passed into the intestine for decompression
Segi 1935 Discovered concentration of basal-granulated cells in intestinal villi of fetus (thesis published in 1936). Structure termed “Segi’s cap” in 1980.
Klass 1950 Diagnosed mesenteric ischemia before infarction. Performed embolectomy without intestinal resection (patient died of acute heart failure).
Shaw & Rutledge 1957 Reported successful superior mesenteric vein embolectomy without bowel resection
Ende 1958 First description of nonocclusive mesenteric ischemia
Skandalakis et al. 1962 Collective review of cases of smooth muscle tumors of the small intestine as reported in the world literature
Aylett 1963 Performed ileorectal anastomosis with proximal loop ileostomy
Root 1965 Used a peritoneal tap to diagnose peritoneal insult (>200 leukocytes/mL)
Kock 1970 Developed continent abdominal ileostomy pouches
Ghanem et al. 1970 Observed increased peritoneal leukocytes after intestinal arterial supply was cut off in dogs and cats
Boley et al. 1971 Edited first textbook on mesenteric ischemia
Guseinov 1975 Studied embryology of lymphatic capillaries in small bowel
Vantrappen et al. 1977 Published first description of human small bowel interdigestive motor complex
Traverso & Longmire 1978 Reported pylorus-sparing pancreaticoduodenectomy
Bookstein 1982 Used angiography to diagnose and treat small bowel bleeding
Saini et al. 1986 Described percutaneous drainage of diverticular abscesses
Gauderer & Stellato 1986 Performed gastrostomy without celiotomy or sutures
McKee et al. 1994 Evaluated diagnostic procedures for diverticular disease (CT scan, contrast enema, ultrasonography)
Zielke et al. 1994
Yacoe et al. 1997

History table compiled by David A. McClusky III and John E. Skandalakis.


Boley SJ, Sammartano RJ, Brandt LJ. Historical perspective. In: Longo WE, Peterson GJ, Jacobs DL. Intestinal Ischemia Disorders. St. Louis: Quality Medical, 1999. pp. 1-16.

Ellis H. The history of small-intestinal surgery. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the Esophagus, Stomach, and Small Intestine (5th ed). Boston: Little, Brown, 1990, pp. 774-782.

Ghanem E, Goodale RL, Spanos P, Tsung MS, Wangensteen OH. Value of leukocyte counts in the recognition of mesenteric infarction and strangulation of shorter intestinal lengths: an experimental study. Surgery 68(4):635-645, 1970.

Khubchandani IT. Evolution of surgical management of ulcerative colitis. Dis Colon Rectum 1989;32:911-917.

Nelson RL. Introduction and history. In: Nelson RL, Nyhus LM (eds.) Surgery of the Small Intestine. Norwalk, CT.: Appleton and Lange, 1987, pp. 3-12.

Peters JH. Historical review of pancreaticoduodenectomy. Am J Surg 1991:161:219-225.

Rachmilewitz D (ed). V International Symposium on Inflammatory Bowel Diseases. Boston: Kluwer, 1997.

Richardson DD, Gray SW, Skandalakis JE. The history of the small bowel. J Med Assoc Ga 1991;80:439-443.

Skandalakis JE, Gray SW, Shepard D, Bourne GH. Smooth Muscle Tumors of the Alimentary Canal: Leiomyomas and Leiomyosarcomas, a Review of 2525 Cases. Springfield, IL: Charles C. Thomas, 1962.

Wangensteen OH, Wangensteen SD. The Rise of Surgery: From Empiric Craft to Scientific Discipline. Minneapolis: University of Minnesota Press, 1978, pp. 106-141.


Normal Development

The distal foregut and the proximal midgut are responsible for the genesis of the three parts of the small bowel (duodenum, jejunum, and ileum). The approximate junction of the distal foregut and proximal midgut lies just distal to the ampulla of Vater in the adult. The demarcation of the small bowel into three parts takes place by the start of the third week of embryonic life.

The position of the duodenum posterior to the superior mesenteric artery is the result of the normal development and rotation of the embryonic gut. According to O’Rahilly and Müller,3 duodenal rotation is unlikely, and the extended peritoneal cavity is responsible for the duodenal mesenteric attachment. The same authors believe that the duodenum’s largely retroperitoneal position is the result of an increase in mesenchyme around the duodenum.

Early in the second month of gestation, the intestines, which elongate faster than the abdominal cavity expands, push a loop out into the umbilical cord (Fig. 16-1). This is the “midgut” of the embryologist, not the “midgut” of the surgeon. The herniated segment extends from approximately the distal one-third of the duodenum through the proximal one-third of the transverse colon. It is supplied by branches of the superior mesenteric artery. The axis of this herniation is the superior mesenteric artery. This artery, together with the celiac axis and the inferior mesenteric artery, is a remnant of the arterial side of the primitive vitelline circulation to the yolk sac. Originally paired and segmentally arranged, the pairs of arteries fuse, and their number is reduced to three by the sixth week of development. At this stage, the superior mesenteric artery continues past the intestine to supply the vitelline stalk, which occasionally persists as Meckel’s diverticulum.

Fig. 16-1.

Development of the small intestine. A. Elongation and herniation of the midgut into the umbilical cord early in the fifth week. (Inset) Late fifth week. B. Primary rotation of the herniated gut around the superior mesenteric artery. Prearterial limb stippled.CA, celiac axis; SMA, superior mesenteric artery; IMA, inferior mesenteric artery. (Modified from Gray SW, Akin JT Jr, Milsap JH Jr, Skandalakis JE. Vascular compression of the duodenum. (Part 1) Contemp Surg 9:37, 1976; with permission.)

Rotation of the intestinal loop counterclockwise through 90° brings the future duodenum and proximal small intestine to the right of the future colon. The axis of this rotation is the superior mesenteric artery. The intestines continue to elongate in the umbilical cord. In the tenth week, they rather suddenly return to the abdomen. The cranial limb of the intestinal loop returns first, so that the duodenum passes behind the superior mesenteric artery. The caudal limb, which will form the distal ileum and the entire colon, returns later, bringing the transverse colon in front of the artery and the duodenum by a further 180° counterclockwise rotation (Fig. 16-2A & B).

Fig. 16-2.

A. Return of the intestines to the abdomen in the tenth week. The prearterial (stippled) limb returns first, passing behind the superior mesenteric artery. B. Final position of the intestines attained shortly after birth. SMA, superior mesenteric artery. (Modified from Gray SW, Akin JT Jr, Milsap JH Jr, Skandalakis JE. Vascular compression of the duodenum. (Part 1). Contemp Surg 9:37, 1976; with permission.)

In the final adult relations, the third part of the duodenum lies in the angle formed by the superior mesenteric artery and the aorta, having passed under the artery. It is this relationship that may lead to duodenal compression by the artery.

Movement of the contents of the duodenum is rarely impeded by the superior mesenteric artery early in life. A few cases in infants are known, but the condition cannot qualify as a frank congenital defect. A predisposition to vascular compression may exist in some individuals and not in others, but it is improbable that it can be recognized. Changes in habitus, posture, and diet later in life seem to be more important than anatomic configuration at birth. Burrington and Wayne4 documented the influence of these extrinsic factors in adolescence.

As early as the beginning of the fifth week, the duodenal epithelium begins to proliferate, especially along the right wall near the origin of the hepatic diverticulum. By the end of the fifth week, only a few luminal clefts remain in the multilayered epithelium.5 The lumen is restored by the eighth week, and the epithelium is a single layer of cells by the tenth week.

The first part of the duodenum retains both dorsal and ventral mesentery. However, during the rotation, the duodenal loop is fixed in the retroperitoneal space. Therefore, the dorsal mesentery of the rest of the duodenum disappears. The “disappearing” dorsal duodenal mesentery remains as an avascular plane of loose connective tissue (the fascia of Treitz) (Fig. 16-3). It is not related to the ligament of Treitz.

Fig. 16-3.

Diagram of the rotation of pancreas and duodenum. A. Primitive relation of dorsal and ventral pancreatic primordia. B. Disappearance of ventral mesentery and rotation of ventral pancreas. C. Final retroperitoneal position of duodenum and pancreas. The plane of fusion of the mesoduodenum is the avascular fascia of Treitz. (Modified from Gray SW, Colborn GL, Pemberton LB, Skandalakis LJ, Skandalakis JE. The duodenum. Part 1: History, embryogenesis, and histologic and physiologic features. Am Surg 55(4):257-261, 1989; with permission.)

A duodenal mesentery is very rare; the authors of this chapter have seen only two cases in 40 years in both the operating room and the anatomy laboratory. This plane is entered into when the Kocher maneuver is performed to lift the second part of the duodenum to the left, thereby exposing the retroduodenal and retropancreatic regions.

As to the maturation of the duodenum, at first there is a single layer of endodermal cells surrounded by undifferentiated mesenchyme cells. By the end of the fourth week, the duodenal mucosa begins to proliferate, especially along the right wall near the origin of the hepatic diverticulum, which arises from the ventral wall during this stage. By the sixth week, only a few luminal clefts remain in the epithelium. By the tenth week, the lumen is completely restored and has become almost entirely single-layered.

Around the turn of the 19th century, it was believed that diverticula, duplications, and atresia resulted from a failure of recanalization of the epithelial plug.6 It now appears that the occlusion is the incidental result of epithelial proliferation, rather than a definite, necessary stage in foregut development. It is probable that some intramural duplications and small diverticula may be the result of persistence of tissue spaces that failed to coalesce with the main portion of the lumina.7

The foregut will differentiate into the pharynx, esophagus, and stomach. The transverse septum, into which the liver cords of endoderm will grow, forms the anterior cranial boundary of the foregut and the open midgut. Posteriorly, the dorsal pancreatic primordium will develop. These structures define the future duodenum.

During the third and fourth weeks, the embryo grows rapidly, but the yolk sac and open midgut do not. By the fifth week, the foregut is as large as the opening of the midgut, which may then be called the yolk stalk, the vitelline duct, or the omphalomesenteric duct. At this time, a ventral swelling of the midgut just caudal to the yolk stalk marks the site of the cecum, and hence, the boundary between the small and large intestine.

Elongation of the midgut, especially of the portion between the yolk stalk and the duodenum, proceeds faster than elongation of the whole body of the embryo. The result of this growth differential is a series of movements that ends with the adult position of the intestines in the abdomen. These movements occur in three well-defined stages that will be described only briefly here. For further details, consult Estrada8 and Skandalakis and Gray.9

Stage 1: Herniation

The midportion of the growing intestine buckles ventrally and protrudes into the coelom of the body stalk in the fifth week (Fig. 16-1A). The apex of the protrusion is marked by the yolk stalk. Its axis is marked by the superior mesenteric artery, which represents part of the primitive blood supply to the yolk sac. This loop of intestine undergoes a counterclockwise twist of 90°, so that the “prearterial” (cranial) limb lies to the right of the postarterial (caudal) limb (Fig. 16-1B). The caudal limb remains nearly straight, while the cranial limb grows rapidly and is thrown into coils.

Stage 2: Return (Reduction)

The intestines return to the abdomen rather suddenly during the tenth week. The cranial limb enters first, to the right of the superior mesenteric artery (Fig. 16-2A & B). The caudal loop enters later: the left colon first; the transverse colon in front of the superior mesenteric artery; and lastly, the cecum with the terminal ileum.

Stage 3: Fixation

From the fourth month until well after birth, the growth of the colon is completed. The mesenteries of the ascending and descending portions become obliterated by fusion with the peritoneum of the body wall. The transverse mesocolon fuses with the posterior leaf of the omental bursa.

Slovis et al.10 reported on 19 patients with incomplete intestinal rotation, six (32%) of whom had normal cecal position and abnormal duodenojejunal junction. Among these six patients midgut volvulus was present in three, and obstructing duodenal bands were present in one. Postnatal fixation of the duodenojejunal junction was accomplished over a ten-month to two-year period in two of the six patients.

Intestinal villi begin to appear in the distal duodenum and the proximal ileum in the eighth week. The whole intestine is provided with villi by the end of the fourth month (the villi of the colon will disappear after birth). Brunner’s glands appear in the third and fourth months, and may be capable of secretion by the end of the fifth month.11 The striate border of the epithelial cells is visible by the third month.

Circular muscle appears in the duodenum late in the fifth week; longitudinal muscle is visible in the third month. Before the longitudinal muscle appears, neuroblasts of the myenteric plexus follow the vagus nerve down the surface of the circular muscle. By the eighth week, all but the distal colon is innervated. The nerve supply is completely in place by the twelfth week.

Congenital Anomalies


Stenoses and Atresias

Stenosis of the duodenum is often associated with an anular pancreas or with aberrant pancreatic tissue in the duodenal wall. Stenosis may also result from a perforated diaphragmatic atresia (see type III below). The aperture may be so small that functional atresia develops later in life.12

We quote from Ladd and Madura13:

Duodenal anomalies are rare in adults. Duodenal webs are best managed by transduodenal excision and duodenoplasty. Annular pancreas is generally best treated by duodenal bypass to the distal duodenum or the jejunum. Annulus division can be carried out if the annulus is extramural, without duodenal stenosis, and if access to the pancreaticobiliary sphincters is necessary.

Atresias may be divided into three types (Fig. 16-4).9

Fig. 16-4.

Types of intestinal atresia. A. The lumen is closed by a mucosal and submucosal diaphragm. B. The atretic segment is a solid fibrous cord. C. There is complete absence of a segment of intestine and its mesentery. Note the dilatation of the intestine proximal to the atresia. (Modified from Colborn GL, Gray SW, Pemberton LB, Skandalakis LJ, Skandalakis JE. The duodenum. Part 3: Pathology. Am Surg 55(7):469-473, 1989; with permission.)

In type A, a membrane composed of mucosa and submucosa closes the duodenal lumen. There may be a secondary perforation. This is the most frequent type. Because it bulges downward under proximal pressure, the diaphragm usually appears to be more distal than is actually the case.

In type B, the proximal and distal ends are blind. They are joined by a fibrous band lying in the edge of the mesentery.

In type C, the proximal and distal blind ends have no connection with each other, and the mesentery between them is absent. This type is rare.

In all three types, the proximal segment is dilated and the distal segment is completely unexpanded. Seventy-five percent of intestinal stenoses and 40 percent of intestinal atresias are found in the duodenum.

Vecchia et al.14 reported that the major causes of morbidity and mortality in patients with intestinal atresia were cardiac anomalies (with duodenal atresia) and ultrashort bowel syndrome (<40 cm), which requires long-term total parenteral nutrition and which can be complicated by liver disease with jejunoileal atresia. They advised that long-term outcomes may be improved by the use of growth factors to enhance adaptation and advances in small bowel transplantation.

Duodenectomy-duodenoplasty for chronic intestinal pseudo-obstruction (megaduodenum) is recommended by Loire et al.15

Duodenal Diverticula

Most duodenal diverticula are found on the concave (pancreatic) wall of the second and third portions of the duodenum. They are usually solitary; however, they may be multiple. Duodenal diverticula are often asymptomatic.

Large symptomatic diverticula should be excised and closed with inversion of the sac. A long T-tube and duodenostomy are recommended for safe dissection of diverticula near the duodenal papilla. Neill and Thompson16 studied complications of duodenal diverticula.

Vassilakis et al.17 reported that Roux-en-Y choleduodenojejunostomy and duodenojejunostomy give satisfactory results for the treatment of complicated duodenal diverticulum.

Chiu et al.18 evaluated a large series of small bowel diverticula and concluded the following:

Duodenal diverticulum was the most common small bowel diverticulum. Abdominal pain and gastrointestinal bleeding were the most common clinical presentations. The small bowel diverticula, except for Meckel’s diverticulum, did not need to be treated if there were no significant symptoms.


Atresias and Stenoses

Congenital intestinal atresia is a major cause of intestinal obstruction in infants. As in the duodenum (see above), jejunoileal atresia occurs in three types (Fig. 16-4).

In type A, obstruction is produced by a diaphragm or a membrane of mucosa and submucosa. It may be complete or may have perforations.

In type B, two blind ends of the intestine are connected by a fibrous cord lying on the edge of the intact mesentery.

In type C, two blind ends of the intestine are not connected with each other, and the mesentery between the ends is absent.

In all except perforated membranes of type A, the proximal segment is greatly dilated and the distal segment is completely unexpanded. If there are multiple atresias, the dilation is proximal to the first one only. Stenoses and all types of atresias are more common in the duodenum than in the ileum and the jejunum.

Matsumoto et al.19 reported on jejunoileal atresia in identical twins, attributing most such cases to environmental influences during gestation. The authors of this chapter have reservations about accepting this etiology for an extremely rare anomaly.

Treatment comprises the excision of the atretic or stenotic segment and anastomosis of the ends. End-to-end anastomosis is rendered difficult by the disparity in size between the dilated proximal segment and the unexpanded distal segment. A side-to-side anastomosis or a Mikulicz exteriorization of the ends, dilation of the distal segment, and subsequent return of the intestines to the abdomen are the procedures of choice. For duodenal atresias, a retrocolic, isoperistaltic, two-layered duodenojejunostomy should be done whenever possible.20 Stenoses should be treated similarly.

Intestinal Duplications

Long intestinal duplications (Fig. 16-5) are the result of a failure of the endoderm to separate from the overlying notochord during the eighteenth to twenty-first day of gestation. Subsequent embryonic growth results in a band of endodermal cells attached to the normal gut at the caudal end and to the notochord at the cranial end. The band of endodermal cells will differentiate into a tubular gutlike structure on the mesenteric side of the normal gut. The notochordal attachment usually fails to persist, but one or more anomalous vertebrae are usually present to indicate the site of the abnormal attachment.

Fig. 16-5.

The formation of dorsal enteric duplications and diverticula. A. Orientation of neural tube notochord and primitive gut. B. Before the fourth week the notochord is attached to the underlying endoderm forming the roof of the primitive gut. C. Separation during the fourth week is normally complete. D, E. Incomplete separation and differences in growth of notochord and endoderm result in a band of endoderm cells pulled from the roof of the gut. F. The band of cells forms a tubular structure similar to and parallel with the normal gut. Note the deformed vertebra. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

The resulting entities may be cystic duplications or long tubular duplications in the mesentery parallel to the normal intestine. They frequently contain gastric or pancreatic mucosa, usually at the proximal end. Communication with the normal intestine is usually at the distal end only.

Cystic duplications and short parallel duplications should be resected entirely, together with the normal intestine served by the same blood vessels (Fig. 16-6A). Longer duplications, and hence, the adjacent intestine, may be preserved by creating a fistula at the distal end of the duplication (Fig. 16-6B), or by extirpation of the common wall (Fig. 16-6C), if there is no ulceration present.

Fig. 16-6.

Intestinal duplication. A. Blood supply to duplications and normal intestine. Resection (at arrows) removes both normal and duplicated segment. B. Resection may be avoided by the creation of a fistula at the blind end of the duplication. C. Extirpation of the common wall between normal and duplicated segments may be feasible. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Meckel’s Diverticulum

A remnant of the proximal portion of the yolk stalk (base of the vitelline stalk) is responsible for the formation of Meckel’s diverticulum. It may be connected to the umbilicus by a fibrous cord that may be patent (ileo-umbilical fistula). Persistence of that portion of the duct between the umbilicus and the ileum results in the diverticulum of Meckel.

Persistence is a misleading term. If the duct fails to degenerate, it not only persists, but usually grows to keep pace with the ileum to which it is attached. Rarely, the entire abdominal portion of the vitelline duct survives as an omphaloileal fistula. Even more rarely, an umbilical sinus or an umbilical polyp may represent the undegenerated distal end of the tract, or an abdominal cyst may indicate disappearance of all but the midportion of the vitelline duct. Much more frequently, a short portion of the ileal end persists and develops into a blindly ending diverticulum of the ileum.

Why epithelial cells of the yolk sac in certain individuals continue to flourish and differentiate instead of following the usual pattern of ceasing to divide during the fifth week of embryonic life is a mystery. Sorokin and Padykula21 reported that rat embryo yolk sac will survive in tissue culture and that regression is not intrinsic to the endoderm. This suggests that it is the mesodermal component which governs epithelial development.

Werner et al.22 reported that Meckel’s diverticulum is the most common congenital anomaly of the gastrointestinal tract and its complications are hemorrhage (due to acid secretion by ectopic gastric mucosa), inflammation (similar to acute appendicitis), and intestinal obstruction (due to intussusception, volvulus, or adhesive bands).

Additional information about Meckel’s diverticulum will be found later in this chapter in the anatomy section.

Small Bowel Diverticulosis

A prevalence of small bowel diverticulosis of 0.3-2.5% was cited by de Lange et al.23

Surgical Anatomy of the Duodenum

Topography and Relations

Relations of the Duodenum

First Part (Superior): 5 cm long. The proximal half is mobile; the distal half is fixed.

The duodenum passes upward from the pylorus to the neck of the gallbladder (Fig. 16-7). It is related (1) posteriorly to the common bile duct, portal vein, inferior vena cava, and gastroduodenal artery; (2) anteriorly to the quadrate lobe of the liver; (3) superiorly to the epiploic foramen; and (4) inferiorly to the head of the pancreas.

Fig. 16-7.

Anterior view of the relationships of the duodenum and pancreas. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

The initial 2.5 cm is freely movable and is covered by the same two layers of peritoneum that invest the stomach. The hepatoduodenal portion of the lesser omentum attaches to the superior border of the duodenum; the greater omentum attaches to its inferior border. The distal 2.5 cm is covered with peritoneum only on the anterior surface of the organ, so that the posterior surface is in intimate contact with the bile duct, the portal vein, and the gastroduodenal artery. The duodenum is separated from the inferior vena cava by a small amount of connective tissue.

Second Part (Descending): 7.5 cm long. It extends from the neck of the gallbladder to the upper border of L4.

This part of the duodenum is crossed by the transverse colon and the mesocolon and consists, therefore, of a supramesocolic portion and an inframesocolic portion. The parts above and below the attachment of the transverse colon are covered with visceral peritoneum. The first and second parts of the duodenum join behind the costal margin a little above and medial to the tip of the ninth costal cartilage and on the right side of the first lumbar vertebra.

The second part of the duodenum forms an acute angle with the first part, and descends from the neck of the gallbladder anterior to the hilum of the right kidney, the right ureter, the right renal vessels, the psoas major, and the edge of the inferior vena cava. It is related anteriorly to the right lobe of the liver, the transverse colon, and the jejunum. At about the midpoint of the second part of the duodenum, the pancreaticobiliary tract opens into its concave posteromedial side. The right side is related to the ascending colon and the right colic flexure.

Third Part (Horizontal or Inferior): 10 cm long. It extends from the right side of L3 or L4 to the left side of the aorta.

The third part of the duodenum begins about 5 cm from the midline, to the right of the lower end of the third lumbar vertebra, at about the level of the subcostal plane. The third, or transverse, part passes to the left, anterior to the ureter, the right gonadal vessels, the psoas muscle, the inferior vena cava, the lumbar vertebral column, and the aorta. It ends to the left of the third lumbar vertebra.

This inframesocolic portion of the duodenum is covered anteriorly by the peritoneum. It is crossed anteriorly by the superior mesenteric vessels and, near its termination, by the root of the mesentery of the small intestine. The third part is related superiorly to the head and uncinate process of the pancreas. The inferior pancreaticoduodenal artery lies in a groove at the interface of the pancreas and the duodenum. Anteriorly and inferiorly, this part of the duodenum is related to the small bowel, primarily to the jejunum.

Fourth Part (Ascending): 2.5 cm long. It extends from the left side of the aorta to the left upper border of L2.

The fourth, or ascending, part of the duodenum is directed obliquely upward. It ends at the duodenojejunal junction to the left and at the level of the second lumbar vertebra at the root of the transverse mesocolon. This junction occurs at about 4 cm below and medial to the tip of the ninth costal cartilage. The fourth part is related posteriorly to the left sympathetic trunk, the psoas muscle, and the left renal and gonadal vessels. Its termination is very close to the terminal part of the inferior mesenteric vein, to the left ureter, and to the left kidney. The upper end of the root of the mesentery also attaches here. The duodenojejunal junction is suspended by the ligament of Treitz, a remnant of the dorsal mesentery, which extends from the duodenojejunal flexure to the right crus of the diaphragm.

Pancreaticobiliary Structures

The fourth (intramural) portion of the common bile duct passes obliquely through the wall of the second part of the duodenum with the main pancreatic duct (Wirsung). Other associated structures are the major and minor papillae, the ampulla of Vater (if present), and the sphincteric mechanism of Boyden. Taken together, they form what Dowdy called the “Vaterian system.”24 This term expresses the anatomic and surgical unity of these structures, but has no functional significance.

The terminal portion of the common bile duct passes through the duodenal wall; it is about 1.5 cm in length, and narrows from 1.0 cm extramurally to 0.54 cm at the papilla. The main pancreatic duct enters the duodenum caudal to the bile duct, also decreasing in diameter. The ducts usually lie side by side, with a common adventitia for several millimeters. The septum between them becomes reduced to a mucosal membrane before actual confluence is reached.

Major Duodenal Papilla

There is confusion in the literature regarding the true definitions of the terms papilla of Vater and ampulla of Vater. The papilla of Vater, which should be called the major duodenal papilla, is a nipplelike formation and projection of the duodenal mucosa through which the distal end of the ampulla of Vater passes into the duodenum. The ampulla of Vater (hepatopancreatic), with its several formations, is the union of the pancreaticobiliary ducts.

The major papilla is on the posteromedial wall of the second (descending) portion of the duodenum to the right of the second or third lumbar vertebra. In older patients, it may lie at a slightly lower level. The distance from the pylorus varies from 7 to 10 cm, with extremes of 1.5 to 12 cm. The distance is decreased in the presence of inflammation of the cap or the postbulbar region of the duodenum.

Viewed from the mucosal surface, the papilla (Fig. 16-8) may be hard to locate because of the mucosal folds; sometimes it is completely overlaid by a transverse fold of duodenal mucosa. Its oval or slitlike orifice lies at its tip, the posterior end of which projects downward, and raises a longitudinal fold, known as the plica longitudinalis. The orifice is frequently filled by villuslike projections called valvules, or valvulae. Occasionally, a diverticulum lying near the papilla can cause difficulty for the surgeon or the endoscopist.

Fig. 16-8.

The T arrangement of duodenal mucosal folds indicating the site of the major duodenal papilla. In some cases, a mucosal fold may cover the orifice of the papilla. The major papilla is rarely as obvious as this illustration. No such arrangement marks the site of the minor papilla. (Originally, in 1775, a plate by Santorini, and reproduced in 1932 by Livingston. Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Ampulla (of Vater)

The ampulla is a dilatation of the common pancreaticobiliary channel within the papilla and below the junction of the two ducts (Fig. 16-9A). If a septum is present as far as the duodenal orifice, the ampulla is said to be absent (Fig. 16-9B). Michels25 collected the findings of 25 investigators in 2500 specimens and concluded that an ampulla was present in 63 percent of cases. By definition, an ampulla was said to be present if the edge of the septum between the two ducts fell short of the tip of the papilla. Actual measurements of the distance between the septal edge and the papillary tip range from 1 to 14 mm, with 75 percent being 5 mm or less.26

Fig. 16-9.

Diagram of the variations in the relation of the common bile duct and main pancreatic duct at the duodenal papilla. A. Minimal absorption of the ducts into the duodenal wall during embryonic development; an ampulla is present. B. Maximum absorption of the ducts into the duodenum. There are separate orifices on the papilla; no ampulla is present. C. Partial absorption of the common channel; no true ampulla is present. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Purists would require a dilatation of the common channel before they would apply the term ampulla. Where the common channel is less than 5 mm long, there is little or no dilatation.27 In such specimens, the presence of a true ampulla becomes a matter of opinion (Fig. 16-9C). We agree with Michels25 that the following classification is the most useful:


Type 1. The pancreatic duct opens into the common bile duct at a variable distance from the opening in the major duodenal papilla. The common channel may or may not be dilated (85 percent).

Type 2. The pancreatic and bile ducts open close to one another but separately on the major duodenal papilla (5 percent).

Type 3. The pancreatic and bile ducts open into the duodenum at separate points (9 percent).

A true dilated ampulla is present in about 75 percent of individuals of type 1, and is absent in types 2 and 3.

The variations in the distance between the pancreaticobiliary junction and the duodenal lumen result from developmental processes.28 In the embryo, the main pancreatic duct arises as a branch of the common bile duct, which in turn arises from the duodenum. Growth of the duodenum absorbs the proximal bile duct up to its junction with the pancreatic duct. When the resorption is minimal, there is a long ampulla, and the junction of the ducts is high in the duodenal wall (type 1), or even extramural. With increased resorption of the terminal bile duct, the junction lies closer to the duodenal orifice and the ampulla is shortened. The maximum resorption results in separate orifices for the main pancreatic duct and the common bile duct (type 3).

Sphincter of Boyden

A complex of several sphincters, composed of circular or spiral smooth muscle fibers, is found around the intramural part of the common bile duct, the main pancreatic duct, and the ampulla, if present. This sphincteric complex is called the sphincter of Boyden.29 The muscle fibers have an embryonic origin separate from that of the duodenal muscularis and are functionally separate from it (Fig. 16-10).

Fig. 16-10.

Diagrammatic representation of the four sphincters making up the sphincter of Boyden. 1. Superior choledochal sphincter. 2. Inferior (submucosal) choledochal sphincter. 3. Sphincter ampullae (papillae). 4. Pancreatic sphincter. The measurements are those of White.179 (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Like the papilla of Vater, another example of a misnamed anatomic entity is the sphincter of Oddi at the duodenal end of the pancreatic and common bile ducts. By priority of description, it should have been named for Francis Glisson.30 In 1654 he described anular fibers around the entire intramural portion of the bile duct, and believed that they guarded the opening against the reflux of the contents of the duodenum. Glisson’s account of his work is found in Boyden.31

Minor Duodenal Papilla

The minor papilla, through which the accessory pancreatic duct (Santorini) opens, is about 2 cm cranial and slightly anterior to the major papilla. It is smaller and less easily identified than the major papilla. The most useful landmark is the gastroduodenal artery, behind which lies the accessory duct and the minor papilla. Duodenal dissection for gastrectomy should end proximal to the artery. The minor papilla may contain no duct or only a microscopic, tortuous channel. A true sphincter (of Helly) is rarely present. In about 10 percent32 of individuals, the duct of Santorini is the only duct draining most of the pancreas. Accidental ligation of this duct, together with the gastroduodenal artery, would result in catastrophic pancreatitis.

Duodenal “Sphincters”

The debates concerning the so-called duodenal sphincters remind the authors of the controversy surrounding the gastroesophageal sphincters in regard to their anatomic or physiologic existence and their relation to duodenal pathology. The authors’ knowledge about duodenal sphincters was obtained from the excellent book by DiDio and Anderson, The “Sphincters” of the Digestive System.33 In addition to the well-known gastroduodenal pyloric sphincter, the duodenum has the following controversial sphincters:


The first duodenal sphincter is said to be located at the distal end of the duodenal bulb and is perhaps related to, if not responsible for, segmental achalasia and “megabulb.”

The sphincter of Villemin is proximal to the ampulla of Vater.34,35

If the so-called “Ochsner muscle” exists, it is probably located below the ampulla of Vater, according to Ochsner, who presented his findings in two publications in 1906.36 In 1907, Boothby expressed doubt as to the existence of the sphincter.37 A sphincter just proximal to the duodenojejunal flexure was also described by both Ochsner and Villemin.

In the introduction to his book about Antonio Scarpa, Monti stated: “Like the poet, and perhaps even more so, the scientist is the product of the period in which [he] lives.”38 It may be that the period in which Ochsner, Boothby, and Villemin lived stimulated them to perform their investigative work. The authors of this chapter agree with DiDio and Anderson that the descriptions of the sphincteric component are vague and that their clinical significance is nonexistent.

Vascular Supply


The blood supply of the duodenum is confusing due to the diverse possibilities of origin, distribution, and individual variations (Fig. 16-11, Fig. 16-12, Fig. 16-13). This is especially true of the blood supply of the first portion of the duodenum. In his fine presentation about the stomach and the duodenum, Griffith39 warned surgeons to be very cautious, because of these variations of the main arteries. Akkinis40 stated that there is no collateral circulation beyond the terminal arcades of the small bowel. Do we have the same phenomenon in the first portion of the duodenum? What about the anemic spot of Mayo that corresponds to the distribution of the supraduodenal artery? Does it exist? Do the variations of the above-named arteries represent, as Griffith states, an underlying factor in necrosis and leakage? The authors of this chapter do not want to take a position on these questions. Our only advice is to use good surgical technique when surgery is definitely required, and not take an overenthusiastic approach when dealing with benign disease.

Fig. 16-11.

Major arterial supply to the duodenum. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Fig. 16-12.

Anterior view of arterial supply of the duodenum and pancreas. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Fig. 16-13.

Posterior view of arterial supply of duodenum and pancreas. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

The first part of the duodenum is supplied by the supraduodenal artery (Fig. 16-11) and the posterior superior pancreaticoduodenal branch of the gastroduodenal artery (retroduodenal artery as described by Edwards, Michels, and Wilkie), which is a branch of the common hepatic artery. In many individuals, the upper part of the first 1 cm is also supplied by branches of the right gastric artery. In some individuals, one may see separate small branches to the superior and posterior aspects of the first part of the duodenum; they can be properly called supraduodenal and retroduodenal, respectively. Each may arise separately, or in various combinations. It is preferable, therefore, that the term retroduodenal not be used as a synonym for the posterior superior pancreaticoduodenal branch, the principal role of which is to supply the second part of the duodenum and pancreatic head. Nomina Anatomica (6th ed)41 also acknowledges the separate identity of the supraduodenal, retroduodenal, and posterior superior pancreaticoduodenal arteries; the supraduodenal artery is frequently absent, however.

After giving origin to the supraduodenal, retroduodenal, and posterior superior pancreaticoduodenal branches, the gastroduodenal artery descends between the first part of the duodenum and the head of the pancreas. It terminates by dividing into the right gastroepiploic and anterior superior pancreaticoduodenal arteries, both supplying twigs to this part of the duodenum.

The remaining three parts of the duodenum are supplied by an anterior and a posterior arcade. From the arcades spring pancreatic and duodenal branches. Those supplying the duodenum are called arteriae rectae; they may be embedded in the substance of the pancreas. Four arteries contribute to the pancreaticoduodenal vascular arcades:


1. The anterior superior pancreaticoduodenal arteries, commonly two in number, arise from the gastroduodenal artery on the ventral surface of the pancreas.

2. The posterior superior pancreaticoduodenal (retroduodenal) artery usually crosses in front of the common bile duct. The artery then spirals to the right and posterior to the duct, descending deep to the head of the pancreas. Several of the retroduodenal artery branches anastomose inferiorly with rami from the posterior branch of the inferior pancreaticoduodenal artery.

3 & 4. Anterior inferior and posterior inferior pancreaticoduodenal arteries arise from the superior mesenteric artery or its first jejunal branch, either separately or from a common stem. Blood reaches the concave surface of the duodenum by the vasa recta from the pancreaticoduodenal arcades. At first supplying the muscularis externa, they form a large plexus in the submucosa, from which arteries pierce the muscularis mucosae and form a second rich plexus just beneath the epithelium of the villi. The surgeon should be sure to ligate only one of the two arcades, the superior or the inferior only.

Lately, Hentati et al.42 proposed a new classification of the arterial supply of the duodenal bulb (Fig. 16-14, Fig. 16-15, Fig. 16-16), as follows:

The two arterial pedicles (infra- and supraduodenal) reach the bulb on its posterior aspect; each pedicle is made up of two sorts of blood currents (right and left); the posterior aspect of the bulb seems to be the most vascularized one, explaining, apart from bleeding from gastroduodenal [artery] erosion, the hemorrhagic character of ulcers of the posterior aspect of the bulb. The predominance of the left-hand currents explains the possible ischemia of the duodenal bulb and/ or rupture of the duodenal stump after their interruption.

Fig. 16-14.

General layout of the vessels on the anterior aspect of the duodenal bulb (classic concept). 1, common hepatic a.; 2, gastroduodenal a.; 3, hepatic a.; 4, right gastric a.; 5, posterior duodenopancreatic a.; 6, right gastroepiploic a.; 7, anterior superior duodenopancreatic a.; ASD, supraduodenal a.; AIP, intrapyloric a.; pylore, pylorus. (Modified from Hentati N, Fournier HD, Papon X, Aube Ch, Vialle R, Mercier Ph. Arterial supply of the duodenal bulb: an anatomoclinical study. Surg Radiol Anat 1999;21:159-64; with permission.)

Fig. 16-15.

General layout of the vessels of the posterior aspect of the bulb (classic concept). 1, common hepatic a.; 2, gastroduodenal a.; 3, hepatic a.; 4, right gastric a.; 5, posterior duodenopancreatic a.; 6, right gastroepiploic a.; 7, anterior superior duodenopancreatic a.; ASD, supraduodenal a.; AIP, intrapyloric a.; pylore, pylorus; a, retroduodenal aa.; b, accessory duodenal aa.; c, poorly vascularized area. (Modified from Hentati N, Fournier HD, Papon X, Aube Ch, Vialle R, Mercier Ph. Arterial supply of the duodenal bulb: an anatomoclinical study. Surg Radiol Anat 1999;21:159-64; with permission.)

Fig. 16-16.

General layout of the vessels of the bulb (concept of Hentati et al.). A, left supraduodenal current; B, right supraduodenal current; C, left intraduodenal current; D, right intraduodenal current; ASD, supraduodenal a.; AIP, intrapyloric a. (Modified from Hentati N, Fournier HD, Papon X, Aube Ch, Vialle R, Mercier Ph. Arterial supply of the duodenal bulb: an anatomoclinical study. Surg Radiol Anat 1999;21:159-64; with permission.)


Veins of the lower first part of the duodenum and the pylorus usually open into the right gastroepiploic veins (Fig. 16-17); they are the subpyloric veins. The upper first part of the duodenum is drained by suprapyloric veins, which open into the portal vein or the posterior superior pancreaticoduodenal vein. Anastomoses between subpyloric and suprapyloric veins pass around the duodenum. One of these has been said to mark the site of the pylorus (prepyloric vein of Mayo).43 It is not a constant indicator of the location of the pylorus.

Fig. 16-17.

The venous drainage of the duodenum and pancreas: anterior view. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

The venous arcades draining the duodenum follow the arterial arcades and tend to lie superficial to them. The anterior superior vein drains into the right gastroepiploic vein while the posterior superior vein usually passes behind the common bile duct to enter the portal vein. The inferior veins can enter the superior mesenteric (Fig. 16-18), the inferior mesenteric, the splenic, or the first jejunal vein. The veins may terminate separately or by a common stem.

Fig. 16-18.

The venous drainage of the duodenum and pancreas and formation of the hepatic portal vein: posterior view. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)


The duodenum is richly supplied with lymphatics (Fig. 16-19). They originate as blind-ending vessels (lacteals) in each villus of the mucosa. These vessels form a plexus in the lamina propria and, piercing the muscularis mucosae, form a second submucosal plexus. Still another lymphatic plexus lies between the circular and longitudinal layers of the muscularis. Collecting trunks pass over the anterior and posterior duodenal wall toward the lesser curvature to enter the anterior and posterior pancreaticoduodenal lymph nodes.

Fig. 16-19.

Diagrammatic presentation of duodenal lymphatics. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

The anterior extramural collecting ducts drain to nodes anterior to the pancreas. The posterior ducts pass to nodes posterior to the head of the pancreas. These follow the veins and arteries to nodes related to the superior mesenteric artery.

At the turn of the 20th century, Bartels44 presented evidence that the valves of the lymphatic vessels connecting the duodenal wall with the head of the pancreas are arranged so that normal lymph flow is from pancreas to duodenum, and not the reverse. This theory has not been confirmed recently. Although the lymphatics of the pancreas have received some attention, those of the duodenum have received very little.


Within the duodenal wall are the two well-known neural plexuses of the gastrointestinal tract, each of which is composed of groups of neurons interconnected by networks of fibers. One plexus (of Meissner) is in the submucosa; another plexus (of Auerbach) is in the connective tissue between the circular and longitudinal layers of muscularis externa. Some of the neuronal cell bodies and processes in the plexuses are assumed to be postganglionic parasympathetic. Several studies indicate that many are related (1) to circuitry for processing information received from various types of sensory receptors, (2) to synaptic complexes for directing neural outflow, and (3) to interconnecting neurons.45

Preganglionic parasympathetic fibers in the plexuses are carried initially by the vagus nerves. Postganglionic sympathetic fibers arise from cell bodies located in the celiac and superior mesenteric ganglia, in sympathetic chain ganglia ranging from T-6 to T-12, or scattered along the course of the splanchnic nerves. The extrinsic nerve supply to the duodenum probably includes contributions which leave the anterior hepatic plexus close to the origin of the right gastric artery. In six out of 100 specimens examined by Skandalakis et al.,46 nerves from the hepatic division of the anterior vagal trunk gave rise to one or more branches that innervated the first part of the duodenum. In most specimens, some branches could be traced upward toward the gastric incisura. The vagaries of the vagus are well known.47,48

Surgical Anatomy of the Jejunum and the Ileum

Topography and Anatomy

Length of the Jejunoileum

For all practical purposes, 60 percent of the length of the GI tract is composed of jejunoileum,49 which performs 90 percent of the absorption.50,51

The beginning and the end of the jejunum and ileum are topographically related to peritoneal pockets or fossae which are usually very shallow. Occasionally, when they are very deep, they may be the cause of internal herniation. At the beginning of the jejunum there are paraduodenal fossae; at the end, ileocecal fossae; in the center, there is nonfusion of the intestinal root.

Touloukian and Smith,52 in an autopsy study of children, reported that total intestinal length ranged from 142 ± 22 cm for preterm infants 19 to 27 gestational weeks to 304 ± 44 cm for preterm infants more than 35 gestational weeks. The same authors reported that the average length of jejunoileum was 248 ± 40 cm for preterm infants more than 35 gestational weeks.

The length of the alimentary tract in humans is surprisingly difficult to measure. In the older literature, reviewed by Bryant,53 the length of the jejunum and ileum in cadavers was reported to be from 10 to 40 feet. Based upon his own studies, Bryant recorded an average length of 20.5 feet (624.8 cm). From his tables, an average of 20 to 22 feet has been widely quoted in textbooks up to the present.

That the “normal” length of 20 to 22 feet bears no relation to the jejunoileum in the living patient was apparent in 1924 when Reis and Schembra54 measured the jejunoileum in living dogs and remeasured it at various intervals after death. In the first 10 minutes, it elongated 23 to 25 percent. Four hours after death, the increase in length reached 135 percent. This occurs because tonus of the longitudinal muscle is lost much faster than that of the circular muscle.

Blankenhorn and associates55 intubated eight patients and from their measurements determined the average length of the duodenum to be about 22 cm (8.5 inches); jejunoileum, 258 cm (8.5 ft); and colon, 110 cm (3 ft, 7 inches). The overall nose-to-anus length of the gastrointestinal tract averaged 452 cm (14 ft, 10 inches). There is some evidence that intestinal length is greater in obese individuals.56

A 1995 study by Nightingale and Lennard-Jones57 found that the normal adult human small intestinal length, measured surgically or at autopsy from the duodenojejunal flexure, ranges from 275 to 850 cm. According to Nordgren et al.,58 in patients with Crohn’s disease the small bowel was significantly shorter than in patients with ulcerative colitis and in a control population.

The surgeon is more concerned with the length of intestine remaining after a resection than with the amount resected. In the older literature there are lists of operations in which 4-5 m or more of intestine were removed, with survival of the patient.59 Undoubtedly, the resected segment was measured only after the resection was completed and the abdomen closed; elongation of the specimen was by then well under way. Accurate measurements should be made before the intestine is removed and with the least manipulation possible. We cannot explain why the older measurements are still widely accepted.

Weser60,61 studied the functional capacity of the jejunoileum. He reported that 50 percent resection can be tolerated well by the patient, but 75 percent resection will produce severe malabsorption syndrome. Winawer and Zamchek62 believed that patient survival is possible with the duodenum in situ following resection of approximately 50 cm of the jejunoileum. Wilmore63 stated that 15 cm of jejunum or ileum with the ileocecal valve in situ can be tolerated, but 40 cm of small bowel is needed if the ileocecal valve is resected. Total parenteral nutrition is an extremely useful treatment with short bowel syndrome in infants as well as in adults.

Thompson64 reported the surgical aspects of the short-bowel syndrome. He stated that:


Ostomy formation is often prudent at the time of initial resection

Factors influencing restoration of intestinal continuity must be considered (Table 16-2)

Prophylactic cholecystectomy is often advisable to avoid cholelithiasis

Surgical therapy includes procedures to slow intestinal transit

Intestinal transplantation may be the most promising therapy

Table 16-2. Factors Influencing Decision to Restore Intestinal Continuity

Factors for restoring intestinal continuity
  Absorptive capacity increased
  Intestinal transit time prolonged
  Effects of short-chain fatty acids enhanced
  Intestinal stoma avoided
Factors against restoring intestinal continuity
  Secretory diarrhea from bile acids
  Perianal complications increased
  Dietary restrictions
  Incidence of nephrolithiasis increased

Source: Thompson JS. Surgical aspects of the short-bowel syndrome. Am J Surg 1995;170:532-536; with permission.

In a more recent publication, the same author stated the following65:

The outcome of short bowel syndrome is influenced by several factors including intestinal disease, remnant length and location, the other digestive organs, and intestinal adaptation…Patients with short bowel syndrome resulting from inflammatory disease appear to have a better nutritional prognosis after the first year. While they are more likely to have had multiple resections and develop short bowel syndrome with longer remnant length, inflammatory disease itself is an important prognostic factor. This may be related to resolution of inflammatory disease or a greater adaptive response.

Dyke and Vinocur66 noted that “pneumatosis cystoides intestinalis has been encountered in a large number of infants with necrotizing enterocolitis and short gut syndrome and in children who are immunosuppressed following liver transplantation.”

In resecting a segment of the proximal part of the jejunoileum, remove at least 10 cm of healthy small bowel on each side of the lesion, as well as a V-like mesenteric excision. In performing a resection of the terminal ileum, surgery by right colectomy is the appropriate procedure, due to the anatomic lymphatic pathway.

Differential Characteristics of the Jejunum and Ileum

There is no good way to identify an isolated loop of small intestine with absolute certainty without following it in one direction to the duodenojejunal junction, or in the other direction to the ileocecal junction. Table 16-3 may be consulted as an additional, but not very satisfactory, guide for distinguishing the jejunum from the ileum. It is our opinion that the clearest distinction between the jejunum and the ileum is based upon the differences between the topographic features of the blood supply to these two regions of the bowel.

Table 16-3. Some Differences between Jejunum and Ileum

Jejunum Ileum
Wall thicker Wall thinner
Lumen larger Lumen smaller
Fat on mesentery Fat on ileum and mesentery
Prominent plicae circulates Less prominent plicae
Single line of arterial arcades Several lines of arterial arcades
Aggregate lymph nodules (Peyer’s patches) sparse Aggregate lymph nodules frequent

Source: Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.

Remember that each typical segment of jejunum characteristically has one or two arterial arcades in the mesentery. These arcades join parallel jejunal arteries, with parallel, long vasa recta arising from the arcades, then pass to the intestinal wall. Such vasa recta have a length of approximately 4 cm. A typical segment of the ileum often has three or more arterial arcades in the mesentery, with great numbers of relatively short vasa recta (approximately 1.5 cm in length) passing to the ileal wall. The great number of short vasa recta is related, presumably, to the large role in absorption played by the ileum. Similarly, the increase in the quantity of fat seen in the mesentery of some individuals correlates with the relative significance of the absorption of fatty elements in the ileum, in comparison with that in the jejunum.

Theoretically, the preceding information is correct; in a virgin peritoneal cavity in a thin patient, these facts may assist in identification. However, in patients with fatty mesentery, even translumination with a sterile lighting device does not help. Our final recommendation is to use the ligament of Treitz and the ileocecal junction to distinguish the jejunum from the ileum.

Vascular Supply


The superior mesenteric artery arises from the aorta below the origin of the celiac trunk. In about one percent of individuals, there is a combined celiacomesenteric trunk.67 The celiac, superior, and inferior mesenteric arteries are the remnants of the paired vitelline arteries of the embryo. The superior mesenteric artery continues beyond the ileal border to supply the Meckel’s diverticulum (if one is present).

The basic patterns of the intestinal arteries have been described by Noer and colleagues,68 Michels and associates,67 and others. On average, the left side of the superior mesenteric artery gives origin to five intestinal arteries above the origin of the ileocolic artery, and 11 arteries below that level. Eight more arteries arise from the ileal branch of the ileocolic artery.67 A few centimeters from the border of the intestine, these intestinal vessels branch to form a series of arterial arcades connecting the intestinal arteries with one another (Fig. 16-20). Proximally, in the jejunum, one to three arcades are present; distally, in the ileum, there is an increased number of arcades.

Fig. 16-20.

The blood supply of the jejunum and ileum. The arcades of the superior mesenteric artery increase in complexity distally. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

The vascular arches form the primary anastomoses of the arterial supply. A complete channel may exist from the posteroinferior pancreaticoduodenal artery, which is parallel to the intestine and joins the marginal artery (of Drummond) of the colon. In some individuals, the pathway is incomplete, usually at the end of the ileum.67 From the arches of the arcades, numerous arteries (the vasa recta) arise, then pass (without cross-communication) to enter the intestinal wall. They may bifurcate to supply each side, or they may pass singly to alternate sides of the intestine (Fig. 16-21).

Fig. 16-21.

A. The vasa recta may divide into two short vessels to the mesenteric side of the intestine and two long vessels supplying the rest of the intestinal wall. B. More frequently, a single long vessel supplies one side of the intestine, alternating with a vessel supplying the other side. C. A single long and short vessel serving one side only. The remaining 34 percent are various combinations of paired or single long or short vessels. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission. Data from Michels NA, Siddharth P, Kornblith PL, Parke WW. The variant blood supply to the small and large intestines: Its import in regional resections. J Int Coll Surg 1963;39:127.)

The vasa recta branch beneath the serosa without anastomosing, before piercing the muscularis externa. There is no collateral circulation between the vasa recta or their branches at the surface of the intestines. This configuration provides the best supply of oxygenated blood to the mesenteric side of the intestine, and the poorest supply to the antimesenteric border.

If we accept that there is no collateral circulation beyond the terminal arcades (in other words, no communication between the vasa recta and/or within the intramural network), then the blood supply of the antimesenteric border of the small bowel is probably relatively poor. Therefore, during surgery, the bowel ought to be opened halfway between the mesenteric and the antimesenteric border. We have made incisions many times at the antimesenteric border, and have had no complications.

Within the intestinal wall, the arteries form a large plexus in the submucosa. From this plexus, short vessels reach the lamina propria to supply a network of capillaries around the intestinal crypts, while longer arteries supply the cores of the intestinal villi (Fig. 16-22). Thus, there are two regions of anastomoses of intestinal arteries: the extramural arches between intestinal arteries, and the intramural submucosal plexus.

Fig. 16-22.

A cast of the blood vascular system of the jejunal wall. 1. Capillaries of villi. 2. Capillaries of intestinal crypts. 3. Submucosa with venules (Ve), veins (Vn), and arteries (Ar). 4. Vessels of the muscularis. Scanning electron microscope x 180. (From Kessel RG, Kardon RH. Tissues and Organs: A Text-Atlas of Scanning Electron Microscopy. San Francisco: Freeman, 1979; with permission.)


One or more small veins originate near the tip of each intestinal villus and travel outward, receiving contributions from a plexus of veins around the intestinal glands. They enter the submucosal plexus, which is drained through the muscular layer by larger veins traveling with the arteries in the mesentery, to reach the superior mesenteric vein. These intestinal veins are interconnected by venous arcades that are similar to, but less complex than, the accompanying arterial arcades. The superior mesenteric vein belongs to the portal system, which drains the intestinal blood into the liver.


Lymphatic vessels (lacteals) arise in the cores of the intestinal villi. They form plexuses at the base of the villi, the base of the crypts, in the muscularis mucosa, in the submucosa, and between the circular and longitudinal layers of the muscularis externa. This series of plexuses is drained by large lymphatics that travel in the mesentery with the arteries and veins. The lymph flows to nodes residing between the leaves of the mesentery. Over 200 small mesenteric nodes lie near the vasa recta and along the intestinal arteries. Drainage from the mesenteric nodes is finally to the large, superior mesenteric lymph nodes at the root of the mesentery. Efferent vessels from these and the celiac nodes form the intestinal lymphatic trunk. This trunk passes beneath the left renal artery and ends in the left lumbar lymphatic trunk (70 percent) or in the cisterna chyli (25 percent).

In summary, the pathways of small bowel lymphatics are as follows:


Intramural: Lacteals mucosal vessels submucosal plexus subserosal plexus

Extramural: Vasa recta lymph nodes along the mesenteric vessels lymph nodes along the superior mesenteric artery and celiac artery cisterna chyli


The innervation of the jejunum and the ileum is by the autonomic system. Pain secondary to small bowel pathology is referred to the 9th, 10th, and 11th thoracic nerves, and usually is periumbilical.

Dimensions of the Mesentery

Shackleford69 stated that the length of the mesentery of the small intestine, measured between the attachment to the intestine and the root of the mesentery, usually does not exceed 20 to 25 cm. This length will permit a loop of intestine to slide down into an inguinal hernia, especially if the mesentery is slightly relaxed at its extraperitoneal attachment. Similarly, it is usually long enough to permit the surgeon to bring a loop up to form an esophagojejunostomy.

There is considerable variation in the breadth of the small bowel mesentery and that of the sigmoid mesentery. In patients with volvulus and intestinal knots, the breadth of the affected mesentery is greater than that found in healthy patients70 (Fig. 16-23). It has not yet been determined whether there are any ethnic differences in these dimensions and their variations. The topographic anatomy and relation of the mesenteric root of the small bowel on its oblique pathway from the left upper quadrant to the right lower quadrant is as follows:


1. The proximal end of the mesenteric root is found at the left side of L2, which is the most likely location of the duodenojejunal junction.

2. The uncinate process of the pancreas is characteristically located (when it is present) between the aorta and the superior mesenteric artery.

3. The mesentery crosses in front of the third, or horizontal, part of the duodenum.

4. It descends obliquely downward to the right, in front of the inferior vena cava.

5. The mesentery attaches to the lateral border of the right common iliac vessels.

6. It passes in front of the psoas major muscle, crossing the right ureter and the right gonadal vessels.

7. The mesentery root terminates at the ileocecal junction; there it contains the ileocolic vessels, in front of the upper end of the right sacroiliac joint.

Fig. 16-23.

The breadth of the mesentery. It is usually long enough to reach the internal inguinal ring. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; data from Vaez-Zadeh K, Dutz W. Ileosigmoid knotting. Ann Surg 172:1027, 1970; with permission.)

In extremely rare cases, the mesentery of the small bowel is not totally fixed in the retroperitoneal space. Such a defect can permit an intestinal loop to enter, and can produce intestinal obstruction.71

To prepare a long loop of jejunum for anastomosis, the following steps can be used, after securing the duodenojejunal junction and drawing the proximal jejunum out of the abdomen:72


1. The peritoneum is incised and the selected loop is isolated and inspected. Fat and lymph nodes are removed to within 1-2 cm from the wall of the intestine.

2. The jejunal vessels are skeletonized of connective tissue, nerve fibers, and lymphatic vessels. The arteries and veins are freed to their bifurcations to form the anastomotic arcades.

3. The exposed blood vessels are again covered with peritoneum. The anatomy of the jejunal arteries and their arcades is examined to determine the feasibility of dividing the necessary number of arteries (usually 3 or 4) required for mobilization of a loop of adequate length.

4. The root of the mesentery is divided as necessary to gain length, if required.

Wind et al.73 presented the anatomic basis of mesenteric elongation and the use of the ileum for tension-free ileo-anal anastomosis. We advise interested surgeons to put this article in their collections, and we present verbatim results along with four anatomic drawings (Fig. 16-24, Fig. 16-25, Fig. 16-26, Fig. 16-27):

Twenty-two fresh cadavers had an ileal J-shaped reservoir of 18 cm fashioned from the last loop of small intestinal loop after section of the root of the mesentery. The gains in length so obtained were measured after section of the ileocolic artery at its origin (group A) or section between the two vascular arches of the last small intestinal group (group B); the superior mesenteric vessels were then injected with colored resin. The gain in length obtained by these two methods was identical (2.3 ± 1.1 cm for group A as against 2.18 ± 0.9 cm for group B), but only if the section of the ileocolic artery was accompanied by section of the mesenteric peritoneum up to the vascular arch formed by the anastomosis between the terminal branch of the superior mesenteric artery and the ileocolic artery. The constancy of this anastomosis always allowed section of the ileocolic artery while preserving good vascular distribution to the entirety of the reservoir. Section between the two arches was difficult when the distance separating them was small.

Fig. 16-24.

Ileocecal region. The staple applicator (A) shows section of the last loop flush with the ileocecal valve. The forceps (B) is located at the site of the future apex of the J-shaped reservoir. 1. superior mesenteric artery. 2. ileocolic artery. 3. terminal ileal branch of superior mesenteric artery. 4. ileal branch of ileocolic artery. 5. recurrent ileal artery. (Modification from Wind P, Chevallier JM, Sauvanet A, Delmas V, Cugnenc PH. Anatomic basis of mesenteric elongation for ileo-anal anastomosis with J-shaped reservoir: comparison of two techniques of vascular selection. Surg Radiol Anat 1996;18:11-16; with permission.)

Fig. 16-25.

Appearance of terminal loop of small intestine after section. The recurrent ileal artery has been sectioned at its origin and the ileocecal artery has been divided below the origin of the ileal branch. (Modified from Wind P, Chevallier JM, Sauvanet A, Delmas V, Cugnenc PH. Anatomic basis of mesenteric elongation for ileo-anal anastomosis with J-shaped reservoir: comparison of two techniques of vascular selection. Surg Radiol Anat 1996;18:11-16; with permission.)

Fig. 16-26.

For elongation of the mesenteric axis, the ileocolic artery has been sectioned at its origin from the superior mesenteric artery. (Modified from Wind P, Chevallier JM, Sauvanet A, Delmas V, Cugnenc PH. Anatomic basis of mesenteric elongation for ileo-anal anastomosis with J-shaped reservoir: comparison of two techniques of vascular selection. Surg Radiol Anat 1996;18:11-16; with permission.)

Fig. 16-27.

For elongation of the mesenteric axis, some vascular connections between the primary arch and the second-order arch have been sectioned. (Modified from Wind P, Chevallier JM, Sauvanet A, Delmas V, Cugnenc PH. Anatomic basis of mesenteric elongation for ileo-anal anastomosis with J-shaped reservoir: comparison of two techniques of vascular selection. Surg Radiol Anat 1996;18:11-16; with permission.)

Anatomy of the Ileocecal Valve

For almost 400 years after its first description by Bauhin in 1579,74 the ileocecal valve was considered to be a slitlike valve with two major lips. As early as 1914, Rutherford noticed the differences between the valve of the cadaver and that of the living patient. With the development of new methods (such as colonoscopy and photography through a cecostomy) for studying the ileocecal area in living patients, it was demonstrated that the “valve” in most patients resembles the cervix protruding into the vagina or the pyloric opening into the duodenum.74

The slitlike orifice of the ileocecal valve appears to be a postmortem artifact. Ulin and colleagues75 illustrated the changes in appearance of the valve, from a “papilla” to a bilabial valve, that take place within the first hour after death (Fig. 16-28). The closing mechanism of the papilla is formed by two rings of thickened circular muscle, one at the base of the papilla and one at the free end.

Fig. 16-28.

The ileocecal valve. A. The papillary appearance of the valve in the living patient. B. The bilabial appearance of the valve in the cadaver. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Terminal Ileum and Appendiceal Abscess

An appendiceal abscess may be palpated by abdominal examination when it is located posteriorly or anteriorly to the terminal ileal loop. The abscess located anteriorly is occasionally referred to as an abscess behind the right rectus abdominis muscle.

Anatomy of Meckel’s Diverticulum

Surgical Anatomy

When present, Meckel’s diverticulum arises from the antimesenteric surface of the ileum about 40 cm from the ileocecal valve in infants, and almost 50 cm in adults. It may be less than 15 cm (4% of cases) or as much as 167 cm from the valve (Fig. 16-29).20 Not less than 5 feet (about 2 meters) of ileum should be inspected to be sure that the diverticulum has not been overlooked.

Fig. 16-29.

Location on the ileum and frequency of occurrence of Meckel’s diverticulum. (Modified from Skandalakis JE, Gray SW (Eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; data from Jay GD III, Margulis RR, McGraw AB, Northrip RR. Meckel’s diverticulum: a survey of one hundred and three cases. Arch Surg 61:158-169, 1950; with permission.)

The diverticulum may be as short as 1 cm or as long as 26 cm: 75 percent will be from 1 to 5 cm; the rest will be longer.9 In spite of these wide variations, there are limits to the possible size and position of vitelline duct remnants. Their length is not measured in meters. They do not arise from the colon, the duodenum, or even from the jejunum (for rare exceptions, see Benson76). Although they may appear to do so, vitelline duct remnants cannot arise from the mesenteric side of the ileum. Remember: very long diverticula, those beyond the boundaries of the ileum, and diverticula on the mesenteric side are not Meckelian in origin.

Three major types of Meckel’s diverticulum are shown in Figure 16-30. The usual condition (Fig. 16-30A) is a blind diverticulum with a free and mobile tip (74 percent). In most of the remainder (24 percent), the tip is attached to the anterior body wall at the umbilicus (Fig. 16-30B). In a few cases (2 percent), the structure is patent to the outside (omphalo-ileal fistula), a solid cord, or a cystic remnant (Fig. 16-30C).

Fig. 16-30.

Major types of Meckel’s diverticulum. A. Diverticulum with free end not attached to body wall. B. Diverticulum connected with the anterior body wall by a fibrous cord. C. Fistula opening through the umbilicus. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

The mucosa of the diverticulum is largely ileal; gastric, pancreatic, or duodenal mucosa may also be present. Gastric mucosa was present in 80 percent of specimens examined by Stewart and Storey.77 Far from being merely an embryologic curiosity, ectopic gastric mucosa with parietal cells leads to ileal ulceration, and is an important conduit of pathology of the diverticulum to the adjacent ileum.

Remember that the independent blood supply of Meckel’s diverticulum originates from an intestinal arcade.

Meckel’s diverticulum is discovered only incidentally during surgery (2 to 4.5 percent of individuals) or at autopsy (1.1 to 2.5 percent of individuals, unless the organ is diseased).9 It is widely stated to be more frequent in males than in females, but this is true only in the presence of disease. Incidentally-found Meckel’s diverticula are equally distributed between the sexes (Fig. 16-31).78

Fig. 16-31.

Difference in age and sex distribution of diseased (symptomatic) and incidental (asymptomatic) Meckel’s diverticulum among 53 children and 71 adults. A sex difference is apparent only in children with diseased Meckel’s diverticulum. Scale indicates the number of cases. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)


Obstruction produced by Meckel’s diverticulum is a complication, rather than a disease of the diverticulum. Since the pathologic findings originate with the diverticulum, Androulakis et al.78 categorized obstruction under Meckel’s diverticulum disease.

Ulceration accounts for about 40 percent of Meckel’s diverticulum disease. It is produced by secretions from ectopic gastric mucosa in the diverticulum. Ulceration acts on unprotected ileal mucosa in the diverticulum or in the ileum distal to it. Bright red or brick red rectal bleeding secondary to ulceration is painless and episodic.79 In 90 percent of cases of bleeding associated with a Meckel’s diverticulum, Tc-99m pertechnetate (nuclear scan with technetium pertechnetate) confirms the clinical diagnosis by demonstrating the ectopic gastric mucosa in the diverticulum.79

Lichtstein and Herskowitz80 reported on a 91-year-old male with massive lower gastrointestinal bleeding secondary to Meckel’s diverticulum with ectopic gastric mucosa.

Obstruction and intussusception together account for about 32 percent of Meckel’s diverticulum disease. Obstruction can be caused by volvulus. A diverticulum attached to the abdominal wall can also cause obstruction by incarceration of an intestinal loop. The diverticulum is the leading point of intussusception. According to Oldham and Wesley,79 five to ten percent of patients with symptomatic diverticular disease present with the clinical picture of intussusception.

Appendicitis-like inflammation, often from the presence of a foreign body and narrow base, accounts for 17 percent of Meckel’s diverticulum disease.79

Neoplasms are found in about 6 percent of Meckel’s diverticulum disease. In order of frequency, these neoplasms are leiomyomas, leiomyosarcomas (malignant gastrointestinal stromal tumors), carcinoid tumors, and adenocarcinomas. Lin et al.81 reported a case of gastric adenocarcinoma of Meckel’s diverticulum which completely obstructed the sigmoid colon. Carcinoid tumors may be the most common neoplastic lesions of the diverticulum.82

Umbilical symptoms (umbilical leakage from an omphaloileal fistula, weeping from an umbilical polyp, or infection of an umbilical sinus) account for the remaining 5 percent of Meckel’s diverticulum disease.9

The symptomatology of Meckel’s diverticulum disease is the clinical picture of acute appendicitis, or symptoms produced by the accompanying pathology (rectal bleeding, intestinal obstruction, etc.).

Incidental Meckel’s Diverticulum

It is our opinion that an asymptomatic Meckel’s diverticulum should always be excised if found during an exploratory laparotomy. The only question is the type of excision: a wide V-wedge excision with intact mesenteric borders, or a minimal segmental bowel resection. We prefer the latter if the general condition of the patient permits, and if the surgeon is not absolutely sure about any possible pathology involving the diverticulum.

We quote Yahchouchy et al.83 on the prophylactic removal of a incidentally discovered Meckel’s diverticulum, “The risk of complications of a Meckel’s diverticulum has not been found to decrease with age. So the benefits of incidental diverticulectomy outweighed its attending morbidity and mortality.”

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Histology and Physiology of the Small Intestine

Histology of the Duodenum

The duodenal wall, from inside to outside, consists of a mucous membrane, a submucosa, a muscularis externa, and an external serosa. The mucosa is thrown up into large crescentic folds (plica circulares, or valves of Kerckring) that project into the intestinal lumen transverse to its long axis. These folds are absent in the proximal 2.5 to 5 cm of the duodenum. The folds are very large and close together just distal to the entrance of the common bile and pancreatic ducts. The duodenal mucosa is characterized by a columnar epithelium on a lamina propria of loose connective tissue, bounded by a thin layer of smooth muscle, the muscularis mucosae. Leaf-shaped villi of mucosa project into the intestinal lumen.

The epithelial surface of the villi contains columnar absorptive intestinal cells capped with microvilli and a glycoprotein surface coat; there are also goblet cells, Paneth cells, argentaffin cells, and a variety of endocrine polypeptide-secreting cells, not all of which are yet understood. The absorptive cells are the most numerous and have the greatest rate of replacement.

Between the villi projecting from the surface into the lumen are openings of simple tubular glands (crypts of Lieberkühn) extending into the lamina propria. Beneath the muscularis mucosa, the submucosa is filled with the coiled tubular glands of Brunner that pierce the muscularis mucosa and open into the bottoms of the crypts. These glands, which are characteristic of the duodenal portion of the small intestine, become less frequent, and finally disappear, in its distal segment. Their secretion is alkaline, probably to neutralize the acid gastric secretion of the stomach. The submucosa is bounded by the muscularis externa, having a deep layer of circular smooth muscle and a superficial layer of longitudinal smooth muscle. These two layers form the contractile basis of peristalsis.

The duodenum, together with the pylorus of the stomach, controls the passage of food to the jejunum and the ileum. The anatomic basis for this action rests on the structure of the proximal duodenum.

At the gastroduodenal junction, the continuity of the circular musculature is interrupted by a ring-shaped septum of connective tissue derived from the submucosa. Proximal to this ring, the circular muscle layer is thickened to form the pyloric sphincter of the stomach. Distal to the ring, there is an abrupt decrease in the thickness of the circular muscle that forms the relatively thin-walled duodenum. At its distal end, the pylorus (“os pylorus”) is surrounded by a duodenal fornix. This arrangement must be kept in mind when performing pyloromyotomy.

The longitudinal external muscle layer, without a change in thickness, is also interrupted at the gastroduodenal junction (except on the side of the lesser curvature, where some peripheral muscle fibers are continuous with fibers of the duodenal musculature). This arrangement may serve to carry peristaltic contractions across the interruption at the connective tissue septum.84

Internally, the appearance of the submucosal glands of Brunner marks the gastroduodenal junction. This may not correspond with the muscular junction. In human beings, the submucosal glands may extend a few centimeters into the pylorus. Occasionally, antral gastric mucosa may prolapse through the pylorus, producing a radiological finding but not a true clinical syndrome.

Where the common bile duct and the main pancreatic duct pass through the wall of the duodenum to open into its lumen, there is an absence of Brunner’s glands. The duodenojejunal junction also is marked internally by the disappearance of Brunner’s glands, and externally by the attachment of the suspensory ligament of Treitz. There is no line of demarcation at this junction.

The suspensory muscle (or, ligament) of Treitz is a fibromuscular band that arises from the right crus of the diaphragm and inserts on the upper surface of the duodenojejunal flexure. It passes posterior to the pancreas and the splenic vein, and anterior to the left renal vein. It may surround the celiac artery or course to its left as the ligament passes toward the terminal region of the duodenum. At its origin, the band contains striated muscle fibers continuous with those of the right crus of the respiratory diaphragm. Near its insertion, the suspensory band contains smooth muscle fibers continuous with those of the longitudinal duodenal muscularis. According to O’Rahilly and Müller,3 the suspensory duodenal muscle, which develops at the beginning of the third trimester, descends from the vicinity of the celiac axis and small intestine down to the duodenojejunal flexure.

The suspensory ligament usually inserts on the duodenal flexure and the third and fourth portions of the duodenum (Fig. 16-32A); it may insert on the flexure only (Fig. 16-32B), or on the third and fourth portions only (Fig. 16-32C). There can also be multiple attachments (Fig. 16-32D). In almost one-fifth of cadavers, the ligament is absent, apparently without associated symptoms.85

Fig. 16-32.

Variations of the attachment of the suspensory muscle (ligament) of Treitz. A. Attachments to the flexure and the third and fourth portions of the duodenum. This is the most common type. B. Attachment to the duodenojejunal flexure. C. Attachments to the third and fourth portions only. D. Multiple separated attachments of the suspensory ligament. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

The proximal half of the first part of the duodenum is completely covered by peritoneum, but all the other parts are located retroperitoneally. The second and third parts are overlapped by the head of the pancreas, so that there is a pancreatic bare area of the duodenum not covered by peritoneum. A second bare area exists on the anterior surface of the second part of the duodenum, where the transverse colon is attached (Fig. 16-33). With pancreatic cancer or pancreatitis, the pancreas and mesocolon, with its middle colic artery, become firmly fixed. The anatomic entities responsible for duodenal fixation are the pylorus, the superior mesenteric vessels, the ligament of Treitz, and, of course, the peritoneum.

Fig. 16-33.

Bare areas of the duodenum. The pancreas is in intimate contact with the duodenum along the concave surface. The attachment of the transverse mesocolon produces an additional bare area. (Modified from Skandalakis JE, Skandalakis LJ, Colborn GL, Pemberton LB, Gray SW. The duodenum. Part 2: Surgical anatomy. Am Surg 55(5):291-298, 1989; with permission.)

Physiologic Characteristics of the Duodenum

Although the duodenum’s control over gastric emptying was known, or at least suspected, in antiquity, the action of the duodenum on the pylorus is far more complex than Rufus of Ephesus could have imagined. Nerve reflexes acting from the duodenum to the pylorus are partly through the extrinsic nerves. Some go via prevertebral sympathetic ganglia, and return through inhibitory sympathetic nerve fibers to the stomach. In addition to extrinsic nerves, the enteric nervous system within the wall of the gastrointestinal tract is now recognized as an independent integrative system with structural and functional properties akin to those of the central nervous system. Thus, the enteric nervous system plays a major role in coordinating and programming gastrointestinal functions within the walls of the duodenum and the stomach.45

We quote from Nemeth et al.86 on the embryology of peristalsis:

[N]eurone density of myenteric plexus is significantly higher in the mesenteric border of the small bowel compared with antimesenteric border in premature infants. The marked morphological differences observed in neurone density in the small bowel of premature infants may contribute to immature small bowel activity.

In addition to the neural mechanisms, there is a humoral effect on the stomach from the duodenum. It appears to respond chiefly to fat in the gastric chyme. The two feedback systems (neural and humoral) work together to inhibit gastric emptying when the duodenum is full or the chyme contains excess acid, protein, or fat. Emptying of the stomach depends upon the amount of chyme to be processed.

Histology of the Jejunum and the Ileum

The intestinal wall (Fig. 16-34) is composed of a serosa of visceral peritoneum, longitudinal and circular muscle, a submucosa of connective tissue, and a mucosa of connective tissue, smooth muscle, and epithelium. The plicae circulares of the small intestine are most obvious in the jejunum. The villi of the jejunum are the most distinctly long, tongue-shaped, or fingerlike projections. The villi of the ileum are shorter and shaped more bluntly, disappearing gradually as the ileocecal valve is approached.

Fig. 16-34.

Section through the wall of the small intestine. The submucosa should be included in stitches forming an anastomosis. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Almost a century ago, Halsted pointed out the importance of the submucosal connective tissue in holding sutures.87 One should remember that when butchers make beef or pork sausage, it is from this layer of the intestine that casings are made; “catgut” sutures also used to be made from this layer. Fear of perforating the mucosa with a stitch makes seromuscular sutures seem to be safer, but the integrity of an anastomosis is greater if the submucosa is included.88-91

The serosa surrounds the jejunum and ileum completely, except at the mesenteric border. Together with the muscular coat, the serosa is the well-known stroma for the application of seromuscular sutures during surgical procedures. The muscular coat, which is formed by the inner circular and outer longitudinal layers, should be considered, at least surgically, as one layer. The muscular coat is responsible for intestinal motility. It contains the myenteric plexus of Auerbach, as well as ganglia for non-myelinated nerve fibers. The submucosa is the home of the very rich network of neuronal elements of Meissner’s plexus, as well as arteries, veins, and lymphatics. It also hosts the Peyer’s patches of isolated and confluent masses of lymphatic nodules in the antimesenteric side of the ileum.

Physiologic Characteristics of the Jejunum and the Ileum

The multitude of villi and their innumerable microvilli vastly increase the surface area of the mucosa of the small intestine that is responsible for absorption and secretion. Intestinal absorptive cells, goblet exocrine cells, and Paneth cells are found in the villi. T-cells and APUD (amine precursor uptake and decarboxylation) cells also are found there. According to Guyton,92 the small intestine absorbs almost all the ingested fluid (about 1.5 liters per day), plus all the fluid from gastrointestinal secretions (approximately 7 liters). The large bowel absorbs only 1.5 liters. The substances absorbed by the small bowel include water, ions, and nutrients (carbohydrates, proteins, and fats).

The small bowel makes the following nonimmunologic contributions:92,93


Degradation of harmful toxins by enteric proteolytic enzymes, lysozymes, and hydrochloric acid

Inhibition of bacteria by mucin, as well as protection of the enteric epithelium

Removal of microbes and parasites by peristaltic activity

Dilution and exclusion of antigens by rapid turnover of the epithelium, minimizing violation of the epithelial surface

Competition for inhibition taking place between the pathologic and the endogenous bacteria

The histologic and functional integrity of the small bowel mucosa is maintained by the genesis of cells that replace the old dying cells. The rapid turnover of the epithelium of the mucosa of the small bowel (in comparison with the slow turnover of that in the large bowel) makes neoplasia of the small bowel unusual. Townsend et al.,94 reporting on growth factors and intestinal neoplasms, wrote that, despite the huge surface area of the small intestines, the interactions of the factors responsible for growth and differentiation are less frequently deranged than in the large bowel. Sarr95 speculates that the following factors may explain why the small bowel has fewer benign and malignant neoplasia in comparison with the stomach and large bowel:


Mucosal cells are replaced rapidly

Small bowel chyme has a high liquid content and is, therefore, less “irritating”

Contents move rapidly through the small bowel, minimizing exposure to carcinogens

Alkaline pH and decreased bacterial concentration minimize the formation of carcinogens from bile and ingested precarcinogens

High activity of the enzyme benzopyrene hydroxylase in the small intestinal mucosa results in detoxification of carcinogens

The small intestine offers humoral and cellular immune surveillance (secretory IgA, abundant immunocompetent lymphoid tissue)

Sarr95 believes that depressed overall immune surveillance by the small intestine may support the genesis of neoplasia in immunocompromised individuals.

Surgery of the Small Intestine

Decalogue of Good and Safe Intestinal Surgery


1. Start by carefully exploring the peritoneal cavity and examining the intraperitoneal organs for primary, secondary, or metastatic disease from the tumor in question, or for metastasis from other tumors, especially melanoma.

2. Inspect and gently palpate the tumor to be resected.

3. Perform good mobilization (both proximal and distal) of the area in question, to avoid tension and to perform an anastomosis without tension.

4. Be extremely careful of the blood supply. Angiography prior to surgery gives the surgeon information about the vascular topography of the duodenum. In a mesentery with a lot of adipose tissue, pulsation of vessels in the mesentery may not be obvious, but gentle palpation can reveal vessels. Very minimal bleeding at the edges is a good sign.

5. Form larger proximal and distal stomata by oblique placement of the noncrushing clamps.

6. After the resection, a good, tension-free apposition of the distal and proximal stomata with serosa-to-serosa approximation is essential.

7. Prepare both stomata for anastomosis by cleaning fat and adhesions approximately 0.5-1.0 cm from the cut edge (especially in the mesenteric border, where leaks always occur).

8. Include the submucosa with the seromuscular layer to better ensure the integrity of the intestinal anastomosis.

9. Avoid hematomata on the anastomotic side.

10. Check anastomotic patency with the thumb and index finger.

Neoplasms of the Small Intestine

The small bowel from the gastroduodenal junction to the ileocecal junction is the home of rare benign and malignant tumors. Because of the differences in anatomic topography of the duodenum and the jejunum/ileum, surgical techniques differ according to the location of the tumor.

The classification and distribution of small bowel neoplasms can be appreciated by study of Table 16-4, Table 16-5, and Table 16-6. Blanchard et al.96 reviewed benign and malignant smooth muscle tumors, and their results are shown in Figure 16-35 and Figure 16-36. According to Sarr,95 the malignant tumors of the small bowel are adenocarcinoma (30-50 percent), leiomyosarcoma (10-20 percent), lymphoma (10-15 percent), and carcinoid tumors (13 percent). Again according to Sarr, adenocarcinoma occurs in the duodenum in 40 percent of cases, in the jejunum in 40 percent, and in the ileum in 20 percent.

Table 16-4. Pathology of Primary Small Bowel Tumors by Cell of Origin

Cell of Origin Benign Malignant
Epithelium Adenoma Adenocarcinoma
Connective tissue Fibroma Fibrosarcoma
Smooth muscle Leiomyoma Leiomyosarcoma
Fat Lipoma Liposarcoma
Vascular endothelium Hemangioma Angiosarcoma
Lymphatics Lymphangioma Lymphangiosarcoma
Lymphoid tissue Pseudolymphoma Lymphoma
Nerve Neurofibroma Neurofibrosarcoma
Ganglioneuroma GAN tumor
Argentaffin cell Carcinoid
Mixed Hamartoma  

Source: Coit DG. Cancer of the small intestine. In: DeVita VT Jr, Hellman S, Rosenberg SA (eds). Cancer: Principles & Practice of Oncology, 5th Ed. Philadelphia: Lippincott-Raven, 1997; with permission.

Table 16-5. Distribution of Malignant Tumors of the Small Bowel by Site in 27 Series

Tumor Duodenum Jejunum Ileum Total
Adenocarcinoma 634 454 301 1389 (44%)
Carcinoid 60 92 781 933 (29%)
Lymphoma 34 183 276 493 (15%)
Sarcoma 61 159 148 368 (12%)
Total 789 (25%) 888 (28%) 1506 (47%) 3183 (100%)

Source: Coit DG. Cancer of the small intestine. In: DeVita VT Jr, Hellman S, Rosenberg SA (eds). Cancer: Principles & Practice of Oncology, 5th Ed. Philadelphia: Lippincott-Raven, 1997; with permission.

Table 16-6. Distribution of Benign Tumors of the Small Bowel by Site in 13 Series

Tumor Duodenum Jejunum Ileum Total
Leiomyoma 24 64 47 135 (37%)
Polyp, adenoma 34 17 17 68 (19%)
Lipoma 11 13 30 54 (15%)
Hemangioma 1 10 26 37 (10%)
Fibroma 4 7 12 23 (6%)
Other 27 8 13 48 (13%)
Total 101 (27%) 119 (33%) 145 (40%) 365 (100%)

Source: Coit DG. Cancer of the small intestine. In: DeVita VT Jr, Hellman S, Rosenberg SA (eds). Cancer: Principles & Practice of Oncology, 5th Ed. Philadelphia: Lippincott-Raven, 1997; with permission.

Fig. 16-35.

Incidence of leiomyomas in the small intestine. n = 886 cases, plus 166 not specified. (Modified from Blanchard DK, Budde JM, Hatch GF III, Wertheimer-Hatch L, Hatch KF, Davis GB, Foster RS Jr, Skandalakis JE. Tumors of the small intestine. World J Surg 24:421-429, 2000; with permission.)

Fig. 16-36.

Incidence of leiomyosarcomas in the small intestine. n =1268 cases, plus 387 not specified. (Modified from Blanchard DK, Budde JM, Hatch GF III, Wertheimer-Hatch L, Hatch KF, Davis GB, Foster RS Jr, Skandalakis JE. Tumors of the small intestine. World J Surg 24:421-429, 2000; with permission.)

Several authors96,97 strongly advise that leiomyoma of the gastrointestinal tract be treated as a malignant tumor, due to the difficulty of diagnosis by frozen or permanent section. This enigmatic presentation dictates radical surgery, even though it may actually be a benign disease. A similar situation exists with sessile villous adenoma. Because of the possibility of malignancy, it should be treated not by enterotomy and excision, but by segmental resection.

 Read an Editorial Comment

Polyps and polyposis present a similar scenario. Sarr95 states that 30 percent of these harbor adenocarcinoma; therefore, radical surgery is the appropriate response. However, since it is not within the scope of this book to present detailed pathologic descriptions of the many lesions that can involve the small bowel, we end the listing of them at this point.

Wängberg et al.98 studied 64 patients with disseminated midgut carcinoids and concluded that an active surgical approach must be recommended to patients with midgut carcinoid syndrome. Figures 16-37 and 16-38 summarize their treatment program and results.

Fig. 16-37.

Treatment program aiming at aggressive tumor reduction in patients with the midgut carcinoid syndrome using surgery and hepatic artery embolization. All interventional procedures were performed under octreotide protection. (From Wängberg B, Westberg G, Tylén U, Tisell L-E, Jansson S, Nilsson O, Johansson V, Scherstén T, Ahlman H. Survival of patients with disseminated midgut carcinoid tumors after aggressive tumor reduction. World J Surg 1996;20:892; with permission.)

Fig. 16-38.

Flow chart of 64 patients with the midgut carcinoid syndrome according to the treatment program in Fig. 16-37. Observation time is given as the mean ± SEM (standard error of mean). (From Wängberg B, Westberg G, Tylén U, Tisell L-E, Jansson S, Nilsson O, Johansson V, Scherstén T, Ahlman H. Survival of patients with disseminated midgut carcinoid tumors after aggressive tumor reduction. World J Surg 1996;20:892; with permission.)

In commenting on the above paper, Farley99 noted that aggressive surgical therapy with improved adjuvant therapy of carcinoid malignancies provides hope for patients with hepatic involvement of midgut carcinoid.

Kirshbom et al.100 stated that metastatic carcinoids of unknown origin behave like midgut carcinoids with respect to hormone production, indolence, and survival.

Surgery of the duodenum can be summarized as follows:


1. With malignancy in the first, third, and fourth part of the duodenum, a segmental resection may be advisable, depending on many other factors.

2. With malignancy of the second part, Whipple resection with regional lymphadenectomy is the procedure of choice. We feel that periampullary carcinoma should be treated radically; occasionally, depending on the age and general condition of the patient, local excision will be performed instead.

3. We agree with the conclusion of Rose et al.,101 and Lillemoe’s concurrence,102 that duodenal carcinoma is biologically comparable to pancreatic and gastric cancer. Therefore, the procedure of choice is pancreatoduodenectomy.

4. According to Farnell and colleagues,103 “Pancreaticoduodenectomy is appropriate for villous tumors containing cancer and may be considered an alternative for select patients with benign villous tumors of the duodenum. If local excision is performed, regular postoperative endoscopic surveillance is mandatory.”

Bleeding, perforation, and obstruction are the complications of small bowel neoplasia. The peculiar anatomy of the lymphatics of the small bowel, together with the above complications, lessens the possibility of a cure if the tumor is malignant.

The mesentery should be inspected for lymph nodes. An excisional biopsy of any enlarged lymph nodes or perhaps two to three suspect lymph nodes should be performed. Careful incision of the overlying peritoneum and excision of the lymph nodes in toto should follow a report of malignancy in the lymph nodes. What appears to be a discolored lymph node may actually be an accessory or ectopic spleen, rather than a lymph node.

Surgical Applications to the Duodenum

First Part of the Duodenum

The relative paucity of collateral pathways in the arterial supply to the first part of the duodenum should cause the surgeon to exercise all possible care in operative procedures in this area. Here, solidly based anatomic knowledge, skillful technique, and conservative skeletonization will produce good results with surgical procedures.

Second Part of the Duodenum

The duodenum is one of the most difficult areas to approach when operating, because of the fixation of the duodenum and the pancreas, the common blood supply for both organs (superior and inferior pancreaticoduodenal arcades), and the opening of the common bile duct and pancreatic ducts. With malignant disease, a pancreaticoduodenectomy should be performed. In the presence of benign disease, a more conservative approach, such as segmental resection, is the preferred treatment. Edwards et al.104 describe two cases in which pancreaticoduodenectomy with en bloc colectomy were attempted as curative procedures for primary malignancies of the duodenum.

Third Part of the Duodenum

The proximal one-third of this part of the duodenum is difficult to deal with because of its relationship posterosuperiorly to the head of the pancreas and the uncinate process. The third part is related posteroinferiorly to the inferior mesenteric artery, which arises from the aorta just behind the duodenum. The surgeon should remember that the third part is crossed ventrally by the superior mesenteric vessels in the vertical plane. The horizontal plane is crossed by the transverse mesocolon, with its marginal artery and the middle colic artery. The surgeon should proceed slowly with the uncinate process, which is closely related to the superior mesenteric vessels. Many small vessels originate from the inferior pancreaticoduodenal arcades. Other small twigs from the superior mesenteric artery are commonly present.

Fourth Part of the Duodenum

The fourth portion of the duodenum is related to two anatomic entities of importance: the ligament of Treitz above, and the inferior mesenteric vein, which is to the left of the paraduodenal fossae. The surgeon should use the fourth portion to begin the exploration of the distal duodenum (third and fourth portions). Remember that mobilization of the right colon and transection of the ligament of Treitz are necessary for good exposure of the distal duodenum. The blood supply here originates from the divisions of the intestinal branches of the superior mesenteric artery, and is similar to that of the rest of the small bowel. The arteries of the fourth part of the duodenum have little or no collateral circulation, and the blood supply is “least efficient” in the “antimesenteric” border (the duodenum loses its mesentery in development but, embryologically, the middle of the anterior wall, which is covered by peritoneum, should be considered its “antimesenteric” border).

Bleeding Duodenal Ulcer

A duodenal ulcer is a peptic ulceration that is located on the posterior wall of the duodenal bulb. When bleeding occurs, it is the gastroduodenal artery that has been eroded, and in most cases the erosion is close to the springing of the transverse pancreatic artery. Turnage105 advised three-point ligation of these vessels to prevent future bleeding.

Remember, in 10 percent32 of the cases there is only one pancreatic duct: the duct of Santorini. The gastroduodenal artery passes “behind” the duodenum and in front of the duct of Santorini. A very deep suture to stop the bleeding can ligate, with catastrophic results, the only pancreatic duct that is present. (See additional information about the accessory pancreatic duct in the section “Surgical Notes to Remember” in this chapter.)

Vascular Compression of the Duodenum

Anatomy of Vascular Compression

A consequence of the erect posture of humans is that the superior mesenteric artery leaves the aorta at a more acute angle than it does in quadrupeds. Through this vascular angle passes the third or fourth part of the duodenum, held in place by the suspensory muscle of Treitz. The posterior limb of the angle is formed by the vertebrae and the paravertebral muscles, as well as by the aorta. The anterior limb is formed by the superior mesenteric artery; the middle and right colic arteries (the superior mesentery artery’s first two branches in the transverse mesocolon) sometimes join in. The most narrow part of the angle, above the duodenum, contains the uncinate process and the left renal vein. The relation of the third portion of the duodenum to the superior mesenteric artery, middle colic artery, aorta, and mesentery is shown in sagittal section in Fig. 16-39. An anterior view of the duodenum, superior mesenteric artery, middle colic artery, and vertebral column is shown in Fig. 16-40.

Fig. 16-39.

Diagrammatic sagittal section through the neck of the pancreas showing the relation of the third portion of the duodenum to the superior mesenteric artery (SMA), middle colic artery (MCA), aorta, and mesentery. (Modified from Akin JT Jr, Gray SW, Skandalakis JE. Vascular compression of the duodenum: presentation of ten cases and review of the literature. Surgery 79(5):515-522, 1976; with permission.)

Fig. 16-40.

Anterior view of the duodenum, superior mesenteric artery (SMA), middle colic artery (MCA), and vertebral column. (Modified from Akin JT Jr, Gray SW, Skandalakis JE. Vascular compression of the duodenum: presentation of ten cases and review of the literature. Surgery 79(5):515-522, 1976; with permission.)

The position of the duodenum beneath the superior mesenteric artery is the result of normal intestinal rotation. Vascular compression syndrome was first described by Rokitansky106 in 1861. Compression in patients with malrotation and grossly altered vascular relationships107 or duodenal compression by anomalous hepatic portal veins108 are not considered here.

Anatomic Variations of Vascular Compression

Three anatomic variations are important in vascular compression:


1. Variations in the length and attachment of the suspensory muscle

2. Variations in the level at which the duodenum crosses the vertebral column

3. Variations in the level of the origin of the superior mesenteric artery

The duodenum usually crosses the vertebral column at the level of the third lumbar vertebra,109 but it may cross at a lower level, especially in women. In a few patients, the crossing may be as high as the second lumbar vertebra. Either the third or the fourth part of the duodenum may lie over the vertebral column.

A lower crossing might seem to allow more room for the duodenum. However, the lumbar curve of the spine reaches its most anterior position at the fourth lumbar vertebra; therefore, the space between the limbs of the angle does not increase. This lumbar curvature is usually more pronounced in females than in males.

The suspensory muscle of the duodenum (ligament of Treitz) connects the right crus of the diaphragm with the duodenojejunal flexure. Variations in insertion are shown in Fig. 16-32; the type shown in Fig. 16-32A is the most common. Multiple separate divisions are not unusual; occurrences of three and four divisions have been reported.110

The duodenum may be pulled higher into the vascular angle if the suspensory muscle is short. Since only the flexure may be raised, the angulation of the fourth part is increased, while the third part remains at the usual level.

According to Cauldwell and Anson,111 in 75 percent of individuals, the superior mesenteric artery arises from the aorta at a level between the upper one-third of the first lumbar vertebra and the disc between the first and second lumbar vertebrae. The artery frequently produces a groove on the anterior surface of the duodenum. Figure 16-39 shows the course of the superior mesenteric artery and its relations to posterior entities.

Compression is occasionally produced by the middle colic artery, which arises from the superior mesenteric artery at the inferior border of the pancreas. This branch lies in the transverse mesocolon and crosses the third part of the duodenum.

The normal angle made by the superior mesenteric artery and the aorta has been measured in cadavers by Derrick and Fadhli112 and Byers and Mansberger, as reported by Mansberger et al.,113 and in living patients by Hearn.114 Of six cases reported by Hearn, five showed radiologic evidence of superior mesenteric artery compression, and the diagnosis was confirmed by surgery in four. The measurements reported in these studies are shown in Table 16-7; it is apparent that the angle is less than normal in two patients in the study by Hearn.

Table 16-7. Aortomesenteric Angles

  No. Average angle(degrees) Range (degrees)
Derrick and Fadhli (1965)a 
64 41.25 20 to 70
Mansberger et al. (1968)b 
31 30 18 to 60
Living subjects [Hearn (1966)]c:  
Normal arteriograms 5 56 45 to 65
Patients with superior mesenteric artery syndrome 2* 11 10 to 12

*One following body cast, one following 30 lb. weight loss (dieting).

a. Derrick JR, Fadhli HA: Surgical anatomy of the superior mesenteric artery. Am Surg 31:545, 1965.

b. Hearn JB: Duodenal ileus with special reference to superior mesenteric artery compression. Radiology 86:305, 1966.

c. Mansberger AR, Hearn JB, Byers RM, et al.: Vascular compression of the duodenum: Emphasis on accurate diagnosis. Am J Surg 115: 89, 1968.

Source: Akin JT, Gray SW, Skandalakis JE. Vascular compression of the duodenum: Presentation of ten cases and review of the literature. Surgery 1976; 79:515-22; with permission.


The chief symptoms of vascular compression of the duodenum are vomiting and epigastric pain after meals. Weight loss commencing after the onset of symptoms is frequent, since the patient regurgitates food or becomes afraid to eat.110


Section or lysis of the suspensory ligament (ligament of Treitz) is the procedure of choice. Occasionally, duodenojejunostomy may be necessary.


Vascular compression of the duodenum, while not rare, can be considered a matter of degree. While many individuals with marked compression are easily diagnosed, many other patients with equally real but less severe compression escape diagnosis and live in discomfort, more or less palliated by medical regimens.

Exposures of the Duodenum

Exposure of the duodenum can be necessary in a search for traumatic injury, for pancreatic procedures, for exploration of the distal common bile duct, for section of the suspensory ligament to relieve duodenal compression, or to reduce a redundant proximal loop of a gastrojejunostomy above the transverse mesocolon.115 The following maneuvers will provide the needed exposures:


1. Mobilization of the second and proximal third portions of the duodenum is obtained by incising the parietal peritoneum along the descending duodenum (second portion), and by retracting the duodenum medially with the head of the pancreas (the “Kocher maneuver”). Madden states that this procedure should bear the name of Jourdain, who described it in 1895.116 This maneuver permits examination of the posterior wall of the duodenum, as well as exploration of the retroduodenal and pancreatic portions of the common bile duct.

2. Exposure of the third portion of the duodenum, proximal to the superior mesenteric vessels, can be obtained by an incision through the transverse mesocolon, an incision through the gastrocolic omentum, or reflection of the right half of the colon.117

3. Exposure of the duodenum distal to the superior mesenteric vessels can be accomplished by incision through the gastrocolic omentum and further reflection of the right colon. In addition, division of the parietal fold just inferior to the paraduodenal fossa will permit visualization of the distal duodenum. Further mobilization of the duodenum can be obtained by transection of the ligament of Treitz.85 In dividing the mesocolon, the surgeon must watch for the right colic, the middle colic, and the marginal vessels. The gastroepiploic arteries lie near the greater curvature of the stomach, within the gastrocolic ligament, and must also be handled appropriately.

Surgical Notes to Remember

(See table “Anatomic Complications of Some Gastric, Duodenal, and Pancreatic Procedures” in stomach chapter).


Duodenectomy alone is impossible because of the fixation of the head of the pancreas to the duodenal loop; pancreaticoduodenectomy is the only practical procedure. However, pancreas-sparing duodenectomy or duodenum-sparing pancreatectomy for benign diseases are new procedures currently being tried, but not used by the majority of surgeons.

Do not ligate both the superior and the inferior pancreaticoduodenal arteries. Ligation of both can cause necrosis of the head of the pancreas and of a great part of the duodenum.

The accessory pancreatic duct (of Santorini) passes deep to the gastrointestinal artery. For safety, ligate the artery away from the anterior medial duodenal wall where the papilla is located. Such a maneuver avoids injury to or ligation of the duct. The well-known phrase “water under the bridge” applies to the relation of the ureter and the uterine artery, as well as to the relation of the accessory pancreatic duct and the gastroduodenal artery. Keep in mind that in 10 percent32 of cases, the duct of Santorini is the only duct draining the pancreas. Therefore, ligation of the gastroduodenal artery with accidental inclusion of the duct will be catastrophic.

With the Kocher maneuver, the surgeon reconstructs the primitive mesoduodenum and achieves mobilization of the duodenum. This is useful for some surgical procedures.

Do not skeletonize more than 2 cm of the first part of the duodenum. If more than 2 cm of skeletonization is done, a duodenostomy may be necessary to avoid blowout of the stump secondary to poor blood supply.

The suspensory ligament can be transected with impunity. It should be ligated before being sectioned, so that bleeding from small vessels contained within it can be avoided. Failure to completely sever the suspensory muscle (which is possible if the insertion is multiple) will, of course, fail to relieve the symptoms of vascular compression of the duodenum (Fig. 16-41).

With a large, penetrating, posterior duodenal or pyloric ulcer, the surgeon should remember the following:


– The proximal duodenum shortens because of the inflammatory process (duodenal shortening)

– The anatomic topography of the distal common bile duct, the opening of the duct of Santorini, and the ampulla of Vater are distorted

– Leaving the ulcer in situ is a wise decision

– The following two procedures are extremely useful:


Careful palpation for, or visualization of, the location of the ampulla of Vater

Common bile duct exploration, with insertion of a catheter into the common bile duct and the duodenum

Chang et al.118 advise partial and complete circular duodenectomy as well as highly selective vagotomy for the treatment of duodenal ulcer with obstruction.

Katkhouda et al.119 stated that a perforated duodenal ulcer may be repaired laparoscopically.

In the majority of cases, the common bile duct is located to the right of the gastroduodenal artery at the posterior wall of the first portion of the duodenum. In many cases, the artery crosses the supraduodenal portion of the common bile duct anteriorly or posteriorly. This phenomenon may also be observed with the posterior superior pancreaticoduodenal artery, which crosses the common bile duct ventrally, to the right, and then dorsally.

According to Nassoura et al.,120 the vast majority of penetrating duodenal injuries should be treated by primary repair or resection and anastomosis. Degiannis121 recommended the addition of pyloric exclusion to the operative management of penetrating duodenal injuries.

A retrospective study by Allen et al.122 of 22,163 cases of blunt trauma identified 35 (0.2%) cases of blunt duodenal injury. Despite modern diagnostic techniques (CT scan, diagnostic peritoneal lavage), diagnosis was delayed (more than 6 hours) in seven (20%) of these 35. Delayed diagnosis was associated with an increase in abdominal complications.

Chou et al.123 concluded after reviewing 309 CT examinations that CT imaging is a reliable method for localizing the duodenojejunal junction because the inferior mesenteric vein can be clearly demonstrated. They identified the junction in 224 examinations.

Bouvier et al.124 stated that duodenojejunal junction tumors may be excised in a single block if the superior mesenteric artery is not involved with the tumor.

Fig. 16-41.

Section of the suspensory ligament usually lowers the duodenum two fingerbreadths below the origin of the superior mesenteric artery (SMA). (Modified from Akin JT Jr., Milsap JH Jr., Gray SW, Skandalakis JE. Pictorial presentation of the vascular compression of the duodenum. III. Contemp Surg 1977;10:52-6. Used with permission.)

Surgical Applications to the Jejunum and Ileum

Diagnostic Procedures for the Jejunum and Ileum

Morphology, topography, functional problems, and pathology may be visualized by several methods, such as:


Barium swallow

Barium enema (if the ileocecal valve permits entrance of the barium into the terminal ileum)

Selective superior mesenteric artery arteriography



Tc-99m pertechnetate (nuclear scan with technetium pertechnetate)

Peck et al.125 advised use of computed tomography for detection of the cause of intestinal obstruction and the presence of strangulation.

Resection of the Jejunum and the Ileum

Pathologic Indications for Resection

Jejunal or ileal resection may be done in response to several pathologic entities of the small bowel. To name a few:


Internal hernia, intussusception

Intestinal obstruction secondary to Crohn’s disease, mesenteric cysts, lymphangioma or other causes126

Mesenteric thrombosis of arterial or venous type, with infarction (ischemia)

Benign or malignant tumors

Intestinal injury secondary to bleeding or penetrating abdominal trauma; traumatic perforation


Obstruction by food, foreign bodies, or gallstones

Volvulus with bowel necrosis

Meckel’s diverticulum

Duplication of the intestine

Atresias and stenoses of the intestine

Bemelman and colleagues127 favored laparoscopic ileocolic resection for Crohn’s disease over open surgery, based on early hospital discharge and improved cosmetic results.

Here we will consider only intussusception, mesenteric cysts, and mesenteric ischemia.


An intussusception is created when a proximal segment of intestine (the intussusceptum) invaginates into the portion of the intestine immediately distal to it (the intussuscipiens) (Fig. 16-42). Intussusceptions are named for their location; the most frequent are ileocolic. They tend to increase in length, frequently appearing at the anus. Figure 16-43 shows the location and extent of 120 intussusceptions in infants and children.128

Fig. 16-42.

Diagram of the anatomy of an intestinal intussusception. Such a formation can enlarge distally until the leading edge reaches the anus. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Fig. 16-43.

Location of 120 intussusceptions in children. The head of the arrow indicates the position of the advancing head of the intussusception. (Modified from Lionakis B, Gray SW, Skandalakis JE, Akin JT Jr. Intussusception in infants and children. South Med J 1960:53:1226; with permission.)

Meckel’s diverticulum is the most common identifiable cause of intussusception in children. Other known causes are intestinal polyps, duplications, atresias, and tumors of the intestine, but 85 percent of our cases of intussusceptions in children could not be assigned to any cause (Fig. 16-44). A seasonal cycle, with more admissions in the spring and the summer, has been observed in children.128

Fig. 16-44.

Cause of intussusception in 23 cases, 14.5% of total cases. The remaining 136 cases had no evident anatomic cause. (Modified from Lionakis B, Gray SW, Skandalakis JE, Akin JT Jr. Intussusception in infants and children. South Med J 1960: 53:1226; with permission.)

The Centers for Disease Control and Prevention129 in Atlanta reported preliminary findings of an increased risk of intussusception among healthy infants who were recipients of the rotavirus vaccine. Perhaps this is another etiologic factor for the genesis of intussusception.

Zapas et al.130 presented ileocecal duplication (cyst), which was the focal point for ileocolic intussusception. The treatment was bowel resection and primary anastomosis.

Oldham and Wesley79 presented a table (Table 16-8) of predisposing factors for the development of intussusception.

Table 16-8. Predisposing Factors to the Development of Intussusception

Anatomic Lead Points  Bleeding Disorders* 
Meckel’s diverticulum Henoch-Schönlein purpura
Polyp Hemophilia
Hypertrophied Peyer patch Leukemia
Appendix Trauma* 
Duplication or enteric cyst Blunt abdominal trauma
Lymphoma Major retroperitoneal operative procedures
Other neoplasm Other 
Ectopic pancreas Cystic fibrosis
Associated Infections   

*These factors are more likely to be associated with small bowel-to-small bowel intussusception than with ileocolic intussusception.

Source: Oldham KT, Coran AG, Wesley JR. Pediatric abdomen. In: Greenfield LJ, ed. Surgery: Scientific Principles and Practice, 2nd Ed. Philadelphia: Lippincot-Raven, 1997; with permission.

In adults, our “two-thirds rule” can be applied131: Two-thirds of adult intussusceptions are from known causes. Of these, two-thirds are due to neoplasms. Of those caused by neoplasms, two-thirds of the neoplasms will be malignant.

The first stage of intussusception is edema of the intussusceptum, owing to lymphatic obstruction. Venous obstruction occurs next, followed by infarction and gangrene. The final stage is necrosis and perforation. Very rarely, the intussusception sloughs, and anastomosis with the normal proximal portion produces a spontaneous cure.

Oldham and Wesley79 stated that ultrasound examination is a very reliable tool, demonstrating intussusception as a mass, with a double lumen resembling a “bull’s eye.” They added that an air contrast enema or a barium enema serves both diagnostic and therapeutic purposes.

As previously noted, reduction of the intussusception can be spontaneous, or it may be achieved by a barium enema, an air enema, or with operation. With operation, reduction can be attempted, or resection with anastomosis of the healthy ends may be necessary. We believe that reduction by enema should be attempted in children. Wang et al.132 reported that pneumatic reduction, with air and fluoroscopic guidance, afforded them a 97 percent success rate for reduction without surgery.

If the reduction is successful, the patient should be watched for 48 hours for possible recurrence. If the enema is unsuccessful or the intussusception recurs, operation should be undertaken at once. For children, we recommend reduction with resection if necessary; for adults, we recommend resection without reduction.

Mesenteric Cysts

Mesenteric cysts are fluid-filled chambers lined by cuboidal or columnar epithelium or without lining. No smooth muscle is present. Blood vessels infrequently adhere to the wall of the cyst.133 The fluid inside may be clear if located in the mesentery of the distal small bowel or colon, or chylous if in the mesentery of the proximal small bowel.133 Baird et al.134 presented a case of mesenteric cyst containing milk of calcium.

Mesenteric cysts are uncommon. Since 1507, only 820 cases of mesenteric cysts have been reported.135 From 1900 to 1926 at the Massachusetts General Hospital only six cases of mesenteric cyst were recorded.136 There were only seven cases at the Mayo Clinic in more than one million patients.137 At Saint Joseph’s Infirmary, Atlanta, Skandalakis138 found only two cases of mesenteric cyst in 67,000 admissions between 1922 and 1955. Mesenteric cysts occur in about 1 in 100,000 general hospital admissions and in 1 in 4000 to 34,000 pediatric admissions.133

Mesenteric cysts may be malignant or benign. They may be unilocular or multilocular, single or multiple.139 The home of mesenteric cysts in most cases is the mesentery of the small bowel (60%) or of the colon (40%)140 (Fig. 16-45). Mourad et al.141 presented a cyst localized in the hepatogastric mesentery and made reference to two similar cases from the literature. Chung et al.142 reported on several cysts located in the mesentery of the small bowel (5 cases), the base of the mesentery with retroperitoneal extension (4 cases), transverse mesocolon (4 cases), and gastrocolic ligament (2 cases).

Fig. 16-45.

Topographic anatomy showing 5 omental and mesenteric cysts (dotted). (Modified from Skandalakis JE, Gray SW [eds]. Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.)

Confusion exists in the literature regarding mesenteric, omental, and retroperitoneal masses; between benign or malignant cystic neoplasms and cysts; and between solid and cystic neoplasms. We do not propose to resolve this issue, other than to point out that benign mesenteric cystic neoplasms and mesenteric cysts are usually assumed to be terms referring to the same pathologic entities, and we do not disagree with that view. For a more detailed presentation of the classification of mesenteric cysts, see Table 16-9.

Table 16-9. Classification

I. Embryonal cysts
  A. Arising from embryonic remnants and sequestrated tissue
    1. Serous
    2. Chylous
    3. Sanguineous
    4. Dermoid
  B. Arising by sequestration from the bowel
    1. Including Meckel’s diverticulum
  C. Of urogenital origin
II. Pseudocysts
  A. Of infective origin
    1. Hydatids
    2. Cystic degeneration of tuberculous nodes
  B. Cystic malignant disease
III. Embryonic and developmental cysts
  A. Enteric
  B. Urogenital
  C. Lymphoid
  D. Dermoid
  E. Embryonic defects in early formation of lymphatic vessels, lymph nodes, etc.
IV. Traumatic or acquired cysts (cyst wall composed of fibrous tissue without a lining membrane)
  A. Those caused by injury
    1. Hemorrhage causing sanguineous cysts
    2. Rupture of lacteals
    3. Extravasation of chyle into surrounding tissue
V. Neoplastic cysts
  A. Benign cysts
    1. Hyperplastic lymph of vessels resolving in lymphangiomata
  B. Malignant cysts
    1. Lymphangioendothelioma
VI. Infective and degenerative cysts
  A. Mycotic
  B. Parasitic
  C. Tuberculous
  D. Cystic degeneration of lymph nodes and other tissue

Classification from Caropreso P. Mesenteric cysts: a review. Arch Surg 1974; 108:242-246. After Ford JR. Mesenteric cyst: review of the literature with report of an unusual case. Am J Surg 1960;99:878-883; with permission.

The incidence may be highest in the fourth decade of life and lowest in the first and sixth.143 Takiff et al.144 stated that cysts are more common in middle-aged adults and more common in women. However, they may occur in either sex and at any age. There is a case in the literature of a cyst in a neonate142 and one in a 72 year old.138

Cystic tumors of the mesentery are rare. They are typically benign. Cystic lymphangiomas are the most common type of benign tumor and are lined by endothelium. Their gross structure is often indistinguishable from that of mesenteric cysts. Knol and Eckhauser133 stated that despite the fact that the incidence of malignant change is low the cystic wall should be examined for “rough, friable, papillary projections that suggest malignancy.”

How these cysts arise is a matter of speculation. Orobitg et al.145 reported a case of mesenteric cyst of lymphatic origin. Lee et al.146 presented a cyst of mullerian origin that was located between the liver and right adnexa. Mullerian cysts of the mesentery and retroperitoneum are extremely rare and may be of urogenital origin.

Some published hypotheses (Table 16-10) suggest that mesenteric cysts may arise from degeneration of lymph nodes,147,148 or result from congenital malformation of lymphatic vessels,149 developmental anomalies,137 and trauma.150 Guthrie and Wakefield151 suggested that mesenteric cysts originate from true diverticula of the small intestine that grow into the mesentery and become pinched off. Gross and Ladd152 described mesenteric cysts as “[m]isplaced bits of lymphatic tissue which proliferate and . . .accumulate fluid because they do not possess communications which allow them to drain properly into the remainder of the lymphatic system.” Beahrs et al.153 stated: “It is felt that chylous cysts do not have a common mode of origin but may come from several sources.”

Table 16-10. Theories on the Etiology of Mesenteric Cysts

Name Theory
Rokitansky Degeneration of lymph nodes
Carson Degeneration of lymph nodes
Hill Congenital malformation of the lymphatic vessels
Godel Neoplasia in the presence of lymph vessel hyperplasia
Handfield-Jones Developmental anomalies
Arzella Developmental anomalies
Lee Traumatic origin
Ewing Traumatic origin
Guthrie-Wakefield Embryologic origin from true diverticula of the small intestine which grew into the mesentery and became pinched off
Gross-Ladd “Misplaced bits of lymphatic tissue which proliferate and they accumulate fluid because they do not possess communications which allow them to drain properly into the remainder of the lymphatic system”
Beahrs et al. “It is felt that chylous cysts do not have a common mode of origin but may come from several sources”

Source: Skandalakis JE. Mesenteric cyst: a report of three cases. J Med Assoc Ga 44(2):75-80, 1955; with permission.

The severity of symptoms correlates with cyst size.133 Cysts may be asymptomatic or may present with abdominal pain, fever, vomitting, diarrhea or constipation, ascites, and abdominal mass. Mohanty et al.154 described a case of mesenteric cyst that presented as an inguinal hernia, and these authors found four more such cases from the English literature. Chung et al.142 reported that several cases presented as appendicitis. Namasivayam et al.155 reported on a mesenteric cyst producing volvulus of the proximal small bowel.

Ultrasonography,156 and CT and MR imaging, together with history and physical examination, is used to diagnose mesenteric cysts.133

Treatment is surgical: (1) resection and primary anastomosis, if the cyst is unduly adherent to the intestine, (2) dissection and enucleation, or (3) marsupialization. The treatment of choice is dissection and enucleation; if this is not possible, resection with anastomosis of the remaining ends may be done. Tuttle et al.157 advised simple enucleation as the treatment of choice for all types of mesenteric cysts.

The first step is to study the cyst through the open abdomen and to make the differential diagnosis between a true mesenteric cyst and an enteric cyst. Then one must try to locate and displace all the important vessels of the mesentery. If this can be done, the dissection is easy. If this is not possible we must think of resection. We cannot agree with Parsons158 that marsupialization is an obsolete procedure. When indicated, it is a necessary evil and “the way of necessity.”

In summarizing the operative aspects of mesenteric cysts, one should emphasize the following:


Always have in mind the blood supply of the intestine

Carefully close the opened mesentery

Avoid rough or ragged areas on bowel or mesentery

Several reports159-161 indicate that laparoscopic surgery for mesenteric cysts can be successful.

Mesenteric Ischemia

Mesenteric ischemia, the acute type, is a real surgical emergency. Divino et al.162 urged that aggressive treatment be immediately instituted when mesenteric vein thrombosis is suspected. We quote Skandalakis et al.163:

Mesenteric venous thrombosis appears to be a distinct clinical entity among the group of conditions generally referred to as mesenteric vascular occlusions. In contrast to catastrophic arterial occlusions, mesenteric venous thrombosis follows a different course. The latter is much nore amenable to surgery, and because of the more insidious onset of symptoms, earlier recognition of this entity offers an opportunity for early and adequate treatment in a large percentage of cases.

According to Hassan and Raufman,164 the following eight conditions are associated with mesenteric venous thrombosis:


previous abdominal surgery

blunt abdominal trauma

hypercoagulable states

oral contraceptive use


portal hypertension

decompression disease, sickle-cell anemia, hypoperfusion syndrome

paroxysmal nocturnal hemoglobulinuria, volvulus, intussusception

Hassan and Raufman found that previous abdominal surgery and hypercoagulable states are the most common of the above conditions. Gewertz,165 in an invited critique of the paper of Mansour,166 wisely stated the following:

The morbidity and mortality of acute mesenteric ischemia has remained high despite heightened sensitivity to the diagnosis. Since the duration of the ischemic episode is the most important determinant of outcome, an aggressive diagnostic and treatment protocol must be maintained. While this stance may precipitate many negative angiographic studies, such an approach is the only opportunity to save in these critically ill patients.

Non-Pathologic Reasons for Resection

Intestinal resection can be performed for inherent disease of the segment resected, or to obtain a normal segment for use elsewhere in the body. Healthy intestinal segments have been used in the gastrointestinal tract in the following ways, both in experimental animals167 and in human patients:168,169


as jejunal loops for stomach reconstruction

as intestinal transplant for chronic short gut syndrome following surgical intervention for necrotizing enterocolitis170

as graft material for treatment of desmoid tumors in patients with familial adenomatous polyposis171

as intestinal loops for esophageal reconstruction

as segments of intestine for biliary tract surgery

as surgical treatment of postgastrectomy syndrome

as mucosal grafts of jejunum for large duodenal defects172

Similar use of the intestine has been successful in such urologic procedures as:


Ileal graft to enlarge the bladder

Ileal loop to reimplant a ureter into the bladder


Ileal pouch formation and ileoanal anastomosis

In addition, the small intestine has been used for:


Vaginal reconstruction

Reinforcement of vascular grafts

Revascularization of the breast

Strictureplasty for obstructing small bowel Crohn’s disease173

Some of these techniques have been abandoned, but several are still being used today very successfully. Few organs are more easily exposed and mobilized than are loops of small intestine. Size reductions of adult cadaveric small bowels can provide suitable grafts for pediatric transplantation.174 Adhesions from previous surgery are the chief obstacles to good mobilization.

Anatomic Complications of Intestinal Resection

Dhar and Kirsner175 reported the possible consequences of ileal resection as follows:


Diarrhea and steatorrhea

Bacterial overgrowth

Nutritional deficiencies


Hyperoxaluria and nephrolithiasis

Gastric hypersecretion

Vascular Injury

Table 16-11 summarizes some of the anatomic complications of resection. The most serious vascular injury by far in resecting the small intestine is that to the superior mesenteric artery. This must be repaired at once. Injury to the mesentery and one or more of the intestinal arteries will require ligation. It will also increase the length of a devitalized segment of intestine and hence, the length of the resection needed.

Table 16-11. Summary of Anatomic Complications of Small Intestine Resections

Procedure Vascular Injury Organ Injury Inadequate Procedure
Intestinal resection Ischemia at antimesenteric border from injury to vasa recta, at mesenteric border from hematoma at junction of mesentery and anastomotic site, from injury to intestinal arteries and arcades supplying intestinal segment to be preserved Peritoneal soiling, adhesions from raw surfaces, tension on anastomosis Too short a segment resected, leakage of anastomosis at suture line, inadequate stoma, failure to look for possible additional distal obstructions, side-to-side anastomosis with long stump of proximal limb

Source: Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.

Any line of resection must be placed where it minimizes injury to the blood supply. Clamps should be placed such that there is at least 1 cm free on either side of the line of transection. Preserve as many vascular arches and vasa recta as possible (Fig. 16-46).

Fig. 16-46.

Recommended position of noncrushing clamps for segmental resection of intestine. The 30° angle from a vertical transection preserves as much of the antimesenteric blood supply as possible (arrows) and slightly increases the functional diameter of the anastomosis. (Modified from Skandalakis JE, Skandalakis PN, Skandalakis LJ. Surgical Anatomy and Technique: A Pocket Manual, 2nd Ed. New York: Springer, 2000; with permission.)

Hematomas at the anastomotic site will cause ischemia, necrosis, and perforation. Hematomas are most common at the junction of the mesentery with the anastomotic site. Here, mesenteric vessels can be occluded, producing local ischemia.

Organ Injury

The only organ at risk, of course, should be the intestine being resected. The abdominal cavity should be well packed before any enterotomy or enterostomy to avoid contamination and future infection with resulting intraperitoneal or abdominal wall abscesses. The surgeon must exercise judgment as to how much intestine is to be resected. There is no excuse for resecting too little; if in doubt, the surgeon should remove the segment in question.

Leakage at the suture line is the result of poor technique and will be followed by a fistula or general peritonitis. The possibility of leakage can be reduced by careful closure of the mesentery at the suture line to avoid damaging blood vessels, use of a nasogastric tube to avoid distention, and avoidance of tension on the anastomosis.

An inadequate stoma will result in stasis of intestinal contents, and possible obstruction. A slightly oblique line of resection will help enlarge the anastomotic opening and will preserve the blood supply to the antimesenteric border. The proper angle is shown in Fig. 16-47. Surgeons must use their judgment in cutting adhesions. They should ligate both distal and proximal ends of adhesion bands to prevent possible bleeding. Simple adhesions are usually avascular; no ligation is needed.

Fig. 16-47.

Side-to-side anastomosis. A. Stoma too proximal. B. Dilated stump of proximal loop resulting in the blind stump syndrome. C. Proper location of the stoma at the distal end of proximal loop. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Surgeons should make every effort to avoid producing raw surfaces during dissection. In very rare cases, raw surfaces should be repaired with 3-0 Vicryl. But the pathobiology of adhesion formation is foreign-body reaction, and sutures serve as the nidus for such reactions. An end-to-end anastomosis is the preferred method for intestinal resection. If a side-to-side anastomosis is to be used, the opening should be carried as close to the blind ends as possible to avoid blowout of the stumps or the blind stump syndrome (Fig. 16-47).

Tension and torsion at the anastomosis must be avoided. The surgeon must be sure that any tension or torsion has not been merely transferred to a more distal or proximal site. The resection of an intestinal obstruction does not preclude the presence of another obstruction distal to the anastomosis. This is of great importance in surgery for intestinal atresias in infancy.152

Complications related to needle catheter jejunostomy were studied by Myers et al.176 These complications are detailed in Table 16-12. North and Nava177 report that it is possible to introduce air into the portal vein during a needle catheter jejunostomy.

Table 16-12. Complications Related to Needle Catheter Jejunostomy in 2022 Consecutive Applications

Category Complication Reoperation Death Complication Reoperation
Abdominal wall infection 3 3 0 2 2
Bowel necrosis 3 3 2 2 2
Pneumatosis intestinalis 3 2 0 0 0
Bowel obstruction 3 3 1 1 1
Fistula 1 0 0 0 0
Intra-abdominal infection 3 3 0 1 1
Central line sepsis 1 0 0 1 0
Subcutaneous abscess 2 0 0 0 0
Dislodgment 10 3 0 10 4
Occlusion 5 1 0 5 2
Total 34 18 3 22 10*

*Two repeat operations involved 2 complications.

Source: Myers JG, Page CP, Stewart RM, Schwesinger WH, Sirinek KR, Aust JB. Complications of needle catheter jejunostomy in 2,022 consecutive applications. Am J Surg 1995;170:547-551; with permission.

Nussbaumer et al.178 reported traumatic perforation of the small bowel as the rare complication of inguinal hernia.


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