Print | Close Window

Note: Large images and tables on this page may necessitate printing in landscape mode.

Skandalakis' Surgical Anatomy > Chapter 18. Large Intestine and Anorectum >

INTRODUCTION
The large intestine is formed by the following anatomic entities:

Ileocecal valve

Appendix

Cecum

Ascending colon

Hepatic flexure

Transverse colon

Splenic flexure

Descending colon

Sigmoid colon

Anorectum

In this book, the appendix has been presented in the preceding chapter.

Following our presentations on the above list of topics is a special section written by
Professor Ahmed Shafik. Dr. Shafik, who is chairman of the Department of Surgery and
Experimental Research at the medical school of Cairo University, Egypt, is such an original
thinker in regard to the large intestine and anorectum that we invited him to share his
unique perspective with our readers. We are grateful to him for interpreting his research
and offering his philosophy to us, and we are honored to provide his excellent work on the
large intestine and anorectum to our readers. We encourage careful thought about Dr.
Shafik's innovative ideas.

NOTE: Some writers use the word "colon" to mean the collectivity of four anatomic entities:
ascending, transverse, descending, and sigmoid colons. Occasionally we will employ the
word "colon" or "colonic" in that manner to mean "large intestine" (e.g. "colonic" wall for
"large intestinal" wall).

HISTORY
The anatomic and surgical history of the large intestine and anorectum is shown in Table
18-1.

Table 18-1. Anatomic and Surgical History of the Large Intestine and Anorectum

Hippocrates ca. 400 Treated hemorrhoids with white-hot iron or by burning them off; treated fistulas by use of seton
B.C.

Aristotle (384-322 Used the word "colon"; noted that congenital malformations occurred more often in boys than
B.C.) girls

Soranos of Performed digital rupture of membranes of the anal canal of newborns

Ephesus (A.D. 98-
138)

Galen (121-201 Named the rectum "apefthismenon"

A.D.)

Paul of Aegina Collected lost works of Heliodorus, Leonidas, and Antyllus, and presented first description of a
(625-690 A.D.) surgical technique for anal atresia

Albertus Magnus Works indicate that anal atresia was well known during Middle Ages
(1193-1280)

John Arderne 1367 Wrote paper that contained the basis of anorectal surgery

Antonius Studied recto-anal agenesis in autopsy; reported recto-anal agenesis with vaginal fistula
Benivenius (1513-
1572)

Tobias Cneulinus ca. Unsuccessful perineal operation for recto-anal agenesis because the rectum could not be
1580 identified

Fabricius Hildanus 1593 Successfully opened anal agenesis by incision, introduction of rectal speculum, dilatation of the
opening, and application of lead carbonate and meninge-dye

J.S. von 1609 Reported the first case of anal agenesis with urethral fistula; reported isolated rectal atresia
Grafenberg without anal atresia

G.T. Drr 1668 Described anus copertus with perineal fistula; incised the anal membrane and the obstructed
anus, curing the child

Hendrik van 1676 Ruptured anal stenosis with a knife and successfully maintained the opening with salves and
Roonhuysen instruments

Physician to King 1686 Conceived of and performed fistulotomy on the king

Louis XIV

Frederik Ruysch ca. Reported spontaneous rupture of anal atresia in a 5-day-old child (who died soon thereafter)
(1638-1731) 1700
Saviard 1702 In a child with no trace of an anus, he inserted a lancet, and entered the blind rectal pouch.
Meconium was released and the child survived.

Littr 1710 Successfully treated imperforate anus by opening colon in left lower quadrant of abdomen

Heister 1718 Operated using a trocar on two children whose rectum ended at the level of upper sacrum;
both died

Barbout 1739 Reported two cases of recto-anal agenesis with recto-cloacal fistula
to
1775

Percivall Pott 1765 British doctor whose writings pointed up the advances Britons had made in colorectal diseases
and surgery

Pillore 1776 Performed cecostomy for cancer of the lower bowel

Petit 1781 Incising for recto-anal agenesis, a tumor, but no rectum, was found. After incision of the tumor,
meconium discharged. Patient died.

Benjamin Bell 1787 Successfully treated 2 cases of recto-anal agenesis; newly formed orifices tended to shrink from
scar tissue

Duret 1793 Successfully treated imperforate anus by opening left lower quadrant of colon

Latta 1795 Successfully treated recto-anal agenesis, but dilatation therapy was required for nine full
months

Callisen 1798 Suggested extraperitoneal colostomy at the lumbar area for imperforate anus

Meckel 1817 Studied embryology of the normal colon

Lisfranc (1790- Operated on colonic tumors

1847)

Frederick Salmon 1835 Salmon was founder and chief surgeon of St. Mark's Hospital in London, which was the
pinnacle of knowledge and treatment of colon and rectal diseases

William At this hospital William Allingham wrote the first textbook devoted entirely to anorectal
Allingham disease; it describes hemorrhoid treatment by excision and ligature

Amussat 1835 Described surgery for imperforate anus.

1839 Adopted Callisen's procedure.

G.M. Bushe 1837 Wrote first American proctology book that later acquired international acclaim

Nlaton 1839 Exposed, fixed, and incised distended loop of bowel proximal to obstruction

Miller 1857 First successful operation for recto-anal agenesis with bladder fistula
J.H. Bigelow 1858 Wrote that at the present state of the art of surgery, children with rectal or anal atresia should
die without operation

W.H. Bodenhamer 1860 First to produce a clear classification of rectal and anal malformations

Teale (1801-1868) Favored exploratory surgery for bowel obstruction

Mason 1873 Reported 80 cases of colostomy for obstruction with 32.5% mortality

Wilks 1875 Described ulcerative colitis

Hutchinson 1878 ". . .exploratory operations for the relief of abdominal obstruction, the cause of which cannot be
diagnosed, are not warrantable." Stated that by the time a surgeon is called, "the stage at which
abdominal taxis is most hopeful has passed."

J.W. Matthews 1878 American physician began teaching in America the principals of anorectal surgery he had
learned at St. Mark's Hospital, London

Edmund Andrews 1878 Co-authored one of the first textbooks on anorectal surgery
& E.W. Andrews

Billroth 1879 Performed sigmoid resection and exteriorization of the proximal bowel as permanent colostomy

Kraske & Kocher ca. Perfected the sacral approach to rectal tumors
1880

Parker 1883 Urged extension of protracted palliative management of intestinal obstruction

Reybard 1884 Reported survival after resection and anastomosis for cancer of the colon

Greves 1885 Advocated operative intervention for intestinal obstruction

Bryant 1885 Reverted to the intraperitoneal maneuvers of Pillore and Duret

Tait (1845-1899) Remarked that accurate diagnosis could only be made by exploration, "which is better
performed before than after death"

H.O. Thomas 1885 Published monograph against surgical intervention for intestinal obstruction, "The Collegian of
1666 and the Collegians of 1885." Stated that cases of acute intestinal obstruction "belonged to
the department of medicine, the surgeon was a mere assistant. . . An operation may be required
in a few hours or it may not be required for weeks."

Mikulicz 1886 Reverting from his formerly more aggressive surgical approach, decided that laparotomy often
offered no hopeful prospect for relief of acute intestinal obstruction

Hirschsprung 1886 Described autopsies of two infants who died from congenital megacolon (Hirschsprung's
disease)

Fitz & Senn 1888 Advised 48-72 hours observation before patient diagnosed with intestinal obstruction was
turned over to the surgeon
Retterer 1890 Studied urorectal septum and cloaca

Bloch & Paul 1892 Development of "obstructive resection," in which portion of bowel with tumor is brought
to outside abdominal cavity; 1-2 days later, it is divided by cautery, forming a "loop" or "double-
1895 barreled" colostomy

Mall 1898 Studied the development and position of the human intestine.

1899 Observed the extraembryonic growth of the intestines and their return to the abdomen.

J.W. Matthews 1899 Became one of founders of American Proctologic Society. Later called "the Father of
Proctology."

Mikulicz 1905 Perfected and popularized obstructive resection

W.E. Miles 1908 British surgeon who described combined abdominoperineal resection for rectal cancer

Chilaiditi 1910 Described hepatic flexure between liver and diaphragm

Morton 1912 Offered a description of congenital absence of the colon using segmental arterial ligation in
dogs

Johnson 1913 Studied development of colonic mucosa

Dott 1923 Developed a classification of abnormalities of intestinal rotation based on embryologic

observations

Henri Hartmann 1923 Described treatment for obstructing carcinoma of the distal colon

Miles 1926 Developed combined abdominoperineal resection

Rankin 1930 Improved the double-barreled colostomy

Cuthbert Dukes 1932 Originated classification for carcinoma of the rectum

Ladd & Gross 1934 Created a new classification of anorectal anomalies that was the standard for many years

Kirschner 1934 German doctor demonstrated a combined synchronous approach to the abdominoperineal
resection

Gilchrist 1938, Published studies of retrograde lymphatic spread in regard to gastrointestinal carcinoma

1952

Swenson 1950 Designed operation for anal sphincter-preserving removal of aganglionic segments of colon

Stephens 1953 Recognized that the puborectalis muscle is the most critical to continence

Scott 1959 Investigated autonomic supply of the rectum and anorectum

Duthie & Gairns 1960 Investigated sensory innervation of the lower anal canal
Skandalakis et al. 1962 Collective review of cases of smooth muscle tumors of the colon, appendix, and rectum as
reported in the world literature

Painter & Burkitt 1971 Studied relationship of low-residue diet to diverticulosis

Stephens & Smith 1984 Classified anorectal anomalies as high, intermediate, low cloacal, and rare

Pea 1990 Recommended posterior sagittal anorectoplasty

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

References

Estrada RL. Anomalies of Intestinal Rotation and Fixation. Springfield IL: Charles C. Thomas, 1958.

Kevorkian J. The Story of Dissection. New York: Philosophical Library, 1959.

Muldoon JP. History of colorectal surgery. In: Mazier WP, Levien DH, Luchtefeld MA, Senagore AJ (eds). Surgery of the
Colon, Rectum, and Anus. Philadelphia: WB Saunders, 1995.

Schrli AF. Malformations of the anus and rectum and their treatment in medical history. Prog Pediatr Surg 11:141-172, 1978.

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.

Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994.

Wangensteen OH, Wangensteen SD. The Rise of Surgery. Minneapolis: University of Minnesota Press, 1978.

Warren R. Surgery. Philadelphia: WB Saunders, 1963.

EMBRYOGENESIS
Normal Development
During herniation of the intestines into the umbilical cord (Fig. 18-1), a slight local
enlargement of the portion posterior to the superior mesenteric artery marks the site of
the future cecum. Growth and differentiation of this postarterial limb lags behind that of
the proximal prearterial limb when the intestines return to the abdomen.

Fig. 18-1.
Diagram of the growth of the embryonic midgut into the umbilical cord. Fifth week of gestation. The distal limb shows a
swelling at the site of the cecum. The three great arteries supplying the stomach and intestines are remnants of the earlier
vitelline arteries. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery.
New York: McGraw-Hill, 1983; with permission.)

Goblet cells and epithelial cells with a striate border may be found in the colon by the
eleventh week. During the third month, villi and glands appear. The villi reach their
maximum development in the fourth month and gradually shorten and disappear with the
enlargement of the colon in the seventh and eighth months.

Langman and Rowland3 reported that the estimated total number of lymphoid follicles in
the large intestine is between 12,761 and 18,432. The average follicular density is 18.4
per cm2 in the cecum, 15.0 per cm2 in the colon, and 25.4 per cm2 in the rectum.
Previously reported numbers were very low; perhaps these new numbers will remind the
physician about the diagnosis of lymphoid hyperplasia.

The circular layer of muscularis externa appears caudally in the ninth week and spreads
cranially. Ganglion cells of the myenteric plexus of Auerbach reach the colon in the
seventh week, and innervation appears to be complete by the twelfth week. 4 The first
longitudinal muscle fibers are present at the anal canal in the tenth week. Above the
sigmoid colon, the longitudinal fibers extend cranially only along the mesenteric border of
the colon, reaching the cecum in the eleventh week. By the fourth month, the entire colon
is covered, but growth of the muscle coat does not keep up with increasing colon
diameter. By the fourth month, the longitudinal muscle coat becomes separated into three
bands, the taeniae coli. Meconium gradually fills the colon and the lower ileum until birth.

Remember

The colon is produced by both the midgut and the hindgut. The midgut is responsible for
the genesis of the cecum, the ascending colon, and the proximal of the transverse
colon. The hindgut is responsible for the remainder of the colon, the rectum, and the
proximal part of the anus. To be more specific, the distal of the transverse colon, the
descending colon, the sigmoid colon, the rectum and the proximal part of the anal canal
develop from the hindgut.

The distal part of the surgical anal canal is not related embryologically to the hindgut. It
most likely originates from the anal pit, which is of ectodermal origin. As O'Rahilly and
Mller5 wrote, "the anal canal is probably derived from the cloaca." To be more
anatomically correct but still speculative about the embryology of the anorectum, we
present the following information by Rowe et al.6 about the cloacal region.

In the fifth week, the embryonic cloaca is an endodermal sac receiving the hindgut
dorsally and the allantoic stalk ventrally. The cloaca (Fig. 18-2A, B) is separated
from the outside by a thin cloacal membrane (proctodeum), which occupies the
embryo's ventral surface between the tail and the body stalk. During the sixth
week, a septum of mesoderm divides the cloaca into a ventral urogenital sinus and
a dorsal rectum (Fig. 18-2C) . This mesodermic septum fuses with the cloacal
membrane in the seventh week to form the perineal body. The cloacal membrane is
divided into a larger, ventral urogenital membrane and a smaller, dorsal anal
membrane. Externally, the anal membrane becomes slightly depressed, forming the
anal dimple.

By the eighth week, the anal membrane ruptures, leaving no trace of itself (Fig. 18-
2D). The pectinate line in the adult is often considered to be at the level of the anal
membrane, but little evidence exists to either support or contradict this view.
Whatever the exact line of demarcation, the rectum and the upper anal canal are
endodermal and are supplied by the inferior mesenteric artery, while the lower anal
canal is ectodermal and is supplied by branches of the internal iliac artery.

On either side of the anal membrane, the somatic mesoderm forms a pair of anal
tubercles. These tubercles fuse dorsally into a horseshoe-shaped structure. By the
tenth week, the ventral tips of the horseshoe fuse with the perineal body. Striated
muscle in this horseshoe-shaped structure will later become the superficial portion
of the external anal sphincter. The anal sphincter will form at the normal location
even if the rectum should end blindly or should open at another site.

Fig. 18-2.
Diagram of stages in development of the anus and rectum from the fifth to tenth weeks of gestation. A, Closing plate
(proctodeum separates the cloaca from the outside). Urorectal septum (arrow) grows downward to divide the
cloaca. B, Cloaca almost separated into dorsal rectum and ventral urogenital sinus. Tailgut is vanishing. C, Fusion of
urorectal septum with closing plate to form the perineal body. D, Closing plates rupture. E, Division into rectum and
urogenital sinus by the perineal body is complete. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd
ed). Baltimore: Williams & Wilkins, 1994; with permission.)

The superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA) provide the
blood supply of the entire colon. In the surgical anal canal, the branches of the internal
pudendal artery participate.

Congenital Anomalies of the Colon

Stenoses and Atresias
Stenoses and atresias occur in the same pattern as those of the small intestine (see
"Stenoses and Atresias" in the small intestine chapter). They are less common in the large
intestine, with an incidence ranging from 4.6 percent7 to 11.7 percent8 of all intestinal
atresias. More type I (diaphragmatic) atresias occur in the ascending and sigmoid colons,
and more type III (complete segmental) atresias occur in the transverse
colon.9 Treatment is the same as that for atresias of the small intestine.

Dalla Vecchia et al.10 reported 277 cases of intestinal atresia and stenosis, detailing the
treatment and results. The obstruction was duodenal in 138 (50%) [79 (57%) female, 59
(43%) male], jejunoileal in 128 (46%) [61 (48%) female, 67 (52%) male], and colonic in
21 (8%) [8 (38%) female, 13 (62%) male]. Patients with colon atresia were managed
with initial ostomy and delayed anastomosis in 18 of 21 patients (86%) and resection with
primary anastomosis in 3 (14%).

We quote from Lambrecht and Kluth11 on hereditary multiple atresias of the

gastrointestinal tract:

Hereditary multiple atresias have several unique features: (1) the abdominal x-ray
shows signs of gastric or duodenal atresia combined with typical large rounded or
oval homogeneous calcifications in the abdominal cavity, (2) intraoperatively
widespread atresias (exclusively type I and II) extending mostly from the stomach
to rectum are found, (3) cystic dilatation of the bile ducts can be present in cases
with both complete pyloric and duodenal or proximal jejunal atresia, (4) the
pathogenesis is still speculative; a combined immunodeficiency should be excluded,
and (5) a fatal outcome is the rule.

Congenital Aganglionic Megacolon (Hirschsprung's Disease)

Aganglionic megacolon is the result of an absence of ganglion cells in a distal segment of
colon. Neurenteric ganglion cells normally originate in the neural crest, enter the cranial
end of the esophagus, and then follow vagus nerve fibers caudally until the entire gut is
innervated. Why the migrating cells sometimes stop short of the rectum is unknown.

As seen in Fig. 18-3, only 4%12 of the aganglionic segments of the colon are found
proximal to the splenic flexure. It is interesting to note that the neural crest cells forming
these intestinal ganglia follow the vagus with a low failure rate to the end of that nerve's
distribution, i.e., approximately up to the splenic flexure. The remainder of the colon and
rectum receive their parasympathetic innervation via the second, third, and fourth sacral
nerves which have a more or less diffuse pathway to the colon themselves. Perhaps they
do not serve as effectively as a "guide" or "transporter" of the neural crest cells for their
migration into the hindgut derivative. Postganglionic fibers from proximal normal ganglia,
as well as preganglionic parasympathetic fibers, are usually present. The aganglionic
segment usually extends into the sigmoid colon, but the whole of the large intestine and
even part of the small intestine can be affected (Fig. 18-3).13

Fig. 18-3.

Relative frequency of aganglionic segments by length of segment affected. Most cases involve the rectum and sigmoid colon
only. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994;
with permission.)

The greatly dilated proximal segment is normal; the narrowed distal segment is without
ganglia (Fig. 18-4). The line of resection must be within the area in which ganglion cells
are present. Because aganglionosis (Fig. 18-5) is not the only cause of megacolon, a
biopsy is necessary to demonstrate the absence of ganglion cells in the narrowed segment
and their presence in the dilated segment.
Fig. 18-4.

Gross appearance and biopsy findings in aganglionic megacolon. On gross examination the normal colon is thought to end
at A, but biopsy findings reveal that the aganglionic segment extends to B. Resection must be through the dilated proximal
portion in which ganglion cells are present. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical
Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Fig. 18-5.
Possible causes of megacolon which must be considered in diagnosis. (Modified from Skandalakis JE, Gray SW.
Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Remember to differentiate between congenital megacolon and massive fecal impaction.

Because massive fecal impaction may lead to megarectum causing abdominal
compartment syndrome and colorectal obstruction, perforation, or necrosis, Lohlun et
al.14 recommend prompt manual disimpaction or appropriate operative treatment.

Wulkan and Georgeson15 recommend primary laparoscopic endorectal pull-through

surgery as a safe and effective procedure for Hirschsprung's disease in infants and
children.

Colonic Malposition
There are several types of malposition. In Chilaiditi syndrome, the hepatic flexure is
situated between the liver and the diaphragm due to anomalies of the hepatic ligaments.
We quote from Balthazar:16

Positional anomalies of the colon may be explained by an arrest in the normal

development of the distal midgut. Aberrations involving the incipient stages of
rotation lead to severe malpositions, while those involving the latter stages to
milder forms. . . There is a high incidence of associated failure of fixation resulting
in mobile colons that can be demonstrated radiographically. In addition, the great
majority of colonic malrotations demonstrate rotational abnormalities involving the
proximal intestinal tract. Their clinical implication is related to the presence of other
incidental congenital anomalies or to complications derived from faulty mesenteric
 fixations such as peritoneal bands, adhesions, kinking, or intestinal volvulus.

DePrima et al.17 reported reversed intestinal rotation due to abnormal rotation and
fixation.

Retropsoas positioned bowel (colonic positioning posterior or posterolateral to the psoas

muscle at a level below the lower kidney pole) may occur in the ascending or descending
colon. Prassopoulos et al.18 advised that this condition be considered when performing
percutaneous diskectomy or other interventional procedures in the posterior
retroperitoneum.

Congenital Short Colon

Congenital short colon is total or partial replacement of the colon by a pouch, as well as
associated anorectal malformation and colourinary fistula. A case of congenital short colon
with imperforate anus was reported by Herman et al.19 An excellent paper about
congenital short colon by Wakhlu et al.20 advised that the initial procedure be a window
colostomy, followed by pouch excision/ coloplasty and pull-through by a combined
abdominal and posterior sagittal approach when the baby is 6 months old.

Congenital Anomalies of the Anorectum

Multiple classifications of anorectal anomalies exist; none is perfect. We present a highly
diagrammatic review of these anomalies with the hope that the student of embryology will
be able to visualize these enigmatic malformations topographicoanatomically (Table 18-2
and Figs. 18-6, 18-7, 18-8, 18-9, 18-10, and 18-11).

Table 18-2. Anatomic Classification of Anorectal Malformations

Female Male

High High

Anorectal agenesis Anorectal agenesis

With rectovaginal fistula With rectoprostatic urethral fistulaa

Without fistula Without fistula

Rectal atresia Rectal atresia

Intermediate Intermediate

Rectovestibular fistula Rectobulbar urethral fistula

Rectovaginal fistula Anal agenesis without fistula

 Anal agenesis without fistula

Low Low

Anovestibular fistulaa Anocutaneous fistulaa

Anocutaneous fistulaa,b Anal stenosisa,c

Anal stenosisc

Cloacal malformationsd

Rare malformations Rare malformations

aRelatively common lesion.

bIncludes fistulae occurring at the posterior junction of the labia minora often called "fourchette fistulae" or "vulvar fistulae."
cPreviously called "covered anus."
dPreviously called "rectocloacal fistulae." Entry of the rectal fistula into the cloaca may be high or intermediate, depending on
the length of the cloacal canal.

Source: Skandalakis JE, Gray SW (eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with
permission.

Fig. 18-6.
Copyright 2006 The McGraw-Hill Companies. All rights reserved.
Privacy Notice. Any use is subject to the Terms of Use and Notice. Additional Credits and Copyright Information.