Pararectal Fascia

The endopelvic fascia is a thick layer of parietal peritoneum that lines the walls and floor of the pelvis. The portion that is closely applied to the periosteum of the anterior sacrum is the presacral fascia. The fascia propria of the rectum is a thin condensation of the endopelvic fascia that forms an envelope around the mesorectum and continues distally to help form the lateral rectal stalks. The lateral rectal stalks or ligaments are actually anterolateral structures containing the middle rectal artery. The stalks reside in close proximity to the mixed autonomic nerves, containing sympathic and parasympathetic nerves, and division of these structures close to the pelvic sidewall may result in injury to these nerves, resulting in impotence and bladder dysfunction (Fig. 52-3).

FIGURE 52-3 Endopelvic fascia.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 10.)

The rectosacral fascia, or Waldeyer’s fascia, is a thick condensation of endopelvic fascia connecting the presacral fascia to the fascia propria at the level of S4 that extends to the anorectal ring. Waldeyer’s fascia is an important surgical landmark, and its division during dissection from an abdominal approach provides entry to the deep retrorectal pelvis. Dissection between the fascia propria and presacral fascia follows the principles of surgical oncology and minimizes the risk for vascular or neural injuries. Disruption of the presacral fascia may lead to injury of the basivertebral venous plexus, resulting in massive hemorrhage. Disrupting the fascia propria during an operation for rectal cancer may significantly increase the incidence of subsequent recurrence of cancer in the pelvis if mesorectum is then left behind.

Pelvic Floor

The muscles of the pelvic floor, like those of the anal sphincter mechanism, arise from the primitive cloaca. The pelvic floor, or diaphragm, consists of the pubococcygeus, iliococcygeus, and puborectalis, a group of muscles that together form the levator ani. The pelvic diaphragm resides between the sacrum, obturator fascia, ischial spines, and pubis. It forms a strong floor that supports the pelvic organs and, with the external anal sphincter, regulates defecation. The levator hiatus is an opening between the decussating fibers of the pubococcygeus that allows egress of the anal canal, urethra, and dorsal vein in men and the anal canal, urethra, and vagina in women. The puborectalis is a strong, U-shaped sling of striated muscle coursing around the rectum just above the level of the anal sphincters. Relaxation of the puborectalis straightens the anorectal angle and permits descent of feces; contraction produces the opposite effect. The puborectalis is in a state of continual contraction, a factor vital to the maintenance of continence. Puborectalis dysfunction is an important cause of defecation disorders. The pubococcygeus and iliococcygeus most likely participate in continence by applying lateral pressure to narrow the levator hiatus (Figs. 52-4 and 52-5).

FIGURE 52-4 Levator muscles.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 18.)

FIGURE 52-5 Hiatal ligament.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 18.)

Arterial Supply and Venous and Lymphatic Drainage

Knowledge of the embryologic development of the intestinal tract provides an excellent foundation for understanding the anatomic blood supply. The foregut is supplied by the celiac artery, the midgut by the SMA, and the hindgut by the IMA (Figs. 52-6 and 52-7). Anatomic redundancy confers survival advantages and, in the intestinal tract, this feature is provided by extensive communication between the major arteries and collateral blood supply (Fig. 52-8). The territory of the SMA ends at the distal portion of the transverse colon and that of the IMA begins in the region of the splenic flexure. A large collateral vessel, the marginal artery, connects these two circulations and forms a continuous arcade along the mesenteric border of the colon. Vasa recta from this artery branch off at short intervals and supply the bowel wall directly (Fig. 52-9). The SMA supplies the entire small bowel, giving off 12 to 20 jejunal and ileal branches to the left and up to three main colonic branches to the right. The ileocolic artery is the most constant of these branches; it supplies the terminal ileum, cecum, and appendix. The right colic artery is absent in 2% to 18% of specimens; when present, it may arise directly from the SMA or as a branch of the ileocolic or middle colic artery. It supplies the ascending colon and hepatic flexure and communicates with the middle colic artery through collateral marginal artery arcades. The middle colic artery is a proximal branch of the SMA. It generally divides into right and left branches, which supply the proximal and distal transverse colon, respectively. Anatomic variations of the middle colic artery include complete absence in 4% to 20% and the presence of an accessory middle colic artery in 10% of specimens. The left branch of the middle colic artery may supply territory also supplied by the left colic artery through the collateral channel of the marginal artery. This collateral circulation in the area of the splenic flexure is the most inconsistent of the entire colon and has been referred to as a watershed area, vulnerable to ischemia in the presence of hypotension. In some studies, up to 50% of specimens were found to lack clearly identified arteries in a small segment of colon at the confluence of the blood supplies of the midgut and hindgut. These individuals rely on adjacent vasa recta in this area for arterial supply to the bowel wall. In practice, surgeons avoid making anastomoses in the region of the splenic flexure, fearing that the blood supply will not be sufficient to permit healing of the anastomosis, a situation that could lead to anastomotic leak and sepsis.

FIGURE 52-6 Arterial supply of the colon.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 23.)

FIGURE 52-7 Arterial supply of the rectum.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 24.)

FIGURE 52-8 Pathologic anatomy and occlusion of the SMA and IMA. A, Occlusion of SMA. B, Occlusion of the IMA. C, Ligating the IMA. 1, Correct location of ligation (see inset); 2, Incorrect location of ligation.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 28.)

FIGURE 52-9 Cross-sectional anatomy of the colon, with vasa brevia and vasa recta.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 26.)

The IMA originates from the aorta at the level of L2 to L3, approximately 3 cm above the aortic bifurcation. The left colic artery is the most proximal branch, supplying the distal transverse colon, splenic flexure, and descending colon. Two to six sigmoid branches collateralize with the left colic artery and form arcades that supply the sigmoid colon and contribute to the marginal artery.

The arc of Riolan is a collateral artery, first described by Jean Riolan (1580-1657), that directly connects the proximal SMA with the proximal IMA and may serve as a vital conduit when one or the other of these arteries is occluded. It is also known as the meandering mesenteric artery and is highly variable in size. Flow can be forward (IMA stenosis) or retrograde (SMA stenosis), depending on the site of obstruction. Such obstruction results in increased size and tortuosity of this meandering artery, which may be detected by arteriography; the presence of a large arc of Riolan thus suggests occlusion of one of the major mesenteric arteries (Fig. 52-10).

FIGURE 52-10 Arc of Riolan.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 27.)

The IMA terminates in the superior rectal (superior hemorrhoidal) artery, which courses behind the rectum in the mesorectum, branching and then entering the rectal submucosa. Here, the capillaries form a submucosal plexus in the distal rectum at the level of the anal columns. The anal canal also receives arterial blood from the middle rectal (hemorrhoidal) and inferior rectal (hemorrhoidal) arteries. The middle rectal artery is a branch of the internal iliac artery. It is variable in size and enters the rectum anterolaterally, passing alongside and slightly anterior to the lateral rectal stalks. It has been reported to be absent in 40% to 80% of specimens studied. The inferior rectal artery is a branch of the pudendal artery, which itself is a more distal branch of the internal iliac. From the obturator canal, it traverses the obturator fascia, ischiorectal fossa, and external anal sphincter to reach the anal canal. This vessel is encountered during the perineal dissection of an abdominoperineal resection.

The venous drainage of the colon and rectum mirrors the arterial blood supply. Venous drainage from the right and proximal transverse colon empties into the superior mesenteric vein, which coalesces with the splenic vein to become the portal vein. The distal transverse colon, descending colon, sigmoid, and most of the rectum drain into the inferior mesenteric vein, which empties into the splenic vein to the left of the aorta. The anal canal is drained by the middle and inferior rectal veins into the internal iliac vein and subsequently the inferior vena cava. The bidirectional venous drainage of the anal canal accounts for differences in patterns of metastasis from tumors arising in this region (Fig. 52-11).

FIGURE 52-11 Venous drainage of the colon and rectum.

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 30.)

Lymphatic drainage also follows the arterial anatomy. The wall of the large bowel is supplied with a rich network of lymphatic capillaries that drain to extramural channels paralleling the arterial supply. Lymphatics from the colon and proximal two thirds of the rectum ultimately drain into the para-aortic nodal chain, which empties into the cisterna chyli. Lymphatics draining the distal rectum and anal canal may drain to the para-aortic nodes or laterally, through the internal iliac system, to the superficial inguinal nodal basin. Although the dentate line roughly marks the level where lymphatic drainage diverges, classic studies by Block and Enquist using dye injection demonstrated that spread through lymphatic channels occurs to adjacent pelvic organs, such as the vagina and broad ligament, when injections are administered as high as 10 cm proximal to the dentate line (Figs. 52-12 and 52-13).

FIGURE 52-12 Lymphatic drainage of the colon.

(From Corman ML [ed]: Colon and rectal surgery, ed 4, Philadelphia,1998, Lippincott-Raven, p 21.)

FIGURE 52-13 Lymphatic drainage of the rectum (A) and anal canal (B).

(From Gordon PH, Nivatvongs S [eds]: Principles and practice of surgery for the colon, rectum and anus, ed 2, St Louis, 1999, Quality Medical Publishing, p 32.)

Lymph nodes are commonly grouped into levels depending on their location. Epicolic nodes are located along the bowel wall and in the epiploic appendices. Nodes adjacent to the marginal artery are paracolic. Intermediate nodes are located along the main branches of the large blood vessels; primary nodes are located on the SMA or IMA. Lymph node invasion by metastatic cancer is an important prognostic factor for patients with colorectal cancer. Accurate pathologic assessment of lymph nodes is essential for accurate staging, which serves as a determinant for treatment of patients with colorectal cancer.

Nerves

Preganglionic sympathetic nerves from T6 to T12 synapse in preaortic ganglia. Postsympathetic fibers then course along blood vessels to reach the right and transverse colons. The right and transverse colon parasympathetic supply comes from the right vagus nerve. Parasympathetic fibers follow branches of the SMA to synapse in the wall of the bowel. The left colon and rectum receive sympathetic supply from the preganglionic lumbar splanchnics of L1 to L3. These synapse in the preaortic plexus located above the aortic bifurcation and the postganglionic elements follow the branches of the IMA and superior rectal artery to the left colon, sigmoid, and rectum. The lower rectum, pelvic floor, and anal canal receive postganglionic sympathetics from the pelvic plexus. The pelvic plexus is adherent to the pelvic sidewalls and is adjacent to the lateral stalks. It receives sympathetic branches from the presacral plexus, which condense at the sacral promontory into the left and right hypogastric nerves. These sympathetic nerves, which descend into the pelvis dorsal to the superior rectal artery, are responsible for delivery of semen to the posterior prostatic urethra. Failure to preserve at least one of the hypogastric nerves during rectal dissection results in ejaculatory dysfunction in males.

The pelvic parasympathetic nerves, or nervi erigentes, arise from S2 to S4. Preganglionic parasympathetic nerves merge with postganglionic sympathetics after the latter emerge from the sacral foramina. These nerve fibers, through the pelvic plexus, surround and innervate the prostate, urethra, seminal vesicles, urinary bladder, and muscles of the pelvic floor. Rectal dissection may disrupt the pelvic plexus and its subdivisions, resulting in neurogenic bladder and sexual dysfunction. Rates of bladder and erectile dysfunction after rectal surgery are as high as 45%. The degree and type of dysfunction are affected by the level of the neurologic injury. A high IMA ligation severing the hypogastric nerves near the sacral promontory results in sympathetic dysfunction characterized by retrograde ejaculation and bladder dysfunction. Injury to the mixed parasympathetic and sympathetic periprostatic plexus results in impotence and an atonic bladder.

Recycling of Nutrients

During the digestive process, ingested nutrients are diluted within the intestinal lumen by biliopancreatic and GI secretions. The small intestine absorbs most ingested nutrients and some of the fluid and bile salts secreted into the lumen. However, the ileal effluent is still rich in water, electrolytes, and nutrients that resist digestion. The colon has the functional ability to recover these substances and avoid unnecessary losses of fluids, electrolytes, nitrogen, and energy. To accomplish this, the colon depends highly on its bacterial flora.

Absorption

The total absorptive area of the colon is estimated at approximately 900 cm². Between 1000 and 1500 mL of fluid is poured into the cecum by the daily ileal effluent. The total volume of water in stool is only 100 to 150 mL/day. This 10-fold reduction in water across the colon represents the most efficient site of absorption in the GI tract per surface area. The net absorption of sodium is even higher. Although the ileal effluent contains 200 mEq/liter of sodium, stool contains only 25 to 50 mEq/liter. One major difference between sodium and water absorption in the colon is that although water is absorbed passively, sodium requires active transport. Sodium is transported against chemical and electrical gradients at the expense of energy consumption.

The colonic epithelium can use various fuels; however, n-butyrate is oxidized in preference to glutamine, glucose, or ketone bodies. Because mammalian cells do not produce n-butyrate, the colonic epithelium relies on luminal bacteria to produce it through the fermentation of dietary fiber. The lack of n-butyrate, such as that resulting from the inhibition of fermentation by broad-spectrum antibiotics, leads to less sodium and water absorption and thus diarrhea. Conversely, the perfusion of the colonic lumen with n-butyrate stimulates sodium and water absorption. n-Butyrate, acetate, and propionate are SCFAs produced through bacterial fermentation; these constitute the main anions in stool. Other physiologic effects of SCFAs on the colon include stimulation of blood flow, mucosal cell renewal, and regulation of intraluminal pH for homeostasis of the bacterial flora.

In addition to recovering sodium and water, the colonic mucosa absorbs bile acids. The colon absorbs bile acids that escape absorption by the terminal ileum, thus making the colon part of the enterohepatic circulation. Bile acids are passively transported across the colonic epithelium by nonionic diffusion. When the colonic absorptive capacity is exceeded, colonic bacteria deconjugate bile acids. Deconjugated bile acids can then interfere with sodium and water absorption, leading to secretory, or choleretic, diarrhea. Choleretic diarrhea is seen early after right hemicolectomy as a transient phenomenon and more permanently after extensive ileal resection.

Secretion

The physiologic role of colon secretion is demonstrated in patients with chronic renal failure. Uremic patients can remain normokalemic while ingesting a normal amount of potassium before requiring dialysis. This phenomenon is associated with a compensatory increase in colonic secretion and fecal excretion of potassium. This effect is blocked by spironolactone, which illustrates the effect of aldosterone on colonic potassium secretion. Potassium secretion requires both Na⁺,K⁺-ATPase and Na⁺-K⁺-2Cl⁻ cotransport on the basolateral membrane and an apical potassium channel.

Many forms of colitis are associated with increased potassium secretion, such as inflammatory bowel disease (IBD), cholera, and shigellosis. In addition, some forms of colitis impair colonic absorption or produce secretion of chloride, such as collagenous and microscopic colitis and congenital chloridorrhea. Chloride is secreted by colonic epithelium at a basal rate, which is increased in pathologic conditions such as cystic fibrosis and secretory diarrhea. Secretion of chloride also requires the coupling of Na⁺,K⁺-ATPase and Na⁺-K⁺-2Cl⁻ cotransport to exit passively through the apical membrane. Calcium and cyclic adenosine monophosphate both stimulate chloride secretion, whereas bicarbonate and SCFAs inhibit chloride secretion.

Colonic secretion of H⁺ and bicarbonate is coupled to the absorption of Na⁺ and Cl⁻, respectively. It is through these exchangers that the colon is linked to systemic acid-base metabolism. The supply of H⁺ and bicarbonate for these exchangers is maintained by the hydration of CO₂, catalyzed by colonic carbonic anhydrase. Changes in systemic pH induce changes in the activity of carbonic anhydrase, eliciting elimination of H⁺ or bicarbonate as needed to bring the systemic pH back to normal.

Motility

Colonic motility is a highly complex process, made difficult to investigate by a lack of standardized terminology and measurements. Additionally, movement through the colon is relatively slow compared with the proximal GI tract, and studies require prolonged observation.

Colonic motility patterns may be more simply divided into two primary patterns, segmental activity and propagated activity. Segmental activity consists of single contractions or rhythmic bursts of contractions. The purpose of these segmental contractions is to propel fecal matter distally via a directed pressure gradient toward the rectum in discrete distances and allow for mixing, which promotes optimal absorption. The second pattern is propagated activity, commonly classified on the basis of amplitude as low-amplitude or high-amplitude propagated contractions.⁵ High-amplitude propagated contractions have been historically referred to as mass movements, or migrating motor complexes whose role is shifting large quantities of contents through the colon. These have an important role in defecation, with mass movements propelling larger volumes of fecal matter to the distal colon and emptying of the descending colon into the sigmoid colon and rectum. Little is known about low-amplitude propagated contractions, but they are associated with distention of the viscous and passage of flatus.

There seems to be a circadian rhythm to colonic motility, with maximum peaks of activity immediately after waking and after meals. Sleep is associated with a decrease in colonic motility.

Not surprisingly, food ingestion results in an increase of overall colonic motility for approximately 2 hours. This reflex is stimulated not only by gastric distention but also by the central nervous system (CNS), initiated by visualization of food. Additionally, meal composition affects colonic responses. Increased activity in response to carbohydrate meals is fairly short-lived, whereas fatty meals elicit longer term responses.

Ultimately, transit in the colon is controlled by the autonomic nervous system. Parasympathetic innervation reaches the colon through the vagus and pelvic nerves. The enteric nervous system in the colon is arranged in several plexuses—subserosal, myenteric (Auerbach), submucosal (Meissner), and mucosal plexuses. Sympathetic innervation originates in the superior and inferior mesenteric ganglia and reaches the colon via perivascular plexuses.

Formation of Stool

The frequency of defecation is just as variable among individuals as is their perception of abnormal stool frequency. An individual who passes more than three loose stools daily is considered as having diarrhea, whereas fewer than three weekly stools is considered constipation. Any frequency within that range is considered normal, although many individuals will still seek medical attention for what they perceive as diarrhea or constipation. Many factors influence colonic transit rate. Colonic transit is longer in women than in men and longer in premenopausal than postmenopausal women. Conversely, colonic transit time is shortened in smokers. In normal subjects, supplementation with NSPs does not shorten colonic transit time, although it does increase fecal weight. In patients with idiopathic constipation, however, NSPs, in the form of psyllium seeds, shorten colonic transit time and increase stool weight.

Defecation

Normal defecation requires adequate colonic transit time, stool consistency, and fecal continence. Fecal continence implies deferment of stool elimination, discrimination among gas, liquid, and solid stool, and selective elimination of gas without stool. There is some controversy regarding the actual role of the rectum under resting conditions. Some have proposed that the rectum is simply a conduit, which under resting conditions should be empty. If stool arrives at the rectum, the anorectal inhibitory reflex is triggered, forcing the subject to hold defecation by voluntary contraction of the external sphincter. However, any surgeon who performs routine rigid proctosigmoidoscopies in the office is well aware that a patient can have a rectum full of stool without any awareness. This leads to the opposing view, which regards the rectum as a reservoir. Just as stool triggers the anorectal inhibitory reflex, it also triggers a rectocolic reflex. This reflex allows continuous filling of the rectum with fecal material until the colon is emptied.

The mechanisms involved in fecal continence are not fully understood. A certain reservoir capacity is needed to achieve fecal continence. A stiff nondistensible rectum, such as in radiation proctitis, may produce incontinence, even when the sphincter muscles are competent. Some of the internal and external sphincter muscle fibers are necessary for adequate continence, although many patients have part of the sphincter severed during a fistulotomy and are still continent. Probably, the only factor needed for fecal continence is innervation of the sphincter. The motor nerve fibers, which produce contraction of the sphincter fibers, and also all the sensory innervation are important to empty the rectum adequately.

Pathogenesis

Diverticula are actually herniations of mucosa through the colon at sites of penetration of the muscular wall by arterioles. These sites are on the mesenteric side of the antimesenteric taeniae. In some cases, the arteriole penetrating the wall can be displaced over the dome of the diverticulum. This close relationship between the artery and diverticulum is responsible for the massive hemorrhage that can occasionally complicate diverticulosis (Fig. 52-15).

FIGURE 52-15 Pathogenesis of diverticular disease. Diverticula are herniations of the mucosa through the points of entry of blood vessels across the muscular wall. Because the diverticula are formed only by the mucosa rather than by the entire wall of the intestine, they are called false diverticula. Note that the diverticula form only between the mesenteric taenia and each of the two lateral taeniae. Because there are no perforating vessels, diverticula do not form on the antimesenteric side of the colon.

There is often a striking hypertrophy of the muscular layers of the colonic wall associated with diverticulosis. This thickening of the colonic wall, usually affecting the sigmoid colon, may precede the appearance of diverticula. Diverticula most commonly affect the sigmoid colon and are confined to the sigmoid in approximately 50% of patients with diverticulosis. The next most common area involved is the descending colon (≈40% of affected individuals), and the entire colon has diverticula in 5% to 10% of patients with diverticulosis. Even in patients with diverticula involving the entire colon, the muscular thickening characteristic of the disease is usually confined to the sigmoid (Fig. 52-16).

FIGURE 52-16 Colonoscopic view of diverticula.

The sigmoid colon, the most common site of diverticula formation, is also the segment of colon with the smallest luminal diameter. If the colonic lumen contains a large volume of fiber, the contractile pressure required to propel the feces forward is low. In such circumstances, the colonic pressure in the sigmoid is only slightly higher than atmospheric pressure. However, with the decreased amount of fiber provided by today’s typical dietary regimens, there is decreased colonic luminal content, requiring the generation of increased colonic pressures to propel the feces forward. Colonic pressures as high as 90 mm Hg can be generated by contraction of the narrow sigmoid colon. These high intraluminal pressures are thought to be responsible for the herniations of mucosa through the anatomically weak points in the colonic wall.

It has long been conjectured that factors contributing to diverticular disease, or at least diverticulitis, is the consumption of nuts, popcorn, and small seeds, such as are found in tomatoes, and patients with diverticular disease are often counseled to avoid these foods. However, a large prospective study of men without known diverticular disease has failed to detect an increase in the risk of diverticulosis or diverticular complications.¹¹