and include proctalgia and/or pain at the injection site, local bruising and inflammatory reaction.

Efficacy data are sparse but one large randomized controlled trial demonstrated improvement in

continence for half the patients treated with SOLESTA.56 The FDA-approved SNS for treatment of fecal

incontinence in 2011. It is a two-stage procedure, in which there is a trial period, involving

percutaneous implantation of an electrode into S3. If there is a >50% improvement in symptoms, the

patient proceeds to the second stage which involves placement of a permanent stimulator. Between 50%

and 92% success rates have been reported with an improvement of ≥50% reduction in the number of

incontinent episodes per week compared to baseline. Perfect continence has been achieved in 40% of

subjects.57–68 Since SNS was approved, it has largely replaced overlapping sphincteroplasty as the first

line treatment. Finally, colostomy is a last resort in patients in whom all other treatment modalities

have failed.

SUMMARY

The colon, rectum, anus all help coordinate very complicated functions. Understanding their physiology

is important in the management of their associated pathology.

References

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19. Higgins PD, Johanson JF. Epidemiology of constipation in North America: a systematic review. Am

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20. Bharucha AE. Constipation. Best Pract Res Clin Gastroenterol 2007;21:709–731.

21. Maron DJ, Fry RD. New therapies in the treatment of postoperative ileus after gastrointestinal

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22. Delaney CP, Wolff BG, Viscusi ER, et al. Alvimopan, for postoperative ileus following bowel

resection: a pooled analysis of phase III studies. Ann Surg 2007;245:355–363.

23. Bohm B, Milsom JW, Fazio VW. Postoperative intestinal motility following conventional and

laparoscopic intestinal surgery. Arch Surg 1995;130:415–419.

24. Frantzides CT, Cowles V, Salaymeh B, et al. Morphine effects on human colonic myoelectric activity

in the postoperative period. Am J Surg 1992; 163:144–148; discussion 8–9.

25. Mann C, Pouzeratte Y, Boccara G, et al. Comparison of intravenous or epidural patient-controlled

analgesia in the elderly after major abdominal surgery. Anesthesiology 2000;92:433–441.

26. Wolff BG, Michelassi F, Gerkin TM, et al. Alvimopan, a novel, peripherally acting mu opioid

antagonist: results of a multicenter, randomized, double-blind, placebo-controlled, phase III trial of

major abdominal surgery and postoperative ileus. Ann Surg 2004;240:728–734; discussion 34–35.

27. Wilmore DW, Kehlet H. Management of patients in fast track surgery. BMJ 2001;322:473–476.

28. Ljungqvist O. ERAS-enhanced recovery after surgery: moving evidence-based perioperative care to

practice. JPEN J Parenter Enteral Nutr 2014;38:559–566.

29. Lubowski DZ. Enhanced recovery after surgery and laparoscopic colorectal surgery: where to now?

ANZ J Surg 2014;84:500–501.

30. Geltzeiler CB, Rotramel A, Wilson C, et al. Prospective study of colorectal enhanced recovery after

surgery in a community hospital. JAMA Surg 2014; 149(9):955–961.

31. Bagnall NM, Malietzis G, Kennedy RH, et al. A systematic review of enhanced recovery care after

colorectal surgery in elderly patients. Colorectal Dis 2014;16(12):947–956.

32. Chambers D, Paton F, Wilson P, et al. An overview and methodological assessment of systematic

reviews and meta-analyses of enhanced recovery programmes in colorectal surgery. BMJ Open

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33. Greco M, Capretti G, Beretta L, et al. Enhanced recovery program in colorectal surgery: a metaanalysis of randomized controlled trials. World J Surg 2014; 38:1531–1541.

34. Walker EA, Roy-Byrne PP, Katon WJ. Irritable bowel syndrome and psychiatric illness. Am J

Psychiatry 1990;147:565–572.

35. Munakata J, Naliboff B, Harraf F, et al. Repetitive sigmoid stimulation induces rectal hyperalgesia

in patients with irritable bowel syndrome. Gastroenterology 1997;112:55–63.

36. Ogilvie H. Large-intestine colic due to sympathetic deprivation. Br Med J 1948;2:671.

37. Saunders MD, Cappell MS. Endoscopic management of acute colonic pseudo-obstruction. Endoscopy

2005;37:760–763.

38. Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of

400 cases. Dis Colon Rectum 1986;29:203–210.

39. Johnson CD, Rice RP, Kelvin FM, et al. The radiologic evaluation of gross cecal distension:

emphasis on cecal ileus. AJR Am J Roentgenol 1985;145:1211–1217.

40. Nanni G, Garbini A, Luchetti P, et al. Ogilvie’s syndrome (acute colonic pseudo-obstruction): review

of the literature (October 1948 to March 1980) and report of four additional cases. Dis Colon

Rectum 1982;25:157–166.

41. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudoobstruction. N Engl J Med 1999;341:137–141.

42. Trevisani GT, Hyman NH, Church JM. Neostigmine: safe and effective treatment for acute colonic

pseudo-obstruction. Dis Colon Rectum 2000; 43:599–603.

43. Saunders MD, Kimmey MB. Systematic review: acute colonic pseudo-obstruction. Aliment Pharmacol

Ther 2005;22:917–925.

44. Rockwood TH, Church JM, Fleshman JW, et al. Patient and surgeon ranking of the severity of

symptoms associated with fecal incontinence: the fecal incontinence severity index. Dis Colon

Rectum 1999;42:1525–1532.

45. Jorge JM, Wexner SD. Etiology and management of fecal incontinence. Dis Colon Rectum

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1993;36:77–97.

46. Byrne CM, Solomon MJ, Young JM, et al. Biofeedback for fecal incontinence: short-term outcomes

of 513 consecutive patients and predictors of successful treatment. Dis Colon Rectum 2007;50:417–

427.

47. Keck JO, Staniunas RJ, Coller JA, et al. Biofeedback training is useful in fecal incontinence but

disappointing in constipation. Dis Colon Rectum 1994;37:1271–1276.

48. Bartlett L, Sloots K, Nowak M, et al. Biofeedback for fecal incontinence: a randomized study

comparing exercise regimens. Dis Colon Rectum 2011;54:846–856.

49. Schwandner T, Konig IR, Heimerl T, et al. Triple target treatment (3T) is more effective than

biofeedback alone for anal incontinence: the 3T-AI study. Dis Colon Rectum 2010;53:1007–1016.

50. Barisic GI, Krivokapic ZV, Markovic VA, et al. Outcome of overlapping anal sphincter repair after 3

months and after a mean of 80 months. Int J Colorectal Dis 2006;21:52–56.

51. Demirbas S, Atay V, Sucullu I, et al. Overlapping repair in patients with anal sphincter injury. Med

Princ Pract 2008;17:56–60.

52. Evans C, Davis K, Kumar D. Overlapping anal sphincter repair and anterior levatorplasty: effect of

patient’s age and duration of follow-up. Int J Colorectal Dis 2006;21:795–801.

53. Fleshman JW, Peters WR, Shemesh EI, et al. Anal sphincter reconstruction: anterior overlapping

muscle repair. Dis Colon Rectum 1991;34:739–743.

54. Jesudason SR, Mathai V, Gladwin G, et al. Functional outcome of overlapping sphincter repair for

anal incontinence. Trop Gastroenterol 1999;20:189–190.

55. Lamblin G, Bouvier P, Damon H, et al. Long-term outcome after overlapping anterior anal sphincter

repair for fecal incontinence. Int J Colorectal Dis 2014;29(11):1377–1383.

56. Graf W, Mellgren A, Matzel KE, et al. Efficacy of dextranomer in stabilised hyaluronic acid for

treatment of faecal incontinence: a randomised, sham-controlled trial. Lancet 2011;377:997–1003.

57. Altomare DF, Ratto C, Ganio E, et al. Long-term outcome of sacral nerve stimulation for fecal

incontinence. Dis Colon Rectum 2009;52:11–17.

58. Boyle DJ, Murphy J, Gooneratne ML, et al. Efficacy of sacral nerve stimulation for the treatment of

fecal incontinence. Dis Colon Rectum 2011;54:1271–1278.

59. Damon H, Barth X, Roman S, et al. Sacral nerve stimulation for fecal incontinence improves

symptoms, quality of life and patients’ satisfaction: results of a monocentric series of 119 patients.

Int J Colorectal Dis 2013;28:227–233.

60. Devroede G, Giese C, Wexner SD, et al. Quality of life is markedly improved in patients with fecal

incontinence after sacral nerve stimulation. Female Pelvic Med Reconstr Surg 2012;18:103–112.

61. George AT, Kalmar K, Panarese A, et al. Long-term outcomes of sacral nerve stimulation for fecal

incontinence. Dis Colon Rectum 2012;55:302–306.

62. Lim JT, Hastie IA, Hiscock RJ, et al. Sacral nerve stimulation for fecal incontinence: long-term

outcomes. Dis Colon Rectum 2011;54:969–674.

63. Maeda Y, Lundby L, Buntzen S, et al. Outcome of sacral nerve stimulation for fecal incontinence at

5 years. Ann Surg 2014;259:1126–1131.

64. Mellgren A, Wexner SD, Coller JA, et al. Long-term efficacy and safety of sacral nerve stimulation

for fecal incontinence. Dis Colon Rectum 2011; 54:1065–1075.

65. Michelsen HB, Thompson-Fawcett M, Lundby L, et al. Six years of experience with sacral nerve

stimulation for fecal incontinence. Dis Colon Rectum 2010; 53:414–421.

66. Takano S, Boutros M, Wexner SD. Sacral nerve stimulation for fecal incontinence. Dis Colon Rectum

2013;56:384.

67. Wexner SD, Coller JA, Devroede G, et al. Sacral nerve stimulation for fecal incontinence: results of

a 120-patient prospective multicenter study. Ann Surg 2010;251:441–449.

68. Wexner SD, Hull T, Edden Y, et al. Infection rates in a large investigational trial of sacral nerve

stimulation for fecal incontinence. J Gastrointest Surg 2010; 14:1081–1089.

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Chapter 65

Acute Gastrointestinal Hemorrhage

Jason S. Mizell and Richard H. Turnage

Key Points

1 Upper gastrointestinal (UGI) hemorrhage accounts for about 80% of cases of acute GI blood loss.

2 The most common cause of acute UGI hemorrhage is peptic ulcer disease and the most common

cause of acute lower gastrointestinal (LGI) hemorrhage is diverticulosis.

3 Upper GI bleeding typically presents with hematemesis (the vomiting of blood) or melena (the

passage of black, tarry stool), whereas lower GI bleeding typically causes hematochezia (the passage

of fresh blood from the rectum).

4 Most patients (about 80%) suffering from GI hemorrhage will stop bleeding spontaneously. Those

who do not stop or those who rebleed are at particularly high risk to suffer an in-hospital

complication, require operative control of their hemorrhage, or die.

5 Esophagogastroduodenoscopy (EDG) is the initial diagnostic study of choice for patients suspected of

bleeding from the esophagus, stomach or duodenum and colonoscopy is the procedure of choice for

evaluating patients with a suspected lower GI hemorrhage.

6 Nonsteroidal anti-inflammatory drugs are an important risk factor for the development of GI

hemorrhage in general and gastroduodenal ulcer formation in particular.

7 Treatment of patients bleeding from gastroduodenal ulcer is intravenous proton pump inhibitor and

endoscopic thermocoagulation or mechanical ligation or clipping of the bleeding vessel.

8 In general, a patient bleeding from esophageal varices should undergo urgent pharmacologic therapy

with intravenous octreotide and endoscopic banding of the bleeding varices.

9 Lower GI hemorrhage due to diverticulosis is generally managed nonoperatively due to a low risk of

persistent or recurrent bleeding.

1 Acute gastrointestinal (GI) hemorrhage is categorized as upper or lower depending upon the location

of the bleeding relative to the ligament of Treitz. Upper GI (UGI) hemorrhage (i.e., bleeding from the

esophagus, stomach, or duodenum) accounts for about 80% of cases of acute GI blood loss, with most of

the remainder coming from the colon. The small intestine is the site of hemorrhage in about 1% to 5%

of cases.1,2 Although it may be decreasing,3 the incidence of UGI bleeding is estimated to be about 37 to

150 episodes per 100,000 individuals depending upon the population sampled,4 whereas the incidence

of lower GI (LGI) bleeding is about 20 cases per 100,000 individuals.5 Overall, GI hemorrhage accounts

for roughly 300,000 hospitalizations and 30,000 deaths annually in the United States.6

2 The differential diagnosis of overt UGI and LGI hemorrhage and the relative frequency of the most

common causes of GI bleeding are shown in Tables 65-1 and 65-2 and Figure 65-1A,B, respectively.

Although the incidence varies by age, overall the most common causes of acute UGI hemorrhage are

peptic ulcer disease (31% to 58%), gastritis and mucosal erosions (9% to 30%), and gastroesophageal

varices (3% to 23%)1,4 whereas diverticulosis (24% to 47%), all forms of colitis (6% to 26%), neoplasms

(9% to 17%), and angiodysplasia (2% to 12%) account for most instances of lower GI

hemorrhage.1,5,7–10

PATIENT CHARACTERISTICS

Patients who suffer significant GI hemorrhage are more commonly older (average age approximately 60

to 70 years)1,4) and male compared with individuals without GI bleeding. Furthermore, these

individuals are more likely to use alcohol, tobacco, aspirin, nonsteroidal anti-inflammatory drugs

(NSAIDs), and anticoagulants.1,11 Predictors of risk for acute GI bleeding are shown in Table 65-3.

Coexisting chronic illnesses are common in patients suffering either a UGI or LGI hemorrhage.

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Various studies have suggested a correlation between GI bleeding and correlates of poor health such as

the use of multiple medications, reduced levels of physical activity, and inability to complete basic selfcare tasks.11 Cardiovascular,11 hepatic, and renal disease12 are particular risk factors for acute GI

bleeding. The presence of these chronic illnesses, as well as chronic obstructive pulmonary disease and

cirrhosis, also greatly increase the risk of rebleeding after endoscopic control.13 Tobacco is also

associated with higher rates of significant GI hemorrhage. A prospective cohort study of 5,888 men and

women found that the multivariate-adjusted hazard ratio for subjects who smoked more than half a pack

per day was 2.14 (95% CI = 1.22, 3.75) for UGI bleeding.11

Certain medications increase the risk of GI hemorrhage. Many studies have related the use of NSAIDs

and aspirin to significant GI bleeding. The risk is particularly elevated for UGI bleeding but NSAIDs

increase the risk of LGI hemorrhage as well. In Vreeburg’s review of 951 patients with UGI hemorrhage,

41% used NSAIDs or aspirin. Van Leerdam reported that more than half of the patients bleeding from

ulcers were actively taking NSAIDs or ASA.14 Mellemkjaer et al.15 found that the observed to expected

ratio of UGI hemorrhage in a cohort of 156,138 users of NSAIDs was 4.1 (95% CI = 3.8, 4.5). Other

medications known to increase the risk of GI hemorrhage include corticosteroids, spironolactone,16 and

the selective serotonin reuptake inhibitors (SSRIs).17,18

The use of anticoagulants is also an important risk factor for acute GI bleeding. Coumadin is a

particularly common cause. Kaplan found the age- and sex-adjusted hazard ratio for GI bleeding in

patients taking oral anticoagulants was 2.59 (95% CI = 1.71, 3.93).11 Vreeburg et al.4 reported that

17% of their patients with UGI hemorrhage were taking coumadin and the international normal ratio

(INR) was greater than 4 in more than half of these patients. Because coumadin metabolism can be

affected by so many interfering substances, inadvertent coumadin toxicity is a common problem, often

presenting with GI hemorrhage. Antiplatelet agents such as clopidogrel and ticlopidine are also

associated with an increased risk of GI hemorrhage.19

Table 65-1 Differential Diagnosis of Acute Upper Gastrointestinal Hemorrhage by

Anatomic Site

CLINICAL PRESENTATION

3 The presentation of GI bleeding can range from mild asymptomatic bleeding to overt GI bleeding.

UGI bleeding typically presents with hematemesis (the vomiting of blood) or melena, whereas LGI

bleeding typically presents with hematochezia. Melena is a black, tarry stool resulting from the

degradation of blood by enteric bacteria. It may occur with the loss of as little as 50 to 200 mL of

blood.20,21 Bleeding from the small intestine or right colon may also appear black if it has remained in

the GI tract for more than 12 to 14 hours.22 Hematochezia is the passage of bright red blood, marooncolored blood, or blood clots from the rectum. However, massive UGI hemorrhage can cause

1679

hematochezia in as many as 11% of patients, but this is typically associated with hemodynamic

instability.23 Patients with acute GI bleeding may present with the hemodynamic consequences of

hemorrhage including light-headedness, dizziness, orthostatic syncope or near syncope, shortness of

breath, or palpitations from tachycardia.

Table 65-2 Differential Diagnosis of Acute Lower Gastrointestinal Hemorrhage by

Anatomic Site

Figure 65-1. A: The relative frequency of the most common causes of upper gastrointestinal hemorrhage in the United States.

These data represent the percentage of patients with each of these causes of UGI hemorrhage for 482 patients in a survey of the

members of the American College of Gastroenterology published by Peura et al.1 in 1997. These data are very similar to that

reported by Vreeburg in a multi-institutional study of 951 patients sustaining a UGI hemorrhage in the hospitals in and

surrounding Amsterdam.4 B: The relative frequency of the most common causes of lower gastrointestinal hemorrhage. These data,

reported by Lingenfelser and Ell5 are the percentage of patients with each of these causes of lower GI hemorrhage in 912 patients

collected in five studies from Europe, the Orient, and the United States

1,7–10

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The medical history and physical examination provide important clues of the etiology of the patient’s

hemorrhage and the potential risk to the patient’s life. The occurrence of melena after several days of

worsening epigastric or upper abdominal pain suggests peptic ulcer disease; whereas hematemesis or

melena following vomiting or retching strongly suggests a Mallory–Weiss tear. Massive, painless UGI

hemorrhage in a patient with cirrhosis suggests bleeding from gastroesophageal varices, although other

etiologies including peptic ulcer disease or a Mallory–Weiss tear must also be considered. The medical

history should elicit the presence of risk factors for GI hemorrhage alluded to in the previous

paragraphs and in Table 65-3 .

A systematic physical examination will document the magnitude of bleeding and the patient’s ability

to compensate. Massive hemorrhage is associated with signs and symptoms of hypovolemic shock,

including cool, clammy, mottled skin, tachycardia, tachypnea, flat jugular veins, oliguria, and perhaps

hypotension. These responses may be altered by advanced age, concomitant medical problems, and

particular medications. Physical examination should also document evidence of cirrhosis and portal

hypertension (i.e., ascites, spider angiomas, hepatosplenomegaly, palmar erythema, and large

hemorrhoidal veins). A rectal examination may demonstrate bright red blood or melena. The clinical

scenario alone will usually not localize the location of the bleeding, so other diagnostic studies are often

required to identify the cause and site of bleeding.

PROGNOSTIC FACTORS

4 Most patients (approximately 80%) suffering from GI hemorrhage will stop bleeding spontaneously.

Those who do not stop or those who rebleed are at particularly high risk to suffer an in-hospital

complication, require operative control of their hemorrhage, or die. Several classification systems have

been developed to separate patients with low risk of complications from those with a high risk of

complications due to acute UGI and LGI hemorrhage. These systems have also been used to stratify

those patients who may be safely managed as an outpatient from those requiring in-hospital care.24 The

BLEED classification system addresses both UGI and LGI hemorrhage and consists of the following

parameters: ongoing bleeding, low systolic blood pressure, elevated prothrombin time, erratic mental

status, and unstable comorbid disease. Patients with at least one BLEED criterion are more likely to

suffer in-hospital complications from UGI bleeding (31% vs. 4%) or LGI bleeding (38% vs. 12%) than

are patients with no criteria.25

Table 65-3 Characteristics of Individuals at an Increased Risk of Developing

Acute Gastrointestinal Bleeding

Table 65-4 Rockall Risk Scoring System and Rates of Rebleeding and Mortality

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left colon, sigmoid colon, rectum, and superior anal canal. The inferior mesenteric vein follows a course

of its own, starting at the left colic artery, and ascends over the psoas muscle in a retroperitoneal plane.

The vein courses under the body of the pancreas to drain into the splenic vein. During an anterior

resection of the rectum, division of the inferior mesenteric vein at the inferior border of the pancreas

can provide additional mobility of the left colon to facilitate a coloanal anastomosis. The superior

hemorrhoidal (rectal) veins drain blood from the rectum and upper part of the anal canal, where the

internal hemorrhoidal plexus is situated, into the portal system via the inferior mesenteric vein. The

middle hemorrhoidal (rectal) veins drain the lower part of the rectum and upper part of the anal canal

into the systemic circulation via the internal iliac veins. The inferior hemorrhoidal (rectal) veins drain

blood from the lower rectum and anal canal, where the external hemorrhoidal plexus is located, via the

internal pudendal veins into the systemic venous circulation via the internal iliac veins. In the setting of

portal hypertension, the superior, middle, and inferior hemorrhoidal veins interact to shunt venous

blood from the portal system into the systemic circulation.

LYMPHATIC DRAINAGE

4 Lymphatic drainage generally follows the arterial blood supply of the colon and rectum. In the anal

canal, lesions above the dentate line drain into the inferior mesenteric lymph nodes. Lesions below the

dentate line drain into the internal iliac lymph nodes but can also drain into the inferior mesenteric

lymph nodes.

Neural Components

The colon possesses extrinsic and intrinsic (enteric) neuronal systems. The extrinsic system consists of

sympathetic and parasympathetic nerves that inhibit or stimulate colonic peristalsis, respectively. The

sympathetic innervation to the right colon originates from the lower thoracic segments of the spinal

cord and travels in the thoracic splanchnic nerves to the celiac and superior mesenteric plexuses.

Postganglionic fibers emerge from here and course along the superior mesenteric artery and its

branches to the right side of the colon. The parasympathetic nerves originate from the right vagus nerve

and travel along with the sympathetic nerves to the right side of the colon. The left side of the colon

and the rectum receive sympathetic fibers that arise from L1 through L3 segments of the spinal cord.

This passes through the ganglionated sympathetic chains and leaves as a lumbar sympathetic nerve to

join the preaortic plexus. It extends along the inferior mesenteric artery as the mesenteric plexus and

then becomes the presacral nerve or superior hypogastric plexus. These hypogastric nerves are

identified at the sacral promontory 1 cm lateral to the midline. The key zones of sympathetic nerve

damage are during ligation of the inferior mesenteric artery and during initial posterior rectal

mobilization adjacent to the hypogastric nerves. The parasympathetic supply to the left side of the colon

and the rectum comes from S2 through S4 spinal cord segments. The sacral nerve fibers become the

nervi erigentes, which join the pelvic plexus at the pelvic side walls. To prevent injury during full

mobilization of the rectum, the lateral ligament should be cut close to the rectal side wall. Both the

sympathetic and parasympathetic nervous systems play a role in erection, in that damage to the

parasympathetics can lead to erectile dysfunction, while retrograde ejaculation can occur with damage

to sympathetic nerve injury.

The intrinsic, or enteric, nervous system consists of two groups of plexuses that are identified by their

location within the colon wall. This system can function independently of the central nervous system

and controls motility and exocrine and endocrine functions of the gut, and is involved in intestinal

immune regulation and inflammatory responses. The Meissner plexus is located in the submucosa

between the muscularis mucosae and the circular muscle of the muscularis propria and is important in

secretory control. The myenteric plexus, also known as the Auerbach plexus, is located between the inner

circular muscle and outer longitudinal muscle layers of the colon and primarily controls intestinal

motility.4

The internal anal sphincter is supplied by the sympathetic and parasympathetic nerves that supply the

lower rectum. The parasympathetic nerves are inhibitory. The external sphincter is supplied by the

inferior rectal branch of the internal pudendal nerve and the perineal branch of S4. Sensation of the anal

canal is from the inferior rectal nerve, a branch of the pudendal nerve.

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PHYSIOLOGY

The colon’s function is to absorb, store, digest carbohydrate and protein residues, and secrete mucus.

Absorption

The colon absorbs water, sodium, and chloride and secretes potassium and bicarbonate. The physiologic

control of colonic water and electrolyte transport requires careful integration of neural, endocrine, and

paracrine components. Although colonic epithelium does not actively absorb glucose or amino acids as

the small-intestinal epithelium does, the colon does absorb short-chain fatty acids and vitamins that are

produced by bacterial breakdown of nonabsorbed carbohydrates and amino acids. These short-chain

fatty acids, which include acetate, butyrate, and propionate, are absorbed in a concentration-dependent

fashion. They are a major (70% of colonic mucosal energy) energy substrate for colonic epithelial cells

and represent the major fecal anions.6

Approximately 1,500 mL of ileal effluent reaches the cecum in a 24-hour period, 90% of which is

reabsorbed in the colon; 100 to 150 mL of water remains in stool. The colon has a tremendous capacity

that allows it to absorb as much as 5 to 6 L of water within a 24-hour period. When colonic capacity is

exceeded, diarrhea results.7 Normally formed feces consist of 70% water and 30% solid material. Almost

half of the solid material is made up of bacteria and the other half is composed of undigested food

material and desquamated epithelium. Water absorption in the colon is a passive process that depends

primarily on the osmotic gradient established by the active transport of sodium across the colonic

epithelium. The composition of ileal effluent and luminal flow rates also play an important role in water

absorption. Upsetting the balance of these three factors results in diarrhea. The absorptive capacity is

not the same throughout each segment of the colon. Salt and water absorption is greatest in the right

colon. Patients undergoing a right hemicolectomy should therefore be counseled preoperatively that

they may experience loose bowel movements in the early postoperative period. Patients should also be

reassured that this will resolve with time as the remaining colon adapts.

Sodium absorption by the colonic epithelium is an active cellular transport process similar to that seen

in small-intestinal and renal epithelial cells.8 Initially, sodium absorption involves the passive movement

of sodium across the apical membrane into the mucosal cell down an electrochemical gradient. To

maintain an adequate electrochemical gradient, intracellular sodium is removed from the cell into the

interstitial space in exchange for potassium at the basolateral membrane. This is an energy-dependent

process that is controlled by Na+-K+-adenosine triphosphatase (ATPase). Mineralocorticoids

(predominantly aldosterone) and glucocorticoids accelerate sodium absorption and potassium excretion

in the colon by increasing Na+-K+-ATPase activity.9 Potassium movement into the colonic lumen is

primarily a passive process that depends on the electrochemical gradient generated by the active

transport of sodium across colonic epithelial cells. Chloride absorption in the colon is generally thought

to be an energy-independent process that is associated with reciprocal exchange for bicarbonate at the

luminal border of the mucosal cell.10 Patients with a ureterosigmoidoscopy may develop

hyperchloremia and secrete excessive amounts of bicarbonate.

Twenty percent of urea synthesized by the liver is metabolized mainly in the colon. This is converted

into 200 to 300 mL of ammonia each day, of which most is absorbed by passive coupled diffusion with

bicarbonate and forms ammonia and carbon dioxide. Ammonia is also derived from dietary nitrogen,

epithelial cells, and bacterial debris. Mucus is produced by goblet cells and secreted into the lumen via

stimulation of the pelvic nerves.

Colonic Flora

5 The bacterial flora of the colon is established soon after birth and depends in large part on dietary and

environmental factors. The colon is populated by approximately 1013 commensal bacteria.10 The vast

majority of the normal colonic flora consists of anaerobic bacteria, with Bacteroides species being most

prevalent, particularly B. fragilis.11 Aerobic colonic bacteria are mainly coliforms and enterococci, with

Escherichia coli being the most predominant coliform. The colonic flora is important for (a) digestion and

absorption of complex macromolecules, (b) protecting the colon against invasion by noncommensal

bacteria, and (c) development of mucosal immunity. Fermentation of carbohydrates generates shortchain fatty acids, including acetic acid, propionic acid, and butyrate, which is the primary nutrient for

the colonic mucosa. Colonic bacteria also produce certain vitamins, such as vitamin K and B12

, which are

absorbed by the host. The enterohepatic circulation of bilirubin and bile acids depends on bacterial

enzymes produced by fecal flora. The degradation of bile pigments by colonic bacteria gives stool its

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characteristic brown color. Colonic bacteria also play an important role in preventing infection by

controlling the growth of potentially pathogenic bacteria such as Clostridium difficile.

6 Host and colonic flora have a mutualistic relationship; however, disturbances of this coexistence can

lead to human disease.12 Changes in diet and use of antibiotics can dramatically alter the microbiome.

Dysregulation of the flora has been implicated in the pathogenesis of inflammatory bowel disease,

obesity and, to a lesser extent, colorectal cancer. Increasingly, dysregulation has also been linked to

nongastrointestinal diseases including autism and other neurologic conditions. In animal studies, mice

with certain immune deficiencies that make them prone to colitis fail to develop colitis when raised

under germ-free conditions. Analysis of the microbiota of patients with inflammatory bowel disease

revealed markedly different flora compositions in ulcerative colitis, Crohn disease, and healthy control

patients. Similarly, certain genetically altered mice with a propensity to develop colorectal cancer fail to

develop tumors in germ-free conditions. Although studies of human flora and colorectal cancer are

limited, preliminary studies have raised interest in modulating the colonic flora as a way to treat and/or

prevent colitis and other diseases of the colon.

Colonic Motility

Motor activity varies greatly throughout the colon. There are two patterns of colonic motility:

segmental contractions, which are single or clustered contractions, and propagated activity, which is

either high-amplitude (>100 mm Hg) propagated contractions (HAPCs) or low-amplitude (<60 mm

Hg) propagated contractions (LAPCs). Segmental contractions are intermittent contractions of the

longitudinal and circular muscles that result in the segmented appearance of the colon.13 These

contractions propel luminal contents in a back-and-forth pattern over short distances, slowing aboral

transit and allowing for water reabsorption.14 Propagated activity consists of strong, propulsive

contractions of the smooth muscle that involve a long segment of colon.15 The LAPCs move luminal

contents forward at a rate of 0.5 to 1.0 cm/s and typically last for 20 to 30 seconds.13 HAPCs occur

three to four times per day, primarily after awakening, exercise, and after meals.

The orderly progression of colonic luminal contents from cecum to anus requires the coordination of

smooth muscle contractions. Calcium-dependent cyclic depolarization and repolarization of the colonic

smooth muscle cell membrane generates a basic electrical pattern of slow-wave activity. This activity

allows each smooth muscle cell to control its own contraction and to couple with adjacent smooth

muscle cells.16 The extrinsic (autonomic) and intrinsic (enteric) neuronal systems also interact to

influence colonic motility.

Defecation

As the fecal mass enters the rectum, the internal anal sphincter relaxes, while the external anal sphincter

contracts to maintain continence. Distention of the rectum in this setting is the primary stimulus for

defecation to begin. At this point, the urge to defecate may be suppressed by conscious contraction of

the external anal sphincter. Receptive relaxation of the rectal ampulla accommodates the fecal mass and

the urge to defecate passes unless the volume of feces is extremely large or the sphincter mechanism is

impaired. If the subject voluntarily accedes to the urge to defecate, a Valsalva maneuver occurs, which

increases the intra-abdominal pressure to overcome the resistance of the external anal sphincter.

Relaxation of the pelvic muscles causes the pelvic floor to descend and the anorectal angle to straighten.

Conscious inhibition of the external anal sphincter then allows passage of the feces. On completion, the

pelvic floor returns to its resting position and the anal sphincter muscles return to their resting activity,

closing the anal canal. Under normal circumstances, this process occurs once every 24 hours; however,

the interval between bowel movements may vary between 8 and 12 hours and 2 to 3 days in normal

subjects.

The frequency of defecation is influenced by multiple environmental and dietary factors. The

gastrorectal reflex occurs as postprandial defecation. An increase in rectal tone results in increased

pressure from the fecal mass on the rectal wall, providing heightened sensation.

Anal Continence

There are varying degrees of anal continence, with a spectrum from complete control to complete lack

of control. Maintaining continence is complex, as both voluntary and involuntary mechanisms play a

role in anal continence. The most important mechanisms involve the internal anal sphincter, which

contributes 52% to 85% of the pressure generated to maintain continence.17,18 The rest of the

contribution to the anal basal pressure includes the following: 30% from the external anal sphincter and

1668

15% from the hemorrhoidal cushions. The internal sphincter is supplied by dual extrinsic innervation:

sympathetic outflow (S5) via the hypogastric nerve provides motor supply and inhibition by

parasympathetic outflow (S1–S3). The external sphincter nerve supply is dependent on the pudendal

nerve (S2–S4) and maintains tonic activity at rest. When stool enters the rectum, the contents of the

rectum are sampled by sensors in the anal canal to determine whether the contents are solid, liquid, or

gas. By discriminating between the consistency of the stool, the pelvic floor and sphincter muscles are

able to coordinate a complex mechanism through angulation of the pelvic floor and contraction of the

anal sphincter muscles. Other mechanisms contributing to continence include stool consistency and

volume. Modification of the stool consistency to more solid and less voluminous stool may allow a

patient to recapture fecal control. Reservoir function of the rectum consists of lateral angulations of the

sigmoid colon and the valves of Houston as a mechanical barrier to slow the progression of stool.

DISORDERS OF COLONIC MOTILITY AND ANAL CONTINENCE

Constipation

7 Constipation is common and may affect up to 15% of people, but only a portion of affected

individuals seek medical help.19 Colorectal surgeons, gastroenterologists, gynecologists, and family

medicine physicians are frequently called upon to treat constipation.20 To evaluate constipation, the

clinician must ask focused questions about bowel function. Constipation can mean infrequent bowel

movements, straining, or hard stools. The Rome criteria were developed to help standardize the

diagnosis (Table 64-1). Constipation can be caused by lifestyle choices, side effects of medications taken

for other reasons, medical conditions (such as hypothyroidism), structural abnormalities of the colon,

pelvic floor dysfunction, and colonic inertia (Table 64-2). Evaluation of the constipated patients includes

a thorough history, a physical examination including a rectal examination, and evaluation for sources of

pelvic floor dysfunction such as rectocele. Colonoscopy may be necessary to eliminate a structural

bowel obstruction as the cause of constipation.

DIAGNOSIS

Table 64-1 Rome III Criteria for the Diagnosis of Constipation

ETIOLOGY

Table 64-2 Causes of Constipation

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After eliminating medication-related or metabolic causes of constipation and in the absence of

systemic symptoms, it may be practical to initiate medical therapy before proceeding with radiologic

testing for rare conditions such as colonic dysmotility or pelvic floor dysfunction. The goal of first-line

medical therapy is to increase stool bulk and physical activity. Fiber intake should be increased to 20 to

30 g/d. To achieve this recommended daily amount, fiber supplementation with either psyllium or

methylcellulose is frequently required. At least eight glasses of water should be ingested daily. Fiber

and water intake increases stool bulk, and bulky bowel movements stimulate colonic motility. If fiber,

water, and exercise do not relieve constipation, then laxatives should be added to the regimen.

Laxatives can be divided into different categories by mechanism of action (Table 64-3). Osmotic

laxatives are usually the first-line treatment for severe constipation. Long-term use of laxatives, which

irritate the colon, should be avoided, however, because they can actually impair colon function.

Melanosis coli, a dark discoloration of the colonic mucosa seen on colonoscopy, is a sign of frequent

laxative use.

TREATMENT

Table 64-3 Laxatives

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Some patients whose constipation does not respond to standard medical therapy will be found to have

slow-transit constipation or pelvic floor dysfunction, both of which require radiologic studies for

diagnosis. The most common technique for evaluating colonic transit is a Sitz marker study (Fig. 64-6).

To complete this test, all laxatives must be stopped 48 hours before the study. On day 0, a set number

of radiopaque markers are ingested; an abdominal radiograph is obtained on day 1 to document that the

markers were ingested and have passed through the small bowel into the colon, and again on day 5 to

determine if the markers have been expelled. Normally, on day 5, more than 80% of the markers should

be evacuated. If more than 20% of the markers remain and they are either clustered in the right colon

or evenly distributed throughout the colon, the patient has slow-transit constipation. Outlet obstruction

is suggested by clustering of the markers in the sigmoid or rectum. Outlet dysfunction can be further

evaluated with defecography, a fluoroscopic study of defecation. Slow-transit constipation is best

treated with surgery, and obstructed defecation with biofeedback therapy.

Figure 64-6. Sitz marker study demonstrating colonic inertia.

Postoperative Ileus

8 9 Postoperative ileus is transient impairment of bowel function after an operation. It is most common

in patients after intra-abdominal surgical procedures, particularly colonic operations. Clinically,

postoperative ileus is manifested by abdominal distention and delayed passage of flatus and, less

1671

frequently, by nausea and vomiting. After an abdominal operation, the colon usually takes 3 to 5 days

to recover, whereas the stomach and small bowel resume normal motor function more rapidly (1 to 2

days and 1 day, respectively).21 In a recent multicenter study, the average length of hospital stay after

bowel resection was 6.6 days, with 11.5% of patients requiring a nasogastric tube for ileus.22

Postoperative ileus is multifactorial. Surgical and anesthetic technique, narcotic use, inactivity, and

postoperative infectious complications all have been implicated in prolonged ileus. Bowel manipulation

has also been suggested to contribute to the development of ileus.22 The observation that postoperative

ileus is shorter after minimally invasive surgery adds credence to this theory.23 Use of the anesthetic

agent halothane, as well as opioid analgesics, can prolong postoperative ileus.21 After surgery,

systemically administered morphine, in addition to binding to μ-opioid receptors in the central nervous

system and promoting analgesia, binds to peripheral μ-opioid receptors in the colon and causes

nonpropulsive electrical activity that can prolong ileus.24 Given this, recent research has focused on

strategies to minimize the use of perioperative narcotics with the goal of preventing or minimizing

postoperative ileus. One of the most promising strategies is the use of a thoracic epidural for

postoperative analgesia. In addition to delivering analgesia with minimal narcotics, thoracic epidural

blocks promote parasympathetic activity by blunting sympathetic inhibition of the gut, thereby

promoting gut motility. The greatest benefit is seen with epidural infusions of local anesthetic (lidocaine

or bupivacaine), as compared to narcotics.21 Other benefits of using thoracic epidurals in the

postoperative period are improved mental acuity and overall better pain control as compared to

traditional narcotic-based regiments, both of which promote early mobility, particularly in elderly

patients.25 Alvimopan, an oral medication that blocks the μ-opioid receptors in the gastrointestinal tract,

is the most studied medication to prevent postoperative ileus. A phase III multicenter study of patients

who had a bowel resection or hysterectomy found that alvimopan (12 mg before surgery, then twice a

day until discharge) decreased hospital stay by 18 hours as compared to placebo, in narcotic naïve

patients.26 As understanding of gut neurophysiology continues to improve, it is anticipated that more

narcotic sparing pain regimens will be available for the management of postoperative pain.

Enhanced recovery protocols are increasingly gaining traction in the United States. Initially called

Fast Track Surgery by Wilmore and Kehlet,27 and later Enhanced Recovery After Surgery (ERAS), they

focus on incorporating evidence-based treatments into clinical pathways with a particular emphasis on

multimodal pain management and avoidance of narcotics.28 General principles of enhanced recovery

protocols include preoperative education, avoidance of preoperative fasting and postoperative

nasogastric tubes, early introduction of enteral feeding, avoidance of parenteral narcotic analgesia.29

The enhanced recovery protocols accelerate surgical recovery and are associated with reductions in

length of hospital stay and decreased 30 postoperative morbidity including infectious complications and

postoperative ileus.30–33 In order to implement protocols and maintain high levels of compliance,

enhanced recovery requires a multidisciplinary team approach with surgeons, anesthesia providers,

nurses and care coordinators collaborating for both the implementation and sustaining of the protocol.

Patient engagement and preoperative expectation setting is essential. Most successful programs have

developed enhanced recovery focused educational materials and report marked increase in patient

satisfaction postprotocol implementation.

Irritable Bowel Syndrome

Irritable bowel syndrome is defined as abdominal pain that is not associated with an anatomic

abnormality and may or may not be associated with alterations in bowel habits. The causes of this

disorder are uncertain. Emotional stress and psychiatric illness have been implicated in the pathogenesis

of the disorder and may exacerbate symptoms.34 Physiologic abnormalities have also been

demonstrated, as has abnormal colonic motility in response to an ingested meal.35 Altered myoelectric

activity and abnormal gut hormone secretion have also been cited as potential causes.

Because no one, clear cause of irritable bowel syndrome has been demonstrated, no specific treatment

regimen has been defined for this disorder. Most patients have asymptomatic periods interrupted by

intervals of symptoms. The approach to treatment begins with an evaluation of the factors associated

with irritable bowel syndrome. Diagnosis and treatment of an underlying psychiatric problem may

resolve the patient’s symptoms. A detailed dietary history should also be taken, and factors that

contribute to constipation or diarrhea should be adjusted appropriately. If these management strategies

are not successful, gradually introducing anticholinergic medications may be helpful. Anticholinergic

agents can reduce the rate of myoelectric activity and decrease tonic contractions in the colon, thereby

relieving the cramping and bloating that many patients experience. Low doses of tricyclic

1672

antidepressants, including imipramine, amitriptyline, and nortriptyline, often decrease or eliminate

abdominal symptoms. Constipation is known to be one major side effect of these agents, which may be

helpful in patients with irritable bowel syndrome and underlying diarrhea, but a problem in patients

with pre-existing constipation. The myriad treatment options described for irritable bowel syndrome

underscores the poor understanding of this clinical entity.

Colonic Pseudo-obstruction

Colonic pseudo-obstruction, also known as Ogilvie syndrome, is massive dilation of the colon without an

actual mechanical obstruction. In 1948, Ogilvie described two patients with colonic pseudo-obstruction

from malignant infiltration of the celiac plexus that he postulated led to sympathetic inhibition.36 In the

intestine, stimulation of the sympathetic nervous system decreases intestinal motility, whereas

activation of the parasympathetic nervous system promotes contractility. Colonic pseudo-obstruction

results from an imbalance in the autonomic nervous system of the gastrointestinal tract. Various

metabolic conditions, pharmacologic agents, and traumatic factors can alter the balance of the intestinal

autonomic nervous system and have been associated with colonic pseudo-obstruction.37 The most

frequent presenting symptoms are abdominal pain and nausea and vomiting. On physical examination,

the abdomen is distended and tympanic and may be mildly tender when palpated. Marked colonic

distention present on an abdominal radiograph is the hallmark of the condition (Fig. 64-7). Fever and

leukocytosis are rare and should raise the concern for perforation.38 First-line management of colonic

pseudo-obstruction is conservative and consists of nasogastric decompression, cessation of oral feedings,

correction of fluid and electrolyte imbalances, and avoidance of narcotics and anticholinergics. If

abdominal radiographs do not show gas throughout the colon, an abdominal computed tomography scan

or a Gastrografin enema should be considered to rule out a mechanical obstruction. With conservative

measures, colonic pseudo-obstruction resolves in more than 75% of cases. When the pseudo-obstruction

persists for more than 6 days and/or the diameter of the cecum on abdominal radiograph is greater than

12 cm, the risk for cecal perforation increases.38,39

Figure 64-7. Pseudo-obstruction of the colon (Ogilvie syndrome).

Colonic pseudo-obstruction is most commonly seen in elderly patients who may have other significant

medical conditions, so when free perforation occurs, it can be associated with significant morbidity and

mortality (up to 40% in one study).40 In patients whose pseudo-obstruction is not responding to

conservative therapy but who have no signs of peritonitis, 2.5 mg of neostigmine given intravenously

over 2 to 3 minutes has been found to decompress the colon promptly in nearly all patients.41,42

Neostigmine is a reversible acetylcholinesterase inhibitor that stimulates the intestinal parasympathetic

receptors, promoting colonic motility.43 In a randomized controlled study, the pseudo-obstruction

resolved promptly in 10 of 11 patients.41 If neostigmine fails to decompress the colon, another

1673

alternative is decompressive colonoscopy. In one series, 69% of patients had resolution of their pseudoobstruction after colonoscopy to remove air.43 Surgery is reserved for patients with obvious peritoneal

signs or whose pseudo-obstruction has not improved after all forms of nonsurgical therapy. In such

patients, when the possibility of cecal perforation is high, a cecostomy can be considered.

Anal Incontinence

Anal incontinence is defined as the inability to control the passage of gas, liquid, or solid stool.

Obstetric trauma from vaginal deliveries is the most common cause of fecal incontinence in adult

women.1 Occult sphincter injury is reported in 25% to 35% of women on endoanal ultrasound after

delivery. Vaginal deliveries that require forceps/vacuum-assistance and/or episiotomies are associated

with increased risk of subsequent fecal incontinence. Others include aging, anorectal surgery,

inflammatory bowel disease, infectious proctitis, anal or rectal neoplasm, congenital malformations

(e.g., spina bifida, imperforate anus, myelomeningocele), traumatic injury, sequelae of radiation,

underlying neurologic disorders (diabetes, multiple sclerosis, pudendal neuropathy and fecal impaction).

Workup consists of obtaining a history focusing on the above etiologic factors, evaluation and

optimization of underlying medical conditions, documentation of bowel habits, and further

characterization of the incontinence. It is important to establish if other pelvic floor disorders are

present as well by eliciting symptoms of rectal and pelvic organ prolapse, as well as urinary

incontinence. The most common scoring system to quantitate fecal incontinence is the Cleveland Clinic

Florida Fecal Incontinence Score (CCF-FIS) (Table 64-4).44,45 Physical examination should note anal

sphincter tone, as well as associated scars from prior anorectal surgery or vaginal delivery. Physiologic

studies to assess incontinence complement the history and physical examination and include anorectal

manometry for evaluation of anal sphincter function, and endoscopic ultrasound for detection of occult

sphincter defects. Other diagnostic studies to consider, based on symptoms include defecography (to

evaluate for pelvic organ prolapse), and colonoscopy (to diagnose occult malignancy or inflammatory

bowel disease).

Table 64-4 Cleveland Clinic Incontinence Score

Initial management is conservative and consists of medication to optimize bowel and biofeedback to

ensure that the anal muscles are squeezing appropriately. A trial with bulking agents, such as fiber and

constipating agents is effective for many patients with loose stools and incontinence; bulky, soft stools

are easiest for the anal sphincter muscles to retain. For patients with incontinence related to fecal

impaction, a laxative regimen including enemas and scheduled disimpactions can improve control.

Biofeedback is a form of physical therapy that retrains muscle (external sphincter and pelvic floor

muscles) and facilitates anal-neuro feedback for discrimination of rectal sensations. Biofeedback has

been shown to improve fecal incontinence in 50% to 86% of patients.46–49 Because it is safe,

inexpensive, and effective, biofeedback should be offered to all patients who do not respond to medical

therapy.

10 The most common surgical interventions are overlapping sphincteroplasty, injectable agents,

sacral nerve stimulation (SNS), and colostomy. Traditionally, overlapping sphincteroplasty has been the

standard of care for patients with fecal incontinence and a sphincter defect on imaging studies. Shortterm success rates have been as high as 70%; however, long-term functional outcomes are poor.50–55 A

newer option, injectable agents augment the anal cushions and are used for mild to moderate degrees of

passive fecal incontinence. Different biomaterials have been used but the most common is SOLESTA

(hyaluronic acid/dextranomer) (Salix Pharmaceuticals, Inc). Complications are minor and self-limiting

1674

 

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SECTION I: COLON AND RECTUM

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Chapter 64

Colon and Rectal Anatomy and Physiology

Sandy H. Fang and Elizabeth C. Wick

Key Points

1 The mesorectum is invested by the fascia propria of the rectum.

2 The ileocolic branch of the superior mesenteric artery supplies the right colon and part of the

transverse colon.

3 The inferior mesenteric artery supplies part of the transverse colon, sigmoid colon, and rectum.

4 The inguinal lymph nodes drain the lymphatics from the anal canal below the dentate line.

5 The colon has 1013 bacteria, which promote mucosal immunity, help digest complex nutrients, and

protect against pathogenic organisms.

6 Alterations in the colonic flora have been associated with inflammatory bowel disease and colorectal

cancer.

7 Constipation is one of the most common conditions treated by physicians, but only rarely is it due to

colonic inertia.

8 During postoperative ileus, the stomach recovers after 1 to 2 days, the small bowel after 1 day, and

the colon after 3 days.

9 Thoracic epidural use after colorectal surgery can shorten postoperative ileus.

10 Sacral nerve stimulation is a newer and effective treatment for fecal incontinence.

INTRODUCTION

While the complex coordination of stool through the colon, rectum, and anus is the main function of the

colon, it also plays a role in the complex digestion and absorption of carbohydrate and protein residue,

creates a balanced environment for bacteria, and lubricates stool for transit. Understanding the anatomy

and physiology of the colon, rectum, and anus is important to treating the pathology associated with it.

EMBRYOLOGY OF THE COLON AND RECTUM

The primitive gut is derived from endoderm and begins to form during the third to fourth week of

gestation. It is divided into three segments: foregut, midgut, and hindgut. Embryologically, the colon is

derived from the midgut, which is supplied by the superior mesenteric artery, and the hindgut, which is

supplied by the inferior mesenteric artery.1 The midgut gives rise to the small intestine distal to the

ampulla of Vater, the cecum and appendix, the ascending colon, and the right half to two-thirds of the

transverse colon. During the sixth gestational week, the midgut herniates from the abdominal cavity

into the extraembryonic coelom, undergoes a 270-degree counterclockwise rotation around the superior

mesenteric artery, and then returns to the abdominal cavity at 10 weeks’ gestation. The hindgut gives

rise to the distal one-third of the transverse colon, descending and sigmoid colon, rectum, and upper

portion of the anal canal. The terminal end of the hindgut is the endoderm-lined pouch termed the

cloaca. During development, the cloaca is partitioned by the urorectal septum into the rectum and upper

anal canal and urogenital sinus. Ultimately, the distal anal canal arises from canalization of the

ectoderm. The pectineal or dentate line marks the junction between tissue derived from endoderm and

ectoderm in the anal canal.

ANATOMY OF THE COLON AND RECTUM

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The colon begins in the right lower quadrant of the abdomen as the cecum. The ileum enters the colon

at the posteromedial aspect at the ileocecal valve.1 Characteristics unique to the colon are (a) taeniae

coli, (b) haustra, and (c) appendices epiploicae, located on the antimesenteric surface of the colon.

There are three taeniae (anterior, posterior medial, and posterior lateral), which are condensations of

the outer longitudinal muscle layer in the colon. They are named according to their attachments: taenia

mesocolica (attached to the mesocolon), taenia omentalis (attached to the greater omentum), taenia

libera (no attachments). The taeniae originate at the base of the appendix, course along the length of

the colon, and then converge at the rectosigmoid junction.

On average, the colon is 150 cm long. The taenia are one-sixth shorter than the colon and are

believed to be responsible for pockets of the colon wall called sacculations or haustra.1 The epiploicae

appendices are fat appendages seen on the colonic serosa.

The colon consists of five layers: mucosa, submucosa, circular muscle layer, longitudinal muscle layer,

and serosa (Fig. 64-1). Microscopically, the colonic mucosa is a columnar epithelium marked by crypts

and goblet cells. Unlike the small intestine, the columnar epithelium of the colon and rectum does not

have villi. The submucosa is the strongest layer of bowel and contains Meissner plexus. The myenteric

plexus of Auerbach is on the external surface of the circular muscle layer. The outer longitudinal

muscles form the taeniae coli. Finally the serosa is not present in the lower portions of the rectum.

The colon begins in the right lower quadrant with the cecum. The cecum extends approximately 6 to

8 cm below the ileocecal valve (where the terminal ileum enters the posteromedial aspect of the cecum)

(Fig. 64-2). The angulation between the ileum and cecum via the superior and inferior ileocecal

ligaments is important in maintaining competence against reflux at the ileocecal junction.2 The cecum is

the widest portion of the colon (7.5 to 8.5 cm in diameter), has the thinnest wall, and is entirely

enveloped by peritoneum. The appendix originates from the lowest portion of the cecum and can be

readily identified by following the converging taeniae. In 85% to 95% of people, the appendix lies

posterior to the cecum, lateral and in line to the terminal ileum, but the position can vary, with the

most frequent variants being retrocecal (toward the psoas muscle), pelvic, and retroileal.3 During

colonoscopy, visualization of the appendiceal orifice and ileocecal valve are the landmarks required in a

complete colonic examination. From the cecum, the right colon ascends to the hepatic flexure

(approximately 15 cm). The hepatic flexure is anterior to the inferior pole of the right kidney and

overlies the second portion of the duodenum. The hepatic flexure is marked by medial, anterior, and

downward angulation of the colon. When the right colon and mesentery are mobilized during a

colectomy, care must be taken to avoid injury to the underlying duodenum. Only the anterior surface of

the right colon is invested with peritoneum; laterally, the white line of Toldt marks the extent of the

peritoneal covering and serves as an important landmark during surgical mobilization of the colon.

Figure 64-1. Layers of the colonic wall.

The transverse colon stretches from the hepatic flexure to the splenic flexure and is the longest

segment of colon (between 30 cm and 60 cm). The transverse colon is suspended by the transverse

mesocolon and is completely intraperitoneal. It is the most mobile portion of the colon and may descend

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to the level of the iliac crests or deep into the pelvis. The greater omentum descends from the greater

curve of the stomach in front of the transverse colon and then ascends to attach to the transverse colon

on its anterosuperior edge. To mobilize the transverse colon or enter the lesser sac, the fusion plane of

the omentum to the transverse colon must be dissected. The splenic flexure is situated high in the left

upper quadrant, more cephalad than the hepatic flexure, and lies anterior to the mid-left kidney and

abuts the lower pole of the spleen. There are attachments from the colon to the diaphragm at the level

of the 10th and 11th ribs and spleen (phrenocolic and splenocolic ligaments), and these must be

carefully divided during mobilization of the splenic flexure to avoid splenic injury.

The descending colon is approximately 25 cm long and courses from the splenic flexure to its junction

with the sigmoid colon at the pelvic brim. It lies anterior to the left kidney and, like the right colon, the

anterior, lateral, and medial portions of the descending colon are covered by peritoneum.

The sigmoid colon extends from the pelvic brim to the sacral promontory, where it continues as the

rectum and generally measures 15 to 50 cm in length. It is completely invested by peritoneum. The

rectosigmoid junction is marked by the convergence of the colonic taenia. The sigmoid colon is

extremely mobile and has a generous mesentery that extends along the pelvic brim from the iliac fossa

across the sacroiliac joint to the second or third sacral segment. Because of its mobile mesentery, the

sigmoid colon can twist and cause an obstruction, termed sigmoid volvulus. The left ureter runs in the

intersigmoid fossa, which is at the base of the mesosigmoid. When a high ligation of the inferior

mesenteric artery is performed during a cancer operation or the sigmoid colon is being mobilized along

the white line of Toldt, the left ureter should be identified to avoid inadvertent injury. Preoperative

placement of urinary stents can be useful for locating the ureter intraoperatively in complex,

reoperative pelvic surgery.

1 At the sacral promontory, the colon becomes the rectum. The outer layer of the rectal wall is

composed of the longitudinal muscle, where the three teniae splay. The rectum measures 12 to 15 cm in

length. It proceeds posterior and caudal along the curvature of the sacrum and coccyx, passing through

the levator ani muscles, at which point it turns abruptly caudal and posteriorly at the anorectal ring,

becoming the anal canal. Anterior to the rectum are the uterine cervix and posterior vaginal wall in

women, and the bladder and prostate in men. Posteriorly, the rectum occupies the sacral concavity

where the median sacral vessels, presacral veins, and sacral nerves run, all of which are invested in the

presacral fascia. The rectum is marked by three curves. The upper and lower curves are convex and to

the right, while the middle is convex and to the left. Within the lumen, these correspond to the valves

of Houston, which separate the lower third, middle third, and upper third of the rectum – important

landmarks when the location of a rectal abnormality is established endoscopically (the lower rectal

valve is at 7 to 8 cm from the anal verge, middle rectal valve at 9 to 11 cm, and upper rectal valve at

12 to 13 cm).4 The valves do not contain all layers of the bowel wall and thus biopsy at this location

carries minimal risk of perforation. The middle valve of Houston is the internal landmark corresponding

to the anterior peritoneal reflection. The anterior and lateral surfaces of the upper third of the rectum

are intraperitoneal, whereas only the anterior surface of the middle third of the rectum is

intraperitoneal in location. The lower third of the rectum is entirely extraperitoneal. The mesorectum is

the term used to describe the areolar tissue surrounding the rectum that contains nerves, lymphatics,

and terminal branches of the superior hemorrhoidal branch of the inferior mesenteric artery. Although it

invests the rectum circumferentially, the mesorectum is most prominent posterior to the rectum. It is

invested by the fascia propria of the rectum, a continuation of the parietal endopelvic fascia (Fig. 64-3).

The fascia propria (investing fascia) includes the distal two-thirds of the posterior rectum and the distal

one-third of the anterior rectum, where it is no longer intraperitoneal. A total mesorectal excision

entails removal of the entire rectum without violating the fascia propria of the rectum. This is

accomplished by mobilizing the rectum using the plane between the fascia propria of the rectum and the

presacral fascia. Anterior to the investing fascia (fascia propria) is a delicate layer of connective tissue

known as Denonvilliers fascia, which separates the rectum from its anterior structures. Waldeyer fascia

(rectosacral fascia) is the presacral fascia that is an extension of the parietal pelvic fascia from the

periosteum of sacral segment four to the posterior wall of the rectum. It contains branches of the sacral

splanchnic nerves. Below Waldeyer fascia is the supralevator or retrorectal space.

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Figure 64-2. General anatomic components of the colon.

Figure 64-3. Fascial relationships of the pelvis.

The surgical anal canal begins at the anorectal ring or levator ani muscles and extends to the anal

verge. It measures 2 to 4 cm and is usually longer in men than in women. The internal anal sphincter

(continuation of the circular smooth muscle of the rectum) and the external anal sphincter (continuation

of the puborectalis muscle) encircle the anal canal and control fecal continence. The internal anal

sphincter relies on autonomic innervation, while the external anal sphincter uses somatic innervation.

The median length and thickness of the female anterior external sphincter is 11 and 13 mm and thus a

small tear sustained during vaginal delivery may cause fecal incontinence.5 There are three layers of the

external sphincter – subcutaneous (traversed by the conjoined longitudinal muscle with some fiber

attachments to the skin), superficial (connective tissue attaches posteriorly, forming the anococcygeal

ligament), and deep (continues with the puborectalis muscle). Between the internal and external anal

sphincters, the longitudinal muscle of the rectum joins fibers of the levator ani and puborectalis muscles

to form the conjoined longitudinal muscle. The dentate line marks the transition between the columnar

epithelium of the intestine and the squamous epithelium of the anal canal. The transition between these

two epithelia is called the anal transitional zone. The Columns of Morgagni are the 6 to 14 longitudinal

folds located at the dentate line. Small pockets between these columns called anal crypts contain anal

glands, which may become obstructed with foreign material to cause an infection. Below the dentate

line is the anoderm, which extends to the anal verge and does not contain accessory skin structures,

such as hair, sebaceous and sweat glands. The autonomic nervous system innervates proximal to the

dentate line and the somatic nervous system supplies the anoderm and distally.

Pelvic Floor

The perineal body is the tendinous insertion of the external anal sphincter, bulbocavernosus, and

superficial and deep transverse perineal muscles. It supports the perineum and separates the vagina

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from the anus.

Three striated muscles that attach to the pubic bone make up the pelvic floor or levator ani muscles:

iliococcygeus, pubococcygeus, and puborectalis. The pelvic floor muscles are supplied by branches from

the third sacral nerve, while the external anal sphincter is supplied by nerve fibers traveling with the

pudendal nerve on the levators undersurface.

The puborectalis originates from the back of the symphysis pubis and forms a U-shaped sling as it

joins the opposite muscle posteriorly. The iliococygeus muscle arises from the ischial spine and posterior

part of the obturator fascia and travels inferiorly, posteriorly, and medially to insert into the last two

segments for the sacrum and coccyx. The pubococcygeus muscle arises from the anterior half of the

obturator fascia and the posterior pubis. Its fibers are directed backward, downward, and medially,

where they decussate with fibers of the opposite side. The decussation is called the anococcygeal raphe.

Anorectal Spaces

The perianal space surrounds the anal canal superficially and contains the external hemorrhoidal plexus.

The ischioanal space extends laterally and goes superiorly to the levator ani from the skin on the

perineum. The levator ani and external sphincter muscles form the medial boundary, while the lateral

wall is formed by the obturator fascia. The superficial postanal space connects the perianal spaces with

each other posteriorly below the anococcygeal ligament, while the deep postanal space lies above the

anococcygeal ligament. The ischioanal and perianal spaces make the ischioanal fossa. The deep postanal

and ischiorectal spaces form a horseshoe configuration that may be involved in a horseshoe abscess.

Below the perianal space between the sphincter muscles is the intersphincteric space. The submucosal

space contains the internal hemorrhoidal plexus and lies between the internal anal sphincter and the

mucosa distal to the dentate line. Proximally, it becomes the submucosa of the rectum. Above the

levator complex is the supralevator space, which extends superiorly to the peritoneum at the rectosacral

fascia. The retrorectal space extends above the rectosacral fascia and lies between the upper two-thirds

of the rectum and sacrum.

Arterial Blood Supply

2 3 The arterial blood supply to the colon, rectum, and anus is highly variable. The following

summarizes the general courses of the arterial blood supply. The superior mesenteric artery arises from

the aorta, runs posterior to the pancreas, and passes anterior to the third portion of the duodenum (Fig.

64-4). In addition to supplying the small bowel through jejunal and ileal branches, the superior

mesenteric artery gives rise to the ileocolic, right colic, and middle colic branches that supply the

cecum, ascending colon, and proximal transverse colon. The right colic arterial anatomy is particularly

variable and can be absent or arise from the ileocolic or the superior mesenteric artery. The middle colic

artery has a right branch that supplies the hepatic flexure and the right portion of the transverse colon,

while the left branch supplies the left portion of the transverse colon. The inferior mesenteric artery

arises from the anterior surface of the aorta, typically 3 to 4 cm above the aortic bifurcation, and

supplies the distal transverse colon, descending colon, sigmoid colon, and upper rectum. The inferior

mesenteric artery gives rise to the left colic artery and sigmoidal branches, then continues in the

sigmoid mesentery, and after crossing the left iliac vessels, is renamed the superior rectal/hemorrhoidal

artery. The inferior mesenteric artery may also function as an important collateral vessel to the lower

extremities during instances of distal aortic occlusion. The superior hemorrhoidal artery descends

behind the rectum and splits into right and left branches in the mesorectum. It is the main blood supply

of the rectum. The middle and inferior rectal/hemorrhoidal arteries arise from either the internal

pudendal arteries or the hypogastric arteries and supply the distal two-thirds of the rectum. The

presence of the middle rectal artery, in particular, can be variable. A series of arterial arcades along the

mesenteric border of the entire colon, known as the marginal artery of Drummond, connect the superior

mesenteric and inferior mesenteric arterial systems. The marginal artery may be attenuated or absent at

the distal transverse colon/splenic flexure, the delineation between the midgut and hindgut, and thus

ischemic colitis most commonly affects this region. The arc of Riolan (“meandering mesenteric artery”)

is a short loop connecting the left branch of the middle colic artery and the trunk of the inferior

mesenteric artery. The inferior rectal/hemorrhoidal arteries traverse the ischioanal fossa and supply the

anal canal and external anal sphincter muscles.

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Figure 64-4. Arterial blood supply of the colon.

Figure 64-5. Venous drainage of the colon by the portal vein.

VENOUS DRAINAGE

The veins that drain the large intestine bear the same terminology and follow a course similar to that of

their corresponding arteries (Fig. 64-5). The veins from the right colon and transverse colon, along with

the veins draining the small intestine, drain into the superior mesenteric vein. The superior mesenteric

vein runs slightly anterior to and to the right of the superior mesenteric artery. The superior mesenteric

vein courses beneath the neck of the pancreas, where it joins with the splenic vein to form the portal

vein. The inferior mesenteric vein is a continuation of the superior rectal vein and drains blood from the

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Follow-up After Resection of Cholangiocarcinoma

Recurrence following resection of ICC is within the liver in 60% of patients. While data are lacking,

there is some evidence to suggest that there is a role for reresection in highly selected patients. The

most likely site of recurrence after resection of hilar cholangiocarcinoma is locally within the bile duct,

regional lymph nodes, or liver. Therapy for recurrence is palliative. Surgical reexcision is usually

impossible because of the challenging anatomic location and the radical procedures that are required for

resection of the primary tumor. The main symptoms of recurrence that demand palliation are pruritus

or cholangitis associated with jaundice. For biliary drainage to relieve jaundice or cholangitis, either

surgical drainage or drainage by PTC can be effective. Endoscopic drainage has little role in the relief of

jaundice in patients who have had Roux-en-Y biliary reconstruction. For limited recurrences,

intraluminal brachytherapy or external beam radiotherapy may improve palliation and, potentially,

survival.132

Routine follow-up consists of office visits every 3 months with physical examination and

measurement of liver function tests. Although a rising alkaline phosphatase level is a reliable indicator

of evolving biliary obstruction, patients recovering from liver resection and biliary obstruction can have

persistent elevations of alkaline phosphatase. Up to 10% of patients with biliary surgical reconstruction,

however, may develop a benign anastomotic stricture. Most patients with recurrence or a benign

stricture will present with jaundice or cholangitis. Surveillance cross-sectional imaging is recommended

every 3 to 6 months for the first 2 years following resection and should be individualized thereafter.

Issues for the Future

Further studies are needed to develop effective adjuvant, and potentially neoadjuvant, therapies for

cholangiocarcinoma. Continued assessment of novel drugs and radiosensitizers, and biologic agents is

warranted. A better understanding of the molecular pathogenesis and genetics of bile duct cancers may

lead to new therapeutic strategies and possibly preventive strategies for high-risk populations.

BENIGN GALLBLADDER NEOPLASMS

Incidence

Benign tumors of the biliary tract are rare, but have been reported more frequently as imaging

modalities (e.g., ultrasound and CT scan) have come into widespread and frequent use. In patients

undergoing cholecystectomy, the reported incidence of benign gallbladder tumors is less than 3%.

Pathology

Polyps and Pseudotumors

Benign gallbladder tumors are most frequently polyps or polypoid lesions. The incidence of polyps in

asymptomatic patients is about 5%.3 Cholesterol polyps (cholesterolosis), accounting for half of all

gallbladder polypoid lesions, result from epithelium-covered, cholesterol-laden macrophages in the

lamina propria.133 These lesions are likely a result of an error in cholesterol metabolism. They extend

from the mucosa on a narrow stalk, grossly appearing as yellow spots on the mucosal surface. Nearly all

are multiple, and most are less than 10 mm in size.133,134 When a polyp is pedunculated, it is benign in

most cases; alternatively, sessile “polyps” are more often malignant (Fig. 63-10). Inflammatory polyps

result from chronic inflammation and extend by a narrow vascularized stalk into the gallbladder lumen.

None of these lesions are considered premalignant, although isolated cases of cholesterolosis associated

with in situ carcinoma have been reported.135

Adenomas

Gallbladder adenomas are found infrequently. They may be tubular or papillary, both arising from the

epithelial layer of the gallbladder. Multiple papillary adenomas, or papillomas, are called papillomatosis.

A direct association between benign adenoma, adenoma containing carcinoma in situ, and invasive

carcinoma has been demonstrated; thus these lesions are considered premalignant.136 Malignant

transformation, however, has only rarely been reported, primarily from large adenomas. In one series,

all benign adenomas were less than 12 mm in diameter, whereas the adenomas with cancerous foci

were greater than 12 mm.135

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Figure 63-10. T2-weighted magnetic resonance imaging scan showing a sessile polyp within the gallbladder (arrow) that was

malignant on histologic examination.

Adenomyomatosis

Adenomyomatosis of the gallbladder is characterized by localized or diffuse hyperplastic extensions of

the mucosa into, and often beyond, a hypertrophied gallbladder muscular layer. Hyperplasia occurs at

outpouchings of the mucosa of the gallbladder through the wall (Rokitansky–Aschoff sinuses) and

through the crypts of Luschka. This can result in focal thickening of the gallbladder wall, resembling

gallbladder adenocarcinoma. The etiology is unknown. This lesion may be premalignant, because cases

of adenocarcinoma arising in or near adenomyomatosis have been reported, but this relationship is

unclear.127,138

Other Benign Gallbladder Tumors

Other benign lesions include tumors arising from the tissue of the gallbladder wall, such as leiomyomas,

lipomas, hemangiomas, granular cell tumors, and heterotopic tissue, including gastric, pancreatic, or

intestinal epithelium.

Clinical Findings

Patients with benign gallbladder tumors typically present with symptoms consistent with

choledocholithiasis, including right upper quadrant pain, fatty food intolerance, and nausea. Many

benign gallbladder lesions are also discovered incidentally after elective cholecystectomy. Therefore,

symptoms caused by benign lesions are difficult to separate from those caused by gallstones. Most

lesions, however, are asymptomatic and are discovered incidentally during imaging for other abdominal

conditions.

Diagnosis

Diagnosis of benign gallbladder polyps is usually made when an ultrasound study is obtained to evaluate

a patient for symptoms consistent with gallstones. On ultrasound, a filling defect that does not change

with position is likely a polyp or carcinoma and not a gallstone. Cholesterol polyps are typically small,

submucosal, multiple, and hyperechoic on ultrasound because of their high cholesterol content. Other

than this typical appearance and the fact that malignant polyps are usually more than 1 cm in size, it is

difficult to differentiate benign from malignant polyps.

Both intravenous contrast-enhanced and unenhanced CT may be important in distinguishing benign

from malignant polyps. In a recent series examining 31 polypoid lesions of the gallbladder, contrastenhanced CT detected all of the lesions. Benign polyps were not visualized with unenhanced CT, unlike

neoplastic tumors, thus improving the ability to distinguish these lesions when both enhanced and

unenhanced CT scans were obtained.9 Endoscopic ultrasound has also been used to image these lesions,

and may be more accurate than transabdominal ultrasound in differentiating benign from malignant

tumors.22

Treatment

Large polyps, greater than 10 mm, have the greatest malignant potential.9,133,134 Without the evidence

of invasion or metastatic disease, however, no radiologic test can reliably differentiate benign from

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malignant lesions. Therefore, if large (>1 cm) polyps are present, even in asymptomatic patients

without stones, cholecystectomy is warranted.139 Additionally, resection is recommended for smaller

pedunculated lesions with evidence of a vascularized stalk. Small pedunculated lesions with the gross

characteristics of a benign cholesterol polyp may be observed and resected only if symptomatic.

Although these lesions have routinely been followed with ultrasound, a recent prospective study

suggested that polyps smaller than 1 cm do not progress to carcinoma.140 Cholecystectomy, however, is

still considered the standard of care if there is any increase in size.

BENIGN BILE DUCT NEOPLASMS

Incidence

Benign bile duct tumors, at times clinically resembling hilar cholangiocarcinoma, are less common,

occurring in less than 1% of patients.4

Pathology

Attesting to the rarity of these lesions, only two cases of benign extrahepatic bile duct disease occurred

in 4,200 biliary tract operations in one institution.141 The most common benign tumors of the

extrahepatic biliary tree arise from the glandular epithelium lining the ducts; about two-thirds of benign

tumors are polyps, adenomatous papilloma, or bile duct adenomas. Most are found in the periampullary

region, but they can be distributed throughout the entire biliary tree (Fig. 63-11). Multiple papillomas

also have been reported throughout the intrahepatic and extrahepatic biliary tree, termed multiple biliary

papillomatosis. Although local recurrence and progression to death from obstructive jaundice and

cholangitis occur frequently in these rare cases, these tumors have little, if any, malignant potential.

Other benign tumors (e.g., cystadenoma, granular cell myoblastoma, leiomyoma, and heterotopic

tissue) have also been reported.

One condition that deserves consideration is the case of “malignant masquerade,” an inflammatory,

fibrotic lesion clinically resembling hilar cholangiocarcinoma, but pathologically consisting only of

extensive fibrosis and inflammatory cells without evidence of dysplasia or preneoplastic change.142–144

In patients being considered for palliative treatment alone with presumed hilar cholangiocarcinoma, it is

essential to obtain a tissue diagnosis. It is inappropriate to treat benign lesions by percutaneous stenting

because of the excellent outcome after resection of these lesions.

Clinical Findings

Biliary obstruction, with resultant jaundice or cholangitis, is frequently the presenting symptom in

patients with benign bile duct tumors. Symptoms may also include epigastric pain or nausea. Because

these tumors are indolent, symptoms may be intermittent or gradually progressive.

Figure 63-11. Distribution of papillomas and adenomas of the biliary tree. The ampulla and common bile duct are the most

frequent sites.

Diagnosis

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Because of the presence of jaundice, benign bile duct tumors are usually initially evaluated with

ultrasound. Many patients then undergo ERCP or PTC and CT scan. A diagnosis of malignant

masquerade should be suspected in patients with mass lesions that resemble hilar cholangiocarcinomas,

but without lobar atrophy or portal vein involvement.

Treatment

Resection and reconstruction are performed to relieve jaundice and cholangitis. The preferred

reconstruction is a Roux-en-Y choledochojejunostomy to decrease the risk of postoperative biliary

stricture or recurrent cholangitis.

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