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

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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

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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

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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

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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

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