topics

11/7/25

2496 PART 10 Disorders of the Gastrointestinal System

(odds ratio 1.57), with a number needed to treat (NNT) of 10.2.

The modest therapeutic gain was similar to that yielded by other

currently available therapies for IBS. However, currently, there are

still insufficient data to recommend routine use of this antibiotic in

the treatment of IBS.

Prebiotics These are nondigestible food ingredients that stimulate growth and/or activity of bacteria in the GI tract. There have

been four randomized trials to examine the effects of prebiotics.

Three of the four studies reported that prebiotics worsened or did

not improve IBS symptoms. This is not surprising given the adverse

effects of a high-carbohydrate diet on IBS symptoms.

Probiotics These are defined as live microorganisms that when

administered in adequate amounts confer a health benefit on the

host. A meta-analysis of 10 probiotic studies in IBS patients found

significant relief of pain and bloating with the use of Bifidobacterium breve, Bifidobacterium longum, and Lactobacillus acidophilus

species compared to placebo. However, there was no change in stool

frequency or consistency. Large-scale studies of well-phenotyped

IBS patients are needed to establish the efficacy of these probiotics.

Low FODMAP Diet A diet rich in FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) often

triggers symptoms in IBS patients. FODMAPs are poorly absorbed

by the small intestine and fermented by bacteria in the colon to

produce gas and osmotically active carbohydrates (Fig. 327-4).

At the same time, on entering the colon, FODMAPs may serve

as nutrients for the colonic bacteria and promote the growth of

gram-negative commensal bacteria, which may induce epithelial damage and subclinical mucosa inflammation. Fructose and

fructans induce IBS symptoms in a dose-dependent manner. In

contrast, a low FODMAP diet reduces IBS symptoms. A systemic

review and meta-analysis of seven studies of IBS patients found

that a low FODMAP diet was associated with reduced global symptoms compared with control interventions. These studies showed

symptomatic benefit of restricting FODMAPs in 50–80% of patients

with IBS. There is increasing support for recommending a low

FODMAP diet as first-line treatment for IBS patients. Given that

between 20 and 50% of patients do not respond to a low FODMAP

diet, the identification of patients who are more likely to respond

to a low FODMAP diet at baseline would be highly beneficial. In a

small clinical study comparing responders to a low FODMAP diet

to nonresponders, fecal volatile organic acid profiling at baseline

accurately predicted response in 97% of cases. This finding needs

to be confirmed by large prospective cohort studies.

SUMMARY

The treatment strategy of IBS depends on the severity of the

disorder (Table 327-3). Most IBS patients have mild symptoms.

They are usually cared for in primary care practices, have little

or no psychosocial difficulties, and do not seek health care often.

Treatment usually involves education, reassurance, and dietary/

lifestyle changes. A smaller portion have moderate symptoms that

are usually intermittent and correlate with altered gut physiology,

e.g., worsened with eating or stress and relieved by defecation.

For IBS-D patients, treatments include gut-acting pharmacologic

agents such as antispasmodics, antidiarrheals, bile acid binders,

and the newer gut serotonin modulators (Table 327-4). In IBS-C

patients, increased fiber intake and the use of osmotic agents

such as polyethylene glycol may achieve satisfactory results. For

patients with more severe constipation, a chloride channel opener

(lubiprostone) or GC-C agonist (linaclotide or plecanatide) may be

considered. For IBS patients with predominant gas and bloating, a

low-FODMAP diet may provide significant relief. Some patients

Bloating, abdominal discomfort, flatulence, diarrhea

Abdominal

distention

Water in intestines Gas production

Small poorly absorbed carbohydrates

Food source for

bacteria Laxative effect

FIGURE 327-4 Pathogenesis of FODMAP-related symptoms. FODMAPs are poorly

absorbed by the small intestine and fermented by gut bacteria to produce gas and

osmotically active carbohydrates. These events act in concert to cause bloating,

flatulence, and diarrhea. FODMAPs may also serve as nutrients for colonic bacteria,

which may induce mucosa inflammation. FODMAP, fermentable oligosaccharides,

disaccharides, monosaccharides, and polyols. (Figure created using data from

http://www.nutritiontoyou.com/wp-content/uploads/2014/06/IBS-symptoms.png.)

TABLE 327-3 Spectrum of Severity in IBS

MILD MODERATE SEVERE

Clinical Features

Prevalence 70% 25% 5%

Correlations with gut physiology +++ ++ +

Symptoms constant 0 + +++

Psychosocial difficulties 0 + +++

Health care issues + ++ +++

Practice type Primary Specialty Referral

TABLE 327-4 Possible Drugs for a Dominant Symptom in IBS

SYMPTOM DRUG DOSE

Diarrhea Loperamide 2–4 mg when necessary/

maximum 12 g/d

Cholestyramine resin 4 g with meals

Alosetrona 0.5–1 mg bid (for severe IBS,

women)

Constipation Psyllium husk 3–4 g bid with meals, then adjust

Methylcellulose 2 g bid with meals, then adjust

Calcium polycarbophil 1 g qd to qid

Lactulose syrup 10–20 g bid

70% sorbitol 15 mL bid

Polyethylene glycol 3350 17 g in 250 mL water qd

Lubiprostone (Amitiza) 24 mg bid

Magnesium hydroxide 30–60 mL qd

Linaclotide (Plecanatide) 290 μg qd/3 mg qd

Prucalopride 2 mg qd

Abdominal pain Smooth-muscle relaxant qd to qid ac

Tricyclic antidepressants Start 25–50 mg hs, then adjust

Selective serotonin

reuptake inhibitors

Begin small dose, increase as

needed

Gas and bloating Low FODMAP diet

Probiotics qd

Rifaximin 550 mg bid

Available only in the United States.

Abbreviation: FODMAP, fermentable oligosaccharides, disaccharides,

monosaccharides, and polyols; IBS, irritable bowel syndrome.

Source: Reproduced with permission from GF Longstreth et al: Functional bowel

disorders. Gastroenterology 130:1480, 2006.

2497 Diverticular Disease and Common Anorectal Disorders CHAPTER 328

may benefit from probiotics and rifaximin treatment. A small

proportion of IBS patients have severe and refractory symptoms,

are usually seen in referral centers, and frequently have constant

pain and psychosocial difficulties. This group of patients is best

managed with antidepressants and other psychological treatments

(Table 327-4). Clinical trials demonstrating success of a low FODMAP diet in improving IBS symptoms and quality of life provide

strong evidence supporting the use of this dietary approach in the

treatment of IBS. These observations, if confirmed, may lead to the

use of the low FODMAP diet as the first line of treatment of IBS

patients with moderate to severe symptoms.

■ FURTHER READING

Bharucha AE, Lacy BE: Mechanisms, evaluation, and management

of chronic constipation. Gastroenterology 158:1232, 2020.

Dionne J et al: A systematic review and meta-anaylsis evaluating the

efficacy of a gluten-free diet and a low FODMAP diet in treating

symptoms of irritable bowel syndrome. Am J Gastroenterol 113:1290,

2018.

Drossman DA: Functional gastrointestinal disorders: History,

pathophysiology, clinical features, and Rome IV. Gastroenterology

150:1262, 2016.

Mayer EA et al: Brain-gut microbiome interactions and functional

bowel disorders. Gastroenterology 146:1500; 2014.

Pittayanon R et al: Gut microbiota in patients with irritable bowel

syndrome: A systematic review. Gastroenterology 157:97, 2019.

Zhou SY et al: FODMAP diet modulates visceral nociception by

lipopolysaccharide-mediated intestinal barrier dysfunction and

intestinal inflammation. J Clin Invest 128:267, 2018.

328 Diverticular Disease

and Common Anorectal

Disorders

Susan L. Gearhart

■ DIVERTICULAR DISEASE

Incidence and Epidemiology In the United States, diverticulosis affects one-third of the population aged >60 years, and in most

instances, there are no associated symptoms. However, 10–25% of

individuals with diverticulosis will develop acute diverticular disease.

In addition, 10–25% of individuals with diverticular disease will experience recurrent symptoms, and up to 10% will develop complications

leading to surgery. Diverticular disease has become the fifth most costly

gastrointestinal disorder in the United States and is the leading indication for elective colon resection. The incidence of diverticular disease is

on the rise, especially among individuals <40 years of age. The majority of patients with diverticular disease report a lower health-related

quality of life and more depression as compared to matched controls,

thus adding to health care costs. Formerly, diverticular disease was

confined to developed countries; however, with the adoption of westernized diets in underdeveloped countries, diverticulosis is on the rise

across the globe. Immigrants to the United States develop diverticular

disease at the same rate as U.S. natives. Although the prevalence among

females and males is similar, males tend to present at a younger age.

Anatomy and Pathophysiology Two types of diverticula occur

in the intestine: true and false (or pseudodiverticula). A true diverticulum is a saclike herniation of the entire bowel wall, whereas a pseudodiverticulum involves only a protrusion of the mucosa and submucosa

through the muscularis propria of the colon (Fig. 328-1). The type of

FIGURE 328-1 Gross and microscopic view of sigmoid diverticular disease. Arrows

mark an inflamed diverticulum with the diverticular wall made up only of mucosa.

diverticulum most commonly affecting the colon is the pseudodiverticulum. The diverticula occur at the point where the nutrient artery,

or vasa recta, penetrates through the muscularis propria, resulting in a

break in the integrity of the colonic wall. This anatomic restriction may

be a result of the relative high-pressure zone within the muscular sigmoid colon. Thus, higher-amplitude contractions combined with constipated, high-fat-content stool within the sigmoid lumen in an area of

weakness in the colonic wall result in the creation of these diverticula.

Consequently, the vasa recta is either compressed or eroded, leading to

either perforation or bleeding.

Diverticula commonly affect the left and sigmoid colon; the rectum

is always spared. However, in Asian populations, 70% of diverticula are

seen in the right colon and cecum as well. Yamanda et al. found rightsided colonic diverticulosis in 22% of Japanese patients undergoing

colonoscopy. Diverticulitis is inflammation of a diverticulum. Previous

understanding of the pathogenesis of diverticulosis attributed a lowfiber diet as the sole culprit, and onset of diverticulitis would occur

acutely when these diverticula become obstructed. However, evidence

now suggests that the pathogenesis is more complex and multifactorial.

Better understanding of the gut microbiota suggests that dysbiosis is

an important aspect of disease. Chronic low-grade inflammation is

thought to play a key role in neuronal degeneration, leading to dysmotility and high intraluminal pressure. As a consequence, pockets or

outpouchings develop in the colonic wall where it is weakest.

2498 PART 10 Disorders of the Gastrointestinal System

Presentation, Evaluation, and Management of Diverticular

Bleeding Hemorrhage from a colonic diverticulum is the most

common cause of hematochezia in patients >60 years, yet only 20% of

patients with diverticulosis will have gastrointestinal bleeding. Patients

at increased risk for bleeding tend to be hypertensive, have atherosclerosis, and regularly use antithrombotic therapy and nonsteroidal

anti-inflammatory agents. Additional risk factors include obesity and

a history of diabetes mellitus. Most bleeds are self-limited and stop

spontaneously with bowel rest. The lifetime risk of rebleeding is 25%.

Initial localization of diverticular bleeding may include colonoscopy,

multiplanar computed tomography (CT) angiogram, or nuclear medicine tagged red cell scan. If the patient is stable, ongoing bleeding is

best managed by angiography. If mesenteric angiography can localize

the bleeding site, the vessel can be occluded successfully with a coil in

80% of cases. The patient can then be followed closely with repetitive

colonoscopy, if necessary, looking for evidence of colonic ischemia.

However, with highly selective coil embolization, the rate of colonic

ischemia is <10%, and the risk of acute rebleeding is <25%. Long-term

results (40 months) indicate that >50% of patients with acute diverticular bleeds treated with highly selective angiography have had definitive

treatment. Alternatively, colonoscopic ligation with banding or placement of a detachable snare has been shown in a recent meta-analysis

to be an effective way to obtain hemostasis if the bleeding site can

be localized. Ligation has been shown to prevent rebleeding or the

requirement of emergent surgery. In the event that these measures

fail to achieve hemostasis, a segmental resection of the colon may be

undertaken. This may be advantageous in patients on chronic anticoagulation and immunosuppression as delayed bleeding and perforation

have been reported in this subpopulation.

If the patient is unstable or has had a 6-unit bleed within 24 h,

current recommendations are that surgery should be performed. If the

bleeding has been localized, a segmental resection can be performed. If

the site of bleeding has not been definitively identified, a subtotal colectomy may be required. In patients without severe comorbidities, surgical resection can be performed with a primary anastomosis. A higher

anastomotic leak rate has been reported in patients who received

>10 units of blood.

Presentation, Evaluation, and Staging of Diverticulitis

Acute uncomplicated diverticulitis (also known as symptomatic

uncomplicated diverticular disease [SUDD]) characteristically presents

with fever, anorexia, left lower quadrant abdominal pain, and obstipation (Table 328-1). In <25% of cases, patients may present with generalized peritonitis indicating the presence of a diverticular perforation.

If a pericolonic abscess has formed, the patient may have abdominal

distention and signs of localized peritonitis. Laboratory investigations

will demonstrate a leukocytosis. Rarely, a patient may present with

an air-fluid level in the left lower quadrant on plain abdominal film.

This is a giant diverticulum of the sigmoid colon and is managed with

resection to avoid impending perforation.

The diagnosis of diverticulitis is best made on a contrast-enhanced

abdominal and pelvic CT scan demonstrating the following findings:

sigmoid diverticula, thickened colonic wall >4 mm, and inflammation within the pericolic fat with or without the collection of contrast

Abscess

Feces

I II

III IV

FIGURE 328-2 Hinchey classification of diverticulitis. Stage I: Perforated

diverticulitis with a confined paracolic abscess. Stage II: Perforated diverticulitis

that has closed spontaneously with distant abscess formation. Stage III:

Noncommunicating perforated diverticulitis with fecal peritonitis (the diverticular

neck is closed off, and therefore, contrast will not freely expel on radiographic

images). Stage IV: Perforation and free communication with the peritoneum,

resulting in fecal peritonitis.

TABLE 328-1 Presentation of Diverticular Disease

Uncomplicated Diverticular Disease—75%

Abdominal pain

Fever

Leukocytosis

Anorexia/obstipation

Complicated Diverticular Disease—25%

Abscess 16%

Perforation 10%

Stricture 5%

Fistula 2%

material or fluid. In up to 20% of patients, an abdominal abscess may

be present. Symptoms of irritable bowel syndrome (Chap. 327) may

mimic those of diverticulitis. Therefore, suspected diverticulitis that

does not meet CT criteria or is not associated with a leukocytosis

or fever is not diverticular disease. Other conditions that can mimic

diverticular disease include an ovarian cyst, endometriosis, acute

appendicitis, and pelvic inflammatory disease.

Although the benefit of colonoscopy in the evaluation of patients

with diverticular disease has been called into question, its use is still

considered important in the exclusion of colorectal cancer. The parallel

epidemiology of colorectal cancer and diverticular disease provides

enough concern for an endoscopic evaluation before operative management. Therefore, a colonoscopy should be performed ~6 weeks after

an attack of diverticular disease.

Complicated diverticular disease is defined as diverticular disease

associated with an abscess or perforation and less commonly with a

fistula (Table 328-1). Perforated diverticular disease is staged using the

Hinchey classification system (Fig. 328-2). This staging system was

developed to predict outcomes following the surgical management of

complicated diverticular disease. In recent years, the Hinchey staging

system has been modified to include the development of a phlegmon

or early abscess (Hinchey stage Ia). A pericolic abscess is then considered Hinchey stage Ib. In complicated diverticular disease with fistula

formation, common locations include cutaneous, vaginal, or vesicle

fistulas. These conditions present with either passage of stool through

the skin or vagina or the presence of air in the urinary stream (pneumaturia). Colovaginal fistulas are more common in women who have

undergone a hysterectomy.

TREATMENT

Diverticular Disease

MEDICAL MANAGEMENT

Asymptomatic diverticular disease discovered on imaging studies

or at the time of colonoscopy is best managed by lifestyle changes.

Although the data regarding dietary risks and symptomatic diverticular disease are limited (Table 328-2), patients may benefit from

2499 Diverticular Disease and Common Anorectal Disorders CHAPTER 328

a fiber-enriched diet that includes 30 g of fiber each day. Supplementary fiber products such as Metamucil, Fibercon, or Citrucel

are useful. The use of fiber decreases colonic transit time and,

therefore, prevents increased intraluminal pressure leading to the

development of diverticulosis. The incidence of complicated diverticular disease appears to also be increased in patients who smoke

and are obese. Therefore, patients should be encouraged to refrain

from smoking and to join a weight loss program. The historical

recommendation to avoid eating nuts is based on no more than

anecdotal data.

SUDD with confirmation of inflammation and infection within

the colon should be treated initially with bowel rest. The routine use

of antibiotics in uncomplicated diverticular disease does not reduce

time to symptom resolution or risk of complications or recurrence.

There is ample evidence establishing the safety of treating SUDD

without antibiotics. The AVOD trial randomly assigned 623 inpatients with CT-confirmed uncomplicated left-sided diverticulitis to

receive intravenous fluids alone or intravenous fluids and antibiotics and found no differences between the treatment groups in terms

of time to recovery, the development of complicated diverticular

disease, and recurrence. The DIABOLO trial from the Dutch Diverticular Disease Collaborative Study Group compared the efficacy

of treating patients with their first episode of sigmoid diverticulitis

with antibiotics or outpatient observation. A total of 528 patients

with CT-proven uncomplicated diverticulitis were randomized to

either a 10-day course of amoxicillin/clavulanic acid or observation

in an outpatient setting. This study demonstrated that antibiotics

made no difference in symptom duration or management, and the

results favored observation over antibiotic therapy for uncomplicated diverticulitis (SUDD). Currently, the practice guidelines of

the American Society of Colon and Rectal Surgery state that “selected

patients with uncomplicated diverticulitis can be treated without

antibiotics.” Hospitalization for acute diverticulitis is recommended if

the patient is unable to take oral therapy, is affected by several comorbidities, fails to improve with outpatient therapy, or has complicated

diverticulitis. Nearly 75% of patients hospitalized for acute diverticulitis will respond to nonoperative treatment with a suitable antimicrobial regimen. The current recommended antimicrobial coverage is

a third-generation cephalosporin or ciprofloxacin and metronidazole

targeting aerobic gram-negative rods and anaerobic bacteria. Unfortunately, these agents do not cover enterococci, and the addition of

ampicillin to this regimen for nonresponders is recommended. Alternatively, single-agent therapy with a third-generation penicillin such

as IV piperacillin or oral penicillin/clavulanic acid may be effective.

The usual course of antibiotics is 7–10 days, although this length of

time is being investigated. Patients should remain on a limited diet

until their pain resolves.

Once the acute attack has resolved, the mainstay medical management of diverticular disease to prevent symptoms has evolved.

The risk of recurrent hospitalization following an episode of acute

diverticular disease is 11%. Established risk factors for symptomatic recurrence include younger age, the formation of a diverticular abscess, more frequent attacks (>2 per year), multimorbidity,

obesity, and smoking. Prevention strategies may include smoking

cessation and weight loss. Diverticular disease is now considered a

functional bowel disorder associated with low-grade inflammation.

The use of anti-inflammatory medications (mesalazine) in randomized clinical trials has shown them to be beneficial at reducing

symptoms and disease recurrence in patients with SUDD. However,

when objective signs of inflammation such as C-reactive protein

and computerized imaging are taken into consideration, no benefit

for the use of mesalazine has been shown.

Treatment strategies targeting dysbiosis in diverticular disease

have also been evaluated using polymerase chain reaction (PCR) on

stool specimens. Stool samples from consumers of a high-fiber diet

have different bacterial content than stool samples from consumers

of a low-fiber, high-fat diet. Probiotics are increasingly used by

gastroenterologists for multiple bowel disorders and may prevent

recurrence of diverticulitis. Specifically, probiotics containing Lactobacillus acidophilus and Bifidobacterium strains may be beneficial;

however, a recent systematic review was unable to show any benefit

to the use of probiotics alone. The addition of fiber or mesalazine

with probiotics has been shown to maintain remission. Rifaximin

(a poorly absorbed broad-spectrum antibiotic), when compared

to fiber alone for the treatment of SUDD, is associated with 30%

less frequent recurrent symptoms from uncomplicated diverticular

disease.

SURGICAL MANAGEMENT

Preoperative risk factors influencing postoperative mortality rates

include higher American Society of Anesthesiologists (ASA) physical status class (Table 328-3) and preexisting organ failure. In

patients who are low risk (ASA P1 and P2), surgical therapy can be

offered to those who do not rapidly improve on medical therapy.

For uncomplicated diverticular disease, medical therapy can be

continued beyond two attacks without an increased risk of perforation requiring a colostomy. However, patients on immunosuppressive therapy, in chronic renal failure, or with a collagen-vascular

disease have a fivefold greater risk of perforation during recurrent

attacks. A multicentered randomized clinical trial (DIRECT trial)

comparing surgery with conservative management for recurrent

SUDD demonstrated that elective surgical resection was associated

with an improved quality of life and was more cost-effective at

5 years following resection as compared to conservative management. Surgical therapy is indicated in all low-surgical-risk patients

with complicated diverticular disease.

The goals of surgical management of diverticular disease include

controlling sepsis, eliminating complications such as fistula or

obstruction, removing the diseased colonic segment, and restoring

intestinal continuity. These goals must be obtained while minimizing morbidity rate, length of hospitalization, and cost in addition to

maximizing survival and quality of life. Table 328-4 lists the operations most commonly indicated based on the Hinchey classification

and the predicted postoperative outcomes. The current options

for uncomplicated diverticular disease include an open or a laparoscopic resection of the diseased area with reanastomosis to the

rectosigmoid. Preservation of portions of the sigmoid colon may

lead to early recurrence of the disease. The benefits of laparoscopic

TABLE 328-2 The Use of Fiber in the Management of Diverticular Disease (DD)

JOURNAL, STUDY YEAR PATIENTS (N) INTERVENTION STUDY LENGTH FINDINGS

Lancet, 1977 18 Wheat or bran crisp bread 3 months Significant reduction of symptoms score

BMJ, 1981 58 Bran, ispaghula, placebo 16 weeks No difference

J Gastroenterol, 1977 30 Methylcellulose 3 months Significant reduction in symptoms

BMJ, 2011 47,033 Vegetarian vs nonvegetarian 11.6 years Vegetarians had a 31% lower risk of DD

Gastroenterology, 2012 2104 Fiber consumption 12 years Fiber associated with great risk of DD

JAMA, 2008 47,288 Nut, corn, popcorn

consumption

18 years Higher nut, corn, and popcorn had lower risk of

recurrence

Ann R Coll Surg Engl, 1985 56 Fiber consumption 66 months Higher fiber associated with 19% reduction in symptom

recurrence

Source: Modified from A Turis et al: Review article: The pathophysiology and medical management of diverticulosis and diverticular disease of the colon. Aliment Parmacol

Ther 42:664, 2015.

2500 PART 10 Disorders of the Gastrointestinal System

TABLE 328-3 American Society of Anesthesiologists Physical Status

Classification System

P1 A normal healthy patient

P2 A patient with mild systemic disease

P3 A patient with severe systemic disease

P4 A patient with severe systemic disease that is a constant

threat to life

P5 A moribund patient who is not expected to survive without the

operation

P6 A declared brain-dead patient whose organs are being removed for

donor purposes

TABLE 328-4 Outcome Following Surgical Therapy for Complicated Diverticular Disease Based on Modified Hinchey Staging

HINCHEY STAGE OPERATIVE PROCEDURE ANASTOMOTIC LEAK RATE, % OVERALL MORBIDITY RATE, %

Ia (pericolic phlegmon) Laparoscopic or open colon resection 43 15

Ib (pericolic abscess) Percutaneous drainage followed by laparoscopic or

open colon resection

3 15

II Percutaneous drainage followed by laparoscopic

or open colon resection +/− proximal diversion with

an ostomy

3 15

III Laparoscopic washout and drainage

Laparoscopic or open resection with proximal diversion

(ostomy)

Hartmann’s procedure

3 30% risk of peritonitis requiring reoperation if

no resection is performed.

Overall morbidity 50%

Overall mortality 15%

IV Hartmann’s procedure

Washout with proximal diversion

— Overall morbidity 50%

Overall mortality 15%

FIGURE 328-3 Methods of surgical management of complicated diverticular

disease. 1. Drainage, omental pedicle graft, and proximal diversion. 2. Hartmann’s

procedure. 3. Sigmoid resection with coloproctostomy. 4. Sigmoid resection with

coloproctostomy and proximal diversion.

resection over open surgical techniques include early discharge (by

at least 1 day), less narcotic use, less postoperative complications,

and an earlier return to work.

The options for the surgical management of complicated diverticular disease (Fig. 328-3) include the following open or laparoscopic procedures: (1) proximal diversion of the fecal stream with

an ileostomy or colostomy and sutured omental patch with drainage, (2) resection with colostomy and mucous fistula or closure of

distal bowel with formation of a Hartmann’s pouch (Hartmann’s

procedure), (3) resection with anastomosis (coloproctostomy), or

(4) resection with anastomosis and diversion (coloproctostomy

with loop ileostomy or colostomy). (5) Laparoscopic technique of

washout and drainage without diversion has been described for

Hinchey III patients; however, a threefold increased risk of recurrent peritonitis requiring reoperation with washout alone has been

reported.

Patients with Hinchey stage Ia are managed with antibiotic therapy only followed by resection with anastomosis at 6 weeks. Patients

with Hinchey stages Ib and II disease are managed with percutaneous drainage followed by resection with anastomosis about

6 weeks later. Current guidelines put forth by the American Society

of Colon and Rectal Surgeons suggest, in addition to antibiotic

therapy, CT-guided percutaneous drainage of diverticular abscesses

that are >3 cm and have a well-defined wall. Abscesses that are

<5 cm may resolve with antibiotic therapy alone. Contraindications

to percutaneous drainage are no percutaneous access route, pneumoperitoneum, and fecal peritonitis. Drainage of a diverticular

abscess is associated with a 20–25% failure rate. Urgent operative intervention is undertaken if percutaneous drainage fails and

patients develop generalized peritonitis, and most will need to be

managed with a Hartmann’s procedure (resection of the sigmoid

colon with end colostomy and rectal stump). In selected cases, nonoperative therapy may be considered. In one nonrandomized study,

nonoperative management of isolated paracolic abscesses (Hinchey

stage I) was associated with only a 20% recurrence rate at 2 years.

More than 80% of patients with distant abscesses (Hinchey stage II)

required surgical resection for recurrent symptoms.

The management of Hinchey stage III disease is under debate.

In this population of patients, no fecal peritonitis is present, and it

is presumed that the perforation has sealed. Historically, Hinchey

stage III has been managed with a Hartmann’s procedure or with

primary anastomosis and proximal diversion. Several studies have

examined short- and long-term outcomes for laparoscopic peritoneal lavage to remove the peritoneal contamination and place

drainage catheters should a communication to the bowel still exist.

However, this procedure has been associated with an increased risk

of requiring reoperation for ongoing peritonitis. Overall, ostomy

rates are lower with the use of laparoscopic peritoneal lavage. No

anastomosis of any type should be attempted in Hinchey stage IV

disease or in the presence of fecal peritonitis. A limited approach to

these patients is associated with a decreased mortality rate.

2501 Diverticular Disease and Common Anorectal Disorders CHAPTER 328

Recurrent Symptoms Recurrent abdominal symptoms following

surgical resection for diverticular disease occur in 10% of patients.

Recurrent diverticular disease develops in patients following inadequate surgical resection. A retained segment of diseased rectosigmoid

colon is associated with twice the incidence of recurrence. The presence of irritable bowel syndrome may also cause recurrence of initial

symptoms. Patients undergoing surgical resection for presumed diverticulitis and symptoms of chronic abdominal cramping and irregular

loose bowel movements consistent with irritable bowel syndrome have

poorer functional outcomes.

COMMON DISEASES OF THE ANORECTUM

■ RECTAL PROLAPSE (PROCIDENTIA)

Incidence and Epidemiology Rectal prolapse is six times more

common in women than in men. The incidence of rectal prolapse

peaks in women >60 years. Women with rectal prolapse have a higher

incidence of associated pelvic floor disorders including urinary incontinence, rectocele, cystocele, and enterocele. About 20% of children

with rectal prolapse will have cystic fibrosis. All children presenting

with prolapse should undergo a sweat chloride test. Less common

associations include Ehlers-Danlos syndrome, solitary rectal ulcer syndrome, congenital hypothyroidism, Hirschsprung’s disease, dementia,

cognitively impaired, and schizophrenia.

Anatomy and Pathophysiology Rectal prolapse (procidentia) is

a circumferential, full-thickness protrusion of the rectal wall through

the anal orifice. It is often associated with a redundant sigmoid colon,

pelvic laxity, and a deep rectovaginal septum (pouch of Douglas).

Initially, rectal prolapse was felt to be the result of early internal rectal

intussusception, which occurs in the upper to mid rectum. This was

considered to be the first step in an inevitable progression to full-thickness external prolapse. However, only 1 of 38 patients with internal

prolapse followed for >5 years developed full-thickness prolapse. Others have suggested that full-thickness prolapse is the result of damage

to the nerve supply to the pelvic floor muscles or pudendal nerves from

repeated stretching with straining to defecate. Damage to the pudendal

nerves would weaken the pelvic floor muscles, including the external

anal sphincter muscles. Bilateral pudendal nerve injury is more significantly associated with prolapse and incontinence than unilateral injury.

Presentation and Evaluation In external prolapse, the majority

of patient complaints include anal mass, bleeding per rectum, and poor

perianal hygiene. Prolapse of the rectum usually occurs following defecation and will spontaneously reduce or require the patient to manually reduce the prolapse. Constipation occurs in ~30–67% of patients

with rectal prolapse. Differing degrees of fecal incontinence occur in

50–70% of patients. Patients with internal rectal prolapse will present

with symptoms of both constipation and incontinence. Other associated findings include outlet obstruction (anismus) in 30%, colonic

inertia in 10%, and solitary rectal ulcer syndrome in 12%.

Office evaluation is best performed after the patient has been given

an enema, which enables the prolapse to protrude. An important

distinction should be made between full-thickness rectal prolapse

and isolated mucosal prolapse associated with hemorrhoidal disease

(Fig. 328-4). Mucosal prolapse is known for radial grooves rather than

circumferential folds around the anus and is due to increased laxity

of the connective tissue between the submucosa and underlying muscle of the anal canal. The evaluation of prolapse should also include

cystoproctography and colonoscopy. These examinations evaluate

for associated pelvic floor disorders and rule out a malignancy or a

polyp as the lead point for prolapse. If rectal prolapse is associated

with chronic constipation, the patient should undergo a defecating

proctogram and a sitzmark study. This will evaluate for the presence

of anismus or colonic inertia. Anismus is the result of attempting to

defecate against a closed pelvic floor and is also known as nonrelaxing

puborectalis. This can be seen when straightening of the rectum fails

to occur on fluoroscopy while the patient is attempting to defecate. In

colonic inertia, a sitzmark study will demonstrate retention of >20% of

markers on abdominal x-ray 5 days after swallowing. For patients with

fecal incontinence, endoanal ultrasound and manometric evaluation,

including pudendal nerve testing of their anal sphincter muscles, may

be performed before surgery for prolapse (see “Fecal Incontinence,”

below).

TREATMENT

Rectal Prolapse

The medical approach to the management of rectal prolapse is

limited and includes stool-bulking agents or fiber supplementation

to ease the process of evacuation. Surgical correction of rectal

prolapse is the mainstay of therapy. Two approaches are commonly

considered: transabdominal and transperineal. Transabdominal

approaches have been associated with lower recurrence rates, but

some patients with significant comorbidities are better served by a

transperineal approach.

Common transperineal approaches include a transanal proctectomy (Altmeier procedure), mucosal proctectomy (Delorme procedure), or placement of a Tirsch wire encircling the anus. The goal

of the transperineal approach is to remove the redundant rectosigmoid colon. Common transabdominal approaches include presacral suture or mesh rectopexy (Ripstein) with (Frykman-Goldberg)

or without resection of the redundant sigmoid. Colon resection,

in general, is reserved for patients with constipation and outlet

obstruction. Ventral rectopexy is an effective method of abdominal repair of full-thickness prolapse that does not require sigmoid

resection (see description below). This repair may have improved

functional results over other abdominal repairs. Transabdominal

procedures can be performed effectively with laparoscopic and,

more recently, robotic techniques without increased incidence of

recurrence. The goal of the transabdominal approach is to restore

normal anatomy by removing redundant bowel and reattaching the

supportive tissue of the rectum to the presacral fascia. The final

alternative is abdominal proctectomy with end-sigmoid colostomy. If total colonic inertia is present, as defined by a history of

A C

B D

FIGURE 328-4 Degrees of rectal prolapse. Mucosal prolapse only (A, B, sagittal

view). Full-thickness prolapse associated with redundant rectosigmoid and deep

pouch of Douglas (C, D, sagittal view).

2502 PART 10 Disorders of the Gastrointestinal System

constipation and a positive sitzmark study, a subtotal colectomy

with an ileosigmoid or rectal anastomosis may be required at the

time of rectopexy.

Previously, the presence of internal rectal prolapse identified

on imaging studies has been considered a nonsurgical disorder,

and biofeedback was recommended. However, only one-third of

patients will have successful resolution of symptoms from biofeedback. Two surgical procedures more effective than biofeedback are

the stapled transanal rectal resection (STARR) and the laparoscopic

ventral rectopexy (LVR). The STARR procedure (Fig. 328-5) is

performed through the anus in patients with internal prolapse. A

circular stapling device is inserted through the anus; the internal

prolapse is identified and ligated with the stapling device. LVR

(Fig. 328-6) is performed through an abdominal approach. An

opening in the peritoneum is created on the left side of the rectosigmoid junction, and this opening continues down anterior on the

rectum into the pouch of Douglas. No rectal mobilization is performed, thus avoiding any autonomic nerve injury. Mesh is secured

to the anterior and lateral portion of the rectum, the vaginal fornix,

and the sacral promontory, allowing for closure of the rectovaginal

septum and correction of the internal prolapse. In both procedures,

recurrence at 1 year was low (<10%), and symptoms improved in

more than three-fourths of patients.

■ FECAL INCONTINENCE

Incidence and Epidemiology Fecal incontinence is the involuntary passage of fecal material for at least 1 month in an individual

with a developmental age of at least 4 years. The prevalence of fecal

incontinence in the United States is 0.5–11%. The majority of patients

are women and aged >65. A higher incidence of incontinence is seen

among parous women. One-half of patients with fecal incontinence

also suffer from urinary incontinence. The majority of incontinence

is a result of obstetric injury to the pelvic floor, either while carrying a

fetus or during the delivery. An anatomic sphincter defect may occur in

up to 32% of women following childbirth regardless of visible damage

to the perineum. Risk factors at the time of delivery include prolonged

labor, the use of forceps, and the need for an episiotomy. Symptoms of

incontinence can present two or more decades after obstetric injury.

Medical conditions known to contribute to the development of fecal

incontinence are listed in Table 328-5.

Anatomy and Pathophysiology The anal sphincter complex

is made up of the internal and external anal sphincter. The internal

sphincter is smooth muscle and a continuation of the circular fibers of

the rectal wall. It is innervated by the intestinal myenteric plexus and

is therefore not under voluntary control. The external anal sphincter

is formed in continuation with the levator ani muscles and is under

voluntary control. The pudendal nerve supplies motor innervation to

the external anal sphincter. Obstetric injury may result in tearing of

the muscle fibers anteriorly at the time of the delivery. This results in

an obvious anterior defect on endoanal ultrasound. Injury may also be

the result of stretching of the pudendal nerves during pregnancy or

delivery of the fetus through the birth canal.

Presentation and Evaluation Patients may suffer with varying

degrees of fecal incontinence. Minor incontinence includes incontinence

to flatus and occasional seepage of liquid stool. Major incontinence is

frequent inability to control solid waste. As a result of fecal incontinence,

patients suffer from poor perianal hygiene. Beyond the immediate

FIGURE 328-5 Stapled transanal rectal resection. Schematic of placement of the

circular stapling device.

FIGURE 328-6 Laparoscopic ventral rectopexy (LVR). To reduce the internal prolapse

and close any rectovaginal septal defect, the pouch of Douglas is opened and mesh

is secured to the anterolateral rectum, vaginal fornix, and sacrum. (Reproduced

with permission from A D’Hoore et al: Long-term outcome of laparoscopic ventral

rectopexy for total rectal prolapse. B J S 91:1500, 2004.)

TABLE 328-5 Medical Conditions That Contribute to Symptoms of

Fecal Incontinence

Neurologic Disorders

• Dementia

• Brain tumor

• Stroke

• Multiple sclerosis

• Tabes dorsalis

• Cauda equina lesions

Skeletal Muscle Disorders

• Myasthenia gravis

• Myopathies, muscular dystrophy

Miscellaneous

• Hypothyroidism

• Irritable bowel syndrome

• Diabetes

• Severe diarrhea

• Scleroderma