# 09 - 339 Diverticular Disease and Common Anorectal Disorders

### 339 Diverticular Disease and Common Anorectal Disorders

patients, increased fiber intake and the use of osmotic agents such as 
PEG may achieve satisfactory results. For patients with more severe 
constipation, a chloride channel opener (lubiprostone) or GC-C ago­
nist (linaclotide or plecanatide) or NHE3 inhibitor (tenapanor) may 
be considered. For IBS patients with predominant gas and bloating, 
a low FODMAP diet may provide significant relief. Some patients 
may benefit from probiotics and rifaximin treatment. A small pro­
portion 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 neuromodulators and other psychological treatments (Table 
338-4). Clinical trials demonstrating success of a low FODMAP diet 
in improving IBS symptoms and quality of life provide strong evi­
dence 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
Chang L et al: AGA Clinical Practice Guideline on the pharmaco­
logical management of irritable bowel syndrome with constipation. 
Gastroenterology 163:118, 2022.
Dionne J et al: A systematic review and meta-analysis 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.
Lembo A et al: AGA Clinical Practice Guideline on the pharmacologi­
PART 10
Disorders of the Gastrointestinal System
cal management of irritable bowel syndrome with diarrhea. Gastro­
enterology 163:137, 2022.
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 lipo­
polysaccharide-mediated intestinal barrier dysfunction and intestinal 
inflammation. J Clin Invest 128:267, 2018.
Susan L. Gearhart

Diverticular Disease 

and Common Anorectal 
Disorders
■
■DIVERTICULAR DISEASE
Incidence and Epidemiology 
In the United States, diverticulosis 
affects one-half of the population aged >60 years, and the majority 
of affected individuals will have no associated symptoms. However, 
studies have shown that ~5% of individuals with diverticulosis will 
develop acute diverticular disease. In addition, 10–25% of individu­
als 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 and most prevalent 
among middle-aged individuals. The majority of patients with diver­
ticular 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 develop­
ing 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. Known risk factors for 
the development of diverticular disease include the use of nonsteroidal 
anti-inflammatory drugs (NSAIDS), aspirin, steroids, opioids, smok­
ing, and sedentary lifestyle.
Anatomy and Pathophysiology 
Two types of diverticula occur 
in the intestine: true and false (or pseudodiverticula). A true diverticu­
lum is a saclike herniation of the entire bowel wall, whereas a pseudo­
diverticulum involves only a protrusion of the mucosa and submucosa 
through the muscularis propria of the colon (Fig. 339-1). The type of 
diverticulum most commonly seen in the colon is the pseudodiver­
ticulum. 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. Diverticula are most com­
monly encountered in the sigmoid colon. This anatomic restriction 
may be a result of the relative high-pressure zone within the muscular 
sigmoid colon. Higher-amplitude contractions combined with consti­
pated, high-fat-content stool within the sigmoid lumen in an area of 
weakness in the colonic wall result in the creation of these diverticula. 
FIGURE 339-1  Gross and microscopic view of sigmoid diverticular disease. Arrows 
mark an inflamed diverticulum with the diverticular wall made up only of mucosa.

Consequently, the vasa recta is either compressed or eroded, leading to 
either perforation or bleeding.
As mentioned above, diverticula commonly affect the left and 
sigmoid colon; the rectum is always spared. However, in Asian popula­
tions, 70% of diverticula are seen in the right colon and cecum. Diver­
ticulitis is inflammation of a diverticulum. Previous understanding of 
the pathogenesis of diverticulosis attributed the disease to poor dietary 
choices, and the onset of diverticulitis would occur acutely when these 
diverticula become obstructed. However, evidence now suggests that 
the pathogenesis is more complex and multifactorial. Better under­
standing 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. Studies have also 
shown that it is more common for patients with diverticular disease 
to have abnormal collagen cross-linking. Researchers hypothesize that 
abnormal collagen cross-linking leads to loss of intestinal compliance 
and, therefore, higher intraluminal pressure, leading to pockets or 
outpouchings.
A newer approach to examine causality in diseases such as diverticu­
litis is to examine genome-wide associations (GWAs) using a variety of 
biobanks. Biobanks from Iceland, Denmark, and the United Kingdom 
have been examined for GWAs in diverticular disease and identified 
LAMB4 and TNFSF15 variants to be associate with early-onset, severe 
diverticular disease in otherwise healthy families. Although the exact 
function these genes play in the development of diverticular disease is 
unknown, the protein encoded by the gene LAMB4 is part of the extra­
cellular matrix lamin family, whereas the protein encoded by the gene 
TNFSF15 is a member of the tumor necrosis family, which has implica­
tions in inflammation.
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 atheroscle­
rosis, and regularly use anticoagulants and NSAIDs. Additional risk 
factors include obesity and a history of diabetes mellitus. Of note, due 
to increased use of anticoagulants in our aging population, there has 
been a rise in the incidence of diverticular bleeding. 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 medi­
cine 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%. Longterm 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, 
placement of a detachable snare, and over-the-scope hemoclip have 
been shown to be effective methods to obtain hemostasis if the bleed­
ing site can be localized. These approaches have 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 refractory to angiographic or endoscopic treatments, 
unstable, or has required a large-volume transfusion, current recom­
mendations 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 

TABLE 339-1  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%
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 characteristically presents with 
fever, anorexia, left lower quadrant abdominal pain, and obstipa­
tion (Table 339-1). 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 without the collection of 
contrast material or fluid. Additional syndromes have been identified 
that relate to the presence of diverticulosis or diverticular disease. 
Symptomatic colitis-associated diverticulosis (SCAD) is uncommon 
(<1% of patients with diverticulosis) and occurs when inflammation 
is identified between the diverticula on endoscopic assessment. Symp­
toms of SCAD mimic irritable bowel disease. Symptomatic uncom­
plicated diverticular disease (SUDD) is a condition seen in patients 
with known diverticular disease and ongoing abdominal pain without 
evidence of overt inflammation on radiographic imaging.
CHAPTER 339
Diverticular Disease and Common Anorectal Disorders 
Complicated diverticular disease is defined as diverticular disease 
associated with an abscess or perforation and less commonly with a 
fistula (Table 339-1). Symptoms of complicated diverticular disease 
may be similar to uncomplicated disease, or patients may exhibit signs 
of peritonitis indicating the presence of a diverticular perforation. If a 
pericolonic abscess has formed, the patient may have abdominal dis­
tention and signs of localized peritonitis. Laboratory investigations 
often demonstrate a leukocytosis. Rarely, a patient may present with 
an air-fluid level in the left lower quadrant on plain abdominal film. 
This should raise a concern for a giant diverticulum of the sigmoid 
colon and is managed with resection to avoid impending perforation.
Perforated diverticular disease is staged using the Hinchey clas­
sification system (Fig. 339-2). This staging system was developed to 
predict outcomes following the surgical management of complicated 
diverticular disease. The Hinchey staging system has been modified 
to include the development of a phlegmon or early abscess (Hinchey 
stage Ia). 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
Medical Management of Diverticular Disease
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 diver­
ticular disease are limited (Table 339-2), patients may benefit from 
a fiber-enriched diet or supplements that include 30 g of fiber 
each day. The use of fiber decreases colonic transit time and, 
therefore, prevents increased intraluminal pressure, leading to the

Abscess
I
II
Feces
III
IV
FIGURE 339-2  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.
PART 10
Disorders of the Gastrointestinal System
development of diverticulosis. The incidence of complicated diver­
ticular 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.
ANTIBIOTICS
The routine use of antibiotics in uncomplicated diverticular disease 
does not appear to reduce time to symptom resolution or reduce the 
risk of complications or recurrence. Two large, randomized trials 
(the AVOD trial and the Diabolo trial) and a large meta-analysis 
demonstrated that immunocompetent patients with uncomplicated 
diverticular disease had no difference in time to symptom resolu­
tion, recurrence rates, development of complicated diverticular 
disease, or surgery if treated with or without antibiotics. Currently, 
patients who are immunocompromised, have findings of extensive 
inflammation on radiographic studies, are at risk for disease pro­
gression, or have computed tomography (CT) findings of compli­
cated diverticular disease should be treated with antibiotics. Known 
risk factors for disease progression included the American Society 
of Anesthesiologists (ASA) classification of III or IV, >5 days of 
TABLE 339-2  The Use of Fiber in the Management of Diverticular Disease (DD)
JOURNAL, STUDY YEAR
PATIENTS (N)
INTERVENTION
STUDY LENGTH
FINDINGS
Lancet, 1977

Wheat or bran crisp bread
3 months
Significant reduction of symptoms score
BMJ, 1981

Bran, ispaghula, placebo
16 weeks
No difference
J Gastroenterol, 1977

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

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

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.

symptoms, and elevation of C-reactive protein (CRP) or white 
blood cell (WBC) count.
If the use of antimicrobial therapy is desired, the current recom­
mended antimicrobial coverage for uncomplicated acute diverticu­
litis is a third-generation cephalosporin (or ciprofloxacin if there is 
a known allergy to cephalosporins) and metronidazole targeting a 
mixed flora. 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 5 days. A 
study compared the use of intravenous (IV) versus oral antibiot­
ics in uncomplicated diverticular disease and noted no difference 
in recovery time or progression of the disease and recommended 
that safe home treatment on oral antibiotics after a 6-h observation 
in the emergency department is reasonable. Exclusion criteria for 
home treatment included complicated diverticular disease, immu­
nocompromised patient, significant active comorbidities, poor 
social support, or a decline during observation.
DIET AND OTHER MEDICAL THERAPIES
Patients should remain on a limited diet until their pain resolves. 
The use of anti-inflammatory medications (mesalazine) in ran­
domized 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 CRP and computer­
ized imaging are taken into consideration, no benefit for the use of 
mesalazine has been shown.
Probiotics are increasingly used by gastroenterologists for mul­
tiple bowel disorders and may prevent recurrence of diverticulitis. 
Specifically, probiotics containing Lactobacillus acidophilus and 
Bifidobacterium strains may be beneficial; however, a systematic 
review was unable to show any benefit to the use of probiotics alone. 
The addition of fiber or mesalazine with probiotics has shown some 
promise in maintaining 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.
COLONOSCOPY
Colonoscopy should be considered ~6 weeks after the first episode 
of uncomplicated diverticular disease and after the development 
of complicated diverticular disease as the overall prevalence of 
colon cancer is low in these patients (<2%) but higher incidence 
has been seen with complicated diverticulitis (6–8%). The parallel 
epidemiology of colorectal cancer and diverticular disease provides 
enough concern for an endoscopic evaluation before operative 
management.
SURGICAL MANAGEMENT OF DIVERTICULAR DISEASE
Preoperative risk factors influencing postoperative mortality rates 
include higher ASA physical status class (Table 339-3) and pre­
existing 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 dis­
ease, medical therapy can be continued beyond two attacks without 
an increased risk of perforation requiring a colostomy. However,

TABLE 339-3  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
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 conserva­
tive 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 com­
pared to conservative management. Surgical therapy is generally 
indicated in all low-surgical-risk patients with complicated diver­
ticular disease. A randomized trial (LASER trial) examined the use 
of laparoscopic surgery for refractory or complicated diverticular 
disease and demonstrated improved quality of life and a reduction 
in recurrent symptoms by 50% when compared to conservative 
treatment.
The goals of surgical management of diverticular disease include 
controlling sepsis, eliminating complications such as fistula or 
obstruction, removing the diseased colonic segment, and restor­
ing intestinal continuity. Table 339-4 lists the operations most 
commonly indicated based on the Hinchey classification and the 
predicted postoperative outcomes. The current options for uncom­
plicated diverticular disease include an open or a minimally inva­
sive 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 minimally 
invasive 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 diver­
ticular disease (Fig. 339-3) include the following open or minimally 
invasive procedures: (1) proximal diversion of the fecal stream with 
an ileostomy or colostomy and sutured omental patch with drain­
age, (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 
TABLE 339-4  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

Ib (pericolic abscess)
Percutaneous drainage followed by laparoscopic or open 
colon resection
II
Percutaneous drainage followed by laparoscopic or open colon 
resection +/− proximal diversion with an ostomy
III
Laparoscopic washout and drainage
or
Laparoscopic or open resection with proximal diversion (ostomy)
or
Hartmann’s procedure
IV
Hartmann’s procedure
or
Washout with proximal diversion

recurrent peritonitis requiring reoperation with washout alone has 
been reported. Robotic surgery resection for complicated diverticu­
lar disease is associated with a lower rate of conversion to an open 
procedure.

Patients with Hinchey stage Ia may be managed with antibiotic 
therapy only or followed by resection with anastomosis following 
further workup and symptom resolution. Patients with Hinchey 
stages Ib and II disease are managed with percutaneous drainage 
followed by resection with anastomosis following further evalu­
ation and symptom resolution. 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 per­
cutaneous 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 percu­
taneous 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 stapling of 
the rectosigmoid distal to the diseased segment). In selected cases, 
nonoperative therapy may be considered.
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 peri­
toneal 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.
CHAPTER 339
Diverticular Disease and Common Anorectal Disorders 
Recurrent Symptoms 
Recurrent abdominal symptoms following 
surgical resection for diverticular disease occur in 10% of patients. 
Recurrent diverticular disease develops in patients following inad­
equate surgical resection. A retained segment of diseased rectosigmoid 
colon is associated with twice the incidence of recurrence. The pres­
ence of irritable bowel syndrome may also cause recurrence of initial 
symptoms. Patients undergoing surgical resection for presumed diver­
ticulitis and symptoms of chronic abdominal cramping and irregular 
loose bowel movements consistent with irritable bowel syndrome have 
poorer functional outcomes.

30% risk of peritonitis requiring 
reoperation if no resection is 
performed.
Overall morbidity 50%
Overall mortality 15%
—
Overall morbidity 50%
Overall mortality 15%

FIGURE 339-3  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.
PART 10
Disorders of the Gastrointestinal System
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 incon­
tinence, 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 syn­
drome, 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 believed 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 pro­
lapse. 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 identified significantly more with full-thickness prolapse and fecal 
incontinence than unilateral injury.
Presentation and Evaluation 
In external prolapse, patient com­
plaints include a palpable anal mass, bleeding per rectum, leakage of 
blood and mucus, 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 

A
C
B
D
FIGURE 339-4  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).
of fecal incontinence occur in 50–70% of patients. Patients with inter­
nal rectal prolapse will present with symptoms of both constipation 
and incontinence. Other associated findings include outlet obstruc­
tion (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 dis­
tinction should be made between full-thickness rectal prolapse and 
isolated mucosal prolapse associated with hemorrhoidal disease 
(Fig. 339-4). 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.
TREATMENT
Rectal Prolapse
The medical approach to the management of rectal prolapse is 
limited and includes stool-bulking agents or fiber supplementa­
tion to ease the process of evacuation. Surgical correction of rectal 
prolapse is the mainstay of therapy. Previously, the presence of 
internal rectal prolapse identified on imaging studies has been con­
sidered a nonsurgical disorder, and biofeedback was recommended. 
However, only one-third of patients will have successful resolution 
of symptoms from biofeedback. 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 proctec­
tomy (Altmeier procedure), mucosal proctectomy (Delorme proce­
dure), 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. Ven­
tral rectopexy is an effective method of abdominal repair of internal 
and full-thickness prolapse that does not require sigmoid resection. 
This repair has been shown to have improved pelvic floor functional 
results over other abdominal repairs. Transabdominal procedures 
can be performed effectively with laparoscopic and robotic tech­
niques. Short- and long-term recurrence rates are low (<10%), and 
symptoms improved in more than three-fourths of patients.
■
■FECAL INCONTINENCE
Incidence and Epidemiology 
Fecal incontinence is the involun­
tary passage of fecal material or the inability to control the initiation 
of defecation. The prevalence of fecal incontinence in adults in the 
United States approaches 15% and is expected to increase given our 
aging population. A higher incidence of incontinence is seen among 
older parous women. One-half of patients with fecal incontinence also 
suffer from urinary incontinence. The cause of fecal incontinence is 
often multifactorial; however, the majority of women with fecal incon­
tinence are parous and may have experienced obstetrical 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 con­
tribute to the development of fecal incontinence are listed in Table 339-5.
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. Fecal incontinence is classified into three 
categories based on the clinical presentation. These categories include 
TABLE 339-5  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

passive incontinence (passage of stool without awareness), urge incon­
tinence (leakage of stool despite attempts at holding), and fecal seep­
age (seepage of residue generally following defecation associated with 
normal continence). Beyond the immediate problems associated with 
fecal incontinence, these patients are often withdrawn and suffer from 
depression. For this reason, quality-of-life measures are an important 
component in the evaluation of patients with fecal incontinence.

The evaluation of fecal incontinence should include a thorough 
history and physical examination including digital rectal examination 
(DRE). Weak sphincter tone on DRE and loss of the “anal wink” reflex 
(S1-level control) may indicate a neurogenic dysfunction. Perianal 
scars may represent surgical injury. Other studies helpful in the diag­
nosis of fecal incontinence include anal manometry, pudendal nerve 
terminal motor latency (PNTML), and endoanal ultrasound. Centers 
that care for patients with fecal incontinence will have an anorectal 
physiology laboratory that uses standardized methods of evaluating 
anorectal physiology. Pudendal nerve studies evaluate the function of 
the nerves innervating the anal canal using a finger electrode placed in 
the anal canal. Stretch injuries to these nerves will result in a delayed 
response of the sphincter muscle to a stimulus, indicating a prolonged 
latency. Finally, endoanal ultrasound will evaluate the extent of the 
injury to the sphincter muscles before surgical repair. Unfortunately, 
all of these investigations are user-dependent, and very few studies 
demonstrate that these studies predict outcome following an interven­
tion. Magnetic resonance imaging (MRI) has also been utilized in the 
evaluation of the sphincter muscle complex in treatment planning for 
fecal incontinence, but its role has not been well-established.
Rarely does a pelvic floor disorder exist alone. The majority of 
patients with fecal incontinence will have some degree of urinary 
incontinence. Similarly, fecal incontinence is a part of the spectrum 
of pelvic organ prolapse. For this reason, patients may present with 
symptoms of obstructed defecation as well as fecal incontinence. Care­
ful evaluation including dynamic MRI or cinedefecography should 
be performed to search for other associated defects. Surgical repair 
of incontinence without attention to other associated defects may 
decrease the success of the repair.
CHAPTER 339
Diverticular Disease and Common Anorectal Disorders 
TREATMENT
Fecal Incontinence
Medical management of fecal incontinence includes strategies to 
bulk up the stool, which help in increasing fecal sensation and 
complete evacuation. Stool bulking agents include fiber supple­
mentation, loperamide, diphenoxylate, and bile acid binders. These 
agents help to bind the stool, resulting in more complete evacuation 
and decreasing the frequency of bowel movements. This can be 
particularly helpful in patients with mild symptoms of fecal incon­
tinence. Patients may be offered a form of physical therapy called 
biofeedback. This therapy helps strengthen the external sphincter 
muscle while training the patient to relax with defecation to avoid 
unnecessary straining and further injury to the sphincter muscles. 
At a minimum, biofeedback is risk-free and most patients will have 
some improvement. For this reason, it should be incorporated into 
the initial recommendation to all patients with fecal incontinence. 
It is important to note that there is no medical or surgical therapy to 
reduce incontinence of flatus. Dietary alterations to reduce gas pro­
duction and the use of probiotics are the only antidotal remedies.
Historically, the “gold standard” for the treatment of fecal incon­
tinence with an isolated sphincter defect has been the overlapping 
sphincteroplasty. The external anal sphincter muscle and scar tis­
sue, as well as any identifiable internal sphincter muscle, are dis­
sected free from the surrounding adipose and connective tissue. An 
overlapping sphincter repair is performed in an attempt to rebuild 
the muscular ring and restore its function. However, long-term 
results following overlapping sphincteroplasty have been poor, with 
a 50% failure rate over 5 years.
Alternative therapies for the treatment of fecal incontinence 
included sacral nerve modulation, collagen-enhancing injectables,

and anal implantable self-expanding prostheses (THD Gatekeeper 
and Sphinkeeper). Sacral nerve stimulation (SNS) was the first 
implantable pacemaker and is a U.S. Food and Drug Administra­
tion (FDA)-approved adaptation of a procedure developed for the 
management of urinary incontinence. SNS is indicated in patients 
with two or more episodes of frank fecal incontinence per week. 
Long-term results for SNS have been promising, with nearly 80% of 
patients having a reduction in incontinence episodes by at least 50%. 
There are inherent challenges with the SNS device, and to avoid these 
challenges, percutaneous or transcutaneous tibial nerve stimulation 
(PTNS or TTNS) is being offered to patients with fecal incontinence. 
PTNS is offered in a clinical setting, while TTNS can be performed at 
home. Both require weekly sessions of stimulation of the tibial nerve, 
which serves to feedback to the third sacral nerve root. Collagenenhancing injectables and anal self-expanding implants have been 
around for several years. Results from randomized trials have been 
variable but support the use of injectables/implantables in patients 
who are not candidates for sacral nerve modulation.

Finally, the use of stem cells to increase the bulk of the sphincter 
muscles is currently being tested. Stem cells can be harvested from 
the patient’s own muscle, grown, and then implanted into their 
sphincter complex. Concern for cost and the need for an additional 
procedure have dampened enthusiasm.
MIXED CONSTIPATION AND FECAL INCONTINENCE
It is estimated that up to 20% of patients presenting for evaluation of 
fecal incontinence have mixed constipation and fecal incontinence. 
Fecal incontinence, in this instance, is related to the large number 
of laxatives required to produce stool evacuation. This condition 
is more difficult to manage and often requires close collaboration 
with different specialties. One promising intervention is the use of 
a transanal irrigation system (Peristeen by Coloplast). This system 
provides daily irrigations of the left side of the colon to assist with 
evacuations and has shown promising results. The daily assistance 
with evacuation leads to less need for oral laxatives and reduced 
episodes of incontinence. One drawback is long-term adherence to 
the irrigations.
PART 10
Disorders of the Gastrointestinal System
■
■HEMORRHOIDAL DISEASE
Incidence and Epidemiology 
Symptomatic hemorrhoids 
affect >1 million individuals in the Western world per year. Hemor­
rhoidal disease can occur at any age and affects females and males 
at similar rates. The prevalence of hemorrhoidal disease is less in 
developing countries. The typical low-fiber, high-fat diet prominent 
in developed countries is associated with constipation and straining 
and the development of symptomatic hemorrhoids. Other risk fac­
tors for hemorrhoids include pregnancy and high-impact activities 
(bike riding).
Anatomy and Pathophysiology 
Hemorrhoidal cushions are a 
normal part of the anal canal. The vascular structures contained within 
this tissue aid in continence by preventing damage to the sphincter 
muscle. Three main hemorrhoidal complexes traversing the anal canal 
include the left lateral, the right anterior, and the right posterior. Pro­
longed engorgement with straining leads to prolapse of this tissue into 
the anal canal. Over time, the anatomic support system of the hemor­
rhoidal complex weakens, exposing this tissue to the outside of the 
anal canal where it is susceptible to injury. Hemorrhoids are commonly 
classified as external or internal. External hemorrhoids originate below 
the dentate line and are covered with squamous epithelium and are not 
associated with an internal component. Internal hemorrhoids originate 
above the dentate line and are covered with mucosa and transitional 
zone epithelium and represent the majority of hemorrhoids.
Presentation and Evaluation 
Patients commonly present to a 
physician for two reasons: bleeding and protrusion. Pain is less com­
mon than with fissures and, if present, is described as a dull ache from 
engorgement of the hemorrhoidal tissue. Severe pain may indicate a 
thrombosed external hemorrhoid. Hemorrhoidal bleeding is described 

as painless bright red blood seen either in the toilet or upon wiping. 
Occasional patients can present with significant bleeding, which may 
be a cause of anemia; however, the presence of a colonic neoplasm 
must be ruled out in anemic patients, especially given the noted rise in 
young patients with colorectal cancer. Patients who present with pro­
truding tissue complain about inability to maintain perianal hygiene 
and anal itching (pruritis) and are often concerned about the presence 
of a malignancy.
The diagnosis of hemorrhoidal disease is made on physical exami­
nation. Inspection of the perianal region for evidence of thrombosis 
or excoriation is performed, followed by a careful digital examination. 
Anoscopy is performed paying particular attention to the known posi­
tion of hemorrhoidal disease. The patient is asked to strain. It is impor­
tant to differentiate the circumferential appearance of a full-thickness 
rectal prolapse from the radial nature of prolapsing hemorrhoids (see 
“Rectal Prolapse,” above). The stage and location of the hemorrhoidal 
complexes are defined.
TREATMENT
Hemorrhoidal Disease
The treatment for bleeding hemorrhoids is based on the stage of the 
disease (Table 339-6). In all patients with bleeding, the possibility 
of other causes must be considered, and further studies should 
include endoscopic assessments.
With rare exceptions, the acutely thrombosed hemorrhoid can be 
excised within the first 48 h by performing an elliptical excision and 
clot extraction. This can often be performed at the bedside with local 
anesthesia; sitz baths, fiber, and stool softeners are prescribed. Addi­
tional nonoperative therapies for bleeding hemorrhoids include rub­
ber band ligation, infrared coagulation, and sclerotherapy. Sensation 
begins at the dentate line; therefore, all procedures can be performed 
without discomfort either endoscopically or in the office. Bands are 
placed around the engorged tissue, causing ischemia and fibrosis. 
This aids in fixing the tissue proximally in the anal canal. Patients 
may complain of a dull ache for 24 h following band application. 
During sclerotherapy, 1–2 mL of a sclerosant (usually sodium tetra­
decyl sulfate) is injected using a 25-gauge needle into the submucosa 
of the hemorrhoidal complex. Care must be taken not to inject the 
anal canal circumferentially, or stenosis may occur.
For surgical management of hemorrhoidal disease, excisional 
hemorrhoidectomy with sharp dissection (Milligan-Morgan 
hemorrhoidectomy), bipolar electrocautery ligation (LigaSure), 
transhemorrhoidal dearterialization (THD), and stapled hemor­
rhoidectomy (“the procedure for prolapse or hemorrhoids” [PPH]) 
are the procedures of choice. All surgical methods of management 
TABLE 339-6  The Staging and Treatment of Hemorrhoids
DESCRIPTION OF 
CLASSIFICATION
TREATMENT
STAGE
I
Enlargement with 
bleeding
Fiber supplementation
Short course of cortisone suppository
Sclerotherapy
Infrared coagulation
II
Protrusion with 
spontaneous reduction
Fiber supplementation
Short course of cortisone suppository
Sclerotherapy
Infrared coagulation
III
Protrusion requiring 
manual reduction
Fiber supplementation
Short course of cortisone suppository
Rubber band ligation
Operative hemorrhoidectomy
IV
Irreducible protrusion
Fiber supplementation
Cortisone suppository
Operative hemorrhoidectomy

are equally effective in the treatment of symptomatic third- and 
fourth-degree hemorrhoids. Current postprocedure outcomes fol­
lowing hemorrhoidectomy target improvements in bleeding, pain, 
and recurrence rates. The sutured hemorrhoidectomy involves the 
removal of redundant tissue down to the anal verge, and unpleasant 
anal skin tags are removed as well. However, pain and postopera­
tive bleeding are more common. The stapled hemorrhoidectomy is 
associated with less discomfort; however, this procedure does not 
remove anal skin tags, and an increased number of complications 
are associated with use of the stapling device. THD uses ultrasound 
guidance to ligate the blood supply to the anal tissue, hence reduc­
ing hemorrhoidal engorgement. Ligation with electrocautery uses a 
bipolar device (LigaSure) to remove the unwanted prolapsed tissue. 
Both THD and ligation with electrocautery have demonstrated 
similar short-term and long-term results; however, ligation with 
electrocautery requires less operative time. No procedures on hem­
orrhoids should be done in patients who are immunocompromised 
or who have active proctitis. Emergent hemorrhoidectomy for 
bleeding hemorrhoids is associated with a higher complication rate.
Acute complications associated with the treatment of hemor­
rhoids include pain, infection, recurrent bleeding, and urinary 
retention. Care should be taken to place bands properly and to 
avoid overhydration in patients undergoing operative hemorrhoid­
ectomy. Late complications include fecal incontinence as a result 
of injury to the sphincter during the dissection. Anal stenosis 
may develop from overzealous excision, with loss of mucosal skin 
bridges for reepithelialization. Finally, an ectropion (prolapse of 
rectal mucosa from the anal canal) may develop. Patients with an 
ectropion complain of a “wet” anus as a result of inability to prevent 
soiling once the rectal mucosa is exposed below the dentate line.
■
■ANORECTAL ABSCESS
Incidence and Epidemiology 
The development of a perianal 
abscess is more common in men than women by a ratio of 3:1. The 
peak incidence is in the third to fifth decade of life. Perianal pain asso­
ciated with the presence of an abscess accounts for 15% of office visits 
to a colorectal surgeon. The disease is more prevalent in immunocom­
promised patients such as those with diabetes, hematologic disorders, 
or inflammatory bowel disease (IBD) and persons who are HIV posi­
tive. These disorders should be considered in patients with recurrent 
perianal infections.
Anatomy and Pathophysiology 
An anorectal abscess is an 
abnormal fluid-containing cavity in the anorectal region. Anorectal 
abscess results from an infection involving the glands surrounding 
the anal canal. Normally, these glands release mucus into the anal 
canal, which aids in defecation. When stool accidentally enters the 
anal glands, the glands become infected, and an abscess develops. 
Anorectal abscesses are perianal in 40–50% of patients, ischiorectal in 
20–25%, intersphincteric in 2–5%, and supralevator in 2.5% (Fig. 339-5).
Presentation and Evaluation 
Perianal pain and fever are the 
hallmarks of an abscess. Patients may have difficulty voiding and have 
blood in the stool. On physical examination, a large fluctuant area is 
usually readily visible. Routine laboratory evaluation shows an elevated 
WBC count. Diagnostic procedures are rarely necessary unless evalu­
ating a recurrent abscess. A CT scan or MRI has an accuracy of 80% 
in determining incomplete drainage. If there is a concern about the 
presence of IBD, a rigid or flexible sigmoidoscopic examination may 
be done at the time of drainage to evaluate for inflammation within the 
rectosigmoid region. A more complete evaluation for Crohn’s disease 
would include a full colonoscopy and small-bowel enterography.
TREATMENT
Anorectal Abscess
As with all abscesses, the “gold standard” is drainage. Office drainage 
of an uncomplicated anorectal abscess may suffice. A small incision 

Fistula
tracts
Abscesses
Supralevator

Intersphincteric
Ischiorectal

Perianal

Intersphincteric

Extrasphincteric

Trans-sphincteric

Suprasphincteric
FIGURE 339-5  Common locations of anorectal abscess (left) and fistula in ano (right).
close to the anal verge is made, and a Mallenkot drain is advanced 
into the abscess cavity. The Mallenkot catheter (a mushroom-shaped 
catheter with grooves) can be maintained by the patient for up to 

1 week before being removed to avoid tissue ingrowth. For patients 
with a complicated abscess or who are diabetic or immunocompro­
mised, drainage should be performed in an operating room under 
anesthesia. These patients are at greater risk for developing necrotiz­
ing fasciitis. The role of antibiotics in the management of anorectal 
abscesses is limited. Antibiotics are only warranted in patients who 
are immunocompromised or have obvious cellulitis on physical exam.
CHAPTER 339
■
■FISTULA IN ANO
Diverticular Disease and Common Anorectal Disorders 
Incidence and Epidemiology 
The incidence of fistulizing peri­
anal disease parallels the incidence of anorectal abscess and is esti­
mated to be 1 in 10,000 individuals. Some 30–40% of abscesses will 
give rise to an anal fistula. Although the majority of the fistulas are 
cryptoglandular in origin, 10% are associated with IBD, tuberculosis, 
malignancy, and radiation.
Anatomy and Pathophysiology 
An anal fistula is defined as 
a communication of an abscess cavity with an identifiable internal 
opening within the anal canal. This identifiable opening is commonly 
located at the dentate line where the anal glands enter the anal canal. 
Patients experiencing continuous drainage at 1 month following the 
treatment of a perianal abscess likely have an anal fistula. These fistulas 
are classified by their relationship to the anal sphincter muscles, with 
70% being intersphincteric, 23% transsphincteric, 5% suprasphincteric, 
and 2% extrasphincteric (Fig. 339-5).
Presentation and Evaluation 
A patient with an anal fistula will 
complain of constant drainage from the perianal region associated with 
tenderness. Examination under anesthesia is the best way to evaluate 
a fistula. However, in cases with a complex fistula, a preoperative MRI 
will identify tracts with an accuracy of 80%. During surgery, hydrogen 
peroxide injected through the external opening will aid in identifying 
the internal opening. Goodsall’s rule states that a posterior external 
fistula will enter the anal canal in the posterior midline, whereas an 
anterior fistula will enter at the nearest crypt. A fistula exiting >3 cm 
from the anal verge may have a complicated upward extension and may 
not obey Goodsall’s rule.
TREATMENT
Fistula in Ano
A newly diagnosed draining fistula is best managed with an opera­
tive intervention including initial placement of a seton catheter 
(a vessel loop or silk tie placed through the fistula tract), which