Priscilla Marsicovetere, JD, PA-C

CE/CME No: CR-1808

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand the pathophysiology of diverticulitis.
• Describe the spectrum of clinical presentations of diverticulitis.
• Understand the diagnostic evaluation of diverticulitis.
• Differentiate the management of uncomplicated and complicated diverticulitis.

FACULTY
Priscilla Marsicovetere is Assistant Professor of Medical Education and Surgery, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, and Program Director for the Franklin Pierece University, PA Program, Lebanon, New Hampshire. She practices with Emergency Services of New England, Springfield Hospital, Springfield, Vermont.

The author has no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through July 31, 2019.

Article begins on next page >>

Treatment of this common complication of diverticular disease is predicated on whether the presentation signals uncomplicated or complicated disease. While some uncomplicated cases require hospitalization, many are amenable to primary care outpatient, and often conservative, management. The longstanding practice of antibiotic treatment of uncomplicated cases is now considered a selective, rather than a routine, option.

Diverticular disease is one of the most common conditions in the Western world and one of the most frequent indications for gastrointestinal-related hospitalization.¹ It is among the 10 most common diagnoses in patients presenting to the clinic or emergency department with acute abdominal pain.² Prevalence increases with age: Up to 60% of persons older than 60 are affected.³ The most common complication of diverticular disease is diverticulitis, which occurs in up to 25% of patients.⁴

The spectrum of clinical presentations of diverticular disease ranges from mild, uncomplicated disease that can be treated in the outpatient setting to complicated disease with sepsis and possible emergent surgical intervention. The traditional approach to diverticulitis has been management with antibiotics and likely sigmoid colectomy, but recent studies support a paradigm shift toward more conservative, nonsurgical treatment.

This article highlights current trends in diagnosis and management of acute diverticulitis.

DEFINITION AND EPIDEMIOLOGY

Diverticular disease is marked by sac-like outpouchings, called diverticula, that form at structurally weak points of the colon wall, predominantly in the descending and sigmoid colon.⁵ The prevalence of diverticular disease is increasing globally, affecting more than 10% of people older than 40, as many as 60% of those older than 60, and more than 70% of people older than 80.^1,3 The mean age for hospital admission for acute diverticulitis is 63.³

Worldwide, males and females are affected equally.³ In Western society, the presence of diverticula, also called diverticulosis, is more often left-sided; right-sided disease is more prevalent in Asia.^3,5

The most common complication of diverticular disease is diverticulitis—inflammation of a diverticulum—which affects 10% to 25% of patients with diverticular disease during their lifetime.^4,5 Diverticulitis can be classified as uncomplicated (characterized by colonic wall thickening or pericolic inflammatory changes) or complicated (characterized by abscesses, fistulae, obstruction, or localized or free perforations).^1,6 As many as 25% of diverticulitis cases are considered complicated.^4,5 The severity of diverticulitis is commonly graded using the Hinchey Classification (Table 1).^1,7

Continue to: PATHOPHYSIOLOGY

Diverticula tend to occur in areas where the colonic wall is weak: namely, between the mesenteric and antimesenteric taeniae, where the vasa recta penetrate the muscle—points of entry of blood vessels through the colonic wall.^1,4 The exact pathogenesis of diverticular disease is not completely understood but is thought to be multifactorial. Microscopic studies have shown muscular atrophy at the sites of diverticula, making them more susceptible to mucosal herniation in the setting of increased intraluminal pressure.¹ Additional potential contributing factors include alterations in colonic microbiota, muscular dysfunction or dysmotility, lifestyle, and genetics.

Diverticulitis is the result of microscopic and macroscopic perforation of diverticula. Historically, the perforations were thought to result from obstruction of a diverticulum by a fecalith, leading to increased pressure within the outpouching, followed by perforation.³ Such obstruction is now thought to be rare. A more recent theory suggests that increased intraluminal pressure is due to inspissated food particles that lead to erosion of the diverticular wall, causing focal inflammation and necrosis and resulting in perforation.³ Microperforations can easily be contained by surrounding mesenteric fat; however, progression to abscess, fistulization, or intestinal obstruction can occur. Frank bowel wall perforation is not contained by mesenteric fat and can lead quickly to peritonitis and death if not treated emergently.

RISK FACTORS

Dietary fiber

In 1971, Burkitt was the first to posit that diverticular disease developed due to small quantities of fiber in the diet that led to increased intracolonic pressures.⁸ His theory was based on the observation that residents of several African countries, who ate a high-fiber diet, had a low incidence of diverticular disease. Burkitt hypothesized that this was due to shorter colonic transit time induced by high dietary fiber.

Several studies conducted since Burkitt made his observations have examined the association of dietary fiber and diverticular disease, with conflicting results. In 1998, Aldoori et al found that a low-fiber diet increases the incidence of symptomatic diverticular disease.⁹ However, in 2012, a large cohort study of patients undergoing colonoscopy found that those who reported the highest fiber intake were at highest risk for diverticulosis.¹⁰ In 2013, Peery et al examined the relationship among bowel habits, dietary fiber, and asymptomatic diverticulosis and found that less-frequent bowel movements and hard stools were associated with a decreased risk for diverticulosis.¹¹ In 2017, a prospective cohort study of nearly 50,000 men without a known history of diverticulosis showed that diets high in red meat were associated with a higher incidence of diverticulitis over nearly three decades of follow-up, whereas a diet high in fiber was associated with a decreased incidence of diverticulitis.¹²

Although no definitive association has been found between dietary fiber intake and risk for diverticulosis, some studies have demonstrated an association between dietary fiber and diverticular complications. In 2014, Crowe et al found that consumption of a high-fiber diet was associated with a lower risk for hospital admission and death from diverticular disease.¹³ Recent guidelines from the American Gastroenterological Association (AGA) on diverticulitis recommend high dietary fiber intake in patients with a history of acute diverticulitis.¹⁴ However, no study has shown a reversal of the process or a reduction in the number of episodes of diverticulitis after adoption of a high-fiber diet.

Continue to: Historically, patients with diverticulitis...

Smoking

Smoking has been linked to diverticulitis and has been associated with a threefold risk for complications, including severe diverticulitis.^16,17 An increased risk for recurrent episodes has also been found in smokers following surgical intervention.¹⁷

Medications

NSAIDs, corticosteroids, and opioids have been associated with an increased risk for perforated diverticulitis.^18,19 A significant association has been found between NSAID use and severity of diverticulitis, including perforation; one study reported a relative risk of 1.25 (95% confidence interval, 10.5 to 1.47) for diverticulitis with regular use of aspirin (≥ 2x/wk).^20,21

More frequent steroid use has been found in patients with complicated diverticulitis, compared to patients with uncomplicated disease (7.3% vs 3.3%; P = .015).²² A systematic review of five studies comparing patients with and without steroid use showed significantly higher odds of diverticular perforation in patients taking a steroid.²³ Pooled data showed significantly increased odds of perforation and abscess formation with use of an NSAID (odds ratio [OR], 2.49), steroid (OR, 9.08), or opioid (OR, 2.52).²²

Continue to: Vitamin D

Vitamin D

In a 2013 retrospective cohort study of 9,116 patients with uncomplicated diverticulosis and 922 patients who developed diverticulitis that required hospitalization, Maguire et al examined the association of prediagnostic serum levels of vitamin D and diverticulitis.²⁴ Among patients with diverticulosis, higher prediagnostic levels of 25-hydroxyvitamin D were significantly associated with a lower risk for diverticulitis—indicating that vitamin D deficiency could be involved in the pathogenesis of diverticulitis.

The association between diverticulitis and vitamin D levels was supported by an additional study in 2015, in which the authors investigated the association between ultraviolet (UV) light and diverticulitis.²⁵ They identified nonelective diverticulitis admissions in the Nationwide Inpatient Sample database and linked hospital locations to geographic UV data. They examined UV exposure in relation to risk for admission for diverticulitis and found that, compared with high-UV (UV4) areas, low-UV (UV1) areas had a higher rate of diverticulitis (751.8/100,000 admissions, compared with 668.1/100,000 admissions, respectively [P < .001]), diverticular abscess (12.0% compared with 9.7% [P < .001]), and colectomy (13.5% compared with 11.5% [P < .001]). They also observed significant seasonal variation, with a lower rate of diverticulitis in winter (645/100,000 admissions) compared with summer (748/100,000 admissions [P < .001]). Because UV exposure largely determines vitamin D status, these findings are thought to support a role for vitamin D in the pathogenesis of diverticulitis.

Genetics

Two studies found an association between genetics and diverticular disease. A 2012 study using The Swedish Twin Registry found that if one twin is affected with the disease, the odds that the other will be affected was 7.15 in monozygotic (identical) twins and 3.20 in dizygotic (fraternal) twins.²⁶ A 2013 Danish twin study found a relative risk of 2.92 in twin siblings compared to the general population.²⁷ Both studies estimated the genetic contribution to diverticular disease to be 40% to 50%.^26,27

Obesity

Several large prospective studies have shown a positive association between high BMI, waist circumference, and waist-to-hip ratio and risk for diverticulitis.⁴ A BMI > 30 was found to increase the relative risk of acute diverticulitis by 1.78, compared with a normal BMI.¹⁷ In a large, prospective, population-based cohort study in 2016, Jamal Talabani et al found that obese persons had twice the risk for admission for acute colonic diverticulitis than normal-weight persons did.²⁸ Waist circumference and waist-to-hip ratio were also independently associated with risk for diverticulitis. The pathophysiology of the associations is not clearly understood but may involve pro-inflammatory changes of adipose tissue, which secrete cytokines that promote an inflammatory response, and changes in gut microbiota.^4,12

Physical activity

Data on the association of physical activity and diverticulitis is inconsistent. Some studies have found as much as a 25% decrease in the risk for diverticulitis with increased physical activity; more recent studies (2013 and 2016), on the other hand, found no association between diverticulosis and physical activity.^11,17,19,28

Continue to: CLINICAL PRESENTATION

The clinical presentation of diverticulitis typically depends on the severity of inflammation and the presence (or absence) of complications. The most common presenting symptom is left lower-quadrant abdominal pain, which occurs in approximately 70% of cases and lasts for longer than 24 hours.²⁹ Fever (usually < 102°F), leukocytosis, nausea, vomiting, and changes in bowel function may also be present.^1,30,31 Approximately 50% of patients report constipation in diverticular disease; 20% to 35% report diarrhea.⁵

Patients may also report dysuria, secondary to irritation of the bladder by an inflamed segment of colon.^3,17 Patients may report fecaluria, pneumaturia, or pyuria, which indicate a colovesical fistula.¹ Passage of feces or flatus through the vagina indicates a colovaginal fistula.

The differential diagnosis of diverticulitis is listed in Table 2.¹⁷

PHYSICAL EXAMINATION

Physical examination in diverticulitis will almost always elicit tenderness to palpation over the area of inflammation, typically in the left lower quadrant. This is due to irritation of the peritoneum.³ A palpable mass may be present in as many as 20% of patients if an abscess is present. Bowel sounds may be hypoactive or hyperactive if there is a bowel obstruction.¹⁷ In cases of frank bowel-wall perforation, patients can present with peritoneal signs of rigidity, guarding, and rebound tenderness.^3,31 Tachycardia, hypotension, and shock are rare but possible findings. Digital rectal examination may reveal tenderness or a mass if a pelvic abscess is present.^17,31

DIAGNOSTICS

The diagnosis of acute diverticulitis can often be made clinically, based on the history and physical examination. Because clinical diagnosis can be inaccurate in as many as 68% of cases, however, laboratory testing and imaging play an important role in diagnosis.³

Continue to: Clinical laboratory studies

Because leukocytosis is present in approximately one-half of patients with diverticulitis, a complete blood count (CBC) should be obtained; that recommendation notwithstanding, approximately one-half of patients with diverticulitis have a normal white blood cell count.^29,30 A urine test of human chorionic gonadotropin should be ordered to exclude pregnancy in all premenopausal and perimenopausal women, particularly if antibiotics, imaging, or surgery are being considered.³¹ Urinalysis can assess for urinary tract infection.

Multiple studies have demonstrated the utility of C-reactive protein (CRP) in the workup of acute diverticulitis. In general, patients with a complicated episode will present with a significantly higher CRP level than that of uncomplicated disease.³² Kechagias et al found that the CRP level at initial evaluation may be helpful in predicting the clinical severity of the attack. A CRP level > 170 mg/L has been found to have a greater probability of severe disease, warranting CT and referral for hospitalization.³³ A low CRP level was more likely to herald a mild course of disease that is amenable to outpatient antibiotic management or supportive care. This finding is consistent with previous reports of the association between CRP levels of 90 to 200 mg/L and the severity of diverticulitis.^32,34

Imaging

Abdominopelvic CT with intravenous (IV) contrast. This imaging study is the gold standard diagnostic tool for diverticulitis, with sensitivity as high as 97%.³ CT can distinguish diverticulitis from other conditions, such as irritable bowel syndrome (based on a history of symptoms and the absence of CT findings), gastroenteritis, and gynecologic disease. It can also distinguish between uncomplicated and complicated diverticulitis and therefore guide therapeutic interventions, such as percutaneous drainage of an intra-abdominal abscess. CT findings associated with uncomplicated diverticulitis include colonic wall thickening and pericolonic fluid and inflammatory changes, such as fat stranding. CT findings associated with complicated disease include abscess (paracolonic or pelvic), peritonitis (purulent or feculent), phlegmon, perforation, fistula, and obstruction.^1,3

Ultrasonography (US) can also be used in the assessment of diverticulitis, although it has lower sensitivity (approximately 61% to 84%) than CT and is inferior to CT for showing the extent of large abscesses or free air.^3,18,30 A typical US finding in acute diverticulitis is a thickened loop of bowel with a target-like appearance.¹⁷ Findings are highly operator-dependent, however, and accuracy is diminished in obese patients. US may be a good option for pregnant women to avoid ionizing radiation.

Magnetic resonance imaging (MRI) is another option for imaging in diverticulitis but is not routinely recommended. It provides excellent soft-tissue detail and does not deliver ionizing radiation, but it is not as sensitive as CT for identifying free air.^18,31 Furthermore, MRI requires prolonged examination time, which may not be tolerated by acutely ill patients, and is not an option for patients with certain types of surgical clips, metallic fragments, or a cardiac pacemaker.

Continue to: Abdominal radiography...

MANAGEMENT

For decades, patients with diverticulitis were managed with antibiotics to cover colonic flora; many underwent urgent or emergent surgery to remove the affected segment of colon. Over the years, however, the treatment paradigm has shifted from such invasive management toward a nonsurgical approach—often, with equivalent or superior outcomes. More and more, management of diverticulitis is dictated by disease presentation: namely, whether disease is uncomplicated or complicated.¹

Current guidelines recommend hospitalization, with possible surgical intervention, in complicated disease (free perforation, large abscesses, fistula, obstruction, stricture) and in patients who cannot tolerate oral hydration, who have a relevant comorbidity, or who do not have adequate support at home.³⁵ Uncomplicated cases may also require hospitalization if certain criteria for admission are met: immunosuppression, severe or persistent abdominal pain, inability to tolerate oral intake, and significant comorbidity.⁵

Absent these criteria, outpatient management of uncomplicated diverticulitis is appropriate. After the treatment setting is determined, choice of intervention and length of treatment should be addressed.

Nonpharmacotherapeutic management

Dietary restrictions, from a full liquid diet to complete bowel rest, have been recommended for the management of acute diverticulitis. This recommendation is not supported by the literature, however. At least two studies have shown no association between an unrestricted diet and an increase in diverticular complications. In a 2013 retrospective cohort study, no increase in diverticular perforation or abscess was found with a diet of solid food compared to a liquid diet, a clear liquid diet, or no food by mouth.³⁶ In a more recent (2017) prospective cohort study of 86 patients with uncomplicated diverticulitis, all of whom were on an unrestricted diet, only 8% developed complications.³⁷

Continue to: There is no high-quality evidence for...

There is no high-quality evidence for instituting dietary restrictions in acute uncomplicated diverticulitis. As such, permitting oral intake as tolerated is a reasonable option.

Pharmacotherapy

Antibiotics have long been the cornerstone of pharmacotherapy for acute diverticulitis, covering gram-negative rods and anaerobes. The rationale for such management is the long-held belief that diverticulitis is caused by an infectious process.³⁸ Common outpatient regimens include

• Ciprofloxacin (500 mg every 12 h) plus metronidazole (500 mg every 8 h)
• Trimethoprim–sulfamethoxazole (1 double-strength tablet every 12 h) plus metronidazole (500 mg every 8 h)
• Amoxicillin (875 mg)–clavulanate (1 tablet every 8 h) or extended-release amoxicillin–clavulanate (2 tablets every 12 h)
• Moxifloxacin (400 mg/d; for patients who cannot tolerate metronidazole or ß-lactam antibiotics).

Providers should always consult their local antibiogram to avoid prescribing antibiotics to which bacterial resistance exceeds 10%.

Despite widespread use of antibiotics for diverticulitis, multiple studies in recent years have shown no benefit to their use for uncomplicated cases. In 2012, Chabok et al investigated the need for antibiotic therapy to treat acute uncomplicated diverticulitis and found no statistically significant difference in outcome among patients treated with antibiotics and those managed conservatively.³⁹ In 2014, Isacson et al performed a retrospective population-based cohort study to assess the applicability of a selective “no antibiotic” policy and its consequences in terms of complications and recurrence; the authors found that withholding antibiotics was safe and did not result in a higher complication or recurrence rate.⁴⁰ Furthermore, in a 2017 multicenter study, Daniels et al conducted a randomized controlled trial comparing observation and antibiotic treatment for a first episode of uncomplicated acute diverticulitis in 528 patients and found no prolongation of recovery time, no increased rate of complications, and no need for surgical intervention in patients who were not treated with antibiotics.⁴¹

These studies are in agreement with the most recent AGA guidelines, which recommend selective, rather than routine, use of antibiotics for acute diverticulitis.¹⁴ This shift in approach may be due, in part, to a change in understanding of the etiology of the disease—from an infectious process to more of an inflammatory process.³⁸

Continue to: For patients who require inpatient management of diverticulitis...

Other agents used to manage diverticulitis include three that lack either strong or any data at all showing efficacy. The most recent AGA guidelines recommend against their use for this indication¹⁴:

Rifaximin. Two recent observational cohort studies, one from 2013 and the other from 2017, compared this poorly absorbed oral antibiotic with mesalamine to placebo or no treatment at all.⁴² Neither provided evidence that rifaximin treats or prevents diverticulitis.

Mesalamine. This anti-inflammatory has also been studied to prevent recurrence of diverticulitis. In a randomized, double-blind, placebo-controlled multicenter trial of 1,182 patients, Raskin et al found that mesalamine did not reduce the rate of recurrence of diverticulitis, time to recurrence, or the number of patients requiring surgery.⁴³ This conclusion was reiterated by a 2016 meta-analysis that found no evidence to support use of mesalamine in the prevention of diverticulitis recurrence.⁴⁴

Probiotics. Despite multiple studies undertaken to assess the efficacy of probiotics in the prevention and treatment of diverticular disease, strong data supporting their use are sparse. In 2016, Lahner et al examined 11 studies in which various probiotics were used to treat diverticular disease and found that, although there was a weak positive trend in the reduction and remission of abdominal symptoms, the evidence was not strong enough to recommend their routine use in managing the disease.⁴⁵

Continue to: Surgical treatment

Surgical treatment

Acute uncomplicated diverticulitis can be treated nonsurgically in nearly all patients, regardless of whether treatment occurs in the inpatient or outpatient setting. For complicated disease, however, approximately 15% to 25% of patients require surgery. The main indication for emergent or urgent surgical intervention is colonic perforation, which can lead to acute peritonitis, sepsis, and associated morbidity and mortality.²⁹

The decision to perform elective surgery should be made case by case, not routinely—such as after a recurrent episode of diverticulitis, when there has been a complication, or in young patients (< 50 years).^1,11 Immunocompromised patients (transplant recipients, patients taking steroids chronically, and patients with HIV infection who have a CD4 count < 200 cells/μL) can pre­sent with more virulent episodes of diverticulitis, have a higher incidence of perforation and fecal peritonitis, and have a greater likelihood of failure of nonsurgical management.¹ Surgical intervention after the first episode of diverticulitis in these patients should therefore be considered.

In 2014, the American Society of Colon and Rectal Surgeons (ASCRS) recommended the laparoscopic Hartmann procedure (primary resection of the affected segment of colon, with end colostomy, followed by colostomy closure) as the gold standard for the treatment of acute perforated diverticular disease when surgery is required.⁴⁶

COLONOSCOPY AFTER DIVERTICULITIS

Although endoscopy is to be avoided during acute diverticulitis because of the risk for perforation, it is recommended six to eight weeks after the acute episode has resolved to rule out malignancy, inflammatory bowel disease, and colitis.^1,3 Interestingly, in 2015, Daniels et al compared the colonoscopic detection rate of advanced colonic neoplasia in patients with a first episode of acute diverticulitis and in patients undergoing initial screening for colorectal cancer, and found no significant difference in the detection rate between the two groups.⁴⁷ The authors concluded that routine colonoscopic follow-up after an episode of acute uncomplicated diverticulitis could be eliminated and that those patients could be screened according to routine guidelines.

Lau et al found a number of cancers and other significant lesions on colonoscopy performed after an episode of acute diverticulitis, with a 2.1% prevalence of colorectal cancer within one year after CT-proven diverticulitis, and an increase in the prevalence of abscess, local perforation, and fistula.⁴⁸ Their study excluded patients who had had a colonoscopy within one year, however. They therefore recommended performing colonoscopy only for patients who have not had a recent colonoscopic exam. This recommendation is in accord with the most recent AGA and ASCRS guidelines. If a patient has had a recent colonoscopy prior to an acute episode of diverticulitis, the value of repeating the study after the episode resolves is unclear.

Continue to: CONCLUSION

As this article shows, the spectrum of clinical presentations for diverticulitis is broad, and management most often requires a case-by-case approach. Treatment is dictated by whether disease presentation is uncomplicated or complicated; outpatient management is appropriate for uncomplicated cases in the absence of specific criteria for hospitalization. Recent evidence supports a paradigm shift away from mandatory dietary restriction and routine antibiotic use.

CE/CME No: CR-1808

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand the pathophysiology of diverticulitis.
• Describe the spectrum of clinical presentations of diverticulitis.
• Understand the diagnostic evaluation of diverticulitis.
• Differentiate the management of uncomplicated and complicated diverticulitis.

FACULTY
Priscilla Marsicovetere is Assistant Professor of Medical Education and Surgery, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, and Program Director for the Franklin Pierece University, PA Program, Lebanon, New Hampshire. She practices with Emergency Services of New England, Springfield Hospital, Springfield, Vermont.

The author has no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through July 31, 2019.

Article begins on next page >>

Treatment of this common complication of diverticular disease is predicated on whether the presentation signals uncomplicated or complicated disease. While some uncomplicated cases require hospitalization, many are amenable to primary care outpatient, and often conservative, management. The longstanding practice of antibiotic treatment of uncomplicated cases is now considered a selective, rather than a routine, option.

Diverticular disease is one of the most common conditions in the Western world and one of the most frequent indications for gastrointestinal-related hospitalization.¹ It is among the 10 most common diagnoses in patients presenting to the clinic or emergency department with acute abdominal pain.² Prevalence increases with age: Up to 60% of persons older than 60 are affected.³ The most common complication of diverticular disease is diverticulitis, which occurs in up to 25% of patients.⁴

The spectrum of clinical presentations of diverticular disease ranges from mild, uncomplicated disease that can be treated in the outpatient setting to complicated disease with sepsis and possible emergent surgical intervention. The traditional approach to diverticulitis has been management with antibiotics and likely sigmoid colectomy, but recent studies support a paradigm shift toward more conservative, nonsurgical treatment.

This article highlights current trends in diagnosis and management of acute diverticulitis.

DEFINITION AND EPIDEMIOLOGY

Diverticular disease is marked by sac-like outpouchings, called diverticula, that form at structurally weak points of the colon wall, predominantly in the descending and sigmoid colon.⁵ The prevalence of diverticular disease is increasing globally, affecting more than 10% of people older than 40, as many as 60% of those older than 60, and more than 70% of people older than 80.^1,3 The mean age for hospital admission for acute diverticulitis is 63.³

Worldwide, males and females are affected equally.³ In Western society, the presence of diverticula, also called diverticulosis, is more often left-sided; right-sided disease is more prevalent in Asia.^3,5

The most common complication of diverticular disease is diverticulitis—inflammation of a diverticulum—which affects 10% to 25% of patients with diverticular disease during their lifetime.^4,5 Diverticulitis can be classified as uncomplicated (characterized by colonic wall thickening or pericolic inflammatory changes) or complicated (characterized by abscesses, fistulae, obstruction, or localized or free perforations).^1,6 As many as 25% of diverticulitis cases are considered complicated.^4,5 The severity of diverticulitis is commonly graded using the Hinchey Classification (Table 1).^1,7

Continue to: PATHOPHYSIOLOGY

Diverticula tend to occur in areas where the colonic wall is weak: namely, between the mesenteric and antimesenteric taeniae, where the vasa recta penetrate the muscle—points of entry of blood vessels through the colonic wall.^1,4 The exact pathogenesis of diverticular disease is not completely understood but is thought to be multifactorial. Microscopic studies have shown muscular atrophy at the sites of diverticula, making them more susceptible to mucosal herniation in the setting of increased intraluminal pressure.¹ Additional potential contributing factors include alterations in colonic microbiota, muscular dysfunction or dysmotility, lifestyle, and genetics.

Diverticulitis is the result of microscopic and macroscopic perforation of diverticula. Historically, the perforations were thought to result from obstruction of a diverticulum by a fecalith, leading to increased pressure within the outpouching, followed by perforation.³ Such obstruction is now thought to be rare. A more recent theory suggests that increased intraluminal pressure is due to inspissated food particles that lead to erosion of the diverticular wall, causing focal inflammation and necrosis and resulting in perforation.³ Microperforations can easily be contained by surrounding mesenteric fat; however, progression to abscess, fistulization, or intestinal obstruction can occur. Frank bowel wall perforation is not contained by mesenteric fat and can lead quickly to peritonitis and death if not treated emergently.

RISK FACTORS

Dietary fiber

In 1971, Burkitt was the first to posit that diverticular disease developed due to small quantities of fiber in the diet that led to increased intracolonic pressures.⁸ His theory was based on the observation that residents of several African countries, who ate a high-fiber diet, had a low incidence of diverticular disease. Burkitt hypothesized that this was due to shorter colonic transit time induced by high dietary fiber.

Several studies conducted since Burkitt made his observations have examined the association of dietary fiber and diverticular disease, with conflicting results. In 1998, Aldoori et al found that a low-fiber diet increases the incidence of symptomatic diverticular disease.⁹ However, in 2012, a large cohort study of patients undergoing colonoscopy found that those who reported the highest fiber intake were at highest risk for diverticulosis.¹⁰ In 2013, Peery et al examined the relationship among bowel habits, dietary fiber, and asymptomatic diverticulosis and found that less-frequent bowel movements and hard stools were associated with a decreased risk for diverticulosis.¹¹ In 2017, a prospective cohort study of nearly 50,000 men without a known history of diverticulosis showed that diets high in red meat were associated with a higher incidence of diverticulitis over nearly three decades of follow-up, whereas a diet high in fiber was associated with a decreased incidence of diverticulitis.¹²

Although no definitive association has been found between dietary fiber intake and risk for diverticulosis, some studies have demonstrated an association between dietary fiber and diverticular complications. In 2014, Crowe et al found that consumption of a high-fiber diet was associated with a lower risk for hospital admission and death from diverticular disease.¹³ Recent guidelines from the American Gastroenterological Association (AGA) on diverticulitis recommend high dietary fiber intake in patients with a history of acute diverticulitis.¹⁴ However, no study has shown a reversal of the process or a reduction in the number of episodes of diverticulitis after adoption of a high-fiber diet.

Continue to: Historically, patients with diverticulitis...

Smoking

Smoking has been linked to diverticulitis and has been associated with a threefold risk for complications, including severe diverticulitis.^16,17 An increased risk for recurrent episodes has also been found in smokers following surgical intervention.¹⁷

Medications

NSAIDs, corticosteroids, and opioids have been associated with an increased risk for perforated diverticulitis.^18,19 A significant association has been found between NSAID use and severity of diverticulitis, including perforation; one study reported a relative risk of 1.25 (95% confidence interval, 10.5 to 1.47) for diverticulitis with regular use of aspirin (≥ 2x/wk).^20,21

More frequent steroid use has been found in patients with complicated diverticulitis, compared to patients with uncomplicated disease (7.3% vs 3.3%; P = .015).²² A systematic review of five studies comparing patients with and without steroid use showed significantly higher odds of diverticular perforation in patients taking a steroid.²³ Pooled data showed significantly increased odds of perforation and abscess formation with use of an NSAID (odds ratio [OR], 2.49), steroid (OR, 9.08), or opioid (OR, 2.52).²²

Continue to: Vitamin D

Vitamin D

In a 2013 retrospective cohort study of 9,116 patients with uncomplicated diverticulosis and 922 patients who developed diverticulitis that required hospitalization, Maguire et al examined the association of prediagnostic serum levels of vitamin D and diverticulitis.²⁴ Among patients with diverticulosis, higher prediagnostic levels of 25-hydroxyvitamin D were significantly associated with a lower risk for diverticulitis—indicating that vitamin D deficiency could be involved in the pathogenesis of diverticulitis.

The association between diverticulitis and vitamin D levels was supported by an additional study in 2015, in which the authors investigated the association between ultraviolet (UV) light and diverticulitis.²⁵ They identified nonelective diverticulitis admissions in the Nationwide Inpatient Sample database and linked hospital locations to geographic UV data. They examined UV exposure in relation to risk for admission for diverticulitis and found that, compared with high-UV (UV4) areas, low-UV (UV1) areas had a higher rate of diverticulitis (751.8/100,000 admissions, compared with 668.1/100,000 admissions, respectively [P < .001]), diverticular abscess (12.0% compared with 9.7% [P < .001]), and colectomy (13.5% compared with 11.5% [P < .001]). They also observed significant seasonal variation, with a lower rate of diverticulitis in winter (645/100,000 admissions) compared with summer (748/100,000 admissions [P < .001]). Because UV exposure largely determines vitamin D status, these findings are thought to support a role for vitamin D in the pathogenesis of diverticulitis.

Genetics

Two studies found an association between genetics and diverticular disease. A 2012 study using The Swedish Twin Registry found that if one twin is affected with the disease, the odds that the other will be affected was 7.15 in monozygotic (identical) twins and 3.20 in dizygotic (fraternal) twins.²⁶ A 2013 Danish twin study found a relative risk of 2.92 in twin siblings compared to the general population.²⁷ Both studies estimated the genetic contribution to diverticular disease to be 40% to 50%.^26,27

Obesity

Several large prospective studies have shown a positive association between high BMI, waist circumference, and waist-to-hip ratio and risk for diverticulitis.⁴ A BMI > 30 was found to increase the relative risk of acute diverticulitis by 1.78, compared with a normal BMI.¹⁷ In a large, prospective, population-based cohort study in 2016, Jamal Talabani et al found that obese persons had twice the risk for admission for acute colonic diverticulitis than normal-weight persons did.²⁸ Waist circumference and waist-to-hip ratio were also independently associated with risk for diverticulitis. The pathophysiology of the associations is not clearly understood but may involve pro-inflammatory changes of adipose tissue, which secrete cytokines that promote an inflammatory response, and changes in gut microbiota.^4,12

Physical activity

Data on the association of physical activity and diverticulitis is inconsistent. Some studies have found as much as a 25% decrease in the risk for diverticulitis with increased physical activity; more recent studies (2013 and 2016), on the other hand, found no association between diverticulosis and physical activity.^11,17,19,28

Continue to: CLINICAL PRESENTATION

The clinical presentation of diverticulitis typically depends on the severity of inflammation and the presence (or absence) of complications. The most common presenting symptom is left lower-quadrant abdominal pain, which occurs in approximately 70% of cases and lasts for longer than 24 hours.²⁹ Fever (usually < 102°F), leukocytosis, nausea, vomiting, and changes in bowel function may also be present.^1,30,31 Approximately 50% of patients report constipation in diverticular disease; 20% to 35% report diarrhea.⁵

Patients may also report dysuria, secondary to irritation of the bladder by an inflamed segment of colon.^3,17 Patients may report fecaluria, pneumaturia, or pyuria, which indicate a colovesical fistula.¹ Passage of feces or flatus through the vagina indicates a colovaginal fistula.

The differential diagnosis of diverticulitis is listed in Table 2.¹⁷

PHYSICAL EXAMINATION

Physical examination in diverticulitis will almost always elicit tenderness to palpation over the area of inflammation, typically in the left lower quadrant. This is due to irritation of the peritoneum.³ A palpable mass may be present in as many as 20% of patients if an abscess is present. Bowel sounds may be hypoactive or hyperactive if there is a bowel obstruction.¹⁷ In cases of frank bowel-wall perforation, patients can present with peritoneal signs of rigidity, guarding, and rebound tenderness.^3,31 Tachycardia, hypotension, and shock are rare but possible findings. Digital rectal examination may reveal tenderness or a mass if a pelvic abscess is present.^17,31

DIAGNOSTICS

The diagnosis of acute diverticulitis can often be made clinically, based on the history and physical examination. Because clinical diagnosis can be inaccurate in as many as 68% of cases, however, laboratory testing and imaging play an important role in diagnosis.³

Continue to: Clinical laboratory studies

Because leukocytosis is present in approximately one-half of patients with diverticulitis, a complete blood count (CBC) should be obtained; that recommendation notwithstanding, approximately one-half of patients with diverticulitis have a normal white blood cell count.^29,30 A urine test of human chorionic gonadotropin should be ordered to exclude pregnancy in all premenopausal and perimenopausal women, particularly if antibiotics, imaging, or surgery are being considered.³¹ Urinalysis can assess for urinary tract infection.

Multiple studies have demonstrated the utility of C-reactive protein (CRP) in the workup of acute diverticulitis. In general, patients with a complicated episode will present with a significantly higher CRP level than that of uncomplicated disease.³² Kechagias et al found that the CRP level at initial evaluation may be helpful in predicting the clinical severity of the attack. A CRP level > 170 mg/L has been found to have a greater probability of severe disease, warranting CT and referral for hospitalization.³³ A low CRP level was more likely to herald a mild course of disease that is amenable to outpatient antibiotic management or supportive care. This finding is consistent with previous reports of the association between CRP levels of 90 to 200 mg/L and the severity of diverticulitis.^32,34

Imaging

Abdominopelvic CT with intravenous (IV) contrast. This imaging study is the gold standard diagnostic tool for diverticulitis, with sensitivity as high as 97%.³ CT can distinguish diverticulitis from other conditions, such as irritable bowel syndrome (based on a history of symptoms and the absence of CT findings), gastroenteritis, and gynecologic disease. It can also distinguish between uncomplicated and complicated diverticulitis and therefore guide therapeutic interventions, such as percutaneous drainage of an intra-abdominal abscess. CT findings associated with uncomplicated diverticulitis include colonic wall thickening and pericolonic fluid and inflammatory changes, such as fat stranding. CT findings associated with complicated disease include abscess (paracolonic or pelvic), peritonitis (purulent or feculent), phlegmon, perforation, fistula, and obstruction.^1,3

Ultrasonography (US) can also be used in the assessment of diverticulitis, although it has lower sensitivity (approximately 61% to 84%) than CT and is inferior to CT for showing the extent of large abscesses or free air.^3,18,30 A typical US finding in acute diverticulitis is a thickened loop of bowel with a target-like appearance.¹⁷ Findings are highly operator-dependent, however, and accuracy is diminished in obese patients. US may be a good option for pregnant women to avoid ionizing radiation.

Magnetic resonance imaging (MRI) is another option for imaging in diverticulitis but is not routinely recommended. It provides excellent soft-tissue detail and does not deliver ionizing radiation, but it is not as sensitive as CT for identifying free air.^18,31 Furthermore, MRI requires prolonged examination time, which may not be tolerated by acutely ill patients, and is not an option for patients with certain types of surgical clips, metallic fragments, or a cardiac pacemaker.

Continue to: Abdominal radiography...

MANAGEMENT

For decades, patients with diverticulitis were managed with antibiotics to cover colonic flora; many underwent urgent or emergent surgery to remove the affected segment of colon. Over the years, however, the treatment paradigm has shifted from such invasive management toward a nonsurgical approach—often, with equivalent or superior outcomes. More and more, management of diverticulitis is dictated by disease presentation: namely, whether disease is uncomplicated or complicated.¹

Current guidelines recommend hospitalization, with possible surgical intervention, in complicated disease (free perforation, large abscesses, fistula, obstruction, stricture) and in patients who cannot tolerate oral hydration, who have a relevant comorbidity, or who do not have adequate support at home.³⁵ Uncomplicated cases may also require hospitalization if certain criteria for admission are met: immunosuppression, severe or persistent abdominal pain, inability to tolerate oral intake, and significant comorbidity.⁵

Absent these criteria, outpatient management of uncomplicated diverticulitis is appropriate. After the treatment setting is determined, choice of intervention and length of treatment should be addressed.

Nonpharmacotherapeutic management

Dietary restrictions, from a full liquid diet to complete bowel rest, have been recommended for the management of acute diverticulitis. This recommendation is not supported by the literature, however. At least two studies have shown no association between an unrestricted diet and an increase in diverticular complications. In a 2013 retrospective cohort study, no increase in diverticular perforation or abscess was found with a diet of solid food compared to a liquid diet, a clear liquid diet, or no food by mouth.³⁶ In a more recent (2017) prospective cohort study of 86 patients with uncomplicated diverticulitis, all of whom were on an unrestricted diet, only 8% developed complications.³⁷

Continue to: There is no high-quality evidence for...

There is no high-quality evidence for instituting dietary restrictions in acute uncomplicated diverticulitis. As such, permitting oral intake as tolerated is a reasonable option.

Pharmacotherapy

Antibiotics have long been the cornerstone of pharmacotherapy for acute diverticulitis, covering gram-negative rods and anaerobes. The rationale for such management is the long-held belief that diverticulitis is caused by an infectious process.³⁸ Common outpatient regimens include

• Ciprofloxacin (500 mg every 12 h) plus metronidazole (500 mg every 8 h)
• Trimethoprim–sulfamethoxazole (1 double-strength tablet every 12 h) plus metronidazole (500 mg every 8 h)
• Amoxicillin (875 mg)–clavulanate (1 tablet every 8 h) or extended-release amoxicillin–clavulanate (2 tablets every 12 h)
• Moxifloxacin (400 mg/d; for patients who cannot tolerate metronidazole or ß-lactam antibiotics).

Providers should always consult their local antibiogram to avoid prescribing antibiotics to which bacterial resistance exceeds 10%.

Despite widespread use of antibiotics for diverticulitis, multiple studies in recent years have shown no benefit to their use for uncomplicated cases. In 2012, Chabok et al investigated the need for antibiotic therapy to treat acute uncomplicated diverticulitis and found no statistically significant difference in outcome among patients treated with antibiotics and those managed conservatively.³⁹ In 2014, Isacson et al performed a retrospective population-based cohort study to assess the applicability of a selective “no antibiotic” policy and its consequences in terms of complications and recurrence; the authors found that withholding antibiotics was safe and did not result in a higher complication or recurrence rate.⁴⁰ Furthermore, in a 2017 multicenter study, Daniels et al conducted a randomized controlled trial comparing observation and antibiotic treatment for a first episode of uncomplicated acute diverticulitis in 528 patients and found no prolongation of recovery time, no increased rate of complications, and no need for surgical intervention in patients who were not treated with antibiotics.⁴¹

These studies are in agreement with the most recent AGA guidelines, which recommend selective, rather than routine, use of antibiotics for acute diverticulitis.¹⁴ This shift in approach may be due, in part, to a change in understanding of the etiology of the disease—from an infectious process to more of an inflammatory process.³⁸

Continue to: For patients who require inpatient management of diverticulitis...

Other agents used to manage diverticulitis include three that lack either strong or any data at all showing efficacy. The most recent AGA guidelines recommend against their use for this indication¹⁴:

Rifaximin. Two recent observational cohort studies, one from 2013 and the other from 2017, compared this poorly absorbed oral antibiotic with mesalamine to placebo or no treatment at all.⁴² Neither provided evidence that rifaximin treats or prevents diverticulitis.

Mesalamine. This anti-inflammatory has also been studied to prevent recurrence of diverticulitis. In a randomized, double-blind, placebo-controlled multicenter trial of 1,182 patients, Raskin et al found that mesalamine did not reduce the rate of recurrence of diverticulitis, time to recurrence, or the number of patients requiring surgery.⁴³ This conclusion was reiterated by a 2016 meta-analysis that found no evidence to support use of mesalamine in the prevention of diverticulitis recurrence.⁴⁴

Probiotics. Despite multiple studies undertaken to assess the efficacy of probiotics in the prevention and treatment of diverticular disease, strong data supporting their use are sparse. In 2016, Lahner et al examined 11 studies in which various probiotics were used to treat diverticular disease and found that, although there was a weak positive trend in the reduction and remission of abdominal symptoms, the evidence was not strong enough to recommend their routine use in managing the disease.⁴⁵

Continue to: Surgical treatment

Surgical treatment

Acute uncomplicated diverticulitis can be treated nonsurgically in nearly all patients, regardless of whether treatment occurs in the inpatient or outpatient setting. For complicated disease, however, approximately 15% to 25% of patients require surgery. The main indication for emergent or urgent surgical intervention is colonic perforation, which can lead to acute peritonitis, sepsis, and associated morbidity and mortality.²⁹

The decision to perform elective surgery should be made case by case, not routinely—such as after a recurrent episode of diverticulitis, when there has been a complication, or in young patients (< 50 years).^1,11 Immunocompromised patients (transplant recipients, patients taking steroids chronically, and patients with HIV infection who have a CD4 count < 200 cells/μL) can pre­sent with more virulent episodes of diverticulitis, have a higher incidence of perforation and fecal peritonitis, and have a greater likelihood of failure of nonsurgical management.¹ Surgical intervention after the first episode of diverticulitis in these patients should therefore be considered.

In 2014, the American Society of Colon and Rectal Surgeons (ASCRS) recommended the laparoscopic Hartmann procedure (primary resection of the affected segment of colon, with end colostomy, followed by colostomy closure) as the gold standard for the treatment of acute perforated diverticular disease when surgery is required.⁴⁶

COLONOSCOPY AFTER DIVERTICULITIS

Although endoscopy is to be avoided during acute diverticulitis because of the risk for perforation, it is recommended six to eight weeks after the acute episode has resolved to rule out malignancy, inflammatory bowel disease, and colitis.^1,3 Interestingly, in 2015, Daniels et al compared the colonoscopic detection rate of advanced colonic neoplasia in patients with a first episode of acute diverticulitis and in patients undergoing initial screening for colorectal cancer, and found no significant difference in the detection rate between the two groups.⁴⁷ The authors concluded that routine colonoscopic follow-up after an episode of acute uncomplicated diverticulitis could be eliminated and that those patients could be screened according to routine guidelines.

Lau et al found a number of cancers and other significant lesions on colonoscopy performed after an episode of acute diverticulitis, with a 2.1% prevalence of colorectal cancer within one year after CT-proven diverticulitis, and an increase in the prevalence of abscess, local perforation, and fistula.⁴⁸ Their study excluded patients who had had a colonoscopy within one year, however. They therefore recommended performing colonoscopy only for patients who have not had a recent colonoscopic exam. This recommendation is in accord with the most recent AGA and ASCRS guidelines. If a patient has had a recent colonoscopy prior to an acute episode of diverticulitis, the value of repeating the study after the episode resolves is unclear.

Continue to: CONCLUSION

As this article shows, the spectrum of clinical presentations for diverticulitis is broad, and management most often requires a case-by-case approach. Treatment is dictated by whether disease presentation is uncomplicated or complicated; outpatient management is appropriate for uncomplicated cases in the absence of specific criteria for hospitalization. Recent evidence supports a paradigm shift away from mandatory dietary restriction and routine antibiotic use.

CE/CME No: CR-1808

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand the pathophysiology of diverticulitis.
• Describe the spectrum of clinical presentations of diverticulitis.
• Understand the diagnostic evaluation of diverticulitis.
• Differentiate the management of uncomplicated and complicated diverticulitis.

FACULTY
Priscilla Marsicovetere is Assistant Professor of Medical Education and Surgery, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, and Program Director for the Franklin Pierece University, PA Program, Lebanon, New Hampshire. She practices with Emergency Services of New England, Springfield Hospital, Springfield, Vermont.

The author has no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through July 31, 2019.

Article begins on next page >>

Treatment of this common complication of diverticular disease is predicated on whether the presentation signals uncomplicated or complicated disease. While some uncomplicated cases require hospitalization, many are amenable to primary care outpatient, and often conservative, management. The longstanding practice of antibiotic treatment of uncomplicated cases is now considered a selective, rather than a routine, option.

Diverticular disease is one of the most common conditions in the Western world and one of the most frequent indications for gastrointestinal-related hospitalization.¹ It is among the 10 most common diagnoses in patients presenting to the clinic or emergency department with acute abdominal pain.² Prevalence increases with age: Up to 60% of persons older than 60 are affected.³ The most common complication of diverticular disease is diverticulitis, which occurs in up to 25% of patients.⁴

The spectrum of clinical presentations of diverticular disease ranges from mild, uncomplicated disease that can be treated in the outpatient setting to complicated disease with sepsis and possible emergent surgical intervention. The traditional approach to diverticulitis has been management with antibiotics and likely sigmoid colectomy, but recent studies support a paradigm shift toward more conservative, nonsurgical treatment.

This article highlights current trends in diagnosis and management of acute diverticulitis.

DEFINITION AND EPIDEMIOLOGY

Diverticular disease is marked by sac-like outpouchings, called diverticula, that form at structurally weak points of the colon wall, predominantly in the descending and sigmoid colon.⁵ The prevalence of diverticular disease is increasing globally, affecting more than 10% of people older than 40, as many as 60% of those older than 60, and more than 70% of people older than 80.^1,3 The mean age for hospital admission for acute diverticulitis is 63.³

Worldwide, males and females are affected equally.³ In Western society, the presence of diverticula, also called diverticulosis, is more often left-sided; right-sided disease is more prevalent in Asia.^3,5

The most common complication of diverticular disease is diverticulitis—inflammation of a diverticulum—which affects 10% to 25% of patients with diverticular disease during their lifetime.^4,5 Diverticulitis can be classified as uncomplicated (characterized by colonic wall thickening or pericolic inflammatory changes) or complicated (characterized by abscesses, fistulae, obstruction, or localized or free perforations).^1,6 As many as 25% of diverticulitis cases are considered complicated.^4,5 The severity of diverticulitis is commonly graded using the Hinchey Classification (Table 1).^1,7

Continue to: PATHOPHYSIOLOGY

Diverticula tend to occur in areas where the colonic wall is weak: namely, between the mesenteric and antimesenteric taeniae, where the vasa recta penetrate the muscle—points of entry of blood vessels through the colonic wall.^1,4 The exact pathogenesis of diverticular disease is not completely understood but is thought to be multifactorial. Microscopic studies have shown muscular atrophy at the sites of diverticula, making them more susceptible to mucosal herniation in the setting of increased intraluminal pressure.¹ Additional potential contributing factors include alterations in colonic microbiota, muscular dysfunction or dysmotility, lifestyle, and genetics.

Diverticulitis is the result of microscopic and macroscopic perforation of diverticula. Historically, the perforations were thought to result from obstruction of a diverticulum by a fecalith, leading to increased pressure within the outpouching, followed by perforation.³ Such obstruction is now thought to be rare. A more recent theory suggests that increased intraluminal pressure is due to inspissated food particles that lead to erosion of the diverticular wall, causing focal inflammation and necrosis and resulting in perforation.³ Microperforations can easily be contained by surrounding mesenteric fat; however, progression to abscess, fistulization, or intestinal obstruction can occur. Frank bowel wall perforation is not contained by mesenteric fat and can lead quickly to peritonitis and death if not treated emergently.

RISK FACTORS

Dietary fiber

In 1971, Burkitt was the first to posit that diverticular disease developed due to small quantities of fiber in the diet that led to increased intracolonic pressures.⁸ His theory was based on the observation that residents of several African countries, who ate a high-fiber diet, had a low incidence of diverticular disease. Burkitt hypothesized that this was due to shorter colonic transit time induced by high dietary fiber.

Several studies conducted since Burkitt made his observations have examined the association of dietary fiber and diverticular disease, with conflicting results. In 1998, Aldoori et al found that a low-fiber diet increases the incidence of symptomatic diverticular disease.⁹ However, in 2012, a large cohort study of patients undergoing colonoscopy found that those who reported the highest fiber intake were at highest risk for diverticulosis.¹⁰ In 2013, Peery et al examined the relationship among bowel habits, dietary fiber, and asymptomatic diverticulosis and found that less-frequent bowel movements and hard stools were associated with a decreased risk for diverticulosis.¹¹ In 2017, a prospective cohort study of nearly 50,000 men without a known history of diverticulosis showed that diets high in red meat were associated with a higher incidence of diverticulitis over nearly three decades of follow-up, whereas a diet high in fiber was associated with a decreased incidence of diverticulitis.¹²

Although no definitive association has been found between dietary fiber intake and risk for diverticulosis, some studies have demonstrated an association between dietary fiber and diverticular complications. In 2014, Crowe et al found that consumption of a high-fiber diet was associated with a lower risk for hospital admission and death from diverticular disease.¹³ Recent guidelines from the American Gastroenterological Association (AGA) on diverticulitis recommend high dietary fiber intake in patients with a history of acute diverticulitis.¹⁴ However, no study has shown a reversal of the process or a reduction in the number of episodes of diverticulitis after adoption of a high-fiber diet.

Continue to: Historically, patients with diverticulitis...

Smoking

Smoking has been linked to diverticulitis and has been associated with a threefold risk for complications, including severe diverticulitis.^16,17 An increased risk for recurrent episodes has also been found in smokers following surgical intervention.¹⁷

Medications

NSAIDs, corticosteroids, and opioids have been associated with an increased risk for perforated diverticulitis.^18,19 A significant association has been found between NSAID use and severity of diverticulitis, including perforation; one study reported a relative risk of 1.25 (95% confidence interval, 10.5 to 1.47) for diverticulitis with regular use of aspirin (≥ 2x/wk).^20,21

More frequent steroid use has been found in patients with complicated diverticulitis, compared to patients with uncomplicated disease (7.3% vs 3.3%; P = .015).²² A systematic review of five studies comparing patients with and without steroid use showed significantly higher odds of diverticular perforation in patients taking a steroid.²³ Pooled data showed significantly increased odds of perforation and abscess formation with use of an NSAID (odds ratio [OR], 2.49), steroid (OR, 9.08), or opioid (OR, 2.52).²²

Continue to: Vitamin D

Vitamin D

In a 2013 retrospective cohort study of 9,116 patients with uncomplicated diverticulosis and 922 patients who developed diverticulitis that required hospitalization, Maguire et al examined the association of prediagnostic serum levels of vitamin D and diverticulitis.²⁴ Among patients with diverticulosis, higher prediagnostic levels of 25-hydroxyvitamin D were significantly associated with a lower risk for diverticulitis—indicating that vitamin D deficiency could be involved in the pathogenesis of diverticulitis.

The association between diverticulitis and vitamin D levels was supported by an additional study in 2015, in which the authors investigated the association between ultraviolet (UV) light and diverticulitis.²⁵ They identified nonelective diverticulitis admissions in the Nationwide Inpatient Sample database and linked hospital locations to geographic UV data. They examined UV exposure in relation to risk for admission for diverticulitis and found that, compared with high-UV (UV4) areas, low-UV (UV1) areas had a higher rate of diverticulitis (751.8/100,000 admissions, compared with 668.1/100,000 admissions, respectively [P < .001]), diverticular abscess (12.0% compared with 9.7% [P < .001]), and colectomy (13.5% compared with 11.5% [P < .001]). They also observed significant seasonal variation, with a lower rate of diverticulitis in winter (645/100,000 admissions) compared with summer (748/100,000 admissions [P < .001]). Because UV exposure largely determines vitamin D status, these findings are thought to support a role for vitamin D in the pathogenesis of diverticulitis.

Genetics

Two studies found an association between genetics and diverticular disease. A 2012 study using The Swedish Twin Registry found that if one twin is affected with the disease, the odds that the other will be affected was 7.15 in monozygotic (identical) twins and 3.20 in dizygotic (fraternal) twins.²⁶ A 2013 Danish twin study found a relative risk of 2.92 in twin siblings compared to the general population.²⁷ Both studies estimated the genetic contribution to diverticular disease to be 40% to 50%.^26,27

Obesity

Several large prospective studies have shown a positive association between high BMI, waist circumference, and waist-to-hip ratio and risk for diverticulitis.⁴ A BMI > 30 was found to increase the relative risk of acute diverticulitis by 1.78, compared with a normal BMI.¹⁷ In a large, prospective, population-based cohort study in 2016, Jamal Talabani et al found that obese persons had twice the risk for admission for acute colonic diverticulitis than normal-weight persons did.²⁸ Waist circumference and waist-to-hip ratio were also independently associated with risk for diverticulitis. The pathophysiology of the associations is not clearly understood but may involve pro-inflammatory changes of adipose tissue, which secrete cytokines that promote an inflammatory response, and changes in gut microbiota.^4,12

Physical activity

Data on the association of physical activity and diverticulitis is inconsistent. Some studies have found as much as a 25% decrease in the risk for diverticulitis with increased physical activity; more recent studies (2013 and 2016), on the other hand, found no association between diverticulosis and physical activity.^11,17,19,28

Continue to: CLINICAL PRESENTATION

The clinical presentation of diverticulitis typically depends on the severity of inflammation and the presence (or absence) of complications. The most common presenting symptom is left lower-quadrant abdominal pain, which occurs in approximately 70% of cases and lasts for longer than 24 hours.²⁹ Fever (usually < 102°F), leukocytosis, nausea, vomiting, and changes in bowel function may also be present.^1,30,31 Approximately 50% of patients report constipation in diverticular disease; 20% to 35% report diarrhea.⁵

Patients may also report dysuria, secondary to irritation of the bladder by an inflamed segment of colon.^3,17 Patients may report fecaluria, pneumaturia, or pyuria, which indicate a colovesical fistula.¹ Passage of feces or flatus through the vagina indicates a colovaginal fistula.

The differential diagnosis of diverticulitis is listed in Table 2.¹⁷

PHYSICAL EXAMINATION

Physical examination in diverticulitis will almost always elicit tenderness to palpation over the area of inflammation, typically in the left lower quadrant. This is due to irritation of the peritoneum.³ A palpable mass may be present in as many as 20% of patients if an abscess is present. Bowel sounds may be hypoactive or hyperactive if there is a bowel obstruction.¹⁷ In cases of frank bowel-wall perforation, patients can present with peritoneal signs of rigidity, guarding, and rebound tenderness.^3,31 Tachycardia, hypotension, and shock are rare but possible findings. Digital rectal examination may reveal tenderness or a mass if a pelvic abscess is present.^17,31

DIAGNOSTICS

The diagnosis of acute diverticulitis can often be made clinically, based on the history and physical examination. Because clinical diagnosis can be inaccurate in as many as 68% of cases, however, laboratory testing and imaging play an important role in diagnosis.³

Continue to: Clinical laboratory studies

Because leukocytosis is present in approximately one-half of patients with diverticulitis, a complete blood count (CBC) should be obtained; that recommendation notwithstanding, approximately one-half of patients with diverticulitis have a normal white blood cell count.^29,30 A urine test of human chorionic gonadotropin should be ordered to exclude pregnancy in all premenopausal and perimenopausal women, particularly if antibiotics, imaging, or surgery are being considered.³¹ Urinalysis can assess for urinary tract infection.

Multiple studies have demonstrated the utility of C-reactive protein (CRP) in the workup of acute diverticulitis. In general, patients with a complicated episode will present with a significantly higher CRP level than that of uncomplicated disease.³² Kechagias et al found that the CRP level at initial evaluation may be helpful in predicting the clinical severity of the attack. A CRP level > 170 mg/L has been found to have a greater probability of severe disease, warranting CT and referral for hospitalization.³³ A low CRP level was more likely to herald a mild course of disease that is amenable to outpatient antibiotic management or supportive care. This finding is consistent with previous reports of the association between CRP levels of 90 to 200 mg/L and the severity of diverticulitis.^32,34

Imaging

Abdominopelvic CT with intravenous (IV) contrast. This imaging study is the gold standard diagnostic tool for diverticulitis, with sensitivity as high as 97%.³ CT can distinguish diverticulitis from other conditions, such as irritable bowel syndrome (based on a history of symptoms and the absence of CT findings), gastroenteritis, and gynecologic disease. It can also distinguish between uncomplicated and complicated diverticulitis and therefore guide therapeutic interventions, such as percutaneous drainage of an intra-abdominal abscess. CT findings associated with uncomplicated diverticulitis include colonic wall thickening and pericolonic fluid and inflammatory changes, such as fat stranding. CT findings associated with complicated disease include abscess (paracolonic or pelvic), peritonitis (purulent or feculent), phlegmon, perforation, fistula, and obstruction.^1,3

Ultrasonography (US) can also be used in the assessment of diverticulitis, although it has lower sensitivity (approximately 61% to 84%) than CT and is inferior to CT for showing the extent of large abscesses or free air.^3,18,30 A typical US finding in acute diverticulitis is a thickened loop of bowel with a target-like appearance.¹⁷ Findings are highly operator-dependent, however, and accuracy is diminished in obese patients. US may be a good option for pregnant women to avoid ionizing radiation.

Magnetic resonance imaging (MRI) is another option for imaging in diverticulitis but is not routinely recommended. It provides excellent soft-tissue detail and does not deliver ionizing radiation, but it is not as sensitive as CT for identifying free air.^18,31 Furthermore, MRI requires prolonged examination time, which may not be tolerated by acutely ill patients, and is not an option for patients with certain types of surgical clips, metallic fragments, or a cardiac pacemaker.

Continue to: Abdominal radiography...

MANAGEMENT

For decades, patients with diverticulitis were managed with antibiotics to cover colonic flora; many underwent urgent or emergent surgery to remove the affected segment of colon. Over the years, however, the treatment paradigm has shifted from such invasive management toward a nonsurgical approach—often, with equivalent or superior outcomes. More and more, management of diverticulitis is dictated by disease presentation: namely, whether disease is uncomplicated or complicated.¹

Current guidelines recommend hospitalization, with possible surgical intervention, in complicated disease (free perforation, large abscesses, fistula, obstruction, stricture) and in patients who cannot tolerate oral hydration, who have a relevant comorbidity, or who do not have adequate support at home.³⁵ Uncomplicated cases may also require hospitalization if certain criteria for admission are met: immunosuppression, severe or persistent abdominal pain, inability to tolerate oral intake, and significant comorbidity.⁵

Absent these criteria, outpatient management of uncomplicated diverticulitis is appropriate. After the treatment setting is determined, choice of intervention and length of treatment should be addressed.

Nonpharmacotherapeutic management

Dietary restrictions, from a full liquid diet to complete bowel rest, have been recommended for the management of acute diverticulitis. This recommendation is not supported by the literature, however. At least two studies have shown no association between an unrestricted diet and an increase in diverticular complications. In a 2013 retrospective cohort study, no increase in diverticular perforation or abscess was found with a diet of solid food compared to a liquid diet, a clear liquid diet, or no food by mouth.³⁶ In a more recent (2017) prospective cohort study of 86 patients with uncomplicated diverticulitis, all of whom were on an unrestricted diet, only 8% developed complications.³⁷

Continue to: There is no high-quality evidence for...

There is no high-quality evidence for instituting dietary restrictions in acute uncomplicated diverticulitis. As such, permitting oral intake as tolerated is a reasonable option.

Pharmacotherapy

Antibiotics have long been the cornerstone of pharmacotherapy for acute diverticulitis, covering gram-negative rods and anaerobes. The rationale for such management is the long-held belief that diverticulitis is caused by an infectious process.³⁸ Common outpatient regimens include

• Ciprofloxacin (500 mg every 12 h) plus metronidazole (500 mg every 8 h)
• Trimethoprim–sulfamethoxazole (1 double-strength tablet every 12 h) plus metronidazole (500 mg every 8 h)
• Amoxicillin (875 mg)–clavulanate (1 tablet every 8 h) or extended-release amoxicillin–clavulanate (2 tablets every 12 h)
• Moxifloxacin (400 mg/d; for patients who cannot tolerate metronidazole or ß-lactam antibiotics).

Providers should always consult their local antibiogram to avoid prescribing antibiotics to which bacterial resistance exceeds 10%.

Despite widespread use of antibiotics for diverticulitis, multiple studies in recent years have shown no benefit to their use for uncomplicated cases. In 2012, Chabok et al investigated the need for antibiotic therapy to treat acute uncomplicated diverticulitis and found no statistically significant difference in outcome among patients treated with antibiotics and those managed conservatively.³⁹ In 2014, Isacson et al performed a retrospective population-based cohort study to assess the applicability of a selective “no antibiotic” policy and its consequences in terms of complications and recurrence; the authors found that withholding antibiotics was safe and did not result in a higher complication or recurrence rate.⁴⁰ Furthermore, in a 2017 multicenter study, Daniels et al conducted a randomized controlled trial comparing observation and antibiotic treatment for a first episode of uncomplicated acute diverticulitis in 528 patients and found no prolongation of recovery time, no increased rate of complications, and no need for surgical intervention in patients who were not treated with antibiotics.⁴¹

These studies are in agreement with the most recent AGA guidelines, which recommend selective, rather than routine, use of antibiotics for acute diverticulitis.¹⁴ This shift in approach may be due, in part, to a change in understanding of the etiology of the disease—from an infectious process to more of an inflammatory process.³⁸

Continue to: For patients who require inpatient management of diverticulitis...

Other agents used to manage diverticulitis include three that lack either strong or any data at all showing efficacy. The most recent AGA guidelines recommend against their use for this indication¹⁴:

Rifaximin. Two recent observational cohort studies, one from 2013 and the other from 2017, compared this poorly absorbed oral antibiotic with mesalamine to placebo or no treatment at all.⁴² Neither provided evidence that rifaximin treats or prevents diverticulitis.

Mesalamine. This anti-inflammatory has also been studied to prevent recurrence of diverticulitis. In a randomized, double-blind, placebo-controlled multicenter trial of 1,182 patients, Raskin et al found that mesalamine did not reduce the rate of recurrence of diverticulitis, time to recurrence, or the number of patients requiring surgery.⁴³ This conclusion was reiterated by a 2016 meta-analysis that found no evidence to support use of mesalamine in the prevention of diverticulitis recurrence.⁴⁴

Probiotics. Despite multiple studies undertaken to assess the efficacy of probiotics in the prevention and treatment of diverticular disease, strong data supporting their use are sparse. In 2016, Lahner et al examined 11 studies in which various probiotics were used to treat diverticular disease and found that, although there was a weak positive trend in the reduction and remission of abdominal symptoms, the evidence was not strong enough to recommend their routine use in managing the disease.⁴⁵

Continue to: Surgical treatment

Surgical treatment

Acute uncomplicated diverticulitis can be treated nonsurgically in nearly all patients, regardless of whether treatment occurs in the inpatient or outpatient setting. For complicated disease, however, approximately 15% to 25% of patients require surgery. The main indication for emergent or urgent surgical intervention is colonic perforation, which can lead to acute peritonitis, sepsis, and associated morbidity and mortality.²⁹

The decision to perform elective surgery should be made case by case, not routinely—such as after a recurrent episode of diverticulitis, when there has been a complication, or in young patients (< 50 years).^1,11 Immunocompromised patients (transplant recipients, patients taking steroids chronically, and patients with HIV infection who have a CD4 count < 200 cells/μL) can pre­sent with more virulent episodes of diverticulitis, have a higher incidence of perforation and fecal peritonitis, and have a greater likelihood of failure of nonsurgical management.¹ Surgical intervention after the first episode of diverticulitis in these patients should therefore be considered.

In 2014, the American Society of Colon and Rectal Surgeons (ASCRS) recommended the laparoscopic Hartmann procedure (primary resection of the affected segment of colon, with end colostomy, followed by colostomy closure) as the gold standard for the treatment of acute perforated diverticular disease when surgery is required.⁴⁶

COLONOSCOPY AFTER DIVERTICULITIS

Although endoscopy is to be avoided during acute diverticulitis because of the risk for perforation, it is recommended six to eight weeks after the acute episode has resolved to rule out malignancy, inflammatory bowel disease, and colitis.^1,3 Interestingly, in 2015, Daniels et al compared the colonoscopic detection rate of advanced colonic neoplasia in patients with a first episode of acute diverticulitis and in patients undergoing initial screening for colorectal cancer, and found no significant difference in the detection rate between the two groups.⁴⁷ The authors concluded that routine colonoscopic follow-up after an episode of acute uncomplicated diverticulitis could be eliminated and that those patients could be screened according to routine guidelines.

Lau et al found a number of cancers and other significant lesions on colonoscopy performed after an episode of acute diverticulitis, with a 2.1% prevalence of colorectal cancer within one year after CT-proven diverticulitis, and an increase in the prevalence of abscess, local perforation, and fistula.⁴⁸ Their study excluded patients who had had a colonoscopy within one year, however. They therefore recommended performing colonoscopy only for patients who have not had a recent colonoscopic exam. This recommendation is in accord with the most recent AGA and ASCRS guidelines. If a patient has had a recent colonoscopy prior to an acute episode of diverticulitis, the value of repeating the study after the episode resolves is unclear.

Continue to: CONCLUSION

As this article shows, the spectrum of clinical presentations for diverticulitis is broad, and management most often requires a case-by-case approach. Treatment is dictated by whether disease presentation is uncomplicated or complicated; outpatient management is appropriate for uncomplicated cases in the absence of specific criteria for hospitalization. Recent evidence supports a paradigm shift away from mandatory dietary restriction and routine antibiotic use.

CE/CME No: CR-1711

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand basic anorectal anatomy and how to perform a thorough anorectal exam.
• Describe the physical exam findings of common benign anorectal conditions.
• Discuss the different treatment options for benign anorectal conditions.
• Differentiate between common benign anorectal symptoms and red flags that should prompt referral to a colorectal specialist.

FACULTY
Priscilla Marsicovetere is an Assistant Professor of Medical Education and of Surgery at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire; Program Director for the Franklin Pierce University PA Program in Lebanon, New Hampshire; and practices with Emergency Services of New England at Springfield Hospital in Vermont. Srinivas Joga Ivatury is an Assistant Professor of Surgery at the Geisel School of Medicine at Dartmouth and practices in the Department of Surgery at the Dartmouth Hitchcock Medical Center in Lebanon, New Hampshire.

The authors have no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through October 31, 2018.

Article begins on next page >>

Anorectal pain and discomfort can stem from several possible etiologies, most of which are benign. As such, many patients with anorectal complaints who present in the primary care setting can be adequately evaluated, diagnosed, and treated without referral to a colorectal specialist. However, the clinician must be able to differentiate between common benign anorectal symptoms and red flags that should prompt referral.

Anorectal disorders are common in the United States and result in numerous primary care visits each year. Presentations range from pain and itching to bleeding and lesions. Common anorectal conditions include hemorrhoids, perianal skin tags, fissures, pruritus ani, perianal abscess, and condyloma. Most are benign and can be managed in the primary care setting.

Before a provider can competently diagnose and treat anorectal conditions, however, a comprehensive history and physical examination must be conducted. Grucela and colleagues documented that physicians’ diagnostic accuracy with anorectal conditions is about 50%—highlighting the need for providers to become more familiar with the history and clinical elements associated with anorectal complaints.¹

This article reviews the assessment of the anorectum, diagnosis of common disorders and their recommended treatments, and red flags for referral to a colorectal specialist.

ANORECTAL ANATOMY

The beginning of the anal canal is demarcated by its moist, hairless appearance. Just inside the anal opening are two palpable circular muscles, the internal and external anal sphincters, separated by an intersphincteric groove. The sphincters are firmly closed in the resting state, which helps maintain continence.

The anal canal is generally 3 to 4 cm long and ends at the dentate line, a series of crypts in the anal mucosa.² The crypts are openings into the anal glands, which are mucus-secreting structures in the anus. The dentate line is easily identified on anoscopy as a discrete change in the appearance of the mucosa. The dentate line is an important landmark because it delineates the boundary between somatic and visceral nerve supplies.³ Tissue proximal to the dentate line is innervated by visceral nerves and is insensate, and thus usually not a cause of pain; tissue distal to the dentate line, however, is highly innervated by somatic nerves and can be intensely painful.²

The anorectal canal is lined by three fibrovascular cushions, located in the left lateral, right posterior, and right anterior positions.⁴ Inside each cushion is a venous structure, called a hemorrhoid, which allows the cushion to enlarge and help maintain continence.⁵

Proximal to the anus is the rectum, the 12- to 15-cm long terminus of the colon. Anorectal examination in the primary care setting will typically not progress beyond the last 2 to 3 cm of the rectum.

TAKING THE HISTORY

A thorough history will provide clues about potential underlying anorectal pathology. Patients may not be forthcoming about symptoms due to embarrassment, fear of a cancer diagnosis, or cultural customs or habits. A thorough history should elicit information about all of the patient’s symptoms (see Table 1), including bleeding, change in bowel habits, and unintended weight loss.

PHYSICAL EXAM

Positioning the patient

Undergoing an anorectal examination can be embarrassing, whether it be from exposure of sensitive body parts or the less-than-desirable prone jackknife positioning. Patients often have preconceived notions that the exam will be humiliating and/or painful. Care should be taken to minimize any embarrassment and discomfort.

Positioning of the patient is a matter of provider preference. Options include the left lateral decubitus, prone jackknife, or lithotomy positions.

Positioning should always be done with draping. Regardless of position, ensure the draping exposes only the perineum. This can be achieved by encircling the patient’s bare bottom with a plain white sheet that exposes only the anus and surrounding skin, keeping the lower back, lateral buttocks, and thighs covered.

Interestingly, data on patient preference for positioning during anorectal exams are limited. In a 2009 study of 178 patients undergoing anorectal exam, more than half of patients (up to 71.4%) expecting to or having already had a proctologic exam reported that no specific type of positioning (eg, Sims, lithotomy with lifted legs, knee-chest, knee-chest with patient’s body bent forward) was most embarrassing to them.⁶ The report revealed that while most patients would favor the Sims position if they had a choice, they deferred to their examiner to choose the position that seemed most suitable to get a reliable diagnosis.⁶

Inspection of the perineum

Once the patient is properly positioned and draped, inspection of the perineum can occur. Begin by gently spreading the buttocks. Describe any abnormality seen (eg, ulcer, lesion, dermatitis, prolapsing tissue, or blood), including size, color, and location.

A common pitfall is to describe the location of abnormalities using a clock face, such as “at 4 o’clock.” This is misleading and should be avoided, because depending on patient position, the clock face can point to different locations (eg, if the patient is in the lithotomy versus prone jackknife position).

A better approach is to divide the perianal area into four anatomic quadrants: right anterior, right posterior, left anterior, left posterior. Using this schematic, the patient's position is irrelevant, and accurate documentation of lesion location is assured.

Digital rectal exam

After visual inspection of the perianal skin, a digital rectal exam (DRE) should be performed. Slowly insert a gloved, lubricated index finger into the anus and lower rectum. Note the tone of the anus at rest (eg, excessively tight vs lax). Palpate the circumference of the anus, sweeping side to side while assessing for any tenderness, mass, or induration—if present, note the anatomic quadrant. If a mass is felt, note whether it is firm or soft, fixed or mobile, and broad-based or pedunculated. When the lubricated finger is removed from the anus, note whether blood is present.

Anoscopy

After DRE, visually inspect the anorectum. The instrument used varies from anoscope to rigid proctoscope to flexible sigmoidoscope. In a primary care setting, the most likely available instrument is an anoscope. The average anoscope is about 7 cm long and 2 cm in diameter, with a beveled tip and an obturator (see Figure 1), and allows a 360° view of the anal canal.⁷

Examination of the anal canal is accomplished by dividing the canal into the four anatomic quadrants described earlier and inserting the lubricated anoscope for inspection of each of the four quadrants. Observe the rectal mucosa and the anus as the scope is slowly withdrawn. If abnormalities are seen, note the location, size, shape, and any other descriptive features.

It is not necessary to perform a Hemoccult test after examination of the anorectum, as the presence of minor blood may be the direct result of the exam itself and thus provides no useful information to the examiner.

COMMON PATHOLOGIES

Once the history and physical exam are complete, a differential diagnosis can be formulated. Most anorectal disorders are benign conditions that pose no immediate health threat and can be managed in the primary care setting. Others, however, can be more serious and should prompt referral to a colorectal specialist for further evaluation. Knowing the difference can spare a patient unnecessary anxiety and referral; it can also lead to prompt, lifesaving interventions if red flags are recognized.

Hemorrhoids

Hemorrhoids are a common anorectal complaint.^8,9 It is estimated that up to 75% of the population will experience symptoms of hemorrhoids during their lifetime.^5,8 Whether internal or external, in their normal, nonpathologic, quiescent state, hemorrhoids are asymptomatic. Hemorrhoids become symptomatic when the supporting structures of hemorrhoidal tissue (ie, the anal cushions) deteriorate, resulting in venous dilation, inflammation, and thrombosis, which in turn lead to swelling, bright red bleeding, and/or prolapse.^2,10 The most common causes of hemorrhoidal disease are chronic constipation and prolonged straining with bowel movements, though chronic diarrhea and pregnancy have also been identified as risk factors.^2,8,11

External hemorrhoids, which are located distal to the dentate line, are typically only visible when they become thrombosed or swollen. In this state, they may manifest as acute-onset, exquisitely painful, large, purple-to-blue bulges at the anal outlet (see Figure 2). The number and size of the lesions can vary. The patient may report pain when sitting or wiping, as well as bleeding from the lesion.^12,13 The pain is typically severe in the first couple of days, then slowly starts to subside.^2,12

For internal hemorrhoids, which are located proximal to the dentate line, the main symptom is usually painless bright red blood per rectum.^8,11,12 Patients may also report a sensation of rectal fullness or experience prolapse of the hemorrhoid through the anus. Prolapse typically occurs with defecation; in more severe cases, it can also occur between bowel movements, usually with any activity that increases intra-abdominal pressure (eg, coughing, heavy lifting, pregnancy, portal hypertension). The prolapse may reduce spontaneously, or may have to be manually reduced. If it cannot be reduced, there is a risk for incarceration or strangulation, potentially leading to gangrene.

The presence of bleeding and/or prolapse determines the classification of internal hemorrhoids (see Table 2). Dietary and lifestyle modification are used in the management of all grades of hemorrhoids. In addition, for grade 1 and 2 lesions, topical medication (eg, anti-inflammatory cream) can be used, whereas grade 3 (and selected grade 2) lesions respond well to rubber band ligation. Given the severity of grade 4 lesions, surgical intervention (eg, hemorrhoidectomy) is usually indicated.¹⁰

About a third of patients with symptomatic hemorrhoids seek clinical treatment.¹⁴ Most are hemodynamically stable and require no imaging and usually no labs (unless anemia is suspected).² Management depends on the location and degree of symptoms (eg, internal vs external, prolapse, or thrombosis). In the event of an acutely thrombosed external hemorrhoid, clot excision for pain relief is appropriate if symptoms have been present for less than 48 to 72 hours; after that amount of time, the pain from the procedure will likely exceed the degree of relief provided, and conservative management should instead be recommended.^2,8,11

Firstline treatment consists of lifestyle modification with a high-fiber diet and daily fiber supplement to ensure stool is soft and easy to pass.^2,8 A meta-analysis of seven clinical trials with a total of 378 patients with hemorrhoids showed that fiber supplementation resulted in a 50% decrease in bleeding risk from internal hemorrhoids.¹⁵

Adequate hydration, preferably with noncaffeinated liquids, is also recommended. This will prevent constipation and the need to strain or spend excessive time on the toilet. Sitz baths can help alleviate pain and discomfort.

Several OTC topical medications are marketed for hemorrhoid relief. Many of these preparations contain steroids for their anti-inflammatory effects or astringents to address skin irritation that can result from anal leakage if prolapsing hemorrhoids prevent the anal outlet from closing. Steroid use should be limited to five to seven days, due to atrophic effects on the skin. While OTC preparations may temporarily alleviate discomfort, they will not address the underlying cause of symptoms.

Indications for referral to a colorectal specialist for symptomatic hemorrhoids include failure to improve with conservative management, persistent patient discomfort, and prolapse, as these indicate potential need for more invasive treatment.

Perianal skin tags

Perianal skin tags, while a nuisance, are not pathologic in most instances and pose no threat to health. They are an outgrowth of normal skin, appearing as loose, flesh-colored perianal tissues (see Figure 3). Tags range in size from a few millimeters to a centimeter long and can occur alone or in multiples.

Perianal skin tags are diagnosed clinically and require no labwork or imaging. Visual inspection is typically sufficient to distinguish tags from pathologic lesions such as condyloma or abscess. If there is uncertainty, however, biopsy or referral to a specialist is warranted.

Certain medical conditions can predispose a patient to development of perianal skin tags. They can be sequelae of thrombosed external hemorrhoids.^8,11 They are also common in patients with Crohn disease.¹¹ Perianal skin tags are not, however, the result of anal intercourse or sexually transmitted infections.

Treatment is usually not indicated for perianal skin tags. If the tags interfere with hygiene or cause perianal discomfort or significantly decreased quality of life, however, patients may seek removal. These patients should be referred to a colorectal specialist for evaluation for excision.

Anal fissures (fissure in ano)

The most common cause of severe anorectal pain is fissure.⁴ A fissure is an elliptical tear, or split, in the lining of the anal canal that causes spasm of the anal sphincters. The tear is distal to the dentate line and thus intensely painful.^2,5 Common cited causes of fissures are trauma from passage of large, hard stools, straining, or diarrhea.¹⁶

Fissures can usually be visualized by spreading the posterior anus apart (see Figure 4). They are most commonly located in the posterior or anterior midline, though they can occur anywhere around the anus.^2,4 Often, a sentinel tag—appearing as a taut, flesh-colored skin tag—is present at the external pole of the fissure.^5,11 DRE and anoscopy should be avoided, as they will trigger intense pain and spasm of the sphincters.

Fissures are characterized as acute (present ≤ 3 months) or chronic (> 3 months).^9,11 Visually, acute fissures typically have clean edges, with the appearance of a paper cut to the mucosa, while chronic fissures have indurated, heaped-up edges, often with exposure of the underlying sphincter muscle.¹⁷

They tend to be exquisitely painful, as the mucosa distal to the dentate line is highly innervated. Patients report pain akin to “passing shards of broken glass” with bowel movements, which is often accompanied by a fear of defecation and bright red blood on the toilet paper or dripping into the water.¹¹ The pain, caused by spasm of the sphincters, typically starts during a bowel movement and lasts minutes to hours afterward.

Initial treatment is aimed at relaxing the sphincters, as well as softening stool to prevent further trauma and allow the fissure to heal. Patients should be educated about the importance of adequate fiber intake to prevent constipation and straining. A daily bulk fiber supplement, in addition to a high-fiber diet (20-25 g/d), has been shown to result in healing of 87% of acute fissures.¹⁶ Sitz baths in plain warm water, three to four times a day, can encourage relaxation of the sphincters and increase local blood flow, both of which help with fissure healing.¹⁶ Topical medications can also be prescribed. These include compounded nitroglycerin 0.2% or nifedipine 2.0%, which act to reduce the spasm by relaxing smooth muscle, as well as increase blood flow to the lesion.^12,14

Most acute fissures will heal with the regimen of high fiber intake, sitz baths, and topical medication. For refractory or chronic fissures, referral to a colorectal specialist for more invasive treatment is appropriate. Additionally, fissures that are not located in the typical posterior or anterior midline might indicate an atypical etiology, such as Crohn disease, tuberculosis, leukemia, or HIV, and thus patients who present with fissures in these locations should also be referred to a colorectal specialist.^2,4,11,18

Pruritus ani

Pruritus ani, known as perianal dermatitis, is a benign condition that presents with intense perianal itching and burning. It is the second most common anorectal condition after hemorrhoids and affects up to 5% of the US population.^2,9,11,19

Pruritus ani often develops secondary to local irritation of the skin (eg, from prolonged exposure to moisture), leading to an inflammatory response within the superficial skin layers. The irritation causes patients to scratch the skin, resulting in trauma, excoriation, and ulcer formation and leading to a cycle of further inflammation, exacerbation of symptoms, and persistent scratching.

Physical exam may reveal circumferential erythematous and irritated perianal skin (see Figure 5). Linear or deep, punched-out excoriations may be present. Chronically, patients may develop lichenification with thick, whitened patches of skin.¹¹ In the absence of red flags such as unintentional weight loss, anemia, rectal bleeding, or a family history of colon cancer, no additional evaluation is required during the initial visit, though anoscopy can be used to rule out associated anorectal pathology.

Many different causes of pruritus ani have been reported (see Table 3). In the case of an identifiable cause, symptoms tend to resolve once the offending agent is eliminated. Up to a quarter of cases, however, are idiopathic, with no identifiable trigger.²⁰

Symptom management is thus key. Patients should be educated about lifestyle modification and informed that scratching will irritate the skin further and aggravate symptoms.^5,11 If incontinence or diarrhea is thought to cause symptoms, dietary modifications, a fiber supplement, dysmotility agents, and Kegel exercises to strengthen the sphincters and decrease anal leakage can be recommended.

The affected skin should be kept clean and dry at all times. Aggressive wiping and overzealous hygiene should be avoided. Sitz baths can help with hygiene. A topical astringent such as witch hazel can help remove excess moisture from the skin. A layer of protective skin barrier cream with zinc oxide, when applied over dry skin, can help protect the skin from leakage throughout the day.

A sedating antihistamine can reduce scratching during sleep. Topical hydro­cortisone 1% cream is effective for itch relief; this should be limited to five to seven days of consecutive use, however, as it can lead to pathologic thinning of the perianal skin. Topical capsaicin 0.006% cream has been shown to help alleviate intractable ­pruritus.^2,21

The goal of these measures is to break the cycle of irritation and inflammation and give the skin an opportunity to heal. If the patient fails to improve, referral to a colorectal specialist or, alternatively, a dermatologist, is warranted for perianal skin biopsy and more invasive treatment options.

Perianal abscess

A perianal abscess is an infected cavity filled with pus under pressure, located near the anus or rectum. It most often results from an acute infection of the anorectal glands located at the dentate line that tracks outward to the perianal skin.¹² Abscesses can also result from another disease process, such as Crohn disease, diabetes, or rectal trauma.^2,11

Localized pain, swelling, and drainage are common presenting symptoms of an abscess.^2,11 Systemic symptoms such as fever and chills may present later in the course but are rare.²

Treatment of the acute process is incision and drainage (I&D).^11,12 This can be accomplished in the office with injection of local anesthesia, followed by excision of an ellipse of skin overlying the cavity large enough to allow full drainage of the abscess. Use of drains and packing of the wound are usually not necessary. There is also no role for antibiotics unless the patient is diabetic or immunosuppressed or cellulitis is present.¹¹ In patients with systemic signs of illness, imaging such as CT or MRI of the pelvis can be used to assess for a deeper infection.^2,12

For most patients, I&D resolves the process. However, up to half of perianal abscesses progress to form a fistula, a tunnel connecting the infected anal gland to the external skin.^2,11,22 Indeed, abscesses and fistulae are part of the same infectious process, with the abscess representing the acute phase of infection and the fistula representing the chronic phase. On physical exam, in addition to the abscess site on the skin, a fistula may manifest as a palpable cord beneath the skin between the anus and the abscess opening.⁹ Additionally, the patient may report the abscess has been recurrent in nature, cyclically increasing in size and pain, then spontaneously draining.

A fistula requires surgical intervention for definitive treatment and should therefore prompt referral to a colorectal specialist. In the absence of fistula, however, a simple perianal abscess can be treated with I&D in the primary care setting.

Condyloma acuminatum

Condyloma acuminatum, also known as genital warts, is the most common sexually transmitted infection in the United States and a frequent anorectal complaint.^23-25 More than 6 million new infections occur annually.²⁵

Condyloma is caused by the human papillomavirus (HPV).²⁴ More than 100 HPV subtypes have been identified.²⁵ Types 6 and 11 are associated with typical condyloma acuminatum, while types 16 and 18 are found more commonly with dysplasia and malignant transformation.^3,26

The lesions are spread by direct skin-to-skin or mucosa-to-mucosa contact, including anal intercourse. They appear as tiny finger-like projections on the perianal or genital skin, often with a cauliflower-like appearance, in clusters or as single entities, and ranging in size from a few millimeters to several centimeters (see Figure 6).

The patient may be asymptomatic or may complain of bleeding with defecation or leakage from the rectum between bowel movements. In up to 90% of perianal condyloma, concomitant anorectal lesions are present.³ Anoscopy is therefore indicated whenever perianal lesions are seen.

Treatment of genital warts varies depending on the number and location of lesions. The goal is lesion removal, but none of the available treatments are curative.²⁴ If only a few small (diameter < 2 mm) warts are seen in the perianal area, with no anal involvement, these can be treated with topical cytotoxic agents. A commonly used agent is podophyllotoxin 0.15% (a derivative of podophyllin), an antimitotic agent that interferes with viral replication and induces necrosis of the wart.²⁶ Podophyllin is effective for small warts, but recurrence rates range from 38% to as high as 79%.^24,26 The most common side effects are local erythema, swelling, pain, and pruritus.

Trichloroacetic acid (TCA), which is considered a form of chemical cautery, has been deemed more effective for tiny warts (diameter 1-2 mm) and better tolerated than podophyllin.²⁴ Unlike podophyllin, however, TCA must be applied in clinic by a specialist, not at home by the patient. It works by chemically burning, cauterizing, and eroding skin and mucosa, thereby destroying old infected cells and allowing for growth of new, healthy cells.²⁴ Using a solution with a higher concentration of TCA (80%-90%) has been shown to be more effective than lower concentration solutions (30%).²⁴ The recurrence rate is high, generally about 36%.²⁷ Due to its low risk for systemic absorption, TCA is safe for use during pregnancy.²⁴

Local application of an immunomodulator, such as imiquimod 2%, 3.75%, or 5% cream, can also be used. Imiquimod works by upregulating tumor necrosis factor, leading to decreased viral replication and subsequent regression of warts.²⁴ The most common side effects of imiquimod are erythema, erosions, burning, and pruritus.²⁴ The higher concentration is associated with increased clearance rates as well as increased adverse effects.²⁷ Therefore, the 3.75% cream is the preferred concentration of most providers.²⁷ Recurrence rates range from 13% to 19%.²⁸

In 2006, the FDA approved polyphenon E, a botanical ointment, to treat anogenital warts. The formulation is composed of eight different sinecatechins extracted from green tea leaves.²⁹ Green tea sinecatechins have been shown to have antioxidant, antiproliferative, and antiviral properties, though the specific mechanisms of action in inhibiting anogenital wart growth have not been well studied to date. In a multicenter, randomized, double-blind, vehicle-controlled, three-arm parallel group phase 3 trial of 495 patients with anogenital warts, sinecatechins ointment 10% or 15% applied three times daily for 16 weeks resulted in complete clearance of warts in 57.2% and 56.3% of patients, respectively, compared to 33.7% clearance in the vehicle patients.³⁰ Partial clearance (≥ 50%) of warts was observed in 78.4% of patients who used the 15% ointment, 74.0% of those who used the 10% ointment, and 51.5% of the vehicle patients. Rates of recurrence were 6.5% and 8.3% with use of the 10% and 15% sinecatechins ointment, respectively, which are much lower than recurrence rates observed with other topical applications (eg, imiquimod and podophyllotoxin).³⁰

For larger warts or when there are anal lesions present, surgical excision and fulguration is required and referral to a colorectal specialist is warranted.

Warts recur from 4.6% to more than 70% of the time, most commonly due to activation of latent virus.²³ Therefore, whether initially treated in an office or operating room, condyloma patients require follow-up on a regular basis, generally every six to 12 months, to assess for recurrent anal lesions so that treatment can be promptly initiated.

In the absence of a cure for anogenital warts, prevention through an HPV vaccine is important. The quadrivalent HPV vaccine (Gardasil) was approved by the FDA in 2006 for prophylactic vaccination of females ages 9 to 26. The vaccine triggers host formation of antibodies against four common subtypes of HPV: 6, 11, 16, and 18.³¹ In 2009, the FDA expanded the use of Gardasil to include males ages 9 to 26; subsequently, Gardasil 9 (which protects against nine types of HPV) was approved for males ages 9 to 15.³² In a group of 4,065 healthy males between the ages of 16 and 26, Gardasil reduced the incidence of external anogenital warts by 90.4%.³³

HPV vaccine is now recommended for females through age 26 and males through age 21. The CDC also recommends HPV vaccine for the following individuals through age 26 if they did not get vaccinated when they were younger:

• Young men who have sex with men
• Young men who identify as gay or bisexual or who intend to have sex with men
• Young adults who are transgender
• Young adults with immunocompromising conditions (including HIV).³⁴

CONCLUSION

Anorectal conditions are a common presentation in the primary care setting. A thorough history and physical exam will usually determine the etiology, and most benign pathologies can be successfully treated in the primary care clinic. Knowing how to perform an anorectal exam and having a thorough understanding of the most common anorectal pathologies can help alleviate examiner discomfort, while ensuring that patients receive prompt and adequate care. At the same time, recognizing the red flags can expedite referral for colorectal specialty evaluation when appropriate. Red flags that should prompt immediate referral to a colorectal specialist include older age, unintentional weight loss, iron deficiency anemia, family history of inflammatory bowel disease or colorectal cancer, and persistent anorectal bleeding or persistent symptoms despite adequate treatment of a suspected benign condition.

CE/CME No: CR-1711

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand basic anorectal anatomy and how to perform a thorough anorectal exam.
• Describe the physical exam findings of common benign anorectal conditions.
• Discuss the different treatment options for benign anorectal conditions.
• Differentiate between common benign anorectal symptoms and red flags that should prompt referral to a colorectal specialist.

FACULTY
Priscilla Marsicovetere is an Assistant Professor of Medical Education and of Surgery at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire; Program Director for the Franklin Pierce University PA Program in Lebanon, New Hampshire; and practices with Emergency Services of New England at Springfield Hospital in Vermont. Srinivas Joga Ivatury is an Assistant Professor of Surgery at the Geisel School of Medicine at Dartmouth and practices in the Department of Surgery at the Dartmouth Hitchcock Medical Center in Lebanon, New Hampshire.

The authors have no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through October 31, 2018.

Article begins on next page >>

Anorectal pain and discomfort can stem from several possible etiologies, most of which are benign. As such, many patients with anorectal complaints who present in the primary care setting can be adequately evaluated, diagnosed, and treated without referral to a colorectal specialist. However, the clinician must be able to differentiate between common benign anorectal symptoms and red flags that should prompt referral.

Anorectal disorders are common in the United States and result in numerous primary care visits each year. Presentations range from pain and itching to bleeding and lesions. Common anorectal conditions include hemorrhoids, perianal skin tags, fissures, pruritus ani, perianal abscess, and condyloma. Most are benign and can be managed in the primary care setting.

Before a provider can competently diagnose and treat anorectal conditions, however, a comprehensive history and physical examination must be conducted. Grucela and colleagues documented that physicians’ diagnostic accuracy with anorectal conditions is about 50%—highlighting the need for providers to become more familiar with the history and clinical elements associated with anorectal complaints.¹

This article reviews the assessment of the anorectum, diagnosis of common disorders and their recommended treatments, and red flags for referral to a colorectal specialist.

ANORECTAL ANATOMY

The beginning of the anal canal is demarcated by its moist, hairless appearance. Just inside the anal opening are two palpable circular muscles, the internal and external anal sphincters, separated by an intersphincteric groove. The sphincters are firmly closed in the resting state, which helps maintain continence.

The anal canal is generally 3 to 4 cm long and ends at the dentate line, a series of crypts in the anal mucosa.² The crypts are openings into the anal glands, which are mucus-secreting structures in the anus. The dentate line is easily identified on anoscopy as a discrete change in the appearance of the mucosa. The dentate line is an important landmark because it delineates the boundary between somatic and visceral nerve supplies.³ Tissue proximal to the dentate line is innervated by visceral nerves and is insensate, and thus usually not a cause of pain; tissue distal to the dentate line, however, is highly innervated by somatic nerves and can be intensely painful.²

The anorectal canal is lined by three fibrovascular cushions, located in the left lateral, right posterior, and right anterior positions.⁴ Inside each cushion is a venous structure, called a hemorrhoid, which allows the cushion to enlarge and help maintain continence.⁵

Proximal to the anus is the rectum, the 12- to 15-cm long terminus of the colon. Anorectal examination in the primary care setting will typically not progress beyond the last 2 to 3 cm of the rectum.

TAKING THE HISTORY

A thorough history will provide clues about potential underlying anorectal pathology. Patients may not be forthcoming about symptoms due to embarrassment, fear of a cancer diagnosis, or cultural customs or habits. A thorough history should elicit information about all of the patient’s symptoms (see Table 1), including bleeding, change in bowel habits, and unintended weight loss.

PHYSICAL EXAM

Positioning the patient

Undergoing an anorectal examination can be embarrassing, whether it be from exposure of sensitive body parts or the less-than-desirable prone jackknife positioning. Patients often have preconceived notions that the exam will be humiliating and/or painful. Care should be taken to minimize any embarrassment and discomfort.

Positioning of the patient is a matter of provider preference. Options include the left lateral decubitus, prone jackknife, or lithotomy positions.

Positioning should always be done with draping. Regardless of position, ensure the draping exposes only the perineum. This can be achieved by encircling the patient’s bare bottom with a plain white sheet that exposes only the anus and surrounding skin, keeping the lower back, lateral buttocks, and thighs covered.

Interestingly, data on patient preference for positioning during anorectal exams are limited. In a 2009 study of 178 patients undergoing anorectal exam, more than half of patients (up to 71.4%) expecting to or having already had a proctologic exam reported that no specific type of positioning (eg, Sims, lithotomy with lifted legs, knee-chest, knee-chest with patient’s body bent forward) was most embarrassing to them.⁶ The report revealed that while most patients would favor the Sims position if they had a choice, they deferred to their examiner to choose the position that seemed most suitable to get a reliable diagnosis.⁶

Inspection of the perineum

Once the patient is properly positioned and draped, inspection of the perineum can occur. Begin by gently spreading the buttocks. Describe any abnormality seen (eg, ulcer, lesion, dermatitis, prolapsing tissue, or blood), including size, color, and location.

A common pitfall is to describe the location of abnormalities using a clock face, such as “at 4 o’clock.” This is misleading and should be avoided, because depending on patient position, the clock face can point to different locations (eg, if the patient is in the lithotomy versus prone jackknife position).

A better approach is to divide the perianal area into four anatomic quadrants: right anterior, right posterior, left anterior, left posterior. Using this schematic, the patient's position is irrelevant, and accurate documentation of lesion location is assured.

Digital rectal exam

After visual inspection of the perianal skin, a digital rectal exam (DRE) should be performed. Slowly insert a gloved, lubricated index finger into the anus and lower rectum. Note the tone of the anus at rest (eg, excessively tight vs lax). Palpate the circumference of the anus, sweeping side to side while assessing for any tenderness, mass, or induration—if present, note the anatomic quadrant. If a mass is felt, note whether it is firm or soft, fixed or mobile, and broad-based or pedunculated. When the lubricated finger is removed from the anus, note whether blood is present.

Anoscopy

After DRE, visually inspect the anorectum. The instrument used varies from anoscope to rigid proctoscope to flexible sigmoidoscope. In a primary care setting, the most likely available instrument is an anoscope. The average anoscope is about 7 cm long and 2 cm in diameter, with a beveled tip and an obturator (see Figure 1), and allows a 360° view of the anal canal.⁷

Examination of the anal canal is accomplished by dividing the canal into the four anatomic quadrants described earlier and inserting the lubricated anoscope for inspection of each of the four quadrants. Observe the rectal mucosa and the anus as the scope is slowly withdrawn. If abnormalities are seen, note the location, size, shape, and any other descriptive features.

It is not necessary to perform a Hemoccult test after examination of the anorectum, as the presence of minor blood may be the direct result of the exam itself and thus provides no useful information to the examiner.

COMMON PATHOLOGIES

Once the history and physical exam are complete, a differential diagnosis can be formulated. Most anorectal disorders are benign conditions that pose no immediate health threat and can be managed in the primary care setting. Others, however, can be more serious and should prompt referral to a colorectal specialist for further evaluation. Knowing the difference can spare a patient unnecessary anxiety and referral; it can also lead to prompt, lifesaving interventions if red flags are recognized.

Hemorrhoids

Hemorrhoids are a common anorectal complaint.^8,9 It is estimated that up to 75% of the population will experience symptoms of hemorrhoids during their lifetime.^5,8 Whether internal or external, in their normal, nonpathologic, quiescent state, hemorrhoids are asymptomatic. Hemorrhoids become symptomatic when the supporting structures of hemorrhoidal tissue (ie, the anal cushions) deteriorate, resulting in venous dilation, inflammation, and thrombosis, which in turn lead to swelling, bright red bleeding, and/or prolapse.^2,10 The most common causes of hemorrhoidal disease are chronic constipation and prolonged straining with bowel movements, though chronic diarrhea and pregnancy have also been identified as risk factors.^2,8,11

External hemorrhoids, which are located distal to the dentate line, are typically only visible when they become thrombosed or swollen. In this state, they may manifest as acute-onset, exquisitely painful, large, purple-to-blue bulges at the anal outlet (see Figure 2). The number and size of the lesions can vary. The patient may report pain when sitting or wiping, as well as bleeding from the lesion.^12,13 The pain is typically severe in the first couple of days, then slowly starts to subside.^2,12

For internal hemorrhoids, which are located proximal to the dentate line, the main symptom is usually painless bright red blood per rectum.^8,11,12 Patients may also report a sensation of rectal fullness or experience prolapse of the hemorrhoid through the anus. Prolapse typically occurs with defecation; in more severe cases, it can also occur between bowel movements, usually with any activity that increases intra-abdominal pressure (eg, coughing, heavy lifting, pregnancy, portal hypertension). The prolapse may reduce spontaneously, or may have to be manually reduced. If it cannot be reduced, there is a risk for incarceration or strangulation, potentially leading to gangrene.

The presence of bleeding and/or prolapse determines the classification of internal hemorrhoids (see Table 2). Dietary and lifestyle modification are used in the management of all grades of hemorrhoids. In addition, for grade 1 and 2 lesions, topical medication (eg, anti-inflammatory cream) can be used, whereas grade 3 (and selected grade 2) lesions respond well to rubber band ligation. Given the severity of grade 4 lesions, surgical intervention (eg, hemorrhoidectomy) is usually indicated.¹⁰

About a third of patients with symptomatic hemorrhoids seek clinical treatment.¹⁴ Most are hemodynamically stable and require no imaging and usually no labs (unless anemia is suspected).² Management depends on the location and degree of symptoms (eg, internal vs external, prolapse, or thrombosis). In the event of an acutely thrombosed external hemorrhoid, clot excision for pain relief is appropriate if symptoms have been present for less than 48 to 72 hours; after that amount of time, the pain from the procedure will likely exceed the degree of relief provided, and conservative management should instead be recommended.^2,8,11

Firstline treatment consists of lifestyle modification with a high-fiber diet and daily fiber supplement to ensure stool is soft and easy to pass.^2,8 A meta-analysis of seven clinical trials with a total of 378 patients with hemorrhoids showed that fiber supplementation resulted in a 50% decrease in bleeding risk from internal hemorrhoids.¹⁵

Adequate hydration, preferably with noncaffeinated liquids, is also recommended. This will prevent constipation and the need to strain or spend excessive time on the toilet. Sitz baths can help alleviate pain and discomfort.

Several OTC topical medications are marketed for hemorrhoid relief. Many of these preparations contain steroids for their anti-inflammatory effects or astringents to address skin irritation that can result from anal leakage if prolapsing hemorrhoids prevent the anal outlet from closing. Steroid use should be limited to five to seven days, due to atrophic effects on the skin. While OTC preparations may temporarily alleviate discomfort, they will not address the underlying cause of symptoms.

Indications for referral to a colorectal specialist for symptomatic hemorrhoids include failure to improve with conservative management, persistent patient discomfort, and prolapse, as these indicate potential need for more invasive treatment.

Perianal skin tags

Perianal skin tags, while a nuisance, are not pathologic in most instances and pose no threat to health. They are an outgrowth of normal skin, appearing as loose, flesh-colored perianal tissues (see Figure 3). Tags range in size from a few millimeters to a centimeter long and can occur alone or in multiples.

Perianal skin tags are diagnosed clinically and require no labwork or imaging. Visual inspection is typically sufficient to distinguish tags from pathologic lesions such as condyloma or abscess. If there is uncertainty, however, biopsy or referral to a specialist is warranted.

Certain medical conditions can predispose a patient to development of perianal skin tags. They can be sequelae of thrombosed external hemorrhoids.^8,11 They are also common in patients with Crohn disease.¹¹ Perianal skin tags are not, however, the result of anal intercourse or sexually transmitted infections.

Treatment is usually not indicated for perianal skin tags. If the tags interfere with hygiene or cause perianal discomfort or significantly decreased quality of life, however, patients may seek removal. These patients should be referred to a colorectal specialist for evaluation for excision.

Anal fissures (fissure in ano)

The most common cause of severe anorectal pain is fissure.⁴ A fissure is an elliptical tear, or split, in the lining of the anal canal that causes spasm of the anal sphincters. The tear is distal to the dentate line and thus intensely painful.^2,5 Common cited causes of fissures are trauma from passage of large, hard stools, straining, or diarrhea.¹⁶

Fissures can usually be visualized by spreading the posterior anus apart (see Figure 4). They are most commonly located in the posterior or anterior midline, though they can occur anywhere around the anus.^2,4 Often, a sentinel tag—appearing as a taut, flesh-colored skin tag—is present at the external pole of the fissure.^5,11 DRE and anoscopy should be avoided, as they will trigger intense pain and spasm of the sphincters.

Fissures are characterized as acute (present ≤ 3 months) or chronic (> 3 months).^9,11 Visually, acute fissures typically have clean edges, with the appearance of a paper cut to the mucosa, while chronic fissures have indurated, heaped-up edges, often with exposure of the underlying sphincter muscle.¹⁷

They tend to be exquisitely painful, as the mucosa distal to the dentate line is highly innervated. Patients report pain akin to “passing shards of broken glass” with bowel movements, which is often accompanied by a fear of defecation and bright red blood on the toilet paper or dripping into the water.¹¹ The pain, caused by spasm of the sphincters, typically starts during a bowel movement and lasts minutes to hours afterward.

Initial treatment is aimed at relaxing the sphincters, as well as softening stool to prevent further trauma and allow the fissure to heal. Patients should be educated about the importance of adequate fiber intake to prevent constipation and straining. A daily bulk fiber supplement, in addition to a high-fiber diet (20-25 g/d), has been shown to result in healing of 87% of acute fissures.¹⁶ Sitz baths in plain warm water, three to four times a day, can encourage relaxation of the sphincters and increase local blood flow, both of which help with fissure healing.¹⁶ Topical medications can also be prescribed. These include compounded nitroglycerin 0.2% or nifedipine 2.0%, which act to reduce the spasm by relaxing smooth muscle, as well as increase blood flow to the lesion.^12,14

Most acute fissures will heal with the regimen of high fiber intake, sitz baths, and topical medication. For refractory or chronic fissures, referral to a colorectal specialist for more invasive treatment is appropriate. Additionally, fissures that are not located in the typical posterior or anterior midline might indicate an atypical etiology, such as Crohn disease, tuberculosis, leukemia, or HIV, and thus patients who present with fissures in these locations should also be referred to a colorectal specialist.^2,4,11,18

Pruritus ani

Pruritus ani, known as perianal dermatitis, is a benign condition that presents with intense perianal itching and burning. It is the second most common anorectal condition after hemorrhoids and affects up to 5% of the US population.^2,9,11,19

Pruritus ani often develops secondary to local irritation of the skin (eg, from prolonged exposure to moisture), leading to an inflammatory response within the superficial skin layers. The irritation causes patients to scratch the skin, resulting in trauma, excoriation, and ulcer formation and leading to a cycle of further inflammation, exacerbation of symptoms, and persistent scratching.

Physical exam may reveal circumferential erythematous and irritated perianal skin (see Figure 5). Linear or deep, punched-out excoriations may be present. Chronically, patients may develop lichenification with thick, whitened patches of skin.¹¹ In the absence of red flags such as unintentional weight loss, anemia, rectal bleeding, or a family history of colon cancer, no additional evaluation is required during the initial visit, though anoscopy can be used to rule out associated anorectal pathology.

Many different causes of pruritus ani have been reported (see Table 3). In the case of an identifiable cause, symptoms tend to resolve once the offending agent is eliminated. Up to a quarter of cases, however, are idiopathic, with no identifiable trigger.²⁰

Symptom management is thus key. Patients should be educated about lifestyle modification and informed that scratching will irritate the skin further and aggravate symptoms.^5,11 If incontinence or diarrhea is thought to cause symptoms, dietary modifications, a fiber supplement, dysmotility agents, and Kegel exercises to strengthen the sphincters and decrease anal leakage can be recommended.

The affected skin should be kept clean and dry at all times. Aggressive wiping and overzealous hygiene should be avoided. Sitz baths can help with hygiene. A topical astringent such as witch hazel can help remove excess moisture from the skin. A layer of protective skin barrier cream with zinc oxide, when applied over dry skin, can help protect the skin from leakage throughout the day.

A sedating antihistamine can reduce scratching during sleep. Topical hydro­cortisone 1% cream is effective for itch relief; this should be limited to five to seven days of consecutive use, however, as it can lead to pathologic thinning of the perianal skin. Topical capsaicin 0.006% cream has been shown to help alleviate intractable ­pruritus.^2,21

The goal of these measures is to break the cycle of irritation and inflammation and give the skin an opportunity to heal. If the patient fails to improve, referral to a colorectal specialist or, alternatively, a dermatologist, is warranted for perianal skin biopsy and more invasive treatment options.

Perianal abscess

A perianal abscess is an infected cavity filled with pus under pressure, located near the anus or rectum. It most often results from an acute infection of the anorectal glands located at the dentate line that tracks outward to the perianal skin.¹² Abscesses can also result from another disease process, such as Crohn disease, diabetes, or rectal trauma.^2,11

Localized pain, swelling, and drainage are common presenting symptoms of an abscess.^2,11 Systemic symptoms such as fever and chills may present later in the course but are rare.²

Treatment of the acute process is incision and drainage (I&D).^11,12 This can be accomplished in the office with injection of local anesthesia, followed by excision of an ellipse of skin overlying the cavity large enough to allow full drainage of the abscess. Use of drains and packing of the wound are usually not necessary. There is also no role for antibiotics unless the patient is diabetic or immunosuppressed or cellulitis is present.¹¹ In patients with systemic signs of illness, imaging such as CT or MRI of the pelvis can be used to assess for a deeper infection.^2,12

For most patients, I&D resolves the process. However, up to half of perianal abscesses progress to form a fistula, a tunnel connecting the infected anal gland to the external skin.^2,11,22 Indeed, abscesses and fistulae are part of the same infectious process, with the abscess representing the acute phase of infection and the fistula representing the chronic phase. On physical exam, in addition to the abscess site on the skin, a fistula may manifest as a palpable cord beneath the skin between the anus and the abscess opening.⁹ Additionally, the patient may report the abscess has been recurrent in nature, cyclically increasing in size and pain, then spontaneously draining.

A fistula requires surgical intervention for definitive treatment and should therefore prompt referral to a colorectal specialist. In the absence of fistula, however, a simple perianal abscess can be treated with I&D in the primary care setting.

Condyloma acuminatum

Condyloma acuminatum, also known as genital warts, is the most common sexually transmitted infection in the United States and a frequent anorectal complaint.^23-25 More than 6 million new infections occur annually.²⁵

Condyloma is caused by the human papillomavirus (HPV).²⁴ More than 100 HPV subtypes have been identified.²⁵ Types 6 and 11 are associated with typical condyloma acuminatum, while types 16 and 18 are found more commonly with dysplasia and malignant transformation.^3,26

The lesions are spread by direct skin-to-skin or mucosa-to-mucosa contact, including anal intercourse. They appear as tiny finger-like projections on the perianal or genital skin, often with a cauliflower-like appearance, in clusters or as single entities, and ranging in size from a few millimeters to several centimeters (see Figure 6).

The patient may be asymptomatic or may complain of bleeding with defecation or leakage from the rectum between bowel movements. In up to 90% of perianal condyloma, concomitant anorectal lesions are present.³ Anoscopy is therefore indicated whenever perianal lesions are seen.

Treatment of genital warts varies depending on the number and location of lesions. The goal is lesion removal, but none of the available treatments are curative.²⁴ If only a few small (diameter < 2 mm) warts are seen in the perianal area, with no anal involvement, these can be treated with topical cytotoxic agents. A commonly used agent is podophyllotoxin 0.15% (a derivative of podophyllin), an antimitotic agent that interferes with viral replication and induces necrosis of the wart.²⁶ Podophyllin is effective for small warts, but recurrence rates range from 38% to as high as 79%.^24,26 The most common side effects are local erythema, swelling, pain, and pruritus.

Trichloroacetic acid (TCA), which is considered a form of chemical cautery, has been deemed more effective for tiny warts (diameter 1-2 mm) and better tolerated than podophyllin.²⁴ Unlike podophyllin, however, TCA must be applied in clinic by a specialist, not at home by the patient. It works by chemically burning, cauterizing, and eroding skin and mucosa, thereby destroying old infected cells and allowing for growth of new, healthy cells.²⁴ Using a solution with a higher concentration of TCA (80%-90%) has been shown to be more effective than lower concentration solutions (30%).²⁴ The recurrence rate is high, generally about 36%.²⁷ Due to its low risk for systemic absorption, TCA is safe for use during pregnancy.²⁴

Local application of an immunomodulator, such as imiquimod 2%, 3.75%, or 5% cream, can also be used. Imiquimod works by upregulating tumor necrosis factor, leading to decreased viral replication and subsequent regression of warts.²⁴ The most common side effects of imiquimod are erythema, erosions, burning, and pruritus.²⁴ The higher concentration is associated with increased clearance rates as well as increased adverse effects.²⁷ Therefore, the 3.75% cream is the preferred concentration of most providers.²⁷ Recurrence rates range from 13% to 19%.²⁸

In 2006, the FDA approved polyphenon E, a botanical ointment, to treat anogenital warts. The formulation is composed of eight different sinecatechins extracted from green tea leaves.²⁹ Green tea sinecatechins have been shown to have antioxidant, antiproliferative, and antiviral properties, though the specific mechanisms of action in inhibiting anogenital wart growth have not been well studied to date. In a multicenter, randomized, double-blind, vehicle-controlled, three-arm parallel group phase 3 trial of 495 patients with anogenital warts, sinecatechins ointment 10% or 15% applied three times daily for 16 weeks resulted in complete clearance of warts in 57.2% and 56.3% of patients, respectively, compared to 33.7% clearance in the vehicle patients.³⁰ Partial clearance (≥ 50%) of warts was observed in 78.4% of patients who used the 15% ointment, 74.0% of those who used the 10% ointment, and 51.5% of the vehicle patients. Rates of recurrence were 6.5% and 8.3% with use of the 10% and 15% sinecatechins ointment, respectively, which are much lower than recurrence rates observed with other topical applications (eg, imiquimod and podophyllotoxin).³⁰

For larger warts or when there are anal lesions present, surgical excision and fulguration is required and referral to a colorectal specialist is warranted.

Warts recur from 4.6% to more than 70% of the time, most commonly due to activation of latent virus.²³ Therefore, whether initially treated in an office or operating room, condyloma patients require follow-up on a regular basis, generally every six to 12 months, to assess for recurrent anal lesions so that treatment can be promptly initiated.

In the absence of a cure for anogenital warts, prevention through an HPV vaccine is important. The quadrivalent HPV vaccine (Gardasil) was approved by the FDA in 2006 for prophylactic vaccination of females ages 9 to 26. The vaccine triggers host formation of antibodies against four common subtypes of HPV: 6, 11, 16, and 18.³¹ In 2009, the FDA expanded the use of Gardasil to include males ages 9 to 26; subsequently, Gardasil 9 (which protects against nine types of HPV) was approved for males ages 9 to 15.³² In a group of 4,065 healthy males between the ages of 16 and 26, Gardasil reduced the incidence of external anogenital warts by 90.4%.³³

HPV vaccine is now recommended for females through age 26 and males through age 21. The CDC also recommends HPV vaccine for the following individuals through age 26 if they did not get vaccinated when they were younger:

• Young men who have sex with men
• Young men who identify as gay or bisexual or who intend to have sex with men
• Young adults who are transgender
• Young adults with immunocompromising conditions (including HIV).³⁴

CONCLUSION

Anorectal conditions are a common presentation in the primary care setting. A thorough history and physical exam will usually determine the etiology, and most benign pathologies can be successfully treated in the primary care clinic. Knowing how to perform an anorectal exam and having a thorough understanding of the most common anorectal pathologies can help alleviate examiner discomfort, while ensuring that patients receive prompt and adequate care. At the same time, recognizing the red flags can expedite referral for colorectal specialty evaluation when appropriate. Red flags that should prompt immediate referral to a colorectal specialist include older age, unintentional weight loss, iron deficiency anemia, family history of inflammatory bowel disease or colorectal cancer, and persistent anorectal bleeding or persistent symptoms despite adequate treatment of a suspected benign condition.

CE/CME No: CR-1711

PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.

EDUCATIONAL OBJECTIVES
• Understand basic anorectal anatomy and how to perform a thorough anorectal exam.
• Describe the physical exam findings of common benign anorectal conditions.
• Discuss the different treatment options for benign anorectal conditions.
• Differentiate between common benign anorectal symptoms and red flags that should prompt referral to a colorectal specialist.

FACULTY
Priscilla Marsicovetere is an Assistant Professor of Medical Education and of Surgery at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire; Program Director for the Franklin Pierce University PA Program in Lebanon, New Hampshire; and practices with Emergency Services of New England at Springfield Hospital in Vermont. Srinivas Joga Ivatury is an Assistant Professor of Surgery at the Geisel School of Medicine at Dartmouth and practices in the Department of Surgery at the Dartmouth Hitchcock Medical Center in Lebanon, New Hampshire.

The authors have no financial relationships to disclose.

ACCREDITATION STATEMENT

This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid through October 31, 2018.

Article begins on next page >>

Anorectal pain and discomfort can stem from several possible etiologies, most of which are benign. As such, many patients with anorectal complaints who present in the primary care setting can be adequately evaluated, diagnosed, and treated without referral to a colorectal specialist. However, the clinician must be able to differentiate between common benign anorectal symptoms and red flags that should prompt referral.

Anorectal disorders are common in the United States and result in numerous primary care visits each year. Presentations range from pain and itching to bleeding and lesions. Common anorectal conditions include hemorrhoids, perianal skin tags, fissures, pruritus ani, perianal abscess, and condyloma. Most are benign and can be managed in the primary care setting.

Before a provider can competently diagnose and treat anorectal conditions, however, a comprehensive history and physical examination must be conducted. Grucela and colleagues documented that physicians’ diagnostic accuracy with anorectal conditions is about 50%—highlighting the need for providers to become more familiar with the history and clinical elements associated with anorectal complaints.¹

This article reviews the assessment of the anorectum, diagnosis of common disorders and their recommended treatments, and red flags for referral to a colorectal specialist.

ANORECTAL ANATOMY

The beginning of the anal canal is demarcated by its moist, hairless appearance. Just inside the anal opening are two palpable circular muscles, the internal and external anal sphincters, separated by an intersphincteric groove. The sphincters are firmly closed in the resting state, which helps maintain continence.

The anal canal is generally 3 to 4 cm long and ends at the dentate line, a series of crypts in the anal mucosa.² The crypts are openings into the anal glands, which are mucus-secreting structures in the anus. The dentate line is easily identified on anoscopy as a discrete change in the appearance of the mucosa. The dentate line is an important landmark because it delineates the boundary between somatic and visceral nerve supplies.³ Tissue proximal to the dentate line is innervated by visceral nerves and is insensate, and thus usually not a cause of pain; tissue distal to the dentate line, however, is highly innervated by somatic nerves and can be intensely painful.²

The anorectal canal is lined by three fibrovascular cushions, located in the left lateral, right posterior, and right anterior positions.⁴ Inside each cushion is a venous structure, called a hemorrhoid, which allows the cushion to enlarge and help maintain continence.⁵

Proximal to the anus is the rectum, the 12- to 15-cm long terminus of the colon. Anorectal examination in the primary care setting will typically not progress beyond the last 2 to 3 cm of the rectum.

TAKING THE HISTORY

A thorough history will provide clues about potential underlying anorectal pathology. Patients may not be forthcoming about symptoms due to embarrassment, fear of a cancer diagnosis, or cultural customs or habits. A thorough history should elicit information about all of the patient’s symptoms (see Table 1), including bleeding, change in bowel habits, and unintended weight loss.

PHYSICAL EXAM

Positioning the patient

Undergoing an anorectal examination can be embarrassing, whether it be from exposure of sensitive body parts or the less-than-desirable prone jackknife positioning. Patients often have preconceived notions that the exam will be humiliating and/or painful. Care should be taken to minimize any embarrassment and discomfort.

Positioning of the patient is a matter of provider preference. Options include the left lateral decubitus, prone jackknife, or lithotomy positions.

Positioning should always be done with draping. Regardless of position, ensure the draping exposes only the perineum. This can be achieved by encircling the patient’s bare bottom with a plain white sheet that exposes only the anus and surrounding skin, keeping the lower back, lateral buttocks, and thighs covered.

Interestingly, data on patient preference for positioning during anorectal exams are limited. In a 2009 study of 178 patients undergoing anorectal exam, more than half of patients (up to 71.4%) expecting to or having already had a proctologic exam reported that no specific type of positioning (eg, Sims, lithotomy with lifted legs, knee-chest, knee-chest with patient’s body bent forward) was most embarrassing to them.⁶ The report revealed that while most patients would favor the Sims position if they had a choice, they deferred to their examiner to choose the position that seemed most suitable to get a reliable diagnosis.⁶

Inspection of the perineum

Once the patient is properly positioned and draped, inspection of the perineum can occur. Begin by gently spreading the buttocks. Describe any abnormality seen (eg, ulcer, lesion, dermatitis, prolapsing tissue, or blood), including size, color, and location.

A common pitfall is to describe the location of abnormalities using a clock face, such as “at 4 o’clock.” This is misleading and should be avoided, because depending on patient position, the clock face can point to different locations (eg, if the patient is in the lithotomy versus prone jackknife position).

A better approach is to divide the perianal area into four anatomic quadrants: right anterior, right posterior, left anterior, left posterior. Using this schematic, the patient's position is irrelevant, and accurate documentation of lesion location is assured.

Digital rectal exam

After visual inspection of the perianal skin, a digital rectal exam (DRE) should be performed. Slowly insert a gloved, lubricated index finger into the anus and lower rectum. Note the tone of the anus at rest (eg, excessively tight vs lax). Palpate the circumference of the anus, sweeping side to side while assessing for any tenderness, mass, or induration—if present, note the anatomic quadrant. If a mass is felt, note whether it is firm or soft, fixed or mobile, and broad-based or pedunculated. When the lubricated finger is removed from the anus, note whether blood is present.

Anoscopy

After DRE, visually inspect the anorectum. The instrument used varies from anoscope to rigid proctoscope to flexible sigmoidoscope. In a primary care setting, the most likely available instrument is an anoscope. The average anoscope is about 7 cm long and 2 cm in diameter, with a beveled tip and an obturator (see Figure 1), and allows a 360° view of the anal canal.⁷

Examination of the anal canal is accomplished by dividing the canal into the four anatomic quadrants described earlier and inserting the lubricated anoscope for inspection of each of the four quadrants. Observe the rectal mucosa and the anus as the scope is slowly withdrawn. If abnormalities are seen, note the location, size, shape, and any other descriptive features.

It is not necessary to perform a Hemoccult test after examination of the anorectum, as the presence of minor blood may be the direct result of the exam itself and thus provides no useful information to the examiner.

COMMON PATHOLOGIES

Once the history and physical exam are complete, a differential diagnosis can be formulated. Most anorectal disorders are benign conditions that pose no immediate health threat and can be managed in the primary care setting. Others, however, can be more serious and should prompt referral to a colorectal specialist for further evaluation. Knowing the difference can spare a patient unnecessary anxiety and referral; it can also lead to prompt, lifesaving interventions if red flags are recognized.

Hemorrhoids

Hemorrhoids are a common anorectal complaint.^8,9 It is estimated that up to 75% of the population will experience symptoms of hemorrhoids during their lifetime.^5,8 Whether internal or external, in their normal, nonpathologic, quiescent state, hemorrhoids are asymptomatic. Hemorrhoids become symptomatic when the supporting structures of hemorrhoidal tissue (ie, the anal cushions) deteriorate, resulting in venous dilation, inflammation, and thrombosis, which in turn lead to swelling, bright red bleeding, and/or prolapse.^2,10 The most common causes of hemorrhoidal disease are chronic constipation and prolonged straining with bowel movements, though chronic diarrhea and pregnancy have also been identified as risk factors.^2,8,11

External hemorrhoids, which are located distal to the dentate line, are typically only visible when they become thrombosed or swollen. In this state, they may manifest as acute-onset, exquisitely painful, large, purple-to-blue bulges at the anal outlet (see Figure 2). The number and size of the lesions can vary. The patient may report pain when sitting or wiping, as well as bleeding from the lesion.^12,13 The pain is typically severe in the first couple of days, then slowly starts to subside.^2,12

For internal hemorrhoids, which are located proximal to the dentate line, the main symptom is usually painless bright red blood per rectum.^8,11,12 Patients may also report a sensation of rectal fullness or experience prolapse of the hemorrhoid through the anus. Prolapse typically occurs with defecation; in more severe cases, it can also occur between bowel movements, usually with any activity that increases intra-abdominal pressure (eg, coughing, heavy lifting, pregnancy, portal hypertension). The prolapse may reduce spontaneously, or may have to be manually reduced. If it cannot be reduced, there is a risk for incarceration or strangulation, potentially leading to gangrene.

The presence of bleeding and/or prolapse determines the classification of internal hemorrhoids (see Table 2). Dietary and lifestyle modification are used in the management of all grades of hemorrhoids. In addition, for grade 1 and 2 lesions, topical medication (eg, anti-inflammatory cream) can be used, whereas grade 3 (and selected grade 2) lesions respond well to rubber band ligation. Given the severity of grade 4 lesions, surgical intervention (eg, hemorrhoidectomy) is usually indicated.¹⁰

About a third of patients with symptomatic hemorrhoids seek clinical treatment.¹⁴ Most are hemodynamically stable and require no imaging and usually no labs (unless anemia is suspected).² Management depends on the location and degree of symptoms (eg, internal vs external, prolapse, or thrombosis). In the event of an acutely thrombosed external hemorrhoid, clot excision for pain relief is appropriate if symptoms have been present for less than 48 to 72 hours; after that amount of time, the pain from the procedure will likely exceed the degree of relief provided, and conservative management should instead be recommended.^2,8,11

Firstline treatment consists of lifestyle modification with a high-fiber diet and daily fiber supplement to ensure stool is soft and easy to pass.^2,8 A meta-analysis of seven clinical trials with a total of 378 patients with hemorrhoids showed that fiber supplementation resulted in a 50% decrease in bleeding risk from internal hemorrhoids.¹⁵

Adequate hydration, preferably with noncaffeinated liquids, is also recommended. This will prevent constipation and the need to strain or spend excessive time on the toilet. Sitz baths can help alleviate pain and discomfort.

Several OTC topical medications are marketed for hemorrhoid relief. Many of these preparations contain steroids for their anti-inflammatory effects or astringents to address skin irritation that can result from anal leakage if prolapsing hemorrhoids prevent the anal outlet from closing. Steroid use should be limited to five to seven days, due to atrophic effects on the skin. While OTC preparations may temporarily alleviate discomfort, they will not address the underlying cause of symptoms.

Indications for referral to a colorectal specialist for symptomatic hemorrhoids include failure to improve with conservative management, persistent patient discomfort, and prolapse, as these indicate potential need for more invasive treatment.

Perianal skin tags

Perianal skin tags, while a nuisance, are not pathologic in most instances and pose no threat to health. They are an outgrowth of normal skin, appearing as loose, flesh-colored perianal tissues (see Figure 3). Tags range in size from a few millimeters to a centimeter long and can occur alone or in multiples.

Perianal skin tags are diagnosed clinically and require no labwork or imaging. Visual inspection is typically sufficient to distinguish tags from pathologic lesions such as condyloma or abscess. If there is uncertainty, however, biopsy or referral to a specialist is warranted.

Certain medical conditions can predispose a patient to development of perianal skin tags. They can be sequelae of thrombosed external hemorrhoids.^8,11 They are also common in patients with Crohn disease.¹¹ Perianal skin tags are not, however, the result of anal intercourse or sexually transmitted infections.

Treatment is usually not indicated for perianal skin tags. If the tags interfere with hygiene or cause perianal discomfort or significantly decreased quality of life, however, patients may seek removal. These patients should be referred to a colorectal specialist for evaluation for excision.

Anal fissures (fissure in ano)

The most common cause of severe anorectal pain is fissure.⁴ A fissure is an elliptical tear, or split, in the lining of the anal canal that causes spasm of the anal sphincters. The tear is distal to the dentate line and thus intensely painful.^2,5 Common cited causes of fissures are trauma from passage of large, hard stools, straining, or diarrhea.¹⁶

Fissures can usually be visualized by spreading the posterior anus apart (see Figure 4). They are most commonly located in the posterior or anterior midline, though they can occur anywhere around the anus.^2,4 Often, a sentinel tag—appearing as a taut, flesh-colored skin tag—is present at the external pole of the fissure.^5,11 DRE and anoscopy should be avoided, as they will trigger intense pain and spasm of the sphincters.

Fissures are characterized as acute (present ≤ 3 months) or chronic (> 3 months).^9,11 Visually, acute fissures typically have clean edges, with the appearance of a paper cut to the mucosa, while chronic fissures have indurated, heaped-up edges, often with exposure of the underlying sphincter muscle.¹⁷

They tend to be exquisitely painful, as the mucosa distal to the dentate line is highly innervated. Patients report pain akin to “passing shards of broken glass” with bowel movements, which is often accompanied by a fear of defecation and bright red blood on the toilet paper or dripping into the water.¹¹ The pain, caused by spasm of the sphincters, typically starts during a bowel movement and lasts minutes to hours afterward.

Initial treatment is aimed at relaxing the sphincters, as well as softening stool to prevent further trauma and allow the fissure to heal. Patients should be educated about the importance of adequate fiber intake to prevent constipation and straining. A daily bulk fiber supplement, in addition to a high-fiber diet (20-25 g/d), has been shown to result in healing of 87% of acute fissures.¹⁶ Sitz baths in plain warm water, three to four times a day, can encourage relaxation of the sphincters and increase local blood flow, both of which help with fissure healing.¹⁶ Topical medications can also be prescribed. These include compounded nitroglycerin 0.2% or nifedipine 2.0%, which act to reduce the spasm by relaxing smooth muscle, as well as increase blood flow to the lesion.^12,14

Most acute fissures will heal with the regimen of high fiber intake, sitz baths, and topical medication. For refractory or chronic fissures, referral to a colorectal specialist for more invasive treatment is appropriate. Additionally, fissures that are not located in the typical posterior or anterior midline might indicate an atypical etiology, such as Crohn disease, tuberculosis, leukemia, or HIV, and thus patients who present with fissures in these locations should also be referred to a colorectal specialist.^2,4,11,18

Pruritus ani

Pruritus ani, known as perianal dermatitis, is a benign condition that presents with intense perianal itching and burning. It is the second most common anorectal condition after hemorrhoids and affects up to 5% of the US population.^2,9,11,19

Pruritus ani often develops secondary to local irritation of the skin (eg, from prolonged exposure to moisture), leading to an inflammatory response within the superficial skin layers. The irritation causes patients to scratch the skin, resulting in trauma, excoriation, and ulcer formation and leading to a cycle of further inflammation, exacerbation of symptoms, and persistent scratching.

Physical exam may reveal circumferential erythematous and irritated perianal skin (see Figure 5). Linear or deep, punched-out excoriations may be present. Chronically, patients may develop lichenification with thick, whitened patches of skin.¹¹ In the absence of red flags such as unintentional weight loss, anemia, rectal bleeding, or a family history of colon cancer, no additional evaluation is required during the initial visit, though anoscopy can be used to rule out associated anorectal pathology.

Many different causes of pruritus ani have been reported (see Table 3). In the case of an identifiable cause, symptoms tend to resolve once the offending agent is eliminated. Up to a quarter of cases, however, are idiopathic, with no identifiable trigger.²⁰

Symptom management is thus key. Patients should be educated about lifestyle modification and informed that scratching will irritate the skin further and aggravate symptoms.^5,11 If incontinence or diarrhea is thought to cause symptoms, dietary modifications, a fiber supplement, dysmotility agents, and Kegel exercises to strengthen the sphincters and decrease anal leakage can be recommended.

The affected skin should be kept clean and dry at all times. Aggressive wiping and overzealous hygiene should be avoided. Sitz baths can help with hygiene. A topical astringent such as witch hazel can help remove excess moisture from the skin. A layer of protective skin barrier cream with zinc oxide, when applied over dry skin, can help protect the skin from leakage throughout the day.

A sedating antihistamine can reduce scratching during sleep. Topical hydro­cortisone 1% cream is effective for itch relief; this should be limited to five to seven days of consecutive use, however, as it can lead to pathologic thinning of the perianal skin. Topical capsaicin 0.006% cream has been shown to help alleviate intractable ­pruritus.^2,21

The goal of these measures is to break the cycle of irritation and inflammation and give the skin an opportunity to heal. If the patient fails to improve, referral to a colorectal specialist or, alternatively, a dermatologist, is warranted for perianal skin biopsy and more invasive treatment options.

Perianal abscess

A perianal abscess is an infected cavity filled with pus under pressure, located near the anus or rectum. It most often results from an acute infection of the anorectal glands located at the dentate line that tracks outward to the perianal skin.¹² Abscesses can also result from another disease process, such as Crohn disease, diabetes, or rectal trauma.^2,11

Localized pain, swelling, and drainage are common presenting symptoms of an abscess.^2,11 Systemic symptoms such as fever and chills may present later in the course but are rare.²

Treatment of the acute process is incision and drainage (I&D).^11,12 This can be accomplished in the office with injection of local anesthesia, followed by excision of an ellipse of skin overlying the cavity large enough to allow full drainage of the abscess. Use of drains and packing of the wound are usually not necessary. There is also no role for antibiotics unless the patient is diabetic or immunosuppressed or cellulitis is present.¹¹ In patients with systemic signs of illness, imaging such as CT or MRI of the pelvis can be used to assess for a deeper infection.^2,12

For most patients, I&D resolves the process. However, up to half of perianal abscesses progress to form a fistula, a tunnel connecting the infected anal gland to the external skin.^2,11,22 Indeed, abscesses and fistulae are part of the same infectious process, with the abscess representing the acute phase of infection and the fistula representing the chronic phase. On physical exam, in addition to the abscess site on the skin, a fistula may manifest as a palpable cord beneath the skin between the anus and the abscess opening.⁹ Additionally, the patient may report the abscess has been recurrent in nature, cyclically increasing in size and pain, then spontaneously draining.

A fistula requires surgical intervention for definitive treatment and should therefore prompt referral to a colorectal specialist. In the absence of fistula, however, a simple perianal abscess can be treated with I&D in the primary care setting.

Condyloma acuminatum

Condyloma acuminatum, also known as genital warts, is the most common sexually transmitted infection in the United States and a frequent anorectal complaint.^23-25 More than 6 million new infections occur annually.²⁵

Condyloma is caused by the human papillomavirus (HPV).²⁴ More than 100 HPV subtypes have been identified.²⁵ Types 6 and 11 are associated with typical condyloma acuminatum, while types 16 and 18 are found more commonly with dysplasia and malignant transformation.^3,26

The lesions are spread by direct skin-to-skin or mucosa-to-mucosa contact, including anal intercourse. They appear as tiny finger-like projections on the perianal or genital skin, often with a cauliflower-like appearance, in clusters or as single entities, and ranging in size from a few millimeters to several centimeters (see Figure 6).

The patient may be asymptomatic or may complain of bleeding with defecation or leakage from the rectum between bowel movements. In up to 90% of perianal condyloma, concomitant anorectal lesions are present.³ Anoscopy is therefore indicated whenever perianal lesions are seen.

Treatment of genital warts varies depending on the number and location of lesions. The goal is lesion removal, but none of the available treatments are curative.²⁴ If only a few small (diameter < 2 mm) warts are seen in the perianal area, with no anal involvement, these can be treated with topical cytotoxic agents. A commonly used agent is podophyllotoxin 0.15% (a derivative of podophyllin), an antimitotic agent that interferes with viral replication and induces necrosis of the wart.²⁶ Podophyllin is effective for small warts, but recurrence rates range from 38% to as high as 79%.^24,26 The most common side effects are local erythema, swelling, pain, and pruritus.

Trichloroacetic acid (TCA), which is considered a form of chemical cautery, has been deemed more effective for tiny warts (diameter 1-2 mm) and better tolerated than podophyllin.²⁴ Unlike podophyllin, however, TCA must be applied in clinic by a specialist, not at home by the patient. It works by chemically burning, cauterizing, and eroding skin and mucosa, thereby destroying old infected cells and allowing for growth of new, healthy cells.²⁴ Using a solution with a higher concentration of TCA (80%-90%) has been shown to be more effective than lower concentration solutions (30%).²⁴ The recurrence rate is high, generally about 36%.²⁷ Due to its low risk for systemic absorption, TCA is safe for use during pregnancy.²⁴

Local application of an immunomodulator, such as imiquimod 2%, 3.75%, or 5% cream, can also be used. Imiquimod works by upregulating tumor necrosis factor, leading to decreased viral replication and subsequent regression of warts.²⁴ The most common side effects of imiquimod are erythema, erosions, burning, and pruritus.²⁴ The higher concentration is associated with increased clearance rates as well as increased adverse effects.²⁷ Therefore, the 3.75% cream is the preferred concentration of most providers.²⁷ Recurrence rates range from 13% to 19%.²⁸

In 2006, the FDA approved polyphenon E, a botanical ointment, to treat anogenital warts. The formulation is composed of eight different sinecatechins extracted from green tea leaves.²⁹ Green tea sinecatechins have been shown to have antioxidant, antiproliferative, and antiviral properties, though the specific mechanisms of action in inhibiting anogenital wart growth have not been well studied to date. In a multicenter, randomized, double-blind, vehicle-controlled, three-arm parallel group phase 3 trial of 495 patients with anogenital warts, sinecatechins ointment 10% or 15% applied three times daily for 16 weeks resulted in complete clearance of warts in 57.2% and 56.3% of patients, respectively, compared to 33.7% clearance in the vehicle patients.³⁰ Partial clearance (≥ 50%) of warts was observed in 78.4% of patients who used the 15% ointment, 74.0% of those who used the 10% ointment, and 51.5% of the vehicle patients. Rates of recurrence were 6.5% and 8.3% with use of the 10% and 15% sinecatechins ointment, respectively, which are much lower than recurrence rates observed with other topical applications (eg, imiquimod and podophyllotoxin).³⁰

For larger warts or when there are anal lesions present, surgical excision and fulguration is required and referral to a colorectal specialist is warranted.

Warts recur from 4.6% to more than 70% of the time, most commonly due to activation of latent virus.²³ Therefore, whether initially treated in an office or operating room, condyloma patients require follow-up on a regular basis, generally every six to 12 months, to assess for recurrent anal lesions so that treatment can be promptly initiated.

In the absence of a cure for anogenital warts, prevention through an HPV vaccine is important. The quadrivalent HPV vaccine (Gardasil) was approved by the FDA in 2006 for prophylactic vaccination of females ages 9 to 26. The vaccine triggers host formation of antibodies against four common subtypes of HPV: 6, 11, 16, and 18.³¹ In 2009, the FDA expanded the use of Gardasil to include males ages 9 to 26; subsequently, Gardasil 9 (which protects against nine types of HPV) was approved for males ages 9 to 15.³² In a group of 4,065 healthy males between the ages of 16 and 26, Gardasil reduced the incidence of external anogenital warts by 90.4%.³³

HPV vaccine is now recommended for females through age 26 and males through age 21. The CDC also recommends HPV vaccine for the following individuals through age 26 if they did not get vaccinated when they were younger:

• Young men who have sex with men
• Young men who identify as gay or bisexual or who intend to have sex with men
• Young adults who are transgender
• Young adults with immunocompromising conditions (including HIV).³⁴

CONCLUSION

Anorectal conditions are a common presentation in the primary care setting. A thorough history and physical exam will usually determine the etiology, and most benign pathologies can be successfully treated in the primary care clinic. Knowing how to perform an anorectal exam and having a thorough understanding of the most common anorectal pathologies can help alleviate examiner discomfort, while ensuring that patients receive prompt and adequate care. At the same time, recognizing the red flags can expedite referral for colorectal specialty evaluation when appropriate. Red flags that should prompt immediate referral to a colorectal specialist include older age, unintentional weight loss, iron deficiency anemia, family history of inflammatory bowel disease or colorectal cancer, and persistent anorectal bleeding or persistent symptoms despite adequate treatment of a suspected benign condition.