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.

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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.

Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

[email protected]

Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

[email protected]

Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

[email protected]

New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

[email protected]

New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

[email protected]

New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

[email protected]

Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The meeting is cochaired by Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, Mich., Christopher B. Zachary, MD, of the University of California, Irvine, and Joseph F. Fowler Jr., MD, of the University of Louisville (Ky).

Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The meeting is cochaired by Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, Mich., Christopher B. Zachary, MD, of the University of California, Irvine, and Joseph F. Fowler Jr., MD, of the University of Louisville (Ky).

Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The meeting is cochaired by Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, Mich., Christopher B. Zachary, MD, of the University of California, Irvine, and Joseph F. Fowler Jr., MD, of the University of Louisville (Ky).

TORONTO – Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News

[email protected]

On Twitter @mitchelzoler

TORONTO – Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News

[email protected]

On Twitter @mitchelzoler

TORONTO – Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News

[email protected]

On Twitter @mitchelzoler

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News

[email protected]

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36