Figure 2. Coronal section of rectum with a
chronic anal fissure
showing: A, Dentate line. B, Anal papilla. C, Fibers of the
internal anal sphincter at the base. D, Sentinel tag. E, Internal
anal sphincter. F, External anal sphincter.
Most patients with anal pain or irritation present to their physicians complaining of hemorrhoids. [43] [51] Many, however, turn out to have another reason for their discomfort. Anal fissures, proctalgia fugax, levator ani syndrome, and pruritis ani are common causes of anorectal pain and irritation. The primary care clinician can diagnose and manage these diseases with confidence, as most patients have uncomplicated cases that respond to simple lifestyle changes and routine medications.
An anal fissure is a longitudinal tear or ulcerated area in the distal anal canal, usually in the posterior or anterior midline and usually extending from the level of the dentate line out to the anal verge. [43] Acute anal fissures have little surrounding inflammation and may spontaneously heal in 2 to 3 weeks. A chronic anal fissure usually is deeper and is
Anal fissures affect men and women equally. Most anal fissures occur in the posterior midline; women are slightly more likely than men to have anterior fissures (Table 1) . A patient with multiple fissures, or whose fissure is not in the midline, is more likely to have an associated colorectal disorder such as Crohn's disease. [19] Although anal fissures are seen in both newborns and the elderly, 87% of chronic sufferers are between 20 and 60 years old, and 54% are between 30 and 50. [55] [65]
In the past, clinicians thought that tearing of the anal skin as the patient passed a hard, dry stool caused anal fissures. In fact, only 25% of patients with fissures have constipation. [50] Furthermore, this theory did not explain why most fissures are in the posterior midline. Klosterhalfen et al, [42] in their study of the inferior rectal artery anatomy in cadavers, proposed an alternative hypothesis. They noted that in most subjects, the capillary system of the inferior rectal artery ended at the posterior commissure, making this site prone to ischemic injury. Using laser Doppler flowmetry in healthy volunteers, Schouten and colleagues [77] confirmed that the blood supply to the posterior anoderm is lower than at the other sides of the canal. Furthermore, patients with anal fissures showed improvement in the posterior commissure blood flow following lateral sphincterotomy. [76] Spasm of the internal anal sphincter may worsen the ischemia and retard healing. Most anal manometric studies show an increase in the resting anal pressure in patients with anal fissures, a finding consistent with chronic internal anal sphincter contraction. [3] [10] [17] [22] [31] [41] [45] [62] [76] [92] Additional risk factors for anal fissures include a low fiber diet and previous anal surgery. [37]
Almost all patients with anal fissures
complain of perirectal pain; many also have rectal bleeding. In a study of 172
persons with chronic
| Gender | Fissure Location | ||
|---|---|---|---|
| Posterior | Anterior | Other | |
| Male | 83%-84% | 6%-9% | 7%-10% |
| Female | 67%-68% | 10%-21% | 11%-14% |
| Both | 75%-76% | 13%-16% | 9%-12% |
A gentle and reassuring manner is necessary to examine someone suffering from
an anal fissure;
many patients tolerate only gradual spreading of the buttocks. The acute anal
fissure looks like a superficial tear in the
anal mucosa. A chronic anal fissure
is deeper and often has an associated proximal anal papilla and distal sentinel
tag (Figs. 1 (Figure Not Available) and 2)
. The fissure margins may be inflamed and fibers of the internal anal sphincter
may be visible at its base. [36]
[43]
[58]
[74]
If the patient has atypical or multiple fissures, the practitioner should search
for an underlying disorder. Causes of atypical or multiple fissures are *
Inflammatory bowel disease
Figure 1. (Figure
Not Available) Chronic anal fissure
showing: A, External hemorrhoid. B, Fibers of the internal anal
sphincter at the base. C, Sentinel tag. (Courtesy of RP Billingham, MD,
Seattle, Washington.)
Figure 2. Coronal section of rectum with a
chronic anal fissure
showing: A, Dentate line. B, Anal papilla. C, Fibers of the
internal anal sphincter at the base. D, Sentinel tag. E, Internal
anal sphincter. F, External anal sphincter.
Anoscopic and digital rectal examinations, although recommended in patients with chronic anal fissures, may be painful. In these circumstances, an anesthetic such as 2% lidocaine jelly applied to the fissure may lessen the examination discomfort. [36] [43]
Anal fissure treatment includes dietary manipulation, medication, anal dilatation, and internal sphincterotomy. [74] Patients with acute anal fissures who have diarrhea or constipation are told to consume high fiber foods. Topical anesthetics and corticosteroids often are recommended as well. [38] Warm sitz baths may help relieve the pain. These simple measures may heal acute anal fissures within 3 weeks in almost 90% of patients.
In contrast to acute anal fissures, only 40% to 60% of patients with chronic anal fissures improve with conservative therapy. [25] [47] Historically, anal dilatation, fissurectomy, or sphincterotomy have been offered to these patients. Anal dilatation has been employed extensively in Europe and Australia; however results have been mixed. [25] [35] [56] [68] Many feel that anal dilatation is simply an uncontrolled sphincterotomy with a higher incontinence rate than other therapies. [58] [74] Compared with lateral internal sphincterotomy, fissurectomy has a lower cure rate and higher incidence of postoperative pain. Therefore, in most of the world, including North America, lateral internal sphincterotomy is the procedure of choice. [43] [51] [58]
Lateral internal sphincterotomy was first described in the 1950s. [15] The lateral is preferred over the posterior approach as it is less likely to produce a keyhole deformity, which causes fecal soiling. [43] [61] Notaras [61] modified the technique in the late 1960s, demonstrating a minimally invasive
Complications of lateral internal sphincterotomy include late healing of the sphincterotomy site, wound infection, fecal or flatus incontinence, and fissure recurrence. [30] [46] [50] [86] Although incontinence rates for flatus vary from 0% to 35%, and for feces from 0% to 5%, [30] [46] [50] [86] most researchers report an incontinence rate for flatus that is 2% or less and for feces a rate that is 1% or less. Similarly, most surgeons note a long-term operative failure rate of less than 3%. [46] [50] [58] [86] Because incontinence may rarely be a problem, the American Society of Colon and Rectal Surgeons advises caution before performing lateral internal sphincterotomy in patients with diarrhea, irritable bowel syndrome, diabetes, or other pre-existing states that predispose them to incontinence. [74] This view has prompted some authors to recommend preoperative anal manometry and endoanal ultrasound in patients with recurrent fissures and in women with a history of episiotomy or third-degree tear during labor. [50] Others regard preoperative anal manometry as unnecessary because presurgical and postsurgical measurement of the internal anal sphincter resting pressure shows no statistically significant correlation. [72]
In the last decade, several researchers have successfully treated chronic anal fissures with the novel use of two medications: topical nitroglycerin and injectable botulin toxin. [52] [75] Recently, O'Kelly [63] and others demonstrated that nitric oxide is the inhibitory neurotransmitter responsible for internal anal sphincter relaxation. Loder et al [48] showed that 0.2% topical nitroglycerin ointment, a nitric oxide donor, produced a 27% decrease in mean resting sphincter pressure. Since that 1994 paper, at least six groups have published their experiences using nitroglycerin to treat chronic anal fissures. [5] [24] [49] [64] [83] [88]
Two randomized, controlled trials of nitroglycerin in patients with anal fissures have been published. [5] [49] Bacher et al [4] noted that after 1 month, 80% of subjects treated with nitroglycerin applied three times daily to the anoderm had healed fissures, compared with only 40% who received topical lidocaine. Similar results were reported in another study in which nitroglycerin was used twice daily. After 8 weeks, the anal fissure resolved in 68% of the treatment cohort, compared with 8% of the placebo group. [49] Compared with placebo, subjects receiving nitroglycerin ointment had a statistically significant fall in internal anal sphincter resting pressure and rise in anodermal blood flow. [5] [49]
All researchers mention a dramatic reduction in anal fissure pain with nitroglycerin. [5] [24] [49] [64] [83] [88] Complications include headache in 20% to 35% and occasional tachyphylaxis. [5] [24] [88] Long-term success rates are not known, but most patients who relapse respond to retreatment. [49]
Injectable botulin toxin also shows promise as a nonsurgical treatment of chronic anal fissures. [28] [39] [53] [54] Jost [39] reported fissure healing in 79 of 100 patients 6 months after 2.5 to 5 U of botulin toxin was injected into the external (not internal) anal sphincter. Seven patients experienced transitory fecal incontinence. In a double-blind, randomized, controlled trial
Most patients with anal fissures respond to conservative treatment such as stool softeners (if necessary), sitz baths, and daily application of 1% hydrocortisone cream to the fissure. Patients who fail to improve after 4 weeks should be offered lateral internal sphincterotomy. Topical nitroglycerin ointment and injectable botulin toxin are experimental treatments requiring further study prior to general acceptance. Neither drug is approved by the Food and Drug Administration for this indication.
Proctalgia, or perirectal pain, was first described in the 19th century. [57] Three terms are used to classify proctalgia: levator ani (or levator spasm) syndrome, proctalgia fugax, and coccygodynia. [51] [91] Levator ani syndrome refers to chronic or recurrent rectal pain or aching, with episodes lasting 20 minutes or longer in the absence of organic disease that could account for the pain. [91] Proctalgia fugax connotes anal or rectal pain, lasting for seconds to minutes and then disappearing for days to months, in the absence of organic disease to account for these symptoms. [91] Coccygodynia usually describes tenderness of the tip of the coccyx and is synonymous with levator ani syndrome. Unfortunately, the three terms have been used interchangeably in the literature, making precise recommendations for treatment difficult.
Both levator ani syndrome and proctalgia fugax are common disorders. It is estimated that 6% of the United States population suffers from levator ani syndrome, while 8% have proctalgia fugax. [12] Proctalgia fugax was at one time thought to be a disorder of perfectionistic young men. [67] It is now apparent that both proctalgia fugax and levator ani syndrome occur slightly more often in women. Both are more common in patients under age 45; psychological factors are not always present (see below). [12]
Thiele generally is acknowledged as the first to recognize the relationship between levator ani muscle spasm and chronic intermittent rectal pain. [84] The levator ani consists of three muscles: the ileococcygeus the puborectalis, and pubococcygeus. These three surround the anus to form
Proctalgia Fugax
The cause of proctalgia fugax is not known, but current theories favor rectal muscle spasm. [4] [60] [91] Anal manometric studies have demonstrated that patients with proctalgia fugax have normal anorectal muscle function at rest, but develop anal smooth muscle dysfunction during a painful attack. [14] [73] Two families with hereditary proctalgia fugax have been studied. Members of both families had endosonographic evidence of thickened internal anal sphincter muscles. Anal manometry of affected persons showed increased resting pressure and prominent ultraslow wave pressure oscillations. The latter were thought to be caused by smooth muscle contractions of the internal anal sphincter, and peaks in pressure were associated with characteristic pain. [9] [40] Furthermore, drugs known to relax smooth muscles may have relieved attacks of proctalgia fugax. [7] [13] [29]
Proctalgia fugax may be associated with functional gastrointestinal disorders. Abdominal pain and distension, frequent loose stools, and a sensation of incomplete evacuation after defecation have been noted more often in patients with proctalgia fugax. The significance of this remains a mystery. [85]
An investigation of the psychological aspects of proctalgia fugax done in the 1960s found most sufferers to be anxious, tense, and perfectionistic. [70] There was, however, no control group for the subjects. Current consensus does not support a psychosomatic origin for either proctalgia fugax or levator ani syndrome, [91] although stressful events may trigger attacks. [23] [73]
Grant et al [27] in an analysis of 316 cases observed that patients with levator ani syndrome complained of a vague, indefinite rectal discomfort or pain. The pain was felt high in the rectum and was sometimes associated with a sensation of pressure like a ball or other intrarectal object. Others note the pain may be aggravated by sitting or by the need to defecate, and relieved by walking or lying down. [18] [23]
By definition, the pain of proctalgia fugax is brief and self limited. Patients with proctalgia fugax complain of sudden onset of intense, sharp, stabbing or cramping pain in the anorectum. The pain occurs at any time of the day and typically awakens the sufferer from a sound sleep. [14] [27] [29] [67] [73]
The physical examination of patients with levator ani syndrome and proctalgia fugax usually is unremarkable. [4] [60] [91] In patients with levator ani syndrome, palpation of the levator muscle while performing a digital rectal examination usually reproduces their pain. Grant noted that in patients with levator ani syndrome, their levator muscle may be felt as a firm band beneath the examining finger as it is passed from a lateral to an anterior
There are no diagnostic studies to exclude or confirm levator ani syndrome or proctalgia fugax. The inexperienced practitioner should consider other causes of anorectal pain and obtain further investigations or consultations as appropriate. [34] [59] [66] [80] Other causes of anorectal pain are *
Management of levator ani syndrome and proctalgia fugax is controversial. No single treatment has been unusually successful in all patients. Patients with levator ani syndrome and proctalgia fugax should be reassured that their painful attacks are benign and often diminish over time.
Levator Ani SyndromeFor patients with levator ani syndrome, initial conservative treatment with hot baths, nonsteroidal anti-inflammatory drugs, muscle relaxants, or levator muscle massage is recommended. [18] [27] [66] Levator muscle massage consists of high, deep, digital pressure over the puborectalis portion of the levator floor. [18] This procedure is repeated every 2 to 3 weeks for two to three courses. [27] One-half to two-thirds of levator ani syndrome sufferers improve with the above measures. [18] [27]
In the 1980s, several researchers tried electrogalvanic stimulation of the levator muscle. Early studies reported a 90% success rate, [59] [80] but subsequent investigations demonstrated a long-term failure rate of 32% to 60%. [6] [34] [66] More recently, researchers using EMG-based biofeedback have shown improvement in pain in some studies. [23] [33] The findings of these studies may be unreliable because of the small number of subjects, lack of controls, and high dropout rate.
Proctalgia FugaxRecommendations for treatment of proctalgia fugax are limited to anecdotal reports and a single randomized controlled trial. Fortunately for most patients, the attacks are brief and infrequent. For patients with frequent attacks, physical modalities such as hot packs or direct anal pressure
Pruritis ani is an unpleasant cutaneous sensation that induces that desire to scratch the skin around the anal orifice. [32] [81] The exact incidence worldwide is unknown; it reportedly occurs in as many as 45% and as few as 1% of the population. [2] [32] It occurs more often in men, with the observed male-to-female ratio varying from 2:1 to 4:1. [11] [44] [81] Most patients are 30 to 70 years old. [79] [87] Pruritis ani can be classified as primary (idiopathic) or secondary.
Causes of secondary pruritis ani are *
Anorectal disorders
Pruritis ani is a symptom complex, not a diagnosis. It is estimated that 25% to 75% of patients with pruritis ani have an associated disorder. [2] [8] [11] [26] [32] [89] [90] These patients with so-called secondary pruritis ani usually respond to treatment of the underlying condition. It has been suggested that psychological factors may play a role in the genesis of anal itching. [87] Research, however, does not support this perception. [44] [79]
Approximately one-half of patients with perianal pruritis have no identifiable anal or rectal disease. These patients can be difficult to treat, but frequently improve following modification of diet and perianal hygiene habits. In 1977 Friend [20] proposed that patients with idiopathic pruritis ani consume enormous quantities of liquids and that certain beverages--coffee, tea, cola, and beer--were especially likely to produce anal itching. He suggested that there is a threshold above which patients develop pruritis ani from certain food items and below which they do not. [20] Furthermore, he observed a 24- to 48-hour delay in the onset of symptoms after the threshold was exceeded. Although most authorities agree that patients with pruritis ani should avoid coffee (including decaffeinated), alcohol, and caffeinated drinks, Friend's hypothesis has never been studied in a randomized controlled trial. [11] [26] [32] [81]
The pathophysiology of all the secondary causes of pruritis ani is beyond the scope of this article. Little is known about the pathogenesis of idiopathic pruritis ani. Smith et al hypothesized that fecal leakage caused skin irritation and subsequent pruritis. They proposed a mechanism whereby several factors including stress, diet, and anatomic anal changes produced accidental fecal soiling. Indeed, anal manometric studies of patients with pruritis ani demonstrate an increase in anal sphincter relaxation and subsequent fluid leak following rectal distension. [1] [16]
Although no difference in fecal microflora in patients with pruritis ani has been found, it is thought that bacterial endopeptidases, exotoxins, and intestinal lysozymes may act as irritating agents. [26] [78] If the sufferer scratches and breaks the sensitive perianal skin, these substances might penetrate into the dermis causing inflammation and release of other irritating compounds. [26] Therefore, more itching and scratching ensue, creating a vicious cycle. Many patients add insult to injury by attempting to clean the area with harsh soaps and vigorous rubbing, or by applying topical medications that further irritate the skin. Other factors such as increased perianal moisture from sweat also may contribute to the problem.
Patients with pruritis ani usually report an escalating pattern of itching and scratching in the perianal region. These symptoms may be worse at night when they are less distracted by usual daily activities. The clinician
Examination of the perianal area may reveal maceration, erythema, excoriation, and lichenification. The practitioner should perform a digital rectal examination and anoscopy to assess the sphincter tone and look for secondary causes of pruritis suggested from the history. Initially, an exhaustive search for associated or causative conditions usually is not necessary. At least one study recommends an aggressive work-up of patients over age 50 or who have had symptoms for several weeks. [11] Patients who fail to respond to 3 or 4 weeks of conservative treatment should undergo further investigations such as skin biopsy and sigmoidoscopy or colonoscopy. [58]
The management of pruritis ani is directed towards the underlying cause. Most patients with secondary pruritis ani improve following treatment of the primary disorder. [71] If the diagnosis is idiopathic, then the patient is taught principles of good anal hygiene and instructed to modify his or her diet. Several patient self-care instructions have been published. [2] [20] [32] [79] [81] In general, pruritis ani sufferers are advised to clean the perianal area with water following defecation, but to avoid using soaps and vigorous rubbing. Following this, the patient should dry the anus with a hair dryer or by patting gently with cotton. Between bowel movements he or she should place a thin cotton pledget dusted with unscented cornstarch against the anus. A high fiber diet is recommended to regulate bowel movements and absorb excess liquid. Finally, the patient should eliminate all foods and beverages that may be exacerbating the itching. Once the symptoms have resolved, the patient can cautiously add these dietary items one at a time, keeping a food and symptom diary to see if there is a threshold phenomenon. [20]
Topical medications generally are not recommended because they may cause further irritation. If used, a bland cream such as zinc oxide or mild corticosteroid such as 1% hydrocortisone cream should be applied sparingly two to three times a day. [2] [26] [32] [81] More potent fluorinated corticosteroids should be avoided as they may worsen the problem by causing skin atrophy. [32] [87] Agents such as aluminum acetate, crotamiton, and magnesium hydroxide in phenol are no better than bland creams in the treatment of pruritis ani. [2]
Systemic therapy with an antihistamine such as diphenhydramine (Benadryl) or hydroxyzine (Atarax, Vistaril) may relieve the itching and allow the patient to sleep. [26] Recalcitrant cases of pruritis ani are uncommon, and clinicians treating these patients should search for a secondary cause of the itching. It is advisable to refer patients with intractable idiopathic pruritis ani to a dermatologist, gastroenterologist, or colorectal surgeon for treatment.
Anal fissures, proctalgia fugax, levator ani syndrome, and pruritis ani are common afflictions. The clinician who obtains a thorough history and performs a complete examination can accurately diagnose these disorders. Ancillary tests are seldom helpful and rarely necessary. Most patients suffering from these conditions readily respond to conservative therapy provided in the primary care practitioner's office. Most patients with anal fissures improve with stool softeners, sitz baths, and application of a mild corticosteroid cream; however, some patients require an operation. New, nonsurgical methods are being developed that may reduce the need for surgical intervention. Patients with perirectal pain should be examined thoroughly for potentially curable causes of their discomfort. If levator ani syndrome or proctalgia fugax are confirmed, the patient should be reassured concerning the benign nature of the attacks. The ideal remedy for levator ani syndrome is not known, but some patients may obtain relief from nonsteroidal anti-inflammatory drugs, muscle relaxants, levator muscle massage, electrogalvanic stimulation, or biofeedback. Proctalgia fugax rarely requires specific treatment since attacks are brief and self-limited. Patients with pruritis ani should be taught principles of good anal hygiene, told to reduce their fluid intake, and avoid anorectal trauma such as rubbing or scratching.
The author acknowledges the Swedish Medical Center Library Staff for their help in obtaining material for this article.