Fissure & Pruritus

Marcus Burnstein, MD
Assistant Professor of Surgery
University of Toronto
Toronto, ONT

Anal Fissure

Anal fissure is a tear in the anal canal extending from just below the dentate line to the anal verge. Fissures occur in both genders and at all ages, most commonly in young and middle age adults. The cardinal symptom is pain during and for minutes to hours following defaecation. Bright red blood is common. Over 90% of anal fissures are located in the posterior midline, with almost all the rest located in the anterior midline. The acute fissure is a "mere crack" in the anoderm. Fissures which fail to heal acquire features of chronicity, including a distal sentinel tag, a proximal hypertrophied anal papilla, fibrotic edges, and exposed internal sphincter fibres.

1. Etiology and Pathogenesis
Understanding of anal fissure has increased tremendously in recent years.(1,2) The initiating factor is trauma, typically overstretching of the anoderm by a large hard stool. The proposed explanation for the posterior midline predominance is a lack of tissue support and maximal stretching at this site. It has been hypothesized that failure to heal is secondary to poor perfusion of the anoderm in the posterior midline. According to this hypothesis, posterior midline ischaemia is the result of arterial anatomy and internal anal sphincter hypertonicity. The evidence in support of this hypothesis is very strong:

• angiographic and anatomic studies of the inferior rectal artery show compromised blood flow in the posterior midline.(3)

• laser Doppler flowmetry demonstrates lower perfusion in the posterior midline and to a lesser extent in the anterior midline.(4)

• there is manometric evidence of sustained hypertonicity of the internal anal sphincter in patients with chronic anal fissure,(5) and an inverse correlation has been demonstrated between anal pressure and anodermal blood flow - the higher the pressure the lower the blood flow.(6)

• successful treatments for chronic anal fissure produce a significant reduction in resting anal tone and a significant increase in anodermal blood flow.(4,7)

Whether internal sphincter hypertonicity is a cause or effect remains uncertain. It has been assumed that hypertonicity is a reaction to anorectal pain. It has also been postulated that increased anal pressure precedes fissure, and that psychological stress produces a sustained rise in internal anal sphincter tone.(8)

2. Treatment

(i) Acute Fissure
Warm baths and a diet sufficiently high in fibre to achieve soft bulky stools allows approximately 80% of acute anal fissures to heal within three weeks. Stool softeners and fibre supplements are reasonable additions. Warm baths have been shown to reduce resting anal pressure. The addition of anaesthetic and steroid ointments, dilators, and local injections, do not increase healing rates and should generally be avoided. Recurrence is common, in the range of 30 - 70%, but can be reduced to 15 - 20% by maintaining a high fibre diet.(2)

Nitric oxide has been identified as the chemical messenger of the intrinsic non-adrenergic, non-cholinergic pathway mediating relaxation of the internal anal sphincter. Topical application of nitroglycerin, a nitric oxide donor, causes a transient lowering of resting anal pressure and an increase in anodermal blood flow. Bacher et al reported a 92% healing rate within two weeks for acute fissures treated with application of 0.2% glyceryl trinitrate ointment t.i.d. (9)

(ii) Chronic Fissure
Chronic fissures are unlikely to heal with warm baths and a high fibre diet. The key to healing chronic fissures is the reduction of resting anal pressure.

(a) Internal Sphincterotomy: Division of the internal anal sphincter is associated with excellent healing rates, but carries a risk of continence deficit. Posterior midline sphincterotomy has been condemned because of slow wound healing and unacceptably high rates of soiling, often associated with a posterior midline gutter or "keyhole" deformity. Lateral internal sphincterotomy (LIS) achieves healing in over 95% within several weeks; keyhole is avoided, and the rate and severity of continence problems are reduced, but are not negligible. The data regarding continence problems following LIS are difficult to interpret for many reasons, including the variety of LIS techniques, the diverse definitions of incontinence, the performance of additional procedures with LIS, and perhaps most importantly, the duration, meticulousness, and technique of follow up. Continence problems are reported in 0 - 35% of patients following LIS.(10)

A prospective randomized study comparing closed LIS (CIS) and open LIS (OIS) found no difference in healing and complication rates. Postoperative pain was lower with CIS.11 A retrospective review of 549 patients showed no difference between OIS and CIS in persistence of symptoms (3.4% OIS vs 5.3% CIS), recurrence of fissure (10.9% vs 11.7%), and need for re-operation (3.4 % vs 4%).12 Differences were found in flatus incontinence (30.3% vs 23.6%), soiling (26.7 vs 16.1) and accidental bowel movements (11.8 vs 3.1%). Over one third of patients complained of some change in continence. Anal deformity was felt to be minimal with both techniques. The difference in continence may be explained by a more complete sphincterotomy with OIS, although physiologic studies by others have not demonstrated a correlation between decrease in resting pressure and post-LIS incontinence. Both OIS and CIS have been shown to produce similar reductions in resting anal pressure, in the range of 20%.(2)

Current practice is to divide the internal sphincter to the level of the dentate line. It has been suggested that the height of LIS should be the lesser of the proximal end of the fissure, or two thirds the length of the sphincter. Littlejohn et al reported their experience with 287 patients who had LIS "tailored" to the length of the fissure.13 Four developed flatus incontinence, one minor staining, and two urgency. Five patients underwent repeat LIS for persistence or recurrence.

(b) Anal Dilatation: This is a crude technique for reducing sphincter pressure. The sphincter injury is uncontrolled and this method should be abandoned. Failure and incontinence rates are higher than with LIS.(2)

(c) Topical Nitroglycerin: Lund et al randomized 80 patients to apply 0.2% glyceryl trinitrate ointment (GTN) or placebo to the lower anal canal b.i.d.(7) Chronicity was defined by symptoms of greater than six weeks duration and fibrosis at the base of the fissure. At eight weeks healing was observed in 68% of the GTN group, and 8% of the placebo group. Median time to healing was six weeks. Resting pressure fell and anodermal blood flow increased in the GTN group. 3/38 patients in the GTN group recurred and each was successfully treated by further GTN. No patients reported impairment of continence. Resting pressure returned to pre-treatment levels with discontinuation of GTN. 58% of patients reported headache; only one patient stopped treatment. Schouten et al treated 34 consecutive patients for 6 - 12 weeks with topical Isosorbide Dinitrate.15 Within ten days anal pain was resolved in all patients. At twelve weeks, there was complete healing in 30/34. Mean duration of follow up was eleven months - fissure relapse was seen in 2/30 (7%). The reversible nature of "chemical sphincterotomy" is particularly attractive in patients at increased risk of impaired continence, e.g. patients who have had LIS. In Lund's trial,(7) five patients in each group were recurrences after LIS; 3/5 healed with GTN.

(d) Botulinum Toxin: Botulinum toxin has been injected into the external and internal sphincters and, with short term follow up, healing rates of 80% have been achieved. This approach is expensive and invasive compared to nitroglycerin.(2)

3. Special Issues

(i) Recurrent Fissure After Sphincterotomy
If non-operative measures fail to heal recurrent or persistent fissure, LIS can be repeated on the opposite side. The data is limited. LIS failure has been endoscopically linked to failure to divide the internal sphincter.(15) Pre-op manometry and endosonography have been recommended. Anal advancement flap has been suggested for patients at increased risk of faecal incontinence, such as elderly patients, diabetics, irritable bowel patients, multiparous women, and patients with recurrent fissure post LIS. Leong et al randomized 40 patients (no prior operation) to OIS or advancement flap (without sphincterotomy).16 There were no failures in the OIS group and three failures in the advancement flap group. There was no faecal incontinence in either group. Sphincterotomy plus anoplasty is indicated when fissure is associated with stenosis.

(ii) Crohn's Disease
Anal fissure is reported in 5 - 43% of patients with Crohn's disease.(17) These fissures are more likely to be asymptomatic (15 - 56%), multiple (14 - 33%), and eccentric ( 8 - 29%). Non-operative treatments, including Metronidazole, Prednisone, and ASA are successful in 44 - 81%, and are the usual approach. Selective operative treatment by Fleshner et al, usually sphincterotomy Ý fissurectomy, achieved healing in 88%. Abscess-fistula and proctectomy rates were not different between patients treated operatively and non-operatively. All of the abscess-fistula disease arose from the base of the unhealed fissure. Resection of proximal disease did not influence fissure healing.

(iii) HIV
In the HIV positive patient, benign fissure and idiopathic AIDS ulcers are distinct processes. Ano-receptive intercourse and diarrhoeal illnesses predispose the HIV positive homosexual to the development of anal fissures which are typical in appearance and response to treatment.18 Idiopathic anal ulcers are characterized by persistent gnawing pain, location above the dentate line, a broad base, deep invasion, a patulous anus, and AIDS. Debridement, excision with mucosal advancement, and Depo-Medrol injection have been successful.

(iv) Postpartum
Cosby et al prospectively evaluated 313 prima gravid women.(19) Twenty nine (9%) developed postpartum acute anal fissure, half in the anterior midline. Anal manometry pre and post delivery was not different in women who did and did not develop fissure. Six weeks after delivery, resting and squeeze pressures fell in both groups. Postnatal constipation was more common in those who developed anal fissure (62% versus 29%). 27/29 were successfully treated conservatively. As the postpartum fissures were associated with reduced pressures the authors suggested sphincter conserving options, such as advancement flaps. Sultan et al warn of the special risk of post-LIS incontinence in women, especially women with previous obstetrical trauma.20 Endoanal ultrasound demonstrated external anal sphincter defects in 19% of primiparous and 29% of multiparous women. LIS tends to be more extensive in women than intended, most likely related to the shorter anal canal.

Pruritus Ani (PA)(21, 22, 23)

The approach to diagnosis and management is simplified by recognizing primary "idiopathic" PA and secondary PA, due to specific pathology. At least half are primary, although it is likely that in some cases an original cause has faded and primary PA has remained.

1. Mechanisms
Numerous factors have been postulated - with inconsistent quality and quantity of evidence - to explain primary PA:

• The area is rich in nerve endings. Pain and itch are likely served by the same receptors and pathways, explaining the effectiveness of pain and counter-irritation in relieving itch. The receptors are located at the dermoepidermal junction so that skin damage increases receptor stimulation.

• The area is prone to wetness from sweat and mucous/faecal seepage, leading to maceration.

• There is exposure to faecal factors - PH, dietary substances, bacteria. Normal PH of perianal skin is acid - the alkalinity of diarrhoeal stools and soaps has been implicated. Substance sensitivities may exist to spices, coffee, milk, chocolates, and beer. Faecal bacteria produce neuraminidases that irritate the skin.

• Over-hygienic behaviour and "the itch-scratch cycle": obsessive "polishing" and scratching damage the skin leaving it more susceptible to irritative stimuli. Overzealous cleansing and poor hygiene may both be etiologic.

• Stress: emotional upset may accentuate the perception of itch.

• Ointments: topical steroids compromise normal skin resistance to trauma and infection. Anaesthetic agents are sensitizing.

A unifying pathophysiologic theory for primary PA has evolved in which impaired sphincter function with resultant seepage is the common underlying disturbance:

• Patients show earlier leakage of infused fluids and an exaggerated rectoanal inhibitory reflex.

• Coffee ingestion is associated with a reduction in anal pressure.

• 50% of patients have a history of poor evacuation.

While disturbed sphincter function has been proposed as causative, it may be a secondary phenomenon.

2. Diagnostic Approach
Potential causative factors should be evaluated by history: hygiene, continence, diet, travel, "exposure" to children, sexual history, topical and oral medications, other skin problems and illnesses, allergies, lactose intolerance, and stress. A complete anorectal examination is performed to look for specific causes of secondary PA (Table I). Primary PA is symmetrical around the anus. Laboratory investigation is not usually warranted; exceptions:

• Persistent, focal, unilateral or otherwise "suspicious" lesions MUST BE BIOPSIED. (Punch biopsy is a useful technique.)

• Diarrhoeal illnesses need appropriate work up.

• "Scotch tape test" for pinworms (children and exposed adults).

• In selected cases - viral and bacterial culture, scrapings for fungus and yeast, blood work for diabetes and blood disorders.

3. Treatment
These patients are frustrated by an embarrassing problem for which they have often received little help. Reassurance, patient education and follow-up are key elements of treatment. Patients must accept that a quick, easy, permanent fix is not realistic. The ASCRS pamphlet on PA is helpful. Berman has summarized patient education (Table II).21 The aim is to achieve clean, dry, intact skin. A two to three week course of 1% hydrocortisone cream after bowel movements and q.h.s. may help to break the itch-scratch cycle. Antifungal and anti-candidal creams are used when secondary infection is suspected. Coffee should be eliminated. Psyllium promotes complete evacuation. Sedatives and anti-pruritics are rarely added. Topical anaesthetics are avoided. Loperamide, by increasing resting anal pressure, may have a role in selected cases.

Less than 15% have a process that is amenable to operative correction. Routine treatment of haemorrhoids and skin tags is not recommended. When extensive tags or prolapsing tissue appear to contribute to poor hygiene, operation may be undertaken. Radiation, undercutting, excision and grafting, and injection are avoided. Biopsy should be readily undertaken for persistent focal or unilateral lesions; squamous cell cancer, basal cell cancer, Bowen's disease and Paget's disease may all present as PA.

Table I. Secondary Pruritus Ani ("The D's")

1. Diseases of the Anorectum

• fistula, fissure, haemorrhoids, ectropion, anal deformity

• venereal infections, herpes, condyloma

• radiation

• anorectal neoplasms

2. Diabetes and Blood Dyscrasias

3. Diseases of Gynaecologic Origin

• pruritus vulvae secondary to vaginal discharge or urinary incontinence may extend posteriorly

4. Diarrhoeal States

5. Drugs

• antibiotics may ( diarrhoea, candidal infection

6. Diet and Vitamin Deficiency

• beer, tea, coffee, chocolates, spices, citrus, tomato...

• vitamin A and B deficiency

• intertrigo - mixed bacterial infection associated with obesity

• erythrasma - Corynebacterium minutissimum infection, fluorescence (porphyrins) under UV light, well demarcated, red, scaly, also in toe webs, groin, axilla, and navel

• contact dermatitis - over the counter preparations and "caine" derivatives; steroids ( thin skin +- striae

• psoriasis – atypical in the perianal region – plaque, pallor, poorly defined, +- scaly; associated with lesions at elbows, knees, trunk, nails

• neurodermatitis - lichenification, evidence of scratching

• parasitic infection - pinworm, scabies, pediculosis

• mycotic infections - candida - vesicles, pustules, satellites, erythema, maceration, vaginitis; fungi - well defined border, unilateral, also at toes (from S. Wexner)

Table II. Treatment of Primary Pruritus Ani(21)

Do's

• Cut fingernails short

• Ensure sufficient dietary bulk

• Evacuate completely

• Wash after elimination

• Bathe effectively but use little soap

• Dry gently after washing

• Apply cotton and talc after drying

• Use lotion or cream as prescribed

Don't

• Scratching

• Dietary "irritants"

• Excessive steroid medications

• Coloured or perfumed toilet papers

• Overuse of soaps

• Mineral oil and topical anaesthetics

References

1. Schoeten WR, Briel JW, Auwerda JJA, et al. Anal fissure: new concepts in pathogenesis and treatment. Scand J Gastroenterol 1996; 31 Suppl 218:78-81.

2. Lund JN, Scholefield JH. Aetiology and treatment of anal fissure. Br J Surg 1996; 83:1335-1344.

3. Klosterhalfen B, Vogel P, Rixen H, et al. Topography of the inferior rectal artery: a possible cause of chronic, primary anal fissure. Dis Colon Rectum 1989; 32:43-52.

4. Schoeten WR, Briel JW, Auwerda JJA, et al. Ischaemic nature of anal fissure. Br J Surg 1996; 83:63-65.

5. Keck JO, Staniunas RJ, Coller JA, et al. Computer generated profiles of the anal canal in patients with anal fissure. Dis Colon Rectum 1995; 38:72-79.

6. Schoeten WR, Briel JW, Auwerda JJA. Relationship between anal pressure & anodermal blood flow. Dis Colon Rectum 1994; 37:664-669.

7. Lund JN, Scholefield JH. A randomized, prospective, double blind, placebo controlled trial of glyceryl trinitrate ointment in treatment of anal fissure. Lancet 1997; 349:11-14.

8. Regadas FSP, Batista LK de O, Albuquerque JLA, et al. Pharmacological study of the internal anal sphincter in patients with chronic anal fissure. Br J Surg 1993; 80:799-801.

9. Bacher H, Mischinger HJ, Werkgartner G, et al. Local nitroglycerin for treatment of anal fissures: an alternative to lateral sphincterotomy? Dis Colon Rectum 1997; 40:849-845.

10. Hananel N, Gordon PH. Lateral internal sphincterotomy for fissure in ano - revisited. Dis Colon Rectum 1997; 40:597-602.

11. Kortbeek JB, Langevin JM, Khoo RE, et al. Chronic fissure in ano: a randomized study comparing open and subcutaneous lateral internal sphincterotomy. Dis Colon Rectum 1992; 35:835-7.

12. Garcia-Aguilar J, Belmonte C, Wong WD, et al. Open vs closed sphincterotomy for chronic anal fissure. Dis Colon Rectum 1996; 39:440-443.

13. Littlejohn DRG, Newstead GL. Tailored lateral sphincterotomy for anal fissure. Dis Colon Rectum 1997; 40:1439-1442.

14. Schoeten WR, Briel JW, Boerma MO, et al. Pathophysiological aspects and clinical outcome of intra-anal application of isosorbide dinitrate in patients with chronic anal fissure. Gut 1996; 39:465-469.

15. Farouk R, Mauson JRT, Duthie GS. Technical failure of lateral sphincterotomy for the treatment of chronic anal fissure; a study using endoanal ultrasonography. Br J Surg 1997; 84:84-85.

16. Leong AFPK, Seow-Choen F. Lateral sphincterotomy compared with anal advancement flap for chronic anal fissure. Dis Colon Rectum 1995; 38:69-71.

17. Fleshner PR, Schoetz DJ Jr, Roberts PL et al. Anal fissure in Crohn's disease: a plea for aggressive management. Dis Colon Rectum 1995; 38:1137-1143.

18. Viamonte M, Dailey TH, Gottesman L. Ulcerative disease of the anorectum in the HIV+ patient. Dis Colon Rectum 1993; 36:801-805.

19. Cosby H, Donnelly VS, O'Herlihy C et al. Anal canal pressures are low in women with postpartum anal fissure. Br. J. Surg 1997; 84:86-88.

20. Sultan AH, Mann MA, Nicholls RJ, et al. Prospective study of the extent of internal anal sphincter division during lateral sphincterotomy. Dis Colon Rectum 1994; 37:1031-1033.

21. Berman IR. Mechanisms, diagnosis and management of anal irritation and itching. In Schrock T (ed): Perspectives in Colon and Rectal Surgery. St. Louis, Quality Medical Publishing, Inc., 1990, 3:82-97.

22. Smith LE. Perianal dermatologic disease. In Gordon PH, Nivatvongs S: Principles and Practice of Surgery for the Colon, Rectum and Anus. St. Louis, Quality Medical Publishing, Inc., 1992:281-300.

23. Friend WG. Pruritus Ani. In Fazio V (ed): Current Therapy in Colon and Rectal Surgery. Toronto, BC Decker Inc., 1990:42-45.