Anal Fissure



Fig. 4.1
Typical chronic anal fissure





4.2 Epidemiology


Fissure in ano is one of the common benign anorectal conditions and can occur at any age. It commonly affects the younger and middle age groups but is sometimes seen at other ages, including infancy and early childhood and has no sex predilection. Ninety percent of anal fissures occur in the posterior midline of the anoderm and are solitary. Ten percent of women and one percent of men may have fissures in the anterior midline (Fig. 4.2). Women who develop symptoms during pregnancy or after childbirth usually have anterior fissure in ano (Jonas et al. 2001). Atypical positions of fissure or multiple fissures (Figs. 4.3 and 4.4) should raise the suspicion of uncommon causes like inflammatory bowel disease, tuberculosis, anal intercourse and anal malignancy, or immunodeficiency syndromes.

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Fig. 4.2
Anterior anal fissure


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Figs. 4.3 and 4.4
Atypical positions of anal fissure


4.3 Classification


Fissures may be classified as primary idiopathic, which is the most common and secondary, based on the etiology. It has also been classified arbitrarily as acute fissure in ano and chronic fissure in ano based on the duration of symptoms and healing. Typically acute anal fissures are those which heal within 6 weeks of duration spontaneously or with medical management. They are superficial and may deepen to expose the underlying internal sphincter. Fissures which have not healed in 6 weeks and developed secondary changes in the form of sentinel tag, hypertrophied anal papilla (Fig. 4.5), induration of the lateral edges of the fissure, relative stenosis secondary to spasm, or fibrosis of the internal sphincter are labeled as chronic, and these often require surgical management (Zaghiyan and Fleshner 2011; Madalinski 2011). Based on location, fissure is classified as typical or atypical. Among the typical sites, posterior fissures are the most common (90 %), while anterior ones are uncommon. Atypical fissures are located at any other site and usually due to some secondary pathology.

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Fig. 4.5
Hypertrophied papillae and sentinel pile


4.4 Pathology


In its early stages, a fissure is a simple split in the skin of the anal canal, but there soon develop in connection with it certain secondary changes. One of the most striking of these is a swelling of the skin at the lower end of the fissure, actually at the level of the anal orifice, so that it forms a tag – like swelling the so-called sentinel pile. This is presumably due to low-grade infection and lymphatic edema, and often the tag has a very inflamed, tense, and edematous appearance (Fig. 4.6); later it may undergo fibrosis and persist as a permanent fibrous skin tag even after the fissure has healed.

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Fig. 4.6
Inflamed, edematous sentinel pile

Quite frequently, the anal valve immediately above the fissure also becomes swollen due to edema and fibrosis and forms a hypertrophied anal papilla. Another feature in a long-standing case is the development of fibrous induration in the lateral edges of the fissure. At any stage, frank suppuration may occur and extend into the surrounding tissues to form a perianal abscess, which may discharge through the fissure into the anal canal or may burst externally to produce a low anal fistula: fissure fistula complex (Fig. 4.7). Usually the external opening of this fistula lies in or close to the midline, a short distance behind the anus, and an anal fissure should always be thought of as the most common cause of such a median low dorsal anal fistula. When the fissure is relatively superficial, the sphincter usually undergoes a tight spasm, but when the fissure deepens and bares the sphincter fibers, this becomes even more pronounced. Eventually after several months, the muscle may become fibrosed in its spastic condition so that a rather fibrotic, tightly contracted, internal sphincter may result.

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Fig. 4.7
Fissure fistula complex


4.5 Etiopathogenesis


The etiology and pathogenesis of this condition is poorly understood and hence the confusion in the choice of optimal modality of treatment. It was known for a long time that the tear in anal fissure is caused by passage of hard fecal mass. In 1994, a theory of inverse relationship of anodermal blood flow in the posterior commissure of the anoderm to the internal sphincter resting pressure was postulated by Schouten et al. (1996). The blood supply to the posterior midline of the anal canal has been demonstrated to be significantly lower using Laser Doppler Flowmetry than anywhere else in the anal canal (Klosterhalfen et al. 1989) and hence the increased propensity of occurrence of anal fissures in this region. It has also been found that there is a decrease in the normal spontaneous cyclical anal sphincter relaxation in patients with anal fissure. No single factor can be attributed to the etiopathogenesis of anal fissures, and a combination of factors may be contributory. These can be discussed under the following subheadings:


4.5.1 Microtrauma to Anal Canal Mucosa


Passage of a hard fecal mass causes a tear in the anoderm distal to the dentate line which is sensitive to pain. This causes severe pricking pain in the anal canal which in turn results in severe anal sphincteric spasm. This vicious cycle perpetuates and progresses to chronic fissure in ano, which is characterized by deep fissure, associated with hypertrophy of split mucosal edges, external skin tag at the distal end, and hypertrophied anal papillae at the proximal end.


4.5.2 Anal Sphincteric Spasm


The resting anal pressure is a function of the internal anal sphincter and is mediated by both alpha-adrenergic nerve fibers and inherent muscle tone. Relaxation of internal anal sphincter on rectal distension automatically is called rectoanal inhibitory reflex (RAIR). It has been observed that in patients with chronic fissure in ano, there is abnormal rectoanal inhibitory reflex along with hypertonicity of the internal anal sphincter and a long high pressure zone (HPZ). The application of pharmacological preparations that relax internal anal sphincter is effective in healing of chronic fissure in ano.


4.5.3 Anal Mucosal Ischemia


It has been demonstrated in cadaveric angiographic studies that there is paucity of vascular supply to the posterior commissure of the anal canal mucosa in patients with fissure. Any mucosal microtrauma in this region has delayed healing and progresses to a chronic condition if the causative factor is not eliminated (Schouten et al. 1996; Klosterhalfen et al. 1989).


4.5.4 Trauma During Childbirth


A small number of women develop chronic anal fissure following traumatic childbirth which is either attributed to indirect shearing forces during vaginal birth or due to tethering of anal mucosa to the underlying internal sphincter due to fibrosis, rendering it susceptible to further trauma.


4.5.5 Other Causes of Secondary Anal Fissure


Rare causes of anal fissure include inflammatory bowel disease like Crohn’s disease, tuberculosis, sexually transmitted diseases like syphilis, anal malignancy, human immunodeficiency syndrome, and anal trauma due to unnatural sexual intercourse or finger digitation. Fissures in these patients may be located anywhere including atypical sites.


4.6 Clinical Features


The most common symptom of fissure in ano is excruciating tearing anal pain after passage of stools associated with passage of minimal amounts of bright red blood which usually lines the stools. Subsequently, it may continue as a severe burning discomfort for few minutes to hours after defecation. To some patients with an anal fissure, the pain is so agonizing that they are frightened to have a motion and may remain in a constipated condition. Some patients complain of perianal pruritus and feeling of wetness in the perianal region. Some patients with a large sentinel tag may become aware of this as a lump at the anus and may complain of having a painful external pile. Sometimes patients with a painful anal fissure develop disturbances of micturition, either dysuria and retention or increased frequency.

During examination, it is essential that extreme gentleness is displayed since fissure in ano is an extremely painful condition and the patient suffering from it is usually very apprehensive of rectal examination. Examination of the perianal region on careful inspection typically shows a superficial mucosal split in acute fissure. This requires gentle parting of the buttocks sufficient to open the anal orifice. A chronic fissure will have raised edges of the mucosal split with varying depth mostly in the posterior midline, exposing the pale-colored internal sphincter at the floor. The induration at the edges gives an impression that of a button hole on palpation. There is often a skin tag at the distal end and a hypertrophied anal papilla at the proximal end (Gupta 2004). Proctoscopy may have to be deferred especially in an acute case in view of pain. The sphincter spasm and the fibrosis may be appreciated during palpation. Occasionally, a fistula may be demonstrated with an infected fissure in ano (Fig. 4.7). Abnormal locations and multiplicity should raise a suspicion, and attempts must be made to rule out specific causes for the occurrence of fissure in ano as described above. Crohn’s fissures are multiple, asymptomatic, and eccentric in location. HIV-disease-related fissures are deep, broad based, or cavitating ulcers with poor sphincter function.


4.7 Differential Diagnosis




(a)

Idiopathic stenosis of internal sphincter:

It is a definite clinical entity. It occurs in certain older patients, usually women, who have been accustomed to taking aperients over many years so that the anal canal has for a long time been spared the regular dilating action of a normal solid motion. As a consequence, the internal sphincter undergoes contraction and may become fixed in this contracted condition by fibrosis, as in a case of chronic anal fissure. There may be no symptoms, or when the contraction becomes extreme, the patient may find difficulty in passing motions. The condition is easily recognized by finding a tightly contracted internal sphincter on palpation, without any evidence of a past or present fissure. If required, it can be treated by internal sphincterotomy exactly as for chronic anal fissure.

 

(b)

Pruritus ani with superficial cracks of the anal skin.

 

(c)

Tuberculous ulcer.

 

(d)

Inflammatory bowel disease with anal ulceration.

 

(e)

Squamous cell carcinoma of the anus or adenocarcinoma of the rectum invading the anal canal or anus.

 

(f)

Syphilitic fissures.

 

(g)

Secondary fissures may be caused by previous anal operations that result in scarring, stenosis, and loss of anoderm. Individuals who have undergone intestinal bypass procedures for obesity may develop anal stenosis associated with a fissure.

 

(h)

Atypical fissures other than in the classical position or multiple fissures warrant detailed history and examination to rule out causes like tuberculosis, inflammatory bowel disease, malignancy, sexually transmitted disease, or unnatural sexual practices.

 


4.8 Management


Management strategies are decided based on the acuteness or chronicity of the fissure clubbed with the patients presenting complaints. Etiological factors and complications of fissures also determine the choice of the treatment offered.


4.8.1 Management of Acute Superficial Anal Fissure


Conservative measures to treat superficial fissure involves breaking the vicious cycle of tear, pain, and anal sphincteric spasm. This includes:

(a)

Measures to soften stools like high-fiber diet, adequate oral fluid intake, and consumption of bulk-forming agents like Isphagula and laxatives (Jensen 1987).

 

(b)

Warm water sitz baths help to soothen the perianal region and relieve sphincter spasm (Dodi et al. 1986).

 

(c)

Measures to relieve anal pain like local application of local anesthetic agents like lignocaine cream before the act of defecation and after (Gupta 2004).

 

(d)

Antibiotics, anti-amoebic, and antihelmintics are prescribed in presence of infections.

 

Fortunately, most of the acute fissures respond well to these measures itself, but the rest may require some form of medical treatment which is no different from that advised for chronic fissure and described below:


4.8.2 Management of Persistent Acute Fissure In Ano and Chronic Anal Fissure



4.8.2.1 Medical Management


Medical management aims at eliminating the factors involved in the etiopathogenesis of anal fissure and consists of facilitating passage of soft stools, anal sphincteric relaxation, and adequate pain relief and thereby promoting fissure healing.

(a)

Warm water sitz baths promote healing by soothening the area and aid in relaxing the sphincter (Dodi et al. 1986).

 

(b)

High dietary fiber intake as maintenance therapy has shown to decrease recurrence rates (Jensen 1987). Recurrence ranges from 30 to 70 % if the high-fiber diet is abandoned after fissure is healed. This rate is reduced to 15–20 % if patient continues to remain on high-fiber diet. Hence, lifelong dietary modification is recommended.

 


4.8.2.1.1 Chemical Sphincterotomy

The one who progresses to chronicity still responds well to nonoperative management available in the form of local ointments of mainly nitrates and calcium channel blockers defined as chemical sphincterotomy agents. The ideal topical treatment for anal fissure should reduce pain and heal the fissure with minimal recurrence, without impairing the continence, and with low side effects.


4.8.2.1.2 Topical Nitroglycerine

Topical nitroglycerine (local application) is a nitrate donor and a vasodilator. It aids in improving local blood flow. It also reduces internal sphincter muscle spasm by release of nitric oxide from glyceryl trinitrate (GTN) metabolism at cellular level. Nitric oxide acts via guanylate cyclase pathway leading to chemical sphincterotomy (Kennedy et al. 1999) and thereby relieves pain and promotes healing. Nitroglycerine local preparation is available in both 0.2 and 0.4 % concentrations. It is applied two to three times per day with a gloved finger for 8 weeks. It relives pain for 2–6 h. Healing has been reported in 70–80 % patients. Its usage has decreased the recurrence rate by 50 % compared to placebo (Nelson et al. 2012). Dose escalation or specialized dose-delivery device 0.75 ml of 0.3 % GTN ointment (2.25 mg) three times intra-anal application using a cannula or transdermal patch has been shown not to improve the healing rate (Bailey et al. 2002). Headache is the main side effect which limits its use. Other side effects include rebound hypertension, syncope, crescendo angina, and allergic dermatitis.


4.8.2.1.3 Topical Diltiazem (2 %)

Topical diltiazem (2 %), a calcium channel blocker, is applied twice a day for 8 weeks. It acts by blocking the calcium channels in the cells which when stimulated do not contract so much. The anal sphincter relaxes which lowers resting anal pressure and promotes healing. Studies have shown promising results and an overall healing rate of 88 %. In contrast to glyceryl trinitrate ointment, topical diltiazem has very limited adverse drug effects (Knight et al. 2001). These include headache, drowsiness, mood swings, and perianal itching. Oral diltiazem 60 mg was fond to be inferior to topical diltiazem (38 %) with more side effects (Jonas et al. 2001).

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May 14, 2017 | Posted by in GASTOINESTINAL SURGERY | Comments Off on Anal Fissure
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