A Comparison of Conservative Treatment Versus Surgical Methods
Manu G Nariani*, Rajeev Chaturvedi**, Jignesh Jatania**
*Assistant Prof. of General Surgery, Consultant Surgeon; **Resident, Gen. Surgery, Bombay Hospital Institute of Medical Sciences.
INTRODUCTIONAnal fissure is the most common cause of severe anal pain. It is the most common cause of bleeding per anus in infants and young children. The pain of anal ulcer is intolerable and always disproportionate to the severity of the physical lesion. It may be so severe that patients may avoid defaecation for days altogether until it becomes inevitable. This leads to hardening of the stools, which further tear the anoderm during defaecation, setting a vicious cycle.
It occurs as a superficial split in the anoderm, that may heal by itself or may progress to a chronic fissure. The physical lesion extends from distal to the dentate line to the anal verge. A well developed idiopathic anal fissure rests directly over the internal sphincter and the circular fibers of this sphincter are visible on the floor of the fissure on naked eye inspection. The internal sphincter undergoes a perpetual state of spasm due to irritation and hypertrophies. This characteristic can be clinically observed during examination of the anal canal. The lower edge of the internal anal sphincter (IAS) is prominent and so is the inter-sphincteric groove. If these are not present then other causes of anal fissure should be suspected.
Secondary changes develop with persistence of the fissure over time - 1) there may be mild induration of the lateral edges of the fissure, 2) on the proximal end of the fissure, an anal papilla hypertrophies that may become as large as a polyp, 3) there may be a swelling at the distal end of the fissure - a tag like swelling, the so called sentinel pile. It forms due to low grade inflammation and lymphatic oedema. This tag may become acutely inflamed, tense and oedematous, it may undergo fibrosis and persist as a permanent tag even after the anal fissure has healed, or it may develop into a perianal abscess or a low and superficial fistula when the abscess communicates with the anal lumen and has burst open in the perianal skin, 4) a perianal fistula may also develop due to an acute suppuration of the fissure.
Surgical anatomy and pressures in anal canal
The anus functions as a continent mechanism for the GIT. The mechanism consists of the internal and external anal sphincters, the puborectalis, and the levator ani muscles. The puborectalis hooks the anal canal to the pubic bones. Anal canal passes through the pelvic diaphragm, therefore, the process of defaecation has to function in close coordination with the pelvic diaphragm - where the levator ani become important. The sphincter apparatus is organized as two concentric muscular tubes, positioned one enclosing the other. The internal anal sphincter (IAS) is the specialized continuation of the circular layer of the rectum. It also has variable amount of longitudinal muscles on luminal as well as the external aspects. It consists of smooth muscles and is supplied by parasympathetic autonomic nerves. The external anal sphincter (EAS) is skeletal muscle under voluntary control.
The tonic resting state pressure of the IAS is called 'anal resting pressure'. It has been found that this pressure is significantly increased in majority of patients with anal fissure. The IAS pressure has been found to display an overshoot phenomenon in the patients with chronic anal fissure; it overshoots the basal resting pressure after physiologic lowering in response to the rectal dilation with balloons. This signifies the internal sphincteric spasm, so characteristic of this condition. The external anal canal when made to contract maximally under command gives the maximum squeeze pressure. It is an indicator of the continence facility of the anus.
Reasons of predilection of the posterior midline of the anal canal for fissures
The anoderm is more adherent to the underlying tissue in the posterior midline. The sphincter fibers form Y-shaped decussation in the posterior midline that is anchored to the mucosa. A perfusion lower than the rest of the anal canal may be responsible for the persistence of the fissure when there is continued constipation and trauma due to hard stools. Angiographic post-mortem studies by Klosterhalfen et al have revealed that the small branches of both inferior rectal arteries passing through the IAS has no or minimal contact at the posterior midline in 85% of cases. Blood supply to the anoderm at the posterior midline was found to be significantly lower. Maria et al have reported that there was deposition of anti-endothelial cell antibody (AECA) complexes on the intima of the small branches of the rectal arteries in the patients with chronic anal fissure, the event which may further compromise the already marginal blood supply. Intense and prolonged internal sphincter spasm further compromises the blood perfusion of the anoderm, which, at least, is important in keeping the fissure from healing.[4-6]
Note that, the reduced blood supply to the lesion is indicated by the absence of granulation tissue at the base of the fissure and a very slow growth of the anoderm even when the traditional conservative treatment eases the trauma due to hard faeces.
1.Warm Water Sitz bath with boric powder, betadine solution, or potassium permanganate. This treatment soothes the pain and relaxes the spasm of the IAS for some time.
2.Adequate analgesia is necessary to break the vicious cycle of pain - avoidance to defaecation for prolonged periods - hard stools - further tearing of the anoderm - increased pain.
3.Stool softeners; soft and formed stools negotiate the rectum and anal canal in non-traumatic physiologic manoeuvre. Plenty of oral fluids will also help to keep the stools soft.
4.High-fiber-diet and bulk-forming agents such as Isaphgula: Green leafy vegetables fibrous fruits were helpful. Five grams of bran per day has been studied in comparative studies and found useful.
5.Reassurance and encouragement for not resisting the urge for defaecation helps prevent hard stools. Later the patient should be encouraged to acquire and maintain a regular bowel habit of once or twice a day. Application of local anaesthetic cream or gel may help avoid the torture experienced in passage of stools in the patients with acute fissures.
6.Topical creams, gels, ointments. A variety of topical preparations are commercially available. The degree of benefit experienced by individual patient is greatly variable. Xylocaine gel/ointment, allantoin creams, antibiotic creams, and hydrocortisone ointments are only a few of them. Jensen studied the effect of xylocaine ointment and hydrocotisone ointment.
7.Chemical cauterization using silver nitrate or phenol-in-glycerine. This procedure may be repeated a couple of times until healing occurs - till 4 to 8 weeks.
Frequent topical application of 0.2% nitroglycerine paste on the anal canal epithelium has been used to relieve the internal sphincteric spasm. Nitroglycerine release NO, a naturally occurring smooth muscle relaxant. Long-term relaxation of the spasm allows the anoderm time for healing. Prolonged use along with the WASH regimen will allow healing in about two-thirds of the patients.
9.Oral Nifedipine : reversible internal anal sphincterolysis.
Nifedipine is an L-type calcium channel antagonist. L-type calcium channels are the principal calcium channels in the GI smooth muscles. It has been used with variable effects in the management of achalasia cardia. In the treatment of anal fissures 20 mg of Nifedipine is given twice daily. Nifedipine relieves the sphincter spasm. It also increases the local blood supply, by an independent mechanism, to allow faster healing.
10.Botulinum toxin type A : Chemical denervation of internal anal sphincter. Injection of 20 Units of type A botulinum toxin diluted to 50 U/mL into the internal anal sphincter ensures a reduction of the internal anal resting pressure for at least 4 months. This allows the fissure time for healing. The toxin exerts its effects on the acetylcholine releasing parasympathetic peripheral nerve endings as well as the ganglionic nerve endings, thereby leading to flaccid paralysis of the internal sphincter.
1.Anal dilation was described by Recamier in 1838. It has undergone several variations and modifications. It is performed under general anaesthesia or local anaesthesia. A gradual insertion and dilation to four to eight fingers lubricated with paraffin, lignocaine jelly, or K-Y jelly achieves reduction of internal sphincteric pressure.
2.Fissurectomy involves excision of the fissure from the anal canal. The wound is left open without suturing.
The internal sphincter is divided completely in its lower part from the dentate line to the lower margin. The objective of the procedure is to relieve the pressure in the anal canal; the part of the sphincter above the dentate line is left intact. It should be noted that the spasm of the internal sphincter is taken as the key pathogenetic mechanism in the initiation and at least maintaining the fissure.[15-18] There are various approaches to the internal sphincterology; (a) Posterior midline, anterior, or lateral sphincterotomy - based on the site of division of the sphincter, (b) open or closed sphincterotomy - based on whether anoderm is incised or not during the procedure, (c) submucosal or the inter-sphincteric approaches.
4.Carbon dioxide laser surgery involves laser vaporization of the fissure locally. The internal sphincter can be incised using this laser. In long-standing fissures anal stenosis is present. It can be used to give relieving incisions in the three quadrants other than the fissure before the fissure is attended. Cryo-analgesia with liquid nitrogen is given to all wounds distal to the anorectal line.
Comparative criticism of various methods of treatment of anal fissures
A 'W-A-S-H' was a popular non-surgical treatment, which used Warm water Sitz baths + Analgesics + Stool softeners + High fiber diet. It has been used as treatment regimen itself and along with the other conservative approaches as well as a pretreatment for the surgical methods. It serves good as either of them. As a regimen by itself it is effective in easing the discomfort by hot fomentation. It also relieves the spasm of the sphincter for a short period of time. About one third to one half of the patients show healing. In these patients the fissure may not recur if the high-fiber diet is continued and a regular bowel habit is observed by the patient. It is a successful measure only in acute fissures: though the regimen definitely makes the life easier even for those with chronic fissure.
Nitroglycerine offers a good non-surgical alternative. Success with this mode of therapy depends upon prolonged use and support with the W-A-S-H regimen. It takes about 4-6 weeks of use for healing, though some patients may require therapy for as long as 8 weeks. Success rate are of the order of 60%. Non-compliance may lead to failure to heal or recurrences. Headaches may occur in the users, which may be severe enough in some patients that it may necessitate discontinuation of the medication. The second problem with nitroglycerine topical treatment is that some patients experience tachyphylaxis, wherein increasing concentrations of the paste are required to maintain the desired effect on the internal anal sphincter. A regimen of weekly escalating dose starting from 0.2%, increasing each week by 0.1% to 0.6% has been documented as resulting in a more rapid healing. However, when the treatment is stopped there is a high rate of relapse.
Oral Nifedipine offers a convenient regimen along with a non-surgical alternative. The healing is good as Nifedipine enhances the local blood supply, by dilatation of vascular smooth muscles, in addition to production of spasmolysis. The principal side-effect of oral Nifedipine is flushing of the face and limbs. This is usually a short-lived phenomenon, lasting for less than an hour of intake of the medication. It usually wanes with continued use. A small number of patients experience mild headaches. These patients responded to simple analgesics. It has been advised that Nifedipine should be avoided in patients who have a history of severe headaches. Nifedipine has little effect on the skeletal muscles and there was no difference in maximum squeeze pressure, which is a function of the external sphincter. Therefore, incontinence does not occur with its use for anal fissures. Interestingly, Nifedipine has been used to treat severe anal pain associated with hypertension to a good effect. One may contemplate a judicious selective use of Nifedipine therapy for patients who have anal fissure and have concurrent hypertension.
Botulinum toxin injections are a good alternative to surgery. These can be given as a clinic procedure. Anaesthesia or bowel preparation is not required. In one study that used saline injections in internal sphincter as control medication, seventy-four to seventy-six per cent patients treated with botulinum toxin showed complete healing of the fissure and symptomatic relief. Those who showed little benefit were later given a second trial with the toxin. The total cure rates with two injections reached almost 90%. A second study with botulinum toxin compared two doses of the toxin for therapy of anal fissure. It found that an injection of 20 Unit of the toxin in the internal anal sphincter is sufficient for one injection trial. A third study compared patient the effect of the site of injection on the internal sphincter. It revealed that the patients who had received injections in the posterior midline or near the posterior midline showed healing less frequently as compared to those who received the injections near the anterior midline. The authors proposed that greater degree of fibrosis in the posterior sites of internal sphincter in patients with anal fissure leads to a restriction of diffusion of the toxin in the internal sphincter muscles, when injected in or near the posterior midline and this led to failure of the parasympathetic denervation of internal sphincter. When accidentally made into the external anal sphincter or the surrounding tissue, has been reported to cause perianal thrombosis.
Fissurectomy, by itself, is an incomplete treatment as the anoderm heals very slowly and the factor initiating and/or aggravating the problem - the internal sphincter spasm - is not tackled. When combined with anal dilatation or sphincterotomy, it may make the procedures more effective.
Sphincterotomy is a very effective procedure. Posterior sphincterotomy is slow to heal and has a tendency to lead to a posterior midline keyhole defect that may cause a persistent seepage or difficulty in continence. It is generally considered an outdated procedure; but it still has its place in selective cases with a posterior midline fissure complicated by a posterior midline fistula and perhaps when a stenotic canal is being repaired with a posteriorly based advancement flap.
The sphincteric mechanism is most weak in the anterior portion, therefore, anterior sphincterotomy should be avoided.
Lateral sphincteromy, especially after the standardization of the closed method, has been chosen by many surgeons. The reasons for this favour are the simplicity of the procedure, minimal anaesthesia requirements, and good results. It takes only 3 to 4 weeks for healing (as compared to 7 to 8 weeks required by posterior sphincterotomy). The success of the procedure depends upon (1) cutting the complete thickness of the internal sphincter in the lower part from dentate line to the lower border of the muscles, and (2) avoiding even a small violation of the integrity of the anoderm and mucosa. If mucosa is punctured, one should convert the procedure to an open internal sphincterotomy. If the above stated simple guidelines are religiously adhered to the recurrence and complication rates of sphincterotomy for primary anal fissures are very low.
The list of complications that can arise due to procedure is formidable; but with careful and experienced hands the procedure is safe and simple. Ecchymosis of the anal canal and perianal skin is the most common complication, it can be quite extensive in the closed technique and Sitz baths are enough for its management; haemorrhage is a rare complication as the bleeding is tamponaded. In open procedure haemorrhage can be managed by careful suturing of the edges of the mucosa. Perianal abscess is associated with only 1% of the closed sphincterotomies; there are always associated with anal fistula and presumed to occur as a result of inadvertent penetration of mucosa by the knife. Recurrence and failure to heal occur in less than 5% cases. If conservative therapy does not help repeat sphincterotomy can be undertaken. Incontinence occurs due to violation of the external sphincter fibers or due to a keyhole deformity due to posterior fissurectomy or posterior midline open sphincterotomy.
Anal dilation has been questioned in relation to its effectiveness, recurrence, and incontinence as a complication. It has been said that the four (2+2) finger stretch method produces an uncontrolled fracturing of the internal sphincter. It has also been claimed that even though it may give an initial relief to the patient, approximately 40% of the patients develop recurrence and a significant proportion on those treated had incontinence of stools or flatus.[24-26]
In our clinic, we advise 'W-A-S-H' therapy for several days before the procedure is undertaken, until the patient decides to undergo the procedure. Anal dilation is performed manually under general anaesthesia and skeletal muscle relaxation or with liberal local anaesthesia using about 20 to 25 mL mixture in equal proportions of 2% Xylocaine and Sensorcaine. The W-A-S-H is continued after discharge from the hospital till the patient becomes asymptomatic. High fiber diet and maintenance of regular bowel habit in order to avoid constipation and hard stools is continued for life long. Antibiotics are prescribed for a few days in the post-operative period. With our own experience of treating anal fissures, we feel that it is the technique of the procedure of anal dilation that determines the success of the anal dilatation for allowing healing of the anal fissure and avoidance of incontinence as a complication. When performed under adequate local anaesthesia or general anaesthesia and skeletal muscle relaxation, gradual dilation up to six (3+3) fingers with gentle circular manoeuvring of the inserted fingers achieves the desired effect. It does not cause any damage to the external anal sphincter (skeletal muscle) and, thus incontinence of stools or flatus are seldom seen. Incontinence after anal dilatation is usually due to stretching of the external sphincter and puborectalis muscle. Some of the patients complained of temporary inability to control bowel movements during the period when skeletal muscle relaxant medication was still acting. All patients resumed bowel and flatus control within 24 hours after the procedure. None of our patients showed recurrence of anal fissure in a one year follow-up. In support of our findings, we found the experiences of Weaver et al who found that manual dilatation of anus had no significant differences in outcomes than the internal sphincterotomy. Crapp and Alexander Williams had described anal dilatation as the procedure of choice for anal fissures.
In our view gentle manual dilatation can be offered to all patients of chronic primary anal fissure or first recurrence after any conservative mode of treatment. The procedure is simple involves no incision or suturing, and, in our experience, has been very effective in achieving its objective. The patient can be discharged one day after the procedure Fissurectomy may be added to treatment for chronic fissure, especially in the cases that require excision of the sentinel pile.
Thus we feel that conservative treatment with nitroglycerine, botulin toxin, and oral Nifedipine are all effective methods that may reduce the need for anaesthesia and surgery in most of the patients. These can be offered to the patients who do not have fitness for anaesthesia. The options should be presented to the patient with complete information about the method, cure rates, complications, and reversibility of the complications and the final choice should be left in their hands. But selection of patients with regard to the adverse effect susceptibility profile and wishes of patient are crucial. Surgery has been carried for primary anal fissures since very long time, we have seen complications and understood the reasons for them in detail. These complications usually occur with inexperienced or reckless hands. Besides, surgery comes as one step treatment option with certain cure rates in careful and experienced approach.
This article is dedicated to the memory of Dr. RK Menda.
1.Morgan, Thompson. Surgical anatomy of the anal canal with special reference to the surgical importance of the internal sphincter and conjoint longitudinal muscles. Ann Roy Coll Surg 1965; 19 : 88.
2.Klosterhalfen B, Vogel P, et al. Typography of the inferior rectal artery: a possible cause of chronic primary fissure. Dis Colon Rectum 1989; 32 : 43-52.
3.Maria G, Brissinda D, et al. Identification of anti-endothelial cell antibodies (EACA) in patients with chronic anal fissures. Surgery 1999; 126 : 535-40.
4.Schouten WR, Briel JW, et al. Relationship between anal pressure and anodermal blood flow : the vascular pathogenesis of anal fissure. Dis Colon Rectum 1994; 37 : 664-9.
5.Abcarian H, Lakshmanan S, et al. The role of internal anal sphincter in chronic anal fissures. Dis Colon Rectum 1982; 25 : 525-8.
6.Gibbons CP, Read NW. Anal hypertonia in fissures : Cause or effect? Br J Surg 1986; 58 : 96.
7.Jensen SL. Diet and other risk factors for fissure-in-ano. Dis Colon Rectum 1988; 31 :770-3.
8.Jensen SL. Treatment of first episode of acute anal fissure - a prospective, randomized study of lignocaine ointment vs hydrocortisone ointment vs warm Sitz bath plus bran. Br Med J 1986; 292 : 1167.
9.Loder PB, Kamm MA, Nicholas RJ, Phillips RKS. Reversible chemical sphincterotomy by local application of glyceryl trinitrate. Br J Surg 1994; 81 : 1386-9.
10.Lund JN, Scholefield JH. A prospective, randomized double-blind placebo controlled trial of glyceryl trinitrate in anal fissure. Lancet 1997; 349 : 11-4.
11.Cook TA, Smilgin Humphreys MM, et al. Oral Nifedipine reduces resting anal pressure and heals chronic anal fissures. Br J Surg 1999; 86 : 1269-73.
12.Maria G, Casetta E, et al. A comparison of botulinum toxin and saline injection for treatment of chronic anal fissure. N Engl J Med 1998; 338 : 217-20.
13.Watts JM, Goligher JC, et al. Stretching of the treatment of fissure-in-ano. Br Med J 1965; 2 : 342.
14.Lund JN, Scholefield JH. A prospective, randomized double-blind placebo controlled trial of glyceryl trinitrate in anal fissure. Lancet 1997; 349 : 11-4.
15.Eisenhammer S. Surgical correction of chronic internal anal sphincter contracture. S Afr Med J 1951; 25 : 486.
16.Bell GA. Laternal internal sphincterotomy in Chronic anal fissure - a surgical technique. Am Surg 1980; 46 : 572-5.
17.Chowcat NL, et al. Internal sphincteromy for Chronic anal fissure : long-term effects on anal pressure. Br J Surg 1986; 73 : 915.
18.Notaras MJ. The treatment of anal fissure by lateral subcutaneous internal sphincterotomy : technique and results. Br J Surg 1971; 58 : 96.
19.Maria G, Casetta E, et al. A comparison of botulinum toxin and saline injection for treatment of chronic anal fissure. N Engl J Med 1998; 338 : 217-20.
20.Maria G, Brisinda G, et al. Botulinum injections in the internal anal sphincter for treatment of chronic anal fissures. Long-term results after two different dose regimens. Ann Surg 1998; 228 : 664-9.
21.Maria G, Brisinda G, et al. Influence of botulinum toxin site of injection on healing rate in patients with chronic anal fissure. Am J Surg 2000; 79 : 46-50.
22.Jost WH, Schanne S, Mlitz H, Schimrift K. Perianal thrombosis following injection therapy into the external anal sphincter using botulinum toxin. Dis Colon Rectum 1995; 38 : 781 (letter).
23.Ferrari BT, Ray JE, Cathright JB (Ed). Complications of colon and rectal surgery. WB Saunders, 1985; 98-100.
24.McDonald P, Driscoll AM, et al. Anal dilation in the conservative management of acute anal fissure. Br J Surg 1983; 70 : 25.
25.Shub HA, et al. Complications of anal dilatation for acute anal fissure. Dis Colon Rectum 1989; 32 : 545.
26.Guttman H, et al. Complications of anal dilatation for acute anal fissure. Dis Colon Rectum 1989; 32 : 545.
27.Weaver et al. Manual dilation of the anus vs lateral subcutaneous sphincterotomy in treatment of chronic fissure-in-ano : results of a prospective randomized clinical trial. Dis Colon Rectum 1987; 30 : 420-3.
28.Crapp AR, Alexander-William J. Fissure-in-ano and anal canal stenosis. Part I : Conservative treatment. Clin Gastroenterol 1975; 4 : 619-28.