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5.7.3 Oral Medication
Flavonoids and their related compounds (e.g., diosmin, hesperidin, and rutin) are the most common ora l venotonic agents used for treating hemorrhoids. They are plant che­micals found mainly in citrus fruits and Ginkgo biloba leaves. They were first described in the treatment of chronic venous insufficiency and edema. In hemorrhoids, flavonoids appeared to relieve symptoms by increasing venous tone, reducing venous capacity, decreasing capillary permeability, facilitatin g lymphatic drainage, and having mild anti­inflammatory effects.
A metaanalysis of 24 randomized controlled trails including more than 2000 patients with hemorrhoids demonstrated that oral flavonoids had beneficial effects on relieving the symptoms of internal hemorrhoids such as bleeding, pruritus, discharge, and leakage, as well as significantly improving the overall symptoms of hemorrhoids. Moreover, post­operative administration of oral flavonoids was associated with a reduction in bleeding, pain, and analgesic consumption after hemorrhoidectomy.
17
Oral flavonoids were given at
1.5–2g/day for 1–2 weeks for treating the acute symptoms of hemorrhoids. A combination of oral flavonoids and fiber supplement ceased bleeding from nonprolapsing internal hemorrhoids quicker than fiber suppl ement alone.
18
However, the role of oral flavonoids for preventing recurrent hemorrhoids is not fully clarified. A small randomized controlled trail in France showed that the administration of micronized purified flavonoid fraction at 1 g/day for 2 months could reduce chronic symp­toms of hemorrhoids from 70% to 40% and decrease the duration of symptomatic epi­sodes from 4.6 to 2.6 days.
19
An open-label study from India showed that perinatal administration (8 weeks before delivery to 4 weeks after deliver y) of combined oral flavo­noids in pregnant individuals with symptomatic hemorrhoids minimized a relapse in acute hemorrhoidal attack in the antenatal period by 54% without any adverse effect on pregnancy and infant.
20
Oral calcium dobes ilate is another drug commonly used in the treatment of acute symptoms of hemorrhoids. This synthetic compound appeared to reduce capillary per­meability, improve lymphatic drainage, inhibit platelet aggregation and thro mbus forma­tion, lower blood hyperviscosity, and increase red cell flexibility thus reducing the swelling of hemorrhoids.
21
Oral calcium dobesilate was given at 1g/day for 1 week and maintained at 0.5 g/day for 5weeks for treating acute hemorrhoid symptoms. However, it is evident that oral calcium dobesilate might be associated with agranulocytosis—a rare idiosyn­cratic (type B) adverse drug reaction.
22
For traditional or herbal medicine, there is no strong evidence concerning the safety and effectiveness of such agents for treating symp­tomatic hemorrhoids.
23
5.7.4 Sclerotherapy
Sclerotherapy involves the injection of a sclerosing agents (e.g., 1%–2% ethoxy-sclerol solution or 2%–5% phenol solution) into the anal submucosa around the pedicles of hem­orrhoids—but not into the hemorrhoids themselves, otherwise it may cause immediate
Chapter 5 • Hemorrhoidal Disease 57
transient precordial and upper abdominal pain.24Sclerotherapy shrinks the vascular channels within hemorrhoid plexus and creates a fixing scar in the anal submucosa (
Fig. 5.3). It is an effective nonsurgical treatment for low-grade hemorrhoids. It is generally
carried out as an ambulatory procedure without any anesthesia, and can be repeated as needed every 2–4 weeks until the lesion disappears.
1
The volume of sclerosing solution
used in each lesion varies between 1 and 3mL.
The proper injection of the solution is crucial because an inappropriate inject ion would lead to serious complications including anal sepsis, anal stricture, or anal fistula (if the sclerosing solution is infiltrated into the muscular wall of the anal canal). Transient bacteremia was reported in 8% of patients after sclerotherapy.
25
As a result, immunocom­promised patients and individuals with valvular heart disease should be given intravenous prophylactic antibiotics within 1 h before stating the procedure.
5.7.5 Rubber Band Ligation
Rubber band ligation is arguably the most common office-based intervention for patients with internal hemorrhoids. A rubber band is applied to the pedicle (base) of the hemor­rhoids, using a suction ligator or conventional Barron ligato r, the blood supply to the hem­orrhoids is reduced causing them to shrink or atrophy (
Fig. 5.4). The rubber band will
spontaneously dislodge within 1–2 weeks as the hemorrhoids disappear. However, sec­ondary anorectal bleeding may occur after the dislodgement of a rubber band—mainly due to insufficient hemostasis. Therefore this intervention is contraindicated in patients with a bleeding disorder and those taking antiplatelet drugs or anticoagulants.
1
This procedure can be safely and effectively performed without anesthesia via an ano­scopy or during the retroflex view of flexible endoscopy. Complications after banding included thrombosed hemorrhoids, severe pain, dysuria, and urinary retention requiring catheterization. There were reports of pelvic sepsis after rubber band ligation in an immu­nocompromised patient. As a result, many physicians avoid performing this procedure in immunocompromised individuals or those with concurrent anorectal infection. Mild pain after rubber band ligation is relatively common and can be treated with oral analgesia, warm sitz baths, and avoidance of hard stools by taking mild laxatives or bulk-forming
FIG. 5.3 Sclerotherapy.
58 ANORECTAL DISORDERS
agents. Several hemorrhoids can be ligated in one session but the risks of postprocedural pain and bleeding may increase. For that reason, some physicians prefer multiple ligation sessions (serial session) every 3–4weeks until the hemorrhoids disappear.
11
A metaanalysis of 18 clinical trials compared short-term outcomes of various interven­tions for symptomatic hemorrhoids including rubber band ligation, sclerotherapy, and conventional hemorrhoidectomy.
26
It showed that rubber band ligation had a lower inci­dence of recurrent symptoms and need of retreatment than sclerot herapy, but it had a higher incidence of postprocedural pain. In order to minimize pain after banding, physi­cians should avoid placing the rubber band too close to the dentate line. In fact, the proper position of banding is at the pedicle of hemorrhoids or over the bleeding site. Although this metaanalysis demonstrated that rubber band ligation had inferior outcomes to hemorrhoidectomy for treating grade III prolapsing hemorrhoids, the authors advocated rubber band ligation as a first-line treatment for such lesions because of its safety, simplic­ity, and no requirement of hospitalization.
A recent multicenter randomized trial comparing the effectiveness of rubber band liga­tion vs. Doppler-guided hemorrhoidal arterial ligation for grade II–III hemorrhoids showed that the surgical arterial ligation had lower recurrence but was more painful than rubber band ligation.
27
Comparing the costs and the clinical outcomes between these two
methods, rubber band ligation appears to be more cost-effective and could be a preferable
FIG. 5.4 Rubber band ligation.
Chapter 5 • Hemorrhoidal Disease 59
choice for treating grade II–III hemorrhoids.28In daily practice, a single lesion of a grade III internal hemorrhoid responds well to rubber band ligation, but several lesions or com­bined hemorrhoids may require surgical interventions such as excisional hemorrhoidect­omy, hemorrhoidal plication, Doppler-guided hemorrhoidal arterial ligation, or stapled hemorrhoidopexy.
11
5.7.6 Other Office-Based Procedures
These procedures include cryotherapy, infrared coagulation, radiofrequency ablation, and laser treatment. Cryotherapy involves the direct application of liquid nitrogen or a cryo­probe onto internal hemorrhoids causing tissue freezing and destruction. Although it was claimed to have less postprocedural pain because cold temperature may decrease in sensory impulses and muscle spasm, several studies showed that prolonged pain, foul­smelling discharge from tissue necrosis, and persistent lesions were frequently seen after cryotherapy.
1
As a result, cryotherapy has fallen out of favor as an outpatient treatment of
uncomplicated hemorrhoids.
Infrared coagulator uses infrared radiation to coagulate tissue and vaporize water in the cell thereby causing the shrinkage of hemorrhoids. The necrotic tissue is dry and seen as a white spot—which eventually heals with fibrosis. Compared with sclerotherapy, infra­red coagulation is less technique-dependent and avoids the potential complications of misplaced scle rosing injection. Infrared coagulation is another simple and effective office-based procedure for low-grade internal hemorrhoids.
1
Radiofrequency ablation and laser therapy are relatively new modalities for treating low-grade or uncomplicated hemorrhoids. An electrode connected to a radiofrequency generator or a laser system is placed into hemorrhoid bundle and causes the contacting tissue to be coagulated and vaporized. Hence, the hemorrhoid venous plexus is reduced and fixed to the underlying tissue by subsequent fibrosis.
1
Both radiofrequency ablation and laser therapy for hemorrhoids may be performed on an outpatient basis with or with­out anesthesia. They appear to be effective for treating internal hemorrhoids with limited mucosal prolapse,
29,30
but special instruments or set-up units are required. More studies especially of the long-term outcomes are warranted before making these novel interven­tions as viable office-based treatment options for hemorrhoids.
5.8 Management of Hemorrhoids in Specific Considerations
5.8.1 Hemorrhoids in Patients Taking Anticoagulants or Antiplatelet Drugs
Anticoagulants or antiplatelet drugs may promote or prolong anal bleeding in patients with internal hemorrhoids and increase the risk of postprocedural or postsurgical bleed­ing. Although bleeding episodes may be mild and self-limited, whether or not the discon­tinuity of such drugs is required depends on the indications of the drugs used, the severity
60 ANORECTAL DISORDERS
of bleeding, and the patient’s hemodynamic status. Sclerotherapy is a preferential proce­dure for bleeding low-grade hemorrhoids refractory to conser vative management. Rubber band ligation is contraindicated in patients taking anticoagulant or antiplatelet drugs due to the risk of secondary bleeding. If rubber band banding or any surgical intervention is scheduled, the cessation of anticoagulants or antiplatelet drugs 5–7 days before and after the procedure is recommended.
5,11
5.8.2 Hemorrhoids in Pregnancy
Hemorrhoids and their symptoms are highly prevalent during pregnancy, especiall y in the third trimester.
31
Since most lesion s or their symptoms will resolve spontaneously after giving birth, the key principle of treatment is to relieve the acute hemorrhoidal symptoms by means of conservative management as previously mentioned. Lying down on the left side may reduce the congestion of the hemorrhoid venous plexus. Avoidance of constipa­tion cou ld minimize the episodes and the severity of bleeding and prolapse. Increased liquid and dietary fiber, topical medication, and a mild laxative are generally safe for preg­nant or breastfeeding women. However, there are a very limited number of studies exam­ining the safety and effectiveness of oral venotonic drugs or other office -based procedures in pregnant women with internal hemorrhoids.
20
In the case of massive bleeding, anal packing could be a simpl e and useful maneuver. Surgical intervention is reserved for strangulated or extensively thrombosed hem orrhoids.
11
5.8.3 Hemorrhoids in Immunocompromised Patients
In general any intervention or operation should be avoided due to a higher risk of anor­ectal sepsis and delayed wound healing in immunocompromised patients.
32
The main­stay for treating symptomatic hemorrhoids in this group of patients is a conservative approach (pharmacological treatment plus dietary and lifestyle modification).
5,11
If needed, sclerotherapy appears to be better and safer than rubber band ligation and sur­gical interventions for bleeding hemorrhoids. The administration of intravenous prophy­lactic antibiotics are advised before performing any intervention due to the possibil ity of bacteremia in immunodeficiency hosts. Individuals achieving good control of HIV viral replication and maintaining high CD4 counts may have an uneventful surgery for high­grade hemorrhoids.
5.8.4 Hemorrhoids in Patients With Crohn’s Disease
Hemorrhoids should be distinguished from Crohn’s disease-associated anal skin tags, which are often large, edematous, tender, and cyanotic as they arise from lymphedema secondary to lymphatic obstruction.
33
However, these two lesions may occur simulta­neously. For patients with Crohn’s disease and active anorectal inflammation, conserva­tive measures are the first-line treatment for hemorrhoids. Aggressive interventions or surgery should be avoided until the disease is in the quiescent state.
Chapter 5 • Hemorrhoidal Disease 61
5.8.5 Hemorrhoids in Patients With Cirrhosis or Portal Hypertension
Internal hemorrho ids must be differentiated from anorectal varices, which are markedly dilated collateral submucosal veins originating above the anal verge. Conservative treat­ment is a preferential approach to bleeding hemorrhoids in such patients, which includes the administration of topical medication and oral flavonoids, as well as the correction of anemia and coagulopathy. If this fails sclerotherapy should be considered. It is worth not­ing that rubber band ligation is contraindicated due to a high risk of profound secondary bleeding. In a refractory case, suture ligation at the bleeder is advised. Hemorrhoidectomy is indicated when bleeding hemorrhoids are refractory to other approaches.
11
References
1.
Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol. 2012;18:2009–2017.
2. Johanson JF, Sonnenberg A. The prevalence of hemorrhoids and chronic constipation. An epidemio-
logic study. Gastroenterology. 1990;98:380–386.
3. Acheson RM. Haemorrhoids in the adult male; a small epidemiological study. Guys Hosp Rep.
1960;109:184–195.
4. Riss S, Weiser FA, Schwameis K, et al. The prevalence of hemorrhoids in adults. Int J Colorectal Dis.
2012;27:215–220.
5. Lohsiriwat V. Approach to hemorrhoids. Curr Gastroenterol Rep. 2013;15:332.
6. Serra R, Gallelli L, Grande R, et al. Hemorrhoids and matrix metalloproteinases: a multicenter study on
the predictive role of biomarkers. Surgery. 2016;159:487–494.
7. Nasseri YY, Krott E, Van Groningen KM, et al. Abnormalities in collagen composition may contribute to
the pathogenesis of hemorrhoids: morphometric analysis. Tech Coloproctol. 2015;19:83–87.
8. Aigner F, Gruber H, Conrad F, et al. Revised morphology and hemodynamics of the anorectal vascular
plexus: impact on the course of hemorrhoidal disease. Int J Colorectal Dis. 2009;24:105–113.
9. Lohsiriwat V, Scholefield JH, Wilson VG, Dashwood MR. Endothelin-1 and its receptors on haemor-
rhoidal tissue: a potential site for therapeutic intervention. Br J Pharmacol. 2017;174:569–579.
10. Han W, Wang ZJ, Zhao B, et al. Pathologic change of elastic fibers with difference of microvessel density
and expression of angiogenesis-related proteins in internal hemorrhoid tissues. Zhonghua Wei Chang Wai Ke Za Zhi. 2005;8:56–59.
11. Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist’s view. World J Gastroenterol. 2015;21:
9245–9252.
12. Lohsiriwat V. Anorectal emergencies. World J Gastroenterol. 2016;22:5867–5878.
13. Alonso-Coello P, Mills E, Heels-Ansdell D, et al. Fiber for the treatment of hemorrhoids complications:
a systematic review and meta-analysis. Am J Gastroenterol. 2006;101:181–188.
14. Lohsiriwat D, Lohsiriwat V. Outpatient hemorrhoidectomy under perianal anesthetics infiltration.
J Med Assoc Thai. 2005;88:1821–1824.
15. Huang YJ, Chen CY, Chen RJ, Kang YN, Wei PL. Topical diltiazem ointment in post-hemorrhoidectomy
pain relief: a meta-analysis of randomized controlled trials. Asian J Surg. 2018;41:431–437.
16. Sammour
T, Barazanchi
AW, Hill AG, Group P. Evidence-based management of pain after excisional
haemorrhoidectomy surgery: a PROSPECT review update. World J Surg. 2017;41:603–614.
62 ANORECTAL DISORDERS
17. Perera N, Liolitsa D, Iype S, et al. Phlebotonics for haemorrhoids. Cochrane Database Syst Rev. 2012;
CD004322.
18. Ho YH, Tan M, Seow-Choen F. Micronized purified flavonidic fraction compared favorably with rubber
band ligation and fiber alone in the management of bleeding hemorrhoids: randomized controlled trial. Dis Colon Rectum. 2000;43:66–69.
19. Godeberge P. Daflon 500 mg in the treatment of hemorrhoidal disease: a demonstrated efficacy in
comparison with placebo. Angiology. 1994;45:574–578.
20. Buckshee K, Takkar D, Aggarwal N. Micronized flavonoid therapy in internal hemorrhoids of preg-
nancy. Int J Gynaecol Obstet. 1997;57:145–151.
21. Arceo A, Berber A, Trevino C. Clinical evaluation of the efficacy and safety of calcium dobesilate in
patients with chronic venous insufficiency of the lower limbs. Angiology. 2002;53:539–544.
22. Ibanez L, Ballarin E, Vidal X, Laporte JR. Agranulocytosis associated with calcium dobesilate clinical
course and risk estimation with the case-control and the case-population approaches. Eur J Clin Phar- macol. 2000;56:763–767.
23. Gan T, Liu YD, Wang Y, Yang J. Traditional Chinese medicine herbs for stopping bleeding from hae-
morrhoids. Cochrane Database Syst Rev. 2010;CD006791.
24. Mann CV, Motson R, Clifton M. The immediate response to injection therapy for first-degree haemor-
rhoids. J R Soc Med. 1988;81:146 – 148.
25. Adami B, Eckardt VF, Suermann RB, Karbach U, Ewe K. Bacteremia after proctoscopy and hemor-
rhoidal injection sclerotherapy. Dis Colon Rectum. 1981;24:373–374.
26. MacRae HM, McLeod RS. Comparison of hemorrhoidal treatments: a meta-analysis. Can J Surg.
1997;40:14–17.
27. Brown SR, Tiernan JP, Watson AJM, et al. Haemorrhoidal artery ligation versus rubber band ligation for
the management of symptomatic second-degree and third-degree haemorrhoids (HubBLe): a multi­centre, open-label, randomised controlled trial. Lancet. 2016;388:356–364.
28. Brown S, Tiernan J, Biggs K, et al. The HubBLe trial: haemorrhoidal artery ligation (HAL) versus rubber
band ligation (RBL) for symptomatic second- and third-degree haemorrhoids: a multicentre rando­mised controlled trial and health-economic evaluation. Health Technol Assess. 2016;20:1–150.
29. Giamundo P, Salfi R, Geraci M, Tibaldi L, Murru L, Valente M. The hemorrhoid laser procedure tech-
nique vs rubber band ligation: a randomized trial comparing 2 mini-invasive treatments for second­and third-degree hemorrhoids. Dis Colon Rectum. 2011;54:693–698.
30. Gupta PJ. Ambulatory hemorrhoid therapy with radiofrequency coagulation. Clinical practice paper.
Rom J Gastroenterol. 2005;14:37–41.
31. Staroselsky A, Nava-Ocampo AA, Vohra S, Koren G. Hemorrhoids in pregnancy. Can Fam Physician.
2008;54:189–190.
32. Morandi E, M
erlini D, Salvaggio A, Foschi D, Trabucchi E. Prospective study of healing time after hemorrhoidectomy: influence of HIV infection, acquired immunodeficiency syndrome, and anal wound infection. Dis Colon Rectum. 1999;42:1140–1144.
33. Bonheur JL, Braunstein J, Korelitz BI, Panagopoulos G. Anal skin tags in inflammatory bowel disease:
new observations and a clinical review. Inflamm Bowel Dis. 2008;14:1236–1239.
Chapter 5 • Hemorrhoidal Disease 63
6
Anal Fissure
Richelle J.F. Felt-Bersma
*,†, Ingrid J.M. Han-Geurts
†
* A M S T E R D A M U M C, A M S TE R D A M , T H E NE T H E R L A ND S†PR O C T O S C L I N IC , B I L T H O V E N,
TH E N E T H E R L A N DS
6.1 Definition
An anal fissure is a linear or oval-shaped tear or ulceration in the anal canal extending from the anal verge to the dentate line (
Fig. 6.1). It was first described in 1934 by
Lockhart-Mummery.
1
Anal fissures can be acute or chronic. A fissure is defined as chronic when it remains symptomatic for more than 6–8 weeks; when there is involvement of the submucosa or the internal anal sphincter (IAS), sometimes accompanied by a sentinel peri-anal skin tag and a hypertrophied papilla; or in cases of recurrent episodes (
Fig. 6.2).
6.2 Etiology/Pathophysiology
The etiology of anal fissures is not entirely clear and has multiple pathogenic factors. Cen­tral to the pathogenesis is trauma to the anal canal. The initial event is often the passage of a hard and/or bulky stool and severe diarrhea with local irritation resulting in a tear in the anoderm. Other less frequent causes are post anorectal surgery, childbirth, and anorecep­tive intercourse.
As a response to the fissure and pain the anal pressure increases. Several studies have
demonstrated increased IAS pressure compared to controls.
2,3
In addition, many patients demonstrate secondary dyssynergia due to the anal pain and are at risk of developing chronic pelvic pain.
4
The increased anal sphincter pressure impairs the blood flow and
subsequently wound healing.
An epidemiological study in the United States showed 0.7 to 1.7 cases per 1000 person­years depending on age (in Ontario, Canada the incidence was 0.75). The overall incidence of 1.1 per 1000 person-years translates to an average life time risk of 7.8%, and thus an anal fissure is indeed a common problem.
5
Fissures are equa lly present in men and women typically at 40 years, although young people and children may also be affected. In 75% of cases the fissures are located in the posterior midline and anteriorly in 25%, and they are more frequent in women after childbirth. Postpartum fissures are related to the per­ineal dynamic changes, ruptures hormonal levels, and dyssynergia.
6
Less than 1% of all fissures are located of the midline and are considered atypical fissures. The etiology of these fissures includes Crohn’s disease, ulcerative colitis, anal cancer, human immunode­ficiency virus (HIV), syphilis, herpes, tuberculosis, and leukemia.
Anorectal Disorders.
https://doi.org/10.1016/B978-0-12-815346-8.00006-0
© 2019 Elsevier Inc. All rights reserved.
65
The reason for the preferential location of the anal fissure posteriorly has several the­ories. One theory is the relatively lower support of the dorsal external sphincter due to its epileptical shape. Furthermore, the relative ischemia of the posterior commissure might be caused by the anatomically lower blood flow, which deteriorates when there is high anal pressure.
7,8
The pa thogenesis in nonclassical fissures without a high pressure is
not so clear but may be related to poor vascularization, scarring, or inflammation.
6.3 Symptoms and Diagnosis
Pain is present in almost all patients. The pain is sharp, increases during defecation, and may be present for minutes to hours. Some patients develop a painful sentinel pine and
FIG. 6.2 Chronic anal fissure in a patient. The deep fissure (F) is visible between the arrows.
FIG. 6.1 Schematic drawing of an anal fissure. IAS, internal anal sphincter; EAS, external anal sphincter.
66 ANORECTAL DISORDERS
believe that this is the cause of the pain. A trace of bright-red blood on the toilet paper or streaking the surface of the stool is seen in more than 70% of patients.
The diagnosis is easy and can be made by the patient’s medical history and physical examination. Inspection of the anus by careful spreading the buttocks and asking the patients to strain makes the fissure visible. Sometimes it is so painful that the even this is impossible. Digit al palpation can be too painful and is not always necessary at first, although with careful patient instruction this is often possible or should be at tempted at the next visit. Besides the anal fissure, dyssynergia can also be diagnosed. A proctoscopy definitely should be avoided at this point. If there is doubt about the diag­nosis at the start or during the course of treatment, further examination needs to be per­formed with conscious sedation. A differential diagnosis includes other benign (hemorrhoids, rectal intussusception, or prolapse) or malignant anorectal disorders (anorectal or colon cancer).
6.4 Additional Investigations
Unless another diagnosis is suspected, besides clinical examination, no testing is required. An endoscopy may be necessary to exclude other causes of rectal blood loss or when there is a protracted course without he aling.
Anal manometry has no direct clinical appliance. However, many studies have been performed in patients with anal fissures.
3
An increased resting tone is invariably present
in the classic anal dorsal fissure (
Fig. 6.3). The cause of the increased resting pressure is
thought to be the result of increased pressure of the IAS. Often, however, there is clinically also dyssynergia due to the pain, which has been suggested in a clinical study.
9
In addition,
ultra slow waves can be found
10
and represent high anal resting pressure.
11
Endoanal ultrasound will normally not reveal any abnormalities. Although in cases of a
deep chronic fissure the anal sphincter can become less demarcated (
Fig. 6.4A); in some
cases of a persisting fissure an inters phincteric abscess (
Fig. 6.4B) can be found.
12
6.5 Therapy
Historically, ointments were applied and manual anal dilation was performed. In 1951 sur­gical therapy in the form of lateral internal sphincterotomy (LIS), sometimes in combina­tion with anal dilat ation, was introduced.
13
The success rate was high, fecal incontinence seemed not to be an issue and therefore this technique was adopted throughout the world. Not until 1989 did reports appear about high rates of fecal incontinence after LIS, with up to 36% for flatus and 12% for solid stool,
14
which were confirmed in another retrospective
study with rates of 30% incontinence for flatus and 12% for solid stool.
15
A systematic review of fecal incontinence following LIS from 22 studies, mostly case series or cohorts, found an overall incontinence rate of 14%, with 1% for solid stool.
16
Since the publication
of fecal incontinence rates after LIS a more conservative approach has been adopted and
Chapter 6 • Anal Fissure 67