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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
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