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Krakovic M (1974) Untersuchungen über die Verteilung der Proktodäaldrüsen beim Menschen in
Bezug auf den Umkreis des Analkanals und ihre Beziehung zur anorektalen Fistel. Langenbecks
Arch Chir 336:141–154
Schwaner S (2002) Operative Behandlung der chronischen Analfissur: Ergebnisse, Rezidive,
Kontinenzleistung nach Fissurektomie bzw. Fissurektomie und lateraler Sphinkterotomie [dis-
sertation]. Universität Mainz
Sentinel Tags
Abcarian H (1975) Lateral internal sphincterotomy. A new technique for treatment of chronic
fissure- in-ano. Surg Clin North Am 55:143–150
Arroyo A, Perez F, Serrano P et al (2004) Open versus closed lateral sphincterotomy performed as
an outpatient procedure under local anesthesia for chronic anal fissure: prospective randomized
study of clinical and manometric longterm results. J Am Coll Surg 199:361–367
Böttcher KJ (1977) Die operative Behandlung der Analfissur [dissertation]. Universität
Erlangen-Nürnberg
Boulos PB, Araujo IGC (1984) Adequate internal sphincterotomy for chronic anal fissure: subcu-
taneous or open technique? Br J Surg 71:360–362
Brühl W, Schmauz R (1999) Schmerzanamnese von Analfissuren mit / ohne hypertrophierte
Analpapille und Vorpostenfalte sowie Ergebnisse nach Behandlung mit Glyceroltrinitratsalbe
0.3%. Coloproctology 21:147–154
Eißer H (1990) Die chirurgische Behandlung der chronischen und akuten Analfissur [dissertation].
Universität Münster
Gupta PJ, Kalaskar S (2003) Removal of hypertrophied anal papillae and fibrous anal polyps
increases patient satisfaction after anal fissure surgery. Tech Coloproctol 7:155–158
Khubchandani IT, Reed JF (1989) Sequelae of internal sphincterotomy for chronic fissure in ano.
Br J Surg 76:431–434
Oh C, Divino CM, Steinhagen RM (1995) Anal fissure. 20-year experience. Dis Colon Rectum
38:378–382
Parellada C (2004) Randomized, prospective trial comparing 0.2 percent isosorbide dinitrate oint-
ment with sphincterotomy in treatment of chronic anal fissure: a two year follow-up. Dis Colon
Rectum 47:437–443
Richard CS, Gregoire R, Plewes EA et al (2000) Internal sphincterotomy is superior to topical
nitroglycerin in the treatment of chronic anal fissure: results of a randomized, controlled trial
by the Canadian Colorectal Surgical Trials Group. Dis Colon Rectum 43:1048–1058
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Universität Mainz
Soß K (1973) Die Behandlung der Analfissur [dissertation]. Universität Erlangen-Nürnberg
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References
25
© Springer International Publishing AG 2017
V. Wienert et al., Anal Fissure, DOI 10.1007/978-3-319-49244-5_3
3
Secondary Anal Fissures
3.1 Associated with Ulcerative Colitis
Only few, mostly older publications on anorectal complications of Colitis ulcerosa
(ulcerative colitis, UC) can be found in medical literature. This is not astonishing,
because contrary to Crohn’s disease, ulcerative colitis affects only the mucous
membrane, but on no account the deeper layer of the bowel wall. Therefore, an
increased rate of anal fissures associated with or induced by ulcerative colitis is not
to be expected. This condition corresponds to our clinical experience. Whereas in
1964 Lockhart-Mummery had described even 23% anal lesions, mostly painful fis-
sures in patients with a documented ulcerative colitis, the corresponding figures of
1972 dropped to only 7%. This result would suggest an improvement in differential
diagnosis.
Prevalence
Figures on the epidemiology of fissures in the general population are not avail-
able. The prevalence rate of fissures in proctological patients is estimated to range
from 6.4 to 13.8%, so that the abovementioned figures definitely lie within the
normal spectrum (cf. Chap. 5 “Epidemiology”). In this context, it is interesting to
note that the German Guidelines of the Association of the Scientific Medical
Societies (“AWMF-Leitlinie”) make no reference to anal complications of ulcer-
ative colitis. Yet, they state the fact that the initial diagnosis “Colitis ulcerosa” had
to be corrected in up to 10% of the cases. Ricketts and Palmer (1946) do not men-
tion a single case of a fissure in 206 patients between 1927 and 1945, likewise
Sloan et al. (1950) who analyzed the data of 2000 ulcerative colitis patients of the
Mayo Clinic between 1918 and 1937. Alexander-Williams and Buchmann (1980)
believe that anal fissure with ulcerative colitis is rather unusual. But Dombal et al.
(1966) found in 17.6% of 465 ulcerative colitis patients (1952–1963) one or more
anorectal complications, of which anal fissure was the most common disorder in
12.3% of the cases.
26
Jackman (1954) found anorectal, mostly multiple complications in 16% of 200
consecutive cases which he had diagnosed with “chronic” ulcerative colitis. Among
these were nine patients (4.5%) suffering from anal fissures.
Notaras (1977) points out that multiple fissures or fissures transgressing cranially
the pectinate line raise the suspicion of more serious diseases such as ulcerative
colitis, Crohn’s disease, tuberculosis, or syphilis. According to Marti and Givel
(1992), 7% of the colitis patients suffer from fissures, of which some were multiple
ones. They describe them as broad, inflamed, and located outside the median line.
Goligher (1975) comments on this subject in a similar way. He, too, regards anorec-
tal septic complications, including fissures, as not at all unusual. Fissures are
extremely painful, often multiple, extramedian, and lead rapidly to the formation of
an abscess or a fistula. Fuzy (1961) specifies the rate of anorectal complications
associated with ulcerative colitis even within the range of 20–25%. Although they
are not life-threatening, they are still very annoying. He regards the colitic fissure as
a partially deroofed, “intracutaneous” (better: intra-anodermal) abscess with insuf-
ficient drainage. According to his experience, these fissures, frequently multiple
ones, often heal spontaneously during the phase of remission, that is, the arrest of
diarrhea.
Dombal et al. (1966) observed that anorectal complications develop almost
exclusively in phases of clinical activity and then increasingly in severe exacerba-
tions. The strongest evidence for them was the fact that only three patients (0.4%)
exhibited fissures in phases of complete remission, but 27 patients (11.3%) in phases
of severe aggravation. Also, the extent of colitis obviously plays a role in anal fis-
sure formation. If the rectum alone was affected, fissures were found in only 2.2%
of cases. If, however, the entire colon was affected, fissures were found in 5.7% of
cases. Dombal et al. (1966) were also able to show that anal complications appear
mostly within the first year of disease.
Therapy
For Dombal et al. (1966), fissures caused by colitis are rarely painful (more typical
of Crohn’s disease). Therefore, they treated anal fissures usually conservatively
with the intention to improve the general condition of the patient. If necessary, they
applied local anesthesia. Fuzy (1961) also recommends pain control with local
treatment (topical anesthetics, cortisone-based suppositories, sitz baths, compresses,
or enemas). Jackman (1954) treats fissures, which he classified as extremely pain-
ful, with fomentation and also with anesthetizing ointments and suppositories.
According to his experience, hot anal irrigations give only temporary relief. In the
case of a possibly existing sentinel tag and undermined or bulging wound edges, he
favors debridement for a better drainage and the removal of anal spasm caused by
this procedure. If conservative therapy fails, then Fuzy (1961) recommends a care-
ful surgical procedure to enable an adequate drainage which exceeds the anal edge
far enough so that the wound can heal from inside. In his opinion, excision of the
fissure is unnecessary and not indicated especially for active colitis. Relapse is rare
after this procedure. He warns expressly against a radical surgical procedure which
entails the danger of incontinence. Without giving any percentages, Hurst describes
3 Secondary Anal Fissures
27
in his publication of 1935 a painful “anositis” with secondary sphincter spasm to be
an absolutely common complication. Whether these findings are possibly fissures
with a reactive anal stenosis cannot be assessed here.
Conclusion
In cases of ulcerative colitis, anal lesions, including fissures, have been described
more frequently in the past. Due to improved differential diagnosis regarding
Crohn’s disease, this high prevalence appears to be wrong from today’s point of
view. It is most likely that in those days no difference was made between genuine
fissures and fissure-like erosions caused by diarrhea or rhagades.
3.2 Associated with Crohn’s Disease
Anal lesions, especially fissures, are very common with Crohn’s disease. In fact,
they provide nothing less than evidence in differential diagnosis to distinguish them
from Colitis ulcerosa (Homan et al. 1976). Statements concerning their frequency
vary considerably. Atwell et al. (1965) state 4% of 172 Crohn’s disease patients;
14% according to Jackson (1958); and Andersson et al. (2003) observed a frequency
ranging from 20 to 80%. In their retrospective study (1957–1990) of 56 Crohn’s
disease patients, Fleshner et al. (1995) found 49 patients (84%) with symptomatic
fissures. Baker and Milton-Thompson (1971) witnessed between 1950 and 1969 in
262 Crohn’s disease patients at St. Mark’s Hospital London, 215 anal lesions (82%),
of which 18 were anal fissures (6.9% of patients or 8.4% of anal lesions, respec-
tively). Corresponding figures concerning children and adolescents lie within the
same range (Markowitz et al. 1984; Palder et al. 1991). Occasionally, anal lesions
supply first evidence of Crohn’s disease (Lockhart-Mummery 1964), particularly if
they are asymptomatic (Fleshner et al. 1995), cause relatively little pain, or even
become asymptomatic in the course of time (Alexander-Williams and Buchmann
1980). Under certain circumstances, they can be the only indication of Crohn’s dis-
ease (Morson et al. 1959; Lockhart-Mummery 1965) and often precede by years the
verification of the primary disease or the appearance of abdominal symptoms,
respectively (Baker and Milton-Thompson 1971; Gray et al. 1965; Homan et al.
1976; Lockhart-Mummery 1965; O’Donoghue and Hyland 1997; Palder et al. 1991;
Wienert et al. 1973). But anal lesions can also occur long after the appearance of
abdominal symptoms or the diagnosis of Crohn’s disease. Anal fissure is partly
regarded as a complication, partly as an anal manifestation of Crohn’s disease.
Krieg et al. (1977) believe that anal or perianal lesions are an indication of “a florid
intestinal affection or a recurrence after an earlier colon resection.”
Pathogenesis
As a possible pathological cause, Andersson et al. (2003) discuss an increased
sphincter tonus which might impair local blood flow and therefore contribute to the
development of anal fissures. Buchmann et al. (1980), however, observed almost
identical conditions of anal pressure at rest in patients with an active or healed anal
3.2 Associated with Crohn’s Disease
28
fissure, respectively. Frequent bouts of diarrhea can also play a role in the develop-
ment of an infection when stool is pressed into the anal crypts (Andersson et al.
2003). Anal lesions in Crohn’s disease occur more often if the colon (Homan et al.
1976; Hobbiss and Schofield 1982; Platell et al. 1996; Sweeney et al. 1988; Williams
et al. 1981) and the rectum in particular are afflicted (Atwell et al. 1965; Lockhart-
Mummery 1965, 1972). Members of either gender are almost equally affected
(Williams et al. 1981, 1979) (Fig. 3.1).
Findings
Characteristically, Crohn’s disease related fissures appear as chronic fissures, are
often multiple (Bernard et al. 1986; Buchmann et al. 1980), and—contrary to the
classic anal fissure—develop not only in a median position. Fleshner et al. (1995),
however, located 66% of the Crohn’s disease related fissures at 6 o’clock and 50%
at 12 o’clock, and 32% (n = 18) of patients had multiple fissures. Hughes (1978)
saw Crohn’s disease related fissures predominantly at 6 and 12 o’clock. Even though
these are very often deep and show undermined wound edges, they are normally
almost pain free. Therefore, they can be easily overlooked or only be found during
a systematic digital and instrumental (speculum) examination. Lockhart-Mummery
(1972) describes them as longitudinal ulcers, which can extend to the anorectal ring.
Signposts for diagnosis are often the moist, livid secondary sentinel tags, which are
Fig. 3.1 Fissure-like Crohn’s lesion at 6 o’clock, with anal fistula at 7 o’clock
3 Secondary Anal Fissures
29
almost pathognomonic for Crohn’s disease (Lentner et al. 1995). These sentinel tags
are edematous, fleshy, larger and coarser than normal skin tags (Alexander-Williams
and Buchmann 1980), and exude a watery secretion (Gray et al. 1965). Bridges of
tissue between the different wound edges as well as subfissural fistulous tracts can
often be found when a speculum examination is carried out.
Development
Among 61 Crohn’s disease patients with anal lesions, Alexander Williams and
Buchmann (1980) found 54 (88.5%) with one or more anal fissures. Seventeen fis-
sures (31.5%) had completely healed after a 10-year follow-up. Ten fissures were
still visible; 27 anal fissure patients and 7 others had developed a relative anal ste-
nosis. Among 53 patients with a Crohn’s disease-related fissure, Buchmann et al.
(1980) observed a spontaneous healing in 43 patients (81%) after 10 years. A func-
tionally ineffective stenosis had developed in 27 patients (51%).
Complications
As with normal fissures, formation of abscess and fistula can occur. Abscesses are
incised and drained. If a fistula appears on the surface of the skin, it is either split or
operated under gentle treatment of the sphincter. During a follow-up of 8 months on
average (1–136 months), Fleshner et al. (1995) saw abscesses or fistulae in 26% of
the patients (n = 13), irrespective of the therapy employed. Interestingly, most of the
fissures in their patients were symptomatic (pain, rectal bleeding, discharge, pruri-
tus). Painful fissures are relatively rare, but if, they were mostly narrow and deep
and according to Buchmann et al. (1980) more likely concomitant in such cases.
These are treated like normal fissures.
Differential Diagnostics
Besides venereal affections, among them first and foremost the luetic primary effect,
anal tuberculosis must be ruled out in patients with documented tuberculosis as well
as in patients from countries affected by TB, and bilharziosis in patients coming
from tropical zones. Further differential diagnoses are dealt with in the following
chapters.
Therapy
Priority must be given to a systemic treatment of the basic disease. Buchmann and
Alexander-Williams (1980) recommend above all a strictly conservative procedure
and favor bed rest. They are fervent opponents of forced dilatation in the case of
constriction, and they very carefully dilate with one finger—if at all. Bernard et al.
(1986) are of the same opinion as well as Buchmann et al. (1980) who dilate with
maximally two fingers because of the imminent danger of incontinence. It is strongly
advised against performing maximum dilatation after Lord’s procedure (Cohen
1990). Many of the fissures heal spontaneously or under medical or surgical therapy
for abdominal Crohn’s disease (Bernard et al. 1986; Lockhart-Mummery 1972;
Hughes 1978; Krieg et al. 1977). The alleviation of the problems caused by fissures
takes precedence over surgery (Hughes and Jones 1983). Sweeney et al. (1988),
3.2 Associated with Crohn’s Disease
30
however, did not notice in 11 out of 61 patients any interaction with the disease
activity. The fissures healed despite floridity.
O’Donoghue and Hyland (1997) believe that a combination of “aggressive inter-
nists and conservative surgeons” is the ideal therapy option. Steroids and azathioprine
seem to be just as effective as bed rest alone (Brooke et al. 1976). Allan (1977) and
also Palder et al. (1991) saw good results after the use of metronidazole. Depending
on the dose, Rankin et al. (1979) successfully treated their patients with salazosulfa-
pyridine (SASP), prednisolone, and azathioprine. Administering the same active
agents, Fleshner et al. (1995) obtained healing rates of 50% with regard to active fis-
sures and of 60% with regard to chronic fissures after surgical therapy. Homan et al.
(1976) see only occasionally an indication for surgical intervention. Then, fissurec-
tomy as well as lateral sphincterotomy are performed. In their opinion, the latter is the
therapy of choice. Also, Sohn et al. (1980) favored this procedure in cases of painful
anal lesions. In the state of remission, wounds caused by surgery heal usually without
complications and delay (Hobiss and Schofield 1982; Wolkomir and Luchtefeld
1993). Surgical procedure is reserved for complications like abscesses or fistulae
(Buchmann 1988). In cases of active Crohn’s disease, local surgical procedures should
be avoided because wound healing is then protracted (Hughes 1978).
Gray et al. (1965) describe the case of a 13-year-old boy who after fissurectomy
had to undergo follow-up surgery because of disturbed wound healing. Healing took
18 months altogether. There are fissures which are suggestive of deep ulcers and—
especially when the rectum is involved—intrude occasionally into the musculature
and the surrounding fatty tissue in a destructive manner. In these cases, Lockhart-
Mummery (1965, 1972) achieved healing not by local excision or protective colos-
tomy, but by resection of the afflicted colon section only. Also, Krieg et al. (1977)
recommend resection of the intestinal focus of disease after futile systemic therapy.
They perform local surgical invasions only by way of exception, if the results were
not too serious and if the response to medical treatment was positive. Wolff et al.
(1985) see an advantage in resecting anal lesions only when no focus of disease
remains and no relapse will occur.
To achieve a better comparability of treatment results, Hughes (1992) propagates
the application of the UFS classification of perianal Crohn’s disease (U = ulceration,
F = fistula/abscess, S = stricture), which he has developed. This scheme also considers
associated conditions, proximal intestinal involvement, and disease activity (APD).
Tables 3.1 and 3.2 list the relevant publications. On average, 85% of Crohn’s
disease patients exhibit anorectal lesions and 51% develop anal fissures.
Conclusion
Next to medical therapy for the basic disease, local conservative measures (oint-
ment, sitz baths) are indicated when uncomplicated fissures are found. Chronic fis-
sures can be treated surgically. The ablation of the callous wound edges under
inclusion of the hypertrophied anal papilla and the resection of the secondary skin
tag with concurrent removal of the subanodermal fistulae permit good drainage and
further wound healing. In English-speaking countries, lateral sphincterotomy for
anal fissures is regarded as the therapy of choice. According to the current state of
3 Secondary Anal Fissures
31
scientific knowledge, however, this procedure cannot be justified any longer because
extremely often cases of incontinence have been documented as late sequelae. This
is especially true for Crohn’s disease.
3.3 Induced by Infectious Pathogens
3.3.1 Syphilis
Syphilis is a venereal disease which is caused by Treponema palladium, a faculta-
tively anaerobic bacterium belonging to the spirochete family. Being a chronic pro-
gressive infection, it passes through various stages. The anorectal manifestation of
Table 3.1 Anorectal lesions
associated with Crohn’s
disease in 15 trials with 4228
patients (in %)
Author (year)
Patients Anorectal lesions
(n) (%)
Farmer et al. (1975) 615 3.4
Sangwan et al. (1996) 1735 3.8
Atwell et al. (1965) 102 10.8
Williams et al. (1979) 123 11.4
Penner and Crohn (1938) n/a 14.0
Homan et al. (1976) 138 28.0
Hobbiss and Schofield (1982) 151 30.0
Jackman and Smith (1943) 114 31.6
Rankin and Watts (1979) 569 36.0
Platell et al. (1996) 306 42.4
Morson et al. (1959) 47 49.0
Markowitz et al. (1984) 149 49.0
Lockhart-Mummery (1975) n/a 61.0
Fielding (1972) 153 76.3
Schmidt et al. (1968) 26 85.0
TO TA L 4228 35.13
Table 3.2 Anal fissures associated with Crohn’s disease in 10 trials with 3178 patients (in %)
Author (year)
Patients Anal fissure
(n) (n) (%)
Rankin and Watts (1979) 569 80 14.0
Hobbiss and Schofield (1982) 151 23 15.2
Sweeney et al. (1988) 233 60 26.0
Platell et al. (1996) 306 84 27.6
Williams et al. (1981) 1098 318 29.0
Homan et al. (1976) 138 41 29.7
Markowitz et al. (1984) 149 51 34.2
Palder et al. (1991) 325 113 34.8
Fielding (1972) 153 78 50.9
Fleshner et al. (1995) 56 47 84.0
TO TA L 3178 895 28.2
3.3 Induced by Infectious Pathogens
32
syphilis is rare (Marino 1964; Wile and Holman 1941). Earlier, it occurred mainly
in women (Lockhart-Mummery 1914). Today, it is evidently a problem among
homosexual men (Gabriel 1963; Hollings 1961; Marino 1964; Nicol 1962; Pradel
et al. 1985; Samenius 1968; Smith 1963; Thompson 1969). The frequency rate of
extragenital syphilis, manifest in the anal canal, varies between 1.5 and 2.6%
(Downing 1939; Wile and Holman 1941). Most likely, anorectal syphilis is far more
common than reported. It can easily be overlooked because of rather unspecific
complaints which could also be ascribed to other anal affections, to the short period
of time of the primary effect (cf. below), and not least because of physicians who
lack experience. This is, inter alia, reflected in the fact that most of the admission
diagnoses are wrong (Hollings 1961; Samenius 1968). Samenius reports about the
case of one patient who had been examined six times by different physicians, but
none of them came even remotely close to the correct diagnosis. There may also be
many patients who are ashamed and therefore delay or fail to see a specialist physi-
cian. This is particularly true of patients with a different cultural background (Menda
et al. 1971). Apart from a noticeable change in sexual behavior, male homosexuals
in particular are responsible for the increased frequency of anal syphilis (Tarr and
Lugar 1960) because they are definitely more promiscuous than heterosexuals.
Findings
At stage 1, anal syphilis appears both as a relatively broad ulcer and as a rather indo-
lent fissure-like lesion which is coarse or indurated (ulcus durum) at its base and its
edges (Goligher 1975; Winkler and Otto 1997). As a rule, this so-called primary affect
(PA) develops about 3 weeks after the infection (time of incubation: 10–90 days).
Because anal syphilis does not show any pathognomonic alterations, examination
results make it very difficult to differentiate between anal syphilis and a “normal” fis-
sure. In contrast to the anal fissure which is mainly found in the commissure, the lat-
eral (60%) and also the multiple manifestation (55%) is perfectly typical of a syphilitic
fissure (Pradel et al. 1985). Characteristically, a symmetrical secondary lesion is often
found at the opposite wall of the anal canal (Gabriel 1963; Goligher 1975).
Ulcers at the anal verge or fissures in the anal canal, which have a coarse texture
to the touch during the bidigital examination (ulcus durum) and are relatively pain-
less during defecation and examination, should raise suspicions of anal syphilis,
especially when (possibly homosexual) men are concerned.
Winkler and Otto (1997), however, describe the luetic fissure of the anal canal as
quite painful, as clearly defined and not undermined. Goligher (1975) also points
out that syphilitic ulcers, contrary to popular opinion, are not at all painless. We, too,
(Toberer et al. 2013) found besides a number of indolent ones an extremely painful
luetic fissure. Luetic lesions at the anal verge are rounded or oval, and those in the
anal canal are linear (Pradel et al. 1985). According to both Marino (1964) and
Pradel, the edges are “poorly defined”; according to Menda et al. (1971) they are
rather flat in shape. The sphincter tonus is not increased (Thompson 1965). Normally,
enlarged, coarse, indolent pelvic lymph nodes are found, which may also be absent,
because in case of anal syphilis, the para-aortic lymph nodes are often affected
(Lautenschlager 2006) (Fig. 3.2).
3 Secondary Anal Fissures
33
Symptoms
As already mentioned, symptoms are rather unspecific: pruritus, oozing, or serous
and evil-smelling discharge, absence of pain or only mild pain particularly during
defecation; sometimes, light hemorrhage.
Diagnostics
A tentative diagnosis is confirmed by direct evidence of pathogens, by dark-field or
fluorescent microscopy of the stimulus secretion, or by serological means (TPHA,
TPPA, FTA-ABS-test). After that, documentation, examination, and possibly
cotreatment of the partner or the partners are just as necessary as the exclusion of
other sexually transmitted diseases (HIV).
Progress
After about 2–4 weeks, the primary luetic affection heals completely, even without
therapy. After a time span of between 9 weeks and 6 months, syphilis will pass into
stage 2 if it remains untreated.
Therapy
Penicillin still is the therapeutic agent of first choice, because no resistances in
Treponema pallidum have been observed so far. Dose and duration of therapy are
stage-dependent. During the primary and secondary stages, for instance, a dose of
IM 1 million units/day clemizole penicillin G for 14 days or one single dose of IM
Fig. 3.2. Syphilitic chancre (Photo: B. Lenhard)
3.3 Induced by Infectious Pathogens