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2.4 million units benzathine penicillin G. In case of penicillin allergy, doxycycline
2 × 100 mg/day is taken orally for 14 days or erythromycin 4 × 0.5 g/day orally for
14 days. To avoid a Jarisch-Herxheimer reaction (cutaneous and general reactions
such as fever, shivering attacks, headache, exanthema as reaction to the toxins of the
disintegrating treponemes), oral administration of a prednisolone equivalent (1 mg/
kg of body weight) is advisable 30–60 min before the first administration of an
antibiotic (AWMF Guidelines). If treated adequately, the primary affection heals
within 7–10 days.
3.3.2 Tuberculosis
Perianal and anal manifestations of tuberculosis (TB) are rare in the Western world.
Only about 0.7% of extrapulmonary TB (Chung et al.: 5%; Kumar et al. 1997:
28.7%) are located there. In the majority of cases, males are afflicted (Alvarez and
McCabe 1984; Alvarez Conde et al. 1992; Chung et al. 1997). According to Bacon
(1949), anorectal TB is classified into four types, as miliary, lupoid, verrucous, and
ulcerous, the latter being the most common type. Normally, anal TB is concurrent
with pulmonary tuberculosis (Jali 1989; Logan 1969; Martin 1947; Nalepa et al.
2006) or abdominal TB. The modes of transmission are hematogenous or lymphatic
dissemination, direct spread from neighboring organs, or swallowing of sputum
which contains tubercle bacilli. Reports on perianal tuberculous ulcers at the anal
verge, particularly in the anal canal, or fissures of the same kind are rare. In a period
of 10 years, only two tuberculous ulcers in the anal canal were found among the 10
male and 2 female patients affected with anorectal TB at St. Mark’s Hospital
between 1958 and 1967 (Logan 1969). Jali (1989) describes one single case of an
anal ulcer in the UK in a period of 10 years. Perianal lesions occur more often
(Akgun et al. 2005; Harland and Varkey 1992; Honig et al. 2000; Nepomuceno et al.
1971; Sarela and Supe 1996; Whalen et al. 1980).
Findings
The ulcerous form of anal TB normally appears as a soft, superficial ulcer show-
ing a neurotic, hemorrhagic, granulated wound bed with a purulent, mucous
coating (Gupta 2005) or a secretion of that kind. The edges of the lesion are
irregular and undermined (Gabriel 1963; Goligher 1975; Logan 1969). It can be
quite difficult to differentiate it from a Crohn’s disease related fissure (Goligher
1975; Logan 1969). We ourselves had one case of a tuberculous ulcer in the
upper anal canal. Findings on palpation and clinical presentation were in no way
different from a deep-seated carcinoma. A preferred location has not yet been
described.
Symptoms
The intra-anal ulcer sometimes causes heavy pain (Jali; Logan; Myers 1994), so that
digital or instrumental examination requires analgesia, whereas the perianal lesion
is relatively asymptomatic. Occasionally, pain is the only symptom (Jali). But
3 Secondary Anal Fissures
35
patients also complain of soreness, pruritus, discharge, or hemorrhage. Sometimes,
there is an inguinal lymph gland swelling (Gupta 2005).
Diagnostics
Apart from the usual digital and instrumental examination such as proctoscopy and
bivalve speculum, diagnostics comprise biopsy as well. In the best case, the Ziehl-
Neelsen stain shows acid-fast rod bacteria (Honig et al.). Suspicious facts, like
poorly or nonhealing wounds despite adequate therapy, tiredness and lack of perfor-
mance, night sweats, coughing/hemoptysis, insidious loss of weight, should be the
reason for further diagnostic measures (biopsy → bacterial culture/PCR). After the
diagnosis, pulmonary TB and immune deficiency (HIV) have to be ruled out.
Therapy
Treatment is carried out after a resistance screening with tuberculostatics, usually as
a four-drug regimen.
3.3.3 Leishmaniasis
Leishmaniases are parasitic protozoa which can afflict skin or mucous membrane
(Leishmania tropica, L. brasiliensis) in their (muco-)cutaneous form and the inner
organs (L. donovani; L. chagasi) in their visceral form (Sunderkötter 2014). Since
the Gulf Wars, a viscerotrope variant of L. tropica is known, which until then had
been regarded to be exclusively responsible for cutaneous manifestations
(Sunderkötter 2014). Leishmaniasis is transmitted by sandflies of different species
in the Old and New World (Sunderkötter 2014).
In medical literature, only two cases of perianal ulcers induced by leishmaniasis
are described (Meis et al. 1999; Schmid et al. 1999), but not a single case of such a
lesion in the anal canal. In one case (Meis et al. 1999), Histoplasma capsulatum was
finally found in the bacterial culture. The perianal ulcer described by Schmid et al.
(1999) is uncommon insofar as L. donovani bodies were found in the bone marrow
of a 51-year-old patient, but not in the perianal lesion.
Among our own patients (Mlitz et al. 2012), there is one case of a 45-year-old
AIDS patient who repeatedly had to undergo chemotherapy because of malignant
non-Hodgkin’s lymphoma. During his first consultation at the end of 1995, he com-
plained of a painful anal syndrome during and after defecation and also of oozing
and pruritus in ano. Examination showed a secondary skin tag at the anal verge at
5 o’clock. Also at 5 o’clock in the anal canal, a broad fissure-like ulcer could be
palpated as far as above the pectinate line. The abscess cavity there, which nearly
extended to the edge of the levator ani muscle, could be entered by the distal pha-
lanx of the index finger. Before the era of HAART therapy, surgeons confined
themselves to perform wound toilet and the excision of secondary skin tag to allow
a better wound drainage. The histopathological examination yields a well-
developed, chronically granulating, scarring, partly also florid, and erosive unspe-
cific inflammation accompanied by enhanced epithelium recovery. During the
3.3 Induced by Infectious Pathogens
36
further course of the disease, the clinical diagnosis of leishmaniasis was histologi-
cally (iliac crest bone graft technique) backed by the evidence of amastigotes. The
follow-up evaluation of the resected tissue revealed also leishmaniasis as well as an
epithelial defect or rather an anal fissure.
3.3.4 Histoplasmosis
Histoplasma capsulatum is a fungus which is endemic to the Mississippi area and the
valley of the Ohio River. It is an opportunistic pathogen which mostly affects the
lungs of immunocompromised patients. There are only few reports on anal ulcers/
fissures, particularly concerning AIDS patients (Kahi et al. 2005; Winburn and Yeh
1999). Winburn and Yeh describe a severe, fast developing anal affliction with increas-
ing pain, discharge, and incontinence. Medical examination was only possible when
the patient was anesthetized. A complete loss of anoderm between the anal verge and
the pectinate line was found. The internal anal sphincter was exposed in its left
hemicircumference. The right dorsal parts of the anal sphincter were melted down, so
that the anococcygeal ligament could be seen. Furthermore, there was a connection to
the right side of the ischiorectal fossa. An antimycotic therapy (itraconazole) achieved
a temporary improvement, 6 months later, however, exitus letalis occurred.
In 1999, Meis et al. published a case report of a perianal ulcer induced by leish-
maniasis; yet, Histoplasma capsulatum was found in the bacterial culture.
3.3.5 Virally Induced
3.3.5.1 HIV/AIDS
Numerous publications on perianal and intra-anal ulcerations associated with HIV
infections or with AIDS patients have appeared in the era before HAART, the Highly
Active Antiretroviral Therapy (Consten et al. 1995; Miles et al. 1990, 1991), which are
no longer found in the industrial societies. These studies revealed that at a rate of
21–40%, homosexual individuals were significantly more often afflicted than intrave-
nous drug users who showed a rate of only 3% (Miles et al. 1992; Wolkomir et al. 1990).
Symptoms
Normally, patients complain of strong pain and tenesmus, rectal hemorrhage, puru-
lent discharge, in some cases, pruritus ani and incontinence (Miles et al. 1990;
Nadal et al. (1999); Safavi et al. 1991). These signs and symptoms persist over a
long time, in some of Nadal’s patients for as long as 18 months.
Diagnostics
Proctologic examination is extremely painful and is therefore generally carried out
under anesthesia. It includes digital palpation of the anorectum and examination by
proctoscope and/or spreadable anal speculum. For bacterial and viral analysis, pap
tests are mostly used.
3 Secondary Anal Fissures
37
Results
Anal fissures or fissure-like ulcers in patients with AIDS are located in the entire
circumference (Miles et al. 1991). They are sometimes multiple (Consten et al.
1995), and deeper and longer than normal fissures and are found further proximally
in the anus, and here mostly in the area of the pectinate line, often in combination
with proctitis (Consten et al. 1995). Therefore, these lesions often escape inspection
when the buttocks are parted. Nadal et al. (1999) and Viamonte et al. (1993) saw the
majority of ulcerations in the midline position, mainly dorsal. Frequently, herpes
simplex and cytomegaloviruses as well as chlamydia can be proved in such ulcers
(Consten et al. 1995; Miles et al. 1991; Abe et al. 2005; Horn and Hood 1990; Puy-
Montbrun et al. 1990). It is not clear whether the viral infection is a secondary
problem or the cause for the ulcers. Because of the fact that drug-addicted hetero-
sexual AIDS patients often show significantly less anal ulcers or fissures (cf. above),
it is rather likely that it is a secondary problem. Presumably, anal ulcers in homo-
sexual patients are mainly due to a traumatic origin like anal intercourse. The
sphincter tonus in many patients is not increased, but rather reduced (Nadal et al.
1999; Viamonte et al. 1993).
Therapy
After the medication directed against the corresponding pathogens had failed, Miles
et al. (1991) excised the ulcers refractory to treatment. Normally, these are situated
perianally or at the anal verge. To their surprise, they achieved analgesia in 44% of
the cases within 4 weeks. Retrospectively, Consten et al. (1995) compared local
excision with mucosal flap advancement, and using this method found excellent
results in 92% of the cases. Nadal et al. (1999) excised the wound edges only, left the
wound base open, and approximated the wound edges with a simple running suture.
Because of the reduced sphincter tonus, they did not consider sphincterotomy.
Subsequently, antibiosis was carried out with metronidazole. After 10 days, patients
had only pain during defecation, as a rule. Viamonte et al. (1993) divided anal lesions
of HIV patients into benign fissures and invasive ulcerated processes, the latter at the
more progressive stages of HIV disease (AIDS). They treated their 33 anal fissure
patients in the same way as HIV-negative patients, which means conservatively, at
first. When treatment failed in 23 patients, they performed lateral sphincterotomy in
13 patients. Twelve patients became free of complaints, and eleven were healed.
Histology
In three cases, Nadal et al. (1999) found squamous cell carcinomas “in situ”, in one
case Morbus Bowen, and in three cases CMV inclusions. The latter ones were also
observed by Consten et al. (1995) in 6 out of 23 patients, although the cultures set
up beforehand were negative.
3.3.5.2 Herpes Simplex Viruses (HSV)
Reports on intra-anal fissural ulcers caused by HSV-1 or HSV-2 were not found in the
medical literature we have reviewed, but we found reports on superficial perianal
ulcers which healed after appropriate medication treatment (Goodell et al. 1981).
3.3 Induced by Infectious Pathogens
38
Furthermore, HSV can be proved in many intra-anal ulcers of HIV-positive homo-
sexuals (Consten et al. 1995; Miles et al. 1991). However, it is impossible to deter-
mine whether they are responsible for the development of these lesions or whether the
colonization of the wound base is secondary (Consten et al. 1995). The fact that drug-
addicted heterosexual AIDS patients often exhibit significantly less anal ulcers than
homosexual patients makes the latter theory appear more realistic. Pradel et al. (1985)
saw four cases of “ulcerous anorectitis,” but do not give any further description.
3.3.5.3 Cytomegaloviruses (CMV)
In many anal fissures of HIV/Aids-infected patients, CMV can be proved by viral cul-
ture (cf. Sect. 3.3.5.1 HIV/Aids). Here, too, it is not clear, whether these viruses are the
cause of the intra-anal ulcers or whether the ulcers are secondarily colonized by them.
3.4 Drug-Induced
3.4.1 Ergotamine
Anorectal ergotism is very rare. Its characteristic lesions—ulcers, proctitis/rectitis, fis-
tula, stenoses—are differential diagnoses of mostly perianal or anorectal Crohn’s dis-
ease lesions. Drug anamnesis, namely the use of suppositories containing ergotamine
(not for sale in Germany any longer) to reduce or prevent migraine attacks, is instru-
mental in finding the correct diagnosis. Between 1980 and 1997, only 15 studies on
this subject were found. Eight studies are concerned with ulcerations in the anal area.
Only 12 cases of perianal or intra-anal ulcers are described, including two cases from
our medical experience (Baptista et al. 1992; Brandt et al. 1997; Eckhardt et al. 1986;
Jost et al. 1991; Jost 1999; Lamesch et al. 1995; Mlitz 2007; Schaarschmidt et al. 1984;
Strohal and Diem 1992; Wienert and Grußendorf 1980). Only women are affected.
The abuse of suppositories containing ergotamine to treat migraine leads to the
cutaneous and mucosal resorption of ergotamine tartrate, an ergot alkaloid.
Ulceration ensues induced by vessel constriction and local ischemia. There is no
correlation between the daily dose, the period of application, and the extent of dam-
age. Anocutaneous ergotism, which appears perianally or in the anal canal, pro-
duces typically a burning pain (“Ignis Sacer”, St. Anthony’s fire) and rectal bleeding
during defecation. Therapy consists in the elimination of noxa. Then, without fur-
ther specific treatment, the ulcers generally heal with scarring after some weeks.
Possible stenoses can be dilated digitally or by gentle use of the bougie.
3.4.2 Nicorandil
Nicorandil is used for the treatment of angina pectoris or cardiac ischemia. It was
introduced in Japan in 1984, and 10 years later in Europe (Katory et al. 2005). It is not
available as a finished medicinal product in Germany and the United States. Nicorandil
is a nicotinic acid derivative drug, and, as a potassium channel opener, it has
3 Secondary Anal Fissures
39
vasodilatory effects on veins and coronary arteries (Kiowski and Riebenfeld 2001). In
1997, Reichert et al. described oral ulcers as an unwanted side effect of nicorandil.
Then, in 2002, Watson et al. reported for the first time on an anal ulceration after
nicorandil therapy. Obviously, the formation of ulcers is primarily dependent on the
dose administered, not on the duration of therapy. After years of application, it is not
uncommon that such ulcers will appear in the anogenital area if the dose is increased
(Al-Hilli et al. 2006; Claeys et al. 2006; Malik et al. 2005; Watson et al. 2002, 2004).
Sporadically, these ulcers also occur peristomally (Williams et al. 2007). It is typical
of these ulcerations that they cannot be successfully treated, neither by local surgery
nor by doing an ileostomy, and that at a time when the pathogenesis was still unknown
(Claeys et al. 2006; Cooke et al. 2006; Williams et al. 2007).
Characteristic features of these ulcers, which often appear as fissures in the anal
area, are intense soreness and their manifestation: the ulcers look as if they were
deeply punched out, internal sphincter fibers are visible at the wound base (Al-Hilli
et al. 2006), and the wound edges are undermined (Watson et al. 2002, 2004). Histology
findings are unspecific. Fatty and connective tissue with fibrosis and chronic inflam-
mation without granulomas and without an indication of malignity are found (Al-Hilli
et al. 2006). In differential diagnosis, chronic inflammatory colon diseases, first of all
Crohn’s disease, anal carcinoma, and also virus-induced anal lesions like HIV/Aids,
syphilis, TB, as well as other possible causes of secondary fissures must be ruled out.
Therefore, a thorough drug anamnesis is absolutely necessary. The origin of
ulceration is still disputed. The cause of the formation of ulcers is supposed to be a
vascular steal phenomenon, probably in combination with the physiological isch-
emia in the area of the posterior commissure and an increased sphincter tone. This
pathomechanism does not apply to perianal, peristomal, genital, and oral ulcers,
however. Local toxic events, which are possibly associated with an electrolyte
imbalance, are also suggested to induce ulcers. Yet, since nicorandil or its metabo-
lites are mainly excreted through the kidneys and only partially through feces, this
explanation is not plausible (Katory et al. 2005). In animal tests, nicorandil had even
a protective effect on induced stomach ulcers (Passeron et al. 2004).
Therapy
Ulcers, refractory to all other treatment and often persistent for years, normally heal
relatively fast after the elimination of the noxa (Katory et al. 2005; Malik et al. 2005;
Passeron et al. 2004). Pain stops already before healing is complete (Renwick et al.
2004). In some cases, in which angina pectoris could obviously not be treated in any
other way, nicorandil had to be administered again. The reduction of the dose did not
lead to a relapse (Renwick et al. 2004). A relapse occurred, when a fresh therapy was
begun, presumably with the same dosage (Katory et al. 2005; Toquero et al. 2006)
3.4.3 Isotretinoin
Isotretinoin is a synthetic retinoid used to treat severe forms of acne like acne nodu-
laris or acne conglobata, which are resistant to standard treatment. The drug may
3.4 Drug-Induced
40
only be prescribed by physicians or under supervision by those physicians who “are
familiar with the application of systemic retinoids in the treatment for severe acne
and who possess far reaching knowledge of the risks of isotretinoin therapy and the
necessary controls” (WINAPO
®
Lauer-Taxe of April 15, 2008).
Unwanted side effects (>10%) are often skin desquamation, pruritus, and thinning
of the skin accompanied with increased vulnerability (15–25%). Looking through the
relevant medical literature, we found one publication on two anal fissures, which in one
case had appeared after “a few days,” in the other case 1 week after the start of therapy
(2 × 20 mg daily), due to a papulonodular erythematous rosacea or a nodular cystic
acne (Radmanesh 2006). The results are described relatively vague as anal fissure and
proctitis (“fissured and xerotic anal mucosa”). After the isotretinoin therapy had been
stopped, the condition of the patient gradually improved within the following 2 weeks.
3.4.4 Chemotherapeutics
We found only one study which associates anal fissures with aggressive chemotherapy
(Proske et al. 2003). This study is about leukemia patients with a severe immunity
weakness caused by an intensive chemotherapy. Proske et al. examined 31 patients
who suffered from myeloblast leukemia (AML), lymphoblast leukemia (ALL), mul-
tiple myeloma, Burkitt’s lymphoma, and AL amyloidosis. The anal pathology was
caused by “acute and subacute anal fissures, sometimes in an atypical location, or by
a crypt inflammation.”. During the medical examination, secondary changes—in
some cases, extensive—were found as an indication of a chronic event, even though
not a single patient had complained of proctological problems prior to the diagnosis
of the malignant underlying disease. During the proctologic examination, the authors
described a “flaming reddening…, the total skin area was very sensitive to pressure,”
whereas the clinical picture was perhaps mitigated by the prophylactic antibiosis.
Rectal examination was only possible under local anesthesia.
The fissures were treated with warm sitz baths, bloodless dilatation carried out
with an anal dilator by the patient himself, but not during the aplasia phase, and by
the administration of antiphlogistics. The fissure in 5 out of 31 patients healed with-
out complication; in 2 patients, fistulae developed which were drained by placing a
seton to prevent an abscess during the remission phase. Patients with a chronic anal
fissure (60%)—those with secondary changes—were operated during the remission
phase. It was found that the postoperative healing process with an average healing
time of 6 weeks was not longer than that of patients without a hematologic disease.
3.5 Other Pathological Causes
3.5.1 Leukemia
Only few, mostly older publications on perianal and anorectal complications in con-
nection with leukemia can be found in medical literature. Kirschbaum and Preuss
3 Secondary Anal Fissures
41
(1943) did not see any anal involvement in 123 consecutive autopsies of patients
who had died of leukemia. Leukemic infiltrates in the rectum are unusual and
extremely rare, whereas they are often initial signs and symptoms of leukemia, par-
ticularly in the oral cavity, and here in children.
Blank (1955) describes the case of a 62-year-old woman who was admitted to
hospital because she had been suffering from anal disorders for 10 days already.
Several areas with skin defects were seen in her anal region. During anamnesis, she
was diagnosed with lymphatic leukemia. The next day, the affected areas were
excised to provide for better drainage. After that, her condition worsened rapidly,
and she died on the third postoperative day. In another case, two infants, both suf-
fering from acute lymphatic aleukemic leukemia, developed a large thrombosis at
the anal verge, which progressively took on a darker color within a short period of
time and quickly exulcerated. The thrombosis caused a large and extremely painful
deep necrosis, which extended partly into the distal rectal ampulla. One infant died
4 days after the anal symptoms first occurred, and the other about 2 months later.
Apart from a further female patient with chronic lymphatic leukemia, who devel-
oped an anal ulcer 2 years after the beginning of her disorder, Blank (1955) saw a
38-year-old patient who suffered from myeloid leukemia and rectal pain after he
had been given a barium contrast enema. Within 4 weeks, an ulcer formed in his
dorsal anal canal. He, too, died shortly afterwards.
Siegal and Bernstein (1965) observed in seven patients with different types of
leukemia an anorectal involvement, mostly ulcerations and abscesses. Only one
patient survived 3 months, while the others succumbed to their disease after a fou-
droyant course maximally 4 weeks later, entirely irrelevant whether the patients had
received conservative treatment, generally damp heat or sitz baths, broad-spectrum
antibiotics and steroids, or surgical treatment. Therefore, the recommendation at
that time was to treat anorectal lesions in leukemia patients conservatively in con-
sideration of their immune deficiency (pain therapy, nursing measures). Abscesses
should be incised (Siegal and Bernstein 1965).
For Sehdev et al. (1973), the combination of symptomatic treatment and radiation
therapy was the method of choice to control the perianal complications (among them,
two anal fissures) due to uncontrolled acute or chronic leukemia. Vanheuverzwyn
et al. (1980) saw among 514 patients with hematologic disorders 31 (6%) with severe
anal lesions, namely inflammatory infiltrates located around the anus or the ischio-
rectal fossa or in the anal canal (n = 4), anodermal ulcers (n = 21), and idiopathic anal
fissures (n = 5). Furthermore, they diagnosed 16 perianal, perirectal, or ischiorectal
abscesses. In six cases (20%), the periproctitic abscess was the first symptom of
hematologic disease. The notion at that time was proved to be true that anorectal
lesions associated with hematologic disease were regarded as a bad omen (Latin:
“signum mali ominis”): 14 out of 31 patients (45%) died within 4 weeks. Causes of
death were sepsis, neurologic or pulmonary complications. They saw a connection
between lethality and hematologic disease because 9 of the 14 deceased patients had
a persistent neutropenia and 11 suffered from acute myeloid leukemia.
Among 83 patients with leukemia, North et al. (1996) found 22 with anal fissure
(26.5%). Proske et al. (2003) saw 31 hemato-oncologic patients with rectal pain
3.5 Other Pathological Causes
42
symptoms undergoing aggressive chemotherapy. They represented about 10% of the
new malignant cases of myeloblastic leukemia (AML), lymphoblastic leukemia
(ALL), multiple myelomata, Burkitt’s lymphomata, and AL amyloidosis, which
were recorded in the Division of Hematology of the University Hospital of Heidelberg
during the years 2001 and 2002. These patients showed acute and subacute anal fis-
sures—sometimes in nontypical locations—and also crypt abscesses and abscess-
like manifestations, without the ripening process of abscesses. During the phase of
aplasia, which was required by therapy, treatment was conservative and included
analgesics, antiphlogistics, and antibiotics as well as sitz baths. During the remission
phase, patients with chronic fissures were operated, and the secondary changes were
concurrently excised. The period of wound healing did not differ from that of non-
hemato-oncologic patients. Obviously, some of the patients have already had asymp-
tomatic chronic fissures before, which exacerbated while receiving chemotherapy in
the aplasia phase. Long before Vanheuverzwyn et al. (1980), the authors Yeomans
(1930), Silvers (1933), and Carmel (1944) had already drawn attention to the tempo-
ral coincidence of ulcerations and neutropenia or agranulocytosis.
3.5.2 Cow’s Milk Allergy
Andiran et al. (2003) retrospectively compared two groups of 30 children each,
aged between 4 months and 3 years old, in terms of their daily cow’s milk consump-
tion, their period of breast-feeding, and other clinical characteristics. They were
able to prove that the daily consumption of cow’s milk was significantly higher in
the group of children with chronic constipation (defecation once or twice a week)
and anal fissures. These children had also been breast-fed for a distinctly shorter
period. In this group, 17 children were found to have a ventral fissure (n = 8), a
dorsal fissure (n = 9), and multiple fissures (n = 13). Also, significantly more cutane-
ous and respiratory atopic symptoms could be observed than in the control group of
30 healthy children. They concluded that constipation and anal fissure might be the
result of cow’s milk allergy.
Iacono et al. (1998) describe the case of a 5-year-old boy who was bottle-fed
with cow’s milk proteins from his day of birth on and contracted infectious enteritis
when he was 2 months old. When he was two and a half years old, he developed anal
fistula and anal fissures. Six months later, a severe constipation occurred because
laxatives had no effect. When he was 4 years old, the fistula was split and the fissure
operated. Nevertheless, both reappeared already after 1 month. At the age of 5, three
anal fissures and the orifice of a fistula were found. There was no clinical evidence
of a chronically inflamed colon. Cow’s milk allergy was then assumed to be causal,
and a week later, after adequate abstention, defecation became normal, that is, one
time a day. After 3 weeks, the anal fissures and the anal fistula had healed com-
pletely. During renewed exposure to cow’s milk, constipation reoccurred and an
anal fissure developed already 4 days later.
Iacono et al. (1998) did another double-blind crossover study which concerned
65 children between 11 and 72 months of age, with chronic constipation defined as
3 Secondary Anal Fissures
43
defecation every 3–15 days. They found again a correlation between an obvious
cow’s milk allergy and chronic constipation or the occurrence of anal fissures. After
the consumption of soy milk, however, the symptoms regressed in most children,
but reoccurred with renewed exposure to cow’s milk.
3.5.3 Behçet’s Disease
In our latitudes, Behçet’s disease is an extremely rare inflammatory disease of
unknown etiology, presumably in the sense of an autoimmune disease. We did not
find any publication in the medical literature which explicitly dealt with anal ulcers
or fissures as symptoms of Behçet’s disease. Such ulcers are only mentioned in a
review by Thompson (1969).
References
Associated with Ulcerative Colitis
Alexander-Williams J, Buchmann P (1980) Perianal Crohn’s disease. World J Surg 4:203–208
AWMF online. Leitlinien. Diagnostik und Therapie der Colitis ulcerosa. http://www.awmf.org/
leitlinien/detail/ll/021-009.html
Dombal de FT, Watts JMK, Watkinson G et al (1966) Incidence and management of anorectal
abscess, fistula and fissure, in patients with ulcerative colitis. Dis Colon Rectum 9:201–206
Fuzy PJ Jr (1961) Surgical management of anorectal complications of chronic ulcerative colitis.
South Med J 54:785–787
Goligher JC (1975) Surgery of the anus rectum and colon, 3rd edn. Baillière Tindall, London
Hurst AF (1935) Prognosis of ulcerative colitis. Lancet 2:1194–1196
Jackman RJ (1954) Management of anorectal complications of chronic ulcerative colitis. Arch
Intern Med 94:420–424
Lockhart-Mummery HE (1964) Anal and perianal ulceration in Crohn’s disease. Proc R Soc Med
57:897–898
Lockhart-Mummery HE (1972) Anal lesions of Crohn’s disease. Clin Gastroenterol 1:377–382
Marti MC, Givel JC (1992) Chirurgie anorektaler Krankheiten. Springer, Berlin
Notaras MJ (1977) Fissure-in-ano. Lateral subcutaneous internal anal sphincterotomy. In: Rob C,
Smith R (eds) Operative surgery. Butterworths, London
Ricketts WE, Palmer WL (1946) Complications of chronic non-specific ulcerative colitis.
Gastroenterology 7:55–66
Sloan WP, Bargen JA, Baggenstoss AH (1950) Local complications of chronic ulcerative colitis
based on the study of 2000 cases. Proc Staff Meet Mayo Clin 25:240–251
Associated with Crohn’s Disease
Alexander-Williams J, Buchmann P (1980) Perianal Crohn’s disease. World J Surg 4:203–208
A-Hilli Z, Pritchard R, Roche-Nagle G et al (2006) Nicorandil related anal ulcer. Ir J Med Sci
175:62–63
Allan RN (1977) Evaluation of metronidazole in the management of Crohn’s disease. Gut 18:422
Andersson P, Olaison G, Hallböök O (2003) Increased anal resting pressure and rectal sensitivity
in Crohn’s disease. Dis Colon Rectum 46:1685–1689
References