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© Springer International Publishing AG 2017
V. Wienert et al., Anal Fissure, DOI 10.1007/978-3-319-49244-5_5
5
Epidemiology and Etiopathogenesis
5.1 Epidemiology
Anal fissure is not at all a rare disease. Astonishingly, there is only one epidemio-
logical study concerning the prevalence of anal fissure in the general population.
Ani (1983) examined 336 adults in West Nigeria and found an anal fissure disease
rate of 23.8%.
But, there are some studies which determine the prevalence of anal fissure in a
defined population. Jost (1999) found a prevalence of 1.9% when he examined 1500
neurological patients. Ajayi et al. (1974) saw anal fissures in 12.6% of 300 procto-
logical patients, Berg (1970) in 13.8% (n = 600), and Wienert (1973) in 6.4% (n =
100). Pescatori and Interisano (1995) conducted a survey in Italian hospitals in 1994
and discovered among 15,161 proctological patients 10% with anal fissure. Corby
et al. (1997) reported anal fissures in 9% of 313 female patients in pregnancy or in
childbed. Martin (1953) found anal fissures in 10.7% (n = 414) and Abramowitz and
Battallan (2003) in 16.4% of 168 women.
Conclusion
About 10% of proctological patients suffer from anal fissure disease.
5.1.1 Anal Fissures in Children and Juveniles
Anal fissures are not at all rare to find in infants and children. Tander et al. saw 62
young patients with anal fissures within 1 year, Demirbag et al. treated 31 young
individuals during the same period of time. Sönmez et al. observed 91 cases within
16 months, and Lambe et al. (2000) treated 37 young patients with anal fissures
within 36 months.
Multiple anal fissures in children are also frequent (Sönmez et al. 2002). Acute
but also chronic anal fissures occur in children just as often as in adults (Apley
56
1956). According to Nwako, 50% of young patients show skin tags; the gender dis-
tribution is almost the same as with adults (Table 5.1).
In contrast to adults, constipation in children seems to play a special role in etio-
pathogenesis. Ellison found constipation in 24.7% among his collective of young
patients, and Kenny et al. observed constipation in even 85% of cases. In this con-
text, reference is made to Sect. 5.2.4. As with adults, the main symptom of anal
fissure is pain during defecation. Anal fissure is the most common cause of rectal
bleeding in children.
Often, clinical therapy trials do not inform on the kind of anal fissure. Yet, this
knowledge is essential because acute, chronic, and secondary anal fissures call for
different therapeutic measures, and prognosis also is different.
In a four-arm RCT, Sönmez et al. treated 102 children suffering from anal fissure
over a period of 10 days. Eighty-six percent of anal fissures healed in the GTN
group (n = 22), 60% in the Emla group (n = 25), 20% in the lidocaine group (n =
24), and 5% in the placebo group (n = 20).
Tander et al. conducted a similarly designed RCT. They too compared the effect
of GTN (n = 31) with that of lidocaine (n = 14) and placebo (n = 17). After 8 weeks,
the healing rate in the first group was 83%, in the second group 21%, and in the
placebo group 35%.
Kenny et al. treated 31 children with GTN ointment and placebo over a period
of 16 weeks and were able to achieve complete healing in 84% of the verum
group. The children, however, received laxatives (sic!) at the same time. Demirbag
et al. treated 31 children with GTN ointment with a healing rate of 84% after 8
weeks.
Some authors carried out surgery after an unsuccessful conservative therapy or
in the case of a relapse.
Lambe et al. (2000) performed fissurectomy in 37 children (14 boys, 23 girls)
between the ages of 17 weeks and 12 years, and postoperatively gave doses of laxa-
tives. After 6 weeks, 81% of the children were free of complaints.
Two authors reported on their experience with lateral internal sphincterotomy.
Nwako performed sphincterotomy in 22 children aged between 6 and 12 (14 boys,
8 girls). He says, “This method is probably the operation of choice for most
cases of therapy- resistant anal fissure”. Cohen and Dehn called lateral internal
Table 5.1 Pediatric anal fissure by gender in seven trials with 443 children
Author (year)
Patients Male Female
(n) (n) (n)
Kenny et al. (2001) 40 18 22
Tander et al. (1999) 62 29 33
Demirbag et al. (2005) 31 12 19
Sönmez et al. (2002) 91 44 47
Ellison (1960) 174 84 90
Cohen and Dehn (1995) 23 14 9
Nwako (1975) 22 14 8
Total 443 215 228
5 Epidemiology and Etiopathogenesis
57
sphincterotomy an effective procedure to treat anal fissure in children. They operated
on 23 children, and all the anal fissures were healed after 8 weeks.
Conclusion
We believe that surgeons should be extremely cautious about surgical therapy for
children.
5.2 Etiopathogenesis
5.2.1 Anal Sphincter Hypertonia
In the past, the hypothesis was put forward that an increased muscle tone of the
internal anal sphincter is a decisive factor for the development of an anal fissure. To
date, however, anal manometric studies could not prove this theory. Moreover, it is
still unclear, whether sphincter hypertonia is the primary or a secondary factor. It is
also not clear, whether sphincter hypertonia is to be considered either as cause or
effect of the anal fissure disease. Nothmann and Schuster (1974), Arabi et al. (1977),
Hancock (1977), Gibbons and Read (1986), Jostarndt et al. (1986), Lin (1989),
Farouk et al. (1994), Keck et al. (1995), Horvath et al. (1995), and Zbar et al. (1999),
they all found an increased anal resting pressure, as opposed to Duthie and Bennett
(1964), Keighley et al. (1976), Abcarian et al. (1982), Braun and Raguse (1985) and
Klug and Eckert (1992), whose findings would not confirm this hypothesis.
Apart from that, clinical examinations of fissure patients (Jostarndt et al.1986)
show that not only the internal sphincter muscle generates anal resting pressure but
also the external sphincter muscle with a 45% share. Schweiger (1982) puts the
share at 30%.
The results of these studies must be evaluated critically because measurements
were done with different instruments, and techniques were applied which are not
approved. Some authors performed rapid pull-through manometry, others, however,
used selective manometry. The measuring instruments used were balloons filled
with either air or water, open-end perfused catheters or electronic pressure sensors.
The diameters of the different balloon systems lay between 1 and 25 mm. If the cali-
ber size of the pressure probe is increased, incorrect pressure values (here, an
increase) have to be expected because an irritation of the anal canal will follow.
Often, the collectives of patients and controls were too small to draw representa-
tive conclusions. Moreover, the measurement results are not only dependent on age,
gender, and time of day but also on the stage of the fissure disease. Thus, an old
chronic anal fissure generally has a lower resting pressure than a fresh one.
The procedure of anal manometry as such can also produce artifacts. The intro-
duction of the catheter increases pain, and a spasm occurs, which means an involun-
tary cramp of both of the anal sphincter muscles. Jostarndt et al. (1986) were able to
establish a clear correlation between pain and resting pressure. The greater the pain,
the higher the resting pressure. As a consequence, the dogma of “anal fissure equal
to elevated anal resting pressure” is not correct, even though all therapy measures
5.2 Etiopathogenesis
58
which aim at the reduction of the muscle tone have been described as more or less
successful (Tables 5.2 and 5.3).
Arabi et al., Nothmann and Schuster (Table 5.2) as well as Duthie and Bennett
(Table 5.3) do not specify the stage of anal fissure development.
Conclusion
There is no evidence whatsoever that anal fissure disease leads to an increase of anal
resting pressure. There is also no evidence that anal fissure disease is induced by
elevated anal resting pressure.
5.2.2 Anal Sphincter Fibrosis
For almost a hundred years, there has been an ongoing discussion in the medical
literature whether an internal anal sphincter fibrosis (sclerosis) is also causally
Table 5.2 Increased anal resting pressure (ARP) in 209 chronic anal fissure patients (in cm H
2
O
or mm Hg*)
Author (year)
Probands Healthy controls Patients
Chronic anal
fissure patients
(n) ARP (n) ARP
Anal resting pressure in cm H
2
O
Arabi et al. (1977) 78 88±34 48 130±43
Hancock (1977) 40 85±20,5 12 116±21.8
Gibbons and Read (1986) 14 73±27 6 114±17,1
Jostarndt et al. (1986) 20 71.2±24.9 20 87.4±38.8
Anal resting pressure in mm Hg
Nothmann and Schuster (1974) 17 50 (25–75) 7 85 (75–100)
Lin (1989) 36 71.2±24.9 29 87.4±38.8
Farouk et al. (1994) 33 94 30 132
Keck et al. (1995) 12 82.6 (50–121) 12 120.5 (81–154)
Horvath et al. (1995) 28 70 (30–108) 28 86 (65–115)
Zbar et al. (1999) 33 60 17 85
*100 cm H
2
O = 73.556 mm Hg
Table 5.3 Normotensive anal resting pressure (ARP) in 70 chronic anal fissure patients (in cm
H
2
O or mm Hg
a
) (in cm/H
2
O and mm/Hg
a
)
Author (year)
Probands Healthy controls Patients
Chronic anal
fissure patients
(n) ARP (n) ARP
Anal resting pressure in cm H
2
O
Keighley et al. (1976) 20 104±18.4 7 106±16.3
Anal resting pressure in mm Hg
Duthie and Bennett (1964) 29 38 8 38
Abcarian et al. (1982) 10 40–110 8 50–105
Braun and Raguse (1985) 15 42.2±9.2 17 41.0±9.7
Klug and Eckert (1992) 30 87% normotensive
a
100 cm H
2
O = 73.556 mm Hg
5 Epidemiology and Etiopathogenesis
59
involved in the formation of anal fissure. Anal sphincter muscle scarring would
occur, and the sphincter muscle would lose elasticity, which is attributed to the loss
of muscle fibers as well as to excessive connective tissue growth. In extreme cases,
an anal stenosis would develop. The passage of solid stool through the ring of scars
could then cause an anal fissure. Yet, it might also be conceivable that a fibrosis
would secondarily develop, which is induced by an existent anal fissure.
Miles (1919) misinterpreted the fibrous internal anal sphincter muscle as a ring
of scars and called this structure “pecten band,” without having it examined histo-
logically, however.
For the first time in 1932, Abel and Lond showed the fibrosis of this pecten band
histologically, but did not differentiate it from the internal sphincter muscle.
Eight years later (1940), Fine and Lawes performed biopsies of the correspond-
ing areas in healthy probands and found smooth musculature, but no pecten band.
In 1956, Morgan and Thompson histologically examined the base of anal fis-
sures; they did not find fibrosis, but smooth musculature only.
Gemsenjäger and Ohnacker (1972) carried out detailed histological examina-
tions involving 32 anal fissure patients and divided the seriousness of fibrosis into
three grades: Grade 0 – only musculature, no fibrosis; Grade I – slight-to-moderate
fibrosis; Grade II – severe fibrosis. Nineteen patients did not show fibrosis; 13
patients exhibited moderate-to-severe fibrosis.
Applying the same gradation, Brown et al. (1989) diagnosed fibrosis in all 18
anal fissure patients of their collective in contrast to the “healthy” controls who had
undergone rectal amputation. Three patients showed slight, four moderate, and
eleven patients severe fibrosis.
In 1992, Topf succeeded in clarifying these apparently contradictory findings.
He histologically examined 47 anal canal samples taken from corpses and divided
the process of fibrosing into four grades. Topf understands the fibrosis of the inter-
nal anal sphincter muscle as a physiological aging process, because the grade of
fibrosis corresponds very well with age: Grade I up to 20 years of age, Grade II from
20 to 40 years of age, Grade III between 40 and 80 years of age, and Grade IV over
80 years of age.
Conclusion
Fibrosis of the internal anal sphincter muscle is a physiological aging process of the
muscle. The pecten band as an anatomical structure does not exist.
5.2.3 Traumata
The origin of an anal fissure is explained again and again – also in proctological
textbooks – by the passage of hard stool balls which cause lesions in the anoderm.
Gabriel (1963) writes that anal fissure is the consequence of a trauma. In his opin-
ion, the reason is hyperextension of the anal canal during the passage of thick, hard
masses of stool which causes lesions in the anoderm. Also, Stirnemann and Halter
(1970) believe that mechanical strain during defecation, for instance, induced by
hard scybala, leads to a rupture in the anal canal. According to Neiger (1987),
5.2 Etiopathogenesis
60
tearing of anoderm during the passage of hard stool balls happens at the weakest
spot, the commissures. Further, Marti and Givel (1992) have no doubts that anal
fissure is a crack in the anoderm as a result of the passage of hard stool.
Bailey and Snyder (2000) write that anal fissure is traditionally ascribed to con-
stipation and the passage of hard stool. It is interesting to note that anal fissure
patients are constipated only in a little more than a quarter of the cases on average
(27.9%), so that presumably other etiopathogenetic factors are worth considering
(cf. Sect. 6.4). Lingemann (2001) believes that the mechanical irritation by hard
stool or diarrhea in combination with a local inflammation (papillitis/cryptitis) leads
to lesion in the anoderm. Brühl et al. (2011) write that it is not only hard stool which
causes anal fissures, but also a pulpy or diarrheic stool. Contrary to the abovemen-
tioned different opinions, patients strikingly often report that fissure symptoms
occur after one single bowel evacuation of hard stool.
Genuine accidents lead only to a very small extent to fissure-like wounds in the
anal area, like the introduction of sharp-edged objects into the anus (Black et al.
1982). Foreign objects that were swallowed, for instance, a flat chicken bone (Pradel
et al. 1986) or a rollmops skewer (author’s case, unpublished), can also injure the
tissue while passing through the anus, although even the swallowing of razor blades
by prison inmates or psychiatric patients mostly remains without consequences.
Conclusion
A trauma may induce a fissure. But, in our opinion, local pathologies should
coexist.
5.2.4 Anal Abuse
A frequent cause of anorectal injuries in children is probably anal abuse. Multiple
and deep fissures are found, often off the median line, which should direct suspicion
toward such a pathogenesis, especially when the perineum is involved (Ameh 2001).
Black et al. (1982) saw several cases of multiple anal fissures, but also such with
severe injury of the continence organ involving the peritoneal cave. The majority of
the victims were younger than 16 years of age. The rate of boys abused is 7.5%
(Black et al. 1982) or 11–16% (Jaffe et al. 1975; Ellerstein and Canavan 1980).
Whereas boys are abused during childhood almost as often as girls, their percentage
drops with increasing age (Black et al. 1982).
Girls often suffer significantly less from injuries than boys while they are anally
abused. Pierce (2004) examined three groups of children with regard to fissures and
scars in the anal area. The first group (n = 81) included children, who gave neither
anamnestically nor clinically any reason for suspicion of sexual abuse. Two children
were found with fissures which could be medically explained. The second group (n
= 83) comprised children, who were suspected to be sexually abused, but anal pen-
etration was denied. Anal fissures or scars were found in nine cases (11%), and four
of the nine girls suffered from significant constipation at times. The third group (n
= 50) consisted of children who all displayed strong signs of anal abuse; 41 of them
5 Epidemiology and Etiopathogenesis
61
(84%) had fissures or scars. There was definite proof of anal abuse in 13 cases
because either a confession or a conviction of the offender existed. The other cases
were considered as not proven, despite corresponding suspicious facts. Anal abuse
is difficult to prove, when neither seminal fluid nor sexually transmitted diseases
can be traced. Often, a lot of time passes between the act itself, its detection, and
medical examination, especially when children are concerned. Therefore, the clas-
sic fresh signs like swellings, contusions, bruising, and multiple anal fissures cannot
serve as evidence any more (Pierce 2004).
Definite signs of anal abuse are in the first place multiple fissures (mostly not
median), which are either fresh or in the phase of healing, and heal without any
further therapy when victim and suspect have been separated. Further hints are sig-
nificant constipation (defecation intervals between 3 and 15 days), stool of a thick
or firm quality, pain during defecation, and/or rectal bleeding. Nzimbala and
Bruyninx (2007) describe the ordeal lasting for years of a female patient with recur-
ring anal fissures, who was also subjected to anal abuse. They point out that persist-
ing or permanently recurring gastrointestinal symptoms in combination with anal
affections should direct suspicion toward anal abuse.
5.2.5 Anal Sexual Practices
Formation of fissures as a consequence of anal sexual practices is not uncommon,
especially when homosexuals are concerned. By analogy, heterosexual anal inter-
course can also lead to injuries of the mucosa. Pradel et al. (1986) describe linear
cracks in the mucosa, anal sphincter ruptures, and even perforations of the rectosig-
moid colon by anal fisting (“fist fornication” or “handballing”). Similar injuries also
occur when foreign objects of any conceivable kind (vibrators, bottles, broomsticks,
air pumps, etc.) are introduced during anal ipsation (Barone et al. 1983).
Therapy Splits in the mucosa and anal fissures, caused by anorectal trauma, gener-
ally heal without complications or, if necessary, after local measures such as sitz
baths, locally anesthetizing gel, or stool softeners (Ameh 2001). Severe anorectal
trauma conditions are treated surgically. Diseases, which can be sexually transmit-
ted (chlamydia, gonorrhea, syphilis, HIV, etc.) should be ruled out or, if necessary,
treated accordingly.
5.2.6 Infection
Anal cryptitis is an abscessing, unspecific inflammation of the cryptoglandular
apparatus. The proctodeal glands, which are found more frequently in the area of
the dorsal circumference, are regarded as pathogenetically important factors. An
occlusion of the gland ducts induced by an inflammatory edema with consecutive
formation of retention cysts, penetration of feces into the lumen of the crypt, and
colonization of the crypts with intestinal germs lead consequently to anal cryptitis.
5.2 Etiopathogenesis
62
It is possible that the inflammatory process in the cryptal area has a causal relation-
ship with anal fissures. Therefore, Dohrenbusch et al. (1986) and Klosterhalfen
et al. (1988) consider cryptitis to be the pathomorphological substratum of chronic
anal fissure. According to Raulf and Kolbert (2006), cryptitis can be seen as the
pioneer of fissure formation. Maceration of the adjacent anoderm with correspond-
ingly increased vulnerability may occur due to inflammatory edematous saturation
of tissue by retention or to increased secretion from the cryptal area. Stool of hard
consistency would then lead to superficial perforation of the crypt roof, which then
results in the development of anal fissure.
Conclusion
It is possible that infection of anal crypts paves the way for anal fissure formation.
5.2.7 Ischemia
There are only a few studies on the hypothesis of decreased tissue perfusion:
Klosterhalfen et al. (1988, 1989) performed 20 postmortem angiographic studies
and discovered that the perfusion of the anal canal takes place almost exclusively
through the inferior rectal artery. In 85% of the angiographies, the posterior com-
missure was not supplied at all. But if it was supplied, then only by small-caliber
branches of the inferior rectal artery. This region was continuously perfused at a rate
of only 15% through the branches of the superior rectal artery.
Lund et al. (1999), too, histologically examined preparations taken from eight
corpses and proved that the arteriolar density in the area of the posterior anal com-
missure is significantly lower than that in the remaining anal canal, and this not only
in the submucosa, but also in the internal anal sphincter muscle.
Gibbons and Read (1986), too, assume local ischemia after the use of laser
Doppler velocimetry (LDV) to measure skin perfusion. The radiation of a helium
neon laser is coupled into the skin. Laser Doppler flux distribution provides a rela-
tive measure for the microvascular blood flow of the skin and is mostly given in
arbitrary units (AU). Absolute flow measurements cannot be gained because the
vessel architecture in the measurement range, the local hematocrit value, the hemo-
globin content, the thickness of the epidermis, and thus the exact penetration depth
(1–6 mm) of the laser beam are all unknown. The signal derived from a white sur-
face corresponds to a flux value zero. The measuring signal on the skin contains
information from capillaries, arterioles, and venules. Because of these parameters,
objective measurement using LDV cannot be expected.
Schouten et al. (1994) used LDV in 9 anal fissure patients and in 31 healthy con-
trols. Concerning the healthy controls, perfusion in the posterior segment of the
anoderm was reduced in contrast to the other sectors (12, 3, and 9 o’clock).
Moreover, with regard to the anal fissure patients, they noticed a significant reduc-
tion of the blood flow in the posterior sector, which was inversely proportional to the
anal resting pressure. After sphincterotomy, the blood flow in 27 anal fissure patients
improved by 65%, while anal resting pressure was reduced by 35%.
5 Epidemiology and Etiopathogenesis
63
Conclusion
It is rather unlikely that restricted perfusion of the anoderm is causal for the patho-
genesis of anal fissure. But it might be possible that restricted perfusion supports
fissure formation or impedes spontaneous healing, respectively.
5.2.8 Anatomical Causes
Lockhart-Mummery (1914) suggested that one cause of anal fissure origin was the
particular anatomical structure of the external anal sphincter muscle in the area of
the posterior and anterior anal commissure. The lower end of the muscle was in
reality not laid out circularly and consisted of only a few muscle fibers at the anal
commissures. Lockhart-Mummery therefore believed that the anoderm in the area
of the commissures would have only little protection through the underlying weak
musculature.
Hiller (1931) assumes a restricted elasticity of the anal commissures caused by
external sphincter muscle fibers, which run dorsally or ventrally and serve for the
fixation of the anal canal.
The distribution pattern of anal crypts (Krakovic 1974) and the possible con-
nection with the location of anal fissures have already been dealt with in Sect.
2.6.2.
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5 Epidemiology and Etiopathogenesis