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factor. On the other hand, it makes defecation possible due to its relaxation
reflex when the rectal ampulla is distended.
The striated external anal sphincter muscle encloses the internal anal
sphincter muscle at the caudal end of the anal canal. Similar to the striated
skeletal musculature, the external sphincter muscle is capable of a maximal
short-period contraction for the purpose of deliberate action. Cranially, the
striated puborectalis muscle follows, which genetically corresponds to the
lowest part of the levator ani muscle. It encases dorsally the rectum like a
sling, while omitting its ventral parts and inserting into the pubic bone (os
pubis) with broad tendons. The contraction of this muscle leads to a diagonal
sealing of the upper anal canal by a ventral shift of the back wall of the lower
rectum like a crimp connection (“gross anal closure”).
Epithelial Portions of the Continence Organ
The epithelial coating of the anorectum consists of three parts. The epithelium
of the distal part of the anal canal, the anatomical anal canal, is especially
important for the continence function. Here lies the dry, nonkeratinizing squa-
mous epithelium of the anoderm, which due to its intensive supply with sensi-
tive nerve endings is capable to differ between the various aggregate conditions
of the colonic contents. Above the pectinate line, in the section of the surgical
anal canal stemming from the endoderm, a columnar epithelium is found
whose structure is similar to that of the rectal mucosa. Between these two
areas lies the zone of the so-called transitional epithelium (transitional cell
area), which is of individually differing width and is also supplied with sensi-
tive nerves. The histological examination discloses a cylindrical structure.
Macroscopically, the transitional cell area shows a whitish color in contrast to
the reddish shimmering mucosa above, which is not innervated sensitive.
Subepithelial Portions of the Continence Organ
Under the mucosa of the upper anal canal, the corpus cavernosum recti is
located immediately below the epithelium. It is in fact a set of venous vascular
cushions which exist in every individual and are colloquially called “hemor-
rhoids” (Aigner et al. 2006, 2009; Engelhardt et al. 2010). The arterial supply
of this vascular plexus takes place cranially in the tunica submucosa, in par-
ticular through the branches of the superior rectal artery (A. rectalis superior).
The venous discharge runs submucosally partly into the superior rectal vein (V.
rectalis superior) and partly into the venous stems of the middle rectal veins
(Vv. rectalis mediae), while taking its course through the internal anal sphinc-
ter. The virtually permanent contraction of this muscle to maintain continence
leads to a partial obstruction of the venous discharge, while the arterial supply
1 Anatomy
3
remains undisturbed. As a result, the vascular cushions are dammed up, and
thus seal effectively the lumen of the upper anal canal (“hermetic seal”). The
caudal portions of the branches of the superior rectal artery pass through the
muscular rectal wall in a straight direction and reach the corpus cavernosum
recti without taking its course through the submucosa. Additionally, there is
arterial supply of the corpus cavernosum recti from the middle rectal artery (A.
rectalis media), so that this redundant vascularization ensures the function of
the corpus cavernosum under all circumstances.
Neural Portions of the Continence Organ
The neural structures make sure that the different functional areas of the con-
tinence organ are connected with each other and also with the superordinate
nerve centers (Raulf 2004). While the internal anal sphincter muscle is auton-
omous and controlled by stretch receptors in the rectal wall and in the puborec-
talis muscle, the striated muscle portions receive their somatic innervation
from the lowermost lumbar plexus and the sacral part of the spinal cord. From
the viewpoint of anatomy, the course of the branches of the pudendal nerve
(N. pudendus) is important. At the level of the pelvic floor, they run laterally
towards the striated muscle fibers. The pudendal nerve branches are situated
at about 2, 4, 8 and 10 o’clock lithotomy position within the ischioanal fossa
(fossa ischiorectalis). By analogy with a clock, the anus is seen in such a way
that 6 o’clock corresponds to the dorsal circumference, that is, toward the tip
of the coccyx (Fig. 1.1).
Anatomie des Anorektum
PLICA RECTALIS
AMPULLA RECTI
M.LEVATOR ANI
M.PUBORECTALIS
ANALE PAPILLE
LINEA DENTATA
PROKTODAEALDRUESE
M.SPHINCTER INTERNUS
M.SPHINCTER EXTERNUS
ANODERM
LINEA ANOCUTANEA
MORGAGNISCHE KRYPTE
PLEXUS HAEMORRHOIDALIS
Fig. 1.1 Anorectal anatomy, schematic (Wienert and Mlitz 1995)
1.1 Anatomy of the Anorectum
4
1.2 Definition of Anal Fissure
Anal fissures are divided into primary — acute or chronic — and secondary fissures.
They are lesions in the lower anal canal. Primary anal fissures develop as local enti-
ties; secondary fissures develop in the context of a basic disease.
Anal fissure is a painful, linear or spindle-shaped, longitudinal defect in the
highly sensitive anoderm. It often causes a reactive sphincter hypertonia, which pos-
sibly triggers a reduced blood circulation with venous stasis. It is found in the ano-
derm between the pectinate line and the anal verge.
Anal fissures can heal either spontaneously or after therapy. They can recur or
turn from acute into chronic anal fissures (Figs. 1.2 and 1.3).
Fig. 1.2 Acute anal fissure dorsal, erosions perianal
1 Anatomy
5
References
Anatomy
Aigner F, Bodner G, Gruber H et al (2006) The vascular nature of hemorrhoids. J Gastrointest Surg
10:1044–1050
Aigner F, Gruber H, Conrad F et al (2009) Revised morphology and hemodynamics of the anorec-
tal vascular plexus: impact on the course of hemorrhoidal disease. Int J Colorectal Dis
24:105–113
Engelhardt V, Lametschwandtner A, Böhler U et al (2010) Microangioarchitecture of haemor-
rhoids. A scanning electron microscopy study of vascular corrosion casts. Phlebologie
39:12–17
Raulf F (2004) Funktionelle Anatomie des Anorektums. Hautarzt 55:233–239
Wienert V, Mlitz H (1995) Einführung in die Proktologie. Schattauer, Stuttgart
Fig. 1.3 Acute anal fissure ventral, erosions dorsal
References
7
© Springer International Publishing AG 2017
V. Wienert et al., Anal Fissure, DOI 10.1007/978-3-319-49244-5_2
2
Chronic Anal Fissure
2.1 Morphology
Chronic anal fissure presents as longitudinal, deep ulcer, sometimes coated with
smear. Secondary changes can occur in their development, such as hypertrophied
anal papillae close to the proximal edge of the fissure at the level of the pectinate
line, also pathologically altered crypts (anal cryptitis) or sentinel tags (secondary
skin tags) with or without incomplete or complete fistula. At this stage, the wound
edges are scarred and bulging, occasionally callused or undermined. Sometimes,
the transversely running, now and then fibrous tissue of the internal anal sphincter
appears at the fissure floor. It is not the duration of the existence of the anal fissure
that is pathognomonic for the chronic anal fissure, but the appearance of the altera-
tions mentioned earlier. The difficulty of a morphologically related definition of the
chronic anal fissure is dealt with in Chap. 4.
2.2 Location
The analysis of 15 trials comprising a total of 6881 patients in Table 2.1 shows that
anal fissures are located at the posterior midline with a frequency rate between 45.1
and 86.9% and at the anterior midline with a rate between 8.0 and 39.3%. In the
other sectors, they appear with a frequency rate between 0.5 and 12.3%. Goligher
(1975) found ventrally located anal fissures significantly more in women than in
men (10:1).
8
Table 2.1 The location of anal fissures in 15 trials with 6881 patients (in %)
Author (year)
Patients
Location of anal
fissure
Posterior midline
Anterior
midline
Other
locations
(n) (%) (%) (%)
Willemsen (1963) 144 45.1 20.8
Mazier (1972) 1000 74.8 16.5
Soß (1973) 269 84.0 11.5 2.2
Böttcher (1977) 508 77.7 13.5
Kühn (1979) 138 82.0 8.0 0.7
Stürmlinger (1986) 153 81.0 9.2 9.8
Khubchandani and Reed
(1989)
1077 62.0 25.2 0.9
Eißer (1990) 131 74.0 14.1 11.9
Kleinilbeck (1990) 735 79.0 10.0 12.3
Jost et al. (1991) 130 86.9 6.2 1.5
Oh et al. (1995) 1047 75.3 12.9
Hananel and Gordon (1997) 876 73.5 16.4 5.8
Schanne (1998) 56 51.8 39.3
Hasse et al. (2004) 209 79.4 16.3 0.5
Lysy et al. (2006) 408 68.4 21.3
Total 6881
Fig. 2.1 Dorsal median
chronic anal fissure with
sentinel tag
2 Chronic Anal Fissure
9
Fig. 2.2 Ventral and
dorsal median chronic anal
fissure with sentinel tag
Fig. 2.3 Dorsal median
chronic anal fissure with
hypertrophied papilla
(dilating speculum)
2.2 Location
10
Fig. 2.4 Dorsal median
chronic anal fissure with
pronounced secondary
changes
Fig. 2.5 Dorsal median
anal fissure with abscess;
purulent discharge visible
at spontaneous perforation
of abscess
Fig. 2.6 Dorsal median
anal fissure with fistula;
surgical hook used for
exploration
2 Chronic Anal Fissure
11
2.3 Age Distribution
The analysis of seven publications which refer to a total of 2346 anal fissure patients
yields the age distribution in Table 2.2.
The peak incidence occurs in patients between 30 and 50 years of age.
Twenty-four clinical trials with a total of 4978 anal fissure patients show a peak
incidence between 38 and 51.2 years of age (Table 2.3). Anal fissures in children are
relatively rare.
Table 2.2 Anal fissure patients by age groups in seven trials with 2346 patients (in %)
Author (year)
Anal fissure
patients
Years of age
0–10 11–20 21–30 31–40 41–50 51–60 61–70 71–80
(n) (%) (%) (%) (%) (%) (%) (%) (%)
Willemsen (1963) 144 0.8 3.3 23.1 28.1 33.1 8.2 3.3 –
Mazier (1972) 1000 0.5 2.9 12.9 25.9 29.4 18.7 8.6 1.2
Böttcher (1977) 508 – 1.5 14.5 37.0 27.4 20.3 – –
Kühn (1979) 138 – – 10.1 30.4 21.7 18.8 16.7 2.2
Wolff (1986) 272 – 0.7 14.4 22.9 25.8 20.7 10.3 4.7
Stürmlinger (1986) 153 – – 15.7 26.8 22.2 19.0 11.8 4.6
Eißer (1990) 131 – 1.5 12.9 22.8 31.9 24.3 6.1 –
Total 2346
Table 2.3 Median age of 4978 anal fissure patients in 24 trials
Author (year)
Anal fissure patients Median age
(n) (years)
Hardy (1967) 59 48
Fischer et al. (1978) 66 41.9
Abcarian (1980) 300 35.7
Bode et al. (1984) 121 46.8
Hsu and MacKeigan (1984) 1753 42.4
Jensen et al. (1984) 58 39
Wolff (1986) 271 46.3
Khubchandani and Reed (1989) 1355 42.8
Jost (1989) 130 46.3
Prohm (1993) 396 43.9
Leong and Seow-Choen (1995) 34 39
Maria et al. (1998) 15 38
Brisinda et al. (1999) 25/25 45.1/39.2
Altomare et al. (2000) 59/60 43.7/42.7
Brisinda et al. (2002) 75/75 43/45
Lindsey et al. (2003) 40 38.1
Mentes et al. (2003) 61 40
Brisinda et al. (2004) 50/50 41.6/42.6
Giral et al. (2004) 10/11 41/39
Massoud et al. (2005) 25 35.5
Arroyo et al. (2005) 40/40 38/41
Jones et al. (2006) 15 46
Brisinda et al. (2007) 50/50 46.2/42.0
Brown et al. (2007) 24/27 51.2/47.9
Total 4978
2.3 Age Distribution
12
2.4 Gender Distribution
The analysis of 28 trials with 11,577 patients (Table 2.4) shows that women and
men are almost equally affected, females at rates from 38 up to 72.1% and males
from 27.9 up to 62%.
Table 2.4 Anal fissure patient distribution by gender in 33 trials with 11,577 patients (in %)
Author (year)
Anal fissure
patients (n) Female (%) Male (%)
Mazier (1972) 1000 49.1 50.9
Böttcher (1977) 508 46.8 53.2
Marby et al. (1979) 253 38.0 62.0
Kühn (1979) 138 43.5 56.5
Abcarian (1980) 300 47.0 53.0
Hsu and MacKeigan (1984) 859 51.0 49.0
Stürmlinger (1986) 153 52.2 47.8
Wolff (1986) 271 47.2 52.8
Vafai and Mann (1987) 696 60.2 39.8
Lewis et al. (1988) 350 63.1 36.9
Khubchandani and Reed (1989) 1077 57.4 42.6
Jost (1989) 1423 41.4 58.6
Kouba (1990) 833 54.5 45.5
Jost et al. (1991) 130 43.5 56.5
Prohm (1993) 396 49.0 51.0
Pernikoff et al. (1994) 500 57.0 43.0
Jost (1997) 100 43.0 57.0
Littlejohn and Newstead (1997) 352 44.3 55.7
Hananel and Gordon (1997) 876 50.1 49.9
Richard et al. (2000) 38 42.1 57.9
Richard et al. (2000) 44 65.9 34.1
Altomare et al. (2000) 59 43.0 57.0
Altomare et al. (2000) 60 46.0 54.0
Bacher et al. (2000) 126 52.4 47.6
Brisinda et al. (2002) 75 44.0 56.0
Brisinda et al. (2002) 75 49.3 50.7
Bailey et al. (2002) 304 45.4 54.6
Mentes et al. (2003) 61 72.1 27.9
Mentes et al. (2003) 50 64.0 36.0
Liratzopoulos et al. (2006) 246 51.2 48.8
Brisinda et al. (2007) 50 48.0 52.0
Brisinda et al. (2007) 50 58.0 42.0
Pascual et al. (2007) 124 53.2 46.8
Total 11,577
2 Chronic Anal Fissure