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 1956). According to Nwako, 50% of young patients show skin tags; the gender distribution is almost the same as with adults (Table 5.1).

In contrast to adults, constipation in children seems to play a special role in etiopathogenesis. 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 context, 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 laxatives. 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 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.

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 caliber 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 representative 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 introduction of the catheter increases pain, and a spasm occurs, which means an involuntary 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 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.