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 fissures 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.

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 anorectal 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 insufficient 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 exacerbations. 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 fissure 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.

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, respectively). 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 disease (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.”

O’Donoghue and Hyland (1997) believe that a combination of “aggressive internists 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 salazosulfapyridine (SASP), prednisolone, and azathioprine. Administering the same active agents, Fleshner et al. (1995) obtained healing rates of 50% with regard to active fissures and of 60% with regard to chronic fissures after surgical therapy. Homan et al. (1976) see only occasionally an indication for surgical intervention. Then, fissurectomy 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 colostomy, 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.