Delley (1855) writes about the symptoms: “In such cases, emptying the bowels is always associated with stabbing pain which in case of an already persistent anal fissure outlasts the act of defecation itself for several hours or even for days and often radiates into the sacral region. In rare cases, but still frequently enough, there are even incidents of loss of consciousness and antiperistaltic movements of the stomach. As a consequence, people afflicted with anal fissure try to delay this painful act as long as possible by deliberately contracting the anal sphincter muscle to reverse defecation for some hours” (translated from the German original).

Likewise, Peters (1920) summarizes the clinical presentation in particular of the acute anal fissure: “Severe, increasing and almost unbearable pain during and especially after defecation, pain which is not restricted to the anus alone but also radiates towards the back, sometimes dull, sometimes nagging, so that in some cases the patient is hampered in his professional activity and has to lie down for hours to go through the same stage of suffering again during the next bowel motion.” Frey (1943) quotes Alexis Boyer mentioning a patient who had to give up his sedentary job and had to accept a place of work where he could stand in order to escape pain attacks.

Nevertheless, Fischl (1927) recommends never to miss out local medical examination, and in case of severe painfulness after prior anesthesia, because “it will keep the physician from ignoring a beginning carcinoma.” According to Passavant (cited by Delley 1855), pain caused by anal fissure can especially develop in children who are infected by worms, and one of them creeps into the fissure during the night. Svehla (1902) describes five cases in which complaints caused by anal fissure were misinterpreted as coxitis. Delley (1855) never or hardly ever states anal fissure in children, but quite often in “the prime of life,” and here preferably in females. Leusden (1925), however, observes anal fissure in twice as many men as in women and also mostly in middle or older age.

Our ancients already recognized and described the polyetiology of anal fissure. For Delley (1855), “the same causes which induce chronic hyperemia, venous stasis and varicose enlargement of the vascular ramifications in the rectal skin” are to be blamed for constipation which could lead to skin cracks in one or more places during the passage of hard, voluminous feces through the anus. Fischl (1927) quotes Boas (1878) who states besides habitual constipation the disproportion between the stool caliber and the lumen of the anus as the most important prerequisite for the development of anal fissure. In more than 50% of all patients with constipation, Fischl (1927) regards anal fissure as the sole reason of their disorder. Rappert (1938) was able to show in animal tests that anal fissure is at least supported by constipation. Delley (1855) believes that a further reason for anal fissure is the “act of giving birth, during which the perineum is pushed forward by the advancing head of the fetus and therefore the anal opening becomes considerably lengthened. Furthermore, severe constipation which usually occurs after birth, slight injuries of the anus, for example, through enemas, cannulas and an unnatural satisfaction of sexual urges” (translated from the German original). Brown (1864, cited by Willemsen 1963) sees a connection between female masturbation and anal fissures and showed that stimulation of the clitoris results in strong sphincter muscle contractions. According to Frey (1943), Boyer also observed in 1818 an accumulated incidence of anal fissures in patients with hemorrhoidal disease or patients who had been surgically treated for this disorder. Leusden (1925) believes hemorrhoidal patients suffering from severe stooling to be also predisposed for anal fissure. In his thesis, Rick (1922) finds anal fissure associated with hemorrhoidal disease in 22 of 34 patients. He quotes Quenu and Hartmann who describe such a coincidence in 70–80% of cases. Besides constipation, Rick (1922) considers also burns, rash, decomposition of sweat, and fecal remains as causes of anal fissure, and also manipulations to increase lust in masturbating women, delivery, and backward fall on the buttocks. Likewise, Hirschmann (cited by Fischl 1927) holds traumata responsible for the development of anal fissure that are caused by passage of abnormally massive stool, introduction or expulsion of foreign bodies, sneezing or coughing, or by faulty use of instruments. Morgagni (1921) and Orbach (1928), too, regard traumata as causes for anal fissure. They particularly mention hard stool, manipulation with foreign objects, pederasty, the birth process, and rubbing when afflicted with pruritus ani. Fischl (1927) however, found traumatic anal fissure to be extremely rare in oriental boys who “professionally” practiced pederasty because they used Vaseline or other lubricants. Leusden (1925) explains that “the mucous membrane in the posterior and anterior commissure is more tightly attached to the anal sphincter muscle below. It is not so movable and therefore more exposed to strains, stretching and possibly also to injuries through hard stool and foreign objects” (translated from the German original). Orbach (1928) explains the persistence of anal fissure chemically as a result of passing stool in the sense of a vicious circle. Blond (1934) attributes the formation of anal fissure to the disintegration of a thrombosed small-caliber knot of varicose veins.

Fischl (1927) states that anal fissures usually occur individually. “If more than one is present, this is a sign of a general tuberculous, gonorrheal, syphilitic infection or a sign of decline of these devastating diseases” (translated from the German original). Morgagni (1921), too, observes anal fissure together with gonorrhea, chancroid (ulcus molle) and syphilis. Peters (1920, cited by Willemsen 1963) assumes a connection between severe itching and oxyuridae, pruritus and anal eczema. The effects of intense scratching would favor anal fissure formation. Meissl (1926) saw anal fissure predominantly in neurasthenic individuals. He is convinced that “the main sign of Fissura ani, namely sphincter muscle spasm, is not the result of one or more cracks in the anal mucous membrane inside or outside the sphincter muscle, but rather the cause of them” (translated from the German original). Rosenbach (1900) concludes from “the fact that primary – not at all or only distantly connected with local irritations – manifestations of spasms occur in other organs, (…) that very likely rectal spasm is not identical with Fissura ani” (translated from the German original). He believes that a “perverse tonic innervation of the anal sphincter muscle apparatus is responsible” for the rectal spasm (translated from the German original). Frey (1943) cites Alexis Boyer who said that he has never observed an anal fissure without spasm, but has observed spasm of the sphincter muscle without an anal fissure.

Fischl (1927) describes fresh anal fissures, which often show a purulent or fibrously adhering coating, and old anal fissures (“I was able to pursue them for twenty years”), which almost always have bulging, indurated, callous edges. Projecting edematous skin at the outer skin of the anus, also called sentinel tag (Peters 1920), is characteristic of the existence of (chronic) anal fissure. To English physicians, this skin tag is known as sentinel pile (Hirschmann 1914). Fischl (1927) points out that “accumulated secretion in the anal fissure prevents wound healing unless excision or ligature of the sentinel tag provided an unobstructed discharge of secretion” (translated from the German original). Leusden (1925) attributes the poor healing tendency to the fact that “to a certain extent, the deliberate immobilization of this opening necessary for healing is not subjected to the owner’s free will” (translated from the German original).

Clinical histories from 1948 through 1958 are the bases of Willemsen’s thesis. Her statistical evaluation gives a high percentage (70.8%) of altered blood counts (in more than 50%, a slight or marked anemia). She discusses a relationship between iron deficiency and the formation of anal fissure, similar to the formation of angular stomatitis.

Delley (1855) describes three stages of anal fissure, namely the linear erosion, the fresh crack in the eroded mucous membrane, and the ulcerous form. Czerny (1903) observes sometimes only a slight laceration of the mucous membrane between hemorrhoidal folds, sometimes rhagades-like ulcers with callous edges. Fischl (1927) describes the anal fissure as a linear defect whose edges become chronically inflamed, indurated, and bulging if they have already existed for a longer period of time. Outside the anus, there is often an inflamed skin fold, similar to a hypertrophied anal papilla. According to Fischl, anal fissure in males is found in nine cases out of ten in the area of the posterior commissure, whereas the rate in females is 60%. The anal fissure in the remaining 40% is found at the anterior commissure or next to it. The reason for this is “that due to the concavity of the sacrum the rectal and anal canals are curved in such a way that the greatest force during the expulsion of stool is directed towards the posterior commissure” (translated from the German original). Acute anal fissures often show a purulent or fibrous coating, whereas chronic anal fissures almost always have bulging, callous edges. For Reichle (1940), too, the posterior commissure is the typical location of anal fissure. In most cases, it is “a flat, linear ulcer of about one cm in length.”