Dear Editor: Anal fissure is a linear ulcer in the squamous epithelium of the distal anal canal, usually located in the posterior midline. Its etiology is not clear yet, but the ischemic cause remains the most commonly supported theory. Pain during defecation is the main symptom indicated by patients, while on physical examination, spasm of the anal canal is a common finding. Although patients may complain of periodic episodes suggesting chronicity, most of the anal fissures at first presentation heal with lifestyle measures, laxatives, and local ointments. Chronicity is widely defined by both chronology and morphology. However, in spite of these treatments, some patients develop a chronic fissure, but so far, the real reason of unhealed fissures has not been investigated. In our practice, we have seen several cases where chronic anal fissure developed into an intersphincteric abscess. The literature is scarce about the subject. Three studies proposed a theory that a chronic anal fissure is the clinical and pathological expression of a coexisting intersphincteric or low transsphincteric fistula [1–3]. Herein, we present a case with anal ultrasound in which a chronic fissure developed into an abscess. A female patient who suffered from anal pain since 3 months was referred to our outpatient clinic. She stated that the pain started after passing hard stools. Her general practitioner had treated her with mononitrate (diltiazem) ointment and macrogol. However, the anal pain persisted and occurred daily during defecation. Her medical history included asthma for which she used inhalation medication with corticosteroids. She had two vaginal births; during the first, an episiotomy was performed. At physical examination, there were no signs of general illness. The peri-anal skin was normal; there was no swelling. A fissure in the posterior midline was noticed. Rectal examination was hardly possible due to the pain, and hypertonia of the (internal) anal sphincter was present. During vaginal examination, there was no suspicion for any pararectal abscess nor signs of dyssynergy of the pelvic floor. Transanal ultrasound revealed a hypo-echogenic reflection in the mucosa that matched a fissure. The macrogol was continued, the topical treatment with diltiazem ointment increased to three times a day to be explicitly applied into the anus. Furthermore, we prescribed oral analgesics and explained the paradoxical functioning of the puborectal muscle during pain and the importance of avoiding straining. After 4 weeks, her pain had almost disappeared. She still used oral analgesics on demand but stopped using the diltiazem. Six weeks later, she returned because the pain had increased. At that time, the pain was continuously present despite the use of oral analgesics. Anal examination revealed a small sentinel polyp posteriorly and hypertonia of the (internal) anal sphincter. On transanal ultrasound, we now saw a hypo-echogenic area posteriorly suspicious for an intersphincteric infection. She was administered oral antibiotics (amoxicillin/clavulanic acid 625 mg), to be taken three times a day during 2 weeks. Three weeks later, she presented with ongoing pain and a painful swelling posterior of the anus. At rectal examination, a * Richelle J. F. Felt-Bersma rjf.felt@vumc.nl