시원항병원
051) 331-7275논문발표
| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 17 | Chronic Idiopathic Anal Pain [2001년 5월 DCR] | 2011-11-12 | 3283 |
|
Analysis of Ultrasonography, Pathology, and Treatment
J. Christiansen, M.D., F.R.C.S., E. Bruun, M.D., B. Skjoldbye, M.D., K. Hagen, M.D.
From the Department of Surgery D and Department of Ultrasonography, Herlev Hospital, University of
Copenhagen, Denmark PURPOSE: This study was undertaken to analyze whether intra-anal ultrasound examination, anorectal physiologic evaluation, and histopathologic examination in patients with chronic idiopathic anal pain presented any common features and whether the results of different treatment modalities
correlated with these findings. METHODS: Eighteen patients who met the criteria for chronic idiopathic anal pain were studied. All had an intra-anal ultrasound examination and a complete anoreetal physiologic evaluation. In a selected group of patients, ultrasound-guided biopsy sampies were taken from pathological areas in the internal and external sphincter. Treatment consisted of analgesics only in four patients, 0.2 percent nitroglycerin ointment in four, and ultrasound injection of botulin Cootulinmn toxin, Botox ®) into the intersphincteric space in nine. Two patients, including one who was previously treated with botulin, ultimately had a colostomy.
RESULTS: Four patients were managed satisfactorily on analgesic treatment under the guidance of the hospital's pain clinic. Nitroglycerin ointment resulted in temporary pain relief in one of four patients.
Injection of botulin resulted in a permanent improvement in four patients, a temporary improvement in one patient, and no effect in four patients. Two patients had a colostomy, resulting in complete pain relief. The effect or tack of effect of nitroglycerin ointment and botulin was not related to changes in anal pressure. CONCLUSION: Chronic idiopathic anal pain is a condition of unknown origin for which no proven therapy exists. As in other syndromes based on muscular dystonia, some patients may benefit from injection of botulin.
DISCUSSION
Chronic idiopathic anal pain (CAP) is part of a rather ill-defined group of disorders termed chronic idiopathic perineal pain, which also includes proctalgia fugax and coccygodynia. The main feature
of these syndromes is that no objective abnormalities are found on clinical examination, and the distinctionbbetween the different groups of perineal pain is based solely on the patient's description of the pain and location of tenderness by palpation. Patients classified as having CAP usually describe a pain located at the anus, often with radiation to the
upper anal canal or lowest part of the rectum. In the majority of patients, the pain is present constantly,although its intensity varies. It is usually aggravated by sitting and by defecation and is relieved by lying down. A feeling of obstructed defecation has also been described. The cause and pathogenesis of the syndrome are unknown, but in a few patients, more advanced, instrumental investigations of the anal canal, such as intra-anal ultrasound and magnetic resonance scan, may reveal treatable organic disorders, such as chronic intrasphincteric abscesses and fistulas.
There is no satisfactory treatment for CAP; nonetheless, anal stretch and internal sphincterotomy are still
used in several patients on the assumption that the pain might be caused by a hypertonic anal sphincter, because no objective changes can be demonstrated. We present the clinical course in 18 consecutive patients with CAP who all had an intra-anal ultrasound
investigation, defecography, and a complete anorectal physiology examination. The present study did not reveal any distinct etiologic or pathogenetic findings. The fact that TRUS
demonstrated abnormal findings in 12 of the 18 patients is difficult to place in a pathogenetic context. In a study of TRUS in patients who previously had undergone anal dilation, we found anal sphincter abnormalities of the same type as in the present study in 13 of 20 patients, but none of them had CAP. The single patient in the present study who had an abnormally thick internal sphincter experienced no effect from either nitroglycerin ointment or botulin administration, although resting pressure was decreased by 30 percent. In a study comprising 12 patients with CAP, 12 anal resting pressure was significantly higher than in a
control group (a mean of 67 vs. 44 mmHg). Nine of these patients also had paradoxical puborectalis contraction. In the present study, anal resting pressure exceeded the laboratory's upper normal value of 140 cm H20 in only one patient. Injection of botulin, which reduced resting pressure by- 20 percent, had no effect on the pain. Neill and Swash found an appreciable degree of perineal descent in 21 of 35 patients with CAP, but
because their study did not include a control group, it is not possible to draw any conclusions about its causal relationship with CAP. We found only two patients with abnormal perineal descent, whereas in a previous study from our department, perineal descent during straining in asymptomatic women with a median age of 54 years was between 2 and 8 cm. The degree of perineal descent during straining was still within the range found in patients with anal incontinence and obstructed defecation, i.e., tess than 14 cm. Thus, the present study does not support either increased anal resting pressure, thickening of the internal anal sphincter, or perineal descent as a pathogenetic factor in CAP. As Neill and Swash stated in 1982, there is no satisfactory treatment for CAP, and this is still true.
Because there is no recognizable disease, we have focused on physiologic and structural differences from the normal population, primarily variations in anal sphincter pressure and variation in sphincter structure as studied by ultrasonography and histopathologic examination. The structural changes found by ultrasonography of the internal sphincter were rather nonspecific (Table
2), as were the histologic findings. In three patients, a fibrous band inside the external sphincter was found, but neither ultrasonographic or histologic findings were clearly related to the effect of treatment; one of the three patients who had an effect from the botulin had a biopsy sample taken from the internal sphincter with abnormal echoic area showing normal smooth muscle. Biopsy from the external sphincter with a circular fibrous band in the two remaining patients showed fibrosis. In the above-mentioned study of 12 patients with CAP and increased resting pressure, biofeedback
reduced pressure to the same level as in the control group, and all patients were relieved of their pain after a mean training period of 8 weeks. Re-education sessions were given monthly for 3 months, followed by sessions every third month, resulting in cure of 11 of 12 patients after a mean follow-up of 18 months. This demonstrates, in contrast to the present study, a surprisingly strong correlation between CAP and anal resting pressure and a convincing therapeutic effect of reducing the pressure. The marked difference in this respect between the two studies could suggest a systematic difference in the definition of CAP in the two series. The use of botulin is based on the successful treatment of dystonia of other muscles such as spasmodic torticollis and strabismus. In addition, anismus has been treated successfully by injection of botulin into the puborectalis. The mechanism of action of botulin remains unclear, but the effect is probably not unconditionally linked to a reduction in resting pressure. A systematic study of the effect of botulin on perineal pain syndromes is currently being performed in our department.
Because the etiology and pathogenesis of CAP are unknown and may- be multifactoriaI, it is not likely
that the same treatment wilt have an effect in all patients. An attempt at pressure reduction by application of nitroglycerin ointment appears to be rational. If pressure reduction is obtained and pain diminishes, a more permanent pressure reduction should be achieved either by botulin injection or biofeedback training. Even in the absence of an effect of pressure reduction, injection of botulin may be tried, because its effect is not necessarily linked to a reduction in anal resting pressure. In severe cases in which the above-mentioned therapies are without effect, a colostomy may be the solution, as it was for two of our patients. Given the unknown etiologT, this treatment may also fail, but because both of our patients experienced aggravation of pain after defecation, we anticipated a favorable effect of fecal diversion. We have no experience with biofeedback, but because anal pressure may be a pathogenetic factor in some patients, it may be worth trying as a first treatment option. |
|||