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Dysmenorrhoea
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SYMPOSIUM
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DYSMENORRHOEA Janice S. Kwon, BA, MD,l Robert L. Reid, MD, FRCSC, 2 1Resident,
2Professor, Department of Obstetrics and Gynaecology, 3Division of Reproductive Endocrinology and Infertility, 1,2Queen's University
ABSTRACT
Dysmenorrhoea affects a significant number of women of childbearing age, and has the potential far severe impairment of their daily lives. This article reviews both primary and secondary dysmenorrhoea and the diagnosis and treatment far each. In addition to conventional therapy, this article outlines some of the newer therapeutic options that may play important roles in the future. RESUME
La dysmenorrhee touche un grand nombre de femmes en age de procn~er, et elle peut alrerer gravement leur vie quotidienne. Dans cet article, on examine aIa fois Ia dysmenorrhee primaire et Ia dysmenorrhee secondaire, le diagnostic et le traitement de chacune des celles-ci. En
plus du traitement classique, on decrit certaines des nouvelles options therapeutiques qui joueront sans doute un role important a I' avenir.
J SOC OBSTET GYNAECOL CAN 1997;19:955-62 KEY WORDS
Dysmenorrhea, primary, prostaglandins, secondary. Received on May 10th, 1996. Revised and accepted on June 25th, 1996.
interfere with normal activities resulting in absenteeism from school or work. 1 Dysmenorrhoea is categorized as being either primary or secondary. Primary dysmenorrhoea occurs in the absence of any identifiable physical abnormalities whereas secondary dysmenorrhoea is caused by demonstrable lesions involving the uterus, tubes, ovaries or pelvic peritoneum (Table 1).1 The terms primary and secondary
INTRODUCTION
Dysmenorrhoea is the presence of cyclic pain associated with menstrual periods. The word "dysmenorrhoea" is derived from a Greek root meaning "difficult monthly flow." It is estimated that up to 50 percent of women of childbearing age suffer from dysmenorrhoea and that about 15 percent of these women suffer sufficient discomfort to
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of primary dysmenorrhoea and should suggest a secondary cause. Examination of the patient with primary dysmenorrhoea should be completely normal with no palpable abnormalities of the uterus or adnexae. The abdomen should be soft and non-tender. The diagnosis of primary dysmenorrhoea should be one of exclusion (of secondary causes). When untreated, the monthly anorexia and vomiting associated with severe dysmenorrhoea have been thought to account for a series of three to four transverse ripples on fingernails and toenails (Beau's lines) typically observed in other situations involving acute protein malnutrition. s The pain of primary dysmenorrhoea is attributed to the action of prostaglandins. In the 1930s, intense uterine contractions were observed in women with dysmenorrhoea. By the 1940s, women with dysmenorrhoea were known to have increased electrical and mechanical uterine activity corresponding to their menstrual pain, but the trigger for this was unknown. In 1958, extracts of menstrual fluid were discovered to be powerful muscle stimulants. Shortly thereafter, prostaglandins were isolated from sloughed endometrium. 6 High PGF2a concentrations were found in the menstrual fluid of dysmenorrhoeic women. Prostaglandins, now accepted as the explanation for dysmenorrhoea, have only been isolated from secretory endometrium implying a one-to-one correlation with ovulatory cycles. 7 The absence of primary dysmenorrhoea during the first three to six menstrual cycles of a young woman can be explained by the absence of ovulatory cycles during this time. The uterine activity stimulated by prostaglandins can be intense. Resting pressure of the uterus is about five to 15 mm Hg. Normally, uterine contractions during menses reach pressures of 50 to 80 mm Hg every three to ten minutes, lasting for 15 to 30 seconds. However, in the dysmenorrhoeic woman, these uterine contractions can be up to 400 mm Hg, lasting more than 90 seconds, with less than 15 seconds resting time. Resting pressures may be as high as 80 to 100 mm Hg.l The frequency and intensity of contractions reduce blood flow to the myometrium creating a sort of uterine "angina."B
'l'ABL~ 1CAUSES OF DYSMENORRHOEA PRIMARY - aberrant prostaglandin .bolism
SECONDARY
- endometriosis - inflammatory processes (endometritis, pelvic inflammatory disease) - adenomyosis - intra-uterine polypslfibroids - cervical stenosis (after cervical trauiD~) - sequestered intra-uterineendotnetrium (after endometrial ablation orin aSsoQation with Asherman's syndrome) - referred musculoskeletal pain - somatization
with respect to dysmenorrhoea do not imply a temporal association as they do with amenorrhoea and infertility. PRIMARY DYSMENORRHOEA
The incidence of primary dysmenorrhoea is greatest in women in their late teens to early 20s, however, it can affect women in their 40s. Although conventional teaching suggests that primary dysmenorrhoea decreases after childbearing, recent evidence indicates that increasing age is more important than increasing parity in this process. 2 Other factors that seem to be associated with primary dysmenorrhoea include smoking and lack of exercise. Women smoking for up to 10 years had a relative risk of dysmenorrhoea of 1.3, and those who smoked for 10 to 20 years had a relative risk of 2.8 compared to never-smokers.) Primary dysmenorrhoea has been reported to be less prevalent in women who engage in sports activities, with the severity of dysmenorrhoea being less in those involved in more intense exercise. 4 No significant association has been found between alcohol use and the severity of dysmenorrhoea.) Patients with primary dysmenorrhoea usually complain of crampy or colicky pain in the suprapubic area. The pain may radiate to the back, sacrum, and inner thighs. This symptom occurs in the first one to three days of menstruation. It may be associated with nausea, vomiting, headache or diarrhoea. The association between premenstrual syndrome and dysmenorrhoea is variable, however in some women, such premenstrual symptoms as irritability, nervousness, and depression may persist into the menses compounding the distress due to dysmenorrhoea. Dyspareunia during menses is not a feature
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SECONDARY DYSMENORRHOEA
The factors that cause secondary dysmenorrhoea are more common in older patients, thus, the incidence increases with age as opposed to the situation with primary dysmenorrhoea. The signs and symptoms of secondary
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, , , polyps or fibroids. Ultrasound can be helpful in the diagnosis of adenomyosis by identifying uterine enlargement and myometrial heterogeneity.I 5 Diagnostic laparoscopy will identify endometriosis and hysteroscopy will identify intra-uterine lesions. Rarely, hysteroscopic biopsy of endometrial and superficial myometrial layers using the resectoscopic wire loop can be used to confirm a diagnosis of adenomyosis.I 6 When all investigations fail to provide a diagnosis, the possibility of somatization must be considered. The patient who presents with multiple physical complaints which seem generalized and vague should be questioned about her psychosocial history, including sexual abuse. Screening for sexual abuse may not always be routine in a gynaecologist's practice. Many women often do not initially disclose abuse. The screening process may be facilitated by interviewing the woman alone and expressing concern about the problem of violence against women. Often these women appear evasive and frightened and they may minimize the abuse. These women need to be made aware of community resources, counselling, and legal options, all of which should be familiar to the physician. I7 Anxiety and depression often accompany somatization disorder, and it is not uncommon for patients with this disorder to be using several prescribed and nonprescribed medications. IS
dysmenorrhoea can be quite variable and are usually determined by the underlying disease. History and physical examination are most important for the diagnosis. In the adolescent, outflow tract obstruction must be ruled out, as imperforate hymen and transverse vaginal septum may be associated with painful but hidden menstruation (cryptomenorrhoea). Cervical stenosis may likewise exacerbate menstrual cramps. Pelvic examination may reveal painful nodules in the cui de sac or restricted movement of the uterus suggesting endometriosis, which is perhaps the most common cause of secondary dysmenorrhoea. It has been suggested that there is a direct association between pain and the production of prostaglandins and other products by endometriotic implants. 9,JQ However, consistent response of dysmenorrhoea secondary to endometriosis with prostaglandin synthetase inhibitors has not been reported. A few studies have shown that the severity of pain with endometriosis is not associated with the stage of the disease. lI -1l Vercellini et al. also reported that the frequency of dysmenorrhoea was significantly lower in women with only ovarian endometriosis as compared to those with lesions at other sites (peritoneum, ovary and peritoneum, or vagina}.1l Symmetric enlargement of the uterus may suggest adenomyosis, a condition in which endometrial glands penetrate deeply into the myometrium; the more extensive the adenomyosis the greater the risk of dysmenorrhoea. I4 Asymmetric enlargement of the uterus may suggest the presence of myomata (fibroids). Small intra-uterine polyps or fibroids which may cause severe dysmenorrhoea will frequently go undetected by physical examination. If treatment of presumed primary dysmenorrhoea is unsuccessful, vaginal ultrasound and/or sonohysterography should be performed to evaluate this possibility. Pelvic inflammatory disease can lead to diffuse abdominal symptoms during or after menses. Laboratory tests playa limited role in the evaluation of dysmenorrhoea, and treatment is usually instituted without the need for bloodwork. When medical interventions fail, a complete blood count (CBC) is sometimes helpfuL An elevated white cell count may point to an inflammatory process and a low haemoglobin level may suggest excessive blood loss due to a fibroid or adenomyosis. Bloodwork other than a CBC is not generally usefuL When treatment of presumed primary dysmenorrhoea fails or when physical examination suggests pelvic disease, endovaginal ultrasound may identify intra-uterine
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TREATMENT OF PRIMARY DYSMENORRHOEA NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(N SAl Ds)
In primary dysmenorrhoea, initial treatment is directed toward reduction of prostaglandin production with anyone of a variety of prostaglandin synthetase inhibitors. The NSAIDs that have been routinely used and shown to eliminate dysmenorrhoea include mefenamic acid, meclofenamate sodium, naproxen, and ibuprofen (now available as an over-the-counter product). Two new NSAIDs, tiaprofenic acid and tolfenamic acid, have been shown in preliminary studies to be more effective than mefenamic acid. 19,20 Therapy with NSAIDs for primary dysmenorrhoea is generally so successful that if some response is not evident, the diagnosis of primary dysmenorrhoea should be reconsidered. There are several classes of these drugs, and patients who receive only partial relief from one should be tried on an NSAID from
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, , , another class. In severe cases where nausea and vomiting preclude ingestion of NSAIDs after the onset of dysmenorrhoea, patients should be instructed to recognize impending menstruation and to take the NSAID in advance. 21 It is important to exclude pregnancy before prescribing, as the safety of NSAIDs for the fetus in early pregnancy is unknown. These medications should be avoided in any woman with a history of gastritis or peptic ulcer disease.
Transcutaneous electrical nerve stimulation has been shown to provide very effective pain relief in visceral pain conditions where the pain is believed to be secondary to local ischaemia. In one study, TENS increased local blood flow to skin flaps and reduced stasis and oedema compared to placebo treatment in patients undergoing reconstructive surgery.26 The approach has also been shown to eliminate anginal pain presumably by decreasing myocardial oxygen consumption rather than increasing coronary blood flowY Because the pathophysiology of primary dysmenorrhoea involves ischaemia, the possibility that TENS influences blood flow or oxygen requirements of the uterus has been considered. However, as TENS causes prompt relief from dysmenorrhoea without decreasing intra-uterine pressure, it is most likely that TENS alters the body's ability to perceive pain by inhibiting pain stimuli to the midbrain28 or by increasing levels of endogenous opiates. 29
ORAL CONTRACEPTIVES
Combined oral contraceptive pills (OCPs) are also very effective for treating dysmenorrhoea although their mode of action is still unclear. The OCPs impede endometrial growth and decrease the prostaglandin content of menstrual fluid. As a result, uterine contractility is reducedY,23 More recently, OCPs have been shown to decrease vasopressin levels which may, in part, account for some of the OCP-induced decrease in uterine activity.24 When the effect of OCPs or NSAIDs is less than optimal, a combination of an OCP with an NSAID may be tried.
EXPERIMENTAL MEDICAL THERAPIES MAGNESIUM PIDOLATE
A 1992 study evaluated the effectiveness of magnesium in the form of magnesium pidolate, 4.5 mg orally t.Ld. from the seventh day preceding menses to the third day of menstruation, and found that there was a significant improvement in first day dysmenorrhoea (but not second and third day dysmenorrhoea).3o Practically speaking, this long term therapy for a short duration of benefit is unlikely to be clinically useful.
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
For various reasons some women are unable to take NSAIDs and/or OCPs. Transcutaneous electrical nerve stimulation (TENS) is a non-pharmacological method that has been shown to be effective for pain relief in a variety of conditions, including dysmenorrhoea. 25 The few reported studies on TENS are small and have failed to control for a placebo response. The role of TENS is likely to be limited to the treatment of dysmenorrhoeic women who cannot take NSAIDs or OCPs and those who wish non-pharmacological intervention. One treatment session of TENS lasting only a few minutes is often enough to break an attack of dysmenorrhoea. In some patients, several short treatment sessions are necessary. Some women report the high intensity TENS to be painful but most willingly accept a short period of pain to obtain relief from their dysmenorrhoea. The equipment is available as a compact, portable unit that can be obtained from a physiotherapist. It delivers a constant current at a set amperage and frequency through electrodes applied to the skin. For relief of dysmenorrhoea, TENS is applied to the lower abdomen suprapubically, right and lefr iliac fossae up to the umbilicus, and sacro-iliac region.
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CALCIUM CHANNEL BLOCKERS
Nicardipine has been described as an effective alternative for an adolescent refractory to standard treatments for dysmenorrhoea. 31 This promising medical approach warrants more detailed study. BETA-2 (~2) RECEPTOR AGONISTS
Such medications as ritodrine and vasodilan which have been used to decrease uterine contractility in preterm labour have yet to be systematically studied for use in dysmenorrhoea. Akerlund et al. reported the efficacy of intravenous terbutaline, a selective ~2 receptor agonist, in 11 women with severe primary dysmenorrhoea. All patients reported pain relief within one minute after injection of terbutaline, but this effect only lasted between one and two hours.32 Further trials with selective ~2 receptor agonists may be warranted.
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, , , DANAZOL
HYSTERECTOMY
Danazol has been found to be effective in reducing dysmenorrhoea in women with endometriosis. 33,34 Its role in the management of primary dysmenorrhoea has not yet been investigated.
Hysterectomy may be indicated in the patient whose childbearing is complete and who is suffering from refractory dysmenorrhoea. 38 TREATMENT OF SECONDARY DYS MEN 0 RRH 0 EA
OMEGA-3 POLYUNSATURATED FATTY ACIDS
Omega-3 fatty acids compete with omega-6 fatty acids (which are abundant in the western diet) for the production of prostaglandins and leukotrienes through incorporation into cell wall phospholipids and competition at the prostaglandin synthetase level. Just before menstruation, omega-6 fatty acids, particularly arachidonic acid, are released from the cell wall which result in a cascade of prostaglandins and leukotrienes in the uterus, resulting in dysmenorrhoea. Hansen et al. found that competitive interaction between omega-3 and omega-6 fatty acids resulted in the production of less potent prostaglandins (POE3) and leukotrienes (LTBs, LTCs).35 Recently, Harel et 01. reported that dietary supplementation with omega-3 fatty acids (fish oil) reduced dysmenorrhoea in adolescents. 36 More studies in different populations are needed to address the limitations as well as the amount and frequency of fish oil that should be used. Fish oil has the advantage of being a natural supplement, and may be viewed favourably as treatment for dysmenorrhoea if proven safe and effective in future studies.
Only specific therapy aimed at correcting the underlying cause of secondary dysmenorrhoea will ultimately be successful, whether it be used for treating endometriosis, removing a myoma, polyp, or intra-uterine contraceptive device. In a prospective randomized double blind trial, laser laparoscopic ablation of minimal, mild, and moderate endometriosis achieved pain control superior to expectant management six months after surgery.39 Presacral neurectomy has been used for the treat- , ment of pelvic pain associated with endometriosis. 40 The role of presacral neurectomy in the treatment of dysmenorrhoea is controversial. Nezhat et 01. reported a significant alleviation of dysmenorrhoea in 92 percent of those undergoing laparoscopic presacral neurectomy one year postoperativelyY Tjaden et al. reported that 88 percent of their subjects with severe dysmenorrhoea and stage III to IV endometriosis who were treated with presacral neurectomy remained pain-free after 42 months of follow-up. None of the subjects who was treated by conservative surgery (resection of endometriotic lesions) was pain-free at follow-upY In contrast, the randomized trial by Candiani et al. reported no difference in pain relief for patients with endometriosis and dysmenorrhoea treated with either presacral neurectomy or conservative surgery, in fact, constipation and urinary urgency developed or worsened in more patients undergoing presacral neurectomy.43 The long term benefits of presacral neurectomy have not been established. Laser ablation of the uterosacral ligaments has also been used by some clinicians at the time of laparoscopic assessment. To date, no controlled trial has demonstrated convincingly the effectiveness of this approach.44.45
SURGERY ENDOMETRIAL ABLATION
This is a relatively new procedure that is usually employed for treatment of refractory menorrhagia. Short term studies have confirmed the efficacy of endometrial ablation not only for excessive menstrual flow but also for associated dysmenorrhoea. 37 Of all menorrhagic women with dysmenorrhoea, 76 percent reported either marked improvement or cure. At times, endometrial ablation may leave a focus of endometrium with no route for the escape of blood, resulting in severe dysmenorrhoea in an apparently amenorrhoeic woman. Ultrasound can establish the diagnosis, and curettage will frequently relieve the obstruction.
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CONCLUSIONS
Primary dysmenorrhoea generally affects adolescents and younger women and occurs in the absence of underlying gynaecologic lesions. Aberrant prostaglandin metabolism or activity increases uterine activity resulting in myometrial ischaemia and pain. The initial treatment for
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, , , 10. Stripling MC, Martin DC, Chatman DL, Vander Swaag R, Poston WM. Subtle appearance of endometriosis. Fertil SteriI1988;49:427. 11. Stout AL, Steege JG, Dodson WC, Hughes CL. Relationship of laparoscopic findings to self-report of pelvic pain. Am J Obstet Gynecol1991 ;164:73. 12. Fedele L, Parazzini F, Bianchi S, Arcaini L, Candiani GB. Stage and localization of pelvic endometriosis and pain. Fertil Steril 1990;53: 155. 13. Vercellini P, Trespidi L, De Giorgi 0, Cortesi I, Parazzini F, Crosignani PG. Endometriosis and pelvic pain: relation to disease stage and localization. Fertil Steril 1996;65:299-304. 14. Nishida M. Relationship between the onset of dysmenorrhea and histologic finding in adenomyosis. Am J Obstet Gynecol1991 ;165:229-31. 15. Brosens JJ, de Sousa NM, Barker FG, Paraschos T, Winston RM. Endovaginal ultrasonography in the diagnosis of adenomyosis uteri; identifying the predictive characteristics. Br J Obstet Gynaecol 1995;102:471-4. 16. McCausland AM. Hysteroscopic myometrial biopsy: its use in diagnosing adenomyosis and its clinical application. Am J Obstet GynecoI1992;166:1619-28. 17. ACOG Technical Bulletin. The battered woman. 1989;124:1-8. 18. Waldinger, RJ. Somatization Disorder. Psychiatry, Second Edition. American Psychiatric Press, Inc. 1990:226.
primary dysmenorrhoea is either with NSAIDs or OCPs, depending on the contraceptive needs and individual characteristics of the affected woman. If one approach fails, the other should be tried and then both in combination. When this combination is unsuitable or ineffective, a trial of transcutaneous electrical nerve stimulation may be warranted. Varieties of other medications have been used in such circumstances but their use must still be considered experimental. Thorough and timely investigation of women who fail to respond to these approaches will usually reveal the underlying cause of secondary dysmenorrhoea. Somatization should always be considered. The long term effects of such newer techniques as presacral neurectomy and laser ablation of uterosacral ligaments have not yet been established, although some clinicians have advocated their use for intractable, debilitating pain. When no cause is found to explain dysmenorrhoea and conventional therapies fail to provide relief, hysterectomy may be considered in women who have completed childbearing. REFERENCES 1. 2.
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19. Tilyard MW, Dovey SM. A comparison of tiaprofenic acid, mefenamic acid and placebo in the treatment of dysmenorrhea in general practice. Aus N Z J Obstet Gynaecol 1992;32: 165-8. 20. Delgado J, Simonin G, Servier C, Garcia R, Yoma J. Tolfenamic acid and mefenamic acid in the treatment of primary dysmenorrhea. Pharmacol Toxico11994;75 suppl 2:89-91. 21. Benassi L, Bertani D, Avanzini A. An attempt at real prophylaxis of primary dysmenorrhea: comparison between meclofenamate sodium and naproxen sodium. Clin Exp Obstet GynecoI1993;20:102-7. 22. Lalos 0, Joelsson I. Effect of an oral contraceptive on uterine tonicity in women with primary dysmenorrhea. Acta Obstet Gynecol Scand 1981 ;60:229-32. 23. Milsom I, Sundell G, Andersch B. The influence of different combined oral contraceptives on the prevalence and severity of dysmenorrhea. Contraception 1990;42:497-506. 24. Ekstrom P, Akerlund M, Forsling M, Kindahl H, Laudanski T, Mrugacz G. Stimulation of vasopressin release in women with primary dysmenorrhoea and after oral con-
Smith RP. Cyclic pelvic pain and dysmenorrhea. Obstet Gynecol Clin North Am 1993;20:753-64. Heisterberg L. Factors influencing spontaneous abortion, dyspareunia, dysmenorrhea and pelvic pain. Obstet Gyneco11993;81 :594-7. Parazzini F, Tozzi L, Mezzopane R, Luchini L, Marchini M, Fedele L. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology 1994;5: 469-72. Izzo A, Labriola D. Dysmenorrhea and sports activities in adolescents. Clin Exp Obstet GynecoI1991;18: 109-16. Colver GB, Dawber RPR. Multiple Beau's lines due to dysmenorrhoea. Br J Dermatol 1984;111 :111-3. Chambers PL, Pickles VR. Plain-muscle stimulants in extracts of menstrual fluid and of endometrial curettings. J PhysioI1958;144:68. Merck Sharp and Dohme Research Laboratories. Primary dysmenorrhea. The Merck Manual, fifteenth edition 1987:1712. Akerlund M, Bengtsson LP, Carter AM. A technique for
traception treatment - effect on uterine contractility. Br J
monitoring endometrial or decidual blood flow with an
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Obstet Gynaecol 1992;99:680-4. 25. Milsom I, Hedner N, Mannheimer C. A comparative study of the effect of high intensity transcutaneous electrical
intra-uterine thermister probe. Acta Obstet Gynecol Scand 1975;54:469-77. Vernon MW, Beard JS, Graves K, Wilson E. Classification
nerve stimulation and oral naproxen on intrauterine pressure and menstrual pain in patients with primary dysmen-
of endometriotic implants by morphologic appearance and capacity to synthesize prostaglandin F. Fertil Steril 1991 ;56:230.
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orrhea. Am J Obstet GynecoI1994;170:123-9.
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, , , 42. Tjaden B, Schlaff WD, Kimball A. Rock JA. The efficacy of presacral neurectomy for the relief of midline dysmenorrhea.ObstetGynecoI1990;76:89-91. 43. Candiani GB, Fedele L, Vercellini P, Bianchi 5, Di Nola G. Presacral neurectomy for the treatment of pelvic pain associated wtih endometriosis: a controlled study. Am J ObstetGynecoI1992;167:100-3. 44. Vercellini P, Fedele L, Bianchi 5, Candiani GB. Pelvic denervation for chronic pain associated with endometriosis: fact orfancy? Am J Obstet GynecoI1991;165:745-9. 45. Lee RB, Stone K, Magelssen D, Belts RP, Benson WI. Presacral neurectomy for chronic pelvic pain. Obstet GynecoI1986;68:517-21.
26. Lundeberg T, Kjartansson J, Samuelsson U. Effect of electrical stimulation on healing of ischaemic skin flaps. Lancet 1988;2:712-4. 27. Mannheimer C, Eliasson T, Andersson B, et a/. The effects of spinal cord stimulation in pacing-induced angina pectoris and possible mechanisms of action. Br Med J 1993;307:477-80. 28. Smith RP, Heltzel JA. Interrelation of analgesia and uterine activity in women with primary dysmenorrhea. J Reprod Med 1991 ;36:260-4. 29. Salar G, Job I, Mingrino 5, et a/. Effect of transcutaneous electrical nerve stimulation on CSF beta-endorphin content in patients without pain problems. Pain 1981;10:169. 30. Benassi L, Barletta FP, Baroncini L, et a/. Effectiveness of magnesium pidolate in the prophylactic treatment of primary dysmenorrhea. Clin Exp Obstet Gynecol 1992;19:176-9. 31. Earl DT, Mercola JM. Calcium channel blockers and dysmenorrhea. J Adol Health 1992;13:107-8. 32. Akerlund M, Andersson KE, Ingemarsson I. Effects of terbutaline on myometrial activity, uterine blood flow and lower abdominal pain in women with primary dysmenorrhoea. Br J Obstet Gynaecol 1976;84:673-8. 33. Cirkel U, Ochs H, Schneider HP. A randomized, comparative trial of triptorelin depot and danazol in the treatment of endometriosis. Eur J Obstet Gynecol Reprod Bioi 1995;59:61-9. 34. Adamson GD, Kwei L, Edgren RA. Pain of endometriosis: effects of nafarelin and danazol therapy. Intemational Journal of Fertility and Menopausal Studies 1994;39:215-7. 35. Hansen HS, Olsen SF. Dietary (n-3)-fatty acids, prostaglandins, and prolonged gestation in humans. Prog Clin Bioi Res 1988;282:305-17. 36. Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-3 polyunsaturated fatty acids: the management of dysmenorrhea in adolescents. Am J Obstet GynecoI1996;174:1335-8. 37. Fraser IS, Angsuwanthana 5, Mahmoud F, Yezerki S. Short and medium term outcomes after rollerball endometrial ablation for menorrhagia. Med J Aus 1993;158:454-7. 38. SOGC Clinical Practice Guidelines, No. 47, April 1996; Clinical Practice Guidelines for Hysterectomy. 39. Sutton CJG, Ewen SP, Whitelaw N, Haines P. Prospective randomized double blind controlled trial of laser laparoscopy in treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril 1994;62:696-700. 40. Candiani GB, Fedele L, Vercellini P, Bianchi 5, Di Nola G. Presacral neurectomy for the treatment of pelvic pain associated with endometriosis: a controlled study. Am J Obstet GynecoI1992;167:100-3. 41. Nezhat C, Nezhat F. A simplified method of laparoscopic presacral neurectomy for the treatment of central pelvic pain due to endometriosis. Br J Obstet Gynaecol 1992;99:659-63.
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SYMPOSIUM
, , , , , , ,
DYSMENORRHOEA Janice S. Kwon, BA, MD,l Robert L. Reid, MD, FRCSC, 2 1Resident,
2Professor, Department of Obstetrics and Gynaecology, 3Division of Reproductive Endocrinology and Infertility, 1,2Queen's University
ABSTRACT
Dysmenorrhoea affects a significant number of women of childbearing age, and has the potential far severe impairment of their daily lives. This article reviews both primary and secondary dysmenorrhoea and the diagnosis and treatment far each. In addition to conventional therapy, this article outlines some of the newer therapeutic options that may play important roles in the future. RESUME
La dysmenorrhee touche un grand nombre de femmes en age de procn~er, et elle peut alrerer gravement leur vie quotidienne. Dans cet article, on examine aIa fois Ia dysmenorrhee primaire et Ia dysmenorrhee secondaire, le diagnostic et le traitement de chacune des celles-ci. En
plus du traitement classique, on decrit certaines des nouvelles options therapeutiques qui joueront sans doute un role important a I' avenir.
J SOC OBSTET GYNAECOL CAN 1997;19:955-62 KEY WORDS
Dysmenorrhea, primary, prostaglandins, secondary. Received on May 10th, 1996. Revised and accepted on June 25th, 1996.
interfere with normal activities resulting in absenteeism from school or work. 1 Dysmenorrhoea is categorized as being either primary or secondary. Primary dysmenorrhoea occurs in the absence of any identifiable physical abnormalities whereas secondary dysmenorrhoea is caused by demonstrable lesions involving the uterus, tubes, ovaries or pelvic peritoneum (Table 1).1 The terms primary and secondary
INTRODUCTION
Dysmenorrhoea is the presence of cyclic pain associated with menstrual periods. The word "dysmenorrhoea" is derived from a Greek root meaning "difficult monthly flow." It is estimated that up to 50 percent of women of childbearing age suffer from dysmenorrhoea and that about 15 percent of these women suffer sufficient discomfort to
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T
T
of primary dysmenorrhoea and should suggest a secondary cause. Examination of the patient with primary dysmenorrhoea should be completely normal with no palpable abnormalities of the uterus or adnexae. The abdomen should be soft and non-tender. The diagnosis of primary dysmenorrhoea should be one of exclusion (of secondary causes). When untreated, the monthly anorexia and vomiting associated with severe dysmenorrhoea have been thought to account for a series of three to four transverse ripples on fingernails and toenails (Beau's lines) typically observed in other situations involving acute protein malnutrition. s The pain of primary dysmenorrhoea is attributed to the action of prostaglandins. In the 1930s, intense uterine contractions were observed in women with dysmenorrhoea. By the 1940s, women with dysmenorrhoea were known to have increased electrical and mechanical uterine activity corresponding to their menstrual pain, but the trigger for this was unknown. In 1958, extracts of menstrual fluid were discovered to be powerful muscle stimulants. Shortly thereafter, prostaglandins were isolated from sloughed endometrium. 6 High PGF2a concentrations were found in the menstrual fluid of dysmenorrhoeic women. Prostaglandins, now accepted as the explanation for dysmenorrhoea, have only been isolated from secretory endometrium implying a one-to-one correlation with ovulatory cycles. 7 The absence of primary dysmenorrhoea during the first three to six menstrual cycles of a young woman can be explained by the absence of ovulatory cycles during this time. The uterine activity stimulated by prostaglandins can be intense. Resting pressure of the uterus is about five to 15 mm Hg. Normally, uterine contractions during menses reach pressures of 50 to 80 mm Hg every three to ten minutes, lasting for 15 to 30 seconds. However, in the dysmenorrhoeic woman, these uterine contractions can be up to 400 mm Hg, lasting more than 90 seconds, with less than 15 seconds resting time. Resting pressures may be as high as 80 to 100 mm Hg.l The frequency and intensity of contractions reduce blood flow to the myometrium creating a sort of uterine "angina."B
'l'ABL~ 1CAUSES OF DYSMENORRHOEA PRIMARY - aberrant prostaglandin .bolism
SECONDARY
- endometriosis - inflammatory processes (endometritis, pelvic inflammatory disease) - adenomyosis - intra-uterine polypslfibroids - cervical stenosis (after cervical trauiD~) - sequestered intra-uterineendotnetrium (after endometrial ablation orin aSsoQation with Asherman's syndrome) - referred musculoskeletal pain - somatization
with respect to dysmenorrhoea do not imply a temporal association as they do with amenorrhoea and infertility. PRIMARY DYSMENORRHOEA
The incidence of primary dysmenorrhoea is greatest in women in their late teens to early 20s, however, it can affect women in their 40s. Although conventional teaching suggests that primary dysmenorrhoea decreases after childbearing, recent evidence indicates that increasing age is more important than increasing parity in this process. 2 Other factors that seem to be associated with primary dysmenorrhoea include smoking and lack of exercise. Women smoking for up to 10 years had a relative risk of dysmenorrhoea of 1.3, and those who smoked for 10 to 20 years had a relative risk of 2.8 compared to never-smokers.) Primary dysmenorrhoea has been reported to be less prevalent in women who engage in sports activities, with the severity of dysmenorrhoea being less in those involved in more intense exercise. 4 No significant association has been found between alcohol use and the severity of dysmenorrhoea.) Patients with primary dysmenorrhoea usually complain of crampy or colicky pain in the suprapubic area. The pain may radiate to the back, sacrum, and inner thighs. This symptom occurs in the first one to three days of menstruation. It may be associated with nausea, vomiting, headache or diarrhoea. The association between premenstrual syndrome and dysmenorrhoea is variable, however in some women, such premenstrual symptoms as irritability, nervousness, and depression may persist into the menses compounding the distress due to dysmenorrhoea. Dyspareunia during menses is not a feature
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SECONDARY DYSMENORRHOEA
The factors that cause secondary dysmenorrhoea are more common in older patients, thus, the incidence increases with age as opposed to the situation with primary dysmenorrhoea. The signs and symptoms of secondary
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, , , polyps or fibroids. Ultrasound can be helpful in the diagnosis of adenomyosis by identifying uterine enlargement and myometrial heterogeneity.I 5 Diagnostic laparoscopy will identify endometriosis and hysteroscopy will identify intra-uterine lesions. Rarely, hysteroscopic biopsy of endometrial and superficial myometrial layers using the resectoscopic wire loop can be used to confirm a diagnosis of adenomyosis.I 6 When all investigations fail to provide a diagnosis, the possibility of somatization must be considered. The patient who presents with multiple physical complaints which seem generalized and vague should be questioned about her psychosocial history, including sexual abuse. Screening for sexual abuse may not always be routine in a gynaecologist's practice. Many women often do not initially disclose abuse. The screening process may be facilitated by interviewing the woman alone and expressing concern about the problem of violence against women. Often these women appear evasive and frightened and they may minimize the abuse. These women need to be made aware of community resources, counselling, and legal options, all of which should be familiar to the physician. I7 Anxiety and depression often accompany somatization disorder, and it is not uncommon for patients with this disorder to be using several prescribed and nonprescribed medications. IS
dysmenorrhoea can be quite variable and are usually determined by the underlying disease. History and physical examination are most important for the diagnosis. In the adolescent, outflow tract obstruction must be ruled out, as imperforate hymen and transverse vaginal septum may be associated with painful but hidden menstruation (cryptomenorrhoea). Cervical stenosis may likewise exacerbate menstrual cramps. Pelvic examination may reveal painful nodules in the cui de sac or restricted movement of the uterus suggesting endometriosis, which is perhaps the most common cause of secondary dysmenorrhoea. It has been suggested that there is a direct association between pain and the production of prostaglandins and other products by endometriotic implants. 9,JQ However, consistent response of dysmenorrhoea secondary to endometriosis with prostaglandin synthetase inhibitors has not been reported. A few studies have shown that the severity of pain with endometriosis is not associated with the stage of the disease. lI -1l Vercellini et al. also reported that the frequency of dysmenorrhoea was significantly lower in women with only ovarian endometriosis as compared to those with lesions at other sites (peritoneum, ovary and peritoneum, or vagina}.1l Symmetric enlargement of the uterus may suggest adenomyosis, a condition in which endometrial glands penetrate deeply into the myometrium; the more extensive the adenomyosis the greater the risk of dysmenorrhoea. I4 Asymmetric enlargement of the uterus may suggest the presence of myomata (fibroids). Small intra-uterine polyps or fibroids which may cause severe dysmenorrhoea will frequently go undetected by physical examination. If treatment of presumed primary dysmenorrhoea is unsuccessful, vaginal ultrasound and/or sonohysterography should be performed to evaluate this possibility. Pelvic inflammatory disease can lead to diffuse abdominal symptoms during or after menses. Laboratory tests playa limited role in the evaluation of dysmenorrhoea, and treatment is usually instituted without the need for bloodwork. When medical interventions fail, a complete blood count (CBC) is sometimes helpfuL An elevated white cell count may point to an inflammatory process and a low haemoglobin level may suggest excessive blood loss due to a fibroid or adenomyosis. Bloodwork other than a CBC is not generally usefuL When treatment of presumed primary dysmenorrhoea fails or when physical examination suggests pelvic disease, endovaginal ultrasound may identify intra-uterine
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TREATMENT OF PRIMARY DYSMENORRHOEA NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(N SAl Ds)
In primary dysmenorrhoea, initial treatment is directed toward reduction of prostaglandin production with anyone of a variety of prostaglandin synthetase inhibitors. The NSAIDs that have been routinely used and shown to eliminate dysmenorrhoea include mefenamic acid, meclofenamate sodium, naproxen, and ibuprofen (now available as an over-the-counter product). Two new NSAIDs, tiaprofenic acid and tolfenamic acid, have been shown in preliminary studies to be more effective than mefenamic acid. 19,20 Therapy with NSAIDs for primary dysmenorrhoea is generally so successful that if some response is not evident, the diagnosis of primary dysmenorrhoea should be reconsidered. There are several classes of these drugs, and patients who receive only partial relief from one should be tried on an NSAID from
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, , , another class. In severe cases where nausea and vomiting preclude ingestion of NSAIDs after the onset of dysmenorrhoea, patients should be instructed to recognize impending menstruation and to take the NSAID in advance. 21 It is important to exclude pregnancy before prescribing, as the safety of NSAIDs for the fetus in early pregnancy is unknown. These medications should be avoided in any woman with a history of gastritis or peptic ulcer disease.
Transcutaneous electrical nerve stimulation has been shown to provide very effective pain relief in visceral pain conditions where the pain is believed to be secondary to local ischaemia. In one study, TENS increased local blood flow to skin flaps and reduced stasis and oedema compared to placebo treatment in patients undergoing reconstructive surgery.26 The approach has also been shown to eliminate anginal pain presumably by decreasing myocardial oxygen consumption rather than increasing coronary blood flowY Because the pathophysiology of primary dysmenorrhoea involves ischaemia, the possibility that TENS influences blood flow or oxygen requirements of the uterus has been considered. However, as TENS causes prompt relief from dysmenorrhoea without decreasing intra-uterine pressure, it is most likely that TENS alters the body's ability to perceive pain by inhibiting pain stimuli to the midbrain28 or by increasing levels of endogenous opiates. 29
ORAL CONTRACEPTIVES
Combined oral contraceptive pills (OCPs) are also very effective for treating dysmenorrhoea although their mode of action is still unclear. The OCPs impede endometrial growth and decrease the prostaglandin content of menstrual fluid. As a result, uterine contractility is reducedY,23 More recently, OCPs have been shown to decrease vasopressin levels which may, in part, account for some of the OCP-induced decrease in uterine activity.24 When the effect of OCPs or NSAIDs is less than optimal, a combination of an OCP with an NSAID may be tried.
EXPERIMENTAL MEDICAL THERAPIES MAGNESIUM PIDOLATE
A 1992 study evaluated the effectiveness of magnesium in the form of magnesium pidolate, 4.5 mg orally t.Ld. from the seventh day preceding menses to the third day of menstruation, and found that there was a significant improvement in first day dysmenorrhoea (but not second and third day dysmenorrhoea).3o Practically speaking, this long term therapy for a short duration of benefit is unlikely to be clinically useful.
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
For various reasons some women are unable to take NSAIDs and/or OCPs. Transcutaneous electrical nerve stimulation (TENS) is a non-pharmacological method that has been shown to be effective for pain relief in a variety of conditions, including dysmenorrhoea. 25 The few reported studies on TENS are small and have failed to control for a placebo response. The role of TENS is likely to be limited to the treatment of dysmenorrhoeic women who cannot take NSAIDs or OCPs and those who wish non-pharmacological intervention. One treatment session of TENS lasting only a few minutes is often enough to break an attack of dysmenorrhoea. In some patients, several short treatment sessions are necessary. Some women report the high intensity TENS to be painful but most willingly accept a short period of pain to obtain relief from their dysmenorrhoea. The equipment is available as a compact, portable unit that can be obtained from a physiotherapist. It delivers a constant current at a set amperage and frequency through electrodes applied to the skin. For relief of dysmenorrhoea, TENS is applied to the lower abdomen suprapubically, right and lefr iliac fossae up to the umbilicus, and sacro-iliac region.
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CALCIUM CHANNEL BLOCKERS
Nicardipine has been described as an effective alternative for an adolescent refractory to standard treatments for dysmenorrhoea. 31 This promising medical approach warrants more detailed study. BETA-2 (~2) RECEPTOR AGONISTS
Such medications as ritodrine and vasodilan which have been used to decrease uterine contractility in preterm labour have yet to be systematically studied for use in dysmenorrhoea. Akerlund et al. reported the efficacy of intravenous terbutaline, a selective ~2 receptor agonist, in 11 women with severe primary dysmenorrhoea. All patients reported pain relief within one minute after injection of terbutaline, but this effect only lasted between one and two hours.32 Further trials with selective ~2 receptor agonists may be warranted.
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, , , DANAZOL
HYSTERECTOMY
Danazol has been found to be effective in reducing dysmenorrhoea in women with endometriosis. 33,34 Its role in the management of primary dysmenorrhoea has not yet been investigated.
Hysterectomy may be indicated in the patient whose childbearing is complete and who is suffering from refractory dysmenorrhoea. 38 TREATMENT OF SECONDARY DYS MEN 0 RRH 0 EA
OMEGA-3 POLYUNSATURATED FATTY ACIDS
Omega-3 fatty acids compete with omega-6 fatty acids (which are abundant in the western diet) for the production of prostaglandins and leukotrienes through incorporation into cell wall phospholipids and competition at the prostaglandin synthetase level. Just before menstruation, omega-6 fatty acids, particularly arachidonic acid, are released from the cell wall which result in a cascade of prostaglandins and leukotrienes in the uterus, resulting in dysmenorrhoea. Hansen et al. found that competitive interaction between omega-3 and omega-6 fatty acids resulted in the production of less potent prostaglandins (POE3) and leukotrienes (LTBs, LTCs).35 Recently, Harel et 01. reported that dietary supplementation with omega-3 fatty acids (fish oil) reduced dysmenorrhoea in adolescents. 36 More studies in different populations are needed to address the limitations as well as the amount and frequency of fish oil that should be used. Fish oil has the advantage of being a natural supplement, and may be viewed favourably as treatment for dysmenorrhoea if proven safe and effective in future studies.
Only specific therapy aimed at correcting the underlying cause of secondary dysmenorrhoea will ultimately be successful, whether it be used for treating endometriosis, removing a myoma, polyp, or intra-uterine contraceptive device. In a prospective randomized double blind trial, laser laparoscopic ablation of minimal, mild, and moderate endometriosis achieved pain control superior to expectant management six months after surgery.39 Presacral neurectomy has been used for the treat- , ment of pelvic pain associated with endometriosis. 40 The role of presacral neurectomy in the treatment of dysmenorrhoea is controversial. Nezhat et 01. reported a significant alleviation of dysmenorrhoea in 92 percent of those undergoing laparoscopic presacral neurectomy one year postoperativelyY Tjaden et al. reported that 88 percent of their subjects with severe dysmenorrhoea and stage III to IV endometriosis who were treated with presacral neurectomy remained pain-free after 42 months of follow-up. None of the subjects who was treated by conservative surgery (resection of endometriotic lesions) was pain-free at follow-upY In contrast, the randomized trial by Candiani et al. reported no difference in pain relief for patients with endometriosis and dysmenorrhoea treated with either presacral neurectomy or conservative surgery, in fact, constipation and urinary urgency developed or worsened in more patients undergoing presacral neurectomy.43 The long term benefits of presacral neurectomy have not been established. Laser ablation of the uterosacral ligaments has also been used by some clinicians at the time of laparoscopic assessment. To date, no controlled trial has demonstrated convincingly the effectiveness of this approach.44.45
SURGERY ENDOMETRIAL ABLATION
This is a relatively new procedure that is usually employed for treatment of refractory menorrhagia. Short term studies have confirmed the efficacy of endometrial ablation not only for excessive menstrual flow but also for associated dysmenorrhoea. 37 Of all menorrhagic women with dysmenorrhoea, 76 percent reported either marked improvement or cure. At times, endometrial ablation may leave a focus of endometrium with no route for the escape of blood, resulting in severe dysmenorrhoea in an apparently amenorrhoeic woman. Ultrasound can establish the diagnosis, and curettage will frequently relieve the obstruction.
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CONCLUSIONS
Primary dysmenorrhoea generally affects adolescents and younger women and occurs in the absence of underlying gynaecologic lesions. Aberrant prostaglandin metabolism or activity increases uterine activity resulting in myometrial ischaemia and pain. The initial treatment for
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, , , 10. Stripling MC, Martin DC, Chatman DL, Vander Swaag R, Poston WM. Subtle appearance of endometriosis. Fertil SteriI1988;49:427. 11. Stout AL, Steege JG, Dodson WC, Hughes CL. Relationship of laparoscopic findings to self-report of pelvic pain. Am J Obstet Gynecol1991 ;164:73. 12. Fedele L, Parazzini F, Bianchi S, Arcaini L, Candiani GB. Stage and localization of pelvic endometriosis and pain. Fertil Steril 1990;53: 155. 13. Vercellini P, Trespidi L, De Giorgi 0, Cortesi I, Parazzini F, Crosignani PG. Endometriosis and pelvic pain: relation to disease stage and localization. Fertil Steril 1996;65:299-304. 14. Nishida M. Relationship between the onset of dysmenorrhea and histologic finding in adenomyosis. Am J Obstet Gynecol1991 ;165:229-31. 15. Brosens JJ, de Sousa NM, Barker FG, Paraschos T, Winston RM. Endovaginal ultrasonography in the diagnosis of adenomyosis uteri; identifying the predictive characteristics. Br J Obstet Gynaecol 1995;102:471-4. 16. McCausland AM. Hysteroscopic myometrial biopsy: its use in diagnosing adenomyosis and its clinical application. Am J Obstet GynecoI1992;166:1619-28. 17. ACOG Technical Bulletin. The battered woman. 1989;124:1-8. 18. Waldinger, RJ. Somatization Disorder. Psychiatry, Second Edition. American Psychiatric Press, Inc. 1990:226.
primary dysmenorrhoea is either with NSAIDs or OCPs, depending on the contraceptive needs and individual characteristics of the affected woman. If one approach fails, the other should be tried and then both in combination. When this combination is unsuitable or ineffective, a trial of transcutaneous electrical nerve stimulation may be warranted. Varieties of other medications have been used in such circumstances but their use must still be considered experimental. Thorough and timely investigation of women who fail to respond to these approaches will usually reveal the underlying cause of secondary dysmenorrhoea. Somatization should always be considered. The long term effects of such newer techniques as presacral neurectomy and laser ablation of uterosacral ligaments have not yet been established, although some clinicians have advocated their use for intractable, debilitating pain. When no cause is found to explain dysmenorrhoea and conventional therapies fail to provide relief, hysterectomy may be considered in women who have completed childbearing. REFERENCES 1. 2.
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19. Tilyard MW, Dovey SM. A comparison of tiaprofenic acid, mefenamic acid and placebo in the treatment of dysmenorrhea in general practice. Aus N Z J Obstet Gynaecol 1992;32: 165-8. 20. Delgado J, Simonin G, Servier C, Garcia R, Yoma J. Tolfenamic acid and mefenamic acid in the treatment of primary dysmenorrhea. Pharmacol Toxico11994;75 suppl 2:89-91. 21. Benassi L, Bertani D, Avanzini A. An attempt at real prophylaxis of primary dysmenorrhea: comparison between meclofenamate sodium and naproxen sodium. Clin Exp Obstet GynecoI1993;20:102-7. 22. Lalos 0, Joelsson I. Effect of an oral contraceptive on uterine tonicity in women with primary dysmenorrhea. Acta Obstet Gynecol Scand 1981 ;60:229-32. 23. Milsom I, Sundell G, Andersch B. The influence of different combined oral contraceptives on the prevalence and severity of dysmenorrhea. Contraception 1990;42:497-506. 24. Ekstrom P, Akerlund M, Forsling M, Kindahl H, Laudanski T, Mrugacz G. Stimulation of vasopressin release in women with primary dysmenorrhoea and after oral con-
Smith RP. Cyclic pelvic pain and dysmenorrhea. Obstet Gynecol Clin North Am 1993;20:753-64. Heisterberg L. Factors influencing spontaneous abortion, dyspareunia, dysmenorrhea and pelvic pain. Obstet Gyneco11993;81 :594-7. Parazzini F, Tozzi L, Mezzopane R, Luchini L, Marchini M, Fedele L. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology 1994;5: 469-72. Izzo A, Labriola D. Dysmenorrhea and sports activities in adolescents. Clin Exp Obstet GynecoI1991;18: 109-16. Colver GB, Dawber RPR. Multiple Beau's lines due to dysmenorrhoea. Br J Dermatol 1984;111 :111-3. Chambers PL, Pickles VR. Plain-muscle stimulants in extracts of menstrual fluid and of endometrial curettings. J PhysioI1958;144:68. Merck Sharp and Dohme Research Laboratories. Primary dysmenorrhea. The Merck Manual, fifteenth edition 1987:1712. Akerlund M, Bengtsson LP, Carter AM. A technique for
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intra-uterine thermister probe. Acta Obstet Gynecol Scand 1975;54:469-77. Vernon MW, Beard JS, Graves K, Wilson E. Classification
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of endometriotic implants by morphologic appearance and capacity to synthesize prostaglandin F. Fertil Steril 1991 ;56:230.
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, , , 42. Tjaden B, Schlaff WD, Kimball A. Rock JA. The efficacy of presacral neurectomy for the relief of midline dysmenorrhea.ObstetGynecoI1990;76:89-91. 43. Candiani GB, Fedele L, Vercellini P, Bianchi 5, Di Nola G. Presacral neurectomy for the treatment of pelvic pain associated wtih endometriosis: a controlled study. Am J ObstetGynecoI1992;167:100-3. 44. Vercellini P, Fedele L, Bianchi 5, Candiani GB. Pelvic denervation for chronic pain associated with endometriosis: fact orfancy? Am J Obstet GynecoI1991;165:745-9. 45. Lee RB, Stone K, Magelssen D, Belts RP, Benson WI. Presacral neurectomy for chronic pelvic pain. Obstet GynecoI1986;68:517-21.
26. Lundeberg T, Kjartansson J, Samuelsson U. Effect of electrical stimulation on healing of ischaemic skin flaps. Lancet 1988;2:712-4. 27. Mannheimer C, Eliasson T, Andersson B, et a/. The effects of spinal cord stimulation in pacing-induced angina pectoris and possible mechanisms of action. Br Med J 1993;307:477-80. 28. Smith RP, Heltzel JA. Interrelation of analgesia and uterine activity in women with primary dysmenorrhea. J Reprod Med 1991 ;36:260-4. 29. Salar G, Job I, Mingrino 5, et a/. Effect of transcutaneous electrical nerve stimulation on CSF beta-endorphin content in patients without pain problems. Pain 1981;10:169. 30. Benassi L, Barletta FP, Baroncini L, et a/. Effectiveness of magnesium pidolate in the prophylactic treatment of primary dysmenorrhea. Clin Exp Obstet Gynecol 1992;19:176-9. 31. Earl DT, Mercola JM. Calcium channel blockers and dysmenorrhea. J Adol Health 1992;13:107-8. 32. Akerlund M, Andersson KE, Ingemarsson I. Effects of terbutaline on myometrial activity, uterine blood flow and lower abdominal pain in women with primary dysmenorrhoea. Br J Obstet Gynaecol 1976;84:673-8. 33. Cirkel U, Ochs H, Schneider HP. A randomized, comparative trial of triptorelin depot and danazol in the treatment of endometriosis. Eur J Obstet Gynecol Reprod Bioi 1995;59:61-9. 34. Adamson GD, Kwei L, Edgren RA. Pain of endometriosis: effects of nafarelin and danazol therapy. Intemational Journal of Fertility and Menopausal Studies 1994;39:215-7. 35. Hansen HS, Olsen SF. Dietary (n-3)-fatty acids, prostaglandins, and prolonged gestation in humans. Prog Clin Bioi Res 1988;282:305-17. 36. Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-3 polyunsaturated fatty acids: the management of dysmenorrhea in adolescents. Am J Obstet GynecoI1996;174:1335-8. 37. Fraser IS, Angsuwanthana 5, Mahmoud F, Yezerki S. Short and medium term outcomes after rollerball endometrial ablation for menorrhagia. Med J Aus 1993;158:454-7. 38. SOGC Clinical Practice Guidelines, No. 47, April 1996; Clinical Practice Guidelines for Hysterectomy. 39. Sutton CJG, Ewen SP, Whitelaw N, Haines P. Prospective randomized double blind controlled trial of laser laparoscopy in treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril 1994;62:696-700. 40. Candiani GB, Fedele L, Vercellini P, Bianchi 5, Di Nola G. Presacral neurectomy for the treatment of pelvic pain associated with endometriosis: a controlled study. Am J Obstet GynecoI1992;167:100-3. 41. Nezhat C, Nezhat F. A simplified method of laparoscopic presacral neurectomy for the treatment of central pelvic pain due to endometriosis. Br J Obstet Gynaecol 1992;99:659-63.
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