The standard teaching and gynaecological approach to period and pelvic pain is to undertake a laparoscopy as the ‘gold standard’ for the identification of endometriosis,¹ to identify the cause of the pain and, ideally, to surgically correct any pathological findings in an effort to try and resolve the pain problem. In the setting of period and pelvic pain, studies suggest that 30–50 per cent of women will have endometriosis found at laparoscopy. A further number will have some adhesions found. So why not laparoscope everyone with significant period and pelvic pain who has not responded to NSAIDs and the oral contraceptive pill (OCP)?

There are a number of reasons, which include my experiences of working at Royal Children’s Hospital (RCH) in Melbourne where there have been many unusual, but very instructive, clinical problems, but also the lack of correlation between pain and endometriosis, the lack of RCTs demonstrating any long-term benefit of laparoscopy for pain and the increasing knowledge regarding the mechanisms associated with pain, pain sensitisation and the development of persistent or chronic pain.

Starting with my experience at RCH; remember that it has often been an unusual presentation of a problem that teaches us something or leads to improved understanding of a condition.

By listening to adolescents with dysmenorrhoea, we recognised that 40 per cent experience nausea, 30 per cent have vomiting and/or diarrhoea, 20 per cent have headaches, 10 per cent feel faint or are dizzy. This is classic primary dysmenorrhoea, which begins a few days prior to menses and lasts usually until day 2 or 3, caused by inflammatory cytokines and prostaglandins.

Extending from this, adolescent girls are seen at RCH with anaphylaxis as well as ICU admissions for severe asthma – occurring only with onset of their menses. Adolescent girls have also been admitted for severe vomiting occurring four-five weekly, prior to their first period, and then with their periods, when they begin. Exacerbations of Crohn’s disease and irritable bowel syndrome occur at times of menses, as do migraines and the symptoms associated with chronic fatigue and fibromyalgia. Most of these events can be attributed to inflammatory cytokines and prostaglandins, which are known to be critically involved in the process of endometrial shedding² and are clearly pretty potent substances.

Again listening to the adolescents with dysmenorrhoea, the pain patterns of those with dysmenorrhoea and heavy menses, but not the prostaglandin-related symptoms, is actually different – with their pain occurring on days of heavy bleeding. We know that 95 per cent of women get retrograde bleeding and that those that bleed heavily are doing more of this.³ Thus, the pain pattern is different, either because they are cramping to expel a blood clot or they have more retrograde bleeding with the peritoneal free fluid causing irritation provoking bladder and bowel symptoms and their different pain pattern.

Through my work at the RCH, I have been involved in the care of more than 100 women with uterovaginal agenesis. Given that one in 10 women are supposed to develop endometriosis, why aren’t there a similar number of women with Mayer-Rokitansky-Küster-Hauser with endometriosis? I have yet to see a case (when there is no endometrial tissue present), and neither are they found in the medical literature. In contrast, I have seen numerous young women with obstructed Müllerian anomalies and most of these have significant endometriosis due to substantial retrograde menses. In young women, it is often not appropriate or possible to operate immediately, so periods are suppressed and the corrective surgery is undertaken some months to years later. In these young women, the endometriosis has invariably resolved by the time of their surgery. This spontaneous resolution, of even moderate to severe endometriosis, has been reported by others.

Bleeding disorders in adolescents with heavy menstrual bleeding (HMB) have long been recognised. On taking a history, including family history, I rapidly realised that the mothers of the adolescents with HMB also had heavy periods (and endometriosis), and we subsequently often identify bleeding disorders in both the teenager and the mother. Kadir has shown that more than 10 per cent of women with HMB in adult gynaecology clinics have a mild bleeding disorder,⁴ but this rate also applies to women with histologically proven endometriosis. Various epidemiological studies have already shown that women who bleed more often, for longer and more heavily, are more likely to have endometriosis.⁵ So, at a clinical level – if you don’t bleed, you do not seem to make endometriosis, and if you bleed lots you are more likely to do so.

Now add to this background the science of pain and central sensitisation. It is the presence of pain that is associated with lower thresholds of pain sensitivity and thus central sensitisation, not the presence or absence of endometriosis.⁶ Additionally, repeated cyclic pain is thought to predispose to persistent or chronic pain.⁷ But further to this, the poor correlation between symptoms, location and pain severity with location of endometriosis raises concerns regarding endometriosis and its failure to fulfil the Bradford-Hill criteria for causality. The relationship between pain and endometriosis is not helped by the trials relating to pain and laparoscopy. There have been three RCTs that have involved women who had presented with pain, and then when endometriosis was identified at the time of laparoscopy, had either sham (diagnostic laparoscopy only) or excision/laser undertaken.^{8 9 10} The initial outcome measures for two of these studies was endometriosis at six-month follow up¹¹ or at their repeat surgery.¹² The study by Abbott demonstrated no difference in pain scores at six or 12 months between those who had delayed or immediate excisional surgery.¹³ Long-term follow up (mean six years) of the former study demonstrated pain recurrence in both groups.¹⁴ Likewise, the study by Jarrell with follow up to 12–14 years, demonstrated no difference between those with sham surgery and those with excision of endometriosis in pain score outcomes, an equal likelihood of repeat surgery and with the only predictor of repeat surgery being pain score prior to first laparoscopy.¹⁵

What about the risk of progression of endometriosis? Several studies have reported on delays of 4–11 years to the diagnosis of endometriosis.¹⁶ Adolescents who have been seen at RCH are likely to be in the 10 per cent of teenagers with significant dysmenorrhoea¹⁷ who should be at high risk, in theory, of having endometriosis. Their management involves reducing menstrual loss and often suppressing menses altogether to manage their symptoms. In a retrospective cohort, we had performed a laparoscopy in only 8 per cent (12/150) and only one had endometriosis. A long-term follow up study of these adolescents located 50 per cent of the young women 5–15 years later, with a 95 per cent participation rate (n=70). 25 per cent had no pain, 25 per cent had some pain, and 50 per cent had ongoing pain. If we follow the argument that endometriosis will progress without excision and specific treatment, then of this adolescent cohort, most, if not all, should have had significant endometriosis by the time they had a laparoscopy as adults. This is particularly the case as others have reported that of adolescents who fail cyclic OCP and NSAIDs, 38–100 per cent^{18 19 20} will have endometriosis at the time of laparoscopy. Yet, in the long-term follow up cohort, only 13 of the 26 who had had a laparoscopy under adult care, had endometriosis – all minimal/mild disease. So despite a long history of dysmenorrhoea and never having had excision of any theoretical/potential spots of endometriosis, there was no moderate or severe endometriosis. The fertility rate among the cohort was as good, if not better, than the state age matched figures. Maybe the outcomes were better than expected due to the reduction in menstrual loss during adolescence. I won’t argue that the ongoing pain in 50 per cent is a problem; but, there were no predictive features of this cohort and I suspect the lack of psychological input may have contributed.

You may argue that adolescents are different, and you may be correct. Nevertheless, in adult women, with normal, careful ultrasounds (and ignoring comments regarding immobile and tender ovaries, due to lack of evidence that this is relevant), I mostly avoid laparoscopies for pain. I admit I do not know who will benefit from a negative laparoscopy, and I am sure there is a cohort, but there is also a significant cohort who will be angry about a negative laparoscopy. There will be 20 per cent who will develop a new pain – often a trigger point on their abdominal wall.

Women report that their period and pelvic pain symptoms are ignored and trivialised, not managed. What I am advocating, and what others are also saying, is that dysmenorrhoea and pelvic pain should not be trivialised and ignored. It needs to be actively managed to endeavour to avoid the development of persistent pelvic pain and central sensitisation, with the incumbent risk for many other chronic pain syndromes. The aim is to manage pain symptoms, rather than excising some endometriosis, which may well return with a subsequent heavy period. The aim is to reduce menstrual loss (tranexamic acid or hormones), plus or minus suppression of menses and ovulation (a potential source of pain), provide and link patients to period and pelvic pain education and seek the assistance of physiotherapists. I know I need to do better at finding psychologists with an interest in pain, as I am sure they will have an impact on pain rumination, magnification and helplessness²¹ and offer patients the skills to better manage the stressors and contributors to pain.

1. SK Agarwal, C Chapron, LC Giudice, et al. Clinical diagnosis of endometriosis: a call to action. Am J Obstet Gynecol. 2019;220(4):354.e1-e12.
2. J Evans, LA Salamonsen. Inflammation, leukocytes and menstruation. Rev Endocr Metab Disord. 2012;13(4):277-88.
3. TM D’Hooghe, CS Bambra, BM Raeymaekers, PR Koninckx. Increased prevalence and recurrence of retrograde menstruation in baboons with spontaneous endometriosis. Hum Reprod. 1996;11(9):2022-5.
4. R Kadir, D Economides, C Sabin, et al. Frequency of inherited bleeding disorders in women with menorrhagia. Lancet. 1998;351(9101):485-9.
5. BPaW Eskenazi, L Marcella. Epidemiology of Endometriosis. Obstetrics and Gynecology Clinics. 1997;24(2):235-57.
6. S As-Sanie, RE Harris, SE Harte, et al. Increased pressure pain sensitivity in women with chronic pelvic pain. Obstet Gynecol. 2013;122(5):1047-55.
7. G Hardi, S Evans, M Craigie. A possible link between dysmenorrhoea and the development of chronic pelvic pain. ANZJOG. 2014;54(6):593-6.
8. CJ Sutton, SP Ewen, N Whitelaw, P Haines. Prospective, randomized, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril. 1994;62(4):696-700.
9. J Abbott, J Hawe, D Hunter, et al. Laparoscopic excision of endometriosis: a randomized, placebo-controlled trial. Fertil Steril. 2004;82(4):878-84.
10. J Jarrell, R Mohindra, S Ross, et al. Laparoscopy and reported pain among patients with endometriosis. J Obstet Gynaecol Can. 2005;27(5):477-85.
11. CJ Sutton, SP Ewen, N Whitelaw, P Haines. Prospective, randomized, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril. 1994;62(4):696-700.
12. J Abbott, J Hawe, D Hunter, et al. Laparoscopic excision of endometriosis: a randomized, placebo-controlled trial. Fertil Steril. 2004;82(4):878-84.
13. J Abbott, J Hawe, D Hunter, et al. Laparoscopic excision of endometriosis: a randomized, placebo-controlled trial. Fertil Steril. 2004;82(4):878-84.
14. KD Jones, P Haines, CJ Sutton. Long-term follow-up of a controlled trial of laser laparoscopy for pelvic pain. JSLS. 2001;5(2):111-5.
15. J Jarrell, R Brant, W Leung, P Taenzer. Women’s Pain Experience Predicts Future Surgery for Pain Associated With Endometriosis. J Obstet Gynaecol Can. 2007;29(12):988-91.
16. SK Agarwal, C Chapron, LC Giudice, et al. Clinical diagnosis of endometriosis: a call to action. Am J Obstet Gynecol. 2019;220(4):354.e1-e12.
17. M Parker, A Sneddon, P Arbon. The menstrual disorder of teenagers (MDOT) study: determining typical menstrual patterns and menstrual disturbance in a large population-based study of Australian teenagers. BJOG. 2010;117(2):185-92.
18. P Vercellini, L Fedele, L Arcaini, et al. Laparoscopy in the diagnosis of chronic pelvic pain in adolescent women. J Reprod Med. 1989;34(10):827-30.
19. MR Laufer, J Sanfilippo, G Rose. Adolescent endometriosis: diagnosis and treatment approaches. J Pediatr Adolesc Gynecol. 2003;16(3 Suppl):S3-11.
20. EC Dun, KA Kho, VV Morozov, et al. Endometriosis in adolescents. JSLS. 2015;19(2).
21. M Sullivan, S Bishop, J Pivik. The Pain Catastrophizing Scale: development and validation. Psychological Assessment. 1995;7(4):524-32.