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JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY
Your partner in paediatric and O&G practice
ISSN 1012-8875 (HONG KONG)
Paediatric Psoriasis Managing Headache in Children
Dysmenorrhoea What Are the Benefits and Risks of HRT?
JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY
J UL/ AUG 2 0 1 2 Vol. 38 No. 4
133 • Proton pump inhibitors and hip fracture in postmenopausal women • Screening for cervical cancer in Europe: Cost-effectiveness of HPV versus cytology screening • Screening and cervical cancer mortality • Nicotine replacement patches in pregnancy: Negative study 134 • Peer-led parenting intervention for disruptive child behaviour • Results of modern paediatric burn care
135 • Chlorhexidine to the umbilical cord in developing countries • Moderate or late preterm birth and health outcomes • Paediatricians influence parental febrile behaviour 136 • Oral amoxicillin for severe early childhood pneumonia in rural Pakistan
Board Director, Paediatrics Professor Pik-To Cheung Associate Professor Department of Paediatrics and Adolescent Medicine The University of Hong Kong Board Director, Obstetrics and Gynaecology Professor Pak-Chung Ho Head, Department of Obstetrics and Gynaecology The University of Hong Kong
Professor Biran Affandi University of Indonesia Dr Karen Kar-Loen Chan The University of Hong Kong Associate Professor Oh Moh Chay KK Women’s and Children’s Hospital, Singapore Associate Professor Anette Jacobsen KK Women’s and Children’s Hospital, Singapore Professor Rahman Jamal Universiti Kebangsaan Malaysia Dato’ Dr Ravindran Jegasothy Hospital Kuala Lumpur, Malaysia Associate Professor Kenneth Kwek KK Women’s and Children’s Hospital, Singapore Dr Siu-Keung Lam Kwong Wah Hospital, Hong Kong Professor Terence Lao Chinese University of Hong Kong Dr Kwok-Yin Leung The University of Hong Kong
Dr Tak-Yeung Leung Chinese University of Hong Kong Professor Tzou-Yien Lin Chang Gung University, Taiwan Professor Somsak Lolekha Ramathibodi Hospital, Thailand Professor Lucy Chai-See Lum University of Malaya, Malaysia Professor SC Ng National University of Singapore Professor Hextan Yuen-Sheung Ngan The University of Hong Kong Professor Carmencita D Padilla University of the Philippines Manila Professor Seng-Hock Quak National University of Singapore Dr Tatang Kustiman Samsi University of Tarumanagara, Indonesia Professor Perla D Santos Ocampo University of the Philippines Associate Professor Alex Sia KK Women’s and Children’s Hospital, Singapore
Dr Raman Subramaniam Fetal Medicine and Gynaecology Centre, Malaysia Professor Walfrido W Sumpaico MCU-DFT Medical Foundation, Philippines Professor Cheng Lim Tan KK Women’s and Children’s Hospital, Singapore Associate Professor Kok Hian Tan KK Women’s and Children’s Hospital, Singapore Dr Surasak Taneepanichskul Chulalongkorn University, Thailand Professor Eng-Hseon Tay Thomson Women’s Cancer Centre, Singapore Professor PC Wong National University of Singapore Dr George SH Yeo KK Women’s and Children’s Hospital, Singapore Professor Hui-Kim Yap National University of Singapore Professor Tsu-Fuh Yeh China Medical University, Taiwan
JPOG JUL/AUG 2012 • i
JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY
J UL/ AUG 2 0 1 2 Vol. 38 No. 4
137 Paediatric Psoriasis Paediatric psoriasis is a common disorder with significant morbidity. New advances in biologic therapy,
as well as recent reviews assessing classification, have led to a greater understanding of the condition of psoriasis. Presented in this review article is an overview of the presentation of psoriasis as well as an up-to-date review of management options. Vyom Sharma, David Orchard
147 Dysmenorrhoea Dysmenorrhoea is a medical condition characterized by severe uterine pain during menstruation
manifesting as cyclical lower abdominal pain. Mainstay treatment is generally supportive providing symptomatic relief, and more directive surgical treatment is reserved for specific secondary causes of dysmenorrhoea or for refractory cases. Therefore, patients with primary dysmenorrhoea may simply need reassurance and simple analgesics, while those with secondary dysmenorrhoea require investigation and treatment of the underlying organic problem. An overview of managing this condition is presented in this article. Shilpa Kolhe, Shilpa Deb
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PUBLISHER: Journal of Paediatrics, Obstetric & Gynaecology (JPOG) is published 6 times a year by UBM Medica, a division of United Business Media. CIRCULATION: JPOG is a controlled circulation for medical practitioners in South East Asia. It is also available on subscription to members of allied professions. SUBSCRIPTION: The price per annum is US$42 (surface mail, students US$21) and US$48 (overseas airmail, students US$24); back issues US$8 per copy. EDITORIAL MATTER published herein has been prepared by professional editorial staff. Views expressed are not necessarily those of UBM Medica. Although great care has been taken in compiling and checking the information given in this publication to ensure that it is accurate, the authors, the publisher and their servants or agents shall not be responsible or in any way liable for the continued currency of the information or for any errors, omissions or inaccuracies in this publication whether arising from negligence or otherwise howsoever, or for any consequences arising therefrom. The inclusion or exclusion of any product does not mean that the publisher advocates or rejects its use either generally or in any particular field or fields. COPYRIGHT: © 2012 UBM Medica. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, in any language, without written consent of copyright owner. Permission to reprint must be obtained from the publisher. ADVERTISEMENTS are subject to editorial acceptance and have no influence on editorial content or presentation. UBM Medica does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature. Philippine edition: Entered as second-class mail at the Makati Central Post Office under Permit No. PS-326-01 NCR, dated 9 Feb 2001. Printed by Fortune Printing International Ltd, 3rd Floor, Chung On Industrial Building, 28 Lee Chung Street, Chai Wan, Hong Kong.
JPOG JUL/AUG 2012 • ii
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Genting Centre. Singapore 088934 Tel: (65) 6223 3788 Fax: (65) 6221 4788 E-mail: enquiry@jpog. Obstetrics and Gynaecology contains articles under licence from UBM Media LLC. This article will focus on the clinical management of headache in children including migraine. WC Leung The Journal of Paediatrics. Elizabeth Farrell 157 Review Article Paediatrics 164 Managing Headache in Children Headache is a common symptom in children. tension headache. LL Chan. OBSTETRICS & GYNAECOLOGY J UL/ AUG 2 0 1 2 Vol. several major studies have substantially resolved these areas of controversy. M A McShane.jpog. WL Lau.com. Case Studies Interesting cases seen in general practice and their management. Copyright © 2011 UBM Media LLC. Review Articles Comprehensive reviews providing the latest clinical information on all aspects of the management of medical conditions affecting children and women.JOURNAL OF PAEDIATRICS. The articles appearing on pages 49–53.com Lisa Low. and pages 67–80 are reprinted with permission of Consultant for Pediatricians. 4 Review Article Gynaecology 157 What Are the Benefits and Risks of HRT? Opinions concerning the benefits and risks of hormone replacement therapy (HRT) have varied over the past decade. S J Hughes Continuing Medical Education 169 Gestational Diabetes 169 Historically. The Cover: Managing Headache in Children © 2012 UBM Medica Pictorial Medicine Vignettes of illustrated cases with clinical photographs. Illustrator JPOG JUL/AUG 2012 • iii . All rights reserved. or contact: The Editor UBM Medica Asia Pte Ltd. there has been a lot of controversy over most aspects of gestational diabetes mellitus (GDM) as well as the relationship between GDM and type II diabetes mellitus. Recurrent or persistent headache is most commonly due to migraine (with and without aura). Recently. For more information. please refer to the Instructions for Authors on our website www. or chronic daily headache. Maintaining and regularly updating one’s knowledge about HRT is paramount so that accurate information can be given to patients. 38 No. No 3 Lim Teck Kim Road.
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Screening and cervical cancer cure: population based cohort study. Screening and cervical cancer mortality OBSTETRICS Nicotine replacement patches in pregnancy: Negative study JPOG JUL/AUG 2012 • 133 .000 person-years among non-users. After adjustment for age. A study in Sweden has shown that Smoking in pregnancy can cause miscarriage. Among smokers. and costs were derived from studies in the Netherlands.230 women who had a diagnosis of invasive cervical cancer between 1999 and 2001 in Sweden. There is uncertainty about whether screening for cervical cancer reduces cervical cancer mortality or simply increases the time from diagnosis to death (lead time). De Kok IMCM et al. there were 893 hip fractures.500 screening policies in five European scenarios. and the effect is independent of lead-time bias. Smear test screening for cervical cancer increases cure rates.51 events per 1. BMJ 2012. BMJ 2012.02 events per 1. During follow-up. Arbyn M et al. 344 (Feb. The model was validated using Dutch data. the cure rate was 92% for cancers detected by smear test screening and 66% for cancers detected because of symptoms. 25): 15 (e372). women who used a PPI for at least 2 years had a 35% increase in risk. Khalili H et al. plascreening might be preferred when the cost of cytology was low and when HPV was highly prevalent and testing for HPV costly. 344 (March 24): 18 (e900). BMJ 2012. a significant difference. Use of proton pump inhibitors and risk of hip fracture in relation to dietary and lifestyle factors: a prospective cohort study. A microsimulation model has been used to compared the costeffectiveness of > 1.000 personyears among PPI users and 1. Primary screening for human papillomavirus compared with cytology screening for cervical cancer in European settings: cost effectiveness analysis based on a Dutch microsimulation model. the use of PPIs increased the risk of hip fracture by 51%. Effect of screening on deaths from cervical cancer in Sweden. For women aged 23–65 years. screening improves prognosis. Screening for cervical cancer in Europe: Cost-effectiveness of HPV versus cytology screening Human papillomavirus (HPV) testing for cervical cancer screening is more sensitive but less specific than cytological screening. The rate of cure was also significantly higher among women screened at recommended intervals than among women overdue for screening. Andrae B et al. HPV screening is often preferable to cytological screening in cervical cancer screening programmes in Europe. the risk increasing with longer use. 344 (March 1): 17 (e670). but there was no significant increase in risk with PPIs in nonsmoking women. A total of 79. The model showed that HPV testing was usually preferable. The rate of hip fracture was 2.899 postmenopausal women in the study provided biennial information on PPI use and other risk factors from 2000 to 2008.Peer Reviewed Journal Watch PPI use by postmenopausal women increas- GYNAECOLOGY Proton pump inhibitors and hip fracture in postmenopausal women es the risk of hip fracture among smokers but not among non-smokers. Cost-effectiveness analyses have given varying results partly because key factors vary between countries. Primary cytological It has been suggested that regular use of a proton pump inhibitor (PPI) may increase the risk of hip fracture. The study included all 1. Data from the US Nurses’ Health Study have confirmed the association in postmenopausal women. Ibid: 11(e804) (editorial).
6% (placebo).4% (nicotine replacement) vs 7. with only 7. Randomization was to intervention or waiting list controls. Data from a single modern paedi- PAEDIATRICS Peer-led parenting intervention for disruptive child behaviour Parents in socioeconomically disadvantaged groups may have difficulty obtaining appropriate advice and management for children with disruptive behaviour problems. 379: 1013–1021. All subjects received behavioural cessation support. preterm birth. improvement in child disruptive behaviour and positive parenting practices was significantly greater in the intervention group compared with the control group. have shown that a peer-led parenting intervention may be effective. The addition of nicotine replacement Day C et al. Tompkins RG. but the value of nicotine replacement therapy is uncertain. cental abruption. Researchers in London. a total of 952 children were treated for burns involving between 30% and > 90% of total body surface area (TBSA). A total of 1. Mean age was 7. and improved life support systems have meant that the prognosis for burns patients has improved in recent decades. It is suggested that children with more than 60% TBSA burns should be transferred immediately to a specialist burns unit. JPOG JUL/AUG 2012 • 134 . Using the parent-reported intensity subscale of the Eyberg child behaviour inventory. Between 1998 and 2008. Evaluation of a peer led parenting intervention for disruptive behaviour problems in children: community based randomised controlled trial.5%. The rate of abstinence from the quit date until delivery (validated by measurements of exhaled carbon monoxide or salivary cotinine) was 9. mostly from black and ethnic minority groups. and 9% developed sepsis (2% to 26%). A trial in England has failed to show benefit from nicotine replacement patches in pregnancy. 344 (March 24): 17 (e1107). England. NEJM 2012. BMJ 2012. The intervention consisted of an 8-week peerled parenting programme based on principles of social learning theory and delivered by trained peer facilitators in a manualized group format at schools and children’s centres. The rates of adverse pregnancy and birth outcomes were similar in the two groups. Stewart-Brown S. A randomized trial of nicotine-replacement therapy patches in pregnancy. and 116 index children with disruptive behavioural problems. Ibid: 10 (e1160) (editorial). a non-significant difference. 366: 808–818. Behavioural support for smoking cessation is effective in pregnancy. Mortality increased rapidly with 62% or greater TBSA involvement.050 women smokers (five or more cigarettes a day) were randomized at seven hospitals to nicotine replacement patches or placebo patches for 8 weeks. Overall.3 years and 66% were boys. Multi-organ failure developed in 16% of patients. new grafting techniques. Survival of children with burn injuries. Lancet 2012. patches to behavioural cessation support was not beneficial. and neonatal morbidity and mortality. however. Ibid: 846–847 (editorial). beginning at 12–24 weeks’ gestation. Oncken C. was poor. The study included 116 families.8% of the placebo group continuing with the patches for more than a month. but compliance was poor. low birth weight.2% of the replacement group and 2. Kraft R et al. Coleman T et al. atric burns unit in Texas have correlated burn area and prognosis. All respondents described their satisfaction with the intervention as ‘a great deal’ or ‘quite a lot’. Ibid: 983–984 (comment). The drop-out rate was 8.replacement for smoking cessation during pregnancy. 6% with 30–39% TBSA involvement and 45% with >90% TBSA involved. Burn size and survival probability in paediatric patients in modern burn care: a prospective observational cohort study. Peer led parenting support programmes. mortality was 13% (3% with 30–39% burns rising to 55% with > 90% burns). Nicotine Results of modern paediatric burn care New drug treatments. The intervention was successful. Compliance.
wheezing.3 per 1.000 (DC). a cluster randomized trial included 133 clusters (29. 379: 1022–1028: Soofi S et al.5 per 1.6 per 1. The UK Millennium cohort study is a nationally Moderate or late preterm birth and health outcomes JPOG JUL/AUG 2012 • 135 . Osrin D. and parental rating of children’s health. Chlorhexidine cord cleansing to reduce neonatal mortality. clusterrandomised trial. cluster-randomised trial. and 28. SC). Birth at 32–36 weeks accounted for 5. Health outcomes in relation to gestational age at birth were assessed at ages 3 and 5 years and included growth. hospital admissions.4% for birth at 32–36 weeks.3 per 1.2 per 1.2 per 1. Now. 2. use of prescribed drugs. In rural Pakistan. but handwashing had no significant effect. but the optimum frequency of application is to be established. 1. Data from Nepal have suggested that the application of chlorhexidine to the umbilical cord after birth could reduce umbilical infection and neonatal mortality. El Arifeen S et al. daily application for 7 days (multiple cleansing. supply of chlorhexidine only. and 4. Topical application of chlorhexidine to neonatal umbilical cords for prevention of omphalitis and neonatal mortality in a rural district of Pakistan: a community-based.4% for birth at 37–38 weeks. Ibid: 984–986 (comment). In general.000 (MC).Peer Reviewed Journal Watch Chlorhexidine to the umbilical cord in developing countries About half of all neonatal deaths around the world are caused by infections. but there was no reduction with handwashing.741 neonates. Birth before 32 weeks accounted for 3. especially in the rural areas of developing countries where hygiene is often poor. a significant reduction with SC. supply of soap for handwashing only.760 neonates) with randomization to one of three options: a single application of chlorhexidine to the cord soon after birth (single cleansing. have confirmed the benefits of cord cleansing with chlorhexidine. the study included 187 population clusters and 9.8% of such children and birth at 37–38 weeks for 7. Hill ZE. Lancet 2012. and 5.7% of children with three or more hospital admissions at ages 9 months to 5 years.7% for birth before 32 weeks. and the umbilicus is regarded as a major point of entry for infective organisms. Chlorhexidine cleansing was associated with a significant 42% reduction in risk of omphalitis compared with dry cord care. The effect of cord cleansing with chlorhexidine on neonatal mortality in rural Bangladesh: a community-based. Neonatal mortality was 22. 26. The rate of severe cord infection (redness and pus) was 3.2%. there was an inverse relationship between gestational age at birth and frequency of adverse health outcomes. compared with DC. a significant reduction with MC. or dry cord care (DC). The greatest number of such outcomes was among children born at moderate or late preterm (32–36 weeks) or at early term (37–38 weeks). compared with DC. Ibid: 1029–1036. the corresponding population attributable fractions were 5. These researchers conclude that cord cleansing with chlorhexidine is effective. Randomization was to one of four options for infants delivered by traditional birth attendants (TBAs): supply of 4% chlorhexidine solution to be applied to the cord by the TBA at birth and then daily by family members for up to 14 days. one in rural Bangladesh and one in rural Pakistan.000 (MC).818 infants born in 2000–2002 and still living in the UK at the age of 9 months. These researchers conclude that cord cleansing with chlorhexidine is effective and that the provision of chlorhexidine in birth kits might reduce neonatal mortality. Similarly. but not with SC. representative prospective cohort study including 18.000 live births (SC). two studies reported in one issue of the Lancet. but not with MC. chlorhexidine was associated with a significant 38% reduction in neonatal mortality. longstanding illness. MC). and supply of soap for handwashing. In Bangladesh. For a limiting longstanding illness.000 (DC).000 (SC). or promotion of dry cord care.
and that they alternated ibuprofen and acetaminophen to treat fever (27% vs 21. paediatricians and parents said that they use sponging or ice packs to reduce fever (78. 344 (March 17): 17 (e896). Bryle EM et al. and the Democratic Republic of the Congo. The study highlighted a number of wrong behaviours. All parents believed that fever could cause harmful effects like delirium. Home treatment with oral amoxicillin was at least as effective as current WHO policy for severe pneumonia.953). The Oral amoxicillin for severe early childhood pneumonia in rural Pakistan In 2008. or given a single dose of oral co-trimoxazole and referred to the nearest health facility for intravenous antibiotic treatment (control clusters). Parental and medical knowledge and management of fever in Italian pre-school children. 89. Black RE. 1.9% believed that fever could cause brain damage or seizures. If left untreated. drugs used for treatment. and 14 days.7% of parents ( P < 0.8%. Educational programmes aimed at paediatricians could help modify parental behaviours as well. and drug administration techniques. Treatment failure by day 6 occurred in 8% (intervention) and 13% (control).4%.4% of paediatricians and 1. The majority of parents (67. India. P = 0. Nigeria. The similarities between many of the attitudes and practices related to fever demonstrate ‘Fever phobia’ describes an attitude of unreasonable fear that parents may have surrounding fever and treatment for fever in their children. a trial in rural Pakistan has shown that the policy is effective for children with severe pneumonia. questionnaire was based on previous similar sur- Paediatricians influence parental febrile behavior veys and recent guidelines from the UK and Italy on fever management. Oral antipyretic administration was correctly preferred by 73. Now. 6. compared with rectal administration. JPOG JUL/AUG 2012 • 136 . included 4. Those with severe pneumonia were prescribed oral amoxicillin syrup (45 mg/kg twice daily) for 5 days at home (intervention clusters). Parents of children aged 0–6 were given an 18-question multiple choice questionnaire on fever management including the definition of fever based on body temperature. Paediatricians were given a similar but terminologically different questionnaire.5% vs 77. China. A survey of 388 parents and 480 physicians from Italy showed that physician attitudes towards febrile children can inform how parents handle their the degree to which parents follow their paediatrician’s lead. Of concern. the World Health Organization (WHO) and United Nations Children’s Fund recommended antibiotic treatment at home given by trained health workers. BMJ 2012. rural Pakistan: a cluster-randomised controlled trial. There were three deaths. Almost half of all deaths in young children occur in Pakistan. The children were screened by lady health workers. instead of hospital referral.1% of paediatricians and 48. 12(1): 97. potential side effects of fever. The children were followed up at 2. Soofi S et al. P = 0. Chiappini E et al. El Arifeen S. and in 2004.0001).2% of parents said that they use acetylsalicylic acid or steroids as a secondchoice therapy to antipyretic drugs (P = 0. two in the intervention group and one in the control group. despite guideline recommendations. 3.867). a non-significant difference. Effects of gestational age at birth on health outcomes at 3 and 5 years of age: population based cohort study.410 children aged 2–59 months with WHO-defined severe pneumonia. Lancet 2012. for non-severe pneumonia in rural areas.8%) said that their paediatrician was their primary source of information on fever and fever management. In similar ratios. Delayed treatment is responsible for many child pneumonia deaths.937). dehydration. or coma. Communitybased treatment of severe childhood pneumonia. child’s illness and may be a driving factor in fever phobia. A cluster randomized trial in rural Sindh province.Modestly preterm birth and early term birth contribute more to the burden of adverse health outcomes than does very preterm birth. 379: 729–737. Pakistan. Effectiveness of community case management of severe pneumonia with oral amoxicillin in children aged 2–59 months in Matiari district. Meta-analyses have confirmed the effectiveness of this policy. pneumonia accounted for 18% of all deaths in children under the age of 5 years. best place to take temperature. Ibid: 692–694 (comment). BMC Pediatr 2012.
About 30–40% of adult cases begin by age 15. MBBS. hyperproliferation of the keratinocyte.and under-expression of certain proteins in psoriatic lesions. MBBS. FRCR. neovascularization. Diagnostic Radiology MBBS. These cells release pro-inflammatory cytokines which trigger a cascade of cytokines that lead to keratinocyte proliferation. This article covers an approach to classification.Sharma. and vasodilation. and inflammatory infiltration. FACD Tang Phua Vyom Hwee. Early diagnosis and treatment can arrest progression to disfiguring states that requires extensive treatment. MMed Diagnostic Radiology Paediatric Psoriasis Vyom Sharma. These actions are mediated by activated T cells and dendritic cells that are present in psoriatic plaques. Its role in active psoriasis is strongly suggested by increase in TNF levels after therapy and increased levels in psoriatic plaques. There is over. David Orchard. MBBS. of which increased levels are found in active plaques. MBBS. JPOG JULY/AUG 2012 • 137 . FRCR. as well as minimize the psychosocial burden imposed by this illness. a pro-inflammatory cytokine. MMed David Orchard. MBBS. PATHOGENESIS AND AETIOLOGY The aetiology of psoriasis is multifactorial. FACD INTRODUCTION Psoriasis is a chronic inflammatory disease characterized by well-demarcated erythematous plaques that demonstrate a characteristic silvery scaling. and provides an up-to-date review of management options. Much of psoriasis is believed to be mediated by tumor necrosis factor (TNF) a. The effects of these expressions are threefold: abnormal keratinocyte differentiation.PA EDIA TRICS I Peer Reviewed Imaging Paediatric Imaging Paediatric Brain Tumours Brain Tumours Paediatric Psoriasis Tang Phua Hwee. provides some popular regimes treatment.
certain individuals with the Cw*0602 allele are four times more likely to develop guttate psoriasis. Other noted associations are of an increased incidence of psoriasis seen in sufferers of Kawasaki disease. more recent studies suggest figures of approximately 70%. munological basis for disease. However. the larger JPOG JUL/AUG 2012 • 138 . Ethnic variation is not clear. environmental factors are believed to play a significant role in the development of the condition. followed by black and then Asian populations. ulcerative colitis and bone marrow transplantation. the site of HLA class I (associated with early onset disease) and II (late onset disease) antigens which are thought to produce differing subtypes of the disease. Genetic influences are suggested by studies which state positive family history in first-degree relatives somewhere between 10% and 73%. Figure 3. EPIDEMIOLOGY One-third of adults with psoriasis report onset in childhood. noted no variance except in the Inuit race. It is postulated that streptococcal antigen activate lymphocytes which induces mitotic activity. Psoriasis in the concha of the ear. with only 35% of monozygotic twins demonstrating psoriasis. all supporting the im- Figure 2. suggested by twin studies demonstrating disparity in concordance. Napkin psoriasis. which has an established association with guttate-type psoriasis. Crohn’s disease. however. postulating the role of omega-3 fatty acids in the prevention of psoriasis. Typical well-demarcated. however. Major gene for psoriasis susceptibility is thought mainly to be located on chromosome 6. Other studies.PAEDIATRIC S PAEDIATRICS I Peer Reviewed Figure 1. A highly relevant environmental factor is streptococcal infection. However. with some studies quoting incidence highest in Caucasian. however. Classically. some authors have observed female preponderance by 2:1. salmon-pink patches with silvery scale.
The inclusion of psoriatic diaper rash drastically increases incidence of psoriasis in children under 2. Itch is variable but mostly not a significant symptom. • lichen planus. Pityriasis rosea. Age distribution in the paediatric population is unclear. Isolated facial involvement can occur and is more common in the paediatric population than in adults. If excluded. In babies. and scalp although these areas are not as typically involved in the paediatric population as compared with adults. • pityriasis rubra pilaris. and there will often be a history of gradual expansion. and the scale is described as ‘trailing’ rather than leading the outer annulus. Pityriasis rosea (Figure 4c) may have a herald patch and have the oval lesions lining along the ribs. Psoriasis in this distribution will generally have no scale and the diagnosis is made on the ‘salmon-pink’ colour of the erythema and the welldemarcated borders of the plaques. Certain sites when involved are highly suggestive of psoriasis and include the umbilicus (Figure 1). including: • atopic dermatitis. the most common pattern of presentation in children of that age group. Discoid (nummular) eczema (Figure 4a) tends to be more pruritic. The predominant areas affected are the knees. • pityriasis rosea. balanitis. studies show identical distribution amongst all age groups. It presents mostly as well-demarcated erythematous lesions with fine or coarse ‘silvery’ scaling (Figure 1). elbows. Tinea corporis (Figure 4b) tends to have a more active edge. a b c JPOG JUL/AUG 2012 • 139 . If psoriasis is extremely aggressive. Figure 4. These diagnoses can be excluded with biopsy if there are difficulties with clinical diagnosis. b. the napkin area is frequently involved (Figure 3). it may DIAGNOSIS Psoriasis primarily is diagnosed clinically and classified on the basis of morphology. and can be oozing. • discoid eczema (nummular dermatitis). a. Intertriginous areas are also commonly affected in children possibly presenting as vulvitis. and the natal cleft. buttocks. c.PA EDIA TRICS I PA ED IATRICS Peer Reviewed studies showed approximately equal gender distribution. • tinea corporis. • drug reactions. however. Differential diagnosis. Differential diagnosis includes other papulosquamous disorders of childhood. the concha of the ear (Figure 2). Tinea corporis. Discoid eczema. is less well defined with more intensity towards the centre. and perianal itching.
whereby the severity of redness. take on the form of pustular psoriasis (Figure 5). Other changes include subungual keratosis and discolouration. in clinical practice the calculations can be contrived with 16 separate variables. Pustular psoriasis requires hospitalization. it composed 40–50% of all cases. Nail Involvement Reports range from 7% to 40%. arms. In the largest study of 1. Mucosal Involvement Mucosal involvement can involve up to 5. it constitutes the overwhelming majority of psoriasis cases. elevated white cell count. The changes that are most common are pitting. While useful in trials. In this setting. Swabbing of pharynx and perianal area is recommended by some. The scores then multiplied by a factor which represents the proportion. however. they are not the mainstay treatment for psoriasis. The pustules are sterile.6% of cases.262 cases in Australia. Some authors recommend post-antibiotic urinalysis to monitor for post-streptococcal glomerulonephritis. thickness and scaling of all plaques on the body. Psoriasis severity is measured commonly by the Psoriasis Area and Severity Index (PASI) whereby four sections of the body (head. fever. there is frequently lethargy. then be followed by a period of typical CLINICAL SUBTYPES Plaque Psoriasis Plaque psoriasis constitutes 34–84% of cases in many JPOG JUL/AUG 2012 • 140 . The simplified PASI for clinical use. The morphology is different with often annular plaques with peripheral postulation. Therapy is not commonly needed. It has explosive onset and high fevers and other constitutional symptoms. and legs) are scored according to severity of psoriasis. and elevated liver transaminases. these three variables are each multiplied by the estimated percentage of body surface area covered by the plaques. Pustular This form is rare in children. longitudinal striations. The thickness of the plaques and degree of scaling can be highly variable from patient to patient although is usually consistent from plaque to plaque on a given patient. It is commonly precipitated by group A b-haemolytic streptococci infection or other viral infections. are estimated on a scale of 1–4. and children mostly will need medical admission and oral medication conducted by a dermatologist. Together with plaque psoriasis. It will often recur. It can involve oral/genital mucosa which demonstrates erythematous patches. followed by onycholysis. Then. as subclinical Streptococcus infection can at times be present. trunk.PAEDIATRIC S PAEDIATRICS I Peer Reviewed Figure 5. large studies. Oral antibiotics can be used to treat the throat or perianal infection. Guttate Guttate (‘drop-like’) psoriasis presents with a sudden onset widespread eruption of papules to small plaques. These are then summed to give the simplified PASI.
elbow. The treatment varies significantly from patient to patient depending on impact of disease. b-blockers. knees. It can be difficult to distinguish psoriatic from rheumatoid arthropathy. who are not bothered by their condition. however. Criteria for psoriatic arthritis proposed by Vasey and Espinoza Criterion I: Psoriatic skin or nail involvement Criterion II: Peripheral pattern 1. whittling of terminal phalanges. Pain and soft tissue swelling with or without limitation of motion of the peripheral joints involved in an asymmetrical peripheral pattern for over 4 weeks. and metatarsophalangeal joints. Trauma to the skin is well known to trigger a flare (Koebner phenomenon). Over time. lithium. and bony ankylosis Non-pharmacological strategies including counselling about the natural history of the disease is important Criterion III: Central pattern Arthropathy Psoriatic arthropathy is rare in children. if required. Grade 3 or 4 unilateral sacroiliitis fatty acid supplementation in adults has demonstrated marginal benefit. Pain and soft tissue swelling with or without limitation of movement of the distal interphalangeal joint for over 4 weeks 2. Complications such as elevated hepatic transaminases and Ig A nephropathy have been documented. Pencil-in-cup deformity. This includes a sausage digit 3. 1. Symmetrical peripheral arthritis for over 4 weeks. It is reasonable to treat minimally in young children. All treatments are considered to be suppressive rather than curative. Spinal pain and stiffness with the restriction of motion present for over 4 weeks 2. metacarpophalangeal joints. Table 1. fluffy periostitis. and ankle. There is no clear research suggesting dietary triggers or therapy in children. more commonly used in children. it can be debilitating. The criteria devised by Vasey and Espinoza have proven to be most sensitive (Table 1). proximal interphalangeal joints of the hand. or. in the absence of rheumatoid factor or subcutaneous nodules 4. it involves the wrists. particularly regarding patient/family fears of permanent disfigurement.PA EDIA TRICS I PA ED IATRICS Peer Reviewed plaque psoriasis. and most therapies are additive in combination. It is often worthwhile using a combination of therapies and encouraging maximum compliance in an attempt to clear the JPOG JUL/AUG 2012 • 141 TREATMENT Non-pharmacological strategies including counselling about the natural history of the disease is important. although omega-3 . It commonly involves the proximal and distal interphalangeal joints of the feet. Pharmacological triggers include chloroquine. Stress has been implicated in adults as an exacerbator of disease severity. withdrawal of systemic and potent topical steroids. hydroxychloroquine. and with aggressive combination therapy in older children. Grade 2 symmetric sacroiliitis according to the New York criteria 3.
tar or salicylic acid or calcipotriol can be used. tachyphylaxis. Hydrocortisone 1% BD 2. Add calcipotriol 0.5 mg/kg up to 500 mg orally BD for 10 days. It remains a popular choice in children because it obviates the systemic steroid absorption. The preparations are in cream or liquid form. zinc. Greasier emollients are easiest to spread and are best for drier skin. LPC= liquor picis carbonis. Coal tars: tar treatment has anti-inflammatory and antipruritic effects. Coal tar prepared 1% lotion topically nocte/BD or LPC (20% coal tar in alcohol solution) 4% + salicylic acid 2% in aqueous cream nocte/BD + moderately potent corticosteroid in the morning (both LPC and salicylic concentrations can be titrated up to 10%. consider addition of tacrolimus/pimecrolimus and/or bursts of more potent topical steroids. • glycerol 10% in sorbolene cream.) 2.005% OD or BD. The more potent preparations are used to treat thicker areas of skin.05% at night + moderate steroid in the morning. BD = twice daily. or roxithromycin (immediate) or cephalexin if penicillin-sensitive When clear. commence phenoxymethylpenicillin 12. (Seek dermatologic participation in management will be required. All treatments are considered to be suppressive rather than curative DISCUSSION OF MODALITIES Topical Emollient: emollients are best used on scaling or irritated skin. 4. LPC 1–2% in aqueous or zinc cream OD for maintenance. Recent streptococcal throat infection To eliminate this precipitant.) Genital area 1. a moderately potent corticosteroid cream applied OD. Add tazarotene 0.to high-potency steroids for limited periods of time. Facial and diaper region can be treated with mild preparations such as 1% hydrocortisone. Steroid: topical corticosteroids have antiinflammatory and anti-mitotic effects. Possible regimes psoriasis and then maintaining with minimal or no therapy (Table 2). Adverse effects include atrophy in areas of thin skin. based on response. although its odour and staining effects on skin affect compliance in older children. striae. Face and flexure LPC 2% + salicylic acid 2% in aqueous cream topically at night (coal tar solution) and hydrocortisone 1% ointment topically in the morning If refractory. preparations include: • aqueous cream ± liquid paraffin. Younger children in nappies: Moderately potent corticosteroid cream and anti-candidal cream (nystatin/imidazole). Its JPOG JUL/AUG 2012 • 142 . Acute pustular This presentation is serious and requires hospital admission. Scalp Shampoos containing corticosteroids. Trunks and limbs can be treated effectively with medium. consider light therapy in older children. or biologics/systemic therapy (see below). and hypothalamicpituitary-adrenal axis suppression. If the above fail. Topical therapy for plaque psoriasis affecting the trunk and limbs 1. OD = once daily. however. In cases of poor response after 2 weeks. • 50/50 liquid and white soft paraffin. and provide prompt relief. a less greasy preparation may be best in hot weather. 3.PAEDIATRIC S PAEDIATRICS I Peer Reviewed Table 2. In order of increasing greasiness.
such as systemic absorption or atrophy. folliculitis. Emollients provide prompt relief of scaling or irritated skin. When used as part of the Goeckerman regimen (daily topical coal tar and exposure to UV-A or UV-B). However. However. a study in children by Zvulunov on 58 children demonstrated remission in 81% and mild skin irritation in 20%. JPOG JUL/AUG 2012 • 143 . maximal effect is initiated after 6 weeks only. However. Tazarotene: tazarotene is a topical synthetic retinoid best used as an adjunct to topical steroid and other therapies if control is not achieved. Tacrolimus is a calcineurin inhibitor that acts by preventing the production of cytokines in T cells and mast cells. Theoretical risk of hypocalcaemia is unlikely if calcipotriene is not used on large surface area. potential increased mutagenicity and temporary genotoxicity. Local irritation is the only common side effect.PA EDIA TRICS I PA ED IATRICS Peer Reviewed adverse effects include local acne. and irritant/contact dermatitis. it has concurrently demonstrated carcinogenic. are of risk. Safety of treatment beyond 1 year’s duration has not been well established. While unsuitable for thick plaques owing to poor penetration and absorption. SYSTEMIC Systemic therapies are usually reserved for chronic severe psoriasis refractory to topical and light therapies. Calcipotriene can be used as an adjunct. it has proven efficacious in the treatment of adults. A small paediatric study in 2007 of 11 patients showed drastic improvement when applied to the face and intertriginous areas. Calcineurin inhibitors: tacrolimus and pimecrolimus are calcineurin blockers. or less commonly as a substitute. but a 20-year follow-up of 29 patients from Mayo Clinic did not find any cases of malignancies. Use in children is rare and only as an adjunct. Systemic therapies are usually reserved for chronic severe psoriasis refractory to topical and light therapies Calcipotriene: this vitamin D derivative can be used where adverse effects of steroids. it has proven to be highly effective in many studies. It can cause staining and troubling irritation. Studies suggest equal or better response than topical steroids and anthralin with reduced side effects. Anthralin: anthralin use remains controversial in children.
JPOG JUL/AUG 2012 • 144 BIOLOGICS Recently. all potential side effects are not known. and pseudotumor cerebri. Use as monotherapy is uncommon. .7 mg/kg/wk) provides excellent clearance according to one study. and can cause liver cirrhosis. Common side effects include nausea and vomiting.PAEDIATRIC S PAEDIATRICS I Peer Reviewed Coal tar medications remain a popular choice in children as they are considered to be safe.5 mg and folate administration. Systemic Retinoid Acitretin and isotretinoin have proven beneficial as single agent therapy for pustular and erythrodermic psoriasis. there have been advances in the use of biologic therapies for paediatric autoimmune disease. skeletal toxicity. Side effects can include skin fragility. Methotrexate Methotrexate (dosed at 0.2–0. with close monitoring of liver function tests and cholesterol. Therapy is generally commenced with 7. however less so for plaque psoriasis. Theoretical risks of malignancy and lymphoproliferative disorders seem to be minimal owing to the low doses and limited durations of treatment in this population. cyclosporine has proven efficacious in paediatric psoriatic patients. Close monitoring for renal function and blood pressure is required. It is often used as an adjunct to light therapy. It is a known abortifactant and teratogen. There have been advances in the use of biologic therapies for paediatric autoimmune disease Cyclosporin At doses of 3–5 mg/kg. Owing to the recent development newness of these therapies. deranged liver enzymes. conferring 75% PASI reduction in most children. Three TNF antagonist drugs have been commonly used in children for conditions such as Crohn’s disease and juvenile idiopathic arthritis.
Etanercept A multicentre. topical and systemic with no side effects. Side effect profile in the treatment of other diseases has been encouraging. Overall. It is given as subcutaneous injection once or twice weekly. Ustekinumab Ustekinumab is a human monoclonal antibody that inhibits interleukin receptor-mediated signalling. of which increased levels are found in active plaques. It is administered as twoweekly intravenous infusion. it has demonstrated success in patients with juvenile idiopathic arthritis. Adverse events including human papillomavirus. Three recent randomized controlled trials have demonstrated 12-weekly subcutaneous ustekinumab to improve clinical and quality-of-life parameJPOG JUL/AUG 2012 • 145 . Multiple studies have demonstrated dose-dependent clinical responses and linear pharmacokinetics. infection. it was well tolerated. with 53% of children achieving a physician’s global assessment of clear by 12 weeks (versus 13% in the placebo group).PA EDIA TRICS I PA ED IATRICS Peer Reviewed Psoriasis is believed to be mediated by tumor necrosis factor. Reports supporting infliximab in psoriasis include two case studies where both patients failed multiple therapies. most commonly associated with upper respiratory tract infection. gastroenteritis and influenza were reported. Adalimumab There is no literature on the use of adalimumab in paediatric psoriasis. randomized controlled trial has demonstrated efficacy versus placebo. but also rare cases of hepatosplenic lymphoma. pneumonia. However. Infliximab Infliximab is used for a variety of paediatric autoimmune diseases.
Conflict of interest: None. Gross J. Biologic modalities offer much promise for the efficacious and safe management of psoriasis in children. it is important to diagnose and establish early management. Pearce DJ. been conducted in children. Louden BA. however.PAEDIATRIC S PAEDIATRICS I Peer Reviewed ters. Version 3. Victoria. Morris A. Gottlieb AB.45:487–498. However. Pediatr Infect Dis J 2000. Side effects include erythema and hyperpigmentation. Available from: http://www. The pathogenesis of psoriasis and the mechanism of action of tazarotene. limit severity of the disease as well as reduce the psy- About the Authors Vyom Sharma is a hospital medical officer at the Royal Melbourne Hospital. The genetics of psoriasis. Martin NG.10:7.17:174–178. psoralen–UV-A therapy is uncommon since the advent of narrowband UV-B.17:364–375. Williams K. Dermatol Ther 2004. Conflict of interest: None. Melbourne. J Am Acad Dermatol 1993. and combination with topical/systemic modalities two to three treatments a week can be common.accessdata. Lebwohl M. Severe psoriasis—oral therapy with a new retinoid. Raychaudhuri SP.4:S129–S133. or infective morbidities. A Simplified Psoriasis Area Severity Index (SPASI) for rating psoriasis severity in clinic patients. US FDA. Henseler T. Childhood psoriasis a clinical review of 1262 cases. malignancies. Mays S. A comparative study of paediatric onset psoriasis with adult onset psoriasis. Australia. and as such their suitability and safety are yet to be assessed completely. Therapeutic guidelines: dermatology. Melbourne. J Am Acad Dermatology 1997. Initially published in Paediatrics and Child Health 2011. Lang W. Carcinogenicity has not been demonstrated. with no indication of links with cardiovascular. Rogers M. Duffy DKL. The relationship between infection with group A beta haemolytic streptococci and the development of psoriasis. Melbourne: Therapeutic Guidelines Limited. Fischer G. Pediatr Dermatol 2001. Fredriksson T. Adverse event rates were favourable. Royal Children’s Hospital.157:238–244. Curr Opin Pediatr 2002. Pediatric psoriasis and psoriatic arthritis.14:404–409. Asano AT. J Am Acad Dermatology 2001. Rogers M. Ongoing studies shall provide data regarding adverse events over a longer period of time.29:428–434. © 2011 Elsevier Ltd. Early intervention can maintain clearance. Rasmussen JE. chological and emotional stress of this disease. Psoriasis in Australian twins.19:153–154. Lewkoweiz D. David Orchard is Staff Specialist in the Department of Dermatology.18:188–198. Hagar C.fda. Spelman LS. Dermatology Expert Group. Dermatologica 1978. Highlights of prescribing information: Stelara™ ustekinumab). Childhood psoriasis. as it has demonstrated an increased risk of squamous cell carcinoma and melanoma. Treatment of psoriasis. Duvic M. 2009. Part 1.gov /drugsatfda_docs/label/2009/125261lbl. Pettersson U. Topical therapy and phototherapy. Narrowband therapy reduces dose of UV. Feldman SR. Dermatol Online J 2004. Psoralen–UV-A A psoralen is administered before UV therapy in this regime as a photosensitizer. either orally for generalized photosensitization or topically for local effect. Parkville.pdf.21(3):126–131. Ali S. CONCLUSION Considering that a significant proportion of adult cases of psoriasis develops in children. Australia.37:S1–S11. J Am Acad Dermatol 1998. Pediatr Dermatol 2000. These studies have not. JPOG JUL/AUG 2012 • 146 . Further Reading LIGHT TREATMENT UV-B UV-B has been demonstrated to be safe and efficacious in children.
increasing from around 40% in girls aged 12 years. MRCOG. The initial onset of primary dysmenorrhoea is usually shortly after menarche (6–12 months). and secondary dysmenorrhoea where there is an identifiable pathological condition known to contribute to painful menstruation. ‘meno’ meaning month. but decreases with advancing age. the reported prevalence is age-related. Shilpa Deb. Shilpa Deb. The term dysmenorrhoea is derived from the Greek words ‘dys’ meaning difficult.G YNA GYNA ECOLOGY ECOLOGY I Peer I Peer Reviewed Reviewed Dysmenorrhoea Dysmenorrhoea Shilpa Kolhe. MD. MD. MRCOG BACKGROUND Dysmenorrhoea is a medical condition characterized by severe uterine pain during menstruation manifesting as cyclical lower abdominal or pelvic pain. MBBS. One systematic review of community and hospital surveys estimated the overall prevalence to be 45–95% whilst a second age-based systematic review suggested 25–50% of adult women and as many as 75% of adolescents experience pain with menJPOG JUL/AUG 2012 • 147 . when ovulatory cycles are established. However. Symptoms of primary dysmenorrhoea begin a few hours before the start of menstruation and are often relieved during the first few days of bleeding. DGO. Secondary dysmenorrhoea can also occur at any time after menarche but is most commonly observed in women in their third and fourth decade of life in association with an existing condition. Since dysmenorrhoea is a symptom that could be perceived differently by different women. to 70% in girls at 17 years of age. MBBS. and ‘rrhea’ meaning flow. An epidemiological study showed that the prevalence of dysmenorrhoea among adolescent females ranges from 60% to 93%. MBBS. MRCOG Shilpa Kolhe. MRCOG. It is commonly divided into primary dysmenorrhoea. where there is no coexistent pathology. DGO. which may also radiate to the back and thighs. painful or abnormal. MBBS. it is difficult to establish its true incidence.
This effect is mediated via myometrial oxytocin and vasopressin V1a receptors. It is also found that the levels of prostaglandins in endometrial fluid in the early follicular phase of menstrual cycle are less than levels in late luteal phase of menJPOG JUL/AUG 2012 • 148 arrhoea and nausea are commonly associated with primary dysmenorrhoea. and feeling depressed. dieting. The other reported factors in the causation of increased myometrial activity are increased levels of circulating vasopressin and leukotrienes. may increase the sensitivity of pain fibres in the uterus. The role of vasopressin may relate to prostaglandin synthesis and release. it is thought that this myometrial activity is modulated and augmented by prostaglandin synthesis. such as cigarette or alcohol use. It is one of the most commonly reported reasons for absenteeism from school or work with some studies suggesting that 10–45% of women miss or reduce time at work. the annual economic loss has been estimated at 600 million work hours and 2 billion dollars. This may reflect the increase in circulating levels of prostaglandin F 2α. PGF 2 and PGE 2 can cause contraction of bronchial. and that the clinical manifestations of dysmenorrhoea are similar to those with prostaglandin-induced labour or medical management of miscarriage. In contrast to the uterine contractions in normal menstruation. (The hypothesis that prostaglandins released from the endometrium at the time of menses contribute to dysmenorrhoea is supported by the observation that endometrial concentrations of prostaglandin E2 (PGE2) and prostaglandin F2 (PGF2) correlate with the severity of dysmenorrhoea. reach higher active pressures (frequently more than 150 mm Hg). contractions in women with primary dysmenorrhoea often begin with elevate basal tone. vomiting.GYNAECOLOGY I Peer Reviewed struation. One community survey of adolescents aged 12–18 years showed dysmenorrhoea as one of the most common biomedical problems causing health risk behaviours and psychosocial problems. Increased endometrial expression of leukotrienes has been demonstrated in women with primary dysmenorrhoea resistant to prostaglandin antagonists. and vascular smooth muscle resulting in bronchoconstriction. bowel. infrequent/never seat belt use. and are non-rhythmic or in coordinate. as well as PGE2. Pain is significant in 5–20% who report severe dysmenorrhoea or pain that prevents them from participating in their usual activities. diarrhoea. Di- PATHOPHYSIOLOGY The most important physiological event reported with dysmenorrhoea is increased myometrial activity with accompanying uterine ischaemia (uterine ‘angina’). These reports suggest a significant socio-economic and psychosocial impact of dysmenorrhoea on female health during the reproductive years. While the pathophysiological mechanisms that cause this are not entirely understood. Psychosocial factors may play a role in the perception and the severity of the pain. which stimulates the type C afferent pain neurones. leukotrienes. In addition to stimulating uterine contractions. CLINICAL FEATURES History is critical in establishing the diagnosis of . nausea. In the United States. that cyclo-oxygenase inhibitors decrease menstrual fluid prostaglandin levels and decrease pain. strual cycle. and hypertension. school or other activities. which is a potent myometrial stimulant and vasoconstrictor. Doppler flow studies have supported this hypothesis by showing higher uterine and arcuate artery resistance on the first day of menses in women with primary dysmenorrhoea than in controls.
which may radiate to the back and along the thighs. irritability (72%). bloating.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed Table 1. cyclicity and severity of pain and associated symptoms such as nausea. dizziness (28%). and provide reassurance through a negative assessment. PRIMARY DYSMENORRHOEA Primary dysmenorrhoea almost invariably occurs in young women with ovulatory cycles and usually appears within a year after menarche. lower backache (60%). One should specifically determine the factors that exacerbate or ameliorate the symptoms. leukotrienes Usually self-limiting. subfertility. intermenstrual. as secondary dysmenorrhoea is more commonly refractory to simple treatments such as non-steroidal anti-inflammatory drugs (NSAIDs) and the combined oral contraceptive (COCP). Associated symptoms – such as malaise and fatigue (85%). Differential characteristics of primary and secondary dysmenorrhoea Primary Age (years) Onset of pain Pathophysiology Symptoms 16–25 Just prior to menstruation (spasmodic) Excess prostaglandins. The pain classically begins just before or with the onset of menstruation lasting through the first 1–2 days and is typically described as spasmodic lower abdominal or pelvic pain superimposed over a constant dull aching pain. The diagnosis of primary dysmenorrhoea is made primarily based on history and then by exclusion of existing pathology. It is then important to exclude the secondary causes of dysmenorrhoea – such as pelvic infection. duration and amount of menstrual flow. diarrhoea and fatigue is essential in the diagnosis of dysmenorrhoea. vomiting. vasopressin. sexually transmitted disease. and subfertility. Social and family history should be considered as they may have direct or indirect bearing on the causation and help in optimizing the treatment (Table 1). dysmenorrhoea and also in differentiating between primary and secondary dysmenorrhoea. NSAIDs = non-steroidal anti-inflammatory drugs. diarrhoea (60%). Pelvic or rectal examination where appropriate may be helpful to exclude common problems of young age such as pelvic inflammatory disease and endometriosis. headache (45%). Menstrual bleeding is usually normal. Psychosexual factors may be contributing to dysmenJPOG JUL/AUG 2012 • 149 . and an assessment of the onset. duration. enlarged. fixed. postcoital bleeding. cycle length and regularity. lasts for first 1–3 days menstruation Responds to COCP and NSAIDs Periods normal or light Unremarkable Secondary 30–45 Pain often progresses through late luteal (congestive) Underlying disorder Associated with other features related to underlying disease Resistant to COCP and NSAIDs Periods often heavy Dependent on cause but may include a tender. abdominopelvic surgery and difficult childbirth – which could present with additional symptoms of deep dyspareunia. retroverted uterus with adnexal tenderness and a mass Signs COCP = combined oral contraceptive. A thorough menstrual history including the age at menarche and at the onset of pain. and nausea and vomiting (89%) – may be present. type. endometriosis.
Endometriosis may be an isolated finding or associated with a uterine abnormality. reiterating the importance of pelvic examination in this group of patients. Similar findings may be seen in adolescents with acute or chronic pelvic inflammatory disease. and unilateral or bilateral adnexal masses. The pain associated with secondary dysmenorrhoea is more likely to coincide or be temporally associated to other gynaecological symptoms. which is largely due to endometriosis. Microscopy and culture of swabs from the endocervix for Chlamydia and gonorrhoea should be obtained together with a high vaginal swab . vaginal discharge. The pain is different to that of primary dysmenorrhoea and is described as pelvic heaviness and back pain increasing progressively throughout the late luteal phase and peaking with the onset of menstruation. dyspareunia. decreased uterine mobility. Women with endometriosis who present with secondary dysmenorrhoea have physical findings approximately 40% of the time. but a full blood count to exclude anaemia should be undertaken in women with associated menorrhagia. SECONDARY DYSMENORRHOEA Secondary dysmenorrhoea mainly occurs in the third and fourth decade of reproductive life. which is largely made on clinical findings. intermenstrual bleeding. such as cycle irregularity. Major Causes of Secondary Dysmenorrhoea Gynaecologic disorders: • Endometriosis • Adenomyosis • Pelvic inflammatory disease • Fibroids • Endometrial polyps • Ovarian cysts • Intrauterine contraceptive device • Intrauterine adhesions • Congenital obstructive mullerian malformations • Pelvic congestion syndrome • Cervical stenosis Non-gynaecologic disorders: • Inflammatory bowel disease • Irritable bowel syndrome • Urogenital disease • Psychogenic disorders The most common cause of secondary dysJPOG JUL/AUG 2012 • 150 INVESTIGATIONS Careful analysis of the clinical findings should be made and investigations directed towards the likely underlying causes. More extensive disease will manifest similarly to that seen in older women with nodular disease over the uterosacral ligaments and rectovaginal septum. ovarian cyst or presence of congenital anomaly in the urogenital tract. menorrhoea is endometriosis. There are no specific tests to diagnose primary dysmenorrhoea. rectovaginal and uterine tenderness associated with cervical excitation is seen in 76% of adolescents with endometriosis. and postcoital bleeding. A small but significant minority of adolescent girls will have secondary dysmenorrhoea. Routine blood tests are not usually indicated in patients with isolated dysmenorrhoea.GYNAECOLOGY I Peer Reviewed orrhoea and should be considered where medical treatment is unsuccessful. This pattern of pain is often referred to as ‘congestive pain’ in contrast to the ‘spasmodic’ pain seen with primary dysmenorrhoea. It is important to remember that absence of abnormal findings does not exclude secondary dysmenorrhoea and should be complemented with a transvaginal ultrasound. heavy periods. Adnexal. which is more likely when dysmenorrhoea occurs during the first or second cycles after menarche.
can prove beneficial in the diagnosis of endometrial pathology. Laparoscopy is the gold standard in investigation of peritoneal endometriosis. B6. to ascertain or clarify diagnosis. Transvaginal ultrasound is preferable to transabdominal as it offers more resolution and can also be used as an extension of the pelvic examination to qualify tenderness and uterine mobility. TENS = transcutaneous electrical nerve stimulation. These tests are non-specific but may be used to monitor disease progression or response to therapy. In certain cases. quality of life scales. Whichever system is used. MANAGEMENT Treatment for dysmenorrhoea is aimed at relieving symptoms and is best treated with analgesics that are prostaglandin inhibitors so as to affect the physiological mechanisms behind menstrual pain and by directing treatment at the underlying pathology. and compound analgesics Magnesium Thiamine Vitamin B1. which is raised in some cases of endometriosis. Four-dimensional ultrasound may have a role in assessing the frequency and intensity of myometrial activity associated with dysmenorrhoea. Table 2.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed from the posterior vaginal fornix for other sexually transmitted diseases. Underlying causes of secondary dysmenorrhoea – such as fibroids. which is shown to be comparable with hysteroscopy in diagnosing endometrial lesions (Tables 1 and 2). consideration should be given to saline infusion sonography. intrauterine contraceptive devices and ovarian cysts including endometriomas – are best assessed with ultrasound. Many studies have employed patient self-reporting using a visual analogue or other pain scale. Evidence-based treatment options for dysmenorrhoea Grade A NSAIDs (other than aspirin) Combined oral contraceptives Grade B & C Aspirin. also allowing treatment at the same time. Additional measures include analysis of the proportion of women requiring analgesics in addition to their assigned treatment and recording the percentage of women reporting activity restriction of social activities or absenteeism from work or school. Hysteroscopy may be indicated to evaluate intrauterine pathology suggested by imaging and may be combined with resection of an endometrial polyp or sub-mucosal fibroid. therefore. adhesions and chronic pelvic inflammatory disease. To improve the sensitivity and specificity of ultrasound in the detection of endometrial lesions including polyps and submucosal fibroids. paracetamol. The same is true of the tumour marker CA-125. Three-dimensional ultrasound offers the benefit of assessing organs in coronal plane and. E Fish oil High-frequency TENS Topical heat (about 39°C) Exercise Japanese and Chinese herbal medicine Unknown Levonorgestrel intrauterine system Surgical interruption of pelvic nerve pathways Acupuncture Behavioural interventions Magnet therapy Vasopressin antagonists Low-frequency TENS No benefit Spinal manipulation NSAID = non-steroidal anti-inflammatory drug. a diagnostic laparoscopy may be required. A raised white cell count suggests infection and may be associated with a raised erythrocyte sedimentation rate and C-reactive protein in patients with chronic pelvic inflammatory disease. grading dysmenorrhoea according to severity of JPOG JUL/AUG 2012 • 151 . or other similar measures such as the menstrual distress or menstrual symptom questionnaires.
Nineteen different types of Cox-1 NSAIDs and two Cox-2 NSAIDs (meloxicam and etoricoxib) were evaluated. 4.GYNAECOLOGY I Peer Reviewed pain and limitation of daily activity will help guide the treatment strategy and catalogue the response to treatment (Table 2). or the concomitant use of medications known to increase the likelihood of upper gastrointestinal adverse events.27). Although known to have reduced gastrointestinal toxicity. because they are generally used for short periods in otherwise healthy young women. It is proposed that NSAIDs relieve primary dysmenorrhoea mainly by suppressing the production of endometrial prostaglandins. A recent Cochrane review analysed 73 randomized controlled trials (RCTs). JPOG JUL/AUG 2012 • 152 . that NSAIDs are associated with adverse effects including headache. meclofenamate) may be preferred. NSAIDs that achieve peak serum concentrations within 30–60 minutes and have a faster onset of action (eg.50. However. While all NSAIDs are thought to be effective. such as corticosteroids and anticoagulants – the potential risks and benefits of using an NSAID should be considered and discussed with the patient. naproxen and ibuprofen appear significantly better than mefenamic acid and aspirin in terms of the need for rescue analgesia. drowsiness.05–3. ibuprofen. they are frequently well tolerated and free of serious toxicity in most patients. Besides. Cox-2 inhibitors are more expensive. CI. NSAIDs (with an exception of aspirin) were significantly superior to placebo in reducing the pain associated with primary dysmenorrhoea (odds ratio. and meloxicam was significantly less effective for pain relief than diclofenac. Etoricoxib did not differ significantly in efficacy from naproxen. 1. Medical Treatments NSAIDs (Other Than Aspirin) NSAIDs are the mainstay of treatment for primary dysmenorrhoea.85– 5. 95% CI. and aspirin hypersensitivity because of their pharmacokinetic and pharmacodynamic drug interactions and possible effects on platelet aggregation. gastrointestinal bleeding. When treating women with risk factors for NSAID-induced ulceration – which include previous clinical history of gastroduodenal ulcer or perforation. thus inhibiting synthesis of prostaglandins. 95% confidence interval.90. probably owing to the short-term administration only. 3. Some recommended doses are as follows: naproxen 250–275 mg four to eight hourly. NSAIDs were also significantly more effective for pain relief than paracetamol (OR. naproxen. with evidence from one systematic review that their use is associated with a reduced restriction of daily activities. NSAIDs are also contraindicated in patients with renal insufficiency. Gastrointestinal ulceration and haemorrhage were less prominent side effects. bleeding diatheses. and the need for additional analgesia compared with placebo. a gastro-protective agent should also be prescribed. there was no significant difference found in their efficacy (P > 0. relieving pain by up to 70%. absenteeism. however. It should be remembered. OR. 1.05). ibuprofen 400 mg three. dizziness and dryness in addition to gastrointestinal effects like nausea and indigestion. In addition. When NSAIDs were compared with each other. there may be direct analgesic action on the central nervous system (Dawood 2006).44). neither Cox-2 NSAIDs differed significantly in tolerability from the Cox-1 comparators. NSAIDs inhibit cyclooxygenase (Cox) type 1 and 2 pathways. thus alleviating cramps and restoring normal uterine activity. It is unclear which NSAIDs have better efficacy or safety and when is the optimal time to initiate treatment. NSAIDs – with the exception of Cox-2 inhibitors – may also benefit social interaction. If an NSAID is offered in this situation.
therefore. Transdermal and vaginal ring contraceptives have a favourable impact on dysmenorrhoea similar to that noted with the use of COCP. Improvement in pain was reported in five studies that compared COCP to placebo (OR. This in turn reduces the amount of prostaglandin produced by glands in the lining of the uterus. nimesulide 50–100 mg twice daily. aspirin or naproxen in two systematic reviews. This method of approach eliminates the risks associated with taking NSAIDs for pain relief. Coproxamol (paracetamol and dextropropoxyphene) appears to be superior to placebo. poorly tolerated or contraindicated. The extended cycle regimen might be associated with less menstrual pain than the monthly regimen.5–15 mg daily.08). future trials comparing the two regimes are warranted. but is associated with more side effects than naproxen and is less effective than mefenamic acid. Over 90% of adolescents with primary dysmenorrhoea report a reduction in pain within 3 months of commencing a COCP containing at least 30 μg of oestrogen. Tricycling COCP has been used to treat women with severe dysmenorrhoea especially that associated with endometriosis. diclofenac 200 mg/day in divided doses. 2. COCP is thought to work by inhibiting ovulation Other hormonal therapies such as progestogens (depomedroxyprogesterone acetate and levonorgestrel). Paracetamol and Compound Analgesics and. However. the oestrogen-dependent proliferation of the endometrium and reduced secretion of progesterone. which then reduces both uterine blood flow and cramps. meloxicam 7. Aspirin.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed four or six times daily. One systematic review found that aspirin was significantly more effective than placebo for pain relief but not as effective as ibuprofen. A Cochrane systematic review on the efficacy of modern COCP (low-dose oestrogen) found COCP as effective as gonadotrophin-releasing hormone analogue in treating painful symptoms of endometriosis. mefenamic acid 250 mg eight hourly.01. Another RCT concluded that one to two tablets of combination of ibuprofen and paracetamol provided superior analgesic efficacy than placebo. Zahradnik et al suggested that COCPs should be used as a first-line therapy in women with dysmenorrhoea who also wish contraception. danazol and gonadotrophin-releasing hormone analogues – again work by inhibiting ovulaJPOG JUL/AUG 2012 • 153 . A Cochrane systematic review of the efficacy of COCPs for primary dysmenorrhoea analysed 10 RCTs out of the 23 identified. Pareek et al found that fixed-dose combination of aceclofenac–drotaverine (NSAID + antispasmodic) was superior to monotherapy with aceclofenac in women with primary dysmenorrhoea. There were no studies identified that directly compared COCP to NSAIDs in the management of dysmenorrhoea. naproxen and mefenamic acid (number needed to treat for aspirin was 10.32–3. Combined oral contraceptive pills containing less than 35 μ g of oestradiol have been shown to control symptoms of dysmenorrhoea effectively and therefore should be the preferred choice of COCP. 95% CI. 1. Combined Oral Contraceptives COCPs are commonly used as second-line therapy for primary dysmenorrhoea where NSAIDs are ineffective. compared with only 2 or 3 for other NSAIDs). There is strong evidence to support the use of COCPs containing low-dose oestrogen for the treatment of dysmenorrhoea. Other Hormonal Therapies Paracetamol was shown to offer no additional pain relief than placebo.
although both active drug and placebo reduced pain. the benefits of magnesium. salpingectomy and ablation or excision of endometriotic deposits or hysteroscopic resection of endometrial polyps. although more research is needed to quantify this effect. The dose and regimen of treatment with magnesium to be used is still unclear. Pyridoxine – pyridoxine (vitamin B 6) is shown to be more effective at reducing pain when compared with placebo and a combination of magnesium and vitamin B 6. Dependent upon the aetiology. however. However. ovarian cystectomy. Vitamin B 1 – one large trial showed vitamin B 1 to be more effective than placebo in reducing pain. results are limited by the poor methodological quality of the trials. In severe cases of endometriosis resistant to medical therapy. A total of 87% of patients were cured up to 2 months after treatment. surgical procedures such as laparoscopic uterine nerve ablation and presacral neurectomy may be performed for symptomatic relief of pain in refractory cases of dysmenorrhoea. These two surgical procedures interrupt most of the cervical sensory nerve fibres (thus diminishing uterine pain). Although there is insufficient evidence to support its routine use. They are frequently used for short periods of no more than 6 months to provide a few months of amenorrhoea and relief from symptoms in women debilitated by their pain. There is some evidence supporting the benefits of a low-fat vegetarian diet on dysmenorrhoea in parous women. Adverse effects associated with fish oil treatment were mild and included nausea and worsening of acne. Magnesium – there is limited evidence on JPOG JUL/AUG 2012 • 154 . Chinese herbal medicine – there is some promising evidence supporting the use of Chinese herbal medicine for primary dysmenorrhoea. this may necessitate conservative laparoscopic or open surgery with adhesiolysis. intrauterine adhesions and sub-mucosal fibroids. hysterectomy. It is generally not indicated for treating primary dysmenorrhoea. Omega-3 fatty acids (fish oil) – one RCT has shown that the use of omega-3 fatty acids may reduce pain. Conservative Treatments Herbal Products and Dietary Supplements Thiamine – a single large randomized controlled trial has shown beneficial effects of thiamine (100 mg daily) on menstrual pain when used for 2 months or more. Surgical Treatments Surgical intervention may be necessary to treat the underlying cause of secondary dysmenorrhoea. Vitamin E – a RCT showed vitamin E alone (500 units per day or 200 units twice per day. The levonorgestrel-releasing intrauterine system. the results of three small trials comparing magnesium with placebo showed that magnesium was more effective than placebo for pain relief and the need for additional medication was less. with or without bilateral oophorectomy. may be required. beginning 2 days before menses and continuing through the first 3 days of bleeding) was more effective than placebo for relieving dysmenorrhoea in adolescents randomly assigned to either therapy. can be of benefit in treating coexistent menorrhagia.GYNAECOLOGY I Peer Reviewed tion and suppressing the menstrual cycle and can occasionally be used for resistant dysmenorrhoea. although not licensed for the treatment of dysmenorrhoea. Japanese herbal medicine – one small trial showed the natural herbal remedy tokishakuyaku-san to be more effective for pain relief than placebo and less use of additional pain medication.
but only one trial noted greater pain reduction in the real versus the sham acupuncture group. there is no evidence to suggest that spinal manipulation is effective in the treatment of primary or secondary dysmenorrhoea. resulting in lower perception of painful uterine signals. The heat wrap provided better pain relief than acetaminophen and was well tolerated. Overall. There are trials underway assessing the role of vasopressin antagonists. biofeedback. Beta-agonists and calcium channel blockers are reported to be of some benefit in dysmenorrhoea. A trial randomly assigned women with dysmenorrhoea to an abdominal heat wrap (40°C) which was worn for 8 hours. electromyographic training. TENS is thought to have two effects: (1) it raises the threshold for pain signals from uterine hypoxia and hypercontractility by sending a volley of afferent impulses through the large diameter sensory fibres of the same nerve root. A larger and better designed RCT found no significant difference between spinal manipulation and placebo manipulation after 1 month. and (2) it stimulates release of endorphins from the peripheral nerves and the spinal cord. hypnotherapy. vitamin K. a placebo wrap. acetaminophen (1. Topical heat treatment – heat to abdomen appears to be as effective as oral analgesics for relief of dysmenorrhoea. More data from controlled trials demonstrating safety and efficacy need to be done before these modalities can be recommended. yoga) for treatment of dysmenorrhoea. Alverine citrate. or placebo pills. Three trials compared acupuncture to sham acupuncture. hence reducing menstrual pain. These include attempts at modification of the way the woman thinks about her pain (eg. Transdermal glyceryl trinitrate is useful as a modulator of uterine contractility and an alternative for the management of primary dysmenorrhoea. four times per day for 1 day). and magnet therapy in the treatment of dysmenorrhoea. all three observed a reduction in pain in both groups. Lamaze exercises. Transcutaneous electrical nerve stimulation – transcutaneous electrical nerve stimulation (TENS) seems to work by altering the body’s ability to receive or perceive pain signals.000 mg every 5 hours. imagery. Spinal manipulation – spinal manipulation may improve spinal mobility and pelvic blood flow. magnesium.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed Alternative remedies Acupuncture – there is limited evidence from controlled trials to support the use of complementary alternative medicine (acupuncture. limited-quality RCTs. but none is licensed for this indication. A meta-analysis from the Cochrane database including three trials (n = 124 women) found that high-frequency (50–120 Hz) TENS was more effective than placebo TENS for relief of dysmenorrhoea but is less effective than ibuprofen. an anticholinergic antispasmodic. is licensed for the treatment of dysmenorrhoea. JPOG JUL/AUG 2012 • 155 . coping strategies) and attempts at modification of her response to pain (eg. This has been reported as an effective alternate treatment for dysmenorrhoea in two small. but there is a lack of published evidence on its efficacy for this indication and it is unlikely to be as effective as NSAIDs or the COCP. desensitization-based procedures. antispasmodics. and relaxation training). Other Non-hormonal Therapies Exercise – systematic review on the use of exercise for relief of dysmenorrhoea included a single randomized trial that provided some evidence that exercise reduces menstrual symptoms. Behavioural interventions – a systematic review concluded that behavioural interventions may be of benefit in treating women with dysmenorrhoea. although is limited by its side effect of headache.
progression and eventual outcome depend on the underlying pathology. Nonsteroidal antiinflammatory drugs for primary dysmenorrhoea. Proctor ML. Behavioural interventions for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev 2007. Conflicts of interest: None declared. Proctor ML. Spinal manipulation for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev 2005.(3):CD002248.GYNAECOLOGY I Peer Reviewed Practice points supportive providing symptomatic relief.(3):CD002119. Roberts H. as its severity. peaking with onset of menstruation • History is critical in establishing the diagnosis of dysmenorrhoea • Treatment is aimed at symptomatic relief with analgesics – especially NSAIDs – and at treating the underlying pathology Further Reading Chantler I. Suckling J. There is no coexisting pathology • Secondary dysmenorrhoea is always associated with an underlying pathology and is characterized by congestive menstrual pain. Cochrane Database Syst Rev 2010.24:39–44.21(11):311–316. Proctor ML. It is a leading cause of absenteeism. Pain Med 2007. Acupuncture for primary dysmenorrhoea: a systematic review. Proctor M. UK. Farquhar C. Oral contraceptive pill for primary dysmenorrhoea. The effect of three cyclo-oxygenase inhibitors on intensity of primary dysmenorrheic pain. Cochrane Database Syst Rev 2002. Fuller A. Shilpa Deb is a Consultant in Obstetrics and Gynaecology at Nottingham University Hospitals NHS Trust. Johnson TC. Nottingham. CONCLUSIONS Dysmenorrhoea has a significant physical. Mainstay treatment is generally JPOG JUL/AUG 2012 • 156 About the Authors Shilpa Kolhe is a Senior Registrar in Obstetrics and Gynaecology at Queen’s Medical Centre. Pattison HM.8:295– 300. Farquhar CM. • Around 40–70% of women suffer with dysmenorrhoea • Increased myometrial activity induced by an excessive production of prostaglandin causing ischaemia is the most accepted pathophysiological mechanism • Primary dysmenorrhoea is seen in young women with ovulatory cycles and is characterized by spasmodic menstrual pain starting just before menstruation lasting for 24–48 hours. which increases progressively through the late luteal phase. Tugay N. Mitchell D. . Conflicts of interest: None declared. UK. Hwang EW. Murphy PA. affecting 40–70% of women of reproductive age. psychological and social impact. behavioural. Effectiveness of transcutaneous electrical nerve stimulation and interferential current in primary dysmenorrhea. Queen’s Medical Centre Campus. Farquhar C. Cochrane Database Syst Rev 2009. Cho SH. Marjoribanks J.(4):CD002120. and more directive surgical treatment should be reserved for specific secondary causes of dysmenorrhoea or for refractory cases. Johnson NP. Hing W. Latthe PM.(4):CD001896. Demirturk F. Exercise for dysmenorrhoea.(1):CD001751. Herbal and dietary therapies for primary and secondary dysmenorrhoea. Initially published in Obstetrics. Brown J. Brown S. Cochrane Reviews PROGNOSIS There are very few longitudinal studies examining the progression and eventual outcome of primary or secondary dysmenorrhoea. et al. Clin J Pain 2008. Gynaecology and Reproductive Medicine 2011. Khan KS. but it probably reflects increased myometrial activity induced by an excessive production of prostaglandin causing ischaemia. BJOG 2010. The prognosis of secondary dysmenorrhoea is not known. Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhoea. Akbayrak T. Proctor ML. Cochrane Database Syst Rev 2010. Wong CL.117:509. Farquhar CM. The exact pathophysiological processes are not fully understood. Cochrane Database Syst Rev 2006.(2):CD004142. Primary dysmenorrhoea often improves in the third decade of a woman’s reproductive life and appears to be reduced after childbirth. © 2011 Elsevier Ltd. Nottingham. Murphy PA.
This article aims to summarize the current position. Over-the-counter alternative products have no better effect than placebo. limiting alcohol intake. Opinions concerning the benefits and risks of HRT have varied over the past decade.G YNA ECOLOGY I Peer Reviewed What Are the Benefits and Risks of HRT? Elizabeth Farrell. and longitudinal studies have shown that significant symptoms may last up to a mean of 8 years. and will depend on the age of the woman at the time of her menopause. About 20% of women will have moderate to severe symptoms that interfere with quality of life. and undertaking regular exercise. and • as a first-line therapy in young women with osteoporosis. with about 10% of women affected having symptoms for 10 years or more. cessation of smoking. This lifestyle plan should include healthy eating. JPOG JUL/AUG 2012 • 157 .and postmenopausal women. in particular for the vasomotor symptoms of hot flushes and sweats and symptoms relating to the atroph- ic changes in the urogenital tract. FRCOG H ormone replacement therapy (HRT) is the most effective treatment for menopause symptoms in peri. as given in the most recent recommendations of the International Menopause Society. AM. being a healthy weight.1 All menopausal women should be advised to develop a healthy lifestyle programme in addition to possibly taking HRT. INDICATIONS FOR HRT The indications for prescribing HRT are • the presence of moderate to severe menopausal symptoms impacting on a woman’s ability to function normally. FRANZCOG.
HRT can be ceased every 4 to 5 years to see if symptoms recur. These younger women often require high-dose therapy. yearly after her regimen is effective in improving her symptoms and quality of life. Combined therapy of oestrogen and a pro- . and gels. cardiovascular disease and perhaps also an increase in mood disorders and dementia. for effective symptom control and to preserve bone density.GYNAECOLOGY I Peer Reviewed All menopausal women should develop a healthy lifestyle. with a yearly risk–benefit analysis being made. or perhaps longer. Recently. The duration of therapy should not be fixed but reassessed yearly. in addition to possibly taking hormone replacement therapy. It is usually advised that these women take HRT at least until they are 50 years of age. PREMATURE AND EARLY MENOPAUSE Women experiencing a premature menopause (before the age of 40 years) or an early menopause (before the age of 45 years) are at greater health risks of early onset of osteoporosis. there has been a reduction in the number of products available for women because pharmaceutical companies have withdrawn various products for financial reasons (not because Some of the menopause symptoms women experience are listed in the box on page 159. The dose of HRT prescribed should be the lowest effective dose that reduces symptoms and improves quality of life. but should always be individualized. it may be required for 5 to 10 years. have her regimen tailored over further visits and then be seen at least JPOG JUL/AUG 2012 • 158 MONITORING OF PATIENTS ON HRT to determine the appropriate combination of hormones. of any safety issues). Regular screening is recommended. sometimes requiring up to 6 months A woman who is prescribed HRT should be reviewed after 2 to 3 months. patches. either HRT or the oral contraceptive pill. HRT PRESCRIBING The HRT products available include tablets.
Cyclical progestogens (E+P) are used in perimenopausal cycling women and continuous progestogen (E+P) after menopause. They are a potential medicolegal hazard for prescribers and should not be advocated. Menopause symptoms1 • Hot flushes – in 80% women – significant in 20% of affected women – last longer than 5 years in 25% of affected women Night sweats Muscle/joint pains Formications Anxiety. the Women’s Health Initiative (WHI) investigators reanalysed their data about coronary heart So-called ‘bioidentical’ or ‘natural’ HRT products. and oestrogen alone (oestrogen replacement therapy.3 JPOG JUL/AUG 2012 • 159 . low libido Fatigue Overall diminished wellbeing A recent follow-up study of the WHI showed a reduced risk of breast cancer in the women who took oestrogen alone for 7 years • • • • • • • • • various medical conditions. are untested for long-term safety and efficacy and avoid the safeguards of Therapeutic Goods Administration registration. The incidences of menopause symptoms and of disease (CHD) that had lead to scare headlines in 2002. which are formulated from imported hormones by local compounding pharmacies. No morbidity was significantly increased in this group.2 They found that there was an ‘absence of excess risk of CHD and the suggestion of reduced total mortality in younger women’. which is the group normally treated with HRT. This offered reassurance to those women initiating HRT under the age of age 60 years for symptom control. This is also reassuring for these women. The research literature needs to be interpreted accordingly and may not necessarily be applicable to all community groups. Tibolone is another option for postmenopausal women. A recent follow-up study of the WHI showed a reduced risk of breast cancer in the women who took oestrogen alone for 7 years. concentration Vaginal dryness. depending on a woman’s country of origin and the length of time she has lived in Australia. ERT) in women who have had hysterectomies. irritability Sleep disturbances Lessened memory. will also vary within our population. Most studies in women using HRT have been in western industrialized countries with mainly Caucasian populations. Meta-analysis of other studies supports this conclusion. such as breast cancer.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed gestogen (E+P) should be prescribed in women with a uterus. NEW MESSAGE ABOUT HRT NEAR MENOPAUSE In 2007. Urogenital symptoms can be treated appropriately with vaginal oestrogen therapy either alone or in combination with HRT.
BENEFITS AND RISKS OF HRT Benefits HRT has the following beneficial effects: • relieves vasomotor symptoms of hot flushes and sweats • reverses urogenital atrophic symptoms. HRT may have beneficial effects on the followJPOG JUL/AUG 2012 • 160 ing menopause symptoms: • aches and pains in joints and muscles • insomnia or sleep problems • loss of libido • mood disturbance • quality of life. If HRT is commenced in healthy women around the time of the final menstrual period. Risks of specific cancers and of other conditions are summarized below. there may be a reduction in cardiovascular risk and a reduction of Alzheimer’s dementia. arteries. Breast Cancer The WHI study has shown no increase in the risk of breast cancer in first-time E+P HRT users 5 years . Risks Most studies on the risks of HRT focus on the risks of cancer associated with its use. HRT may also improve sexual function. and intervertebral discs. loss of lubrication • prevents bone loss due to oestrogen deficiency associated with menopause • decreases osteoporosis fractures in the spine and hip • reduces risk of diabetes • improves connective tissues in skin.GYNAECOLOGY I Peer Reviewed Each woman should be counselled about the benefits and risks of hormone replacement therapy to enable her to make an informed decision. and the specific HRT conjugated equine oestrogens plus medroxyprogesterone acetate when used for more than 4 years may reduce the risk of colon cancer. joints. such as vaginal dryness.
progestogens. Therefore. JPOG JUL/AUG 2012 • 161 . Mammographic breast density is increased with HRT. Ovarian Cancer The risk of endometrial cancer is increased in women with an intact uterus taking unopposed oestrogen therapy. Cessation of HRT leads to a lowering of risk. The WHI and the Nurses’ Health Study have shown that there was no increase in risk of breast cancer after 7 to 15 years of use of ERT. If HRT is commenced in healthy women around the time of the final menstrual period. Tibolone use is not associated with an increase in the risk of hyperplasia or endometrial cancer.000 women per year of use). and this may decrease the ability to interpret mammograms accurately.1% per year or fewer than 1 per 1. Endometrial Cancer proliferative effect of oestrogen. routes of administration of oestrogen. and after 5 years the risk is the same as the general population of the same age. women should always be given a progestogen to protect the endometrium against the There is no evidence showing an increased risk of ovarian cancer in women taking combined HRT.and postmenopausal women. Hormone replacement therapy is the most effective treatment for menopause symptoms in peri. there may be a reduction in cardiovascular risk and a reduction of Alzheimer’s dementia Little information is available on different doses. A very small increase in risk has been shown with long-term oestrogen-only therapy. An adequate progestogen dose will reduce the risk of endometrial hyperplasia and cancer. progesterone. It has shown a small increase 4 to 5 years after treatment initiation in those with prior use (less than 0.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed after treatment initiation. and androgens. The risk will increase with increasingly higher doses of oestrogen and will remain for many years even after the oestrogen has been stopped.
transdermal oestradiol at doses of 50 μg or less showed no increase in risk of stroke. In an observational study. The WHI and the Nurses’ Health Study both showed an increase in risk in women taking oral E+P or ERT of one additional stroke per 1. Tibolone is associated with a small increase in risk of stroke in older women. but there was no increased risk in women in the 50.to 59-year-old group. Coronary Artery Disease The age of the woman. Venous Thromboembolism Increasing age at time of initiation of HRT has been shown to lead to increased risk of coronary events. especially in older women with pre-existing coronary disease.GYNAECOLOGY I Peer Reviewed Most studies on the risks of hormone replacement therapy focus on the risks of cancer associated with its use. Lung Cancer Stroke A statistically significant small increase in the risk of non-small cell lung cancer has been shown in older women taking HRT for 5 years. JPOG JUL/AUG 2012 • 162 Venous thromboembolism (VTE) is the major risk associated with the taking of oral oestrogens. her cardiovascular risks (such as hypertension) and the route of administration of E+P or ERT are all factors that influence the risk of stroke. The events are increased in the first year of therapy.000 person-years. The . No increased risk of coronary events was shown when HRT was initiated near the menopause. and there may even be possible protection.
Australia.000 person-years. Chlebowski RT. on behalf of the International Menopause Society Writing Group. Lancet Oncol 2012. Effects of conjugated equine oestrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial. FURTHER READING Anderson GL. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. Tibolone is not associated with an increased risk of VTE. Aragaki AK.288:321–333. Southern Health. About the Author Dr Farrell is Head of the Menopause Unit. Pines A. obesity. JPOG JUL/AUG 2012 • 163 . et al. ERT leads to an excess risk of 1. Management of cardiovascular risk in the perimenopausal women: a consensus statement of European cardiologists and gynecologists. particularly the vasomotor symptoms and the atrophic changes. Women’s Health Initiative Steering Committee. Rossouw JE. Climacteric 2007. Prentice RL. © 2012 Medicine Today Pty Ltd.000 person-years and E+P to an excess risk of 2. et al. Gall Bladder Disease The risk of gall bladder disease (and cholecystectomy) is increased with E+P. Updated IMS recommendations on postmenopausal hormone therapy and preventive strategies for midlife health.2 per 1. Casey C. Climacteric 2011. JAMA 2004:291:1701–1712. JAMA 2002. Anderson GL. Declaration of interests: Dr Farrell has been on advisory committees and received educational and research grants from various pharmaceutical companies over the past 10 years but does not think these associations have influenced the content of this article. Monash Medical Centre. Maintaining and regularly updating one’s knowledge about the menopause and HRT is paramount for each professional to be able to give information accurately. Prentice RL. 3. and Past President of the Australasian Menopause Society. Anderson GL. Manson JE. REFERENCES 1. Limacher M. and may vary according to the type of progestogen being taken. Sturdee DW. Assaf AR. Rosano G. et al. There is an increase in dementia in older women commenced on E+P/ERT.13:476–486. Writing Group for the Women’s Health Initiative Investigators. Written or website information will also help her to confirm her decision.3 per 1. Victoria. Rossouw JE. Initially published in Medicine Today April 2012. In the 65 to 79 years age group. Melbourne. CONCLUSION HRT remains the most effective treatment for menopause symptoms.297:1465–1477.13(4):59–61.10:508–526. Conjugated equine oestrogen and breast cancer incidence and mortality in postmenopausal women with hysterectomy: extended follow-up of the Women’s Health Initiative randomised placebo-controlled trial. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. 2. related to the avoidance of the first-pass pathway of metabolism. Reprinted with permission. Transdermal oestrogens seem to have a lower risk of VTE. JAMA 2007.14:302–320.G YNA ECOLOGY YNA ECOLOGY I GPeer Reviewed risk also increases with increasing age. Alzheimer’s Dementia Each woman should be counselled about the benefits and risks of HRT in a manner that allows her to make an informed decision. et al. Collins P. and thrombophilias. et al.
MBBS. MB BCh.PAEDIATRICS PAEDIATRICS II Peer Peer Reviewed Reviewed Managing Imaging Paediatric Headache Managing Headache in Children Brain in Tumours Children M A McShane. MB BCh. MBBS. There are many good reviews of head- ache and its treatment in the clinical journals. Headache in the very young (children less than 5 years) also needs to be JPOG JUL/AUG 2012 • 164 . This paper will focus on the clinical management of headache in children including migraine and will not dwell on classification or diagnosis. persistent early morning headache. and a recent paper published in the Archives of Diseases in Childhood (2010) provides a guideline to help identify those children who might have a tumour. cognitive decline. and hormonal disturbance (for example evidence of diabetes insipidus or growth failure). Sufficient time is required to allow a good consultation in the child presenting with headache. The classification system for headache introduced in 1998 by the International Headache Society has been updated and is widely used in research and clinical papers. physical symptoms such as altered gait or visual symptoms. short but escalating history. FRCR. making clear definition difficult in clinical practice. Diagnostic Radiology M A McShane. MBBS. S J Hughes. MRCPCH H eadache is a common symptom in children. the importance of a detailed history and clinical examination cannot be overemphasized. S JMMed Hughes. Headache including migraine affects up to 30% of the population and often begins in childhood. Recurrent or persistent headache is most commonly due to one of three main headache types: migraine (with and without aura). Symptom overlap between the various headache syndromes is particularly common in children. MRCP(UK). MRCPCH Tang Phua Hwee. All parents are concerned that there may be serious underlying pathology. tension headache. Delay in making a diagnosis of brain tumour occurs in many children and adolescents. DIAGNOSIS When considering the management of the child with headache. particularly chronic headache. and chronic daily headache. MRCP(UK). and particular features which might suggest a tumour include a change in headache symptom. It is important not to miss serious pathology.
serious disorders such as tumours and conditions such as a Chiari 1 malformation are relatively rare causes of headache. It may not be possible to recognize any particular stress in every patient. such as insufficient sleep. but enquiry is essential and measures to reduce stress encouraged. It is important to ask about bedtime. There is also some evidence that weight loss in such patients may reduce the impact of migraines. but in addition these problems tend to increase the frequency of headache. Advice aimed to improve sleep has the potential to reduce migraines. Time well spent at this first appointment may avoid unnecessary anxiety and repeated GP and hospital visits. Analgesic headache is now well recognized. we usually advise the family about non-medical interventions that might help the symptoms. Sleep is important for all children. Often simply stopping regular analgesic treatment can improve the headache symptoms particularly in those who report that the medicine is of no benefit. Children who are obese have increased frequency and increased disability from attacks. In those who have migraines triggered by sport. After taking a good history and undertaking a thorough examination. then investigation is unlikely to be helpful. Stress has also been historically suggested as a cause for headache. and a self-perpetuating cycle of analgesic overuse can easily occur. Missing meals with resultant relatively low blood sugar seems to be a particular trigger in some individuals. Psychological interventions are an emerging area of interest JPOG JUL/AUG 2012 • 165 HEADACHE MANAGEMENT (SIMPLE AND NON-PHARMACOLOGICAL MEASURES) When we see a child with migraine or tension headache. In clinical practice. daytime sleepiness and night waking. most of us would accept that stress contributes to headache severity and frequency. but with increasing anxiety about the potential danger associated with X-radiation this should be with magnetic resonance imaging if done routinely.PA EDIA TRICS I PA ED IATRICS Peer Reviewed managed with caution. Children and adolescents with migraines not only have a higher rate of sleep disturbance. and poor sleep is a common association in those with chronic headache. We often recommend that individuals with chronic headache increase fluid intake although evidence supporting this strategy is lacking. Dietary factors may be important in some individuals. There is a place for organizing a scan in some patients for reassurance. most patients can be reassured following discussion and formulation of a management plan. but restrictive diets in growing children are best avoided. There is good evidence that lifestyle issues impact upon headaches and migraines. Parents need to be aware that many fizzy drinks contain caffeine and that it is best to drink plain tap water for thirst rather than sugary drinks. a small snack before activity can be beneficial. be warned that there may be some initial rebound. While it may not necessarily be the cause. If there is a typical history for migraine or tension headache and a thorough clinical examination is normal. and eating meals at regular intervals may be helpful for many patients. Reducing caffeine intake is often advised although most children are not heavy tea and coffee drinkers. We feel that giving some responsibility to the parent and patient in terms of adapting their lifestyle can have a positive effect on symptoms possibly by giving them some control. The clinician also needs to be aware that it is not uncommon for magnetic resonance imaging to reveal unexpected abnormalities often with no relevance to the presenting symptom. encourage a regular calm settling regime and recommend removal of distractions such as sound systems and televisions from the bedroom. although the patient needs to .
magnesium and coenzyme Q10.PAEDIATRIC S PAEDIATRICS I Peer Reviewed in the treatment of migraine. The serotonin (5-HT) 1 agonists are not licensed for use in children. If first-line analgesics are unsuccessful in migraine headaches. In children with migraine. phenothiazines and antihistamines. possibly owing to the anti-emetic action. show statistical significance in the acute treatment of migraine. then simple measures should be employed. It is important to balance the side effects of any treatments against the disabling effects of the migraine. We rarely advise these interventions. but lack of effect in a clinical trial has led to it becoming less popular. and some have been shown to have efficacy including butterbur (Petasites hybridus ). The BMJ review paper suggests that in adults. NSAIDs. but extrapyramidal side effects need to be mentioned. Ergot derivatives are now rarely used in adult practice and never in children. NSAIDS (non-steroidal anti-inflammatory drugs). then triptans are now the recommended second-line acute treatment. we recommend that they try to sleep or at least rest after taking an analgesic until the JPOG JUL/AUG 2012 • 166 Acute Treatment of Migraine First-line treatments consist of routine analgesics: paracetamol. mineral supplements and vitamins are sometimes used by patients who dislike drug treatment. A recent BMJ review (2011) notes that herbal remedies. the combined oral contraceptives is usually avoided. In the older adolescent patient with migraine with aura. but these are not without their potential side effects and uncertainty about dosage may have practical limitations for use particularly in children. with the aim to minimize the requirement for medication where possible. Formulations combining paracetamol. If the migraine is infrequent and not severe. There is some evidence that relaxation strategies are helpful for the individual in both preventing and treating migraine episodes. This should always be done in consultation with child and family. Anti-emetics mentioned in the British National Formulary for Children (BNFc) include metoclopramide. Biofeedback techniques and behavioural therapies such as cognitive behaviour therapy can have a positive effect on disabling chronic illness including chronic daily headache. simple analgesics should be used on no more than 15 days per month and migraine-specific acute drugs should be used no more than 10 days per month. and in some individuals the pill can exacerbate headaches. Sumatriptan can be prescribed from 6 years and older and zolmitriptan from 12 years. but the BNFc does give dosage recommendations for the drugs sumatriptan and zolmitriptan. Both need to . Feverfew was often used as a headache treatment. Regular and long-term use should be avoided. codeine and an anti-emetic are available and can be helpful for some patients. PHARMACOLOGICAL TREATMENT Treatment is generally undertaken in a stepwise fashion. headache has resolved. There have been few studies assessing the effectiveness of simple analgesics in non-malignant chronic pain disorders including migraine. such as ibuprofen. Chronic analgesics use (abuse) can produce a persisting ‘analgesic headache’. The Lancet Neurology paediatric paper suggests that simple analgesia should be used on no more than 3 days per week and migraine-specific drugs no more than 6 days per month. and weak opiates such as codeine. and all simple analgesics are most effective when taken early in the episode. Rectal preparations are available. but some patients will research and use alternative medicine sometimes with useful effect. domperidone.
β-blockers. Caution is needed with this treatment particularly when on other prescribed medications. but much depends on the response of the acute headaches to simple measures and the disability caused by the attacks. The adverse effects of treatment also need to be discussed. an atypical neuroleptic malignant syndrome. but side effects can be troublesome including fatigue. but these are rarely a problem in children. The 5-HT agonists can be administered orally or as melt-in-the-mouth tablets. Occasional behavioural disturbance is described. Adverse effects include increased appetite and drowsiness. but in our practice if significant headaches are occurring more than once weekly. as well as increased responsiveness to acute treatment during an attack Headache and Migraine Prophylaxis There are no agreed guidelines on when prophylactic treatment should be used. In older children. it is widely used. These are pizotifen. JPOG JUL/AUG 2012 • 167 Aims of prophylactic treatment include reduction of attack frequency. It does have mild anticholinergic actions and can potentially cause problems such as urinary retention and worsening of glaucoma. but we rarely use this drug in younger children and often find that it is not well tolerated in some older children. as well as increased responsiveness to acute treatment during an attack. Despite this lack of evidence. can be triggered. We generally use pizotifen as first-line prophylactic treatment but giving this as a single dose at night to avoid daytime sedation. Aims of prophylactic treatment include reduction of attack frequency. Recent evidence in adults has suggested efficacy for oxygen treatment in cluster headache.PA EDIA TRICS I PA ED IATRICS Peer Reviewed be initiated by a specialist and should be avoided in children with cardiac disease. The BNFc gives a dose schedule from 2 years and older. severity and duration. Triptans are generally well tolerated in the paediatric age group. Pizotifen is not recommended for children with epilepsy. There is good evidence that β-blockers are effective in migraine. The decision to start a prophylactic drug requires careful discussion. cold extremities and poor sleep. but it is recommended that they be given as monotherapy. It is relatively rare for us to recommend triptans in children in our clinical practice. and many parents will choose to avoid regular medication for their children because of anxieties about drug-related side effects. . The BNFc suggests more than two attacks per month. and anti-epileptics. but fortunately this particularly distressing headache syndrome is rare in children. daily prophylaxis should be considered. hypertension. but the evidence that it is an effective treatment for migraine is limited. they can be administered subcutaneously via an auto-injector or be given by the intranasal route. Propranolol is the most commonly used β -blocker for migraine prophylaxis. The BNFc gives doses from 5 years and older. The BNFc mentions three prophylactic drug groups for use in children. Pizotifen has antihistamine and anti-serotonin actions. It should not be given to patients with a history of asthma and bronchospasm. Postural hypotension may be a problem in some teenagers. severity and duration. and epilepsy. These drugs can interact with other medications and the ‘serotonin syndrome’.
Clinical trials have shown efficacy for topiramate and sodium valproate. It is recommended that throughout treatment.21(11):518–520. Walker D. Koller K. They are also useful for patients who fail to respond to other prophylactic agents. Current approaches to the diagnosis and management of paediatric migraine. . © 2011 Elsevier Ltd. Dev Med Child Neurol 2006. Arch Dis Child 2010. an old antidepressant. using simple lifestyle strategies and a range of medications. Once diagnosed. but their use is not licensed for this indication and we rarely use them other than for extremely rare conditions such as alternating hemiplegia. expectations when changing medications should occur with the patient and their family. UK. We rarely use this in children younger than 12 years. Wilne S. Kennedy C. Grundy R. Conflicts of interest: none declared. An approach to children with chronic daily headache. Reading.342:d583. BMJ 2011.48:997–1000. CONCLUSIONS Headache is a common symptom in children and young people and requires careful clinical assessment. The BNFc recommends that these medications should be initiated and supervised by a specialist. Regular medications should be reviewed after a 1-month period. Levin M.9:190–204.95:534–539. Pharmacological prevention of migraine. but this has not been well studied in the paediatric population yet. it is often possible to stop prophylaxis after a period of time. treatment should progress in a stepwise fashion. Ward T. UK. Initially published in Paediatrics and Child Health 2011.d583. Botulinum toxin has recently obtained approval for use in chronic headache in both the UK and USA in adults. This treatment is not yet widely accepted as effective in the adult population and we would think indications for use in children will be very limited. Mack KJ. Further Reading Fenstermacher N. Advice on the timing of cessation of prophylaxis is not well studied. Anticholinergic side effects are described but rarely troublesome in children in the small doses used for this indication. doi:10. Side effects include drowsiness and sometimes agitation. Treatment goals and expectations should be agreed with patient and their family. Conflicts of interest: none declared. There is also some emerging evidence in adults that certain nutrients such as coenzyme. S J Hughes is a Consultant in Paediatric Neurodisability at the Royal Berkshire Hospital. Oxford. riboflavin and magnesium may be helpful. We do not recommend long-term treatment in children. Carbamazepine may also be an effective treatment in some individuals and may have a better side effect profile. Amitriptyline. Lancet Neurol 2010. setting goals and reviewing JPOG JUL/AUG 2012 • 168 About the Authors M A McShane is a Consultant Paediatric Neurologist at the Children’s Hospital at the John Radcliffe Hospital. using diary recording for evidence of effectiveness. Collier J. as necessary. Hershey AD. Calcium channel blocker agents can be used to treat migraine. The diagnosis of brain tumours in children: a guideline to assist healthcare professionals in the assessment of children who may have a brain tumour. Length of Treatment In children. is widely used in the management of chronic pain disorders in children and adults. We recommend reviewing the effectiveness of prophylactic treatment after 1 month and continuing treatment for 3–6 months. Longterm treatment in children should be avoided with breaks in treatment at 3–6 monthly intervals.1136/bmj. A number of other treatments are available to treat children with chronic headache.PAEDIATRIC S PAEDIATRICS I Peer Reviewed Anti-epileptics drugs are useful in the management of migraine and other disorders with chronic pain.
and 31. and Canada described 3. 21. MBBS. Prince of Wales Hospital. MRCOG. treatment. Recently.1 The first case report of GDM appeared in 1824.2 the Australian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS). found that the prevalence of GDM was 14. MBBS. there has been a lot of controversy over most aspects of GDM. Historically. Another study 9 performed in a different university teaching hospital in Hong Kong. FHKAM (O&G).5% (20–24 years). The United States reported an incidence of 3–8%. polyuria and glycosuria and the death of a macrosomic infant from shoulder impaction. a study 8 performed in a university teaching hospital.2%. JPOG JUL/AUG 2012 • 169 Medicine Units Network treatment of mild gestational diabetes (MFMUN-GDM) clin4 in more recent publications. which will be discussed further in this article.2%. and the relationship between GDM and type II diabetes mellitus. body build. WC Leung. WL Lau. from the youngest to the oldest cohort ( P < 0. including screening. which described a mother with thirst. ethnic origins). MD. the Hyperglycaemia and Adverse Pregnancy Outcomes (HAPO) study. age. In our hospital. The United Kingdom reported an incidence of 2% 6 ical trials. studied (eg.2% INCIDENCE The reported varies with diagnostic criteria and characteristics of the population being . MBBS. FHKAM (O&G). risks.000 deliveries per year. diagnosis. It is defined by the National Diabetes Data Group in 1985 as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. the prevalence of GDM increased from 1. the incidences of GDM in 2008 and 2009 were 13.3% ( ≤ 20 years). respectively.8%.9% ( ≥ 40 years).Continuing Medical Education Gestational Diabetes LL Chan. a regional hospital with around 6. several major studies have substantially resolved these areas of controversy. FRCOG. 2. eg. Cert RCOG (Maternal & Fetal Medicine) INTRODUCTION Gestational diabetes mellitus (GDM) is a controversial subject in obstetrics. with a rising trend 5 (25–29 years). 10. showed that of the 16.7% (35–39 years). 7 In Hong Kong.2% and 14.383 women incidence of GDM managed in the period 1998–2001.3% (30–34 years). and the Maternal-Fetal 3 Diagnosis and treatment of gestational diabetes can help reduce the risk of many adverse pregnancy outcomes due to this condition. Queen Mary Hospital.001). 6. respectively. FRCOG.
They also take into account the continuous association between maternal blood glucose concentrations and adverse perinatal outcomes as seen in HAPO. the IADPSG JPOG JUL/AUG 2012 • 170 . according to the current guidelines for the diagnosis of pre-existing diabetes. HbA1c. but < 7. the IADPSG suggests that an abnormal 1-hour plasma glucose is adequate for the diagnosis. GDM = gestational diabetes mellitus. and fetal body weight being greater than the 90th percentile. or 2hG ≥ 8. HbA1c = glycated haemoglobin A1c. the International Association of Diabetes and Pregnancy Study Groups (IADPSG) established a new set of diagnostic guidelines (Figure 1). relative to the odds of those outcomes at mean glucose values. IADPSG = The International Association of Diabetes and Pregnancy Study Groups.1 mmol/L. DM = diabetes mellitus. RG = random glucose.Figure 1.1 mmol/L Normal GDM if FG ≥ 5. fasting plasma glucose. 2hG = 2-hour plasma glucose in 75-g oral glucose tolerance test. and these criteria were not designed to identify pregnant women at increased risk for adverse perinatal outcomes but rather women at higher risk for the development of diabetes after pregnancy. FG = fasting glucose. The agreed thresholds represent an odds ratio of 1.1 mmol/L and 7.0 mmol/L. hence lowering the thresholds of GDM in most guidelines. cord C-peptide. Moreover. SCREENING AND DIAGNOSIS The diagnostic criteria of GDM were initially established more than 40 years ago.0 mmol/L GDM if FG ≥ 5. As more and more women suffer from 10 recommends screening women with risk factors at the booking visit by using random plasma glucose.0 mmol/L. all or high-risk women should have FG.75 for birth weight. Applying this system of testing and di- diabetes before pregnancy. RG tested DM if FG ≥ 7. or HbA1c ≥ 6. or 1hG ≥ 10. or RG ≥ 11. OGTT = oral glucose tolerance test.0 mmol/L 75-g OGTT at 24–28 weeks DM if FG ≥ 7. Following the publication of the HAPO study. GDM can be diagnosed at the booking visit with a fasting plasma glucose between 5.5%. Flow chart showing guidelines as suggested by IADPSG10 At booking visit.0 mmol/L. In contrast to the World Health Organization criteria which use an abnormal fasting or 2-hour plasma glucose for the diagnosis of diabetes.1 mmol/L.5 mmol/L 1hG = 1-hour plasma glucose in 75-g oral glucose tolerance test. or glycated haemoglobin A1c paired with diagnostic thresholds. They also recommend that all women who do not have diabetes should be screened at 24–28 weeks’ gestation with the 75-g oral glucose tolerance test.
multicentre study. neonatal hyperbilirubinaemia. linear. Exclusion criteria include fasting plasma glucose > 5.3 1. 255–267. Pridjian et al. 37(2).9 mmol/L. birth weight > 90th percentile.13 The risk factors and health risks of GDM are summarized in Tables 1 and 2. JPOG JUL/AUG 2012 • 171 . cord plasma C-peptide level reflective of fetal hyperinsulinemia. It showed an unambiguous.6 2. Risks factors of gestational diabetesa RISKS The HAPO study2 was a 10-year. ie. shoulder dystocia or birth injury.2 7.9 b b b b References Torloni et al.6 1. 2010. 11 Table 1. caesarean section. Relative risk compared with white race. Risk factors Overweight Obesity Severe obesity Prior gestational diabetes Prior macrosomic infant Maternal age greater than 25 y Maternal age greater than 35 y Multiple gestation South East Asian Hispanic African American Polycystic ovarian syndrome Parent with diabetes Sibling with diabetes Periodontal disease Low maternal birth weight a b Odds ratio 2 3. excess neonatal adiposity. 2010. or the 2-hour plasma glucose ≥ 11. blinded. women diagnosed with GDM in the late second and early third trimesters were randomized to two groups.7 7 23 3. with permission from Elsevier. 255–267. In both studies which were double blind. or a random plasma glucose ≥ 8. Update on gestational diabetes. It aimed at studying the associations between the risks of adverse pregnancy outcomes and the degrees of maternal glucose intolerance less severe than overt diabetes. Chu et al Torloni et al.2 7. Intervention in both trials included Large for gestational age/ macrosomia Birth trauma Hypomagnesaemia Hyperviscosity Polycythaemia Hyperbilirubinaemia Cardiomyopathy a Reprinted from Obstetrics and Gynecology Clinics of North America.8 mmol/L.3 2. pre-eclampsia).Continuing Medical Education agnostic criteria will probably double the incidence of GDM. neonatal hypoglycaemia. positive association between maternal glycaemia and adverse pregnancy outcomes (eg. routine care or intervention. prospective. Update on gestational diabetes.4 2.505 pregnant women. with permission from Elsevier. Pridjian et al.8 2. Table 2. which enrolled 25.4 1. 37(2).2 mmol/L. Chu et al Torloni et al. Chu et al McGuire et al McGuire et al Cypryk et al Xiong et al Rauh-Hain et al Dornhorst et al Dooley et al Dooley et al Toulis et al Kim et al Kim et al Xiong et al Seghieri et al Reprinted from Obstetrics and Gynecology Clinics of North America.1 2.9 3. 12. Health risks of gestational diabetesa Mother Birth trauma Increased caesarean delivery Pre-eclampsia/ Gestational hypertension Type 2 diabetes Metabolic syndrome Fetus Hyperinsulinaemia Cardiomyopathy Stillbirth Newborn Respiratory distress syndrome Hypoglycaemia Hypocalcaemia Child/Adult Obesity Type 2 diabetes Metabolic syndrome TREATMENT The ACHOIS3 and the MFMUN-GDM4 clinical trials demonstrated that diagnosis and treatment of GDM were worthwhile because these reduced the risk of many adverse pregnancy outcomes of GDM.
In the ACHOIS trial. weight gain.20 One study showed that in women with GDM.07. reduced rates of caesarean sections for macrosomia and cephalopelvic disproportion. bone fracture. a 30% caloric restriction help to avoid ketonuria or an increase in free fatty acids. carbohydrate restriction to < 42% led to fewer LGA infants. Rates of induction of labour and of admission to the neonatal unit were increased by treatment in the ACHOIS trial only. A more severe caloric restriction is not recommended. 97% CI. and nerve palsy) was reduced by diagnosis and intervention (adjusted odds ratio. a composite measure 3 the MFMUN-GDM trial only. blood glucose monitoring. if needed.72–1. 0. shoulder dystocia. 16 was not statistically significant (relative risk. insulin treatment. the . habits.75.87. financial needs. kg/m2 should restrict caloric intake (to 25 kcal/kg/day or less) and engage in moderate exercise (of at least 30 minutes daily).21 dietary modification. 0. Referral to nutritional counselling should ideally occur within 48 hours of the diagnosis of GDM. CI. 0. 15 The first meeting with a professional dietitian should be arranged within 1 week of the referral.14–0. The goal of fractionating food intake into three meals and two to three snacks in between meals is to distribute the glucose intake throughout the day in order to control the postprandial glucose. The Dietary Reference Intakes recommends no increase in calories for the first trimester but an additional 340 kcal/ day during the second trimester and 452 kcal/day during the third trimester. and blood glucose goals. and a total of three visits are suggested.01). Generally. 17 In obese women with GDM. P = 0. culture. but this must be individualized. 95% confidence interval. while at the same time maintaining a satisfactory nutritional intake. and. and reduced need for insulin treatment.18 while improving glycaemic control. these two trials showed that identification and treatment of GDM with a standard approach improved pregnancy outcomes. physical activity. Generally. In both studies. pre-eclampsia and maternal pregnancy weight gain were reduced by intervention. of serious perinatal complications (defined as one or more of death. The National Institute for Clinical Excellence (NICE) guidelines19 in the UK recommend that women with GDM whose prepregnancy body mass index is above 27 Few studies have focused on the benefit of carbohydrates with a low glycaemic index.14). P = 0.33. A similar composite measure in the MFMUN-GDM trial was also decreased but 4 DIETARY MODIFICATION The scientific evidence for making nutritional recommendations for women with GDM is limited. rates of large-for-gestational-age (LGA)/macrosomia. 0. 40–45% of the calories in the daily diet come from carbohydrates. The evening snack decreases the night-time ketogenesis related to fasting.diet should be adjusted and individualized to meet the patient’s food choice. Rates of shoulder dystocia and caesarean section were significantly decreased by treatment in JPOG JUL/AUG 2012 • 172 Throughout the pregnancy. compared with a higher carbohydrate content (45–50%).
0–5. Preliminary studies showed that it was effective in decreasing postprandial hyperglycaemia in GDM. sions to neonatal units. but subsequent insulin was indicated in 46. guidelines 19 22 The NICE ences between the insulin and glyburide groups with regard to birthweight.5 mmol/L. but its use has been limited by its side effects. which is a measure of how much each gram of available carbohydrate in the food increasing a person’s blood glucose level following consumption of the food. high levels of fasting glucose.25 The Metformin in Gestational Diabetes (MiG) trial26 of 751 women showed similar perinatal complications in both the metformin and insulin groups. are not common and do not differ very much from those resulting from insulin therapy. health carers can reassure them that the rates of congenital malformations with the use of oral hypoglycaemic agents and insulin do not differ with the peak level at 2–4 hours after intake. It binds to receptors that are associated with the adenosine triphosphate-dependent potassium channels of pancreatic β cells to increase insulin secretion and insulin sensitivity of peripheral tissues. while food with carbohydrates that break down more slowly. like abdominal crampJPOG JUL/AUG 2012 • 173 Oral Hypoglycaemic Agents Glyburide (or glibenclamide) is a second-generation sulfonylurea. Early neonatal complications. admis- recommend drug treatment if diet and exercise cannot control the . Because it acts as an insulin sensitizer in peripheral tissues rather than as an insulin analogue.7–7. 5. But no proof exists that extra dietary fibre intake is beneficial in these women. as it may reduce the postprandial blood glucose. relative to consumption of glucose. with better acceptability in the metformin group. tend to have a low GI. or neonatal hypoglycaemia. despite dietary modification. blood glucose for 1–2 weeks. but the fetal response to various dosages of glyburide is not completely known.1 mmol/L. Acarbose . The Fifth International Workshop-Conference on Gestational Diabetes recommends the following blood glucose concentrations: fasting plasma glucose. The maternal glucose control (fasting blood glucose and 2-hour postprandial) by oral hypoglycaemic agents and insulin is also comparable. LGA/ macrosomia. When counselling patients. Long-term safety data on infants whose mothers were treated with glyburide or metformin are lacking. The onset of action takes approximately 1 hour When counselling patients. Food with carbohydrates that break down quickly during digestion and release glucose rapidly into the bloodstream tend to have a high GI. Studies on the placental transfer of glyburide are contradictory. health carers can reassure them that the rates of congenital malformations with the use of oral hypoglycaemic agents and insulin do not differ. < 7. gestation at delivery. and stimulates glucose uptake in peripheral tissues. has been used less often. or if ultrasound shows possible fetal macrosomia (abdominal circumference above the 70th percentile) at diagnosis. releasing glucose more gradually into the bloodstream. 23 A meta-analysis by Moretti et al reported no differ24 PHARMACOTHERAPY Drug treatment is necessary in 7–20% of women with GDM when.Continuing Medical Education Few studies have focused on the benefit of carbohydrates with a low glycaemic index (GI). Metformin belongs to the biguanide group. In vitro studies showed minimal placental transfer. there is insufficient glucose control. Metformin does cross the placenta. The onset of action takes approximately 1 hour with the peak level at 4 hours after intake. It inhibits hepatic gluconeogenesis and glucose absorption. such as hypoglycaemia. or persistent hunger sensation. suboptimal weight gain (due to caloric restriction). an alpha glucosidase inhibitor. There have been no randomized studies with sufficient sample size to draw a conclusion on the benefits of carbohydrates with a low GI. it is believed that fetal metabolism is less likely to be affected. and 2-hour postprandial plasma glucose.3% of women taking metformin. < 6. Increased dietary fibre intake is traditionally recommended for women with GDM.8 mmol/L. 1-hour postprandial plasma glucose.
echo19 cardiography. Insulin therapy should be stopped in women who have not taken insulin before pregnancy. lin analogue lispro has also been shown to be safe in observational studies.ing. The short-acting insuJPOG JUL/AUG 2012 • 174 ANTENATAL MANAGEMENT Once GDM is diagnosed. or have other obstetric complications. have macrosomic or growth-restricted fetuses. The mode and timing of delivery of POSTPARTUM MANAGEMENT Approximately 50% of women with GDM will develop type 2 diabetes within 5 to . During labour.1% vs 33. P < 0.000 to 4.27 Further studies are needed to better evaluate the potential placental transfer of this drug. tests of fetal wellbeing after 38 weeks’ gestation). The short-acting insulin analogue aspart has been shown to be safe in pregnancy in a randomized trial 28 and has been registered for this indication. no strong evidence exists to support earlier induction of labour. there is no safety data available on the long-acting insulin analogues detemir and glargine. while those women who are taking insulin for pre-existing diabetes should resume their pre-pregnant insulin dosages. Another issue is the inaccuracy of ultrasound in estimating fetal weight. In an attempt to prevent macrosomia and to guide the treatment. Recommendations concerning the lower estimated fetal weight thresholds for prophylactic caesarean section vary from 4. growth scan at 28. One study30 failed to detect a benefit to expectant management beyond 38 weeks’ gestation. as the rate of caesarean delivery was not reduced but rather the rates of LGA infants and shoulder dystocia were increased. There is no consensus on the frequency and timing of antenatal surveillance tests in women with GDM. Induction of labour in women with insulin-treated diabetes at 38 weeks’ gestation is intended to reduce the risk of stillbirth. There are two types of insulin: human insulin and insulin analogue. and additional health-care costs. Insulin Traditionally.500 g. For uncomplicated GDM. Both the American College of Obstetricians and Gynecologists and the Royal College of Obstetricians and Gynaecologists recommend prophylactic caesarean section if the estimated fetal weight is > 4.005). especially in breastfeeding women. require drugs. caesarean-associated maternal and fetal morbidities. blood pressure measurement. 31 Prophylactic pre-labour caesarean section using estimated fetal weight by ultrasound has been proposed but is controversial. followed by a gradual decrease during the rest of the day. a randomized trial compared ultrasound performed at 29 32 weeks’ gestation with ultrasound at both 28 and 32 weeks’ gestation. which was also confirmed by a Cochrane review of randomized trials on elective delivery in women with diabetes. who do not comply with advice.500 g. visits to health carers or dietitians by the pregnant women should be made at least every 1–2 weeks and more frequently if complications occur. long-acting human insulin should be used instead. After the second trimester. glycaemic control must be relaxed to prevent maternal hypoglycaemia. shortacting insulin should be used to achieve optimal glucose levels of between 4 and 8 mmol/L and to prevent neonatal hypoglycaemia.3%. and urine albumin testing to diagnose preeclampsia are also essential at every visit. Therefore. Women in the first trimester are at risk of hypoglycaemic events because of emesis. History review. as small amounts of acarbose can be absorbed into the bloodstream. and blood glucose levels should be closely monitored with appropriate adjustment of insulin. as though they had pre-existing diabetes and to begin close antenatal monitoring (eg. insulin requirements rise. which leads to an increase in unnecessary caesarean deliveries and. women with GDM is controversial because sufficient data are lacking to make a recommendation. insulin has been regarded as the standard treatment for diabetes. After delivery. However. especially when diet and exercise fail to control the maternal blood glucose and there is no risk of placental transfer of insulin to the fetus. Insulin requirements are not constant throughout the day: it is low at night with a sharp rise at dawn. It is crucial to manage women. both are prescribed offlabel. therefore. 32 and 36 weeks’ gestation. The rate of macrosomia was significantly higher in the group assessed only at 32 weeks (71. the NICE guidelines suggest anomaly scan.
New consensus criteria for GDM: problem solved or Pandora’s box? Diabetes Care 2010. Crowther CA. Sipe M. Am J Obstet Gynecol 2010. 19. and drugs. 2002.6:1–161. Bonet B. Griffin ME. Ho LF.58:453–459. risk factor-based screening for gestational diabetes mellitus: detection rates. et al. Ann Pharmacother 2008. 6. gestation at diagnosis and outcome. Knopp RH. 28. 14. et al. 31. HAPO Study Cooperative Research Group. Women with GDM should be treated with dietary modification.to 23-year follow-up study in Denmark. Insulin-requiring diabetes in pregnancy: a randomized trial of active induction of labor and expectant management.10:649–667. McPhee AJ. Koren G. In a large 4. International Association of Diabetes and Pregnancy Study Groups. 30. JPOG JUL/AUG 2012 • 175 . American Diabetes Association. 16. It is unclear whether a traditional 2-hour 75-g oral glucose tolerance test or fasting plasma glucose test may be more useful at this time. Safety of glyburide for gestational diabetes: a meta-analysis of pregnancy outcomes. Elliott BD. Benedetti T. and Dr Lau and Dr Leung are consultants. Maternal age and prevalence of gestational diabetes mellitus. Rowan JA. HAPO Study Cooperative Research Group. Dyer AR. Rezvani M. 68% of the 481 women with previously diagnosed GDM had impaired glucose regulation. Diabetes Spectrum 2001. Prior gestational hyperglycemia: a long-term predictor of the metabolic syndrome. Landon MB. Without a uniform diagnosis. Diabetes Care and Education Dietetic Practice Group. 2008 March. Batting MR. Metzger BE. Chan BC. 17. Fetal and perinatal outcomes in type 1 diabetes pregnancy: a randomized study comparing insulin aspart with human insulin in 322 subjects. Diabetes Care 2007. 12. Am J Obstet Gynecol 2008.(2):CD001997. Monge L.29:485–486. Wyckoff J. 18.e1–186.346:393–403. Damm P. Splett P. Prevalence of gestational diabetes mellitus in Hong Kong based on the 1998 WHO criteria. 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CME Questions This continuing medical education service is brought to you by the Medical Progress Institute. 2. Name in BLOCK CAPITALS: Signature: Date: Please mail your completed answer sheet back to: The Secretariat Hong Kong College of Obstetricians & Gynaecologists Room 805. 3. The incidence of GDM in Hong Kong is 25%. Aberdeen.75 for birth weight and cord C-peptide. The National Institute for Clinical Excellence recommends fortnightly growth scans in women with GDM from 32 weeks’ gestation. The Royal College of Obstetricians and Gynaecologists recommends prophylactic caesarean section if the estimated fetal weight is greater than 4. In obese women with GDM. The selected thresholds in the International Association of Diabetes and Pregnancy Study Groups guidelines represent an odds ratio of 1. Hong Kong Academy of Medicine Jockey Club Building 99 Wong Chuk Hang Road. an institute dedicated to CME learning. Hong Kong JPOG JUL/AUG 2012 • 176 False CME Answers for JPOG Jan/Feb 2012 of Pregnancies With Previous Caesarean Section Answers 1 2 3 4 5 6 7 8 9 10 T F F T T T T T T F HKCOG CME Article: Management . 10. 6. 5. True 1. Glyburide can cause fetal hyperinsulinaemia. The 75-g oral glucose tolerance test is the recommended test in the postnatal period of women with GDM. relative to the odds of those outcomes at mean glucose values. 9. CME Article Gestational Diabetes Answer True or False to the questions below. Rates of shoulder dystocia and caesarean section were significantly reduced by treatment in the ACHOIS and MFMUN-GDM trials. 8. there should be a 40% restriction of caloric intake. 7. Read the article ‘Gestational Diabetes’ and answer the following questions. 4. Gestational diabetes mellitus (GDM) can present in the first trimester.000 g. This JPOG article has been accredited for CME by the Hong Kong College of Obstetricians and Gynaecologists. Metformin is registered and approved for use in pregnancy.
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