JAN/FEB 2012 MAR/APR 2012 Vol. Vol. 38 38 No. No.

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JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY

Your partner in paediatric and O&G practice

IN PRACTICE

ISSN 1012-8875 (HONG KONG)

JOURNAL WATCH

PAEDIATRICS

Type 1 Diabetes Mellitus in Childhood Atopic Dermatitis in Children: A Practical Approach

GYNAECOLOGY

Bacterial Vaginosis
CME ARTICLE

Screening for Group B Streptococcus in Pregnancy
www.jpog.com

JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY

MAR/ APR 2012 Vol. 38 No. 2

Journal Watch

45 • Bevacizumab for ovarian cancer • Induction of labour at term: Transcervical Foley catheter vs vaginal prostaglandin E2 gel 46 • Early versus delayed clamping of the umbilical cord • Malaria and bacteraemia in children • Speed of intravenous rehydration for children 47 • Influenza in children worldwide

47

48 • Hospital-acquired bacteraemia in children in a Kenyan hospital Review Articles
Paediatrics

49 Type 1 Diabetes Mellitus in Childhood Type 1 diabetes mellitus (T1DM) is the most common chronic metabolic condition in youth, and its
incidence is increasing worldwide. Care of the child and adolescent with T1DM should be multidisciplinary and involve professionals experienced in childhood diabetes, including a physician, nurse, dietitian and social worker. Maintenance of excellent glycaemic control and regular screening for complications should be emphasized, all in the context of a healthy and supportive physical and psychosocial environment.

Rayzel M Shulman, Denis Daneman

49

Editorial Board
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 MAR/APR 2012 • i

JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY

MAR/ APR 2012 Vol. 38 No. 2

In Practice 59 Rotting Teeth in a Young Girl
Simon Wooley, Kaye Roberts-Thomson

Review Articles
Gynaecology

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60 Bacterial Vaginosis Bacterial vaginosis is the commonest cause of abnormal vaginal discharge in women of childbearing
age, with a prevalence as high as 50% in some communities. Bacterial vaginosis is a risk factor for acquisition of sexually transmitted infections including HIV, and for post-abortion endometritis and adverse pregnancy outcomes such as late miscarriage and preterm birth. Studies of antibiotics in pregnancy have not consistently shown reduced adverse outcomes, so better strategies need to be studied to improve pregnancy outcome. Phillip Hay

60

Ben Yeo
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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.

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JPOG MAR/APR 2012 • ii

5 3 2.0102 vs control Friso Gold with Unique * Stool frequency after 28 days of feeding Stool consistency after 28 days of feeding The key to enhancing intestinal health in infants and growing children * The Friso Gold range with – comprises a key prebiotic and two probiotics to support a healthy stool pattern. Professional advice should be given to pregnant women and new mothers to impart that proper maternal nutrition is important in preparation for breastfeeding and its maintenance.55 p=0.33 p=0.33 Control 3.5 0 2. use and store infant formula as directed to avoid health hazards. 4.01 vs baseline 5 1.55 Mean number of stools per day 2.hk References: 1. Bifidobacterium are added as supplements in Friso 3 Gold and Friso 4 Gold Baseline For medical professionals’ reference only. Mothers should also consider social and financial implications in selecting the suitable infant feeding method. Arch Dis Child Fetal Neonatal Ed 2002. Ben XM.33 Control Mean number of stools per day 2. 3=seedy. et 5 al. present in the entire Friso Gold range. 5=hard Galacto-oligosaccharides (GOS) stimulate intestinal microflora production to improve stool frequency and consistency in children1 Bifidobacterium lactis and Lactobacillus paracasei further increase bowel movements to target age-specific needs in growing children2 Bowel movements/week 10 Percentage of children with hard stools (%) Friso 1 Gold 0–6 months p=0. Introducing partial bottle-feeding may disadvantage breastfeeding.5 1 0.0079 vs control p<0. Proper feeding practices should be observed so as not to prevent mothers from breastfeeding. Prepare.117:927-931. 2 weeks . Central.5 0 p<0.5 0 p<0.0003 vs control p=0. World J Gastroenterol 2008. Chin Med 2004.0001 vs control 2. Shun Tak Centre West Tower 200 Connaught Road. Nutr J 2007.74 Bowel movements/week 3.2 Stool consistency scores 2.2 Stool consistency scores 2.0003 vs control p=0.33 p=0.0079 vs control p<0. 4=formed. et al. Bekkali N. et al. Infant formula is an accepted breast milk substitute for mothers who do not breastfeed.friso. 2. It is difficult to reverse a decision to avoid or discontinue breastfeeding.75 2. 2=soft.5 2 1.74 1.Human milk 3 Oligosaccharide formula 4 3.5 2 1.4. a prerequisite for optimal intestinal health in children Human milk 3 Oligosaccharide formula 4 3.0001 vs control 2. stimulate intestinal microflora production in term infants. Hong Kong Baseline Tel: 852 2859 3705 Fax: 852 2858 3093 www.009 vs baseline Friso 2 Gold 6–12 months Friso 3 Gold 40 1–3 years 35 35 30 25 20 15 10 Friso 4 Gold 3 years onwards 20 5 FrieslandCampina (Hong 0 Kong) Limited Room 1702-5.5 2 1. Ben XM. Breast milk is best for babies.75 2.14:6564-6568 2 weeks 4 weeks 0 lactis and Lactobacillus paracasei *Galacto-oligosaccharides. et al.5 2 1.5 1 0.0102 vs control Stool frequency after 28 days of feeding Stool consistency after 28 days of feeding 0 Baseline 2 weeks 4 weeks Stool consistency score: 1=fluid.com.5 0 2. Breast milk provides superior nutrition for babies. similar to levels in breastfed infants3.5 3 2. 3.01 vs baseline p=0.009 vs baseline 10 p=0. Boehm G. 17/F.86:F178-F181.6:17.5 1 0.5 1 0.

The Cover: ‘Atopic Dermatitis in Children’ © 2012 UBM Medica Pictorial Medicine Vignettes of illustrated cases with clinical photographs. KY Leung. Review Articles Comprehensive reviews providing the latest clinical information on all aspects of the management of medical conditions affecting children and women. Case Studies Interesting cases seen in general practice and their management. Genting Centre. OBSTETRICS & GYNAECOLOGY MAR/ APR 2012 Vol. All should be done through a multidisciplinary approach and liaison with primary care. Mazin Alfaham 68 79 In Practice (Answer) Continuing Medical Education 81 Screening for Group B Streptococcus in Pregnancy Group B Streptococcus (GBS) is the most frequent cause of severe early-onset neonatal infection. Art Director Connie Lim. Triveni Shekariah. For more information. poor compliance and psychological factors. Singapore 088934 Tel: (65) 6223 3788 Fax: (65) 6221 4788 E-mail: enquiry@jpog. Thomas Li. and pages 67–80 are reprinted with permission of Consultant for Pediatricians. Illustrator JPOG MAR/APR 2012 • iii . which is associated with a high rate of morbidity and mortality. The articles appearing on pages 49–53. Manjunatha Kalavala. Teresa WL Ma. Copyright © 2011 UBM Media LLC. and a pilot study in Hong Kong. This review article discusses the current screening methods for GBS in pregnancy.com Rowena Sim.JOURNAL OF PAEDIATRICS. please refer to the Instructions for Authors on our website www. All rights reserved. usually staphylococcal or streptococcal. and the focus thus lies in disease prevention. KKW To. Obstetrics and Gynaecology contains articles under licence from UBM Media LLC. CW Law. The clinical assessment involves an enquiry about triggers as well as details of therapy. 38 No. Because the early-onset disease develops shortly and rapidly after birth. the updated guidelines by the Centers for Disease Control and Prevention. Resistant eczema should raise the suspicion of secondary infection. KY Wong. No 3 Lim Teck Kim Road.com. 2 Review Articles Paediatrics 68 Atopic Dermatitis in Children: A Practical Approach Atopic dermatitis is a common condition that takes a significant time from the daily work of general paediatricians. there has been little improvement in the disease treatment. Sarah Morag McGhee 81 The Journal of Paediatrics.jpog. or contact: The Editor UBM Medica Asia Pte Ltd. the improvement in laboratory techniques.

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1 months (CB). a total of 1. 17%) than in the control group (7%). a nonsignificant difference. Canada. Among high-risk patients. NEJM 2011. A phase 3 trial of bevacizumab in ovarian cancer. The rate of caesarean section was 23% Bevacizumab is a humanized monoclonal antibody against vascular endothelial growth factor (VEGF). At the time of analysis.1 months (BT). included a total of 824 women with a singleton. progression-free survival was 22.2%. BT). Cervical ripening may be promoted by mechanical or pharmacological means. and IIB-IV ovarian cancer. Hypertension was more common in the bevacizumab groups (BT. The maximum effect of bevacizumab was at 12 months. the corresponding figures were 14. an unfavourable cervix. and an indication for induction of labour. BI. one uterine perforation and one Induction of labour at term: Transcervical Foley catheter vs vaginal prostaglandin E2 gel Worldwide.Peer Reviewed Journal Watch the BI and control groups. In both of these trials. Hypertension occurred in 18% of patients induction of labour. the addition of bevacizumab to chemotherapy improved survival with greater benefit for high-risk patients.873 women with newly diagnosed stage III or IV ovarian cancer had debulking surgery and were then randomized at 336 centres to 22 × 3-week cycles of chemotherapy (paclitaxel plus carboplatin) plus either bevacizumab in cycles 2–22 (bevacizumab throughout. no history of caesarean section. Randomization was to transcervical Foley catheter (inflated with 30 mL of saline or water) or use of prostaglandin E2 vaginal gel. at 12 centres. 11.8%.8 months (CB) vs 20. respectively. at the end of planned bevacizumab treatment.3 months (controls). and it had diminished by 24 months. and 1.1 months and overall survival 28. Investigators in the Netherlands have compared transvaginal Foley catheter inflation with use of a prostaglandin E2 vaginal gel. and placebo in cycles 7–22 (bevacizumab-initiation.4 months (C) vs 24. both in the vaginal prostaglandin group.2 months (BI). The time from the start of induction to birth of the infant was significantly longer with the Foley catheter method (29 hours vs 18 hours) probably because of a longer time to the onset of labour. a total of 1. Incorporation of bevacizumab in the primary treatment of ovarian cancer. but there was no significant difference between on bevacizumab.6%. one in the USA. or Fallopian tube cancer were randomized at 263 centres to chemotherapy with (CB) or without (C) bevacizumab. and 14. BI). At 42 months.3 months (C). In the second of these trials. GYNAECOLOGY Bevacizumab for ovarian cancer overall survival was 76% with no differences in survival between the three groups. and oxytocin infusion started at least 6 hours after the last dose of vaginal gel and with a Bishop score of 6 or more. Gastrointestinal wall disruption needing treatment occurred in 2. The study. Australia and New Zealand.8 vs 36. Canada. and one in eight European countries. OBSTETRICS (Foley catheter) vs 20% (prostaglandin gel). Two trials. and VEGF is implicated as a promoter of ovarian cancer. In the first of the trials. Amniotomy was performed.6 months. peritoneal cancer. or bevacizumab in cycles 2–6. BT was associated with a significant 28% reduction in progression or death compared with control treatment. Perren TJ et al. South Korea and Japan. Median progression-free survival was 10.528 women with stage I. have assessed the benefits of bevacizumab for women with ovarian cancer. some 20–30% of deliveries follow uterine rupture. Median mean progression-free survival at 36 months was 21. IIa. or placebo in cycles 2–22 (controls). term pregnancy in cephalic presentation with intact membranes. 2. Burger RA et al. There was a significant 19% reduction in risk of progression or death with bevacizumab. Ibid: 2484–2496.5 months vs 18. Sig- JPOG MAR/APR 2012 • 45 . 365: 2473–2483. There were two serious adverse events. 23%.

they performed a longitudinal case-control study with 1. 378: 1316–1323. but the rates of anaemia at age 2 days were 1. but in developed countries early clamping remains the rule. Sickle-cell trait (HbAs). and hospital admissions for bacteraemia. Delayed cord clamping and improved infant outcomes. Lancet 2011.000 childyears because of more effective malaria control.5 to 3.3%. provides protection against malaria. they studied 292 children aged 3 months to 13 years with bacteraemia and 528 bacteraemia including cases due to non-typhoidal salmonella. Bacteraemia was associated with sickle-cell disease. Anderson O et al. PAEDIATRICS Malaria and bacteraemia in children Bacteraemia is common in children in sub-Saharan Africa. Intracervical Foley catheter for induction of labour: Ibid: 2054–2055 (comment). largely Gram-negative Early versus delayed clamping of the umbilical cord months. a significant difference in favour of delayed clamping. Foley catheter versus vaginal prostaglandin E2 gel for induction of labour at term (PROBAAT trial): an open-label. however. At the same time. undernutrition. ter birth) cord clamping. randomised controlled trial. A meta-analysis including this and two other studies showed that the Foley catheter method was associated with significantly less risk of hyperstimulation or postpartum haemorrhage. 378: 2095–2103. Delayed cord clamping reduced the rate of early neonatal anaemia and reduced the rate of iron deficiency. case-control study and a longitudinal study. HIV infection.45 per 1. Delayed clamping would prevent one case of iron deficiency for every 20 children born. Ibid: 1281–1282 (comment). A total of 400 term infants born after a lowrisk pregnancy were randomized to early (within 10 seconds of birth) or delayed (at least 3 minutes afis also thought to make children susceptible to invasive bacterial infections. malnutrition. Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. Malaria parasitaemia increased the risk of bacteraemia 6. decreased in parallel with those for malaria. Ibid: 1233–1234 (d7127) (editorial). First. Scott JAG et al.7-fold.45 admissions per 1.nificantly more women in the prostaglandin group (3% vs 1%) were treated for suspected intrapartum infection. Stock S. and hyperbilirubinaemia were similar in the two groups. Between 1999 and 2007. and sickle-cell disease all contribute to the susceptibility. Van Rheenan P. JPOG MAR/APR 2012 • 46 . Greenwood B.2% vs 6. the rate of hospital admission for malaria fell from 28. Relation between falciparum malaria and bacteraemia in Kenyan children: a population-based. 343: 1244 (d7157). from 2.000 child-years. the protection provided by sicklecell trait against bacteraemia fell.454 cases (children with bacteraemia) and 10. but the Foley catheter method is associated with less maternal and neonatal risk. but not of anaemia. The prevalence of iron deficiency was reduced by 90% with delayed rather than early clamping. A study in Sweden has re-emphasized the benefits. Mean serum ferritin levels at 4 months of age were significantly 45% higher with delayed clamping (117 vs 81 µg/L). Sickle-cell trait was associated with a 64% reduction in risk of bacteraemia. These researchers conclude that the two methods are similarly effective.749 controls. The rates of neonatal respiratory problems. Malaria The benefits of delaying clamping of the umbilical cord have been promoted for many years. HIV infection. Malaria control should reduce the prevalence of bacteraemia. In 1999. The two groups had similar haemoglobin levels at age 4 months. Obaro S. and researchers in Kenya have taken advantage of this to perform a mendelian randomization study. Lancet 2011.59 to 1. Malaria and bacteraemia in African children. BMJ 2011. and leukocyte haemozoin pigment. Norman JE. Next. A BMJ editorialist calls for more units to practice delayed clamping. and 62% of cases of bacteraemia were attributed to malaria. polycythaemia. at the age of 4 control children. Jozwiak M et al. the prevalence of parasitaemia in the community was 29%.

Lancet 2011. accounting for 22% of ALRI episodes in young children. Speed of intravenous rehydration for children A recent trial in sub-Saharan Africa showed that JPOG MAR/APR 2012 • 47 . Now. with almost all (99%) of these deaths occurring in developing countries. Data were obtained from studies published between Jan 1.000 and 111. and 16 unpublished population-based studies. Global burden of respiratory infections due to seasonal influenza in young children: a systematic review and meta-analysis. The 43 studies included about 8 million children younger than 5 years. 378: 1917–1930. 20 million cases of ALRI due to influenza. It was estimated that in 2008. Nair H et al. 2010. The estimated number of deaths from ALRI due to influenza viruses in children < 5 years old in 2008 was between 28. and 1 million cases of severe ALRI from this cause. until now.Peer Reviewed Journal Watch Influenza in children worldwide Acute lower respiratory infections (ALRI) were the cause of 1. Around the world. 1995 and Oct 31. The most common pathogen is respiratory syncytial virus. the available data have been analysed in a systematic review and meta-analysis of 43 studies. Zambon M. Assessment of the burden of influenza in children. there have been no estimates of the global burden of disease from this cause. there were 90 million new cases of influenza in this age group. It has been suspected that seasonal influenza viruses cause many childhood episodes of ALRI but.56 million deaths in young children in 2008.500. Influenza is a common cause of ALRI in young children worldwide. about 13% of all cases of ALRI and 7% of cases of severe ALRI in young children were caused by influenza viruses. Ibid: 1897–1898 (comment).

5–33 kg) presenting with gastroenteritis and mild to moderate dehydration to the emergency department of a children’s hospital were treated initially with oral rehydration. Mortality was 53% for hospital-acquired bacteraemia and 24% for community-acquired bacteraemia. but the time to hospital discharge was significantly longer in the rapid rehydration group (6. rising during the study period by 27% per year. and severe malnutrition and unnecessary blood transfusion were contributory factors. common in children in sub-Saharan Africa. 18 bacterial pathogens were isolated. Nager AL. group D streptococci. Feasy N. about 40 times the local Hospital-acquired bacteraemia in children in a Kenyan hospital rate of community-acquired bacteraemia. of 15 years (14% aged 0–28 days. Molyneux E. Freedman SB et al. These researchers suspect that the increase is related to increased hospital stays because of an increasing proportion of neonates and fewer short stays with malaria.000 days in hospital. Lancet 2011. The main infecting organisms were Escherichia coli and Klebsiella pneumoniae. Now. The incidence was 1. In the Kilifi District Hospital in Kenya between 16 April 2002 and 30 September 2009.0 per 1.9% saline 60 mL/kg over 1 hour) or standard intravenous rehydration (20 mL/kg over 1 hour). each accounting for around 20% of rapid bolus intravenous fluid administration was potentially lethal for children with dehydration. Rapid intravenous rehydration in paediatric gastroenteritis. in all. Acinetobacter species.9 per 1. and 58% over 1 year).than standard rehydration. Ibid: 1183 (d7083) (editorial). Rapid rehydration did not give better results Although community-acquired bacteraemia is cases. a non-significant difference. and non-typhi Salmonella species (9%). The main pathogens differed from those of communityacquired bacteraemia. has shown no advantage from rapid rehydration compared with standard rehydration. there are few data about hospital-acquired bacteraemia. Yeasts were isolated in 5% of cases. Prolonged treatment was needed by 52% vs 43% (non-significant difference).3 vs 5. The main pathogen in community-acquired bacteraemia was Streptococcus pneumoniae (29%). overall. When oral rehydration had failed. Acinetobacter species (10%). A total of 226 children > 90 days old (weight. Hospital-acquired bacteraemia was uncommon in this study but carried a high mortality.000 admissions overall. Risk and causes of paediatric hospital-acquired bacteraemia in Kilifi District Hospital. Canada. there were 33. Ibid: 1982–1983 (comment). Clinical rehydration at 2 hours was achieved in 36% (rapid) vs 30% (standard). Rapid versus standard intravenous rehydration in paediatric gastroenteritis: pragmatic blinded randomised clinical trial. Factors associated with hospital-acquired bacteraemia included severe malnutrition and blood transfusion in the absence of severe anaemia. fever.188 admissions of children up to the age JPOG MAR/APR 2012 • 48 . 343: 1190 (d6976). they were randomized to rapid intravenous rehydration (0. 3% 29–59 days. BMJ 2011. Keep it clean: hospital-acquired infections in children. A 7-year survey in a single hospital has been reported. to rapid rehydration being effective and safe. Kenya: a prospective cohort study. Aiken AM et al. Staphylococcus aureus. 378: 2021–2027. a study in Toronto.0 hours). The writer of a largely critical editorial insists that currently available evidence points. and poor peripheral perfusion. and Pseudomonas aeruginosa each accounted for slightly less than 10% of cases and. 25% 60 days to 1 year. The rate of hospital-acquired bacteraemia (> 48 hours after admission) was 5. followed by Staphylococcus aureus (13%). Survivors of hospital-acquired bacteraemia spent an extra 10 days in hospital compared with patients who did not become bacteraemic.

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000/year) and Canada (21. The incidence of type 2 diabetes (T2DM) is increasing most notably in the adolescent age group. MD. JPOG MAR/APR 2012 • 49 .4/100. both sexes.3 T1DM affects children of all ages.000 children with T1DM. from the highest in Finland (57. in parallel with the rise in obesity throughout the world.6 Data are lacking about the incidence of T1DM in some developing countries in sub-Saharan Africa and South and East Asia. in which the diagnosis may be being missed.7/100.3 The overall annual incidence is increasing at a rate of about 3%4 with the greatest increase in the youngest age group.2 EPIDEMIOLOGY Worldwide.000/year) to the lowest reported in China (0. and 76.000/year).6/100. MBBCh.000/year) and Venezuela (0. FRCP(C) INTRODUCTION Type 1 diabetes mellitus (T1DM) is the most common chronic metabolic condition in children and adolescents. The classification of DM is described by the American Diabetes Association.5 Several hypotheses to explain this changing incidence have been proposed. such as rapid growth in early childhood.1/100. Denis Daneman. there are approximately 480. but none is widely accepted.PAEDIATRICS I Peer Reviewed Type 1 Diabetes Mellitus in Childhood Rayzel M Shulman. or both.000 new cases are diagnosed each year. and all ethnic groups. environmental exposures. 3 Incidence rates of T1DM in children and adolescents under 15 years of age vary greatly by geographical region. resulting in hyperglycaemia and associated abnormalities in carbohydrate. Diabetes mellitus (DM) comprises a group of heterogeneous conditions involving defects in insulin secretion or action. and reduced early exposure to pathogens.1 T1DM is by far the most common type seen in childhood. FRCPC. protein and fat metabolism.

It most commonly results from autoimmune destruction of insulin-producing β-cells in the pancreas. a CLINICAL PRESENTATION AND DIAGNOSIS The presentation of T1DM can range from a clinically stable child with symptoms of polyuria. Hispanic and Native North Americans). obesity. dietary factors or toxins. DQ 0201/0302. might trigger the development of T-cell-dependent autoimmunity in genetically susceptible individuals.5% OR 2) Fasting plasma glucose 7.8 A number of genetic loci in the major histocompatibility region are associated with increased susceptibility to developing T1DM.1 Type 2 Diabetes (T2DM) In the pubertal age group.000/year. Only rarely are repeated blood glucose measurements and/or an oral glucose tolerance test required to make the diagnosis of T1DM in children (Table 1). Asian. criteria 1–3 should be confirmed by repeat testing. but key factors include genetic predisposition (> 80% have a positive family history). a random plasma glucose ≥ 200 mg/dL (≥ 11. coeliac disease. In PATHOPHYSIOLOGY T1DM is the result of a combination of genetic and environmental influences. Addison’s disease. DR 4/4. sex.55/100. intrauterine environment.1 mmol/L) during an oral glucose tolerance test. Devendra et al proposed that one or more environmental factors. To date.PA EDIATRICS I Peer Reviewed Table 1. T1DM must be differentiated from T2DM. TrialNet. includJPOG MAR/APR 2012 • 50 the presence of these classical symptoms of hyperglycaemia. the diagnosis should not be delayed. and DQ 0300/0302. and insulin resistance. and myasthenia gravis. American Diabetes Association criteria for the diagnosis of diabetes ing the alleles DR3/4. using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in watera OR 4) In a patient with classic symptoms of hyperglycaemia or a hyperglycaemic crisis. These patients are susceptible to other autoimmune diseases. Insulitis with gradual β -cell destruction leads to pre-diabetes and finally to overt DM. Ongoing research by international networks is exploring ways to prevent. ethnicity (more common in African-American. The risk of T1DM is approximately 5% if there is an affected first-degree relative and slightly higher if the affected parent is the father rather than the mother. A Canadian population-based surveillance study of non-type 1 diabetes in children under 18 years of age found an incidence rate of 1.10 The aetiology of T2DM is multifactorial. such as enteroviruses.0 mmol/L (fasting is defined as no caloric intake for at least 8 hoursa) OR 3) 2-hour plasma glucose ≥ 200 mg/dL (≥ 11. In such situations. such as Hashimoto’s thyroiditis. interventional trials have failed to delay the onset or prevent T1DM in those genetically at risk.1 mmol/L is sufficient to make the diagnosis of DM. Both secretion and action of insulin are usually dis- . treatment should be initiated urgently to prevent or reverse DKA.9 1) HbA1c ≥ 6.7 Autoimmunity is manifest by detectable antibodies to ICA512/ IA-2. The test should be performed as described by the World Health Organization. a single blood glucose measurement > 11. delay or reverse the progression of T1DM (eg. enuresis and weight loss to a severely dehydrated child with diabetic ketoacidosis (DKA). polydipsia.1 mmol/L) In the absence of unequivocal hyperglycaemia. Forty genetic loci have been associated with T1DM by a genome-wide association study and meta-analysis. TRIGR). insulin autoantibody and glutamic acid decarboxylase.

EKG = electrocardiography.5–5 mL/kg/hr • Oral hydration • S/C insulin (see illness rules) After 1st hour of IV fluids • If history of voiding within last hour and potassium <5. electrolytes. • DO NOT GIVE BOLUS OF INSULIN • Continuous cardio-respiratory monitoring (with EKG tracing) Neurological deterioration • Headache.3 • Bicarbonate >18 mmol/L • Start S/C insulin • Stop IV insulin ½ hour after S/C dose of rapid-acting or 1 hour after S/C dose of regular insulin • Determine cause of DKA • Contact regional Pediatric Diabetes Education Centre • Hourly.5 ml/kg/hr of standard solution as above • Contact Tertiary Pediatric Diabetes Centre • Admit to ICU Observation and monitoring • Hourly blood glucose (capillary) • Aim for a decrease in blood glucose of 5 mmol/L/h • Strict hourly documentation of fluids input/output • Calculate and review fluids balance at least every 4 hours • Improvement • Clinically well • Tolerating oral fluids • pH >7.4–0. venous gases – then Q2–4h • Follow effective osmolality = (2x measured sodium + measured blood glucose) • Avoid a decrease of >2–3 mmol/L/hr in effective osmolality by increasing IV sodium concentration Adapted from: Ontario Ministry of Health and Long-term Care.04-0. Q2–4h = every 2–4 hours. PALS = Pediatric Advanced Life Support.5 mmol/L. Emergency room (ER) management guidelines for the child with type 1 diabetes in diabetic ketoacidosis (DKA) History (some or all of) • Polyuria • Polydipsia • Weight loss • Abdominal pain • Tiredness • Vomiting • Confusion • Difficulty breathing Clinical signs generally include • Deep sighing respirations – (Kussmaul breathing) with no wheeze or rhonchi • Smell of ketones on breath • Lethargy/drowsiness • Dehydration – mild to severe • Urine ketones/glucose • Capillary glucose STAT in ER • Venous blood – glucose. IV = intravenous. Emergency Room Management for the Child with Type 1 Diabetes. Available at: www.ca/english/providers/pub/diabetes/child_poster. Inotrope-resistant shock 3.4–0. irritability. decreased level of consciousness. Include this amount in total fluid intake.3 • Consult paediatrician immediately Vascular decompensation (with or without coma) • Hypotension (see box) • Decreased level of consciousness No vascular decompensation Resuscitation • Assess airway and breathing • Apply 100% oxygen by mask • Normal saline 10 mL/kg to expand vascular space THEN • Decrease to 5–7 mL/kg/hr with potassium chloride as noted below • Only infuse sodium bicarbonate (1–2 mEq/kg over 1 hour) if: 1. urea. © Queen’s Printer for Ontario. STAT = statim. 2009. Cardiac arrest • Clinically dehydrated • Hyperventilating OR • Vomiting • Normal BP (lying and sitting) • Minimally dehydrated • Tolerating fluids orally • Normal bowel sounds • Normal mental status Normal saline 7 mL/kg over 1st hour with potassium chloride as noted below THEN 3.04–0. gases.pdf. assessment of neurological status for a minimum of 24 hours • 2–4 hours after start of IV – electrolytes. creatinine • Other as indicated Confirm DKA • Ketonuria • Serum bicarbonate < 18 mmol/L • Glucose > 11 mmol/L Hypotension (PALS values) Age Systolic BP (mm Hg) < 1 month < or = 60 1 month to 1 year < or = 70 1 to 10 years < or = 70 + (2 x age in years) > 10 years < or = 90 • pH < 7.05 U/kg/hr = 0.gov. D5 = 5% dextrose.health. ICU = intensive care unit.1 units/kg/hr = 1mL/kg/hr (of solution of 25 units of regular insulin in 250 mL normal saline). HR = heart rate. Reproduced and adapted with permission. Life-threatening hyperkalaemia 2. JPOG MAR/APR 2012 • 51 .5 mL/kg/hr of standard solution as above • Blood glucose < 10 mmol/L change to IV fluids • 20% mannitol 5 mL/kg over 20 minutes • If sodium has declined. decreased HR • First rapidly exclude hypoglycemia by capillary blood glucose measurement THEN • Treat for cerebral oedema Acidosis not improving (in 3–4 hours) • Check insulin delivery system • Consider sepsis • Contact Tertiary Pediatric Diabetes Centre Acidosis improving • Blood glucose <15 mmol/L OR • Blood glucose falls >5 mmol/L/h after 1st hour of fluids • Change IV to D5/normal saline with potassium as above • Decrease insulin to 0.PAEDIATRICS I PAEDIATRICS Peer Reviewed Figure 1.on. BP = blood pressure. administer 2–4 ml/kg of 3% saline over 10–20 min THEN Normal saline at maintenance IV rate • Decrease insulin to 0. at least. add 40 mEq/L of potassium chloride to IV fluid • Aim to keep potassium between 4–5 mEq/L • Continuous insulin infusion 0.05 U/kg/hr = 0. S/C = subcutaneous.

and obesity). hyperglycaemia (blood glucose > 11 mmol/L). the presence of psychiatric disorders. Identifying this diagnosis is important to predict the course of disease. DKA may also be present in up to 25% of young people presenting with T2DM. the incidence of DKA has been reported to be 8 episodes per 100 patient-years.0–7.5 mmol/L) fasting hyperglycaemia. severe insulin resistance.5–8. 14 insulin omission or insulin pump failure. DIABETIC KETOACIDOSIS Diabetic keoacidosis results from absolute insulin insufficiency. Insulin resistance may manifest clinically with acanthosis nigricans (a velvety thickening of the dermis found especially on the posterior neck and axillae). although one feature may predominate.0–10. guide management. rarely.32(suppl 1). and ketonuria. and genetic testing is available for all of the identified mutations. formerly known as maturityonset diabetes of the young. and aid in diagnosis and management of similarly affected family members. 13 In those with established T1DM in the United States. explain associated clinical features. JPOG MAR/APR 2012 • 52 .12 DKA is present at T1DM presentation in 15–67% of children.0–10. Monogenic Diabetes Occasionally. Can J Diabetes 2008. and features of metabolic syndrome (hypertension.5 Careful avoidance of hypoglycaemia in this age group owing to risk of cognitive impairment Adapt targets to patient’s age Appropriate for most patientsa 6–12 13–18 ≤ 8.0–6. leading to metabolic acidosis (pH < 7. ordered at clinical presentation. HbA1c ≥ 6. especially if young or familial • Diabetes associated with extra-pancreatic features Specific genetic defects are listed in Table 1.0 4. Glycaemic and HbA1c targets according to the 2008 Clinical Practice Guidelines of the Canadian Diabetes Association Age (y) HbA1c (%) Plasma glucose (mmol/L) 6. features of polycystic ovarian syndrome (hyperandrogenism.0 2-hour postprandial plasma glucose (mmol/L) – Considerations <6 ≤ 8. T1DM must be differentiated from monogenic diabetes.0 mmol/L. fasting/preprandial plasma glucose 4. longer duration of diabetes. a In adolescents in whom it can be safely achieved. and 2-hour postprandial plasma glucose 5.0–8.0 ≤ 7.PA EDIATRICS I Peer Reviewed Table 2. 11 Monogenic diabetes should be considered in the following clinical scenarios11: • Neonatal diabetes and diabetes diagnosed within the first 6 months of life • Familial diabetes with an affected parent • Mild (5. Risk factors that predict DKA include female sex. dyslipidaemia.0%. ketonaemia. consider aiming toward normal PG range (ie.0–12.0 Source: Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada.0 – 5. Monogenic forms of diabetes result from single gene mutations that cause impaired β-cell function or.0 4. higher reported insulin dose. higher mean HbA 1c.0 mmol/L). menstrual irregularity).3 or bicarbonate < 15 mmol/L). its frequency being inversely related to the incidence of T1DM in that area.

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insulin dose adjustment. The starting total daily dose is 0.9%. or greater costs. Families of children with T1DM should have a clear understanding of the rationale for blood glucose and HbA 1c targets for their child. DKA is the major cause of hospitalization.PAEDIATRICS I PAEDIATRICS Peer Reviewed DKA should be treated as a medical emergency by an experienced medical team. It is essential that from the moment of diagnosis. morbidity and mortality in young people with T1DM. and detection and treatment of hypoglycaemia. A meta-analysis of homebased management at DM onset suggests that in comparison to routine hospital admission. The most serious complication is cerebral oedema. or cardiac arrest. Boluses of fluid and insulin should be avoided. greater hypocapnia after adjusting for the degree of acidosis. acute diabetic complications or psychosocial outcomes. 12 ed that support services are available and that no other medical or social conditions exist that would place the child in danger. After initial stabilization and education. 15 Early ‘survival skills’ to be mastered include insulin injections.and long-term implications. diabetes nurse. usually lower in younger children. and an attenuated rise in the measured serum sodium during treatment. Demographic risk factors associated with increased risk for cerebral oedema include younger age. children presenting without DKA can be safely managed on an ambulatory basis provid- ercise. and longer duration of symptoms. The treatment algorithm used at our centre is outlined in Figure 1. Treatment of DKA in children differs in several respects from that in adults: first. effects of ex- MANAGEMENT OF T1DM IN CHILDHOOD The diagnosis of T1DM is a pivotal moment for the child as well as for his/her family. including a physician. which occurs in 0. Insulin initiation varies greatly among different centres but generally consists of two to four injections per day. In the subsequent weeks. these families receive expert care from a team of health professionals experienced in childhood diabetes. Risk factors that are present at the time of diagnosis or during treatment are increased serum urea. dietitian and social worker. outpatient care is not associated with worse metabolic control. T1DM is a lifelong condition with serious short. basic nutrition planning. Fluid repletion should occur gradually with sodium chloride 0. and is adjusted on a daily basis until target blood glucose is achieved (Table 2). blood glucose monitoring. This includes regular JPOG MAR/APR 2012 • 53 . administration of sodium bicarbonate. with 25% mortality.0% of DKA episodes. children and their families enter the long-term followup phase of their diabetes.5–1. both fluids and insulin are calculated on a per kilogram rather than an empirical basis.6 units/kg body weight/day. new-onset diabetes. more detailed information is provided about diabetes management (patho- Families need to be forewarned of the natural history of T1DM so that they do not develop false hope that their child’s diabetes is ‘going away’ physiology. and sick days). At onset. Bicarbonate should be given only in the setting of life-threatening hyperkalaemia.4–0. severe acidosis. inotrope-resistant shock.

and individual and family preferences. associated conditions (hypothyroidism. Special attention must be paid to those children and their families.20 Generic name Rapid-acting Lispro Aspart Short-acting Regular human insulin Intermediate-acting (NPH) NPH human insulin Basal insulin Glargine Detemir Onset 10–30 min Peak 30 min–3 h Duration 3–5 h 30–60 min 2–5 h Up to 12 h 90 min– 4h 45 min– 4h 4–12 h Up to 24 h Minimal peak action Up to 24 h Source: Insulin action. and duration of action of commonly used insulin preparations demonstrated conclusively that intensive glycaemic control delays and prevents the microvascular and macrovascular complications of T1DM.html. Families need to be forewarned of the natural history of T1DM so that they do not develop false hope that their child’s diabetes is ‘going away’. Increasingly. with insulin doses calculated to match carbohydrate intake and ambient blood sugar.22 CSII is a more sophisticated form of basal-bolus regimen whereby fast-acting The Diabetes Control and Complications Trial (DCCT) JPOG MAR/APR 2012 • 54 GLYCAEMIC AND HbA1c TARGETS insulin analogue is administered by continuous in- . Most children and teenagers now start their treatment with a combination of intermediate-acting insulin or basal insulin analogue (insulin glargine or insulin detemir). INSULIN REGIMENS follow-up visits with their diabetes team with surveillance for psychosocial problems. peak. coeliac disease). The choice of regimen should be tailored to the child’s age. See Table 3 for the onset. and duration of action of commonly used insulin preparations.joslin. peak. this basal-bolus approach can help to achieve and maintain near-normal glycaemia. who have the greatest difficulty meeting the considerable demands of their diabetes regimen. 19. 2010 Joslin Diabetes Center. children and teenagers with T1DM are using continuous subcutaneous insulin infusion (CSII) pumps. and microvascular and macrovascular complications. Onset. The duration of the honeymoon phase is proportional to the age of the child. Available from: www. most patients enter a transient remission or ‘honeymoon’ phase when exogenous insulin requirements decrease as a result of residual β-cell secretion.18 Multiple studies attest to the difficulties in achieving these goals in all children with T1DM. Severe hypoglycaemia in young children has been associated with mild cognitive deficits later in life. most frequently the youngest children and adolescents. although the cause-and-effect relationship remains controversial. duration of diabetes. This demands that age-appropriate targets be set and that progressively tighter control be sought as the child grows older. Soon after initial presentation. Approaches to insulin therapeutics vary from one centre to another. 16. targets of metabolic control.org/info/insulin_action. daily routines. 21 When rigorously applied. combined with rapid-acting insulin analogues (insulin lispro or insulin aspart) given two or more times daily.PA EDIATRICS I Peer Reviewed Table 3.17 Intensification of therapy is associated with an increased risk of hypoglycaemia that can be a limiting factor in achieving good metabolic control. Table 2 summarizes the glycaemic goals published in the 2008 Clinical Practice Guidelines of the Canadian Diabetes Association.

BLOOD GLUCOSE MONITORING Children and adolescents with T1DM are encouraged to monitor blood glucose at least four times per day (before each meal and at bedtime). Families should have injectable glucagon at home to treat severe hypoglycaemia (coma. Co-morbidities JPOG MAR/APR 2012 • 55 The goal of diabetes management should be to maintain the lowest possible HbA1c without severe or prolonged hypoglycaemia or hyperglycaemia.9 mmol/L or 70 mg/dL) is a common unwanted effect in people treated with insulin and occurs when there is an imbalance in insulin dose.28 Recognition of symptoms of hypoglycaemia can be difficult in young children with T1DM. 16. rarely. Methods for adjusting insulin and carbohydrate intake to accommodate exercise have been proposed. blood pressure. and therefore increased monitoring of blood glucose when hypoglycaemia might be expected (overnight. NUTRITION Recommendations for nutritional intake in young people with T1DM should aim to support optimal glycaemic control. weighted more heavily toward the most recent 4 weeks. food consumed and activity. A systematic review and meta-analysis of randomized controlled trials comparing CSII to multiple daily injection in children with T1DM found a modest improvement (0.23 HbA1c is a measure of glycaemic control over the previous 4–12 weeks. strenuous exercise. more frequent monitoring with either insulin dose adjustment or appropriate food intake are needed to avoid the extreme hypoglycaemia that can occur with activity. Maintenance of a blood glucose logbook is essential to follow patterns and to make appropriate dose adjustments. although in some cases rigorous exercise may induce a stress response leading to hyperglycaemia. Hypoglycaemia has been associated with reduced cognitive functioning and can.26. insulin doses can be calculated . seizure. Quality of 5 based on the number of grams of carbohydrates consumed and on deviation from the target blood glucose.25 PHYSICAL ACTIVITY Physical activity in general leads to increased glucose utilization.17 HYPOGLYCAEMIA Hypoglycaemia (blood glucose < 3. after insulin dose adjustment. The cost of 6 CSII is considerable and cannot be accommodated by many families and health-care systems. or illness) is recommended. Nutritional requirements for children with T1DM do not differ from those of healthy children and adolescents. Lower HbA1c values have been associated with fewer and delayed microvascular and macrovascular complications.24%) in HbA 1c in the CSII group and found no differences in DKA or severe hypoglycaemia between groups. or severe confusion). and fit with the insulin regimen. and lipid profiles. Symptoms include autonomic (adrenergic) activation and/or neurological dysfunction (neuroglycopenia). Diabetes should not limit the ability of a child to participate in sport.PAEDIATRICS I PAEDIATRICS Peer Reviewed fusion (basal rate) with intermittent boluses given before carbohydrate ingestion or to correct hyperglycaemia.27 life and patient satisfaction have been reported to be at least equal or improved with CSII. be a cause of death in young people with T1DM. For children and teenagers involved in exercise activities. Continuous glucose monitoring technologies have been developed and are increasingly being used in clinical care as an adjunct to intermittent monitoring. If carbohydrate 24 counting is used.

In anticipation of this. Teenagers should also have private time with the members of the diabetes care team as this promotes independence and responsibility. DM is also a major risk factor for macrovas- . and higher body mass index percentile in teenage girls with T1DM have been shown to predict the onset of eating disturbances JPOG MAR/APR 2012 • 56 COMPLICATION SURVEILLANCE Chronic hyperglycaemia is associated with subsequent development of microvascular complications (retinopathy. intensification of the insulin regimen. TRANSITION TO ADULT CARE The transition period from paediatric to adult DM care can be a daunting time for the patient and family. body image concerns. Insulin omission may be one method by which the teenager may attempt to control his/her weight. adolescents with DM should be encouraged to take an increasingly active role in their diabetes care from an early stage. Adolescents should be offered regular sexual health and contraception counselling. In the context of universal health-care funding. SICK-DAY MANAGEMENT Diabetes control may deteriorate during periods of intercurrent illness. Alternatively. and disorders29 and should therefore be assessed in the routine diabetes care in this population. a phenomenon termed metabolic memory. Tight metabolic control delays and slows the progression of these complications. Frequent monitoring of blood glucose and ketones. leading to hyperglycaemia and ketosis. Illnesses associated with decreased oral intake may predispose to hypoglycaemia. the stress of some illnesses may lead to a vigorous counter-regulatory hormone response. Poorly controlled T1DM is a risk factor for maternal and fetal complications. Diabetes is not an absolute contraindication to using oral contraception. dyslipidaemia. and family history. Adolescents who plan to or hold a driver’s licence should always check their blood glucose before driving. ADOLESCENTS WITH T1DM Given the association of smoking with both microvascular and macrovascular complications of DM. longer duration of disease. Suboptimal metabolic control has been shown to have an enduring negative effect on the development and progression of microvascular complications even if glycaemic control is subsequently ameliorated. and timely emergency department attendance for those with repeated vomiting should help to prevent metabolic deterioration. Depression. and the effect of alcohol and illicit drugs on blood glucose. 31 Other risk factors for long-term complications include younger age of DM onset. hypertension. adolescents should be counselled in smoking prevention and cessation. Unstable glycaemic control and severe hypoglycaemic events may limit their ability legally to obtain or maintain a driver’s licence.PA EDIATRICS I Peer Reviewed such as coeliac disease and Addison’s disease can increase the risk of hypoglycaemia. continuation of insulin therapy with appropriate dose adjustment. neuropathy and nephropathy). although the risk is less for youth who transfer to a new allied health team but maintain physician continuity. It is important to address the risk of severe hypoglycaemia associated with an unpredictable daily activity schedule. 30 Formal transition programmes may facilitate transfer to adult care and prevent the high rates of drop-out reported in some centres. smoking. there is an increased rate of DM-related hospitalizations in the 2 years after transition to adult care.

such as amylin analogues (pramlintide).33 Other strategies to improve the effectiveness of subcutaneous insulin action in T1DM have been proposed. and an effective algorithm to alter insulin delivery based on real-time glucose sensor inputs. This system involves an insulin pump to deliver insulin. pharmacological interventions for high-risk young people with T1DM will provide cardio-renal protection. and insulin-sensitizing and other adjunctive agents may lead to improved therapies for the management of T1DM in the future JPOG MAR/APR 2012 • 57 . These procedures carry significant risks related to the procedures themselves and the need for chronic immunosuppression. and the organization of health services. Recommendations for screening for complications are summarized by the Canadian Diabetes Association 2008 Clinical Practice Guidelines. Preventive measures include maintaining normal blood pressure. FUTURE DEVELOPMENTS Pancreatic and islet-cell transplantation has been performed in adults with T1DM for end-stage renal disease or persistent metabolic instability. The long-term safety and effectiveness of these agents for the management of T1DM in young people remain uncertain. and glucagon-like peptide 1 analogues have also been studied. avoiding smoking. peripheral artery. These substantial advances should be made known to young people and their families as reason for hope. especially in the area of genetic susceptibility.18 Research to develop an effective extracorporeal artificial pancreas is ongoing. A multidisciplinary approach to the care of young people with T1DM should are ongoing to determine whether. Furthermore. a continuous glucose sensor. and participating in regular exercise. alpha glucosidase inhibitors (acarbose). in addition to optimizing glycaemic control. Advances continue in the understanding of the pathogenesis of DM. insulin preparations and delivery mechanisms. emphasizing the proven benefit of excellent glycaemic control. many children and adolescents (especially) with T1DM fail to achieve their age-appropriate glycaemic targets • Ongoing research in the area of islet-cell transplantation.PAEDIATRICS I PAEDIATRICS Peer Reviewed cular complications (coronary artery. or cardiac arrest • Despite advances in monitoring devices. inotrope-resistant shock. bicarbonate should be given only in the setting of life-threatening hyperkalaemia. Other agents that may improve postprandial blood glucose. including insulin-sensitizing therapies such as recombinant human insulin-like growth factor 1. and cerebrovascular disease). growth hormone suppressors or antagonists. Patient and 32 family education about complications should begin early and be ongoing. Cardiovascular disease is the most important cause of the excess mortality associated with diabetes. closedloop insulin delivery systems. correcting dyslipidaemia. What’s new? • The incidence of type 1 diabetes mellitus (T1DM) is increasing worldwide at a rate of approximately 3% per year with the greatest increase in the youngest age group • Genetic loci associated with T1DM are being discovered by genome-wide association studies • In the management of diabetic ketoacidosis. and direct insulin-sensitizing agents (metformin. CONCLUSION T1DM in young people remains a common and challenging condition. Significant improvements have been made in the development of glucose monitors. insulin formulations and delivery systems. Trials 18 thiazolidinediones). and as an impetus to maintain the best possible metabolic control. only 10% of patients were insulin-independent at 5 years after islet-cell transplantation.

Pinhas-Hamiel O. Waugh N. Copeland K.6:50–62.28:186–212. Factors influencing glycemic control in young people with type 1 diabetes in Scotland: a population-based study (DIABAUD2). Donaghue KC. Predictors of acute complications in children with type 1 diabetes. et al.89:188–194. Assessment and management of hypoglycemia in children and adolescents with diabetes. Diabetes Care 2007. Incidence trends for childhood type 1 diabetes in Europe during 1989–2003 and predicted new cases 2005–20: a multicentre prospective registration study.38:777–790. Wherrett DK.10(suppl 12):134–145. 33.33(suppl 1):S62–69. Scottish Study Group for the Care of the Young D. et al. Pediatrics 2009. Klingensmith G. 14. Rebrin K. Shalitin S.44(suppl 3):B75–B80. Rydall AC. Transition to adult care for youths with diabetes mellitus: findings from a Universal Health Care System. 8. Lancet 2009. Clayton DG. 11. 32. Donaghue KC. Daneman D. Diabetes Care 2005. Silverstein J. Self-monitoring of blood glucose in children and teens with diabetes. Hub R. Paradis G. 28. Further Reading Daneman D. Rodin GM. Buccino J. Prevention of type 1 diabetes. Swift PG.23:857–866. References 1. Barrett TG.89:188–194. Chase HP. Rachmiel M. Competing interests: Rayzel Shulman received the 2009/10 Canadian Pediatric Endocrine Group (CPEG) Fellowship sponsored by Novo Nordisk Canada. Mackenzie T. N Engl J Med 2005. ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. Geographical variation of presentation at diagnosis of type I diabetes in children: the EURODIAB study. N Engl J Med 1993. Diabetes Care 2010. The rise of childhood type 1 diabetes in the 20th century. 29. The use of insulin pump therapy in the pediatric age group. Dunger DB. 19. Bangstad HJ. 2. 18. Thomas S. Sperling MA. Pediatr Diabetes 2007. Federation ID. Dunger DB. Sperling MA. 24. 17.287:2511–2518. Barrett JC. Denis Daneman is Paediatrician-in-Chief at SickKids and Chair of the Department of Pediatrics at the University of Toronto. 15.30:72–79. Incidence and trends of childhood type 1 diabetes worldwide 1990–1999. Green A.5:656–665. Gyurus E.30:2245–2250.63:75–85. Dahms W. Ranke MB. 22. Levy-Marchal C. Beneficial effects of intensive therapy of diabetes during adolescence: outcomes after the conclusion of the Diabetes Control and Complications Trial (DCCT). Pediatr Diabetes 2005. Porter JR. Nat Genet 2009. Danne T. Olmsted MP. Pediatr Diabetes 2009. Status and rationale of renoprotection studies in adolescents with type 1 diabetes. JAMA 2002. Goldstein D. Acquired non-type 1 diabetes in childhood: subtypes. Zeitler P. Early diabetes-related complications in adolescents. Guttmann A. Backlund JY. Saad MF. Diabet Med 2006. Bruining J.353:2643–2653. et al. Neu A.139:804–812.328:750–754. Colton PA. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. Acerini CL.PA EDIATRICS I Peer Reviewed emphasize optimal metabolic control with minimal hypoglycaemia. Tamborlane WV. Perkins B. Diabetes Care 2010. Routine hospital admission versus out-patient or home care in children at diagnosis of type 1 diabetes mellitus. Dunger D. and management. Eisenbarth GS.32(suppl 1). EURODIAB ACE Study Group. ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. Cochrane Database of Syst Rev 2007. Concannon P. 16. et al. Canada. in the context of a healthy and supportive physical and psychosocial environment.10:468–473.10:347–355. Njolstad P. Pediatr Endocrinol Rev 2007.124:e1134–e1141. Competing interests: Denis Daneman has been a member of the Hvidøre International Study Group for Childhood Diabetes sponsored by Novo Nordisk Inc. 2009. Dunger DB. To T. Dean HJ. et al. diagnosis. Patterson CC. 4. Pediatr Diabetes 2009. Cleary PA. Klingensmith GJ.33:786–791. Perlman K. 5. Acerini CL. Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes. Diabetologia 2001.(2):CD004099. 3. Diabetes Care 2007. 27. et al. Diabetes Educ 2009. 25. 6. Patterson CC. Panagiotopoulos C. medication-induced diabetes. Deeb LC. J Pediatr 2005. Daneman D. Type 2 diabetes mellitus in children and adolescents is still a rare disease in Germany: a population-based assessment of the prevalence of type 2 diabetes and MODY in patients aged 0–20 years. © 2010 Elsevier Ltd. Type 2 diabetes. JPOG MAR/APR 2012 • 58 . Pediatr Diabetes 2009. Arch Dis Child 2004. The diagnosis and management of monogenic diabetes in children and adolescents. et al. Can J Diabetes 2006.41:703–707. Skinner CT. 13. Bui H. Hariri F. Malone J. Daneman D. Gale EAM. Feldhahn L. Endocrinol Metab Clin North Am 2009. Daneman D. J Pediatr 2001. 10. Brussels: Federation ID.373:2027–2033.146:693–700. Exercise and type 1 diabetes mellitus in youth. Swift PGF. 12. 20. Insulin treatment. Canada. Are children with type 1 diabetes consuming a healthful diet? A review of the current evidence and strategies for dietary change. White NH. Daneman D. Diabetes 2006. Diabetes Atlas. Arch Dis Child 2004. Rewers A.10 (suppl 12):1–2. BMJ 2004. 7. Pediatr Diabetes 2009.51:3353– 3361. 21. 23. Horm Res 2008. Pediatr Diabetes 2009.35:97– 107.38(12): 679–685. Cleary PA. Nathan DM. 9. Hanas R. Feasibility of automating insulin delivery for the treatment of type 1 diabetes. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. et al. Amed S. Arch Dis Child 2004. Type 1 diabetes: recent developments. Initially published in Medicine 2010. et al. Swift PG.30:2245– 2250. Marcovecchio ML. Diabetes Care 2008.70:14–21. et al. Diagnosis and classification of diabetes mellitus. Type 1 diabetes and exercise: using the insulin pump to maximum advantage. Clarke W. ISPAD clinical practice consensus guidelines 2006–2007. Dahlquist GG.55:3344–3350. Devendra D. de Beaufort CE. Liu E.31:1978– 1982. Continuing stability of center differences in pediatric diabetes care: do advances in diabetes treatment improve outcome? The Hvidøre Study Group on Childhood Diabetes. The global spread of type 2 diabetes mellitus in children and adolescents. DIARY Group Baden- Württemberg. Nansel TR. Shield J.10(suppl 12):33–42. Diabetes Care 2001.89:1138–1144. Rovner AJ. Rewers A. Darwin C.8:88–102. 31. 26. Jones T. Phillip M. Klingensmith G.329:977–986. et al. Continuing stability of center differences in pediatric diabetes care: do advances in diabetes treatment improve outcome? The Hvidøre Study Group on Childhood Diabetes. Riddell M. Hattersley A. About the Authors Rayzel M Shulman is currently pursuing a PhD at the University of Toronto. de Beaufort CE. Horm Res 2005. Skinner CT. Diabetes 2002. 30. Prediction of the onset of disturbed eating behavior in adolescent girls with type 1 diabetes.24:239–244. Ontario. Clar C. Ontario. and monogenic diabetes in Canadian children: a prospective national surveillance study. Steil GM. review and recommendations. EURODIAB Study Group. Nakhla M. ISPAD clinical practice consensus guidelines 2009 compendium. Tossavainen PH. Care of children and adolescents with type 1 diabetes. Can J Diabetes 2008. Ehehalt S. The Diabetes Control and Complications Trial Research Group.

BDSc. How should the current situation be handled? Will the secondary dentition suffer? (Answers on p. An opportunistic health check revealed that three of her top front teeth had rotted away to below the gum line.IN P ractice I IN PRACTICE Peer Reviewed Clinical Case Rotting Teeth in a Young Girl Simon Wooley. MPH Figure 1 CASE SCENARIO Tracey. MPHC. BDS. Her mother denied that Tracey excessively consumed sweets or sweet drinks. Kaye Roberts-Thomson. confirmed that Tracey brushed her teeth and rather defensively asserted that Tracey had been born with ‘soft teeth’. She also had several carious teeth towards the back of her mouth. was brought in to my clinic from an outlying rural community to receive her immunizations before starting school. 79) JPOG MAR/APR 2012 • 59 . aged 5 years old.

A meta-analysis has concluded that bacterial vaginosis has the characteristics of an STI: being associated with partner change and other STIs. the prevalence of bacterial vaginosis is 10–20%. FRCR. B acterial vaginosis is the most common cause of abnormal vaginal discharge in women of childbearing age. The diagnosis can be confirmed by microscopy ± additional tests.3 The debate about whether bacterial vaginosis is an STI or merely sexually associated continues. accompanied by loss of the usual vaginal acidity. In 1983. FRCP Tang Phua Hwee. but it may be as high as 36% in women attending STI clinics and 28% in those seeking elective termination of pregnancy. Bacterial vaginosis is associated with infective complications in pregnancy and following gynaecological surgery. It is a syndrome of unknown cause characterized by depletion of the normal Lactobacillus population and an overgrowth of vaginal EPIDEMIOLOGY In unselected populations in the UK. MBBS. About 50% of cases are asymptomatic. MBBS.GYN PA AECOLOGY EDIATRICS I Peer Reviewed Imaging Paediatric Bacterial BrainVaginosis Tumours Phillip Hay. and is a risk factor for the acquisition of sexually transmitted infections (STIs) including human immunodeficiency virus (HIV).4 The strongest evidence against it being an STI has come from studies reporting similar rates in self-reported virgin and non-virgin women. 5–7 This has been chalJPOG MAR/APR 2012 • 60 . the term ‘bacterial vaginosis’ replaced the older term ‘Gardnerella vaginitis’. fishy-smelling discharge that is most noticeable after unprotected intercourse or at the time of menstruation. MMed Diagnostic Radiology anaerobes.1 Women with symptomatic bacterial vaginosis report an offensive. 2 A prevalence of more than 50% was reported in rural Uganda. This recognized the fact that many anaerobic or facultative anaerobic bacteria are present and that classical signs of inflammation are absent.

DIAGNOSIS Bacterial vaginosis should be suspected in any woman presenting with an offensive. The description of the biofilm that develops in bacterial vaginosis by Swidsinski and colleagues places Gardnerella vaginalis once again at the centre of pathogenesis of bacterial vaginosis. The organisms classically associated with bacterial vaginosis using culture and those more recently identified using molecular techniques 9. defensins. Table 1.5 • Release of a fishy smell on addition of alkali (10% potassium hydroxide) • Characteristic discharge on examination • Presence of ‘clue cells’ on microscopy of vaginal fluid mixed with normal saline At least three of the four criteria must be fulfilled to make a diagnosis of bacterial vaginosis. The triggers for bacterial vaginosis are probably multiple. . Amsel criteria (Table 2) have been the mainstay of diagnosis in settings such as genitourinary medicine clinics where microscopy can be performed.5–4. be misleading: • The appearance of vaginal secretions may be JPOG MAR/APR 2012 • 61 are shown in Table 1.0 is observed. Epithelial cells covered with so many small bacteria that the border is fuzzy are termed ‘clue cells’ because their presence is a clue to the diagnosis.5 to as high as 7. which reduces the inhibitory effect of H 2O 2 on anaerobic growth. the lactobacilli reduce in concentration and may disappear whilst there is an increased concentration of anaerobic and facultative anaerobic organisms. although other organisms may be present in small numbers. typically fishy-smelling vaginal discharge.12 Any of the Amsel criteria can. It is not known how often bacterial vaginosis occurs in post-menopausal women. The condition often arises spontaneously around the time of menstruation and may resolve spontaneously in mid-cycle. however. it is associated with black race and intrauterine device use. and bacteriocins. Composite (Amsel) criteria for the diagnosis of bacterial vaginosis • Vaginal pH > 4. The organisms classically associated with bacterial vaginosis using culture are shown in the first column and those more recently identified through molecular techniques in the second Gardnerella vaginalis Bacteroides (Prevotella) Mycoplasma hominis Mobiluncus species Atopobium vaginae BVAB1-3 (Clostridiales) Megasphaera Sneathia Leptotrichia AETIOLOGY AND PATHOGENESIS Lactobacilli dominate the normal vaginal flora. Lactobacilli produce inhibitory mediators including lactic acid. white or yellow discharge adherent to the walls of the vagina. H2O2.8 In many studies.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed lenged by a detailed study that reported no bacterial vaginosis in women denying any oral or digital genital contact. Speculum examination shows a thin. homogeneous. Gardnerella accounted for 90% of bacteria seen in the biofilm. Lactobacilli predominated in women with normal flora but did not form a biofilm. Hormonal changes and inoculation with organisms from a partner might also be important. When bacterial vaginosis develops. with Atopobium vaginae the only other numerically important organism. 11 In some women. the biofilm covered the entire biopsy. in others. An increase in vaginal pH from the normal 3. it was more patchy.10 Table 2.

Gram-stained vaginal smear from a woman with normal flora. typical of Mobiluncus mulieris. Large. JPOG MAR/APR 2012 • 62 . curved rods. Clue cells are not part of most scoring systems for bacterial vaginosis. some Gram-positive and some Gram-negative.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed Figure 1. are present. and none are seen in this field. There are many small bacteria present. Epithelial cells and their nuclei can be seen clearly. Figure 2 Gram-stained vaginal smear from a woman with bacterial vaginosis. Gram-positive rods are typical of lactobacilli.

GYNAECOLOGY I GYNAECOLOGY Peer Reviewed altered by factors such as recent intercourse and douching. a high vaginal swab can be sent to the microbiology laboratory for examination by wet mount or Gram staining. use in genitourinary medicine clinics in preference to the Amsel criteria. Typical lactobacilli are large. Recent studies have concluded that there is a continuum from normal Gram Staining Examination of a Gram-stained vaginal smear is a quick and relatively simple means of diagnosis. • Both Candida and trichomoniasis can give a similar clinical appearance. Recognition of intermediate categories can be more difficult and entails subjective assessment of the morphotypes. • Detection of clue cells is the single most sensitive and specific criterion. Recent studies have concluded that there is a continuum from normal Lactobacillus-dominated flora to ‘severe bacterial vaginosis’. The normal flora includes plentiful sis there are large numbers of Gram-negative cocci and small rods (Figure 2). If the pH is high. A pH of less than 4. Curved rods (Mobiluncus species) may be present.5 almost excludes bacterial vaginosis. all of which can also coexist with bacterial vaginosis. Debris or degenerate cells can be mistaken for clue cells. • Vaginal pH may be elevated during menstruation or by the presence of semen. Scoring systems (eg. However. In cervicitis. It enables recognition of intermediate flora. This is recognized in Gram-stain scoring systems but not with Amsel criteria. candidiasis and trichomoniasis. whereas in bacterial vagino. • A positive potassium hydroxide test may be found in the presence of semen. In routine practice. there may be contact bleeding. When the history is highly suggestive of the condition but the tests are negative. and stored slides can be subsequently evaluated independently in research studies. vaginal pH can be measured using pH-sensitive paper. offer further testing if symptoms return. 14 Other Tests Commercially available tests detect biochemical changes in vaginal fluid associated with bacterial vaginosis. and purulent discharge may be visible in the external os. Candida typically causes a curd-like discharge and is associated JPOG MAR/APR 2012 • 63 tem (Hay–Ison criteria) has been recommended for . but the interpretation of microscopy is subjective. A simplified scoring sys13 Other common causes of vaginal discharge are cervicitis caused by Chlamydia or gonorrhoea. the relatively high cost of the currently available tests compared with use of the Gram stain or Amsel criteria has limited their uptake. the Nugent) have attempted to reduce interobserver variability. and lactobacilli sometimes adhere to epithelial cells in low numbers.(TABLE 3) negative coccus. Gardnerella is usually a Gram- Lactobacillus-dominated flora to ‘severe bacterial vaginosis’ DIFFERENTIAL DIAGNOSIS lactobacilli (Figure 1). Gram-positive rods with blunt ends.

but after 4 weeks this declines to 80% in openlabel studies and less than 70% in blinded studies. termination of pregnancy) or in pregnancy. 18 Oral clindamycin can induce rashes and occasionally pseudomembranous colitis. The cure rate immediately after treatment with metronidazole is up to 95%. a metallic taste.0 Microscopy ± 4.5 Microscopy and culture ++ 4. homogeneous Trichomoniasis +++ May be offensive Yellow or green Thin. About 10% of women develop symptomatic candidiasis following Antibiotics Antibiotics targeting anaerobic organisms should be effective in bacterial vaginosis. the value of treating asymptomatic bacterial vaginosis has not been established. These organisms can be sought using specific diagnostic tests. The standard treatment for bacterial vaginosis is metronidaJPOG MAR/APR 2012 • 64 . and metronidazole can be used in pregnancy. Treatment should therefore be prescribed for control of symptoms and in situations in which it might prevent complications of a procedure (eg. Trichomonas causes a more purulent discharge and is associated with soreness and erythema.5–7.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed Table 3. Differential diagnosis of vaginal discharge Symptoms and signs Itching or soreness Smell Colour Consistency Other signs Potassium hydroxide test pH Confirmation Candidiasis ++ May be ‘yeasty’ White Curdy Bacterial vaginosis – Offensive. There is also no evidence that treatment reduces the prevalence in the community. tests for Chlamydia and gonorrhoea – < 4.15. Allergic rashes occur occasionally. or tinidazole 2 g which is more expensive. fishy White or yellow Thin. MANAGEMENT Bacterial vaginosis is sometimes distressing and must be managed with sensitivity. Adverse Effects of Treatment Oral metronidazole is associated with nausea.17 Topical treatments with intravaginal 2% clindamycin cream or 0. zole.0 Microscopy and culture with itching. They are more expensive than oral metronidazole but have similar efficacy and can be useful when systemic treatment is not desirable. Initial concerns about potential teratogenicity have not been substantiated.5–7.16 An alternative is a 2-g single dose. homogeneous Cervicitis – – Clear or coloured Mucoid Purulent mucus at cervical os – < 4.5 Microscopy. Because it has a relapsing–remitting course in many women. Metronidazole and clindamycin are obvious choices. 400 mg orally 12-hourly for 5–7 days. and alcohol intolerance.75% metronidazole gels are licensed for the treatment of bacterial vaginosis.

Many physicians advocate screening for STIs in the partners of women with recurrent bacterial vaginosis. Another approach is to use lactic acid gel to acidify the vagina. accompanied by an antifungal agent if there is a history of candidiasis. Male Partners Four double-blind. If the woman washes her hair in the shower. possibly including bacterial vaginosis. Bacterial vaginosis is sometimes distressing and must be managed with sensitivity.0.4–7. otherwise regular antibiotic treatment is the only option. although it was associated with increased rates of candidiasis. tinidazole or clindamycin. bacterial vaginosis recurs frequently following treatment. If available. the probiotics or lactic acid gel may help to prevent relapse. It is thought that women with bacterial vaginosis are at increased risk of chorioamnionitis.22 Several studies have assessed the value of screening for and treatment of bacterial vaginosis in preventing adverse outcomes in pregnancy. The results have been variable. placebo-controlled trials have failed to show any difference in bacterial vaginosis relapse rates following treatment of male partners with metronidazole. Relapses In some women. It is sensible to use condoms with new sex partners to protect against infections. The author usually prescribes metro21 COMPLICATIONS Pregnancy Bacterial vaginosis is associated with second-trimester miscarriage and preterm birth. It is reasonable to screen the sex partner for infections. some studies showed a benefit with treatment in terms of reducing preterm birth JPOG MAR/APR 2012 • 65 nidazole in the dosage and preparation preferred by the woman to self-treat at the first sign of relapse. so there is insufficient evidence to support their routine use in current guidelines. One study showed that use of metronidazole gel twice weekly reduced the rate of relapse. which can stimulate preterm birth through the release of proinflammatory cytokines. 19.20 bubble bath should be avoided. Management of such cases is difficult. but this is not based on prospective studies. she should avoid contact between the shampoo and the vulval area. but several vaginal strains are now available. The reported odds ratio is 1.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed treatment of bacterial vaginosis. Both approaches have been evaluated in small studies of variable quality. Vaginal lactobacilli differ from those considered optimal for the gut. Alternative Treatments Probiotics and prebiotics have been studied as a treatment for gastrointestinal conditions. Patient Advice and Self-help Vaginal douching and the use of shower gel and .

The potential role of bacterial vaginosis in infections following intrauterine device insertion.2% in a placebo-treated group and 3. but the largest study to date showed no benefit from treatment with short courses of metronidazole. This was confirmed by the most recent Cochrane review.8% in those prescribed oral metronidazole before termination. it cannot be concluded that antibiotic treatment of bacterial vaginosis in pregnancy will universally reduce the incidence of preterm birth.75% metronidazole gel • Routine screening and treatment in pregnancy to prevent preterm birth are not recommended.26 Other Gynaecological Surgery Bacterial vaginosis has been associated with vaginal cuff cellulitis. 24 a fourfold reduction in infective complications with clindamycin cream compared with placebo.25 A more recent randomized controlled trial in Sweden found rates. wound infection and abscess formation after hysterectomy. hysteroscopy. and dilatation and curettage has not been systematically studied.23 On the basis of these studies. A double-blind. placebo-controlled trial in Sweden showed that the risk of endometriJPOG MAR/APR 2012 • 66 HIV and STIs HIV has spread rapidly through sub-Saharan Africa . Termination of Pregnancy Women infected with Chlamydia trachomatis who undergo elective termination of pregnancy are at high risk of endometritis and pelvic inflammatory disease. but symptomatic women should be treated tis in women without Chlamydia was 12. it is not known how to prevent it Practice points • Metronidazole 400 mg twice daily for 5–7 days remains the firstline treatment for bacterial vaginosis • The frequency of recurrence can be reduced by regular application of 0. including Atopobium vaginae • The description of a vaginal biofilm containing predominantly Gardnerella vaginalis places the organism as central in pathogenesis again • The biofilm also offers the opportunity to study potential new treatments for bacterial vaginosis • Probiotics and lactic acid gels need further study as alternative treatments to antibiotics Because the aetiology of bacterial vaginosis is not fully understood. No randomized trials have been performed to investigate the value of screening and treatment before such surgery.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed What’s new? • Molecular techniques have identified several new organisms in bacterial vaginosis. Bacterial vaginosis also confers an increased risk and may be present in almost 30% of such women.

25. Cochrane Database Syst Rev 2007. Burtin P.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis.342:1500–1507. it is not known how to prevent it. Am J Obstet Gynecol 1995. Intrauterine infection and preterm delivery. et al. Sexually transmitted diseases treatment guidelines.29:297–301.3 reported bacterial vaginosis to be associated with HIV acquisition during pregnancy and the postnatal period. Workowski KA. Schwebke J. Hauth JC. 2. Ison CA. et al.38(6): 281–285. Fredricks DN. et al. Gray RH. which included a course of metronidazole. High prevalence of bacterial vaginosis in adolescent girls in a tropical area of Ecuador. 15. Bump RC. Vaca M. A randomized. et al. Bacterial vaginosis and disturbances of vaginal flora: association with increased acquisition of HIV. Boyer CB. Thejls H. Ariburnu O. MendlingW. Bacterial vaginosis has also been associated with an increased incidence of non-gonococcal urethritis in male partners. Platz-Christensen JJ. Klebanoff MA. Antibiotics for treating bacterial vaginosis in pregnancy. Taha TE. Verhelst R. 11. Easmon CS. Bacterial vaginosis in sexually experienced and non-sexually experienced young women entering the military. 13. AIDS 1998. intermittent ‘mass treatment’. 12. Suppressive antibacterial therapy with 0. Dalaker K.78:413–415. Dukes CD. UK. Clin Infect Dis 2008. Indications for therapy and treatment recommendations for bacterial vaginosis in nonpregnant and pregnant women: a synthesis of data. 27. Additionally. Sobel JD. randomized study. Hogan V.12:1699–1706. 8. Cloning of 16S rRNA genes amplified from normal and disturbed vaginal microflora suggests a strong association between Atopobium vaginae. National guideline for the management of bacterial vaginosis. Clin Infect Dis 2002.org/documents/62/62. Yen S. Hocking JS. JPOG MAR/APR 2012 • 67 . Am J Obstet Gynecol 1988. 16. 6. et al. Nugent RP. 9. Curr Opin Infect Dis 2009. Metronidazole to prevent preterm delivery in pregnant women with asymptomatic bacterial vaginosis. 18. relapse is relatively common. Larsson PG. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. Gardnerella vaginalis and bacterial vaginosis. et al. Hoover DR. Brocklehurst P. Safety of metronidazole in pregnancy: a meta-analysis.102:927–933. Health gains from screening for infection of the lower genital tract in women attending for termination of pregnancy. Am J Obstet Gynecol 2006. Platz-Christensen JJ.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed and South East Asia in the last two decades.68:134–138. Am J Obstet Gynecol 1992. BMC Microbiol 2004. except in pregnant women. Berman SM.55:1–94. 4.79:390–396. Fethers KA. Fiedler TL. Ison CA. Hay PE. N Engl J Med 2005. Einarson TR. Morton A. Bacterial vaginosis emerged as a cofactor for HIV acquisition in the Rakai study in rural Uganda. Obstet Gynecol 2005.117:225–228. References 1. About the Author Phillip Hay is Reader in Genitourinary Medicine at St George’s University of London. multicenter study. Koren G. N Engl J Med 2000. Treatment with 2% clindamycin vaginal cream prior to first trimester surgical abortion to reduce signs of postoperative infection: a prospective.200:1662–1670.342:206–210. Pahlson C. Marrazzo JM.353:1899–1911. Fethers KA. Gurrin LC. J Clin Microbiol 1991. Gardner HL. Acta Obstet Gynecol Scand 2000. Lancet 1993. 10. Hay P. Haemophilus vaginalis vaginitis. Genitourin Med 1992. et al. 5. 14. Bradshaw CS. Buesching WJ. 17. Barrons R. therefore.69:962–976. hydrogen peroxide produced by lactobacilli can inhibit HIV in vitro and is absent in most women with bacterial vaginosis. Wawer MJ. Tassone D. Initial reports identified genital ulcer STIs as co-factors for transmission. AIDS 1998 September 10. Early sexual experiences and risk factors for bacterial vaginosis. Carey JC. Loening-Baucke V. http://www. did not reduce the prevalence of bacterial vaginosis. Fairley CK. Incidence of pelvic inflammatory disease after first-trimester legal abortion in women with bacterial vaginosis after treatment with metronidazole: a doubleblind. Wareham K. Adherent biofilms in bacterial vaginosis. Sexual risk factors and bacterial vaginosis: a systematic review and meta-analysis. 20. Sewankambo NK. Thomas PD. Am J Obstet Gynecol 1955. McDonald HM. Forsum U. Verstraelen H.166:100–103. Hillier SL.30:453–468. In the Rakai study.106:1013–1023. Emery SJ. Flinn SD. Molecular identification of bacteria associated with bacterial vaginosis.(1):CD000262. 2006. Shafer MA.35(suppl 2):S152–S172. 7. British Association for Sexual Health and HIV. Clinical Effectiveness Group.12:1211– 1225. N Engl J Med 2000 May 18. A study of pregnant women in Malawi 3 PREVENTION Because the aetiology of bacterial vaginosis is not fully understood. Sex Transm Infect 2002. Potential mechanisms by which bacterial 27 vaginosis might increase HIV transmission include effects on local immune mediators. Initially published in Medicine 2010. Erazo S. Andrews WW. 24. Dallabetta GA. If bacterial vaginosis is established as an important risk factor for HIV spread. double-blinded. Markowitz LE. Krohn MA. 22. Recurrent bacterial vaginosis. community trial of intensive sexually transmitted disease control for AIDS prevention. Use of Lactobacillus probiotics for bacterial genitourinary infections in women: a review. Hauth JC. Gordon A. Clin Ther 2008. Bacterial vaginosis in virginal and sexually active adolescent females: evidence against exclusive sexual transmission. © 2010 Elsevier Ltd.47:1426–1435. Guadalupe I.194:1283–1289. Bacterial vaginosis: a diagnostic approach. Obstet Gynecol 2003. J Infect Dis 2009. Swidsinski A. Claeys G. 21. 3. pdf.bashh. Moncada J. Hay PE.4:16.172:525–529. Koumans EH. Fairley CK. Validation of a simplified grading of Gram stained vaginal smears for use in genitourinary medicine clinics. Campbell CJ.342:534–540. et al. MMWR Recomm Rep 2006. Ferris D. Antibiotics inhibit growth of the anaerobes but do not necessarily eliminate the factors that led to the development of bacterial vaginosis. Larsson PG. 2006. Blackwell AL. et al. BJOG 2010. Uganda. A newly defined specific infection previously classified ‘‘nonspecific’’ vaginitis. its control will become an important public health issue in many countries. 23.158:935– 939. placebo-controlled. 26. Rakai. Goldenberg RL. Taddio A. 19.22:82–86.

AD is frequently the first disorder of the atopic triad. supporting the role of environmental factors in the expression of AD. It is possible that epicutaneous sensitization to allergens predisposes to development of asthma and allergic rhinitis. asthma and allergic rhinitis are known as the ‘atopic triad’. FRCP. whereas it continues to increase in younger children. MD.PA EDIATRICS I Peer Reviewed Atopic Dermatitis in Children: A Practical Approach Triveni Shekariah. by 5 years of age. inflammatory. The concept of ‘atopic march’ evolved from clustering of these conditions in the same individuals and families. by 1 year of age in 60%. Prevalence in children in UK is up to 20%. DDVL. Mazin Alfaham. MRCP. MBBS. 50% of children with early AD and a strong family history of allergy had allergic airway disease or asthma compared with 12% in patients without AD or a family history of atopy. AD. This is paralleled by increases in the prevalence of asthma. FRCPCH. Migrant studies reveal that AD prevalence increases in populations that move from an area of low to high prevalence. Up to 70% of children have a spontaneous remission before adolescence. JPOG MAR/APR 2012 • 68 . In a large multicentre study. and by 5 years of age in 85% of affected infants and children. Manjunatha Kalavala. However. eosinophilic oesophagitis. MD EPIDEMIOLOGY Atopic dermatitis (AD) is a chronic pruritic. allergic rhinoconjunctivitis. The prevalence of AD in children has increased steadily over the last three decades of the 20th century. AD is one of the most common skin disorders in children. MBChB. recent data suggests that AD and hay fever prevalence might have levelled off or decreased over the last 10 years in those aged 12 years or older. skin disease that typically begins in early childhood. and gastroenteritis. Disease onset typically occurs by 6 months of age in 45%.

Complex interaction of defects in skin barrier function. pain. irritability. This results in increased trans-epidermal water loss and dry skin. restricted activities. May overlap with seborrhoeic dermatitis. AETIOLOGY The pathophysiology of AD is not completely understood. . Parental atopy. Figure 1. and decreased participation in sport and other social activities. a key protein in barrier function. might play an important part in early-onset AD and asthma. environmental factors and infectious agents in a genetically susceptible individual are thought to result in AD. Dry scaly lesions on the scalp. Filaggrin mutations are identified in 30% of European patients with AD. exhaustion. and adverse social interactions. quality of life is impaired owing to pruritus. Mutations in the genes coding for filaggrin. Severe AD may result in poor school performance. The concordance rate for AD is higher among monozygotic twins (77%) than among dizygotic twins (15%). and worry owing to their child’s disease. host immune response. is significantly associated with the manifestation and severity of early AD in children. behavioural problems. sleep disturbance. low self-esteem. In children with AD.PAEDIATRICS I PAEDIATRICS Peer Reviewed IMPACT ON THE CHILD AND FAMILY AD has the potential to be a major handicap with considerable personal. Erythematous papules and plaques with background oedema typical of infantile atopic dermatitis. social and financial consequences. Parents of children with moderate to severe AD experience sleep disturbance. frustration. Defective epidermal barrier function is a hallmark of AD. Reduced ceramide levels. It will also allow increased trans-epidermal penetration of environmental allergens and triggers inflammation. in particular AD. The family stress related to the care of children with moderate or severe AD is significantly greater than that of the care of children with type 1 diabetes mellitus. and genetic variaJPOG MAR/APR 2012 • 69 Figure 2.

Early-onset AD usually emerges in the absence of detectable IgE-mediated allergic sensitization. Inflammation in AD is biphasic. Antigen-specific IgE is the major recognition structure for allergens on basophils and JPOG MAR/APR 2012 • 70 mast cells. and food. S aureus enterotoxins increase the inflammation in AD and provoke the generation of enterotoxin-specific IgE. an initial Th2 phase precedes a chronic phase in which Th0 cells and Th1 cells are predominant. which correlates with the severity of disease. house dust mite products. Discrete lichenified papules on the dorsum of hands. Exogenous proteases from Staphylococcus aureus and house dust mites. IgE-mediated sensitization occurs several weeks or months later.PA EDIATRICS I Peer Reviewed Figure 3. Figure 4. tion in stratum corneum tryptic enzyme and epidermal collagen may also play a role. Scratching increases the binding of S aureus to skin. Defective barrier function allows penetration of high-molecular-weight allergens in pollens. Atopic dermatitis on extensor surface of extremities. Lichenified plaques on cubital fossae. Enterotoxins also contrib- . and the use of soaps and detergents further damage the barrier function. Keratinocytes in atopic skin produce cytokines that signal dendritic cells to drive helper Tcell (Th)2 polarization. S aureus colonization with or without clinical signs of infection occurs in more than 90% of patients with AD and contributes to the severity of inflammation. Figure 5. microbes.

The lesions show significant oedema.PAEDIATRICS I PAEDIATRICS Peer Reviewed Figure 6. The lesions may remain localized to the face or extend to the trunk and extensor aspects of the JPOG MAR/APR 2012 • 71 . Clinical Features During the first few months of life. The cytokines generated during inflammation in AD downregulate the natural production of antimicrobial peptides in the epidermis – cathelicidin and defensin. AD typically affects face and scalp. leading to oozing and crusting unrelated to secondary infection. This argues against a prominent role for histamine in causing AD-related pruritus. Pruritus and dry scaling of scalp are common (Figure 2). Flare-up of lesions around mouth is common with teething and initiation of solid foods. It is important to keep in mind contact urticaria to food when the lesions are predominantly around mouth. Nummular lesions on the trunk. This results in increased susceptibility to colonization with Staphylococcus and the yeast Malassezia furfur . Antihistamines are not always effective in relieving the pruritus. AD is more prevalent in urban. Periorbital and perioral areas are relatively spared. The scalp lesions may represent overlap with seborrhoeic dermatitis. the latter plays an important role in head and neck eczema. which has potent antiviral activity. Neuropeptides. are not known. nuclear families compared with rural areas. proteases. The underlying mechanisms for pruritus. Intensely pruritic erythematous papules affect cheeks and forehead (Figure 1). This is probably due to irritation caused by saliva and foods. Figure 7. Patients with AD are predisposed to eczema herpeticum and eczema vaccinatum because of a reduced production of cathelicidin. improvement in personal amenities and higher standards of the personal cleanliness have reduced the opportunity for infections in young children and increased susceptibility to AD. kinins and cytokines may play an important role in inducing pruritus. the most important symptom of AD. The ‘hygiene hypothesis’ postulates that declining family size. Atopic dermatitis with secondary infection. ute to emergence of resistance to topical corticosteroid (TCS) treatment.

Lymphadenopathy in the severely affected area may be prominent owing to inflammation and secondary bacterial infection. This is because of the combination of increased hydration in the diaper area. Involvement of the antecubital and popliteal fossae. ill-defined erythematous patches. and neck is more common in older children and adolescents (Figure 4). However. feet. and inaccessibility to scratching and rubbing. Older children are less likely to have the exudative lesions of infancy and. leading to sleep disturbances. and anterior thighs Round collections of numerous. typical dry scaling erythematous patches of AD. protection from triggers by the diaper. The lesions on the trunk and extremiJPOG MAR/APR 2012 • 72 es are transient and are reversible when the underlying inflammation is controlled. In children 1 year of age or older. In Africaribbean children. upper arms Accentuated markings on the palms and soles Groove of the lower eyelid. perhaps because of the friction associated with crawling (Figure 3). tiny. hands. sometimes with fine scale. sharply defined erythematous scaly plaques (nummular lesion – Figure 6) might accompany the more Keratosis pilaris Lichen spinulosus Pityriasis alba Hyperlinear palms Atopic pleat (Dennie– Morgan fold) Allergic shiners White dermographism Follicular-based keratotic papules. exhibit more lichenified papules and plaques representing more chronic disease (Figure 5). Post-inflammatory hypopigmentation or hyperpigmentation is common. Nummular lesions tend to be more recalcitrant to topical therapy and are frequently secondarily infected. Scarring is not a prominent feature but might result from secondary infection and deeply excoriated areas. ankles. skin-coloured to hypopigmented dry spiny papules ≥ 1 cm hypopigmented patches. coin-shaped. Eczema herpeticum. some children show an ‘inverse’ pattern with primarily involvement of extensor areas. the lesions of AD are often more papular (follicular AD). Clinical features seen with increased frequency in children with atopic dermatitis ties are often symmetric. Alhough flexural areas are commonly involved. often present from infancy Slate-grey to violaceous infraorbital discolouration with or without swelling Paradoxical blanching of skin on stroking firmly with a blunt pointed object Figure 8. the extensor surface of the arms and legs are involved. extensor aspects of arms.PA EDIATRICS I Peer Reviewed Table 1. Hyperpigmentation is particularly common in lichenified areas. Pruritus is frequently severe. . AD typically spares diaper area. instead. It is important not to confuse them with tinea corporis. wrist periorbital area. lateral aspects of face. Generalized dry skin (xerosis) is common. The pigmentary chang- extremities. scattered. especially in darker skinned children. By 8–10 months of age. especially on face. these sites might also be affected in infants and young children. perioral area.

Table 2 lists the UK Working Party’s diagnostic criteria. History of involvement of the skin creases such as folds of elbows. A history of a general dry skin in the last year. Molluscum contagiosum lesions are often associated with pruritus and eczema around them. Children with AD are also prone to disseminated viral infections. Positive bacterial cultures in the right clinical context are helpful in diagnosing S aureus infecJPOG MAR/APR 2012 • 73 . and puspresent with similar clinical features and require prompt treatment with systemic antibiotics. CyA = cyclosporin A. CyA) or UV therapy ity of di se Moderate to severe AD as Step 3 Mid–high potency TCS and/or TCI* e In Mild to moderate AD te Step 2 Low–mid potency TCS and/or TCI* ns Dry skin only Step 1 Basic treatment Skin hydration. UV = ultraviolet. Absence of xerosis in the background skin is a clue to scabies. or around the neck (including cheeks in children under 10). crusting. due to accidental infection with vaccinia virus when children come in contact with adults receiving small pox vaccination. Molluscum contagiosum. During infective episodes. fronts of ankles. 2. and also cause flare-up of AD. Several clinical signs (Table 1) are seen with increased frequency in children with AD. secondary to herpes simplex virus infection (Figure 8). severe AD Step 4 Systemic therapy (eg. avoidance of irritants. tends to be more disseminated and difficult to treat. Management strategy for atopic dermatitis (AD) (adopted from Akdis et al). TCI = topical calcineurin inhibitors. emollients. based on morphology and distribution of lesions. 3. Visible flexural eczema (or eczema involving the cheeks/forehead and outer limbs in children under 4). UK Working Party’s diagnostic criteria for atopic dermatitis Must have An itchy skin condition (or parental report of scratching or rubbing in a child) Plus three or more of the following 1. 5. Clustering and umbilication of vesicles are characteristic. Eczema vaccinatum is disseminated vaccinia viral lesions. Recalcitrant. A personal history of asthma or hay fever (or history of atopic disease in a first-degree relative in children under 4). identification and addressing of specific trigger factors TCS = topical corticosteroids. Diagnosis Diagnosis is often clinical. a common cutaneous viral infection in children. Repeated S aureus infections are common (Figure 7).PAEDIATRICS I PAEDIATRICS Peer Reviewed Table 2. Onset under the age of 2 (not used if child is under 4). Eczema herpeticum (Kaposi’s varicelliform eruption) is an explosive development of vesiculopustular eruption in the patches of AD. Beta-haemolytic streptococcal infections can Figure 9. tules. 4. exudation. pruritus and chronicity of the disease. behind the knees. S aureus infections are characterized by intense erythema. patients might experience flareup of AD or fail to respond to appropriate therapy. Various diagnostic criteria have been proposed. It is important to keep scabies in mind in a child presenting with generalized pruritic rash. although they do occur in non-atopic children.

generally speaking. When diagnosis is in doubt. Age-appropriate educational sessions for parents are shown to improve objective severity of eczema and quality of life scores. Educating the family about the nature of the disease and setting the realistic expectations about the treatment outcomes are crucial. A positive IgE or skin prick test does not necessarily indicate an underlying ongoing allergy and might be representing past sensitization. This will help ensure compliance with the treatment. Biopsy is rarely performed for diagnosis of AD. smears taken by scraping the floor of the vesicle show multinucleate viral giant cells. Psychological support from the health-care professionals. particularly if associated with gut dysmotility or failure to thrive. Recognition of psychological factors and involvement of child psychologist will go a long way in reducing the stress involved in coping with a chronic condition like AD. egg or soya. Potential triggers for atopic dermatitis is important. Direct fluorescent assay helps in rapid diagnosis of eczema herpeticum while viral cultures are confirmatory. Early recognition and treatment of infections help prevent flare-ups. although some cases are not IgE-mediated. Specific serum IgE for food and skin prick tests in the context of a thorough allergy history might be helpful. school and support groups JPOG MAR/APR 2012 • 74 Avoidance of Triggers Potential triggers for AD vary among patients. Common triggers are listed in Table 3. • • • • • • • Harsh detergents/soaps. Food allergy may be associated with AD in up to 30% of patients. Food allergy should be considered in children who have reacted previously to a food with immediate symptoms or in infants and young children with moderate to severe atopic eczema that has not been controlled by optimum management. Step-wise treatment strategy is depicted in Figure 9. A team approach with doctor and nurse experienced in the management of AD works well. It is important to emphasize that avoidance of triggers may result in improvement in AD but not complete cure. MANAGEMENT Developing good rapport with the child and the family is the cornerstone of successful management of AD. or fragrances Abrasive clothing (wool or synthetics) Inhalant allergens – dust mite. animal dander. Chronicity of AD. When these tests are not available. Atopy patch testing might be useful in some cases with suspected allergy to cow’s milk. Substitution of soaps and detergents with bath emollients and emollient-based soap substitutes prevent further dryness and damage to the epidermal barrier. family. histology of skin biopsy shows spongiotic dermatitis. A therapeutic/diagnostic trial of food exclusion might be justified and is easier to try in infants owing to the limited dietary variety required at that age and. Careful history and food diaries are essential. astringents. Any management decisions have to be made in agreement with the family. pollen Infections Overheating/sweating Psychological stress Food allergens tion. punctuated with flare-ups and secondary infections are frustrating for the child and the parents. toiletries containing alcohol. particularly when associated with allergic rhinitis. Dietary restrictions should only be recommended in cases of an established diagnosis of food hypersensitivity. accept- . Oral antihistamines are beneficial when aeroallergens are suspected to be triggering AD.PA EDIATRICS I Peer Reviewed Table 3.

Further studies are needed to establish the role of these products in the management of AD. Ointments tend to be greasy. Re- Bathing Bathing in lukewarm water with a bath emollient is helpful in skin hydration and removal of exudates and crusts. chlorine in swimming pool water is beneficial in reducing S aureus colonization. The current British system of classification stratifies TCSs into four groups based on the vasoconstrictor assay: mild. potent and very potent. gently pat the skin dry with a towel. TCSs have anti-inflammatory. Emollients Regular application of emollients remains the mainstay of general management of AD. anti-proliferative. The choice of the emollient depends on the individual skin status. The difference in potency between groups is often dramatic. There is no evidence to support delayed introduction of solid foods beyond the sixth month of life having an impact on AD and atopic sensitization at 2 years of age. It is important to stress that emollients need to be applied continuously even when the skin is not inflamed. prolonged bathing in very hot water with strong detergent or bubble baths cause further dryness of the skin. in addition to intermittent intranasal mupirocin ointment. Swimming for 20 minutes three times a week is helpful. However. An involvement of a paediatric dietician is crucial. fish. If this is not practical. and seasonal and climatic conditions. However. Clobetasol propionate 0. The role of breastfeeding in the prevention of AD is debatable. This applies for foods thought to be highly allergenic such as cow’s milk. Parents should be cautioned against uncontrolled restriction diets. time of the day. cently. Exclusive breastfeeding for the first 4 months decreases the cumulative incidence of AD in the first 2 years of age in high-risk infants. while creams and lotions are cosmetically more appealing for application during daytime. Application of emollient immediately after the bath (‘soak and seal’) prevents drying up of skin.05% ointment (very potent) is JPOG MAR/APR 2012 • 75 . an emollient needs to be applied immediately after coming out of the pool to prevent dryness of skin. Children with eczema who are suspected of having food allergy as a trigger might benefit from being reviewed in a paediatric clinic with a special interest in allergy. immunosuppressive. In patients with repeated S aureus infections. are also shown to reduce the severity of eczema by reducing S aureus infection and colonization. Topical Corticosteroids Topical corticosteroids remain the first-line treatment for control of flare-ups. Data on the role of probiotics in the prevention of AD in high-risk infants are conflicting. There is lack of evidence for the role of maternal diet during pregnancy or lactation. Further studies are needed to clarify this issue. Long-term bleach baths. and vasoconstrictive actions. eggs and peanuts.PAEDIATRICS I PAEDIATRICS Peer Reviewed ance of alternative milk products. After bath. rather than rubbing. patients are asked to try samples of emollients and prescription is issued for the emollient of patient’s choice. Exclusive breastfeeding beyond 4 months does not confer specific additional benefit. In our clinic. particularly in adolescents. Emollients reduce dryness of skin. a ‘swimming pool’ can be created at home by adding a small amount of household bleach to bath water. moderate. several emollients with ingredients claimed to have anti-inflammatory properties have been introduced as steroid-sparing agents. Bleach baths reduce the number of infections and the need for antibiotics. A combination of cream/lotion during the day and ointment during night is useful. reduce trans-epidermal water loss and also help in reducing pruritus and inflammation.

they are useful treatment options for sensitive skin areas such as face and intertriginous area. Intermittent twice weekly application of fluticasone propionate 0. rosacea. Local side effects include atrophy. TCIs are not associated with increased incidence of bacterial infections. and reduced bone mineral density. telangiectasia.03% ointment twice daily for 2–6 weeks. Systemic absorption might result in suppression of hypothalamic-pituitary-adrenal axis. TCIs are not associated with atrophy as they do not inhibit collagen synthesis. these complications are rare when TCSs are used judiciously. A frequently observed side effect is transient burning sensation at the application site. Topical Calcineurin Inhibitors Tacrolimus 0. the frequency of topical tacrolimus is reduced to two or three times a week for a period of up to 12 months. Ointments are preferred for treatment of dry lichenified patches as they are associated with better penetration and efficacy. Initial control of flareup with TCS is followed by 2–3 times a week application of TCI for a period of up to 1 year to maintain remission. Relatively new TCS preparations like mometasone furoate and fluticasone propionate have lower atrophogenic potential. this sensation will subside. which may include areas of broken skin. striae. but they should not be used in the presence of infection. However. They provide an effective. A potent TCS can be used intermittently for short periods of time to control the flare-ups. Therefore.03% ointment and pimecrolimus 1% cream are approved for second-line treatment of moderate to severe AD in children above 2 years of age for short-term continuous use (up to 6 weeks) and long-term non-continuous use (up to 12 months). Sequential use of TCIs with TCSs reduces the number of flare-ups. TCIs have high molecular weight (more than 800 kDa). perioral dermatitis. acne. Concerns about lymphomas and systemic .PA EDIATRICS I Peer Reviewed ~1. S aureus enterotoxin contributes to the emergence of resistance to TCSs. Clearance of patches of eczema by application of appropriate-strength TCSs for few days is followed by application of tacrolimus 0. Prolonged use of potent TCSs is associated with local and systemic side effects. cataracts. One study showed slightly increased risk of herpes simplex virus infection. and glaucoma. Only mild to moderately potent preparations should be used on genital. However. Addressing these conJPOG MAR/APR 2012 • 76 cerns is important to ensure compliance and avoid suboptimal treatment. with continued use. hypopigmentation. an initial therapy with a potent TCS.800 times more potent than hydrocortisone 1% ointment (mild). if skin lesions remain well controlled. Molecules above 500 kDa have limited potential for systemic absorption. After this period. Prolonged use of TCSs might result in loss of efficacy by ‘tachyphylaxis’. Children with atopic eczema and their caregivers should be informed that TCSs and TCIs should be applied only to areas of active atopic eczema. The choice of an adequate vehicle is important to achieve optimal therapeutic effect. TCSs are also used sequentially with topical calcineurin inhibitors (TCIs).05% cream up to 24 weeks is shown to reduce the number of flare-ups. Cushing’s syndrome. Repeated studies involving much higher concentrations of TCIs failed to show systemic absorption. Concerns about adverse effects have resulted in ‘steroid phobia’ in parents. growth retardation. followed by changeover to low-potency preparation for longer period is also effective. steroid-free therapeutic alternative in the management of AD. TCIs block the production and release of proinflammatory cytokines after antigen-specific or non-specific activation of T cells and mast cells. TCS preparations should be applied no more than twice daily. Alternatively. facial and intertriginous areas.

and serve as an effective barrier to scratching. Wet wraps increase skin hydration. Topical emollients with antiseptics may help Wet Wraps Wet wraps are useful in treating the refractory areas. defined as the amount of topical medication extending from the tip to the distal interphalangeal crease on the palmar aspect of the index finger. Topical antibiotics should be used with caution to prevent emergence of resistant strains and contact sensitization. Non-sedating antihistamines are less useful for relieving pruritus. One FTU is 0. Application of topical agents is time-consuming. Wet wraps with once-daily application of TCSs is an effective short-term intervention. and infections are frequent. risks and benefits have to be discussed in detail and parents be given sufficient time to make decisions. and some of the topical preparations can sting particularly during acute flare-ups. Adjunctive Therapy Sedating antihistamines such as hydroxyzine and chlorpheniramine maleate are useful in improving sleep during flare-ups. azathioprine. reduce colonization of S aureus. The fingertip unit (FTU). Antimicrobial Agents The skin of children with AD is heavily colonized with S aureus . although they probably do not have direct effects on the pruritus associated with AD. Prompt recognition and treatment with topical and oral antibiotics will help clear the infection and control the flare-up of AD.PAEDIATRICS I PAEDIATRICS Peer Reviewed malignancy have not been substantiated by large population-based studies. Long-term follow-up studies and careful photo-protection measures are advisable. Printed information leaflets available on the British Association of Dermatology website (www.bad. Such treatments are initiated after involving a dermatologist. Viral and fungal infections need to be recognized early and treated promptly to prevent dissemination. However.org. and mycophenolate are reserved for severe AD not responding to optimum topical therapy. Bleach baths in addition to topical nasal mupirocin will help reduce the number of infections and need for antibiotics. particularly on the limbs. effects of longterm use of TCIs on immune surveillance in the skin are not known. Incorrect use of wet wraps may cause maceration of the skin and secondary infections. As these modalities involve frequent visits to the hospital and blood tests for monitoring side effects.uk) are useful. is a useful guide to estimate the amount of topical medication needed to cover a given area. promote penetration of topical medications. Wet wraps should not be used in the presence of infection. However.5 g of ointment or cream. or promote skin dryness. Both the child and parents need constant encouragement and advice on quantity of medication to be used. Fusidic acid resistance remains high in spite of local community guidelines to restrict the use of this topical antibiotic. melatonin has been beneficial in some cases. they may benefit patients with allergic triggers. CONCLUSIONS AD is a common. Systemic Therapies Second-line therapies in the form of phototherapy or systemic immunomodulatory medications such as prednisolone. cyclosporine. A wide variety of wet-wrap techniques have been used. chronic skin disease that starts JPOG MAR/APR 2012 • 77 . One FTU is sufficient to cover an area of two adult hand areas. Patient education and close supervision by experienced medical staff are essential. Anecdotally.

timing of introduction of complementary foods. and other health-care proJPOG MAR/APR 2012 • 78 About the Authors Triveni Shekariah is Core Medical Trainee Doctor at The Welsh Institute of Dermatology. Asthma and Immunology/PRACTALL Consensus Report.131:406– 416. Mills CM. behavioural therapists. • Moisturizing the skin with regular daily topical emollients would help to reduce itching and minimize the frequency of relapses. UK. III. • Intermittent topical corticosteroids (TCSs) are the main antiinflammatory agents in the management of atopic dermatitis (AD).138:293–296. • Under-treatment. the overall management depends on (1) educating caregivers about AD’s chronic. particularly those who are prone to frequent flares and need AD treatment in sensitive skin areas. Is eczema really on the increase worldwide? J Allergy Clin Immunol 2008. Cardiff. Allergy 2006. (3) approaching trigger avoidance carefully and with the understanding that.61:969–987. December 2007. Finlay AY. UK.K. in general. Br J Dermatol 1998. Kemp AS. . Worldwide variation in prevalence of symptoms of asthma. Further Reading Akdis CA.nice. Clinical guidelines CG57. AD is a multifactorial disease. Long CC.21:105–113. TCIs have been shown to provide an effective. • The use of topical calcineurin inhibitors (TCIs) would decrease the need for TCSs. Cardiff. breastfeeding. unpredictable course characterized by flares that can occur despite best efforts. A practical guide to topical therapy in children. and hydrolyzed formulas. (2) appreciating the compromised epidermal barrier and the importance of proper skin care. Heath Park. Regular use of emollients and intermittent use of TCSs remain the cornerstone of therapy.351:1225–1232. usually through fear of side effects. PRACTALL Consensus Group. Concern about skin cancer from TCIs seems unfounded. is harmful and leaves the child in distress continuously. • Children with difficult AD and certainly those that might require systemic therapy should be reviewed by a dermatologist with expertise in children’s eczema. Pediatrics 2008. Bieber T. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction. and (4) using a team-oriented approach that includes primary care physicians. steroid-sparing alternative for appropriate patients. N Engl J Med 2008. • Food allergy should be sought for especially in the first 2 years of life and mainly in those with a severe degree of AD and/or those with concomitant history of immediate reactions. psychologists. Mazin Alfaham is Consultant Paediatrician at the Children’s Hospital. © 2011 Elsevier Ltd. In conjunction with these pharmacological treatments. Asthma and Immunology/PRACTALL Consensus Report. Initially published in Paediatrics and Child Health 2011. and atopic eczema: ISAAC. University Hospital of Wales. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/ American Academy of Allergy.org. Allergy 2006. Working Party’s diagnostic criteria for atopic dermatitis. • Management should include a holistic approach.38:441–446. Manjunatha Kalavala is Consultant in Dermatology and Paediatric Dermatology at The Welsh Institute of Dermatology. Br J Dermatol 1994. allergic rhinoconjunctivitis. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/ American Academy of Allergy. Independent hospital validation. et al. University Hospital of Wales. Cardiff. Pharmacoeconomics 2003. Cost of illness of atopic dermatitis in children: a societal perspective. Atopic dermatitis. early in life and can adversely affect a child’s overall health and development. University Hospital of Wales. American Academy of Pediatrics Committee on Nutrition and Section on Allergy and Immunology. specialists. ISAAC Phase One and Three Study Groups. Bieber T.PA EDIATRICS I Peer Reviewed Learning points fessionals to better achieve long-term success for patients with AD. Heath Park. Heath Park. Glamorgan House. but a careful approach with dose and duration is always prudent.61:969–987. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Glamorgan House.358:1483–1494.121:947– 954. Available at: http://guidance. Nat Genet 2006. nurses. Akdis M.21(3):112–118.uk/CG57.121:183–191. UK. Management of atopic eczema in children from birth up to the age of 12 years. The U. Lancet 1998.

8. It is also a timely opportunity to introduce information about the causes and prevention of tooth decay in general and early childhood caries (or baby bottle caries/decay) with the parent and child in a non-blaming manner. Treatment recommended by a dental practitioner would be subject to a detailed history and examination.IN P ractice I IN PRACTICE Peer Reviewed Clinical Case Rotting Teeth in a Young Girl Simon Wooley. were hospitalized for dental extractions and restorations. MPH Answer: COMMENTARY This case is a stark reminder that few preschool children access dental care. BDS. This information would be reinforced by the dental clinician. Kaye Roberts-Thomson. and to improve the early identification and referral (to public or private practitioners) of children experiencing tooth decay (see www. To this end.sadental. most of which were preventable. including assessment of the expected exfoliation of the deciduous teeth in question. Early childhood caries generally affects the upper front deciduous teeth but can affect all teeth. All GPs and other health providers who are visited for health and immunization checks can play a key role in the prevention and management of dental caries (tooth decay) in this age group.000 Australian children. the ‘lift the lip’ strategy was introduced by the South Australian Dental Service and has been adopted in other states and territories as a response to the decline in oral health of children. The need for a general anaesthetic is a real possibility. MPHC. this being especially difficult in rural and remote areas. 28. It is typically associated with prolonged exposure (such as comfort sucking while sleeping) to JPOG MAR/APR 2012 • 79 Figure 1 .sa.au for details. In 2008/2009. In the case scenario presented here.gov. the first priority is to highlight to Tracey’s mother the need for prompt dental referral and assessment.000 of whom were younger than 5 years of age. and the ability of the child to cope with treatment in the dental chair. the severity and extent of the decay in general. including a photographic guide/tool to assist caries identification). BDSc.

Reprinted with permission. Adelaide. Australian hospital statistics 2008–09. Health services series no. this should begin at 18 months of age • inadequate oral hygiene and plaque removal. Australian Institute of Health and Welfare. an abscessed deciduous tooth has the potential to affect the development of the permanent successor.IN Practice PRACTICE In I Peer Reviewed a sweet drink (eg. Risk or demineralization factors include: • a high frequency or prolonged consumption of fermentable carbohydrates and sugary foods or drinks • comfort sucking with a sweet drink (even plain milk). Dental statistics and research series no. Canberra: Australian Institute of Health and Welfare. soft drink. Although uncommon. no. there is an increased risk of space loss and crowding in the secondary dentition. © 2011 Medicine Today Pty Ltd. Initially published in Medicine Today July 2011. parents should assist children with brushing up to about the age of 8 years. Professor Roberts-Thomson is the Director of the Australian Research Centre for Population Oral Health. adult toothpaste should be used from 6 years of age • children should be told to spit but not rinse after brushing to maximize the fluoride benefit from toothpaste • professionally applied fluoride agents such as fluoride varnish should be used in children at high risk of tooth decay • fissure sealing of selected teeth is recommended. This risk is greater for early loss of posterior deciduous teeth as compared with anteriors. 80% is experienced by 20% of young children (those under the age of 6 years). HSE 84. Further Reading Armfield JM. Aust Dent J 2005. 2009. Aust Dent J 2006. no. which is potentially reversible when confined to enamel.12(7):63–64. Cat. Good oral health is important to general health. Dental health of Australia’s teenagers and pre-teen children: the Child Dental Health Survey.au (accessed June 2011). Deciduous and permanent teeth can have development defects of enamel and dentine (hypoplasia). infant-feeding cups rather than infant-feeding bottles are preferred for drinks other than formula or breast milk JPOG MAR/APR 2012 • 80 • twice daily plaque removal with a soft brush and junior fluoride toothpaste (from 18 months to 6 years).51:130–139. which might otherwise have been avoidable. subject to the severity and timing of the infection to coincide with the development of the successor crown. 2010. Should a deciduous tooth require premature extraction. Bill CJ. particularly sleeping with a bottle • delaying commencement of tooth brushing with a junior fluoride toothpaste. Risk factors for dental caries in the five-year-old SA population. the outer layer of the tooth. juice). The notion of ‘soft teeth’ is often a misconception of a parent seeking a cause for the decay outside of their control and therefore their responsibility. however. All health practitioners can play an active role in the prevention of tooth decay and early intervention if they ‘lift the lip’. Protective or remineralization factors include the following: • tap water is the best drink (fluoridated ideally) to satisfy thirst • after 6 months of age. South Australian Dental Service [website]. Cat. Canberra: Australian Institute of Health and Welfare. Of the total incidence of tooth decay. Australian Research Centre for Population Oral Health. Do LG.sa. Spencer AJ. The model of decay as a ‘balance’ between demineralization (risk factors) and remineralization (protective factors) of teeth is useful. CONCLUSION Good oral health in young children is declining. DEN 199. to tip the ‘balance’ in favour of remineralization. these are relatively uncommon and are often not carious. High caries children in Australia: a ‘tail’ of caries distribution.sadental. Australia. Almost 44% of 5-year-olds in Australia have tooth decay. Decay is a dynamic process of demineralization/ remineralization.50:204–206. Available online at: www. Brennan DS. based on the remote Anangu Pitjantjatjaraku Yankunytjatjaraku Lands of South Australia. Slade GD. This may necessitate space maintenance for the permanent successor and/or future orthodontic assessment and intervention. This is especially so in rural and remote areas where exposure to fluoride and access to clinical dental care may be problematic. 52. Sanders AE.gov. cordial. 17. University of Adelaide. Upper permanent incisors usually have completed their crown development by a year or two before the expected eruption at about 6 years of age. Australia 2003–04. . SA. About the Authors Dr Wooley is a Dental Practitioner with Nganampa Health Council. The aim is to minimize the risk factor exposure and maximize the protective factors – that is.

et al.. Menopause 1998. ASBMR 1998 3) Keil D. 62. 2) Mc Clung M et al..Recommend low dose HRT.the progestogen makes the difference: . Novofem® Start in time with convincing cycle regulation. Low dose human oestrogen NETA ..proven additive e ect on bone protection2 Convincing cycle regulation3 Easy administration with the unique dispenser References: 1) Notelovitz M et al. 991-995 1mg 17 -Estradiol + 1mg Norethisterone Acetate Further information is available on request : DKSH Hong Kong Limited Tel : (852) 2895 9668 Fax : (852) 2895 9548 HRT-D-201002 . Geburtsh Frauenheilk 2002. 5(4): 250-251.proven additive e ect on hot ushes1 .

which screening method to use to identify high-risk women is controversial. MBBS. MBBS. FHKAM(O&G). Teresa WL Ma. 7 a 1-year pilot study on universal prenatal swab-based screening was conducted in a public hospital in Hong Kong to study the cost-effectiveness. 4 However. The aim of this review article is to discuss the current screening methods for GBS in pregnancy. and the focus thus lies in disease prevention. MBChB(HK). MBBS. which is used in the US and some European countries. FHKAM (O&G). Sarah Morag McGhee. 0.17). 0. DRCOG. BA. Because the early-onset disease develops shortly and rapidly after birth. was recommended by the Royal College of Obstetricians and Gynaecologists. FHKAM (Paediatrics). PhD Glas. FHKAM (Paediatrics). Because of the lack of local data. KY Wong. FHKAM(O&G).5 while the universal swab-based strategy. . INTRODUCTION Group B Streptococcus (GBS) is the commonest cause of severe early-onset neonatal infection. there has been little improvement in the disease treatment. which is associated with a high rate of morbidity and mortality (5–10%). FHKCPaed. MRCP. GBS colonization in the maternal gastrointestinal and/or genital tracts is a prerequisite for early-onset GBS (EOGBS) disease. and a pilot study in Hong Kong. the updated CDC guidelines. MBBS. DCG(HKCOG).6 was recommended JPOG MAR/APR 2012 • 81 GBS culture remains the reference standard for the detection of GBS colonization in pregnant women. MRCOG. KKW To. MBBS. MRCP. MD. Recent re- About half of GBS meningitis will be complicated by neurodevelopment impairment. FRCOG. The conventional laboratory test for GBS is culture. Thomas Li. It is well documented that intrapartum antibiotics prophylaxis (IAP) given to high-risk women can reduce the GBS colonization rate of newborns (odds ratio [OR]. FRCOG. FFPH (RCP) UK in the Centers for Disease Control and search has focused on the improvement of microbiological techniques to detect GBS colonization and infection. The clinical risk strategy. CW Law. FRCPath. the improvement in laboratory techniques. MRCP. providing that there has been at least 2 hours of exposure to the prophylactic antibiotics during labour. FHKAM (Pathology). BSc.1) and the incidence of EOGBS disease (OR. which is used in the UK. 1–3 Prevention (CDC) guidelines in 2002 and 2010.Continuing Medical Education Screening for Group B Streptococcus in Pregnancy KY Leung.

12 If the vaginal/rectal swab or urine cultures show the presence of GBS.14 1.7. Besides. and the current obstetric practice. Universal swab-based screening urinary tract infection or asymptomatic bacteriuria with GBS during pregnancy is indicated. 15–17 Furthermore. 2. Under the risk-based strategy. In the US. Routine vaginal/rectal swab for GBS screening in women at 35–37 weeks of gestation. GBS = group B Streptococcus. the prevalence of clinical risk factors in EOGBS disease. the risk of EOGBS disease will be low even if the woman has one of the risk factors. there will still be affected infants who lack the typical intrapartum risk factors for GBS infection.13 If the vaginal/rectal swab shows the presence of GBS. are born to mothers with a negative GBS screen. universal swab-based strategy may not be accepted by some women because giving IAP in screen-positive cases will affect their autonomy and the feasibility of home birth.10 If the GBS status is unknown during term labour in the current pregnancy.12 UNIVERSAL SCREENING OR GBS screening will be required in her cur. antenatal antibiotics treatment cannot prevent EOGBS disease because per oral antibiotic treatment does not eliminate vaginal or rectal colonization. increasing use of IAP can lead to an increase in Gram-negative or drug-resistant early- CLINICAL RISK FACTORS The clinical risk factors for EOGBS disease are well known and are listed in Table 1. treatment of Table 2.9 colonized with GBS at delivery. Give intrapartum antibiotics a) if the vaginal/rectal swab or urine cultures show the presence of GBS. IAP is given to a woman without taking a swab if she has one or more of the risk factors. 8.000) or rarely death (1:100. Side effects of IAP include anaphylaxis (1 in 10. risk factors will be used to determine the . If a woman gives a history of maternal GBS colonization in her previous pregnancy but without neonatal disease.7 If the GBS screening is negative.Table 1. or if the woman has given birth to an infant with invasive GBS disease. or represent missed opportunities for prevention. IAP will be given to the mother. or b) if the woman has given birth to an infant with invasive GBS disease. prenatal rent pregnancy as the recurrence risk is more than one-third. Besides. this risk-based strategy cannot identify a subset of pregnant women who do not have any risk factors but are JPOG MAR/APR 2012 • 82 If the GBS status is unknown. and a risk factor (as in Table 1) is present. universal swab-based strategy has However.18 Health-care providers should remain alert for signs of sepsis in any newborn infant. 10 UNIVERSAL SWAB-BASED STRATEGY Current American and Canadian guidelines recommend routine vaginal/rectal 35–37 weeks of gestation (Table 2). Clinical risk factors for early-onset group B Streptococcus (GBS) disease A previous delivery of a newborn with GBS disease Antenatal GBS bacteriuria Membrane rupture of 18 hours or more Gestation < 37 weeks Intrapartum fever administration of IAP.swab for GBS screening of women at NOT? Whether to implement universal swabbased strategy or not depends on the local incidence of EOGBS disease. IAP will be given. or c) if the GBS status is unknown.000).2 On the other hand. 7. the risk-based approach may inappropriately expose 65–85% of women with risk factors who are GBS-negative to antibiotics. 11 onset neonatal infection. However.

Rapid test for group B Streptococcus 1. Latex agglutination test 3.5 per 1. Nucleic acid amplification tests needed for taking lower vagina swabs. the clinical riskbased strategy has been recommended in the UK because of the low prevalence of EOGBS disease (0. the swabs can be placed into the enrichment broth immediately after collection. vent 67% of EOGBS by giving IAP to 17% of pregnant women. 7 BY WHOM? The vaginal–rectal swabs are usually taken by a health-care provider. The use of 23 It is unclear whether it is cost-effective to add a routine urine test for asymp­ tomatic bacteriuria on top of vaginal–rectal swabs at 35–37 weeks’ gestation. intermittent or transient. these two swabs can be stored in one transport medium as there is no need to differentiate between these two sites for screen-positive cases. such as Todd-Hewitt broth supplemented with nalidixic acid and either gentamicin or colistin.27 If processing is delayed. 19 11 Universal swab- based strategy was found to be not cost- However. re-incubation and re-inspection will be required at 48 hours. data are WHICH SITE? GBS colonization in the maternal gastrointestinal and/or genital tracts is a prerequisite for EOGBS disease. The colonization can be permanent. To increase the detection rate of GBS colonization. Less-educated women may be more reluctant to collect their own samples. An alternative is to take perineal swabs which may be preferred by women. DNA probes 5. If GBS is not identified. Processing the swabs within 24 hours of collection is recommended. Optical immunoassays and enzyme immunoassays 4. After having been given appropriate instructions. To save laboratory cost. The latter is inspected for GBS after incubation for 18–24 hours.Continuing Medical Education been adopted because of the high prevalence of EOGBS (1. effective in the UK. 24 ate non-nutritive transport medium which can help sustain the viability of GBS in settings where immediate laboratory processing is not possible. A speculum is not WHEN TO TAKE THE SWABS? A recent systematic review in 2010 con- PROCESSING The swabs will be placed into an appropri- firms the recommendations to screen for GBS at 35–37 weeks’ gestation. This risk-based strategy can pre5 Table 3. pregnant women can collect their own vaginal–rectal screening specimens and give similar GBS yield.29 Selective broth medium. still limited.000 births) even in the absence of systematic screening or widespread IAP and high prevalence (60–70%) of clinical risk factors in EOGBS disease.11 On the other hand. Taking rectal swabs may cause discomfort or pain. The broth is then subcultured to a blood agar plate.20–22 Perinatal colonization rate is around 50%.30 The negative predictive value of GBS cultures JPOG MAR/APR 2012 • 83 . 25 two separate swabs is preferred over the use of one swab for both sites because of hygienic problem. swabs are taken from both the lower vagina (vaginal introitus) and the rectum (through the anal sphincter) instead of from one site alone. Fluorescence in situ hybridization 2. refrigeration (at 4ºC) will be used for storage. 28 Alternatively. The use of selective broth media can facilitate GBS isolation by preventing the overgrowth of other commensal bacteria in vagina/rectum. The colonization rate varies from 10% to 30%.8 per 1. This swab-based strategy can prevent 75% of EOGBS disease by giving IAP to 31% of pregnant women. but only 1% becomes infected. 26 25 However.000 births) and low prevalence (38%) of clinical risk factors in EOGBS disease. A recent study showed that agreement was high (96%) between the vaginal–rectal and the vaginal–perianal collection methods. is inoculated and incubated at 35–37ºC in ambient air or 5% CO2. they may prefer a health professional to collect their swabs.

.

However. but preterm newborns are at high risk of developing EOGBS disease. specificity and cost. While the sensitivity of NAAT for GBS can be as high as 92. latex agglutination test. availability of 24hour service. GBS colonization early in pregnancy is not predictive of EOGBS disease because the coloniza­ t ion can be transient. staffing requirements. Therefore.33 Consequently. were not sensitive and specific enough to replace the established culture method. Ideally. Studies have JPOG MAR/APR 2012 • 84 Recently. but it usually takes 24–72 hours to get the results. 35–41 It is recommended that a swab for GBS screening be taken at 35–37 weeks’ gestation. women who deliver before 35 weeks of gestation are not screened for GBS. 30 GBS colonization can be intermittent during pregnancy. molecular testing meth42 ods have been developed. The performance of commercially available NAAT on non-enriched samples was variable and not adequate in comparison with culture.or overtreatment with IAP may be resulted. optical immunoassays and enzyme immunoassays. 41 A rapid test may be useful for women at term with unknown GBS status and without risk factors. including fluorescence in situ hybridization. including DNA probes and nucleic acid amplification 43 tests (NAAT) such as polymerase chain reaction (PCR). culture-based testing is suitable for antepartum but not intrapartum screening.5–100. the latter increases the turnaround time.32 Second. or amniotic fluid. meconium. the current evidence does not support their use in replace­ ment of antenatal culture or risk-based assessment of women with CULTURE OR RAPID TEST? GBS culture remains the reference standard for the detection of GBS colonization. there are two disadvantages.34 the culture method may not provide a timely result to guide IAP.0% with use of an enrichment step. First.31 It will be appropriate to take a swab for GBS screening at 35–37 weeks. and costs. However. under. based on its current sensitivity. Universal screening using a rapid test was not cost-effective.45 More data are needed.performed within 5 weeks before delivery is very high (95–98%) but declines beyond 5 weeks. A change in the GBS colonization status from screening to delivery can occur in 9% of women. lack of antimicrobial susceptibility. shown that the rapid tests (Table 3). there are concerns on the real-world turnaround time. viable or low-count bacteria 44 and is not affected by the presence of blood. Although the results of intrapartum swabs can reflect the GBS status more accurately than those of antepartum swabs. the use of a highly sensitive and specific test with rapid turnaround time can assess intrapartum GBS colonization and hence guide IAP.33 The turnaround time of this rapid real-time PCR test can be within 1 hour.18 About 6% of GBS carriers remaining undetected in antenatal cultures.42 A rapid PCR test can detect non- . On the other hand. up to 67% of infants with EOGBS were delivered by mothers who were negative on prenatal GBS screening. 7.

The main reasons for declining GBS screening included (1) unwillingness to undergo screening (35. GBS screening for GBS.Yuk Hospital to determine the cost-effecly if the woman is not in true labour or if tiveness of prenatal universal screening the GBS culture is negative. EOGBS is associated with maternal GBS bacteriuria (generally >105 colony-forming units/mL of urine). IAP should be given for unknown GBS status or a positive GBS screen within 5 Preterm Prelabour Rupture of Membranes If a woman is admitted with leaking before 37 weeks’ gestation. A working group including obstetricians.542 were eligible for screening at 35–37 weeks’ gestation.4%). all the public hospitals in Hong Kong used the clinical risk-based strategy to prevent EOGBS disease.908 pregnant women.7–1.46 Few data are available on the risk with low (< 10 4) colony-count GBS bacteriuria.890. Otherwise.2%). if any. all pregnant women tion. After reviewing the procedures of swab taking. and (5) plan to deliver in a private or other hospital (8. and the incidence of EOGBS was around 0.4%). ‘pregnancy’ should be specified when sending urine samples to a laboratory. During the study period from April should be repeated at 35–37 weeks’ gesta. GBS screening should be performed unless it was performed within 5 weeks. the screen-positive rate increased to around 9.SCREENING FOR GBS IN fied on antenatal swabs for GBS screening. ‘penicil. seeking antenatal care were invited to participate in this study. However. If antibiotics are given to prolong latency for preterm prelabour rupture of membranes.5% in subsequent months. Pilot Study There are racial or ethnic differences in EOGBS disease. This was consistent with the results of another local study that the prevalence JPOG MAR/APR 2012 • 85 . IAP was given to screen-positive women. Newborn infants born to mothers with GBS colonization were managed according to a protocol. and its availability is limited. 47 All the swab specimens were sent to the microbiology laboratory of Queen Mary Hospital for testing for GBS. GBS screening should be performed unless it was performed within 5 weeks. THE EFFECTS OF UPDATED CDC GUIDELINES7 ON OBSTETRIC PRACTICE Bacteriuria To ensure proper testing.000 births. weeks. NAAT testing is optional. 90% or 3.2009 to March 2010. 82% of these eligible women accepted the screening. a 1-year pilot study was conducted in Queen Mary Hospital and Tsan Maternal GBS Colonization Rate During the pilot project which involved 3.1 per 1. 46 Antibiotic Susceptibility To ensure laboratory testing for antimicrobial susceptibility to clindamycin. Because of the lack of local data. HONG KONG Intra Partum NAAT can be used to detect GBS in women with unknown GBS status and without any risk factors during intra partum. We noticed a low screen-positive rate (4.2%) in the first month of screening. In the past. (4) planned elective Caesarean section (10. transport medium and laboratory testing. (3) screening deemed unnecessary (20.6%. After explanation and counseling on GBS screening by a midwife. Threatened Preterm Labour If a woman is admitted with signs and symptoms of labour before 37 weeks’ gestation. The latter should report GBS in urine culture specimens when present at concentrations of ≥ 10 4 colony-forming units/mL in pure culture or mixed with a second microorgan­ i sm.7%). (2) screening done privately (24. paediatricians. should be speci.UNIVERSAL PRENATAL lin-allergic’ history. The overall incidence of maternal GBS colonization was 9. The total number of women who underwent GBS screening was 2.4%). an additional GBS prophylaxis should be given for 48 hours unless a GBS screen performed within the preceding 5 weeks was negative. GBS testing results should not affect the duration of antibiotics which are given to prolong latency. GBS screening was performed according to the 2002 CDC guidelines. and then discontinued subsequent. and microbiologists was formed to study the prevention strategy in 2008.Continuing Medical Education unknown GBS status during intra partum. the antibiotics should also be able to cover GBS adequately.

22 ance to the protocol was. colonization rate was significantly higher in health-care professionals (19. as even those with negative results would be better off treated to reduce the risk of EOGBS disease. It seems that the universal swab-based strategy would likely cost more but probably avoid more cases of EOGBS disease than the clinical risk factor-based strategy. based on the best evidence we have available at present.9%) (P < 0. The effectiveness of IAP and the rate of receiving IAP were less important. One of them developed meningitis as well. There were three cases of EOGBS disease presented with septicaemia. processing and reporting of culture results may prevent additional Babies During the pilot project. either a health-care professional or a woman with a parity of 3 or above was not a good screening marker as they constituted only a small proportion of the pregnant women. collection. However. Around 8% of women did not return at 35– 37 weeks’ gestation for GBS screening. in general. and disability. the mothers declined screening while the screening result was negative in the remaining one.19 GBS screening in high-risk women would not be cost-effective. There was no major maternal complications related to GBS.4%.004).770 swabs (including gastric aspirate.000 vs US$3. However.9% of women with GBS colonization. The cost-effectiveness acceptability curves show that using the World Health Organization benchmark for value of a lifeyear (one to two times per capita gross do- LOGISTIC PROBLEMS There were no major logistic difficulties. US$12. and the current obstetric practice.3%) than women with a parity below 3 (9.22 Like another local study. The ICER was most sensitive to the rates of maternal colonization. the neonate was not infected. mestic product). Tracing the GBS reports from our electronic medical system was preferred over paper records. COST-EFFECTIVENESS ANALYSIS The cost-effectiveness analysis was performed by the Department of Community Medicine using a prediction model. a risk factor was present in only 12.001). and cost-effectiveness. There were no adverse events or complaints by patients. Varying the number of days in hospital and the proportion of days in the neonatal intensive care unit for EOGBS cases did not have an important impact on the cost-effectiveness of the strategies. universal prenatal screening cannot prevent all affected infants because of a false-negative result. 11 The incremental cost-effectiveness ratio (ICER) was HK$255. ear. The compliJPOG MAR/APR 2012 • 86 . This modelling study has shown that.4%) than in housewives (7. a cost-effectiveness study has shown that culture-based testing of women with no risk factors or rupture of membranes ≥ 18 hours with treatment for all preterm and high-risk term women would be the most cost-effective strategy. Surprisingly. In two of them. but at a larger cost than the risk-factor strategy (75% vs 54%. a total of 1. This result was compatible with the 4% false-negative rate which was reported in the literature. In the UK.of GBS on booking was 10. vertical transmission. good the GBS except for one screen-positive case in which IAP was not given. and blood) were taken from the babies. Fortunately. This finding is consistent with a study in the US that universal screening was predicted to prevent more EOGBS disease.000).367 (about US$32. the swab-based strategy in Hong Kong would likely cost more but probably avoid more cases of EOGBS than the cur- CONCLUSION Whether to implement universal swabbased strategy or clinical risk-based strategy depends on the local incidence of EOGBS disease. over 80% of simulations found that the swab-based strategy was more cost-effective than the current clinical risk factor-based strategy. mortality. The GBS colonization rate was also higher in women with a parity of 3 or above (27. the lack of the typical intrapartum risk factors for GBS infection.000) per life-year gained. Improved management of preterm deliveries and improved communication. or missed opportunities for screening. which might not be available during the intrapartum period.5%) (P = 0. the prevalence of clinical risk factors in EOGBS disease.18 There was no neonatal mortality related to GBS. Universal swabbased strategy and clinical risk-based strategy differ in the proportion of women being given IAP. rent clinical risk factor-based strategy.

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GBS colonization rate was significantly higher in health-care professionals than in housewives in Hong Kong. True False 1. For GBS screening. Maternal temperature of 38. If the vaginal/rectal swab shows the presence of GBS. In the UK. 9. Administration of intrapartum antibiotic prophylaxis for GBS is indicated in a woman who goes into labour at 38 weeks’ gestation with unknown GBS status and gives a history of maternal GBS colonization in her previous pregnancy but without neonatal disease. Name in BLOCK CAPITALS: Signature: Date: Please mail your completed answer sheet back to: The Secretariat Hong Kong College of Obstetricians & Gynaecologists Room 805.CME Questions This continuing medical education service is brought to you by the Medical Progress Institute. 6. If a woman is admitted with painful uterine contractions at 35 weeks’ gestation and unknown GBS status. 7. 5. Hong Kong JPOG MAR/APR 2012 • 88 CME Answers for JPOG Jan/Feb 2012 of Pregnancies With Previous Caesarean Section Answers 1 T 2 F 3 F 4 T 5 T 6 T 7 T 8 T 9 T 10 F HKCOG CME Article: Management . antenatal antibiotics treatment will be required to eradicate GBS. Hong Kong Academy of Medicine Jockey Club Building 99 Wong Chuk Hang Road. Aberdeen. This JPOG article has been accredited for CME by the Hong Kong College of Obstetricians and Gynaecologists. It is recommended to take swabs for GBS screening at 35–37 weeks’ gestation. GBS screening should be performed and intrapartum antibiotic prophylaxis for GBS given. CME Article Screening for Group B Streptococcus in Pregnancy Answer True or False to the questions below. an institute dedicated to CME learning. 8. 4. culture-based testing of women with no risk factors while being given intrapartum antibiotics for GBS for all preterm and high-risk term women is the most cost-effective strategy. 2. Read the article ‘Screening for Group B Streptococcus in Pregnancy’ and answer the following questions. 3. swabs are taken from both the high vagina and the anus.8ºC during the intra partum is a risk factor for early-onset group B Streptococcus (GBS) disease. 10. Delayed processing of the swabs for more than 24 hours does not affect the laboratory detection of GBS. The performance of a rapid test for GBS on non-enriched swab samples is as good as the culture method.

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