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JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY
Your partner in paediatric and O&G practice
ISSN 1012-8875 (HONG KONG)
Type 1 Diabetes Mellitus in Childhood Atopic Dermatitis in Children: A Practical Approach
Screening for Group B Streptococcus in Pregnancy
JOURNAL OF PAEDIATRICS, OBSTETRICS & GYNAECOLOGY
MAR/ APR 2012 Vol. 38 No. 2
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
48 • Hospital-acquired bacteraemia in children in a Kenyan hospital Review Articles
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
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
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
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Marisa Lam Greg Town
Deputy Managing Editor Associate Editor
Edwin Yu, Ho Wai Hung, Jasmine Chay
Minty Kwan Jenny Lim
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
et al.com. 3=seedy.33 Control 3.75 2.0003 vs control p=0. 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. Shun Tak Centre West Tower 200 Connaught Road.55 p=0. It is difficult to reverse a decision to avoid or discontinue breastfeeding.6:17.5 1 0.33 Control Mean number of stools per day 2. 3.01 vs baseline 5 1.2 Stool consistency scores 2.0102 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.0079 vs control p<0.0003 vs control p=0.5 2 1.hk References: 1.5 1 0.5 0 2.friso.4. Mothers should also consider social and financial implications in selecting the suitable infant feeding method. Hong Kong Baseline Tel: 852 2859 3705 Fax: 852 2858 3093 www. 4=formed. stimulate intestinal microflora production in term infants.5 2 1.14:6564-6568 2 weeks 4 weeks 0 lactis and Lactobacillus paracasei *Galacto-oligosaccharides. present in the entire Friso Gold range. Chin Med 2004. World J Gastroenterol 2008.5 3 2. Boehm G.2 Stool consistency scores 2. Infant formula is an accepted breast milk substitute for mothers who do not breastfeed.5 2 1.33 p=0. Ben XM. et al.5 1 0.86:F178-F181. use and store infant formula as directed to avoid health hazards. 2 weeks .75 2. 2=soft.74 Bowel movements/week 3. et al. Prepare.5 1 0.0001 vs control 2.55 Mean number of stools per day 2. a prerequisite for optimal intestinal health in children Human milk 3 Oligosaccharide formula 4 3.5 0 p<0. Bekkali N.009 vs baseline 10 p=0.117:927-931.Human milk 3 Oligosaccharide formula 4 3.009 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. 4.01 vs baseline p=0. et 5 al.5 0 p<0.33 p=0. Proper feeding practices should be observed so as not to prevent mothers from breastfeeding. 17/F. Nutr J 2007. Breast milk provides superior nutrition for babies. Bifidobacterium are added as supplements in Friso 3 Gold and Friso 4 Gold Baseline For medical professionals’ reference only. similar to levels in breastfed infants3.0001 vs control 2.5 0 2.0079 vs control p<0.74 1. 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. Breast milk is best for babies. Arch Dis Child Fetal Neonatal Ed 2002. Introducing partial bottle-feeding may disadvantage breastfeeding.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.5 3 2.5 2 1. Central. 2. Ben XM.
38 No. poor compliance and psychological factors. and the focus thus lies in disease prevention. Thomas Li. the updated guidelines by the Centers for Disease Control and Prevention. Review Articles Comprehensive reviews providing the latest clinical information on all aspects of the management of medical conditions affecting children and women. Genting Centre. Because the early-onset disease develops shortly and rapidly after birth. All rights reserved. This review article discusses the current screening methods for GBS in pregnancy. there has been little improvement in the disease treatment. Singapore 088934 Tel: (65) 6223 3788 Fax: (65) 6221 4788 E-mail: enquiry@jpog. KKW To.com. Teresa WL Ma. No 3 Lim Teck Kim Road. Sarah Morag McGhee 81 The Journal of Paediatrics. 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. usually staphylococcal or streptococcal. or contact: The Editor UBM Medica Asia Pte Ltd. KY Leung. Case Studies Interesting cases seen in general practice and their management. OBSTETRICS & GYNAECOLOGY MAR/ APR 2012 Vol. Triveni Shekariah. All should be done through a multidisciplinary approach and liaison with primary care. and a pilot study in Hong Kong.com Rowena Sim. and pages 67–80 are reprinted with permission of Consultant for Pediatricians. Resistant eczema should raise the suspicion of secondary infection. Illustrator JPOG MAR/APR 2012 • iii . The clinical assessment involves an enquiry about triggers as well as details of therapy. Obstetrics and Gynaecology contains articles under licence from UBM Media LLC. KY Wong. 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.jpog. Copyright © 2011 UBM Media LLC. which is associated with a high rate of morbidity and mortality.JOURNAL OF PAEDIATRICS. the improvement in laboratory techniques. The articles appearing on pages 49–53. CW Law. Art Director Connie Lim. Manjunatha Kalavala. For more information. The Cover: ‘Atopic Dermatitis in Children’ © 2012 UBM Medica Pictorial Medicine Vignettes of illustrated cases with clinical photographs. please refer to the Instructions for Authors on our website www.
The maximum effect of bevacizumab was at 12 months. Sig- JPOG MAR/APR 2012 • 45 . have assessed the benefits of bevacizumab for women with ovarian cancer. and 1. and IIB-IV ovarian cancer. IIa. or Fallopian tube cancer were randomized at 263 centres to chemotherapy with (CB) or without (C) bevacizumab. or bevacizumab in cycles 2–6.2%. and 14.5 months vs 18. At 42 months. Hypertension was more common in the bevacizumab groups (BT. Median progression-free survival was 10. The study. peritoneal cancer. The rate of caesarean section was 23% Bevacizumab is a humanized monoclonal antibody against vascular endothelial growth factor (VEGF). progression-free survival was 22. 2.8 months (CB) vs 20. term pregnancy in cephalic presentation with intact membranes.1 months and overall survival 28. In both of these trials.1 months (CB). an unfavourable cervix. Investigators in the Netherlands have compared transvaginal Foley catheter inflation with use of a prostaglandin E2 vaginal gel.4 months (C) vs 24. at 12 centres. 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.3 months (controls).2 months (BI).1 months (BT). In the first of the trials. and VEGF is implicated as a promoter of ovarian cancer. BT was associated with a significant 28% reduction in progression or death compared with control treatment. There were two serious adverse events. OBSTETRICS (Foley catheter) vs 20% (prostaglandin gel). South Korea and Japan. and placebo in cycles 7–22 (bevacizumab-initiation. A phase 3 trial of bevacizumab in ovarian cancer. but there was no significant difference between on bevacizumab. and oxytocin infusion started at least 6 hours after the last dose of vaginal gel and with a Bishop score of 6 or more. BT). no history of caesarean section.6%. BI). Canada. the corresponding figures were 14.873 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. Hypertension occurred in 18% of patients induction of labour.6 months. Australia and New Zealand. Incorporation of bevacizumab in the primary treatment of ovarian cancer. Amniotomy was performed.Peer Reviewed Journal Watch the BI and control groups. There was a significant 19% reduction in risk of progression or death with bevacizumab. at the end of planned bevacizumab treatment. Median mean progression-free survival at 36 months was 21. Canada. and one in eight European countries. the addition of bevacizumab to chemotherapy improved survival with greater benefit for high-risk patients. a nonsignificant difference. included a total of 824 women with a singleton. 11. Among high-risk patients.3 months (C). one uterine perforation and one Induction of labour at term: Transcervical Foley catheter vs vaginal prostaglandin E2 gel Worldwide. both in the vaginal prostaglandin group. 23%. one in the USA. In the second of these trials. Two trials. 17%) than in the control group (7%). GYNAECOLOGY Bevacizumab for ovarian cancer overall survival was 76% with no differences in survival between the three groups. or placebo in cycles 2–22 (controls). Cervical ripening may be promoted by mechanical or pharmacological means. Randomization was to transcervical Foley catheter (inflated with 30 mL of saline or water) or use of prostaglandin E2 vaginal gel. a total of 1.528 women with stage I. a total of 1.8%. Ibid: 2484–2496.8 vs 36. Perren TJ et al. NEJM 2011. and it had diminished by 24 months. Gastrointestinal wall disruption needing treatment occurred in 2. At the time of analysis. 365: 2473–2483. Burger RA et al. and an indication for induction of labour. respectively. some 20–30% of deliveries follow uterine rupture.
2% vs 6. Obaro S.5 to 3. case-control study and a longitudinal study. A BMJ editorialist calls for more units to practice delayed clamping. These researchers conclude that the two methods are similarly effective.59 to 1. Malaria parasitaemia increased the risk of bacteraemia 6. PAEDIATRICS Malaria and bacteraemia in children Bacteraemia is common in children in sub-Saharan Africa. In 1999. decreased in parallel with those for malaria. the prevalence of parasitaemia in the community was 29%. randomised controlled trial. Between 1999 and 2007. Foley catheter versus vaginal prostaglandin E2 gel for induction of labour at term (PROBAAT trial): an open-label. The rates of neonatal respiratory problems. Jozwiak M et al. at the age of 4 control children. At the same time. Ibid: 1233–1234 (d7127) (editorial). First. provides protection against malaria. The prevalence of iron deficiency was reduced by 90% with delayed rather than early clamping. Malaria The benefits of delaying clamping of the umbilical cord have been promoted for many years. The two groups had similar haemoglobin levels at age 4 months. JPOG MAR/APR 2012 • 46 . Delayed clamping would prevent one case of iron deficiency for every 20 children born. from 2. polycythaemia. Lancet 2011. the protection provided by sicklecell trait against bacteraemia fell. HIV infection. Malaria control should reduce the prevalence of bacteraemia. Relation between falciparum malaria and bacteraemia in Kenyan children: a population-based. they performed a longitudinal case-control study with 1. but the Foley catheter method is associated with less maternal and neonatal risk. Intracervical Foley catheter for induction of labour: Ibid: 2054–2055 (comment). Sickle-cell trait was associated with a 64% reduction in risk of bacteraemia. 378: 1316–1323. Lancet 2011. ter birth) cord clamping. and sickle-cell disease all contribute to the susceptibility.749 controls. 343: 1244 (d7157). Scott JAG et al. BMJ 2011. 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. Delayed cord clamping reduced the rate of early neonatal anaemia and reduced the rate of iron deficiency.000 child-years. Stock S. a significant difference in favour of delayed clamping. and researchers in Kenya have taken advantage of this to perform a mendelian randomization study. and hyperbilirubinaemia were similar in the two groups. Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. Sickle-cell trait (HbAs). Malaria and bacteraemia in African children. Delayed cord clamping and improved infant outcomes. Ibid: 1281–1282 (comment). 378: 2095–2103. 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. however. but in developed countries early clamping remains the rule.45 admissions per 1. malnutrition. Van Rheenan P. Greenwood B. but not of anaemia.nificantly more women in the prostaglandin group (3% vs 1%) were treated for suspected intrapartum infection.000 childyears because of more effective malaria control. Mean serum ferritin levels at 4 months of age were significantly 45% higher with delayed clamping (117 vs 81 µg/L). they studied 292 children aged 3 months to 13 years with bacteraemia and 528 bacteraemia including cases due to non-typhoidal salmonella. but the rates of anaemia at age 2 days were 1. largely Gram-negative Early versus delayed clamping of the umbilical cord months. and hospital admissions for bacteraemia. Next.3%. Norman JE. and 62% of cases of bacteraemia were attributed to malaria. and leukocyte haemozoin pigment. Anderson O et al. undernutrition. HIV infection.7-fold.45 per 1. Bacteraemia was associated with sickle-cell disease. A study in Sweden has re-emphasized the benefits.454 cases (children with bacteraemia) and 10. the rate of hospital admission for malaria fell from 28.
Influenza is a common cause of ALRI in young children worldwide. 1995 and Oct 31. The 43 studies included about 8 million children younger than 5 years. 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. Nair H et al.56 million deaths in young children in 2008. Ibid: 1897–1898 (comment). and 16 unpublished population-based studies. Zambon M.500. The most common pathogen is respiratory syncytial virus. Global burden of respiratory infections due to seasonal influenza in young children: a systematic review and meta-analysis. Assessment of the burden of influenza in children. Now. the available data have been analysed in a systematic review and meta-analysis of 43 studies. 378: 1917–1930. Speed of intravenous rehydration for children A recent trial in sub-Saharan Africa showed that JPOG MAR/APR 2012 • 47 . 20 million cases of ALRI due to influenza. and 1 million cases of severe ALRI from this cause. until now.000 and 111. Lancet 2011. The estimated number of deaths from ALRI due to influenza viruses in children < 5 years old in 2008 was between 28. 2010. Data were obtained from studies published between Jan 1. It was estimated that in 2008. It has been suspected that seasonal influenza viruses cause many childhood episodes of ALRI but. Around the world. about 13% of all cases of ALRI and 7% of cases of severe ALRI in young children were caused by influenza viruses. with almost all (99%) of these deaths occurring in developing countries.Peer Reviewed Journal Watch Influenza in children worldwide Acute lower respiratory infections (ALRI) were the cause of 1. accounting for 22% of ALRI episodes in young children.
Acinetobacter species. and 58% over 1 year). Risk and causes of paediatric hospital-acquired bacteraemia in Kilifi District Hospital. Factors associated with hospital-acquired bacteraemia included severe malnutrition and blood transfusion in the absence of severe anaemia. Kenya: a prospective cohort study. Ibid: 1982–1983 (comment). Freedman SB et al. 3% 29–59 days. in all. Now.188 admissions of children up to the age JPOG MAR/APR 2012 • 48 . Rapid rehydration did not give better results Although community-acquired bacteraemia is cases. Lancet 2011. 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. of 15 years (14% aged 0–28 days. Feasy N. Clinical rehydration at 2 hours was achieved in 36% (rapid) vs 30% (standard). 343: 1190 (d6976). 378: 2021–2027. a study in Toronto. Hospital-acquired bacteraemia was uncommon in this study but carried a high mortality. Ibid: 1183 (d7083) (editorial). The rate of hospital-acquired bacteraemia (> 48 hours after admission) was 5.9 per 1. Nager AL. 18 bacterial pathogens were isolated. The incidence was 1. and poor peripheral perfusion. there were 33.than standard rehydration. each accounting for around 20% of rapid bolus intravenous fluid administration was potentially lethal for children with dehydration. Prolonged treatment was needed by 52% vs 43% (non-significant difference). A total of 226 children > 90 days old (weight. rising during the study period by 27% per year. Survivors of hospital-acquired bacteraemia spent an extra 10 days in hospital compared with patients who did not become bacteraemic. The main pathogens differed from those of communityacquired bacteraemia. Molyneux E. Staphylococcus aureus.9% saline 60 mL/kg over 1 hour) or standard intravenous rehydration (20 mL/kg over 1 hour). The main pathogen in community-acquired bacteraemia was Streptococcus pneumoniae (29%). The main infecting organisms were Escherichia coli and Klebsiella pneumoniae. there are few data about hospital-acquired bacteraemia. and non-typhi Salmonella species (9%).0 hours). about 40 times the local Hospital-acquired bacteraemia in children in a Kenyan hospital rate of community-acquired bacteraemia. common in children in sub-Saharan Africa. fever.000 admissions overall. group D streptococci. and severe malnutrition and unnecessary blood transfusion were contributory factors. Aiken AM et al. The writer of a largely critical editorial insists that currently available evidence points. BMJ 2011. they were randomized to rapid intravenous rehydration (0. but the time to hospital discharge was significantly longer in the rapid rehydration group (6. Rapid versus standard intravenous rehydration in paediatric gastroenteritis: pragmatic blinded randomised clinical trial.000 days in hospital. Mortality was 53% for hospital-acquired bacteraemia and 24% for community-acquired bacteraemia. Keep it clean: hospital-acquired infections in children. a non-significant difference. 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. A 7-year survey in a single hospital has been reported. to rapid rehydration being effective and safe. overall. In the Kilifi District Hospital in Kenya between 16 April 2002 and 30 September 2009. When oral rehydration had failed. 25% 60 days to 1 year.0 per 1. has shown no advantage from rapid rehydration compared with standard rehydration. Rapid intravenous rehydration in paediatric gastroenteritis. and Pseudomonas aeruginosa each accounted for slightly less than 10% of cases and. followed by Staphylococcus aureus (13%). Yeasts were isolated in 5% of cases. Canada. Acinetobacter species (10%).3 vs 5.
000/year) to the lowest reported in China (0.4/100.000/year). in parallel with the rise in obesity throughout the world.5 Several hypotheses to explain this changing incidence have been proposed. but none is widely accepted. FRCP(C) INTRODUCTION Type 1 diabetes mellitus (T1DM) is the most common chronic metabolic condition in children and adolescents. FRCPC. and reduced early exposure to pathogens.000/year) and Canada (21. from the highest in Finland (57. such as rapid growth in early childhood. resulting in hyperglycaemia and associated abnormalities in carbohydrate. there are approximately 480.1/100.000 children with T1DM. The classification of DM is described by the American Diabetes Association. 3 Incidence rates of T1DM in children and adolescents under 15 years of age vary greatly by geographical region. or both.000 new cases are diagnosed each year. and 76.6/100. and all ethnic groups. JPOG MAR/APR 2012 • 49 . Denis Daneman. MBBCh.3 The overall annual incidence is increasing at a rate of about 3%4 with the greatest increase in the youngest age group.PAEDIATRICS I Peer Reviewed Type 1 Diabetes Mellitus in Childhood Rayzel M Shulman. both sexes.000/year) and Venezuela (0.3 T1DM affects children of all ages. MD. in which the diagnosis may be being missed. Diabetes mellitus (DM) comprises a group of heterogeneous conditions involving defects in insulin secretion or action.7/100.1 T1DM is by far the most common type seen in childhood.2 EPIDEMIOLOGY Worldwide. The incidence of type 2 diabetes (T2DM) is increasing most notably in the adolescent age group.6 Data are lacking about the incidence of T1DM in some developing countries in sub-Saharan Africa and South and East Asia. environmental exposures. protein and fat metabolism.
10 The aetiology of T2DM is multifactorial. obesity.1 mmol/L) during an oral glucose tolerance test.1 mmol/L is sufficient to make the diagnosis of DM.PA EDIATRICS I Peer Reviewed Table 1. includJPOG MAR/APR 2012 • 50 the presence of these classical symptoms of hyperglycaemia. Forty genetic loci have been associated with T1DM by a genome-wide association study and meta-analysis. a single blood glucose measurement > 11. and DQ 0300/0302. criteria 1–3 should be confirmed by repeat testing. The test should be performed as described by the World Health Organization. intrauterine environment. 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. 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. sex. polydipsia. To date. enuresis and weight loss to a severely dehydrated child with diabetic ketoacidosis (DKA). T1DM must be differentiated from T2DM.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. delay or reverse the progression of T1DM (eg. ethnicity (more common in African-American. treatment should be initiated urgently to prevent or reverse DKA. and insulin resistance. a CLINICAL PRESENTATION AND DIAGNOSIS The presentation of T1DM can range from a clinically stable child with symptoms of polyuria. A Canadian population-based surveillance study of non-type 1 diabetes in children under 18 years of age found an incidence rate of 1.1 mmol/L) In the absence of unequivocal hyperglycaemia. the diagnosis should not be delayed. dietary factors or toxins. TRIGR). TrialNet. such as Hashimoto’s thyroiditis.1 Type 2 Diabetes (T2DM) In the pubertal age group. Both secretion and action of insulin are usually dis- . DQ 0201/0302. Asian. These patients are susceptible to other autoimmune diseases. Insulitis with gradual β -cell destruction leads to pre-diabetes and finally to overt DM. DR 4/4. might trigger the development of T-cell-dependent autoimmunity in genetically susceptible individuals.000/year. American Diabetes Association criteria for the diagnosis of diabetes ing the alleles DR3/4. 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).7 Autoimmunity is manifest by detectable antibodies to ICA512/ IA-2. interventional trials have failed to delay the onset or prevent T1DM in those genetically at risk. coeliac disease.5% OR 2) Fasting plasma glucose 7. but key factors include genetic predisposition (> 80% have a positive family history). insulin autoantibody and glutamic acid decarboxylase. It most commonly results from autoimmune destruction of insulin-producing β-cells in the pancreas. such as enteroviruses.9 1) HbA1c ≥ 6. Hispanic and Native North Americans). Ongoing research by international networks is exploring ways to prevent. In PATHOPHYSIOLOGY T1DM is the result of a combination of genetic and environmental influences.55/100. and myasthenia gravis. Addison’s disease. a random plasma glucose ≥ 200 mg/dL (≥ 11. Devendra et al proposed that one or more environmental factors.8 A number of genetic loci in the major histocompatibility region are associated with increased susceptibility to developing T1DM. In such situations.
Include this amount in total fluid intake. • DO NOT GIVE BOLUS OF INSULIN • Continuous cardio-respiratory monitoring (with EKG tracing) Neurological deterioration • Headache. gases. JPOG MAR/APR 2012 • 51 .ca/english/providers/pub/diabetes/child_poster. 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 3.5 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.04-0.04–0. D5 = 5% dextrose.5 mmol/L. 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.05 U/kg/hr = 0. ICU = intensive care unit. administer 2–4 ml/kg of 3% saline over 10–20 min THEN Normal saline at maintenance IV rate • Decrease insulin to 0. IV = intravenous. S/C = subcutaneous. EKG = electrocardiography.pdf.gov. electrolytes. Q2–4h = every 2–4 hours. HR = heart rate. at least. irritability. add 40 mEq/L of potassium chloride to IV fluid • Aim to keep potassium between 4–5 mEq/L • Continuous insulin infusion 0. urea.4–0. Inotrope-resistant shock 3.health.PAEDIATRICS I PAEDIATRICS Peer Reviewed Figure 1. Life-threatening hyperkalaemia 2.3 • 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. decreased level of consciousness. Reproduced and adapted with permission. PALS = Pediatric Advanced Life Support.4–0. 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 0.05 U/kg/hr = 0.5 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 >7.3 • 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. 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. BP = blood pressure. STAT = statim.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 <5.1 units/kg/hr = 1mL/kg/hr (of solution of 25 units of regular insulin in 250 mL normal saline). assessment of neurological status for a minimum of 24 hours • 2–4 hours after start of IV – electrolytes. Available at: www.on. 2009. Emergency Room Management for the Child with Type 1 Diabetes. © Queen’s Printer for Ontario. 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.
longer duration of diabetes. DKA may also be present in up to 25% of young people presenting with T2DM. consider aiming toward normal PG range (ie. and aid in diagnosis and management of similarly affected family members.0 mmol/L. DIABETIC KETOACIDOSIS Diabetic keoacidosis results from absolute insulin insufficiency.PA EDIATRICS I Peer Reviewed Table 2. 14 insulin omission or insulin pump failure. and obesity). higher mean HbA 1c. JPOG MAR/APR 2012 • 52 .0 ≤ 7.3 or bicarbonate < 15 mmol/L).0–10.0 4. a In adolescents in whom it can be safely achieved. and ketonuria. Glycaemic and HbA1c targets according to the 2008 Clinical Practice Guidelines of the Canadian Diabetes Association Age (y) HbA1c (%) Plasma glucose (mmol/L) 6.5–8.0–10.0 Source: Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada.12 DKA is present at T1DM presentation in 15–67% of children. higher reported insulin dose. and genetic testing is available for all of the identified mutations.0 4. hyperglycaemia (blood glucose > 11 mmol/L). Insulin resistance may manifest clinically with acanthosis nigricans (a velvety thickening of the dermis found especially on the posterior neck and axillae). rarely. formerly known as maturityonset diabetes of the young. its frequency being inversely related to the incidence of T1DM in that area. explain associated clinical features. the presence of psychiatric disorders.0 2-hour postprandial plasma glucose (mmol/L) – Considerations <6 ≤ 8.0–8. Identifying this diagnosis is important to predict the course of disease.5 mmol/L) fasting hyperglycaemia. and features of metabolic syndrome (hypertension. dyslipidaemia. 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 (5.0–7. especially if young or familial • Diabetes associated with extra-pancreatic features Specific genetic defects are listed in Table 1. guide management. 13 In those with established T1DM in the United States.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. fasting/preprandial plasma glucose 4. ketonaemia. T1DM must be differentiated from monogenic diabetes. leading to metabolic acidosis (pH < 7. Risk factors that predict DKA include female sex.0%. ordered at clinical presentation. although one feature may predominate. HbA1c ≥ 6.0 – 5.32(suppl 1).0–6. Monogenic Diabetes Occasionally. severe insulin resistance. features of polycystic ovarian syndrome (hyperandrogenism. the incidence of DKA has been reported to be 8 episodes per 100 patient-years.0 mmol/L). menstrual irregularity).0–12. Can J Diabetes 2008. and 2-hour postprandial plasma glucose 5. Monogenic forms of diabetes result from single gene mutations that cause impaired β-cell function or.
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Bicarbonate should be given only in the setting of life-threatening hyperkalaemia. and detection and treatment of hypoglycaemia. inotrope-resistant shock. children presenting without DKA can be safely managed on an ambulatory basis provid- ercise. Insulin initiation varies greatly among different centres but generally consists of two to four injections per day. 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. Families of children with T1DM should have a clear understanding of the rationale for blood glucose and HbA 1c targets for their child. and is adjusted on a daily basis until target blood glucose is achieved (Table 2). and sick days). these families receive expert care from a team of health professionals experienced in childhood 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. At onset. morbidity and mortality in young people with T1DM. Boluses of fluid and insulin should be avoided. or greater costs. blood glucose monitoring.0% of DKA episodes.PAEDIATRICS I PAEDIATRICS Peer Reviewed DKA should be treated as a medical emergency by an experienced medical team. Demographic risk factors associated with increased risk for cerebral oedema include younger age. This includes regular JPOG MAR/APR 2012 • 53 . outpatient care is not associated with worse metabolic control. both fluids and insulin are calculated on a per kilogram rather than an empirical basis. administration of sodium bicarbonate.5–1. DKA is the major cause of hospitalization. and longer duration of symptoms. new-onset diabetes.4–0. It is essential that from the moment of diagnosis. In the subsequent weeks. Risk factors that are present at the time of diagnosis or during treatment are increased serum urea. severe acidosis. The starting total daily dose is 0. Fluid repletion should occur gradually with sodium chloride 0. The most serious complication is cerebral oedema. T1DM is a lifelong condition with serious short. which occurs in 0. diabetes nurse. dietitian and social worker.6 units/kg body weight/day. children and their families enter the long-term followup phase of their diabetes. basic nutrition planning. with 25% mortality. usually lower in younger children. acute diabetic complications or psychosocial outcomes. insulin dose adjustment.9%. A meta-analysis of homebased management at DM onset suggests that in comparison to routine hospital admission.and long-term implications. After initial stabilization and education. 12 ed that support services are available and that no other medical or social conditions exist that would place the child in danger. The treatment algorithm used at our centre is outlined in Figure 1. or cardiac arrest. Treatment of DKA in children differs in several respects from that in adults: first. 15 Early ‘survival skills’ to be mastered include insulin injections. greater hypocapnia after adjusting for the degree of acidosis. including a physician. and an attenuated rise in the measured serum sodium during treatment.
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.html. and individual and family preferences.17 Intensification of therapy is associated with an increased risk of hypoglycaemia that can be a limiting factor in achieving good metabolic control. and duration of action of commonly used insulin preparations. most frequently the youngest children and adolescents. Increasingly. See Table 3 for the onset. Severe hypoglycaemia in young children has been associated with mild cognitive deficits later in life. associated conditions (hypothyroidism. daily routines. The choice of regimen should be tailored to the child’s age. Onset. 19. Soon after initial presentation.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- . Available from: www. 16. The duration of the honeymoon phase is proportional to the age of the child. Special attention must be paid to those children and their families. most patients enter a transient remission or ‘honeymoon’ phase when exogenous insulin requirements decrease as a result of residual β-cell secretion.PA EDIATRICS I Peer Reviewed Table 3. Most children and teenagers now start their treatment with a combination of intermediate-acting insulin or basal insulin analogue (insulin glargine or insulin detemir). children and teenagers with T1DM are using continuous subcutaneous insulin infusion (CSII) pumps. Table 2 summarizes the glycaemic goals published in the 2008 Clinical Practice Guidelines of the Canadian Diabetes Association. This demands that age-appropriate targets be set and that progressively tighter control be sought as the child grows older. duration of diabetes. 21 When rigorously applied. peak. 2010 Joslin Diabetes Center. this basal-bolus approach can help to achieve and maintain near-normal glycaemia. 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. peak. combined with rapid-acting insulin analogues (insulin lispro or insulin aspart) given two or more times daily. with insulin doses calculated to match carbohydrate intake and ambient blood sugar. 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’. although the cause-and-effect relationship remains controversial. INSULIN REGIMENS follow-up visits with their diabetes team with surveillance for psychosocial problems. who have the greatest difficulty meeting the considerable demands of their diabetes regimen. Approaches to insulin therapeutics vary from one centre to another.18 Multiple studies attest to the difficulties in achieving these goals in all children with T1DM.joslin. and microvascular and macrovascular complications. coeliac disease). targets of metabolic control.org/info/insulin_action.
For children and teenagers involved in exercise activities.25 PHYSICAL ACTIVITY Physical activity in general leads to increased glucose utilization. Quality of 5 based on the number of grams of carbohydrates consumed and on deviation from the target blood glucose. after insulin dose adjustment.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. Maintenance of a blood glucose logbook is essential to follow patterns and to make appropriate dose adjustments. 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.23 HbA1c is a measure of glycaemic control over the previous 4–12 weeks. insulin doses can be calculated . or illness) is recommended. seizure. or severe confusion). 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). NUTRITION Recommendations for nutritional intake in young people with T1DM should aim to support optimal glycaemic control.28 Recognition of symptoms of hypoglycaemia can be difficult in young children with T1DM. Nutritional requirements for children with T1DM do not differ from those of healthy children and adolescents. Symptoms include autonomic (adrenergic) activation and/or neurological dysfunction (neuroglycopenia). strenuous exercise. Lower HbA1c values have been associated with fewer and delayed microvascular and macrovascular complications. and fit with the insulin regimen. 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. food consumed and activity. and lipid profiles.26. Hypoglycaemia has been associated with reduced cognitive functioning and can. although in some cases rigorous exercise may induce a stress response leading to hyperglycaemia.27 life and patient satisfaction have been reported to be at least equal or improved with CSII. Diabetes should not limit the ability of a child to participate in sport.24%) in HbA 1c in the CSII group and found no differences in DKA or severe hypoglycaemia between groups. 16. 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. Methods for adjusting insulin and carbohydrate intake to accommodate exercise have been proposed. The cost of 6 CSII is considerable and cannot be accommodated by many families and health-care systems.17 HYPOGLYCAEMIA Hypoglycaemia (blood glucose < 3. and therefore increased monitoring of blood glucose when hypoglycaemia might be expected (overnight. more frequent monitoring with either insulin dose adjustment or appropriate food intake are needed to avoid the extreme hypoglycaemia that can occur with activity. be a cause of death in young people with T1DM. Families should have injectable glucagon at home to treat severe hypoglycaemia (coma. weighted more heavily toward the most recent 4 weeks. blood pressure.PAEDIATRICS I PAEDIATRICS Peer Reviewed fusion (basal rate) with intermittent boluses given before carbohydrate ingestion or to correct hyperglycaemia. rarely.
Adolescents should be offered regular sexual health and contraception counselling. the stress of some illnesses may lead to a vigorous counter-regulatory hormone response. neuropathy and nephropathy). and disorders29 and should therefore be assessed in the routine diabetes care in this population. Illnesses associated with decreased oral intake may predispose to hypoglycaemia. dyslipidaemia. and family history. ADOLESCENTS WITH T1DM Given the association of smoking with both microvascular and macrovascular complications of DM. Depression. Insulin omission may be one method by which the teenager may attempt to control his/her weight. and the effect of alcohol and illicit drugs on blood glucose. 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. Diabetes is not an absolute contraindication to using oral contraception. Unstable glycaemic control and severe hypoglycaemic events may limit their ability legally to obtain or maintain a driver’s licence. although the risk is less for youth who transfer to a new allied health team but maintain physician continuity. 31 Other risk factors for long-term complications include younger age of DM onset. adolescents should be counselled in smoking prevention and cessation. intensification of the insulin regimen. Poorly controlled T1DM is a risk factor for maternal and fetal complications. Tight metabolic control delays and slows the progression of these complications. 30 Formal transition programmes may facilitate transfer to adult care and prevent the high rates of drop-out reported in some centres. Frequent monitoring of blood glucose and ketones. continuation of insulin therapy with appropriate dose adjustment. longer duration of disease. body image concerns. It is important to address the risk of severe hypoglycaemia associated with an unpredictable daily activity schedule. 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. Adolescents who plan to or hold a driver’s licence should always check their blood glucose before driving. DM is also a major risk factor for macrovas- . and timely emergency department attendance for those with repeated vomiting should help to prevent metabolic deterioration. Teenagers should also have private time with the members of the diabetes care team as this promotes independence and responsibility. hypertension. In the context of universal health-care funding. smoking. adolescents with DM should be encouraged to take an increasingly active role in their diabetes care from an early stage. leading to hyperglycaemia and ketosis.PA EDIATRICS I Peer Reviewed such as coeliac disease and Addison’s disease can increase the risk of hypoglycaemia. SICK-DAY MANAGEMENT Diabetes control may deteriorate during periods of intercurrent illness. there is an increased rate of DM-related hospitalizations in the 2 years after transition to adult care. a phenomenon termed metabolic memory. TRANSITION TO ADULT CARE The transition period from paediatric to adult DM care can be a daunting time for the patient and family. In anticipation of this. Alternatively.
These substantial advances should be made known to young people and their families as reason for hope. and the organization of health services. and direct insulin-sensitizing agents (metformin. Furthermore. Advances continue in the understanding of the pathogenesis of DM. and cerebrovascular disease). or cardiac arrest • Despite advances in monitoring devices.18 Research to develop an effective extracorporeal artificial pancreas is ongoing. alpha glucosidase inhibitors (acarbose). Recommendations for screening for complications are summarized by the Canadian Diabetes Association 2008 Clinical Practice Guidelines. Trials 18 thiazolidinediones). such as amylin analogues (pramlintide). bicarbonate should be given only in the setting of life-threatening hyperkalaemia. closedloop insulin delivery systems. a continuous glucose sensor. Cardiovascular disease is the most important cause of the excess mortality associated with diabetes. Patient and 32 family education about complications should begin early and be ongoing. peripheral artery. correcting dyslipidaemia. Other agents that may improve postprandial blood glucose. FUTURE DEVELOPMENTS Pancreatic and islet-cell transplantation has been performed in adults with T1DM for end-stage renal disease or persistent metabolic instability. insulin formulations and delivery systems. Preventive measures include maintaining normal blood pressure. in addition to optimizing glycaemic control. The long-term safety and effectiveness of these agents for the management of T1DM in young people remain uncertain. only 10% of patients were insulin-independent at 5 years after islet-cell transplantation. especially in the area of genetic susceptibility. and as an impetus to maintain the best possible metabolic control. including insulin-sensitizing therapies such as recombinant human insulin-like growth factor 1. CONCLUSION T1DM in young people remains a common and challenging condition. growth hormone suppressors or antagonists. insulin preparations and delivery mechanisms.33 Other strategies to improve the effectiveness of subcutaneous insulin action in T1DM have been proposed. This system involves an insulin pump to deliver insulin. and glucagon-like peptide 1 analogues have also been studied. avoiding smoking. and participating in regular exercise. emphasizing the proven benefit of excellent glycaemic control. 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 an effective algorithm to alter insulin delivery based on real-time glucose sensor inputs. inotrope-resistant shock. 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 . Significant improvements have been made in the development of glucose monitors.PAEDIATRICS I PAEDIATRICS Peer Reviewed cular complications (coronary artery. pharmacological interventions for high-risk young people with T1DM will provide cardio-renal protection. These procedures carry significant risks related to the procedures themselves and the need for chronic immunosuppression. many children and adolescents (especially) with T1DM fail to achieve their age-appropriate glycaemic targets • Ongoing research in the area of islet-cell transplantation. A multidisciplinary approach to the care of young people with T1DM should are ongoing to determine whether.
146:693–700. and management. N Engl J Med 2005. 22. Rebrin K. Bruining J. Further Reading Daneman D. Barrett JC. Pediatr Diabetes 2009. Neu A. Daneman D. Nat Genet 2009. 5.55:3344–3350. ISPAD clinical practice consensus guidelines 2009 compendium. 6. Insulin treatment. Tamborlane WV. Deeb LC. Tossavainen PH. Sperling MA. Incidence trends for childhood type 1 diabetes in Europe during 1989–2003 and predicted new cases 2005–20: a multicentre prospective registration study. et al.31:1978– 1982. Clar C. Mackenzie T. Guttmann A. Panagiotopoulos C.30:2245– 2250. Colton PA. Skinner CT. Diabetes Care 2008.89:188–194. The use of insulin pump therapy in the pediatric age group. 2009. Zeitler P. 29. Saad MF.30:72–79. Diabetes Atlas. Pediatr Diabetes 2009. et al. Routine hospital admission versus out-patient or home care in children at diagnosis of type 1 diabetes mellitus. de Beaufort CE. Goldstein D. Geographical variation of presentation at diagnosis of type I diabetes in children: the EURODIAB study. Continuing stability of center differences in pediatric diabetes care: do advances in diabetes treatment improve outcome? The Hvidøre Study Group on Childhood Diabetes. 10. Thomas S. de Beaufort CE. Arch Dis Child 2004. Buccino J. and monogenic diabetes in Canadian children: a prospective national surveillance study. Olmsted MP. Rewers A. White NH. Feasibility of automating insulin delivery for the treatment of type 1 diabetes. N Engl J Med 1993. Chase HP. Malone J. ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. Wherrett DK. 23. Pinhas-Hamiel O. Diabetes Care 2005. Rewers A. EURODIAB Study Group. Brussels: Federation ID. Diabetes Care 2010. Type 2 diabetes. Donaghue KC.287:2511–2518. Diabet Med 2006. Donaghue KC. Diabetes 2006. References 1.373:2027–2033. Shalitin S.89:1138–1144. Dunger DB. Feldhahn L. Pediatrics 2009. Dunger DB. 3.51:3353– 3361. Arch Dis Child 2004. Transition to adult care for youths with diabetes mellitus: findings from a Universal Health Care System. Predictors of acute complications in children with type 1 diabetes. Patterson CC. Hanas R.139:804–812. 17. Dunger D. Diabetes Care 2007. Rydall AC. Rovner AJ. Hattersley A. Dean HJ. 15. Diabetologia 2001. diagnosis. Pediatr Diabetes 2009. 33. 32. et al. et al. 24. 14.23:857–866. medication-induced diabetes. Shield J. To T. Dahlquist GG. 4. Federation ID. Early diabetes-related complications in adolescents. 27. Perlman K. Competing interests: Denis Daneman has been a member of the Hvidøre International Study Group for Childhood Diabetes sponsored by Novo Nordisk Inc.28:186–212.33:786–791. Bangstad HJ.10(suppl 12):33–42. Sperling MA.353:2643–2653. 25. Daneman D. Rachmiel M. Levy-Marchal C.124:e1134–e1141. et al. Pediatr Diabetes 2005. 8. 19.10 (suppl 12):1–2. Green A. 31. Daneman D. Acerini CL. JPOG MAR/APR 2012 • 58 . Pediatr Diabetes 2009. © 2010 Elsevier Ltd. Daneman D. JAMA 2002.41:703–707. Canada. Dahms W. ISPAD clinical practice consensus guidelines 2006–2007. 18. Pediatr Endocrinol Rev 2007. Patterson CC. Type 1 diabetes and exercise: using the insulin pump to maximum advantage. Skinner CT.10:468–473. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. et al. Cleary PA. Self-monitoring of blood glucose in children and teens with diabetes. Perkins B. Backlund JY. About the Authors Rayzel M Shulman is currently pursuing a PhD at the University of Toronto. Hub R.24:239–244. Gale EAM. Ranke MB. Hariri F. Nathan DM. Exercise and type 1 diabetes mellitus in youth. Cleary PA. Dunger DB. Can J Diabetes 2008. 28. 16. Arch Dis Child 2004. Swift PGF. 2. Silverstein J. Care of children and adolescents with type 1 diabetes. et al. J Pediatr 2005. 13. Diabetes Educ 2009. EURODIAB ACE Study Group.70:14–21.(2):CD004099. Status and rationale of renoprotection studies in adolescents with type 1 diabetes.30:2245–2250. Concannon P.38(12): 679–685.5:656–665. Riddell M. The rise of childhood type 1 diabetes in the 20th century. 12. et al. Njolstad P. The global spread of type 2 diabetes mellitus in children and adolescents. Cochrane Database of Syst Rev 2007. Klingensmith G. 30. Acquired non-type 1 diabetes in childhood: subtypes. Swift PG. Denis Daneman is Paediatrician-in-Chief at SickKids and Chair of the Department of Pediatrics at the University of Toronto. et al. Klingensmith G. DIARY Group Baden- Württemberg. Eisenbarth GS. Steil GM. Horm Res 2005. Nakhla M. Assessment and management of hypoglycemia in children and adolescents with diabetes. in the context of a healthy and supportive physical and psychosocial environment. Endocrinol Metab Clin North Am 2009.329:977–986. 26. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. Gyurus E. review and recommendations. Type 1 diabetes: recent developments. Rodin GM. Diagnosis and classification of diabetes mellitus.35:97– 107.10(suppl 12):134–145. Incidence and trends of childhood type 1 diabetes worldwide 1990–1999. ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. Lancet 2009. Continuing stability of center differences in pediatric diabetes care: do advances in diabetes treatment improve outcome? The Hvidøre Study Group on Childhood Diabetes. Can J Diabetes 2006. 7. Liu E. Clayton DG.328:750–754. et al. Pediatr Diabetes 2009. Marcovecchio ML. Diabetes 2002. Ontario. BMJ 2004.44(suppl 3):B75–B80.38:777–790.PA EDIATRICS I Peer Reviewed emphasize optimal metabolic control with minimal hypoglycaemia. Amed S. Diabetes Care 2007. Factors influencing glycemic control in young people with type 1 diabetes in Scotland: a population-based study (DIABAUD2). Diabetes Care 2010. Pediatr Diabetes 2007. Scottish Study Group for the Care of the Young D. Bui H. Waugh N. Klingensmith GJ. The Diabetes Control and Complications Trial Research Group. Paradis G. Devendra D. 11. Porter JR. Swift PG. Acerini CL. Genome-wide association study and meta-analysis find that over 40 loci affect risk 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.6:50–62. Beneficial effects of intensive therapy of diabetes during adolescence: outcomes after the conclusion of the Diabetes Control and Complications Trial (DCCT). Horm Res 2008.89:188–194. Jones T.63:75–85.32(suppl 1). Prediction of the onset of disturbed eating behavior in adolescent girls with type 1 diabetes. 21. Barrett TG. Competing interests: Rayzel Shulman received the 2009/10 Canadian Pediatric Endocrine Group (CPEG) Fellowship sponsored by Novo Nordisk Canada. The diagnosis and management of monogenic diabetes in children and adolescents. Ehehalt S. Canada. Prevention of type 1 diabetes. Daneman D.10:347–355. Danne T. Initially published in Medicine 2010. Phillip M. Diabetes Care 2001. et al. 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.8:88–102. Darwin C. 20. Copeland K. J Pediatr 2001. Nansel TR. Are children with type 1 diabetes consuming a healthful diet? A review of the current evidence and strategies for dietary change. Clarke W.33(suppl 1):S62–69. Ontario. 9.
MPHC. aged 5 years old. An opportunistic health check revealed that three of her top front teeth had rotted away to below the gum line. BDS. MPH Figure 1 CASE SCENARIO Tracey. confirmed that Tracey brushed her teeth and rather defensively asserted that Tracey had been born with ‘soft teeth’. Kaye Roberts-Thomson.IN P ractice I IN PRACTICE Peer Reviewed Clinical Case Rotting Teeth in a Young Girl Simon Wooley. Her mother denied that Tracey excessively consumed sweets or sweet drinks. was brought in to my clinic from an outlying rural community to receive her immunizations before starting school. 79) JPOG MAR/APR 2012 • 59 . BDSc. She also had several carious teeth towards the back of her mouth. How should the current situation be handled? Will the secondary dentition suffer? (Answers on p.
accompanied by loss of the usual vaginal acidity. About 50% of cases are asymptomatic. 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. the prevalence of bacterial vaginosis is 10–20%. MBBS. In 1983.1 Women with symptomatic bacterial vaginosis report an offensive.GYN PA AECOLOGY EDIATRICS I Peer Reviewed Imaging Paediatric Bacterial BrainVaginosis Tumours Phillip Hay. This recognized the fact that many anaerobic or facultative anaerobic bacteria are present and that classical signs of inflammation are absent.4 The strongest evidence against it being an STI has come from studies reporting similar rates in self-reported virgin and non-virgin women. fishy-smelling discharge that is most noticeable after unprotected intercourse or at the time of menstruation. The diagnosis can be confirmed by microscopy ± additional tests. B acterial vaginosis is the most common cause of abnormal vaginal discharge in women of childbearing age. MBBS. FRCR. and is a risk factor for the acquisition of sexually transmitted infections (STIs) including human immunodeficiency virus (HIV). Bacterial vaginosis is associated with infective complications in pregnancy and following gynaecological surgery. FRCP Tang Phua Hwee. the term ‘bacterial vaginosis’ replaced the older term ‘Gardnerella vaginitis’.3 The debate about whether bacterial vaginosis is an STI or merely sexually associated continues. MMed Diagnostic Radiology anaerobes. A meta-analysis has concluded that bacterial vaginosis has the characteristics of an STI: being associated with partner change and other STIs. 5–7 This has been chalJPOG MAR/APR 2012 • 60 . but it may be as high as 36% in women attending STI clinics and 28% in those seeking elective termination of pregnancy. 2 A prevalence of more than 50% was reported in rural Uganda.
with Atopobium vaginae the only other numerically important organism. defensins. the biofilm covered the entire biopsy. Table 1. The triggers for bacterial vaginosis are probably multiple. 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. Gardnerella accounted for 90% of bacteria seen in the biofilm. The organisms classically associated with bacterial vaginosis using culture and those more recently identified using molecular techniques 9. typically fishy-smelling vaginal discharge. 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. it was more patchy. Speculum examination shows a thin. which reduces the inhibitory effect of H 2O 2 on anaerobic growth. H2O2. although other organisms may be present in small numbers.12 Any of the Amsel criteria can. When bacterial vaginosis develops. An increase in vaginal pH from the normal 3. Composite (Amsel) criteria for the diagnosis of bacterial vaginosis • Vaginal pH > 4. DIAGNOSIS Bacterial vaginosis should be suspected in any woman presenting with an offensive. Amsel criteria (Table 2) have been the mainstay of diagnosis in settings such as genitourinary medicine clinics where microscopy can be performed.5 to as high as 7. in others. homogeneous.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.10 Table 2. Lactobacilli predominated in women with normal flora but did not form a biofilm. be misleading: • The appearance of vaginal secretions may be JPOG MAR/APR 2012 • 61 are shown in Table 1. the lactobacilli reduce in concentration and may disappear whilst there is an increased concentration of anaerobic and facultative anaerobic organisms.5–4. 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. It is not known how often bacterial vaginosis occurs in post-menopausal women. however. and bacteriocins. it is associated with black race and intrauterine device use. Hormonal changes and inoculation with organisms from a partner might also be important.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed lenged by a detailed study that reported no bacterial vaginosis in women denying any oral or digital genital contact. Lactobacilli produce inhibitory mediators including lactic acid. . white or yellow discharge adherent to the walls of the vagina. 11 In some women. The condition often arises spontaneously around the time of menstruation and may resolve spontaneously in mid-cycle.8 In many studies.0 is observed.
Gram-positive rods are typical of lactobacilli.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed Figure 1. Large. curved rods. JPOG MAR/APR 2012 • 62 . some Gram-positive and some Gram-negative. Figure 2 Gram-stained vaginal smear from a woman with bacterial vaginosis. Clue cells are not part of most scoring systems for bacterial vaginosis. and none are seen in this field. are present. There are many small bacteria present. Epithelial cells and their nuclei can be seen clearly. typical of Mobiluncus mulieris. Gram-stained vaginal smear from a woman with normal flora.
In cervicitis. and stored slides can be subsequently evaluated independently in research studies. 14 Other Tests Commercially available tests detect biochemical changes in vaginal fluid associated with bacterial vaginosis. the relatively high cost of the currently available tests compared with use of the Gram stain or Amsel criteria has limited their uptake. 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).GYNAECOLOGY I GYNAECOLOGY Peer Reviewed altered by factors such as recent intercourse and douching. • A positive potassium hydroxide test may be found in the presence of semen. Recognition of intermediate categories can be more difficult and entails subjective assessment of the morphotypes. • Both Candida and trichomoniasis can give a similar clinical appearance. It enables recognition of intermediate flora. Debris or degenerate cells can be mistaken for clue cells. Gardnerella is usually a Gram- Lactobacillus-dominated flora to ‘severe bacterial vaginosis’ DIFFERENTIAL DIAGNOSIS lactobacilli (Figure 1). This is recognized in Gram-stain scoring systems but not with Amsel criteria. A simplified scoring sys13 Other common causes of vaginal discharge are cervicitis caused by Chlamydia or gonorrhoea. candidiasis and trichomoniasis. and purulent discharge may be visible in the external os. vaginal pH can be measured using pH-sensitive paper. Curved rods (Mobiluncus species) may be present. In routine practice. 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. Candida typically causes a curd-like discharge and is associated JPOG MAR/APR 2012 • 63 tem (Hay–Ison criteria) has been recommended for . Scoring systems (eg. a high vaginal swab can be sent to the microbiology laboratory for examination by wet mount or Gram staining. • Vaginal pH may be elevated during menstruation or by the presence of semen. and lactobacilli sometimes adhere to epithelial cells in low numbers. offer further testing if symptoms return. • Detection of clue cells is the single most sensitive and specific criterion.5 almost excludes bacterial vaginosis. whereas in bacterial vagino. When the history is highly suggestive of the condition but the tests are negative. all of which can also coexist with bacterial vaginosis. the Nugent) have attempted to reduce interobserver variability. but the interpretation of microscopy is subjective. Typical lactobacilli are large. A pH of less than 4. there may be contact bleeding. use in genitourinary medicine clinics in preference to the Amsel criteria. Gram-positive rods with blunt ends. If the pH is high.(TABLE 3) negative coccus. However.
5–7. Treatment should therefore be prescribed for control of symptoms and in situations in which it might prevent complications of a procedure (eg.0 Microscopy and culture with itching.5 Microscopy and culture ++ 4. Initial concerns about potential teratogenicity have not been substantiated. the value of treating asymptomatic bacterial vaginosis has not been established. homogeneous Cervicitis – – Clear or coloured Mucoid Purulent mucus at cervical os – < 4.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed Table 3.0 Microscopy ± 4.17 Topical treatments with intravaginal 2% clindamycin cream or 0. The cure rate immediately after treatment with metronidazole is up to 95%. About 10% of women develop symptomatic candidiasis following Antibiotics Antibiotics targeting anaerobic organisms should be effective in bacterial vaginosis.75% metronidazole gels are licensed for the treatment of bacterial vaginosis. 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. These organisms can be sought using specific diagnostic tests. Metronidazole and clindamycin are obvious choices. or tinidazole 2 g which is more expensive. but after 4 weeks this declines to 80% in openlabel studies and less than 70% in blinded studies. 18 Oral clindamycin can induce rashes and occasionally pseudomembranous colitis. They are more expensive than oral metronidazole but have similar efficacy and can be useful when systemic treatment is not desirable. zole.5 Microscopy. a metallic taste.5–7. MANAGEMENT Bacterial vaginosis is sometimes distressing and must be managed with sensitivity. tests for Chlamydia and gonorrhoea – < 4. homogeneous Trichomoniasis +++ May be offensive Yellow or green Thin. and alcohol intolerance. Adverse Effects of Treatment Oral metronidazole is associated with nausea. The standard treatment for bacterial vaginosis is metronidaJPOG MAR/APR 2012 • 64 . termination of pregnancy) or in pregnancy. Because it has a relapsing–remitting course in many women. Allergic rashes occur occasionally. There is also no evidence that treatment reduces the prevalence in the community.15.16 An alternative is a 2-g single dose. and metronidazole can be used in pregnancy. fishy White or yellow Thin. 400 mg orally 12-hourly for 5–7 days. Trichomonas causes a more purulent discharge and is associated with soreness and erythema.
accompanied by an antifungal agent if there is a history of candidiasis. Management of such cases is difficult. It is thought that women with bacterial vaginosis are at increased risk of chorioamnionitis. The author usually prescribes metro21 COMPLICATIONS Pregnancy Bacterial vaginosis is associated with second-trimester miscarriage and preterm birth. Many physicians advocate screening for STIs in the partners of women with recurrent bacterial vaginosis. The reported odds ratio is 1.22 Several studies have assessed the value of screening for and treatment of bacterial vaginosis in preventing adverse outcomes in pregnancy. One study showed that use of metronidazole gel twice weekly reduced the rate of relapse. the probiotics or lactic acid gel may help to prevent relapse. she should avoid contact between the shampoo and the vulval area. placebo-controlled trials have failed to show any difference in bacterial vaginosis relapse rates following treatment of male partners with metronidazole. possibly including bacterial vaginosis. Male Partners Four double-blind.4–7. but this is not based on prospective studies.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed treatment of bacterial vaginosis.20 bubble bath should be avoided. so there is insufficient evidence to support their routine use in current guidelines. It is reasonable to screen the sex partner for infections. bacterial vaginosis recurs frequently following treatment. If available. Vaginal lactobacilli differ from those considered optimal for the gut. Alternative Treatments Probiotics and prebiotics have been studied as a treatment for gastrointestinal conditions. although it was associated with increased rates of candidiasis. Relapses In some women. Patient Advice and Self-help Vaginal douching and the use of shower gel and . 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.0. but several vaginal strains are now available. tinidazole or clindamycin. The results have been variable. If the woman washes her hair in the shower. Bacterial vaginosis is sometimes distressing and must be managed with sensitivity. 19. It is sensible to use condoms with new sex partners to protect against infections. Both approaches have been evaluated in small studies of variable quality. which can stimulate preterm birth through the release of proinflammatory cytokines. otherwise regular antibiotic treatment is the only option. Another approach is to use lactic acid gel to acidify the vagina.
2% in a placebo-treated group and 3. A double-blind.GYNAECOLO GY G YNAECOLOGY I Peer Reviewed What’s new? • Molecular techniques have identified several new organisms in bacterial vaginosis. 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. hysteroscopy. but symptomatic women should be treated tis in women without Chlamydia was 12. The potential role of bacterial vaginosis in infections following intrauterine device insertion. wound infection and abscess formation after hysterectomy. and dilatation and curettage has not been systematically studied. 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 . 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.23 On the basis of these studies.26 Other Gynaecological Surgery Bacterial vaginosis has been associated with vaginal cuff cellulitis. No randomized trials have been performed to investigate the value of screening and treatment before such surgery. Bacterial vaginosis also confers an increased risk and may be present in almost 30% of such women. This was confirmed by the most recent Cochrane review. it cannot be concluded that antibiotic treatment of bacterial vaginosis in pregnancy will universally reduce the incidence of preterm birth.25 A more recent randomized controlled trial in Sweden found rates. 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 the largest study to date showed no benefit from treatment with short courses of metronidazole. 24 a fourfold reduction in infective complications with clindamycin cream compared with placebo.8% in those prescribed oral metronidazole before termination.75% metronidazole gel • Routine screening and treatment in pregnancy to prevent preterm birth are not recommended.
Safety of metronidazole in pregnancy: a meta-analysis. 3. Ison CA. Obstet Gynecol 2005. its control will become an important public health issue in many countries. Gordon A. Burtin P. Clinical Effectiveness Group. Am J Obstet Gynecol 1955. hydrogen peroxide produced by lactobacilli can inhibit HIV in vitro and is absent in most women with bacterial vaginosis. AIDS 1998. Shafer MA. Treatment with 2% clindamycin vaginal cream prior to first trimester surgical abortion to reduce signs of postoperative infection: a prospective.342:1500–1507.106:1013–1023. Goldenberg RL. Fethers KA. Haemophilus vaginalis vaginitis. Ison CA. Clin Infect Dis 2008. et al. British Association for Sexual Health and HIV. Hay P. 12. 8. Buesching WJ.117:225–228. BMC Microbiol 2004. Hay PE. Campbell CJ.200:1662–1670. Additionally. Initial reports identified genital ulcer STIs as co-factors for transmission. 10. Platz-Christensen JJ. BJOG 2010. J Infect Dis 2009. 9. 2006. N Engl J Med 2005. Obstet Gynecol 2003. Platz-Christensen JJ.55:1–94. et al.79:390–396. Bacterial vaginosis in virginal and sexually active adolescent females: evidence against exclusive sexual transmission. Adherent biofilms in bacterial vaginosis.GYNAECOLOGY I GYNAECOLOGY Peer Reviewed and South East Asia in the last two decades. MendlingW. et al. Sexual risk factors and bacterial vaginosis: a systematic review and meta-analysis. placebo-controlled.22:82–86. Am J Obstet Gynecol 1988. Ferris D.342:534–540. Bump RC. therefore. et al. Genitourin Med 1992. et al. N Engl J Med 2000. which included a course of metronidazole. Gray RH. Tassone D. Am J Obstet Gynecol 2006. intermittent ‘mass treatment’. Sexually transmitted diseases treatment guidelines. A randomized. Curr Opin Infect Dis 2009. Larsson PG. Antibiotics for treating bacterial vaginosis in pregnancy. Morton A. Swidsinski A. Intrauterine infection and preterm delivery. Initially published in Medicine 2010. 13.194:1283–1289.org/documents/62/62. Gardner HL. Clin Ther 2008. Fiedler TL. did not reduce the prevalence of bacterial vaginosis.172:525–529.353:1899–1911.12:1211– 1225. 6. Blackwell AL. Taddio A.69:962–976. Hauth JC.342:206–210. Bacterial vaginosis in sexually experienced and non-sexually experienced young women entering the military. Boyer CB. et al. 22. Pahlson C. Koumans EH. Dukes CD. Bradshaw CS. Potential mechanisms by which bacterial 27 vaginosis might increase HIV transmission include effects on local immune mediators. Nugent RP. 17. 26. Molecular identification of bacteria associated with bacterial vaginosis. Bacterial vaginosis: a diagnostic approach. Rakai. it is not known how to prevent it. Dallabetta GA. MMWR Recomm Rep 2006. 20. © 2010 Elsevier Ltd. Indications for therapy and treatment recommendations for bacterial vaginosis in nonpregnant and pregnant women: a synthesis of data. Incidence of pelvic inflammatory disease after first-trimester legal abortion in women with bacterial vaginosis after treatment with metronidazole: a doubleblind. except in pregnant women. pdf. multicenter study. J Clin Microbiol 1991. 21. Forsum U. Validation of a simplified grading of Gram stained vaginal smears for use in genitourinary medicine clinics.29:297–301. A study of pregnant women in Malawi 3 PREVENTION Because the aetiology of bacterial vaginosis is not fully understood. Loening-Baucke V. Barrons R. 18. Schwebke J.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Hillier SL. Marrazzo JM. About the Author Phillip Hay is Reader in Genitourinary Medicine at St George’s University of London. JPOG MAR/APR 2012 • 67 . 14.38(6): 281–285. Antibiotics inhibit growth of the anaerobes but do not necessarily eliminate the factors that led to the development of bacterial vaginosis. 25. Recurrent bacterial vaginosis. Thomas PD. Sewankambo NK. Am J Obstet Gynecol 1995. 24. Brocklehurst P. Berman SM. Cochrane Database Syst Rev 2007. Cloning of 16S rRNA genes amplified from normal and disturbed vaginal microflora suggests a strong association between Atopobium vaginae. 2006. relapse is relatively common. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. Verhelst R. UK. 5. et al. Sobel JD. Wareham K. Claeys G. 7. References 1. Flinn SD. Klebanoff MA. Am J Obstet Gynecol 1992. Bacterial vaginosis emerged as a cofactor for HIV acquisition in the Rakai study in rural Uganda. 11. Acta Obstet Gynecol Scand 2000. et al. Hogan V. Larsson PG. 27. community trial of intensive sexually transmitted disease control for AIDS prevention. Yen S.78:413–415. Hocking JS.35(suppl 2):S152–S172. et al. Koren G. Fairley CK.(1):CD000262. Thejls H. Carey JC. McDonald HM. Early sexual experiences and risk factors for bacterial vaginosis. 23.158:935– 939. Wawer MJ. If bacterial vaginosis is established as an important risk factor for HIV spread. Hay PE. Gardnerella vaginalis and bacterial vaginosis. Ariburnu O. A newly defined specific infection previously classified ‘‘nonspecific’’ vaginitis. In the Rakai study. Easmon CS. Einarson TR. High prevalence of bacterial vaginosis in adolescent girls in a tropical area of Ecuador. Bacterial vaginosis has also been associated with an increased incidence of non-gonococcal urethritis in male partners. Use of Lactobacillus probiotics for bacterial genitourinary infections in women: a review. Hoover DR. Hauth JC. Moncada J.102:927–933. Health gains from screening for infection of the lower genital tract in women attending for termination of pregnancy. 2. Erazo S. Guadalupe I. 16. N Engl J Med 2000 May 18.30:453–468. Fredricks DN.68:134–138. Gurrin LC. double-blinded. Bacterial vaginosis and disturbances of vaginal flora: association with increased acquisition of HIV. Markowitz LE. Taha TE. Lancet 1993. randomized study.4:16. Krohn MA. Clin Infect Dis 2002. Fethers KA. Fairley CK. Vaca M. 15. 19. Suppressive antibacterial therapy with 0. AIDS 1998 September 10.47:1426–1435.166:100–103.12:1699–1706. 4. Emery SJ. Sex Transm Infect 2002. http://www. Metronidazole to prevent preterm delivery in pregnant women with asymptomatic bacterial vaginosis. Verstraelen H.bashh. National guideline for the management of bacterial vaginosis. Dalaker K. Andrews WW. Uganda. Workowski KA.3 reported bacterial vaginosis to be associated with HIV acquisition during pregnancy and the postnatal period.
However. by 1 year of age in 60%.PA EDIATRICS I Peer Reviewed Atopic Dermatitis in Children: A Practical Approach Triveni Shekariah. Migrant studies reveal that AD prevalence increases in populations that move from an area of low to high prevalence. Prevalence in children in UK is up to 20%. supporting the role of environmental factors in the expression of AD. Disease onset typically occurs by 6 months of age in 45%. AD is one of the most common skin disorders in children. by 5 years of age. MD. It is possible that epicutaneous sensitization to allergens predisposes to development of asthma and allergic rhinitis. JPOG MAR/APR 2012 • 68 . The prevalence of AD in children has increased steadily over the last three decades of the 20th century. The concept of ‘atopic march’ evolved from clustering of these conditions in the same individuals and families. allergic rhinoconjunctivitis. inflammatory. This is paralleled by increases in the prevalence of asthma. DDVL. Manjunatha Kalavala. Up to 70% of children have a spontaneous remission before adolescence. whereas it continues to increase in younger children. FRCP. 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. eosinophilic oesophagitis. and gastroenteritis. asthma and allergic rhinitis are known as the ‘atopic triad’. MBChB. AD is frequently the first disorder of the atopic triad. MBBS. MD EPIDEMIOLOGY Atopic dermatitis (AD) is a chronic pruritic. and by 5 years of age in 85% of affected infants and children. skin disease that typically begins in early childhood. MRCP. AD. Mazin Alfaham. FRCPCH. 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. In a large multicentre study.
Filaggrin mutations are identified in 30% of European patients with AD. sleep disturbance. Defective epidermal barrier function is a hallmark of AD. is significantly associated with the manifestation and severity of early AD in children. Dry scaly lesions on the scalp. quality of life is impaired owing to pruritus. AETIOLOGY The pathophysiology of AD is not completely understood. Parents of children with moderate to severe AD experience sleep disturbance. The concordance rate for AD is higher among monozygotic twins (77%) than among dizygotic twins (15%). a key protein in barrier function. Reduced ceramide levels. environmental factors and infectious agents in a genetically susceptible individual are thought to result in AD. Mutations in the genes coding for filaggrin. 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 decreased participation in sport and other social activities. Severe AD may result in poor school performance. Erythematous papules and plaques with background oedema typical of infantile atopic dermatitis. In children with AD. behavioural problems. in particular AD. frustration. exhaustion. host immune response. social and financial consequences. May overlap with seborrhoeic dermatitis. Figure 1. This results in increased trans-epidermal water loss and dry skin. low self-esteem. pain. and adverse social interactions. Complex interaction of defects in skin barrier function. restricted activities. . and worry owing to their child’s disease. irritability. might play an important part in early-onset AD and asthma. It will also allow increased trans-epidermal penetration of environmental allergens and triggers inflammation.PAEDIATRICS I PAEDIATRICS Peer Reviewed IMPACT ON THE CHILD AND FAMILY AD has the potential to be a major handicap with considerable personal. and genetic variaJPOG MAR/APR 2012 • 69 Figure 2. Parental atopy.
Scratching increases the binding of S aureus to skin. tion in stratum corneum tryptic enzyme and epidermal collagen may also play a role.PA EDIATRICS I Peer Reviewed Figure 3. Enterotoxins also contrib- . IgE-mediated sensitization occurs several weeks or months later. which correlates with the severity of disease. house dust mite products. Figure 5. Atopic dermatitis on extensor surface of extremities. Inflammation in AD is biphasic. Early-onset AD usually emerges in the absence of detectable IgE-mediated allergic sensitization. Exogenous proteases from Staphylococcus aureus and house dust mites. and food. Keratinocytes in atopic skin produce cytokines that signal dendritic cells to drive helper Tcell (Th)2 polarization. and the use of soaps and detergents further damage the barrier function. S aureus enterotoxins increase the inflammation in AD and provoke the generation of enterotoxin-specific IgE. Lichenified plaques on cubital fossae. 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. an initial Th2 phase precedes a chronic phase in which Th0 cells and Th1 cells are predominant. Antigen-specific IgE is the major recognition structure for allergens on basophils and JPOG MAR/APR 2012 • 70 mast cells. Defective barrier function allows penetration of high-molecular-weight allergens in pollens. Discrete lichenified papules on the dorsum of hands. Figure 4. microbes.
leading to oozing and crusting unrelated to secondary infection. Flare-up of lesions around mouth is common with teething and initiation of solid foods. This argues against a prominent role for histamine in causing AD-related pruritus. kinins and cytokines may play an important role in inducing pruritus. The lesions may remain localized to the face or extend to the trunk and extensor aspects of the JPOG MAR/APR 2012 • 71 . The cytokines generated during inflammation in AD downregulate the natural production of antimicrobial peptides in the epidermis – cathelicidin and defensin. Atopic dermatitis with secondary infection. the latter plays an important role in head and neck eczema. ute to emergence of resistance to topical corticosteroid (TCS) treatment. Periorbital and perioral areas are relatively spared. Antihistamines are not always effective in relieving the pruritus. Nummular lesions on the trunk. AD is more prevalent in urban. Figure 7. The ‘hygiene hypothesis’ postulates that declining family size. are not known. 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. proteases. Clinical Features During the first few months of life. The underlying mechanisms for pruritus. The scalp lesions may represent overlap with seborrhoeic dermatitis. which has potent antiviral activity. It is important to keep in mind contact urticaria to food when the lesions are predominantly around mouth. AD typically affects face and scalp. Intensely pruritic erythematous papules affect cheeks and forehead (Figure 1). Patients with AD are predisposed to eczema herpeticum and eczema vaccinatum because of a reduced production of cathelicidin. The lesions show significant oedema.PAEDIATRICS I PAEDIATRICS Peer Reviewed Figure 6. nuclear families compared with rural areas. Pruritus and dry scaling of scalp are common (Figure 2). the most important symptom of AD. Neuropeptides. This results in increased susceptibility to colonization with Staphylococcus and the yeast Malassezia furfur . This is probably due to irritation caused by saliva and foods.
and anterior thighs Round collections of numerous. Alhough flexural areas are commonly involved. hands. Lymphadenopathy in the severely affected area may be prominent owing to inflammation and secondary bacterial infection. tiny. Generalized dry skin (xerosis) is common. The lesions on the trunk and extremiJPOG MAR/APR 2012 • 72 es are transient and are reversible when the underlying inflammation is controlled. especially on face. scattered. Involvement of the antecubital and popliteal fossae. In Africaribbean children. Nummular lesions tend to be more recalcitrant to topical therapy and are frequently secondarily infected. typical dry scaling erythematous patches of AD. and inaccessibility to scratching and rubbing. 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. perioral area. the lesions of AD are often more papular (follicular AD). sometimes with fine scale. In children 1 year of age or older. skin-coloured to hypopigmented dry spiny papules ≥ 1 cm hypopigmented patches. upper arms Accentuated markings on the palms and soles Groove of the lower eyelid. 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. ankles. Eczema herpeticum. It is important not to confuse them with tinea corporis. instead. ill-defined erythematous patches. extensor aspects of arms. This is because of the combination of increased hydration in the diaper area. lateral aspects of face. Hyperpigmentation is particularly common in lichenified areas. Pruritus is frequently severe. the extensor surface of the arms and legs are involved. Post-inflammatory hypopigmentation or hyperpigmentation is common. protection from triggers by the diaper. and neck is more common in older children and adolescents (Figure 4). The pigmentary chang- extremities. these sites might also be affected in infants and young children. feet. wrist periorbital area. AD typically spares diaper area. some children show an ‘inverse’ pattern with primarily involvement of extensor areas. . Older children are less likely to have the exudative lesions of infancy and.PA EDIATRICS I Peer Reviewed Table 1. exhibit more lichenified papules and plaques representing more chronic disease (Figure 5). However. Scarring is not a prominent feature but might result from secondary infection and deeply excoriated areas. By 8–10 months of age. leading to sleep disturbances. Clinical features seen with increased frequency in children with atopic dermatitis ties are often symmetric. coin-shaped. perhaps because of the friction associated with crawling (Figure 3). especially in darker skinned children.
A personal history of asthma or hay fever (or history of atopic disease in a first-degree relative 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. based on morphology and distribution of lesions. Various diagnostic criteria have been proposed. Eczema herpeticum (Kaposi’s varicelliform eruption) is an explosive development of vesiculopustular eruption in the patches of AD. exudation. severe AD Step 4 Systemic therapy (eg. secondary to herpes simplex virus infection (Figure 8).PAEDIATRICS I PAEDIATRICS Peer Reviewed Table 2. Molluscum contagiosum lesions are often associated with pruritus and eczema around them. and puspresent with similar clinical features and require prompt treatment with systemic antibiotics. Recalcitrant. It is important to keep scabies in mind in a child presenting with generalized pruritic rash. Management strategy for atopic dermatitis (AD) (adopted from Akdis et al). Clustering and umbilication of vesicles are characteristic. Diagnosis Diagnosis is often clinical. S aureus infections are characterized by intense erythema. UV = ultraviolet. 5. Absence of xerosis in the background skin is a clue to scabies. pruritus and chronicity of the disease. Visible flexural eczema (or eczema involving the cheeks/forehead and outer limbs in children under 4). Repeated S aureus infections are common (Figure 7). 3. CyA = cyclosporin A. Positive bacterial cultures in the right clinical context are helpful in diagnosing S aureus infecJPOG MAR/APR 2012 • 73 . Children with AD are also prone to disseminated viral infections. Onset under the age of 2 (not used if child is under 4). emollients. 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. Several clinical signs (Table 1) are seen with increased frequency in children with AD. A history of a general dry skin in the last year. a common cutaneous viral infection in children. identification and addressing of specific trigger factors TCS = topical corticosteroids. History of involvement of the skin creases such as folds of elbows. due to accidental infection with vaccinia virus when children come in contact with adults receiving small pox vaccination. Molluscum contagiosum. 4. fronts of ankles. or around the neck (including cheeks in children under 10). TCI = topical calcineurin inhibitors. Table 2 lists the UK Working Party’s diagnostic criteria. crusting. avoidance of irritants. patients might experience flareup of AD or fail to respond to appropriate therapy. behind the knees. During infective episodes. tends to be more disseminated and difficult to treat. Beta-haemolytic streptococcal infections can Figure 9. and also cause flare-up of AD. although they do occur in non-atopic children. 2. tules. Eczema vaccinatum is disseminated vaccinia viral lesions.
pollen Infections Overheating/sweating Psychological stress Food allergens tion. Dietary restrictions should only be recommended in cases of an established diagnosis of food hypersensitivity. egg or soya. Food allergy may be associated with AD in up to 30% of patients. Chronicity of AD. Potential triggers for atopic dermatitis is important. generally speaking. Direct fluorescent assay helps in rapid diagnosis of eczema herpeticum while viral cultures are confirmatory. A team approach with doctor and nurse experienced in the management of AD works well. accept- . Oral antihistamines are beneficial when aeroallergens are suspected to be triggering AD. 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. Age-appropriate educational sessions for parents are shown to improve objective severity of eczema and quality of life scores. toiletries containing alcohol. When diagnosis is in doubt. Educating the family about the nature of the disease and setting the realistic expectations about the treatment outcomes are crucial. Psychological support from the health-care professionals. It is important to emphasize that avoidance of triggers may result in improvement in AD but not complete cure. Careful history and food diaries are essential. astringents. Substitution of soaps and detergents with bath emollients and emollient-based soap substitutes prevent further dryness and damage to the epidermal barrier. punctuated with flare-ups and secondary infections are frustrating for the child and the parents. 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. A positive IgE or skin prick test does not necessarily indicate an underlying ongoing allergy and might be representing past sensitization. • • • • • • • Harsh detergents/soaps. Atopy patch testing might be useful in some cases with suspected allergy to cow’s milk. Biopsy is rarely performed for diagnosis of AD. smears taken by scraping the floor of the vesicle show multinucleate viral giant cells. particularly when associated with allergic rhinitis. Specific serum IgE for food and skin prick tests in the context of a thorough allergy history might be helpful.PA EDIATRICS I Peer Reviewed Table 3. school and support groups JPOG MAR/APR 2012 • 74 Avoidance of Triggers Potential triggers for AD vary among patients. 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. or fragrances Abrasive clothing (wool or synthetics) Inhalant allergens – dust mite. Step-wise treatment strategy is depicted in Figure 9. Early recognition and treatment of infections help prevent flare-ups. particularly if associated with gut dysmotility or failure to thrive. although some cases are not IgE-mediated. family. Any management decisions have to be made in agreement with the family. MANAGEMENT Developing good rapport with the child and the family is the cornerstone of successful management of AD. animal dander. This will help ensure compliance with the treatment. histology of skin biopsy shows spongiotic dermatitis. When these tests are not available. Common triggers are listed in Table 3.
The role of breastfeeding in the prevention of AD is debatable. an emollient needs to be applied immediately after coming out of the pool to prevent dryness of skin. Exclusive breastfeeding beyond 4 months does not confer specific additional benefit. potent and very potent. cently. Further studies are needed to clarify this issue. It is important to stress that emollients need to be applied continuously even when the skin is not inflamed. while creams and lotions are cosmetically more appealing for application during daytime.05% ointment (very potent) is JPOG MAR/APR 2012 • 75 . a ‘swimming pool’ can be created at home by adding a small amount of household bleach to bath water. The current British system of classification stratifies TCSs into four groups based on the vasoconstrictor assay: mild. Long-term bleach baths. are also shown to reduce the severity of eczema by reducing S aureus infection and colonization. eggs and peanuts. Emollients reduce dryness of skin. 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. In patients with repeated S aureus infections. There is lack of evidence for the role of maternal diet during pregnancy or lactation. Further studies are needed to establish the role of these products in the management of AD. Swimming for 20 minutes three times a week is helpful. After bath. time of the day. 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. anti-proliferative. Clobetasol propionate 0. Parents should be cautioned against uncontrolled restriction diets. A combination of cream/lotion during the day and ointment during night is useful. Application of emollient immediately after the bath (‘soak and seal’) prevents drying up of skin. in addition to intermittent intranasal mupirocin ointment. rather than rubbing. and seasonal and climatic conditions. 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.PAEDIATRICS I PAEDIATRICS Peer Reviewed ance of alternative milk products. Ointments tend to be greasy. moderate. If this is not practical. chlorine in swimming pool water is beneficial in reducing S aureus colonization. patients are asked to try samples of emollients and prescription is issued for the emollient of patient’s choice. particularly in adolescents. and vasoconstrictive actions. fish. gently pat the skin dry with a towel. Emollients Regular application of emollients remains the mainstay of general management of AD. TCSs have anti-inflammatory. Exclusive breastfeeding for the first 4 months decreases the cumulative incidence of AD in the first 2 years of age in high-risk infants. reduce trans-epidermal water loss and also help in reducing pruritus and inflammation. immunosuppressive. Re- Bathing Bathing in lukewarm water with a bath emollient is helpful in skin hydration and removal of exudates and crusts. In our clinic. An involvement of a paediatric dietician is crucial. Topical Corticosteroids Topical corticosteroids remain the first-line treatment for control of flare-ups. However. This applies for foods thought to be highly allergenic such as cow’s milk. The choice of the emollient depends on the individual skin status. Data on the role of probiotics in the prevention of AD in high-risk infants are conflicting. The difference in potency between groups is often dramatic. prolonged bathing in very hot water with strong detergent or bubble baths cause further dryness of the skin. However.
facial and intertriginous areas. Intermittent twice weekly application of fluticasone propionate 0. Repeated studies involving much higher concentrations of TCIs failed to show systemic absorption.PA EDIATRICS I Peer Reviewed ~1. A frequently observed side effect is transient burning sensation at the application site. TCIs have high molecular weight (more than 800 kDa). Prolonged use of TCSs might result in loss of efficacy by ‘tachyphylaxis’. they are useful treatment options for sensitive skin areas such as face and intertriginous area. Sequential use of TCIs with TCSs reduces the number of flare-ups.05% cream up to 24 weeks is shown to reduce the number of flare-ups. followed by changeover to low-potency preparation for longer period is also effective. Prolonged use of potent TCSs is associated with local and systemic side effects. rosacea. with continued use. growth retardation. but they should not be used in the presence of infection.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). Addressing these conJPOG MAR/APR 2012 • 76 cerns is important to ensure compliance and avoid suboptimal treatment. After this period. However. telangiectasia. and reduced bone mineral density. this sensation will subside. Concerns about lymphomas and systemic . Relatively new TCS preparations like mometasone furoate and fluticasone propionate have lower atrophogenic potential. Therefore. 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. hypopigmentation. steroid-free therapeutic alternative in the management of AD. The choice of an adequate vehicle is important to achieve optimal therapeutic effect.800 times more potent than hydrocortisone 1% ointment (mild). Clearance of patches of eczema by application of appropriate-strength TCSs for few days is followed by application of tacrolimus 0. Ointments are preferred for treatment of dry lichenified patches as they are associated with better penetration and efficacy. these complications are rare when TCSs are used judiciously. TCS preparations should be applied no more than twice daily. perioral dermatitis. Alternatively. the frequency of topical tacrolimus is reduced to two or three times a week for a period of up to 12 months. S aureus enterotoxin contributes to the emergence of resistance to TCSs.03% ointment twice daily for 2–6 weeks. acne. Local side effects include atrophy. Topical Calcineurin Inhibitors Tacrolimus 0. A potent TCS can be used intermittently for short periods of time to control the flare-ups. cataracts. They provide an effective. Molecules above 500 kDa have limited potential for systemic absorption. Cushing’s syndrome. Concerns about adverse effects have resulted in ‘steroid phobia’ in parents. TCIs block the production and release of proinflammatory cytokines after antigen-specific or non-specific activation of T cells and mast cells. One study showed slightly increased risk of herpes simplex virus infection. However. Children with atopic eczema and their caregivers should be informed that TCSs and TCIs should be applied only to areas of active atopic eczema. Systemic absorption might result in suppression of hypothalamic-pituitary-adrenal axis. TCIs are not associated with atrophy as they do not inhibit collagen synthesis. striae. if skin lesions remain well controlled. Only mild to moderately potent preparations should be used on genital. TCSs are also used sequentially with topical calcineurin inhibitors (TCIs). TCIs are not associated with increased incidence of bacterial infections. which may include areas of broken skin. and glaucoma. an initial therapy with a potent TCS.
One FTU is 0. Application of topical agents is time-consuming. Such treatments are initiated after involving a dermatologist. Anecdotally. CONCLUSIONS AD is a common. However. Systemic Therapies Second-line therapies in the form of phototherapy or systemic immunomodulatory medications such as prednisolone. Wet wraps increase skin hydration. Topical emollients with antiseptics may help Wet Wraps Wet wraps are useful in treating the refractory areas.5 g of ointment or cream. Antimicrobial Agents The skin of children with AD is heavily colonized with S aureus . chronic skin disease that starts JPOG MAR/APR 2012 • 77 . promote penetration of topical medications. defined as the amount of topical medication extending from the tip to the distal interphalangeal crease on the palmar aspect of the index finger. Printed information leaflets available on the British Association of Dermatology website (www. reduce colonization of S aureus. Non-sedating antihistamines are less useful for relieving pruritus. and infections are frequent. Fusidic acid resistance remains high in spite of local community guidelines to restrict the use of this topical antibiotic. The fingertip unit (FTU). Wet wraps with once-daily application of TCSs is an effective short-term intervention. they may benefit patients with allergic triggers.org. Bleach baths in addition to topical nasal mupirocin will help reduce the number of infections and need for antibiotics.PAEDIATRICS I PAEDIATRICS Peer Reviewed malignancy have not been substantiated by large population-based studies. azathioprine. Wet wraps should not be used in the presence of infection. risks and benefits have to be discussed in detail and parents be given sufficient time to make decisions. is a useful guide to estimate the amount of topical medication needed to cover a given area. Topical antibiotics should be used with caution to prevent emergence of resistant strains and contact sensitization. melatonin has been beneficial in some cases. Both the child and parents need constant encouragement and advice on quantity of medication to be used. although they probably do not have direct effects on the pruritus associated with AD. A wide variety of wet-wrap techniques have been used. Patient education and close supervision by experienced medical staff are essential. or promote skin dryness.bad. cyclosporine. As these modalities involve frequent visits to the hospital and blood tests for monitoring side effects. Incorrect use of wet wraps may cause maceration of the skin and secondary infections. effects of longterm use of TCIs on immune surveillance in the skin are not known. Long-term follow-up studies and careful photo-protection measures are advisable. and mycophenolate are reserved for severe AD not responding to optimum topical therapy. and serve as an effective barrier to scratching. However. Prompt recognition and treatment with topical and oral antibiotics will help clear the infection and control the flare-up of AD.uk) are useful. Adjunctive Therapy Sedating antihistamines such as hydroxyzine and chlorpheniramine maleate are useful in improving sleep during flare-ups. and some of the topical preparations can sting particularly during acute flare-ups. Viral and fungal infections need to be recognized early and treated promptly to prevent dissemination. One FTU is sufficient to cover an area of two adult hand areas. particularly on the limbs.
A practical guide to topical therapy in children.358:1483–1494. Long CC. and (4) using a team-oriented approach that includes primary care physicians. Glamorgan House. 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. but a careful approach with dose and duration is always prudent.21:105–113.K. Lancet 1998. Available at: http://guidance.org. • The use of topical calcineurin inhibitors (TCIs) would decrease the need for TCSs. UK. Manjunatha Kalavala is Consultant in Dermatology and Paediatric Dermatology at The Welsh Institute of Dermatology. Glamorgan House. particularly those who are prone to frequent flares and need AD treatment in sensitive skin areas. nurses. Worldwide variation in prevalence of symptoms of asthma. Cardiff. 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.21(3):112–118. Atopic dermatitis. Regular use of emollients and intermittent use of TCSs remain the cornerstone of therapy. Heath Park. Independent hospital validation. in general. psychologists. Br J Dermatol 1994.61:969–987. . Heath Park. Allergy 2006. Concern about skin cancer from TCIs seems unfounded. In conjunction with these pharmacological treatments. Working Party’s diagnostic criteria for atopic dermatitis. (3) approaching trigger avoidance carefully and with the understanding that. Asthma and Immunology/PRACTALL Consensus Report. specialists.38:441–446. Cardiff. timing of introduction of complementary foods. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction. III. University Hospital of Wales. Mazin Alfaham is Consultant Paediatrician at the Children’s Hospital. • 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.PA EDIATRICS I Peer Reviewed Learning points fessionals to better achieve long-term success for patients with AD. • Moisturizing the skin with regular daily topical emollients would help to reduce itching and minimize the frequency of relapses. Nat Genet 2006. December 2007. early in life and can adversely affect a child’s overall health and development. • Under-treatment. steroid-sparing alternative for appropriate patients. Bieber T. Is eczema really on the increase worldwide? J Allergy Clin Immunol 2008. Bieber T. University Hospital of Wales. University Hospital of Wales.61:969–987. and atopic eczema: ISAAC.131:406– 416. Cardiff. PRACTALL Consensus Group. TCIs have been shown to provide an effective. Kemp AS. American Academy of Pediatrics Committee on Nutrition and Section on Allergy and Immunology. Br J Dermatol 1998. behavioural therapists.121:947– 954.uk/CG57. Initially published in Paediatrics and Child Health 2011. breastfeeding. Pediatrics 2008. Mills CM. • Management should include a holistic approach. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/ American Academy of Allergy. Management of atopic eczema in children from birth up to the age of 12 years. (2) appreciating the compromised epidermal barrier and the importance of proper skin care. ISAAC Phase One and Three Study Groups. Heath Park. N Engl J Med 2008. Akdis M. Finlay AY. et al. © 2011 Elsevier Ltd. the overall management depends on (1) educating caregivers about AD’s chronic.351:1225–1232. Clinical guidelines CG57. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis.121:183–191.138:293–296. Cost of illness of atopic dermatitis in children: a societal perspective. UK. Allergy 2006. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/ American Academy of Allergy. and hydrolyzed formulas. Asthma and Immunology/PRACTALL Consensus Report. • Intermittent topical corticosteroids (TCSs) are the main antiinflammatory agents in the management of atopic dermatitis (AD). The U. allergic rhinoconjunctivitis. usually through fear of side effects. Pharmacoeconomics 2003. UK. unpredictable course characterized by flares that can occur despite best efforts. AD is a multifactorial disease. Further Reading Akdis CA.nice.
the first priority is to highlight to Tracey’s mother the need for prompt dental referral and assessment.sa. 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. were hospitalized for dental extractions and restorations. 8. 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. and to improve the early identification and referral (to public or private practitioners) of children experiencing tooth decay (see www. including assessment of the expected exfoliation of the deciduous teeth in question. This information would be reinforced by the dental clinician. Treatment recommended by a dental practitioner would be subject to a detailed history and examination. It is typically associated with prolonged exposure (such as comfort sucking while sleeping) to JPOG MAR/APR 2012 • 79 Figure 1 . BDSc.000 of whom were younger than 5 years of age. BDS. In the case scenario presented here.000 Australian children. The need for a general anaesthetic is a real possibility. MPH Answer: COMMENTARY This case is a stark reminder that few preschool children access dental care.IN P ractice I IN PRACTICE Peer Reviewed Clinical Case Rotting Teeth in a Young Girl Simon Wooley. and the ability of the child to cope with treatment in the dental chair. this being especially difficult in rural and remote areas. most of which were preventable. To this end. the severity and extent of the decay in general.au for details.sadental. 28. MPHC. including a photographic guide/tool to assist caries identification). 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. In 2008/2009.gov. Kaye Roberts-Thomson. Early childhood caries generally affects the upper front deciduous teeth but can affect all teeth.
© 2011 Medicine Today Pty Ltd.au (accessed June 2011).12(7):63–64. Dental health of Australia’s teenagers and pre-teen children: the Child Dental Health Survey. SA. which might otherwise have been avoidable. Australia. this should begin at 18 months of age • inadequate oral hygiene and plaque removal. Aust Dent J 2005. Sanders AE. All health practitioners can play an active role in the prevention of tooth decay and early intervention if they ‘lift the lip’. Available online at: www.IN Practice PRACTICE In I Peer Reviewed a sweet drink (eg. there is an increased risk of space loss and crowding in the secondary dentition. Professor Roberts-Thomson is the Director of the Australian Research Centre for Population Oral Health. This is especially so in rural and remote areas where exposure to fluoride and access to clinical dental care may be problematic. Spencer AJ. The model of decay as a ‘balance’ between demineralization (risk factors) and remineralization (protective factors) of teeth is useful. . Protective or remineralization factors include the following: • tap water is the best drink (fluoridated ideally) to satisfy thirst • after 6 months of age. Decay is a dynamic process of demineralization/ remineralization. Should a deciduous tooth require premature extraction. Adelaide. Brennan DS. which is potentially reversible when confined to enamel. University of Adelaide. these are relatively uncommon and are often not carious. Australian Institute of Health and Welfare. Reprinted with permission. The aim is to minimize the risk factor exposure and maximize the protective factors – that is.gov. Deciduous and permanent teeth can have development defects of enamel and dentine (hypoplasia). Australian Research Centre for Population Oral Health. Australian hospital statistics 2008–09. 52.sa. Canberra: Australian Institute of Health and Welfare. HSE 84. Health services series no. Of the total incidence of tooth decay. Canberra: Australian Institute of Health and Welfare. Further Reading Armfield JM. juice). Do LG. based on the remote Anangu Pitjantjatjaraku Yankunytjatjaraku Lands of South Australia. subject to the severity and timing of the infection to coincide with the development of the successor crown. Slade GD. 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). parents should assist children with brushing up to about the age of 8 years. 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. 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. Dental statistics and research series no. High caries children in Australia: a ‘tail’ of caries distribution. Bill CJ.50:204–206. the outer layer of the tooth.sadental. an abscessed deciduous tooth has the potential to affect the development of the permanent successor. 2009. Initially published in Medicine Today July 2011. Although uncommon. DEN 199. Risk factors for dental caries in the five-year-old SA population. Good oral health is important to general health. 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). particularly sleeping with a bottle • delaying commencement of tooth brushing with a junior fluoride toothpaste. Upper permanent incisors usually have completed their crown development by a year or two before the expected eruption at about 6 years of age.51:130–139. cordial. 2010. CONCLUSION Good oral health in young children is declining. no. 80% is experienced by 20% of young children (those under the age of 6 years). This risk is greater for early loss of posterior deciduous teeth as compared with anteriors. Cat. South Australian Dental Service [website]. About the Authors Dr Wooley is a Dental Practitioner with Nganampa Health Council. Almost 44% of 5-year-olds in Australia have tooth decay. Cat. 17. to tip the ‘balance’ in favour of remineralization. This may necessitate space maintenance for the permanent successor and/or future orthodontic assessment and intervention. however. soft drink. Australia 2003–04. Aust Dent J 2006. no.
proven additive e ect on hot ushes1 . ASBMR 1998 3) Keil D. et al.Recommend low dose HRT. Novofem® Start in time with convincing cycle regulation.. 5(4): 250-251. Low dose human oestrogen NETA . 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...proven additive e ect on bone protection2 Convincing cycle regulation3 Easy administration with the unique dispenser References: 1) Notelovitz M et al. Menopause 1998. 62.the progestogen makes the difference: . 2) Mc Clung M et al.
MBBS. providing that there has been at least 2 hours of exposure to the prophylactic antibiotics during labour. FHKAM(O&G). there has been little improvement in the disease treatment. 0.5 while the universal swab-based strategy. MD. which is associated with a high rate of morbidity and mortality (5–10%). MBBS. FHKAM (Paediatrics). 0. FRCPath. FHKAM (Pathology). which is used in the UK. which screening method to use to identify high-risk women is controversial. FRCOG. FRCOG. MRCOG. and the focus thus lies in disease prevention. MBBS. Recent re- About half of GBS meningitis will be complicated by neurodevelopment impairment. BSc. KKW To. BA. MBBS. FHKAM (Paediatrics). FHKCPaed. MRCP. Thomas Li. 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. Because the early-onset disease develops shortly and rapidly after birth. FHKAM(O&G).17). The clinical risk strategy. MBBS. MRCP. The conventional laboratory test for GBS is culture. The aim of this review article is to discuss the current screening methods for GBS in pregnancy. 4 However. was recommended by the Royal College of Obstetricians and Gynaecologists. . INTRODUCTION Group B Streptococcus (GBS) is the commonest cause of severe early-onset neonatal infection. Because of the lack of local data. Teresa WL Ma. which is used in the US and some European countries. Sarah Morag McGhee. KY Wong.1) and the incidence of EOGBS disease (OR. 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].6 was recommended JPOG MAR/APR 2012 • 81 GBS culture remains the reference standard for the detection of GBS colonization in pregnant women.Continuing Medical Education Screening for Group B Streptococcus in Pregnancy KY Leung. and a pilot study in Hong Kong. the updated CDC guidelines. MRCP. 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. DRCOG. FHKAM (O&G). CW Law. MBChB(HK). DCG(HKCOG). GBS colonization in the maternal gastrointestinal and/or genital tracts is a prerequisite for early-onset GBS (EOGBS) disease. 1–3 Prevention (CDC) guidelines in 2002 and 2010. the improvement in laboratory techniques. PhD Glas.
IAP is given to a woman without taking a swab if she has one or more of the risk factors. or b) if the woman has given birth to an infant with invasive GBS disease.000) or rarely death (1:100. or represent missed opportunities for prevention. If a woman gives a history of maternal GBS colonization in her previous pregnancy but without neonatal disease. Universal swab-based screening urinary tract infection or asymptomatic bacteriuria with GBS during pregnancy is indicated.18 Health-care providers should remain alert for signs of sepsis in any newborn infant. prenatal rent pregnancy as the recurrence risk is more than one-third. IAP will be given to the mother.Table 1. the risk-based approach may inappropriately expose 65–85% of women with risk factors who are GBS-negative to antibiotics. there will still be affected infants who lack the typical intrapartum risk factors for GBS infection. the risk of EOGBS disease will be low even if the woman has one of the risk factors. 11 onset neonatal infection. risk factors will be used to determine the .14 1.12 UNIVERSAL SCREENING OR GBS screening will be required in her cur. universal swab-based strategy has However. 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. are born to mothers with a negative GBS screen.9 colonized with GBS at delivery. 10 UNIVERSAL SWAB-BASED STRATEGY Current American and Canadian guidelines recommend routine vaginal/rectal 35–37 weeks of gestation (Table 2).12 If the vaginal/rectal swab or urine cultures show the presence of GBS.2 On the other hand. Side effects of IAP include anaphylaxis (1 in 10. and the current obstetric practice.7. or c) if the GBS status is unknown.swab for GBS screening of women at NOT? Whether to implement universal swabbased strategy or not depends on the local incidence of EOGBS disease. 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. Give intrapartum antibiotics a) if the vaginal/rectal swab or urine cultures show the presence of GBS. Besides.7 If the GBS screening is negative. 8. treatment of Table 2. 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. 2. GBS = group B Streptococcus. Under the risk-based strategy. IAP will be given. 15–17 Furthermore. 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.000). antenatal antibiotics treatment cannot prevent EOGBS disease because per oral antibiotic treatment does not eliminate vaginal or rectal colonization. and a risk factor (as in Table 1) is present.13 If the vaginal/rectal swab shows the presence of GBS. 7. Routine vaginal/rectal swab for GBS screening in women at 35–37 weeks of gestation. In the US. the prevalence of clinical risk factors in EOGBS disease. or if the woman has given birth to an infant with invasive GBS disease.10 If the GBS status is unknown during term labour in the current pregnancy. However. Besides.
28 Alternatively. Taking rectal swabs may cause discomfort or pain. The broth is then subcultured to a blood agar plate. 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. The colonization rate varies from 10% to 30%. still limited.30 The negative predictive value of GBS cultures JPOG MAR/APR 2012 • 83 . If GBS is not identified. pregnant women can collect their own vaginal–rectal screening specimens and give similar GBS yield. Less-educated women may be more reluctant to collect their own samples.27 If processing is delayed. The latter is inspected for GBS after incubation for 18–24 hours. Latex agglutination test 3. intermittent or transient. 24 ate non-nutritive transport medium which can help sustain the viability of GBS in settings where immediate laboratory processing is not possible. The colonization can be permanent.29 Selective broth medium. To save laboratory cost. the clinical riskbased strategy has been recommended in the UK because of the low prevalence of EOGBS disease (0. Rapid test for group B Streptococcus 1. After having been given appropriate instructions. This risk-based strategy can pre5 Table 3.20–22 Perinatal colonization rate is around 50%. such as Todd-Hewitt broth supplemented with nalidixic acid and either gentamicin or colistin. but only 1% becomes infected. This swab-based strategy can prevent 75% of EOGBS disease by giving IAP to 31% of pregnant women. 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. The use of selective broth media can facilitate GBS isolation by preventing the overgrowth of other commensal bacteria in vagina/rectum. 7 BY WHOM? The vaginal–rectal swabs are usually taken by a health-care provider.11 On the other hand. refrigeration (at 4ºC) will be used for storage. the swabs can be placed into the enrichment broth immediately after collection. Optical immunoassays and enzyme immunoassays 4. 25 two separate swabs is preferred over the use of one swab for both sites because of hygienic problem. effective in the UK. re-incubation and re-inspection will be required at 48 hours. DNA probes 5. Processing the swabs within 24 hours of collection is recommended.8 per 1. is inoculated and incubated at 35–37ºC in ambient air or 5% CO2. Fluorescence in situ hybridization 2. 19 11 Universal swab- based strategy was found to be not cost- However. they may prefer a health professional to collect their swabs. data are WHICH SITE? GBS colonization in the maternal gastrointestinal and/or genital tracts is a prerequisite for EOGBS disease. swabs are taken from both the lower vagina (vaginal introitus) and the rectum (through the anal sphincter) instead of from one site alone.Continuing Medical Education been adopted because of the high prevalence of EOGBS (1.000 births) even in the absence of systematic screening or widespread IAP and high prevalence (60–70%) of clinical risk factors in EOGBS disease. An alternative is to take perineal swabs which may be preferred by women. vent 67% of EOGBS by giving IAP to 17% of pregnant women.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.5 per 1. 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. Nucleic acid amplification tests needed for taking lower vagina swabs. To increase the detection rate of GBS colonization. 26 25 However.
Although the results of intrapartum swabs can reflect the GBS status more accurately than those of antepartum swabs. under. women who deliver before 35 weeks of gestation are not screened for GBS. staffing requirements. However. GBS colonization early in pregnancy is not predictive of EOGBS disease because the coloniza t ion can be transient. A change in the GBS colonization status from screening to delivery can occur in 9% of women. the latter increases the turnaround time. However. viable or low-count bacteria 44 and is not affected by the presence of blood. meconium. there are concerns on the real-world turnaround time.0% with use of an enrichment step. were not sensitive and specific enough to replace the established culture method. and costs. 7. shown that the rapid tests (Table 3).18 About 6% of GBS carriers remaining undetected in antenatal cultures. While the sensitivity of NAAT for GBS can be as high as 92.45 More data are needed. The performance of commercially available NAAT on non-enriched samples was variable and not adequate in comparison with culture. or amniotic fluid. 41 A rapid test may be useful for women at term with unknown GBS status and without risk factors. the use of a highly sensitive and specific test with rapid turnaround time can assess intrapartum GBS colonization and hence guide IAP. First. On the other hand. Universal screening using a rapid test was not cost-effective. including DNA probes and nucleic acid amplification 43 tests (NAAT) such as polymerase chain reaction (PCR). specificity and cost. Ideally.42 A rapid PCR test can detect non- . 35–41 It is recommended that a swab for GBS screening be taken at 35–37 weeks’ gestation. including fluorescence in situ hybridization. but it usually takes 24–72 hours to get the results. but preterm newborns are at high risk of developing EOGBS disease. 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. based on its current sensitivity.or overtreatment with IAP may be resulted.34 the culture method may not provide a timely result to guide IAP. optical immunoassays and enzyme immunoassays. Studies have JPOG MAR/APR 2012 • 84 Recently. latex agglutination test.33 The turnaround time of this rapid real-time PCR test can be within 1 hour.5–100. culture-based testing is suitable for antepartum but not intrapartum screening.performed within 5 weeks before delivery is very high (95–98%) but declines beyond 5 weeks.31 It will be appropriate to take a swab for GBS screening at 35–37 weeks.33 Consequently. lack of antimicrobial susceptibility. up to 67% of infants with EOGBS were delivered by mothers who were negative on prenatal GBS screening. molecular testing meth42 ods have been developed.32 Second. Therefore. 30 GBS colonization can be intermittent during pregnancy. availability of 24hour service. there are two disadvantages.
82% of these eligible women accepted the screening. EOGBS is associated with maternal GBS bacteriuria (generally >105 colony-forming units/mL of urine).46 Few data are available on the risk with low (< 10 4) colony-count GBS bacteriuria. 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. GBS screening for GBS. the antibiotics should also be able to cover GBS adequately. (2) screening done privately (24.6%. paediatricians. GBS screening should be performed unless it was performed within 5 weeks. Because of the lack of local data. THE EFFECTS OF UPDATED CDC GUIDELINES7 ON OBSTETRIC PRACTICE Bacteriuria To ensure proper testing.890.UNIVERSAL PRENATAL lin-allergic’ history. (4) planned elective Caesarean section (10. and the incidence of EOGBS was around 0. if any. Threatened Preterm Labour If a woman is admitted with signs and symptoms of labour before 37 weeks’ gestation. Pilot Study There are racial or ethnic differences in EOGBS disease.1 per 1. IAP was given to screen-positive women. and its availability is limited. a 1-year pilot study was conducted in Queen Mary Hospital and Tsan Maternal GBS Colonization Rate During the pilot project which involved 3. After reviewing the procedures of swab taking. 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. In the past. (3) screening deemed unnecessary (20. A working group including obstetricians. NAAT testing is optional. transport medium and laboratory testing.4%). and (5) plan to deliver in a private or other hospital (8.7–1. and then discontinued subsequent. 47 All the swab specimens were sent to the microbiology laboratory of Queen Mary Hospital for testing for GBS. The main reasons for declining GBS screening included (1) unwillingness to undergo screening (35. all pregnant women tion. We noticed a low screen-positive rate (4. seeking antenatal care were invited to participate in this study.SCREENING FOR GBS IN fied on antenatal swabs for GBS screening. all the public hospitals in Hong Kong used the clinical risk-based strategy to prevent EOGBS disease.4%). However.Continuing Medical Education unknown GBS status during intra partum. and microbiologists was formed to study the prevention strategy in 2008. If antibiotics are given to prolong latency for preterm prelabour rupture of membranes. GBS screening should be performed unless it was performed within 5 weeks.5% in subsequent months.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.7%).908 pregnant women. ‘pregnancy’ should be specified when sending urine samples to a laboratory. After explanation and counseling on GBS screening by a midwife. This was consistent with the results of another local study that the prevalence JPOG MAR/APR 2012 • 85 . ‘penicil. should be speci. During the study period from April should be repeated at 35–37 weeks’ gesta. 46 Antibiotic Susceptibility To ensure laboratory testing for antimicrobial susceptibility to clindamycin. 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. the screen-positive rate increased to around 9. The total number of women who underwent GBS screening was 2. Newborn infants born to mothers with GBS colonization were managed according to a protocol. weeks.000 births. an additional GBS prophylaxis should be given for 48 hours unless a GBS screen performed within the preceding 5 weeks was negative.2%) in the first month of screening.2009 to March 2010. GBS testing results should not affect the duration of antibiotics which are given to prolong latency.542 were eligible for screening at 35–37 weeks’ gestation.4%). Otherwise. GBS screening was performed according to the 2002 CDC guidelines.2%). The overall incidence of maternal GBS colonization was 9. 90% or 3.
5%) (P = 0.4%. Improved management of preterm deliveries and improved communication. or missed opportunities for screening. Surprisingly. However.22 Like another local study. The effectiveness of IAP and the rate of receiving IAP were less important. One of them developed meningitis as well.9% of women with GBS colonization. mestic product). the lack of the typical intrapartum risk factors for GBS infection. This result was compatible with the 4% false-negative rate which was reported in the literature. 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. This modelling study has shown that. The ICER was most sensitive to the rates of maternal colonization. This finding is consistent with a study in the US that universal screening was predicted to prevent more EOGBS disease. a risk factor was present in only 12.3%) than women with a parity below 3 (9. There were no adverse events or complaints by patients. The GBS colonization rate was also higher in women with a parity of 3 or above (27. vertical transmission. rent clinical risk factor-based strategy. and blood) were taken from the babies.18 There was no neonatal mortality related to GBS. COST-EFFECTIVENESS ANALYSIS The cost-effectiveness analysis was performed by the Department of Community Medicine using a prediction model. and disability. but at a larger cost than the risk-factor strategy (75% vs 54%. Around 8% of women did not return at 35– 37 weeks’ gestation for GBS screening. the prevalence of clinical risk factors in EOGBS disease. the neonate was not infected. over 80% of simulations found that the swab-based strategy was more cost-effective than the current clinical risk factor-based strategy. There were three cases of EOGBS disease presented with septicaemia. 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. which might not be available during the intrapartum period. 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.004). the mothers declined screening while the screening result was negative in the remaining one. Fortunately.000) per life-year gained. based on the best evidence we have available at present. mortality.000 vs US$3. processing and reporting of culture results may prevent additional Babies During the pilot project.367 (about US$32.of GBS on booking was 10.9%) (P < 0. US$12. collection. There was no major maternal complications related to GBS. The compliJPOG MAR/APR 2012 • 86 . 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. 22 ance to the protocol was.770 swabs (including gastric aspirate. and cost-effectiveness. However. 11 The incremental cost-effectiveness ratio (ICER) was HK$255.001). In two of them.000). a total of 1. colonization rate was significantly higher in health-care professionals (19. Tracing the GBS reports from our electronic medical system was preferred over paper records. good the GBS except for one screen-positive case in which IAP was not given. 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. ear. 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. and the current obstetric practice. In the UK. in general.19 GBS screening in high-risk women would not be cost-effective. as even those with negative results would be better off treated to reduce the risk of EOGBS disease.4%) than in housewives (7. universal prenatal screening cannot prevent all affected infants because of a false-negative result. Universal swabbased strategy and clinical risk-based strategy differ in the proportion of women being given IAP.
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Neonatal early-onset Escherichia coli disease: the effect of intrapartum ampicillin. 17. Evaluation of a novel real-time PCR test based on the ssrA gene for the identification of group B streptococci in vaginal swabs. Real-time PCR assay provides reliable assessment of intrapartum carriage of group B Streptococcus . Shaffer LE. Prevention of early-onset group B streptococcal disease in newborns.117:1055–1066. The University of Hong Kong. Sandhu G. Pearce C.org.35:267–280. Dekker FW. Benitz WE. Crook D. 2003. Kaczorowski J. Ke D. Sharma M.179:879– 883. Colbourn TE. Rapid screening for Streptococcus agalactiae in vaginal specimens of pregnant women by fluorescent in situ hybridization. Rapid diagnosis of vaginal carriage of group B beta haemolytic streptococcus by an enrichment cum antigen detection test. Elfstrom L. 33. 44. Obstet Gynecol 2004. Indian J Med Res 2004. Boyer KM. Obstet Gynecol 2011. May 2001. Am J Obstet Gynecol 2011. Clinical features and epidemiology of septicaemia and meningitis in neonates due to Streptococcus agalactiae in Copenhagen County. 29. 5. Carr MH.Continuing Medical Education cases of EOGBS disease. et al.41:2170– 2173. N Engl J Med 2009. UK. Vaginalperianal compared with vaginal-rectal cultures for detecting group B streptococci during pregnancy. 30. Intrapartum antibiotics for group B streptococcal colonisation. Earlyonset group B streptococcal disease in the era of maternal screening. Leung TN. Alfa MJ. Bergh K. 41. The DEVANI European project. Schrag S. 2.39:1129–1135. 22. Mennemeyer ST. HoutmanRoelofsen RL. 45. 36. J Clin Microbiol 2010. Dörr PJ. Philipson EH. New DNA-based PCR approaches for rapid real-time detection and prevention of group B streptococcal infections in newborns and pregnant women. Schrag SJ. Bergeron MG. Carriage of group B streptococcus in pregnant women from Oxford.104:1062–1076. Smaill F. 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3.8ºC during the intra partum is a risk factor for early-onset group B Streptococcus (GBS) disease. 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. If the vaginal/rectal swab shows the presence of GBS. CME Article Screening for Group B Streptococcus in Pregnancy Answer True or False to the questions below. 7. 4. It is recommended to take swabs for GBS screening at 35–37 weeks’ gestation. Hong Kong Academy of Medicine Jockey Club Building 99 Wong Chuk Hang Road. GBS colonization rate was significantly higher in health-care professionals than in housewives in Hong Kong. 6. antenatal antibiotics treatment will be required to eradicate GBS. 8. 9. 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 . Name in BLOCK CAPITALS: Signature: Date: Please mail your completed answer sheet back to: The Secretariat Hong Kong College of Obstetricians & Gynaecologists Room 805. This JPOG article has been accredited for CME by the Hong Kong College of Obstetricians and Gynaecologists. The performance of a rapid test for GBS on non-enriched swab samples is as good as the culture method.CME Questions This continuing medical education service is brought to you by the Medical Progress Institute. Delayed processing of the swabs for more than 24 hours does not affect the laboratory detection of GBS. For GBS screening. 5. If a woman is admitted with painful uterine contractions at 35 weeks’ gestation and unknown GBS status. 2. True False 1. GBS screening should be performed and intrapartum antibiotic prophylaxis for GBS given. Aberdeen. Read the article ‘Screening for Group B Streptococcus in Pregnancy’ and answer the following questions. 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. 10. In the UK. swabs are taken from both the high vagina and the anus. Maternal temperature of 38. an institute dedicated to CME learning.
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