Oxford Handbook of Clinical Specialties PDF

OXFORD HANDBOOK OF CLINICAL SPECIALTIES NINTH EDITION JUDITH COLLIER MURRAY LONGMORE KEITH AMARAKONE 3 3 Great Clarendon Street, Oxford OX2 6DP Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and certain other countries. Published in the United States by Oxford University Press Inc., New York © Oxford University Press, 2013 The moral rights of the authors have been asserted First published 1987 Fifth edition 1999 Translations: Greek Second edition 1989 Sixth edition 2003 Spanish Romanian Third edition 1991 Seventh edition 2006 German Russian Polish Fourth edition 1995 Eighth edition 2008 Hungarian Portuguese 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, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by licence or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above. You must not circulate this book in any other form and you must impose the same condition on any acquirer. British Library Cataloguing in Publication Data Data available Library of Congress Cataloging in Publication Data Data available Typeset by GreenGate Publishing Services, Tonbridge, UK; printed in China on acid-free paper through CC Offset Printing Co. Ltd ISBN 978-0-19-959118-3 Drugs Except where otherwise stated, recommendations are for the non-pregnant adult who is not breastfeeding. To avoid excessive doses in obese patients it may be best to calculate doses on the basis of ideal body weight (IBW): see p621. We have made every effort to check this text, but it is still possible that drug or other errors have been missed. OUP makes no representation, express or implied, that doses are correct. Readers are urged to check with the most up-to-date product information, codes of conduct, and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text, or for the misuse or misapplication of material in this work. For updates/corrections, see oup.co.uk/academic/medicine/handbooks/updates. Contents Front cover Back cover Drugs ii Preface to the ninth edition iv Preface to the first edition v Conflicts of interest: none declared v Understanding our patients vi What happens when ward rounds collide? vii Dedication viii Acknowledgments ix How to use this book x A note on the use of pronouns x Symbols and abbreviations xi 1 Obstetrics 1 2 Paediatrics 98 3 Gynaecology 240 4 Psychiatry 312 5 Ophthalmology 410 6 Primary care 466 7 Ear, nose and throat diseases 534 8 Dermatology 582 9 Anaesthesia 612 10 Unusual eponymous syndromes 638 11 Orthopaedics and trauma 656 12 Pre-hospital immediate care 790 Index 817 The content of each chapter is detailed on each chapter’s first page. Preface T his is the first medical textbook to take the health of its readers serious- ly on the grounds that the health of one person (a patient) must not be bought at the expense of another (their doctor). It is an unsettling paradox that when we study medicine our own health goes out of the window (fig 1), with long hours of coal-face working often without joy or sustenance as our health is shattered by the weight of an over-full curriculum (no doubt because there are too many organs and we know far too much about them). What can a book do about this defenestration (fig 1)? First of all the ideal book can (must!) be brief with a clear distinction between work and play. Secondly, such a book must furnish the mind: as we drill down into the minute structure of disease, there must be a corresponding search for the macroscopic, the human, and the universal. This book intends to make plain the idea that for every such spiral of down-drilling, there is a corresponding upward spiral (the swarf, fig 2) towards the Fig 1. Defenestration infinite—and we aim the help the reader find the jumping-off point where these spirals intersect, so that the movement down (reductionism) is complemented by a movement up (integrative medicine). Can this influence the heath of our readers? The answer lies in a single word: enlightenment. The spiral illuminations at the beginning of each chapter (and scat- tered throughout the book) remind us to follow the movement up as well as the movement down. Fol- low the swarf! We should do this in our consultations, as well as in our reading. Never pass over an opportunity to widen the horizons of your patients, or to have your own horizons widened by your patient: what better way is there of reducing the Fig 2. Swarf size of their (and our) insoluble prob- “The way up is the way down… lems? Here, it is enough to point out Whether on the shores of Asia, or in the Edg- ware Road.” that the well-furnished mind confers The dry salvages TS Eliot; 1941 resilience to the body. We all know that stress brings on physical disease—and from this premise it is a short step to accept that a resilient mind is central to maintaining heath. We aim to find magnetic correspondences in the jumping-off points between the down- ward-drilling helix and the upward-spinning swarf-spirals using philosophy, literature, humour, and tinctures of hope. Ultimately we would like readers to develop their own methods, thereby converting passive acceptance of an overfull curriculum into wealth, life, and beauty. JABC, KM & JML—Preface to the 9th edition—Cape Clear iv Preface to the 1st Edition W hen someone says that he is ‘doing obstetrics’—or whatever, this should not hide the fact that much more is being done besides, not just a little of each of medicine, psychiatry, gynaecology and paediatrics, but also a good deal of work to elicit and act upon the patient’s unspoken hopes and fears. At the operating table he must concentrate minutely on the problem in hand; but later he must operate on other planes too, in social and psychological dimensions so as to understand how the patient came to need to be on the operating table, and how this might have been prevented. All the best special- ists practise a holistic art, and our aim is to show how specialism and holism may be successfully interwoven, if not into a fully watertight garment, then at least into one which keeps out much of the criticism rained upon us by the proponents of alternative medicine. We hope that by compiling this little volume we may make the arduous task of learning medicine a little less exhausting, so allowing more energy to be spent at the bedside, and on the wards. For a medical student coming fresh to a specialty the great tomes which mark the road to knowledge can numb the mind after a while, and what started out fresh is in danger of becoming exhausted by its own too much. It is not that we are against the great tomes themselves—we are simply against reading them too much and too soon. One starts off strong on ‘care’ and weak on knowledge, and the danger is that this state of affairs becomes reversed. It is easier to learn from books than from patients, yet what our patients teach us may be of more abiding significance: the value of sympathy, the uses of compassion and the limits of our human world. It is at the bedside that we learn how to be of practical help to peo- ple who are numbed by the mysterious disasters of womb or tomb, for which they are totally unprepared. If this small book enables those starting to explore the major specialties to learn all they can from their patients, it will have served its purpose—and can then be discarded. Because of the page-a-subject format, the balance of topics in the follow- ing pages may at first strike the reader as being odd in places. However, it has been our intention to provide a maximally useful text rather than one which is perfectly balanced in apportioning space according to how common a particular topic is—just as the great Terrestrial Globes made by George Phil- lips in the 1960s may seem at first to provide an odd balance of place names, with Alice Springs appearing more prominently than Amsterdam. To chart a whole continent, and omit to name a single central location out of respect for ‘balance’ is to miss a good opportunity to be useful. George Phillips did not miss this opportunity, and neither we hope, have we. It is inevitable that some readers will be disappointed that we have left out their favoured subjects (the Phillips’ Globe does not even mention Oxford!). To these readers we offer over 300 blank pages by way of apology. JABC & JML—Preface to the 1st edition—Ferring, 1987 Conflicts of interest: none declared Because of numerous and well-publicized occasions where writers of guidelines recommending certain drugs turn out to have undisclosed financial contacts with the pharmaceutical industries concerned,1 we wish to place on record that we have no contacts with any pharmaceutical company, and no pharmaceutical company employs us in any capacity, and neither have we received any financial input bearing upon our research for this publication. We v have a policy of not seeing representatives from the pharmaceutical industry, or receiving their gifts or hospitality. We assert that the drugs recommended in this book have been selected on the basis of the best available evidence. DRs LONGMORE, COLLIER, and AMARAKONE, 2012 Understanding our patients Most of the time we treat our patients quite well, without ever really understanding them. The idea that we should strive to understand and empathize with all our patients is unreasonable. Out-patient clinics and surgeries would grind to a halt, and urgent visits would never get done. It is also possible that to do so would be counter-productive from the patient’s point of view. For two human beings to understand each other’s inner life is a rare event, and if we offered this understanding to all our patients they might become addict- ed to us, and be unable to get on with the rest of their lives. Nevertheless, it is good practice to try to understand some patients. Doing so may entail swallowing an alien world and digesting it rather slowly. Paradoxically, to achieve this, we very often need to keep our mouths shut, particularly with those in whom we have reached a therapeutic impasse—for example if the illness is untreatable, or the patient has rejected our treatment, or if the patient seems to be asking or appealing for something more. Eye contact is important here. One of the authors (JML) recalls forever his very first patient—found on a surgical ward recovering from the repair of a perforated duodenal ulcer: a nice simple surgical patient, ideal for beginners. I asked all the questions in the book, and knew all his answers and his physical features, even the colour of his eyes. Luckily, the house officer who was really looking after him did not ask so many questions, and knew how to interpret the appeal for help behind those eyes, and in his busy day found space to receive the vital clue beyond my grasp—that my patient was a drug addict and under great stress as he could no longer finance his activity. So, the first step in trying to understand a patient is to sit back and listen. Next, if possible, it is very helpful to see your patient often, to establish rap- port and mutual respect. If the relationship is all one way, with the doctor finding out all about the patient, but revealing nothing of him or herself, this mutual respect can take a very long time to grow. But beware of sharing too much of your own inner life with your patients: you may overburden them, or put them off. Different patients respond to different approaches. Understand- ing patients inevitably takes time, and it may be hard in a series of short ap- pointments. A visit to the patient’s home may be very revealing, but for many doctors trapped in hospital wards or clinics, this is impossible. But it is usually possible to have a longish private interview, and take whatever opportunity arises. We once worked with a consultant who infuriated his junior staff on busy ward rounds by repeatedly selecting what seemed to us the most bor- ing and commonplace medical ‘cases’ (such as someone with a stroke) and proceeding to draw the curtain around the patient’s bed to exclude us, and engage in what seemed like a long chat with the patient, all in very hushed voices, so that we never knew what he said—until Sister told us that he never said anything much, and simply received anything that was on the patient’s mind. For the most part, he was swallowing their world in silence. We came to realize that there was nothing that these patients, robbed as they were of health and wholeness, appreciated more in their entire hospital stay. vi What happens when two ward rounds collide? We once worked with a splendid consultant, Dr B—, who, among other ec- centric but lovable traits, believed that data such as an ECG should be inter- preted according to the mood of the day and in the light of bedside nuances. He would not let us label old ECGs with the diagnosis accorded at the time of their recording, in case this conflicted with later nuances. So during ward rounds old ECGs would be unearthed and reinterpreted by the great man, as if he were a conductor wringing new meaning from a well-known score. Ward rounds tended to be rather slow and it so happened that faster, newer consultants would start overtaking us on ward rounds. But we noticed that some of their entourage would take this moment of impact to hive off from the fast ward round, and attach themselves to ours. The faster ward round moved on to some trite destination leaving us to tussle with the great questions of medicine. Let us consider further this moment of instability and choice when the two ward rounds collide. As Paul Verlaine wrote, “There is nothing more precious than a song which is cloudy from the joining of the indistinct with the precise”. We tend to over-value the precise and undervalue the indistinct. Like Dr B—, we need to re-interpret patients’ exact words as if they were a musical score. All too often, though, we rely on summaries of our patients’ stories, massacred by eloquent, but treacherous, medical jargon. Paul Verlaine knew what to do: “Take eloquence, and wring its neck” is his advice, if it’s truth we are after. In its place he recommends systematic ambiguity and giving nuance free rein.... C ar nous voulons la Nuance encor, Pas la couleur, rien que la Nuance! Oh! la nuance seule fiance For we want nuance, Not colour, nothing but nuance! Only nuance joins Le rêve au rêve et la flûte au cor! Dream to dream and flutes to horns! Paul Verlaine, Art poétique So what are the facts? Give me hard facts and I will give you a diagnosis. That was the alluring but dangerous message from the fast ward round. And we all have to make our choice of when to hive off from this ward round and join Dr B—. If we can accord some ambiguity to the facts we may start to be of real use to our patients. After all, they have to live with the facts, so we may as well let the facts breathe and have a complicated life of their own. There is something undefined in every fact. Find what it is, and use the undefined as a vehicle to explore your patient’s subtleties and contradictions. So, in memory of Dr B—, we propose a new section in the Medical Notes called Nuances, to be placed before the Functional Enquiry and after the History of the Presenting Complaint. “The patient pointed to his ear when he said this” or “He was obviously frightened reliving this moment...” or “The patient ran out of language at this point...” Running out of language is a sure sign that you are getting somewhere with our patient. Too much eloquence is fatal: this is Paul Verlaine’s worthless jewel (“ce bijou d’un sou”) that sounds hollow and fake when put to the test. We have to accept that language is not very good at dealing with pain—or any internal state. vii Dedication viii Acknowledgements We thank those who have contributed their time and wisdom to previous editions: Dr Steven Emmet for detailed help in reading proofs; Professor Tor Chiu for his help with the ENT chapter; Natalie Langdown for help with autism; Pro- fessor Mark Lowenthal for his indefatigable help with Paediatrics and other chapters. We thank all the authors who have joined us for previous editions: Ju- dith Harvey, Tim Hodgetts, Duncan Brown, Peter Scally, Mark Brinsden, Ahmad R. Mafi, and Tom Turmezei. Specialist Readers We are hugely indebted to our Specialist Readers for their advice, encouragement, and constructive criticism. Each chapter in this book has benefitted from their trustworthy oversight. They are thanked individually at the beginning of each chapter. Junior Readers It was our great pleasure to welcome a new team of Read- ers to the ninth edition of this book. Our Junior Readers showed commitment, intelligence, and ingenuity in their contributions to the referencing and cross- referencing of this edition. We have a better book for it. Thank you to Mathura- nayagham Niroshan, Shahzad Arain, Rashmi Singh, Josh Hurn, Konstantinos Kritikos, Mark Cassar, William Hunt, David Lee, Aaron Lai, Winnie Chen, Yong De Jun, Pooja Sarkar, Xuebin Dong, Roland Bensted, and Fandy Wang. Reader participation We have been very fortunate to receive so many well- considered suggestions and corrections to the book from readers. Their contributions have enhanced the book and we are grateful. Over the years the list has grown too large to accommodate in the book, so we now have a dedicated webpage for the purpose: www.oup.com/uk/ohcs9acknowledgements. If you would like to give us feedback, correct a mistake, or make a suggestion, you can do so by filling in the comment card enclosed in this volume and posting it to us, or by going to our website: www.oup.com/uk/ohcs9efeedback. ix How to use this book This book has some useful features to help you get the most out of the information inside. Quick chapter look-ups Index on the back cover refers to and aligns with the coloured tabs on the sides of the pages. References (1) Every reference has an individual identification indicated by a pink superscript number. The full details of every reference are held online at www.oup.com/ohcs9refs. Cross references There are cross references to other chapters within the book, to the Oxford Handbook of Clinical Medicine (OHCM), and to other titles in the Oxford Medical Handbooks series. Reference intervals Included inside the back cover. Conversion factors to and from SI units are given on the bookmark. Right-hand vertical comments At the side of some tables and topics, an alternative opinion of the content inside. Symbols and abbreviations See opposite. Corrections and suggestions Found a mistake? Have a suggestion for the next edition? Let us know at www.oup.com/uk/ohcs9efeedback. Major changes are announced online at www.oup.co.uk/academic/series/oxhmed/updates. A note on the use of pronouns For brevity, the pronoun ‘he’ or ‘she’ has been used in places where ‘he or she’ would have been appropriate. Such circumlocutions do not aid the reader in forming a vivid visual impression, which is one of the leading aims of good au- thorship. Therefore, for balance and fairness, and where sense allows, we have tried alternating he with she. x Symbols and abbreviations ........don’t dawdle! Prompt action C3..........complement xi xi saves lives Ca.........carcinoma ...........this phrase is important CBRN....chemical, biological, radiological,  (†) more (or less) vital topic; a rough guide for 1st-time readers nuclear CBT.......cognitive-behaviour therapy .......an opportunity for holistic/non- CCDC....consultant in communicable reductionist thinking disease control.......conflict (controversial topic) CCF.......combined (right & left sided) 1,2,3 , ,.......references at oup.co.uk/ohcs9refs cardiac failure 1 2 3.......drug dose not in BNF, see CHC.......combined hormonal oup.co.uk/ohcs9refs contraception #...........fracture ChVS.....chorionic villus sampling .........differential diagnosis CI..........contraindications  : .....male to female ratio CIN........cervical intra-epithelial neoplasia ............decreased CMV......cytomegalovirus; controlled .........normal (eg plasma level) mandatory ventilation ............increased CNS.......central nervous system ~...........about CoC.......combined oral contraceptive ≈............approximately equal COM......chronic otitis media –ve.......negative CPA.......care programme approach +ve......positive CPAP.....continuous +ve airways pressure ............on account of/because of CPR.......cardiopulmonary resuscitation ............therefore CRP.......c-reactive protein A&E.......emergency department CRPS.....complex regional pain syndrome A2A.......angiotensin 2 receptor (blockers) CSF.......cerebrospinal fluid ABC.......air, breathing, circulation CT..........computer tomography A(P)LS..advanced (paediatric) life support CVP.......central venous pressure manuals CVS.......cardiovascular system ABR.......audiological brainstem responses CXR.......chest x-ray AC..........ante cibum (before food) D............dimension (or dioptre) ACE(i)...angiotensin-converting enzyme D&C.......dilatation (cervix) & curettage (inhibitor) D&V......diarrhoea and vomiting ACLS.....advanced cardiac life support dB..........decibel ACTH.....adrenocorticotrophic hormone DHS.......dynamic hip screw ADD.......attention deficit disorder DIC........disseminated intravascular ADH......antidiuretic hormone coagulation AFP....... -fetoprotein (=alpha) DIP........distal interphalangeal AIDS.....acquired immunodeficiency syn. DKA......diabetic ketoacidosis Alk.......alkaline (phos=phosphatase) dL..........decilitre ALL.......acute lymphoblastic leukaemia DM........diabetes mellitus ALT........alanine aminotransferase DMSA...dimercaptosuccinic acid ANA......antinuclear antibody DNA......deoxyribonucleic acid ANF.......antinuclear factor DOH.......Department of Health (NHS) ANS.......autonomic nervous system DPL.......diagnostic peritoneal lavage AP.........anteroposterior DRG.......dorsal root ganglion APH.......antepartum haemorrhage DSM-IV Diagnostic & Statistical Manual, 4e APLS.....advanced paediatric life support DUB.......dysfunctional uterine bleeding APM......auto-premotor syndrome DVT.......deep venous thrombosis ARF.......acute renal failure E-BM....evidence-based medicine ARM......artificial rupture of membranes EBV.......Epstein–Barr virus ASD.......atrioseptal defect ECG.......electrocardiogram ASO.......antistreptolysin O (titre) ECT.......electroconvulsive therapy ASW.....approved social worker EEG.......electroencephalogram ATLS.....Advanced Trauma Life Support EIA........enzyme immunoassay manual; see www.trauma.org ENT.......ear, nose and throat ATN.......acute tubular necrosis ERPC.....evacuation of retained products AV.........atrioventricular of conception AVM......arteriovenous malformation ESR.......erythrocyte sedimentation rate HCG.....-human chorionic gonadotrophin ET..........endotracheal BJGP.....British Journal of General Practice FB..........foreign body BMJ......British Medical Journal FBC.......full blood count BNA......borderline nuclear abnormality FCR.......flexor carpi radialis BNF.......British National Formulary FDP.......flexor digitorum profundus xi xi BNF......children’s BNF C FDS.......flexor digitorum sublimis BP..........blood pressure FH..........family history ©..........courtesy of the copyright holder FNA.......fine needle aspiration FNT.......fetal nuchal translucency LHRH....luteinizing hormone-releasing FSH.......follicle-stimulating hormone hormone xi xi G............gauge LMP......day 1 of last menstrual period xi g............gram LMWH..low molecular weight heparin G()GT.gamma()glutamyl trans- LP..........lumbar puncture peptidase LVH.......left ventricular hypertrophy G6PD....glucose-6-phosphate μ(g)......micro(gram) dehydrogenase MAOI....monoamine oxidase inhibitor GA.........general anaesthesia MCP......metacarpophalangeal GCS.......Glasgow coma scale MCV......mean cell volume GFR.......glomerular filtration rate MEA......microwave endometrial ablation GH.........growth hormone MET......meta-analysis GI..........gastrointestinal mg........milligrams (μg=microgram=mcg) GP.........general practitioner MHA.....Mental Health Act h............hour MI.........myocardial infarction Hb..........haemoglobin ML.........millilitre HBsAg..hepatitis B surface antigen mmHg millimetres of mercury HBV.......hepatitis B virus MRI.......magnetic resonance imaging HCG.......human chorionic gonadotrophin MSU......midstream urine culture HDL.......high-density lipoprotein MTP......metatarsophalangeal HFOV.....high-frequency oscillatory mU.........milliunit(s) ventilation MVA......motor vehicle accident HIV........human immunodeficiency virus N=20*...reference to a randomized trial HLA.......human leucocyte alleles of 20 patients (* or what ever HPA.......Health Protection Agency number follows N) HPO.......hypothalamic–pituitary–ovarian n=63*...reference to a non-randomized HPV.......human papilloma virus trial of 63 patients (* or what HRT.......hormone replacement therapy ever number follows n) HVS.......high vaginal swab N2O.......nitrous oxide ibid.......ibidem (Latin, in the same place) NaCl......sodium chloride IBW......ideal body weight NAI.......non-accidental injury ICP........intracranial pressure NBM......nil by mouth (no solids or fluids) IE..........infective endocarditis NEJM....New England Journal of Medicine Ig...........immunoglobulin NEPE.....non-epileptic paroxysmal events IHD........ischaemic heart disease NGT.......nasogastric tube IM.........intramuscular NHS.......National Health Service INR........international normalized ratio of NICE.....National Institute for Health and prothrombin time Clinical Excellence IOP........intraocular pressure NICU.....neonatal intensive care unit IP..........interphalangeal NMJ......neuromuscular junction IPPV.....intermittent positive pressure NOF.......neck of femur ventilation NSAID..non-steroidal anti-inflammatory IPT........interpersonal therapy drug(s) IQ..........intelligence quotient OAE.......otoacoustic emissions ISQ........in status quo (Latin, no change) OED.......Oxford English Dictionary, OUP ISS........injury severity score OHCM...Oxford Handbook of Clinical ITP........idiopathic thrombocytopenic Medicine 8e, OUP purpura OM........otitis media ITU........intensive therapy unit OME......otitis media with effusion IU/iu.....international unit OMV......open mouth view IUCD.....intrauterine contraceptive device ON.........omni nocte (take at night) IUI.........intrauterine insemination ORh–ve.blood group O, Rh negative IV..........intravenous ORIF.......open reduction and internal fixation IVF........in vitro fertilization OT..........occupational therapist IVI.........intravenous infusion PA..........posteroanterior IVU........intravenous urography PaCO2...partial pressure of CO2 in arterial JVP.......jugular venous pressure blood K+..........potassium PAN.......polyarteritis nodosa kg.........kilogram pANCA.perinuclear antineutrophil kpa.......kilopascal cytoplasmic antibody L............litre PaO2......partial pressure of oxygen in LA..........local anaesthesia arterial blood LBC.......liquid-based cytology PC..........post cibum (after food) xii LCR.......ligase chain reaction PCA.......patient-controlled anaesthesia xi LDH.......lactate dehydrogenase PCOS.....polycystic ovarian syndrome xi xi LFT........liver function test PCR.......polymerase chain reaction LH..........luteinizing hormone PCV.......packed cell volume PDA.......patent ductus arteriosus SGA.......small-for-gestational age PE..........pulmonary embolus SLE........systemic lupus erythematosus xi PET.......pre-eclamptic toxaemia SNHL....sensorineural hearing loss xi xi PG.........pemphigoid gestations SpO2.....pulse oximetry estimated PGD........preimplantation genetic diagnosis SaO2; no allowance for PICU.....paediatric intensive care unit carboxyhaemoglobin PID........pelvic inflammatory disease SSRI.....selective serotonin reuptake PIP........proximal interphalangeal inhibitor(s) PKU.......phenylketonuria stat.......statim (Latin for once); single dose PMB......postmenopausal bleeding STD.......sexually transmitted disease PMS......premenstrual syndrome STI........ Sexually transmitted infection PO.........per os (Latin for by mouth) SUFE.....slipped upper femoral epiphysis PoP........progesterone-only pill SVC.......superior vena cava POP.......plaster of Paris SVP.......saturation vapour pressure PPH.......postpartum haemorrhage syn.......syndrome PR..........per rectum T°..........temperature, degrees Centigrade PTR.......prothrombin ratio t½..........half life PUO.......pyrexia of unknown origin T3..........triiodothyronine PUVA....psoralen-ultraviolet A T4..........thyroxine PV.........per vaginam (via the vagina) TB..........tuberculosis QOF.......quality & outcomes framework TBW.....tension band wiring ...........treatment (prescribing drugs) TCRE.....transcervical resection of RA.........rheumatoid arthritis; regional endometrium anaesthesia TED.......transverse elastic graduated RBC.......red blood cell TENS.....transcutaneous electrical nerve RCGP....Royal College of General stimulation Practitioners TFT........thyroid function tests RCOG....Royal College of Obstetricians TIA........transient ischaemic attack and Gynaecologists ToP........termination of pregnancy RCT.......randomized controlled trial TPH.......transplacental haemorrhage REM......rapid eye movement TPR.......temperature, pulse, and RMO......registered medical officer respirations RSD.......reflex sympathetic dystrophy TRTS.....triage revised trauma score RSI........repetitive strain injury; rapid TSH.......thyroid-stimulating hormone sequence induction TSOH....transient synovitis of the hip RTA.......road traffic accident(s) U............unit(s) RTS.......revised trauma score U&E.......urea and electrolytes RUQ.......right upper quadrant UK.........United Kingdom RVH.......right ventricular hypertrophy URTI.....upper respiratory tract infection S1 S2...... 1 and 2 heart sounds st nd US(S)...ultrasound (scan) SAD.......seasonal affective disorder UTI........urinary tract infection SALT.....speech and language therapist UV.........ultraviolet SAO2.....arterial blood O2 saturation, ≈ SpO2 VLBW...very low birthweight infant (allows for carboxyhaemoglobin) VSD.......ventriculoseptal defect SBE.......subacute bacterial endocarditis VTE.......venous thromboembolism SC..........subcutaneous VUR.......vesico-ureteric reflux SCBU....special care baby unit WCC.....white blood cell count SE..........side-effects wt.........weight sec........second(s) WR........Wasserman reaction SFH.......symphysis fundal height yrs, y....years SERM....selective oestrogen receptor ZN.........Ziehl–Neelsen (stain for TB) modulator xiii Fig 1. This plan is rendered almost unintelligible by over-use of abbreviations. It might mean: xi xi If in status quo (ISQ=no change in state) in 2 days’ time (/7 in this context means days; /52 would mean weeks), refer to the Sexually Transmitted Infections clinic for treatment ()— if it turns out he does not arrive (DNA), follow-up at the out-patient department.2 1 Obstetrics Pre-pregnancy counselling 2 Hypertension & eclampsia1 48 Care plans 3 Prematurity 50 Booking criteria 4 Small for gestational age 52 Physiological changes in Large for gestational age 53 pregnancy 6 Postmaturity 54 Obesity 7 Fetal distress 55 Antenatal care 8 Obstetric shock 55 Anti-D 9 Antepartum haemorrhage 56 Prenatal diagnosis 10 Normal labour 58 Tests for Down’s syndrome 12 Membrane rupture 60 Preimplatation tests 13 Induction of labour 62 Placenta 14 Active management of labour 64 Thromboprophylaxis 16 Pain relief in labour 66 Minor symptoms 17 Multiple pregnancy, IVF 68–9 Hyperemesis gravidarum 18 Breech 70 Pregnancy & medical conditions Other malpresentations 71 – Sickle-cell disease 19 Prolapsed cord 72 – Cardiac disease 20 Impacted shoulders 72 – Psychopharmacology 21 Meconium-stained liquor 73 – Anaemia 22 Dystocia 74 – HIV 23 Forceps/ventouse 76 – Diabetes mellitus 24 Caesarean section 78 – Thyroid disease 25 Uterine rupture 80 – Jaundice 26 Mendelson’s syndrome 80 – Malaria 27 Stillbirth 82 – Renal disease 28 Postpartum haemorrhage 84 – Epilepsy 29 Retained placenta 86 – Connective tissue disease 30 Uterine inversion 86 – Hypertension 31 DIC and coagulation defects 88 – Thromboembolism 32 Amniotic fluid embolism 89 – Thrombophilia 33 Birth injuries 90, Ante/perinatal infection 34–7 maternal 91 Abdominal pain 38 Episiotomy and tears 92 Abdominal palpation 40 Puerperium 94 Pelvis and head 42 Contraception after a baby 95 Fetal monitoring 44–5 Maternal mortality 96 Ultrasound 46 Perinatal mortality 97 Sources RCOG Green Top guidelines; Saving Mothers’ Lives (Confidential En- quiry). 1 Mat mort 2011 Cochrane database (www.liv.ac.uk/lstm/ehcap/pc/nwc-pcl.html). Relevant topics elsewhere: Neonatology, p107–22; breastfeeding, p124–6; rhesus disease, p116; ectopic pregnancy, p262; miscarriage/termination, p258–60; trophoblastic disease, p264; fibroids in pregnancy, p277; preterm/light-for- dates babies, p128; chickenpox in pregnancy, p144; parvovirus B19, p142; postnatal depression, p408. 1 The term pregnancy-induced hypertension with proteinuria is tending to replace the term pre-eclampsia. We have not followed this trend as to do so obscures the vital fact about pre- eclampsia: it may lead on to eclampsia. We favour pre-eclampsia because it is short and sends the shadow of a shiver down our spines, being a reminder of how dangerous it can be. We thank Ms Alison Peattie, our Specialist Reader, and Mathuranayagham Niroshan, our Junior Reader, for their contribution to this chapter. The essence of reproductive health 1 Pregnancy is a risky affair for babies and mothers. The textbook causes of maternal mortality in the UK are pulmonary embolism, eclampsia, haemorrhage, infection, and cardiac diseases, with all the other causes being rare. But if an obstetrician could be granted one wish, it would not be to abol- ish these; rather it would be to make every pregnancy planned and desired by the mother. Worldwide, a woman dies every minute from the effects of pregnancy, and most of these women never wanted to be pregnant in the first place—but either had no means of contraception, or were without the skills, authority, and self-confidence to negotiate with their partners. So the real killers are poverty, ignorance, and the unwieldy desires of men, and the real solutions entail literacy, economic growth, and an equality of dialogue Obstetrics between the sexes. Any obstetric or governmental initiatives in reproductive health which do not recognize these facts are doomed. 2 School-based sex education This can be effective, if linked to easy access to contraceptive services. This is the conclusion of a meta-analysis, taking into account cohort studies (if meta-analyses confine themselves to the 15 or so randomized studies, no benefit is shown). 3 It may be necessary to foster a knowledge-sharing, skill-promoting environment that is part of a continuing process, and not a ‘one-off ’ affair—for educational programmes to work. Adolescent pregnancy rates: USA : 116/1000; UK : 57/1000; Canada: 50/1000. In 2007 in England & Wales 160 pregnancy were terminated in those 1 month pre-conception till 13wks (5mg/day if past NTD, on antiepileptics, p29, obese (BMI ≥30), HIV+ve on co-trimoxazole prophylaxis, 8 diabetic 9 or sickle cell disease p19). Foods with >0.1mg of folic acid/serving: brussels sprouts, asparagus, spinach, blackeye beans, fortified cereals. Avoid liver & vit. A (vit. A embryopathy) & caffeine. Smoking decreases ovulations, causes abnormal sperm production (± less penetrating capacity),  rates of miscarriage (≈2), and is associated with preterm labour and lighter-for-dates babies (mean is 3376g in non-smoker; smoker: 3200g), placenta Search for those who praevia and abruption. 10 Reduced reading ability in need counselling most smokers’ children up to 11yrs old shows that long- Diabetes mellitus term effects are important. ~17% of smoking moth- Tropical travellers ers stop before or in pregnancy. Frequent miscarriage Alcohol consumption High levels of consump- Hypothyroidism tion are known to cause the fetal alcohol syndrome Epilepsy (p138). Mild drinking eg 1–2U/wk has not been shown Rubella-susceptible to adversely affect the fetus but alcohol does cross Pet-owners (toxo- the placenta and may affect the fetal brain. Miscar- plasmosis risk is ) riage rates are higher among drinkers of alcohol. NICE Phenylketonuria recommends 5U/session) is BP  especially harmful. 11 To cut consumption: see p513. SLE Spontaneous miscarriage (SM) Risk of miscarriage Genetic history, eg: is 8.9% in women aged 20–40yrs, rising to 74.7% for spina bifida etc. women ≥45yrs. After 3 miscarriages, risk of next preg- thalassemia nancy failure is 44.6% for nullips aged 25–29yrs, and Duchenne’s 35.4% for parous women.12 cystic fibrosis et al Recurrent spontaneous miscarriage See p261. Individualized care plans—eg for diabetes mellitus9 3 For optimal care, when there are many features that need to be addressed an individualized care plan can help. The example below is of a care plan for diabetic women. The care plan is a chance for dialogue between the mother and her carers: all must sign-up to it. Placed in her notes it should be consulted throughout pregnancy when the woman is seen. In the case of a diabetic pregnancy the woman should be seen in a joint clinic where a multidisciplinary team is available comprising obstetrician, diabetes physician, diabetic specialist nurse, diabetes midwife, and dietician. The care plan should cover the antenatal period and up to 6 weeks post-partum. It can be individualized, and generally includes advice about: Aspirin 75mg/24h PO until delivery to reduce pre-eclampsia risk. 13 Targets for glycaemic control (p24 for levels; pregnant mother to liaise every Obstetrics 2 weeks with diabetic team concerning blood readings). Retinal digital screening with mydriasis schedule (as soon as possible after pregnancy confirmed if not screened in previous 12 months; after 1st antenatal appointment and again at 16–20 weeks if retinopathy seen on initial screen in pregnancy and at 28 weeks if none seen at initial screening). 1 4 Up to 20% develop proliferative retinopathy. Renal screening schedule (for microalbuminuria as well as dipstix protein, at 1st appointment if not screened in previous 12 months). Refer to nephrologist if creatinine ≥120μmol/L or protein excretion >2g/day. Give thromboprophylaxis if protein excretion >5g/day. Fetal surveillance (eg 4 chamber and outflow tract echo at 20 weeks; ultrasounds at 28, 32, and 36 weeks for fetal growth and amniotic fluid depth and cardiotocogram eg twice weekly from 38 weeks if she chooses to await spontaneous labour rather than accepting induction/caesarean section when offered at 38 weeks) earlier if growth restriction seen. Plan for delivery. If co-morbidity such as neuropathy or obesity arrange anaesthetic assessment at 36 weeks. Diabetes care after delivery. If macrosomia is found on ultrasound the consultant obstetrician should then write a clear plan to determine follow-up scans, fetal surveillance, and mode and time of delivery. For postnatal care the care plan should include, as a minimum: Plan for managing glycaemic control (eg return to pre-pregnancy regimen). Neonatal care: feed as soon as possible then 2–3hrly to prevent hypoglycaemia. Check glucose level at 2–4h after birth, and if signs of hypoglycaemia. Give IV glucose to baby if symptomatically hypoglycaemic. Tube feed or give IV glucose if 2 consecutive readings 24h old, feeding well and able to maintain glucose levels. Contraception (currently mothers with the worst obstetric outcomes are the least likely to receive contraceptive advice). Follow-up care after discharge from hospital (eg glucose tolerance test 6 weeks postpartum and annually to see if still diabetic in gestational diabetes). How to access pre-pregnancy review prior to subsequent pregnancies.  The advantage of care plans is that by documenting the plan, it enables members of the team (including the mother and father, for they are frequently the most reliable at making sure things happen if they know what is expected) to check that pregnancy is monitored as planned. 4 Booking criteria and home delivery Most women in the UK have ‘shared obstetric care’—ie most of their antenatal care is from the community midwife (±GP), with limited (or no) visits (usually 2) to the hospital to see the consultant under whose care they are delivered, returning home (eg after 6–72h) for postnatal care. A minority receive their complete care from hospitals and the usual reasons for this are that the complications envisaged make full consultant care desirable. Some women are cared for by community midwives and their GP, but increasingly, low-risk women are receiving all their care from midwives, with doctors involved only if complications arise. Delivery may be in hospital in consultant- or midwife-led units, or, more rarely, at home. There is quite good evidence that consultant input into antenatal care of normal pregnancies achieves no added benefits (p8)—but risk factors making specialist visits and booking desirable are generally agreed (see MINIBOX). Is it safe for low-risk mothers to deliver in high- Risk factor—vis à vis: technology hospitals? Here interventions with their The mother complications are more common. In the UK this >40yrs old question is usually academic (unless a midwife-led Nullip 34yrs delivery unit is available) as most GPs are reluctant History of infertility to conduct births—and 6 months’ training in obstet- ≥5 past pregnancies Obstetrics rics gives scant skill. The rising birth rate and service Multip 35 constitute 15% of PPH mothers dying, and almost 50% of those dying Maternal mortality Feeding by bottle Obstetrics from thromboembolism are obese. As mothers may be more motivated to accept lifestyle modifications, pregnancy is a period during which obesity can be more effectively man- aged. Control of body weight during this period is vital. Aim to encour- age weight loss well before embarking on planned pregnancy. NB: dieting during pregnancy may not be wise as low weight gain during pregnancy correlates with lighter babies more prone to postnatal problems. 26 Good evidence is lacking. Lowest neonatal mortality is for birth weights of 3500–4500g and maternal weight gain depending on BMI: 27 BMI 29 2*–6kg *Assuming personal coaching and using a food diary (“I didn’t eat the cake as I knew I’d have to write it down, so I chose fruit instead...”). Some may need no weight gain. medicinenet.com/script/main/art.asp?articlekey=100897 2010 CMACE /RCOG guidelines recommend giving 5mg folic acid from 1 month before conception and for the first trimester if BMI ≥30 to prevent increased risk of neural tube defects. Obese women are more prone to vitamin D deficiency so ensure they are taking 10μg vitamin D supplementation while pregnant and breastfeeding. If BMI ≥30, screen for diabetes, eg oral glucose tolerance test at 24–28 weeks and consider heparin throm- "Eating for 2 is the only nice thing about being pregnant" boprophylaxis for 7 days postnatally if one additional thrombotic risk factor (p16), with addition of TED stockings if 2 risk factors. Mobilize all obese women early. If women with BMI ≥30 require caesarean section, give IV prophylactic antibiotics and, if subcutaneous fat is >2cm thick, suture that separately, to prevent infection. Women with BMI ≥40 should always receive 7-day postnatal heparin prophylaxis and TED stockings whatever the mode of delivery. They should have an antenatal consultation with an obstetric anaesthetist with an anaesthetic plan made for labour and delivery, and need 3rd trimester assessment to plan manual handling requirements and provision of appropriate TED stockings. When in labour inform anaesthetist. They should have continuous midwifery care and should have an IV sited early in labour. If opera- tive delivery is required the attending anaesthetic should be a consultant (or signed off obese-competent) obstetric anaesthetist. 8 Antenatal care  The aims of antenatal care are to: Detect any disease in the mother Ameliorate the discomforts of pregnancy Monitor and promote fetal wellbeing Prepare mothers for birth Monitor trends to prevent or detect any early complications of pregnancy: BP is the most important variable (eclampsia, p48). Is thromboprophylaxis (p16) or aspirin (p3 and p31) needed? Who should give antenatal care? Midwives may manage care, calling in doctors if risks (p4) or specific needs arise. Book by 12 weeks: see within 2 weeks if already ≥12 weeks pregnant. Women with BMI ≥35 need consultant care. The 1st antenatal visit is very comprehensive. Find a language interpreter if she needs one. Avoid using relatives (confidentiality issues). History: Usual cycle length; LMP (a normal period?); see Naegele’s rule (p1). Contraception; drugs; past history, eg surgery to abdomen or pelvis. Any fertility problems; outcome and complications of past pregnancies. Is there family history of diabetes, BP, fetal abnormality, or twins? Does she have concurrent illness (p20–35)? Has she been ‘cut’ (p247). If past or family history of DVT or embolism, screen for thrombophilia. Is gestational diabetes (GDM) a risk? Screen (75g glucose tolerance test) at 18 ± 28wks) if previous (GDM); at 24wks if BMI >30, previous baby >4.5kg, 1st Obstetrics degree relative diabetic, family origin (FO) from area of high risk of diabetes. Past mental illness? If serious (schizophrenia, bipolar disorder) or past postnatal problems, get antenatal assessment; put management plan in notes. Is she poor (eg gas/electricity supply cut off)? Unmarried? Unsupported? Subject to domestic violence? (p514) A substance abuser? (p362). ‘Healthy Start Vitamins for Women’—folic acid + vitamins C & D (10μg/d) are free to some during pregnancy and for 1 year after birth (Healthy Start Scheme UK). Avoid pâtés & blue/soft cheese (eg Brie, Camembert, to avoid listeria, p35); Toxoplasmosis advice: p34. Avoid liver (p2). Advise UK mothers to have vitamin D (above) if family of origin is African, or as listed below,1 or housebound, covered when outdoors, have BMI >30, or are diet vit. D depleted.2 Examination: Check heart, lungs, BP, weight (record BMI), and abdomen. Is a cervical smear needed? Varicose veins? Sensitively ask if genitally ‘cut’ (p246). Tests: Blood: Hb, group (antibodies if Rh–ve, p116), syphilis & rubella (±chick- en-pox) serology, HBs Ag (p36 & p26) HIV test; sickle test if black, Hb electro- phoresis (p22) and 25-hydroxyvitamin D if relevant. 28 Take an MSU (protein; bacteria). Arrange tests to exclude Down’s (p12). If she is foreign, a TB contact, or a hospital worker, consider CXR after 14 weeks. Offer early ultrasound to establish dates, exclude multiple pregnancy and aid with Down’s tests and an 18–20-week anomaly scan. Suggest: Parentcraft/relaxation classes; dental visit. Enquire about problems and anxieties. Consider need for iron and folate (p85 and p22). Advise on: Smoking, alcohol, diet, correct use of seat belts (above or below the bump, not over it) and adequate rest. Ensure knowledge of social secu- rity benefits. Usual exercise and travel are OK (avoid malarious areas) up to 36 weeks (singleton): 29 check with airline. Intercourse OK if no vaginal bleeding. Later visits Check urine for albumin, BP, fundal height. Check lie and presentation at 36 weeks. Do Hb and Rh antibodies at 28 & 34 weeks and give anti-D then if needed (p9). Visits are at 4mL, especially after manual removal of placenta, and with caesarean section. A Kleihauer test is especially important in stillbirth, as massive spontaneous transplacental haemorrhage can be the cause of fetal death. Where >4mL TPH is suggested by the Kleihauer screen, a formal estimation of the TPH volume is required and 500U anti-D given for every 4mL fetal cells transfused (maximum 5000U anti-D at 2 IM sites/24h). Note: Kleihauer tests can be negative where there is ABO incompatibility as fetal cells are rapidly cleared from the maternal circulation. Liaise with the transfusion service. Check maternal blood every 48h to determine clearance of cells and need for continuing anti-D. Any mother receiving anti-D prenatally (see below), should also receive it postnatally unless she delivers an Rh-negative baby. Use of anti-D in miscarriage in Rh–ve mothers 1 Anti-D should be given to all having surgical or medical terminations of pregnancy or evacuation of hytadiform mole (p264), unless they are already known to have anti-D antibodies. Give 250U if 20+0 weeks’ gestation. 2 Anti-D should always be given where spontaneous miscarriage is followed by medical or surgical evacuation. 3 Anti-D should be given where spontaneous complete miscarriage occurs after 12+0 weeks’ gestation. 4 Threatened miscarriage ≥12+0 weeks give anti-D; if bleeding continues in- termittently give anti-D 6-weekly until delivery. 5 Routine anti-D is not recommended with threatened miscarriage before 12 weeks’ gestation (but consider if viable fetus, heavy or repeated bleeding, and abdominal pain). Use of anti-D in pregnancy in Rh–ve mothers 1 Give anti-D 500U at 28 and 34 weeks to rhesus negative women (primip antenatal sensitization falls from 0.95% to 0.35%). Anti-D may still be detect- able in maternal blood at delivery. Still give postnatal anti-D, if indicated (as above). Take 28-week blood sample for antibodies before 28-week anti-D. 2 When significant TPH may occur: with chorionic villus sampling; external cephalic version; APH; uterine procedures (eg amniocentesis, fetal blood sampling); abdominal trauma; intrauterine death. Use 250U before 20 weeks’ gestation, 500U (and do Kleihauer) after 20 weeks. 3 Anti-D should be given in cases of ectopic pregnancy. 4 For threatened miscarriage, see above. 10 Prenatal diagnosis  ‘The first half of pregnancy can become a time of constant “exams” to see if the baby can be allowed to graduate to the second half of pregnancy’. Those at high and, increasingly, those at low risk of having an abnormal baby are offered prenatal diagnosis to allow better treatment of the expected defect, or (more often) if they would wish to terminate any abnormal fetus. Cell-free fetal DNA circulating in maternal blood may be useful in the future. High-risk pregnancies Maternal age >35 (chromosome defects). Previous abnormal baby or family history of inherited condition. Problems Anxiety while false +ve results are sorted out is a big problem. Terminating normal fetuses, eg  fetus of carriers of X-linked conditions. Most abnormalities are in low-risk groups ( missable by selective screening). Services available, their quality, and populations made eligible vary widely. Termination of female fetuses in cultures valuing males more highly. Devaluation of positive view of handicapped or ‘special needs’ children. Ultrasound at 11+0–13+6 weeks dates pregnancy, screens for nuchal translucency (see BOX) and chorionicity (p68). Further anomaly scan is at ~18 weeks. Skilled operators detect many structural anomalies. See BOX opposite and p46. Ultra- Obstetrics sound best detects externally impinging structural abnormality, eg anenceph- aly/spina bifida. Internal structural abnormality detection rate, eg for heart disease and diaphragmatic hernia, remains 3mm at 10–13 weeks’ gestation (as did 4.5% of chromosomally normal fetuses). The greater the extent of FNT, the greater the risk of abnormality. Nuchal translucency screening may be used to see who may benefit from more invasive chorionic villus sampling (or amniocentesis p10, which may delineate the precise chromosomal abnormality, eg trisomies). Note: positive predictive value of screening is 4% so 96% of women with a ‘positive’ test undergo an ‘unnecessary’ invasive procedure (chorionic villus sampling in the first trimester or amniocentesis in the second trimester). If nuchal screening was used as the only screening test 2 or 3 normal pregnancies would be lost after chorionic villus sampling, and 1 after amniocentesis, for every 4 pregnancies correctly detected with trisomy 21. It is useful for screening twins as early detection is best, for if selective fetocide is to be used risk of miscarriage is 3-fold higher if done after 16 weeks. Monochorionic twins have a higher false +ve rate for nuchal translucency thickness than dichorionic twins or singletons. In the 25% of monochorionic twins with FNT discordance of >20 %, more than 30% had early fetal death or severe twin–twin transfusion syndrome (10% if less discordance). 37 Note that the degree of neck flexion during the ultrasound examination may influence nuchal measurements. Other ‘soft markers’ for Down’s syndrome are fetal nasal bone appearance, the Doppler velocity wave form in the ductus venosus and tricuspid regur- gitation. 38 Systematic review shows that of all chromosomally normal fetuses (eu- ploid) with significant nuchal thickening, 70–90% have normal outcome, 2.2–10.6% miscarry, 0.5–12.7% have neurodevelopmental problems, and 2.1–7.6% of malformations were undiagnosed before birth. 39 12 Tests to detect Down’s syndrome  The 1st antenatal diagnosis of Down’s syndrome was in 1968. Initially there was amniocentesis for older mothers (Penrose noted an association with mater- Maternal age & Down’s1 nal age in 1933; see table). Then screening by blood Age of Fetuses Live mother with births test was introduced, then nuchal screening (p11). (yrs) 40 Down’s at with From 2007, the UK NHS has aimed for screening 16 weeks1 Down’s tests giving detection rates of 75% with a false 15–19 — 1 : 1250 +ve rate of 1 : 250 (~5% of pregnancies) she will 33 1 : 420 1 : 625 be offered tests such as chorionic villus sampling 34 1 : 325 1 : 500 (p10) and amniocentesis (p10). Early ultrasound is 351 1 : 250 1 : 350 vital for dating pregnancies for these tests. 36 1 : 200 1 : 275 The combined test combines nuchal translucency 34 1 : 150 1 : 225 (NT) + free -human chorionic gonadotrophin (HCG) 38 1 : 120 1 : 175 39 1 : 100 1 : 140 + pregnancy associated plasma protein (PrAP-A or 40 1 : 75 1 : 100 PAPP-A) + the woman’s age. Used between 10 weeks Obstetrics 41 1 : 60 1 : 85 3 days and 13 weeks 6 days. It achieves detection 42 1 : 45 1 : 65 rates of 95% of all aneuploides, 86% trisomy-21, and 43 1 : 35 1 : 50 100% of trisomy-18 and trisomy-13. PrAP-A levels are 44 1 : 30 1 : 40 ~19.6% lower in smokers. 41 In multiple pregnancy ≥45 1 : 20 1 : 25 risk is calculated per pregnancy if monochorionic; per fetus when dichorionic or trichorionic. 42 The integrated test This is better than the combined test if there are good facilities for NT measurements available and the woman is prepared to wait for 2nd trimester results. It involves NT + PrAP-A in the 1st trimester + the quadruple test in the 2nd trimester. Do not use 2nd trimester tests for triplets. 42 The quadruple test combines maternal -fetoprotein (AFP) + unconjugated estriol + free HCG or total HCG + inhibin-A + the woman’s age in the 2nd trimester. Use between 15 weeks + 0 days and 20 weeks + 0 days so useful for women presenting in the 2nd trimester. The emotional cost to the mother is impossible to calculate:43 56 out of every 57 women under 37yrs old who had a +ve test proved, after amniocentesis, not to have an affected fetus. Amniocentesis causes fetal loss (~0.86%44), and these losses will sometimes be of normal babies. New screening regimens in the 1st trimester go some way to mitigating distress and anxiety. We have no idea of the best way of counselling parents before the test. If we just hand out a leaflet, few will read it, and then when it comes to amniocentesis and termination, many will refuse—and the screening test wastes money, as well as laying health authorities open to litigation: “I never understood that I might lose a normal baby…” The alternative is to provide full details at the time of the initial blood test. The irony is that gaining informed consent is then the most expensive part of the test, and one which itself could cause much distress. Imagine an overjoyed expectant mother arriving in the clinic serene- ly happy in fulfilling her reproductive potential: the quintessence of health. She leaves only after being handed ethical conundrums of quite staggering proportions, involving death, disease, and human sacrifices, and a timetable for their resolution that would leave even the most fast-moving philosopher breathless and disorientated, and which may leave her forever bereft of one of Nature’s most generous gifts: the fundamental belief in one’s own wholeness. 1 Sources vary: if we look just at births to mothers aged 35, the proportion with Down’s in 4 studies was 1 : 265; 1 : 270; 1 : 35040,45 and 1 : 400 (ACOG 1999)46 Why the difference between 16wks and time of birth? Because of spontaneous miscarriages of fetuses with Down’s syndrome between 16wks and birth. Preimplantation genetic diagnosis 13 Preimplantation genetic diagnosis (PGD) is an early form of prenatal diagnosis in which embryos created in vitro are analysed for well-defined genetic defects. Defect-free embryos are then used for implantation. It is used in those with high risk of genetic disease, eg carriers of monogenic disease or chromosome structural abnormalities (eg translocations) who have repeatedly terminated pregnancies due to prenatal tests showing abnormality, who have concurrent infertility, who have had recurrent miscarriage (as occurs with translocation carriers), and for those with moral or religious objections to termination. It has also been used to screen for aneuploidy (PGD -AS) in those undergoing in vitro fertilization hoping to enhance chance of ongoing pregnancy (eg in the case for women >37–40 years old—but see below). Obstetrics Pioneered in the early 1990s, PGD has resulted in >1200 pregnancies (pregnancy rate 24%), of which 5% of babies had some kind of abnormality. PGD selection of embryos by HLA type so that a child born after using this technology can be used as a stem cell donor to save a sibling from certain conditions (eg with Fanconi anaemia,  thalassaemia, or leukaemia) is controversial, but possible. Some clinics select sex of implanted embryo eg for ‘family balancing’. Genetic analysis at the single cell level occurs using 1st polar body of an egg, or 2nd polar body (extruded after fertilization and completion of second meiotic division), or using blastomeres from cleavage-stage embryos. The blastocyst is the latest stage from which cells can be used but is little used as it leaves little time for analysis as embryos must be transferred before day 5 or 6. Biopsied surplus embryos can be cryopreserved but implantation rate for these is only 12%. Fluorescence in situ hybridization (FISH) is used for analysis of chromosomes and polymerase chain reaction (PCR) for analysis of genes in monogenic diseases. PGD can currently be applied for detecting 33 monogenic diseases. Gene analysis for X-linked conditions has the advantage that healthy male embryos and non-carrier female embryos can be transferred. Sexing embryos for X- linked conditions remains useful for conditions where the single gene is not known (eg non-fragile-X X-linked mental retardation), has been judged too dif- ficult a search, and for women eg over 37 who do not wish to wait for specific tests to be developed. Pregnancy rates are 17% after testing for structural chromosome abnormality (including translocations), 16% after sexing, 21% after testing for monogenic diseases. This is lower than the expected rate of 20–25% expected for regular IVF. For PGD -AS 25% pregnancy rates are achieved overall for women of previously poor prognosis due to advanced maternal age (a lower proportion than those where preimplantation genetic screening is not used), 47 repeated IVF failure (but only 8% do get pregnant), and recurrent miscarriage (28% pregnancy rate achieved). 14 The placenta  The placenta is the organ of respiration, nutrition, and excretion for the fetus. It produces hormones for maternal wellbeing. It immunologically protects the fetus from rejection and allows the passage of maternal IgG antibodies. Development At term the placenta weighs 1/7th the weight of the baby. It has a blood flow of 600mL/min. The placenta changes throughout pregnancy as calcium is deposited in the villi and fibrin on them. Excess fibrin may be deposited in diabetes and rhesus disease, so  fetal nutrition. Placental types Velamentous insertion (1%): umbilical vessels go within the membranes before placental insertion. Placenta succenturia: (5%) There is a separate (succenturiate) lobe away from the main placenta which may fail to separate normally and cause a PPH or puerperal sepsis. Vasa praevia: Fetal vessels from velamentous insertion or between lobes (succenturia, or bilobe placenta) risk damage at membrane rupture causing fetal haemorrhage. Caesarean delivery is needed (urgent if fetal compromise at membrane rupture, elective if detected antenatally by ultrasound). Placenta membranacea (1/3000) a thin placenta surrounds the baby. Some is in the lower segment so predisposes to APH. It may fail to separate in the 3rd stage. Placenta accreta: There is abnormal (morbid) adherence of all or part of the placenta to the Obstetrics uterus, termed placenta increta myometrium inflitrated, placenta percreta if penetration reaches the serosa. These 3 types predispose to PPH and need hysterectomy. Incidence  with the number of previous caesarean sections. Diagnose prenatally (colour doppler US/MRI p78). Placenta praevia The placenta lies in the lower uterine segment. It is found in ~0.5% of pregnancies. Risks are of significant haemorrhage by mother and fetus. Avoid PV examinations, advise against penetrative intercourse.10 Associations: Caesarean section; sharp curette TOP; multiparity; multiple pregnancy; mother >40 years; assisted conception; deficient endometrium-manual removal of placenta, D&C, fibroids, endometritis. Ultrasound (US) at 24%). Poor lower segment contractility predisposes to postpartum haemorrhage. Caesarean section should be consultant-performed or supervised with consultant anaesthetic attendance at 38wks, (36–7wks with steroid cover, crossmatched blood + haematologist available, 48 if accreta suspected), at a hospital with blood bank and level 2 critical care beds. 49 Ad- mitting those with major placenta praevia at ≤35 weeks’ gestation so that immediate help is available, is controversial, and not practised by many UK units but admit at 34wks if major praevia and there has been bleeding. After delivery Examine the placenta for abnormalities (clots, infarcts, am- nion nodosum, vasa praevia, single umbilical artery). Weigh the placenta (weight >25% of the baby suggests congenital nephrotic syndrome). Blood may be taken from the cord for Hb, Coombs’ test, LFTs, and blood group (eg for rhesus disease), or for infection screens, if needed. 15 Fig 1. Seven spiral arteries are here seen to have been successfully invaded by Obstetrics trophoblast and they are now flooding the vast intervillous spaces with hot maternal blood—producing the slow whooshing crescendos heard by the ultrasound probe as the backdrop to the faster fetal heart beat. To get to the fetus proper, nutrients have a 6-part journey: maternal blood space  syncytiotrophoblast  trophoblast basement membrane  capillary basement membrane  capillary endothelium  fetal blood. 50 In pre-eclampsia, trophoblast invasion is too shallow: there is no progress beyond the superficial portions of the uterine spiral arterioles. So these spiral arterioles retain their endothelial linings and remain narrow-bore, high-resistance vessels, resulting in poor maternal blood flow. The mother may raise her blood pressure to compensate for this—but the price may be eclampsia (p49). 51 Plasma chemistry in pregnancy Non-pregnant Trimester 1 Trismester 2 Trimester 3 Centile 2.5 97.5 2.5 97.5 2.5 97.5 2.5 97.5 Na+ mmol/L 138 146 135 141 132 140 133 141 Ca2+ mmol/L 2 2.6 2.3 2.5 2.2 2.2 2.2 2.5 *corrected 2.3 2.6 2.25 2.57 2.3 2.5 2.3 2.59 Albumin g/L 44 50 39 49 36 44 33 41 AST IU/L 7 40 10 28 11 29 11 30 ALT IU/L 0 40 6 32 6 32 6 32 TSH 0 4 0 1.6 1 1.8 7 7.3 *Calcium corrected for plasma albumin (OHCM p670) Other plasma reference intervals (not analysed by trimester) Non-pregnant Pregnant Alk phos IU/L 3–300 ≤450 (can be  in normal pregnancies) Bicarbonate mmol/L 24–30 20–25 Creatine μmol/L 70–150 24–68 Urea mmol/L 2.5–6.7 2–4.2 Urate μmol/L 150–390 116–276 (24wks), 110–322 (32wks), 120–344 (36wks) C-reactive protein does not change much in pregnancy. Platelets ≥150 ≈ 109/L (beware if 120 ≈ 109/L see p48). TSH may be low 40, or caesarean in labour, give LMWH for 7 days postpartum. Thromboprophylaxis after vaginal delivery: Risk factors Risk factors: (Thrombophilia/past thromboem- Age >35 years old bolism considered separately.) If BMI >40 offer Early pregnancy BMI >30 treatment. Offer to all women with two of the Smoker risk factors opposite (see MINIBOX). Parity ≥3 Obstetrics Multiple pregnancy Treatment: Treat with low molecular weight Assisted reproduction heparin (LMWH) eg enoxaparin starting as soon Gross varicose veins as possible after delivery (as long as no postpar- Paraplegia tum haemorrhage and ≥4h after epidural cathe- Sickle cell disease/SLE ter siting or removal—6h if that was traumatic). Nephrotic syndrome Continue for 7 days including at home. Dose of Some cardiac causes 1 enoxaparin: if the early pregnancy weight (EPW) Past thromboembolism Thrombophilia is 50–90kg, give 40mg/24h SC; if EPW 170kg Hyperemesis/dehydration give 0.6mg/kg/24h SC. If heparin is contraindi- Pre-eclampsia cated, use TED compression stockings (TED= Immobility for ≥3 days eg transverse elastic graduated). If 3 or more risk symphysis pubis dysfunc- factors give stockings and LMWH. tion Ovarian hyperstimulation Women with past venous thromboembolism Major infection (eg pyelo- (VTE ) ± thrombophilia: Action depends on risk: nephritis, wound infection) VH = very high; HR = high risk; IR = intermediate so hospital admission risk. Labour lasting >24h (VH) If recurrent VTE (+antiphospholipid syn- Mid-cavity forceps drome or antithrombin deficiency) or already Elective caesarean on long-term warfarin, use high-dose pro- Blood loss >1L/transfused phylactic LMWH, eg enoxaparin 40mg/12h SC Surgery in puerperium if 50–90kg EPW (or 75% of weight adjusted eg evacuation of retained products of conception therapeutic dose (WATD)). WATD=1mg/kg/12h Postpartum sterilization (kg is the EPW), prenatally and 1.5mg/kg/24h Long travel time (≥4h) postnatally. This is given prenatally. Withhold at onset of labour (halve to /24h the day before and the day of induction). Give for 6wks postpartum or revert to warfarin day 5–7 postnatally. (HR) Previous VTE unprovoked/idiopathic or oestrogen (or pregnancy)-related; or VTE + (1st degree relative with VTE or thrombophilia); or VTE + docu- mented thrombophilia: give LMWH antenatally and 6 weeks postpartum. (IR) If a single previous VTE provoked by major risk factor no longer present and no other risk factors give LMWH for 6wks postpartum (PP). Women with asymptomatic thrombophilia: See p33. 1 Non-oestrogen related provoked thromboembolism eg previous major surgery is not a risk factor. 17 Minor symptoms of pregnancy Before prescribing any drug, think—Is it necessary? Is it safe? Consult Data-sheets ± a national teratology information service (tel 0191 232 1525uk). Symptoms and signs in the first 10 weeks: Early symptoms are amenor- rhoea, nausea, vomiting, and bladder irritability. Breasts engorge, nipples enlarge (darken at 12 weeks), Montgomery’s tubercles (sebaceous glands on nipples) become prominent. Vulval vascularity increases and the cervix sof- tens and looks bluish (4 weeks). At 6–10 weeks the uterine body is more globu- lar. Temperature rises (5% of pre-pregnancy weight) and ketosis. It affects 1% of pregnant women. Risk is increased in youth, non-smokers, primips, working outside home, pre- existing diabetes, hyperthyroidism, psychiatric illness, family history, those with previous eating disorders and multiple or molar pregnancy (hence the idea that excessively high HCG levels may be the cause—whereas steeply rising oestrogens may cause the very common feature of morning sickness). Rarely, hyperemesis has been fatal. Recurrence rate 15% (10% if changed paternity). 53 Presentation Inability to keep food or fluids down; weight  (2–5kg) ± nutritional deficiency, dehydration, hypovolaemia, tachycardia, postural hypoten- sion, electrolyte disturbance with hypokalaemia and hyponatraemic shock, polyneuritis (B vitamins ), behaviour disorders, liver and renal failure. There may be ptyalism (inability to swallow saliva) and spitting. Tests Do PCV and U&E to help guide IV fluid regimen. 50% have abnormal LFTs (usually raised aminotransferase and bilirubin). TFTs are abnormal in 60% of those with hyperemesis. This is biochemical hyperthyroidism with raised free thyroxine and suppressed TSH. In women with hyperemesis thyroxine is con- verted to reverse tri-iodothyronine in the tissues which is physiologically in- Obstetrics active so stimulating metabolic rate less and conserving energy stores. The severity of hyperemesis correlates with the degree of biochemical hyperthyroidism, and those with abnormal TFTs require longer hospitalization to prevent readmission. The biochemical hyperthyroidism settles as vomiting settles so does not require treatment in its own right. Chart losses, weigh, record pulse and standing and lying blood pressure. Exclude UTI. Do ultrasound scan to exclude twins or hydatidiform mole. Treatment Admit to hospital. Give thromboprophylaxis (eg enoxaparin 40mg/24h SC) and anti-embolic stockings. Spend time optimizing psychological wellbeing. Is she worried about how her other children are being cared for? Most settle with due care and attention. If not too severe it may settle with rest, ginger, pyridoxine, dry bland food, and carbonated drinks. Rou- tine thiamine supplementation is wise for all women admitted (eg thiamine 25–50mg/8h PO) or if IV required 100mg diluted in 100mL normal saline given over 60min, repeated at weekly intervals. This is to prevent development of Wernicke’s encephalopathy (see OHCM p707)—which is then associated with 40% fetal loss. Correct dehydration with IV infusion (eg with normal saline infusion with potassium added to each bag as guided by U & E). Beware rapid reversal of hyponatraemia which can cause fatal central pontine myelinosis. 54 If condition does not improve after rehydration anti-emetics may be needed eg cyclizine 50mg/8h PO/IM or IV. Other recognized anti-emetics used: meto- clopramide, prochloperazine, chlorpromazine, domperidone, ondansetron. 55 Phenothiazines can cause drowsiness, extrapyramidal side effects, and ocu- logyric crisis. Those resistant to conventional treatments may respond to steroid treatment, eg hydrocortisone 100mg twice daily followed by 40mg prednisolone/24h tapering down. Prednisolone can then usually be reduced to 2.5–10mg/24h by 20 weeks' gestation. If it is needed long-term screen for UTI and gestational diabetes. Prednisolone is metabolized by the placenta, fetal blood levels are low and adverse fetal effects have not been reported. Parenteral nutrition may, very rarely, be needed—OHCM p574. If nutritional support is required both nasojejunal tube feeding and percutaneous endoscopic gastrostomy have been successfully used. 56 Parenteral nutrition has been found to be associated with serious complications (eg line sepsis). Get a dietician’s help. Sickle-cell disease in pregnancy57 19 Sickle-cell disease (SCD) is caused by a group of haemoglobin disorders (single gene recessive) which predispose to ‘sickling’ of red cells in low oxygen conditions causing vaso-occlusion in small vessels, and cells prone to increased haemolytic breakdown. Disease complications include painful crises, stroke, pulmonary hypertension, renal dysfunction, leg ulcers, retinal disease, avascu- lar necrosis (eg of hip). Pregnancy complications include maternal painful crises, prematurity and fetal growth restriction. Some studies suggest increased maternal infection, thromboembolic events and pre-eclampsia. Most prevalent in those of African descent it is also prevalent in the Caribbean, Middle East, Mediterranean, parts of India, South and Central America. There are 100–200 pregnancies in women with SCD in the UK annually. Obstetrics Preconception Women with SCD should be under annual clinic review to monitor disease. Arrange sickle specialist preconception review. Advice should cover factors affecting sickling crises (cold, hypoxia, dehydration-hence nausea and vomiting of pregnancy, over-exertion, stress). Pregnancy worsens anaemia, so  risk of crises and acute chest syndrome (ACS)-chest pain, cough, tachypnoea and new infiltrates on CXR: treat as for pneumonia+blood transfusion. Screen for red cell antibodies (if present risk of haemolytic disease of newborn). Pregnancy  risks of infection (especially UTI). Address  risk of fetal growth restriction (hence  induction, caesarean section rates). Address chance of fetus being affected (partner’s blood to check carrier/haemoglobinopathy status: genetic counselling if needed). Assess current disease: echocar- diography if not done in last year to exclude pulmonary hypertension (tricuspid regurgitant jet velocity >2.5m/s high risk, p20); BP & urinalysis, U &E, LFT ; retinal screening (proliferative retinopathy common); screen for iron overload if mul- tiply transfused (if significantly overloaded, preconception chelation therapy is advised). SCD is a hyposplenic state; advise daily penicillin or erythromycin and update vaccines: hepatitis B, single dose haemophilus influenza B & menin- gococcal C, 5-yearly pneumococcal, and annual H1N1 with seasonal influenza. Stop ACE /A2A drugs & hydroxycarbamide ≥3 months), preconceptually. Give 5mg folic acid daily (p2) preconceptually (requirement  as haemolysis). Antenatal care Ensure preconception measures addressed. Manage by specialist multidisciplinary team if possible; if not, by ‘high-risk’ team using protocols. If fetus has haemoglobinopathy risk, offer prenatal testing by 8–10 weeks. From 12 weeks give 75mg aspirin daily to reduce risk of developing pre- eclampsia. Suggest graduated compression stockings in pregnancy. If hospi- talized, give heparin thromboprophylaxis. Check BP at all antenatal visits and an MSU monthly. Offer viability scan at 7–9 weeks, dating scan at 11–14, anomaly scan at 20, and growth scan 4-weekly from 24 weeks. Only supplement iron if proven deficiency. Blood transfusion is not routine; if needed for sickling complication use fully compatible rhesus C,D,E and Kell typed CMV-negative blood (if so, transfusion regimen may be needed for rest of pregnancy). Top up transfusions may be needed if Hb falls to 6 or by 2g/dL from booking. Crises affect 27–50%. Admit if fever, severe or atypical pain, chest pain, or breathless. If pain needs IV opiates use morphine/diamorphine (not pethidine, it risks fits); give nasal O2 if oxygen sats non- pregnant levels by  heart rate and stroke volume. Twins  CO 30% more. Heart disease affects 8 weeks apart) ± past arterial thrombosis, venous thrombosis, or recurrent pregnancy loss. It may be primary, or follow other connective tissue disorder (usually SLE in which it occurs in 10%). Outcome: Untreated, 160/110) advise opera- tive delivery. Continue antenatal hypotensives postnatally (as above), reducing treatment if BP 24h since last dose LMWH. If caesarean section, use drains and wound clips or inter- rupted sutures in case of wound haematoma. Restart heparin 3h post-op (or >4h from epidural; do not remove epidural catheter within 12h of LMWH use). Postpartum enoxaparin can be reduced to 1.5mg/kg/24h. If warfarin chosen (after 3rd day) postpartum, monitor INR meticulously. Treat for at least 6 weeks postpartum and 3 months from thrombosis. Compression stockings should be worn for 2 years (reduces post-thrombotic syndrome incidence from 23% to 11%). 8 9 Both heparin and warfarin are fine if breastfeeding. Prophylaxis See p16. 33 Thrombophilia in pregnancy Thrombophilia is a tendency to increased clotting and many underlying causes are now known to contribute. Collectively, the conditions below affect at least 15% of Western populations, but are found in 50% of those with episodes of venous thromboembolism. Conditions include: Factor V Leiden mutation* decreases factor V breakdown by protein C (ac- tivated protein C (APC) resistance). This affects ~4% of the population and increases thrombotic risk 5–8.3 times (heterozygotes). Homozygous individu- als have 10–34 times the risk of venous thromboembolism. Protein C deficiency* (affects 0.3% of population; increasing thrombotic risk 2–4.8 times). Protein S deficiency* (affects 2% of population;  thrombotic risk 3.2 times). Obstetrics Antithrombin III deficiency* (affects 0.02% of population; thrombotic risk is increased 4.7–10 times). Acquired thrombophilia. This is lupus anticoagulant ± cardiolipin antibody*. Women with lupus anticoagulant risk arterial and venous thrombosis; in atypical veins, eg portal or arm. G20210A mutation of the prothrombin gene (1% of the population). Thrombotic risk is increased 3–10 times for heterozygotes, 26.4 times in homozygotes Homozygosity for the thermolabile variant of methylene tetrahydrofolate reductase (C677T MTHFR), which leads to homocysteinaemia (10% of the population). No association was found between venous thromboembolism and homozygosity for C677T MTHFR mutation, perhaps because plasma homo- cysteine reduces in pregnancy and folic acid supplements ameliorate hyper- homocysteinaemia. Dysfibrinogenaemia is rare, and the thrombotic risk variable. Pregnancy is an acquired risk factor for venous thromboembolism; the postnatal period being especially risky. The difficulty is to know who has thrombophilia, and what risk this poses to a pregnant woman. Past thrombosis increases risk, as does family history so thromboprophylaxis is recommended for those with history of thromboembolism and known thrombophilia or family history of thromboembolism (p16) both antenatally and postnatally. Treat- ment is stratified according to risk. For risks see p16. Women with asymptomatic thrombophilia: Women without past thromboembolic history but with the higher risk thrombophilias ie antithrombin deficiency, more than one thrombophilic defect (including homozygous factor V Leiden, homozygous G20210A mutation, and compound heterozygotes of factor V Leiden and G20210A mutations); and women with other thrombophilias but additional risk factors need expert advice as to whether antenatal thromboprophylaxis is required in addition to postnatal use on an individual basis. Women with lower risk thrombophilias but no additional risk factors can have careful surveillance antenatally and 7 days of postnatal low molecular weight heparin. It is not felt that all women should be screened for thrombophilia; although screening is recommended for those with a family history of thromboembolism and those with past history of idiopathic, or unprovoked thromboembolism (ie not oestrogen or pregnancy related). Screening is also recommended in those with second-trimester pregnancy loss, severe or recurrent eclampsia, and intrauterine growth restriction. Low molecular weight heparin is recommended for those with thrombophilia and past history of thromboembolism (see p16). The thrombophilias marked * above, and acquired protein c resistance are risk factors for developing pre-eclampsia so aspirin 75mg/24h PO is recommended from 12 weeks until delivery. 90 34 Infection: 1 † Investigating rash in pregnancy91 Investigate maculopapular rashes for rubella and parvovirus B19 (p142) (both these can infect the fetus) and measles. If maternal measles within 6 days before or after birth, the neonate needs human normal immune globulin 0.6mL/kg to max 5mL to prevent infection. Maternal chickenpox (p144) in 1st 24h of rash, from 20 weeks’ gestation merits oral aciclovir. Hospitalize her for IV aciclovir if immunosuppressed, very dense or haemorrhagic lesions, neurological or respiratory symptoms. Mothers in contact with rashes (15min, same household or room, face to face contact); test for parvovirus B19 (asymptomatic infections affect fetus as often as symp- tomatic), and rubella (unless vaccinated ≈2 or antibody level ≥10IU/mL ≈2, or 1 of each). If she has chickenpox contact and is susceptible (confirmed by urgent blood test), varicella zoster immune globulin (VZIG) can be given within 10 days of exposure but still manage her as if infectious 8–24 days post VZIG: and advise her to see GP if she develops a rash as protection not always effective. Rubella Childhood vaccination prevents rubella susceptibility. Asymptomatic reinfection can occur making serology essential in all pregnant rubella contacts. Routine antenatal screening finds those needing puerperal vaccination (avoid pregnancy for 1 month: vaccine is live). Symptoms (p142) are absent in Obstetrics 50%. The fetus is most at risk in the 1st 16 weeks’ gestation. 50–60% of fetuses are affected if maternal primary infection is in the 1st month of gestation: 90% asymptomatic). Intracranial calcification, hydro-

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