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Practical General Practice
For Buttenvorth-Heinemann: Commissioning Editor: Heidi Allen Project Development Manager: Robert Edwards Project Manager: Andrea Hill Designer: George Ajayi
Practical General Practice Guidelines for Effective Clinical Management
Edited by AleX KhOt MA, MB, BChir, DCH General Practitioner, East Sussex, UK
Andrew PolrnearMA,Msc,FRcp FRCGP Senior Research Fellow, Academic Unit of Primary Care, The Trafford Centre for Graduate Medical Education and Research, University of Sussex, UK
BUTTERWORTH-HEINEMANN An imprint of Elsevier Science Limited © Reed Educational and Professional Publishing Ltd 1999 © 2003, Elsevier Science Limited. 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, without either the prior permission of the publishers, or a licence permitting restricted copying in the United Kingdom issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London WIT 4LP. Permissions may be sought directly from Elsevier's Health Sciences Rights Department in Philadelphia, USA: phone: (+1) 215 238 7869, fax: (+1) 215 238 2239, e-mail: [email protected] You may also complete your request on-line via the Elsevier Science homepage (http://www.elsevier.com), by selecting 'Customer Support' and then 'Obtaining Permissions'. First edition 1988 Second edition 1992 Third edition 1999 Fourth edition 2003 Reprinted 2003 ISBN 0 7506 4911 9 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Note Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The editors and the publishers have taken care to ensure that the information given in this text is accurate and up to date. However, readers are strongly advised to confirm that information, especially with regard to drug usage, complies with the latest legislation and standards of practice. Disclaimer The clinical advice and the organizational details contained in this book refer to the United Kingdom, unless otherwise stated. The book is intended for the use of medical practitioners and not for patients. While strenuous efforts have been made to ensure the accuracy of the information in this book, it is the responsibility of the doctor who is caring for the patient to make his or her own judgement on the best treatment for that patient at that time. Some of the information contained in this book will become out of date. Some of it may even be wrong, written as it is by mere human beings. In particular, we recommend that prescribing details are checked with the British National Formulary or equivalent, or with the manufacturers' date sheets. We do not even attempt to list contraindications or adverse effects, nor do we always point out when a product is unlicensed for the use we are suggesting. The authors, editors and publishers cannot accept liability for information that is subsequently shown to be wrong. your source for books, journals and multimedia in the health sciences
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17. Substance abuse
The structure of the book ix
18. Ear, nose and throat problems 335
19. Eye problems
20. Skin problems
Feedback and updating List of contributors
List of abbreviations
21. Allergic problems 383
22. Older people 389 23. Disability 403
1. General 1 2. Infectious diseases
24. Haematology 415
3. Sexually transmitted infections 41 4. Childhood problems 51
26. Health promotion and screening 441
5. Cardiovascular problems 89
6. Respiratory problems 115 7. Gastroenterological problems
8. Endocrine problems 147 9. Rheumatological problems
25. Pain, palliative care and bereavement 421
10. Neurological problems 189 11. Gynaecological problems 209 12. Contraception and sexual problems 227
Appendix 1 Routine schedule of immunizations 459 Appendix 2 Incubation period and infectivity of common diseases 459 Appendix 3 A suggested schedule of immunization for travellers 460
13. Obstetric problems 253
Appendix 4 Notification of infectious diseases 460
14. Urinary problems 275
Appendix 5 Child health promotion 460
15. Surgical problems 287
Appendix 6 Injury prevention strategies 461
16. Psychiatric problems 301
Appendix 7 Stages of child development
Appendix 8 Stages of puberty 465
Appendix 20 Testing peripheral nerves 479
Appendix 9 Predicted normal peak flow values in children (under 15 years of age) 466
Appendix 21 Drug levels 480
Appendix 10 Peak expiratory flow in normal subjects 467 Appendix 11 FEV^FVC charts 468 Appendix 12A Management of chronic asthma in schoolchildren and young adults 469 Appendix 12B Management of asthma in children under 5 471 Appendix 13 Pill ladders 472 Appendix 14 Obstetrical table 473 Appendix 15 Edinburgh Postnatal Depression Scale 474 Appendix 16 International prostate symptom score (IPSS) 475 Appendix 17 Body mass index 476 Appendix 18 Blood data 477 Appendix 19 Dermatomes and myotomes 478
Appendix 22 Suggestions for monitoring patients taking disease-modifying anti-rheumatic drugs 481 Appendix 23 Problems associated with specific causes of disability 484 Appendix 24 The Community Dependency Index 486 Appendix 25 Nottingham Extended Activities of Daily Living Questionnaire (EADL) 487 Appendix 26 Admission procedures for patients with mental health problems 487 Appendix 27 The early warning form for use in psychotic illness 488 Appendix 28 Drug stabilities 489 Appendix 29 Guidelines for the urgent referral of patients with suspected cancer 491 Index 497
In the preface to the first edition of this book we wrote about our belief that it was possible 'to draw up guidelines of management which are logical and justifiable on the evidence'. The subsequent development of evidence-based medicine and of clinical guidelines shows that we were not alone in our belief and the evidence on which guidelines can now be based is far more extensive than it was then. For this reason we have recruited other authors to write some of the chapters, and they have indeed brought a new breadth to the book. We want to stress that this is a manual of clinical practice, not a collection of national guidelines. Each section is structured to try to mirror the thought processes of the doctor (see The structure of the book) in a way that few national guidelines do. Even less is it a textbook designed to give the reader an all-round knowledge of the subject. Anything that does not help the doctor decide what to do with the patient in the consulting room has been purged. Furthermore, we are deeply suspicious of textbooks as instruments of stagnation. We urge our readers to realize that this book will have started to go out of date by the time it goes on sale. Our hope is that the reader will use it as a template on which to write new information and new management strategies. This new edition is different from previous editions in a number of ways: 1. The search for evidence has been conducted in a more systematic way than before. Each author has searched for national guidelines, in the UK and abroad. If a reliable guideline was not found,
a search for evidence was conducted by working through the Cochrane Library, Clinical Evidence, Evidence-Based Medicine, Bandolier, Drug and Therapeutics Bulletin, Effective Health Care, Medline and other sources of evidence until reliable information was found. 2. The use of new authors has allowed us to submit the material for peer review. All chapters, except those submitted too late to allow time for review, were posted on a dedicated website. Authors reviewed each others' work and submitted comments to the editors. These comments were then argued over until they were accepted or rejected. 3. Contributors to three chapters have come from abroad - Australia, New Zealand and Mexico. The chapters that they have contributed therefore contain practical information, about patient organizations for instance, local to those authors, as well as the equivalent information for the UK. In some ways this has been a trial run. We have learnt what we suspected: that the core of the book is applicable to any country where a system of primary care exists that resembles that in the UK. We have also learnt that the local details differ so much that a single book cannot contain them. The way forward, for the fifth edition, must be multiple editions, differing electronic versions or a combination of the two. We therefore ask that you excuse our inconsistency in this edition. Our move to an international version is not due to unbounded ambition, but to our realization that previous editions have sold well abroad, and that we need to respond to what is clearly a need in
countries other than the UK. Indeed, the first Spanish edition of the book is in preparation. 4. The book contains many more references than previous editions. This partly reflects the systematic way in which the evidence has been collected,
but also it serves as a fairly complete guide to the literature on clinical management in primary care. Alex Khot Andrew Polmear
The structure of the book
ASTERISKS AND BULLETS
Central to the structure are instructions preceded by an asterisk:
These are used to highlight information that might otherwise get lost in the text: guidelines, a list of tests as a 'work-up' for a patient with a particular condition, or patient organizations.
* Ask the patient x, y and z; * Examine for a, b and c; * Take blood for d, e and f, etc. At the same time the reasons for these steps are explained, either in the same sentence or nearby, signalled by a round bullet. LISTS Where we present a list in no particular order we use (a) chest pain; (b) hypotension; or (c) heart failure. Where the order is important we number the list: 1. Sit the patient up. 2. Give oxygen.
3. Give diamorphine ...
REFERENCES Our aim is to reference every statement of fact. Where such a statement is not accompanied by a reference, the reader can assume it is taken from the reference in a box at the start of that section. Most instructions are, however, not referenced because they are original to this book.
We would like to thank the staff at ButterworthHeinemann for their help and support, especially Melanie Tait, Zoe Youd, Heidi Allen, Robert Edwards and Andrea Hill in the production of this edition; Caroline Makepeace, Mary Seager and Geoff Smaldon for previous editions; and Sue Deeley, our original editor, whose faith in our book from the start made the whole project possible. We are deeply grateful to Trish Maxwell at the University of Sussex for her work in transforming the work of so many authors into a single
format. As editors we would like to thank the contributors for their work and for their willingness to shrink their masterpieces into the required format. In turn the contributors would like to thank Professor R West (Chapter 17), Professor David Price, Dr Ron Neville, Dr David Bellamy, Dr Mike Thomas, Dr Daryl Freeman, Dr Rachel Joce, Dr Angela Iveson (Chapter 6) and the NHS R&D National Primary Care Award Scheme (for support of Dr A Sheikh).
Feedback and updating
We are keen to receive feedback from readers that could inform a future edition. This could take the form of ideas for new topics, new evidence that should be incorporated, or correction of errors of fact or judgement. A reader who would like to provide feedback should email [email protected]
A reader who does not have access to email may provide feedback by post by writing to Product Manager - General Practice, Elsevier Science, 32 Jamestown Road, London, NW1 7BY, UK.
List of contributors
Alex Khot, MA, MB, BChir, DCH General Practitioner, Portslade on Sea, East Sussex, UK
Hilary Pinnock, MB, ChB, MRCGP General Practitioner, Whitstable Medical Practice, GPIAG Clinical Research Fellow, Dept of General Practice & Primary Care, University of Aberdeen, UK
Andrew Polmear, MA, MSc, FRCP, FRCGP Senior Research Fellow, Academic Unit of Primary Care, The Trafford Centre for Graduate Medical Education and Research, The University of Sussex, Falmer, UK
Nurse Adviser Primary Care & Public Health
Ross Lawrenson, MD, MRCGP, MFPHM, FAFPHM Professor of Primary Health Care, University of Surrey, Guildford, UK
Jackie Cassell, MSc, MRCP, Dip GUM, DFFP Clinical Research Fellow, Department of Sexually Transmitted Diseases, Royal Free and University College Medical School, London, UK Barbara Rasburn, MB BS, BSc (Rons), MRCGP, DRCOG, DSFP General Practitioner, South Islington, London, UK
Marilyn Eveleigh, BA(Hons), PGCE, RGN, SCM, HV, FWT, NP, FRSH
Chapter 9 Kevork Hopayian, MB BS, BSc, FRCGP, DCH, DRCOG General Practitioner, Aldeburgh, Suffolk, UK
Pierre Pellegrino, MD Associate Specialist, Department of Sexually Transmitted Diseases, Royal Free and University College Medical School, London, UK
Stephen Cox, MSc, MB BS, MRCGP, DRCOG General Practitioner, Ardingly, West Sussex, UK
Multiple sclerosis and essential tremor
Paul Seddon, MB ChB, DCH, FRCP, FRCPCH Consultant Paediatrician, Brighton and Sussex University Hospitals, NHS Trust, East Sussex, UK
William A Rhoton, MD Planning & Development Unit, Hospital Civil de Guadalajara, Guadalajara, Mexico
LIST OF CONTRIBUTORS xiii
Fernando Petersen-Aranguren, MD, FACC Chair of Medicine, University of Guadalajara, Guadalajara, Mexico
Chapter 11 Lisa Argent, MB BS, DRCOG General Practitioner, GP Tutor, Hospital Practitioner in Obstetrics and Gynaecology, Brighton, East Sussex, UK
Chapter 20 CB Del Mar, MA, MD, MB BChir, FRACGP, FAFPHM Professor of General Practice, University of Queensland Medical School, Australia Geoff Mitchell, MB BS, FRACGP, FAChPM
Senior Lecturer in General Practice, University of Queensland Medical School, Australia
Chapter 21 Aziz Sheikh, BSc, MSc, MB BS, MRCGP, MRCP, DCH, DRCOG, DFFP
Sam Rowlands, MD, MRCGP, MFFP, DCH, DRCOG Lead Clinician in Reproductive & Sexual Health, South East Hertfordshire Primary Care Trust, General Practitioner, Luton, UK
NHS R&D National Primary Care Training Fellow, Department of Primary Health Care & General Practice, Imperial College of Science, Technology & Medicine, London, UK
Des Holden, BSc, PhD, MB BS, MRCOG Consultant Obstetrician, Brighton and Sussex University Hospitals, NHS Trust, East Sussex, UK
Ngaire Kerse, PhD, MBChB, FRNZCGP General Practitioner and Senior Lecturer in General Practice
Chapter 15 David Lewis, B Med Sci, FRCSEd, MRCGP, DFFP General Practitioner, Watford, UK
Matthew Parsons, BSc (Hons), MSc, PhD, RGN Senior Lecturer in Gerontology, Faculty of Medical and Health Sciences, University of Auckland, New Zealand
Ben Essex, MB BS, MSc, FRCGP, FRCP Medical Advisor, Lewisham Primary Care Trust, London, UK
Jane Crawford-White, DipCOT, BSc (Hons), SROT Lead Practitioner Occupational Therapist, East Cambridgeshire and Fenland Primary Care Trust Disability
Steven Laitner, MB BS, MSc, MRCP(UK), DCH, MRCGP DFPHM Specialist Registrar, Public Health Medicine, Brent and Harrow Health Authority, Middlesex and General Practitioner, St Albans, UK
Nick Lennox, MB BS, B Med SC, Dip Obst, FRACGP Director, Developmental Disability Unit, School of Population Health, University of Queensland, Australia
Philip Cotton, MRCGP Lecturer, Department of General Practice, University of Glasgow, UK
Catherine Neden, MA, FRCP, FRCGP, Dip Pall Med John Neden, MA, FRCGP, Dip Pall Med General Practitioners, Ramsgate, Kent, UK
List of abbreviations
5-FU 5-HT A/C AA AAA ABI ABPM ACBS ACE AD ADHD AF AFP AI AIDS ALP ALT AOM APTT APV AS ASO ASW a-v AV b.d. BA BBT BCC BCG BMA BMD BMI BMJ BNF
5-fluorouracil 5-hydroxytryptamine albumin/creatinine ratio attendance allowance abdominal aortic aneurysm ankle-brachial index ambulatory pressure monitoring Advisory Committee on Borderline Substances angiotensin converting enzyme Alzheimer's disease attention deficit (hyperactivity) disorder atrial fibrillation alpha-fetoprotein aortoiliac acquired immune deficiency syndrome actinomyces-like organism alanine transferase acute otitis media activated partial thromboplastin time acellular pertussis vaccine ankylosing spondylitis antistreptolysin O (titre) approved social worker arteriovenous atrio-ventricular twice daily (bis die) Benefits Agency basal body temperature basal cell carcinoma bacillus Calmette-Guerin British Medical Association bone mineral density body-mass index British Medical Journal British National Formulary
BP BSER BTB CABG CCF CDH CDSC CEG CF CHD CI CIN CJD CMO CMV CNS COAD COC COMA COPD CPAP CPHM CPK CPN CPR CRP CSA CSF CSM CSOM CT CTD CVA CVB CVD
blood pressure brainstem evoked response breakthrough bleeding coronary artery bypass graft congestive cardiac failure congenital dislocation of the hip Communicable Disease Surveillance Centre clinical effectiveness guidelines cystic fibrosis coronary heart disease confidence interval cervical intraepithelial neoplasia Creutzfeld-Jakob disease Chief Medical Officer cytomegalovirus central nervous system chronic obstructive airways disease combined oral contraceptive Committee on Medical Aspects of Food and Nutrition Policy chronic obstructive pulmonary disease continuous positive airways pressure Consultant in Public Health Medicine creatine phosphokinase community psychiatric nurse cardiopulmonary resuscitation c-reactive protein child sexual abuse cerebrospinal fluid Committee on Safety of Medicines chronic suppurative otitis media computerized tomography connective tissue disease cerebrovascular accident chorionic villus biopsy cardiovascular disease
LIST OF ABBREVIATIONS
CXR D&C DC DEET DEXA DLA DMARD DMPA DNA DoH DRO DSM DSS DTB DTP DU DVLA DVT DXR DXT ECG ED EDD EEG EIA ELISA EMA ENT EPA ERPC ESR FAP FBC FBS FDA FEVj FHSA FM3 FM5 FM6 FOB FP FPA FSH FT3 FT4 FTU FVC GA GCA
chest X-ray dilatation and curettage direct current diethyltoluamide dual energy X-ray absorptiometry disability living allowance disease-modifying antirheumatic drug depot medroxyprogesterone deoxyribonucleic acid Department of Health disablement resettlement officer Diagnostic and Statistical Manual Department of Social Security (now the Department of Work and Pensions) Drug and Therapeutics Bulletin diphtheria, tetanus and pertussis duodenal ulcer Driver and Vehicle Licensing Agency deep vein thrombosis deep radiotherapy deep radiotherapy electrocardiogram extended delivery expected date of delivery electroencephalogram enzyme immunoassay enzyme-linked immunosorbent assay endomysial antibody ear, nose and throat enduring power of attorney evacuation of the retained products of conception erythrocyte sedimentation rate familial adenomatous polyposis full blood count fetal blood sample Food and Drugs Administration (USA) forced expiratory flow volume in 1 second Family Health Services Authority Form Med 3 Form Med 5 Form Med 6 faecal occult blood femoropopliteal Family Planning Association follicle stimulating hormone free tri-iodothyronine free thyroxine fingertip unit forced vital capacity general anaesthetic giant cell arteritis
GCS GGT GI CMC GORD GP GPC GTN GTT GUM H2 HA ART Hb HbAlc HBeAg HBIG HBsAg HCG HDL HGV Hib HIV HMSO HNIG HNPCC HR HRT HSE HSV HTN HV HVS IBS IDD IFG IgG IgM IGT IHD im 1MB INR IOP IQ ISA ISDN ISMN ITP iu IUCD IUD
Glasgow Coma Scale gamma-glutamyl transferase gastrointestinal General Medical Council gastro-oesophageal reflux disease general practitioner General Practitioners' Committee (of the BMA) glyceryl trinitrate glucose tolerance test genitourinary medicine histamine receptor type 2 highly active antiretroviral therapy haemoglobin glycated haemoglobin hepatitis B virus e antigen hepatitis B immunoglobulin hepatitis B virus surface antigen human chorionic gonadotrophin high density lipoprotein heavy goods vehicle Haemophilus influenzae b human immunodeficiency virus Her Majesty's Stationery Office normal human immunoglobulin hereditary non-polyposis colorectal cancer heart rate hormone replacement therapy Health and Safety Executive herpes simplex virus hypertension health visitor high vaginal swab irritable bowel syndrome insulin dependent diabetes impaired fasting glycaemia immunoglobulin G immunoglobulin M impaired glucose tolerance ischaemic heart disease intramuscular intermenstrual bleeding international normalized ratio intraocular pressure intelligence quotient intrinsic sympathomimetic activity isosorbide dinitrate isosorbide mononitrate idiopathic thrombocytopenic purpura International Units intrauterine contraception device intrauterine device
LIST OF ABBREVIATIONS
IUGR IUS iv IVU JVP KUB LBC LDL LFT LH LHRH LMP LNG-IUS LOC LR LSCS LTOT LVF MA MAOI MASTA MCP MCV MDA MDI MI miu MMR MMSE MR MRI MS MSBP MSU MTP NE NETOEN NHS NI NICE NIDD NNH NNT NRT NSAID NSF NSPCC NSU o.d.
intrauterine growth retardation intrauterine system intravenous intravenous urogram jugular venous pressure kidneys, ureter and bladder liquid-based cytology low-density lipoprotein liver function test luteinizing hormone luteinizing hormone releasing hormone last menstrual period levonorgestrel releasing intrauterine system loss of consciousness likelihood ratio lower segment caesarean section long-term oxygen therapy left ventricular failure Maternity Allowance monoamine oxidase inhibitor Medical Advisory Service for Travellers Abroad metacarpophalangeal mean cell volume Misuse of Drugs Act metered dose inhaler myocardial infarction millions of international units measles, mumps and rubella Mini-mental State Examination modified release magnetic resonance imaging multiple sclerosis Munchausen's syndrome by proxy mid-stream urine metatarsophalangeal norethisterone enantate 1,9-nortestosterone National Health Service National Insurance National Institute for Clinical Excellence non-insulin dependent diabetes number needed to harm number needed to treat nicotine replacement therapy non-steroidal anti-inflammatory drug National Service Framework National Society for the Prevention of Cruelty to Children non-specific urethritis every day
o.m. OA OME OR ORS OT OTC p.r.n. PA PAM PCO PCOS PCP PE PEFR PEG PET PF PFI PHLS PHN PID PIH PIP PKU PMR PMS POP PPH PPI PPm PSA PSV PTA PUVA PV PVD q.d.s RA RAST RCGP RCP RCT RDC REM RIDDOR RMO RMS RNA RR RR
every night (omni node) osteoarthritis otitis media with effusion odds ratio oral rehydration salts occupational therapy/therapist over the counter as necessary posteroanterior postauricular myogenic response primary care organization polycystic ovary syndrome Pneumocystis carinii pneumonia pulmonary embolus peak expiratory flow rate percutaneous endoscopic gastrostomy positron emission tomography peak flow pill-free interval Public Health Laboratory Service post-herpetic neuralgia pelvic inflammatory disease pregnancy-induced hypertension proximal interphalangeal phenylketonuria polymyalgia rheumatica premenstrual syndrome progestogen-only pill post-partum haemorrhage proton pump inhibitor parts per million prostate-specific antigen public service vehicle post-traumatic amnesia psoralens with UVA plasma viscosity peripheral vascular disease to be taken four times a day (quarter die sumendum) rheumatoid arthritis radioallergosorbent testing Royal College of General Practitioners Royal College of Physicians randomized controlled trial research diagnostic criteria rapid eye movement Reporting of Injuries, Disease and Dangerous Occurrences Regulations Regional Medical Officer Regional Medical Service ribonucleic acid relative risk (according to context) respiratory rate (according to context)
LIST OF ABBREVIATIONS
RRR RUQ SBE sc SCC SD SHBG SIDS SK SLE SLR SMP SpA SPECT SPF SSD SSM SSP SSRI stat STD STI t.d.s. T4 TB TCA TENS
relative risk reduction right upper quadrant subacute bacterial endocarditis subcutaneous squamous cell carcinoma standard deviation sex hormone binding globulin sudden infant death syndrome solar keratosis systemic lupus erythematosus straight leg raising statutory maternity pay spondylarthropathies single photon emission computerized tomography sun protection factor Social Services department superficial spreading melanoma statutory sick pay selective serotonin reuptake inhibitor immediately sexually transmitted disease sexually transmitted infection to be taken three times a day (ter die sumendum) thyroxine tuberculosis tricyclic antidepressant transcutaneous electrical nervous stimulation
TFT TIA TIBC TM TOP TPHA TSH TURF TV U&Es UPSI URTI USS UTI UV UVA UVB UVC VA VAT VDRL VF VTE VZIG WB WBC WHO
thyroid function test transient ischaemic attack total iron-binding capacity temporomandibular termination of pregnancy Treponema pallidum haemagglutination (test) thyroid stimulating hormone transurethral resection of the prostate Trichomonas vaginalis urea and electrolytes unprotected sexual intercourse upper respiratory tract infection ultrasound scan urinary tract infection ultraviolet ultraviolet wavelength A ultraviolet wavelength B ultraviolet wavelength C visual acuity value added tax Venereal Disease Reference Laboratory ventricular fibrillation venous thromboembolism varicella-zoster immunoglobulin withdrawal bleed white blood cell (count) World Health Organization
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CHAPTER CONTENTS Medical certificates 1 Statutory Sick Pay 1 The Medical Service of the Benefits Agency Employment rehabilitation 3 Food handlers 4 Maternity benefits 4 Financial benefits for patients 4 If you disagree with the BA decision
Fitness to drive 7 Common medical problems that affect driving 8 Driving and the elderly 10 Driving for the disabled 10 Exemption from the wearing of a car seat belt 11 Fitness to fly
Fitness to scuba dive Mental capacity
Victims of crime or accidents 16 Rape and indecent assault 16 Occupational disease reporting 17 References
MEDICAL CERTIFICATES (SOCIAL SECURITY, STATUTORY SICK PAY AND MATERNITY BENEFITS) Advice: Benefits Agency (BA) booklet Medical Evidence for SSP, SMP and Social Security Incapacity Benefit Purposes: A Guide for Registered Medical Practitioners leaflet IB 204 available from local BA offices. Details are also available on www.dwp.gov.uk/index.htm
Patients are deemed unfit for work because of: (a) illness; or (b) the danger of their passing on infection; or (c) the fact that they are receiving treatment on a regular basis (e.g. dialysis, chemotherapy or radiotherapy). STATUTORY SICK PAY To qualify for Statutory Sick Pay (SSP), a patient must be employed, be under age 65 and have been sick for 4 consecutive days. This includes days when the patient would not normally have worked. A leaflet for patients (NI224 SSP) is available from local Benefits Agency offices. Periods of sickness that are =£ 8 weeks apart count as one. An employee not eligible for SSP may claim incapacity benefit instead. Self certification: If patients are sick for 4 to 7 days they should, on the last day of illness, certify themselves on form SCI if claiming incapacity benefit or form SC2 if claiming SSP. The GP is not 1
required to fill in a certificate for the first 7 days of illness. * Use form Med 3 (FM3) if the patient has been seen and examined not more than 1 day before. Otherwise use form Med 5 (FM5). * Assess whether patients are fit to work at their normal occupation. If unemployed, consider the patients' fitness for their last job, or the job for which they are registered with the Employment Service.
Notes on form Med 3 Open certificates
(a) If the patient is not expected to return to work within 2 weeks, an 'open' certificate should be issued, i.e. in Section (b) write in an appropriate number of weeks. In the first 6 months of illness, this period should not exceed 6 months. (b) If the patient is unfit continuously for more then 6 months then the statement can be filled in for longer periods and, in cases of severe illness, 'until further notice' can be used. (c) If an 'open' statement is issued, a patient cannot return to work without a 'closed' certificate. Closed certificates
If a patient is expected to return to work within 2 weeks, a 'closed' statement can be issued (i.e. in Section (b), after the phrase 'OR until', the date that the patient is expected to return to work should be filled in). Backdating
The GP cannot backdate a certificate. However, when a patient has either failed to consult a doctor at the start of the illness or has allowed a gap to occur between expiry of one 'open' Med 3 and the signing of the next, the GP can, in the space for comments, write: 'continuously unfit since ....
If a certificate is lost a duplicate can be issued, but 'DUPLICATE' should be written in the space for comments.
Notes on form Med 5 Use it if:
(a) no statement has been issued since the patient was examined and the GP wishes to issue a certificate more than 1 day after examination; or (b) it is felt, on the basis of a report from another doctor (not more than 1 month previously), that the patient should refrain from work; or (c) the patient has returned to work without a 'closed' form Med 3 (see below). Note: Form Med 5 should not be issued for a future period of more than 1 month.
Diagnosis The diagnosis should be as precise and as accurate as possible, unless the patient's interests dictate otherwise. If the GP does not wish to write the precise diagnosis, an imprecise diagnosis can be used. At the same time, form Med 6 (FM6) (one copy with each pad of FM3s) should be filled in with the correct diagnosis and sent to the local Benefits Agency office.
Notes on form Med 4 Form Med 4 (FM4) is issued when requested by patients, who will have been instructed to ask for it by the Benefits Agency. This usually happens after 28 weeks illness. The doctor should: (a) certify whether patients should refrain from their usual occupation; and (b) give the full diagnosis and further information, on which the BA will base the decision whether patients are fit for any work (the Personal Capability Assessment).
Once given, the GP is not required to issue further certificates.
THE MEDICAL SERVICE OF THE BENEFITS AGENCY The Medical Service may be involved: (a) at the request of an employee because the employer has refused to pay SSP. This happens when an employer does not accept that the employee is unfit to work; (b) where an employer asks for a second opinion, as in the case of prolonged or frequent illness, e.g. more than four periods of illness of 4 to 7 days each in any one year; (c) where an adjudication officer at the local BA office cannot find sufficient reason to grant incapacity benefit to a patient who is claiming it. Doctors who want a second opinion while continuing to issue certificates may refer cases to the Medical Service via the local BA office using form RM7 (one copy with each pad of FM3s). Patients will not be told that the GP made the referral. The Service is, however, unlikely to review patients if they are claiming SSP and not incapacity benefit.
When the GP disagrees with the decision of the BA When an adjudication officer declares that a patient is fit for work, a GP may only continue to issue form Med 3 if the patient's condition has deteriorated or the diagnosis has changed. It is important to detail the change under 'Doctor's remarks'. If neither of these circumstance applies, the patient should appeal against the decision of the adjudication officer to the Independent Tribunal Service. The GP can assist the appeal by: (a) writing in support of the patient; (b) asking a consultant for an opinion; (c) referring the patient to the Disability Employment Adviser for an opinion; (d) advising the patient to obtain support from a trade union or local rights organization.
EMPLOYMENT REHABILITATION As soon as it becomes clear that a patient will never be fit to return to previous work, consider whether rehabilitation or a change of job would be advisable. It is worth raising this topic before the BA applies the Personal Capability Assessment.
Options when the patient may be fit for alternative work (a) Issue a closed form Med 3, and in the comments section write 'fit within limits'. State what work might be suitable; or (b) continue to issue an open form Med 3 and refer, with the patient's consent, to the Disability Employment Adviser at the Jobcentre. Write a letter or complete form DP99 (available from the Jobcentre). The Adviser can arrange for the patient to be registered as disabled, which can lead to a number of facilities including retraining and placement in sheltered workshops or in vacancies reserved for the disabled. The Adviser also has access to schemes which provide special equipment and assistance with fares, and to the Job Introduction Scheme (which finances a disabled person in a job for a 6-week trial); or (c) continue to issue an open form Med 3 and recommend that the patient takes on part-time or light work as therapy. This can be done without loss of benefits, provided the doctor recommends it as therapeutic and the patient earns less than a certain amount and works for fewer than 16 hours a week. After April 2002 it will be called 'permitted work' and prior approval by a doctor will not be required. Prior approval from the local BA office is necessary before starting work to avoid accusations of 'moonlighting'.
Council tax discount Patients are entitled to a council tax discount if they are 'substantially and permanently disabled' or severely mentally impaired or they come into certain categories of carers.
FOOD HANDLERS Advice: Department of Health (DoH). Food Handlers' Fitness to Work. London: HMSO, 1995. Available from DoH, PO Box 410, Wetherby, LS23 7LN
Food handlers with diarrhoea or vomiting that is likely to be infectious should refrain from work and not return until 48 hours after the diarrhoea or vomiting has ceased. Indicators of infection are the presence of fever, or more than one episode of diarrhoea or vomiting. They should be notified as suspected food poisoning. Negative stool samples will only be needed from those with Salmonella typhi or paratyphi (six samples) or toxin-producing Escherichia coli (two samples). Food handlers with hepatitis A may return to work 7 days from the onset of symptoms. Food handlers with a staphylococcal or streptococcal infection may return to work once the lesion has healed, or sooner if it can be adequately covered. This applies to infections of the skin, eye, ear or mouth.
starting the time during which she draws her allowance until, at the latest, 1 week after the baby's birth. SMP or maternity allowance may be paid for a shorter period if a woman: (a) continues to work into the last 6 weeks of pregnancy (i.e. after 34 weeks of pregnancy); or (b) claims late.
Form Mat B1 * A form Mat B1(A) should be issued either by the GP or by the midwife not earlier than 20 weeks before the expected week of delivery (i.e. after 20 weeks of pregnancy). Examination may have been before this time. * If maternity allowance is claimed after confinement, use form Mat Bl (B).
FINANCIAL BENEFITS FOR PATIENTS
MATERNITY BENEFITS Guidance: The Benefits Agency. A Guide to Maternity Benefits. Leaflet Nl 17A from local BA offices.
Review: Teale C. Money problems and financial help. BMJ 1996; 313: 288-90. Guidance: www.dwp.gov.uk/index.htm
Most working women will be entitled to Statutory Maternity Pay (SMP) or Maternity Allowance (MA). The regulations are complex, and it is for the woman's employer to tell her the details. A woman not entitled to SMP nor to MA should claim incapacity benefit from 6 weeks before the expected date of delivery (HDD) until 2 weeks after the birth. The woman should: (a) inform her employer at least 21 days before she intends to stop work (she must not stop work earlier than 14 weeks before the expected delivery, i.e. when 26 weeks pregnant); (b) hand in medical evidence of the expected date of confinement (form Mat Bl, see below). Both SMP and maternity allowance are paid for a maximum of 18 weeks from, at the earliest, 11 weeks before the expected week of confinement (i.e. 29 weeks pregnant). A woman may delay
Figures in brackets (below) refer to the BA leaflet number, and these leaflets are available from local BA offices. It is worth the GP using the same terminology as the BA when writing in support of patients' claims.
Patients with a low income and little savings In 2001 the threshold for savings was £8000 for patients aged 40dB) hearing impairment is 1.16 per 1000. (A number acquire this severe loss of hearing bringing this figure to 1.3 per 1000. These children require a hearing aid). • At least a further 0.3 per 1000 have a hearing loss which is less than 40 dB but is sufficient for the child to need a hearing aid. • If all high-risk factors are considered, between 40 and 70% of all cases could be identified by testing 5-10% of all babies. • The following are at a high risk of congenital deafness: (a) survivors of intensive care, gestation 50 with angina, hypertension or heart failure. The reduction in mortality risk (RRR 20%, NNT 48) appears to be long term.
110 CARDIOVASCULAR PROBLEMS
* Prescribe an angiotensin converting enzyme (ACE) inhibitor to any patient who has had an MI and who has heart failure or left ventricular systolic dysfunction. Also consider them for patients who meet the criteria of the HOPE study (see p. 98). * Diabetes. Patients with diabetes should have their blood sugar and blood pressure meticulously controlled, with a target for the latter of < 140/80 or below (see p. 90). Lipids and their treatment: The NSF recommendations for secondary prevention The targets: (a) lower the total cholesterol to 0.75 jjig daily) have an increased risk of adrenal suppression, cataracts, reduced bone density and bruising.19 Risks should be balanced against benefits and alternatives considered (see box below).
1. Consider an objective trial of long-acting bronchodilators. 2. Monitor response with symptoms and peak flow charting. 3. If no response, stop the additional therapy and consider an alternative (e.g. leukotriene antagonists, increased dose of inhaled steroid). 4. If poor response to any of the options, consider the need for referral.
Beta2-agonists provide symptomatic relief and should be prescribed on an 'as required' basis.12,14,20 They are less effective than inhaled steroids in the management of mild persistent asthma.14,21 * Patients requiring relief medication more than once a day should be considered for regular prevention with inhaled steroids.12 * Exercise-induced asthma which persists despite good asthma control with inhaled steroids may be prevented by using a beta2-agonist prior to exercise. Long-acting bronchodilators are given regularly twice a day as 'add-on therapy' to asthmatics not controlled on inhaled steroids. The addition of long-acting bronchodilators improves lung function, symptom control, reduces the need for relief medication and reduces the exacerbation rate compared with increasing the dose of inhaled steroids.22,23 Leukotriene antagonists are mediator antagonists and are an option as 'add-on therapy'. Their role in comparison with other established therapies is still being investigated.1,12 Other therapeutic options
Management of patients not controlled on a moderate dose of inhaled steroids That is, adult maximum daily maintenance dose: beclomethasone 1000 ug, budesonide 800ug or fluticasone 500 ug. That is, childhood maximum daily maintenance dose: beclomethasone 400 |xg daily, budesonide 400 ug daily or fluticasone 250 u,g. Assessment: (a) Is the diagnosis correct? (b) Is the patient complying with the regular use of inhaled steroids? (c) Can the patient use his or her inhaler device? (d) Does the patient also have uncontrolled rhinitis? (e) Are there any environmental factors?
* Sodium cromoglicate has a small overall treatment effect and should not be first line treatment for the prevention of asthma.24 * Theophyllines may be an option as 'add on therapy' for a minority of patients.1,12 * A short 'rescue' course of oral steroids may be needed at any time and at any step12 but consideration of maintenance therapy with oral steroids should prompt referral to a respiratory physician.1
Devices The effectiveness of inhaled therapy depends on inhaler technique and the particle size produced
by the device.16 Inhaler devices should be selected for individual patients taking into consideration: (a) The patient's ability to use a device. This should always be checked before an inhaler is prescribed, and re-checked regularly. Effective delivery is achieved in about half the patients studied.16 Technique should be observed for: - the patient's inspirational flow rate compared to flow rate recommended by the manufacturer for efficient actuation and inhalation; - hand/breath coordination; - ability to follow the instructions for correct use. (b) The drug and dosage required. High doses of inhaled steroid should be given by a spacer device. (c) MCE guidelines recommend the use of spacers (with masks for infants) for children under the age of five.25 Choice of spacer device should be guided by the information in the Summary of Product Characteristics (see: www.nice.org.uk). (d) Patient preference and lifestyle issues may be relevant. (e) Cost of the device.26
Choice of inhaler device for different age groups Age
Devices to consider
MDI + spacer (with a mask for infants) MDI + spacer
Dry powder devices
Breath actuated devices MDI
Breath-actuated devices Dry powder devices MDI, measured-dose inhaler.
Recommended for inhaled steroids because it reduces oral deposition Once a child has adequate inspiration and can be relied on not to blow by mistake Once inspiration is adequate If technique is adequate. Should be used with a spacer to deliver high doses of inhaled steroid
Follow-up Review may be undertaken by GPs or trained asthma nurses and should encompass: * Specific morbidity questions. The Royal College of Physicians recommend that the following three questions should be asked at every asthma review consultation:27 1. Have you had difficulty sleeping because of your asthma symptoms (including cough)? 2. Have you had your usual asthma symptoms during the day (cough, wheeze, tight chest or breathlessness)? 3. Has your asthma interfered with your usual activities (housework, work or school, etc.)? * Review of medication, considering the need to step up or the possibility of stepping down treatment.12 * Review of inhaler technique. * Education and self-management. Patients should be encouraged to discuss issues of importance to them. Education should aim to empower patients to be in control of their asthma and should include the provision of written self-management plans.28
Indications for outpatient referral Referral to a respiratory physician or paediatrician should be considered:12,24 (a) If the diagnosis is not clear. (b) If the patient is not controlled with moderate doses of inhaled steroids ± add-on therapy and their inhaler technique is satisfactory. (c) If there is a possibility of occupational asthma. (d) If there is a history of life-threatening attacks or brittle asthma.
Self-management plans Education involving self-monitoring and written action plans reduce hospitalizations, emergency consultations, reduction in days off work or school, and nocturnal asthma.28 * Offer all asthmatics written self-management plans which should: (a) be tailored to the individual patient, taking into account his or her clinical condition and preference for autonomy;
(b) involve self-monitoring, based on peak flows and/or symptoms; (c) provide information about features which indicate that the patient's asthma is worsening; (d) advise what action the patient should take.
National Asthma Campaign 'Be in Control' action plan Symptoms are:
Peak flow is:
>80% of patient's best
Normal - continue treatment or talk to doctor/nurse about taking less treatment
Getting a cold, symptoms during daytime and/or night time
40°C, RR >30/minute, BP 20 years ago;§ (o) with known dysplasia,§ atrophic gastritis§ or intestinal metaplasia;§ or (p) jaundice.§
§ Referral is urgent (to be seen within 2 weeks) in these conditions.4
* Check Hb in all the above. * Give antacids while referral is proceeding. If the endoscopy is likely to be delayed for more than 4 weeks, consider giving a course of acid suppression for 2-4 weeks but complete the course at least 4 weeks before the endoscopy to avoid masking the pathology. * If endoscopy is negative and symptoms do not respond to acid suppression, consider alternative investigations: ultrasound of the gall bladder and pancreas, serum amylase or lipase, and LFTs during an exacerbation of pain. Consider other causes of abdominal pain.
Patients less likely to have positive endoscopic findings It is customary to treat these patients empirically, with endoscopy reserved for those who fail to respond or who relapse frequently. Against this approach is the fact that a response to acid suppression does not select those patients who will subsequently have a positive endoscopy. There is insufficient evidence to say that one approach is superior to the alternatives. The main options are therefore: (a) treat symptomatically with antacids, stepping up to an H2 antagonist then to a proton pump inhibitor (PPI) if necessary; or (b) test and treat; i.e. test all dyspeptics for H. pylori and eradicate it in those who are positive, without endoscopy; or (c) early endoscopy for all, which may be no more expensive than empirical treatment.5 Other options are: (d) test and endoscope if positive. This has been shown to increase endoscopy rates without any benefit to the patient.6 * In the absence of an authoritative current national guideline, the Primary Care Society for Gastroenterology7 recommends option (a), proceeding to option (b) or (c), according to local policy, in patients who relapse frequently or
whose symptoms are severe or do not respond to symptomatic treatment.
Patients in whom the diagnosis has been established Duodenal ulcer
Testing for H. pylori Use a breath test, or, if unavailable, a laboratory serology test enzyme-linked immunosorbent assay (ELISA).The bedside dipstick test on whole blood is unreliable.8 * Stop a proton pump inhibitor (PPI) 2 weeks before the breath test. Wait 4 weeks after eradication before repeating the test. * Serology cannot be used to assess response to eradication. It remains positive for 6-12 months.
Initial management * Explore the patient's fears and reassure as far as is justified. Worry about the seriousness of symptoms is the most significant factor in bringing patients with dyspepsia to their GP.9 * Advise the patient to stop smoking, to reduce coffee and alcohol intake and to avoid aspirin and NSAIDs. * Categorize the patient according to the Chicago Working Party report as follows:10 1. Peptic ulcer-like symptoms and any who are undefinable * Give antacids half-hourly if necessary. Avoid NSAIDs. * // there is no response after 1 week: check Hb and prescribe an H2-antagonist for 2-4 weeks. 2. Reflux-like symptoms * Advise the patient about general measures for reflux oesophagitis (see below). * Prescribe antacids ± alginates in adequate dosage, e.g. magnesium trisilicate or gaviscon 10-20 ml after meals + at night. * If the above fails, prescribe a PPI for 2-4 weeks. 3. Dysmotility-like symptoms Patients complain of bloating, nausea, retching and inability to eat a full meal. They may have symptoms of irritable bowel syndrome (IBS) as well. * Prescribe a prokinetic agent, e.g metoclopramide or, especially in the younger female, domperidone.
* Eradicate H. pylori without prior testing. At the time of writing the current regimen is to give 1 week of: (a) PPI at double the standard dose (in two divided doses); and (b) amoxycillin 1 g b.d.; and (c) clarithromycin 500 mg b. d. If the patient is intolerant of clarithromycin or amoxycillin, either can be changed to metronidazole 400 mg b.d. Alternatively, metronidazole may be used in place of amoxycillin first-line, provided the patient is not from an area of high metronidazole resistance (e.g. a developing country or a UK inner city with a large immigrant community). * If eradication is being given for an active ulcer, or for GI bleeding or to a patient on an NSAID, continue the proton pump inhibitor for a second week at the same dosage. * Only confirm that eradication is successful in complicated or refractory ulcers. Use the breath test, not serology, for confirmation, and delay testing until at least 4 weeks after treatment is completed. If the breath test is positive, give a second course of eradication therapy. * Patients who are still breath-test positive or who relapse after successful H. pylori eradication may have an antibiotic-resistant organism or may need longterm acid suppression. Refer to a gastroenterologist. Gastric ulcer * Test for H. pylori and eradicate if positive. Continue the PPI for 2 months, and ensure that follow-up endoscopy is performed until the ulcer is healed. NSAID-induced peptic ulcer * Stop the NSAID and treat the ulcer as above (but with H. pylori eradication only if testing for H. pylori is positive); or * Continue the NSAID in patients who cannot do without it, and prescribe a healing dose of a
134 GASTROENTEROLOGICAL PROBLEMS
PPI followed by a maintenance dose for as long as the patient continues to take the NSAID. H. pylori testing and eradication is unlikely to benefit the patient, who would anyway remain on long-term acid suppression.11 * Consider use of a COX II selective inhibitor or another newer NSAID, which is less toxic to gastric mucosa. The National Institute for Clinical Excellence (NICE) warns that even COXII-selective inhibitors should be used with caution in patients with a history of peptic ulcer, of GI bleeding or of perforation. NICE'S recommendations for the use of COX II selective inhibitors are summarized in the box below. Recommendations on the use of COX-ll-selective inhibitors12 Use them only in patients at high risk of serious adverse GI adverse effects: (a) Age 65 and over; (b) On concomitant medication which increases the risk of upper GI adverse effects (but not low-dose aspirin); (c) With serious comorbidity; or (d) When prolonged use at maximum dosage is contemplated.
* The benefit from acid suppression is modest.15 PPIs are slightly more effective than H2 antagonists.16 * The benefit from H. pylori eradication in those who are positive is small with a mere 9% (95% CI 40% to 4%) reduction in the number of patients still suffering after treatment.14 * Continue the general measures above, with extra attention to an explanation of the nature of the condition. * Explore whether psychological factors are playing a part. * Give antacids for acid-like symptoms or an prokinetic agent for dysmotility-like symptoms. * Control more severe symptoms with short courses of acid suppression. Before repeating or continuing acid suppression, remember that the placebo response in non-ulcer dyspepsia is marked.17 Consider an antidepressant, even in patients who are not clinically depressed. * Consider referral for counselling or psychotherapy for those in whom the psychological component appears to be large.18
They should not be combined with a gastroprotective agent.
Duodenitis * Erosive duodenitis is part of the spectrum of duodenal ulcer disease and should be treated in the same ways as duodenal ulcer. Non-erosive duodenitis and gastritis should be treated symptomatically without H. pylori eradication, even if they are H. pylori positive. Patients on long-term acid suppression for a proven peptic ulcer * Consider H. pylori eradication, without further investigation, as for newly diagnosed patients.13 Established diagnosis of non-ulcer dyspepsia • This is the final diagnosis in 90% of patients with dyspepsia under the age of 45 and 75% of such patients who are H. pylori positive.14
GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD) • The diagnosis is made either by a classical history or by the finding of oesophagitis on endoscopy • A normal endoscopy does not exclude the diagnosis. As many as 50% of patients whose symptoms are due to reflux will have no visible oesophagitis. • Endoscopy is, however, essential in the diagnosis of Barrett's oesophagus and stricture. These patients need long-term acid suppression and regular endoscopy. Otherwise, the aim in patients with or without oesophagitis is to control symptoms. • Advise the patient to: (a) elevate the bed head by 6 inches; (b) stop smoking (two cigarettes in 20 minutes reduces lower oesophageal sphincter pressure by 50% and increases acid secretion);
(c) avoid fatty foods, alcohol, coffee, onions, peppermint, citrus fruits, tomatoes and other foods known to make symptoms worse. Weight loss in the obese may help symptoms; (d) avoid aspirin and other NSAIDs; (e) avoid lying down with a full stomach, and preferably eat 4 hours before going to bed. * Mild symptoms: 'step-up' as follows, moving to the next step if the previous one fails to control symptoms: 1. Antacids and/or alginates in adequate doses after meals and at night. Raft antacids cost about four times as much, but appear to give better relief of symptoms than antacids alone. 2. Acid suppression: a PPI daily for 4-8 weeks. This controls symptoms in 83% and heals oesophagitis in 78%, as opposed to 60% and 50% for H2 antagonists. Continuous use of a PPI gives the best results in heartburn19 but is not recommended in the UK for mild-moderate symptoms for reasons of cost (see box on NICE guidance below). 3. Prakinetic agents may be helpful in individual patients, either alone or in combination with a proton pump inhibitor. * Severe symptoms: 'step-down' treatment, starting with a PPI, and reducing to an H2 antagonist or antacid as symptoms resolve. If symptoms are only controlled by a PPI, continue it at the lowest dose that gives control. Patients who do not respond should be referred for endoscopy as below. * Surgery: consider referral of young patients (e.g. under age 50) uncontrolled by the above measures to a surgeon who specializes in fundoplication.20 Also consider referral in those in whom reflux has led to inhalation of gastric contents with respiratory symptoms, and in those in whom a hiatus hernia is causing mechanical problems. Fundoplication, however, frequently causes difficulty with swallowing, belching and dyspepsia.
Guidance on the use of PPIs from the National Institute for Clinical Excellence NICE. Guidance on the use of proton pump inhibitors in the treatment of dyspepsia. London: NICE, 2001. Online. Available: www.nice.org.uk
PPIs are appropriate: (a) When a patient on an NSAID must continue it and has a documented NSAID-induced ulcer. The dose should be stepped down for maintenance. (b) As part of an H. pylori eradication programme. (c) For GORD, either where symptoms are severe or with proven pathology (oesophageal ulceration or Barrett's oesophagus). The dose should be 'stepped down' except in cases of complicated oesphagitis (stricture, ulcer or haemorrhage). (d) In other situations, including undiagnosed dyspepsia, a short course may be indicated where other symptomatic treatment has failed.
COLORECTAL CANCER Guidelines: SIGN. Colorectal cancer: a national guideline recommended for use in Scotland by the Scottish Intercollegiate Guidelines Network. Scottish Intercollegiate Guidelines Network, 1997. Online. Available: www.sign.ac.uk Department of Health. Guidelines for the urgent referral of patients with suspected cancer. London: DoH, 2000. Online. Available: www.doh.gov.uk/ cancer/referral.htm
* Refer patients for screening if they have a sufficiently strong family history (see p. 136). * Refer patients of any age urgently (to be seen within 2 weeks21) who have a new occurrence of: (a) a right-sided abdominal mass; or (b) a rectal (not pelvic) mass; or (c) rectal bleeding and a change in bowel habit to looser stools and/or increased frequency of defecation persistent for 6 weeks; or (d) iron deficiency anaemia without an obvious cause (Hb 5-10 years is associated with a 50% increase in breast cancer and the beneficial effects of HRT may be lost a few years after cessation (see p. 219). * Depending on the drug used, the population studied, length of follow-up and which fracture Table 9.5
* Consider prescribing calcium 0.5-1 g daily and vitamin D 400 iu daily. * Consider falls risk assessment, advice and referral, e.g. to physiotherapy (walking aids, hip protectors) or occupational therapy.78 For those at high risk, or with established osteoporosis with or without fracture * Consider referral to specialist for DEXA scan or refer directly to imaging unit. Only refer if the result is likely to alter your management. * Treat according to the result as follows: -T score above —1: Reassure and give lifestyle advice.79 -T score —1 to —2.5: Lifestyle advice and recommend pharmacological therapy if previous fracture. -T score below —2.5: Lifestyle advice and recommend pharmacological therapy. Postmenopausal women * Use HRT or a bisphosphonate, or calcitonin second line. * If using a bisphosphonate for prevention, use alendronate 5mg daily or, for treatment, 10 mg
Estimating dietary intake of calcium
Calcium content mg
Glass, 200 ml
Cheddar cheese Low-fat fruit yoghurt White or brown bread Wholemeal bread Baked beans Canned sardines in tomato sauce with bones Broccoli
30 g Pot(150g) 2 slices of large loaf 31 g 2 slices of large loaf 31 g 1 small can, 150g 100g
237-249 (depending on whether full fat, semi-skimmed or skimmed) 216 225 72 39 80 460
Cooked, 85 g
Source: The Calcium Counter, National Dairy Council, 5-7 John Princes Street, London.
daily or 70 mg once a week; or use cyclical etidronate with calcium; or risedronate 5 mg daily. Steroid-induced osteoporosis * Prescribe alendronate 5mg daily for prevention or treatment but 10 mg if postmenopausal and not on HRT; or use cyclical etidronate with calcium; or risedronate 5 mg daily. Premenopausal women or men 4% at the spine or >7% at the hip. Then recheck the DEXA scan 1-3 yearly according to the risk. * Intermittent steroids. Manage the patient as above if the total dose over 6 months is equivalent to the doses given above. This means considering prophylactic drugs if intermittent steroid use equates to 7.5 mg daily over 6 months.
Management of fracture In vertebral collapse, exercises are contraindicated and recovery is likely to take 3 months. * Refer to domiciliary physiotherapy and occupational therapy to keep the patient mobile and independent. * Prescribe analgesics. * If analgesia is insufficient, prescribe calcitonin 50-100 iu sc or im injection, three times a week or daily. Reduce the frequency of dosing as the pain is controlled. The maximum duration of treatment is 3 months.81 It should be combined with calcium (at least 600 mg/day) and vitamin D (400 iu daily). Its analgesic action is independent of its effect on the osteoporosis.
POLYMYALGIA RHEUMATICA/TEMPORAL ARTERITIS 183
Patient information: ARC. www.arc.org.uk (choose 'index' then 'O' for osteoporosis). The National Osteoporosis Society, Camerton, Bath BA2 OPJ, tel. 01761 471771; Helpline 01761 472721; www.nos.org.uk
POLYMYALGIA RHEUMATICA/ TEMPORAL ARTERITIS Review: Swannell AJ. Polymyalgia rheumatica and temporal arteritis: diagnosis and management. BMJ 1997; 314:1329. Guideline: Polymyalgia, clinical recommendation from prodigy, 1999. Online. Available: www.prodigy.nhs.uk/ guidance/crs/Polymyalgia%20Rheumatica.htm
Background (a) About half of patients with giant cell arteritis (GCA) have symptoms of polymyalgia rheumatica (PMR), and 15-50% of patients with PMR have GCA.82 (b) In PMR, the inflammation affects mainly the shoulder and pelvic girdle muscles. (c) They are both conditions predominantly of the elderly, rarely occurring under the age of 50.
POLYMYALGIA RHEUMATICA Management objectives • To control symptoms of stiffness and pain (plus associated constitutional symptoms, e.g. fatigue, weight loss). • To reduce the risk of the complication of temporal arteritis. • To minimize the risks of steroid therapy.
Diagnosis • The patient is being committed to at least 2 years of steroid therapy. As no single test reliably confirms the diagnosis, the history is important. • The typical history in PMR is of pain, stiffness, or both, affecting the upper arms and upper legs
with diurnal variation, that is, say, worse in the mornings. This history is present in 95% of cases.83 • Confidently diagnose PMR if three or more of the diagnostic criteria (see box below) are present or if one criterion is associated with a clinical or pathological abnormality of the temporal artery. The sensitivity for this criterion-based test is 92% (i.e. it will correctly identify 92% of all cases) and the specificity is 80% (i.e. it will correctly exclude 80% of normals).84 Features of polymyalgia rheumatica (a) Bilateral shoulder pain or stiffness. (b) Onset of illness 40mm/h. (d) Age 65 years or more. (e) Depression and/or weight loss. (f) Bilateral tenderness in the upper arms.
Investigations * Check ESR or plasma viscosity. Note that the ESR will be normal in 20% of cases. * Check FBC; a normocytic normochromic anaemia is common.
Initial management * Measure weight, BP and test urine for sugar before starting steroids. * Prescribe prednisolone 15 mg daily. Higher starting doses are rarely needed and are more likely to cause adverse effects.85 * Review within a fortnight. Expect a dramatic response within days. * Consider these alternative diagnoses if there is no response to steroids: (a) cervical spondylosis (the commonest differential diagnosis); (b) rheumatoid arthritis; (c) malignancy especially lung cancer; (d) connective tissue disease - polymyositis; (e) myeloma; (f) hypothyroidism. * Therefore, retake history, re-examine and consider the following investigations: (a) CXR;
(b) FBC; (c) biochemistry screen: U&E, calcium, LFTs, TFTs; (d) protein electrophoresis - to exclude myeloma; (e) creatine kinase - to exclude polymyositis. * Raise the dose of prednisolone to 30 mg daily if you have confidently excluded other diagnoses.
Maintenance steroid therapy * The risk of relapse is highest early on in treatment and at doses below 10 mg. Temporal arteritis is more likely to develop at doses below 10 mg daily. * Treatment needs to be maintained for at least 2 years. Even then, only a quarter of patients can stop steroids after this time.86 * Over half of patients with PMR (and GCA) will develop complications of steroids, the commonest being weight gain.87 * Reduce prednisolone dose to the lowest possible to maintain control. A suggested routine is as follows:88 * Prescribe 15 mg daily for the first month. Check inflammatory markers after 2-6 weeks. * Reduce by 2.5 mg each fortnight until 10 mg daily is reached, providing there is no relapse of symptoms or rise in inflammatory markers. * Review the patient 1 week after each dose reduction. * Reduce the daily dose by 1 mg every 6 weeks until 5-7 mg daily is reached. * Maintenance dose: 5-7 mg for 12 months providing there is no relapse of symptoms or inflammatory markers. * Final reduction: Reduce the daily dose by 1 mg every 6 to 8 weeks, providing symptoms and (less importantly) inflammatory markers remain controlled. * If symptoms suggest continuing disease in presence of normal inflammatory markers, give more weight to the former. * Warn patients that symptoms may return and advise early consultation. A return of symptoms is a more reliable early indication of relapse than inflammatory markers.
Referral * Refer patients when: (a) Symptom control requires a high maintenance dose of steroids or the patient develops significant adverse steroid effects on lower doses (steroid sparing drugs may be considered). (b) There is doubt about the diagnosis, particularly when there is synovitis and anaemia suggestive of rheumatoid arthritis.
Patient education * Advise patients to seek urgent attention if they develop a unilateral headache, tenderness in the scalp or jaw claudication (facial pain on chewing). * Advise patients about the risks of steroids (see below) and precautions to take. * Offer the ARC booklet, available: www.arc. org.uk (choose 'index' then 'P' for polymyalgia rheumatica).
TEMPORAL ARTERITIS • Temporal arteritis is the commonest form of GCA but other arteries may be involved. After headache or pain in the temple, the next most common syndrome is jaw claudication. • It is almost exclusively a disease of white people. • A normal ESR, PV or negative temporal artery biopsy do not rule out the disease. The chance of obtaining a positive biopsy after 1 week of steroid therapy falls to 10%.82 • Steroid therapy should not be delayed pending the results of investigations because untreated GCA carries a risk of visual loss in 40% of patients.89
Initial management82 * Visual loss: If vision is impaired, give prednisolone up to 80 mg immediately and make an urgent referral to an ophthalmologist. If there is likely to be a delay, continue that dose daily. * Clear clinical diagnosis without visual loss: (a) Take blood for an ESR and FBC; (b) Start prednisolone 40 mg daily;
POLYMYALGIA RHEUMATICAfi'EMPORAL ARTERITIS
(c) See the patient after 48 hours: If the symptoms have virtually gone, the diagnosis is confirmed (see below for maintenance doses). If the symptoms are still present, discuss the patient with a rheumatologist/ophthalmologist urgently. Temporal artery biopsy is likely to be needed, and should be performed as soon as possible after starting steroids. * Suspected diagnosis: Check ESR or PV, start steroids 40 mg daily and arrange for the patient to be seen within 48 hours by a rheumatologist/ ophthalmologist.
Maintenance treatment * Reduce the dose by 5 mg every 4 weeks down to 10 mg daily, then as for polymyalgia rheumatica. * If long-term maintenance is needed, keep the dose as low as possible, e.g. about 3 mg daily.
Steroids Adverse effects will develop in up to 50% of patients. The risk is positively associated with the dose.82 * Educate the patient about the risks. (a) weight gain; (b) hypertension; (c) osteoporosis; (d) development of diabetes/worsening of diabetic control; (e) infection risk, especially chicken pox; (f) risk of GI perforation in combination with NSAIDs; (g) adrenal suppression. * Ensure the patient has an up-to-date steroid card. * Advise the patient not to stop steroids suddenly. * Advise the patient that it may be necessary to increase the dose of steroids during intercurrent illness and to seek medical advice. * Warn the patient to avoid contagious contacts with chicken pox and shingles (there is a risk of fatal disseminated chickenpox if not immune). Advise them to seek urgent medical advice if they are exposed. Obtain specialist advice if such exposure occurs (see p. 31).
* Consider testing immune status for chickenpox when commencing steroid therapy. * Check weight, BP and urine (or blood) for glucose every 3 months. * Patients are likely to be on 7.5 mg or more prednisolone daily for 6 months so should be started on prophylaxis against osteoporosis (see Osteoporosis, above). * Advise flu vaccination if on high doses of steroid over the winter months.
FIBROMYALGIA Review: Doherty M, Jones A. ABC of rheumatology: Fibromyalgia syndrome. BMJ1995; 310: 386-9.
* This is a distinctive syndrome90 with the following features: (a) diffuse pain; (b) fatigue and non-restorative sleep; (c) multiple points of extreme tenderness, usually neck and low back, trapezius, chest wall, lateral humeral epicondyle, upper outer quadrant of buttock, greater trochanter and knee. * Some deny its existence as a syndrome.91 Its preponderance in women (90% of sufferers), the presence of fatigue and poor sleep, and its association with anxiety and depression have led to the view that it is a form of somatisation. However, these facts do not de facto prove it to be a psychosomatic disease, since they apply to several rheumatic problems, e.g. rheumatoid arthritis.
Management * Find out the patient's concerns and worries and answer appropriately. * Explain that there is no serious pathology but do not imply that the symptoms are not genuine.92 * Advise gradual increasing exercise.92 * Explain the value of tricyclics in raising the pain threshold and improving sleep. Prescribe low dose amitriptyline 25 mg o.n. and increase according to the response.93 * In severe unremitting cases, consider referral to a multidisciplinary team.
Patient information: ARC leaflet. Online. Available: www.arc.org.uk (choose 'index' then 'F' for fibromyalgia).
Patient support group: Fibromyalgia Association UK, PO Box 206, Stourbridge, DY9 8YL, tel. 01384 820052; www.fmsni.freeserve.co.uk
REFERENCES 1. Superio-Cabuslay E, Ward MM, Lorig KR. Patient education interventions in osteoarthritis and rheumatoid arthritis: a meta-analytic comparison with nonsteroidal anti-inflammatory drug treatment. Arthritis Care Res 1996; 9: 292-301. 2. Donovan JL, Blake DR. Qualitative study of interpretation of reassurance among patients attending rheumatology clinics: 'just a touch of arthritis, doctor?' BMJ 2000; 320: 541-4. 3. Bird HA. When are NSAIDs appropriate in osteoarthritis? Drugs Aging 1998; 12: 87-95. 4. Eccles M, Freemantle N, Mason J et al. North of England evidence based guideline development project: summary guideline for non-steroidal anti-inflammatory drugs versus basic analgesia in treating the pain of degenerative arthritis. BMJ 1998; 317: 526-30. 5. PCRS. The management of osteoarthritis - patient-centred not disease-focused. Primary Care Rheumatology Society. Online. Available: www.liv.ac.uk/HumanAnatomy/phd/pcr/ 6. Chard J, Dieppe P. Glucosamine for osteoarthritis: magic, hype, or confusion? BMJ 2001; 322: 1439^0. 7. Moore RA, Tramer MR, Carroll D et al. Quantitative systematic review of topically applied non-steroidal anti-inflammatory drugs. BMJ 1998; 316: 333-8. 8. Eccles M, Freemantle N, Mason J et al. North of England evidence based guideline development project: summary guidelines for non-steroidal anti-inflammatory drugs versus basic analgesia in treating the pain of degenerative arthritis. BMJ 1998; 317: 526-30. 9. Zhang WY, Li Wan Po A. The effectiveness of topically applied capsaicin: a meta-analysis. Eur J Clin Pharmacol 1994; 46: 517-22. 10. Creamer P. Intra-articular corticosteroid injections in osteoarthritis: do they work and if so, how? Ann Rheum Dis 1997; 56: 634-6. 11. DTB. Hyaluronan for knee osteoarthritis. Drug Ther Bull 1999, 37. 12. Gam AN, Johannsen F. Ultrasound therapy in musculoskeletal disorders: a meta-analysis. Pain 1995; 63: 85-91. 13. Puett DW, Griffin MR. Published trials of non-medicinal and non-invasive therapies for hip and knee osteoarthritis. Ann Intern Med 1994; 121: 133^0. 14. Royal College of Radiologists. Making the best use of a department of clinical radiology. London: RCR, 1998. 15. Scott DL, Shipley M, Dawson A et al. Strategies for improving clinical effectiveness. London: British Rheumatology Society. Online. Available: www.rheumatology.org.uk 16. Towheed TE, Hochberg MC. Health-related quality of life after total hip replacement. Semin Arthritis Rheumatism 1996, 26: 483-91.
17. Callahan CM, Drake BG, Heck DA et al. Patient outcomes following tricompartmental total knee replacement: a meta-analysis. JAMA 1994, 271: 349-57. 18. Garellick G et al. Survival of hip replacements. Clin Orthop Rel Res 2000; 375: 157-67. 19. Moran CG, Horton TC. Total knee replacement: the joint of the decade. BMJ 2000; 320: 820. 20. National Institutes for Health. Total hip replacement. MH Consensus Statement 1994; 12: 1-31. 21. Simmons N, Ball A, Cawson R et al. The case against antibiotic prophylaxis for dental treatment of patients with joint prostheses. Lancet 1992; 339: 310. 22. Nachemson A, Jonsson E (Eds). Neck and back pain. Philadelphia: Lippincott Williams & Wilkins, 2000. 23. Mason V. The prevalence of back pain in Great Britain. London: OPCS HMSO, 1994. 24. Garvey T, Marks M, Wiesel S. A prospective, randomized, double-blind evaluation of trigger-point injection therapy for low-back pain. Spine 1989; 14: 962-4. 25. Waddell G, Feder G, Lewis M. Systematic reviews of bed rest and advice to stay active for acute low back pain. Br J Gen Pract 1997; 47: 647-52. 26. Tulder MV, Malmivaara A, Esmail R, Koes B. Exercise therapy for low back pain (Cochrane Review). The Cochrane Library, Issue 2. Oxford: Update Software, 2000. 27. Guzman J, Esmail R, Karjalainen K et al. Multidisciplinary rehabilitation for chronic low back pain: systematic review. BMJ 2001; 322: 1511-16. 28. Vroomen P, de Krom M, Knotterus J. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation: a systematic review. / Neurol 1999; 246: 899-906. 29. Hazard R, Haugh L, Reid S et al. Early physician notification of patient disability risk and clinical guidelines after low back injury: a randomized, controlled trial. Spine 1997; 22: 2951-8. 30. Koes BW, Assendelft WJ, van der Heijden GJ et al. Spinal manipulation for low back pain: an updated systematic review of randomized clinical trials. Spine 1996; 21: 2860-71. 31. DoH. Referral guidelines for suspected cancer. London: Department of Health, 2000. Online. Available: www.doh.gov.uk/cancer/referral.htm 32. Royal College of Radiologists. Making the best use of a department of clinical radiology. London: RCR, 1998. 33. Frank A. Low back pain. BMJ 1993; 306: 90. 34. Nachemson A, Jonsson E (Eds). Neck and back pain. Philadelphia: Lippincott Williams & Wilkins, 2000. 35. Aker P, Gross A, Goldsmith C et al. Conservative management of mechanical neck pain: systematic overview and meta-analysis. BMJ 1996; 313: 1291-6.
36. Gam AN, Johannsen F. Ultrasound therapy in musculoskeletal disorders: a meta-analysis. Pain 1995; 63: 85-91. 37. Yassi A. Repetitive strain injuries. Lancet 1997; 349: 943-7. 38. Speed C, Hazelman B. Shoulder pain. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. 39. Assendelft W, Hay E, Adshead R et al. Corticosteroid injections for lateral epicondylitis: a systematic overview. BJGP 1996; 46: 209-16. 40. Marshall S, Tardif G, Ashworth N. Local corticosteroid injection for carpal tunnel syndrome (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2001. 41. Speed C. Corticosteroid injections in tendon lesions. BMJ 2001; 323: 382-6. 42. Silver T. Joint and soft tissue injection. Injecting with confidence, 2nd edition. London: Radcliffe Medical Press, 1999. 43. Gotzsche PC. Non-steroidal anti-inflammatory drugs. BMJ 2000; 320: 1058-61. 44. British National Formulary. Non-steroidal antiinflammatory drugs. 2001, 41: Section 10.1.1. Online. Available: http://BNF.org 45. Silverstein FE, Faich G, Goldstein JL et al. Gastrointestinal toxicity with celecoxib vs. nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis. The CLASS study: a randomised controlled trial. JAMA 2000; 284: 1247-55. 46. Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure: a meta-analysis. Ann Intern Med 1994,121: 289-300. 47. Anon. GI, renal and cardiac AEs of NSAIDs. Bandolier 2000; 79: 6. Online. Available: www.jr2.ox.ac.uk/bandolier/index.html 48. Henry D, Lim LL, Garcia Rodriguez LA et al. Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis. BMJ 1996; 312:1563-6. 49. Anon. Cox-2 roundup. Bandolier 2000; 75. 50. Rostom A, Wells G, Tugwell P et al. Prevention of NSAID-induced gastroduodenal ulcers (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2000. 51. The diagnosis and management of anaphylaxis. / Allergy Clin Immunol 1998; 101 (6 Pt 2): S465-S528. 52. NICE. Cox II selective inhibitors, celecoxib, rofecoxib, meloxicam, and etodolac for osteoarthritis and rheumatoid arthritis. Technology Appraisal Guidance No. 27, London: NICE, July 2001. 53. Eccles M, Freemantle N, Mason J. North of England evidence based guideline development project: summary guideline for non-steroidal anti-inflammatory drugs versus basic analgesia in treating the pain of degenerative arthritis. BMJ 1998; 317: 526-30. 54. British National Formulary. Non-steroidal anti-inflammatory drugs. 2001, 42: Section 10.1.1. Online. Available: http://BNF.org 55. PRODIGY. Gout, clinical recommendations: 1999. Available on www.prodigy.nhs.uk 56. Ralston S, Capell H, Sturrock R. Alcohol and response to treatment of gout. BMJ 1988; 296: 1641-2. 57. Egsmose C, Lund B, Borg G et al. Patients with rheumatoid arthritis benefit from early second line
62. 63. 64. 65. 66.
67. 68. 69. 70.
therapy: 5 year follow up of a prospective double blind placebo controlled study. / Rheumatol 1995; 22: 2208-13. Arnett FEA. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31: 315-24. Scott D, Shipley M, Dawson A et al. The clinical management of rheumatoid arthritis and osteoarthritis: strategies for improving clinical effectiveness. Br J Rheumatol 1998; 37: 546-54. Royal College of Radiologists. Making the best use of a department of clinical radiology. London: RCP, 1998. Calin A, Elswood J, Klouda P. Destructive arthritis, rheumatoid factor HLA DR4: susceptibility versus severity: a case-control study. Arthritis Rheum 1989; 32: 1221-5. Brooks P, Day R. Non-steroidal anti-inflammatory drugs: differences and similarities. New Engl J Med 1991; 324: 1716-25. British National Formulary. Antimetabolites. 2001; 42: Section 8.1.3. Online. Available: http://BNF.org Thurtle O. Whose guidelines should you follow? Musculoskel Med 1993; 3: 4. PRODIGY. Rheumatoid arthritis, clinical recommendations: 1999. Available on www.prodigy.nhs.uk American College of Rheumatology. Guidelines for the management of rheumatoid arthritis 1996. Online. Available: www.rheumatology.org (choose 'publications' then 'treatment guidelines'). Palinkas L, Kabongo M. The use of complementary and alternative medicine by primary care patients. Practice 2000; 49: 1121-30. Fortin P, Lew R, Liang M et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. / Clin Epidemiol 1995; 48: 1379-90. Jacobs JC. Spondyloarthritis and enthesopathy. Current concepts in rheumatology. Arch Intern Med 1983; 143: 103-7. Van den Hoogen HMM, Koes BW, Van Eijk JTM, Bouter LM. On the accuracy of history, physical examination, and erythrocyte sedimentation rate in diagnosing low back pain in general practice: a criteria-based review of the literature. Spine. 1995; 20: 318-27. Calin A, Porta J, Fries JF, Schurman DJ. Clinical history as a screening test for ankylosing spondylitis. JAMA 1977; 237: 2613^. Kraag G et al. The effects of comprehensive home physiotherapy and supervision on patients with ankylosing spondylitis. A randomised controlled trial. Rheumatol 1990; 17: 228-33. Koh WH, Pande I, Samuels A et al. Low dose amitriptyline in ankylosing spondylitis: a short term, double blind, placebo controlled study. / Rheumatol 1997; 24: 2158-61. Maugars Y et al. Assessment of the efficacy of sacroiliac corticosteroid injections in spondyloarthropathies: a double blind study. Br J Rheumatol 1996; 35: 767-70. Clegg DO, Reda DJ et al. Comparison of sulfasalazine and placebo in the treatment of ankylosing spondylitis. A Department of Veterans Affairs Cooperative Study. Arthritis Rheum 1996; 39: 2004-12. Creemers MC, Franssen MJ, Van de Putte LB et al. Methotrexate in ankylosing spondylitis: an open study. / Rheumatol 1996; 22: 1104-7.
77. Royal College of Physicians and The Bone and Tooth Society of Great Britain. Osteoporosis: clinical guidelines for prevention and treatment. Update on pharmacological interventions and an algorithm for management. London: RCP, 2000. Online. Available: www.rcplondon.ac.uk 78. Close ], Ellis M, Hooper REA. Prevention of falls in the elderly trial (PROFET: a randomised controlled trial). Lancet 1999; 353: 93-7. 79. Ernst E. Exercise for female osteoporosis. A systematic review of randomised clinical trials. Sports Medicine 1998; 25: 359-68. 80. National Osteoporosis Society. The prevention and management of corticosteroid induced osteoporosis. Bath: NOS, 1998. 81. British National Formulary. Drugs affecting bone metabolism. 2001, 42: Section 6.6. Online. Available: http://BNF.org 82. Fountain G, Hazleman B. Polymyalgia rheumatica and giant cell arteritis. BMJ 1995; 310: 1057-9. 83. Bahlas A, Ramos-Remos C, Davis P. Clinical outcome of 149 patients with polymyalgia rheumatica and giant cell arteritis. / Rheumatol 1998; 25: 99-104. 84. Bird H, Esselinckx W, Dixon ASJ et al. An evaluation of criteria for polymyalgia rheumatica. Ann Rheum Dis 1979; 38: 434-9. 85. Kyle V, Hazleman B. Treatment of polymyalgia rheumatica and giant cell arteritis. I. Steroid regimens in the first two months. Ann Rheum Dis 1989; 48: 658-61.
86. Kyle V, Hazleman B. Clinical and laboratory course of polymyalgia rheumatica/giant cell arteritis after the first two months of treatment. Ann Rheum Dis 1993; 52: 847-50. 87. Kyle V, Hazleman B. Treatment of polymyalgia rheumatica and giant cell arteritis. II. Relation between steroid dose and steroid-associated side effects. Ann Rheum Dis 1989; 48: 662-6. 88. PRODIGY. Polymyalgia, clinical recommendations: 1999. Available on www.prodigy.nhs.uk 89. Birkhead N, Wagener H, Shick R. Treatment of temporal arteritis with adrenal corticosteroids: results in 55 cases in which the lesion was proven at biopsy. / Am Med Assoc 1957; 163: 821-7. 90. Wolfe F. The relation between tender points and fibromyalgia symptom variables: evidence that fibromyalgia is not a discrete disorder in the clinic. Ann Rheum Dis 1997; 56: 268-71. 91. Makela M. Is fibromyalgia a distinct clinical entity? The epidemiologist's evidence. Bailliere's Best Pract Res Clin Rheumatol 1999; 13: 415-19. 92. Gowans S, deHueck A, Voss S et al. A randomized, controlled trial of exercise and education for individuals with fibromyalgia. Arthritis Care Res 1999; 12: 120-8. 93. O'Malley P, Balden E, Tomkins G et al. Treatment of fibromyalgia with antidepressants: a meta-analysis. / Gen Intern Med 2000; 15: 659-66.
CHAPTER CONTENTS Migraine 189 Menstrual migraine 191 Cluster headaches 191
Non-migrainous headache 191 Tension-type headache 191 Chronic paroxysmal hemicrania 192 Exertional and coital headache 192 Thunder-clap' headache 192 Raised intracranial pressure 192 Epilepsy
Parkinson's disease 196 Stroke 198 TIA and minor stroke
Motor neurone disease Multiple sclerosis
Paraplegia 204 Essential tremor References 205
Guidelines: British Association for the Study of Headache. Guidelines for all doctors in the diagnosis and management of migraine and tension-type headache. March 1999. Available from the British Association for the Study of Headache, Wood Dene, Stanton Lees, Mr Matlock, Derbyshire DE4 2LQ www.bash.org.uk William EM et al. Guidelines for the diagnosis and management of migraine in clinical practice. Can Med Assoc J1997; 156: 1273-87.
Treatment of the acute attack Standard advice for every attack
(a) Advise patients to remove themselves to a quiet place and sleep if possible. Consider giving a benzodiazepine if sleeping has helped in the past. (b) Give: dispersible aspirin 900 mg or soluble paracetamol 1 g, or ibuprofen 400 mg, at the first sign of the attack; and metoclopramide lOmg or domperidone 10 mg orally or a 30 mg suppository. This will reduce nausea and lead to quicker absorption of analgesics. Do not use codeine or other opioids: they tend to worsen nausea and are more prone to lead to analgesic-overuse headache. Severe attacks
* Give diclofenac lOOmg suppositories and domperidone 30 mg suppositories. 189
* Consider a 5-HTj agonist, whether by tablet, wafer, nasal spray or self-administered injection. The tablets or spray will abort 70% of attacks at whatever stage they are given,1 the injection 85%.2 They may be less effective during an aura.3 If one 5-HTx agonist fails or causes side-effects, consider a trial of another. * Hold ergotamine in reserve for use only if the above fail and observe the restrictions on its use listed in the BNF. Oral ergotamine is ineffective, being almost entirely removed by first-pass metabolism. The benefits of ergotamine are usually outweighed by its problems: side-effects are common (20%), especially nausea and abdominal pain; overuse leads to headache, which is only relieved by taking further ergotamine; it should not be used in those with vascular disease, nor in those on propranolol or methysergide, nor if sumatriptan has been taken in the previous 6 hours. If the doctor is called * Administer either a 5-HTi agonist (e.g. sumatriptan sc) unless two injections have already been given in the last 24 hours or one dose in the last hour; or diclofenac 75 mg im plus metoclopramide 10 mg im or prochlorperazine 12.5 mg im for vomiting. * Admit the patient with a prolonged attack who is becoming dehydrated.
Prevention * Encourage the patient to discover the triggers of an attack and see how they can be altered, e.g. stress, excitement, certain foods, hunger, fatigue, exertion, oversleeping and coitus. * Stop combined oral contraceptives (COCs) in a woman whose migraine starts or worsens when taking them, especially if focal symptoms develop. Their use is associated with an increased risk of cerebral thrombosis. If stopping the COC is unacceptable, give low-dose aspirin daily, and use the lowest oestrogen pill acceptable. * Consider prophylaxis in anyone whose life is sufficiently disturbed by attacks.
Self-help group: Migraine Action Association, Unit 6, Oakley Hay Lodge Business Park, Great Folds Road, Great Oakley, Northants NN18 9AS, tel. 01536 461333; www.migraine.org.uk
Prophylaxis Three or more attacks per month is the usual criterion for prophylaxis, but a patient with severe attacks may choose prophylaxis with far fewer than that. * Explain that most of the prophylactic drugs have the same efficacy, reducing the frequency of severity of attacks by about 50%, but that individual patients respond to some and not others so a trial of drugs will be necessary. * Continue a drug that is effective for at least 6 months, and tail off slowly (except methysergide, see below). Try each for 2 months before abandoning it. Ask the patient to monitor attacks with a diary. * Use only one prophylactic drug at a time, except as an extreme measure. (a) Beta-blockers without intrinsic sympathomimetic activity (ISA). Propranolol, atenolol, metoprolol, nadolol and timolol. Start at a low dose, e.g. propranolol 10 mg t.d.s., and increase monthly up to 160 mg daily. A patient may fail to respond to one beta-blocker but respond to another. (b) Pizotifen helps 60% of patients, but side-effects of sleepiness and weight gain are common. Start at 1.5mg at night. If tolerance develops, increase the dose. (c) NSAIDs. Aspirin 75-500 mg daily helps up to 30% of patients.4 Ibuprofen, naproxen and flurbiprofen may help about 50%,5 but are not appropriate for long-term use; the risk of side-effects does not abate with time. (d) Calcium channel blockers. Nifedipine, verapamil and diltiazem are effective in conventional doses but not licensed for use in migraine. (e) Tricyclic antidepressants, e.g. amitriptyline 10-75mg at night, may be helpful and are especially useful combined with propranolol in patients with a combination of migraine and tension headaches.
(f) Sodium valproate may be helpful although unlicensed for use in migraine. Start at 200 mg b.d. (g) Methysergide still has a role where all other prophylaxis has failed, but it should be given under specialist supervision for 4 months at a time with 1 month between courses to reduce the risk of retroperitoneal fibrosis. (h) Feverfew 200 mg daily may help,6 although not prescribable. Benefit only occurs after 6 weeks of use. Once started, patients should always buy the same product, because the constituents are not standardized. (i) Acupuncture but may help, although the evidence is not convincing.7
MENSTRUAL MIGRAINE * NSAIDs, e.g. naproxen 250-500 mg b.d., starting at the onset of bleeding. * Percutaneous oestrogen, e.g. Estraderm TTS patch (an unlicensed use) applied 2 days before the migraine is likely to start and left on for 4 days. Start with the 50 juig patch and adjust the strength up or down according to the response. Do not use oestrogens in women with focal migraine. * Women already on the COC. Consider the tricycle regimen (see p. 230).
CLUSTER HEADACHES (MIGRAINOUS NEURALGIA) * 5-HT^ agonists will abort three-quarters of all attacks within 15 minutes.8 * Ergotamine (see p. 190) taken half an hour before an attack is due will prevent some attacks. * Verapamil 20 mg t.d.s. will stop two-thirds of episodes once attacks begin. If it fails, use a betablocker or pizotifen. * Methysergide may be used more readily than in migraine because it will be needed for 3 months or less. * Lithium carbonate is probably the most effective prophylactic, and should be used as for manicdepressive illness (see p. 308). * Prednisolone 40 mg daily for 5 days then reducing to the lowest dose that will control attacks is justified if other prophylactic treatments fail.
NON-MIGRAINOUS HEADACHE • A history and simple examination (BP, fundi and a search for focal neurological signs) permit a clinical diagnosis in most patients. An ESR may be needed in patients over 50 to exclude giant cell arteritis. Cervical spondylosis, sinusitis, intracranial haemorrhage and other conditions of which headache is a symptom will need treatment in their own right. • Analgesic headache may complicate management, and is most likely to occur in patients taking analgesics combined with benzodiazepines or opioids such as dextropropoxyphene. Analgesics for headaches should not be taken on more than 15 days per month.9
TENSION-TYPE HEADACHE Guideline: DTB. Management of tension-type headache. Drug Ther Bull 1999; 37: 41-4.
* Exclude conditions which can cause secondary tension headache, e.g. cervical spondylosis, poor neck posture, temporomandibular (TM) joint dysfunction, sinus pain or eye muscle disorders. * Explain that the condition is real and benign. * Explore the tensions in the patient's life. * Advise relaxation techniques: yoga, massage, 'time-out' from a stressful day or more formal stress management.10 * Assess whether depression is present. * Check whether medication overuse is contributing to the headache. * Recommend paracetamol or aspirin over the counter. * Prescribe: (a) an NSAID, e.g. ibuprofen 400 mg t.d.s. if needed, but for no more than 3 days per week; (b) a tricyclic antidepressant, e.g. amitriptyline 10-75mg at night; or (c) propranolol 10^0 mg t.d.s.
CHRONIC PAROXYSMAL HEMICRANIA These are repeated attacks of unilateral headache lasting less than 45 minutes. * NSAIDs, e.g. indomethacin 25 mg t.d.s. reducing to 25 mg daily, will prevent most attacks.
EXERTIONAL AND COITAL HEADACHE * Give an NSAID or propranolol before attacks once a pattern is established.
THUNDER-CLAP' HEADACHE * Refer urgently if the first attack is sufficiently severe to present acutely. It may be a subarachnoid haemorrhage, presaging a more severe bleed.
RAISED INTRACRANIAL PRESSURE This is rarely the cause of headache in a patient without vomiting, papilloedema or neurological signs. However, exceptions occur. * Refer patients with a short history of headache (less than 4 months), especially if it is localized, worse on waking, worse on coughing or straining, and especially in the older patient.11
2. Prevent onlookers from restraining the fitting patient. 3. Do not give drugs initially - the fit is likely to have stopped before they can act. Give drugs if the fit is continuing without signs of abating after 5 minutes. 4. Admit any patient with a fit if there is suspicion that the fit is secondary to other illness; if the patient fails to recover completely after the fit (other than feeling sleepy); or if there is status epilepticus. Status epilepticus exists if more than one seizure occurs without the patient regaining consciousness, or if the fitting continues for over 30 minutes; 5 minutes of fitting is a more reasonable guide to when drugs should be given. 1. Give lorazepam 4mg iv slowly, and repeat every 15 minutes until the fits are controlled. Diazepam lOmg may be given iv or rectally, but is probably less effective.12 iv administration by paramedics (using half those doses) can reduce respiratory or circulatory complications from 20%, with placebo, to 10% with the benzodiazepine. 2. Check the blood sugar with a test strip. 3. Arrange immediate admission even if the fits are controlled - the patient may need other measures to prevent cerebral oedema.
Subsequent management EPILEPSY Guidelines: British Epilepsy Association. Principles of epilepsy management 1999. Online. Available: www.epilepsy.org.uk Crawford P, Appleton R, Betts T et al. Best practice guidelines for the management of women with epilepsy. Se/zt/re1999;8:201-17. MeReC. The treatment of epilepsy parts 1 and 2. MeReC Bull 1995; 6:17-20, 25-8.
Management of a major fit 1. Turn the patient into the coma position and ensure that the airway is not obstructed.
• A single fit is not necessarily epilepsy. It is only followed by recurrence in 40% of patients over 15. If the EEG is normal, the chance of further fits is only about 10% and does not warrant anticonvulsants.13 • Refer for neurological assessment, to be seen within 4 weeks, because of the need to exclude an underlying cause and because of the implications for work and driving. Refer more urgently if there are multiple seizures or focal neurological signs. The only patient who need not be referred is a child aged 18 months to 5 years who has recovered promptly from a febrile convulsion. • Discuss with the specialist the need to start an antiepileptic drug before the patient has been seen if there has been a previous fit in the
preceding 12 months or if the waiting list is longer than 4 weeks. * Once the diagnosis of epilepsy has been made and a decision taken about drug treatment, the GP is best placed to take over management, calling on a specialist for advice if in difficulties. Follow-up must, however, be structured, and defaulters sought out. Repeat prescriptions of drugs and a policy of waiting until a patient complains of problems are inadequate.14 * Re-referral is needed where: (a) control is poor or the drugs are causing side-effects; (b) seizures have continued for 5 years; (c) there are pointers to a previously unsuspected cause for the fits; (d) concurrent illness complicates management; or (e) the patient needs preconceptual advice.
Initial management * Find out how much the patient and his or her family understand about epilepsy, and answer their questions. Issues to discuss are: (a) Heredity. If one parent has epilepsy the risk for a child is increased from 0.5-1% to 4%. If both parents have epilepsy the risk increases to 15-20%.15 (b) Underlying pathology. It is not usually evidence of a brain tumour. Only 5% of those having their first fit over 21 years old have cerebral pathology. For those aged 45-55 it is still only 10%. (c) Prognosis. In 80% of patients with epilepsy, fits can be controlled by drug treatment and most of those patients need drug treatment for less than 5 years.16 * Acknowledge the distress and anger the patient and family feel at the disruption this diagnosis has brought to their lives. * Driving. Advise the patient of the need to notify the DVLA and the insurance company of any seizure, however minor. Document this advice. A licence is likely to be withdrawn until: (a) free from fits for 1 year; or (b) if the patient's fits in the last year have been while asleep and the patient has had fits
while asleep for >3 years with no fits while awake in that time (see p. 8). Fits at the time of waking or falling asleep count as 'daytime' fits. * Employment. Advise the patient not to work at heights or near dangerous machinery. An HGV or PSV licence will be lost until fit free for 10 years. * Lifestyle. Stress the positive side of how few changes there need to be. Swimming is possible provided someone else is present who could lifesave if necessary. Cycling in traffic is probably unwise. Counsel the patient about disclosing the diagnosis to friends and employers. It appears that more than half do not tell their fiancees.
Self-help groups: Epilepsy Action, New Anstey House, Gate Way Drive, Yeadon, Leeds LS19 7XY www.epilepsy.org.uk, helpline 0808 800 5050 The National Society for Epilepsy, Chalfont St Peter, Bucks SL9 ORJ, tel. 01494 601400 for details of local groups and also as an excellent source of information, www.epilepsynse.org.uk
Drug treatment • The British Epilepsy Association recommends prescribing by brand name because of evidence that generic prescribing leads to patients being switched between brands, and this carries a 10% risk of a worsening of seizure control.17 • Most patients are treated with one of three firstline drugs: sodium valproate, carbamazepine or phenytoin. In most types of seizure they are equally effective and the choice is made on their side-effect profile. Sodium valproate is first choice in primary generalized, absence and myoclonic seizures, while it is first equal with carbamazepine in partial seizures. • Phenytoin is very much third choice because of its narrow therapeutic window and the frequency of side-effects.18 Phenobarbitone is rarely used because adverse effects are greater.19 • If control is not achieved with a single firstline drug, a newer add-on drug is given as well.
Procedure 1. Start at a low dose as follows, and increase until fits are controlled or side-effects occur: (a) Carbamazepine 100 mg daily, increasing every week by lOOmg daily to a maximum of 600 mg b.d. Doses up to 2000 mg a day can be used with consultant advice. (b) Sodium valproate 300 mg b.d. increasing by 200 mg daily every 3 days to 1 g b.d. Doses up to 2500 mg daily can be used with consultant advice. (c) Phenytoin 200 mg daily, increasing every week by 100 mg daily to 600 mg a day. A blood level should be performed 1 week after each change of dose once 300 mg a day has been reached because of the narrow therapeutic window. 2. If the control of fits is unsatisfactory despite the prescription of adequate doses: check compliance; if using carbamazepine, check the blood level. If it is below the therapeutic range, check compliance again. If it seems satisfactory, continue to increase the dose with repeat blood levels; if using sodium valproate, do not check blood levels; they are not a guide to efficacy. 3. Abandon a drug if control is poor despite maximum dosage, but only after a sufficiently long trial (e.g. 2 months at full dosage), or, if fits are infrequent, the time in which three to five fits would be expected to occur.20 4. Tail-off one drug only when the patient is established on the next. 5. Only if some, but not enough, benefit has been obtained from the first drug should it be continued as well as the second. Even then a single firstline drug plus a newer add-on drug is probably better. Practical points * Phenytoin can be given once daily, and sodium valproate and carbamazepine (unless given in the slow-release form) twice a day. * Monotherapy. Use one drug at a time if possible. The addition of a second drug may only give a further 10% of control. * Compliance. Explain the importance of not missing doses and, especially, of not stopping
treatment abruptly. Poor compliance may be a sign that the patient does not fully accept the diagnosis. * Alcohol. Explain that moderate drinking of 1 to 3.5 units per day twice a week has no effect on seizure control.21 1 to 2 units a day is probably safe. Heavier drinking may induce a fit as well as interact with antiepileptic drugs. * Aspirin. Warn patients taking sodium valproate against taking intermittant aspirin. It displaces valproate from protein-binding sites and so potentiates it. If regular aspirin is needed, the dose of valproate may need to be reduced to allow for this. * Pregnancy. (a) Warn women of child-bearing age to seek advice about the use of their drugs before trying to become pregnant. No drug seems any safer than any other.22 The principle is to maintain a woman who needs drugs on a single drug at the lowest effective dose. Dose adjustment may be needed; absorption may be poor and the drug will be diluted by the increased blood volume (see p. 267). If a woman gets pregnant unintentionally, she should not stop treatment. Any damage will already have been done, and she merely risks losing her baby if she subsequently fits. (b) Women taking sodium valproate or carbamazepine should be offered mid-trimester screening for neural tube defects. (c) Advise women to take folic acid 5 mg daily before trying to conceive and throughout pregnancy. (d) Give vitamin K in the last month of pregnancy and to the newborn. Antiepileptic drugs can increase the risk of haemorrhagic disease of the newborn. * Contraception. Remember that women taking phenytoin, phenobarbitone or carbamazepine need, if requiring COC, either an increased oestrogen dosage (see p. 230) or a change to sodium valproate. Measure the blood progesterone on day 21 to confirm that ovulation has been suppressed. Doses of oestrogen of up to 100 |jig may be needed. Three packs may be run into one, without a break. If the patient is using the progestogen-only pill, the dose should be doubled or the method changed.
* Short-lived exacerbations of epilepsy. Clobazam is useful to tide patients over times when fits are more likely, e.g. menstruation and tiredness. It can be used to control fits occurring in clusters. Tolerance prohibits longer-term use. * Add-on drugs. Vigabatrin, lamotrigine, gabapentin, tiagabine, topiramate and zonisamide may be initiated by a specialist. They seem to be equally effective.23 The GP needs to know that: (a) they do not interfere with oral contraceptives; (b) their half-life may be affected by other anticonvulsants, e.g. sodium valproate prolongs the half-life of lamotrigine. Conversely, lamotrigine can precipitate carbamazepine toxicity, topiramate can precipitate phenytoin toxicity, while vigabatrin can lower phenytoin concentrations.
Follow-up (a) Review any fits (preferably recorded on a chart) and their precipitating causes. (b) Review the patient's attitude to the epilepsy and any social problems that have arisen. Encourage the family to attend, whether the patient is an adult or a child. The epilepsy may put other members of the family under considerable stress. (c) Review drug compliance, by checking the frequency of repeat prescriptions. (d) Review side-effects. (e) Do not check anticonvulsant serum levels routinely except with doses of phenytoin above 300 mg a day. The serum level should not determine the anticonvulsant dose; the correct dose is the smallest dose that controls the seizures. With the exception of phenytoin, only check serum levels when control is poor, there is concern about toxicity, higher than usual doses are being considered, more than one drug is being given, compliance is in doubt, or in renal or hepatic impairment.24 (f) Blood tests. It is traditional to recommend yearly checks of FBC, calcium, phosphate and alkaline phosphatase, advice which is traditionally ignored. Abnormalities are uncommon and minor and only worth testing for inpatients
on high doses. The one potentially fatal sideeffect, hepatotoxity due to sodium valproate, occurs in only 1 in 10,000, mainly in mentally handicapped children under 3 years old, and routine testing would not predict it anyway. Tests of serum electrolytes in patients on carbamazepine in order to detect hyponatraemia may be worthwhile.25
Stopping treatment • Specialist advice is wise before withdrawing drugs in a patient who has been free from fits for a number of years. Ultimately it is the patient who must make the decision, weighing the problems of drug-taking against the upset of a further fit with its implications for driving, employment and family distress. Patients who stop their drugs and remain fit-free have higher morale than those who are fit-free on drugs.26 • Withdrawal may be considered in grand mal when the patient has been free of fits for 2 years, although there is no evidence on which to base this.27 It is likely to be followed by relapse in half of adults and 20% of children in the first year, against a recurrence rate of 33% for adults who remained on medication. Recurrence does not worsen the overall prognosis.28 • Withdrawal is most likely to be successful in patients with: (a) primary generalized epilepsy; (b) epilepsy controlled on a single drug with no seizures on treatment; (c) a normal EEC; (d) a few seizures over a short space of time; (e) childhood or teenage onset; (f) no family history of mental retardation or cerebral pathology.29 • Maximum dose reduction. In adults the maximum reduction each time should be: carbamazepine 200 mg; phenytoin 50 mg; sodium valproate 200 mg; phenobarbitone 30 mg; primidone 125 mg. • Speed of withdrawal. Withdrawal should take at least 6 months. If a drug is being withdrawn and being replaced by another it can be withdrawn faster, but in steps not shorter than one every 3 weeks.
PARKINSON'S DISEASE Guideline: The Primary Care Task Force of the Parkinson's Disease Society (UK). Parkinson's aware in primary care. 1999. Online. Available: www.parkinsons.org.uk
• The disease should be confirmed by a specialist in all cases; 25% of referrals to a Parkinson's disease clinic were found not to have Parkinson's disease.30 • 'Parkinsonism', whether due to drugs, multiple small strokes or other causes, does not respond to treatment with levodopa and must not be confused with Parkinson's disease.
Management The diagnosis of Parkinson's disease has huge medical, psychological and social implications for the patient and family. The key worker, who may be a GP, specialist nurse or consultant, is needed to coordinate the professionals involved. The medical aspects of care will be shared between specialist and GP. While the specialist will initiate treatment, the GP is often responsible for coping with adverse effects or altering drug doses. * Find out what specific problems the patient has. Treatment should be individually tailored to these problems. * Explain the diagnosis and the management plan. Stress that almost everybody enjoys prolonged benefit from treatment. * Explain the problem that lies at the heart of drug treatment: that levodopa is the most effective drug for the relief of disability but that prolonged use leads to the problems described below. Delaying its use and keeping its dose low may mean that it will remain effective later in the disease: hence the use of other agents early, and of levodopa-sparing agents later. * Depression. Use antidepressants as you would in other depressed patients. Depression occurs in
almost half of patients and is part of the disease, not merely a reaction to the disability. * Dementia occurs in 10%, and is likely to be missed unless specifically tested for. Its discovery has important implications in planning treatment. * Constipation should be treated by encouraging mobility, a high-fibre diet if the patient can swallow it, and laxatives. * Physiotherapy may be helpful though the evidence is sparse.31 One meta-analysis found that physiotherapy could improve walking speed and the activities of daily living.32 * Occupational therapy can help with difficulties with feeding and dressing, and provide alterations to the bed, chair and bath although, again, the evidence is sparse.33 Difficulties with speech and swallowing. Referral to speech therapy may help to make the voice more forceful.34 There is no evidence either way on benefit for dysphagia. * Financial benefits. Many patients are eligible for benefits for the disabled (see p. 4). * Carers. Assess, and reassess, the ability of the carer to cope. * Driving. Advise drivers to notify the DVLA and the insurance company. * Surgery. A few patients will be candidates for destructive surgery. They are likely to be those under 70, with no other cerebral disease, who have severe unilateral tremor or dyskinesia. Self-help group: The Parkinson's Disease Society, 215 Vauxhall Bridge Road, London SW1V 1EJ, tel. 020 7931 8080 has information for patients and carers and organizes local groups. Helpline: 0808 800 0303; www.parkinsons.org.uk
Drug treatment Choice and timing of drug therapy depends on the age of the patient, because of the limited time for which levodopa is likely to be effective. The approach for patients under 50 and over 70 is fairly clear. Patients between the ages of 50 and 70 are in a borderline area where individual circumstances will influence the decision.
The younger patient Start drugs only when they are needed for symptom control. Options are: (a) Anticholinergics, which may be given especially for tremor. They are very prone to cause confusion in the elderly and in these patients the only strong indication for them is excessive salivation. A convenient choice is benzhexol 2mg daily increasing up to a maximum of 5mg t.d.s., or orphenadrine 50-100 mg t.d.s. If the main side-effect is a dry mouth, take before food; If the main side-effect is nausea, take after food. (b) Amantadine at a dose of 100 mg b.d. is of modest benefit but has few side-effects. (c) Dopamine agonists: bromocriptine, pergolide, lysuride or one of the newer drugs can all relieve symptoms. Initial treatment with bromocriptine rather than levodopa appears to be slightly less effective in reducing disability but with fewer motor complications.35 Dopamine agonists are very likely to cause initial nausea or vomiting and domperidone may be needed. (d) Selegiline postpones the time when levodopa is needed.36 Earlier hopes that this was due to a neuroprotective effect are probably unfounded,37 and one trial has raised the possibility that it causes an increase in mortality.38 (e) Levodopa (see below) should be started when symptoms interfere sufficiently with the patient's life, despite the above. The older patient * Levodopa. Start levodopa when symptoms are interfering significantly with the patient's life. Not only is there less need to 'save' levodopa for later, but also the levodopa-sparing drugs are more likely to give rise to adverse effects in the elderly. (a) Warn patients about the immediate sideeffects, e.g. nausea and postural hypotension. Give the tablets after food to avoid nausea. Be aware, however, that a protein meal can compete with levodopa for absorption. If an antiemetic is needed, use domperidone. Check
the standing blood pressure before and after starting the drug. (b) Use a preparation that combines levodopa with a decarboxylase inhibitor. (c) Agree on a specific goal that treatment should achieve, e.g. being able to walk to the shops. (d) Start with a low dose, containing levodopa 50 mg t.d.s., and increase by 50 mg a week until the goal has been achieved. (e) Monitor the response. As well as asking about the benefit, set the patient a task (e.g. unbuttoning a coat or walking to the door) and time it for an objective assessment. Stop increasing the dose as soon as sufficient benefit has been achieved. * Add amantadine, dopamine agonists or selegeline (see above) but not anticholinergics when levodopa alone is not sufficient. Later problems with levodopa These may not begin for some years after the drug is started: (a) end-of-dose deterioration; (b) dyskinesia, usually at peaks of levodopa levels but also as the dose wears off; (c) on-off motor fluctuations unrelated to levodopa dose; (d) nausea and vomiting; (e) psychiatric side-effects and acute confusion (see Psychiatric problems, below). * Management of motor complications: (a) Give a smaller amount more often to avoid the peaks and troughs of drug levels. In extreme cases, 2-hourly doses may be needed. Alternatively, change to a controlled-release preparation. (b) Add selegiline, which will improve end-ofdose deterioration in 50% of patients and permit a reduction in levodopa dose, which will help any dyskinesia. (c) Add a dopamine agonist, e.g. bromocriptine 1.25mg daily, increasing slowly as detailed in the BNF. Reduce the dose of levodopa by one-third. Confusion and postural hypotension
often limit the value of this drug. One of the newer dopamine agonists may suit an individual patient better. (d) Arrange for admission for initiation of apomorphine injections which the patient or carer can then give at home. Apomorphine is useful in patients with fluctuating motor responses, on-off oscillations and dyskinesias. It works within 20 minutes, but benefit only lasts for about an hour.39 * Nausea and vomiting: (a) ensure that doses are taken after meals; (b) decrease the dose of levodopa while increasing the dose of decarboxylase inhibitor. The intention is to lower the extracerebral level of levodopa without lowering the intracerebral level; (c) add domperidone.
Psychiatric problems In addition to the difficulty that a patient is likely to have in adjusting to the condition, Parkinson's disease and its treatment cause a whole range of psychiatric disorders. • Levodopa can cause anxiety, agitation, elation, depression, insomnia, paranoia, hallucinations and delusions. Dose reduction is more effective than trying to treat the reaction with further drugs. • Depression may be part of the disease rather than a reaction to the disease. It responds to antidepressants. Choose a first generation tricyclic if anticholinergic action is required as well, e.g. in excessive salivation. If constipation is already a problem or the patient is already on an anticholinergic drug, choose one with less anticholinergic activity such as lofepramine or a selective serotonin reuptake inhibitor (SSRI). • Psychosis may be due to Parkinson's disease or to the medication. Withdraw the latter in the manner outlined below. If part of the disease, neuroleptics may be needed despite the detrimental effect they are likely to have on the parkinsonism. • Organic confusion is likely to be due to the medication. Stop the drug most recently added. If there has been no recent change, stop drugs in the following order: anticholinergics, selegiline,
amantadine and dopamine agonists. Levodopa is the drug least likely to cause confusion, but its dose may need to be altered. Palliative care of the terminal patient A time will come when no further alteration in drugs will be helpful, and the patient and family will need an increased amount of support. Adequate analgesia and sedation of the patient will be needed, as in any palliative situation.
STROKE Guidelines: The Intercollegiate Working Party on Stroke. National Clinical Guidelines for Stroke. London: The Royal College of Physicians, 2000. Available from the RCR 11 Saint Andrews Place, Regent's Park, London NW1 4LE; www.rcplondon.ac.uk/ceeu_stroke_ concise.htm Scottish Intercollegiate Guidelines Network (SIGN). Management of patients with stroke; Parts 1-4; Online. Available: www.sign.ac.uk/guidelines/ The National Service Framework for Older People. London: Department of Health, 2001. Online. Available: www.doh.gov.uk/nsf/olderpeople.htm
• Management of stroke patients in a stroke unit is associated with a sustained reduction in mortality40 and improvement in the quality of life.41 • Rehabilitation, physiotherapy, occupational therapy and psychological support are all part of well-organized stroke care. This can dramatically reduce mortality and disability.42 • Brain imaging by CT or MRI scanning should be undertaken to detect intracerebral or subarachnoid haemorrhage, and to exclude other causes of the stroke syndrome, in all patients within 48 hours of onset unless there are good clinical reasons for not doing so.43 • Thrombolysis in selected patients reduces the risk of death or deterioration after a stroke with an NNT of approximately 20.44 It is only suitable for patients who can be admitted to a specialist unit with experience of thrombolysis within 3, or at the outside, 6 hours of the onset of the stroke.45
Acute stroke Admit all patients unless:^3 (a) the diagnosis is clear and examination allows the localization of the damage to one cerebral area; and (b) brain imaging can be arranged within 48 hours unless there is a good clinical reason not to do so; and (c) the diagnosis can be reviewed by an experienced clinician; and (d) cardiovascular status can be reviewed; and (e) care services can provide support within 24 hours; and (f) a specialist stroke service is part of those services. If managing the patient at home, the key action points (in liaison with the specialist stroke services) are: * Maintain the airway. * Ensure that hydration is maintained. * Explain the situation to the patient and carers and give support. * Give aspirin (300 mg) as soon as possible after the onset of stroke symptoms if a diagnosis of haemorrhage is considered unlikely (NNT = 77).45 * Assess the patient's cardiovascular state, including heart, carotid arteries and blood pressure. Do not lower blood pressure in the acute phase.46 * Assess the patient's neurological state including motor and sensory function regularly until stable. * Check swallowing. Can the patient swallow saliva? If so, can he or she swallow a teaspoon of water? Clinically detectable dysphagia occurs in about half of patients with first stroke47 and is often unrecognized.45 Patients with dysphagia need urgent assessment by a speech therapist. A nasogastric tube or gastrostomy may be needed to avoid aspiration pneumonia. * Control the blood glucose in diabetics. * Control pyrexia with paracetamol, fan and treat any underlying cause. * Monitor pressure areas if there is immobility. * Check urinary function and continence, and catheterize if necessary.
* Apply a full length compression stocking to a weak or paralysed leg to prevent venous thrombosis.
Longer-term management * Early discharge is only appropriate if a specialist community stroke rehabilitation team is available. If so, early discharge may improve outcomes48 but at the risk of worsening the mental health of the carers.49 * Depression has been found in as many as half of patients 3 months after a stroke and at 12 months. The prevalence in carers is almost as high.50 A further 20% suffer from poststroke emotional lability.51 * Refer to a specialist rehabilitation team, if not already involved. This team will manage the rehabilitation process but may need support from the GP. * Check that a multidisciplinary assessment has been performed, including assessment of consciousness level, swallowing, pressure sore risk, nutritional status, cognitive impairment, movement and handling needs. * Check that carers and family have been involved closely with the planning of discharge from inpatient care. * Muscular spasm. Use antispasmodics as needed to prevent or treat spasticity, e.g. baclofen 10 mg up to four times daily or diazepam 2-1 Omg three times daily, but with caution because of the risk of sedation. * Depression. Monitor for depression with a screening questionnaire (see p. 309) giving information and advice, and considering antidepressant drug treatment (see p. 311). Tricyclic antidepressants and SSRIs are effective in major depression52 and emotional lability.51
Secondary prevention The risk of recurrence is 8% per year.53 * Lifestyle changes. Assist smokers to stop (see p. 331) and urge weight reduction, dietary change, and exercise where appropriate (see p. 108).
* Aspirin. Prescribe 75 mg daily unless the stroke is likely to have been haemorrhagic or aspirin is contraindicated. In patients with a previous ischaemic stroke, it will prevent 39 events per 10,000 patients over a mean of 37 months but at the expense of 12 haemorrhagic strokes.54 * Blood pressure. Once the initial phase of the stroke is over (usually about 2 weeks), control any hypertension to < 140/85 or < 140/80 in diabetics (see p. 90). * Atrial fibrillation. Arrange anticoagulation with warfarin whether valvular disease is present or not. * ACE inhibition. Give ramipril (increasing to lOmg daily) in all in whom it is not contraindicated. It can reduce the risk of future stroke by 32% independent of its effect on BP (The HOPE Study 2002). * Co-incidental cardiac disease. Arrange echocardiography in patients with stroke and cardiac disease (other than atrial fibrillation). Almost 20% will be found to have an intracardiac source of an embolus.55 The commonest cardiac pathologies are mitral valve disease, prosthetic valves, left atrial enlargement and myocardial infarction in the last 3 months.43 * Raised cholesterol. Use a statin and diet to lower cholesterol as recommended in the prevention of coronary heart disease (see p. 109). Other routine matters * Explain the prognosis if requested (65% are likely to achieve independence). Those with a better prognosis are those who are continent, who have regained power on the affected side within 1 month and who are progressing towards walking within 6 weeks. Improvement is likely to continue for some months. * Driving. Explain that the patient should not drive for at least 1 month after a stroke or transient ischaemic attack (TIA) and that the DVLA and the insurance company should be informed. * Arrange relief admissions and other support for the carers (e.g. attendance allowance) in consultation with the stroke team.
Primary prevention Prevention should be targeted towards patients with one or more of these factors. * Hypertension. Control blood pressure to systolic blood pressure 4.5 (pH paper is cheap and readily available). (d) Release of fishy odour on adding alkali (10% KOH).
PELVIC INFLAMMATORY DISEASE (PID) Guideline: Clinical Effectiveness Group of the Association for Genitourinary Medicine and the Medical Society for the study of Venereal Diseases. Guidelines
PELVIC INFLAMMATORY DISEASE
for the management of pelvic infection, 2001. Online. Available: www.mssvd.org.uk/CEG/ceguidelines.htm Systematic review: Ross J. Pelvic Inflammatory disease. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. Available: www.clinicalevidence.org
• PID is usually the result of ascending infection from the endocervix. Neisseria gonorrhoeae and Chlamydia trachomatis have been identified as causative agents, whilst Gardnerella vaginalis, anaerobes and other organisms commonly found in the vagina may also be implicated. • PID has a high morbidity; about 20% of affected women become infertile, 20% develop chronic pelvic pain, and 10% of those who conceive have an ectopic pregnancy.27 • Repeated episodes of PID are associated with a four- to sixfold increase in the risk of permanent tubal damage.28 • PID may be asymptomatic. • Symptoms can include lower abdominal pain, dyspareunia, abnormal bleeding, abnormal vaginal or cervical discharge. • 10-20% of women with PID will develop perihepatitis. • It is likely that delaying treatment increases the risk of long-term sequelae such as ectopic pregnancy, infertility and pelvic pain. Because of this, and the lack of definitive diagnostic criteria, a low threshold for the empiric treatment of PID is recommended.
Diagnosis Clinical diagnosis is correct in only 65% of cases compared to laparoscopy. Even laparoscopy can miss mild cases but it remains the most reliable investigation. In the UK it is not recommended in all cases because of the cost implications. • If not referring perform the following: (a) Endocervical swabs for gonococcus and chlamydia. Negative microbiological tests do not exclude a diagnosis of PID; in at least 50% of cases no specific organism is identified; (b) Urinanalysis, pregnancy test, and MSU specimen to look for other causes of lower abdominal pain;
(c) Blood for ESR or C-reactive protein. A raised level would support the diagnosis.29 * Recommend rest and provide adequate analgesia. * Recommend that unprotected intercourse be avoided until the woman and her partner(s) have completed treatment and follow up. * If an IUD is in situ, and this is the preferred method of contraception, leave it in place. Remove it only if the condition fails to respond to treatment and other causes of pain have been excluded.30'31'32 * Drug treatment. (a) ofloxacin 400 mg b.d for 14 days plus metronidazole 400 mg b.d. for 14 days; or (b) doxycycline 100 mg b.d for 14 days plus metronidazole for 14 days (add in ciprofloxacin 500 mg stat dose if the infection was acquired abroad or there is a high incidence of gonococcal infection in the local population); or (c) erythromycin 500 mg b.d for 14 days plus metronidazole 400 mg b.d. for 14 days. * Review daily in case admission becomes necessary.
Admission Admit patients if (a) the illness is severe; (b) not responding after 3 days of oral therapy; (c) unable to tolerate oral drugs; (d) a pelvic mass is present; (e) the patient is pregnant; (f) there is diagnostic uncertainty; (g) the patient suffers from immunodeficiency; (h) the patient is above the normal age for PID. An alternative diagnosis, e.g. ovarian carcinoma, is more likely.
Follow-up for all patients * Trace, investigate and treat the woman's partner^) if an STD is diagnosed.33 One study of women with acute salpingitis found that 30 out of 34 male contacts had urethritis.34 Another study found that 60% of contacts had relevant infections, and that in most of these it was asymptomatic.35 * Discuss with the patient her need for safer sex.
* Advise the patient to ask for antibiotic cover (e.g. doxycycline 200 mg stat) if she ever needs a termination of pregnancy (TOP) or a dilatation and curettage (D&C). * Advise the patient to seek advice promptly if the symptoms return.
(b) Stress management. Explain that although it is not the cause of the syndrome, stress is harder to cope with during the premenstrual period. Relaxation methods, yoga, meditation and exercise can be of benefit.
Therapeutic options Patient information: www.patient.co.uk. (choose 'women's health' then 'pelvic inflammatory disease').
PREMENSTRUAL SYNDROME Systematic review: Premenstrual syndrome. Clinical Evidence, Issue 4. London: BMJ Publishing Group, 2000. Online. Available: www.clinicalevidence.com Guideline: National Association for Premenstrual Syndrome. Treatment guidelines for premenstrual syndrome. Guidelines 2001,15. Online. Available: www.eGuidelines.co.uk
* 95% of women have symptoms related to their menstrual cycle; in 5% they are disabling. More than 150 symptoms have been reported. * Diagnosis depends not on the type of symptom, but on the timing of the symptoms and their cyclicity. Symptoms present 1-14 days prior to menstruation and disappear at the onset or on the day of the heaviest flow. If behavioural symptoms persist throughout the cycle then consider a psychological/psychiatric disorder. * Ask the patient to keep a menstrual and symptom diary for at least 2 months. She can score symptoms according to their severity. * Listen sympathetically. It is a real entity. This alone can be therapeutic. * Give simple advice: (a) Dietary advice. Explain that some women seem more sensitive to blood sugar changes at this time of the cycle, and this may be the cause of food cravings, panic reactions, irritability and aggression. Advise patients to reduce their refined sugar intake as well as their caffeine intake. Small frequent carbohydrate snacks seem effective in about 30% of women.
* Oestrogens may improve or in some cases worsen the situation. The COC can prove helpful, especially in those women requiring contraception. Women who experience symptoms during their pill-free week can take three consecutive packets back-to-back. A lower dose of oestrogen, as HRT, may help some women but cyclical progestogens must be used in women with an intact uterus. * Prostaglandin inhibitors, e.g mefenamic acid, may be of value for breast and pelvic pain, joint pains and headache. They may be taken from day 14, or from the start of symptoms, until symptoms abate. * Antidepressants may help even if depressive symptoms are absent. SSRIs, e.g fluoxetine 20^40 mg show improvements in both physical and psychological symptoms.36 * Vitamin B6 50-100 mg daily.37 This recommendation is based on limited information from poor quality trials, but looks as if B6 may be of benefit.38 * Breast tenderness. Treatment options include: (a) bromocriptine 1.25mgb.d. (b) danazol 200 mg daily. Note: Progestogens have been found unhelpful in the treatment of PMS.39 Note: Evening primrose oil. There is no evidence from high quality studies that it is helpful in PMS.40
Patients not responding * Refer to a gynaecologist for the consideration of suppression of ovarian function. Treatment options include high-dose danazol, high-dose oestrogen, gonadotrophin-releasing hormone analogues with add-back HRT. Patient support: The National Association for Premenstrual Syndrome (NAPS), 41 Old Road,
THE MENOPAUSE 217
East Peckham, KentTN12 SAP, helpline 0870 7772177; www.pms.org.uk Premenstrual Society, PO Box 429, Addlestone, Surrey KT15 1DZ, helpline 01932 872560 (11 a.m.-6 p.m., weekdays only).
GESTATIONAL TROPHOBLASTIC DISEASE: HYDATIDIFORM MOLE AND CHORIOCARCINOMA RCOG. The management of gestational trophoblastic disease. Guideline No. 18. London: Royal College of Obstetricians and Gynaecologists, 1999.
• Gestational trophoblastic disease is a rare event in the UK, with a calculated incidence of 1.54 per 1000 live births.41 • In the UK there is an effective registration and treatment programme with high cure rates. • Once the diagnosis of hydatidiform mole has been made, follow-up will be needed for between 6 months and 2 years. The aim is to detect the occurrence of choriocarcinoma. • Serum estimations of levels of human chorionic gonadotrophin (HCG) levels should be performed according to protocols from the regional expert units (London, Sheffield and Dundee). • The combined oral contraceptive pill and hormone replacement are safe to use after HCG levels have reverted to normal. • Women should be advised not to conceive until the HCG level has been normal for 6 months or follow-up has been completed (whichever is the sooner). Patient information: The Hydatidiform Mole and Choriocarcinoma UK information service, www.hmolechorio.org.uk
Screening centres Trophoblastic Tumour Screening and Treatment Centre Department of Oncology, Charing Cross Hospital, Fulham Palace Road, London W6 8RF
Tel. 020 8846 1409, fax 020 8748 5665 Trophoblastic Tumour Screening and Treatment Centre Weston Park Hospital, Whitham Road, Sheffield. S10 2SJ Tel. 0114 226 5202. Fax. 0114 226 5511 Hydatiform Mole Follow-up (Scotland) Department of Obstetrics and Gynaecology, Ninewells Hospital, Dundee DD1 9SY Tel. 01382 632748. Fax. 01382 632096
THE MENOPAUSE Information: Prodigy guidance. Menopausal management (HRT), June 2001. Online. Available: www.prodigy.nhs.uk/guidance National Prescribing Centre. The benefits and risks of HRT. MeReC Bulletin 2001; No. 16, www.npc.co.uk Rymer J, Morris E. Menopausal symptoms. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001, pp. 1303-10. Online. Available: www.clinicalevidence.com Rees M, Purdie DW. Management of the menopause. Handbook of the BMS. London: BMS Publications, 1999.
Establishing the diagnosis • FSH levels fluctuate markedly during the perimenopause and so are of limited value in symptomatic women, in whom a clinical history can form the basis of diagnosis. • There is little place for LH, oestradiol and progesterone levels in clinical practice.42 • No investigations are routinely indicated before starting HRT. • Consider taking serial FSH measurements in the following circumstances: (a) Women with symptoms under the age of 40 because of the implications of premature ovarian failure. (b) Women with symptoms who have had a hysterectomy with ovarian conservation. They are at risk of an early menopause. (c) Women over the age of 45 who are still on hormonal contraception who wish to establish
whether they are menopausal. The hormonal contraception can mask the menopause (see p. 222 contraception in the perimenopause). * Take FSH levels 4-8 weeks apart when the woman is not on HRT or hormonal contraception. FSH levels of greater than 30 iu/L are generally considered to be in the postmenopausal range. * Abnormal bleeding. Refer women, without starting HRT, if they give a history of abnormal bleeding, e.g. sudden change in menstrual pattern, intermenstrual bleeding, postcoital bleeding or a postmenopausal bleed.42'43
Initial management * Counsel women about the menopause. Ideally, all perimenopausal women should be given the opportunity to discuss the menopause, with particular reference to the symptomatology, common misconceptions and treatment options. * Take the opportunity to discuss lifestyle issues (smoking cessation, diet and exercise). * Osteoporosis. Identify those patients at high risk of osteoporosis and assess whether HRT is indicated (see p. 180 Osteoporosis). * Vasomotor symptoms. (a) HRT is extremely effective in controlling these symptoms.44 (b) Consider clonidine for those unable to take HRT.45-46 (c) Diet. Discuss the limited evidence that suggests that phytoestrogens may be helpful in relieving vasomotor symptoms.47'48 They are plant substances similar to oestrogen, found in soya beans, chickpeas and cereals. * Vaginal dryness. Treatment options include: (a) HRT (see below). (b) Local oestrogens. These can be given per vaginum daily until symptoms have ceased, then twice weekly for 3 to 6 months. There is some systemic absorption of the oestrogens and therefore if using long-term oral progestogen should be taken for 10 days of each month.49 (c) Vaginal lubricants. These include KY jelly, Replens (a non-hormonal aqueous moisturizer) and Senselle (a water-based lubricant), although the latter two are not available on the NHS.
* Urinary symptoms. (a) Symptoms related to urogenital atrophy will respond to oestrogen by any route. Maximum benefit takes between 1 and 3 months of therapy.50 (b) Stress incontinence is unlikely to respond to oestrogen replacement therapy alone. Refer patients who are sufficiently troubled to a gynaecologist. * Psychological symptoms. Psychological symptoms may relate to a woman's hormonal status but, equally, the menopause may become a 'scapegoat' for patients with underlying emotional problems.51 Counselling may be helpful, but many will improve when their physical symptoms improve.52 Depression may need treatment in its own right.
HORMONE REPLACEMENT THERAPY (HRT) Information: National Prescribing Centre. The benefits and risks of HRT. MeReC Bulletin 2001; 16. Online. Available: www.npc.co.uk
• Relatively few eligible women use HRT, and those that do often stop it within the first few months. The main reasons for this are the fear of breast cancer and the return of withdrawal bleeding.53 Also many women express concerns around weight gain on HRT (see below). • There is evidence from randomized trials that the use of unopposed oestrogens or combined oestrogen/progestogen therapy does not cause extra weight gain in addition to that normally gained at the time of the menopause.54 • HRT can be considered for all peri and postmenopausal women, especially in those: (a) who have had a premature menopause; (b) who have marked symptoms and want symptom relief; (c) at high risk of osteoporosis (see p. 180).
Contraindications Oestrogen replacement therapy is absolutely contraindicated in very few patients. Even in women in whom treatment appears contraindicated,
oestrogen therapy may be prescribed under supervision of a specialist menopause clinic if the women's symptoms are particularly severe.55 • Absolute contraindications include: (a) acute-phase myocardial infarction, pulmonary embolism or deep vein thrombosis (DVT); (b) active endometrial or breast cancer; (c) pregnancy; (d) undiagnosed breast mass; (e) uninvestigated abnormal vaginal bleeding; (f) severe active liver disease. Note: Many contraindications given in prescribing data sheets are derived from high-dose combined oral contraceptives, and are, in the view of most experts, not applicable to HRT.55 HRT use in women with comorbidity (relative contraindications) (a) Thromboembolic disease (personal or family history) Women with a personal or family history suggestive of thrombophilia (see p. 418) should be offered thromboembolic screening before starting. (b) Past history of breast or endometrial cancer. Refer women who want to consider HRT to the appropriate specialist. Although conventional advice is that oestrogens are contraindicated, small studies of breast cancer survivors have not shown an adverse effect on survival. (c) Diabetes and gall bladder disease. Use a transdermal preparation. (d) Liver disease. Refer to a specialist clinic. (e) Endometriosis. Refer to a specialist clinic. (f) Fibroids. HRT may enlarge fibroids, causing heavy or painful withdrawal bleeds. Warn patients to report pain or pressure effects on the bladder or bowel.
Benefits and risks Benefits (a) Symptom relief. Improvement in vasomotor symptoms occur in a few weeks, and vaginal symptoms in 3 months. (b) Osteoporosis prevention (Table 11.1). Oestrogen therapy at sufficient doses is effective for the
Table 11.1 Minimum doses of oestrogen needed for bone conservation Drug
Estradiol Oral conjugated equine oestrogens
1.5g (two measures)
daily 6 monthly
Transdermal estradiol patch Estradiol gel Estradiol implants
* Although 1 mg or 2mg oral estradiol can be used for prevention of osteoporosis, the bone protective effect is dose related. Some products are licensed for osteoporosis prevention at 2 mg only, while others are licenced at 1 mg and 2mg.
prevention of osteoporosis.56 This bone protection lasts as long as HRT is taken, but bone loss begins as soon as HRT is stopped. Evidence that HRT prevents fractures is less strong. Observational studies show a reduction in fracture risk of65%.57 Unproven benefits (a) Primary prevention of cardiovascular disease. The majority of the evidence comes from observational studies and so firm recommendations cannot be made until the results of ongoing randomized, controlled trials (RCTs) are known. There is insufficient data to suggest that HRT should be initiated solely for the purpose of primary prevention of cardiovascular disease (CVD). (b) Secondary prevention of cardiovascular disease. HRT does not appear to prevent the progression of cardiovascular disease.58 At present it is recommended that: -HRT should not be initiated for the secondary prevention of CHD; -the decision to continue long-term HRT in women with CVD should be based on noncoronary benefits and risks and on patient preference; and -if a woman has an acute cardiovascular event while taking HRT it is prudent to consider stopping HRT therapy. Reinstitution should be based on non-coronary benefits and risks and patient preference.59
(c) Dementia and cognitive function. Evidence on the effect of HRT on the onset of dementia is conflicting and HRT should not be given for the prevention of dementia at the present time. Risks (a) Breast cancer -Short-term use (less than 5 years) does not appear to increase the risk of breast cancer.60 - Long-term use (more than 5 years) is associated with a small increase in the cases of breast cancer.61 -How big is the risk? The 20-year risk is as follows:62 (i) women aged 50 not using HRT: 45 per 1000; (ii) women using HRT for 5 years: 47 per 1000; (iii) women using HRT for 10 years: 51 per 1000; (iv) women using HRT for 15 years: 57 per 1000. - Once a woman has stopped HRT for 5 years or more she loses the excess risk. - Breast cancer in HRT users appears to have a better prognosis than in non-users.63 (b) Endometrial cancer. Unopposed oestrogen therapy enhances the development of endometrial hyperplasia and increases the risk of endometrial cancer. Addition of progestogens reduces the risk. (c) Venous thromboembolism. The excess risk is 16-23 per 100,000 HRT users per year, compared to a base-line risk of 8-11 per 100,000 per year. This increased risk disappears once HRT is stopped.64
Initial assessment * Take a history and assess menopausal status. * Check for contraindications to HRT therapy. * Give lifestyle advice, as above. * Check BP. * Advise the woman about breast awareness. Check that mammography screening is in place if over 50 years. Mammography is not needed before commencing HRT unless the woman is at high risk of breast cancer.65
* Check that regular cervical screening is taking place.
Treatment General principles Oestrogens: * Start at the lowest possible dose of oestrogen (especially in the older women who tend to get more oestrogenic side-effects) and increase at 3-monthly intervals if necessary to achieve optimum symptom control. * Give oestrogens continuously, and only give them without progestogens if the woman has had a hysterectomy. Progestogens: These must be added for endometrial protection in women with a uterus. Most products contain either C-19 derivatives (norethisterone/levonorgestrel) which are more androgenic, or C-21 derivatives (medroxyprogesterone acetate/dydrogesterone) which are less androgenic. * Change to a less androgenic preparation if the patient is troubled by progestogenic side-effects. Perimenopausal women with an intact uterus:
* Use a cyclical regimen (monthly or 3-monthly). The majority of women will have a bleed towards the end of the progestogen phase. Postmenopausal women with a uterus:
* Use: (a) a cyclical regimen; or (b) a continuous combined regimen. Continuous regimens induce an atrophic endometrium and so do not produce a withdrawal bleed, although irregular bleeding can occur in the first 4-6 months. Bleeding should be investigated if it persists for longer than 6 months, becomes heavier rather than less, or if it occurs after amenorrhoea; or (c) tibolone. This combines oestrogenic and progestogenic activities, and weak androgenic activity. It is indicated for the treatment of vasomotor symptoms and osteoporosis prophylaxis. It must only be started at least 1 year after the menopause. There is evidence that it improves libido.66'67
Alternative modes of delivery (a) Oestrogen implants. Repeat every 4-8 months. Occasionally there can be a recurrence of vasomotor symptoms with supraphysiological plasma concentrations of oestradiol (tachyphylaxis). Check plasma estradiol levels have returned to normal (less than lOOOpmol/L) before inserting a new implant. (b) Transdermal patches and gels. These avoid the first-pass metabolism in the liver and deliver a more constant level of hormone. Patches come as either reservoir or matrix patches. Skin reactions are less common with the matrix patches. (c) Intrauterine system. The levonorgestrel releasing system (LNG-IUS) is not licensed for HRT, but would be an alternative route for the delivery of progestogen to protect the endometrium. A recent 5-year follow-up concludes that the LNGIUS effectively protects against endometrial hyperplasia.68 It provides contraception, and it is the only way a non-bleed regime may be achieved in the perimenopause.
5% of women, but pregnancy needs to be excluded in perimenopausal women. * Refer if there is: (a) a change in the pattern of withdrawal bleeds and breakthrough bleeding that persists for more than 3 months; (b) unexpected or prolonged bleeding that persists for more than 4 weeks after stopping HRT: refer urgently. Bleeding on continuous combined therapy or tibolone * Explain to patients that the risk of bleeding is 40% in the first 4-6 months. * Make sure the patient was at least 1 year postmenopausal before she started the regimen. * Bleeding beyond 6 months requires further investigation. * Bleeding that occurs after a period of amenorrhoea requires further investigation. Oestrogen-related side-effects
Managing the side-effects of HRT Bleeding on cyclical combined therapy * Check when the bleeding occurs. These regimes should produce regular predictable bleeds starting towards or soon after the end of the progestogenic phase. * Consider poor compliance, drug interactions or gastrointestinal upset. * Try stopping HRT to see if it is the cause of the bleeding. * If bleeding problems are due to HRT, alter the progestogen: (a) heavy or prolonged bleeding: increase the dose or duration of progestogen, or change type of progestogen to a more androgenic type (see p. 220). (b) bleeding early in the progestogenic phase: increase dose or change type of progestogen. (c) painful bleeding: change type of progestogen. (d) Irregular bleeding: change regime or increase dose of progestogen. * No bleeding whilst taking a cyclical regime reflects an atrophic endometrium and occurs in
* Oestrogenic side effects include fluid retention, bloating, breast tenderness and enlargement, nausea, headache, leg cramps and dyspepsia. * Encourage the patient to persist with therapy for 12 weeks, as most side-effects resolve with time. * For persistent side-effects consider (a) reducing the dose; or (b) changing the oestrogen type (swap between the two main forms of oestrogen: estradiol and conjugated equine oestrogens); or (c) changing the route of delivery. * Nausea and gastric upset. Change the timing of the oestrogen dose, e.g. try taking it with food or at bedtime. Progestogen-related side-effects Progestogen-related side-effects tend to occur in a cyclical pattern during the progestogenic phase of cyclical HRT. Continuous combined products contain lower doses of progestogens and sideeffects are less likely. Side-effects include fluid retention, breast tenderness, headaches, mood
swings, depression, acne, lower abdominal pain and backache. * Encourage the patient to persist with therapy for about 12 weeks, as some side-effects will resolve. * Various changes in the progestogens may be helpful, but remember not to reduce the dose or duration below that which protects the endometrium. Options: (a) reduce the duration but not below 10 days; (b) reduce the dose of progestogen; or (c) change the progestogen type (either C-19 or C-21 derivatives; see p. 220); or (d) change the route of progestogen (oral, transdermal, vaginal or intrauterine); or (e) reduce the frequency of how often the progestogen is taken by switching to a longcycling regime. Progestogens are administered for 14 days every 3 months (but only suitable for women with scant periods or postmenopausal); or (f) change to a continuous combined therapy which often reduces progestogenic side-effects with established use, but it is only suitable for postmenopausal women.
Follow-up of women on HRT * See after 3 months, then 6 monthly. * Check for compliance, bleeding patterns and side-effects. * Check that the patient is up to date with her cervical smears and mammograms. Note: There is no need to check the BP except as good practice in any well-person screening.
How long to continue? * Symptomatic relief. Give HRT until there is a reasonable chance that the symptoms will not return. If troublesome symptoms recur on withdrawal HRT can be restarted for 6-12 months at a time. * Osteoporosis prevention. Five years treatment is the minimum, and 10 years is believed to give the optimum risk/benefit ratio. The fact that the benefit rapidly drops-off after stopping HRT must be
set against the risk of breast cancer associated with longer-term use.
Stopping treatment * HRT may be stopped abruptly or gradually. For gradual reduction: (a) cyclical therapy. Reduce the oestrogen dose progressively over 3 months but maintain the progestogen as before; (b) continuous therapy. Reduce both the oestrogen and progestogen dose by 50% for a few weeks then stop. * Review after a few months. If troublesome symptoms have recurred consider restarting therapy at the lowest possible dose and titrating up as necessary. If only local symptoms persist use a vaginal preparation.
HRT and contraception * Perimenopausal women cannot be assumed to be infertile. * Routine HRT preparations do not suppress ovulation and do not provide contraceptive cover. * Contraception should be continued for 1 year after the last menstrual period (LMP) for women over 50 years, or for 2 years after the LMP for women under the age of 50 years. * Perimenopausal women may use: (a) barrier methods, IUD or LND-IUS, as well as HRT; or (b) the COC instead of HRT; or (c) the progestogen-only pill (POP), possibly combined with HRT, although there are theoretical concerns that the oestrogen component of HRT may interfere with the action of the POP on the cervical mucus.69
When has the menopause occurred when masked by HRT or COC? It is important to know this so a realistic idea of how long the women needs to remain on contraception can be calculated (see above); 80% of women are postmenopausal by the age of 54 years.70
CERVICAL SCREENING 223
* Discontinue HRT or COC for 6-8 weeks then check FSH and repeat after a further 4-8 weeks.71 If both FSH levels are above 30 iu/L, stop contraception after a further year. If a spontaneous period occurs, or FSH less than 30 iu/L, continue contraception and repeat the test in 1 year. * Women on the POP. Check the FSH without stopping the POP. Patient organisations: British Menopause Society. 36, West Street, Marlow, Bucks SL7 2NB, tel. 01628 890199; www.the-bms.org The Amarant Trust. 11-13 Charterhouse Buildings, London EC1M 7AN, helpline 01293 413000. Women's Health Information Service. 52 Featherstone Street, London EC1Y 8RT, tei. 020 7251 6333; helpline 0845 125 5254; www.womenshealthlondon.org.uk
CERVICAL SCREENING Guidance: NHSCSR Publication No 8. Guidelines for clinical practice and programme management, 2nd edition. Sheffield: NHSCSP Publications, 1997. NHS Cancer Screening Programme. Online. Available: www.cancerscreening.nhs.uk/cervical
number of false negatives and inadequate samples. The National Institute for Clinical Excellence (NICE) has considered the evidence about LBC and has recommended pilot studies to evaluate controlled introduction of LBC into the NHS cervical screening programme.
Taking a smear • In England in 1991-2, 6.3% of smears were inadequate.74 • Extended-tip spatulas appear to be better for collection of cytology samples than the Ayre spatula.75 * Repeat an inadequate smear within 3 months. If there are two further inadequate smears, refer for colposcopy. * If the smear result is inflammatory and the laboratory cannot comment on whether the smear is positive or negative: (a) perform HVS and endocervical swabs; (b) treat patient and partner for the specific organism; (c) repeat the smear.
Terminology Table 11.2 Terminology used during cervical screening
• The NHS screening programme requires that all women between the age of 20 and 64 are offered a smear every 3 years. • Women reaching the age of 65, who have had at least two normal smears need not have further smears. The last smear should be no more than 5 years before her 65th birthday. • There were 2740 new cases of invasive cervical cancer in England and Wales in 1997. This is a 26% fall in incidence over the previous 5 years.72 • According to the Imperial Cancer Research Fund, cervical screening prevents between 1,100 and 3,900 cases of cervical cancer each year.73 • Coverage of the target age group by the NHS cervical screening programme has increased from 45% in 1988-89 to 83.7% in 1999-2000. • New developments to improve the accuracy of cervical cytology are in the pilot stage. It is likely that liquid-based cytology (LBC) will reduce the
Mild dyskaryosis Moderate dyskaryosis Severe dyskaryosis
CIN 1 (mild dysplasia) CIN 2 (moderate dysplasia) CIN 3 (severe dysplasia or carcinoma in situ)
CIN, cervical intraepithelial neoplasia. The correlation between status on smear and on histology is not close.
Follow-up Borderline or mild dyskaryosis ±'human papilloma virus In the absence of signs or symptoms: (a) treat vulval warts if present (see p. 44); (b) repeat the smear in 6 months. If unchanged, refer for colposcopy. If negative; then
224 GYNAECOLOGICAL PROBLEMS
(c) repeat in a further 6 months. If this is still negative the woman can revert to 3-yearly smears. Note: An alternative view is that referral of all women with mild dyskaryosis would be more cost-effective.76 The possibility that a woman is likely to default from follow-up would sway the balance in favour of immediate referral. Moderate or severe dyskaryosis
* Refer for early colposcopy. Stress that this is part of the screening process and does not mean that the patient has cancer. * Advise the woman to continue her contraception, including the COC; pregnancy makes management more difficult.
After colposcopy and treatment
* Follow-up at 6 and 12 months (by gynaecologist). * Then smear yearly for 5 years (GP or gynaecologist). * If normal, then revert to 3-yearly smears. After hysterectomy with a CIN history
* Perform vault smears at 6 and 12 months. Further smears every 3 years are only needed if there is a suspicion that the condition was not completely removed.
REFERENCES 1. Zhang WY, Po AL. Efficacy of minor analgesics in primary dysmenorrhoea: a systematic review. Br J Obst Gyn 1998; 105(7): 780-89. 2. Wilson M, Farquhar C. Dysmenorrhoea. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. Available: www.clinicalevidence.org 3. Gokhale LB. Curative treatment of primary (spasmodic) dysmenorrhoea. Indian J Med Res 1996; 103: 227-31. 4. Wilson ML, Murphy PA. Herbal and dietary therapies for primary and secondary dysmenorrhoea. Cochrane Review. In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. 5. Farquhar C, Sutton C. The evidence for the management of endometriosis. Curr Opin Obst Gynaecol 1998; 10 (4): 321-32. 6. Moore J, Kennedy S, Prentice A. Modern combined oral contraceptives for pain associated with endometriosis (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. 7. Farquhar C. Endometriosis. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. Available: www.clinicalevidence.org 8. Vercellini P, Cortesi I, Crosignani PG. Progestogens for symptomatic endometriosis - a critical analysis of the evidence. Fertil Steril 1997; 68(3): 393-401. 9. DTB. Managing endometriosis. Drug Ther Bull 1999; 37: 25-9. 10. Pattie MA, Murdoch BE, Theodoras D, Forbes K. Voice changes in women treated for endometriosis & related conditions: the need for comprehensive vocal assessment. / Voice (US) 1998; 12: 366-71. 11. DTB. Surgical management of menorrhagia. Drug Ther Bull 1994; 32: 70-2. 12. RCOG. The initial management of menorrhagia. Evidence-based clinical guidelines, No. 1.
13. 14. 15. 16. 17.
18. 19. 20.
London: Royal College of Obstetricians and Gynaecologists, 1999. Lethaby A, Farquhar C, Cooke I. Antifibrinolytics for heavy menstrual bleeding (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. Centre for Reviews and Dissemination. The management of menorrhorragia. Effective Health Care, 1995. DTB. Levonorgestrel intra-uterine system for menorrhagia. Drug Ther Bull 2001; 39 (11). Iyer V, Farquhar C, Jepson R. Oral contraceptive pills for heavy menstrual bleeding (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. Lethaby A, Irvine G, Cameron I. Cyclical progestogens for heavy menstrual bleeding (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. Gannon MJ et al. A randomised trial comparing endometrial resection and abdominal hysterectomy for the treatment of menorrhagia. BMJ 1991; 303: 1362-4. Soloman CG. The epidemiology of polycystic ovary syndrome. Prevalence and associated disease risk. Endocrinol Metab Clin N Am 1999; 28 (2): 247-63. Wild S, Pierpoint T, Mckeigue P, Jacobs H. Cardiovascular disease in women with PCOS at long term follow up: a retrospective cohort study. Clin Endocrinol 2000; 52: 595-600. Farquhar C, Lee O, Toomath R, Jepson R. Spironolactone versus placebo or in combination with steroids for hirsutism and/or acne (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2000. Moghetti P, Castello R, Negri C et al. Metformin effects on clinical features, endocrine and metabolic profiles and insulin sensitivity in polycystic ovary syndrome: a randomised, double blind, placebo-controlled 6-month trial, followed by open, long-term clinical evaluation. / Clin Endocrinol Metab 2000; 85: 139-46.
23. Bingham JS. What to do with patients with recurrent vulvovaginal candidiasis. Sex Transm In/1999; 75: 225-7. 24. Watson MC, Grimshaw JM, Bond CM et al. Oral versus intra-vaginal imidazole and triazole anti-fungal treatment of uncomplicated vulvovaginal candidiasis (thrush) (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. 25. Bisschop MP, Merkus JM, Scheyground H, van Clusen J. Co-treatment of the male partner in vaginal candidosis: a double blind randomised controlled study. Br } Obstet Gynaecol 1986: 93: 79-81. 26. Potter J. Should sexual partners of women with bacterial vaginosis receive treatment? Br J Gen Pract 1999; 49: 913-18. 27. Metters JS, Catchpole M, Smith C et al. Chlamydia trachomatis; summary and conclusions of CMO's expert advisory group. London: Department of Health,1998. 28. Hills SD, Owens LM, Marchbanks PA et al. Recurrent chlamydial infections increase the risks of hospitalisation for ectopic pregnancy and pelvic inflammatory disease. Am f Obstet Gynecol 1997; 176: 103-7. 29. Miettinen AK, Heinonen PK, Laippala P, Paavonen J. Test performance of ESR & C-reactive protein in assessing the severity of acute PID. Am J Obstet Gynecol 1993; 169: 1143-9. 30. Teisala K. Removal of an IUD and the treatment of acute PID. Ann Med 1989; 21: 63-5. 31. Larsson B, Wennergren M. Investigation of Cu-IUD for possible effect on frequency and healing of PID. Contraception 1981; 24: 137-49. 32. Soderberg G, Lingren S. Influence of an IUD on the course of acute salpingitis. Contraception 1981; 24: 137-43. 33. Robinson AJ, Kell P. Male partners of women with pelvic infection should be traced (letter). BMJ 1995; 311: 630. 34. Kinghorn GR et al. Clinical and microbiological investigation of women with acute salpingitis and their consorts. Br } Obst Gyn 1986; 93: 869-80. 35. Kamwendo F et al. Gonorrhoea, genital chlamydia infection and non-specific urethritis in male partners of hospitalized women treated for acute pelvic inflammatory disease. Sex Trans Dis 1993; 20: 143-6. 36. Dimmock PW, Wyatt KM, Jones PW, O'Brien PM. Efficacy of selective serotonin re-uptake inhibitors in premenstrual syndrome: a systematic review. Lancet 2000; 356: 1311-36. 37. Wyatt KM, Dimmock PW, Jones PW, O'Brien SP. Efficacy of vitamin B-6 in the treatment of premenstrual syndrome: systematic review. BMJ 1999; 318: 1375-81. 38. Anon. Vitamin B6 for premenstrual syndrome. Bandolier Jan 2000. 39. Wyatt KM, Dimmock PW, Ones P et al. Efficacy of progesterone and progestogens in the management of PMS. BMJ 2001; 323 (7316): 776-80. 40. Anon. Evening primrose oil for premenstrual syndrome. Bandolier Aug 2000. 41. Bagshawe KD, Dent J, Webb J. Hydatiform mole in England and Wales 1973-1983. Lancet 1986; 2: 673-7. 42. Hope S, Rees M, Brockie J 1999. Hormone replacement therapy - a guide for primary care. Oxford: Oxford University Press, 1999. 43. Korhonen MO, Symons JP, Hyde BM et al. Histological classification and pathological findings for endometrial biopsy specimens obtained from 2964 perimenopausal
and postmenopausal women undergoing screening for continuous hormone replacement therapy. Am J Obstet Gynaecol 1997; 176: 377-80. 44. MacLennan A, Lester S, Moore V. Oral oestrogen replacement therapy versus placebo for hot flushes (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. 45. Edington RF, Chagnon JP. Clonidine for menopausal flushing. Can Med Assoc J 1980; 123: 23-6. 46. Nagamani M, Kelver ME, Smith ER. Treatment of menopausal flashes with transdermal administration of clonidine. Am J Obstet Gynecol 1987; 156: 561-5. 47. Scambia G, Mango D, Signorile PG et al. Clinical effects of a standardised soy extract in postmenopausal women: a pilot study. Menopause 2000; 7: 105-11. 48. Anon. Alternatives for the menopause. Bandolier Oct 1998; 56-9. 49. Weiderpass E, Baron JA, Adami HO et al. Low potency oestrogen and risk of endometrial cancer: a case control study. Lancet 1999; 353: 1824-8. 50. Cardozo L, Bachmann G, McClish D et al. Meta-analysis of estrogen therapy in the management of urogenital atrophy in postmenopausal women: second report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol 1998; 92: 722-7. 51. Hunter MS. Depression and the menopause. BMJ 1996; 313: 350-1. 52. Gath D et al. Depression and the menopause. BMJ 1990; 300: 1287-8. 53. MeReC. Hormone replacement therapy 2: new preparations. MeReC Bulletin 1997; 8: 17-20. 54. Norman RJ, Flight IHK, Rees MCP. Oestrogen and progestogen hormone replacement therapy for perimenopausal and post-menopausal women: weight and body fat distribution (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001. 55. Rees M, Purdie DW. Management of the menopause. The handbook of the BMS. London: BMS Publications, 1999. 56. Writing group for the PEPI trial. Effects of hormone therapy on bone mineral density. Results from the postmenopausal estrogen/progestin interventions (PEPI) trial. JAMA 1996; 276: 1389-95. 57. Royal College of Physicians and The Bone and Tooth Society of Great Britain. Osteoporosis: clinical guidelines for prevention and treatment. Update on pharmacological interventions and an algorithm for management. London: RCP, 2000. Online. Available: www.rcplondon.ac.uk 58. Hulley S, Grady D, Bush T et al. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and estrogen/progestin replacement study (HERS) research group. JAMA 1998: 280(7): 605-13. 59. Mosca L, Collins P et al. Hormone replacement therapy and cardiovascular disease. A statement for healthcare professionals from the American Heart Association. Circulation 2001; 104: 499-503. 60. New Zealand Guidelines Group. Best practice evidencebased guidelines for the appropriate prescribing of hormone replacement therapy. Online. Available: www.nzgg.org.uk 61. Collaborative Group on Hormonal Factors in Breast Cancer (1997). Breast cancer and HRT: collaborative re-analysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Lancet 1997; 350: 1047-59.
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62. Committee on Safety of Medicines. EPINET message from the chairman 9.10.97. 63. Gapstur SM, Morrow M, Sellers TA. Hormone replacement therapy and risk of breast cancer with a favorable histology: results of the Iowa Women's Health Study. JAMA 1999; 28: 2091-7. 64. CSM. Risk of venous thromboembolism with hormone replacement therapy. Curr Prob Pharmacovigil 1996; 22. Online. Available: www.mca.gov.uk 65. Hope S, Rees M, Brockie J. Hormone replacement therapy a guide for primary care. Oxford: Oxford University Press, 1999. 66. Nathorst-Boos }, Hammer M. Effect on sexual life a comparison between tibolone and a continuous estradiol-norethisterone acetate regimen. Maturitas 1997; 26:15-20. 67. Kokcu A, Cetinkaya MB, Yanik F et al. The comparison of effects of tibolone and conjugated estrogenmedroxyprogesterone acetate therapy on sexual performance in postmenopausal women. Maturitas 2000; 36: 75-80. 68. Varila E, Wahlstrom T, Rauramo I. A 5-year study of the use of a levonorgestrol intra-uterine system in women receiving hormone replacement therapy. Fertil Steril 2001; 76: 969-73.
69. Pitkin J. Contraception and the menopause. Maturitas 2000; 1: S29-S36. 70. DTB. Hormone replacement therapy. Drug Ther Bull 1994; 34: 81-4. 71. Gebbie AE. Contraception for women over 40. The management of the menopause, annual review (Ed. John Studd). London: Parthenon Publishing, 1998, pp. 67-80. 72. NHS Cancer Screening Programmes. Cervical cancer - incidence, mortality and risk factors, 2002. Available: www.cancerscreening.nhs.uk/cervical/ risks.html 73. Sasieni PD, Cuzick J, Lynch-Farmery E et al. Estimating the efficacy of screening by auditing smear histories of women with and without cervical cancer. Br J Cancer 1996; 73: 1001-5. 74. Austoker J. Screening for cervical cancer. BMJ 1994; 309: 241-8. 75. Martin-Hirsch P, Jarvis G, Kitchener H, Lilford R. Collection devices for obtaining cervical cytology samples (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2001. 76. Hammond R. Management of women with smears showing mild dyskaryosis. BMJ 1994; 308: 1383-4.
CHAPTER CONTENTS Hormonal contraception 228 The combined oral contraceptive pill 228 The progestogen-only pill 234 Injectable progestogens 236 Etonogestrel-releasing implant: Implanon 238 Non-hormonal methods of contraception Intrauterine devices 238 Barrier methods 241 Emergency contraception
Contraception and sexual problems
Contraception in special cases 243 Contraception and young people 243 Contraception and older women 244 Contraception and learning disability 244 Sterilization 244 Termination of pregnancy Infertility
Adoption 247 Sexual problems 247 References
245 Advice: Glasier A, Gebbie A. Handbook of family planning and reproductive healthcare, London: Churchill Livingstone, 2000. Rowlands S. Managing family planning in general practice. London: Radcliffe Medical Press, 1997. Faculty of Family Planning & Reproductive Health Care. Online. Available: www.ffprhc.org.uk.
When giving contraceptive advice it is good practice if this is backed up with appropriate and accessible written information. The Family Planning Association (fpa) provides a range of leaflets covering all methods, which is regularly revised and is available through the local Health Promotion Unit. These leaflets should be used when a patient is deciding on a method, initiating a method and from time to time as a refresher. Recording that a patient has been given the relevant leaflet, has read it and discussed it will help to reduce litigation risk.1 Patients wanting to go to a family planning clinic or who are being referred from general practice can get details of a convenient clinic from:
fpa, 2-12 Pentonville Road, London N1 9FP, tel. 020 7837 4044; www. (the web site allows a search on a map with details right down to street level).
CONTRACEPTION AND SEXUAL PROBLEMS
HORMONAL CONTRACEPTION THE COMBINED ORAL CONTRACEPTIVE (COC) PILL Assessment of the patient
The following are the essential components of the assessment before initiating the COC: (a) menstrual and obstetric history; (b) history of migraine - presence of aura/focal nature; (c) past or current illnesses which might represent contraindications; (d) family history of venous thromboembolism (VTE), MI, cerebrovascular accident (CVA), hypertension and breast cancer; (e) current drug therapy (prescribed and OTC); (f) allergies; (g) BP measurement (defer starring the COC until 8 weeks after delivery in women who have had pre-eclampsia, even if the BP is normal); (h) baseline height/weight: BMI (important, as it is both an arterial and a venous risk factor).
Contraindications The World Health Organization gives four categories of condition in which use of the COC is (or is not) contraindicated:2 • WHO1 is a condition for which there is no restriction on use of the method. • WHO2 is when the advantages of the method generally outweigh the theoretical or proven risks. Table 12.1
• WHO3 is when the theoretical or proven risks usually outweigh the advantages but the method can be used with caution and additional care as a 'method of last choice'. • WHO4 is a condition which represents an unacceptable health risk and the method should not be used.
Absolute contraindications (WHO4) Cardiovascular
(a) Any past arterial or venous thrombosis. (b) Ischaemic heart disease and cardiomyopathies. (c) Severe or combined risk factors for venous or arterial disease (see Tables 12.1 and 12.2). (d) Migraine, if severe or focal.3 The following suggest transient ischaemia and preclude use of the COC: loss of a part of the visual field; unilateral weakness/parasthesiae; disturbance of speech; first ever migraine attack after starting COC; status migrainosus. Migraine without aura is safe (this includes blurred vision, photophobia, phonophobia and flashing lights affecting the whole visual field). (e) Transient ischaemic attacks (TIAs). (f) Hyperlipidaemia - avoid COC if total cholesterol >8mmol/L or triglyceride >4.5mmol/L. (g) Thrombophilias - inherited, e.g. factor V Leiden mutation, or acquired, e.g. lupus anticoagulant. (h) Post-splenectomy if platelet count >500 X 109/L.
Risk factors for venous thromboembolism4
Family history of VTE in 1 st degree relative age 39 Confined to bed Leg in plaster Past thrombosis Sclerosing treatment >50
Normal coagulation factors including factor V Leiden, protein C, protein S, antithrombin III BMI 30-39 Confined to wheelchair
Varicose veins Age
Extensive varicose veins >35
Adapted from Handbook of family planning and reproductive healthcare, Glasier A, Gebbie A (Eds), 2000, by permission of the publisher Churchill Livingstone.
(i) Other conditions predisposing to thrombosis: blood dyscrasias; autoimmune disorders, e.g. SLE; Klippel-Trenaunay syndrome; severe polycythaemia; elective major or leg surgery (see p. 232); during leg immobilization; before and after all varicose vein treatments (see Table 12.1 and p. 232); travel to above 4500 m; inflammatory bowel disease (ulcerative colitis and Crohn's disease, both are associated with hypercoagulability during exacerbations and so the COC should not be used during such exacerbations or in those with severe disease). (j) Past cerebral haemorrhage, (k) Vascular malformations of the brain. (1) Structural heart disease, e.g. septal defects and valvular pathology because of the risk of systemic emboli in the presence of arrythmias or shunts, (m) Pulmonary hypertension. Liver (a) Active liver disease with abnormal LFTs (safe to start COC 3 months after LFTs have returned to normal). (b) Cholestatic jaundice if induced by COC or history of this condition in pregnancy. (c) Dubin-Johnson or Rotor syndrome. (d) Liver adenoma, carcinoma or focal nodular hyperplasia. (e) Gallstones. (f) The acute hepatic porphyrias.
Sex-steroid-COC-induced conditions (a) Chorea. (b) COC-induced hypertension. (c) Acute pancreatitis linked with hypertriglyceridaemia. (d) Pemphigoid gestationis. (e) Haemolytic uraemic syndrome or thrombotic thrombocytopenic purpura. (f) Otosclerosis. (g) Stevens-Johnson syndrome. (h) Trophoblastic disease - until HCG levels are undetectable. (i) SLE (also because of thrombotic risk). Pregnancy Undiagnosed genital tract bleeding Oestrogen-dependent neoplasms These (e.g. breast cancer) are absolute contraindications. Anxiety about COC safety If not relieved by counselling.
Relative contraindications (WHO2 and WHO3) (a) Risk factors for venous and arterial disease (Tables 12.1 and 12.2). The presence of a single risk
Table 12.2 Risk factors for arterial disease4 Risk factor
Family history of arterial CVS disease in 1 st degree relative age 39 Migraine with focal aura Severe migraine Rx Ergot derivative
Normal lipid profile 1st attack in relative age 45 or more 5-30 per day BMI 30-39 Migraine without aura Migraine with non-focal aura Rx 5-HTi agonist
BP > 160/95 Retinopathy, nephropathy or neuropathy Duration of diabetes mellitus >20 years Age 30+
BP 140-159/90-95 No complications Age 35. (d) Lactating mothers - progestogen in the breast milk has no adverse effect on the baby.18 (e) Those who choose it, especially those aged over 25 or 30 years, and who accept that it is less reliable than the COC.
Absolute contraindications (WHO4) (a) Severe arterial disease or at very high risk. (b) Serious side-effect on COC not clearly due to oestrogenic component. (c) Undiagnosed genital tract bleeding. (d) Actual or possible pregnancy. (e) Recent trophoblastic disease - until HCG levels are undetectable. (f) Acute porphyria - history of an actual attack. (g) Anxiety about POP safety - if not relieved by counselling.
Relative contraindications (WHO2 and WHO3) (a) Risk factors for arterial disease, e.g. hypertension and hyperlipidaemia. (b) Past subarachnoid haemorrhage (WHO2). (c) Breast cancer (WHO3). (d) Current liver disorders (WHO2). (e) Acute porphyria - latent without a past attack. (f) Previous ectopic pregnancy (WHO2). (g) Functional ovarian cysts. (h) The young - because of the strict adherence necessary and its lower efficacy than the COC.
HORMONAL CONTRACEPTION 235
Taking the POP: procedure and advice Starting the POP: (a) Day 1. If starting on day 1 (i.e. the first day of the period) then no other precautions need be taken. (b) Later in the cycle. Extra precautions should be taken for the first 7 days. (c) Switch from COC. If changing from a COC, go straight on to the POP without a 7-day break. Extra precautions are not necessary but it may be necessary to take the pill at a different time of day. (d) Postpartum. Start at 3 weeks postpartum. Extra precautions are only needed for the next 7 days if starting later than that. Note: Time of day. The pill must be taken regularly at the same time each day (ideally at least 4 hours before the most frequent time of intercourse to ensure maximal mucus-thickening effect). Advice (a) Efficacy. Explain that, in women aged 40 or over, the POP has a similar efficacy to the COC in women aged 25. The efficacy is lowest in women with no alteration in cycle activity and is greatest in those with complete suppression of cycles and consequent amenorrhoea (roughly 40% of women continue to ovulate, in 40% there is variable interference with the follicular and luteal phase, and in 20% ovulation is inhibited completely). (b) Bleeding pattern. From (a) it follows that 40% have similar cycles to their normal pattern, 40% have shorter cycles (which may gradually lengthen towards normal over time) with episodes of spotting or breakthrough bleeding and 20% have long cycles or amenorrhoea. (c) Safety. There is no evidence of an increased risk of thrombosis. However, there is some evidence of an increased risk of breast cancer for use in the previous 5 years; relative risk 1.17 (SD = 0.09, p = 0.06), but no increase 10 or more years after stopping.15 (d) Antibiotics. The POP is not affected by antibiotics, except rifampicin and griseofulvin (see (h) below).
(e) Missed pills. If a pill is missed or delayed for more than 3 hours then alternative precautions need to be taken for 7 days. (f) Diarrhoea or vomiting. If vomiting or diarrhoea occur, continue to take the pill regularly but take extra precautions during the attack and for the next 7 days. (g) Obesity. Give patients weighing over 70 kg two pills per day. (h) Enzyme-inducing drugs. Epileptics and others on enzyme-inducing drugs are probably best advised not to rely on POPs, even if more than one pill daily is given.
Side-effects Non-menstrual These are the usual progestogenic ones such as headaches, tender breasts, acne, depression, weight gain and loss of sexual drive. But because the dose of progestogen is so low, these sideeffects are not that common and often not severe. Irregular bleeding * Examine to exclude a pathological cause. * Do not change to another POP. There is no suggestion that with the current range of POPs changing brand will improve menstrual or nonmenstrual side-effects. This situation will change when the POP containing 75 jag of desogestrel is launched as this inhibits ovulation to a greater degree.19 * Suggest a change to another method. Abdominal pain of gynaecological origin * Consider ectopic pregnancy. If it can be excluded, then refer for ultrasound. It may be due to a functional ovarian cyst. Such a cyst usually resolves without treatment. Amenorrhoea when cycles have been present * Exclude pregnancy before assuming that it is due to the POP.
CONTRACEPTION AND SEXUAL PROBLEMS
* Encourage the woman to persevere with the POP. She is in the group least likely to become pregnant with it.
Relative contraindications (WHO2 and WHO3)
* Depot medroxyprogesterone acetate (DMPA) Depo-Provera: 150 mg in 1 ml. Shake the preloaded syringe thoroughly before administration. * Norethisterone enantate (NE) - Noristerat: 200 mg in 1ml. Warm the vial close to body temperature before administration.
(a) Risk factors for arterial disease, e.g. hypertension and hyperlipidaemia. (b) Breast cancer (WHO3). (c) Current liver disorders (WHO3). (d) Past severe depression. (e) Women planning a pregnancy in the reasonably near future. (f) Women with risk factors for osteoporosis (WHO3). (g) Women aged over 45 - to ensure optimal bone mineral density on entering the menopause (see below).
Note: NE is not licensed for long-term use. When used for longer than 16 weeks, this use outside the licence must be discussed with the patient.
INJECTABLE PROGESTOGENS Preparations
Discuss with the patient the following:
Indications The indications are similar to those for the POP. Patients for whom injectable progestogens are especially indicated are women:
(a) likely to forget (or to worry about forgetting) to take daily pills; (b) for whom higher dose long-term progestogens are beneficial, e.g. those with fibroids or endometriosis; (c) with sickle-cell disease: DMPA improves the blood picture and reduces the number of crises.20
Injectables are effective and independent of coitus, with no oestrogenic side-effects. They are 'invisible', which may be important to some women, e.g. those in controlling or abusive relationships. They may enhance lactation and relieve premenstrual and menstrual symptoms. Seizure control has been reported to be improved in some epileptics. In addition, they afford some protection against pelvic infection and may improve endometriosis and sickle-cell disease.
Absolute contraindications (WHO4)
(a) Severe arterial disease or at very high risk. (b) Serious side-effect on COC not clearly due to oestrogenic component. (c) Liver adenoma, severe liver impairment, severe past steroid-associated cholestatic jaundice. (c) Undiagnosed genital tract bleeding. (d) Actual or possible pregnancy. (e) Recent trophoblastic disease - until HCG levels are undetectable. (f) Acute porphyria. (g) hypoestrogenism - not amenorrhoea alone, (h) Anxiety about safety of injectables - if not relieved by counselling.
Injectables are a very effective means of contraception: DMPA failure rates are 30 should lose weight whether ovulatory or not. (f) Men should avoid soaking in hot baths, wearing tight underwear and remaining seated for many hours at a time. (g) Couples should be advised to have regular intercourse throughout the cycle; there is no evidence that use of temperature charts and LH detection tests to time intercourse improves pregnancy rates. Use of clomifene in general cannot be justified in general practice in view of the increased risk of multiple pregnancy and ovarian cancer. An exception to this is if a woman, who previously conceived using it, presents again with anovulatory cycles. The role of the GP after referral * Administer the drugs for assisted conception according to a protocol agreed with the specialist clinic. * Support the couple throughout the drawn-out process of investigation and treatment. Self-help organizations who supply literature and run support networks: ISSUE, 114 Lichfield Street, Walsall, WS1 1SZ, tel. 01922 722888; www.issue.co.uk CHILD, 3 St Leonard's Road, Bexhill-on-Sea TN40 1JA, tel. 01424 732361; www.child.org.uk Books and videos about assisted conception are also available from The Human Fertilization and Embryology Authority, Paxton House, 30 Artillery Lane, London E1 7LS, tel. 020 7377 5077; www.hfea.gov.uk
ADOPTION Patient contact: The Director, British Agencies for Adoption and Fostering, Skyline House, 200 Union Street, London SE1 OLX, tel. 020 7593 2000; www.baaf.org.uk
SEXUAL PROBLEMS Review: Tomlinson J (Ed). ABC of sexual health. London: BMJ Books, 1999.
• Sexual problems may have a physical or psychological origin, but often they are mixed. • All patients with sexual problems develop 'performance anxiety', where they are not relaxed and spontaneous in love making, are alert to further failure and become a spectator of their own sexual performance. • In about 30% of patients, the partner also has a problem. • In any consultation about sexual problems it is important to ascertain: (a) what is the real complaint? (b) why is the problem being presented now? (c) is the desire for change real? (d) who is really complaining, the patient or the partner? (e) what are the expectations of the patient? • Consider the following psychological aspects in any patient presenting with a problem: (a) Ignorance and misunderstanding. This includes faulty sex education and technique, inability to communicate sexual needs, and unrealistic expectations due to stereotyped views of expected behaviour and performance. (b) Anger and resentment. This often remains unresolved, with the couple unable to communicate their feelings to each other clearly. It often arises where the partners are unable to express their feelings as children because of excessive unresolved anger in their parents. It may occur in response to relationship difficulties, financial difficulties, children, in-laws or stress at work. (c) Shame, embarrassment and guilt. This may be due to a negative sexual attitude laid down in childhood, where the parents looked upon sexuality as 'bad'. Traumatic sexual experiences may add to these fears. (d) Anxiety/fear about sex. Fear of closeness, vulnerability, letting go and failure may lead to a self-perpetuating cycle of anxiety.
CONTRACEPTION AND SEXUAL PROBLEMS
(e) Poor self-image may contibute to lack of interest in sex and sexual response. Changes in women may occur after operations, especially mastectomy or hysterectomy postmenopausally and after childbirth. Both sexes commonly suffer after redundancy and when depressed. Information for patients: Litvinoff S. The Relate guide to sex in loving relationships. Vermilion, 1999. Self-help material on the internet: the 'Sex and relationships' section at www.netdoctor.co.uk Advice for disabled people: SPOD, 286 Camden Road, London N7 OBJ, tel. 020 7607 8851. www.spod-uk.org Referrals for sex therapy: via local family planning clinic or Relate.
Lack of sexual desire This is the commonest presenting female sexual dysfunction, is often the hardest to treat and usually needs specialist help. Underlying psychological difficulties are frequent. These may relate specifically to sex, e.g. previous sexual abuse, or they may relate to a more widespread psychological disorder. Physical illness and drugs/ substances are also possible causes. Women specifically lose sexual desire: (a) postpartum; (b) because of pain; (c) where their partner's performance repeatedly leads to frustration, as in premature ejaculation.
Erectile dysfunction Guideline: Ralph D, McNicholas T. UK management guidelines for erectile dysfunction. BMJ200Q; 321:499-503.
Erectile dysfunction occurs in 10-15% of men but varies with age, with some degree of dysfunction being experienced by 40% of men at age 40 and by 70% at age 70. Patients who have the courage to mention it should be told that much can be
done to help. Although at least 50% of the patients referred to specialist clinics have an organic component, anxiety about the situation will make things worse. * From the history, assess particularly whether: (a) the impotence has arisen suddenly, with a precipitating cause, and is variable, with erections occurring in the early morning but not during intercourse. These patients are likely to have a psychological cause for the problem. (b) the onset was gradual, is constant, with partial or poorly sustained erections and no full early morning erections. These patients are likely to have a physical cause, although a psychological component is frequently superimposed. * Be alert to psychiatric problems including generalized anxiety states (excessive adrenergic constrictor tone), depression, psychosis, body dysmorphic disorder, gender identity problems and alcoholism. * Check for the cause being an adverse drug reaction to beta-blockers, thiazides, spironolactone, cimetidine, antidepressants, phenothiazine antipsychotics and, especially, alcohol. * Examine: (a) blood pressure. Check blood sugar. (b) genitalia (includes testicular size, fibrosis in the shaft of the penis and retractibility of the foreskin). Further examination may sometimes be indicated by age or findings in the history especially cardiovascular, neurological, endocrine and urinary systems.
Work-up (a) blood glucose; (b) testosterone (if history or examination suggest possible hypogonadism or if required to reassure patient).
Treatment in general practice52 (a) Oral sildenafil. The number of men needed to be treated with sildenafil for one additional man to experience an improvement in his erections is 1.86.53 Disadvantages are that it is a facilitator
SEXUAL PROBLEMS 249
rather than an initiator of erections and that it has a slower onset of action than injected or transurethral alprostadil (see below). Prescribe sildenafil at NHS expense to men with any of the conditions approved by the Department of Health, marking the prescription SLS, and giving enough (usually) for one treatment a week. A private prescription can be issued to any patient who does not come within the DoH guidelines (Health Services Circular HSC 1999/148 available at www.doh.gov.uk/publications/coinh.html). (b) Sublingual apomorphine - takes only 20 minutes to produce an erection. Like sildenafil, it is on the NHS 'grey list' (Schedule 11). Counselling may be successful in psychogenic impotence, and is appropriate for couples who do not wish to be referred: * See the couple together. * Recommend a manual, e.g. The Relate guide to sex in loving relationships (see box above). * Instruct the couple on the sensate focus programme. Instructions can be downloaded from the web, e.g. atwww.personalmd.com/healthtopics/ crs/touch.htm * Set 'homework' assignments for the couple; these can be tailored to meet specific needs.
Referral * Refer those not responding for sex therapy via the local family planning clinic or Relate. The outcome is successful in 50-80% of cases. * Refer for relationship counselling those whom you sense have larger relationship or personality problems. * Refer to a urologist those with physical causes, those who have not responded to sildenafil/ apomorphine or who have contraindications to it and those with psychological causes that are proving intractable. Possible treatments are: (a) hormone replacement therapy in those with hypogonadism; (b) alprostadil - as injections into the corpus cavernosum or transurethrally; (c) vacuum devices; (d) penile prostheses.
Details of therapists are available from: British Association for Sexual and Relationship Therapy, PO Box 13686, London SW20 9ZH, www.basrt.org.uk Institute of Psychosexual Medicine, 11 Chandos Street, London W1M 9DE, tel. 020 7580 0631; www.ipm.org.uk
Dyspareunia Eight per cent of women aged 35-59 admit that sexual intercourse usually causes discomfort.54 The functional problems may be primary, or secondary to a physical cause, and considerable skill may be needed to unravel the problem. * Distinguish from the history and examination between: (a) lack of lubrication due to lack of interest; (b) vaginismus, which usually becomes apparent at vaginal examination (see below); (c) vulval or vaginal causes: infections, vulvar vestibulitis syndrome, lichen sclerosus, lichen planus, urethral caruncle, postmenopausal vaginitis, postepisiotomy syndrome. Those for whom there is no specific treatment may benefit from 5% lignocaine ointment applied 20 minutes before sexual intercourse; (d) pelvic causes with tenderness on rocking the cervix or palpating the fornices, e.g. endometriosis, pelvic infection, ovarian pathology; (e) psychogenic causes, where vulval burning or pain is due to somatization of other difficulties. Vaginismus This consists of a phobia of penetration and involuntary spasm of the pubococcygeal and associated muscles surrounding the lower third of the vagina. * Explore the root cause. It may be: (a) fear of the unknown or the patient's ignorance of her own anatomy; (b) a past history of unpleasant experiences such as rape, sexual abuse or severe emotional trauma; or previous dyspareunia; (c) a defence mechanism against growing up and becoming a woman. (A common pattern is
250 CONTRACEPTION AND SEXUAL PROBLEMS
for the patient to live close to her parents, remaining the daughter and marrying an unassertive man.) * Desensitize simple cases by encouraging the women to examine herself, and also encourage her partner to be confident enough to insert a finger into the vagina. Some women may prefer to use vaginal dilators. * Refer to a sex therapist if this simple approach fails. * Give the patient details of Resolve - the Vaginismus Support Group, PO Box 820, London N10 SAW.
the glans between finger and thumb during relaxation phases. * Clomipramine 25 mg daily or paroxetine 20 mg each evening are effective in delaying ejaculation.52 Retarded ejaculation
This is usually a sign of long-standing sexual inhibition. Often the patient can ejaculate by masturbation, but not intravaginally. * Explore any feelings of anxiety and guilt. * Start a sensate focus programme (see above). * If 'home therapy' fails, refer for psychosexual counselling.
Disorders of orgasm Anxiety tends to delay a woman's orgasm, but accelerates a man's. Premature ejaculation
This is present when ejaculation occurs sooner than either partner would wish, usually before penetration or soon after. Interest in sex may be reduced in both partners. * Advise the patient that, with practice, he can learn to delay ejaculation. The stop/start technique can be taught by therapists or learnt from the book cited above. In essence, when during caressing or during intercourse a man feels he is close to climax he should stop being stimulated and relax for 30 seconds. Stimulation can then recommence until he is close to climax again, when the relaxation is repeated. If this fails, the woman should squeeze the penis at the base of
Orgasmic problems in women
* A woman who has never achieved an orgasm may have deep-seated psychological reasons for being afraid to let go. She may need 'permission' to investigate her body's own responses further, either by masturbation or vibrator. When she has learnt how to relax, she should be encouraged to tell her partner and incorporate caressing into their usual lovemaking. * Women who have lost the ability to achieve orgasm may need counselling, especially about their current relationship or a recent loss of selfimage. * Check that she is not taking drugs that inhibit orgasm, e.g. clonidine, and that her failure to achieve orgasm is not due to neurological disease or pelvic surgery. Contrary to the results of some poorly executed studies, total hysterectomy does not impair ability to achieve orgasm.55
REFERENCES 1. Brown ADG. Legal aspects of family planning. In Glasier A, Gebbie A (Eds). Handbook of family planning and reproductive healthcare. London: Churchill Livingstone, 2000, pp. 231-48. 2. Anonymous. Improving access to quality care in family planning: medical eligibility criteria for contraceptive use. Geneva: World Health Organization, 2000. 3. MacGregor EA, Guillebaud J. Combined oral contraceptives, migraine and ischaemic stroke. Br J Fam Planning 1998; 24: 55-60.
4. Guillebaud J. Combined oral contraception. In Glasier A, Gebbie A (Eds). Handbook of family planning and reproductive healthcare. London: Churchill Livingstone, 2000, pp. 29-76. 5. Anonymous. Combined oral contraceptives containing desogestrel or gestodene and the risk of venous thromboembolism. Curr Prob Pharmacovigil 1999; 25: 12. 6. Kemmeren JM, Algra A, Grobbee DE. Third generation oral contraceptives and risk of venous thrombosis: meta-analysis. BMJ 2001; 323: 131-4.
7. Walker AM. Newer oral contraceptives and the risk of venous thromboembolism. Contraception 1998; 57: 169-81. 8. Anonymous. First prescription of combined oral contraception: recommendations for clinical practice. Br } Fam Planning 2000; 26: 27-38. 9. Stewart FH, Harper CC, Ellertson CE, Grimes DA, Sawaya GF, Trussell J. Clinical breast and pelvic examination requirements for hormonal contraception. JAMA 2001; 285: 2232-9. 10. O'Brien MD, Gilmour-White S. Epilepsy and pregnancy. BMJ 1993; 307: 492-5. 11. Rosenberg MJ, Long SC. Oral contraceptives and cycle control: a critical review of the literature. Adv Contracep 1992; 8 (Suppl. 1): 35-45. 12. Guillebaud J. Contraception and sterilization. In Turnbull A, Chamberlain G (Eds). Obstetrics. Edinburgh: Churchill Livingstone, 1989, pp. 1135-52. 13. Poulter NR. Oral contraceptives and blood pressure. In Hannaford PC, Webb AMC (Eds). Evidence-guided prescribing of the pill. Carnforth: Parthenon, 1996, pp. 77-88. 14. Fernandez E, La Vecchia C, Balducci A, Chatenoud L, Franceschi S, Negri E. Oral contraceptives and colorectal cancer risk: a meta-analysis. Br J Cancer 2001; 84: 722-7. 15. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53,297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies. Lancet 1996; 347: 1713-27. 16. Rosenberg MJ, Waugh MS, Stevens CM. Smoking and cycle control among oral contraceptive users. Am J Obstet Gynecol 1996; 174: 628-32. 17. Hampton N. The role of hormonal contraceptives in acne. Br J Sex Med 1995; May/June: 11-14. 18. Fotherby K. The progestogen-only pill. In Filshie M, Guillebaud J (Eds). Contraception: science and practice. London: Butterworths, 1989, pp. 94-108. 19. Rice C, Killick S, Hickling D, Coelingh Bennink H. Ovarian activity and vaginal bleeding patterns with a desogestrel-only preparation at three different doses. Hum Repro 1996; 11: 737-40. 20. Bhathena RK. The long-acting progestogen-only contraceptive injections: an update. Br J Obstet Gynaecol 2001; 108: 3-8. 21. Kaunitz AM. Injectable contraception. Obst Gynecology Clin N Am 2000; 27: 741-80. 22. WHO. A multicentred phase III comparative trial of depot-medroxyprogesterone acetate given three-monthly at doses of lOOmg or 150mg: II. The comparison of bleeding patterns. Contraception 1987; 35: 591-610. 23. Merki-Feld GS, Neff M, Keller PJ. A prospective study on the effects of depot medroxyprogesterone acetate on trabecular and cortical bone after attainment of peak bone mass. Br J Obstet Gynaecol 2000; 107: 863-9. 24. Tang OS, Tang G, Yip PSF, Li B. Further evaluation on long-term depot-medroxyprogesterone acetate use and bone mineral density: a longitudinal cohort study. Contraception 2000; 62: 161-4. 25. Fotherby K, Howard G. Return of fertility in women discontinuing injectable contraceptives. / Obstet Gynaecol 1986; 6: S110-S15.
26. Croxatto HB, Makarainen L. The pharmacodynamics and efficacy of Implanon. Contraception 1998; 58: 91S-7S. 27. Mascarenhas L. Insertion and removal of Implanon. Contraception 1998; 58: 79S-83S. 28. Affandi B. An integrated analysis of vaginal bleeding patterns in clinical trials of Implanon. Contraception 1998; 58: 99S-107S. 29. Urbancsek J. An integrated analysis of nonmenstrual adverse events with Implanon. Contraception 1998; 58: 109S-15S. 30. Rowlands S, Hampton N. Intrauterine contraception. In Kubba A, Sanfilippo J, Hampton N, eds. Contraception and office gynecology: choices in reproductive healthcare. London: WB Saunders, 1999, pp. 93-112. 31. Grimes D. Intrauterine device and upper-genital-tract infection. Lancet 2000; 356: 1013-19. 32. Grimes D, Schulz KF. Antibiotic prophylaxis for intrauterine contraceptive device insertion (Cochrane Review). The Cochrane Library, Issue 4. Oxford: Update Software, 2000. 33. The Clinical and Scientific Committee. Recommendations for clinical practice: actinomyces like organisms and intrauterine contraceptives. Br J Fam Planning 1998; 23: 137-8. 34. Grimes D, Schulz K, Stanwood N. Immediate postabortal insertion of intrauterine devices (Cochrane Review). The Cochrane Library, Issue 3, Oxford: Update Software, 2000. 35. Hicks D. The risks and benefits of contraceptive method regarding sexually transmitted infections. Br J Fam Planning 1996; 22: 34-6. 36. Mindel A. Condoms. London: BMJ Books, 2000. 37. Longworth JCD, Marable E. Recent advances in barrier contraception: review and report of clinical trial of the Oves® cervical cap. Rev Gijnaecolog Pract 2001; 1: 89-99. 38. European Natural Family Planning Study Groups. Prospective European multi-center study of natural family planning (1989-1992): interim results. Adv Contracep 1993; 9: 269-83. 39. Bonnar J, Flynn A, Freundl G, Kirkman R, Royston P, Snowden R. Personal hormone monitoring for contraception. Br J Fam Planning 1999; 24: 128-34. 40. Anonymous. Emergency contraception: recommendations for clinical practice. Br J Fam Planning 2000; 26: 93-6. 41. Cheng L, Giilmezoglu AM, Ezcurra E, Van Look PFA. Interventions for emergency contraception (Cochrane Review). The Cochrane Library, Oxford: Update Software, 2000. 42. Task Force on Postovulatory Methods of Fertility Regulation. Randomised controlled trial of levonorgestrel versus the Yuzpe regimen of combined oral contraceptives for emergency contraception. Lancet 1998; 352: 428-33. 43. Rodrigues I, Grou F, Joly J. Effectiveness of emergency contraceptive pills between 72 and 120 hours after unprotected intercourse. Am J Obstet Gynecol 2001; 184: 531-7. 44. Wilcox AJ, Dunson DB, Weinberg CR, Trussell J, Baird DD. Likelihood of conception with a single act of intercourse: providing benchmark rates for assessment of post-coital contraceptives. Contraception 2001; 63: 211-15. 45. Trussell J, Ellertson C. Efficacy of emergency contraception. Fertil Control Rev 1995; 4: 8-11.
CONTRACEPTION AND SEXUAL PROBLEMS
46. Donovan C, Hadley A, Jones M, et al. Confidentiality and young people. London: Royal College of General Practitioners and Brook, 2000. 47. Gebbie A. The menopause. In Glasier A, Gebbie A (Eds). Handbook of family planning and reproductive healthcare. London: Churchill Livingstone, 2000, pp. 371-94. 48. Cooper E. Couples with learning disabilities. In Killick S (Ed). Contraception in practice. London: Martin Dunitz, 2000, pp. 229-40. 49. Royal College of Obstetricians and Gynaecologists. Male and female sterilisation: evidence-based clinical guidelines, No. 4. London: RCOG Press, 1999. 50. Frank P, McNamee R, Hannaford PC, Kay CR, Hirsch S. The effect of induced abortion on
51. 52. 53.
subsequent fertility. Br ] Obstet Gynaecol 1993; 100: 575-80. Gilchrist AC. Psychological sequelae of abortion. Trends in urology, gynaecology and sexual health 1998; March: 9-10. Holmes S. Treatment of male sexual dysfunction. Br Med Bull 2000; 56: 798-808. Burls A, Gold L, Clark W. Systematic review of randomised controlled trials of sildenafil (Viagra®) in the treatment of male erectile dysfunction. Br J Gen Pract 2001; 51: 1004-12. Osborn M, Hawton K, Gath D. Sexual dysfunction among middle aged women in the community. BMJ 1988; 296: 959-62. Farrell SA,. Kieser K. Sexuality after hysterectomy. Obstet Gynecol 2000; 95: 1045-51.
CHAPTER CONTENTS Prepregnancy care 253 Genetic disorders 253 Previous obstetric history 254 Medical history 255 Lifestyle 256 Infection 256 Nutrition 256
13 Obstetric problems
Routine antenatal care 256 Prenatal diagnosis and screening 258 Problems in pregnancy 259 Vaginal bleeding and miscarriage 259 Abdominal pain 261 Infection or contact with infectious disease 261 Vomiting and reflux 263 Pruritus 263 Excessive weight gain 263 Fundal height 263 Hypertension 264 Anaemia 265 Rhesus-negative mothers 266 Abnormal lie 266 High head 266 Post-maturity 266 Specific medical conditions and pregnancy 267 Drug misuse 268 Intrapartum care Postnatal care References
Policy statement: The role of general practice in maternity care. Occasional paper 72. London: Royal College of General Practitioners, 1995.
PREPREGNANCY CARE The GP has an important role in identifying risk factors before conception. This can be done either at a specific consultation or when the opportunity arises, e.g. as part of contraceptive care, or when seeing patients with diabetes or hypertension. GENETIC DISORDERS All couples should be referred for genetic counselling if they request it, or there are risk factors which need further investigation. The list of identifiable conditions is increasing, and recent studies in the UK suggest clinicians across specialties are poor at appreciating which conditions have identifiable genetic components.1 If there is any doubt, contact the nearest department of clinical genetics for advice. Children or adults with a major abnormality or disease, even if not at present thought to be genetic in origin, should have blood stored at a regional genetics laboratory for later analysis. Those at higher risk are: (a) Couples with a personal or family history of an abnormality that is presumed to be genetic in origin. They should be referred for genetic 253
counselling or have blood taken by the GP on the advice of the geneticist. Important examples are: - cystic fibrosis; - Huntington's chorea; - Duchenne and other muscular dystrophies; -polycystic kidneys; -mental retardation, which may be due to fragile-X syndrome. (b) Couples belonging to a high risk ethnic group (see below). (c) Older women. The risk of having a baby with Down syndrome is 1:400 at age 35, rising to 1:100 at age 40 and 1:30 at age 45. After the age of 37 the risk of chromosomal abnormality is greater than the risk of miscarriage after amniocentesis. Apart from this, neonatal outcome is not affected by maternal age, although women having their first pregnancy over age 35 are more likely to have hypertension, diabetes or placental abruption. (d) Consanguinous couples. First-degree cousins have a slight but significant increase in congenital malformations. This is likely to be higher if there is a family history of congenital disease. Caucasian first-degree cousins should be offered screening for cystic fibrosis, even where there is no family history.
High-risk ethnic groups African-Caribbean: Sickle-cell and thalassaemia * Exclude sickle-cell trait in the parents by checking their Hb and asking for sickle solubility test. If positive, request Hb electrophoresis. * Refer all couples who are both heterozygous, or where the mother is and the father has thalassaemia minor or is unknown. Patient leaflets: Sickle Cell Society, 54 Station Road, London NW10 4UA, tel. 020 8961 7795; www.sicklecellsociety.org
Indian subcontinent, Far East and Southern Europe: Thalassaemia * Check Hb and, if the mean cell haemoglobin is below 25 pg, arrange Hb electrophoresis; or * Screen for haemoglobinopathy regardless of the MCH, if that is local policy.
Note: If both partners have thalassaemia trait, refer for specialist genetic advice. Patient leaflets: UK Thalassaemia Society, 19 The Broadway, Southgate Circus, London N14 6PH, tel. 020 8882 0011; www.ukts.org
Jewish population: Tay Sachs * Consider referral for the exclusion of Tay Sachs trait. One in 30 of Ashkenazi Jewish descent is positive. Telephone the Tay Sachs carrier testing centre at Guy's Hospital, tel. 020 7955 4648, or the Regional Genetics Centre.
PREVIOUS OBSTETRIC HISTORY (a) Down syndrome: make certain that all women who have had a previous Down syndrome baby have received genetic counselling, regardless of the age at which they conceived. (b) Previous miscarriages (see also p. 260): inform all patients, if asked, that the overall incidence of miscarriage is around 15%. However, women whose last pregnancy was normal have a 5% chance of miscarriage, whereas women whose last pregnancy ended in miscarriage have a 20-25% chance of a miscarriage.2 Women with three consecutive miscarriages have a 40% chance of the next pregnancy ending in miscarriage. (c) Recurrent miscarriages: refer to a gynaecologist for assessment all women who have had three consecutive miscarriages. Reassure them, however, that they still have a 60% chance of a normal pregnancy. Consider early referral if: - there is a history of cycle irregularity; - there is a family history of miscarriage or of congenital disease; - there is a relevant medical problem; - the miscarriage was mid trimester; or - there is an urgency to achieve a live birth, as in the older woman. Hospital work-up for recurrent miscarriage: (a) Blood sugar; (b) TFTs; (c) LH on day 7; (d) Blood group and antibodies;
PREPREGNANCY CARE 255
(e) (f) (g) (h) (i)
Antiphospholipid antibodies; Factor V Leiden; Karyotyping of both partners; Pelvic ultrasound; Hysterosalpingography if miscarriages are late.
(d) Family history or previous infant with neural tube defects: All women in this category should receive folic acid prior to conception. Give 5mg daily, starting 1 month prior to stopping contraception, and continue throughout the first trimester. This will reduce the incidence of further neural tube defects by 70% (DoH letter, 12 August 1991). Women should also receive advice about antenatal diagnosis (see below). (e) Size, gestation and maturity of previous infants: -previously large babies: consider screening for type 2 diabetes. -previous intrauterine growth retardation: stress the importance of not smoking and drinking alcohol. The woman should be referred early in pregnancy for consideration of uterine artery Doppler as a screening test, and for serial growth scans from 24 weeks gestation. MEDICAL HISTORY Hypertension (see p. 264) * This should be assessed before a woman gets pregnant, as it may be masked by the fall in blood pressure in the first half of pregnancy. * Discuss the most appropriate drug with the relevant specialist before conception. Diabetes (see p. 267) * Explain that diabetes is associated with an increase in congenital abnormalities (about double), but that this can be decreased significantly by good control of the blood sugar prior to and during pregnancy.3
multiplied by two for every further drug taken.4 Sodium valproate increases the risk of neural tube defects 50 times, to about 1.5%. With carbamazepine the rate is 1%. Otherwise abnormalities are not specific to individual drugs. There is little data on the safety of newer drugs. There is no convincing evidence that any one drug is safer than another.5 * Discuss with the neurologist: (a) whether to stop anticonvulsants in any woman who has been free of convulsions for 2 years; but counsel the patient about the risks of untreated epilepsy in pregnancy. Convulsions may lead to stillbirth; or (b) whether to change anticonvulsants or reduce their dose in those in whom they cannot be stopped. * Make it clear that even on anticonvulsants there is a 90% chance of a normal outcome, that prenatal diagnosis is effective in picking up neural tube defects (see below) and that many defects can be corrected after birth. * Ensure that all epileptics are offered: (a) Folic acid. Those continuing antiepileptic medication should take folic acid 5mg daily from 3 months before conception until the end of the 12th week. Those stopping their drugs need only take 400 |xg daily from 1 month before conception; (b) an anomaly ultrasound examination at 18/19 weeks; and (c) Vitamin K. Give vitamin K 20 mg orally daily for the last 4 weeks of pregnancy to women on enzyme-inducing antiepileptic treatment. * Educate a woman's partner about what to do should she fit, as epilepsy may be less predictable.
Other medication A decision should be taken about the need to stop other drugs which are associated with fetal abnormalities, e.g. warfarin and lithium.
Epilepsy The risk of fetal abnormality in births to epileptic mothers not on treatment is probably the same as that of the general population (2-3%). This rises to 4-9% if one antiepileptic drug is taken and is
Psychiatric history The Confidential Enquiry into Maternal Deaths in the UK for 1997-9 recognized that the second commonest indirect cause of death was associated
256 OBSTETRIC PROBLEMS
with psychiatric disease (30 deaths over the 3-year period). They recommend seeking a history early in pregnancy and ensuring effective follow up in late pregnancy and the early postnatal period.
(f) Genital herpes and warts (see p. 262). Management to protect the neonate is only an issue in the last weeks of pregnancy.
* Alcohol/smoking. Counsel the couple to stop smoking and women to reduce their alcohol consumption to a maximum of 1 unit a day.
* Check Hb in all women with a previous history or at high risk of anaemia, e.g. vegans, multiple pregnancies, and those with a short interval between pregnancies. * Check the serum ferritin in those women who have a history of iron-deficiency anaemia, even if the haemoglobin is normal.
INFECTION (a) Rubella. All women should have rubella antibodies tested before each pregnancy; immunity can be lost between one pregnancy and the next. In 1986 in the UK, 2% of pregnant women are still not immune.6 (b) Hepatitis B. Women from high-risk countries (especially Vietnam and other areas of South East Asia) or those at risk by virtue of occupation or lifestyle should be screened for hepatitis B. The case for nationwide screening in pregnancy is strong/ and many units now offer this routinely. (c) Listeria. Advise women to avoid soft cheeses, 'cook-chill' foods (unless thoroughly reheated) and pates prior to and during pregnancy. They should avoid contact with sheep at lambing time, and with silage. In 1990 there were 24 cases of listeriosis in pregnant women in England and Wales.8 (d) Toxoplasmosis. Women contemplating pregnancy should be warned about the risks of handling soil, cat faeces or raw meat, and of eating undercooked meat and unwashed vegetables and fruits. Eighty per cent of British women are not immune at the time of pregnancy. There are currently no plans to offer widespread screening in the UK. (e) HIV. Most maternity units in the UK offer screening to all women booking for antenatal care, as precautions taken at delivery (antiretroviral medication and caesarean section) are highly effective at reducing vertical transmission. Several studies have suggested that screening only by risk factor will miss significant numbers of HIV positive women.9
Calcium * Consider giving calcium supplements to all patients at high risk, e.g. those economically deprived, Asian immigrants, repeated pregnancies, women who breast-fed for a prolonged period.
Diet * Advise a balanced diet high in fibre to avoid later constipation. * Recommend that all women take 400 |xg of folic acid a day from before conception until the end of the 12th week. This will prevent 95% of neural tube defects.10
Liver * Advise the woman not to eat liver or liver products, e.g. sausage or pate, because of the high vitamin A content11 or to reduce consumption to no more than 50 g of liver per week or lOOg of pate.12 Furthermore, see Listeria above.
ROUTINE ANTENATAL CARE Antenatal care varies from entirely hospital-based to entirely GP and community midwife-based, which gives equally good results in low-risk
ROUTINE ANTENATAL CARE 257
women.13 It is usually shared between the two. The right setting is that which best meets the needs of the woman concerned.14 Indications for referral for hospital-based antenatal care are: (a) (b) (c) (d) (e)
the patient's own choice; a poor obstetric history; a relevant medical problem; an obstetric complication in this pregnancy; multiple pregnancy.
Antenatal care should cover the following.
Booking (a) Age, ethnic origin of both parents, medical history, obstetric history, family history, alcohol, smoking, social circumstances, and diet. Recommend folic acid 400 jxg daily until week 12 if the patient is not already taking it. (b) Estimate expected date of delivery (EDD). (c) Check blood pressure, heart, weight, height, urine, oedema, teeth. (d) Blood tests: Hb, group and antibodies, rubella, syphilis serology and hepatitis B and HIV, after counselling. Tests for sickle-cell trait and thalassaemia if at risk. (e) MSU: Asymptomatic bacteriuria carries a high risk of overt infection during pregnancy (see p. 265). (f) Decide whether the patient is at normal or higher risk. (g) Discuss the place and mode of delivery, a plan for pain relief and involvement of partner. (h) Book an ultrasound scan for dating, placental site, multiple pregnancy, and gross anomalies. A patient with a history of a previous ectopic pregnancy or with other high risk factors (see below) for an ectopic should have an ultrasound scan as soon as pregnancy is suspected. (i) Counsel for Down syndrome screening by serum biochemistry, or by fetal nuchal scan (or in some centres by a combination test), (j) Arrange for a blood sugar 2 hours after a glucose load, at a later date, according to local policy. The WHO definition of gestational diabetes is a fasting sugar of 7mmol/L or above or a 2-hour sugar of 7.8mmol/L or above.15
Risk factors for ectopic pregnancy (a) (b) (c) (d) (e) (f)
A history of pelvic inflammatory disease; Previous tubal surgery; Previous ectopic pregnancy; Sterilization; Assisted reproduction; Progesterone IUD.
A patient in any of these categories should have an urgent USS as soon a pregnancy is suspected. An intrauterine pregnancy should be visible at 5-6 weeks gestation, or the serum (3HCG concentration should exceed lOOOmiu/L. Diagnosis of an ectopic pregnancy may not only be life-saving, but may also permit medical treatment with methotrexate provided the pregnancy is less than 3.5cm.16
Follow-up appointments What evidence there is suggests that reducing the number of visits is not associated with worse outcomes, except that women may be less satisfied.17 The Royal College of Obstetricians and Gynaecologists recommends a minimum of four appointments, after booking, at the following times: 20-22, 28-32,36 and 40 weeks. In addition, primagravida need a blood pressure check at 26,34 and 38 weeks. The case for fewer routine visits is, however, far from clear.18 Repeated weighing is no longer routinely offered.19
At each appointment check: (a) the patient's general health; (b) BP; (c) urine; (d) oedema; (e) symphysis-fundal height; (f) fetal movements or fetal heart sounds; (g) presentation (after 32 weeks). In addition: (a) at 16 weeks check that USS and alpha-fetoprotein (AFP) have been arranged, if wanted; (b) at 28 and 36 weeks take blood for Hb and ABO and rhesus antibodies; (c) screen for gestational diabetes according to local protocols.
258 OBSTETRIC PROBLEMS
PRENATAL DIAGNOSIS AND SCREENING A GP should be aware of the techniques of prenatal diagnosis in order to: (a) identify all women who might benefit from early assessment by the obstetrician; (b) counsel patients about the accuracy and risk of prenatal diagnosis; (c) make sure that the opportunity for prenatal diagnosis is not overlooked by the obstetrician. Prenatal diagnosis is generally performed to; (a) allow termination of pregnancy when a fetal abnormality is detected; (b) reassure parents when a fetus is unaffected; (c) prepare the parents and the neonatal unit for the birth of an abnormal baby. Women are routinely offered screening in the form of ultrasound, or by maternal serum testing using the 'triple test' (human chorionic gonadotrophin, estriol and alpha-fetoprotein). Several groups in the UK are now looking at combining ultrasound and serum screening either sequentially or concurrently, although the results of these studies are not yet available.
medication, need an informed discussion. For some abnormalities, early diagnosis is available by transvaginal scanning in tertiary centres (e.g. some cardiac anomalies, gastroschisis). For others USS at 18-19 weeks, or sometimes even later, is required (see below).
Down syndrome Triple test: a composite risk score, performed at 16-20 weeks, based on maternal age, serum alphafetoprotein, unconjugated estriol and human chorionic gonadotrophin. If the threshold for offering amniocentesis is set at a risk of 1 in 250, then about 5% of women will screen positive. About 1 in 40 of these will be shown to have an affected fetus.20 Detection rates of only 60% are claimed even if all women proceed to diagnostic testing. In reality, few centres achieve near 100% uptake for screening and advantages over screening on maternal age alone may be less than has previously been published.21 An integrated test, based on screening in the first and second trimesters, is more reliable but not widely available.22
Tests involved Chorionic villus biopsy (CVB)
All women who have a personal or family history of neural tube or other structural defect should be offered an ultrasound examination at 18-19 weeks. Ordinary ultrasound practised by a suitably trained operator should detect 90-95% of all cases of spina bifida, and all cases of anencephaly. Where ultrasonography of adequate quality is not available women should, ideally, be offered a scan in a region where it is, or a serum alpha-fetoprotein at 16-18 weeks (this detects 80% of open defects and about 90% of those with anencephaly). Confirmation by ultrasound is then needed.
This is usually performed after 11 weeks and allows termination of pregnancy in the first trimester, but has a miscarriage rate of 1.2%. There is also a further 1-2% chance of needing an amniocentesis to establish the diagnosis. CVB performed before 10 weeks may rarely cause limb abnormalities.23 It is indicated for, e.g. early diagnosis of chromosomal disorders, inborn errors of metabolism amenable to DNA analysis, haemophilia A and B, sickle-cell disease, alpha- and beta-thalassaemia, cystic fibrosis, muscular dystrophies, Huntington's chorea, alpha-1-antitrypsin deficiency, osteogenesis imperfecta, adult polycystic kidneys, tuberous sclerosis and von Recklinghausen's disease.
Women with a personal or family history of other abnormalities, or who have been put at risk by
This is usually performed at 15-16 weeks, which will allow termination by 20 weeks. It is associated
Spina bifida, anencephaly or other structural abnormality
PROBLEMS IN PREGNANCY
with a miscarriage rate of 1%. Many laboratories now use polymerase chain reaction technology to give results for Down and Edward syndromes in 48 hours, usually backed by culture results for other chromosomal anomalies available 2 weeks later.
72 hours of the bleeding starting, although, if a longer period has elapsed, it may still give some protection. In the second half of pregnancy the dose can be adjusted according to the results of the maternal Kleihauer test.
Ectopic pregnancy Ultrasonography
Routine ultrasonography can detect grosser forms of congenital abnormality, e.g. cranial and neural tube defects, severe skeletal dysplasia and abnormalities of the heart, chest and abdominal organs between 17 and 20 weeks. Hydrocephalus may be detected later. As technology and training improve the range of anomalies detectable prenatally continues to increase. Fetoscopy
Visualization of the fetus is necessary for assessment of some external malformations. It is also used for laser treatment of twin-to-twin transfusion syndrome.
PROBLEMS IN PREGNANCY VAGINAL BLEEDING AND MISCARRIAGE Guideline: Stillbirth and Neonatal Death Society. Pregnancy loss and the death of a baby: guidelines for professionals. London: SANDS, 1995.
* Rhesus status. If a rhesus-negative patient bleeds, anti-D immunization is recommended by the DoH at any stage of pregnancy, whether the bleeding leads to loss or continuation of the pregnancy. There is, however, no evidence that this is of benefit in threatened or naturally completed miscarriages, and it is reasonable to withhold anti-D immunoglobulin in miscarriages without evacuation of the retained products of conception (ERPC) under 12 weeks.24 * If anti-D immunoglobulin is needed, the dose depends upon the preparation used. Give it within
Ectopic pregnancy is usually associated with mild vaginal bleeding as well as pain. A negative pregnancy test (i.e. an HCG level below 50mU/ml) virtually excludes an ectopic. Intrauterine pregnancies should be visible on transvaginal ultrasound when serum HCG exceeds 1000 mU/L. * Admit any patient in whom the possibility of an ectopic is anything more than remote. It is the commonest cause of death in the first trimester and remains in the top five causes of death in pregnancy.25
Suspected miscarriage up to 14 weeks pregnancy Guidance: Ankum WM, Wieringa-de Waard M, Bindels PJE. Management of spontaneous miscarriage in the first trimester: an example of putting informed shared decision making into practice. SMJ2001; 322: 1343-6. Cahill DJ. Managing spontaneous first trimester miscarriage. 6M/2001; 322: 1315-16.
* Women referred to specialist care tend to undergo surgical evacuation, sometimes unnecessarily. * Expectant management at home can avoid referral in a large proportion of cases with possibly better outcomes. * Perform a vaginal examination to assess the cervix. * Do not use a pregnancy test to see whether the pregnancy is viable; too many false positives and false negatives occur. Threatened miscarriage
* If there is modest loss, minor pain and the os is closed, manage at home. Rest will reduce the
amount of loss, although it will not affect the outcome. * Prepare the patient for what may happen; 50% will miscarry. * Arrange for an ultrasound detection of fetal heart movements. They are reliably detectable from the 7th week, and may be detectable from the 6th. If they are present, the pregnancy has a 95% chance of continuing.26 If bleeding and pain settle: * Advise the patient that, if the pregnancy continues, the risk of fetal abnormality is no greater than in patients who have not bled. (There is a higher risk of antepartum haemorrhage and early neonatal death, but it is difficult to justify telling the patient this unless asked.) * Arrange an ultrasound scan to confirm that the pregnancy is viable. * If a vaginal examination has not been performed, do so to look for local causes of bleeding, e.g. erosion, polyp or carcinoma. * The use of the triple test at 16 weeks is less reliable. Inevitable miscarriage
* If there is considerable loss, pain and the os is open, refer to hospital. * Remove any products of conception felt within the vagina. Send them to hospital with the patient. * If bleeding is heavy, give Syntometrine 1 ml im while awaiting the ambulance. The decision as to whether to perform a ERPC will be made by the gynaecologists. Not performing ERPC is as effective in four out of five women, but requires greater follow-up.27 Complete miscarriage
* If products have been lost, pain and bleeding have stopped and the os is closed: (a) inform the patient that the miscarriage is probably complete; (b) tell the patient to contact you if more bleeding occurs; (c) discuss with the parents whether to send the products of conception for histology. Some
may wish to have some tissue returned to them so that a burial service can be held. This can provide a focus for their grief. Even if no tissue is available, it is possible for a memorial service to be held. (d) Repeat the pregnancy test after 1 week. A negative test helps to exclude an ectopic. Follow-up after miscarriage
* Arrange to meet all patients who have miscarried about 4 weeks afterwards. Be aware that the patient has suffered a bereavement, and may need counselling; 50% are still likely to feel depressed.28 A quarter are likely to be suffering from post-traumatic stress disorder (PTSD).29 PTSD is also found in a fifth in the third trimester of the next pregnancy30 and is more likely if the next pregnancy follows within a year of the miscarriage. It may be more likely if the mother sees and holds the dead infant. * Attend to any physical issues and the possible need for contraception. The traditional advice to have two normal periods before trying to conceive again may be more important to allow time for the grieving process than for any physical reason. * Be aware that women are distressed by the fact that no reason for the miscarriage can usually be given. Explain that early miscarriage is due either to an abnormality of fetal development, or to a failure of implantation. * Explain that one miscarriage is followed by a slight or even no increase in risk of subsequent miscarriages.31 Investigations are unlikely to be fruitful unless three or more pregnancies have miscarried (see p. 254). Having three consecutive miscarriages gives a patient a subsequent risk of 40%. Referral for investigation is then traditional, but earlier referral would be justified as discussed above. Patient information and support: The Miscarriage Association, c/o Clayton Hospital, Northgate, Wakefield, West Yorkshire, WF1 3JS, helpline 01924 200799; administration 01924 200795 for leaflets about all aspects of miscarriage and ectopic pregnancy; www. miscarriageassociation .org. uk
PROBLEMS IN PREGNANCY
Suspected miscarriage after 14 weeks pregnancy The more advanced the pregnancy, the more advisable it is to admit the patient to hospital at the onset of bleeding, whether or not there has been pain. After 14 weeks, painless bleeding is due to placenta praevia until proved otherwise. Bleeding with severe pain is likely to be due to abruptio placentae. Do not do a vaginal examination in these patients. Patient information and support: For parents whose baby is stillborn or dies soon after birth: SANDS (the Stillbirth and Neonatal Death Society), 28 Portland Place, London W1N 4DE, helpline 020 7436 5881; administration 020 7436 7940; www.uk-sands.org
ABDOMINAL PAIN Abdominal pain may be due to a variety of causes, some of which are serious and which may present in an atypical way. Any cause which could occur outside pregnancy (e.g. renal calculus) must be considered. In the first 20 weeks, consider: (a) miscarriage; (b) ectopic pregnancy; (c) urinary infection; (d) appendicitis; (e) impaction of a retroverted uterus; (f) red degeneration of a fibroid (the maximum incidence is 12-18 weeks, but it may occur at any time); (g) torsion of an ovary or tube; (h) haematoma of the round ligament; (i) accident to an ovarian cyst. After 20 weeks, consider, in addition: (a) (b) (c) (d) (e) (f)
labour; abruptio placentae; haematoma of the rectus abdominis; red degeneration of a fibroid; uterine rupture; dehiscence of the pubic symphysis.
INFECTION OR CONTACT WITH INFECTIOUS DISEASE Rubella contact • If a pregnant woman is infected with rubella, the risk to the fetus is greatest up to 11 weeks but 30% of fetuses between 11 and 16 weeks are affected. • Infection occurring before 16 weeks is usually considered to be grounds for termination, if requested. • If a pregnant woman is affected between 16 and 19 weeks, the risk of fetal damage is less than 2%. Deafness is the most likely problem. This is not usually considered to be sufficient grounds for termination. • After 19 weeks there appears to be no risk.32 • Accidental immunisation in pregnancy has not been associated with embryopathy. Rubella contact before 16 weeks
If the pregnancy is less than 16 weeks (regardless of whether the woman has had rubella or the vaccination or antibodies were previously detected:33 • Take blood for rubella antibodies. (a) If IgG is present and the blood was taken within 12 days of contact, inform the woman that she is immune and that there is little need to worry. (b) If IgG is present but the blood was taken more than 12 days after contact, request IgM levels. If IgM shows recent infection, discuss the risks of fetal abnormality and the question of termination of pregnancy. (c) If IgG is absent, repeat IgM 2 weeks later. If she has seroconverted, discuss the question of termination of pregnancy as above. The value of immunoglobulin in protecting the fetus is doubtful (see p. 27). (d) Any IgG-negative woman should be immunised in the puerperium. Note: If a woman contracts rubella and decides to continue the pregnancy, fetal blood sampling (from the umbilical vein) from 20 weeks onwards can indicate whether the baby has contracted it by assessing fetal IgM.
Varicella (chickenpox) A congenital varicella syndrome, including limb deformities and scarring, may occur in 3% of pregnancies where the mother contracts chickenpox (although not shingles) in the first trimester.34 * A woman who is not known to be immune and who is in contact with chickenpox in the first trimester: check her varicella antibodies, and give VZIG if not immune (see p. 31). Give aciclovir if she develops varicella. * Offer an ultrasound anomaly scan to women contracting chickenpox before 20 weeks gestation. Note: A mother who contracts chickenpox in the week before giving birth, or just after, and delivers an unaffected baby, should be isolated from the baby until no longer contagious.35 Neonatal chickenpox in the first 10 days of life has a mortality of 30%. The baby needs VZIG.
Cytomegalovirus (CMV) CMV infection is now the commonest congenital infection in the UK. The birth incidence is between 0.2-2.5%, and 10% of these infections will produce an affected neonate. Two-thirds of congenital infection are thought to result from primary maternal infection and one-third from recurrent infection in the mother. Ganciclovir is effective in the neonate but has not been proven to be of benefit if given to the mother during pregnancy. Advice to a woman who seroconverts to CMV during pregnancy is difficult and such rare cases should be referred for tertiary centre advice.
Toxoplasmosis Toxoplasmosis causes fetal infection in about 15% of cases in the first trimester, rising to 70% in the third. The risk of serious fetal damage if the fetus is infected is however greater in early pregnancy. Overall, up to 90% of infected babies escape longterm damage. Most maternal cases are asymptomatic. The incidence of children born with definite or probable toxoplasmosis in the UK is very low. In 1989 only 14 cases were notified.36
* Where there is concern, check serology as soon as possible after conception and monthly thereafter. IgM may stay positive for months; timing infection in relation to pregnancy stage requires IgG avidity testing at the National Reference Laboratory. In the case of infection, the woman may be offered USS and amniocentesis to detect fetal abnormality, and fetal blood sampling between 20 and 24 weeks. Even if FBS demonstrates fetal infection, it cannot indicate whether the fetus has been damaged.36 Treatment with spiramycin in pregnancy is safe but of unproven benefit.
Listeria Maternal infection may be asymptomatic or associated with fever. The infection carries a risk of miscarriage, stillbirth or the birth of an infected baby. Symptoms in the mother are so non-specific that the diagnosis is rarely made during the acute illness, especially as the only useful diagnostic test is blood culture. Women with fever for 48 hours who are pregnant and who have no obvious other source of infection should have a blood culture specifying listeria. Treatment is with iv ampicillin.
Hepatitis A Reassure the mother that the infant will not be harmed, although it may be infected if occurring shortly before term.
Hepatitis B Hepatitis B is not influenced by pregnancy, but if the mother is infected there is a risk of acute infection of the fetus or neonate. For the management of babies born to HBsAg positive mothers, see p. 24.
Herpes genitalis Primary infection at delivery gives a 20-50% risk of neonatal herpes, which is frequently fatal. Recurrent herpes at delivery gives a risk of 1-2%. Lower segment caesarean section (LSCS) is usually only recommended if the patient is suffering
PROBLEMS IN PREGNANCY
her first attack during labour. Viral shedding is less in subsequent attacks and maternal IgG crosses the placenta to provide some fetal protection. There is probably little value in taking viral swabs in the last month of pregnancy in those with a history of infection but without active lesions.37 Aciclovir in the last month of pregnancy reduces viral shedding and vertical transmission.38
more effective but toxicity has occurred in animal studies. * In late pregnancy exclude: UTI, pre-eclampsia and surgical causes of vomiting. * Hyperemesis gravidarum. Admit if the weight loss is more than 5% with ketosis. She needs iv fluids and possibly thiamine.
PRURITUS Genital warts See p. 44.
HIV • A mother who is HIV positive has a risk of fetal infection of 15-25%, but this can be substantially reduced by delivery by caesarean section and/or antiretroviral therapy. Most maternity units offer screening to all women. Some babies will be HIV-antibody-positive at birth due to maternal antibody, but will become negative as maternal antibody is cleared. • Breast-feeding doubles the chance of vertical transmission and is not recommended. If a woman must breast feed then exclusive breastfeeding rather than mixed feeding should be recommended as neonatal seroconversion may be greatest with the bowel inflammation secondary to artificial feeds. • Zidovudine can reduce the chance of vertical transmission if given to the mother antenatally and during labour, and to the baby postpartum.39 • Pregnancy does not appear to hasten the onset of AIDS in women who are HIV positive.
VOMITING AND REFLUX • Advise: (a) a biscuit before getting up; (b) small frequent meals; (c) a low-sodium, low-sugar antacid for heartburn; (d) stop iron if it is making symptoms worse. • Prescribe ranitidine 150mg b.d. to patients not controlled on the above measures. A lesser dose is no better than placebo.40 A PPI is likely to be
Pruritus, without jaundice, is the commonest manifestation of obstetric cholestasis, which, in turn, is associated with premature birth in 60%, fetal distress in up to 33% and intrauterine death in up to 2%.41 * Check LFTs. Transaminases are raised in 60% of cases, though only 25% have a raised bilirubin. * Refer all affected patients. Ursodeoxycholic acid will relieve pruritis. Most obstetricians will deliver the baby at 37 weeks.
EXCESSIVE WEIGHT GAIN * The average weight gain is 10-12.5 kg (0.65kg first quarter, 4 kg by midpregnancy, 8.5 kg by the third quarter, 12.5kg by term). Over a quarter of the total gain is due to fat deposition in the middle two quarters of pregnancy. * Excessive weight gain is associated with an increased incidence of pre-eclampsia. Check BP, urine and the presence of oedema.
FUNDAL HEIGHT * At 22 weeks the fundus should have reached the umbilicus, and at 32 weeks the lower rib border. * The symphysis-to-fundus height in centimetres should be within two of the number of weeks gestation between 20 and 36 weeks. * If the fundus is over 3 cm less than dates, refer for exclusion of fetal intrauterine growth retardation (IUGR) or oligohydramnios. * If the fundus is 3 cm more than dates, refer for assessment for possible multiple pregnancy or hydramnios.
HYPERTENSION • Blood pressure falls early in the first trimester as the fall in peripheral resistance exceeds the rise in cardiac output. Blood pressure reaches its nadir by 16 weeks, plateaus until 22 weeks and then increases towards term. • Pregnancy-induced hypertension (PIH): Blood pressure which rises to exceed 90 mmHg diastolic on more than one occasion, in the second half of pregnancy, resolves after delivery and is not complicated by proteinuria. The International Society for the Study of Hypertension in Pregnancy has chosen this definition, rather than one based on a relative rise in diastolic pressure, because of the fact that any rise in pressure varies according to when the baseline was taken; and because a relative rise seems to correlate less well with outcomes than the use of an absolute cut-off point. • Pre-eclampsia: This is defined in the same way as above, but is complicated by proteinuria of >300mg/24h. The terms PIH and pre-eclampsia should not be used interchangeably as the former is not associated with poor maternal or fetal outcome, whilst pre-eclampsia is a leading cause of maternal and fetal morbidity. • Women with pre-existing hypertension are prone to develop pre-eclampsia as well, but, if this does not occur, moderate hypertension is compatible with a normal pregnancy. • Antihypertensives do not lessen the risk of developing PIH or alter its progression, but may be necessary for maternal health. • Aspirin prophylaxis (75 mg daily) may prevent the development of pre-eclampsia and moderate the condition once it has started. • Measuring the blood pressure. Use phase 4 diastolic pressure and not phase 5, which may be misleadingly low in pregnancy.42
Pre-existing hypertension • Ideally, all women should have their blood pressure measured preconceptually. If the first measurement is made in the first trimester, the vasodilation of normal pregnancy may mask a higher figure. A blood pressure of >140/90 before 20 weeks suggests pre-existing hypertension and needs specialist assessment.
Anti-hypertensives may reduce the chance that mild hypertension will become severe. Whether one drug is better than another is not clear.43
Pre-eclampsia * Arrange for the patient to be seen at the first available clinic, and: (a) consider aspirin 75 mg daily; (b) start a daily kick chart, with instructions to report if there has been a 50% drop in kicks by noon or less than 10 kicks by noon; (c) daily checks on urine for protein; (d) twice-weekly BP checks. * Admit if: (a) the BP is over 160/100. The patient needs antihypertensives; or (b) the urine has one plus or more of protein; or (c) there is evidence of intrauterine growth retardation; or (d) there are symptoms related to pre-eclampsia, e.g. headache, nausea, visual disturbance and epigastric pain. Admit these patients as an emergency.
Eclampsia • This is a medical emergency with a high maternal mortality. The patient must be resuscitated, and transferred to hospital as fast as possible. There is now good evidence that the anticonvulsant of choice to prevent further fits is magnesium sulphate. • Recurrence and follow up: many women will have PTSD when their normal physiological pregnancy has been taken from them. It is important to explain what happened and the relatively low chance of recurrence in future pregnancies (20%). Many units offer uterine artery Doppler as a screening test in subsequent pregnancies, with the possibility that aspirin, or vitamin C and E (antioxidants44), can reduce this rate further.
Proteinuria A trace of protein is acceptable. It may be due to contamination with vaginal secretions or to a delay since the urine was passed.
PROBLEMS IN PREGNANCY 265
One plus or more in the absence of raised BP * Arrange for an MSU for culture and microscopy. If negative, check the serum creatinine, the 24-hour urinary protein and refer. * Arrange to see the patient again within 2 days looking for clinical deterioration; 10% of patients who develop eclampsia have proteinuria without a raised BP.45
• Warn the patient of her 20-30% chance of developing diabetes in the next 5 years. This risk can be decreased, or postponed by maintenance of a 'diabetic diet' after pregnancy.
• As the plasma volume increases in pregnancy, the haemoglobin falls. Only a haemoglobin 65 suffer from incontinence, as do up to 7% of women aged 250mg/L or a protein/creatinine ratio of >20mg/mmol if they also have a raised creatinine or hypertension; (c) with haematuria and any degree of proteinuria. * If proteinuria is present but does not meet the criteria for referral, repeat the tests 6 monthly.
ASYMPTOMATIC HAEMATURIA Guideline: SIGN. Investigation of asymptomatic microscopic haematuria in adults. Scottish Intercollegiate Guidelines Network, 1997. Online. Available: www.sign.ac.uk
RENAL DISEASE ASYMPTOMATIC PROTEINURIA Guideline: SIGN. Investigation of asymptomatic proteinuria in adults. Scottish Intercollegiate Guidelines Network, 1997. Online. Available: www.sign.ac.uk
Work-up if the dipstick shows proteinuria (a) Blood pressure; (b) MSU and a dipstick for haematuria; (c) 24-hour urinary protein or protein/creatinine ratio; (d) Serum creatinine and electrolytes; (e) Fasting blood sugar.
Macroscopic haematuria This is rarely due to glomerular disease. Refer to a urologist.
Microscopic haematuria • A finding of one + or more is significant, as is the repeated finding of a trace. About half of these patients will have glomerular disease.32
* Check that the test was not carried out shortly after strenuous exercise, during menstruation or during a UTI. * Check the MSU. More than five red cells per high power field is abnormal. If normal, repeat the test for blood with a dipstick. If still positive, ignore the negative MSU result. Red cells lyse easily in urine in the time it takes for an MSU to reach the laboratory. * Check serum creatinine, abdominal X-ray and ultrasound of the urinary tract. * Refer: (a) children and young adults, and patients with red cell casts or a raised creatinine, without evidence of urinary obstruction, to a nephrologist; (b) older adults (e.g. over 40 years old) to a urologist. Ten per cent of asymptomatic haematuria in adults is due to malignancy, mainly in those over 40. They need a cystoscopy.
* Check that there is no remediable cause for the decline in renal function: (a) drugs, especially NSAIDs, diuretics or ACE inhibitors; (b) dehydration; (c) gastrointestinal bleeding. * Refer to a renal physician for diagnosis and, if appropriate, for the management of the uraemia. * Patients not regularly followed up by a renal physician should:
(a) be regularly reviewed to try to reduce the rate of progression of the renal disease and to reduce the risk of cardiovascular disease. Screen for hypertension, anaemia, dyslipidaemia, hyperparathyroidism and hyperphosphataemia; (b) be referred back to the renal physician if the creatinine reaches 250 mmol/L unless a decision has been made to offer no further treatment. Even if the patient does not wish to have dialysis or transplantation, the quality of life might be improved with dietary advice, treatment of renal bone disease, and erythropoietin.
Review: Walker R. General management of end-stage renal disease. BMJ 1997; 315: 1429-32.
REFERENCES 1. Hamilton-Miller JM. The urethral syndrome and its management. / Antimicrobial Chemother 1994; 33 (Suppl. A): 63-73. 2. Brumfitt W, Hamilton-Miller JMT. Consensus viewpoint on management of urinary infections. / Antimicrobial Chemother 1994; 33 (Suppl. A): 147-53. 3. Barry HC, Hickner J, Ebell MH et al. A randomized controlled trial of telephone management of suspected urinary tract infections in women. J Fam Pract 2001; 50: 589-94. 4. Urinary tract infection. MeReC Bulletin 1995; 6 (8): 29-32. 5. Committee for Safety of Medicines. Revised indications for co-amoxiclav. Curr Prob Pharmacovigil 1997; 23: 8. Available on www.mca.gov.uk/ 6. Baerheim A. Empirical treatment of uncomplicated cystitis. BMJ 2001; 323: 1197-8. 7. Kontiokari T, Sundqvist K, Nuutinen M et al. Randomised trial of cranberry-lingonberry juice and lactobacillus GC drink for the prevention of urinary tract infections in women. BMJ 2001; 322: 1571-3. 8. Anon. The mysterious 'urethral syndrome' (letter). BMJ 1991; 303: 361-2. 9. McNaughton Collins M, MacDonald R, Wilt T. Interventions for chronic abacterial prostatitis (Cochrane
10. 11. 12. 13. 14. 15.
16. 17. 18.
Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2001. MeReC. Urinary incontinence in adults. MeReC Bulletin 1997; 8: part 1: 33-6; part 2: 41-4. Burgio KL et al. Prevalence, incidence and correlates of urinary incontinence in healthy middle-aged women. / Lira/ 1991; 146: 1255-9. Duckett JRA. Women with urinary incontinence should be referred to a specialist. BMJ 1996; 313: 754. O'Brian J, Long H. Urinary incontinence: long-term effectiveness of nursing intervention in primary care. BMJ 1995; 311: 1208. US Department of Health and Human Services. Urinary incontinence in adults. Rockville MD: Agency for Health Care and Policy Research (AHCPR), 1992. Malone-Lee JG, Walsh IB, Maugourd M-F et al. Tolterodine: a safe and effective treatment for older patients with overactive bladder. J Am Geriatr Soc 2001; 49: 700-5. DTB. Managing urinary tract infection in women. Drug Ther Bull 1998; 36: 30-2. Foster MC et al. Urological myths. BMJ 1990; 301: 1421-3. Abrams P. Managing lower urinary tract symptoms in older men. BMJ 1995; 310: 1113-17.
19. Ball AJ et al. The natural history of untreated 'prostatism'. Br J Urol 1981; 53: 613-16. 20. Wasson JH, Reda DJ, Bruskevitz RC et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. New Engl J Med 1995; 332: 75-9. 21. Farmer A, Noble J. Drug treatment for benign prostatic hyperplasia. BMJ 1997; 314: 1215-16. 22. Lepor H et al. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group. The efficacy of terazocin, finasteride, or both in benign prostatic hyperplasia. New Engl J Med 1996; 335: 533-9. 23. Emberton M et al. The effect of prostatectomy on symptom severity and quality of life. Br J Urol 1996; 77: 233-47. 24. Woolf SH. Should we screen for prostate cancer? BMJ 1997; 314: 989-90. 25. NHS Centre for Reviews and Dissemination. Screening for prostate cancer. Effectiveness Matters 1997: 2(2). 26. Schroder FH. Detection of prostate cancer. BMJ 1995; 310: 140-1.
27. MRC Prostate Cancer Working Party Investigators Group. Immediate versus deferred treatment for advanced prostatic cancer: initial results of the Medical Research Council trial. Br J Urol 1997; 79: 235-46. 28. NHS Centre for Reviews and Dissemination. Screening for prostate cancer: the evidence. Information for men considering or asking for PSA tests. Effectiveness Matters 1997: 2 (2). Available on www.york.ac.uk/inst/crd/ welcome.htm 29. Chan ECY, Sulmasy DP. What should men know about prostate-specific antigen screening before giving informed consent? Am J Med 1998; 105: 266-74. 30. Dawson C, Whitfield H. Urological emergencies in general practice. BMJ 1996; 312: 838-40. 31. Prodigy. Guidance on the national electronic library for health guidelines database. Online. Available: www.prodigy.nhs.uk (choose 'urology' then 'renal colic-acute'). 32. Topham PS et al. Glomerular disease as a cause of isolated microscopic haematuria. Quarterly J Med 1994; 87: 329-35.
CHAPTER CONTENTS Head injury 287 Head injury in young children 288 Treatment after any head injury 288 Rehabilitation after a head injury 289
Orthopaedic trauma in primary care 289 Whiplash injury 289 Acute knee injury 289 Acute ankle injury 290 Breast problems 290 Peripheral vascular disease 292 Buerger's disease 294 Raynaud's phenomenon 294 Abdominal aortic aneurysm 294 Gallstones 295 Cholecystitis 295
Superficial wounds 296 Burns 296 Dog bites 296 Lacerations 297 Common postoperative complications Returning to work after operations References
Indications for referral for skull X-ray or CT scan1,2,3 (a) history of unconsciousness; or post-traumatic amnesia (PTA) of more than 10 minutes; (b) history of severe trauma including, in a child under 5, a fall of over 60 cm on to the head; (c) suspected foreign body or penetrating injury; (d) convulsion; (e) severe persistent headache; (f) persistent vomiting; (g) clinical signs of skull fracture e.g. crepitus, skull depression, 'bogginess', serious scalp laceration or haematoma, blood or cerebrospinal fluid (CSF) in the nose or ear, or CSF in the wound; (h) altered conscious state at the time of the examination (Glasgow Coma Scale (GCS; Table 15.1) 7 days. Do not give repeat prescriptions without review. Do not give >100g per month of a moderately potent teroid. Try to rotate steroids with alternative treatments. Only use potent or very potent steroids under specialist supervision.
Guttate psoriasis should resolve in a few months without treatment. If treatment is needed: * Use an emollient for dryness. * Use a mild tar and steroid cream or calcipotriol to suppress the lesions if the patient prefers a more active approach. * Refer early for phototherapy if the psoriasis is widespread and troubles the patient.
Referral Refer when:
Widespread plaque psoriasis * Refer. Systemic treatment will probably be needed.
Scalp psoriasis * Shampoo daily with a tar shampoo, e.g. Polylar. * Exacerbations. Continue coal tar shampoo and also apply a daily steroid scalp application or calcipotriol scalp solution twice a day (but not prior to shampooing). Diprosalic scalp application has
(a) the diagnosis is uncertain; (b) the psoriasis is severe; (c) the psoriasis fails to respond to the above treatments; (d) the patient needs more intensive education or counselling than is possible in primary care; (e) there is psoriatic arthropathy; (f) there is widespread guttate psoriasis; (g) there is generalized pustular or erythrodermic psoriasis. Referral is urgent: it may be lifethreatening. It is especially likely to occur if potent steroids are used and then withdrawn.
Patient groups: Australia: The Psoriasis Association Inc. 16 Musgrave Street, Kirra, Queensland 4225, tel. 190 2272 100 or e-mail [email protected] New Zealand: The Psoriasis Association of New Zealand Inc. Online. Available: www.everybody.co.nz/support/psoriasis.html l/AOThe Psoriasis Association. 7 Milton Street, Northampton NN2 7JG, tel. 01604 711129.
SKIN INFECTIONS VIRAL INFECTIONS Warts (other than genital warts) Systematic reviews: Gibbs S, Harvey I, Sterling JC et al. Local treatments for cutaneous warts (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software, 2001. DTB. Tackling warts on the hands and feet. Drug Ther Bull 1998; 36: 22-4.
• Human papilloma virus (HPV) causes a wide range of different lesions, from cauliflower-like lesions to flat mosaic lesions. Many wart infections are completely asymptomatic, yet shed virus to transmit them. • Genital warts are of greatest concern because they are associated with malignancy, particularly some subtypes with cervical cancer. • Warts will probably always remit spontaneously but the time to remission may be very variable. • First-line topical treatment remains salicylic acid. Between 67% and 84% of warts are cleared by 3 months of daily treatment.10 • Surgical treatment includes of a wide range of destructive methods, including cryotherapy cautery, laser treatment, and excision. They may be no more effective than chemical methods. • There is not enough evidence to establish whether any one is superior to another (either in establishing cure or reducing the chance of recurrence, which ranged from 5-35%), or that treatment reduces infectivity (among genital warts).
* If the patient is not troubled by the wart, suggest that it is left alone. The majority will disappear spontaneously as immunity is gained. However, if the patient elects for treatment, explain that the wart must be rubbed down with an emery board before application of a topical agent. Pare down thick warts with a scalpel in the surgery. * Choose agents from the following groups. Explain that 3 months treatment may be needed and that the agent should not touch normal skin. (a) salicylic acid for a wart anywhere except on the face; (b) podophyllin, glutaraldehyde or formalin for plantar warts. * Plantar warts. Prescribe a salicylic acid gel for children who wish to use swimming pools, and give them a note to confirm that they do not need a verruca sock. * Filiform warts. Curette them under local anaesthetic. * Plane warts should be left to resolve spontaneously. * Surgery. Warts not responding to treatment after 3 months, or those that are a particular nuisance, are candidates for freezing or curettage and cautery. Children under 10 tolerate these procedures badly.
Referral Refer: (a) if the diagnosis is uncertain, especially if sites other than hands, feet or face are affected; (b) if the patient is immunosuppressed; (c) when there is a sudden widespread eruption of warts. Malignancy may be the cause; (d) warts that have failed to clear after 3 months intensive topical treatment; (e) facial warts if cryotherapy is not available.
HERPES SIMPLEX LABIALIS * Topical aciclovir appears to speed resolution, with agents in a lipophilic base more effective than those of a hydrophilic base. * Oral aciclovir (200 mg five times daily for 10 days), valaciclovir (500 mg three times daily for
374 SKIN PROBLEMS
7 days) and famciclovir (250 mg three times daily for 7 days) similarly reduce the duration of the disease. • Topical local anaesthetic cream (e.g. Xylocaine gel) may ease the pain. • There is some evidence that a course of oral aciclovir or famciclovir before exposure to intense UV light reduces the incidence and duration of attacks. Sunscreen prophylaxis similarly reduces the risk of attacks.
(b) the immunocompromised; or (c) patients in moderate to severe acute pain; or (d) older patients, e.g. over age 50. Starting the drug after 72 hours may be of value if new vesicles are still appearing. * Corticosteroids/idoxuridine. The evidence is too weak to recommend their use.
Systematic reviews: Lancaster T, Silagy C, Gray S. Primary care management of acute herpes zoster: systematic review of evidence from randomized controlled trials. Br J Gen Pract 1995; 45:39-45. Yaphe J, Lancaster T. Postherpetic neuralgia. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. Available: www.clinicalevidence.org
* The prevention of post-herpetic neuralgia (PHN) and the prompt treatment of ophthalmic zoster are the most important issues. PHN follows shingles in 50% of patients aged over 60 and 75% of patients over 70, of whom half will still be suffering 1 year later.11 * Oral aciclovir (800 mg five times daily for 5 days), famciclovir (250 mg t.d.s. for 7 days), and valaciclovir (1 g t.d.s for 7 days) taken within 72 hours of the appearance of the rash can shorten the duration and severity of the rash, and reduce the risk of persistent post-herpetic pain. The latter two have better bioavailability than aciclovir and may be more effective in reducing the risk of PHN.12,13
Acute herpes zoster * The patient with zoster on exposed skin should remain isolated until the last lesion scabs over. They can transmit the virus to non-immune individuals, who can contract chicken pox. * Give adequate analgesia. Opioids may be required. * Oral antiviral agents. Prescribe at high dose for 7 days, starting within 72 hours of the start of the rash, for: (a) ophthalmic zoster; or
For treatment of PHN, see p. 424.
* Check for diabetes in recurrent or unusually severe skin infections. * Topical antibiotics inevitably lead to colonization of the skin with resistant organisms. Do not therefore use antibiotics topically which may be needed systemically. * Topical neomycin, if used for less than 10 days, rarely leads to allergy.
Cellulitis and erysipelas * Use oral penicillin or erythromycin. Antibiotics effective against streptococcus (penicillin, ceftriaxone, roxithromycin and flucloxacillin) are equally useful, so penicillin is usually the drug of choice. Oral versus intravenous antibiotics have not been tested in a controlled trial. * Narrow-spectrum penicillin derivatives (flucloxacillin and dicloxacillin) can cause elevation of hepatic enzymes and should not be used as first line therapies. * There is no good evidence that routine microbiological tests improve treatment outcomes.14
Impetigo * Treat isolated lesions with topical antibiotic preparations, such as mupirocin, neomycin or soframycin. * Widespread lesions: give oral antibiotics, e.g. cephalexin or erythromycin. * Reduce the skin bacterial load to limit the extent of the current infection and recurrences. Try regular baths using an antiseptic solution or soap.
* Reduce the nasal and perianal carry rates of staphylococcus by the use of topical antibacterial agents (again mupirocin, neomycin or soframycin). * Treat all family members simultaneously if cross infection is a problem. Children should not attend school until the lesions have crusted over and there is no discharge.
Other bacterial infections * Boils should be drained. Daily washes with chlorhexidine will prevent spread. Oral flucloxacillin is needed for ill patients. * Recurrent staphylococcal skin infections. Patients with recurrent staphylococcal infections often carry staphylococci in sites not cleared by systemic antibiotics, especially the nose and the perineum. Bath daily with triclosan bath concentrate. Prescribe chlorhexidine and neomycin nasal cream or mupirocin nasal ointment. * Hidmdenitis suppuritiva. If the axilla is infected, give: (a) erythromycin 500 mg b.d. or oxytetracycline 500 mg b.d. for 1 month in the first instance, but 6 months treatment may be needed; or (b) topical clindamycin for 3 months. * Erythrasma is due to a corynebacterium, and is often mistaken for axillary tinea. Use a topical imidazole or oral tetracycline or erythromycin for 2 weeks. * Hair follicles: (a) folliculitis: use topical antiseptics or topical antibiotics; (b) furunculosis: use oral antibiotics (e.g. flucloxacillin). * Caruncle. Refer for surgical excision and drainage. The patient will also need antibiotics if unwell, or if there is associated cellulitis. Reduce the risk of recurrence by clearing the skin and nose of pathogenic staphylococci as above.
Ketoconazole is slightly more expensive. Terbinafine is yet more expensive but appears to be slightly more effective15 and need only be applied for 1 week. • Use imidazoles for 2 weeks after clinical healing to avoid recurrence. • Nystatin is effective against yeasts, but not against other fungi. • Oral ketoconazole, fluconazole, itraconazole and terbinafine should only be used for severe fungal infections.
Candidiasis • Occurs in napkin dermatitis, intertrigo and angular stomatitis. Use nystatin cream, or an imidazole, with a steroid if there is inflammation.
Pityriasis versicolor * Explain that: (a) it does not need treatment if the patient does not mind the appearance; (b) killing the organism, which can be done by means of topical or even systemic antifungals, will not solve the cosmetic issue until old discoloured skin has been desquamated in the usual way; and will not prevent recurrence in susceptible people if treatment is stopped. * If the patient wishes treatment, use a low toxicity fungal poison such as zinc piridinthione, selenium sulfide, or a sulpha compound, often made up into a shampoo, which can be used several times a week indefinitely. * If there is extensive skin involvement, consider using itraconazole 200 mg daily for 5 days.
Seborrhoeic dermatitis and dandruff See p. 368.
FUNGAL INFECTIONS • There is little to choose between the topical imidazoles: clotrimazole, econazole and miconazole.
Tinea capitis Send skin scrapings before starting treatment. Use oral itraconazole or terbinafine. Topical antifungals are ineffective.
Tinea pedis, cruris and corporis (a) Stress the importance of drying any moist areas. (b) Use an imidazole cream for 3 weeks or terbinafine cream for 1 week. (c) Consider oral terbinafine in resistant cases. (d) Avoid relapse by using dusting powders.
FUNGAL INFECTIONS OF NAILS Guidelines: Denning DW et al. Fungal nail disease: a guide to good practice (report of a Working Group of the British Society for Medical Mycology). BMJ1995; 311:1277-81. MeReC. Fungal nail infections. MeReC Bulletin 1997; 8: 45-8.
* Most people are not troubled by it. Oral antifungals are not without side-effects. * If planning to treat, confirm the diagnosis by sending scrapings, taken with a blunt scalpel, or nail clippings. These should be transported in a folded square of paper. Pus from the nail fold is valuable in chronic paronychia. Specify microscopy and culture for fungi. * Dermatophyte infection (infection with Trichophyton species). Give terbinafine 250 mg daily for 6 weeks (fingernails) or 3 months (toenails). Patients who prefer not to take oral drugs, or whose disease is confined to one or two nails, may use amorolfine nail lacquer or tioconazole nail solution. * Infection with yeasts, non-dermatophyte moulds or mixed infections. Give itraconazole 200 mg daily for 3 months or 'pulsed', i.e. 200 mg b.d. for 1 week every month for 2 (fingernails) or 3 (toenails) months. * Explain that the infection may continue to respond after the end of the course of treatment. Terbinafine and itraconazole persist in nail keratin for up to 9 months after the end of treatment.
LICHEN PLANUS * This condition may follow contact sensitivity to certain chemicals and drugs, or in response to chronic graft-versus-host disease.
* The rash is a collection of dark shiny, pearly papules about 2-4 mm across. They have a lacy pattern on the surface. The papules are distributed most commonly to flexor surfaces of the body, most commonly the wrist. * The lesions are self-limiting and usually resolve in a year. * Examine the mouth and genital mucosa. Asymptomatic white lines across the buccal, anal or genital mucosa confirm the diagnosis. * If drugs are suspected, they should be withdrawn. * Topical steroids may assist in reducing the size of the papules.
ALOPECIA With scarring * Take skin scrapings. Treat with antifungals if positive. If negative, refer for skin biopsy for conditions such as discoid lupus erythematosis.
Patchy without scarring * If there is a rash, scrape off scales and send for microscopy. If positive, treat with oral itraconazole or terbinafine. * Alopecia areata. Reassure the patient that regrowth is likely to occur within 1 year. Steroid creams are often prescribed, but there is little evidence of value. * Trichotillomania. Consider mechanical damage, especially in children.
Diffuse without scarring * 80% of men and 35% of women have frontal/ temporal pattern balding by the age of 60. Men usually progress to baldness of the crown; women do so less often. Work-up when hair loss is unexpected (a) FBC; (b) Ferritin; (c) TFTs; (d) Calcium phosphate.
SKIN INFESTATIONS 377
* Exclude drugs as a cause, e.g. cytotoxics, anticoagulants, antithyroid drugs, retinoids. * Acute hair loss. Explain that there is a cycle in the growth of each hair. Stress and illness can bring the majority of hairs to the end of the cycle at the same time so that they all fall out. They will then regrow together. * Postpartum acute hair loss. Explain that the hairs have been held back in their natural cycle during pregnancy, and that now that the pregnancy is over they have caught up and come out at the same time. They will regrow, but it may take many months. Exclude anaemia and thyroid dysfunction. * Consider referral for counselling, which may be available through the local dermatology department, and for a NHS wig. Advise men with male pattern baldness that minoxidil lotion will reduce the loss in 70% of cases and promote new hair growth in 30%, with a good cosmetic result in 10%. It is only available in the UK on a private prescription, and should be applied for 3 months before judging benefit. Once stopped the benefit is lost. * Discuss the option of surgery. Self-help groups: Hairline International: the Alopecia Patients' Society, Lyons Court, 1668 High Street, Knowle, Solihull, West Midlands B93 OLY, tel. 01564 775281. Alopecia Areata Support Association (Australia), PO Box 89, Camberwell, Victoria 3124, Melbourne, Australia, tel. 03 9513 8580; www.alopecia.auz.com
* Malathion may be effective, but there is no RCT evidence. * Gamma benzene hexachloride may have rare adverse events - aplastic anaemic and fits in patients treated for extensive disease. * Treat all members of a household and all sexual contacts simultaneously. Where transmission is sexual, screen for other STDs (see p. 42). * Instructions: 1. Apply the selected treatment to all areas below the neck before retiring, and wash off in the morning. Children and those with compromised immunity need to have the cream applied to the neck, face, ears and scalp as well. Wash all bedclothes, bed linen and underclothes in hot water that day. 2. Repeat the treatment in one week to eradicate the hatched mites. * Give appropriate antibiotics (cephalexin or erythromycin) if pustules are present. Note: The itch may persist longer than the mites. Repeated use of antiscabetic lotions does not accelerate resolution. Specific antipruritic measures are more appropriate.
LICE Head lice Guideline: MeReC. Management of head louse infection. MeReC Bulletin 1999; 10:17-20. Systematic review: NHS Centre for Reviews and Dissemination. Treating head lice and scabies. Effectiveness Matters. June 1999; 4 (1).
SKIN INFESTATIONS SCABIES Systematic review: Walker G, Johnstone P. Scabies. Clinical Evidence, Issue 5. London: BMJ Publishing Group, 2001. Available: www.clinicalevidence.org
• Pyrethrin (permethrin) has been found to cure 90% of affected individuals. It is more effective than gamma benzene hexachloride or crotamiton though both these latter agents are effective in their own right.
• Overuse of insecticides has led to resistance. Current guidelines stress that treatment should only be given if a living, i.e. moving, louse is found. Nits are egg cases stuck to hairs and do not necessarily mean there is active infestation. • Bug-busting (wet-combing of the hair to remove lice) is ineffective as treatment.16 The place of wetcombing is in detection (see box below). • Make sure the whole household is checked and ask the parents to notify the school nurse so that the rest of the class can be examined. UK guidelines stress that the affected child should not be
excluded from school. Any transmission will already have taken place. * Prescribe the recommended parasiticidal preparation: malathion, permethrin or carbaryl. Health districts will rotate from one preparation to the other every 3 years to avoid resistance. It is important to cooperate with this policy. Local chemists or the local pharmaceutical advisers will know the current recommendations. * Practicalities: two applications are needed 7 days apart; lotions, liquids or creme rinses should be used, not shampoos. Note: Asthmatics or young children should use aqueous malathion. Note: Carbaryl has been found to cause cancer in laboratory animals after prolonged exposure to high doses. There is therefore a theoretical risk that it may be carcinogenic in humans, although the CMO advises that any risk is exceedingly small.17 Detection combing 1. Buy a fine tooth detector comb. 2. Wash the hair and leave it wet. Comb first with an ordinary comb then with the detector comb, beginning at the top of the head. The comb must be touching the scalp and be drawn right to the ends of the hairs. 3. Look for lice on the comb. 4. Continue to comb until the whole scalp and all the hair has been covered - it should take 10-15 minutes. 5. If you find something that could be a louse, stick it to a piece of paper with clear sticky tape and take it to a nurse, doctor or pharmacist for confirmation.
Genital lice (crab lice) * Treat all intimate contacts. It is usually spread by sexual contact in adults, but finding it in a child does not necessarily raise suspicion of sexual abuse. It can survive for 24 hours in clothes or bedding. * Use aqueous preparations of malathion, permethrin, phenothrin or malathion to the whole body, not just the pubic hair, for 12 hours and repeated after 7 days.
Body lice * Wash clothes in hot water. No other treatment is necessary.
PAPULAR URTICARIA Fleas * Deflea the cat, dog or rabbit. * Treat the house. Spray insecticide on carpets and soft furnishings, and around where the pet sleeps.
Bed bugs * Wash bed linen. * Call in the Environmental Health Department to treat the house. The bugs live behind wallpaper and skirting boards, not in the beds themselves.
Animal mites * Treat the pet, who is likely to have signs of the disease (e.g. mange).
Bird mites * Clear birds' nests from outside the bedroom window if bird mites are suspected.
MALIGNANCY There are three main groups of primary skin cancer: 1. basal call carcinoma (BCC), arising from the basal cells of the germinal layer; 2. squamous cell carcinoma (SCC) arising from squamous cells; and 3. melanoma, arising from pigmented cells. Although all are common in white-skinned people living in sunny climates, the prognosis of each is very different.
BASAL CELL CARCINOMAS (BCCs) • These are the most common skin cancers. They are most common on head and upper trunk. • Although they do not metastasize without undergoing squamous transformation, delay in diagnosis can lead to disaster from loss of wide areas of tissue, or underlying organs such as the eye.
* A trial of sun-screen failed to show benefit for preventive BCCs.
Management * If there is any doubt about diagnosis, biopsy is indicated. * Treatment is by excision, or in the elderly, superficial X-ray therapy. * Superficial ones can be treated with local destruction, such as liquid nitrogen cryotherapy or imiquimod cream.
SQUAMOUS CELL CARCINOMAS (SCCs) * These are also common skin cancers. They are most common on sun-exposed areas including extremities. * Referral. In the UK, urgent referral, to be seen within 2 weeks, is indicated for any patient with: (a) an indurated lesion in which there has been documented expansion over the last 1-2 months; or (b) a positive biopsy; or (c) any new or growing skin lesion in a patient who is immunosuppressed. * If there is any doubt about diagnosis, biopsy is indicated. * Treatment is by excision (SCCs are much less radiosensitive to superficial X-ray therapy than BCCs). * Stress the importance of further prevention. Use of a sun-screen has been shown to decrease the later formation of SCCs in a randomized trial. Use of a hat and clothing is even more effective in avoiding solar damage.
MELANOMA * Melanomas are the most dangerous form of skin cancer, and are also related to past sun exposure. * Of several forms, the most common is the superficial spreading melanoma (SSM) for which early diagnosis of thin lesions is critical because it conveys such a better prognosis compared to
those left to grow thicker. Nodular, and acral forms (on palms and feet) carry a worse prognosis, although this is very variable. • They are pigmented (except in the case of the rare amelanotic form). SSMs especially can be hard to distinguish from benign skin naevi ('moles'), and also flat seborrhoeic keratoses. • Special distinguishing characteristics of melanomas include asymmetry, size greater than 6 mm, irregular edges or surface, or non-uniform pigmentation. Unfortunately, early SSMs are often difficult to diagnose.
Management * If there is any doubt about diagnosis, biopsy. * In the UK, patients qualify for referral urgently, to be seen within 2 weeks, if they have a pigmented lesion which shows one or more of the following: growing in size, changing shape, irregular outline, changing colour, mixed colour, ulceration, or inflammation. * Definitive treatment is by excision, leaving at least 5 mm of healthy skin around the specimen. Lesions with a histology report indicating less than 0.075 mm thickness have a very good prognosis. There is no evidence that any immunotherapy, chemotherapy or radiotherapy provides any significant improvement in mortality or morbidity.
SOLAR KERATOSES • Solar keratoses (SKs) are keratotic lesions on sun-exposed skin caused by solar damage. • They may be precursors of SCCs. However, most SKs spontaneously remit without progress into SCCs. Fewer than 1 in 1000 SKs transform into SCCs.18 Moreover, many SCCs arise from previously normal skin rather than SKs. • Some patients worry about skin cancer (for which SKs are indeed a risk factor), and the hardness of the lesions can be irritating on clothing. * If there is any doubt about the diagnosis of cancer, biopsy. * Destructive treatment of SKs (by cryotherapy, or excision biopsy if there is diagnostic doubt) may be required for local symptomatic treatment.
* Symptomatic treatment of SKs can be achieved by use of topical applications such as salicylic ointment (5%) or urea cream (10%) or by topical diclofenac. * Treating SKs as a preventive to developing SCCs is unjustified. * Preventive activity in the form of sunscreens has been shown to decrease the later formation of solar keratoses. * 5-fluorouracil cream (5-FU): people with damaged skin can benefit from applying 5-FU daily to affected areas, such as the forehead or forearms. Stop the cream after 2-3 weeks, when the patient experiences an inflammatory reaction. The skin will then regenerate, leaving a cosmetically improved surface. Only prescribe it if reasonably experienced in its use. Before treatment: (a) warn the patient that the treatment is unpleasant; the inflammatory reaction will cause erythema and possibly ulceration; (b) check carefully for malignancy in the area; 5-FU can mask an SCC or a BCC.
HYPERHIDROSIS GENERALIZED HYPERHIDROSIS A cause is not usually found, but consider: (a) autonomic nervous system imbalance, as in the menopause; (b) autonomic neuropathy, with areas of hypohidrosis and compensatory hyperhidrosis elsewhere; (c) hyperthyroidism; (d) hyperpituitarism.
HYPERHIDROSIS OF THE PALMS, SOLES AND AXILLAE * Use daily aluminium chloride hexahydrate applied at night to dry skin and washed off in the morning, until benefit is achieved. Do not apply within 12 hours of shaving or using depilatories. Use hydrocortisone cream if the preparation causes irritation. Reduce to weekly applications once control is achieved.
* For treatment failures, discuss the availability of iontophoresis or injections of botulinum toxin with the local physiotherapy department or dermatologist.19 * Otherwise consider referral for sympathectomy for palmar sweating and axillary skin excision for axillary sweating. Both have their problems; infection following skin excision, and surgical disasters following sympathectomy. * If odour is a problem apply an antibacterial b.d., e.g. chlorhexidine cream or dusting powder.
GRAVITATIONAL ULCERS Systematic reviews: Nelson EA, Cullum N, Jones J. Venous leg ulcers. Clinical Evidence, Issue 5. London. BMJ Publishing Group, 2001. Available: www. clinicalevidence.org Compression therapy for venous leg ulcers. Effective Health Care 1997; 3 (4).
• Firm, but not excessive compression dressings of the legs have been shown to reduce healing time. Compression devices (e.g. TED stockings) also reduce recurrence of venous ulcers. • The type of dressing used does not appear to influence healing time. • Oxpentiphylline and flavinoids improve healing rates but they are not recommended by current guidelines.20,21
Management * Check the arterial supply before compression bandages are applied. The ratio of ankle to brachial systolic blood pressure (see p. 293) should be measured by Doppler. Compression should not be applied if the ratio is 12 years 10-20mg
Diagnosis • There is no uniformly accepted objective definition of anaphylaxis.15 • Diagnosis depends on the identification of a constellation of symptoms and signs which may involve a number of organ systems: (a) skin: erythema, pruritis, urticaria and angioedema; (b) eyes: injection of conjunctiva, tearing and itching; (c) airways: sneezing, rhinorrhoea, laryngeal oedema, cough, wheeze and dyspnoea; (d) gastrointestinal: tongue swelling, abdominal cramps, vomiting and diarrhoea; (e) cardiovascular: palpitations, light-headedness and collapse. • A working diagnosis of anaphylaxis can be made by identifying features of a systemic allergic reaction accompanied by either respiratory difficulty or symptoms/signs suggestive of hypotension.17
Chlorpheniramine (im or slow iv) Hydrocortisone (im or slow iv) Crystalloid fluid (iv)
1-6 years: 50 mg 6-1 2 years: 100mg >12 years: 1 00-500 mg Children: 20 ml/kg of body weight Adults: 1-2 litres
4. Give inhaled beta2-agonist if there is severe bronchospasm. 5. Repeat adrenaline 5 minutes after first dose if there is no clinical improvement. 6. Give chlorpheniramine im (or by slow iv injection). 7. Give iv crystalloid fluid infusion if symptoms of hypotension persist (a repeat dose may be necessary).20 8. Give hydrocortisone im (or by slow iv injection). 9. Admit to hospital as a later relapse in symptoms may occur.21
Management • Management is best considered in two stages: treatment of the acute attack and follow-up care.18 Acute management (see Table 21.3) 1. Commence life support (basic and advanced) if indicated. 2. Give oxygen. 3. Give adrenaline (epinephrine) 1:1000 solution (im) if not already administered (many patients with a history of anaphylaxis will have been issued with adrenaline for self-injection). The Chief Medical Officer cautions against the use of the iv route except by experienced practitioners treating profound shock.19 A 10-fold dilution is needed.
Follow-up care * Trigger. Refer to an allergist in order to objectively identify the trigger and for consideration of desensitization therapy.22 This will involve a detailed history and subsequent investigations, which may include skin-prick testing, serumspecific IgE tests and allergen challenge. * Allergen avoidance. Reinforce any allergen advice issued; dietetic referral may be indicated in cases of food allergy. * Adrenaline. Issue adrenaline for self-administration (for example, EpiPen, Anapen or Ana-Guard) and educate the patient on when and how to use it. * Alert bracelet. Recommend purchase of a MedicAlert bracelet/necklace documenting history of anaphylaxis, noting where adrenaline is
kept should the patient be found in a collapsed state. * Asthma control. Optimize asthma control in those with a history of asthma as the risk of fatality is increased in this group.22
* Liaise with nursery/school/work as appropriate.23
USEFUL CONTACTS For patients Anaphylaxis Campaign PO Box 275, Farnborough, Hampshire GU14 6SX Tel. 01252 542029; fax 01252 377140; website: www.anaphylaxis.org.uk British Allergy Foundation Deepdene House, 30 Bellegrove Road, Welling, Kent, DA16 SPY Helpline 020 8303 8583; tel. 020 8303 8525; website: www.allergyfoundation.com MedicAlert Foundation 1 Bridge Wharf, 156 Caledonian Road, London Nl 9UU
Tel. 020 7833 3034; fax 020 7278 0647; website: www.medicalert.co.uk For professionals British Society for Allergy & Clinical Immunology 66 Weston Park, Thames Ditton, Surrey KT7 DHL Tel. 020 8398 9240; fax 020 8398 2766; website: www.soton.ac.uk/~bsaci National Asthma & Respiratory Training Centre The Athenaeum, 10 Church Street, Warwick CV34 4AB Tel. 01926 493313; fax 01926 493224; website: www.nartc.org.uk
REFERENCES 1. Sampson HA. Food allergy. In: Kay AB (Ed). Allergy and allergic diseases. Oxford: Blackwell Science, 1997: 1517-49. 2. Clough J. Allergies at your fingertips. London: Class, 1997: 120-49. 3. Young E, Stoneham MD, Petruckevitch et al. A population study of food intolerance. Lancet 1994; 343: 1127-30. 4. Bruinjzeel-Koomen CA, Ortolani C, Aas K et al. Position paper. Adverse reactions to foods. Allergy 1995; 50: 623-36. 5. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment. Peanut allergy. London: Department of Health, 1998. 6. Wood SF. CP guide to the diagnosis and management of allergic disorders in children. London: Mosby, 1999: 33-8. 7. Bindslev-Jensen C. Food allergy. In: Durham SR (Ed). ABC of allergies. London: BMJ Books, 1998: 44-7. 8. Joint Task Force on Practice Parameters for Allergy and Immunology. Practice parameters for allergy diagnostic testing. Ann Allergy Asthma Immunol 1995; 75: 543-625. 9. Royal College of Physicians Committee on Clinical Immunology and Allergy. Allergy: conventional and alternative concepts. London: RCP, 1992. 10. National Asthma & Respiratory Training Centre. Management of allergy in primary care. Warwick: NARTC, 2001: Unit 8. 11. Radcliffe MJ. Food allergy and intolerance. In: Jackson WJ (Ed). Allergic disorders. London: Mosby-Wolfe, 1997: 91-107. 12. Chief Medical Officer. Health advice on peanut allergy. CEM/CMO/98/9. Online. Available: www.doh.gov.uk/cmo/cmo989.htm
13. Pumphrey RS. Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy 2000; 308: 1144-50. 14. Sheikh A, Alves B. Hospital admissions for acute anaphylaxis: time trend study. BMJ 2000; 320: 1441. 15. Project team of the Resuscitation Council (UK). Emergency medical treatment of anaphylactic reactions. / Accid Emerg Med 1999; 16: 243-8. 16. Project team of the Resuscitation Council (UK). Update on the emergency medical treatment of anaphylaxis reactions for first medical responders and for community nurses. Resuscitation 2001: 48: 241-3. 17. Ewan PW. Anaphylaxis. BMJ 1998; 316: 1442-5. 18. Sheikh A. Anaphylaxis. Update 1999; 58: 984-8. 19. Professional letter - Chief Medical Officer. Current vaccine and immunisation issues. PLCMO(2001)1. 20. Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials. BMJ 1998: 316: 961-4. 21. Joint Task Force on Practice Parameters, Work Group on Diagnosis and Management of Anaphylaxis. The diagnosis and management of anaphylaxis. / Allergy Clin Immunol 1998; 101: S465-S528. 22. Lane SJ, Lee TH. Anaphylaxis. In: Kay AB (Ed). Allergy and allergic diseases. Oxford: Blackwell Science, 1997: 1550-72. 23. Vickers DW, Maynard L, Ewan PW. Management of children with potential anaphylactic reactions in the community: a training package and proposal for good practice. Clin Exp Allergy 1997; 27: 898-903.
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CHAPTER CONTENTS Keeping older people healthy
Managing frailty 390 Supporting older people at home 390 Acute confusion, agitation, loss of mobility
Subacute deterioration without acute illness: depression or dementia 393 Dementia
Falls 396 Lower limb problems 398 Night cramps 398 Restless legs syndrome 398 Postural ankle oedema 399 Elder abuse Legal aspects
KEEPING OLDER PEOPLE HEALTHY
Screening and prevention * Continue screening programmes for mammography and cervical screening until older age. There is little evidence that screening is no longer worthwhile and most programmes recommend continuing to age 75 years, although in the UK routine screening ends at 65. * Screening for and management of hypertension in particular and cardiovascular disease in general is more important for older people1 as they are at higher absolute risk. Ten older people with hypertension and diabetes or twenty older people treated for hypertension for 5 years will prevent one cardiovascular event. * Influenza vaccination is indicated for all persons age 65 years and over and in some countries (although not the UK) pneumococcal vaccination as well.
Smoking * Advise smoking cessation for all older people as stopping reduces mortality by 50%.l * Simple advice from primary care doctors is effective in smoking cessation.2
Alcohol • Although alcohol consumption decreases with age, 17% of men and 7% of older women exceed limits of regular consumption of alcohol. 1-5% of 389
older people who drink more than occasionally report that they are 'problem drinkers' and males more so than females.3 • Alcohol misuse in the elderly contributes towards falls, stroke, depression and osteoporosis. • Simple advice from the GP is effective in reducing alcohol consumption.4
Exercise • 30 to 60 minutes of sustained low level activity, such as walking, on at least 3 days per week5 will result in moderate health benefits such as reduced fatigue, weight loss, increased socialization, improved control of type II diabetes, less shortness of breath on exertion.6 • No adverse effects of low to moderate activity have been observed in trials promoting physical activity for community dwelling older people.7 • Advise regular, safe, physical activity as part of daily activities. Simple advice delivered in primary care is effective in increasing activity for older patients.8 • Recommend exercise which mimics the activities of daily living (ADL) such as repetitive sit to stand and walking. This is more acceptable and beneficial for older people. • Referral to physiotherapy for strength and balance training will reduce falls by 40% in women over age 80 years.9
MANAGING FRAILTY • Frailty is best regarded as 'a condition or syndrome which results from a multi-system reduction in reserve capacity to the extent that a number of physiological systems are close to, or passed the threshold of symptomatic clinical failure. As a consequence, the frail person is at increased risk of disability and death from minor external stresses'.10 • General practice, as part of the primary healthcare network, is well placed to detect and treat emerging frailty and prevent further deterioration. • The Nottingham Extended Activities of Daily Living (EADL; see Appendix 25) scale may be
useful in detecting unsuspected functional decline (see p. 405).
Early intervention * Preventive home visits with health professionals or lay people trained in case-finding reduce mortality and admission to residential care and may promote independence and improve quality of life for frail older people.11 * Effective management of minor ailments, such as painful foot problems, may halt declining mobility and improve long term outcomes. * Maximizing management of chronic problems and minimizing polypharmacy may halt functional decline. The UK National Service Framework12 recommends an annual review of medication for people aged 75 and over, with a 6-monthly review for those taking four or more medicines.
SUPPORTING OLDER PEOPLE AT HOME • There is considerable variation in availability of services for older people internationally and within countries, although care can be broadly divided into formal and informal provision. Generally, there is a multitude of services available aimed at either maintaining function or providing rehabilitation. • Services can be accessed either by direct referral or through specialist geriatric services. • A comprehensive assessment is recommended before referring to services. • In general, services are accessed in the UK through a social worker; Australia, by direct referral or through Geriatric Assessment Services; and New Zealand, the Needs Assessment Coordinator.
Difficulty maintaining living arrangements • Refer to an occupational therapist for assessment of activities of daily living (ADL) function at home and provision of equipment.
ACUTE CONFUSION, AGITATION, LOSS OF MOBILITY
* Refer to a social worker to set up home carer for housework. * Refer to a social worker for Meals-on-Wheels (daily hot food or weekly frozen meal deliveries). * Refer to a podiatrist/chiropodist for foot care.
(c) the occupational therapist, physiotherapist for functional assessment and provision of equipment; (d) the social worker for temporary provision of personal care and housework.
Isolation * Refer to Age Concern for provision of a volunteer/befriending service. * Refer to a social worker for day centre placement. * Refer to Dial-a-driver or social worker to access subsidised taxi service for transport. Carer stress (see p. 408) * Ascertain reason for stress. * Refer for access to respite services, including day and night respite, and residential home placement for short periods. * Refer for home care for personal assistance. * Refer to occupational therapist, for assessment of ADL function and equipment.
Functional deterioration at home Refer to: (a) a geriatrician for a comprehensive assessment; (b) a day hospital, for multidisciplinary assessment and treatment; (c) physiotherapy for musculoskeletal assessment and exercises; (d) occupational therapy for ADL functional assessment, provision of equipment and treatment; (e) a social worker for personal home care; (f) the district nurses for bathing service; (g) a speech language therapist if the condition affects communication or swallowing; (h) a dietician.
Poor recovery after an acute episode * Consider referral to: (a) the appropriate hospital service; (b) the district nursing service;
ACUTE CONFUSION, AGITATION, LOSS OF MOBILITY • A change in mental or physical status of usually well independent older people should be taken seriously and treated urgently. Symptoms of serious illness are often masked and fever is seldom higher than 37.5°C even in overwhelming infection. • Acute change can be due to serious disease without overt symptomatology related to that disease. Confusion can be as simple as 'the patient has suddenly changed, something is wrong, the level of function has deteriorated'. • Agitation may occur and can be defined as 'inappropriate verbal, vocal, or motor activity that is not explained by needs' and may be due to undiagnosed pain, acute illness, or simply the inability to communicate needs. • A loss of mobility or 'taken to the bed' may be due to serious illness. • Establishing the onset of deterioration and prior function is essential to identify delirium characterized by a fluctuating level of consciousness, disorientation, global cognitive deficit. This is almost always due to organic cause, usually infection. • The classic triad of confusion, incontinence and falls should alert the clinician to the presence of serious illness.13
Diagnosis A diagnosis of acute serious illness or medication toxicity should be assumed until proven otherwise. There are many causes for acute confusion including:14 (a) infection, most commonly, pneumonia and urinary tract infection;
392 OLDER PEOPLE
(b) cardiovascular disorder, especially myocardial infarction and congestive heart failure; (c) neurological disorder, most commonly stroke; (d) medication interaction or toxicity, particularly psychotropic medications or cardiovascular medications; (e) acute alcohol withdrawal; (f) acute psychiatric disorder, including psychosis; (g) electrolyte disturbance, dehydration, hyponatremia; (h) endocrine disorder, thyroid disease, diabetes; (i) acute change in hearing or vision; (j) faecal impaction or retention of urine; (k) neoplasia; (1) acute surgical emergency, such as peritonitis from appendicitis or gall bladder disease; (m) undiagnosed fracture.
Specific evaluation A thorough history and physical examination are necessary including: (a) History of prior functional level, social support, medications and medical problems. Involving caregivers or family member to get a history may be necessary. (b) Examination of cardiovascular and neurological systems. (c) Musculo-skeletal examination, especially for those with reduced mobility. Suspect undiagnosed fracture after apparent minor injury with excessive disability. (d) Abdominal examination to exclude an acute abdomen. (e) Rectal examination. (f) Examination of the fundi. (g) Investigations will be guided by the history and physical (see box below).
Possible investigations FBC and ESR; U&Es; LFTs; TFTs; MSU; blood glucose; calcium;
blood cultures; ECG; CXR and other X-rays as suggested by the examination.
Management Delirium, acute confusion * Refer for admission to acute medical ward or geriatric assessment ward if the diagnosis cannot be clearly identified and the patient cannot be managed at home. * Refer for admission to acute hospital if pneumonia or stroke is evident and the patient cannot be cared for at home. If treating the patient at home: * Treat any infection with an appropriate antibiotic. * Stop medications with potential toxicity, especially sedative/hypnotics if they are suspected of causing acute confusion. * Treat dehydration with fluids with attention to cardiovascular function. * Deal with faecal impaction in the usual way, with attention to follow up bowel function. Fluids, exercise and fibre are all needed for adequate bowel function in older people. Agitation * Treat the cause as above, especially undiagnosed pain. * Refer for admission to geriatric or psychogeriatric assessment ward if the patient cannot be managed at home. * Refer to a psychiatrist for evaluation if psychosis is suspected. * If no cause is found and the patient has underlying dementia, see below (p. 394). * Behavioural management is useful for any agitated patient including: (a) allowing wandering in a safe environment; (b) relocation to alternative living arrangements if agitation becomes a constant problem and cannot be managed in current living arrangement;
SUBACUTE DETERIORATION WITHOUT ACUTE ILLNESS: DEPRESSION OR DEMENTIA
(c) encouraging participation in usual activities; (d) avoiding confrontation if aggression is a feature; (e) physical restraint should be avoided as it causes injury. * See p. 395 for services available. * Medication. Treat with haloperidol if no cause is found and behavioural management fails. * Benzodiazepines should be avoided. Even short-acting benzodiazepines accumulate in the older person and worsen the confusion. Loss of mobility
* Treat acute illness as for acute confusion above. * If minor injury is the cause, and significant disability has resulted and there is no fracture: (a) give adequate pain relief; (b) mobilize as soon as possible; (c) refer to community physiotherapy or outpatients department or day hospital services for rehabilitation.15 * Consider giving vitamin D with calcium co-supplementation. This may reduce the risk of hip fracture in frail older people16 (see p. 180). * Refer the patient to a day hospital, which can improve overall functional outcome and service utilization when compared with no comprehensive care.15 * Refer for comprehensive inpatient geriatric assessment and management if overall function has deteriorated without apparent cause.
SUBACUTE DETERIORATION WITHOUT ACUTE ILLNESS: DEPRESSION OR DEMENTIA • Deterioration in mental or physical status can be slow and progressive and not apparently due to acute illness (i.e. not delirium). • If the onset is slow and workup has not shown a treatable acute cause then the differential diagnoses of dementia or depression must be considered.
Diagnosis * The diagnosis of depression is often missed in older people as the prominence of physical symptoms compounds the diagnosis. * Dementia is of more insidious onset than depression. * Cognition and physical deterioration in depression is worse in the mornings. * In depression insight is present, whereas those with dementia rarely have insight. * Orientation is poor in dementia and reasonable in depression. * Memory loss is characteristically worse for recent events in dementia, but can be similar for recent and remote events in depression.
Specific evaluation * Ask about a family and personal history of depression. * Ask about recent significant events. Bereavement and relocation predispose to social isolation and depression. * Check functional status and independence in living activities. * Check the patient's social and financial supports. * Ask about driving. Specific driving assessment may be necessary later. * The geriatric depression scale is useful in diagnosing depression in those without severe dementia.17 * Assess the patient's cognitive state formally using one or both of the following tests: • Clock drawing is a useful, non-threatening test of mental function. Simply draw a circle and ask the patient to 'make it into a clock with the time at 10 to two'. If numbers are not spread throughout all four quadrants then the test is positive. • A standardized mental test score, such as the Abbreviated Mental Test Score, see box. It is only reliable if used precisely.18 Abbreviated Mental Test Score Each question scores 1. A score of 6 or less suggests dementia. 1. Age (exact number of years); 2. Time (to the nearest hour);
3. A simple address, e.g. 42 West Street, to be repeated by the patient at the end of the test; 4. Year (the current year); 5. The place (exact address or the name of the surgery or hospital); 6. Recognition of two persons present (by name or role); 7. Date of birth (correct day and month); 8. Year of the First World War (1914 or 1918 is enough); 9. Name of the monarch (must be current monarch); 10. Count backwards from 20 to 1 (with no mistakes, or with mistakes which the patient corrects without prompting).
Management * Treatment of dementia is outlined in the next section. * Refer for geriatric medical or geriatric psychiatric assessment if the diagnosis is not clear. * Treat depression, if present, with: (a) a SSRI or a TCA (see p. 311);19 and/or (b) psychological therapy including cognitive behaviour therapy. Access to publicly funded counselling services may limit availability. * Follow-up is essential to ensure recovery of function.
DEMENTIA Guidelines: Practice parameter: Diagnosis of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001; 56:1143-53. Practice parameter: Management of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2W\; 56:1154-66.
• Dementia affects 10% of those over age 65 years and 20% of those over age 80 years. • Absolute numbers of those with dementia will increase exponentially in the next two decades as the world population ages. • New therapies recently available and currently under investigation mean that identification of early dementia will be more important in the future.
Diagnosis * Suspect dementia when the patient has: (a) impairment in short and long-term memory, abstract thinking, judgement, other higher cortical function or personality change; and (b) the disturbance is severe enough to interfere significantly with work, social activities or relationships; and (c) delirium is absent.20 * Confirm it with a formal assessment using the Abbreviated Mental Test Score or the clock drawing test (see above). * Determine, from the history and examination, whether it is possible to decide on the cause of the dementia (see below). This entails examination of the patient's mental state and cognition, a neurological and cardiovascular examination and a screen for depression. However, many patients have atypical or non-specific presentations. * Exclude the few cases of reversible cognitive impairment as detailed below. The box lists the clinical features of the types of dementia.
Types of dementia listed in order of prevalence Dementia - Alzheimer's type • Accounts for the majority of dementia cases • Insidious onset over several years • Global deficits Vascular dementia • Accounts for 10% of dementia cases, although 29-41% of dementia cases autopsied have some vascular pathology • Stepwise progression • Bilateral neurological signs • A history of cardiovascular disease such as HTN suggests vascular dementia • Risk factors, or a history of risk factors for cardiovascular make vascular dementia more likely Dementia with Lewy bodies Dementia plus Balance and gait disorder Prominent hallucinations and delusions Sensitivity to antipsychotics Fluctuations in alertness Frontotemporal dementia • Early loss of personal awareness • Early loss of social awareness • Hyperorality • Stereotyped, perseverative behaviours
Prion disease (Creutzfeld-Jakob disease; CJD) • Rapidly progressive symptoms • Characteristic EEG pattern of periodic sharp wave complexes • Pathological brain tissue diagnosis • CSF 14-3-3 protein (high sensitivity and specificity for diagnosis of CJD)
Specific evaluation * History from caregiver or source other than the patient. * Screen for depression. * Examination of mental state, cognition, neurological system. * Examination of cardiovascular system. * Investigations: (a) vitamin B12 level; (b) thyroid function; (c) FBC, U&Es, LFTs, calcium, glucose, ESR; (d) CXR, MSU; (e) Syphilis screening may no longer be needed unless there is a specific risk factor or they are from certain parts of the USA. * Imaging with CT or MRI. Availability will limit access in some regions. * Imaging with single photon emission computerized tomography (SPECT) or positron emission tomography (PET) is not recommended for routine use. * Genetic testing and genotyping is not currently recommended. * The CSF 14-3-3 protein may become available and is useful for confirming or rejecting the diagnosis of CJD in clinically appropriate circumstances.
Management General * It is widely accepted that most patients with dementia should be assessed by a psychogeriatrician or geriatrician. * Cognition, function, mood and behaviour as well as general health should be evaluated in patients with dementia every 6 months.
* Refer for intensive long-term education and support for caregivers (if available) to delay time to residential care placement. * Offer or refer for education for family caregivers to reduce caregiver stress. * Refer for home support (see supporting older people at home). * Refer for placement in dementia specific longterm care. This reduces behavioural problems and use of chemical and physical restraints. For patients in residential care * Offer residential care staff education about the behavioural management patients with Alzheimer's disease (AD). * Explain that a safe wandering space is essential for the older person with dementia to avoid agitation and unnecessary restraint, although there is no direct evidence of benefit.21 This is especially useful for 'sundowning' (increased agitation in the late afternoon). * Scheduled toileting and prompted voiding reduces urinary incontinence. * Music therapy, simulated natural sounds and intensive multimodality group training may improve overall function. Medications for cognitive symptoms Alzheimer's disease22 * Treatment with cholinesterase inhibitors should be considered in patients with mild to moderate AD. Accessibility to subsidized medications will limit availability in some countries. The UK National Institute for Clinical Excellence23 recommends that any of the drugs below (except tacrine) may be given to people with mild to moderate AD, but only if the Mini-Mental State Examination (MMSE) score is above 12, the diagnosis of AD has been made in a specialist clinic and treatment has been initiated by a specialist. Studies show a small average degree of improvement in cognition and behavioural control but no effect on the eventual progression of the disease. These include: (a) Tacrine: 10 mg four times daily for 4 weeks, then 20 mg four times daily for 4 weeks, then
396 OLDER PEOPLE
30 mg four times daily for 4 weeks then 40 mg four times daily with dose escalation as tolerated; (b) Donepezil: 5mg daily increased to 10 mg daily after 4 weeks; (c) Rivastigmine: 1.5 mg twice daily for 2 weeks, then 3 mg twice daily for 2 weeks, then 4.5 mg twice daily for 2 weeks to 6 mg twice daily; (d) Galantamine: 16 to 24 mg daily. * Vitamin E may slow the progression of AD, although evidence is limited.24 Ischemic dementia
* Evidence-based data supporting pharmacological efficacy of agents to treat non-AD dementia is lacking. However, the patient with vascular dementia would benefit from measures used in other cardiovascular diseases, e.g. aspirin, if the quality of life makes such measures appropriate. Medications for non-cognitive symptoms Behavioural disturbance Treatment of delirium, an acute change in mental status characterized by fluctuation in level of consciousness, is empirical. It is more complex in those with dementia.25 * Look for an organic cause, most commonly undiagnosed pain, infection and cardiovascular disorder as with well older people. * Use behavioural and environmental modification. * Treat agitation and psychosis with psychotropic medications. Risperidone or haloperidol are the drugs of choice. Start at the lowest dose and titrate to the lowest possible effective dose. Financial and legal aspects (UK) * Assess whether the patient is eligible for exemption from the Council tax (see p. 3). * Assess whether it is appropriate for someone else to be given power of attorney (see p. 14 and 399). Support groups: Alzheimer's New Zealand, PO Box 2808, Christchurch, New Zealand, tel. 64 3 365 1590; www.alzheimers.org.nz
Alzheimer's Association Australia, PO Box 108, Higgins 2615, tel. 61 2 6254 4233; www.alzheimers.org.au Alzheimer's Society, Gordon House, 10 Greencoat Place, London SW1P 1PH, tel. 020 7306 0606; www.alzheimers.org.uk Details of Alzheimer's Associations in other countries can be found on the website of the Alzheimer's Disease International. Website: www.alz.co.uk Age Concern New Zealand, PO Box 10-688, Wellington, New Zealand, tel. 64 4 471 2709; www.ageconcern.org.nz Age Concern England, Astral House, 1268 London Road, London SW16 4ER, tel. 020 8765 7200; www.ageconcern.org.uk Details of other UK branches of Age Concern can be found on the UK website above.
FALLS Guideline: American Geriatrics Society, British Geriatrics Society, American Academy of Orthopaedic Surgeons Panel on Falls Prevention. Guideline for the prevention of falls in older persons. J Am Geriatric Soc 2001; 49: 664-72.
Falls are serious and common for those over age 75 years. Risk factors have been identified and specific interventions proven to reduce falls.
Risk factors (a) age over 80 years; (b) cognitive impairment; (c) history of fall and fall-related injury; (d) arthritis; (e) depression; (f) use of mobility aid; (g) gait and balance impairment; (h) lower limb muscle weakness; (i) visual deficit; (j) impaired daily functioning, or a low score on the Nottingham EADL scale (see p. 405); (k) use of psychotropic medications. Those with multiple risk factors are at a higher risk of falls.
Diagnosis * Distinguish between 'hot' and 'cold' falls. (a) 'Hot' falls result from major medical conditions such as stroke, myocardial infarction or seizure. Treatment of the acute illness usually entails admission to hospital. (b) 'Cold' falls occur in the absence of serious acute illness. * Case-finding in primary health care for those with a high risk of falls is recommended although clear evidence of benefit is lacking. Case-finding could include a process where every adult over the age of 75 years is asked if they have sustained a fall over the previous year. This part of the chapter deals with management of cold falls and those with high risk of falls. The UK National Service Framework for Older People12 recommends that those who have fallen and those at high risk of falling are referred to a Falls Centre. Specific evaluation Those presenting with a single or recurrent falls or those who have a gait and balance deficit should undergo a fall assessment including: (a) history of fall circumstances; (b) medication review; (c) review of chronic medical problems including alcohol misuse; (d) examination of: - vision; - gait and balance (see below); - lower leg strength; -neurological system, especially proprioceptive and coordination function and including mental status; -cardiovascular system, especially heart rate and rhythm, lying and standing blood pressure and the murmurs of valvular disease. (e) the environment in which the falls occurred, with attention to: -hazards such as loose mats, cords and unstable furniture; - lighting levels; (f) investigations including FBC and ECG.
Simple gait assessment Ask the patient to stand from a chair, without using the arms, walk several paces, turn around and return (the Get Up and Go test26). Unsteadiness or difficulty completing this in less than 30 seconds shows a gait and balance deficit and further evaluation is needed.
Management * Results of the evaluation will guide specific management. In general, multiple risk factors are present. * Multifactorial intervention is more effective than single intervention in preventing future falls.27 * All older people over age 75 years should be asked whether they have had a fall in the last year. * Refer all with a history of loss of consciousness to a physician. Investigations, such as a 24-hour ECG, may reveal a cause. * Treat any injury resulting from the fall in the usual way * Treat those at high risk of recurrent falls as follows: Community-dwelling older people at high risk of recurrent falls27 * Refer for a programme of muscle strengthening and balance retraining and advice on use of assistive devices. This depends on the local availability of a falls clinic or falls-related exercise groups. * Encourage increased exercise such as walking or refer to an exercise programme with a balance component. * Refer for Tai Chi C'uan exercise. A 15-week course reduces falls by 50%.28 The availability of classes may be limited. * Review medications and reduce psychotropics. * Home environment. Refer for modification of environmental hazards according to the availability of occupational therapy. * Review all medical conditions. Treat cardiovascular disorders, including postural hypotension and any cardiac arrhythmia.
* Osteoporosis. Consider giving vitamin D3 with calcium co-supplementation to reduce the risk of vertebral fracture.16 Older people in residential care and assisted living settings at high risk of recurrent falls * Refer to physiotherapy for gait and balance training and advice on use of assistive devices. This depends on the availability of physiotherapy services in long-term care. * Review medications and reduce medication use, especially psychotropics. * Educate staff about falls reduction. * Consider giving vitamin D3 with calcium co-supplementation to reduce the risk of hip fracture.16 * Offer hip protective devices and garments to reduce hip fracture.29
LOWER LIMB PROBLEMS NIGHT CRAMPS Nocturnal leg cramps are common occurrences among older, generally healthy adults.
Diagnosis The history, physical exam, and laboratory testing can uncover treatable causes: (a) (b) (c) (d) (e)
endocrine; neurological; vascular disorders; treatment with certain drugs; occupational factors.
However, a significant portion of cases are idiopathic. Possible investigations FBC and ESR; U & Es; LFTs; blood glucose; calcium; TFTs.
Management * Treat the underlying cause whenever possible. * Massaging and stretching is the recommended first-line treatment for idiopathic cases. * Quinine sulfate also appears to offer safe and effective symptom management, although its efficacy has not been definitively established in clinical trials.30 RESTLESS LEGS SYNDROME Review: Chaudhuri KR, Appiah-Kubi LS, Trenkwalder C. Restless legs syndrome. J A/euro/ Neurosurg Psychiatry 2001; 71:143-6.
• The minimum diagnostic criteria proposed by the International Restless Legs Syndrome Study Group31 are: (a) a desire to move limbs, usually associated with para/dysaesthesia; (b) motor restlessness; (c) symptoms worse or exclusively present at rest: partial/temporary relief with activity; (d) symptoms worse in the evening or at night. • Iron deficiency with or without anaemia is found in a third of elderly patients with restless legs. • A positive family history is present in 63% to 92% of patients with the idiopathic syndrome. Work-up (a) RBC; (b) serum ferritin; (c) folic acid; (d) B12; (e) U & Es.
* Examine to exclude peripheral neuropathy. * Review the patient's drugs. Possible causes are neuroleptics, lithium, beta-blockers, TCAs, anticonvulsants, H2-blockers. * Consider drug treatment for patients with symptoms that are sufficiently severe. Dopaminergic drugs are effective but prone to causing adverse effects. Levodopa itself appears to cause augmentation, that is, symptoms appear to start earlier in the day and may spread to the upper
LEGAL ASPECTS 399
limbs. Start each drug with a low dose at first, administered at least 2 hours before the patient goes to bed. If one drug fails, try one from another group. Options are: (a) levodopa (+decarboxylase inhibitor) starting with a low dose (100-200 mg); (b) bromocriptine 7.5 mg daily; (c) clonazepam 0.5-2 mg daily; (d) carbamazepine 100-300 mg daily.
POSTURAL ANKLE OEDEMA Many patients are given diuretics inappropriately for postural oedema. * Assess carefully to exclude a cardiac, renal or hepatic cause. * Treat postural oedema by advising the patient to: (a) keep active; (b) elevate legs when sitting; and (c) use support hosiery. * Give a diuretic only where the oedema is too severe to permit the patient to pull on a support stocking, and even then only give it for a maximum of 3 weeks. * Consider a trial without diuretics for those already started on them. In one study, 85% of those suitable were successfully withdrawn from diuretics.32 Be aware that even patients who do not need their diuretics are likely to suffer an initial increase in oedema as a rebound phenomenon, which may take 6 weeks to settle.
ELDER ABUSE • A UK study has shown the prevalence of abuse in the patient's own home to be significant, with physical abuse in 2%, verbal in 5% and financial in 2%.33 Forty-five per cent of carers of the elderly in respite care admitted to some form of abuse.34 • There are no statutory guidelines or legislation. Intervention should always be interdisciplinary. • Abuse may take the form of: (a) physical: hitting, pushing, restraining; (b) psychological: threats, insults, left alone unaware of when the caregiver will return;
(c) sexual: unwanted advances, rape; (d) financial: theft of money or property; (e) neglect: failure of adequate personal care / food / medication/ continence /pressure relief etc.; (f) lack of privacy: especially intimate functions; (g) misuse of medications: especially sedatives; (h) routines: e.g. rigid meal, bed and bath times; (i) overstimulation. * The following may suggest abuse: (a) delay in seeking medical help; (b) differing histories from patient and carer, especially if explanations are implausible; (c) inconsistencies on examination; (d) frequent calls for visits by the GP or A & E attendances; (e) carer not accompanying patient when that would be expected; (f) abnormal behaviour in the presence of the carer, e.g. fear or withdrawal. * Discuss the situation with the patient, carer and involved care agencies. Further action will depend on the wishes and competence of the patient and the nature and severity of the abuse. * Discuss the case with Action on Elder Abuse (see box below). Professional and patient information: Action on Elder Abuse, Astral House, 1268 London Road, London SW16 4ER, tel. 020 8765 7000; helpline 080 8808 8141; www.elderabuse.org.uk
LEGAL ASPECTS Power of attorney At an early stage of declining mental function, suggest to the family that they consult a solicitor about an Enduring Power of Attorney (EPA) before the patient is incapable of signing the form. In order to sign, the patient must be capable of understanding the implications of so doing, and may be capable of this even if incapable of managing his or her affairs. If it is left too late, it is then necessary to apply to the Court of Protection to appoint a receiver, and this is much more
400 OLDER PEOPLE
cumbersome. Note that this is different from the registration of an EPA with the Court of Protection. This becomes necessary when the person who signed it becomes incapable of managing his or her own affairs (see p. 14).
Detention of an older person Guideline: UK: Section 47 of the National Assistance Act and Article 10, The Human Rights Act 1999.
The National Assistance Act allows for the 'detention and maintenance in suitable premises of persons in need of care and attention'. It enables a local authority to seek an order from a magistrates court for the removal of a person from his or her home on the grounds that: (a) He is suffering from a grave chronic disease or, being aged, infirm or physically incapacitated, is living in insanitary conditions; (b) He is unable to look after himself and is not receiving proper care and attention from anyone else; and (c) His removal is necessary in his own interests or for preventing injury to the health or, serious nuisance to, other persons. Following the court hearing, an order can be made to remove a person by a specified officer of the appropriate authority. The order authorizes the person's detention and maintenance, but does not provide for medical treatment to be given without the person's consent. The initial order can
last up to 3 months although it can be extended. If after 6 weeks an appeal is successful, the order can be revoked. There is now some discussion that The Human Rights Act 1999, which came into force on 2 October 2000, will prove contrary to the National Assistance Act, as Section 6 (1) of the former makes it unlawful for a public authority to act in a way which goes against the European Convention on Human Rights, such as everyone has the right to 'liberty and security of person' and 'respect for his private and family life, his home and his correspondence.' However, if the person is removed under Section 47, this can be undertaken under 'protection for health,' although it remains a possibility that removals may be appealed at some stage in the future. * Refer for comprehensive assessment by social worker, geriatrician, or psychogeriatrician, as part of application to the magistrate. This is not technically required under the Act. Note: The Act should not be used for patients with mental disorder, who are covered by the Mental Health Act. * In Australia and New Zealand, refer to the local geriatric assessment team if there is a need for legal intervention to ensure patient safety and wellbeing.
Mental capacity See p. 13.
REFERENCES 1. Curb }, Pressel S, Cutler } et al. Effect of diuretic-based antihypertensive treatment on cardiovascular disease risk in older diabetic patients with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group. / Am Med Assoc 1996; 276: 1886-92. 2. Vetter N, Ford D. Smoking prevention among people aged 60 and over: a randomized controlled trial. Age Ageing 1990; 19: 164-8. 3. DHSS. Living in Britain: Results from the 1994 General Household Survey. Norwich: The Stationery Office, 1994.
4. Anderson P. Effectiveness of general practice interventions for patients with harmful alcohol consumption. Br J Gen Prac 1993; 43: 386-9. 5. Manley A. Physical activity and health. A report of the Surgeon General. Pittsburgh: US Department of Health and Human Services, 1996. 6. Rooney E. Exercise for older patients: Why it's worth the effort. Geriatrics 1993; 48: 68-72. 7. Elward K, Larson E. Benefits of exercise for older adults. A review of existing evidence and current recommendations for the general population. Clin Geriatric Med 1992; 8: 35-50.
8. Kerse N, Jolley D, Arroll B et al. Improving health behaviours of the elderly: a randomised controlled trial of a general practice educational intervention. Br Med J 1999; 319: 683-7. 9. Campbell A, Robertson M, Gardner M et al. Randomised controlled trial of a general practice programme of home based exercise to prevent falls in elderly women. Br Med J 1997; 315: 1065-9. 10. Campbell A, Buchner D. Unstable disability and the fluctuation of frailty. Age Ageing 1997; 26: 315-18. 11. Elkan R, Kendrick D, Dewey M et al. Effectiveness of home based support for older people: systematic review and meta-analysis. Commentary: When, where, and why do preventive home visits. Br Med J 2001; 323: 719. 12. Department of Health. National Service Framework for Older People. London: Department of Health, 2001. Online. Available: www.doh.gov.uk/nsf/olderpeople.htm 13. Mold J. Principles of geriatric care. American Health Consultants. Primary Care Reports 1996; 2: 2-9. 14. O'Keefe K, Sanson T. Elderly patients with altered mental status. Emerg Med Clin N Am 1998; 16: 701-15. 15. Forster A, Young J, Langhorne P. Medical day hospital care for the elderly versus alternative forms of care (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. 16. Gillespie W, Avenell A, Henry D et al. Vitamin D and vitamin D analogues for preventing fractures associated with involutional and post-menopausal osteoporosis (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. 17. Montorio I, Izal M. The Geriatric Depression Scale: a review of its development and utility. International Psychogeriatrics 1996; 8:103-12. 18. Holmes J, Gilbody S. Differences in use of the Abbreviated Mental Test Score by geriatricians and psychiatrists. BMJ 1996; 313: 465. 19. Wilson K, Mottram P, Sivanranthan A et al. Antidepressants versus placebo for the depressed elderly (Cochrane review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. 20. American Psychiatric Association. Diagnostic and Statistical manual of mental disorder, 3rd edition, revised 1987. Washington DC: American Psychiatric Association, 1987. 21. Price J, Hermans D, Grimley Evans J. Subjective barriers to prevent wandering of cognitively impaired people
30. 31. 32. 33. 34.
(Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. Doody R, Stevens I, Beck C et al. Practice parameter: management of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001; 56: 1154-66. UK National Institute for Clinical Excellence, Technology appraisal guidance No. 19. London: National Institute for Clinical Excellence, 2001. Online. Available: www.nice.org.uk Tabet N, Birks J, Grimley Evans J et al. Vitamin E for Alzheimer's disease (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. Britton A, Russell R. Multidisciplinary team interventions for delirium in patients with chronic cognitive impairment (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. Mathias S, Nayak U, Isaacs B. Balance in elderly patients: the 'Get up and Go' test. Arch Phys Med Rehabil 1986; 67: 387-9. Gillespie L, Gillespie W, Robertson M et al. Interventions for preventing falls in elderly people (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. Wolf S, Barnhart H, Kutner N et al. Reducing frailty and falls in older persons: an investigation of Tai Chi and computerized balance training. Atlanta FICSIT Group. Frailty and Injuries: Cooperative Studies of Intervention Techniques. / Am Geriatric Soc 1996; 44: 489-97. Parker M, Gillespie L, Gillespie W. Hip protectors for preventing hip fractures in the elderly (Cochrane Review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. Kanaan N, Sawaya R. Nocturnal leg cramps. Clinically mysterious and painful - but manageable. Geriatrics 2001; 56: 39-42. Walters A. Towards a better definition of restless legs syndrome. The International Restless Legs Syndrome Study Group. Movement Disord 1995; 10: 634-42. de Jonge J et al. Short term effect of withdrawal of diuretic drugs prescribed for ankle oedema. BMJ 1994; 308: 511-13. Ogg J, Bennett G. Elder abuse in Britain. BMJ 1992; 305: 998-9. Homer A, Gilliard C. Abuse of elderly people by their carers. BMJ 1990; 301: 1359-62.
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Physical disability and rehabilitation 403 Carers
People with learning disability (UK) or intellectual disability (Australia) 409 Down syndrome References
PHYSICAL DISABILITY AND REHABILITATION • A person is defined as disabled if blind, deaf, dumb, or suffering from mental disorder, or substantially and permanently handicapped by illness, injury or congenital deformity or other such disabilities (The Chronically Sick and Disabled Persons Act 1970). • Clear evidence exists for the benefit of rehabilitation in patients with stroke,1 heart failure1 and falls due to poor balance. • Physiotherapy can reduce pain and improve mobility.2 • The provision of equipment and alterations to the home can improve outcomes.3 Every patient with a significant disability needs: (a) a key worker, who may be a GP, who will coordinate all aspects of care; (b) an assessment of overall disability, by the occupational therapist (OT) as a minimum; (c) an identification of a person who is a carer. The GP needs to become familiar with the medical condition that has caused the disability. Where the condition is a rarity, the GP will not gain the confidence of the family without this knowledge and will not be able to take a proactive role. Check the following: (a) Can the patient's physical state be improved? (b) Can the patient's mental state, including self-esteem, be improved? 403
(c) Can the patient's ability to live independently be improved? (d) Can the patient's mobility inside and outside be improved? (e) Is there any work that the patient may be able to undertake? (f) Can the patient be helped to enjoy leisure and social activities? (g) Would the carer benefit from more support? (h) Can the patient's or carer's financial state be improved (see Chapter 1)? Patient information and organizations: Department of Health. A practical guide for disabled people: where to find information, services and equipment (HB6). London: Department of Health, 2002. Royal Association for Disability and Rehabilitation (RADAR), 12 City Forum, 250 City Road, London EC1V 8AF, tel. 020 7250 3222; e-mail: [email protected] Disablement Information and Advice Line (DIAL), St Catherine's, Tickhill Road, Doncaster, South Yorkshire DN4 8QN, tel. 01302 310123; e-mail: [email protected]
Referral Consider referral to the appropriate agency if: (a) the cause of the disability is unknown; or (b) there is new impairment, disability or handicap; or (c) there is deterioration in existing impairment, disability and handicap; or (d) the disabled person and/or their carer are barely coping.
Eligibility Section 2 of the Chronically Sick and Disabled Persons Act 1970 lists the arrangements that the Local Authority has a duty to make: (a) the provision of practical assistance for that person in his or her home; (b) the provision for that person of, or assistance to that person in obtaining wireless, television, library or similar recreational facilities; (c) the provision for that person of lectures, games, outings ... and taking advantage of educational facilities that are available; (d) the provision of facilities or assistance in travelling to and from his or her home for the purposes of participating in any services provided; (e) the provision of assistance for that person in arranging for the carrying out of any works of adaptation in the home or the provision of additional facilities designed to secure his or her greater safety, comfort or convenience; (f) facilitating the taking of holidays; (g) the provision of meals for that person in his or her home or elsewhere; (h) the provision for that person in obtaining a telephone and any special equipment necessary to enable him or her to use a telephone.4
Where rehabilitation services can be located
With the overall reduction of hospital bed numbers there has been expansion of rehabilitation services accessible to the GP and provided in community settings. GPs need to be familiar with the provision in their local area. Awareness of the eligibility criteria of the different services are essential in managing patients' expectations.
(a) unidentified medical problems, e.g. anaemia, heart failure, hypothyroidism, Parkinson's disease; (b) occult depression; (c) occult dementia that may be masked by intact social skills; (d) communication problems, e.g. poor vision or hearing.
(a) Social Services for the OT team, and visual and hearing impairment teams. (b) Intermediate care: often integrated health and social services multidisciplinary teams for defined periods of rehabilitation either up to 2 weeks (rapid response) or 6 weeks. They may provide home-based services or alternative beds outside the acute hospital setting.
PHYSICAL DISABILITY AND REHABILITATION 405
(c) Community rehabilitation teams: for specific clinical conditions such as stroke, physical disability, learning disability, etc.
Assessment of level of disability and dependency In addition to the assessment of the underlying condition a broader picture of how the person is coping with managing daily tasks can assist in deciding where referrals need to be made. Activities of daily living can be categorized into: (a) personal care: feeding, dressing, toiletting, grooming and indoor mobility; (b) extended care: managing domestic tasks and the wider environment in cooking, shopping, working, and socializing. The Community Dependency Index (CDI) (see Appendix 24) is a standardized assessment of personal care and is recommended to use when: (a) there is high level dependency, the patient is predominantly housebound, reliant on informal carers; (b) when a package of care from statutory services appears to be indicated. The CDI will help decide on the frequency and extent of support needed. A score of less than 75 usually represents a moderate disability and a score of less than 50 represents a severe disability.5'6 The Nottingham Extended Activities of Daily Living Questionnaire (see Appendix 25) is more appropriate when there are low or moderate levels of dependency and the person is able to access the wider environment.7
Assessment and improvement of the home environment Refer for an OT assessment if the home environment is presenting a barrier to the person managing daily tasks independently. The following are the most common areas that the GP can observe, or ask questions about, to identify difficulties: • Access Are the steps and stairs at the entrance way and within the house negotiable by the person?
Is there level access or do thresholds or door widths present a barrier? Is there adequate space to manoeuvre in corridors and in rooms with mobility equipment? Do the floor coverings present a hazard? • Controls Can the person reach sockets and light switches? Is the home adequately heated? Is the lighting, door and window security adequate? Can the person get to the door to respond to callers? • Kitchen Can the person reach the oven and hob to handle hot items safely? Can the person reach into both high and low cupboards? Is the sink and work surface a suitable height? Can the person open jars and tins, and prepare vegetables? • Toilet and bathroom Is the person able to get in and out of the bath/ shower? Can the person get on and off the toilet? Can the person manage taps? • Bedroom and living rooms Can the person get in and out of his or her bed and chair? Can the person easily reach the telephone from his or her bed or chair? Self assessment for patients on reducing home hazards: Clemson L. Westmead Home Safety Assessment.8 Forms can be purchased through Winslow, tel. 0845 921 1777; e-mail: [email protected]
Role of GP in rehabilitation assessment To enable the OT or rehabilitation team to plan appropriate short- and long-term intervention they often require detailed information on the client's disability, diagnosis and prognosis. In complicated cases it is useful to discuss the issues to reach realistic long-term solutions and to ensure resources are appropriately allocated for major equipment and adaptation.
Community interventions Following assessment the OT or rehabilitation team may: 1. plan interventions to reduce the impairment and prevent complications through goal-focused, patient-centred home activity programmes that are reviewed and progressed; 2. reduce the disability through advice on, and in some cases supply of, specialist equipment; 3. recommend environmental adaptations both minor and major or if necessary provide rehousing reports. These three broad areas of intervention are generally considered to form a hierarchy and are covered in more detail in the rest of this section. Throughout, advice, support and training can be given to formal and informal carers alongside liaison with other involved parties. Community rehabilitation The following areas of rehabilitation may be included in a patient's programme. Referrals for specific services may be made either by the GP or the therapist, or for some services the therapist may need to approach the GP for authorization. (a) Physical rehabilitation: to improve balance, muscle power and joint range of movement, reduce pain, maintain positioning, seating, the management of tone and spasms, referral for splints or prosthetics. Passive movements need to be completed regularly by a carer trained by the therapist to prevent contractures. GPs and therapists will need to work closely together to achieve optimum dosage of medication for spasticity in order to reduce spasm without reducing tone to such an extent that function is adversely effected. (b) Cognitive rehabilitation: problem solving, perceptual difficulties, memory strategies, compensation techniques. (c) Vocational rehabilitation: assessment of vocational aptitudes, referral to the Disability Employment Advisor, sources of equipment to support employment (see Chapter 1). (d) Community access: refer for shop mobility schemes, taxi-card schemes, dial-a-ride, driving
assessment centres, motability scheme for adapted vehicles for a disabled person as a driver or as a passenger (see Chapter 1). (e) Leisure: the importance of leisure activities for self-esteem and motivation should not be overlooked; accessing clubs and community education classes, socializing and a balance of active and sedentary pastimes. Community equipment services A wide range of large-scale equipment can be loaned to patients for use both in the long term and short term. Increasingly, health and social services are required to integrate their provision into a single service.9 There may be some charges for loans. Small-scale equipment such as dressing, feeding and kitchen equipment may not be available for loan. GPs can encourage patients to return equipment that they no longer use. Commonly available equipment includes: (a) nursing equipment: hoists, beds, pressurerelieving equipment, commodes, urinals, palliative care equipment; (b) mobility and positioning equipment: sticks, crutches, frames, wheelchairs, cushions, wedges, transfer belts and boards, multiglide sheets; (c) daily living equipment: toilet seats and frames, bath boards, seats and hoists, trolleys, perching stools, bed and chair raisers, modified cutlery, tap turners. Alternative sources of equipment Retail outlets: Look up Yellow Pages index under 'disabled equipment and vehicles' Mail order catalogues for equipment: • Ways and Means, Novara House, Excelsior Road, Ashby Park, Ashby de la Zouch, Leicestershire LE65 1NG, tel. 01530 418916. • Smith and Nephew, PO Box 5665, Kirkby-in-Ashfield, Notts NG17 7QX, tel. 01623 722337; http://www.snrehab.com Mail order catalogues for special shoes: • Hotter Comfort Concept, tel. 0800 525 893. • Cosyfeet, 5 The Tanyard, Leigh Road, Street, Somerset, BA16 OHR, tel. 01458 447275. Mail order catalogues for adapted clothes: • Rolli Moden, tel. 0049 6226 960 208; www.rolli-moden.de
PHYSICAL DISABILITY AND REHABILITATION
• Silvalea Textiles, Unit 3-4, Silverhills Buildings, Decoy Industrial Estate, Newton Abbot, DevonTQ12 5LZ, tel. 01626 333793; www.silvaleatextiles.co.uk
• All patients who use powered vehicles should be advised to take out at least third party liability insurance.
Assist!ve technologies for profound disability.
For patients who depend on these assistive technologies, a 24-hour call-out service for breakdown maintenance and servicing arrangement is essential.12
GPs and community therapists will need to consider the need for, and know where to refer for, the following: (a) (b) (c) (d)
communication aids; environmental control systems; sensory alarm systems; wheelchairs.
Wheelchairs. GPs and therapists can requisition the issuing of a manual wheelchair from a standard limited range. Assessment needs to include the frequency and location of use, height and weight of the patient, whether the patient will self propel, fitness of the main carer for attendantpropelled wheelchairs, whether the wheelchair will be transported in a car and, if being used in the home, whether any adaptations to the house are required. If a patient has a very clear idea of a nonstandard type of wheelchair he or she requires, the patient should be advised about the voucher scheme. There are two options: (a) The independent option to contribute to the cost of a more expensive wheelchair of the patient's choice. The patient will own the wheelchair and be responsible for its maintenance and repair. (b) The partnership option to contribute to the cost of a more expensive wheelchair of the patient's choice from a range selected by the local wheelchair service. The NHS will own the wheelchair and be responsible for its maintenance and repair.10 Powered wheelchairs
• Referral should be made to the local wheelchair service for electrically powered indoor chairs (EPIC), electrically powered indoor/outdoor chairs (EPIOC) and special seating clinics for wheelchair postural supports. • OTs can advise on suitable electric scooters. Patients who receive mobility allowance can use this to hire or hire/purchase a scooter through the Motability scheme11 (www.motability.co.uk).
Home adaptation: grants Assistance towards housing adaptations for people with permanent and substantial physical disability is available via the Disabled Facilities Grant, for which there is a means test. The OT's role is to assess and advise on what is necessary and appropriate.13 If the disabled person wishes, the OT can make a referral to the local council for a grant. The grant process is lengthy and works cannot be started prior to grant approval. At the present time grants can be mandatory or discretionary. Indications for mandatory grants (a) Access in, out and around the property to the principal rooms: kitchen, bathroom, toilet, living room, bedroom. (b) To ensure the safety of the disabled person and his or her carer. (c) Access to essential facilities: bathing, cooking, lighting, heating. (d) To enable the disabled person to care for dependants or visa versa. Discretionary grants. In some circumstances, a grant may be available for a disabled person's accommodation, welfare or employment needs, e.g. a safe play area for a disabled child or to enable a housebound disabled person to work from home. Other grants. Renovation grants are available for properties in serious disrepair. Home assistance grants are for smaller works. The disabled person should be advised to apply direct to the council. In all cases, the council will need to check that proposed works are necessary, appropriate, reasonable and practical. There are plans to phase out the discretionary grants, renovation grants and home assistance grants. New options include assistance to move to a new property, preferential loans to top-up
the mandatory grant for meeting the costs of a home owner's contribution and equity release loans. Councils will be required to publish their local housing strategy.14 For information on the grants and schemes in operation, apply to the local council or the Home Improvement Agency. Other sources of information for adaptations and equipment Patients who have above the financial savings threshold for grants or compensation cases may wish to seek assistance privately to avoid waiting for assessment and advice. Alternatives could include the following: (a) Private OT: lists obtainable through College of Occupational Therapists (UK), 106-114 Borough High Street, Southwark, London, SE1 1LB, tel. 020 7357 6480; www.cot.co.uk (b) Independent Living Centres and Disability Resource Centres. (c) National exhibitions: Naidex, Independent Living, Care and Rehabilitation. (d) Centre for Accessible Environments for architectural advice, consultancy, training and publications for new build homes, public buildings and spaces. Nutmeg House, 60 Gainsford Street, London SE1 2NY, tel. 020 7357 8182; e-mail [email protected] globalnet.co.uk (e) Disabled Living Foundation - a registered charity that provides information on equipment that promotes independence. It runs an equipment centre, telephone helpline, training events and publishes the Hamilton Index, a comprehensive database of equipment and suppliers (available on subscription), tel. 020 7289 6111; e-mail [email protected] dlf.org.uk; www.dlf.org.uk (f) Care and Repair England supports a network of home improvement agencies dedicated to offering home repair and adaptations for older and disabled people to live independently in their own homes for as long as they wish. 3rd Floor, Bridgford House, Pavilion Road, West Bridgford, Nottingham NG2 5GJ, tel. 0115 982 1527; e-mail [email protected]; www.careandrepair-england.org.uk (g) Joseph Rowntree Foundation for research on housing and social issues. Details of Part M
building standards, lifetime home standards and smart homes are on their website. The Homestead, 40 Water End, York, North Yorkshire YO30 6WP, tel. 01904 629241; e-mail: info® jrf.org.uk; www.jrf.org.uk (h) Mandelstram M. How to get equipment for disability, 3rd edition. London: Jessica Kingsley and Kogan Page for the Disabled Living Foundation, 1993.
Supports for home living Refer to Social Services for: (a) home care assessment, identification of needs, commissioning care through private care agencies for personal care tasks only, 24-hour live-in carer schemes; (b) meals; (c) respite care including sitting service, day care and short or long stays in residential/nursing homes; (d) personal alarm systems; (e) assessment of carer's needs.
CARERS Guideline: The National Strategy for Carers. London: Department of Health, 2001. Online. Available: www.carers.gov.uk
• Six million people in the UK are carers, of these 1.5 million care for more than 20 hours per week. Family and friends provide 70% of the care. The Australian Bureau of Statistics15 estimates that there are 2.3 million carers in Australia, or one in every five households. Of these carers, about 500,000 are providing substantial or full-time care. • Caring imposes a strain on the health of the carer. Twenty per cent have never had a break from caring, and 65% admit that their own health has suffered.16 • Carers need good information on the needs and treatment of the person they are caring for. One study found that only a third of carers had received any information, training or guidance in
PEOPLE WITH LEARNING DISABILITY (UK) OR INTELLECTUAL DISABILITY (AUSTRALIA)
relation to the patient's medication, dressings or other health-care needs.17
Services UK local services have a duty to assess the ability of the carer to provide care, and to increase support services they provide to the household if the carer cannot cope (Carers (Recognition and Services) Act 1995). Parents who care for disabled children can ask for a separate assessment under the Children Act or Section 2 of The Chronically Sick and Disabled Persons' Act. Young people under 18 often act as carers and have the same right to an assessment and to provision of services as an older carer.18
Common problems for carers (a) Poor health and exhaustion. (b) A restricted social life. (c) Damage to their relationships with the person with care needs or with their partner. (d) Emotional problems: -anger with the situation, with the person they are caring for, and with those who provide services; -feeling undervalued, especially by health professionals, if they think they are being patronized; (e) Financial limitations: -loss of earnings; -increased wear and tear on clothing, upholstery, etc; - the need to purchase special items; - increased heating and laundry bills. * Consider whether keeping an index of carers would help to foster an awareness of their needs. * During every consultation with a patient or carer consider: (a) whether the carer and patient know everything they need to know about the illness. Information can, however, only be passed to the carer with the patient's consent;19 (b) whether more is expected of the carer than he or she has been educated for, e.g. simple nursing procedures;
(c) the impact of caring under the categories above. * Discuss with every carer the need for extra support, with a view to referral to Social Services for assessment. * Direct the carer to appropriate local or national voluntary organizations to provide emotional support as well as practical advice (e.g. eligibility for financial benefits or the provision of breaks). Support and advice for carers Australia: Carers Australia: www.carers.asn.au Carer Resource Centres: freecall 1800 242 636 (10 a.m.-4 p.m. Monday to Friday). Provide support and information for carers. Carer Respite Centres: freecall 1800 059 059. Provide emergency assistance 24 hours per day. UK: Carers' National Association: tel. 0345 573369; www.carersuk.demon.co.uk; Helpline 0808 808 7777 (10 a.m.-12 noon and 2 p.m.-4 p.m.).
Princess Royal Trust for Carers: 020 7480 7788; www.carers.org Crossroads - Caring for Carers: tel. 01788 573653; www.crossroads.org.uk Contact a Family: tel. 020 7383 3555.
PEOPLE WITH LEARNING DISABILITY (UK) OR INTELLECTUAL DISABILITY (AUSTRALIA) • Poor communication is a major barrier to care. It can be minimized by people with an intellectual disability, where able, or their carers, providing high quality health information. Clinicians can only make informed assessments and management recommendations if symptoms or signs, such as records of seizures, behaviour, bowel chart or menstruation, and past history, are clearly documented. It is the responsibility of paid carers and their organizations to provide such information.20 • The GP is the professional most in contact with people with an intellectual disability and the one responsible for the provision of medical care. Proactive care is especially important as, at times,
such patients will not seek care or be able to describe subjective experience crucial to assessment and diagnosis. Investigations may be indicated where a clear history is lacking. • The possibility that the aetiology of an individual's disability can be identified becomes more likely as genetic knowledge increases. Accurate diagnosis may have major ramifications for the family and for the person with the disability. • There are high levels of undiagnosed and undermanaged conditions.16 The RCGP has recommended regular medical review21 and some evidence exists to support yearly health review byGPs.18'22 * Refer when the suspicion of learning disability arises. Re-refer if there is weight change, change in behaviour or if the patient's carer or a close relative dies.23 * Check the aetiology of the patient's condition, if it is unknown: (a) Send blood for karyotyping and screening for fragile X. (b) Send urine for screening for inborn errors of metabolism. (c) Consider review by a genetics service.
Areas of concern24 (a) Gastrointestinal disorders -Constipation is present in up to 70%, with the attendant risk of faecal impaction, atonic bowel and obstruction. -Reflux oesophagitis is present in 30% of people with an intellectual disability with an IQ