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13th Edition CHAMBERLAIN’S SYMPTOMS AND SIGNS IN CLINICAL MEDICINE An Introduction to Medical Diagnosis This page intentionally left blank 13th Edition CHAMBERLAIN’S SYMPTOMS AND SIGNS IN CLINICAL MEDICINE An Introduction to Medical Diagnosis Edited by Andrew R Houghton MA(Oxon) DM FRCP(Lond) FRCP(Glasg) Consultant Physician and Cardiologist, Grantham and District Hospital, Grantham, and Visiting Fellow, University of Lincoln, Lincoln, UK David Gray DM MPH BMedSci BM BS FRCP(Lond) FRSPH Reader in Medicine and Honorary Consultant Physician, Department of Cardiovascular Medicine, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre, Nottingham, UK First published in Great Britain in 1936 Second edition 1938 Third edition 1943 Fourth edition 1947 Fifth edition 1952 Sixth edition 1957 Seventh edition 1961 Eighth edition 1967 Ninth edition 1974 Tenth edition 1980 Eleventh edition 1987 Twelfth edition 1997 This thirteenth edition published in 2010 by Hodder Arnold, an imprint of Hodder Education, an Hachette Livre UK Company, 338 Euston Road, London NW1 3BH http://www.hodderarnold.com © 2010 Edward Arnold (Publishers) Ltd All rights reserved Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the publishers or in the case of reprographic production in accordance with the terms of licences issued by the Copyright Licensing Agency In the United Kingdom such licences are issued by the Copyright Licensing Agency: Saffron House, 6-10 Kirby Street, London EC1N 8TS Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the editors nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made In particular (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed Furthermore, dosage schedules are constantly being revised and new sideeffects recognized For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book 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 ISBN-13 978 340 974 254 10 Commissioning Editor: Production Editor: Production Controller: Cover Designer: Indexer: Joanna Koster Jane Tod Kate Harris Amina Dudhia Linda Antoniw Typeset in 10 pt Minion by Phoenix Photosetting, Chatham, Kent Printed and bound in India What you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hodderarnold.com Contents Instructions for companion website Preface List of contributors Chamberlain and his textbook of symptoms and signs Acknowledgements Section A - The Basics Taking a history An approach to the physical examination Devising a differential diagnosis Ordering basic investigations Medical records Presenting cases Section B - Individual Systems 10 11 12 13 14 15 16 17 18 19 20 21 The cardiovascular system The respiratory system The gastrointestinal system The renal system The genitourinary system The nervous system Psychiatric assessment The musculoskeletal system The endocrine system The breast The haematological system Skin, nails and hair The eye Ear, nose and throat Infectious and tropical diseases Section C - Special Situations 22 23 24 25 26 Assessment of the newborn, infants and children The acutely ill patient The patient with impaired consciousness The older patient Death and the dying patient Further reading Index vi vii viii x xii 11 20 23 29 35 40 82 108 137 160 185 209 233 254 269 286 306 329 351 370 390 425 434 438 458 466 467 INSTRUCTIONS FOR COMPANION WEBSITE This book has a companion website available at: http://www.hodderplus.com/chamberlainssymptomsandsigns To access the image library and multiple choice questions included on the website, please register on the website using the following access details: Serial number: kwlt294ndpxm Once you have registered, you will not need the serial number but can log in using the username and password you will create during registration Preface The student of medicine has to learn both the ‘bottom up’ approach of constructing a differential diagnosis from individual clinical findings, and the ‘top down’ approach of learning the key features pertaining to a particular diagnosis In this textbook we have integrated both approaches into a coherent working framework that will assist the reader in preparing for academic and professional examinations, and in everyday practice In so doing, we have remained true to the original intention of E Noble Chamberlain who, in 1936, wrote the following in the preface to the first edition of his textbook: As the title implies, an account has been given of the common symptoms and physical signs of disease, but since his student days the author has felt that these are often wrongly described divorced from diagnosis An attempt has been made, therefore, to take the student a stage further to the visualisation of symptoms and signs as forming a clinical picture of some pathological process In each chapter some of the commoner or more important diseases have been included to illustrate how symptoms and signs are pieced together in the jig-saw puzzle of diagnosis E Noble Chamberlain Symptoms and Signs in Clinical Medicine, 1st edition (1936) We have split this textbook into three sections The first section introduces the basic skills underpinning much of what follows – how to take a history and perform an examination, how to devise a differential diagnosis and select appropriate investigations, and how to record your findings in the case notes and present cases on ward rounds The second section takes a systems-based approach to history taking and examining patients, and also includes information on relevant diagnostic tests and common diagnoses for each system Each chapter begins with the individual ‘building blocks’ of the history and examination, and ends by drawing these elements together into relevant diagnoses A selection of self-assessment questions pertaining to each chapter is also available on the companion website so you can test what you have learnt The third and final section of the book covers ‘special situations’, including the assessment of the newborn, infants and children, the acutely ill patient, the patient with impaired consciousness, the older patient and death and the dying patient We are grateful to all of our contributors for sharing their expertise in the chapters they have written We hope that today’s reader finds the 13th edition of Chamberlain’s Symptoms and Signs in Clinical Medicine to be as useful and informative as previous generations have done since 1936 Andrew R Houghton David Gray 2010 List of contributors Guruprasad P Aithal MD PhD FRCP Consultant Hepatobiliary Physician, Nottingham Digestive Disease Centre; NIHR Biomedical Research Unit, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK David Baldwin MD FRCP Consultant Respiratory Physician, Respiratory Medicine Unit, David Evans Centre, Nottingham University Hospitals NHS Trust, City Campus, Nottingham, UK Christine A Bowman MA FRCP Consultant Physician in Genitourinary Medicine, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK Stuart N Cohen BMedSci (Hons) MMedSci (Clin Ed) MRCP Consultant Dermatologist, Department of Dermatology, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Declan Costello MA MBBS FRCS(ORL-HNS) Specialist Registrar in Otolaryngology, Ear, Nose and Throat Department, John Radcliffe Hospital, Oxford, UK Robert N Davidson MD FRCP DTM&H Consultant Physician in Infection and Tropical Medicine, Department of Infection and Tropical Medicine, Lister Unit, Northwick Park Hospital, Harrow, Middlesex, UK Alastair K Denniston PhD MA MRCP MRCOphth Clinical Lecturer and Honorary Specialist Registrar in Ophthalmology, Academic Unit of Ophthalmology, University of Birmingham, Birmingham and Midland Eye Centre, City Hospital, Birmingham, UK Chris Dewhurst MbChB MRCPCH PgCTLCP Specialist Registrar in Neonatology, Liverpool Women’s Hospital, Liverpool, UK John S C English FRCP Consultant Dermatologist, Department of Dermatology, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Jennifer Eremin MBBS DMRT FRCR Senior Medical Researcher and Former Consultant Clinical Oncologist, United Lincolnshire Hospitals NHS Trust, Lincoln, UK Oleg Eremin MB ChB MD FRACS FRCSEd FRCST(Hon) FMedSci DSc (Hon) Consultant Breast Surgeon and Lead Clinician for Breast Services, United Lincolnshire Hospitals NHS Trust, Lincoln, UK David Gray DM MPH BMedSci BM BS FRCP(Lond) FRSPH Reader in Medicine and Honorary Consultant Physician, Department of Cardiovascular Medicine, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Alan J Hakim MA FRCP Consultant Physician and Rheumatologist, Associate Director for Emergency Medicine and Director of Strategy and Business Improvement, Whipps Cross University Hospital NHS Trust, London, UK Rowan H Harwood MA MSc MD FRCP Consultant Physician in General, Geriatric and Stroke Medicine, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Andrew R Houghton MA(Oxon) DM FRCP(Lond) FRCP(Glasg) Consultant Physician and Cardiologist, Grantham and District Hospital, Grantham, and Visiting Fellow, University of Lincoln, Lincoln, UK Martin R Howard MD FRCP FRCPath Consultant Haematologist York Hospital, and Clinical Senior Lecturer, Hull, York Medical School, Department of Haematology, York Hospital, York, UK List of contributors Prathap Kumar Kanagala MBBS MRCP Specialist Registrar in Cardiology, Department of Medicine, Grantham and District Hospital, Grantham, UK Peter Mansell DM FRCP Associate Professor and Honorary Consultant Physician, Department of Diabetes and Endocrinology, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Philip I Murray PhD FRCP FRCS FRCOphth Professor of Ophthalmology, Academic Unit of Ophthalmology, University of Birmingham, Birmingham and Midland Eye Centre, City Hospital, Birmingham, UK Leena Patel MD FRCPCH MHPE MD Senior Lecturer in Child Health and Honorary Consultant Paediatrician, University of Manchester, Royal Manchester Children’s Hospital, Central Manchester University Hospitals Foundation Trust, Manchester, UK Hina Pattani BSc MBBS MRCP Specialist Registrar in Intensive Care and Respiratory Medicine, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham Basant K Puri MA PhD MB BChir BSc(Hons)MathSci MRCPsych DipStat PGCertMaths MMath Professor and Honorary Consultant in Imaging and Psychiatry, Hammersmith Hospital and Imperial College London, London, UK Venkataraman Subramanian DM MD MRCP Walport Lecturer, Nottingham Digestive Disease Centre: NIHR Biomedical Research Unit, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK Peter Topham MD FRCP Senior Lecturer in Nephrology, John Walls Renal Unit, University Hospitals of Leicester, Leicester, UK Ian H Treasaden MB BS LRCP MRCS FRCPsych LLM Honorary Clinical Senior Lecturer in Psychiatry, Imperial College London, London, and Consultant Forensic Psychiatrist Three Bridges Medium Secure Unit, West London Mental Health NHS Trust, Middlesex, UK Adrian Wills BSc(Hons) MMedSci MD FRCP Consultant Neurologist, Department of Neurosciences, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham Bob Winter DM FRCP FRCA Consultant in Intensive Care Medicine, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK ix The genitourinary system 174 mucosal infection is frequent Most have arthritis or arthralgia as a principal symptom Septic arthritis may be very joint destructive There are two clinical syndromes, which may represent different stages of DGI: ● ● triad of tenosynovitis, dermatitis and polyarthralgia: ● small sterile joint effusions ● blood cultures only positive if taken within two days of acute onset purulent arthritis without associated skin lesions: ● usually affects one joint, often the knee, ankle or wrist N gonorrhoeae can be isolated from aspirated effusion ● blood cultures negative Rare complications include endocarditis, meningitis, osteomyelitis History: ● sexual history – assess recent risks of exposure to N gonorrhoeae ● genital symptoms – urethral/vaginal discharge ● proctitis – pain on defecation, blood or discharge per rectum ● joint symptoms – which affected, pain, swelling, redness, decreased range of movement ● skin lesions ● systemic symptoms, fever and malaise Examination: ● There may be a polyarthralgia (usually affecting knees, wrists, small joints of hand, ankles and elbows) with small sterile effusions or septic arthritis – red, hot, tender joint(s) Figure 11.6 Disseminated gonococcal infection lesion on palm ● Skin lesions start as red macules and become either vesiculopapular then pustular or haemorrhagic then purpuric (especially on palms and soles) Small in number, painful and often close to affected joint, they last 4–5 days but cropping may occur (Fig 11.6) Diagnosis: ● ● ● All patients should have full STI screen Blood cultures Aspirate joint effusions for microscopy and culture Genital ulceration Genital herpes Genital herpes is caused by HSV types and Following primary infection, HSV ascends sensory nerves from the site of initial infection and becomes latent in local sensory ganglia Viral reactivation causes episodes of recurrent herpes or asymptomatic shedding (asymptomatic shedding is common and often the source of onward transmission) Seventyfive per cent of people infected with HSV are not aware that they have genital herpes either because their symptoms are very mild/absent or because the symptoms have been assumed to be due to something else (most commonly thrush) History: ● sexual history including cold sores in sexual partners and oral sex ● previous similar episodes ● painful genital lesions – blisters or ulcers ● may be preceded by prodromal symptoms of tingling in same area or pain in the back, buttock and back of leg ● itching, soreness, discharge which may mimic candidiasis with vulval/perineal/perianal itch, soreness and vaginal/urethral discharge ● swelling of vulva or prepuce ● tender or swollen groin lymph nodes ● dysuria ● difficulty passing urine – may become intensely painful/acute urinary retention ● systemic symptoms – malaise, fever, headache, myalgia Common diagnoses Figure 11.7 Recurrent herpes on penis Examination: ● tender, superficial ulceration: ● women may have extensive involvement of vulva, perineum and cervix associated with labial oedema especially in primary herpes It may be too painful to pass a speculum during an acute episode ● men commonly get ulcers on the glans penis, prepuce or penile shaft (Fig 11.7) ● perianal and intra-anal/rectal lesions can occur ● in recurrent episodes localized small clusters of superficial painful blisters which progress to tender ulcers are common ● tender lymph nodes in groins Complications: ● ● ● ● ● ● psychological adhesions secondary infection of lesions sacral radiculopathy – leading to urinary retention, constipation aseptic meningitis erythema multiforme Diagnosis: ● ● ● Initial provisional diagnosis is based on clinical history and examination Confirmation by HSV culture or PCR on swabs from ulcers/blisters HSV serology is not used routinely in the UK because of the limitations in usefulness and poor predictive value in low prevalence populations Complement fixation tests (CFTs) are of poor specificity in differentiating between HSV type and type Positive CFTs may simply reflect previous perioral cold sores IgM antibody response to primary infection may take many weeks to develop More specific glycoprotein G antibody tests are expensive but better at differentiating between past infections with the two strains However, 50 per cent of primary genital HSV is due to HSV type infection ● Dark ground tests if primary syphilis possible ● Syphilis serology and HIV serology ● Full STI screen when symptoms allow Genital ulcer differential diagnosis: ● genital herpes ● excoriations (e.g secondary to vulvovaginitis) ● syphilis, primary and secondary ● HIV including seroconversion illness ● herpes zoster ● idiopathic ulceration ● erythema multiforme Behỗets disease tropical ulcers Syphilis Syphilis is caused by the spirochaete Treponema pallidum The incidence of syphilis in the UK has increased since 2000 There have been recent outbreaks in both heterosexual and MSM sexual networks Long-term complications occur in 30–40 per cent of untreated individuals and include gummatous disease (a granulomatous nodule with a necrotic centre and fibrous capsule), cardiovascular syphilis and neurosyphilis Pregnant women with infectious syphilis have a high risk of vertical transmission with fetal intrauterine death or congenital syphilis Syphilis significantly increases the risk of HIV transmission Infectious syphilis (early syphilis) This occurs in the first years after infection The infection may be divided into primary, secondary or early latent syphilis on the basis of clinical findings and serology results Primary syphilis History: ● Lesions appear 9–90 days (commonly 2–3 weeks) after exposure: one or more painless chancre(s) develop at the site of inoculation 175 The genitourinary system 176 Figure 11.8 Chancre of primary syphilis ● Concealed lesions may go unnoticed and resolve without treatment within 3–10 weeks Examination: ● ● ● ● classical chancre – round ulcers with a welldefined, indurated margin and a clean base that readily yields exudates on pressure (Fig 11.8) commonly found on the genitals, perianally or in the mouth enlarged regional lymph nodes less classical presentations with painful primary lesions, without associated regional lymphadenopathy, are now common Figure 11.9 Palmar lesions in a patient with secondary syphilis ● ● ● ● Examination (commonest findings): ● Diagnosis: ● ● ● Syphilis serology may take 6–12 weeks to become positive after infection so may be negative in very early infection Spirochetes may be visible in exudate from the base of ulcerative lesions viewed under a highpower, dark ground microscope Multiplex PCR tests that detect syphilis, chancroid, HSV type and HSV type are available from Colindale virus reference laboratory and will become more widely available Secondary syphilis ● ● This usually presents weeks to months after exposure (but may be up to years) Systemic infection that can affect every organ system ● ● ● ● generalized rash wart-like lesions in genital and perianal areas Skin – generalized rash often affecting palms/ soles (Fig 11.9) Appearance of rash varies and different forms may occur together Earliest lesions are rose pink, round and macular Coppery papular lesions then develop Papulosquamous lesions look similar to psoriasis Pustular lesions are rare Ano-genital area – primary chancre may still be visible Localized or diffuse mucocutaneous ulceration of genitals Condylomata lata are wartlike fleshy papular lesions which occur in moist areas (e.g vulval and perianal) Mouth – localized or diffuse mucocutaneous ulceration of mouth Lymph nodes – generalized lymphadenopathy (firm, easily palpated, non-tender lymph nodes) Examination (less common findings): ● ● ● History: ● ulceration of mouth and genitals generalized lymphadenopathy malaise, fever, anorexia headache or signs of focal neurology – suggesting early neurosyphilis ● ● alopecia uveitis and choroidoretinitis meningovascular disease ● headache ● cranial nerve palsies (third, sixth, eighth) ● hemiplegia (uncommon) periostitis (e.g painful tibia) arthritis/arthralgia Common diagnoses CLINICAL PEARL The symptoms of secondary syphilis are very similar to those of HIV seroconversion syndrome and HIV testing should be done in all patients presenting in this way ● ● ● glomerulonephritis hepatitis splenomegaly Diagnosis: ● ● ● Serology strongly positive in secondary syphilis with high titres of venereal disease research laboratory (VDRL) and Treponema pallidum particle agglutination (TPPA); IgM positive Beware the prozone effect! VDRL may falsely appear negative until serum is diluted Dark ground microscopy of syphilitic mucocutaneous lesions positive for spirochetes Late syphilis This is seen in patients presenting more than years after untreated infection History: ● ● ● Examination: ● ● i IMPORTANT All patients suspected of having syphilis should be referred to GUM for diagnosis, treatment and contact tracing Early latent syphilis ● ● ● ● ● This occurs within the first years of infection The patient is infectious but has no obvious signs or symptoms of disease Some patients may pass into this stage following symptoms of primary or secondary syphilis, others never develop obvious symptoms Detected on serological screening Requires treating as for infectious syphilis above If early syphilis is untreated, the disease passes into a late latent phase after years Serious, potentially fatal, long-term complications develop in 30–40 per cent of patients: ● ● ● gummatous lesions in 15 per cent neurological lesions in 10 per cent cardiovascular lesions in 10 per cent Ask about risk factors and sexual history, any known previous episodes of syphilis including treatment and follow-up, previous symptoms suggestive of primary or secondary syphilis Late latent syphilis: ● No signs or symptoms but positive syphilis serology Gummatous syphilis: ● Occurs 3–15 years after untreated primary infection ● A gumma is a granulomatous nodule with a necrotic centre and fibrous capsule The nodules may ulcerate ● Gummas may develop in skin, mucous membranes, bones, cartilage and viscera ● groups of painless, firm, coppery red ulcers ‘tissue paper scarring’ where lesions have healed ‘punched out’ ulcers on the hard and soft palate, tongue, pharynx or nasal septum Neurosyphilis In asymptomatic neurosyphilis there are cerebrospinal fluid (CSF) and serum abnormalities only but it may progress Meningovascular disease (2–7 years after infection) History: ● ● ● ● ● headache visual disturbance limb weakness – may present as a stroke with hemianopia or hemiplegia hearing difficulties convulsions Examination: ● ● third, sixth, seventh and eighth cranial nerve palsies Argyll Robertson pupils – small and unequal, accommodate but not react to light 177 The genitourinary system 178 Parenchymatous disease (10–20 years after untreated initial infection) Chronic progressive meningoencephalitis causing cerebral atrophy – dementia and general paralysis of the insane (GPI) History: ● ● ● may come from carers or relatives – poor memory, dulling of intellect, lack of insight and judgement, delusions and confusion, mood swings convulsions incontinence Cardiovascular syphilis ● May develop 10–30 years after infection in about 10 per cent of untreated patients ● Aortitis: ● coronary artery ostia stenosis ● calcification and aneurysm of ascending aorta ● aortic regurgitation History: ● ● Examination: ● ● ● ● ● assess mental status look for: ● fine tremor of lips, tongue and hands ● dysarthria examine pupils (Argyll Robertson pupils in about 25 per cent) examine tendon reflexes and plantar response (hyperactive tendon reflexes and extensor plantar responses from pyramidal tract lesions) spastic paraplegia Tabes dorsalis (15–25 years after infection) History: ● ● ● ● attacks of severe pains ● acute ‘lightning’ attacks often affecting the legs ● acute onset episodes of epigastric pain and vomiting (gastric crisis) ● symptoms of other tabetic crises due to smooth muscle spasm which can affect rectum, bladder, urethra, kidneys and larynx unsteadiness (ataxia) incontinence impotence Examination: ● ● ● ● ● ● high-stepping gait loss of tendon reflexes and impaired deep pain, vibration and position sense Positive Romberg’s sign (dorsal column degeneration) bilateral ptosis Argyll Robertson pupils in about 50 per cent optic atrophy Charcot’s joints initially asymptomatic later symptoms include: ● dull substernal pain ● angina ● paroxysmal nocturnal dyspnoea (left ventricular failure) ● stridor, cough, dysphagia and Horner’s syndrome (pressure symptoms from the aneurysm) Examination: ● signs of aortic regurgitation Diagnosis of late syphilis: ● ● ● ● clinical findings syphilis serology – raised VDRL and TPPA CSF – raised white cell count, protein and positive VDRL/FTA/TPPA chest X-ray Congenital syphilis Untreated early infectious syphilis in a pregnant woman has a 70–100 per cent risk of transmission to the baby resulting in stillbirth in up to a third of cases Early congenital syphilis – presenting within years of birth Signs include snuffles, vesiculo-bullous lesions, condylomata lata, lymphadenopathy and hepatosplenomegaly Late congenital syphilis – presenting over years old ● Examine: ● face – saddle nose, flat face with frontal bossing, linear scars (rhagades) at corners of mouth ● teeth – Hutchinson’s incisors (small, pegged and centrally notched) and Moon’s molars (rounded) ● eyes – choroido-retinitis ● bones – sabre tibia ● neurological deficits, e.g deafness Common diagnoses CLINICAL PEARL Problems with syphilis serology: ● ● ● ● ● May be negative in early primary infection Low grade positive serology often persists after successful treatment Unable to distinguish syphilis from other treponemal infections, e.g yaws, endemic syphilis and pinta Acute false-positive VDRL occurs after immunizations and with viral infections Chronic false-positive VDRL occurs with autoimmune diseases (sometimes before they declare themselves) and leprosy Lymphogranuloma venereum Lymphogranuloma venereum is an STI caused by C trachomatis serovars L1, L2 and L3 It is highly prevalent in parts of Africa, Asia and South America but it is rare in western Europe Recent outbreaks have been detected in some European cities in MSM (most of whom were also HIV positive) It is a marker of ‘unsafe’ sex and associated with other STIs, HIV and hepatitis C LGV may cause unpleasant symptoms and long-term complications It may be misdiagnosed (e.g as Crohn’s or cancer) History: ● ● Chancroid Chancroid is an STI caused by Haemophilus ducreyi It is uncommon in the UK History: ● ● ● recent sexual contacts in high prevalence areas e.g Africa and Asia (incubation period is 3–10 days) painful ulcers on genitals or perianally tenderness in groins Examination: ● ● ● ● One or more painful ulcers at the site of bacterial inoculation These so called ‘soft sores’, are not indurated, have a necrotic base, ragged undermined edge, and bleed easily Tender groin lymphadenopathy which progresses to form fluctuant buboes Complications are more common in men who may develop phimosis or partial loss of tissue of the glans penis (‘phagedenic ulcer’) Systemic spread does not occur with chancroid Diagnosis: ● ● ● Often made on clinical grounds with exclusion of other causes of genital ulceration Culture of H ducreyi is rarely available PCR tests are very sensitive and usually done as part of the multiplex PCR, which also looks for syphilis and HSV types and sexual history and risk factors painless erosions/ulcers on genitals, perianal region or in mouth – the primary lesion (appears after incubation for 3–30 days) is transient and may be unnoticed Examination: A painless papule/pustule/shallow erosion may be seen at site of bacterial inoculation – the primary lesion is transient and may be unnoticed ● Secondary lesions (usually 10–30 days after primary): ● Inflamed and swollen regional lymph glands, e.g in groin (inguinal syndrome) ● acute haemorrhagic proctitis (anorectal syndrome) ● periadenitis and bubo formation occurs and may ulcerate, discharging pus and creating chronic fistulas ● 15–20 per cent develop the ‘groove sign’: lymph nodes in femoral and inguinal systems separated by inguinal ligament ● systemic spread is associated with fever, arthritis, pneumonitis, perihepatitis ● Tertiary phase lesions: ● proctitis ● acute proctocolitis ● fistulae ● strictures ● chronic granulomatous disfiguring condition of the vulva (‘esthiomene’) Long-term complications: ● lymphoedema of genitals (elephantitis) with persistent suppuration and pyoderma ● association with rectal cancer ● 179 The genitourinary system 180 Diagnosis: ● swabs from ulcers/inflamed rectal mucosa for NAAT (PCR) for Chlamydia If positive, reconfirm and send to reference lab for serotyping ● if bubo present aspirate and send for PCR as above ● serology (e.g CFT, micro-IF) Donovanosis (granuloma inguinale) Donovanosis is caused by Klebsiella granulomatis It is not commonly seen in the UK, and it is seen only in patients with sexual contacts in tropical countries Figure 11.10 Warts at base of penis History: ● ● sexual history and risk factors ano-genital ulcers and enlarged lymph nodes Examination: ● ● ● painless friable ano-genital ulcers or hypertrophic lesions associated with enlarged regional lymph nodes abscesses and pseudo-buboes in tissues overlying the groin lymph nodes untreated the lesions may spontaneously resolve or slowly spread causing local tissue destruction and rarely haematogenous spread to bones and viscera Figure 11.11 Wart on frenulum Diagnosis: ● commonly made by identifying Donovan bodies in smears or tissue biopsies Genital lumps Genital warts Genital warts are caused by human papilloma virus (HPV) There are over 100 strains of HPV, but only a few (mainly types and 11) cause external genital warts These HPV types are not associated with cervical cancer HPV infections are very common About 80 per cent of the sexually active population will carry HPV in their genital tract at some time Most infections (90 per cent) not result in visible warts but are subclinical (they may still be infectious to others) Most infections are self-limiting over time though it may take several months or even years to clear during which the visible warts may recur Figure 11.12 Close-up of wart History: ● ● ● warty lumps on genitals or around anus vaginal discharge genital itch – may occur with warts especially when the virus is becoming more active prior to warts appearing Common diagnoses Examination: ● ● warts may vary in size, number and appearance (Figs 11.10–11.12) usually feel ‘gritty’ to fingertip Molluscum contagiosum Molluscum contagiosum is caused by a pox virus, and is often misdiagnosed as genital warts History: ● ● ● ● small, smooth, umbilicated, papular skin lesions in immunocompromised HIV patients, lesions may be found in other sites (e.g the face) Molluscum contagiosum occurs in children in nongenital locations (e.g the arms) resulting from innocent non-sexual contact The lesions are self-limiting but may cause itch Scratching the lesions may autoinoculate the virus into adjacent skin ● ● ● Public lice look like small brown freckles – you may see them move The eggs attached in the hairs Pubic lice may be found in hairs on the legs and abdomen of more hirsute patients and in eyelashes and eyebrows They not thrive in the denser hair of the head Scabies Scabies is an infestation caused by the Sarcoptes scabiei mite which burrows into skin and then lays its eggs Transmission is by skin to skin contact as may occur in both sexual and non-sexual contact Fomite spread may also occur – mites can survive up to 72 hours away from the body The symptoms may take 4–6 weeks to develop History: ● Infestations Pediculosis pubis – pubic lice/‘crabs’ (Phthirus pubis) Pubic lice (Fig 11.13) may be spread by intimate contact with an infested contact or by shared bedding and clothing of a heavily infested person Sexual contact is not essential pubic itch sometimes patients notice the lice moving or see the eggs attached in the hairs Examination: itchy lumps – in adults these lesions are usually found on the genitals, buttocks, thighs or abdomen Examination: ● History: generalized pruritus (often sparing the head and neck) worse at night, caused by a hypersensitivity reaction to the mite’s excrement Examination: ● ● ● ● Burrows may be seen between the fingers and at the wrists and elbows Lesions in the genital area are often papular or nodular Immunocompromised patients including those with HIV may develop crusted lesions that are highly transmissible (Norwegian scabies) Diagnosis is usually made on the basis of clinical appearance but scrapings from burrows examined under light microscopy can confirm the infestation Blood-borne viruses HIV Primary HIV infection (PHI)/seroconversion illness History: Figure 11.13 Pediculosis pubis – the crab louse ● PHI may be asymptomatic 181 The genitourinary system 182 ● Symptoms of PHI usually occur 2–6 weeks after acquiring HIV and vary in severity from mild and transient to acutely debilitating: ● generalized rash ● generalized lymphadenopathy, pharyngitis (glandular fever-like symptoms) ● acute oro-genital ulceration ● myalgia, arthralgia, fever, headache (flu-like or viral meningitis-like symptoms) ● acute nausea, anorexia and diarrhoea Patients with HIV-related immunodeficiency History: ● ● ● ● ● ● Examination: ● ● ● ● ● ● pyrexia widespread maculo-papular rash superficial ulceration or deeper aphthous ulcers in mouth and ano-genital areas pharyngitis generalized lymphadenopathy and hepatosplenomegaly neck stiffness and photophobia Diagnosis: ● ● ● ● ● ● Early in seroconversion the HIV antibody test may be negative Newer fourth generation tests detect HIV earlier by identifying both HIV IgM and p24 antigen Always specify ‘possible seroconverter’ on request form If tests negative repeat after weeks Patients with HIV usually experience several years without any symptoms following recovery from seroconversion Patients remain infectious during this period and at risk of progression to AIDS and death Since 1996 drug therapy with highly active antiretroviral therapy (HAART) has had a huge impact on life expectancy and quality of life of patients living with HIV With appropriate healthcare HIV-positive patients may now live a near normal lifespan HAART has also reduced the risk of motherto-child HIV transmission from 20–40 per cent (dependent on mother’s health and co-factors for transmission) to less than per cent Undiagnosed and untreated, HIV infection progressively destroys the immune system ● ● ● ● ● prolonged episodes of herpes simplex persistent frequently recurrent candidiasis oral candidiasis odd-looking mouth lesions, e.g oral hairy leucoplakia, Kaposi’s sarcoma recently developed or worsened seborrhoeic dermatitis or psoriasis molluscum contagiosum on the face unexplained weight loss or night sweats persistent diarrhoea gradually increasing shortness of breath and dry cough recurrent bacterial infections including pneumocystis pneumonia (PCP; Fig 11.14) indicator diseases, e.g tuberculosis, lymphoma and PCP Diagnosis: ● It is important to consider testing for HIV in any patient with symptoms that might suggest HIVrelated disease Figure 11.14 Pneumocystis pneumonia in a patient with human immunodeficiency virus infection Summary Hepatitis B ● ● ● ● ● ● The hepatitis B virus (HBV) is a DNA virus that can be easily transmitted by sexual contact It is readily transmitted vertically from mother to child at delivery Other routes of transmission include injecting drug use with shared contaminated equipment, needlestick injury, exposure to infected blood products/tissues Sexually acquired HBV is more common among MSM, intravenous drug users, commercial sex workers, patients from high prevalence areas and their sexual contacts High-risk patients are therefore screened for current HBV infection (surface antigen present) and evidence of previous infection and natural immunity (core antibody) or successful previous vaccination (surface antibody) Patients vulnerable to infection are then offered hepatitis B vaccination HBV infection may cause acute hepatitis with jaundice or remain asymptomatic Patients with chronic hepatitis are at risk of cirrhosis and hepatoma See Viral hepatitis for more details (p 381) Hepatitis C ● The hepatitis C virus (HCV) is much more difficult to transmit sexually or vertically than HBV ● The risk of sexual transmission of HCV is, however, significantly increased in individuals with HIV and in MSM practising high-risk sexual activities e.g ‘fisting’ (insertion of a fist into the sexual partner’s rectum for sexual gratification), which may traumatize the ano-rectal epithelium ● More common routes of HCV transmission include injecting drug use with shared contaminated equipment, needle-stick injury, exposure to infected blood products/tissues ● HCV infection may cause acute hepatitis with jaundice or remain asymptomatic Patients with chronic hepatitis are at risk of cirrhosis and hepatoma ● See Viral hepatitis for more details (p 381) SUMMARY History – common presenting symptoms in patients with an STI or other genitourinary condition: ● ● ● women ● vaginal discharge ● vulval itching and/or soreness ● dyspareunia (pain on intercourse) ● pelvic and lower abdominal pain ● irregular bleeding per vagina men ● urethral discharge ● dysuria ● pain and swelling in the testicles/epididymis both sexes ● painful genital ulceration ● genital warts and other skin lumps ● skin rashes ● itchy skin ● rectal pain or discharge (if receptive anal sex) Sexual history – ask the following details about the last sexual contact: ● ● ● ● ● When was it? What kind of sex? Casual or regular contact? In a higher risk group/known to have an STIs or HIV? Where? (local/UK/abroad) Also ask about: ● ● ● other sexual contacts in the last and 12 months lifetime exposure to higher risk activities condom use Other important history: ● current contraception, current or previous pregnancies and LMP ● previous urinary or genital symptoms? ● other medical conditions that may predispose to genital symptoms 183 184 The genitourinary system Examination indicated: ● ● ● ● – general examination when look for systemic signs look for skin rashes examine inside mouth generalized lymphadenopathy? Genital examination: ● ● examine groin for lymph nodes ?skin rashes/folliculitis in the pubic area/visible pubic lice or their eggs In men: ● ● ● ● ● examine penis, prepuce, scrotum and perianal area look for inflammation and erythema, blisters, ulceration, warts, molluscum contagiosum ?urethral discharge examine the scrotal contents for swelling/pain if history of receptive anal intercourse pass a proctoscope to look for inflammation/ ulceration/pus/bleeding/warts In women: ● ● ● ● examine the vulva, introitus, perineum and perianal area using a vaginal speculum assess vaginal discharge and cervix bimanual PV examination pregnancy test on urine if abdominal pain Investigations – all new patients attending GUM clinics are encouraged to have testing for: ● ● ● ● ● C trachomatis by NAAT on a first-catch urine in men and a cervical swab in women N gonorrhoea both by NAAT and by swabs from urethra, cervix, pharynx and rectum as appropriate for microscopy, culture and sensitivity on selective media syphilis – by serological testing or by dark ground microscopy if a suspicious ulcerative lesion is found HIV – by blood test other tests may be offered on sexual history, symptoms and signs, e.g herpes PCR, microscopy for BV/trichomoniasis/Candida FURTHER READING British Association for Sexual Health and HIV (BASHH) guidelines Available at: www.bashh org/guidelines Pattman R, Snow M, Handy P, et al (eds) 2005 Oxford handbook of genitourinary medicine, HIV and AIDS Oxford: Oxford University Press 12 The nervous system Adrian Wills INTRODUCTION CLINICAL HISTORY In spite of rapid technological advances, the successful diagnosis of neurological disease depends on the ability to take a thorough history from patients, relatives and eyewitnesses Skilled neurologists often have slightly obsessive personalities and may spend long hours perusing the medical records looking for a previously unrecognized nugget of clinical information which reveals the diagnosis The three fundamental questions that need answering are always: Headache ● ● ● Where is the lesion? What is the pathology? What is the treatment? Inexperienced clinicians often order sophisticated (and expensive!) investigations hoping that the diagnosis may be revealed, but sadly this rarely happens Many investigations are relatively sensitive but not necessarily disease specific: for instance, white matter lesions revealed by magnetic resonance imaging (MRI) of the brain have an entirely different significance in younger and elderly patients The neurological examination should be thought of as a form of hypothesis testing, scrutinizing ideas generated by the patient’s history However, students and trainee doctors are often assessed on their ability to perform a competent neurological examination, and in exams such as MRCP PACES, the neurology and cardiology stations are the main pass/fail discriminators in borderline candidates The examination should be practised by rote so that it becomes almost reflexive in nature With experience the most relevant components can be cherrypicked but to accomplish this safely may take years of training This chapter is confined mainly to the discussion of neurological illness in adults; paediatric neurology is a separate specialty and is covered in Chapter 22 Headache is an extremely common symptom and most people experience some form of headache at some stage in their lives There are numerous headache classification systems but the most practical strategy is to differentiate between acute and chronic syndromes: acute headaches may indicate sinister pathology, chronic headaches rarely Acute headaches may be hyperacute (instantaneous) or evolve over hours to days Instantaneous headaches may be extremely severe (‘worst ever’) and associated with loss of consciousness, meningism and focal neurological signs The most common cause is a subarachnoid haemorrhage (Fig 12.1) but there are many others (see Box 12.1) BOX 12.1 CAUSES OF INSTANTANEOUS HEADACHE (LIFE-THREATENING CAUSES IN BOLD) ● ● ● ● ● ● Subarachnoid haemorrhage Venous sinus thrombosis Cerebral haemorrhage (especially posterior fossa) Phaeochromocytoma Low pressure headache Thunderclap and ice pick headaches Headaches that evolve over days to hours may be sinister, particularly in a headache-naïve patient, although it is important to remember that even a first attack of migraine may lead to an urgent hospital admission Meningism (neck stiffness, photophobia) demands urgent investigation and may be caused by bacterial (including tuberculosis) and viral meningitis or encephalitis (also associated with altered mentation, seizures and focal neurological signs) Migraine (throbbing headache), 186 The nervous system Aneurysm Figure 12.1 T2-weighted magnetic resonance image showing a large aneurysm in the right temporal lobe often lasting several hours, is usually paroxysmal and associated with photophobia, visual symptoms (including scotomas, phosphenes and fortification spectra), phonophobia, nausea and/or vomiting and a desire to lie still or even sleep This contrasts with other idiopathic paroxysmal headache disorders such as cluster headache, in which the pain is relieved by movement and is associated with autonomic features (see Box 12.2) BOX 12.2 SYMPTOMS IN AUTONOMIC HEADACHE (INCLUDING CLUSTER) ● ● ● ● ● Eye watering Nasal stuffiness Horner’s syndrome (paroxysmal) Isolated ptosis Conjunctival injection Chronic headaches are usually benign and most often caused by tension headache or chronic daily headache (with or without associated analgesic overuse) The pain may be quite diffuse, nondescript, maximal over the vertex with no particular exacerbating or relieving factors ‘Red flags’ that should prompt further investigation include: ● ● ● ● ● pain worsened by lying flat, or pain that wakes the patient at night focal neurological symptoms/signs visual obscurations (transient blurring on standing – may indicate imminent coning) jaw claudication, shoulder aching and scalp tenderness (temporal arteritis in elderly patients) loss of visual acuity or haloes (glaucoma) Acute glaucoma may cause marked systemic upset including headache, nausea, vomiting and malaise Other caused of chronic headache are shown in Box 12.3 Trigeminal neuralgia is a particularly unpleasant lancinating pain (lasting seconds), mainly affecting the cheek and precipitated by speaking or touching the affected area Low-pressure headaches are relatively common after neurosurgical shunt insertion or lumbar puncture (headache worse on standing up) but can occur ‘spontaneously’ because of leakage of cerebrospinal fluid (CSF) via the meninges (usually spinal) Clinical history BOX 12.3 RARER CAUSES OF CHRONIC HEADACHE ● ● ● ● ● ● ● ● ● ● ● Chronic carbon monoxide poisoning Obstructive sleep apnoea Hypercapnia Drugs Malignant hypertension (including eclampsia) Idiopathic intracranial hypertension Low pressure headaches Venous sinus thrombosis Post-traumatic (medico-legal cases) Subdural haematoma Polycythaemia Loss of consciousness The most common dilemma in everyday practice is differentiating between: BOX 12.4 RARER CAUSES OF LOSS OF CONSCIOUSNESS ● ● ● ● ● more likely to be benign in younger patients but note that structural heart disease and arrhythmias are not confined to elderly people Patients may use the term ‘blackout’ and this covers a wide range of symptoms including: loss of consciousness pre-syncope (may be a white out) paroxysmal visual loss vertigo or dizziness falls ● ● ● ● ● ● seizure disorders cardiovascular syncope non-epileptic attacks (pseudoseizures) The comments of an eyewitness are absolutely crucial; without this it is often impossible to make a diagnosis, although this is often revealed with the passage of time (watchful waiting) Table 12.1 shows the main historical discriminators Other rarer causes are shown in Box 12.4 Syncopal attacks are Vertebro-basilar strokes, transient ischaemic attacks (TIAs) and migraine Hydrocephalic attacks Carotid sinus sensitivity Insulinoma Poor diabetes control ● ● Drop attacks may be idiopathic (sudden fall due to loss of tone in the legs without loss of consciousness) or precipitated by emotion e.g laughter (cataplexy) often associated with other features of narcolepsy including vivid dreams and sleep paralysis CLINICAL PEARL Table 12.1 Distinguishing between epilepsy, syncope and non-epileptic attacks Epilepsy Syncope Non-epileptic attack disorder Pallor – + – Prodrome – + – Situational – + + stress orthostatic Incontinence ++ + + Lateral tongue biting ++ – – Jerking ++ + brief prolonged +++ very prolonged Pelvic thrusting – – +++ Gaze aversion – – +++ Nausea – ++ – ● ● ● Vertebro-basilar insufficiency and thoracic outlet syndrome are both rare conditions; try to think of alternative common diagnoses when a patient complains of dizziness on head movement or tingling in the hand (e.g benign positional vertigo and carpal tunnel syndrome) Carpal tunnel syndrome can cause symptoms involving the whole arm Isolated vertigo is rarely caused by migraine or epilepsy Weakness Hyperacute weakness is usually caused by vascular disease (stroke) and is most commonly unilateral, reflecting transient or permanent loss of perfusion in the cerebral hemispheres or brainstem TIAs are classically defined as lasting up to 24 hours but in 187 188 The nervous system clinical practice are usually of much shorter duration Bilateral weakness (usually lower limb) or quadriplegia is a marker of spinal cord disease Acute weakness Acute weakness (evolving over hours to days) may also be unilateral or paraparetic, reflecting inflammatory or neoplastic disease involving the brain and spinal cord, respectively Rapidly evolving quadriplegia may be associated with sensory symptoms (Guillain–Barré syndrome/diphtheria) or not (myasthenic crisis, botulism, polymyositis, polio) Most of these conditions can also lead to diaphragmatic involvement and bulbar dysfunction Chronic or progressive weakness Chronic or progressive weakness may be indicative of a range of organic (Table 12.2) and non-organic pathologies (chronic fatigue syndrome/abnormal illness behaviour) Proximal weakness presents with difficulty on stairs, getting out of a chair or combing hair Distal weakness usually manifests as ‘trips’ over pavements or uneven surfaces or difficulty doing up buttons, writing, etc Fatiguability (as a symptom rather than sign) can be a remarkably unhelpful discriminator and is seen in a range of conditions other than myasthenia gravis Sensory symptoms Positive (tingling, dysaesthesia, paraesthesia) and negative (numbness) sensory symptoms can reflect pathology anywhere in the sensory pathways The presence of positive sensory symptoms can be useful in discriminating between genetic (Charcot–Marie Tooth, CMT) and acquired (chronic inflammatory demyelinating polyneuropathy, CIDP) neuropathies as well as epilepsy/migraine (positive) versus stroke (negative) Neuropathic pain (cf diabetes) is often lower limb predominant and described as burning, stinging or throbbing Allodynia is defined as pain caused by normally non-painful stimuli (e.g touch), whereas hyperpathia implies a lowered pain threshold Bladder symptoms Urinary urgency, frequency (see Chapter 10) and nocturia are associated with an ‘upper motor neurone (UMN)’ bladder and characteristic of spinal cord disease, especially demyelination A ‘neuropathic’ bladder (cauda equina, rarely caused by neuropathy) causes loss of bladder sensation with dribbling incontinence Cord transection (usually traumatic) leads to complete loss of voluntary bladder control although automatic reflexive manoeuvres (e.g stroking the thigh) can be utilized to assist bladder emptying Frontal lobe disorders may lead to loss of inhibition with urination taking place in socially embarrassing (for the relatives rather than patient) situations Autonomic symptoms A variety of neurological pathologies (Box 12.5) may lead to autonomic dysfunction and consequent symptoms including: Table 12.2 Causes of chronic progressive weakness (with associated features) Distribution Cranial nerve symptoms Bladder symptoms Sensory symptoms Neuropathy Distal Rare Rare Common Myopathy Proximal Unusual Rare Rare Neuromuscular junction Proximal Common Rare Rare Radiculopathy Asymmetrical Rare Common (lumbosacral) Common (pain) Anterior horn Asymmetrical Common Rare Rare Spinal cord Pyramidal Never Common Common Brainstem Pyramidal Common Rare Common Cerebral cortex Pyramidal Common Rare (cf frontal) Common .. .13 th Edition CHAMBERLAIN S SYMPTOMS AND SIGNS IN CLINICAL MEDICINE An Introduction to Medical Diagnosis This page intentionally left blank 13 th Edition CHAMBERLAIN S SYMPTOMS AND SIGNS IN CLINICAL. .. physical examination Devising a differential diagnosis Ordering basic investigations Medical records Presenting cases Section B - Individual Systems 10 11 12 13 14 15 16 17 18 19 20 21 The cardiovascular... Campus, Nottingham, UK ix Chamberlain and his textbook of symptoms and signs The first edition of Symptoms and Signs in Clinical Medicine: An Introduction to Medical Diagnosis was published in 19 36