Macleod's Clinical Diagnosis

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Macleod’sDiagnosis Clinical 2nd Edition

Alan G Japp meb ksf MBChB(Hons) BSc(Hons) MRCP PhD Consultant Cardiologist, Royal Infirmary of Edinburgh; Honorary Clinical Senior Lecturer, University of Edinburgh UK Colin Robertson BA(Hons) MBChB FRCPGlas FRCSEd FICP(Hon)ooks eeFSAScot com Honorary Professor of Accident and Emergency eb oks Medicine and Surgery, me o om University of Edinburgh UK

Co-authors Rohana J Wright MBChB MD FRCPEd Consultant Physician, St John’s Hospital, Livingston, and Edinburgh Centre for Endocrinologyo om andooksfree. Diabetes, Edinburgh, UK Matthew J Reed MA(Cantab) MB BChir MRCS FCEM MD Consultant and NRS Career Researcher Clinician in Emergency Medicine, Royal Infirmary of Edinburgh; Honorary Reader, University of Ed nburgh UK Andrew Robson MA (Cantab) BM BCh FRCS PhD Specialist Registrar in General Surgery, Royalooks Infirmary of e. Edinburgh, o UK

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First edition 2013 Second edition 2018

ISBN 9780702069611 International ISBN 9780702069628

Notices Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence orooksfre otherwise, or from any c use or operation of any methods, products, instructions, or ideas contained in the material herein. booksfre

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Printed in Poland Last digit is the print numbero 9 8 7 6 5 4 3 2 1 Contentsme

Preface vii Acknowledgements viii Abbreviations ix

SECTION fr1 PRINCIPLES om OF CLINICAL ASSESSMENT 1 1. What’s in a diagnosis? 3 2. Assessing patients: a practical guide 7 3. The diagnostic processeb fr 17

SECTION 2 ASSESSMENT OF COMMON PRESENTING PROBLEMS 22

4. Abdominal pain 24 5. comBreast lump 46 6. Chest pain 50 7. Coma and altered consciousness 72 8. Confusion: delirium and odementia sf 78 9. Diarrhoea 90 10. Dizziness 96 11. Dysphagia 108 12. Dyspnoea 112 13. Fatiguem 130 14. Fever 138 15. Gastrointestinal haemorrhage: haematemesisee and rectal bleeding 150 16. Haematuria 158 17. Haemoptysis 162k 18. Headache 166 19. Jaundice 174 vi • CONTENTS

e20. Joint swelling 184 21. Leg swelling 190s 22. Limb weakness 196 23. Low back pain 208 24. Mobility problems: falls and immobility 214 25. Nausea and vomitingm 222 26. Palpitation 232 27. Rash:om acute generalized skin eruption 240 28 Red eye 250 29. Scrotal swelling 258 30. Shock 264s 31. Transient loss of consciousness: syncope and seizures 270 32. Urinary incontinence 282 33. Vaginal bleeding 288 34. Weight loss m b o 294

Appendix 301 Indexom 305 Prefacem

‘Ninety per cent of diagnoses are made from examination have been marginalized by novel the history.’ imaging techniques and disease biomarkers. ‘Clinical examination is the cornerstone of Nevertheless, a focused clinical examination is assessment.’ critical to recognizing the sick patient, raising red flags identifying unsuspected problems and, These, or similar platitudes, will be familiar to in some cases, revealing signs that cannot be most students in clinical training. Many, however, identified with tests (for example, the mental notice a ‘disconnect’ between the importance state examination). ascribed to basic clinical skills during teaching Our aim is to show you how to use your core andoo the apparent s r reliance on m sophisticated inves- clinical skills to maximum advantage. We offer tigations in the parallel world of clinical practice. a grounded and realistic approach to clinical Modern diagnostics have radically altered the diagnosis with no bias towards any particular face of medical practice; clinical trainingmebo is still element sfree.com of the assessment. Wheremeboo appropriate, sf catching up. We recognize that teachers and we acknowledge the limitations of the history textbooks frequently fall into the trap of eulogizing and examination and direct you to the necessary clinical assessment rather than explaining its investigation. We also highlight those instances actual role in contemporary diagnosis. where diagnosis is critically dependent on basic Yet we come to praise the clinical assessment, clinical assessment, thereby demonstrating its not to bury it The history may not, by itself, vital and enduring importance. We wish you deliver the diagnosis in 90% of cases but it every success in your training and practice, and is essential in all cases to generate a logical hope that this book provides at least some small differential diagnosis and to guide rational measure of assistance. investigation and treatment. In many ‘developed’ Alan Japp countries,ooksf some ee so-called com classical physica Colin Robertson signs are rare and certain aspects of the clinicalboo sfree com Edinburgh, 2018 eboo f Acknowledgementsm

On behalf of the editors and authors, I would Edinburgh (Chapter 28, Red eye); Dr Lydia Ash, like to thank Laurence Hunter for encouraging Specialty Registrar, Obstetrics & Gynaecology, and facilitating this new edition; and Helen Leng Edinburgh (Chapter 33, Vaginal bleeding), Mr for once again providing the perfect blend of Andrew Duckworth, Specialty Registrar, Ortho- tolerance, support and discipline. We also thank paedic Surgery, Edinburgh (Chapter 20, Joint everyone who volunteered suggestions and swelling) and Mr Neil Maitra, Locum Consultant ideas for the 2nd edition, particularly Dr Vicky Urologist, Lanarkshire (Chapter 16, Haematuria) Tallen ire, Dr Michael MacMahon and Dr Dean and everyone else who has volunteered ideas, Kerslake. Finally we gratefully acknowledge a comments, assistance or a friendly ear. valuable contribution to individual chapters from ooksfAJ booksDr Mark Wright, ree.com Consultant Ophthalmologist, ebo sfree.com Abbreviationsme

Abbreviations that do not appear in this list are spelled out in the main text. ABCDE airway, breathing, circulation, DMARD disease-modifying anti-rheumatic disability exposure drug ABG arterial blood gas ECG electrocardiogram/ ACE angiotensin-converting enzyme electrocardiography ACPA anti-citrullinated protein antibody EEG electroencephalogram/ ACTH adrenocorticotrophic hormone frelectroencephalography .com AIDS acquired immunodeficiency ENA extractable nuclear antigen syndrome ENT ear, nose and throat ALPooalkaline ree.com phosphatase ERCP endoscopic retrograde ALT alanine aminotransferase cholangiopancreatography ANA antinuclear antibody ESR erythrocyte sedimentation rate ANCA antineutrophil cytoplasmic antibody FBC full blood count meb APTT activated partial thromboplastin FiO2 fraction of inspired oxygen time GCS Glasgow Coma Scale (score) ASMA anti-smooth muscle antibody GFR glomerular filtration rate ASO anti-streptolysin O GGT gamma-glutamyl transferase AST aspartate aminotransferase GI gastrointestinal AXR abdominal X-ray GP general practitioner BMI body mass index GU genitourinary BP blood pressure Hb haemoglobin bpm beats per minute hCGsfhuman com chorionic gonadotrophin BS breath sound HIV human immunodeficiency virus CBG capillary blood glucose HR heart rate CLOocampylobacter free com-like organism ICP intracranial pressure CK creatine kinase ICU intensive care unit CKD chronic kidney disease ID infectious disease CNS central nervous system IM intramuscular(ly) m ok COPD chronic obstructive pulmonary INR international normalized ratio disease IV intravenous(ly) CPET cardiopulmonary exercise test IVU intravenous urogram/urography CRP C-reactive protein JVP jugular venous pulse CRT capillary refill time LDH lactate dehydrogenase CSF cerebrospinal fluid LFT liver function test CSU catheter specimen of urine LIF left iliac fossa CT computed tomogram/tomography LKMsfliver .com kidney microsomal CTPA computed tomographic pulmonary (antibodies) angiography LLQ left lower quadrant CVPocentral ree.co venous pressure LP lumbar puncture CXR chest X-ray LUQ left upper quadrant DC direct current MRA magnetic resonancem angiography x • ABBREVIATIONS

MRCP magnetic resonance RLQ right lower quadrant cholangiopancreatography RR respiratory rate MRI magnetic resonance imaging RUQ right upper quadrant

MSU midstream urine (specimen) SaO2 oxygen saturation of arterial blood NSAID non-steroidal anti-inflammatory drug SC subcutaneous(ly)

PaCOoo2 partial re pressure of carbon dioxide SIRS systemic inflammatory response in arterial blood syndrome

PaO2 partial pressure of oxygen in arterial SLE systemic lupus erythematosus

blood m boSpO sf2 peripheral (capillary)m oxygen b ok PCR polymerase chain reaction saturation PEFR peak expiratory flow rate SSRI selective serotonin re-uptake PET positron emission tomography inhibitor PFTs pulmonary function tests SVT supraventricular tachycardia PR per rectum TFT thyroid function test PRN pro re nata; whenever required TIA transient ischaemic attack PSA prostate-specific antigen TNF tumour necrosis factor PT prothrombin time TWI T wave inversion PV per vaginam Usfr+E urea .com and electrolytes qSOFA quick Sepsis Related Organ Failure UGIE upper gastrointestinal endoscopy oAssessment ree com UMN upper motor neuron QTc corrected QT interval USS ultrasound scan RF rheumatoid factor VT ventricular tachycardia RIF right iliac fossa WBC white blood countme o Section 1 Principles of clinical assessment m sf me ks

1. What’s in a diagnosis? 3 2. Assessingc patients: a practical guide 7 3. The diagnostic process 17 This page intentionally lefto blank What’s ins a diagnosis? 1ks

From differential diagnosis next step would be to establish the cause of to final diagnosis the anaemia. If subsequent laboratory investigations revealed evidence of iron deficiency, you A diagnosis is simply shorthand for a patient’s need to determine the cause. Gastrointestinal condition or disease process. The ability to investigations might uncover a gastric tumour diagnose accurately is fundamental to clinical but, even then, further assessment would still practice Only with a correct diagnosis, or a be required to establish a tissue diagnosis and short-list of possible diagnoses, can you: stage the tumour. The eventual ‘final diagnosis • formulate an appropriate sequence of might be of iron-deficiency anaemia secondary to investigationsoks ree.c m blood loss from a T3, N1, M1 gastric carcinoma • begin correct treatment and assess its with metastasis to liver and peritoneum. Clearly, effectiveness the diagnosis of ‘anaemia’ would have been • give an informed prognosis and make grossly inadequate. follow-up arrangements. m sfreeSome conditions, com especiallymebooksf functional disor- Producing a differential diagnosis – a list of ders such as irritable bowel syndrome, lack a diagnoses, placed in order of likelihood, which definitive confirmatory test; here diagnosis relies may be causing the presentation – is a stepping- upon recognising characteristic clinical features stone to the final diagnosis. This list may be and ruling out alternative diagnoses – especially lengthy at the outset of assessment but will serious or life-threatening conditions. Such become progressively shorter as you accumu- disorders are often referred to as diagnoses of late information about the patient’s condition exclusion. through your history-taking, examination and investigations. When one diagnosis begins to Probability and risk stand out from the rest as the most likely cause Diagnostic tests are inherently imperfect, so ofooksfree.com the patient’s presentation, it is often referred regard diagnoses as statements of probability to as the working diagnosis. Investigations are rather than hard facts. In practice, a disease is then directed toward confirming (or refuting) this ‘ruled in’ when the probability of it being present condition and thereby arriving at a finalmebo diagnosis. is deemed free.com to be sufficientlymebo high, and ‘ruled This entire process may happen very rapidly; for out’ when the probability is sufficiently low. example, establishing a final diagnosis of acute The degree of ce tainty required depends on ST segment elevation myocardial infarction in a factors such as the consequences of missing the patient presenting with acute chest pain should particular diagnosis, the side-effects of treatment usually take less than 10 minutes. and the risks of further testing. Doctors must Frequently the identification of an abnormality not become so ‘paralysed’ by the implications of is only the first step in the diagnostic process and m ssing a diagnosis that they admit the patient additional assessment is required to characterize unnecessarily to hospital and/or investigate to a condition in greater detail or search for an levels that are not in the patient’s best inte ests underlying cause. For example, in a middle-aged and are unacceptable because of time, expense manooksfree.com presenting with fatigue, you might identify and intrinsic risk, e.g. radiation exposure. On anaemia as the cause of his symptoms, but the the other hand, a high threshold of certainty, diagnostic process would not stop there. The i.e. very low probability, is required to exclude mebo ksfree.com mebooksf What’s in a diagnosis? 4

potentially life-threatening conditions. If the situ- Special situations ation is explained appropriately, most patients will accept tests that yield a diagnostic accu- Medically unexplained symptoms racy of less than 1% for acute life-threatening Sometimes it is difficult to correlate patients’ conditions. symptoms with a specific disease This does not ooksfreThe current diagnostic m approach to suba- mean that the symptoms with which they present rachnoid haemorrhage (SAH) illustrates this. are factitious or that they are malingering – merely For a middle-aged patient who presents, fully that we are unable to provide a physical cause conscious, with a history of sudden (withinmeb a few re meboo for the symptoms. For patients in primary care, seconds) onset of ‘the worst headache ever’, the over 70% have symptoms that cannot be readily chances of a diagnosis of SAH are approximately explained by a specific diagnosis. Nevertheless, 10–12%. The presence of some clinical findings, the symptoms are very real to the patient and e.g. photophobia, neck stiffness, cranial nerve one of the major challenges, intellectually and palsies, subhyaloid haemorrhage – will increase practically, is to recognize which patients have these chances markedly but these features may physical disease. take time to develop. Even if clinical examination Clusters of symptoms in recognisable patterns, is unequivocally normal, the chances of SAH are in the absence of physical and investigational 8–10% Currently, there is no simple bedside test abnormalities, are called functional syndromes for SAH and the initial investigation is normally (Table 1.1). a non-contrast CT scan. A positive scan will ooksfree com In general, the greater the number of symp- prompt appropriate treatment, possibly involving toms, the greater the likelihood that there is a neurosurgical or neuroradiological intervention. psychological component to the presentation. A negative scan does not, however, exclude meboRemember sfree.com that patients with chronicmeb disease oks are an SAH. The accuracy of CT scanning in more likely to demonstrate psychological aspects detecting SAH depends upon the experience of their condition, especially depression, which of the reporting individual, the nature of the may, in turn, affect the mode of presentation. scanner (principally, its resolution) and the time Avoiding excessive and inappropriate investigation interval between the onset of symptoms and the scan (accuracy falls with time). A scan 1 performed within 12 hours by most modern Table 1 1 Common functional syndromes scanners and interpreted by a skilled radiolo- Syndrome Symptoms gist has a diagnostic accuracy of approximately 2 98% But, given the morbidity and mortality of Chronic fatigue Persistent fatigue unrecognized and untreated SAH, even this syndrome level of diagnostic accuracy is inadequate. Irritable bowel Abdominal pain, altered bowel booksFor this reason, ree.com patients with a negative CT syndrome habit (diarrhoea or constipation) and abdominal bloating scan have a lumbar puncture. The CSF obtained must be examined by spectrophotometrymebo in Chronic f e pain comPersistent painmeb in one or more the laboratory for xanthochromia (direct visual syndrome parts of the body, sometimes following injury but which inspection of the fluid is insufficiently accurate). outlasts the original trauma2 Xanthochromia (produced from haemoglobin Fibromyalgia Pain in the axial skeleton with breakdown within the CSF) takes some time trigger points (tender areas in to develop and the sensitivity of this test peaks the muscles)2 at about 12 hours after symptom onset. The Chronic back Pain, muscle tension or stiffness combination of a negative CT scan performed pain localized below the costal margin within 12 hours of symptom onset and normal and above the inferior gluteal CSF findings at 12 hours reduces the chances folds, with or without leg pain2 of the patient’s symptoms being caused by an 1 SAH to well below 1% – a level of probability In all cases, physical examination and investigation fail to reveal ooksfree.com an underlying physical cause. acceptable to most clinicians and, if appropriately 2Symptoms must have lasted more than 3 months. explained, to their patient. ebo fre m e o k What’s in a diagnosis? 5

10 1e Organics cause m 8

4 3-year incidence (%) 2

Fatigue Oedema Dizziness Insomnia Chest pain Headache Back painDyspnoeaook Numbness

Abdominal pain Fig. 1.1 Common symptoms and disease. (From Douglas JG, Nicol F, Robertson C. Macleod’s Clinicalm Examination, 13th edn. Edinburgh: Churchill Livingstone, 2013.)

specific situations this may be life-saving as Box 1.1 Symptoms and their relationship to well as diagnostic. In any patient with altered physical disease consciousness or acute neurological dysfunction More commonly without a clearly identifiable cause, two conditions • Chest pain need to be excluded and treated immediately. • Breathlessness sfree.coHypoglycaemia can mimic conditions such • Syncope as epilepsy and hemiplegia. Check the CBG. • Abdominaloksf pain e c If the value is low, take a formal blood sample Less commonly for laboratory blood glucose determination, but • Fatigue do not wait for this result before giving treat- • Back pain ment – give glucose or glucagon immediately. • Headache If hypoglycaemia is the causemebooks of the patient’s • Dizziness symptoms, response will normally occur within 5–10 minutes (rarely, in cases where there has been severe, prolonged hypoglycaemia, this may to ‘exclude’ diagnoses is important, especially if take longer and residual neurological deficit may patients have no specific ‘red flags’ in relation to persist). their history, they are not in a recognized at-risk Opioid intoxication is usually associated with group, and there are no abnormalities on clinical al ered consciousness, reduced respiratory ra e examination and simple bedside tests (Fig. 1.1 and depth, and small pupils. The diagnosis is and Box 1.1). rarely difficult in younger patients with a history or ksfree co other features of illicit drug use. However, these Treatment before diagnosis features are not always present, and chronic Sometimes, accurate diagnosis depends upon opioid toxicity may develop over hours/days, the patient’s response to treatment. In a few particularly in elderly patients or those with renal meb sfree com mebooksf What’s in a diagnosis? 6 impairment Naloxone is a highly specific opioid to medical conditions through the media and antagonist with no agonist activity. Give 0.8 mg the Internet. A patient who has previously had naloxone (SC, IM or IV) immediately. If there is a condition that has recurred, e.g. asthma or any response, further doses of naloxone will be urinary tract infection, or who has a flare-up required until no further reversal is achieved. of a chronic condition, e.g. inflammatory bowel Rememberooksfre that the half-life m of naloxone is much disease, will often present in this way. Remember shorter than that of the opioid that has been that many patients will be worrying about a spe- taken, so repeated stat. doses or an infusion cific diagnosis causing their presenting complaint. are likely to be needed. meboThis sfre is particularly the case mebooksffor breast lumps, There is one other situation where treatment is rectal bleeding and chronic headache, where necessary before, or to achieve, diagnosis. It is the perception may be that the only possible unnecessary, unhelpful and inhumane to leave a diagnosis is cancer. patient in pain from whatever cause. Put yourself Self-diagnosis may also cause a delay in in the patient’s place. There is never any seeking medical help because the patient does indication to withhold analgesia from a patient not appreciate the significance of a symptom in pain. Concerns that you will ‘mask’ clinical or subconsciously may not want to consider signs, e.g. by giving opioids to a patient with the possibility of serious disease. Common an ‘acute abdomen, encourage opioid toler- examples include attributing ischaemic chest ance or addiction, and impair informed consent pain to ‘indigestion’ and assuming that rectal areooksfree completely unfounded. com In fact, diagnostic bleeding is due to haemorrhoids. accuracy is improved by making the patient One way of initially handling patients who come more co-operative, aiding the performance of with a diagnosis is to let them express this openly investigations such as ultrasoundmebo and pain and s then ree to acknowledge com theirmeb concerns. oksf You relief brings additional benefits in reducing must respect these (indeed, the patient may catecholamine stimulation, improving respiratory well be right) while taking care not to miss a and cardiovascular function. The ‘pain ladder’ more likely diagnosis. In particular, do not take approach is useful, but for patients in acute or shortcuts with any of the components of history severe pain, IV opioids titrated to the clinical taking, examination and investigation that may response are usually needed. be required. Patients with rare or unusual diseases often know much more about their condition than you The patient who comes with a diagnosis Use this golden opportunity. There is no loss Many patients have an idea of their own condi- of face in admitting your ignorance. Patients tionoo and, sfindeed, e.commay begin the consultation by will respect you for your honesty and you can telling you their perceived diagnosis. In part this learn much from them about the diseasebooksf and relates to improved education, greater exposureebo its sfree treatment comand effects. Assessing patients: a practical guide oksfre 2 Introduction circulation, disability, exposure [ABCDE] assessment’) for life-threatening disorders Before you can diagnose patients you must first and major derangements meof physiology ooksf obtain the necessary clinical and investigative • patients who are stable, including those information. Diagnostic success depends upon initially assessed by the ABCDE approach, the accuracy and completeness of this initial data should have a full history and clinical gathering so your history-taking and examination examination, as outlined below (‘full clinical skills are crucial During clinical training, you may assessment’), alongside basic tests relevant have been taught a fairly idealized and rigid to the specific presentation ‘method’ of patient assessment. However, in • the approach to frail, elderly patients may everyday practice, a more flexible, fluid approach need to be modified to take account is preferable; this will allow you to adapt to of differences in the nature of illness the c inical situation and acquire the essential presentation, e.g. multi- versus single organ informationooksfree in the most com efficient manner pathology; significant functional decline Traditionally, the assessment of patients has secondary to minor illness. boo been divided into two distinct phases: • the clinical assessment: history andmeb o ree.com physical examination Rapid assessment of the sick patient • diagnostic investigations The ABCDE assessment (see Clinical tool, p. 8) At least in the hospital setting, this distinction combines prompt identification of life-threatening is highly artificial due to the easy and real-time pathology with immediate management of any availability of basic tests such as ECG, CXR, abnormalities detected, prioritising those that are glucose meter reading and ABG, and routine most rapidly fatal. Take an ABCDE approach if laboratory blood tests such as FBC, U+E and the patient: LFTs. Wherever appropriate, these simple tests • appears unwell or is unresponsive should be carried out in tandem with the clinical • exhibits evidence of acute physiological assessment to form a ‘routine patient work-up derangement on basic observations (HR, The information from all of these sources is com- ooksfree com RR, BP, arterial oxygen saturation [SpO2], bined to form a working or differential diagnosis. temperature) Where necessary, further targeted investigation • has features of a serious acute problem in can then be undertaken to confirm themebo suspected any free.com organ system. m book diagnosis, narrow the differential diagnosis, e.g. Repeat the process to assess the effects of exclude high-risk conditions, inform prognosis interventions or in the event of any further and guide management deterioration. Protect the spine at all times if Thus, in this book, we advocate the following there is any suspicion of recent trauma. system for patient evaluation: • the routine work-up: history, physical examination and basic tests Routine assessment of the stable patient: • targeted supplementary investigations. the full clinical assessment The optimal approach to the routine work-up Use Macleod’s Clinical Examination for a varies, depending on the stability and illness comprehensive guide to history taking and severityooksfree of the patient: c systems-based clinical examination. The following • acutely unwell patients require a rapid, is an aide-mémoire with an emphasis on practical targeted evaluation (‘airway, breathing, tips and avoidance of common pitfalls. me fre com mebook Assessing patients: a practical guide 8

Clinical tool The ABCDE assessment What to look for How to respond A Aioksfre way m A1 Ask ‘How are you feeling?’ If signs of obstruction: If patient can speak normally, airway is patent – move • Get help! straight to B. e • Try simple airway manoeuvres: head tilt/chin lift; jaw thrust (Fig. 2.1) me A2 Assess for airway obstruction • Remove foreign bodies/secretions from pharynx under • Lack of airflow at the mouth (complete obstruction) direct vision • Throat or tongue swelling • Insert Guedel or nasopharyngeal airway • Gurgling, snoring, choking, stridor If obstruction persists: • Paradoxical breathing (indrawing of chest with • Get expert assistance immediately expansion of abdomen on inspiration; vice-versa • Consider laryngeal mask airway or tracheal intubation on expiration) • In the context of anaphylaxis (see below), if throat or Only move to B once airway patent tongue swelling, give IM adrenaline (0.5 mg) B. Breathing

B1 G ve high concentration O2 initially if hypoxaemic

B2 Assess rate, depth and symmetry of breathing If respiratory effort inadequate: onoting: k f ee com • Get help! • Poor respiratory effort: ↓↓RR, feeble, shallow • Manually ventilate via bag-valve-mask Breaths ebo• Consider ee.com a trial of naloxone, if any suspicion of opiate • High respiratory effort: RR >20/min, use of toxicity m Accessory muscles, visibly tiring • Asymmetrical chest expansion

B3 Check for tracheal deviation If severe respiratory distress and signs of tension pneumothorax (p. 264), perform immediate needle B4 Percuss and auscultate chest, noting: aspiration. • Dullness – suggesting pleural effusion, collapse, If widespread wheeze, check for signs of anaphylaxis (see consolidation below) If present, manage as described; otherwise, • ↓breath sounds – suggesting collapse give nebulized bronchodilator. pneumothorax,sfree. pleural om effusion • Wheeze – suggesting bronchospasm Crackles – suggesting pulmonary oedema, fibrosis consolidation • Bronchial breathing suggesting consolidatione o free co B5 Record SpO2 If chronic type 2 respiratory failure or severe chronic obstructive pulmonary disease (COPD),m titrate fraction

of inspired oxygen (FiO2) to patient’s baseline SpO2 (if known) or 90–92%. In all other critically ill patients, continue high FiO2. m Assessing patients: a practical guide 9

Clinical tool—cont’d The ABCDE assessment 2 What to look for Hows to respond C. Cioksfre culation C1 Check colour & temperature of hands In patients with evidence of shock, e.g. ↑CRT, cold • Cold, clammy, blue, mottled? peripheries, thready pulse, ↑HR, ↓BP: • Pink and warm? Secure IV access (large bore if possible) If ventricular tachycardia (VT), attemptm defibrillation b with C2 Measure capillary refill time (CRT) a synchronized DC shock (ask anaesthetist to sedate if Press firmly over fingertip for 5 sec, release pressure conscious). then record time taken for skin to return to normal If bradycardia: colour • Give atropine 0.5–3 mg • ≤2 sec is normal • if no response or HR <40/min, get expert help and • ≥2 sec suggests ↓peripheral perfusion consider IV adrenaline or transcutaneous pacing If tongue/throat swelling, severe respiratory distress, C3 Palpate radial and carotid pulse: widespread wheeze and/or a new rash, assume • Tachycardia: >100 bpm anaphylaxis: • Bradycardia: <60 bpm (or inappropriately slow for • Stop any potential trigger context) • Give 0.5 mg IM adrenaline (anterolateral aspect of • ksfreThready, weak – csuggesting m ↓cardiac output, e.g. middle 1/3 of the thigh) hypovolaemia • Give fast IV fluids • Bounding – suggesting hyperdynamic circulation, • Get immediate anaesthetic help e.g. early sepsis bOtherwise, sfree.co give fluid challenge unless evidence of pulmonary oedema. e C4 Measure blood pressure

C5 Assess height of JVP at 45°

C6 Auscultate the heart for: • Murmurs • 3rd heart sound/gallop rhythm

C7 Attach ECG monitor and review rhythm: • Regular broad complex tachycardia – likely ven ricular tachycardia (VT) (p. 234) • Regular narrow complex tachycardia, e.g. sinus ksfretachycardia, supraventricular co tachycardia (SVT), a trial flutter (p. 232) • Irregular tachycardia – likely atrial fibrillation (p. 232) • Bradycardia ≤40 bpm, e.g. 2nd or 3rd degree atrioventricular (AV) block (p. 234) me

C8 Perform a 12-lead ECG if chest pain or arrhythmia D. Disability D1 Check capillary blood glucose (CBG) If CBG <3 mmol/L: • Send blood for formal lab glucose measurement • Give immediate IV dextrose D2 Record Glasgow Coma Scale (p. 73) If ↓GCS sf e. • sfree.Perform an ABG if any suspicion of hypercapnia, e g chronic lung disease, depressed ventilation • Give 0.8–2 mg IV naloxone if ↓pupil size or no obvious cause • Assess response after 1 min and consider further doses if partial response e ook Assessing patients: a practical guide 10

Clinical tool—cont’d The ABCDE assessment What to look for How to respond D3 oksfreTake a ‘3D’ history m Description of symptoms Drugs and allergies Disorders/Disability prior to this illness

D4 Examine pupils with a pen torch: • Bilateral pinpoint – suggests opioid intoxication or pontine lesion • Bilateral dilated – suggests cocaine/amphetamine or tricyclic antidep essant intoxication or atropine • Unilateral fixed, dilated suggests↑ intracranial pressure or 3rd nerve palsy E. Exposure E1 Record body temperature If temperature <34°C, confirm core temperature with a low-reading thermometer and start rewarming E2 Fully expose the body (preserve dignity), looking measures. ofor: sf e.com oRepeat sf the ABCDE assessment if a significant abnormality • Bleeding or injuries was noted at any stage. • Rashes Refer to the relevant chapter for further assessment of • Jaundice specific presentations, e.g. dyspnoea, shock, chest • Medic alert bracelet pain, ↓GCS, abdominal pain, headache.me o E3 Examine the abdomen for distension, tenderness, guarding, rigidity m

A B

Fig. 2.1 Simple airway manoeuvres. A Head-tilt, chin-lift method. B Jaw-thrust method – preferred in patients with suspected neck injury. (From Douglas G, Nicol F, Robertson C. Macleod s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone,free 2009.) free Assessing patients: a practical guide 11

The history questions initially and give the patient time. Only then should you move to more focused, ‘closed’ Think of the history, not as a series of questions questions. 2 to be asked, but as a body of information that In particular, note: needs to be gathered using all available sources • a supplementary account of the current (Table 2.1 and Boxes 2.1–2.3). History taking is, ooks re problem is essential in patients presenting usually, the single most important component in with confusion or transient loss of the diagnostic process. It is also the one area consciousness ebo f that many doctors perform inadequately. Let the mebo• sfre details of the past medical history are usually patient tell their story (the presenting complaint) in better established from the GP record and their own words without interrupting. Use ‘open’ medical case notes than by simply asking the patient, particularly with respect to the

Box 2.1 Features of alcohol dependence in the outcome of previous investigations history • if available, use a repeat prescription or GP record to obtain the specific names • A strong, often overpowering, desire to take alcohol and dosages of drugs, then ask patients • Inability to control starting or stopping drinking and the amount that is drunk if they are actually taking the medicines • Drinking alcohol in the morning as prescribed. Ask about the use of any • Tolerance,oksfre where increased c doses are needed to additional over-the-counter or herbal achieve the effects originally produced by lower remedies. Also ask the patient about doses side-effects of any current or previous • Withdrawal state when drinking is stopped or medications. ebook reduced, including tremor, sweating, rapid heart rate, anxiety, insomnia and occasionally seizures,m ree. om disorientation or hallucinations (delirium tremens). It The clinical examination is relieved by more alcohol A routine ‘screening’ clinical examination (see • Neglect of other pleasures and interests Clinical tool, p 12) is required in most patients. • Continuing to drink in spite of being aware of the harmful consequences Some elements of the clinical examination that have traditionally been considered routine are only

Table 2.1 Key information required from the history

Information to be established Specific details Sources of information Presenting complaint Full details of recent symptoms and events Patient, relatives, ook om carers, witnesses, GP Past history Current and previous medical disorders Medical case notes, GP Previousm investigations o and results e.com record,m patient book Efficacy of previous treatments Drugs and allergies All prescribed and over-the-counter medications Repeat prescription, and doses; adherence to prescription; recent GP record, patient, changes to medications; adverse drug reactions relatives, carers (what drug? what happened?) Environmental risk factors Smoking, alcohol (see Box 2.1) drug misuse1 (see Patient, relatives Box 2.2), travel, pets, sexual history1 (see Box 2.3) Impact and consequences of Ability to mobilize, self-care, undertake activities Patient, relatives, illnessok (if relevant) e (work, driving, hobbies) friends, carers,o GP Effects on employment,ook family, free finance, comconfidence 1Only if appropriate. Assessing patients: a practical guide 12

Box 2.2 Non-prescribed drug history Box 2.3 Sexual history questions

• What drugs are you taking? • Do you have a regular sexual partner at the moment? • How often and how much? • Is your partner male or female? • How long have you been taking drugs? • Have you had any (other) sexual partners in the last ooks• Any periods r of abstinence? If m so, when and why did 12 months? you start using drugs again? • How many were male? How many female? • What symptoms do you have if you cannot obtain • Do you use barrier contraception – sometimes,ebooks drugs? always or never? • Do you ever inject? meb• Have fre you ever had a sexually transmitted infection? • Do you ever share needles, syringes or other drug paraphernalia? • Do you see your drug use as a problem? • Do you want to make changes in your life or change the way you use drugs?com

Clinical tool The 20-step clinical examination 1. Assess general demeanour, appearance, Sit the patient up at 90° movements, odour, nutrition and hydration. 12. Inspect the trunk (front and back) for rashes, moles, 2. Record routine observations, including temperature, spider naevi, scars etc. pulse, BP, RR and SpO2. me 13. Palpate for lymphadenopathy andme goitre; check for 3. Examine the hands: temperature, capillary refill, bony/renal angle tenderness, sacral oedema. colour, nails, tremor, asterixis and joints. 14. Examine the lung fields from the back. 4. Feel the radial and brachial pulses. 5. Inspect the face and eyes (Table 2.2). Lay the patient flat 6. Examine the mouth: dental hygiene, cyanosis, 15. Examine the abdomen and hernial orifices. tonsillar inflammation, ulcers, blisters and 16. Examine the legs. candidiasis. • Inspect for swelling, colour, rashes, skin changes. • Feel for pitting, temperature, pulses, capillary Position the patient at 45° refill. 7. Assess the height and waveform of the JVP and feel 17. Perform a neurological examination of the legs. the carotid pulse. • Check tone, look for wasting, abnormal 8. Inspectksfre and palpate com the trachea: check centrality and movements. cricosternal distance. o s• Assess ee.co power: flexion/extension of hips, knees, 9. Inspect and palpate the praecordium. ankles. 10. Auscultate the heart. • Check reflexes: knees, ankle jerks, plantar 11. Examine the lung fields from the front. response. e o Assessing patients: a practical guide 13

Clinical tool—cont’d The 20-step clinical examination 2 • Testsfre sensation: L2–S1 dermatomes (see Fig. 19. Screen for cranial nerve abnormalities. 22.1, p. 200). • Test visual acuity and pupillary reactions; check • Test coordination: heel–shin test (Fig. 2.2B). for homonymous field defects. • Assess transfer and gait (p. 215). • Check eye movements (characterize nystagmus) Sit the patient up and hearing in each ear. • Test sensation above the upper lip and over the 18. Perform a neurological examination of them arms. maxillae and eyelids. m boo • Check tone, look for wasting, abnormal • Facial movements: raise eyebrows, show teeth, movements. close eyes against resistance, blow out cheeks. • Assess power: abduction/adduction of shoulders, 20. Perform urinalysis and bedside capillary blood fingers; flexion/extension of elbows, wrists; grip glucose measurement. strength. • Check reflexes: supinator, biceps, triceps. om • Test sensation: C5–T1 dermatomes (see Fig. 22.1, p. 221). • Test coordination: rapid alternating movements and free.cfinger–nose test (Fig. m 2.2A).

Table 2.2 Characteristic faces and their features,e including facial expression Disorder Appearance Acromegaly Coarsening with enlarged features, e.g. nose, lips, orbital ridges and jaw (prognathism) Hypothyroidism Pale, puffy skin with loss of lateral third of eyebrows Hyperthyroidism Startled appearance with lid ret action Cushing’s disease ‘Moon face’, plethoric complexion and buffalo hump over lower cervical–upper thoracic spine Parkinsonism Expressionless faces and drooling Myasthenia gravis Expressionless faces with bilateral ptosis Myotonia dystrophica Frontal baldness and bilateral ptosis ooSuperior sfrvena caval obstruction Plethoric, oedematous face and neck, chemosis of conjunctivae, prominent veins and venules Malar flush Dusky redness of cheeks seen in low cardiac output e.g. mitral mebooksfree.comstenosis; also seen in myxoedema m bo Systemic lupus erythematosus Rash over nose and cheeks – ‘butterfly rash’ Progressive systemic sclerosis Taut skin around mouth with ‘beaking’ of nose m Assessing patients: a practical guide 14 m

Fig. 2.2 Tests of coordination. A Finger–nose test. B Heel–shin test (From Ford MJ, Hennessey I, Japp A Introduction to Clinical Examination, 1 2 8th edn. Edinburgh: Churchill ksf Livingstone, 2005.)

required in specific circumstances. These include examination of the fundi, rectum, genitalia, breasts Box 2 4 Abbreviated mental test and individual joints. (Score 1 for each correct response) Additional steps • How old are you? • Youoksf will gain ee an impression of higher • What is the time just now? • What year is it? mental function through taking the history. • What is the name of this place? (Where are we just If you suspect impairment, perform an now?) Abbreviated Mental Test (AMT; Box 2.4). Please memorize the following address: 42 West Street • If you detect a relevant abnormalitymeb on the • s When re is your birthday (date and mebmonth)? routine examination, perform a detailed • What year did the First World War begin? examination of the relevant system (see • What is the name of the Queen? Macleod’s Clinical Examination). • Can you recognize … ? Two people? • Additional examination steps required for a • Count backwards from 20 to 1 • Repeat the address that I gave you specific presentation are described in the relevant chapters: Normal score: 8–10 • testicular examination (p. 258) Source: Hodkinson HM 1972. Evaluation of a mental test score • breast examination (p. 49) for assessment of mental impairment in the elderly. Age Ageing. • examination for meningeal irritation (p. 169) 1:233–238. • examinationksfree.com of lumbar spinal movements (p. 211) • ‘confusion assessment method’ for detection of delirium (p. 80) e sfr e com Assessing patients: a practical guide 15

• assessment of gait (p. 215) focused approach to identify important problems • head thrust test (p. 101) rapidly and reliably, and to produce a useful list • Dix–Hallpike manoeuvre (p. 103) of differential diagnoses. 2 • jawksfre jerk (p. 109). Chronological age is a poor marker for identifying who would benefit from a tailored ‘geriatric’ Basic investigations assessment. Some elderly patients present with a single specific acute pathology, e.g. the fit 90-year- The specific tests required for a routine work-up old with an acute myocardial infarction. This patient depend on the presenting problem. For example, memay sfre require rapid coronary revascularizationmebook rather f an ECG is mandatory in patients with acute chest than a comprehensive geriatric assessment. pain but not in those with chronic low back pain. Conversely, a 59-year-old with multiple medical The recommended tests for different clinical problems and medications, and an inability to presentations are specified in the relevant chapters mobilize may benefit greatly from a geriatric in Part 2. In several chapters we give detailed assessment. Frailty is the increased vulnerability in guidance on interpreting these tests, including: reserve and function across multiple physiological • the ECG in chest pain (p. 54) systems such that the ability to withstand acute • arterial blood gases (p. 116) stressors is compromised. Identification of frailty is • pulmonary function tests (p. 127) difficult, and debate continues over robust criteria. • pleural tap and analysis of pleural fluid (p. 129) Formal frailty scores such as the Edmonton Frailty • lumbar puncture and CSF analysis (p. 170) oksfree.com Scale (www.nscphealth.co.uk/edmontonscale-pdf) • a septic screen (p. 142) ooksfree com can be used to grade the degree of frailty and • anaemia (p. 136) various screening tools have been developed • renal failure (p. 230) for use in acute settings to help identify patients • hyponatraemia (p. 88). mebooksf most likely to benefit from comprehensive geriatric assessment. As a guide, the presence of two or Approach to the frail, elderly patient more of these criteria suggests frailty: Frail, elderly patients comprise a major proportion • functional decline, e.g. inability to perform of acute medical and surgical admissions and basic activities of daily living (ADLs) are frequently challenging to assess and treat. • confusion (delirium, dementia) They often present in a vague, non-specific way, • polypharmacy and in many cases with acute delirium. This can • care home resident result in difficulty identifying the specific culprit for • recent immobility or falls the acute deterioration, especially as many will • ≥1 unplanned admissions in the past have a background of multiple chronic comorbidi 3 months o ties and functional limitation. One unfortunate • difficulty in walking booksfree.comconsequence of this is the tendency to categorize • malnutrition elderly patients into a small number of ‘diagnostic • incontinence. dustbins’. Instead of a differential diagnosis,mebo the ree com impression at the end of the clerking may read Specific tips for assessment of the elderly/ ‘Off legs’, ‘Mechanical fall , ‘Social admission’ frail patient or ‘Collapse ?Cause’ Such impressions could be correct, but they are not diagnoses. An accurate history is important in the frail, elderly The challenges of acute assessment in the patient, but may be significantly more difficult elderly are often compounded by a misconcep- to obtain tion that the process must always be painstaking • Use open questions sparingly. and laborious. Comprehensive geriatric assess- • Clarify vague terms, e.g. ‘a while’, and ment does require time and input from multiple question inconsistencies, e.g. if patients health professionals but it is often preferable cannot recall the details of their ‘fall , how toooksfree.com defer this for a period than to undertake it do they know that they did not black out? poorly in the midst of a busy acute admission. • Wherever possible, complement the Where time and personnel are limited, use a patient’s history with collateral information mebo ree co mebook Assessing patients: a practical guide 16

from witnesses, carers, relatives, other Elderly patients with abdominal pathology may health professionals and previous notes. present ‘atypically’. Frail patients may tire easily during the history • Consider perforation of a viscus or and examination: ischaemic bowel, even in the absence of • Ifoksfre necessary, perform the m assessment in abdominal rigidity – have a low threshold for ‘bite-sized’ chunks. imaging • If there are multiple symptoms, address • Percussion and palpation of the bladder them in order of importance to the patient, may reveal ‘asymptomatic’ urinary retention unless they are ‘red-flag’. mein fre patients with non-specificme deterioration. ook • If the list of established diagnoses is long, Most elderly patients can follow the instructions determine which problems are ‘active’ required for a standard neurological examination (‘When did you last have angina?’) and • Try to overcome sensory impairment with explore those re evant to the current aids (put the hearing aid in!), repetition and presentation in detail. demonstration Prioritize important and common problems in • If the patient struggles to cooperate, the systemic enquiry. obtain equivalent information by observing • How far can you walk? movement, passive or provoked • Can you manage a flight of stairs? • Pay close attention to muscle bulk, gait • Whatoksfree.com stops you? (p. 215), visual acuity and functional • Do you have a cough? movements of the arms and hands • When did you last move your bowels? • Assess joint movements in conjunction • Do you have any difficulty passing urine? with the neurological examination. • Have you been incontinent? meScreening ree.com for cognitive impairmentmeboo • Have you lost weight? is an integral part of examination in the • Have you fallen or blacked out? elderly: use objective tests, e.g. AMT • Do you get dizzy? (see Box 2.4) or 4AT (p. 80), rather than • Do you have any weakness or numbness in general impressions. Record the score, your face or limbs? even if the patient appears to have intact • Are you forgetful? cognition – documentation of a normal baseline may aid a subsequent diagnosis An exhaustive ‘social history’ during the initial of delirium. assessment is often unproductive. Depression is common in elderly hospitalized • Establish the key information regarding patients and is a well-recognized mimicker of functionaloksfree.c status and social/care m dementia. arrangements but avoid replicating work that will be undertaken by other health • Maintain a high index of suspicion professionals, e.g. occupational therapist. but remember that low mood may be • Do not overlook specific issues inmeb the social situational free.com and appropriateme (‘stuck in ook history, e.g. alcohol intake, driving. hospital’). • Exclude organic disease before attributing ‘biological symptoms’ to depression. Inspection Basic investigations have a higher yield in Certain aspects of the examination demand elderly patients due to the increased prevalence closer attention in the elderly. of disease and the frequent absence of charac- • Observe carefully for evidence of teristic clinical features. dehydration, malnutrition, constipation, • Perform FBC, U+E, ECG and CXR in injuries and pressure sores in frail, any elderly patient with non-specific dependentoksfree. or demented patients. deterioration. • Consider a formal swallow test to exclude • Have a low threshold for considering aspiration in patients with recurrent badditional free.com tests such as CRP, LFTs, pneumonia. calcium or TFTs. eb The diagnostic process ks 3o sf

With time and practice, most trainees will acquire they recognize a bird by its ‘jizz’ – a combination the skills necessary to take a history, perform of its appearance movement and behaviour. a competent physical examination and interpret Some medical conditions, e.g. Parkinsonism, basic tests. The next stage is to translate the are readily identified in a similar way. resulting raw clinical data into a diagnosis. The Pattern recognition can be a powerful primary aim of this book is to show you how technique, particularly when employed by an this can be achieved. experienced clinician. In theory, it requires you to have experienced an identical, or at least very Diagnostic methods similar, presentation previously, and so is less The exact method by which a diagnosis is suited to the newcomer. However, the diagnostic reached may seem mysterious to newcomers to method most commonly utilized by medical clinicaloo medicine. s ee The com best diagnosticians invari- students and junior doctors is actually a variant ably use several complementary skills which have of this approach. The major difference is that been honed through years or decades of experi- their ‘database’ of patterns corresponds to the ence; these are often applied subconsciouslymebo and descriptions sfree of com signs and symptomsmebooksf provided in hence are difficult to explain. Consequently, the textbooks rather than previous real-life examples. diagnostic process may be taught poorly and, This has several major disadvantages. Firstly, most often, is simply experienced at second descriptions of physical signs from textbooks or hand, by observation. lectures, e.g pill-rolling tremor or festinating gait, As an inexperienced clinician you cannot are poor substitutes for experiencing them at first expect to achieve diagnostic skills overnight, hand Textbooks also tend to present an idealized but this book aims to show you how to make account of the way in which illnesses present a diagnosis in the great majority of the most emphasising classical signs and symptoms commonly encountered and important clinical that are often relatively rare in everyday clinical presentations. As a first step, it helps to consider practice. Similarly, a reliance on textbook learning twoooksfree. well-established, contrasting om approaches does not allow you to appreciate the multiple to diagnosis: pattern recognition and prob- subtle variations in presentation that exist for the ability analysis. These methods illustrate some same disorder. Pattern recognition may fail even fundamental principles of diagnosticmebo reasoning ksfree.comthe most experienced clinicianmebooksf when conditions but both have major drawbacks that limit their present atypically or when characteristic features application in everyday practice. are masked, e.g. the patient with acute coronary syndrome who has sharp chest pain rather than Pattern recognition crushing or heavy discomfort, or the diabetic The diagnosis is made by recognising character- patient who has no pain or discomfort at all istic features of the patient’s illness that you have because of coexistent autonomic neuropathy. encountered previously in other patients with the This tendency is greatly amplified when these same disorder. For most people, visual informa- conditions have not been experienced repeatedly tion is a strong prompt to memory recall, so the in the real world. techn que is particularly helpful for conditions with Probability analysis anooksfree. obvious abnormality omof appearance, e g. skin conditions. Moving visual images are even more For the great majority of conditions, no single evocative. Ornithologists commonly describe how symptom, sign or test will have sufficient power meboo sfree com me sf The diagnostic process 18 to enable you to rule in or rule out a diagnosis. area of considerable uncertainty. In practice, it However, each will alter the probability of the is not usually possible to combine more than diagnosis to a greater or lesser extent. The two or three LRs outside a validated scoring diagnostic weighting of a particular symptom, system. For readers interested in using LRs to sign or test can be expressed as a likelihood ratio calculate diagnostic probabilities, we recommend (LR).ooks The LRre is the proportion m of patients with Evidence Based Physical Diagnosis, by Steven the specific disease who exhibit the particular McGee (4th edn, 2017, Elsevier). finding, divided by the proportion without the In everyday practice, this approach has two disease who also exhibit the same finding.mebo Note major sfre applications. Firstly, knowledgemebooksf of LRs that the finding may be positive, e.g. presence for different symptoms, risk factors or clinical of a particular sign, or negative, e.g. absence signs allows you to identify those with the of a particular sign. highest diagnostic value. As a rough rule of If the LR value is >1, the chance of the disease thumb, LR values between 0.5 and 2 are rarely is increased; the higher the value, the greater helpful, whereas values ≥5 or ≤0.2 are usually the likelihood of the disease. If the LR value is clinically useful. Secondly, for some conditions, <1, the chance of the disease being present is LRs have been used to develop and validate reduced. For example, an LR of 5 increases the diagnostic algorithms that allow the condition absolute probability of a disease by approximately to be ruled in or ruled out based on thresholds 30% and an LR of −0.2 decreases it by 30%. of probability. Examples are the Wells scores for LRsoksfree.com are available for many clinical features and deep vein thrombosis (p. 193) and pulmonary tests. In theory, this allows you to use the infor- thromboembolism (p. 120). mation derived from your assessment to calculate A different approach: tailored the probability of a disease. However, before mebodiagnostic sf ee guides com m booksf you can do this, you need to know the pre-test probability of the patient having the disease in For the inexperienced clinician, neither fuzzy question – in other words, the prevalence of pattern recognition nor rigid probability analysis the disease in a population with similar baseline offers a practical and satisfactory approach to characteristics to your patient. Among other diagnostic reasoning. We therefore advocate things, the pre-test probability may be influenced an alte native system that takes positive by a patient’s age, sex, ethnic origin, occupation, elements from both of these methods but is social background and past history, as well as easy to apply in everyday practice and does the clinica setting within which you work (rural not rely on vast amounts of clinical experi- versus urban environment, primary care versus ence. We set out this system in the form secondary care). For example, the probability of of individual ‘diagnostic guides’ for all of Plasmodiumooksfree.com falciparum malaria being the cause the major presenting clinical problems. With of headache, myalgia and fever in a previously fit, experience, you will start to use your own 19-year-old in the UK in the middle of a winter unique methods but, at the outset, following influenza epidemic is vanishingly small,meboo but it an sf established ee.com framework maymebooksf help to prevent will be very much higher for a similar individual crass, potentially damaging, errors. returning from sub-Saharan Africa. Each chapter in Part 2 is a diagnostic guide or Another problem with using LRs to calculate ‘road-map’ for a common clinical presentation. probability lies in trying to combine information The purpose of the guides is not to tell you which from multiple symptoms, physical signs and questions to ask and which examination steps to test results. This is hampered by a need for the perform – this was outlined in Chapter 2 and will be broadly similar for most presentations. Rather, findings tofree.com be independent of each other – an free com f The diagnostic process 19

it is to explain how to use the information you narrower differential diagnosis (dysphagia or have extracted from the history, examination and haemoptysis in the examples above). initial tests to work toward a diagnosis. After you have decided on which guide to To do this, we focus on the most valuable use, the format is simple to follow: 3 pieces of diagnostic data – those symptom char- • each begins with the differential diagnosis: acteristics,ooksfre signs and test results with the greatest a rundown of the important diagnoses potential to narrow the differential diagnosis or to consider for the particular presenting to rule in/rule out suspected conditions. problem ebo ks The guides follow a logical and meboconsistent • we fre then present m an overview of approach designed to reflect contemporary assessment: this is essentially a flowchart medical practice. They provide a secure frame- that lays out the route to diagnosis. It is work to work within but are not rigid protocols vital that you understand the format of the and allow ample scope for clinical judgement. overview so an example is provided in Fig. The highest priority is always given to imme- 3.1 and is explained below diately life-threatening problems. In some cases, • each overview is accompanied by a this means focusing on aims of assessment other step-by-step assessment. This is a textual than diagnosis, e.g. gauging illness severity or companion to the overview that explains determining resuscitation requirements. The next and expands on each individual step aim is, wherever necessary, to exclude major • some chapters also contain details on pathology;ooksfree for each of com the most serious potential further assessment of common disorders or disorders, the guides will identify those patients abnormalities that may have been identified who require further investigation to rule in or during the initial assessment rule out the diagnosis. Thereafter we prioritize meboThe example ree. in Fig. om 3.1 showsmebo the initial stages of diagnostic information with the highest yield the overview of assessment for jaundice (shown whilst avoiding data that do not significantly alter fully in Ch. 19). probabilities or help to target investigation. In • Blue boxes are stages of action – they situations where the information obtained from contain the steps of assessment that you the routine work-up is unlikely to yield a clear need to undertake. This will always include working diagnosis we may opt to provide a one of the two principal methods of clinical strategy for further investigation to help narrow assessment outlined in Chapter 2 (‘airway, the differential diagnosis. breathing, circulation, disability, exposure [ABCDE]’ or ‘full clinical assessment’) p us How to use the diagnostic guides the essential basic tests, e.g. ECG CXR Theoo first step free.com is to determine which guide if any, and any necessary additional examination is the most appropriate for the patient in front of steps. Note: The diagnostic process that you. Ensure that you have clarified the true nature follows assumes that you have performed of the problem; a patient who presentsmebo with a fall these free.co steps and extractedmebook the relevant may have had a black out, whilst a patient who clinical information. has had a ‘funny turn’ may have experienced • Yellow boxes are stages of diagnostic focal limb weakness. In general, you should reasoning – they do not show ‘what to do match the guide to the patient’s predominant now’ but rather ‘what to think about now’. complaint. However if the presentation entails Each numbered step in the diagnostic two or more related symptoms, e.g. abdominal process is accompanied by a detailed pain + dysphagia; dyspnoea + haemoptysis, we explanation in the step-by-step assessment recommendfree.com choosing the symptom with the sectionree.com (see above). The diagnostic process 20

ABCDE + ECG, CXR ± ABG fre m Yes Treat and 1 Cause requiring immediate correction? Final diagnosis reassess

2 Assess effort and adequacy of oxygenationm and ventilation

Yes 3 Underlying COPD? See Further assessment of acute dyspnoea in patients with COPD (p. 121) No Yes 4 Evidence of respiratory tract infection? See Further assessment of respiratory tract infection (p. 123)

No bFig. 3.1 A guide fr to using the o ‘overview of assessmentb . r co The diagnostic process 21

• Red boxes represent important elements with the yellow boxes, explanatory text is of the assessment that are independent of provided in the accompanying step-by- the diagnostic process, e.g. evaluation step assessment. In some cases, further of illness severity or resuscitation investigation may be required to confirm the 3 requirements.oksfre diagnosis, refine it, assess severity or guide • Green boxes represent the potential optimal management; if so, the necessary endpoints of the diagnostic process eAs steps re will be outlined m in the text.ebook Sectionooks 2 Assessment of common me o presenting problems

4. Abdominal pain 24 5. Breast lump 46 6. Chestsfree. pain 50s 7 Coma and altered consciousness 72 8. Confusion: delirium and dementia 78 9. Diarrhoea 90 10. Dizziness 96 11. Dysphagia 108 12. Dyspnoea 112 13. Fatigue 130 14. Fever 138 15. Gastrointestinal haemorrhage: haematemesis andsf rectal bleeding 150 16. Haematuria 158ks 17.o Haemoptysis sf 162 18. Headache 166 19. Jaundice 174 20. Joint swelling 184 21. Leg swelling 190 22. Limb weakness 196 23. Low back pain 208 24. Mobility problems: falls and immobility 214 25. Nauseasfr and e vomiting c 222 ks 26. Palpitation 232 27. Rash: acute generalized skin eruption 240 28. Red eye 250 29. Scrotal swelling 258 30 Shocks re 264s 31. Transient loss of consciousness: syncope ando seizures 270 32. Urinary incontinence 282 33. Vaginal bleeding 288 34. Weight loss 294 Abdominal pain s 4ks

Acute abdominal pain • diabetic ketoacidosis/hypercalcaemia/ adrenal crisis (diffuse) Acute abdominal pain has a vast differential • functional abdominal pain (any region diagnosis. The spectrum of disease severity is or diffuse). also wide, ranging from the life-threatening to the innocuous. Effective assessment requires the rapid recognition of critically unwell patients Key questions and, where appropriate, targeted investigations. What are the characteristics of the pain? Causes of acute abdominal pain are listed below. An educated analysis of a patient’s abdominal The numbers in brackets correspond to the pain symptoms yields immeasurable information. different regions of the abdomen, as displayed The mnemonic ‘SOCRATES’ is often helpful: booksfreein Fig. 4.1, at which comthe pain is typically mostboo consider s e the Site, com Onset, Character, Radiation, prominent: Associated features, Timing, Exacerbating factors • cholecystitis/cholangitis (1) and Severity of the pain. Basedmebook on these features, • biliary colic (1, 2) it should be possible to distinguish between most • hepatitis (1, 2) of the above causes of pain. • pneumonia (1 or 3) Visceral pain is conducted by autonomic nerve • peptic ulcer disease/gastritis (2) fibres, so its location corresponds to the embryo- • acute coronary syndrome (2) logical origin of the affected structure (Fig. 4.2). • pancreatitis (2, 5) The pain may arise from distension or excessive • ruptured abdominal aortic aneurysm (AAA) contraction (spasm) of hollow organs. It also arises (2, 5) from tissue damage (inflammation), ischaemia or • splenic rupture (3, diffuse) direct chemical stimulation of pain receptors in • renal calculus (4, 7 or 6, 9) organs. It is typically dull and poorly localized and is • pyelonephritisoks ee.co (4 or 6) not associated with abdominal guarding or rigidity. • early appendicitis (5, diffuse) True ‘colicky’ pain reflects intermittent episodes of • established appendicitis (7) intense smooth muscle contraction that produce • terminal ileitis, e.g. Crohn’s disease, short-lived spasms of discomfort lasting seconds Yersinia (7) mtosfree.com minutes before subsiding. Somemebooksf disorders are • mesenteric adenitis (7, diffuse) described as ‘colic’ but are actually pseudocolic, • diverticulitis (7 or 9) (e.g. renal or biliary colic). In these cases, the pain • colitis (7, 8, 9) builds to a crescendo over several minutes before • ectopic pregnancy (7, 8, 9) reaching a steady peak that may last for several • pelvic inflammatory disease/endometriosis hours before easing. Visceral pain may also be (7, 8, 9) constant, for example in bowel ischaemia. • ovarian torsion/cyst rupture (7, 8, 9) Somatic pain arises from irritation and • lower urinary tract infection (UTI)/cystitis (8) inflammation of the parietal peritoneum and is • intestinal obstruction (diffuse) conducteds ree.com by somatic nerves. It is sharp, well • perforationoksfre (diffuse) .c localized, constant and often associated with • mesenteric ischaemia (diffuse) local tenderness and guarding Widespread • gastroenteritis (diffuse mid-/ inflammation of the parietal peritoneum produces upper-abdominal) generalized peritonitis. ebooksf Abdominal pain 25 Differential diagnosis

Referred pain is perceived at a site remote may thereby contribute to the diagnostic process. from its source and arises due to convergence In some patients, the presence of inflammatory of nerve fibres at the same spinal cord level features may assist the interpretation of uncertain (Fig. 4.3). physical signs, e.g. mild localized abdominal tenderness, reinforcing suspicion of local peritonitis. Is there a systemic inflammatory response? In patients without a clear cause for pain, these Manyo serious ksfre causes of acute abdominal pain 4 features may suggest the need for admission either stem from or provoke an inflammatory and further investigation. By the same token, process within the abdominal cavity. The pres- mebthe s absence re of othese featuresmebooksf can, when used ence of fever, ↑CRP or ↑WBC with neutrophilia correctly, help to exclude important inflammatory suggests that the patient is mounting an acute pathology. Finally, recognising and grading the systemic inflammatory response (Box 4.1) and m presence of a systemic inflammatory response are central to the assessment of illness severity. Note that the significance of an individual result depends on the clinical context, particularly with respect to CRP. In general, the higher the result, 132 the greater the extent of systemic inflammation. A sfreemarginal rise com in CRP, e.g. <30 mg/L, does not provide compelling evidence of a major 5 inflammatory process. However if the test is 46being used to help ‘rule out’ a condition, then it is safer to regard any limit above the upper range of normal as elevated mebooksf 7 9 8 Box 4.1 Indicators of systemic inflammation

• Fever (>38°C) • ↑CRP (>10 mg/L)1 • WBC >11 × 109/L or <4 × 109/L Fig. 4.1 Regions of the abdomen. See text for typical sites of pain (From Ford MJ, Hennessey I, Japp A. 1The significance of the result depends on the clinical Introduction to Clinical Examination, 8th edn. Edinburgh: contextfr – see e.c text. m Churchi lksfre Livingstone, 2005.) Abdominal pain 26 Differentialcom diagnosis

Foregut – pain localises to epigastric area Midgut – pain localises to periumbilical area Hindgutmeboo – pain localises to suprapubic area

Fig. 4.2 Abdominal pain. Pe ception of visceral pain is localized to the epigastric, umbilical or suprapubic region, according to the embryolog cal origin of the affected organ. (From Douglas G, Nico F, Robertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009.) om com Abdominal pain 27 Doifferential diagnosis

Rightk shoulder

Diaphragm 4 Tip of scapula

Gall bladder

Ureter Inguinal canal free

Gallbladder pain Diaphragmatic pain Ureteric pain

Fig. 4.3 Characteristic radiation of pain from the gallbladder, diaphragm and ureter. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009.) Abdominal pain 28 Differential diagnosis

Chronic/episodic abdominal pain Choledocholithiasis (stone in the common bile duct – CBD) causes cholestatic jaundice Chronic abdominal pain is common and challeng- (see Ch. 19) with less severe upper abdominal ing to assess. Careful evaluation with targeted pain, or indeed no pain. In ascending cholangitis, investigation is required to exclude organic pathol- infection of the biliary tree occurs upstream from ogy.ooksfre Most younger patients com will have a functional a blockage in the CBD (gallstone, tumour, liver disorder, e.g. irritable bowel syndrome (IBS), but fluke). Patients present with significant sepsis this should be a diagnosis of exclusion. In older (pyrexia), jaundice and abdominal discomfort patients with new, persistent abdominalmebo pain, (Charcot’s sfre triad). mebooksf the priority is to exclude underlying malignancy. Pancreatic pain Gastroduodenal disorders Acute pancreatitis causes severe upper abdomi- Peptic ulcer disease is a common cause of nal pain that radiates to the back, often with chronic upper abdominal pain. Almost all repeated vomiting. It is associated, depending duodenal ulcers and 70% of gastric ulcers are on the severity, with a systemic inflammatory attributable to H. pylori infection. Typical features response and may progress to multiorgan failure include recurrent episodes of burning or gnawing The majority of cases are caused by gallstones discomfort, relationship to food (variable), and passing down the common bile duct and irritating associated dyspeptic symptoms, e.g. nausea, the pancreas or by alcohol directly injuring the belchingooksfree. and relief with antacids. m Classically, pain pancreas. Chronic pancreatitis develops in a from gastric ulcers occurs several minutes after subset of patients with recurrent episodes of eating whereas pain from duodenal ulcers occur acute pancreatitis. In some patients, it is constant hours later and may be relieved by food.meboand sfree.co unremitting, while in others,mebooksf episodes are Gastritis without frank ulceration may produce provoked by drinking alcohol or eating. Associ- similar symptoms. ated features include weight loss, anorexia and, Gastric cancer occurs more frequently in in advanced disease, diabetes mellitus (endocrine patients >55 years In addition to pain, associ- deficiency) and steatorrhoea (exocrine insuffi- ated symptoms include early satiety, unintentional ciency). The majority of cases are due to chronic weight loss and vomiting. All of the above disor- alcohol excess. Diagnosis is usually made by CT ders are best diagnosed by upper gastrointestinal but endoscopic ultrasound with biopsy may be endoscopy (UGIE). required to rule out malignancy. Unlike acute pancreatitis, serum amylase is usually unhe pful; Gallstoneso sfree co ↓faecal elastase indicates pancreatic exocrine insufficiency. Most gallstones are asymptomatic. Pancreatic cancer may cause severe, unrelent- Biliary colic occurs when a gallstone obstructs ing pain in the upper abdomen that radiates to the cystic duct, causing gallbladder distension. It the back (50% patients), and is usually associated tends to occur 1–6 hours after a meal, memanifesting sfree.com meb oksf with cachexia ± cholestatic jaundice. as intense, dull, RUQ or epigastric pain ± radiation to the back or scapula (see Fig. 4.3). The pain Mesenteric ischaemia builds to a crescendo over minutes, and may last several hours before subsiding. It does not cause Chronic mesenteric ischaemia is a rare cause of jaundice, deranged LFTs or abdominal signs. USS chronic abdominal pain that tends to occur in should confirm the presence of gallstones or, rarely, patients with widespread severe atherosclerotic demonstrate pathological gallbladder changes. In disease. Dull periumbilical or lower abdominal cholecystitis, infection of the gallbladder due to pain develops approximately 30 minutes after gallstones obstructing the cystic duct occurs. The eating (‘abdominal angina’) and may be associ- pain classically persists over time, is associated ated with bloody diarrhoea. This may lead to withooksfree.com a fever and there may be jaundice in cases a fear of eating so weight loss is common. of Mirizzi’s syndrome (where a large gallstone However, even the patient who eats ‘normally’ is and inflamed gallbladder wall causes extrinsic often cachectic due to poor absorption. The diag- compression of the common hepatic meboduct). nosis sfree.com is made by CT mesentericmebooksf angiography. Abdominal pain 29 Differential diagnosis

Acute mesenteric ischaemia presents very differ- Non ulcer dyspepsia causes symptoms that ently: acute, agonizing, constant diffuse abdominal may be indistinguishable from peptic ulcer. UGIE pain with minimal examination findings (poor and mucosal biopsies are normal. localization, no peritonism), systemic upset and, IBS causes abdominal pain that is relieved usually, lactic acidosis. It is a surgical emergency by defecation or is associated with a change withooksfre a high mortality. It is due either to mesenteric in bowel habit. Diagnostic criteria are shown 4 embolism 50% (patients may have atrial fibrillation), in Box 9.1, page 90. Symptoms tend to follow thrombosis in situ 25% (atherosclerotic disease), a relapsing and remitting course, and are congestive venous infarction due to mesentericmebo vein often sfre exacerbated o by psychosocialmebook stress. It is f thrombosis (5%) or due to non-occlusive causes essential to rule out other organic causes of these (20%) such as cardiac failure or septic shock. symptoms, including inflammatory bowel disease, malignancy, coeliac disease and tropical sprue. Inflammatory bowel disease Renal tract disorders Colitis due to either Crohn’s disease or ulcerative colitis may cause cramping lower abdominal pain, Infrequent, discrete attacks of severe loin pain usually in association with bloody diarrhoea. Small radiating to the groin ± haematuria suggest renal bowel inflammation in Crohn’s disease is often stone disease. Chronic dull, aching or ‘dragging manifest by persistent cramping periumbilical or discomfort may be due to cancer, adult polycystic RLQ pain ± diarrhoea (non-bloody) and constitu- kidney disease (APKD), loin pain–haematuria tionalooksfree upset. Subacute com small bowel obstruction syndrome or chronic obstruction/pyelonephritis. due to oedema or fibrosis (strictures) may lead Patients with acute renal colic typically writhe in pain to colicky postprandial abdominal discomfort. and are unable to find a comfortable position (in Both disorders are also associated withmebo a range ksfreecontrast to patients c mwith peritonitismebooksf who lie very still). of extraintestinal features (see Box 9.3, p. 91). Gynaecological conditions

Colon cancer Sudden onset lower abdominal pain in women of reproductive age may represent ovarian torsion This is a common cancer in men and women. (around a cyst) or ruptured ectopic pregnancy. In many countries, screening programmes Both are surgical emergencies. Recurrent epi- detect tumours before they cause symptoms. sodes of acute lower abdominal pain that regularly However, patients may present with colicky lower occur midway through the menstrual cycle may abdominal pain (from partial or complete bowel be a manifestation of ovulation (mittelschmerz). obstruction). Other important features include The pain typically occurs suddenly, as the graafian a history of weight loss, change in bowel habit follicle ruptures, and subsides over 24 hours. (alternatingooksfree.c between constipation and diarrhoea An ovarian cancer or cyst may present with as liquid faeces bypasses around firmer stool non-specific persistent lower abdominal discom- that is partially held up), rectal bleeding and iron fort ± evidence of a pelvic mass on abdominal/ deficiency anaemia. Tenesmus is mebooa feature of PV sfree.com examination. mebooksf low rectal tumours. Right-sided cancers present Endometriosis (endometrial tissue outside the insidiously with vague pain and iron deficiency uterus) and pelvic inflammatory disease (PID; anaemia. This is because the proximal colon is infection of the upper reproductive tract) are more distensible and contains liquid faeces, so common causes of chronic lower abdominal obstructive features are not seen and blood loss is pain in women of reproductive age. occult. Diagnosis is usually made by colonoscopy. CT colonography may be used for frail patients Other diagnostic possibilities who are unfit for endoscopic colonoscopy. • Constipation. • Hypercalcaemia. Functional disorders • Small bowel ulcers/tumours. Theseoo are freeextremely com common, particularly in • Acute intermittent porphyria. younger adults. Diagnosis is based on typical • Giardiasis. clinical features in the absence of apparent • Abdominal tuberculosis. organic disease. mebo• Coeliac e disease. com Abdominal pain 30 Acute abdominal pain: overview

ABCDE fre com Yes Resuscitate, urgent surgical review 1 Evidence of shock? Consider ruptured AAA / ectopic pregnancy / spleeno No

Yes Erect CXR 2 Generalised peritonitis? Likely perforated viscus Urgent surgical review No

Full clinical assessment, FBC, U+E, CRP

Yes Abdominal 3 Features of intestinal obstruction? Intestinal obstruction re co X-rayre No

Yes 4 Acute and/or bloody diarrhoea? Gastroenteritis / colitis

Yes CT Kidney, 5 Unilateral loin or flank pain? Likely renal colic ureter and bladder No

Pain localised to upper or lower Yes See Assessment of upper abdominal pain 6 abdomen?ree or lower abdominal pain No

Consider mesenteric ischaemia, Crohn s disease, gastroenteritis, irritable bowel syndrome 7 ‘medical causes’. Surgical review ± CT boabdomen if any reeconcern b Abdominal pain 31 Acute abdominal pain: step-by-step assessment

1 Evidence of shock? 2 Generalized peritonitis? Rapidly identify patients who are shocked with Generalized peritonitis is usually the mani- hypotension and evidence of tissue hypoperfu- festation of a perforated hollow viscus with sion (see Box 30.1, p. 267). inevitable spillage of enteric fluid, e.g stomach, ooksfreRemember that young, fit patients can often duodenum or colon. Suspect it if there is severe, 4 maintain BP in the face of major fluid losses; in non-colicky abdominal pain that is worse on these patients hypotension occurs late, so look movement, coughing or deep inspiration, and carefully for early features such as ↑meboHR, ↑RR, kswhich is e associated co with inflammatorymebooks features narrow pulse pressure, anxiety, pallor, cold sweat and generalized abdominal rigidity. The patient or light-headedness on standing ± postural ↓BP. will usually be lying still, taking shallow breaths, If the patient has overt or incipient shock, and will be in obvious distress or discomfort; secure two large-bore IV lines; send blood for reconsider the diagnosis if the patient appears cross-match, U+E, FBC, amylase and LFTs; and well or is moving freely. begin aggressive resuscitation. Patients require aggressive resuscitation, The diagnoses to consider first are rupture of antibiotics and immediate surgical referral. Free an AAA, ectopic pregnancy or other viscus, as air under the diaphragm on erect CXR (present these may require immediate surgical intervention. in 50–75% of cases) confirms the diagnosis • Suspectksfree ruptured comAAA in any patient with (Fig. 4.4); if CXR non-diagnostic consider CT known AAA, a pulsatile abdominal mass with oral and IV contrast. A very high index of or risk factors, e.g. male >60 years old, suspicion is required in the elderly and in patients who experiences sudden-onset, severe taking systemic steroids; signs areebooksf often subtle, abdominal/back or loin pain followedmeb rapidly so sfree reassess frequently. com by haemodynamic compromise. Localized peritonitis (or peritonism) occurs • Suspect ruptured ectopic pregnancy in any where the parietal peritoneum is irritated, for pregnant woman or woman of child-bearing example by an inflamed appendix or diverticular age with recent-onset lower abdominal abscess. This results in focal abdominal rigidity pain or PV bleeding; perform an immediate over the area affected and may precede progres- bedside pregnancy test. sion to generalized peritonitis should the patient’s • Consider splenic rupture in any shocked condition deteriorate. patient with abdominal pain who has a history of recent trauma, e.g. road traffic accident. If any of these diagnoses is suspected, arrange immediate surgical review prior to imaging. booksfree.comIn the absence of these conditions perform an ECG, CXR, urinalysis and ABG, continue to assess for an underlying cause, asmebo described ee.com below, and refer for urgent surgical review. Other important diagnoses to consider include: • perforated viscus • acute mesenteric ischaemia • acute inflammatory conditions, e.g. pancreatitis, colitis, cholangitis • medical conditions, e.g. diabetic ketoacidosis, myocardial infarction, adrenal crisis, pneumonia • anyoksfree.c condition associated m with repeated vomiting, e.g. intestinal obstruction,

gastroenteritis. Fig. 4.4 Free air under the diaphragm Abdominal pain 32 Acute abdominal pain: step-by-step assessment

3 Features of intestinal obstruction? Distended loops of small bowel Stomach Suspect intestinal obstruction if abdominal pain is colicky and accompanied by vomiting, absolute constipation and/or abdominal distension. The predominantooks symptoms e com will vary, depending on the site of obstruction; in high small bowel obstruction vomiting and pain are pre-eminent, whereas in low colonic lesions constipation andmebo distension e c are more pronounced. If any of these features are present, perform an abdominal X-ray (AXR) (Fig. 4.5) to confirm the diagnosis and estimate the level of the obstruction. Examine for an incarcerated hernia in any patient with suspected bowel obstruction. Consider fu ther imaging and rectal examination to confirm an obstructing lesion and differentiate from pseudo-obstruction in patients with large bowel obstruction. Patientsoksfree may be comprofoundly dehydrated – check U+E, provide adequate fluid resuscitation, A insert a large-bore nasogastric tube and consider a urinary catheter. Refer to surgery for further assessment and management. mebo

4 Acute and/or bloody diarrhoea? Recent onset of acute diarrhoea with cramping abdominal pain ± vomiting suggests infective gastroenteritis. Suspect colitis (infective, inflammatory or ischaemic) if the patient has bloody diarrhoea with cramping lower abdominal pain ± tenesmus and features of systemic inflammation (see Box 4.1). Always consider the possibility of ischaemic colitis if the patient is elderly or hasooksfree known vascular comdisease/atrial fibrillation; if ischaemic colitis is suspected, arrange a CT mesenteric angiogram. Otherwise, send stool for culture and assess as described in meboChapter 9.

5 Unilateral loin or flank pain? B Suspect renal tract obs ruction (usually due to a calculus) if there is severe, colicky loin pain (see above) that radiates to the groin ± testes/ Very distended Distended low-lying labia. Patients will typically writhe in pain, unable caecum transverse colon to find a comfortable position (in contrast to Fig. 4.5 Intestinal obstruction. A Small bowel. patients with peritonitis who lie very still). Visible B Large bowel. (From Begg JD. Abdominal X-rays Made (macroscopic) or dipstick (microscopic) haema- Easy, 2nd edn. Edinburgh: Churchill Livingstone, 2006.) turia is present in 90% of cases and vomiting is oks commonooksfree.com during bouts of pain. o s ee. Abdominal pain 33 Acute abdominal pain: step by-step assessment

Exclude an AAA if the patient is at high risk, Consider other causes ± surgical review e.g. male >60 years with vascular disease, or 7 or further imaging if any concern if the presentation is atypical, e.g. absence of haematuria/restlessness/radiation to groin: Organize CT angiography to look for features request an urgent USS and, if this confirms of mesenteric ischaemia in any patient with theooks presence re of an AAA, arrange immediate severe, diffuse pain, shock or unexplained lactic 4 surgical review. Otherwise, organize non-contrast acidosis – especially if patients are elderly or have abdominal CT (or IVU if CT is not available) to vascular disease/atrial fibrillation The abdominal confirm the presence of a stone. m boexamination e may co be unremarkablemebook until advanced In patients with a confirmed stone, check renal stages. function and look for features of infection proximal Consider atypical presentations of common disorders such as acute appendicitis or inflam- to the obstruction including ↑temperature/WBC/ CRP or leucocytes/nitrites on urinalysis. If you matory bowel disease. A retrocaecal appendix suspect proximal infection, take urine and blood may present with flank pain while any area of the cultures, give IV antibiotics and refer urgently gut may develop a Crohn’s inflammatory mass. to urology. Bo h gastroenteritis and hypercalcaemia may Suspect pyelonephritis if flank pain is non-colicky cause abdominal discomfort with conspicuous and associated with inflammatory features (see vomiting and minimal abdominal signs – measure Box 4.1), leucocytes and nitrites (produced by serum calcium and enquire about infectious bacteria) on urine dipstick, or loin/renal angle contacts and recent ingestion of suspicious ooksf e com foodstuffs. tenderness ± lower urinary tract symptoms. Consider alternative diagnoses, e.g. acute Functional disorders, e.g. IBS are a frequent cholecystitis, appendicitis, if there ismebo prominent cause sfree of acute com abdominal pain.me The diagnosis ooksf abdominal tenderness/guarding or if urinalysis is of IBS is discussed on page 90, but enquire negative for both leucocytes and nitrites. Take about a background of longstanding intermittent blood and urine cultures, start IV antibiotics abdominal pain with altered bowel habit and and arrange prompt renal USS to exclude a review the notes for previous similar admissions. perinephric collection or renal obstruction. A period of observation with repeated clinical evaluation is very often the key to successful Pain localized to upper or diagnosis; for example, abdominal pain that was 6 lower abdomen? or ginally central and non-specific may, on repeat examination, have migrated to the RIF, suggest- The localization of pain within the abdomen ing a diagnosis of acute appendicitis. Pat ents can be very helpful in narrowing the differential who remain systemically well and whose pain diagnosisooksfre (see Figs 4.1 c and m 4.2). appears to be settling can usually be discharged • If the patient has predominantly RUQ, LUQ, safely, with outpatient review. Those with marked epigastric or generalized upper abdominal systemic upset or other features causing concern pain, proceed to Acute upper abdominalmeb obut sfree.com no clear underlying causemebooksf require further pain (p. 34). investigation ± surgical review. • If the patient has RIF, LIF, suprapubic or bilateral lower abdominal pain, proceed to Acute lower abdominalom pain (p. 38). Abdominal pain 34 Acute upper abdominal pain: overview

Amylase, LFT, erect CXR, ECG fre com Yes Likely perforated 1 Free air on CXR? Urgent surgical review hollow viscus

Yes 2 ECG evidence of ischaemia? Consider acute coronary syndromem o

Yes Urgent surgical 3 Amylase >500 U/L? Likely acute pancreatitis review

Yes Common bile duct obstruction 4 Jaundice? USS s co s cocholangitis, hepatitis

5 Inflammatory response?

No Yes

Yes RUQ pain / tenderness?m Likely cholecystitis USS Yes

Consider pneumonia, pancreatitis, subphrenic abscess, pyelonephritis, appendicitis, gastroenteritis,sf inflammatory bowel m disease

Yes 6 Characteristics of biliary colic? Likely biliary colic USSe No

7 Consider acute gastritis, peptic ulcer, gastroenteritis, non-specific abdominalm pain Observation / surgom cal review if any concern Abdominal pain 35 Acute upper abdominal pain: step-by-step assessment

1 Free air on CXR? 3 Amylase >500 U/L? Perform an erect CXR in all unwell patients with Measure serum amylase in any patient with acute acute upper abdominal pain; the presence of free severe epigastric pain. Patients with an amylase air under the diaphragm (see Fig. 4.4) indicates >3× the reference range are 95% likely to have perforationooks of re a hollow viscus. Secure IV access, pancreatitis; levels >1000 U/L are considered 4 cross-match for blood, resuscitate with IV fluids diagnostic. and refer immediately to surgery. ebo sfIf amylase e colevels are normal or equivocal, If the CXR fails to demonstrate free air or continue to suspect the diagnosism if books the history is equivocal but clinical suspicion is high, e.g. is characteristic and: sudden-onset severe pain with epigastric tender- • there has been a delay in presentation OR ness and guarding, consider an abdominal CT, • there is a history of alcoholism – especially but first check amylase and ECG as described if the patient has had previous episodes of in steps 2 and 3. pancreatitis. In these patients, consider CT with intravenous ECG evidence of ischaemia? 2 contrast (provided renal function is satisfactory) Acute coronary syndromes, particularly inferior to look for evidence of pancreatic inflammation myocardial infarction (MI), may present atypically Once the diagnosis has been made, evalu- with epigastric pain. However, hypotension or ate repeatedly for evidence of complications, severeooksfre bleeding in patients com with acute abdominal e.g. shock, hypoxia (acute respiratory distress pathology may provoke or exacerbate ischaemia syndrome, ARDS), disseminated intravascular in patients with stable coronary artery disease; in coagulation (DIC); calculate the Glasgow these circumstances, administration ofmeboo powerful prognostic sfree criteria com score (Boxmebooksf 4.2) or other antithrombotic agents may have catastrophic validated prognostic score; and monitor CRP. consequences. • Perform an ECG in all patients. 1 • Refer immediately to cardiology if there are Box 4.2 Modified Glasgow criteria for features of an ST elevation MI (see Box 6.1, assessing prognosis in acute pancreatitis p. 51). • Age >55 years • In patients with ST depression, evaluate • PaO2 <8 kPa (60 mmHg) carefully for hypotension, sepsis, hypoxia • WBC >15 × 109/L and bleeding before attributing changes to • Albumin <32 g/L • Serum calcium 2.00 mmol/L (8 mg/dL) (corrected) an acuteksfre coronary com event. < • Glucose >10 mmol/L (180 mg/dL) • In patients with non-specific T wave • Urea >16 mmol/L (45 mg/dL) (after rehydration) changes (see Box 6.1, p. 51), measure • ALT >200 U/L boo cardiac biomarkers to assist diagnosis and • LDH >600 U/L continue to search for alternative causes. me1Severity ree and prognosis co worsen as the number of these factors • Seek cardiology input if there is any increases. More than three implies severe disease. diagnostic doubt. Abdominal pain 36 Acute upper abdominal pain: step-by-step assessment

Manage all patients with severe or high-risk acute inflammatory features accompanied by any of pancreatitis (shock, organ failure, Glasgow score the following: ≥3 or peak CRP >210 mg/L) in a critical care unit. • localized RUQ pain Perform an abdominal USS to look for gallstones • direct tenderness to palpation in the RUQ and an MRCP if there is jaundice or a dilated • positive Murphy’s sign (sudden arrest commonooksfre bile duct (CBD) com on USS. Rarely, those of inspiration while taking a deep breath with severe pancreatitis may require urgent ERCP during palpation of the gallbladder). and stone extraction. Consider CT after five days In the absence of acute cholecystitis, the USS to assess the extent of pancreatic injury and meboomay frereveal an coalternative causemeboo for the presenta- look for evidence of complications, e.g. infection, tion, e.g. pyelonephritis, hepatitis, subphrenic particularly in patients with persistent organ failure collection. or a systemic inflammatory response. In cases of If none of these features is present, consider diagnostic uncertainty, an earlier CT may be helpful. alternative disorders: • basal pneumonia if there is clinical or 4 Jaundice? CXR evidence of basal consolidation (see Organize an urgent abdominal USS for all patients Figs 12.3 and 12.4, p. 118), especially with acute upper abdominal pain and jaundice if accompanied by productive cough or to look for evidence of biliary obstruction or dyspnoea hepatitis. • gastroenteritis in patients with an acute ooksfrAssume biliary sepsis, com at least initially, if the vomiting illness and no abdominal guarding patient is unwell with high fever ± rigors or or rigidity (reassess regularly) cholestatic jaundice (p. 176); give IV antibiotics • acute pyelonephritis if urinalysis is positive and, if the USS confirms a dilated meCBD, refer o for ree.co leucocytes/nitrites. m boo immediately to surgery for further investigation Otherwise, consider USS/CT to exclude (MRCP) and biliary decompression (ERCP). atypical presentations of acute appendicitis/ Assess as described in Chapter 19 if there pancreatitis/cholecystitis, Crohn’s disease or are clinical or USS features of acute hepatitis. other acute inflammatory pathology.

5 Inflammatory response? 6 Characteristics of biliary colic? At this stage, use the presence or absence of a systemic inflammatory response (see Box 4.1) Biliary colic is a common cause of acute severe to narrow the differential diagnosis. upper abdominal pain in patients who are Arrangeoksf prompt e abdominal com USS to confirm or otherwise well and do not exhibit evidence of a exclude acute cholecystitis in any patient bowith systemic s e inflammatory com response. Abdominalboo US sS Abdominal pain 37 Acute upper abdominal pain: step by-step assessment can assist the diagnosis by demonstrating the ingestion of suspicious foodstuffs are likely to presence of gallstones. However, asymptomatic have gastroenteritis. gallstones are very common and so the history Suspect acute gastritis if the patient reports is critical to making an accurate diagnosis. new-onset gnawing, burning or vague epigastric Lookoksfre for the following suggestive features: discomfort ± mild tenderness – especially if this • onset of pain a few hours after a meal (may is associated with dyspeptic symptoms, e.g. 4 waken the patient from sleep) nausea, belching, heartburn or a history of recent • duration ≤6 hours followed by complete alcohol excess/NSAID use; consider peptic ulcer resolution of symptoms m bdisease fre if there co is a backgroundmebooks history of similar • the main site is the epigastrium or RUQ ± symptoms. radiation to the back In many cases, no definite diagnosis is • constant, vague, aching or cramping reached. Admit for observation ± surgical review discomfort (it is not, strictly speaking, if symptoms are not improving or there are wor- ‘colicky’) rying features on examination. Otherwise, patients • history of previous similar episodes. can usually be discharged, with further outpatient assessment if symptoms recur or persist. Arrange abdominal USS only in patients with a suggestive history. ksfr e co Consider other causes ± observation/ 7 surgical review if any concern Systemically well patients with an acute vomiting illness and recent infectious contactme or free com Abdominal pain 38 Acute lower abdominal pain: overview

Urgent Known pregnancy, positive Yes Ectopic pregnancy / 1 gynaecological pregnancy test or PV bleeding? fre other cause sfre com review No

2 Pain predominantly in RIF?

No Yes

Pain migration + RIF tenderness Yes Urgent surgical Likely appendicitis + ↑WBC / CRP?m m review

Yes Consider urgent Any of above features? Possible appendicitis USS / CT

LLQ pain, tenderness + Yes Surgical review 3 Consider diverticulitis b f inflammatory response? + CT

Pelvic examination

Gynaecological Yes review Acute pelvic inflammatory 4 Suspect acute gynaecological pathology? e ± USS disease, ovarian cyst / ee c torsion No

Yes 5 Leucocytes / nitrites on urinalysis? Likely urinary tract infection

Consider atypical appendicitis, endometriosis, terminal ileitis, mesenteric adenitis, renal stone 6 Observation / surgical review if any concern Abdominal pain 39 Acute lower abdominal pain: step-by-step assessment

Known pregnancy, positive pregnancy An ↑WBC and ↑CRP are not specific for 1 test or PV bleeding? appendicitis but the diagnosis is unlikely if both are within normal limits. Nevertheless, a Perform a bedside pregnancy test in any pre surgical review is mandatory if the presentation or peri-menopausal woman with acute lower is otherwise typical – especially if <12 hours from abdominalook frepain. If positive or the patient has onset of symptoms. 4 vaginal bleeding, request an urgent gynaecologi- Maintain a high index of suspicion for appen- cal review with transabdominal ± transvaginal USS dicitis in any patient with RLQ pain. Request to exclude ectopic pregnancy. If the mebopregnancy prompt sfre surgical co review andme consider ooksf urgent test is negative but there is ongoing suspicion of imaging to assist diagnosis if pain is accompa- pregnancy, e.g. missed period, vaginal bleeding, nied by either of the two clinical features listed send blood for formal laboratory measurement above or an ↑WBC/↑CRP. of beta-human chorionic gonadotrophin. Abdominal USS may help to confirm the Request a gynaecological review for assess- diagnosis rapidly or, in females, identify pelvic ment of pregnancy-related complications in any pathology, e.g. ovarian cyst/torsion. woman with known intra-uterine pregnancy CT offers greater diagnostic accuracy and who develops acute lower abdominal pain, but may be considered in males or if diagnostic consider alternative diagnoses, including acute uncertainty persists after USS. appendicitis. oksfree com LLQ pain, tenderness + inflammatory 2 Pain predominantly in RIF? 3 response? The two most helpful clinical characteristics of Exclude sigmoid diverticulitis in any patient with acute appendicitis are: me ksacuteree.com LLQ pain and tendernessm ( bo± guarding) sf • migration of pain from the periumbilical with evidence of systemic inflammation (see region to the RLQ Box 4.1) – especially if >40 years. Even in the • RLQ tenderness or signs of local absence of overt tenderness or inflammatory peritonism. features, maintain a high degree of suspicion In the absence of previous appendectomy, if the patient is elderly or has known diverticular acute appendicitis is highly likely if both of these disease. Arrange urgent CT to confirm the features are present, alongside mild fever or an diagnosis and identify complications, e.g. ↑WBC or ↑CRP. In these circumstances, imaging abscess, or to seek an alternative cause for f is unlikely to contribute to the diagnosis and the presentation. patients should be referred immediately to the o sfre com on-callooksfree. surgeon. m Abdominal pain 40 Acute lower abdominal pain: step-by-step assessment

4 Suspect acute gynaecological pathology? • adnexal tenderness on bimanual vaginal examination. Have a high index of suspicion for acute The diagnosis is often one of exclusion gynaecological pathology in any woman of and, in the emergency setting, it is prudent to child-bearing age with acute pelvic or lower seek formal gynaecological input; in difficult abdominal pain. ooksfre com cases, diagnostic laparoscopy may be required. Organize an urgent USS if there is a history of Whenever the diagnosis is considered, take abrupt-onset, severe, unilateral pelvic or lower endocervical swabs for chlamydia and gonor- abdominal pain with any of the following features: me orhoea, re and treat o in all cases mebif positive. oks • associated nausea and vomiting • unilateral tenderness 5 Leucocytes/nitrites on urinalysis? • adnexal tenderness or palpable adnexal mass Suprapubic pain/tenderness is common in UTI • age <35 years. but the absence of nitrites and leucocytes on urinalysis makes the diagnosis unlikely. The principal aim of USS is to look for evidence Acute appendicitis may cause dysuria, fre- of ovarian torsion but it may reveal an alternative quency and urgency with positive urinalysis, e g. diagnosis, e.g. ovarian cyst. Request a gynaecol- haematuria, leucocytes, if the inflamed appendix ogy review if you have a strong clinical suspicion lies adjacent to the bladder or ureter always of torsion or the USS result is equivocal. consider this possibility, particularly in males (in In the absence of features suggesting ovarian ooksfree m whom cystitis is rare). However, in the absence torsion, consider acute pelvic inflammatory of other worrying features, a positive urinalysis disease (PID). Suspect the diagnosis if there is for both leucocytes and nitrites, especially in bilateral lower abdominal pain and tenderness mebowomen, sfree suggests com UTI; send mebooksfan MSU and start ± fever associated with any of the following empirical treatment. features: • abnormal vaginal or cervical discharge • tenderness on moving the cervix during bimanual vaginal examinationcom (‘cervical excitation’) Abdominal pain 41 Acute lower abdominal pain: step by-step assessment

Consider other causes ± observation/ radiates to the testes/labia or is associated with 6 surgical review if any concern visible/dipstick haematuria. The diagnosis of acute urinary retention is Consider atypical presentations of appendicitis usually obvious but should be excluded in con- resulting from variations in the position of the fused patients with lower abdominal tenderness appendix;ook for fre example, an inflamed appendix that and distress. Clinical examination should be 4 lies within the pelvis may only be tender on rectal diagnostic but a bladder scan may be helpful. examination. Alternative diagnoses in patients In female patients, consider the possibility of with inflammatory features include terminalmebo ileitis alternative fre pelvic co pathology, e.g.mebooks endometriosis and mesenteric adenitis. Seek a formal surgical or mittelschmerz (recurrent episodes of lower opinion if the diagnosis is uncertain. abdominal pain that regularly occur midway Consider mesenteric ischaemia in any patient through the menstrual cycle), especially if there who appears unwell or has an unexplained lactic is a background of previous similar episodes at acidosis – especially if they have known vascular the midpoint of their menstrual cycle. disease or atria fibrillation. In many patients, a precise diagnosis remains An obstructed renal stone most commonly elus ve and, as with upper and generalized presents with loin pain but, once descended abdominal pain, functional disorders are a f to the ureter, may cause more localized tender- commonsfree cause. com nessoksfree.com in the RLQ or LLQ; suspect this if the pain Abdominal pain 42 Chronic/relapsing abdominal pain: overview

Full clinical assessment, PR exam, FBC, LFTs, ESR, CRP, Ca2+, coeliac serology f e com r Upper GI symptoms with Yes Peptic ulcer disease, 1 UGIE alarm features? gastric cancer, gastritis

Lower GI symptoms with Yes 2 Colonoscopy Colon cancer, colitis alarm features?

Jaundice, abnormal LFTs, hepatomegaly, Yes 3 Abdominal Hepatobiliary cancer, biliary ascites or typical history of biliary colic? USS colic, (or other diagnosis)

Yes Renal cancer, stone d sease, 4 Loin pain + mass or haematuria? oRenal eeUSS adult polycystic kidney o ee. (± CT) disease oo No

Consider pelvic malignancy, Cyclical pain, pelvic mass, dyspareunia Yes 5 endometriosis, pelvic inflammatory or abnormal PV bleeding / discharge? disease

Cancer, Crohn’s disease, Palpable mass, weight loss, systemic Yes 6 Abdominal chronic pancreatitis upset or unexplained jaundice? free CT (or other diagnosis) No

Clinical or laboratory features Yes 7 oFurther e investigation ± refer GI suggesting organic disease?

Likely functional disorder, e.g. irritable bowel syndrome Reassess or refer GIm / gynaecology if persistent troublesome symptomsm / organic features Abdominal pain 43 Chronic/relapsing abdominal pain: step-by-step assessment

1 Upper GI symptoms with alarm features? 2 Lower GI symptoms with alarm features? Arrange prompt UGIE if there is upper abdominal Arrange urgent lower GI endoscopy in any discomfort ± other dyspeptic symptoms with patient with: any of the following: • rectal bleeding • ooksf weight loss e • a palpable rectal mass 4 • dysphagia • iron deficiency anaemia • persistent vomiting or early satiety • change in bowel habit and >45 years or • abdominal distension m ksfrecent e weight co loss. m s • haematemesis or iron deficiency Consider flexible sigmoidoscopy as the first-line anaemia investigation in patients <45 years, colonoscopy • ≥55 years with new-onset persistent if >45 years. Obtain the biopsy results of any symptoms. suspicious lesions or sections of GI mucosa. If a gastric ulcer is identified, ensure that a biopsy is sent to exclude malignancy, prescribe Jaundice, abnormal LFTs, hepatomegaly, H. pylori eradication therapy if the CLO test is 3 ascites or typical history of biliary colic? positive recheck the history for NSAID use, and consider an interval UGIE to ensure satisfactory The combination of new-onset jaundice and healing. persistent/recurrent abdominal discomfort ooksfreeEradicate H. pylori in any m patient with a duo- suggests hepatitis, choledocholithiasis or, most denal ulcer and confirm successful eradication frequently, malignancy, e.g. biliary, ampullary, with a urea breath test. ebopancreatic f e or comhepatocellular cancer or hepatic In patients with macroscopic appearances of metastases. USS may revealmebook the cause but, if an upper GI tumour, obtain the formal biopsy inconclusive, further investigation, e.g. CT or result and consider a staging CT scan. MRCP, is mandatory. m Abdominal pain 44 Chronic/relapsing abdominal pain: step-by-step assessment

Arrange USS and perform a diagnostic ascitic lower abdominal pain. The features of PID are tap in any patient with ascites (send for biochem- described above; if present, take endocervical istry microbiology and cytology). If the ascites is or vaginal swabs for gonorrhoea and chlamydia exudative and USS fails to reveal an underlying – treat if positive. cause, organize an abdominal CT scan. Consider endometriosis in any woman of ooksfreThe features of biliary com colic are described reproductive age with severe dysmenorrhoea, above. If present, arrange USS to look for or chronic lower abdominal pain and any of the gallstones. Note that gallstones are a very following features: eboo sf frequent finding in asymptomatic mebpatients so, • sfre variation with co menstrual cycle unless the history is typical or there is evidence • deep dyspareunia of a complication, e.g. dilated CBD, chronic • other prominent cyclical or perimenstrual cholecystitis, they are unlikely to explain the symptoms. presentation. Establishing a definitive diagnosis of endome- Refer to a GI specialist if there is a convincing triosis may be challenging – refer to a gynaecolo- history of biliary pain in the absence of gallstones, gist for further assessment, e.g. laparoscopy if especially if associated with abnormal LFTs or symptoms are severe. a dilated CBD.free c m Palpable mass, weight loss, systemic 4 Loin pain + mass or haematuria? 6 upset or unexplained jaundice? You must exclude upper renal tract cancer in At this stage, organize an abdominal CT if the any patient presenting with persistent oin pain patient has any of the above features. Patients associated with a mass or haematuria (visible or with a palpable mass may have been investigated dipstick). Renal USS is a first-line investigationmeb with free.cother modalities m in steps meb1–5 above b out CT and may reveal alternative causes, e.g. APKD or is more likely to identify certain masses, e.g. chronic hydronephrosis. Consider CT ± urology pancreas, small bowel, renal tract and omental, referral if the cause remains unclear, especially and should be performed if the cause remains in patients >40 years. uncertain. In patients with abdominal pain and significant weight loss or other major constitu- Cyclical pain, pelvic mass, dyspareunia or tional upset, e.g. fevers, night sweats or ↑↑ESR, 5 abnormal PV bleeding/discharge? CT may reveal evidence of lymphoma, solid organ Organize a pelvic USS in any patient with a malignancy or inflammatory disease, e.g. chronic pelvic mass or any postmenopausal patient pancreatitis, abscess, Crohn’s disease sf withooksfree PV bleeding or c recent-onset, m persistento sfree.com Abdominal pain 45 Chronic/relapsing abdominal pain: step by-step assessment

Clinical or laboratory features suggest if evidence of vascular disease elsewhere, e.g. 7 organic disease? angina, intermittent claudication. Assess any patient with associated diarrhoea Further investigation is usually required if the Even in the absence of diarrhoea, consider further patient is >45 years with recent-onset symptoms, investigation for small bowel Crohn’s disease, weightook loss, fr constitutional co upset or abnormal e.g. enteroscopy, barium follow-through or small 4 screening investigations. Important organic bowel MRI in a young patient with unexplained causes of pain that may easily be missed mouth ulcers, ↑ESR/CRP, extraintestinal mani- include chronic pancreatitis, chronic mebomesenteric festations fre (see co Box 9.3, p. 91)mebooks or persistent RLQ ischaemia and Crohn’s disease. tenderness. Consider chronic pancreatitis in any patient If none of the above is present, a functional with a background of chronic alcohol excess or cause, e.g. IBS is likely – particularly when typical steatorrhoea. Check faecal elastase, perform an symptoms are present (see Box 9.1, p. 90). abdominal CT and consider specialist referral for However, patients with persistent, troublesome further assessment. symptoms may require specialist assessment Exclude mesenteric ischaemia (CT mesenteric and investigation to exclude organic disease angiography) if there is a close relationship free com betweenksfree eating and the com onset of pain, especially Breast lump 5o s

Breast lump is the most common presenting Breast abscess feature of breast cancer. All breast lumps must be referred to a specialist breast service for The lump usually develops rapidly and is tender. evaluation by triple assessment, comprising There is often overlying erythema; there may be clinical, radiological and pathological evaluation. fever and evidence of a systemic inflammatory The majority of referrals to breast services are response benign. Results of malignant lumps should be In lactating women, breast abscesses occur managed in a multidisciplinary team setting. most frequently in the first 12 weeks post-partum; USS is the imaging modality of choice in painful, cracked nipples are common. It may be women <35 years due to the high density difficult to distinguish an abscess if breast tissue ofooksfree.com breast tissue. MRI scanning is suitable for is grossly indurated due to mastitis; in these cases selected patients. Older women should have referral should be made for further booksassessment mammography ± USS. Pathological assess- and ultrasound imaging. ment is undertaken by ultrasound-guidedmebo core sfreeIn non-lactating com women, abscesses are biopsy, fine needle aspiration (for cystic lesions) uncommon and an underlying inflamma- or occasionally excision biopsy. tory cancer should be excluded. Subareolar abscesses are the most common form, typically Breast cancer associated with a periductal mastitis; there is a The breast is the most common site of cancer in strong association with smoking. women; 1 in 9 women in the UK are affected by Fibroadenoma breast cancer in their lifetime. The risk increases with age and the mean age at diagnosis is 60 Fibroadenoma is a common benign neoplasm years. Risk factors are shown in Box 5.1. Features that occurs after puberty in younger women of a breast lump that suggest cancer are shown usually <30 years. It typically presents as a in Box 5.2. However, it is not possible to exclude discrete, mobile, non-tender mass with a rubbery ooksfree.c m consistency. The diagnosis should be confirmed cancer by clinical examination alone and all palpable booksf masses should be regarded as potentially malignantebo by sfr triple assessment. e com until proven otherwise. Fibrocystic change Fibrocystic change is a benign condition associated with tender, lumpy breasts that may affect up to 50% of women between 20 and 50 years but is Box 5.1 Risk factors for breast cancer

• Previous breast cancer • Increasing age Box 5.2 Suspicious features of breast lump • Family history • Oral contraceptive pill • Hardness • Hormone replacement therapy • Immobilityfree m • Ea ly menarche • Skin tethering/puckering • Late menopause • Skin changes (peau d’orange, eczema) • Nulliparityoksfre c m • Nipple retraction • First pregnancy >35 years • Lymphadenopathy • Current smoker • Bloody nipple discharge Breast lump 47 Differential diagnosis rare after menopause. Features often vary over nodules, and resolves over weeks. Galactocoele the course of the menstrual cycle due to hormone is a rare cystic lesion of the breast. It contains fluctuations. Areas of firm, lumpy breast tissue milk and most commonly occurs in lactating without a discrete mass are often termed nodular women; occurrence in non-lactating women breast tissue; if this is localized or asymmetrical and requires further endocrine investigation. persistsooksfre throughout the cycle, referral should be made to exclude underlying cancer. Breast cysts Nipple lesions 5 are firm, smooth, well-defined lumps which may These must be investigated (triple assessment) cause discomfort if enlarging. USS confirms their mebotosfre rule out an underlying o cancer.m Causes ooksf include cystic nature. If needle aspiration yields bloody fluid, Paget’s disease of the nipple (95% association this should be sent for cytological examination. with cancer), nipple adenoma, eczema of the Fat necrosis nipple, basal cell carcinoma, melanoma and Bowen’s disease. Fat necrosis is a benign condition that arises after trauma or surgery. It may present as a firm, Male breast disease irregular mass with tethering to overlying skin, making it difficult to distinguish from malignancy. Breast lumps in men are rare. Gynaecomastia Irrespective of recent trauma, all lumps with most commonly presents as a rubbery button suspicious features should be regarded as of tissue, concentric to the areola. It occurs potentiallyooksfree malignant cand mevaluated urgently byo frequently sfre at compuberty and necessitates careful triple assessment. testicular examination and assessment of sexual development. Around 25% are idiopathic. Other Other causes causes include drugs (~20%), e.g. spironolac- Skin and subcutaneous lesions, such as epi- tone, anabolic steroids, liver cirrhosismebooks (decreased dermoid cysts and lipomata, may occur on the metabolism of oestrogen, <10%), gonadal failure breast. Phylloides tumours are rare and share (decreased androgens, <10%) and testicular many clinical features with fibroadenomas but tumours (increased oestrogen production, are typically more aggressive; metastasis is ~3%). Male breast cancer (1% of all breast rare but can occur. Superficial thrombophlebitis cancers) typically presents as a hard, fixed lesion, (spontaneous thrombosis of superficial breast sometimes with overlying skin involvement, and veins) presentsfree.com with palpable, erythematous linear is usuallyree.com eccentric to the areola. Breast lump 48 Overview

Full clinical assessment + breast examination f e 1 Discrete lump palpable?

Yes No

Asymmetrical or localised No m Re-examine and consider breast imaging. nodularity?

Yes

Refer for triple assessment if patient >35 years or lump persists aftere menstruation c m

Yes

Yes 2 Evidence of abscess? Refer to on-call breast specialist

Features of/risk factors for Yes 3 Refer urgently for triple assessment breast cancer?

Refer for triplee assessment

A B C

Fig. 5.1 Positions for inspecting the breast. A Hands pressed into hips. B Hands above head. C Leaning forward. (From Ford MJ, Hennessey I, Japp A. Introductionme to Clinical Examination, 8th edn. Edinburgh: Churchillme Livingstone, 2005.) Breast lump 49 Step-by-step assessment

1 Discrete lump palpable? breast/surgical team. Refer to a breast specialist to exclude an abscess in any breast-feeding If you are unable to locate a lump, ask the patient woman with gross mastitis and induration to attempt to find it and examine in different positions, e.g. supine and upright. In the absence Features of/risk factors for ofooks a discrete lump, re assess carefully for nodularity. 3 Refer any patient >35 years old with a localized breast cancer? 5 area of nodularity or discrete lump for urgent triple Refer any patient with a palpable breast lump assessment. If the patient is <35 years,mebo refer for s specialist re triple co assessmentm to exclude breast f for triple assessment if the localized nodularity cancer. persists at review after menstruation. Request urgent review if: If no lump or nodularity is detected, consider • patient has risk factors for breast cancer ultrasound or mammography as appropriate to (Box 5.1) exclude underlying impalpable pathology. • lump is rapidly enlarging • lump has features of breast cancer (Box 2 Evidence of abscess? 5.2) Suspect breast infection if there is an acute, • patient ≥30 years with a new discrete lump painful swelling with overlying erythema, fever or • patient <30 years with a major risk factor, a systemic inflammatory response; start antibiotic e.g. personal or family history of breast treatmentooksfre and refer comas an emergency to theo cancer. ree. om ooks

Clinical tool Breast examination • Obtain consent and offer a chaperone; ensure privacy against the chest wall using the palmar surface of the and a warm room. fingers held flat on the surface of the breast. Palpate • Enquire whether the patient has noticed any breast clockwise to cover all of the breast tissue, including lumps and ask her to point them out. under the nipple. • With the patient sitting comfortably, hands resting on • Record the size, position, attachments, mobility, the thighs, inspect for asymmetry, local swelling, skin su face, edge and consistency of any lumps and look changes, e.g. dimpling, redness and nipple inversion or for associated signs of inflammation (tenderness, discharge. warmth, redness). • Repeat the inspection (Fig. 5.1) with the patient’s • Palpate for axillary lymph nodes. Ask the patient to sit handsoksfree.com pressed against her hips (contracting the facing you and support the full weight of her arm at the pectoral muscles), raised above her head (stretching wrist with your opposite hand. After warning of possible the pectoral muscles) and sitting forward with the discomfort, use your other hand to palpate all around breasts dependent. the axilla, compressing its contents against the chest • With the patient supine, and hands under the head, wall. Repeat on the other side. palpate each breast: compress the breastmeb tissue free.com mebook Chest pain 6o sf

Chest pain is one of the most common presenta- and 20% relative increase) and a decrease in tions encountered in both emergency medicine the diagnosis of unstable angina. and medical outpatient clinics. The diagnostic Unstable angina or NSTEMI may also occur approach to acute chest pain is different from in the absence of acute plaque rupture if hypox- that of intermittent chest pain and they should aemia, anaemia, tachyarrhythmia or hypotension be considered as distinct clinical entities. is superimposed upon stable coronary artery disease (CAD). Acute chest pain The pain of myocardial ischaemia is desc ibed below (see ‘angina pectoris’). Theo primary k reeaim is to com identify acute coronary • In unstable angina, the pain: syndromes (ACSs) and other life-threatening • is of new onset and severe causes, such as aortic dissection and pulmonary • occurs at rest or embolism (PE). ECG analysis, CXR andmebo biomark- sfree• occurs comwith increasing mfrequency, ksf ers, e.g. troponin, D-dimer, play a central role duration or intensity. in evaluation and are intimately linked with the • In STEMI, the pain is typically severe, clinical assessment. Pleuritic chest pain has a with an abrupt onset, and is persistent, sharp or stabbing character and varies with unrelieved by glyceryl trinitrate (GTN) respiration (worse on inspiration); it should be spray and accompanied by autonomic differentiated from non-pleuritic pain at an early upset (sweating, nausea and vomiting). stage, as it suggests a different range of possible • The presentation of NSTEMI may lie diagnoses anywhere between these two extremes; it is distinguished from unstable angina by Acute coronary syndromes biochemical evidence of infarction Acute thrombus formation in a ruptured or eroded (↑troponin), and from STEMI by ECG atheromatousook f ee.comcoronary artery plaque causes an features (Boxes 6.1 and 6.2). ACS. Sudden total occlusion of a major vessel • Certain groups of patients, e g elderly or causes ischaemia of a full-thickness segment diabetic, may have no or minimal pain. of myocardium resulting in acute STmebo elevation ree.com me o myocardial infarction (STEMI). The mainstay of Aortic dissection treatment in these patients is immediate reperfu- This is a tear in the wall of the aorta. It typically sion by primary angioplasty or fibrinolytic therapy. causes sudden onset, intense, unrelenting chest With incomplete occlusion or a good collateral pain that radiates to the back, between the blood supply there is less extensive ischaemia, shoulder blades (this may be the main site of which is usually associated with a degree of pain). The character of the pain is often described cardiomyocyte necrosis (non-ST elevation as ‘ripping’, ‘tearing’ or, most frequently, ‘sharp’. myocardial infarction; NSTEMI). Less frequently, Autonomic upset is common; syncope or focal myocardial ischaemia can occur without cell neurological deficit may occur. Mortality is high loss (unstable angina). The introduction of (1% per hour in the initial phase). Aortic dissection high-sensitivityooksfree.com cardiac troponin measurements must be suspected in any patient presenting (with gender-specific cut-offs) has resulted in an with coexisting cardiovascular and neurological increase in the detection of MI (~4% absolute symptoms or signs. ebooksf mebo sfree.com Chest pain 51 Differential diagnosis

Box 6.1 ECG abnormalities in acute Box 6.2 Universal definition of coronary syndromes myocardial infarction

ECG abnormalities in STEMI Outside the context of sudden death, percutaneous 1 o≥1 mm sfr ST elevation in at least 2 adjacent limb coronary intervention or coronary surgery, acute leads, e.g. II and III; I and aVL OR myocardial infarction (MI) should be used when there 2. ≥2 mm ST elevation in at least 2 adjacent is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these praecordial leads, e.g. V2 and V3; V5 and V6 OR 3. Left bundle branch block of new onset conditions any one of the following criteria meets the mdiagnosis fr for MI. o meboo 6 Major ischaemic ECG changes (strongly suggestive • Detection of a rise and/or fall of cardiac biomarker of myocardial ischaemia) values (preferably cardiac troponin [cTn]) with at least 1. ST changes that vary with onset and offset of pain one value above the 99th percentile upper reference (‘dynamic’ changes) limit (URL) and w th at least one of the following: 2. ≥1 mm horizontal ST depression in ≥2 adjacent • symptoms of ischemia leads • new or presumed new significant ST-segment–T 3. Deep symmetrical T wave inversion wave (ST–T) changes or new left bundle branch Minor ischaemic ECG changes (less specific for blockee.com (LBBB) myocardial ischaemia) development of pathological Q waves in the ECG • imaging evidence of new loss of viable 1 <1 mm horizontal ST depression myocardium or new regional wall motion 2 oNew or sfre evolving T wave c inversion or flattening abnormality • identification of an intracoronary thrombus by angiography or autopsy.

Source: Thygesen K, Alpert JS, Jaffe AS et al. 2012. Universal Pulmonary embolism definition of myocardial infarction. Eur Heartm J. 33:2551–2567. b Pain due to PE depends on the site and size of the embolism. Small emboli commonly produce pleuritic symptoms due to distal pulmonary infarction and may produce few other clinical signs; usually presents with ‘heartburn’: a hot or burning large emboli may produce severe, sudden-onset, retrosternal discomfort that radiates upwards; central chest pain that mimics MI due to central some patients experience severe episodes of pulmonary occlusion. Most patients with large pain that mimic cardiac pain, possibly due to embol are dyspnoeic and have other features reflux-induced spasm. Important clues include such as haemoptysis, syncope or shock. The onset after eating, aggravation of symptoms majority of emboli arise from lower limb deep by lying supine or bending over, and, often, veinooksfree thrombosis (DVT), com but clinical features of a history of recent weight gain Oesophageal DVT are inconsistent and often absent rupture is often diagnosed late and carries a high mortality. It should be suspected in any Acute pericarditis meboopatient sfree who develops c chest painmebooksf after vomiting. This typically causes constant retrosternal pain with a sharp, stabbing character that may radiate Pneumothorax to the shoulders, arm or trapezius ridge. It is Pneumothorax causes unilateral, sudden-onset usually more localized than ischaemic pain and pleuritic chest pain, often associated with may be accompanied by a rub on auscultation. breathlessness. In large pneumothoraces there Pain is often, but not invariably, worsened by may be ↓breath sounds and hyper-resonance inspiration lying down, with movement or during to percussion. Diagnosis is usually confirmed swallowing, and eased by sitting forward. on CXR. Gastro-oesophageal disorders Pneumonia Oesophagealoo sfree.com spasm can cause severe This may cause pleuritic pain, usually accom- retrosternal discomfort that mimics cardiac panied by other clinical features such as fever, pain. Gastro-oesophageal reflux disease (GORD) cough, purulent sputum and breathlessness. mebo sfree.co mebo f Chest pain 52 Differential diagnosis

Musculoskeletal problems Box 6.3 Estimating the likelihood of coronary A common cause of chest discomfort with a wide artery disease1 variety of presentations. The pain often varies with High risk posture or movement, and may be reproduced or exacerbated by local palpation. Rib fracture • Previously documented CAD or other vascular ooksfre co disease, e.g. stroke, peripheral arterial disease typically causes severe pain following trauma but • Male >60 years OR >50 years with ≥2 risk factors most cases are due to minor soft tissue injuries. OR >40 years with ≥3 risk factors Even these can be symptomatic formebo up to 6 • sfr Female >60 years with ≥3 risk factorsmebo weeks. Malignant chest wall invasion produces Moderate risk constant, unremitting, localized pain that is not • All patients not in high-risk or low-risk group related to respiration and may disturb sleep. Low risk Anxiety • Age <30 years A common cause of chest pain. Occasionally, • Female <40 years with no risk factors presentations are dramatic, with patients report- 1Risk factors: cigarette smoking, diabetes mellitus, hypertension, ing intense symptoms. Associated features may hypercholesterolaemia (total cholesterol ≥6.5 mmol/L), family include breathlessness with ‘inability to take h story of premature CAD. enough air’ and tingling around the mouth; the onset of symptoms may coincide with stressful situationsooksfree or emotional distress. m o sfree.c m ‘pressure’ and ‘heaviness’ but many others, e.g. Other causes ‘burning’ are recognized. Many patients do not perceive angina as painful but most feel a sense • Intrathoracic malignancy or connective me of ‘discomfort’ – if you only ask about ‘pain’, tissue disorders, e.g. systemic lupus you may miss the diagnosis. erythematosus, rheumatoid arthritis, may Stable angina is almost always due to ath- involve the pleura and present with pleuritic erosclerotic narrowing in one or more coronary pain pleural effusion. ± arteries. In considering the likelihood of angina, it • Subdiaphragmatic inflammatory pathology, is therefore important to consider the underlying e.g. abscess, can mimic pneumonia risk of CAD (Box 6.3). Myocardial blood flow (pleuritic pain, fever, small pleural effusion). is adequate under resting conditions but is • Mediastinal masses, e.g. thymoma or insufficient to meet metabolic demands during lymphoma, tend to cause a dull, periods of increased cardiac work. Consequently, constant, progressive retrosternal pain that oksfree.com episodes of angina tend to be precipitated by a disturbs sleep. predictable degree of exertion and rapidly relieved • Herpes zoster may cause severe pain, by rest and/or GTN spray, with episodes typically sometimes preceded by tingling or burning, lasting <10 minutes. Less commonly, angina followed by development of a vesicular me omay sfree result from com tachyarrhythmiasmebooksf (especially on rash in a dermatomal distribution. The rash a background of significant coronary narrowing) has often not manifested at the time of or transient coronary artery spasm. presentation, making diagnosis difficult. Gastro-oesophageal disorders Intermittent chest pain Gastro-oesophageal reflux typically causes a hot, burning retrosternal discomfort which radi- Angina pectoris ates upwards; it is often provoked by bending or lying flat, e.g. in bed, and there may be a Angina is the symptomatic manifestation of relationship with food. Symptoms are relieved myocardial ischaemia. It tends to be perceived as by antacids. Oesophageal spasm can cause a ookdiffuse retrosternal fr e. discomfort m that may radiate severe retrosternal discomfort that closely to the left (or right) shoulder/arm, throat, jaw or mimics cardiac pain and may be worsened by back. Typical descriptions include ‘tightness’, exertion and relieved by nitrates. There is often mebo sfree.com mebooksf Chest pain 53 Differential diagnosis an associated history of dysphagia, dyspepsia breathlessness and cough, and precipitants other or typical heartburn. than exertion may be apparent, e.g. common allergens, viral upper RTI. Musculoskeletal disorders These are a common cause of chest discomfort Anxiety withook a wide fre variety of presentations; most are Emotional distress is a very common cause of due to minor soft tissue injuries. The pain typi- chest pain and many suspected angina attacks cally varies with posture or movement and may are actually ‘panic attacks’. Presentations are respond to NSAIDs. In costochondritis,mebo there is often sfre quite dramatic, o with mebpatients reporting f 6 well-localized tenderness of the costochondral throat tightness, a ‘choking’ sensation and/or junctions that is exacerbated by local pressure. difficulty taking a breath. There may be evidence of hyperventilation with tingling around the mouth Asthma and extremities and ↓PaCO2 on ABG. Episodes Patients with asthma may describe exertional tend to arise incom the context of stress rather than chest ‘tightness’ on account of bronchospasm, exertion. which may be difficult to distinguish from angina. There is usuallyfree an associated c m history of wheeze, Chest pain 54 Clinical tool: the ECG in acute chest pain

Clinical tool ECG abnormalities in chest pain The ECG in STEMI recognized by reciprocal anterior ST depression and a

dominant R wave (reciprocal Q wave) in V1. Further ECG Acute transmural ischaemia produces ST elevation in leads changes occur as the infarct progresses (Fig. 6 4): loss of ooksfrethat ‘look at’ the affected region o of myocardium: o the R wave, followed by development of Q waves and T • in anterior MI (Fig. 6.1), V2–V5 wave inversion (TWI). ST segments typically return to • in lateral MI, V5, V6, I and aVL baseline; persistent ST elevation may indicate the • in inferior MI (Fig. 6.2), II, III and aVF. development of a left ventricular aneurysm.meboo Extensive There may be associated ST depression in the opposing anteroseptal infarction may cause new left bundle branch leads (‘reciprocal change’). Posterior MI (Fig. 6.3) is block (Fig. 6.5) rather than ST elevation.

I aVR C1 C4

II aVL C2 C5

III aVF C3 C6

Fig. 6.1 Acute anterior ST elevation myocardial infarction. (From Douglas G, Nicol F mRobertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh:om Churchill Livingstone, 2009.)

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.2 Acute inferior ST elevation myocardial infarction. (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.) e ree Chest pain 55 Clinical tool: the ECGco in acute chest pain Clinical tool—cont’d ECGfre abnormalities in chest pain

I aVR V1 V4

II aVL V2 V5 6

III aVF V3 V6

Fig. 6.3 Acute inferoposterior ST elevation myocardial infarction. (From Grubb NR, Newby DE. Churchill’s Pocketbooks Cardi logy,ks 2nd edn. Edinburgh: Churchill Livingstone, 2006.) ks

I aVR V1 V4

II aVL V2 V5

III aVF V s 3 V6

Fig. 6.4 Evolving anterior ST elevation myocardial infarction.bo s

I aVR V1 V4

II aVL V2 V5

IIIf aVF V3 V6

Fig. 6.5 Left bundle branch block.

Continued Chest pain 56 Clinical tool: the ECG in acute chest pain

Clinical tool—cont’d ECG abnormalities in chest pain

ST elevation in leads V2–V5 can be a normal finding (‘high the presenting hospital ECG with that obtained by the pre- take off’) and, in the absence of a previous ECG, may hospital ambulance service. On the other hand, slight ST cause diagnostic confusion. With high take-off, the ST depression, especially if up-sloping, may be normal ooksfreelevation is typically concave co and frequently associated TWI may be the only ECG evidence of ischaemia. Biphasic with notching in the terminal portion of the QRS complex TWI in leads V2–V3 (Fig. 6.8) or deep symmetrical (Fig. 6.6). Appearances remain stable over time and there TWI in these leads +/− other praecordial leads are no reciprocal changes. ECG features that mebfavour acute (Fig. 6.9) suggests critical obstruction mebookof the left anterior pericarditis from STEMI include: widespread ST elevation descending artery (Wellens’ syndrome). Other patterns of (not corresponding to the territory of a single coronary TWI are less specific. Lateral TWI, together with artery); PR depression; the absence of reciprocal changes, downward-sloping ST depression, is a common feature of Q wave formation or R wave loss; and TWI only after left ventricular hypertrophy (Fig. 6.10) or digitalis normalization of ST segments. treatment; comparison with previous ECGs is very helpful.

TWI confined to leads 1V –V3 (Fig. 6.11) suggests right The ECG in unstable angina/NSTEMI heart strain and favours a diagnosis of PE over ACS. TWI New horizontal ST depression suggests active ischaemia also occurs with cardiomyopathies, pericarditis, (Fig. 6.7); the extent and depth of depression correlate myocarditis, cerebrovascular events (especially with severity of ischaemia and risk of adverse outcomes. subarachnoid haemorrhage), electrolyte abnormalities and ‘Dynamic ST segment changes – those that coincide hyperventilation. However, in the appropriate with pain and normalize with resolution of pain – strongly clinical context, new or evolving TWI supports a diagnosis ooksfree.comsuggest ischaemia. It is therefore important to compare of ACS. ook bo sfree com

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.6 ‘High take-off’ ST segments. (From Hampton JR. The ECG Made Easy, 7th edn. Edinburgh: Churchill Livingstone, 2008.) m Chest pain 57 Clinical tool: the ECGco in acute chest pain Clinical tool—cont’d ECGfre abnormalities in chest pain I VR V1 V4

II VL V2 V5 6

III VF V3 V6

Fig. 6.7 Ischaemic anterolateral ST segment depression. (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone,fre 2008.) re

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V5 ooFig. 6.8 Biphasic T wave inversion in leads V2–V3.

I aVR V1 V4

II aVL V2 V5

III aVF V f 3 V6

Fig. 6.9 Deep symmetrical T wave inversion

Continued Chest pain 58 Clinical tool: the ECG in acute chest pain

Clinical tool—cont’d ECG abnormalities in chest pain

The ECG in acute pericarditis V1, TWI in leads V1–V3 (Fig. 6.11) or right bundle branch block (Fig. 6.13). The ‘classical’ ECG finding of a deep Acute pericarditis characteristically produces diffuse, slurred S wave in I with a Q wave and TWI in III S1Q3T3’) ooksfreconcave (upward-sloping) co ST elevation in most leads, with is rare. ook ST depression in aVR (Fig. 6.12). Associated PR segment depression (with PR elevation in aVR) is highly suggestive. The ECG in aortic dissection Unlike STEMI, ST elevation typically persists for many days. T waves are upright during ST changes but subsequentlymebo The ECG may be normal or show non-specific invert. abnormalities. If the dissection flap involves the ostium The ECG in PE of a coronary artery, there may be ECG changes of a STEMI (usually inferior) The ECG may change rapidly, In most cases, the ECG is normal or shows only sinus i.e. changes of STEMI may resolve then recur, due to tachycardia. Specific abnormalities suggestive of PE differential changes in blood pressure in the true and false include new right axise.co deviation, a dominant R wave in lead aortic lumens.

I VR V1 V4

II VLeV2 e com V5

III VF V3 V6

Fig. 6.10 Left ventricular hypertrophy. (From Hampton JR. The ECG Made Easy, 7th edn. Edinburgh: Churchill Livingstone, 2008.) fre sfre

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.11 Anterior T wave inversion due to acute right heart strain. (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.) bo e bo Chest pain 59 Clinical tool: the ECGco in acute chest pain Clinical tool—cont’d ECGfre abnormalities in chest pain

I VR V1 V4

6 II VL V2 V5

III VF V3 V6

Fig. 6.12 Acute pericarditis. (From Hampton JR 150b ECG Problems, 3rd edn. Edinburgh: Churchill Livingstone,b 2008.)

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.13 Right bundle branch block. (From Hampton JR. 150 ECG Problems, 3rd edn. Edinburgh: Churchill Livingstone, 2008.) m m Chest pain 60 Acute chest pain: overview

ABCDE, ECG fre co ECG changes suggest STEMI Yes Refer urgently to 1 Likely STEMI (see Box 6.1)? Cardiology oo No See Further ‘Major’ ischaemic ECG changes Yes 2 Likely ACS assessment of (see Box 6.1)? NSTEMI / unstable angina (p. 65) No

Suspect aortic dissection / PE / Yes Aortic dissection, pulmonary 3 Urgent oesophageal rupture? embolism, oesophageal imaging rupture, other No

Yes 4 o>1 diagnostic r e.c features of pericarditis? oPericarditis ee No

Yes 5 Clear history of pleuritic pain? See acute pleuritic pain (p. 64) No

6 History cons stentco with ACS? No Yes

Full clinical assessment, repeat ECG, cardiacks biomarkers, CXR, FBC, U+E

See Further assessment Any ischaemic ECG changes Yes Likely ACS; consider 7 of NSTEMI / unstable (see Box 6.1) or ↑troponin? alternative causes angina (p. 63)

No meb

Yes See Further assessment 8 High clinical probability of ACS? Likely ACS of NSTEMI / unstable angina (p. 63) No

Lowe clinical probability m of ACS No 9 or features suggest alternative Consider further investigation for underlying diagnosis? coronary artery disease

Yes

10 Consider GI, musculoskeletal, respiratorby mediastinal fre and psychological causes Chest pain 61 Acute chest pain: step-by-step assessment

ECG changes suggest STEMI Box 6 4) and proceed to further assessment of 1 (see Box 6.1)? NSTEMI/unstable angina. Seek expert help if there is any doubt regarding ECG interpretation Patien s with acute chest pain and ECG changes If the ECG is non-diagnostic, e.g. old left compatible with STEMI (see Box 6.1) are likely bundle branch block, paced ventricular rhythm: to benefit from immediate reperfusion therapy, ook fre • manage as per NSTEMI/unstable angina e.g. primary angioplasty or thrombolysis. if clinical features strongly suggest ACS, Unless ECG changes are old, the history is e.g. pulmonary oedema or presenting incompatible with ACS (Box 6.4) or there is a mebo sfresymptoms co very similar to previousmebooksf MI 6 strong clinical suspicion of aortic dissection (see • consider a near-patient troponin assay, below), make a diagnosis of STEMI. if available (these are specific, i.e. good • Attach cardiac monitoring and repeat to rule in, but not sensitive, i.e. not good ABCDE (p. 8) regularly. enough to rule out, for MI) • Establish the duration of the pain and • otherwise, await laboratory troponin whether it is ongoing. results – check on admission; if negative, • In younger patients with few or no risk repeat up to 12 hours after maximal pain factors for CAD, ask specifically about depending on your local protocol and cocaine or amphetamine use. local troponin assay. Some high sensitive • Seekoksfree urgent Cardiology com input if there is troponin assays are more than 99% diagnostic doubt, haemodynamic instabi ity sensitive for MI at 6 hours after maximal or if primary angioplasty services are pain, or even 3 hours at lower threshold available. values. ebo k • If angioplasty is not available, confirm eligibility for thrombolysis (see Box 22.3, p. 207m). o ree.com Suspect aortic dissection, PE or If ST elevation is present but does not meet 3 oesophageal rupture? the above criteria, repeat the ECG at frequent regular intervals and manage as per NSTEMI/ In the absence of clear ECG evidence of unstable angina. ischaemia/infarction, consider other life- Seek urgent Cardiology input if there is threatening conditions such as aortic dissection, any uncertainty regarding diagnosis or ECG massive PE and oesophageal rupture. For all of interpretation. these a high index of suspicion is vital since delay in diagnosis may prove fatal and characteristic Major’k free. ischaemic omECG changes ‘textbook’ clinical features are often absent. 2 (see Box 6.1)? You must exclude aortic dissection in patients with severe acute chest pain and ANY of the If the ECG shows ‘major’ ischaemic changes, features in Box 6.5. In the absence of these clarify that the history is consistent with ACSeb (see sfree.com ebooksf

Box 6.4 What symptoms are consistent with Box 6.5 Features suggestive of acute acute coronary syndrome? aortic dissection

Symptoms of myocardial ischaemia vary widely and often • Pain reaches maximal intensity within seconds differ from textbook descriptions so, when confronted of onset with compelling ECG evidence of ischaemia, you are • Main site of pain is interscapular likely to find that very few accounts of chest discomfort • Character of pain described as ‘tearing’ or ‘ripping’ are inconsistent with ACS. • Syncope or new focal neurological signs Any pain in the chest (or arms/jaw) that lasts >10 • Newfree. early diastolic o murmur (aortic regurgitation) minutes or that occurs repeatedly for minutes at a time • Asymmetrical pulses (not previously documented) with little or no exertion, is consistent with ACS. The task • Inter-arm blood pressure differential greater than is tooksfree.co determine (using the ECG, cardiac biomarkers, the 20 mmHg ok description of the pain and the underlying likelihood of • Marfan’s syndrome CAD) whether the pain is likely to represent ACS • Widened mediastinum on CXR Chest pain 62 Acute chest pain: step-by-step assessment features, consider the diagnosis in any patient More than one diagnostic features with a first presentation of severe acute chest 4 of pericarditis? pain and no clear alternative diagnosis, especially f e if: Diagnose pericarditis if more than one of the following features is present: • thereo is sfre a background co of hypertension, previous aortic surgery, trauma or • pain radiating to the trapezius ridge (highly pregnancy, or specific for pericarditis) or has typical • the pain is described as ‘sharp’ or radiates features (see p. 51) ebo k to the back. • pericardial friction rub (85% of cases) • typical ECG changes (p. 58; present in 80% A normal CXR does not exclude the diagnosis. of cases). There are two characteristic age presentation peaks for dissection; by far the most common is Request an echocardiogram to detect any in the 7th decade (majority male and associated associated effusion (urgently if any features of with atheroscle osis) but there is also a small tamponade – p. 265) and assess LV function peak in the 3rd decade that mustn’t be forgotten (may be impaired if associated myocarditis). (mainly females and associated with connective tissue disease). 5 Clear history of pleuritic pain? If you suspect dissection, arrange immediate If the patient reports pain that clearly and contrast enhanced thoracic CT or transoe- consistently varies with respiratory movements, sophagealooksfree.com echo; in unstable patients, consider especially if described as ‘sharp’ ‘knife-like’, bedside transthoracic echo, which will identify ‘stabbing’ or ‘catching’, then proceed to Acute most type A dissections (but does not exclude pleuritic pain (p. 66). If there is any doubt, con- the diagnosis). mebotinue s on ee the diagnostic co pathwaymeboo for non-pleuritic Consider massive PE if there is sudden-onset, pain initially and reconsider if no clear diagnosis severe chest pain associated with any of the emerges or the patient’s description becomes following features: more suggestive of pleuritic pain. • marked dyspnoea or hypoxaemia in the absence of pulmonary oedema 6 History consistent with ACS? • high risk of PE, e.g. malignancy, recent Further assessment for ACS is generally not surgery, prolonged immobility or clinical required in patients with: evidence of DVT • syncope or signs of shock (Box 30.1, • a single short-lived episode of pain, e.g 10 minutes poksfree.com 267) – especially with ↑JVP < • suggestive ECG changes (p. 58). • a typical episode of stable exertional angina • a clear alternative cause for pain, e.g. In hypotensive or peri-arrest patients, consider herpes zoster; recent chest wallebo injury with urgent transthoracic echo to look for evidence of tenderness on palpation acute right heart strain and excludeme alternative • an fre atypical history om and very low risk of for diagnoses, e.g. cardiac tamponade and consider CAD, e.g. <30 years with no risk factors. thrombolysis (after excluding contraindications; Box 22.3, p. 207). Otherwise, arrange prompt Otherwise, consider admission for repeat ECG CT pulmonary angiography. and cardiac biomarkers. Suspect oesophageal perforation if acute Any ischaemic ECG changes severe chest pain arises after vomiting/retching 7 (see Box 6.1) or ↑troponin? or oesophageal instrumentation. Arrange immediate CXR if ≥1 hour after perforation (may show Repeat the ECG at least once and also during subcu aneous emphysema, pneumomediastinum any further episodes of pain. Measure serum or pleural effusion); otherwise, request water- troponin concentration up to 12 hours from the solubleooksfree contrast barium com swallow/CT and surgicalo onset sf of ee. maximal om pain, depending on the assay review. being used. If the ECG is non-diagnosticbooks but you Chest pain 63 Acute chest pain: step by-step assessment

Box 6.6 Conditions associated with Box 6.7 Angina symptom score elevation of serum troponin other than acute coronary syndrome Retrosternalsfr discomfort co without atypical 1 point ksfre features1 k • Acute decompensated heart failure Discomfort arises during physical exertion2 1 point • Tachy- or bradyarrhythmias Discomfort is relieved by rest or GTN within 1 point • Myocarditis/myopericarditis 5–10 minutes • Aortic dissection • Pulmonary embolism 1Atypical pain features include a ‘sharp or ‘stabbing’ quality; 6 • Prolonged severe hypotension/cardiac arrest significant variation with inspiration or position; or a high degree • Severe sepsis or burns of localisation, e.g. point with tip of finger. • Cardiac trauma/surgery/ablation 2Do not score point if discomfort is fleeting; occurs after but not • Acute neurological disease, e.g. stroke, subarachnoid during exertion; is induced only by specific movements/actions; haemorrhage or has inconsisten relationship, e.g. also occurs regularly • Congestive cardiac failure without any provocation. • Infiltrative card ac diseases, e.g. sarcoidosis, amyloidosis • End-stagefr renal failure e.c m

suspect ACS, check troponin early (laboratory episodes of chest discomfort occurring on or ‘near-patient’ testing) to expedite diagnosis, minimal exertion or at rest, especially if: but always repeat at an appropriate interval after • the symptoms mimic previous episodes of maximal pain if the initial test is negativemeb (12 anginal chest com discomfort, mebor hours with conventional assays but often less • the patient has established CAD or high with high sensitivity assays) likelihood of CAD (see Box 6.7) and the Diagnose ACS in patients with a convincing pain is characteristic of myocardial history of ischaemic chest pain accompanied ischaemia (see above). by troponin or any ECG evidence of ischaemia ↑ Refer patients with these features (or in (see Box 6.1). whom the suspicion of ACS is otherwise high) In patients with an atypical history or to cardiology for further assessment. low underlying risk of CAD, first consider alternative causes of troponin (Box 6.6) and ECG ↑ Low clinical probability of ACS or features changes (see Box 6.1), e.g. PE, myopericarditis 9 suggest alternative diagnosis? or aorticoksfre dissection, com but proceed to further assessment of ACS if there is no clear alternative In the absence of the features above, unstable cause. eboangina free.com is unlikely if any of the following is present: • low likelihood of CAD (Boxmeb 6.3) o 8 High clinical probability of ACS? • the pain persisted at high intensity for Now try to identify the subset of patients >1 hour (would expect troponin rise with unstable angina but no ECG evidence of if ischaemic pain) and an ECG during ischaemia or significant myocyte necrosis. This maximal pain was normal presentation has become much less common • the symptoms mimic previous episodes of since the advent of high sensitivity troponin chest discomfort that are not suggestive of assays. ACS is unlikely if biomarkers remain angina (Box 6.7). normal despite pain persisting at high intensity Seek an alternative explanation for chest pain for a prolonged period, e.g. >1 hour since this in these patients. degree of ischaemia would be expected to cause Further investigation (Box 6.8) may be helpful myocyteooksfree necrosis. However, com consider unstable in patients who do not fall into either category, to angina if the patient reports repeated shorterboo lived look free.comfor evidence of underlying obstructive CAD. eboo s Chest pain 64 Acute chest pain: step-by-step assessment

Consider non-cardiac causes of Box 6.8 Investigations in suspected angina 10 chest pain • Investigations are used to seek evidence of myocardial ischaemia during cardiac stress or to • Make a clinical diagnosis of GORD, confirmoks and/or r refute co underlying CAD. musculoskeletal pain or herpes zoster if • Exercise ECG and other ‘stress tests’ seek to there are typical features (see p. 52). establish whether increases in cardiac work induce • Consider paroxysmal tachyarrhythmia if the myocardial ischaemia. During exercise, pain was accompanied by rapid palpitation the development of typical symptoms with ST and an ECG was not obtained during segment shift >1 mm suggests angina. Absenceme of f e meboo symptoms. symptoms and ECG changes at high workload argues against angina. • Re-evaluate for aortic dissection or PE and • Exercise ECG is often inconclusive and has a high consider echocardiogram/thoracic CT if ‘false-positive’ rate in low isk patients. Other forms ongoing pain haemodynamic compromise of stress testing, e.g myocardial perfusion scan or or other clinical concern. dobutamine stress echo, offer higher sensitivity/ • Consider thoracic or respiratory review if specificity and are particularly useful when the there is an unexplained CXR abnormality, resting ECG is abnormal, e.g. left bundle branch block or the patient is unable to perform treadmill e.g. mediastinal/hilar mass. exercise. • Reassess for pericarditis and arrange an • Stress tests are contraindicated in unstable angina, echocardiogram to look for pericardial decompensatedoksfree.com heart failure or severe hypertension. effusion, if there are any suggestive features • Coronary angiography is the definitive test for (see step 4, above) or cardiomegaly on defining the presence, extent and severity of CAD. CXR. Severe stenosis in one or more vessels st ongly suggests ischaemia as the cause of pain whilstme the • Consider free hyperventilation com mor anxiety book if there absence of significant coronary stenosis effectively are suggestive clinical features (see p. 52) excludes angina. associated with ↓PaCO2 (with normal PaO2) • In patients with a relatively low risk of CAD, CT and PE has been excluded. coronary angiography is a useful, non-invasive m method to rule out stable angina by excluding the presence of significantcom CAD. Chest pain 65 Acute chest pain: further assessment

Further assessment of NSTEMI/ • evaluate the response to GTN spray; if pain unstable angina improves, consider IV GTN infusion. Consider paroxysmal tachyarrhythmia, e.g. Step 1 Identify critically unwell patients atrial fibrillation, as the mechanism for NSTEMI Attach cardiac monitoring to all patients with in patients who did not have an ECG during ongoingook chest fre pain and review regularly with pain, e.g. if pain associated with palpitation or repeat ECG. Admit to a CCU/HDU and arrange previous history of arrhythmia urgent Cardiology review if you identify any of the following: meboStep s 3 reIdentify high-risk co patientsm book 6 • shock (p. 267) Risk-stratify patients using a validated scoring • pulmonary oedema system such as the GRACE score (http://www • ventricular arrhythmia, complete heart block .gracescore.org/website/WebVersion.aspx). The (see Fig. 31.2, p. 279) GRACE score predicts the risk of in-hospital and • ST elevation or refractory pain. 6 month death in patients with ACS and can be used to aid the selection of patients for clinical Step 2 Consider all potential factors contributing to and interventional procedures. myocardial ischaemia Step 4 Use cardiac biomarkers to differentiate In patients with ongoing pain: unstable angina from NSTEMI • maintain SpO2 ≥94% Measure serum troponin I or T up to 12 hours • identifyoksfre and treat tachyarrhythmias co from the onset of maximal pain (can often be • if any suspicion of anaemia or acute measured earlier with highly sensitive assays). bleeding, e.g. pallor, haematemesis, If ↑, classify as NSTEMI; otherwise, classify as melaena, check Hb urgently (prior to giving unstable angina. antiplatelet agents/anticoagulants)m ks ee.com meboo • if tachycardic, assess and treat any ongoing pain, then consider beta-blockade (if no contraindications)om Chest pain 66 Acute pleuritic pain: overview

1 Diagnostic CXR abnormality? fre co No Yes

Yes Pneumothorax? Pneumothorax

Yes See Further assessment Consolidation? Likely pneumonia of respiratory tract infection (p. 123) No

Yes Pleurale effusion? See Furthere assessment of pleural effusion (p. 129) No

Yes Bony lesion at site of pain? Fracture, tumour, metastasis

Clinical signs of consolidation + Yes See Further assessment 2 Likely pneumonia features of respiratory tract infection? of respiratory tract infection (p. 123) No

Clinical o CXR suspicion of Yes Malignancy or other 3 Consider CT chest malignancy?ee. cause No

Full clinical assessment, FBC D-dimer, +/- CRPo, ABG e

Pericardial rub or ‘pericarditic’ Yes 4 Pericarditis ECG changes?

Wells score >4 or raised D-dimer Yes . Pulmonary embolism 5 CTPA (or V/Q scan) or unexplained hypoxaemia? c or other cause Nor .co

6 Likely musculoskeletal pain or viral infection Consider other causes Chest pain 67 Acute pleuritic pain: step-by-step assessment

1 Diagnostic CXR abnormality? Pe icardial rub or ‘pericarditic’ 4 ECG changes? Look carefully for: • pneumothorax (see Fig. 12.5, p. 118) – Diagnose pericarditis if pleuritic pain is accom- smalloksfre pneumothoraces are easily missed panied by typical ECG features of pericarditis • consolidation (see Figs 12.3 and 12.4, (see Box 6.1) or a pericardial rub. p. 118) – if present, go to further assessment of respiratory tract infection Wells score >4 or raised D-dimer or (RTI) (p. 123), especially if accompaniedm by 5 funexplained e co hypoxaemia?m ook 6 cough, purulent sputum, dyspnoea or fever • pleural effusion (see Fig. 12.6, p. 119) – if You must exclude PE in any patient with acute present, assess as on page 129 pleuritic pain and no other obvious cause. A • rib fractures or metastatic deposits – if the negative D-dimer test in patients with a Wells latter are present, investigate for a primary score ≤4 (see Fig. 12.7, p. 120) effectively rules lung, renal, thyroid, breast or prostate out the diagnosis makes the diagnosis unlikely. cancer or multiple myeloma. Arrange further investigation with CTPA if the Wells score is >4 (irrespective of D-dimer), D-dimer is positive, or clinical suspicion is otherwise high, Clinical signs of consolidation features + e.g. unexplained hypoxaemia, features of right 2 ofk respiratory free tract com infection? heart strain on ECG (see Box 6.1). Even in the absence of definitive CXR changes, CTPA may provide an alternative cause for pneumonia is the likely diagnosis if pleuritic pain the presentation in patients without PE. is accompanied by: eb sfree.com eb oksf • focal chest signs, e.g. crackles, bronchial Likely musculoskeletal pain or viral breathing, and 6 infection. Consider other causes • symptoms of RTI: productive cough, acute dyspnoea or fever Seek a respiratory opinion and consider further imaging in patients with dyspnoea or a new If present, assess as per on page 123. CXR abnormality other than those described above. Consider drug-induced pleuritis, e.g. 3 Clinical or CXR suspicion of malignancy? amiodarone, methotrexate, or pleurisy seconda y Consider further investigation with CT chest ± to a connective tissue disorder, e.g. history or bronchoscopy in patients >40 years or with a clinical features of systemic lupus erythematosus/ history of smoking/asbestos exposure if pain is rheumatoid arthritis. accompaniedooksfr by: c m Otherwise, the most likely diagnoses are • a history of weight loss viral pleurisy or musculoskeletal pain. Suspect • recurrent or unexplained haemoptysis the former if there is fever, coryzal or ‘flu-like’ • recent change in voice msymptoms sfree.com or a pleural rub; mebosuspect the latter ksf • persistent cervical lymphadenopathy if there is any recent injury, prolonged severe • finger clubbing coughing, unusually strenuous upper body activ- • suspicious CXR changesm (see Box 17.1, ity, marked exacerbation of pain on movement p. 163). or obvious tendernessom on palpation. Chest pain 68 Intermittent chest pain: overview

Full clinical assessment, ECG f e co See Further Angina score = 3 OR Yeks Possible stable assessment 1 Angina score = 2 + high / angina of suspected moderate risk of CAD anginabook (p. 71) No

Consider unstable angina / Characteristic description of Yes 2 tachyarrhythmia / vasospastic angina / ‘ischaemic-type’ pain? oesophageal spasm

No m

Retrosternal discomfort that is: Yes 3 (a) hot or burning, (b) relieved by antacids Gastro-oesophageal reflux disease or (c)free provoked by food / lying down?

Pain highly localised, induced by specific Yes 4 Musculoskeletal pain movements or reproduced by palpation? meb No

Yes 5 Wheeze, breathlessness, cough? Consider bronchospasmm No

Pain provoked by stress / strong Yes 6 emotion or associated with features of Consider anxiety / panic attacks hyperventilation?sfr

Evaluate for angina in patients with high risk of CAD 7 Look for evidence of underlying manxiety / depressive disorder Consider trial of simple analgesia or acid suppression therapy Chest pain 69 Intermittent chest pain: step-by-step assessment

Angina score = 3 OR Angina score = 2 + spasm may closely mimic ischaemic-type dis- 1 high/moderate risk of CAD? comfort and also lacks a consistent relationship to exertion. The hallmark of stable angina is a correlation Consider these diagnoses in patients with between symptoms and alterations in cardiac characteristic ischaemic-type discomfort that work.ook Retrosternal fre discomfort that consistently lacks a predictable relationship to exertion or arises during exertion and is rapidly relieved (with the exception of unstable angina) in whom (<5 minutes) by rest strongly suggests angina. stress testing fails to demonstrate inducible The quality of the discomfort may varymebo widely myocardial sfre ischaemia. co meboo f 6 and is frequently vague or non-specific. The Suspect unstable angina and refer to cardiol- likelihood of angina also depends on the risk of ogy if any of the following: underlying CAD. With rare exceptions, coronary • new onset of symptoms within the atherosclerosis is cen ral to the pathogenesis of preceding 2 weeks angina, so patients with a low risk of CAD have • episodes of discomfort previously related to a correspondingly low risk of angina. exertion but now occurring at rest • Calculate the ‘angina score’ based on • new abnormality on resting ECG the three criteria in Box 6.7, then broadly (see Box 6.1). stratify the a priori risk of CAD based on Suspect paroxysmal arrhythmia if any of the age, sex and risk factors (see Box 6.3). following: • Ifoksfree angina score = 3, com go to further assessment of possible angina, irrespectiveb • palpitation ree compreceding or during of risk factors. symptoms • If angina score = 2, go to further • previously documented tachyarrhythmia assessment of possible angina unless • infrequent episodes of variablem duration. ok ‘low-risk’ of CAD. If suspected, attempt to document the rhythm • Consider further assessment for possible during a typical episode of symptoms. angina in patients at high risk of CAD in Suspect vasospastic angina if any of the whom the history is vague or unclear. following: • no apparent triggers Characteristic description of • sudden onset of intense symptoms ± 2 ‘ischaemic-type’ pain? autonomic features • short duration of episodes (2–5 minutes) The typical manifestation of myocardial ischae- • episodes occurring in clusters. mia is a diffuse, poorly localized, retrosternal If suspected, consider a trial of Holter ECG discomfortook frethat radiates com to the neck, jaw and left (or right) shoulder and/or arm, and has a monitoring to look for evidence of ST elevation tight, constricting, pressure-like, aching or heavy during symptomatic episodes quality. It is frequently described as meboodiscomfort Suspect ree. oesophageal om spasmm if boany of the rather than pain. Patients often illustrate the following: sensation by placing a hand or fist over the • intermittent dysphagia centre of the chest. • history or typical symptoms of GORD (see Intermittent episodes of myocardial ischaemia below) unrelated to exertion may occur with critical • discomfort occurring predominantly at night coronary obstruction due to plaque rupture and or after eating. thrombus formation (unstable angina), coronary If the history suggests GORD, consider reas- artery spasm (vasospastic angina) or paroxysmal sessment after a trial of a proton pump inhibitor; tachyarrhythmia (especially in the presence of otherwise, refer to the GI team for consideration an underlyingoksfree. coronary ostenosis). Oesophageal oof sfree.cupper GI endoscopy/oesophageal m manometry.oksf Chest pain 70 Intermittent chest pain: step-by-step assessment

Retrosternal discomfort that is: (a) hot or Pain provoked by stress/strong emotion 3 burning, (b) relieved by antacids or (c) 6 or associated with features provoked by food/lying down? of hyperventilation? If the pain is unlikely to be cardiac, seek typical Attributing episodes of chest pain to anxiety can featuresoo of sfre other disorders. co The above features be challenging. Emotional distress increases suggest GORD; a symptomatic response to acid cardiac work and may provoke angina, but suppression therapy, e.g. proton pump inhibitor, symptoms that occur exclusively in this context effectively confirms the diagnosis.meboo Upper GI are more e likely c to have a psychologicalmeboo origin. endoscopy is usually not required but consider Associated features of panic or hyperventilation if symptoms are refractory during episodes, e.g breathlessness with ‘inability to take in enough air’ or a choking sensation, Pain highly local zed, induced by specific tingling in the extremities and light-headedness, 4 movements or reproduced by palpation? support the diagnosis. Seek specialist input before attributing a new presentation of chest Musculoskeletal pain may present in a multitude pain to anxiety in patients with a high risk of CAD. of ways. The above features are suggestive, as is a history of recent injury, strain or uncharacteristi- Evaluate for angina in patients at high cally vigorous activity. Further investigation is 7 risk of CAD. Consider other causes. rarely necessary; a symptomatic response to simpleooksfree analgesia helps co to confirm the diagnosis. In many patients it is not possible to reach a defi- bonite diagnosis. ee.com Reassess those with inconclusive 5 Wheeze, breathlessness, cough? investigations for angina or with a high likelihood of CAD (see Box 6.3) if symptoms persist. Where Asthma and chronic obstructive pulmonary mebo k a cardiac cause has been ruled out and no other disease may be difficult to distinguish from angina cause is apparent, patients often respond to on clinical grounds if symptoms are provoked simple reassurance. However, a minority by exertion and produce a sensation of chest experience severe, refractory symptoms and ‘tightness’. Helpful diagnostic features may may merit specialist assessment for underlying include a history of cough or wheeze (especially psychological factors and/or management of nocturnal), diurnal variation in symptoms, the chronic pain. presence of wheeze on auscultation, a history of atopy and absence of risk factors for CAD. If ree.com asthma or chronic obstructive pulmonary disease is suspected,oksfree.com evaluate as described in Chapter 12 Chest pain 71 Intermittent chest pain: further assessment

Further assessment of suspected angina clinical suspicion and are unable to identify a clear alternative cause. Step 1 Consider unstable angina and structural If results are equivocal, e.g. suboptimal test, heart disease minor abnormality, or typical symptoms without An abrupt onset or sudden worsening of exer- ECG changes), consider an alternative stress test tionalooks chest pain re indicates unstable angina - see or coronary angiography to clarify the diagnosis. p. 65. Arrange echocardiography to exclude aortic Step 3 Assess symptom severity and risk stenosis and hypertrophic cardiomyopathym if bo the The freseverity coof angina is basedm booksnot on the 6 patient has an ejection systolic murmur, exertional intensity of pain but the frequency of symptoms, syncope or ECG features of left ventricular impairment of exercise capacity and consequent hypertrophy (see Fig. 6.8). functional limitation As this information is used to Step 2 Confirm or refute the diagnosis guide treatment and monitor response, quantify In patients >40 years with a typical history (angina symptoms accurately and determine their impact score 3) and moderate/high likelihood of CAD on work, hobbies and daily activities. Persistence (see Box 6.3), make a clinical diagnosis of stable of limiting symptoms despite anti-anginal therapy angina and proceed to step 3. is an indication for angiography with a view to If the risk of CAD is low (see Box 6.3), consider revascularisation. CT coronary angiography, if available, as a first Exercise ECG may identify high risk patients lineooksfree.com investigation (Box 6.8). If negative, return to whose prognosis could be improved by revas- the algorithm for intermittent chest pain (re-enter cularisation. Refer patients for angiography if at step 3). If positive, proceed to a stress test there are any of the following abnormalities on or invasive angiography. meboexercise sfree.com ECG: meboo sf Otherwise, consider a stress test (Box 6.8). If • ST elevation positive, diagnose stable angina and proceed to • severe or widespread ST depression step 3. If negative, i.e. no evidence of inducible • ST depression at low workload or for a ischaemia at high stress return to the algorithm prolonged period in recovery for intermittent chest pain (re-enter at step 3). • fall or failure to rise in BP Seek input from ecardiology com if you have a high • ventr culare comarrhythmia. Coma and alteredsf consciousness 7ok

Consciousness is a poorly defined, ill-understood from witnesses, relatives or ambulance crew. In term. ‘Normal’ consciousness requires: particular, ask about: • an intact ascending reticular activating • the circumstances in which the patient system (located in the brainstem and was found, e.g. exposure to temperature responsible for arousal) and extremes or poisons • normal function of the cerebral cortex, • the speed, nature and surrounding thalamus and their connections events, e.g. sudden onset – subarachnoid (responsible for cognition). haemorrhage, seizure, trauma; Altered consciousness results if either malfunc- gradual – expanding intracranial lesion, tions. Minor defects, e.g. memory impairment metabolic conditions; fluctuating – recurrent disorientationooksfree.com or slow cerebration, can be subtle seizures; recent flu-like illness – meningitis, and difficult to detect, especially if there are co- sepsis existent language, visual or speech problems. • trauma, e.g. road traffic accident, falls, Consider multi-factorial causes contributingmebo to assault ree.com m boo altered consciousness, e.g. a patient who has • drug history (prescribed and over-the- taken alcohol falls in the street, sustaining a head counter), alcohol and recreational injury, lying unnoticed for hours and becoming drug use hypothermic. • past medical history. Important causes to The Glasgow Coma Scale (GCS; Table 7.1) was consider are listed below. developed to assess/prognosticate head injury and is commonly used to record conscious level Metabolic causes although it is less well validated in non-traumatic • Hypo-/hyper-glycaemia. condit ons. A GCS score <15/15 indicates • Hypo-/hyper-thermia. altered consciousness. ‘Coma’ denotes a patient • Hypo-/hyper-natraemia. with no eye response and a GCS ≤8/15. Do not ooksfree. om • Hypothyroidism. use terms such as semi-conscious, stuporous, • Metabolic acidosis. obtunded, etc. ebo fre co Minor disturbance of consciousness is a central feature of delirium, see Chapter 8. The Drugs/toxins assessment pathway in this chapter is appropri- • Alcohol. ate for patients with a GCS 15 and: < • Opioids, benzodiazepines, tricyclic • E <3, V <4 or M <5 i e. >1 point drop in at antidepressants, barbiturates etc. least one domain • ‘Recreational’ drugs, e.g. • known or suspected head injury gamma-hydroxybutyrate (GHB), ketamine, • a clinical picture not suggestive of delirium. mephedrone,ree.com etc. As the patient is unlikely to be able to give a • Carbon monoxide/other cellular toxins, e.gs clear history,ksfree it is essential com to obtain a history cyanide. Coma and altered consciousness 73 Differential diagnosis

CNS causes Table 7. Glasgow Coma Scale • Trauma:fre intracranial o bleeding (extradural, Criter on Score subdural, intracerebral, subarachnoid), Eye opening diffuse axonal injury. Note that patients ookSpontaneous fr 4 taking anticoagulants or with bleeding To speech 3 disorders may have intracranial bleeding To pain 2 following minor, unrecognized trauma. • Infection: meningitis, encephalitis,meboo cerebral No response 1 abscess, cerebral malaria. Verbal response • Stroke: cortex or brainstem. 7 Orientated 5 • Subarachnoid haemorrhage. Confused: talks in sentences but 4 • Epilepsy. disorientated • Intracranial space-occupying lesion, e.g. Verbalizes: words not sentences 3 primary or secondary tumour. • Hypertensive encephalopathy. Vocalizes: sounds (groans or grunts) not 2 words • Psychogenic.free c m No vocalization 1 Organ failure Motor response • Shock. ookObeys commands ree co 6 • Respiratory failure (hypoxia and/or Localizes to pain, e.g. brings hand up 5 hypercapnia). eb beyond chin to supra-orbital pain • Renal failure (uraemic encephalopathy). Flexion withdrawal to pain: no localisation 4 • Liver failure (hepatic encephalopathy). to supra-orbital pain but flexes elbow to nail bed pressure Abnormal flexion to pain 3 Extension to pain: extends elbow to nail 2 bed pressure No response 1 Record the GCS as a total and its three separate componentsks e.g. r GCS 9/15: c E3, V2, M4 Coma and altered consciousness 74 Overview

ABCDE + collateral history fre m Yes 1 Respiratory failure, shock or CBG <3.0? Treat immediately and re-evaluate

Yes Urgent cultures, 2 Suspect CNS infection? Infection confirmed and CT brain ± LP m

Yes Rewarm and 3 Core temperature <34ºC? Hypothermia c reassess No

Yes 4 Anys suspicion coof opioid toxicity? Naloxone trial Opioid toxicity

Yes 5 Witnessed seizure activity? See seizure (p. 276)

GCS £8, head injury, headache or Yes 6 Urgent CT brain Intracranial lesion evidence of intracranial pathology?

2+ Full clinical assessment, collateral history, FBC, U+Es LFTs, glucose, o Ca , TFTs Yes o7 Major s metabolic omderangement? Correct (slowly if necessary) and reassess No

Yes 8 Suspicion of drug/alcohol toxicity? Collateral history; toxicology screen/drug levels

Consider hepatic/hypertensive encephalopathy, non-convulsive status epilepticus, CNS toxicity/ 9 infection and psychogenic presentation. CT brain and toxicology screen if not already performed; MRI/LP/EEG if cause remains unclear ree. free. Coma and altered consciousness 75 Step-by-step assessment

1 Respiratory failure, shock or CBG <3.0? 3 Co e temperature <34°C? Ensure a patent airway and provide cervical Measure core temperature with a low-reading spine control if you suspect trauma. As the rectal thermometer in any patient with a tympanic GCS falls, particularly if GCS ≤8, definitive airway reading <35°C or clinical suspicion of hypother- management,ook f ee.g. tracheal intubation, is likely mia, e.g. prolonged immobility or exposure to to be required, so seek expert anaesthetic help wet and cold conditions. early. Look for and treat rapidly reversible causes Suspect a contribution to altered conscious- of ↓GCS as per the ABCDE assessment:meboness sf from e hypothermia co if them core temperature books • assess oxygenation and ventilation by is <34°C. Rewarm and reassess whilst searching ABG analysis (p. 115). Treat hypoxia and for additional causes Check TFTs and consider 7 hypercapnia urgently treatment with IV tri-iodothyronine (T3) or • give a therapeutic/diagnostic trial of IV levothyroxine (T4) (preceded by IV cortico-

naloxone (see below) if PaCO2 is ↑ or any steroid) if there is any suspicion of myxoedema evidence of respiratory depression coma. • look for shock (see Box 30.1, p. 267); if present, assess and treat as per Chapter 4 Any suspicion of opioid toxicity? 30 sfree co • check a capillary blood glucose reading Give a therapeutic/diagnostic trial of naloxone if (‘CBG’); if <3.0 mmol/L, send blood for the patient has received any opioid medication, formal laboratory glucose measurement but is a known or suspected ‘recreational’ user, has treat immediately with IV dextrose or IV/IM small pupils or has no obvious alternative cause glucagon without waiting for the resultmeb. In for altered consciousness. com Anymeboo rapid improve- patients with malnutrition/chronic alcohol ment in conscious level, increase in respiratory excess, consider slow IV thiamine to rate/depth or pupil dilation indicates that opioids prevent the (theoretical) risk of precipitating are contributing, at least in part, to the clinical Wernicke’s encephalopathy. state. The half-life of naloxone is shorter than most opioid/opioid metabolites, so further doses Reassess if confusion persists despite effective or an infusion are likely to be needed. correction of all of the above.

2 Suspect CNS infection? 5 Witnessed seizure activity? Suspect CNS infection in any patient with ↓GCS A clear, detailed history from an eyewitness is accompanied by meningism (Box 18.2, p. 169), crucial. ↓GCS is common post-ictal, but seizures a ooksfrnew-onset maculopapular e.com or purpuric rash, can be precipitated by a wide spectrum of or fever. If malaria is a possibility, e.g. recent conditions including hypoglycaemia, head injury travel to endemic area, perform thick and thin ± intracranial haematoma, alcohol withdrawal, blood films and seek immediate expertmebo advice. drug overdose, e.com e.g. tricyclicmebook antidepressants, Otherwise, take blood cultures and throat swabs, infection etc. give empirical IV antibiotics/antivirals and arrange In status epilepticus, associated hypoxia/ an urgent brain CT. If there is no clinical or CT hypercapnia aggravates the cerebral injury and contraindication, perform LP for CSF analysis mortality is ~10%. Assess further as described (see Table 18.1, p. 171com). in Chapter 31com Coma and altered consciousness 76 Step-by-step assessment

GCS ≤8 head injury, headache or calcium, magnesium or phosphate, only if 6 evidence of intracranial pathology? derangement is severe.

Once you have identified and treated major 8 Suspicion of drug/alcohol toxicity? physiological derangement, life-threatening infectionook and fre rapidly reversible com causes of ↓GCS, Even in patients with a history or features of it is vital to identify an intracranial cause of altered acute or chronic alcohol intake, never assume consciousness. In general, immediate brain CT that altered consciousness is due to alcohol is required in patients with any of: meboalone. fre The correlation betweenmebo breath or blood alcohol levels and conscious level is poor, so • GCS ≤8 • a history of headache, focal neurological beyond confirming that alcohol is present, these symptoms, or lateralising neurological values are of limited help and can be potentially signs, e.g. unilateral pupillary abnormality, misleading. In particular, look for (and treat) absence of limb movement or extensor alcohol-related hypoglycaemia, occult head injury, intracranial bleeding and recreational drug use plantar response, or signs of ↑ICP (Box 22 2, p. 199) or overdose. • known or suspected head injury Examine for characteristic clinical ‘toxidromes’ • CSF shunt in situ. (Table 7.2) in any patient with suspected overdose but remember that mixed overdoses or cocktails Pa ients must be accompanied throughout by of drugs (often with alcohol) are common and anooksfree individual who can com provide advanced airway/ ooksf breathing support as intubation and controlled ventilation may be needed. ebo sfree.com

7 Major metabolic derangement? Table 7.2 Common toxidromes associated with coma/altered consciousness Decreased GCS is common in hypo- and Symptom/signs Drug hypernatraemia. It tends to reflect the rate of sodium alteration rather than absolute values Respiratory depression, Opioids small pupils (see p. 88). If the disturbance is known to be acute, correct promptly then reassess; otherwise, Dilated pupils, tachycardia, Tricyclic hyper reflexia, muscle antidepressants correct cautiously, at a slow rate, with frequent ↑ tone, urinary retention. If remeasurement to avoid excessive neuronal fluid severe: cardiac rhythm/ shifts and consequent cerebral oedema or central ECG abnormalities, ↓BP, pontine myelinolysis. There may be a lag between seizures correctionooksfree.com of the metabolic derangement and Hypotension, respiratory Barbiturates, return of normal conscious level. depression, bradycardia, benzodiazepines Decreased GCS may be a feature of diabetic ↓ muscle tone eb ketoacidosis (DKA). Always considerm DKA if bo the Tachycardia, sfree ↑ coBP, Sympathomimetics, patient has Type 1 diabetes mellitus; confirm the arrhythmias, dilated cocaine, ecstasy, diagnosis by identifying metabolic acidosis on pupils, tremor, agitation amphetamines, SSRIs ABG, ketonuria on urinalysis or blood ketones. Agitation, myoclonus, Gamma- Suspect Hyperosmolar Hyperglycaemic State seizures, nausea, hydroxybutyrate (GHB) (HHS), (formally HyperOsmolar Non-Ketotic coma bradycardia, coma - HONK) rather than DKA if there is marked Vivid hallucinations, Ketamine and hyperglycaemia (>30 mmol/L) and hyperos- agitation, dysphoria, phencyclidine (PCP) molarity (>320 mOsm/kg) without significant nystagmus, autonomic disturbance, seizures, hyperketonaemia (<3.0 mmol/L) or acidosis (pH coma >7 3 bicarbonate >15 mmol/L) – hypovolaemia and altered consciousness are common features. Euphoria, drowsiness, Solvents o ksfree.com arrhythmias, Suspect a contribution to altered conscious- laryngospasm ness from uraemia or disturbances of plasma meboo sfree com Coma and altered consciousness 77 Step by-step assessment respiratory/cardiovascular depression (hypoten- Consider further investigation if no clear sion, arrhythmias etc.) may predominate in any 9 cause identified severe poisoning. Measure paracetamol and If the cause remains unclear, arrange CT brain salicylate levels (± lithium and iron, if indicated) and, if there is a strong suspicion of illicit drug and send a toxicology screen if not already per- use,ooksfre perform a urine toxicology screen See formed. Consider hepatic encephalopathy if the www.npis.org or http://www.toxbase org for patient has known or suspected liver disease, or further information. ebohypertensive f e en cocephalopathy if BP is consistently Consider carbon monoxide poisoning. The fea- >180/120 mmHg with hypertensivemebook retinopathy or evidence of renal involvement. Otherwise, tures of CO poisoning are non-specific; the ‘classic’ 7 description of cherry-red mucous membranes/ seek neurological and/or critical care input and skin is very rare. Severe metabolic acidosis and consider MRI (brainstem pathology), EEG (non- ECG changes of ischaemia/infarction with convulsive sta us, hepatic encephalopathy) and arrhythmias and hypotension may be found. LP (CNS infection). Some pulse oximeters can measure carboxyhae- Psychogenic unresponsiveness is a diagnosis moglobin (COHb), but confirm with measurement of exclusion, but consider it if comprehensive of COHb on arterial or venous blood sample. The investigation fails to reveal an underlying cause COHb value at presentation is not a good guide and there are suggestive signs, e.g. response to to conscious level and the half-life of COHb (~4 tickling, resistance to passive eye opening and hoursooksfree.com breathing room air) will be significantly less gaze deviating towards the floor in anyooksf position. if the patient has been given oxygen. Extrapola- tion back to the time of exposure will indicate the peak level more accurately. meboo sfree com Confusion: delirium and dementia ksf k 8o sf

Confusion (impaired cognition) is global impair- • Lithium. ment of mental function. • Corticosteroids (especially high-dose). Delirium is an abrupt decline in cognitive function • Baclofen. that follows a fluctuating course and is accompa- • Levodopa/dopamine agonists. nied by impaired attention, (e.g. easily distracted, • Digoxin. unable to maintain focus) and disturbed conscious- *indicates that confusion may arise from either ness (‘hyperalert /agitated or drowsy/↓awareness). drug effects or withdrawal. Common associated features include reversal of the sleep–wake cycle, hallucinations, delusions and Metabolic/physiological disturbance altered emotion/psychomotor behaviour. • Hypoxia. Dementia is a chronic, progressive dec ine • Hypercapnia. bin cognitive oksfree function com without disturbance of • Shock. consciousness. • Hypo/hyperthermia. The initial challenge with confusedm patients ois • sfree Hypo/hyperglycaemia. co finding them (sometimes literally). Agitated, rest- • Hyponatraemia. less patients rapidly attract attention but those • Hypo/hypercalcaemia. with ‘hypoactive delirium’ are quiet, withdrawn and • Dehydration easily missed. In patients with pre-existing demen- • Uraemia. tia, delirium may be overlooked unless baseline • Metabolic acidosis. cognitive function is established. It is also pos- • Hepatic encephalopathy. sible to mislabel dysphasic, deaf or depressed • Hypo/hyperthyroidism. patients as confused. Infection Delirium • CNS infection: o free.com • meningitis (bacterial, viral, fungal, The differential diagnosis of delirium is wide and, tuberculosis) o in patients with a ‘vulnerable brain’ (Box 8.1), • encephalitis includes almost any acute physical, mental or • cerebral abscess environmental insult. Causes are listedmeb below; sf• cerebral ee.c malaria. those shown in bold are unlikely to be solely • Non-CNS infection: responsible for delirium, except in patients with • sepsis a ‘vulnerable brain’. • pneumonia • urinary tract Drugs • biliary/intra-abdominal • Alcohol*. • endocarditis. • Opioids* Intracranial causes • Benzodiazepines*. fr e.co • An iconvulsants. • Seizures (post-ictal state). • Tricyclicksf antidepressants*. m • Haemorrhage. • Anticholinergics. • Space-occupying lesion. • Antihistamines. • Head injury. • Antipsychotics*. • ↑intracranial pressure. Confusion: delirium and dementia 79 Differential diagnosis

‘Reversible’ causes Box 8.1 Delirium and the ‘vulnerable brain’

• Vitamin B12/folate deficiency. When assessing delirium, consider predisposing factors, as • Subdural haemorrhage. well as acute precipitants. Elderly patients (especially >80 • Hypothyroidism. years)ok and those r with pre-existing cognitive impairment (diagnosed or undiagnosed), frailty, multiple sensory • Normal pressure hydrocephalus. deficits, chronic alcohol excess or any significant underlying • HIV. b brain disorder, e.g. cerebrovascular disease, Parkinson’s • Neurosyphilis. disease, multiple sclerosis have a reduced thresholdme for • Wilson’s fre disease. om developing delirium. These patients have a ‘vulnerable brain’ and delirium may result from relatively minor insults Other causes that would not normally impair cognitive function in healthy • Frontotemporal dementias. patients without such predisposing factors. 8 • Korsakoff’s psychosis. • Multiple sclerosis. • Progressive multifocal Other causes leucoencephalopathy. • Pain. • Subacute sclerosing panencephalitis. • Postoperative. • (Variant) Creutzfeldt–Jakob • Constipation.ks e om disease. • Urinary retention. • Huntington’s disease. • Acute abdominal pathology (pancreatitis, Disorders that may mimic appendicitis). eb ree.com e • Myocardial infarction. confusion • Carbon monoxide. • Acute thiamine deficiency (Wernicke’s • Depression. encephalopathy). • Dysphasia. • Paraneoplastic syndromes. • Deafness. • Cerebral vasculi is • Acute psychosis. • Acute intermittent porphyria. • Behavioural disturbance. • Heavy metal poisoning, e.g. lead, arsenic. • Amnesic syndromes. • Unusual stimuli and sensory impairment. ee.co Dementia/chronic cognitive impairmentook free.co Common causes • Alzheimer’s disease. • Vascular disease. • Lewy body dementia. Confusion: delirium and dementia 80 Confusion: overview

Full clinical assessment, collateral history, AMT (Box 2.4) & 4-AT test (Box 8.2) f e com fre Yes Consider depression/dysphasia/deafness 1 Normal cognitive function? behavioural disturbance o No

Yes Go to Delirium 2 Normal baseline cognitive function? Likely delirium (p. 82)

Go to Delirium Acute cognitive function, fluctuating Yes Likely delirium with 3 ↓ (p. 82) course, altered consciousness/attention? underlying dementia

Nor e.c Consider treatment Mood/motivation/enjoyment, or Yes 4 ↓ kPossible e.c depression and/or expert Geriatric Depression Scale score >4? assessmentook No Go to further assessment 5 Likely dementia of chronic confusion (p. 89)

Clinical tool The 4AT: rapid assessment test for delirium and cognitive impairment The 4AT is a validated, sensitive tool for diagnosing [3] Attention delirium. It contains four elements. Scored as follows: Ask the patient to recite the months of the year in ≥4: possible delirium +/– cognitive impairment backwards order, starting at December. One prompt is 1–3:oks possible reecognitive impairment permitted to assist initial understanding. 0: delirium or cognitive impairment unlikely (but delirium Achieves 7 months or more correctly 0 still possible if [4] information incomplete) b sfreStarts but scores <7 months/refuses to start 1 Untestable (cannot start because unwell, drowsy, [1] Alertness inattentive) 2 me o Normal 0 Mild sleepiness for <10 seconds after waking, then [4] Acute change or fluctuating course normal 0 Is there evidence of significant change or fluctuation Clearly abnormal 4 in alertness/cognition/other mental function, e.g. This includes patients who are drowsy, or agitated/ paranoia/hallucinations arising over last 2 weeks and hyperactive. Attempt to rouse with speech or gentle touch. still evident in comlast 24 hours No 0 [2] AMT4 Yes 4 Age, date of birth, place (name of hospital or building), current year No mistakes 0 1oksfr mistake 1 co 2 or more mistakes/untestable 2 Confusion: delirium and dementia 81 Confusion: step-by-step assessment

1 Normal cognitive function? acute change. Spend time speaking with the patient and observing behaviour. In addition to Disorientation, forgetfulness and muddled think- direct observation, seek evidence of fluctuation ing may be apparent from normal conversation through discussion with nursing staff or review but confirm with an objective assessment, e.g. of overnight reports. Delirium is frequently theooks abbreviated re mental test (AMT; Box 2.4, superimposed on dementia (acute on chronic p. 14) or mini-mental state examination (MMSE). confusion) – look for important clues such as Use these tools to screen for confusion in all sudden decline in cognitive abilities, alteration of patients with a ‘vulnerable brain mebo(Box 8.1). consciousness, sfre com fluctuating coursemebooksf and difficulty Ensure that apparent cognitive impairment is concentrating. not due to communication problems (deafness, dysarthria, language barriers) or an isolated ↓Mood/motivation/enjoyment, or 8 disorder of comprehension (receptive dysphasia), 4 Geriatric Depression Scale score >4? word-finding difficulty (expressive dysphasia), memory (amnesic syndrome), behaviour or mood. Depression can mimic or exacerbate dementia. Patients with depression often score poorly Ask patients if they feel low in mood but also in formal testing through refusal to volunteer enquire about things they take pleasure in (do answers rather than making mistakes – if these they still enjoy them?), as well as biological patients are encouraged (or treated), performance symptoms (early morning waking, ↓appetite, may improve. ↓weight). During conversation, note expressions ooksfree com of guilt, worthlessness, pessimism and other 2 Normal baseline cognitive function? negative thoughts (especially if exaggerated or incongruent with circumstances) and look for Establish baseline cognitive function and any m opsychomotor sfree retardation, o lackmebooksf of depth or variety recent change in mental status by speaking to in affect, and poor eye contact. Scoring systems, relatives/friends/carers and checking previous e.g. the geriatric depression scale (GDS), may cognitive assessments. Thorough questioning is assist diagnosis. If uncertain, refer for specialist important as relatives may have the impression evaluation or reassess after a trial of treatment. that baseline cognition was normal – as the patient was in a familiar environment, seeing familiar people talking about familiar topics and 5 Likely dementia not being pressed on recent events – even if There is no absolute division between acute and baselineksfree cognition was, com in fact, impaired. chronic confusion in terms of timing or causes. Even if the cause has been removed, it can take many Acute cognitive function, fluctuating ↓ weeks for a delirium to resolve fully. Further, chronic 3 course, altered consciousness/attention? confusion can fluctuate. However, if confusion has Use the 4AT assessment test (Clinical tool, p. 80) persisted for >12 weeks without an obvious acute to diagnose delirium. Having establishedm baseline b cause sf or e evidence com of improvement,mebooks see ‘Further cognitive function, look for any evidence of an assessment of chronic confusion’ (p. 89). Confusion: delirium and dementia 82 Delirium: overview

ABCDE f e com 1 Capillary BG < 3.0 / deranged Yes Treat immediately and re-evaluate physiology?

Yes Urgent blood cultures and antibiotics 2 Suspect meningitis? LP if no contraindication

Yes Urgent 3 High risk of intracranial pathology? Intracranial lesion neuroimaging Nor c

Full clinical assessment, collateral history, FBC U+E, LFTs, glucose, Ca2+, TFTs, CRP ok e. Yes 4 Metabolic disturbance? Correct and reassess Seek underlyingeb cause No

Yes Collateral history; toxicology screen/drug levels 5 Likely drug toxicity? Consider discontinuation/dose adjustment/antidote

Yes Consider intoxication/withdrawal/ 6 Alcohol excess/dependence? e Wernicke’sree encephalopathy m No

Yes 7 Known or suspected liver disease? Consider hepatic encephalopathy

Baseline cognitive impairment or Yes 8 See Delirium in the vulnerable brain (p. 86) ↑susceptibility to delirium?

Yes 9 Evidence or high risk of infection? Must exclude CNS infection

Neuroimaging and toxicology screen if not already performed 10oReview f eeenvironmental exposures; reconsider alcohol withdrawal Neurology ± Psychiatry review bo ee Confusion: delirium and dementia 83 Delirium: step-by-step assessment

1 Capillary BG <3.0/deranged physiology? explained by hypoglycaemia, hypothyroidism or, if severe: dehydration, acidosis, ↓Na+ (especially Evaluate and treat respiratory failure (Ch. 12), <120 mmol/L), ↑Ca2+ (>3.0 mmol/L) or hyper- shock (Ch. 30), depressed consciousness (Ch glycaemia, e.g. hyperosmolar hyperglycaemic 7), hypothermia and seizure (Ch. 31) before con- state (p. 297 [Ch. 34]). Uraemia is an unusual sideringooks other re causes of delirium. Exclude new or cause of acute confusion in the non vulnerable worsening hypercapnia in any patient with chronic brain but may result in toxic accumulation of type 2 respiratory failure or significant chronic medication. ebooksf lung disease. If the capillary BG is <3mebo 0 mmol/L, sfreThe vulnerable com brain is more sensitive to send blood for laboratory glucose measurement metabolic derangement – even mild dehydration, but treat immediately, without waiting for the renal impairment or glycaemic/electrolyte/thyroid result. Reassess if confusion persists despite disturbance may impair cognition. Correct any 8 effective correction disturbances but continue to search for additional contributing factors. 2 Suspect meningitis? See ‘Further assessment of hyponatraemia’ + Assume meningitis/encephalitis if the patient (p. 88) in any patient with unexplained ↓Na . has meningism (Box 18.2, p. 169), a purpuric rash or a febrile illness with headache, seizures, 5 Likely drug toxicity? focal neurological signs or no obvious alternative source.ooks Take r blood e cultures m and throat swabs Illicit drug use or poisoning and give empirical IV antibiotics immediately. If Substance abuse is a common cause of acute there are no contraindications, perform an LP confusion/psychosis in younger patients. If it is (p. 170). Request CT prior to LP if seizure, focal mebosuspected, ree use com all available mesources of infor- neurological signs, GCS <15 or papilloedema. mation to establish what has been taken and when. Look for characteristic clinical features of 3 High risk of intracranial pathology? toxicity (see Table 7.2, p. 76) and consider a Consider urgent CT brain to exclude a structural urine toxicology screen. See www.npis.org for CNS cause if any of the following are present: further information. Give naloxone in patients with • new focal neurological signs or ataxia features of acute opioid toxicity – a response • first seizure should occur within seconds to minutes; observe • drowsiness (if you suspect opioid toxicity, closelysfree.com for symptoms of acute opioid withdrawal give a trial of naloxone before CT) (sweating, tremor, agitation, seizures). • recentoksfree.c head injury m Prescribed medication • sudden severe headache • any fall/trauma in a patient on Anticonvulsants, lithium, sedatives and opioids anticoagulation. can cause confusion, even in healthy brains. In patients with active malignancy, immunosup- Many other drugs may precipitateme delirium sfin pression or recent falls, look for other causes the vulnerable brain (see Box 8.1), especially of delirium, but have a low threshold for early tricyclic antidepressants, anticholinergics, e.g. neuroimaging to exclude intracranial metastases/ oxybutynin, antipsychotics and antihistamines. abscess/haemorrhage. Even if they are normally well tolerated, these agents may contribute to delirium in the context of other acute insults. Benzodiazepines can have 4 Metabo ic disturbance? a paradoxical effect, worsening confusion and Review blood chemistry for metabolic distur- agitation. Abrupt withdrawal of benzodiazepines bance check laboratory glucose, even if capillary and opioids can also precipitate delirium, often BG is within the normal range. The healthy brain several days after stopping. is ooksrelatively resistant re to com metabolic insult so do not Verify all drugs and dosages with the patient/ attribute confusion solely to modest biochemical relatives/carers. Check how frequently PRN derangement. However, delirium is likely to be medications, especially benzodiazepines and mebo sfree.com mebo ksf Confusion: delirium and dementia 84 Delirium: step-by-step assessment

opioids, are used at home and ensure they if first fit, focal neurological signs or evidence have not been inadvertently omitted, reduced of head injury. or reinstated in hospital. Consider a trial cessation or ↓dose of any drug with potential CNS side Wernicke’s encephalopathy effects (see Table 7.2, p. 76), especially if recently Consider thiamine deficiency and the need booksfreintroduced or increased. com Weigh the likelihood of for supplementation in all patients with acute toxicity against ongoing treatment benefit and confusion on a background of chronic alcohol predictable problems on discontinuation. Where excess. Give immediate IV thiamine if there is necessary, taper the dose graduallymebo to avoid short-term fre memory loss, diplopia,mebo gaze palsy, withdrawal symptoms. nystagmus, ataxia or severe malnutrition.

6 Alcohol excess/dependence? 7 Known or suspected liver disease? Suspect hepatic encephalopathy in any patient Acute alcohol intoxication with an existing diagnosis or clinical features of Acute alcohol intoxication is the most common cirrhosis. Constructional apraxia (inability to draw cause of altered mental status in the emergency a star) and/or asterixis (Fig. 19.1, p. 180), together department but may coexist with other pathology, with the absence of florid hallucinations/adrenergic e.g. head injury, liver injury, nutritional deficiency. features may differentiate hepatic encephalopathy Confirmooksfree. the presence oof alcohol with breath or from alcohol withdrawal in patients wi h alcoholic blood tests but always search for additionalbo liver sfree disease. coIf you suspect encephalopathy, causes of confusion. seek and treat potential precipitants, including spontaneous bacterial peritonitis (an ascitic tap Alcohol withdrawal is mandatory if ascites is present),mebooksf other infections, This may present early, e.g. 6–12 hours after dehydration, constipation, subclinical GI bleeding cessation of drinking, or late, e.g. 2–3 days after and drugs with CNS toxicity. hospital admission. Typ cal symptoms include Consider acute liver failure and seek urgent confusion, agitation, hallucinations and adrenergic expert advice in patients without cirrhosis over-stimulation (tremor, sweating, tachycardia). who have jaundice and very high ALT or ↑PT. The diagnosis is obvious in patients with a Perform an ABG to exclude hypercapnia if there florid presentation and clear history of alcohol is asterixis without features of liver disease. excess/dependence but consider it in all cases Baseline cognitive impairment or of unexplained delirium. Screen all patients for 8 ↑susceptibility to delirium? alcohol problems (Box 2.1, p. 11), identify elderly patientsooksfree with subtle comalcohol dependence, e.g. The diagnostic approach now depends on the ‘large’ daily sherry. If in doubt, obtain a collateral underlying threshold for developing delirium. If history and look for an isolated increase in GGT/ any feature in Box 8.1 is present, proceed to mean cell volume. Seizures may mecomplicate oo ‘Delirium free. in the vulnerable om brain:meb overview of further severe withdrawal but consider neuroimaging assessment’. Confusion: delirium and dementia 85 Delirium: step by-step assessment

9 Evidence or high risk of infection? disease. If CT is non-diagnostic, consider MRI brain. Check carboxyhaemoglobin levels for Suspect CNS infection in patients with carbon monoxide toxicity if there is associated ↑temperature/WBC/CRP or ↑susceptibility headache or if the patient has been exposed to (foreign travel, immuno suppression, animal bite). smoke/exhaust fumes (though levels may cor- Doooksfre not attribute confusion to minor non-CNS relate poorly with symptoms). Measure urinary infections. porphyrins (liaising with the biochemistry labora- Seek urgent input from an ID unit if the patient tory in advance), especially if there is associated has recently travelled to the developingm world, boo abdominal sfre pain. com Test for HIV.mebooksf has received an animal or tick bite, is HIV-positive If the cause is still not apparent, seek expert or is taking immunosuppressive therapy, e.g. neurological ± psychiatric input. EEG may assist in long-term steroids, chemotherapy. Send blood the diagnosis of atypical seizures, toxic encepha- 8 for thick and thin films if travel to a malaria- lopathies or unusual neurodegenerative diseases. endemic region has been undertaken within Other tests to consider include autoimmune/ the last 3 months Otherwise, undertake LP to vasculitis antibodies (cerebral vasculitis?), syphilis/ exclude CNS infection. Lyme disease serology, antineuronal antibodies If CNS infection has been excluded, treat any (paraneoplastic syndrome?) and heavy metal other apparent source of infection but continue levelssfree in blood com and urine. sf to searchoksfree.c for additional causes m of confusion. Neuroimaging and toxicology screen. 10 Consider other causes. Neurology ± Psychiatry review If not already carried out, perform neuroimaging and LP to exclude CNS infection and structural Confusion: delirium and dementia 86 Delirium in ‘vulnerable brain’: overview

Systemic inflammatory response or Yes Confirm source/organism 1 apparentfre source om of infection? Consider empirical antibiotics

Yes Relieve distress; gradually up-titrate 2 Pain present? analgesia; target assessment b

Exclude silent MI Clinical or ECG evidence of acute Yes 3 Correct hypoxia/hypotension; optimise cardiac disorder? treatment ofom heart failure/arrhythmia No

Yes 4 Palpabler bladder? om Insert/replace catheter; send CSU

Yes Exclude bowel obstruction 5 Constipated? Treat with laxatives/enemas

Yes 6 Sensory impairment? Reorientate, check glasses and hearing aids

Consider other causes, e.g. viral illness, depression 7 Neuroimaging to exclude structural CNS disease if confusion persists or deteriorates Establishfre accurate baseline function; reassess and reorientate regularly sfr m Confusion: delirium and dementia 87 Delirium in ‘vulnerable brain’: step-by-step assessment

Likely sou ce of infection or systemic Check troponin and assess further for acute 1 inflammatory response? coronary syndrome if there are other indicative ECG changes (p. 51). Cardiac failure may con- In the vulnerable brain, even minor infections can tribute to delirium through hypoxia or cerebral trigger delirium. Infections may present ‘atypically’ hypoperfusion. Avoid hypotension where possible lackingook characteristic fre symptoms and signs. (review medication) and correct hypoxia and In patients with ↑temperature/WBC/CRP, take anaemia. Treat any brady- or tachyarrhythmias blood cultures and look for a septic focus (p. and consider diuretic if there is fluidebooksf overload. 142). Also consider atypical presentationsmebo of acute sfre com abdominal pathologies, e.g. perforation, pan- Palpable bladder/Constipated/Sensory 4-6 creatitis, appendicitis, cholecystitis or diverticulitis. impairment? Re-examine regularly, check amylase and have a Actively look for and treat urinary retention, constipa- 8 low threshold for abdominal imaging – especially tion and nutritional deficiency (including B /folate). if there is any pain/tenderness or deranged LFTs. 12 If a urinary catheter is required, it may be possible Consider LP if the source remains elusive. to withhold anticholinergic drugs for detrusor Even in the absence of ↑temperature/WBC/ instability. Patients with moderate to severe demen- CRP, consider empirical antibiotic treatment if tia are at high risk of becoming acutely confused there s a convincing focus of infection, e.g. when presented with unusual surroundings, positive MSU or new purulent sputum, but people and stimuli. Provide frequent reassurance weigh the likelihood of bacterial infection against and reorientation, encourage visits from family complicationsooksfree such as com GI upset or Clostridium members, check that patients have their normal difficile diarrhoea. boo sfree.co glasses and hearing aids, and ensure adequate 2 Pain present? lighting. mebooksf Pain can cause or contribute to delirium in the Consider other causes. Neuroimaging. 7 vulnerable brain and may be difficult to assess Establish baseline function if the patient is agitated or muddled. Wherever In the absence of another indication for brain possible, identify and treat the underlying cause imaging, it may be reasonable to persevere with using simple analgesia/non-pharmacological the above measures for several days. However, measures as first-line treatment but do not leave arrange CT brain to exclude subdural haem- patients in distress. Where opioids are required, orrhage and other structural pathology if the carefu ly up-titrate and monitor. patient fails to improve or deteriorates. Review ksfree.com medications daily and reassess regular y for Clinical or ECG evidence of acute pain, metabolic disturbance or infection. Make 3 cardiac disorder? a detailed assessment of baseline cognitive Occasionally, myocardial infarction (MI) presents ability and level of function Finally, consider as delirium. Seek urgent cardiology minput if the rarer sfree.com causes, as described for mebooksfthe non-vulnerable ECG meets the criteria for ST elevation MI. brain. Confusion: delirium and dementia 88 Confusion: further assessment

Further assessment of hyponatraemia • ‘hypovolaemic’ if there is evidence of fluid depletion, e.g. dry mucous membranes, Step 1 Confirm true hyponatraemia ↓skin turgor, thirst, ↓JVP Apparent hyponatraemia may result from drip • ‘euvolaemic’ if neither of the above are arm contamination, laboratory/labelling error, or present. ‘pseudohyponatraemia’ooks re com due to hyperlipidaemia, The most common causes of hypervolaemic hyperproteinaemia, hyperglycaemia or high hyponatraemia are cardiac failure, cirrhosis, plasma ethanol. Check plasma osmolality (usually oliguric renal failure and nephrotic syndrome. If normal in pseudohyponatraemia) andmebo recheck the cause re is not obvious, checkmeb for proteinuria, o + Na if the result appears spurious. perform an echocardiogram and assess for Step 2 Estimate the rate of Na+ decline evidence of cirrhosis (p. 176). + A rapid ↓ in plasma Na+ may lead to life- In hypovolaemic hyponatraemia there is Na + threatening cerebral oedema, and requires and water depletion, with relatively greater Na prompt correction. In contrast a gradual ↓ in Na+ loss. The most common causes are excessive allows osmotic adaptation by cerebral neurons diuretic therapy and acute diarrhoea/vomiting. + and rapid correction may lead to irreversible and If the source of Na and water loss is not brainstem damage (central pontine myelinolysis). obvious, measure urine sodium. The normal It is therefore critical to distinguish acute (<72 response of the kidneys to salt and water + hours) from chronic (>72 hours) hyponatraemia depletion is to minimize Na excretion If urine + Suspectooksfre chronic if any .com of the following features Na is appropriately low (<20 mmol/L), suspect is present: GI tract losses, e.g. diarrhoea, vomiting or ‘third space’ losses, e.g. pancreatitis, burns. If urine • recent U+E results demonstrating a Na+ is ( 20 mmol/L), then there is a contribution progressive decline in plasma Nam+ bo sfree.com> mebo ksf to salt and water depletion from renal losses, • slowly progressive onset of symptoms, e.g. e.g. adrenal insufficiency, renal tubular acidosis anorexia, lethargy, confusion or ‘salt-wasting’ renal disease. • asymptomatic or only mild symptoms with a plasma Na+ ≤125 mmol/L Step 4 If euvolaemic, or if cause unclear, measure • no clear cause for a sudden decrease in urine sodium and osmolality + plasma Na (see below). If feasible, discontinue any diuretics for 10 days In these patients, correct Na+ with extreme and recheck U+E alongside plasma and urine care Recheck U+E every 2–4 hours, and aim osmolality and urine Na+. for a rise in plasma Na+ of ≤8 mmol/day. Low urine Na+ (<20 mmol/L) implies that Suspectoksfree.com acute hyponatraemia if: ↓plasma Na+ is not due to excessive renal • abrupt onset of symptoms within the last Na+ losses. The cause may be hypovolaemic 48 hours OR hyponatraemia due to extra-renal losses (see • major symptoms (severe confusion, ↓ GCS, above) but without obvious clinical manifestations seizures) with Na+ ≥ 120 mmol/L,m bof sfree.chypovolaemia. In m this case,meboo urine osmolality f especially with a history of sudden increase in free will be ↑ (>150 mmol/kg) due to the presence of water intake, e.g., excessive IV dextrose administra- other solutes. If urine osmolality is <150 mmol/ tion (especially postoperatively) or polydipsia. kg, the likely cause is excessive water intake. In If you suspect acute hyponatraemia, seek hospitalized patients check for recent administra- urgent expert advice but, in an emergency, aim tion of hypotonic IV fluids, e.g. 5% dextrose. In to increase plasma Na+ by 4–6 mmol/L over 1–2 non-hospitalized patients consider psychogenic hours then reassess. polydipsia. If hyponatraemia is accompanied by ↑urine Step 3 Assess volume status Na+ (>20 mmol/L) and osmolality (>150 mmol/ Clear evidence of either ↑ or ↓ECF volume is kg), consider diuretic use, adrenal insufficiency, veryook helpful free.comin determining the underlying cause. hypothyroidism, salt-wasting renal disease and the Categorize the patient as: syndrome of inappropriate ADH secretion (SIADH). • ‘hypervolaemic’ if there is evidence of fluid Check TFTs and a 9 a.m cortisol. High or overload, e.g. oedema, ↑JVP, ascitesm bohigh–normal sfree plasma com urea/uricmebooks acid may indicate Confusion: delirium and dementia 89 Confusion: further assessment subtle ↓ECF volume; if present, consider Consider psychiatric illness salt-wasting diseases or occult diuretic use. Perform an objective measure of cognition Otherwise, the likely diagnosis is SIADH. (at least MMSE) to ensure the presentation fits If you suspect SIADH, look for an underlying with a chronic decline in cognition dementia. cause (Box 8.2). Consider trial cessation of any Depression can mimic or exacerbate dementia suspectedooksf causative e agent. If the cause remains and may be difficult to diagnose. Consider using unclear, request a CXR and CT brain and assess tools such as the Cornell scale to assist diag- the response to fluid restriction <( 1 L/day). nosis and, if you suspect depression, reassess meboocognitive sfre function c after m a trial mebooksfof anti-depressant Further assessment of chronic confusion therapy. The approach to progressive cognitive decline Assess for reversible causes over a period of months to years differs from Perform a CT brain in every patient with chronic 8 the approach to acute confusion. Exclude the confusion. This may identify reversible causes, reversible causes from p. 79 with a CT brain and e.g. subdural haemorrhage or normal pressure blood tests; if no reversible cause is identified, hydrocephalus (ataxia and incontinence should refer for specialist evaluation and care. raise the index of suspicion), or suggest possible aetiological factors, e.g. vascular disease Measure TFTs in all patients, as hypothyroidism

Box 8.2 Causes of SIADH can present as dementia and responds to treat- oo free com ment. Take a careful alcohol history and consider • Tumours, especially small-cell lung cancer Wernicke–Korsakoff syndrome in any patient with • CNS disorders: stroke, trauma, infection • Pulmonary disorders, e.g. pneumonia, tuberculosis chronic alcohol misuse. Look for and correct • Drugs mnutritional sf ee.com deficiencies, e.g. mebooks12B , folate. • Anticonvulsants, e.g. carbamazepine Consider rare causes • Psychotropics, e.g. haloperidol • Antidepressants, e.g. fluoxetine Perform a more intensive work-up if the patient • Cytotoxics, e.g. cyclophosphamide has an unusual pattern of cognitive impairment, • Hypoglycaemics, e.g. chlorpropamide e.g. preserved recent memory or personality/ • Opioids, e.g morphine speech change, unexplained neurological find- • Proton-pump inhibitors, e.g. omeprazole ings on examination, a rapid course of cognitive • Sustained pain, stress, nausea, e.g. postoperative decline or onset at a young age. This should state usually include an HIV test, copper studies, Lyme/ • Acute porphyria sfree.com • Idiopathic syphilis serology, MRI brain and LP ± furtherksf oksfree.com specialist assessment, e.g. EEG. Diarrhoea 9oksf

Diarrhoea may be defined as the passage of ≥3 Irritable bowel syndrome loose or liquid stools/day. Patients often have difficulty describing their stools. The Bristol Stool Irritable bowel syndrome is the most common Form Scale https://www.niddk.nih.gov/health- cause of chronic diarrhoea. The predominant information/health-communication-programs/ bowel habit may alternate between diarrhoea bowel-contro awareness-campaign/Documents/ and constipation, and diagnosis is based on Bristol_Stool_Form_Scale_508.pdf can be helpful. typical clinical features (Box 9.1) in the absence The differential diagnosis depends on symptom of apparent organic disease. Symptoms tend to duration. Acute diarrhoea (<2 weeks) is usually follow a relapsing and remitting course, often infectious but occasionally is due to drugs or a exacerbated by psychosocial stress firstooksfree.com presentation of inflammatory bowel disease. Drugs Chronic/relapsing diarrhoea may reflect colorectal cancer or inflammatory bowel disease, but the Many drugs, including numerous over-the- most frequent cause is irritable bowelmeboo syndrome. counter sfree preparations, com cause diarrhoeam (Box 9.2 ksf). Infectious diarrhoea Colorectal cancer Infectious diarrhoea is due to faecal–oral trans- Colorectal cancer may present with diarrhoea, mission of viruses, bacteria, bacterial toxins or especially if left-sided/distal. Suggestive features parasites. Most cases are self-limiting and a include weight loss, rectal bleeding, a palpable pathogen is rarely identified. Viruses and toxins mass or ron-deficiency anaemia, but the absence predominantly affect the stomach and small of these features DOES NOT exclude malignancy. bowel, causing large-volume, watery diarrhoea and pronounced vomiting; in toxin-mediated diarrhoea, e.g. Staphylococcus aureus, the incubation period is typically <12 hours. Invasive ooksfree com Box 9.1 Rome III criteria for diagnosis of intestinal pathogens, including certain strains of irritable bowel syndrome Escherichia coli, and Shigella, may cause bloody diarrhoea, often with severe abdominal cramps Recurrent abdominal pain or discomfort on at least 3 meboodays reeper monthcom during the previous m3 months b that is and systemic upset (dysentery). Clostridium associated with two or more of the following: difficile infection (CDI) is an important cause of • relieved by defecation hospital-acquired diarrhoea, especially following • onset associated with a change in stool frequency broad-spectrum antibiotic therapy; CDI ranges • onset associated with a change in stool form or from mild diarrhoeal illness to life-threatening appearance. pseudomembranous colitis. Diarrhoea that Supporting symptoms include: persists for >10 days is unlikely to be infective, • altered stool frequency but consider protozoal infections, e.g. giardiasis, • altered stool form • altered stool passage (straining and/or urgency) amoebiasis or Cryptosporidium infection, in free.com • mucorrhoea patients who are immunocompromised or have • abdominal bloating or subjective distension. ecentlyooksfree.com travelled to the tropics. Diarrhoea 91 Differential diagnosis

Box 9.2 Drugs that frequently cause diarrhoea Box 9.3 Extra-intestinal features of inflammatoryfre bowel o disease • Laxatives (including occult laxative abuse) • Antibiotics (especially macrolides) • General: fever, malaise, weight loss • Alcohol (especially chronic alcohol excess) • Eyes: conjunctivitis, episcleritis, iritis ooks• NSAIDs r • Joints: arthralgia of large joints, sacroiliitis/ankylosing • Metformin spondylitis • Colchicine • Skin: mouth ulcers, erythema nodosum, pyoderma • Orlistat (steatorrhoea) gangrenosum • Proton pump inhibitors • Liver: fatty liver, gallstones, sclerosingmebo cholangitis, • SSRIs cholangiocarcinoma (ulcerative colitis) • Nicorandil • Cytotoxic agents 9

The diagnosis must be considered in any patient Disorders causing malabsorption >45 years with new-onset, persistent diarrhoea and is usually confirmed by colonoscopy with Fat malabsorption causes pale, greasy, offen- biopsy. sive stools that float and are difficult to flush (steatorrhoea). Other features of malabsorption Inflammatoryooksfre bowel disease include undigested foodstuffs in stool, weight Ulcerative colitis (UC) is confined to the large loss, bloating and nutritional deficiencies. The bowel and typically presents with bloody diar- usual underlying cause is small bowel disease, rhoea and cramping lower abdominalmeb pain ± e.g. s coeliac e disease, Crohn’smebooks disease, tropical tenesmus, mucus discharge, fever and constitu- sprue, lymphoma, small bowel resection or tional upset. Crohn’s disease can affect any part pancreatic insufficiency. of the alimentary tract and may present with large Other causes bowel symptoms simi ar to those of UC, or with small bowel symptoms, e.g. watery, non-bloody • Diverticulitis, ischaemic colitis. diarrhoea accompanied by abdominal pain and • Hyperthyroidism, autonomic neuropathy. weight loss Both disorders are associated with • Carcinoid tumour, gastrinoma, VIPoma. a range of extra-intestinalfree.com features (Box 9.3). • Severeree.c constipation with overflow. Diarrhoea 92 Acute diarrhoea: overview

Full clinical assessment, rectal exam ± stool culture f e co 1 Assess resuscitation requirements and illness severity.k f

Yes

Yes Consider dysentery, diverticulitis, ischaemic 2 Bloody diarrhoea? colitis, inflammatory bowel diseasem No

Yes Urgent stool for 3 Risk of C. difficile nfection? C. difficile toxin ± C. difficile infection empirical treatment No

Yes 4 Risk of protozoal infection? Stool sample for ova, Confirm infection s o cysts and parasites No

Yes Discontinue drug 5 Likely drug culprit? Drug related diarrhoea eif possible ks

No me

Likely gastroenteritis 6 Liaise with ID/GI if symptoms persist >10 days

Assess resuscitation requirements and AKI occurs in the context of bloody diarrhoea, 1 illness severity look for features of haemolytic uraemic syndrome, e.g. ↓Hb, ↓platelets, ↑bilirubin/LDH/reticulocytes. Stepo 1 Are k there features of o shock? Look for ↑HR, ↓BP (a late sign) or evidence of Step 3 Does the patient otherwise require IV fluids/ tissue hypoperfusion (see Box 30 1, p. 267). If hospital admission? e ooks present, provide aggressive IV fluidme resuscita- Patients s with clinical evidence of dehydration tion and reassess. Although hypovolaemia from (thirst, dry mucous membranes, ↓skin turgor) GI losses is the likeliest cause of shock, also and concomitant vomiting, or those who are consider intra-abdominal SIRS/sepsis, medication unable to match oral intake to ongoing losses and adrenal insufficiency (diarrhoea is a common require IV fluids feature of acute adrenal crisis). Other features that may indicate a need for hospital admission include Step 2 Is there acute renal impairment? • fever Hypovolaemia may result in severe ‘pre-renal’ • ↑WBC acute kidney injury (AKI), especially if compounded • bloody diarrhoea by antihypertensive or nephrotoxic medication • abdominal tenderness/guarding/rigidity eo g. diuretics, ksfre ACE inhibitors, com NSAIDs. Patients • frail, elderly or immunocompromised patient with AKI require IV rehydration with close moni- • significant comorbidity, e.g. heart/renal/ toring of fluid balance, urine output and +U E. If hepatic failure. eboo mebo ree com Diarrhoea 93 Acute diarrhoea: step-by-step assessment

2 Bloody diarrhoea? Box 9.4 Assessing the severity of Clostridium The frequent passage of bloody stools suggests difficile infection either Mild WBC not elevated • infectiono s with re invasive organisms, e.g. <3 episodes of loose stools/day Campylobacter, Shigella or Amoeba, or Moderate ↑WBC (but <15 × 109/L) cytotoxin-producing organisms, e.g C 3–5 loose stools/day e fre co 9 difficile, E. coli O157 OR Severe WBC >15 × 10 /L or • non-infectious colitis, e.g. ischaemic colitis Serum creatininemeboo >50% above inflammatory bowel disease. baseline or Temp >38.5°C or It is often difficult to differentiate dysentery from Evidence of severe colitis (abdominal a first attack of inflammatory bowel disease in or radiological signs) the early stages: both may be accompanied by Life-threatening Signs of shock (p. 267) 9 abdominal pain, tenesmus, mucus, constitutional Partial or complete ileus upset and a systemic inflammatory response Toxic megacolon or (see Box 14 1, p. 141). CT evidence of severe disease

• Send FBC, CRP and three stool samples Adapted from Public Health England 2013. Updated guidance on in all patients, plus blood cultures if fever is the management and treatment of Clostridium difficile infection. present.oksfree.com Public Health England. http://www.hpa.org.uk ok • Test stool for C. difficile toxin (CDT) if the patient has risk factors (see below), severe systemic upset or ↑↑WBC. eb s c m 3 months or is >65 years. In high-risk patients • Liaise with the ID team and request analysis send ≥3 samples before ruling out the diagnosis. of stool for ova, cysts and parasites if If C. difficile confirmed, assess severity at least recent foreign travel. daily (Box 9.4). • Request an abdominal X-ray to look for colonic dilatation (see Fig. 4.5B, p. 32) if 4 Risk of protozoal infection? there is abdominal tenderness/distention or a pronounced systemic inflammatory Send three stool samples on consecutive days response. for ova, cysts and parasites in patients with a history of recent foreign travel, when there is If the duration of symptoms is ≤7 days, suspect an infectious cause unless there are known or suspected immunocompromised, specific pointers to an alternative diagnosis e.g. chemotherapy, HIV or in men whooksf have Considerooksfr ischaemic e comcolitis if bloody diarrhoea sex with men. was preceded by sudden onset of left-sided 5 Likely drug culprit? lower abdominal pain or in any patient >50 years with known atherosclerotic disease ormebo a source Suspect sfree drug-related co diarrhoea if the onset of of systemic embolism, e.g. atrial fibrillation. symptoms corresponds with initiation or ↑dose Refer any patient with known inflammatory of drug, especially those listed in Box 9.2. Seek bowel disease, extra-intestinal manifestations (see an alternative explanation if diarrhoea does not Box 9.3), previous sim lar episodes or symptoms resolve on drug discontinuation. >7 days for specialist GI evaluation. Seek an urgent surgical review if there is Likely gastroenteritis. Liaise with ID/GI if 6 evidence of peritonism or toxic megacolon, or symptoms persist >10 days you suspect ischaemic colitis or diverticulitis. Most cases are self-limiting viral or toxin-mediated infections and do not require further investigation 3 Risk of C. difficile infection? or antimicrobial treatment. If symptoms persist Sendo stool k for free CDT in comany patient who lives in an >10 days, seek specialist advice and consider institution, e.g. nursing home, has recently been further assessment as for chronic/relapsingbooks hospitalized, received antibiotics within the last diarrhoea (see below). mebo sf ee om Diarrhoea 94 Chronic/relapsing diarrhoea: overview

Full clinical assessment, rectal exam ± FBC f e co Yes Treat and 1 Hard or impacted stool in rectum? Likely overflow diarrhoea reassesso No

Yes Investigate 2 Steatorrhoea? Likely malabsorption disorder for cause

Yes Urgent lower Colorectal cancer, ulcerative 3 Alarm features? bowel Investigation colitis, Crohn’s disease, other

Yes Discontinue 4 Likely drug culprit? Drug-related diarrhoea s c drugs if possible c No

Yes 5 Specific infection risk? Consider protozoa, HIV, C. difficile

2+ FBC, U+E, LFTs, TFTs, Ca , CRP, ESR, coeliac serology ± ferritin, B12, folate

Clinical or laboratory features Yes 6 Further investigation ± refer GI suggesting organic disease? ree m No

Likely functional disorder, e.g. irritable bowel syndrome 7 Reassess or refer GI if persistent troublesome symptoms/organic features ebo ee om Diarrhoea 95 Chronic/relapsing diarrhoea: step-by-step assessment

1 Hard or impacted stool in rectum? time and restart the drug if symptoms continue unaltered. Always ask about alcohol excess. Have a high index of suspicion for overflow diarrhoea in frail, immobile or confused elderly patients 5 Specific infection risk? Always do a rectal examination. If the stool is hardooks or impacted, r treat with faecal softeners and Exclude protozoal infection in patients with a laxatives, then reassess. If the rectal examination history of travel to the tropics, e.g giardiasis, is normal, overflow diarrhoea is unlikely (90% of amoebiasis, or with known HIV infection/other impactions are rectal), but consider anmebo abdominal immunocompromised, fre co e.g. cryptosporidiosismebo – X-ray if there is strong clinical suspicion. send three fresh stool samples for examination for ova cysts and parasites. Liaise with the ID 2 Steatorrhoea? team if stool samples are negative but there is ongoing clinical suspicion of infection. Test for Steatorrhoea signifies fat malabsorption but HIV in any pat ent with chronic diarrhoea and 9 its absence does not exclude a malabsorptive risk factors. disorder. If steatorrhoea is present, ensure C difficile diarrhoea may be chronic or relaps- that the patient is not taking orlistat (available ing – send stool to test for CDT in any patient over the counter in the UK) and check coeliac with risk factors (see above). serology and faecal elastase (↓in pancreatic insufficiency). If ↓faecal elastase or a strong Clinical or laboratory features suggesting suspicionooksfree.c of pancreatic disease, e.g. suggestive 6 organic disease? symptoms or cystic fibrosis, consider pancreatic Screen for hyperthyroidism, hypercalcaemia and imaging (CT/MRCP); otherwise, consider small coeliac disease. Refer to GI for further small bowel investigation, e.g. duodenal biopsy, MRI. mebobowel sf investigation ee com if large-volume,me non-bloody oo f Screen for nutritional deficiencies, e.g. iron, B , 12 stool, previous gastric/small bowel surgery or folate, Ca2+, Mg2+, PO 3−, albumin, in any patient 4 evidence of nutritional deficiencies: albumin, B , with suspected malabsorption. 12 2+ 2+ 3− folate, Ca , Mg , PO4 . Exclude inflammatory bowel disease if there 3 Alarm features? is a positive family history, mouth ulcers, fever, Expedite lower bowel investigation to exclude ↑CRP/ESR or extra-intestinal manifestations (see colorecta cancer/inflammatory bowel disease if Box 9.3). Refer to GI for further evaluation if the patient has persistent diarrhoea associated any of the above features is present or there with any of the following: aresf other ee findings com that suggest organic disease, • rectaloksfree bleeding m e.g. weight loss, anorexia, painless diarrhoea, • palpable rectal/abdominal mass prominent nocturnal symptoms or recent onset • weight loss of symptoms in a patient >45 years. Faecal • iron deficiency anaemia calprotectin levels can assist in the differentia- • new presentation in a patient >45 years. tion between inflammatory andmebooksf non-inflammatory Consider flexible sigmoidoscopy as a first-line bowel disease. investigation in patients <45 years or colonoscopy if >45 years. 7 Likely functional disorder If none of the above is present, a functional 4 Likely drug culprit? cause, e g irritable bowel syndrome, is likely – Look for a temporal relationship between particularly when typical symptoms are present potential drug culprits (see Box 9.2) and the (Box 9.1). Provide reassurance and explanation onset of diarrhoea. Consider trial discontinuation but refer to GI if symptoms are progressive, where feasible but change only one agent at any distressing or disabling. ksf oksfree. m o sfree.co Dizziness 10oksfre

The key to assessing dizziness lies in establish- nystagmus tend to be constant and protracted. ing the exact nature of the patient’s symptoms. Vertebrobasilar transient ischaemic attacks Occasionally, transient alteration of conscious- (TIAs) may cause recurrent, transient episodes ness or focal neurological deficit will be described of vertigo. as a dizzy turn However, most patients with dizziness have vertigo, light-headedness/presyn- Other causes cope or a sensation of unsteadiness. These include migraine-associated vertigo Disorders causing vertigo ototoxicity, e.g. gentamicin, furosemide, cisplatin herpes zoster oticus (Ramsay Hunt syndrome) Vestibularoksfree.com neuronitis and perilymphatic fistula. This is inflammation of the vestibular nerve, pos- Disorders causing presyncope/ sibly due to viral infection. There is abrupt onset light-headedness e oksf of severe vertigo, associated with nausea and vomiting. Labyrinthine involvement (labyrinthitis)meb sfrReflex e presyncope om (vasovagal episode) causes tinnitus and/or hearing impairment. Reflex vasodilatation and/or bradycardia occur in Benign paroxysmal positional response to a ‘trigger’ such as intense emotion vertigo (BPPV) or noxious stimuli, e.g. venesection. There is a prodrome of nausea, sweating and ‘greying-out’ BPPV is caused by particles in the semicircular of vision loss of peripheral vision. Syncope often canals which alter endolymph flow. Brief episodes ensues but may be averted by lying down. of vertigo, typically lasting 10–60 seconds, are provoked by changes in head position. Orthostatic hypotension Ménière’s disease Orthostatic hypotension may result from antihypertensive medication, hypovolaemia (dehy- Recurrento sfree. attacks of vertigo, m fluctuating low- dration, blood loss) or autonomic dysfunction, frequency hearing loss, tinnitus and a sense of especially in elderly or diabetic patients. aural fullness are caused by increased volume eboo of endolymph in the semicircular canals.mebArrhythmia free.com Brady- and tachyarrhythmia can reduce cardiac Acoustic neuroma output and thereby compromise cerebral perfu- This cerebellopontine angle tumour usually pre- sion. There may be associated palpitation, ECG sents with unilateral sensorineural hearing loss. abnormalities or a cardiac history. Vertigo may occur but is rarely the predominant problem. Structural cardiac disease Severe left ventricular outflow tract obstruction, Brainstem pathology e g. aortic stenosis or hypertrophic obstructive Vertigo may be due to infarction, haemorrhage, cardiomyopathy, can result in light-headedness demyelination or a space-occupying lesion. There by reducing cardiac output. Episodes may be willook usually be f associated .co features of brainstem provoked by exertion. There will usually be abnor- dysfunction, e.g. diplopia, dysarthria or cranial malities on examination, e.g. systolic murmur, nerve palsies. Vertigo, nausea, vomiting and and ECG, e.g. left ventricular hypertrophy. meboo sfree.com mebooksf Dizziness 97 Differential diagnosis

Disorders causing unsteadiness motor endplate or muscle) can result in unsteadiness due to weakness. Ataxia Other causes Lack of coordination of muscle movements mayo cause ks profound re unsteadiness and difficulty Loss of confidence, joint problems, Parkin walking; it is most commonly due to cerebellar son’s disease and gait dyspraxia may all cause pathology. ebounsteadiness. fre o Other disorders causing dizziness Multisensory impairment m b Many other conditions can cause dizziness, Balance requires input from multiple sensory including hypoglycaemia, partial (temporal lobe) modalities (visual, vestibular touch, propriocep- seizure, migraine variants, normal pressure tive); reduced function in more than one of these hydrocephalus, hyperventilation and anxiety. modalities, even if relatively minor, may cause com unsteadiness. This is most often seen in the elderly. 10e Weakness Lesions anywhere in the motor tract (cerebral cortex,oksfr upper motor e neuron, c m lower motor neuron, Dizziness 98 Initial assessment: overview

Full clinical assessment f e co Y s Loss of consciousness? k See Transient loss of consciousness (Ch. 29) 1 o No

Yes 2 Transient focal neurological deficit? Likely transient ischaemic attack

Yes 3 Illusory sense of motion? Go to Ve tigoco (p. 100) No

Yes 4 Light-headednesss co or presyncope? Go to Presyncope (p. 104)

Sense of unsteadiness or Yes 5 Go to Assessment of unsteadiness (p. 107) impaired balance? m No

Exclude anaemia and postural hypotension 6 Consider hypoglycaemia,co complex partial seizure, migraine, hyperventilation,c anxiety Dizziness 99 Initial assessment: step-by-step assessment

1 Loss of consciousness? Sense of unsteadiness or 5 impaired balance? Establish this first, as loss of consciousness requires a different diagnostic approach (see In some patients with dizziness, the principal Ch. 31). If at all possible, obtain an eyewitness problem is impaired sense of balance associated accountooks of rethe episode; otherwise, suspect with falls or the feeling that one might fall. This transient loss of consciousness if there is a usually occurs while standing and is aggravated history of ‘coming to’ on the ground or if facial by walking. The patient may need to hold on injuries were sustained. meboto furniture e orco other people. Examinationmebook of the gait (p. 215) may be revealing. The underlying 2 Transient focal neurological deficit? problem is often impaired central processing of the body’s position in space, e.g. cerebellar A TIA is often described by the patient as a ‘funny disorders, impaired proprioception, peripheral turn’ and careful questioning may be required to neuropathy, visual loss, poorly compensated elicit a history of transient focal neurological dis- vestibular disorders, which may be exacerbated turbance (usually 3 hours). The most common 10 < by reduced muscle strength or confidence, presentat ons include hemiparesis, hemisensory particularly in the elderly. disturbance, facial droop, speech disturbance, diplop a and monocular visual loss (amaurosis fugax). Vertigo may occur with a vertebrobasilar 6 Consider other causes TIA,ooksfree.com usually accompanied by other brainstem features. boIf the free description com of dizziness is unclear, ask for more details: ‘Imagine you are having one of your 3 Illusory sense of motion? dizzy turns now. Talk me throughmeb exactly what e happens and what you feel.’ If the account is Vertigo is an illusory sensation of motion (usually not consistent with any of the above categories, spinning or rotatory). When present, it is invariably consider alternative causes. aggravated by movement. If the nature of the • Suspect hypoglycaemic attacks if the dizziness is not apparent from the patient’s own patient is taking insulin or sulphonylurea account, then ask: ‘When you have dizzy spells, drugs or reports relief of symptoms with do you simply feel light-headed or do you see sugar intake; a CBG and lab glucose the world spin around you as if you had just measurement taken during an episode will got off a playground roundabout?’ The latter confirm or exclude the diagnosis. indica es vertigo. ksfree.com • Seek neurological advice if there are repeated episodes of amnesia, 4 Light-headedness or presyncope? altered consciousness or unusual Consider presyncope in patients who describe behaviour. a feeling of light-headedness, ‘as if I might faint • In all patients with orthostatic symptoms, or pass out’, or one that is akin to theme familiar perform ree an com FBC to excludem anaemia bo and transient sensation experienced after standing measure erect and supine BP. up quickly. If any of the episodes has been • Anxiety is the most common cause of associated with blackout, assess as described ‘dizzy turns’ in patients under 65 years but for transient loss of consciousness (Ch. 31). is a diagnosisom of exclusion. com Dizziness 100 Vertigo: overview

Full clinical assessment ± ENT exam and Dix–Hallp ke manoeuvre (Fig. 10.1) f e co fre Yes 1 Red flag features (see Box 10.1)? Must exclude central lesion

Yes Likely vestibular neuronitis. Consider neuroimaging 2 New-onset sustained vertigo? if atypical features or symptoms persistm >2 weeks

Recurrent transient episodes Yes 3 provoked by changes in Likely benign paroxysmalc positional vertigo head position?

Recurrent episodes associated Yes Refer for audiometry o4 with rhearing e loss/tinnitus/ear co Likely Ménière’s disease ± exclusion of fullness? acousticboo neuroma No

New-onset recurrent spontaneous Yes Possible vertebrobasilar 5 Urgent MRA episodes lasting minutes? transient ischaemic attacks

Yes 6 Associated migraine? Likely migraine-associated vertigo fre m No

Consider Ménière’s disease, ototoxicity, central lesion 7 Refer ENT if persistent unexplained true vertigo Consider non-vertiginous causes of dizziness if atypical presentation meb fre m Dizziness 101 Vertigo: step-by-step assessment

1 Red flag features (Box 10.1)? Consider neuroimaging (preferably MRI) if the patient has a negative head thrust test, is unable The presence of any of the features in Box to stand without support or has a history of 10.1 raises the possibility of serious intracranial vascular disease – primarily to exclude acute pathology. cerebellar stroke. ooksIf the presentation re is sudden, consider acute In vestibular neuronitis, severe vertigo typically haemorrhagic or ischaemic stroke and arrange persists for several days and full recovery occurs urgent neuroimaging. Where less acute, the main within 3–4 weeks; reassess if symptoms persist concern is to exclude intracranial massmebo lesion. beyond sfre this period. co m b oksf CT is usually the initial imaging modality but MRI offers superior visualization of the posterior Recurrent transient episodes provoked by fossa. All patients with progressive sensorineural 3 changes in head position? hearing loss require MRI to exclude acoustic A history of repeated, brief episodes of vertigo neuroma. provoked by changes in head position, e.g. turning over in bed or looking up, strongly 10 2 New-onset sustained vertigo? suggests BPPV. Episodes may occur in bouts In the absence of red flag features, new-onset lasting several weeks interspersed with periods sustained vertigo is most likely due to vestibular of remission. A positive Dix–Hallpike test (Fig. neuronitis. The usual story is of abrupt-onset 10.1) confirms the diagnosis but, even if negative, severeooksfre vertigo with nausea om and vomiting but BPPV remains the likely diagnosis. without hearing loss or tinnitus. The patient has booksf e difficulty walking but can usually stand unsup- ported. There is unilateral nystagmusmebo enhanced sfree. m by asking the patient to look to the side or by Box 10.2 The head thrust test blocking visual fixation (place a blank piece of paper a few inches in front of the eyes and With intact vestibula function, changes in head position inspect from the side). A positive head thrust trigger reflex eye movements in the opposite direction to maintain visual fixation via the vestibulo-ocular reflex test (Box 10.2) confirms the diagnosis. (VOR). The head thrust test assesses the VOR on both sides Stand in front of the patient, grasp his/her head in your hands and instruct him/her to focus on your nose. Turn the head as rapidly as possible to one side by 15° Box 10.1 Red flag features in vertigo (do not perform in patients with known or suspected • Focal neurological symptoms or signs: dysarthria, neck pathology) and observe eye movements. Failure diplopia,o sf facial weakness, com swallowing difficulties, to maintain fixation on the target is evidenced by the dysdiadochokinesis or focal limb weakness need for a voluntary, corrective eye movement back • Papilloedema, drowsiness or ↓GCS towards the target. This indicates peripheral vestibular • Inability to stand or walk dysfunction on the side to which the head was turned. • Atypical nystagmus (down-beating, bi-directional Perform the test in both directions. Unilateral impairment gaze evoked, pure torsional, not suppressedm with of sfree.com VOR is seen in vestibular neuronitismeboo and excludes a fixation on object) central cause for vertigo. See the video at the website of • New-onset headache: sudden onset and severe or the Journal of Neurology, Neurosurgery, and Psychiatry: worse in morning/lying down http://jnnp.bmj.com/content/suppl/2007/09/13/ • Progressive unilateral hearingom loss jnnp.2006.109512.DC1/78101113webonlymedia.mpgom Dizziness 102 Vertigo: step by-step assessment

Recurrent episodes associated with the diagnostic criteria for migraine (see Table 18.2, 4 hearing loss/tinnitus/ear fullness? p. 173) and have episodic vertigo with no other obvious cause have probable migraine- Diagnosis of Ménière’s disease requires the associated vertigo; definitive diagnosis requires following criteria: a temporal association between vertigo and • ook recurrent fre attacks coof vertigo lasting minutes migraine headache or aura. to hours (± nausea and vomiting) • fluctuating sensorineural hearing loss, 7 Consider other causes/ENT referral especially for low frequencies (audiometrym b is s re m ooksf usually required to detect this) In Ménière’s disease, the patient is often unaware • tinnitus or a sense of pressure/fullness in of low-frequency hearing loss or tinnitus during the ear. attacks, and hearing may have returned to normal by the time of audiometry. In these To exclude acoustic neuroma, consider ENT circumstances, recurrent attacks of spontaneous referral for any patient with unilateral hearing vertigo may be the only presenting feature. loss and vertigo, especially if the presentation is Suspect ototoxicity in any patient with new- recent in onset or atypical for Ménière’s disease. onset vertigo or other balance/hearing disturbance if gentamicin, furosemide or cisplatin has New-onset recurrent spontaneous recently been prescribed. Persistent symptoms 5 episodesk free.com lasting minutes? despite drug cessation may indicate irreversible Vertebrobasilar TIAs are normally associated vestibulocochlear dysfunction. with other neurological features, e.g. diplopia, Reassess all patients for red flag features dysarthria, facial numbness, but occasionally and arrange an MRI of the brain if there is any present with episodes of vertigo asmeb the only suspicion sfree.com of a central lesion.me ooksf symptom. Patients with a crescendo pattern Patients with dizziness present constantly over of symptoms may have impending thrombosis weeks or whose dizziness is not improved by and require prompt referral for imaging of the remaining still are unlikely to have true vertigo. posterior circulation, e g. MR angiography. Otherwise, refercom to ENT for further evaluation. 6 Associated migraine? Enquire about possible migrainous symptoms in all patientssfr with episodic e om vertigo. Those who fulfil Dizziness 103 Vertigo: stepco by-step assessment

A B 10

Fig. 10.1 The Dix–Hallpike test. Start with the patient sitting upright on the couch. Explain what you are going to do. A Rapidly lie the patient supine with the head (supported by your hands) extended over the end of the couch and turned to the r ght. Maintain this position for at least 30 seconds, asking the patient to report any symptoms whilst observing for nystagmus. B Repeat with the head turned to the left. The test is positive if the patient develops symptoms of vertigo and nystagmus. (From Boon NA, Colledge NR, Walker BR. Davidson’s Principles & Practice of Medicine, 20th edn Edinburgh: Churchillooksfr Livingstone, 2006.) ooksfr ooks e Dizziness 104 Light-headedness/presyncope: overview

Yes 1 Featuresfre of shock? co Assess as per Chapter 30 No

Postural symptoms + orthostatic Yes 2 Orthostatic presyncope hypotension?

Clinical or ECG featu es that suggest Yes 3 Echocardiogram Cardiac syncope structural heart disease?

Clinical or ECG features that suggest Yes Document 4 Intermittent arrhythmia arrhythmia?sfr om rhythm

Yes 5 Typical precipitant or prodrome? Likely reflex presyncope

Diagnosis uncertain; consider other causes of dizziness If recurrent presyncope,om consider tilt test, Holter monitor, implantableo loop recorder or refer Cardiology Dizziness 105 Light-headedness/presyncope: step-by-step assessment

1 Features of shock? • a history or clinical signs of aortic stenosis/ hypertrophic cardiomyopathy Acute light-headedness may signify haemody- • clinical features of cardiac failure namic instability. Look for shock (Box 30.1, p • relevant ECG abnormalities, e.g. severe left 267), including early features, e.g. ↑HR, narrow ventricular hypertrophy, right heart strain, pulseooksf pressure, e pallor or postural ↓BP. If present, deep anterior T-wave inversion assess as described in Chapter 30. bo re co Clinical or ECG features that Postural symptoms + orthostatic 4 suggest arrhythmia? m oo 2 hypotension? Suspect an arrhythmic aetiology if episodes A secure diagnosis of orthostatic presyncope of light-headedness are associated with palpita- requires: tion or occur whilst supine, if there are significant • a clear temporal relationship between light- ECG abnormalities (see Box 31.3, p. 273), or if headedness and standing up the patient has a history of myocardial infarction. • demonstration of a significant postural The key to clinching the diagnosis is to 10 BP drop (≥20 mmHg in systolic BP or document the rhythm during a typical episode ≥10 mmHg in diastolic BP within 3 minutes If episodes are relatively frequent, arrange Holter of changing from a lying to a standing monitoring, e.g. 24-hour tape; if less frequent, a position).oksfree. om patient-activated external recorder or implantable If orthostatic presyncope is detected, search loop recorder may be more helpful. for underlying causes, e.g. antihypertensives,eb sfree.com dehydration, autonomic neuropathy. 5 Typical precipitant or prodrome?m booksf e Consider whether episodes of light-headedness Clinical or ECG features that suggest 3 structural heart disease? occurred while the patient was standing and had a clear precipitating trigger, e.g. intense Consider echocardiog aphy to exclude structural emotion, venepuncture or prolonged standing heart disease in patients with: and/or were accompanied by other ‘prodromal’ • exertional presyncope features such as nausea, sweating and distur- • a family historyee of comsudden unexplained bance of vision. A tilt test may help to clinch death the diagnosis.free.com Dizziness 106 Unsteadiness: overview

Yes Consider trial 1 Likely drug culprit? Drug-induced unsteadiness fre co discontinuationre No

Yes 2 Ataxia or cerebellar signs? Neuroimaging ± refer Neurology

Nystagmus, hearing disturbance or Yes 3 Possible vestibular dysfunction Refer ENT positive Dix–Hallpike manoeuvre?

Yes 4 Elderlyre frail or multiple m comorbidities? See Gait assessment (p. 215) No

Diagnosis uncertain; consider anxiety or reassessment of presentation Refer ENT or Neurology if persistent oreb disabling disturbance e of balance m Dizziness 107 Unsteadiness: step-by-step assessment

1 Likely drug culprit? previous alcohol intake and consider an MRI of the brain and/or neurology referral. Drug causes of unsteadiness are numerous and fre co common but close attention should be paid to Nystagmus, hearing disturbance or the following agents: 3 positive Dix–Hallpike manoeuvre? • alcohol ooksfre Even if the patient’s account of dizziness is not • antihypertensives suggestive of vertigo, the presence of nystagmus, • sedatives, e.g. benzodiazepines hearing disturbance or a positive Dix–Hallpike • antipsychotics, e.g. haloperidol manoeuvre suggests vestibularmeb dysfunction. • antidepressants, e.g. amitriptyline Refer to ENT. • anticonvulsants, e.g. carbamazepine. If safe to do so, discontinue potential drug 4 Elderly, frail or multiple comorbidities? culprits and reassess Multiple factors may contribute to unsteadiness, particularly in the elderly, including limb weakness, 2 Ataxia or cerebellar signs? 10 sensory neuropathy, impaired proprioception, Suspect cerebellar dysfunction if there is joint disease, impaired visual acuity and loss of ataxia (broad-based, unsteady gait; inability to confidence. Several factors commonly coexist. heel–toe walk) or other typical clinical features, If the patient has evidence of more than one e.g.ooks intention e tremor, com dysdiadochokinesis, of these, is frail/elderly or exhibits unsteadiness past-pointing, dysarthria or nystagmus If any during walking, assess as describedbooksf for mobility e of these is present, enquire about currenteb and problems sfree (Ch. co 24). Dysphagia 11ok fre

Patients with dysphagia require prompt assess- Parkinson’s disease and stroke ment to exclude serious pathology. Unless the history clearly points to a functional oropharyngeal These frequently cause swallowing difficulty but cause, oesophageal investigation is necessary to other features are usually more prominent. rule out mechanical obstruction – in particular, Inadequate saliva malignancy. Inadequate saliva, e.g. anticholinergics, connec- Oropharyngeal dysphagia tive tissue disease, such as Sjögren’s syndrome, s .com may lead to problems with forming a manageable Bulbar palsy bolus.

Lower motor neuron palsies of cranial nerves IX– Other causes XII result in weakness of the tongue and muscles of chewing/swallowing. The tongue is flaccid These include myopathies, myotonic dystrophy with fasciculation, often with a changemeb in voice and sfree.com tumours of the pharynx mor larynx. ksf (Table 11.1). Causes include motor neuron Oesophageal dysphagia (structural) disease (MND) and brainstem tumour or infarction. Both structural disease and dysmotility may cause dysphagia Structural causes usually cause Pseudobulbar palsy dysphagia for solids; motility disorders may cause Bilateral upper motor neuron lesions of cranial dysphagia for solids and liquids. nerves IX XII produce a small, contracted and Food bolus obstruction slowly moving tongue and pharyngeal muscles with a brisk jaw jerk (Fig. 11.1). There may be There is sudden onset of complete dysphagia, associated speech disturbance and emotional often with an inability to swallow even saliva. The labilityooksfree (Table 11.1). cCauses m include cerebro- diagnosis is usually obvious from the history but vascular disease, demyelination and MND. it may be the first manifestation of an underlying ebostricture. ee com ebook Myasthenia gravis Malignant stricture Fatigability of oropharyngeal muscles causes increasing swallowing difficulty after the first few Patients with oesophageal cancer typically mouthfuls. Dysphagia may occur before other present with progressive, painless dysphagia features of myasthenia are readily apparent. to solid foods Weight loss may be marked, especially if presentation is delayed. Cachexia Pharyngeal pouch and lymphadenopathy are suggestive but physi- The pouch is formed by posterior herniation of cal signs are typically absent. the pharyngeal mucosa between the thyroph- Benign stricture aryngeus and cricopharyngeus muscle, and is usually found in elderly patients. In addition to Most commonly, benign stricture is due to dysphagia,ooksfr there e.com is classically regurgitation of gastro-oesophageal reflux, especially in the undigested food, halitosis, the feeling of a lump elderly. Rarer causes include oesophageal webs in the neck and gurgling after swallowing liquids. (seen in iron deficiency, typically posterior to mebo free com mebo Dysphagia 109 Differential diagnosis

Table 11.1 Comparison of signs in bulbar and Hiatus hernia pseudobulbar palsy Hiatus hernia with an associated intrathoracic Bulbar Pseudobulbar stomachs re can present o with dysphagia and vom- Speecho freNasal tone; ’Donald duck’ iting. Urgent treatment is required to preventoks difficulty forming voice strangulation of the stomach. consonants (especially ‘R’); Extrinsic compression may become slurred Lung cancer, thyroid goitre, mediastinal nodes, an enlarged left atrium or a thoracic aortic Tongue Weak, wasted Small, stiff with fasciculation aneurysm may, rarely, produce dysphagia by compressing the oesophagus. Jaw jerk Normal or absent Brisk Gag reflex Absent Present Oesophageal dysphagia (dysmotility) Emotions Normal Labile (e.g. Achalasia e.com uncontrollable laughing/crying) This is an uncommon disorder characterized by 11 losssfree of peristalsis com in the distal oesophagus and impaired relaxation of the lower oesophageal sphincter. Dysphagia is of slow onset (often years), occurs for liquids and solids and may initially be intermittent. Dysphagia for liquids is the most prominent symptom. Retrosternal discomfort and regurgitation mebooksfare common.

Chagas disease Chagas disease can present with achalasia; consider it in patients originating from endemic areas in Central and South America and confirm with serological testing.

Scleroderma Oesophageal involvement is seen in ~90% Fig 11.1 The jaw jerk. To elicit the jaw jerk, ask the of cases; impaired peristalsis results from patient to let his/her mouth hang open, place your index fingeroo on the patient’s chin and strike your finger with a replacement of muscle with fibrous tissues tendon hammer. (From Ford MJ, Hennessey I, Japp A. and severe gastro-oesophageal reflux occurs Introduction to Clinical Examination, 8th edn Edinburgh: due to incompetence of the lower oesophageal Churchill Livingstone, 2005.) mebsphincter. f ee. Other o features of mebookscleroderma, e.g. calcinosis, Raynaud’s disease, telangiectasia, may be apparent. the cricoid), Schatzki rings (benign idiopathic Diffuse oesophageal spasm strictures of the lower oesophagus), ingestion of caustic substances, eosinophilic oesophagitis This may cause transient episodes of dysphagia, or, rarely, benign oesophageal tumours and although episodic chest pain that mimics angina radiotherapy.free.com is usuallyree. the predominant o symptom. Dysphagia 110 Overview

Full clinical assessment f e No 1 Difficulty in swallowing food or fluids? k Consider globus/odynophagia

Yes

2 Suspect oropharyngeal cause?

Upperco GI endoscopy Stricture/oesophagitis/motilityco disorder

Contrast swallow / manometry Motility disorder/pharyngeal pouch

Yes

Yes Cerebrovascular accident/bulbar palsy/ Neurological abnormality? 3 pseudobulbar palsy/Parkinson’s disease

No me

Yes 4 Fatigability/muscle weakness? Myasthenia gravis/myopathy/myositis

Yes 5 Abnormality on ENT investigation? Oropharyngeal cancer / pharyngeal pouch fre m No

Consider upper GI endoscopy if not already performed 6 CT if any suspicion of head and neck tumour Refer to GI or speech and languagemeb therapy if symptoms epersist m

1 Difficulty in swallowing foods or fluids? 2 Suspect oropharyngeal cause? Features of true dysphagia include difficulty initiat- Suspect oropharyngeal dysphagia if the patient ing swallowing or the sensation of food ‘sticking’ does NOT report food sticking in the lower throat after swallowing. Globus is the sensation of a or retrosternum and one or more of the following lump in the throat; it is unrelated to swallowing features is present: andooksfree. often associated with anxiety or strong • drooling/spillage of food from the mouth emotion. Odynophagia is pain on swallowing and • immediate sensation of a bolus catching’ suggests oesophageal inflammation or ulceration. in the neck ebo ksf mebo sfree. Dysphagia 111 Step-by-step assessment

• difficulty initiating swallow – repeated • muscle fatigability (ask the patient to attempts are required to clear the bolus count to 50 or hold the arms above the • choking/coughing on swallowing. head). Refer to a Neurologist if you suspect If none of these features are present, investigate the diagnosis. for an oesophageal cause. Arrange a UGIE to look for a structural cause, especially oesopha- b oksfre 5 Abnormality on ENT investigation? geal cancer. UGIE may also reveal features of e s certain motility disorders, e.g. achalasia, but can Exclude oropharyngeal cancer if the patient has be normal, especially in sclerodermameboo or diffuse an oropharyngeal re co pattern of dysphagia (see step oesophageal spasm. 2) without evidence of underlying neurological/ If no cause is identified on UGIE, consult a GI neuromuscular disorder – especially if risk specialist, as further investigation for a motility factors (smoking, alcohol, human papillomavirus disorder, e.g. contrast swallow or oesophageal infection) or other suggestive clinical features, e.g. manometry, may be required. If all GI investiga- palpable neck lump, halitosis, cough, hoarseness, tions are reassuring, re-evaluate for a possible sore throat, ear pain (referred pain), weight loss. oropharyngeal cause. Refer to an ENT specialist for investigation, e.g 11 nasendoscopy and CT/MRI scanning. 3 Neurological abnormality? Investigate for a pharyngeal pouch e.g. contrast swallow or nasoendoscopy, if there is f the history suggests an oropharyngeal aetiol associated regurgitation or a lump in the neck ogyo for k dysphagia, free.com neurological evaluat on that appears after eating (occasionally may is essential. Although swallowing difficulty is be compressed by hand, expunging the food common in stroke, Parkinson’s disease and contents of the pouch), /– halitosis (from food multiple sclerosis, it is very rarely themebo primary sfree.com + meboo f lodged in the pouch), weight loss, aspiration or presenting problem. However, dysphagia may chronic cough. be the principal complaint in bulbar palsy and pseudobulbar palsy so look carefully for the relevant clinical features (Table 11.1); if they are Consider further investigation/referral to present, look for other features of MND and 6 GI or speech and language therapy perform neuroimaging to exclude vascular or If not already done, arrange urgent UGIE structural brainstem disease. unless there is clear evidence of neurological or neuromuscular dysfunction. Request a CT if 4 Fatigability/muscle weakness? you suspect cancer of the head and neck, e.g. Myasthenia gravis is rare and easily missed. The local mass or lymphadenopathy. Once significant dysphagiao k typically free.com presents with increasing dif- pathology of the oropharynx and oesophagus is ficulty in swallowing after the first few mouthfuls actively excluded, refer patients with suspected and difficulty in chewing. Ask specifically about/ oropharyngeal dysphagia of uncertain cause to examine for: mebothe sfree.c speech and language therapymebooksf team for a • fatigable weakness of muscles: initial detailed swallow evaluation with formal speech strength is normal but there is a rapid and ± videofluoroscopy. This will confirm the decline with activity presence of oropharyngeal dysfunction and help • weak voice with prolonged speaking to clarify the mechanism. If you still suspect • diplopia com oesophageal dysphagia, refer to a GI specialist • ptosis for furtheree.com assessment. Dyspnoea 12ok fre

The sensation of breathlessness occurs when Parenchymal lung disease there is a mismatch between instructions for ventilation sent by the brainstem, and sensory • Pneumonia feedback from the thorax. When evaluating a • Lobar collapse. patient with breathlessness, remember that • Acute respiratory distress syndrome severity is highly subjective. Some individuals (ARDS). may not experience dyspnoea despite severe impairment of gas exchange. Other respiratory causes • Pneumothorax. • Pleural effusion. Acuteo sfree.comdyspnoea • Pulmonary embolism (PE). • Acute chest wall injury. Acute dyspnoea is defined here as new-onset or abruptly worsening breathlessnessm within the Cardiovascular f e.co causes preceding 2 weeks. When accompanied by severe hypoxaemia, hypercapnia, exhaustion or • Acute cardiogenic pulmonary oedema. ↓GCS, it may herald life threatening pathology. • Acute coronary syndrome. The diagnosis can usually be made by combin- • Cardiac tamponade. ing clinical evaluation and monitoring with key • Arrhythmia. investigations including CXR, ECG and ABG. In • Acute valvular heart disease. the initial phase of assessment, diagnosis and treatment should be concurrent, and the cycle of Other causes intervention and reassessment should continue • Metabolic acidosis. until the patient is stable. Important causes of o• Psychogenic fr e.com breathlessness (acute acuteooksfree.com dyspnoea are listed below. hyperventilation). Upper airway obstruction Chronic dyspnoea • Inhaled foreign body. • Anaphylaxis. Chronic dyspnoea is defined here as breathless- • Epiglottitis. ness of >2 weeks’ duration. Use the Medical • Extrinsic compression, e.g. rapidly Research Council (MRC) dyspnoea scale (Box expanding haematoma. 12.1) to assess the severity of breathlessness. Important causes of chronic dyspnoea are Lower airway disease listed below. • Acute bronchitis. For many causes, the diagnosis can be made • Asthma. by combining clinical evaluation with PFTs, ECG, • Acute exacerbation of chronic obstructive CXR,sfree FBC and com pulse oximetry. However, early pulmonary disease (COPD). presentations of common problems, such as • Acuteoksf exacerbation e .com of bronchiectasis. COPD and congestive cardiac failure may have • Anaphylaxis. no clinical signs and a normal CXRbooksf In 1 in 3 Dyspnoea 113 Differential diagnosis

• Interstitial lung disease (ILD), e.g. Box 12.1 MRC dyspnoea scale sarcoidosis, idiopathic pulmonary fibrosis, Grade 1 Not troubled by breathlessness except on extrinsic allergic alveolitis. strenuous exercise • Chronic pulmonary thromboembolism Grade 2 Short of breath when hurrying or walking up • Bronchiectasis. ooksa slight hill r • Cystic fibrosis. Grade 3 Walks slower than contemporaries on level • Pulmonary hypertension (primary or ground because of breathlessness, or has to stop for secondary). e o breath when walking at own pace Grade 4 Stops for breath after walking aboutme 100 m or • Pulmonary re vasculitis. o after a few minutes on level ground • Tuberculosis (TB). Grade 5 Too breathless to leave the house, or • Laryngeal/tracheal stenosis, e.g. extrinsic breathless when dressing or undressing compression, malignancy. Source: Adapted from Fletcher CM, Elmes PC, Fairbairn MB Cardiovascular causes et al. 1959. The significance of respiratory symptoms and the diagnosis of chronic bronchitis in a working population. Br Med • Chronic heart failure. J. 2:257–266. ee.c m • Coronary artery disease (‘angina equivalent’). • Valvular heart disease. 12 • Paroxysmal arrhythmia. • Constrictive pericarditis. patients, there is more than one underlying • Pericardial effusion. diagnosis to explain dyspnoea, so assess dysp- • Cyanotic congenital heart disease. noeic patients thoroughly, even afterme a possible re c m m Other causes explanation has been found, particularly if the severity of pathology found is not commensurate • Severe anaemia. with the severity of symptoms. • Obesity. • Chest wall disease, e.g. kyphoscoliosis. Respiratory causes • Physical deconditioning. • Asthma. • Diaphragmatic paralysis. • COPD • Psychogenic hyperventilation. • Pleural effusion. • Neuromuscularree.co disorder, e.g. myasthenia • Lung cancer: bronchial carcinoma, gravis, muscular dystrophies. mesothelioma,oksf lymphangitis com • Cirrhosis (hepatopulmonary syndrome).o carcinomatosis. • Tense ascites. Dyspnoea 114 Acute dyspnoea: overview

ABCDE + ECG, CXR ± ABG fre co Yes Treat and 1 Cause requiring immediate correction? Final diagnosis reassess

2 Assess effort and adequacy of oxygenationm and ventilation

Yes Likely left ventricular failure; consider acute 5 Clinical/CXR features of heart failure? b erespiratory r co distress syndrome No

Yes 6 Generalised wheeze with ↓PEFR? Acute asthma See Further assessment of acute asthma (p. 122) No

Yes Pneumothorax/pleural effusion/ 7 Diagnostic CXR abnormality? re m lobar collapse/other No

Yeos re 8 Ischaemic ECG changes (see Box 6.1)? Likely acute coronary syndrome

ABG shows primary metabolic acidosis Yes Consider diabetic ketoacidosis/salicylate 9 with normal PaO2? poisoning/uraemia/shock

Clinical suspicion of pulmonary Yes Pulmonary embolism 10 CTPA / embolismfre or unexplained hypoxaemia? perfusion scan (or alternative diagnosis) No

Diagnosis uncertain: seek respiratory input if hypoxia, hypercapnia, haemoptysis or abnormal CXR Consider primary hyperventilation if ebABG shows respiratory re alkalosis mwith normal PaOeb2 Dyspnoea 115 Acute dyspnoea: step-by-step assessment

1 Cause requiring immediate correction? Distinguish acute and acute-on-chronic ventilatory failure from chronic compensated As part of the ABCDE assessment process hypercapnia.sfre co (p. 8), dentify and provide immediate corrective Look for reversible factors contributing to treatment for: ventilatory impairment, e.g. bronchospasm, seda- • ooks airway obstruction re tion, respiratory depressants. Be vigilant for loss • tension pneumothorax of hypoxic drive in patients with chronic type 2

• anaphylaxis respiratory failure receiving supplemental O2 but • arrhythmia with cardiac compromise. suspect an alternative cause,meboo e.g. exhaustion, f Seek specialist input if necessary and repeat airways obstruction, if the patient exhibits marked the assessment following intervention. breathlessness or increased effort of breathing. Seek input from the critical care team and consider the need for respiratory support, e.g. Assess effort and adequacy of 2 non-invasive ventilation or tracheal intubation oxygenation and ventilation and mechanical ventilation if any of the following This is undamental to the assessment of features is present: acute respiratory compromise and should be • impending exhaustion reassessed frequently to monitor progress and • acute/acute-on-chronic ventilatory 12 evaluate the effects of interventions. failure not resolving with the measures ooksfrAssess the effort e cof breathing m by repeated described above clinical observation of rate, depth and pattern • progressively rising PaCO2 of respiration; look for use of accessory muscles • SpO2 <90% or PaO2 <8 kPa despite maximal respiratory assistance and features of exhaustion. Monitormebo the SpO2 free com m oo by pulse oximetry in all patients and perform • progressively rising FiO2 requirements to ABG analysis if any of the following features is maintain target SpO2. present: • a need for airway or ventilatory support 3 Underlying COPD? • SpO2 <92% (or unreliable), central cyanosis See ‘Further assessment of acute dyspnoea or high O2 requirements • features of hypercapnia: drowsiness, in COPD’ if the patient has known or suspected confusion, asterixis COPD. • severe, prolonged or worsening respiratory In the absence of a pre-existing diagnosis, distress suspect COPD in any patient with a smoking • backgroundoksf ee of COPD co and/or chronic type 2 history and either: respiratory failure • clinical (Fig. 12.1) or CXR features of • smoke inhalation (carboxyhaemoglobin) hyperinflation, or • suspected metabolic acidosis or meprimary o• sfree.co chronic exertional dyspnoeam with b wheeze oks hyperventilation. and/or a chronic productive cough.

Use the SpO2 ± PaO2 to assess adequacy Evidence of respiratory tract of oxygenation. 4 Correct hypoxia by administration of supple- infection (RTI)? mental O2. Titrate the inspired O2 concentration Having considered the above conditions, go to (FiO2) to the minimum required to achieve a target ‘Further assessment of respiratory tract infection’ SpO2: if any of the following features is present: • 94–98% for previously well patients. • new cough with purulent sputum or • normal baseline SpO2 for patients with significant increase in purulent sputum chronicoks hypoxia. e co • temperature ≥38°C or <35°C Monitor FiO2 requirements carefully to maintain • acute illness with sweating, shivers and the target SpO2. myalgia

Use the PaCO2 to assess adequacy of ventila- • clinical/CXR signs of consolidation tion (see Clinical tool, p. 116). m bo(Figs free 12.2 comand 12.3) with ↑mWBC/CRP. bo Dyspnoea 116 Acute dyspnoea: step-by-step assessment

Clinical tool Interpretation of arterial blood gases Assessment of ventilation is clearly impaired, suggesting the presence of important

lung disease. However, this PaO2 would usually result in PaCO2 is directly determined by alveolar ventilation – the an SaO2 (arterial oxygen saturation) >90%, a level which volume of air transported between the alveoli and the ooksfre co will allow adequate delivery of O2 to tissues (provided that outside world in any given time. Therefore, ↑PaCO2 haemoglobin and cardiac output are normal) (hypercapnia) implies ventilatory failure – type 2 respiratoryeb ebook failure. Assessment of acid–base status

A slow, gradual rise in PaCO2 (chronic type 2 respiratory An acidosis is any process that acts to lower blood pH failure) is usually accompanied by an increase in (↑H+); an alkalosis is one that acts to raise blood pH (↓H+). − HCO3 that serves to maintain overall acid–base balance An ↑PaCO2 indicates a respiratory acidosis; a ↓PaCO2 (H+ within normal range). However, this metabolic indicates a respiratory alkalosis. compensation occurs over days/weeks so any acute rise in − − A ↓HCO3 indicates a metabolic acidosis; an ↑HCO3 PaCO (acute or acute-on-chronic type 2 respiratory failure) 2 indicates a metabolic alkalosis. will lead to an increase in H+ (Table 12.1). A respiratory or metabolic acid–base disturbance usually In type 2 respirato y failure, the rate of rise in PaCO and 2 triggers an adjustment by the other system to limit the associated increase in H+ provide a better guide to the change in blood pH (compensation). Respiratory severity than the absolute value of PaCO . 2 compensation happens over minutes; metabolic A ↓PaCO2 implies hyperventilation. If PaO2 is also lowered compensation takes days to weeks. (or just within normal limits), the hyperventilation is Having identified the presence of any metabolic or probably an appropriate response to hypoxia. Alternatively, ooksfree.com respiratory disturbances, look next at H+ (or pH) to assess if HCO − is decreased, it may reflect respiratory 3 the overall impact on acid–base status If the metabolic compensation for a primary metabolic acidosis, e.g. and respiratory processes oppose each other, the H+ diabetic ketoacidosis. A PaCO with normal PaO and ↓ 2 2 helps to differentiate the primary disturbance from the HCO − (on room air) suggests primary (psychogenic)m bo sfree.com meb 3 compensatory response: an ↑H+ (or upper limit of normal) hyperventilation but this is a diagnosis of exclusion (see suggests that the acidosis is the primary disturbance and below). vice versa. Assessment of oxygenation Primary respiratory acidosis (ventilatory failure) and alkalosis (hyperventilation) are dealt with above. A ↓PaO2 implies impairment of oxygenation. A corresponding normal PaCO2 indicates that this is due to Causes of metabolic acidosis and alkalosis are shown in ventilation/perfusion mismatch – type 1 respiratory failure. Box 12 2. If there is a primary metabolic acidosis, calculate

In contrast ↑PaCO2 indicates that it is due, at least in part, the anion gap: to failure of ventilation – type 2 respiratory failure. ++ −− Anion gapN=+()aK−+()Cl HCO3 The administration of supplemental O2 makes ABG analysis []Normal =−10 18 mmolL moreoksfree.co complex as it can be difficult to judge whether the PaO2 is appropriate for the FiO2 and, hence, whether oxygenation is impaired. A useful rule of thumb is that the

difference between FiO2 (%) and PaO2 (in kPa) should be Table 12.1 Arterial blood gases in different ≤10. A patient breathing room air (FiO2 of 21%) should patterns of type 2 respiratory failure − have a PaO2 of at least 11 kPa. If subtle impairmentmeb is free.co PaCO2 meHCO3 opH suspected, repeat the ABG on room air. Acute ↑ → ↓ It is important to note the distinction between impaired

oxygenation (↓PaO2) and inadequate oxygenation Chronic ↑ ↑ → (insufficient PaO2 to support normal aerobic metabolism). Acute-on-chronic ↑ ↑ ↓ Consider a patient with a PaO2 of 8.5 kPa: oxygenation

5 Clinical/CXR features of heart failure? • a recent history of orthopnoea, nocturnal dyspnoea or progressively worsening Acute decompensated heart failure is the likely exertional dyspnoea cause of breathlessness if any of the following • signs of fluid overload: peripheral areook present: fr com oedema, ↑JVP • CXR evidence of pulmonary oedema or Always suspect the diagnosis in patients congestion (Fig. 12.4) e fr c with a background of chronicme heart failure or Dyspnoea 117 Acute dyspnoea: step by-step assessment

Pursed lips

Increased rate and depthoo of breathing f co

Intercostal indrawing

Sitting forward and gripping bed (increases action of accessory muscles) 12 Signs of hyperinflation ↑Antero-posterioroo ee. diameter Intercostal indrawing Decreased cricosternal distance Poor chest expansion (<5 cm)

Fig. 12.1 Clinical features of COPD.

Box 12.2 Causes of metabolic acidosis and alkalosis

− Metabolic acidosis (low HCO3 ) With raised anion gap • Lactic acidosis, e.g. hypoxaemia, shock, sepsis, infarction • Ketoacidosis (diabetes, starvation, alcohol excess) • Renaloksfree failure o • Poisoning (aspirin, methanol, ethylene glycol) With normal anion gap • Renal tubular acidosis • Diarrhoea • Ammonium chloride ingestion • Adrenal insufficiency Fig. 12.2 Pneumonia of the right middle lobe.

− Metabolic alkalosis (high HCO3 ) • Vomiting that acute heart failure can also present de • Potassium depletion, e.g. diuretics novo. • Cushing’s syndrome Difficulty may arise when the CXR is not • Conn’s syndrome (primary hyperaldosteronism) diagnostic, e.g. in early or mild cases, and when auscultatory findings resemble those heard in other predisposing cardiac condition, e.g. other disorders, e.g. pulmonary fibrosis, bilat- previous MI, LV systolic dysfunction or valvular eral pneumonia. A therapeutic trial may assist diseaseook but eeassess carefully m for alternative diagnosis: rapid improvement of symptoms causes of acute decompensation (especially if with vasodilators/diuretics is strongly suggestive the above features are absent) and remember of heart failure as the aetiology of dyspnoea. mebo sfree co mebooksf Dyspnoea 118 Acute dyspnoea:co step-by-step assessment

Fig. 12.3 Right upper lobe pneumonia containing air bronchograms. co

Figs 12.5 Right pneumothorax.

However, BNP is also raised in a w de variety of other cardiac and non-cardiac conditions so elevated levels do not automatically confirm a diagnosis of acute heart failure.meb

6 Generalized wheeze with ↓PEFR? See ‘Further assessment of acute asthma exacerbation’ in patients with known asthma and either: • generalized wheeze, or

Fig. 12.4 Left ventricular failure. Note the hazy perihilar • ↓PEFR. shadowing (‘bat’s wings’), the prominent, dilated upper Consider other causes of acute dyspnoea, lobe veins and the basal Kerley B lines, all characteristic of pulmonary oedema. There is also cardiomegaly. e.g. pneumothorax or PE, if neither of these ooksf features is present. Suspect a first presentation of asthma (and proceed to ‘Further assessment of acute asthma Consider non-cardiogenic pulmonary oedema exacerbation’) if there is widespread wheeze with in acutely dyspnoeic patients with bilateralm pul- ree c m meb ok no evidence of COPD, anaphylaxis or pulmonary monary infiltrates but no other evidence of heart oedema (see above). Assess with pulmonary failure – especially in the setting of severe acute function tests (PFTs) ± PEFR diary following pathology such as trauma, burns, pancreatitis resolution of the acute episode. or sepsis. Echocardiography, to assess ventricular and 7 Diagnostic CXR abnormality? valvular function, is a key diagnostic test and is particularly useful in patients without a pre- CXR may be more sensitive than clinical examina- existing diagnosis of heart failure or in those with tion for detecting some lung abnormalities, e.g possible non-cardiogenic pulmonary oedema. pneumothorax (Fig. 12.5), pleural effusion (Fig. If available, brain-type natriuretic peptide (BNP) 12.6) or lobar collapse (see Figs 17.3 and 17.4, testingooksfree. can help to rule om out acute heart failure. p. 163). Low plasma BNP (<100 pg/mL) or N-terminal-pro See below (p. 129) for ‘Further assessment BNP (<300 pg/mL) make the diagnosis unlikely. of pleural effusion’. eb oksf meboo sfree. om Dyspnoea 119 Acute dyspnoea: step by-step assessment

Table 12.2 Clinical and chest X-ray findings in patients with suspected PE in the emergency departmentsfre (with co and without confirmed PE on further investigation) Confirmed PE No PE identified Feature (n = 1,880) (n = bo528) k Clinical findings Dyspnoea at 50% 51% rest Pleuritic chest 39% 28% pain Cough 23% 23% Haemoptysis 8% 5% Syncope 6% 6% Signs of DVT 24% 18% (unilateral limb swelling) Fig. 12.6 Left pleural effusion. CXR findings Normal 40% 41% 12 If the patient has lobar collapse, consider Atelectasis 17% 15% furoo her investigation, s e.g. bronchoscopy to Infiltrate 14% 14% exclude a proximal obstructing lesion. Pleural effusion 16% 14%

If CXR appearances are non-specific or uncer- Adapted from Pollack CV et al. 2011. Clinical characteristics, tain, continue through the diagnosticme process oo management, sfree and outcomes m of patients diagnosedm with b acute and attempt to correlate with clinical findings. pulmonary embolism in the emergency department: initial report of Consider further imaging, e.g. CT thorax, or EMPEROR (Multicenter Emergency Medicine Pulmonary Embolism in the Real World Registry) J Am Coll Cardiol. 57(6):700–706. specialist respiratory input if no firm diagnosis emerges. 10 Clinical suspicion of PE? Ischaemic ECG changes 8 (see Box 6.1, p. 51)? PE is under-diagnosed. Clinical and CXR findings, in isolation, lack diagnostic sensitivity and Dyspnoea may be the predominant manifestation specificity (Table 12.2). Use a clinical decision of myocardial ischaemia/infarction. If there is ECG tool such as that shown in Fig. 12.7 and Table evidence of ischaemia (Box 6.1) and no obvious 12.3 to evaluate for PE in patients with acute alternative cause for breathlessness, assess as dyspnoea and any of the following: describedooksf in Chapter ee. 6. m • relevant risk factors, e.g. active malignancy, recent surgery or prolonged immobility ABG shows primary metabolic acidosis 9 m o• sf haemoptysis, ee c pleuritic chestmeb pain or oksf with normal PaO2? evidence of deep vein thrombosis (DVT) Identify the presence of metabolic acidosis by • unexplained hypoxaemia ABG analysis (see Clinical tool, p. 116). If present, • ECG features of right heart strain (see p. 58) look for an underlying cause (see Box 12.2) • no clear alternative diagnosis • examine for evidence of shock or D-dimer is less useful in hospitalized patients mesenteric infarction so in this setting consider further investigation • test urine for glucose and ketones if the Wells score is ≥2. Have a low threshold • check U & E for performing ABG as subtle oxygenation • measure plasma glucose, lactate, salicylate abnormalities may not be detected by SpO2. levelsksfree com Where imaging is performed to exclude PE, CT • calculate the anion gap. pulmonary angiography offers greater sensitiv- Do not attribute dyspnoea solely to metabolic ity than a ventilation/perfusion scan and may acidosis if there is evidence of hypoxaemia. demonstrate an alternative diagnosis. meb sfree com mebooksf Dyspnoea 120 Acute dyspnoea:co step-by-step assessment

Assess clinical Table 12.3 Wells score (pulmonary embolism) probability, using fr Wells score (Table 12.3) Clinical variable Po ntsk Clinical signs and symptoms of DVT1 3 PE PE No alternative diagnosis is more likely 3 unlikely likely than PE Heart rate >100 bpm 1.5 Immobilisation or surgery in the 1.5 D-dimer* +ve CTPA previous 4 weeks Previous DVT/PE 1.5 –ve –ve +ve Haemoptysis 1 Active malignancy (treatment within 1 last 6 months or palliative) PE Diagnosis Score >4: PE likely; ≤4: PE unlikely excluded PE 1Minimum of leg swelling and pain elicited upon palpation of thes deep veins. e.c Fig. 12.7 Algorithm for the assessment of suspected pulmonary embolism using the Wells score. *Highly sensitiveoo assay. f Dyspnoea 121 Acute dyspnoea: further assessment

Further assessment of acute dyspnoea in objective estimate of disease severity patients with COPD and look for evidence of chronic hypercapnia (see above). Step 1 Clarify cause for acute deterioration • Trajectory of disease: consider changes • Ensureok that fre there is no new CXR in the above severity measures over time, abnormality: look carefully for evidence the frequency of admissions and previous of collapse, consolidation, pneumothorax requirement for respiratory support, e.g. or pleural effusion. If there are features of non-invasive and invasive ventilation. consolidation, treat as pneumoniameb rather • Previous re sputum co cultures: antibioticmeboo prescribing should than ‘infective exacerbation of COPD’. be guided by local protocols but knowledge of previous pathogens may permit more effective tailored therapy; • Ask about cough and sputum: treat as an discuss with the microbiology team if unusual or resistant infective exacerbation of COPD if there is organisms have been grown on previous cultures. an increase in sputum volume or purulence with no evidence of consolidation. Step 3 Compare current status to baseline and • If wheeze is predominant and there monitor response to treatment are no features of infection, the likely • Oxygenation and ventilation: compare diagnosis is non-infective exacerbation current ABG values and SpO2 to previous of COPD. Look for precipitants, e.g. records. Give supplemental O2 to return 12 beta-blocker,ksfree non-compliance com with inhalers SpO2/PaO2 to baseline. If the patient has environmental trigger. chronic type 2 respiratory failure, monitor • Evaluate for PE (see Fig. 12.7) if there is for loss of ventilatory drive and repeat an a sudden increase in breathlessness or ABG after any increase in FiO2. hypoxia without wheeze, change mein sputum • Airways ree.com obstruction: assessmebook PEFR or new CXR abnormality. and the presence/extent of wheeze; monitor changes to gauge response to Step 2 Establish pre-exacerbation status and details bronchodilator therapy. of previous exacerbations • Functional reserve: assess overall work of This provides a comprehensive picture of breathing (rate, depth, use of accessory underlying disease severity, helping to guide muscles). Very high respiratory work cannot the goals and limits of therapy. be maintained for long; refer to critical care • Baseline performance: quantify normal if there is impending exhaustion. exercise tolerance, ask about activities that • Following recovery, record pre-discharge

provoke dyspnoea and ascertain ability to PEFR, SpO2 and ABG on air. performoksfree activities comof daily living (ADLs). • Baseline lung function: refer to previous ABG/ SpO2 measurements and PFTs to provideebo an ree com Dyspnoea 122 Acute dyspnoea: further assessment

Further assessment of acute asthma Step 2 Look for treatable precipitants exacerbation Seek evidence of infection, e.g. pyrexia pu ulent sputum, ↑WBC, physical/CXR signs Step 1 Assess severity and need for of consolidation (see Figs 12.2 and 12.3) and hospital admission flitting upper lobe infiltrates, suggesting allergic Assessook severity fre in any co patient with suspected bronchopulmonary aspergillosis. Culture sputum acute asthma according to Table 12.4; perform if this is purulent and blood if temperature is an ABG if there are life-threatening features ≥38° C. Carefully review the CXR to exclude or SpO2 <92%. Admit patients to mebohospital if pneumothorax sfre (see Fig. 12.5mebooksf). they have: Step 3 Assess baseline control • any life-threatening features Establish: • features of a severe attack persisting after initial treatment • frequency and severity of exacerbations • baseline symptoms between exacerbations • PEFR <75% or significant ongoing symptoms after 1 hour of treatment • best PEFR • other features causing concern, e.g. • current inhaler regimen, technique and previous near-fatal asthma, poor compliance compliance. frequency of PRN inhaler use • frequency of oral steroids (need for bone If there are ongoing features of a severe attack, protection?) monitor in a critical care environment with ooksfree c m • current smoking status. repeated assessment of SpO2, PEFR, RR, HR Look for avoidable precipitants, e g. pollen, pets, and work of breathing ± ABG. Refer urgently cold air, exercise, smoking, occupational triggers, to the intensive care unit if PaCO2 ismebo >6 kPa or ree.co me o rising, or there is worsening hypoxia, exhaustion beta-blockers, NSAIDs. or ↓GCS.

Table 12.4 Clinical features of severe asthma

Severity PEFR or Other features Moderate 50–75% best or predicted Increased symptoms Severe 33–50% best or predicted Any of: oks e. RR >25 HR >110 Inability to complete sentences in one breath Life-threatening <33% best or predicted Any of: e m o PaO2 <8 kPa ‘Normal’ PaCO2 (>4.6–6.0 kPa) SpO2 <92% Silent chest Cyanosis Exhaustion/altered conscious level Poor respiratory effort Arrhythmia Hypotension

Near-fatal PaCO2 >6 kPa

Modified from British Thoracic Society, Scottish Intercollegiate Guidelines Network 2014. British guideline on the management of asthma. Thorax. 69(Suppl 1):1–192. o e.co o oo s Dyspnoea 123 Acute dyspnoea: further assessment

Further assessment of respiratory Table 12.5 CURB-65 score tract infection

Step 1 Classify the type of RTI Feature Score In patients with features of RTI, distinguish Confusion Abbreviated Mental Test <8/10 pneumoniaook frefrom non-pneumonic infection by Urea >7 mmol/L the presence of focal chest signs, e.g. crackles, RR ≥30/min bronchial breathing and/or new CXR shadowing BP Systolic 90 or diastolic 60 mmHg (see Figs 12.2 and 12.3). Classify as community-mebo fr co < m< oo acquired pneumonia (CAP) if infection has been Age ≥65 years acquired out of hospital, and hospital-acquired Total score 30-day mortality risk pneumonia (HAP) if the onset of illness occurred 0 0.6% 1 3.2% ≥2 days after hospital admission or within 90 days 2 13.0% of discharge from hospital after an admission 3 17.0% of 2 or more days. In previously well patients 4 41.5% without focal chest signs or CXR abnormality, the 5 57.0% likely diagnosis is non-pneumonic RTI, e.g. acute bronchitis. In patients with known bronchiectasis, L m W, et al. 2003. Defining community acquired pneumonia severity on presentation to hospital: an international derivation 12 consider an infective exacerbation if the sputum and validation study. Thorax. 58(5):377–382. becomesooksfree more purulent com or offensive; assessment of patients with underlying COPD is describedbo s m above. discrete or flitting shadows on CXR, especially Step 2 Assess severity IV drug users. m ok The CURB-65 score (Table 12.5) can help to Step 4 Gather information to inform risk-stratify patients with CAP Consider referral to antimicrobial choice critical care for monitoring/intervention in patients In any patient requiring hospitalisation for RTI, with a CURB-65 score >2. Patients with a low culture blood and sputum, perform serological CURB-65 may still require admission to hospital assessment for atypical pathogens and (during if they require supplementary oxygen. influenza outbreaks) take a viral throat swab. Step 3 Look for predisposing factors In patients with severe pneumonia (CURB-65 Assess for factors associated with immunocom- >2), send urine (Legionella) and blood/sputum promise, e.g. chronic disease (AIDS, diabetes (Pneumococcus) for rapid antigen detection by cirrhosis, malnutrition), acute disease (any critical PCR. Aspirate pleural fluid for microscopy and illness),ooksfr drugs (steroids, e com cancer chemotherapy) culture if there is an associated parapneumonic or previous splenectomy. Suspect aspiration in effusion. Send multiple sputum samples (induced patients with a history of swallowing difficulty, with nebulized hypertonic saline if necessary) for stroke, alcoholism or recent unconsciousness.meboo Ziehl–Neelsen s ree.com staining and TBmebooksf culture if there is Pneumonia may occur distal to a bronchial a suspicion of TB: carcinoma – repeat the CXR to ensure resolution • significant immunocompromise or debility of changes in patients with risk factors and con- • previous residence in an endemic TB area sider further investiga ion, e.g. bronchoscopy, if • recent close contact with a smear-positive there are persistent symptoms/CXR features or TB patient recurrent pneumonia at the same site. Preceding • CXR evidence of previous TB viral infection, especially influenza, may predis- • a background of persistent productive pose to severe secondary bacterial infection. coughree.com with weight loss, night sweats or Considerk endocarditis fr e com in patients with multiple other constitutional symptoms. Dyspnoea 124 Chronic dyspnoea: overview

Full clinical assessment, SpO , FBC, ECG, CXR e co 2

No Consider asthma, hyperventilation, 1 Dyspnoea related to exertion? paroxysmal arrhythmia Yes

Yes 2 Pleural effusion or ↓Hb? Investigate and treat then reassess

No Yes 3 Any alarm features (Box 12.4)? Exclude lung cancer/other serious pathology

Yes Interstitial lung disease, cancer, bronchiectasis, 4 Significant CT abnormality? re m emphysema, other No fre m

5 Abnormal PFTs?

No Yes Yes Obstructive defect? Likely COPD or chronic asthma

Yes Consider interstitial lung disease, chest wall Restrictive defect? deformity, obesity, neuromuscular 6 Significant echo abnormality?

No Yes Yes Left ventricular impairment? Chronic heart failure ee oNo Yes Valvular disease, cardiomyopathy, pulmonary Other diagnostic abnormality? s e m hypertension, pericardial constriction/effusion

Unexplained hypoxia or ↑risk of Yes Pulmonary embolism/ 7 CTPA venous thromboembolism? other lung pathologyeb No Clinical suspicion of coronary Yes Investigate 8 Likely angina artery disease (Box 6.8, p. 64)

Consider obesity, physical deconditioning, psychogenic dyspnoea, neuromuscular disorder 9 PFTs, echoee. ± CPET/respiratory input if limiting, progressiveee. or unexplained symptoms Dyspnoea 125 Chronic dyspnoea: step-by-step assessment

1 Dyspnoea related to exertion? be functional. Suspect this if the patient exhibits typical features (Box 12.3) in the absence of Chronic dyspnoea arising from organic disease objective evidence of cardiorespiratory disease is almost always provoked or exacerbated by (normal examination, SpO2, CXR ± PFTs/serial exertion, so episodic dyspnoea unrelated to PEFR). Refer for specialist assessment if there is exertionooksfre has a limited range of diagnoses. diagnostic doubt or symptoms are troublesome Suspect asthma if there is: booor sfredisabling despite co explanation and reassurance. • associated cough or wheeze ebooksf • a reproducible precipitant for episodes, e.g. 2 Pleural effusion or ↓Hb? cold air, pollen, house dust, pets Consider these conditions early as they can be • diurnal variation in symptoms with easily confirmed or excluded. Go to ‘Further prominent nocturnal or early morning evaluation of pleural effusion’ if there is CXR ± symptoms (especially if sleep is disturbed), clinical evidence of unilateral effusion (see Fig. or 12.6). Always check Hb in patients with exertional • a history of atopy. dyspnoea, as pallor is an insensitive sign. If Hb Seek objective evidence of airflow reversibility is decreased, evaluate as described on page or variability to confirm the diagnosis: the former 136 but consider other causes – especially if Hb by spi ometry (≥15% improvement in FEV1 fol- is only slightly decreased or symptoms persist 12 lowing inhaled bronchodilators), the latter by despite correction. askingooksfree the patient to comkeep a diary of peak-flow recordings (look for >20% diurnal variation on 3 Any alarm features (Box 12.4)? ≥3 days/week for 2 weeks). Consider specialist assessment if the diagnosis is mebouncertain, Change sfr in e.com voice or stridor mayme indicate laryngeal/ ksf especially if occupational asthma is suspected. tracheal obstruction secondary to intrinsic cancer Paroxysmal tachyarrhythmia may present with or extrinsic compression (lymphoma, thyroid discrete episodes of breathlessness without any tumour or retrosternal goitre); if present, refer clear precipitant (although dyspnoea, when the patient urgently for endoscopic evaluation, present, is usually aggravated by exertion). e.g. fibre optic bronchoscopy/nasoendoscopy. Consider this if Refer for urgent specialist evaluation with bronchoscopy CT to exclude lung cancer if • dyspnoea is accompanied by palpitation ± the patient has risk factors ( 40 years or smoking • episodes arise ‘out of the blue’ with an > history) accompanied by any suspicious clinical abrupt onset, or or CXR features (see Box 12.4); these include • the ECG shows evidence of pre-excitation (seeoksfre Fig. 26.2, p. 233 com). If paroxysmal tachyarrhythmia is suspected, Box 12.4 Alarm features in chronic dyspnoea attempt to document the rhythm during symptoms e oksf (see p. 237) if necessary using an ambulatoryme Clinical sfree features com recorder or smart phone ECG monitor. • Stridor Dyspnoea that occurs predominantly at rest • Haemoptysis with no consistent relationship to exertion may • Weight loss • Change in voice • Persistent or non-tender cervical lymphadenopathy • Finger clubbing Box 12.3 Features suggestive of psychogenic dyspnoea CXR features (see also Box 17.1, p. 163) • Lungree. mass o • Provoked by stressful situations • Cavitation • Inability to take a deep breath or ‘get enough air’ • Hilar enlargement • Frequent deep sighs • Lobar collapse (persistent) • Digital/perioraloks ee. tingling m • ↓PaCO2 with normal PaO2 on ABG N.B. These features are especially worrying if the patient is a • Short breath-holding time smoker, is >40 years or has had asbestos xposure.eb Dyspnoea 126 Chronic dyspnoea: step-by-step assessment lobar collapse, which may indicate a proximal Refer for specialist evaluation if CT shows obstructing tumour. evidence of ILD or other serious pathology In younger non-smokers consider initial further e.g. cancer, bronchiectasis. Arrange further evaluation with CT thorax; refer for specialist investigation with PFTs, if these have not been assessment if CT suggests malignant disease, performed already, if the CT shows features of failsooksfr to reveal a clear co alternative cause or is emphysema. ooksf not readily available. Evaluate patients with haemoptysis as described in Chaptermebo 17. 5 sfre Abnormal PFTs? Have a low threshold for requesting PFTs (Box 4 Significant CT abnormality? 12.5 and Tables 12.6 and 12.7).

Arrange high-resolution CT to look for evidence of Diagnose COPD if FEV1/FVC is <70% ILD if the patient has any of the relevant features (indicating airways obstruction) with a post- listed in Box 12.5. bronchodilator FEV1 <80% predicted (indicating incomplete reversibility). Look for other characteristic abnormalities, including ↑TLC and RV (which helps to differentiate from ILD in borderline Box 12 5 Criteria for investigations in cases) and ↓gas transfer (indicative of significant chronic dyspnoea emphysema). Exclude alpha1-antitrypsin defi- PFTs if there is: ciency in younger patients. If SpO2 is ≤92%, ooks• wheeze om perform an ABG to identify patients with type • prominent nocturnal or early morning symptoms 2 respiratory failure or those who might qualify • symptoms precipitated by cold weather or common for home oxygen therapy. ebooksf allergens me sfree.comDiagnose asthma if there is an obstructive • history of atopy • clinical or CXR features of hyperinflation ventilatory defect with ≥15% improvement in FEV1 (see Fig. 12.2) following inhaled bronchodilators. If not, consider • smoker aged >40 years further assessmentm with repeat spirometry, PEFR • chronic productive cough (≥3 consecutive months for ≥2 successive years) • occupational dust exposure, treatment with methotrexate/amiodarone or previous radiotherapy

• ↓SpO2 (at rest or on exertion) with no apparent alternative cause • major or progressive decrease in effort tolerance w thout other obvious cause. ooksfree.coEchocardiogram if there is: • significant ECG abnormality, e.g. left bundle branch block, evidence of LVH, pathological Q waves, frequent ventricular ectopics, atrial fibrillationme • previous MI or chronic hypertension (especially if target organ damage) • ↑JVP or peripheral oedema • murmur (not previously investigated) • clinical/CXR evidence of pulmonary congestion, cardiomegaly or pulmonary hypertension • elevated BNP (BNP ≥35 pg/mL; N-terminal-pro BNP ≥125 pg/mL). High-resolution CT thorax if there is: • interstitial shadowing on CXR (Fig. 12.8) • unexplained restrictive lung defect or ↓gas transfer • strongoksfree clinical suspicion com of interstitial lung disease, e.g. hypoxia or end-inspiratory crackles in a patient with previous exposure to birds, dust or hay. b Fig. 12.8 CXR in interstitial lung disease. m Dyspnoea 127 Chronic dyspnoea: step by-step assessment

Table 12 6 Pulmonary function tests

Test Description Measures Examples of relevant diagnoses

Spirometryo fr Airflow at the mouth is FEV1, FVC Obstructive lung disease: disproportionate reduction measured during a in FEV1 (FEV1:FVC ratio <0.8) forced exhalation Restrictive lung disease: proportionate reduction in FEV1 and FVC

Reversibility Spirometry is repeated after FEV1, FVC Complete reversibility of obstruction is common in giving bronchodilatorsm okasthma, incomplete co reversibilitymeboo common in COPD Lung volumes Gas dilution or whole-body TLC, RV COPD (normal or increased TLC), restrictive lung plethysmography disease (reduced TLC and RV) Diffusion Carbon monoxide uptake DLCO, Dm Interstitial pneumonitis (low DLCO, low Dm), capacity from alveoli is measured pulmonary haemorrhage (high DLCO, normal Dm)

DLCO – lung diffusion of carbon monoxide; Dm – membrane component of diffusion; FEV1 – forced expired volume in 1 second; FVC – forced vital capacity; RV – residual volume; TLC – total lung capacity ee com fre com 12

and an intrapulmonary cause, e.g ILD, if there Table 12.7 Severity of airflow obstruction is a proportionate decrease in TLCe and RV. Severity FEV1 Significant echocardiographic Mild 50–80% predicted 6 abnormality? Moderate 30–49% predicted Refer for cardiology evaluation if the echo shows Severe <30% predicted major valvular abnormality, e.g. severe mitral regurgitation or aortic stenosis or pericardial Source: Modified from Boon NA, Colledge NR, Walker BR, Hunter JAA. Davidson s Principles and Practice of Medicine, effusion 20th edn. Edinburgh: Churchill Livingstone, 2006 (Box 19.30, In chronic heart failure, exertional dyspnoea p. 680). may be the sole presenting feature, but significant cardiac dysfunction is unlikely in the absence of the features in Box 12.5. The presence and severity of left ventricular systolic dysfunction can diaryo or specialist ree evaluation if there is high clinical be determined by echocardiography Consider suspicion or borderline spirometry results. cardiology referral if left ventricular systolic In patients with a restrictive lung defect (see function is normal but the patient has clinical Table 12.6), evaluate for an underlyingmebo cause: features sfre suggestive c m of heart failure,mebooksf e.g. elevated • arrange echocardiography and reassess JVP, oedema or CXR evidence of pulmonary following treatment if there is evidence of congestion – especially if there is left ventricular pulmonary congestion hypertrophy/left atrial dilatation (heart failure with • look for major chest wall deformity, e.g. preserved ejection fraction) or a history of previ- severe kyphoscoliosis ous cardiac surgery/radiotherapy (constrictive • exclude ILD with high-resolution CT if there pericarditis). are suggestive clinical/CXR features (Fig. If the echo suggests pulmonary hypertension 12.8) or there is no clear alternative cause without significant LV impairment or valvular • measure BMI to identify massive obesity, disease, evaluate fully for underlying chronic e.g.oksfree BMI >40. com lung disease, e.g. PFTs, high-resolution CT Suspect extrapulmonary compression (e g. chest, sleep studies, CTPA. In the absence of neuromuscular disorder, chest wall deformity) hypoxaemia or significant lung disease, refer for if there is a decrease in TLC with normal RV, specialist assessment. ebooksf mebo sfree com Dyspnoea 128 Chronic dyspnoea: step-by-step assessment

Unexplained hypoxia or ↑risk of venous are frequently responsible for exertional breath- 7 thromboembolism? lessness and ↓exercise capacity; suspect this in patients with ↑BMI (especially >30), recent Exclude chronic thromboembolic disease in any weight gain or a sedentary lifestyle. patient with unexplained hypoxia or risk factors If there are features of hyperventilation (see forook DVT. Ventilation/perfusion fre co lung scanning may Box 12.3) or symptoms are disproportionate to have higher sensitivity for detection of chronic objective findings, perform an ABG on room air PE but CT pulmonary angiography is more likely (ideally during symptoms) and consider referral to identify alternative lung pathology,mebo e.g. ILD, for sfre formal evaluation of psychogenicmeboo dyspnoea. sf emphysema. At this stage, review any abnormalities detected and determine whether they are suf- Clinical suspicion of coronary ficient to account for the presentation. In patients 8 artery disease? with multiple possible causes for dyspnoea, e.g. Angina occasionally manifests as a sensation obesity, left ventricular impairment and airways of breathlessness without chest discomfort. disease, cardiopulmonary exercise testing (in Evaluate for angina with an exercise ECG or which ECG, respiratory gas exchange and minute other stress test (see Box 6.8, p. 63) if the patient ventilation are recorded during exercise) may has risk factors for coronary artery disease (see help to establish the predominant mechanism. Box 6.3, p. 52) and symptoms are consistently Patients with a major change or progressive provokedooks by ree. exertion and m relieved within 5 decline in exercise capacity without adequate minutes by rest. Relief of symptoms with anti- explanation require further evaluation; arrange anginal therapy or coronary revascularisation an echocardiogram and PFTs if these have not confirms the diagnosis. meboyet sfree been performed, com and considermebooksf referral for specialist evaluation, e.g. cardiac catheterisation Consider other causes. Further or cardiopulmonary exercise testing. 9 investigation if limiting, progressive or unexplained symptoms Obesity rarely causes significant cardiorespiratory impairment unless BMI is >40. However, lesser degrees of obesity and/or physical deconditioning free com Dyspnoea 129 Chronic dyspnoea: further assessment

Box 12.6 Causes of abnormal pleural Box 12.7 Light’s criteria for differentiation of fluid collections pleuralfr exudate co and transudate

Serous effusions The pleural fluid is likely to be an exudate if≥ 1 of the Transudateo sfr following criteria is present: • Cardiac failure • pleural fluid protein : serum protein ratio >0.5 • Hepatic failure • pleural fluid LDH : serum LDH ratio >0.6 • Renal failure • pleural fluid LDH> two-thirds of the upper limit of • Nephrotic syndrome normal serum LDH. meboo • Hypoalbuminaemia • Peritoneal dialysis • Constrictive pericarditis • Hypothyroidism • Meigs’ syndrome (pleural effusion, benign ovarian Further assessment of pleural effusion fibroma and ascites) Box 12.6 lists the causes of abnormal collections Exudate of fluid in the pleura. Initial assessment depends • Parapneumonic (usually bacterial) on laboratory analysis of the fluid. • Bronchial carcinoma • TB • Usefree.co Light’s criteria to distinguish exudative • Connective tissue disease from transudative effusions (Box 12 7). 12 • Pancreatitisok fre co • Review pleural fluid biochemistry. The • Mesothelioma presence of amylase indicates pancreatitis; • Post-MI syndrome pH <7.3 suggests bacterial infection • Sarcoidosis or cancer; rheumatoid factor suggests Other fluids connective tissue disease.meboo s Pus • Identify evidence of infection: Gram stain, • Empyema; most commonly caused by acute bacterial culture, microscopy for acid-fast bacilli. TB infection of the pleura culture may take months. Chyle • Look for evidence of malignancy: cytology • Chylothorax; caused by lymphatic obstruction, most may identify malignant cells; CT thorax commonly by metastatic cancer ± needle biopsy may reveal malignancy; Blood • Haemothorax; causes acute dyspnoea, usually pleural biopsy of regions identified as following trauma abnormalfree may com provide a diagnostic sfr e.c specimen. Fatigue 13ok fre

Fatigue is physical and/or mental exhaustion. It Respiratory causes is very common and non specific, so identifying significant underlying disease is difficult. Acute • Obstructive sleep apnoea. fatigue is usually caused by self-limiting infec- • Chronic obstructive pulmonary disease. tions or transient life circumstances. This guide pertains to fatigue of at least 2 weeks’ duration. Cardiac causes A care ul history may reveal that the problem • Congestive cardiac failure. is actually something other than fatigue, e.g. • Bradyarrhythmias. breathlessness, in which case this should be pursued. If a localizing or more specific feature, e.g.ooksfree.com haemoptysis, fever, jaundice, comes to light, Haematological causes make it the primary focus of assessment. • Anaemia. Causes of fatigue are shown below, with an • Haematological malignancy, e.g. emphasis on conditions that frequentlymebo present lymphoma. r e com m with fatigue as the chief complaint. Important problems to differentiate from fatigue are Endocrine causes described in Box 13.1. • Hypothyroidism. Non-organic causes • Hypercalcaemia. • Psychological stress/overwork. • Diabetes mellitus. • Depress on. • Adrenal insufficiency. • Fibromyalgia. • Hypopituitarism.ree com • Chronic fatigue syndrome. ksfree c Infection Medications • Infectious mononucleosis. • Beta-blockers. • Tuberculosis. • Chronic alcohol excess. • HIV. • Benzodiazepines and other sedatives. • Infective endocarditis. • Corticosteroids. • Lyme disease. • Chemotherapeutic agents. Chronic inflammatory conditions Malignancy • Rheumatoid arthritis. • Haematological. • Inflammatory bowel disease. • Solid organ. • Connective tissue disorders, e.g. systemic • Disseminated.free m lupusfree.co erythematosus. Fatigue 131 Differential diagnosis

Box 13.1 Presentations that must be distinguished from fatigue

Exertional dyspnoea longer participates in hobbies, interests and other activities. ‘Tiredness’ or ‘lack of energy’ is often cited as the reason Establish if the true complaint is reduced exercise for giving up these activities and careful questioning may ookstolerance. Quantify r how far the patient can walk in be required to distinguish true physical limitation from a meters/other tangible distance. Assess as described inb lack s of rinclination or owill. book Chapter 12. General debility Muscle weakness Ask about a change in weight, appearance or clothes size. Ask specifically about muscle weakness and formally Measure weight and compare with previous records if assess muscle group power (see Table 22.1). If detected, available. Look for evidence of malnutrition and reduced evaluate muscle weakness as per Chapter 22. muscle bulk. If present, evaluate thoroughly for an Excessive sleepiness underlying malignant inflammatory, GI or endocrine cause. This may result from depression, insomnia or sleep Concealed concerns disordered breathing, e.g. obstructive sleep apnoea (OSA). Fatigue may act as a ‘proxy’ complaint for an issue that Assess with the Epworth sleep score. Ask the patient’s the patient is reluctant to raise directly, e.g. problems partner about snoring and episodes of apnoea/hypoapnoea with finances, employment, alcohol or personal/sexual during sleep. If OSA is suspected, refer the patient for relationships. Enquire with tact, allow time and opportunity formal sleep studies. for the patient to voice concerns and ask specifically about Lossoksfree. of motivation m alcohol intake (see Box 2.1, p. 11). ok 13 This may result from depression, chronic stress or other psychosocial problems – consider it whenever a patient no me sfre com Fatigue 132 Overview

Full clinical assessment f e Yes Consider trial Fatigue secondary to drug 1 Likely drug culprit? discontinuation therapy

FBC, U+E, LFTs, TFTs, ESR, CRP, Ca2+, glucose, urinalysis ± pregnancy test

Anaemia/uraemia/hypothyroidism/ Clear cause identified on initial Yes hypercalcaemia/pregnancy/diabetes mellitus/ 2 screening bradyarrhythmia/drug-related

Fever, night sweats or Yes 3 Assess as per Pyrexia of unknown origin (p. 148) ↑sfinflammatory markers? m

Yes Further targeted 4 Other indicator of organic disease? Organic cause mevaluation s om m No

Yes Consider HIV/tuberculosis/Lyme disease/ 5 Specific infection risk? tropical infection

Yes 6 Lowfr mood, anhedonia? Likely depression No

Explore psychosocial factors. Assess impact on lifestyle and employment 7 Consider obesity/physical deconditioning If persistent and otherwise unexplained,meb consider chronic fr fatigue syndrome m Fatigue 133 Step-by-step assessment

1 Likely drug culprit? Diabetes mellitus Review all medications – prescribed and over- Formally evaluate for diabetes if the patient the-counter. Suspect a drug cause if there is has other suggestive symptoms or an ele ated a temporal relationship between a likely culprit fasting or random blood glucose (see Clinical tool: (seeooksfre above) and the onset of symptoms. If pos- Diagnosing diabetes and glycaemic complica- sible, stop or replace suspect medications and tions, p. 299). review symptoms after an appropriate interval. Poor glycaemic control in known diabetes Alcohol in excess or used chronicallymeboo can cause cases s re may cause co fatigue. Reviewm books the blood fatigue. Toxic environmental exposures, e.g. glucose diary and HbA1c to determine whether carbon monoxide, lead, mercury, arsenic, are control is adequate and, if not, reassess the less common, but potentially reversible causes. fatigue after correction. Repeated episodes of hypoglycaemia may also cause fatigue, and Definite cause identified on examination should be addressed. 2 or screening investigations? Hypothyroidism If any of the abnormalities listed below are Ask about symptoms of cold intolerance, detected, reassess fatigue after appropriate constipation and weight gain, and look for evaluation and treatment. oksfr e c m hypothyroid facies, dry skin, brittle hair and Anaemia nails, myxoedema and goitre. In patients with 13 known hypothyroidism, consider whether thy- This may cause fatigue but is also a common roxine replacement is adequate and ask about feature of chronic disease. See ‘Further assess- compliance. ↑TSH and ↓T4 confirms primary ment of anaemia’ (p. 136) in any patientme with ↓Hb. hypothyroidism. s e com Beware the mebookslow TSH with low Renal failure T4 – this may indicate secondary hypothyroidism so perform a full pituitary hormone profile. Uraemia is a cause of fatigue. If there is new or worsening renal impairment, see ‘Further Bradycardia assessment of renal failure’ (p. 230). If HR is <60 bpm, perform an ECG and consider Hyperca caemia a 24-hour tape. Refer to a cardiologist if there is evidence of complete heart block, a resting HR Fatigue and other symptoms, e.g. abdominal <50 bpm or a blunted HR response to exercise. pain, vomiting, constipation, polyuria, confusion and anorexia, may occur if corrected serum Pregnancy calciumooksfree.co is >3.0 mmol/L. Hypercalcaemia may Consider in any woman of child-bearing age reflect serious underlying disease, e g. bony and, if necessary, perform a pregnancy test. metastases, squamous cell lung cancer and eb sf multiple myeloma. mebo sfree.c Fever, night sweats m or 3 Firstly, check a parathyroid hormone (PTH) ↑inflammatory markers? level: Fatigue is a common, and often predominant, • an ↑ or →PTH suggests primary symptom in patients with systemic inflammatory hyperparathyroidism. Refer to or malignant disease, e.g. lymphoma, endocar- Endocrinology ditis, myeloma, tuberculosis. If there is a history • if ↓PTH, examine the breasts (p. 48) and of fever or night sweats or an ESR/CRP, review prostate, perform a CXR, a radioisotope ↑ as described for fever and pyrexia of unknown bone scan and myeloma ‘screen’, review origin (Chapter 14). drugs (especially calcium or vitamin D supplements). If no cause is identified, oksfree co 4 Other indicator of organic disease? consider a CT scan of the chest, abdomen and pelvis to look for underlying Look for the following indicators of organic malignancy. edisease sfree during com your assessment. me o f Fatigue 134 Step-by-step assessment

Abnormalities on FBC or blood film Features of chronic liver disease or deranged LFTs High or low cell counts, abnormal cells, e.g. blasts, or morphological abnormalities, e.g. target Look for stigmata of chronic liver disease (Box cells may indicate important haematological or 19.5, p. 176). If jaundiced, assess as per Ch. systemicooksfre disease. Seek co haematological advice 19. If LFTs are abnormal, enquire about alcohol for any unusual or unsuspected abnormality. intake and discontinue hepatotoxic drugs; if the eboabnormality re persists, consider a ‘liver screen’ Lymphadenopathy (Box 19.7, p. 181). mebook Enlarged lymph nodes may occur with malignancy (lymphoma, leukaemia or secondary Features of adrenal insufficiency deposits) or in reaction to infection/inflammation. Look for pigmentation of sun-exposed areas, The most important conditions to consider are recent scars palmar creases and mucosal mem- HIV, tuberculosis (TB), infectious mononucleosis branes; vitiligo/other autoimmune conditions; and malignancy postural hypotension and ↓Na+/↑K+. Confirm • Search for a local source of infection/ with a short ACTH (Synacthen) stimulation test. inflammation if swelling is localized to one lymph node group. 5 Specific infection risk? • Suspect haematological malignancy Consider HIV if the patient: ifoksfre there is generalized com painless lymphadenopathy. • has had unprotected sex, a blood • Consider lymph node biopsy if the cause is transfusion, done health-care work or has not apparent or you suspect malignancy. been resident in an HIV endemic area me• has eengaged .com in high-risk sexualmeb activity f Evidence of cardiorespiratory dysfunction • is an IV drug user, past or present. Consider a CXR ± Mantoux test if the patient • Look for features of cardiac failure has: (↑JVP, peripheral oedema, pulmonary • had previous TB or been resident in a TB congestion) or a new murmur; if present, endemic area arrange an ECG and echocardiogram. • had recent exposure to a patient with • Check SpO2 at rest ± on exertion; if low, active TB perform an ABG on room air and look for • immunosuppression. an underlying cause. • Askoks about ree.com smoking history and consider Consider Lyme serology if the patient has: CXR/pulmonary function tests (see Table • a history of a recent tick bite 12.5, p. 126). • a history of an erythema chronicum migrans • recently travelled to an endemic area. Some patients find it difficult to differentiate between fatigue and dyspnoea; if therem is a clear b Discuss ree.c with an mID unit if themeb patient has: o history or objective evidence of reduced effort • recently undertaken foreign travel beyond tolerance, consider a similar approach to that Europe and North America of chronic exertional dyspnoeam (see Ch. 12). • a history of a recentm animal bite. Fatigue 135 Step by-step assessment

6 Low mood, anhedonia? Box 13.2 Diagnostic criteria for chronic Suspect depression if the patient has lost fatigue syndrome enjoyment or interest in life (ask about previous interests, hobbies and so on), reports low mood Fatigue for ≥4 months with all of the following: • a clear starting point or expresses negative thoughts (guilt, pessimism, ooksfre • persistent and/or recurrent symptoms low self-esteem) out of proportion to the circum- • unexplained by other conditions stances. Look for blunted affect, psychomotor • a substantial reduction in activity level retardation and biological symptoms, meboe.g. loss of • characterized fr co by post-exertional mmalaise and/or libido, early morning waking. Consider psychiatric fatigue (feeling worse after physical activity) referral or a trial of antidepressants. and one or more of the following: • difficulty sleeping or insomnia • muscle and/or joint pain without inflammation Explore psychosocial factors and impact • headaches 7 on lifestyle. Consider obesity, physical • painful lymph nodes that are not enlarged deconditioning, chronic fatigue syndrome • sore throat or general malaise or flu-like symptoms • cognitive dysfunction, such as difficulty with thinking If the pat ent has a BMI >30 or lacks physical • physical or mental exertion that makes fitness, encourage appropriate lifestyle changes symptoms worse and reassess. If not already excluded consider • dizziness and/or nausea coeliac disease, infectious mononucleosis and • palpitation, without heart disease 13 Lymeooksfree.co borreliosis. Chronic fatigue syndrome is a diagnosis of exclusion with specific criteriabo free.com (Box 13.2). Fatigue 136 Further assessment of anaemia

anaemia less likely (present in 90% of cases). Further assessment of anaemia Seek Haematology advice in difficult cases.

Step 1 Use he mean cell volume (MCV) to narrow the If B12 and folate are normal, exclude hypo- differential diagnosis thyroidism, pregnancy and alcoholic liver disease, In the UK, microcytic anaemia (MCV <76 fL) is and then evaluate for haemolysis (Step 2) and usuallyooks due to re iron deficiency. co myelodysplasia (Step 3), as described below.

First, confirm iron deficiency. Serum ferritin is Measure iron studies and vitamin B12/folate in more indicative of total body iron than serum patients with normocytic anaemia, as combined iron but may be increased by liver medisease or o iron freand B12 or folate deficiencies,mebooks e.g. nutritional systemic inflammation. deficiency, small bowel disease, may result in a • ↓ferritin confirms iron deficiency. normocytic picture. • If ferritin is normal, transferrin saturation Step 2 Investigate for haemolysis <20% suggests iron deficiency. Consider haemolysis in patients with normal or If iron deficiency is confirmed, identify the ↑MCV. underlying cause. Seek evidence of ↑red cell destruction: • Review the diet and consider inadequate • ↑bilirubin/LDH iron intake, especially in vegetarians. • ↑urinary urobilinogen • Ask about blood loss: haematemesis, • red cell fragments on blood film melaena,o sfree.com haemoptysis, epistaxis, and a compensatory increase in red cell haematuria, menorrhagia, trauma. production: • Arrange UGIE and colonoscopy unless b there is a clear non-GI source of bleeding, • ↑reticulocytes e.g. menorrhagia, haematuria. me• polychromasia re co • nucleated red cell precursors on blood film. Where the cause remains unclear If present, distinguish intravascular from • exclude coeliac disease: serology ± extravascular haemolysis to narrow the differential duodenal biopsy at the time of UGIE diagnosis. • refer to GI for further investigation, e.g. Intravascular haemolysis, e.g. in microangio- small bowel pathology. pathic haemolytic anaemia (MAHA), defective Reassess symptoms and FBC after iron sup- mechanical heart valve, malaria – releases free plementation and treatment of any underlying Hb into the plasma, leading to cause • ↓plasma haptoglobins (mop up free Hb Refer patients with a ↓MCV and normal then cleared by the liver) iron stores to a haematologist for investigation • methaemalbuminaemia (once haptoglobin ofook alternative free.com diagnoses, e.g. thalassaemia, binding is saturated) sideroblastic anaemia. • haemosiderinuria (once albumin binding In patients with a macrocytic anaemia (MCV capacity exceeded) >98 fL), measure vitamin B12 and fastingm serum boo sfree c m m bo k f • haemoglobinuria (black urine if fulminant, folate. e.g. in malaria). In the absence of pregnancy, causative drugs, e.g. methotrexate, phenytoin, or haemolysis (see With extravascular haemolysis, e.g. hereditary below), ↓folate is likely to be due to poor dietary spherocytosis, autoimmune haemolysis or red intake (fruit, leafy vegetables) but always check cell enzymopathies, these features are absent coeliac serology. and there is often clinical or USS evidence of splenomegaly (the site of red cell breakdown) ↓B12 is unlikely to be due to dietary deficiency unless the patient is a strict vegan. Check for In either case, review the blood film for previous gastrectomy or small bowel surgery, diagnostic abnormalities: then investigate for pernicious anaemia. Intrinsic • malaria parasites on thick and thin films factorooksfree.com antibodies are diagnostic but only present (mandatory if recent travel to malaria in 60% of cases; anti-parietal cell antibodies are endemic region) non-specific but their absence makes pernicious • sickle cells – sickle cell anaemia mebo ksfree.com meboo sf Fatigue 137 Further assessment of anaemia

• red cell fragments – MAHA, e.g. electrophoresis and urine for measurement of haemolytic uraemic syndrome, Bence Jones protein. Discuss with a haematolo- thrombotic thrombocytopenic purpura; gist if these are positive or if there is clinical defective mechanical heart valve, march suspicion, e.g. bone pain, pathological fracture, haemoglobinuriaoksfre lytic bone lesions, unexplained ↑Ca2+ or ESR. • spherocytes – autoimmune haemolytic anaemia or hereditary spherocytosis bStep sfre 4 Consider co chronic non-haematological disease • Heinz bodies, bite cells – G-6-PD Consider chronic kidney disease as a potential deficiency. cause for normocytic (↓erythropoietinme production) ooksf if GFR <60 mL/min/1.73 m2, and especially if Discuss immediately with a haematologist if <30 mL/min/1.73 m2. Measure ferritin and you suspect haemolytic uraemic syndrome or transferrin saturation to ensure that the patient thrombotic thrombocytopenic purpura, e.g. AKI, is iron-replete (ferritin >100 ng/mL; transferrin neurological features, acute diarrhoeal illness. saturation >20%) and discuss with a nephrologist. If spherocytes are present, perform a direct The most common cause of normocytic Coombs test to help differentiate autoimmune anaemia is chronic inflammatory disease, e.g. haemolyt c anaemia from hereditary spherocy- rheumatoid arthritis, polymyalgia rheumatica, tosis. If the cause is unclear, consider enzyme chronic infection or malignancy. Consider the assays (G-6-PD or pyruvate kinase deficiency) diagnosis if: and Hb electrophoresis (haemoglobinopathies) 13 andooksfree refer to a haematologist. om • other causes of ↓Hb have been excluded (including iron, B12, folate deficiency) Step 3 Seek evidence of bone marrow failure or • there is no evidence of active bleeding haematological malignancy e oo sfree.com • anaemia is mild, e.g. Hb>80 g/L, and Review the FBC and blood film for: mebo ks • unexplained weight loss, fever, ↑ESR/ • deficiencies in other cell lines CRP or ↓albumin – search for an (↓WBC, ↓platelets) underlying cause. • ↑WBC, e.g. chronic myeloid leukaemia, chronic lymphocytic leukaemia Step 5 Refer to a haematologist • atypical cells, e.g. blasts. Seek input from a haematologist if the cause of Examine for lymphadenopathy and splenomegaly, anaemia is still unclear, you suspect a serious or and refer for further investigation, e.g. bone unusual haematological disorder or the patient marrow evaluation. fails to respond to therapy. f Look for evidence of a paraproteinaemia, e.g.ooks multiple ree.comyeloma: send serum for proteino sfree.c m Fever 14oksfre

Fever (or pyrexia) is a body temperature >99th • Viral hepatitis. percentile of the healthy adult maximum; in • Diverticulitis. clinical practice, a temperature ≥38°C is usually • Intra-abdominal TB. regarded as significant. Extreme fever >( 41°C) • Hepatic abscess. is life threatening and tends to occur with gram negative bacteraemia, drug reactions, e.g. neuro- Skin/soft tissue leptic malignant syndrome, intracranial pathology • Cellulitis. (leading to central temperature dysregulation) • Erysipelas. or extreme environmental conditions. Pyrexia • Necrotizing fasciitis. of unknown origin (PUO) is documented fever • Pyomyositis. thatooksfree.com persists without explanation for 2–3 weeks • Infected pressure sore. despite investigation. • Wound infection. Fever occurs most commonly as part of the acute phase response to infection.m Sepsis bo is e co Musculoskeletal causes defined as ‘life-threatening organ dysfunction due to a dysregulated host response to • Septic arthritis (native and prosthetic joint). infection’*; it carries a significant mortality and • Osteomyelitis. must be recognized and managed quickly. Other • Discitis. causes of fever are malignancy, connective tissue • Epidural abscess. disease, drug reactions, miscellaneous causes and fictitious fever. Genitourinary tract *Singer M Deutschman CS, Seymour CW, et re c m Lower urinary tract infection (UTI), al. The Third International Consensus Definitions e.g. cystitis, prostatitis. for Sepsis and Septic Shock (Sepsis-3). JAMA • Upper UTI (pyelonephritis). 2016 Feb 23;315(8):801-10. ooksfree com • Perinephric collection. Infection • Pelvic inflammatory disease. • Epididymo-orchitis. Respiratory system • Syphilis.

• Acute bronchitis. CNS • Pneumonia. • Influenza. • Meningitis (bacterial, viral, fungal, TB). • Empyema. • Encephalitis. • Infective exacerbation of bronchiectasis/ • Cerebral abscess. COPD. • Tuberculosis (TB). ENTr e.co GI causes • Upper respiratory tract infection (RTI), e.g.k o fr e tonsillitis. • Gastroenteritis. • Otitis media. • Appendicitis. • Quinsy. • Biliary sepsis. • Dental abscess. Fever 139 Differential diagnosis

• Mumps/parotitis. • Solid tumours, especially renal, liver, colon, • Glandular fever (Epstein–Barr virus; EBV). pancreas. • Sinusitis. Connective tissue disorders Immunocompromisedo sfre patients • Giant cell arteritis/polymyalgia rheumatica. • Pneumocystis jiroveci (carinii) pneumonia.b• Rheumatoid re oarthritis. • Aspergillosis. • Systemic lupus erythematosuse oo • TB. • Polymyositis. • Atypical mycobacterial infection, e.g. • Polyarteritis nodosa. Mycobacterium avium intracellulare. • Wegener’s granulomatosis. • Cytomegalovirus (CMV) infection. • Churg–Strauss disease. • Toxoplasmosis. • Cryoglobulinaemia. • Cryptococcal meningitis. • Adult-onset Still’s disease. • Nocardia infection. Drugs • Disseminated herpes/fungal infection. • Drugr fevercom (almost any drug). Returning travellers • Antipsychotics (neuroleptic malignant syndrome). • Malaria. • Anaesthetics (malignant hyperthermia). • Typhoid.o s ee.c m • Cocaine, amphetamines, ecstasy • Infective diarrhoea, e.g. cholera, boo 14 amoebiasis, Shigella. Other causes • Amoebic liver abscess. • Strongyloides infection. • Transfusion-associated. • Schistosomiasis. • Thyrotoxicosis, thyroiditis. • Dengue. • Phaeochromocytoma. • Chikungunya • Deep vein thrombosis (DVT)/pulmonary embolism (PE). Other infectious causes • Pancreatitis. • Alcoholic hepatitis/delirium tremens. • Leptospirosis. • Rheumatic fever. • Brucellosis. • Inflammatoryfree com bowel disease. • Lyme disease. • Sarcoidosis. • Qoksfree. fever. • Atrial myxoma. • HIV. • Familial Mediterranean fever. • Toxoplasmosis. • Erythroderma/Stevens–Johnson syndrome. • Fungal infection. • Fictitious (fever or apparent fever • Measles, rubella. surreptitiously engineered by the patient). • Herpes zoster infection (chickenpox or me shingles). Malignancy • Haematological malignancy, including lymphoma, leukaemia,e.c myeloma. Fever 140 Overview

Full clinical assessment, FBC ± CRP f e Yes Seek source of 1 New qSOFA score >1 (Box 14.1) or k Probable sepsis 1 high-risk feature? infection > ook No

Yes Consider transfusion reaction / malignant 2 Suspect non-infective cause? hyperthermia / neuroleptic malignant syndrome

Septic screen (see Clinical tools: ‘Septic screen’ +/–e. ‘Extensions of the septic screen in specific patient groups’) ee Yes 3 Specific risk factor for infection? Further targeted investigation

Clinical findings / initial tests Yes 4 Confirm diagnosis ± empirical treatment suggest a likely source? m

Yes 5 Positive cultures? Seek sourceco ± specific antimicrobial therapy No

Yes 6 Persistent fever? See Further assessment of pyrexia of unknown s c origin No

Likely self-limiting viral infection Investigate as per pyrexia of unknown origin if persistently ↑CRP/ESR, recurrent fever or major systemic upset m m Fever 141 Step-by-step assessment

New qSOFA score >1 (Box 14.1) or >1 potentially life-threatening and important to 1 high risk feature? recognize immediately; they may be overlooked if not specifically considered at the outset Unless you suspect a non-infective cause for If the patient is receiving blood products, stop fever (see step 2) use the qSOFA score (Box the transfusion, ensure the patient’s ID matches 14.1 ook) to rapidly fre identify sepsis pending lab data/ that on the unit, and check that the ABO and ABG/urine output trends: diagnose sepsis if RhD groups in the transfused blood are compat- qSOFA score >1 (assume baseline score of ible with the patient. Contact the blood bank zero unless known pre-existing organmebo dysfunc- and sfre seek immediate co Haematologymebook input if there f tion). Also diagnose sepsis if >1 of the following is any suspicion of ABO incompatibility or other features is present: major transfusion reaction. Otherwise, monitor • Hypoxia (e.g. PaO2/FiO2 <53.3 KPa or temperature and vital signs, and consider restart- supplemental O2 required to maintain SpO2 ing the transfusion at a slower rate if observations >94%) are stable, the patient is systemically well and • Hypotension (e.g. MAP <70 mmHg; SBP the rise in temperature is 1.5°C. <100 mmHg or need for inotropes) < • GCS <15 Suspect neuroleptic malignant syndrome if the • Oliguria: (e.g. not passed urine for ≥12 hours patient has received neuroleptics, e.g. haloperidol, or urine output <0.5 ml/kg/hr) within the past 1–4 weeks and exhibits muscular • Serum creatinine >110 µmol/L or >50% rise rigidity, tremor and excessive sweating and/or fromoksf baseline. ee om altered mental status, especially in association • Bilirubin >20 µmol/L with ↑CK. 9 14 • Platelets <150 × 10 /L If appropriate, ask the patient about recent Manage all patients with suspectedm sepsis in use sfree of cocaine, com ecstasy orm amphetamines; ooksf accordance with the Surviving Sepsis guidelines consider toxic hyperthermia if temperature (http://www.survivingsepsis.org/GUIDELINES/ is >39°C, especially if there are features of Pages/default.aspx) while searching for a focus excessive sympathomimetic activity, e.g. ↑BP, of infection – see Clinical tool: A septic screen ↑HR, dilated pupils, aggression, psychosis or (p. 142). serotonin syndrome, e.g. rigidity, hyper-reflexia. Assess haemodynamic status frequently Measure CK, U+E, LFTs and coagulation, and (see Ch. 30) and manage as septic shock if monitor ECG, HR, BP and urine output, to identify there is persistent hypotension (mean arterial complications such as rhabdomyolysis, acute renal pressure [MAP] <65 mmHg) and ↑serum failure, arrhythmia, disseminated intravascular lactate (>2 mmol/L) despite adequate volume coagulation and acute liver failure. esuscitation. Assume malignant hyperthermia if the patient oo sfree. om develops severe pyrexia with tachycardia ± 2 Suspect non-infective cause for fever? rhabdomyolysis during administration of, or within e1–2 sfree hours of exposure com to, a volatile anaesthetic, Most acute febrile illnesses are caused by e.g. halothane or succinylcholine.mebo ksf infection, but the following conditions are Suspect heatstroke if the patient has had sustained exposure to very hot weather, e.g. Box 14.1 qSOFA (quick SOFA) criteria during a heatwave or has been undertaking prolonged severe exertion in high temperatures. • Respiratory rate ≥ 22/min 1 point In all of the above cases continue to evaluate • Altered mentat on (e.g. GCS <15) 1 point • Systolic blood pressure ≤ 100 mmHg 1 point for infection and other causes if there is any ee c m diagnostic doubt. free.com Fever 142 Step-by-step assessment

Clinical tool A septic screen The septic screen combines clinical assessment with • If new-onset jaundice, arrange an abdominal USS and laboratory analysis and imaging studies to identify a source serology for viral hepatitis of infection.ok It fre may also reveal co non-infectious causes • Treat empirically for biliary sepsis and of pyrexia, e.g. malignancy. The full screen may not be arrange surgical review if there is a cholestatic required in all patients, especially if there is an obvious pattern of jaundice (p. 176) or USS shows dilated focus of infection. e o bile ducts. eb k General • Send blood and urine samples for leptospirosis culture and serology ± PCR if symptoms include • ≥2 sets of blood cultures, urinalysis, FBC, U+E, LFTs, purpura, ↓platelets or conjunctival congestion, CRP, CXR. or there has been recent exposure to potentially Respiratory contaminated water, e.g. freshwater sports, sewage worker – liaise with the ID team. • Assess suspected RTI e.g. new/worsening • Check amylase and assess as described cough with purulent sputum or CXR consolidation as in Chapter 4 if acute abdominal pain with tenderness per page 123. or guarding. • Perform a pleural tap and send fluid for biochemical, • If palpable abdominal mass investigate for infective, microbiological and cytological analysis if unilateral e.g. diverticular or appendiceal abscess, and non- pleural effusion (p. 129). infective, e.g. carcinoma, lymphoma, causes with USS • If other respiratory features, e.g. haemoptysis, non- or CT ± aspiration or biopsy. specificoksfree.c CXR hypoxia, consider further investigation, e.g. CT, bronchoscopy to exclude atypical infection, Urinary tract lung cancer and PE. b free.com • Send an MSU if new-onset urinary tract symptoms, Abdominal an indwelling urinary catheter or leucocytes/nitrites on • Send stool samples for microscopy, culture and urinalysis (bacterial UTI highly unlikelyme in the absence k sensitivity testing ± Clostridium difficile toxin if acute of either nitrites or leucocytes.) diarrhoea. • Arrange USS to exclude renal obstruction, calculus • Investigate for inflammatory bowel disease, e.g. flexible or a perinephric collection if loin pain or renal angle sigmoidoscopy, if persistent bloody diarrhoea. tenderness. • Perform an urgent ascitic tap in any febrile patient • Exclude urinary ract cancer ± inflammatory renal with ascites; treat empirically as spontaneous disease (see Ch. 16) if persistent haematuria bacterial peritonitis (SBP), pending culture, if >250 (visible or non-visible) or loin pain with repeated neutrophils/µL ascitic fluid. Consider TB and negative MSU. malignancy if fluid is exudative and initial cultures • Send swabs for Neisseria gonorrhoeae and Chlamydia negative. sfree.cif urethral or PV discharge. m ksfree.com Fever 143 Step by-step assessment

Clinical tool—cont’d A septic screen Skin and soft tissue Cardiovascular • Send swabs from any wounds or sites discharging pus • Investigate for endocarditis (Box 14.2) with a • Suspectoksfre cellulitis if there is an area of acutely hot transthoracic echocardiogram and ≥3 sets of blood erythematous and painful skin; look for potential entry cultures if new murmur, vasculitic/embolic phenomena sites, e.g. peripheral cannulae, skin breaks or a predisposing cardiac lesion with no obvious • Seek immediate surgical assessment and give IV alternative source of infection. antibiotics if any features of severe necrotizingm b• sConsider a transoesophageal co echocardiogrammebo if infection, e.g. rapid spread, crepitus, anaesthesia over transthoracic images equivocal or persistent high lesion, major haemodynamic compromise or pain out clinical suspicion. of proportion with clinical findings. ENT • DVT may produce a low-grade fever – exclude as described on page 193 if acutely swollen limb. • Consider a throat swab for influenza during outbreaks • Consider investigation for osteomyelitis, e.g. bone or the autumn/winter season. scan, if persistent non-healing ulcer. • Send a swab for Streptococcus pyogenes if pustular • Examine the whole body for rashes – seek urgent exudates. dermatology advice if blistering, mucosal involvement • If parotitis or tender lymphadenopathy, or pustules (see Ch. 27). consider a throat swab for mumps PCR and, if age-appropriate, check EBV serology (>95% of CNS patients >35 years will have evidence of previous • Assumeoksfree CNS infection, com initially, if severe exposure). headache, meningism, purpuric rash, focal 14 neurological signs, new-onset seizures or unexp ained Musculoskeletal ↓GCS. Give immediate empirical treatment after blood • If acutely swollen, painful joint, seek urgent orthopaedic cultures, arrange urgent neuroimaging and,me assessment free and co perform diagnosticm aspiration oo to if no contraindications (p. 170), perform lumbar exclude septic arthritis (see Ch. 20). puncture. • If unexplained back pain with no other obvious source • If meningitis suspected, send a throat swab for for fever, take ≥3 blood cultures and arrange spinal Neisseria meningitidis PCR.om MRI to exclude discitis.om Fever 144 Step-by-step assessment

Specific risk factor for infection? 3 Box 14.2 Modified Duke criteria for the diagno- Infections other than those discussed above may sis of infective endocarditis need to be considered in patients returning to or Major criteria entering the UK from abroad (especially from the Positive blood culture tropics)ooksfre and those who co are immunocompromised • Typical organism from two cultures or with IV drug use. • Persistent positive blood cultures taken >12 hours If the patient has come from an at-risk apart e region for viral haemorrhagic feverm and bohas • ≥ fr3 positive cultures taken over >1 hour unexplained bleeding, discuss urgently with Endocardial involvement the health protection team (before admission). • Positive echocardiographic findings of vegetations • New valvular regurgitation Otherwise, complete a septic screen as per ‘Clinical tool: Extensions to the septic screen Minor criteria in specific patient groups’. The prevailing strains • Predisposing valvular or cardiac abnormality and resistance patterns of common infections • IV drug misuse such as pneumonia may differ in other parts of • Pyrexia ≥38°C • Embolic phenomenon the world so seek input from an ID specialist • Vasculitic phenomenon at an early stage. • Blood cultures suggestive – organism grown but not Immunocompromised patients may experi- achieving major criteria enceooksfree more severe comsequelae from infection • Suggestive echocardiographic findings with common pathogens and are at greater Definite endocarditis: two major, or one major and three risk of opportunistic infections, especially minor, or five minor with mycobacteria, viruses and fungi.mebo Follow Possible ree endocarditis: c mone major andmeb one minor, k the additional steps for immunocompromise or three minor (Clinical tool: Extensions to the septic screen Modified from Boon NA, Colledge NR, Walker BR, Hunter JAA. in specific patient groups) if the patient has an Davidson’s Principles and Practice of Medicine, 20th edn. acquired or congenital immunodeficiency (includ- Edinburgh: Churchill Livingstone, 2006. ing HIV); is receiving treatment with high-dose steroids, immunosuppressants, DMARDs or anti- TNF drugs; or is neutropenic for any reason. Clinical findings/initial tests suggest More specific forms of immunocompromise 4 a likely source? include asplenia (↑susceptibility to encapsulated organisms and malaria) and the presence of Following appropriate cultures, treat immediately indwelling vascular access devices or other with antibiotics according to the likely source and prosthetic material. Test for HIV in patients who local guidelines in patients with severe sepsis. If booksfree.comare at high risk or who present with an atypical no clear source is identified or the patient has infection or other indicators of HIV – see http:// neutropenia (especially if the neutrophil count www.bhiva.org/documents/Guidelines/Testing/mebois <1.0 × 109/L) om or other significantmebook immuno- GlinesHIVTest08.pdf. compromise, provide empirical broad-spectrum Ask about all forms of drug use in any patient antibiotic ± antifungal therapy. The choice of presenting with unexplained fever. If there has antimicrobials will depend on patient factors and been IV drug use, establish frequency, duration local resistance patterns – discuss with Microbiol- and sites of injection. Maintain awareness of any ogy and other relevant specialties, e.g. Oncology, local/national outbreaks, as unusual organisms Haematology. Refine the antibiotic regimen in may be implicated, e.g. anthrax skin infections. discussion with the Microbiology team on the Always consider the possibility of underlying basis of subsequent culture results. blood borne infection, e.g. hepatitis B or C, Patients with recurrent fever, or fever in the HIV. Discuss with the ID team if the patient absence of immunocompromise, neutropenia or isooksfree haemodynamically com compromised or fails to haemodynamic disturbance can often wait for improve on standard therapy. bothe sfree.com results of cultures before antibiotic therapy ebook f Fever 145 Step by-step assessment is started. If there is a clear source of infection, bottles, confirm an infective aetiology and help start empirical antibiotic therapy and adjust as to guide further investigation; for example, blood necessary in light of the culture results and culture results are central to the diagnosis of sensitivity testing; otherwise, reassess daily whilst infective endocarditis (see Box 14.2). awaiting the full results of the septic screen. Persistently positive blood cultures despite ooksfre appropriate antibiotic therapy suggest a deep- 5 Positive cultures? seated infection; the source must be identified and removed, e.g. debridement, drainage. Re-evaluate your initial diagnosis andm treatment sfre co meboo sf in the light of culture results. 6 Persistent fever? Positive cultures may confirm a suspected source of infection, e.g. MSU, sputum and Acute fever is frequently a manifestation of self- guide the most appropriate antibiotic therapy. limiting viral illnesses. In the absence of continuing On the other hand, blood cultures that yield pyrexia, ongoing symptoms or signs, or worrying an unexpected organism may challenge your investigation results, no further action is required. working diagnosis and prompt re-evaluation for Recurrent fever, especially with persistent an alternative source, e.g. Staphylococcus aureus elevation of inflammatory markers or significant in suspected UTI. constitutional upset, mandates further evaluation; In the patient with no obvious source of fever, if present, proceed to ‘Further assessment of positive blood cultures, especially in multiple pyrexia of unknown origin’. oksf ooksfree.com o sfree.com 14 Fever 146 Step-by-step assessment

Clinical tool Extensions to the septic screen in specific patient groups Recent travel or residence abroad • Check dengue fever serology if recent return from • Documentksfre exactly where co the patient has been, specific the tropics/subtropics and an acute febrile illness dates of travel and activities undertaken (including associated with a rash (generalized, blanching, macular a sexual history). Ask about vaccinations/malaria in the initial stages), headache or severe aches and prophylaxis prior to and during travel. pains. Discuss immediately with the ID team if any • Consult an ID specialist at an early stage for any suspicion of dengue haemorrhagic fever (epistaxis, GI returning traveller with unexplained fever.m b sfrbleeding, petechia, purpura, ↓platelets,meboo coagulopathy) • Exclude malaria if they are a recent traveller to an or dengue shock syndrome (↓BP, ↓capillary refill time, endemic region (http://www.cdc.gov/malaria/about/ organ dysfunction). distribution.html) with three sets of blood films± • Send blood for Chikungunya serology/viral PCR if malaria antigen card: recent travel to an endemic region. • use the antigen card to facilitate rapid diagnosis, particularly if acutely unwell, but also send films as Immunocompromise the card may miss parasitaemia of <0.5% and is • In patients with HIV, check the most recent CD4 not accurate for speciation count and repeat if >3 months ago. Fungal and viral • take films over a 72-hour period, ideally after a infections are more likely if CD4 count <200 but can fever spike, as this is when parasitaemia is highest occur at higher counts. Check compliance with anti- • discussksfree any positive com case immediately with an ID retroviral therapy/antimicrobial prophylaxis. specialist and refer to the British Infection • Seek early advice from a respiratory specialist if Society treatment guidance at http:// there are respiratory symptoms or an abnormal CXR www.journalofinfection.com/article/s0163- (especially cavitation) cavitation, or a high suspicion of 4453(16)00047-5/fulltext. Pneumocystis pneumonia due to any of the following • If fever is accompanied by diarrhoea, isolate the patient features: and note all recent travel history on stool specimenm • freesubacute, e.g. com over 2–3 weeks,mebo or progressive requests. Discuss immediately with Microbiology and shortness of breath ID teams if any suspicion of cholera, e.g. refugee/aid • non-productive cough worker in high-risk area. • diffuse bilateral perihilar infiltrates on CXR or non- • Send blood and stool cultures for typhoid if high specific changes fever, constitutional upset and recent travel to Asia • unexplained hypoxaemia (including desaturation (especially the Indian subcontinent), Africa (especially on exercise). sub-Saharan) or Latin America. Discuss urgently with • Send sputum, for microscopy (acid-fast bacilli, the ID team, especially if suggestive clinical features, fungal), histopathological analysis (Pneumocystis) e.g. rose coloured spots over the trunk, relative and mycobacterial culture; if necessary, induce bradycardia, constipation. sputum by nebulized hypertonic saline in a • Consider acute schistosomiasis if exposure to negative-pressure environment and discuss need for potentiallyoksfree.com infested water, e.g. freshwater swimming, other diagnostic procedures, e.g. bronchoalveolar rafting, water sports in Africa, South America or lavage. Asia, within the past 8 weeks, +/− eosinophilia, • If prominent GI symptoms, send blood for Strongyloides hepatosplenomegaly, RUQ tenderness, bloody serology and consider investigation for CMV colitis, e.g. diarrhoea or urticarial rash. Send blood for serology flexible sigmoidoscopy+ biopsy and intra-abdominal and discuss with an ID specialist. meTB, free.com e.g. CT abdomen/pelvis ± targetedmeboo biopsy (samples • Arrange USS to exclude amoebic abscess if must be sent in saline, not formalin, as acid-fast bacilli previous travel to the tropics and RUQ discomfort ± are destroyed). palpable liver. m Fever 147 Step by-step assessment

Clinical tool—cont’d Extensions to the septic screen in specific patient groups • If CNS features, investigate as per the general septic • Discuss early with the relevant specialty if you suspect screen but send blood for Toxoplasma serology, infection of prosthetic material, e.g. valve prosthesis, requestoksfre CSF staining for Cryptococcus and TB, and pacemaker and prosthetic joint. biopsy any space-occupying lesion. IV drug use • Request a dermatology review and biopsy of any • Take ≥3 sets of blood cultures prior to starting suspicious or unusual rashes, e.g. cutaneous T-cell antibiotic therapy. e ok lymphomas, Kaposi’s sarcoma. me• sfrLook at all new co and old injection sites; if inflamed or • Prolonged indwelling vascular access catheters, e.g. tender, consider USS to exclude an underlying abscess. Hickman lines, tunnelled lines, carry a substantial risk • Arrange a Doppler USS to exclude DVT if there is any of bacterial/fungal infection; suspect line infection in all groin or leg swelling cases where there is no clear alternative source, even • Exclude ilio-psoas abscess by CT if there is groin or if the entry point looks clean. lower back pain with difficulty extending the leg. • Take blood cultures from the line and, if feasible, • Arrange an echocardiogram ± transoesophageal remove sending the tip for culture. echoca diography if there is no clear alternative source • Conside echocardiography to look for endocarditis of fever or there is evidence of septic emboli on CXR in patients with confirmed bacteraemia – especially (see Box 14.2). S aureus or persistent fever. free.com sfree.com

14 Fever 148 Further assessment

Further assessment of pyrexia of blood film abnormality, e.g. atypical unknown origin lymphocytes. • Arrange muscle biopsy if ↑CK, to exclude Perform additional screening investigations (Box inflammatory myositis. 14.3) in any patient with persistent unexplained • Perform a radioisotope bone scan to fever.ook These fre may reveal co a diagnosis or provide look for evidence of malignancy or useful leads for further investigation. osteomyelitis if persistent bony pain, ↑Ca2+, • Discuss the significance of any positive ↑prostate-specific antigen or↑ alkaline serology with the ID/Microbiologym team boophosphatase re (with otherwisemebo normal LFTs). s and a positive ANA, ENA or ANCA with the • If LFTs persistently deranged or Rheumatology team. hepatomegaly without an obvious cause, • Biopsy any suspicious masses or request a liver biopsy (with material for lymphadenopathy (including bilateral hilar culture) to look for TB, sarcoidosis and lymphadenopathy) detected clinically or granulomatous hepatitis. radiologically • If persistent haematuria/proteinuria with • If an abscess is identified, request a negative MSU, discuss with the Renal surgical opinion regarding drainage. teamfree and consider com renal biopsy to exclude • Discuss with Haematology and consider glomerulonephritis. bone marrow examination if Bence Jones • Use the Duke (see Box 14.2) and Jones protein,oksfre paraproteinaemia .com or a significant criteria (Box 14.4) to confirm or refute a suspected diagnosis of endocarditis or rheumatic fever respectively

Box 14.3 Further screening tests in pyrexia of meboo s unknown origin

Ensure that a full septic screen (see above) is carried Box 14.4 Jones criteria for the diagnosis of out, plus: rheumatic fever Clinical Major manifestations • Repeat a full clinical assessment, including travel, • Carditis sexual occupational and recreational history; lymph • Polya thritis nodes skin and eye examination; urinalysis; PR; • Chorea breast and testicular examination. • Erythema marginatum • Subcutaneous nodules Microbiological Minor manifestations • Serologyoksfree for HIV, viral hepatitis m (A–E), EBV, CMV, toxoplasmosis, Q fever, Lyme disease, brucellosis • Fever syphilis, Chlamydia, Bartonella and Yersinia. • Arthralgia • Serology for leishmaniasis, amoebiasis, • Previous rheumatic fever trypanosomiasis and schistosomiasis if therem has b• ↑ freeESR or CRP c m been travel to the developing world. • Leucocytosis • Tuberculin (Mantoux) test and three early morning • First-degree atrioventricular block urine specimens for TB microscopy and culture. PLUS • Antistreptolysin O titre. • Supporting evidence of preceding streptococcal Biochemistry/immunology/haematology infection: recent scarlet fever, raised antistreptolysin • ANA, RF, ANCA O or other streptococcal antibody titre, positive throat • FBC with peripheral blood film, ferritin, LDH, CK, culture 2+ Ca , plasma electrophoresis, TFTs, prostate-specific N.B. Evidence of recent streptococcal infection antigen (if male patient >50 years). is particularlyfree.co important if there is only one major • Urine for Bence Jones protein. manifestation. Radiological oksfree c m From Boon NA, Colledge NR, Walker BR, Hunter JAA. Davidson’s • CT chest/abdomen/pelvis. Principles and Practice of Medicine, 20th edn. Edinburgh: • Echocardiogram. Churchill Livingstone, 2006 (p. 617). bo Fever 149 Further assessment

• Consider an ANCA-negative systemic • Suspect adult-onset Still’s disease vasculitis if palpable purpura, skin ulceration if microbiological and autoimmune or livedo reticularis. Measure serum investigations are consistently negative and cryoglobulins (cryoglobulinaemic vasculitis); there are recurrent joint pains or a transient, consideroksfre arteriography, e.g. renal, non-pruritic, salmon-pink maculopapular mesenteric or tissue biopsy if polyarteritis rash that coincides with fever, especially if nodosa is suspected, e.g. eosinophilia, ↑↑↑ferritin. renal impairment, ↑BP, constitutional upset. • Review all drugs: discontinue one at a time • If ↑ESR in a patient >50 years: mebfor re 72 hours and then reinstatem if books fever • treat for giant cell arteritis and arrange persists. temporal artery biopsy if there is • If the cause remains unclear, consider a headache, visual loss, scalp tenderness whole body PET scan to look for evidence or an inflamed, thickened, pulseless or of occult malignancy (e.g. lymphoma) tender temporal artery or vasculitis, bone marrow biopsy or • diagnose polymyalgia rheumatica if there liver biopsy, and consider diagnoses of is any proximal joint pain or stiffness exclusion, e.g. Behçet’s disease, familial – review the diagnosis if there is no Mediterraneanfree com fever, fictitious fever. response to systemic steroids within 72ksfree hours. com 14 Gastrointestinal haemorrhage: haematemesis ok and rectal bleeding o 15 book fre

Haematemesis is the vomiting of blood from the Mallory–Weiss tear upper GI tract. Bright red blood or clots imply active This is a mucosal tear in the oesophago-gastric bleeding and are a medical emergency. Altered junction following increased gastric pressure. blood with a dark granular appearance (‘coffee- 90% of these bleeds stop spontaneously. grounds’) suggests that bleeding has ceased or The history is characteristic: forceful retching has been relatively modest. Melaena is the passage with initially non-bloody vomit, followed by of black tarry stools, usually due to acute upper haematemesis. GI bleeding (see ‘Haematemesis’ below), but occasionallyooksfree due to bleeding com within the small bowe Oesophageal/gastric varices or right side of the colon. Haematochezia is the These are collateral veins that form in response passage of fresh red or maroon blood per rectum; to portal hypertension and allow portal blood it is usually due to colonic bleeding, but 15% of mebooto sfr bypass e.co the liver and enterme the systemic sf cases result from profuse upper GI bleeding. circulation directly. The most common cause Haematemesis is hepatic cirrhosis Segmental varices from portal vein thrombosis (pancreatitis) may occasionally With major upper GI haemorrhage, resuscitation occur. Patients typically present with massive must take place alongside assessment. Diagnosis upper Gl bleeding. is secondary and will usually be established at upper GI endoscopy (UGIE). Many units have Upper GI malignancy a major haemorrhage protocol with which you There is often a background of weight loss should be familiar. anorexia, early satiety or dysphagia; a palpable Pepticoksfree.co ulcer epigastric mass or signs of metastatic disease may rarely be evident. Peptic ulcer is the most common cause of upper GI bleeding (50%) and an important cause of massive Other uncommon causes haemorrhage. It is often accompanied by epigastric Congenital malformations of the vascular tree, pain. Important aetiological factors includemeb Helico- s re .com m oks e.g. Dieulafoy’s lesion, can produce major bacter pylori infection (95% of duodenal, 75% of haemorrhage. An aorto-duodenal fistula will gastric ulcers) and NSAIDs/aspirin. usually present with massive haematemesis – Gastritis/duodenitis suspect this if patient has had previous surgery for abdominal aortic aneurysm. Gastritis/duodenitis (30%) is typically accompanied by dyspepsia, epigastric discomfort and nausea. Most commonly, it is due to excess Rectal bleeding alcohol consumption or NSAIDs/aspirin. The majority of patients have a benign cause In acute rectal bleeding, assessment of bleed- Oesophagitis ing severity and adequate resuscitation take Thisoo is usually sfree due to comgastro-oesophageal reflux. precedence over diagnosis. The pattern of There may be a history of heartburn, indigestion bleeding guides the location. Anorectal bleed- or painful swallowing. eboing s typically e presents c m with intermittent episodes mebooks Gastrointestinal haemorrhage: haematemesis and rectal bleeding 151 Differential diagnosis of minor, fresh bright red bleeding during or abdominal pain and, often, systemic upset. after defecation, which is not mixed with the Endoscopy and biopsy of the lower bowel stools Distal colon bleeding is darker red and confirm the diagnosis; inflammatory markers may be partially mixed with the stools; proximal (CRP, faecal calprotectin) provide a useful guide colon bleeding is dark red and fully mixed with to disease activity. Perianal Crohn’s disease is stools.ooksfre Remember that large m volume upper GI or often associated with complex perianal fistulas. proximal colon bleeding can present with fresh booksf bright red bleeding (and shock). ebo sfreIschaemic colitis om Perianal disorders Ischaemic colitis tends to occur in older patients, typically resulting in severe lower abdominal These are a common cause of rectal bleeding pain associated with rectal bleeding. It results in all age groups. Bright red bleeding is often from occlusion of the inferior mesenteric artery, associated with other anorectal symptoms such which is usually due to situ thrombosis in ath- as discomfort, mucus discharge or pruritus. erosclerosis. (In contrast, acute embolus more Causes include haemorrhoids, fissure-in-ano, commonly affects the superior mesenteric artery perianal Crohn’s disease and anal cancer. Be territory.) aware that haemorrhoids can cause major bleeds. Always examine the anus of a patient Angiodysplasia (arteriovenous presenting with rectal bleeding: diagnosis is made malformation) byooksfree PR examination comand proctoscopy. Severe pain, especially during defecation, suggests These are degenerative vascular malformations anal fissure, and the patient will not tolerate and are an important cause of severe lower GI bleeding, predominantly in the elderly. Typical 15 PR examination. Always consider a mebooconcurrent free com meb proximal bleeding source. endoscopic features may be apparent but diagnosis is often challenging (CT angiography, Diverticular disease labelled red cell scan) and bleeding frequently Diverticular disease is the most common cause of recurs. severe acute rectal bleeding and typically occurs Other causes in older patients. Bleeding occurs due to erosion of a vessel in the neck of a diverticulum and is GI infections may cause bloody diarrhoea by mostly fresh blood; it may be life-threatening causing local invasion of the mucosa, usually with but stops spontaneously in 75% of patients. systemic upset. Other small intestinal sources of rectal blood loss include Meckel’s diverticulum Colorectal carcinoma o sfree.co (melaena) and intussusception (‘currant jelly’ Colorectal carcinoma is a common cancer in men bleeding) in young patients. Acute small bowel and women. Recent weight loss, tenesmus, a ischaemia may be associated with rectal bleeding change or alternating bowel habit or symptoms but the predominant feature is severe abdominal of colicky lower abdominal pain may bemeb present. pain sfre and the . patient m is severelymebooksf unwell. Small However, the presentation is frequently insidious bowel tumours are rare and present with intermit- with minimal symptoms. Polyps may also cause tent bleeding (may require capsule endoscopy). rectal bleeding. Diagnosis is made by colonic Radiation proctocolitis should be considered imaging (sigmoidoscopy/colonoscopy or CT colo- in any patient with a history of pelvic radiation, nography in patients who are unfit for endoscopic e.g. for prostatic or gynaecological malignancy; investigation ) most present within 2 years of radiotherapy. Colonic ulcer is an uncommon cause of Inflammatory bowel disease bleeding, usually related to use of NSAIDs Colorectal inflammation in ulcerative colitis or Rectal ulcers are poorly understood, typ cally Crohn’s disease may cause rectal bleeding. The occur in young adults and usually respond to passageook of frfrank blood com ± mucus and tenesmus conservative treatment (bulking agents and may occur in proctitis. Colitis produces bloody laxatives). Nicorandil is associated with oral, diarrhoea with intermittent cramping lower rectal and anal ulcers. ebooksf mebo s ree com Gastrointestinal haemorrhage: haematemesis and rectal bleeding 152 Haematemesis: overview

ABCDE, urgent FBC, U+E, LFTs, coagulation screen, cross match fre com 1 Resuscitation requirements assessed? (Boxeso 15.1 and re15.2) m Yes

Urgent UGIE Active bleeding, features of shock Yes 2 after adequate Final diagnosis or suspected variceal bleed? resuscitation

Yes Consider 3 Rockall risk scorec >0 (Table 15.1)? Final diagnosis inpatiente. UGIE No

Full clinical assessment

Yes 4 Background of alarm features? Consider upper GI malignancy UGIE

Haematemesis preceded by Yes 5 Probable Mal ory–Weiss tear forceful retching / vomiting? m

Consider gastritis / duodenitis / oesophagitis UGIEsfr if diagnosis omunclear or ongoing symptoms Gastrointestinal haemorrhage: haematemesis and rectal bleeding 153 Haematemesis: step-by-step assessment

Box 15.1 Resuscitation in acute haemorrhage First steps

• A+B before C: recheck airway frequently, especially if ↓GCS/vomiting. Give high concentration O2 • Getoks help: one r pair of hands is m not enough. If necessary call the medical emergency or cardiac arrest team Secure IV access and monitoring • 2 large bore cannulae in antecubital veins or equivalent • Central venous cannulation, e.g. femoral line if peripheral access difficult • Get expert help immediately if you cannotm obtain adequate oo access com • Urgent FBC, U+E, LFTs, coagulation screen and cross-match (inform blood bank) • Measure pulse, BP, RR, GCS and reassess peripheral perfusion every 10–15 min • Insert urinary catheter; monitor hourly urine output Resuscitate and reassess Early shock features (see Box 15.2) or any ongoing blood Advanced shock features (see Box 15.2) or ongoing major loss: blood loss: • 0.5–1 L stat of IV crystalloid or colloid • 1–2 L stat of IV crystalloid • 2 units of red cells if Hb <8 g/dL, ongoing bleeding or • use red cells as soon as available >2 L IV crystalloid or colloid given • consider O negative blood if significant delay in Reassessoksfr e com cross-matching (use group specific blood as soon as • If advanced shock features or major blood possible) loss on reassessment, resuscitate as per the Reassess adjacent column. • If ongoing advanced shock features or major blood • Otherwise, continue with treatment and discuss with loss, activate the major haemorrhage protocol: 15 haematologist if any of the following: m sfree.administer red cell concentrate (RCC)me and fresh o • known coagulopathy/anticoagulant therapy frozen plasma (FFP) and consider platelets and • INR >1.4 cryoprecipitate. • platelets <100 × 109/L • Seek specialist input, e.g. ICU, GI, surgical, as • fibrinogen< 1 g/L appropriate and discuss haemostatic support, with • ≥4 L IV fluid in any form haematologist.

Box 15 2 Clinical features of hypovolaemic shock Early Advanceds om • HR >100 bpm • Systolic BP <100 mmHg (or ↓40 mmHg from baseline) • Capillaryo refill r time (CRT) c > 2s • HR >120 bpm o • Narrow pulse pressure • RR >20 breaths/min • ↓Postural BP • Cold, mottled peripheries • Pale, sweaty, anxious, thirsty • Confused, lethargic, ↓GCS

Resuscitation requirements assessed? is profound. Remember that heart rate may be 1 (Boxes 15.1 and 15 2) misleading in patients on rate-limiting medications, e.g. beta-blockers, calcium channel blockers, or Resuscitation is the top priority. Use Box 15.1 as with fixed-rate pacemakers, and that compensa- a framework for evaluating resuscitation needs but tory vasoconstriction may not occur in patients on tailor your assessment to the individual. Monitoring vasodilators. In patients who present with fresh, red trends of the parameters in Box 15.2 provides haematemesis, the subsequent vomiting of ‘coffee far more information than a single ‘snapshot’ grounds’ or passage of black tarry stools may assessment and is essential for evaluating simply be a manifestation of the original bleed, but response to treatment. Do not rely exclusively further bright red haematemesis or haematochezia onooksfree.com this framework and you should be aware that implies continued active bleeding. ooksf patients may respond differently to haemorrhage: young patients may compensate until blood loss mebo sfree.com Gastrointestinal haemorrhage: haematemesis and rectal bleeding 154 Haematemesis: step-by-step assessment

Active bleeding, features of shock or assessment and observation; most need inpatient 2 suspected variceal bleed? UGIE to calculate the full score and establish the diagnosis. All pat ents with haematemesis accompanied by features of shock (see Box 15.2) or evidence of 4 Background of alarm features? ongoingook bleeding fre should com have an urgent UGIE after adequate resuscitation. Variceal bleeds have Request UGIE to exclude upper GI malignancy a high mortality (30–50%) and usually require if the patient has any of the following alarm urgent UGIE following resuscitation andmeboo correc- features: sfre m meb f tion of coagulopathy. Assume variceal bleeding in • weight loss any patient with known hepatic cirrhosis, clinical • anorexia or early satiety features of chronic liver disease (see Box 19.5, p. • dysphagia 176) or deranged LFTs with evidence of impaired • epigastric mass hepatic synthetic function (↑PT, ↓albumin). • lymphadenopathy • jaundice 3 Rockall risk score >0 (Table 15.1)? • age ≥50 years. In the absence of continued active bleeding, haem dynamic compromise or oesophageal Haematemesis preceded by forceful 5 retching/vomiting? varices, use a risk scoring system to guide the needooksfre for hospital admission com and UGIE. The Rockall With a characteristic history of Mallory–Weiss risk score comprises clinical (pre-endoscopic) tear, the diagnosis can often be made clinically, and diagnostic (post-endoscopic) elements. A without the need for UGIE. In other cases, a pre-endoscopic score of 0 predicts anmebo extremely diagnosis ree of gastritis co and oesophagitismebo may be low risk of death (0.2%) and rebleeding (0.2%), suggested by the history. Consider UGIE where but predicted mortality rises to 2.4% for a score there is no obvious explanation for symptoms of 1 and 5.6% for a score of 2. Admit patients or repeated haematemeses.m with a pre-endoscopy Rockallom score >0 for further Gastrointestinal haemorrhage: haematemesis and rectal bleeding 155 Haematemesis: step by-step assessment

Table 15 1 Rockall risk score

Score Variable 0 1 2 3 ooAge r<60 years m 60–79 years ≥80 years Pre endoscopy: Shock ‘No shock’, systolic ’Tachycardia’, ‘Hypotension’, Initial score criteria BP ≥100 mmHg, systolic BP systolic BP ebo pulse <100 bpm ≥meb100 mmHg, <100 mmHg com pulse ≥100 bpm Comorbidity No major Cardiac failure, Renal failure, comorbidity ischaemic heart liver failure, disease, any disseminated major comorbidity malignancy Diagnosis Mallory–Weiss All other Upper GI tract Post-endoscopy: tear, no lesion diagnoses cance Additional criteria identified and no ee c m for full score stigmata of recent haemorrhage Major stigmata None, or dark spot Blood in upper GI ooof recent only e. m tract, adherent haemorrhage clot, visible or spurting vessel 15 Gastrointestinal haemorrhage: haematemesis and rectal bleeding 156 Rectal bleeding: overview

1 Acute rectal bleed? fre com No Yes

ABCDE, PR examination, urgent FBC, U+E, LFTs, coagulation screen, cross-matchb 2 Resuscitation requirementsm bo assessed? (Boxes 15.1 & 15.2) m Yes

Yes 3 Suspectedo upper GI source? Assess as per haematemesis

No Admit; Yes Cancer / polyp / arteriovenous 4 High-risk bleed (Box 15.3)? colonic malformation / colitis / imaging diverticular disease No

Manage as outpatient unless other worrying features or ongoing rectale bleeding me r co

Full clinical assessment, PR examination, FBC

Cancer / polyp / arteriovenous Risk factors for major Yes Colonic 5 malformation / colitis / colorectal pathology? imaging ee. m diverticular disease No Yeso e 6 Clinical features of anal disorder? Likely haemorrhoids or anal fissure o No

Refer GI if persistent or troublesome symptoms

1 Acute rectal bleed? Resuscitation requirements assessed? 2 (see Boxes 15.1 and 15.2) Regard any prolonged, profuse or ongoing episode of bright red/maroon PR blood loss Make adequate resuscitation your top priority within the previous 24 hours as acute rectal Evaluate and address resuscitation requirements bleeding. Assess patients with melaena in the as described for haematemesis, step 1. same way as those with haematemesis (see 3 Suspected upper GI source? above).ooksf Where ee the cpredominant problem is bloody diarrhoea, evaluate as described on page Assume, initially, that melaena reflects upper 93. In the absence of acute bleeding, proceed GI bleeding and assess as ebdescribed for sf to step 5. meboohaematemesis sfree.c. Gastrointestinal haemorrhage: haematemesis and rectal bleeding 157 Rectal bleeding: step-by-step assessment

Brisk bleeding from the upper GI tract may haemodynamic instability despite resuscitation present with a fresh red PR bleed and implies or high transfusion requirements. severe, life-threatening haemorrhage. The diagnosis is straightforward if there is concomitant Risk factors for major 5 haematemesis but otherwise a high index of colorectal pathology? suspicionooksfre is essential. Proceed m with a working Refer the patient for urgent lower GI investiga- diagnosis of lower GI bleeding in patients without tion (usually colonoscopy) to exclude colorectal haemodynamic instability but suspect an upper cancer if any of the criteria in Box 15.4 is present. GI source in those with features of hypovolaemicmebo Also fre consider com lower GI endoscopicmeb assessment shock. If present, seek senior GI input and if the patient has: consider UGIE as the first-line investigation • systemic/extraintestinal features of following resuscitation especially if there are inflammato y bowel disease (see Box 9.3, any recent upper GI symptoms, e.g. epigastric p. 91) pain, or known/suspected oesophageal varices. • a history of pelvic radiotherapy • recent-onset, persistent bleeding when 4 High-risk bleed (Box 15.3)? the patient is ≥50 years or has a strong Consider non-admission or early discharge family history of colorectal cancer, e.g. a (with outpatient follow-up) if the patient has no first-degree relative< 45 years at diagnosis, high-risk features (see Box 15.2) or evidence of or two or more first-degree relatives. ongoingooksfre bleeding – especially com if there is evidence of a benign anal disorder. Do not discharge a 6 Clinical features of anal disorder? patient without making a clear decision as to the 15 likely cause of bleeding. Admit any patientmeboo with Perform ree. careful omrectal examinationme and ookproctos- risk factors for uncontrolled or recurrent bleeding copy in all patients to look for an anal disorder. (see Box 15.3). Once adequately resuscitated Do not forget to look for anal cancer. If a benign and clinically stable, arrange colonic imaging anorectal pathology one is identified, provide to establish the site and cause of bleeding. reassurance but refer the patient for outpatient The majority of rectal bleeding settles with colorectal evaluation if there is diagnostic doubt conservative management. Colonoscopy is most or symptoms persist despite conservative informative when the bleeding has stopped. CT management. angiography requires active ongoing bleeding of Arrange further GI investigation and/or referral a sufficient rate to be detected. in all patients without an obvious anorectal cause, Seek urgent senior surgical input in any in whom bleeding persists or recurs. patientooksfree with continued com active bleeding, ongoing bo sfree com Box 15.4 High-risk features for colorectal cancer in patients with rectal bleeding Box 15.3 Risk factors for adverse outcomes in me ks acute lower GI bleeding • Rectal bleeding ≥4 weeks with change of bowel habit (↓ or ↑frequency or alternating bowel habit) • Any haemodynamic instability • Tenesmus • Initial haematocrit <35% or need for red blood cell • Palpable rectal or abdominal mass transfusion • Significant we ght loss, e.g.≥ 6 kg • Any visualized red blood PR • Previous excision of colorectal cancer or polyps • INR >1.4 or current anticoagulant use (warfarin, • History of inflammatory bowel disease novel oral anticoagulants, aspirin/NSAID) • Family history of colorectal cancer, polyps or • Significant comorbidity, e.g. cardiorespiratory, renal, inheritedfree.co colorectal cancer syndromes hepatic impairment or current hospital inpatient • Age >50 years without anal symptoms, e.g. • Ageoksfree. >60 years om discomfort, itching, lumps, prolapse Haematuria k 16oksfre

Haematuria, or blood in the urine, may be visible or other stone types (10%) comprising urate (macroscopic) or non-visible (microscopic), (excessive meat consumption or chemotherapy) detected only by dipstick testing or urine and struvite (staghorn calculi, associated with microscopy. Visible haematuria strongly suggests chronic urinary tract infection) and cysteine (rare significant urological disease and always requires inherited disorders). Ureteric obstruction typically further evaluation. Non-visible haematuria (defined presents with renal ‘colic’ – acute, severe loin in the UK as ≥1+ haematuria on 2 out of 3 urine pain radiating to the groin ± genitalia that builds to dipstick tests) is a common incidental finding in a crescendo of intensity over a few minutes, often asymptomatic patients and the challenge lies accompanied by restlessness (a key difference in differentiating benign causes from serious to peritonism where patients lie still) nausea pathology.ooksfree com and vomiting. The pain persists until obstruction It is important to differentiate haematuria from: is relieved. Visible haematuria may occur and • contamination in menstruating women dipstick is positive in 90% of cases. • other causes of urine discolourationmebo sfree.com mebooksf (Box 16.1). Bacterial urinary tract infection Women who are sexually active, pregnant, or are Tumours postmenopausal are prone to UTIs. UTIs in men 60% of renal cancers and 80% of bladder <50 years old are uncommon. Sexually transmit- cancers present with haematuria. Both tumour ted infections should be specifically investigated types are rare below the age of 40. Associated in this cohort. Common clinical features of lower features may include loin pain, abdominal mass UTI include frequency, dysuria, urgency, malodor- and systemic upset (renal cancer) or lower urinary ous urine and visible or dipstick haematuria In tract symptoms (LUTS), e.g. dysuria, frequency, acute pyelonephritis (with ascending infection urgency and hesitancy (bladder cancer). to the renal tract) there is typically loin pain, However,ooksfree.c in the majority of cases, haematuria fever, rigors and significant systemic upset. UTI is the sole symptom and examination is normal. is likely if a dipstick test is positive for either Risk factors are listed in Box 16.2. Around 12% nitrite or leucocyte esterase, but is unlikely if both of prostate cancers present with haematuriamebo are sfree.com absent. A pure growth ofmebooksf >105 organisms/ (more commonly microscopic). mL of fresh MSU confirms the diagnosis and permits sensitivity testing. A subset of patients Stones (particularly women) develop recurrent UTIs. It is Stones may cause obstruction anywhere along important to rule out renal tract stones (sources the urinary tract, though typically at sites of nar- of chronic infection), incomplete bladder emptying rowing, e.g. the pelvi-ureteric junction, pelvic (e.g. prostatic hypertrophy in men) and diabetes. brim and vesico-ureteric junction. Those in Rarely, a renal tract malignancy may present the renal pelvis or bladder may remain asymp- with recurrent UTIs due to necrotic tissue with tomat c for years and present incidentally with secondary infection. dipstick haematuria. Stones may be formed from Atypical infection calciumooksfree.co oxalate (80%, associated with hypercal- ciuria), from calcium phosphate (10% linked to Urinary tuberculosis (TB) may cause visible renal tubular acidosis and hyperparathyroidism), haematuria ± other urinary tract symptoms, mebo sfree com meb f Haematuria 159 Differential diagnosis

Box 16.1 Causes of urine discolouration other Box 16.2 Risk factors for urinary tract cancer than haematuria • Smoking Orange • Occupational exposure to chemicals/dyes (benzenes, • Concentratedo s r normal urine, e.g. dehydration aromatic amines) • Conjugated bilirubin • Irritative voiding symptoms • Rifampicin, isoniazid (also in tears/saliva/sweat), • Previous pelvic irradiation Senna e• Cyclophosphamide fr o exposure • Rhubarb, carrots • Schistosomiasis – increases riskm of bladder o • Any cause of red urine squamous cell carcinoma (rather than transitional cell carcinoma) Red • Chronic inflammation of other causes • Myoglobinuria (rhabdomyolysis) • Porphyrins • Beetroot, blackberries • Chlorpromazine metronidazole, nitrofurantoin, warfarin (glomerulonephritis). Associated features include • Mercury and lead poisoning (rare) proteinuria, hypertension, oedema and renal Brown failure. Those most likely to result in haematuria • Conjugated bilirubin include anti-glomerular basement membrane • okMuddy brown’ fr urine e.c – red cell m casts in acute tubular disease (Goodpasture’s syndrome), small-vessel necrosis (ATN) vasculitis, e.g. Wegener’s granulomatosis, post- • Homogentisic acid (in alkaptonuria or ochronosis) estreptococcal sfre glomerulonephritis, m SLE and Black (rare) immunoglobulin A (IgA) nephropathy.mebooksf In IgA • Drugs: L-dopa nephropathy there may be intermittent episodes 16 • Phenol and copper poisoning of visible haematuria coinciding with upper res- Blue/Green piratory tract infections. Diagnosis of glomerular • Drugs/dyes, e.g. propofol, fluorescein, methylene blue disease is made by renal biopsy. Inherited renal • Pseudomonal urine nfection disorders, such as Alport’s syndrome and adult polycystic kidney disease, may also present with visible or non-visible haematuria. pulmonary manifestations and constitutional Other causes upset Urinalysis is positive for WBC but routine culture is negative. Diagnosis requires a fresh • Trauma: direct urethral trauma; blunt or early morning urine sample for acid-/alcohol-fast penetrating abdominal/pelvic injury. bacilliooksfr and TB culture. coPainless visible haematuria • Iatrogenic: renal biopsy, transurethral toward the end of voiding is the most common resection of prostate, cystoscopy, urinary initial presenting feature of Schistosoma haema- catheterisation. eboo tobium infection, most commonly acquiredmebo in • Vascular: f ee.com arterio-venous malformations; Egypt/East Africa, e.g. by swimming in freshwater renal vein thrombosis. lakes. Clues to diagnosis include travel history • Coagulopathy. and eosinophilia. Non-visible haematuria is also • Renal cysts common in bacterial endocarditis. • Acute tubular necrosis. • Thin basement membrane disease Renal disease (common, benign, often familial). Haematuria may occur as a result of disorders • Loin pain-haematuria syndrome. that disrupt the glomerular basement membrane • Extremefree exertion, co e.g. distance running. sfre com Haematuria 160 Overview

Full clinical assessment, urinalysis, U+E f e

Visible, symptomatic or No 1 Transient or spurious haematuria persistent haematuria? o

Yes Imaging + Yes 2 Renal colic? Likely renal stone further investigations

Evidence of UTI or recent instrumentation Yes Traumatic Treat / 3 of urinary tract? haematuriae / UTI reassess

Visible haematuria, LUTS, age >40 or Yes Imaging and 4 Anatomical lesion ohigh-risk efeatures? c cystoscopy

GFR, proteinuria, BP or clinical Yes Refer to 5 ↓ ↑ Renal disease suspicion of renal disorder? Nephrology

Thin basement membrane disease / arteriovenous malformation / stone / cyst 6 Monitor regularly for new or recurrent visible haematuria / lower urinary tract symptoms / proteinuria / ↓GFR fre sfre m Haematuria 161 Step-by-step assessment

Visible, symptomatic or Consider infective endocarditis if there is fever, 1 persistent haematuria? splinter haemorrhages, predisposing lesion or new murmur. Consider other causes of urine discoloration (see Do not attribute haematuria to anticoagulation Box 16.1) that may mimic visible haematuria. Use or antiplatelet treatment alone without further dipstickook testing fre (at least 1+) on a freshly voided investigation. sample to detect non-visible haematuria; send urine for microscopy only in uncertain cases, e.g. Visible haematuria, LUTS age >40 or suspicion of myoglobinuria. Ask specificallymebo about 4 sfrehigh-risk co features? m ook f episodes of visible haematuria in any patient with a positive dipstick test. Repeat dipstick testing In the absence of renal colic and following at a later date if the test was performed during treatment/exclusion of transient causes of menstruation, shortly after strenuous exercise haematuria, you must exclude cancer if any of or following urinary catheterization. the following features is present: Evaluate further for haematuria as described • visible haematuria below if the patient has: • LUTS • age 40 years • visible haematuria ree.com> • high-risk features for urinary tract cancer • non-visible haematuria with loin pain or (see Box 16.2). LUTS • 2oksfree.com out of 3 positive dipstick tests for Refer such patients to Urology for further haematuria at different times. investigation, e.g. renal USS ± IVU or CT urogram and cystoscopy. bo 2 Renal colic? ↓GFR, proteinuria, ↑BP or clinical The combination of haematuria and renal colic 5 suspicion of renal disorder? 16 (see above) suggests ureteric obstruction, usually from a stone or, less commonly, from clots or Refer to a nephrologist for further evaluation ± sloughed renal papilla. Confirm the presence and renal biopsy if any of the following features is position of a stone with a CT of the kidneys, present: ureters and bladder (CT KUB). Dipstick the urine • proteinuria, e.g. albumin : creatinine ratio for infection (nitrites and leucocytes). Observe ≥30 closely for decreased urine output and symp- • renal impairment (GFR <60 mL/min) • ↑BP in a patient <40 years toms of infection. Perform further investigations • connective tissue disease, e.g. SLE to establish an underlying cause, e.g. chemical • family history of Alport’s syndrome/adult composition of stone; plasma calcium/phosphate/ polycystic kidney disease uricooks acid. Refer ree.com to Urology for further management. • episodes of visible haematuria coinciding with upper urinary tract infections. Evidence of UTI or recent instrumentation eb o 3 of urinary tract m boo ree. om 6 Likely benign cause. Monitor periodically. Refer to Urology if visible haematuria follows Isolated microscopic haematuria is common and surgical or invasive procedures of the renal tract, usually due to benign disease, e.g. thin basement e.g. renal biopsy, ureteroscopy, transurethral membrane disease. Provided that the above resection of prostate, or abdominal/pelvic/ causes have been excluded, reassure patients genital trauma. that further investigation is not necessary but The absence of leucocytes and nitrites on continue to monitor (e.g. annually) for features dipstick effectively excludes UTI in most cases. such as new urinary tract symptoms, visible If dipstick testing is positive or there is strong haematuria, proteinuria or renal impairment. clinical suspicion, send a midstream urine sample ksf for culture; treat confirmed infection then recheck forooksfre non-visible haematuria. com o sfree.com Haemoptysis ks 17ok e

Haemoptysis, coughing up blood, requires or blood-streaked sputum for ≥2 weeks strongly thorough evaluation to exclude serious pathol- suggests malignancy. Massive haemoptysis may ogy such as lung cancer, tuberculosis (TB) and occur with erosion of tumour into a large vessel. pulmonary embolism (PE); many patients will Weight loss, recent-onset cough, finger clubbing require detailed imaging and specialist assess- and lymphadenopathy are well-recognized fea- ment. Massive haemoptysis (>500 mL/24 hours) tures CXR may show a variety of abnormalities may be life-threatening. (Box 17.1) but is sometimes normal.

Respiratory tract infections Pulmonary embolism Respiratory tract infections (RTIs) are the most Frank haemoptysis occurs due to pulmonary commonook cause free.com of haemoptysis. They typically infarction, usually accompanied by sudden-onset cause blood-stained purulent sputum rather than dyspnoea and pleuritic pain. A pleural rub or frank blood, and have associated features such signs of deep vein thrombosis (DVT) are present as cough, fever and dyspnoea. In acutemebo bronchi- in a fminority ee.com of cases. CXR maymeboo show a wedge- tis, mucosal inflammation can rupture superficial shaped peripheral opacity or pleural effusion, blood vessels; patients with chronic obstructive but is most often normal. pulmonary disease may have haemoptysis during an infective exacerbation. Pneumonia may cause Bronchiectasis frank haemoptysis, especially with invasive There is typically a background of chronic cough bacteria, e.g. Staphylococcus aureus, Klebsiella with copious foul-smelling purulent sputum. spp. or fungi; patients are usually profoundly Finger clubbing and coarse inspiratory crackles unwell. Mycetoma, lung abscess and TB may may be evident on examination. cause massive haemoptysis. More commonly, TB produces chronic cough with small haemoptyses Other causes fever, night sweats, weight loss and characteristic ooksfree.com Pulmonary oedema may cause pink, frothy CXR changes. bosputum sfree.co but dyspnoea is almost always the domi- Lung tumours nant complaint. Other causes include pulmonary hypertension (especially associatedmebo with mitral f Haemoptysis is common in primary bronchial stenosis), coagulopathies, foreign body inhalation, tumours but rare in secondary lung tumours. Risk chest trauma, Wegener’s granulomatosis and factors are smoking (especially ≥40 pack-years) Goodpasture’s syndrome.m and age >40 years; repeatedom small haemoptyses Haemoptysis 163 Differential diagnosis

Box 17.1 The CXR in lung cancer

Common abnormalities on CXR in patients with lung cancer • consolidation (see Figs 12.3 and 12.4, p. 118) that include: fails to resolve or recurs in the same lobe. • aok discrete mass r (see Fig. 17.1) or cavitating lesion (see In a substantial proportion of cases, the CXR is normal. Fig. 17.2) • collapse of a lobe secondary to tumour obstruction (see bo k Figs 17.3 and 17.4) • unilateral hilar enlargement or pleural effusionme (see Fig. o o 12.6, p. 119)

Fig. 17.1 A solitary lung mass (From Douglas G, Nicol Fig. 17.2 A cavitating lung lesion. (From Corne J, 17 F, Robertson C. Macleod’s Clinical Examination, 12th edn. Pointon K. Chest X-ray Made Easy, 3rd edn. Edinburgh: Edinburgh: Churchill Livingstone,om 2009.) Churchill Livingstone,om 2010.)

Fig. 17.3 Left lower lobe collapse. The changes in left lower lobe collapse may be subtle and easily overlooked; Fig 17.4 Right upper lobe collapse. Note the right note the triangular opacification behind the heart, giving upper zone opacification, loss of volume in the right lung the appearance of an unusually straight left heart border field and tracheal deviation. (From Corne J, Pointon K (From Boon NA, Colledge NR, Walker BR. Davidson’s Chest X-ray Made Easy, 3rd edn. Edinburgh: Churchill ooksfrPrinciples & Practice of Medicine, 20th edn. Edinburgh: Livingstone, 2010.) ook Churchill Livingstone, 2006.) b ks Haemoptysis 164 Overview

ABCDE fre No 1 True haemoptysis? Consider haematemesis / epistaxis

Yes

Yes 2 Massive haemoptysis? Resuscitation + emergency treatmentm

Full clinical assessment, CXR, FBC, coagulation screen

3 Typical features of RTI Treat and reassess fre co

Clinical suspicion of pulmonary Yeos re 4 Assess for PE Confirmed PE embolism (PE)? (Fig. 12.7, p. 120) No CT chest + Yes Lung cancer / 5 Lung cancer risk features? respiratory parenchymal disease opinion No

Consider other causes CT ± specialist respiratory input if: 6 1 haemoptysis persistent or recurrent 2 agefree. > 40 years or smoker 3. CXR abnormal

1 True haemoptysis? 2 Massive haemoptysis? A clear history of blood being coughed up or Bleeding is difficult to quantify clinically but mixed with sputum reliably indicates haemoptysis. estimate the volume and rate of blood loss, Blood that suddenly appears in the mouth e.g. by direct observation, with a graduated without coughing suggests a nasopharyngeal container. The major risk is asphyxiation through origin; ask about nosebleeds and look for flooding of alveoli or airway obstruction. Use epistaxis or a bleeding source within the mouth. the ABCDE approach (Chapter 2) and seek Blood originating from the GI tract is typically immediate anaesthetic help if any of the following dark,ooksfree.co acidic (test pH) and may contain food is present: particles; blood that is frothy, alkaline and bright • large blood volume, e.g. >50 mL red or pink suggests a respiratory source. in 1 hour e oksf mebo sfree. om Haemoptysis 165 Step-by-step assessment

• airway compromise if smoker >40 years) for further assessment ± • haemodynamicfre instability. bronchoscopy even if CT is normal. Consider other causes/ 3 Typical features of RTI? 6 further investigation Haemoptysis for <1 week with purulent sputum Perform a coagulation screen in any patient on and/or fever suggests acute RTI; assess as anticoagulant therapy, with a history of bleeding described on page 123 and arrange follow-up disorder or with evidence of bleeding elsewhere, review after treatment to ensure that haemoptysismebo or if frethere is no co clear alternativemeb cause. has resolved. Also arrange a follow-up CXR Chronic cough with daily mucopurulent sputum within 6 weeks for any patient with radiographic production or persistent coarse inspiratory consolidation to ensure resolution. crackles suggests bronchiectasis – confirm the diagnosis with high-resolution thoracic CT. Clinical suspicion of Consider TB if any of the following features 4 pulmonary embolism? is present: PE is easily forgotten and easily missed. Physical • prior residence in an endemic area and CXR findings are unreliable so maintain a • immunosuppression (HIV, malnutrition, high index of suspicion. Consider PE and assess general debility) as shown in Fig. 12.7 (p. 120) if haemoptysis is • suggestive clinical features, e.g. night acuteooksfr and accompanied e c by m any of the following: sweats, fever, weight loss • rapid-onset pleuritic pain or dyspnoea • suggestive CXR findings, e.g. a cavitating • symptoms or signs of DVT ebolesion ree (seecom Fig. 17.2), persistent • specific risk factors, e.g. active malignancy, consolidation, miliary TB. me o recent surgery If suspected, obtain ≥3 sputum samples for • new-onset frank haemoptysis with no acid-fast bacilli and mycobacterial culture, and 17 other obvious cause (e.g. no typical seek expert respiratory input. features of RTI). Exclude Goodpasture’s syndrome and Wegener’s granulomatosis if there is evidence of renal involvement, e.g. haematuria, proteinuria, 5 Lung cancer risk features? ↓GFR: check for anti-glomerular basement You must exclude lung cancer, even if another membrane and anti-PR3 (c-ANCA) antibodies diagnosis appears more likely, in any patient with and seek renal input. persistent haemoptysis (>2 weeks) and: Arrange an ECG if the patient has: • ooksf history of cigarette e smoking om • a history of rheumatic fever • weight loss, finger clubbing, Horner’s • exertional dyspnoea, orthopnoea, syndrome, cervical lymphadenopathy paroxysmal nocturnal dyspnoea • mass, cavitating lesion, persistentm • sfree.com signs of mitral stenosis, emeb g. loud S1, sf consolidation/collapse or unilateral hilar low-pitched mid-diastolic murmur adenopathy/pleural effusion on CXR • signs of pulmonary hypertension, e.g. loud (see Box 17.1). P2, right ventricular heave. Thoracic CT is a useful first-line investigation If the cause is still unclear, consider CT and and may reveal a tumour or other cause for specialist respiratory input – especially if >40 haemoptysis, e g. bronchiectasis; but refer years, smoking history, ongoing symptoms or the patient to eea respiratory co specialist (urgently any CXR abnormality. f ee com Headache 18oksfre

Headache is extremely common and usually Vertebrobasilar dissection: may cause acute- benign. The challenge is to identify the small onset occipital/posterior neck pain with brainstem minority of patients with serious underlying signs and symptoms. pathology and those with disorders that respond to specific treatments. Meningitis Classically presents with headache, fever and Subarachnoid haemorrhage (SAH) meningism. The onset of headache is typically The headache is typically of sudden onset over hours rather than sudden. Viral meningitis (reaches maximal intensity within a few seconds), is usually self-limiting, with headache the most occipital and very severe. Distress and photo- prominent clinical feature. Bacterial meningitis phobiaooksfr are common e c but m neck stiffness may is life-threatening; presenting features include take hours to develop. Large bleeds may be ↓GCS, signs of shock (see Box 30.1, p. 267), complicated by ↓GCS, seizure or focal neurologi- purpuric rash (see Fig. 27.13, p. 244) and focal cal signs. Most cases are evident onmeb CT but LP neurological sfree signs. om LP (see Clinicalmeb tool, p. oksf 170) is required in suspected cases with normal CT. is helpful in the diagnosis but must not delay IV Benign thunderclap headache mimics the antibiotics therapy. Beware atypical presentations headache of SAH but investigation reveals no in immunocompromised, pregnant or alcoholic evidence of an intracranial vascular disorder. It patients. may be associated with coitus or exercise. Migraine Other vascular causes Recurrent severe headaches lasting several hours Intracerebellar haemorrhage: typically presents to a few days, usually accompanied by photo- with acute-onset headache, nausea, vomiting, phobia, phonophobia and nausea ± vomiting. In dizziness and ataxia ± ↓GCS. one-third there are associated focal neurological ooksfree.comSpontaneous intracerebral or intraventricular features – an ‘aura’ (Box 18.1). The headache haemorrhage: the onset of headache is usually is typically intense, throbbing and unilateral. The over minutes to hours accompanied by a focal patient usually prefers to lie in a quiet, darkened neurological deficit± ↓GCS. mebroom. sfr Triggers e include om cheese,mebooksf chocolate, alcohol Chronic subdural haematoma: may present and oral contraceptives. A first attack aged> 40 insidiously with headache +/− confusion and/ years is uncommon. or balance problems The headache may be exacerbated by straining, bending or exercise. Cluster headache At least one quarter of patients have no clear This refers to severe, unilateral, retro-orbital history of head trauma so have a high index of headache with restlessness, agitation and suspicion particularly in older patients or those ipsilateral lacrimation, conjunctival injection taking anticoagulants. and rhinorrhoea. Attacks are short-lived (15–90 Cerebral venous thrombosis: headache is minutes) but occur frequently and repeatedly common but variable, e.g. ‘thunderclap’, throb (often at the same time each day) in ‘clusters’ bing,ooksfree ‘band-like’, as are com associated features, e g. lasting days to weeks; these are separated by nausea, vomiting, seizures, cranial nerve palsies, months without symptoms. The male to female hemiparesis, ataxia and ↓GCS. eboratio sfree is 5 : 1. com ebooksf Headache 167 Differential diagnosis

young women taking the oral contraceptive pill, Box 18.1 What constitutes a migraine aura? or secondary to an intracranial space-occupying lesion. In the latter case, there may be focal Auras are focal neurological phenomena that precede neurological signs, change in personality or new- or accompany a migrainous headache. They occur in 20–30%ok of rpatients, usually developing gradually onset seizures. Headache tends to be worse over 5–20 minutes and lasting <60 minutes. Most are in the morning and on lying flat, coughing or visual but they may also be sensory or motor. Common straining. There may be associated vomiting, examples include: eboften s rewithout nausea o +/− papilloedema. • ‘fortification spectra’: shimmering zigzag lines that me ooksf move across the visual field Sinusitis • flashing lights or spots This causes a dull, throbbing headache associ- • temporary loss of vision • numbness/dysaesthesia on one side of the body ated with facial pain over the sinuses. It tends • expressive dysphasia. to be worse on bending forward. There are invariably associated nasal symptoms, e.g. congestion or discharge. Sinusitis lasting >8 Temporal arteritis (giant cell arteritis) weeks requires CT to confirm the diagnosis. A large vessel vasculitis, closely associated with Medication overuse headache polymyalgia rheumatica, more common in women A common cause of chronic frequent head- and unusual in patients <50 years. Clinical ache (often daily) caused by excessive use of features include localized headache (temporal/ ooksf e o analgesics, ergotamines or triptans. Treatment of occipital), scalp tenderness, jaw claudication, choice is withdrawal of the overused medication. visual loss, constitutional upset (malaise, night sweats, pyrexia, weight loss), and anmebo abnormal Tension sfree headache com me oo temporal artery (inflamed, tender, non-pulsatile). The headache is usually bilateral (often general- ESR/CRP are almost always raised. The potential ized or frontal) and described as ‘dull’, ‘tight’ or for rapid-onset irreversible visual loss necessitates ‘pressing’ in nature Unlike migraine, nausea and urgent treatment with steroids. Temporal artery 18 photophobia are uncommon and the patient can biopsy may confirm the diagnosis but should often continue with normal activities. not delay steroid treatment. Other causes Acute glaucoma • Carbon monoxide poisoning. Acute glaucoma, an ophthalmological emergency, • Hypercapnia. occurs due to a sudden increase in intraocula • Drugs: vasodilators, e.g. nitrates, pressure. The typical patient is long-sighted, ‘recreational’ drugs, e.g. solvents middle-agedooksfr or elderly, e com and presents with peri- • Trigeminal neuralgia (brief, repetitive orbital pain (± frontal headache), nausea and episodes of intense shooting/stabbing/ vomiting, blurred vision with halos around lights ‘electric shock’-like pain in II and III divisions and conjunctival injection. Urgent ophthalmologymeboo free.com meb of trigeminal nerve). referral is mandatory. • Trauma: extradural haemorrhage, subdural Raised intracranial pressure haemorrhage, concussion.m May occur as a primary disorder (idiopathic intracranial hypertension) especially in overweight e.com Headache 168 Overview

ABCDE, CNS and eye examination f e 1 First or worst’ presentation?

Yes IV antibiotics + Yes 2 Any features of meningitis? urgent Meningitis m investigation m No

Suspect acute intracranial Yes Immediate 3 Intracranial lesion pathology?co CT brain No abnormality: Re-evaluate No +/- LP / MRI / neuro input

Meets criteria for ‘sudden-onset’ Yes CT brain 4 Subarachnoid haemorrhage headache? ± LP (or alternative diagnosis

SAH excluded: likely benign No b ok cause

Yes Ophthalmology 5 Suspect acute glaucoma? review Acute glaucoma

ESR >50 Age >50 years + any features of Yes 6 or strong Likely temporal arteritis temporal arteritis (Box 18.3) clinical suspicion?e Nor e.cNo m

Full clinical assessment

Yes Neuro- 7 Red flag features (Box 18.4)? Intracranial cause imaging e No

Yes 8 Frontal headache + nasal symptoms? Likely sinusitis

Features of primary headache Yes Migraine / cluster headache / 9 d sorderfree (Table 18.2)? m tension-type headache No

Consider temporal arteritis in patient >50 years with any persistent headache Review medication regimen Outpatient Neurology referral if persistent troublesome symptoms m b ee Headache 169 Step-by-step assessment

1 ‘First or worst’ presentation? SAH may also present with severe headache and meningism, but is less likely if the headache Acute severe pathology is less likely in patients onset was not sudden (see below). with recurrence of a longstanding problem than If you suspect meningitis, take blood cultures in patients with a first presentation of headache. and throat swabs and give IV antibiotics imme- However,ooksf patients e with a pre-existing headache diately. If there are no contraindications, perform disorder, e.g. migraine, may also present acutely LP for CSF analysis (see Clinical tool). If you with another diagnosis such as SAH. If a patient suspect raised intracranial pressure, perform CT with chronic headaches presents withmebo a new prior sfre to LP. It cois difficult to distinguishmebook viral from f headache that is markedly different in severity early bacterial meningitis clinically, so manage or character to normal, assess it as new-onset as bacterial meningitis pending CSF analysis. headache. 2 Any features of meningitis? 3 Suspect acute intracranial pathology? Identifying patients with bacterial meningitis is the Arrange immediate neuroimaging to exclude top priority to allow rapid, potentially life-saving, life-threatening intracranial pathology, e.g. antibiotic treatment. Patients may lack classical haemorrhage or space-occupying lesion wi h features but, in almost all cases, there will be mass effect, if any of the following is present: at least one of: • ↓GCS • focal neurological signs • feveroksfree (≥38° C) c • rash (not always petechial) • new-onset seizures • signs of shock (see Box 30.1, p. 267) • history of recent head injury • acute-onset headache, e.g. over mhours with • sfree. anticoagulation om or coagulopathy.m sf meningism (Box 18.2).

Box 18.2 Meningism? 18 Meningism (neck stiffness, photophobia, positive Kernig’s indicate neck stiffness. To test for Kernig’s sign, flex one of sign) denotes irritation of the meninges. To test for neck the patient’s legs at the hip and knee with your left hand stiffness, lie the patient supine with no pillow, place your placed over the medial hamstrings. Extend the knee with fingers behind their head and gently attempt to flex the your right hand maintaining the hip in flexion (Fig. 18.1B). head until the chin touches the chest (Fig. 18.1A); firm Resistance to extension by spasm in the hamstrings ± resistance to passive flexion and rigidity in the neck muscles flexionsfree.c of the other leg indicates a positive test. ksfree.c

A B

Fig. 18.1 Testing for meningeal irritation. Headache 170 Step-by-step assessment

Clinical tool LP and CSF interpretation Contraindications to LP in the CSF. If there is any possibility of bacterial • Infected skin over the needle entry site. meningitis, treat the patient with antibiotics pending • Radiologicaloksfre evidence coof raised intracranial pressure further investigation, e.g. blood/CSF culture • Clinical suspicion of raised intracranial pressure: • If there is a ↑lymphocyte count, send CSF for viral ↓GCS, focal neurological signs, papilloedema new PCR, including herpes and enterovirus seizures. e o • Symptoms and signs in tuberculous meningitis are • Coagulopathy or platelets <50 × 109/L. often mild or obscure – consider itm if the patient b has o • Severe agitation and restlessness. immunocompromise or is from an endemic TB region, especially if the CSF results suggest the diagnosis (see CSF interpretation above). If suspected, send CSF for acid-fast bacilli and mycobacterial PCR and culture. Routine interpretation of CSF results includes (Table 18.1): • Non-infective disorders can produce a lymphocytic • opening pressure (supine position) picture, including lupus, sarcoidosis and malignant • protein mening tis. Check autoantibodies and discuss with • glucose (always compare with blood glucose) Rheumatology if there are any other suggestive • cell count features. Additional tests, e.g. culture, PCR, oligoclonal bands, may • A difficult procedure may result in a ‘traumatic tap’, i.e be required in some circumstances. red cells in the CSF. This can complicate interpretat on ksfree co of the WBC. A rule of thumb is that 1 white cell Additional points to consider per 1000 red cells is normal. However, if the CSF • Early bacterial meningitis may be mistaken for viral picture is unclear, then the clinical history mustbo be k meningitis as there is a predominance of lymphocyteseb sfree.comtaken into account. Headache 171 Step by-step assessment /L) 6

s 10 ove for r co : often in thousands Red cells ( × 0 ↑ 0 0 0 0 but + xanthochromia (haem breakdown product) 0 /L) 6 10 100 > ve 1 is + Neutrophils ( × 0 0 0 May be 0 in very early stages 0 0 Usually ≥ 0 /L) s6 com 10 as a cause ↑ neutrophils but 50 > ve red cel s, then 1 white : usually < 50 5 is + 5 Lymphocytes ( × 0; if ↑ cell per 1000 red cells is normal of aseptic meningitis 0 Occasionally 100% > 0 > Usually ↑ may be predominant cell type in early stages < me oo 50% 18

f e .c sf . 60% of blood glucose 60% of blood glucose 60% of blood glucose but > 30% of blood glucose 60% blood glucose 50% of blood glucose 60% of b ood glucose CSF glucose (mmol/L) > > < < > < > 3–5 1000 > 100 : may be may : or normal ↑ : may be > CSF protein (mg/L) ↑ ↑ ↑ ↑ ↑ ↑ 200–450 O 2 cm H

or normal or normal or normal Opening pressure 5–18 ↑ ↑ ↑ ↑ ↑ ↑ Interpretation of CSF results o e c Table 18.1 Condition Normal Subarachnoid haemorrhage Viral meningitis TB meningitis Late subarachnoid haemorrhage Vasculitis Bacterial meningitis e oo Headache 172 Step-by-step assessment

LP may be required to exclude meningitis or SAH if CT does not yield a diagnosis and no Box 18.3 Features suggesting temporal arteritis alternative cause is apparent, e.g. toxicity, • Pain localized to temporal or occipital region metabolic derangement. Review the presentation • Inflamed, thickened, pulseless or tender temporal and, if appropriate, evaluate for seizure (p. 276), artery comaooksfre (see Ch. 7) or ‘Limb co weakness’ (see Ch. 22). • Scalp tenderness Seek urgent Neurology input if the cause remains • Jaw claudication • Visual loss (may be temporary initially) unclear. ebo fr • Constitutional symptoms: fever, malaise, fatigue, night sweats, weight loss me o Meets criteria for ‘sudden-onset’ 4 • Symptoms of polymyalgia rheumatica (proximal pain, headache? stiffness, etc.) Exclude SAH in any patient with a severe ‘first or worst’ headache that reaches peak intensity within 5 min of onset and persists for >1 hour. Box 18 4 Red flag features Headache in SAH may not be instantaneous • New-onset headache/change in headache in patients in onset but almost always reaches maximal over 50 years intensity within 5 min and rarely resolves in <1 • Focal CNS signs, ataxia or new cognitive or hour In these circumstances, no clinical features behavioural disturbance can reliably rule out the diagnosis so neuroimag- • Persistent visual disturbance • Headache that changes with posture or wakes the ing ± CSF analysis is mandatory. CT has almost booksfr e.co patient up 100% sensitivity for SAH when performed within • Headache brought on by physical exertion 6 hours on a contemporary multi-slice scanner • Papilloedema and reported by a qualified radiologist.mebo Beyond • New-onset re . headache in a patientmebo with HIV, active 6 hours, if the CT is normal, then LP, at least malignancy or immunocompromised 12 hours from the onset of headache, must be performed to look for xanthochromia; its absence highly likely. In these circumstances, or where effectively excludes SAH. The major differential clinical suspicion is high, e.g. >2 features from diagnosis is benign thunderclap headache; Box 18.3, start steroid therapy immediately. A however, all sudden-onset severe headaches prompt response to steroids essentially confirms should, ideally, be discussed with a neurologist. the diagnosis, though, ideally, temporal artery biopsy should be performed within 2 weeks of 5 Suspect acute glaucoma? starting steroids. Acute glaucoma is sight-threatening. Request urgento kOphthalmology free.com review if the patient has 7 Red flag features (Box 18.4)? acute-onset headache (especially frontal or Regardless of headache duration, you must periorbital) accompanied by any of themebo following exclude sfree.co serious underlying intracranialme pathology sf features: if any features in Box 18.4 are present. Arrange • conjunctival injection CT brain ± MRI and if normal, seek input from a • clouding of the cornea neurologist. Consider benign intracranial hyper- • irregular/non-reactive pupil tension in patients with features of ↑intracranial • ↓visual acuity or blurred vision pressure but no mass on neuroimaging. • sees coloured ‘halos’ around lights. 8 Frontal headache + nasal symptoms? Age >50 years + any features of temporal Whilst frontal headache may raise the suspicion 6 arteritis (Box 18.3)? of sinusitis, the diagnosis should only be madeks Suspect temporal arteritis in patients >50 years when there are associated nasal symptoms Look withoo new-onset sfr e.headache o and any features for at least two of: shown in Box 18.3. Check ESR and CRP • nasal blockage/congestion urgently; ESR >50 mm/hour makes the diagnosis • rhinorrhoea/discharge mebo sf e com Headache 173 Step by-step assessment

Table 18 2 Diagnostic criteria for headache

Migraine Cluster Tension-type Episodeso fr≥5 headache episodes ≥5 okepisodes of headache co with: ≥10 episodes of meeting the following criteria, headache with the or ≥2 episodes associated with following criteria: typical aura (see Box 18.1) 1. Headache duration of 4–72 Severe, unilateral orbital, Duration 30 minutes to hours supraorbital or temporal pain 7 daysmebo lasting 15–180 minutes 2. ≥2 of: Frequency of attacks: ≥2 of: Unilateral location 1 per 2 days to 8 per day Bilateral location Pulsating quality Pressing or tightening Moderate to severe intensity (non-pulsating) quality Disabling1 Mild to moderate intensity e.co Non-disabling2 3. ≥1 of: ≥1 of: None of: Nausea ± vomiting, Restlessness/agitation or Photophobia Photophobia + phonophobia Ipsilateral facial signs3 Phonophobia Nausea Vomiting

1Aggravation by or causing avoidance of routine physical activity, e.g. walking or climbing stairs. 2Not aggravated by or causing avoidance of routine physical activity, e.g. walking or climbing stairs. 3Conjunctival injection, lacrimation, nasal congestion,m rhinorrhoea, forehead oks and facial sweating, miosis, ptosis, eyelid oedema.Modified from Headache Classification Committee of the International Headache Society (IHS) 2013. The International Classification of Headache Disorders, 3rd edn (beta version). Cephalalgia. 33(9):629–808. 18

• loss of smell Diagnosis relies on associated features and pat- • facial pressure or tenderness. terns of presentation (see Table 18.2). By defini- Further investigation is not necessary in acute tion, they cannot be diagnosed on the basis of a sinusitis but refer the patient to ENT if there are single episode. However, where the presentation chronic symptoms. is typical, it may be reasonable to class a case as ooksfre a likely first presentation of a primary headache Features of primary headache disorder disorder. Where a recurrent headache does not 9 (Table 18.2)? efit sfre neatly into a diagnostic category, refer to a neurologist. mebooksf Primary headache disorders, e.g. tension headache, migraine are responsible for most headaches. Jaundice 19oksfre

Jaundice describes the yellow pigmentation also be obstruction of biliary canaliculi due to of skin, sclerae and mucous membranes that inflammation and oedema. There is typically a results from accumulation of bilirubin within disproportionate increase in ALT and AST rela- tissues. This may result from ↑red cell breakdown tive to ALP and GGT. Extensive liver damage (haemolysis), ↓uptake/conjugation by the liver may cause acute liver failure, characterized (hepatocellular dysfunction) or impaired biliary by jaundice, encephalopathy (Table 19.1) and drainage (cholestasis). Jaundice is often further coagulopathy (typically INR >1.5) in the absence classified according to the anatomic location of of pre-existing liver disease. Causes of acute the lesion: pre-hepatic – haemolysis; hepatic – liver failure are shown in Box 19.2. hepatocellular dysfunction and/or intrahepatic bile Potential causes of acute drug-induced liver ductooksfree obstruction; post-hepatic com – extrahepatic bile injury are listed in Box 19.3. LFTs may take duct obstruction. It is important to remember that months to normalize after drug cessation, patients may have more than one aetiology (e.g. especially with cholestatic injury. alcoholic hepatitis on a background mebooksfreeof cirrhosis Acute alcoholic com hepatitis maymeboo occur in individu sf- due to chronic hepatitis C infection). als without chronic liver disease following intensive binge drinking and presents with jaundice, Pre-hepatic causes of jaundice constitutional upset, tender hepatomegaly and Haemolytic disorders (Box 19.1) cause accumula- fever. tion of unconjugated bilirubin in plasma due to In acute viral hepatitis, jaundice is usually ↑red cell destruction. LFTs are otherwise normal, preceded by a 1–2-week prodrome of malaise, but there may be anaemia with evidence of hae- arthralgia, headache and anorexia. Hepatitis molysis on blood tests and film. Clinical features A–E viruses are responsible for most cases; of pre hepatic jaundice include normal coloured lesssfree.c common causes m include cytomegalovirus urine and dark stools. Biochemically there is an (CMV), Epstein–Barr virus (EBV) and herpes unconjugated hyperbilirubinaemia. simplex. Diagnosis is confirmed by serology. ooksfree com Recovery occurs over 3–6 weeks in most Hepatic causes of jaundice cases, but chronic infection develops in up to Problems with conjugation 10% of patients with hepatitis B and 80% with hepatitis C. mebooksf Gilbert’s syndrome is a benign congenital A rare cause of infective jaundice is icteric condition affecting 2–5% of the population. leptospirosis (Weil’s disease), a severe illness Decreased glucuronyl transferase activity limits characterized by deep jaundice, fever, bleeding, bilirubin conjugation and therefore excretion into e.g. epistaxis, haematemesis, renal failure and, the bile, causing mild jaundice during periods often, a purpuric rash. of fasting or intercurrent illness. There are no Autoimmune hepatitis most often presents other clinical/biochemical features of liver disease. with established cirrhosis but 25% of cases manifest as an acute hepatitis with jaundice and consti- Acute liver injury tutional symptoms. It is more common in females Toxic, infective, autoimmune, metabolic (ratio 3 : 1), and there is an association with other andooksfree vascular liver insults com may lead to acute autoimmune conditions. Serum immunoglobulin hepatitis. Jaundice results from impaired biliru- (IgG) levels are raised and serum autoantibodies bin transport across hepatocytes. There may may be present. ebooksf mebo sfree.com Jaundice 175 Differential diagnosis

Table 19.1 West Haven grading of hepatic Box 19.1 Causes of haemolysis encephalopathy Stage Alteration of consciousness Hereditary 0 k freNo change in personality or behaviour • Erythrocyte membrane defects No asterixis • Hereditary spherocytosis • Hereditary elliptocytosis 1 Impaired concentration and attention • Erythrocyte enzyme defects span • Glucose-6-phosphate dehydrogenase deficiency Sleep disturbance, slurredme speech, o• Haemoglobinopathies fr o m asterixis, agitation or depression • Thalassaemia 2 Lethargy, drowsiness, apathy or • Sickle cell aggression Acquired Disorientation, inappropriate behaviour, slurred speech • Immune • Autoimmune haemolytic anaemia 3 Confusion and disorientation, bizarre • Alloimmune: haemolytic transfusion reaction, e.combehaviour haemolytic disease of the newborn Drowsiness or stupor Fragmentation syndromes Asterixis usually absent Microangiopathic haemolytic anaemia, e.g. 4 Comatose with no response to voice haemolytic uraemic syndrome/thrombotic commands thrombocytopenic purpura Minimal or absent response to painful • Mechanical heart valves stimuli o• Drugs, free.c e.g. dapsone • Infections, e.g. malaria • Paroxysmal nocturnal haemoglobinuriam

Box 19.3 Drugs causing acute hepatotoxicity Box 19.2 Causes of acute liver failure Acute hepatitis Drugs/toxins • Paracetamol (in overdose) 19 • Paracetamol overdose1 • Cocaine ecstasy • Anti-tuberculous drugs • Aspirin, NSAIDs • Ecstasy • Halothane • Halothane • Anti-tuberculous therapy: pyrazinamide, isoniazid, • Amanita phalloides rifampicin • Carbonoksf tetrachloride ee o • Antifungals: ketoconazole Infection • Antihypertensives: methyldopa, hydralazine, dronedarone • Acute viral hepatitis (A, B, E)1 b • Cytomegalovirus (CMV), Epstein–Barr virus (EBV) Cholestasis/cholestatic hepatitis Vascular m• Antibiotics: ree penicillins, c m e.g. flucloxacillin, co- amoxiclav, ciprofloxacin, macrolides, e.g. • Shock/ischaemic hepatitis erythromycin • Budd–Chiari syndrome • Chlorpromazine Other • Azathioprine • Wilson’s disease • Oestrogens (including the oral contraceptive pill) • Autoimmune hepatitis • Amitriptyline • Acute fatty liver of pregnancy • Carbamazepine • Extensive malignant infiltration • ACE inhibitors • Cimetidine/ranitidineree co 1Denotes commonsfree. cause. • Sulphonamides Jaundice 176 Differential diagnosis

Box 19.4 Causes of cirrhosis Boxfr 19.5 Stigmata of chronic liver disease • Chronic alcohol excess • Spider naevi • Chronic viral hepatitis (hepatitis B or C) • Digital clubbing • Non-alcoholic fatty liver disease (NAFLD) • Palmar erythema ooks• Autoimmune r hepatitis co • Loss of axillary/pubic hair • Cholestatic • Parotid swelling • Primary sclerosing cholangitis • Gynaecomastia • Primary biliary cirrhosis • Testicular atrophy • Secondary biliary cirrhosis • Metabolic Modified from Headache Classification Committee of the • Hereditary haemochromatosis International Headache Society (IHS) 2013. The International Classification of Headache Disorders, 3rd edn (beta version). • Wilson’s disease Cephalalgia. 33(9) 629–808. • Alpha1-antitrypsin defic ency • Cystic fibrosis • Venous obstruction • Cardiac failure Hepatic tumours • Budd–Chiari syndrome • Drugs e.g. methotrexate Malignant infiltration by primary or, more com- • Cryptogenic monly, metastatic tumours may cause jaundice ksfree om due to intrahepatic duct obstruction or extensive replacement of liver parenchyma Common associated features include cachexia, malaise, Wilson’s disease, an inherited disorder of RUQ pain (stretching of the liver capsule) and copper metabolism, can present with acute hepatomegaly. hepatitis, and occasionally causes meacute liver sf e om mebooks Post-hepatic/biliary causes of jaundice failure. A ↓serum caeruloplasmin is highly suggestive. Jaundice due to biliary obstruction is associ- Hepatic vein thrombosis (Budd–Chiari syn- ated with a pronounced rise in ALP and GGT drome) typically presents with upper abdominal (produced in the biliary epithelium). Clinical pain, hepatomegaly and marked ascites due to features may include pale stools, dark urine and liver outflow venous congestion. itch. A raised PT may occur due to vitamin K Cardiac failure may cause hepatic injury due malabsorption from the GI tract. to vascular congestion with resultant jaundice and ↑ALT. Gallstones Ischaemic hepatitis (‘shock liver’) may result Gallstones are the most common cause of fromooks impaired ree.co hepatic perfusion in a patient with extrahepatic cholestasis; the onset of jaundice shock; the ALT is usually markedly raised. is relatively rapid, may be intermittent and is ebotypically free. accompanied om by epigastric/RUQ pain. Cirrhosis Cholecystitis is diagnosed on meboabdominal USS by Chronic liver injury from any cause (Box 19.4) an inflamed gallbladder (thick-walled) containing results in extensive hepatocellular loss, fibrosis gallstones. A dilated common bile duct on USS and disturbance of the normal hepatic archi- implies extrahepatic biliary obstruction and may tecture. Hepatocellular insufficiency leads to be due to gallstones lodged in the common jaundice, coagulopathy and ↓albumin. Portal bile duct (choledocholithiasis). The presence of hypertension and consequent porto-systemic RUQ pain, fever and rigors suggests bacterial shunting of blood result in oesophageal varices infection proximal to the obstruction (ascending and hepatic encephalopathy (see Table 19.1). cholangitis) and requires prompt antibiotics and Portal hypertension, ↓albumin and generalized decompression (ERCP). salt and water retention, due to haemodynamic Mirizzi’s syndrome arises from extrinsic andooksfree endocrine abnormalities, com lead to ascites. compression of the common hepatic duct by There may be characteristic ‘stigmata’ on a large stone within the gallbladder, with features examination (Box 19.5). eboof sfobstructive ee com jaundice. eboo sf Jaundice 177 Differential diagnosis

Benign strictures Malignancy Benign strictures may result from trauma, particu- Painless jaundice may represent a malignant larly during biliary surgery or as a consequence of cause of obstructive jaundice. Cancer of the inflammation within the biliary tree, e.g. recurrent head of the pancreas typically presents with cholangitis,ooksfre pancreatitis. oinsidious, s re progressive o jaundice due to extrinsic compression of the common bile duct, often with Autoimmune marked weight loss, nausea and anorexia. Pain In primary biliary cirrhosis, there is progressive may be absent in the early stages.mebooks destruction of the intrahepatic bile ducts. Ninety Cholangiocarcinoma is a malignant tumour of percent of patients are female. Pruritus usually the intra-hepatic or extrahepatic biliary tree that precedes jaundice. The presence of anti- most commonly presents with painless jaundice, mitochondrial antibodies is diagnostic. Primary often with pruritus. sclerosing cholangitis causes inflammation, Other important causes of malignant extrinsic fibrosis and str ctures of the intrahepatic and biliary compression include duodenal ampullary extrahepatic biliary tree. It is more common in tumours and enlarged lymph nodes at the porta men and 75%free of patients com have ulcerative colitis. hepatis.free com

19 Jaundice 178 Overview

Full clinical assessment + LFTs, FBC, U+E, coagulat on screen f e Yes 1 Evidence of chronic liver disease? k freSee Further assessment of chronic liver disease (p. 182) o No

Yes 2 Normal liver enzymes, PT, albumin? Likely haemolysis or Gilbert’s syndrome

3 Evidence of obstructive jaundice / cholestasis? co

Yes

Yes Fever / Rigors / RUQ pain? Suspect acute cholangitis

Yes Seek underlying Dilated bile ducts on USS? Extrahepatic obstruction m k cause

No No

ALT >500 U/L, PT or Yes Acute liver injury (viral / autoimmune / 4 ↑ features of encephalopathy? metabolicco / ischaemic / toxic) Nor co

Palpable liver / Yes Abdominal 5 Structural liver disease suspected malignancy? USS / CT o

Chronic alcohol excess or Yes 6 Consider alcoholic hepatitis recent sustained alcohol binge?

Yes Discontinue 7 Likely drug culprit? Drug hepatotoxicity drug Nor e.

Consider viral / autoimmune hepatitis, hepatocellular carcinoma, metabolic liver disease 8 Targeted investigation if suspected cause; oootherwise full liver e screen + abdominal USS Jaundice 179 Step-by-step assessment

1 Evidence of chronic liver disease? red cell fragments on blood film)± evidence of ↑red cell production (e.g. ↑reticulocytes In the absence of an established diagnosis, look polychromasia). Further assessment is described for signs of chronic liver disease, particularly on page 136. physical stigmata (see Box 19.5) and evidence of complications of cirrhosis, e.g. portal ooksfre Evidence of obstructive hypertension. 3 jaundice/cholestasis? • Multiple spider naevi, in the absence of pregnancy/pro-oestrogenic drugs,m strongly boo A srise re in ALP/GGT co out of proportionm to ALT/ sf suggest chronic liver disease. The other AST suggests that jaundice is due to impaired stigmata lack specificity individually but are biliary excretion, especially if accompanied by helpful in combination pale stools/dark urine. If there are features of • Ascites, especially in association with sepsis, take b ood cultures, give IV antibiotics, dilated, superficial periumbilical veins arrange urgent abdominal USS and discuss (‘caput medusae’), is a useful pointer with the surgical team. Otherwise, perform to portal hypertension but may have USS to look for bile duct dilatation (indicating other causes in jaundiced patients, e.g. extrahepatic obstruction) and an underlying intra abdominal malignancy or right heart cause, e.g. gallstones. failure with hepatic congestion. The rapid If USS does not show dilated bile ducts, onsetoksf of ascites, ee jaundice, com hepatomegaly proceed to step 4. and abdominal pain suggests acute Budd– If USS shows dilated bile ducts but does not Chiari syndrome. reveal the underlying cause arrange further • Hepatic encephalopathy (see Tablem 19.1 b) imaging. sfree.com MRCP provides excellentmeb definition o f and synthetic dysfunction (see below) of the biliary tree – request it if you suspect may occur in acute liver failure but are gallstones (acute or recurrent RUQ pain), or highly suggestive of chronic liver disease if there is a past history of biliary pathology. when they occur against a background of CT allows better visualization of the pancreas previous clinical/biochemical evidence of – arrange if jaundice is painless with an insidious, liver disturbance. progressive onset, especially in the elderly, to 19 • Abdominal USS can demonstrate exclude pancreatic cancer. ERCP also provides morphologic features of cirrhosis, e.g. useful diagnostic information but is more often coarse echotexture, ↑nodularity and undertaken subsequently to allow removal of provide supportive evidence of portal gallstones or stenting of the ducts. hypertensionoksfree (splenomegaly, com reversed flow in the portal vein). In difficult cases, biopsy ALT >500 U/L, ↑PT or features of 4 may be required to confirm the diagnosis encephalopathy? b sf and suggest the aetiology. ebo sfree com Identify patients with acute liver failure Evaluate any patient with jaundice and a background of established or suspected cirrhosis Look for features of acute liver failure in all jaun- as described in ‘Further assessment of chronic diced patients without pre-existing liver disease liver disease’ (p. 182). or extrahepatic biliary obstruction, especially if there is evidence of extensive hepatocellular injury (↑↑ALT). 2 Normal liver enzymes, PT, albumin? Hepatic encephalopathy (see Table 19.1) If there are no features of haemolysis or may be subtle; look closely for ↓concentration/ chronic liver disease, jaundice is mild (bilirubin alertness, mild disorientation, behavioural <100 µmol/L) and LFTs are otherwise normal, changes and reversal of the sleep/wake the likelyoksfr diagnosis e. is Gilbert’s m syndrome. cycle. Test specifically for constructional Consider haemolysis if features of liver disease apraxia, e.g. ask the patient to draw a five- are absent and blood results suggest ↑red cell pointed star or clock face and asterixis breakdown (e.g. ↓Hb, ↑LDH, ↓haptoglobin, (Fig. 19.1). Exclude hypoglycaemia and other mebo sfree com mebooksf Jaundice 180 Step-by-stepco assessment

Box 19.6 King’s College Hospital criteria for liverfr transplantation in acute liver failure Paracetamol overdose • H+ >50 nmol/L (pH <7.3) at or beyond 24 hours following the overdose or • Serum creatinine >300 µmol/L plus PT >100 seconds (INR > \6.5) plus encephalopathym o grade 3 or 4 Non-paracetamol cases • PT >100 seconds (INR >6.5) or Fig. 19.1 Examining for asterixis. Asterixis (hepatic flap) • Any three of the following: is a repetitive, jerky tremor of the outstretched hands • jaundice to encephalopathy time >7 days resulting in transient loss of extensor muscle tone at the • age <10 or >40 years wrist. It is due to metabolic brainstem dysfunction and is • indeterminate (non-A, non-B hepatitis) or drug- common in ventilatory failure, hepatic encephalopathy, induced causes renal fa lure and cardiac failure. (From Douglas G, Nicol F, • bilirubin >300 µmol/L Robertson C. Macleod’s Clinical Examination, 12th edn. • PT >50 seconds (INR >3.5) Edinburgh: Churchill Livingstone, 2009.) ooksfree.c Creatinine of 300 µmol/L ≅ 3.38 mg/dL. Bilirubin of 300 µmol/L ≅ 17.6 mg/dL. metabolic abnormalities and consider CT brain to exclude intracranial pathology, especially if Modified from O’Grady JG, Alexander GJ, Hayllar KM, Williams there are focal neurological abnormalities.me EEG R, 1989. ee Early indicators com of prognosis inm fulminant bo hepatic failure. Gastroenterology. 97(2):439–445. may assist the diagnosis. An ↑PT (in the absence of anticoagulation, pre- existing coagulopathy or extensive cholestasis) • metabolic acidosis indicates hepatic synthetic function; measure in ↓ • renal failure (develops in >50%, often all patients with jaundice – daily if there is ↑↑ALT necessitating haemofiltration) or worsening jaundice. If , do not correct unless ↑ • cerebral oedema with ↑intracranial pressure there is major haemorrhage. • bacterial or fungal infection. Seek cause of acute liver injury Use the King’s College criteria (Box 19.6) to identify patients who may require transplantation. Enquire about alcohol and paracetamol intake, Liaise early and closely with a specialist liver unit all recent drugs (prescribed or otherwise) and ooksfree com to enable timely transfer if necessary. possible exposure to environmental/occupational toxins, e.g. carbon tetrachloride. Check viral serol- 5 Palpable liver/suspected malignancy? ogy (IgM antibodies to hepatitis B coremebo antigen ree.co m books (HBc), hepatitis A virus (HAV), hepatitis E virus Consider abdominal USS or CT to exclude (HEV) CMV and EBV), serum caeruloplasmin, malignant or other structural liver disease if the autoantibodies (ANA, ASMA, LKM) and gamma- patient has: globulins, and perform a full toxicology screen. • clinical evidence of hepatomegaly Arrange abdominal USS to exclude Budd–Chiari • known malignancy with metastatic potential syndrome and extensive malignant infiltration. • a palpable abdominal/rectal mass or lymphadenopathy Repeatedly monitor and reassess patients • ascitesfree in the co absence of chronic liver with acute liver failure disease Monitor closely in ICU or a high dependency • unexplained weight loss/cachexia/ unitoo (HDU) sfr for complications e com including: lymphadenopathy. • hypoglycaemia Any abnormal lesions identified may require • hyperkalaemia biopsy for a tissue diagnosis. eb Jaundice 181 Step by-step assessment

Chronic alcohol excess or recent e.g. the patient recently started co-amoxiclav 6 sustained alcohol binge? or anti-tuberculous therapy.

Establ sh alcohol intake in all jaundiced patients. Consider other causes. Targeted Be tactful but persistent. Start with a general 8 investigation or full liver screen enquiryook before fre quantifying typical weekly intake. In addition to the total number of drinks, consider If the cause remains uncertain, screen for viral, the alcohol content (ask about brand if necessary) autoimmune, hereditary and metabolic conditions and, for spirits, the measure per drink.mebo Screen (Box fre 19.7), arrange co an abdominalmeb USS if not for potential problem drinking (see Box 2.1, already performed and confirm alcohol intake. p. 11). Seek a collateral history from relatives If there is fever, purpura, ↓platelets, conjunctival and friends, and observe closely for features of congestion or recent exposure to potentially alcohol withdrawal if you suspect covert alcohol contaminated water (e.g. freshwater sports, abuse. sewage worker), send blood and urine samples Suspect alcoholic hepatitis in any patient with for leptospiral culture, serology ± PCR (liaise longstanding excessive consumption, e.g. >40 with the microbiology laboratory) and consider units/week or recent binge drinking (e.g. >100 empirical antibiotic treatment. Liver biopsy may units/week), or who develops severe withdrawal be required if jaundice persists without a clear symptoms after 24–48 hours in hospital. Helpful cause and potential drug culprits have beenksf supporting features include tender hepatomegaly removed. andooksfree an AST : ALT ratio of om >1. Once the diagnosis is made, calculate the Glasgow alcoholic hepatitis score to assess prognosis and guide treatment. mebooBox sfree.com 19.7 Screening investigations in jaundice/ suspected liver disease 7 Likely drug culprit? Serology Enquire about ALL drugs taken within the • Hepatitis B surface antigen (HBsAg), Hepatitis C preceding 6 weeks including over-the-counter, antibodies HCV Ab (+ IgM antibodies to HBc, HAV, e.g. NSAIDs, paracetamol and herbal remedies. HEV, CMV and EBV if acute) Box 19.2 contains some common causes of 19 Metabolic hepatotoxicity but there are many others; consult with a pharmacist or review the literature if Ferritin, alpha1-antitrypsin level, caeruloplasmin uncertain. Wherever possible, discontinue any Autoimmune suspected drug culprit and observe the effect • AMA, ASMA, ANA, LKM, immunoglobulins on bilirubinoksfree and LFTs. com Liver biochemistry may Other take months to normalize, so consider further • Abdominal USS, alpha-fetoprotein, paracetamol level, investigations (see below) in the interim unless toxicology screen eb clinical suspicion of drug toxicity is mebovery high, re co Jaundice 182 Further assessment

Further assessment of chronic • ensure that an abdominal USS has been liver disease performed within the last 6 months. Additionally, in patients with encephalopathy: Step 1 Establish the underlying cause • seek evidence of upper GI bleeding (stool Try to determine the underlying aetiology in all evaluation, ↓Hb, ↑urea) new presentations of cirrhosis or in situations ook fre co • look for and correct constipation (PR where the cause is unclear. Assess alcohol intake examination, stool chart)/dehydration/ and perform screening investigations as listed in electrolyte disturbance Box 19.7. Exclude treatable causes (e.g. Wilson’s mebo• s minimize re use of opioids andmeb other sedative ok disease, haemochromatosis). Consider referral drugs. for liver biopsy if the cause remains uncertain. In cases of worsening ascites, evaluate salt and Step 2 Look for evidence of complications/ water intake and compliance with diuretics, decompensation exclude spontaneous bacterial peritonitis and Assess all patients with known or suspected consider Budd–Chiari syndrome. cirrhosis for complications. Evaluate for hepatic encephalopathy and examine for ascites, Step 4 Assess prognosis oedema jaundice and malnutrition. Measure Use the Child–Pugh classification (Table 19 2) album n and PT to assess hepatic synthetic to assess prognosis in patients with cirrhosis. function, as well as bilirubin, U+E (hyponatraemia, Other poor prognostic factors include ↑creatinine hepatorenalooksfree syndrome) om and FBC (anaemia, and ↓Na+, a small liver and variceal haemor- thrombocytopenia). Consider investigation for rhage. Consider referral to a transplant centre pulmonary complications such as pleural effu- for patients with Child–Pugh grade B or C. sion, hepatopulmonary syndrome andmebo pulmonary Absolute sfree.com contraindications mebooksto transplantation hypertension in patients with breathlessness, include metastatic malignancy, active sepsis, cyanosis or ↓SpO2. If not already done screen cholangiocarcinoma and active alcohol or IV for oesophageal varices with UGIE and for drug abuse. hepatocellular carcinoma with 6–12-monthly abdominal USS; USS will also detect small- volume ascites and splenomegaly. Table 19.2 Child–Pugh classification Step 3 Seek precipitants of decompensation of cirrhosis Patients with cirrhosis have limited hepatic meta- Score 1 2 3 bolic reserve and many factors can precipitate acute decompensation including spontaneous Bilirubin (µmol/L) <34 34–50 >50 bacterialooksfr peritonitis, e.com other intercurrent infection, Albumin (g/L) >35 28–35 <28 surgery, alcohol excess, hepatotoxic drugs and Ascites None Mi d Marked hepatocellular carcinoma. ebo sfre Encephalopathy None Mild Marked In a cirrhotic patient who develops jaundice, me o coagulopathy or encephalopathy: Prolongation of <4 4–6 >6 PT (seconds) • perform a full sepsis screen (see Clinical tool, p. 142), including an ascitic tap for Child A = Score <7: 1-year survival 82% Child B = Score 7–9: 1-year survival 62% microscopy and culture if ascites is present Child C = Scoreom >9: 1-year survival 42% • review all drugs andcom alcohol intake This page intentionally lefto blank Joint swelling 20 ks ooksfre

This chapter relates primarily to acute swelling or excluded early. Haematogenous spread is of the knee, hip, elbow, shoulder and ankle. the usual route of infection, but local skin or Swelling may arise from periarticular structures bone infection may occur. Common organisms (bursae, tendons, muscles) or the joint. Condi- are S. aureus, N. gonorrhoeae and Salmonella tions affecting the joint itself usually cause diffuse spp. Risk factors include a prosthetic joint, swelling, warmth, tenderness and restriction in skin infection, joint surgery, diabetes mellitus, both active and passive movement. In contrast, increasing age, immunocompromise and IV drug bursitis/tendinopathies cause localized tender- use. Pain, swelling, tenderness and erythema ness and swelling in the area of the joint but develop over a few hours. The joint is often with minimal restriction in joint movement. Pain held in slight flexion with the patient extremely isooksfree.com limited to certain planes of movement and is reluctant to move it. Fever and ↑WBC/CRP may worse with active rather than passive movement. be present but are unreliable features, particularly eboin sfree.compatients taking steroids or NSAIDs and in the Periarticular conditions immunosuppressed. mebooksf Bursitis is most commonly caused by repetitive movement, particularly if pressure is applied over Trauma the bursa during the process. Symptoms may Trauma may result in haemarthrosis if there is arise after unaccustomed activity. Less often it injury to a vascular structure within the joint (a may result from infection, rheumatoid disease fracture or ligamentous injury) or to a traumatic or gout. Common sites of bursitis are pre-/infra- effusion, e.g. from a meniscal tear in the knee. patellar (knee) olecranon (elbow), trochanteric Any local penetrating injury predisposes to (hip) and subacromial (shoulder). infection and requires urgent surgical debride- Tendinopathies and enthesopathies (where ment and washout. the tendon attaches to the bone) are usually caused by overuse or by repetitive minor Crystal arthropathy trauma. Other causes include infection and booksfree com The two most common forms are gout (uric systemic conditions, e.g. rheumatoid disease, acid) and pseudogout (calcium pyrophosphate). gout/pseudogout, Reiter’s disease ankylosing A past history of gout, alcohol excess, spondylitis. Tenderness over the tendon,mebo with s ree.co me sf diuretic use and renal stones are risk factors, discomfort aggravated by movement, is usual as are conditions that cause high cell turnover and crepitus may be detected. Common sites (polycythaemia, lymphoma, psoriasis). In acute for enthesopathies are the elbow (lateral and gout the meta arso-phalangeal joint of the great medial epicondyles) and knee. Osgood-Schlatter toe is most frequently affected, followed by the disease (inflammation of the patellar tendon at ankle, knee, small joints of the feet/hands, wrist the tibial tuberosity) is a common disorder in and elbow. Onset is often sudden and exquisitely adolescents experiencing rapid growth spurts. painful. The affected joint is hot, red and swollen, Articularksfree conditions om with shiny overlying skin. Septic arthritis Reactive arthritis Septic arthritis may lead to irreversible cartilage Reactive arthritis is an autoimmune, non-purulent and joint destruction, and so should be identified arthritis that arises as a result of infection meb sfree com meb f Joint swelling 185 Differential diagnosis

elsewhere in the body, typically within 4 weeks Table 20.1 The 2010 American College of of GI or GU infection (Chlamydia, Campylobacter, Rheumatology/European League Against Yersinia, Salmonella, Shigella). The swelling may Rheumatism classification criteria for appear suddenly or develop over a few days rheumatoid arthritis following an initial spell of joint stiffness in the Criterion Score1 joints. The disorder most commonly affects men booksfrebetween 20–50 years old and typically lasts for A. Joint involvement 1 large joint 0 2–6 months. The most commonly affected joints >1 large joints 1 are lower limb large joints and sacroiliacmebo joints. 1–3 fre small joints ( o± involvement of 2 The classic triad of reactive arthritis comprises large joints) non-infectious urethritis, conjunctivitis/anterior 4–10 small joints (± involvement of 3 uveitis and arthritis. However, this is found only large joints) in a minority of patients. 10 joints (at least 1 small joint) 5 B. Serology Polyarthropathy presenting as Negative RF and negative ACPA 0 monoarthropathy Low-positive RF or low-positive ACPA 2 High-positive RF or high-positive ACPA 3 Osteoarthritis commonly affects the hands, C Acute-phase reactants feet, spine and the large weight-bearing joints, Normal CRP and normal ESR 0 such as the hips and knees. Acute single-joint Abnormal CRP or abnormal ESR 1 exacerbationsooksf may ee follow com minor trauma. It usually D. Duration of symptoms evolves insidiously over months to years but <6 weeks 0 may present with an acute exacerbation. Other ≥6 weeks 1 polyarthopathies such as rheumatoid arthritis (RA) meboo1A score free of ≥6/10 indicates om definite RA. or psoriatic arthritis may occasionally present ACPA – Anti-citrullinated protein antibody. with disproportionate or isolated swelling of a Source modified from Aletaha D, Neogi T, Silman AJ et al. single joint but definitive diagnosis of RA requires 2010. Rheumatoid arthritis classification criteria: an American involvement of more than one joint (Table 20.1). College of Rheumatology/European League Against Rheumatism collaborative in tiative. Arthritis Rheum. 62(9):2582–2591. Bone cancer and secondary deposits Any bone tumour near a joint can potentially 20e cause swelling, although pain is usually the presenting feature. The most common cancers to metastasize to bone are those of the breast, lung,ooksfree. kidney, prostate and om thyroid. Most lesions are visible on X-ray. Be careful to investigate patients who present with joint swelling following (minor) trauma that fails to settle as thismeboo may be com a presentation of bone malignancy. Joint swelling 186 Overview

Full clinical assessment ± FBC, CRP, uric acid, blood cultures f e fre X-ray Yes Fracture or 1 Significant trauma? +/– orthopaedic haemarthrosis review No

Yes X-ray + orthopaedic 2 Prosthetic joint? review

3 Indication for jointco aspiration? Yes

Yes Urgent Positive Gram stain? Septic arthritis orthopaedic review k No

Yes Crystals? Likely gout / pseudogout

Yes High-risk features (see text)? Orthopaedic review o No No

Acute presentation adequately Yes 4 Soft tissue injury explainedsf by recent o trauma?

Recent GI/GU infection or evidence of Yes 5 Likely reactive arthritis urethritis / conjunctivitis? m

Consider rheumatoid arthritis / Yes Rheumatology 6 Evidence of other joint involvement? osteoarthritis / seronegative review spondyloarthritis No

Consider periarticular cause, haemarthrosis, rheumatic fever 7 s c or monoarticular presentation of oligo- or polyarthritis (see Step 6) oks co Joint swelling 187 Step-by-step assessment

1 Significant trauma? absence of trauma, if you suspect septic arthritis. Aspiration of the knee is relatively simple but the Perform plain X-rays if the patient has a history other joints, especially the hip and ankle, require of recent trauma. If a fracture is identified, refer expert technique – seek orthopaedic help. Never to an orthopaedic specialist. aspirate through infected overlying tissues. ooksSuspect haemarthrosis re if severe joint swelling A joint aspirate that shows organisms on arises within 30–60 minutes of injury or occurs Gram stain is diagnostic of septic arthritis but in a patient with impaired coagulation Aspiration is only positive in 30–50% of cases. Elevated of a tense, traumatic haemarthrosismebo may help WBC sfre detected co in joint aspiratemebooksf suggests infection alleviate pain – consult an orthopaedic specialist (Table 20.2), even if the Gram stain fails to and correct any coagulation abnormalities prior demonstrate organisms – seek expert advice. to aspiration (under strict aseptic technique). Crystal-induced arthropathy is suggested In the absence of a coagulation abnormality, by the microscopic identification of monoso- swelling that develops 24 hours or more after joint dium urate in gout or calcium pyrophosphate injury is likely to represent a traumatic effusion. dehydrate (CPP) in pseudogout crystals (see Table 20.2). However, this does not rule out a 2 Prosthetic joint? superimposed infection. In the absence of crystals or a positive Gram In patients with a swollen/tender prosthetic joint, stain, seek orthopaedic review if the aspirate perform an X-ray and consult an orthopaedic is bloody or there is any ongoing suspicion of specialist.ooksf Do not e aspirate com a prosthetic joint septic arthritis, e.g. typical clinical presenta- without prior orthopaedic consultation because tion, inflammatory aspirate (see Table 20.2) or of the risk of introducing infection. Aspiration immunocompromised patient. of prosthetic joints is typically undertakenmebo by sfree com mebook orthopaedic specialists in a sterile operating Acute presentation adequately explained theatre environment. 4 by recent trauma? A significant proportion of acute large joint swell- 3 Indication for joint aspiration? ings in the context of trauma, with a normal Take blood for FBC, CRP, urate and blood X-ray, are soft tissue injuries with variable degrees cultures, but note that a normal WBC, and CRP of ligamentous/cartilaginous/tendinous injury If 20 do not exclude septic arthritis. Strongly consider the history is diagnostic, and joint examination plain X rays if not undertaken already. features are consistent with a soft tissue injury, Perform joint aspiration (using strict aseptic and the X-ray is reassuring, manage the patient technique)ooksfree with urgent cGram stain and microscopy, conservatively. Consider referral to physiotherapy followed by culture and sensitivity, in any patient if there are specific concerns regardingbooks joint e with an acutely swollen, painful, warm joint in the function and tissue injury. mebo sfree com Joint swelling 188 Step-by-step assessment

Table 20 2 Features of inflammatory and non-inflammatory joint aspirates

Non-inflammatory synovial aspirate Inflammatory synovial aspirate oMacroscopic fr features co Volume Small Large Appearance Clear, straw coloured Cloudy or opaque due to pus, red due to blood Viscosity High (hyaluronatem present) Low fr (hyaluronate breakdown) m Microscopic features Cellularity Low High (turbid fluid) WBC Low High (infection, RA, gout) (neutrophil predominance suggests bacterial infection, eosinophilia suggests RA, tuberculosis, arthritis, Lyme disease) Crystals Absent Gout negatively birefringent MSU crystals Pseudogout: positively birefringent CPP crystals Glucose Slightly lower than serum Significantlysfree.co lower than serum in infection P otein Normal Elevated ookGram stain No organisms Assess for bacterial species Microbiological culture Negative Bacterial growth if present

Recent GI/GU infection or evidence of The diagnostic criteria for RA are shown in 5 urethritis/conjunctivitis? Table 20.1. Consider a seronegative arthritis if there is prominent axial involvement/sacroiliitis or In a young patient with non-traumatic acute a history/clinical features of inflammatory bowel arthritis in whom septic arthritis has been disease or psoriasis. excluded, the presence of any of the following Unless the diagnosis is clearly osteoarthritis, features is highly suggestive of reactive arthritis: refer for specialist rheumatological assessment • diarrhoea • urinary frequency 7 Consider other causes • dysuriaoksfree or urgency com • urethral discharge within the preceding 6 Use USS to detect/assess effusions of the hip weeks (typically 1–3 weeks) and shoulder joints and periarticular conditions – • genital ulceration or circinate balanitis tendinopathies, bursitis and muscle haematoma. • symptoms/signs of conjunctivitis mor iritis, b Always free.com consider spontaneousmebo haemarthrosis in f e.g. pain, irritation, tearing, discharge or patients with coagulopathy (including those on redness. anticoagulation or with haemophilia). Evaluate for rheumatic fever if there is a flitting arthritis associated with other characteristic features (see Evidence of other joint involvement? 6 Box 14.4, p. 148). Seek Rheumatology advice if Examine all joints carefully, looking for evidence of you suspect a monoarticular presentation of RA swelling and/or tenderness; note the distribution (see Table 20.1), osteoarthritis or seronegative and symmetryfree.co of additional joint involvement. arthritis.free. om This page intentionally lefto blank Leg swelling 21 ks ooksf e

The predominant cause of leg swelling is oedema tamponade) or primary right heart pathology (e.g. – the abnormal accumulation of fluid within the pulmonary/tricuspid valve disease, RV infarction, interstitial space. Oedema may result from: arrhythmogenic RV cardiomyopathy). • hydrostatic pressure in the venous ↑ Renal failure system due to ↑intravascular volume or obstruction In advanced renal failure, ↓salt and water • ↓plasma proteins, mainly albumin, that excretion results in fluid retention and ↑system c retain fluid within the vascular compartment venous hydrostatic pressure. Chronic renal failure (↓‘oncotic’ pressure), or and heart failure commonly co-exist (cardiorenal • obstructionoksfr to e.com lymphatic drainage: syndrome) and may both contribute to general- ‘lymphoedema’. ized oedema. ooksf Unilateral oedema usually indicates localized Hypoalbuminaemia pathology, e.g. venous or lymphatic obstruction. Bilateral oedema may be due to a localme cause Hypoalbuminaemia sfre c m produces oedema by but more often represents the combination of ↓plasma oncotic pressure. Causes include generalized fluid overload and gravity. Oedema is nephrotic syndrome (↑albumin loss in urine); frequently multifactorial, so search for additional chronic liver disease (↓hepatic synthesis of causes, even if you identify a possible culprit. albumin); systemic inflammatory processes (leakage of albumin from the intravascular Generalized oedema space due to increased capillary permeability ± persistent synthesis of ‘acute-phase proteins’ Cardiogenic causes such as CRP in preference to albumin); protein- losing enteropathy (leakage of albumin into the Cardiogenic lower limb oedema is typically gut due to lymphatic obstruction or mucosal accompanied by other signs of volume overload ± disease); and advanced malnutrition. structuralooks heart e disease com (Fig. 21.1). In congestive cardiac failure (CCF), salt and water retention Iatrogenic causes b oksf due to persistent neurohormonal activation leads Box 21.1 lists drugs that cause oedema. to an ↑ in intravascular volume. Highmeboo systemic sfree com venous hydrostatic pressure may also be caused Idiopathic cyclic oedema by high right ventricular filling pressures if there is concomitant right heart failure. In CCF, right Idiopathic cyclic oedema commonly affects heart failure may reflect involvement of the right women, most frequently of child-bearing age. ventricle (RV) in the underlying disease process Bilateral leg oedema progresses through the (e.g. dilated cardiomyopathy) but is more often day and is most prominent in the evening. The due to chronically high left sided filling pressures aetiology is unclear. which leads in turn to pulmonary hypertension. In the absence of left heart disease, right heart Local causes of oedema failure may arise from other causes of pulmo Deep vein thrombosis naryooksfree hypertension (e.g. com chronic lung disease, thromboembolism or primary pulmonary vascular Deep vein thrombosis (DVT) causes local oedema disease), pericardial disease (e.g. constriction, due to physical obstruction of venous drainage. mebo free co meb Leg swelling 191 Differential diagnosis

Box 21.2 Skin changes in chronic venous Pulmonary insufficiencyfr o oedema Raised JVP • Haemosiderin pigmentation • Atrophy Displacedo k • Hair loss apex beat • Varicose eczema • Induration and fibrosis of subcutaneous tissues Pleural • Ulceration effusions Ascites m

Pelvic mass A pelvic mass may obstruct local venous drainage and increase hydrostatic pressure by compressing pelvic veins. With ovarian tumours, Pitting oedema is usually unilateral. Bilateral oedema oedema is sfree.ccommon in pregnancy because of ↑blood volume and bilateral venous compression by the Fig. 21.1 Clinical features of heart failure. gravid uterus but the diagnosis is usually obvious; o suspect DVT if there is a sudden increase in leg swelling, particularly in the third trimester.ebooksf Box 21.1 Drugs causing oedema Lymphoedema • Calcium channel blockers Causes include malignancy (lymphatic invasion • IV fluids or lymphoma), previous lymph node surgery or • Corticosteroids radiotherapy, filariasis and congenital lymphatic • Mineralocorticoids (fludrocortisone) • Thiazolidinediones ( glitazones’) abnormalities. Early lymphoedema may be indis- • Withdrawal of diuretics tinguishable from other forms of oedema but • NSAIDs with progression it becomes firm and non-pitting • Oestrogens with characteristic skin changes (see below). • Progestogens 21 • Te tosterone Other causes • Growth hormone oksfr e.co Compartment syndrome (↑pressure, vascular compromise and tissue injury within a fascial compartment), rupture of a Baker’s cyst (a Clinical features are notoriously unreliable; swelling of the semi-membranous bursa at the D-dimer and/or Doppler ultrasound arem integral back free of the knee) com or gastrocnemiusmeboo, superficial to diagnosis. Rarely, bilateral or inferior vena thrombophlebitis and cellulitis may all present caval thrombosis may cause bilateral swelling. with an acutely painful, swollen leg. Lipoedema is not true oedema but an accu- Chronic venous insufficiency mulation of excess subcutaneous fat. There is The most common cause of chronic unilateral typically bilateral symmetrical leg swelling that is and bilateral leg swelling. Incompetent valves in non-pitting and spares the dorsum of the feet. the deep and perforating veins impair venous P etibial myxoedema is an abnormal dermal return with a rise in hydrostatic pressure. There accumulation of connective tissue components may be varicose veins and characteristic skin in Graves’ disease. It causes areas of non-p tting changes (Box 21.2). Dependent/gravitational oedema on the anterior or lateral aspects of oedemaooksfree is a variant of com this condition, to be con- the legs, with pink/purple plaques or nodules. sidered if immobility is an issue, e.g. post strokeboo Most sfree.com patients will have evidence of Graves’ patients. ophthalmopathy. ebooksf Leg swelling 192 Overview

Full clinical assessment ± D-dimer (see text) f e 1 Unilateral swelling?

No Yes

Yes Doppler Wells score >1 or +ve D-dimer? Deep vein thrombosis 2 e USS e No Yes Consider cellulitis, thrombophlebitis, 3 Acute onset + pain / inflammation? compartment syndrome, ruptured Baker’s cyst / gastrocnemius No

Recent onset, progressive swelling Yes 4 Must exclude underlying malignancy or clinical suspicion of malignancy?

CT abdo / Non-pitting oedema or previous local Yes 5 Likely lymphoedema pelvis olymph e. node dissection m / radiotherapy? oo e m Seek expeo t advice No Yes 6 Signs of venous insufficiency? Likely chronic venous insufficiency

Possible venous insufficiency; consider imaging to exclude deep vein thrombosis and malignancy if not yet performed

Urinalysre s, ECG, co U+E, LFTs, albumin 7 ≠JVP, pulmonary congestion or symptoms Yes CCF / right heart Echocardiogram of heart failure? kfailure / renal om failure No

Yes Seek underlying Serum albumin 30 mmol/L? e o 8 < Hypoalbuminaemia cause No

Yes Consider dose reduction 9 Likely drug culprit (Box 21.1)? Iatrogenic oedema or discontinuation No Yes 10 Evidence of structural heart disease? Echocardiogram CCF / right heart failure Nor e m

Assess as per unilateral swelling if not already done 11 Likely diagnoses are venous insufficiency or idiopathic oedema Consider lipoedema, pretibial myxoedemaboo ee Leg swelling 193 Step-by-step assessment

1 Unilateral swelling? • Ar ange Doppler USS in all pregnant patients with suspected DVT, as exclusion Examine both limbs for evidence of swelling and by D-dimer has not been validated in this pitting If there is bilateral lower limb swelling group. even if asymmetrical, go to step 7. ooks re 3 Acute onset + pain/inflammation? 2 Wells score >1 or +ve D-dimer? Consider cellulitis if swelling is accompanied by a Consider DVT in any patient with unilateral limb discrete area of erythema, heat, swelling and pain swelling, even without apparent riskm factors or re co m b ± fever or ↑WBC/CRP; negative blood cultures/ other signs or symptoms. Pre-test clinical predic- skin swabs do not rule out the diagnosis. In tion tools, e.g. Wells score (Table 21.1), can superficial thrombophlebitis, signs are localized, guide further investigation Evaluate for bilateral with redness and tenderness along the course DVT in any patient with risk factors and bilateral of a vein, which may be firm and palpable. leg swelling. A ruptured Baker’s cyst may be clinically • If Wells score is ≥2, DVT is likely – arrange indistinguishable from DVT; USS will reveal the a Doppler USS scan to confirm/refute the diagnosis and exclude DVT. diagnosis. sfreeConsider gastrocnemius com muscle rupture in • If Wells score is <2, perform a D-dimer patients with sudden onset of pain during sport- blood test. If negative, DVT is excluded; if oksfre com ing activity ± pain on muscle palpation (maximal positive, arrange a Doppler USS scan at the medial musculotendinous junct on) – USS may be helpful. Consider compartment syndrome if unilateral limb swelling is accompaniedm by bookany of the Table 21.1 Wells score (deep vein thrombosis) features in Box 21.3; if suspected, check CK Clinical feature Score (rhabdomyolysis) and arrange urgent orthopaedic review. Active cancer (treatment within +1 point m last 6 months or palliative) Paralysis, paresis or recent plaster +1 point immobilization of leg Recently bedridden >3 days or +1 point 21 major surgery under general/ Box 21.3 Features of compartment syndrome regional anaesthesia in previous k 12 weeks Clinical context ooksfreeLocal tenderness along codistribution +1 point Lower limb fracture, trauma, crush injury, vascular injury of deep venous system b Drug overdose or ↓GCS Entire leg swollen +1 point Symptoms Calf swelling >3 cm compared +1 point Pain (especially if increasing or deep/aching) to asymptomatic leg (measured Paraesthesia/numbness1 10 cm below tibial tuberosity) Paresis/paralysis1 Pitting oedema confined to +1 point Signs symptomatic leg Pain on passive muscle stretching Collateral superficial veins (non- +1 point Tense, firm or ‘woody’ feel on palpation varicose) ↓Capillary refill or absent distal pulses1 Muscle contracture1 Alternative diagnosis at least −2 points as likely as DVT, e.g. cellulitis, Investigationssfree c thrombophlebitisksfr e. o ↑↑CK S urce: Wells PS et al. 1997. Value of assessment of pretest 1Numbness, paraesthesia, paralysis, absent pulse and probability of deep-vein thrombosis in clinical management contracture are late features; their absence does not exclude Lancet. 350(9094):1795–1798. the diagnosis. bo Leg swelling 194 Step-by-step assessment

Recent onset, progressive swelling or • longstanding pitting oedema with diurnal 4 clinical suspicion of malignancy? variation in a patient >50 years. If none of these is present, reconsider the need A pelv c or lower abdominal mass may produce to exclude underlying DVT and malignancy, and leg swelling by compressing the pelvic veins or assess as described for bilateral leg swelling to lymphatics. Exclude underlying malignancy if any ook fre co look for a cause of generalized oedema. of the following is present: bo s re • weight loss ↑JVP, pulmonary congestion or • previous pelvic cancer 7 symptoms of heart failure?m books • postmenopausal or intermenstrual PV bleeding ↑JVP signifies high central venous pressure • a palpable mass or local lymphadenopathy (due to volume overload and/or ↑cardiac filling • any new-onset, progressive, unilateral pressures) and therefore implies a cardiogenic/ leg swelling with no clear alternative renal cause for bilateral pitting oedema rather than explanation. local venous obstruction or low oncotic pressure. Assume CCF if patients also have suggestive Perform a rectal ± vaginal examination, check symptoms (orthopnoea, paroysmal nocturnal a PSA level (males) and arrange imaging with dyspnoea, recent-onset exertional dyspnoea), USS ( ransabdominal or transvaginal) or CT as a background of LV dysfunction, myocardial appropriate. infarction or left sided valve disease or (irrespective ooksfre com of the JVP) clinical or CXR features of pulmonary Non-pitting oedema or previous local congestion. Bear in mind the possibility of right 5 lymph node dissection/radiotherapy? heart failure secondary to pulmonary hypertension Distinguish lymphoedema from otherme causes (or sfree less commonly com right heart disease)mebooksf in patients of swelling, as it is unlikely to respond to with severe chronic lung disease or clear lung conventional treatments and should prompt fields. In either case, arrange an echocardiogram consideration of an underlying malignancy (new to assess cardiac structure and function including or recurrent). Consider the diagnosis if any of LV/RV size and function, valvular function and the following is present: pulmonary artery pressure. Even in the absence of • previous pelvic malignancy, local ↑JVP or obvious pulmonary congestion, consider radiotherapy or lymph node dissection CCF and arrange an echocardiogram in patients • known or family history of congenital with recent-onset exertional or nocturnal dysp- lymphatic anomaly noea since these signs can be challenging to • oedemaoksfree.com that is firm and non-pitting detect or subtle. • inability to pinch the dorsal aspect of skin at Consider renal impairment as a cause or con- the base of the second toe (Stemmer sign) tributor to fluid retention if GFR<30; see ‘Further • thickening of overlying skin with warty or assessment of renal failure’ p. 230) and seek ‘cobblestone’ appearance. mebrenal sfree advice if com new presentation,mebo major change ksf from baseline or severe oliguria. If you suspect lymphoedema, seek expert advice and consider CT of the pelvis and 8 Serum albumin <30 mmol/L? abdomen to look for evidence of underlying malignancy. Hypoalbuminaemia may cause or contribute to oedema particularly when <25 g/L. Search for an underlying cause. 6 Signs of venous insufficiency? Screen for nephrotic syndrome by urinalysis, Suspect chronic venous insufficiency if any of looking for proteinuria. If the test is positive the fo owing is present: collect a 24-hour urine sample; >3 g protein/24 • characteristicksf e skin changes om (Box 21.2) hours confirms the diagnosis. • prominent varicosities in the affected limb Suspect ↓hepatic synthetic function if there • previous DVT or vein stripping/harvesting in are deranged LFTs or features of chronic liver the affected limb ebdisease sfree (Box 19.5 com, p. 176) and PT is prolonged. mebo ksf Leg swelling 195 Step by-step assessment

A persistent acute-phase response (resulting in • a past history of MI, cardiac surgery, ↓albumin synthesis) may occur in chronic infect- valvular disease, pulmonary embolism ion, inflammatory illness or occult malignancy. or chronic lung disease (e.g. COPD, Suspect this if the patient has a persistently obstructive sleep apnoea) ↑CRP/ESR, recurrent pyrexia, lymphadenopathy, • Heart murmur, S3, displaced apex beat or constitutionalooksfre upset (fever, sweats, malaise, parasternal heave weight loss) or local signs or symptoms, e.g. • Cardiomegaly on CXR palpable mass, active synovitis – investigate • Significant ECG abnormality, e.g. Q waves, as for fever/pyrexia of unknown originmeboo (p. 148). left re or right co bundle branchm block; see oo Box Consider protein-losing enteropathy and seek 6.1, p. 51. GI advice if there is a history or symptoms of GI disorder. Malnutrition must be prolonged and Assess as per unilateral swelling. Likely severe to cause a significant decrease in serum 11 venous insufficiency or idiopathic oedema albumin and is a diagnosis of exclusion. If there is bilateral swelling, first return to step 1 9 Likely drug culprit (see Box 21.1)? and assess for ‘unilateral’ causes, e.g. bilateral DVT. Drug causes are listed in Box 21.1. Where Venous insufficiency is the likeliest cause in feasible, review after trial discontinuation. patients >50 years or in those with skin changes/ oksf e com predisposing factors. Idiopathic cyclic oedema 10 Evidence of structural heart disease? is a common cause in women of child-bearing Bilateral lower limb oedema is less likely to have a age (mechanism not understood) but consider cardiogenic cause if there are no accompanyingme an fechocardiogram ee.co to excludemebooks pulmonary signs or symptoms of heart failure. However, hypertension. Gravitational oedema may occur in the absence of any clear alternative cause, with longstanding immobility. consider echocardiography if there are any point- If pitting is absent, consider lipoedema or ers toward underlying structural heart disease pretibial myxoedema. including: om om

21 Limb weakness 22 ks ooksfre

Limb weakness may be focal or generalized. to the underlying pathology, e.g. malignancy, Diagnosis relies on careful clinical assessment, or a source of septic emboli such as infective complemented, in most cases, by appropriate endocarditis. brain or spinal imaging. Current stroke manage- Spinal cord lesions ment mandates urgent evaluation of unilateral limb weakness However, focal limb weakness Transverse lesions produce bilateral UMN limb can be caused by many non-stroke pathologies weakness (para/tetraparesis), with loss of all and these should not be overlooked in the rush sensory modalities below the spinal cord level to definitive management. and disturbance of sphincter function. Unilateral lesions (Brown–Séquard syndrome) cause ipsilat- Stroke eral UMN weakness and loss of proprioception Strokeoo is sfree.comthe most common cause of unilateral below the cord level, with contralateral loss of limb weakness. Patients typically present with pain and temperature sensation. sudden onset of weakness of the arm, leg or Causes may be compressive lesions, e.g. facial muscles, on one side. Symptomsmebo persist ksfreeintervertebral codisc prolapse, mebooksftrauma, vertebral for >3 hours and often do not resolve. An initial metastases or intrinsic pathology, e.g. transverse

flaccid paresis progresses to upper motor neuron myelitis, glioma, spinal infarct, vitamin B12 defi- (UMN) weakness days later. There may be ciency. Circumferential pain across or sensory associated signs of cortical dysfunction (Box loss below a thoracic or lumbar dermatome 22.1) or other sensory, visual or coordination suggests cord compression (but is not always problems. Aside from rare examples, such as present) – the level should correlate with neu- those affecting certain areas of the brainstem, rological examination of the lower limbs. Saddle symptoms and signs are consistently unilateral. anaesthesia, bilateral leg pain, urinary retention and reduced anal tone suggest cauda equina Transient ischaemic attack (TIA) syndrome, and should prompt urgent imaging. TIAs are temporary, focal, ischaemic insults to the brain. Symptoms and signs usually last Peripheral nerve lesions bookfor at least free10 minutes com and are comparable to Lower motor neuron (LMN) weakness may result stroke but resolve entirely without permanent from generalized disease of peripheral nerves neurological sequelae. The traditionalmebo definition (peripheral sfree.com neuropathy), or fromme lesions affecting oksf of TIA describes a syndrome lasting less than a plexus (plexopathy), spinal root (radiculopathy) a day, but this does not correlate with modern or single nerve (mononeuropathy). In peripheral knowledge of stroke – symptoms >3 hours are neuropathy, the longest nerves tend to be likely to show permanent ischaemic damage to affected first, leading to a ‘glove-and-stocking’ the brain on advanced imaging. With rare excep- pattern of weakness and sensory loss; in the tions, TIAs do not cause loss of consciousness. other lesions, weakness and sensory loss reflect the muscles/skin regions innervated by the Space-occupying lesions affected nerve(s) or nerve root. Space-occupying lesions, e.g. tumour, abscess, chronic subdural haematoma, can cause Motor neuron disease symptomsook and free.com signs mimicking stroke but the A chronic degenerative condition that presents onset is typically more gradual and progressive. with gradual, progressive weakness and a There may be features of raised ICP or clues combination of UMN and LMN signs. There may meboo sf ee.com mebo f Limb weakness 197 Differential diagnosis

altered consciousness. Multiple sclerosis can Box 22.1 Signs of cortical dysfunction present with almost any pattern of UMN limb • Visual field defect weakness,sfre though o paraparesis secondary to • Dysphasia transverse myelitis is most typical. Transient • Dyspraxia focal limb weakness can occur immediately ooks• Neglect r after a focal seizure (Todd’s paresis). Migraine • Sensory or visual inattention. occasionally causes limb weakness (hemiplegic migraine) but this is a diagnosis of exclusion. Myasthenia gravis causes ‘fatigability’mebooksf of limb be bulbar involvement but sensory features are muscles. Generalized muscle weakness may absent. result from congenital/inflammatory myopathy, e.g. polymyositis, endocrine or metabolic distur- Other causes bance, e.g. Cushing’s syndrome, hypokalaemia, Encephalitis may cause limb weakness as or drugs/toxins, e.g. corticosteroids, alcohol; it part of a constellation of central neurological is also a common, non-specific presentation of symptoms including confusion, seizures and acute illness in frail, elderly patients. f ee c free com

22 Limb weakness 198 Bilateral limb weakness: overview

Full clinical assessment, capillary blood glucose f e com Yes 1 Weakness strictly unilateral? k See Unilateral limb weakness (p. 204) No

Check limb Acute-onset or rapidly Yes Cord compression or 2 perfusion then progressive paraparesis? intrinsic pathology urgent MRI

Upper motor neuron signs, sensory 3 level or sphinctere.c disturbance? Yes

Yes Abnormal MRI spine? k Cord compression or intrinsic pathology

No Consider motor neuron disease, B12 No deficiency, bilateral intracranialme lesions Yes 4 Sensory signs or symptoms? Likely peripheral neuropathy

Yes 5 Muscle atigability? Myastheniae. gravis / myasthenic syndrome Nor e

FBC, U+E, CK, ESR, Ca, TFTs, glucose

Proximal weakness with Yes 6 Likely myositis tenderness or ↑CK

Consider peripheral neuropathy, motor neuron disease, mononeuritis multiplex, myopathy, 7 generalised weakness secondary to acute illness, functional weakness Refer to neurologist if no cause identified co e co Limb weakness 199 Bilateral limb weakness: step-by-step assessment

1 Weakness strictly unilateral? If MRI excludes cord compression (and does not yield a definitive alternative diagnosis) Assess power in all four limbs and grade accord- consider spinal stroke if the onset of weakness ing to the MRC scale (Table 22.1). Ask about was very sudden, especially if accompanied any pre-existing limb weakness that predates by severe back pain. Examine for sparing of theooksf current presentation, e e.g. old stroke, and proprioception and vibration sense, and look whether it has changed recently. In any rapid- specifically for MRI changes of spinal infarction. onset weakness, perform a CBG; if <3.0 mmol/L, Otherwise, seek urgent neurological review and send blood for lab glucose measurementmebo but continue sfre to assess co as describedmebooksf below. treat immediately with IV dextrose and then reassess. Upper motor neuron signs, sensory level If the current presentation of limb weakness is 3 or sphincter disturbance? confined to one side of the body assess as per Bilateral weakness associated with UMN signs unilateral limb weakness (this includes patients ( tone, brisk reflexes, extensor plantar response), with contralateral facial weakness). Otherwise, ↑ a sensory level (Fig. 22.1) and/or bladder/bowel continue on the current diagnostic pathway, even dysfunction suggests myelopathy. if signs are markedly asymmetrical. sfree com Arrange an MRI spine to exclude cord Acute-onset or rapidly progressive compression and structural intrinsic 2 paraparesis? spinal disease, e.g. syringomyelia, glioma, abscess. In any patient with sudden-onset or rapidly • If neither is present, check whether the progressive paraparesis or tetraparesis: patient has had previous radiotherapy • immobilize the cervical spine pendingm (post-radiation free.c myelopathy) m me and measure oo imaging, if there is suspicion of recent plasma vitamin B12 levels to exclude trauma subacute combined degeneration of the • discuss immediately with a vascular cord. surgeon if weakness is accompanied by • Suspect transverse myelitis if the MRI features of acute limb ischaemia, e.g. pain; shows evidence of inflammatory change cold/pale/mottled skin; absent pulses and the time from first onset of symptoms • otherwise, arrange urgent spinal imaging, to maximal weakness was between 4 usually MRI, to exclude cord compression hours and 21 days – refer to a neurologist or raumatic injury. for further evaluation, e.g. CSF analysis If MRI confirms a compressive lesion, discuss autoimmune and infective screen. 22 withooksfree a neurosurgeon comor oncologist, depending • Suspect motor neuron disease on the clinical context and likely cause. bo(amyotrophic free com lateral sclerosis) if weakness is slowly progressive and sensory features are absent, especiallymeb if there are ks Table 22.1 Medical Research Council (MRC) associated LMN signs, e.g. fasciculation, or power rating bulbar involvement. Grade Findings on examination 1 No movement, not even muscle flicker 2 Flicker of muscle contraction only Box 22 2 Symptoms and signs suggestive of 3 Movement possible only when action raised intracranial pressure ofee.com gravity is removed and against no resistance • Severe headache • ↓GCS 4 Can move against gravity but not • VI nerve palsy or unilateral pupillary dilatation completely against full active resistance • Vomiting 5 Normal power against full active o• Bradycardia/systolic ee. hypertension resistance • Papilloedema Limb weakness 200 Bilateral limbcom weakness: step-by-step assessment

Fig. 22.1 Dermatomes. The blue dots indicate recommended sites for testing each dermatome. C2 To assess for a sensory level test light touch and pinprick sensation in each dermatome on both sides. If sensation is abnormal in the C3 lower dermatomes, move e c progressively upwards through the C4 truncal/uppermebooks limb dermatomes C4 until it normalizes. (From Ford MJ, Th2 C5 Hennessey I, Japp A. Introduction to Clinical Examination, 8th edn. C5 Th2 3 Edinburgh: Churchill Livingstone, 3 4 2005.) 4 5 5 6 6 Th 7 2 C6 7 8 8 9 Th 10 9 Th 1 11 1 10 12 C 11 L1 6 C8 12 L2 L1 m b f S S C8 2 4 C L2 L L C7 2 4 m7 S3 L5 L3

S1 L5 o Limb weakness 201 Bilateral limb weakness: step by-step assessment

Consider brain imaging to exclude bilateral Consider Guillain–Barré syndrome if distal intracranial lesions, e.g. cerebral emboli/ lower limb numbness or tingling is followed by metastases, venous stroke, demyelination, in any rapidly ascending weakness and absent tendon patient with bilateral UMN limb weakness and: reflexes (Table 22.2). • nooksf evidence e of myelopathy, i.e. normal • Measure urinary porphyrins to exclude MRI spine, no sensory level/sphincter acute intermittent porphyria. disturbance), or • Confirm the diagnosis with nerve • associated cortical signs (see Box 22.1), conduction studies and LP (↑CSF protein features of ↑ICP (Box 22.2), cranialm nerve sfrewith normal co cell count andme glucose). o sf lesions or cerebellar involvement. • Check and monitor vital capacity for Consider CT angiography of the Circle of evidence of respiratory depression. Willis to exclude basilar artery thrombosis in • Refer early to a neurologist for further patients with bilateral but asymmetrical neurol- evaluation. ogy associated with drowsiness and change in Slowly progressive limb weakness that is behaviour with a normal CT brain (seek expert more marked distally with a ‘glove-and-stocking’ advice). Obtain specialist neurological input in pattern of sensory loss strongly suggests a any suspected case of motor neuron disease or sensorimotor peripheral neuropathy, e.g. chronic multiple sclerosis, or if the cause remains unclear. inflammatory demyelinating polyneuropathy, oksfree.com hereditary sensorimotor neuropathy 4 Sensory signs or symptoms? • Arrange nerve conduction studies to In the absence of UMN signs, sphincter dys- confirm peripheral nerve disease and function or a sensory level, the combination differentiate demyelination from axonal of bilateral or generalized limb weaknessme with sfree.cdegeneration. m meb oksf sensory disturbance is usually due to peripheral • Investigate for an underlying cause, e.g. neuropathy. serum protein electrophoresis, HIV test, urinary porphyrins, fasting blood glucose. Consider spinal imaging to exclude bilateral Table 22.2 Clinical features of radiculopathy if sensory loss and motor signs Guillain–Barré syndrome follow a nerve root distribution (see Table 22.4). Remember these as the five ‘A’s: Acute course: Time from onset to maximal 5 Muscle fatigability? weakness = hours to 4 weeks 22 Ascendingo sfree. Initially in legs, progressing to Consider myasthenia gravis if the history or weakness: arms ± respiratory/bulbar/ examination findings suggest fatigable muscle facial muscles weakness: initially normal muscle power that At presentation 60% have rapidly weakens with sustained or repeated weakness in all four limbs; activity. Ocular and bulbar muscles tend to be 50% have facial weaknessm b s ee.com meboo affected before limb muscles. Areflexia: Absence of tendon reflexes helps Ask about the effect of exercise and other to distinguish Guillain–Barré activities on weakness. syndrome from myelopathy • Enquire specifically about diplopia during Associated Distal numbness, tingling or pain reading, weakening of the voice and sensory often precedes weakness symptoms: Loss of proprioception more difficulty in chewing/swallowing after the common than pain and fi st few mouthfuls of food. temperature • Examine for ptosis. Autonomic Sinus tachycardia, postural • Observe patients as they hold their arms involvement: hypotension, impaired above their head for a sustained period. ok comsweating often present • Listen while the patient counts to 50. Urinary retention and constipation are later features In suspected cases, consider a Tensilon test eif rapid free confirmation com is required, e.g. myasthenic mebook Limb weakness 202 Bilateral limb weakness: step-by-step assessment crisis or severe global weakness; otherwise, 7 Consider other causes check for anti-acetylcholine receptor antibodies, arrange a thoracic CT to exclude thymoma and Advanced myopathy may cause a degree of seek expert neurological input. muscle wasting and diminished tendon reflexes Tendon reflexes are normal in myasthenia but suspect an LMN lesion if there is flaccidity, gravis.ooksfre If muscle fatigability com is accompanied absent reflexes and/or fasciculation. by absent tendon reflexes that can be elicited • Consider Guillain–Barré syndrome if there following sustained muscle contraction, con- is new-onset, progressive limb weakness: sider Lambert–Eaton myasthenic mebosyndrome, sthe efeatures c in Table 22.2 mebdistinguish oksfrom a paraneoplastic syndrome – check for serum other causes. If suspected, confirm with LP antibodies to voltage-gated calcium channels, and nerve conduction studies. arrange electrophysiological studies and screen • Suspect lumbosacral plexopathy if there for an underlying malignancy. is severe pain and progressive weakness/ wasting of quadriceps with absent knee Proximal weakness with tenderness 6 reflexes – arrange imaging to exclude or ↑CK malignant infiltration of the plexus and Suspect myositis if symmetrical proximal muscle check fasting blood glucose to exclude weakness is accompanied by ↑CK. If the patient diabetes mellitus (diabetic amyotrophy) is taking statins reassess after a period of dis- • Exclude other causes of motor neuropathy continuation.ooks r Otherwise, e com send an autoantibody – check serum lead and urinary porphyrins screen, including anti-synthetase antibodies, e.g. and arrange nerve conduction studies. anti Jo-1 (associated with polymyositis); exclude • If nerve conduction studies are normal, other toxic causes, e.g. cocaine; andmebo arrange the free most likely com diagnosis ismebook motor neuron muscle biopsy. disease (progressive muscular atrophy) – Even if the CK is normal, consider further arrange electromyography and refer the investigation with muscle biopsy in any patient patient to a neurologist. with symmetrical proximal muscle weakness In patients w th a ‘patchy’ pattern of weakness, associated with aching, tenderness, pyrexia or examine to exclude multiple discrete peripheral ↑ESR. nerve lesionse com (Fig. 22.2), i.e. mononeuritis

Sensoryk Motor com Sensory Motor Sensory Motor Abductor pollicis Finger extensors Small muscles brevis of the hand except Thumb extensors abductors pollicis Opponens and abductors brevisboo pollicis Wrist extensors Ulnar half of flexor Brachioradialis digitorum profundus

A B C Flexor carpi ulnaris

Sensory Motor Toe dorsiflexors

Foot dorsiflexors

Foot evertors

Fig.o 22.2 Clinical signs in peripheral nerve lesions. A Median nerve. B Radial nerve. C Ulnar nerve D Common peroneal nerve. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009.) eb eb Limb weakness 203 Bilateral limb weakness: step by-step assessment multiplex; if suspected, arrange neurophysiologi- parathyroid hormone, if osteomalacia cal assessment and investigate for an underlying considered. At risk groups include the malignant vasculitic or infiltrative disorder. elderly, cirrhotic, malnourished patients and In patients with proximal muscle weakness ethnic minority groups, but this is overall a ± wasting and no associated neurological more common problem than is recognized. abnormality,ooksfre screen for underlying metabolic, Assess frail, elderly patients with generalized nutritional, endocrine and drug-related causes.eboweakness re as codescribed in Ch 24. • Enquire about alcohol intake. Consider a functional aetiology if there are no • Consider trial discontinuation of any objective features of organicmebooks disease and the potentially causative medication, e.g. statin, severity or pattern of weakness is inconsistent fibrate. – especially if the patient has a background of • Check for an underlying biochemical other functional disorders, e.g. irritable bowel disorder, e.g. ↓K+, ↑Ca2+. syndrome, fibromyalgia. • Look for clinical/biochemical features of Refer for specialist neurological evaluation if diabetes, Cushing’s syndrome, Addison’s the cause remains unclear. disease, thyroid disorders and acromegaly. ee.com • Check 25(OH) cholecalciferol alongside serumksf calcium, ee.com alkaline phosphatase and

22 Limb weakness 204 Unilateral limb weakness: overview

1 Sudden onset? fre com No Yes

Yes Consider ischaemia, fracture, Painful? compartment syndrome

Yes Total duration <3 hours? Likely transient ischaemic attack No See Further Likely stroke assessment of stroke (p. 207)

Seizure(s) or evidence of ICP / cortical Yes Consider space- 2 ↑ Neuroimaging dysfunction / CNS infection? occupyingre c lesion, fre meningoencephalitis No

3 Upper motor neuron signs?

Yes

Yes Contralateral sensory loss? Unilateral cord lesion MRI spine

No No Consider space-occupying lesion, stroke, multiple sclerosis, motor neuron disease

Yes 4 Signsf referable to single m nerve root / nerve? Radiculopathy / mononeuropathy

5 Consider plexopathy, multi-root compression, stroke, motor neuron disease, migraine, functional weakness e r e.c m Limb weakness 205 Unilateral limb weakness: step-by-step assessment

1 Sudden onset? Table 22.3 ABCDD score in TIA Evaluate weakness as ‘sudden-onset’ if it reaches maximal intensity within a few minutes 1 2 from the first appearance of symptoms. Age ≥60 ooksfIf there is painful e weakness of a single limb, Blood Systolic ≥140 or consider vascular and orthopaedic causes: pressure diastolic ≥90 • compare pulses, colour, temperature and Clinical Speech disturbance Unilateral capillary refill with the unaffectedmebo limb – features fr cono weakness m weakness seek immediate vascular review if there is Duration 10–59 minutes ≥60 minutes any suspicion of acute limb ischaemia of attack • request an X-ray of the limb if there is any Diabetes Yes history of trauma • measure CK and request an urgent orthopaedic review if there are features of compartment syndrome (see Box 21.3, p. 193). • Otherwise, consider discharge Consider post-ictal weakness (Todd’s paresis) with appropriate secondary if the history suggests seizure activity immediately prevention and specialist follow up priorooksfree to the onset of cweakness m – arrange rapid within a week. neuroimaging unless the cause of seizures is • Arrange neuroimaging prior to discharge in already established, the post-ictal phase is known any patient taking warfarin. e oo to include limb weakness and the weaknessmebo is o improving. Seizure activity or evidence of Acute non-neurological illness or hypotension 2 ↑intracranial pressure/cortical may exacerbate established limb weakness dysfunction/CNS infection? from an old stroke – suspect this if the current weakness is confined to the same territory as a New-onset seizures, signs of cortical dysfunction previously documented persistent neurological (see Box 22.1) or evidence of ↑ICP (see Box deficit and there are other clinical/laboratory 22.2) suggest underlying brain pathology. features to suggest acute systemic illness, but • Arrange prompt neuroimaging (usually CT maintain a low threshold for further neuroimaging. brain) to identify the cause. In the absence of the above causes, sudden- • Seek anaesthetic review prior to scanning if 22 onset unilateral weakness is highly likely to GCS <8 or signs of airway compromise. representooksfree.com a stroke or TIA. If symptoms persist • See page 276 for further assessment of for >3 hours, then proceed, in the first instance, seizures. to ‘Further assessment of stroke’ (p. 207). • In all cases, seek expert neurological advice Diagnose TIA if symptoms havemebo resolved and ree.c consider further m investigationm book with LP completely and lasted <3 hours. ± MRI if CT fails to reveal an underlying • Evaluate for risk factors and sources of cause. embolism as described under ‘Further Consider meningoencephalitis if there is onset assessment of stroke’. of limb weakness over hours accompanied by • Assess the risk of impending stroke using fever, meningism (Box 18.2, p. 169), purpuric the ABCDD score (Table 22.3). rash or features of shock (Box 30.1, p. 267). If • Admit or arrange next-day specialist meningoencephalitis is suspected, obtain blood referral for any patient with >1 TIA cultures, give empirical IV antibiotics/antivirals nksfree.com a week or an ABCDD score ≥4 for and arrange urgent CT brain; thereafter, perform urgent control of risk factors and carotid an LP for CSF analysis unless contraindicated Doppler USS. o(p. sfree.co 170). ooksf Limb weakness 206 Unilateral limb weakness: step-by-step assessment

3 Upper motor neuron signs? nerve root (Table 22.4), or a mononeuropathy if they correspond to a single peripheral nerve A UMN pattern of weakness indicates a lesion (see Fig. 22.2). If radiculopathy is suspected, proximal to the anterior horn cell; progressive consider a spinal MRI, particularly if weakness onset of weakness suggests a space-occupying is progressive. lesionooksf whilst a erapid onset om favours a vascular or inflammatory cause. 5 Consider other causes Exclude a unilateral cord lesion if there is dis- sociated sensory loss (ipsilateral proprioception/m boPerform sfre 2 lesion co or demyelinationm in any patient oksf vibration; contralateral pain/temperature) or a presenting with hemiparesis, even if there are clear sensory level. Otherwise, arrange neuro- no obvious UMN features; if results are normal, imaging; CT is the usual first-line modality but consider hemiplegic migraine. consider MRI if CT is inconclusive, especially if If weakness is confined to a single limb, there are brainstem features, e.g. contralateral consider mu ti-level root compression (see Table cranial nerve palsies or cerebellar signs. 22.4) or plexopathy, e.g. lumbosacral plexopathy Consider an atypical presentation of motor (see above) or brachial plexopathy. neuron disease (usually bilateral) if neuroimaging Otherwise, consider mononeuritis multiplex fails to reveal a cause and sensory features are (seesfree.com above), an atypical presentation of motor absent, especially if there are associated LMN neuron disease (usually bilateral) or functional signs. weakness. ooksf ee com Seek expert neurological input in any case Signs referable to single nerve where the diagnosis remains unclear.eb oksf 4 root/nerve? In the absence of UMN signs, suspect a radiculopathy if clinical signs are referable to a single

Table 22.4 Clinical signs of nerve root compression

Root Weakness Sensory loss (see Fig. 22.1) Reflex loss C5 Elbow flexion (biceps), arm and shoulder Upper lateral arm Biceps abduction (deltoid) oC6 Elbow ree flexion (brachioradialis) Lower lateral arm, thumb, index finger Supinatoro C7 Elbow (triceps), wrist and finger extensors Middle finger Triceps L4 Inversion of foot e ksfrInner calf Knee L5 Dorsiflexion of hallux/toes Outer calf and dorsum of foot S1 Plantar flexion Sole and lateral foot Ankle Limb weakness 207 Further assessment

Further assessment of stroke Step 3 Evaluate for risk factors/underlying cause In any patient with ischaemic stroke, identify modifi- Step 1 Assess eligibility for thrombolysis/mechanical able risk factors for vascular disease, including clot retrieval hypertension, hypercholesterolaemia, smoking and If facilities are available, refer immediately to diabetes; arrange Doppler USS to determine the strokeooks team refor consideration of thrombolysis/ presence and severity of carotid stenosis unless the mechanical clot retrieval in any patient with a affected territory is within the posterior circulation potentially disabling stroke whose first onset of or the patient is unfit for vascular surgery. symptoms occurred within the lastmebo 4.5 hours sfreSuspect a cardiac source ofmebooksf cerebral embolism (potentially longer time frame if mechanical clot if the patient has retrieval available). Where the time of onset is • current or previous evidence of atrial fibrillation uncertain, e.g. symptoms present on awakening, • a recent myocardial infarction define it as the last time the patient was known • clinical features suggesting endocarditis, to be well. Assess rapidly for contraindications e.g. fever and new murmur (Box 22.3) in conjunction with the on-call stroke • ≥2 cerebral infarcts (especially in different team. In patients who meet clinical eligibility territories) criteria, arrange immediate CT brain to exclude • other systemic embolic events, e.g. lower haemorrhagic stroke. limb ischaemia. Step 2 Classify stroke according to clinical and Consider further investigation with transthoracic radiologicalooksfree findings com and, in selected cases, transoesophageal Arrange neuroimaging to differentiate haemor- echocardiography. rhagic stroke from ischaemic stroke and to Investigate for an unusual cause of stroke in exclude non-stroke pathology, emeb g. space- younger free patients com without vascularm risk boo factors. s occupying lesion. Perform a CT brain urgently if • Perform a vasculitis and thrombophilia screen. • the patient is eligible for thrombolysis • Request a bubble contrast echocardiography (see above) to detect a right-to-left shunt, e.g. patent • coagulation is impaired foramen ovale that would permit ‘paradoxical • ↓GCS embolism from the venous circulation. • symptoms include a severe headache • Consider MRA to exclude carotid/vertebral • there is a rapidly progressive neurological artery dissection. deficit • cerebellar haemorrhage is suspected (to exclude obstructive hydrocephalus). Box 22.4 Bamford classification of stroke 22 Otherwise, perform CT within 12 hours of ooks ree. o This separates stroke into four clinical presentations that presentation. Irrespective of CT findings, use the relate to the affected vascular territory and correlate with Bamford classification (Box 22.4) to categorizeebo prognosis. ree.com ebo stroke. TACS (total anterior circulation stroke) • All three of: 1 Box 22.3 Contraindications to thrombolysis 1. weakness/sensory deficit affecting 2 out of 3 of face/arm/leg • Seizure at stroke onset 2. homonymous hemianopia • Symptoms suggestive of subarachnoid haemorrhage 3. cortical dysfunction, e.g. dysphasia, apraxia • Prior intracranial haemorrhage • Intracranial tumour PACS (partial anterior circulation stroke) • Stroke or serious head trauma within last 3 months • Two out of three of the TACS criteria, or cortical • Arterial puncture at a non-compressible site or LP dysfunction alone within 1 week LacS (lacunar stroke) • Active haemorrhage • Suspectedoksfree.co acute pericarditis or aortic dissection • Causes limited motor/sensory deficits withno co tical • Systolic BP >185 mmHg or diastolic BP >110 mmHg dysfunction • INR >1.7, thrombocytopenia or bleeding disorder PoCS (posterior circulation stroke) • Pregnancy ebo• Causes ree a variety com of clinical syndromes, including 1Most are relative contraindications – seek guidance from the homonymous hemianopia, cerebellarm dysfunction o and on-call stroke team if the patient is otherwise eligible. the brainstem syndromes Low back pain 23 ks ooksf e

Low back pain is defined as posterior pain Lumbar spine stenosis between the lower rib margin and the buttock creases; it is acute if the duration is <6 weeks, Narrowing of the lumbar spinal canal typically persistent if it lasts for 6 weeks to 3 months, and occurs in patients >50 years as a result of chronic if it is present for >3 months. In 90% of degenerative spinal changes and may cause patients no specific underlying cause is found lumbosacral nerve root compression. Patients – the pain is thought to originate from muscles often have longstanding, non-specific low and ligaments, and is termed ‘mechanical’. back pain before developing dull or cramp- Radicular pain (‘sciatica’) originates in the lower ing discomfort in the buttocks and thighs back and radiates down the leg in the distribu precipitated by prolonged standing walking tiono ofksfree ≥1 lumbosacral com nerve roots (typically and eased by sitting or lying down (neurogenic L4–S2) ± a corresponding neurological deficit claudication). (radiculopathy). Vertebral trauma and fracture A thorough history and examination,m sup bo- sfree com m ooksf plemented where necessary by spinal imaging, This most commonly follows a fall, road traffic is critical to identify patients with low back pain accident or sporting injury, but may occur who have serious and/or treatable pathology. with minimal or no trauma in patients with osteoporosis or spinal conditions, e.g. anky- Mechanical back pain losing spondylitis. A patient with localized low This is by far the most common cause of low back pain following trauma requires imaging to back pain. The pain tends to be worse during evaluate instability and involvement of the spinal activity, relieved by rest, and is not associated canal/cord. with sciatica, leg weakness, sphincter distur- Spondyloarthritides (inflammatory bance, claudication or systemic upset. An acute back pain) episode is often precipitated by bending, lifting oroo straining. sfree.com In most cases, the pain resolves These chronic inflammatory joint diseases include after a few weeks but recurrence or persistent ankylosing spondylitis and psoriatic arthritis, and low-grade symptoms are relatively common. predominantly affect the sacroiliac joints and axial Risk factors for developing chronic,mebo disabling skeleton; free.com they have a strong geneticmeb association pain include depression, job dissatisfaction, with HLA-B27. Ankylosing spondylitis typically disputed compensation claims and a history of presents in early adulthood with an insidious other chronic pain syndromes. onset of progressive back pain and stiffness over months to years. Lumbar disc herniation This is the most common cause of sciatica. It Spinal tumour predominantly affects young and middle-aged Vertebral metastases from breast, lung, prosta e adults, often following bending or lifting. Symp- or renal cancer are far more common than toms may be exacerbated by sneezing, coughing primary vertebral or other spinal tumours The or straining. The diagnosis is largely clinical and spine is frequently involved in patients with mostooksfree cases resolve within com 6 weeks. Imaging is multiple myeloma. Red flag features (see Box needed for patients with persistent pain and/orbo 23.1 sfree) may suggest com the diagnosis whichbooksf is best neurological deficit. confirmed with MRI. Low back pain 209 Differential diagnosis

Box 23.1 Red flags for possible spinal cancer Box 23.2 Factors that increase the risk of spinalfre infection o • New-onset pain in a patient >55 years • Active or previous cancer • Diabetes mellitus • Constant, unremitting or night pain • General debility ooks• Focal bony retenderness • Indwelling vascular catheters • Unexplained weight loss • IV drug abuse • Fever, sweats, malaise, anorexia • Previous TB infection • Immunosuppression, e.g. HIV infection, chronic steroid therapy m Spinal infections Pyogenic vertebral osteomyelitis, epidural referral for decompression. Diagnosis is best abscess, ‘discitis’ or vertebral tuberculosis (TB) confirmed by MRI. may produce severe, progressive pain, often Other causes with localized tenderness and reduced range of movement. Typical associated features include • Spondylolisthesis (forward slippage of one fever, sweats, malaise and ↑WBC/inflammatory vertebra on another): may cause back and markers Risk factors for spinal infection are radicular pain, and occasionally requires shown in Box 23.2. MRI is sensitive for detecting operative decompression. infection and differentiating from tumour. • Pelvic pathology, e.g. prostate cancer, ooksf ee com pelvic inflammatory disease. Cauda equina syndrome • Renal tract pathology, e.g. stones,e ocancer, k Compression of the collection of nerve roots at pyelonephritis. the base of the spine due to central discm prolapse, • Abdominal free. aortic om aneurysm. trauma or haematoma may lead to irreversible • Shingles. neurological damage and needs emergency • Pregnancy. m

23 Low back pain 210 Overview

Full clinicale assessment m + lumbar spine examination

Bilateral lower limb neurology, sphincter Yes Immediate 1 Cauda equina / other cause dysfunction or ↓perianal sensation? oMRI f spine o

MRI spine Pyrexia, ↑inflammatory markers or Yes 2 + Spinal infection / other cause high clinical suspicion of infection? blood cultures

Sudden-onset pain + known / Yes Spinal 3 Vertebral fracture suspectedree osteoporosis? X raye No

Yes 4 ‘Red flags’ for cancer (Box 23.1)? MRI spine Spinal tumour / other cause bo No

Yes Refer to 5 Inflammatory features? Likely spondyloarthritis rheumatologist

Yes 6 Radicular pain? Likely disc herniation or spinal stenosis

Nor e.

Yes 7 Neurogenic claudication? oLikely spinal e stenosis MRI spine o No

Likely mechanical back pain. Consider MRI spine if progressive / persistent symptoms 8 Otherwise assess for adverse prognostic factors Low back pain 211 Step-by-step assessment

Clinical tool Examination of the lumbar spine • Look for abnormal posture (scoliosis/loss of lordosis) • Test for sciatic nerve root compression (Fig. 23.2): from the back and side when the patient is standing. with the patient supine, slowly flex the hip to 90° • Feeloksfre for tenderness over the bony prominences and with the knee fully extended; limitation of flexion by paraspinal muscles. pain radiating down the back of the leg to the foot • Observe extension, flexion and lateral flexion of the (increased by dorsiflexing the ankle) indicates L4/L5/S1 lumbar spine (Fig. 23.1). nerve root tension (usually due to L3/4, L4/5 or L5/S1 • Assess spinal flexion using Schober’s test:me locate the lumbar disc herniation). co meboo line between the posterior superior iliac crests (L3/L4 • Test for femoral nerve root compression (Fig. 23.3): interspace); mark two points 10 cm above and 5 cm with the patient prone, flex the knee to 90°; then, if below this line. Ask the patient to bend forward as far pain-free, slowly extend the hip. Pain radiating from the as possible, with the knees extended. Lumbar flexion is back down the front of the leg to the knee indicates L2/ restricted if the points separateom by <5 cm. L3/L4 nerve root tension. com

Fig. 23.1 Movements of the spine. A Extension. B Flexion. C Lateral flexion. (From Ford MJ, Hennessey I, Japp A Introduction to Clinical Examination, 8th edn. Edinburgh: Churchill Livingstone, 2005.) mebook

A B C

Fig. 23.2 Stretch test – sciatic nerve roots A Neutral; nerve roots slack. B Straight leg raising limited 23 by tension of root over prolapsed A disc. (From Ford MJ Hennessey I, Japp A. Introduction to Clinical Examination, 8thmebook edn. Edinburgh: Churchill Livingstone, 2005.)

B Low back pain 212 Step-by-stepcom assessment

Fig. 23.3 Stretch test – femoral nerve. A Patient prone and free from pain because femoral roots are slack. B When femoral roots are A tightened by flexion of the knee +/− extension of the hip pain may be felt in the back. (From Ford MJ, Hennessey I, Japp A. Introduction to Clinical Examination, 8th edn. Edinburgh: Churchillmebooks Livingstone, 2005.)

Bilateral lower limb neurology, sphincter Pyrexia, ↑inflammatory markers or high 1 2 dysfunction or ↓perianal sensation? clinical suspicion of infection Ask specifically about: Check WBC, CRP and ESR and perform spinal • ooksf change in urinary frequency X-rays if the patient has risk factors for spinal • any new difficulty in starting or stopping infection (see Box 23.2), localized spinal tender- micturition e ness or a history of night sweats, shivers or • a change in the sensation of toilet paper constitutional upset. Take threemeboo blood cultures when wiping after defecation and arrange urgent MRI spine if any of the • episodes of urinary/faecal incontinence. following is present: If there is any suspicion of bowel/bladder • pyrexia >37.9°C dysfunction, perform a PR examination to • ↑WBC/CRP/ESR assess anal tone and measure bladder volume • high clinical suspicion in a patient with an immediately after voiding by bedside USS or indwelling vascular catheter, IV drug abuse catheterisation; >200 mL suggests urinary or immunosuppression retention • X-ray features suggestive of osteomyelitis Enquire also about weakness or unusual • A known focus of infection, e.g. abscess sensations, e.g. numbness, tingling in the lower cellulitis. limbs;ooksfree.com examine the legs carefully for reduced power, diminished reflexes and sensory disturbo- free com Sudden-onset pain known/suspected bance, and test perianal sensation + e k 3 osteoporosis? Arrange immediate MRI spine to exclude cauda equina syndrome in any patient with low back Perform plain X-rays to look for lumbar com- pain (irrespective of its characteristics) associated pression fractures if the patient has new and with any of: abrupt onset of pain and known/suspected • urinary or faecal incontinence osteoporosis Suspect osteoporosis if: • urinary retention (significant post-void • long-term systemic steroids have been residual urine or ↑bladder volume with no taken urge) • >65 years of age with loss of height, • altered perianal sensation/↓anal tone kyphosis or previous radial/hip fracture. • bilateral lower limb neurological signs or Seek an alternative cause if the X-ray reveals symptoms. no fracture or one that does not correspond to ooksfRequest emergency e com orthopaedic/neurosurgical the level of pain. Consider further investigation review if the MRI confirms cauda equinabo if there fre are any c red m flag features, other than compression. age (see below). ebook Low back pain 213 Step by-step assessment

4 ‘Red flags’ for cancer (Box 23.1)? Suspect lumbar spinal stenosis if the patient is >50 years with a slow progressive onset Investigate for vertebral metastases, e.g. radio- of symptoms and/or features of neurogenic isotope bone scan if the patient has a history claudication (see below). of active or previous lung/prostate/breast/renal/ Consider referral for further investigation if: thyroidooksf cancer. ePerform a breast examination and • persistent pain myeloma screen, measure PSA (in males) Ca2+ • evidence of >1 nerve root involvement and ALP, and consider MRI spine in any other • major disability e ooksf patient with ‘red flag’ features. meboo• s suspected reco lumbar spinal stenosis.

5 Inflammatory features? 7 Neurogenic claudication? Check ESR/CRP and perform plain spinal Consider neurogenic claudication if low back X-rays if gradual onset of low back pain and pain is accompanied by bilateral thigh or leg stiffness. discomfort, e.g. burning, cramping, tingling, that Refer to rheumatology for further evaluation arises during walking or on standing and is rapidly of possible inflammatory back pain if there are relieved by sitting, lying down or bending forward. X-ray features of spondylitis, e.g. squaring of the Evaluate first for vascular claudication if the vertebral bodies/sacroiliitis or >1 of the following: patient has a history of atherosclerotic disease, • morningoksfre stiffness clasting m >30 minutes >1 vascular risk factor, e.g. diabetes mellitus, • improvement of symptoms with exercise smoking, ↑BP, ↑cholesterol or signs of peripheral but not rest arterial disease, e.g. diminished pulses, femoral • nocturnal back pain that arises in the bruit, trophic skin changes Check the ankle: second half of the night mbrachial sfree pressure com index (ABPI)mebooksf and request a • radiation of pain into the buttocks vascular opinion if <1.0. • restricted lumbar spine movements If neurogenic claudication is still suspected, • sacroiliac tenderness consider MRI spine to confirm the presence of • ↑ESR/CRP with no alternative explanation. lumbar spinal stenosis, especially if symptoms are disabling. 6 Radicular pain? Likely mechanical back pain. Pain is ‘radicular’ if it radiates to the lower limb 8 Consider MRI spine if progressive/ beyond the knee with any of: persistent symptoms • dermatomaloksfre distribution om (see Fig. 22.1, Refer to orthopaedics if neurological dysfunction p. 200) or spinal deformity. In the absence of neurological, 23 • evidence of radiculopathy structural, infective, red flag or radicular features, • positive sciatic or femoral stretch test provide reassurance and analgesia, recommend (Figs 23.2 and 23.3). mthat the patient e.com stays active andmebo reassess after a Suspect lumbar disc herniation in acute-onset period of 6–12 weeks. If pain persists, look for radicular pain, especially if the nerve stretch test features of depression and explore other potential is positive. In the absence of red flags or other psychosocial factors. Spinal imaging is unlikely concerning features, reassess after 6–12 weeks to be helpful but seek specialist input if there are of analgesia physiotherapy. persistent or comprogressive disabling symptoms. ± e. om Mobility problems: falls and immobility 24 oksfre ooksf

Patients may present with falls, difficulty dizziness, joint pains or focal limb weakness. In mobilizing or complete immobility. Younger these cases, assessment should focus, initially, patients can usually be rapidly categorized on the underlying primary problem to determine into an underlying aetiology, but evaluation the cause. Some patients with apparent falls may of elderly patients is more complex. Normal actually be experiencing blackouts and, again, physiological changes of ageing – increased body this necessitates a different diagnostic approach. sway, reduced muscle bulk (sarcopenia) and Acute illness or drug reaction impaired reaction time – increase the likelihood of mobili y problems. Moreover, mobility problems In elderly/frail patients, a sudden decline in may be self-reinforcing, as reduced activity leads mobility (acute fall, inability to mobilize) may be toooksfree loss of muscle function com and confidence. A the principal manifestation of any acute medical, thorough, systematic approach is essential to surgical or psychiatric illness or a side-effect of identify adverse consequences of immobility, certain medications (Box 24.1). In those with serious underlying pathology and mebopotentially chronic free.com underlying mobility problems,mebook a relatively reversible contributing factors. minor insult may lead to a major deterioration in mobility. Accidental trip Multifactorial mobility problems Some falls are the unavoidable consequence of a trip or stumble. In the absence of significant In patients with recurrent falls or other chronic injury, recurrent mobility problems or other mobility problems, there is often no single concerns these patients do not require detailed identifiable cause but rather multiple contributing assessment. However, many elderly patients factors, e.g. muscle weakness, balance disorder, exhibit post hoc rationalization of their fall (‘I must po ypharmacy, cognitive impairment, arthritis, have tripped on the carpet’), so falls should only ↓visual acuity, hearing loss. A comprehensive be classified as accidental if there is unequivocal and multidimensional approach to assessment evidenceooksf for this. e co is essential. ooksf ‘Secondary’ mobility presentations Immobility and instability may occurm as a con oo- sfre .c m sequence of other specific problems such as Mobility problems: falls and immobility 215 Differential diagnosis

Box 24.1 Drugs associated with increased risk of falls • Alcohol • sBenzodiazepines om • Anticonvulsants • Diuretics • Antidepressants • Digoxin ooks• Antihypertensives r • Opioids • Antipsychotics • Diabetes medications (oral hypoglycaemicse and insulin)

Clinical tool How to perform a gait assessment • Ask patient to stand from sitting position disease, pain); short, shuffling steps (Parkinson’s Look for: need for assistance; necessary use of disease1 diffuse cerebrovascular disease); high- upper limbs stepping gait (foot-drop, sensory ataxia); broad- • Ask patient to continue standing based/unsteady gait (cerebellar lesion, normal Ask about: light-headedness/sensation of spinning or pressure hydrocephalus) movement • Ask the patient to walk for a longer distance Lookksfree.co for: ability to continue standing safely/ Ask about: chest pain, calf pain, breathlessness, unsteadiness/stooped posture fatigue • Ask patient to move feet together – ensure he/she is Look for: ↑RR, laboured breathing, need standing close by bto ree.c stop Look for: increasing unsteadiness • Repeat, if necessary, after correction of any reversible • Ask patient to close eyes (Romberg’s test) factors, e.g. treatment of acute illness,m effective pain Look for: increasing unsteadiness (be ready to control, rehydration, removal of offending drug catch patient) • Ask patient to open eyes, walk 3 metres, then turn around and walk back, using an aid if required Look for: overall safety and stability; unilateral gait abnormality (stroke, peripheral nerve lesion, joint

1Other features of Parkinsonian gait include reduced arm-swing, stooped postur and, sometimes, difficulty in starting and stopping (‘festinant’ gait) e fre com

24 Mobility problems: falls and immobility 216 Mobility problems: overview

Full clinicalre assessment com + collateral history

Significant injuries or other Yes Evaluate and treat: fractures / wounds / head injury 1 sequelae of fall / immobility? / pain / hypothermia / rhabdomyolysis / dehydrationoo No

Fall related to stumble / trip Yes 2 Accidental trip with none of features in Box 24.3?

Primary prob em = focal limb weakness Yes Mobility secondary Presentation-specific 3 ↓ / blackoutree / dizziness / acute joint pain? to specificee cause assessment (see text) No

Yes Likely acute illness / Identify and treat 4 Abrupt decline in mobility? new drug (see text)bo No

Assess gait (Box 24.4), cognition and visual acuity

Yes 5 Gait or neurological abnormality? See Gait abnormalities

No*

Yes Review medications; consider trial 6 On >3 drugs / high-risk drug (Box 24.1)? r m discontinuationfre / ↓dose m No*

Yes 7 Cognitive impairment / confusion? See Assessment of confusion (Ch 8)

No*

Yes 8 Sensory impairment? Consider referral to optician / ophthalmologist

No*

Yes 9 High fracture risk? Consider bone protection

No*

Multifactorial mobility problem: 10oFunctional ee assessment with input from multidisciplinary team in all cases Consider referral to falls clinic / day hospitalebo if ongoing mobility e problems m * Or problem reviewed / dealt with Mobility problems: falls and immobility 217 Mobility problems: step-by-step assessment

Significant injuries or other sequelae of not ‘normal’ and the visual impairment that led 1 fall/immobility? to the trip or the poor balance that turned it into an injurious fall might be reversible. On the other In all patients who have fallen (or who have been hand, exhaustive assessment is inappropriate found on the floor), perform a rapid but thorough in patients with a genuinely accidental fall and surveyook of the fre entire body for injuries. Fractures, no underlying mobility problems. Have a low lacerations or bruising may be not immediately threshold for further evaluation if any of the apparent, and the cognitively impaired patient features in Box 24.3 is present or events leading may not bring them to your attention. meboAssess the up sfre to the fall comare unclear. mebooksf perfusion and function of any limb with bruising, deformity, pain or swelling and consider the need Primary problem = focal limb weakness/ for X-rays. Pain will compound any existing mobility 3 blackout/dizziness/acute joint pain? problems – ensure it is adequately treated. If there is a history of head injury, arrange neuroimaging if If you identify new limb weakness on examination, any of the features in Box 24.2 is present. assess as described in Chapter 22. In patients with a prolonged period of immobil- If mobility problems are consequent on diz- ity, e.g. lying on the floor or confined to bed, ziness, evaluate firstly for symptomatic postural check temperature to exclude hypothermia, look hypotension: a fall of ≥20 mmHg in systolic BP for clinical/biochemical evidence of dehydration or ≥10 mmHg in diastolic BP within 3 minutes and examine the heels and sacrum for pressure of changing from a lying to standing position, sores.ooksfree.com Consider aspiration/hypostatic pneumonia accompanied by a feeling of light headedness/ in patients with hypoxia, lung crackles or CXR pre-syncope. If this is detected, search for changes. If there has been significant soft tissue underlying causes, e.g. antihypertensives, pressure damage or any prolonged timemebo on the dehydration, sfree.c autonomic m neuropathy.mebooksf Otherwise, floor, check CK and urinary myoglobin (sug- assess as in Chapter 10, but complete a full gested by haematuria on urinalysis with no red mobility assessment, especially if no specific cells on microscopy) to exclude rhabdomyolysis disorder is identified. and be vigilant for compartment syndrome (Box Consider whether an apparent fall could have 21.3, p. 191). been a blackout. Beware of accepting rationaliza- tions for the event (‘I must have tripped’) and Fall related to stumble/trip with none of make every attempt to obtain an eyewitness 2 features in Box 24.3? account of the current episode or previous ones. If patients cannot recall how they came to be Take care in making this diagnosis – a simple trip lying on the ground, assess, in the first instance, on ao loose sfre carpet tile com at walking pace is usually as per transient loss of consciousness (see Ch. 31). Also suspect transient loss of consciousness if the patient was witnessed as having a period of 24 Box 24.2 Indications for early neuroimaging in patients with head injury1 m ounresponsiveness, sfree com sustained facialmebooksf injuries during the fall (most conscious patients can protect Immediate CT brain the face) or experienced palpitation, chest pain, • ↓GCS <12 or persistently <15 breathlessness or a pre-syncopal prodrome prior • Focal neurological signs • Persistent headache or vomiting • Features of basal skull fracture Box 24.3 Features not consistent with a diag- • Coagulopathy or anticoagulation nosis of simple accidental trip CT brain within 8 hours • Recurrent or multiple falls • Seizure • Recentfr edecline c in mobility m or functional status • >65 years + episode of loss of consciousness • Inability to get up from the ground • Retrogradeksfree amnesia co • Implausible mechanism for fall • Evidence of skull fracture • Witnessed period of unresponsiveness • Inability to recall landing on ground 1Based on SIGN guideline 110. • Facial injuries Mobility problems: falls and immobility 218 Mobility problems: step-by-step assessment to ‘falling’. Have a lower threshold for further 5 Gait or neurological abnormality? evaluation of possible syncope in patients with ECG abnormalities (see Box 31.3, p. 273) or a Assessment of walking pattern is key to under- history of major cardiac disease. standing mobility problems. It is a fundamental If oksfremobility problems com are secondary to an element of the neurological examination and can acutely painful joint, assess as in Chapter 20. reveal abnormalities not elicited on gross testing boof sfindividual e modalities. It may also unmask 4 Abrupt decline in mobility? impaired effort tolerance due to cardiorespiratory or lower limb disease. Finally, themebooks gait assessment An abrupt decline in mobility (acute fall, new is an opportunity to assess falls risk, even in the onset of recurrent falls or being ‘off legs’) is absence of specific findings. Check that patients one of the classical atypical presentations of are safe to mobilize, equip them with their normal acute illness in the elderly. Characteristic signs/ walking aid and follow the steps in Clinical tool: symptoms of the specific precipitant may be Assessment of gait. Go to ‘Gait abnormalities’ absent and ‘screening’ investigations (Box 24.4) (p. 220) if any abnormalities are detected. are often required to uncover the problem or identify a focus for further assessment. 6 On >3 drugs/high-risk drug (Box 24.1)? Review all new drugs (including over-the- counter ones) started within the previous weeks Medications are one of the most readily modifi- and consider trial discontinuation of any high- able of all factors influencing mobility problems riskooksfree.com agents (see Box 24.1). If significant loss of but indiscriminate changes may do more harm mobility was preceded by a fall, consider the than good. Individual medications that increase possibility of fracture or head injury – ensure the risk of falling are listed in Box 24.1. Polyp- pain is adequately treated. meboharmacy ( e≥5 regular com medications)mebook is a risk factor Weight loss, muscle wasting, hypoalbumi- for falls. Review the indications for all drugs: naemia and chronic anaemia may suggest a are they still required? Look for opportunities to progressive disorder ‘coming to a head’. Suspect rationalize treatment, consider alternatives and significant acute illness in patients whose baseline consider decreasing the dose. mobility is relatively normal. Once this has been A gradual approach will allow the impact of addressed, complete a full assessment to identify individual changes to be assessed and is essential underlying mobility problems and reversible risk with psychotropic medication where abrupt with- factors for falling. drawal may be worse than the toxic syndrome. In patients with a background of progressive Explore a possible contribution from alcohol in mobility decline/deteriorating functional status/ all cases – in patients with underlying mobility/ generalooksfree frailty, the acute com precipitant may be minor balance problems it may critically impair stability, – do not over-emphasize it in comparison with even when consumed within recommended limits. the underlying contributory factors. ebo ksfree com 7 Cognitive impairment/confusion?mebooks Acute delirium is a common cause of reduced mobility, and may not be readily apparent if it is hypoactive or superimposed on chronic impair- Box 24.4 Screening investigations to identify ment. Vigilance and collateral history are essential acute illness in elderly patients counterparts to objective measures of cognitive • Capillary BG function; an Abbreviated Mental Test score of • PR examination 6/10 is difficult to interpret without knowledge of • Urine dipstick and MSU/CSU (avoid diagnosing a baseline ability. Chronic cognitive impairment is urinary tract infection purely on the basis of abnormal alsosfree a risk factor com for falls, but difficult to amelio- dipstick results) rate. Consider silent precipitants of wandering/ • Bloodoksfre tests – FBC, U+ coE, LFTs, glucose, CRP getting out of bed, such as urinary urgency (minimum) • CXR or nicotine withdrawal. Further assessment of confusion is detailed in Chapter 8. mebooksf Mobility problems: falls and immobility 219 Mobility problems: step by-step assessment

8 Sensory impairment? fractures or a bone mineral density T-score of −2 5 or less and in those taking long-term or Visual impairment increases the risk of falls and frequent courses of systemic steroids. In other may be reversible, e.g. refractory errors, cataracts cases, consider using the Q-fracture risk assess- Screen for ↓visual acuity. If detected, refer to ment tool, http://qfracture.org. anooks ophthalmologist re (or an optician if a refractory error is suspected). Hearing loss may also Multifactorial mobility problem: arrange contribute to instability and increased risk of 10 falling, particularly in combination withmeboo some of sfremultidisciplinary com team assessmentm oksf the other risk factors. All patients with recurrent falls or ↓mobility should be referred to physiotherapy/occupational therapy 9 High fracture risk? for assessment of functional ability, environmental Fractures, especially of the hip, are a devastating contributors to the presentation, and scope for consequence of falls and selected patients may benefit from measures such as walking aids/ benefit from bone protection. This is a contro- strength and balance training/home alarms. versial area and specific indications change, In patients with ongoing problems, consider but treatment, e.g. bisphosphonates, should referralsfree.com to day hospital or a specialist falls clinicsf be consideredksfree.co in patients with previous fragility for comprehensive assessment.

24 Mobility problems: falls and immobility 220 Gait abnormalities: overview

Yes Consider focal weakness / proximal 1 Unable to stand up unaided? fr com myopathyfre / pain / acute illness No

Yes Consider postural hypotension / 2 Unsteady with eyes open? cerebellar ataxia / vertigo

Yes Seek underlying 3 Positive Romberg test? Sensory ataxia cause

Yes Likely Parkinson’s Refer to 4 Features of Parkinsonism? e disease Elderly Medicine

Yes Consider cerebellar lesion / cerebrovascular 5 Gait abnormality? odisease ree / apraxia / peripheral neuropathy / normal pressure hydrocephalus oo No

Yes Consider angina / dyspnoea (Ch. 12) / 6 Reduced exercise tolerance? claudication

Return to Mobility Problems: Overview (Step 6)

1 Unable to stand up unaided? associated features of cerebellar disease, e.g. intention tremor, dysdiadochokinesis dysmetria Lowero klimb weakness c may limit the ability to rise (past-pointing), dysarthria, nystagmus. from a chair or necessitate use of the chair arms boo or pulling on nearby furniture. Systemic illness, 3 Positive Romberg test? toxic insults or metabolic derangement may cause mebo A marked increase in unsteadiness after eye mild generalized weakness. If weakness is per- closing is a positive test, suggesting a sensory sistent, asymmetrical or associated with wasting/ (proprioceptive or vestibular) rather than cer- neurological abnormalities, see Chapter 22. ebellar cause of ataxia. Reduction in sensation may be a normal part of ageing, e.g. reduced 2 Unsteady with eyes open? vibration sense in the feet is common and of Check lying/standing BP if the patient feels faint limited significance in the older patient. Examine or light-headed. Consider vertigo if the patient the patient during walking for an unsteady, has a sensation of spinning or movement. ataxic or ‘lead boot’ gait. The list of possible Observe standing posture, identify reduction in causes of peripheral neuropathy is vast but joint function, and evaluate pain. If patients can screen routinely for diabetes mellitus alcohol remainooksfree standing without c assistance, m ask them excess, liver disease, malnutrition (check vitamin to move their feet close together – inability B12) or iatrogenic causes, e.g. anticonvulsants, to do so indicates significant ataxia. Look for chemotherapy. ebo ksf mebo sfree com Mobility problems: falls and immobility 221 Gait abnormalities: step-by-step assessment

4 Features of Parkinsonism? The gaits associated with Parkinsonism and sensory ataxia are described above. Suspect Look for the typical features of Parkinson’s cerebellar ataxia if the gait is unsteady and disease: broad-based with an inability to heel–toe walk • tremor:oksf coarse, e slow (5 Hz) and usually (as if inebriated with alcohol). A hemiplegic gait is asymmetrical; present at rest, absent usually obvious and will be associated with focal during sleep; decreased by volunta y neurological signs. Bilateral lower limb proximal movement; increased by emotion; muscle weakness may produce a ‘waddling’ gait. adduction–abduction of the thumbme with sfrePain can limit com exertion or altermebooksf gait, leading to flexion–extension of the fingers (‘pill-rolling’) a decrease in function or an increased risk of • ↑tone: ‘lead-pipe’ rigidity or (in the falling. The patient will typically place the foot presence of tremor) ‘cog-wheel’ with a jerky of the affected side delicately on the floor for feel as little time as possible to avoid the pain of • bradykinesia: slow initiation of weight-bearing (‘antalgic’ gait). Osteoarthritis is movement, ↓speed of fine movements, frequently responsible but is usually chronic and expressionless face slowly progressive, and thus unlikely to lead to • gait: delayed initiation, ↓arm swing, hospital admission without additional factors. stooped posture, short, shuffling steps, Acutely painful joints require careful assessment. difficultyksfree turning. c m Consider gait apraxia if no specific neurological The presence of these features makes idi- abnormality or gait pattern is noted but the gait opathic Parkinson’s disease (PD) more likely, but is none the less abnormal. Apraxia, the inability Parkinsonism has other causes: most commonly, to conduct learned, purposeful movements diffuse cerebrovascular disease. Themebo classical properly sfree (in the com absence of amebooksf focal insult), is a description of vascular Parkinsonism is of signs result of general or frontal cerebral insults such of PD below the waist, with relative sparing of as dementia, cerebrovascular disease, normal the arms. pressure hydrocephalus, sedation or metabolic New presentations or progression of PD derangement. are usually assessed in an outpatient setting. Psychological causes of reduced mobility Mobility-related admissions in patients with (especially the fear of falling) can also reduce PD are more likely to be connected with a mobil ty and increase the risk of falls, and may superimposed acute illness or a medication only be elicited by asking the patient to mobilize problem. Make certain that hospitalized patients greater distances. with PD receive their medication at the correct doseooksfree.co and time to ensure that their mobility doeso 6 sfree.c Reduced exercise m tolerance? not deteriorate further. Observe for/ask about exertional dyspnoea, chest discomfort and claudication. The latter may 24 be due to peripheral vascular disease (dimin- 5 Gait abnormality? me f ished pulses, skin changes, vascular disease Gait screening is sensitive for neuromotor, elsewhere) but consider neurogenic claudication sensory and musculoskeletal abnormalities in the secondary to spinal stenosis, especially if the lower limbs because walking is a complex task in discomfort responds to postural change, e.g. comparison with the tests of neurological function bending over, sitting down, more quickly than used in the standarde.com screening examination. standing still.e.com 25 Nausea andsf vomiting ooksf e

Nausea is the unpleasant sensation of being colicky abdominal pain (see Ch. 4) and abso- about to vomit. Vomiting is the forceful expul- lute constipation +/– abdominal distension. The sion of gastric contents often preceded by characteristics of the vomitus may suggest the nausea. Vomiting should be differentiated from location of obstruction: gastric juices – gastric regurgitation, where there is appearance of gastric outlet obstruction; bilious material – small bowel contents without any effort. The assessment of obstruction; feculent material – distal obstruction acute (≤10 days) nausea and vomiting (N&V) differs (or coloenteric/cologastric fistula). from chronic presentations reflecting a different range of likely diagnoses. Other GI tract disease This chapter focuses on N&V as a principal Peptic ulcer disease may present with N&V, presentingooksfree.com complaint. Refer to the relevant typically associated with epigastric discomfort or chapter if a more specific clinical feature is a history of dyspeptic symptoms. Gastroparesis present, e.g. jaundice, headache, chest pain. results in vomiting after food ingestion due to See Chapter 15 if the vomitus comprisesmeboo fresh delayed free.com gastric emptying; suspectmeboo this in patients or altered blood. with poorly controlled diabetes/multiple diabetes- related complications, scleroderma or previous Infection gastric surgery. N&V may be a prominent feature Gastroenteritis is by far the most common cause of acute inflammatory abdominal pathology, e.g. of acute N&V. It may affect any age group but acute pancreatitis/appendicitis/cholecystitis, but has a higher incidence in children, young adults abdominal pain is almost always the principal and the elderly. The aetiology is usually viral, complaint (Ch. 4). Severe constipation may lead e.g. norovirus, rotavirus, adenovirus. Bacterial to N&V, particularly in frail elderly patients. pathogens tend to come from poorly prepared/ cooked foodstuffs, and can include Bacillus Medications cereusooksfree.co and Staphylococcus aureus. There may Numerous medications or toxins can result in be known contacts with similar symptoms, or nausea or vomiting; some of the more common a history of travel, eating out or eating unusual culprits are listed in Box 25.1 Alcohol misuse is foods in recent days. Vomiting mediatedmebo by a very free frequent com cause of both mebacute and chronic f a bacterial toxin tends to develop within 1–6 N&V. Heavy cannabis use can result in chronic hours. Accompanying features may include fever, vomiting, which may be cyclical, and tends to abdominal cramping and diarrhoea. be alleviated by baths and showers. Other infections, e g. urinary tract infection, meningitis, hepatitis or otitis media may also Metabolic disturbance cause N&V, part cularly in more vulnerable groups Chronic renal failure with uraemia tends to such as children and the elderly. However, other present non-specifically and nausea+ /− vomiting clinical features usually predominate. is often a prominent feature. Conversely, severe N&V is an important cause of acute kidney injury GI obstruction due to hypovolaemia. The assessment of renal Mechanicaloo free.cobstruction of mthe GI tract, e g. due failure is discussed on page 230 to tumour, adhesions or incarcerated hernia, Diabetic ketoacidosis (DKA) and, to a lesser may cause vomiting, usually accompanied by extent, hyperosmolar hyperglycaemic state (HHS), mebo sfre c m mebooksf Nausea and vomiting 223 Differential diagnosis

Box 25.1 Common toxic/therapeutic causes of Box 25.2 Clinical / biochemical features often nausea and vomiting present in patients with adrenal insufficiency

Alcohol Digoxin Symptoms (often insidious) Anti-arrhythmics NSAIDs • Lethargy, fatigue ooAnticonvulsants s r Oestrogen and progestogen- • Anorexia, weight loss containing drugs • Nausea and vomiting Antibiotics (esp. Oestrogen and progestogen- • Postural hypotension erythromycin) containing drugsm b fr om Anti-Parkinsonian Opioids Physical signs treatments • Pigmentation (skin, mucous membranes) Cannabinoids Psychotropic meds • Vitiligo Chemotherapy agents Theophylline • Postural hypotension Blood • Hyponatraemia • Hyperkalaemia may present with N&V. Suggestive features • Hypoglycaemia (fasting or spontaneous) include a history of polyuria and/or polydipsia • Normal-anion gap metabolic acidosis (mild) and a background of diabetes (particularly type 1). Other N&V may be the main presenting symptom in • History of other autoimmune disorders hypercalcaemia, especially since other features booksfretend to be non-specific. mUnderlying causesbo are free. o discussed on page 297. GI upset, including N&V is also common in N&V accompanied by vertigo suggests ves- adrenal insufficiency, including acute adrenal tibular or brainstem pathologym (Ch. 10). Vomiting crisis. Hypotension and illness severity are usually may also occur in CNS infection, e.g. meningitis disproportionate to the degree of vomiting. Other but usually not as the main presenting feature. suggestive features are shown in Box 25.2. Other causes CNS causes Always consider pregnancy in women of child- Raised intracranial pressure may produce bearing age with new-onset nausea +/− vomiting. vomiting, often without nausea. When chronic, Symptoms are not always confined to morning e.g. space occupying lesion, vomiting classically and may occur at any time of the day. In eating occurs shortly after wakening and is associated disorders, recurrent vomiting may be concealed with headache (worse on lying, bending or by the patient and brought to light by a family straining)ooksfree and papilloedema. om In acute causes, member. There is frequently a history of psy- e.g. intracerebral haemorrhage, there may be chiatric disorder, deliberate self harm, laxative sudden onset headache initially followed by abuse or evidence of altered body image. a progressive decline in GCS. Nausea,mebo with ksfree.cFunctional vomiting is a diagnosismebooksf of exclu- 25 or without vomiting, occurs during episodes sion; symptoms are typically worse after eating of migraine in ~80% of patients and is often with vomiting of undigested or chewed food. severe; however headache +/− aura is usually There may also be a history of early satiety and the dominant symptomom (Ch. 19). epigastric fullness.om Nausea and vomiting 224 Acute nausea and vomiting: overview

ABCDE fre co 1 Assess illness severity and resuscitation requirements

Full clinical assessment, FBC, U&E, LFTe, Ca2+, oglucose

Yes Test for 2 Pregnancy possible? N&V of pregnancy pregnancy No

3 Associated features suggest a diagnosis?

Yes Constipations + c abdo pain / distension? Likely GI obstruction No

Yes Headache? Consider raised ICP / meningitis e/ migraine No

Yes Vertigo? Likely vestibular neuronitis or acute brainstem pathology No

Yes Chest / jaw / arm pain? Consider acute coronary syndrome

Nor e Yes 4 Metabolic abnormality? Hypercalcaemia / hyperglycaemic emergency / renal failure / adrenal insufficiency ok No

Yes 5 Associated diarrhoea, infectious Likely gastroenteritis contacts or ingestion of ‘suspiciousm k e m foodstuffs’?

Yes Reassess 6 Likely drug or toxic culprit? (see Box 25.1) after trial Drug-induced N&V discontinuation No

7 Acutelys e unwell c or suspicion of Yes Consider ACS / acute abdominal pathology / atypical presentation sepsis k No

8 Probable GI infection. If symptoms persist, see chronic N&V m e. Nausea and vomiting 225 Acute nausea and vomiting: step-by-step assessment

Assess illness severity and resuscitation Other features that may indicate a need for 1 requirements hospital admission include • evidence of sepsis (Ch. 14) Step 1 Are there features of shock? • acute kidney injury Look for ↑HR, ↓BP (a late sign) or evidence of • frail, elderly or immunocompromised patient tissueook hypoperfusion fre (see Box 30.1, p 267). • significant comorbidity, e.g. heart/renal/ If present, reassess following aggressive IV hepatic failure. bo fluid resuscitation and monitor urine output (consider urinary catheterization if necessary).mebo fre com Exclude diabetic ketoacidosis (see Clinical tool, 2 Pregnancy possible? p. 299) if ↑CBG, known type 1 diabetes or recent Ask about last menstrual period and formally polydipsia/polyuria. Suspect adrenal insufficiency test for pregnancy in any women of reproductive in patients with a history of Addison’s disease (or age present ng with N&V. other autoimmune disease), chronic corticosteroid use or suggestive clinical features (Box 25.2); also consider whenever the severity of shock 3 Associated features suggest a diagnosis? appears disproportionate to fluid losses: take blood for random cortisol and treat immediately Perform an AXR if N&V is accompanied by with intravenous hydrocortisone. absent bowel movements and abdominal pain or distension. Consider acute gastritis peptic Stepooksfree 2 Is there acute renal com impairment? ulcer disease or pancreatitis if there is severe Hypovolaemia may result in severe ‘pre-renal’ acute upper abdominal pain. In either case, assess kidney injury (AKI), especially if compounded by as per Chapter 4. ebooks antihypertensive or nephrotoxic medicationme such sfHeadache e may com occur secondary to dehydra- as diuretics, ACE inhibitors or NSAIDs. Patients tion in acute vomiting but consider the possibility with AKI due to volume depletion require IV of serious CNS pathology. Assess as per Chapter rehydration with close monitoring of fluid balance, 18 if headache is a prominent feature, especially urine output and U+E. However, consider other if the onset is acute or there are any other potential drivers of both AKI and nausea/ concerning features, e.g. recent head injury, vomiting, (e.g. sepsis, drug toxicity) in patients anticoagulant therapy, meningism, fever, reduced without clinical evidence of hypovolaemia. GCS, papilloedema or focal neurology. Consider renal failure as the cause of N&V in Acute onset of N&V accompanied by vertigo patients with severe impairment. See page 230 (dizziness with an illusion of movement, e.g. for further assessment of renal failure. spinning) is likely to represent either vest bular Stepooksfree.com 3 Does the patient otherwise require IV fluids/ neuronitis or acute brainstem pathology such hospital admission? as infarction or haemorrhage; assessbooks as per Patients with clinical evidence of dehydration Chapter 10. (thirst, dry mucous membranes, ↓skinmeb turgor) Suspect free ACS com and assess as per Chapter 6 if 25 and ongoing vomiting, require IV hydration. N&V occurs with chest, jaw, neck or arm pain. Nausea and vomiting 226 Acute nausea and vomiting: step-by-step assessment

4 Metabolic abnormality? viral or toxin-mediated infections and do not require further investigation or antimicrobial Test for diabetes and exclude ketoacidosis in treatment. However, consider AXR (to exclude any patient without a pre-existing diagnosis who colonic dilatation) and surgical review if there has ↑CBG lab glucose (p. 299). Consider HHS are concerning features such as bloody diar- inooks patients with re known co diabetes and markedly rhoea, abdominal pain or an excessive systemic ↑BG (p. 299). inflammatory response. Re-evaluate if symptoms Assess patients with renal failure as described persist >10 days. ebooksf on page 230. m bo sfre co 2+ If ↑Ca (corrected for albumin), assess further Likely drug or toxic culprit? as described on page 297 Reassess symptoms 6 (see Box 25.1) after rehydration and other corrective treatment; remember that N&V may be due to the underlying Always ask about recent changes to drugs or cause, e.g. malignancy rather than ↑Ca2+ per se. dosages - including over-the-counter medi- Consider adrenal insufficiency in patients with cines – and check what the patient is actually ↓Na+/↑K+ o ↓blood glucose, especially if there taking. Enquire about recreational drug use and are suggestive clinical features (Box 25.2). If alcohol intake. In drugs with a narrow therapeutic suspected, check a morning cortisol level +/− window, e.g. digoxin or some anticonvulsants, ACTH stimulation test (‘Short Synacthen Test’). check serum levels to exclude toxicity. Resolution oks ree.com of symptoms with drug discontinuation (where ooksf Associated diarrhoea, infectious contacts possible) confirms the diagnosis. 5 or ingestion of ‘suspicious foodstuffs ? Suspect acute gastroenteritis if anymeb of these sfree co features are present. Most cases are self-limiting Nausea and vomiting 227 Acute nausea and vomiting: step by-step assessment

Acutely unwell or suspicion of a low threshold for AXR +/− further abdominal 7 atypical presentation? imaging, e.g. CT or USS. Severe constipation may lead to N&V in immobile, frail or elderly Consider non-specific presentation of major patients so enquire about bowel movements pathology in patients who appear seriously and consider PR exam +/− AXR. oksf unwell,ooksfre (e.g. autonomic upset, physiological derangement). Be mindful of atypical presenta- 8 Probable GI infection tions in frail elderly patients or those with cognitive impairment, immunocompromisemebo (including In sfrethe absence com of alternative pathology, GI chronic corticosteroid treatment) or longstanding infection is the most likely cause; it is almost diabetes. Perform an ECG to look for evidence of always self-limiting so further investigation myocardial infarction/ischaemia (p. 51) and check is usually not required. Re-evaluate if the blood chemistry (including CRP and amylase) and patient is unwell or deteriorating. Proceed to urinalysis. Undertake a septic screen (p. 142) if assessment of chronic N&V symptoms persist there is fever or e↑inflammatory com markers. Have for >10 days.e com

25 Nausea and vomiting 228 Chronic nausea and vomiting: overview

Full clinical assessment, FBC, U&E, LFT, glucose, ca cium f e co fr Yes Targeted 1 Major abnormality on exam / further Confirm diagnosis routine bloods? investigation

Yes 2 Associated upper GI symptoms? UGIE Upper GI cancer / peptic ulcer / gastritis No

Yes Imaging 3 Weight loss / anorexia? Malignancy / other c studies diagnosis

Yes 4 Likely drug / toxic culprit? (see Box 25.1) Trial Drug-induced N&V discontinuation No

Yes 5 Associated headache or vertigo?m k Consider CNS / vestibular disorderm No Gastric Yes 6 Longstanding / poorly controlled emptying Gastroparesis diabetes or previous gastric surgery? studies Noe co Seek Yes 7 Suspect eating disorder? expert Bulimia nervosa / other opinion eating disorder No

Refer for GI review +/- further investigation 8 Consider functional disorder m

Major abnormality on examination/ USS, review alcohol intake/all recent medications 1 routine bloods? and assess further as described in Chapter 19 but continue to look for alternative causes of N&V Screen patients with persistent or recurrent if only minor LFT derangement without jaundice. N&V for the following abnormalities to narrow the differential diagnosis. ksfree.c Palpable abdominal or pelvic mass Deranged LFTs / jaundice + − Arrange urgent imaging to exclude underlying If known chronic liver disease assess as per malignancy. Consider USS initially, particularly page 179. Otherwise, arrange urgent abdominal for pelvic masses or hepatomegaly but arrange me free.co mebo f Nausea and vomiting 229 Chronic nausea and vomiting: step-by-step assessment

CT abdomen/pelvis if no cause is found (or to suspect a toxic aetiology if there is a clear further characterize/stage abnormalities). temporal relationship between starting the drug and symptom onset. Reassess after trial Renal failure discontinuation (if safe to do so) and look for Severe renal failure frequently presents non alternative causes if symptoms persist Check specificallyo k frewith nausea+ /− vomiting, lethargy, serum levels to exclude toxicity in drugs with a anorexia. Distinguish this from ‘pre-renal’ renal narrow therapeutic window, e.g digoxin, lithium, impairment due to protracted vomiting and theophylline. Establish alcohol intake and ask assess for an underlying aetiology (p.meb 230). specifically sfre about com cannabis mebooksfuse.

Anaemia 5 Associated headache or vertigo? Arrange urgent upper GI endoscopy in any Consider ↑intracranial pressure if vomiting is patient with persistent N&V and evidence of associated with recurrent headache that is: most iron deficiency anaemia. In patients without prominent on waking from sleep; aggravated by iron-deficiency, continue anaemia work-up bending, straining or lying; or accompanied by but consider other causes of N&V if no clear papilloedema – arrange urgent CT brain. See explanation identified. Chapter 10 for assessment of patients with Hypercalcaemiao sfree.co vertigo. 2+ Assess as described on page 297. If mildly ↑Ca Longstanding/poorly controlled diabetes continue to evaluate for other causes ofeb N&V. 6 sfreeor previous com gastric surgery? 2 Associated upper GI symptoms? Suspect gastroparesis in diabeticmeb patients with ksf longstanding poor control and/or significant Associated symptoms of dysphagia, early satiety, microvascular complications or in patients with epigastric discomfort or dyspepsia suggest upper previous gastric surgery (including weight reduc- GI tract pathology such as oesophageal/gastric tion surgery). Delayed gastric emptying on a cancer; peptic ulcer disease or gastritis. Ask about nuclear scintigraphy scan confirms the diagnosis. NSAID use/alcohol intake and arrange upper GI endoscopy if any of these are present or if vomit- Suspect eating disorder? ing persists for >4 weeks (urgently if weight loss, 7 dysphagia or new onset symptoms in patient aged Consider this in patients with persistent/recurrent ≥50 years). Refer for formal GI review if persistent vomiting despite reassuring GI investigation who symptoms with no cause identified on endoscopy have evidence of low mood or self esteem, a ooksfree.com ohistory sf of psychiatric .com disorder or where family 3 Weight loss/anorexia? members raise concern. Typically, vomiting Investigate for underlying malignancy if N&V is occurs after eating and is not mebooksdirectly witnessed. 25 accompanied by significant weight loss, (e.g. Explore the issue sensitively and, if suspected, ≥5% of body weight in ≤12 months) +/− anorexia, seek expert input at an early stage. especially in patients with relatively recent onset of symptoms. Arrange upper GI endoscopy if 8 Refer for GI review/further investigation not already performed and, if normal, request CT Arrange UGIE (if not already performed) and refer abdomen/pelvis If no cause identified, continue for GI evaluation if symptoms persist without a to assess as below. Consider chronic presenta- clear cause. Investigate for chronic pancreatitis if tion of adrenal insufficiency if there are other there is associated epigastric discomfort, a history suggestive clinical features (Box 25.2). of chronic alcohol excess and/or steatorrhoea; ksfree com check faecal elastase and arrange abdominal 4 Likely drug/toxic culprit? CT. Consider functional vomiting if investigations Ask about all medications (including over are consistently reassuring but bebooks vigilant for the counter), particularly those in Box 25.2; underlying eating disorder. me sfree.c Nausea and vomiting 230 Further assessment

Further assessment of renal failure if there are ECG changes – titrate up to 10 mL until changes resolve Step 1 Recognize renal impairment • give treatment to lower K+, e.g. IV dextrose Diagnostic criteria for AKI and CKD are shown and insulin, especially if K+ >6.0 mmol/L in Box 25.3 and Table 25.1. or ECG changes. Repeat U+E and ECG Stepooks 2 Identify reand treat co hyperkalaemia following treatment ↑K+ may cause life-threatening arrhythmias and • consider the need for urgent renale review ooks cardiac arrest. Perform an ECG if ≥5.5 mmol/L (Box 25.4). to look for: me re Step 3 Distinguish CKD from AKI • early changes: tall, peaked T waves Previous U+E results are the best guide to the • advanced changes: flattened P waves, ↑PR chronicity of renal impairment. If unavailable, interval, ↑QRS duration. possible clues to CKD include: Treat as follows: • evidence of metabolic bone disease • give IV calcium, e.g. 10% calcium (especially ↑parathyroid hormone) gluconate, with continuous ECG monitoring • bilateral small kidneys on USS • gradual onset of oedema over weeks to months. Box 25.3 Diagnostic criteria for acute kidneyok injury ree om Assume AKI, at least initially, if none of these features is present and there are no previous 1. Increase in serum creatinine by ≥26 µmol/L from U+E results for comparison. baseline within 48 hours 2. Increase in serum creatinine ≥1.5-fold from Step 4 If de novo presentation, perform a full baseline within 1 week m bdiagnostic free work-up com m oo 3. Urine output <0.5 mL/kg/hr for >6 consecutive hours • Assess volume status: renal hypoperfusion Source: Kidney Disease: Improving Global Outcomes. 2010. (‘pre-renal’ failure) is the most common Clinical practice guideline on acute kidney injury. Available cause of AKI Look for: online at http://www.kdigo.org • predisposing factors (diarrhoea, vomiting, blood loss, ↓oral intake, diuretics), Table 25.1 Classification of chronic kidney disease • features of dehydration (↓skin turgor, d y mucous membranes, thirst) and GFR (mL/min/ Stage Category 1.73 m2) • signs of shock (see Box 30.1, p. 267). If you suspect hypovolaemia, assess the response 1 oEvidence fre of chronic om ≥90 kidney damage1 with of urine output and U+E to fluid resuscitation and normal GFR correction of underlying causes 2 Evidence of chronic 60–89 • Exclude obstruction: bladder outflow kidney damage1 with mobstruction ree com occurs most frequentlym book in males f mild impairment of GFR

3 Moderate impairment 30–59 Box 25.4 Reasons for urgent renal referral of GFR • Indication for urgent renal replacement therapy 4 Severe impairment 15–29 + of GFR • ↑K or pulmonary oedema refractory to medical management 5 End-stage renal failure <15 • Severe metabolic acidosis • Uraemic pericarditis 1 Evidence of chronic kidney damage includes: Uraemic encephalopathy • persistent microalbuminuria/proteinuria/haematuria • Progressive increase in serum creatinine despite fluid • structural kidney abnormalities on imaging resuscitation/withholding of nephrotoxins • featuresoksf of chronic e glomerulonephritis com on renal biopsy. Source: Kidney Disease Outcome Quality Initiative 2002. K/ • Persistently oliguric or anuric patients DOQI clinical practice guidelines for chronic kidney disease: • Suspected glomerular disease evaluation, classification, and stratification. Am J Kidneye D s. • CKD ee.co patients with increasing symptoms of uraemia 39(2 Suppl 2):S1–246. or likely progression to stage 5 CKDme k Nausea and vomiting 231 Further assessment

with prostatic enlargement. Insert a urinary (dipstick haematuria with no red cells on catheter if there is a palpable bladder microscopy suggests myoglobinuria). or ↑post-void residual urine on bladder • Send plasma for protein electrophoresis scanning. Request a renal USS to exclude and urine for Bence Jones protein if upperoksfre renal tract obstruction. you suspect multiple myeloma, e g. • Review all recent prescriptions and ask hypercalcaemia, bone pain pathological about non-prescribed drugs. Common fractures, or if the cause of renal culprits include radiographic contrast dysfunction remains unclear. media, NSAIDs, ACE inhibitors/angiotensinmeb re m mebo receptor blockers, antimicrobials Step 5 If acute-on-chronic impairment, consider (gentamicin, vancomycin penicillins, reasons for deterioration amphotericin B) and ciclosporin. Acute deterioration is often due to • Seek evidence of sepsis (Box 14.1, p. 141), • dehydration and, if present, perform a full septic screen • infection as per Chapter 14. • hypotension • Consider other causes: suspect • nephrotoxic agent (see above). glomerulonephritis in any patient with Identify and reverse these causes, monitor renal heavy, e.g. ≥3+, haematuria/proteinuria on function and discuss with the renal team if here dipstick. Evaluate for multisystem disease is any further decline in GFR. (rash,oksfree joint disease, com haemoptysis), perform serological investigations (Table 25.2) and Step 6 If stable CKD, seek evidence discuss urgently with the renal team. of complications • Consider haemolytic uraemic syndrome/m boSequelae s ree of CKD c mshould bem sought and cor ks- thrombotic thrombocytopenic purpura if rected, if possible. AKI is accompanied by an acute diarrhoeal • Renal anaemia: this may result from illness or neurological features. Review inadequate renal production of erythropoietin. the FBC/blood film for:↓ Hb, ↓platelets, Measure ferritin and transferrin saturation to ↑reticulocytes and red cell fragments. Seek ensure that he patient is iron-replete (ferritin immediate expert advice if suspected. >100 ng/mL; transferrin saturation >20%), • Consider rhabdomyolysis in patients with a exclude other causes of anaemia (p. 136) and history of trauma, a long period lying on the referree.com to a nephrologist for consideration of floor or recreational drug use, e.g. cocaine. erythropoiesis-stimulating agents. Check CK (>×5 upper limit of normal) and • Metabolic acidosis: this is indicated by performoksfree.com urinalysis +/− urine microscopy a low venous bicarbonate and can be corrected by oral sodium bicarbonate.

Table 25.2 Serological investigations in • Metabolic bone disease: ↓phosphate suspected glomerulonephritis excretion and ↓renal activation of vitamin 3− 2+ meboo 25 Test Underlying diagnosis D result in ↑PO4 , ↓Ca and ↑parathyroid hormone (secondary hyperparathyroidism). ANA Connective tissue disease, Treat with phosphate binders and vitamin D e g. SLE analogues, aiming to maintain plasma Ca2+ 3− Anti ds-DNA and PO4 within normal limits. Extractable nuclear • Volume overload: in advanced CKD, oliguria antigens may result in significant fluid overload, with Anti GBM antibodies Goodpasture’s disease peripheral ± pulmonary oedema. Liaise with ANCA frVasculitis, m e.g. a nephrologist if this is refractory to diuretic granulomatosis with therapy and salt restriction. polyangiitis • Hypertension: ↑BP is common in CKD, Antistreptolysin Post-streptococcal accelerates the decline in renal function O titre glomerulonephritis and increases cardiovascular risk. Cryoglobulins Cryoglobulinaemia Monitor BP and aim for strict targets, e.g. m<130/80 ree. mmHg. om meboo sf Palpitation 26 ks ooksfre

Palpitation is an unpleasant awareness of the Paroxysmal supraventricular tachycardia heartbeat. Patients may describe the sensation as skipping, fluttering, racing, pounding, thudding ‘Supraventricular tachycardia’ (SVT) refers or jumping. Episodes can be unpleasant and to atrioventricular nodal re-entry tachycardia frightening but most are benign and less than half (AVNRT) and AV re-entry tachycardia (AVRT). are due to a heart rhythm abnormality. In most AVNRT is due to right atrial and AV node re-entry, cases, the key to diagnosis lies in documenting usually in structurally normal hearts; AVRT (known the cardiac rhythm during symptoms. Establish assfree.com Wolff–Parkinson–White syndrome) is caused the frequency, intensity and impact of symptoms by a re-entry circuit formed from the AV node and as this is essential to guide treatment. an ‘accessory pathway’ – an abnormal band of ooksfree.com conducting tissue connecting atria and ventricles. Heightened awareness of Both produce episodes of regular tachycardia normal heartbeat (± light-headedness and breathlessness) with Awareness of the normal heartbeat is common an abrupt onset and offset. Themebooksf ECG shows a but may produce anxiety in patients with psy- regular narrow-complex tachycardia at 140–220/ chosocial stress or health concerns, e.g. recent min (Fig. 26.1). heart ‘scare’, death of family member. It is most In 50% of patients with an accessory pathway, commonly noted when lying awake in bed or the ECG in sinus rhythm shows a short PR interval sitting at rest. and slurring of the QRS upstroke (‘delta wave’) due to premature activation of ventricular tissue Sinus tachycardia/↑stroke volume by the pathway – ‘pre-excitation’ (Fig. 26.2). Causes of sinus tachycardia are shown in Box Most cases of AVNRT and AVRT are curable 26.1; anxiety is the most frequent aetiology, with with radiofrequency catheter ablation. patients typically reporting episodes of a fast, Atrial arrhythmias (atrial tachycardia, regular, pounding heartbeat that builds up and flutter and fibrillation) resolvesooksfree over minutes. com Increased stroke volume due to aortic regurgitation or vasodilator drugs Atrial tachycardia produces symptoms similar to may produce a forceful heartbeat without SVT; the ECG shows a regular narrow-complex tachycardia. mebotachycardia sfree with com abnormal Pme waves. oo Atrial flutter is caused by a large re-entry circuit Extrasystoles within the right atrium that generates an atrial rate Atrial or ventricular extrasystoles (ectopics or of 300/min. This is usually associated with AV premature beats) do not usually cause symptoms block, resulting in a ventricular rate of 150/min (2 : 1 but, in some patients, produce a sensation of block) or 100/min (3 : 1). Symptoms are similar to dropped beats (due to ↓stroke volume of the SVT. The ECG shows a regular narrow-complex ectopic beat), ‘jolts’ or ‘thumps’ (due to ↑stroke tachycardia with ‘saw-toothed’ flutter waves (Fig. volume of the post-ectopic sinus beat), or, if 26 3). With 2 : 1 block these may be obscured so frequent, an irregular heartbeat. Extrasystoles suspect atrial flutter in any patient with a regular are common in healthy individuals and usually narrow-complex tachycardia of 150/min benign,ooksfree.co but frequent ventricular extrasystoles, Atrial fibrillation is common. Underlying causes particularly in older patients may indicate are shown in Box 26.2. Atrial activity is chaotic underlying structural or coronary heart disease. and the ventricles are activated rapidly and mebo sfree.com mebo ksf Palpitation 233 Differential diagnosis

irregularly. Patients with paroxysmal atrial fibril- Box 26.1 Causes of sinus tachycardia la ion experience an erratic or irregular heartbeat • Anxiety or panic disorder thatsfre is usually fast o and may be associated with • Stress or strong emotion breathlessness, light-headedness or ↓effort • Drugs:oks beta r2 agonists, anticholinergics, cocaine, tolerance. The ECG shows an irregular narrow- amphetamines complex tachycardia with no P wa es (Fig. 26.4). • Anaemia Patients with atrial fibrillation or flutter are at • Thyrotoxicosis greater risk of thromboembolic complications, • Fever • Pregnancy including stroke. mebooksf • Phaeochromocytoma

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 26.1 Supraventricular tachycardia. (From Hampton JR 150 ECG Problems, 3rd edn. Edinburgh: Churchill Livingstone,oks 2008.)

I VRe s V1 V4 m 26

II VL V2 V5

III VF V3 V6

Fig. 26.2 Pre-excitation: sinus rhythm in Wolff–Parkinson–White syndrome. (From Hampton JR. Thee ECG Made Easy, 7th edn. Edinburgh: Churchill Livingstone,me 2008.) e Palpitation 234 Differentialco diagnosis I VR Ve1 V4

II VL V2 V5

III VF V3 V6

Fig. 26.3 Atrial flutter with 2 : 1 AV block. (From Hampton JR. The ECGe in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.)fre

Fig. 26.4 Atrial fibrillation with a rapid ventricular response. (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.)

hearts. Rapid palpitation is often accompanied Box 26.2 Common causes of atrial fibrillation by pre-syncope (a feeling of faintness and • Hypertension near-collapse), syncope, breathlessness or chest • Ischaemic heart disease pain. In patients with significant underlying left • Valvular heart disease (especially mitral stenosis) ventricularsfree.c impairment, palpitation is frequently • Alcohol absent. The ECG shows a regular broad-complex • Cardiomyopathyoksfree. tachycardia (Fig. 26.5). A variant, torsades de • Sick sinus syndrome pointes, with a characteristic ECG appearance • Congenital heart disease • Constrictive pericarditis (Fig. 26.6), may occur in patientsebooksf with a pro- • Hyperthyroidism longed QT interval. • Idiopathic (‘lone’ atrial fibrillation) Bradyarrhythmia, e.g. sick sinus syndrome, intermittent AV block Bradyarrhythmias more commonly present with light-headedness or syncope but the patient may Ventricular tachycardia report intermittent episodes of a slow but forceful Ventricular tachycardia (VT) is a potentially heartbeat Associated ECG findings include sinus life-threatening arrhythmia that most frequently pauses, junctional bradycardia and intermittent occurs in patients with previous MI or cardio- second- or third-degree AV block (Figs 31 1 f myopathy but can arise in structurally normal andsfree 31.2, p. 279 com). ksfree c Palpitation 235 Differentialo diagnosis

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 26.5 Ventricular tachycardia. (From Hampton JR. The ECG in Pract ce, 5th edn. Edinburgh: Churchill Livingstone, 2008.)ee.

Fig. 26.6 Torsades de pointes. (From Boon NA, Colledge NR, Walker BR. Davidson’s Principles & Practice of Medicine, 20th edn. Edinburgh: Churchill Livingstone, 2006.)m e. m

26 Palpitation 236 Overview

Yes Feel pulse, 1 Symptoms present during consultation? Diagnosis fre performfre ECG No

Full clinical assessment, ECG

Yes 2 Clear history of extrasystoles? Symptomatic extrasystoles

Heartbeat regular and normal Yes 3 ↑S roke volume / awareness of normal heartbeat speed during symptoms? free No

Attempt to document rhythm during symptomsbo e

See Further assessment of Rhythm documented during Yes palpitation with 4 Diagnosis typical symptoms? documented rhythm (p. 239) No

Yes Further attempt to document rhythm / 5 Alarm features or highly symptomatic? re refer Cardiology / empirical treatment No

Cause uncertain: reassure; refer Cardiology if recurrent troublesome symptoms bo ree Palpitation 237 Step-by-step assessment

1 Symptoms present during consultation? • Use Holter monitoring if symptoms are occurring frequently. A 24-hour Holter If the patient has symptoms during the consulta- monitor is useful only in patients who tion feel the pulse straight away and perform an have at least daily symptoms, a 48-hour ECG as soon as possible. This may sound overly Holter monitor can be used in those with simpleooksfre but much of the difficulty in diagnosing symptoms on most days, and a 7-day palpitation lies in trying to document the rhythm monitor is useful for those w th weekly during a typical episode of symptoms. Do not symptoms, eboo miss the opportunity! mebo• If symptoms re co are occurring less than weekly, consider more prolonged ambulatory 2 Clear history of extrasystoles? monitoring through a wireless ECG patch It is not always possible to distinguish frequent recorder or an external patient-activated extrasystoles from sustained arrhythmias such recorder Ambulatory smart phone monitors as atrial fibrillation on the history alone. However, are now available that are patient activated a clear history of an occasional ‘jolt’ or ‘jump’ and allow an ECG to be recorded and sent in the chest or isolated ‘dropped’ or ‘skipped’ to the clinician. beats is highly suggestive – such patients can • If symptoms are very infrequent, ask the usually be reassured without further investigation patient to phone for an ambulance or report ksfree.com to their family doctor or to an emergency Heartbeat regular and normal speed department during an episode (advise 3 during symptoms? not to drive) or, depending on symptom severity, consider referral for insertion of an Many patients with palpitation describe the implantable loop recorder. heartbeat as ‘forceful’ or ‘strong’ ratherm than fast, free com mebooks • If symptoms are induced by physical exertion, slow or irregular. This may reflect stroke volume, ↑ refer for a supervised exercise ECG. e.g. aortic regurgitation, anaemia, vasodilators, or simply awareness of the normal heartbeat but, in either case, it argues strongly against an Rhythm documented during 4 arrhythmic cause Look for underlying physical typical symptoms? and psychosocial factors, but further investigation Diagnose arrhythmia as the cause of palpita- is usually unnecessary unless there is a specific tion if you obtain an ECG recording of rhythm additional concern. sfree.com disturbance that corresponds with symptoms – proceed to ‘Further assessment of palpitation Attempt to document rhythm during symptoms with documented rhythm’. Clear documentation of sinus rhythm during This is a key diagnostic step. The chosen method a typical attack excludes an arrhythmiceb oksfcause will be dictated predominantly by the frequency for symptoms. of symptoms. me sfreeAsymptomatic co rhythm disturbances may • Consider inpatient telemetry if the patient occur during prolonged ECG monitoring. The 26 has experienced a recent episode, e.g. patient may need further assessment for the in the last 72 hours, with syncope or specific arrhythmia but symptoms should not pre-syncope, or has other high-risk features automatically be attributed to it – especially if (p. 280). com typical symptoms occur during periods of sinus e.com Palpitation 238 Step-by-step assessment rhythm. Consult a cardiologist if there is any subsequently become more frequent or intrusive. doubt as to the significance of an ECG recording. Persist with attempts to document the rhythm Continue to step 5 if the patient did not experi- in patients with symptoms that are frequent, ence a typical episode of palpitation during the unpleasant or which interfere with occupation period of rhythm monitoring. or lifestyle. ooksfre co Irrespective of symptom frequency and 5 Alarm features or highly symptomatic? intensity, refer patients with any of the following features to cardiology for further investigation: The lengths to which you should go tome document sfre meb oksf the ECG during symptoms depends on both the • palpitation associated with syncope or severity of symptoms and the estimated risk of a pre-syncope life-threatening arrhythmia, e.g. VT or complete • family history of sudden cardiac death or heart block. inheritable cardiac conditions Consider reassurance without further investiga- • significant abnormality on resting ECG tion for patients with mild, infrequent symptoms • risk factors for VT, e.g. previous MI, and no high-risk features; reassess if symptoms ventricular surgery, cardiomyopathy.

Table 26.1 CHA2DS2-VASc thromboembolic Table 26.2 HAS-BLED bleeding risk score oorisk score ee.c Thromboembolic risk factor PointsbBleeding ee.com risk factor Points Congestive heart failure: clinical 1 Hypertension: uncontrolled hypertension 1 evidence of heart failure or reduced (systolic BP >160 mmHg) LV ejection fraction m o Abnormal renal/liver function: Hypertension 1 Dialysis or serum creatinine >200 1 Age: ≥75 years 2 micromol/L Cirrhosis or bilirubin >2× normal or ALT 1 Diabetes mellitus 1 >3× normal Stroke: previous stroke, TIA or 2 Stroke: previous stroke 1 systemic embolism Bleeding: previous major bleed or 1 Vascular disease: history of MI, 1 predisposition to bleeding peripheral arterial disease or aortic atheroma Labile INR: time in therapeutic range 1 <60% Age: 64–75 years 1 Elderly: age >65 years 1 ooksfree.Sex: female sex 1 Drugs/alcohol: Risk of thromboembolic events (event rate/100 e Concomitant ree.com use of antiplatelet or 1 person years) according to score non-steroidal anti-inflammatory Score 0 = low risk (0.78) drugs m Score 1 = intermediate risk (2.01) ≥8 alcoholic drinks per week 1 Score ≥2 = high risk (8.82) Score ≥3 indicates higher risk of major Modified from Kirchhof P et al. 2016. 2016 ESC Guidelines for bleeding. the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 37(38):2893–2962 and Olesen Modified from Pisters R et al. 2010. A novel user-friendly JB et al. 2011. Validation of risk stratification schemes for score (HAS-BLED) to assess 1-year risk of major bleeding in predicting strok and thromboembolism in patients with atrial patients with atrial fibrillation: the Euro Heart Survey. Chest. 138(5):1093–1100. fibrillation: nationwidefree.co cohort study. Br Med J. 342:d124. free.c m Palpitation 239 Further assessment

Further assessment of palpitation with Atrial flutter/fibrillation documented rhythm • Perform echocardiography to Assess the frequency and intensity of symptoms exclude structural heart disease, and the impact on occupation and lifestyle. e.g. cardiomyopathy, left ventricular Establishook the fre efficacy and side-effects of previous hypertrophy, valvular disease. treatments. bo• Seek f e causative or exacerbating factors: measure BP, electrolytes and TFT; enquire Sinus tachycardia about alcohol intake and symptomsmebo of • Review all prescribed and ‘recreational’ angina. drugs, screen for anaemia and • Use the CHA2DS2-VASc score (Table 26.1) hyperthyroidism with FBC/TFTs and, where to assess thromboembolic risk in patients appropriate, perform a pregnancy test. with non-valvular atrial fibrillation (all patients • If ↑BP or if episodes are associated with with mitral stenosis are at high risk) and the headache, flushing or GI upset, measure HAS BLED score (Table 26.2) to assess the 24-hour urinary metanephrines to exclude risk of major bleeding. phaeochromocytoma. • Refer to Cardiology if symptoms are • Request an echocardiogram if there are any frequent, distressing or disabling features to suggest structural heart disease despite first-line medical therapy, e.g. e.g.oksf unexplained ee murmur, com signs of heart beta-blockers. o failure. • Look for evidence of an anxiety or panic Ventricular tachycardia disorder. me• Perform ree.com an ECG to look for evidence of underlying structural heart disease, e.g. Extrasystoles cardiomyopathy. • Seek potential exacerbating factors • Enquire about previous MI and symptoms including ↓K+, ↓Mg2+, drugs, e.g. tricyclic of/risk factors for ischaemic heart disease. antidepressants, digoxin, alcohol, tobacco • Measure the QT interval on the ECG in or (possibly) caffeine consumption. sinus rhythm. • Consider further investigation, e.g. • Measure electrolytes – especially K+, Mg2+ echocardiography, exercise ECG if frequent and Ca2+. or associated with other signs/symptoms of • Refer all patients to Cardiology for further CVS disease. investigation, risk stratification and k oksfree com treatment. Supraventricular tachycardia Bradyarrhythmia • Look for pre-excitation on resting ECG (see Fig. 26.2) to suggest an accessorym • Seek free.c an underlying m cause: check TFTs and pathway-mediated tachycardia. review drugs for rate-limiting agents, e.g. 26 • Refer to cardiology for electrophysiology digoxin, beta-blockers, verapamil. study ± radiofrequency ablation if • Refer symptomatic bradyarrhythmia or symptoms are frequent, disabling or asymptomatic second-degree AV block unpleasant or if there are side-effects on (Mobitz type 2), complete heart block or medical therapy.e com sinus pauses >3 seconds to Cardiology. ee.com Rash: acute generalized skin eruption 27 oksfre ooksf e

The accurate diagnosis of skin disease is usually Psoriasis based on visual pattern recognition developed through experience rather than analytical Psoriasis, a very common papulosquamous rule-based approaches. This is a step-by-step eruption, is characterized by well-demarcated approach to assist identification of important erythematous or purple papules and plaques, acute generalized eruptions that require urgent topped with silvery scale. There are three forms advice and treatment. of acute eruption: erythroderma (see above), pustular psoriasis (Fig. 27.4) – a form that can Erythroderma deteriorate rapidly and guttate psoriasis (Fig. Erythroderma (red skin) describes inflamma 27.5) – with characteristic widespread multiple toryoo skinsfree.c disease manifesting m predominantly ‘drop-like’ lesions, most commonly seen in as erythema and involving >90% of the body young adults in association with streptococcal surface area (BSA; Fig. 27.1). The term ‘sub- pharyngitis. Pityriasis rosea is often confused erythrodermic’ is sometimes used tomebo describe with sfree psoriasis. com It may be meboa reaction to ksf a extensive erythema covering <90% BSA. Acute viral infection and initially presents with a single erythroderma can be life-threatening and most ‘herald patch’ followed by the subsequent cases need hospitalization and urgent dermatol- development of multiple lesions on the torso ogy review. The major causes are eczema (40%), (Fig. 27.6). psoriasis (25%), cutaneous lymphoma (15%) and Toxic epidermal necrolysis, drug eruptions 10%). Stevens Johnson syndrome Eczema and erythema multiforme ‘Eczema’ and ‘dermatitis’ are interchangeable Toxic epidermal necrolysis (TEN) is the severe terms. Dermatitis is used to denote a group end of a spectrum of acute eruptions caused by of non-infective inflammatory skin diseases a cell-mediated cytotoxic reaction against epider- thatooks represent a e.com reaction pattern to various mal cells (Fig. 27.7). It is characterized by fever stimuli. Dermatitis may be classified by aetiology (>38° C), widespread tender erythema affect- (atopic, irritant, allergic/contact, venous/stasis), ing >30% of the skin surface, and mucosal morphology (seborrhoeic, discoid) or sitemebo (palmar, involvement sfree.c (see below). m Erythemamebooks is followed plantar, pompholyx). All produce the same key by extensive, full-thickness, cutaneous and clinical feature: pruritic, erythematous lesions mucosal necrosis and denudation within a couple with typically indistinct margins. The lesions can of days. Similar features involving <10% of the progress through a number of phases: acute body surface are termed Stevens–Johnson (with vesicles and bullae – Fig. 27.2), subacute syndrome (SJS), also known as ‘erythema (with scaling and crusting) and chronic (with multiforme major’; if 10–30% of body surface acanthosis, lichenification and fissuring). Lesions area is affected, this is often classified as TEN/ may become secondarily infected by bacteria SJS overlap. Drugs, e.g. allopurinol, anticonvul- forming a crusted yellow exudate (‘impetigo’) (Fig. sants, NSAIDs, cause >80% of cases and have 27 3) or by viruses, e.g. herpes simplex, produc- usually been commenced 1–3 weeks prioroks to ingo a vesicular ksfree pattern com (‘eczema herpeticum’) presentation. bo sfree com Rash: acute generalized skin eruption 241 Doifferential diagnosis

Fig. 27.1k Erythroderma. (From Gawkrodger DJ. Dermatology kICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)

Impetigo. (From Kumar P, Clark M. Kumar & Fig. 27.2 Acute dermatitis. (From Gawkrodger DJ. Fig. 27.3 Dermatology ICT, 4th edn. Edinburgh: Churchill Clark’s Clinical Medicine, 7th edn. Edinburgh: Churchill Livingstone,sfr 2009.) Livingstone,ksfr 2008.)

Fig. 27.4 Pustular psoriasis. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchillm Livingstone, 2008.) Rash: acute generalized skin eruption 242 Differentialco diagnosis Erythema multiforme (minor) represents a similar but milder type of cytotoxic reaction Classically,sfre it presents with ‘target’ lesions, consisting of three zones: a dark or blistered centre (bull’s-eye) surrounded by a pale zone and an outer rim of erythema (Fig. 27.8). The lesions predominantly occur on the hands/feet and affect <10% of the BSA without mucous membrane involvement. Themebooksf underlying cause is more often viral (especially herpes simplex) than drug-induced. Pemphigus/pemphigoid/dermatitis herpetiformis Fig. 27.5 Guttate psoriasis. (From Bolognia J, Jorizzo J, Rapini R. Dermatologye 1st c edn. London: Mosby, 2003.) Separation of keratinocytes from each other, or from the underlying dermis, produces blistering. The three most common blistering disorders are pemphigussfree (Fig. co 27.9), pemphigoid (Fig. 27 10) ksf

Fig. 27.6 Pityriasis rosea. (From Gawkrodger DJ. Fig.s 27.8 Erythema multiforme-target lesions. (From Dermatology ICT, 4th edn. Edinburgh: Churchill Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn. Livingstone, 2008.) London: Mosby, 2003.) ok ooks

Fig. 27.7 Toxic epidermal necrolysis. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.) Rash: acute generalized skin eruption 243 Doifferential diagnosis

Fig. 27.9 Pemphigus. (Fromc Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn.c London: Mosby, 2003.)

Fig. 27.10o Pemphigoid. (From Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn. London: Mosby, 2003.) and dermatitis herpetiformis (Fig. 27.11) which is commonly associated with coeliac disease. me o Urticaria/angioedema Urticaria (Fig. 27.12) is oedema within the dermis secondary to mast cell degranulation, and is a 27 common skin reaction Angioedema results from oedema deeper within the dermis and subcutaneous tissues, and may occur in up to 40% of cases. Although commonly thought to be allergic, most cases of acute urticaria are not mediated by immunoglobulin E (IgE). Those that are, arise in response to drugs (especially antibiotics), foods (peanuts, eggs, shellfish) and skin contact (latex, ooksfree.com Fig. 27.11 Dermatitis herpetiformis. (From Gawkrodger plants, bee/wasp stings), and may progress to DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill anaphylaxis. Non-IgE causes include concurrentebo Livingstone, 2008.) eb Rash: acute generalized skin eruption 244 Differentialco diagnosis

Fig. 27.12 Urticaria. (From Gawkrodger DJ. Dermatologyb ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)b

infection (especially upper respiratory tract infections), drugs that promote mast cell degranulation (opiates, aspirin, NSAIDs, ACE inhibitors) and foods that contain salicylates and additives.

Purpura (including vasculitis) Purpura (Fig. 27.13) is fixed staining of the skin by leakage of blood from the intravascular spaceooks and needs r e.comto be distinguished from simple bruising. Causes include: • septic emboli from systemic infectious diseases m oo • haematological disorders • thrombosis involving microcirculation • vasculitis (inflammation in vessel walls).

Acute exanthems ‘Exanthem’ simply means ‘breakout’ and, although the term is mostly used for rashes with an infectious aetiology, it may be regarded as a pseudonym for any acute eruption or rash. Drug eruptions are common and do not necessarily indicate allergy; ~3% of all patients ooksfree m Fig. 27.13 Vasculitis/purpura. (From Gawkrodger DJ. admitted to hospital have an eruption due to Dermatology ICT, 4th edn. Edinburgh: Churchill adverse drug reactions. Those most commonlyeboo Livingstone, 2008.) eb Rash: acute generalized skin eruption 245 Differential diagnosis

implicated are listed in Box 27.1. In hospital, Box 27.1 Drugs that cause rashes in >1% rashes are commonly attributed to and often of the population causedsfre by medications, o but similar cutaneous • Penicillins signs can be due to underlying or intercurrent • Carbamazepineo sfr illness, e.g. viral or bacterial exanthems or internal • Allopurinol disease, non-specific reactions to treatment, • Gold e.g. sweat rash due to prolonged bed-rest or • Sulphonamides previously unidentified independent skin disease. • NSAIDs • Phenytoin Infective exanthems are largelyme viral. Many ooksf of the • Isoniazid conditions described above could be considered • Chloramphenicol specific examples of infective exanthems, e.g. • Erythromycin erythema multiforme post-herpes simplex, guttate • Streptomycin psoriasis post-pharyngitiscom and pityriasis rosea.

27 Rash: acute generalized skin eruption 246 Overview

Ful clinical assessment fre Yes Urgent 1 >90% body surface area erythematous? k Erythroderma Dermatologyo input No

2 Blisters present?

No Yes Stevens-Johnson Yes syndrome / toxic Urgent Mucous membrane involvement? m epidermal necrolysis / Dermatology input acute pemphigus No

Yes Consider bullous pemphigoid, erythema Blisters ≥5 mm? multiforme, fixed drug eruption, acute dermatitis, insect bite No

Consider herpes simplex / zoster, dermatitis herpetiformis, chickenpox, impetigo, acute dermatitis bo e com

3 Purpura present?

No Yes

Yes Evidencec of infection? Consider meningococcal sepsis / endocarditis No Coagulopathy, anticoagulant therapy, Yes disseminated intravascular coagulation, Platelets or PT / APTT? ↓ ↑ idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura No Consider vasculitis or drug reactione (see text) e c Yes 4 Pustules present? Likely pustular psoriasis or systemic infection

Yes 5 Wheals present? Urticaria Seek precipitant

Noe c Yes 6 Underlying chronic dermatosis? Consider acute flare

7 Likely drug reaction or infective exanthem.e Refer Dermatology if persistent or severe symptoms me Rash: acute generalized skin eruption 247 Step-by-step assessment

1 >90% body surface area erythematous? when erosions and ulceration (with subsequent crusting) occur on oral, genital and ocular Estimate the proportion of skin that is erythe- epithelium; examine these sites in any acute matous using the guide in Box 27.2; >90% of severe skin eruption. BSA indicates erythroderma. Admit any patient Suspect TEN if there is extensive blistering with withooks acute erythroderma e to hospital, assess and peeling of the skin to reveal bright red oozing stabilize as described in Box 27.3 and arrange dermis (see Fig. 27.6), along with mucous mem- urgent dermatology review. Subsequent treat- brane involvement; seek immediate Dermatology ment is based on the exact diagnosis meboand guided review sfre and manage co in a burnsmeboo or critical care sf by expert dermatological assessment. unit. If bullae and mucosal lesions are present but blistering is less extensive, consider SJS 2 Blisters present? and pemphigus (see Fig. 27.9) – arrange prompt Blisters form when fluid separates the layers of dermatological review in all cases. the skin; blisters <5 mm diameter are termed In the absence of mucous membrane involve- ‘vesicles’, those >5 mm are called ‘bullae’. ment look for target lesions (see Fig. 27.8) on Mucous membranes are involved (Fig. 27.14) the hands and feet suggestive of erythema multiforme; otherwise, consider bullous pemphigoid (see Fig. 27.10), fixed drug eruption or,

Box 27.2 Calculating body surface area if lesions are well localized, an insect bite or o fre .c contact dermatitis. Originally developed for calculating surface area for burn If the patient has a painful eruption of vesi- victims, in adults a simple way of calculating the BSA cles, suspect infection with herpes simplex if it affected by a cutaneous disorder is the ‘Wallace rule is confined to the face, lip or finger (herpetic of nines’. This system allocates to different bodymeb parts ksfree com meb oksf 9% (or half thereof) of the total BSA. In extensive skin whitlow) and herpes zoster (shingles; Fig. 27.15) disease it is sometimes easier to identify unaffected if it follows a dermatomal distribution. In febrile skin, and assessment is aided by remembering that the patients with widespread vesicles consider patient’s hand is approximately 1% of BSA.

Rule of 9s Box 27.3 Assessment and immediate management of skin dysfunction 4 5%e . om 4.5% The mainstay of emergency dermatology treatment is 9% 9% to provide surrogate skin function until the underlying condition has resolved or is suppressed with suitable 4.5% 4.5% medication. Look for evidence of shock (see Box 30.1, 9% 9% p. 267) and dehydration, and monitor U+E regularly. 4.5% 4.5% Replenish fluid lost through defective skin barrier 1% b f ee. m function with IV fluids and supplementary electrolytes. 9% 9% 9% 9% Take swabs of all areas of suspected infection and, if the patient is pyrexial, take blood culturesmebook before commencing antibiotic therapy. Use strict aseptic technique for blood cultures, ideally through non- affected skin, to try to avoid contaminants (more likely 27 in dermatologica patients due to ↑skin flora load). Remember that many acute cutaneous eruptions are associated with pyrexia, due not to systemic infection Anterior Posterior but to loss of temperature homeostasis through vasodilatation. Maintain body temperature with a warm room and regular antipyretics. Assess the extent of skin Palmar method compromisesfree.com as detailed above and restore its barrier (patient’s palm) 1% function with regular application of thick emollients ok e (liquid paraffin : white soft paraffin, 50: 50). Remove any potential exacerbates by discontinuing all oo unnecessary medication. Rash: acute generalized skin eruption 248 Step-by-stepco assessment

Fig. 27.15 Herpes zoster. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone,free 2008.)

liver disease, discuss with Haematology if there is coagulopathy or ↓platelets. B If ↓platelets are present with normal coagulation, look for associated features of thrombotic Fig. 27.14 Mucous membrane involvement in m bo Stevens–Johnson syndrome. A Oral. B Ocular. (From thrombocytopenic purpura: Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: • ↓Hb without an obvious alternative cause Churchill Livingstone, 2008.) • red cell fragmentation on blood film • ↑↑LDH • neurological abnormalities (↓GCS, chickenpox or, if there is known eczema, eczema headache, seizures). herpeticum Suspect dermatitis herpetiformis if If any of these is present, seek immedia e the vesicles are intensely itchy and occur on the Haematology input, as urgent plasma exchange extensor surfaces (see Fig. 27.11). may be life-saving. ksfree Suspect a systemic vasculitis, e.g. polyarteritis 3 Purpura present? nodosa, Henoch–Schönlein purpura, microscopic polyangiitis, cryoglobulinaemia, rheumatoid vas- Classify the rash as purpuric if there are dark red culitis or other systemic inflammatory disorder – if or purple macules/patches that do not blanch there is palpable purpura accompanied by fever, with pressure (see Fig. 27.13). me s ree c m meboo sf ↑ESR/CRP, constitutional upset, joint disease Take urgent blood cultures and treat empiri- and/or renal involvement (↓GFR, proteinuria, cally for meningococcal sepsis pending further haematuria). Perform a full vasculitis/autoimmune investigation if the patient has fever, shock, ‘screen’ and consider skin biopsy ± biopsy of drowsiness or meningism (see Box 18.2, p. other affected organs. 169). Consider septic emboli from endocarditis Also consider cholesterol embolization or drug if the patient is febrile and has a predisposing reaction – seek Dermatology input if the cause cardiac lesion or a new murmur. remains unclear. Look for evidence of an underlying bleeding tendency – ask about/examine for ecchy- 4 Pustules present? moses, epistaxis, GI bleeding, menorrhagia haemarthrosisooksfree.com and mucosal haemorrhage, and Pustules are best thought of as small blisters check FBC, PT and APTT. Unless the cause is filled with pus (see Fig. 27.3). The key diagnostic obvious, e.g. excessive anticoagulation chronic conundrum is whether they are infective or sterile. mebo free.com mebo Rash: acute generalized skin eruption 249 Step by-step assessment

In both cases, the patient may be unwell, with patients to miss their dermatological medica- significant constitutional upset. tions due to lack of prescription or interruption Assume an infective pustulosis, at least initially, of their regular topical application routine; if this if the patient has a fever and the lesions have a is the case, suspect an acute flare and look for follicular appearance (individual, palpably raised resolution of the rash after reinstating routine lesions, following the distribution of hair follicles). treatment. booksfrSuspect sterile pustulosis due to either pustular psoriasis or drug reaction if the pustules have Likely drug reaction or infective a subcorneal appearance (more meboosuperficial, 7 sfrexanthem. co Refer to Dermatologym if ooksf often confluent lesions). In either case, admit persistent or severe symptoms the patient and seek an urgent dermatological Occasionally, serious acute drug eruptions lack opinion. the specific features detailed above; seek prompt dermatological advice in any patient with signs 5 Wheals present? of significant systemic upset, mucous membrane Classify the rash as urticaria if there are wheals: involvement or associated lymphadenopathy, or if symptoms are persistent and troublesome. transient (<24 hours), erythematous, intensely pruritic raised skin lesions (see Fig. 27.12). Consider guttate psoriasis and pityriasis rosea Look for swelling of the lips, face and throat, if there is an acute papulosquamous eruption (see suggesting associated angioedema; patients may above) over the trunk. Suspect the former if the describeooksfree. the skin sensation mas burning rather than lesions are ‘drop-like’ (see Fig. 27.5) and there itchy. Take a careful food and drug history to is a history of upper respiratory tract infection identify possible precipitants, although in many within the past 2–3 weeks; suspect the latter if cases a cause cannot be identifiedmebo (idiopathic the lesions free.com form a ‘Christmas tree’mebooks pattern on the urticaria). Other than avoidance of any identified back (see Fig. 27.6) and follow a ‘herald patch’. precipitant, the mainstay of treatment is regular Precise identification of infective exanthems is antihistamines; most cases subside quickly with seldom required as most do not need specific avoidance of the precipitant and/or antihistamine treatment and wil settle conservatively, but seek specialist advice if the patient is a returning treatment. Refer patients with persistent (>24 traveller with fever or an unusual rash. hours) or chronic (>6 weeks) lesions for outpatient dermatological assessment. Review all recent medications, both prescribed and over-the-counter drugs. There is significant variation in the morphology and exposure-to- 6 Underlying chronic dermatosis? onset time (minutes to years) of cutaneous drug Ask about previous skin disease, recent changes eruptions. If a drug reaction is suspected, e.g. boto dermatological k free.com or other medications and spe- a drug from Box 27.1 is involved or there is a cifically whether the present eruption resembles clear temporal association, attempt to confirm previous rashes. It is very common formebo hospital by sfree trial discontinuation com wherevermebooksf feasible.

27 28 Red eye ooksf e

The acute red eye (or eyes) is a common pres- (Fig. 28.2). Bacterial and viral conjunctivitis usually entation. Check visual acuity (VA) in all cases. produce a mucopu ulent discharge and are highly Patients with associated reduced ↓VA, severe contagious. Patients may have difficulty opening pain or photophobia require urgent specialist the eye after sleep because the discharge ‘glues’ ophthalmology referral. the eyelid margins together. Photophobia and VA are unlikely. Conjunctivitis ↓ Foreign body Inflammation of the conjunctiva is common. It can be infective: viral – commonly adenoviruses The patient often reports a sensation of some- and Herpes simplex; bacterial (Streptococcus thing going into the eye – often wind-blown. pneumoniae,ooksfree.com Staphylococcus aureus, Haemophi- There is redness and often copious watering. On lus influenzae, Chlamydia trachomatis, Neisseria examination a small foreign body will be seen, gonorrhoeae; or fungal; allergic or chemical. It superficially adherent to, or embedded in, the can affect one or both eyes and mebocommonly cornea, free.com or under the upper ormebook lower eyelid (Fig. presents with eye redness, eyelid swelling 28.3). Photophobia and discomfort may occur, (usually mild), gritty discomfort and discharge aggravated by blinking if the foreign body is

Clinical tool Acute red eye examination • Ask about subjective VA in both eyes, unilateral of pus cells; hypopyon) or trauma (collection of blood; versus bilateral symptoms, pain, itchiness, burning hyphaema) and grittiness, eye discharge and its character • Assess the pattern of redness. Diffuse redness (mucopurulent, watery), abnormality of eyelashes, involving inner eyelid suggests conjunctivitis. eyelid or eye closure, photophobia and a history of a Segmental redness may indicate episcleritis or scleritis foreignoksfree.c body going into the eye (and the mechanism, (although this may be generalized with deeper scleral e.g. hammering, grinding, blowing in with wind) vessel engorgement). Ciliary injection occurs in iritis • If the patient is uncomfortable, put topical anaesthetic and corneal conditions. Well-demarcated red eye with drops (e.g. oxybuprocaine 0.4%) into the eye Warn quiet adjacent conjunctiva is seen with subconjunctival the patient that this stings for a few seconds before it haemorrhage. works. meb• sfreeWith the slit lamp, carefully inspectmebook the ocular and • Examine eye movements and if appropriate visual corneal surfaces for ulceration, foreign bodies, fields. Pain on eye movement is suggestive of abrasions and trauma. Examine the anterior chamber scleritis or orbital cellulitis. Look at the fundus with an for pus cells. ophthalmoscope. • In addition to carefully examining the cornea and globe • Always check and document objective VA in BOTH for foreign bodies, look in the lower lid by gently pulling eyes with their spectacles or a pinhole using a it down and also evert the upper lid with a cotton wool Snellen chart bud (Fig 28.1). • Check the position of the lid margins and the position • Instil fluorescein and with the slit lamp and with the of the lashes. blue light, carefully re-inspect the ocular and corneal • Assess pupil size, shape, symmetry and reactivity. surfaces for uptake suggesting ulceration, abrasions Assess the clarity of the iris. A hazy iris suggests and trauma. cornealoksfree.c oedema (such as in macute angle glaucoma) or • Irrespective of the suspected diagnosis, if ↓VA inflammatory cells in the anterior chamber (such as ± severe pain ± photophobia, get emergency in iritis). A fluid level may be seen in iritis (co lection Ophthalmology review. b k eb free.com Red eye 251 Doifferential diagnosis

Fig. 28.1 Everting the upper eyelid to look at the conjunctiva. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinicalo Examination, 13th edn. Edinburgh: Churchill Livingstone, 2013.) oo boo

Subconjunctival haemorrhage This is benign self-limiting bleeding from under- neath the conjunctiva (Fig. 28.4). It is most often idiopathic, but is associated with hypertension, straining (coughing, sneezing, Valsalva manoeuvre), NSAIDs, anticoagulants and bleeding disorders, and febrile illnesses, e.g. meningococcaemia, typhoid, malaria. The appearance may be dramatic, butsfre is usually casymptomatic, m painless, and with normal VA. If covering the entire conjunctiva there can be associated oedema (chemosis). Ectropion/entropion/trichiasis/blepharitis Ectropion occurs when the eyelid turns outward. Fig. 28.2 Conjunctivitis. (From Batterbury M, Bowling B, With entropion the eyelid turnsme in (Fig. 28.5 ooks). Both Murphy C. Ophthalmology, 3rd edn. Edinburgh: Churchill more commonly affect the lower lid and cause Livingstone, 2009.) redness, irritation, and watering and increased vulnerability to infections such as conjunctivitis. lodged under the tarsal plate, but ↓VA is unlikely Trichiasis is due to eyelashes that grow back 28 unless the foreign body is in the centre of the towards the eye causing pain and eye redness. cornea. Fluorescein staining will aid identification. Blepharitis is an inflammation (usually chronic) Suspect an intraocular foreign body (i.e. one of the eyelids. which has penetrated the anterior chamber or globe) with trauma from mechanical saws, Keratitis grinding or hammering which can produce high Keratitis is an inflammation/ulceration of the velocityooksfree.co foreign bodies, or if ↓VA, a hyphaema cornea causing an intensely painful red eye with (blood in the anterior chamber) or an abnormal photophobia and watering. VA may be ↓ and pupil is present. ebothe sfree. eyelids swollen. om Keratitis can be infective, meboo Red eye 252 Differentialco diagnosis

Fig. 28.3 Fore gn body. (From Atkinson P, Kendall R, Rensburg LV. Emergency Medicine, 1st edn. Edinburgh: Churchill Livingstone, 2010.)re e

patients and may be associated with systemic diseases including seronegative spondyloarthropa- thies, inflammatory bowel disease, rheumatoid disease, SLE, sarcoid, HIV, etc.mebo Presents with (usually unilateral) eye redness, typically ciliary or limbal (at the junction of the cornea and sclera), blurred vision/↓VA watering, photophobia (experienced when a light is shone into the affected eye and also the normal eye) and pain. Pain may be aggravated by reading or close work. The pupil is commonly small and irregular. Episcleritis/scleritissfree com In episcleritis there is localized inflammation of Fig 28.4 Subconjunctival haemorrhage. (From Scully the episclera (which lies between the conjunctiva Coo Medical Problems in Dentistry, 6th edn. Edinburgh: Churchill Livingstone, 2010.) and the sclera) (Fig. 28.7). Pain is usually mild and there is redness and watering and a nodule may be seen or felt by the patient. Scleritis is a more serious localized inflammationmeboo of the sclera (Fig. 28.8). Pain is a dominant feature and is e.g. viral (herpes simplex infection can produce more severe than with episcleritis and it is often corneal ulcers with a characteristic dendritic recurrent. It responds poorly to analgesics, is branching pattern), bacterial, fungal, amoebic or worse with eye movements and can radiate to parasitic; environmental, e.g. exposure, ultraviolet the periorbital region, forehead, temple and jaw. (as in snow blindness or welder’s arc); chemi- Both conditions are associated with autoimmune cal; traumatic or due to contact lens wearing; diseases and rheumatoid arthritis. ↓VA is unlike y the main risk factor for keratitis is contact lens in episcleritis but present in up to 20% with use Keratitis, if untreated or severe, can lead scleritis. to sight-threatening complications. oksfree.com Acute angle-closure glaucoma Acute iritis (anterior uveitis) A sight-threatening ophthalmic emergency Inflammation of the iris, which is often recurrent caused by sudden blockage of aqueous humour (Fig. 28.6), occurs in young and middle-agedm leading sfree.com to ↑↑↑intraocular pressureme (Fig. 28.9 sf). Red eye 253 Doifferential diagnosis

Fig. 28.5 Senile entropion of the lower lid. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinical Examination, 13th edn. Edinburgh: Churchill Livingstone, 2013.) e. ee.

Fig. 28.6 Iritis (anterior uveitis). (From Swartz MH. Fig. 28.7 Episcleritis. (From Rutter P. Community Textbook of Physical Diagnosis: History and Examination, Pharmacy, 2nd edn. Edinburgh: Churchill Livingstone, 2009.) 6th edn. Philadelphia: Saunders, 2009.) e c ee.c

Fig. 28.8 Scleritis. (From Kanski JJ. Clinical Diagnosis in Ophthalmology, 1st edn. St Louis: Mosby, 2006.) Fig. 28.9 Acute angle-closure glaucoma. Arrows show 28 dilated conjunctival vessels at corneal edge. Note hazy cornea (From Roberts JR, Hedges JR. Clinical Procedures in Emergency Medicine, 5th edn. Philadelphia: Saunders, 2010 )

Middle-aged/elderly, long-sighted patients with Presentation is with acute, usually unilateral, shallow anterior chambers are at particular risk severe eye pain with redness, ↓VA, seeing halos Pupilook dilation can precipitate co the condition so around lights, nausea and vomiting, a cloudy the onset may be more common in the evening cornea and a fixed, mid-dilated non-reactive, and be precipitated by sympathomimetic, often oval-shaped, pupil. The globe feels ‘hard’ anticholinergic and other drugs. meboon (gentle) free.c palpation throughmebook the eyelid. f Red eye 254 Overview

Eye examination (see clinical tool) f e 1 Is eye redness bilateral?

No Yes

Yes Photophobia or severe pain? Consider bilateral iritis / keratitis / m scleritis m No

Yes Itchy? Likely allergic conjunctivitis

Likely infective conjunctivitis

Yes Ectropion / entropion / blepharitis 2 Abnormality of eyelashes, eyelid or eye closure? / trichiasis / Bell’s palsy No

Yes 3 Does cornea stain with fluorescein?m oKeratitis o / foreignm body o No

Yes 4 Is pupil larger in the red eye? Acute angle-closure glaucoma

Yes 5 Is photophobia present? eLikely o iritis fre o No

Yes 6 Severe pain / tenderness? Consider scleritis

7 Is the eye redness localised?

No Yes

Yes Asymptomaticc + ‘quiet’ adjacent conjunctiva Subconjunctival haemorrhage No

Probable episcleritis

Consider unilateral conjunctivitis / extra-ocular causes of red eye (Box 28.1) / episcleritis 8 Urgent ophthalmology review if decreasedbo VA, severe pain or photophobia c Red eye 255 Step-by-step assessment

1 Is the eye redness bilateral? A foreign body or trauma and acute glaucoma are usually unilateral. Conjunctivitis often starts unilaterally and then becomes bilateral. Iritis andooks keratitis can e be bilateral although are more commonly unilateral. Allergic conjunctivitis is almost always bilateral; it is often seasonal, worse in the morning,m itchy bo co and there may be a history of atopy. Viral and bacterial conjunctivitis cannot be reliably differentiated based on clinical features; however, a watery discharge is more commonly seen with viral infection and a mucopurulent discharge with bacterial infection. Severe purulent Fig. 28 10 Dendritic conjunctival ulcer. Fluorescein discharge is common in gonococcal infection. staining showing branching dendritic ulcer. (From Douglas Take conjunctival swabs for culture and sensitivity G Nicol F, Robertson C. Macleod’s Clinical Examination, 13th edn. Edinburgh: Churchill Livingstone, 2013.) and to ksfreeguide antibiotic/antiviral com therapy. Abnormality of eyelashes, eyelid the diagnosis and antimicrobial/antivi al therapy. 2 or eye closure? Many foreign bodies can be simply removed with a cotton bud. Embedded metallic corneal Check the position of the lid margins and the foreign bodies require specialist review for position of the lashes. The appearancesm of removal sfree and treatment of associatedmebo ‘rust-rings’. ectropion, entropion and trichiasis are usually A history consistent with penetrating injury or of obvious. Fluorescein staining may be present if hammering/grinding mandates specialist review the lashes have rubbed on the cornea. and imaging. Bell’s palsy commonly presents with unilateral mouth droop and an inability to close the eye on the affected side. Differentiate from acute 4 Is the pupil larger in the red eye? stroke as the forehead is not spared (patient Suspect acute angle-closure glaucoma in any is unable to wrinkle forehead). Bell’s palsy can patient with periorbital pain, blurred vision/visual cause eye redness because of drying and/or defect and a mid-dilated non-reactive pupil The corneal abrasion/ulceration and temporary taping pain is usually severe and may be mistaken for atooksfree night can help prevent com exposure keratitis and other causes of severe headache e.g migraine corneal ulceration. In blepharitis the lid margins/boor sfree. subarachnoid mhaemorrhage. Similarly, the lashes are inflamed and crusty. associated nausea/vomiting/abdominal pain may lead to a misdiagnosis of gastroenteritis.mebooksf The 3 Does the cornea stain with fluorescein? decreased VA may be profound, e.g. detection of hand movements only. The cornea is usually Examine carefully for fluorescein staining and cloudy and the pupil irregular and unreactive. foreign bodies as described (see Clinical tool). Acute angle-closure is a medical emergency, Infective causes of keratitis and corneal ulceration any time delay in diagnosis and treatment may 28 can be rapidly sight-threatening and may be compromise sight drastically. Get emergency caused by viral, bacterial, fungal or amoebic ophthalmological advice and review. Keep the infection. Herpes simplex virus infection may patient supine if possible and do not cover the eye. produce characteristic dendritic staining of the Analgesics and anti-emetics may be indicated cornea (Fig. 28.10). In addition to examining the cornea with fluorescein staining for ulceration 5 Is photophobia present? lookooksfree for cloudiness or com frank pus (hypopyon) in the anterior chamber; seek urgent specialist Photophobia indicates iritis or corneal epithelial ophthalmological review regarding confirmation of disturbance. Ask about previous similar episodes mebo sfree c m meb sf Red eye 256 Step-by-step assessment

(common in iritis) and underlying systemic conditions (e g. ankylosing spondylitis, reactive Box 28.1 Extraocular causes for a red eye arthritis, inflammatory bowel disease, connec- • Orbital cellulitis tive tissue disorders) known to be associated • Cavernous sinus thrombosis with iritis or scleritis. Cloudiness or hypopyon • Carotid-cavernous fistula ofooksfre the anterior chamber co may be present. Get • Cluster headache emergency ophthalmological review. bo fre

6 Severe pain/tenderness?

Consider scleritis if the red eye is associated with Box 28.2 Features suggestive of a benign cause severe pain (present in ≥80% of cases) or is very for a red eye tender. Typically the redness will be localized • Pupils exhibit normal size and reactivity but in severe cases it can involve most of the • Normal VA (NB: occasionally a central corneal sclera. If suspected refer urgently for specialist abrasion can reduce visual acuity) assessment. • Clear cornea • Clear anterior chamber • No proptosis 7 Is the eye redness localized? • Eyeball not tender on palpation Diagnose subconjunctival haemorrhage if there is • Normal extraocular eye movements a oolocalized s region e.comof redness with no associated symptoms (except possibly mild dryness) and normal appearances of the surrounding con- concerning features, e.g. photophobia or reduced junctiva. Suspect episcleritis if there is segmental meboVA. free.coThough usually localized,m both scleritis and redness associated with mild pain, eye watering episcleritis may cause diffuse eye redness. or injection of the adjacent vessels. Consider Reconsider the possibility of acute angle closure scleritis if there is localized redness associated glaucoma if there are any suggestive features, with reduced VA or pain that radiates to the e.g. cloudy cornea, severe orbital/periorbital pain periorbital region, forehead, temple or jaw. or reports of seeing halos around objects. In the absence of a definite diagnosis, Box 28.2 lists 8 Consider other causes (Box 28.1) features that would point to a benign underlying Infective conjunctivitis may be unilateral, particu- cause. Irrespective of the suspected diagnosis, larly in the early stages; consider the diagnosis get emergency Ophthalmology review if there if thereoksf is associated e com discharge and no other ois sfreedecreased comVA, severe pain or photophobia.oksf This page intentionally lefto blank 29 Scrotal swellingsf ooksfre

Most causes of scrotal swelling are benign, but some have an underlying inflammatory or, rarely, germ cell tumours are a leading cause of malig- malignant process. nancy in young men whilst testicular torsion and strangulated herniae are surgical emergencies. Orchitis It is important to ascertain whether the scrotal This may arise as a complication of epididymitis swelling arises from within the scrotum or from (epididymo-orchitis) or, with mumps (now rare outside (inguinal hernia). due to vaccination). It presents with acute scrotal pain and swelling, over days rather than hours, Indirect inguinal hernia often accompanied by fever, urinary symptoms Inguinal hernia (Fig. 29.1) may occur at any age and/or urethral discharge. There may be a tender, butooksfree.com is increasingly common from middle age and swollen (soft) epididymis/testis or aooksf reactive is the most frequent cause of scrotal swelling. hydrocoele. Herniated bowel passes through the inguinal ring and may descend into the scrotal sac.mebo Left-sided sfree.Testicular tumour hernias may contain the sigmoid colon. As the These typically present as painless, irregular, firm swelling arises from the abdominal cavity, it is not testicular lumps. Non-seminomatous germ cell possible to ‘get above’ it Typically, the swelling tumours (NSGCT) (see Fig. 29.1) are the most is more prominent on standing, associated with common malignancy amongst men aged 20–30 a cough impulse and can be pushed back into years. These comprise yolk sac tumours, cho- the abdomen (‘reduced’). A non-reducible or riocarcinoma, mixed type or embryonal tumours. ‘incarcerated’ hernia may lead to bowel obstruc- Seminomatous tumours present later in life and tion or strangulation with ischaemia. have a slightly less aggressive course. Scrotal Scrotal swellings USS confirms the diagnosis and CT thorax/ abdomen/pelvis is used in staging Tumours Scrotaloo swellings free may com arise from either the con- are very chemosensitive (platinum-based tents of the scrotum or the skin of the scrotum. chemotherapy) and 5-year su vival is greater Abnormalities of the contents should be divided than 90% even if metastasis has occurred. into spermatic cord, epididymis andmebo testicular The sfree.com tumour markers alpha-fetoproteinmebooksf (yolk sac pathologies. tumours), beta-human chorionic gonadotropin Testicular abnormalities (choriocarcinomas) and LDH (tumour burden) should be tested Suspected testicular cancer Hydrocoele requires urgent inpatient management due to the Hydrocoele (see Fig 29.1) is the most common very rapid progression of these tumour types. cause of scrotal swelling, especially in older Torsion of the testis men. Fluid accumulates within the tunica vaginalis (analogous to the peritoneal space Twisting of the testis may compromise its own in the abdomen), producing a painless, cystic blood supply; initially impeding venous ou flow swelling that typically transilluminates. With until the pressure in the testis reached mean substantialooksfree. swelling, the underlying testes may arterial pressure and arterial inflow is then be impalpable. Most cases are idiopathic,ebo but occluded. s e Acute, com severe, unilateralebooks testicular Scrotal swelling 259 Differential diagnosis

Normal Hydrocoele Fig. 29.1 Common causes of e scrotal swelling.

Spermatic cord

Epididymism e o

Testis

Indirect inguinale. hernia Epididymitise

Varicocoele Tumour of testicle.

29e Scrotal swelling 260 Differential diagnosis pain is the dominant presenting symptom, renal tumours (e.g. tumour thrombus of renal often accompanied by nausea and vomiting. cell carcinoma). On examination there may be a red, swollen, exquisitely tender hemiscrotum (often too tender Other spermatic cord pathologies to palpate), with the testis lying in a high posi- Other abnormalities uncommonly include lipomas tionooksfr due to shortening com of the spermatic cord. of the cord (usually identified whilst undertaking Patients are typically young adolescent males but an inguinal hernia repair) and, rarely, adeno- consider torsion in all acute scrotal presentations. myoma and liposarcoma of the cord. Suspected torsion mandates immediatemebo surgical fre m bo correction (de-torsion and pexy), as any delay Abnormalities of the scrotal skin threatens testicular viability. Scrotal wall oedema Epididymis abnormalities This is the most common abnormality of the scrotal skin, presenting as thickened, indurated Epididymo-orchitis skin, usually as a result of congestive cardiac Inflammation of the epididymis± testis (see fa lure or other causes of peripheral oedema. Fig. 29 1) is usually due to sexually transmitted Lymphatic filariasis Wuchereria( bancrofti [90%] infection (mainly chlamydia and gonorrhoea) in Brugia malayi, and Brugia timori) causes oedema younger men, and urinary tract infection (UTI) of the legs and genitals due to parasitic inva- inooksfr older men. Acute e. epididymo-orchitis o may be sion of the pelvic lymphatics. Treatment is with difficult to distinguish clinically from torsion. anti-parasitic agents such as mebendazole. ebooThe sfree.com scrotum may rarely become enormously Epididymal cyst enlarged, for example necessitatingmebooksf carriage These are common, benign, simple cysts arising of the scrotum in a wheelbarrow. In instances from the head of the epididymis. They may be such as these, debulking scrotal surgery is multiple or bilateral. They are palpable separately required. from the testis. Differential diagnosis includes hydrocele, spermatocoele (which is similar to Cellulitis/Fournier’s gangrene an epididymal cyst but contains sperm) and Fournier s gangrene refers to necrotizing fasciitis haematocoele (collection of blood in the tunica of the genitalia, perineum or perianal region; it is vaginalis following trauma). Symptoms include a a life-threatening emergency requiring immedi- dragging or painful sensation due to the weight atesfree surgical debridement c m and broad spectrum of the cyst. antibiotics. Infection is typically polymicrobial with oksfree com both aerobic and anaerobic bacteria, including Spermatic cord abnormalities streptococcus, staphylococcus, enterobacte- riacea and clostridium species. The condition Varicocoele tends to arise in older patients,mebooksf with diabetes as Varicocoeles, varicosities of the gonadal vessels the main risk factor. Intense genital pain and and their tributaries (see Fig. 29.1), are the com- tenderness is the clinical hallmark and, impor- monest abnormalities of the spermatic cord. They tantly, the overlying inflammatory skin changes typically present with a dragging sensation of the (erythema, oedema) may be relatively mild or testis and feel like a ‘bag of worms’ on palpa- even absent in the early stages. In advanced tion. Left-sided varicocoeles may be caused by disease there may be subcutaneous crepitation outflow obstructionee.com of the left renal vein due to or frankee.com gangrene. Scrotal swelling 261 Differentialo diagnosis

Clinical tool Examination of the scrotum Testicular examination • If you cannot ‘get above’ the swelling, check for a • Obtainksfre consent and offer a chaperone. cough impulse and attempt to reduce the swelling by • With the patient standing, then supine, inspect the very gently ‘massaging’ it back into the abdomen. scrotum for redness, swelling and position of the • Determine whether the swelling transilluminates using testes. a pen-torch. • Wearing gloves, palpate each testis in turn between • In patients with an acutely painful scrotum or tender/ forefinger and thumb; identify the spermaticm cord and inflamed scrotal swelling, check them cremasteric boo epididymis and assess any irregularity, swelling or reflex. With the patient’s thigh abducted and externally tenderness. rotated, stroke the upper medial aspect – normally, the • Use your fingers to see whether you can feel above the testis on that side will rise briskly. swelling (Fig. 29.2); if so, it originates in the scrotum. m

Fingersr can om ‘get above’ mass Fingers cannot ‘get above’ mass

Fig. 29.2 Assessing the origin of a scrotal swelling. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone,me 2009.) me

29e Scrotal swelling 262 Overview

Full clinical assessment + testicular examination fre m Inflammation present and Yes Urgent surgical 1 confined to scrotal / surrounding Cellulitis / Fournier’s gangrene review skin? oo

Yes 2 Isolated scrotal skin oedema? Dependent oedema / filariasis

Painful and / or inflamed scrotal Yes Torsion / epididymo-orchitis / Urgent surgical 3 contents? strangulatedee. hernia review Nof ee.

Yes 4 Unable to feel above swelling? Likely inguinal hernia or varicocoele

No Consider USS to Yes delineate 5 Transilluminates? Likely hydrocoele underlying scrotal structures No

Yes 6 Any palpable swelling? Scrotal USS Tumour / spermatocoele / other Nor c

Reassure; consider follow-up evaluation Scrotal swelling 263 Step-by-step assessment

Inflammation present and confined to testicular torsion. There may be associated 1 scrotal/surrounding skin? features as below: • nausea or vomiting Consider Fournier’s gangrene in any patient with • pain duration <24 hours inflammatory skin changes affecting the scrotal • high position of the testis skin (+/– surrounding perineal/perianal regions). ook fre • abnormal cremasteric reflex. Seek immediate surgical review if any of the following are present: eboConsider fre initial co investigation with scrotal USS if the clinical presentation suggests an alterna- • severe pain or tenderness (especially if tive diagnosis such as epididymo-orchitis,me e.g. disproportionate to skin appearances) urethral discharge, tenderness localized to • dusky appearance of skin, fluctuation, epididymis, age 30 years and none of the above crepitation or gangrene > are present. In all other cases, arrange immediate • systemically unwell e.g. sepsis surgical review without delay for imaging. (see Ch. 14), shock (see Ch. 30). In the absence of these features, consider 4 Unable to feel above swelling? scrotal ce lulitis but monitor frequently and have a If it is not possible to palpate above the swelling, very low threshold for surgical review, particularly the swelling is likely to originate from outside in older or diabetic patients. ksfree com the scrotum. Suspect a varicocoele if it feels like a ‘bag of 2 Isolated scrotal skin oedema? worms’; confirm with scrotal USS and exclude In patients with scrotal wall oedema, look underlying renal cell carcinoma f sudden onset, for evidence of generalized oedema, ascites, unilateral and left-sided or not reducible in supine ↑JVP and/or pleural effusions. ↑JVPme indicates position. sfr e com mebo sf systemic venous congestion and strongly Otherwise, suspect an inguinal hernia – look suggests a cardiogenic cause, e.g. cardiac for bowel obstruction (p. 32) and arrange urgent failure or severe pulmonary hypertension/cor surgical review if it is non-reducible. If easily pulmonale. Also consider a cardiac cause in reducible, refer for outpatient surgical evaluation. patients with a significant cardiac history (e.g. previous myocardial infarction, valve disease, 5 Transilluminates? cardiomyopathy), severe chronic lung disease Suspect hydrocoele if there is a painless swelling or exertional/nocturnal dyspnoea. Check U+E of the scrotum that transilluminates. (Epididymal and serum albumin to exclude severe renal cyst and spermatocoeles also transilluminate and failure/hypoalbuminaemia and consider ECG are part of the differential.) Consider USS to assess andooksfree.com or cardiology review. Suspect filariasis if for testicular abnormality (e.g. tumour, inflamma- other causes are excluded and the clinical history tory mass) if there is tenderness systemic upset is suggestive, e.g. from endemic area – seek or difficulty in palpating the testicular structures. expert advice. meboo sfr e.com mebooksf 6 Any palpable swelling? 3 Painful and/or inflamed scrotal contents? USS is the investigation of choice in scrotal swell- Suspect a strangulated hernia if the swelling ing and differentiates malignant tumours from arises from the inguinal canal (see above), is other masses, e.g. spermatocoele, with a high not reducible (or severe pain persists despite degree of accuracy. Arrange scrotal USS in any reduction) and is tender, hot and red, or patient with a detectable scrotal lump or swelling. 29 associated with systemic toxicity. Seek urgent Testicular tumours grow extremely rapidly so surgical review, as there is a risk of bowel admit for urgent testicular USS and urology ischaemia. referral +/– tumour markers and CT stag ng if If the swelling arises from the scrotum (or there is a high suspicion of malignancy, e.g. painooksfree.co prohibits examination) and is painful, tender, painless testicular lump in a young man. Refer inflamed and/or accompanied by acute severe to Urology in any case for further assessment/ unilateral scrotal pain, you MUST excludeebo treatment sfree if the com diagnosis remains uncertain. mebooksf e Shock 30o sfre

Shock is a clinical syndrome characterized Other fluid losses by inadequate systemic and specific organ Hypovolaemia may result from burns, diarrhoea, perfusion. It is recognized by features of tissue vomiting, polyuria or from prolonged dehydration, hypoperfusion (Box 30.1), usually with hypoten- particularly in the elderly. Significant volumes of sion; however, BP may be maintained until the fluid may also be lost into the ‘third space’, e.g. advanced stages of shock, particularly in young, in conditions such as bowel obstruction and fit individuals. acute pancreatitis. Three processes may cause shock: hypovolaemia, pump failure (cardiogenic shock) Cardiogenic shock and vasodilatation (distributive shock). These processesooksfree.com can be difficult to distinguish, as Cardiac disorders may cause valvular or myocar- components of the circulation are interdependent dial dysfunction, and extracardiac disorders may and different mechanisms often coexist, e.g. impede cardiac inflow or outflow (also known as vasodilatation, myocardial suppressionmeboo and ‘obstructive’ free shock). com Peripheralmebo signs are similar relative hypovolaemia may occur simultaneously to those of hypovolaemia but the JVP is usually in sepsis. raised (reflecting right heart failure) and there may Many presentations in this book may be com- be pulmonary oedema (reflecting left heart failure) plicated by shock but here shock is considered as well as features specific to the underlying as the primary presenting problem detected on cause. ECG is often diagnostic. routine observa ions or on targeted examination of a severely or non-specifically unwell patient. Myocardial infarction Shock may result from large infarcts, particularly Hypovolaemic shock in the anterior wall; from smaller infarcts in patients with pre-existing ventricular impairment; Decreased intravascular volume reduces or from structural complications of myocardial cardiacook filling free pressures com and cardiac output A infarction (MI), such as papillary muscle rupture, compensatory increase in heart rate and systemic ventricular septal defect or tamponade. vascular resistance occurs. Characteristic findings are ↓JVP, tachycardia, ↓pulse volumemebo and sfreLeft ventricular com dysfunctionmebooks cool, clammy peripheries. Tachycardia may be without infarction absent in patients on rate-limiting medications, e.g. beta-blockers, calcium channel antagonists. This includes tachy- or bradyarrhythmias, acute myocarditis and end-stage cardiomyopathy. Haemorrhage Valve disorders Blood loss is not always visible; it may be left at the scene of an accident or concealed within Examples of valve disorders include prosthetic surgical drains. The pelvis, retroperitoneum, valve dysfunction, endocarditis and critical aortic peritoneum, thorax and thighs can accommodate stenosis. several litres of extravascular blood. In addition Tension pneumothorax toooksfre trauma, important causes om include GI bleed (see Ch. 15), ruptured abdominal aortic aneurysm The urgency of treatment mandates a clinical (AAA) and ectopic pregnancy. ebodiagnosis. sfree. Typical o findings include increasing meb sf Shock 265 Differential diagnosis respiratory distress, ↓ipsilateral breath sounds, major systemic inflammatory response, e.g. acute tachycardia and hypotension. Tracheal deviation pancreatitis. Features of relative hypovolaemia is often absent. Immediate decompression is may predominate initially. An arterial or venous essential. lactate of 4 mmol/L or greater has been associ- oksfre ated with increased mortality in sepsis Cardiac tamponade Accumulation of fluid in the pericardial space Anaphylaxis (pericardial effusion) impedes cardiac filling. As This produces a very rapid onset of broncho little as 200 mL of fluid may cause metamponade constriction, sfre widespread o erythematousm ooksf rash if accumulation is rapid, e.g. trauma, aortic and severe distributive shock. A precipitant dissection, myocardial rupture. Hypotension, (foodstuffs, drugs – particularly antibiotics, insect tachycardia, ↑JVP and pulsus paradoxus are stings) may be identified. A related problem is usually present. The e may also be muffled heart transfusion reaction; ABO incompatibility may sounds, Kussmaul’s sign (a ‘paradoxical’ rise in present with shock as the only initial sign, particu- JVP on inspiration) and small ECG complexes. larly in unconscious or sedated patients. In severe ECG will confirm the presence of an effusion, anaphylaxis, severe shock or even cardiac arrest provide evidence of cardiac compromise and may occur without other symptoms or signs. guide therapeutic drainage. ks ree.com Drug causes Pulmonary embolism Antihypertensives and anaesthetic agents Massive pulmonary embolism (PE) typically (particularly epidural and spinal anaesthesia) presents with sudden onset of chest pain, may cause distributive shock through excessive dyspnoea and hypoxia with shock.me The JVP peripheral sfree.com vasodilatation. meb f is usually elevated and the ECG may show features of right heart strain. In critically unwell Adrenal crisis patients, bedside echocardiography may assist Glucocorticoid deficiency may result in distribu- the diagnosis. tive shock, particularly during acute stress, e.g. Distributive shock infection, surgery. In distributive shock, peripheral vasodilatation Neurogenic shock causes a drop in systemic vascular resistance and ‘relative hypovolaemia’ (↑size of vascular Neurogenic shock is a rare form of distribu- space without corresponding increase in tive shock associated with direct injury to the ntravascular volume). A compensatory rise in sympathetic fibres that control vascular tone from cardiacooksfree. output is insufficient m to maintain blood a traumatic spinal injury. ooks pressure. Tachycardia and hypotension are often accompanied by warm peripheries and ↑pulse volume. mebo s r e.co

Systemic inflammatory response syndrome/sepsis Distributive shock may complicate sepsis (p. 141) or non-infective e.cconditions m associated with a 30e Shock 266 Overview

ABCDE, ECG, ABG fre No 1 Clinical features of shock (Box 30.1)? k Incipient shock OR consider alternative causes of organ dysfunction / hypotension o Yes

Yes See Box 15.1 2 Obvious bleeding source? Likely hypovolaemic shock and treat cause

Cause that requires immediate specific Yes Treat and 3 Confirm diagnosis treatment? reassess No e o Yes Urgent echo and 4 Evidence of cardiac failure? Likely cardiogenic shock Cardiology opinion to establish cause No

5 Ongoing assessment and treatmentm of shock physiology during diagnostic work-upm (Fig. 30.1) oks

Urgent surgical Suspect pelvic or intra-abdominal Yes 6 opinion Acute surgical cause pathology? ± abdominal USS/CT

Yes Likely systemic inflammatory 7 SIRS criteria or immunocompromise? Seek source fr m responsefre syndrome o / sepsis No

Yes Treat and 8 Suspect adrenal insufficiency? reassess; Acute adrenal crisis check random cortisol b No

No 9 Distributive or cardiogenic pattern? Likely hypovolaemic shock Identify cause

Yes

Further diagnostic work-up guided by shock physiology pattern with invasive monitoring. Involve ICU. Arrange echo and cardiology input if suspect cardiogenic shock Maintainsfree suspicion of sepsis; m consider rarer causes esfre g. neurogenic shock Shock 267 Step-by-step assessment

1 Clinical features of shock (see Box 30.1)? as part of the ABCDE assessment (p. 8). If one of these disorders is suspected but the diagnosis Use the features in Box 30.1 to identify shock. remains uncertain, seek urgent expert assistance, Tissue hypoperfusion is the defining feature e.g. Cardiology review. Absolute values of HR and BP are less informa- tiveooks than monitoring re of trends over time. Some 4 Evidence of cardiac failure? patients may maintain BP within normal limits despite organ dysfunction, but consider local Pulmonary oedema suggests cardiogenic shock. pathology if there is single organ dysfunction,mebo e.g. The sfre most common co cause is severeme left ventricular ksf oliguria, without clear evidence of haemodynamic dysfunction from acute MI. Perform (serial) ECG to compromise. If the patient falls short of the criteria look for evidence of infarction or ischaemia (see in Box 30.1 but you suspect significant circula- Box 6.1, p. 51). Arrange bedside ECG to assess tory compromise, pursue a working diagnosis left ventricular function and exclude mechanical of ‘incipient shock’ and continue through the causes (especially acute mitral regurgitation). diagnostic pathway. Patients without pulmonary oedema but with ↑JVP ± peripheral oedema may have a 2 Obvious bleeding source? cardiogenic component to shock. Those with right ventricular infarction (suspect with inferior Where shock arises from acute haemorrhage, the or posterior MI in the previous 72 hours) chronic initial aims of treatment are to minimize further right heart failure or tricuspid regurgitation may be blood loss and restore adequate circulating ook f e com inadequately filled despite ↑JVP and will respond volume. Assess resuscitation requirements and to fluid challenge. Otherwise, echocardiography is monitor response to treatment as described in mandatory to look for evidence of right ventricular Box 15.1, page 153. In patients withmebo traumatic dysfunction, sfree.com tamponade andmebooksf PE. haemorrhage, always consider the possibility of Patients with cardiogenic shock require an additional cause of shock, e.g. tamponade, invasive monitoring and specialist interventions; tension pneumothorax. if appropriate, urgent Cardiology and ICU referral is essential. Cause that requires immediate 3 specific treatment? Ongoing assessment and treatment In some cases, specific interventions to reverse 5 of shock physiology during diagnostic the underlying cause of shock offer the only work-up (Fig. 30.1) effective treatment (e.g. decompression of a In the absence of obvious haemorrhage, major tension pneumothorax) and take precedence cardiac dysfunction or a rapidly reversible cause over further investigation or supportive measures ooksfr e c m of shock, the next step is to initiate treatment (Table 30.1). Most will be identified and treated and assess response. As shown in Fig. 30.1, ebothe effect ee of repeated om fluid challenge on haemo-

Box 30.1 Clinical features of shock dynamic variables and tissue mebooperfusion helps to delineate the mechanism(s) of shock and guide Haemodynamic further resuscitation and treatment. This process • Systolic BP <100 mmHg or a drop of >40 mmHg should be carried out in parallel with continued from baseline evaluation for a specific underlying cause. Beware • Pulse >100/min concealed bleeding. Haemorrhagic shock is fre- Tissue hypoperfusion quently missed in the early stages. Haemoglobin/ • Skin: capillary refill time> 2 sec or cold/pale/mottled haematocrit levels may be misleading as they 30 extremities are usually normal in acute haemorrhage, and • Renal: oliguria (<0.5 mL/kg/hr) or ↑serum creatinine sfree.com (acute) only fall following fluid replacement. Lactate • CNS: GCS <15, confusion or agitation clearance (change in blood lactate levels over ooksfree• Global: ↑lactate (in the absence m of hypoxaemia) time) is a proxy for monitoring response to treat- ≥2 of the above indicate shock ment. Bedside USS of the inferior vena cava (IVC) and its degree of collapsibility has also mebooksf e Shock 268 Step-by-step assessment

Table 30 1 Rapidly reversible causes of shock

Reversible cause Suspect if Test to confirm Specific intervention Tensionoksfr pneumothorax co Respiratory distress/tracheal Nil – treat immediately Needle aspiration deviation/unilateral hyper- resonance, ↓breath sounds Tachyarrhythmia Ventricular tachycardia (VT) or Nil – treat immediately DC cardioversion supraventricularmeboo tachycardia m ook (SVT) >150 bpm Bradyarrhythmia 3rd degree atrioventricular Nil – treat immediately Atropine, adrenaline, block or HR <40 bpm external or transvenous pacing Anaphylaxis Respiratory distress, stridor, Nil – treat immediately Adrenaline, IV fluid wheeze, angioedema, rash, precipitant ST elevation myocardial Chest pain, ECG criteria Nil – treat immediately Primary angioplasty infarction (MI) (see Box 6.1, p. 51) or thrombolysis Pulmonary embolism Dyspnoea, hypoxia (especially CTPA if stable; urgent Thrombolysis oksfr with clear lung fields), chest ECG if unstable; nil if pain, ↑JVP risk factors, ECG peri-arrest changes (p. 58) Cardiac tamponade ↑JVP, pulsus paradoxus, ECG Pericardiocentesis small QRS complexesm book on ECG r c m

Absolute or relative hypovolaemia: • A brief, transient in JVP/CVP, BP urine output suggests redistribution of fluid or ongoing fluid loss • If no response or a deterioration, larger fluid challenges may be indicated • Consider CVP monitoring if JVP difficult to interpret, known LV impairmen or Give fluid challenge shock persists after ≥3 L IV fluid Corrected hypovolaemia: e.g. 250 mL over 2–5 min oLook for underlying causes, e.g. blood loss ook • Monitor closely for recurrent shock boo Yes No

Shock resolved? Sustained in JVP/CVP to high / normal?

No No

Yes Pulmonary oedema? Cardiogenic +/or distributive shock: • Cool peripheries, thready pulses and/or Yes poor LV function on echocardiography favour cardiogenic • Warm peripheries, bounding pulses Cardiogenic shock: and/or good LV function on • Obtain urgent cardiology and ICU echocardiography favour distributive input to optimise monitoring and • Invasive monitoring usually required to identify / treat the underlying cause accurately define shock physiology and guide use of inotropes / vasopressors request urgent ICU assistance b Fig. 30.1 Shock physiology: The cycle of assessment.m Shock 269 Step by-step assessment been shown to be useful in both diagnosing p. 142) to identify a likely source but do not shock type and guiding response to treatment. delay antibiotics. Assume sepsis in any patient In a spontaneously breathing, previously healthy with immunocompromise until proven otherwise person, variations in pleural cavity pressure with See ‘Surviving Sepsis’ guidelines (http:// breathing are transmitted to the right atrium. www.survivingsepsis.org/GUIDELINES/Pages/ Thisooksfre leads to a reduction of about 50% in default.aspx). IVC diameter on inspiration. Volume depleted spontaneously breathing patients will have a 8 Suspect adrenal insufficiency? reduction of greater than 50% sometimesmebo leading sf e co m ooksf to complete collapse of the IVC on inspiration. Adrenal insufficiency is often overlooked, as many patients have fever and are assumed, at Suspect pelvic or intra-abdominal least initially, to have septic shock. Always 6 pathology? consider the diagnosis and look for clinical/ biochemical features. Useful indicators include Request urgent surgical review if you suspect prominent GI symptoms (almost always present acute abdominal or pelvic pathology. AAA or but non-specific), pigmentation of recent scars, ruptured ectopic pregnancy require immediate palmar creases and mucosal membranes, intervention. Suspect ruptured AAA in patients vitiligo, ↓Na+, ↑K+ and hypoglycaemia. Even >60 years, those with known AAA, a pulsatile a blood glucose at the low end of normal abdominal mass or sudden-onset, severe (3.5–4.5 mmol/L) suggests an inadequate ‘stress abdominal/back;ooksfree. perform an immediate bedside response’. If you suspect adrenal insufficiency, USS, withhold fluid resuscitation if the patient is send blood for a random cortisol level then treat fully conscious and contact a vascular surgeon with IV hydrocortisone without waiting for the as an emergency. meboo sfree com mebo ksf results. A short ACTH (Synacthen) test may Suspect ruptured ectopic pregnancy in any be helpful but takes 30 minutes to perform woman of child-bearing age with recent-onset and should not delay empirical treatment in lower abdominal pain, shoulder-tip pain or critically unwell patients. Remember that any PV bleeding; perform an immediate bedside patient taking systemic steroids for ≥3 months urine pregnancy test and consider bedside will have some adrenal suppression. transabdominal USS to look for free fluid. A more extensive scan to locate a pregnancy can be performed by the Gynaecology team if the 9 Distributive or cardiogenic pattern? patient is stable. Other pointers to an underlying Identify the presence of relative or absolute surgical cause include severe abdominal pain hypovolaemia (see Fig. 30.1). Look for con- / tenderness/guarding/peritonism, air under +ooksfree− com cealed sources of haemorrhage dehydration the diaphragm on CXR or amylase. Look for ↑ (reduced skin turgor, dry mucous membranes) intestinal obstruction on abdominal X ray in and causative/contributory factors, e.g. history of patients with abdominal pain/distension and mebodiarrhoea e.comand vomiting, reducedmebook intake, diuretics, repeated vomiting. Request an urgent surgical antihypertensives. review. See Chapter 4 for further details. Check for ketonuria and metabolic acidosis to exclude diabetic ketoacidosis. If the response to Evidence of infection/inflammation or IV fluids suggests a distributive or cardiogenic 7 predisposition to infection? element, involve ICU, institute appropriate Look for features of sepsis (p. 141). If present, (invasive) monitoring and consider urgent perform a fullee. septic oscreen, (Clinical tool, echocardiography.re com 30e Transient loss of consciousness: syncope and seizures 31o sf e ok fre

Transient loss of consciousness (T-LOC) presents caused by antihypertensive medications or a particular diagnostic challenge. The event has autonomic neuropathy. usually resolved by the time of assessment and • Reflex (neurally mediated) – reflex since critical elements of the history are unknown vasodilatation and/or bradycardia occurs to the patient, witness accounts are crucial. Risk in response to a particular ‘trigger’, e.g. stratification of patients may identify those at ‘vasovagal’ or ‘carotid sinus’ syncope. risk of cardiac or arrhythmia-related syncope requiring admission for further investigation and Seizure those at low risk (often with a diagnosis of reflex Disordered electrical activity affecting the whole or orthostatic syncope) who can be evaluated brain (‘generalized’ seizure) can lead to T-LOC. as outpatients. ooksfree.com oThis s may ee.com be primary or result from a focal (partial) Syncope seizure that spreads to the whole brain (secondary generalization). In the absence of secondary ‘Syncope’ denotes T-LOC resulting from global generalization, partial seizures meboomay cause altered cerebral hypoperfusion, typically associated consciousness (complex partial seizures) without with a BP <60 mmHg for ≥6 seconds. It is T-LOC. Epilepsy is the tendency to have recurrent characterized by rapid onset, short duration seizures. Factors that may provoke seizures in and spontaneous comp ete recovery. patients with epilepsy are shown in Box 31.1. Syncope can be divided into four aetiological subtypes: Hypoglycaemia • Arrhythmia related – due to transient Hypoglycaemia may cause impairment of compromise of cardiac output by a consciousness that resolves with prompt cor- tachy- or bradyarrhythmia, e.g. ventricular rection of capillary blood glucose. Most cases tachycardia,ksfre complete com heart block. are iatrogenic, from treatment of diabetes • Cardiac – due to structural heart with insulin or sulphonylurea drugs. Causes of disease, especially left ventricular outflow ‘spontaneous’ hypoglycaemia include alcohol, obstruction, e.g. severe aortic stenosis, liver failure, insulinoma and adrenal insufficiency. hypertrophic obstructive cardiomyopathy.meb sfree.com mebooksf Acute pulmonary embolism (PE) or aortic Functional disorders (apparent T-LOC) dissection may also cause syncope. ‘Pseudoseizure’ and ‘pseudosyncope’ are • Orthostatic – due to failure of homeostatic terms used to describe episodes that resemble maintenance of BP onom standing, e.g. seizure and syncopeom respectively but do not Transient loss of consciousness: syncope and seizures 271 Differential diagnosis

Box 31.1 Trigger factors for seizures Box 31.2 Atypical features in apparent T-LOC

• Alcohol excess or withdrawal • Prolonged duration (>5 minutes) of episodes • Recreational drug misuse • Eyes closed during episode • Sleep deprivation • Numerous attacks in single day ooks• Physical/mental r exhaustion • Purposeful movements during apparent period of • Intercurrent infection T-LOC • Metabolic disturbance (↓Na+, ↓Mg2+, ↓Ca2+, • Established diagnosis of other functional disorder, uraemia, liver failure) e.g. chronic fatigue syndrome • Non-compliance with medication or drug interactionm fre om meb • Flickering lights have an underlying somatic mechanism, i.e. no rarer causes such as cataplexy, narcolepsy epileptiform activity or cerebral hypoperfusion. and atypical seizures, e.g. absence, as well They can present major diagnostic difficulty and as conditions which may mimic T-LOC, may requ re specialist assessment. Features that including falls, functional disorders, drug/ may raise suspicion of a functional aetiology for alcohol intoxication. Transient ischaemic symp oms over true loss of consciousness are attacks present with focal neurological signs shown in Box 31.2. and symptoms and very rarely cause T LOC. Concussion is a common cause of T-LOC Otherooksfree causes co associated with head trauma. booksf For clinical presentations not suggestive of either tonic-clonic seizure or syncope,me consider sfree.co

31 Transient loss of consciousness: syncope and seizures 272 Transient loss of consciousness: overview

ABCDE fr com No 1 Definite loss of consciousness? Consider dizziness / fall / stroke / transient ischaemic attack

Yes

No 2 Features of shock? Assess as per shock (Ch. 30)

Yes

No 3 Complete recovery of consciousness? Assess as per ↓oGCS (Ch. 7) Yes

Documented CBG <3.0 mmol/L or strong Yes 4 Likely hypoglycaemia clinicals suspicion oof hypoglycaemia?

Full clinical assessment, collateralm history, ECG Yes 5 Any red flag cardiac features (Box 31.3)? Admit and refer to Cardiology

>1 seizure features (Box 31.4) OR 1 Yes 6 Likely seizure See Seizure (p. 276) seizureree feature and no syncope features? e No

>1 syncope features (Box 31.5) and no Yes 7 Likely syncope See Syncope (p. 278) seizure features b

Likely seizure or syncope – make working diagnosis if possible 8 Consider functional causem if atypical features (Box 31.2) Transient loss of consciousness: syncope and seizures 273 Transient loss of consciousness: step-by-step assessment

1 Definite loss of consciousness? administration of carbohydrate/glucagon and was preceded by symptoms of autonomic activation In the absence of a clear witness account this (sweating, trembling, hunger)/neuroglycopenia may be difficult to establish – ask the patient to (poor concentration, confusion, incoordination) recount the events in as much detail as possible. or occurred in a patient taking insulin or a ooksfreAssume T-LOC if: osulphonylurea. sfre com • a witness confirms a period of unresponsiveness Any red flag cardiac features 5 • the patient describes ‘waking up’ or (see Box 31.3)? m ooksf ‘coming to’ on the ground, especially if Always exclude a serious underlying cardiac there is no recollection of falling cause for T-LOC if any of the features in Box • there are facial injuries (most conscious 31.3 is present. Continue through the diagnostic patients can protect their face as they fall). pathway but admit the patient to hospital and T-LOC is unlikely if: discuss with a cardiologist. • there was no loss of postural tone • the patient recalls landing on the ground >1 seizure feature (see Box 31.4) OR 1 6 • a witness account suggests interaction seizure feature and no syncope features? with or awareness of the environment Differentiating between seizure and syncope is throughout the episode. oksfree com a key step in the assessment process. Features that strongly suggest seizure are listed in Box 2 Features of shock? 31.4. Descriptions of ‘jerking , ‘twitching’ or Syncope may be a manifestation of majorm haemo- ‘fitting’ are e.com unhelpful since ‘seizure-like’meboo move s- dynamic compromise, e.g. massive PE, severe ments may occur in up to 90% of syncopal GI bleed. If you find evidence of shock (see Box episodes. In contrast to seizure, the abnormal 30.1, p. 267) during the ABCDE assessment, movements in syncope are usually non-rhythmic evaluate further as per Chapter 30. and brief (<15 seconds).

3 Complete ecovery of consciousness? Box 31 3 Red flag cardiac features The diagnostic pathway below is appropriate only for a transient episode of loss of consciousness. • T-LOC during exertion If there is evidence of persistently ↓GCS during • Severe valvular heart disease, coronary artery the ABCDE assessment, evaluate in the first disease or cardiomyopathy • Family history of unexplained premature sudden instance as described in Chapter 7. ooksfree. om death • Previous ventricular arrhythmia or high risk for Documented CBG <3.0 mmol/L or strong 4 ventricular arrhythmia, e.g. prior MI or ventricular clinical suspicion of hypoglycaemia? surgery me• Sustained ee or non-sustained om ventricularmeboo tachycardia Attributing an episode of reduced consciousness on telemetry to hypoglycaemia requires: • High-risk ECG abnormality: • demonstration of low blood glucose in • bifascicular or trifascicular block (see Fig. 31.3) association with T-LOC • new T wave or ST segment changes (see Box 6.1, • recovery with restoration of p. 51) normoglycaemia. • sinus bradycardia <50 bpm or sinus pause >3 seconds Corroborate a low CBG with a formal lab • second-degree AV block or complete heart block glucose measurement whenever feasible (see Figs 31.1 and 31.2) but do not wait for the result to initiate treatment. • evidence of pre-excitation (see Fig. 26.2, p. 233) 31 Patients may have had corrective treatment prior • marked QT interval prolongation, e.g. QTc >500 milliseconds to assessment without a CBG, e.g. from ambu- ooksfree com • Brugada pattern: RBBB with ST elevation in leads lance crew. In these circumstances, suspect V1–V3 (see Fig. 31.5) b ok hypoglycaemia if the episode resolved with mebo ee om Transient loss of consciousness: syncope and seizures 274 Transient loss of consciousness: step-by-step assessment

The episode of T-LOC is highly likely to have features may be helpful: amnesia for events been a seizure if >1 of the features in Box 31.4 before and after the episode, and headache are present. Seizure is also likely if any of these or aching muscles after the episode suggest features are present, and there are no specific a seizure diagnosis; previous episodes of pointers to syncope (Box 31.5). In both cases, pre-syncope, witnessed pallor during T-LOC, proceedooksfre to ‘Seizure’ (p. om 276). known cardiovascular disease and an abnormal ECG favour syncope. Urinary incontinence is ≥1 syncope features (see Box 31.5) and not a useful discriminating feature. Consider a 7 no seizure features m ofunctional sfr aetiology co if atypical featuresm booksf are present Suspect syncope if any of the features in Box (see Box 31.2). Have a low threshold for specialist 31.5 and none of those in Box 31.4 are present input if the cause remains unclear. – proceed to ‘Syncope’ (p. 278).

Likely seizure or syncope – make working 8 diagnosis if possible. Consider functional cause if atypical features (see Box 31.2) Where differentiation between seizure and syncopeoksfree. is not straightforward, om other clinical o m Transient loss of consciousness: syncope and seizures 275 Transient loss of consciousness: step by-step assessment

Box 31.4 Clinical features strongly suggestive Box 31.5 Clinical features strongly suggestive of seizure of syncope

• T LOC preceded by typical aura, e.g. unusual smell, • T-LOC preceded by chest pain, palpitation, ‘rising’os sensation r in abdomen, o déjà vu dyspnoea, light-headedness or typical ‘pre-syncopal’ • A witness account of abnormal tonic-clonic limb prodrome, e.g. lightheadedness, warmth, nausea, movements that are: vomiting • coarse and rhythmic • T-LOC after standing up, after prolonged standing, • maintained for >30 seconds (ask witness to during exertion or following a typical precipitant: demonstrate movements) m• fre unpleasant com sight, sound, smellm or pain boo • A witness account of head-turning to one side, • venepuncture unusual posturing, cyanosis or automatisms such as • micturition chewing or lip-smacking during the episode • cough • Severely bitten, bleeding tongue or bitten lateral • large meal border of tongue • Brief duration of T-LOC (<1 minute) • A prolonged period (>5 minutes) of confusion or • Rapid return of clear-headedness after T-LOC drowsiness after the episode e.c ee.com

31 Transient loss of consciousness: syncope and seizures 276 Seizure: overview

Full clinical assessment, U+E, Mg2+, Ca2+, LFTs, FBC

f e com Urgent laboratory Yes Likely hypoglycaemic 1 CBG <3.0 mmol/L? glucose and seizure correction No

>10 min continuous seizure / recurrent Yes 2 If ongoing, treat as status epilepticus seizures without full recovery in between?m k f m oo s

Yes

Urgent High suspicion of underlying Yes 3 neuroimaging CNS pathology intracranial pathology? ± LPe. No

Yes 4 oEstablished r e.c diagnosis of epilepsy? Assess triggers and treatment No

Yes Correct / treat 5 Clear precipitating factor? Likely provoked seizure underlying cause Further seizure activity No

Probable new diagnosis of epilepsy. Provide appropriate safety advice 6 Refer to first-fit clinic if rapidly available and no further seizures.co Seek inpute.co from Neurology if any concerns

1 CBG <3.0 mmol/L? requires >30 minutes of continuous seizure activity or repeated seizures withoutme full recovery in Consider hypoglycaemia at the outset because it: between, but a lower time threshold facilitates • is easily identified and corrected early recognition and action. • will cause permanent neurological damage Provide appropriate anticonvulsant therapy, if not corrected e.g. IV diazepam, and supportive measures • needs to be excluded prior to assessment concurrently with clinical assessment. Rapidly for other causes. exclude or correct reversible factors (see below) If CBG <3.0 mmol/L, assess and treat as and seek urgent input from ICU ± the Neurology described above.free c m team. 10 min continuous seizure/recurrent High suspicion of underlying > 3 2 seizures without full recovery in between? intracranial pathology? Status epilepticus is a medical emergency Seizure may be a manifestation of important requiring urgent intervention. Formal diagnosis underlying intracranial pathology, such as meb free.com meb Transient loss of consciousness: syncope and seizures 277 Seizure: step-by-step assessment

5 Clear precipitating factor? Box 31.6 Indications for urgent neuroimaging in seizure Important causes of seizure in adults without epilepsy include: alcohol (excess or withdrawal), • Status epilepticus • Focaloksfr or partial onset seizure recreational drug misuse, e.g. cocaine, ampheta- • Confusion, ↓GCS or focal neurological signs >30 mines, drug overdose, e.g. theophylline, tricyclic minutes post-fit antidepressants, severe metabolic disturbance • Recent head injury ↓Na+, ↓Mg2+, ↓Ca2+ and CNS infection. Look for all • Acute severe headache preceding seizure of these factors and refer for specialist neurological • Known malignancy with potential for brainm sf e com mebooks evaluation (see below) if none is evident. metastases • Immunosuppression (especially HIV) Probable new diagnosis of epilepsy. Refer • Meningism, fever or persistent headache and 6 suspicion of CNS infection to a neurologist as inpatient or outpatient • Anticoagulated or bleeding disorder Admit any patient with repeated seizures or a significant causative factor that requires inpatient treatment. Consider early discharge haemorrhage, infarction, infection or space- only if patients have fully recovered, exhibit no occupying lesion. neurological abnormalities and have a respon- Arrange urgent neuroimaging, usually CT, if sible adult to accompany and stay with them. the patient is at risk of these pathologies (Box Seek advice from a neurologist if you have any 31.6ooksfr). Consider neuroimaging com to exclude new concerns. intracranial pathology in any patient with known Arrange neuroimaging for all first-fit episodes epilepsy with a change in seizure type/pattern in patients >20 years or with focal features. without an apparent precipitating factor.meboo sfree. om mebooksf Depending on local resources, imaging may Provided there are no contraindications, be performed as an outpatient – provided perform a lumbar puncture (p. 170), following there are no indications for urgent imaging CT, if any features suggest CNS infection, e.g. (see Box 31.6) and a ‘first-fit’ follow-up service fever, meningism, rash. is available. Further investigation may not be required in patients with a pre-existing diagnosis 4 Established diagnosis of epilepsy? of epilepsy who have fully recovered following In patients with known epilepsy, address all a typical, uncomplicated fit. factors that may have lowered seizure threshold Prior to discharge, inform all patients of (see Box 31.1) or triggered the event. Measure- statutory driving regulations (in the UK see ment of anticonvulsant drug levels is not routinely www.dft.gov.uk/dvla/medical/ataglance.aspx) booksfreeindicated but considerom it if there has been a and advise them to avoid activities where T-LOC recent change in medication or you suspectebo may sfree be dangerous, com e.g. swimming,ebooks operating non-compliance. machinery, cycling, etc.

31 Transient loss of consciousness: syncope and seizures 278 Syncope: overview

1 Risk-stratify to determine need for inpatient investigat on f e com Yes Arrhythmia-related syncope OR 2 Diagnostic ECG recording? oCardiac fr ischaemia-related syncope No

Clinical suspicion of PE, aortic Yes Urgent 3 Confirm diagnosis dissection or occult bleeding? imaging

Clinical or ECG features that suggest Yes 4 Echo- Cardiac syncope structural heart disease? cardiogram

Nof ee.

Clinical or ECG features that suggest Yes Document 5 o ee Arrhythmia-related syncope arrhythmia-related syncope? rhythm o

Syncope after standing up with Yes 6 Orthostatic syncope documented postural hypotension?

Yes Consider carotid 7 Typical p ecipitant or prodrome? Likely reflex syncope sinus massage f e m if >40 years No

Diagnosis uncertain (40% of cases): If single episode, low risk, no further investigations required If atypical features (Box 31.4), consider pseudosyncope If recurrent syncope, consider tiltmeb test, Holter monitor, implantable e loop mrecorder or mrefer Cardiology Transient loss of consciousness: syncope and seizures 279 Syncope: step-by-step assessment

Risk-stratify to determine need for syncope. Acute coronary syndrome (ACS) is 1 inpatient investigation unlikely in the absence of chest pain or ECG evidence of ACS. Admit all syncopal patients with red flag cardiac Discuss urgently with a cardiologist if any of features (see Box 31.3) and discuss promptly the above features is present. withook the Cardiology fre team. Clinical decision rules and risk prediction tools, e.g. the San Francisco Clinical suspicion of PE, aortic dissection Syncope Rule may be useful, but lack sensitivity 3 or occult bleeding? e o f and specificity. Consider discharge mebowith outpa- sfre com tient investigation (preferably in a syncope clinic These conditions may present with syncope, but if available) if the patient has recovered fully and this is rarely the predominant symptom. Exclude has no other medical problems or no red flag PE and aortic dissection if syncope occurs in features; otherwise, admit for a period of observa- the context of sudden-onset chest pain with tion and investigation (monitoring +/– ambulatory no obvious alternative explanation. Also con- monitoring and ECG). Syncope observation units, sider PE in syncopal patients with dyspnoea, if available, facilitate rapid investigation while the hypoxia, evidence of DVT or major thrombo- patient is under observation for 6 to 24 hours. embolic risk factors. Suspect aortic dissection if there is a new early diastolic murmur pulse 2 Diagnostic ECG recording? deficit or widened mediastinum on CXR (see Ch. 6). Consider subarachnoid haemorrhage Mobitz type II 2nd degree atrioventricular (AV) o k free.com if there is associated headache (see Ch. 18) block (Fig. 31.1), complete heart block (Fig. 31.2), and ruptured ectopic pregnancy or abdominal prolonged pauses, ventricular tachycardia or very aortic aneurysm if there is abdominal pain (see rapid supraventricular tachycardia (>180/min) on meboCh. sfree.com 4). mebooksf the presenting ECG or telemetry establish an arrhythmic cause of syncope. Arrhythmia-related Clinical or ECG features that suggest syncope is also highly likely with persistent sinus 4 structural heart disease? bradycardia <40 bpm, alternating left and right bundle branch block (LBBB and RBBB) or ECG may identify ‘structural’ causes of cardiac pacemaker malfunction with pauses. syncope e.g. severe aortic stenosis, hypertrophic ECG evidence of acute ischaemia suggests cardiomyopathy, prolapsing atrial myxoma or an arrhythmia secondary to ischaemia, e.g. ven- conditions that predispose to arrhythmia, e g. tricular tachycardia,sfree.com or cardiac ischaemia-related severesfree left ventricular c m (LV) systolic impairment. ksf

PP PPPPPPPPP Fig. 31.1 Mobitz type II atrioventricular block. (From Boon NA, Colledge NR, Walkerm BR. Davidson’s Principles & Practice of Medicine, 20th ednom Edinburgh: Churchill Livingstone, 2006.)

** 31

Fig. 31.2 Complete heart block. Arrows indicate P waves. (From Douglas G, Nicol F, Robertson C. Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009.) e me Transient loss of consciousness: syncope and seizures 280 Syncope: step-by-step assessment

Request an ECG if there is exertional syncope, • evidence of pre-excitation (see Fig. 26.2, a family history of sudden unexplained death p. 233) (especially <40 years), a new murmur, clinical • prolonged QT interval (QTc >440 features of cardiac failure, or (unless performed milliseconds in men or >460 recently) a history of myocardial infarction (MI), milliseconds in women) cardiomyopathy,ooksfre valvular com heart disease or con- • Brugada pattern: RBBB with ST genital heart disease. Discuss with a cardiologist elevation in leads V1–V3 (Fig 31.5) if any relevant abnormalities are detected. • features of arrhythmogenic right meboventricular e cardiomyopathy:meb negative T Clinical or ECG features that suggest waves in leads V –V and epsilon waves 5 1 3 arrhythmia-related syncope? • pathological Q wave. Suspect an arrhythmic aetiology for syncope in • any ECG abnormality or history of the following circumstances: cardiovascular disorder in the absence of a • sudden-onset palpitation rapidly followed typical prodrome or precipitant for reflex or by syncope orthostatic syncope. • syncope during exertion or while supine The correlation of a syncopal episode with • previous MI or significant structural heart a sfree.comdocumented rhythm disturbance is the gold disease, e.g. cardiomyopathy, aortic standard for diagnosis of arrhythmia-mediated stenosisoksfree.com syncope. This is frequently challenging, particu- • any of the following ECG abnormalities: larly when syncopal episodes are infrequent. The • LBBB (see Fig. 6.5, p. 55), bi- or choice of investigation and degree of persistence trifascicular block (Fig. 31.3) depend on the risk of life-threatening arrhythmia • sinus bradycardia <50 bpm and frequency of syncope. mebooksf • Mobitz type I 2nd degree AV block Admit patients with red flag cardiac features (Fig. 31.4) (see Box 31.3) immediately for continuous inpa- • sinus pause >3 seconds tient ECG monitoring. Arrange Holter (1 to 7 day o . om I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 31.3 Trifascicular block.co (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.)

P PPPPP PPPPP P P

Fig. 31.4 Mobitz type I atrioventricular block (From Boon NA, Colledge NR, Walker BR. Davidson’s Principles & Practice of Medicine, 20th edn. Edinburgh: Churchill Livingstone, 2006.) e me co Transient loss of consciousness: syncope and seizures 281 Syncope: stepcom by-step assessment

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 31.5 Brugada syndrome. (From Hampton JR. The ECG in Practice, 5th edn. Edinburgh: Churchill Livingstone, 2008.) tape) or ambulatory patch monitoring (14 days) autonomic neuropathy and drugs, e.g. antihy- if symptoms occur relatively frequently. Consider pertensives, vasodilators (especially sublingual an event recorder (external or implanted) if there nitroglycerine) and diuretics, particularly in the sooksf a high suspicion of c arrhythmia but episodes elderly. are infrequent or prove difficult to captureboo by sf c other methods. 7 Typical precipitant or prodrome?m oks Syncope after standing up with A clear precipitating trigger, e.g. intense emotion, 6 documented postural hypotension? venepuncture or prolonged standing (vasovagal syncope) or coughing, sneezing or micturition Diagnose orthostatic syncope if there is: (situational syncope), together with typical prodro- • a history of light-headedness shortly after mal symptoms, strongly suggests reflex syncope, standing, followed by brief T-LOC especially in patients with no ECG or clinical • a documented postural BP drop (of evidence to suggest structural heart disease or ≥20 mmHg in systolic BP or ≥10 mmHg arrhythmia. Consider tilt-table testing in cases of in diastolic BP within 3 minutes of moving diagnostic doubt. Carotid sinus hypersensitiv- from lying to standing). ity is a form of reflex syncope and is usually ooksfreeIn other circumstances, com it may be difficult to diagnosed with carotid sinus massage (CSM). distinguish orthostatic from reflex syncope, e.g. CSM should be avoided in patients with a history when symptoms occur with prolonged standing. of cerebrovascular accident/transient ischaemic Look for an underlying cause of posturalmebo hypo- attack sfree or a carotid com bruit, and requiresmebooksf continuous tension. In severe form it may reflect fluid loss, ECG monitoring; it is diagnostic if syncope is e.g. major haemorrhage or severe dehydration. reproduced in the presence of asystole lasting Other causes include Parkinson’sm syndromes, >3 seconds.

31 Urinary incontinence ks 32o sfre

Urinary incontinence (UI), the involuntary leakage disease, e.g. multiple sclerosis, spina bifida but of urine, affects 15% of women and 10% of men is more often due to intrinsic bladder activity aged >65 years. Treatment or amelioration of UI (‘detrusor overactivity’). Lower UTI may produce can greatly enhance quality of life but it tends acute transient urge incontinence. to be under-reported and under-recognized in clinical practice. UI is frequently multifactorial, Mixed incontinence particular y in frail elderly patients, so seek to A combination of stress and urge incontinence; identify all potentially modifiable contributing treatment should be aimed at the more dominant factors. Take care also to evaluate the impact aspect. of symptoms on daily activities and quality of life. Overflow incontinence Stressooksfree. incontinence om The involuntary passage of urine from an overfull Urine leakage is provoked by an increase in bladder which may or may not be accompanied intra-abdominal pressure, such as during m oby sfr a sensation e com of urgency. Incompleteme bladder ksf coughing, sneezing, effort or exertion. It is emptying may result from: usually due to insufficient urethral support from the pelvic floor muscles but can also be caused • bladder outflow obstruction: benign by intrinsic weakness of the urethral sphincter, prostatic hyperplasia (BPH), prostate e.g. post-pelvic surgery. Stress incontinence cancer, bladder tumour, urethral stenosis, is far more common in females than males severe constipation and most often relates to obstetric trauma. It • bladder atonia in neurological disease, frequently accompanies pelvic organ prolapse e.g. cauda equina or conus medullaris and may also occur with atrophic vaginitis. Stress compression, autonomic neuropathy incontinence in males is usually a complication • drugs with anticholinergic effects such as of prostatectomy. antipsychotics or antidepressants. ooksfree com Treatment of overflow incontinence is with Urge incontinence relief of obstruction (e.g. resection of prostate Urine leakage occurs due to intense bladder cancer, medical treatment of BPH) or intermittent contraction and is preceded by them sensation catheterization. ree.com meb ok of urgency. This can result from neurological Urinary incontinence 283 Differential diagnosis

Box 32.1 Aggravating factors Box 32.2 Medications potentially aggravating incontinence • Polydipsia/polyuria including: poorly controlled sfre o diabetes mellitus, diabetes insipidus, • Diuretics hypercalcaemia,oks r psychogenic polydipsia • Drugs with cholinergic effects1 • Caffeine • Drugs with anticholinergic effects2 • Alcohol overuse/misuse • Alpha-agonists • Mobility problems (see Ch. 24) • Calcium channel blockers • Visual impairment • Beta-agonists • Obesity • Sedatives • Respiratory disease • Lithium • Smoking • Cognitive impairment, e.g. delirium or dementia 1May cause or aggravate urge incontinence. 2 (see Ch. 8) May cause or aggravate overflow incontinence.

Continuous incontinence Functional/multifactorial incontinence Constant leakage of urine throughout the day This occurs when the person is aware of the (and night) suggests the presence of a fistula need to urinate, but for one or more physical betweenook the fr bladder and mthe urethra or vagina. or cognitive reasons are unable to get to the Underlying causes include urogynaecological toilet in time. Potential contributing factors are cancer, previous pelvic surgery/radiotherapy shown in Box 32.1 and aggravating medications or obstetric trauma. meboin sfBox 32.2. om mebooks

32 Urinary incontinence 284 Overview

Full clinical assessment, urinalysis +/- post-void residual / perineal examination f e m fre Yes Cauda equina / 1 Suspect spinal pathology? Urgent MRI spine conus medulla is + /- neurosurgical review syndrome oo No

Confirm with Symptoms of UTI + positive Yes + 2 Likely UTI MC S and urinalysis? reassess UI after treatment No

Yes Evaluate for 3 ↑Post-void residual urine volume? Overflow incontinence e. e. underlying cause No

Yes Reassess after 4 Acute illness? Possible transient UI treatment of underlying illness No ook

Yes 5 Continuous urine leak? Exclude fistula

Evidence of atrophic vaginitis / Yes Atrophic vaginitis 6 Treat and reassess urethritis? / urethritis Noe co Yes Detrusor overactivity / 7 Prominent urge symptoms? neurogenic UI

Yes 8 UI on coughing / sneezing / effort? Stress incontinence m s c No

Likely functional / multifactorial UI 9 Refer Urology if suspicion of urinary tract disease, e.g. younger patientso / associated GU symptoms / previous pelvicco surgery or radiotherapy Urinary incontinence 285 Step-by-step assessment

1 Suspect spinal pathology? an underlying cause, particularly in frail elderly patients, with rectal exam +/− abdominal X-ray Arrange urgent spinal MRI to exclude cauda Seek a neurological opinion if there is a history of equina/conus medullaris syndrome in any patient neurological disorder or associated symptoms/ with recent onset of UI associated with lower limb signs of neurological disease, e.g. lower limb weakness,ooksfre altered perianal/perineal sensation weakness. Otherwise, consider CT abdomen/ (does toilet paper feel normal when wiping?), pelvis and refer to Urology for further assessment faecal incontinence or new low back or leg pain. and investigation, e.g. cystoscopy. Seek immediate neurosurgical/neurologymeboo input sfre co mebooksf if concerning imaging features or unexplained 4 Acute illness? neurological findings. Suspect transient UI as a non-specific manifestation of illness in elderly patients with frailty or multi- 2 Symptoms of UTI and positive urinalysis? morbidity who are acutely unwell, have experienced Suspect UTI if there is a short history of UI an abrupt decline in function, mobility or cognition accompanied by fever, dysuria, frequency or or who have evidence of newly-deranged physiol- malodourous urine; the absence of leucocytes ogy. Seek and treat the underlying illness then and nitrites on dipstick makes UTI very unlikely. re-evaluate continence once the patient has If dipstick testing is positive or there is strong returned to baseline status. clinical suspicion, send an MSU for culture; treat confirmedooksfree. infection then o re-evaluate to ensure 5 Continuous urine leak? that UI resolves. Evaluate for prostatic disease Suspect a fistula between the bladder (or ureter) (see Step 3) in men with >1 UTI andmeb arrange oand sfree.com the vagina/urethra if UI isme continuous rather sf renal tract imaging (USS initially) in women with than intermittent – especially if there is a history of >2 UTI; in both cases consider referral to Urology previous pelvic surgery/radiotherapy or a complex for further specialist investigation. obstetric history. Request an IV urogram and refer to Urology for specialist assessment. 3 ↑Post-void residual (PVR) urine volume? 6 Evidence of atrophic vaginitis/urethritis? Measure PVR in all patients with unexplained UI using a bladder USS scan (correlates well Suspect this as a cause of UI (usually stress-type) with urinary catheter volumes). Suspect overflow in postmenopausal women with symptoms of incont nence due to incomplete bladder emptying urethral irritation (e.g. burning, frequency, painful if the PVR is >100 mL (or >50 mL in younger intercourse) but negative urine dipst ck and patients).ooksfree In men, ask c about m other symptoms culture or with mucosal pallor or erythema on of bladder outlet obstruction, e.g. hesitancy, perineal examination. Reassess symptoms after poor stream, check a PSA (prior to rectal exam) treatment with topical oestrogen for at least 14 and evaluate the prostate by rectalmeboo examina- days. sfree. Continue to om seek other causesmebooksf of UI unless tion. Exclude constipation/faecal impaction as symptoms fully resolve.

32 Urinary incontinence 286 Step-by-step assessment

8 UI on coughing/sneezing/effort? Box 32.3 IQ questionnaire Evaluate as stress incontinence if urine leakage 1. During the past 3 months, have you leaked urine (even a small amount)? consistently coincides with manoeuvres that oksfr• Yes – move to question com 2 increase intra-abdominal pressure, e.g coughing, • No – stop questionnaire. sneezing, laughing, sitting/standing-up – espe- 2. During the past 3 months did you leak urine: cially if there is no associated sensation of • when performing physical activity (coughing, urgency. Where the history is unclear, inspect for sneezing, lifting, exercising)? leakage of urine while asking the patient to cough • when felt urge to empty your bladder,me but not sf e mebooks or, again, consider using the 3 IQ questionnaire able to get to the toilet in time? • neither of the above circumstances. (see Box 32.3) or a voiding diary. 3. During the past 3 months did you leak urine Refer to Gynaecology if there is uterine/ MOST often: vaginal prolapse. Consider potentially aggravating • when performing physical activity (coughing, factors such chronic lung disease (cough) or sneezing, lifting, exercising)? Stress medications (see Box 32.2). In women with incontinence predominant uncomplicated stress UI, reassess after simple • when felt urge to empty your bladder, but not able to get to the toilet in time? Urge measures such as pelvic muscle retraining but incontinence predominant considersfree surgical com evaluation if symptoms remain ksfreeneither of the above c circumstances. m Other severe. Refer male patients with stress UI for cause (neither urge incontinence or stress Urology assessment. incontinence) • both of the above circumstances equally as Likely functional/multifactorial UI. often. Mixed urinary incontinence. 9 Specialist urological assessment in selected cases me oksf In frail or elderly patients UI is very often due to a constellation of factors that prevent timely toileting (funct onal incontinence) rather than a single specific urinary tract pathology. Consider specialist urological assessment/investigation 7 Prominent urge symptoms? if there are associated genitourinary (GU) Evaluate as urge incontinence if the patient symptoms such as haematuria or pelvic pain a reports a clear and consistent history of urgency complex obstetric history, previous pelvic surgery to void prior to leakage of urine. Consider using or radiotherapy, or where functional incontinence the 3 IQ questionnaire (Box 32.3) or a voiding seems unlikely, e.g. younger patients or those diaryooksf if the history e is unclear or the pattern of without significant comorbidity. UI is variable. Otherwise, systematically address all factors Ensure you have excluded urinary retention: that may be contributing to UI (see Box 32.1). repeat post-void bladder scan if initialm results bo Review sfree.com medications (see Boxme 32.2) and ooksf amend equivocal and perform post-void catheterization where necessary. Establish whether the patient if there is a strong clinical suspicion. Consider a has awareness of the need to void. If not, try neurogenic aetiology and obtain specialist input prompted toileting (particularly after diuretics). If in patients with a history of neurological disorder the patient has awareness of the need to void (e.g. multiple sclerosis, spina bifida) or associated but can’t reach the toilet in time, assess mobility neurological signs or symptoms. (see Ch. 24) and consider the need for walking In the absence of urinary retention or neurologi- aids, a downstairs toilet or commode. Evaluate cal features, assume detrusor overactivity as the the effectiveness of continence aids such as likely diagnosis. Refer for specialist urological pads, urisheath or commode. Finally, determine assessment, e.g. urodynamic studies if the the level of distress caused by symptoms and diagnosisooksfree.com is uncertain or symptoms fail to the overall impact on quality of life Consider respond to standard treatments. boreferral sf ee.comfor comprehensive geriatric assessment. ebooksf This page intentionally lefto blank Vaginal bleedings 33o sf e

Vaginal bleeding is a distressing symptom with a placenta praevia (a low-lying placenta with sub- wide variety of potential causes. These may be sequent bleeding from the placental edge) and categorized broadly according to the reproduc- placental abruption (bleeding due to placental tive age of the patient, their pregnancy status, separation f om the uterus; 1% pregnancies). the duration of symptoms and any associated Placenta praevia is diagnosed on USS and features. Examine the patient carefully to identify causes painless bleeding. Placental abruption rectal, urethral, vaginal and cervical sources of is essentially a clinical diagnosis based on blood; if necessary, place a urinary catheter abdominal pain and vaginal bleeding, since the to differentiate between vaginal bleeding and absence of a retro-placental haematoma on USS haematuria. Be sensitive and empathetic, but does not exclude the diagnosis. Be aware that ensureooksfree.com that the assessment is thorough. Arrange placental abruption may be ‘concealed’ – with urgent gynaecological/obstetric review in any no/minimal visible PV bleeding. In this situation, patient with major PV bleeding. eboblood sfree.com loss may still be significant but remains contained within the uterine cavity.mebooksf The patient Pregnancy-related bleeding will have haemodynamic instability out of keeping First trimester with the apparently absent/small volume PV bleeding together with a ‘woody hard’ uterus Vaginal bleeding in the first trimester is very due to blood accumulation. The treatment for common. Bleeding may be due to miscarriage placental abruption is delivery of the baby and or ectopic pregnancy, or may have a benign placenta explanation in the presence of an ongoing intrauterine pregnancy. Miscarriages may be Heavy menstrual bleeding threatened (the foetus is still viable), partial Heavy menstrual bleeding (HMB; previously (non viable products of conception remain in known as menorrhagia) may be defined objec- the uterus) or complete (products of conception tively or subjectively. The objective definition haveooksfr been passed). e.co In miscarriage, patients may is blood loss greater than 80 mL in a cycle, describe a loss of pregnancy-related symptoms. but in practice diagnosis is based on women Miscarriages and ectopic pregnancies are often subjectively reporting using more tampons/pads associated with abdominal pain. Miscarriagesmebo than sfr usual, using com pads and tamponsmebooks together or typically present with central, crampy, menstrual- soaking through protection onto clothing. like lower abdominal pain In ectopic pregnancy, Pathological causes of HMB may be structural the pain is unilateral and constant since there or non-structural. Structural causes include may be bleeding into the peritoneal cavity causing fibroids (leiomyomas) (20–30%), endometrial peritoneal irritation. Unilateral lower abdominal and cervical polyps (5–10%), adenomyosis (5%) pain in females of reproductive age (regardless and malignancy or hyperplasia. Non-structural of PV bleeding) should be assumed to be an causes include coagulopathy (e.g. von Willebrand ectopic pregnancy until ruled out. disease, anticoagulants), ovulatory dysfunction endometrial disorders (e.g. endometritis), iatro- Second and third trimester genic causes (e.g. contraceptives, tamoxifen). Bleedingoo sfreeduring the second com and third trimesters After investigation, approximately 40 60% of is abnormal and must be investigated Serious patients with HMB have no identifiable uterine, and potentially life-threatening causes include endocrine, haematological or infective pathology. mebo ksfree.com mebooksf Vaginal bleeding 289 Differential diagnosis

Intermenstrual bleeding contraception may cause abnormal menstrual bleeding. Intermenstrual bleeding is usually low volume. Uncommonly, low-volume mid-cycle bleeding The pattern of bleeding may be related to may be due to ovulation (when the Graafian contact such as postcoitus, or intermenstrual follicle ruptures and hormonal balance becomes bleedingooks with re no clear precipitants. Causes of predominantly progesterone-based, resulting in contact bleeding are typically cervical, such a shed of blood from the endometrium). This is as cervical ectropion, cervical cancer, cervical associated with acute, unilateral, lower abdominal polyps or infections (typically chlamydiam bobut pain fre(mittelschmerz, om ‘middle pain’)mebooks lasting hours also gonorrhoea). Non-contact, intermenstrual to days, which is often the presenting problem. bleeding has a wide range of causes. There is a continuum between intermenstrual and Postmenopausal bleeding irregular menstrual bleeding that can be difficult Postmenopausal bleeding (PMB) is defined to differentiate. However, in many instances, the as vaginal bleeding >12 months after the last treatment is similar. Causes include endometrial menstrual cycle. Up to 10% of women with PMB lesions (cancer polyps), fibroids (although more have endometrial cancer. Other malignant causes commonly cause HMB), contraceptives, sexually include cervical, vaginal, vulval and, rarely, ovarian transmitted infections and, rarely, medical causes cancer. Atrophic vaginitis with contact bleeding such as coagulopathies and hypothyroidism. due to postmenopausal dryness, pessary devices Oralooksfree contraception comand intrauterine deviceo or sfree intercourse c is a mdiagnosis of exclusion.ooksf

33 Vaginal bleeding 290 Overview

Full clinical assessment + vaginal examination (see C inical tool) f e m fre Yes 1 Evidence of shock? Resuscitate

Ectopic pregnancy / USS (viability/ Yes placenta location) 2 Pregnant? miscarriage / placental abruption / then PV exam+ placenta praevia speculum No

Yes 3 Postmenopausal? Endometrial cancer / atrophic vaginitise / polyps No

Yes Seek underlying 4 Bleeding confined to menstruation? Heavy menstrual bleeding o r e. cause o No

Yes 5 Contact/postcoital bleed? Likely cervical cause

Consider endometrial pathology (fibroids / cancer), STI (chlamydia / gonorrhoea), trauma, cervical 6 disease, oral contraception / IUD, follicle rupture (mittelschmerz),.c bleeding tendency (e.g. coagulopathy)e co Vaginal bleeding 291 Step-by-step assessment

Clinical tool Examination of the female genitalia Vaginal examination is not routine but is often indicated The vaginal examination of females with an intact hymen if inflammatory or neoplastic disease of the genitourinary should be avoided, particularly as the information requ red organsok is suspected fre (Fig. 33.1). Its intimate nature raises can often be obtained by digital examination of the ectum. medicolegal considerations necessitating both informed Vaginal examination of minors requires the consent of a consent and the presence of a chaperone throughout the parent or guardian. book examination. ebo com

2 Pregnant? Test for pregnancy by urine dipstick and/or serum β-HCG, which is quantitative and more sensitivesfr in e very c early pregnancy, in all women of reproductive age with vaginal bleeding. Perform urgent USS in all first trimester patients (including newly diagnosed) as part of the initial assessment to determine foetal viabil ty and location (intrauterine or ectopic) as well as the location of the placenta. For women inmebooksf the second and third trimester, exclude placenta praevia by USS prior to bimanual examination or speculum to avoid disruption of the placenta–cervical junction and catastrophic bleeding. When performing bimanual and speculum examination, assess the volume of passed blood, check for adnexal tenderness (ectopic pregnancy) and identify products of conception at the cervix that require removal.

Fig 33.1 Vaginal examination. (From Ford MJ, 3 Postmenopausal? Hennesseyo I, Japp A. Introduction to Clinical Examination, 8th edn. Edinburgh: Churchill Livingstone, 2005.) bLook sfree.com for associated features of gynaecological cancer such as pelvic pain, pelvic mass, obstructive GI or urinary tractme symptoms or sf weight loss, but exclude malignancy in all patients 1 Evidence of shock? with PMB. Use Boxes 15.1 and 15.2 (p. 153 [GI haemor- Identify sources of lower reproductive tract rhage]) as a framework for assessing resuscitation (endocervix vagina, vulva) bleeding through requirements in acute severe vaginal bleeding. careful examination and biopsy any visible Remember that young patients, especially lesions. Arrange transvaginal USS to image the pregnant women, may maintain relatively normal ovaries and endometrium and proceed to endo- physiological parameters until shock is profound. metrial biopsy if the endometrium is thickened Assume major blood loss if there are features (e.g. >3 mm). Even if the USS appears no mal, of intraperitoneal bleeding, e.g. peritonism consider hysteroscopy and biopsy to exclude shoulder-tipo ksfree.co pain or cervical excitation. Arrange endometrial cancer if bleeding persists Arrange immediate gynaecological/obstetric review in any cervical smear cytology to rule out cervical 33 patient with major vaginal bleeding ebo ksfreecancer, especially co if endometrial pathology is mebooksf Vaginal bleeding 292 Step-by-step assessment excluded. Biopsy all visible cervical lesions even Remember that 40–60% of patients with if the cytological smear is apparently normal. HMB have no identifiable uterine, endocrine Do not rely on gynaecological tumour markers haematological or infective pathology. such as CA125 to rule in or rule out underlying Establish the degree of distress caused by malignancy in patients with PMB. bleeding and the impact on quality of life as this ooksfreConsider other common com causes of PMB such may influence treatment options. Non-hormonal as atrophic vaginitis and polyps only once treatment comprises tranexamic acid (antifibrino- malignancy is excluded. Take vaginal/cervical lytic) or NSAIDs such as mefenamic acid (inhibit swabs if the history raises suspicion mebof sexually prostaglandin sfre response) duringmebook menstruation. f transmitted infection. Hormonal treatment is progesterone (oral/IUD) or combined contraception. Surgical options include 4 Bleeding confined to menstruation? endometrial ablation, myomectomy (removal of fibroids), or, if all other avenues are unsuccessful Most patients are unable to quantify menstrual and the patient wishes for no more children, blood loss accurately so ask about the func- hysterectomy. tional effect of menstruation to identify HMB: is the patient using more sanitary products 5 Contact/postcoital bleed? (tampons, pads, etc.) than normal, do they Examine carefully for vaginal and cervical pathol- require double protection (tampons and pads ogy (see clinical toolkit – vaginal examination) together), are they experiencing flooding (soiling and take high vaginal/endocervical swabs in any ofooksfree clothes through the cosanitary products) or clots? patient who reports postcoital or other contact Check FBC to exclude iron deficiency anaemia. bleeding. Arrange cervical smear cytology unless Enquire carefully about associated postcoital or recently performed and biopsy any visible cervical intermenstrual bleeding – if present meboassess as e com mebook lesion even if the cytological smear is apparently per step 5. normal. Ask specifically about contraceptive use – IUDs are associated with HMB; conversely recent Consider other causes of discontinuation of an oral contraceptive may 6 intermenstrual bleeding lead to increased menstrual blood loss. Check thyroid function tests if there are Establish the pattern and nature of symptoms clinical features of hypothyroidism (p. 133, Ch. – this may range from low-volume ‘spotting’ 13) and prolactin levels if there is a history of between defined periods to apparently totally galactorrhoea. irregular and excessively frequent periods of Screen for coagulopathy if the patient has had variable duration. Intermenstrual bleeding unrelated HMBooksfree. since the onset of om periods; has a family to intercourse/contact is more likely to have an history of bleeding disorder; or reports spontane- endometrial or systemic cause. Enquire about ous bruising, troublesome epistaxis or unexplained contraception use and, in particular, any recent GI bleeding. Enquire about anticoagulantmebo use but changes: sfre the cocombined oralmebooksf contraceptive pill only attribute HMB to anticoagulation once other typically causes breakthrough bleeding (small causes have been excluded volume spotting between the monthly bleed when Take high vaginal and endocervical swabs omitting the tablets for 7 days). Progesterone- if there is any suspicion of infection. Consider based contraceptives (depot preparations such as gynaecological referral for further investigation Nexplanon, hormonal coil such as Mirena) typically including USS (pelvic +/– transvaginal) and/or result in an irregular pattern of bleeding. Consider hysteroscopy, especially if there is persistent/ screening for coagulopathy if there are sugges- troublesome bleeding, associated pelvic pain or tive features (see step 4). Refer any patient with a palpable pelvic mass on abdominal/bimanual persistentsfree unexplained com intermenstrual bleeding examination.oksfree com for gynaecology review and further investigation.oksf This page intentionally lefto blank Weight loss ks 34o sf

Unintentional weight loss of >5% body weight vomiting. Weight loss is also one of several in ≤12 months requires investigation. Lesser non-specific presenting symptoms in chronic degrees of weight loss may also signify underlying adrenal insufficiency (Box 25.2, p. 223). pathology, particularly in the frail elderly. Establish Chronic disease how much weight has been lost, and over what time frame; whether there has been a change In severe non-malignant disease such as in clothes size; and whether there has been a advanced COPD, heart failure or chronic kidney corresponding change in appetite. If present, disease, several mechanisms may contribute to use ‘system-specific’ symptoms or signs (e.g weight loss including poor appetite, persistent haemoptysis, altered bowel habit) to narrow catabolic state and polypharmacy. Prominent theooksfree.com differential diagnosis and guide appropriate weight loss is also a feature of chronic infection, bo ksfreee.g. tuberculosis, com infective endocarditis and HIV. investigation. ebooksf Malignancy Neurological disorder In observational studies, 16–36% of adult Motor neuron disease, Parkinson’s disease, patients with unintentional weight loss have multiple sclerosis and stroke may lead to weight underlying malignancy. Of these, approximately loss through dysphagia (see Ch. 11). Limb weak- 50% originate within the GI tract. Weight loss ness and impaired functional abilities can present in non-GI cancers tends to be associated with a significant barrier to food preparation and more advanced disease. consumption. Multifactorial weight loss is also common in dementia, particularly in advanced Non-malignant GI disease stages. Weight loss is frequently observed in disorders Medication that lead to swallowing difficulty (see Ch. 11), malabsorption (e.g. coeliac disease) or persistent Drug side effects such as anorexia, dry mouth, inflammation (e.g. inflammatory bowel disease). altered taste sensation, nausea, vomiting or booksfrIn peptic ulcer disease, e com mesenteric ischaemia sedation may result in reduced calorie intake and chronic pancreatitis, the pain associated (Box 34.1). Certain drugs are misused to facilitate with eating may lead to weight lossmeboo through weight sfree.com loss, e.g. laxatives or methyroxine. oo avoidance of food. However, weight loss is not Psychiatric an expected feature of functional GI disorders such as irritable bowel syndrome. Low mood can lead to low appetite, or lack of motivation to prepare meals, resulting in weight Endocrine disorders loss. This is a more common phenomenon in Persistent hyperglycaemia due to uncontrolled elderly people with mood disorders. The preva- or undiagnosed diabetes causes weight loss, lence of depression in older adults (>65 years alongside polydipsia and polyuria. In thyro- old) is estimated at around 35%, and higher still toxicosis weight loss occurs despite normal or in those living in institutional settings. Addressing increased appetite. Patients with hypercalcaemia the underlying depressive illness can lead to mayooksfree experience weight com loss due to underlying improved oral intake and weight gain. Primary malignant disease or the direct effects of ↑Ca2+, eating disorders (anorexia and bulimia) are most e.g. osmotic diuresis, anorexia, nausea and commonly identified in younger women, but are meboo sfree com mebooksf Weight loss 295 Differential diagnosis

Other Box 34.1 Drug causes of weight loss Explore possible social causes for weight loss Direct weight loss effect suchsfre as lack of o money to buy food social Diuretics (‘pseudo’ weight loss) isolation and/or chronic alcohol excess Poor Levothyroxine (if excessive dosage) dentition or ill-fitting dentures may also contribute ooksTopiramate (mechanism r uncertain) Appetite suppressants, e.g. Lorcaserin to undernutrition. Glucagon-like peptide-1 (GLP-1) analogues, e.g. Unintentional weight loss is a concerning but Liraglutide non-specific symptom. Refer,m initially, books to the Sympathomimetic agents, e.g. methylphenidate, relevant chapter if one of the following symptoms dextroamphetamine is present: Breast lump (Ch. 5), Dysphagia (Ch. Sodium-glucose Cotransporter 2 (SGLT2) inhibitors, e.g. 11), GI haemorrhage (Ch. 15), Haematuria (Ch. Empagliflozin 16), Haemoptysis (Ch. 17), Jaundice (Ch. 19), Other drug-induced mechanisms of weight loss Scrotal swelling (Ch. 29), Vaginal bleeding (Ch. Nausea and vomit ng: see Box 25.1, p. 223 33). Return to this pathway if no cause for weight Altered sense of taste, e.g. Allopurinol, Zopiclone, loss is identified. Metronidazole Dry mouth, e.g. anticholinergics, clonidine, diuretics Sedat on,ksfree.c e.g. opiates, benzodiazepines, m antipsychotics increasingly recognized in young men; the patient may deny that a problem exists and concerns are often raised by relatives and friendsmeb who free com have noticed a change in eating behaviour or physical appearance.

34 Weight loss 296 Overview

Full clinical assessment, breast, genital & rectal examination, FBC, U&E, LFT, calcium, glucose, TFTre +/- CXR fre

1 Clear cause identified on initial assessment:

No Yes See Clinical tool, Yes ↑↑plasma glucose? Uncontrolled diabetes ‘Diagnosing diabetes andme glycaemic No complications’ (p.299) Yes Suppressedm TSH, ↑T4/T3? Hyperthyroidism No

Seek underlying ↑corrected calcium? Hypercalcaemia cause

Yes 2 ‘System-specific’ findings? Taksrgeted investigation ee (see text) No

Yes 3 Suspect infection? Septic screen (p. 142)

Yes Trial discontinuation 4 Potential drug culprit (Box 34.1)? (if possible) Drug-related weight loss No

Yes 5 Alcohol/drugc misuse? Reassess after treatment / support No

Yes Reassess 6 Features of low mood? Likely depression after treatment No

Yes 7 Suspect eating disorder? oRefer s for specialist assessment c / treatment

Yes 8 Severe systemic illness? Cachexia from chronic disease

Yes Refer old age 9 Cognitive impai ment? Consider dementia o psychiatry No

No clear cause identified? Monitor weight; consider GI investigation / food diary 10 Explore potential contributing factors r c Weight loss 297 Step-by-step assessment

Clear cause identified on initial Request an urgent CXR in patients with 1 screening? persistent respiratory symptoms (>3 weeks) or in those >40 years with a history of smoking or Hyperglycaemia asbestos exposure. Refer for respiratory investigation (usually CT chest /– bronchoscopy) in Consider new-onset diabetes in patients without + patients with an abnormal CXR ( 95% of patients a ookpre-existing fre diagnosis (see Clinical tool p. 299): > with symptomatic lung cancer) or respiratory check for ketoacidosis and, if present, admit for symptoms for 6 weeks despite a normal CXR. urgent treatment. In the absence of ketoacidosis, > Refer patients with concerning GI symptoms refer to your local diabetes service formebo treatment sfre co mebooksf or unexplained iron deficiency anaemia for urgent initiation. Remember that a mild, transient increase endoscopic evaluation: upper GI endoscopy if in blood glucose level may occur in any severe dysphagia, vomiting or upper abdominal pain/ acute illness (stress hyperglycaemia). In older discomfort; colonoscopy if altered bowel habit, patients with new-onset diabetes and weight tenesmus or lower abdominal pain/discomfort; loss consider underlying pancreatic malignancy, upper and lower GI endoscopy if iron-deficiency especially if there is associated abdominal pain. anaemia. CT colonogram provides a less-invasive In patients with known diabetes, use alternative to colonoscopy and may be more plasma HbA1c to gauge the severity of recent appropriate in selected patients, e.g. frail or hyperglycaemia; consider hyperglycaemia as a multimorbid. contributor to weight loss if control is suboptimal Arrange appropriate imaging if you palpate an (especiallyooksfree.com in type 1 diabetes) but continue to abdominal or pelvic mass. USS is often a helpful search for alternative causes. boo sfree com initial investigation, particularly for pelvic masses, Thyrotoxicosis (TSH) but CT is frequently requiredmebo for further char ksf- acterisation +/– staging of malignant tumours. Suppressed TSH with T /T level is diagnostic ↑ 4 3 Check a PSA level in males with prostatic of hyperthyroidism. Look for associated clinical symptoms. Measure PSA prior to the rectal exam features including tremor, poor sleep, heat to avoid false positive tests. Refer patients with intolerance and increased bowel activity +/– eye a hard irregular prostate or ↑PSA (≥3 ng/mL if and skin changes in Graves’ disease. Check <60 years; ≥4 ng/mL if 60–69 years; ≥5 ng/mL thyroid receptor antibody (TRAB) levels to help if ≥70 years) for urgent urological assessment. identify the underlying aetiology and refer to Bear in mind that localized prostate cancer is Endocrinology. unlikely to account for significant weight loss so Hypercalcaemia continue to seek alternative causes unless there are features of advanced disease, e.g. bone pain, Checko plasma sf parathyroid ee.com hormone (PTH) levels to biochemical evidence of skeletal metastases (e.g. identify the likely cause. PTH should be suppressed ↑ALP) or a markedly ↑PSA, e.g. >20 ng/mL. by hypercalcaemia so ↑ or ‘inappropriately normal’ Lymphadenopathy, either local or generalized, PTH suggests primary hyperparathyroidism.mebo If may sfree signify infection, com inflammation,mebooksf e.g. connec- ↓PTH, consider malignancy (e.g. skeletal metas- tive tissue disease, haematological malignancy or tases, multiple myeloma or tumour secretion of solid organ cancer with lymphatic involvement. PTH-related peptide). Other causes, particularly if Check LDH (often ↑ in haematological malig- hypercalcaemia is mild, include sarcoidosis, thiazide nancy) and screen for infection and autoimmune diuretics and vitamin D analogues. disease. In persistent lymphadenopathy consider CT chest/abdomen/pelvis and arrange lymph node biopsy to establish a tissue diagnosis. 2 ‘System-specific’ findings? Consider underlying malignancy in any patient 3 Suspect infection? with unexplained weight loss. Look for clues inooksf the history, physical com examination and Perform a septic screen in patients with fever or routine tests that may help to target furtherbo elevated free.com white cell count/inflammatory markers investigation. (see Clinical tool, p. 142). Ask about foreign travel, mebo 34 Weight loss 298 Step-by-step assessment infectious contacts and risk factors for HIV. loss fear of gaining weight, preoccupation with Examine carefully and repeatedly for murmurs weight issues) or concerns raised by friends/ and peripheralsfre stigmata co of endocarditis. family members, e.g. skipping meals, concealing food. Be sensitive and tactful but persistent in 4 Potential drug culprit? questioning and refer to specialist services if Review all medications, prescribed and non- significant concern. ooksf prescribed, including any ‘nutritional supplements’. In patients with reduced dietary intake 8 Severe systemic illness? ask about symptoms such as drymeb mouth, sfre Assess the severity and trajectory of chronic drowsiness, altered taste sensation or nausea disease, e.g. heart failure, COPD or renal failure and look for potential drug culprits (Box 34.1). using symptom status, functional performance, If you suspect a drug cause, reassess weight frequency of hospitalization and objective markers and symptoms after trial discontinuation (if (e.g. GFR FEV1). Weight loss and anorexia may appropriate). occur in advanced disease. Seek specialist input 5 Alcohol/drug misuse? to optimize management but consider the need for dietetic and/or palliative care input. Enquire about alcohol intake (Box 2.1, p. 11) and recreational drug use, e.g. cocaine, ampheta- Cognitive impairment? minesooksfr in a non-judgmental com manner. Where 9 possible seek collateral history from friends or Assess cognition formally with a mini mental family (who may have raised the concerns re: state examination or Addenbrooke’s cognitive weight loss). Explore associated factorsmebo that may examination-III sfree com in patients withmeb either established f be contributing to weight loss such as appetite or suspected or cognitive impairment. Wherever suppression, replacement of meals with alcohol possible, obtain a collateral history from friends, intake, lack of money to buy food or co-existent relatives or carers to evaluate the contribution mood disorders. from cognitive impairment to weight loss, e.g. forgetting meals, unable to prepare food, para- 6 Features of low mood? noid ideas about food. In patients with more Look for evidence of low mood such as anhedo- advanced dementia enquire about the patient’s nia (loss of pleasure in life), undue pessimism or ability to transfer food from plate to mouth and feelings of guilt/worthlessness pessimism as well any swallowing problems. Refer patient for as biological features of depression, e.g. lack specialist evaluation, e.g. psychiatry of old age. ofooksfree. energy, poor sleep (early m morning waking), reduced libido. Consider undertaking a depres- Consider further investigation and/or sion score, such as the Geriatric Depression 10 food diary. Explore factors contributingeb oksf to Scale in the elderly, or the PHQ-9 in younger reduced food intake adults. If you suspect depression as themebo cause of sfree.com If weight loss persists with no clear cause, weight loss reassess weight and other symptoms consider GI investigation/referral +/– CT if not after a period of treatment. already performed. Use a food diary to record calorie intake. Reconsider the possibility of a 7 Suspect eating disorder? primary eating disorder or depression. Explore Consider the possibility of an eating disorder possible contributing factors to inadequate food particularly in younger women with amenorrhoea intake including inadequate dentition, swallowing or a background of psychiatric or psychological problems, lack of motivation (or money), impaired problems. Be alert for important clues such as mobility (unable to get to shop) or subtle cogni- distorted attitudes to weight or body image tive impairment. Refer frail, elderly patients for (e.g.ooksfree underplaying the c seriousness m of weightoo comprehensive sfree c geriatric m assessment ooksf Weight loss 299 Step by-step assessment

Clinical tool Diagnosing diabetes and glycaemic complications Diagnosis of diabetes diabetes). It develops rapidly over hours. Severity can be graded as mild/moderate/severe depending on the degree (Definition and diagnosis of diabetes mellitus and of biochemical abnormality and presence of altered mental ooksfreintermediate hyperglycaemia. WHO 2006; update 2011.) status (Table 34.2). Mortality is 0.2–2% (with higher rates Typical presenting symptoms of diabetes include thirst, in developing countries). polyuria and unexplained weight loss. These will be more Hyperosmolar hyperglycaemic state (HHS) is usually a prominent, with a shorter history, in type 1 diabetes,meb due to complication sf of poorly co controlled type m2 diabetes, book often absolute insulin deficiency. In type 2 diabetes, there may with insidious onset over days to weeks. Blood glucose be little in the way of symptoms, or they may go unnoticed is very high, with high osmolality and hypercoagulability. due to their insidious onset. Biochemical cut-offs to clinch It is life threatening, with a 15–20% mortality rate. the diagnosis are described in Table 34.1. In symptomatic The frail elderly are most at risk. It can be complicated patients, one laboratory measure is required to confirm by myocardial infarction, stroke or peripheral arterial hyperglycaemia. In asymptomatic people, two confirmatory thrombosis In addition, overly rapid correction of metabolic tests at separate t mes are needed. abnormalities can lead to complications such as seizures, Assessment of long-term glycaemic control cerebral oedema and central pontine myelinolysis. It is, therefore, vital to correct abnormalities gradually and to The target HbA1c in the ongoing management of diabetes, carefully monitor the plasma osmolality ([2 × Na] + urea + to avo d the development of long-term complications, is glucose) during treatment. widely accepted as <58 mmol/mol (<7.5%). There has beenoksfree.com a recent move in updated NICE guidance (2015) to Hypoglycaemia a tighter target of 48 mmol/mol (6.5%), if able to achieve Whilst there is no clear consensus on the biochemical this without unacceptable hypoglycaemia or impact on definition of hypoglycaemia, it is largely accepted that co-morbidities. American Diabetes Association guidance a blood glucose <4 mmol/L (72 mg/dL) would be an recommends a target of <53 mmol/mol (7.0%).meb These appropriate sfree level to com trigger treatment inmeb a person with k targets should, of course, be individualized in consultation diabetes. Severe hypoglycaemia is defined by the with the person with diabetes. requirement for external assistance to restore normal Acute complications of diabetes blood glucose (whether relatives or emergency services). Symptoms (Table 34.3) will usually alert a person with Hyperglycaemic crises diabetes to the development of hypoglycaemia, but it Diabetic ketoacidosis (DKA) is a medical emergency, and is important to be aware that some people lose their involves a triad of diabetes, ketosis and acidosis. It is the hypoglycaemia warning symptoms, known as impaired result of insulin deficiency (absolute – type 1 diabetes/ hypoglycaemia awareness, and they are at high risk of pancreatic disease;free or relative c – m poorly controlled type 2 severefree hypoglycaemia com as a result.

34 Weight loss 300 Step-by-step assessment

Table 34.1 Biochemical criteria for diagnosis of Table 34.3 Symptoms of hypoglycaemia diabetes mellitus Diabetes Autonomic Neuroglycopenic Non-specific Fasting plasma ≥7.0 mmol/L (126 mg/dL) glucose Palpitation Confusion Tiredness ookRandom plasma f e co≥11.1 mmol/L (200 mg/dL) Sweating Weakness Nausea glucose Tremor Dizziness Headachebook 2-hour plasma ≥11.1 mmol/L (200 mg/dL) glucose on OGTT1 Hunger Reduced HbA1c2 ≥48 mmol/mol (6.5%)m b fr concentration Impaired fasting glycaemia Anxiety Incoordination Fasting plasma 6 1–6.9 mmol/L D owsiness glucose (110–125 mg/dL) Speech difficulty Impaired glucose tolerance om 2-hour plasma 7.8–11.0 mmol/L glucose on OGTT (140–200 mg/dL)

1OGTT – Oral glucose tolerance test: venous plasma glucose in fasting state administer 75 g oral glucose load, repeat venous plasma glucose at 2 hours. 2Not suitable as a diagnostic test in children and young people or inoksf the context of: suspected c type m1 diabetes, symptoms for <2 months, acute illness, pregnancy, treatment with medications that cause rapid glucose rise (e.g. steroids, antipsychotics) or acute pancreatic damage/surgery.

Table 34.2 Criteria for diagnosis of DKA and HHS

DKA Severe DKA HHS Plasma glucose1 >13.9 mmol/L (>250 mg/dL) – >33.3 mmol/L (>600 mg/dL) Osmolality >320 mOsm/kg Arterial pH <7.3 <7.0 >7.3 Serum bicarbonate <18 mmol/L <10 mmol/L >18 mmol/L2 ooksfreBlood ketones (capillary sample) o >1.5 mmol/L – Negative/small Urine ketones Positive – Negative/small Mental status Alert orm drowsy Stupor/coma e. Stupor/comame 1If a patient with DKA has started treatment with supplementary insulin, they may present with a normal blood glucose, but still have ketosis and acidosis and be at risk of clinical deterioration. 2In some patients metabolic acidosis may be present due either to relative insulin deficiency (check ketones) or to intercurrent acute illness (lactic acidosis or AKI). Adapted from Kitabchi AE et al 2006. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association Diabetesc Care. m 29(12):2739–2748. c m Appendixm

Normal values for biochemical tests in venous blood

Reference range1 Analyte SI units Non-SI units Alanine amino-transferase (ALT) 10–50 U/L – Albumin 35–50 g/L 3.5–5.0 g/dL Alkaline phosphatase (ALP) 40–125 U/L – Aspartate amino-transferase (AST) 10–45 U/L – Bilirubin (total) 2–17 µmol/L 0.12–1.0 mg/dL ooksCalcium (total) e m 2.12–2.62 mmol/L 4.24–5 24 meq/L or boo 8 50–10.50 mg/dL Chloride 95–107 mmol/L 95–107meboo meq/L Cholesterol (total) Mild increase 5.2–6.5 mmol/L 200–250 mg/dL Moderate increase 6.5–7.8 mmol/L 250–300 mg/dL Severe increase >7.8 mmol/L >300 mg/dL C-reactive protein (CRP) <5 mg/L Highly sensitive CRP assays also exist which may be useful in estimating cardiovascular risk Creatine kinase (CK) (total) Male 55–170 U/L – Female 30–135 U/L – Creatine kinase MB isoenzyme <6% of total CK – ooksCreatinine re 60–120 µmol/L 0.68–1.36 mg/dL Gamma-glutamyl transferase (GGT) 5–55b U/L k e – Glucose (fasting) 3.6–5.8 mmol/L 65–104 mg/dL

Glycated haemoglobin (HbA1c) 5.0–6.5% –m o Lactate 0.6–2.4 mmol/L 5.40–21.6 mg/dL Lactate dehydrogenase (LDH) (total) 208–460 U/L – Phosphate (fasting) 0.8–1.4 mmol/L 2.48–4.34 mg/dL Potassium (plasma) 3.3–4.7 mmol/L 3.3–4.7 meq/L Potassium (serum) 3.6–5.1 mmol/L 3.6–5.1 meq/L Protein (total) 60–80 g/L 6–8 g/dL Sodium 135–145 mmol/L 135–145 meq/L Triglycerides (fasting) 0.6–1.7 mmol/L 53–150 mg/dL ookUrate fr e m Male 0 12–0.42b oks mmol/L 2.0–7 0 mg/dL Female 0.12–0.36 mmol/L 2.0–6eb 0 mg/dL Urea 2.5–6.6 µmol/L 15–40 mg/dL

1Note these values may vary according to local laboratory calibration. 302 • APPENDIX

Arterial blood analysis

Reference range Analysis SIoks units Non-SI units ooBicarbonate fr(HCO3) 21–29 mmol/L 21–29 meq/L Hydrogen ion (H+) 37–45 nmol/L pH boo7.35–7.43

PaCO2 4.5–6.0 kPa 34–45 mmHg

PaO2 12–15 kPa 90–113 mmHg 1,2 Oxygen saturation (SpO2) >97%

1Breathing room air. 2Varies with age.

Haematologicalk values Reference range Analysis SI units Non-SI unitsb Bleeding time (Ivy) <8 min – Blood volume Male 75 ± 10 mL/kg – Female 70 ± 10 mL/kg Coagulation screen Prothrombin time 10.5–13.5 sec – Activated partial thromboplastin time 26–36 sec – D-dimer Routine <0.2 mg/L – Sensitive (for venous thromboembolism) Variable threshold (dependent on method) Erythrocyte sedimentation rate (ESR) Higher values may be normal in older patients Adulto male fr c oksfr0–10 mm/hr – Adult female 3–15 mm/hr – Ferritin Male 17–300 µg/L 17–300 ng/mL Premenopausal female 7–280 µg/L 7–280m ng/mL Postmenopausal female 4–233 µg/L 4–233 ng/mL Fibrinogen 1.5–4.0 g/L 0.15–0.4 g/dL Folate Serum 2.0–13.5 µg/L 2.0–13.5 ng/mL Red cell 95–570 µg/L 95–570 ng/mL Haemoglobin Male 130–180 g/L 13–18 g/dL Female 115–165 g/L 11.5–16.5 g/dL Haptoglobin 0 4–2.4 g/L 0.04–0.24 g/dL Iron ks k fre Male 14–32 µmol/L 78–178 µg/dL Female 10–28 µmol/L 56–156 µg/dL Leukocytes (adults) 4.0–11.0 × 109/L 4.0–11.0ebo × 103/mm3 303 • APPENDIX

Haematological values—cont’d

Reference range Analysis oksSI units Non-SI units ooDifferential white fr cell count Neutrophil granulocytes 2.0–7.5 × 109/L 2.0–7 5 × 103/mm3 Lymphocytes 1.5–4.0 × 109/L 1 5–4.0 × 103/mm3 Monocytes 0.2–0.8 × 109/L 0.2–0.8 × 103/mm3 Eosinophil granulocytes 0.04–0.4 × 109/L 0.04–0.4meb × 103/mm3 Basophil granulocytes 0.01–0.1 × 109/L 0.01–0.1 × 103/mm3 Mean cell haemoglobin (MCH) 27–32 pg – Mean cell volume (MCV) 78–98 fL – Packed cell volume (PCV) or haematocrit Male 0.40–0.54 – Female 0.37–0.47 – Platelets 150–350 × 109/L 150–350 × 103/mm3 Red cell count Male 4.5–6.5 × 1012/L 4.5–6.5 × 106/mm3 Femaleoks c o3.8–5.8 fr× 1012/L 3.8–5.8 × 106/mm3 Red cell lifespan oo Mean 120 days – Half-life (51Cr) 25–35 days – Reticulocytes (adults) 25–85 × 109/L 25–85 × 103/mm3 Transferrin 2.0–4.0 g/L 0.2–0.4 g/dL Transferrin saturation Male 25–56% – Female 14–51% –

Vitamin B12 130–770 pg/mL – Source: Reproducedfr with permission from Innes JA. Davidson’s Essentials of Medicine.fr e Edinburgh: Churchill Livingstone, 2009. This page intentionally lefto blank Index

Page numbers followed by ‘f ’ indicate figures, ‘t’ indicate tables, and ‘b’ indicate boxes.

A low clinical probability of, 52b, Acute rectal bleeding, 156 Abbreviated Mental Test score, 63, 63b–64b Acute red eye, 250, 250b 218 Acute delirium, 218 Acute renal impairment, nausea ABCDE assessment process, 7, Acute diarrhoea, 25b, 32 and vomiting and, 225, 8b–10b, 115 Acute drug eruptions, 249 230–231, 230b Abdominal pain, 24–45, 30f Acute drug-induced liver injury, Acute small bowel ischaemia, acute 24–25, 25f 174, 175b 151 gynaecological pathology, Acute dyspnoea 112 Acute viral hepatitis, 174 40ksfree co cardiovascular causes of, 112 Addenbrooke’s cognitive lower, 38f in COPD, 115 examination-III, 298 bedside pregnancy test in lower airway disease, 112 Adrenal crisis, 265 patient with, 39 overview for, 114f Adrenal insufficiency, 134 chronic relapsing, 42, 42f parenchymal lung disease, nausea and vomiting and, clinical/laboratory features 112 223, 223b suggesting organic disease, respiratorymebook causes of fre, 112 oAdult-onset Still’sme disease, 149 45 step-by-step assessment for, Advanced myopathy, 202 cyclical pain and, 44 115–119 Airflow obstruction, severity of, jaundice, 43–44 upper airway obstruction, 112 127t left lower quadrant, 25b, 39 Acute erythroderma, 240 Airway leucocytes/nitrites on Acute febrile illnesses, 141 assessment of, 8b–10b urinalysis, 40 Acute fever, 145 obstruction, 121 loin pain/haematuria, 44 Acute generalized skin eruption, Alanine amino-transferase (ALT), lower GI symptoms with 240–249 normal values of, 302t alarm features, 43 Acute glaucoma, headache and, Albumin, normal values of, 302t palpable mass, weight loss, 167, 172 Alcohol intoxication, acute, 84 systemic upset/unexplained Acute haemorrhage, Alcohol toxicity, 76–77, 76t jaundice, 44 resuscitation in, 153b Alcohol withdrawal, 84 upperoksfree GI symptoms co with Acute iritis, 252 Alcoholic hepatitis, 181 alarm features, 43 Acute large joint swellings, 187 Alkaline phosphatase (ALP), Abnormal pleural fluid Acute liver failure, 174, 175b normal values of 302t collections, 129b identify patients with, Allopurinol, 240 Abrupt decline, in mobility, 218 mebook179–180 f ee omAltered consciousnessm bo, 72–77, ks Accidental trip, 214, 216f liver transplantation in, 180b 74f diagnosis of, 217b monitor and reassess patients confusion and, 81 Achalasia, 109 with, 180 Ambulatory smart phone Acid-base status, assessment Acute liver injury monitors, 237 of, 116b cause of, 180 American College of Acoustic neuroma, vertigo and, jaundice and, 174–176 Rheumatology/European 96 Acute mesenteric ischaemia, League Against Rheumatism Acute alcoholic hepatitis, 174 28–29 classification criteria, for Acute angle closure glaucoma, Acute non-neurological illness, rheumatoid arthritis, 185t 252–253, 253f, 255 205 Amylase, 35–36 Acute asthma exacerbation, Acute pancreatitis, 28 Amyotrophic lateral sclerosis, assessment of, 122, 122t modified Glasgow criteria 199 Acute chest pain, 50–52, 60f and, 35b Anaemia Acuteooksfree coronary syndrome c, m50, Acute pericarditis, 51 assessment of, 136–137 51b ECG in, 54b–58b, 59f fatigue and, 133 clinical probability of, 63 Acute pyelonephritis, haematuria nausea and vomitingebo and, k history consistent with, 62 andmebooksfre, 158 m229 306 • INDEX

Anaphylaxis 265, 268t Bacterial conjunctivitis, 250 colorectal carcinoma and, ANCA-negative systemic Bacterial urinary tract infection, 151 vasculitis, 149 haematuria and, 158 diverticular disease and, Angina Balance, impaired 99 151 assessment of, 71 Bamford classification, of stroke, high-risk, 157, 157b chronic dyspnoea and, 128 207, 207b inflammatory bowel disease ooksfrepectoris, 52 Baseline cognitive function, and, 151 symptom score, 63b normal, 81 ischaemic colitis and, 151 Angiodysplasia (arteriovenous Baseline cognitive impairment, overview of 156, 156f malformation), 151 delirium and, 84 perianal disorders and, 151 Angioedema, 243–244 Baselinemebooksfre lung function, 121 resuscitationme in, 156 oo Anhedonia, 135, 298 Bedside pregnancy test, in risk factor for, 157, 157b Ankylosing spondylitis, 208 patient with abdominal pain, upper GI source of, Anorectal bleeding, 150–151 39 156–157 Anorexia, 294–295 Bell’s palsy, 255 risk score, 238t nausea and vomiting and, Benign paroxysmal positional vaginal, 288–292 229 vertigo (BPPV), vertigo and, assessment of, 290f Anterior uveitis 252 96 examination of, 291b, 291f Anticonvulsants 240 Benign stricture, 108–109 in first trimester, 288 Anxiety, 52–53 jaundice and, 177 pregnancy and, 291 Aortic dissection, 50, 61–62, Benign thunderclap headache, in second and third 61b 166 trimester, 288 ECG in, 54b–58b Bilateral limb weakness shock in, 291 Appendicitis, 39 acute-onset, 199 Blepharitis, 251 Apraxiaooksfree, 221 m muscle fatigability, 201–202 Blisters, present of, 247–248 Arrhythmia, 96 overview of, 198, 198f Blood Arrhythmia-related syncope, 270 proximal weakness with analysis, arterial, 303t Arterial blood analysis, 303t mebootenderness, 202 sfre film, abnormalitiesm b on, 134 Arterial blood gases, 116b, 116t sensory signs or symptoms normal values for biochemical analysis, metabolic acidosis of, 201 tests in venous, 302t by, 119 upper motor neuron signs of, Blue boxes, 19, 20f Ascites, 179 199–201 Body surface area Aspartate amino-transferase Bilateral lower limb neurology, erythematous, 247, 247b (AST), normal values of, 302t 212 Bone cancer, and secondary Asplenia, 144 Bilateral lower limb oedema, deposits, 185 Assessment, 7–16 195 Bone marrow failure, 137 clinical examination, 11–15, Bilateral oedema, 190–191 BPPV. see Benign paroxysmal 13t Biliary colic, 27f, 28 positional vertigo history 11, 11b–12b, 11t characteristics of, 36–37 Bradyarrhythmias, 234, 268t inspection, 16 Bilirubin, normal values of, 302t assessment of, 239 investigations, 15 Binge drinking, 181 Bradycardia, fatigue and, 133 Asterixis,ooksfre examining for co, 180f Biochemical tests, in venous Brainstem pathology, vertigo Asthma, 53 blood, normal values for, 302t and, 96 Asymptomatic rhythm Blackout, mobility problems, Brain-type natriuretic peptide disturbances, 237–238 217–218 (BNP) testing, 118 Ataxia, 220 Bladder,mebooksf palpable, 87 eBreast m abscessmebook, 46 unsteadiness and, 97 Bleeding Breast cancer, 46, 46b Atrial fibrillation, 232–233, 234f anorectal, 150–151 Breast lump, 46–49, 48f assessment of, 239 assessment of, 290f abscess, evidence of, 49 causes of, 234b bright red, 151 discrete lump palpable, 49 Atrial flutter, 232, 234f confined to menstruation, 292 features of/risk factors for assessment of, 239 heavy menstrual, 288 breast cancer, 46b, 49, Atrial tachycardia, 232–233 intermenstrual, 289, 292 49b Atrophic vaginitis, 285 postcoital, 292 Breathing, assessment of, Atypical infection, haematuria postmenopausal, 289, 8b–10b and, 158–159 291–292 Bright red bleeding, 151 Autoimmune causes, of pregnancy-related, 288 Bronchiectasis, 162, 165 jaundice, 177 rectal, 150–157 Brugada syndrome, 281f Autoimmune hepatitis, 174 acute 156 Budd-Chiari syndrome. see ooksfree.c angiodysplasia Hepatic vein thrombosis B (arteriovenous Bulbar palsy, 108, 109t Bacillus cereus, gastroenteritis ebookmalformation) and fr, 151 Bulimia m , 294–295 caused by, 222 clinical features of, 157 Bursitis, 184 m boo 307 • INDEX

C related to exertion, 125 disorders mimicking, 79 Calcium, normal values of, 302t respiratory causes of, 113 normal cognitive function, 81 Cancer step-by-step assessment for, overview, 80, 80f of breast, 46, 46b 125–128 Congestive cardiac failure (CCF), of colon, 29 unexplained hypoxia, 128 190 red flags for, 213 Chronic fatigue syndrome, 4t, Conjunctivitis, 188, 250, 251f Carbonook monoxide fr poisoning, 77 135, 135b allergic, 255 Cardiac syncope, 270 Chronic heart failure, chronic Connective tissue disorders, Cardiac tamponade, 265, 268t dyspnoea and, 127 fever and, 139 Cardiogenic lower limb oedema, Chronic liver disease, 134, 176b Consciousness, 72 190 assessmentmeboo of, 182 sfre altered, 72–77,mebook 74f Cardiogenic shock, 264, 269 evidence of, 179 Constipation, 87 Cardiorespiratory dysfunction Chronic mesenteric ischaemia, nausea and vomiting, 222 134 28–29 Continuous incontinence, 283 Cataplexy, 271 Chronic non-haematological Conus medullaris syndrome, Cauda equina syndrome, 209 disease, 137 285 Cavitating lung lesion, 163f Chronic obstructive pulmonary Coordination, tests of, 14f CCF. see Congestive cardiac disease (COPD) COPD. see Chronic obstructive failure assessment of acute pulmonary disease CDI. see Clostridium difficile dyspnoea in, 115, 121 Core temperature, 75 infection clinical features of, 117f Coronary artery disease, 128 Cellulit s, 260 Chronic pain syndrome, 4t Cortical dysfunction, 197b Central nervous system Chronic pancreatitis, 28 C-reactive protein (CRP) normal causes, 73 Chronic relapsing abdominal values of, 302t ooksfinfection, 75 e.c m pain, 42 42f Creatinine, normal values of, Cerebral venous thrombosis, Chronic renal failure, 222, 230t 302t 166 Chronic subdural haematoma, Creatinine kinase (CK), normal Chagas disease, 109 166mebooksfrvalues m of, 302mt b o Chest pain, 50–71, 54b–58b Chronic venous insufficiency, leg Creatinine kinase MB acute, 50–52, 60f swelling and, 191, 191b, 194 isoenzyme, normal values of, aortic dissection, 50 Chronological age, 15 302t intermittent, 52–53 Circle of Willis, CT angiography, Crohn’s disease, rectal bleeding non-cardiac causes of 64 201 and, 151 Chest X-ray (CXR) Circulation, assessment of, Crystal arthropathy, joint abnormality, acute dyspnea 8b–10b swelling and, 184 and, 118–119, 118f Cirrhosis, 176, 176b Crystal-induced arthropathy, in lung cancer, 163b Clinical examination 11–15, 187 Child-Pugh classification, of 12b–13b, 13t CURB-65 score, 123, 123t cirrhosis, 182, 182t Clostridium diffici e infection Chloride, normal values of, 302t (CDI), 90 D Cholangiocarcinoma, 177 Cluster headache, 166 Deep vein thrombosis (DVT), Cholecystitisooksfree.c, 176 Coagulation, problems with, oedema and, 190–191 Choledocholithiasis, 28 jaundice and, 174 Delirium, 78–79 79b Cholesterol, normal values of, Cognitive function, normal, alcohol excess/dependence, 302t 81 84 Chronic abdominal pain, 28–29 Cognitivemebooks impairment, 80 rb, 218, assessment m meboo test for, 80b Chronic alcohol excess, 181 298 capillary BG, 83 Chronic back pain, 4t chronic, 79 causes, 79 Chronic cognitive impairment, Colon cancer, 29 drug toxicity and, 83–84 79 Colonic ulcer, 151 drugs and, 78 Chronic dermatosis, 249 Colonoscopy, 157 infection and, 78 Chronic dyspnoea Colorectal cancer, 90–91, high risk of, 85 abnormal PFTs in, 126–127 151 intracranial causes, 78 alarm features in, 125–126, Coma, 72–77, 74f intracranial pathology, high 125b Compartment syndrome, 191, risk of, 83 cardiovascular causes of, 113 193, 193b liver disease, suspected, 84 coronary artery disease and, Confusion, 78–89 meningitis, suspect, 83 128 acute cognitive function, metabolic disturbance, 83 CToks abnormality ree in, 126, om 126b fluctuating course, altered metabolic/physiological echocardiographic consciousness/attention, 81 disturbance, 78 abnormality in, 127 assessment method, 14 normal baseline cognitive overview for, 124f chronic, 89 function, 81 pleural effusion in, 125 depressionmebook, 81 froverview m , 82,meboo 82f 308 • INDEX

Delirium (Continued) malabsorption, disorders coronary artery disease in vulnerable brain, 86, 86f causes, 91 and, 128 step-by-step assessment, overview, 92, 92f CT abnormality in, 126, 87 protozoal infection, risk of, 93 126b Dementia, 78 shock and 92 echocardiographic causesoksfre, 79 Dieulafoy’s lesion, 150 abnormality in 127 chronic cognitive impairment, Differential diagnosis, 3 overview for, 124f 79 Diffuse oesophageal spasm, pleural effusion in, 125 reversible causes, 79 109 related to exertion, 125 Dendritic conjunctival ulcer, 255f Diffusion capacity, 127t respiratory causes of, 113 Dependent/gravitational Disability,mebooks assessment of, e step-by-stepmebo assessment oedema, 191 8b–10b for, 125–128 Depression Disc herniation, lumbar, 208 unexplained hypoxia, 128 in elderly, 16 examination, 210f weight loss and, 294–295 Distributive shock, 265, 269 E Dermatitis, 240, 241f Diverticular disease, 151 Eating disorder, nausea and Dermatitis herpetiformis, Dix-Hallpike test, 101, 103f vomiting and, 229 242–243, 243f 247–248 Dizziness, 96–107 Echocardiography Dermatomes, 200f disorders causes, 97 abnormality, in chronic Diabetes mellitus initial assessment, overview, dyspnoea, 127 diagnosis of, 300t 98, 98f for heart failure, 118 fatigue and, 133 illusory sense of motion, 99 Ectopic pregnancy, bleeding nausea and vomiting and, impaired ba ance, 99 due to, 288 oksfree229 co light-headedness, 99 Ectropion, 251 weight loss and, 299b loss of consciousness, 99 Eczema, 240 Diabetic ketoacidosis (DKA), presyncope, 99 Eczema herpeticum, 240 222–223, 299b transientebook focal neurological fr oEmbolism, pulmonary criteria for diagnosis of, 300t deficit, 99 assessmentme of suspected,k Diagnosis, 3–6 unsteadiness, 99 120f of exclusion, 3 mobility problems, 217–218 clinical suspicion of, 119, patient comes with, 6 DKA. see Diabetic ketoacidosis 119t treatment before, 5–6 Drugs, 72 Wells score, 120f, 120t Diagnostic ECG recording, 279 diarrhoea caused by, 90, 91b Emotional distress, 53 Diagnostic guides, 19–21, 20f shock caused by, 265 Encephalitis, 197 Diagnostic methods, 17–18 toxicity, 76–77, 76t Encephalopathy, hepatic pattern recognition, 17 Duodenitis, 150 features of, 179–180 probability analysis, 17–18 DVT. see Deep vein thrombosis West Haven grading of, 175t, Diagnostic process, 17–21 Dysphagia, 108–111 179 Diagnostic tests, 3–4 oesophageal Endocrine disorders, weight loss Diarrhoea, 90–95 dysmotility, 109 and, 294 acute renal impairment, 92 structural, 108–109 Endometriosis, 44 ooksfreebloody, 91b, 93 co oropharyngeal, 108 ENT investigation, abnormality causes, 91 Dyspnoea, 112–129 on, 110f, 111 chronic/relapsing, overview, acute, 112 Enthesopathies 184 94, 94f cardiovascularebook causes re of, Entropion m , 251, 253f alarm features, 95 112 Epididymal cystmebo, 260 ksf drug culprit, 94f, 95 in COPD, 115 Epididymitis, 259f, 260 infection risk, 95 lower airway disease, 112 Epididymo-orchitis, 260 organic disease, clinical/ overview for, 114f Ep lepsy, 270 laboratory features, 95 parenchymal lung disease, diagnosis of, 277 steatorrhoea, 95 112 Episcleritis, 252, 253f stool, hard/impacted, 95 respiratory causes of, 112 Episodic abdominal pain, Clostridium di ficile infection, step-by-step assessment 28–29 93, 93b for, 115–119 Erythema multiforme, 240–242, dehydration, clinical evidence upper airway obstruction, 242f of, 92 112 Erythroderma, 240, 241f drug related, 90, 91b, 93 chronic, 112–113 acute, 240 infectious, 90 abnormal PFTs in, 126–127 Exanthem, 244–245 inflammatoryoksfr bowel e com disease, alarm features in, 125–126, Exercise tolerance, 221 91, 91b 125b Exposure, assessment of, irritable bowel syndrome, 90, cardiovascular causes of, 8b–10b 90b ebook113 fr e omExtrahepatic cholestasis, 176 mebo 309 • INDEX

Extrasystoles 232 Fournier’s gangrene, 260 H assessment of, 239 Frail, elderly patient, assessment Haematemesis, 150–157 history of, 237 of, 15–16 active bleeding in, 154 Extravascular haemolysis, 136 Frank haemoptysis 162 forceful retching/vomiting in, Extrinsic compression, 109 Frank pus, 255 154 Eyelashes, abnormality of, 255 Free air on CXR, 31f, 35 gastritis/duodenitis and, 150 Eyelid,ooksfre abnormality of, 255 Frontal headache, 172–173 Mallory-Weiss tear and, 150 Full clinical assessment, 7–15 oesophageal/gastric varices F Functional disorders, 29 and, 150 Fat necrosis, 47 Functional incontinence, 283 oesophagitis and, 150 Fatigue, 130–137, 238 Functionalmebook syndrome, 4, fre 4t overview ofmebo, 152, 152f k cardiac causes for, 130 peptic ulcer and, 150 chronic inflammatory G resuscitation in, 153, 153b conditions for, 130 Gait upper GI malignancy and, endocrine causes fo , 130 abnormality, 221 150 haematological causes for, apraxia, 221 variceal bleeding in, 154 130 assessment, 215b, 220f Haematological malignancy, infection and 130 Gallstones, 28 137 malignancy of, 130 jaundice and, 176 Haematological values, medications for, 130 Gamma-glutamyl transferase 303t–304t non-organic causes of, 130 (GGT), normal values of, 302t Haematuria, 158–161 overview for, 132f Gastric cancer, 28 abdominal pain and, 44 presentations of, 131b Gastric varices, 150 atypical infection and respiratory causes for, 130 Gastritis, 37, 150 158–159 ooksfreestep-by-step assessment co for, Gastrocnemius muscle rupture, bacterial urinary tract infection 133–135 193 and, 158 FBC abnormalities, 134 Gastroduodenal disorders, 28 benign cause of, 161 Fever, 138–149 Gastroenteritism booksfr, 222, 226 clinical m suspicionm of b, acute, 145 Gastro-esophageal disorders, 161 clinical findings/initial tests for, 51–53 overview of, 160, 160f 144–145 Gastrointestinal haemorrhage, persistent, 161 CNS and, 138 150–157 renal colic and, 161 connective tissue disorders Gastrointestinal obstruction, 222 renal disease and, 159 and, 139 Gastro-oesophageal reflux, stones and, 158 drugs, 139 benign stricture and, 108–109 symptomatic, 161 ENT and, 138–139 Gastroparesis, 222 tumours and, 158 genitourinary tract and, 138 Generalized oedema, 190 urine discoloration other than, GI causes for, 138 Generalized peritonitis, 31, 31f 159b immunocompromised patients Generalized wheeze 118 UTI and, 161 and, 139 Geriatric Depression Scale, 81, visible, 161 infection and, 138–139, 144 298 Haemolysis, investigate for, ooksfremalignancy of, 139 o GGT. see Gamma-glutamyl 136–137 musculoskeletal causes for, transferase Haemolytic disorders, 174, 138 Giant cell arteritis. see Temporal 175b non-infective cause for, 141 arteritis Haemolytic uraemic syndrome, overview of, 140, 140f Gilbert’smebooksfre syndrome, 174 .231 m meboo f persistent, 145 Glasgow Coma Scale, 72, Haemoptysis, 162–165 recurrent, 145 73t bronchiectasis and, 162 respiratory system and 138 Glomerulonephritis, 231 lung tumours and, 162 returning travellers and, 139 Glucocorticoid deficiency, 265 massive, 164–165 skin/soft tissue and, 138 Glucose (fasting), normal values other causes/further step-by-step assessment for, of, 302t investigation for, 165 141–145 Glycated haemoglobin, normal overview of, 164, 164f Fibroadenoma, 46 values of, 302t pulmonary embolism and, Fibrocystic change, 46–47 Gout, 184 162 Fibromyalgia, 4t Green boxes, 20f, 21 respiratory tract infections Filariasis lymphatic, 260 Guillain-Barré syndrome, 201, and, 162 Fluorescein staining, 255 201t true, 164 Focal limb weakness, 217–218 Guttate psoriasis, 240, 242f, Haemorrhage, 264 Food bolus obstruction, 108 249 Head injury, 76 booksfreForeign body, in the eye com, Gynaecological conditions, 29 neuroimaging of, 217b 250–251, 252f Gynaecomastia, 47 Head thrust test 101b me ooks e m me 310 • INDEX

Headache, 166–173 Hypercalcaemia Inflammatory bowel disease, 29, acute glaucoma and, 167, fatigue and, 133 91, 91b, 151 172 nausea and vomiting and, Inflammatory response, 25b, 36 acute intracranial pathology 223, 229 Inguinal hernia, 258, 259f of, 169–172 Hyperglycaemia, weight loss Inspection, 14b, 16 cluster, 166 and, 297 Instability, 214 ooksfreCSF results in, 171t Hyperinflation, 117f Intermenstrual bleeding, 289, diagnostic criteria for, 173t Hyperosmolar hyperglycaemic 292 features of, 173, 173t state (HHS), 222–223 Intermittent chest pain, 52–53 ‘first or worst’ presentation criteria for diagnosis of, 300t overview, 51b–52b, 63b–64b, of, 169 Hypertensionmeboo, 231 s 68, 68f meb frontal, 172–173 pulmonary, chronic dyspnoea Interstitial lung disease, 126f LP and CSF interpretation in, and, 127 Intestinal obstruction, 32, 32f 170b Hypoactive delirium, 78 Intracerebellar haemorrhage, medication overuse, 167 Hypoalbuminaemia, leg swelling 166 meningitis and, 166 and, 190, 194 Intracranial pressure, raised migraine and, 166, 167b Hypoglycaemia, 5, 270, 273, and headache, 167 nausea and vomiting and, 276, 299b symptoms and signs 229 symptoms of, 300t suggestive of, 199b overview of, 168, 168f Hyponatraemia, 88–89 Intravascular haemolysis, 136 raised intracranial pressure Hypotension, 141, 205 Investigations, 15 and, 167 Hypothyroidism, fatigue and, Iritis, 253f sinusitis and, 167 133 Iron deficiency, 136 subarachnoid haemorrhage Hypovolaemic shock, 264–265 Irritable bowel syndrome, 4t, ooksfrand, 166 e.c m clinical features of, 153b, 154 90, 90b ‘sudden-onset’, 172 Hypoxia 141 Ischaematic ECG changes, 51b, temporal arteritis (giant cell unexplained, 128 61–63, 61b arteritis) and, 167 mebo ksfIschaemia, m ECGme evidence o of, 35 tension, 167 I Ischaemic colitis, 151 vascular causes of, 166 Icteric leptospirosis (Weil’s Ischaemic ECG changes, in Head-tilt, chin-lift method, 10f disease), 174 acute dyspnoea, 119 Heart block, 279f Idiopathic cyclic oedema, 190 Ischaemic hepatitis (‘shock Heart failure Idiopathic intracranial liver’), 176 clinical features of, 116–118, hypertension, 167 Isolated scrotal skin oedema, 191f Illicit drug use or poisoning, 263 symptoms of, 194 delirium and, 83 Heartbeat, normal, 232, 237 Illusory sense of motion, 99 J Heatstroke, 141 Immobility, 214 Jaundice, 36, 174–182, Heavy menstrual bleeding, 288 Immunocompromised patients, 228 Hemiplegic gait, 221 fever and, 139 abdominal pain and, 43–44 Hepatic encephalopathy Immunoglobulin E (IgE), drug culprit for, 181 ooksfreefeatures of, 179–180 c m 243–244 full liver screen in, 181 West Haven grading of, 175t, Impetigo, 240, 241f hepatic causes of 174–176 179 Incontinence overview of, 178, 178f Hepatic tumours, jaundice and, continuous, 283 post-hepatic/biliary causes of, 176 functional/multifactorialmeboo sfre, m176–177mebook Hepatic vein thrombosis (Budd- 283 pre-hepatic causes of, 174 Chiari syndrome), 176 mixed, 282 screening investigations in, Hepatocellular insufficiency, 176 overflow, 282 181b Herniated bowel, 258 stress, 282 Jaw jerk, 108, 109f Herpes simplex virus infection, urge, 282 Jaw-thrust method, 10f 255 urinary, 282–286 Joint aspiration, 187, 188t Herpes zoster, 248f Infection Joint swelling, 184–188 HHS. see Hyperosmolar delirium and, 78 acute large, 187 hyperglycaemic state fatigue and, 130 articular conditions for, Hiatus hernia, 109 fever and, 138–139, 144 184–185 High fracture, 219 shock and, 269 evidence of, 188 High systemic venous vomiting and, 222 overview of, 186, 186 hydrostatic pressure, 190 weight loss and, 297–298 periarticular conditions of, Historyooksfree, 11, 11b–12b,co 11t Infectious diarrhoea, 90 184 HIV infection, risk of, 134 Infective endocarditis, 144b significant trauma of, 187 Holter monitoring, 237 Infective pustulosis, 249 Jones criteria, for diagnosis of Hydrocoele, 258, 263 Inflammatorymebooks back pain, 208 omrheumatic feverme, 148b oo 311 • INDEX

K Liver transplantation, in acute Mesenteric ischaemia, 28–29 Keratitis, 251–252 liver failure, 180b CT angiography for, 33 King’s College Hospital criteria, Lobar collapse, 119 Metabolic acidosis, 117b, 231 for l ver transplantation in Local lymph node dissection/ Metabolic alkalosis, 117b acute liver failure, 180b radiotherapy, 194 Metabolic bone disease 231 Kussmaul’s sign, 265 Loin pain, 44 Metabolic causes, 72 ooksfr Loss of consciousness, 99 Migraine, 166, 167b, 197 L Low back pain, 208–213 Minor disturbance, of Lactate, normal values of, 302t Lower airway disease, 112 consciousness, 72 Lactate dehydrogenase (LDH), Lower limb weakness, 220 Mirizzi’s syndrome, 176 normal values of, 302t Lumbarmebooks disc herniation, 208 e Miscarriage, bleedingmeboo due to, Lambert-Eaton myasthenic examination, 210f 288 syndrome, 202 Lumbar spine stenosis, 208 Mixed incontinence, 282 LDH. see Lactate examination, 210f, 211b Mobility problems, 214–221 dehydrogenase movements of, 211f abrupt decline in, 218 Left lower lobe collapse, 163f Lump, in breast, 46–49 accidental trip, 214 Left ventricular dysfunction, 264 Lung cancer, 165 acute illness, 214, 215b, Left ventricular failure, 118f Lung tumours, haemoptysis 216f, 218b Left-sided hernias, 258 and, 162 blackout/dizziness, Leg swelling, 190–195 Lung volumes, 127t 217–218 acute onset, 193 Lymphadenopathy gait assessment for, 215b overview of, 192, 192f fatigue and, 134 multifactorial, 214, 216f, We ls score, 193, 193t weight loss and, 297 219 Light-headedness, 99 Lymphatic filariasis, 260 related to stumble, 217 ooksfree.cdisorders causing, 96 Lymphoedema, leg swelling secondary, 214 overview, 104, 104f and, 191 significant injuries, 217 step-by-step assessment, ebookstep-by-step m assessment, 105 M 217–219me Likelihood ratio (LR), 17–18 Macleod’s Clinical Examination, Mobitz type I atrioventricular Limb weakness, 196–207 7 block, 280f bilateral Malaria parasites, 136 Mobitz type II atrioventricular acute-onset, 199 Male breast disease, 47 block, 279f overview of, 198, 198f Malignancy, of jaundice, 177 Modified Duke criteria, for proximal weakness with Malignant hyperthermia, 141 diagnosis of infective tenderness, 202 Malignant stricture, 108 endocarditis, 144b sensory signs or symptoms Mallory-Weiss tear, 150 Modified Glasgow criteria, for of, 201 Mantoux test, 134 acute pancreatitis prognosis upper motor neuron signs Massive haemoptysis, 35b of, 199–201 164–165 Monoarthropathy, motor neuron disease and, MCV. see Mean cell volume polyarthropathy presenting oksfree.co196–197 Mean cell volume (MCV), 136 as, 185 peripheral nerve lesions and, Mechanical back pain, 208, 213 Motor neuron disease, limb 196 Medical Research Council weakness and, 196–197, 206 space-occupying lesions and, (MRC) MRI spine, 212 196 dyspnoea scale, 112, 113b Multifactorial incontinence, spinal cord lesions and, 196 powermeboo rating, for limb s 283 m m boo stroke and, 196 weakness, 199, 199t Multifactorial mobility problems, transient ischaemic attack Medically unexplained 214, 216f and, 196 symptoms, 4–5 Multiple sclerosis, 197 unilateral, 199, 204, 204f Medication, prescribed, delirium Multiple spider naevi, 179 overview of, 204, 204f and, 83–84 Multisensory impairment, signs referable to, 206 Medication overuse headache, unsteadiness and, 97 sudden onset, 205 167 Muscle fatigability, 110f, 111, upper motor neuron signs Ménière’s disease, vertigo and, 201–202 of, 206 96 Muscle weakness, 110f, 111 Lipoedema, 191 Meningism, 169b, 169f Musculoskeletal disorders, 53 Liver failure, acute, 174, Meningitis chest pain and, 52 175b features of 169 Myasthenia gravis, 108, 197, identify patients with, headache and, 166 201 ooksfree179–180 com Meningococcal sepsis, 248 tendon reflex in, 202 liver transplantation in, 180b Meningoencephalitis, 205 Myocardial infarction, 51b, 264, monitor and reassess patients Menorrhagia, 288 268t eb o with, 180 Mentalmeboo test, 14–15, s14b e omMyositis, 202 312 • INDEX

N Oedema, 190 chronic/episodic, 28–29 Naloxone, 5–6, 75 bilateral, 190–191 referred, 25, 27f Narcolepsy, 271 cardiogenic lower limb, 190 somatic, 24 Nausea and vomiting, 222–231 dependent/gravitational, 191 true ‘colicky’, 24 acute renal impairment in, generalized, 190 in upper/lower abdomen oks225, 230–231, r 230b iatrogenic causes of, 190, 25f–26f, 33, 34f adrenal insufficiency and, 191b, 195 visceral, 24, 26f 223, 223b idiopathic cyclic, 190 Painless visible haematuria, anaemia and, 229 local causes of, 190–191 158–159 anorexia and, 229 non-pitting, 194 Palmar method, 247f assessment of, 224f unilateralmebooks, 190, 193, 195 Palpable abdominal,meb nausea o atypical presentation in, 227 Oesophageal dysphagia and vomiting, 228–229 blood examination for, dysmotility, 109 Palpable liver/suspected 228–229 structural, 108–109 malignancy, 180 causes of, 223b Oesophageal spasm, 52–53 Palpitation, 232–239, 236f chronic, 223, 228 228f Oesophageal varices, 150 assessment of, 239 diabetes and, 229 Oesophageal webs, 108–109 rhythm of, 237 diagnosis of, 225 Oesophagitis, 150 symptoms of, 237 eating disorder and, 229 Oliguria, 141 Pancreatic cancer, 28 functional vomiting, 223 Opioid toxicity, 5–6, 75 Pancreatic pain, 28 GI infect on and, 227, 229 Orchitis, 258 Paraproteinaemia, 137 headache and, 229 Organ failure, 73 Parenchymal lung disease, 112 hypercalcaemia and, 223, Oropharyngeal dysphagia, 108, Parkinsonism, features of, 221 oksfree229 o 110–111 110f Parkinson’s disease 108 illness severity of, 225 Orthostatic hypotension, 96 weight loss and, 294 infection and, 222 Orthostatic syncope, 270 Paroxysmal tachyarrhythmia, IV fluids for, 225 Osteoarthritis, 185 125 eboo medications and, 222, 226 Osteoporosismeboo, 212 fPattern m recognition, 17 metabolic abnormality in, 226 Overflow incontinence, 282 PE. see Pulmonary embolism metabolic disturbance and, Oxygenation Pelvic mass, leg swelling and, 222–223 adequacy of, in acute 191 pregnancy and, 223, 225 dyspnoea, 115 Pemphigoid, 242–243, 243f, raised intracranial pressure assessment of, 116b 247 and, 223 Pemphigus, 242–243, 243f renal failure and, 229 P Peptic ulcer disease, 28, 150, Nerve root compression, 206, Pain 222 206t of abdomen, 24–45, 30f Perianal disorders, 151 Neurogenic claudication, 213 acute, 24–25, 25f Perianal sensation, 212 Neurogenic shock, 265 acute gynaecological Pericarditis, diagnostic features Neuroleptic malignant pathology, 40 of, 62 syndrome, 141 acute lower, 38f Peripheral nerve lesions limb Neurologicalooks abnormality ee.co, 110f, bedside pregnancy test in weakness and, 196, 202f 111, 218, 220f patient with, 39 Persistent fever, 145 New-onset seizures, 205 chronicebooksf relapsing abdominal e PFTs. m see Pulmonaryebooks function Nicorandil, 151 pain, 42, 42f tests Nipple lesions, 47 clinical/laboratory features Pharyngeal pouch, 108 Non-pitting oedema, 194 suggest organic disease, Phosphate (fasting), normal Non-seminomatous germ cell 45 values of, 302t tumours (NSGCTs), 258 endometriosis and, 44 Photophobia, 250–251, Non-ST elevation myocardial jaundice, 43–44 255–256 infarction (NSTEMI). see left lower quadrant, 25b, 39 Phylloides tumours, 47 Unstable angina/NSTEMI leucocytes/nitrites on Pityriasis rosea, 240, 242f, 249 Non-ulcer dyspepsia, 29 urinalysis, 40 Placenta praevia, 288 Non-visible haematuria, 158 loin pain/haematuria 44 Pleural effusion, 119f Normocyt c anaemia, 136–137 lower GI symptoms with assessment of, 129 NSGCT see Non- alarm features 43 Pleural transudate, 129b sem nomatous germ cell palpable mass weight Pleuritic pain tumours loss, systemic upset/ history of, 62 oksfree com unexplained jaundice, 44 overview, 66, 66f O upper GI symptoms with Pneumonia, 51, 117f Obesity, chronic dyspnoea and, alarm features, 43 haemoptysis and, 162 128 characteristics of, 24–25 right upper lobe, 118f Obstructive shock, 264 inmebooksfre chest, 50–71 comPneumothoraxmeb, 51, 118, 118f 313 • INDEX

Polymyalgia rheumatica, 149 Pustular psoriasis, 240 241f nausea and vomiting and, Polypharmacy, 218 Pustules, 248–249 229 Polyps, 151 Pyrexia, 138, 212 Renal impairment, 194 Poor glycaemic control, 133 Pyrexia of unknown origin Renal tract disorders, 29 Po tal hypertension, 176 (PUO), 138 Respiratory failure, 75 Positive cultures, for fever, 145 assessment of, 148–149, Respiratory tract infection (RTI) Postcoital bleeding, 292 148b assessment of, 123 booksfrePost-ictal weakness (Todd’s classify type of 123 paresis), 205 Q evidence of, 115 Postmenopausal bleeding, 289, qSOFA score, 141, 141b features of, 123, 165 291–292 m book e gather informationmeboo to inform Post-radiation myelopathy, 199 R antimicrobial choice, 123 Post-void residual, 285 Radiation proctocolitis, 151 haemoptysis and, 162 Potassium, normal values of Radicular pain, 208, 213 predisposing factors of, 123 302t Radioisotope bone scan, 148 severity of, 123 Practical guide, 7–16 Rapid assessment, 7 Resuscitation Pregnancy Rapidly progressive paraparesis, in acute haemorrhage, 153b ectopic, bleeding due to, 288 199 in haematemesis, 153, 153b fatigue and, 133 Rash, 240–249 in rectal bleeding, 156 nausea and vomiting, 223, assessment of, 246f Returning travellers, fever and, 225 drugs that cause, 245b 139 vaginal bleeding and, 291 Reactive arthritis, 184–185 Reversibility, 127t Pregnancy-related bleeding, 288 Rectal bleeding, 150–157 Rhabdomyolysis, 231, 231t Presyncope, 99, 234 acute, 156 Rheumatic fever, Jones criteria ookdisorders freecausing, 96 c m angiodysplasia (arteriovenous for, 148b Pretibial myxoedema, 191 malformation) and, 151 Right heart failure, 190 Primary biliary cirrhosis, 177 clinical features of, 157 Right upper lobe collapse, 163f Primary headache disorders, colorectalmebooksf carcinoma and, .Rockall m risk scoreme, 154, oo 155t 173 151 Romberg’s test, 215b, 220 Primary sclerosing cholangitis, diverticular disease and, 151 RTI. see Respiratory tract 177 high-risk, 157, 157b infection Probability and risk, 3–4 inflammatory bowel disease Prosthetic joint, 187 and, 151 S Protein (total), normal values ischaemic colitis and, 151 SAH. see Subarachnoid of, 302t overview of, 156, 156f haemorrhage Proximal muscle weakness, 203 perianal disorders and, 151 Saliva, inadequate, 108 Pruritus, 77 resuscitation in, 156 San Francisco Syncope Rule, Pseudobulbar palsy, 108, 109t risk factor for, 157, 157b 279 Pseudoseizure, 270–271 upper GI source of, 156–157 Schatzki rings, 108–109 Pseudosyncope, 270–271 Recurrent fever, 145 Schistosoma haematobium Psoriasis, 240 Red boxes, 20f, 21 infection, 158–159 Psychogenicooksfree dyspnoea c, 125b Red cell fragments, 137 Sciatica, lumbar disc herniation Pulmonary congestion, 194 Red eye, 250–256, 251f and, 208 Pulmonary embolism (PE), 51, benign cause of, 256b Scleritis, 252, 253f 265, 268t bilateral, 255 Scleroderma, 109 assessment of suspected, examinationmebooksf of, 254f omScrotal kin, abnormalitiesmeboo of, 120f extraocular causes for, 256b 260 clinical suspicion of, 119, larger pupil in, 255 Scrotal swelling, 258–263 119t, 165 localized, 256 assessment of, 261f–262f, ECG in, 54b–58b, 59f severe pain in, 256 262 haemoptysis and, 162 Red flag features, 172b common causes of, 259f Wells score, 120f, 120t Referred pain, 25, 27f inflammation in, 263 Pulmonary funct on tests (PFTs), Reflex presyncope (vasovagal painful, 263 118, 127t episode), 96 palpable, 263 abnormal, in chronic Reflex syncope, 270 Scrotal wall oedema, 260 dyspnoea, 126–127 Renal anaemia, 231 Scrotum, examination of, 261b Pulmonary hypertension, chronic Renal colic, haematuria and, Seizures, 75, 205, 270–281 dyspnoea and, 127 161 assessment of, 276f, 278f Pulmonary oedema, 267 Renal disease, haematuria and, factors of, 277 ooksfrhaemoptysis and e.co, 162 159 features of, 273 274, 275b PUO. see Pyrexia of unknown Renal failure functional cause of, 274 origin fatigue and, 133 inpatient investigation for, 279 Purpura, 244, 248 legmebo swelling and ks, 190 eneuroimaging m meb in, 277b o s 314 • INDEX

Seizures (Continued) Spirometry, 127t Symptoms and disease, 5b, 5f pathology of, 276–277 Spondyloarthritides, 208 Synacthen test, 269 recurrent, 276 examination of, 210f Syncope, 270–281 trigger factors for, 271b Spondylolisthesis, 209 arrhythmia-related, 280–281 Self-diagnosis, 6 Spontaneous intracerebral assessment of, 276f, Sensory impairment, 87, 219 haemorrhage, 166 278f Sepsisooksfre, 138, 265 Spontaneous intraventricular features, 274, 275b Septic arthritis, 184 haemorrhage, 166 functional cause of, 274 Septic screen, 142b–143b ST elevation myocardial inpatient investigation for, 279 in specific patient groups, infarction (STEMI), ECG in, occult bleeding in, 279 146b–147b 51mebooksfrb, 54b–58b, 54f–56f, 61, with posturalmeb hypotension,k Serum albumin, oedema and, 61b 281 194–195 Stable angina, 52 precipitant of, 281 Sexually transmitted infections, Staphylococcus aureus, shock and, 273 haematuria and, 158 gastroenteritis caused by, 222 Syndrome of inappropriate ADH Shock, 31, 264–269 Status epilepticus, 276 secretion (SIADH), causes adrenal insufficiency and, 269 Steatorrhoea, 95 of, 89b assessment, 266f, 267–269 Stenosis, lumbar spine, 208 Systemic inflammatory bleeding in, 267 examination, 210f 211b response, abdominal pain cardiac failure and, 267 movements of, 211f and, 25, 25b clinical features of, 267, 267b Stevens-Johnson syndrome, Systemic inflammatory response diarrhoea and, 92 240–242, 248f syndrome, 265 immediate treatment of, 267 Still’s disease adult-onset, 149 infectionoksfree. and, 269 m Stones, haematuria and, 158 T intra-abdominal pathology, Stress incontinence, 282 Tachyarrhythmia, 268t 269 Stretch test paroxysmal, 125 physiology, 268f femoral nerve, 212f Tailored diagnostic guides, rapidly reversible causes of, sciaticmebooksfre nerve roots, 211f om18–19 meb s 268t Stroke, 108 Telemetry, 237 ‘Shock liver.’ see Ischaemic Bamford classification of, Temporal arteritis (giant cell hepatitis 207, 207b arteritis), and headache, 167, Simple airway manoeuvres, 10f limb weakness and, 196, 207 172, 172b Sinus tachycardia, 232 Stroke volume, 232 TEN. see Toxic epidermal assessment of, 239 Structural cardiac disease, 96 necrolysis causes of, 233b Structural heart disease, 195 Tendinopathies, 184 Sinusitis, headache and, 167 Subarachnoid haemorrhage Tendon reflexes, in myasthenia Skin disease, 240 (SAH), 166 gravis, 202 Skin dysfunction, 247b Subconjunctival haemorrhage, Tension headache, 167 Skin lesions, 47 251, 252f Tension pneumothorax, SOCRATES ( Site, Onset, Subcutaneous lesions, 47 264–265, 268t Character, Radiation, Sub-erythrodermic, 240 Testicular abnormalities, ooksfreeAssociated features, c Timing, m ‘Sudden onset’ headache, 172 258–260 Exacerbating factors and Superficial thrombophlebitis, Testicular tumour, 258, 259f Severity of the pain, 24 193 Thromboembolic risk factor, Sodium, normal values of, 302t Supraventricular tachycardia 238t eb Solitary lung mass, 163f (SVT)meboo, 232, 233f sf eeThrombolysis, m contraindications Somatic pain, 24 assessment of, 239 to, 207b Space-occupying lesions, limb SVT. see Supraventricular Thyrotoxicosis, weight loss and, weakness and, 196 tachycardia 294, 297 Speech/language therapy, Swallowing, difficulty, 110, TIA. see Transient ischaemic investigation/referral to, 110f, 110f attack 111 Swelling Tilt-table testing, 281 Spermatic cord abnormalities, leg, 190–195 Tissue hypoperfusion, 267 260 acute onset, 193 T-LOC. see Transient loss of Spherocytes, 137 overview of, 192, 192f consciousness Sphincter dysfunction, 212 Wells score, 193, 193t Todd’s paresis. see Post-ictal Spinal cancer, red flags for scrotal, 258–263 weakness possible, 209b assessment of, 261f–262f, Torsades de pointes, 235f Spinal cord lesions, limb 262 Torsion of the testis, 258–260 ooksfrweakness and, e.co196 common causes of, 259f Toxic epidermal necrolysis Spinal imaging, 213 inflammation in, 263 (TEN), 240–242, 242f Spinal infections, 209, 209b painfulebooksfr, 263 Toxins m, 72 Spinal tumour, 208 palpable, 263 Trajectory of diseasem boo, 121 315 • INDEX

Transient focal limb weakness, acute illness in, 285 W 197 aggravating factors of, 283b Weakness Transient focal neurological assessment of, 284f limb, 196–207 deficit 99 atrophic vaginitis in, 285 bilateral. see Bilateral limb Transient ischaemic attack (TIA), on coughing/sneezing, 286 weakness 271 medications aggravating, motor neuron disease and, ookslimb weakness e and, 196, 283b 196–197 205t multifactorial, 286 peripheral nerve lesions Transient loss of consciousness spinal pathology for, 285 and, 196 (T-LOC), 270–281 urge symptoms, 286 space-occupying lesions assessment of, 272f urinemebooksfr leak in, 285 and, 196me o k atypical features in, 271b Urinary tract cancer, risk factors spinal cord lesions and, cardiac features for, 273 for, 159b, 161 196 273b Urinary tract infection (UTI), stroke and, 196 complete recovery of, 273 symptoms of, 285 transient ischaemic attack definite, 273 Urinary tuberculosis, 158–159 and, 196 episode of, 274 Urticaria, 243–244, 244f unilateral, 199, 204, 204f Transverse myelitis, 199 UTI. see Urinary tract infection unsteadiness and, 97 Trauma, joint swelling and, 184 Weight loss, 294–298 Travellers, returning, fever and, V alcohol misuse and, 298 139 VA. see Visual acuity assessment of, 296, 296f Treatment, before diagnosis, Vaginal bleeding, 288–292 chronic disease and, 294 5–6 assessment of, 290f cognitive impairment and, 298 Trichiasis, 251 examination of, 291b, diabetes and, 299b Trifascicularook freeblock, 280f o 291f drug causes of, 295b Triglycerides, normal values of, in first trimester, 288 eating disorder and, 298 302t pregnancy and, 291 endocrine disorders and, 294 Troponin, elevation of, 62–63, inme second ooksand third trimester e, factors contributingmeb to, o298 63b 288 hypercalcaemia in, 297 True ‘colicky’ pain, 24 shock in, 291 hyperglycaemia in, 297 True haemoptysis, 164 Valve disorders, 264 infection and, 297–298 Tumours, haematuria and, 158 Varicocoele, 259f, 260 low mood and, 294–295, 298 Vasculitis, 244, 244f malignancy in, 294, 297 U Venous blood, normal values for medication and, 294, 298 UC. see Ulcerative colitis biochemical tests in, 302t neurological disorder and, Ulcerative colitis (UC), 91 Ventilation 294 rectal bleeding and, 151 adequacy of, in acute non-malignant GI disease Unilateral limb weakness, 199 dyspnoea, 115 and, 294 overview of, 204, 204f assessment of 116b screening for, 297 signs referable to, 206 Ventricular tachycardia (VT), severe systemic illness and, suddenoksfree. onset of, 205 m 234, 235f 298 upper motor neuron signs assessment of, 239 unintentional, 295 of, 206 Vertebral trauma and fracture, Weil’s disease. see Icteric Unilateral loin/flank pain, 32–33 208 leptospirosis Unilateral oedema, 190, 193, Vertigo Wells score 195 disordersmebooksfr causing, 96 cdeep m vein thrombosismeb, 193, o Unstable angina/NSTEMI overview of, 100, 100f 193t assessment of, 65 migraine and, 102 pulmonary embolism, 120f, ECG in, 54b–58b, 57f–58f red flag features in, 101, 120t Unsteadiness, 99 101b Wernicke’s encephalopathy, 84 disorders causes, 97 step-by-step assessment, Wheals, 249 overview, 106, 106f 101–102, 101b Wilson’s disease, 176 Unsteady with eyes open, 220 Vestibular neuronitis, vertigo Wolff-Parkinson-White Upper airway obstruction, 112 and, 96 syndrome, 232, 233f Upper GI malignancy, 150 Viral conjunctivitis, 250 Working diagnosis, 3 Urate, normal values of, 302t Visceral pain, 24, 26f Urea, normal values of, 302t Visible haematuria 158 X Urethritis, 188 high-risk features of, 161 Xanthochromia, 4 Urge incontinence, 282 Visual acuity (VA), 250 X-rays, for lumbar compression Urinalysisooksfree.c, 285 m Volume overload, 231 fractures, 212–213 for abdominal pain, 40 Vomiting. see Nausea and Urinary incontinence, 282–286, vomiting Y 286b VT.mebooksf see Ventricular tachycardia omYellow boxes,m 19, 20 bof This page intentionally lefto blank