Macleod’s

Clinical Diagnosis For Elsevier Commissioning Editor: Laurence Hunter Development Editor: Helen Leng Project Manager: Caroline Jones Designer/Design Direction: Miles Hitchen Illustration Manager: Jennifer Rose Illustrator: Antbits Diagnosis Macleod’sClinical Edited by Alan G Japp MBChB(Hons) BSc(Hons) MRCP Cardiology Registrar Royal Infirmary of Edinburgh Edinburgh, UK

Colin Robertson BA(Hons) MBChB FRCPEd FRCSEd FSAScot Honorary Professor of Accident and Emergency Medicine University of Edinburgh Edinburgh, UK

Associate Editor Iain Hennessey MBChB(Hons) BSc(Hons) MRCS Speciality Trainee in Paediatric Surgery Alder Hey Children’s Hospital Liverpool, UK

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First published 2013

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Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

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Printed in China Preface

‘Ninety per cent of diagnoses are made from the have been marginalised by the emergence history.’ of novel imaging techniques and disease ‘Clinical examination is the cornerstone of biomarkers. However, a focused clinical assessment.’ examination is critical to recognising the sick patient, raising red flags, identifying These, or similar platitudes, will be familiar unsuspected problems and, in some cases, to most students in clinical training. Many, revealing signs that cannot be identified however, will have noticed a glaring ‘dis­ with tests (for example, the mental state connect’ between the importance ascribed examination). to basic clinical skills during teaching and Our aim is to show you how to use your the apparent reliance on sophisticated core clinical skills to maximum advantage. investigations in the parallel world of clini­ We offer a grounded and realistic approach cal practice. Modern diagnostics have radi­ to clinical diagnosis with no bias towards cally altered the face of medical practice; any particular element of the assessment. clinical training is still catching up. We Where appropriate, we acknowledge the recognise that both teachers and textbooks limitations of the history and examination frequently fall into the trap of eulogising the and direct you to the necessary investi­ clinical assessment rather than explaining gation. However, we also highlight those its actual role in contemporary diagnosis. instances where diagnosis is critically Yet we come to praise the clinical assess­ dependent on basic clinical assessment, ment not to bury it. The history may not, by thereby demonstrating its vital and endur­ itself, deliver the diagnosis in 90% of cases ing importance. We wish you every success but it is essential in all cases to generate a in your training and practice, and hope that logical differential diagnosis and to guide this book provides at least some small rational investigation and treatment. Some measure of assistance. physical signs are now vanishingly rare and AJ certain aspects of the clinical examination CR

v Acknowledgements

On behalf of the editors and authors, I On a more personal note, I would like would like to thank Laurence Hunter for his to acknowledge the teaching of Mike Ford trust and support; Helen Leng for her as a major inspiration for this book and careful scrutiny and remarkable tolerance; to thank Deepa Japp for her encourage- Caroline Jones and Wendy Lee for their ment, optimism and extraordinary patience hard work and support; and everyone else throughout the long months of writing and who has volunteered ideas, comments, editing. assistance or a friendly ear. AJ

Figure sources

Figs 1.1, 2.1A&B, 4.2, 4.3, 6.1, 12.4, 12.5, 12.6, Figs 6.10, 6.12, 25.1: Hampton JR. 150 ECG 17.1, 18.1, 22.2, 27.2, 29.2: Douglas G, Problems, 3rd edn. Edinburgh: Churchill Nicol F, Robertson C. Macleod’s Clinical Livingstone, 2008. Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009. Figs 10.1, 12.3, 17.3, 25.6, 29.1, 29.4: Boon NA, Colledge NR, Walker BR. Figs 2.2A–C, 4.1, 5.1, 11.1, 12.2, 19.1, 22.1, Davidson’s Principles & Practice of Medicine, 23.1, 23.2, 23.3, 23.4: Ford MJ, Hennessey I, 20th edn. Edinburgh: Churchill Livingstone, Japp A. Introduction to Clinical Examination, 2006. 8th edn. Edinburgh: Churchill Livingstone, 2005. Figs 12.1, 12.8, 17.2, 17.4: Corne J, Pointon K. Chest X-ray Made Easy, Fig. 4.5A&B: Begg JD. Abdominal X-rays 3rd edn. Edinburgh: Churchill Livingstone, Made Easy, 2nd edn. Edinburgh: Churchill 2010. Livingstone, 2006. Figs 26.1, 26.2, 26.4, 26.6, 26.7, 26.11, 26.12, Figs 6.2, 6.7, 6.11, 25.3, 25.4, 25.5, 29.3, 29.5: 26.13, 26.14, 26.15, 26.17: Gawkrodger DJ. Hampton JR. The ECG in Practice, 5th edn. Dermatology ICT, 4th edn. Edinburgh: Edinburgh: Churchill Livingstone, 2008. Churchill Livingstone, 2008.

Fig. 6.3: Grubb NR, Newby DE. Churchill’s Fig. 26.3: Kumar P, Clark M. Kumar and Pocketbooks Cardiology, 2nd edn. Clark Clinical Medicine, 7th edn. Edinburgh: Edinburgh: Churchill Livingstone, 2006. Churchill Livingstone, 2009.

Figs 6.6, 6.8, 25.2: Hampton JR. The ECG Figs 26.5, 26.8, 26.9, 26.10: Bolognia J, Made Easy, 7th edn. Edinburgh: Churchill Jorizzo J, Rapini R. Dermatology, 1st edn. Livingstone, 2008. London: Mosby, 2003. vi Contributors

R Benjamin Aldridge Colin Mitchell MBChB MSc MRCP MRCS MBChB MRCP Clinical Research Fellow in Dermatology, Consultant Geriatrician, St Mary’s University of Edinburgh; Specialty Hospital, London, UK Registrar in Plastic and Reconstructive Surgery, Canniesburn Unit, Glasgow Jonathan C L Rodrigues Royal Infirmary, UK BSc(Hons) MBChB(Hons) MRCP(UK) Specialist Registrar in Clinical Radiology, Roland C Aldridge Severn School of Radiology, Bristol, UK MSc MRCS MRCP Clinical Lecturer, University of Edinburgh; Lynn M Urquhart Honorary Specialty Registrar in General MBChB, MRCP, DTMH Surgery, South East Scotland, Edinburgh, Specialty Registrar in Infectious Diseases UK and Clinical Research Fellow Medical Education, Ninewells Hospital and J Kenneth Baillie Medical School, Dundee, UK BSc(Hons) MRCP FRCA Clinical Lecturer, Department of Critical Hugh B Waterson Care Medicine, University of Edinburgh, MRCSEd Edinburgh, UK Specialist Registrar Trainee in Orthopaedics, Royal Infirmary of Xavier L Griffin Edinburgh, Edinburgh, UK MA MSc MRCS Specialist Registrar in Trauma and Orthopaedic Surgery, Warwick Medical School, University of Warwick, Warwick, UK

vii This page intentionally left blank Contents Abbreviations ...... xi . .

Part 1 Principles of clinical assessment 1 What’s in a diagnosis? ...... 3 2 Assessing patients: a practical guide ...... 7 3 The diagnostic process ...... 19 Part 2 Assessment of common presenting problems 4 Abdominal pain ...... 26 5 Breast lump ...... 44 6 Chest pain ...... 48 7 Coma and altered consciousness ...... 70 8 Confusion: delirium and dementia ...... 76 9 Diarrhoea ...... 88 10 Dizziness ...... 94 11 Dysphagia ...... 106 12 Dyspnoea ...... 110 13 Fatigue ...... 128 14 Fever ...... 136 15 Gastrointestinal haemorrhage: haematemesis and rectal bleeding ...... 148 16 Haematuria ...... 156 17 Haemoptysis ...... 160 18 Headache ...... 164 19 Jaundice ...... 172 20 Joint swelling ...... 182 21 Leg swelling ...... 186 22 Limb weakness ...... 196 23 Low back pain ...... 210 24 Mobility problems: falls and ‘off legs’ ...... 216 25 Palpitation ...... 224 26 Rash: acute generalised skin eruption ...... 232 27 Scrotal swelling ...... 242 28 Shock ...... 246 29 Transient loss of consciousness: syncope and seizures ...... 252 Appendix ...... 264 Index ...... 267 ix This page intentionally left blank Abbreviations

Abbreviations that do not appear in this list are spelled out in the main text.

ABG arterial blood gases GP general practitioner ACE angiotensin-converting enzyme Hb haemoglobin ACPA anti-citrullinated protein antibodies HIV human immunodeficiency virus AIDS acquired immunodeficiency HR heart rate syndrome ICP intracranial pressure ALP alkaline phosphatase ID infectious disease(s) ALT alanine aminotransferase IM intramuscular(ly) ANA antinuclear antibody INR International Normalised Ratio ANCA antineutrophil cytoplasmic IV intravenous(ly) antibodies IVU intravenous urogram/urography APTT activated partial thromboplastin time JVP jugular venous pulse ASMA anti-smooth muscle antibodies LDH lactate dehydrogenase ASO anti-streptolysin O LFTs liver function tests AST aspartate aminotransferase LIF left iliac fossa BM blood glucose meter reading LKM liver kidney microsomal (antibodies) BMI body mass index LLQ left lower quadrant BP blood pressure LP lumbar puncture bpm beats per minute LUQ left upper quadrant BS breath sounds MRA magnetic resonance angiography CK creatine kinase MRCP magnetic resonance CNS central nervous system cholangiopancreatography CPET cardiopulmonary exercise test MRI magnetic resonance imaging CRP C-reactive protein MSU midstream urine (specimen) CRT capillary refill time NSAID non-steroidal anti-inflammatory drug CSF cerebrospinal fluid PCR polymerase chain reaction CSU catheter specimen of urine PEFR peak expiratory flow rate CT computed tomogram/tomography PFTs pulmonary function tests CTPA computed tomographic pulmonary PR per rectum angiography PRN pro re nata; whenever required CVP central venous pressure PSA prostate-specific antigen CXR chest X-ray PT prothrombin time DC direct current PV per vaginam DMARDs disease-modifying anti-rheumatic RF rheumatoid factor drugs RIF right iliac fossa ECG electrocardiogram/ RLQ right lower quadrant electrocardiography RR respiratory rate EEG electroencephalogram/ RUQ right upper quadrant electroencephalography SC subcutaneous(ly) ENA extractable nuclear antigen SIRS systemic inflammatory response ENT ear, nose and throat syndrome ERCP endoscopic retrograde SSRI selective serotonin re-uptake cholangiopancreatography inhibitor ESR erythrocyte sedimentation rate TFTs thyroid function tests FBC full blood count TNF tumour necrosis factor GCS Glasgow Coma Scale (score) U+E urea and electrolytes GFR glomerular filtration rate UGIE upper gastrointestinal endoscopy GGT gamma-glutamyl transferase USS ultrasound GI gastrointestinal WBC white blood count

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Principles of clinical assessment

What’s in a diagnosis?...... 3 Assessing patients: a practical guide...... 7 The diagnostic process...... 19 This page intentionally left blank WHAT’S IN A DIAGNOSIS? 1

From differential diagnosis cause. For example, in a middle-aged man to final diagnosis presenting with fatigue, you might identify anaemia as the cause of his symptoms, but A diagnosis is simply shorthand for a the diagnostic process would not stop there. patient’s condition or disease process. The The next step would be to establish the ability to diagnose accurately is fundamen- cause of the anaemia. If subsequent labora- tal to clinical practice. Only with a correct tory investigations revealed evidence of diagnosis, or a short-list of possible diag- iron deficiency, you would need to - deter noses, can you: mine the cause of this. Gastrointestinal • formulate an appropriate sequence of investigations might uncover a gastric investigations tumour but, even then, further assessment • begin correct treatment and assess its would still be required to establish a effectiveness tissue diagnosis and stage the tumour. The • give an informed prognosis and make eventual ‘final diagnosis’ might be: iron- follow-up arrangements. deficiency anaemia secondary to blood loss from a T3, N1, M1 gastric carcinoma with In most cases, the construction of a dif- metastasis to liver and peritoneum. Clearly, ferential diagnosis is a stepping-stone to the the diagnosis of ‘anaemia’ would have been final diagnosis. This is a list of diagnoses, grossly inadequate! usually placed in order of likelihood, which Some conditions, especially functional may be causing the presentation. This list disorders such as irritable bowel syndrome, may be lengthy at the outset of assessment lack a definitive confirmatory test; here but will become progressively shorter as diagnosis relies upon recognising charac- you accumulate information about the teristic clinical features and ruling out patient’s condition through your history- alternative diagnoses – especially serious taking, examination and investigations. or life-threatening conditions. Such dis­ When one diagnosis begins to stand out orders are often referred to as diagnoses from the rest as the most likely cause of the of exclusion. patient’s presentation, it is often referred to as the working diagnosis. Investigations are Probability and risk then directed toward confirming (or refut- As almost all diagnostic tests are inherently ing) this condition and thereby arriving at imperfect, diagnoses should be regarded as a final diagnosis. This entire process may statements of probability rather than hard happen over a very short period of time; for facts. In practice, a disease is ‘ruled in’ example, establishing a final diagnosis of when the probability of it being present is acute ST elevation myocardial infarction in deemed to be sufficiently high, and ‘ruled a patient presenting with acute chest pain out’ when the probability is sufficiently should usually take less than 10 minutes. low. The degree of certainty required will Frequently, the identification of an abnor- depend on factors such as the consequences mality may only be the first step in the diag- of missing the particular diagnosis, the nostic process and additional assessment side-effects of treatment and the risks of is required to characterise a condition in further testing. Doctors must not become so greater detail or search for an underlying ‘paralysed’ by the implications of missing a 3 What’s in a diagnosis? 1 diagnosis that they admit the patient unnec- accurate). Xanthochromia (produced from essarily to hospital and/or investigate to haemoglobin breakdown within the CSF) levels that are not in the patient’s best inter- takes some time to develop and the sensi- ests and are unacceptable because of time, tivity of this test peaks at about 12 hours expense and intrinsic risk, e.g. radiation after symptom onset. The combination exposure. On the other hand, a high thresh- of a negative CT scan performed within 12 old of certainty, i.e. very low probability, hours of symptom onset and normal CSF is required to exclude potentially life- findings at 12 hours reduces the chances threatening conditions. In general, if the of the patient’s symptoms being caused situation is explained appropriately, most by an SAH to well below 1% – a level of patients will accept tests that will yield a probability acceptable to most clinicians diagnostic accuracy of less than 1% for and, if appropriately explained, to their acute life-threatening conditions. patient. The current diagnostic approach to sub- arachnoid haemorrhage (SAH) illustrates Special situations this. For a middle-aged patient who presents, fully conscious, with a history of Medically unexplained symptoms sudden (within a few seconds) onset of ‘the Sometimes it is difficult to correlate patients’ worst headache ever’, the chances of a diag- symptoms with a specific disease. This does nosis of SAH are approximately 10–12%. not mean that the symptoms with which The presence of some clinical findings, e.g. they present are made up or that patients photophobia, neck stiffness, cranial nerve are malingering – merely that we are not palsies, subhyaloid haemorrhage – will able to provide a physical cause for the increase these chances markedly but these symptoms. For patients in primary care, features may take time to develop. Even over 70% have symptoms that cannot be if clinical examination is unequivocally readily explained by a specific diagnosis. normal, the chances of SAH are 8–10%. Cur- Nevertheless, the symptoms are very real to rently, there is no simple bedside test for the patient and one of the major challenges, SAH and the initial investigation is nor- intellectually and practically, in primary mally a non-contrast CT scan. A positive care is to recognise which patients have scan will prompt appropriate treatment, physical disease. possibly involving neurosurgical or neuro- Clusters of symptoms in recognisable radiological intervention. A negative scan patterns, in the absence of physical and does not, however, exclude an SAH. The investigational abnormalities, are called accuracy of CT scanning in detecting SAH functional syndromes (Table 1.1). depends upon the experience of the report- In general, the greater the number ing individual, the nature of the scanner of symptoms, the greater the likelihood (principally, its resolution) and the time that there is a psychological component to interval between the onset of symptoms the presentation. Remember that patients and the scan (accuracy falls with time). A with chronic disease are more likely to scan performed within 12 hours by most demonstrate psychological aspects of their modern scanners has a diagnostic accuracy condition, especially depression, which of approximately 98%. But, given the mor- may, in turn, affect the mode of presenta- bidity and mortality of unrecognised and tion. Avoiding excessive and inappropriate untreated SAH, even this level of diagnostic investigation to ‘exclude’ diagnoses is accuracy is inadequate. For this reason, important, especially if patients have no patients with a negative CT scan have a specific ‘red flags’ in relation to their history, lumbar puncture. The CSF obtained must they are not in a recognised at-risk group, be examined by spectrophotometry in the and there are no abnormalities on clinical laboratory for xanthochromia (direct visual examination and simple bedside tests (Fig. inspection of the fluid is insufficiently 1.1 and Box 1.1). 4 What’s in a diagnosis? 1

Table 1.1 Common functional syndromes1 Treatment before diagnosis Sometimes, accurate diagnosis depends Syndrome Symptoms upon the patient’s response to treatment. Chronic fatigue Persistent fatigue2 In a few specific situations this may be syndrome life-saving as well as diagnostic. In any Irritable bowel Abdominal pain, altered patient with altered consciousness or acute syndrome bowel habit (diarrhoea or neurological dysfunction without a clearly constipation) and abdominal identifiable cause, two conditions need to bloating be excluded and treated immediately. Chronic pain Persistent pain in one or syndrome more parts of the body, Box 1.1 Symptoms and their relationship to sometimes following injury physical disease but which outlasts the More commonly original trauma2 • Chest pain Fibromyalgia Pain in the axial skeleton with trigger points (tender • Breathlessness areas in the muscles)2 • Syncope Chronic back Pain, muscle tension or • Abdominal pain pain stiffness localised below Less commonly the costal margin and above the inferior gluteal • Fatigue folds, with or without leg • Back pain 2 pain • Headache 1 In all cases, physical examination and investigation fail to reveal an • Dizziness underlying physical cause. 2Symptoms must have lasted more than 3 months. 10

Organic cause 8

6

4 3-year incidence (%) 2

0

Fatigue Oedema Dizziness Insomnia Chest pain Headache Back painDyspnoea Numbness

Abdominal pain Fig. 1.1 Common symptoms and disease. From Douglas JG, Nicol F, Robertson C. Macleod’s Clinical Examination 12E Edinburgh: Churchill Livingstone; 2009.

5 What’s in a diagnosis? 1

Hypoglycaemia can mimic conditions such cardiovascular function. The ‘pain ladder’ as epilepsy and hemiplegia. Check the approach is useful, but for patients in acute blood glucose level using a Stix test on a or severe pain, IV opioids titrated to the finger-prick sample. If the value is low, take clinical response are usually needed. a formal blood sample for laboratory blood glucose determination, but do not wait The patient who comes with for this result before giving treatment – a diagnosis give glucose or glucagon immediately. If Many patients have an idea of their own con- hypoglycaemia is the cause of the patient’s dition and, indeed, may begin the consulta- symptoms, response will normally occur tion by telling you their perceived diagnosis. within 5–10 minutes (rarely, in cases where In part this relates to improved education, there has been severe, prolonged hypogly- greater exposure to medical conditions caemia, this may take longer and residual through the media and the Internet. A neurological deficit may persist). patient who has previously had a condition Opioid intoxication is usually associated that has recurred e.g. asthma or urinary tract with altered consciousness, reduced respi- infection, or who has a flare-up of a chronic ratory rate and depth, and small pupils. The condition e.g. inflammatory bowel disease, diagnosis is rarely difficult in younger will often present in this way. Remember patients with a history or other features that many patients will be worrying about a of illicit drug use. However, these features specific diagnosis causing their presenting are not always present, and chronic opioid complaint. This is particularly the case for toxicity may develop over hours/ breast lumps, rectal bleeding and chronic days, particularly in elderly patients or headache, where the perception may be that those with renal impairment. Naloxone the only possible diagnosis is cancer. is a highly specific opioid antagonist with Self-diagnosis may also cause a delay in no agonist activity. Give 0.8 mg naloxone seeking medical help because the patient (SC, IM or IV) immediately. If there is any does not appreciate the significance of a response, further doses of naloxone will symptom or subconsciously may not want be required until no further reversal is to consider the possibility of serious disease. achieved. Remember that the half-life of Common examples include attributing naloxone is much shorter than that of the ischaemic chest pain to ‘indigestion’ and opioid that has been taken, so repeated stat. assuming that rectal bleeding is due to doses or an infusion are likely to be needed. haemorrhoids. There is one other situation where treat- One way of initially handling patients ment is necessary before, or to achieve, who come with a diagnosis is to let them diagnosis. It is unnecessary, unhelpful and express this openly and then to acknowl- inhumane to leave a patient in pain from edge their concerns. You must respect whatever cause. Put yourself in the patient’s these (indeed, the patient may well be right) place. There is never any indication to while taking care not to miss a more likely withhold analgesia from a patient in pain. diagnosis. In particular, do not take short- Concerns that you will ‘mask’ clinical signs cuts with any of the components of history e.g. by giving opioids to a patient with an taking, examination and investigation that ‘acute’ abdomen, encourage opioid toler- may be required. ance or addiction, and impair informed Patients with rare or unusual diseases consent are completely unfounded. In fact, often know much more about their condi- diagnostic accuracy is improved by making tion than you. Use this golden opportunity. the patient more cooperative, aiding the There is no loss of face in admitting your performance of investigations such as ignorance. Patients will respect you for ultrasound, and pain relief brings addi- your honesty and you can learn much from tional benefits in reducing catecholamine them about the disease and its treatment stimulation, improving respiratory and and effects. 6 ASSESSING PATIENTS: A PRACTICAL GUIDE 2

Introduction • the routine work-up: history, physical Before you can diagnose patients you must examination and basic tests targeted, supplementary investigations first obtain the necessary clinical and inve­ • . stigative information. Diagnostic success The optimal approach to the routine work- depends upon the accuracy and complete- up varies, depending on the stability and ness of this initial data gathering so your illness severity of the patient: history-taking and examination skills are • Acutely unwell patients require a crucial. During clinical training, you may rapid, targeted evaluation (‘ABCDE have been taught a fairly idealised and rigid assessment’) for life-threatening ‘method’ of patient assessment. However, disorders and major derangements of in everyday practice, a more flexible, fluid physiology. approach is preferable; this will allow you • Patients who are stable, including to adapt to the clinical situation and acquire those initially assessed by the ABCDE the essential information in the most effi- approach, should have a full history and cient manner. clinical examination, as outlined below Traditionally, the assessment of patients (‘full clinical assessment’), alongside basic has been divided into two distinct phases: tests relevant to the specific presentation. • The approach to frail, elderly patients • the clinical assessment: history and may need to be modified to take account physical examination of differences in the nature of illness • diagnostic investigations. presentation, e.g. multi- versus single- organ pathology; significant functional At least in the hospital setting, this dis- decline secondary to minor illness tinction is highly artificial due to the easy (p. 15). and real-time availability of basic tests such as ECG, CXR, glucose meter reading and Rapid assessment of ABG, and routine laboratory blood tests the sick patient such as FBC, U+E and LFTs. Wherever The ABCDE assessment (see Clinical Tool: appropriate, these simple tests should be the ABCDE assessment) combines prompt carried out in tandem with the clinical identification of life-threatening pathology assessment to form a ‘routine patient work- with immediate management of any abnor- up’. The information from all of these malities detected, prioritising those that sources is combined to form a working or are most rapidly fatal. Take an ABCDE differential diagnosis. Where necessary, approach if the patient: further targeted investigation can then be undertaken to confirm the suspected diag- • appears unwell or is unresponsive nosis, narrow the differential diagnosis e.g. • exhibits evidence of acute physiological exclude high-risk conditions, inform prog- derangement on basic observations (HR, nosis and guide management. RR, BP, SpO2, temperature) Thus, in this book, we advocate the fol- • has features of a serious acute problem lowing system for patient evaluation: in any organ system. 7 Assessing patients: A practical guide 2

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

B1 Give high concentration O2 B2 Assess rate, depth and symmetry If respiratory effort inadequate: of breathing, noting: • Get help! • poor respiratory effort: ↓↓ RR, feeble, • Manually ventilate via bag-valve-mask shallow breaths • Consider a trial of naloxone. • high respiratory effort: RR > 20/min, use of accessory muscles, visibly tiring • asymmetrical chest expansion B3 Check for tracheal deviation If severe respiratory distress and signs of tension B4 Percuss and auscultate chest, noting: pneumothorax (p 246), perform immediate • Hyperresonance – suggesting needle aspiration. pneumothorax If widespread wheeze, check for signs of • Dullness – suggesting pleural effusion, anaphylaxis (see below). If present, manage collapse, consolidation as described; otherwise, give nebulised • ↓ breath sounds – suggesting collapse bronchodilator. pneumothorax, pleural effusion, • Wheeze – suggesting bronchospasm • Crackles – suggesting pulmonary oedema, fibrosis, consolidation • Bronchial breathing suggesting consolidation

B5 Record SpO2 on high FiO2 If chronic type 2 respiratory failure or severe

COPD, titrate FiO2 to patient’s baseline SpO2 (if known) or 90-92%. In all other critically ill

patients, continue high FiO2.

8 Assessing patients: A practical guide 2

Clinical tool: The ABCDE assessment—cont’d What to look for How to respond C. CIRCULATION C1 Check colour & temperature of hands In patients with evidence of shock, e.g. ↑CRT, • Cold, clammy, blue, mottled? cold peripheries, thready pulse, ↑HR, ↓BP: • Pink and warm? Secure IV access (large bore if possible) C2 Measure capillary refill time (CRT) If VT, attempt defibrillation with a synchronised Press firmly over fingertip for 5s, release DC shock (ask anaesthetist to sedate if pressure then record time taken for skin to conscious) return to normal colour If bradycardia: • ≤2 s is normal • give atropine 0.5–3 mg • ≥2 s suggests ↓peripheral perfusion • if no response or HR < 40/min, get expert C3 Palpate radial and carotid pulse: help and consider IV adrenaline or • tachycardia: >100 bpm transcutaneous pacing • bradycardia: <60 bpm (or inappropriately If tongue/throat swelling, severe respiratory slow for context) distress, widespread wheeze and/or a new • Thready, weak – suggesting ↓cardiac rash, assume anaphylaxis: output, e.g. hypovolaemia • Stop any potential trigger • Bounding – suggesting hyperdynamic • Give 0.5 mg IM adrenaline (anterolateral circulation, e.g. early sepsis aspect of middle 1/3 of the thigh) C4 Measure blood pressure • Give fast IV fluids C5 Assess height of JVP at 45° • Get immediate anaesthetic help C6 Auscultate the heart for: Otherwise, give fluid challenge unless evidence • Murmurs of pulmonary oedema • 3rd heart sound/gallop rhythm C7 Attach ECG monitor and review rhythm: • Regular broad complex tachycardia – likely VT (p. 227) • Regular narrow complex tachycardia, e.g. sinus tachy, SVT, A flutter (p. 225) • Irregular tachycardia – likely atrial fibrillation (p. 226) • Bradycardia ≤40 bpm, e.g. 2nd or 3rd degree AV block (p. 261) C8 Perform a 12-lead ECG if chest pain (p. 52) or arrhythmia D. DISABILITY D1 Check blood glucose meter reading If BM < 3 mmol/L: (‘BM’) • Send blood for formal lab glucose measurement D2 Record Glasgow Coma Scale (p. 71) • Give immediate IV dextrose If ↓GCS • 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 minute and consider further doses if partial response

9 Assessing patients: A practical guide 2

Clinical tool: The ABCDE assessment—cont’d What to look for How to respond D3 Take a ‘3D’ history Description of symptoms Drugs and allergies Disorders/Disability prior to this illness D4 Examine pupils with a pen torch: • Bilateral pinpoint – suggesting opioid intoxication or pontine lesion • Bilateral dilated – suggesting cocaine/ amphetamine intoxication or atropine • Unilateral fixed, dilated suggesting ↑ intracranial pressure or 3rd nerve palsy E. EXPOSURE E1 Record body temperature If temperature < 34°C, confirm core temperature E2 Fully expose the body (preserve dignity), with a low-reading thermometer and start looking for: rewarming measures • Bleeding or injuries Repeat the ABCDE assessment if a significant • Rashes abnormality was noted at any stage. • Jaundice Refer to the relevant chapter for further • Medic alert bracelet assessment of specific presentations, e.g. E3 Examine the abdomen for distension, dyspnoea, shock, chest pain, ↓GCS, tenderness, guarding, rigidity abdominal pain, headache.

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.

10 Assessing patients: A practical guide 2

Repeat the process to assess the effects of record and medical case notes than by interventions or in the event of any further simply asking the patient, particularly deterioration. Protect the spine at all times with respect to the outcome of previous if there is any suspicion of recent trauma. investigations. • If available, use a repeat prescription or Routine assessment of GP record to obtain the specific names the stable patient: The full and dosages of drugs, then ask patients clinical assessment if they are actually taking the medicines Use Macleod’s Clinical Examination, for a as prescribed. Ask about the use of any comprehensive guide to history taking and additional over-the-counter or herbal systems-based clinical examination. The remedies. Also ask the patient about following is an aide-mémoire with an em­ side-effects of any current or previous phasis on practical tips and avoidance of medications. common pitfalls. The history Think of the history, not as a series of ques- Box 2.1 An alcohol history tions to be asked, but as a body of informa- tion that needs to be gathered using all • Quantity and type of drink available sources (Table 2.1 and Boxes • Daily/weekly pattern (especially binge 2.1–2.3). drinking and morning drinking) In particular, note: • Usual place of drinking • A supplementary account of the current • Alone or accompanied problem is essential in patients • Purpose of drinking presenting with confusion or transient • Amount of money spent on alcohol loss of consciousness. • Details of the past medical history are • Attitudes to alcohol usually better established from the GP

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 Patient, relatives, carers, events witnesses, GP Past history Current and previous medical disorders Medical case notes, GP Previous investigations and results record, patient Efficacy of previous treatments Drugs and allergies All prescribed and over-the-counter Repeat prescription, GP medications and doses; adherence to record, patient, relatives, prescription; recent changes to carers medications; adverse drug reactions (what drug? what happened?) Environmental risk factors Smoking, alcohol (Box 2.1), drug Patient, relatives misuse* (Box 2.2), travel, pets, sexual history* (Box 2.3) Impact and consequences Ability to mobilise, self-care, undertake Patient, relatives, friends, of illness (if relevant) activities (work, driving, hobbies) carers, GP Effects on employment, family, finance, confidence *Only if appropriate.

11 Assessing patients: A practical guide 2

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 • How often and how much? moment? • How long have you been taking drugs? • Is your partner male or female? • Any periods of abstinence? If so, when and • Have you had any (other) sexual partners in why did you start using drugs again? the last 12 months? • What symptoms do you have if you cannot • How many were male? How many female? obtain drugs? • Do you use barrier contraception – • Do you ever inject? sometimes, always or never? • Do you ever share needles, syringes or • Have you ever had a sexually transmitted other drug paraphernalia? infection? • 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?

elements of the clinical examination that have traditionally been considered routine The clinical examination are only required in specific circumstances. A routine ‘screening’ clinical examination These include examination of the fundi, (see Clinical tool: The 20-step clinical exam- rectum, genitalia, breasts and individual ination) is required in most patients. Some joints.

Clinical tool: The 20-step clinical examination 1. Assess general demeanour, appearance, 9. Inspect and palpate the praecordium. movements, odour, nutrition and 10. Auscultate the heart. hydration. 11. Examine the lung fields from the front. 2. Record routine observations, including

temperature, pulse, BP, RR and SpO2. Sit the patient up at 90° 3. Examine the hands: temperature, capillary 12. Inspect the trunk (front and back) for refill, colour, nails, tremor, asterixis and rashes, moles, spider naevi, scars etc. joints. 13. Palpate for lymphadenopathy and goitre; 4. Feel the radial and brachial pulses. check for bony/renal angle tenderness, 5. Inspect the face and eyes (Tables 2.2 and sacral oedema. 2.3). 14. Examine the lung fields from the back. 6. Examine the mouth: dental hygiene, cyanosis, tonsillar inflammation, ulcers, Lay the patient flat blisters, candidiasis. 15. Examine the abdomen and hernial Position the patient at 45° orifices. 16. Examine the legs: 7. Assess the height and waveform of the • Inspect for swelling, colour, rashes, JVP and feel the carotid pulse. skin changes. 8. Inspect and palpate the trachea: check • Feel for pitting, temperature, pulses, centrality and cricosternal distance. capillary refill.

12 Assessing patients: A practical guide 2

Clinical tool: The 20-step clinical examination—cont’d 17. Perform a neurological examination of the • Check reflexes: supinator, biceps, legs: triceps. • Check tone, look for wasting, abnormal • Test sensation: C5–T1 dermatomes movements. (see Fig. 22.1, p. 200). • Assess power: flexion/extension of • Test coordination: rapid alternating hips, knees, ankles. movements and finger–nose test • Check reflexes: knees, ankle jerks, (Fig. 2.2A). plantar response. 19. Screen for cranial nerve abnormalities: • Test sensation: L2–S1 dermatomes • Test visual acuity and pupillary (see Fig. 22.1, p. 200). reactions; check for homonymous field • Test coordination: heel–shin test defects. (Fig. 2.2B). • Check eye movements (characterise • Assess transfer and gait (p. 217). nystagmus) and hearing in each ear. • Test sensation above the upper lip and Sit the patient up over the maxillae and eyelids. 18. Perform a neurological examination of the • Facial movements: raise eyebrows, arms: show teeth, close eyes against • Check tone, look for wasting, abnormal resistance, blow out cheeks. movements. 20. Perform urinalysis and bedside blood • Assess power: abduction/adduction of glucose measurement (‘BM’). shoulders, fingers; flexion/extension of elbows, wrists; grip strength.

Table 2.2 Characteristic facies and their features, 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 retraction Cushing’s disease ‘Moon face’, plethoric complexion and buffalo hump over lower cervical– upper thoracic spine Parkinsonism Expressionless facies and drooling Myasthenia gravis Expressionless facies with bilateral ptosis Myotonia dystrophica Frontal baldness and bilateral ptosis Superior vena caval Plethoric, oedematous face and neck, chemosis of conjunctivae, obstruction prominent veins and venules Malar flush Dusky redness of cheeks seen in low cardiac output, e.g. mitral stenosis; also seen in myxoedema Systemic lupus Rash over nose and cheeks – ‘butterfly rash’ erythematosus Progressive systemic Taut skin around mouth with ‘beaking’ of nose sclerosis

13 Assessing patients: A practical guide 2

• If a relevant abnormality is detected on Table 2.3 Signs of systemic disorders affecting the routine examination, perform a the eyes detailed examination of the relevant Colour of sclera Disorder system (see Macleod’s Clinical Blue Chronic iron deficiency Examination). Osteogenesis imperfecta • Additional examination steps required Yellow Jaundice but not for a specific presentation are described carotenaemia in the relevant chapters: Red Scleritis in vasculitic disorders • testicular examination (p. 244) and rheumatoid disease • breast examination (p. 47) • examination for meningeal irritation Black Scleromalacia in rheumatoid (p. 167) disease • examination of lumbar spinal movements (p. 213) Additional steps • ‘confusion assessment method’ for • You will have gained an impression of detection of delirium (p. 78) higher mental function whilst taking the • assessment of gait (p. 217) history. If you suspect impaired mental • head thrust test (p. 99) function, perform an Abbreviated • Dix–Hallpike manœuvre (p. 101) Mental Test (AMT; Box 2.4). • jaw jerk (p. 107).

Fig. 2.2 Tests of coordination. A. Finger–nose test. B. Heel–shin test. 1 2

A

B

14 Assessing patients: A practical guide 2

Box 2.4 Abbreviated Mental Test Approach to the frail, elderly patient (Score 1 for each correct response) Frail, elderly patients comprise a major pro- • How old are you? portion of acute medical and surgical • What is the time just now? admissions and are frequently challenging to assess. They often present in a vague, • What year is it? non-specific way and it can be difficult to • What is the name of this place? (Where are tease out a specific culprit for the acute we just now?) deterioration against a background of mul- Please memorise the following address: 42 tiple chronic comorbidities and functional West Street limitation. One unfortunate consequence of • When is your birthday (date and month)? this is the tendency to categorise elderly patients into a small number of ‘diagnostic • What year did the First World War begin? dustbins’. Instead of a differential diagno- • What is the name of the Queen? sis, the impression at the end of the clerking • Can you recognise … ? Two people? may read ‘Off legs’, ‘Acopia’, ‘Mechanical • Count backwards from 20 to 1 fall’, ‘Social admission’ or ‘Collapse ?Cause’. Such impressions could be correct, but they • Repeat the address that I gave you are not diagnoses. Normal score: 8–10 The challenges of acute geriatric assess- Source: Hodkinson HM 1972 Evaluation of a mental test score ment are often compounded by a miscon- for assessment of mental impairment in the elderly. Age and ageing. 1: 233–238. ception that the process must always be painstaking and laborious. Comprehensive geriatric assessment does require time and Basic investigations input from multiple health professionals but it is often preferable to defer this for The specific tests required for a routine a period than to undertake it poorly work-up will depend on the presenting in the midst of a busy acute admission. problem. For example, an ECG is manda- Where time and personnel are limited, a tory in patients with acute chest pain but focused approach is required to identify not in those with chronic low back pain. important problems rapidly and reliably, The recommended tests for different clini- and to produce a useful list of differential cal presentations are specified in the rele- diagnoses. vant chapters in Part 2. In several chapters Chronological age is a poor marker for we have also provided detailed guidance identifying who would benefit from a tai- on how to interpret the results of these tests, lored ‘geriatric’ assessment. Some elderly including the following: patients present with a single specific acute • the ECG in chest pain (p. 52) pathology, e.g. the fit 90-year-old with an • interpretation of arterial blood gases acute myocardial infarction. This patient (p. 114) may require rapid coronary revascularisa- • interpretation of pulmonary function tion rather than a comprehensive geriatric tests (p. 125) assessment. Conversely, a 59-year-old with • pleural tap and analysis of pleural fluid multiple medical problems and medica- (p. 127) tions, and an inability to mobilise may • lumbar puncture and CSF analysis (p. 168) benefit greatly from a geriatric assessment. • a septic screen (p. 140) Identification of frailty is difficult, and • further assessment of anaemia (p. 134) debate continues over robust criteria. An • further assessment of renal failure (p. 192) inclusive approach to identify as many • further assessment of hyponatraemia patients as possible that would benefit (p. 86). from comprehensive geriatric assessment is

15 Assessing patients: A practical guide 2 preferable, but no method can be fully sen- • How far can you walk? sitive or specific. As a guide, the presence • Can you manage a flight of stairs? of more than one of these criteria suggests • What stops you? frailty: • Do you have a cough? • inability to perform basic activities of • When did you last move your bowels? daily living (ADLs) in the 3 days prior • Do you have any difficulty passing to admission urine? • a stroke in the past 3 months • Have you been incontinent? • depression • Have you lost weight? • dementia • Have you fallen or blacked out? • a history of falls • Do you get dizzy? • one or more unplanned admissions in • Do you have any weakness or the past 3 months numbness in your face or limbs? • difficulty in walking • Are you forgetful? • malnutrition An exhaustive ‘social history’ during the • prolonged bed rest initial assessment is often unproductive: • incontinence. • Establish the key information regarding Specific tips for assessment functional status and social/care arrangements but avoid replicating of the elderly/frail patient work that will be undertaken by other An accurate history is important in the frail, health professionals, e.g. occupational elderly patient, but may be significantly therapist. more difficult to obtain: • Do not overlook specific issues in the • Use open questions sparingly. social history, e.g. alcohol intake, • Clarify vague terms e.g. ‘a while’, and driving. question inconsistencies e.g. if patients Inspection cannot recall the details of their ‘fall’, Certain aspects of the examination demand how do they know that they did not closer attention in the elderly: black out? • Wherever possible, complement the • Observe carefully for evidence of patient’s history with collateral dehydration, malnutrition, constipation, information from witnesses, carers, injuries and pressure sores in frail, relatives, other health professionals and dependent or demented patients. previous notes. • Consider a formal swallow test to exclude aspiration in patients with Frail patients may tire easily during recurrent pneumonia. the history and examination: Elderly patients with abdominal • If necessary, perform the assessment in pathology may present ‘atypically’: ‘bite-sized’ chunks. • If there are multiple symptoms, address • Consider perforation of a viscus or them in order of importance to the ischaemic bowel, even in the absence of patient, unless they are ‘red-flag’. abdominal rigidity – have a low • If the list of established diagnoses is threshold for imaging. long, determine which problems are • Percussion and palpation of the bladder ‘active’ (‘When did you last have may reveal ‘asymptomatic’ urinary angina?’) and explore those relevant to retention in patients with non-specific the current presentation in detail. deterioration. Prioritise important and common Most elderly patients are perfectly problems in the systemic enquiry: capable of following the instructions

16 Assessing patients: A practical guide 2

required for a standard neurological may aid a subsequent diagnosis of examination. delirium. • Try to overcome sensory impairment Depression is common in elderly with aids (put the hearing aid in!), hospitalised patients: repetition and demonstration. • Maintain a high index of suspicion but • If the patient is struggling to cooperate, remember that low mood may be obtain equivalent information through situational and appropriate (‘stuck in simple observation of the patient’s hospital’). movement, passive or provoked. • Exclude organic disease before • Pay close attention to muscle bulk, gait attributing ‘biological symptoms’ to (p. 217), visual acuity and functional depression. movements of the arms and hands. • Assess joint movements in conjunction Basic investigations have a higher with the neurological examination. yield in elderly patients due to the Screening for cognitive impairment is an increased prevalence of disease and the integral part of examination in the frequent absence of characteristic clinical elderly: features: • Use objective tests, e.g. AMT (see Box • Perform FBC, U+E, ECG and CXR in 2.4) or confusion assessment method any elderly patient with non-specific (p. 78), rather than general impressions. deterioration. • Record an AMT score, even if the • Have a low threshold for considering patient appears to have intact cognition additional tests such as CRP, LFTs, – documentation of a normal baseline calcium or TFTs.

17 This page intentionally left blank THE DIAGNOSTIC PROCESS 3

With time and practice, most trainees in is particularly helpful for conditions clinical medicine will acquire the skills nec­ where there is an obvious abnormality of essary to take a patient’s history, perform a appearance, e.g. skin conditions. Moving competent physical examination and inter­ visual images can be even more evocative. pret basic tests. The next stage is to translate Ornithologists commonly describe how the resulting raw clinical data into a diag­ they recognise a bird by its ‘jizz’ – a com­ nosis. The primary aim of this book is to bination of its appearance, movement and show you how this can be achieved. behaviour. Some medical conditions, e.g. Parkinsonism, are readily identified in a Diagnostic methods similar way. The exact method by which a diagnosis is Pattern recognition can be a powerful reached may seem somewhat mysterious to technique, particularly when employed by newcomers to clinical medicine. The best an experienced clinician. In theory, it diagnosticians invariably use several com­ requires you to have experienced an identi­ plementary skills which have been honed cal, or at least very similar, presentation through years or decades of experience; previously, and so is less suited to the new­ these are often applied subconsciously and comer. However, the diagnostic method hence are difficult to explain. Consequently, most commonly utilised by medical stu­ the diagnostic process may be taught poorly dents and junior doctors is actually a variant and, most often, is simply experienced at of this approach. The major difference is second hand, by observation. that their ‘database’ of patterns corresponds As an inexperienced clinician you cannot to the descriptions of signs and symptoms expect to achieve diagnostic skills over­ provided in textbooks rather than previous night, but this book aims to show you how real-life examples. This has several major to make a diagnosis in the great majority disadvantages. Firstly, descriptions of of the most commonly encountered and physical signs from textbooks or lectures, important clinical presentations. As a first e.g. pill-rolling tremor or festinating gait, step, it will be helpful to consider two are a poor substitute for experiencing them well-established and sharply contrasting at first hand. Textbooks also tend to present approaches to diagnosis: pattern recogni­ an idealised account of the way in which tion and probability analysis. These illnesses present, emphasising classical methods illustrate some fundamental prin­ signs and symptoms that are often rela­ ciples of diagnostic reasoning but both have tively rare in everyday clinical practice. major drawbacks that limit their applica­ Similarly, a reliance on textbook learning tion in everyday practice. does not allow you to appreciate the multi­ ple subtle variations in presentation that Pattern recognition exist for the same disorder. Pattern recogni­ The diagnosis is made by recognising char­ tion may fail even the most experienced acteristic features of the patient’s illness clinician when conditions present atypi­ that you have encountered previously in cally or when characteristic features are other patients with the same disorder. For masked, e.g. the patient with acute coro­ most people, visual information is a strong nary syndrome who has sharp chest pain prompt to memory recall, so the technique rather than crushing or heavy discomfort, 19 The diagnostic process 3 or the diabetic patient who has no pain or cause of headache, myalgia and fever in a discomfort at all because of coexistent auto­ previously fit, untravelled, 19-year-old in nomic neuropathy. This tendency is greatly the UK in the middle of a winter influenza amplified when these conditions have not epidemic is vanishingly small, but it will be been experienced repeatedly in the real very much higher for a similar individual world. seen in sub-Saharan Africa. Another problem with using LRs to Probability analysis calculate probability lies in trying to com­ For the great majority of conditions, no bine information from multiple symptoms, single symptom, sign or test will have suf­ physical signs and test results. This can be ficient power to enable you to rule in or done to a limited extent but is hampered by rule out a diagnosis. However, each will a need for the findings to be independent alter the probability of the diagnosis to a of each other – an area of considerable greater or lesser extent. The diagnostic uncertainty. In practice, it is not usually weighting of a particular symptom, sign possible to combine more than two or three or test can be expressed as a likelihood LRs outside a validated scoring system. For ratio (LR). The LR is the proportion of readers interested in using LRs to calculate patients with the specific disease who diagnostic probabilities, we recommend exhibit the particular finding, divided by Evidence Based Physical Diagnosis, by the proportion without the disease who Steven McGee (2nd edn 2007, Saunders). also exhibit the same finding. Note that In everyday practice, this approach has the finding may be positive e.g. presence of two major applications. Firstly, knowledge a particular sign, or negative e.g. absence of of LRs for different symptoms, risk factors a particular sign. or clinical signs allows you to identify those If the LR value is >1, the chance of the with the highest diagnostic value. As a disease is increased; the higher the value, rough rule of thumb, LR values between 0.5 the greater the likelihood of the disease. If and 2 are rarely helpful, whereas values ≥5 the LR value is <1, the chance of the disease or ≤0.2 are usually clinically useful. Sec­ being present is reduced. For example, an ondly, for some conditions, LRs have been LR of 5 increases the absolute probability of used to develop and validate diagnostic a disease by approximately 30% and an LR algorithms that allow the condition to be of −0.2 decreases it by 30%. ruled in or ruled out based on thresholds of LRs are available for many clinical fea­ probability. Good examples are the Wells tures and tests. In theory, this allows you to scores for deep vein thrombosis (p. 189) and use the information derived from your pulmonary thromboembolism (p. 118). assessment to calculate the probability of a disease. However, before you can do this, A different approach: you need to know the pre-test probability of the patient having the disease in question Tailored diagnostic guides – in other words, the prevalence of the For the inexperienced clinician, neither disease in a population with similar base­ fuzzy pattern recognition nor rigid prob­ line characteristics to your patient. Among ability analysis offers a practical and satis­ other things, the pre-test probability may be factory approach to diagnostic reasoning. influenced by a patient’s age, sex, ethnic We therefore advocate an alternative system origin, occupation, social background and that takes positive elements from both past history, as well as the clinical setting of these methods but is easy to apply in within which you work (rural versus urban everyday practice and does not rely on vast environment, primary care versus second­ amounts of clinical experience. We set out ary care). For example, the probability of this system in the form of individual ‘diag­ Plasmodium falciparum malaria being the nostic guides’ for all of the major presenting

20 The diagnostic process 3 clinical problems. As your experience How to use the diagnostic extends and deepens, you will start to use guides your own unique methods but, at the outset, The first step in using the guides is to deter­ following an established framework may mine which, if any, is the most appropriate help to prevent crass and potentially dam­ for the patient in front of you. Ensure that aging errors. you have clarified the true nature of the Each chapter in Part 2 is a diagnostic problem; a patient who presents with a fall guide or ‘road-map’ for a common clinical may have had a blackout, whilst a patient presentation. The purpose of the guides is who has had a ‘funny turn’ may have expe­ not to tell you which questions to ask and rienced focal limb weakness. In general, which examination steps to perform – this you should match the guide to the patient’s was outlined in Chapter 2 and will be predominant complaint. However, if the broadly similar for most presentations. presentation entails two or more related Rather, it is to explain how to use the infor­ symptoms e.g. abdominal pain dysphagia; mation you have extracted from the history, + dyspnoea haemoptysis, we recommend examination and initial tests to work toward + choosing the symptom with the narrower a diagnosis. differential diagnosis (dysphagia or haemo­ To do this, we focus on the most valuable ptysis in the examples above). pieces of diagnostic data – those symptom After you have decided on which guide characteristics, signs and test results with to use, the format is simple to follow: the greatest potential to narrow the differ­ ential diagnosis or to rule in/rule out sus­ • Each begins with the differential pected conditions. diagnosis: a rundown of the important All of the guides follow a logical and diagnoses to consider for the particular consistent approach and are designed to presenting problem. reflect contemporary medical practice. • We then present an overview of They provide a secure framework to work assessment: this is essentially a within but are not rigid protocols and allow flowchart that lays out the route to ample scope for clinical judgement. diagnosis. It is vital that you understand The highest priority is always given to the format of the overview, so an immediately life-threatening problems. In example is provided in Figure 3.1 and is some cases, this means focusing on aims explained below. of assessment other than diagnosis, e.g. • Each overview is accompanied by a gauging illness severity or determining step-by-step assessment. This is a textual resuscitation requirements. The next aim companion to the overview that is, wherever necessary, to exclude major explains and expands on each pathology; for each of the most serious individual step. potential disorders, the guides will identify • Some chapters also contain details on those patients who require further investi­ further assessment of common gation to rule in or rule out the diagnosis. disorders or abnormalities that may Thereafter we prioritise diagnostic informa­ have been identified during the initial tion with the highest yield whilst avoiding assessment. data that do not significantly alter probabil­ The example in Figure 3.1 shows the ities or help to target investigation. In initial stages of the overview of assessment situations where the information obtained for jaundice (shown fully in Ch 19). from the routine work-up is unlikely to yield a clear working diagnosis we may • The blue boxes are stages of action – opt to provide a strategy for further inves­ they contain the steps of assessment tigation to help narrow the differential that you need to undertake. This will diagnosis. always include one of the two

21 The diagnostic process 3

Full clinical assessment + LFTs, FBC, U+E, coagulation screen

Yes See Further assessment of 1 Evidence of chronic liver disease? chronic liver disease (p. 181)

No

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

No

3 Evidence of cholestasis?

Yes Yes Fever / rigors / RUQ pain? Suspect acute cholangitis

No Yes Seek Dilated bile ducts on USS? Extrahepatic cholestasis underlying cause No No

ALT >500 U/L, ↑PT or features Yes Acute viral/autoimmune hepatitis or 4 of encephalopathy? toxic/ischaemic liver injury

No

Fig. 3.1 A guide to using the ‘overview of assessment’.

22 The diagnostic process 3

principal methods of clinical assessment diagnostic process is accompanied by a outlined in Chapter 2 (‘ABCDE’ or ‘full detailed explanation in the step-by-step clinical assessment’) plus the essential assessment section (see above). basic tests, e.g. ECG, CXR, and any • The green boxes represent the potential necessary additional examination steps. endpoints of the diagnostic process. As Note: The diagnostic process that with the yellow boxes, explanatory text follows assumes that you have is provided in the accompanying performed these steps and extracted the step-by-step assessment. In some cases, relevant clinical information. further investigation may be required to • The yellow boxes are stages of thought confirm the diagnosis, refine it, assess and reasoning – they do not show ‘what severity or guide optimal management; to do now’ but rather ‘what to think if so, the necessary steps will be about now’. Each numbered step in the outlined in the text.

23 PART 2

Assessment of common presenting problems

Abdominal pain...... 26 Breast lump...... 44 Chest pain...... 48 Coma and altered consciousness...... 70 Confusion: delirium and dementia...... 76 Diarrhoea...... 88 Dizziness...... 94 Dysphagia ...... 106 Dyspnoea...... 110 Fatigue...... 128 Fever...... 136 Gastrointestinal haemorrhage: haematemesis and rectal bleeding...... 148 Haematuria...... 156 Haemoptysis...... 160 Headache...... 164 Jaundice...... 172 Joint swelling...... 182 Leg swelling...... 186 Limb weakness...... 196 Low back pain...... 210 Mobility problems: falls and ‘off legs’...... 216 Palpitation...... 224 Rash: acute generalised skin eruption...... 232 Scrotal swelling...... 242 Shock...... 246 Transient loss of consciousness: syncope and seizures...... 252 4 ABDOMINAL PAIN

Acute abdominal pain • gastroenteritis (diffuse mid-/upper abdominal) Acute abdominal pain has a vast differen- • diabetic ketoacidosis/hypercalcaemia/ tial diagnosis. The spectrum of disease adrenal crisis (diffuse) severity is also wide, ranging from the • functional abdominal pain (any region life-threatening to the innocuous. Effective or diffuse). assessment requires the rapid recognition of patients with critical illness and, where Key questions appropriate, targeted investigation to iden- What are the characteristics of the pain? tify other potentially serious conditions. Visceral pain arises from distension or Causes of acute abdominal pain are listed excessive contraction of hollow organs. It is below. The numbers in brackets correspond conducted by autonomic nerve fibres, so its to the different regions of the abdomen, as location corresponds to the embryological displayed in Figure 4.1, at which the pain is origin of the affected structure (Fig. 4.2). typically most prominent: The pain is typically dull and poorly local- ised and is not associated with abdominal • cholecystitis/cholangitis (1) guarding or rigidity. True ‘colicky’ pain • biliary colic (1, 2) reflects intermittent episodes of intense • hepatitis (1, 2) smooth muscle contraction that produce • pneumonia (1 or 3) short-lived spasms of discomfort lasting • peptic ulcer disease/gastritis (2) seconds to minutes before subsiding. In • acute coronary syndrome (2) some other disorders described as ‘colic’, • pancreatitis (2, 5) e.g. renal or biliary colic, the pain actually • ruptured abdominal aortic aneurysm builds to a crescendo over a period of (AAA) (2, 5) minutes before reaching a steady peak that • splenic rupture (3, diffuse) may last for several hours before easing. • renal calculus (4, 7 or 6, 9) Somatic pain arises from irritation and • pyelonephritis (4 or 6) inflammation of the parietal peritoneum • early appendicitis (5, diffuse) and is conducted by somatic nerves. It is • established appendicitis (7) sharp, well localised, constant and, often, • terminal ileitis, e.g. Crohn’s disease, associated with local tenderness and guard- Yersina (7) ing. Widespread inflammation of the • mesenteric adenitis (7, diffuse) parietal peritoneum produces generalised • diverticulitis (7 or 9) peritonitis. • colitis (7, 8, 9) Referred pain is perceived at a site remote • ectopic pregnancy (7, 8, 9) from its source and arises due to conver- • pelvic inflammatory disease/ gence of nerve fibres at the same spinal cord endometriosis (7, 8, 9) level (Fig. 4.3). • ovarian torsion/cyst rupture (7, 8, 9) • lower urinary tract infection (UTI)/ Is there a systemic inflammatory cystitis (8) response? • intestinal obstruction (diffuse) Many serious causes of acute abdominal • perforation (diffuse) pain either stem from or provoke an inflam- • mesenteric ischaemia (diffuse) matory process within the abdominal 26 Abdominal pain Differential diagnosis 4 cavity. The presence of fever, ↑CRP or of uncertain physical signs, e.g. mild local- ↑WBC with neutrophilia suggests that the ised abdominal tenderness, reinforcing patient is mounting an acute systemic in- suspicion of local peritonitis. In patients flammatory response (Box 4.1) and may without a clear cause for pain, these fea- thereby contribute to the diagnostic process. tures may suggest the need for admission In some patients, the presence of inflamma- and further investigation. By the same tory features may assist the interpretation token, the absence of these features can, when used correctly, help to exclude im- portant inflammatory pathology. Finally, Box 4.1 Indicators of systemic inflammation recognising and grading the presence of a systemic inflammatory response are central • Fever (>38°C) to the assessment of illness severity. • ↑CRP (>10 mg/L*) Note that the significance of an individ- ual result depends on the clinical context, • WBC 11 109/L or 4 109/L > × < × particularly with respect to CRP. In general, *The significance of the result depends on the clinical context – see text. the higher the result, the greater the extent of systemic inflammation. A marginal rise in CRP e.g. <30 mg/L, does not provide compelling evidence of a major inflamma- tory process. However, if the test is being used to help ‘rule out’ a condition, then it is 1 2 3 safer to regard any limit above the upper range of normal as elevated.

5 4 6 Chronic/episodic abdominal pain Chronic abdominal pain is very common 7 9 and challenging to assess. Most younger 8 patients will have a functional disorder, e.g. IBS, but careful evaluation ± targeted investigation is required to exclude organic pathology. In older patients with new, Fig. 4.1 Regions of the abdomen. See text for persistent abdominal pain, the priority is typical sites of pain. to exclude underlying malignancy.

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

Fig. 4.2 Abdominal pain. Perception of visceral pain is localised to the epigastric, umbilical or suprapubic region, according to the embryological origin of the affected organ.

27 Abdominal pain 4 Differential diagnosis

Right shoulder

Diaphragm Tip of scapula

Gallblader

Ureter Inguinal canal

Gallbladder pain Diaphragmatic pain Ureteric pain Fig. 4.3 Characteristic radiation of pain from the gallbladder, diaphragm and ureter.

Gastroduodenal disorders after a meal, manifesting as intense, dull, Peptic ulcer disease is a common cause of RUQ or epigastric pain ± radiation to the chronic upper abdominal pain. Almost all back or scapula (see Fig. 4.3). The pain duodenal ulcers and 70% of gastric ulcers builds to a crescendo over minutes, and are attributable to H. pylori infection. Typical may last several hours before subsiding. features include recurrent episodes of It does not cause jaundice, deranged LFTs burning or gnawing discomfort, relation- or abdominal signs. USS may confirm the ship to food (variable), associated dyspeptic presence of gallstones or demonstrate path- symptoms e.g. nausea, belching, water- ological gallbladder changes. brash, and relief with antacids. Choledocholithiasis (stone in the CBD) may Gastritis without frank ulceration may cause recurrent episodes of upper abdomi- produce similar symptoms. nal pain associated with cholestatic jaun- Gastric cancer occurs more frequently in dice (see Ch. 19). patients >55 years; associated symptoms Pancreatic pain include dysphagia, early satiety, weight loss and vomiting. All of the above disor- Chronic pancreatitis causes severe upper ders are best diagnosed by upper gastroin- abdominal pain that often radiates to the testinal endoscopy (UGIE). back. In some patients, it is constant and unremitting, while in others, episodes are Gallstones provoked by eating. Associated features Most gallstones are asymptomatic. include weight loss, anorexia, diabetes Biliary colic occurs when a gallstone mellitus (endocrine deficiency) and, in obstructs the cystic duct, causing gallblad- advanced disease, steatorrhoea (exocrine der distension. It tends to occur 1–6 hours insufficiency). The majority of cases are due 28 Abdominal pain Differential diagnosis 4 to chronic alcohol excess. Diagnosis is typical clinical features in the absence of usually made by CT but ERCP may be apparent organic disease. required in difficult cases. Unlike acute Non-ulcer dyspepsia causes symptoms that pancreatitis, serum amylase is usually may be indistinguishable from peptic ulcer. unhelpful; ↑faecal elastase indicates pan- UGIE and mucosal biopsies are normal. creatic exocrine insufficiency. IBS causes abdominal pain that is relieved Pancreatic cancer may cause severe, unre- by defecation or is associated with a change lenting pain in the upper abdomen that in bowel habit. Diagnostic criteria are radiates to the back, and is usually associ- shown in Box 9.1, p. 88. Symptoms tend to ated with cachexia ± cholestatic jaundice. follow a relapsing and remitting course, Mesenteric ischaemia and are often exacerbated by psychosocial stress. Mesenteric ischaemia is a rare cause of chronic abdominal pain that tends to occur Renal tract disorders in patients with widespread severe athero- Infrequent, discrete attacks of severe loin sclerotic disease. Dull epigastric or peri­ pain radiating to the groin ± haematuria umbilical pain develops approximately 30 suggest renal stone disease. Chronic dull, minutes after eating (‘abdominal angina’). aching or ‘dragging’ discomfort may be due This may lead to a fear of eating and so to cancer, adult polycystic kidney disease weight loss is common. The diagnosis is (APKD), loin pain–haematuria syndrome made by mesenteric angiography. or chronic obstruction/pyelonephritis. Inflammatory bowel disease Gynaecological conditions Colitis due to either Crohn’s disease or An ovarian cancer or cyst may present with ulcerative colitis may cause cramping lower non-specific persistent lower abdominal abdominal pain, usually in association with discomfort ± evidence of a pelvic mass on bloody diarrhoea. Small bowel inflamma- abdominal/PV examination. tion in Crohn’s disease is often manifest Endometriosis (endometrial tissue out­ by persistent cramping periumbilical or side the uterus) and PID (infection of the RLQ pain ± diarrhoea (non-bloody) and upper reproductive tract) are common constitutional upset. Subacute small bowel causes of chronic lower abdominal pain in obstruction due to oedema or fibrosis may women of reproductive age. lead to colicky postprandial abdominal dis- Recurrent episodes of lower abdominal comfort. Both disorders are also associated pain that regularly occur midway through with a range of extra-intestinal features (see the menstrual cycle may be a manifestation Box 9.3, p. 89). of ovulation (mittelschmerz). Colon cancer Other diagnostic possibilities This is a common cancer in men and • Constipation. women, and may present with colicky • Hypercalcaemia. lower abdominal pain. Other important fea- • Small bowel ulcers/tumours. tures include weight loss, change in bowel • Acute intermittent porphyria. habit, rectal bleeding and iron-deficiency • Giardiasis. anaemia. Diagnosis is usually made by • Abdominal tuberculosis. colonoscopy. • Yersinia infection. Functional disorders • Coeliac disease. These are extremely common, particularly in younger adults. Diagnosis is based on

29 Abdominal pain 4 Acute abdominal pain: overview

ABCDE

Yes Resuscitate, urgent surgical review 1 Evidence of shock? Consider ruptured AAA / ectopic pregnancy / spleen

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 X-ray

No

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

No

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? or lower abdominal pain

No

Consider mesenteric ischaemia, Crohn’s disease, gastroenteritis, irritable bowel syndrome, 7 ‘medical causes’. Surgical review ± CT abdomen if any concern

30 Abdominal pain Acute abdominal pain: step-by-step assessment 4

1 Evidence of shock? • medical conditions, e.g. diabetic ketoacidosis, myocardial infarction, Rapidly identify patients who are shocked adrenal crisis, pneumonia with hypotension and evidence of tissue • any condition associated with repeated hypoperfusion (see Box 28.1, p. 249). vomiting, e.g. intestinal obstruction, Remember that young, fit patients can gastroenteritis. often maintain BP in the face of major fluid losses; in these patients hypotension occurs 2 Generalised peritonitis? late, so look carefully for early features such as ↑HR, ↑RR, narrow pulse pre­ Generalised peritonitis occasionally results ssure, anxiety, pallor, cold sweat or light- from acute pancreatitis but is usually the headedness on standing ± postural ↓BP. manifestation of a perforated hollow viscus, If the patient has overt or incipient e.g. stomach, duodenum or colon. Suspect shock, secure two large-bore IV lines; it if there is severe, non-colicky abdominal send blood for cross-match, U+E, FBC, pain that is worse on movement, coughing amylase and LFTs; and begin aggressive or deep inspiration, and which is associated resuscitation. with inflammatory features and general- The diagnoses to consider first are rupture ised abdominal rigidity. The patient will of an AAA, ectopic pregnancy or other usually be lying still, taking shallow breaths, viscus, as these may require immediate sur- and will be in obvious distress or discom- gical intervention. fort; reconsider the diagnosis if the patient appears well or is moving freely. • Suspect ruptured AAA in any patient Patients require aggressive resuscitation, with known AAA, a pulsatile abdominal antibiotics and immediate surgical referral. mass or risk factors e.g. male >60 years, Free air under the diaphragm on erect CXR who experiences sudden-onset, severe (present in 50–75% of cases) confirms the abdominal/back pain followed rapidly diagnosis; if CXR non-diagnostic consider by haemodynamic compromise. contrast CT (Fig. 4.4). Serum amylase may • Suspect ruptured ectopic pregnancy in help to differentiate perforation from pan- any pregnant woman or woman of creatitis. A very high index of suspicion is child-bearing age with recent-onset required in the elderly and in patients lower abdominal pain or PV bleeding; taking systemic steroids; signs are often perform an immediate bedside subtle, so reassess frequently. pregnancy test. • Consider splenic rupture in any shocked 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. In the absence of these conditions, perform an ECG, CXR, urinalysis and ABG, continue to assess for an underlying cause, as described below, and refer for urgent surgical review. Other important diagnoses to consider include: • perforated viscus • mesenteric ischaemia • acute inflammatory conditions, e.g. pancreatitis, colitis, cholangitis Fig. 4.4 Free air under the diaphragm. 31 Abdominal pain 4 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 vomit- ing, absolute constipation and/or abdomi- nal distension. The predominant symptoms will vary, depending on the site of obstruc- tion; in high small bowel obstruction vomit- ing and pain are pre-eminent, whereas in low colonic lesions constipation and disten- sion are more pronounced. If any of these features is present, perform an AXR (Fig. 4.5) to help confirm the diagnosis and esti- mate the level of the obstruction. Examine for an incarcerated hernia in any patient with suspected small bowel obstruction. Consider further imaging and rectal examination to confirm an obstruct- ing lesion and differentiate from pseudo- obstruction in patients with large bowel obstruction. A Patients may be profoundly dehydrated – check U+E, provide adequate fluid resuscitation, insert a large-bore nasogastric tube and consider a urinary catheter. Refer to surgery for further assessment and management.

4 Acute and/or bloody diarrhoea? Recent onset of acute diarrhoea with cramp- ing abdominal pain ± vomiting suggests infective gastroenteritis. Suspect colitis (infective, inflammatory or ischaemic) if the patient has bloody diarrhoea with cramp- ing 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 has known vascular disease/atrial fibrilla- tion; if ischaemic colitis is suspected, arrange a CT mesenteric angiogram. Other- B wise, send stool for culture and assess as described in Chapter 9. A Very distended Distended low-lying caecum transverse colon 5 Unilateral loin or flank pain? Fig. 4.5 Intestinal obstruction. A. Small bowel. Suspect renal tract obstruction (usually due B. Large bowel. to a calculus) if there is severe, colicky loin pain (see above) that radiates to the groin ± testes/labia. In contrast to peritonitis, renal tract obstruction causes patients to be

32 Abdominal pain Acute abdominal pain: step-by-step assessment 4 typically restless and unable to lie still. proceed to Acute lower abdominal pain Visible or dipstick haematuria is present in (p. 38). 90% of cases and vomiting is common Consider other causes surgical review during bouts of pain. 7 ± Exclude an AAA if the patient is at high or further imaging if any concern risk e.g. elderly male with vascular disease, Organise CT angiography to look for fea- or the presentation is atypical e.g. absence tures of mesenteric ischaemia in any of haematuria/restlessness/radiation to patient with severe, diffuse pain, shock groin: request an urgent USS and, if this or unexplained lactic acidosis – especially confirms the presence of an AAA, arrange if patients are elderly or have vascular immediate surgical review. Otherwise, disease/atrial fibrillation. The abdominal organise abdominal CT (or IVU if CT is examination may be unremarkable until not available) to confirm the presence of a advanced stages. stone. Consider atypical presentations of In patients with a confirmed stone, check common disorders such as acute appendi- renal function and look for features of infec- citis or inflammatory bowel disease. A tion proximal to the obstruction including retrocaecal appendix may present with an ↑temperature/WBC/CRP or leucocytes/ flank pain while any area of the gut may nitrites on urinalysis. If you suspect proxi- develop a Crohn’s inflammatory mass. mal infection, take urine and blood cul- Both gastroenteritis and hypercalcaemia tures, give IV antibiotics and refer urgently may cause abdominal discomfort with con- to urology. spicuous vomiting and minimal abdominal Suspect pyelonephritis if flank pain is signs – measure serum calcium and enquire non-colicky and associated with inflamma- about infectious contacts and recent inges- tory features (see Box 4.1), leucocytes and tion of suspicious foodstuffs. nitrites on urine dipstick, or loin/renal Functional disorders, e.g. irritable bowel angle tenderness ± lower urinary tract syndrome (IBS), are a frequent cause of symptoms. Consider alternative diagnoses acute abdominal pain. The diagnosis of IBS e.g. acute cholecystitis, appendicitis, if is discussed on page 88, but enquire about there is prominent abdominal tenderness/ a background of longstanding intermittent guarding or if urinalysis is negative for both abdominal pain with altered bowel habit leucocytes and nitrites. Take blood and and review the notes for previous similar urine cultures, start IV antibiotics and admissions. arrange prompt renal USS to exclude a A period of observation with repeated perinephric collection or renal obstruction. clinical evaluation is very often the key to successful diagnosis; for example, abdomi- 6 Pain localised to upper or lower abdomen? nal pain that was originally central and The localisation of pain within the abdomen non-specific may, on repeat examination, can be very helpful in narrowing the dif- have migrated to the RIF, suggesting a ferential diagnosis (see Figs 4.1 and 4.2). diagnosis of acute appendicitis. Patients who remain systemically well and whose • If the patient has predominantly RUQ, pain appears to be settling has settled can LUQ, epigastric or generalised upper usually be discharged safely, with outpa- abdominal pain, proceed to acute upper tient review. Those with marked systemic abdominal pain (p. 34). upset or other features causing concern but • If the patient has RIF, LIF, suprapubic no clear underlying cause require further or bilateral lower abdominal pain, investigation ± surgical review.

33 Abdominal pain 4 Acute upper abdominal pain: overview

Amylase, LFT, erect CXR, ECG

Yes Likely perforated 1 Free air on CXR? Urgent surgical review hollow viscus

No

Yes 2 ECG evidence of ischaemia? Consider acute coronary syndrome

No

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

No

Yes Common bile duct obstruction 4 Jaundice? USS cholangitis, hepatitis

No

5 Inflammatory response?

No Yes

Yes RUQ pain / tenderness? Likely cholecystitis USS

Yes

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

Yes 6 Characteristics of biliary colic? Likely biliary colic USS

No

7 Consider acute gastritis, peptic ulcer, gastroenteritis, non-specific abdominal pain Observation / surgical review if any concern

34 Abdominal pain Acute upper abdominal pain: step-by-step assessment 4

1 Free air on CXR? If amylase levels are normal or equivocal, continue to suspect the diagnosis if the Perform an erect CXR in all unwell patients history is characteristic and: with acute upper abdominal pain; the pres- • there has been a delay in presentation ence of free air under the diaphragm(s) (see OR Fig. 4.4) indicates perforation of a hollow • there is a history of alcoholism – viscus. Secure IV access, cross-match for especially if the patient has had blood, resuscitate with IV fluids and refer previous episodes of pancreatitis. immediately to surgery. If the CXR fails to demonstrate free air or In these patients, consider contrast is equivocal but clinical suspicion is high CT to look for evidence of pancreatic e.g. sudden-onset severe pain with epigas- inflammation. tric tenderness and guarding, consider an Once the diagnosis has been made, evalu- abdominal CT, but first check amylase and ate repeatedly for evidence of complica- ECG as described in steps 2 and 3. tions, e.g. shock, hypoxia (acute respiratory distress syndrome, ARDS), disseminated 2 ECG evidence of ischaemia? intravascular coagulation (DIC); calculate the Glasgow prognostic criteria score (Box Acute coronary syndromes, particularly 4.2) or other validated prognostic score; inferior myocardial infarction (MI), may and monitor CRP. Manage all patients present atypically with epigastric pain. with severe or high-risk acute pancreatitis However, hypotension or severe bleeding (shock, organ failure, Glasgow score ≥3 or in patients with acute abdominal pathology peak CRP >210 mg/L) in a critical care unit. may provoke or exacerbate ischaemia in Perform an abdominal USS to look for patients with stable coronary artery disease; gallstones; those with severe pancreatitis in these circumstances, administration of may require urgent ERCP and stone extrac- powerful antithrombotic agents may have tion, especially if there is jaundice or a catastrophic consequences. dilated common bile duct (CBD). Consider • Perform an ECG in all patients. CT to assess the extent of pancreatic injury • Refer immediately to cardiology if there are features of an ST elevation MI (see Box 6.1, p. 49). • In patients with ST depression, evaluate carefully for hypotension, sepsis, Box 4.2 Modified Glasgow criteria* for hypoxia and bleeding before assessing prognosis in acute pancreatitis attributing changes to an acute • Age >55 years coronary event. • In patients with non-specific T wave • PaO2 <8 kPa (60 mmHg) changes (see Box 6.1, p. 49), measure • WBC >15 × 109/L cardiac biomarkers to assist diagnosis • Albumin <32 g/L and continue to search for alternative • Serum calcium <2.00 mmol/L (8 mg/dL) causes. (corrected) • Seek cardiology input if there is any diagnostic doubt. • Glucose >10 mmol/L (180 mg/dL) • Urea >16 mmol/L (45 mg/dL) (after 3 Amylase >500 U/L? rehydration) Measure serum amylase in any patient with • ALT >200 U/L acute severe epigastric pain. Patients with • LDH >600 U/L an amylase >3× the reference range are 95% *Severity and prognosis worsen as the number of these factors likely to have pancreatitis; levels >1000 U/L increases. More than three implies severe disease. are considered diagnostic. 35 Abdominal pain 4 Acute upper abdominal pain: step-by-step assessment and look for evidence of complications, e.g. • acute pyelonephritis if urinalysis is infection, particularly in patients with per- positive for leucocytes/nitrites. sistent organ failure or a systemic inflam- Otherwise, consider USS/CT to exclude matory response. atypical presentations of acute appendicitis/ pancreatitis/cholecystitis, Crohn’s disease 4 Jaundice? or other acute inflammatory pathology. Organise an urgent abdominal USS for all patients with acute upper abdominal pain 6 Characteristics of biliary colic? and jaundice to look for evidence of biliary Biliary colic is a common cause of acute obstruction or hepatitis. severe upper abdominal pain in patients Assume biliary sepsis, at least initially, if who are otherwise well and do not exhi­ the patient is unwell with high fever ± bit evidence of a systemic inflammatory rigors or cholestatic jaundice (p. 177); give response. Abdominal USS can assist the IV antibiotics and, if the USS confirms a diagnosis by demonstrating the presence dilated CBD, refer immediately to surgery of gallstones. However, asymptomatic for biliary decompression. gallstones are very common and so the Assess as described in Chapter 19 if history is critical to making an accurate there are clinical or USS features of acute diagnosis. hepatitis. Look for the following suggestive features: 5 Inflammatory response? • onset of pain a few hours after a meal At this stage, use the presence or absence of (may waken the patient from sleep) a systemic inflammatory response (see Box • duration ≤6 hours followed by complete 4.1) to narrow the differential diagnosis. resolution of symptoms Arrange prompt abdominal USS to • the main site is the epigastrium or RUQ confirm or exclude acute cholecystitis in ± radiation to the back any patient with inflammatory features • constant, vague, aching or cramping accompanied by any of the following: discomfort (it is not, strictly speaking, • localised RUQ pain ‘colicky’) • direct tenderness to palpation in the • history of previous similar episodes. RUQ Arrange abdominal USS only in patients • positive Murphy’s sign (sudden arrest with a suggestive history. If the pain has of inspiration while taking a deep settled and LFTs are not deranged, USS breath during palpation of the may be performed in the outpatient gallbladder). department. In the absence of acute cholecystitis, the Consider other causes observation/ USS may reveal an alternative cause for the 7 ± presentation, e.g. pyelonephritis, hepatitis, surgical review if any concern subphrenic collection. Systemically well patients with an acute If none of these features is present, con- vomiting illness and recent infectious sider alternative disorders: contact or ingestion of suspicious foodstuffs • basal pneumonia if there is clinical or are likely to have gastroenteritis. CXR evidence of basal consolidation Suspect acute gastritis if the patient (see Figs 12.3 and 12.4, pp. 116 and 117), reports new-onset gnawing, burning or especially if accompanied by productive vague epigastric discomfort ± mild tender- cough or dyspnoea ness – especially if this is associated with • gastroenteritis in patients with an acute dyspeptic symptoms e.g. nausea, belching, vomiting illness and no abdominal heartburn, or a history of recent alcohol guarding or rigidity (reassess regularly) excess/NSAID use; consider peptic ulcer 36 Abdominal pain Acute upper abdominal pain: step-by-step assessment 4 disease if there is a background history of there are worrying features on examination. similar symptoms. Otherwise, patients can usually be dis- In many cases, no definite diagnosis is charged, with further outpatient assess- reached. Admit for observation ± surgical ment if symptoms recur or persist. review if symptoms are not improving or

37 Abdominal pain 4 Acute lower abdominal pain: overview

Urgent Known pregnancy, positive Yes Ectopic pregnancy / 1 gynaecological pregnancy test or PV bleeding? other cause review

No

2 Pain predominantly in RIF?

No Yes

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

No

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

No

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

No

Pelvic examination

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

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

No

Consider atypical appendicitis, endometriosis, terminal ileitis, mesenteric adenitis, renal stone 6 Observation / surgical review if any concern

38 Abdominal pain Acute lower abdominal pain: step-by-step assessment 4

Known pregnancy, positive pregnancy test clinical features listed above or an 1 or PV bleeding? ↑WBC/↑CRP. Abdominal USS may help to confirm the Perform a bedside pregnancy test in any diagnosis rapidly or, in females, identify pre-menopausal woman with acute lower pelvic pathology, e.g. ovarian cyst/torsion. abdominal pain. If positive or the patient CT offers greater diagnostic accuracy and has PV bleeding, request an urgent gynae- may be considered in males or if diagnostic cological review with transabdominal ± uncertainty persists after USS. transvaginal USS to exclude ectopic preg- nancy. If the pregnancy test is negative but LLQ pain, tenderness inflammatory 3 + there is ongoing suspicion of pregnancy response? e.g. missed period, PV bleeding, send blood for formal laboratory measurement of beta- Exclude sigmoid diverticulitis in any human chorionic gonadotrophin. patient with acute LLQ pain and tenderness Request a gynaecological review for (± guarding) with evidence of systemic assessment of pregnancy-related complica- inflammation (see Box 4.1) – especially if tions in any woman with known intra- >40 years. Even in the absence of overt ten- uterine pregnancy who develops acute derness or inflammatory features, maintain lower abdominal pain, but consider a high degree of suspicion if the patient is alternative diagnoses, including acute elderly or has known diverticular disease. appendicitis. Arrange urgent CT to confirm the diagnosis and identify complications e.g. abscess, 2 Pain predominantly in RIF? or to seek an alternative cause for the presentation. The two most helpful clinical characteristics of acute appendicitis are: 4 Suspect acute gynaecological pathology? • migration of pain from the periumbilical Have a high index of suspicion for acute region to the RLQ gynaecological pathology in any woman of • RLQ tenderness or signs of local child-bearing age with acute pelvic or lower peritonism. abdominal pain. In the absence of previous appendec- Organise an urgent USS if there is a tomy, acute appendicitis is highly likely if history of abrupt-onset, severe, unilateral both of these features are present, alongside pelvic or lower abdominal pain with any of mild fever or an ↑WBC or ↑CRP. In these the following features: circumstances, imaging is unlikely to • associated nausea and vomiting contribute to the diagnosis and patients • unilateral tenderness should be referred immediately to the • adnexal tenderness or palpable adnexal on-call surgeon. mass An ↑WBC and ↑CRP are not specific for • age <35 years. appendicitis but the diagnosis is unlikely if both are within normal limits. Neverthe- The principal aim of USS is to look for less, a surgical review is mandatory if evidence of ovarian torsion but it may the presentation is otherwise typical – reveal an alternative diagnosis, e.g. ovarian especially if <12 hours from onset of cyst. Request a gynaecology review if you symptoms. have a strong clinical suspicion of torsion or Maintain a high index of suspicion for the USS result is equivocal. appendicitis in any patient with RLQ pain. In the absence of features suggesting Request prompt surgical review and con- ovarian torsion, consider acute pelvic sider urgent imaging to assist diagnosis if inflammatory disease (PID). Suspect the dia­ pain is accompanied by either of the two gnosis if there is bilateral lower abdominal

39 Abdominal pain 4 Acute lower abdominal pain: step-by-step assessment pain and tenderness ± fever associated with position of the appendix; for example, an any of the following features: inflamed appendix that lies within the • abnormal vaginal or cervical discharge pelvis may only be tender on rectal exami- • tenderness on moving the cervix during nation. Alternative diagnoses in patients bimanual vaginal examination (‘cervical with inflammatory features include termi- excitation’) nal ileitis and mesenteric adenitis. Seek a • adnexal tenderness on bimanual vaginal formal surgical opinion if the diagnosis is examination. uncertain. Consider mesenteric ischaemia in any The diagnosis is often one of exclusion patient who appears unwell or has an and, in the emergency setting, it is prudent unexplained lactic acidosis – especially to seek formal gynaecological input; in dif- if they have known vascular disease or ficult cases, diagnostic laparoscopy may be atrial fibrillation. required. Whenever the diagnosis consid- An obstructed renal stone most com- ered, take endocervical swabs for chlamy- monly presents with loin pain but, once dia and gonorrhoea, and treat in all cases if descended to the ureter, may cause more positive. localised tenderness in the RLQ or LLQ; suspect this if the pain radiates to the testes/ 5 Leucocytes/nitrites on urinalysis? labia or is associated with visible/dipstick Suprapubic pain/tenderness is common in haematuria. UTI but the absence of nitrites and leuco- The diagnosis of acute urinary retention cytes on urinalysis makes the diagnosis is usually obvious but should be excluded unlikely. in confused patients with lower abdominal Acute appendicitis may cause dysuria, tenderness and distress. frequency and urgency with positive uri- In female patients, consider the possibil- nalysis e.g. haematuria, leucocytes, if the ity of alternative pelvic pathology, e.g. inflamed appendix lies adjacent to the endometriosis or mittelschmerz (recurrent bladder or ureter; always consider this pos- episodes of lower abdominal pain that reg- sibility, particularly in males (in whom cys- ularly occur midway through the menstrual titis is rare). However, in the absence of cycle), especially if there is a background of other worrying features, a positive dipstick previous similar episodes at the midpoint for both leucocytes and nitrites, especially of their menstrual cycle. in women, suggests UTI; send an MSU and In many patients, a precise diagnosis start empirical treatment. remains elusive and, as with upper and generalised abdominal pain, functional dis- Consider other causes observation/ orders are a common cause. 6 ± surgical review if any concern Consider atypical presentations of appen­ dicitis resulting from variations in the

40 Abdominal pain Chronic/relapsing abdominal pain: overview 4

Full clinical assessment, PR exam, FBC, LFTs, ESR, CRP, Ca2+, coeliac serology

Upper GI symptoms with Yes Peptic ulcer disease, 1 UGIE alarm features? gastric cancer, gastritis

No

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

No

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

No

Yes Renal cancer, stone disease, 4 Loin pain + mass or haematuria? Renal USS adult polycystic kidney (± CT) disease No

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

No

Cancer, Crohn’s disease, Palpable mass, weight loss, systemic Yes 6 Abdominal chronic pancreatitis upset or unexplained jaundice? CT (or other diagnosis)

No

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

No

Likely functional disorder, e.g. irritable bowel syndrome Reassess or refer GI / gynaecology if persistent troublesome symptoms / organic features

41 Abdominal pain 4 Chronic/relapsing abdominal pain: step-by-step assessment

1 Upper GI symptoms with alarm features? cancer or hepatic metastases. USS may reveal the cause but, if inconclusive, Arrange prompt UGIE if there is upper further investigation, e.g. CT or MRCP, abdominal discomfort ± other dyspeptic is mandatory. symptoms with any of the following: Arrange USS and perform a diagnostic • weight loss ascitic tap in any patient with ascites. If the • dysphagia ascites is exudative and USS fails to reveal • persistent vomiting or early satiety an underlying cause, organise an abdomi- • abdominal distension nal CT scan. • haematemesis or iron deficiency The features of biliary colic are described anaemia above. If present, arrange USS to look for • ≥55 years with new-onset persistent gallstones. Note that gallstones are a very symptoms. frequent finding in asymptomatic patients so, unless the history is typical or there If a gastric ulcer is identified, ensure that is evidence of a complication e.g. dilated a biopsy is sent to exclude malignancy, pre- CBD, chronic cholecystitis, they are unlikely scribe H. pylori eradication therapy if the to explain the presentation. CLO test is positive, recheck the history for Refer to a GI specialist for investigation NSAID use, and consider an interval UGIE of sphincter of Oddi dysfunction if there is to ensure satisfactory healing. a convincing history of biliary pain in the Eradicate H. pylori in any patient with a absence of gallstones, especially if associ- duodenal ulcer and confirm successful ated with abnormal LFTs or a dilated CBD. eradication with a urea breath test. In patients with macroscopic appear- 4 Loin pain + mass or haematuria? ances of an upper GI tumour, obtain the You must exclude upper renal tract cancer formal biopsy result and consider a staging in any patient presenting with persistent CT scan. loin pain associated with a mass or haema- 2 Lower GI symptoms with alarm features? turia (visible or dipstick). Renal USS is a first-line investigation and may reveal Arrange urgent lower GI endoscopy in any alternative causes, e.g. APKD or chronic patient with: hydronephrosis. Consider CT ± urology referral if the cause remains unclear, espe- • PR bleeding cially in patients >40 years. • a palpable rectal mass • iron deficiency anaemia Cyclical pain, pelvic mass, dyspareunia or 5 • change in bowel habit and >45 years or abnormal PV bleeding/discharge? recent weight loss. Organise a pelvic USS in any patient with a Consider flexible sigmoidoscopy as the pelvic mass or any postmenopausal patient first-line investigation in patients< 45 years, with PV bleeding or recent-onset, persis­ colonoscopy if >45 years. Obtain the biopsy tent lower abdominal pain. The features results of any suspicious lesions or sections of PID are described above; if present, of GI mucosa. take endocervical swabs for gonorrhoea and chlamydia – treat if positive. Jaundice, abnormal LFTs, hepatomegaly, 3 Consider endometriosis in any woman of ascites or typical history of biliary colic? reproductive age with severe dysmenor- The combination of new-onset jaundice and rhoea, or chronic lower abdominal pain and persistent/recurrent abdominal discomfort any of the following features: suggests hepatitis, choledocholithiasis or, most frequently, malignancy, e.g. biliary, • variation with menstrual cycle ampullary, pancreatic or hepatocellular • deep dyspareunia 42 Abdominal pain Chronic/relapsing abdominal pain: step-by-step assessment 4

• other prominent cyclical or symptoms, weight loss, constitutional upset perimenstrual symptoms. or abnormal screening investigations. Establishing a definitive diagnosis of Important organic causes of pain that may endometriosis may be challenging – refer to easily be missed include chronic pancreati- a gynaecologist for further assessment, e.g. tis, mesenteric ischaemia and Crohn’s laparoscopy if symptoms are severe. disease. Consider chronic pancreatitis in any Palpable mass, weight loss, systemic patient with a background of chronic 6 upset or unexplained jaundice? alcohol excess or steatorrhoea. Check faecal elastase, perform an abdominal CT and At this stage, organise an abdominal CT if consider specialist referral for further the patient has any of the above features. assessment, e.g. ERCP. The pancreas is often poorly visualised on Exclude mesenteric ischaemia if there is USS, so CT is required to exclude an a close relationship between eating and obstructing pancreatic tumour in any the onset of pain especially if evidence of patient with abdominal pain and unex- vascular disease elsewhere, e.g. angina, plained jaundice. Patients with a palpable intermittent claudication. mass may have been investigated with Assess any patient with associated diar- other modalities in steps 1–5 above but CT rhoea. Even in the absence of diarrhoea, is more likely to identify certain masses, e.g. consider further investigation for small small bowel, renal tract and omental, and bowel Crohn’s disease, e.g. enteroscopy, should be performed if the cause remains barium follow-through in a young patient uncertain. In patients with abdominal pain with unexplained mouth ulcers, ↑ESR/CRP, and significant weight loss or other major extra-intestinal manifestations (see Box 9.3, constitutional upset, e.g. fevers, night p. 89) or persistent RLQ tenderness. sweats or ↑↑ESR, CT may reveal evidence If none of the above is present, a func- of lymphoma, solid organ malignancy or tional cause, e.g. IBS, is likely – particularly inflammatory disease, e.g. chronic pancrea- when typical symptoms are present (see titis, abscess, Crohn’s disease. Box 9.1, p. 88). However, patients with per- sistent, troublesome symptoms may require Clinical or laboratory features suggest 7 specialist assessment and investigation to organic disease? exclude organic disease. Further investigation is usually required if the patient is >45 years with recent-onset

43 5 BREAST LUMP

Breast lump is the most common presenting Breast abscess feature of breast cancer. All breast lumps The lump usually develops rapidly and is must be referred to a specialist breast tender. There is often overlying erythema; service for evaluation by triple assessment, there may be fever and evidence of a sys- comprising clinical, radiological and patho- temic inflammatory response. logical evaluation. In lactating women, breast abscesses Ultrasound (USS) is the imaging modal- occur most frequently in the first 12 weeks ity of choice in women <35 years due to the post-partum; painful, cracked nipples are high density of breast tissue. Older women common. It may be difficult to distinguish should have mammography ± USS. Patho- an abscess if breast tissue is grossly indu- logical assessment is undertaken by fine rated due to mastitis; in these cases referral needle aspiration cytology, core biopsy or should be made for further assessment and occasionally excision biopsy. imaging. Breast cancer In non-lactating women, abscesses are uncommon and an underlying inflamma- The breast is the most common site of tory cancer should be excluded. Subareolar cancer in women; 1 in 9 women in the UK abscesses are the most common form, typi- are affected by breast cancer in their life- cally associated with a periductal mastitis; time. The risk increases with age and the there is a strong association with smoking. mean age at diagnosis is 60 years. Risk factors are shown in Box 5.1. Features of a Fibroadenoma breast lump that suggest cancer are shown Fibroadenoma is a common benign neo- in Box 5.2. However, it is not possible to plasm that occurs after puberty in younger exclude cancer by clinical examination women, usually <30 years. It typically alone and all palpable masses should be presents as a discrete, mobile, non-tender regarded as potentially malignant until mass with a rubbery consistency. The proven otherwise. diagnosis should be confirmed by triple assessment.

Box 5.1 Risk factors for breast cancer

• Previous breast cancer • Age Box 5.2 Suspicious features of breast lump • Family history • Oral contraceptive pill • Hardness • Hormone replacement therapy • Immobility • Early menarche • Skin tethering/puckering • Late menopause • Skin changes (peau d’orange, eczema) • Nulliparity • Nipple retraction • First pregnancy >35 years • Lymphadenopathy • Current smoker • Bloody nipple discharge

44 Breast lump Differential diagnosis 5

Fibrocystic change Other causes Fibrocystic change is a benign condition Skin and subcutaneous lesions, such as epi- associated with tender, lumpy breasts that dermoid cysts and lipomata, may occur on may affect up to 50% of women between 20 the breast. Phylloides tumours are rare and and 50 years but is rare after the meno- share many clinical features with fibroade- pause. Features often vary over the course nomas but are typically more aggressive; of the menstrual cycle due to hormone fluc- metastasis is rare but can occur. Galacto- tuations. Areas of firm, lumpy breast tissue coele is a rare cystic lesion of the breast. It without a discrete mass are often termed contains milk and most commonly occurs nodular breast tissue; if this is localised or in lactating women; occurrence in non- asymmetrical and persists throughout the lactating women requires further endocrine cycle, referral should be made to exclude investigation. underlying cancer. Breast cysts are firm, Male breast disease smooth, well-defined lumps which may cause discomfort if enlarging. USS confirms Breast lumps in men are rare. Gynaeco­ their cystic nature. If needle aspiration mastia most commonly presents as a yields bloody fluid, this should be sent for rubbery button of tissue, concentric to the cytological examination. areola. It occurs frequently at puberty and necessitates careful testicular examination Fat necrosis and assessment of sexual development. Fat necrosis is a benign condition that often Around 25% are idiopathic; other causes arises after trauma or surgery. It may include drugs (~20%), e.g. spironolactone, present as a firm, irregular mass with liver cirrhosis (<10%), gonadal failure tethering to overlying skin, making it diffi- (<10%) and testicular tumours (~3%). Breast cult to distinguish from malignancy. Irre- cancer typically presents as a hard, fixed spective of recent trauma, all lumps with lesion, sometimes with overlying skin suspicious features should be regarded involvement, and is usually eccentric to the as potentially malignant and evaluated areola. urgently by triple assessment.

45 Breast lump 5 Overview

Full clinical assessment + breast examination

1 Discrete lump palpable?

Yes No

Asymmetrical or localised No Reassure. Consider review to re-examine nodularity?

Yes

Review after next menstruation Refer for triple assessment if lump remains palpable

Yes

Yes 2 Evidence of abscess? Refer for emergency aspiration / drainage

Features of/risk factors for Yes 3 Urgent referral for triple assessment breast cancer?

No

Non-urgent referral for triple assessment

A B C Fig. 5.1 Positions for inspecting the breast. A. Hands pressed into hips. B. Hands above head. C. Leaning forward.

46 Breast lump Step-by-step assessment 5

1 Discrete lump palpable? start antibiotic treatment and refer as an emergency to the breast/surgical team. If you are unable to locate a lump, ask the Consider referral to exclude an abscess in patient to attempt to find it and examine in any breast-feeding woman with gross mas- different positions e.g. supine and upright. titis and induration. In the absence of a discrete lump, assess carefully for nodularity. Features of/risk factors for 3 Refer any postmenopausal patient with a breast cancer? localised area of nodularity for urgent triple Refer any patient with a palpable breast assessment. If the patient is premenopausal, lump for specialist triple assessment to repeat the examination after the next men- exclude breast cancer. strual period and refer for triple assessment Request urgent review if: if the localised nodularity persists. If no lump or nodularity is detected, • lump is rapidly enlarging or has reassure but arrange review for repeat features of breast cancer (Box 5.2) examination. • patient > 30 years with a discrete lump persistent over the menstrual cycle 2 Evidence of abscess? • patient < 30 years with a major risk factor, e.g. personal or family history of Suspect breast infection if there is an acute, breast cancer painful swelling with overlying erythema, fever or a systemic inflammatory response;

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

47 6 CHEST PAIN

Chest pain is one of the most common pres- • In unstable angina the pain: entations encountered in both emergency • is of new onset and severe medicine and medical outpatient clinics. • occurs at rest or The diagnostic approach to acute chest pain • occurs with increasing frequency, is different from that of intermittent chest duration or intensity. pain and they should be considered as dis- • In STEMI, the pain is typically severe, tinct clinical entities. with an abrupt onset, and is persistent, unrelieved by glyceryl trinitrate (GTN) Acute chest pain spray and accompanied by autonomic upset (sweating, nausea and vomiting). The primary aim is to identify acute coro- • The presentation of NSTEMI may lie nary syndromes and other life-threatening anywhere between these two extremes; causes, such as aortic dissection and pulmo- it is distinguished from unstable angina nary embolism (PE). ECG analysis, CXR by biochemical evidence of infarction and biomarkers e.g. troponin, D-dimer, (↑troponin), and from STEMI by ECG play a central role in evaluation and are features (Boxes 6.1 and 6.2). intimately linked with the clinical assess- • Certain groups of patients, e.g elderly or ment. Pleuritic chest pain has a sharp or diabetic may have no or minimal pain. stabbing character and varies with respira- tion (worse on inspiration); it should be Aortic dissection differentiated from non-pleuritic pain at an This is a tear in the wall of the aorta. It typi- early stage, as it suggests a different range cally causes sudden-onset, intense, unre- of possible diagnoses. lenting chest pain that radiates to the back, between the shoulder blades (this may be Acute coronary syndromes (ACS) the main site of pain). The character of the Rupture of an atheromatous plaque causes pain is often described as ‘ripping’, ‘tearing’ acute thrombus formation in a coronary or, most frequently, ‘sharp’. Autonomic artery. Sudden total occlusion of a major upset is common; syncope or focal neuro- vessel causes ischaemia of a full-thickness logical deficit may occur. Mortality is high segment of myocardium, resulting in acute (1% per hour in the initial phase). ST elevation myocardial infarction (STEMI). With incomplete occlusion or a good col- Pulmonary embolism lateral blood supply there is less extensive Pain due to PE depends on the site and size or no infarction, producing unstable angina of the embolism. Small emboli commonly or non-ST elevation myocardial infarction produce pleuritic symptoms; large emboli (NSTEMI). Unstable angina or NSTEMI may produce severe, sudden-onset, central may also occur in the absence of acute chest pain that mimics MI. Most patients plaque rupture if hypoxaemia, anaemia, are dyspnoeic and other features may tachyarrhythmia or hypotension is super- include haemoptysis, or (in massive PE) imposed upon stable coronary artery syncope or shock. The majority of emboli disease (CAD). arise from lower limb deep vein thrombosis The pain of myocardial ischaemia is (DVT), but clinical features of DVT are described below (see ‘angina pectoris’). inconsistent and often absent. 48 Chest pain Differential diagnosis 6

Box 6.1 ECG abnormalities in acute coronary Box 6.2 Universal definition of myocardial syndromes infarction ECG abnormalities in STEMI Outside the context of sudden death, 1. ≥1 mm ST elevation in at least 2 adjacent percutaneous coronary intervention or coronary limb leads e.g. II and III; I and aVL OR surgery, myocardial infarction is defined by the 2. ≥2 mm ST elevation in at least 2 adjacent following criteria:

praecordial leads e.g. V2 and V3; V5 and V6 • Detection of rise* and/or fall of cardiac OR biomarkers (preferably troponin), together 3. Left bundle branch block of new onset with evidence of myocardial ischaemia with at least one of the following: Major ischaemic ECG changes (strongly suggestive of myocardial ischaemia) • symptoms of myocardial ischaemia 1. ST changes that vary with onset and offset • ECG changes indicative of new of pain (‘dynamic’ changes) ischaemia or development of pathological Q waves (see Fig. 6.4) 2. ≥1 mm horizontal ST depression in ≥2 adjacent leads • imaging evidence of new loss of viable myocardium or new regional wall motion 3. Deep symmetrical T wave inversion abnormality. Minor ischaemic ECG changes (less specific for *At least one value above the 99th percentile of the upper myocardial ischaemia) reference limit. Source: Thygesen K, Alpert JS, White HD et al. 2007. Universal 1. <1 mm horizontal ST depression definition of myocardial infarction. Circulation. 27 Nov; 116(22):2634–2653. 2. New or evolving T wave inversion or flattening

recent weight gain. Oesophageal rupture is often diagnosed late and carries a high Acute pericarditis mortality. This typically causes constant retrosternal Pneumothorax pain with a sharp, stabbing character that Pneumothorax causes unilateral, sudden- may radiate to the shoulders, arm or trape- onset pleuritic chest pain, often associated zius ridge. It is usually more localised than with breathlessness. In large pneumothora- ischaemic pain and may be accompanied ces there may be ↓ breath sounds and by a rub on auscultation. Pain is often, hyper-resonance to percussion. Diagnosis is but not invariably, worsened by inspiration usually confirmed on CXR. and lying down, and eased by sitting forward. Pneumonia Gastro-oesophageal disorders This may cause pleuritic pain, usually accompanied by other clinical features such Oesophageal spasm can cause severe retro- as fever, cough, purulent sputum and sternal discomfort that mimics cardiac pain. breathlessness. Gastro-oesophageal reflux disease (GORD) usually presents with ‘heartburn’: a hot or Musculoskeletal problems burning retrosternal discomfort that radi- A common cause of chest discomfort with ates upwards; some patients experience a wide variety of presentations. The pain severe episodes of pain that mimic cardiac often varies with posture or movement, and pain, possibly due to reflux-induced spasm. may be reproduced or exacerbated by local Important clues include onset after eating, palpation. Rib fracture typically causes aggravation of symptoms by lying supine severe pain following trauma but most or bending over, and, often, a history of cases are due to minor soft tissue injuries. 49 Chest pain 6 Differential diagnosis

Malignant chest wall invasion produces Box 6.3 Estimating the likelihood of coronary constant, unremitting, localised pain that is artery disease (CAD)* not related to respiration and may disturb High risk sleep. • Previously documented CAD or other Anxiety vascular disease e.g. stroke, peripheral A common cause of chest pain. Occasion- arterial disease ally, presentations are dramatic, with • Male >60 years OR >50 years with ≥2 risk patients reporting intense symptoms. Asso- factors OR >40 years with ≥3 risk factors ciated features may include breathlessness • Female >60 years with ≥3 risk factors with ‘inability to take enough air’ and tin- gling around the mouth; the onset of symp- Moderate risk toms may coincide with stressful situations • All patients not in high-risk or low-risk or emotional distress. group Other causes Low risk • Intrathoracic malignancy or connective • Age <30 years tissue disorders, e.g. systemic lupus • Female <40 years with no risk factors erythematosus, rheumatoid arthritis, *Risk factors: cigarette smoking, diabetes mellitus, may involve the pleura and present hypertension, hypercholesterolaemia (total cholesterol with pleuritic pain ± pleural effusion. ≥6.5 mmol/L), family history of premature CAD. • Subdiaphragmatic inflammatory pathology, e.g. abscess can mimic pneumonia (pleuritic pain, fever, small pleural effusion). coronary arteries. In considering the likeli- • Mediastinal masses, e.g. thymoma or hood of angina, it is therefore important to lymphoma, tend to cause a dull, consider the underlying risk of CAD (Box constant, progressive retrosternal pain 6.3). Myocardial blood flow is adequate that disturbs sleep. under resting conditions but is insufficient • Herpes zoster may cause severe pain, to meet metabolic demands during periods sometimes preceded by tingling or of increased cardiac work. Consequently, burning, followed by development of a episodes of angina tend to be precipitated vesicular rash in a dermatomal by a predictable degree of exertion and distribution. rapidly relieved by rest and/or GTN spray, with episodes typically lasting <10 minutes. Intermittent chest pain Less commonly, angina may result from Angina pectoris tachyarrhythmias (especially on a back- ground of significant coronary narrowing) Angina is the symptomatic manifestation of or transient coronary artery spasm. myocardial ischaemia. It tends to be per- ceived as a diffuse retrosternal discomfort Gastro-oesophageal disorders that may radiate to the left (or right) Gastro-oesophageal reflux typically causes shoulder/arm, throat, jaw or back. Typical a hot, burning retrosternal discomfort descriptions include ‘tightness’, ‘pressure’ which radiates upwards; it is often pro- and ‘heaviness’ but many others e.g. voked by bending or lying flat e.g. in ‘burning’ are recognised. Many patients do bed, and there may be a relationship with not perceive angina as painful but most feel food. Symptoms are relieved by antacids. a sense of ‘discomfort’ – if you only ask Oesophageal spasm can cause severe retro- about ‘pain’, you may miss the diagnosis. sternal discomfort that closely mimics Stable angina is almost always due to cardiac pain and may be worsened by exer- atherosclerotic narrowing in one or more tion and relieved by nitrates. There is often 50 Chest pain Differential diagnosis 6 an associated history of dysphagia, dyspep- associated history of wheeze, breathless- sia or typical heartburn. ness and cough, and precipitants other than Musculoskeletal disorders exertion may be apparent e.g. common allergens, viral upper RTI. These are a common cause of chest discom- fort with a wide variety of presentations; Anxiety most are due to minor soft tissue injuries. Emotional distress is a very common cause The pain typically varies with posture or of chest pain and many suspected angina movement and may respond to NSAIDs. In attacks are actually ‘panic attacks’. Pre­ costochondritis, there is well-localised ten- sentations are often quite dramatic, with derness of the costochondral junctions that patients reporting throat tightness, a is exacerbated by local pressure. ‘choking’ sensation and/or difficulty taking Asthma a breath. There may be evidence of hyper- ventilation with tingling around the mouth Patients with asthma may describe exer- and extremities, and ↓PaCO2 on ABG. Epi- tional chest ‘tightness’ on account of bron- sodes tend to arise in the context of stress chospasm, which may be difficult to rather than exertion. distinguish from angina. There is usually an

51 Chest pain 6 Clinical tool: the ECG in acute chest pain

Clinical tool: ECG abnormalities in chest pain

The ECG in STEMI dominant R wave (reciprocal Q wave) in V1. Acute transmural ischaemia produces ST Further ECG changes occur as the infarct elevation in leads that ‘look at’ the affected progresses (Fig. 6.4): loss of the R wave, region of myocardium: followed by development of Q waves and T wave inversion (TWI). ST segments typically • in anterior MI (Fig. 6.1), V2–V5 return to baseline; persistent ST elevation may • in lateral MI, V5, V6, I and aVL • in inferior MI (Fig. 6.2), II, III and aVF. indicate the development of a left ventricular There may be associated ST depression in aneurysm. Extensive anteroseptal infarction the opposing leads (‘reciprocal change’). may cause new left bundle branch block Posterior MI (Fig. 6.3) is recognised by (Fig. 6.5) rather than ST elevation. reciprocal anterior ST depression and a

I aVR C1 C4

II aVL C2 C5

III aVF C3 C6

II

Fig. 6.1 Acute anterior ST elevation myocardial infarction.

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.2 Acute inferior ST elevation myocardial infarction.

52 Chest pain Clinical tool: the ECG in acute chest pain 6

Clinical tool: ECG abnormalities in chest pain—cont’d

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Fig. 6.3 Acute inferoposterior ST elevation myocardial infarction.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Fig. 6.4 Evolving anterior ST elevation myocardial infarction.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II

Fig. 6.5 Left bundle branch block.

53 Chest pain 6 Clinical tool: the ECG in acute chest pain

Clinical tool: ECG abnormalities in chest pain—cont’d

ST elevation in leads V2–V5 can be a normal pain – strongly suggest ischaemia. On the finding (‘high take-off’) and, in the absence of other hand, slight ST depression, especially if a previous ECG, may cause diagnostic up-sloping, may be normal. Downward-sloping confusion. With high take-off, the ST elevation ST depression in the lateral leads +/− TWI, is a is typically concave and frequently associated common feature of left ventricular hypertrophy with notching in the terminal portion of the (Fig. 6.8) or digitalis treatment. QRS complex (Fig. 6.6). Appearances remain TWI may be the only ECG evidence of stable over time and there are no reciprocal ischaemia. New deep symmetrical TWI across changes. ECG features that favour acute the praecordial leads (Fig. 6.9) suggests pericarditis from STEMI include: widespread ST critical obstruction of the proximal left coronary elevation (not corresponding to the territory of artery but other patterns are less specific. a single coronary artery), PR depression; the Lateral TWI is a common feature of left absence of reciprocal changes, Q wave ventricular hypertrophy and digitalis treatment; formation or R wave loss; and TWI only after comparison with previous ECGs is very helpful.

normalisation of ST segments. TWI confined to leads V1–V3 suggests right heart strain and favours a diagnosis of PE over The ECG in unstable angina/NSTEMI ACS. TWI also occurs with cardiomyopathies, New horizontal ST depression suggests active pericarditis, myocarditis, cerebrovascular ischaemia (Fig. 6.7); the extent and depth of events (especially subarachnoid haemorrhage), depression correlate with severity of ischaemia electrolyte abnormalities and hyperventilation. and risk of adverse outcomes. ‘Dynamic’ However, in the appropriate clinical context, ST segment changes – those that coincide new or evolving TWI supports a diagnosis with pain and normalise with resolution of of ACS.

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.6 ‘High take-off’ ST segments.

54 Chest pain Clinical tool: the ECG in acute chest pain 6

Clinical tool: ECG abnormalities in chest pain—cont’d

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.7 Ischaemic anterolateral ST segment depression.

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.8 Left ventricular hypertrophy.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V1 Fig. 6.9 Deep symmetrical T wave inversion.

55 Chest pain 6 Clinical tool: the ECG in acute chest pain

Clinical tool: ECG abnormalities in chest pain—cont’d The ECG in acute pericarditis suggestive of PE include new right axis Acute pericarditis characteristically produces deviation, a dominant R wave in lead V1, TWI diffuse, concave (upward-sloping) ST elevation in leads V1–V3 (Fig. 6.11) or right bundle in most leads, with ST depression in aVR branch block (Fig. 6.12). The ‘classical’ ECG (Fig. 6.10). Associated PR segment depression finding of a deep, slurred S wave in I with a Q (with PR elevation in aVR) is highly suggestive. wave and TWI in III (‘S1Q3T3’) is rare. Unlike STEMI, ST elevation typically persists for The ECG in aortic dissection many days. T waves are upright during ST changes but subsequently invert. The ECG may be normal or show non-specific abnormalities. If the dissection flap involves The ECG in PE the ostium of a coronary artery, there may be In most cases, the ECG is normal or shows ECG changes of a STEMI (usually inferior). only sinus tachycardia. Specific abnormalities

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.10 Acute pericarditis.

56 Chest pain Clinical tool: the ECG in acute chest pain 6

Clinical tool: ECG abnormalities in chest pain—cont’d

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.

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 6.12 Right bundle branch block.

57 Chest pain 6 Acute chest pain: overview

ABCDE, ECG

ECG changes suggest STEMI Yes Refer urgently to 1 Likely STEMI (see Box 6.1)? Cardiology

No See Further ‘Major’ ischaemic ECG changes Yes 2 Likely ACS assessment of (see Box 6.1)? NSTEMI / unstable angina (p. 63) No

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

Yes 4 >1 diagnostic features of pericarditis? Pericarditis

No

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

6 History consistent with ACS?

No Yes

Full clinical assessment, repeat ECG, cardiac 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

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

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

Yes

10 Consider GI, musculoskeletal, respiratory, mediastinal and psychological causes

58 Chest pain Acute chest pain: step-by-step assessment 6

ECG changes suggest STEMI Seek urgent Cardiology input if there is 1 (see Box 6.1)? any uncertainty regarding diagnosis or ECG interpretation. Patients with acute chest pain and ECG changes compatible with STEMI (see Box ‘Major’ ischaemic ECG changes 2 6.1) are likely to benefit from immediate (see Box 6.1)? reperfusion therapy, i.e. primary angi- oplasty or thrombolysis. If the ECG shows ‘major’ ischaemic changes, Unless ECG changes are old, the history clarify that the history is consistent with is incompatible with ACS (Box 6.4) or there ACS (see Box 6.4) and proceed to further is a strong clinical suspicion of aortic dis­ assessment of NSTEMI/unstable angina. section (see below), make a diagnosis Seek expert help if there is any doubt of STEMI. regarding ECG interpretation. If the ECG is non-diagnostic e.g. old left • Attach cardiac monitoring and repeat bundle branch block, paced ventricular ABCDE (p. 9) regularly. rhythm: • Establish the duration of the pain and whether it is on-going. • manage as per NSTEMI/unstable • In younger patients with few or no risk angina if clinical features strongly factors for CAD, ask specifically about suggest ACS, e.g. pulmonary oedema or cocaine or amphetamine use. presenting symptoms very similar to • Seek urgent Cardiology input if there is previous MI diagnostic doubt, haemodynamic • consider a near-patient troponin assay, instability or if primary angioplasty if available services are available. • otherwise, await laboratory troponin • If angioplasty is not available, confirm results – check on admission; if eligibility for thrombolysis (see Box 22.4, negative, repeat 12 hours after maximal p. 209). pain. If ST elevation is present but does not Suspect aortic dissection, PE or 3 meet the above criteria, repeat the ECG at oesophageal rupture? frequent regular intervals and manage as per NSTEMI/unstable angina. In the absence of clear ECG evidence of ischaemia/infarction, consider other life- threatening conditions such as aortic dis- Box 6.4 What symptoms are consistent with section, massive PE and oesophageal acute coronary syndrome? rupture. For all of these, a high index of Symptoms of myocardial ischaemia vary widely suspicion is vital since delay in diagnosis and often differ from textbook descriptions so, may prove fatal and characteristic ‘text- when confronted with compelling ECG evidence book’ clinical features are often absent. of ischaemia, you are likely to find that very You must exclude aortic dissection in few accounts of chest discomfort are patients with severe acute chest pain and inconsistent with ACS. ANY of the features in Box 6.5. In the absence of these features, consider the diag- Any pain in the chest (or arms/jaw) that lasts nosis in any patient with a first presentation >10 minutes, or that occurs repeatedly for of severe acute chest pain and no clear alter- minutes at a time with little or no exertion, is native diagnosis, especially if: consistent with ACS. The task is to determine (using the ECG, cardiac biomarkers, the • there is a background of hypertension, description of the pain and the underlying previous aortic surgery, trauma or likelihood of coronary artery disease) whether pregnancy, or the pain is likely to represent ACS. • the pain is described as ‘sharp’ or radiates to the back. 59 Chest pain 6 Acute chest pain: step-by-step assessment

Box 6.5 Features suggestive of acute aortic retching or oesophageal instrumentation. dissection Arrange immediate CXR if ≥1 hour after perforation (may show subcutaneous em­ • Pain reaches maximal intensity within physema and/or pneumomediastinum); seconds of onset otherwise, request water-soluble contrast • Main site of pain is interscapular barium swallow/CT and surgical review. • Character of pain described as ‘tearing’ or ‘ripping’ 4 >1 diagnostic features of pericarditis? • Syncope or new focal neurological signs Diagnose pericarditis if more than one of • New early diastolic murmur (aortic the following features is present: regurgitation) • pain radiating to the trapezius ridge • Asymmetrical pulses (not previously (highly specific for pericarditis) or has documented) typical features (see p. 49) • Marfan’s syndrome • pericardial friction rub (85% of • Onset of pain following deceleration injury cases) • typical ECG changes (p. 56; present in • Widened mediastinum on CXR 80% of cases). Request an echocardiogram to detect any associated effusion (urgently if any features of tamponade – p. 247 and assess A normal CXR does not exclude the LV function (may be impaired if associated diagnosis. myocarditis). If you suspect dissection, arrange imme- diate thoracic CT or transoesophageal 5 Clear history of pleuritic pain? echo; in unstable patients, consider bedside transthoracic echo, which will identify most If the patient reports pain that clearly and type A dissections (but does not exclude consistently varies with respiratory move- the diagnosis). ments, especially if described as ‘sharp’, Consider massive PE if there is sudden- ‘knife-like’, ‘stabbing’ or ‘catching’, then onset, severe chest pain associated with any proceed to Acute pleuritic pain (p. 64). If of the following features: there is any doubt, continue on the diagnos- tic pathway for non-pleuritic pain initially • marked dyspnoea or hypoxaemia in the and reconsider if no clear diagnosis emerges absence of pulmonary oedema or the patient’s description becomes more • high risk of PE e.g. malignancy, recent suggestive of pleuritic pain. surgery, prolonged immobility or clinical evidence of DVT 6 History consistent with ACS? • syncope or signs of shock (p. 249) – especially with ↑JVP Further assessment for ACS is generally not • suggestive ECG changes (p. 56). required in patients with: In hypotensive or peri-arrest patients, • a single short-lived episode of pain, e.g. exclude contraindications to thrombolysis <10 minutes (see Box 22.4) and consider urgent transtho- • a typical episode of stable exertional racic echo to look for evidence of acute angina right heart strain and exclude alternative • a clear alternative cause for pain, e.g. diagnoses e.g. cardiac tamponade. Other- herpes zoster; recent chest wall injury wise, arrange prompt CT pulmonary with tenderness on palpation angiography. • an atypical history and very low risk of Suspect oesophageal perforation if acute for CAD, e.g. < 30 years with no risk severe chest pain arises after vomiting/ factors. 60 Chest pain Acute chest pain: step-by-step assessment 6

Otherwise, consider admission for repeat 8 High clinical probability of ACS? ECG and cardiac biomarkers, especially troponin. Now try to identify the subset of patients with unstable angina but no ECG evidence Any ischaemic ECG changes (see Box 6.1) of ischaemia or significant myocyte necro- 7 or ↑troponin? sis. Do this by considering the characteris- tics of the pain alongside the risk of Repeat the ECG at least once and also underlying CAD (Box 6.3). Except in de during any further episodes of pain. Mea­ novo presentations of chest pain, the most sure serum troponin concentration ≥12 helpful feature is the relationship of the hours from the onset of maximal pain. If the current symptoms to previous episodes of ECG is non-diagnostic but you suspect discomfort. ACS, check troponin earlier (laboratory or Unstable angina is highly likely if: ‘near-patient’ testing) to expedite diagnosis, but always repeat at 12 hours if the initial • the symptoms mimic previous episodes test is negative. of anginal chest discomfort but are now Diagnose ACS in patients with a convinc- of longer duration, or occur with ing history of ischaemic chest pain accom- minimal provocation or at rest panied by ↑troponin or any ECG evidence • the symptoms closely resemble a of ischaemia (see Box 6.1). previous documented ACS In patients with an atypical history or low • the patient has established CAD or high underlying risk of CAD, first consider alter- likelihood of CAD (see Box 6.7) and the native causes of ↑troponin (Box 6.6) and pain is characteristic of myocardial ECG changes (see Box 6.1), e.g. PE, myoperi- ischaemia, including at least one of: carditis or aortic dissection, but proceed to • radiation to one or both arms further assessment of ACS if there is no • worsening of discomfort with exertion clear alternative cause. • pressure-like or constricting discomfort associated with sweating or nausea and vomiting. Refer patients with these features (or in Box 6.6 Conditions associated with elevation whom the suspicion of ACS is otherwise of serum troponin other than acute coronary high) to cardiology for further assessment. syndrome Low clinical probability of ACS or features • Acute decompensated heart failure 9 suggest alternative diagnosis? • Tachy- or bradyarrhythmias • Myocarditis/myopericarditis In the absence of the features above, unsta- ble angina is unlikely if any of the following • Aortic dissection is present: • Pulmonary embolism • low likelihood of CAD (Box 6.3) • Prolonged severe hypotension/cardiac arrest • the pain persisted at high intensity for • Severe sepsis or burns >1 hour (would expect troponin rise if • Cardiac trauma/surgery/ablation ischaemic pain) and an ECG during maximal pain was normal • Acute neurological disease e.g. stroke, • the symptoms mimic previous episodes subarachnoid haemorrhage of chest discomfort that are not • Congestive cardiac failure suggestive of angina (Box 6.7). • Infiltrative cardiac diseases e.g. sarcoidosis, Seek an alternative explanation for chest amyloidosis pain in these patients. • End-stage renal failure Further investigation (Box 6.8) may be helpful in patients who do not fall into 61 Chest pain 6 Acute chest pain: step-by-step assessment either category, to look for evidence of • Consider thoracic or respiratory review underlying obstructive CAD. if there is an unexplained CXR abnormality e.g. mediastinal/hilar 10 Consider non-cardiac causes of chest pain mass. • Reassess for pericarditis and arrange an • Make a clinical diagnosis of GORD, echocardiogram to look for pericardial musculoskeletal pain or herpes zoster if effusion, if there are any suggestive there are typical features (see p. 49). features (see step 4, above) or • Consider paroxysmal tachyarrhythmia cardiomegaly on CXR. if the pain was accompanied by rapid • Consider hyperventilation or anxiety if palpitation and an ECG was not there are suggestive clinical features (see obtained during symptoms. p. 49) associated with ↓PaCO (with • Re-evaluate for aortic dissection or PE 2 normal PaO ) and PE has been excluded. and consider echocardiogram/thoracic 2 CT if ongoing pain haemodynamic compromise or other clinical concern.

62 Chest pain Acute chest pain: further assessment 6

Further assessment of NSTEMI/ Table 6.1 The TIMI score unstable angina Step 1 Identify critically unwell patients Risk factor Points Age >65 years 1 Attach cardiac monitoring to all patients with ongoing chest pain and review regu- ≥3 CAD risk factors* 1 larly with repeat ECG. Admit to a CCU/ ≥2 episodes of angina in last 24 hours 1 HDU and arrange urgent Cardiology Aspirin use in past 7 days 1 review if you identify any of the Known CAD (stenosis >50%) 1 following: ST segment deviation ≥0.5 mm on ECG 1 • shock (p. 249) ↑Troponin 1 • pulmonary oedema (p. 113) For risk of death or MI in next 14 days: • ventricular arrhythmia, complete heart Score 0–3 3–5% block (see Fig. 29.2, p. 261) Score 4–5 7–12% • ST elevation or refractory pain. Score 6–7 19%

*Risk factors: ↑BP, ↑cholesterol, smoking, diabetes, family history Step 2 Consider all potential factors of CAD. contributing to myocardial ischaemia In patients with ongoing pain: with palpitation or previous history of • maintain SpO2 ≥94% arrhythmia. • identify and treat tachyarrhythmias Step 3 Identify high-risk patients • if any suspicion of anaemia or acute bleeding, e.g. pallor, haematemesis, Risk-stratify patients using the TIMI score melaena, check Hb urgently (prior to (Table 6.1) or other validated scoring giving antiplatelet agents/ system. Irrespective of the presence of com- anticoagulants) plications or ongoing pain, consider con- • if tachycardic, assess and treat any tinuous ECG monitoring for all medium-risk ongoing pain, then consider beta- patients e.g. TIMI score 4–5, and admission blockade (if no contraindications) to a CCU/HDU for high-risk patients e.g. • evaluate the response to GTN spray; if TIMI score >5. pain improves, consider IV GTN Step 4 Use cardiac biomarkers to infusion. differentiate unstable angina from NSTEMI Consider paroxysmal tachyarrhythmia Measure serum troponin I or T 12 hours e.g. atrial fibrillation, as the mechanism from the onset of maximal pain. If ↑, clas- for NSTEMI in patients who did not have sify as NSTEMI; otherwise, classify as an ECG during pain, e.g. if pain associated unstable angina.

63 Chest pain 6 Acute pleuritic pain: overview

1 Diagnostic CXR abnormality?

No Yes

Yes Pneumothorax? Pneumothorax

No

Yes See Further assessment Consolidation? Likely pneumonia of respiratory tract infection (p. 120) No

Yes Pleural effusion? See Further assessment of pleural effusion (p. 127)

No

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

No

Clinical signs of consolidation + Yes See Further assessment 2 Likely pneumonia features of respiratory tract infection? of respiratory tract infection (p. 127) No

Clinical or CXR suspicion of Yes Malignancy or other 3 Consider CT chest malignancy? cause

No

Full clinical assessment, FBC D-dimer, +/- CRP, ABG

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

No

Wells score >4 or raised D-dimer Yes .. Pulmonary embolism 5 CTPA (or V/Q scan) or unexplained hypoxaemia? or other cause

No

6 Likely musculoskeletal pain or viral infection Consider other causes

64 Chest pain Acute pleuritic pain: step-by-step assessment 6

1 Diagnostic CXR abnormality? Pericardial rub or ‘pericarditic’ ECG 4 changes? Look carefully for: Diagnose pericarditis if pleuritic pain • Pneumothorax (see Fig. 12.5, p. 117) is accompanied by typical ECG features – small pneumothoraces are easily of pericarditis (see Box 6.1) or a pericar­ missed. dial rub. • Consolidation (see Figs 12.3 and 12.4, pp. 116 and 117) if present, go to further Wells score 4 or raised D-dimer or 5 > assessment of respiratory tract infection unexplained hypoxaemia? (RTI) (p. 120), especially if accompanied by cough, purulent sputum, dyspnoea You must exclude PE in any patient with or fever. acute pleuritic pain and no other obvious • Pleural effusion (see Fig. 12.6, p. 117) if cause. A negative D-dimer test in patients present, assess as on page 127. with a Wells score ≤4 (see Fig. 12.7, p. 118) • Rib fractures or metastatic deposits – if effectively rules out the diagnosis makes the latter are present, investigate for a the diagnosis unlikely. Arrange further primary lung, renal, thyroid, breast or investigation with CTPA if the Wells score prostate cancer or multiple myeloma. is >4 (irrespective of D-dimer), D-dimer is positive, or clinical suspicion is otherwise Clinical signs of consolidation features high, e.g. unexplained hypoxaemia, fea- 2 + of respiratory tract infection? tures of right heart strain on ECG (see Box 6.1). Even in the absence of definitive CXR CTPA may provide an alternative cause changes, pneumonia is the likely diagnosis for the presentation in patients without PE. if pleuritic pain is accompanied by: • focal chest signs e.g. crackles, bronchial Likely musculoskeletal pain or viral 6 breathing, and infection. Consider other causes • symptoms of RTI: productive cough, Seek a respiratory opinion and consider acute dyspnoea or fever. further imaging in patients with dyspnoea If present, assess as per on page 120. or a new CXR abnormality other than those described above. Consider drug-induced 3 Clinical or CXR suspicion of malignancy? pleuritis, e.g. amiodarone, methotrexate, or Consider further investigation with CT pleurisy secondary to a connective tissue chest ± bronchoscopy in patients >40 years disorder, e.g. history or clinical features of or with a history of smoking/asbestos systemic lupus erythematosus/rheumatoid exposure if pain is accompanied by: arthritis. Otherwise, the most likely diagnoses are • a history of weight loss viral pleurisy or musculoskeletal pain. • recurrent or unexplained haemoptysis Suspect the former if there is fever, coryzal • recent change in voice or ‘flu-like’ symptoms or a pleural rub; • persistent cervical lymphadenopathy suspect the latter if there is any recent • finger clubbing injury, prolonged severe coughing, unusu- • suspicious CXR changes (see Box 17.1, ally strenuous upper body activity, marked p. 161). exacerbation of pain on movement or obvious tenderness on palpation.

65 Chest pain 6 Intermittent chest pain: overview

Full clinical assessment, ECG

See Further Angina score = 3 OR Yes Possible stable assessment 1 Angina score = 2 + high / angina of suspected moderate risk of CAD angina (p. 69)

No

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

No

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

No

Pain highly localised, induced by specific Yes 4 Musculoskeletal pain movements or reproduced by palpation?

No

Yes 5 Wheeze, breathlessness, cough? Consider bronchospasm

No

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

No

Evaluate for angina in patients with high risk of CAD 7 Look for evidence of underlying anxiety / depressive disorder Consider trial of simple analgesia or acid suppression therapy

66 Chest pain Intermittent chest pain: step-by-step assessment 6

Angina score 3 OR Angina score 2 1 = = + Box 6.7 Angina symptom score high/moderate risk of CAD? Retrosternal discomfort without 1 point The hallmark of stable angina is a correla- atypical features1 tion between symptoms and alterations in Discomfort arises during physical 1 point cardiac work. Retrosternal discomfort that exertion2 consistently arises during exertion and is rapidly relieved (<5 minutes) by rest Discomfort is relieved by rest or GTN 1 point strongly suggests angina. The quality of the within 5–10 minutes discomfort may vary widely and is fre- 1Atypical pain features include a ‘sharp’ or ‘stabbing’ quality; significant variation with inspiration or position; or a high quently vague or non-specific. The likeli- degree of localisation e.g. point with tip of finger. hood of angina also depends on the risk of 2Do not score point if discomfort is fleeting; occurs after but not underlying CAD. With rare exceptions, during exertion; is induced only by specific movements/actions; or has inconsistent relationship e.g. also occurs regularly coronary atherosclerosis is central to the without any provocation. pathogenesis of angina, so patients with a Source: Modified from Diamond GA, Forrester JS 1979. Analysis of probability as an aid in the clinical diagnosis of low risk of CAD have a correspondingly coronary artery disease. New Engl J Med. 300:1350–1358. low risk of angina.

• Calculate the ‘angina score’ based on the three criteria in Box 6.7, then broadly an underlying coronary stenosis). Oesopha- stratify the a priori risk of CAD based geal spasm may closely mimic ischaemic- on age, sex and risk factors (see Box 6.3). type discomfort and also lacks a consistent • If angina score = 3, go to further relationship to exertion. assessment of possible angina, Consider these diagnoses in patients with irrespective of risk factors. characteristic ischaemic-type discomfort • If angina score = 2, go to further that lacks a predictable relationship to assessment of possible angina unless exertion or (with the exception of unstable ‘low-risk’ of CAD. angina) in whom stress testing fails to dem- • Consider further assessment for possible onstrate inducible myocardial ischaemia. angina in patients at high risk of CAD Suspect unstable angina and refer to car- in whom the history is vague or unclear. diology if any of the following: Characteristic description of 2 • new onset of symptoms within the ‘ischaemic-type’ pain? preceding 2 weeks • episodes of discomfort previously The typical manifestation of myocardial related to exertion but now occurring at ischaemia is a diffuse, poorly localised, ret- rest rosternal discomfort that radiates to the • new abnormality on resting ECG neck, jaw and left (or right) shoulder and/ (see Box 6.1). or arm, and has a tight, constricting, pressure-like, aching or heavy quality. It is Suspect paroxysmal arrhythmia if any of frequently described as discomfort rather the following: than pain. Patients often illustrate the sen- • palpitation preceding or during sation by placing a hand or fist over the symptoms centre of the chest. • previously documented tachyarrhythmia Intermittent episodes of myocardial • infrequent episodes of variable duration. ischaemia unrelated to exertion may occur with critical coronary obstruction due to If suspected, attempt to document the plaque rupture and thrombus formation rhythm during a typical episode of symp- (unstable angina), coronary artery spasm toms (p. 229). (vasospastic angina) or paroxysmal tach- Suspect vasospastic angina if any of the yarrhythmia (especially in the presence of following: 67 Chest pain 6 Intermittent chest pain: step-by-step assessment

• no apparent triggers angina on clinical grounds if symptoms are • sudden onset of intense symptoms ± provoked by exertion and produce a sensa- autonomic features tion of chest ‘tightness’. Helpful diagnostic • short duration of episodes (2–5 minutes) features may include a history of cough or • episodes occurring in clusters. wheeze (especially nocturnal), diurnal vari- If suspected, consider a trial of Holter ation in symptoms, the presence of wheeze ECG monitoring to look for evidence of ST on auscultation, a history of atopy and elevation during symptomatic episodes. absence of risk factors for CAD. If asthma Suspect oesophageal spasm if any of the or chronic obstructive pulmonary disease following: is suspected, evaluate as described in Chapter 12. • intermittent dysphagia • history or typical symptoms of GORD Pain provoked by stress/strong emotion or (see below) 6 associated with features of • discomfort occurring predominantly at hyperventilation? night or after eating. Attributing episodes of chest pain to anxiety If the history suggests GORD, consider can be challenging. Emotional distress reassessment after a trial of a proton pump increases cardiac work and may provoke inhibitor; otherwise, refer to the GI team for angina, but symptoms that occur exclu- consideration of upper GI endoscopy/ sively in this context are more likely to have oesophageal manometry. a psychological origin. Associated features of panic or hyperventilation during epi- Retrosternal discomfort that is: (a) hot or sodes, e.g. breathlessness with ‘inability to 3 burning, (b) relieved by antacids or (c) take in enough air’ or a choking sensation, provoked by food/lying down? tingling in the extremities and light- If the pain is unlikely to be cardiac, seek headedness, support the diagnosis. Seek typical features of other disorders. The specialist input before attributing a new above features suggest GORD; a sympto- presentation of chest pain to anxiety in matic response to acid suppression therapy, patients with a high risk of CAD. e.g. proton pump inhibitor, effectively con- firms the diagnosis. Upper GI endoscopy is Evaluate for angina in patients at high usually not required but consider if symp- 7 risk of coronary artery disease. Consider other causes toms are refractory. In many patients it is not possible to reach Pain highly localised, induced by specific 4 a definite diagnosis. Reassess those with movements or reproduced by palpation? inconclusive investigations for angina or Musculoskeletal pain may present in a mul- with a high likelihood of CAD (see Box 6.3) titude of ways. The above features are if symptoms persist. Where a cardiac cause suggestive, as is a history of recent injury, has been ruled out and no other cause is strain or uncharacteristically vigorous apparent, patients often respond to simple activity. Further investigation is rarely nec- reassurance. However, a minority experi- essary; a symptomatic response to simple ence severe, refractory symptoms and may analgesia helps to confirm the diagnosis. merit specialist assessment for underlying psychological factors and/or management 5 Wheeze, breathlessness, cough? of chronic pain. Asthma and chronic obstructive pulmonary disease may be difficult to distinguish from

68 Chest pain Intermittent chest pain: further assessment 6

Further assessment of Box 6.8 Investigations in suspected angina suspected angina Step 1 Consider unstable angina and • Investigations are used to seek evidence of structural heart disease myocardial ischaemia during cardiac stress or to confirm and/or refute underlying CAD. An abrupt onset or sudden worsening of exertional chest pain indicates unstable • Exercise ECG and other ‘stress tests’ seek angina - see page 63. to establish whether increases in cardiac Arrange echocardiography to exclude work induce myocardial ischaemia. During aortic stenosis and hypertrophic cardiomy- exercise, the development of typical opathy if the patient has an ejection systolic symptoms with ST segment shift >1 mm murmur, exertional syncope or ECG fea- suggests angina. Absence of symptoms and tures of left ventricular hypertrophy (see ECG changes at high workload argues Fig. 6.8). against angina. Step 2 Confirm or refute the diagnosis • Exercise ECG is often inconclusive and has a high ‘false-positive’ rate in low risk In patients >40 years with a typical history patients. Other forms of stress testing, e.g. (angina score 3) and moderate/high likeli- myocardial perfusion scan or dobutamine hood of CAD (see Box 6.3), make a clinical stress echo, offer higher sensitivity/ diagnosis of stable angina and proceed to specificity and are particularly useful when step 3. the resting ECG is abnormal, e.g. left bundle If the risk of CAD is low (see Box 6.3), branch block or the patient is unable to consider CT coronary angiography, if avail- perform treadmill exercise. able, as a first-line investigation (Box 6.8). If negative, return to the algorithm for inter- • Stress tests are contraindicated in unstable mittent chest pain (re-enter at step 3). If angina, decompensated heart failure or positive, proceed to a stress test or invasive severe hypertension. angiography. • Coronary angiography is the definitive test for Otherwise, consider a stress test (Box 6.8). defining the presence, extent and severity of If positive, diagnose stable angina and CAD. Severe stenosis in one or more vessels proceed to step 3. If negative i.e. no evi- strongly suggests ischaemia as the cause of dence of inducible ischaemia at high stress, pain whilst the absence of significant coronary return to the algorithm for intermittent stenosis effectively excludes angina. chest pain (re-enter at step 3). Seek input • In patients with a relatively low risk of CAD, from cardiology if you have a high clinical CT coronary angiography is a useful, suspicion and are unable to identify a clear non-invasive method to rule out stable angina alternative cause. by excluding the presence of significant CAD. If results are equivocal e.g. suboptimal test, minor abnormality, or typical symp- toms without ECG changes), consider an therapy is an indication for angiography alternative stress test or coronary angiogra- with a view to revascularisation. phy to clarify the diagnosis. Exercise ECG may identify high risk pati­ Step 3 Assess symptom severity and risk ents whose prognosis could be improved The severity of angina is based not on the by revascularisation. Refer patients for angi- intensity of pain but the frequency of symp- ography if there are any of the following toms, impairment of exercise capacity and abnormalities on exercise ECG: consequent functional limitation. As this • ST elevation information is used to guide treatment and • severe or widespread ST depression monitor response, quantify symptoms accu- • ST depression at low workload or for a rately and determine their impact on work, prolonged period in recovery hobbies and daily activities. Persistence of • fall or failure to rise in BP limiting symptoms despite anti-anginal • ventricular arrhythmia. 69 7 COMA AND ALTERED CONSCIOUSNESS

Consciousness is a poorly defined, ill- history from witnesses, relatives or ambu- understood term. ‘Normal’ consciousness lance crew. In particular, ask about: requires: • the circumstances in which the patient • an intact ascending reticular activating was found, e.g. exposure to temperature system (located in the brainstem and extremes or poisons responsible for arousal) and • the speed, nature and surrounding • normal function of the cerebral cortex, events e.g. sudden onset – subarachnoid thalamus and their connections haemorrhage SAH, seizure, trauma; (responsible for cognition). gradual – expanding intracranial lesion, Altered consciousness results if either metabolic conditions; fluctuating malfunctions. Minor defects, e.g. memory – recurrent seizures; impairment, disorientation or slow cerebra- recent flu-like illness – meningitis, tion, can be subtle and difficult to detect, sepsis) especially if there are coexistent language, • trauma, e.g. road traffic accident, falls, visual or speech problems. Consider the assault possibility of multi-factorial causes contrib- • drug history (prescribed and over-the- uting to altered consciousness: for example, counter), alcohol and recreational a patient who has taken alcohol and then drug use falls in the street, sustaining a head injury, • past medical history. lying unnoticed for hours and becoming Important causes to consider are listed hypothermic. below. The Glasgow Coma Scale (GCS; Table 7.1) was developed to assess/prognosticate Metabolic causes head injury and is commonly used • Hypo/hyper-glycaemia. (although less well validated) to record con- • Hypo/hyper-thermia. scious level in non-traumatic conditions. A • Hypo/hyper-natraemia. GCS score <15/15 indicates altered con- • Hypothyroidism. sciousness. ‘Coma’ denotes a patient with • Metabolic acidosis. no eye response and a GCS ≤8/15. Do not use terms such as semi-conscious, stuper- Drugs/toxins ose, obtunded etc. • Alcohol. Minor disturbance of consciousness is a • Opioids, benzodiazepines, tricyclic central feature of delirium, considered in antidepressants, barbiturates etc. Chapter 8. The assessment pathway in this • ‘Recreational’ drugs, e.g. gamma- chapter is appropriate for patients with a hydroxybutyrate (GHB), ketamine, GCS <15 and: mephadrone etc. • E <3, V <4 or M <5 i.e. >1 point drop in • Carbon monoxide/other cellular toxins, at least one domain e.g. cyanide. • known or suspected head injury • a clinical picture not suggestive of CNS causes delirium. • Trauma: intracranial bleeding As the patient is unlikely to be able to give (extradural, subdural, intracerebral, a clear history, it is essential to obtain a subarachnoid), diffuse axonal injury. 70 Coma and altered consciousness Differential diagnosis 7

• Infection: meningitis, encephalitis, Table 7.1 Glasgow Coma Scale cerebral abscess, cerebral malaria. Criterion Score • Stroke: cortex or brainstem. Eye opening • Subarachnoid haemorrhage. Spontaneous 4 • Epilepsy. To speech 3 • Intracranial space-occupying lesion, e.g. primary or secondary tumour. To pain 2 • Hypertensive encephalopathy. No response 1 • Psychogenic. Verbal response Orientated 5 Organ failure Confused: talks in sentences but 4 • Shock. disorientated • Respiratory failure (hypoxia and/or hypercapnia). Verbalises: words not sentences 3 • Renal failure (uraemic encephalopathy). Vocalises: sounds (groans or grunts) 2 • Liver failure (hepatic encephalopathy). not words No vocalisation 1 Motor response Obeys commands 6 Localises to pain, e.g. brings hand 5 up beyond chin to supra-orbital pain Flexion withdrawal to pain: no 4 localisation to supra-orbital pain but flexes elbow to nail bed pressure Abnormal flexion to pain 3 Extension to pain: extends elbow to 2 nail bed pressure No response 1

71 Coma and altered consciousness 7 Overview

ABCDE + collateral history

Yes 1 Respiratory failure, shock or BM <3.0? Treat immediately and re-evaluate

No

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

No

Yes Rewarm and 3 Core temperature <34ºC? Hypothermia reassess

No

Yes 4 Any suspicion of opioid toxicity? Naloxone trial Opioid toxicity

No

Yes 5 Witnessed seizure activity? See Further assessment of seizure (p. 258)

No

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

No

Full clinical assessment, collateral history, FBC, U+E, LFTs, glucose, Ca2+, TFTs

Yes 7 Major metabolic derangement? Correct (slowly if necessary) and reassess

No

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

No

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

72 Coma and altered consciousness Step-by-step assessment 7

1 Respiratory failure, shock or BM <3.0? with a tympanic reading <35°C or clinical suspicion of hypothermia, e.g. prolonged Ensure a patent airway and provide cervical immobility or exposure to wet and cold spine control if you suspect trauma. As the conditions. GCS falls, definitive airway management, Suspect a contribution to altered con- e.g. tracheal intubation, may be required, so sciousness from hypothermia if the core seek expert anaesthetic help early. Look for temperature is <34°C. Rewarm and reassess and treat rapidly reversible causes of ↓ GCS whilst searching for additional causes. as per the ABCDE assessment: Check TFTs and consider treatment with IV • Assess oxygenation and ventilation by tri-iodothyronine (preceded by IV cortico­ ABG analysis. Treat hypoxia and steroid) if there is any suspicion of myx­ hypercapnia urgently (p. 113). oedema coma. • Give a therapeutic/diagnostic trial of naloxone (see below) if there is 4 Any suspicion of opioid toxicity? ↑PaCO or any evidence of respiratory 2 Give a therapeutic/diagnostic trial of depression. naloxone if the patient has received any • Look for evidence of shock (see Box opioid medication, is a known or suspected 28.1, p. 249); if present, assess and treat ‘recreational’ user, has small pupils or has as per Chapter 28. no obvious alternative cause for altered • Check a blood glucose meter reading consciousness. Any rapid improvement in (‘BM’); if the BM is < 3.0 mmol/L, send conscious level, increase in respiratory blood for formal laboratory glucose rate/depth or pupil dilation indicates that measurement but treat immediately with opioids are contributing, at least in part, to IV dextrose or IV/IM glucagon without the clinical state. The half-life of naloxone is waiting for the result. In patients with shorter than most opioid/opioid metabo- malnutrition/chronic alcohol excess, lites, so further doses or an infusion are consider slow IV thiamine to prevent likely to be needed. the (theoretical) risk of precipitating Wernicke’s encephalopathy. 5 Witnessed seizure activity? Reassess if confusion persists despite effective correction of all of the above. A clear and detailed history from an eyewit- ness is crucial. Whilst ↓ GCS is common 2 Suspect CNS infection? in the post-ictal phase, remember that seizures can be precipitated by a wide Suspect CNS infection in any patient with ↓ spectrum of conditions including hypog­ GCS accompanied by meningism (Box 18.2, lycaemia, head injury ± intracranial p. 167), a new-onset maculopapular or haematoma, alcohol withdrawal, drug purpuric rash, or fever. If malaria is a possi- overdose e.g. tricyclic antidepressants, bility, e.g. recent travel to endemic area, infection etc. perform thick and thin blood films and seek In status epilepticus, associated hypoxia/ immediate expert advice. Otherwise, take hypercapnia aggravates the cerebral injury blood cultures and throat swabs, give empir- and mortality is ∼10%. Assess further as ical IV antibiotics/antivirals and arrange an described on p. 258. urgent brain CT. If there is no clinical or radiological contraindication, perform LP GCS 8, head injury, headache or 6 ≤ for CSF analysis (see Table 18.1, p. 169). evidence of intracranial pathology? Once you have identified and treated major 3 Core temperature <34°C? physiological derangement, life-threatening Measure core temperature with a low- infection and rapidly reversible causes of reading rectal thermometer in any patient ↓GCS, it is vital to identify an intracranial 73 Coma and altered consciousness 7 Step-by-step assessment cause of altered consciousness. In general, 8 Suspicion of drug/alcohol toxicity? immediate brain CT is required in patients with any of the following: Even in patients with a history or features of acute or chronic alcohol intake, never • GCS ≤8 assume that altered consciousness is due • a history of headache or focal to alcohol alone. The correlation between neurological symptoms, lateralising breath or blood alcohol levels and conscious neurological signs, e.g. unilateral level is poor, so beyond confirming that pupillary abnormality, absence of limb alcohol is present, these values are of movement or extensor plantar response, limited help and can be potentially mislead- or signs of ↑ICP (Box 22.2, p. 201) ing. In particular, look for (and treat) • known or suspected head injury alcohol-related hypoglycaemia, occult head • CSF shunt in situ. injury, intracranial bleeding and recrea- Patients must be accompanied by an indi- tional drug use or overdose. vidual who can provide advanced airway/ Examine for characteristic clinical ‘toxid- breathing support as intubation and con- romes’ (Table 7.2) in any patient with trolled ventilation may be needed before the scan is performed. Table 7.2 Common toxidromes associated with 7 Major metabolic derangement? coma/altered consciousness Decreased GCS is common in hypo- and Symptom/signs Drug hypernatraemia, and tends to reflect the rate Respiratory depression, Opioids of sodium alteration rather than the absolute small pupils value (see p. 86). If the disturbance is known Dilated pupils, Tricyclic to be acute, correct promptly then reassess; tachycardia, hyper- antidepressants otherwise, correct cautiously, at a slow rate, reflexia, ↑muscle tone, with frequent remeasurement to avoid urinary retention. If excessive neuronal fluid shifts and conse- severe: cardiac rhythm/ quent cerebral oedema or central pontine ECG abnormalities, ↓BP, myelinolysis. There may be a lag between seizures correction of the metabolic derangement Hypotension, respiratory Barbiturates, and return of normal conscious level. depression, bradycardia, benzodiazepines Decreased GCS may be a feature of dia- ↓muscle tone betic ketoacidosis (DKA). Always consider Tachycardia, ↑BP, Sympathomimetics, DKA if the patient has type 1 diabetes mel- arrhythmias, dilated cocaine, ecstasy, litus; confirm the diagnosis by identifying pupils, tremor, agitation amphetamines, metabolic acidosis on ABG and ketonuria SSRIs on urinalysis. Agitation, myoclonus, Gamma- Suspect hyperosmolar non-ketotic coma seizures, nausea, hydroxybutyrate (HONK) rather than DKA if there is severe bradycardia, coma (GHB) hyperglycaemia e.g. >50 mmol/L, with Vivid hallucinations, Ketamine and hyperosmolarity e.g. >320 mOsm/kg, and agitation, dysphoria, phencyclidine (PCP) dehydration in the absence of significant nystagmus, autonomic ketosis – altered consciousness is a central disturbance, seizures, feature. coma Suspect a contribution to altered con- sciousness from uraemia or disturbances of Euphoria, drowsiness, Solvents plasma calcium, magnesium or phosphate, arrhythmias, only if derangement is severe. laryngospasm

74 Coma and altered consciousness Step-by-step assessment 7 suspected overdose but remember that Consider further investigation if no clear 9 mixed overdoses or cocktails of drugs (often cause identified with alcohol) are common and respiratory/ cardiovascular depression (hypotension, If the cause remains unclear at this stage, arrhythmias etc.) may predominate in any arrange CT brain and send a toxicology severe poisoning. Measure paracetamol screen if not already performed. Consider and salicylate levels (± lithium and iron, if hepatic encephalopathy if the patient has indicated) and, if there is a strong suspicion known or suspected liver disease, or hyper- of illicit drug use, perform a urine toxicol- tensive encephalopathy if BP is consistently ogy screen. See www.npis.org for further >180/120 mmHg with hypertensive retin- information. opathy or evidence of renal involvement. Consider the possibility of carbon monox- Otherwise, seek neurological and/or criti- ide poisoning. The features of CO poisoning cal care input and consider MRI (brainstem are non-specific; the classic description pathology), EEG (non-convulsive status, of cherry-red mucous membranes/skin is hepatic encephalopathy) and LP (CNS very rare. An associated severe metabolic infection). acidosis and ECG changes of ischaemia/ Psychogenic unresponsiveness is a diag- infarction with arrhythmias and hypoten- nosis of exclusion, but consider it if com­ sion may be found. Some pulse oximeters prehensive investigation fails to reveal an can measure COHb. Confirm with formal underlying cause and there are suggestive measurement of COHb on arterial or venous signs, e.g. response to tickling, resistance to blood sample. Remember that the half-life passive eye opening, and gaze deviating of COHb (∼4 hours if breathing room air) towards the floor in any position. will be significantly less if the patient has been breathing oxygen.

75 8 CONFUSION: DELIRIUM AND DEMENTIA

Confusion (impaired cognition) is global • Antipsychotics* impairment of mental function. • Lithium Delirium is an abrupt decline in cogni­ • Corticosteroids (especially high-dose) tive function that follows a fluctuating • Baclofen course and is accompanied by impaired • Levodopa/dopamine agonists attention e.g. easily distracted, unable to • Digoxin maintain focus, and disturbance of con­ (*indicates that confusion may arise sciousness (‘hyperalert’/agitated or drowsy/ from either drug toxicity or ↓awareness). Common associated features withdrawal). include reversal of the sleep–wake cycle, hallucinations, delusions and altered Metabolic/physiological disturbance emotion/psychomotor behaviour. • Hypoxia Dementia is a chronic, progressive decline • Hypercapnia in cognitive function without disturbance • Shock of consciousness. • Hypo/hyperthermia The initial challenge with confused • Hypo/hyperglycaemia patients is finding them (sometimes liter­ • Hyponatraemia ally). Agitated, restless patients rapidly • Hypo/hypercalcaemia attract attention but those with ‘hypoactive • Dehydration delirium’ are quiet, withdrawn and easily • Uraemia missed. In patients with pre-existing • Metabolic acidosis dementia, delirium may be overlooked • Hepatic encephalopathy unless baseline cognitive function is estab­ • Hypo/hyperthyroidism lished. It is also possible to mislabel dys­ phasic, deaf or depressed patients as Infection confused. • CNS infection: Delirium • Meningitis (bacterial, viral, fungal, The differential diagnosis of delirium is tuberculosis) wide and, in patients with a ‘vulnerable • Encephalitis brain’ (Box 8.1) includes almost any acute • Cerebral abscess physical, mental or environmental insult. • Cerebral malaria Causes are listed below; those shown in • Non-CNS infection: bold are unlikely to be solely responsible • Sepsis for delirium, except in patients with a ‘vul­ • Pneumonia nerable brain’. • Urinary tract • Biliary/intra-abdominal Drugs • Endocarditis • Alcohol* • Opioids* Intracranial causes • Benzodiazepines* • Seizures (post-ictal state) • Anticonvulsants • Haemorrhage • Tricyclic antidepressants* • Space-occupying lesion • Anticholinergics • Head injury • Antihistamines • ↑Intracranial pressure 76 Confusion: Delirium and dementia Differential diagnosis 8

Box 8.1 Delirium and the ‘vulnerable brain’ • Unusual stimuli and sensory impairment When assessing delirium, consider predisposing factors, as well as acute Dementia/chronic cognitive precipitants. Elderly patients (especially >80 impairment years) and those with pre-existing cognitive Common causes impairment (diagnosed or undiagnosed), • Alzheimer’s disease multiple sensory deficits, general physical • Vascular disease frailty, chronic alcohol excess or any significant • Lewy body dementia underlying brain disorder e.g. cerebrovascular disease, Parkinson’s disease, multiple sclerosis ‘Reversible’ causes

have a reduced threshold for developing • BVitamin 12/folate deficiency delirium. These patients have a ‘vulnerable • Subdural haemorrhage brain’ and delirium may result from relatively • Hypothyroidism minor insults that would not normally impair • Normal pressure hydrocephalus cognitive function in healthy patients without • HIV such predisposing factors. • Neurosyphilis • Wilson’s disease

Other causes • Frontotemporal dementias Other causes • Korsakoff’s psychosis • Pain • Multiple sclerosis • Postoperative • Progressive multifocal • Constipation leucoencephalopathy • Urinary retention • Subacute sclerosing panencephalitis • Acute abdominal pathology • (Variant) Creutzfeld–Jakob disease (pancreatitis, appendicitis) • Huntington’s disease • Myocardial infarction • Carbon monoxide Disorders that may mimic confusion • Acute thiamine deficiency (Wernicke’s • Depression encephalopathy) • Dysphasia • Paraneoplastic syndromes • Deafness • Cerebral vasculitis • Acute psychosis • Acute intermittent porphyria • Behavioural disturbance • Heavy metal poisoning e.g. lead, arsenic • Amnesic syndromes

77 Confusion: Delirium and dementia 8 Confusion: Overview

Full clinical assessment, collateral history, AMT (Box 2.4) & Confusion Assessment Method (Box 8.2)

Yes Consider depression/dysphasia/deafness 1 Normal cognitive function? behavioural disturbance

No

Yes Go to Delirium 2 Normal baseline cognitive function? Likely delirium (p. 80)

No

Go to Delirium Acute cognitive function, fluctuating Yes Likely delirium with 3 ↓ (p. 80) course, altered consciousness/attention underlying dementia

No

Consider treatment Mood/motivation/enjoyment, or Yes 4 ↓ Possible depression and/or expert Geriatric Depression Scale score >4 assessment

No Go to further assessment 5 Likely dementia of chronic confusion (p. 87)

Clinical tool Confusion assessment method The Confusion Assessment Method is a difficulty keeping track of what is being sensitive tool for diagnosing delirium. It said? contains four elements. Delirium is diagnosed 3. Disorganised thinking if both 1 and 2 are present, plus at least one Is the conversation rambling or irrelevant? of 3 and 4. Is the flow of ideas unclear or illogical? 1. Acute change in mental status and Do they switch unpredictably from subject fluctuating course to subject? Is there evidence of an acute change in 4. Altered level of consciousness mental status from the patient’s Is the patient ‘hyperalert’? baseline? Does this fluctuate during the Is the patient drowsy or difficult to rouse? day (come and go; ↑ and ↓ in severity)? 2. Inattention Does the patient have difficulty focusing attention, e.g. easily distractible, or have

Source: Inouye S, van Dyck C, Alessi C et al. 1990. Clarifying confusion: the confusion assessment method. Annals of Internal Medicine. 113(12):941–948.

78 Confusion: Delirium and dementia Confusion: step-by-step assessment 8

1 Normal cognitive function? change. Spend time speaking with the patient and observing behaviour. In Disorientation, forgetfulness and muddled addition to direct observation, seek evi­ thinking may be apparent from normal dence of fluctuation through discussion conversation but confirm with an objective with nursing staff or review of overnight assessment, e.g. the abbreviated mental test reports. Delirium is frequently superim­ (AMT; Box 2.4, p. 15) or mini-mental state posed on dementia (acute on chronic confu­ examination (MMSE). Use these tools to sion) – look for important clues such as screen for confusion in all patients with a sudden decline in cognitive abilities, altera­ ‘vulnerable brain’ (Box 8.1). Ensure that tion of consciousness, fluctuating course apparent cognitive impairment is not due and difficulty concentrating. to communication problems (deafness, dys­ arthria, language barriers) or an isolated Mood/motivation/enjoyment, or Geriatric 4 ↓ disorder of comprehension (receptive dys­ Depression Scale score >4? phasia), word-finding difficulty (expressive Depression can mimic or exacerbate demen­ dysphasia), memory (amnesic syndrome), tia. Ask patients if they feel low in mood behaviour or mood. Patients with depres­ but also enquire about things they take sion often score poorly in formal testing pleasure in (do they still enjoy them?), as through refusal to volunteer answers rather well as biological symptoms (early morning than making mistakes – if these patients are waking, ↓appetite, ↓weight). During con­ encouraged (or treated), performance may versation, note expressions of guilt, worth­ improve. lessness, pessimism and other negative 2 Normal baseline cognitive function? thoughts (especially if exaggerated or incongruent with circumstances) and look Establish baseline cognitive function and for psychomotor retardation, lack of depth any recent change in mental status by or variety in affect, and poor eye contact. speaking to relatives/friends/carers and Scoring systems, e.g. the geriatric depres­ checking previous cognitive assessments. sion scale (GDS), may assist diagnosis. If Thorough questioning is important as rela­ uncertain, refer for specialist evaluation or tives may have the impression that baseline reassess after a trial of treatment. cognition was normal – as the patient was in a familiar environment, seeing familiar 5 Likely dementia people, talking about familiar topics and There is no absolute division between acute not being pressed on recent events – even if and chronic confusion in terms of timing or baseline cognition was, in fact, impaired. causes. Even if the cause has been removed, Acute cognitive function, fluctuating it can take weeks for a delirium to resolve 3 ↓ course, altered consciousness/attention? fully. Further, chronic confusion can fluctu­ ate. However, if confusion has persisted for Use the Confusion Assessment Method >2 weeks without an obvious acute cause (CAM; Clinical tool) to diagnose delirium. or evidence of improvement, see ‘Further Having established baseline cognitive func­ assessment of chronic confusion’ below. tion, look for any evidence of an acute

79 Confusion: Delirium and dementia 8 Delirium: Overview

ABCDE

Yes 1 BM < 3.0 / deranged physiology? Treat immediatedly and re-evaluate

No

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

No

Yes Urgent 3 High risk of intracranial pathology? Intracranial lesion neuroimaging

No

Full clinical assessment, collateral history, FBC, U+E, LFTs, glucose, Ca2+, TFTs, CRP

Yes 4 Metabolic disturbance? Correct and reassess Seek underlying cause

No

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

No

Yes Consider intoxication/withdrawal/ 6 Alcohol excess/dependence? Wernicke’s encephalopathy

No

Yes 7 Known or suspected liver disease? Consider hepatic encephalopathy

No

Baseline cognitive impairment or Yes 8 See Delirium in the vulnerable brain (p. 84) ↑susceptibility to delirium?

No

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

No

Neuroimaging and toxicology screen if not already performed 10 Review environmental exposures; reconsider alcohol withdrawal Neurology ± Psychiatry review

80 Confusion: Delirium and dementia Delirium: step-by-step assessment 8

1 BM <3.0/deranged physiology? is relatively resistant to metabolic insult so confusion should not be attributed Evaluate and treat respiratory failure solely to modest biochemical derangement. (Ch 12), shock (Ch 28), depressed con­ However, delirium is likely to be explained sciousness (Ch 7), hypothermia and seizure by hypoglycaemia or severe dehydration, (Ch 29) before considering other causes of metabolic acidosis, ↓Na+ (especially delirium. If the BM is <3.0 mmol/L, send <120 mmol/L), ↑Ca2+ (>3.0 mmol/L) or blood for laboratory glucose measurement hyperglycaemia e.g. hyperosmolar non- but treat immediately, without waiting for ketotic coma. Uraemia is an unusual cause the result. Reassess if confusion persists of acute confusion in the non-vulnerable despite effective correction. brain but may result in toxic accumulation of medication. 2 Suspect meningitis? The vulnerable brain is more sensitive to Assume meningitis/encephalitis if the metabolic derangement – even mild dehy­ patient has meningism (Box 18.2, p. 167), a dration, renal impairment or glycaemic/ purpuric rash or a febrile illness with head­ electrolyte/thyroid disturbance may impair ache, seizures, focal neurological signs or cognition. Correct any disturbances but no obvious alternative source. Take blood continue to search for additional contribut­ cultures and throat swabs immediately. ing factors. Give empirical IV antibiotics/antivirals. If See ‘Further assessment of hyponatrae­ there are no contraindications, perform mia’ (below) in any patient with unex­ + an LP (p. 168). Request CT prior to LP if plained ↓Na . seizure, focal neurological signs, drowsi­ ness or papilloedema are present. 5 Likely drug toxicity?

3 High risk of intracranial pathology? Illicit drug use or poisoning Consider urgent CT brain to exclude a Substance abuse is a common cause of acute structural CNS cause if any of the following confusion/psychosis in younger patients. is present: If it is suspected, use all available sources of information to establish what has been • new focal neurological signs or ataxia taken and when. Look for characteristic • first seizure clinical features of toxicity (see Table 7.2, • drowsiness (if strong suspicion of opioid p. 74) and consider a urine toxicology toxicity, consider a trial of naloxone screen. See www.npis.org for further infor­ prior to the CT scan) mation. Give naloxone in patients with fea­ • recent head injury tures of acute opioid toxicity – a response • sudden severe headache should occur within seconds to minutes; • any fall/trauma in a patient on observe closely for symptoms of acute anticoagulation opioid withdrawal (sweating, tremor, agita­ In patients with active malignancy, tion, seizures). immunosuppression or recent falls without Prescribed medication definite head injury, it is reasonable to Anticonvulsants, lithium, sedatives and explore other causes of delirium first, but opioids can cause confusion, even in healthy have a low threshold for early neuroimag­ brains. Many other drugs may precipitate ing to exclude intracranial metastases/ delirium in the vulnerable brain (see Box abscess/haemorrhage. 8.1), especially tricyclic antidepressants, anticholinergics e.g. oxybutynin, antipsy­ 4 Metabolic disturbance? chotics, and antihistamines. Even if they are Check laboratory glucose, even if BM is normally well tolerated, these agents may within the normal range. The healthy brain contribute to delirium in the context of 81 Confusion: Delirium and dementia 8 Delirium: step-by-step assessment other acute insults. Benzodiazepines can but consider neuroimaging if this is a first have a paradoxical effect, worsening confu­ fit, or if focal neurological signs, head injury sion and agitation. Abrupt withdrawal of or poor response to benzodiazepines is benzodiazepines and opioids can also pre­ present. cipitate delirium, often several days after Wernicke’s encephalopathy stopping. Verify all drugs and dosages with the Consider thiamine deficiency and the need patient/relatives/carers. Check how fre­ for supplementation in all patients with quently PRN medications, especially ben­ acute confusion on a background of chronic zodiazepines and opioids, are used at home alcohol excess. Give immediate IV thiamine and ensure they have not been inadvert­ if there is short-term memory loss, diplopia, ently omitted, reduced or reinstated in hos­ gaze palsy, nystagmus, ataxia or severe pital. Consider a trial cessation or ↓dose of malnutrition. any drug with potential CNS side-effects 7 Known or suspected liver disease? (see Table 7.2, p. 74), especially if recently introduced or increased. Weigh the likeli­ Suspect hepatic encephalopathy in any hood of toxicity against ongoing treat­ patient with an existing diagnosis or clinical ment benefit and predictable problems on features of cirrhosis. The presence of con­ discontinuation. Where necessary, taper structional apraxia (inability to draw a the dose gradually to avoid withdrawal star) and/or asterixis (Fig. 19.1, p. 178) and symptoms. absence of florid hallucinations/adrenergic features may differentiate hepatic encepha­ 6 Alcohol excess/dependence? lopathy from alcohol withdrawal in patients with alcoholic liver disease. If encephalopa­ Acute alcohol intoxication thy is suspected, seek and treat potential Acute alcohol intoxication is the most precipitants, including spontaneous bacte­ common cause of altered mental status in rial peritonitis (an ascitic tap is mandatory the emergency department but may coexist if ascites is present), other infections, dehy­ with other pathology e.g. head injury, liver dration, constipation, subclinical GI bleed­ injury, nutritional deficiency. Confirm the ing and drugs with CNS toxicity. presence of alcohol with breath or blood Consider acute liver failure in patients tests but always search for additional causes without cirrhosis who exhibit construc­ of confusion. tional apraxia ± asterixis in association with jaundice, ↑ALT or ↑PT. Perform an ABG to Alcohol withdrawal exclude hypercapnia if there is asterixis This may present early, e.g. 6–12 hours after without these features. cessation of drinking, or late, e.g. 2–3 days after hospital admission. Typical symptoms Baseline cognitive impairment or 8 include confusion, agitation, hallucinations ↑susceptibility to delirium? and adrenergic over-stimulation (tremor, The diagnostic approach now depends on sweating, tachycardia). The diagnosis is the underlying threshold for developing obvious in patients with a florid presenta­ delirium. If any feature in Box 8.1 is present, tion and clear history of alcohol excess/ proceed to ‘Delirium in the vulnerable dependence but consider it in all cases brain: overview of further assessment’ of unexplained delirium. Use the CAGE below. questionnaire to screen for alcohol pro­ blems, identify elderly patients with 9 Evidence or high risk of infection? subtle dependence e.g. ‘large’ daily sherry, obtain a collateral history and look for an Suspect CNS infection in patients with isolated increase in GGT/mean cell volume. ↑temperature/WBC/CRP or ↑susceptibil­ Seizures may complicate severe withdrawal ity (foreign travel, immunosuppression, 82 Confusion: Delirium and dementia Delirium: step-by-step assessment 8 animal bite). Do not attribute confusion to and structural disease. If CT is non- minor non-CNS infections. diagnostic, consider MRI brain. Check Seek urgent input from an ID unit if the carboxyhaemoglobin levels for carbon patient has recently travelled to the devel­ monoxide toxicity if there is associated oping world, has received an animal or tick headache or if the patient has been exposed bite, is HIV-positive or is taking immuno­ to smoke/exhaust fumes (though levels suppressive therapy, e.g. long-term ster­ may correlate poorly with symptoms). oids, chemotherapy. Send blood for thick Measure urinary porphyrins (liaising with and thin films if travel to a malaria-endemic the biochemistry laboratory in advance), region has been undertaken within the last especially if there is associated abdominal 3 months. Otherwise, LP is mandatory to pain. Test for HIV. exclude CNS infection. If the cause is still not apparent, seek If CNS infection has been excluded, treat expert neurological ± psychiatric input. any other apparent source of infection but EEG may assist in the diagnosis of atypical continue to search for additional causes of seizures, toxic encephalopathies or unusual confusion. neurodegenerative diseases. Other tests to consider include autoimmune/vasculitis Neuroimaging and toxicology screen. antibodies (cerebral vasculitis?), syphilis/ 10 Consider other causes. Neurology ± Lyme disease serology, antineuronal anti­ Psychiatry review bodies (paraneoplastic syndrome?) and If not already carried out, perform neu­ heavy metal levels in blood and urine. roimaging and LP to exclude CNS infection

83 Confusion: Delirium and dementia 8 Delirium in ‘Vulnerable Brain’: Overview

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

No

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

No

Exclude silent MI Clinical or ECG evidence of acute Yes 3 Correct hypoxia/hypotension; optimise cardiac disorder? treatment of heart failure/arrhythmia

No

Yes 4 Palpable bladder? Insert/replace catheter; send CSU

No

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

No

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

No

Consider other causes, e.g. viral illness, depression 7 Neuroimaging to exclude structural CNS disease if confusion persists or deteriorates Establish accurate baseline function; reassess and reorientate regularly

84 Confusion: Delirium and dementia Delirium in ‘Vulnerable Brain’: step-by-step assessment 8

Likely source of infection or systemic ST elevation MI. Check troponin and assess 1 inflammatory response? further for acute coronary syndrome if there are other indicative ECG changes. In the vulnerable brain, even minor infec­ Cardiac failure may contribute to delirium tions can trigger delirium. Infections may through hypoxia or cerebral hypoperfusion. present ‘atypically’ lacking characteristic Avoid hypotension where possible (review symptoms and signs. medication) and correct hypoxia and In patients with ↑temperature/WBC/ anaemia. Treat any brady- or tachyarrhyth­ CRP, take blood cultures and look for mias and consider diuretic if there is fluid a septic focus (p. 140). Also consider overload. atypical presentations of acute abdominal pathologies, e.g. perforation, pancreatitis, Palpable bladder/Constipated/Sensory 4-6 appendicitis, cholecystitis or diverticulitis. impairment? Re-examine regularly, check amylase and have a low threshold for abdominal imaging Actively look for and treat urinary reten­ – especially if there is any pain/tenderness tion, constipation and nutritional deficiency or deranged LFTs. If there is still no cause (including B12/folate). If a urinary catheter apparent, consider LP. is required, it may be possible to withhold Even in the absence of ↑temperature/ anticholinergic drugs for detrusor inst­ WBC/CRP, consider empirical antibiotic ability. Patients with moderate to severe treatment if there is a convincing focus dementia are at high risk of becoming of infection, e.g. positive MSU or new puru­ acutely confused when presented with lent sputum, but weigh the likelihood of unusual surroundings, people and stimuli. bacterial infection against complications Provide frequent reassurance and reorien­ such as GI upset or Clostridium difficile tation, encourage visits from family diarrhoea. members, check that patients have their normal glasses and hearing aids, and ensure 2 Pain present? adequate lighting. Consider other causes. Neuroimaging. Pain can cause or contribute to delirium in 7 the vulnerable brain and may be difficult to Establish baseline function assess if the patient is agitated or muddled. In the absence of another indication for Wherever possible, identify and treat the brain imaging, it may be reasonable to per­ underlying cause using simple analgesia/ severe with the above measures for several non-pharmacological measures as first-line days. However, CT brain may be required treatment but do not leave patients in dis­ to exclude subdural haemorrhage and other tress. Where opioids are required, carefully structural pathology if the patient fails to up-titrate and monitor. improve or deteriorates. Review medica­ tions daily and reassess regularly for pain, Clinical or ECG evidence of acute cardiac 3 metabolic disturbance or infection. Make a disorder? detailed assessment of baseline cognitive Occasionally, myocardial infarction (MI) ability and level of function. Finally, con­ presents as delirium. Seek urgent cardiol­ sider rarer causes, as described for the non- ogy input if the ECG meets the criteria for vulnerable brain.

85 Confusion: Delirium and dementia 8 Confusion: further assessment

Further assessment of hyponatraemia Step 3 Assess volume status Step 1 Confirm true hyponatraemia Clear evidence of either ↑ or ↓ECF volume Apparent hyponatraemia may result is very helpful in determining the underly­ from drip arm contamination, laboratory/ ing cause. Categorise the patient as: labelling error, or ‘pseudohyponatraemia’ • ‘hypervolaemic’ if there is evidence of due to hyperlipidaemia, hyperproteinae­ fluid overload, e.g. oedema, ↑JVP, mia, hyperglycaemia or high plasma ascites ethanol. Check plasma osmolality (usually • ‘hypovolaemic’ if there is evidence of normal in pseudohyponatraemia) and fluid depletion, e.g. dry mucous + recheck Na if the result appears spurious. membranes, ↓skin turgor, thirst, ↓JVP Step 2 Estimate the rate of Na+ decline The most common causes of hypervolae­ + A rapid ↓ in plasma Na may lead to life- mic hyponatraemia are cardiac failure, cir­ threatening cerebral oedema, and requires rhosis, oliguric renal failure and nephrotic prompt correction. In contrast a gradual ↓ syndrome. If the cause is not obvious, check + in Na allows osmotic adaptation by cere­ for proteinuria, perform an echocardio­ bral neurons and rapid correction may lead gram and assess for evidence of cirrhosis to irreversible and brainstem damage (cer­ (p. 177). ebral pontine myelinolysis). In hypovolaemic hyponatraemia there is It is therefore critical to distinguish acute Na+ and water depletion, with relatively (<72 hours) from chronic (>72 hours) greater Na+ loss. The most common causes hyponatraemia. Suspect chronic if any of are excessive diuretic therapy and acute the following features is present: diarrhoea/vomiting. + • Urecent +E results demonstrating a If the source of Na and water loss is progressive decline in plasma Na+ not obvious, measure urine sodium. The • slowly progressive onset of symptoms, normal response of the kidneys to salt + e.g. anorexia, lethargy, confusion and water depletion is to minimise Na + • asymptomatic or only mild symptoms excretion. If urine Na is appropriately with a plasma Na+ ≤125 mmol/L low (<20 mmol/L), suspect GI tract losses, • no clear cause for a sudden decrease in e.g. diarrhoea, vomiting or ‘third space’ plasma Na+ (see below) losses, e.g. pancreatitis, burns. If urine Na+ is (>20 mmol/L), then there is a contri­ + In these patients, correct Na with bution to salt and water depletion from extreme care. Recheck U+E every 2–4 hours, renal losses, e.g. adrenal insufficiency, renal + and aim for a rise in plasma Na of tubular acidosis or ‘salt-wasting’ renal ≤8 mmol/day. disease. Suspect acute hyponatraemia if: Step 4 If cause unclear, measure urine • abrupt onset of symptoms within the sodium and osmolality last 48 hours OR If feasible, discontinue any diuretics for 10 • major symptoms (severe confusion, days and recheck U+E alongside plasma ↓GCS, seizures) with Na+ ≥120 mmol/L, and urine osmolality and urine Na+. especially with a history of sudden increase Low urine Na+ (<20 mmol/L) implies in free water intake, e.g. excessive IV dex­ that ↓ plasma Na+ is not due to excessive trose administration (especially postopera­ renal Na+ losses. The cause may be hypo­ tively) or polydipsia. volaemic hyponatraemia due to extra-renal If you suspect acute hyponatraemia, seek losses (see above) but without obvious clin­ urgent expert advice but, in an emergency, ical manifestations of hypovolaemia. In this aim to increase plasma Na+ by 4–6 mmol/L case, urine osmolality will be ↑ (>150 mmol/ over 1–2 hours then reassess. kg) due to the presence of other solutes. If

86 Confusion: Delirium and dementia Confusion: further assessment 8 urine osmolality is <150 mmol/kg, the Further assessment of chronic likely cause is excessive water intake. In confusion hospitalised patients check for recent The approach to progressive cognitive administration of hypotonic IV fluids, e.g. decline over a period of months to years 5% dextrose. In non-hospitalised patients differs from the approach to acute con­ consider psychogenic polydipsia. fusion. Exclude the reversible causes from If hyponatraemia is accompanied by p. 77 with a CT brain and blood tests then ↑urine Na+ (>20 mmol/L) and osmolality refer. Dementia is best managed by experts (>150 mmol/kg), consider diuretic use, so, after following the steps below, refer adrenal insufficiency, hypothyroidism, salt- patients without a reversible cause for spe­ wasting renal disease and the syndrome of cialist evaluation and care. inappropriate ADH secretion (SIADH). Check TFTs and perform a short Syn­ Consider psychiatric illness acthen test. High or high–normal plasma Perform an objective measure of cognition urea/uric acid may indicate subtle ↓ECF (at least MMSE) to ensure the presentation volume; if present, consider salt-wasting fits with a chronic decline in cognition diseases or occult diuretic use. Otherwise, dementia. Depression can mimic or exacer­ the likely diagnosis is SIADH. bate dementia and may be difficult to diag­ If SIADH is suspected, look for an under­ nose. Consider using tools such as the lying cause (Box 8.2). Consider trial cessa­ Cornell scale to assist diagnosis and, if you tion of any suspected causative agent. If the suspect depression, reassess cogntive func­ cause remains unclear, request a CXR and tion after a trial of anti-depressant therapy. CT brain and assess the response to fluid Assess for reversible causes restriction (<1 L/day). Perform a CT brain in every patient with chronic confusion. This may identify revers­ ible causes, e.g. subdural haemorrhage or normal pressure hydrocephalus (ataxia and incontinence should raise the index of Box 8.2 Causes of SIADH suspicion), or suggest possible aetiological • Tumours, especially small-cell lung cancer factors, e.g. vascular disease. Measure TFTs in all patients, as hypothyroidism can • CNS disorders: stroke, trauma, infection present as dementia and responds to treat­ • Pulmonary disorders, e.g. pneumonia, ment. Take a careful alcohol history and tuberculosis consider Wernicke–Korsakoff syndrome in • Drugs any patient with chronic alcohol misuse. • Anticonvulsants, e.g. carbamazepine Look for and correct nutritional deficien­ cies, e.g. B12, folate. • Psychotropics, e.g. haloperidol Consider rare causes • Antidepressants, e.g. fluoxetine Perform a more intensive work-up if the • Cytotoxics, e.g. cyclophosphamide patient has an unusual pattern of cognitive • Hypoglycaemics, e.g. chlorpropamide impairment e.g. preserved recent memory • Opioids, e.g. morphine or personality/speech change, unexplained • Sustained pain, stress, nausea, e.g. neurological findings on examination, a postoperative state rapid course of cognitive decline, or onset at a young age. This should usually include • Acute porphyria an HIV test, copper studies, Lyme/syphilis • Idiopathic serology, MRI brain and LP ± further spe­ cialist assessment, e.g. EEG.

87 9 DIARRHOEA

Diarrhoea may be defined as the passage diagnosis is based on typical clinical fea­ of ≥3 loose or liquid stools/day. The dif­ tures (Box 9.1) in the absence of apparent ferential diagnosis depends on symptom organic disease. Symptoms tend to follow a duration. Acute diarrhoea (<2 weeks) is relapsing and remitting course, often exac­ usually infectious but occasionally is due erbated by psychosocial stress. to drugs or a first presentation of inflam­ Drugs matory bowel disease. Chronic/relapsing diarrhoea may reflect colorectal cancer Many drugs, including numerous over- or inflammatory bowel disease, but the the-counter preparations, cause diarrhoea most frequent cause is irritable bowel (Box 9.2). syndrome. Colorectal cancer Infectious diarrhoea Colorectal cancer may present with diar­ rhoea, especially if left-sided/distal. Sug­ Infectious diarrhoea is due to faecal–oral gestive features include weight loss, rectal transmission of viruses, bacteria, bacterial bleeding, a palpable mass or iron-deficiency toxins or parasites. Most cases are self- anaemia, but their absence DOES NOT limiting and a pathogen is rarely identified. exclude malignancy. The diagnosis must Viruses and toxins predominantly affect the be considered in any patient >45 years stomach and small bowel, causing large- with new-onset, persistent diarrhoea and is volume, watery diarrhoea and pronounced usually confirmed by colonoscopy with vomiting; in toxin-mediated diarrhoea e.g. biopsy. Staphylococcus aureus, the incubation period is typically <12 hours. Invasive intestinal pathogens, including certain strains of Box 9.1 Rome III criteria for diagnosis of Escherichia coli, and Shigella, may cause irritable bowel syndrome bloody diarrhoea, often with severe abdom­ Recurrent abdominal pain or discomfort on at inal cramps and systemic upset (dysentery). least 3 days per month during the previous 3 Clostridium difficile infection (CDI) is an months that is associated with 2 or more of important cause of hospital-acquired diar­ the following: rhoea, especially following broad-spectrum • relieved by defecation antibiotic therapy; CDI ranges from mild diarrhoeal illness to life-threatening pseu­ • onset associated with a change in stool domembranous colitis. Diarrhoea that frequency persists for >10 days is unlikely to be infec­ • onset associated with a change in stool tive, but consider protozoal infections, e.g. form or appearance. giardiasis, amoebiasis or Cryptosporidium Supporting symptoms include: infection, in patients who are immunocom­ • altered stool frequency promised or have recently travelled to the tropics. • altered stool form Irritable bowel syndrome • altered stool passage (straining and/or urgency) Irritable bowel syndrome is the most • mucorrhoea common cause of chronic diarrhoea. The predominant bowel habit may alternate • abdominal bloating or subjective distension. between diarrhoea and constipation, and 88 Diarrhoea Differential diagnosis 9

Box 9.2 Drugs that frequently cause diarrhoea Box 9.3 Extra-intestinal features of inflammatory bowel disease • Laxatives (including occult laxative abuse) • General: fever, malaise, weight loss • Antibiotics (especially macrolides) • Eyes: conjunctivitis, episcleritis, iritis • Alcohol (especially chronic alcohol excess) • Joints: arthralgia of large joints, sacroiliitis/ • NSAIDs ankylosing spondylitis • Metformin • Skin: mouth ulcers, erythema nodosum, • Colchicine pyoderma gangrenosum • Orlistat • Liver: fatty liver, gallstones, sclerosing cholangitis, cholangiocarcinoma (ulcerative • Proton pump inhibitors colitis) • SSRIs • Nicorandil • Cytotoxic agents Disorders causing malabsorption Fat malabsorption causes pale, greasy, offensive stools that float and are difficult Inflammatory bowel disease to flush (steatorrhoea). Other features of malabsorption include undigested food­ Ulcerative colitis (UC) is confined to the stuffs in stool, weight loss, bloating and large bowel and typically presents with nutritional deficiencies. The usual underly­ bloody diarrhoea and cramping lower ing cause is small bowel disease e.g. coeliac abdominal pain ± tenesmus, mucus dis­ disease, Crohn’s disease, tropical sprue, charge, fever and constitutional upset. lymphoma, small bowel resection, or pan­ Crohn’s disease can affect any part of the creatic insufficiency. alimentary tract and may present with large bowel symptoms similar to those of UC, or Other causes with small bowel symptoms, e.g. watery, • Diverticulitis, ischaemic colitis. non-bloody diarrhoea accompanied by • Hyperthyroidism, autonomic abdominal pain and weight loss. Both dis­ neuropathy. orders are associated with a range of extra- • Carcinoid tumour, gastrinoma, VIPoma. intestinal features (Box 9.3). • Severe constipation with overflow.

89 Diarrhoea 9 Acute diarrhoea: Overview

Full clinical assessment, PR exam ± stool culture

1 Resuscitation requirements and illness severity assessed?

Yes

Yes Consider dysentery, diverticulitis, ischaemic 2 Bloody diarrhoea? colitis, inflammatory bowel disease

No

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

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

Yes Discontinue drug 5 Likely drug culprit? Drug-related diarrhoea if possible

No

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

Resuscitation requirements and illness inhibitors, NSAIDs. Patients with AKI 1 severity assessed? require IV rehydration with close monitor­ ing of fluid balance, urine output and U+E. Step 1 Are there features of shock? If AKI occurs in the context of bloody diar­ Look for ↑HR, ↓BP (a late sign) or rhoea, look for features of haemolytic evidence of tissue hypoperfusion (See uraemic syndrome, e.g. ↓Hb, ↓platelets, Box 28.1, p. 249). If present, provide ↑bilirubin/LDH/reticulocytes. aggressive IV fluid resuscitation and reas­ Step 3 Does the patient otherwise require sess. Although hypovolaemia from GI IV fluids/hospital admission? losses would be the likeliest cause, also consider intra-abdominal SIRS/sepsis, Patients with clinical evidence of dehydra­ medication and adrenal insufficiency (diar­ tion (thirst, dry mucous membranes, ↓skin rhoea is a common feature of acute adrenal turgor) and concomitant vomiting, or those crisis). are unable to match oral intake to ongoing losses require IV fluids. Step 2 Is there acute renal impairment? Other features that may indicate a need Hypovolaemia may result in severe ‘pre- for hospital admission include: renal’ acute kidney injury (AKI), especially • fever if compounded by antihypertensive or • ↑WBC nephrotoxic medication e.g. diuretics, ACE • bloody diarrhoea 90 Diarrhoea Acute diarrhoea: Step-by-step assessment 9

• abdominal tenderness/guarding/ atherosclerotic disease or a source of sys­ rigidity. temic embolism e.g. atrial fibrillation. • frail, elderly or immunocompromised Refer any patient with known inflamma­ patient tory bowel disease, extra-intestinal mani­ • significant comorbidity e.g. heart/ festations (see Box 9.3), previous similar renal/hepatic failure. episodes or symptoms >7 days for specialist GI evaluation. 2 Bloody diarrhoea? Seek an urgent surgical review if there is evidence of peritonism or toxic megaco­ The frequent passage of bloody stools sug­ lon, or you suspect ischaemic colitis or gests either: diverticulitis. • infection with invasive organisms, e.g. Campylobacter, Shigella or Amoeba, or 3 Risk of C. difficile infection? cytotoxin-producing organisms, e.g. Send stool for CDT in any patient who lives C. difficile, E. coli O157 OR in an institution e.g. nursing home, has • non-infectious colitis, e.g. ischaemic recently been hospitalised, received antibi­ colitis inflammatory bowel disease otics within the last 3 months or is >65 It is often difficult to differentiate dysen­ years. In high-risk patients send ≥3 samples tery from a first attack of inflammatory before ruling out the diagnosis. bowel disease in the early stages: both may be accompanied by abdominal pain, tenes­ 4 Risk of protozoal infection? mus, mucus, constitutional upset and a sys­ Send three stool samples on consecutive temic inflammatory response (see Box 14.1, days for ova, cysts and parasites in patients p. 139). with a history of recent foreign travel, when • Send FBC, CRP and three stool samples there is known or suspected immunocom­ in all patients, plus blood cultures if promise e.g. chemotherapy, HIV or in men fever is present. who have sex with men. • Test stool for C. difficile toxin (CDT) if the patient has risk factors (see below), 5 Likely drug culprit? severe systemic upset or ↑↑WBC. Suspect drug-related diarrhoea if the onset • Liaise with the ID team and request of symptoms corresponds with initiation analysis of stool for ova, cysts and or ↑dose of drug, especially those listed parasites if recent foreign travel. in Box 9.2. Seek an alternative explanation • Request an abdominal X-ray to look for if diarrhoea does not resolve on drug colonic dilatation (see Fig. 4.5B, p. 32) discontinuation. if there is abdominal tenderness/ distention or a pronounced systemic Likely gastroenteritis. Liaise with ID/GI if 6 inflammatory response. symptoms persist >10 days Unless there are specific pointers to an Most cases are self-limiting viral or toxin- alternative diagnosis, suspect an infectious mediated infections and do not require cause if the duration of symptoms is <8 days. further investigation or antimicrobial treat­ Consider ischaemic colitis if bloody diar­ ment. If symptoms persist >10 days, seek rhoea was preceded by sudden onset of specialist advice and consider further left-sided lower abdominal pain or assessment as for chronic/relapsing diar­ in any patient >50 years with known rhoea (see below).

91 Diarrhoea 9 Chronic/relapsing diarrhoea: Overview

Full clinical assessment, PR exam ± FBC

Yes Treat and 1 Hard or impacted stool in rectum? Likely overflow diarrhoea reassess

No

Yes Investigate 2 Steatorrhoea? Likely malabsorption disorder for cause

No

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

No

Yes Discontinue 4 Likely drug culprit? Drug-related diarrhoea drug if possible

No

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

No

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?

No

Likely functional disorder, e.g. irritable bowel syndrome 7 Reassess or refer GI if persistent troublesome symptoms/organic features

92 Diarrhoea Chronic/relapsing diarrhoea: step-by-step assessment 9

1 Hard or impacted stool in rectum? one agent at any time and restart the drug if symptoms continue unaltered. Always Have a high index of suspicion for overflow ask about alcohol excess. diarrhoea in frail, immobile or confused elderly patients. Always do a PR examina­ 5 Specific infection risk? tion. If hard or impacted, treat with faecal softeners and laxatives, then reassess. If the Exclude protozoal infection in patients PR is normal, overflow diarrhoea is unlikely with a history of travel to the tropics (90% of impactions are rectal), but consider e.g. giardiasis, amoebiasis, or with known an abdominal X-ray if there is strong clini­ HIV infection/other immunocompromise cal suspicion. e.g. cryptosporidiosis – send three fresh stool samples for examination for ova cysts 2 Steatorrhoea? and parasites. Liaise with the ID team if stool samples are negative but there is Steatorrhoea signifies fat malabsorption but ongoing clinical suspicion of infection. Test its absence does not exclude a malabsorp­ for HIV in any patient with chronic diar­ tive disorder. If steatorrhoea is present, rhoea and risk factors. ensure that the patient is not taking orlistat C. difficile diarrhoea may be chronic (available over the counter in the UK) and or relapsing – send stool to test for CDT check coeliac serology and faecal elastase in any patient with risk factors (see (↓in pancreatic insufficiency). If ↓faecal above). elastase or a strong suspicion of pancreatic disease e.g. cystic fibrosis or symptoms Clinical or laboratory features suggesting 6 suggestive of chronic pancreatitis, consider organic disease? pancreatic imaging (CT/MRCP); otherwise, consider small bowel investigation e.g. Screen for hyperthyroidism, hypercalcae­ duodenal biopsy, MRI. Screen for nutri­ mia and coeliac disease. Refer to GI for 2+ tional deficiencies e.g. iron, B12, folate, Ca , further small bowel investigation if large- 2+ 3− Mg , PO4 , albumin, in any patient with volume, non-bloody stool, previous gastric/ suspected malabsorption. small bowel surgery or evidence of nutri­ 2+ tional deficiencies: albumin, B12, folate, Ca , 2+ 3− 3 Alarm features? Mg , PO4 . Exclude inflammatory bowel disease if Expedite lower bowel investigation to there is a positive family history, mouth exclude colorectal cancer/inflammatory ulcers, fever, ↑CRP/ESR or extra-intestinal bowel disease if the patient has persistent manifestations (see Box 9.3). Refer to GI for diarrhoea associated with any of: further evaluation if any of the above fea­ • PR bleeding tures is present or there are other findings • palpable rectal/abdominal mass that suggest organic disease, e.g. weight • weight loss loss, anorexia, painless diarrhoea, promi­ • iron deficiency anaemia nent nocturnal symptoms or recent onset of • new presentation in a patient >45 years. symptoms in a patient >45 years. Consider flexible sigmoidoscopy as a first-line investigation in patients <45 years 7 Likely functional disorder or colonoscopy if >45 years. If none of the above is present, a functional 4 Likely drug culprit? cause, e.g. irritable bowel syndrome, is likely – particularly when typical symp­ Look for a temporal relationship between toms are present (Box 9.1). Provide reassur­ potential drug culprits (see Box 9.2) and the ance and explanation but refer to GI if onset of diarrhoea. Consider trial discon­ symptoms are progressive, distressing or tinuation where feasible but change only disabling. 93 10 DIZZINESS

The key to assessing dizziness lies in estab- Vertigo, nausea, vomiting and nystagmus lishing the exact nature of the patient’s tend to be constant and protracted. Ver­ symptoms. Occasionally, transient altera- tebrobasilar transient ischaemic attacks tion of consciousness or focal neurological (TIAs) may cause recurrent, transient epi- deficit will be described as a dizzy turn. sodes of vertigo. However, most patients with dizziness Other causes have vertigo, light-headedness/presyncope or a sensation of unsteadiness. These include migraine-associated vertigo, ototoxicity e.g. gentamicin, furosemide, cis- Disorders causing vertigo platin, herpes zoster oticus (Ramsay Hunt Vestibular neuronitis syndrome) and perilymphatic fistula. This is inflammation of the vestibular nerve, Disorders causing presyncope/ possibly due to viral infection. There is light-headedness abrupt onset of severe vertigo, associated Reflex presyncope (vasovagal episode) with nausea and vomiting. Labyrinthine involvement (labyrinthitis) causes tinnitus Reflex vasodilatation and/or bradycardia and/or hearing impairment. occur in response to a ‘trigger’ such as intense emotion or noxious stimuli, e.g. Benign paroxysmal positional venesection. There is a prodrome of nausea, vertigo (BPPV) sweating and ‘greying-out’ of vision/loss of BPPV is caused by particles in the semicir- peripheral vision. Syncope often ensues but cular canals which alter endolymph flow. may be aborted by lying down. Brief episodes of vertigo, typically lasting Orthostatic hypotension 10–60 seconds, are provoked by changes in head position. Orthostatic hypotension may result from antihypertensive medication, hypovolae- Ménière’s disease mia (dehydration, blood loss) or autonomic Recurrent attacks of vertigo, fluctuating dysfunction, especially in elderly or dia- low-frequency hearing loss, tinnitus and betic patients. a sense of aural fullness are caused by Arrhythmia increased volume of endolymph in the semicircular canals. Brady- and tachyarrhythmias can reduce cardiac output and thereby compromise Acoustic neuroma cerebral perfusion. There may be associated This cerebellopontine angle tumour usually palpitation, ECG abnormalities or a cardiac presents with unilateral sensorineural history. hearing loss. Vertigo may occur but is rarely Structural cardiac disease the predominant problem. Severe left ventricular outflow tract obstr­ Brainstem pathology uction e.g. aortic stenosis; hypertrophic Vertigo may be due to infarction, haemor- obstructive cardiomyopathy, can result rhage, demyelination or a space-occupying in light-headedness by reducing cardiac lesion. There will usually be associated fea- output. There will usually be abnormalities tures of brainstem dysfunction, e.g. diplo- on examination e.g. systolic murmur, and pia, dysarthria or cranial nerve palsies. ECG e.g. left ventricular hypertrophy. 94 Dizziness Differential diagnosis 10

Disorders causing unsteadiness motor neuron, motor endplate or muscle) Ataxia can result in unsteadiness due to weakness. Lack of coordination of muscle movements may cause profound unsteadiness and dif- Other causes ficulty walking; it is most commonly due to Loss of confidence, Parkinson’s disease and cerebellar pathology. gait dyspraxia may all cause unsteadiness. Multisensory impairment Other disorders causing dizziness Balance requires input from multiple Many other conditions can cause dizziness, sensory modalities (visual, vestibular, including hypoglycaemia, partial (temporal touch, proprioceptive); reduced function in lobe) seizure, migraine variants, normal more than one of these modalities, even if pressure hydrocephalus, hyperventilation relatively minor, may cause unsteadiness. and anxiety. This is most often seen in the elderly. Weakness Lesions anywhere in the motor tract (cere- bral cortex, upper motor neuron, lower

95 Dizziness 10 Initial assessment: overview

Full clinical assessment

Yes 1 Loss of consciousness? See Transient loss of consciousness (Ch. 29)

No

Yes 2 Transient focal neurological deficit? Likely transient ischaemic attack

No

Yes 3 Illusory sense of motion? Go to Vertigo (p. 98)

No

Yes 4 Light-headedness or presyncope? Go to Presyncope (p. 102)

No

Sense of unsteadiness or Yes 5 Go to Assessment of unsteadiness (p. 104) impaired balance?

No

Exclude anaemia and postural hypotension 6 Consider hypoglycaemia, complex partial seizure, migraine, hyperventilation, anxiety

96 Dizziness Initial assessment: step-by-step assessment 10

1 Loss of consciousness? Sense of unsteadiness or impaired 5 balance? Establish this first, as loss of consciousness requires a different diagnostic approach In some patients with dizziness, the princi- (see Ch. 29). Eyewitness accounts of the pal problem is impaired sense of balance dizzy episode are extremely helpful; other- associated with falls or the feeling that one wise, transient loss of consciousness may be might fall. This usually occurs while stand- inferred from a history of ‘coming to’ on the ing and is aggravated by walking. The ground, or suspected from the presence of patient may need to hold on to furniture facial injuries sustained during the episode. or other people. Examination of the gait (p. 217) may be revealing. The underlying 2 Transient focal neurological deficit? problem is often impaired central process- ing of the body’s position in space e.g. cer- A TIA is often described by the patient as a ebellar disorders, impaired proprioception, ‘funny turn’ and careful questioning may peripheral neuropathy, visual loss, poorly be required to ilicit a history of transient compensated vestibular disorders, which focal neurological disturbance (usually <3 may be exacerbated by reduced muscle hours). The most common presentations strength or confidence, particularly in the include hemiparesis, hemisensory distur- elderly. bance, facial droop, speech disturbance, diplopia and monocular visual loss (amau- 6 Consider other causes rosis fugax). Vertigo may occur with a ver- tebrobasilar TIA, usually accompanied by If the description of dizziness is unclear, ask other brainstem features. for more details: ‘Imagine you are having one of your dizzy turns now. Talk me through 3 Illusory sense of motion? exactly what happens and what you feel.’ If the account is not consistent with any of Vertigo is an illusory sensation of motion the above categories, consider alternative (usually spinning or rotatory). When causes. present, it is invariably aggravated by movement. If the nature of the dizziness • Suspect hypoglycaemic attacks if is not apparent from the patient’s own the patient is taking insulin or account, then ask: ‘When you have dizzy sulphonylurea drugs or reports relief of spells, do you simply feel light-headed or do you symptoms with sugar intake; a BM and see the world spin around you as if you had just lab glucose measurement taken during got off a playground roundabout?’ The latter an episode will confirm or exclude the indicates vertigo. diagnosis. • Seek neurological advice if there are 4 Light-headedness or presyncope? repeated episodes of amnesia, altered Consider presyncope in patients who consciousness or unusual behaviour. describe a feeling of light-headedness, ‘as if • Perform an FBC to exclude anaemia I might faint or pass out’, or one that is akin and measure erect and supine BP, to the familiar transient sensation experi- in all patients with orthostatic enced after standing up quickly. If any of symptoms. the episodes has been associated with • Anxiety is the most common cause of blackout, assess as described for transient ‘dizzy turns’ in patients under 65 years, loss of consciousness (Ch 29). but is a diagnosis of exclusion.

97 Dizziness 10 Vertigo: overview

Full clinical assessment ± ENT exam and Dix–Hallpike manoeuvre (Fig. 10.1)

Yes 1 Red flag features (see Box 10.1)? Must exclude central lesion

No

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

No

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

No

Recurrent episodes associated Yes Refer for audiometry 4 with hearing loss/tinnitus/ear Likely Ménière’s disease ± exclusion of fullness? acoustic neuroma

No

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

No

Yes 6 Associated migraine? Likely migraine-associated vertigo

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

98 Dizziness Vertigo: step-by-step assessment 10

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

99 Dizziness 10 Vertigo: step-by-step assessment

Recurrent episodes associated with Those who fulfil the diagnostic criteria for 4 hearing loss/tinnitus/ear fullness? migraine (see Box 18.6, p. 171) and have episodic vertigo with no other obvious Diagnosis of Ménière’s disease requires the cause have probable migraine-associated following criteria: vertigo; definitive diagnosis requires a tem- • recurrent attacks of vertigo lasting poral association between vertigo and minutes to hours (± nausea and migraine headache or aura. vomiting) • fluctuating sensorineural hearing loss, 7 Consider other causes/ENT referral especially for low frequencies In Ménière’s disease, the patient is often (audiometry is usually required to unaware of low-frequency hearing loss or detect this) tinnitus during attacks, and hearing may • tinnitus or a sense of pressure/fullness have returned to normal by the time of in the ear. audiometry. In these circumstances, recur- Consider ENT referral, to exclude acous- rent attacks of spontaneous vertigo may be tic neuroma, for any patient with unilateral the only presenting feature. hearing loss and vertigo, especially if the Suspect ototoxicity in any patient with presentation is recent in onset or atypical new-onset vertigo or other balance/hearing for Ménière’s disease. disturbance if gentamicin, furosemide or cisplatin has recently been prescribed. Per- New-onset recurrent spontaneous sistent symptoms despite drug cessation 5 episodes lasting minutes? may indicate irreversible vestibulocochlear dysfunction. Vertebrobasilar TIAs are normally associ- Reassess all patients for red flag features ated with other neurological features and arrange an MRI brain if there is any e.g. diplopia, dysarthria, facial numbness, suspicion of a central lesion. but occasionally present with episodes of Patients with dizziness present constantly vertigo as the only symptom. Patients with over weeks or whose dizziness is not a crescendo pattern of symptoms may have improved by remaining still are unlikely to impending thrombosis and require prompt have true vertigo. Otherwise, refer to ENT referral for imaging of the posterior circula- for further evaluation. tion, e.g. MRA.

6 Associated migraine? Enquire about possible migrainous symp- toms in all patients with episodic vertigo.

100 Dizziness Vertigo: step-by-step assessment 10

A B 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 right. 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.

101 Dizziness 10 Light-headedness/presyncope: overview

Yes 1 Features of shock? Assess as per Chapter 28

No

Postural symptoms + orthostatic Yes 2 Orthostatic presyncope hypotension?

No

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

No

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

No

Yes 5 Typical precipitant or prodrome? Likely reflex presyncope

No

Diagnosis uncertain; consider other causes of dizziness If recurrent presyncope, consider tilt test, Holter monitor, implantable loop recorder or refer Cardiology

102 Dizziness Light-headedness/presyncope: step-by-step assessment 10

1 Features of shock? • a history or clinical signs of aortic stenosis/hypertrophic cardiomyopathy Acute light-headedness may signify haemo- • clinical features of cardiac failure dynamic instability. Look for shock (Box • relevant ECG abnormalities, e.g. severe 26.1, p. 237), including early features, e.g. left ventricular hypertrophy, right ↑HR, narrow pulse pressure, pallor or pos- heart strain, deep anterior T-wave tural ↓BP. If present, assess as described in inversion. Ch 28. Clinical or ECG features that suggest Postural symptoms orthostatic 4 2 + arrhythmia? hypotension? Suspect an arrhythmic aetiology if episodes A secure diagnosis of orthostatic presyn- of light-headedness are associated with cope requires: palpitation or occur whilst supine, if there • a clear temporal relationship between are significant ECG abnormalities (see Box light-headedness and standing up, and 29.3, p. 257), or if the patient has a history • demonstration of a significant postural of MI. BP drop (≥20 mmHg in systolic BP or The key to clinching the diagnosis is to ≥10 mmHg in diastolic BP within 3 document the rhythm during a typical minutes of changing from a lying to episode. If episodes are relatively frequent, standing position). arrange Holter monitoring e.g. 24-hour tape; if less frequent, a patient-activated If orthostatic presyncope is detected, external recorder or implantable loop search for underlying causes, e.g. anti­ recorder may be more helpful. hypertensives, dehydration, autonomic neuropathy. 5 Typical precipitant or prodrome? Clinical or ECG features that suggest Consider whether episodes of light- 3 structural heart disease? headedness occurred while the patient was standing and had a clear precipitating Consider echocardiography to exclude trigger, e.g. intense emotion, venepuncture structural heart disease in patients with: or prolonged standing and/or were accom- • presyncopal symptoms on exertion panied by other ‘vagal’ features such as • a family history of sudden unexplained nausea, sweating and disturbance of vision. death A tilt test is often valuable in clinching the diagnosis.

103 Dizziness 10 Unsteadiness: overview

Yes Consider trial 1 Likely drug culprit? Drug-induced unsteadiness discontinuation

No

Yes 2 Ataxia or cerebellar signs? Neuroimaging ± refer Neurology

No

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

No

Yes 4 Elderly, frail or multiple comorbidities? See Gait assessment (p. 217)

No

Diagnosis uncertain; consider anxiety or reassessment of presentation Refer ENT or Neurology if persistent or disabling disturbance of balance

104 Dizziness Unsteadiness: step-by-step assessment 10

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

105 11 DYSPHAGIA

Patients with dysphagia require prompt Parkinson’s disease and stroke assessment to exclude serious pathology. These frequently cause swallowing diffi- Unless the history clearly points to an culty but other features are usually more oropharyngeal problem, oesophageal inves- prominent. tigation is necessary to rule out mechanical obstruction – in particular, malignancy. Inadequate saliva Inadequate saliva e.g. anticholinergics, con- Oropharyngeal dysphagia nective tissue disease, such as Sjögren’s Bulbar palsy syndrome, may lead to problems with Lower motor neuron palsies of cranial forming a manageable bolus. nerves IX–XII result in weakness of the Other causes tongue and muscles of chewing/ These include myopathies, myotonic dys- swallowing. The tongue is flaccid with fas- trophy and tumours of the pharynx or ciculation, often with a change in voice larynx. (Table 11.1). Causes include motor neuron disease (MND) and brainstem tumour or Oesophageal dysphagia (structural) infarction. Both structural disease and dysmotility may cause dysphagia. Structural causes Pseudobulbar palsy usually cause dysphagia for solids; motility Bilateral upper motor neuron lesions of disorders may cause dysphagia for solids cranial nerves IX–XII produce a small, con- and liquids. tracted and slowly moving tongue and pha- Malignant stricture ryngeal muscles with a brisk jaw jerk (Fig. 11.1). There may be associated speech dis- Patients with oesophageal cancer typically turbance and emotional lability (Table 11.1). present with progressive, painless dys- Causes include cerebrovascular disease, phagia to solid foods. Weight loss may be demyelination and MND. marked, especially if presentation is delayed. Cachexia and lymphadenopathy Myasthenia gravis are suggestive but physical signs may be Fatigability of oropharyngeal muscles absent. causes increasing swallowing difficulty Benign stricture after the first few mouthfuls. Dysphagia Most commonly, benign stricture is due to may occur before other features of myasthe- gastro-oesophageal reflux, especially in the nia are readily apparent. elderly. Rarer causes include oesophageal webs (seen in iron deficiency), Schatzki rings Pharyngeal pouch (benign idiopathic strictures of the lower The pouch is formed by herniation of oesophagus), ingestion of caustic sub- the pharyngeal mucosa through the stances, eosinophilic oesophagitis, benign cricopharyngeus muscle, and is usually oesophageal tumours and radiotherapy. found in elderly patients. In addition to dysphagia, there may be regurgitation of Food bolus obstruction undigested food, halitosis, the feeling of a There is sudden onset of complete dys- lump in the neck and gurgling after swal- phagia, often with an inability to swallow lowing liquids. even saliva. The diagnosis is usually 106 Dysphagia Differential diagnosis 11

obvious from the history but it may be Table 11.1 Comparison of signs in bulbar and the first manifestation of an underlying pseudobulbar palsy stricture. Bulbar Pseudobulbar Extrinsic compression Speech Nasal tone; ‘Donald duck’ Lung cancer, thyroid goitre, mediastinal difficulty forming voice nodes, an enlarged left atrium or a thoracic consonants aortic aneurysm may, rarely, produce dys- (especially ‘R’); phagia by compressing the oesophagus. may become slurred Oesophageal dysphagia (dysmotility) Tongue Weak, wasted Small, stiff Achalasia with This is a rare disorder characterised by fasciculation loss of peristalsis in the distal oesophagus Jaw jerk Normal or Brisk and impaired relaxation of the lower absent oesophageal sphincter. Dysphagia is of Gag reflex Absent Present slow onset (often years), occurs for liquids Emotions Normal Labile (e.g. and solids, and may initially be intermit- uncontrollable tent. Retrosternal discomfort and regurgita- laughing/ tion are common. crying) Chagas disease Chagas disease can present with achalasia; consider it in patients originating from endemic areas in South America and confirm with serological testing. Scleroderma Oesophageal involvement is seen in ~90% of cases; impaired peristalsis results from replacement of muscle with fibrous tissues and severe gastro-oesophageal reflux occurs due to incompetence of the lower oesopha- geal sphincter. Other features of sclero- derma e.g. calcinosis, Raynaud’s disease, telangiectasia, may be apparent. Diffuse oesophageal spasm Fig. 11.1 The jaw jerk. To elicit the jaw jerk, ask This may cause transient episodes of dys- the patient to let his/her mouth hang open, place phagia, although episodic chest pain that your index finger on the patient’s chin, and strike mimics angina is usually the predominant your finger with a tendon hammer. symptom.

107 Dysphagia 11 Overview

Full clinical assessment

No 1 Difficulty in swallowing food or fluids? Consider globus/odynophagia

Yes

2 Suspect oropharyngeal cause?

No

Upper GI endoscopy Stricture/oesophagitis/motility disorder

Barium swallow / manometry Motility disorder/pharyngeal pouch

Yes

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

No

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

No

Abnormality on speech and language Yes 5 Oropharyngeal disorder therapy assessment or videofluoroscopy?

No

Consider upper endoscopy if not already performed 6 CT if any suspicion of head and neck tumour Refer to GI if symptoms persist

108 Dysphagia Step-by-step assessment 11

1 Difficulty in swallowing foods or fluids? complaint in bulbar palsy and pseudo­ bulbar palsy so look carefully for the Features of true dysphagia include diffi- relevant clinical features (Table 11.1); if culty initiating swallowing or the sensation they are present, look for other features of food ‘sticking’ after swallowing. Globus of MND and perform neuroimaging to is the sensation of a lump in the throat; it exclude vascular or structural brainstem is unrelated to swallowing and often asso­ disease. ciated with anxiety or strong emotion. Odynophagia is pain on swallowing and 4 Fatigability/muscle weakness? suggests oesophageal inflammation or ulceration. Myasthenia gravis is rare and easily missed. The dysphagia typically presents with 2 Suspect oropharyngeal cause? increasing difficulty in swallowing after the first few mouthfuls and difficulty Suspect oropharyngeal dysphasia if the in chewing. Ask specifically about/ patient does NOT report food sticking in examine for: the lower throat or retrosternum and ≥1 of • fatigable weakness of muscles: initial the following features is present: strength is normal but there is a rapid • drooling/spillage of food from the decline with activity mouth • weak voice with prolonged speaking • immediate sensation of a bolus • diplopia ‘catching’ in the neck • ptosis • 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 If none of these features are present, suspect the diagnosis. investgate first for an oesophageal cause. Abnormality on speech and language Arrange an upper GI endoscopy (UGIE) to 5 therapy assessment or videofluoroscopy? look for a structural cause, especially oesophageal cancer. UGIE may also reveal Refer all patients with suspected oropha- features of certain motility disorders e.g. ryngeal dysphagia of uncertain cause to achalasia, but can be normal, especially in the speech and language therapy (SALT) scleroderma or diffuse oesophageal spasm. team for a detailed swallow evaluation If no cause is identified on UGIE, consult with formal speech and ± videofluoros- a GI specialist, as further investigation for a copy. This will confirm the presence of motility disorder, e.g. barium swallow or oropharyngeal dysfunction and help to oesophageal manometry, may be required. clarify the mechanism. If all GI investigations are reassuring, re-evaluate for a possible oropharyngeal 6 Consider further investigation/refer GI cause. Reconsider the possibility of oesophageal dysphagia and arrange urgent UGIE if a 3 Neurological abnormality? formal SALT assessment/videofluoroscopy If the history suggests an oropharyngeal fails to identify any problem with the aetiology for dysphagia, neurological eval- swallow mechanism and there is no evi- uation is essential. Although swallowing dence of neurological or neuromuscular difficulty is common in stroke, Parkinson’s dysfunction. Request a CT if you suspect disease and multiple sclerosis, it is very cancer of the head and neck, e.g. local mass rarely the primary presenting problem. or lymphadenopathy. Otherwise, refer to a However, dysphagia may be the principal GI specialist for further assessment.

109 12 DYSPNOEA

The sensation of breathlessness occurs • Acute respiratory distress syndrome when there is a mismatch between instruc- (ARDS). tions for ventilation sent by the brainstem, and sensory feedback from the thorax. Other respiratory causes When evaluating a patient with breathless- • Pneumothorax. ness, remember that its severity is highly • Pleural effusion. subjective. Some individuals may not expe- • Pulmonary embolism (PE). rience dyspnoea despite severe impairment • Acute chest wall injury. of gas exchange. Cardiovascular causes Acute dyspnoea • Acute cardiogenic pulmonary oedema. • Acute coronary syndrome. Acute dyspnoea is defined here as new- • Cardiac tamponade. onset or abruptly worsening breathlessness • Arrhythmia. within the preceding 2 weeks. When accom- • Acute valvular heart disease. panied by severe hypoxaemia, hypercap- nia, exhaustion or ↓GCS, it may herald Other causes life-threatening pathology. The diagnosis • Metabolic acidosis. can usually be made by combining clinical • Psychogenic breathlessness (acute evaluation and monitoring with key inves- hyperventilation). tigations including CXR, ECG and ABG. In the initial phase of assessment, diagnosis and treatment should be concurrent, and Chronic dyspnoea the cycle of intervention and reassessment should continue until the patient is stable. Chronic dyspnoea is defined here as breath- Important causes of acute dyspnoea are lessness of >2 weeks’ duration. Use the listed below. Medical Research Council (MRC) dyspnoea Upper airway obstruction scale (Box 12.1) to assess the severity of breathlessness. • Inhaled foreign body. Important causes of chronic dyspnoea are • Anaphylaxis. listed below. • Epiglottitis. For many causes, the diagnosis can be • Extrinsic compression e.g. rapidly made by combining clinical evaluation with expanding haematoma. PFTs, ECG, CXR, FBC and pulse oximetry. Lower airway disease However, early presentations of common • Acute bronchitis. problems, such as COPD and congestive • Asthma. cardiac failure, may have no clinical signs • Acute exacerbation of chronic obstructive and a normal CXR. In 1 in 3 patients, there pulmonary disease (COPD). is more than one underlying diagnosis • Acute exacerbation of bronchiectasis. to explain dyspnoea, so assess dyspnoeic • Anaphylaxis. patients thoroughly, even after a possible explanation has been found, particularly Parenchymal lung disease if the severity of pathology found is • Pneumonia. not commensurate with the severity of • Lobar collapse. symptoms. 110 Dyspnoea Differential diagnosis 12

Box 12.1 MRC dyspnoea scale • Chronic pulmonary thromboembolism. Grade 1 Not troubled by breathlessness • Bronchiectasis. except on strenuous exercise • Cystic fibrosis. • Pulmonary hypertension (primary or Grade 2 Short of breath when hurrying or secondary). walking up a slight hill • Pulmonary vasculitis. Grade 3 Walks slower than contemporaries • TB. on level ground because of • Laryngeal/tracheal stenosis, e.g. breathlessness, or has to stop for extrinsic compression, malignancy. breath when walking at own pace Grade 4 Stops for breath after walking about Cardiovascular causes 100 m or after a few minutes on • Chronic heart failure. level ground • Coronary artery disease (‘angina Grade 5 Too breathless to leave the house, equivalent’). or breathless when dressing or • Valvular heart disease. undressing • Paroxysmal arrhythmia. Source: Adapted from Fletcher CM, Elmes PC, Fairbairn MB • Constrictive pericarditis. et al. 1959. The significance of respiratory symptoms and the • Pericardial effusion. diagnosis of chronic bronchitis in a working population. British Medical Journal. 2:257–266. • Cyanotic congenital heart disease.

Other causes • Severe anaemia. Respiratory causes • Obesity. • Asthma. • Chest wall disease, e.g. kyphoscoliosis. • COPD. • Physical deconditioning. • Pleural effusion. • Diaphragmatic paralysis. • Lung cancer: bronchial carcinoma, • Psychogenic hyperventilation. mesothelioma, lymphangitis • Neuromuscular disorder, e.g. carcinomatosis. myasthenia gravis, muscular • Interstitial lung disease (ILD), e.g. dystrophies. sarcoidosis, idiopathic pulmonary • Cirrhosis (hepatopulmonary syndrome). fibrosis, extrinsic allergic alveolitis. • Tense ascites.

111 Dyspnoea 12 Acute dyspnoea: overview

ABCDE + ECG, CXR ± ABG

Yes Treat and 1 Cause requiring immediate correction? Final diagnosis reassess

No

2 Assess effort and adequacy of oxygenation and ventilation

Clinical/CXR features of pulmonary Yes Likely left ventricular failure; consider acute 3 oedema? respiratory distress syndrome

No Yes 4 Underlying COPD? See Further assessment of acute dyspnoea in patients with COPD (p. 119) No

Known asthma with typical flare or Yes 5 Acute asthma See Further assessment generalised wheeze with ↓PEFR? of acute asthma (p. 119) No

Yes 6 Evidence of respiratory tract infection? See Further assessment of respiratory tract infection (p. 120) No

Yes Pneumothorax/pleural effusion/ 7 Diagnostic CXR abnormality? lobar collapse/other

No

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

No

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

No

Clinical suspicion of pulmonary Yes Pulmonary embolism 10 CTPA / embolism 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 ABG shows respiratory alkalosis with normal PaO2

112 Dyspnoea Acute dyspnoea: step-by-step assessment 12

1 Cause requiring immediate correction? Use the PaCO2 to assess adequacy of ven- tilation (see Clinical Tool, p. 114). As part of the ABCDE assessment process Distinguish acute and acute-on-chronic (p. 8), identify and provide immediate ventilatory failure from chronic compen- corrective treatment for: sated hypercapnia. • airway obstruction Look for reversible factors contributing to • tension pneumothorax ventilatory impairment, e.g. bronchospasm, • anaphylaxis sedation, respiratory depressants. Be vigi- • arrhythmia with cardiac compromise. lant for loss of hypoxic drive in patients with chronic type 2 respiratory failure receiving Seek specialist input if necessary and repeat supplemental O2 but suspect an alternative the assessment following intervention. cause, e.g. exhaustion, airways obstruction, if the patient exhibits marked breathlessness Assess effort and adequacy of oxygenation 2 or increased effort of breathing. and ventilation Seek input from the critical care team and This is fundamental to the assessment of consider the need for respiratory support, acute respiratory compromise and should e.g. non-invasive ventilation or tracheal be reassessed frequently to monitor progress intubation and mechanical ventilation if and evaluate the effects of interventions. any of the following features is present: Assess the effort of breathing by repeated • impending exhaustion clinical observation of rate, depth and • acute/acute-on-chronic ventilatory pattern of respiration; look for use of acces- failure not resolving with the measures sory muscles and features of exhaustion. described above Monitor the SpO 2 in all patients and perform • progressively rising PaCO2

ABG analysis if any of the following fea- • SpO2 <90% or PaO2 <8 kPa despite tures is present: maximal respiratory assistance • a need for airway or ventilatory support • progressively rising FiO2 requirements to maintain target SpO2. • SpO2 <92% (or unreliable), central

cyanosis or high O2 requirements Clinical/CXR features of pulmonary • features of hypercapnia: drowsiness, 3 oedema? confusion, asterixis • severe, prolonged or worsening Diagnose pulmonary oedema if there are respiratory distress characteristic CXR appearances (Fig. 12.1) • background of COPD and/or chronic in association with bi-basal inspiratory type 2 respiratory failure crackles ± wheeze. • smoke inhalation (carboxyhaemoglobin) Difficulty may arise when the CXR is not • suspected metabolic acidosis or primary diagnostic, e.g. in early or mild cases, and hyperventilation. when auscultatory findings resemble those heard in other disorders, e.g. pulmonary Use the SpO2 ± PaO2 to assess adequacy of oxygenation. fibrosis, bilateral pneumonia. In these cases, Correct hypoxia by administration of look for supporting evidence of cardiac failure including: supplemental O2. Titrate the inspired O2 concentration (FiO2) to the minimum • progressive ankle swelling/orthopnoea/ required to achieve a target SpO2: exertional dyspnoea prior to acute deterioration • 94–98% for previously well patients • signs of fluid overload: peripheral • normal baseline SpO for patients with 2 oedema, ↑JVP chronic hypoxia. • predisposing cardiac condition, e.g. LV

Monitor FiO2 requirements carefully to impairment, valvular disease, acute maintain the target SpO2. arrhythmia 113 Dyspnoea 12 Acute dyspnoea: step-by-step assessment

Clinical tool Interpretation of arterial blood gases

Assessment of ventilation oxygenation (insufficient PaO2 to support normal aerobic metabolism). Consider a patient with a PaCO2 is directly determined by alveolar ventilation – the volume of air transported PaO2 of 8.5 kPa. Oxygenation is clearly impaired, between the alveoli and the outside world suggesting the presence of important lung disease. However, this PaO2 would usually result in any given time. Therefore ↑PaCO2 (hypercapnia) implies ventilatory failure – type in an SaO2 >90%, allowing adequate delivery of 2 respiratory failure. O2 to tissues (provided that haemoglobin and cardiac output are normal). A slow, gradual rise in PaCO2 (chronic type 2 respiratory failure) is usually accompanied by Assessment of acid–base status an increase in HCO3 that serves to maintain overall acid–base balance (H+ within normal An acidosis is any process that acts to lower range). However, this metabolic compensation blood pH (↑H+); an alkalosis is one that acts + occurs over days/weeks so any acute rise in to raise blood pH (↓H ). A ↑PaCO2 indicates

PaCO2 (acute or acute-on-chronic type 2 a respiratory acidosis; a ↓PaCO2 indicates respiratory failure) will lead to an increase in a respiratory alkalosis. + − H (Table 12.1). A ↓HCO3 indicates a metabolic acidosis; a − In type 2 respiratory failure, the rate of rise ↑HCO3 indicates a metabolic alkalosis. + in PaCO2 and the associated increase in H A respiratory or metabolic acid–base provide a better guide to severity than the disturbance usually triggers an adjustment by

absolute value of PaCO2. the other system to limit the change in blood

A ↓PaCO2 implies hyperventilation. If PaO2 pH (compensation). Respiratory compensation is also lowered (or just within normal limits), happens over minutes; metabolic compensation the hyperventilation is probably an appropriate takes days to weeks.

response to hypoxia. Alternatively, if HCO3 Having identified the presence of any is decreased, it may reflect respiratory metabolic or respiratory disturbances, look compensation for a primary metabolic acidosis next at H+ (or pH) to assess the overall impact

e.g. diabetic ketoacidosis. A ↓PaCO2 with on acid–base status. If the metabolic and + normal PaO2 and HCO3 (on room air) suggests respiratory processes oppose each other, the H primary (psychogenic) hyperventilation but this helps to differentiate the primary disturbance is a diagnosis of exclusion (see below). from the compensatory response: an ↑H+ (or upper limit of normal) suggests that the acidosis Assessment of oxygenation is the primary disturbance and vice versa. Primary respiratory acidosis (ventilatory A ↓PaO2 implies impairment of oxygenation. failure) and alkalosis (hyperventilation) are A corresponding normal PaCO2 indicates that this is due to ventilation/perfusion mismatch dealt with above. – type 1 respiratory failure. In contrast, Causes of metabolic acidosis and alkalosis are shown in Box 12.2. If there is a primary ↑PaCO2 indicates that it is due, at least in part, to failure of ventilation – type 2 metabolic acidosis, calculate the anion gap: + + -- -- respiratory failure. Anion gap==()( Na ++ K -- Cl ++ HCO3 ) The administration of supplemental O2 [Normal==10 -- 18 mmol/L] makes ABG analysis more 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 Table 12.1 Arterial blood gases in different

is that the difference between FiO2 and PaO2 patterns of type 2 respiratory failure (in kPa) should be 10. However, if subtle − ≤ PaCO2 HCO3 pH impairment is suspected, repeat the ABG on Acute ↑ → ↓ room air. Chronic It is important to note the distinction between ↑ ↑ → Acute-on-chronic ↑ ↑ ↓ impaired oxygenation (↓PaO2) and inadequate Dyspnoea Acute dyspnoea: step-by-step assessment 12

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) • Renal failure • Poisoning (aspirin, methanol, ethylene glycol) With normal anion gap Fig. 12.1 Left ventricular failure. Note the hazy perihilar shadowing (‘bat’s wings’), the prominent, • Renal tubular acidosis dilated upper lobe veins and the basal Kerley B • Diarrhoea lines, all characteristic of pulmonary oedema. • Ammonium chloride ingestion There is also cardiomegaly. • Adrenal insufficiency

Metabolic alkalosis (high HCO3) • rapid improvement with vasodilators/ • Vomiting diuretics. • Potassium depletion e.g. diuretics Consider non-cardiogenic pulmonary • Cushing’s syndrome oedema in acutely dyspnoeic patients with • Conn’s syndrome (primary bilateral pulmonary infiltrates; pathology hyperaldosteronism) consistent with ARDS e.g. trauma, burns, pancreatitis, sepsis; and no evidence of cardiac failure. If suspected, arrange echocardiography to assess ventricular and • generalised wheeze, or valvular function. • ↓peak expiratory flow rate (PEFR). 4 Underlying COPD? Consider other causes of acute dyspnoea, e.g. pneumothorax or PE, if neither of these See ‘Further assessment of acute dyspnoea features is present. in COPD’ if the patient has known or sus- Suspect a first presentation of asthma pected COPD. (and proceed to ‘Further assessment of In the absence of a pre-existing diagnosis, acute asthma exacerbation’) if there is wide- suspect COPD in any patient with a smoking spread wheeze with no evidence of COPD, history and either: anaphylaxis or pulmonary oedema (see • clinical (Fig. 12.2) or CXR features of above). Assess with pulmonary function hyperinflation, or tests (PFTs) ± PEFR diary following resolu- • chronic exertional dyspnoea with tion of the acute episode. wheeze and/or a chronic productive cough. Evidence of respiratory tract infection 6 (RTI)? 5 Generalised wheeze with ↓PEFR? Having considered the above conditions, go See ‘Further assessment of acute asthma to ‘Further assessment of respiratory tract exacerbation’ in patients with known infection’ if any of the following features is asthma and either: present: 115 Dyspnoea 12 Acute dyspnoea: step-by-step assessment

Pursed lips

Increased rate and depth of breathing

Intercostal indrawing

Sitting forward and gripping bed (increases action of accessory muscles)

Signs of hyperinflation ↑Antero-posterior diameter Intercostal indrawing Decreased cricosternal distance Poor chest expansion (<5 cm) Fig. 12.2 Clinical features of COPD.

• new cough with purulent sputum or significant increase in purulent sputum • temperature ≥38°C or <35°C • acute illness with sweating, shivers and myalgia • clinical/CXR signs of consolidation (Figs 12.3 and 12.4) with ↑WBC/CRP.

7 Diagnostic CXR abnormality? CXR may be more sensitive than clinical examination for detecting some lung abnor- malities, e.g. pneumothorax (Fig. 12.5), pleural effusion (Fig. 12.6) or lobar collapse Fig. 12.3 Pneumonia of the right middle lobe. (see Figs 17.3 and 17.4, p. 161). See below (p. 127) for ‘Further assessment of pleural effusion’. CT thorax, or specialist respiratory input if If the patient has lobar collapse, consider no firm diagnosis emerges. further investigation, e.g. bronchoscopy to Ischaemic ECG changes (see Box 6.1, exclude a proximal obstructing lesion. 8 p. 49)? If CXR appearances are non-specific or uncertain, continue through the diagnostic Dyspnoea may be the predominant mani- process and attempt to correlate with clini- festation of myocardial ischaemia/infar- cal findings. Consider further imaging e.g. ction. If there is clear ECG evidence of

116 Dyspnoea Acute dyspnoea: step-by-step assessment 12

Fig. 12.4 Right upper lobe pneumonia containing air bronchograms.

Fig. 12.6 Left pleural effusion.

• Check U & E. • Measure plasma glucose, lactate, salicylate levels. • Calculate the anion gap. Do not attribute dyspnoea solely to metabolic acidosis if there is evidence of hypoxaemia.

Clinical suspicion of PE or unexplained 10 hypoxaemia? PE is under-diagnosed. Physical, CXR, ABG and ECG findings are notoriously unrelia- Fig. 12.5 Right pneumothorax. ble. Evaluate for PE as shown in Figure 12.7 in any patient with acute dyspnoea and any ischaemia (Box 6.1) and no obvious alterna- of the following: tive cause for breathlessness, assess as • relevant risk factors, e.g. active described in Chapter 6. malignancy, recent surgery or prolonged immobility ABG shows primary metabolic acidosis 9 • signs or symptoms of deep vein with normal PaO ? 2 thrombosis (DVT) Identify the presence of metabolic acidosis • haemoptysis by ABG analysis (see Clinical Tool, p. 114). • no clear alternative explanation. If present, look for an underlying cause (see In patients who require imaging to Box 12.2): exclude PE, CT pulmonary angiography • Examine for evidence of shock or offers greater sensitivity than a ventilation/ mesenteric infarction. perfusion scan and may demonstrate an • Test urine for glucose and ketones. alternative diagnosis.

117 Dyspnoea 12 Acute dyspnoea: step-by-step assessment

Assess clinical Table 12.2 Wells score (pulmonary embolism) probability, using Clinical variable Points Wells score Clinical signs and symptoms of DVT* 3 No alternative diagnosis is more likely 3 PE PE than PE unlikely likely Heart rate >100 bpm 1.5 Immobilisation or surgery in the 1.5 previous 4 weeks D-dimer +ve CTPA Previous DVT/PE 1.5 –ve –ve +ve Haemoptysis 1 Active malignancy (treatment within 1 last 6 months or palliative) Score >4: PE likely; ≤4: PE unlikely PE Diagnosis excluded PE *Minimum of leg swelling and pain elicited upon palpation of the deep veins. Fig. 12.7 Algorithm for the assessment of suspected pulmonary embolism using the Wells score.

118 Dyspnoea Acute dyspnoea: further assessment 12

Further assessment of acute dyspnoea pathogens may permit more effective in patients with COPD tailored therapy; discuss with the Step 1 Clarify cause for acute deterioration microbiology team if unusual or resistant organisms have been grown on • Ensure that there is no new CXR previous cultures. abnormality: look carefully for evidence of collapse, consolidation, Step 3 Compare current status to baseline pneumothorax or pleural effusion. If and monitor response to treatment there are features of consolidation, treat • Oxygenation and ventilation: compare

as pneumonia rather than ‘infective current ABG values and SpO2 to

exacerbation of COPD’. previous records. Give supplemental O2

• Ask about cough and sputum: treat as to return SpO2/PaO2 to baseline. If the an infective exacerbation of COPD if patient has chronic type 2 respiratory there is an increase in sputum volume failure, monitor for loss of ventilatory or purulence with no evidence of drive and repeat an ABG after any

consolidation. increase in FiO2. • If wheeze is predominant and there are • Airways obstruction: assess PEFR and no features of infection, the likely the presence/extent of wheeze; monitor diagnosis is non-infective exacerbation changes to gauge response to of COPD. Look for precipitants, e.g. bronchodilator therapy. β-blocker, non-compliance with inhalers, • Functional reserve: assess overall work environmental trigger. of breathing (rate, depth, use of • Evaluate for PE (see Fig. 12.7) if there is accessory muscles). Very high a sudden increase in breathlessness or respiratory work cannot be maintained hypoxia without wheeze, change in for long; refer to critical care if there is sputum or new CXR abnormality. impending exhaustion. • Following recovery, record pre- Step 2 Establish pre-exacerbation status discharge PEFR, SpO2 and ABG on air. and details of previous exacerbations This provides a comprehensive picture of underlying disease severity, helping to Further assessment of acute guide the goals and limits of therapy. asthma exacerbation • Baseline performance: quantify normal Step 1 Assess severity and need for exercise tolerance, ask about activities hospital admission that provoke dyspnoea and ascertain Assess severity in any patient with sus- ability to perform activities of daily pected acute asthma according to Table living (ADLs). 12.3; perform an ABG if there are life- • Baseline lung function: refer to previous threatening features or SpO2 <92%. Admit ABG/SpO2 measurements and PFTs patients to hospital if they have: to provide an objective estimate of disease severity and look for evidence • any life-threatening features of chronic hypercapnia (see above). • features of a severe attack persisting • Trajectory of disease: consider changes after initial treatment in the above severity measures over • PEFR <75% or significant ongoing time, the frequency of admissions and symptoms after 1 hour of treatment previous requirement for respiratory • other features causing concern, e.g. support, e.g. non-invasive and invasive previous near-fatal asthma, poor ventilation. compliance. • Previous sputum cultures: antibiotic If there are ongoing features of a severe prescribing should be guided by local attack, monitor in a critical care environ-

protocols but knowledge of previous ment with repeated assessment of SpO2, 119 Dyspnoea 12 Acute dyspnoea: further assessment

Table 12.3 Clinical features of severe asthma Severity PEFR or Speech or Other features Moderate 50–75% best or predicted Full sentences Severe 33–50% best or predicted Unable to finish sentences RR >25 or HR >110 Life-threatening <33% best or predicted Single words or no speech Any of: PaO2 <8 kPa PaCO2 >4.6 kPa Silent chest Cyanosis Exhaustion Altered conscious level Arrhythmia

Near-fatal PaCO2 >6 kPa

PEFR, RR, HR and work of breathing ± Further assessment of respiratory ABG. Refer urgently to the intensive care tract infection unit if PaCO2 is >6 kPa or rising, or there is Step 1 Classify the type of RTI worsening hypoxia, exhaustion or ↓GCS. In patients with features of RTI, distinguish Step 2 Look for treatable precipitants pneumonia from non-pneumonic infection by the presence of focal chest signs, e.g. Seek evidence of infection, e.g. pyrexia, crackles, bronchial breathing and/or new purulent sputum, ↑WBC, physical/CXR CXR shadowing (see Figs 12.3 and 12.4). signs of consolidation (see Figs 12.3 and Classify as community-acquired pneumo- 12.4) and flitting upper lobe infiltrates, nia (CAP) if infection has been acquired out suggesting allergic bronchopulmonary of hospital, and hospital-acquired pneumo- aspergillosis. Culture sputum if this is nia (HAP) if the onset of illness occurred ≥2 purulent and blood if temperature is ≥38°C. days after hospital admission. In previously Carefully review the CXR to exclude pneu- well patients without focal chest signs or mothorax (see Fig. 12.5). CXR abnormality, the likely diagnosis is non-pneumonic RTI, e.g. acute bronchitis. Step 3 Assess baseline control In patients with known bronchiectasis, con- Establish: sider an infective exacerbation if the sputum • frequency and severity of exacerbations becomes more purulent or offensive; assess- • baseline symptoms between ment of patients with underlying COPD is exacerbations described above. • best PEFR Step 2 Assess severity • current inhaler regimen, technique and The CURB-65 score (Table 12.4) can help to compliance risk-stratify patients with CAP. Consider • frequency of PRN inhaler use referral to critical care for monitoring/ • frequency of oral steroids (need for bone intervention in patients with a CURB-65 protection?) score >2. • current smoking status. Look for avoidable precipitants, e.g. Step 3 Look for predisposing factors pollen, pets, cold air, exercise, smoking, Assess for factors associated with immuno- occupational triggers, β-blockers, NSAIDs. compromise, e.g. chronic disease (AIDS, 120 Dyspnoea Respiratory tract infection: further assessment 12

site. Preceding viral infection, especially Table 12.4 CURB-65 score influenza, may predispose to severe sec- Feature Score ondary bacterial infection. Consider endo- Confusion Abbreviated Mental Test <8/10 carditis in patients with multiple discrete or Urea >7 mmol/L flitting shadows on CXR, especially IV drug users. RR ≥30/min BP Systolic <90 or diastolic Step 4 Gather information to inform <60 mmHg antimicrobial choice Age ≥65 years In any patient requiring hospitalisation for Total score 30-day mortality risk RTI, culture blood and sputum, perform 0 0.6% serological assessment for atypical patho- 1 3.2% gens and (during influenza outbreaks) take a viral throat swab. In patients with severe 2 13.0% pneumonia (CURB-65 >2), send urine 3 17.0% (Legionella) and blood/sputum (Pneumococ- 4 41.5% cus) for rapid antigen detection by PCR. 5 57.0% Aspirate pleural fluid for microscopy and Lim W, et al. Thorax. 2003; 58(5): 377-382. culture if there is an associated parapneu- monic effusion. Send multiple sputum samples (induced with nebulised hyper- diabetes, cirrhosis, malnutrition), acute tonic saline if necessary) for Ziehl–Neelsen disease (any critical illness), drugs (steroids, staining and tuberculosis (TB) culture if cancer chemotherapy) or previous splenec- there is a suspicion of TB: tomy. Suspect aspiration in patients with • significant immunocompromise or a history of swallowing difficulty, stroke, debility alcoholism or recent unconsciousness. • previous residence in an endemic Pneumonia may occur distal to a bronchial TB area carcinoma – repeat the CXR to ensure • recent close contact with a smear- resolution of changes in patients with positive TB patient risk factors and consider further inves­ • CXR evidence of previous TB tigation, e.g. bronchoscopy, if there are • a background of persistent productive persistent symptoms/CXR features or cough with weight loss, night sweats or recurrent pneumonia at the same other constitutional symptoms.

121 Dyspnoea 12 Chronic dyspnoea: overview

Full clinical assessment, SpO2, FBC, ECG, CXR

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

No

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

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 Signicant echo abnormality?

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

Unexplained hypoxia or ↑risk of Yes Pulmonary embolism/ 7 CTPA venous thromboembolism? other lung pathology

No Clinical suspicion of coronary Yes 8 Investigate (p. 000) Likely angina artery disease

No

Consider obesity, physical deconditioning, psychogenic dyspnoea, neuromuscular disorder 9 PFTs, echo ± CPET/respiratory input if limiting, progressive or unexplained symptoms

122 Dyspnoea Chronic dyspnoea: step-by-step assessment 12

1 Dyspnoea related to exertion? Box 12.3 Features suggestive of psychogenic dyspnoea Chronic dyspnoea arising from organic disease is almost always provoked or exac- • Provoked by stressful situations erbated by exertion so episodic dyspnoea • Inability to take a deep breath or ‘get unrelated to exertion has a limited range of enough air’ diagnoses. • Frequent deep sighs Suspect asthma if there is: • Digital/perioral tingling • associated cough or wheeze • ↓PaCO2 with normal PaO2 on ABG • a reproducible precipitant for episodes e.g. cold air, pollen, house dust, pets • Short breath-holding time • diurnal variation in symptoms with prominent nocturnal or early morning symptoms (especially if sleep is diagnostic doubt or symptoms are trouble- disturbed), or some or disabling despite explanation and • a history of atopy. reassurance.

Seek objective evidence of airflow revers- 2 Pleural effusion or ↓Hb? ibility or variability to confirm the diag­ nosis: the former by spirometry (≥15% Consider these conditions at an early stage as they can be easily confirmed or excluded. improvement in FEV1 following inhaled bronchodilators), the latter by asking the Go to ‘Further evaluation of pleural effu- patient to keep a diary of peak-flow sion’ if there is CXR ± clinical evidence of recordings (look for >20% diurnal variation unilateral effusion (see Fig. 12.6). Always on ≥3 days/week for 2 weeks). Consider check Hb in patients with exertional dysp- specialist assessment if the diagnosis is noea, as pallor is an insensitive sign. If Hb uncertain, especially if occupational asthma is decreased, evaluate as described on page is suspected. 134 but consider other causes – especially if Paroxysmal tachyarrhythmia may Hb is only slightly decreased or symptoms present with discrete episodes of breath- persist despite correction. lessness without any clear precipitant 3 Any alarm features (Box 12.4)? (although dyspnoea, when present, is usually aggravated by exertion). Consider Change in voice or stridor may indicate this if: laryngeal/tracheal obstruction secondary to intrinsic cancer or extrinsic compression • dyspnoea is accompanied by palpitation (lymphoma, thyroid tumour or retrosternal • episodes arise ‘out of the blue’ with an goitre); if present, refer the patient urgently abrupt onset, or for endoscopic evaluation, e.g. fibre optic • the ECG shows evidence of pre- bronchoscopy/nasoendoscopy. excitation (see Fig. 25.2, p. 225). Refer for urgent specialist evaluation If paroxysmal tachyarrhythmia is sus- with bronchoscopy ± CT to exclude lung pected, attempt to document the rhythm cancer if the patient has risk factors (>40 during symptoms (see p. 229). years or smoking history) accompanied by Dyspnoea that occurs predominantly any suspicious clinical or CXR features (see at rest with no consistent relationship to Box 12.4); these include lobar collapse, exertion may be functional. Suspect this which may indicate a proximal obstructing if the patient exhibits typical features (Box tumour. 12.3) in the absence of objective evidence of In younger non-smokers consider initial cardiorespiratory disease (normal examina- further evaluation with CT thorax; refer tion, SpO2, CXR ± PFTs/serial PEFR). for specialist assessment if CT suggests Refer for specialist assessment if there is malignant disease, fails to reveal a clear 123 Dyspnoea 12 Chronic dyspnoea: step-by-step assessment

Box 12.4 Alarm features in chronic dyspnoea Box 12.5 Criteria for investigations in chronic dyspnoea Clinical features PFTs if there is: • Stridor • Wheeze • Haemoptysis • Prominent nocturnal or early morning • Weight loss symptoms • Change in voice • Symptoms precipitated by cold weather or • Persistent or non-tender cervical common allergens lymphadenopathy • History of atopy • Finger clubbing • Clinical or CXR features of hyperinflation (see Fig. 12.2) CXR features (see also Box 17.1, p. 161) • Smoker aged >40 years • Lung mass • Chronic productive cough (≥3 consecutive • Cavitation months for ≥2 successive years) • Hilar enlargement • Occupational dust exposure, treatment with • Lobar collapse (persistent) methotrexate/amiodarone or previous N.B. These features are especially worrying if the patient is a radiotherapy smoker, is >40 years or has had asbestos exposure. • ↓SpO2 (at rest or on exertion) with no apparent alternative cause • Major or progressive decrease in effort alternative cause or is not readily available. tolerance without other obvious cause Evaluate patients with haemoptysis as Echocardiogram if there is: described in Chapter 17. • Previous MI or chronic hypertension 4 Significant CT abnormality? (especially if target organ damage) • JVP or peripheral oedema Arrange high-resolution CT to look for evi- ↑ dence of ILD if the patient has any of the • Murmur (not previously investigated) relevant features listed in Box 12.5. • Clinical/CXR evidence of pulmonary Refer for specialist evaluation if CT shows congestion, cardiomegaly or pulmonary evidence of ILD or other serious pathology, hypertension e.g. cancer, bronchiectasis. Arrange further • Occupational dust exposure, treatment with investigation with PFTs, if these have not methotrexate/amiodarone or previous been performed already, if the CT shows radiotherapy features of emphysema. • Major or progressive decrease in effort 5 Abnormal PFTs? tolerance with normal PFTs and no other obvious cause Have a low threshold for requesting PFTs (Box 12.5 and Table 12.5). High-resolution CT thorax if there is:

Diagnose COPD if FEV1/FVC is <70% • Interstitial shadowing on CXR (Fig. 12.8) (indicating airways obstruction) with a • Unexplained restrictive lung defect or ↓gas post-bronchodilator FEV1 <80% predicted transfer (indicating incomplete reversibility). Look • Strong clinical suspicion of interstitial lung for other characteristic abnormalities, disease e.g. hypoxia or end-inspiratory including ↑TLC and RV (which helps to crackles in a patient with previous exposure differentiate from ILD in borderline cases) to birds, dust or hay and ↓gas transfer (indicative of significant emphysema). Exclude alpha1-antitrypsin 124 Dyspnoea Chronic dyspnoea: step-by-step assessment 12

Table 12.5 Pulmonary function tests Test Description Measures Examples of relevant diagnoses

Spirometry Airflow at the mouth is FEV1, FVC Obstructive lung disease: disproportionate

measured during a reduction in FEV1 (FEV1:FVC ratio <0.8) forced exhalation Restrictive lung disease: proportionate

reduction in FEV1 and FVC

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

deficiency in younger patients. If SpO2 is ≤92%, perform an ABG to identify patients with type 2 respiratory failure or those who might qualify for home oxygen therapy. Diagnose asthma if there is an obstructive ventilatory defect with ≥15% improvement in FEV1 following inhaled bronchodilators. If not, consider further assessment with repeat spirometry, PEFR diary or specialist evaluation if there is high clinical suspicion or borderline spirometry results. In patients with a restrictive lung defect (see Table 12.5), evaluate for an underlying cause: • Arrange echocardiography and reassess following treatment if there is evidence of pulmonary congestion. • Look for major chest wall deformity, e.g. severe kyphoscoliosis. • Exclude ILD with high-resolution CT if Fig. 12.8 CXR in interstitial lung disease. there are suggestive clinical/CXR features (see Fig. 12.8) or there is no clear alternative cause. e.g. ILD, if there is a proportionate decrease • Measure BMI to identify massive in TLC and RV. obesity, e.g. BMI >40. 6 Significant echo abnormality? Suspect extrapulmonary compression (e.g. neuromuscular disorder, chest wall In compensated cardiac failure, exertional deformity) if there is a decrease in TLC with dyspnoea may be the sole presenting normal RV, and an intrapulmonary cause feature, but significant cardiac dysfunction 125 Dyspnoea 12 Chronic dyspnoea: step-by-step assessment

exercise ECG or other stress test (see Box Table 12.6 Severity of airflow obstruction 6.8, p. 69) if the patient has risk factors for

Severity FEV1 coronary artery disease (see Box 6.7, p. 67) Mild 50–80% predicted and symptoms are consistently provoked Moderate 30–49% predicted by exertion and relieved within 5 minutes by rest. Relief of symptoms with anti- Severe <30% predicted anginal therapy or coronary revascularisa- Source: Modified from Boon NA, Colledge NR, Walker BR, Hunter tion confirms the diagnosis. JAA 2006. Davidson’s Principles and Practice of Medicine. 20th edn. Box 19.30, p. 680. Consider other causes. Further 9 investigation if limiting, progressive or unexplained symptoms is unlikely in the absence of the features listed in Box 12.5. Obesity rarely causes significant cardiores- Refer for cardiology evaluation if the piratory impairment unless BMI is >40. echo shows ventricular dysfunction, major However, lesser degrees of obesity and/or valvular abnormality e.g. severe mitral physical deconditioning are frequently regurgitation or aortic stenosis or pericar- responsible for exertional breathlessness dial effusion/constriction: and ↓exercise capacity; suspect this in If the echo suggests pulmonary hyperten- patients with ↑BMI (especially >30), recent sion without significant LV impairment weight gain or a sedentary lifestyle. or valvular disease, evaluate fully for If there are features of hyperventilation underlying chronic lung disease, e.g. PFTs, (see Box 12.3) or symptoms are dispropor- high-resolution CT chest, sleep studies, tionate to objective findings, perform an CTPA. In the absence of hypoxaemia or ABG on room air (ideally during symp- significant lung disease, refer for specialist toms) and consider referral for formal eval- assessment. uation of psychogenic dyspnoea. At this stage, review any abnormalities Unexplained hypoxia or risk of detected and determine whether they are 7 ↑ venous thromboembolism? sufficient to account for the presentation. In patients with multiple possible causes Exclude chronic thromboembolic disease for dyspnoea, e.g. obesity, left ventricular in any patient with unexplained hypoxia impairment and airways disease, cardio­ or risk factors for DVT. Ventilation/ pulmonary exercise testing (in which ECG, perfusion lung scanning may have higher respiratory gas exchange and minute venti- sensitivity for detection of chronic PE but lation are recorded during exercise) may CT pulmonary angiography is more likely help to establish the predominant mecha- to identify alternative lung pathology, e.g. nism. Patients with a major change or pro- ILD, emphysema. gressive decline in exercise capacity without adequate explanation require further evalu- Clinical suspicion of coronary artery 8 ation; arrange an echocardiogram and PFTs disease? if these have not yet been performed, and Angina occasionally manifests as a sensa- consider referral for specialist evaluation, tion of breathlessness without chest dis- e.g. cardiac catheterisation or cardiopulmo- comfort. Evaluate for angina with an nary exercise testing.

126 Dyspnoea Chronic dyspnoea: further assessment 12

Box 12.6 Causes of abnormal pleural Box 12.7 Light’s criteria for differentiation of fluid collections pleural exudate and transudate Serous effusions The pleural fluid is likely to be an exudate if ≥1 Transudate of the 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 • Nephrotic syndrome limit of normal serum LDH • Hypoalbuminaemia • Peritoneal dialysis • Constrictive pericarditis Further assessment of pleural effusion • Hypothyroidism The causes of abnormal collections of fluid • Meigs’ syndrome (pleural effusion, benign in the pleura are listed in Box 12.6. Initial ovarian fibroma and ascites) assessment depends on laboratory analysis of the fluid. Exudate • Use Light’s criteria to distinguish • Parapneumonic (usually bacterial) exudative from transudative effusions • Bronchial carcinoma (Box 12.7). • TB • Review pleural fluid biochemistry. • Connective tissue disease The presence of amylase indicates pancreatitis; pH <7.3 suggests bacterial • Pancreatitis or cancer; rheumatoid factor suggests • Mesothelioma connective tissue disease. • Post-MI syndrome • Identify evidence of infection: Gram • Sarcoidosis stain, culture, microscopy for acid-fast bacilli. TB culture may take months. Other fluids • Look for evidence of malignancy: Pus cytology may identify malignant cells; CT thorax ± needle biopsy may reveal • Empyema; most commonly caused by acute malignancy; pleural biopsy of regions bacterial infection of the pleura identified as abnormal may provide a Chyle diagnostic specimen. • Chylothorax; caused by lymphatic obstruction, most commonly by metastatic malignancy Blood • Haemothorax; causes acute dyspnoea, usually following trauma

127 13 FATIGUE

Fatigue is physical and/or mental exhaus- Respiratory causes tion. It is very common and non-specific, so • Obstructive sleep apnoea identifying significant underlying disease is • Chronic obstructive pulmonary disease difficult. Acute fatigue is usually caused by self-limiting infections or transient life cir- Cardiac causes cumstances. This guide pertains to fatigue • Congestive cardiac failure of at least 2 weeks’ duration. • Bradyarrhythmias A careful history may reveal that the Haematological causes problem is actually something other than • Anaemia fatigue, e.g. breathlessness, in which case • Haematological malignancy, e.g. this should be pursued. If localising or more lymphoma specific features, e.g. haemoptysis, fever, jaundice, come to light, these should become Endocrine causes the primary focus of assessment. • Hypothyroidism Causes of fatigue are shown below, with • Hypercalcaemia an emphasis on conditions that frequently • Diabetes mellitus present with fatigue as the chief complaint. • Adrenal insufficiency Important problems to differentiate from • Hypopituitarism fatigue are described in Box 13.1. Infection Non-organic causes • Infectious mononucleosis • Psychological stress/overwork • Tuberculosis • Depression • HIV • Fibromyalgia • Infective endocarditis • Chronic fatigue syndrome • Lyme disease Medications Chronic inflammatory conditions • Beta-blockers • Rheumatoid arthritis • Chronic alcohol abuse • Inflammatory bowel disease • Benzodiazepines and other sedatives • Connective tissue disorders, e.g. • Corticosteroids systemic lupus erythematosus • Chemotherapeutic agents Malignancy • Haematological • Solid organ • Disseminated

128 Fatigue Differential diagnosis 13

Box 13.1 Presentations that must be distinguished from fatigue

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

129 Fatigue 13 Overview

Full clinical assessment

Yes Consider trial Fatigue secondary to drug 1 Likely drug culprit? discontinuation therapy

No

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

No

Fever, night sweats or Yes 3 Assess as per Pyrexia of unknown origin (p. 146) ↑inflammatory markers?

No

Yes Further targeted 4 Other indicator of organic disease? Organic cause evaluation

No

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

No

Yes 6 Low mood, anhedonia? Likely depression

No

Explore psychosocial factors. Assess impact on lifestyle and employment 7 Consider obesity/physical deconditioning If persistent and otherwise unexplained, consider chronic fatigue syndrome

130 Fatigue Step-by-step assessment 13

1 Likely drug culprit? pelvis to look for underlying malignancy. Review all medications – prescribed and over-the-counter. Suspect a drug cause if Diabetes mellitus there is a temporal relationship between a Check a fasting blood glucose (FBG) if you likely culprit (see above) and the onset of detect glycosuria or a random blood glucose symptoms. If possible, stop or replace >7 mmol/L. An FBG >7 mmol/L on two suspect medications and review symptoms occasions or a positive oral glucose toler- after an appropriate interval. Alcohol in ance test confirms the diagnosis. excess or used chronically can cause fatigue. Poor glycaemic control in known diabe- Toxic environmental exposures e.g. carbon tes may cause fatigue. Review the blood monoxide, lead, mercury, arsenic, are less glucose diary and HbA1c to determine common, but potentially reversible, causes. whether control is adequate and, if not, reassess the fatigue after correction. Definite cause identified on examination or 2 screening investigations? Hypothyroidism Ask about symptoms of cold intolerance, If any of the abnormalities listed below is constipation and weight gain, and look for detected, reassess fatigue after appropriate hypothyroid facies, dry skin, brittle hair evaluation and treatment. and nails, myxoedema and goitre. In Anaemia patients with known hypothyroidism, con- This may cause fatigue but is also a common sider whether thyroxine replacement is feature of chronic disease. See ‘Further adequate and ask about compliance. A assessment of anaemia’ (below) in any ↑TSH and ↓T4 confirm hypothyroidism. patient with ↓Hb. Bradycardia Renal failure If HR is <60, perform an ECG and consider a 24-hour tape. Refer to a cardiologist if Uraemia is a cause of fatigue. If there is new there is evidence of complete heart block, a or worsening renal impairment, see ‘Further resting HR <50/min or a blunted HR assessment of renal failure’ (p. 192). response to exercise. Hypercalcaemia Pregnancy Fatigue and other symptoms, e.g. abdomi- Consider in any woman of child-bearing nal pain, vomiting, constipation, polyuria, age and, if necessary, perform a pregnancy confusion and anorexia, may occur if cor- test. rected serum calcium is >3.0 mmol/L. Hypercalcaemia may reflect serious under- Fever, night sweats or inflammatory 3 ↑ lying disease, e.g. bony metastases, squa- markers? mous cell lung cancer and multiple myeloma. Fatigue is a common, and often predomi- Examine the breasts (p. 47) and prostate, nant, symptom in patients with systemic perform a CXR and check a parathyroid inflammatory or malignant disease e.g. hormone (PTH) level: lymphoma, endocarditis, myeloma, tuber- culosis. If there is a history of fever or • A ↑ or →PTH suggests primary night sweats or an ↑ESR/CRP, review as hyperparathyroidism. described for fever and pyrexia of unknown • If ↓PTH, perform a radioisotope bone origin (p. 146). scan and myeloma ‘screen’, review drugs (especially calcium or vitamin D 4 Other indicator of organic disease? supplements), check plasma vitamin D levels. If no cause is identified, consider Look for the following indicators of organic a CT scan of the chest, abdomen and disease during your assessment. 131 Fatigue 13 Step-by-step assessment

Abnormalities on FBC or blood film persists, consider a ‘liver screen’ (Box 19.7, High or low cell counts, abnormal cells p. 180). e.g. blasts, or morphological abnormalities Features of adrenal insufficiency e.g. target cells, may indicate important Look for pigmentation of sun-exposed haematological or systemic disease. Seek areas, recent scars, palmar creases and haematological advice for any unusual or mucosal membranes; vitiligo; postural unsuspected abnormality. + + hypotension; and ↓Na /↑K . Confirm Lymphadenopathy with a short ACTH (Synacthen) stimulation Enlarged lymph nodes may occur with test. malignancy (lymphoma, leukaemia or sec- ondary deposits) or in reaction to infection/ 5 Specific infection risk? inflammation. The most important condi- In patients with specific risk features it is tions to consider are HIV, TB, infectious necessary to exclude certain infections, mononucleosis and malignancy. even in the absence of specific clinical • Search for a local source of infection/ features. inflammation if swelling is localised to Consider HIV if the patient: one lymph node group. • has had unprotected sex, a blood • Suspect haematological malignancy if transfusion, done health-care work or there is generalised painless has been resident in an HIV endemic lymphadenopathy. area • Consider lymph node biopsy if the • has engaged in high-risk sexual activity cause is not apparent or you suspect • is an IV drug user, past or present. malignancy. Evidence of cardiorespiratory dysfunction Consider a CXR ± Mantoux test if the patient has: • Look for features of cardiac failure (↑JVP, peripheral oedema, pulmonary • had previous TB or been resident in a congestion) or a new murmur; if TB endemic area present, arrange an ECG and • had recent exposure to a patient with echocardiogram. active TB

• Check SpO2 at rest ± on exertion; if low, • immunosuppression. perform an ABG on room air and look Consider Lyme serology if the patient for an underlying cause. has: • Ask about smoking history and consider CXR/pulmonary function tests (see • a history of a recent tick bite Table 12.5, p. 125). • a history of an erythema chronicum migrans Some patients find it difficult to differen- • recently travelled to an endemic area. tiate between fatigue and dyspnoea; if there is a clear history or objective evidence of Discuss with an ID unit if the patient has: reduced effort tolerance, consider a similar • recently undertaken foreign travel approach to that of chronic exertional dys- beyond Europe and North America pnoea (see Ch 12). • a history of a recent animal bite. Features of chronic liver disease or deranged LFTs 6 Low mood, anhedonia? Look for stigmata of chronic liver disease Suspect depression if the patient has lost (Box 19.5, p. 177). If jaundiced, assess enjoyment or interest in life (ask about pre- as per Ch 19. If LFTs are abnormal, enquire vious interests, hobbies and so on), reports about alcohol intake and discontinue low mood or expresses negative thoughts hepatotoxic drugs; if the abnormality (guilt, pessimism, low self-esteem) out of 132 Fatigue Step-by-step assessment 13

Box 13.2 Diagnostic criteria for chronic fatigue proportion to the circumstances. Look for syndrome blunted affect, psychomotor retardation and biological symptoms, e.g. loss of libido, Fatigue for ≥4 months with all of the following: early morning waking. Consider psychiat- • a clear starting point ric referral or a trial of antidepressants. • persistent and/or recurrent symptoms Explore psychosocial factors and impact • unexplained by other conditions 7 on lifestyle. Consider obesity, physical • a substantial reduction in activity level deconditioning, chronic fatigue syndrome • characterised by post-exertional malaise If the patient has a BMI >30 or lacks physi- and/or fatigue (feeling worse after physical cal fitness, encourage appropriate ­life activity) style changes and reassess. If not already and one or more of the following: excluded consider coeliac disease, infec- • difficulty sleeping or insomnia tious mononucleosis and Lyme borreliosis. Chronic fatigue syndrome is a diagnosis of • muscle and/or joint pain without exclusion with specific criteria (Box 13.2). inflammation • headaches • painful lymph nodes that are not enlarged • sore throat or general malaise or flu-like symptoms • cognitive dysfunction, such as difficulty with thinking • physical or mental exertion that makes symptoms worse • dizziness and/or nausea • palpitation, without heart disease

133 Fatigue 13 Further assessment

Further assessment of anaemia bowel surgery, then investigate for perni- Step 1 Use the mean cell volume (MCV) to cious anaemia. Intrinsic factor antibodies narrow the differential diagnosis are diagnostic but only present in 60% of cases; anti-parietal cell antibodies are non- In the UK, microcytic anaemia (MCV <76 fl) specific but their absence makes pernicious is usually due to iron deficiency. anaemia less likely (present in 90% of cases). First, confirm iron deficiency. Serum fer- Seek Haematology advice in difficult cases. ritin is more indicative of total body iron If B and folate are normal, exclude than serum iron but may be increased by 12 hypothyroidism, pregnancy and alcoholic liver disease or systemic inflammation. liver disease, and then evaluate for haemo- • ↓ferritin confirms iron deficiency. lysis (step 2) and myelodysplasia (step 3), • If ferritin is normal, transferrin as described below.

saturation <16% suggests iron Measure iron studies and vitamin B12/ deficiency. folate in patients with normocytic anaemia, as If iron deficiency is confirmed, identify combined iron and B12 or folate deficiencies the underlying cause. e.g. nutritional deficiency, small bowel disease, may result in a normocytic picture. • Review the diet and consider inadequate iron intake, especially in vegetarians. Step 2 Investigate for haemolysis • Ask about blood loss: haematemesis, Consider haemolysis in patients with melaena, haemoptysis, epistaxis, normal or ↑MCV. haematuria, menorrhagia, trauma. Seek evidence of ↑red cell destruction: • Arrange upper GI endoscopy (UGIE) • ↑bilirubin/LDH and colonoscopy unless there is a clear • ↑urinary urobilinogen non-GI source of bleeding, e.g. • red cell fragments on blood film menorrhagia, haematuria. and a compensatory increase in red cell Where the cause remains unclear: production: • Exclude coeliac disease: serology ± • ↑reticulocytes duodenal biopsy at the time of UGIE. • polychromasia • Refer to GI for further investigation, e.g. • nucleated red cell precursors on blood small bowel pathology. film. Reassess symptoms and FBC after iron If present, distinguish intravascular from supplementation and treatment of any extravascular haemolysis to narrow the dif- underlying cause. ferential diagnosis. Refer patients with a ↓MCV and normal Intravascular haemolysis – e.g. in iron stores to a haematologist for inves­ microangiopathic haemolytic anaemia tigation of alternative diagnoses, e.g. (MAHA), defective mechanical heart valve, thalassaemia, sideroblastic anaemia. malaria – releases free Hb into the plasma, In patients with a macrocytic anaemia leading to: (MCV >98 fl), measure vitamin B12 and fasting serum folate. • ↓plasma haptoglobins (mop up free Hb In the absence of pregnancy, causative then cleared by the liver) drugs e.g. methotrexate, phenytoin, or • methaemalbuminaemia (once haemolysis (see below), ↓ folate is likely to haptoglobin binding is saturated) be due to poor dietary intake (fruit, leafy • haemosiderinuria (once albumin binding vegetables) but always check coeliac capacity exceeded) serology. • haemoglobinuria (black urine if fulminant, e.g. in malaria). ↓B12 is unlikely to be due to dietary defi- ciency unless the patient is a strict vegan. With extravascular haemolysis, e.g. Check for previous gastrectomy or small hereditary spherocytosis, autoimmune 134 Fatigue Further assessment 13 haemolysis or red cell enzymopathies, these Examine for lymphadenopathy and features are absent and there is often clini- splenomegaly, and refer for further investi- cal or USS evidence of splenomegaly (the gation, e.g. bone marrow evaluation. site of red cell breakdown). Look for evidence of a paraproteinaemia, In either case, review the blood film for e.g. multiple myeloma: send serum for diagnostic abnormalities: protein electrophoresis and urine for meas- urement of Bence Jones protein. Discuss • malaria parasites on thick and thin films with a haematologist if these are positive or (mandatory if recent travel to malaria if there is clinical suspicion, e.g. bone pain, endemic region) pathological fracture, lytic bone lesions, • sickle cells – sickle cell anaemia unexplained ↑Ca2+ or ESR. • red cell fragments – MAHA e.g. haemolytic uraemic syndrome, Step 4 Consider chronic thrombotic thrombocytopenic purpura; non-haematological disease defective mechanical heart valve, march Consider chronic kidney disease as a haemoglobinuria potential cause for normocytic (↓erythro- • spherocytes – autoimmune haemolytic poietin production) if GFR <60 mL/min/ anaemia or hereditary spherocytosis 1.73 m2, and especially if <30 mL/min/ • Heinz bodies, bite cells – G-6-PD 1.73 m2. Measure ferritin and transferrin deficiency. saturation to ensure that the patient is Discuss immediately with a haemato­ iron-replete (ferritin >100 ng/mL; transfer- logist if you suspect haemolytic uraemic rin saturation >20%) and discuss with a syndrome or thrombotic thrombocytopenic nephrologist. purpura e.g. AKI, neurological features, The most common cause of normocytic acute diarrhoeal illness. If spherocytes are anaemia is chronic inflammatory disease present, perform a direct Coombs test to e.g. rheumatoid arthritis, polymyalgia help differentiate autoimmune haemolytic rheumatica, chronic infection, or malig- anaemia from hereditary spherocytosis. If nancy. Consider the diagnosis if: the cause is unclear, consider enzyme assays • other causes of ↓Hb have been excluded

(G-6-PD or pyruvate kinase deficiency) and (including iron, B12, folate deficiency) Hb electrophoresis (haemoglobinopathies) • there is no evidence of active bleeding and refer to a haematologist. • anaemia is mild e.g. Hb >80 g/L, and Step 3 Seek evidence of bone marrow • unexplained weight loss, fever, ↑ESR/ failure or haematological malignancy CRP or ↓albumin – search for an underlying cause. Review the FBC and blood film for: • deficiencies in other cell lines (↓WBC, Step 5 Refer to a haematologist ↓platelets) Seek input from a haematologist if the cause • ↑↑WBC, e.g. chronic myeloid leukaemia, of anaemia is still unclear, you suspect a chronic lymphocytic leukaemia serious or unusual haematological disorder • atypical cells, e.g. blasts. or the patient fails to respond to therapy.

135 14 FEVER

Fever is a core body temperature ≥38°C; if Genitourinary tract it persists >3 weeks without explanation it • Lower urinary tract infection (UTI), e.g. is termed pyrexia of unknown origin (PUO). cystitis, prostatitis. Fever occurs most commonly as part of the • Upper UTI (pyelonephritis). acute phase response to infection. Infection • Perinephric collection. causing a systemic inflammatory response • Pelvic inflammatory disease. (sepsis) has a significant mortality and must • Epididymo-orchitis. be recognised and managed quickly. Other • Syphilis. causes of fever are malignancy, connective tissue disease, drug reactions, miscellane- CNS ous causes and factitious. • Meningitis (bacterial, viral, fungal TB). • Encephalitis. Infection • Cerebral abscess. Respiratory system ENT • Acute bronchitis. • Upper respiratory tract infection (RTI), • Pneumonia. e.g. tonsillitis. • Influenza. • Otitis media. • Empyema. • Quinsy. • Infective exacerbation of bronchiectasis/ • Dental abscess. COPD. • Mumps/parotitis. • Tuberculosis (TB). • Glandular fever (Epstein–Barr virus; GI causes EBV). • Gastroenteritis. • Sinusitis. • Appendicitis. Immunocompromised patients • Biliary sepsis. • Viral hepatitis. • Pneumocystis jiroveci (carinii) • Diverticulitis. pneumonia. • Intra-abdominal TB. • Aspergillosis. • Hepatic abscess. • TB. • Atypical mycobacterial infection, e.g. Skin/soft tissue Mycobacterium avium intracellulare. • Cellulitis. • Cytomegalovirus (CMV) infection. • Erysipelas. • Toxoplasmosis. • Necrotising fasciitis. • Cryptococcal meningitis. • Pyomyositis. • Nocardia infection. • Infected pressure sore. • Disseminated herpes/fungal infection. • Wound infection. Returning travellers Musculoskeletal causes • Malaria. • Septic arthritis (native and prosthetic • Typhoid. joint). • Infective diarrhoea, e.g. cholera, • Osteomyelitis. amoebiasis, Shigella. • Discitis. • Amoebic liver abscess. • Epidural abscess. • Strongyloides infection. 136 Fever Differential diagnosis 14

• Schistosomiasis. • Cryoglobulinaemia. • Dengue. • Adult-onset Still’s disease. Other infectious causes Drugs • Leptospirosis. • Drug fever (almost any drug). • Brucellosis. • Antipsychotics (neuroleptic malignant • Lyme disease. syndrome). • Q fever. • Anaesthetics (malignant • HIV. hyperthermia). • Toxoplasmosis. • Cocaine, amphetamines, ecstasy. • Fungal infection. • Measles, rubella. Other causes • Herpes zoster infection (chickenpox or • Transfusion-associated. shingles). • Thyrotoxicosis, thyroiditis. Malignancy • Phaeochromocytoma. • Haematological malignancy, including • Deep vein thrombosis (DVT)/ lymphoma, leukaemia, myeloma. pulmonary embolism (PE). • Solid tumours, especially renal, liver, • Pancreatitis. colon, pancreas. • Alcoholic hepatitis/delirium tremens. • Rheumatic fever. Connective tissue disorders • Inflammatory bowel disease. • Giant cell arteritis/polymyalgia • Sarcoidosis. rheumatica. • Atrial myxoma. • Rheumatoid arthritis. • Familial Mediterranean fever. • Systemic lupus erythematosus. • Erythroderma/Stevens–Johnson • Polymyositis. syndrome. • Polyarteritis nodosa. • Factitious (fever or apparent fever • Wegener’s granulomatosis. surreptitiously engineered by the • Churg–Strauss disease. patient).

137 Fever 14 Overview

ABCDE, FBC ± CRP

Consider transfusion reaction / malignant Exposure to blood products, anaesthetic, Yes 1 hyperthermia / neuroleptic malignant antipsychotics or stimulants? syndrome

No

Systemic inflammatory HR >90, RR >20 or abnormal Yes Assess severity + 2 response syndrome / WBC/CRP? seek source Sepsis

No

Full clinical assessment + septic screen (See Clinical tools: ‘Septic screen’ +/– ‘Extensions of the septic screen in specific patient groups’)

Yes 3 Specific risk factor for infection? Further targeted investigation

No

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

No

Yes 5 Positive cultures? Seek source ± specific antimicrobial therapy

No

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

Likely self-limiting viral infection Investigate as per pyrexia of unknown origin if persistently ↑CRP/ESR, recurrent fever or major systemic upset

138 Fever Step-by-step assessment 14

Exposure to blood products, anaesthetic, to, a volatile anaesthetic, e.g. halothane, or 1 antipsychotics or stimulants? succinylcholine. In all of the above cases continue to eval- The vast majority of acute febrile illnesses uate for infection and other causes if there are caused by infection, but the following is any diagnostic doubt. conditions are potentially life-threatening and important to recognise immediately; 2 HR >90, RR >20 or abnormal WBC/CRP? they may be overlooked if not specifically considered at the outset. Assess patients for a systemic inflammatory If the patient is receiving blood products, response syndrome (SIRS)/sepsis (Box stop the transfusion, ensure the patient’s ID 14.1). Recognise and manage haemody- matches that on the unit, and check that the namic compromise and organ dysfunction, ABO and RhD groups in the transfused (Chapter 28). Admit patients with severe blood are compatible with the patient. sepsis/septic shock to a high-dependency/ Contact the blood bank and seek immediate intensive care unit (HDU/ITU), as inten­ Haematology input if there is any suspicion sive monitoring and treatment will be of ABO incompatibility or other major required; manage in accordance with the transfusion reaction. Otherwise, monitor Surviving Sepsis guidelines (http:// temperature and vital signs, and consider www.survivingsepsis.org/GUIDELINES/ restarting the transfusion at a slower rate if Pages/default.aspx). Early and appropriate observations are stable, the patient is sys- antibiotic treatment is essential to minimise temically well and the rise in temperature mortality. Search for a focus of infection – is <1.5°C. see Clinical Tool: a septic screen (p. 140). Suspect neuroleptic malignant syndrome if the patient has received neuroleptics, e.g. haloperidol, within the past 1–4 weeks Box 14.1 Criteria for determining SIRS, sepsis, and exhibits muscular rigidity, tremor and severe sepsis and septic shock excessive sweating and/or altered mental SIRS status, especially in association with ↑CK. Two or more of: If appropriate, ask the patient about 1. Temperature 38°C or 36°C recent use of cocaine, ecstasy or ampheta- > < mines; consider toxic hyperthermia if 2. HR >90 bpm temperature is >39°C, especially if there 3. RR >20/min are features of excessive sympathomimetic 9 9 4. WBC >12 × 10 /L or <4 × 10 /L or >10% activity, e.g. ↑BP, ↑HR, dilated pupils, immature forms; or ↑CRP* aggression, psychosis or serotonin syn- drome e.g. rigidity, hyper-reflexia. Measure Sepsis CK, U+E, LFTs and coagulation, and • SIRS + suspected or proven infection monitor ECG, HR, BP and urine output, to identify complications such as rhabdomy- Severe sepsis olysis, acute renal failure, arrhythmia, dis- • Sepsis + organ dysfunction or hypotension seminated intravascular coagulation and (see Box 28.1, p. 249) acute liver failure. Septic shock Assume malignant hyperthermia if the patient develops severe pyrexia with tachy- • Severe sepsis that persists despite cardia ± rhabdomyolysis during adminis- adequate fluid resuscitation tration of, or within 1–2 hours of exposure

139 Fever 14 Step-by-step assessment

Clinical tool: A septic screen The septic screen combines clinical • If new-onset jaundice, arrange an abdominal assessment with laboratory analysis and USS and serology for viral hepatitis: imaging studies to identify a source of infection. • Treat empirically for biliary sepsis and It may also reveal non-infectious causes of arrange surgical review if there is a pyrexia, e.g. malignancy. The full screen may cholestatic pattern of jaundice (p. 177) or not be required in all patients, especially if USS shows dilated bile ducts. there is an obvious focus of infection. • Send blood and urine samples for leptospirosis culture and serology ± PCR General if symptoms include purpura, ↓platelets or conjunctival congestion, or there has • ≥2 sets of blood cultures, urinalysis, FBC, been recent exposure to potentially U+E, LFTs, CRP, CXR. contaminated water e.g. freshwater sports, sewage worker – liaise with the Respiratory ID team. • Assess suspected RTI, e.g. new/worsening • Check amylase and assess as described on cough with purulent sputum or CXR page 30 if acute abdominal pain with consolidation as per page 120. tenderness or guarding. • Perform a pleural tap and send fluid for • If palpable abdominal mass investigate for biochemical, microbiological and cytological infective e.g. diverticular or appendiceal analysis if unilateral pleural effusion (p. 127). absces, and non-infective e.g. carcinoma, • If other respiratory features, e.g. lymphoma, causes with USS or CT ± haemoptysis, non-specific CXR hypoxia, aspiration or biopsy. consider further investigation, e.g. CT, bronchoscopy to exclude atypical infection, Urinary tract lung cancer and PE. • Send an MSU if new-onset urinary tract symptoms, an indwelling urinary catheter, Abdominal or leucocytes/nitrites on urinalysis (bacterial • Send stool samples for microscopy, culture UTI highly unlikely in the absence of either and sensitivity testing ± Clostridium difficile nitrites or leucocytes.) toxin if acute diarrhoea. • Arrange USS to exclude renal obstruction, • Investigate for inflammatory bowel disease, calculus or a perinephric collection if loin e.g. flexible sigmoidoscopy, if persistent pain or renal angle tenderness. bloody diarrhoea. • Exclude urinary tract cancer ± inflammatory • Perform an urgent ascitic tap in any febrile renal disease (see Ch 16) if persistent patient with ascites; treat empirically as haematuria (visible or non-visible) or loin spontaneous bacterial peritonitis (SBP), pain with repeated negative MSU. pending culture, if >250 neutrophils/µL • Send swabs for Neisseria gonorrhoeae ascitic fluid. Consider TB and malignancy if and Chlamydia if urethral or PV fluid is exudative and initial cultures negative. discharge.

140 Fever Step-by-step assessment 14

Clinical tool: A septic screen – cont’d Skin and soft tissue Cardiovascular • Send swabs from any wounds or sites • Investigate for endocarditis (Box 14.2) with a discharging pus. transthoracic echocardiogram and ≥3 sets • Suspect cellulitis if there is an area of of blood cultures if new murmur, vasculitic/ acutely hot, erythematous and painful skin; embolic phenomena, or a predisposing look for potential entry sites, e.g. peripheral cardiac lesion with no obvious alternative cannulae, skin breaks. source of infection. • Seek immediate surgical assessment and • Consider a transoesophageal give IV antibiotics if any features of severe echocardiogram if transthoracic images necrotising infection, e.g. rapid spread, equivocal or persistent high clinical crepitus, anaesthesia over lesion, major suspicion. haemodynamic compromise or pain out of proportion with clinical findings. ENT • DVT may produce a low-grade fever – exclude as described on page 189 if • Consider a throat swab for influenza acutely swollen limb. during outbreaks or the autumn/winter • Consider investigation for osteomyelitis, e.g. season. bone scan, if persistent non-healing ulcer. • Send a swab for Streptococcus pyogenes if • Examine the whole body for rashes – seek pustular exudates. urgent dermatology advice if blistering, • If parotitis or tender lymphadenopathy, mucosal involvement or pustules (see consider a throat swab for mumps PCR and, Ch. 26). if age-appropriate, check EBV serology (>95% of patients >35 years will have CNS evidence of previous exposure). • Assume CNS infection, initially, if severe headache, meningism, purpuric rash, focal Musculoskeletal neurological signs, new-onset seizures or • If acutely swollen, painful joint, seek urgent unexplained ↓GCS. Give immediate orthopaedic assessment and perform empirical treatment after blood cultures, diagnostic aspiration to exclude septic arrange urgent neuroimaging and, if no arthritis (see Ch 20). contraindications (Chapter 28), perform • If unexplained back pain with no other lumbar puncture. obvious source for fever, take ≥3 blood • If meningitis suspected, send a throat swab cultures and arrange spinal MRI to exclude for Neisseria meningitidis PCR. discitis.

141 Fever 14 Step-by-step assessment

Box 14.2 Modified Duke Criteria for the The prevailing strains and resistance pat- diagnosis of infective endocarditis terns of common infections such as pneu- Major criteria monia may differ in other parts of the world, so seek input from an ID specialist Positive blood culture at an early stage. • Typical organism from two cultures Immunocompromised patients may experience more severe sequelae from • Persistent positive blood cultures taken 12 > infection with common pathogens and are hours apart at greater risk of opportunistic infections, • ≥3 positive cultures taken over >1 hour especially with mycobacteria, viruses and Endocardial involvement fungi. Follow the additional steps for immunocompromise (Clinical tool: Exten- • Positive echocardiographic findings of sions to the septic screen in specific patient vegetations groups) if the patient has acquired or con- • New valvular regurgitation genital immunodeficiency (including HIV); Minor criteria is receiving treatment with high-dose ster- oids, immunosuppressants, DMARDs or • Predisposing valvular or cardiac abnormality anti-TNF drugs; or is neutropenic for any • IV drug misuse reason. More specific forms of immuno- • Pyrexia ≥38°C compromise include asplenia (↑susceptibil- ity to encapsulated organisms and malaria) • Embolic phenomenon and the presence of indwelling vascular • Vasculitic phenomenon access devices or other prosthetic material. • Blood cultures suggestive – organism Test for HIV in patients who are at high risk grown but not achieving major criteria or with an atypical infection or other indica- • Suggestive echocardiographic findings tors of HIV – see http://www.bhiva.org/ documents/Guidelines/Testing/ Definite endocarditis: two major, or one major GlinesHIVTest08.pdf. and three minor, or five minor Ask about all forms of drug use in any Possible endocarditis: one major and one patient presenting with unexplained fever. minor, or three minor If there has been IV drug use, establish Modified from Boon NA, Colledge NR, Walker BR, Hunter JAA frequency, duration and sites of injection. 2006. Davidson’s Principles and Practice of Medicine. 20th edn. Maintain awareness of any local/national outbreaks, as unusual organisms may be implicated, e.g. anthrax skin infections. Always consider the possibility of underly- ing blood-borne infection e.g. hepatitis 3 Specific risk factor for infection? B or C, HIV. Discuss with the ID team if the patient is haemodynamically compro- Infections other than those discussed mised or fails to improve on standard above may need to be considered in patients therapy. returning to or entering the UK from abroad (especially from the tropics) and those with Clinical findings/initial tests suggest a 4 immunocompromise or IV drug use. likely source? If the patient has come from an at-risk region for viral haemorrhagic fever and has Following appropriate cultures, treat imme- unexplained bleeding, discuss urgently diately with antibiotics according to the with the health protection team (before likely source and local guidelines in patients admission). Otherwise, complete a septic with severe sepsis. If no clear source is iden- screen as per Clinical Tool: Extensions to tified or the patient has neutropenia (espe- the septic screen in specific patient groups. cially if the neutrophil count is <1.0 × 109/L) 142 Fever Step-by-step assessment 14 or other significant immunocompromise, cultures that yield an unexpected organism provide empirical broad-spectrum antibi- may challenge your working diagnosis and otic ± antifungal therapy. The choice of anti- prompt re-evaluation for an alternative microbials will depend on patient factors source e.g. S. aureus in suspected UTI. and local resistance patterns – discuss with In the patient with no obvious source of microbiology and other relevant specialties, fever, positive blood cultures, especially in e.g. Oncology, Haematology. Refine the multiple bottles, confirm an infective aetiol- antibiotic regimen in discussion with the ogy and help to guide further investigation; Microbiology team on the basis of subse- for example, blood culture results are quent culture results. central to the diagnosis of infective endo- Patients with recurrent fever, or fever in carditis (see Box 14.2). the absence of immunocompromise, neu- Persistently positive blood cultures tropenia or haemodynamic disturbance can despite appropriate antibiotic therapy often wait for the results of cultures before suggest a deep-seated infection; the source antibiotic therapy is started. If there is a must be identified and removed e.g. debri- clear source of infection, start empirical dement, drainage. antibiotic therapy and adjust as necessary in light of the culture results and sensitivity 6 Persistent fever? testing; otherwise, reassess daily whilst Acute fever is frequently a manifestation of awaiting the full results of the septic self-limiting viral illnesses. In the absence of screen. continuing pyrexia, ongoing symptoms or signs, or worrying investigation results, no 5 Positive cultures? further action is required. Re-evaluate your initial diagnosis and treat- Recurrent fever, especially with persist- ment in the light of culture results. ent elevation of inflammatory markers or Positive cultures may confirm a -sus significant constitutional upset, mandates pected source of infection e.g. MSU, further evaluation; if present, proceed to sputum, and guide the most appropriate ‘Further assessment of pyrexia of unknown antibiotic therapy. On the other hand, blood origin’.

143 Fever 14 Step-by-step assessment

Clinical tool: Extensions to the septic screen in specific patient groups Recent travel or residence abroad hepatosplenomegaly, RUQ tenderness, • Document exactly where the patient has bloody diarrhoea or urticarial rash. Send been, specific dates of travel and activities blood for serology and discuss with an ID undertaken (including a sexual history). Ask specialist. about vaccinations/malaria prophylaxis prior • Arrange USS to exclude amoebic abscess if to and during travel. previous travel to the tropics and RUQ • Consult an ID specialist at an early stage for discomfort ± palpable liver. any returning traveller with unexplained • Check dengue fever serology if recent return fever. from the tropics/subtropics and an acute • Exclude malaria if recent travel to an febrile illness associated with a rash endemic region (http://cdc-malaria.ncsa. (generalised, blanching, macular in the initial stages), headache or severe aches uiuc.edu/) with three sets of blood films ± malaria antigen card: and pains. Discuss immediately with the • Use the antigen card to facilitate rapid ID team if any suspicion of dengue diagnosis, particularly if acutely unwell, haemorrhagic fever (epistaxis, GI bleeding, but also send films as the card may miss petechia, purpura, ↓platelets, coagulopathy) or dengue shock syndrome ( BP, capillary parasitaemia of <0.5% and is not ↓ ↓ accurate for speciation. refill time, organ dysfunction). • Take films over a 72-hour period, ideally Immunocompromise after a fever spike, as this is when parasitaemia is highest. • In patients with HIV, check the most recent • Discuss any positive case immediately CD4 count and repeat if >3 months ago. with an ID specialist and refer to the Fungal and viral infections are more likely if British Infection Society treatment CD4 count <200 but can occur at higher guidance at http://www.britishinfection. counts. Check compliance with anti- org/drupal/sites/default/files/ retroviral therapy/antimicrobial prophylaxis. malariatreatmentBIS07.pdf. • Seek early advice from a respiratory • If fever is accompanied by diarrhoea, isolate specialist if there are respiratory symptoms the patient and note all recent travel history or an abnormal CXR (especially cavitation) on stool specimen requests. Discuss cavitation, or a high suspicion of immediately with microbiology and ID teams Pneumocystis pneumonia due to any of the if any suspicion of cholera, e.g. refugee/aid following features: worker in high-risk area. • subacute e.g. over 2–3 weeks, or • Send blood and stool cultures for typhoid progressive shortness of breath (and start empirical treatment) if high fever, • non-productive cough constitutional upset and recent travel to Asia • diffuse bilateral perihilar infiltrates on (especially the Indian subcontinent), Africa CXR or non-specific changes (especially sub-Saharan) or Latin America. • unexplained hypoxaemia (including Discuss urgently with the ID team, desaturation on exercise). especially if suggestive clinical features, e.g. Send sputum, for microscopy (acid-fast rose-coloured spots over the trunk, relative bacilli, fungal), histopathological analysis bradycardia, constipation. (Pneumocystis) and mycobacterial culture; if • Consider acute schistosomiasis if exposure necessary, induce sputum by nebulised to potentially infested water, e.g. freshwater hypertonic saline in a negative-pressure swimming, rafting, water sports in environment and discuss need for other Africa, South America or Asia, within the diagnostic procedures, e.g. bronchoalveolar past 8 weeks, +/− eosinophilia, lavage.

144 Fever Step-by-step assessment 14

Clinical tool: Extensions to the septic screen in specific patient groups – cont’d • If prominent GI symptoms, send blood for • Consider echocardiography to look for Strongyloides serology and consider endocarditis in patients with confirmed investigation for CMV colitis, e.g. flexible bacteraemia – especially Staphylococcus sigmoidoscopy + biopsy and intra- aureus or persistent fever. abdominal TB, e.g. CT abdomen/pelvis ± • Discuss early with the relevant specialty if targeted biopsy (samples must be sent in you suspect infection of prosthetic material, saline, not formalin, as acid-fast bacilli are e.g. valve prosthesis, pacemaker, prosthetic destroyed). joint. • If CNS features, investigate as per the general septic screen but send blood for IV drug use Toxoplasma serology, request CSF staining • Take ≥3 sets of blood cultures prior to for Cryptococcus and TB, and biopsy any starting antibiotic therapy. space-occupying lesion. • Look at all new and old injection sites; if • Request a dermatology review and biopsy of inflamed or tender, consider USS to exclude any suspicious or unusual rashes, e.g. an underlying abscess. cutaneous T-cell lymphomas, Kaposi’s • Arrange a Doppler USS to exclude DVT if sarcoma. there is any groin or leg swelling. • Prolonged indwelling vascular access • Exclude ilio-psoas abscess by CT if there is catheters, e.g. Hickman lines, tunnelled groin or lower back pain with difficulty lines, carry a substantial risk of bacterial/ extending the leg. fungal infection; suspect line infection in all • Arrange an echocardiogram ± cases where there is no clear alternative transoesophageal echocardiography if there source, even if the entry point looks clean. is no clear alternative source of fever or • Take blood cultures from the line and, if there is evidence of septic emboli on CXR feasible, remove sending the tip for (see Box 14.2). culture.

145 Fever 14 Further assessment

Further assessment of pyrexia and a positive ANA, ENA or ANCA of unknown origin with the Rheumatology team. • Biopsy any suspicious masses or Perform additional screening investigations lymphadenopathy (including bilateral (Box 14.3) in any patient with persistent hilar lymphadenopathy) detected unexplained fever. These may reveal a clinically or radiologically. diagnosis or provide useful leads for further • If an abscess is identified, request a investigation. surgical opinion regarding drainage. • Discuss the significance of any positive • Discuss with Haematology and consider serology with the ID/Microbiology team bone marrow examination if Bence Jones protein, paraproteinaemia or a significant blood film abnormality, e.g. Box 14.3 Further screening tests in pyrexia atypical lymphocytes. of unknown origin • Arrange muscle biopsy if ↑CK, to Ensure that a full septic screen (see above) is exclude inflammatory myositis. carried out, plus: • Perform a radioisotope bone scan to look for evidence of malignancy or Clinical osteomyelitis if persistent bony pain, • Repeat a full clinical assessment, including ↑Ca2+, ↑prostate-specific antigen or travel, sexual, occupational and recreational ↑alkaline phosphatse (with otherwise history; lymph nodes, skin and eye normal LFTs). examination; urinalysis; PR; breast and • If LFTs persistently deranged or testicular examination. hepatomegaly without an obvious Microbiological cause, request a liver biopsy (with material for culture) to look for TB, • Serology for HIV, viral hepatitis (A–E), EBV, sarcoidosis and granulomatous CMV, toxoplasmosis, Q fever, Lyme disease, hepatitis. brucellosis, syphilis, Chlamydia, Bartonella • If persistent haematuria/proteinuria and Yersinia. with negative MSU, discuss with the • Serology for leishmaniasis, amoebiasis, Renal team and consider renal biopsy to trypanosomiasis and schistosomiasis if exclude glomerulonephritis. there has been travel to the developing • Use the Duke (see Box 14.2) and Jones world. criteria (Box 14.4) to confirm or refute a • Tuberculin (Mantoux) test and 3 early suspected diagnosis of endocarditis or morning urine specimens for TB microscopy rheumatic fever respectively. and culture. • Consider an ANCA-negative systemic • Antistreptolysin O titre. vasculitis if palpable purpura, skin ulceration or livedo reticularis. Measure Biochemistry/immunology/haematology serum cryoglobulins (cryoglobulinaemic • ANA, RF, ANCA. vasculitis); consider arteriography e.g. renal, mesenteric, or tissue biopsy if • FBC with peripheral blood film, ferritin, LDH, polyarteritis nodosa is suspected, e.g. CK, Ca2+, plasma electrophoresis, TFTs, eosinophilia, renal impairment, ↑BP, prostate-specific antigen (if male patient constitutional upset. >50 years). • If ↑ESR in a patient >50 years: • Urine for Bence Jones protein. • Treat for giant cell arteritis and Radiological arrange temporal artery biopsy if there is headache, visual loss, scalp • CT chest/abdomen/pelvis. tenderness or an inflamed, • Echocardiogram. thickened, pulseless or tender temporal artery. 146 Fever Further assessment 14

Box 14.4 Jones Criteria for the diagnosis • Diagnose polymyalgia rheumatica if of rheumatic fever there is any proximal joint pain or Major manifestations stiffness – review the diagnosis if there is no response to systemic • Carditis steroids within 72 hours. • Polyarthritis • Suspect adult-onset Still’s disease if • Chorea microbiological and autoimmune investigations are consistently negative, • Erythema marginatum and there are recurrent joint pains or a • Subcutaneous nodules transient, non-pruritic, salmon-pink Minor manifestations maculopapular rash that coincides with fever, especially if ↑↑ferritin. • Fever • Review all drugs: discontinue one at a • Arthralgia time for 72 hours and then reinstate if • Previous rheumatic fever fever persists. • ↑ESR or CRP • If the cause remains unclear, pursue further investigation with a labelled • Leucocytosis white cell scan, radioisotope bone scan, • First-degree atrioventricular block Doppler USS and/or liver biopsy, and PLUS consider diagnoses of exclusion, e.g. Behçet’s disease, familial Mediterranean • Supporting evidence of preceding fever, factitious fever. streptococcal infection: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, positive throat culture N.B. Evidence of recent streptococcal infection is particularly important if there is only one major manifestation. Boon NA, Colledge NR, Walker BR, Hunter JAA 2006. Davidson’s Principles and Practice of Medicine. 20th edn. p. 617.

147 GASTROINTESTINAL HAEMORRHAGE: 15 HAEMATEMESIS AND RECTAL BLEEDING

Haematemesis is the vomiting of blood from and nausea. Most commonly, it is due to the upper GI tract. Bright red blood or clots excess alcohol consumption or NSAIDs/ imply active bleeding and are a medical aspirin. emergency. Altered blood with a dark, Oesophagitis granular appearance (‘coffee-grounds’) suggests that bleeding has ceased or has This is usually due to gastro-oesophageal been relatively modest. Melaena is the reflux. There may be a history of heartburn, passage of black tarry stools, usually due to indigestion or painful swallowing. acute upper GI bleeding (see ‘Haemateme- Oesophageal/gastric varices sis’ below), but occasionally due to bleeding These are collateral veins that form in within the small bowel or right side of response to portal hypertension and allow the colon. Haematochezia is the passage of portal blood to bypass the liver and enter fresh red or maroon blood per rectum; it the systemic circulation directly. The most is usually due to colonic bleeding but 15% common cause is hepatic cirrhosis. Patients of cases result from profuse upper GI typically present with massive upper Gl bleeding. bleeding. Upper GI malignancy Haematemesis There is often a background of weight loss, With major upper GI haemorrhage, resusci- anorexia, early satiety or dysphagia; a pal- tation must take place alongside assess- pable epigastric mass or signs of metastatic ment. Diagnosis is secondary and will disease may be evident. usually be established at upper GI endos- Mallory–Weiss tear copy (UGIE). Many units have a major haemorrhage protocol with which you This is a mucosal tear in the oesophago- should be familiar. gastric junction, following increased gastric pressure. 90% of these bleeds stop sponta- Peptic ulcer neously. The history is characteristic: force- Peptic ulcer is the most common cause of ful retching with initially non-bloody vomit, upper GI bleeding and an important cause followed by haematemesis. of massive haemorrhage. It is often accom- Other causes panied by epigastric pain. Important aetio- logical factors include Helicobacter pylori Congenital malformations of the vascular infection (90% of duodenal, 60% of gastric tree, e.g. Dieulafoy’s lesion, can produce ulcers) and NSAIDs/aspirin. major haemorrhage. An aorto-duodenal fistula will usually present with massive Gastritis/duodenitis haematemesis – suspect this if patient has Gastritis/duodenitis is typically accompa- had previous surgery for abdominal aortic nied by dyspepsia, epigastric discomfort aneurysm.

148 GASTROINTESTINAL HAEMORRHAGE Differential diagnosis 15

Rectal bleeding Inflammatory bowel disease Colorectal inflammation in ulcerative colitis The majority of patients have a benign or Crohn’s disease may cause rectal bleed- cause. In acute rectal bleeding, assess­ ing. The passage of frank blood ± mucus ment of bleeding severity and adequate and tenesmus may occur in proctitis. Colitis resuscitation take precedence over diagno- produces bloody diarrhoea with inter­ sis. Important causes are listed below. mittent cramping lower abdominal pain Benign anal disorders and, often, systemic upset. Endoscopy and These are a common cause of rectal bleed- biopsy of the lower bowel confirm the diag- ing in all age groups. They typically present nosis; inflammatory markers provide a with intermittent episodes of minor fresh useful guide to disease activity. red bleeding during or after defecation, Arteriovenous malformations although haemorrhoids can cause major These are an important cause of severe bleeds. Associated symptoms of haemor- lower GI bleeding, especially in the elderly. rhoids include discomfort, mucus discharge Typical endoscopic features may be appar- or pruritus. Severe pain, especially during ent but diagnosis is often challenging and defecation, suggests anal fissure. Diagnosis bleeding frequently recurs. is usually made by PR examination and proctoscopy, but always consider a concur- Other causes rent proximal bleeding source. Severe upper GI bleeding from any cause Diverticular disease may present with haematochezia. Invasive GI infections may cause bloody Diverticular disease is the most common diarrhoea, usually with systemic upset. cause of severe acute rectal bleeding. Bleed- Ischaemic colitis, due to acute occlusion ing occurs due to erosion of a vessel in the of the inferior mesenteric artery, tends to neck of a diverticulum; it may be life- occur in elderly patients and may result in threatening but stops spontaneously in 75% severe bleeding with lower abdominal of patients. pain. Colorectal carcinoma Radiation proctocolitis should be consid- Colorectal carcinoma is a common cancer in ered in any patient with a history of pelvic men and women. Recent weight loss, radiation, e.g. for prostatic or gynaecologi- change in bowel habit or colicky lower cal malignancy; most present within 2 years abdominal pain may be present but the of radiotherapy. presentation is frequently insidious with Colonic ulcer is an uncommon cause minimal symptoms. Polyps may also cause of bleeding, usually related to use of rectal bleeding. Diagnosis is usually made NSAIDs. by colonoscopy.

149 GASTROINTESTINAL HAEMORRHAGE 15 Haematemesis: overview

ABCDE, urgent FBC, U+E, LFTs, coagulation screen, cross-match

1 Resuscitation requirements assessed? (Boxes 15.1 and 15.2)

Yes

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

No

Full clinical assessment

Yes Consider 3 Rockall risk score >0 (Table 15.1)? Final diagnosis inpatient UGIE

No

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

No

Haematemesis preceded by Yes 5 Probable Mallory–Weiss tear forceful retching / vomiting?

No

Consider gastritis / duodenitis / oesophagitis UGIE if diagnosis unclear or ongoing symptoms

calcium channel blockers, or with fixed-rate Resuscitation requirements assessed? 1 pacemakers, and that compensatory vaso- (Boxes 15.1 and 15.2) constriction may not occur in patients on Resuscitation is the top priority. Use Box vasodilators. Monitoring trends of the 15.1 as a framework for evaluating resusci- parameters in Box 15.2 provides far more tation needs but tailor your assessment to information than a single ‘snapshot’ assess- the individual. Remember that heart rate ment and is essential for evaluating may be misleading in patients on rate- response to treatment. In patients who limiting medications e.g. beta-blockers, present with fresh, red haematemesis, the 150 GASTROINTESTINAL HAEMORRHAGE Haematemesis: step-by-step assessment 15

Box 15.1 Resuscitation in acute haemorrhage

First steps

• A+B before C: Recheck airway frequently, especially if ↓GCS/vomiting. Give high concentration O2 • Get help: one pair of hands is not enough. If necessary, call the medical emergency or cardiac arrest team • Activate the major haemorrhage protocol, if available

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 cannot obtain adequate access • 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 (Box 15.2) or any ongoing Advanced shock features (Box 15.2) or ongoing blood loss: major blood loss: • 0.5–1 L stat of IV crystalloid or colloid • 1–2 L stat of IV crystalloid or colloid • 2 units of red cells if Hb < 8 g/dL, ongoing • Use red cells as soon as available bleeding or >2 L IV crystalloid or colloid given • Consider O negative blood if significant delay Reassess in cross-matching • If advanced shock features or major blood Reassess loss on reassessment, move to opposite • If no ongoing advanced shock features or column major blood loss, move to opposite column • Otherwise, continue as above and discuss • If ongoing advanced shock features or major with haematologist if any of the following: blood loss give red cells/fluid as fast as • Known coagulopathy/anticoagulant therapy possible, seek specialist input, e.g. ICU, GI, • INR > 1.4 surgical, as appropriate and discuss haemostatic support, e.g. fresh frozen • Platelets < 100 x 109/L plasma, with haematologist. • Fibrinogen < 1 g/L • ≥4 L IV fluid in any form

Box 15.2 Clinical features of hypovolaemic shock Early Advanced • HR >100 bpm • Systolic BP <100 mmHg (or ↓40 mmHg from • Capillary refill time (CRT) >2s baseline) • Narrow pulse pressure • RR >20 breaths/min • ↓Postural BP • Cold, mottled peripheries • Pale, sweaty, agitated, thirsty • ↓GCS

151 GASTROINTESTINAL HAEMORRHAGE 15 Haematemesis: step-by-step assessment

subsequent vomiting of ‘coffee grounds’ or low risk of death (0.2%) and rebleeding passage of black tarry stools may simply (0.2%), but predicted mortality rises to 2.4% be a manifestation of the original bleed, for a score of 1 and 5.6% for a score of 2. but further bright red haematemesis or Admit patients with an initial Rockall score haematochezia implies continued active >0 for further assessment and observation; bleeding. most need inpatient UGIE to calculate the full score and establish the diagnosis. Active bleeding, features of shock or 2 suspected variceal bleed? 4 Background of alarm features? All patients with haematemesis accompa- Request UGIE to exclude upper GI malig- nied by features of shock (see Box 15.2) or nancy if the patient has any of the following evidence of ongoing bleeding should have alarm features: an urgent UGIE after adequate resuscita- • weight loss, anorexia or early satiety tion. Variceal bleeds have a high mortality • dysphagia (30–50%) and usually require urgent UGIE • epigastric mass following resuscitation and correction of • lymphadenopathy coagulopathy. Assume variceal bleeding in • jaundice any patient with known hepatic cirrhosis, • age ≥50 years. clinical features of chronic liver disease (see Box 19.4, p. 175) or deranged LFTs with Haematemesis preceded by forceful 5 evidence of impaired hepatic synthetic retching/vomiting? function (↑PT, ↓albumin). With a characteristic history of Mallory– 3 Rockall risk score >0 (Table 15.1)? Weiss tear, the diagnosis can often be made clinically, without the need for UGIE. In In the absence of continued active bleeding, other cases, a diagnosis of gastritis and haemodynamic compromise or oesopha- oesophagitis may be suggested by the geal varices, use a risk scoring system to history. Consider UGIE where there is no guide the need for hospital admission and obvious explanation for symptoms or UGIE. The Rockall risk score comprises repeated haematemeses. clinical and endoscopic elements. A pre- endoscopic score of 0 predicts an extremely

152 GASTROINTESTINAL HAEMORRHAGE Haematemesis: step-by-step assessment 15

Table 15.1 Rockall risk score Score Variable 0 1 2 3 Age <60 years 60–79 years ≥80 years Initial score Shock ‘No shock’, ‘Tachycardia’, ‘Hypotension’, criteria systolic BP systolic BP systolic BP ≥100 mmHg, ≥100 mmHg, <100 mmHg pulse <100 bpm pulse ≥100 bpm Comorbidity No major Cardiac failure, Renal failure, comorbidity ischaemic heart liver failure, disease, any disseminated major malignancy comorbidity Diagnosis Mallory–Weiss All other Malignancy of Additional tear, no lesion diagnoses upper GI tract criteria for identified and no full score stigmata of recent haemorrhage Major stigmata None, or dark Blood in upper of recent spot only GI tract, haemorrhage adherent clot, visible or spurting vessel

153 GASTROINTESTINAL HAEMORRHAGE 15 Rectal bleeding: overview

1 Acute rectal bleed?

No Yes

ABCDE, PR examination, urgent FBC, U+E, LFTs, coagulation screen, cross-match

2 Resuscitation requirements assessed? (Boxes 15.1 & 15.2)

Yes

Yes 3 Suspected upper GI source? Assess as per haematemesis

No Admit; Yes Cancer / polyp / arteriovenous 4 High-risk bleed (Box15. 3)? colonic malformation / colitis / imaging diverticular disease No

Manage as outpatient unless other worrying features Re-evaluate if further bleeding

Full clinical assessment, PR examination, FBC

Cancer / polyp / arteriovenous Risk factors for major Yes Colonic 5 malformation / colitis / colorectal pathology? imaging diverticular disease

No

Yes 6 Clinical features of anal disorder? Likely haemorrhoids or anal fissure

No

Observe; refer GI if persistent or troublesome symptoms

as described on page 91. In the absence of 1 Acute rectal bleed? acute bleeding, proceed to step 5. Regard any prolonged, profuse or ongoing Resuscitation requirements assessed? episode of bright red/maroon PR blood 2 (see Boxes 15.1 and 15.2) loss within the previous 24 hours as acute rectal bleeding. Assess patients with Make adequate resuscitation your top pri- melaena in the same way as those with hae- ority. Evaluate and address resuscitation matemesis (see above). Where the predomi- requirements as described for haemateme- nant problem is bloody diarrhoea, evaluate sis, step 1.

154 GASTROINTESTINAL HAEMORRHAGE Rectal bleeding: step-by-step assessment 15

3 Suspected upper GI source? Seek urgent senior surgical input in any patient with continued active bleed- Assume, initially, that melaena reflects ing, ongoing haemodynamic instability upper GI bleeding and assess as described despite resuscitation, or high transfusion for haematemesis. requirements. Brisk bleeding from the upper GI tract may present with a fresh red PR bleed and Risk factors for major colorectal 5 implies severe, life-threatening haemor- pathology? rhage. The diagnosis is straightforward if Refer the patient for urgent lower GI inves- there is concomitant haematemesis but tigation (usually colonoscopy) to exclude otherwise a high index of suspicion is colorectal cancer if any of the criteria in Box essential. Proceed with a working diagnosis 15.4 is present. of lower GI bleeding in patients without Also consider lower GI endoscopic haemodynamic instability but suspect an assessment if the patient has: upper GI source in those with features of hypovolaemic shock. If present, seek senior • systemic/extraintestinal features of GI input and consider UGIE as the first-line inflammatory bowel disease (Box 9.3, investigation following resuscitation, espe- p. 89) cially if there are any recent upper GI • a history of pelvic radiotherapy symptoms e.g. epigastric pain, or known/ • recent-onset, persistent bleeding when suspected oesophageal varices. the patient is ≥50 years or has a strong family history of colorectal cancer, e.g. 4 High-risk bleed (Box 15.3)? a first-degree relative <45 years at diagnosis, or two or more first-degree Consider non-admission or early discharge relatives. (with outpatient follow-up) if the patient has no high-risk features (see Box 15.2), 6 Clinical features of anal disorder? especially if there is evidence of a benign anal disorder. Perform careful rectal examination and Admit any patient with risk factors for proctoscopy in all patients to look for an uncontrolled or recurrent bleeding (see Box anal disorder. If one is identified, provide 15.3). Once adequately resuscitated and reassurance but refer the patient for outpa- clinically stable, arrange colonic imaging to tient colorectal evaluation if there is diag- establish the site and cause of bleeding – nostic doubt or symptoms persist despite usually colonoscopy or CT angiography. conservative management. Arrange further GI investigation and/or referral in all patients without an obvious anorectal cause, in whom bleeding persists Box 15.3 Risk factors for adverse outcomes in or recurs. acute lower GI bleeding • Any haemodynamic instability Box 15.4 High-risk features for colorectal cancer in patients with rectal bleeding • Initial haematocrit <35% or need for red blood cell transfusion • Rectal bleeding ≥6 weeks with change of • Any visualised red blood PR bowel habit (↑frequency or looser stools) • INR >1.4 or current aspirin/NSAID use • Palpable rectal or abdominal mass • Significant comorbidity e.g. • Significant weight loss e.g. ≥6 kg cardiorespiratory, renal, hepatic impairment, • Previous excision of colorectal cancer or current hospital inpatient • Age >60 years without anal symptoms, • Age >60 years e.g. discomfort, itching, lumps, prolapse

155 16 HAEMATURIA

Haematuria, or blood in the urine, may be vomiting and restlessness. The pain persists visible (macroscopic) or non-visible (micro- until obstruction is relieved. Visible haema- scopic), detected only by dipstick testing turia may occur and dipstick is positive in or urine microscopy. Visible haematuria 90% of cases. strongly suggests significant urological disease and always requires further evalu- Infection ation. Non-visible haematuria is a common Common clinical features of lower urinary incidental finding in asymptomatic patients tract infection (UTI) include frequency, and the challenge lies in differentiating dysuria, urgency, malodorous urine and benign causes from serious pathology. visible or dipstick haematuria. In acute Painless haematuria is most often caused pyelonephritis there is typically loin pain, by urinary tract cancer or tuberculosis (TB). fever, rigors and significant systemic upset. It is important to differentiate haematuria UTI is likely if a dipstick test is positive for from: either nitrite or leucocyte esterase, but is unlikely if both are absent. A pure growth • contamination in menstruating women of >105 organisms/mL of fresh MSU con- • other causes of red urine (Box 16.1). firms the diagnosis and permits sensitivity Tumours testing. Urinary TB may cause visible hae- 60% of renal cancers and 80% of bladder maturia ± other urinary tract symptoms/ cancers present with haematuria. Both are pulmonary manifestations/constitutional rare below the age of 40. Associated fea- upset. Urinalysis is positive for WBC but tures may include loin pain, abdominal routine culture is negative. Diagnosis mass and systemic upset (renal cancer) or requires a fresh early morning urine sample lower urinary tract symptoms (LUTS), e.g. for acid-/alcohol-fast bacilli and TB culture. dysuria, frequency, urgency and hesitancy Painless visible haematuria toward the end (bladder cancer). However, in the majority of voiding is the most common initial pre- of cases, haematuria is the sole symptom senting feature of Schistosoma haematobium and examination is normal. Risk factors are infection, most commonly acquired in listed in Box 16.2. Around 12% of prostate Egypt/East Africa e.g. by swimming in cancers present with haematuria (more freshwater lakes. Clues to diagnosis commonly microscopic). include travel history and eosinophilia. Dipstick haematuria is also common in bac- Stones terial endocarditis. Stones may cause obstruction anywhere along the urinary tract, though typically at Renal disease sites of narrowing, e.g. the pelvi-ureteric Haematuria may occur as a result of dis­ junction, pelvic brim and vesico-ureteric orders that disrupt the glomerular base- junction. Those in the renal pelvis or bladder ment membrane (glomerulonephritis). may remain asymptomatic for years and Those most likely to result in haematuria present incidentally with dipstick haematu- include anti-glomerular basement mem- ria. Ureteric obstruction typically presents brane disease (Goodpasture’s syndrome), with renal ‘colic’ – acute, severe loin pain small-vessel vasculitis e.g. Wegener’s gran­ radiating to the groin ± genitalia that builds ulomatosis, post-streptococcal glomeru- to a crescendo of intensity over a few lonephritis, systemic lupus erythematosus minutes, often accompanied by nausea, and immunoglobulin IgA nephropathy. 156 Haematuria Differential diagnosis 16

Box 16.1 Causes of urine discolouration Box 16.2 Risk factors for urinary tract cancer

Orange-brown • Smoking • Conjugated bilirubin • Occupational exposure to chemicals/dyes • Rhubarb, senna (benzenes, aromatic amines) • Concentrated normal urine, e.g. very low • Irritative voiding symptoms fluid intake • Previous pelvic irradiation Red-brown • Cyclophosphamide exposure • Blood, myoglobin, free haemoglobin, • Chronic inflammation, e.g. schistosomiasis porphyrins • Beetroot, blackberries • Drugs: rifampicin, metronidazole, warfarin Brown-black such as Alport’s syndrome and adult poly- cystic kidney disease, may also present • Conjugated bilirubin with haematuria. • Drugs: l-dopa Other causes • Homogentisic acid (in alkaptonuria or • Trauma: direct urethral trauma; blunt or ochronosis) penetrating abdominal/pelvic injury. Blue-green • Iatrogenic: renal biopsy, transurethral • Drugs/dyes, e.g. propofol, fluorescein resection of prostate, cystoscopy, urinary catheterisation. • Vascular: arterio-venous malformations; renal vein thrombosis. Associated features include proteinuria, • Bleeding diathesis. hypertension, oedema and renal failure. In • Renal cysts. IgA nephropathy there may be intermittent • Acute tubular necrosis. episodes of visible haematuria coinciding • Thin basement membrane disease with upper respiratory tract infections. (common, benign, often familial). Diagnosis of glomerular disease is made by • Loin pain-haematuria syndrome. renal biopsy. Inherited renal disorders, • Extreme exertion e.g. distance running.

157 Haematuria 16 Overview

Full clinical assessment, urinalysis, U+E

Visible, symptomatic or No 1 Non-significant haematuria persistent haematuria?

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

No

Evidence of UTI, menstruation or Yes Traumatic / ‘transient’ Treat / 3 recent trauma / vigorous exercise? haematuria reassess

No

Visible haematuria, LUTS, age >40 or Yes Imaging and 4 Anatomical lesion high-risk features? cystoscopy

No

GFR, proteinuria, BP or clinical Yes Consider 5 ↓ ↑ Renal disease suspicion of renal disorder? renal biopsy

No

Unexplained haematuria: likely thin basement membrane disease / arteriovenous malformation / 6 stone / cyst Monitor regularly for new or recurrent visible haematuria / lower urinary tract symptoms / proteinuria / ↓GFR

158 Haematuria Step-by-step assessment 16

Visible, symptomatic or persistent Consider infective endocarditis if there is 1 haematuria? fever, splinter haemorrhages, predisposing lesion or new murmur. Check for other causes of urine discolora- Do not attribute haematuria to antico­ tion (see Box 16.1). In the UK, dipstick agulation or antiplatelet treatment alone testing (at least 1+) is used to detect non- without further investigation. visible haematuria; routine urine micros- copy is not recommended but can be Visible haematuria, LUTS, age 40 or 4 > performed in uncertain cases, e.g. suspicion high-risk features? of myoglobinuria. If a dipstick test is posi- tive, ask specifically about episodes of In the absence of renal colic and following visible haematuria. treatment/exclusion of transient causes of Evaluate further as described below if haematuria, you must exclude cancer if any there is: of the following features is present: • visible haematuria • visible haematuria • LUTS • loin pain or LUTS • age >40 years • 2 out of 3 positive tests over time in an • high-risk features (Box 16.2). asymptomatic patient. Refer such patients to urology for further 2 Renal colic? investigation, e.g. CT urogram (or renal USS ± IVU) and cystoscopy. The combination of haematuria and renal colic (see above) suggests ureteric obstruc- GFR, proteinuria, BP or clinical 5 ↓ ↑ tion, usually from a stone or, less com- suspicion of renal disorder? monly, from clots or sloughed renal papilla. Confirm the presence and position ofa Refer to a nephrologist for further evalua- stone with an intravenous urogram (IVU) tion ± renal biopsy if any of the following or, preferably, spiral CT. Observe closely features is present: for ↓urine output or evidence of infection • proteinuria e.g. albumin : creatinine and perform further investigations to estab- ratio ≥30 lish an underlying cause, e.g. chemical • renal impairment (GFR <60 mL/min) composition of stone; plasma calcium/ • ↑BP in a patient <40 years phosphate/uric acid. • Connective tissue disease, e.g. SLE • family history of Alport’s syndrome/ Evidence of UTI, menstruation or recent 3 adult polycystic kidney disease trauma/vigorous exercise? • episodes of visible haematuria Refer to urology if visible haematuria coinciding with URTIs. follows surgical or invasive procedures of the renal tract e.g. renal biopsy, ureteros- 6 Unexplained haematuria. Monitor regularly copy, transurethral resection of prostate, or Isolated microscopic haematuria is common abdominal/pelvic/genital trauma. and usually due to benign disease e.g. thin The absence of leucocytes and nitrites on basement membrane disease. Provided that dipstick effectively excludes UTI in most the above causes have been excluded, reas- cases. If dipstick testing is positive or there sure patients that further investigation is is strong clinical suspicion, send an MSU; not necessary but monitor for worrying fea- treat confirmed infection then recheck for tures such as new urinary tract symptoms, non-visible haematuria. visible haematuria, proteinuria or renal Repeat dipstick testing at a later date if impairment. the test was performed during menstrua- tion or shortly after strenuous exercise or urinary catheterisation. 159 17 HAEMOPTYSIS

Haemoptysis, or coughing up blood, blood-streaked sputum for ≥2 weeks requires thorough evaluation to exclude strongly suggests malignancy. Massive serious pathology such as lung cancer, haemoptysis may occur with erosion of tuberculosis (TB) and pulmonary embolism tumour into a large vessel. Weight loss, (PE); many patients will require detailed recent-onset cough, finger clubbing and imaging and specialist assessment. Massive lymphadenopathy are well-recognised fea- haemoptysis (>500 mL/24 hours) may be tures. CXR may show a variety of abnor- life-threatening. malities (Box 17.1) but is sometimes normal. Respiratory tract infections Pulmonary embolism Respiratory tract infections (RTIs) are the Frank haemoptysis occurs due to pulmo- most common cause of haemoptysis. They nary infarction, usually accompanied by typically cause blood-stained purulent sudden-onset dyspnoea and pleuritic pain. sputum rather than frank blood, and have A pleural rub or signs of deep vein throm- associated features such as cough, fever bosis (DVT) are present in a minority of and dyspnoea. In acute bronchitis, mucosal cases. CXR may show a wedge-shaped inflammation can rupture superficial blood peripheral opacity or pleural effusion, but vessels; patients with chronic obstructive is most often normal. pulmonary disease may have haemoptysis Bronchiectasis during an infective exacerbation. Pneu­ monia may cause frank haemoptysis, There is typically a background of chronic especially with invasive bacteria, e.g. Sta- cough with copious foul-smelling purulent phylococcus aureus, Klebsiella spp. or fungi; sputum. Finger clubbing and coarse patients are usually profoundly unwell. inspiratory crackles may be evident on Mycetoma, lung abscess and TB may cause examination. massive haemoptysis. More commonly, TB Other causes produces chronic cough with small haemo- Pulmonary oedema may cause pink, frothy ptyses, fever, night sweats, weight loss and sputum but dyspnoea is almost always the characteristic CXR changes. dominant complaint. Other causes include Lung tumours pulmonary hypertension (especially associ- Haemoptysis is common in primary ated with mitral stenosis), coagulopathies, bronchial tumours but rare in secondary foreign body inhalation, chest trauma, lung tumours. Risk factors are smoking Wegener’s granulomatosis and Goodpas- (especially ≥40 pack-years) and age >40 ture’s syndrome. years; repeated small haemoptyses or

160 Haemoptysis Differential diagnosis 17

Box 17.1 The CXR in lung cancer

Common abnormalities on CXR in patients with • consolidation (see Figs 12.3 and 12.4, lung cancer include: pp. 116 and 117) that fails to resolve or recurs • a discrete mass (Fig. 17.1) or cavitating in the same lobe. lesion (Fig. 17.2) In a substantial proportion of cases, the CXR is • collapse of a lobe secondary to tumour normal. obstruction (Figs 17.3 and 17.4) • unilateral hilar enlargement or pleural effusion (see Fig. 12.6, p. 117)

Fig. 17.1 A solitary lung mass. Fig. 17.2 A cavitating lung lesion.

Fig. 17.3 Left lower lobe collapse. The changes in left lower lobe collapse may be subtle and Fig. 17.4 Right upper lobe collapse. Note the easily overlooked; note the triangular opacification right upper zone opacification, loss of volume in behind the heart, giving the appearance of an the right lung field and tracheal deviation. unusually straight left heart border.

161 Haemoptysis 17 Overview

ABCDE

No 1 True haemoptysis? Consider haematemesis / epistaxis

Yes

Yes 2 Massive haemoptysis? Resuscitation + emergency treatment

No

Full clinical assessment, CXR, FBC, coagulation screen

Clinical suspicion of pulmonary Yes 3 Assess for PE Confirmed PE embolism (PE)? (Fig. 12.7, (p. 118)) No CT chest + Yes Lung cancer / 4 Lung cancer risk features? respiratory parenchymal disease opinion No

Yes 5 Coagulopathy or acute reversible illness? Treat and observe for up to 2 weeks

No Recurrent or persistent haemoptysis Consider other causes CT ± specialist respiratory input if: 6 1. haemoptysis persistent or recurrent 2. age > 40 years or smoker 3. CXR abnormal

1 True haemoptysis? 2 Massive haemoptysis? A clear history of blood being coughed up Bleeding is difficult to quantify clinically or mixed with sputum reliably indicates but estimate the volume and rate of blood haemoptysis. loss, e.g. by direct observation, with a grad- Blood that suddenly appears in the mouth uated container. The major risk is asphyxi- without coughing suggests a nasopharyn- ation through flooding of alveoli or airway geal origin; ask about nosebleeds and look obstruction. Use the ABCDE approach

for epistaxis or a bleeding source within the (with high-flow O2 and IV resuscitation) mouth. and seek immediate anaesthetic help if any Blood originating from the GI tract is of the following is present: typically dark, acidic (test pH) and may contain food particles; blood that is frothy, • large blood volume e.g. >50 mL in 1 hour alkaline and bright red or pink suggests a • airway compromise respiratory source. • haemodynamic instability. 162 Haemoptysis Step-by-step assessment 17

3 Clinical suspicion of pulmonary embolism? evidence of bleeding elsewhere, or if there is no clear alternative cause. PE is easily forgotten and easily missed. Physical and CXR findings are unreliable so 6 Consider other causes/further investigation maintain a high index of suspicion. Con- sider PE and assess as shown in Figure 12.7 Chronic cough with daily mucopurulent (p. 118) if haemoptysis is acute and accom- sputum production or persistent coarse panied by any of the following: inspiratory crackles suggests bronchiectasis – confirm the diagnosis with high-resolution • rapid-onset pleuritic pain or dyspnoea thoracic CT. • symptoms or signs of DVT Consider TB if any of the following fea- • specific risk factors, e.g. active tures is present: malignancy, recent surgery • new-onset frank haemoptysis with no • prior residence in an endemic area other obvious cause. • immunosuppression (HIV, malnutrition, general debility) 4 Lung cancer risk features? • suggestive clinical features, e.g. night sweats, fever, weight loss You must exclude lung cancer, even if • suggestive CXR findings, e.g. a another diagnosis appears more likely, in cavitating lesion (see Fig. 17.2), any patient with: persistent consolidation, miliary TB. • blood-streaked sputum for >2 weeks If suspected, obtain ≥3 sputum samples • smoker >40 years for acid-fast bacilli and mycobacterial • weight loss, clubbing, Horner’s culture, and seek expert respiratory input. syndrome, cervical lymphadenopathy Exclude Goodpasture’s syndrome and • mass, cavitating lesion or unilateral hilar Wegener’s granulomatosis if there is evi- adenopathy/pleural effusion on CXR dence of renal involvement, e.g. hae­ (Box 17.1). maturia, proteinuria, ↓GFR: check for Thoracic CT is a useful first-line investi- anti-glomerular basement membrane and gation and may reveal a tumour or other anti-PR3 (c-ANCA) antibodies and seek cause for haemoptysis, e.g. bronchiectasis; renal input. but refer the patient to a respiratory special- Arrange an echocardiogram if the ist for further assessment ± bronchoscopy patient has: even if CT is normal. • a history of rheumatic fever • exertional dyspnoea, orthopnoea, 5 Coagulopathy or acute reversible illness? paroxysmal nocturnal dyspnoea Haemoptysis for <1 week with cough and • signs of mitral stenosis, e.g. loud S1, purulent sputum suggests acute RTI; assess low-pitched mid-diastolic murmur as described on page 120 and arrange • signs of pulmonary hypertension, e.g. follow-up review after treatment to ensure loud P2, right ventricular heave. that haemoptysis has resolved. If the cause is still unclear, consider CT Perform a coagulation screen in any and specialist respiratory input – especially patient on anticoagulant therapy, with if > 40 years, smoking history, ongoing a history of bleeding disorder or with symptoms or CXR abnormality.

163 18 HEADACHE

Headache is extremely common and usually with headache the most prominent clini­ benign. The challenge is to identify the cal feature. Bacterial meningitis is life- small minority of patients with serious threatening; presenting features include underlying pathology and those with disor- ↓GCS, signs of shock (see Box 28.1, p. 249), ders that respond to specific treatments. purpuric rash (see Fig. 26.15, p. 240) and Subarachnoid haemorrhage (SAH) focal neurological signs. LP (see Clinical tool p. 168) is helpful in the diagnosis but The headache is typically of sudden onset must not delay IV antibiotics therapy. (often near-instantaneous), occipital and Beware atypical presentations in immuno- very severe. Distress and photophobia are suppressed, pregnant or alcoholic patients. common but neck stiffness may take hours to develop. Large bleeds may be compli- Migraine cated by ↓GCS, seizure or focal neurologi- Recurrent severe headaches lasting several cal signs. Most cases are evident on CT but hours to a few days, usually accompanied LP is required in suspected cases with by photophobia and nausea ± vomiting. In normal CT. one-third there are associated focal neuro- Benign thunderclap headache mimics the logical features – an ‘aura’ (Box 18.1). The headache of SAH but investigation reveals headache is typically intense, throbbing no evidence of an intracranial vascular dis- and unilateral, causing the patient to cease order. It is a diagnosis of exclusion. normal activities in favour of bed-rest in a Other vascular causes quiet, darkened room. Common triggers include cheese, chocolate, alcohol and the Intracerebellar haemorrhage: typically oral contraceptive pill. A first attack aged > presents with abrupt-onset headache, 40 years is uncommon. nausea, vomiting, dizziness and ataxia ± ↓GCS. Cluster headache Spontaneous intracerebral or intraven- This refers to severe, unilateral, retro-orbital tricular haemorrhage: the onset of headache headache with restlessness, agitation and is usually over minutes to hours accompa- ipsilateral lacrimation, conjunctival injec- nied by a focal neurological deficit ± ↓GCS. tion, rhinorrhoea and facial sweating. Cerebral venous thrombosis: headache is Attacks are short-lived (15–90 minutes) but common but variable, e.g. ‘thunderclap’, occur frequently and repeatedly (often at throbbing, ‘band-like’, as are associated the same time each day) in ‘clusters’ lasting features, e.g. nausea, vomiting, seizures, days to weeks; these are separated by cranial nerve palsies, hemiparesis, ataxia, months without symptoms. The male : ↓GCS. female ratio is 5 : 1. Vertebrobasilar dissection: may cause Temporal arteritis (giant cell arteritis) acute-onset occipital/posterior neck pain with brainstem signs and symptoms. A large-vessel vasculitis, closely associated with polymyalgia rheumatica, more Meningitis common in women and unusual in patients Classically presents with headache, fever <50 years. Clinical features include local- and meningism. The onset of headache is ised headache (temporal/occipital), scalp typically over hours rather than sudden. tenderness, jaw claudication, visual loss, Viral meningitis is usually self-limiting, constitutional upset (malaise, night sweats, 164 Headache Differential diagnosis 18

Box 18.1 What constitutes an aura? contraceptive pill, or secondary to an intra­ cranial space-occupying lesion. In the Auras are focal neurological phenomena that latter case, there may be focal neurological precede or accompany a migrainous headache. signs, change in personality or new-onset They occur in 20–30% of patients with seizures. Headache tends to be worse migraine, usually developing gradually over in the morning and on lying flat, cough­ 5–20 minutes and lasting <60 minutes. Most ing or straining. There may be associated are visual in nature but they may also be vomiting, often without nausea +/− sensory or motor. Common examples include: papilloedema. • ‘fortification spectra’: shimmering zigzag Sinusitis lines that move across the visual field This causes a dull, throbbing headache • flashing lights or spots associated with facial pain over the sinuses. • temporary loss of vision It tends to be worse on bending forward. There are invariably associated nasal symp- • numbness/dysaesthesia on one side of the toms, e.g. congestion or discharge. Sinusitis body lasting > 8 weeks requires CT to confirm the • expressive dysphasia. diagnosis. Analgesic headache This refers to headache associated with pyrexia, weight loss), and an abnormal chronic analgesic use especially opioids temporal artery (inflamed, tender, non- such as codeine. Headaches are usually pulsatile). ESR/CRP are almost always bilateral and occur prior to the next dose of raised. The potential for rapid-onset irre- analgesia. versible visual loss necessitates urgent Tension headache treatment with steroids. Temporal artery biopsy may confirm the diagnosis but The headache is usually bilateral (often should not delay steroid treatment. generalised or frontal) and described as ‘dull’, ‘tight’ or ‘pressing’ in nature. Unlike Acute glaucoma migraine, nausea and photophobia are Acute glaucoma, an ophthalmological usually absent and the patient can often emergency, occurs due to a sudden increase continue with normal activities. in intraocular pressure. The typical patient Other causes is long-sighted, middle-aged or elderly, and presents with periorbital pain (± frontal • Carbon monoxide poisoning. headache), nausea and vomiting, blurred • Hypercapnia. vision with halos around lights and con- • Drugs: vasodilators e.g. nitrates, junctival injection. Urgent ophthalmology ‘recreational’ drugs e.g. solvents. referral is mandatory. • Trigeminal neuralgia (brief, repetitive episodes of intense shooting/ Raised intracranial pressure stabbing/‘electric shock’-like pain in II May occur as a primary disorder (idiopathic and III divisions of trigeminal nerve). intracranial hypertension) especially in • Trauma: extradural haemorrhage, overweight young women taking the oral subdural haemorrhage, concussion.

165 Headache 18 Overview

ABCDE, CNS and eye examination

1 ‘First or worst’ presentation?

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

Suspect acute intracranial Yes Immediate 3 Intracranial lesion pathology? 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 cause

Yes Ophthalmology 5 Suspect acute glaucoma? review Acute glaucoma

No

ESR >50 Age >50 years + any features of Yes 6 or strong Likely temporal arteritis temporal arteritis (Box 18.3) clinical suspicion?

No No

Full clinical assessment

Yes Neuro- 7 Red flag features (Box 18.4)? Intracranial cause imaging

No

Yes 8 Frontal headache + nasal symptoms? Likely sinusitis

No

Features of primary headache Yes Migraine / cluster headache / 9 disorder (Boxes 18.5–18.7)? tension-type headache

No

Consider temporal arteritis in patient >50 years with any persistent headache Review analgesic regimen (analgesic headache?) and other drugs Outpatient Neurology referral if persistent troublesome symptoms

166 Headache Step-by-step assessment 18

1 ‘First or worst’ presentation? • fever (≥38°C) • rash (not always petechial) Acute severe pathology is less likely in • signs of shock (see Box 28.1, p. 249) patients with recurrence of a longstanding • acute-onset headache e.g. over hours problem than in patients with a first pres- with meningism (Box 18.2). entation of headache. However, patients with a pre-existing headache disorder, e.g. SAH may also present with severe migraine, may also present acutely with headache and meningism, but is less likely another diagnosis such as SAH. If a patient if the headache onset was not sudden (see with chronic headaches presents with a below). new headache that is markedly different in If you suspect meningitis, take blood cul- severity or character to normal, assess it as tures and throat swabs immediately. Give new-onset headache. IV antibiotics and, if there are no contrain- dications, perform LP for CSF analysis (see 2 Any features of meningitis? over - Clinical Tool). If you suspect raised Identifying patients with bacterial menin­ intracranial pressure, perform CT prior to gitis is the top priority to allow rapid, LP. It is often difficult to distinguish viral potentially life-saving, antibiotic treatment. from early bacterial meningitis clinically, so Patients may lack classical features but, in manage as bacterial meningitis pending almost all cases, there will be at least one of: CSF analysis.

Box 18.2 Meningism?

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

A B Fig. 18.1 Testing for meningeal irritation.

167 Headache 18 Step-by-step assessment

Clinical tool: LP and CSF interpretation Contraindications to LP there is any possibility of bacterial • Infected skin over the needle entry site. meningitis, treat the patient with antibiotics • Radiological evidence of raised intracranial pending further investigation, e.g. blood/CSF pressure. culture. • Clinical suspicion of raised intracranial • If there is a ↑lymphocyte count, send CSF for viral PCR, including herpes and pressure: ↓GCS, focal neurological signs, papilloedema, new seizures. enterovirus. 9 • The history in TB meningitis is often indolent • Coagulopathy or platelets <50 × 10 /L. • Severe agitation and restlessness. – consider it if the patient has known immunocompromise or is from an endemic CSF interpretation TB region, especially if the CSF results suggest the diagnosis (see above). If Routine interpretation of CSF results includes suspected, send CSF for acid-fast bacilli (Table 18.1): and mycobacterial PCR and culture. • opening pressure (supine position) • Non-infective disorders can produce a • protein lymphocytic picture, including lupus, • glucose (always compare with blood sarcoidosis and malignant meningitis. glucose) Check auto-antibodies and discuss with • cell count. Rheumatology if there are any other Additional tests, e.g. culture, PCR, suggestive features. oligoclonal bands, may be required in some • A difficult procedure may result in a circumstances. ‘traumatic tap’, i.e. red cells in the CSF. This can complicate interpretation of the Additional points to consider WCC. A rule of thumb is that 1 white cell • Early bacterial meningitis may be mistaken per 1000 red cells is normal. However, if for viral meningitis as there is a the CSF picture is unclear, then the clinical predominance of lymphocytes in the CSF. If history must be taken into account.

168 Headache Step-by-step assessment 18 /L) 6 + ve for 0 Red cells ( × 10 0 0 0 ↑ : often in thousands 0 but xanthochromia (haem breakdown product) 0 /L) 6 > 100 + ve Neutrophils ( × 10 0 0 ≥ 1 is Usually May be 0 in very early stages 0 0 0 0 /L) 6 ↑ as a cause < neutrophils > 50 + ve ↑ red cells, then 1 < 5 Lymphocytes ( × 10 ↑ : usually but may be predominant cell type in early stages > 5 is Usually 100% > 50 0; if white cell per 1000 red cells is normal 0 0 Occasionally of aseptic meningitis > 50% > 60% of blood glucose 3–5 CSF glucose (mmol/L) < 50% of blood glucose < 60% of blood glucose but < 30% of blood glucose > 60% of blood glucose > 60% blood glucose > 60% of blood glucose CSF protein (mg/L) 200–450 ↑ ↑ or normal ↑ : may be > 1000 ↑ ↑ ↑ : may be > 100 O 2 cm

Opening pressure 5–18 H ↑ or normal ↑ or normal ↑ ↑ ↑ or normal ↑ Table 18.1 Interpretation of CSF results CSF of Interpretation 18.1 Table Condition Normal Bacterial meningitis Viral meningitis TB meningitis Subarachnoid haemorrhage Late subarachnoid haemorrhage Vasculitis

169 Headache 18 Step-by-step assessment

3 Suspect acute intracranial pathology? accompanied by any of the following features: Arrange immediate neuroimaging to • conjunctival injection exclude life-threatening intracranial pathol- • clouding of the cornea ogy, e.g. haemorrhage or space-occupying • irregular/non-reactive pupil lesion with mass effect, if any of the follow- • ↓visual acuity or blurred vision ing is present: • sees coloured ‘halos’ around lights. • ↓GCS Age 50 years any features of temporal • focal neurological signs 6 > + • new-onset seizures arteritis (Box 18.3)? • history of recent head injury Suspect temporal arteritis in patients >50 • anticoagulation or coagulopathy. years with new-onset headache and any of Where CT does not yield a diagnosis the features shown in Box 18.3. Check ESR and no alternative cause is apparent e.g. and CRP urgently; ESR >50 mm/hour toxicity, metabolic derangement, LP may makes the diagnosis highly likely. In these be required to exclude meningitis or SAH. circumstances, or where clinical suspicion Review the presentation and, if appropriate, is high e.g. >2 features from Box 18.3, start evaluate for seizure (p. 258), coma (Ch 7) or steroid therapy immediately. A prompt ‘Limb weakness’ (Ch 22). Seek urgent Neu- response to steroids essentially confirms the rology input if the cause remains unclear. diagnosis, though, ideally, temporal artery biopsy should be performed within 2 weeks Meets criteria for ‘sudden-onset’ of starting steroids. 4 headache? 7 Red flag features (Box 18.4)? Exclude SAH in any patient with a severe ‘first or worst’ headache that reaches peak Regardless of headache duration, you must intensity within 5 min of onset and persists exclude serious underlying intracranial for >1 hour. pathology if any of the features in Box 18.4 Headache in SAH may not be instantane- is present. Arrange CT brain ± MRI and, if ous in onset but almost always reaches normal, seek input from a neurologist. Con- maximal intensity within 5 min and rarely sider benign intracranial hypertension in resolves in <1 hour. If a headache meets patients with features of ↑intracranial pres- these criteria, then there are no clinical fea- sure but no mass on neuroimaging. tures that can reliably rule out the diagnosis so neuroimaging ± CSF analysis is manda- tory. CT within 24 hours will detect 95% Box 18.3 Features suggesting temporal arteritis of bleeds. If normal, then LP, ≥12 hours from the onset of headache, must be per- • Pain localised to temporal or occipital formed to look for xanthochromia; its region absence effectively excludes SAH. The • Inflamed, thickened, pulseless or tender major differential diagnosis is benign thun- temporal artery derclap headache; however, all sudden- • Scalp tenderness onset severe headaches should, ideally, be • Jaw claudication discussed with a neurologist. • Visual loss (may be temporary initially) 5 Suspect acute glaucoma? • Constitutional symptoms: fever, malaise, Acute glaucoma is sight-threatening and fatigue, night sweats, weight loss easily missed. Request urgent Ophthalmol- • Symptoms of polymyalgia rheumatica ogy review if the patient has acute-onset (proximal pain, stiffness etc.) headache (especially frontal or periorbital)

170 Headache Step-by-step assessment 18

Box 18.4 Red flag features Box 18.5 Diagnostic criteria for migraine

• New-onset headache/change in headache Five or more headache episodes meeting the in patients over 50 years following criteria, or two or more episodes • Focal CNS signs, ataxia or new cognitive or associated with typical aura (see Box 18.1): behavioural disturbance 1. headache duration of 4–72 hours • Persistent visual disturbance 2. ≥2 of unilateral location/pulsating quality/ • Headache that changes with posture or moderate to severe intensity/disabling* wakes the patient up 3. ≥1 of nausea ± vomiting/photophobia + • Headache brought on by physical exertion phonophobia. *Aggravation by or causing avoidance of routine physical activity • Papilloedema e.g. walking or climbing stairs. • New-onset headache in a patient with known HIV or active malignancy

Box 18.6 Diagnostic criteria for cluster 8 Frontal headache + nasal symptoms? headache Whilst frontal headache may raise the sus- Five or more episodes of headache with: picion of sinusitis, the diagnosis should 1. severe and unilateral orbital, periorbital or only be made when there are associated temporal pain nasal symptoms. Look for at least two of: 2. duration 15–180 minutes and frequency 1 • nasal blockage/congestion per 2 days to 8 per day • rhinorrhoea/discharge 3. ≥1 of restlessness/agitation or ipsilateral • loss of smell facial signs.* • facial pressure or tenderness. *Conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, eyelid Further investigation is not necessary in oedema. acute sinusitis but refer the patient to ENT if there are chronic symptoms.

Features of primary headache disorder 9 (Boxes 18.5–18.7)? Box 18.7 Diagnostic criteria for tension-type headache Primary headache disorders, e.g. tension Ten or more episodes of headache with the headache, migraine are responsible for following criteria: most headaches. Diagnosis relies on associ- 1. Duration 30 minutes to 7 days ated features and patterns of presentation (Boxes 18.5–18.7). By definition, they cannot 2. ≥2 of bilateral location/tight or pressing be diagnosed on the basis of a single quality/mild to moderate intensity/ episode. However, where the presentation non-disabling* is typical, it may be reasonable to class a 3. None of: photophobia/phonophobia/nausea/ case as a likely first presentation of a vomiting. primary headache disorder. Where a recur- *Not aggravated by or causing avoidance of routine physical rent headache does not fit neatly into a activity e.g. walking or climbing stairs. diagnostic category, refer to a neurologist.

171 19 JAUNDICE

Jaundice describes the yellow pigmentation Icteric leptospirosis (Weil’s disease) is a of skin, sclerae and mucous membranes severe illness characterised by deep jaun- that results from accumulation of bilirubin dice, fever, bleeding e.g. epistaxis, hae­ within tissues. This may result from ↑red matemesis, renal failure and, often, a cell breakdown (haemolysis), ↓uptake/ purpuric rash. conjugation by the liver or impaired biliary Autoimmune hepatitis most often pre­ drainage (cholestasis). sents with established cirrhosis but 25% of Acute liver injury cases manifest as an acute hepatitis with jaundice and constitutional symptoms. The Infective, autoimmune, toxic, metabolic female : male ratio is 3 : 1 and there is an or vascular liver insults may lead to acute association with other autoimmune condi- hepatitis. Jaundice results from impaired tions. Serum immunoglobulin (IgG) levels bilirubin transport across hepatocytes ± are raised and serum autoantibodies may obstruction of biliary canaliculi due to be present. inflammation and oedema. There is typi- Wilson’s disease, an inherited disorder of cally a disproportionate increase in ALT copper metabolism, can present with acute and AST relative to ALP and GGT. Exten- hepatitis, sometimes recurrent, and occa- sive liver damage may cause acute liver sionally causes acute liver failure. A ↓serum failure, characterised by encephalopathy caeruloplasmin is highly suggestive. (Table 19.1) and coagulopathy (typically Hepatic vein thrombosis (Budd–Chiari INR >1.5) in the absence of pre-existing syndrome) typically presents with upper liver disease; jaundice is present in abdominal pain, hepatomegaly and marked most cases and often correlates with the ascites. degree of injury. Causes are shown in Cardiac failure may cause hepatic injury Box 19.1. due to vascular congestion with resultant Potential causes of acute drug-induced jaundice and ↑ALT. liver injury are listed in Box 19.2. LFTs Ischaemic hepatitis (‘shock liver’) may may take months to normalise after result from impaired hepatic perfusion in a drug cessation, especially with cholestatic patient with shock; the ALT is usually ↑↑↑. injury. Acute alcoholic hepatitis may occur in Cirrhosis individuals without chronic liver disease Chronic liver injury from any cause (Box following intensive binge drinking and 19.3) results in extensive hepatocellular presents with jaundice, constitutional upset, loss, fibrosis and disturbance of the normal tender hepatomegaly and fever. hepatic architecture. Hepatocellular fail­ In acute viral hepatitis, jaundice is usually ure leads to jaundice, coagulopathy and preceded by a 1–2-week prodrome of ↓albumin. Portal hypertension and conse- malaise, arthralgia, headache and anorexia. quent porto-systemic shunting of blood Hepatitis A–E viruses are responsible for result in oesophageal varices and hepatic most cases; less common causes include encephalopathy (Table 19.1). Portal hyper- CMV, EBV and herpes simplex. Diagnosis tension, ↓albumin and generalised salt and is confirmed by serology. Recovery occurs water retention, due to haemodynamic and over 3–6 weeks in most cases but chronic endocrine abnormalities, leads to ascites. infection develops in up to 10% of patients There may be characteristic ‘stigmata’ on with hepatitis B and 80% with hepatitis C. examination (see Box 19.5). 172 Jaundice Differential diagnosis 19

Table 19.1 West Haven grading of hepatic Box 19.1 Causes of acute liver failure encephalopathy Drugs/toxins Stage Alteration of consciousness • Paracetamol overdose* 0 No change in personality or • Anti-tuberculous drugs behaviour No asterixis • Ecstasy 1 Impaired concentration and • Halothane attention span • Amanita phalloides Sleep disturbance, slurred speech, • Carbon tetrachloride asterixis, agitation or depression 2 Lethargy, drowsiness, apathy or Infection aggression • Acute viral hepatitis (A, B, E)* Disorientation, inappropriate • Cytomegalovirus (CMV), Epstein–Barr virus behaviour, slurred speech (EBV) 3 Confusion and disorientation, Vascular bizarre behaviour Drowsiness or stupor • Shock/ischaemic hepatitis Asterixis usually absent • Budd–Chiari syndrome 4 Comatose with no response to Other voice commands Minimal or absent response to • Wilson’s disease painful stimuli • Autoimmune hepatitis • Acute fatty liver of pregnancy • Extensive malignant infiltration *Denotes common cause. Hepatic tumours Malignant infiltration by primary or, more commonly, metastatic tumours may cause jaundice due to extensive replacement of more common in men and 75% of patients liver parenchyma or intrahepatic duct have inflammatory bowel disease. obstruction. Common associated features A dilated common bile duct on USS include cachexia, malaise, RUQ pain implies extrahepatic biliary obstruction. (stretching of the liver capsule) and The presence of RUQ pain, fever and hepatomegaly. rigors suggests bacterial infection proximal to the obstruction (ascending cholangitis) Biliary disease and requires prompt antibiotics and Jaundice due to biliary obstruction causes a decompression. predominant rise in ALP and GGT, fre- Gallstones are the most common cause of quently associated with pale stools, dark extrahepatic cholestasis; the onset of jaun- urine and itch. An ↑PT may occur due to dice is relatively rapid and often accompa- vitamin K malabsorption. nied by colicky, epigastric/RUQ pain. In primary biliary cirrhosis, there is pro- Benign strictures may result from trauma, gressive destruction of the intrahepatic bile particularly during biliary surgery or ducts. 90% of patients are female. Pruritus inflammation within the biliary tree, e.g. usually precedes jaundice. The presence of pancreatitis. anti-mitochondrial antibodies is diagno­ Cholangiocarcinoma is a malignant stic. Primary sclerosing cholangitis causes tumour of bile ducts that most commonly inflammation, fibrosis and strictures of the pre­sents with painless jaundice, often with intra- and extrahepatic biliary tree. It is pruritus. 173 Jaundice 19 Differential diagnosis

Box 19.2 Drugs causing acute hepatotoxicity Box 19.3 Causes of cirrhosis

Acute hepatitis • Chronic alcohol excess • Paracetamol (in overdose) • Chronic viral hepatitis (hepatitis B or C) • Cocaine, ecstasy • Non-alcoholic fatty liver disease • Aspirin, NSAIDs • Autoimmune hepatitis • Halothane • Cholestatic • Anti-tuberculous therapy: pyrazinamide, • Primary sclerosing cholangitis isoniazid, rifampicin • Primary biliary cirrhosis • Antifungals: ketoconazole • Secondary biliary cirrhosis • Antihypertensives: methyldopa, hydralazine • Metabolic Cholestasis/cholestatic hepatitis • Hereditary haemochromatosis • Antibiotics: penicillins e.g. flucloxacillin, • Wilson’s disease co-amoxiclav, ciprofloxacin, macrolides • Alpha -antitrypsin deficiency e.g. erythromycin 1 • Cystic fibrosis • Chlorpromazine • Venous obstruction • Azathioprine • Cardiac failure • Oestrogens (including the oral contraceptive pill) • Budd–Chiari syndrome • Amitriptyline • Drugs e.g. methotrexate • Carbamazepine • Cryptogenic • ACE inhibitors • Cimetidine/ranitidine Jaundice in the absence of • Sulphonamides hepatobiliary disease Haemolytic disorders (Box 19.4) cause accu- mulation of unconjugated bilirubin in plasma due to ↑red cell destruction. LFTs Pancreatic carcinoma typically presents are otherwise normal, though Hb may be with insidious, progressive jaundice due to decreased, with evidence of haemolysis on extrinsic compression of the common bile blood tests and film. Gilbert’s syndrome is a duct, often with marked weight loss, nausea benign congenital condition affecting 2–5% and anorexia. Pain may be absent in the of the population. Decreased enzymatic early stages. Other causes of extrinsic biliary activity limits bilirubin conjugation, causing compression include duodenal ampullary mild jaundice during periods of fasting or tumours or enlarged lymph nodes at the intercurrent illness with no other clinical/ porta hepatis. biochemical features of liver disease.

174 Jaundice Differential diagnosis 19

Box 19.4 Causes of haemolysis

Hereditary Acquired • Erythrocyte membrane defects • Immune • Hereditary spherocytosis • Autoimmune haemolytic anaemia • Hereditary elliptocytosis • Alloimmune: haemolytic transfusion • Erythrocyte enzyme defects reaction, haemolytic disease of the newborn • Glucose-6-phosphate dehydrogenase deficiency • Fragmentation syndromes • Haemoglobinopathies • Microangiopathic haemolytic anaemia e.g. haemolytic uraemic syndrome/ • Thalassaemia thrombotic thrombocytopenic purpura • Sickle cell • Mechanical heart valves • Drugs e.g. dapsone • Infections e.g. malaria • Paroxysmal nocturnal haemoglobinuria

175 Jaundice 19 Overview

Full clinical assessment + LFTs, FBC, U+E, coagulation screen

Yes 1 Evidence of chronic liver disease? See Further assessment of chronic liver disease (p. 181) No

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

No

3 Evidence of cholestasis?

Yes

Yes Fever / Rigors / RUQ pain? Suspect acute cholangitis

No

Yes Seek underlying Dilated bile ducts on USS? Extrahepatic cholestasis cause

No No

ALT >500 U/L, PT or Yes Acute liver injury (viral / autoimmune / 4 ↑ features of encephalopathy? metabolic / ischaemic / toxic)

No

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

No

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

No

Yes Discontinue 7 Likely drug culprit? Drug hepatotoxicity drug

No

Consider viral / autoimmune hepatitis, hepatocellular carcinoma, metabolic liver disease 8 Targeted investigation if suspected cause; otherwise full liver screen + abdominal USS

176 Jaundice Step-by-step assessment 19

1 Evidence of chronic liver disease? cases, biopsy may be required to confirm the diagnosis and suggest an In the absence of an established diagnosis, aetiology. look for indicators of chronic liver disease, Evaluate any patient with jaundice and a particularly physical stigmata (Box 19.5) background of established or suspected cir- and evidence of complications of cirrhosis rhosis as described in ‘Further assessment e.g. portal hypertension. of chronic liver disease’ (p. 181). • Multiple spider naevi, in the absence of pregnancy/pro-oestrogenic drugs, 2 Normal liver enzymes, PT, albumin? strongly suggest chronic liver disease. Consider haemolysis in jaundiced patients The other stigmata lack specificity without associated features of liver disease individually but are helpful in and with evidence of ↑red cell breakdown, combination. e.g. ↓Hb, ↑LDH, ↓haptoglobin, blood film • Ascites, especially in association with abnormalities e.g. red cell fragments, ± evi- dilated, superficial periumbilical veins dence of ↑red cell production, e.g. ↑reticu- (‘caput medusae’), is a useful pointer locytes, polychromasia. Further assessment to portal hypertension but may have is described on page 134. If there are no other causes in jaundiced patients, features of haemolysis or chronic liver e.g. intra-abdominal malignancy or disease, jaundice is mild (bilirubin right heart failure with hepatic <100 µmol/L) and LFTs are otherwise congestion. The rapid onset of ascites, normal, the likely diagnosis is Gilbert’s jaundice, hepatomegaly and abdominal syndrome. pain suggests acute Budd–Chiari syndrome. 3 Evidence of cholestasis? • Hepatic encephalopathy (Table 19.1) and synthetic dysfunction (see below) may A rise in ALP/GGT out of proportion to occur in acute liver failure but strongly ALT/AST suggests cholestasis, especially suggest chronic liver disease when they with pale stools/dark urine. If there are fea- occur against a background of previous tures of sepsis, take blood cultures, give IV clinical/biochemical evidence of liver antibiotics, arrange urgent abdominal USS disturbance. and discuss with the surgical team. Other- • Abdominal USS can demonstrate wise, perform USS to look for bile duct dila- morphologic features of cirrhosis e.g. tation (indicating extrahepatic cholestasis) coarse echotexture, ↑nodularity, and and an underlying cause e.g. gallstones. provide supportive evidence of portal If USS does not show dilated bile ducts, hypertension (splenomegaly, reversed proceed to step 4. flow in the portal vein). In difficult If USS shows dilated bile ducts but not the underlying cause, arrange further imaging. Magnetic resonance imaging Box 19.5 Stigmata of chronic liver disease (MRCP) provides excellent definition of the biliary tree – request it if you suspect gall- • Digital clubbing stones e.g. acute onset, associated abdomi- nal pain, or there is a past history of biliary • Palmar erythema pathology. CT allows better visualisation of • Spider naevi the pancreas – arrange if jaundice is pain- • Loss of axillary/pubic hair less with an insidious, progressive onset, • Parotid swelling especially in the elderly, to exclude pancre- atic cancer. ERCP also provides useful • Gynaecomastia diagnostic information but is more often • Testicular atrophy undertaken subsequently to allow removal of gallstones or stenting of the ducts. 177 Jaundice 19 Step-by-step assessment

ALT 500 U/L, PT or features of Seek cause of acute liver injury 4 > ↑ encephalopathy? Enquire about alcohol and paracetamol intake, all recent drugs (prescribed or Identify patients with acute liver failure otherwise) and possible exposure to Look for features of acute liver failure in all environmental/occupational toxins, e.g. jaundiced patients without pre-existing carbon tetrachloride. Check viral serology liver disease or extrahepatic biliary obstruc- (IgM anti-HBc, anti-HAV, anti-HEV, anti- tion, especially if there is evidence of exten- CMV, anti-EBV), serum caeruloplasmin, sive hepatocellular injury (↑↑ALT). autoantibodies (ANA, ASMA, LKM) and Hepatic encephalopathy (Table 19.1) may gamma-globulins, and perform a full toxi- be subtle; look closely for ↓concentration/ cology screen. Arrange abdominal USS to alertness, mild disorientation, behavioural exclude Budd–Chiari syndrome and exten- changes and reversal of the sleep/wake sive malignant infiltration. cycle. Test specifically for constructional apraxia e.g. ask the patient to draw a five- Repeatedly monitor and reassess patients pointed star or clock face, and asterixis (Fig. with acute liver failure 19.1). Exclude hypoglycaemia and other Monitor closely in ITU/HDU for complica- metabolic abnormalities and consider CT tions including: brain to exclude intracranial pathology, especially if there are focal neurological • hypoglycaemia abnormalities. EEG may assist the • hyperkalaemia diagnosis. • metabolic acidosis An ↑PT (in the absence of anticoagula- • renal failure (develops in >50%, often tion, pre-existing coagulopathy or extensive necessitating haemofiltration) cholestasis) indicates ↓hepatic synthetic • cerebral oedema with ↑intracranial function; measure in all patients with jaun- pressure dice – daily if there is ↑↑ALT or worsening • bacterial or fungal infection. jaundice. If ↑, do not correct unless there is major haemorrhage. Use the King’s College criteria (Box 19.6) to identify patients who may require trans- plantation. Liaise early and closely with a specialist liver unit to enable timely transfer if necessary.

5 Palpable liver/suspected malignancy? Consider abdominal USS or CT to exclude malignant or other structural liver disease if the patient has: • clinical evidence of hepatomegaly • known malignancy with metastatic potential • a palpable abdominal/rectal mass or Fig. 19.1 Examining for asterixis. Asterixis is a lymphadenopathy repetitive, jerky tremor of the outstretched hands • ascites in the absence of chronic liver resulting in transient loss of extensor muscle tone disease at the wrist. It is due to metabolic brainstem • unexplained weight loss/cachexia/ dysfunction and is common in ventilatory failure, lymphadenopathy. hepatic encephalopathy, renal failure and cardiac Any abnormal lesions identified may failure. require biopsy for a tissue diagnosis.

178 Jaundice Step-by-step assessment 19

Box 19.6 King’s College Hospital criteria for e.g. >40 units/week or recent binge drink- liver transplantation in acute liver failure ing, e.g. >100 units/week, or who develops Paracetamol overdose severe withdrawal symptoms after 24–48 hours in hospital. Helpful supporting fea- + • H >50 nmol/L (pH <7.3) at or beyond 24 tures include tender hepatomegaly and an hours following the overdose AST : ALT ratio of >1. Once the diagnosis is or made, calculate the Glasgow alcoholic hep- • Serum creatinine >300 µmol/L plus PT atitis score (Table 19.2) to assess prognosis >100 seconds plus encephalopathy grade 3 and guide treatment. or 4 7 Likely drug culprit? Non-paracetamol cases Enquire about ALL drugs taken within the • PT 100 seconds > preceding 6 weeks including over-the- or counter e.g. NSAIDs, paracetamol, and • Any three of the following: herbal remedies. Box 19.2 contains some common causes of hepatotoxicity but there • Jaundice to encephalopathy time >7 days are many others; consult with a pharmacist or review the literature if uncertain. Wher- • Age <10 or >40 years ever possible, discontinue any suspected • Indeterminate or drug-induced causes drug culprit and observe the effect on • Bilirubin >300 µmol/L bilirubin and LFTs. Liver biochemistry may take months to normalise, so consider • PT >50 seconds further investigations (see below) in the Creatinine of 300 µmol/L ≅ 3.38 mg/dL. interim unless clinical suspicion of drug Bilirubin of 300 µmol/L ≅ 17.6 mg/dL. toxicity is very high e.g. the patient recently Boon NA, Colledge NR, Walker BR, Hunter JAA 2006. Davidson’s Principles and Practice of Medicine. 20th edn. started co-amoxiclav or anti-tuberculous p. 953. therapy.

Consider other causes. Targeted 8 Chronic alcohol excess or recent sustained investigation or full liver screen 6 alcohol binge? If the cause remains uncertain, screen for Establish alcohol intake in all jaundiced viral, autoimmune, hereditary and meta- patients. Be tactful but persistent. Start with bolic conditions (Box 19.7), arrange an a general enquiry before quantifying typical abdominal USS if not already performed weekly intake. In addition to the total and confirm alcohol intake. If there is fever, number of drinks, consider the alcohol purpura, ↓platelets, conjunctival conges- content (ask about brand if necessary) and, tion or recent exposure to potentially con- for spirits, the measure per drink. Screen for taminated water e.g. freshwater sports, potential problem drinking (Box 2.1, p. 11). sewage worker, send blood and urine Seek a collateral history from relatives and samples for leptospiral culture, serology ± friends, and observe closely for features of PCR (liaise with the microbiology labora- alcohol withdrawal if you suspect covert tory) and consider empirical antibiotic alcohol abuse. treatment. Liver biopsy may be required if Suspect alcoholic hepatitis in any patient jaundice persists without a clear cause and with longstanding excessive consumption, potential drug culprits have been removed.

179 Jaundice 19 Step-by-step assessment

Table 19.2 Glasgow alcoholic hepatitis score Box 19.7 Screening investigations in jaundice/ suspected liver disease Score 1 2 3 Serology Age <50 ≥50 – • HbsAg, HCV Ab (+ IgM anti-HAV, anti-HBc, WBC (109/L) 15 15 – < ≥ anti-HEV, anti-CMV, anti-EBV if acute) Urea (mmol/L) <5 ≥5 – Metabolic PT ratio or INR <1.5 1.5–2.0 >2.0 Bilirubin (µmol/L) <125 125–250 >250 • Ferritin, alpha1-antitrypsin level, caeruloplasmin An overall score of 5–12 is obtained. ≥9 is associated with a poor prognosis Autoimmune Source: Forrest EH et al. 2007. Gut. Dec; 56(12):1743–1746. • AMA, ASMA, ANA, LKM, immunoglobulins 2007. doi: 10.1136/gut.2006.099226. Other • Abdominal USS, alpha-fetoprotein, paracetamol level, toxicology screen

180 Jaundice Further assessment 19

Further assessment of chronic liver Table 19.3 Child–Pugh classification disease of cirrhosis Step 1 Establish the underlying cause Score 1 2 3 Try to determine the underlying aetiology Bilirubin (µmol/L) <34 34–50 >50 in all new presentations of cirrhosis or in Albumin (g/L) 35 28–35 28 situations where the cause is unclear. Assess > < alcohol intake and perform screening Ascites None Mild Marked investigations as listed in Box 19.7. Exclude Encephalopathy None Mild Marked treatable causes e.g. Wilson’s disease, PT (seconds) <4 4–6 >6 haemochromatosis. Consider referral Child A = Score <7: 1-year survival 82% for liver biopsy if the cause remains Child B = Score 7–9: 1-year survival 62% uncertain. Child C = Score >9: 1-year survival 42% Step 2 Look for evidence of complications/ decompensation microscopy and culture if ascites is Assess all patients with known or suspected present cirrhosis for complications. Evaluate for • review all drugs and alcohol intake hepatic encephalopathy and examine for • ensure that an abdominal USS has been ascites, oedema, jaundice and malnutrition. performed within the last 6 months. Measure albumin and PT to assess hepatic synthetic function, as well as bilirubin, U+E Additionally, in patients with (hyponatraemia, hepatorenal syndrome) encephalopathy: and FBC (anaemia, thrombocytopenia). • seek evidence of upper GI bleeding Consider investigation for pulmonary com- (stool evaluation, ↓Hb, ↑urea) plications such as pleural effusion, hepat- • look for and correct constipation (PR opulmonary syndrome and pulmonary examination, stool chart)/dehydration/ hypertension in patients with breathless- electrolyte disturbance ness, cyanosis or ↓SpO2. If not already done • minimise use of opioids and other screen for oesophageal varices with UGIE sedative drugs. and for hepatocellular carcinoma with In cases of worsening ascites, evaluate 6–12-monthly abdominal USS; USS will salt and water intake and compliance with also detect small-volume ascites and diuretics, exclude spontaneous bacterial splenomegaly. peritonitis and consider Budd–Chiari Step 3 Seek precipitants of syndrome. decompensation Step 4 Assess prognosis Patients with cirrhosis have limited hepatic Use the Child–Pugh classification Table ( metabolic reserve and many factors can 19.3) to assess prognosis in patients with precipitate acute decompensation, e.g. cirrhosis. Other poor prognostic factors spontaneous bacterial peritonitis, other include ↑creatinine and ↓Na+, a small liver intercurrent infection, surgery, alcohol and variceal haemorrhage. Consider refer- excess, hepatotoxic drugs and hepatocellu- ral to a transplant centre for patients lar carcinoma. with Child–Pugh grade B or C. Absolute In a cirrhotic patient who develops jaun- contraindications to transplantation in­ dice, coagulopathy or encephalopathy: clude metastatic malignancy, active sepsis, • perform a full sepsis screen (see Box cholangiocarcinoma and active alcohol or 14.1, p. 139), including an ascitic tap for IV drug abuse.

181 20 JOINT SWELLING

This chapter relates primarily to acute gonorrhoeae and Salmonella spp. Risk factors swelling of the knee, hip, elbow, shoulder include a prosthetic joint, skin infection, and ankle. Swelling may arise from peri- joint surgery, diabetes mellitus, increasing articular structures (bursae, tendons, age, immunocompromise and IV drug use. muscles) or the joint. In general, bursitis/ Pain, swelling, tenderness and erythema tendinopathies cause localised tenderness develop over a few hours. The joint is often and swelling with minimal restriction in held in slight flexion with the patient joint movement limited to certain planes of extremely reluctant to move it. Fever and movement and becoming worse with active ↑WBC/CRP may be present but are rather than passive movement. Conditions unreliable features, particularly in patients affecting the joint itself usually cause taking steroids or NSAIDs and in the more diffuse swelling, warmth, tenderness immunosuppressed. and restriction in active and passive movement. Trauma Trauma may result in haemarthrosis if Periarticular conditions there is injury to a vascular structure within Bursitis is most commonly caused by (unac- the joint (a fracture or ligamentous injury) customed) repetitive movement, particu- or to a traumatic effusion, e.g. from a menis- larly if pressure is applied over the bursa cal tear in the knee. during the process. Less often it may result Any local penetrating injury predisposes from, or be exacerbated by, infection, rheu- to infection and requires urgent surgical matoid disease or gout. Common sites of debridement and washout. bursitis are pre-/infrapatellar (knee), ole- cranon (elbow), trochanteric (hip) and sub- Crystal arthropathy acromial (shoulder). The two most common forms are gout Tendinopathies and enthesopathies (where (uric acid) and pseudogout (calcium the tendon attaches to the bone) are usually pyrophosphate). caused by overuse or by repetitive minor A past history of gout, alcohol excess, trauma. Other causes include infection diuretic use and renal stones are risk factors, and systemic conditions, e.g. rheumatoid as are conditions that cause high cell turno- disease, gout/pseudogout, Reiter’s disease, ver (polycythaemia, lymphoma, psoriasis). ankylosing spondylitis. Tenderness over In acute gout the metatarso-phalangeal the tendon, with discomfort aggravated by joint of the great toe is most frequently movement, is usual and crepitus may be affected, followed by the ankle, knee, small detected. Common sites for enthesopathies joints of the feet/hands, wrist and elbow. are the elbow (lateral and medial epi- Onset is often sudden and exquisitely condyles) and knee. painful. The affected joint is hot, red and swollen, with shiny overlying skin. Septic arthritis Septic arthritis may lead to irreversible car- Reactive arthritis tilage and joint destruction, and so should Reactive arthritis is an acute, non-purulent be identified or excluded early. Haematog- arthritis that arises as a result of infection enous spread is the usual route of infection, elsewhere in the body, typically within 1–3 but local skin or bone infection may weeks of GI or GU infection. The swelling occur. Common organisms are S. aureus, N. may appear suddenly or develop over a 182 Joint swelling Differential diagnosis 20 few days following an initial spell of joint Table 20.1 The 2010 American College of stiffness in the joints. Rheumatology/European League Against Polyarthropathy presenting as Rheumatism classification criteria for monoarthropathy rheumatoid arthritis Osteoarthritis commonly affects the hands, Criterion Score* feet, spine and the large weight-bearing A. Joint involvement joints, such as the hips and knees. Acute 1 large joint 0 single-joint exacerbations may follow minor >1 large joints 1 trauma. It usually evolves insidiously over months to years but may present with an 1–3 small joints (± involvement of 2 acute exacerbation. Other polyarthopathies large joints) polyarthropathies such as rheumatoid 4–10 small joints (± involvement of 3 arthritis or psoriatic arthritis may occasion- large joints) ally present with disproportionate or iso- 10 joints (at least 1 small joint) 5 lated swelling of a single joint but definitive B. Serology diagnosis of rheumatoid arthritis requires Negative RF and negative ACPA 0 involvement of >1 joint (Table 20.1) Low-positive RF or low-positive ACPA 2 Bone cancer and secondary deposits High-positive RF or high-positive 3 Any bone tumour near a joint can poten- ACPA tially cause swelling, although pain is C. Acute-phase reactants usually the presenting feature. The most Normal CRP and normal ESR 0 common cancers to metastasise to bone are Abnormal CRP or abnormal ESR 1 those of the breast, lung, kidney, prostate D. Duration of symptoms and thyroid. Most lesions are visible on <6 weeks 0 X-ray. ≥6 weeks 1 Avascular necrosis ACPA: Anti-citrullinated protein antibody. This most commonly affects the hip, shoul- *A score of ≥6/10 indicates definite rheumatoid arthritis. der or knee, causing joint swelling and Source: Modified from Aletaha D, Neogi T, Silman AJ et al. 2010. Rheumatoid arthritis classification criteria: an American College of collapse. It may occur with prolonged Rheumatology/European League Against Rheumatism collaborative steroid use or certain occupations/sports, initiative. Arthritis Rheum. Sep; 62(9):2582–2591. e.g. diving.

183 Joint swelling 20 Overview

Full clinical assessment ± FBC, CRP, uric acid, blood cultures

Yes 1 Significant trauma or prosthetic joint? Orthopaedic review ± X-ray, joint aspiration

No

2 Indication for joint aspiration?

Yes

Yes Urgent Positive Gram stain? Septic arthritis orthopaedic review No

Yes Crystals? Likely gout / pseudogout

No

Yes High-risk features (see text)? Orthopaedic review

No No

Recent GI/GU infection or evidence of Yes 3 Likely reactive arthritis urethritis / conjunctivitis?

No

Consider rheumatoid arthritis / Yes Rheumatology 4 Evidence of other joint involvement? osteoarthritis / seronegative review spondyloarthritis No

Consider periarticular cause, haemarthrosis, rheumatic fever 5 or monoarticular presentation of oligo- or polyarthritis (see Step 4)

1 Significant trauma or prosthetic joint? correct any coagulation abnormalities prior to aspiration. Perform plain X-rays if the patient has a In patients with a swollen/tender pros- history of recent trauma. thetic joint, perform an X-ray and consult Suspect haemarthrosis if severe joint an orthopaedic specialist. Do not aspirate a swelling arises within 30–60 minutes of prosthetic joint without prior orthopaedic injury or occurs in a patient with impaired consultation because of the risk of introduc- coagulation. Aspiration of a tense, trau- ing infection. matic haemarthrosis may help alleviate In the absence of a coagulation abnormal- pain – consult an orthopaedic specialist and ity, swelling that develops 24 hours or more 184 Joint swelling Step-by-step assessment 20 after joint injury is likely to represent a trau- following features is highly suggestive of matic effusion. reactive arthritis: • diarrhoea 2 Indication for joint aspiration? • urinary frequency Perform joint aspiration (using strict aseptic • dysuria or urgency technique) with urgent Gram stain and • urethral discharge within the preceding microscopy, followed by culture and sensi- 6 weeks (typically 1–3 weeks) tivity, in any patient with an acutely • genital ulceration or circinate balanitis swollen, painful, warm joint in the absence • symptoms/signs of conjunctivitis or of trauma. Aspiration of the knee is rela- iritis, e.g. pain, irritation, tearing, tively simple but the other joints, especially discharge or redness. the hip and ankle, require expert technique 4 Evidence of other joint involvement? – seek orthopaedic help. Never aspirate through infected overlying tissues. Examine all joints carefully, looking for Take blood for FBC, CRP and blood cul- evidence of swelling and/or tenderness; tures, but note that a normal peripheral note the distribution and symmetry of WBC, and CRP do not exclude septic additional joint involvement. arthritis. The diagnostic criteria for rheumatoid A joint aspirate that shows organisms on arthritis are shown in Table 20.1. Consider Gram stain is diagnostic of septic arthritis a seronegative arthritis if there is prominent but is only positive in 30–50% of cases. An axial involvement/sacroiliitis or a history/ ↑ joint aspirate WBC suggests infection, clinical features of inflammatory bowel even if the Gram stain fails to demonstrate disease or psoriasis. organisms – seek expert advice. Unless the diagnosis is clearly osteoar- The identification of monosodium urate thritis, refer for specialist rheumatological (gout) or calcium pyrophosphate dihydrate assessment. (pseudogout) crystals on microscopy sug- gests crystal-induced arthropathy but does 5 Consider other causes not rule out a superimposed infection. Use USS to detect/assess effusions of the In the absence of crystals or a positive hip and shoulder joints and periarticu­ Gram stain, seek orthopaedic review if the lar conditions – tendinopathies, bursitis, aspirate is bloody or there is any ongoing muscle haematoma. Always consider spon- suspicion of septic arthritis e.g. typical clini- taneous haemarthrosis in patients with cal presentation, ↑aspirate WBC or immu- coagulopathy (including those on antico- nocompromised patient. agulation). Evaluate for rheumatic fever if there is a flitting arthritis associated with Recent GI/GU infection or evidence of 3 urethritis/conjunctivitis? other characteristic features (see Box 14.3, p. 146). Seek rheumatology advice if you In a young patient with non-traumatic suspect a monoarticular presentation of acute arthritis in whom septic arthritis has rheumatoid arthritis (see Table 20.1), osteo- been excluded, the presence of any of the arthritis or seronegative arthritis.

185 21 LEG SWELLING

The predominant cause of leg swelling is ‘acute-phase proteins’ such as CRP in pref- oedema – the abnormal accumulation of erence to albumin); protein-losing entero­ fluid within the interstitial space. Oedema pathy (leakage of albumin into the gut may result from: due to lymphatic obstruction or mucosal • ↑(hydrostatic) pressure in the venous disease); and advanced malnutrition. system due to ↑intravascular volume or Iatrogenic causes obstruction Box 21.1 lists drugs that cause oedema. • ↓plasma proteins, mainly albumin, that retain fluid within the vascular Idiopathic cyclic oedema compartment (↓‘oncotic’ pressure), or Idiopathic cyclic oedema commonly affects • obstruction to lymphatic drainage: women, most frequently of child-bearing ‘lymphoedema’. age. Bilateral leg oedema progresses through Unilateral oedema usually indicates the day and is most prominent in the localised pathology e.g. venous or lym- evening. The aetiology is unclear. phatic obstruction; bilateral oedema may Local causes of oedema be due to a local cause but often represents Deep vein thrombosis the combination of generalised fluid over- load and gravity. Oedema is frequently Deep vein thrombosis (DVT) causes local multifactorial, so search for additional oedema due to physical obstruction of causes, even if you identify a possible venous drainage. Clinical features are noto- culprit. riously unreliable; D-dimer and/or Doppler ultrasound are integral to diagnosis. Rarely, Generalised oedema bilateral or inferior vena caval thrombosis Cardiac failure may cause bilateral swelling. Left or right ventricular failure may cause Chronic venous insufficiency oedema through ↑venous hydrostatic pres- The most common cause of chronic unilat- sure. Pulmonary hypertension, even in eral and bilateral leg swelling. Incompetent the absence of right ventricular failure, is valves in the deep and perforating veins an under-recognised cause of peripheral impair venous return with a rise in hydro- oedema. static pressure. There may be varicose veins Renal failure and characteristic skin changes (Box 21.2). In advanced renal failure, ↓salt and water Pelvic mass excretion results in fluid retention and A pelvic mass may obstruct local venous ↑venous hydrostatic pressure. drainage and increase hydrostatic pressure Hypoalbuminaemia by compressing pelvic veins. With ovarian Hypoalbuminaemia produces oedema by tumours, oedema is usually unilateral. ↓plasma oncotic pressure. Causes include Bilateral oedema is common in pregnancy nephrotic syndrome (↑albumin loss in because of ↑blood volume and bilateral urine); chronic liver disease (↓hepatic syn­ venous compression by the gravid uterus thesis of albumin); systemic inflammatory but the diagnosis is usually obvious; suspect processes (leakage of albumin from the DVT if there is a sudden increase in intravascular space due to increased capil- leg swelling, particularly in the third lary permeability ± persistent synthesis of trimester. 186 Leg swelling Differential diagnosis 21

Box 21.1 Drugs causing oedema Box 21.2 Skin changes in chronic venous insufficiency • Calcium channel blockers • Haemosiderin pigmentation • IV fluids • Atrophy • Corticosteroids • Hair loss • Mineralocorticoids (fludrocortisone) • Varicose eczema • Thiazolidinediones (‘glitazones’) • Induration and fibrosis of subcutaneous • Withdrawal of diuretics tissues • NSAIDs • Ulceration • Oestrogens

bursa at the back of the knee) or gastrocne- Lymphoedema mius, superficial thrombophlebitis and cellulitis Causes include malignancy (lymphatic may all present with an acutely painful, invasion or lymphoma), previous lymph swollen leg. node surgery or radiotherapy, filariasis and Lipoedema is not true oedema but an congenital lymphatic abnormalities. Early accumulation of excess subcutaneous fat. lymphoedema may be indistinguishable There is typically bilateral symmetrical leg from other forms of oedema but with pro- swelling that is non-pitting and spares gression it becomes firm and non-pitting the dorsum of the feet. with characteristic skin changes (see below). Pretibial myxoedema is an abnormal dermal accumulation of connective tissue compo- Other causes nents in Graves’ disease. It causes areas Compartment syndrome (↑pressure, vascular of non-pitting oedema on the anterior or compromise and tissue injury within a lateral aspects of the legs, with pink/purple fascial compartment), rupture of a Baker’s plaques or nodules. Most patients will have cyst (a swelling of the semi-membranous evidence of Graves’ ophthalmopathy.

187 Leg swelling 21 Overview

Full clinical assessment ± D-dimer (see text)

1 Unilateral swelling?

No Yes

Yes Doppler Wells score >1 or +ve D-dimer? Deep vein thrombosis 2 USS 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?

No

CT abdo / Non-pitting oedema or previous local Yes 5 Likely lymphoedema pelvis lymph node dissection / radiotherapy? Seek expert advice No Yes 6 Signs of venous insufficiency? Likely chronic venous insufficiency

No

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

Urinalysis, ECG, U+E, LFTs, albumin

Yes Seek underlying 7 Serum albumin <30 mmol/L? Hypoalbuminaemia cause No

See Further New GFR or significant decrease Yes 8 ↓ Renal failure assessment of from baseline? renal failure (p. 192) No Yes 9 Clinical or echo evidence of heart failure? Likely cardiac failure No

Yes Consider dose reduction 10 Likely drug culprit (Box 21.1)? Iatrogenic oedema or discontinuation No

Assess as per unilateral swelling if not already done 11 Likely diagnoses are venous insufficiency or idiopathic oedema Consider lipoedema, pretibial myxoedema

188 Leg swelling Step-by-step assessment 21

1 Unilateral swelling? • Arrange Doppler USS in all pregnant patients with suspected DVT, as Examine both limbs for evidence of swell- exclusion by D-dimer has not been ing and pitting. If there is bilateral lower validated in this group. limb swelling, even if asymmetrical, go to step 7. 3 Acute onset + pain/inflammation?

2 Wells score >1 or +ve D-dimer? Consider cellulitis if swelling is accompa- nied by a discrete area of erythema, heat, Consider DVT in any patient with unilat- swelling and pain ± fever or ↑WBC/CRP; eral limb swelling, even without apparent negative blood cultures/skin swabs do not risk factors or other signs or symptoms. rule out the diagnosis. In superficial throm- Pre-test clinical prediction tools, e.g. Wells bophlebitis, signs are localised, with redness score (Table 21.1), can guide further inves- and tenderness along the course of a vein, tigation. Evaluate for bilateral DVT in any which may be firm and palpable. patient with risk factors and bilateral leg A ruptured Baker’s cyst may be clinically swelling. indistinguishable from DVT; USS will • If Wells score is ≥2, DVT is likely reveal the diagnosis and exclude DVT. – arrange a Doppler USS scan to Consider gastrocnemius muscle rupture in confirm/refute the diagnosis. patients with sudden onset of pain during • If Wells score is <2, perform a D-dimer sporting activity ± pain on muscle palpa- blood test. If negative, DVT is excluded; tion (maximal at the medial musculotendi- if positive, arrange a Doppler USS scan. nous junction) – USS may be helpful. Consider compartment syndrome if unilat- Table 21.1 Wells score (deep vein thrombosis) eral limb swelling is accompanied by any of the features in Box 21.3; if suspected, check Clinical feature Score Active cancer (treatment within +1 point Box 21.3 Features of compartment syndrome last 6 months or palliative) Clinical context Paralysis, paresis or recent plaster +1 point immobilisation of leg Lower limb fracture, trauma, crush injury, vascular injury Recently bedridden >3 days or +1 point major surgery under general/ Drug overdose or ↓GCS regional anaesthesia in previous Symptoms 12 weeks Pain (especially if increasing or deep/aching) Local tenderness along +1 point distribution of deep venous Paraesthesia/numbness* system Paresis/paralysis* Entire leg swollen 1 point + Signs Calf swelling >3 cm compared to +1 point Pain on passive muscle stretching asymptomatic leg (measured 10 cm below tibial tuberosity) Tense, firm or ‘woody’ feel on palpation Pitting oedema confined to +1 point ↓Capillary refill or absent distal pulses* symptomatic leg Muscle contracture* Collateral superficial veins +1 point Investigations (non-varicose) Alternative diagnosis at least as −2 points ↑↑CK likely as DVT e.g. cellulitis, *Numbness, paraesthesia, paralysis, absent pulse and contracture are late features; their absence does not exclude thrombophlebitis the diagnosis. Wells PS et al. Lancet. 1997; 350(9094):1795-8.

189 Leg swelling 21 Step-by-step assessment

CK (rhabdomyolysis) and arrange urgent 6 Signs of venous insufficiency? orthopaedic review. Suspect chronic venous insufficiency if any Recent onset, progressive swelling or of the following is present: 4 clinical suspicion of malignancy? • characteristic skin changes (Box 21.2) • prominent varicosities in the affected limb A pelvic or lower abdominal mass may • previous DVT or vein stripping/ produce leg swelling by compressing the harvesting in the affected limb pelvic veins or lymphatics. Exclude under- • longstanding pitting oedema with lying malignancy if any of the following is diurnal variation in a patient >50 years. present: If none of these is present, reconsider the • weight loss need to exclude underlying DVT and malig- • previous pelvic cancer nancy, and assess as described for bilateral • postmenopausal or intermenstrual PV leg swelling to look for a cause of general- bleeding ised oedema. • a palpable mass or local lymphadenopathy 7 Serum albumin <30 mmol/L? • any new-onset, progressive, unilateral leg swelling with no clear alternative Hypoalbuminaemia may cause or contrib- explanation. ute to oedema, particularly when <25 g/L. Search for an underlying cause. Perform a rectal ± vaginal examination, Screen for nephrotic syndrome by uri- check a PSA level (males), and arrange nalysis, looking for proteinuria. If the imaging with USS (transabdominal or test is positive, collect a 24-hour urine transvaginal) or CT as appropriate. sample; >3 g protein/24 hours confirms the diagnosis. Non-pitting oedema or previous local 5 Suspect ↓hepatic synthetic function if lymph node dissection/radiotherapy? there are deranged LFTs or features of Distinguish lymphoedema from other chronic liver disease (p. 177) and PT is causes of swelling, as it is unlikely to prolonged. respond to conventional treatments and A persistent acute-phase response (result- should prompt consideration of an under- ing in ↓albumin synthesis) may occur in lying malignancy (new or recurrent). Con- chronic infection, inflammatory illness or sider the diagnosis if any of the following occult malignancy. Suspect this if the pati­ is present: ent has a persistently ↑CRP/ESR, recurrent pyrexia, lymphadenopathy, constitutional • previous pelvic malignancy, local upset (fever, sweats, malaise, weight loss) radiotherapy or lymph node or local signs or symptoms e.g. palpable dissection mass, active synovitis – investigate as for • known or family history of congenital fever/pyrexia of unknown origin (p. 146). lymphatic anomaly Consider protein-losing enteropathy and • oedema that is firm and non-pitting seek GI advice if there is a history or symp- • inability to pinch the dorsal aspect of toms of GI disorder. Malnutrition must be skin at the base of the second toe prolonged and severe to cause a significant (Stemmer sign) decrease in serum albumin and is a diagno- • thickening of overlying skin with warty sis of exclusion. or ‘cobblestone’ appearance. New GFR or significant decrease from If you suspect lymphoedema, seek expert 8 ↓ baseline? advice and consider CT of the pelvis and abdomen to look for evidence of underlying Patients with advanced chronic kidney malignancy. disease (CKD) and, less commonly, acute 190 Leg swelling Step-by-step assessment 21 kidney injury (AKI) may develop signifi- failure. If one or more are present, consider cant fluid overload. There will be ­bioche echocardiography to assist diagnosis; sup- mical evidence of renal impairment; see portive findings include ↓left ventricular ‘Further assessment of renal failure’ (p. 192). systolic function, left ventricular hypertro- phy with diastolic dysfunction, severe val- 9 Clinical or echo evidence of heart failure? vular heart disease and/or ↑pulmonary artery pressure. Suspect cardiac failure or pulmonary hypertension as the cause of oedema if 10 Likely drug culprit (see Box 21.1)? there is: Drug causes are listed in Box 21.1. Where • a past history of MI, cardiomyopathy, feasible, review after trial discontinuation. valvular disease, pulmonary embolism or chronic lung disease, e.g. COPD Assess as per unilateral swelling. Likely 11 (‘cor pulmonale’) or obstructive sleep venous insufficiency or idiopathic oedema apnoea • orthopnoea, paroxysmal nocturnal If there is bilateral swelling, first return to dyspnoea or exertional breathlessness step 1 and assess for ‘unilateral’ causes e.g. • ↑JVP, bi-basal crackles, gallop rhythm, bilateral DVT. loud P2 or right ventricular heave Venous insufficiency is the likeliest cause • pulmonary venous congestion and/or in patients >50 years or in those with skin cardiomegaly on CXR (see Fig. 12.1, changes/predisposing factors. Idiopathic p. 115). cyclic oedema is a common cause in women • significant ECG abnormality e.g. Q of child-bearing age but consider an echo­ waves, left or right bundle branch block; cardiogram to exclude pulmonary hyper- see Box 6.1, p. 49. tension. Gravitational oedema may occur with longstanding immobility. In none of these features is present, If pitting is absent, consider lipoedema or oedema is very unlikely to be due to cardiac pretibial myxoedema.

191 Leg swelling 21 Further assessment

Further assessment of renal failure Table 21.2 Classification of chronic kidney Step 1 Recognise renal impairment disease Diagnostic criteria for AKI and CKD are GFR (mL/ shown in Box 21.4 and Table 21.2. Stage Category min/1.73 m2) Step 2 Identify and treat hyperkalaemia 1 Evidence of chronic ≥90 ↑K+ may cause life-threatening arrhythmias kidney damage* with and cardiac arrest. Perform an ECG if normal GFR ≥5.5 mmol/L to look for: 2 Evidence of chronic 60–89 • Early changes: tall, peaked T waves kidney damage* with • Advanced changes: flattened P waves, mild impairment of ↑PR interval, ↑QRS duration. GFR 3 Moderate impairment 30–59 Treat as follows: of GFR • Give IV calcium e.g. 10% calcium 4 Severe impairment of 15–29 gluconate, with continuous ECG GFR monitoring if there are ECG changes 5 End-stage renal failure <15 – titrate up to 10 mL until changes resolve. *Evidence of chronic kidney damage includes: • persistent microalbuminuria/proteinuria/haematuria • structural kidney abnormalities on imaging Box 21.4 Diagnostic criteria for acute kidney • features of chronic glomerulonephritis on renal biopsy. injury Kidney Disease Outcome Quality Initiative. 2002. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, 1. Increase in serum creatinine by ≥26 µmol/L classification, and stratification. Am J Kidney Dis. 39(2 Suppl from baseline within 48 hours 2):S1–246. 2. Increase in serum creatinine ≥1.5-fold from baseline within 1 week 3. Urine output <0.5 mL/kg/hr for >6 consecutive hours Source: Kidney Disease: Improving Global Outcomes. 2010. Clinical practice guideline on acute kidney injury. Available online at www.kdigo.org

192 Leg swelling Further assessment 21

Box 21.5 Reasons for urgent renal referral Assume AKI, at least initially, if none of these features is present and there are no • Indication for urgent renal replacement previous U+E results for comparison. therapy Step 4 If de novo presentation, perform a • ↑K+ or pulmonary oedema refractory to full diagnostic work-up medical management • Assess volume status: renal hypoperfusion • Severe metabolic acidosis (‘pre-renal’ failure) is the most common • Uraemic pericarditis cause of AKI. Look for: • predisposing factors (diarrhoea, • Uraemic encephalopathy vomiting, blood loss, ↓oral intake, • Progressive increase in serum creatinine diuretics), despite fluid resuscitation/withholding of • features of dehydration (↓skin turgor, nephrotoxins dry mucous membranes, thirst) and • Persistently oliguric or anuric patients • signs of shock (see Box 28.1, p. 249). If you suspect hypovolaemia, assess • Suspected glomerular disease the response of urine output and U+E • CKD patients with increasing symptoms of to fluid resuscitation and correction of uraemia or likely progression to stage 5 underlying causes. CKD • Exclude obstruction: bladder outflow obstruction occurs most frequently in males with prostatic enlargement. Insert a urinary catheter if there is a palpable bladder or ↑post-void residual urine • Give treatment to lower K+ e.g. IV on bladder scanning. Request a renal dextrose and insulin, especially if K+ USS to exclude upper renal tract >6.0 mmol/L or ECG changes. Repeat obstruction. U+E and ECG following treatment. • Review all recent prescriptions and ask • Consider the need for urgent renal about non-prescribed drugs. Common review (Box 21.5). culprits include radiographic contrast Step 3 Distinguish CKD from AKI media, NSAIDs, ACE inhibitors/ angiotensin receptor blockers, Previous U+E results are the best guide to antimicrobials (gentamicin, vancomicin, the chronicity of renal impairment. If una- penicillins, amphotericin B) and vailable, possible clues to CKD include: ciclosporin. • evidence of metabolic bone disease • Seek evidence of sepsis (Box 14.1, p. 139), (especially ↑parathyroid hormone) and, if present, perform a full septic • bilateral small kidneys on USS screen as per Chapter 14. • gradual onset of oedema over weeks to • Consider other causes: suspect months. glomerulonephritis in any patient with

193 Leg swelling 21 Further assessment

heavy e.g. ≥3+, haematuria/proteinuria Box 21.6 Serological investigations in on dipstick. Evaluate for multisystem suspected glomerulonephritis disease (rash, joint disease, haemoptysis), perform serological Test Underlying diagnosis investigations (Box 21.6) and discuss ANA Connective tissue urgently with the renal team. disease e.g. SLE Consider haemolytic uraemic syndrome/ Anti ds-DNA thrombotic thrombocytopenic purpura if Extractable nuclear AKI is accompanied by an acute antigens diarrhoeal illness or neurological Anti GBM antibodies Goodpasture’s disease features. Review the FBC/blood film for: ↓Hb, ↓platelets, ↑reticulocytes and ANCA Vasculitis e.g. Wegener’s red cell fragments. Seek immediate Granulomatosis expert advice if suspected. Antistreptolysin O Post-streptococcal Consider rhabdomyolysis in patients titre glomerulonephritis with a history of trauma, a long period Cryoglobulins Cryoglobulinaemia lying on the floor or recreational drug use, e.g. cocaine. Check CK (>×5 upper limit of normal) and perform urinalysis +/− urine microscopy (dipstick haematuria with no red cells on Step 5 If acute-on-chronic impairment, microscopy suggests myoglobinuria). consider reasons for deterioration Send plasma for protein electrophoresis and urine for Bence Acute deterioration is often due to: Jones protein if you suspect multiple • dehydration myeloma, e.g. hypercalcaemia, bone pain • infection pathological fractures, or if the cause of • hypotension renal dysfunction remains unclear. • nephrotoxic agent (see above).

194 Leg swelling Further assessment 21

Identify and reverse these causes, monitor • Metabolic bone disease: ↓phosphate renal function and discuss with the renal excretion and ↓renal activation of 3− 2+ team if there is any further decline in GFR. vitamin D result in ↑PO4 , ↓Ca and Step 6 If stable CKD, seek evidence ↑parathyroid hormone (secondary hyperparathyroidism). Treat with of complications phosphate binders and vitamin D Sequelae of CKD should be sought and cor- analogues, aiming to maintain plasma rected, if possible: 2+ 3− Ca and PO4 within normal limits. • Renal anaemia: this may result from • Volume overload: in advanced CKD, inadequate renal production of oliguria may result in significant fluid erythropoietin. Measure ferritin and overload, with peripheral ± pulmonary transferrin saturation to ensure that the oedema. Liaise with a nephrologist if patient is iron-replete (ferritin >100 ng/ this is refractory to diuretic therapy and mL; transferrin saturation >20%), salt restriction. exclude other causes of anaemia (p. 134) • Hypertension: ↑BP is common in CKD, and refer to a nephrologist for accelerates the decline in renal function consideration of erythropoiesis- and increases cardiovascular risk. stimulating agents. Monitor BP and aim for strict targets, • Metabolic acidosis: this is indicated by a e.g. <130/80 mmHg. low venous bicarbonate and can be corrected by oral sodium bicarbonate.

195 22 LIMB WEAKNESS

Limb weakness may be focal or generalised. cause symptoms and signs mimicking Diagnosis relies on careful clinical assess- stroke but the onset is typically more ment, complemented, in most cases, by gradual and progressive. There may be appropriate brain or spinal imaging. features of raised intracranial pressure Current stroke management mandates (ICP) or clues to the underlying pathology, urgent evaluation of unilateral limb weak- e.g. malignancy, or a source of septic emboli ness. However, focal limb weakness can be such as infective endocarditis. caused by many non-stroke pathologies Spinal cord lesions and these should not be overlooked in the rush to definitive management. Transverse lesions produce bilateral UMN limb weakness (para/tetraparesis), with Stroke loss of all sensory modalities below the Stroke is the most common cause of unilat- spinal cord level and disturbance of sphinc- eral limb weakness. Patients typically ter function. Unilateral lesions (Brown– present with sudden onset of weakness of Séquard syndrome) cause ipsilateral UMN the arm, leg or facial muscles, on one side. weakness and loss of proprioception below Symptoms persist for >3 hours and often the cord level, with contralateral loss of do not resolve. An initial flaccid paresis pain and temperature sensation. progresses to upper motor neuron (UMN) Causes may be compressive lesions e.g. weakness days later. There may be associ- intervertebral disc prolapse, trauma, verte- ated signs of cortical dysfunction (Box 22.1) bral metastases, or intrinsic pathology e.g. or other sensory, visual or coordination transverse myelitis, glioma, spinal infarct, problems. Aside from rare examples, such vitamin B12 deficiency. Circumferential pain as those affecting certain areas of the brain- across or sensory loss below a thoracic or stem, symptoms and signs are consistently lumbar dermatome suggests cord compres- unilateral. sion (but is not always present) – the level should correlate with neurological exami- Transient ischaemic attack (TIA) nation of the lower limbs. Saddle anaesthe- TIAs are temporary, focal, ischaemic insults sia, bilateral leg pain, urinary retention and to the brain. Symptoms and signs usually reduced anal tone suggest cauda equina last for at least 10 minutes and are compa- syndrome. rable to stroke but resolve entirely without permanent neurological sequelae. The tra- Peripheral nerve lesions ditional definition of TIA describes a syn- Lower motor neuron (LMN) weakness may drome lasting less than a day, but this does result from generalised disease of periph- not correlate with modern knowledge of eral nerves (peripheral neuropathy), or stroke – symptoms >3 hours are likely to from lesions affecting a plexus (plexopa- show permanent ischaemic damage to the thy), spinal root (radiculopathy) or single brain on advanced imaging. With rare nerve (mononeuropathy). In peripheral exceptions, TIAs do not cause loss of neuropathy, the longest nerves tend to be consciousness. affected first, leading to a ‘glove-and-stock- ing’ pattern of weakness and sensory loss; Space-occupying lesions in the other lesions, weakness and sensory Space-occupying lesions, e.g. tumour, loss reflect the muscles/skin regions inner- abscess, chronic subdural haematoma, can vated by the affected nerve(s) or nerve root. 196 Limb weakness Differential diagnosis 22

Box 22.1 Signs of cortical dysfunction Table 22.1 Medical Research Council (MRC) power rating • Visual field defect Grade Findings on examination • Dysphasia 1 No movement, not even muscle • Dyspraxia flicker • Neglect 2 Flicker of muscle contraction only • Sensory or visual inattention 3 Movement possible only when action of gravity is removed and against no resistance Motor neuron disease 4 Can move against gravity but not A chronic degenerative condition that completely against full active presents with gradual, progressive weak- resistance ness and a combination of UMN and LMN 5 Normal power against full active signs. There may be bulbar involvement but resistance sensory features are absent.

Other causes causes limb weakness (hemiplegic migraine) Encephalitis may cause limb weakness as but this is a diagnosis of exclusion. Mya­ part of a constellation of central neurologi- sthenia gravis causes ‘fatigability’ of limb cal symptoms including confusion, seizures muscles. Generalised muscle weakness and altered consciousness. Multiple sclero- may result from congenital/inflammatory sis can present with almost any pattern of myopathy e.g. polymyositis, endocrine UMN limb weakness, though paraparesis or metabolic disturbance e.g. Cushing’s secondary to transverse myelitis is most syndrome, hypokalaemia, or drugs/toxins typical. Transient focal limb weakness can e.g. corticosteroids, alcohol; it is also a occur immediately after a focal seizure common, non-specific presentation of acute (Todd’s paresis). Migraine occasionally illness in frail, elderly patients.

197 Limb weakness 22 Bilateral limb weakness: overview

Full clinical assessment, BM

Yes 1 Weakness strictly unilateral? 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

No

Upper motor neuron signs, sensory 3 level or sphincter disturbance?

Yes

Yes Abnormal MRI spine? Cord compression or intrinsic pathology

No Consider motor neuron disease, B12 No deficiency, bilateral intracranial lesions

Yes 4 Sensory signs or symptoms? Likely peripheral neuropathy

No

Yes 5 Muscle fatigability? Myasthenia gravis / myasthenic syndrome

No

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

Proximal weakness with Yes 6 Likely myositis tenderness or ↑CK

No

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

198 Limb weakness Bilateral limb weakness: step-by-step assessment 22

1 Weakness strictly unilateral? Upper motor neuron signs, sensory level 3 or sphincter disturbance? Assess power in all four limbs and grade according to the MRC scale (Table 22.1). Bilateral weakness associated with UMN Ask about any pre-existing limb weakness signs (↑tone, brisk reflexes, extensor plantar that predates the current presentation e.g. response), a sensory level (Fig. 22.1) and/ old stroke, and whether it has changed or bladder/bowel dysfunction suggests recently. In any rapid-onset weakness, myelopathy. perform a Stix test for blood glucose; if • Arrange an MRI spine to exclude cord <3.0 mmol/L, send blood for lab glucose compression and structural intrinsic measurement but treat immediately with spinal disease e.g. syringomyelia, IV dextrose and then reassess. glioma, abscess. If the current presentation of limb weak- • If neither is present, check whether the ness is confined to one side of the body patient has had previous radiotherapy assess as per unilateral limb weakness (this (post-radiation myelopathy) and includes patients with contralateral facial measure plasma vitamin B levels to weakness). Otherwise, continue on the 12 exclude subacute combined current diagnostic pathway, even if signs degeneration of the cord. are markedly asymmetrical. • Suspect transverse myelitis if the MRI Acute-onset or rapidly progressive shows evidence of inflammatory change 2 paraparesis? and the time from first onset of symptoms to maximal weakness was In any patient with sudden-onset or rapidly between 4 hours and 21 days – refer to a progressive paraparesis or tetraparesis: neurologist for further evaluation, e.g. • Immobilise the cervical spine pending CSF analysis, autoimmune and infective imaging, if there is suspicion of recent screen. trauma. • Suspect motor neuron disease • Discuss immediately with a vascular (amyotrophic lateral sclerosis) if surgeon if weakness is accompanied by weakness is slowly progressive and features of acute limb ischaemia, e.g. sensory features are absent, especially if pain; cold/pale/mottled skin; absent there are associated LMN signs, e.g. pulses. fasciculation, or bulbar involvement. • Otherwise, arrange urgent spinal Consider brain imaging to exclude imaging, usually MRI, to exclude cord bilateral intracranial lesions e.g. cerebral compression or traumatic injury. emboli/metastases, venous stroke, demy- If MRI confirms a compressive lesion, elination, in any patient with bilateral UMN discuss with a neurosurgeon or oncologist, limb weakness and: depending on the clinical context and likely • no evidence of myelopathy i.e. normal cause. MRI spine, no sensory level/sphincter If MRI excludes cord compression (and disturbance), or does not yield a definitive alternative diag- • associated cortical signs (see nosis), consider spinal stroke if the onset of Box 22.1), features of ↑ICP (Box 22.2), weakness was very sudden, especially if cranial nerve lesions or cerebellar accompanied by severe back pain. Examine involvement. for sparing of proprioception and vibration sense, and look specifically for MRI changes Seek specialist neurological input in any of spinal infarction. Otherwise, seek urgent suspected case of motor neuron disease or neurological review and continue to assess multiple sclerosis, or if the cause remains as described below. unclear.

199 Limb weakness 22 Bilateral limb weakness: step-by-step assessment

Fig. 22.1 Dermatomes. The C2 blue dots indicate recommended sites for testing each dermatome. C3 To assess for a sensory level, test C4 light touch and C4 C5 pinprick sensation Th2 in each dermatome C5 Th2 3 on both sides. If 3 4 sensation is 4 5 abnormal in the 5 6 lower dermatomes, 6 Th 7 2 move progressively C6 7 8 upwards through 8 9 the truncal/upper Th 10 9 Th limb dermatomes 1 11 1 until it normalises. 10 12 C 11 L1 6 C8 12 L2 L1 S S C8 2 4 C L2 L L C7 2 4 7 S3 L5 L3

S1

S2

L4

L5

L4

S1

S1 L5

200 Limb weakness Bilateral limb weakness: step-by-step assessment 22

Box 22.2 Symptoms and signs suggestive of Box 22.3 Clinical features of Guillain–Barré raised intracranial pressure syndrome • Severe headache Remember these as the five ‘A’s: • ↓GCS Acute course: Time from onset to maximal • VI nerve palsy or unilateral pupillary weakness = hours to 4 weeks dilatation Ascending Initially in legs, progressing to • Vomiting weakness: arms ± respiratory/bulbar/facial • Bradycardia/systolic hypertension muscles • Papilloedema At presentation 60% have weakness in all four limbs; 50% have facial weakness Areflexia: Absence of tendon reflexes 4 Sensory signs or symptoms? helps to distinguish Guillain– Barré syndrome from In the absence of UMN signs, sphincter dys- myelopathy function or a sensory level, the combination Associated Distal numbness, tingling of bilateral or generalised limb weakness sensory or pain often precedes with sensory disturbance is usually due to symptoms: weakness peripheral neuropathy. Consider Guillain–Barré syndrome if Loss of proprioception more distal lower limb numbness or tingling is common than pain and followed by rapidly ascending weakness temperature and absent tendon reflexes (Box 22.3). Autonomic Sinus tachycardia, postural • Measure urinary porphyrins to exclude involvement: hypotension, impaired sweating acute intermittent porphyria. often present • Confirm the diagnosis with nerve Urinary retention and conduction studies and LP (↑CSF constipation are later features protein with normal cell count and glucose). • Check and monitor vital capacity for evidence of respiratory depression. Consider spinal imaging to exclude bilat- • Refer early to a neurologist for further eral radiculopathy if sensory loss and motor evaluation. signs follow a nerve root distribution (see Table 22.3). Slowly progressive limb weakness that is more marked distally with a ‘glove- 5 Muscle fatigability? and-stocking’ pattern of sensory loss strongly suggests a sensorimotor periph- Consider myasthenia gravis if the history eral neuropathy, e.g. chronic inflammatory or examination findings suggest fatigable demyelinating polyneuropathy, hereditary muscle weakness: initially normal muscle sensorimotor neuropathy. power that rapidly weakens with sustained • Arrange nerve conduction studies to or repeated activity. Ocular and bulbar confirm peripheral nerve disease and muscles tend to be affected before limb differentiate demyelination from axonal muscles. degeneration. Ask about the effect of exercise and other • Investigate for an underlying cause, e.g. activities on weakness. serum protein electrophoresis, HIV test, • Enquire specifically about diplopia urinary porphyrins, fasting blood during reading, weakening of the glucose. voice and difficulty in chewing/ 201 Limb weakness 22 Bilateral limb weakness: step-by-step assessment

swallowing after the first few mouthfuls weakness: the features in Box 22.3 of food. distinguish from other causes. If • Examine for ptosis. suspected, confirm with LP and nerve • Observe patients as they hold their arms conduction studies. above their head for a sustained period. • Suspect lumbosacral plexopathy if • Listen while the patient counts to 50. there is severe pain and progressive weakness/wasting of quadriceps with In suspected cases, consider a Tensilon absent knee reflexes – arrange imaging test if rapid confirmation is required e.g. to exclude malignant infiltration of the myasthenic crisis or severe global weak- plexus and check fasting blood glucose ness; otherwise, check for anti-acetylcholine to exclude diabetes mellitus (diabetic receptor antibodies, arrange a thoracic CT amyotrophy). to exclude thymoma, and seek expert neu- • Exclude other causes of motor rological input. neuropathy – check serum lead and Tendon reflexes are normal in ­ mya urinary porphyrins and arrange nerve sthenia gravis. If muscle fatigability is conduction studies. accompanied by absent tendon reflexes • If nerve conduction studies are normal, that can be elicited following sustained the most likely diagnosis is motor muscle contraction, consider Lambert– neuron disease (progressive muscular Eaton myasthenic syndrome, a paraneo- atrophy) – arrange electromyography plastic syndrome – check for serum and refer the patient to a neurologist. antibodies to voltage-gated calcium chan- nels, arrange electrophysiological studies In patients with a ‘patchy’ pattern of and screen for an underlying malignancy. weakness, examine to exclude multiple discrete peripheral nerve lesions (Fig. 22.2), Proximal weakness with tenderness or 6 i.e. mononeuritis multiplex; if suspected, ↑CK arrange neurophysiological assessment and Suspect myositis if symmetrical proximal investigate for an underlying malignant, muscle weakness is accompanied by ↑CK. vasculitic or infiltrative disorder. If the patient is taking statins reassess after In patients with proximal muscle weak- a period of discontinuation. Otherwise, ness ± wasting and no associated neuro­ send an autoantibody screen, including logical abnormality, screen for underlying anti-synthetase antibodies, e.g. anti Jo-1 metabolic, nutritional, endocrine and drug- (associated with polymyositis); exclude related causes: other toxic causes, e.g. cocaine; and arrange • Enquire about alcohol intake. muscle biopsy. • Consider trial discontinuation of any Even if the CK is normal, consider further potentially causative medication, e.g. investigation with muscle biopsy in any statin, fibrate. patient with symmetrical proximal muscle • Check for an underlying biochemical weakness associated with aching, tender- disorder, e.g. ↓K+, ↑Ca2+. ness, pyrexia or ↑ESR. • Look for biochemical/clinical features of Cushing’s syndrome, Addison’s 7 Consider other causes disease, thyroid disorders and Advanced myopathy may cause a degree acromegaly. of muscle wasting and diminished ten- • Check 25(OH) cholecalciferol to exclude don reflexes but suspect an LMN lesion if osteomalacia in elderly, cirrhotic or there is flaccidity, absent reflexes and/or malnourished patients. fasciculation. Assess frail, elderly patients with • Consider Guillain–Barré syndrome if generalised weakness as described in there is new-onset, progressive limb Ch 24. 202 Limb weakness Bilateral limb weakness: step-by-step assessment 22

Consider a functional aetiology if there dis­orders, e.g. irritable bowel syndrome, are no objective features of organic disease fibromyalgia. and the severity or pattern of weakness Refer the patient for specialist neuro­ is inconsistent – especially if the patient logical evaluation if the cause remains has a background of other functional unclear.

203 Limb weakness 22 Unilateral limb weakness: overview

1 Sudden onset?

No Yes

Yes Consider ischaemia, fracture, Painful? compartment syndrome

No

Yes Total duration <3 hours? Likely transient ischaemic attack No See Further Likely stroke assessment of stroke (p. 208)

Seizure(s) or evidence of ICP / cortical Yes Consider space- 2 ↑ Neuroimaging dysfunction / CNS infection? occupying lesion, 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 Signs referable to single nerve root / nerve? Radiculopathy / mononeuropathy

No

5 Consider plexopathy, multi-root compression, stroke, motor neuron disease, migraine, functional weakness

204 Limb weakness Unilateral limb weakness: step-by-step assessment 22

Sensory Motor Sensory Motor Sensory Motor

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

A B C Flexor carpi ulnaris

Sensory Motor Toe dorsiflexors

Foot dorsiflexors

Foot evertors

D Fig. 22.2 Clinical signs in peripheral nerve lesions. (A) Median nerve. (B) Radial nerve. (C) Ulnar nerve. (D). Common peroneal nerve.

1 Sudden onset? Acute non-neurological illness or hypo- tension may exacerbate established limb Evaluate weakness as ‘sudden-onset’ if it weakness from an old stroke – suspect reaches maximal intensity within a few this if the current weakness is confined minutes from the first appearance of to the same territory as a previously symptoms. documented persistent neurological deficit If there is painful weakness of a single and there are other clinical/laboratory limb, consider vascular and orthopaedic features to suggest acute systemic illness, causes: but maintain a low threshold for further • Compare pulses, colour, temperature neuroimaging. and capillary refill with the unaffected In the absence of the above causes, limb – seek immediate vascular review sudden-onset unilateral weakness is highly if there is any suspicion of acute limb likely to represent a stroke or TIA. If symp- ischaemia. toms persist for >3 hours, then proceed, in • Request an X-ray of the limb if there is the first instance, to ‘Further assessment of any history of trauma. stroke’ (p. 208). • Measure CK and request an urgent Diagnose TIA if symptoms have resolved orthopaedic review if there are features completely and lasted <3 hours. of compartment syndrome (see Box 21.3, • Evaluate for risk factors and sources of p. 189). embolism as described under ‘Further Consider post-ictal weakness (Todd’s assessment of stroke’. paresis) if the history suggests seizure activ- • Assess the risk of impending stroke ity immediately prior to the onset of weak- using the ABCDD score (Table 22.2). ness – arrange rapid neuroimaging unless • Admit or arrange next-day specialist the cause of seizures is already established, referral for any patient with >1 TIA in the post-ictal phase is known to include a week or an ABCDD score ≥4 for limb weakness, and the weakness is urgent control of risk factors and improving. carotid Doppler USS. 205 Limb weakness 22 Unilateral limb weakness: step-by-step assessment

Table 22.2 ABCDD score in TIA 3 Upper motor neuron signs? 1 2 A UMN pattern of weakness indicates a Age ≥60 lesion proximal to the anterior horn cell; progressive onset of weakness suggests a Blood Systolic ≥140 or space-occupying lesion whilst a rapid onset pressure diastolic ≥90 favours a vascular or inflammatory cause. Clinical Speech Unilateral Exclude a unilateral cord lesion if features disturbance, no weakness there is dissociated sensory loss (ipsila­ weakness teral proprioception/vibration; contralateral Duration 10–59 minutes ≥60 minutes pain/temperature) or a clear sensory level. of attack Otherwise, arrange neuroimaging; CT is the Diabetes Yes usual first-line modality but consider MRI if CT is inconclusive, especially if there are brainstem features e.g. contralateral cranial nerve palsies or cerebellar signs. • Otherwise, consider discharge with Consider an atypical presentation of appropriate secondary prevention and motor neuron disease (usually bilateral) if specialist follow-up within a week. neuroimaging fails to reveal a cause and • Arrange neuroimaging prior to sensory features are absent, especially if discharge in any patient taking warfarin. there are associated LMN signs.

Seizure activity or evidence of 4 Signs referable to single nerve root/nerve? 2 ↑intracranial pressure/cortical dysfunction/CNS infection? In the absence of UMN signs, suspect a radiculopathy if clinical signs are referable New-onset seizures, signs of cortical dys- to a single nerve root (Table 22.3), or a function (see Box 22.1) or evidence of ↑ICP mononeuropathy if they correspond to a (see Box 22.2) suggest underlying brain single peripheral nerve (see Fig. 22.2). If pathology. radiculopathy is suspected, consider a • Arrange prompt neuroimaging (usually spinal MRI, particularly if weakness is CT brain) to identify the cause. progressive. • Seek anaesthetic review prior to scanning if GCS <8 or signs of airway 5 Consider other causes compromise. Perform neuroimaging to exclude a stroke, • See page 258 for further assessment of space-occupying lesion or demyelination in seizures. any patient presenting with hemiparesis, • In all cases, seek expert neurological even if there are no obvious UMN features; advice and consider further if results are normal, consider hemiplegic investigation with LP ± MRI if CT fails migraine. to reveal an underlying cause. If weakness is confined to a single limb, Consider meningoencephalitis if there is consider multi-level root compression onset of limb weakness over hours accom- (see Table 22.3) or plexopathy, e.g. lum- panied by fever, meningism (Box 18.2, bosacral plexopathy (see above) or brachial p. 167), purpuric rash, SIRS criteria (Box plexopathy. 14.1, p. 139) or features of shock (Box 28.1, Otherwise, consider mononeuritis multi- p. 249). If meningoencephalitis is suspected, plex (see above), an atypical presentation of obtain blood cultures, give empirical IV motor neuron disease (usually bilateral) or antibiotics/antivirals and arrange urgent functional weakness. CT brain; thereafter, perform an LP for CSF Seek expert neurological input in any analysis unless contraindicated (p. 168). case where the diagnosis remains unclear. 206 Limb weakness Unilateral limb weakness: step-by-step assessment 22

Table 22.3 Clinical signs of nerve root compression Root Weakness Sensory loss (see Fig. 22.1) Reflex loss C5 Elbow flexion (biceps), arm and Upper lateral arm Biceps shoulder abduction (deltoid) C6 Elbow flexion (brachioradialis) Lower lateral arm, thumb, Supinator index finger C7 Elbow (triceps), wrist and finger Middle finger Triceps extensors L4 Inversion of foot Inner calf Knee L5 Dorsiflexion of hallux/toes Outer calf and dorsum of foot S1 Plantar flexion Sole and lateral foot Ankle

207 Limb weakness 22 Further assessment

Further assessment of stroke Step 3 Evaluate for risk factors/ Step 1 Assess eligibility for thrombolysis underlying cause If facilities are available, consider throm- In any patient with ischaemic stroke, iden- bolysis in any patient with a potentially tify modifiable risk factors for vascular disabling stroke whose first onset of symp- disease, including hypertension, hyper­ toms occurred within the last 3 hours. cholesterolaemia, smoking and diabetes; Where the time of onset is uncertain e.g. arrange Doppler USS to determine the pres- symptoms present on awakening, define it ence and severity of carotid stenosis unless as the last time the patient was known to be the affected territory is within the posterior well. Assess rapidly for contraindications circulation or the patient is unfit for vascu- (Box 22.4) and seek expert guidance from lar surgery. the on-call stroke team. In patients who Suspect a cardiac source of cerebral meet clinical eligibility criteria, arrange embolism if the patient has: immediate CT brain to exclude haemor- • current or previous evidence of atrial rhagic stroke. fibrillation Step 2 Classify stroke according to clinical • a recent myocardial infarction and radiological findings • clinical features suggesting endocarditis, e.g. fever and new murmur Arrange neuroimaging to differentiate • ≥2 cerebral infarcts (especially in haemorrhagic stroke from ischaemic stroke different territories) and to exclude non-stroke pathology, e.g. • other systemic embolic events, e.g. space-occupying lesion. Perform a CT brain lower limb ischaemia. urgently if: Consider further investigation with • the patient is eligible for thrombolysis transthoracic and, in selected cases, (see above) transoesophageal echocardiography. • coagulation is impaired Investigate for an unusual cause of stroke • ↓GCS in younger patients without vascular risk • symptoms include a severe headache factors: • there is a rapidly progressive neurological deficit • Perform a vasculitis and thrombophilia • cerebellar haemorrhage is suspected (to screen. exclude obstructive hydrocephalus). • Request a bubble-contrast echocardiography to detect a right-to- Otherwise, perform CT within 24 hours left shunt, e.g. patent foramen ovale that of presentation. Irrespective of CT findings, would permit ‘paradoxical embolism’ use the Bamford classification (Box 22.5) to from the venous circulation. categorise stroke. • Consider MRA to exclude carotid/ vertebral artery dissection.

208 Limb weakness Further assessment 22

Box 22.4 Contraindications to thrombolysis* Box 22.5 Bamford classification of stroke

• Seizure at stroke onset This separates stroke into four clinical • Symptoms suggestive of subarachnoid presentations that relate to the affected haemorrhage vascular territory and correlate with prognosis. • Prior intracranial haemorrhage TACS (total anterior circulation stroke) • Intracranial tumour • All three of: • Stroke or serious head trauma within last 3 1. Weakness/sensory deficit affecting 2 out months of 3 of face/arm/leg • Arterial puncture at a non-compressible site 2. Homonymous hemianopia or LP within 1 week 3. Cortical dysfunction e.g. dysphasia, • Active haemorrhage apraxia • Suspected acute pericarditis or aortic PACS (partial anterior circulation stroke) dissection • Two out of three of the TACS criteria, or • Systolic BP >185 mmHg or diastolic BP cortical dysfunction alone >110 mmHg LacS (lacunar stroke) • INR >1.7 thrombocytopenia or bleeding disorder • Causes limited motor/sensory deficits with • Pregnancy no cortical dysfunction *Most are relative contraindications – seek guidance from the PoCS (posterior circulation stroke) on-call stroke team if the patient is otherwise eligible. • Causes a variety of clinical syndromes, including homonymous hemianopia, cerebellar dysfunction and the brainstem syndromes

209 23 LOW BACK PAIN

Low back pain is defined as posterior pain for patients with persistent pain and/or between the lower rib margin and the neurological deficit. buttock creases; it is acute if the duration is <6 weeks, persistent if it lasts for 6 weeks Lumbar spine stenosis to 3 months, and chronic if it is present for Narrowing of the lumbar spinal canal typi- >3 months. In 90% of patients no specific cally occurs in patients >50 years as a result underlying cause is found – the pain is of degenerative spinal changes and may thought to originate from muscles and liga- cause lumbosacral nerve root compression. ments, and is termed ‘mechanical’. Patients often have longstanding, non- Radicular pain (‘sciatica’) originates in the specific low back pain before developing lower back and radiates down the leg in the dull or cramping discomfort in the buttocks distribution of ≥1 lumbosacral nerve roots and thighs precipitated by prolonged (typically L4–S2) ± a corresponding neuro- standing/walking and eased by sitting or logical deficit (radiculopathy). lying down (neurogenic claudication). A thorough history and examination, Vertebral trauma and fracture supplemented where necessary by spinal This most commonly follows a fall, road imaging, is critical to identify patients with traffic accident or sporting injury, but may low back pain who have serious and/or occur with minimal or no trauma in patients treatable pathology. with osteoporosis or spinal conditions, Mechanical back pain e.g. ankylosing spondylitis. A patient with This is by far the most common cause of low localised low back pain following trauma back pain. The pain tends to be worse requires imaging to evaluate instability and during activity, relieved by rest, and is not involvement of the spinal canal/cord. associated with sciatica, leg weakness, Spondyloarthritides sphincter disturbance, claudication or sys- temic upset. An acute episode is often pre- (inflammatory back pain) cipitated by bending, lifting or straining. In These chronic inflammatory joint diseases most cases, the pain resolves after a few include ankylosing spondylitis and psori- weeks but recurrence or persistent low- atic arthritis, and predominantly affect the grade symptoms are relatively common. sacroiliac joints and axial skeleton; they Risk factors for developing chronic, disa- have a strong genetic association with bling pain include depression, job dissatis- HLA-B27. Ankylosing spondylitis typically faction, disputed compensation claims and presents in early adulthood with an insidi- a history of other chronic pain syndromes. ous onset of progressive back pain and stiff- ness over months to years. Lumbar disc herniation This is the most common cause of sciatica. Spinal tumour It predominantly affects young and middle- Vertebral metastases from breast, lung, aged adults, often following bending or prostate or renal cancer are far more lifting. Symptoms may be exacerbated by common than primary vertebral or other sneezing, coughing or straining. The diag- spinal tumours. The spine is frequently nosis is largely clinical and most cases involved in patients with multiple mye­ resolve within 6 weeks. Imaging is needed loma. Red flag features (see Box 23.1) may 210 Low back pain Differential diagnosis 23 suggest the diagnosis, which is best con- Box 23.1 Red flags for possible spinal cancer firmed with MRI. Spinal infections • New-onset pain in a patient >55 years Pyogenic vertebral osteomyelitis, ‘discitis’ • Active or previous cancer or vertebral tuberculosis (TB) may produce • Constant, unremitting or night pain severe, progressive pain, often with local- • Focal bony tenderness ised tenderness and reduced range of movement. Typical associated features • Unexplained weight loss include fever, sweats, malaise and ↑WBC/ • Fever, sweats, malaise, anorexia inflammatory markers. Risk factors for spinal infection are shown in Box 23.2. MRI is sensitive for detecting infection and dif- Box 23.2 Factors that increase the risk of ferentiating from tumour. spinal infection Cauda equina syndrome • Diabetes mellitus Compression of the collection of nerve roots • General debility at the base of the spine due to central disc prolapse, trauma or haematoma may lead • Indwelling vascular catheters to irreversible neurological damage and • IV drug abuse needs emergency referral for decompres- • Previous TB infection sion. Diagnosis is best confirmed by MRI. • Immunosuppression, e.g. HIV, infection, Other causes chronic steroid therapy • Spondylolisthesis (forward slippage of one vertebra on another): may cause back and radicular pain, and • Renal tract pathology, e.g. stones, occasionally requires operative cancer, pyelonephritis. decompression. • Abdominal aortic aneurysm. • Pelvic pathology, e.g. prostate cancer, • Shingles. pelvic inflammatory disease. • Pregnancy.

211 Low back pain 23 Overview

Full clinical assessment + lumbar spine examination

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

No

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

No

Sudden-onset pain + known / Yes Spinal 3 Vertebral fracture suspected osteoporosis? X-ray

No

Yes 4 ‘Red flags’ for cancer (Box 23.1)? MRI spine Spinal tumour / other cause

No

Yes Refer to 5 Inflammatory features? Likely spondyloarthritis rheumatologist

No

Yes 6 Radicular pain? Likely disc herniation or spinal stenosis

No

Yes 7 Neurogenic claudication? Likely spinal stenosis MRI spine

No

Likely mechanical back pain. Consider MRI spine if progressive / persistent symptoms 8 Otherwise assess for adverse prognostic factors

212 Low back pain Step-by-step assessment 23

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

Fig. 23.1 Movements of the spine. A. Extension. B. Flexion. C. Lateral flexion.

A B C

Fig. 23.2 Stretch test – sciatic nerve roots A. Neutral; nerve roots slack. B. Straight leg raising limited by tension of root A over prolapsed disc.

B

213 Low back pain 23 Step-by-step assessment

Fig. 23.3 Stretch test – femoral nerve. A. Patient prone and free from pain because femoral roots are A slack. B. When femoral roots are tightened by flexion of the knee +/− extension of the hip pain may be felt in the back.

B

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 • change in urinary frequency spinal X-rays if the patient has risk factors • any new difficulty in starting or for spinal infection (see Box 23.2), localised stopping micturition spinal tenderness or a history of night • a change in the sensation of toilet paper sweats, shivers or constitutional upset. when wiping after defecation Take three blood cultures and arrange • episodes of urinary/faecal incontinence. urgent MRI spine if any of the following is present: If there is any suspicion of bowel/bladder dysfunction, perform a PR examination to • pyrexia (>37.9°C) assess anal tone and measure bladder • ↑WBC/CRP/ESR volume immediately after voiding by • high clinical suspicion in a patient with bedside USS or catheterisation; >200 mL an indwelling vascular catheter, IV drug suggests urinary retention. abuse or immunosuppression Enquire also about weakness or unusual • X-ray features suggestive of sensations, e.g. numbness, tingling in the osteomyelitis. lower limbs; examine the legs carefully for Sudden-onset pain known/suspected reduced power, diminished reflexes and 3 + sensory disturbance, and test perianal osteoporosis? sensation. Perform plain X-rays to look for lumbar Arrange immediate MRI spine to exclude crush fracture if the patient has new and cauda equina syndrome in any patient with abrupt onset of pain and known/suspected low back pain (irrespective of its character- osteoporosis. Suspect osteoporosis if: istics) associated with any of: • urinary or faecal incontinence • long-term systemic steroids • urinary retention (significant post-void • >65 years of age with loss of height, residual urine or ↑bladder volume with kyphosis or previous radial/hip no urge) fracture. • altered perianal sensation/↓anal tone Seek an alternative cause if the X-ray • bilateral lower limb neurological signs reveals no fracture or one that does not or symptoms. correspond to the level of pain. Consider Request emergency orthopaedic/ further investigation if there are any neurosurgical review if the MRI confirms red flag features, other than age (see cauda equina compression. below). 214 Low back pain Step-by-step assessment 23

4 ‘Red flags’ for cancer (Box 23.1)? Suspect lumbar spinal stenosis if the patient is >50 years with a slow progressive Investigate for vertebral metastases, e.g. onset of symptoms and/or features of neu- radioisotope bone scan if the patient has a rogenic claudication (see below). history of active or previous lung/prostate/ Consider referral for further investi­ breast/renal/thyroid cancer. Perform a gation if: breast examination and myeloma screen, • persistent pain measure PSA (in males), Ca2+ and ALP, and • evidence of >1 nerve root involvement consider MRI spine in any other patient • major disability with ‘red flag’ features. • suspected lumbar spinal stenosis. 5 Inflammatory features? 7 Neurogenic claudication? Check ESR/CRP and perform plain spinal Consider neurogenic claudication if low X-rays if gradual onset of low back pain and back pain is accompanied by bilateral thigh stiffness. or leg discomfort, e.g. burning, cramping, Refer to rheumatology for further evalu- tingling, that arises during walking or on ation of possible inflammatory back pain if standing and is rapidly relieved by sitting, there are X-ray features of spondylitis, e.g. lying down or bending forward. squaring of the vertebral bodies/sacroiliitis Evaluate first for vascular claudication if or >1 of the following: the patient has a history of atherosclerotic • morning stiffness lasting >30 minutes disease, >1 vascular risk factor, e.g. diabetes • improvement of symptoms with exercise mellitus, smoking, ↑BP, ↑cholesterol or but not rest signs of peripheral arterial disease, e.g. • nocturnal back pain that arises in the diminished pulses, femoral bruit, trophic second half of the night skin changes. Check the ankle : brachial • radiation of pain into the buttocks pressure index (ABPI) and request a vascu- • restricted lumbar spine movements lar opinion if <1.0. • sacroiliac tenderness If neurogenic claudication is still sus- • ↑ESR/CRP with no alternative pected, consider MRI spine to confirm the explanation. presence of lumbar spinal stenosis, espe- cially if symptoms are disabling. 6 Radicular pain? Likely mechanical back pain. Consider MRI Pain is ‘radicular’ if it radiates to the lower 8 spine if progressive/persistent symptoms limb beyond the knee with any of: Refer to orthopaedics if neurological dys- • dermatomal distribution (see Fig. 22.1, function or spinal deformity. In the absence p. 200) of neurological, structural, infective, red • evidence of radiculopathy flag or radicular features, provide reassur- • positive sciatic or femoral stretch test ance and analgesia, recommend that the (Figs 22.2 and 22.3). patient stays active, and reassess after a Suspect lumbar disc herniation in acute- period of 6–12 weeks. If pain persists, look onset radicular pain, especially if the nerve for features of depression and explore stretch test is positive. In the absence of other potential psychosocial factors. Spinal red flags or other concerning features, reas- imaging is unlikely to be helpful but seek sess after 6–12 weeks of analgesia ± specialist input if there are persistent or physiotherapy. progressive disabling symptoms.

215 24 MOBILITY PROBLEMS: FALLS AND ‘OFF LEGS’

Patients may present with falls, difficulty ‘Secondary’ mobility presentations mobilising or complete immobility (‘off Immobility and instability may occur as a legs’). Younger patients can usually be consequence of other specific problems rapidly categorised into an underlying such as dizziness, joint pains or focal limb aetiology, but evaluation of elderly patients weakness. In these cases, assessment should is more complex. Normal physiological focus, initially, on the underlying primary changes of ageing – increased body sway, problem to determine the cause. Some reduced muscle bulk (sarcopenia) and patients with apparent falls may actually be impaired reaction time – increase the likeli- experiencing blackouts and, again, this hood of mobility problems. Moreover, necessitates a different diagnostic approach. mobility problems may be self-reinforcing, as reduced activity leads to loss of muscle Acute illness or drug reaction function and confidence. A thorough, sys- In elderly/frail patients, a sudden decline tematic approach is essential to identify in mobility (acute fall, ‘off legs’) may be adverse consequences of immobility, serious the principal manifestation of any acute underlying pathology and potentially medical, surgical or psychiatric illness or a reversible contributing factors. side-effect of certain medications (Box 24.1). In those with chronic underlying mobility Accidental trip problems, a relatively minor insult may lead to a major deterioration in mobility. Some falls are the unavoidable consequence of a trip or stumble. In the absence of sig- Multifactorial mobility problems nificant injury, recurrent mobility problems In patients with recurrent falls or other or other concerns, these patients do not chronic mobility problems, there is often require detailed assessment. However, no single identifiable cause but rather many elderly patients exhibit post hoc multiple contributing factors, e.g. muscle rationalisation of their fall (‘I must have weakness, balance disorder, polypharmacy, tripped on the carpet’), so falls should cognitive impairment, arthritis, ↓visual only be classified as accidental if there is acuity. A comprehensive and multidimen- unequivocal evidence for this. sional approach to assessment is essential.

216 Mobility problems: Falls and ‘off legs’ Differential diagnosis 24

Box 24.1 Drugs associated with increased risk of falls

• Alcohol • Benzodiazepines • Anticonvulsants • Diuretics • Antidepressants • Digoxin • Antihypertensives • Opioids • Antipsychotics

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

*Other features of Parkinsonian gait include reduced arm-swing, stooped posture and, sometimes, difficulty in starting and stopping (‘festinant’ gait).

217 Mobility problems: Falls and ‘off legs’ 24 Mobility problems: Overview

Full clinical assessment + collateral history

Significant injuries or other Yes Evaluate and treat: fractures / wounds / head injury 1 sequelae of fall / immobility? / pain / hypothermia / rhabdomyolysis / dehydration

No

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

No

Primary problem = focal limb weakness Yes Mobility secondary Presentation-specific 3 ↓ / blackout / dizziness / acute joint pain? to specific cause assessment (see text)

No

Yes Likely acute illness / Identify and treat 4 Abrupt decline in mobility? new drug (see text)

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)? discontinuation / ↓dose

No*

Yes 7 Cognitive impairment / confusion? See Assessment of confusion (Ch 24)

No*

Yes 8 Visual impairment? Consider referral to optician / ophthalmologist

No*

Yes 9 High fracture risk? Consider bone protection

No*

Multifactorial mobility problem: 10 Functional assessment with input from multidisciplinary team in all cases Consider referral to falls clinic / day hospital if ongoing mobility problems * Or problem reviewed / dealt with. 218 Mobility problems: Falls and ‘off legs’ Mobility problems: step-by-step assessment 24

Significant injuries or other sequelae of to exclude rhabdomyolysis and be vigilant 1 fall/immobility? for compartment syndrome (Box 21.3, p. 189). In all patients who have fallen (or who have been found on the floor), perform a rapid Fall related to stumble/trip with none of 2 but thorough survey of the entire body for features in Box 24.3? injuries. Fractures, lacerations or bruising may be not immediately apparent, and the Take care in making this diagnosis – a cognitively impaired patient may not bring simple trip on a loose carpet tile at walking them to your attention. Assess the perfusion pace is usually not ‘normal’ and the visual and function of any limb with bruising, impairment that led to the trip or the poor deformity, pain or swelling and consider balance that turned it into an injurious fall the need for X-rays. Pain will compound might be reversible. On the other hand, any existing mobility problems – ensure exhaustive assessment is inappropriate in it is adequately treated. If there is a history patients with a genuinely accidental fall of head injury, arrange neuroimaging if any and no underlying mobility problems. of the features in Box 24.2 is present. Have a low threshold for further evaluation In patients with a prolonged period of if any of the features in Box 24.3 is present immobility, e.g. lying on the floor or -con or events leading up to the fall are unclear. fined to bed, check temperature to exclude Primary problem focal limb weakness/ hypothermia, look for clinical/biochemical 3 = blackout/dizziness/acute joint pain? evidence of dehydration, and examine the heels and sacrum for pressure sores. Con- If you identify new limb weakness on sider aspiration/hypostatic pneumonia in examination, assess as described in patients with hypoxia, lung crackles or CXR Chapter 22. changes. If there has been significant soft If mobility problems are consequent on tissue pressure damage or any prolonged dizziness, evaluate firstly for symptomatic time on the floor, check CK and urinary postural hypotension: a fall of ≥20 mmHg myoglobin (suggested by haematuria on in systolic BP or ≥10 mmHg in diastolic BP urinalysis with no red cells on microscopy) within 3 minutes of changing from a lying to standing position, accompanied by a feeling of light-headedness/pre-syncope. If Box 24.2 Indications for early neuroimaging in this is detected, search for underlying patients with head injury* causes e.g. antihypertensives, dehydr­ Immediate CT brain ation, autonomic neuropathy. Otherwise, assess as in Chapter 10, but complete a full • ↓GCS <12 or persistently <15 • Focal neurological signs • Persistent headache or vomiting Box 24.3 Features not consistent with a • Features of basal skull fracture diagnosis of simple accidental trip • Coagulopathy or anticoagulation • Recurrent or multiple falls CT brain within 8 hours • Recent decline in mobility or functional status • Seizure • Inability to get up from the ground • >65 years + episode of loss of consciousness • Implausible mechanism for fall • Retrograde amnesia • Witnessed period of unresponsiveness • Evidence of skull fracture • Inability to recall landing on ground *Based on SIGN guideline 110. • Facial injuries

219 Mobility problems: Falls and ‘off legs’ 24 Mobility problems: step-by-step assessment

mobility assessment, especially if no spe- Review all new drugs (including over- cific disorder is identified. the-counter ones) started within the previ- Consider whether an apparent fall could ous weeks and consider trial discontinuation have been a blackout. Beware of accepting of any high-risk agents (see Box 24.1). If rationalisations for the event (‘I must have significant loss of mobility was preceded by tripped’) and make every attempt to obtain a fall, consider the possibility of fracture or an eyewitness account of the current epi­ head injury – ensure pain is adequately sode or previous ones. If patients cannot treated. recall how they came to be lying on the Weight loss, muscle wasting, hypoalbu- ground, assess, in the first instance, as per minaemia and chronic anaemia may suggest transient loss of consciousness (see Ch 29). a progressive disorder ‘coming to a head’. Also suspect transient loss of consciousness Suspect significant acute illness in pat­ if the patient was witnessed as having a ients whose baseline mobility is relatively period of unresponsiveness,­ sustained normal. Once this has been addressed, facial injuries during the fall (most complete a full assessment to identify conscious patients can protect the face) or underlying mobility problems and reversi- experienced palpitation, chest pain, breath- ble risk factors for falling. lessness or a pre-syncopal prodrome prior In patients with a background of progres- to ‘falling’. Have a lower threshold for sive mobility decline/deteriorating func- further evaluation of possible syncope in tional status/general frailty, the acute patients with ECG abnormalities (see precipitant may be minor – do not over- p. 262) or a history of cardiac disease. emphasise it in comparison with the under- If mobility problems are secondary to lying contributory factors. an acutely painful joint, assess as in Chapter 20. 5 Gait or neurological abnormality? Assessment of walking pattern is key to 4 Abrupt decline in mobility? understanding mobility problems. It is a An abrupt decline in mobility (acute fall, fundamental element of the neurological new onset of recurrent falls or being ‘off examination and can reveal abnormalities legs’) is one of the classical atypical presen- not elicited on gross testing of individual tations of acute illness in the elderly. Char- modalities. It may also unmask impaired acteristic signs/symptoms of the specific effort tolerance due to cardiorespiratory precipitant may be absent and ‘screening’ or lower limb disease. Finally, the gait investigations (Box 24.4) are often required assessment is an opportunity to assess to uncover the problem or identify a focus falls risk, even in the absence of specific for further assessment. findings. Check that patients are safe to mobilise, equip them with their normal walking aid and follow the steps in Clinical Box 24.4 Screening investigations to identify tool: Assessment of gait. Go to ‘Gait abnor- acute illness in elderly patients malities’ (p. 222) if any abnormalities are • Glucose meter reading (‘BM’) detected.

• PR examination 6 On >3 drugs/high-risk drug (Box 24.1)? • Urine dipstick and MSU/CSU (avoid diagnosing a urinary tract infection purely Medications are one of the most readily on the basis of abnormal dipstick results) modifiable of all factors influencing mobil- ity problems but indiscriminate changes • Blood tests – FBC, U E, LFTs, glucose, CRP + may do more harm than good. Individual (minimum) medications that increase the risk of falling • CXR are listed in Box 24.1. Polypharmacy (>3 regular medications) is a risk factor for falls. 220 Mobility problems: Falls and ‘off legs’ Mobility problems: step-by-step assessment 24

Review the indications for all drugs: are cataracts. Screen for ↓visual acuity. If they still required? Look for opportunities detected, refer to an ophthalmologist (or an to rationalise treatment, consider alterna- optician if a refractory error is suspected). tives, and decreasing the dose. A gradual approach will allow the impact 9 High fracture risk? of individual changes to be assessed and is Fractures, especially of the hip, are a devas- essential with psychotropic medication tating consequence of falls and selected where abrupt withdrawal may be worse patients may benefit from bone protection. than the toxic syndrome. Explore a possible This is a controversial area and specific contribution from alcohol in all cases – in indications change, but treatment e.g. patients with underlying mobility/balance bisphosphonates, should be considered in problems it may critically impair stability, patients with previous fragility fractures even when consumed within recommended or a bone mineral density T-score of −2.5 limits. or less and in those taking long-term or frequent courses of systemic steroids. In 7 Cognitive impairment/confusion? other cases, consider using the WHO Acute delirium is a common cause of fracture risk assessment tool or FRAX™ reduced mobility, and may not be readily score, www.shef.ac.uk/FRAX/tool.jsp. apparent if it is hypoactive or superim- Multifactorial mobility problem: arrange posed on chronic impairment. Vigilance 10 and collateral history are essential counter- multidisciplinary team assessment parts to objective measures of cognitive All patients with recurrent falls or ↓mobil- function; an Abbreviated Mental Test score ity should be referred to physiotherapy/ of 6/10 is difficult to interpret without occupational therapy for assessment of knowledge of baseline ability. Chronic cog- functional ability, environmental contribu- nitive impairment is also a risk factor for tors to the presentation, and scope for falls, but difficult to ameliorate. Consider benefit from measures such as walking silent precipitants of wandering/getting aids/strength and balance training/home out of bed, such as urinary urgency or nico- alarms. In patients with ongoing problems, tine withdrawal. Further assessment of con- consider referral to day hospital or a fusion is detailed in Chapter 8. specialist falls clinic for comprehensive assessment. 8 Visual impairment? Visual impairment increases the risk of falls and may be reversible e.g. refractory errors,

221 Mobility problems: Falls and ‘off legs’ 24 Gait abnormalities: Overview

Yes Consider focal weakness / proximal 1 Unable to stand up unaided? myopathy / pain / acute illness

No

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

No

Yes Seek underlying 3 Positive Romberg test? Sensory ataxia cause

No

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

No

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

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

No

Return to Mobility Problems: Overview (Step 6)

1 Unable to stand up unaided? move their feet close together – inability to do so indicates significant ataxia. Look for Lower limb weakness may limit the ability associated features of cerebellar disease, to rise from a chair or necessitate use of the e.g. intention tremor, dysdiadochokinesis, chair arms or pulling on nearby furniture. dysmetria (past-pointing), dysarthria, Systemic illness, toxic insults or metabolic nystagmus. derangement may cause mild generalised weakness. If weakness is persistent, asym- 3 Positive Romberg test? metrical or associated with wasting/ A marked increase in unsteadiness after eye neurological abnormalities, see Chapter 22. closing is a positive test, suggesting a 2 Unsteady with eyes open? sensory (proprioceptive or vestibular) rather than cerebellar cause of ataxia. Check lying/standing BP if the patient Reduction in sensation may be a normal feels faint or light-headed. Consider part of ageing e.g. reduced vibration sense vertigo if the patient has a sensation of in the feet is common and of limited signifi- spinning or movement. Observe standing cance in the older patient. Examine the posture, identify reduction in joint function, patient during walking for an unsteady, and evaluate pain. If patients can remain ataxic or ‘lead boot’ gait. The list of possible standing without assistance, ask them to causes of peripheral neuropathy is vast 222 Mobility problems: Falls and ‘off legs’ Gait abnormalities: Step-by-step assessment 24 but screen routinely for diabetes mellitus, The gaits associated with Parkinsonism alcohol excess, liver disease, malnutrition and sensory ataxia are described above.

(check vitamin B12) or iatrogenic causes, e.g. Suspect cerebellar ataxia if the gait is anticonvulsants, chemotherapy. unsteady and broad-based with an inability to heel–toe walk (as if inebriated with 4 Features of Parkinsonism? alcohol). A hemiplegic gait is usually obvious and will be associated with focal Look for the typical features of PD: neurological signs. Bilateral lower limb • tremor: coarse, slow (5 Hz) and usually proximal muscle weakness may produce a asymmetrical; present at rest, absent ‘waddling’ gait. during sleep; decreased by voluntary Pain can limit exertion or alter gait, movement; increased by emotion; leading to a decrease in function or an adduction–abduction of the thumb with increased risk of falling. The patient will flexion–extension of the fingers typically place the foot of the affected side (‘pill-rolling’) delicately on the floor for as little time as • ↑tone: ‘lead-pipe’ rigidity or (in the possible to avoid the pain of weight-bearing presence of tremor) ‘cog-wheel’ with a (‘antalgic’ gait). Osteoarthritis is frequently jerky feel responsible but is usually chronic, and • bradykinesia: slow initiation of slowly progressive, and thus unlikely to movement, ↓speed of fine movements, lead to hospital admission without addi- expressionless face tional factors. Acutely painful joints require • gait: delayed initiation, ↓arm swing, careful assessment. stooped posture, short, shuffling steps, Consider gait apraxia if no specific neu- difficulty turning. rological abnormality or gait pattern is The presence of these features makes idio- noted but the gait is none the less abnormal. pathic Parkinson’s disease (PD) more likely, Apraxia, the inability to conduct learned, but Parkinsonism has other causes: most purposeful movements properly (in the commonly, diffuse cerebrovascular disease. absence of a focal insult), is a result of The classical description of vascular Parkin- general or frontal cerebral insults such as sonism is of signs of PD below the waist, dementia, cerebrovascular disease, normal with relative sparing of the arms. pressure hydrocephalus, sedation or meta- New presentations or progression of PD bolic derangement. are usually assessed in an outpatient setting. Psychological causes of reduced mobility Mobility-related admissions in patients (especially the fear of falling) can also with PD are more likely to be connected reduce mobility and increase the risk of with a superimposed acute illness or a falls, and may only be elicited by asking the medication problem. Make certain that patient to mobilise greater distances. hospitalised patients with PD receive their medication at the correct dose and time to 6 Reduced exercise tolerance? ensure that their mobility does not deterio- Observe for/ask about exertional dysp- rate further. noea, chest discomfort and claudication. The latter may be due to peripheral vascu- 5 Gait abnormality? lar disease (diminished pulses, skin changes, Gait screening is sensitive for neuromotor, vascular disease elsewhere) but consider sensory and musculoskeletal abnormalities neurogenic claudication secondary to in the lower limbs because walking is a spinal stenosis, especially if the discomfort complex task in comparison with the tests responds to postural change e.g. bending of neurological function used in the stand- over, sitting down, more quickly than ard screening examination. standing still.

223 25 PALPITATION

Palpitation is an unpleasant awareness of former is due to right atrial and AV node the heartbeat. In most cases, the key to re-entry, usually in structurally normal diagnosis lies in documenting the cardiac hearts; the latter (known as Wolff–Parkinson– rhythm during symptoms. Establishing the White syndrome) is caused by a re-entry frequency, intensity and impact of symp- circuit formed from the AV node and an toms is essential to guide treatment. ‘accessory pathway’ – an abnormal band Heightened awareness of of conducting tissue connecting atria and ventricles. normal heartbeat Both produce episodes of regular tachy- Awareness of the normal heartbeat is cardia (± light-headedness and breathless- common but may produce anxiety in ness) with an abrupt onset and offset. The patients with psychosocial stress or health ECG shows a regular narrow-complex concerns e.g. recent heart ‘scare’, death of tachycardia at 140–220/min (Fig. 25.1). family member. It is most commonly noted In 50% of patients with an accessory when lying awake in bed or sitting at rest. pathway, the ECG in sinus rhythm shows a Sinus tachycardia/↑stroke volume short PR interval and slurring of the QRS upstroke (‘delta wave’) due to premature Causes of sinus tachycardia are shown in activation of ventricular tissue by the Box 25.1; anxiety is most frequently respon- pathway – ‘pre-excitation’ (Fig. 25.2). sible, with patients typically reporting Most cases of AVNRT and AVRT are episodes of a fast, regular, pounding heart- curable with radiofrequency catheter beat that builds up and resolves over ablation. minutes. Increased stroke volume due to aortic regurgitation or vasodilator drugs Atrial arrhythmias (atrial tachycardia, may produce a forceful heartbeat without flutter and fibrillation) tachycardia. Atrial tachycardia produces symptoms Extrasystoles similar to SVT; the ECG shows a regular Atrial and ventricular extrasystoles (ectop- narrow-complex tachycardia, but with ics or premature beats) are common in abnormal P waves. healthy individuals but may indicate struc- Atrial flutter is caused by a large re-entry tural or coronary heart disease. They do not circuit within the right atrium that gener- usually cause symptoms but, in some ates an atrial rate of 300/min. This is usually patients, produce a sensation of dropped associated with AV block, resulting in a beats (due to ↓stroke volume of the ectopic ventricular rate of 150/min (2 : 1 block) or beat), ‘jolts’ or ‘thumps’ (due to ↑stroke 100/min (3 : 1). Symptoms are similar to volume of the post-ectopic sinus beat), or, if SVT. The ECG shows a regular narrow- frequent, an irregular heartbeat. complex tachycardia with ‘saw-toothed’ flutter waves (Fig. 25.3). With 2 : 1 block Paroxysmal supraventricular these may be obscured, so suspect atrial tachycardia flutter in any patient with a regular narrow- The term ‘supraventricular tachycardia’ complex tachycardia of 150/min. (SVT) is typically applied to atrioventricu- Atrial fibrillation is common. Underlying lar nodal re-entry tachycardia (AVNRT) causes are shown in Box 25.2. Atrial activity and AV re-entry tachycardia (AVRT). The is chaotic and the ventricles are activated 224 Palpitation Differential diagnosis 25

Box 25.1 Causes of sinus tachycardia rapidly and irregularly. Patients with par- oxysmal atrial fibrillation experience an • Anxiety or panic disorder erratic or irregular heartbeat that is usually fast and may be associated with breathless- • Stress or strong emotion ness, light-headedness or ↓effort tolerance. • Drugs: beta2 agonists, anticholinergics, The ECG shows an irregular narrow- cocaine, amphetamines complex tachycardia with no P waves (Fig. • Anaemia 25.4). Patients with atrial fibrillation or • Thyrotoxicosis flutter are at greater risk of thromboembolic complications, including stroke. • Fever • Phaeochromocytoma Ventricular tachycardia • Pregnancy Ventricular tachycardia (VT) is a potenti­ ally life-threatening arrhythmia that most

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 25.1 Supraventricular tachycardia.

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 25.2 Pre-excitation: sinus rhythm in Wolff–Parkinson–White syndrome. 225 Palpitation 25 Differential diagnosis

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 25.3 Atrial flutter with 2 : 1 AV block.

II

Fig. 25.4 Atrial fibrillation with a rapid ventricular response.

Box 25.2 Common causes of atrial fibrillation frequently occurs in patients with previous myocardial infarction or cardiomyopathy • Ischaemic heart disease but can arise in structurally normal hearts. Patients experience an abrupt onset of • Valvular heart disease (especially mitral rapid palpitation often associated with pre- stenosis) syncope (a feeling of faintness and near- • Hypertension collapse), syncope, breathlessness or chest • Cardiomyopathy pain. The ECG shows a regular broad- • Sick sinus syndrome complex tachycardia (Fig. 25.5). A variant, torsades de pointes, with a characteristic • Alcohol excess ECG appearance (Fig. 25.6), may occur in • Congenital heart disease patients with a prolonged QT interval. • Constrictive pericarditis Bradyarrhythmia e.g. sick sinus • Hyperthyroidism syndrome, intermittent AV block • Idiopathic (‘lone’ atrial fibrillation) Bradyarrhythmias more commonly present with light-headedness or syncope but the patient may report intermittent episodes of a slow but forceful heartbeat. Associated ECG findings include sinus pauses, junc- tional bradycardia and intermittent second- or third-degree AV block (Figs 29.1, 29.2, p. 261).

226 Palpitation Differential diagnosis 25

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 25.5 Ventricular tachycardia.

Fig. 25.6 Torsades de pointes.

227 Palpitation 25 Overview

Yes Feel pulse, 1 Symptoms present during consultation? Diagnosis perform ECG

No

Full clinical assessment, ECG

Yes 2 Clear history of extrasystoles? Symptomatic extrasystoles

No

Heartbeat regular and normal Yes 3 ↑Stroke volume / awareness of normal heartbeat speed during symptoms?

No

Attempt to document rhythm during symptoms

See Further assessment of Rhythm documented during Yes palpitation with 4 Diagnosis typical symptoms? documented rhythm (p. 231) No

Yes Further attempt to document rhythm / 5 Alarm features or highly symptomatic? refer Cardiology / empirical treatment

No

Cause uncertain: reassure; refer Cardiology if recurrent troublesome symptoms

228 Palpitation Step-by-step assessment 25

1 Symptoms present during consultation? • If symptoms are occurring less than weekly, consider an external patient- If the patient has symptoms during the con- activated recorder. sultation, feel the pulse straight away and • If symptoms are very infrequent, ask the perform an ECG as soon as possible. This patient to report to hospital during an may sound overly simple but much of the episode (advising him not to drive) or, difficulty in diagnosing palpitation lies in depending on symptom burden and trying to document the rhythm during a severity, consider referral for insertion typical episode of symptoms. Do not miss of an implantable loop recorder. the opportunity! • If symptoms are induced by physical exertion, refer for a supervised 2 Clear history of extrasystoles? exercise ECG.

It is not always possible to distinguish fre- Rhythm documented during typical 4 quent ventricular extrasystoles from sus- symptoms? tained arrhythmias such as atrial fibrillation on the history alone. However, a clear Diagnose arrhythmia as the cause of palpi- history of an occasional ‘jolt’ or ‘jump’ in tation if you obtain an ECG recording of the chest or isolated ‘dropped’ or ‘skipped’ rhythm disturbance that corresponds with beats is highly suggestive – such patients symptoms – proceed to ‘Further assessment can usually be reassured without further of palpitation with documented rhythm: investigation. further assessment’. Clear documentation of sinus rhythm Heartbeat regular and normal speed during a typical attack excludes an arrhyth- 3 during symptoms? mic cause for symptoms. Asymptomatic rhythm disturbances may Many patients with palpitation describe occur during prolonged ECG monitoring. the heartbeat as ‘forceful’ or ‘strong’ rather The patient may need further assessment than fast, slow or irregular. This may reflect for the specific arrhythmia but symptoms ↑stroke volume e.g. aortic regurgitation, should not automatically be attributed to it anaemia, vasodilators, or simply awareness – especially if typical symptoms occur of the normal heartbeat but, in either case, during periods of sinus rhythm. Consult a it argues strongly against an arrhythmic cardiologist if there is any doubt as to the cause. Look for underlying physical and significance of an ECG recording. psychosocial factors but further investiga- Continue to step 5 if the patient did not tion is usually unnecessary unless there is a experience a typical episode of palpitation specific additional concern. during the period of rhythm monitoring.

Attempt to document rhythm during 5 Alarm features or highly symptomatic? symptoms The lengths to which you should go to doc- This is a key diagnostic step. The chosen ument the ECG during symptoms depends method will be dictated predominantly by on both the severity of symptoms and the the frequency of symptoms. estimated risk of a life-threatening arrhyth- • Use inpatient telemetry if the patient mia, e.g. VT or complete heart block. has experienced a recent episode e.g. Patients with mild, infrequent symptoms in the last 72 hours, with syncope or and no high-risk features may be reassured pre-syncope, or has other high-risk without further investigation and reas- features (p. 262). sessed later if symptoms become more fre- • Holter monitoring for 1–7 days is quent or intrusive. However, it is important suitable if symptoms are occurring to pursue repeated attempts to document frequently (≥1/week). the rhythm in patients with symptoms that 229 Palpitation 25 Step-by-step assessment

are frequent or unpleasant or which inter- • risk factors for VT, e.g. previous fere with occupation or lifestyle. myocardial infarction, ventricular Irrespective of the frequency and inten- surgery, cardiomyopathy sity of palpitation, investigate further to Refer to cardiology for further investiga- exclude a serious underlying arrhythmia in tion, e.g. invasive electrophysiology study, patients with: implantable loop recorder, risk stratifica- • syncope or pre-syncope tion and treatment. • significant abnormality on resting ECG

230 Palpitation Further assessment 25

Palpitation with documented rhythm: cardiomyopathy, left ventricular further assessment hypertrophy, valvular disease. • Seek causative or exacerbating factors: Assess the frequency and intensity of symp- measure BP, electrolytes and TFT; toms and the impact on occupation and enquire about alcohol intake and lifestyle. Establish the efficacy and side- symptoms of angina. effects of previous treatments. • Use the CHA2DS2VASc score (http:// Sinus tachycardia www.escardio.org/guidelines-surveys/ • Review all prescribed and ‘recreational’ esc-guidelines/GuidelinesDocuments/ drugs, check FBC and TFTs, and, where guidelines-afib-FT.pdf) to assess appropriate, perform a pregnancy test. thromboembolic risk in patients with • If ↑BP or episodes are associated with non-valvular atrial fibrillation (all headache, flushing or GI upset, measure patients with mitral stenosis are at 24-hour urinary metanephrines to high risk). exclude phaeochromocytoma. • Refer to Cardiology if symptoms are • Request an echocardiogram if any frequent, distressing or disabling despite features suggest structural heart disease, first-line medical therapy, e.g. e.g. unexplained murmur, signs of heart beta-blockers. failure. Ventricular tachycardia • Look for evidence of an anxiety or panic • Perform an echocardiogram to look for disorder. evidence of underlying structural heart Extrasystoles disease e.g. cardiomyopathy. • Seek potential exacerbating factors • Enquire about previous MI and including ↓K+, ↓Mg2+, drugs e.g. tricyclic symptoms of/risk factors for ischaemic antidepressants, digoxin, excessive heart disease. alcohol, tobacco or (possibly) caffeine • Measure the QT interval on the ECG in consumption. sinus rhythm. • Consider further investigation, e.g. • Measure electrolytes – especially K+, echocardiography, exercise ECG if Mg2+ and Ca2+. frequent or associated with other signs/ • Refer all patients to Cardiology for symptoms of CVS disease. further investigation, risk stratification Supraventricular tachycardia and treatment. • Look for pre-excitation on resting ECG Bradyarrhythmia (see Fig. 25.2) to suggest an accessory • Seek an underlying cause: check TFTs pathway-mediated tachycardia. and review drugs for rate-limiting • Refer to cardiology for electrophysiology agents, e.g. digoxin, beta-blockers, study ± radiofrequency ablation if verapamil. symptoms are frequent, disabling or • Refer symptomatic bradyarrhythmia unpleasant or if there are side-effects on or asymptomatic second-degree AV medical therapy. block (Mobitz type 2), complete heart Atrial flutter/fibrillation block or sinus pauses >3 seconds to Cardiology. • Perform echocardiography to exclude structural heart disease, e.g.

231 26 RASH: ACUTE GENERALISED SKIN ERUPTION

The accurate diagnosis of skin disease can bacteria forming a crusted yellow exudate be difficult for the non-expert, as successful (‘impetigo’) (Fig. 26.3), or by viruses, e.g. diagnosis is usually based on visual pattern herpes simplex, producing a vesicular recognition developed through experience pattern (‘eczema herpeticum’). rather than analytical rule-based appro­ Psoriasis aches. This is a step-by-step approach to assist identification of important acute gen- Psoriasis, a very common papulosqua­ eralised eruptions that require urgent der- mous eruption, is characterised by well- matology advice and treatment. demarcated erythematous or purple papules and plaques, topped with silvery Erythroderma scale. There are three forms of acute erup- Erythroderma (red skin) describes inflam- tion: erythroderma (see above), pustular matory skin disease manifesting predomi- psoriasis (Fig. 26.4) – a form that can nantly as erythema and involving >90% of deteriorate rapidly, and guttate psoriasis the body surface area (BSA; Fig. 26.1). The (Fig. 26.5) – with characteristic widespread term ‘sub-erythrodermic’ is sometimes multiple ‘drop-like’ lesions, most com- used to describe extensive erythema cover- monly seen in young adults in association ing < 90% BSA. Acute erythroderma can be with streptococcal pharyngitis. Pityriasis life-threatening and most cases need hospi- rosea is often confused with psoriasis. It talisation and urgent dermatology review. may be a reaction to a viral infection and The major causes are eczema (40%), psoria- initially presents with a single ‘herald sis (25%), cutaneous lymphoma (15%) and patch’ followed by the subsequent deve­ drug eruptions (10%). lopment of multiple lesions on the torso (Fig. 26.6). Eczema Toxic epidermal necrolysis, ‘Eczema’ and ‘dermatitis’ are interchange- able terms. Dermatitis is used to denote a Stevens–Johnson syndrome and group of non-infective inflammatory skin erythema multiforme diseases that represent a reaction pattern to Toxic epidermal necrolysis (TEN) is the various stimuli. Dermatitis may be classi- severe end of a spectrum of acute eruptions fied by aetiology (atopic, irritant, allergic/ caused by a cell-mediated cytotoxic reac- contact, venous/stasis), morphology (seb- tion against epidermal cells (Fig. 26.7). It is orrhoeic, discoid) or site (palmar, plantar, characterised by fever (>38°C), widespread pompholyx). All produce the same key tender erythema affecting >30% of the clinical feature: pruritic, erythematous skin surface, and mucosal involvement (see lesions with typically indistinct margins. below). Erythema is followed by exten­ The lesions can progress through a number sive, full-thickness, cutaneous and mucosal of phases: acute (with vesicles and bullae necrosis and denudation within a couple of – Fig. 26.2), subacute (with scaling and days. Similar features involving <10% of the crusting) and chronic (with acanthosis, body surface are termed Stevens–Johnson lichenification and fissuring). Lesions may syndrome (SJS), also known as ‘erythema also become secondarily infected by multiforme major’; if 10–30% of body 232 Rash: Acute generalised skin eruption Differential diagnosis 26

Fig. 26.1 Erythroderma.

Fig. 26.2 Acute dermatitis. Fig. 26.3 Impetigo.

Fig. 26.4 Pustular psoriasis. 233 Rash: Acute generalised skin eruption 26 Differential diagnosis

surface area is affected, this is often classi- fied as TEN/SJS overlap. Drugs, e.g. allopu- rinol, anticonvulsants, NSAIDs, cause >80% of cases and have usually been commenced 1–3 weeks prior to presentation. Erythema multiforme (minor) represents a similar but milder type of cytotoxic reac- tion. Classically, 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 ery­ thema (Fig. 26.8). The lesions predomi- nantly occur on the hands/feet and affect Fig. 26.5 Guttate psoriasis. <10% of the BSA without mucous mem- brane involvement. The underlying cause is more often viral (especially herpes simplex) than drug-induced.

Fig. 26.6 Pityriasis rosea. Fig. 26.8 Erythema multiforme-target lesions.

Fig. 26.7 Toxic epidermal necrolysis.

234 Rash: Acute generalised skin eruption Differential diagnosis 26

Fig. 26.9 Pemphigus.

Fig. 26.10 Pemphigoid.

Pemphigus/pemphigoid/dermatitis herpetiformis Separation of keratinocytes from each other, or from the underlying dermis, produces blistering. The three most common blister- ing disorders are pemphigus (Fig. 26.9), pemphigoid (Fig. 26.10) and dermatitis her- petiformis (Fig. 26.11) which is commonly associated with coeliac disease.

Urticaria/angioedema Urticaria (Fig. 26.12) is oedema within the dermis secondary to mast cell degranula- tion, and is a common skin reaction. Fig. 26.11 Dermatitis herpetiformis.

235 Rash: Acute generalised skin eruption 26 Differential diagnosis

Fig. 26.12 Urticaria.

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 medi- ated by immunoglobulin IgE. Those that are, arise in response to drugs (especially antibiotics), foods (peanuts, eggs, shellfish) and skin contact (latex, plants, bee/wasp stings), and may progress to anaphylaxis. Non-IgE causes include concurrent infec- tion (especially upper respiratory tract infections), drugs that promote mast cell degranulation (opiates, aspirin, NSAIDs, ACE inhibitors), and foods that contain sali- cylates and additives. Purpura (including vasculitis) Purpura (Fig. 26.13) is fixed staining of the skin by leakage of blood from the intravas- cular space and needs to be distinguished from simple bruising. Causes include: • septic emboli from systemic infectious diseases Fig. 26.13 Vasculitis/purpura. • haematological disorders • thrombosis involving microcirculation • vasculitis (inflammation in vessel walls).

236 Rash: Acute generalised skin eruption Differential diagnosis 26

Acute exanthems Box 26.1 Drugs that cause rashes in >1% of ‘Exanthem’ simply means ‘breakout’ and, the population although the term is mostly used for rashes • Penicillins with an infectious aetiology, it may be regarded as a pseudonym for any acute • Carbamazepine eruption or rash. • Allopurinol Drug eruptions are common and do not • Gold necessarily indicate allergy; ~3% of all • Sulphonamides patients admitted to hospital have an erup- tion due to adverse drug reactions. Those • NSAIDs most commonly implicated are listed in Box • Phenytoin 26.1. In hospital, rashes are commonly • Isoniazid attributed to and often caused by medica- • Chloramphenicol tions, but similar cutaneous signs can be due to underlying or intercurrent illness, • Erythromycin e.g. viral or bacterial exanthems or internal • Streptomycin disease, non-specific reactions to treatment, e.g. sweat rash due to prolonged bed-rest or previously unidentified independent skin disease. Infective exanthems are largely viral. Many of the conditions described above could be considered specific examples of infective exanthems, e.g. erythema multi- forme post-herpes simplex, guttate psoria- sis post-pharyngitis and pityriasis rosea.

237 Rash: Acute generalised skin eruption 26 Overview

Full clinical assessment

Yes Urgent 1 >90% body surface area erythematous? Erythroderma Dermatology input No

2 Blisters present?

No Yes Stevens-Johnson Yes syndrome / toxic Urgent Mucous membrane involvement? 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

3 Purpura present?

No Yes

Yes Evidence 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 reaction (see text)

Yes 4 Pustules present? Likely pustular psoriasis or systemic infection

No

Yes 5 Wheals present? Urticaria Seek precipitant

No

Yes 6 Underlying chronic dermatosis? Consider acute flare

No

7 Likely drug reaction or infective exanthem. Refer Dermatology if persistent or severe symptoms

238 Rash: Acute generalised skin eruption Step-by-step assessment 26

1 >90% body surface area erythematous? 2 Blisters present? Estimate the proportion of skin that is Blisters form when fluid separates the erythematous using the guide in Box layers of the skin; blisters < 5 mm diameter 26.2; >90% of BSA indicates erythroderma. are termed ‘vesicles’ whilst those >5 mm Admit any patient with acute erythroderma are called ‘bullae’. Mucous membranes are to hospital, assess and stabilise as described involved (Fig. 26.14) when erosions and in Box 26.3 and arrange urgent dermatol- ulceration (with subsequent crusting) occur ogy review. Subsequent treatment is based on oral, genital and ocular epithelium; on the exact diagnosis and guided by expert examine these sites in any acute severe skin dermatological assessment. eruption. Suspect TEN if there is extensive blister- ing with peeling of the skin to reveal bright red oozing dermis (see Fig. 26.6), along with mucous membrane involvement; Box 26.2 Calculating body surface area seek immediate Dermatology review and manage in a burns or critical care unit. If Originally developed for calculating surface bullae and mucosal lesions are present but area for burn victims, in adults a simple way of blistering is less extensive, consider SJS and calculating the body surface area (BSA) pemphigus (see Fig. 26.9) – arrange prompt affected by a cutaneous disorder is the dermatological review in all cases. ‘Wallace rule of nines’. This system allocates to different body parts 9% (or half thereof) of the Box 26.3 Assessment and immediate total BSA. In extensive skin disease it is management of skin dysfunction sometimes easier to identify unaffected skin, The mainstay of emergency dermatology and assessment is aided by remembering that treatment is to provide surrogate skin function the patient’s hand is approximately 1% of BSA. until the underlying condition has resolved or is suppressed with suitable medication. Look for Rule of 9s evidence of shock (Box 28.1, p. 249) and 4.5% 4.5% dehydration, and monitor U+E regularly. Replenish fluid lost through defective skin barrier 9% 9% function with IV fluids and supplementary

4.5% 4.5% electrolytes. Take swabs of all areas of 9% 9% suspected infection and, if the patient is pyrexial, 4.5% 4.5% take blood cultures before commencing 1% antibiotic therapy. Use strict aseptic technique for blood cultures, ideally through non-affected 9% 9% 9% 9% skin, to try to avoid contaminants (more likely in dermatological patients due to ↑skin flora load). Remember that many acute cutaneous eruptions are associated with pyrexia, due not to systemic infection but to loss of temperature homeostasis through vasodilatation. Maintain body Anterior Posterior temperature with a warm room and regular antipyretics. Assess the extent of skin compromise as detailed above and restore its Palmar method barrier function with regular application of thick 1% (patient’s palm) emollients (liquid paraffin : white soft paraffin, 50 : 50). Remove any potential exacerbates by discontinuing all unnecessary medication.

239 Rash: Acute generalised skin eruption 26 Step-by-step assessment

A

Fig. 26.15 Herpes zoster.

Take urgent blood cultures and treat empirically for meningococcal sepsis pen­ ding further investigation if the patient has fever, shock, drowsiness or meningism (see Box 18.2, p. 167). Consider septic emboli B from endocarditis if the patient is febrile Fig. 26.14 Mucous membrane involvement. and has a predisposing cardiac lesion or a A. Oral. B. Ocular. new murmur. Look for evidence of an underlying bleed- ing tendency – ask about/examine for In the absence of mucous membrane ecchymoses, epistaxis, GI bleeding, menor- involvement, look for target lesions (see Fig. rhagia, haemarthrosis and mucosal haem- 26.8) on the hands and feet suggestive of orrhage, and check FBC, PT and APTT. erythema multiforme; otherwise, consider Unless the cause is obvious e.g. excessive bullous pemphigoid (see Fig. 26.10), fixed anticoagulation, chronic liver disease, drug eruption or, if lesions are well local- discuss with Haematology if there is coagu- ised, an insect bite or contact dermatitis. lopathy or ↓platelets. If the patient has a painful eruption of If ↓platelets are present with normal vesicles, suspect infection with herpes coagulation, look for associated features of simplex if it is confined to the face, lip or thrombotic thrombocytopenic purpura: finger (herpetic whitlow), and herpes zoster • ↓Hb without an obvious alternative (shingles; Fig. 26.15) if it follows a der- cause matomal distribution. In febrile patients • red cell fragmentation on blood film with widespread vesicles consider chicken- • ↑↑LDH pox or, if there is known eczema, eczema • neurological abnormalities (↓GCS, herpeticum. Suspect dermatitis herpeti- headache, seizures). formis if the vesicles are intensely itchy If any of these is present, seek immediate and occur on the extensor surfaces (see Haematology input, as urgent plasma Fig. 26.11). exchange may be life-saving. Suspect a systemic vasculitis, e.g. polyar- 3 Purpura present? teritis nodosa, Henoch–Schönlein purpura, Classify the rash as purpuric if there are microscopic polyangiitis, cryoglobulinae- dark red or purple macules/patches that do mia, rheumatoid vasculitis or other sys- not blanch with pressure (see Fig. 26.13). temic inflammatory disorder – if there is 240 Rash: Acute generalised skin eruption Step-by-step assessment 26 palpable purpura accompanied by fever, 6 Underlying chronic dermatosis? ↑ESR/CRP, constitutional upset, joint disease and/or renal involvement (↓GFR, Ascertain whether the patient has a back- proteinuria, haematuria). Perform a full ground of skin disease. Enquire about vasculitis/autoimmune ‘screen’ and con- recent changes to dermatological or other sider skin biopsy ± biopsy of other affected medications and ask specifically whether organs. the present eruption resembles previous Also consider cholesterol embolisation or rashes. It is very common for hospital drug reaction – seek Dermatology input if patients to miss their dermatological medi- the cause remains unclear. cations due to lack of prescription or inter- ruption of their regular topical application 4 Pustules present? routine; if this is the case, suspect an acute flare and look for resolution of the rash after Pustules are best thought of as small blisters reinstating routine treatment. filled with pus (see Fig. 26.3). The key diag- nostic conundrum is whether they are Likely drug reaction or infective exanthem. infective or sterile. In both cases, the patient 7 Refer dermatology if persistent or severe may be unwell, with significant constitu- symptoms tional upset. Assume an infective pustulosis, at least Occasionally, serious acute drug eruptions initially, if the patient has a fever and the lack the specific features detailed above; lesions have a follicular appearance (indi- seek prompt dermatological advice in any vidual, palpably raised lesions, following patient with signs of significant systemic the distribution of hair follicles). Suspect upset, mucous membrane involvement or sterile pustulosis due to either pustular pso- associated lymphadenopathy, or if symp- riasis or drug reaction if the pustules have toms are persistent and troublesome. a subcorneal appearance (more superficial, Consider guttate psoriasis and pityriasis often confluent lesions). In either case, rosea if there is an acute papulosquamous admit the patient and seek an urgent der- eruption (see above) over the trunk. Suspect matological opinion. the former if the lesions are ‘drop-like’ (see Fig. 26.5) and there is a history of upper 5 Wheals present? respiratory tract infection within the past 2–3 weeks; suspect the latter if the lesions Classify the rash as urticaria if there are form a ‘Christmas tree’ pattern on the back wheals: transient (<24 hours), erythema- (see Fig. 26.6) and follow a ‘herald patch’. tous, intensely pruritic raised skin lesions Precise identification of infective -exan (see Fig. 26.12). Look for swelling of the thems is seldom required as most do not lips, face and throat, suggesting associated need specific treatment and will settle angioedema; when this is present, patients conservatively, but seek specialist advice may describe the skin sensation as burning if the patient is a returning traveller with rather than itchy. Take a careful food and fever or an unusual rash. drug history to identify possible precipi- Review all recent medications, both tants, although in many cases a cause prescribed and over-the-counter drugs. cannot be identified (idiopathic urticaria). There is significant variation in the mor- Other than avoidance of any identified pre- phology and exposure-to-onset time cipitant, the mainstay of treatment is regular (minutes to years) of cutaneous drug erup- antihistamines; most cases subside quickly tions. If a drug reaction is suspected, e.g. with avoidance of the precipitant and/or a drug from Box 26.1 is involved or there antihistamine treatment. Refer patients is a clear temporal association, attempt to with persistent (>24 hours) or chronic (>6 confirm by trial discontinuation wherever weeks) lesions for outpatient dermatologi- feasible. cal assessment. 241 27 SCROTAL SWELLING

Most causes of scrotal swelling are benign, Torsion of the testis but germ cell tumours are a leading cause Twisting of the testis may occlude its own of malignancy in young men whilst testicu- blood supply. Acute, severe, unilateral tes- lar torsion and strangulated herniae are ticular pain is the dominant presenting surgical emergencies. symptom, often accompanied by nausea Inguinal hernia and vomiting. On examination there may be a red, swollen, exquisitely tender hemis- Inguinal hernia (Fig. 27.1) may occur at any crotum (often too tender to palpate), with age but is increasingly common from the testis lying in a high position due to middle age and is the most frequent cause shortening of the spermatic cord. Suspected of scrotal swelling. Herniated bowel passes torsion mandates immediate surgical cor- through the inguinal ring and may descend rection, as any delay threatens testicular into the scrotal sac. As the swelling arises viability. from the abdominal cavity, it is not possible to ‘get above’ it. Typically, the swelling is Epididymo-orchitis more prominent on standing, associated Inflammation of the epididymis ± testis with a cough impulse and can be pushed (Fig. 27.1) is usually due to sexually trans- back into the abdomen (‘reduced’). A non- mitted infection in younger men, and reducible or ‘incarcerated’ hernia may lead urinary tract infection (UTI) in older men. to bowel obstruction or strangulation with Orchitis without epididymitis occurs in ischaemia. mumps (now less common due to vaccina- Hydrocoele tion). Acute epididymo-orchitis may be dif- ficult to distinguish clinically from torsion. Hydrocoele (Fig. 27.1) is a common cause of It presents with acute scrotal pain and scrotal swelling, especially in older men. swelling, over days rather than hours, often Fluid accumulates within the tunica vagi- accompanied by fever, urinary symptoms nalis, producing painless, cystic swelling and/or urethral discharge. There may be a that typically transilluminates. Most cases tender, swollen epididymis/testis or a reac- are idiopathic, but some have an underly- tive hydrocoele. ing inflammatory or malignant process. With substantial swelling, the underlying Other causes testes may be impalpable. Varicocoeles (Fig. 27.1) are varicosities of Testicular tumour the gonadal vessels and their tributaries that may impair testicular function and feel Germ cell tumours (Fig. 27.1) are the most like a ‘bag of worms’ on palpation. A hae- common malignancy amongst men aged matocoele (collection of blood in the tunica 20–30 years, typically presenting as the inci- vaginalis) may occur following trauma. dental discovery of a painless testicular Epididymal cysts are discrete fluid-filled lump. Scrotal USS confirms the diagnosis swellings arising from the epididymis; and CT thorax/abdomen is used in stag­ spermatocoeles are similar but contain ing; >90% are curable, even if metastasis sperm. Both may occasionally cause dis- has occurred. Alpha-fetoprotein and beta- comfort but are almost always benign. human chorionic gonadotrophin are raised in extensive disease and act as ‘tumour markers’. 242 Scrotal swelling Differential diagnosis 27

Normal Hydrocoele Fig. 27.1 Common causes of scrotal swelling.

Spermatic cord

Epididymis

Testis

Indirect inguinal hernia Epididymitis

Varicocoele Tumour of testicle

243 Scrotal swelling 27 Overview

Full clinical assessment + testicular examination

Yes Torsion / epididymo-orchitis / Urgent surgical 1 Painful and/or inflamed? strangulated hernia review

No

Yes 2 Unable to feel above swelling? Likely inguinal hernia or varicocoele

No Consider USS to Yes delineate 3 Transilluminates? Likely hydrocoele underlying scrotal structures No

Yes 4 Any palpable swelling? Scrotal USS Tumour / spermatocoele / other

No

Reassure; consider follow-up evaluation

Clinical tool: Examination of the scrotum Testicular examination • If you cannot ‘get above’ the swelling, check • Obtain consent and offer a chaperone. for a cough impulse and attempt to reduce • With the patient standing, then supine, the swelling by very gently ‘massaging’ it inspect the scrotum for redness, swelling, back into the abdomen. and position of the testes. • Determine whether the swelling • Wearing gloves, palpate each testis in turn transilluminates using a pen-torch. between forefinger and thumb; identify the • In patients with an acutely painful scrotum spermatic cord and epididymis and assess or tender/inflamed scrotal swelling, check any irregularity, swelling or tenderness. the cremasteric reflex. With the patient’s • Use your fingers to see whether you can thigh abducted and externally rotated, feel above the swelling (Fig. 27.2); if so, it stroke the upper medial aspect – normally, originates in the scrotum. the testis on that side will rise briskly.

toxicity. Seek urgent surgical review, as 1 Painful and/or inflamed? there is a risk of bowel ischaemia. Suspect a strangulated hernia if the swell- If the swelling arises from the scrotum (or ing arises from the inguinal canal (see pain prohibits examination) and is painful, above), is not reducible (or severe pain per- tender, inflamed and/or accompanied by sists despite reduction) and is tender, hot acute severe unilateral scrotal pain, you and red, or associated with systemic MUST exclude testicular torsion. 244 Scrotal swelling Step-by-step assessment 27

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

Fig. 27.2 Assessing the origin of a scrotal swelling.

Consider initial investigation with scrotal non-reducible. If easily reducible, refer for USS if the clinical presentation suggests an outpatient surgical evaluation. alternative diagnosis such as epididymo- orchitis, e.g. urethral discharge, tenderness 3 Transilluminates? localised to epididymis, age >30 years, and none of the following is present: Make a diagnosis of hydrocoele if there is a painless swelling of the scrotum that trans­ • nausea or vomiting illuminates. Consider USS to delineate the • pain duration <24 hours underlying scrotal structures and exclude • high position of the testis an underlying tumour or inflammatory • abnormal cremasteric reflex. mass – especially if there is tenderness, con- In all other cases, arrange immediate sur- stitutional upset or difficulty in palpating gical review without delay for imaging. the testicular structures.

2 Unable to feel above swelling? 4 Any palpable swelling? If it is not possible to palpate above the USS is the investigation of choice in swelling, the swelling is likely to originate scrotal swelling and differentiates malig- from outside the scrotum. nant tumours from other masses, e.g. sper- Suspect a varicocele if it feels like a ‘bag matocoele, with a high degree of accuracy. of worms’; confirm with scrotal USS and Arrange scrotal USS in any patient with a exclude underlying renal cell carcinoma if detectable scrotal lump or swelling – sudden onset, unilateral and right-sided or promptly if there is a high suspicion of not reducible in supine position. malignancy, e.g. painless testicular lump Otherwise, suspect an inguinal hernia – in a young man. Refer to Urology for look for bowel obstruction (p. 32) and further assessment/treatment if the diagno- arrange urgent surgical review if it is sis remains uncertain. 245 28 SHOCK

Shock is a clinical syndrome characterised Other fluid losses by inadequate systemic and specific organ Hypovolaemia may result from burns, diar- perfusion. It is recognised by features of rhoea, vomiting polyuria or from prolonged tissue hypoperfusion (see Box 28.1 below), dehydration, particularly in the elderly. usually with hypotension; however, BP Significant volumes of fluid may also may be maintained until the advanced be lost into the ‘third space’, e.g. in condi- stages of shock, particularly in young, fit tions such as bowel obstruction and acute individuals. pancreatitis. Three processes may cause shock: hypo- volaemia, pump failure (cardiogenic shock) Cardiogenic shock and vasodilatation (distributive shock). Cardiac disorders may cause valvular or These processes can be difficult to distin- myocardial dysfunction, and extracardiac guish, as components of the circulation are disorders may impede cardiac inflow or interdependent and different mechanisms outflow (also known as ‘obstructive’ shock). often coexist e.g. vasodilatation, myocardial Peripheral signs are similar to those of suppression and relative hypovolaemia hypovolaemic shock but the JVP is may occur simultaneously in sepsis. usually raised and there may be pulmonary Many presentations in this book may be oedema as well as features specific to the complicated by shock but here shock is con- underlying cause. Echocardiography is sidered as the primary presenting problem often diagnostic. detected on routine observations or on tar- Myocardial infarction geted examination of a severely or non- Shock may result from large infarcts, par- specifically unwell patient. ticularly in the anterior wall; from smaller Hypovolaemic shock infarcts in patients with pre-existing ven- Decreased intravascular volume reduces tricular impairment; or from structural cardiac filling pressures and cardiac output. complications of myocardial infarction (MI), A compensatory increase in heart rate and such as papillary muscle rupture, ventricu- systemic vascular resistance occurs. Char- lar septal defect or tamponade. acteristic findings are ↓JVP, tachycardia, Left ventricular dysfunction without ↓pulse volume and cool, clammy peripher- infarction ies. Tachycardia may be absent in patients This includes tachy- or bradyarrhy­ on rate-limiting medications, e.g. beta- thmia, acute myocarditis and end-stage blockers, calcium channel antagonists. cardiomyopathy. Haemorrhage Valve disorders Blood loss is not always visible; it may be Examples of valve disorders include pros- left at the scene of an accident or concealed thetic valve dysfunction, endocarditis and within surgical drains. The pelvis, retro- critical aortic stenosis. peritoneum, peritoneum, thorax and thighs can accommodate several litres of extravas- Tension pneumothorax cular blood. In addition to trauma, impor- The urgency of treatment mandates a clini- tant causes include GI bleed (see Ch cal diagnosis. Typical findings include 15), ruptured abdominal aortic aneurysm increasing respiratory distress, tachycar­ (AAA) and ectopic pregnancy. dia and ↓ipsilateral air entry. Tracheal 246 Shock Differential diagnosis 28 deviation is often absent. Immediate decom- accompanied by warm peripheries and pression is essential. ↑pulse volume. Cardiac tamponade Systemic inflammatory response Accumulation of fluid in the pericardial syndrome (SIRS)/sepsis space (pericardial effusion) impedes cardiac In SIRS (see Box 14.1, p. 139), distributive filling. As little as 200 mL of fluid may shock occurs as a result of infection (sepsis) be sufficient if accumulation is rapid, e.g. or other systemic inflammatory response trauma, aortic dissection. Hypotension, e.g. acute pancreatitis. Features of relative tachycardia, ↑JVP and pulsus paradoxus hypovolaemia may predominate initially. are usually present. There may also be Anaphylaxis muffled heart sounds, Kussmaul’s sign (a paradoxical rise in JVP on inspiration) This produces a very rapid onset of bron- and small complexes on ECG. Echocardiog- choconstriction, widespread erythematous raphy will confirm the presence of an rash and severe distributive shock. A pre- effusion, provide evidence of cardiac cipitant (foodstuffs, drugs – particularly compromise and guide therapeutic antibiotics, insect stings) may be identified. drainage. A related problem is transfusion reaction; ABO incompatibility may present with Pulmonary embolism shock as the only initial sign, particularly in Massive pulmonary embolism (PE) typi- unconscious or sedated patients. cally presents with sudden onset of chest Drug causes pain, dyspnoea and hypoxia with shock. Antihypertensives and anaesthetic agents The JVP is usually elevated and the ECG (particularly epidural and spinal anaesthe- may show features of right heart strain. In sia) may cause distributive shock through critically unwell patients, bedside echocar- excessive peripheral vasodilatation. diography may assist the diagnosis. Adrenal crisis Distributive shock Glucocorticoid deficiency may result in dis- In distributive shock, peripheral vasodilata- tributive shock, particularly during acute tion causes a drop in systemic vascular stress e.g. infection, surgery. resistance and ‘relative hypovolaemia’ (↑size of vascular space without corre- Neurogenic shock sponding increase in intravascular volume). Neurogenic shock is a rare form of distribu- A compensatory rise in cardiac output is tive shock associated with direct injury to insufficient to maintain blood pressure. the sympathetic fibres that control vascular Tachycardia and hypotension are often tone.

247 Shock 28 Overview

ABCDE, ECG, ABG

No 1 Clinical features of shock (Box 28.1)? Incipient shock OR consider alternative causes of organ dysfunction / hypotension Yes

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

No

Cause that requires immediate specific Yes Treat and 3 Confirm diagnosis treatment? reassess

No

Yes Urgent echo and 4 Evidence of cardiac failure? Likely cardiogenic shock Cardiology opinion to establish cause No

5 Ongoing assessment and treatment of shock physiology during diagnostic work-up (Fig. 28.1)

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

No

Yes Likely systemic inflammatory SIRS criteria or immunocompromise? Seek source 7 response syndrome / sepsis

No

Yes Treat and 8 Suspect adrenal insufficiency? reassess; Acute adrenal crisis check random cortisol 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 Maintain suspicion of sepsis; consider rarer causes, e.g. neurogenic shock

248 Shock Step-by-step assessment 28

1 Clinical features of shock (Box 28.1)? Cause that requires immediate specific 3 treatment? Use the features in Box 28.1 to identify shock. Tissue hypoperfusion is the defining In some cases, specific interventions to feature. Absolute values of HR and BP are reverse the underlying cause of shock offer less informative than monitoring of trends the only effective treatment and take prec- over time. Some patients may maintain BP edence over further investigation or sup- within normal limits despite organ dys- portive measures (Table 28.1). Most will be function, but consider local pathology if identified and treated as part of the ABCDE there is single organ dysfunction, e.g. oligu- assessment (p. 8). If one of these disorders ria, without clear evidence of haemody- is suspected but the diagnosis remains namic compromise. If the patient falls short uncertain, seek urgent expert assistance, of the criteria in Box 28.1 but you suspect e.g. cardiology review. significant circulatory compromise, pursue a working diagnosis of ‘incipient shock’ 4 Evidence of cardiac failure? and continue through the diagnostic Pulmonary oedema suggests cardiogenic pathway. shock. The most common cause is severe 2 Obvious bleeding source? left ventricular dysfunction from acute MI. Perform (serial) ECG to look for evi- Where shock arises from acute haemor- dence of infarction or ischaemia (Box 6.1, rhage, the initial aims of treatment are to p. 49). Arrange bedside echocardiography minimise further blood loss and restore to assess left ventricular function and adequate circulating volume. Assess resus- exclude mechanical causes (especially acute citation requirements and monitor response mitral regurgitation). to treatment as described in Chapter 15, Patients without pulmonary oedema but Box 15.1. In patients with traumatic haem- with ↑JVP ± peripheral oedema may have orrhage, always consider the possibility of a cardiogenic component to shock. Those an additional cause of shock, e.g. tampon- with right ventricular infarction (suspect ade, tension pneumothorax. with inferior or posterior MI in the previous 72 hours), chronic right heart failure or tri- cuspid regurgitation may be inadequately filled despite↑ JVP and will respond to fluid challenge. Otherwise, echocardiography Box 28.1 Clinical features of shock is mandatory to look for evidence of Haemodynamic right ventricular dysfunction, tamponade and PE. • Systolic BP <100 mmHg or a drop of Patients with cardiogenic shock require >40 mmHg from baseline invasive monitoring and specialist inter- • Pulse >100/min ventions; if appropriate, urgent cardiology Tissue hypoperfusion and ICU referral is essential. • Skin: capillary refill time >2 sec or cold/ pale/mottled extremities Ongoing assessment and treatment of 5 shock physiology during diagnostic • Renal: oliguria (<0.5 mL/kg/hr) or ↑serum work-up (Fig. 28.1) creatinine (acute) • CNS: GCS <15, confusion or agitation In the absence of obvious haemorrhage, major cardiac dysfunction or a rapidly • Global: lactate (in the absence of ↑ reversible cause of shock, the next step is to hypoxaemia) initiate treatment and assess response. As ≥2 of the above indicate shock shown in Fig. 28.1, the effect of repeated fluid challenge on haemodynamic variables 249 Shock 28 Step-by-step assessment

Table 28.1 Rapidly reversible causes of shock Reversible cause Suspect if Test to confirm Specific intervention Tension Respiratory distress/tracheal Nil – treat Needle aspiration pneumothorax deviation/unilateral hyper- immediately resonance, ↓ breath sounds Tachyarrhythmia VT or SVT >150 bpm Nil – treat DC cardioversion immediately Bradyarrhythmia 3rd degree atrioventricular Nil – treat Atropine, adrenaline, block or HR <40 bpm immediately external or transvenous pacing Anaphylaxis Respiratory distress, stridor, Nil – treat Adrenaline, IV fluid wheeze, angioedema, rash, immediately precipitant ST elevation MI Chest pain, ECG criteria Nil – treat Primary angioplasty (Box 6.1, p. 49) immediately or thrombolysis Pulmonary embolism Dyspnoea, hypoxia (especially CTPA if stable; Thrombolysis with clear lung fields), chest urgent pain, ↑ JVP risk factors, ECG echocardiogram changes (p. 56) if unstable; nil if peri-arrest Cardiac tamponade ↑ JVP, pulsus paradoxus, Echocardiogram Pericardiocentesis small QRS complexes on ECG

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 impairment or Give fluid challenge shock persists after ≥3 L IV fluid Corrected hypovolaemia: e.g. 250 mL over 2–5 min • Look for underlying causes, e.g. blood loss • Monitor closely for recurrent shock 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. Fig. 28.1 Shock physiology: The cycle of assessment

250 Shock Step-by-step assessment 28 and tissue perfusion helps to delineate the 8 Suspect adrenal insufficiency? mechanism(s) of shock and guide further resuscitation and treatment. This process Adrenal insufficiency is often overlooked, should be carried out in parallel with con- as many patients have fever and are tinued evaluation for a specific underlying assumed, at least initially, to have septic cause. shock. Always consider the diagnosis and look for clinical/biochemical features. Suspect pelvic or intra-abdominal Useful indicators include prominent GI 6 pathology? symptoms (almost always present but non-specific), pigmentation of recent scars, Request urgent surgical review if you palmar creases and mucosal membranes, suspect acute abdominal or pelvic pathol- vitiligo, ↓Na+, ↑K+ and hypoglycaemia. ogy. AAA or ruptured ectopic pregnancy Even a blood glucose at the low end of require immediate intervention. Suspect normal (3.5–4.5 mmol/L) suggests an inad- ruptured AAA in patients >40 years with equate ‘stress response’. If you suspect known AAA, a pulsatile abdominal mass adrenal insufficiency, send blood for a or sudden-onset, severe abdominal/back. random cortisol level then treat with IV Suspect ruptured ectopic pregnancy in any hydrocortisone without waiting for the woman of child-bearing age with recent- results. A short ACTH (Synacthen) test may onset lower abdominal pain or PV bleeding; be helpful but takes 30 minutes to perform perform an immediate bedside urine preg- and should not delay empirical treatment nancy test and consider USS if sufficiently in critically unwell patients. Remember stable. Other pointers to an underlying sur- that any patient taking systemic steroids gical cause include severe abdominal pain for ≥3 months will have some adrenal +/− tendernes/guarding/peritonism, air suppression. under the diaphragm on CXR or ↑amylase. Look for intestinal obstruction on abdomi- 9 Distributive or cardiogenic pattern? nal X-ray in patients with abdominal pain/ distension and repeated vomiting. Request Identify the presence of relative or absolute an urgent surgical review. See Chapter 4 for hypovolaemia (see Fig. 28.1). Look for con- further details. cealed sources of haemorrhage, dehydra- tion (reduced skin turgor, dry mucous Evidence of infection/inflammation or membranes) and causative/contributory 7 predisposition to infection? factors, e.g. history of diarrhoea and vomiting, reduced intake, diuretics, Look for features of SIRS and sepsis antihypertensives. (Box 14.1, p. 139). If present, perform a Check for ketonuria and metabolic acido- full septic screen, (see p. 140) to identify a sis to exclude diabetic ketoacidosis. If the likely source but do not delay antibiotics. response to IV fluids suggests a distributive Assume sepsis in any patient with immuno­ or cardiogenic element, involve ICU, insti- compromise until proven otherwise. See tute appropriate (invasive) monitoring and ‘Surviving Sepsis’ guidelines (http:// consider urgent echocardiography. www.survivingsepsis.org/GUIDELINES/ Pages/default.aspx).

251 TRANSIENT LOSS OF CONSCIOUSNESS: 29 SYNCOPE AND SEIZURES

Transient loss of consciousness (T-LOC) • Reflex (neurally mediated) syncope presents a particular diagnostic challenge. – reflex vasodilatation and/or The event has usually resolved by the time bradycardia occurs in response to a of assessment and critical elements of the particular ‘trigger’ e.g. ‘vasovagal’ or history are unknown to the patient. Witness ‘carotid sinus’ syncope. accounts are therefore extremely valuable. Seizure Diagnosis often relies on the problem recur- ring and careful risk stratification of patients Disordered electrical activity affecting the is essential to identify those who require whole brain (‘generalised’ seizure) can lead admission and those who can be safely to LOC. This may be primary or result from evaluated as outpatients. a focal (partial) seizure that subsequently spreads to the whole brain (secondary gen- Syncope eralisation). In the absence of secondary ‘Syncope’ denotes T-LOC resulting from generalisation, partial seizures may cause global cerebral hypoperfusion, typically altered consciousness (complex partial sei- associated with a BP <60 mmHg for ≥6 zures) without LOC. Epilepsy is the ten- seconds. Syncope can be divided into dency to have recurrent seizures. Factors four subtypes, based on the underlying that may provoke seizures in patients with aetiology: epilepsy are shown in Box 29.1. • Arrhythmia-related syncope – due to Hypoglycaemia transient compromise of cardiac output Hypoglycaemia may cause impairment of by a tachy- or bradyarrhythmia, e.g. consciousness that resolves with correction ventricular tachycardia, complete heart of blood glucose. Most cases are iatrogenic, block. from treatment of diabetes with insulin • Cardiac syncope – due to structural or sulphonylurea drugs. Causes of ‘spon­ heart disease, especially left taneous’ hypoglycaemia include alcohol, ventricular outflow obstruction e.g. liver failure, insulinoma and adrenal severe aortic stenosis, hypertrophic insufficiency. obstructive cardiomyopathy. Acute pulmonary embolism (PE) or aortic Functional disorders (apparent T-LOC) dissection may also cause syncope. ‘Pseudoseizure’ and ‘pseudosyncope’ are (Arrhythmia-related syncope and terms used to describe episodes that cardiac syncope are often grouped resemble seizure and syncope respectively together under the term ‘cardiac but do not have an underlying somatic syncope’ but it is useful to consider mechanism i.e. no epileptiform activity or them separately). cerebral hypoperfusion. They can present • Orthostatic syncope – due to failure of major diagnostic difficulty and may require homeostatic maintenance of BP on specialist assessment. Features that may assuming an upright posture e.g. raise suspicion of a functional aetiology for caused by antihypertensive symptoms over true loss of consciousness medications. are shown in Box 29.2. 252 TRANSIENT LOSS OF CONSCIOUSNESS Differential diagnosis 29

Box 29.1 Trigger factors for seizures Box 29.2 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 • Physical/mental exhaustion • Purposeful movements during apparent • Intercurrent infection period of LOC • Metabolic disturbance (↓Na+, ↓Mg2+, ↓Ca2+, • Established diagnosis of other functional uraemia, liver failure) disorder e.g. chronic fatigue syndrome • Non-compliance with medication or drug interaction • Flickering lights absence, as well as conditions which may mimic T-LOC, including falls, functional disorders, drug/alcohol intoxication. Tran- Other causes sient ischaemic attacks present with focal When the clinical picture is not suggestive neurological signs and symptoms and very of either tonic-clonic seizure or syncope, rarely cause T-LOC. Concussion is a consider rarer causes such as cataplexy, common cause of T-LOC associated with narcolepsy and atypical seizures, e.g. head trauma.

253 TRANSIENT LOSS OF CONSCIOUSNESS 29 Transient loss of consciousness: overview

ABCDE

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

Yes

No 2 Features of shock? Assess as per shock (Ch. 28)

Yes

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

Yes

Documented BM <3.0 mmol/L or strong Yes 4 Likely hypoglycaemia clinical suspicion of hypoglycaemia?

No

Full clinical assessment, collateral history, ECG

Yes 5 Any red flag cardiac features (Box 29.3)? Admit and refer to Cardiology

No

>1 seizure features (Box 29.4) OR 1 Yes 6 Likely seizure See Seizure (p. 258) seizure feature and no syncope features?

No

>1 syncope features (Box 29.5) and no Yes 7 Likely syncope See Syncope (p. 260) seizure features

No

Likely seizure or syncope – make working diagnosis if possible 8 Consider functional cause if atypical features (Box 29.2)

254 TRANSIENT LOSS OF CONSCIOUSNESS Transient loss of consciousness: step-by-step assessment 29

1 Definite loss of consciousness? measurement whenever feasible but do not wait for the result to initiate treatment. In the absence of a clear witness account Some patients may have had corrective this may be difficult to establish – ask the treatment prior to assessment without a BM patient to recount the events in as much recording. In these circumstances, suspect detail as possible. hypoglycaemia if the episode resolved with Assume T-LOC if: administration of carbohydrate/glucagon • a witness confirms a period of and was preceded by symptoms of auto- unresponsiveness nomic activation (sweating, trembling, • the patient describes ‘waking up’ or hunger)/neuroglycopenia (poor concen­ ‘coming to’ on the ground, especially if tration, confusion, incoordination) or there is no recollection of falling occurred in a patient taking insulin or a • there are facial injuries (most conscious sulphonylurea. patients can protect their face as they fall). 5 Any red flag cardiac features (Box 29.3)? T-LOC is unlikely if: Always, exclude a serious underlying • there was no loss of postural tone cardiac cause for LOC if any of the features • the patient recalls landing on the in Box 29.3 is present. Continue through the ground diagnostic pathway but admit the patient to • a witness account suggests interaction hospital and discuss with a cardiologist. with or awareness of the environment 1 seizure feature (Box 29.4) OR 1 seizure throughout the episode. 6 > feature and no syncope features? 2 Features of shock? Differentiating between seizure and Syncope may be a manifestation of major syncope is a key step in the assessment haemodynamic compromise, e.g. massive process. Features that strongly suggest PE, severe GI bleed. If you find evidence of seizure are listed in Box 29.4. Note that shock (Box 28.1, p. 249) during the ABCDE vague descriptions of ‘jerking’, ‘twitching’ assessment, assess as per Chapter 28. or ‘fitting’ are unhelpful since ‘seizure-like’ movements may occur in up to 90% of 3 Complete recovery of consciousness? syncopal episodes. In contrast to seizure, the abnormal movements in syncope The diagnostic pathway below is appropri- are usually non-rhythmic and brief (<15 ate for a transient episode of LOC. If there seconds). is evidence of persistently ↓GCS during the The episode of T-LOC is highly likely to ABCDE assessment, evaluate in the first have been a seizure if >1 of the features in instance as described in Chapter 7. Box 29.4 are present. Seizure is also likely if Documented BM 3.0 mmol/L or strong any of these features are present, and there 4 < clinical suspicion of hypoglycaemia? are no specific pointers to syncopeBox ( 29.5). In both cases, proceed to ‘Seizure’ Attributing an episode of reduced con- (p. 258). sciousness to hypoglycaemia requires: 1 syncope features (Box 29.5) and no • demonstration of low blood glucose in 7 ≥ association with LOC seizure features • recovery with restoration of Suspect syncope if any of the features in normoglycaemia. Box 29.5 and none of those in Box 29.4 Corroborate a low capillary blood glucose are present – proceed to ‘Syncope’ meter reading (‘BM’) with a laboratory (p. 260).

255 TRANSIENT LOSS OF CONSCIOUSNESS 29 Transient loss of consciousness: step-by-step assessment

episode favour a diagnosis of seizure; pre- Likely seizure or syncope – make working vious episodes of pre-syncope, witnessed 8 diagnosis if possible. Consider functional pallor during LOC, known cardiovascular cause if atypical features (Box 29.2) disease and an abnormal ECG favour Where differentiation between seizure and syncope. Urinary incontinence is not a syncope is not straightforward, other clini- useful discriminating feature. Consider a cal features may be helpful: amnesia for functional aetiology if atypical features are events before and after the episode, and present (Box 29.2). Have a low threshold for headache or aching muscles after the specialist input if the cause remains unclear.

256 TRANSIENT LOSS OF CONSCIOUSNESS Transient loss of consciousness: step-by-step assessment 29

Box 29.3 Red flag cardiac features Box 29.4 Clinical features strongly suggestive of seizure • T-LOC during exertion • LOC preceded by typical aura e.g. • Severe valvular heart disease, coronary unusual smell, ‘rising’ sensation in artery disease or cardiomyopathy abdomen, déjà vu. • Family history of unexplained premature • A witness account of abnormal tonic-clonic sudden death limb movements that are: • Previous ventricular arrhythmia or high • coarse and rhythmic risk for ventricular arrhythmia e.g. prior • maintained for >30 seconds (ask myocardial infarction or ventricular surgery witness to demonstrate movements) • Sustained or non-sustained ventricular • A witness account of head-turning to one tachycardia on telemetry side, unusual posturing, cyanosis or • High-risk ECG abnormality: automatisms such as chewing or lip- • Bifascicular or trifascicular block (see smacking during the episode Fig. 29.3) • Severely bitten, bleeding tongue or bitten • New T wave or ST segment changes lateral border of tongue (see Box 6.1, p. 49) • A prolonged period (>5 minutes) of • Sinus bradycardia <50 bpm or sinus confusion or drowsiness after the episode pause >3 seconds • Second-degree AV block or complete heart block (Figs 29.1, and 29.2) Box 29.5 Clinical features strongly suggestive • Evidence of pre-excitation (see Fig. 25.2, of syncope p. 225) • LOC preceded by chest pain, palpitation, • Marked QT interval prolongation e.g. dyspnoea, light-headedness or typical QTc 500 milliseconds > ‘pre-syncopal’ prodrome • Brugada pattern: right bundle branch • LOC after standing up, after prolonged block with ST elevation in leads V –V 1 3 standing, during exertion or following a (see Fig. 29.5) typical precipitant: • unpleasant sight, sound, smell or pain • venepuncture • micturition • cough • large meal • Brief duration of LOC (<1 minute) • Rapid return of clear-headedness after LOC

257 TRANSIENT LOSS OF CONSCIOUSNESS 29 Seizure: overview

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

Urgent laboratory Yes Likely hypoglycaemic 1 BM <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?

Yes

Urgent High suspicion of underlying Yes 3 neuroimaging CNS pathology intracranial pathology? ± LP

No

Yes 4 Established 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 Seek input from Neurology if any concerns

1 BM <3.0 mmol/L? diagnosis requires >30 minutes of continu- ous seizure activity or repeated seizures Consider hypoglycaemia at the outset without full recovery in between, but a because it: lower time threshold facilitates early recog- • is easily identified and corrected nition and action. • can cause permanent neurological Provide appropriate anticonvulsant damage if not corrected therapy e.g. IV diazepam, and supportive • needs to be excluded prior to measures concurrently with clinical assess- assessment for other causes. ment. Rapidly exclude or correct reversible factors (see below) and seek urgent input If the bedside glucose reading is from ICU ± the Neurology team. <3.0 mmol/L, assess and treat as described High suspicion of underlying intracranial above. 3 pathology? 10 min continuous seizure/recurrent 2 > seizures without full recovery in between? Seizure may be a manifestation of impor- tant underlying intracranial pathology, Status epilepticus is a medical emergency such as haemorrhage, infarction, infection and requires urgent intervention. Formal or space-occupying lesion. 258 TRANSIENT LOSS OF CONSCIOUSNESS Seizure: step-by-step assessment 29

Box 29.6 Indications for urgent neuroimaging 5 Clear precipitating factor? in seizure Important causes of seizure in adults • Status epilepticus without epilepsy include alcohol (excess • Confusion, ↓GCS or focal neurological signs or withdrawal), recreational drug misuse >30 minutes post-fit e.g. cocaine, amphetamines, drug overdose • Recent head injury e.g. theophylline, tricyclic antidepressants, severe metabolic disturbance ↓Na+, ↓Mg2+, • Acute severe headache preceding seizure ↓Ca2+ and CNS infection. Look for all of • Meningism these factors and refer for specialist neuro- • Known malignancy with potential for brain logical evaluation (see below) if none is metastases evident. • Immunosuppression (especially HIV) Probable new diagnosis of epilepsy. Refer 6 to a neurologist as inpatient or outpatient Admit any patient with repeated seizures or a significant causative factor that requires Arrange urgent neuroimaging, usually inpatient treatment. Consider early dis- CT, if the patient is at risk of these patho­ charge only if patients have fully recovered, logies (Box 29.6). Also consider neur­ exhibit no neurological abnormalities and oimaging to exclude new intracranial have a responsible adult to accompany and pathology in any patient with known stay with them. Seek advice from a neurolo- epilepsy who exhibits a change in seizure gist if you have any concerns. type or pattern without an apparent Arrange neuroimaging for all first-fit epi- precipitating factor. sodes in patients >20 years or with focal Provided there are no contraindications, features. Depending on local resources, perform a lumbar puncture (p. 168), follow- imaging may be performed through the ing CT, if there are features suggestive of outpatient clinic, provided there are no CNS infection, e.g. unexplained fever, men- indications for urgent imaging (see Box ingism, new rash. 29.6) and a ‘first-fit’ follow-up service is 4 Established diagnosis of epilepsy? available. Further investigation may not be required in patients with a pre-existing In patients with known epilepsy, address diagnosis of epilepsy who have fully recov- all factors that may have lowered seizure ered following a typical, uncomplicated fit. threshold (see Box 29.1) or triggered the Prior to discharge, inform all patients of event. Routine checking of anticonvul­ statutory driving regulations (in the UK see sant drug levels is usually not indicated www.dft.gov.uk/dvla/medical) and advise but consider it if there has been a then to avoid activities where LOC may be recent change in medication or suspected dangerous e.g. swimming, operating heavy non-compliance. machinery, cycling.

259 TRANSIENT LOSS OF CONSCIOUSNESS 29 Syncope: overview

1 Risk-stratify to determine need for inpatient investigation

Yes Arrhythmia-related syncope OR 2 Diagnostic ECG recording? Cardiac ischaemia-related syncope

No

Clinical suspicion of pulmonary Yes Urgent 3 Confirm diagnosis embolism or aortic dissection? imaging

No

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

No

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

No

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

No

Yes Consider carotid 7 Typical precipitant or prodrome? Likely reflex syncope sinus massage if >40 years No

Diagnosis uncertain (40% of cases): If single episode, low risk, no further investigations required If atypical features (Box 29.4), consider pseudosyncope If recurrent syncope, consider tilt test, Holter monitor, implantable loop recorder or refer Cardiology

260 TRANSIENT LOSS OF CONSCIOUSNESS Syncope: step-by-step assessment 29

Risk-stratify to determine need for 2 Diagnostic ECG recording? 1 inpatient investigation Mobitz type II 2nd degree AV block (Fig. Admit all syncopal patients with red flag 29.1), complete heart block (Fig. 29.2), pro- cardiac features (see Box 29.3) and discuss longed pauses, ventricular tachycardia or promptly with the Cardiology team. Risk very rapid supraventricular tachycardia prediction tools like the San Francisco (>180/min) on the presenting ECG or Syncope Rule (Box 29.7) can help to pre­ telemetry establish an arrhythmic cause of vent unnecessary admissions. Consider dis- syncope. Arrhythmia-related syncope is charge with outpatient investigation if also highly likely with persistent sinus the patient has recovered fully and has no bradycardia <40 bpm, alternating left and other medical problems and none of the San right bundle branch block or pacemaker Francisco Syncope Rule risk factors; other- malfunction with pauses. wise, admit for a period of observation ECG evidence of acute ischaemia sug- and investigation. gests an arrhythmia secondary to ischae- mia, e.g. ventricular tachycardia, or cardiac Box 29.7 San Francisco Syncope Rule ischaemia-related syncope. Discuss urgently with a cardiologist if • History of congestive cardiac failure any of the above features is present. • Haematocrit/packed cell volume <30% Clinical suspicion of PE or aortic 3 • ECG abnormality* dissection? • Dyspnoea These conditions may present with syncope, • Systolic BP <90 mmHg at presentation although this is rarely the predominant Treat as high-risk if any of the above features symptom. You must exclude both if syncope is present occurs in the context of sudden-onset chest 75–98% sensitivity but only ~50% specificity pain with no obvious alternative explana- for an adverse event in the next 30 days tion. Also consider PE in syncopal patients *Any rhythm other than sinus rhythm or any new change with dyspnoea, hypoxia, evidence of deep compared with previous ECG. Quinn J, et al. Ann Emerg Med. vein thrombosis or major thromboembolic 2006;47(5):448–54. risk factors. Suspect aortic dissection if there is a new early diastolic murmur, pulse

PPPPPPPPPPP Fig. 29.1 Mobitz type II atrioventricular block.

* *

Fig. 29.2 Complete heart block. Arrows indicate P waves. 261 TRANSIENT LOSS OF CONSCIOUSNESS 29 Syncope: step-by-step assessment

deficit or widened mediastinum on CXR. • previous MI or significant structural See Chapter 6 for further details. heart disease, e.g. cardiomyopathy, aortic stenosis Clinical or ECG features that suggest 4 • any of the following ECG abnormalities: structural heart disease? • LBBB (Fig. 6.5, p. 53), bi- or Echocardiography may identify ‘structural’ trifascicular block (Fig. 29.3) causes of cardiac syncope e.g. severe aortic • sinus bradycardia <50 bpm stenosis, hypertrophic cardiomyopathy, • Mobitz type I 2nd degree AV block prolapsing atrial myxoma, or conditions (Fig. 29.4) that predispose to arrhythmia e.g. severe • sinus pause >3 seconds LV systolic impairment. • evidence of pre-excitation (Fig. 25.2, Request an echocardiogram if there is p. 225) exertional syncope, a family history of • prolonged QT interval (QTc >440 sudden unexplained death, a new murmur, milliseconds in men or >460 clinical features of cardiac failure, or (unless milliseconds in women) performed recently) a history of MI, cardio- • Brugada pattern: RBBB with ST myopathy, valvular heart disease or con- elevation in leads V1–V3 (Fig. 29.5) genital heart disease. Discuss with a • features of arrhythmogenic right cardiologist if any relevant abnormalities ventricular cardiomyopathy: negative are detected. T waves in leads V1–V3 and epsilon waves Clinical or ECG features that suggest • pathological Q wave. 5 arrhythmia-related syncope? • any ECG abnormality or history of cardiovascular disorder in the absence Suspect an arrhythmic aetiology for syncope of a typical prodrome or precipitant for in the following circumstances: reflex or orthostatic syncope. • sudden-onset palpitation rapidly followed by syncope The correlation of a syncopal episode • syncope during exertion or while supine with a documented rhythm disturbance is

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 29.3 Trifascicular block.

P P PPP PPPPP PP P Fig. 29.4 Mobitz type I atrioventricular block. 262 TRANSIENT LOSS OF CONSCIOUSNESS Syncope: step-by-step assessment 29

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 29.5 Brugada syndrome. the gold standard for diagnosis of Look for an underlying cause of postural arrhythmia-mediated syncope. This is fre- hypotension. In severe form it may reflect quently challenging, particularly when syn- fluid loss, e.g. major haemorrhage or copal episodes are infrequent. The choice severe dehydration. Other causes include of investigation and degree of persistence Parkinson’s syndromes, autonomic neu- depend on the risk of life-threatening ropathy and drugs, e.g. antihypertensives, arrhythmia and frequency of syncope. vasodilators (especially sublingual nitro- Admit patients with red flag cardiac fea- glycerine) and diuretics, particularly in tures (see Box 29.3) immediately for con- the elderly. tinuous inpatient ECG monitoring. Arrange Holter monitoring (1–7-day tape) if symp- 7 Typical precipitant or prodrome? toms are occurring frequently. Consider an A clear precipitating trigger, e.g. intense event recorder (external or implanted) if emotion, venepuncture or prolonged there is a high suspicion of arrhythmia but standing (vasovagal syncope) or coughing, episodes are infrequent or prove difficult to sneezing or micturition (situational syn­ capture by other methods. cope), together with typical prodromal symptoms, strongly suggests reflex syn­ Syncope after standing up with 6 documented postural hypotension? cope, especially in patients with no ECG or clinical evidence to suggest structural heart Diagnose orthostatic syncope if there is: disease or arrhythmia. Consider tilt-table • a history of light-headedness shortly testing in cases of diagnostic doubt. Carotid after standing, followed by brief LOC sinus hypersensitivity is a form of reflex • a documented postural BP drop (of syncope and is usually diagnosed with ≥20 mmHg in systolic BP or ≥10 mmHg carotid sinus massage (CSM). CSM should in diastolic BP within 3 minutes of be avoided in patients with a history of cer- moving from lying to standing). ebrovascular accident/transient ischaemic attack or a carotid bruit, and requires con- In other circumstances, it may be difficult tinuous ECG monitoring; it is diagnostic if to distinguish orthostatic from reflex syncope is reproduced in the presence of syncope, e.g. when symptoms occur with asystole lasting >3 seconds. prolonged standing.

263 APPENDIX

Normal values for biochemical tests in venous blood Reference range 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 10–45 U/L – (AST) Bilirubin (total) 2–17 µmol/L 0.12–1.0 mg/dL Calcium (total) 2.12–2.62 mmol/L 4.24–5.24 meq/L or 8.50–10.50 mg/dL Chloride 95–107 mmol/L 95–107 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

CO2 (total) 22–30 mmol/L 22–30 meq/L C-reactive protein (CRP) <5 mg/L Highly sensitive CRP assays also exist which measure lower values and 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 – Creatinine 60–120 µmol/L 0.68–1.36 mg/dL Gamma-glutamyl transferase 5–55 U/L – (GGT) Glucose (fasting) 3.6–5.8 mmol/L 65–104 mg/dL

Glycated haemoglobin (HbA1c) 5.0–6.5% – Lactate 0.6–2.4 mmol/L 5.40–21.6 mg/dL Lactate dehydrogenase (LDH) 208–460 U/L – (total) 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 Urate Male 0.12–0.42 mmol/L 2.0–7.0 mg/dL Female 0.12–0.36 mmol/L 2.0–6.0 mg/dL Urea 2.5–6.6 µmol/L 15–40 mg/dL

264 APPENDIX 

Arterial blood analysis Reference range Analysis SI units Non-SI units Bicarbonate 21–29 mmol/L 21–29 meq/L Hydrogen ion 37–45 nmol/L pH 7.35–7.43

PaCO2 4.5–6.0 kPa 34–45 mmHg

PaO2 12–15 kPa 90–113 mmHg

Oxygen saturation (SpO2) >97%

Haematological values Reference range Analysis SI units Non-SI units Bleeding time (Ivy) <8 min – Blood volume Male 75 ± 10 mL/kg – Female 70 ± 10 mL/kg – Coagulation screen Prothrombin time 8.0–10.5 sec – Activated partial thromboplastin time 26–37 sec – D-dimer Routine <0.2 mg/L Sensitive (for venous thromboembolism) Variable threshold – (dependent on method) Erythrocyte sedimentation rate Higher values in older patients are not necessarily abnormal Adult male 0–10 mm/hr – Adult female 3–15 mm/hr – Ferritin Male 17–300 µg/L 17–300 ng/mL Pre-menopausal female 7–280 µg/L 7–280 ng/mL Post-menopausal 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 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 4.0–11.0 × 103/mm3

265 APPENDIX 

Reference range Analysis SI units Non-SI units Differential white 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 0.04–0.4 × 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 Female 3.8–5.8 × 1012/L 3.8–5.8 × 106/mm3 Red cell lifespan 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: Reproduced with permission from Innes JA 2009. Davidson’s Essentials of Medicine. Edinburgh: Churchill Livingstone.

266 INDEX

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

A electrocardiographic airway abbreviated mental test, 14, 15b, abnormalities associated assessment of, 8b–10b, 10f 79, 221 with, 52b–56b manoeuvres for opening, 10f ABCDE assessment approach, 7, non-cardiac causes of, 62 obstruction of, 8b–10b 8b–10b overview of, 58f alcohol abdomen acute cholecystitis, 36 acute intoxication, 82 palpable mass in, 43 acute coronary syndromes. See altered consciousness caused regions of, 27f also myocardial infarction by, 74 abdominal aortic aneurysm, 31, acute chest pain caused by, chronic excess of, 179 33, 251 48–50 delirium caused by, 82 abdominal computed clinical probability of, 61 withdrawal from, 82 tomography, 43 electrocardiographic alcohol history, 11b abdominal pain abnormalities in, 49b alcoholic hepatitis, 172, 179, 180t acute epigastric pain associated alpha-fetoprotein, 242 assessment of, 31–33 with, 35 altered consciousness causes of, 26–27 history-taking findings, 60 assessment of, 73–75 characteristics of, 26 symptoms of, 59b causes of, 70–75 lower, 33, 38f, 39–40 acute diarrhoea, 32, 90–93, 90f overview of, 72f overview of, 30f acute dyspnoea toxidromes associated with, upper, 33, 34f, 35–36 arterial blood gases, 115b 74–75, 74t chronic assessment of, 113, 115, 115b, American College of assessment of, 42–43 119–126 Rheumatology/European differential diagnosis of, causes of, 110 League Against 27–43 in chronic obstructive Rheumatism, 183t overview of, 41f pulmonary disease, 115, amylase, 35 lower, 29 119 amyotrophic lateral sclerosis, ABO incompatibility, 139 definition of, 110 199 abscess, breast, 44 overview of, 112f anaemia accidental trip, 216–223, 219b acute exanthems, 237 assessment of, 134–135 achalasia, 107 acute gastritis, 36–37 fatigue caused by, 131–135 acid–base status, 115 acute glaucoma, 165, 170 microangiopathic haemolytic, acidosis, 115b, 195 acute gynaecological pathology, 134 metabolic, 115b, 117, 195, 39 microcytic, 134 251 acute haemorrhage, 151b normocytic, 135 respiratory, 115b acute hepatitis, 172 anal disorders, 149–155 acoustic neuroma, 94 acute hyponatraemia, 86 analgesic headache, 165 acromegaly, 12b–13b, 13t acute kidney injury, 90, 190, anaphylaxis, 8b–10b, 247, 250t ACTH test, 251 192b, 193 angina pectoris activities of daily living, 16 acute liver failure, 82–83, 172, assessment of, 69 acute abdominal pain 173b, 178–181 coronary artery disease and, assessment of, 31–33 acute liver injury, 172–174, 67–68 causes of, 26–27 178–179 intermittent chest pain caused characteristics of, 26 acute pancreatitis, 35b by, 50–65 lower, 33, 38f, 39–40 acute pericarditis, 49, 52b–56b, laboratory investigations for, overview of, 30f 56, 56f, 60 69b, 126 upper, 33, 34f, 35–36 acute right heart strain, 52b–56b, manifestations of, 126 acute alcohol intoxication, 82 57f severity of, 69 acute alcoholic hepatitis, 172 acute urinary retention, 40 stable, 67, 69 acute appendicitis, 33–35, acute viral hepatitis, 172 unstable. See unstable angina 39–40 acute-phase response, 190 angina symptom score, 67, 67b acute chest pain adrenal crisis, 247 angioedema, 235–236 algorithm for, 58f adrenal insufficiency, 132–133, anhedonia, 132 assessment of, 59–62 251 ankle : brachial pressure index, causes of, 48–50 airflow obstruction, 126t 215

267 INDEX 

ankylosing spondylitis, 210 atrial flutter with 2: 1 AV block, fibrocystic change as cause of, ‘antalgic’ gait, 223 224, 226f, 231 45 anticonvulsants, 258 atrial tachycardia, 224 palpable, 47 anxiety atrioventricular nodal re-entry suspicious features of, 44b acute chest pain caused by, 50 tachycardia, 224 ultrasound evaluations, 44 intermittent chest pain caused aura, 164, 165b breathing assessment, 8b–10b by, 51–62, 68 auscultation of heart, 8b–10b bronchial tumours, 160 aortic dissection, 48, 56, 59, 60b, autoimmune hepatitis, 172 bronchiectasis, 160, 163 62, 261 avascular necrosis, 183–185 Brown-Séquard syndrome, 196 aortic stenosis, 69 axillary lymph nodes, 47b Brugada pattern, 262, 263f aorto-duodenal fistula, 148–152 Budd–Chiari syndrome, 172, 177 appendicitis, acute, 33–35, 39–40 B bulbar palsy, 106, 107t, 109 arms bacterial meningitis, 164, 168 bursitis, 182 neurological examination of, Baker’s cyst, 187, 189 12b–13b Bamford classification of stroke, C weakness of. See limb 208, 209b CAGE questionnaire, 179 weakness benign paroxysmal positional calcium pyrophosphate arrhythmias. See also specific vertigo, 94, 99 dihydrate crystals, 185 arrhythmia benign thunderclap headache, cancer diagnosis of, 229 164 bone, 183 presyncope caused by, 94, benzodiazepines, 81–82 breast, 44–47, 44b 103 beta-human chorionic colon, 29 syncope caused by, 252, gonadotrophin, 242 colorectal, 88, 93, 149, 155b 261–262 bilateral limb weakness gastric, 28 arterial blood gases, 115b assessment of, 199, 201–202 lung, 111, 161b, 163 arteriovenous malformations, overview of, 198f oesophageal, 106 149 biliary colic, 28, 36, 42 ovarian, 29 arthritis biliary disease, 173–174 pancreatic, 29, 174 reactive, 182–183 biliary sepsis, 36 renal tract, 42 rheumatoid, 183t, 185 bladder outflow obstruction, 193 urinary tract, 157b septic, 182 bleeding. See also haemorrhage capillary refill time, 8b–10b ascending cholangitis, 173 lower gastrointestinal, 155b carbon monoxide poisoning, 75 ascites, 172, 177 rectal. See rectal bleeding cardiac disease, structural asphyxiation, 162 upper gastrointestinal, 149 echocardiography of, 262 assessment. See also specific variceal, 152 presyncope caused by, 94, 103 disorder, assessment of blisters, 239 cardiac syncope, 252 clinical. See clinical blood glucose, 73 cardiac tamponade, 247, 250t assessment bloody diarrhoea, 32, 91 cardiogenic shock, 246–247, of elderly patients, 15–17 body surface area, 237–241, 239b 249–251 of frail patients, 15–17 body temperature, 73 cardiorespiratory dysfunction, phases of, 7 bone cancer, 183 132 of sick patient, 7–11 bowel obstruction carotid pulse, 8b–10b step-by-step, 21 large, 32f carotid sinus massage, 263 asterixis, 82, 178f small cellulitis, 140b–143b, 187, 189 asthma radiographs of, 32f central nervous system acute exacerbation of, subacute, 29 infection, 73, 82–83 119–120, 120t bradyarrhythmia, 226–231, 250t cerebellar ataxia, 223 angina versus, 68 bradycardia, 8b–10b, 131 cerebral embolism, 208 intermittent chest pain caused bradykinesia, 223 cerebral venous thrombosis, 164 by, 51 breast abscess, 44 cerebrospinal fluid analysis, severe, 120t breast cancer, 44–47, 44b 168b–171b, 169t

signs and symptoms of, 123 breast cysts, 45 CHADS2 score, 231 ataxia, 95, 105, 222–223 breast infection, 47 Chagas disease, 107 atrial extrasystole, 224, 229, 231 breast inspection, 46f, 47b chest pain atrial fibrillation, 224–225, 226b, breast lump acute 226f, 231 assessment of, 46f, 47 algorithm for, 58f

268 INDEX 

assessment of, 59–62 chronological age, 15–16 coronary artery disease causes of, 48–50 chylothorax, 127b angina and, 67–68 electrocardiographic circulation assessment, 8b–10b likelihood factors, 50, 50b abnormalities associated cirrhosis, 172, 174b, 181, 181t cortical dysfunction, 197b with, 52b–56b clinical assessment, 7 crackles, 8b–10b non-cardiac causes of, 62 clinical examination, 12–14, cranial nerve screening, 12b–13b overview of, 58f 12b–13b, 14t C-reactive protein, 27 intermittent history, 11, 11b, 11t Crohn’s disease, 29, 43, 149 assessment of, 65–69 investigations, 15, 17 Cryptosporidium, 88 causes of, 50–69 clinical examination, 12–14, crystal arthropathy, 182 overview of, 66f 12b–13b, 14t CURB-65 score, 120, 121t pleuritic, 48, 60, 64f, 65 Clostridium difficile infection, 88, Cushing’s disease, 12b–13b, 13t chest radiographs 91, 93 lung cancer, 161b cluster headache, 164, 171b D pneumonia, 116, 117f cognitive impairment, 87. D-dimer test, 65 pneumothorax, 117f See also dementia deep vein thrombosis, 48, 160, 186 Child–Pugh classification of ‘colicky’ pain, 26 dehydration, 90, 193 cirrhosis, 181, 181t colitis, 32, 149 delirium cholangiocarcinoma, 173 colon cancer, 29 causes of, 76–77, 77b choledocholithiasis, 28 colonic ulcer, 149–155 consciousness disturbances cholestasis, 177 colorectal cancer, 88, 93, 149, associated with, 70 chronic back pain, 5t 155b definition of, 76 chronic cognitive impairment, coma dementia and, 79 77–85 assessment of, 73–75 differential diagnosis of, chronic diarrhoea, 92f, 93 overview of, 72f 76–77, 77b chronic dyspnoea toxidromes associated with, mobility problems caused by, alarm features in, 123, 124b 74–75, 74t 221 assessment of, 123–126, 123b compartment syndrome, 187, overview of, 80f causes of, 110–127 189–190, 189b in ‘vulnerable brain’, 77b, 79, definition of, 110 complete heart block, 261f 81, 84f, 85 echocardiographic evaluation computed tomography coronary dementia of, 125 angiography, 69 causes of, 77–85 investigations for, 124b concussion, 253–255 definition of, 76 overview of, 122f confusion delirium and, 79 pulmonary function tests, 124, assessment of, 77–79 differential diagnosis of, 125t chronic, 87 77–s85 chronic fatigue syndrome, 5t, conditions that mimic, dengue fever, 144, 144b–145b 133b 77–85 depression, 87 chronic hyponatraemia, 86 definition of, 76 dermatitis, 232, 233f chronic iron deficiency, 12b–13b, hyponatraemia as cause of, dermatitis herpetiformis, 235, 14t 86–87 235f, 240 chronic kidney disease, 135, overview of, 78f dermatomes, 200f 192t, 193, 195 Confusion Assessment Method, dermatosis, 241 chronic liver disease, 132, 78b, 79 diabetes mellitus, 131 174–181, 177b, 186 conjunctivitis, 185 diabetic ketoacidosis, 74 chronic obstructive pulmonary connective tissue disorders, 50 diagnosis disease consciousness definition of, 3 acute dyspnoea in, 115, 119 altered. See altered of exclusion, 3 angina versus, 68 consciousness by patient, 6 clinical features of, 116f loss of. See loss of pattern recognition method pulmonary function tests for, consciousness of, 19–20 124–125, 125t normal, 70 probability analysis method chronic pain syndrome, 5t consolidation, 65 of, 20 chronic pancreatitis, 28–29, 43 constructional apraxia, 82 process involved in, 3, 19–23, chronic venous insufficiency, coordination tests, 12b–13b, 22f 186, 187b, 190–191 14f self-diagnosis, 6

269 INDEX 

treatment before, 5–6 causes of, 110 Mobitz type II atrioventricular working, 3 in chronic obstructive block, 261f diagnostic guides, 20–23 pulmonary disease, 115, non-ST elevation myocardial diaphragm, free air under, 31f 119 infarction, 54 diaphragmatic pain, 28f definition of, 110 pulmonary embolism, 56 diarrhoea overview of, 112f ST elevation myocardial acute, 32, 90–93, 90f chronic infarction, 49b, 52–54, assessment of, 43 alarm features in, 123, 124b 52b–56b, 59 bloody, 32, 91 assessment of, 123–126, ST segment depression, chronic, 92f, 93 123b 52b–56b, 55f Clostridium difficile infection as causes of, 110–127 trifascicular block, 262f cause of, 88, 91, 93 definition of, 110 T-wave inversion, 52, 54, definition of, 88 echocardiographic 55f drugs that cause, 88, 89b, 93 evaluation of, 125 unstable angina, 54 infectious, 88–93 investigations for, 124b Wolff-Parkinson-White irritable bowel syndrome as overview of, 122f syndrome, 225f cause of, 88, 93 pulmonary function tests, emotional distress, 68 relapsing, 92f, 93 124, 125t empyema, 127b Dieulafoy’s lesion, 148–152 exertional, 125, 129b encephalitis, 81, 197–199 differential diagnosis, 3, 21 Medical Research Council endocarditis, 140b–143b, 141 diffuse oesophageal spasm, scale of, 111b endometriosis, 29, 40, 42–43 107–109 psychogenic, 123b enthesopathies, 182 diffusion capacity, 125t at rest, 123 epidermoid cysts, 45 direct Coombs test, 135 dysuria, 40 epididymal cysts, 242–243 disability, 8b–10b epididymitis, 243f disease, symptoms and, 4, 5b, 5f E epididymo-orchitis, 242, 243f distributive shock, 247–251 ectopic pregnancy, 31, 251 epigastric pain, 29 diverticular disease, 149 eczema, 232 epilepsy, 252, 259. See also status Dix-Hallpike test, 99, 101f, 105 elderly patients epilepticus dizziness acute illness in, 220b erythema multiforme, 232–234, assessment of, 97 assessment of, 15–17 234f causes of, 94–105 inspection of, 16–17 erythroderma, 232–237, 233f overview of, 96f mobility problems in. See Escherichia coli, 88 drug(s) mobility problems examination falls caused by, 217b, 220 unsteadiness in, 105 breast, 46f, 47b fatigue caused by, 131 electrocardiography clinical, 12–14, 12b–13b, 14t jaundice caused by, 179 acute chest pain, 52b–56b exanthems, 237 liver injury caused by, 172 acute coronary syndrome, exclusion, diagnoses of, 3 oedema caused by, 187b 49b exercise tolerance, 223 drug eruptions, 237 acute pericarditis, 52b–56b, exertional dyspnoea, 125, 129b drug history, 12b 56, 56f exertional syncope, 262 drug toxicity, 74 angina pectoris, 69 exposure, 8b–10b Duke criteria, for infective aortic dissection, 56 extrasystoles, 224, 229, 231 endocarditis, 142b atrial fibrillation, 224–225, eyes, 12b–13b, 14t duodenitis, 148 226b, 226f dysentery, 91 atrial flutter, 224 F dysphagia atrial tachycardia, 224 falls assessment of, 109 Brugada syndrome, 263f blackout as cause of, 220 oesophageal, 106–109 complete heart block, 261f causes of, 216–223 oropharyngeal, 106–109 description of, 8b–10b drugs associated with, 217b overview of, 108f left bundle branch block, hip fractures caused by, 221 dyspnoea 52b–56b, 53f visual impairment as risk acute left ventricular hypertrophy, factor for, 221 arterial blood gases, 115b 52b–56b, 55f fat malabsorption, 89 assessment of, 113, 115, Mobitz type I atrioventricular fat necrosis, 45 115b, 119–126 block, 262f fatigability, 109, 201

270 INDEX 

fatigue gastroenteritis, infective haemolytic uraemic syndrome, acute, 128 abdominal pain caused by, 32 193–194 assessment of, 131–135 diarrhoea caused by, 91 haemoptysis chronic fatigue syndrome, gastrointestinal infections, 149 assessment of, 162–163 133b gastro-oesophageal disorders causes of, 160–163, 175b definition of, 128 acute chest pain caused by, 49 definition of, 160 differential diagnosis of, 129b intermittent chest pain caused overview of, 162f overview of, 130f by, 50–51 haemorrhage. See also bleeding femoral nerve, 214f gastro-oesophageal reflux acute, 151b fever disease hypovolaemic shock caused acute, 143 acute chest pain caused by, 49 by, 246 assessment of, 139, 142–143, benign stricture caused by, intracerebellar, 164 144b–147b, 146–147 106 intracerebral, 164 causes of, 136–147 intermittent chest pain caused intraventricular, 164 definition of, 136 by, 50–51, 68 subarachnoid, 4, 164–167, in immunocompromised generalised oedema, 186–191 170 patients, 144–145 generalised peritonitis, 31 subdural, 85, 87 overview of, 138f generalised skin eruption haemothorax, 127b recurrent, 142–143 assessment of, 237–241, 239b head injury, 219b in travelers, 144 causes of, 232–237, 233f–236f, head thrust test, 99, 99b fibroadenoma, 44 237b headache fibrocystic change, in breasts, 45 overview of, 238f analgesic, 165 fibromyalgia, 5t geriatric depression scale, 79 assessment of, 167, 170–171 finger–nose test, 12b–13b, 14f giant cell arteritis, 164–165 benign thunderclap, 164 flank pain, 32 Gilbert’s syndrome, 174 cerebrospinal fluid analysis flexible sigmoidoscopy, 42 Glasgow alcoholic hepatitis assessment, 168b–171b, focal limb weakness, 219 score, 180t 169t food bolus obstruction, 106–107 Glasgow Coma Scale, 70, 71t, cluster, 164, 171b frail patients. See also elderly 73–74 frontal, 171 patients glaucoma, acute, 165, 170 lumbar puncture assessment, assessment of, 15–17 globus, 109 168b–171b inspection of, 16–17 glomerulonephritis, 156–157, migraine, 164, 165b, 171b mobility problems in. See 194b overview of, 166f mobility problems glucocorticoid deficiency, 247 primary, 171, 171b unsteadiness in, 105 Goodpasture’s syndrome, red flag features for, 171b free air 156–157, 163 subarachnoid haemorrhage as on chest radiographs, 35 Graves’ ophthalmopathy, cause of, 164–167 under diaphragm, 31f 187–189 ‘sudden-onset’, 170 frontal headache, 171 Guillain-Barré syndrome, tension, 165, 171b functional syndromes, 4, 5t 201–202, 201b head-tilt, chin-lift method, 10f guttate psoriasis, 234f, 241 heart auscultation, 8b–10b G gynaecomastia, 45 heart failure, 191 gait heartbeat awareness, 224–231 abnormalities of, 222–223, 222f H heel–shin test, 12b–13b, 14f assessment of, 217b, 220 haemarthrosis, 182, 184 Helicobacter pylori, 28, 42 screening of, 223 haematemesis hemiplegic gait, 223 gait apraxia, 223 assessment of, 150, 152 hemiscrotum, 242 galactocele, 45 causes of, 148–152 hepatic encephalopathy, 82, gallbladder pain, 28f definition of, 148 173t, 177–178, 181 gallstones, 28, 173 overview of, 150f hepatic tumours, 173 gastric cancer, 28 haematocoele, 242–243 hepatic vein thrombosis, 172 gastric ulcers, 42 haematuria hepatitis gastric varices, 148 causes of, 156–159 acute, 172 gastritis, 28, 148 definition of, 156 acute viral, 172 gastrocnemius muscle rupture, overview of, 158f autoimmune, 172 189 haemolysis, 134–135 ischaemic, 172

271 INDEX 

hepatobiliary disease, 174 spinal, 211, 211b J hepatotoxicity, 174b urinary tract, 156, 159, 242 jaundice, 12b–13b, 14t, 36, 42 hereditary spherocytosis, 135 infectious diarrhoea, 88–93 acute liver injury as cause of, hernia infective endocarditis, 142b 172–174 incarcerated, 32 infective exanthems, 237, 241 assessment of, 174–181 ‘incarcerated’, 242 infective gastroenteritis biliary disease as cause of, inguinal, 242–243, 243f, 245 abdominal pain caused by, 32 173–174 strangulated, 244 diarrhoea caused by, 91 causes of, 172–174 herpes zoster, 50 infective pustulosis, 241 definition of, 172 herpetic whitlow, 240 inflammation hepatic tumours as cause of, herpetic zoster, 240, 240f acute cholecystitis as cause of, 173 hip fractures, 221 36 in hepatobiliary disease, 174 history, 11, 11b, 11t systemic, 27b overview of, 176f hydrocoele, 242, 243f, 245 inflammatory back pain, 210 screening investigations for, hypercalcaemia, 131 inflammatory bowel disease 180b hyperinflation, 116f diarrhoea caused by, 89 jaw jerk, 107f hyperkalaemia, 192–193 extra-intestinal features of, jaw-thrust method, 10f hyperosmolar non-ketotic coma, 89b joint aspiration, 185 74 pain caused by, 29 joint swelling hyperresonance, 8b–10b rectal bleeding caused by, 149 assessment of, 184–185 hypertension, 195 inguinal hernia, 242–243, 243f, causes of, 182–185 hyperthyroidism, 12b–13b, 13t 245 overview of, 184f hypertrophic cardiomyopathy, inspection Jones criteria, for rheumatic 69 breast, 46f, 47b fever, 147b hyperventilation, 62, 126 of elderly/frail patients, 16–17 hypervolaemic hyponatraemia, intermittent AV block, 226–230 K 86 intermittent chest pain Kernig’s sign, 167b hypoalbuminaemia, 186, 190 assessment of, 65–69 ketonuria, 251 hypoglycaemia, 6, 81, 252, 255 causes of, 50–69 King’s College criteria, 178, hypoglycaemic attacks, 97 overview of, 66f 179b hyponatraemia, 86–87 interstitial lung disease, 111, Kussmaul’s sign, 247 hypothermia, 73 125f hypothyroidism, 12b–13b, 13t, intestinal obstruction L 131 abdominal pain caused by, 32 laboratory investigations, 15, 17 hypovolaemia, 90, 193 large bowel, 32f Lambert-Eaton myasthenic hypovolaemic shock, 151b, small bowel syndrome, 202 246–251 radiographs of, 32f large bowel obstruction, 32f hypoxia, 113, 126 subacute, 29 left bundle branch block, intracerebellar haemorrhage, 52b–56b, 53f, 262 I 164 left ventricular dysfunction, 246, icteric leptospirosis, 172 intracerebral haemorrhage, 164 249 idiopathic cyclic oedema, 186, intracranial pressure, 165, 201b left ventricular failure, 115f, 186 191 intravenous drug use, 144b– left ventricular hypertrophy, idiopathic intracranial 145b, 145 52b–56b, 55f hypertension, 165 intraventricular haemorrhage, left ventricular outflow tract IgA nephropathy, 156–157 164 obstruction, 94 illicit drug use, 81 iron deficiency, 134 leg swelling impetigo, 233f irritable bowel syndrome assessment of, 189–195, 189b, incarcerated hernia, 32 description of, 5t, 29, 33, 43 189t infection diarrhoea caused by, 88, 93 oedema as cause of. See breast, 47 Rome III diagnostic criteria oedema central nervous system, 73, for, 88b overview of, 188f 82–83 ischaemia, 35. See also unilateral, 189 Clostridium difficile, 88, 91, 93 myocardial ischaemia legs gastrointestinal, 149 ischaemic colitis, 32, 91, 149 neurological examination of, protozoal, 91, 93 ischaemic hepatitis, 172 12b–13b 272 INDEX 

weakness of. See limb lumbar disc herniation, 210, 215 monosodium urate crystals, 185 weakness lumbar puncture, 168b–171b motor neuron disease, 197 leucocytes, 40 lumbar spine multiple myeloma, 193–194 light-headedness, 94, 97, 102f, examination of, 213b–215b multiple sclerosis, 197–199 103 stenosis of, 210, 215 Murphy’s sign, 36 Light’s criteria, 127b lumbosacral plexopathy, 202 muscle fatigability, 201 likelihood ratio, 20 lung cancer, 111, 161b, 163 muscle weakness, 129b limb weakness lung tumours, 160 musculoskeletal conditions or bilateral lung volumes, 125t disorders assessment of, 199, 201–202 Lyme serology, 132 acute chest pain caused by, overview of, 198f lymphadenopathy, 132 49–50 causes of, 196–208 lymphoedema, 187, 190 intermittent chest pain caused stroke as cause of, 196 by, 51 transient ischaemic attack as M musculoskeletal pain, 68 cause of, 196 malabsorption, 89 myasthenia gravis, 12b–13b, 13t, unilateral malar flush, 12b–13b, 13t 106, 109 assessment of, 203–206, 208, male breast disease, 45–47 myocardial infarction 209b malignant stricture, 106 definition of, 49b description of, 199 Mallory–Weiss tear, 148, 152 delirium as presenting overview of, 204f Mantoux test, 132 symptom of, 85 sudden-onset, 203–205 mean cell volume, 134 non-ST elevation. See non-ST upper motor neuron mechanical low back pain, elevation myocardial pattern of, 206 210–211, 215 infarction lipoedema, 187 mediastinal masses, 50 shock caused by, 246 lipomata, 45 Medical Research Council ST elevation. See ST elevation liver dyspnoea scale, 111b myocardial infarction acute failure of, 82–83, 172, power rating, 197t, 199 myocardial ischaemia 173b, 178–181 medically unexplained contributing factors, 63 acute injury of, 172–174, 173b, symptoms, 4 dyspnoea as symptom of, 116 178–179 Meigs’ syndrome, 127b pain associated with, 48, 67 chronic disease of, 132, Ménière’s disease, 94 symptoms of, 59b 174–181, 177b, 186 meningism, 167b myopathy, 202 malignancy of, 178 meningitis, 81, 164 myositis, 202 transplantation of, 179b meningoencephalitis, 206 myotonic dystrophica, 12b–13b, liver function tests, 132 mesenteric ischaemia, 29, 40, 43 13t loin pain, 32, 42 metabolic acidosis, 115b, 117, loss of consciousness 195, 251 N dizziness and, 97 metabolic alkalosis, 115b naloxone, 6, 81 transient. See transient loss of metabolic bone disease, 195 nephrotic syndrome, 190 consciousness microangiopathic haemolytic nerve root compression, 207t low back pain anaemia, 134 neurogenic claudication, 210, acute, 210 microcytic anaemia, 134 215 assessment of, 215 migraine headache, 164, 165b, neurogenic shock, 247–251 chronic, 210 171b neuroleptic malignant definition of, 210 mittelschmerz, 29, 40 syndrome, 139 mechanical, 210–211, 215 mobility problems neurological examination, overview of, 212f assessment of, 219–221 12b–13b lower abdominal pain, 29 causes of, 216–223 neutropenia, 142 lower airway disease, 110 delirium as cause of, 221 nitrites, 40 lower gastrointestinal bleeding, overview of, 218f non-cardiogenic pulmonary 155b psychological causes of, 223 oedema, 115 lower gastrointestinal Mobitz type I atrioventricular non-pitting oedema, 190 endoscopy, 42 block, 262, 262f non-ST elevation myocardial lower limb weakness, 222 modified Glasgow criteria, 35b infarction lower motor neuron weakness, monoarthropathy, 183 acute chest pain caused by, 48 196 mononeuritis multiplex, 206 assessment of, 63–65

273 INDEX 

clinical presentation of, 48 treatment of, before diagnosis, pleural fluid collections, 127b electrocardiography of, 54 6 pleural rub, 65, 160 unstable angina versus, 63–65 ureteric, 28f pleuritic chest pain, 48, 60, 64f, non-ulcer dyspepsia, 29 visceral, 26, 27f 65 normal pressure hydrocephalus, palpitation pneumonia 87 assessment of, 229, 231 acute chest pain caused by, normocytic anaemia, 135 causes of, 224–231, 225b–226b, 49 nystagmus, 99, 105 225f–227f chest radiographs of, 116, 117f definition of, 224 pneumothorax O overview of, 228f acute chest pain caused by, 49 oedema pancreatic cancer, 29, 174 chest radiograph of, 117f drug-induced, 187b pancreatic pain, 28–29 tension, 8b–10b, 246–247, 250t generalised, 186–191 pancreatitis polyarthropathy, 183 idiopathic cyclic, 186, 191 acute, 35b polypharmacy, 220 local causes of, 186–191 chronic, 28–29, 43 porphyrins, 83 lymphoedema, 187, 190 ‘panic attacks’, 51–59 portal hypertension, 172 pulmonary, 113, 115, 160–162, paradoxical breathing, 8b–10b postmenopausal patients, breast 249 paraparesis, 199 lump evaluations in, 47 oesophageal cancer, 106 paraproteinaemia, 135 postural hypotension, 263 oesophageal dysphagia, 106–109 parenchymal lung disease, 110 pregnancy test, 39 oesophageal perforation, 60 Parkinsonism, 12b–13b, 13t, 223 prescription medications, oesophageal rupture, 49, 59 Parkinson’s disease delirium caused by, oesophageal spasm, 49–51, 68 dysphagia caused by, 106, 109 81–82 oesophageal varices, 148, 172 features of, 223 presenting complaint, 11t oesophageal webs, 106 gaits associated with, 223 presyncope oesophagitis, 148 tremors associated with, 223 assessment of, 103 ‘off legs’, 216 parotitis, 140b–143b, 141 disorders that cause, 94 opioid intoxication, 6 paroxysmal arrhythmia, 67 light-headedness versus, 97 opioid toxicity, 73 paroxysmal supraventricular overview of, 102f oropharyngeal dysphagia, tachycardia, 224, 225f, 231 pretibial myxoedema, 187–189 106–109 paroxysmal tachyarrhythmia, primary biliary cirrhosis, 173 orthostatic hypotension, 94, 62, 123 primary headache disorders, 103 past medical history, 11, 11t 171, 171b orthostatic syncope, 263 patient evaluation, 7 probability, 3–4 osteoarthritis, 183, 223 pattern recognition, 19–20 probability analysis, 20 osteogenesis imperfecta, pelvic inflammatory disease, progressive systemic sclerosis, 12b–13b, 14t 39–40, 42 12b–13b, 13t osteoporosis, 214 pelvic mass, 186, 190 prolonged QT interval, 262 ototoxicity, 100 pemphigoid, 235, 235f protein-losing enteropathy, 186, ovarian cancer, 29 pemphigus, 235, 235f 190–191 ovarian torsion, 39 peptic ulcer, 148–152 protozoal infection, 91, 93 oxygen supplementation, 115b peptic ulcer disease, 28 pseudobulbar palsy, 106, 107t, oxygenation, 113, 115 pericardial rub, 65 109 pericarditis, acute, 49, 52b–56b, ‘pseudoseizure’, 252 P 56, 56f, 60 ‘pseudosyncope’, 252

PaCO2, 115b peripheral nerve lesions, 196, psoriasis, 232, 233f pain 205f psychogenic dyspnoea, 123b abdominal. See abdominal peritonitis, generalised, 31 psychogenic unresponsiveness, pain periumbilical pain, 29 75 delirium associated with, 85 pharyngeal pouch, 106 pulmonary embolism diaphragmatic, 28f phylloides tumours, 45 chest pain caused by, 48, 59, gallbladder, 28f pityriasis rosea, 234f, 241 62, 65 low back. See low back pain Plasmodium falciparum, 20 description of, 117, 118f pancreatic, 28–29 pleural effusion, 117f, 123, 127, electrocardiography of, 56 referred, 26, 28f 127b haemoptysis caused by, 160, somatic, 26 pleural exudate, 127b 163

274 INDEX 

shock caused by, 247, 250t retrosternal pain, 49 shock, 103 syncope caused by, 252, 261 rhabdomyolysis, 193–194 assessment of, 249, 251 pulmonary function tests, 124, rheumatic fever, 147b, 185 cardiogenic, 246–247, 249–251 125t rheumatoid arthritis, 183t, 185 characteristics of, 246 pulmonary hypertension, 186 rib fracture, 49–50 clinical features of, 90–93, 249, pulmonary oedema, 113, 115, right bundle branch block, 249b 160–162, 249 52b–56b, 57f diarrhoea and, 90–93 pulse, 8b–10b right ventricular infarction, 249 distributive, 247–251 pupillary examination, 8b–10b risk, 3–4 hypovolaemic, 151b, 246–251 purpura, 236, 236f, 240 Rockall risk score, 152, 153t neurogenic, 247–251 pustular psoriasis, 233f Romberg test, 222 overview of, 248f pustules, 241 physiology of, 250f pustulosis, infective, 241 S reversible causes of, 250t pyelonephritis, 33 saliva, 106 septic, 139b pyrexia of unknown origin, San Francisco Syncope Rule, sick patient assessment, 7–11 146–147, 146b 253b, 261 sick sinus syndrome, 226–230 Schatzki rings, 106 sigmoid diverticulitis, 39 R Schistosoma haematobium, 156 sinus tachycardia, 224, 231 radial pulse, 8b–10b Schober’s test, 213b–215b, 213f sinusitis, 165 radiation proctocolitis, 149 sciatic nerve roots, 213b–215b, skin eruption, generalised. See radicular pain, 210, 215 213f generalised skin eruption rapidly progressive paraparesis, sciatica, 210 sleepiness, 129b 199 scleritis, 12b–13b, 14t small bowel obstruction rash scleroderma, 107 radiographs of, 32f drugs that cause, 237b scleromalacia, 12b–13b, 14t subacute, 29 generalised skin eruption. See scrotal examination, 244b–245b somatic pain, 26 generalised skin eruption scrotal swelling space-occupying lesions, 196 reactive arthritis, 182–183 assessment of, 244–245, 245f speech and language therapy rectal bleeding causes of, 242–243, 243f assessment, 109 assessment of, 154–155 overview of, 244f spermatocoeles, 242–243 causes of, 149–155 seizures. See also status sphincter of Oddi dysfunction, 42 overview of, 154f epilepticus spider naevi, 177 referred pain, 26, 28f assessment of, 258–259 spinal cancer, 211b reflex presyncope, 94 clinical features of, 257b spinal cord lesions, 196 reflex syncope, 252 description of, 73 spine. See also lumbar spine relapsing diarrhoea, 92f, 93 intracranial pathology as examination of, 213b–215b renal anaemia, 195 cause of, 258 infections of, 211, 211b renal colic, 159 neuroimaging of, 259, 259b movements of, 212f renal disease, 156–157 overview of, 258f tumours of, 210–211 renal failure referrals for, 259 spirometry, 125t assessment of, 192–195 syncope versus, 255–256 spondylarthritides, 210 fatigue caused by, 131 tonic-clonic, 253–255 spondylolisthesis, 211 leg swelling caused by, 186 transient loss of consciousness ST depression, 52, 52b–56b, 55f renal stone obstruction, 40 caused by, 252, 253b ST elevation myocardial renal tract cancer, 42 self-diagnosis, 6 infarction renal tract disorders, 29 sepsis acute anterior, 52b–56b, 52f renal tract obstruction, 32 biliary, 36 acute chest pain caused by, 48 respiratory acidosis, 115b diagnostic criteria for, 139b acute inferior, 52b–56b, 52f respiratory alkalosis, 115b shock caused by, 247, 251 acute inferoposterior, respiratory failure, 73 septic arthritis, 182 52b–56b, 53f respiratory tract infection septic screen, 140b–143b anterior, 52b–56b, 53f dyspnoea caused by, 115, septic shock, 139b electrocardiographic 120–126 severe sepsis, 139b abnormalities in, 49b, haemoptysis caused by, sexual history, 12b 52–54, 52b–56b, 52f–53f, 160–163 Shigella, 88 59 retrosternal discomfort, 67–68 shingles. See herpetic zoster shock caused by, 250t

275 INDEX 

stable angina, 67, 69 assessment of, 261–263, 261b, toxidromes, 74–75, 74t status epilepticus, 73–74, 258 261f–263f transient ischaemic attacks steatorrhoea, 93 clinical features of, 257b ABCDD score in, 206t Stemmer sign, 190 exertional, 262 limb weakness caused by, step-by-step assessment, 21 orthostatic, 263 196, 205–206 Stevens–Johnson syndrome, overview of, 260f vertebrobasilar, 94, 97 232–234 San Francisco Syncope Rule, transient loss of consciousness Still’s disease, 147 253b, 261 assessment of, 255–256, 257b stones, 156 seizures versus, 255–256 cardiac features, 257b stool impaction, 93 trigger factors, 263 causes of, 252–263 straight leg raising, 213f syndrome of inappropriate features of, 253b strangulated hernia, 244 antidiuretic hormone overview of, 254f Streptococcus pyogenes, 140b– secretion, 87, 87b transverse myelitis, 199 143b, 141 systemic inflammatory trauma stress testing, 69 response, 26–27, 186 joint swelling caused by, 182, stretch test systemic inflammatory response 184 of femoral nerve, 214f syndrome, 139, 139b, 247, vertebral, 210 of sciatic nerve roots, 213f 251 ‘traumatic tap’, 168 strictures, 106, 173 systemic lupus erythematosus, trifascicular block, 262f stroke 12b–13b, 13t trigeminal neuralgia, 165 assessment of, 208 systemic vasculitis, 240–241 troponin, 61 Bamford classification of, 208, tuberculosis 209b T haemoptysis caused by, 160 classification of, 208, 209b tachyarrhythmia, 250t vertebral, 211 dysphagia secondary to, 106 tachycardia tumours limb weakness secondary to, atrial, 224 haematuria caused by, 196–208 atrioventricular nodal 156–159 risk factors for, 208 re-entry, 224 hepatic, 173 thrombolysis for, 208, 209b description of, 8b–10b spinal, 210–211 structural cardiac disease paroxysmal supraventricular, testicular, 242, 243f echocardiography of, 262 224, 225f, 231 T-wave inversion, 52, 54, 55f presyncope caused by, 94, sinus, 224, 231 20-step clinical examination, 103 ventricular, 225–226, 227f, 231 12–14, 12b–13b, 14t subacute small bowel temporal arteritis, 164–165, 170, obstruction, 29 170b U subarachnoid haemorrhage, 4, tendinopathies, 182 ulcerative colitis, 89, 149 164–167, 170 tendon reflexes, 202 ultrasound subdural haemorrhage, 85, 87 Tensilon test, 202 acute gynaecological substance abuse-related tension headache, 165, 171b pathology, 39 delirium, 81 tension pneumothorax, 8b–10b, acute upper abdominal pain, ‘sudden-onset’ headache, 170 246–247, 250t 36 superficial thrombophlebitis, testicular examination, breast lump, 44 187, 189 244b–245b scrotal swelling, 245 superior vena caval obstruction, testicular torsion, 242 unilateral limb weakness 12b–13b, 13t testicular tumour, 242, 243f assessment of, 203–206, 208, suprapubic pain, 40 thrombolysis, 208, 209b 209b supraventricular tachycardia, thrombotic thrombocytopenic description of, 199 224, 225f, 231, 261 purpura, 193–194, 240 overview of, 204f swelling. See joint swelling; TIMI score, 63, 63t sudden-onset, 203–205 scrotal swelling Todd’s paresis, 197–199, 205 upper motor neuron pattern symptoms tonic-clonic seizure, 253–255 of, 206 disease and, 4, 5b, 5f torsades de pointes, 225–226, unstable angina medically unexplained, 4 227f assessment of, 63–65, 69 syncope, 252–263 torsion, of testis, 242 cardiac biomarkers for, arrhythmia-related, 252, toxic epidermal necrolysis, 63–65 261–262 232–234, 234f, 239 description of, 48

276 INDEX 

electrocardiography of, 54 vasovagal episode, 94 visceral pain, 26, 27f symptoms of, 61, 67 venous insufficiency, chronic, visual impairment, 221 unsteadiness, 95, 97, 104f, 105 186, 187b, 190–191 volume overload, 195 upper airway obstruction, 110 venous thromboembolism, 126 ‘vulnerable brain’, 77b, 79, 81, upper gastrointestinal bleeding, ventilation, 113, 115 84f, 85 149 ventricular extrasystole, 224, upper gastrointestinal 229, 231 W endoscopy, 28, 42, 109, ventricular tachycardia, 225–226, weakness, limb. See limb 152 227f, 231 weakness upper gastrointestinal vertebral fracture, 210 Wegener’s granulomatosis, 163 malignancy, 148 vertebral metastases, 210–211, Weil’s disease, 172 upper motor neuron weakness, 215 Wells score, 65, 118f, 118t, 189, 196 vertebral trauma, 210 189t uraemia, 131 vertebral tuberculosis, 211 Wernicke-Korsakoff syndrome, ureteric obstruction, 156 vertebrobasilar dissection, 164 87 ureteric pain, 28f vertebrobasilar transient Wernicke’s encephalopathy, urethritis, 185 ischaemic attacks, 94, 97 82–85 urinary tract cancer, 157b vertigo wheals, 241 urinary tract infection, 156, 159, assessment of, 99–100 wheeze, 8b–10b, 115 242 disorders that cause, 94–105 Wilson’s disease, 172 urine discolouration, 157b head thrust test for, 99, 99b Wolff-Parkinson-White urine sodium, 86–87 illusory sensation of motion syndrome, 224, 225f urticaria, 235–236, 236f associated with, 97 working diagnosis, 3 overview of, 98f V red flag features in, 99, 99b X variceal bleeding, 152 vestibular neuronitis, 94, 99–100 xanthochromia, 4 varicocoeles, 242–243, 243f, 245 videofluoroscopy, 109 vasculitis, 236, 236f viral hepatitis, 140b–143b Z vasospastic angina, 67–68 viral meningitis, 164 Ziehl–Neelsen staining, 121–123

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