Cardiology

Endocrinology

Gastroenterology

General Hepato-pancreato-biliary

Medicine
Haematology

Immunology & allergy

& Surgery Neurology

Renal
medical student revision guide Respiratory

Surgical principles

The acute abdomen

✓ everything you need to prepare for exams

� Gastrointestinal surgery

✓ diagrams, flowcharts, colour coding

� The breast
and summary boxes
✓ includes all core topics for medical
� Vascular surgery
finals & foundation years Urology
✓ peer-reviewed with the latest guidelines
�
Critical illness

Emergency presentations

Rebecca Richardson Rheumatology

& Ricky Ellis
Trauma & orthopaedics
 General
Medicine
& Surgery
medical student revision guide
“I like the unique style … It is simple,
engaging and easy to read, whatever your
learning preferences (I particularly like
the colour coding!). It also covers topics
comprehensively, making it not only a
great aide-memoire but also a very useful
everyday book on the ward.”
From the Foreword by
Professor Farah Bhatti OBE
Consultant Cardiothoracic Surgeon

General Medicine and Surgery.indb 1 11-Jan-23 3:01:40 PM

 Student Ambassadors
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General Medicine and Surgery.indb 2 11-Jan-23 3:01:42 PM

 Cardiology

Endocrinology

Gastroenterology

General Hepato-pancreato-biliary

Medicine
Haematology

Immunology & allergy

& Surgery Neurology

Renal
medical student revision guide Respiratory

Surgical principles

The acute abdomen

Rebecca Richardson Gastrointestinal surgery
BMBS, BMedSci
Junior Doctor, Royal Derby Hospital, Derby
The breast
Ricky Ellis
PhD, MRCS, MBChB, BSc, DPD, MFSTEd, FHEA Vascular surgery
Urology Specialist Registrar, Royal Derby
Hospital, Derby
Urology

Critical illness

Emergency presentations

Rheumatology

Trauma & orthopaedics

General Medicine and Surgery.indb 3 11-Jan-23 3:01:44 PM

 © Scion Publishing Ltd, 2023
First published 2023

All rights reserved. No part of this book may be reproduced or transmitted, in any form
or by any means, without permission.

A CIP catalogue record for this book is available from the British Library.

ISBN 9781914961182

Scion Publishing Limited

The Old Hayloft, Vantage Business Park, Bloxham Road, Banbury OX16 9UX, UK

www.scionpublishing.com

Important Note from the Publisher

The information contained within this book was obtained by Scion Publishing Ltd from
sources believed by us to be reliable. However, while every effort has been made to
ensure its accuracy, no responsibility for loss or injury whatsoever occasioned to any
person acting or refraining from action as a result of information contained herein can
be accepted by the authors or publishers.

Readers are reminded that medicine is a constantly evolving science and while the
authors and publishers have ensured that all dosages, applications and practices are
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not to be considered unprotected by law.

Typeset by Medlar Publishing Solutions Pvt Ltd, India

Printed in the UK

Last digit is the print number: 10 9 8 7 6 5 4 3 2 1

General Medicine and Surgery.indb 4 11-Jan-23 3:01:44 PM

 Contents
Foreword................................................................................... viii
Preface..........................................................................................ix
Acknowledgements...................................................................x
About the authors.......................................................................x
Peer reviewers.............................................................................xi
General abbreviations............................................................ xii
How to use this book............................................................. xiii

Chapter 1: CARDIOLOGY 1 Chapter 4: HEPATO-PANCREATO-BILIARY 47

Acute coronary syndrome....................................................... 2 Hepatitis..................................................................................... 48

Chronic stable angina .............................................................. 4 Ascites......................................................................................... 50
Heart valve disease.................................................................... 5 Liver neoplasms....................................................................... 51
Infective endocarditis............................................................... 7 Chronic pancreatitis................................................................ 52
Congestive cardiac failure........................................................ 8 Haemochromatosis................................................................. 52
Acute pulmonary oedema....................................................... 9 The spleen.................................................................................. 53
Syncope...................................................................................... 10 Jaundice..................................................................................... 54
Atrial fibrillation....................................................................... 11 Gallbladder disease................................................................. 55
Miscellaneous cardiac conditions........................................ 12 Pancreatic neoplasms............................................................. 57

Chapter 2: ENDOCRINOLOGY 15 Chapter 5: HAEMATOLOGY 59

Diabetes mellitus..................................................................... 16 Haematological lineage......................................................... 60

Pituitary disorders.................................................................... 20 Anaemia overview................................................................... 61
Adrenal disease........................................................................ 22 Anaemia from reduced RBC production............................ 62
Thyroid disease......................................................................... 26 Haemolytic anaemias............................................................. 63
Parathyroid disease................................................................. 29 Thalassaemias........................................................................... 65
Sodium imbalance................................................................... 31 Sickle cell disease..................................................................... 66
Pancytopenia............................................................................ 67
Chapter 3: GASTROENTEROLOGY 33
Myeloproliferative disorders................................................. 68
Clinical nutrition....................................................................... 34 Multiple myeloma.................................................................... 69
Gastro-oesophageal reflux disease..................................... 35 Leukaemia................................................................................. 70
Peptic ulcer disease................................................................. 36 Lymphoma................................................................................. 72
Gastro-intestinal haemorrhage............................................ 37 Haemostasis.............................................................................. 73
Dysphagia.................................................................................. 38 Coagulation disorders............................................................. 74
Oesophageal cancer................................................................ 39 Investigating bleeding problems......................................... 76
Gastric cancer............................................................................ 40 Blood transfusion..................................................................... 77
Coeliac disease......................................................................... 41
Chapter 6: IMMUNOLOGY AND ALLERGY 81
Obesity........................................................................................ 41
Acute diarrhoea........................................................................ 42 Allergic disorders..................................................................... 82
Irritable bowel syndrome....................................................... 43 Autoimmune & immunodeficiency disorders.................. 83
Inflammatory bowel disease................................................. 44

General Medicine and Surgery.indb 5 11-Jan-23 3:01:44 PM

 vi Contents

Chapter 7: NEUROLOGY 85 Lung cancer.............................................................................135

Sarcoidosis...............................................................................136
Nervous system structure & function
Interstitial lung disease........................................................137
Areas of the brain..................................................................... 86
Occupational lung disease..................................................138
Vision........................................................................................... 87
Spinal cord tracts..................................................................... 88 Chapter 10: GENERAL SURGICAL
Nervous system investigations PRINCIPLES 139
Lumbar puncture..................................................................... 90
Wound healing.......................................................................140
Imaging with CT & MRI........................................................... 91
Postoperative care.................................................................141
Acute neurological disease
Postoperative assessment...................................................143
Acute spinal problems............................................................ 92
Fluid therapy...........................................................................144
Neuromuscular emergencies................................................ 93
Acute hydrocephalus.............................................................. 94 Chapter 11: THE ACUTE ABDOMEN 147
Cortical venous sinus thrombosis........................................ 95
Neuro-oncology....................................................................... 96 General overview...................................................................148
CNS infection............................................................................ 97 Acute pancreatitis..................................................................150
Brain abscess............................................................................. 98 Meckel’s diverticulum...........................................................152
Long-term neurological conditions Acute appendicitis.................................................................153
Multiple sclerosis...................................................................... 99 Diverticular disease...............................................................154
Epilepsy....................................................................................101 Gastrointestinal perforation................................................155
Neuropathies..........................................................................104 Intestinal obstruction...........................................................156
Motor neurone disease.........................................................107 Hernias......................................................................................158
Myasthenia gravis..................................................................108 Chapter 12: GASTROINTESTINAL SURGERY 161
Myopathies..............................................................................109
Essential tremor......................................................................110 Perianal disease......................................................................162
Headaches...............................................................................111 Colorectal cancer...................................................................164
Anal cancer..............................................................................166
Chapter 8: RENAL 113
Chapter 13: THE BREAST 167
Acute kidney injury...............................................................114
Chronic kidney disease.........................................................116 Breast conditions...................................................................168
Glomerular disease................................................................118 Chapter 14: VASCULAR DISEASE 171
Urinary tract infection...........................................................120
Haematuria..............................................................................120 Hypertension..........................................................................172
Carotid artery disease...........................................................174
Chapter 9: RESPIRATORY 121 Aneurysms...............................................................................175
Respiratory failure..................................................................122 Acute aortic syndromes........................................................176
Pneumothorax........................................................................123 Chronic peripheral arterial disease....................................177
Pleural effusion.......................................................................124 Acute limb ischaemia............................................................180
Pneumonia..............................................................................125 Amputation.............................................................................181
Tuberculosis.............................................................................126 Vasospastic disorders............................................................182
Covid-19...................................................................................127 Thoracic outlet syndrome ...................................................183
Asthma.....................................................................................128 Varicose veins..........................................................................184
Chronic obstructive pulmonary disease..........................130 Leg ulcers.................................................................................185
Bronchiectasis.........................................................................132 Venous thromboembolic disease......................................186
Sleep apnoea..........................................................................133 Lymphoedema ......................................................................188
Cystic fibrosis...........................................................................134

General Medicine and Surgery.indb 6 11-Jan-23 3:01:44 PM

 Contents vii

Chapter 15: UROLOGY 189 Crystal-associated arthritis..................................................235

Rheumatoid arthritis.............................................................237
Stone disease (nephrolithiasis)...........................................190
Seronegative spondyloarthritis..........................................239
Urinary tract malignancy.....................................................191
Multisystem connective tissue disease............................241
Bladder outlet obstruction..................................................193
Systemic vasculitis.................................................................244
Bladder trauma.......................................................................195
Polymyalgia rheumatica.......................................................245
Scrotal lumps..........................................................................196
Miscellaneous musculoskeletal conditions.....................246
Testicular tumours.................................................................198
Conditions of the penis........................................................199 Chapter 19: TRAUMA & ORTHOPAEDICS 249

Chapter 16: CRITICAL ILLNESS 201 Musculoskeletal conditions

Bone and joint infection.......................................................250
The critically ill patient..........................................................202
Musculoskeletal malignancy...............................................252
The semi-conscious/unconscious patient.......................203
Diseases of the bone.............................................................254
Organ support........................................................................204
Osteoarthritis .........................................................................256
Chapter 17: EMERGENCY PRESENTATIONS 207 Trauma
Primary survey........................................................................257
Acid–base disorders..............................................................208
Secondary survey ..................................................................258
Electrolyte abnormalities.....................................................209
Head injuries...........................................................................259
Overdoses................................................................................211
Spinal cord injury...................................................................262
Seizures....................................................................................212
Chest injuries...........................................................................264
Sepsis........................................................................................213
Major haemorrhage..............................................................265
Shock.........................................................................................214
Burns ........................................................................................266
Life-threatening arrhythmia...............................................216
Fractures
Cardiac arrest..........................................................................218
General fracture principles..................................................268
Specific presentations...........................................................219
Pathological fractures...........................................................272
Chapter 18: RHEUMATOLOGY 223 Common adult fractures......................................................273
Common paediatric fractures.............................................279
Regional periarticular pain..................................................224
Neck & back pain....................................................................229 Figure acknowledgements..................................................281
Peripheral nerve entrapment.............................................233 Index of conditions................................................................283
Fibromyalgia...........................................................................234

General Medicine and Surgery.indb 7 11-Jan-23 3:01:44 PM

 viii 

Foreword
A book such as this takes time, effort and dedication from all the contributors who do this alongside their already busy clinical work.
It is heartening to see this commitment to supporting the education and advancement of the next generation of doctors and allied
health professionals.

I like the unique style which is based on Dr Richardson’s personal notes whilst a medical student. It is simple, engaging and easy to
read, whatever your learning preferences (I particularly like the colour coding!) It also covers topics comprehensively, making it not
only a great aide-memoire but also a very useful everyday book on the ward. The judicious use of references (e.g. NICE guidelines and
BMJ Best Practice) also enables readers to look into subjects in depth if needed, without affecting the flow of the text.

Once again, I commend the authors on their remarkable efforts and wish everyone who picks up this book well in their careers.

Professor Farah Bhatti OBE

Consultant Cardiothoracic Surgeon

General Medicine and Surgery.indb 8 11-Jan-23 3:01:44 PM

  ix

Preface
I remember it well. Countless evenings sat at my desk, desperately trying to work out what I needed to know, and how I was going
to know it. Hours spent trudging through textbooks, soaking up line after line of information, only to be left certain that after a week
on my new placement, it would all be forgotten. Medical school is tough. The vast volume of knowledge that must be acquired and
retained, to achieve the standards expected of a safe and successful doctor, is a daunting task. But as you will find at every stage in
your medical career, help is always available if you know where to look. For you, I hope this book can be your help. I present it as
your trusted companion, a loyal friend that will stand by your side through good times and bad, something to turn to when you need
guidance, reassurance, or simply just a place to start!

There is no end of resources available for medical students, all designed to make the journey from student to doctor that little bit
easier. For me, I found this wealth of information to be just as much of a curse as it was a blessing. Not only was I faced with the
overwhelming task of learning it all, but I first had to find and dissect the parts that were relevant to me. Wouldn’t it be easier if
everything I needed to know was in the same place? The simple answer – yes. And that is how I started to write this book.

My first goal when creating the Medical Student Revision Guides was to bring together all the key topics needed for medical school
exams and life as a junior doctor in one readily available place. I did this through summarising a variety of recognised resources,
including textbooks, articles and clinical guidelines. This has been supplemented by the expert knowledge of specialists in each
field, who have reviewed each chapter to ensure it is accurate and reflects the most up-to-date guidance.

My second goal was to do everything I could to help you remember this information. I appreciate everyone is unique in the way
they learn, but with most of us relying on vision as our dominant sense, it seemed illogical not to utilise its power. As such, I have
specifically designed this book with an extensive use of colour, diagrams and summary tables, to create a resource that is visually
striking and a refreshing change from your current textbooks. The informal ‘notes-style’ layout and dedicated column that allows for
your own annotations on each page, are features that I hope make the content feel more accessible and easier to engage with.

It is my sincere hope that you find this book useful, whether it be as your comprehensive revision resource, or a quick reminder of a
condition that you come across on the ward. I am forever grateful for any feedback that can help me to better help you, so please
do leave a review with your honest thoughts.

I wish you luck with your exams, and all the best for your future careers.

Rebecca Richardson

Disclaimer
It is important to note that this book is designed as a revision tool and aide-memoire. It is not intended to give an in-depth understanding of each condition, but
rather to focus on the key points that often appear in undergraduate exams. It should not be solely relied upon in clinical situations; please always check the most
current and local guidelines before implementing management or administering any treatment.
Every attempt has been made to ensure that the most up-to-date information has been included at the time of writing this book. However, due to the continuously
evolving nature of the medical profession, and with variations in clinical practice between hospital Trusts, this cannot be guaranteed. It is therefore advised that
you correlate these notes to other resources, and supplement them with your own clinical encounters, to ensure a complete learning experience. Readers should
also ensure that they learn all elements of their own medical school curriculum, regardless of whether they are covered in this book.

General Medicine and Surgery.indb 9 11-Jan-23 3:01:45 PM

 x 

Acknowledgements
I must firstly say a huge thank you to the team at Scion Publishing for making this book a reality. A special mention to Jonathan and
Clare, for your tireless work overcoming layout issues and design problems, to ensure the end product was everything I had hoped it
would be.

Secondly, I would like to thank my co-author, Ricky. Your advice and guidance have been invaluable in this process. Your wealth of
experience in the field of medical education has undoubtedly benefited the book and its readers, and remains an inspiration for my
future work.

My thanks are extended to all those who have contributed time and expertise as a chapter reviewer. I will be eternally grateful
that you could see the potential in my work in its early stages and gave up your own time to help me achieve it. The abundance of
knowledge and experience you have brought is priceless and will underpin the learning of many future doctors.

Finally, to my loved ones. To Mum and Dad, for the years of selflessness and sacrifice that allowed me the opportunities to achieve all
that I have today. To my brother, Chris, whose artistic talent never fails to amaze me, and has inspired the covers and diagrams of both
my books. To Nana, Gran, Grandad and Margaret, for the timeless wisdom and unconditional love that only grandparents can provide.
And to Martin, for your endless patience, support and encouragement in all that I do.

Thank you.

About the authors

Rebecca Richardson is a junior doctor currently working in Ricky Ellis is a Urology Specialist Registrar, Honorary Clinical
the East Midlands. After graduating from the University of Senior Lecturer and Research Associate for the Intercollegiate
Nottingham as one of the top students in her year, with first Committee for Basic Surgical Examinations (ICBSE). Ricky is an
class honours, she became passionate about helping others to award-winning trainer and regularly organises teaching courses
follow in her footsteps. Her revision notes have already helped including the internationally delivered ‘Urology Boot Camp for
hundreds of medical students across the UK prepare for their Medical Students’. He is passionate about improving training
exams. Rebecca has continued her mission to support students for medical students and junior doctors and was awarded the
and trainees through creating content for a variety of medical prestigious Association of Surgeons in Training and Faculty of
education platforms, as well as running regular virtual teaching Surgical Trainers Silver Suture Award for contributions to and
sessions to help students practise for their clinical examinations. excellence in surgical training.

General Medicine and Surgery.indb 10 11-Jan-23 3:01:45 PM

  xi

Peer reviewers
Section Peer reviewer
Cardiology Dr Manish Gandhi
Consultant Cardiologist, Royal Devon University Healthcare NHS Foundation Trust
Endocrinology Dr David Hughes
Consultant in Diabetes, Endocrinology & Bariatric Medicine, University Hospitals of Derby and Burton NHS Trust
Gastroenterology Dr J H Williams
Hepatobiliary Consultant Gastroenterologist, University Hospitals of Derby and Burton NHS Foundation Trust

Haematology Dr M Bishton
Clinical Associate Professor, University of Nottingham, School of Translational Sciences
Honorary Consultant Haematologist Nottinghamshire University Hospitals NHS Trust
National Cancer Registration and Analysis Service (NCRAS) lead for Haemato-oncology NHS-Digital
Neurology Dr S L Toh
Consultant Neurologist, University Hospitals of Derby and Burton NHS Foundation Trust
Dr M Kolappan
Consultant Neurologist, Neuro-ophthalmologist and Headache Specialist, University Hospitals of Derby and Burton NHS
Foundation Trust
Renal medicine Dr Nitin Kolhe
Consultant Nephrologist and Clinical Director for Specialist Medicine at University Hospitals of Derby and Burton NHS Trust
Respiratory Dr NJ Withers
Consultant in CF/Respiratory Medicine, Royal Devon University Healthcare NHS Foundation Trust
General surgery Miss Ruth Parks
GI surgery General Surgery Registrar (East Midlands North), Clinical Research Fellow (University of Nottingham)

Vascular surgery Mr Andrew Duncan

Vascular Registrar and Honorary Research Fellow, University of Leicester
Urology Mr Ricky Ellis
Urology Specialist Registrar, University Hospitals of Derby and Burton NHS Foundation Trust
Critical illness Dr Emily Howells
Emergency presentations Consultant in Intensive Care Medicine and Anaesthetics, Royal Devon University Healthcare NHS Foundation Trust

Trauma Dr Chris Leighton

Advanced Trainee Intensive Care Medicine and Anaesthetics, University Hospitals Plymouth NHS Trust
Rheumatology Dr Clare Webb
Senior Clinical Educator in Rheumatology, University Hospitals of Derby and Burton NHS Foundation Trust and Honorary
(Consultant) Assistant Professor University of Nottingham
Dr Adam Munks
Senior Clinical Educator in Musculoskeletal Medicine, University Hospitals of Derby and Burton NHS Foundation Trust and
Honorary (Consultant) Assistant Professor University of Nottingham
Trauma & orthopaedics Mr Tony Bateman
Consultant Trauma, Orthopaedic and Spine Surgeon, University Hospitals of Derby and Burton NHS Trust

General Medicine and Surgery.indb 11 11-Jan-23 3:01:45 PM

 xii 

General abbreviations
Each chapter begins with a set of abbreviations specific for that chapter.

2ww – 2 week wait eGFR – Estimated GFR PCR – Polymerase chain reaction
a. – Arterial ENT – Ear, nose and throat PE – Pulmonary embolism
ABCDE – Airways, Breathing, Circulation, EPO – Erythropoeitin PET – Positron emission tomography
Disability, Exposure ESR – Erythrocyte sedimentation rate PHx – Past history
ABG – Arterial blood gas FBC – Full blood count PNS – Peripheral nervous system
ABX – Antibiotics FHx – Family history PO – (per ora) Orally
AXR – Abdominal X-ray G&S – Group & save PR – Per rectum
BB – Beta-blocker GA – General anaesthetic PRN – Pro re nata (as required)
BD – Twice a day GCS – Glasgow Coma Score/Scale pulm. – Pulmonary
BG – Blood glucose GFR – Glomerular filtration rate QDS – Four times a day
BMI – Body mass index GI – Gastrointestinal RA – Rheumatoid arthritis
BP – Blood pressure GP – General practitioner RBC – Red blood cell
ca – Cancer h – Hour RFT – Renal function test
Ca – Calcium Hb – Haemoglobin RHS – Right-hand side
CBT – Cognitive behavioural therapy HF – Heart failure r/o – Risk of
CCB – Calcium channel blocker HIV – Human immunodeficiency virus R/V – Review
CCF – Congestive cardiac failure HR – Heart rate re – Regarding
CF – Cystic fibrosis HTN – Hypertension RF – Risk factor
CHF – Chronic heart failure ICP – Intracranial pressure RR – Respiration rate
CI – Contraindication Ig – Immunoglobulin s – Second
CK – Creatine kinase IHD – Ischaemic heart disease SALT – Speech and language therapy
CKD – Chronic kidney disease IM – Intramuscular SBP – Systolic blood pressure
CMV – Cytomegalovirus inc. – Including SC – Subcutaneous
CN – Cranial nerve IV – Intravenous SD – Standard deviation
CNS – Central nervous system IVDU – Intravenous drug user SE – Side-effect
CPAP – Continuous positive airway pressure Ix – Investigation SL – Sublingual
CPR – Cardiopulmonary resuscitation JVP – Jugular venous pressure SLE – Systemic lupus erythematosus
Cr – Creatinine LFT – Liver function test SOB – Shortness of breath
CRP – C-reactive protein LHS – Left-hand side SSRI – Selective serotonin reuptake inhibitor
CRT – Capillary refill time LMWH – Low molecular weight heparin Sx – Symptoms
CSF – Cerebrospinal fluid LOC – Loss of consciousness TB – Tuberculosis
CT – Computed tomography m – Month TCA – Tricyclic antidepressant
CV – Cardiovascular mcg – Microgram TDS – Three times a day
CVA – Cerebrovascular accident MCS – Microscopy, culture and sensitivity TFT – Thyroid function test
CVD – Cardiovascular disease MDT – Multidisciplinary team TIA – Transient ischaemic attack
CXR – Chest X-ray MI – Myocardial infarction TNM – Tumour, nodes, metastases
D&V – Diarrhoea and vomiting min – Minute Tx – Treatment
d – Day MND – Motor neurone disease U&Es – Urea & electrolytes
DBP – Diastolic blood pressure MRI – Magnetic resonance imaging USS – Ultrasound scan
DDx – Differential diagnosis Mx – Management UTI – Urinary tract infection
DM – Diabetes mellitus NBM – Nil by mouth VBG – Venous blood gas
DOAC – Direct oral anticoagulant NSAID – Non-steroidal anti-inflammatory vit – Vitamin
DRE – Digital rectal examination drug VTE – Venous thromboembolism
DVLA – Driver and Vehicle Licensing Agency N&V – Nausea & vomiting W – Week
Dx – Diagnosis OCD – Obsessive–compulsive disorder WBC – White blood cell
ECG – Electrocardiogram OD – Once a day WCC – White cell count
ECT – Electroconvulsive therapy O/E – On examination WHO – World Health Organization
EEG – Electroencephalogram OT – Occupational therapist y – Year

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  xiii

How to use this book

The underlying principle of this book is to present information in a way that is eye-catching, clear and easy to remember.
This page will explain some of the key layout features that have been used to achieve this.

1. Notes column – each page is divided into a main text section, and a tinted notes column. The notes column is used to house
additional information, and to provide space for your own notes, should you wish to make any.

Notes column Main text section

2. Text colour
• chapter coloured text – used to expand on a point / provide extra information
• grey text – used for less important information
• red text – used for red flags and emergency points
• blue text – used for extra points / annotations

3. Highlighting – words/phrases that have been highlighted are linked to extra information. Look for another highlight of the same
colour on the page to find this information. The below example uses green highlighting to link ‘Skin fold’ to the additional information
'Normal fold thickness'.

4. Box colours – a variety of different boxes are used to display information.

• Yellow tinted box – for triggers / risk factors, complications & prognosis
• Blue tinted box – for differential diagnoses
• Red box – for red flags / emergency points
• Chapter coloured box – for all other types of information

Yellow-tinted Blue-tinted Red

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 2  Chapter 1: Cardiology

Acute coronary syndrome

→ STEMI, NSTEMI & unstable angina (not stable angina)

Key differentials: Pathogenesis

• Coronary spasm • PE
• Pericarditis/ • Pneumothorax 1. Atherosclerosis: fatty deposition in artery wall causes plaque build-up
myocarditis • GORD
2. ACS when: Plaque rupture → Thrombosis → Vasoconstriction → Ischaemia
• Aortic dissection • PUD
± distal thromboembolism
• MSK
(costochondritis) Results in a transmural or subendocardial infarct (circumferential infarct if global
hypoperfusion)

Risk factors Clinical presentation

• Smoking • Diabetes mellitus
• Hypertension • FHx → Severe, ‘crushing’ chest pain (at rest)
• Alcohol • Previous IHD • retrosternal, radiating to arm/neck/jaw
*Angina is <20min /
• lasts >20min & NOT RELIEVED by 3× GTN sprays*
relievable
→ Sympathetic symptoms: sweating, palpitations, dyspnoea, nausea
• sense of ‘impending doom’
BEWARE ATYPICAL PRESENTATION: ‘silent MI’
= ACS with no chest pain On examination
Instead: syncope / pulmonary oedema / 
epigastric pain → in elderly/diabetics/females • Sympathetic Sx: pallor, sweating, tachycardia
• Myocardial impairment: hypotension,  JVP, basal creps, 3rd heart sound,
Serial troponin: shows continued rise at 6h, pulmonary/peripheral oedema
peak at 24h
Multiple of Troponin without reperfusion Investigations Other causes  troponin:
cut-off level
Troponin with reperfusion • myocarditis/pericarditis
100
CK-MB without reperfusion 1. Bloods:  lipids,  glucose, clotting • post-PCI
50 CK-MD with reperfusion 2. Serial troponin:  on admission + 6–12h later → • ventricular strain / HF
20
3. ECG: within 10min of presentation • burns/sepsis
10
4. Other: CXR, ECHO, angiogram • PE
5
2
(r/o DDx, assess prognosis & determine • renal failure
1
Cut-off level best Tx) But these show
consistently high levels
0 1 2 3 4 5 6 7
Fig. 1.1 Days after symptoms onset

STEMI ECG CHANGES: *New LBBB + chest pain = assumed STEMI*

STEMI: complete occlusion
= ST elevation AND  troponin
NSTEMI: partial occlusion
= ST depression / T wave inversion OR normal
ECG AND  troponin
UA: partial occlusion
= ST depression/ T wave inversion WITHOUT  At onset of pain Within 1h Following Tx 24h later Days/months
troponin normal sinus ST elevation T-wave inversion ST normalised deep Q-wave
complex Deep Q waves T-wave inversion (tissue death)
Fig. 1.2
ST-elevation criteria:
Widespread concave ST elevation = pericarditis
>1 mm in ≥2 contiguous* limb leads
OR
>2mm in ≥2 contiguous* chest leads NSTEMI ECG CHANGES (IF PRESENT):
+ ST depression in reciprocal leads ≥0.5mm ST depression in ≥2 contiguous* leads
AND >1mm T depression in leads with +ve QRS
Posterior STEMI:
ST depression in ≥2 chest leads V1–4
Takotsubo: ‘broken heart syndrome’ (stress cardiomyopathy):
AND ≥0.5mm ST elevation in any V7–9
appears with Sx & ECG changes of STEMI but normal angiogram
*contiguous = represent same territory
Medicine

General Medicine and Surgery.indb 2 11-Jan-23 3:01:47 PM

 Chapter 1: Cardiology  3

Management1

NSTEMI/UA STEMI
Acute Morphine + metoclopramide (5–10mg) Remember acute management as 'MONA(A)'
Oxygen (if sats <90%)
Nitrates (GTN spray)
Antiplatelets (300mg chewable aspirin + loading dose ticagrelor/clopidogrel/prasugrel)
Anticoagulant (fondaparinux 2.5mg for 72h)
1. GRACE score: assess inpatient & 6m First line: primary PCI ideally if
mortality <120min from onset (95% success)
2. DAPT score: predicts who will benefit Target 150min call → balloon time
from dual antiplatelet therapy
Second line: thrombolysis
3. Angiographic assessment
(rarely used as many contraindications)
4. Revascularisation options: PCI, CABG
Long- A 1. Lifelong Aspirin: 75mg OD
RETURN TO DRIVING:
term A 2. Continue 2nd Antiplatelet: ticagrelor/clopidogrel/prasugrel (for 1y)
Angina: if Sx controlled
BB 3. Lifelong Beta-Blocker: bisoprolol (HR at 60bpm)
PCI: 1w
A 4. Lifelong Atorvastatin
CABG: 4w
A 5. ACEi: ramipril
ICD: 6m
6. Treat underlying problems: HF/HTN (BP<140/90)
Rehab Optimise physical, psychological & social functioning + stabilise/slow atherosclerosis
Patient education: about risk factors for CVD
Exercise programme: gradual return
Return to work: usually after 2w (depends on job)

GRACE score parameters to predict inpatient & 6m mortality NSTEMI: dual antiplatelet therapy
1. Age Aspirin + ticagrelor/clopidogrel/prasugrel
Although GRACE score has good predictive value → consider lower dose if high bleeding risk
2. HR of mortality, it is often not used in practice.
3. SBP (HASBLED score)
4. Creatinine Local logistics determines speed of cardiac → consider stopping if going for CABG
5. Any CHF catheterisation. STEMI have primary PCI revascularisation
6. Cardiac arrest at admission immediately on arrival, NSTEMI and unstable → consider GI protection with PPI if >65y or Hx
7. ST segment changes angina have inpatient cardiac catheterisation as of GORD/PUD
8. Elevated cardiac markers soon as feasible, prior to discharge.

Complications of ACS

D Death
A Arrhythmia AF, VF, VT, bradyarrhythmias (VF = most common complication)
R Rupture Of papillary muscles / ventricular wall / septum (causes MR, VSD & LVF)
Beck’s triad:
T Tamponade Due to ventricular wall rupture = Beck’s triad
H Heart failure May be due to VSD = cardiogenic shock 1.  JVP
2.  BP
3. Quiet heart sounds
V Valve problem Due to papillary muscle dysfunction/rupture = new murmur
A Aneurysm of Due to weakened ventricular wall
ventricle Dressler’s syndrome:
D Dressler’s syndrome Immune-mediated pericarditis (usually 2–3w later) 1. Fever
E Emboli From thrombus forming over damaged left ventricle wall 2. Chest pain
3. Exertional dyspnoea
R Recurrence
4. Pericardial effusion

1 NICE (2020) Acute coronary syndromes [NG185]

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 20  Chapter 2: Endocrinology

Pituitary disorders
The pituitary gland sits below the hypothalamus & optic chiasm

Mass effects of pituitary adenoma: Pituitary adenoma: BENIGN

• Bitemporal hemianopia = from pressure on 1. Microadenoma <1cm
optic chiasm 2. Macroadenoma >1cm = mass effects Fig. 2.3  Visual fields in
• Ocular palsies = from pressure on cavernous • Functioning: secrete hormones (70–80%) bitemporal hemianopia.
sinus (CN 3,4,6)
• Non-functioning: not secretory (20–30%)
• Headache from  ICP
• Altered appetite/thirst/sleep = from pressure (GH-RH) Growth hormone-releasing hormone
on hypothalamus (TRH) Thyrotropin-releasing hormone
• Hypopituitarism from destruction of (CRH) Corticotropin-releasing hormone NEUROSTIMULATION
(GnRH) Gonadotropin-releasing hormone
functional tissue (SRIF) Somatotropin release inhibiting
• Hyperprolactinaemia from stalk effect factor / somatostatin inhibitor
Ant Post Oxytocin
(DA) Dopamine Breasts &
GH uterus
Bones, ADH
‘The stalk effect’ muscles ACTH Kidneys
Prolactin TSH
→ Dopamine released from hypothalamus Breasts LH Thyroid
FSH Adrenal
reaches pituitary gland via pituitary stalk gland
gland
Ovaries &
→ Normally dopamine INHIBITS prolactin testes T3 & T4
→ Damaged/compressed stalk =  DA = Aldosterone
cortisol
 inhibition = HYPERPROLACTINAEMIA Oestrogen
Progesterone
→ Secretory prolactinoma plus compression Testosterone

effects = MASSIVE PROLACTIN  (>10,000) Fig. 2.4  Functions of the pituitary gland.

Hypopituitarism

Hypopituitarism: Hormone Clinical effects Management

• Sx = vague & non-specific lacking
• General Mx = HORMONE REPLACEMENT GH Children: short stature GH analogue
Typical order of hormone loss

• Ix & Tx of specific cause Adults: no Sx / abnormal body

composition / fatigue
LH/FSH ( sex Children: delayed puberty Testosterone (males)
hormones) Adults: no Sx / hypogonadism /  or HRT (females)
amenorrhoea
TSH ( T3/T4) Hypothyroidism (cold, weight loss, tired) Thyroxine
ACTH ( cortisol) Lethargy, weight loss,  glucose,  Na Hydrocortisone/prednisolone
DDx hypopituitarism:
PROLACTIN Failed lactation –
Pituitary Hypothalamic
ADH Diabetes insipidus (polyuria/polydipsia) Desmopressin
• Non-functioning • Craniopharyngioma
adenoma • Infarction
• Metastatic tumour • Infection INVESTIGATIONS:
• Surgical resection of • Sarcoid 1. History & examination: including visual fields & cranial nerves
gland 2. Pituitary hormones:
• Apoplexy (vascular
• All except prolactin: LOW/normal
insult)
• PROLACTIN
→ 500–1000: (micro-prolactinoma) or (non-functioning tumour
compressing stalk) or (other cause of  prolactin*) • Renal impairment
→ >1000: (micro-prolactinoma AND stalk compression) • Antipsychotics
or (macroprolactinoma) • Pregnancy/OCP
3. Effector gland hormones: LOW (T3/T4, FSH*, IGF-1, 9am cortisol)
    *FSH should be high if post-menopausal as  oestradiol (no more follicles)

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 Chapter 2: Endocrinology  21

4. Stimulation tests: LOW / no response

• For ACTH deficiency: insulin When given insulin, blood glucose
stress test (IST) drops → hypoglycaemia triggers ACTH
• For acromegaly: OGTT → GH release – no  ACTH suggests deficiency
suppression
• For non-pituitary cause of
adrenal disease: Synacthen test When given glucose in OGTT, GH
should be suppressed
5. Imaging: CT/MRI – determine
No suppression suggests acromegaly (check
pathology
IGF-1 levels)

Secretory/functional adenomas
→ can produce >1 hormone

Type of adenoma Hormonal effect Symptoms Treatment

Prolactinoma 35% HYPERPROLACTINAEMIA • Galactorrhoea (+ female amenorrhoea) DA agonist* *SE: pulmonary
(F:M = 5:1)  basal prolactin •  Fertility,  libido, hypogonadism • carbergoline fibrosis (need CXR)
• Complications: osteoporosis • bromocriptine
GH-secreting 20% ACROMEGALY/GIGANTISM •  Size hands/feet slow onset 1. Surgery: transsphenoidal
 IGF-1 & glucose • Coarse facies, wide-spaced teeth 2. Radiotherapy
• Vision loss 3. Medical
• Tired, headache, sweaty,  libido • DA agonist
• Complications: DM, HTN, OSA • somatostatin analogue
ACTH-secreting 10% CUSHING DISEASE •  Weight, DM,  libido
 cortisol • Hair, striae, hump
TSH-secreting rare HYPERTHYROIDISM •  Weight, fatigue
 T3/4 • Hot, sweaty, palpitations

Raised TSH & T4 usually indicates poor compliance with LT4 treatment
LH-/FSH-secreting adenoma = VERY RARE

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 Chapter 3: Gastroenterology  39

Oesophageal cancer
→ UK prevalence: 14 in 100,000 (increasing due to RFs)
→ M:F = 2:1
Presents late & POOR PROGNOSIS4
Squamous cell (20%): upper 2/3 oesophagus
RF = smoking, alcohol, Asian, achalasia Stage 5y Survival
Adenocarcinoma (80%): lower 1/3 oesophagus 1 53%
RF = smoking, alcohol, obesity, Barrett’s oesophagus (GORD) 2 30%
3 16%
Symptoms
4 0%
• Progressive dysphagia: solids → • Retrosternal chest pain Overall 17%
liquids → saliva • Lymphadenopathy
• Weight loss & anorexia • ± cough, aspiration, hoarseness

Investigations
• OGD & biopsy – histological grading
• CT chest, abdo, pelvis – TNM staging
• Endoscopic USS – more detailed T&N staging
• PET scan – detects metabolically active mets
TNM staging
Tumour Nodes Metastases
Tis – tumour in situ N0 none M0 no mets
T1a – invades lamina propria N1 1–2 LNs M1 distant mets
T1b – invades submucosa N2 3–6 LNs
T2 – invades muscularis propria N3 7+ LNs
T3 – invades adventitia
T4 – invades adjacent tissues

Management5 Management requires an MDT approach

Adenocarcinoma
Tis or T1a (N0, M0) Endoscopic mucosal resection/dissection (EMR/EMD)
T1b (N0, M0) or >75yrs Surgical resection or definitive chemoradiotherapy
Complications of upper GI surgery:
T2, T3, T4 (M0) Neoadjuvant chemo → surgery + adjuvant chemo
• Weight loss – need dietetic support
Squamous cell carcinoma • Dysphagia – due to strictures
T1a (N0) EMR/EMD • Reflux
All others (M0) Neoadjuvant chemo → surgery + adjuvant chemo • Delayed emptying
Any histology with mets (M1) = palliative care
1. Chemo ± radiotherapy
2. Symptom relief: stents, analgesia
SURGICAL OPTIONS:
Ivor Lewis oesophagectomy (2 stage → open or keyhole) Oesophagus
Part removed Stomach
Stage 1 (abdominal): re-joined
• mobilise / free stomach from blood supply
Stage 2 (thoracic):
• mobilise & resect affected part of oesophagus
• pass ‘free’ stomach through hiatus & staple to remaining oesophagus
• pylorectomy to improve gastric emptying post-op
NB. Oesophageal surgery = high morbidity & mortality Fig. 3.2  Ivor Lewis oesophagectomy.
→ need careful pre-op assessment for suitability
4 Cancer survival by stage at diagnosis for England, 2019. ONS.
5 NICE (2018) Oesophago-gastric cancer [NG83] Medicine

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 40  Chapter 3: Gastroenterology

Gastric cancer
→ UK prevalence*: 10 in 100,000 → 5th most common cancer worldwide6
*prevalence is increasing globally due to increased → M:F = 3:1 → Peak age: 50–70y
prevalence of modifiable RFs
Types
Risk factors:
→ Internal: pernicious anaemia, H. pylori, 1. Adenocarcinoma (85%)
polyps 2. Other (15%) – lymphoma, leiomyosarcoma, GISTs
→ External: smoking, high salt/nitrate
(red meat) Symptoms
→ Genetic: Japanese, HNPCC, Group A blood
• Epigastric pain / dyspepsia
• Early satiety
Presents late & POOR PROGNOSIS7 often non-specific & mimic PUD
• N&V, anorexia, weight loss
Stage 5y Survival • Dysphagia
1 65%
2 36% Investigations
3 24% • OGD & multiple ulcer edge biopsies – histological grading & location
4 0% • CT chest, abdo, pelvis – TNM staging (same as oesophageal)
Overall 20% • Endoscopic USS – more detailed T&N staging

Signs O/E
• Epigastric mass (50%)
• Virchow’s node enlargement only in late stage / metastases
• Hepatomegaly, ascites
• Jaundice, acanthosis nigricans

Management8

Any histology with mets = palliative care Adenocarcinoma

1. Chemo ± radiotherapy Tis or T1a (N0, M0) Endoscopic mucosal resection
2. Symptom relief: stents, bypass, analgesia T1b (N0, M0) or >75y Direct to surgery
T2, T3, T4 (M0) Neoadjuvant chemo → surgery + adjuvant chemo

SURGICAL OPTIONS:
Siewert class Location Management
Gastrectomy complications: 1 1–5cm above GOJ Oesophagectomy
• Vit B12 / iron deficiency 2 <1cm above or <2cm below GOJ Oesophagectomy or total gastrectomy
• Early satiety / weight loss
• Osteoporosis/osteomalacia 3 2–5cm below GOJ Total gastrectomy
Distal Near pylorus Distal gastrectomy

Total gastrectomy + Roux-en-Y reconstruction:

1. Resection of stomach
2. Connect proximal jejunum to lower oesophagus
3. Reconnect distal duodenum further down jejunum to allow
passage of bile
Duodenum / Distal gastrectomy:
Part removed jejunum
re-joined 1. Resection of distal part of stomach
2. Various reconstruction options (Roux-en-Y = better outcome
but  risk)
Fig. 3.3  Distal gastrectomy.
6 InternationalAgency for Research on Cancer, WHO 2020
7 Cancer survival by stage at diagnosis for England, 2019. ONS.
Medicine 8 NICE (2018) Oesophago-gastric cancer [NG83]

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 Chapter 4: Hepato-pancreato-biliary  55

Gallbladder disease
→ Gallbladder stores and concentrates bile
→ Fatty acids / amino acids in duodenum stimulate CCK release
Contents of bile:
→ CCK stimulates gallbladder contraction & bile release
• Water (97%)
Investigations • Bile salts / pigments
• Cholesterol
1. History & abdo exam + pregnancy test + urine dip
• Phospholipids
2. Bloods: FBC, CRP/ESR, LFTs, clotting (± amylase)
3. Imaging:
→ USS (shows GB/duct dilation) → ERCP (Dx & Tx but invasive) USS = FIRST-LINE imaging
→ MRCP (95% sensitive to detect stone) → CT if concerned about tumour

Types of bile stone

1. CHOLESTEROL – crystallisation of excess cholesterol Risk factors*: *Crohn’s & ileal resection = additional RFs as  bile
2. PIGMENT – contain calcium bilirubinate salt absorption
Fat Female
• Black: haemolytic conditions (SCA, malaria) Fair Fertile
• Brown: biliary stasis or infection Forty FHx

Complications of gallstones
most gallstones = asymptomatic, until complications
1. In gallbladder: biliary colic (cystic duct obstruction), acute cholecystitis,
perforation*, carcinoma *needs emergency cholecystectomy
2. In bile ducts: biliary colic (common duct obstruction) → ascending cholangitis Mirizzi’s syndrome:
or acute pancreatitis
Gallstone impacts in cystic duct / Hartmann’s
3. In intestine: gallstone ileus (stone erodes through gallbladder = fistula to
pouch
duodenum → intestinal obstruction) AXR shows air in biliary tree • Extrinsic compression of hepatic duct
• Obstructive jaundice without dilation of CBD
Management4
• C. perfringens
• Klebsiella
OBSTRUCTION INFLAMMATION INFECTION • E. coli

BILIARY COLIC ACUTE CHOLECYSTITIS ASCENDING CHOLANGITIS

= temporary duct obstruction = long-term cystic duct obstruction = long-term common bile duct
Systemically well! causes inflammation of GB wall obstruction causes duct infection
Symptoms: Systemically unwell! Symptoms:
• Colicky RUQ / diffuse pain Symptoms: Charcot’s triad:
(visceral) Initially: biliary colic 1. High swinging
▶ crescendos (stop if stone moves) With inflammation: (localised pain) fever (chills Reynolds’ pentad:
▶ radiates to back/shoulder • Fever & vomiting + rigors) + 4. Confusion
▶ worse with food (esp. fatty) • Severe RUQ pain + peritonism 2. RUQ pain + 5. Shock
• ± N&V 3. Jaundice (ICU admission)
O/E:
• Obstructive jaundice Investigations:
Guarding & rigidity + Murphy’s sign
if common duct blocked/Mirizzi’s • Bloods:  WCC, CRP, ESR
Investigations:
Investigations: • LFTs: obstructive picture
• Bloods:  WCC, CRP, ESR
• Bloods = normal Management: ABCDE + Sepsis 6
• USS/MRCP (dilation, thick GB wall)
• USS/MRCP (shows dilation/stones) • IV fluids, analgesia + IV ABX
Management: ABCDE
Management: (e.g. cefuroxime + metronidazole)
• IV fluid, analgesia + IV ABX
• Bed rest, fluid, analgesia, NBM • Emergency ERCP ± stenting
• Elective cholecystectomy (by 1w
• Elective cholecystectomy (by 6w)
but ideally within 72h)

Key DDx: GORD, PUD, acute pancreatitis, Murphy’s sign: press over GB – patient has sharp pain during inspiration as
IBD, acute hepatitis, pyelonephritis peritoneum hits your hand
4 BMJ Best Practice (2021) Gallstones, acute cholecystitis, acute cholangitis
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 56  Chapter 4: Hepato-pancreato-biliary

Other gallbladder pathologies

Courvoisier’s law:
CARCINOMA OF THE GALLBLADDER
Painless, obstructive jaundice with palpable → Uncommon (occurs in elderly)
gallbladder = unlikely due to gallstones → Associated with long-standing gallstones
→ think carcinoma of pancreas
Symptoms:
• RUQ pain
Sx occur late (& then mimic
• Weight loss chronic cholecystitis)
• Obstructive jaundice & palpable mass (late sign)

Management: poor prognosis as late presentation

• Radical cholecystectomy (± liver resection if affected)

CHOLANGIOCARCINOMA (adenocarcinoma of bile ducts / ampulla)

→ Common sites = at ductal confluences
→ Mostly in elderly patients
→ Can be 2° to PSC/IBD

Symptoms:
• Painless progressive jaundice Sx occur late & mimic
• Weight loss PANCREATIC CANCER

Management: poor prognosis as late presentation

• Whipple’s procedure (if operable)
• Palliative stenting (relieves jaundice & helps gastric emptying)

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 Chapter 5: Haematology  61

Anaemia overview
Anaemia is defined as Hb <130g/L in men & <115g/L in women
Key questions to ask:

Causes 1. Isolated anaemia or pancytopenia?

(pancytopenia suggests BM failure)
1.  RBC production e.g. IDA (most common), BM disorders, cytotoxic 2. What is the MCV?
drugs / chemotherapy, CKD, aplastic anaemia
2.  RBC destruction e.g. SCD, thalassaemias, G6PD deficiency, autoimmune
haemolysis All patients are screened for anaemia
3. Blood loss (rare in children) e.g. vWD, Meckel diverticulum before surgery

→ If <100g/L check haematinics and replace

Signs/symptoms if low
General signs/symptoms → If <60g/L as above, but transfuse if active
• Fatigue/weakness bleeding
• Pallor (conjunctiva) Symptoms occur if Hb <60–70g/L
• SOB/tachycardia/dizziness
DDx microcytic anaemia: TAILS
Specific signs/symptoms • Thalassaemia (α or β-thalassaemia trait)
→ Koilonychia: IDA • Anaemia of chronic disease e.g. renal failure
→ Jaundice: haemolytic anaemia • Iron-deficiency anaemia
→ Leg ulcers: sickle cell disease • Lead poisoning
→ Tingling fingers/toes: B12 deficiency • Sideroblastic anaemia

Investigations
DDx macrocytic anaemia: ABCDEF
• FBC – MCV (size of RBC) & MHC (Hb per RBC), reticulocytes • Alcohol & liver disease
• Iron studies – serum iron & ferritin, TIBC • B12 deficiency
• Blood film – size, shape, colour of red cells • Compensatory reticulocytosis (blood loss)
• Serum bilirubin – high in haemolysis • Drugs (cytotoxic)
• Hb HPLC or Hb electrophoresis – shows amount of each Hb type • Endocrine (hypothyroidism)
(HbS, HbA, HbF) • Folate deficiency

Types of haemoglobin
DDx normocytic anaemia: CHARMD
Fetal (HbF): 2α chains + 2γ chains → higher O2 affinity
• Chronic disease ( iron +  ferritin)
Adult (HbA): 2α chains + 2β chains → lower O2 affinity
• Haemolysis
Adults normally have 2 HbA alleles (HbAA). Patients with haemoglobinopathies such as • Acute blood loss
thalassaemia or SCD have at least one abnormal allele, causing non-HbA haemoglobins • Renal anaemia (causing low EPO levels)
(e.g. HbSS, HbAS) • Marrow disorder
• Deficiencies combined (iron + B12)

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 62  Chapter 5: Haematology

Anaemia from reduced RBC production

Must r/o GI bleed
in older patients
Iron-deficiency anaemia
→ most common anaemia worldwide (especially menstruating females)
Causes:
• Inadequate intake – Fe-deficient diet e.g. vegetarian
• Malabsorption – coeliac, gastrectomy
• Increased requirements – pregnancy
NB. Ferritin will be raised in
• Chronic blood loss – menorrhagia / GI bleed
inflammation
Dietary advice for IDA Diagnosis:
High Fe foods: 1. FBC:  MCV = microcytic
• Red meat, liver • Oily fish 2. Iron studies:  serum iron &  serum ferritin,  TIBC (body tries to  Fe uptake)
• Pulses, beans, peas • Fortified cereals 3. Blood film: abnormally shaped, small, hypochromic (pale) RBCs
• Leafy, green veg • Dried fruit / nuts Management1: e.g. GI malignancy
Vit C (fruit & veg) helps Fe absorption 1. Determine cause: thorough Hx & exam → r/o serious causes
Foods to avoid: ▶ OGD/colonoscopy, anti-tTG, menorrhagia Hx
• Excess cow’s milk (only 10% Fe is absorbed) 2. Treat underlying cause
• Tannin (tea) (inhibits Fe absorption) 3. Dietary advice
4. Oral iron supplements e.g. ferrous sulphate/fumarate
▶ TDS until Hb normal then minimum 3m OD
▶ Can use IV iron if oral not tolerated/absorbed
NB: if no response to Tx consider Ix for other causes (esp. malabsorption)

B12 & folate deficiency

Intrinsic factor binds B12 in stomach to → causes pernicious anaemia
enable absorption in the terminal ileum Causes of B12 deficiency:
• Low dietary intake – vegan/vegetarian
B12 = coenzyme needed for folate conversion • Malabsorption (in terminal ileum) – e.g. Crohn’s, gastrectomy
Folate = needed for RBC synthesis • Low intrinsic factor – e.g. autoimmune (pernicious anaemia)
Causes of folate deficiency:
B12 deficiency can cause peripheral neuropathy, • Low dietary intake
subacute spinal cord degeneration & angular • Malabsorption (in duodenum/jejunum) – e.g. coeliac, jejunal resection
cheilitis • Increased requirements – pregnancy, haemolytic anaemia
Diagnosis:
If B12 AND folate deficient, must replace 1. FBC:  MCV = macrocytic – often >125
B12 first to avoid subacute combined 2. Blood film: hypersegmented neutrophils (>5 lobules) & tear-drop cells
degeneration of the spinal cord 3. Iron & B12 studies:  B12,  serum folate,  cobalamin
4. Intrinsic factor antibodies B12 = eggs, fortified cereals, dairy
Management2: Folate = broccoli, peas, brown rice
• If not pernicious anaemia, dietary advice
• IM B12 & folic acid (5mg OD) supplements (4m)
• If pernicious anaemia: lifelong IM B12 replacement (hydroxocobalamin)

RBC aplasia
→ failure of RBC synthesis
Diagnostic results in RBC aplasia:  Hb, Causes:
 reticulocytes, normal BR, Coombs test –ve • Diamond–Black anaemia = rare, congenital → raised MCV ± short stature,
abnormal thumbs
• Transient erythroblastopenia = triggered by viral infection in children
• Parvovirus B19 – infects young RBCs – only causes RBC aplasia in children/
adults with inherited haemolytic anaemia
1 BNF Treatment Summary – Anaemia, Iron Deficiency
2 BNF Treatment Summary – Anaemia, Megaloblastic
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 88  Chapter 7: Neurology Nervous system structure & function

Spinal cord tracts

The descending spinal tracts
Corticobulbar tract innervates each cranial
nerve bilaterally except for: Pyramidal tracts = voluntary control (cerebral cortex → brainstem & spinal cord)

1. Facial nerve (CN VII): Corticospinal: voluntary movement of Corticobulbar: voluntary movement of face &
→ Forehead = bilateral representation contralateral body neck
→ Branch to lower face = unilateral → Originate in motor cortex → Originate in motor cortex
representation → Decussate in medullary pyramids → Terminates in brainstem
→ UMN lesion spares frontalis → Synapse with LMNs in spinal cord → Synapse with cranial nerves
2. Hypoglossal (CN XII):
→ Each half of tongue supplied by contralateral The ascending tracts
corticobulbar tract
→ Lesion causes contralateral weakness, so Dorsal column medial Spinothalamic Spinocerebellar
tongue deviates towards weak side lemniscus (DCML)
Fine touch, vibration, Pain & temperature Unconscious proprioception (ipsilateral)
proprioception (contralateral) (awareness of position & movement of
(contralateral) body parts in space without conscious
thought)

UMNs Upper motor neurones vs. lower motor neurone lesions

Cerebral
cortex UMNs: motor cortex → internal capsule → brainstem → spinal cord
Head & Neck LMNs: anterior horn cell → nerve root → peripheral nerve → NMJ → muscle
Brainstem Cranial n. muscles
Upper motor neurone lesion Lower motor neurone lesion
(brain + spinal cord) (peripheral nerves)
Limb
Spinal n. muscles Signs • Hypertonia • Hypotonia
Spinal • Hyper-reflexia • Hypo-reflexia
cord
LMNs • Pyramidal weakness* • Proximal/distal weakness
Fig. 7.3  Pathway of UMNs & LMNs. • Clonus • Wasting
• +ve Babinski • Fasciculations
• Spastic gait
*Pyramidal weakness:
Upper limbs: extensor muscles weaker than Causes • Stroke / brain tumour • Peripheral neuropathy (DM, alcohol, drugs)
flexors • Spinal tumour / injury • Polio (anterior horn cells) / Guillain–Barré
= results in flexed elbow & wrist • Cerebral palsy / MS • MND
Lower limbs: flexor muscles weaker than • Myasthenia gravis
extensors
= results in extended knee/ straight leg Facial weakness

Upper motor neurone lesion Lower motor neurone lesion

Signs • Contralateral weakness • Ipsilateral weakness
• Frontalis spared • Whole face
Causes • Stroke / brain tumour • Bell’s palsy
• Subdural haematoma • GBS (usually bilateral)
• MS • Infection (HSV, CMV, EBV, Lyme disease)
• Trauma

Bulbar palsy: LMN lesion causing dysarthria Pseudobulbar palsy: bilateral UMN lesion causing dysarthria = damage to medullary
= weakness of muscles supplied by CN IX, X, XII cranial nerves
→ Nasal speech / dysarthria → ‘Donald Duck’ speech (spastic dysarthria)
→ Hyporeflexia: jaw jerk & gag reflex absent → Hyperreflexia: jaw jerk & gag reflex increased
→ Tongue: weak & wasted & fasciculations → Tongue: weak & spastic

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 Nervous system structure & function Chapter 7: Neurology  89

Dermatomes Myotomes

Nerve root Motor function

L1 C5 Elbow flexion
C4 L2
L1 C6 Wrist extension
T2
S2
S3 C7 Wrist flexion, finger extension, elbow extension
S5 S4
L2 C8 Finger flexion
C5 T1 Finger abduction
L1,2 Hip flexion
T1 S2
L3
L3 Knee extension
L4 Ankle dorsiflexion
L5 Knee flexion, big toe extension
C6
S1 Knee flexion, ankle plantarflexion, big toe flexion
L4 L5
L5 L4

Deep tendon reflex Nerve roots

C8 S1 Biceps + brachioradialis C5, C6
C7
Triceps C7, C8
S1
Knee jerk L3, L4
Fig. 7.4 Ankle jerk S1, S2

Focal peripheral nerve lesions

Lesion Symptoms Sensory loss Motor loss Causes

Median nerve • Pain/tingling in Dorsal & palmar aspect • Middle & index fingers (L) • Repetitive motion
(C5–T1) hand of lateral 3.5 digits • Thenar muscles (OAF) • DM/thyroid
Carpal tunnel • Thenar muscle Lumbricals • RA/OA
wasting Opponens • Pregnancy
Abductor pollicis brevis
Flexor opponens
Ulnar nerve • Pain/tingling in Dorsal & palmar aspect All small hand movement except LOAF • Elbow trauma
(C8–T1) hand of medial 1.5 digits (interossei/lumbricals) • Idiopathic
Cubital tunnel • Weak grip • Finger abduction & adduction
• Ulnar claw • Thumb adduction
(paradox) • Little & ring finger flexion
• Wrist flexion
Radial nerve • Wrist drop Dorsal hand & 1st web Brachioradialis: Wrist extension • Humerus fracture
(C5–T1) space Extensor digitorum: Finger extension
Brachial plexus • Erb’s palsy Shoulder & arm Deltoid, biceps, brachialis, rotator cuff, • Idiopathic
(C4–T1) (weakness, serratus anterior • Trauma
sensory loss & • Damage from assisted delivery at birth
muscle atrophy) • Compression
• Inflammatory
Axillary nerve • Deltoid wasting Regimental badge area Deltoid: shoulder abduction • Proximal humerus fracture
(C5–C6)
Common • Foot drop Lateral calf & dorsum Tibialis anterior: dorsiflexion & eversion • Sporting injury
peroneal nerve of foot   (direct trauma near knee)
(L4–S2) • Fibular head fracture
• Habitual leg crossing
Medicine

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 116  Chapter 8: Renal

Chronic kidney disease = progressive & irreversible

deterioration of renal function (>3m)

Classification
Factors increasing risk of needing RRT
→ use to identify those most at risk of needing RRT
• Younger age • Male gender Base on 2 factors:
• Lower eGFR • Higher ACR Persistent albuminuria
1. GFR
2. Albuminuria A1 A2 A3

Signs/symptoms: <3mg/mmol 3–30mg/mmol >30mg/mmol

GFR (ml/min/1.73m2) G1 ≥90
Early stages = asymptomatic
• Anaemia: pallor, fatigue G2 60–89
• Bone disease: osteomalacia/fractures G3a 45–59
• Hyperkalaemia: palpitations, dizziness, G3b 30–44
chest pain
• Fluid overload: peripheral oedema, SOB G4 15–29
• Early uraemia: fatigue, anorexia, N&V, G5 <15
pruritus, hiccups Table based on KDIGO AKI staging system.
• Late uraemia: confusion
• Metabolic acidosis:  HR & RR, vomiting,
Causes of deteriorating GFR
fatigue, headache
• Other: sexual dysfunction = common
Diabetes mellitus (38%) Glycation of efferent arteriole =  pressure & sclerosis
** CKD associates with cardiovascular events Hypertension (25%) Thickened walls of afferent arteriole = hypoperfusion
& AKI **
Chronic glomerulonephritis (16%) Inflammation & damage to vessels
Investigations: Chronic pyelonephritis Urinary reflux or recurrent infection

1. Urine dip & BP Obstructive uropathy Back-up of pressure = hydronephrosis & damage
→ Urine protein–creatinine ratio → neurogenic bladder, BPH, malignancy, stones
for nephrotic syndromes Polycystic kidney disease (PKD) → Auto dominant form presents in adults
→ Urine albumin–creatinine ratio (ACR) → Fluid-filled cysts press on nephrons = atrophy
for CKD → Sx: back pain, headaches, haematuria, HTN
2. Bloods:
→ U&Es – compare to previous eGFR → Risk factors for CKD decline: HTN, DM, smoking, infection, NSAIDs/ACEis
→ Bicarbonate – acid–base balance lost
→ Hb – normocytic anaemia Management of CKD4
→ PTH ( if bone disease & also  ALP)
→ Glucose (for DM)
RISK REDUCTION of CVD: lifestyle factors are important
→ ANA, ANCA, complement 1. BP control: ACEi/ARB if proteinuria (BP<140/90 or <130/80 if diabetic)
3. USS kidney (kidneys may be small) 2. Cholesterol control: statin
Advise low salt & phosphate diet
4. Renal biopsy – if still unsure of cause 3. Comorbidity control: diabetes control
5. CXR – for pulmonary oedema 4. Stop smoking
5. Weight management

Pathogenesis of renal bone disease: TREAT/MANAGE COMPLICATIONS

1. Anaemia – IV iron + EPO stimulating agents (r/o B12/folate deficiency first)
 Vit D activation in kidneys =  Ca absorption 2. Bone disease – vit D & calcium supplements if deficient, phosphate binders
= 2° hyperparathyroidism ( PTH) 3. Oedema – careful fluid monitoring ± diuretics
 PTH causes  osteoclastic activity
=  Ca resorption from bone to restore serum Ca
= leaves bone weak
In kidney transplant patients, parathyroid
gland may become autonomous in spite
of normal renal function = tertiary
hyperparathyroidism

4 NICE (2021) Chronic kidney disease [NG203]

Medicine

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 Chapter 8: Renal  117

MANAGE MEDICATIONS
1. Stop drugs that worsen glomerular function / acute nephrotoxics
2. Alter dose of medications if GFR is low e.g. stop metformin if GFR <30

REFER TO NEPHROLOGY: if GFR <30 or  >15 in 1y or 5y risk of needing

RRT >5% (using kidney failure risk equation5)
→ assess & manage symptoms/complications & prep for RRT

Renal replacement therapy options

ensure patients are fully informed of all options &
DIALYSIS: usually started around eGFR 10, unless there are complications supported in decision-making
Haemodialysis Peritoneal dialysis
Method Blood pumped out of body Dialysate solution infused into peritoneal cavity
through ‘artificial kidney’ (peritoneum acts as filtering membrane)
Access AV fistula / semi-permanent Catheter into peritoneum
jugular or subclavian catheter
Complications Site infection, hypotension, Peritonitis, catheter problems, hernia, fluid
air embolus, N&V, endocarditis retention, weight gain
Frequency 3 × 4h sessions each week Continuous ambulatory = 4 × 20min each
day while active
Automated = overnight (3–5 exchanges over
8–10h)

KIDNEY TRANSPLANT: gold standard for those with end-stage CKD

→ but only 40% of patients with CKD 5 are suitable Who is suitable?
• Generally fit for general anaesthetic
Process: • At least 5y left to live
→ Transplant placed in iliac fossa & anastomoses of vessels made • No underlying malignancy
→ Usually leave native kidney in place • No other significant comorbidities
• Good vascular supply to legs
Post-transplant treatment:
→ Lifelong immunosuppression = tacrolimus or ciclosporin plus azathioprine/ + a suitable match is found:
MMF → ABO, tissue type, age & gender
→ 6m of steroids to prevent acute rejection e.g. prednisone + Need to assess suitability of donor:
→ Aspirin, antihypertensives, PPI, bone protection urine dip, U&Es, USS & general fitness
Complications:
• Immediate: graft thrombosis, ureteric leak/obstruction, bleeding, rejection
• 3–6m: rejection, HTN, ileus, infections (urinary or respiratory)
• Long-term: cancer, interstitial fibrosis (2° to ciclosporin/tacrolimus),
cardiac disease, infections

Ethical issue: waiting list of >4500 (avg. wait = 3y)

Transplant rejection: 10–20%
Points to consider for transplant: → Often asymptomatic (concern if rise in Cr)
Pros Cons → RFs: non-concordance, drug interactions,
• Medication burden poor match
•  Longevity (80% 10y survival)
• Immunosuppressive SEs → Tx: IV methylprednisolone &
•  Quality of life (free from dialysis)
• Frequent hospital visits  immunosuppressants

et al. (2019) The Kidney Failure Risk Equation for prediction of end stage renal disease in UK
5 Major,

primary care. PLOS Medicine, 16:e1002955

Medicine

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 124  Chapter 9: Respiratory

Pleural effusion
Accumulation of fluid in pleural cavity
Types of fluid
Empyema: pus (infection) Symptoms Signs
Chylothorax: lymphatic fluid
May be asymptomatic •  Expansion
Haemothorax: blood (trauma)
• SOB ± pleurisy • Stony dull percussion
Fluid: transudate or exudate
• Sx of underlying cause • Absent breath sounds
•  Vocal resonance / tactile fremitus
• Tracheal deviation away if massive

Investigations

1. CXR – blunted CPAs, homogenous consolidation (only detect if >300ml)

2. USS – identify location & volume
3. Pleural tap (US guidance)* *1–2 intercostal spaces below
upper border of effusion
• Microbiology: MCS
• Clinical chemistry: protein, LDH, glucose, pH
• Cytology: 80% sensitive for malignancy
4. Further Ix if no obvious cause:
• Pleural biopsy – r/o malignancy/TB
Fig. 9.2  Left-sided pleural effusion.
• CT with contrast – shows pleural thickening

Types of pleural effusion

Transudate Exudate
Pathophysiology Movement of fluid from circulation → pleural space Production & secretion of fluid into pleural space
 Capillary hydrostatic pressure or  Capillary permeability
 Capillary oncotic pressure
Causes • Congestive heart failure ( hydrostatic pressure) Inflammation: trauma, RA, sarcoid, SLE
• Renal failure ( oncotic pressure  albumin) Infection: pneumonia, TB
• Liver failure ( oncotic pressure  albumin) Infarction: PE, post-MI (Dressler’s)
• Hypothyroidism Malignancy: 25% of effusions
Medication: MTX, amiodarone, phenytoin
Presentation Bilateral Unilateral
Fluid Lower protein, lower LDH Higher protein, higher LDH
<25g/L protein +  LDH >30g/L protein +  LDH
Management Usually improve with Tx of underlying cause Pleural tap all with pneumonic illness or suspected malignancy + effusion
→ Usually do not need tapping/drainage Treat cause & drain if moderate/large

LIGHT’S CRITERIA Specific management of pleural infection (empyema)2

used to distinguish transudate & exudate if
protein 25–35g/L 1. Pleural tap: pH <7.2, low glucose, high LDH
• Simple parapneumonic infection = straw colour with no orgs
Transudate Exudate • Loculated empyema = pockets of semi-solid pus
Pleural:serum <0.5 ≥0.5 2. IV ABX for minimum 2w
protein 3. Chest drainage: if frank pus / organisms cultured / pH <7.2 / no improvement
4. Decortication (VATS: video-assisted thoracoscopy): remove restrictive layer
Pleural:serum <0.6 ≥0.6
LDH of fibrous tissue → if long-standing pus / thickened pleura
Sx of empyema =
Pleural fluid <2/3 upper >2/3 upper effusion + FEVER
Organisms causing empyema:
LDH limit of normal limit of normal
Strep. milleri, H. influenzae, E. coli, Staph. aureus, Pseudomonas

2 BMJ Best Practice (2021) Pleural effusion

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 Chapter 9: Respiratory  125

Pneumonia = signs of respiratory tract infection + new shadowing on CXR

Community-acquired pneumonia Hospital-acquired pneumonia

Primary or secondary to lung disease >48h after admission or within 10d Risk factors for pneumonia:
of discharge • Immunocompromised
• Strep. pneumoniae (80%) • Gram-negatives: • Hospitalised
• H. influenzae (more common in COPD) ▶ Klebsiella • Chronic lung disease
• Mycoplasma pneumoniae* (younger patients) ▶ E. coli • Elderly/young/male
• Chlamydia pneumoniae* (elderly patients) ▶ Pseudomonas • Alcoholic/smoker/IVDU
• Legionella pneumoniae* *Atypicals • MRSA / Staph. aureus
• Viral: RSV, influenza, Covid-19 (15%)
Aspiration pneumonia: in stroke, neuromuscular disease,  GCS

Clinical presentation
• Fever, rigors, malaise, anorexia
• Productive cough – rusty sputum / haemoptysis
• Dyspnoea
• Pleuritic chest pain

On examination
•  RR,  HR,  temp •  expansion
•  O2 sats / cyanosis • coarse crackles
•  GCS / delirium – if elderly • pleural rub, bronchial breathing
• Signs of consolidation • dull percussion
•  vocal resonance Fig. 9.3  Right upper zone consolidation.

Investigations3 Risk stratification: CURB65 score

• Bedside: basic obs, urine dip
C Confusion MMSE ≤8 or disorientated
• Bloods: U Urea >7mmol/L
▶ FBC, U&Es, CRP, LFT, glucose ▶ ABG ▶ Atypical serology
R Resp rate ≥30/min
• Microbiology:
▶ Sputum & blood cultures (guide ABX choice) B BP SBP <90 or DBP <60
▶ Urine antigens (atypical orgs) 65 Age >65y
▶ Throat swab (if suspect viral)
Mild: 0–1 = home Tx
• Chest X-ray: consolidation = DIAGNOSTIC
Mod: 2 = hospital Tx
Severe: ≥3 = consider ICU
Management3
1. Conservative: analgesia, O2, antipyretics, IV fluids, chest physio Complications of pneumonia:
2. Antibiotics: follow local antimicrobial guideline (see table below for common • Pleural effusion • Lung abscess
examples) • Resp. failure • Bronchiectasis
1st line If penicillin allergy Duration & • Sepsis • Pneumothorax
route • Empyema • Lobe collapse
CAP Mild Amoxicillin 500mg TDS Doxycycline 5d PO
Mod Amoxicillin 500mg TDS + Doxycycline + clarithromycin 7d PO Repeat CXR after 6w to ensure resolution & no
clarithromycin 500mg TDS underlying malignancy / lung abnormalities
Severe Co-amoxiclav + clarithromycin Levofloxacin + vancomycin 10d IV
HAP Mild Doxycycline PO 5d PO
Severe Co-trimoxazole PO 5–7d IV
Aspiration Amoxicillin + metronidazole 5–7d IV
3. Long-term: smoking cessation advice, influenza vaccine if high risk
3 BMJ Best Practice (2021) Community acquired pneumonia Medicine

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 Chapter 10: General surgical principles  141

Postoperative care
Summary of postoperative problems

Immediate Delayed Common sources of post-op pyrexia

• Primary haemorrhage • Infection (pneumonia, UTI, wound) & infection
• Shock • Pressure sores Chest (infection)
• Low urine output • Paralytic ileus Catheter (UTI)
• Pain • Secondary haemorrhage (7–10d post) Start SEPSIS 6 if
Cut (infection) potential sepsis
• N&V • Acute MI (in first 72h) Cannula (infection)
• Confusion/delirium (qSOFA score ≥2 /
Immobilisation: Calves (DVT) clinical judgement)
• DVT, PE, stroke – give LMWH/aspirin Central line (infection)
• Urinary retention & AKI Collections (abdo/pelvis)
• Chest infections – in elderly/ventilated 1–3d: respiratory
• Atelectasis 3–5d: urinary
• Pressure sores & muscle wasting 5–7d: wound/abscess/leak
Ix: blood cultures, CXR, urine dip / MCS, cannula
Anastomotic leak site, surgical wound swab, CT/USS of surgical site

AETIOLOGY: leak of luminal contents from a surgical join → important

complication of GI surgery

RISK FACTORS:
Patient risk factors Surgical risk factors
• Medication (steroids/ • Emergency surgery
immunosuppressants) • Longer intra-operative time
• Smoking/alcohol • Oesophageal–gastric or rectal anastomosis
• DM, obesity, malnutrition • Peritoneal contamination (by free pus or faeces)

CLINICAL PRESENTATION: 5–7d post-op (often due to ischaemia)

• Abdo pain ± peritonism
• Fever, tachycardia, new atrial fibrillation
→ consider in any patient failing to progress post GI resection

INVESTIGATIONS:
• FBC, CRP, U&Es, LFT, clotting, VBG
• Group & save
• CT with contrast = diagnostic

MANAGEMENT:
• SEPSIS 6 (IV ABX)
• Larger leaks may need drainage or laparoscopic exploration / surgical
intervention

Intra-abdominal abscess
RISK FACTORS:
• Intra-abdominal infection (e.g. appendicitis, diverticulitis)
• Recent intra-abdominal surgery

CLINICAL PRESENTATION: CT abdo with contrast

= diagnostic
• Fever
• Anorexia/N&V
• Abdominal pain
• Altered bowel habit / prolonged ileus

MANAGEMENT:
• IV ABX + drainage (+ send fluid for culture)
• May need to return to theatre Surgery

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 142  Chapter 10: General surgical principles

Paralytic ileus
AETIOLOGY: reduced intestinal motility → very common following abdo/
pelvic surgery

RISK FACTORS:
Patient risk factors Surgical risk factors
• Increased age • Use of anti-cholinergic/opioid medication
• Electrolyte derangement (e.g. Na+, K+ • Pelvic/abdominal surgery
and Ca2+) • Extensive intra-operative intestinal
• Neurological disorders (e.g. dementia/ handling
Parkinson’s) • Peritoneal contamination (by free pus or
faeces)
CLINICAL PRESENTATION:
Ix are done to rule out
• Failure to pass faeces/flatus more serious pathologies
• Abdo distension & absent bowel sounds
• N&V

MANAGEMENT: INVESTIGATIONS:
• IV fluids & daily bloods (electrolytes) • FBC, CRP, U&Es
• Encourage mobilisation • Electrolytes (Ca2+, PO4–, Mg2+)
• Review analgesia (opiates) in • Consider imaging: AXR ± CT
conjunction with pain team (to rule out other pathology
• Consider if need to be NBM ± NG e.g. obstruction)
tube (remove stomach contents
to reduce vomiting)

Post-op haemorrhage
Primary bleed – within intra-operative period → resolved during operation &
close monitoring post-op
Reactive bleed – within 24h of operation → usually a missed vessel / slipped
ligature
More detail on haemorrhagic shock in Chapter 16: Secondary bleed – 7–10d post-op → usually erosion of a vessel 2° to infection
Critical illness
SIGNS/SYMPTOMS: tachycardia, tachypnoea, dizziness, reduced urine output
(NB: hypotension = late sign)

INVESTIGATIONS: thorough examination for signs of bleeding/swelling/

discolouration/tenderness/peritonism

MANAGEMENT:
1. ABCDE → IV fluid resuscitation + direct pressure on bleeding site if visible
2. Urgent senior review → may need to return to theatre
3. Urgent blood transfusion – if moderate/severe bleeding (activate major
haemorrhage protocol if necessary)

Urinary retention
Risk factors for urinary retention:
• >50y • Opiates, PRESENTATION: MANAGEMENT:
• Spinal/epidural antimuscarinics • Reduced output • Withdraw causative agents
• Neuro comorbidity • Infection/sepsis • Suprapubic mass/pain • Catheter
• Paralytic ileus • Constipation
• Pelvic/uro surgery INVESTIGATIONS: Work-up for AKI:
• USS bladder (residual volume) • Fluid status • Urine dip
• Kidney function: eGFR, U&Es • FBC, CRP, U&Es, LFT • USS KUB
Surgery

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 148  Chapter 11: The acute abdomen

General overview
ANY REGION
• Pancreatitis • AAA rupture
• Gallstone disease • Peptic ulcer • Mesenteric ischaemia*
▶ Biliary colic • Inferior MI • Obstruction
▶ Cholecystitis • Oesophagitis/
▶ Cholangitis GORD *Mesenteric ischaemia:
• Hepatitis consider in patients with
• Liver abscess out of proportion pain ±
metabolic acidosis
Right Left
Epigastric
• Early appendicitis hypochondriac hypochondriac
region
• Bowel obstruction region region • Splenic abscess
• Strangulated hernia • Splenic rupture
(paraumbilical/umbilical)

Right Umbilical Left lumbar

• Renal calculi lumbar region region region • Renal calculi
• Pyelonephritis • Pyelonephritis
• UTI • UTI

Right iliac Hypogastric Left iliac

region region region

• Appendicitis • Meckel’s • Testicular torsion • Diverticulitis • Sigmoid

(late) diverticulitis • Urinary retention • Ulcerative volvulus
• Ureteric colic • PID • Cystitis colitis • Constipation
• Crohn’s • Ovarian cyst • PID • Testicular • PID
• Testicular torsion • Salpingitis torsion • Ovarian cyst
• Ectopic pregnancy • Hernia • Ectopic • Salpingitis
pregnancy • Hernia

Fig. 11.1  This diagram should be used as a guide to the differentials of acute abdominal pain. It is important to note that any of the mentioned
pathologies can present with pain in any area of the abdomen, and thus it is important to correlate location of pain with other clinical signs and
investigations, and not to rule out differentials based on the location of pain alone.

Medical causes of acute abdominal pain

• DKA • Hypercalcaemia
• UTI • Spontaneous bacterial peritonitis
• Basal lobe pneumonia • Mesenteric adenitis
• Poisoning/overdose • Constipation
• Addison’s disease

Patterns of pain

Type of pathology
Inflammatory Obstructive Perforation Visceral
Peritonitic pain Colicky pain (waves of pain) Sudden localised then peritonitic pain Poorly localised pain (referred)
→ fever, tachycardia → vomiting, constipation → shock ( HR, RR,  BP) → specific Sx e.g. jaundice
→  WCC, ESR, CRP → distension, tinkling sounds → N&V

Peritonitic pain = worse on inspiration & movement → lie still, shallow breaths, rigidity & guarding
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 Chapter 11: The acute abdomen  149

Investigations & management

INVESTIGATIONS: NB: Not all acute abdominal pathologies
• Obs: BP, HR, RR, sats, temp, ECG present with pain – often absent in the
• Pregnancy test: in all females of child-bearing age elderly, children, diabetics & pregnant women
• Bloods: FBC, U&Es, LFT, CRP, amylase, glucose, clotting, ABG (lactate)
• Urinalysis: protein, nitrates, leukocytes, blood, glucose, pH Amylase can be raised in some pathologies
• Imaging: USS, erect CXR, abdo CXR, CT other than pancreatitis e.g. perforated
• Specialist tests: MRCP/ERCP, MRI, barium swallow, OGD, colonoscopy duodenum
→ not always indicated Erect CXR: may show air under diaphragm;
however, a negative erect CXR does not
INITIAL MANAGEMENT: early senior input if concerned exclude pneumoperitoneum
• ABCDE + targeted Mx of suspected cause

Things to consider:
• Nutritional and feeding status – keep NBM if surgery likely soon or vomiting
• Hydration and fluid balance – IV or oral fluid maintenance, consider catheter
• Are antibiotics indicated? – signs consistent with infection
• Investigations to guide/aid management – blood cultures, ABG, G&S, CXR, ECG
• Is blood transfusion / major haemorrhage protocol required?
• Is theatre / surgical intervention needed? – NBM, consent, book theatre slot

IMAGING INDICATIONS:
X-ray Abdo USS CT
• Obstruction • Biliary pathologies • AAA/vascular
• Toxic megacolon • Kidneys, ureter, bladder • Malignancy/mass
• Foreign body • Gynae pathologies • Complications of obstructions
• Appendix (in a female patient, no role • Appendix if >50y
in male)

CONSIDERATIONS FOR SURGERY:

Patient health:
• Anaesthetic review
• Comorbidities/frailty
• Ceiling of care: ReSPECT form / DNACPR ReSPECT = Recommended Summary
• Morbidity/mortality calculation e.g. P-POSSUM score Plan for Emergency Care and Treatment,
a patient-held form
Patient wishes:
• Current wishes
• Advance directives / ReSPECT forms
• Discussion with family
NB: the decision to operate is a complicated one and many factors should be
considered.
See Chapter 16: Critical illness (and Chapter 10: Anaesthetics in the companion
Clinical Specialties book) for further details.

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 164  Chapter 12: Gastrointestinal surgery

Colorectal cancer
↳ most = adenocarcinomas
→ 3rd most common cancer → Peak age: >60y
→ 2nd most common cause of → M>F
cancer deaths → 1 in 30 risk
Risk factors
Familial adenomatous polyposis (FAP):
• Polyps (UC, HNPCC, FAP) → identify & remove Polypectomy + follow-up
Auto dominant mutation in APC gene • Age (90% are aged >50 y) endoscopy (complications =
• Diet – low fibre, high fat, processed meat bleeding & perforation)
→ Hundreds of polyps
→ Presents at 35–45y (consider if <50y with • Smoking/alcohol/obesity
colorectal cancer) • IBD (UC especially)
→ Colonoscopy every 2y from 25 to 75y • Genetics (FAP & HNPCC / Lynch syndrome) • FHx
Clinical presentation
HNPCC / Lynch syndrome:
4%
Auto dominant mutation in DNA repair 3%
genes 3%
→ Cancers of colon, endometrium, ovary, Liver = common site of colorectal
stomach, bladder, brain, skin 7% cancer metastases
→ Presents >40y (consider if <50y with 5%
colorectal cancer)
→ Colonoscopy every 2y from 25 to 75y 14%
NB: non-polyposis condition (no polyps
present) 27%
Amsterdam criteria to Dx
37%
Rectum Sigmoid
Bowel cancer screening programme3:
qFIT (quantifiable faecal immunochemical Fig. 12.4  Sites of colorectal cancer.
test)
→ if >120mcg/g refer for colonoscopy to Right side Left side Rectal
remove any polyps = Late presentation • Weight loss / fatigue • Weight loss / fatigue
Every 2y from the age of 50y • Weight loss / fatigue • Change in bowel habit • Tenesmus
• IDA • Obstruction • Bright PR bleed
± Abdo pain/mass • Blood-streaked stools • DRE: palpable mass
May present as an acute emergency:
± Abdo pain/mass
• Bowel obstruction → 20% present with signs of disseminated disease e.g. liver mets = jaundice
• Bowel perforation
• Extreme pain Investigations
1. DRE 4. Colonoscopy & biopsy = gold
2. Bloods – FBC (for IDA), LFTs, U&Es standard
3. Tumour marker: CEA (not specific – 5. MRI – if rectal cancer
use for monitoring) 6. CT (chest, abdo, pelvis) – for TNM
staging

Red flags for 2ww referral4: Classification & staging

1. ≥40y with unexplained weight loss & abdo Stage Duke’s stage Features 5y survival5 Duke’s criteria or TNM staging
pain
2. ≥50y with unexplained rectal bleeding 1 A Mucosa only 90–95%
3. ≥60y with altered bowel habit or IDA 2 B1 Into muscularis 80–85%
4. Occult blood present when faeces tested B2 Through wall
Also consider if: 3 C1 T2 + nodes 60–65%
• Rectal or abdominal mass
C2 T3 + nodes
• ≤50y with rectal bleeding and any of:
▶ Abdominal pain 4 D Distant mets <11%
▶ Altered bowel habit
▶ Weight loss 3 Bowel cancer screening programme (www.gov.uk/guidance/bowel-cancer-screening-
▶ IDA programme-overview)
4 NICE (2015, updated 2021) Suspected cancer: recognition and referral [NG12]
5 Cancer survival by stage at diagnosis for England, 2019. ONS.

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 Chapter 12: Gastrointestinal surgery  165

Management of colorectal cancer6

Lymph drainage:
→ colectomy + ‘en bloc’ lymph node removal ± chemotherapy
→ Ascending & transverse drain to superior
Different levels of resection: = location of tumour mesenteric LNs
→ Descending & sigmoid drain to inferior
Left hemicolectomy Right hemicolectomy Sigmoid colectomy mesenteric LNs
→ Rectum (above pectinate line) to internal
iliac LNs

Hartmann’s
= sigmoid colectomy with colostomy
(stoma formation)

Anterior resection Abdominoperineal resection Panproctocolectomy Panproctocolectomy

= if synchronous cancer or inflammatory bowel
disease

Stoma formation:
Elective or emergency

Fig. 12.5 Decision depends on:

• location of resection
• indication for operation
MANAGEMENT OF OBSTRUCTING COLON CANCER: emergency
• patient comorbidities
1. ABCDE • patient lifestyle/preference
2. Analgesia + NG tube decompression
3. CT scan if no small bowel distension = competent ileocaecal valve = BAD
4. Endoscopic stenting or colectomy (often with stoma) → colectomy type
depends on obstruction location

Management of rectal cancer6

1. Total mesorectal excision (removal of rectum)

• Low tumours <5cm above anus: abdominoperineal excision
(resect + stoma)
• Higher tumours >5cm from anus: anterior resection
(resect + anastomosis)
2. ± Chemotherapy ± radiotherapy

Colorectal cancer follow-up

Follow-up for 5y post-surgery
1. CEA – check every 6m
2. CT CAP – annually 20–30%
3. Colonoscopy – at 1 & 5y recurrence

MDT input
including stoma nurse / specialist nurse

6 NICE (2020, updated 2021) Colorectal cancer [NG151]

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 Chapter 14: Vascular disease  177

Chronic peripheral arterial disease

Causes
Fontaine classification:
1. Atherosclerosis: DM, smoking, age, male, HTN, obesity, inactivity, cholesterol
2. Vasculitis: Buerger’s disease → common in young, heavy smokers Asymptomatic
3. Fibromuscular dysplasia → non-inflammatory arterial wall thickening
Intermittent claudication
4. Other: cystic adventitial disease, iliac endofibrosis, popliteal artery entrapment

Pathogenesis: endothelial dysfunction → inflammation → macrophages → fatty streaks Ischaemic rest pain
→ plaque → rupture → platelet adherence → thrombus
Ulceration/gangrene
Signs and symptoms

Intermittent claudication Ischaemic rest pain Peripheral neuropathy Ischaemic rest pain >2w
Often coexists alongside PAD in DM + ABPI <0.4 or TP <30mmHg
Pathology Insufficient perfusion during Constant insufficient perfusion Damaged peripheral nerves = critical limb-threatening
exercise ischaemia (CLTI)
Symptoms Cramping muscle pain Continuous, severe, burning/ Tingling/numbness ± pain can cause development of ulcers
→ on exercise (limits walking*) aching → glove & stocking distribution & gangrene ( risk if DM)
→ relieved by rest → worse at night → no relief dangling foot / cold & needs urgent Ix & Tx to
→ reproduced walking same → relieved by dangling leg out floor prevent limb loss
distance of bed → prone to wounds = infection risk
→ relieved by walking on a cold
floor Infection more likely if coexisting PAD
Signs • Absent/weak peripheral pulses • Peripheral pulses present Leriche syndrome: occluded distal
*Claudication • Cold, pale, hairless legs • No pallor with Buerger’s aorta, iliac & femoro-popliteal
distance vessels
• Buerger’s angle <20° (angle leg raised
→ bilateral buttock/thigh pain
before pallor) ± erectile dysfunction

DDx of intermittent claudication Intermittent Spinal stenosis

claudication
• Spinal stenosis • Sciatica = shooting pain
Fixed claudication Leg pain may be present at
• Venous claudication • Popliteal artery entrapment
distance rest ± back pain
▶ bursting pain from start of ▶ normal pulses
walking ▶ younger, active, Sx when Not precipitated by Worsened by  time
▶ relieved by elevation exercising  time standing standing
Worse walking uphill Better walking
Investigations uphill / bending forward
→ needs full cardiovascular screen O/E: absent O/E: pulses present but
1. History & examination: peripheral 4. Duplex USS: show site & degree of peripheral pulses neurological Sx
vascular exam + BP, ECG stenosis = non-invasive
2. Bloods: FBC, lipids 5. MR/CTA: image larger aorto–iliac right ankle pressure
3. ABPI ± treadmill test vessels = invasive ABPIright =
highest brachial pressure

Management10
ABPI Interpretation9 Action
MEDICAL Action is based on severity of symptoms
>1.3 Calcification (diabetes) TBPI (toe BPI)
• Lifestyle: stop smoking, weight loss, exercise programmes (weekly for 3m)
1–1.3 Normal No action
• Optimise comorbidities: HTN, DM, cholesterol (high dose statin)
• Antiplatelets: 75mg clopidogrel (or 2.5mg rivaroxaban BD + 75mg aspirin) 0.4–0.9 Mild–moderate PAD Routine
• Vasoactive drugs: consider use in claudicants e.g. naftidrofuryl or cilostazol (intermittent referral
claudication)
9 Cronenwett JL & Johnston KW (2014) Rutherford's Vascular Surgery. 8th edition. Elsevier Health <0.4 Severe PAD (rest pain)
Urgent
Sciences
10 European Society for Vascular Surgery (2019) Clinical practice guideline on management of chronic <0.3 Impending gangrene referral
limb-threatening ischemia
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 178  Chapter 14: Vascular disease

SURGICAL → consider in more severe cases or where medical treatment has failed
• Percutaneous transluminal angioplasty (PTA) or stenting
Common sites of atherosclerosis
• Surgical reconstruction (bypass graft)
• Coronary arteries • Amputation = last resort
• Major branches of the aortic arch
• Visceral branches of abdo aorta Chronic mesenteric vascular occlusive disease
• Terminal abdominal aorta + branches
→ atherosclerosis of SMA, coeliac trunk & IMA*, causing inadequate perfusion for
*Good collateral blood supply so symptoms only digestion → ‘gut claudication’
likely to occur if ≥2 vessels affected
CLINICAL PRESENTATION: (at least 3m duration)
• Postprandial epigastric pain: 10min to 3h after eating
Risk factors for chronic mesenteric vascular • Gross weight loss & fear of eating (but appetite unaffected)
occlusive disease: as for all arterial disease • Non-specific GI symptoms: altered bowel habits, N&V
(+ typically females >60y) • ± other vascular comorbidities e.g. HTN, DM, smoking etc.

INVESTIGATIONS: diagnosis of exclusion (extensive GI examination needed

to r/o other causes)
Complications: • History & examination: may have epigastric bruit & tenderness
• Malabsorption / weight loss • Routine bloods: often normal → may be nutritional deficiencies
• Bowel infarction • Duplex ultrasound of mesenteric vessels
• CT angiography → diagnostic

MANAGEMENT11: urgent if significant weight loss, diarrhoea ± continuous

pain SMA is the most important
1. Modify risk factors: diet & exercise, stop smoking vessel to keep patent
2. Antiplatelet (75mg clopidogrel) & high dose statin (e.g. 80mg atorvastatin)
3. Percutaneous mesenteric stenting: less invasive than surgery
*If not suitable for endovascular intervention, 4. Surgery: bypass graft*
endovascular intervention failed, or young with
complex non-atherosclerotic lesions
Other causes of gut ischaemia
Presentation of gut ischaemia: ACUTE OCCLUSIVE MESENTERIC ISCHAEMIA: due to embolism
Sx: severe, sudden abdominal pain
Triad of Sx: clinical diagnosis
RF: AF, vascular disease
1. Out of proportion pain
2. Diarrhoea &/or vomiting Ix: negative d-dimer can rule out → do not use lactate to diagnose or rule out
3. Source of embolus e.g. AF Mx: surgical embolectomy ± retrograde stenting; may need bowel resection

NON-OCCLUSIVE MESENTERIC ISCHAEMIA (NOMI): hypoperfusion

causes ischaemia despite patent mesenteric vessels
Sx: severe abdominal pain
Causes: vasopressors, cocaine, abdominal compartment syndrome (ACS), dialysis,
severe burns, cardiac surgery
Mx: surgical/endovascular revascularisation ± treatment of ACS with
decompressive laparotomy

ISCHAEMIC COLITIS: acute, transient reduction in blood supply to large bowel

Sx: severe pain ± bloody stools
Causes: low BP / shock, thromboembolism,  age, cocaine
Mx: supportive ± colectomy if peritonitic

11 European Society for Vascular Surgery (2017) Clinical practice guideline on management of the

diseases of mesenteric arteries and veins

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 Chapter 15: Urology  193

Bladder outlet obstruction

Common causes
Ureter
→ BPH
→ Prolapse Uterus
Urinary
→ Post-incontinence surgery bladder
→ Bladder calculi Pubic bone Cervix
Rectum
→ Urethral strictures Urethra
Vagina
Clitoris
→ Malignancy (bladder/urethral/prostatic) Labium minora Anus
→ External compression Labium majora
→ Neurological disease Fig. 15.4  Female genitourinary anatomy.

Clinical presentation
Urinary bladder
1. Lower urinary tract symptoms (LUTS) rapid onset Pubic bone Ureter

2. Acute urinary retention: suprapubic pain, palpable bladder, anuria Ductus Seminal
vesicle
deferens
3. Chronic urinary retention: LUTS, renal impairment, palpable bladder, Prostate
Urethra gland
overflow incontinence, large residual urine volume
Penis
Rectum
Epididymis
Voiding symptoms Storage symptoms Anus
Testis
Hesitancy Frequency
Poor flow Urgency ± urge incontinence ‘FUN’ Fig. 15.5  Male genitourinary anatomy.
Post-void dribbling Nocturia
Dysuria (bedwetting / overflow Incontinence)
(sensation of incomplete emptying) IPSS: score/questionnaire to determine how
much symptoms impact daily life
Present in obstruction Present if bladder dysfunction
(can be 2° to chronic obstruction)

Bladder calculi Management of acute urinary retention:

PATHOGENESIS: crystallisation of minerals in urine if it becomes concentrated 1. ABCDE
(if incomplete emptying / urine stasis) 2. Bloods: FBC, U&Es (deranged U&Es = HPCR
Often uric acid or calcium stones (or struvite if UTI-related) → need USS KUB & urology R/V)
CAUSES: 3. Catheter (3-way if haematuria)
4. Full Hx and examination (including DRE &
Outlet obstruction Neurogenic retention Other neuro exam)
• BPH / prostate • Stroke / spinal cord injury • Infection (UTIs) 5. Monitor fluid and electrolyte balance
carcinoma • Spina bifida • Dehydration
• Bladder tumour • Diabetes • Foreign body / catheter
• Urethral stricture • Augmentation cystoplasty • Passage of renal calculi into
• Prolapse (in women) bladder

CLINICAL PRESENTATION: MANAGEMENT7:

• LUTS: voiding & storage Transurethral cystolitholapaxy
• Dysuria & haematuria at end of 1. Cystoscope passed up urethra to
stream identify stones
• Lower abdo pain 2. Crush stones or fragment with
± recurrent UTI laser / pneumatic device
3. Bladder irrigation to remove
INVESTIGATIONS: fragments
• Hx & exam: abdo & pelvic + DRE
• Bloods: FBC, CRP, U&Es, Ca, PO4, OR Open cystolithotomy = surgical Bladder calculi increase risk of bladder cancer
urate, glucose, VBG (HCO3) removal of bladder stones via a lower
• Urine dip & MCS – r/o infection abdominal incision
• Basic imaging: USS
• Specialist imaging: CT KUB

7  European Society of Urology (2021) Guidelines on bladder stones Surgery

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 194  Chapter 15: Urology

Benign prostatic hyperplasia (BPH)

→ 50% of over 50s
→ affect transitional zone of prostate

PATHOGENESIS: occurs with age due to androgens stimulating increase in

number of prostate cells

CLINICAL PRESENTATION:
• Voiding symptoms ± secondary storage symptoms
• ± Haematuria
Chronic urinary retention
• Enlarged, smooth prostate on DRE
Chronic obstruction can lead to chronic urinary • Acute retention (sometimes occurs = rapid & painful)
retention → gradual stretching of bladder over
years (painless) INVESTIGATIONS:
• Symptoms: asymptomatic or LUTS, palpable 1. History & examination: IPSS score & remember DRE
bladder, overflow incontinence, large residual 2. Urinalysis: dip & MCS
volume of urine 3. Uroflowmetry: <10ml/sec suggests obstruction
• Complications: UTIs, calculi, high pressure 4. Bloods: including PSA
chronic retention (HPCR) → renal impairment 5. Transrectal USS + biopsy: definitive diagnosis
& hydronephrosis
MANAGEMENT8: depends on symptom severity

Mild Moderate Severe

1. Reassurance Pharmacotherapy Surgery:
Possible complications of TURP: 2. Lifestyle 1. Alpha blockers (e.g. tamsulosin) 1. TURP = gold standard
Acute: bleeding, UTI (fluid intake) = relax smooth muscle 2. Other: e.g. laser/steam
Chronic: retrograde ejaculation, impotence, 3. Follow-up → SEs: retrograde ejaculation, postural treatment
incontinence, bladder neck stenosis / urethral hypotension, dizziness, headache
3. Prostatic artery
stricture 2. ± 5-alpha-reductase inhibitors embolisation
(e.g. finasteride)
4. Self-catheterisation / 
= inhibits testosterone → DHT conversion
long-term catheter
→ pros:  prostate size
→ cons: take 6w to 6m to work
→ SEs: loss of libido, impotence
3. ± Anti-cholinergics (e.g. oxybutynin/
solifenacin)
In combination with above to treat 2° storage
LUTS

8  NICE (2010, updated 2015) Lower urinary tract symptoms in men [CG97]
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 Chapter 17: Emergency presentations  209

Electrolyte abnormalities
Hyperglycaemia (DKA & HHS)
DIAGNOSIS:
DKA HHS
1. Hyperglycaemia: random BG >11mmol/L 1. Profound hyperglycaemia: random BG
2. Ketosis: capillary ketones >3mmol/L or >30mmol/L
urinary ketones ++ 2. No ketosis & pH >7.3
3. Acidosis: HCO3− <15 or pH <7.35 3. High osmolality: >320mosmol/kg

MANAGEMENT OF HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS)1

1. ABCDE & confirm Dx with lab results & osmolality (VBG)
2. IV FLUIDS 0.9% saline (infusion over 24h)
3. Do not start insulin (until rate of fall in glucose is <5mmol/L per hour)
→ then give fixed rate insulin at half dose of DKA (0.05 units/kg/h)
4. K+ replacement with KCl if K+ drops to <5.5mmol/L
5. Prophylactic anticoagulation – LMWH for full duration of admission

MANAGEMENT OF DIABETIC KETOACIDOSIS (DKA)2

1. ABCDE
2. Confirm Dx with lab results (VBG)
3. Consider HDU if:
• CBK >6mmol/L
• HCO3− <5mmol/L
• pH <7.0
• GCS <12

*Avoid rapid
IV fluids*
rehydration as risk
0.9% saline (1L over 1h)
cerebral oedema
Tests:
VBG for pH, HCO3−, glucose, ketones
U&Es, FBC, CRP, CXR, ECG

Fixed rate high dose insulin

(0.1 units/kg/h)

Potassium replacement Glucose replacement

(KCl) AND (10% glucose)
if K+ drops to <5.5mmol/L when BG <14mmol/L

Monitor hourly:
Identify & treat underlying cause •  Blood glucose
e.g. ABX if septic •  Blood ketones
•  VBG (pH, HCO3−, K+)

Also monitor:
Once stable •  Urine output
• switch to SC insulin •  U&Es (K+, Cr, urea)
• encourage regular feeding & fluids •  Neurological state
Fig. 17.2  DKA management in adults.

1 Diabetes UK (2012) The management of hyperosmolar hyperglycaemic state (HHS) in adults with
diabetes
2 Diabetes UK (2021) The management of diabetic ketoacidosis in adults

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 210  Chapter 17: Emergency presentations

Hypoglycaemia3
CAUSES:
• Reduced oral intake Hypoglycaemia = blood glucose <4mmol/L
• Intense exercise
• Binge drinking
• Taking too much insulin (if diabetic)

SYMPTOMS:
• Irritable, anxious, confused
• Hungry or nauseous
• Shaky, dizzy, light-headed
• Seizures if severe

MANAGEMENT:
1. Oral rapid-acting glucose or IV glucose 100ml 20% / IM glucagon 1mg
2. Long-acting carbohydrate e.g. toast (once CBG >4mmol/L)
3. Look for cause (document, monitor and get specialist review if needed)

Hyperkalaemia
CAUSES:
• CKD / renal failure
• Drugs (ACEis/ARBs, NSAIDs, spironolactone, potassium supplements)
• Burns / trauma / tissue injuries
• Hormonal disorders e.g. Addison’s Hyperkalaemia = K+ >5.2mmol/L
Severe hyperkalaemia = K+ >6mmol/L
SYMPTOMS:
• Chest pain / palpitations
• Dizziness/weakness
• Abdominal pain / vomiting

INVESTIGATIONS:
• U&Es
• ECG – tented T waves, flattened P wave, shortened QT interval

MANAGEMENT:
1. 10ml 10% calcium gluconate
2. IV insulin + 25g glucose
3. Salbutamol nebs
4. Treat cause

3 NICE BNF – Treatment summary: Hypoglycaemia

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 Chapter 18: Rheumatology  229

Neck & back pain

Red flags: need urgent MRI
• New onset in <20y or >55y • Saddle anaesthesia • Fever
• Constant night pain • Bladder/bowel incontinence • Steroid use
• Progressive motor weakness • Hx of trauma/cancer • Recent infection
• Thoracic back pain • Unexplained weight loss

Differentials of neck/back pain

Structural Inflammatory Destructive Metabolic Referred pain

• Mechanical • Spondyloarthropathies • Malignancy (1° or 2°) • Osteoporosis • Major viscera
• Disc prolapse • Sacroiliitis • Infection (discitis, • Osteomalacia • Uro-genitary
• Spinal stenosis • Polymyalgia osteomyelitis, TB) • Paget’s • Aorta
• Spondylolisthesis rheumatica • Hip

Cervical radiculopathies Radiculopathies = conditions where ‘pinched’

nerve roots cause pain, paraesthesia,
CERVICAL SPONDYLOSIS → cervical radiculopathy caused by age-related weakness in a dermatomal distribution
degenerative changes to spine (unilateral)
• Ageing causes disc degeneration (dehydration & flattening) =  shock → LMN signs (hyporeflexia, hypotonia)
absorption
• Results in bony changes of vertebrae → osteophyte development
• Osteophytes ‘pinch’ nerve roots as they leave spinal canal Myelopathies = conditions where compressed
• May develop into myelopathy spinal cord causes pain, paraesthesia,
weakness bilaterally + other neurological
Symptoms: symptoms
• Pain in neck (radiating down arm as a • Tingling/numbness in one → UMN signs (hyperreflexia, hypertonia,
‘dull ache’/‘toothache’) → ‘brachial dermatome spasticity)
neuralgia’ • ± Weakness in one arm
On examination:
• Pain reproduced with lateral neck flexion towards affected side Upper limb dermatomes
• Motor signs: modest upper muscle weakness ↳ ‘Spurling sign’
C5 ‘Regimental badge area’
• Sensory signs: reduced pin-prick sensation discrimination (in one dermatome)
• LMN signs: hyporeflexia, hypotonia C6 Thumb & index finger
Diagnosis: usually clinical C7 Middle finger
→ Neurological examination: myotomes, dermatomes, reflexes
→ MRI if no improvement / considering surgery
Management: mostly self-limiting in 6–12w
1. Conservative:
• Rest, physiotherapy, analgesia (NSAIDs or neuropathic – TCAs)
• Hard collar for neck immobilisation
2. Surgical:
• ACDF (anterior cervical discectomy & fusion) if persistent/worsening/severe Sx

CERVICAL DISC PROLAPSE = seen in those aged 30–40y; usually Hx of mild

neck trauma
Symptoms: Management:
• Pain in neck 1. Conservative: rest, physiotherapy,
• Tingling/numbness/paraesthesia in analgesia (NSAIDs or neuropathic
one dermatome of arm – TCAs)
• ± weakness in one arm 2. Surgical: microdiscectomy
Investigation:
→ Neurological examination: myotomes, dermatomes, reflexes
→ MRI → recommended for cervical spine (assess need for surgery)
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 230  Chapter 18: Rheumatology

Cervical myelopathy
CERVICAL CANAL STENOSIS → cord compression = more serious than
cervical radiculopathy
Causes:
• Age-related degeneration: osteophyte formation & ligament hypertrophy
• Disc bulging/herniation: consider in younger patients
Affects middle-aged/elderly
Symptoms: gradual onset so late presentation & Dx
• Gait abnormalities: spastic & ataxic
• Loss of fine motor skills → difficulty fastening buttons, writing etc.
• Later = tingling in fingers (may be misdiagnosed as carpal tunnel syndrome)
± sphincter dysfunction
Hoffman’s sign: flick middle finger & watch for On examination:
reflexive movement of index/thumb • Gait abnormalities: spastic & ataxic
→ positive in UMN pathology e.g. spinal cord • Wasting on shoulder girdle muscles
compression • UMN signs: spasticity, clonus, +ve Hoffman’s/Babinski, hyperreflexia,
hypertonia
Investigations: X-ray & MRI
Management:
Surgical intervention: laminectomy → recommended as progressive
deterioration

Lumbar radiculopathies
Lower limb dermatomes LUMBAR DISC PROLAPSE = common in those aged 25–55y
L4 Inner shin, below knee Pathology:
L5 Buttock, lateral calf, big toe • With age = increased risk of prolapse through defect in surrounding annulus
fibrosus
S1 Post. thigh & calf, little toe • Results in compression of nerve roots
Symptoms: often onset during lifting/
Prolapsed nucleus
bending/twisting Vertebra presses on nerve root
Usually posterolateral herniation of disc, • Stabbing lower back pain
therefore compresses nerve root below → radiating down the leg/buttock
i.e. herniated L5/S1 disc will compress S1 • Numbness/tingling (in one leg)
nerve root On examination:
Nerve root
• Pain reproduced with straight leg
raise Nucleus
Sciatica = pain along path of sciatic nerve • Motor signs: modest lower muscle pulposus
(radiates down to toe) due to disc prolapse, weakness (usually unilateral)
Annulus fibrosus
stenosis or osteophytes affecting nerve • Sensory signs: reduced pin-prick
Fig. 18.9  Anatomy of disc prolapse.
roots L4–S1 sensation discrimination
(one dermatome)
• LMN signs: hyporeflexia, hypotonia
Discs are named after vertebra above & below • May be scoliosis due to paravertebral muscle spasm
e.g. L4/5 or L3/4 Diagnosis: usually clinical
• Neurological examination: myotomes, dermatomes, reflexes
• MRI if no improvement / considering surgery
Management: 90% self-limiting in 6–12w
Complications of surgery  :
Nerve damage, CSF leak, infection, haemorrhage, 1. Conservative: rest, physiotherapy, analgesia (NSAIDs or neuropathic – TCAs)
back pain 2. Surgical: if no improvement in 6w
• Nerve root block (under fluoroscopic guidance)
• Microdiscectomy (remove piece of prolapsed disc)
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 252  Chapter 19: Trauma & orthopaedics Musculoskeletal conditions

Musculoskeletal malignancy
Soft tissue swellings
*Urgent referral if red flags:
1. 2ww for USS Benign Malignant
2. If USS worrying/unclear: 2ww cancer • <5cm or slow-growing • >5cm or rapid increase in size*
pathway (MRI & biopsy) • Painless • Painful*
• Superficial to fascia • Penetrates fascia (deep within muscle)*
If no worrying features:
• Well-circumscribed • Irregular border / not contained
observe or biopsy + histology
• Homogeneous appearance • Heterogeneous radiological appearance
e.g. lipoma, leiomyoma, schwannoma e.g. sarcoma

Primary bone tumours

Osteosarcoma (most common) Chondrosarcoma Ewing’s sarcoma

Epidemiology → Children/adolescents (M>F) Adults >50y Children/adolescents (rare)
→ 2nd peak in old age
(in Paget’s / post radiotherapy)
Common sites Distal femur, proximal tibia & humerus Flat bones: pelvis, scapula, rib Diaphysis of bones
Associated Sx Lung mets Pain, mechanical Sx, Systemic upset
pathological fractures (weight loss, fever,  ESR)
Treatment 1. Chemotherapy Not sensitive to chemo 1. Chemotherapy
2. Surgery (+ more chemo) 1. Surgery 2. Surgery
5y survival No mets at Dx: 60–65% Low grade: 90% 50%
Mets at Dx: 20% High grade: 60%

Multiple myeloma
→ malignancy of plasma cells of bone marrow: proliferation of one type of
plasma cell producing one type of Ig

SYMPTOMS:
• Bone pain (commonly backache)
• Fractures of long bones & vertebral collapse Average age: >70y
• Hypercalcaemia (due to increased osteolytic activity)
• Anaemia, neutropenia, thrombocytopenia RF: Afro-Caribbean
• ± Renal impairment & recurrent infections

INVESTIGATIONS:
• FBC: anaemia,  WCC,  ESR/CRP
• U&Es, LFTs: deranged renal function in 20% Poor prognosis:
• Bone profile: hypercalcaemia 6y median survival
• Plasma electrophoresis:  monoclonal Igs
• Urine microscopy: Bence Jones proteins (monoclonal light chains)
• X-rays: punched-out osteolytic lesions (‘pepper-pot’)
• Bone scintigraphy: may have cold spots
• Bone marrow biopsy: >10% clonal plasma cells

MANAGEMENT:
• Supportive for complications e.g. anaemia, renal failure
• Localised disease: radiotherapy
• Widespread disease: chemotherapy

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 Musculoskeletal conditions Chapter 19: Trauma & orthopaedics  253

Metastatic bone disease

→ most common cause of destructive bone disease in adults
→ 70% in axial skeleton (mostly in spinal column)
SYMPTOMS:
• Bone pain (unremitting, dull ache → night pain) Common origins of bone mets:
• Pathological fractures (sudden worsening of pain) PB-KTL (‘lead kettle’)
• Hypercalcaemia Prostate Kidneys
• Spinal cord compression Breast Thyroid
• B Sx: weight loss, night sweats Lung

ON EXAMINATION:
• Bony tenderness
• Swelling Differentials:
• Reduced ROM in joints • Multiple myeloma
• Lymphadenopathy NB: if no Hx of • Lymphoma
• Anaemia cancer, consider • Bone infection
primary bone tumour
• Neurological deficit

INVESTIGATIONS: find primary source

• FBC: anaemia,  WCC,  ESR/CRP
• U&Es, LFTs, TFTs, bone profile: hypercalcaemia
• Tumour markers: PSA for prostate cancer
• Myeloma screen: electrophoresis + urinalysis
• X-rays: lytic or sclerotic lesions
• CT/MRI: for primary tumour (chest, abdo, pelvis)
• Bone scintigraphy: hot spots
• CXR
• CT-guided biopsy: if uncertain of Dx

MANAGEMENT:
1. Find primary source: X-ray, CT, MRI, bone scan
2. Supportive
• Pain relief
• Bone protection: splints/bisphosphonates (assess fracture risk)
3. Chemo/radiotherapy
4. Surgery:
• Stabilisation if risk of fracture in long bones / vertebrae
• Arthroplasty if joint involvement

Sclerotic lesions: white areas

Lytic lesions: dark areas

Fig. 19.1 Fig. 19.2

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