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Emergency topics
Arrests
Adult resuscitation E pp. 232–3
Obstetric resuscitation E p. 244
Neonatal resuscitation E pp. 242–3
Paediatric resuscitation E pp. 238–40
Trauma resuscitation E pp. 236–7
Emergencies
Abdominal pain E p. 294
Aggressive behaviour E p. 370
Anaphylaxis E pp. 484–5
Bradyarrhythmia E p. 262
Breathlessness E p. 276
Burns E pp. 480–1
Chest pain E p. 246
Clotting abnormalities E p. 418
Coma E pp. 344–5
Diabetic ketoacidosis (DKA) E p. 330
Disseminated intravascular coagulation (DIC) E p. 417
GI bleed E p. 304
Hepatic encephalopathy E p. 318
High INR E p. 418
Hyperglycaemia E p. 330
Hyperkalaemia E p. 399–403
Hyperosmolar non-ketotic state (HONK) E p. 332
Hypertension E p. 268
Hypoglycaemia E p. 328
Hypokalaemia E pp. 399–403
Hypotension E p. 488–9
Hypoxia E p. 276
Limb pain E p. 458
Liver failure E p. 318
Overdose E p. 506
Paediatric seizure E p. 349
Psychosis E p. 378–81
Rash E p. 424
Red eye E pp. 440–2
Reduced GCS Epp. 344–5
Renal failure/kidney injury E p. 386
Shock E pp. 490–5
Shortness of breath E p. 276
Stridor E p. 290
Stroke E p. 354
Tachyarrhythmia E p. 254
Seizures E p. 348
Normal values
Despite national efforts to standardise laboratory testing and reporting,
exact ranges vary between hospitals, these figures serve as a guide.
Haematology see E p. 580
Hb–men
Hb–women
130–180g/L
115–160g/L
WBC
MCV
76–96fl
Plts
150–400 x 10 /l
Ferritin
TIBC
12–200micrograms/l B12
42–80µmol/l
Folate
• NØ
• LØ
9
• EØ
4–11 x 109/l
2.0–7.5 x 109/l
(40–75%)
1.3–3.5 x 109/l
(20–45%)
0.04–0.44 x
109/l (1–6%)
197–866pg/ml
2–20micrograms/l
Clotting see E p. 581
INR
PT
Fibrinogen
0.8–1.2
11–16s
1.5–4.0g/l
APTTr
APTT
D–dimer
0.8–1.2
35–45s
<0.3mg/ml
(<300ng/ml)
Ca2+ (adjusted)
PO43–
Mg2+
HCO3–
Cl–
2.2–2.6mmol/l
0.8–1.5mmol/l
0.7–1.0mmol/l
22–29mmol/l
95–108mmol/l
30–130units/l
3–35units/l
10–55units/l
Bilirubin
Albumin
Total protein
3–21micrograms/l
35–50g/l
60–80g/l
0–120units/l
3.5–6.0mmol/l
24–37g/l
<6mmol/l
0.5–1.9mmol/l
CRP
ESR
CK
LDH
PSA
<5mg/l
<20mm/h
25–195units/l
70–250units/l
0–4ng/ml
PaO2
PaCO2
10.6–13.3kPa
4.7–6.0kPa
U+Es see E p. 582
Na+
K+
Urea
Creatinine
Osmolality
133–146mmol/l
3.5–5.3mmol/l
2.5–7.8mmol/l
70–150µmol/l
275–295mOsmol/kg
LFTs see E p. 583
ALP
ALT
γGT
Other
Amylase
Fasting glucose
Immunoglobulins
Cholesterol
Triglycerides
Blood gases see E pp. 598–9
pH
Base excess
7.35–7.45
±2mmol/l
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Fifth Edition
Tim Raine
Consultant Gastroenterologist,
Cambridge University Hospitals NHS Foundation Trust, UK
George Collins
Cardiology Registrar
Barts Health NHS Trust, UK
Catriona Hall
General Practitioner,
James Wigg Practice, Kentish Town, London, UK
Nina Hjelde
Anaesthetic registrar,
Manchester University NHS Foundation Trust, UK
Consultant Editors
James Dawson
Consultant Anaesthetist,
Nottingham University Hospitals NHS Trust, UK
Stephan Sanders
Assistant Professor, UCSF School of Medicine, USA
Simon Eccles
Consultant in Emergency Medicine, St Thomas Hospital, UK
1
1
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Third Edition published in 2011
Fourth Edition published in 2014
Fifth Edition published in 2018
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v
Preface
It seems that every new edition of this book has arrived fresh on the tail
of some major change impacting the training and lives of junior doctors
in the NHS. Previous new appointments into the Foundation Programme
had to contend with the traumas of the introduction of ‘Modernising
Medical Careers’. More recently, we have seen the treatment of junior
doctors reach the national media once more with the new junior doctors’
contract and the ensuing, unprecedented industrial relations dispute of
2015–​2016. If there is a theme, beyond the constant upheaval that our
junior doctors are being subjected to, it is the increasing void between
those delivering healthcare on the ‘shop floor’ and those planning what
is best for the health service, often based upon misinformation and misunderstanding. In a landscape where a Secretary of State for Health so
wilfully misquotes data as to lead to questions regarding his honesty and
his intelligence, what message of hope can we send to newly appointed
junior doctors? And as we wrote in a previous preface, through all of this
turbulence, the fact remains that the leap from being a final year medical
student to a junior doctor remains immense. No matter what elements
may be introduced to final year curricula, or to Foundation Programme
inductions, the psychological and professional gear-​shift is a change that
many feel unprepared for. Overnight the new doctor inherits huge responsibility, an incessantly active bleep, and an inflexible working rota.
But something else happens, overnight. The new doctor also becomes
a valued member of the medical team, someone who patients look to
for help and someone with the capacity to provide that help to both patients and their relatives. Despite changes in training structure, the new
doctor has the potential and flexibility to learn and shape a career in just
about any area of medicine they wish to pursue. And if the assault of
politicians might well distress some, take solace in over two decades of
UK polling data, showing doctors as representing the profession consistently rated highest for trustworthiness, with politicians languishing consistently at the very opposite end of the spectrum.
Nevertheless, such is the burden that comes with the new professional
status, that nothing can make the transition that a student doctor must
go through easy. At the very least, we hope that this book can act as a
guide, a manager of expectations, but above all else, as a companion
on this difficult journey. Carry the book with you. Turn to it when you
feel most exposed or most worried. We have tried to make sure that,
whatever the situation, there will be at least something that you can read
and use to start you off along the right path. And if there isn’t? Don’t
panic—​make sure you have spoken with someone senior, and take heed
of the advice on p. xxviii. Finally, when the dust has settled, please take
the time to let us know and to help us continue to improve this book by
sending comments and suggestions to: Mohfp.uk@oup.com
TR, 2017
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To every doctor who’s ever stood there thinking:
‘What on earth do I do now?’
vii
Acknowledgements
The authors would like to say a huge ‘thank you’ to many people for
their wisdom, knowledge, and support:
• Tim thanks Lucy for her patience and support and Beatrice, Felix, and
Max for their carefree good humour
• George would like to thank Mel, Mark and Charlie, whose support
and space made this authorship possible
• Catriona would like to thank her former Foundation colleagues for
their friendship, encouragement, and resilience, and her colleagues in
General Practice for their mentorship and unfailing support
• Nina would like to dedicate this work to her husband for his endless
support through yet another one of her ventures
Specific thanks for assistance with specialist material go to Dr Daniel
Neville (Respiratory), Dr Sam O’Toole (Endocrinology), Dr Simon Vann
Jones (Psychiatry), Drs Bjorn Thomas and Duncan Leadbetter (Skin and
eyes), and Dr Elaine Church (Emergencies).
This book builds upon the efforts of authors of all previous editions.
In particular, we are grateful for the vision of Simon Eccles and the hard
work of James Dawson and Stephan Sanders, without whom this book
would never have come to be.
We would also like to thank all the staff at Oxford University Press
for their help and for making our writing into a book. In particular, Liz
Reeve and Kate Smith for their terrific efforts and support in making
the OHFP5e such a pleasure to work on, along with the rest of the
OUP team:
• Michael Hawkes
• Fiona Chippendale
ix
Contents
Symbols and abbreviations
Introduction
10 tips on being a safe junior doctor
10 tips on being a happy doctor
1 Being a doctor
2 Life on the wards
3 History and examination
4 Prescribing
5 Pharmacopoeia
6 Resuscitation
7 Cardiovascular
8 Respiratory
9 Gastroenterology
10 Endocrinology
11 Neurology
12 Psychiatry
13 Fluids and renal
14 Haematology
15 Skin and eyes
16 Emergency department
17 Procedures
18 Interpreting results
Appendices
Index
x
xxv
xxvii
xxviii
1
67
125
169
183
225
245
275
293
327
343
369
385
405
423
447
523
579
613
629
x
Symbols and
abbreviations
K
I
E
T
2
3
M
i
d
l
±
>
<
♀
♂
A+E
AAA
ABG
ABPI
ABx
ACCS
ACEi
ACF
ACR
ACS
ACTH
ADH
ADL
AED
AF
AFB
αFP (AFP)
AIDS
AKI
ALL
definition
topics covered elsewhere
cross reference
supplementary information
emergency
don’t dawdle
website
increased
decreased
leading to
plus/​minus
greater than
less than
female
male
accident and emergency
abdominal aortic aneurysm
arterial blood gas
ankle–​brachial pressure index
antibiotics
acute care common stem
angiotensin-​converting enzyme inhibitor(s)
academic clinical fellowship
albumin:creatinine ratio
acute coronary syndrome
adrenocorticotrophic hormone
antidiuretic hormone
activities of daily living
automated external defibrillator/​anti-​epileptic drug
atrial fibrillation
acid-​fast bacilli
α-​fetoprotein
acquired immunodeficiency syndrome
acute kidney injury
acute lymphoblastic leukaemia
Symbols and abbreviations
ALP
ALS
ALT
AML
AMPH
AMPLE
ANA
ANCA
AoMRC
AP
APH
APLS
APTT
AR
ARB
ARDS
ARVC
AS
ASA
ASAP
ASD
AST
AT
ATLS
ATN
AV
AVN
AVR
AXR
Ba
BAL
BBB
BCG
bd
BE
β-​hCG
BIH
BiPAP
BKA
BLS
alkaline phosphatase
Advanced Life Support®
alanine aminotransferase
acute myeloid leukaemia
approved mental health professional
Allergies; Medications; Past medical history; Last meal;
Events leading to presentation
antinuclear antibody
antineutrophil cytoplasmic antibody
Academy of Medical Royal Colleges
anteroposterior
antepartum haemorrhage
Advanced Paediatric Life Support
activated partial thromboplastin time
aortic regurgitation
angiotensin receptor blocker
acute respiratory distress syndrome
arrhythmogenic right ventricular cardiomyopathy
aortic stenosis
American Society of Anesthesiologists
as soon as possible
atrial septal defect
aspartate transaminase
angiotensin
Advanced Trauma Life Support
acute tubular necrosis
atrioventricular
atrioventricular node
aortic valve replacement
abdominal X-​ray
barium
bronchoalveolar lavage
bundle branch block
bacille Calmette–​Guérin (TB vaccination)
bis die (twice daily)
base excess
β-​human chorionic gonadotrophin
benign intracranial hypertension
biphasic positive airways pressure
below knee amputation
Basic Life Support
xi
xii
Symbols and abbreviations
BM
BMA
BMI
BNF
BNP
BP
BPH
BX
C+S
Ca
Ca2+
CABG
CAD
CAH
CAPD
CBD
CBG
CBT
CCF
CCG
CCT
CCU
CD
CDT
CEA
CEPOD
CEX
cf
CHD
CI
CJD
CK
CK-​MB
CKD
CLL
CLO
CML
CMV
CNS
CO
Boehringer Mannheim meter (capillary blood glucose) or
bone marrow
British Medical Association
body mass index
British National Formulary
brain natriuretic peptide
blood pressure
benign prostatic hypertrophy
biopsy
culture and sensitivity
carcinoma
calcium
coronary artery bypass graft
coronary artery disease
congenital adrenal hyperplasia
continuous ambulatory peritoneal dialysis
case-​based discussion/​common bile duct
capillary blood glucose
cognitive behavioural therapy
congestive cardiac failure
clinical commissioning group
Certificate of Completion of Training
coronary care unit
controlled drug
Clostridium difficile toxin
carcinoembryonic antigen
Confidential Enquiry into Perioperative Deaths
Clinical Evaluation Exercise
compared with
coronary heart disease
contraindication
Creutzfeldt–​Jakob disease
creatine kinase
heart-​specific creatine kinase (MB-​isoenzyme)
chronic kidney disease
chronic lymphocytic leukaemia
Campylobacter-​like organism
chronic myeloid leukaemia
cytomegalovirus
central nervous system
carbon monoxide
Symbols and abbreviations
CO2
COAD
COC
COPD
CPAP
CPK
CPN
CPR
CQC
CRP
CRT
CSF
CSU
CT
CTCA
CTG
CTPA
CVA
CVP
CVS
CXR
d
D+C
D+V
DBS
DC
DCCV
DCM
DEXA
DH
DHS
DI
DIB
DIC
DIPJ
DKA
DLB
DM
DMARD
DNA
DNAR
carbon dioxide
chronic obstructive airway disease
combined oral contraceptive
chronic obstructive pulmonary disease
continuous positive airway pressure
creatine phosphokinase
community psychiatric nurse
cardiopulmonary resuscitation
care quality commission
C-​reactive protein
capillary-​refill time/​cardiac resynchronization therapy
cerebrospinal fluid
catheter specimen of urine
computed tomography/​Core Training/Core Trainee
CT coronary angiogram
cardiotocograph
CT pulmonary angiogram
cerebrovascular accident
central venous pressure
cardiovascular system
chest X-​ray
day(s)
dilatation and curettage
diarrhoea and vomiting
Disclosure and Barring Service
direct current
direct current cardioversion
dilated cardiomyopathy
dual-​energy X-​ray absorptiometry (DXA)
drug history/​Department of Health
dynamic hip screw
diabetes insipidus
difficulty in breathing
disseminated intravascular coagulation
distal interphalangeal joint
diabetic ketoacidosis
dementia with Lewy bodies
diabetes mellitus
disease-​modifying anti-​rheumatic drug
deoxyribonucleic acid/​did not attend
do not attempt resuscitation
xiii
xiv
Symbols and abbreviations
DOAC
DoB
DOPS
DRE
DSM-​5
DTP
DU
DVLA
DVT
d/​w
Dx
EBM
EBV
ECG
Echo
ECV
ED
EDD
EEG
EMD
EMG
ENP
ENT
EO
EPO
ERCP
ERPC
ESM
ESR
ESRF
ET
EtOH
ETT
EUA
EVD
EWTD
F1/​F2
FAST
FB
direct oral anticoagulant
date of birth
Direct Observation of Procedural Skills
digital rectal examination
Diagnostic and Statistical Manual of Mental Disorders
5th edition
diphtheria, tetanus, and pertussis
duodenal ulcer
Driver and Vehicle Licensing Agency
deep vein thrombosis
discuss(ed) with
diagnosis
evidence-​based medicine
Epstein–​Barr virus
electrocardiogram
echocardiogram
external cephalic version
emergency department (formerly A+E)
expected due date (pregnancy)
electroencephalogram
electromechanical dissociation or pulseless electrical
activity (PEA)
electromyogram
emergency nurse practitioner
ear, nose, and throat
eosinophil
erythropoietin
endoscopic retrograde cholangiopancreatography
evacuation of retained products of conception
ejection systolic murmur
erythrocyte sedimentation rate
end-​stage renal failure
endotracheal
ethanol (alcohol)
endotracheal tube
examination under anaesthetic
extra-​ventricular drain
European Working Time Directive
Foundation year one/​two
focused assessment with sonography in trauma
foreign body
Symbols and abbreviations
FBC
FDP
FEV1
FFP
FH
FiO2
FNA
FOB
FOOSH
FP
FPP
FRC
FSH
FTSTA
FVC
G+S
G6PD
GA
GB
GBS
GCS
GFR
γGT (GGT)
GH
GI
GMC
GN
GORD
GOSWH
GP
GTN
GTT
GU(M)
h
h@N
HAART
HAI
HAV
Hb
HbA1c
HBV
full blood count
fibrin degradation product
forced expiratory volume in one second
fresh frozen plasma
family history/foetal heart
fraction of inspired oxygen
fine needle aspiration
faecal occult blood
fall on outstretched hand
Foundation Programme
flexible pay premia
functional residual capacity
follicle stimulating hormone
fixed-term specialty training appointment
forced vital capacity
group and save
glucose-6-phosphate dehydrogenase
general anaesthetic
gall bladder
Group B Streptococcus/Guillain–Barré syndrome
Glasgow Coma Scale
glomerular filtration rate
gamma-glutamyl transpeptidase
growth hormone/gynae history
gastrointestinal
General Medical Council
glomerulonephritis
gastro-oesophageal reflux disease
guardian of safe working hours
general practitioner
glyceryl trinitrate
glucose tolerance test
genitourinary (medicine)
hour(s)
hospital at night
highly active antiretroviral therapy
hospital-acquired infection
hepatitis A virus
haemoglobin
glycosylated haemoglobin
hepatitis B virus
xv
xvi
Symbols and abbreviations
HCA
HCC
hCG
HCM
HCSA
HCT
HCV
HDL
HDU
HEE
HELLP
HHS
HIV
HLA
HMMA
HOCM
HONK
HPA
HPC
HR
HRCT
HRT
HSP
HSV
HTN
HUS
HVS
I+D
IBD
IBS
ICD
ICD-​10
ICP
ICS
ICU
ID
IE
IFG
Ig
IGT
healthcare assistant
hepatocellular carcinoma
human chorionic gonadotrophin
hypertrophic cardiomyopathy
Hospital Consultants and Specialists Association
haematocrit
hepatitis C virus
high-​density lipoprotein
high dependency unit
Health Education England
haemolysis, elevated liver enzymes, low platelets
(syndrome)
hyperglycaemic hyperosmolar state
human immunodeficiency virus
human leucocyte antigen
4-​hydroxy-​3-​methoxymandelic acid (phaeochromocytoma)
hypertrophic obstructive cardiomyopathy
hyperosmolar non-​ketotic state
Health Protection Agency
history of presenting complaint
heart rate/​human resources
high-​resolution computed tomography scan
hormone replacement therapy
Henoch–​Schönlein purpura
herpes simplex virus
hypertension
haemolytic uraemic syndrome
high vaginal swab
incision and drainage
inflammatory bowel disease
irritable bowel syndrome
implantable cardiac defibrillator
International Classification of Diseases 10th revision
intracranial pressure
inhaled corticosteroid
intensive care unit
identification/​infectious diseases
infective endocarditis
impaired fasting glucose
immunoglobulin
impaired glucose tolerance
Symbols and abbreviations
IHD
ILS
IM
Imp
IN
INH
INR
ITP
ITU
IU
IUCD
IUP
IV
IVDU
IVI
IVP
IVU
Ix
JDC
JVP
K-​nail
kPa
KUB
K-​wire
L
LA
LABA
LACS
LAD
LAMA
LBBB
LDH
LDL
LETB
LFT
LH
LHRH
LIF
LMA
LMN
LMP
ischaemic heart disease
Immediate Life Support
intramuscular
impression (clinical)
intranasal
by inhalation
international normalized ratio
idiopathic thrombocytopenic purpura
intensive care unit/​intensive therapy unit
international unit
intrauterine contraceptive device
intrauterine pregnancy
intravenous
intravenous drug user
intravenous infusion
intravenous pyelogram
intravenous urogram
investigation(s)
Junior Doctors’ Committee of BMA
jugular venous pressure
Küntscher nail
kilopascal
kidneys, ureter, bladder (X-​ray)
Kirschner wire
litre(s)
local anaesthetic/​left atrium
long-​acting β-​agonist
lacunar circulation stroke
left axis deviation/​left anterior descending
long acting muscarinic agonist
left bundle branch block
lactate dehydrogenase
low-​density lipoprotein
Local Education and Training Board
liver function test
luteinizing hormone
luteinizing hormone releasing hormone
left iliac fossa
laryngeal mask airway
lower motor neuron
last menstrual period
xvii
xviii
Symbols and abbreviations
LMWH
LN
LØ
LOC
LP
LRTI
LSCS
LTFT
LTOT
LUQ
LVEF
LVF
LVH
MAOI
mane
MAP
M,C+S
MCPJ
MCV
MDR
MDT
MDU
ME
MEWS
mg
MI
min
mL
MMC
mmH2O
mmHg
MMR
MMSE
MND
MPS
MR
MRA
MRCP
MRI
MRSA
MS
low-​molecular-​weight heparin
lymph node
lymphocyte
loss of consciousness
lumbar puncture
lower respiratory tract infection
lower segment Caesarean section
less than full-time training
long-​term oxygen therapy
left upper quadrant
left ventricular ejection fraction
left ventricular failure/​left ventricular function
left ventricular hypertrophy
monoamine oxidase inhibitor
in the morning
mean arterial pressure
microscopy, culture, and sensitivity
metacarpal phalangeal joint
mean cell volume
multi-​drug resistant
multidisciplinary team
Medical Defence Union
myalgic encephalitis
Modified Early Warning Score
milligram(s)
myocardial infarction
minute(s)
millilitre(s)
Modernising Medical Careers
millimetres of water
millimetres of mercury
measles, mumps, and rubella
Mini-​mental State Examination
motor neuron disease
Medical Protection Society
mitral regurgitation/​modified release/​magnetic resonance
mineralocorticoid receptor antagonist
magnetic resonance cholangiopancreatography
magnetic resonance imaging
meticillin-​resistant Staphylococcus aureus
multiple sclerosis/​mitral stenosis
Symbols and abbreviations
MSF
MSSA
MST
MSU
MTPJ
mth
MVR
N+V
NAD
NAI
NBM
NEB
NG
NHS
NHSI
NICE
NICU
NJ
NNU
NØ
NOAC
nocte
NPA
NPSA
NSAID
NSTEMI
NTN
NVD
NYHA
OA
Obs
OCD
OCP
od
OD
OGD
OHA
OHAM
OHCC
OHCLI
OHCM
multisource feedback
meticillin-​sensitive Staphylococcus aureus
morphine sulfate
mid-​stream urine
metatarsal phalangeal joint
month(s)
mitral valve replacement
nausea and vomiting
nothing abnormal detected
non-​accidental injury
nil by mouth
by nebulizer
nasogastric
National Health Service
NHS improvement
National Institute for Health and Care Excellence
neonatal intensive care unit
nasojejunal
neonatal unit
neutrophil
non-​vitamin K antagonist oral anticoagulant
at night
nasopharyngeal aspirate
National Patient Safety Agency
non-​steroidal anti-​inflammatory drug
non-​ST-​elevation myocardial infarction
national training number
normal vaginal delivery
New York Heart Association
osteoarthritis
observations
obsessive–​compulsive disorder
oral contraceptive pill/​ova, cysts and parasites
omni die (once daily)
overdose
oesophagogastroduodenoscopy
Oxford Handbook of Anaesthesia
Oxford Handbook of Acute Medicine
Oxford Handbook of Critical Care
Oxford Handbook of Clinical and Laboratory Investigation
Oxford Handbook of Clinical Medicine
xix
xx
Symbols and abbreviations
OHCS
OHEM
OHFP
OHGP
OHOG
om
on
ORIF
OSA
OSCE
OT
OTC
P
PA
PaCO2
PACS
PAD
PAN
PaO2
PAT
PBC
PCA
pCO2
PCOS
PCR
PCT
PCV
PD
PDA
PE
PEA
PEEP
PEFR
PERLA
PET
PICU
PID
PIP
PIPJ
PMETB
Oxford Handbook of Clinical Specialties
Oxford Handbook of Emergency Medicine
Oxford Handbook for the Foundation Programme
Oxford Handbook of General Practice
Oxford Handbook of Obstetrics and Gynaecology
omni mane (in the morning)
omni nocte (at night)
open reduction and internal fixation
obstructive sleep apnoea
objective structured clinical examination
occupational therapy
over the counter
pulse
posteroanterior
partial pressure of arterial carbon dioxide
partial anterior circulation stroke/​picture archiving and
communication systems
peripheral arterial disease
polyarteritis nodosa
partial pressure of arterial oxygen
Peer Assessment Tool
primary biliary cirrhosis
patient-​controlled analgesia
partial pressure of carbon dioxide
polycystic ovary syndrome
polymerase chain reaction
primary care trust
packed cell volume
Parkinson’s disease
patent ductus arteriosus
pulmonary embolism
pulseless electrical activity
positive end-​expiratory pressure
peak expiratory flow rate
pupils equal and reactive to light and accommodation
positron emission tomography
paediatric intensive care unit
pelvic inflammatory disease
peak inspiratory pressure
proximal interphalangeal joint
Postgraduate Medical Education and Training Board (obsolete)
Symbols and abbreviations
PMH
PMT
PND
PNS
PO
pO2
PoC
POCS
PONV
POP
PPH
PPI
PR
PRHO
PRN
PROM
PRV
PSA
PSH
PT
PTH
PU
PUD
PUO
PV
PVD
qds
RA
RAST
RBBB
RBC
RDW
REM
RF
Rh
RhF
RIF
ROM
ROS
RR
past medical history
pre-​menstrual tension
paroxysmal nocturnal dyspnoea
peripheral nervous system
per os (by mouth)
partial pressure of oxygen
products of conception
posterior circulation stroke
postoperative nausea and vomiting
plaster of Paris/​progesterone-​only pill
postpartum haemorrhage
proton pump inhibitor
per rectum (by rectum)
pre-​registration house officer (old training system but still
occasionally used)
pro re nata (as required)
premature rupture of membranes (pregnancy)
polycythaemia rubra vera
prostate-​specific antigen/​prescribing safety exam
past surgical history
prothrombin time
parathyroid hormone
passed urine/​peptic ulcer
peptic ulcer disease
pyrexia of unknown origin
plasma viscosity/​per vagina
peripheral vascular disease
quater die sumendus (four times daily)
rheumatoid arthritis
radioallergosorbant test
right bundle branch block
red blood cell
red cell distribution width
rapid eye movement (sleep stage)
rheumatic fever
rhesus
rheumatoid factor
right iliac fossa
range of movement
review of systems
respiratory rate
xxi
xxii
Symbols and abbreviations
RS
RSI
RTA
RTI
RUQ
RVH
Rx
s
SABA
SAH
SALT
SAMA
SARS
Sats
SBE
SBP
SC
SCBU
SCC
SE
SH
SHDU
SHO
SIADH
SIRS
SJS
SL
SLE
SOA
SOB
SOBAR
SOBOE
SOL
SOT
SpO2
SpR
SR
SSRI
STAT
ST
respiratory system
rapid sequence induction
road traffic accident
road traffic incident
right upper quadrant
right ventricular hypertrophy
prescription
second(s)
short-​acting β-​agonist
sub-​arachnoid haemorrhage
speech and language therapy
short acting muscarinic agonist
severe acute respiratory syndrome
O2 saturation
sub-​acute bacterial endocarditis
systolic blood pressure
subcutaneous
special care baby unit
squamous cell carcinoma
side effects
social history
surgical high dependency unit
senior house officer (old training system but still
widely used)
syndrome of inappropriate antidiuretic hormone secretion
systemic inflammatory response syndrome
Stevens–​Johnson syndrome
sublingual
systemic lupus erythematosus
swelling of ankles
short of breath
short of breath at rest
short of breath on exertion
space-​occupying lesion
shape of training
oxygen saturation in peripheral blood
specialist registrar (old training system but still widely used)
slow release/​sinus rhythm
selective serotonin re-​uptake inhibitor
statim (immediately)
Specialty Training/​Trainee
Symbols and abbreviations
STD
STEMI
STI
STOP
StR
SVC
SVR
SVT
Sx
T3
T4
TAB
TACS
TB
TBG
TCA
tds
TEDS
Temp
TEN
TENS
TFT
THR
TIA
TIBC
TIMI
TIPS
TKR
TLC
TMJ
TNM
TnT
TOE
TPHA
TPN
TPR
TSH
TTA
TTO
TTP
TURP
sexually transmitted disease
ST elevation myocardial infarction
sexually transmitted infection
surgical termination of pregnancy
Specialty Training Registrar
superior vena cava
systemic vascular resistance
supraventricular tachycardia
symptoms
tri-​iodothyronine
thyroxine
Team Assessment of Behaviour
total anterior circulation stroke
tuberculosis
thyroxine-​binding globulin
tricyclic antidepressant
ter die sumendus (three times daily)
thromboembolism deterrent stockings
temperature
toxic epidermal necrolysis
transcutaneous electrical nerve stimulation
thyroid function test
total hip replacement
transient ischaemic attack
total iron binding capacity
Thrombolysis in Myocardial Infarction
transjugular intrahepatic porto-​systemic shunting
total knee replacement
total lung capacity/​tender loving care
temporomandibular joint
tumour, nodes, metastases –​cancer staging
troponin T
transoesophageal echocardiogram
treponema pallidum haemagglutination assay
total parenteral nutrition
total peripheral resistance
thyroid-​stimulating hormone
to take away
to take out
thrombotic thrombocytopenic purpura
transurethral resection of prostate
xxiii
xxiv
Symbols and abbreviations
TWOC
Tx
u/​U
U+E
UA
UC
UMN
UO
URTI
US(S)
UTI
UV
V/​Q
VA
VC
VDRL
VE
VF
VMA
VP shunt
VSD
VT
VZV
WB
WBC
WCC
WCT
WHO
wk
WPW
wt
X-​match
yr
ZN
trial without catheter
treatment
units (write out ‘units’ when prescribing)
urea and electrolytes
unstable angina
ulcerative colitis
upper motor neuron
urine output
upper respiratory tract infection
ultrasound scan
urinary tract infection
ultraviolet
ventilation/​perfusion scan
visual acuity
vital capacity
venereal disease research laboratory (test)
vaginal examination/​ventricular ectopic
ventricular fibrillation
vanillylmandelic acid
ventriculoperitoneal shunt
ventriculoseptal defect
ventricular tachycardia
varicella-​zoster virus
weight bear(ing)
white blood cell
white cell count
wide complex tachycardia
World Health Organization
week(s)
Wolff –​Parkinson–​White (syndrome)
weight
crossmatch
year(s)
Ziehl–​Neelsen
Introduction
Introduction
Welcome to the 5th edition of the Oxford Handbook for the Foundation
Programme—​the ultimate FP doctor’s survival book. It is set out differently from other books; please take 2 minutes to read how it works:
Being a doctor (E pp. 1–66) covers the non-​clinical side of being a
junior doctor:
• The FP (E pp. 2–3) how to get a place, what it’s all about, the ePortfolio
• Starting as an F1 (E p. 12) essential kit, efficiency, being organized
• Communication (E pp. 20–1) breaking bad news, translators,
languages
• Quality and ethics (E pp. 27) confidentiality, consent, capacity
• When things go wrong (E p. 32) errors, incident forms, hating your job
• Boring but important stuff (E pp. 38–9) NHS structure, money, benefits
• Your career (E p. 45) exams, CVs, getting ST posts, audits, research.
Life on the wards (E pp. 67–123) is the definitive guide to ward
jobs; it includes advice on ward rounds, being on-​call, night shifts, making
referrals, and writing in the notes. A section on common forms includes
TTOs and ‘fit’ notes. There’s an important section on death—​covering
attitudes, palliative care, certifying, death certificates, and cremation
forms as well as new material on the structure of the NHS. Ward
­dilemmas including nutrition, pain, death, and aggression are covered in
detail, along with a section designed to help surgical juniors pick their
way through the hazards of the operating theatre and manage their
­patients perioperatively.
History and examination (E pp. 125–67) covers these old medical
school favourites, from a ‘real-​world’ perspective, to help you rapidly
identify pathology and integrate your findings into a diagnosis.
Prescribing (E pp. 169–82) and Pharmacopoeia (E pp. 169–82)
cover how to prescribe, best practice, complex patients, interactions,
and specific groups of drugs; commonly prescribed drugs are described
in detail, with indications, contraindications, side effects, and dosing
advice.
Clinical chapters (E pp. 225–44) These chapters cover common clinical and ward cover problems. They are described by symptoms b
­ ecause
you are called to see a breathless patient, not someone having a PE:
• Emergencies The inside front cover of this handbook has a list of
emergencies according to symptom (cardiac arrest, chest pain,
seizures) with page references. These pages give step-​by-​step
instructions to help you resuscitate and stabilize an acutely ill patient
whilst waiting for senior help to arrive
• Symptoms The clinical pages are arranged by symptom; causes
are shown for each symptom, along with what to ask and look
for, relevant investigations, and a table showing the distinguishing
xxv
xxvi
Introduction
features of each disease. Relevant diseases are described in the pages
following each symptom
• Diseases If you know the disease you can look it up in the index to find
the symptoms, signs, results, and correct management.
Procedures (E pp. 523–77) contains instructions on how to perform specific procedures, along with the equipment needed and
contraindications.
Interpreting results (E pp. 579–611) provides a guide to understanding investigations including common patterns, the important features to note, and possible causes of abnormalities.
Appendices (E pp. 613–27) are several pages of useful information
including contact numbers, growth charts, unit conversion charts, driving
regulations, blank timetables, and telephone number lists.
10 tips on being a safe junior doctor
10 tips on being a safe junior doctor
These tips are adapted from the National Confidential Enquiry into
Patient Outcome and Death (NCEPOD) report An Acute Problem?1
NCEPOD is an independent body which aims to improve the quality and
safety of patient care. The report summarizes a survey over one month
of admissions to UK intensive care units. The findings are now more
than a decade old, but sadly remain as relevant and current as when they
were first written.
1) More attention should be paid to patients exhibiting physiological
abnormalities. This is a marker of increased mortality risk (E p. 226)
2) The importance of respiratory rate monitoring should be
highlighted. This parameter should be recorded at any point that
other observations are being made (E p. 226)
3) Use of early warning scores can help to monitor patients and
trigger appropriate escalation of care. Use them with care as they
can still miss some acutely unwell patients (E pp. 226–7)
4) It is inappropriate for referral and acceptance to ICU to happen at
junior doctor (<ST3) level (E pp. 228–9)
5) Training must be provided for junior doctors in the recognition of
critical illness and the immediate management of fluid and oxygen
therapy in these patients (E p. 230)
6) Consultants must supervise junior doctors more closely and should
actively support juniors in the management of patients rather than
only reacting to requests for help
7) Junior doctors must seek advice more readily. This may be from
specialized teams such as outreach services or from the supervising
consultant
8) Each hospital should have a track and trigger system that allows
rapid detection of the signs of early clinical deterioration and an
early and appropriate response (E pp. 226–7)
9) All entries in the notes should be dated and timed and should
end with a legible name, status, and contact number (bleep or
telephone) (E p. 76)
10) Each entry in the notes should clearly identify the name and grade of
the most senior doctor involved in the patient episode (E p. 76).
The full report and several other NCEPOD reports are available online1
and are well worth reading; there are many learning points for doctors
of all grades and specialties.
1
An Acute Problem? NCEPOD (2005) at Mwww.ncepod.org.uk/​2005aap.html See also Emergency
Admissions: A journey in the right direction? (2007) at Mwww.ncepod.org.uk/​2007ea.html, Deaths
in Acute Hospitals: Caring to the End? (2009) at Mwww.ncepod.org.uk/​2009dah.html, and
Knowing the risk (2011) at Mwww.ncepod.org.uk/​2011poc.html
xxvii
xxviii
10 tips on being a happy doctor
10 tips on being a happy doctor
1) Book your annual leave Time off is essential; failing to take leave
doesn’t make you hard-​working or any more likely to get ahead, but
making a major error due to cumulative fatigue will have repercussions
for both the affected patient and your career. Spend leave doing
something you really enjoy with people you really like. If you have
fixed leave, at least you'll get what you're owed (hopefully), but swaps
can be a pain and take a lot of persistence. If you have to book time
off, it will usually be your responsibility to swap on-​calls. You usually
need to book your leave 6wk in advance and summer is always
popular. Sit down early with your team and discuss your leave plans
2) Be organized This is important but difficult when you first start
as a doctor. Come in early, keep a list of useful names and numbers
(there are pages in the appendix to help you with this, E p. 622),
and pick up hints and tips from your predecessors
3) Smile You cannot cure most diseases, you cannot make procedures
pleasant, you cannot help the fact that you, ward staff, and patients
are in the hospital, but smiling and being friendly can make all the
difference. Above all else, never shout at anyone. Shouting or being
insulting is unprofessional. If you have a problem it should be addressed
in private. The job rapidly becomes unpleasant if you get a reputation
for being rude and reputations (good and bad) travel quickly
4) Don’t underestimate the impact of night shifts on your
energy levels and health Consider your plans before, during, and
after night shifts carefully to allow sufficient time to sleep and recover.
Everyone will give advice on how best to cope with night shifts, so try
various approaches until you find the best routine for you
5) Ask for senior help Never feel you cannot ask for help, even for
something you feel you ‘should’ know. It is always better to speak to
someone senior rather than guess, even if it is in the middle of the night
6) Check in the BNF If you are not familiar with a drug then
always check in the BNF before you give it. Trust nobody: it will be
your name next to the prescription
7) Look at the obs Acutely ill patients nearly always have abnormal
observations. Always remember to look at the respiratory rate as
this is the observation most commonly ignored by junior doctors
Stay calm It is easy to panic the first time you are called to an acutely
8) ill patient, but staying calm is important to help you think clearly about
how to manage the situation. Take a deep breath, work through the
‘ABC’ while performing initial investigations and resuscitation (the
emergency pages will guide you through this) and call someone senior
9) Be reliable If you say you are going to do something then do it.
If you are unable to do so then let someone know—​nursing staff
in particular also have many things to remember and constantly
reminding doctors of outstanding jobs is frustrating
10) Prepare for the future Medicine is competitive, you need to
give yourself the best chance. Over the first 2 years you should:
• Present interesting cases
• Think about your career
• Organize specialty taster sessions
• Create a CV and portfolio
• Get good referees and mentors • Consider sitting examinations
• Enjoy being a ‘proper’ doctor.
• Participate in audit
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1
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sible for signingwyou off; this r­esponsibility may
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Professor Sir John Temple, ‘Time for Training’, 2010 Crown Copyright available free at
Mwww.mee.nhs.uk/​pdf/​JCEWTD_​Final%20report.pdf
Professor John Collins, ‘Foundation for Excellence: An Evaluation of the Foundation Programme’
available at Mwww.mee.nhs.uk/​pdf/​401339_​MEE_​FoundationExcellence_​acc.pdf
Health Education England, ‘Better Training, Better Care’, available at Mhttps://​www.hee.nhs.uk/​
our-​work/​hospitals-​primary-​community-​care/​learning-​be-​safer/​better-​training-​better-​care-​btbc
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et1.1 The FP hierarchy .net
et
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your annual progress. Responsible for signing off on
successful completion of each foundation year
Acute trusts provide the employment contract, salary, and
HR for foundation doctors. For community placements
(eg GP practice), the responsibility for education passes
to this ‘Local Education Provider’ but the contract of
employment remains with the acute trust. There can be
conflicts between the needs of the acute trusts (doctors on
the wards delivering services to patients) and some of the
educational requirements of the FP (E p. 59)
Doctor responsible for the training of individual
foundation doctors. Ideally for a whole year but
occasionally for a single attachment. Will review your
progress regularly, check that your assessments are up
to date, and help you plan your career
Doctors who supervise your learning and training, day
to day, for each attachment. In some posts (often your
1st) the roles of the educational supervisor and clinical
supervisor may be merged
Those undertaking an academic FP (which includes a
designated period of research) will be assigned an individual
to oversee academic work and provide feedback
Individuals in each trust and Foundation school who help
with FP registration and administration
Leadership position(s) where willing trainees voluntarily
facilitate two-​way feedback between their peers and
their local or regional educationalists
This is you! You are an adult learner with responsibilities
for your own learning. You are expected to integrate with
the educational processes of the FP, including providing
feedback on the programme to your supervisors, trainee
representatives, and via local and national training surveys
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wBeing a doctor
4
ww
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Chapter 1
t
t
t
.ne
.ne
.ne
Applying
to
the
Foundation
Programme
X
X
X
ok applications to the FPooarekthrough the online FP Application
ok System
o
Bo All
B
B
(FPAS) at Mwww.foundationprogramme.nhs.uk.
stages.
w.FPAS You will need to bewThere
w. are several
w
Registration
for
nominated.
For
final
year ww
w
w
students in the UK your medical school will do this for you. Those applying
from outside the UK should contact the UKFPO Eligibility Office in good
etotallow checks to take place..nBefore
et nomination you can register
efort
time
n
n
.
.
an
account
but
cannot
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form.
X
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X
ok Completing the application
ok form Within a designated
ok window
o
o
o
B
each year (usually in .early
October), nominated applicants
wB
w.B will be able to w
access the application
form. This has a number of
parts:
w
w
w contact details, DoB, and relevant
w personal health.
w
Personal Name,
Eligibility GMC status, right to work in the UK, and immigration status.
Fitness
convictions and fitness
proceedings.
etCriminal
etto practise
eoft
n
n
n
.
.
.
Referees
Details
of
2
referees
(1
academic,
1
clinical).
Their
knowledge
Xyour performance is more important
X than their seniority because
X
ok contribute
ok checks
ofork work)they
o
o
o
to
your
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suitability
raB
.B
.B
ther than your actual
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w
w
w
Competencesw
Educational
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ww
4
Evidence You will be asked to list any additional degrees for scoring
against a very specific system and to upload a copy of certificates; 5 total
percentage points are available for your degree, with 2 further points for
publications (proof is required and will be assessed).
Clinical skills You will be asked to self-​assess against a list of practical
skills—​this does not form part of the assessment process but will be
used by Foundation schools to coordinate training.
Academic selection If applying to the academic FP (E p. 6).
UoA preferences Foundation schools are grouped into Units of Application
(UoA) that process applications jointly. You will be asked to rank all UoA
in order of preference, with successful applicants allocated to UoA in
score order (you will be allocated to your highest preference UoA that
still has places when your turn comes). Tables showing vacancies and
competition ratios for previous years are available on the UKFPO website but these do tend to vary between years (see Box 1.1).
Equal opportunities To monitor NHS recruitment practices.
Declaration You are required to sign various declarations of probity.
Linked applications Two applicants can join their applications (E pp. 6–7).
Scoring Your application will be scored based upon 2 components:
Educational Performance Measure (50 points) This comprises a score between 34 and 43 based upon which decile your medical school decides
your performance falls in, relative to your peers (this is locally determined) with 7 further points for education achievements detailed on the
application form as previously mentioned.
Situational Judgement Test (50 points) See Boxes 1.2 and 1.3.
et
et
.n
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o
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o
o
w.B
o
ww
et
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These include evidence of the right to work in the UK; of having taken medical training solely in English
or having IELTS scores of ≥7.5; of complying with GMC requirements for provisional registration
which may include passing Professional and Linguistic Assessment Board test; a statement of support
from your medical school dean; academic transcripts; proof of medical qualifications; and a practical
clinical assessment exam. You should allow sufficient time for this complex process of verification.
o
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Applying to the Foundation Programme
5w
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t
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.ne1.1 Units of Application
.neand 2017 competition
.data
Box
X
X
X
k
k
ok Anglia 257 (47%) ooNW
o(84%)
o
Wales 322
of England 786
Bo East
B
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292 (100%)
Essex, Beds and Herts .
w (99%)
w. Midlands
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Northern 381 (77%) wWest
304 (25%)
w
w
ww
Leicester, Northampton,
and Northern Ireland w 176 (131%)
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240 (100%)
Rutland 153 (54%)
(32%)
Oxford 215 (99%)
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t (75%)
t (77%) 250
t
e
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Peninsulan189
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160 (348%)
.
.
.
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792
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X
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okHumber
o
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B
B in April 2017 NC
.B
The 21 UoA shown arew
the Foundation Schools for the 2017 application.
w.Note,
and NE Thames merged
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Foundation School. Vacancy
w
w
numbers for 2017
ware shown, with figures in brackets representing
w the number of applicants
ww
ranking the UoA as their first preference, expressed as a percentage of this number of jobs.
Source: data from Mwww.foundationprogramme.nhs.uk
et 1.2 Situational Judgement
et Test (SJT)
et
n
n
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.
.
.
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Box
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ok These computer-​markedotests
okof 70 questions sat under examination
ok cono
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B
ditions over 2h 20min.B
you with situations in which
you might be
w confront
w.B There
placed as an F1w
doctor,
and ask how you wouldw
respond.
are two
basic response
w formats: (i) rank five possiblewresponses in order and (ii) ww
choose three from eight possible responses. Marks are assigned according
to how close to an ‘ideal’ answer you come, with marks for near misses
and no negative marking. Raw scores are subject to statistical normalization and scaling to generate a final mark out of 50. Officially, you cannot
‘revise’ for the test, as it is an assessment of attitudes, but there is a strong
weighting on medical ethics which can be revised, and you can familiarize
yourself with what is expected and try to understand model answers.5
When introduced into FP selection for 2013 appointments, problems with
SJT marking led to hundreds of altered offers. Ongoing controversy surrounds SJTs as a means of selection, the thin evidence base behind them,
and the heavy weighting they receive. One prominent researcher and SJT
advocate closely involved in the pilots is also a director of a company that
provides SJTs, as well as being a key figure behind the selection process
that so spectacularly failed during the 2007 MMC reforms. Nonetheless,
it is difficult to argue that previous systems based upon answering generic questions or students competing to get references from a few blessed
Professors were any better. Our advice for now: ‘Get studying!’
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Prescribing is a fundamental part of the FP and it is now a requirement for
UK FP applicants to demonstrate their knowledge of the safe and effective
use of medicines through completion of this national pass/​fail prescribing
skills assessment. Piloted in 2010 in response to a GMC-​sponsored survey
which showed that 9% of hospital prescriptions contain errors, applicants
are tested on common prescriptions, medications, drug calculations, and
monitoring regimens that are encountered during the FP. Exams take place
at UK medical schools between February and June each year, and non-​UK
trainees can sit it during F1.6
o
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Practice paper available on UKFPO website. Mock questions available in
(Oxford Assess and Progress), third edition (Metcalfe D, et al.), 2018. Oxford University Press.
More information available at Mhttps://​prescribingsafetyassessment.ac.uk
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6
Chapter 1
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t
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t
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asp?file=academic_​rough_​guide_​2013_​interactive_​web_​version_​final.pdf
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visors but also other work colleagues in the form of a Team Assessment
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both are equally
important. The burden of what many see as a tick-​box exercise is still
significant, though improving slowly with each FP curriculum revision.
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other assessments:
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1 per procedure during F1
By the end of F1 you need to be signed off as competent in 15 core procedures:
• Venepuncture
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• IV cannulation
• SC injection (eg insulin or LMWH)
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medications and injections
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of fluids
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Team assessment of behaviour (TAB)
1 per year
You will be required to engage in a Maoist process of self-​criticism, then select a
minimum of 10 colleagues who will be invited to provide anonymous feedback,
including at least 2 consultants/​GPs, 1 other doctor >FY2, 2 senior nurses >band 5,
and 2 allied health professionals/​other team members (eg ward clerks, secretaries,
and auxiliary staff). Similar feedback comes from your Placement Supervision Group
but they are nominated by your supervisor rather than by you. Your educational
supervisor will then collate all the results and share them with you.
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should avoid recording patient identifiable information within your ePortfolio, since this is not the
purpose for which it was collected. Using hospital numbers rather than names, or completely
obscuring personal details is considered acceptable.
Separate meetings: your clinical supervisor should address what is expected of you and what is
available to you; your educational supervisor should take an overview of your progress and goals.
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healthcare policy and overseeing the NHS in England. Health and Social Care
Act A 2012 parliament act and the largest NHS reorganization since 1948, legislated for more healthcare regulation and patient involvement, and decentralization of healthcare/​budget responsibility. Allowed business to compete with
NHS providers for service provision. Commissioners With two-​thirds of the total
NHS budget, GPs, nurses, hospital doctors, and lay members now lead >200
clinical commissioning groups (CCGs) in buying (commissioning) local services
(including secondary care, mental health, and community services). GPs themselves as well as highly specialized services are still commissioned nationally.
Providers Commissioners purchase services from providers, which can be GPs,
the private sector, voluntary sector, or hospitals. Most trusts are ‘Foundation’
Trusts, that is, have more financial and managerial freedom (the intention being
to provide more flexibility to better suit local patient needs).
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Trade unions Represent doctors and if supported by members can call for industrial taction over employment disputes.
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promotes and coordinates their work. Faculty of Medical Management and
Leadership A faculty of the Academy of Royal Colleges that is dedicated to
medical leadership. A good resource for trainees interested in medical leadership and management.
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t
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n
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main organizations; all offer 24h helplines (E pp. 614–15):
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t 10 for F1, £20 for F2 net
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for those planning a career in hospital medicine. Benefits include employment advice, contract checking, personal injury service, and legal
services. Annual cost is £100 for foundation trainees.
Income protection Pays a proportion of your basic salary ± a lump sum (rates
vary) until retirement age if you are unable to work for health reasons.
Check if it covers mental health problems, and if it still pays if you are capable of doing a less demanding job. NHS sickness benefits are not comprehensive (providing F1s 1mth full pay, 2mth half pay, and F2s 2mth full pay,
2mth half pay): Available from various providers, typically starting at £24/​
mth as an F1, rising according to age, pay, illness, and risks.
2015 NHS Pension Scheme A proportion of your pay is put into the
scheme to be returned, with additional interest and employer contributions, during your retirement. Despite bringing the retirement age in line
with the state pension, an increase in the cost of personal contributions,
and a shift from final salary to career-​averaged earnings, the 2015 NHS
Pension Scheme remains the best pension available; do not opt out.
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P45/​P60 tax form When you leave a job you will receive a P45; if you continue in the same job you will receive a P60 every April. These need to
be shown when starting a new job.
Bank details Account number, sort code, and proof of address.
Hepatitis B You need proof of hep B immunity and vaccinations. You
should keep validated records of your immunizations and test results.
GMC registration certificate This proves you are a registered doctor.
Disclosure and Barring service (DBS) certificate (formerly CRB checks) It is the
employer’s responsibility to perform these checks. You must complete all
paperwork in good time, but payment is the responsibility of the trust.10
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In theory, the medical staffing department of your trust should sort a lot of this out in advance
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ID badge Used
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areas’. If the card doesn’t give access then return it or get it fixed.
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food from machines. For problems, contact the mess president.
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Chapter 1
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Occupational
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sible for ensuring that. the hospital is a safe environment
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t that affects your abilityntoetwork may require a consultation.
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• If you arew
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• Keep your clothes clean and roll up long sleeves to be bare below the
elbows in clinical areas
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• Avoid jewellery (plain metal rings are acceptable) and wrist watches
• Clean your stethoscope with a chlorhexidine swab after each use
• Wash your hands or use alcohol gel after every patient contact,
even when wearing gloves; rinsing all the soap off reduces irritation.
Clostridium difficile spores are resistant to alcohol, so always wash your
hands after dealing with affected patients
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• Use antibiotics appropriately and follow local prescribing policies. For
more information, contact your local infection control team.
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As a doctor you will come into contact with bodily fluids daily. It is important to develop good habits so that you are safe on the wards:
• Wear gloves for all procedures that involve bodily fluids or sharps.
Gloves reduce disease transmission if penetrated with a needle—​
consider wearing two pairs for treating high-​risk patients
• Dispose of all sharps immediately; take the sharps bin to where you are
using the sharps and always dispose of your own sharps
• Vacutainers are safer than a needle and syringe. Most hospitals now
stock safety cannulas and needles for phlebotomy, use of which
decreases the risk of needle-​stick injuries yet further
• Mark bodily fluid samples from HIV and hepatitis B+C patients as ‘High
Risk’ and arrange a porter to take them safely to the lab
• Consider wearing goggles if bodily fluids might spray
• Cover cuts in your skin
• Avoid wearing open-​toed shoes or sandals
• Make sure your hepatitis B boosters are up to date.
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Pen-​torch Useful for looking in mouths and eyes; very small LED torches
are available in ‘outdoors’ shops or over the Internet and can fit onto a
keyring or be attached to stethoscopes to prevent colleagues borrowing
and not returning them.
Tendon hammer These are hard to find on wards. Collapsible pocket-​sized
versions can be bought for £12–​15.
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searching, and can be more ‘predictable’ than those on the ward.
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Shoes A pair of smart, comfy shoes is essential—​you will be on your feet
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K Box 1.7 Social
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wand
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16
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Chapter 1
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Being a doctor
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wYou are not expected to knoww
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et
n
n
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.
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w
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ww
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et
n
n
n
.
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being cared for in the right environment. While there are many factors that
slow down patient flow, patients, clinicians, and management staff will thank
you if high-​quality discharge letters are prepped well in advance. Keeps tabs
on estimated discharge dates and if you’re not sure, enquire with your colleagues about who may be going home tomorrow.
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17w
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w
w and management plans. ww
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but writing it down reduces errors. They are usually electronic and may
be manually or automatically generated, allowing every team member to
carry a copy. Lists can be invaluable for discussing/​referring a patient while
away from the ward but must be kept confidential and disposed of securely
(E p. 83).
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ww
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.
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Along with ward rounds and clinicalw
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wwequipment Finding equipment
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t To make your day runnasesmoothly
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t
t early in the day is important
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eblood
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n
n
n
.
.
.
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X
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the risk of forgetting what you were asked to do. Consider whether there
is anyone else you could delegate simple tasks to, such as nurse practitioners or ward staff while you attend to more urgent tasks.
t
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t through jobs in order.nTry
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doctor performing the procedure or one trained in taking consent for
that particular procedure
Bookmark online or get a copy of your hospital guidelines/​protocols,
eg pre-​op investigations, anticoagulation, DKA, pneumonia etc.
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Remember the names and faces of your colleagues and patients
Talk to your predecessors to get hints and tips specific to your ward.
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care. Healthcare was. done to people rather than with
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ok these can be very powerful.
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o
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.B illness of relainclude: religious beliefs,
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tives with similar
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Treatment expectations
t
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Patients may have clear expectations of their treatment (eg an operation
or being given a prescription). These expectations are important sources
of discontentment when not fulfilled. Find out what their expectations
are and why. Useful questions may include: ‘What do you think is wrong
with you?’ ‘What are you worried about?’ ‘What were you expecting
we’d do about this?’
oo
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o
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Make time to imagine yourself in your patient’s shoes. Isolation or communication difficulties will heighten fear at an already frightening time.
Long waits without explanation are sadly common. Aggression from
friends or relatives is often simply a manifestation of anxiety that not
enough is being done. Ask yourself ‘How would I want my family treated
under these circumstances?’ then do this for every patient.
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Hospitals can rob people of their dignity. Wherever and whenever possible help restore this:
• Keep your patients covered (including during resuscitation)
•Ensure the curtains are around the bed on the ward round
• Make sure they have their false teeth in to talk and glasses/​wigs on
whenever possible
• Help them self-​care when possible.
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ok Patients areforoften
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w
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o
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to gain more insight about their condition or to allow a training doctor
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22
.B
w
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Chapter 1
Being a doctor
.B
w
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t
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Communication
and
X
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k and colleagues is a vital part
ok
opatients
okof the job.
communication with
o
o
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B
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All communication
w.
w.
w
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Whenever you
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professional (see ww
w
w
Box 1.9), include your name and role, the patient’s name, location, and
primaryt problem, what you would like tthem to do and how urgently, and
ethey can contact you if there.are
eany problems
et
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n
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.
.
X
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ok T Box 1.9 Handover
ok
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o
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o
B
.B
Reductions in working
shift-​based rotas, and
w.B hours, a move towardsww
w
the increased
w cross-​cover between specialties
w mean the number of ww
doctors caring for a patient during their stay has increased, making the
effective transfer of information more important. Handover occurs at
et and end of every shift, and
eit tis vital that it is given enough.ntime
et
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n
n
.
.
and
thought.
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handover
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X
X
kX must
ok while others are more informal.
ok Either way, the incomingoodoctor
o
o
get
a
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idea
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the
situation
including
the
names,
locations,
and
B
.B
.Breview, as well
w
clinical details forwunwell patients and those needing
other outstanding
ww tasks that need going. Giving
ww and receiving a good ww
handover is a key skill and one you should pride yourself on perfecting.
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net communicationX.net
net
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.
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p. 76.
letters E p. 84.
ok ClinicalnotesnotesEEp. 82.
ok Referral
ok
o
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TTOs E pp. 80–1.
Bo Sick
B
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. wants to discharge themselves,
Self-​discharge If your
wpatient
w. speak to them, w
w
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ask why, manage
their concerns, and explain why
they need hospital manw
w
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agement and what may happen if they leave. If they have capacity, then ask
them to sign a ‘self-​discharge form’ and do a TTO as normal.
t
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conduct
.ne
.ne
.ne
X
X
X
you are a respected
member of society and a representative
ok As a doctor
oandk people
okin a certain
medical profession,
will expect you tooact
o
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B
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this does. not mean you cannot be yourself,
there is a big
w school and you must be aware
w.of expectations:
change from medical
w
w
w yourself, especially overwthe telephone or when
ww
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answering a bleep; ‘Hello’ is not enough
t
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et your
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X
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handover or ward rounds
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ward staff or your seniors. Ask for help if you feel overrun with tasks.
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Communication and conduct
23w
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X
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o
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wcallprevents
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t staff will be present net
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etot explain
ediscuss
n
n
.
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the patient’s progress. in a
X
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o
oork ask them
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o
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ww
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ok Patient communication
ok
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o
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o
B A patient’s perception
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B largely on
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ware
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Remember that patients
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w
wfeel powerless, and are worried
w about their
ww
onment, often
health.
B
Introductions Always introduce yourself to patients and clearly state your
name and position. Ask your patient how they wish to be addressed (eg
Denis or Mr Smith). Patients meet many staff members daily so reintroduce yourself each time you see them (see Box 1.10).
General advice Try to avoid using medical jargon. Be honest with your
replies to them, and give direct answers when asked a direct question. If
you do not know the answer, be honest about this too.
Results Explain why a test was done, what it shows, and what it means.
Diagnosis Try to give the everyday name rather than a medical one (heart
attack instead of MI). Explain why this has happened. A patient who
understands their condition is more likely to comply with treatment.
Prognosis Along with the obvious questions about life expectancy
(E p. 86), patients are most interested in how their life will be affected.
Pitch your explanation in terms of activities of daily living (ADLs), walking,
driving (E p. 619), and working. Bear in mind that patients may want to
know about having sex, but are often too embarrassed to ask.
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X
Kate Granger was a geriatrician, patient, and campaigner for compassionate and personalized care who sadly died at the age of 34 in 2016.
She was diagnosed with terminal cancer in 2011 and spent her subsequent years campaigning for better communication between doctors
and patients. Frustrated at the lack of introductions from healthcare
staff caring for her in hospital, she started the #hellomynameis campaign in 2013. Founded on the simple idea of reminding staff that a
confident introduction is often all that is needed to put patients at ease,
the campaign raised £250,000 for cancer charities and has received
widespread public and professional support. It is a reminder to us all
never to forget something as simple as introducing ourselves properly.
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24
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Chapter 1
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w
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Being a doctor
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X
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k always be done by a senior
ok
oshould
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o
o
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B
B
termined time when.relatives and friends ± specialist. nurses can be preware likely to be involved inw
w bad news, often w
sent. In reality,w
breaking
wItyou
w
while on-​call.
can be a positive experiencew
if done well.
Preparation Read the patient’s notes carefully and ensure that all ret Be clear in your mind nabout
earet up to date and for the right
epatient.
et
sults
n
n
.
.
.
the
sequence
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events
and
the
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X discuss with a senior. kX furkXther management and likelyoprognosis—​
k
o
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oo
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B
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(E p. 31, p. 29) .ABpatient has a right
w
w before the in- w
to know what w
is going on or to choose not tow
w know.If Ask
vestigations w
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a patient does not w
want their relatives to know about their diagnosis you must respect this.
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etask, do not assume—​many.nfamilies
et have complex dynamics..net
n
.
Warning
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Give
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X bad news is imminentksoXit is not
ok completely out of the blue,
oegk ‘I have the results from . .o. would
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B
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anyone else here when
I tell you them/​shall we go to .aB
quiet room?’.
.
w
w
How to do itw
w The SPIKES model is often used:
ww
ww
B
Setting Ask a colleague to hold your bleep, set aside suitable time (at least
30min), silence your mobile phone, use a quiet room, and invite a nurse
who has been involved in the patient’s care. Arrange the seats so you can
make eye contact and remove distractions. Introduce yourself and find
out who everyone is.
Perception Find out what the patient already knows by asking them directly; this will give you an idea of how much of a shock this will be and
their level of understanding to help you give appropriate information.
Invitation Explain that you have results to give them and ask if they are
ready to hear them. It helps to give a very brief summary of events so
they understand what results you are talking about.
Knowledge Break the bad news, eg ‘A doctor has looked at the sample
and I’m sorry to say it shows a cancer’. Give the information time to sink
in and all present to react (shock, anger, tears, denial). Once the patient
is ready, give further information about what this means and the expected management. Give the information in small segments and check
understanding repeatedly. Prognosis can be difficult; never give an exact
time (‘months’ rather than ‘4 months’). Be honest and realistic. Try to
offer hope even if it is just symptom improvement or leaving hospital.
Empathy Acknowledge the feelings caused by the news; offer sympathy.
This will take place alongside the ‘Knowledge’ step. Listen to their concerns, fears, and worries. This will guide what further information you
give and help you to understand their reactions.
Summary Repeat the main points of the discussion and arrange a time for
further questions, ideally with a senior and yourself present. Give a clear
plan of what will happen over the next 48h. Document the discussion in
the patient’s notes (diagnosis, prognosis, expectations) with your name
and contact details.
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Cross-cultural communication
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1.11).
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Professional
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n
n
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.
X
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ww can accompany the ww
patient for future appointments.
Never assume you know what the patient wants without asking them.
t
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.ne members as interpreters
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Family
X
X
X
k not be
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and friends o
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o
o
Nevertheless,
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w
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patient’s response
w
w
family member was used for interpretation in the notes.
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e drawbacks are the lack.nofetconfidentiality
ethet
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and the bias
n
.
.nwhen
X
X
X
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ok underlying family issues are
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o
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. for their parents from an early
.Bage,o but again their
w
w
views can bias the
and its outcomew
sexual health and vulw consultation
w
wand
w (eg
nerable adults)
even routine clinical questions
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etof interests If you think the relative
etyouis biasing
etotit
n
n
n
.
.
is an
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are professionally obliged
X a trained interpreter.kX
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o on behalf of adults (Eop.o31).
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Box 1.11 w
Who can interpret?
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ww
Hospital interpreters
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26
.B
w
ww
Chapter 1
Being a doctor
.B
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t
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Outside
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X
X
X
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okinclude: poagencies who could
o
o
Bo Outside
B
B
.
lice, media, solicitors,. fire brigade, paramedics, GP, researchers,
and the
wPatient confidentiality mustwbewrespected.
patient’s employer.
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n
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.
X• Do they have any right to the
Xinformation they are seeking?kX
ok GPs, healthcare professionals,
ok and ambulance staff may
o well
o
o
omany
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B
B
B
.
.
others do notw
w
witwbe a more senior
• Should you
be the one discussing this or should
w
w
ww
member of the team?
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et have
et andyour hospital unless: .net
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the patient’s permission,
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.
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and
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o
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• Do not ‘chat’w
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a patient,
no matter what
the allegedwcircumstances; all patients havew
an equal right to privacy
ww
•
•
•
•
• Breaching a patient’s confidentiality without good cause is treated as
misconduct by the GMC.
t
t
t
.ne
.ne
.ne
Confidentiality
and the police
X
X
X
investigation of assaults
The police may well ask the
conok Immediate
o‘Iskit life-​
okclinical
o
o
of an assault victim.
t
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.
.
this question is tow
know how thoroughly to investigate
w the crime scene. w
wto give
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of w
severity.
w
w
In the public interest In situations where someone may be at risk of serious
injury, disclosure
is permitted by the GMC.
t
edecision.
et This should be a consultant-​
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n
n
net
.
.
.
X
X
X
Traffic Act Everyonekhas a duty to provide the policekwith inforok The Roadwhich
may lead to
identification of a driver who
oothe
oo is alleged to
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.
have committed a driving
offence. You are obliged .to
supply the name
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and address, not
wclinical
wwseniors first.
w
w
ww
Being a witness in court
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e you are a professional.witness
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knowledge/​experience.
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w
w
w
w
ww
Medical research
et
n
.
kX
o
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You may be asked to provide patient details for research. Ask the researcher to provide you with ID and if they have consent from the patient. Unless the researcher has specific permission to screen medical
notes, they may ask you to seek initial permission from any potential participant before passing on the patient’s details to the researcher.
et
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Clinical governance/quality
27w
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.ne governance/​
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Clinical
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k NHS
ok definition: ‘Clinical governance
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o
o
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are accountable for continuously
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w. standards ofimproving
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and safeguarding
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in
w
w
w
ww
which clinicalw
excellence will flourish.’
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t responsible for your clinical
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eare
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et
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which you should be
n
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n
.
.
Xaiming to continuously improve
kX the standard of your opractice
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ok • You need a mechanismoforoassessing
o
o
trainer as part
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.B have
wmay
of your regular appraisal process. Additionally, you
audits and
w
w
regular departmental
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w
w
ww
• You should be aiming to continuously learn and improve your care for
patients.
while still in training, tthis almost goes without saying; t
et forAgain,
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revising
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n
.
X
X
kX
this means for you
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ok What
oktoasdepartmental
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o
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o
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.Bprocedures for which you have
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w.Bnotaudits,
wwto participate
w
• You will bew
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usually
w
ww
of morbidity and mortality. These are used to ensure consistency of
practice and to pick up problems early
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grand rounds to keep up to date with changes
• You should answer any responses to complaints promptly.
t
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X
k
oo
et
oo
B
.
w
t
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X
k
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kX
oo
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The clinical governance
w structure in every hospital
wwincludes:
w
w
ww
• Audit of practice (eg reattendances within 1wk or wound infections)
• Appraisal and revalidation structures
t and mortality) to allow t
• Regular
meetings (eg morbidity
net departmental
.clinicians
.nehighlight common concernsX.ne
to compare their care and
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routes of accountability
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. is responsible for fixing w.
but seemingly now
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w
• A risk management
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jeopardize
wpatient care
ww which
ww
high-​quality
(critical incident reporting,
E p. 34)
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lessons
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et
n
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n
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.
.
department
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kX
governance/​quality
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ensures
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w.B governance/​quality mechanisms
w.B are measured w
Compliance with
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w
w
both regionally
w and nationally through qualitywboards.
w
B
Clinical governance/​quality mechanisms
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o
et
n
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et
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kX
t
o
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w
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28
.B
w
ww
Chapter 1
.B
w
w
ww
w
Being a doctor
t
t
t
.ne
.ne
.ne
Medical
ethics
X
X
X
ok
ok
ok
o
o
is medical ethics?
Bo What
B
B
Ethics are moral values,
w. and in the context of medicine
w. are supported by w
w
w
four main underlying
principles:
w
w
w
Autonomy This is the right for the individual to make decisions for themselves, tand not be overtly pressurized
or swayed by others (namely
e nurses, relatives, etc). Patients
et should
et
doctors,
be allowed to contribute
n
n
n
.
.
.
Xwhen decisions are made about their care. If an individual lacks
Xcapacity
ok (E p. 30) then it might onotokbeXappropriate to let them omake
okimportant
o
B
autonomous decisions.
.B
w.Bfor the patient and w
Beneficence Thisw
isw
concerned with doing what w
is right
w best interests. This does notwnecessarily mean we should w
what is in their
do everything to keep a 90-​year-​old patient alive who has widespread
metastatic
disease. There will be times
it is beneficent to keep
etcomfortable,
etot diewhen
eta
n
n
n
patient
and allow them
naturally.
.
.
.
X maleficence This ensureskX
X to
givers refrain from doing
ok Non-​
o orcare-​
okof harm
o
o
o
the patient, whether physical
psychological. An example
a breach
B
.B be if a patient came towharm
.B as a result
in nonmaleficencew
would
of a
w inadequate training or ww
doctor performing
ww a procedure in which theywhad
B
supervision.
Justice This requires that all individuals are treated equally and that both
the benefits and burdens of care are distributed without bias. Justice also
covers openness within medical practice and the acknowledgement that
some activities may have certain consequences—​specifically legal action.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
Two further principles are important to consider:
Dignity This should be retained for both the patient and the people
delivering their healthcare.
Honesty This is a fundamental quality which doctors (as well as other
care-​givers) and patients should be expected to exhibit in order to
strengthen the doctor–​patient relationship.
ww
o
Bo
t
.ne
X
k
t
.ne
X
k
w
t
o
o
w.B
Ethical conflict
et
.ne
X
k
oo
B
.
w
.n
kX
Ethical dilemmas frequently arise in clinical practice and are probably not
discussed enough. While the principles listed do not necessarily provide
an immediate answer, they do create a framework on which the various
components of the conflict can be teased out and addressed individually.
All doctors should be able to discuss common ethical dilemmas by analysing how each principle is relevant and weighing them up against one
another. In ethics there are no right answers, but careful thought and discussion of situations can allow a harmonious solution to be found.
ww
t
e
X.n
ww
.ne
X
k
t
ww
et
n
.
X
ww
k
ok
oo
oo
Bo Ethics and communication
B
B
.
.
wwthat apparently complexwethical
wwissues arise because ww
It is quite common
w
of a failure in communication between the patient or their loved ones
and healthcare
professionals. The solution
most of these conflictstis
et
et to lines
the
establishment
of effective and.transparent
of communication.
n
n
.
.ne
X
X
X
k
k
ok
oo
oo
Bo
B
B
.
.
w
w
ww
ww
ww
B
.B
w
w
.B
w
w
w
w
w
Patient confidentiality
29w
t
t
t
.ne
.ne
.ne
Patient
confidentiality
X
X
X
ok breach patient confidentiality
ok is unlawful and unprofessional;
ok several
o
o
Bo To
B
B
doctors are disciplined. and even struck off the medical
each year
wbe careful when talking aboutwpatients
w. register
for this. You should
in public places,
w
w
wthe hospital environment, andw
including within
only disclose patient informa- w
tion to recognized healthcare staff as appropriate. Pieces of paper with patient information
on must never leave e
the
t
t hospital and should be shredded
eare
et
n
n
n
if they
no longer required. Do not
leave patient lists lying around. Personal
.
.
.
X
X be disguised so individual
databases of patients
kXpatients
ok electronic
ok should
cannot be identified. Electronic
devices on which patientoo
information is
o
o
B stored outside of thewhospital
B under the
.B should be encrypted and
registered
w.(names
Data Protectionw
Act. You avoid giving any information
nature of
w
w
wpolice, press, or other enquirers;wask your seniorsorfor
injuries) to the
advice w
when dealing with these (E p. 26).
Publications
Medical journals will often
et
et insist that any article which
ein-t
n
n
n
.
.
.
volves
a
patient
must
be
accompanied
by
written
consent
from
the
patient
X the publication of the material,
Xirrespective of how difficultkitX
ok for
okpatient.
o
o
oo would be
to
track
down
and
identify
that
B
B
B
.
.
w
wabout a patient to a
Presentations
and images If you are talking
group of healthcare
ww workers in your own hospital
ww you do not need to ww
obtain consent, but doing so is courteous. If you are talking to an audience
from outside your hospital it is advisable you seek the patient’s consent
unless the patient is fully anonymized. Equally, if you want to keep copies
of radiographs or digital images, ensure these are made anonymous and
if this isn’t possible obtain the patient’s written consent. Bear in mind that
presentations can easily end up online and be accessed by those other
than your original audience.11
Relatives Your duty lies with your patient and if a relative asks you a
question about the patient, it is essential you obtain verbal consent from
the patient to talk to the relative; alternatively offer to talk to the relative
in the presence of the patient. Relatives do not have any rights to know
medical information. If the patient lacks capacity then seek senior advice
before talking to the relatives. Document all conversations in the notes.
Children As described for adults, if the child has capacity to give consent (see ‘Gillick competence’/​Fraser guidelines E p. 30), you must seek
verbal consent from the patient to tell the relatives (parents) about their
health. If the patient refuses, then offer to talk to the patient about their
condition in the presence of their relatives. If you sense the situation will
be difficult, seek senior advice/​support.
Telephone calls Wards receive many telephone calls asking how patients are and if they have had tests or operations yet. The potential to
break patient confidentiality here is great. Often there is a telephone by
each bed, so encourage callers to speak to the patient directly. Otherwise,
inform the patient who the caller is and relay a message from the patient
to the caller. Apologize to the caller for not being able to offer any further
information and suggest that you could talk things over with both themselves and the patient when they visit. See ‘Outside agencies’ E p. 26.
et
et
.n
kX
o
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o
o
w.B
o
ww
et
et
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o
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o
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ok
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t
ok
o
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e
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ok
o
w.B
ww
t
t
e
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ok
o
B
.
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ww
ww
t
e
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e
X.n
ok
o
B
.
w
For a good discussion of the ethical issues, see Draper H, Rogers W. Re-​evaluating confidentiality: using patient information in teaching and publications APT 2005;11:115, available free at
Mapt.rcpsych.org/​content/​11/​2/​115.full.pdf
11
ww
t
e
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et
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ww
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et
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w
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wBeing a doctor
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Someone who has capacity can comprehend and retain information material relevant to the decision, especially as to the consequences of not
having the intervention in question, and must be able to use and weigh
this information in the decision-​making process.
For a patient to have capacity they must:
• Be able to understand the information relevant to making the decision
and consequences of refusal
• Retain the information long enough to allow for decision-​making
• Weigh up the information to arrive at a decision
• Be able to communicate the decision they have made.
Remember that:
• Patients may have the capacity to make certain decisions and
not others
• Capacity in the same patient may fluctuate over time.
Capacity is most often impaired by chronic neurological pathology such
as dementia, learning difficulties, and psychiatric illness, but is also impaired by acute states such as delirium, acute severe pain, alcohol and
drug intoxication (both recreational and iatrogenic—​eg morphine).
Children and capacity Children under 16yr of age were once regarded as lacking capacity to give consent, but now if the child meets the
criteria then they are regarded as having ‘Gillick’ competence (Fraser
guidelines12), and may give consent (Box 1.12). It is always advisable, however, to involve the parent or guardian in discussions about the patient’s
care if the patient allows (see also E p. 417).
ww
t
t
e
X.n
ok
Bo
ok
o
w.B
ok
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ok
o
w.B
t
ok
o
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.
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e
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ok
o
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.
w
ww
et
et
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kX
o
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o
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w.B
ww
ww
No capacity When the patient does not have capacity and is over 18,
family and friends are not able to make a decision on the patient’s behalf; their views should, however, be listened to. Where the patient lacks
capacity and there is no next of kin to consult, an Independent Mental
Capacity Advocate (IMCA)13 may need to be appointed who advises clinicians in making decisions on behalf of the patient in their best interests. In
an emergency situation, the patient is treated under the ‘doctrine of necessity’, that is, doing what is in the patient’s best interests until they attain
capacity to make the decisions themselves.
et
et
.n
kX
o
o
.n
kX
o
o
w.B
ww
ww
t
t
ok
Bo
e
X.n
ok
ok
o
w.B
ww
ww
t
t
e
X.n
ok
Bo
e
X.n
Although 16 years is the usual age at which people are automatically allowed to give their own consent, younger people can consent to most
treatments or operations if they are capable. This follows a famous case
in 1986 when Victoria Gillick went to the courts to get authority to be
informed if her daughters sought contraceptive treatments. The law disagreed and decided that if a child was competent, he/​she could consent to
treatment without parental knowledge—​this is often referred to as being
‘Gillick’ competent when a child meets the criteria in that case.
o
w.B
ok
o
B
.
w
ww
ww
t
e
X.n
e
X.n
ok
o
B
.
w
Wheeler R. Gillick or Fraser? A plea for consistency over competence in children. BMJ
2006;332:807.
13
Mental Capacity Act (2005); Mwww.legislation.gov.uk/​ukpga/​2005/​9/​section/​35
12
ww
t
K Box 1.12 Gillick competence/​Fraser guidelines
e
X.n
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et
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w
Chapter 1
t
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Capacity
X
k
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.B
w
w
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w
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t
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Consent
X
k
o
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w
w
oo
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.
w
t
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X
k
Consent
et
o
w.B
o
Understanding consent and obtaining it satisfactorily can be difficult. If
you are ever unsure, seek senior help.
ww
ww
tient should be aware of the risks and benefits and be able to communicate the procedure in a language that the patient will understand. If you do
not regularly perform the procedure yourself or are not trained to take consent
for the procedure then you must not obtain consent for it. Obtaining consent
satisfactorily is a skill that can be learned from senior colleagues, so initially
shadow your seniors when they are taking consent from a patient to learn
how to do it properly, then have a senior colleague supervise you the first
few times to ensure you include all the relevant information.
et
n
.
kX
t
ok
.B
w
ww
ww
Informed consent In order to give informed consent, patients must
ok
et
n
.
X
Bo
et
n
.
X
ok
ww
t
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k
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o
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et
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X
ok
first be deemed to have capacity to consent under the specific circumstances (E p. 30). Consent should reflect the fact that the patient is aware
of what is going to happen and why. They should be aware of the consequences of not undergoing the procedure, the potential benefits, and any
alternatives, and be free from any coercion. The common risks and side
effects should be discussed, as should the potentially rare but serious consequences of the procedure. As a rule, any risks which might affect the decision of a normal person should be discussed—​plus any risks that might
be of specific importance for the individual patient, such as where the profession of the patient makes a normal trivial risk of special importance (eg
a tiny risk of postoperative vertigo might be of particular importance for a
window cleaner). The patient should be provided with information well in
advance of the procedure to allow them to think it over and prepare any
questions they may wish to ask.
o
B
.
w
ww
et
n
.
kX
oo
e
X.n
o
w.B
31w
.n
kX
Obtaining consent The individual who obtains consent from the pa-
o
Bo
B
.B
w
w
.n
kX
w
oo
B
.
ww
Types of consent There are three main types of consent:
ww
t
.ne
X
k
ww
tThe patient offers you theirnearmt as you approach them with
ta
Implied
.ne and syringe to take blood.
.
.ne
needle
X
X
X
kthat you are going to perform
You explain
ok Expressed—​byverbal
oprocedure
ok a lumbar
o
o
describing
the
and potential complications,
and
Bo puncture,
B
B
the patient agreesw
to .have it done.
w.
w
w
Expressed—​ww
ritten The patient is given an extensive
w explanation of the ww
procedure and complications and informed of the alternatives. A record
of the tconsultation is made which both
t patient and doctor sign. This
e
e
et
document
should be completed prior
to the planned treatment ornpron
n
.
.
.
Xcedure, and consent verified katXthe time of the procedure. kX
ok Difficult situations There
o
o
situations whereoproblems
arise
o
B with consent issues.wIf.Bin odoubt,areseekmany
senior advicew
or.B
consult one of the
medical defencew
24hw
telephone support.
w unions (E p. 2) which have w
ww
If a patient has capacity to give or withhold consent, and chooses not to
receivettreatment even in the face of tdeath, then treating that patient
e their will is potentially a criminal
e offence. This includes patients
et
against
n
n
n
.
.
.
Xwith psychiatric illness. Note kthat
X this situation is distinct fromkXthat of a
ok patient with a psychiatric oillness
o who may lack capacity toomake
o decisions
o
B regarding psychiatricwtreatment,
B and may be detainedwand
Bgiven psychiatric
.
.
(but not medicalw
treatment) under the Mental Health
Act (E p. 371).
w
ww
ww
B
32
.B
w
ww
Chapter 1
Being a doctor
.B
w
w
ww
w
t
t
t
.ne
.ne
.ne
Medical
errors
X
X
X
ok
ok from the trivial and correctable
ok to the sedoctor makes mistakes,
o
o
Bo Every
B
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vere and avoidable. .
w
w.
w
w
What to do
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once/​
w
ithin
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w
w
ww
• Stabilize the patient, call for senior help early
• Do not
the error by tryingt to cover it up or ignoring it
et compound
eto the patient as appropriate.net
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where possible, apologizing
n
n
.
X• Don’t underestimate the seriousness
X of the situation kX
ok • If serious and you haveotime,
ok start documenting events,oincluding
o times
o
• If after the error you
wish to add more details, then.do
so but make it
B
B
B
.
w
clear when theyw
w were added. This is perfectly
wacceptable
• Amendingw
notes, without making it clear that
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w
ww
retrospectively and with a clear date and time, is serious misconduct.
t
Serious
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erare
et
n
n
n
.
.
.
•
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X patient early. Apologizekthat
X the event has taken placek(Box
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ok the
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o 1.13),
o
o
o
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• Inform your senior/​
immediately. If you
w.Bconsultant
wshould
w
w
has caused
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w
w
defence organization (E p. 614) as soon as practical.
t you from working temporarily
neexclude
net pending preliminaryXenquiries.
net
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.
.
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X
a judgemental act but
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ok This isbenotinformed
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. organization at
to others involved. If .this happens, speak with your defence
w
w
once. You should
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the hospital and
w within
w
ww for more than 2wk withoutwreview.
cannot be excluded
Let the hospital and w
others know how to get hold of you. Less serious errors should be treated
as training
and dealt with by youreconsultant
or tutor. A period of close
t
t
et issues
n
n
supervision
or retraining may be appropriate.
.
.
.ne
X
X
X
ok Sources of help ook
ok
o
Bo Clinical events Consultant,
B
B
supervisors
and
defence
organizations.
.
w
w.dean, the BMA.
Non-​clinical events
Your consultant, the postgraduate
w
w
w these events resolve very ww
Don’t forgetw
friends and family, and remember
slowly, sometimes years in big cases, so don’t expect answers quickly.
et
et
et
n
n
n
.
.
.
K
Box
1.13
Duty
of
candour
X
kXprofesok Candour is being openooandkXhonest. While our ethicalooand
o
B
sional duties of candour
trusts and
.B are well established, since
w
w.B2015
their employees
have a legal duty of candourwtowards
their patients.
w
If an unexpected/​
w unintended incident occurs
w that could/​did result in ww
Disciplinary procedures If you have made a serious error the hospital
et
n
.
kX
o
Bo
death, psychological harm for >28d, permanent reduction in function
or non-​permanent but significant physical harm needing an increase in
treatment (e.g. longer admission, another procedure, treatment cancellation, transfer to higher-​level care), then trusts are legally obliged to
apologize and explain to the patient, and notify them as investigations
evolve. Failure to do so may result in prosecution by the CQC.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
w
t
.ne
Complaints
X
k
o
Bo
oo
B
.
w
w
Complaints
t
.ne
X
k
33w
et
o
w.B
.n
kX
o
Every doctor has complaints made about them. These can be about your
clinical ability, conduct, or communication skills. They may be justified or
spurious but they are inevitable, therefore do not feel your world has
fallen apart when you are told a complaint has been made about you.
ww
ww
ww
How the system handles complaints There are two types of
o
Bo
et
n
.
kX
t
ok
o
w.B
.B
ww
How to respond to a complaint
et
n
.
X
ok
et
n
.
X
ok
o
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.
w
t
.ne
X
k
oo
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oo
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et
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o
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w
ww
ww
et
n
.
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ok
o
w.B
• Preventable death of a patient
• Significant harm to a patient, in a predictable way
• Disciplinary offences including:
• substance abuse
• being drunk on duty
• sexual/​racial harassment.
et
n
.
kX
.n
kX
t
Box 1.14 Serious errors
o
oo
B
.
w
o
o
w.B
ww
et
.ne
X
k
.ne
X
k
ww
t
.ne
X
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ww
t
e
X.n
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o
B
.
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t
et
oo
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.
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ww
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X
ok
.n
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ww
o
w
ww
• All formal complaints are collated centrally in the hospital. In the rare
event you are sent a complaint personally, do not respond but pass it to
the complaints department. In most trusts, the department that handles
complaints is known as PALS (Patient Advice and Liaison Service). They
also provide more general advice and support for patients
• If a patient makes a complaint to you about care they have received
from a colleague (doctor, nurse, or other) then listen to them but try
to avoid appearing to agree or support their position, no matter how
much you may share their opinions. Depending on the seriousness of
their allegations (Box 1.14), either offer to feedback the comments or
advise them to discuss matters further with PALS
• If a complaint has been made about the care of a patient you saw, you
may be asked for a statement. This is an internal document and should
be written as a letter, but bear in mind that if the case goes to court,
this document could be requested by the patient’s lawyers
• Simply state the facts as you see them, do not try to apportion blame.
You may be able to expand on your notes, particularly the details of
conversations which may not have been documented
• Do not take it personally
• If you feel it is clear how any error could be avoided in future then state
this as well. Patients are often satisfied by knowing that any mistake they
suffered will not be repeated for others
• All the statements made by the staff involved are then collated and a
letter is written on behalf of the chief executive (and usually signed by
them) to the patient. This usually ends the matter
• There are further steps, both with the trust and then regionally, if this
is not enough.
ww
Bo
et
n
.
kX
oo
e
X.n
complaints—​formal and informal. If a patient complains to you informally
it is in everyone’s best interest, and will save many hours of clinical time, if
you are able to resolve the situation to the patient’s satisfaction there and
then. If you are unable to do so, but feel the problem may be solvable by
more senior input, then call for help. Don’t agree to do something which
you are unable to carry out.
Bo
B
.B
w
w
w
ww
ww
t
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
wBeing a doctor
34
ww
w
Chapter 1
t
t
t
.ne
.ne
.ne
Incident
reporting
X
X
X
ok
okare defined as:
ok
o
o
incidents B
These
Bo Clinical
B
. patients’ care or disruptswcritical
. treatment
• Anything whichw
w harms
w
• An event w
which
could potentially lead to harm
if
allowed
to progress
w
ww
(‘near misses’). They range from minor incidents, eg incorrect results,
to life-​
group
t threatening, eg wrong blood
t in a blood transfusion.net
e
e
n
n
Non-​
c
linical
incidents
These
include:
.
.
.
kX• Incidents which involve staff,
kXrelatives, or visitors
kX
o
o
o
o
Bo • Incidents whichwinvolve
.Bonon-​clinical equipment orwproperty.
.Bincidents
The aim of incident reporting is to highlight adverse
or ‘near
w
was a result. Ultimately
misses’, assess
them, and review clinical practice
it is ww
w
w
designed to reduce clinical risks and improve overall quality of patient care.
t occurs
When
a clinical incident/​nearemiss
et sure
et
n
n
.
• .Make
the patient is safe .n
X
X
kX reporting form (usually online)
a trust critical o
incident
ok •• Complete
ok if
o
o
o
Forward
the
form
to
the
clinical
risk
coordinator
(usually
automatic
B
form is electronic)
w.Bare aware of what has happened
w.B
w
w
•Ensure your seniors
w
w
ww
• Consider completing some formal reflective practice in your ePortfolio.
t
net samples from two different
nepatients
net
• .Blood
being confused
.
.
X
X
X
or follow-​k
ok • Failure to report
o up abnormal results
ok
failure
o
o
Bo •Equipment
B
B
• Drugs prescribed to
who have a documented
w. mpatients
w. allergy
• Delay in treatment/​
anagement.
w
w
w
w
ww
Completing incident forms
• Fill intan incident form as soon as yout can after the event so that yout
e
ne forget any relevant information
ne
.don’t
.nform.
.online
• Check you are filling in the correct
All NHS trusts now use
X
X
X
ok incident reporting systems
okthough there may be paper backups
ok
o
o
Bo • Include the time,wdate,
B
B
staff
involved,
as
well
as
the
issues
being
.
. form reported
wthe
• Check if the w
named consultant needs to fill in/​
sign
w
• If you are w
reporting an incident involving your
wcolleagues, inform them ww
and explain the situation. Learn from their mistakes without judging them.
t risk directors for evaluation
The critical
incident form is copied toeclinical
et meetings,
et
n
n
n
.
at.panel
where changes.to
clinical practice are discussed.
X
X
X
ok Hints and tips ook
ok
o
o
B
• If a critical incident.B
is filed involving yourself, .don’t
w form
w B assume
you’re a badw
doctor;
use it as a learning experience
w
wreason and circumstances andwclarify the situation with the ww
• Find out the
Examples of all-​too-​common clinical incidents
14
person filing the report
• Go over the incident and review your actions, asking if there is
anything you would change; if it helps, discuss it with a colleague.
t
ok
Bo
t
e
X.n
e
X.n
ok
o
B
.
w
t
e
X.n
ok
o
B
.
w
See Mhttps://improvement.nhs.uk/documents/2266/Never_Events_list_2018_FINAL_v5.pdf for
a list of events that should never happen (but sadly, still sometimes do).
14
ww
ww
ww
B
.B
w
ww
.B
w
w
w
w
Colleagues and problems
35w
t
t
t
.ne
.ne
.ne
Colleagues
and
problems
X
X
X
k
ok
ok with a colleague who
oworried
of us may have oworked
us
o
Bo Many
B
B
. want to be treated by Dr
.X’. When does this
professionally—​‘I wouldn’t
w
w
become enoughwto do something? And what dow
w
w you do?
ww
Clinical incompetence
• The GMC
is quite clear that we all havet a clinical duty to report
t who
t
e
e
colleagues
we believe to be incompetent.
This does not equate
toe
n
n
n
.
.
.
that you
Xpointing out every fault of every
Xother doctor but it does meankX
ok cannot ignore serious concerns
ok if you believe patients areoatorisk
of harm
o
o
B • Serious concernswabout
B a trainee should be passedwto.Bthe relevant
.
consultant. Ask to see them in private. It may be easiest to open the
conversation
with a question, to ask them to
ww
wputwyour mind at rest:
ww
‘I don’t know if you are aware that Dr X does not use chaperones? I’ve
always
told we should use them fortintimate examinations. I’m here t
et been
ehad felt uncomfortable with Dr .X.’ne
because
two women told me that they
n
.
.nthen
X
X
X
•
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ok another consultant or, ifoitoiskvery serious,youtheshould
okto
medical director
o
o
B • If you are unsurewwhether
then
.B a problem exists, or how
w.Bseriousoritais,clinical
talk to a friendly
consultant informally (eg your
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w
w
lecturer you
wgot on with at medical school).w
ww
Recreational drugs/​alcohol
t is a clear difference between
t
• There
nemuch
neatdoctor occasionally drinking
.too
.ne
while off-​duty and X
one. who helps themselves to controlled
X
X
has developed
ok drugs or who
ok an alcohol problem between
ok what
o
regardless.B
of o
substance, there is a difference
Bo • Likewise,
B
someone does that
w only affects themselves andwactions
w. which affect
w
quality of patient
care.
Any
colleague
who
appears
w
w on duty while badly ww
hungover is a potential risk to patient care and should be removed from
clinical
(and should be encouraged
to recover in the mess or go t
t should
et duties
ekind
home).
Repetitive behaviour of this
be discussed with n
n
n
.
.
. thee
colleague, and/​or their educational
supervisor
X
X
X
k arriving drunk, or use of ocontrolled
k
ok • Drinking during workingoohours,
o
and
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duty
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your
Bo drugs are totallywunacceptable
B
B
.
w. the GMC
consultants to any such problem. They will consider
w
w
guidance and
w following a meeting with thewindividual involved will
ww
decide if GMC referral is appropriate or if a local warning and period
of ‘probation’
is needed These problems
are better tackled early t
etsolvable than
et patient
while
left until they.n
cause
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n
.
.ne
X
X
X
k
k
problems
ok Psychological
oo serious psychological illnesses
oo just like
year, doctors B
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Bo •Every
B
.
.
the rest of the population
and doctors are just as
diagnosis
w
wwbad atandself-​
• The more common
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ww problems include frankwdepression
ww
et
n
.
kX
o
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the rare include psychosis and schizophrenia (E p. 14); the symptoms
often come on gradually such that even close colleagues may not notice
the transition from mildly eccentric to frankly pathological
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about their health.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
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X
ok
.Bo
ww
B
36
.B
w
ww
Chapter 1
.B
w
w
ww
w
Being a doctor
t
t
t
.ne your job X.ne
.ne
Hating
X
X
k is common and usually transient.
ok
owork
ok If you
problems at
o
o
Bo Experiencing
B
B
. try to identify the problem.
. However diffifind things do not improve,
wpolite,
cult things are w
at w
work, you should always remain
and
w
wdon’t, you may be the one perceived
w to be thepunctual,
ww
helpful. If you
problem.
Stress at the workplace
et
et a doctor, the demands of.nyour
et
The
responsibility
that comes with.nbeing
n
.
expectations from peers and patients
Xjob, fear of litigation, and highkX
X can
ok leave you physically and omentally
o exhausted. If you feel things
okare getting
o
o
on top of you, reassess
B
.B your workload. Speak towcolleagues
.B to find out
if there are easierw
ways of doing things. Take annual
leave and upon your
w
w
return approach
w your work schedule differently
w to help regain control ww
of things. Ensure you have time to relax away from work and keep up
your outside
If things don’t timprove, talk to a friend, contact
et (Einterests.
ediscuss the situation with a trusted
et
the
BMA
p. 614) for advice, .or
n
n
n
.
.
X or mentor.
X
X
ok senior
ok
ok
o
o
o
Handing
in
your
resignation
B
.B
.B
If you can find now
other option and you are clearw
medicine isn’t for you,
w
w
you can always
leave
your
job.
Find
out
how
much
notice you are re- ww
w
w
quired to give and who to direct your letter of resignation to. During
your last weeks, stay an active member of the team rather than taking a
short-​timer’s attitude. Complete any outstanding work and tidy up loose
ends before leaving.
t
t
t
.ne
.ne
.ne
X
X
X
k
ok
ok
at work oo
o
Bo Bullying
B
B
.your seniors, peers, other healthcare
Bullying can be from
wrelatives.
w. professionals, w
patients, or their
If you feel you are
being bullied, discuss it
w
w
w either at work or independently
w (eg the BMA). Speak to w
with someone,
your predecessors to find out if they had similar difficulties and how they
t the problem. Keep a diarynoferelevant
t events, together withnewit-t
handled
.ne and approach your consultant.
. If it is your consultant who
nesses,
is the
X
X
X. counk problem, approach anotherokconsultant you trust or contactokBMA
o
Bo selling (E p. 614).w.Bo
.Bo
w
Sexual harassment
This may start
wwvery innocently and gradually
wwescalate into intimidating ww
behaviour which may affect your work, social life, and confidence. In
the first instance, make it clear that their advances are not welcome and
confide in someone you trust. Find out if other colleagues are also being
harassed and report the harassment to your educational supervisor.
Again, the BMA can be a useful source of advice.
t
e
X.n
.ne
X
k
t
et
n
.
X
k
ok
o
oo
Bo Discriminationw.Bo
B
.
w
ww policy that includes ww
All employers
must abide by an equal opportunities
w
w
standards on treating all employees. Before deciding to take things further, confide
Keep a record of any events
t in a trusted senior colleague.
et documenting
eandt
thatne
stand out as being discriminatory,
dates, times,
n
n
.
.
.
witnesses.
Contact
the
BMA
for
advice.
You
may
have
to
submit
X
X toa
kX so make sure you areokprepared
ok formal letter outlining your
oconcerns,
o
o
o
pursue a formal complaint
before committing yourself
on paper.
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
t
.ne
Relaxation
X
k
o
Bo
oo
B
.
w
t
.ne
X
k
et
o
w.B
.n
kX
o
ately. Leave the ward, ask someone to hold your bleep, and take 5min
to unwind. Take deep breaths and concentrate on the feeling of the air
rushing in and out of your lungs. Count the breaths and try to clear your
mind. Try squeezing the muscles in your feet then feeling them relax; do
this with all the muscle groups from your legs to your neck. Think about
something you are looking forward to.
Do not let medicine take over your life. In particular, value and cultivate
your non-​medical friendships—​these can be hard to sustain under the
strains of shiftwork but you will value an external perspective on life beyond the NHS. It may not take much to make life seem better; try to:
et
n
.
kX
ww
t
ok
o
w.B
.B
w
ww
• Go for a walk
• Watch a film
• Go shopping
•Exercise
• Watch a comedy
• Take a long bath
• Go out for a meal
et
n
.
X
•
•
•
•
•
•
•
Talk to friends
Watch sport
Play a game
Have a good cry
Go to the pub
Have a massage
Cook
et
n
.
X
ok
o
B
.
w
ww
•
•
•
•
•
•
•
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et
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.
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e
X.n
ww
ok
Bo
37w
Have a break There are few problems that must be solved immedi-
ww
o
Bo
w
Causes of stress
Plan a holiday
Talk to parents
Have a lie-​in
Listen to music
Have an early night
Join a class/​club
Read (another) book.
ww
t
.ne
X
ok
o
B
.
w
ww
ww
Try to avoid
t
t
net
.ne sleeping tablets
.ne
• .Smoking
• Drugs/​
X
X
X
ok •Excessive alcohol ook •Excessive caffeine.
ok
o
Bo
B
B
w.
w.
w
Causeswofw stress
w
ww
Attitude
t you have no control over;neit tis
Thereeist no point worrying about things
.n to feel concerned aboutXfuture
.ne events
natural
but almost everything
X
X. will
k turn out well in the end, even
k
k
if it is not as you have planned
it.
o
o
o
o
Bo The job
.Bowith time; these
w.B
w
See E p. 19 onw
being
efficient. The job gets much
easier
w
skills becomew
second nature and you performw
individual tasks quicker.
ww
Yourself
t
e
X.n
ok
Bo
.ne
X
k
t
et
n
.
X
Be honest with yourself: are you tired? Everything is harder, slower, and
more stressful when you have not had enough sleep.
Think about what makes you stressed and whether this is a problem
with your attitude, the way you do the job, other people, or the nature
of the job. Try to accept, change, or avoid these stressors.
ok
o
o
w.B
ww
Other people
ww
o
w.B
If someone is annoying you then consider telling them so. Plan how you
will tell them, do it in private, and do not blame them; just explain how it
makes you feel. Most people will be apologetic and try to change.
et
n
.
kX
et
n
.
kX
ww
t
.ne
X
k
o 2 If you feel it is all getting otooomuch and/​or nobody cares, try speaking
oo200to:169
Bo BMA counselling (you
B
B
.
.
don’t
need to be a member)
08459
w
w
Samaritans
ww
ww 08457 90 90 90
ww
B
38
.B
w
ww
Chapter 1
.B
w
w
ww
w
Being a doctor
t
t
t
.ne and contractsX.ne
.ne
Pay
X
X
ok
ok
ok
o
o
doctors’ contract
Bo Junior
B
B
. junior doctors’ terms andwconditions
.
In August 2017, the
of service
wwnew
w
replaced thew
previous
2002 contract (updated
in
2008).
The most signifi- ww
w
cant changes were pay increments rewarding responsibility rather than time
served, new safeguards against poor training and overwork (Box 1.15), and
et of normal working hours
etuntil 9pm on weekdays. However,
et
an n
extension
n
n
.
.
.
many
details
were
contentious
and
despite
concessions
on
both
sides,
X
X the country bore witnesskXto an unok sticking points remained.oAsoka result,
o
o
oNHS
precedented and lengthy
dispute between the BMA and
Employers
B
B
B
.
.
w of the contract (see Box 1.16).
wEven now, employers, w
over the precise terms
w
w
trainers, andw
trainees are getting to grips withwthe details, with national re- w
views planned for 2018 and transitional arrangements until 2022. You should
read your
carefully as we provide
only a summary, the details are
et contract
et unfamiliar
et
important,
and your seniors may be.n
quite
with its intricacies.
n
n
.
.
X
X
X
ok Box 1.15 Limits onoworking
ok hours
ok
o
o
B
.B are responsible for doctors’
.Bsafe working
•Employees and doctors
winclude
wduring
• Limits on hours
no more than 48h work
the average
w
w
w Working Time
ww
working w
week (56h if opted out of the European
B
directive), or 72h in any 7d stretch. The average working week
is defined as starting at midnight between Sunday and Monday, is
averaged over 26wk, and includes locums (E p. 40)
Mandatory 11h rest between shifts, with time off within 24h if less
No shift (except non-​resident ‘availability’ shifts) should exceed 13h
Consecutively no more than 8d of work, 5 long shifts (10h+), 4
long shifts that finish after 11pm, or any 4 shifts that include 3 of the
hours between 11pm–​6am (with 2d mandatory break after each)
30m break during a 5h shift or 2 during a 9h shift; not within an hour of
starting/​finishing, ideally in the middle, and can be merged into 1h
Safeguards are there for breaches or inadequate training (E p. 39).
t
.ne
X
k •
oo •
•
•
o
et
•.n
X
k
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
t
.ne
X
k
w
t
.ne
X
k
ww
et
.n
kX
oo
oo
B
B
.
.
The following elements
w vary depending on yourwrota
w but are added up to w
w
generate your
salary (payslip E p. 41):
w
w
w
Basic salary Depends on grade and responsibility, based on 40h/​week.
Additional
hours An allowance for up tot8h extra per week.
et allowance
ebasic salary depending on the
efre-t
Weekend
A % added to .the
n
n
n
.
.
X of weekends you work
X(3% for 1 in 7, 10% for 1 in 2).kX
ok quency
okbasic
Night duty 37% on top ofothe
salary for hours worked
o
oo9pm–​7am.
B
B
B
.
.
Availability allowance 8%
on
top
of
the
basic
salary
for
when
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>48h during the average working week (Box 1.15), >72h in any consecutive 7d, or have <8h rest between consecutive shifts. Contractual
breaches not meeting these criteria are reciprocated with time off or pay
for all work done. Complete an ‘exception report’ as soon as possible.
Exception reporting The way of informing trusts when work varies from
the agreed schedule (e.g. differences in hours, breaks, patterns, training,
or support). If patient safety is at risk, it must be raised orally at the time
to the responsible senior clinician, otherwise electronic forms distribute
the details and should be submitted within 14d (7d if claiming pay, 24h if
patient safety breach). Outcomes may be fines, extra income, time off, a
work schedule review, or system change.
Work schedule review To ensure that schedules remains fit for purpose.
Triggered in writing by doctors, supervisors, employers, exception reports, or the guardian of safe working hours. If dissatisfied, escalate to a
level 2 work schedule review and then a ‘formal grievance procedure’.
Guardian of safe working hours (GOSWH) ‘Independent’ champion of safe
working hours (but employed by the trust and approved by junior doctors). Responsible for escalating working hours problems to senior
management, distributing money from fines, and reviewing exception reports. Accountable to junior doctors and the executive board.
Junior doctors’ forum A forum for junior doctors to raise concerns and
decide on the allocation of fines (from fines, 1.5× basic pay goes to
the individual and 2.5× to training/​trainees). Made up of elected junior
doctor representatives, the GOSWH, the chair of the local negotiating
committee, and the director of postgraduate education.
Director of postgraduate education Responsible for training in the trust.
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wBeing a doctor
40
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Chapter 1
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w. torecords
w
in your self-​assessment
the Inland Revenue at the
end of each tax year.
w
w
w projects being undertaken ww
Research w
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tot a week-​long study and in most
circumstances the volunteerseare
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kXsickness
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can be internal or external. Internal
locums have
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w.Bat the hospital and arewworking
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their substantive post
w
from the NHS
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w staff bank. External locums w
base hospital (or do not have one), often on behalf of private locum agencies. There
locum agencies that
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n
n
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.
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ok rates, seems to have hadolittle
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15
cap to be broken has been widely used by many trusts, with several continuing to pay rates similar to or above those offered before the introduction of the cap. Rates of pay will vary and can still be negotiated, but an F1
can expect pre-​tax rates of £20–​30/​h, and F2s £25–​35/​h. The second
new measure is a clause in the 2016 junior doctors’ contract specifying
that those doctors planning to take locum work must initially offer their
services for the proposed shift time to their employing trust staff bank.
The trust must respond in a timely manner indicating if they require the
doctor’s services. The doctor is under no obligation to take any extra shifts
on, but would not be able to take an agency locum if the trust had offered
staff bank work at an appropriate level (not a lower grade). Importantly,
you should discuss locum shifts with your supervisor and include them in
your work schedule to ensure contractual limits on individual and average
weekly working hours (48h or 56h depending on if you’ve opted out of
the EWTD) are not exceeded.
Cremation certificates The cremation form has two parts
(E pp. 100–1). The first is completed by a ward doctor (usually the F1)
and the second by a senior doctor, often from another department. Under
arrangements prior to 2017, junior doctors were paid around £70 for completing the form; this fee is under review as part of ongoing reforms (E pp.
100–1). The bereavement office handles the forms and issues any cheques.
Make sure you see the body, checking identity and that there is no implantable
device that needs removing (E p. 100); they really do explode if incinerated.
Gifts The GMC is clear in its message that you should not encourage patients or their families to give, lend, or bequeath gifts to yourself, others,
or to organizations.16 If you are given a gift, then it is acceptable to take it
as long as it has negligible financial value. If you are given money, then pass
this to the ward sister to put into ward funds.
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Always check your payslips carefully, before storing them safely: make backups of electronic payslips and
never throw paper copies away. They can be a useful record of tax, pension, and loan payments long after
you have enjoyed spending the money. If you think a mistake has been made, contact the salaries and wages
division of the HR office for your trust, quoting your assignment number (employee number). In the event of
significant underpayment, you can request an interim payment be made pending the resolution.
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This is the total annual basic salary for your nodal pay point (‘1’ for FY1s, ‘2’ for FY2s). Latest updates are released as
‘Pay Circulars’ on the NHS Employers website Mwww.nhsemployers.org
This is the date when you are next due to go a point up the pay scale, usually 12 months of full time employment after your previous
date (or date of first starting working as a doctor). When changing trusts mistakes can be made so always check this date is correct.
Your tax code shows the amount of income you are entitled to earn in the current tax year that you do not pay any tax on. This
figure should be multiplied by 10 to give your total allowance. This will be the basic personal allowance for the tax year, as set by the
government, adjusted to take account of any under- or over-payments you may have made in previous years. Each tax year runs
from April to April. After your first tax year in paid employment, you will receive a P60 summarising your tax paid during that year
with the code that should apply to you in the next tax year. A copy should also be sent to your trust, but if you move trusts around
this time, the new trust may not receive the correct information unless you show them your copy of the P60. If your new trust does
not know the correct code for you, they will use an ‘emergency’ code, set as the basic personal allowance, which may or may not be
correct. The letter after the code should be an ‘L’ unless very specific circumstances apply to you. See also Mwww.hmrc.gov.uk
This will be approximately 1/12 of your basic annual salary.
This lists the pay you receive on top of your basic pay for additional hours over 40h, nights, and weekends. Details of how these
are calculated are provided in the pay circulars and related junior doctor contract information available from the NHS employers
website. Do check that the medical staffing department have provided correct details of your rota to the payroll team since early
evidence from the introduction of the new contract would suggest a number of instances of errors in this regard.
Under the ‘Pay as you earn’ scheme (PAYE), your trust will automatically deduct your tax from your income each month. Both
your basic pay and your pay for additional hours, nights, and weekends are taxable. In your first few months of employment,
you may not pay any tax until your income has risen above the personal allowance for that year. Enjoy this while it lasts!
National Insurance contributions pay for certain state benefits, including your state pension. These are not optional, and will be deducted
automatically, according to thresholds. The current rate is 12% of income over £157/week, though this is subject to annual review.
The NHS pension scheme remains a very good deal, although terms and conditions have been changed significantly
in recent years and are subject to further negotiations. Your pension contributions are not taxed and will also be
deducted automatically according to various earnings thresholds, unless you opt out of the scheme. Pension contributions are calculated from your basic pay (including any London weighting) - pay for additional hours, nights, and
weekends is not subject to any deductions. See also Mwww.nhsbsa.nhs.uk/nhs-pensions
Repayment for any student loan is taken automatically from your pre-tax earnings when your income reaches a certain threshold.
Although the landscape around tuition fees, repayment thresholds and interest rates is constantly changing, in 2017/2018 the
minimum contribution is 9% of earnings above the threshold. Specific thresholds and repayment timings then depend on when and
where you trained. If you trained in Scotland or Northern Ireland, or in England or Wales and started before 1st September 2012,
repayments start in the April of the first year after you graduate (the start of the financial year) and are taken from any pre-tax earnings
above an annual threshold of £17,775. In this case pay slips before April in the first year after you graduate may not contain loan deductions. If your course was in England or Wales but started on or after 1st September 2012, student loan contributions are taken as
soon as you graduate on any monthly pre-tax earnings over £1,750 (equivalent threshold of £21,000 per year). You can repay faster
if you wish. Keep a record of all payments you make and check them against annual statements. Errors are common when changing
trusts. Payments that appear to have gone missing can be credited to your account easily if you can provide a copy of your payslips.
See Mwww.studentloanrepayment.co.uk.
The numbers in this section will keep a tally of your total payments from that employer during the current tax year. If
you change trusts, the numbers will be reset, but your tax thresholds should not be.
Your NI letter reflects the contribution group you fall into. For almost all of those in the NHS pension scheme, this will be ‘A’.
Pensionable pay does not include any pay for additional hours, nights, and weekends.
Pay dates will vary between trusts but are generally around the last Thursday in the month. It can be difficult to get
paid on time at the start of employment with a new trust.
Trusts will transfer the money into your bank account by BACS transfer. These can take up to 3 working days.
Your taxable pay includes your basic pay (including London weighting) and pay for additional hours, nights, and weekends, less any pension contributions.
Don’t get too excited by this number…
…and try not to get too sad about this one…
... because this is what you’re going to have to spend until next month comes around.
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42
Chapter 1
Being a doctor
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ok level of medical graduate
okdebt has increased markedlyoinorecent
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On average, new FP trainees
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wloans.
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include maintenance
Financial manw
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w
w have therefore changed drastically.
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agement priorities
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comprehensive but aims to give some important pointers and warnings.
etclearance
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X types of debt:
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okdebts (eg credit cards ± overdraft,
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o
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full charge). Pay .these
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.B Try not to
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(2) Medium-​w
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et loans At very low ratesnofetinterest—​
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17
Think ‘total cost’ not just ‘monthly repayments’.
Some basic rules for financial planning
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Short
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X
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and you will bew
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taken care of,
to save for the deposit on a w
property (even if just £100/​mth). With interest rates currently low, home
t is an attractive option if you
t raise a deposit. Bear in mindnethatt
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Financial advice
ww
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wwhave a salary that increases w
Since you now
incrementally and is virtually w
guaranteed for life, finance companies will swarm round you like wasps
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no altruism here:
.
.
X independent financialkadvice
X is hard to obtain—​ask how
X
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.B for any
• Firms must noww
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Ercolani MG, et al. The lifetime cost to English students of borrowing to invest in a medical
degree: a gender comparison using data from the Office for National Statistics.
2015;5:e007335.
17
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etrevisit your retirement planning
etat regular intervals through.nyour
et
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Now that you are earning a salary you will be paying tax. Most will be
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• Professional subscriptions, eg GMC, BMA, MDU/​MPS, Royal College
•Examination fees and course fees (previously not deductible, but
HMRC has relented on this since 2012).
Tax reclaims may be made through full self-​assessment, but this is not
essential. If you pay tax through PAYE, simply send a letter to HM
Revenue and Customs, Pay As You Earn, PO Box 1970, Liverpool. L75
1WX, stating your name, NI number, and detailing your professional expenses as listed above. You must also include details of any additional,
undeclared income, including cremation forms. Your tax code for subsequent years will be adjusted accordingly.
Tax returns A tax return is an online form asking for details of all the money
you have received which may have tax owing on it. This includes your salary
and other income whether earned (eg locum shifts or cremation fees) or
unearned (eg lodger/​flatmate, bank interest, and dividend yields).
• If you are asked to complete one then obtain a Government Gateway
ID (Mwww.gov.uk) and password. This takes time, don’t leave it until
January
• Fill it in online and the maths is done automatically
• Return it before 31 January otherwise you will be fined £100 (if <3mth
late), or more if >3mth late (depends on how late, and how much is due)
• Claim your deductible allowances but also list your additional income.
The Inland Revenue has been known to ask an undertaker to list all payments to doctors and then cross-​check. If your tax is simple then tax returns
are not hard to do, otherwise pay a company/​accountant to do it for you.
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wBeing a doctor
44
ww
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Chapter 1
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w
w
w for any questions is your medical
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Foundation school. Always ask for copies of their written policies.
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them know. Ask for the rota position which is off for those dates
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Specialty training
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The ‘Shape of Training’ report marks the evolution of a number of
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‘Foundation for Excellence’) examining how we can best adapt training programmes to the changing needs of society. Published in 2013 by Professor
David Greenaway, it sets out a structure by which changes in patients
(e.g. multiple comorbidities, complex conditions, ageing populations) and
healthcare (rapidly shifting technologies and NHS restructuring) might be
matched by medical training, without destabilizing current training and service delivery. In brief, the report advocates training clinicians who are more
generalist, engaged, and adaptable to change. The 19 wide-​ranging recommendations include full GMC registration after medical school, broader
and longer training programmes after the FP (e.g. women’s health, child
health, mental health), transferrable competencies allowing easier transition between programmes, postgraduate opportunities to work in recognized related fields (similar specialties, management, education), and
subspecialty ‘credentialing’ (subspecialization only after ‘Completion of
Specialty Training’ as driven by patient and work-​force needs). Although
officially independent, questions of political interference were raised after a
Freedom of Information request uncovered minutes from a series of previously undisclosed meetings between representatives from the Department
of Health, the GMC, and Professor Greenaway. The recommendations
were accepted by the government. Organizations including the AoMRC
and GMC have ongoing workstreams mapping out the practical implications of the report. Early changes are expected in the next few years, with
longer-​term changes likely to take between 10 and 15 years.
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wBeing a doctor
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w
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or a ‘lead’ LETB using a web-​based application system. A small number of
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teria
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tration, rightw
to work in the UK, language skills,
w prior experience.
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offices taccording to a nationally agreedt timetable.
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wwa long list of supporting ww
this is not always
documentation, including your portfolio (E p. 8). Formats will vary between a traditional panel-​based interview (eg core training programmes) or
performing a number of exercises in front of assessors (eg GP).
Offers Are made electronically through the UK offers system according
to a coordinated timetable. You will be asked to rank all LETBs where
you would accept a job; successful applicants are then allocated to LETBs
in score order (you will be allocated to your highest preference that still
has places when your turn comes). You then have 48h to review offers
and decide whether to accept, hold, or reject. You may also elect to receive automatic ‘upgrades’ if a higher ranking choice becomes available.
Re-​advertisement To unfilled posts will take place in a 2nd application
round. If you accept a job in round 1, you may still apply for a different
post in round 2, but you need to inform all those concerned.
Employment checks And contract signing—​remarkably NHS employers
claim to need up to 2 months after you start work to get around to
issuing a contract and some manage to miss even this. Speak to your
BMA representative in the event of contract problems.
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48
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Chapter 1
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are 21 different training
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w
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w
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w
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t specialties other than those
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Specialty training options
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.ne 1.3 Specialty training programmes
.ne at CT1/​ST1 (2018) X.ne
X
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Recruitment
ok Specialty
ok contact details ook
o
Bo Run-​through specialties
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w.NIHR Trainees CoordinatingwCentre
w.BMnihr.ac.uk
ACFs
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w Health Education WessexwMwessexdeanery.nhs.uk
ww
Cardiothoracic
surgery
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wMheeoe.hee.nhs.uk/​
reproductive health
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t and the Humber net
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et
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medicine
org.uk
ACCS—​anaesthetics Health Education West Mids Manro.wm.hee.nhs.uk
ACCS—​emergency
London recruitment Mhttp://​www.lpmde.ac.uk/​
medicine
Anaesthetics
Health Education West Mids Manro.wm.hee.nhs.uk
Core medical training Royal College of Physicians Mwww.ct1recruitment.
org.uk
Core surgical training London recruitment Mhttp://​www.lpmde.ac.uk/​
Core psychiatry
Health Education North West Mnwpgmd.nhs.uk/​
training
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wBeing a doctor
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Chapter 1
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wBeing a doctor
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Chapter 1
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Choosing
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which specific jobs to. do. There are also jobs outside.of specialty training
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Priorities Before looking for a job, write a list of factors that matter to
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.
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Location Could you move?
far would you commute?
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different post, providing you notify all those concerned. Outside of this formal
process, it is unacceptable to turn down a post you have already accepted unless you have an extremely good reason. The GMC take a clear position on
your obligation to protect patient care by not compromising the recruitment
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wSpecialties in medicine 53ww
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merous specialties shown
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20
Acute internal medicine
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Anaesthesia
• Paediatric anaesthesia
• Obstetric anaesthesia
• Pain management
Audiovestibular medicine
Aviation and space medicine
Cardiology
Cardiothoracic surgery
• Congenital cardiac surgery
Chemical pathology
• Metabolic medicine
Child and adolescent psychiatry
Clinical genetics
Clinical neurophysiology
Clinical oncology
Clinical pharmacology and therapeutics
Clinical radiology
• Interventional radiology
Community sexual health and
reproductive medicine
Dermatology
Diagnostic neuropathology
Emergency medicine (EM)
• Paediatric emergency medicine
• Pre-​hospital emergency medicine
Endocrinology and diabetes mellitus
Forensic psychiatry
Gastroenterology
• Hepatology
General internal medicine
General practice
General psychiatry
• Liaison psychiatry
• Rehabilitation psychiatry
• Substance misuse psychiatry
General surgery
• Breast surgery
• Colorectal surgery
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Genito-​urinary medicine
Geriatric medicine
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For more details on the career options available to doctors, including all of the above, see
Want To Be A Brain Surgeon? (Eccles S et al.), Oxford University Press, 2009.
20
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Paediatrics
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• Neonatal medicine
• Paediatric oncology
Palliative medicine
Pharmaceutical medicine
Plastic surgery
Psychiatry of learning disability
Public health medicine
Rehabilitation medicine
Renal medicine
Respiratory medicine
Rheumatology
Sport and exercise medicine
Trauma and orthopaedic surgery
• Hand surgery
• Spinal surgery
Tropical medicine
Urology
Vascular surgery
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54
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Chapter 1
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Chapter 1
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w.B0121231 (full)
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Personal statement
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McBurney City Hospital
F1 to Dr Mallory, Gastroenterology
McBurney City Hospital
F1 to Dr Haler, Respiratory Medicine
McBurney City Hospital
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I have organized several climbing
to Scotland
wI.B
w.Btrips
and one to the w
Alps.
am interested in medical w
journalism
and have spent
wJournal of Thrombophlebitis. ww
a week in thew
editorial office of the International
Publications
etCJ. Letter: Student debt. Students’
et Journal 2016;35(2):101 .net
• Flint
n
n
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ww
ww
ww
References
Dr Ian Haler, Educational Supervisor, Department of Respiratory Medicine,
McBurney’s Medical Centre, McBurney’s Point, McBurney, McB1 7TS Tel
0111 924 9924 ext 2370. ian.haler@mcburney.ac.uk
t
t
t
.ne
.ne
.ne
X
X
X
k
ok
oportfolio
ok
o
o
Bo Box 1.19 Thewpaper
B
B
.
w. evidence of your w
Most interviews require a folder containing physical
w
w
achievements.
w Use the following structurewas a guide to gather evi- w
dence long before interviews. Sections should be subdivided for ease
of navigation.
t
t
net print on high quality paper.
Curriculum
the.back,
.ne vitae At the front or X
.ne
X
X
form For interviewers
to refer back to.
k
ok Copy of application
ok
oPhD,
o
o
and qualifications
Diplomas, PGCerts, BSc, MSc,BMD,
etc.
Bo Degrees
B
.
. postgraduate.
Prizes, awards, andw
grants Local/​national, undergraduate/​
w
Oral and poster
presentations Local, regional, national,
ww
ww or international.
ww
Books, abstracts, and other publications First/​last author or co-​author.
Teaching experience Small group, lectures, or courses (with feedback).
Clinical audit and quality improvement Results, reports, and presentations.
Commitment to specialty Skills, membership exams, experience, etc.
Courses and conferences attended Local, national, or international.
References, testimonials, and feedback Feedback/​
testimonials from patients and colleagues can show reflective practice and professionalism.
Research projects Give a summary, your exact role, and any reports.
Logbook of practical procedures Including supervised and unsupervised.
Work-​place based assessments Notable DOPS, CBDs, and CEX forms.
Management and leadership Trainee representation, committees, etc.
Reflective practice To demonstrate that you learn through reflection.
Achievements outside medicine Shows that you are well-​rounded.
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58
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Chapter 1
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Being a doctor
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.
.
the interview itself;
them as much notice
wtry toforgiveinformation
w as possible. Look at
wwebsite
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the recruitment
about
the format, questions, and ww
w
w
what to bring; try to talk to previous applicants and arrange mocks.
Interview
at the interview
plenty of time, allow for tall
t with
eoft delaysdayonArrive
eeven
e
sorts
the roads or train,
if this means you have to
read
n
n
.
.
.ncandiX
X
X
the
newspaper
for
an
hour.
Relax
and
be
yourself
with
the
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k
ok before you are calledooin;kmost of them will have similar
ooqualifications
Bo dates
B
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and experience as yourself
and will be just as nervous.
Dress smartly in a
.
.
w or skirt). You will
simple suit andw
tiew
for men and suit for women w
(trouser
w specific instructions as to what
w documentation to bring, ww
normally receive
which you should follow exactly; as a minimum, bring a copy of your CV
(E pp.t54–5) and a summary printout from
ePortfolio (E p. 8). t
einterview Relax. The worst.nethatt canyour
n
.
.nenot
The
happen is that you are
X
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k of the world. The formatoofk interviews
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o 2–​3 end
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are usually
interviewers; introduceB
yourself
Bo varies,
B
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the panel and wait w
to be offered a seat. For some posts
there
w will be a series
of panels, each with
ww a different brief (eg CV verification,
ww clinical scenarios, per- ww
Bo
B
Interview preparation Employers must allow you time off to attend
sonal skills), and you will rotate between panels. Take a few moments to think
about the questions before answering and ask for a question to be rephrased
if you don’t understand it. Always make good eye contact with all members of
the panel and be aware of your own body language.
Common questions It is impossible to predict the questions you
will be asked, but they are likely to include questions about your portfolio, relevant clinical scenarios, and current medical news/​issues. Many
questions have no correct answer and will test your communication skills,
common sense, and ability to think under pressure:
• Talk us through your portfolio; what are you most proud of in it?
• What is missing from your portfolio?
• What qualities can you offer our training programme?
• Why have you chosen a career in . . .?
• What do you understand by ‘clinical governance’?
• Tell us about your audit. Why is audit important?
• If you were the Secretary for Health, where would your priorities lie?
• How would you manage . . . [specific clinical scenario]?
• Where do you see yourself in 5, 10 years’ time?
• If you were the CT1 in the hospital alone at night and you were
struggling with a clinical problem, what would you do?
• Tell us about your teaching experiences. What makes a good teacher?
Clinical scenarios Interviewers should not ask you specific medical questions (eg ‘What is the dose of . . .’); they can pose scenarios to discuss your
management of a situation. These often focus on key issues such as communication, prioritization, calling for senior help when appropriate, multidisciplinary
teams, and clinical safety. For some specialties, a few formal OSCE-​style stations may be included—​you should be told about this in advance.
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Membership exams
59w
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Membership
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k you will need to complete
ok progress beyond the oSToyears
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are difficult and w
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w E p. 43). Most membership
w exams take place 2–​3 ww
tax deductible
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past, e
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B Medicine Regionalwexamination
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.Band overseas; all
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et clinical skills, £657, <7yr.since
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w Part A, and 4 attempts to pass
wpart B: are permitted 6 ww
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• Part A MCQ (Basic sciences and Principles of Surgery in General), £513,
eligible from graduation
• Part B OSCE £930, eligible after part A.
To apply for an ST3 position in surgery you need to have completed the
entire MRCS.
General practice You need to be a GP registrar to take the MRCGP
exams. There are 3 parts and no time limits though the GP registrar post is
a year long; 10% fee reductions apply to associate RCGP members:
• AKT (written exam) £501
• CSA (clinical skills) OSCE stations, £1325
• ePortfolio similar to the FP portfolio. Access costs £611, but is free
among other benefits for RCGP members (£163 registration, plus
£369 annual cost).
You need to complete the MRCGP to become a GP.
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Other membership exams in the Foundation years
Emergency medicine (MRCEM) Three-​part exam (two written and one
clinical) required to apply for ST4. Part A may be sat as early as F1, but
all parts must be passed within 7 years of passing Part A.
Anaesthetics (FRCA) Full primary (MCQ and OSCE) exam only open to
anaesthetic trainees, though F1 and F2 doctors can attempt MCQ component. Applications to ST3 are only permitted when all parts of the
primary FRCA are passed.
Obstetrics and Gynaecology (MRCOG) Part 1 (written) eligible after graduation; part 2 (written + OSCE) within 7 years of passing part 1.
Pathology MRCPath normally completed during ST.
Paediatrics (MRCPCH) 3 written papers (attempted in any order after graduation); clinical exam after 12mth paeds experience and passing all written.
Radiology (FRCR) Can only be attempted after gaining training post.
Psychiatry (MRCPsych) Different requirements for part A (GMC registration), part B (psychiatry training), and the practical (24mth experience).
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(3) Compare data to standards (87% of cannulas replaced in 72h)
(4) Change practice (present data to colleagues and propose new
approaches, eg date of placement written on cannula dressings)
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(6) Reaudit (repeat data collection after 3mth—​has anything changed?).
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B
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conclusions and indicate where further research may be directed. Thank
the appropriate parties and invite questions/​
discussion. See audit/
​research section E p. 61, p. 66.
Journal club Begin with a brief explanation of why you have chosen to discuss
the particular clinical topic and list the articles which you have appraised. Aim
to include why the study was undertaken, the appropriateness of the study,
the methods and statistics used, the validity of the study, and make comparisons between different studies. Include latest guidelines and invite discussion
regarding how the research may affect current clinical practice. Finish with
a summary of the studies undertaken, their results, and where they were
published for future reference (see Box 1.20).
Case presentation The presentation should tell a story about a patient
and let the audience try and work out the diagnosis as though they are
clerking the patient for the first time. Name the talk something cryptic,
eg ‘Headache in the traveller’. Refer to your patient by initials only and
make sure patient details are blanked on all images and test results.
Present the history and physical examination. Invite audience suggestions
for the diagnosis and management. Give the results of investigations and
again invite the audience to comment. Give the diagnosis and discuss
subsequent management. Summarize with an outline of the topic and
management; end with a question/​discussion session.
Teaching session It is helpful to base a topic around a patient if this is appropriate. Keep the session interactive; have question slides where the audience
can discuss answers. Summarize with learning points; it is helpful to provide
a handout of your slides for people to take away (E p. 65).
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The medical team 68
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none of these remain, but you will still hear the term.
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to a SpR but not working towards a CCT award.
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need to secure an ST3/​4 post afterwards.
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patients. Their presence on the ward varies between specialties.
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Medical students Medical students are present in most hospitals and
should be allowed and encouraged to be part of the medical team.
Medicine is both a science and a vocation, and although studying for
exams is important, many of the clinical and non-​clinical skills needed to
succeed as a doctor are not written in textbooks and can only be learned
in a supervised way either on the wards or in the clinic.
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Life on the wards
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t
t stressed people who nareetin
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.B physiotherDischarge coordinators
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apists, and occupational
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help in finding social and intermediate care placements (E Box 2.1 p. 73).
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o
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w
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nulation), and assist in theatre. Most cannot prescribe, although there are
some who are qualified to use the nurses’ formulary (E p. 70).
Specialist nurses These include stoma, respiratory, pain, cardiac, diabetes, tissue viability, and Macmillan nurses. They are excellent for giving
advice and are an important first port of call for the junior doctor.
Occupational therapists These work with patients to restore,
­develop, or maintain practical skills such as personal care. Assess patients’
homes for changes required to help with activities. Many elderly patients
require OT assessment before discharge—​nurses usually make the referral. OTs work in primary and secondary care (E Box 2.1 p. 73).
Pharmacists These dispense drugs and advise you on medication. They
check the accuracy of every prescription that is written. Some hospitals
have a medicines information ​line which you can call for prescribing advice.
Phlebotomists These are professional vampires who appear on the
wards with the sole aim of taking blood. They often appear at unpredictable times and may not come at all at weekends, so leave blood forms out
early. Some can take blood from central lines and perform blood cultures.
If asked nicely they may accept requests mid phleb-​round.
Physiotherapists These use physical exercises and manipulation to treat
injuries and relieve pain. Chest physios are commonly found on respiratory
and surgical wards to help improve respiratory function and sputum expectoration by teaching specific breathing exercises. Involve them early in patient
management—​nurses usually make the referral, but do not hesitate to discuss
your patient’s needs or progress directly with them (E Box 2.1 p. 73).
Social workers These support patients’ needs in the community. They
assess patients and help organize care packages (invaluable for elderly
­patients). Where residential care is required, they help guide the family and
patient through the decision-​making process and financial issues. They are
also involved in child protection and vulnerable adult safeguarding work.
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for you (E p. 87)! ... ‘Just for my learning, what is the reason for...?’
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readily accepted and queries can be discussed directly
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educational opportunities like this are good for your career planning as well.
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Box 2.1 Discharge planning
This is a multidisciplinary process that should start on admission and continue
throughout. Medical, discharge planning, and therapy teams complete social
needs assessments, asking 4 key questions: (i) what support is there? (ii) Now
they have become unwell, do they need more? (iii) Is there potential to improve? (iv) Where would they prefer to go? We aim to give patients both
safety and independence. Options include (i) social care (from home adaptations, mobility aids and home carers to residential homes and nursing homes),
(ii) intermediate care for those with potential to improve (home re-​ablement,
rehabilitation, or community hospitals), and (iii) community healthcare (district
nurses, nursing agencies, and community therapy). It is a complex process due
to variations in personal preferences, family situations, local services, national
structures, and funding streams, but take the time to learn the local process.
Your contribution to this important multidisciplinary conversation can be critical and failure to engage will inevitably lead to discharge delays.
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t how urgently they neednseeing,
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needs doing, a half-​full box is part done, and a full box is a job done)
• Visit all the areas you cover in order and tell the wards this is what
you’ll be doing; ask them to compile a list of non-​urgent tasks for when
you arrive
• When you order a test on-​call, make a note to check the result as it’s
easy to forget.
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w
w
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a constant supply of work that can usually wait. Breaks are not just about
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keep you alert and reducetstress and tension headaches.tIt
t patients’
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interests that you
n
ne
.
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Few doctors look forward to their night shifts, especially if they are doing
several in a row. Don’t underestimate how tired you feel during and
after a run of nights. That said, on nights you will gain a lot of experience.
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Things to take with you
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.
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t number
et isofnow
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n
.
.nduty
at night. Some hospitals use mobile
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(eg lumbar punctures). They can then call you to observe or be supervised.
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shift; getting up early the morning before can help with this
• Go to bed for at least 7h each day, even if you don’t sleep you’ll rest
• Make your room dark and quiet—​eye masks/​earplugs help; ensure
anyone else in the house knows you are working nights
•Eat plenty and have regular meals, even if you don’t feel like it
• Travel home safely. If you feel too tired to travel home safely, trusts
are obliged to provide a place to rest or transport to take you home.
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The potential to make mistakes during night shifts is greater than during
the day. If you are unsure, double check. The following are some of the
common problem areas:
• Poor handover; ensure you know who needs review (E p. 22)
• Failing to appreciate a sick patient and not calling for help
• Fluid prescriptions (eg failing to note renal/​heart failure, DM,
electrolyte imbalance)
• Warfarin prescriptions with INRs coming back out of hours.
• Check you’ve got the right patient when documenting/​seeing results.
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76
.B
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Chapter 2
Life on the wards
.B
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t
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everyone, irrespective
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wThe
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et
ethave the date and time. It is.nuseful
et
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Each entry should
n
n
.
.
to
have
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patient
and
Xyour surname and bleep number
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Chapter 2
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Life on the wards
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on the local system as part of induction. They form a point of reference at
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t provide clinical coding informaet
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the patient is likely to be discharged. This allows the drugs to be dispensed
from pharmacy as soon as possible so that the patient’s discharge is not
delayed. See Fig. 2.5.
• Begin to enter information on the TTO at the earliest opportunity; check
any queries with your team, particularly regarding the principal diagnosis
• Check the duration of the medication for discharge (eg ABx) and stop
any unnecessary drugs (eg prophylactic low-​molecular-​weight heparin)
• Check drug doses and frequencies with the BNF, your seniors, a
pharmacist, or by calling your hospital’s drug information-​line
• Check required follow-​up appointments, give details, and be clear on
who will arrange them (eg the ward clerk or the clinic administrators)
• Phone the GP if the patient needs an early check-​up, has a poor social
situation, or self-​discharges. It may take several days for a TTO to reach
the GP: written instructions such as ‘check K+ in 3/​7’ are unsafe
•Hand the TTO and the patient’s drug chart to the patient’s nurse or
inform them that you have completed it to avoid unnecessary bleeps
• If you are unsure whether the TTO has been done check the drug chart;
there is often a tick in a box showing if TTOs have been dispensed
• Discuss the diagnosis, results, and discharge plan with your patient; if
they understand the management plan they are more likely to comply.
Controlled drugs for TTOs These are slightly more complex, but
can still be written by F1 doctors in most trusts. They must include all the
information in Table 2.2. CD prescriptions are only valid for 28d from the
date of signing and only 30d of CDs can be dispensed on a single prescription. See also Fig. 2.6 and Box 2.3.
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o Morphine, diamorphine,oopethidine, fentanyl, alfentanil,ooremifentanil,
o
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Box 2.3 Examples of controlled drugs
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wDISCHARGE SUMMARIES 81ww
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82
Chapter 2
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Life on the wards
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. Med 3) will usually fall to you.
of Fitness for Work, Form
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w
w sick pay and social securitywpayments. You can advise that ww
and enables statutory
a patient is ‘not fit for work’ or ‘may be fit for work’ under restricted conditions.
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et form (Form Med 10) maynbe
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and date the form. You need to give an appropriate amount of time for the
patient to recover from their illness as reasonably anticipated at the time of
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M https://​www.gov.uk/​government/​uploads/​system/​uploads/​attachment_​data/​
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under the Open Government Licence v3.0.
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Referring a patient to another medical team can be one of the most
difficult parts of the job. The other doctor is often very busy and will
inevitably know more about the patient’s condition than you (hence
the referral). At times it can feel like they are trying to make you feel
stupid—​this is rarely the case. Consider this from the point of view of
the other doctor: They need to establish:
•How unwell the patient is
•How urgently they need to be seen
• What investigations have already been done and what still need to be
done to assist them in their review
• If they are the right person to see the patient.
You will often be asked to refer a patient by your senior. Ask them directly:
• To help my referral and for my learning, why do they need referring?
• What do they want the other team to do (advise over the phone,
formal review, take over care, see in clinic, procedure/​operation)?
•How urgent is the referral?
Next, think about what information the other doctor will want. Many specialties have additional components to history and examination that you will
need to be able to describe, see the pages in the history and examination
chapter (Box 2.4); if necessary, go and see/​examine the patient yourself:
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et 2.4 Additional components
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X
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ok Breast surgery E p. 143 Haematology
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o
Neurology
Renal.B
E p. 387
Bo Cardiology E pp. 130–1
B
. Obstetrics EE pp.pp. 134–8
w
w
Dermatology E pp. 140–1
160–1 Respiratory
w Oncology E p. 142wwRheumatology EE pp.p. 132148–54 ww
w
Endocrine
E p. 139
ENT
Ophthalmology E pp. 144–5 Urology
E p. 146
E pp. 156–7
t
t
Gastroet
Orthopaedics E
E p. 133
pp. 148–54 Vascular
E pp. 130–1
e
.n E pp. 158–9 PaediatricsX.nE pp. 166–7 surgery
.ne
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w
w
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t relevant specialist, introduce
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X-​rays These exploit the different absorbance of a pulse of X-​ray radiation
by different anatomical structures and foreign bodies. This allows the visualization and distinction of metal, bone, soft tissue, fat, fluid, and air.
Fluoroscopy This uses X-​ray images acquired in real time, often with addition of a contrast material, eg coronary angiogram or barium swallow.
CT This uses a series of 2D X-​ray images acquired in different planes to
construct cross-​sectional 3D images. IV or PO contrast can be used to
accentuate, eg blood vessels or the GI tract.
MRI This uses strong magnetic fields to align hydrogen nuclei (protons)
within tissues. Disturbance of the axis of these protons by radiowaves
allows the recording of radiowaves emitted as the protons return to
baseline. MRI offers excellent soft tissue imaging and does not require
ionizing radiation exposure. Image acquisition can be slow and require
multiple different ‘sequences’ while the patient lies in a cramped space.
Ultrasound This exploits the differential reflection of high-​frequency sound
waves to visualize structures, including soft tissues in real time. Overlying air
and fat compromise signal quality, and bone penetration is poor.
Nuclear medicine This depends upon the detection of radiation emitted
by the decay of radiolabels attached to substances with affinity for certain body tissues. Positron emission tomography (PET) is a specific form of
nuclear medicine that typically uses radiolabelled glucose analogues to
detect regions of metabolic activity, eg in cancer. These techniques are
especially powerful when combined with anatomical imaging approaches
such as CT/​MRI to increase localization (eg PET/​CT or PET/​MRI).
Requesting Selecting, performing, interpreting, and managing medical imaging resources falls to the specialty of radiology. These doctors often have
little direct contact with your patient and depend upon effective communication from you to select and prioritize imaging modalities (including appropriate
use of contrast agents and imaging sequences), as well as inform their image
interpretation; always include specific clinical questions on request forms.
Radiologists have a vital duty to limit unnecessary exposure to ionizing radiation. Doses involved can range from minimal (eg CXR: <1% annual background radiation exposure) to substantial (eg contrast CT C/​A/​P: 710yr
background radiation). Even a trivial radiation exposure will be associated
with an appreciable cancer risk to a population if performed often enough.3
Always ensure you know why any investigation you are asked to request
is needed, how urgent it is, and how it will change the patient’s management. For less urgent investigations or simple X-​rays, it is usually enough
to submit a request giving sufficient clinical information. For more urgent
or specialist imaging, request the scan or fill in the form, then phone or go
to the radiology department, and speak to the duty radiologist. Be polite,
explain why the test has been requested (and by whom), and ask if there
is any way it could be performed today if necessary. If this fails and the test
is very urgent, your registrar should discuss with the radiologist directly.
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general principle must be to keep exposure As Low As Reasonably Possible (ALARP).
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2 Worrying features diHR, diBP, diRR, dGCS, sweating,
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abdominal pain (E pp. 295–303), back pain (E pp. 360–1), limb pain
(E p. 462), infection (E pp. 496–505). Common Postoperative, musculoskeletal, chronic pain.
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• Paracetamol 1g/​4h, max 4g/​24h PO/​PR/​IV.
NSAIDS Good for inflammatory pain, renal or biliary colic, and bone pain;
Contraindications (BARS) Bleeding (pre-​op, coagulopathy), Asthma, Renal disease,
Stomach (peptic ulcer or gastritis). 10% of asthmatics are NSAID-​sensitive, try a
low dose if they have never used them before. Avoid use in the elderly. Increased
risk of CVA/​MI; Side effects Worsen renal function, GI bleeding (upper and
lower—​co-​prescribe a PPI or high-​dose H2-​blocker for those at risk: ≥65yrs,
­previous peptic ulcer, use of other medicines with GI side effects, or major
comorbidity). Both NSAIDs and COX-​2 inhibitors are associated with increased
risk of MI and CVA; use with caution in those at risk.
• Ibuprofen 400mg/​6h, max 2.4g/​24h PO, weaker anti-​inflammatory
action, but less risk of GI ulceration
• Diclofenac 50mg/​8h, max 150mg/​24h PO/​PR (also IM/​IV, see BNF).
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Ward round Assess daily the effectiveness of analgesia (whether pain
hinders activity (coughing, getting out of bed etc)) and about side effects
(drowsiness, nausea, vomiting, and constipation).
Ask about (SOCRATES) Site, Onset, Character, Radiation, Alleviating
factors, Timing (duration, frequency), Exacerbating factors, Severity, associated features (sweating, nausea, vomiting). PMH Stomach problems (acid
reflux, ulcers), asthma, cardiac problems; DH Allergies, tolerance of NSAIDs,
analgesia already taken and perceived benefit; SH ?Drug abuse.
Obs iHR and iBP suggests pain; RR, pupil size and GCS if on opioids.
Look for Source/​cause of pain, masses, tenderness, guarding.
Investigations These should be guided by your history and examination;
none are specifically required for pain.
Treatment No patient should be left in severe pain, consider titrating
an IV opioid after an antiemetic (E pp. 310–11). Use the steps of the
WHO pain ladder (Table 2.3). Ensure regular analgesia is prescribed, with
adequate PRN analgesia for breakthrough pain. If a patient has moderate
or severe pain start at step 3 or 4; using paracetamol and NSAIDs reduces
opioid requirement and consequently side effects.
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better to prescribe the components separately in hospital:
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PO, nurses must give 8/​500 dose if 30/​500 not specified
• Co-​dydramol 10mg dihydrocodeine and 500mg paracetamol; two
tablets/​6h PO
• Co-​proxamol Contained dextropropoxyphene and has been withdrawn
owing to its potential toxicity and poor analgesic properties. Some
patients may still be taking this, but it is not prescribed to new patients.
Strong opioids Morphine is used for severe pain. Use regular fast-​acting opioids for acute pain with regular laxatives and PRN or regular antiemetics.
See ‘weak opioids’ for cautions, side effects, and toxicity. Use only one
method of administration (ie PO, SC, IM, or IV) to avoid overdose:
• Oral eg Sevredol® or Oramorph® 10mg/​2–​4h
• SC/​IM Morphine 10mg/​2–​4h or diamorphine 5mg/​2–​4h
• IV titrate to pain; dilute 10mg morphine into 10mL H2O for injections
(1mg/​mL), give 2mg initially and wait 2min for response. Give 1mg/​2min
until pain settled observing RR and responsiveness.
Long-​acting opioids These are used after major surgery or in chronic
pain. Use standard opioids initially until morphine requirements known
(E p. 95) then prescribe a regular long-​acting dose along with PRN fast-​
acting opioids to cover breakthrough pain (equivalent to 15% or one-​
sixth of daily requirements). Laxatives will be needed.
• Oral MST® dose = half total daily oral morphine requirement
(E p. 95) given every 12h, usually 10–​30mg/​12h, max 400mg/​24h
• Topical Fentanyl patch lasts 72h, available in 12–​100micrograms/​h doses.
Naloxone This given orally antagonizes the constipating effects of opioids,
but is metabolized on ‘first pass’ through the liver and does not interfere
with analgesic effects. Compound preparations oxycodone/​naloxone
preparations (eg Targinact®) may be of benefit for chronic pain relief in
those who develop painful constipation despite regular laxatives.
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t
Other
adjuncts
.ne analgesic options/​X
.ne
.ne
X
X
opioid analgesia
be given with paracetamol,
ok Nefopam Aandnon-​
ok that canEpilepsy
ok Side
o
o
opioids; Contraindications
and convulsions;
Bo NSAIDs,
B
B
­effects Urinary retention,
w. pink urine, dry mouth,wlight-​
w. headedness.
• Nefopam 30–​w
90mg/​8h PO.
w
w
ww
Hyoscine butylbromide This gives good analgesia in colicky abdo pain;
Contraindications Paralytic ileus, prostatism, glaucoma, myasthenia gravis,
et Side effects Constipation,.ndryetmouth, confusion, urine retention.
et
porphyria;
n
n
.
.
•
Buscopan
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6
h
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I
M/​
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X
kX relaxant, eg spasm withokback
ok Diazepam This acts as oa omuscle
pain;
o
o
B
B
Contraindications Respiratory
compromise/​failure, sleep.B
apnoea. Side effects
.
Drowsiness, confusion,
(use
ww physical dependencew
wforwshort-​term only). ww
• Diazepamw
2mg/​8h PO.
Quinine This is used for nocturnal leg cramps; Contraindications Haemoglobinuria, optic
neuritis, arrhythmias; Side effects
et 200mg/​
et Abdo pain, tinnitus, confusion.
et
n
n
n
.
.
• .Quinine
24h PO—​at night.
X
X
kXa bolus
ok Patient-​controlled analgesiao(PCA)
ok This is a syringe driver that
ogives
o
o
of
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opioid
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morphine,
but
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tramadol
B
B or fentanyl)
.B
.infusion
w
when the patient w
activates a button. A background
rate, bolus
w to prevent
dose, and maximum
over- ww
ww bolus frequency can bewadjusted
B
®
dose/​pain; changes to the PCA are usually undertaken by the pain team
(see Box 2.6). The patient must be alert, cooperative, have IV access,
and their pain under control before starting. Check hospital protocols.
Epidurals These are inserted by the anaesthetist in theatre usually prior
to surgery. A local anaesthetic infusion (± opioid) anaesthetizes the
spinal nerves, and usually produces a sensory level below which the patient has little or no feeling; if this level rises too high (higher than T4
(nipples)) there is risk of respiratory failure. The anaesthetist or pain
team (see Box 2.6) usually look after epidurals and their dosing post-​op.
Complications include local haematoma, abscess (causes cord compression, E p. 361), or local infection; if there are concerns about an epidural speak to the anaesthetist covering acute pain immediately.
Syringe driver These are used mainly for palliative analgesia and symptom
control (E p. 95).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
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X
k
t
ok
o
o
w.B
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
et
n
.
X
Most hospitals have pain teams, often subdivided into acute and
chronic services. These comprise nurses and a pain specialist (usually an anaesthetist). The acute pain service is sometimes run by the
Outreach Team.
In-​patients with pain issues can be referred to the teams for assessment, though ensure all simple measures have been undertaken to
address the patient’s pain first, namely identify and treat cause of
pain, and ensure the patient is receiving adequate simple analgesia
(regular paracetamol, NSAIDs (if not contraindicated), and an opioid,
if appropriate).
et
n
.
kX
o
Bo
oo
B
.
w
.n
kX
ww
t
e
X.n
ww
et
.ne
X
k
K Box 2.6 Pain team
ok
Bo
w
t
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Pain
91w
t
t
t
Neuropathic
and chronic pain
.ne
.ne
.ne
X
X
X
pain is caused bykdamage to or chronic stimulation
ok Neuropathic
o
ok of nerve
o
eg radiculopathy o
(nerve root pain), peripheral neuropathy,
and
Bo fibres,
B
B
. pain tends to be difficult towdescribe
.
phantom limb pain.
The
or pinpoint
w
and is often aching,
throbbing, or shooting
in nature. Chronic
w
wwcauseburning,
ww pancreatitis,
conditions can
significant pain, eg chronic
arthritis, w
post-​traumatic, DM, trigeminal neuralgia; there is frequently a psychot
genic e
component.
Standard analgesia e
istoften ineffective and the services
et
n
.
of .anchronic pain specialist should.n
be sought. See Box 2.7. Commoner
X pain therapies include:kX
X
ok chronic
o at a low dose; Contraindications
okrecent MI,
o
o
o
Tricyclic
antidepressants
Given
B arrhythmias; Side w
.B
.B
effects Dry mouth, constipation,wsedation. This is the
w
w
first-​line treatment
w for neuropathic pain according
w to NICE guidance. ww
• Amitriptyline 10–​75mg/​24h PO.
Pregabalin
Hypersensitivity,
lactation; Side
t Contraindications
t Canpregnancy,
eDizziness,
esigns.
et
­effects
tiredness, cerebellar
be used instead of
amin
n
n
.
.
.
Xtriptyline as first-​line treatmentkXfor neuropathic pain.
X
ok • Pregabalin 75–​300mg/​1o2hoPO.
ok
o
o
B Duloxetine Contraindications
Uncontrolled hypertension,
.Bpregnancy, seizw.B dizziness,
wmouth.
ures; Side effectsw
Nausea,
somnolence,
dry
First line for
w
w neuropathy. Avoid abrupt discontinuation.
w
ww
painful diabetic
4
• Duloxetine 60–​120mg/​24h PO.
If first-​line drugs are unsuccessful, combination therapy with two or
more agents can be considered. If this is unsuccessful then referral for a
specialist opinion should be considered. The following are examples of
more advanced therapies a pain specialist may prescribe.
TENS Transcutaneous Electrical Nerve Stimulation is believed to affect
the gate mechanism of pain fibres in the spine and/​or to stimulate the
production of endorphins. Use at a high frequency for acute pain or slow
frequency for chronic/​neuropathic pain.
Steroids and nerve blocks Injections of steroids combined with local anaesthetic into joints or around nerves can reduce pain for long periods. This
needs to be done by a specialist.
Sympathectomy and nerve ablation The ablation of sensory and sympathetic nerves by surgery or injection; used as a last resort in some forms
of chronic pain.
Acupuncture Effective in some trials and with a greater evidence base than
most complementary therapies.
Counselling and cognitive behavioural therapy (CBT) to develop coping strategies
are widely studied in chronic pain and may be considered by appropriately skilled
specialists. Concern remains that it makes things worse for some patients.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
o
w.B
ok
o
o
w.B
t
ok
o
w.B
e
X.n
ok
ww
o
w.B
ww
ww
Allodynia
Seemingly harmless stimuli such as light touch can provoke pain
Hyperpathia A short episode of discomfort causes prolonged, severe pain
Hyperalgesia Discomfort which would otherwise be mild is felt as severe pain
t
t
e
X.n
ok
4
e
X.n
ok
ww
o
B
.
w
ww
t
e
X.n
Box 2.7 Some terms in chronic pain
Bo
.n
kX
ww
t
e
X.n
ww
et
.n
kX
ww
Bo
.n
kX
o
w.B
ww
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et
.n
kX
t
e
X.n
ok
ww
o
B
.
w
NICE guidelines available at Mguidance.nice.org.uk/​CG173
ww
B
92
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne
.ne
.ne
Thinking
about
death
X
X
X
k delay it.
ok Death is inevitable and
okeven the best medicine canooonly
o
Bo KPatients
B
B
often die in .hospital and as a trainee you will. have a vital role in
wand relatives through it. Aswwith
w
supporting patients
in mediw
ww knowledge,
w everything
cine this requires
skills, and compassion,
and getting it right w
can be challenging but rewarding. The following should help guide you.
t of dying, however be naware
etIt is natural for patients to.benescared
et
Fears
n
.
.
that
many
are
not
and
are
entirely
at
ease
with
the
idea.
If
they
are
afraid,
X to find out why. It may bekX
X
the loss of dignity/​control, o
theksymptoms
ok try
o
o
o
o
(suffocation or pain),.B
their relatives seeing them suffering,
B
.B or the unpleasant death of w
a loved one. Many of these canw
now be carefully manw
w
aged or avoided.
w When death is not expectedwor deterioration is sudden, ww
then your role in talking to the patient and allaying their fears cannot be
overstated.
This will be emotionally difficult
etsupport
et and you must never hesitate
et
to seek
yourself.
n
n
n
.
.
.
X
X
X
bad news E p.k24.
ok Breaking
o Even with sudden deteriorations
ok there are
o
o
o
Other
sources
of
help
B
many other sources
wof.Bhelp:
w.B
w
w
• Macmillanw
nurses and the palliative care team
w (E p. 93)
ww
B
• The acute pain team (usually part of anaesthetics)
• The chaplaincy.
Do not forget you’re working with nursing staff who may know the patient much better than you, so discuss their care with them.
Sorting arrangements Needless to say, marching in and offering a priest
and solicitor will be insensitive, but the hospital will be able to provide legal
support or an appropriate religious official if asked. Many patients’ strongest
wish is to die in comfort, often in their own home. Get the Macmillan and/​or
palliative care team involved early as this can frequently be arranged.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
et
nenot
netat
Do
resuscitate orders.n
Towards the end of life, attempts
.
.
X
X
X
can be more harm
than good; however, the decisions
k are
ok ­resuscitationaround
oforms
okinitiated and
DNAR
complex and shouldobe
at a
o
Bo discussions
B
B
. level. Patients must now bewinvolved
. in discussions
registrar or consultant
w
unless it may lead
w to ‘psychological harm towthe
w patient’ (see Box 2.8). ww
Nursing staffw
must always be informed.
K Box
et 2.8 Tracey v Cambridge
etUniversity Hospitals 2014
et
n
n
n
.
.
.
decisions
XThis case helped clarify the law on when to not discuss DNARkX
ok with patients. Janet TraceyoohadkXterminal cancer with a prognosis
o of 9mth
o
o
and was admitted to.B
ITU with a cervical spine injury.B
after a road traffic
B
w despite a desire to w
accident. After extubation,
be w
involved in her care, a
w
DNAR wasw
placed without consulting her orw
her family. The DNAR was ww
then removed, however the judge ruled that the DNAR was in breach of
UK and
law (Convention ontHuman Rights, Article 8, ‘right to
et European
e DNARs can be distressing .tonepa-t
a.private
life’) because while discussing
n
n
.
Xtients, unless doctors feel thatk‘the
X distress might cause physicalkorXpsychook logical harm’ the risks of otheodiscussion
obenefits (eg
are outweighed byo
the
o
B
B
to autonomy, dignity,.B
and their right to a private life and
second opinion).
.
w
w
ww
ww
ww
B
.B
w
ww
.B
w
w
w
w
Palliative care
93w
t
t
t
.ne
.ne
.ne
Palliative
care
X
X
X
k
k fook
ooriginally
care is the non-​
co
urative treatment of a disease;
o
o
Bo Palliative
B
B
. but now covers other w
.
cused on terminal cancer,
disorders.
In practice,
cancer patientsw
arew
still able to access more services,
including the excelw
w nurses who should be involved
w as early as possible. The ww
lent Macmillan
aim is to provide the best quality of life for as long as possible—​this may
include
t
etadmission to a hospice (often
etemporarily).
et
n
n
n
.
.
.
Pain
(E
pp.
88–91)
This
is
a
common
problem
in
palliative
care;
opioids
X
X
X
ok are often used. It is important
okto use all modalities of treatment.
okConsider:
o
o
o
(urinary retention, bowel spasm,
bony mets)
B • Treating the source
w.B(nerve blocks, TENS, neuropathic
w.B pain)
• Non-​opioid analgesia
w
w
• Alternative
wroutes (intranasal, PR, transdermal,
w SC, IM, IV).
ww
Table 2.5 is a guide to converting between opioids, it is not an exact scit changes need to be monitored
ence e
and
et for over-​or under-​dosing..net
n
n
.
.
X 2.5 Opioids and theirkpotency
X relative to PO morphine kX
ok Table
oTypical dose
o
o
o
Opioid
Route
24h max Bo Relative
B
B
.
.
0.1
w
Codeine
PO
60mg/​4h
240mgw
w
0.1
Dihydrocodeine
30mg/​4–​6h
wwPO
w240mg
ww
B
Tramadol
Oral morphine
Oxycodone
Morphine
Diamorphine
Fentanyl
.
kX
o
o
net
PO
PO
PO
SC/​IM/​IV
SC
Topical
50mg/​4h
10mg/​1–​4h
5mg/​4–​6h
5mg/​1–​4h
2.5mg/​1–​4h
25micrograms/​h
oo
B
.
w
ww
t
.ne
kX
600mg
N/​A
400mg
N/​A
N/​A
2400micrograms
oo
B
.
ww
w
0.2
1
2
2
3
100–​150
t
.ne
X
k
Other symptoms Many of the treatments listed in Table 2.6 can be
ww
t
t
et information on prescribing
used
For.n
further
.nein non-​palliative patients. X
.nein
palliative problems see E BNF and
OHCM10 p. 532.
X
X
ok
ok
ok
o
o
Bo Table 2.6 Symptom
B
B
care .
w. management in palliative w
w
w
Symptom wwTreatments
w
w
Breathlessness
O , open windows, fans, diamorphine, benzodiazepines,
steroids, helium and oxygen
t
t (for stridor), SC furosemidenet
e
e
Constipation
E
pp.
316–17,
also
bisacodyl
n
n
.
X. simple/​codeine linctus,kmorphine
X.
Saline nebs, antihistamines,
kXCough
k
o
o
o
ice or pineapple chunks,
Bo Dry mouth Chlorhexidine,
.Bo(thrush)sucking
.Bo consider
Candida
infection, synthetic w
saliva
w
w
Hiccups
eg Maalox , Gavisconw
, chlorpromazine,
haloperidol
wwAntacids,
ww
Itching
Emollients, chlorphenamine, cetirizine, colestyramine
jaundice), ondansetron
t
et vomiting (obstructive
et
Nausea/​
E pp. 310–11, also
levomepromazine
and haloperidol.ne
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
2
®
®
B
.B
w
w
.B
w
w
wLife on the wards
94
ww
w
Chapter 2
t
t
t
.ne dying patientX.ne
.ne
The
X
X
ok patients who have reached
ok the final stage of their illness
okand are not
o
o
Bo For
B
B
expected to survive,. the decision may be taken by.a senior doctor to
w
wthe patient comfort- w
withdraw active
and focus on keeping
wtreatment
wwemotive
able. Thesew
decisions and discussions are highly
and should be w
handled with consideration and skill (E p. 92). Much emphasis has been
placed
better deaths foreallt dying patients (see Box 2.9). et
eton achieving
n
n will often (but not always)Xbe.nbed-​
.
Identifying
the dying The patient
Xbound with minimal oral intakekand
X.reduced
GCS. This simpleodefinition
k
k has
o
oo for recovery, while timescales
o can be difficult
specificity, with potential
Bo poor
B
B
.
.
to predict. Since considerable
uncertainty will always
effective and
wpersist,
ww is vital, along with regular
wreview
honest communication
of treatment deciw
w
ww
sions by the senior responsible clinician.
Communication Wherever possible, discussions should happen with
t
et and their relatives well.nineadvance;
et
thenpatient
all views should be n
docu.
.
mented
and
used
to
draw
up
a
care
plan.
Even
where
an
illness
progresses
X the withdrawal of active
X treatment needs to be carefully
kX conok rapidly,
okto discuss
owithdrawal
o
o
o
sidered
and
every
effort
made
with
the
relatives;
of
B
.B
.B
care by junior staffw
during out-​of-​hours periods should
be avoided.
w
w
Stopping w
medications Administering drugs
wwmay cause unnecessary ww
5
distress, particularly those aimed at prophylaxis of long-​term conditions.
Review all medications with a senior and stop those deemed to be unnecessary. The decision to stop antibiotics can be a particularly difficult one,
but again, this is made easier by well-​documented prior conversations.
et
et
.n
kX
o
Bo
o
o
w.B
o
o
w.B
ww
During our lives, the care we receive focuses on increasing both the quality
and quantity of life, and with advances in modern medicine the options
available for both are vast. However, as we approach death, life-​prolonging
treatments start to fail, therapies pursuing quantity of life become futile and
therefore harmful, and the care we receive rightly focuses on quality of life
instead. At these crucial junctures in life, the support we offer must be complete, flexible, and holistic, focusing on each patient’s individual physical, psychological, familial, spiritual, and social needs. In recent years, many reports
have identified serious misgivings with the way this process is managed in the
UK. A 2015 report from the Health Service Ombudsman found inadequacies in the recognition of dying patients, effective symptom control, communication, out-​of-​hours cover, and advanced care planning.6 Therefore, in 2016
the government committed to a series of ambitious and far-​reaching independent recommendations striving for ‘excellence in palliative care for every
dying person’.7 These include improving care quality (eg sharing best practice, investing in research, and MDTs), personalizing care (eg individualized
care plans, personal budgets, care coordinators, and named consultants),
better education (eg improved workforce training and community resilience
programmes), and more accountability (eg CQC inspections, and quality
standard frameworks). A 2017 review found good progress but expect to
see significant changes in the provision of palliative care until at least 20218.
et
et
.n
kX
o
o
o
w.B
ok
Bo
o
o
w.B
t
ok
o
w.B
5
6
7
8
e
X.n
ok
o
w.B
ww
t
t
e
X.n
e
X.n
ok
o
B
.
w
Mhttps://​www.nice.org.uk/​guidance/​ng31
Mhttps://​www.ombudsman.org.uk/​publications/​dying-​without-​dignity-​0
Mhttps://​www.gov.uk/​government/​publications/​choice-​in-​end-​of-​life-​care-​government-​response
Mhttps://www.gov.uk/government/uploads/system/uploads/attachment_data/file/645631/
Government_response_choice_in_end_of_life_care.pdf
ww
ww
t
e
X.n
ok
o
B
.
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ww
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e
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ww
ok
.n
kX
ww
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e
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et
.n
kX
ww
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kX
K Box 2.9 Current changes in end of life care
ww
Bo
et
.n
kX
ww
ww
B
.B
w
ww
.B
w
w
w
w
The dying patient
95w
t
t
t
Resuscitation
Attempts at cardiopulmonary
resuscitation in patients
.ne
.ne
.ne
X
X
X
stage disease are inappropriate
(see Box 2.9). Although
k
ok with end-​
oresponsible,
ok thein derests with the senior
patients must beoinvolved
the
o
Bo cision
B
B
. feel it would cause them
.‘physical or psychoconversation unless clinicians
w
w
logical harm’ tow
w discuss it (E p. 92 and Box 2.8wp.w90).
ww
Investigations These may be unnecessary. This includes routine blood
tests, where the outcome will not influence clinical management, but will
et to the taking of nursing .observations
et in the final stages of .illness.
et
alsonextend
n
n
.
X and fluid A loss of appetite
X terminal stages of diseasekisXcommon
ok Food
oknotinbetheforced.
o fluids should
and at this stage nutrition should
The intake of o
oral
o
o
B be supported as longwas.B
tolerated, even if this incurs a risk .ofBaspiration. Beyond
wonly where it increases w
this stage, artificial
(IV or SC) should be used
wwhydration
wwBear
comfort, although
regular mouth care may continue.
in mind that studies w
have shown no clear benefit to length or quality of life in a palliative setting.
t and overuse of syringe drivers
et Not all dying patients are.ninepain,
et
Analgesia
n
n
.
.
is
inappropriate.
However,
where
present,
it
is
vital
to
control
pain
while
X oversedation (E p. 93).kX
X
Always exclude a treatable cause,
ok avoiding
opatient
ok eg urinary
o
o
o
retention,
constipation.
If
the
is
currently
in
pain
give
an
immediate
B morphine bolus (2.5–​
.B
.Bon diamorphinedia-or
5mg SC max 1hrly if not currently
w
w
give 1/​6th ofw
24hw
dose 1hrly if already on diamorphine).
ww Where pain is regular ww
9
and predictable, discuss starting a syringe driver with a SC diamorphine infusion giving a total 24h dose equivalent to current cumulative opioid requirements (use Table 2.5 (E p. 93) to convert between opioids).
t
t
t
.ne
.ne
.ne
X
X
X
This may be a sign
ok Agitation
okof pain. Try PRN doses initially;
okadd a syro
driver (with additional
PRN dose) if regular doses areorequired:
Bo inge
B
B
PRN Levomepromazine
w. 12.5–​25mg SC 6–​12hrly,worw.
w
PRN Midazolam
2.5–​
w 5mg/​4h SC max 4hrly w
ww
Syringe driver Levomepromazine 50–​150mg/​24h and/​or midazolam 10–​
20mg/​2t4h SC (higher doses up to 60mg/​
24h may be required).
t
e and vomiting Continue
etexisting
n
n
Nausea
antiemetics in a syringe
.
.
.ne
X
X
X
are controllingkthe symptoms; if there is no nausea
then
ok driver if they
oadd a syringe driver if it is needed
okregularly.
PRN cyclizine and
o
o
Bo prescribe
B
B
. required use a 5HT antagonist
. (eg ondansetron).If
further antiemeticsw
are
w
PRN Cyclizine 50mg/​
ww 8h SC
ww
ww
Syringe driver Levomepromazine 5–​12.5mg/​24h SC.
Secretions
patient’s breathing may
t Thewith
t become rattly due to the nbuild-​
esecretions
eupt
up.of
a poor cough/​
se
wallow reflex. Sitting the patient
n
n
.
.
promptly.
Xslightly may help; medication improves
X the symptoms if startedkX
ok Start with a PRN dose andoadd
oka syringe driver if regular doses
oare required:
o
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B PRN Glycopyrronium
200–​400micrograms SC 6hrly
wSC.B6hrly.
w.B or hyoscine w
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w
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Syringe driver Glycopyrronium 1.2–​2mg/​24h SC or hyoscine butylbromide
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et
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oo Database
.BCochrane
Further care Review the patient regularly. Ask the patient and/​or rela-
o
Bo
tives if there are any new symptoms and adjust medications accordingly. If
you are unable to control symptoms, ask for a palliative care review.
9
o
o
B
.
w
ww
Good P, et al. Medically assisted hydration to assist palliative care patients.
Syst Rev 2014;4:CD006273 . Mwww.cochrane.org/​CD006273/​SYMPT_​medically-​assisted-​
hydration-​to-​assist-​palliative-​care-​patients
w
ww
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.B
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96
Chapter 2
ww
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Life on the wards
t
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Death
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o
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oo
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You will often be w
to declare that a patient has
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w
until it is done. There may be other members of staff who can do this if
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et it for the first time, ask another
et
fortable
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kXColleges has guidance onothekXdiagnosis
ok The Academy of MedicalooRoyal
o
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w
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wwmay have specific guidelineswwhich
1. Confirming cardiorespiratory arrest
You should
the patient for a minimum
of five minutes to confirm
et observe
et occurred:
et
irreversible
cardiorespiratory arrest
has
n
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.
.
.
X•Listen for heart sounds in two
Xplaces, for one minute in each
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ok (total two minutes), then
ok
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o
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.Bartery
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•Listen for breath
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w
w
(total twow
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w
ww
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Declaring death
10
It is common to hear transmitted gastrointestinal sounds when auscultating
the chest, which should be ignored. However, in a very recently deceased
patient it is also not uncommon for a lone complex to appear on the ECG,
or for them to take a ‘last’ (agonal) breath. This or any other spontaneous
return of cardiac or respiratory activity during your period of observation
should prompt a further five-​minute observation from the next point of
cardiorespiratory arrest, unless the patient is for active resuscitation.
t
.ne
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2. Confirming the absence of motor response
o
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t
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t
et
After five minutes of continued cardiorespiratory arrest confirm the absence of motor response in the patient:
• Absence of the pupillary response to light; the pupils will often be
dilated and they should not change when exposed to a bright light
source (eg pen torch)
• Absence of the corneal reflex; passing rolled up cotton wool over the
edge of the cornea should not elicit a blinking response
• Absence of any motor response to supra-​orbital pressure; applying
firm supra-​orbital pressure should not elicit any motor response.
o
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X3. Documentation kX
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ok The time of death is recorded
o as the time at which theseocriteria
ok are fulo
o
B
filled (Fig. 2.9). Remember
w.B to sign and print yourwname
w.Band bleep number. w
w
w
w
w
et
et
et
n
n
n
.
.
.
X
X
X
ok
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ok
o
o
o
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w.B
w.B
w
w
w
w
ww
Academy of Medical Royal Colleges ‘A Code of Practice for the Diagnosis and Confirmation of
Death’, 2010. Mhttp://​www.aomrc.org.uk/​publications/​reports-​guidance/​ukdec-​reports-​and-​
guidance/​code-​practice-​diagnosis-​confirmation-​death/​
10
B
.B
w
ww
t
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X
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o
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.
.
X happens to the patient
X after death?
X
ok What
ok prepare
okclosing the
When a patient dies the o
nurses
the body, including:
o
o
B curtains, lying the w
body
.Bflat with one pillow, closingwthe
.Beyes and closing
the jaw (this may
need to be propped closed with
a rolled towel under the
w
w
w
wthe body, using pads to absorb w
chin), washing
any leakage from the urethra, w
vagina, or rectum, and removing attachments (eg fluids, pumps). Lines
and tubes
will
t are not removed since these
t be inspected if a post-​mortem
net
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patient
.ne is undertaken. The X
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k
k
have been declared
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ok Oncearetheytaken
oo dead
oo prepared,
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in a portable coffin. .Curtains
and portBo they
B
able partitions arew
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ww around death ww
ww
Communication
On occasion, it will be your duty to inform others of the death of a
t This will produce strongneemotions,
t
lovedeone.
even when the news
etis
.n and calls for skilful and
. sensitive communication (EX.p.n24).
expected,
X
X
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acok Ensure youyouarewherever
ok to know
ok toin the
o
o
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the identity of everyone
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B
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. the notes beroom, and that the
w.environment is appropriate.
wStudy
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w
w
w
w
ww
Fig. 2.9 Example of what to write in the notes when a patient dies.
11
to the death—​if you are still unsure of details, be honest and offer to
check. Ask if they would like to see the body at that time, and be clear
that there will be later opportunities too. The most important element
is to give those receiving the news time—​both silence and emotion are
completely acceptable and to be expected and should not be talked
over or hurried. You will not be able to remove sorrow, but your empathy and professionalism may just help to soften a painful memory that
will be mentally revisited many times in the coming months and years.
t
e
X.n
ok
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.ne
X
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t
ok
o
o
w.B
ww
et
n
.
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ww
o
w.B
Always remember to inform the GP of the patient’s death, especially if
it was unexpected. This is both courteous and prevents any unfortunate
phone calls from the GP enquiring about the patient’s health.
Bo
o
et
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.
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o
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Henry C, Wilson J. Personal care at the end of life and after death.
8 May 2012,
available free online at: Mwww.nursingtimes.net/​Journals/​2012/​05/​08/​h/​i/​z/​120805-​Innov-​
endoflife.pdf
11
ww
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B
.B
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98
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
Medical
.ne Certificate of Cause
.nofe Death
.ne
X
X
X
in the United Kingdom
k registrar’s
ok K All deaths
ok must be registered withoa olocal
In order for this toohappen, a doctor may issue a ‘medical
certificate
Bo office.
B
B
. confusingly often referred
.to as a ‘death
of cause of death’ w
(MCCD),
certifiw
cate’. Alternatively,
where the cause of death isw
not clear or there are any
w
wrequiring clarification, the coroner’s
w office must be informed ww
circumstances
(E p. 102). In Scotland, different legislation applies and a slightly different
MCCD
etis used and the procurator fiscal
ettakes the coroner’s role. .net
n
n
.
.
Eligibility
In
hospital,
it
is
ultimately
the
responsibilityX
to ensure
X but consultant’s
kXthe MCCD is properly completed
k
it can be delegated tooakmember of
o
o
othe patient in the last 14d of life
o in Northern
team who ‘attended’
(28d
Bo the
.toBthose
.Bcare
Ireland). This applies
involved in the patient’s
and who reliw
w
w and course of in-​patientwstay.
w Where circumstances
ably know the
history
w
ww
­require involvement of the coroner’s office/​procurator fiscal (E p. 102),
do not complete the MCCD unless they instruct you to do so.
et the MCCD Most of the.entries
et are self-​explanatory: .net
Completing
n
n
.
X• Name of deceased: full namekXof the deceased
X
ok • Date of death as statedotoome:
ok
eg fifteenth day of Augusto2016
o
B
• Age as stated to me:.B
92 years
.B
w eghospital,
wdied
• Place of death:
ward,
and city where w
they
w
• Last seen w
alive by me: eg fourteenth day ofw
August 2016
ww
B
Then circle just one of these (most commonly option ‘3’):
1. The certified cause of death takes account of information obtained from
post-​mortem.
2. Information from post-​mortem may be available later.
3. Post-​mortem not being held.
4. I have reported this death to the Coroner for further action.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
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.Bo
As part of the reforms to death certification that are being proposed, the new role of Medical
Examiner (Medical Reviewer in Scotland) will provide an additional source of advice (E p. 102).
12
ww
ok
o
o
w.B
ww
et
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.
kX
o
.ne
X
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w
Then circle just one of these (most commonly option ‘a’):
a. Seen after death by me.
b. Seen after death by another medical practitioner but not by me.
c. Not seen after death by a medical practitioner.
Cause of death This can be difficult: it is important to take advice from the consultant
the patient was under.12 It is important to think of this as a sequence of events
leading up to the death of the patient. The pathology listed in I(a) is whatever ultimately resulted in the patient dying (eg intraventricular haemorrhage, myocardial
infarction, meningococcal septicaemia); avoid using modes of death (Table 2.7) as
this may lead to delays later in the process. The I(b) and I(c) entries should be the
pathology/​sequence of events which led up to I(a). Include pathology in II which
likely contributed to death but might not have necessarily been part of the main
sequence of events leading up to the death. It is not compulsory to have entries in
I(b), I(c) or II and these can be left blank. Avoid abbreviations.
Approximate interval between onset and death This gives the sequence of
events a time frame.
An example
I(a) Pulmonary embolism
6 hours
(b) Fractured femur
7 days
(c) Osteoporosis
30 years
II Ischaemic heart disease
30 years
t
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X
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ok
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ww
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.B
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w
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Death
99w
t
t
et
The.n
death might have been due to or contributed
.ne to by the employmentXfollowed
.ne
X
X
by the deceased Ifkyou think the death was in any k
related
ok at some time
oindustrial disease you should refer
oway
employment or an
the case to
o
o
Bo tothetheir
B
B
coroner/​procurator
for their consideration..
w.Thisfiscal
w
wwand medical qualifica- ww
Signing the certificate
requires
your signature
w
w
tions, alongside which your local office will usually ask you to print your
name and often your GMC number. For Residence it is acceptable to
t For deaths in hospital: younalso
ethet name of the hospital and.the
ecity.
et
enter
n
n
.
.
need
to
enter
the
name
of
the
patient’s
consultant
at
the
time
of
death.
X
X
kXside of
ok Completing the sides Makeosure
okyou complete the stubs onooeither
o
B the main form, copying
exactly your entries off the main
wIf.Byou
w.B form.
w
Completing the back
have spoken to thew
coroner’s or procurator
w for you to complete ww
fiscal’s office,w
and they have decided it is appropriate
the MCCD, they may ask you to circle one of the options and initial in
t the reverse of the MCCD.net
box Aeon
et
n
n
.
.
.
Post-​
m
ortem
There
are
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types
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post-​
m
ortem
(PM):
those
mandated
X
X
X
ok by the coroner or procurator
okfiscal, and those undertakenoafter
ok a medical
o
o
B request (a ‘hospitalwPM’).
.B
w.B
The coroner’s PMw(Procurator fiscal in Scotland.)wUndertaken to find out
wdied and to inform the decision
w on whether an inquest is ww
how someone
B
needed or not. The next of kin is informed, but not asked for permission, as the law requires a PM to be performed.
A hospital PM This is usually undertaken at a doctor’s request to provide
more information about an illness or the cause of death. Consent must
be given by the patient before they died, or by the next of kin after their
death. The hospital bereavement office can assist with this should you be
asked to gain consent.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
ww
Table 2.7 Causes and modes of death
w
oo
B
.
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t
.ne
X
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ww
t
t
t
Causes
of death
.ne of death (use these terms)
.ne Modes
.ne
X
X
X
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these
terms)
k
ok
oarrhythmia
ok
infarction, cardiac
Cardiac arrest, syncope
o
o
Bo Myocardial
B
B
.
Sepsis, hypovolaemia,
Hypotension,
whaemorrhage,
w.shock, off legs
anaphylaxis
w
w
w
w
ww
Congestive cardiac failure, pulmonary
Heart failure, cardiac failure,
oedema
failure
t
t ventricular
e
e
et
Bronchopneumonia,
pulmonary embolism,
Respiratory failure,
n
n
n
.
.
.
asthma,
chronic
obstructive
pulmonary
respiratory
arrest
X
kX
kX
ok disease
o
o
o
o
o
Cerebrovascular accident
Collapse
B
.B failure, uraemia
w.B diabetic Liver failure,
wrenal
Cirrhosis, glomerulonephritis,
w
w
nephropathyw
w
ww
Carcinomatosis, carcinoma of the . . .
Cachexia, exhaustion
t
t
e
e
et
n
n
n
.
.
.
X
X
X
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ok
ok
o
o
o
B
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w.B
w
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w
w
ww
B
.B
w
w
.B
w
w
wLife on the wards
100
ww
w
Chapter 2
t
t
t
Cremation
forms
.ne
.ne
.ne
X
X
X
individual crematoria
k or regions may have slightly
k different
ok Statute While
othey
oand
o
o
cremation forms,
all follow a similar pattern
very
Bo looking
B
B
.
.cremation ask
similar questions.wGuidance
on how to complete
forms is
w
freely availablew
online, though the bereavement
w office will also be able ww
to guide youw
and answer your questions. w
Cremation form nomenclature The main form to be completed for adult cret
mation
Ireland)—​see ‘Completing
etis ‘Cremation 4’ (Form B .inneNorthern
et
n
n
.
.
Cremation
4’
E
p.
101.
The
senior
doctor
(who
must
be
fully
registered
kX>5 years) who checks and overifies
kX the details in Cremation 4osubsequently
kX for
o
o cremation
‘Cremation.B
5’ o
(Form C in Northern Ireland).
Bo completes
.BOther
forms are availablew
for stillbirths, and for the cremation
of body parts.
w
w in hospital, it is expectedwthat
w the person completing ww
Eligibility Forw
deaths
Cremation 4 treated the deceased during their last illness and to have
seen the
deceased within 14 days of death.
Medical practitioners cometCremation
et to practise
et
pleting
4 must hold a licence
with the GMC,.n
which
n
n
.
.
Xincludes temporary or provisional
X registration.
X
ok Examining the body If youooarek completing a cremation oform
ok you were
o
B
Bpatient’s identity
previously required .to
the body to check the
w B see
w.them
(wrist band and
physical
appearance) and examine
to see if they
w
w
w which may cause a problem
w during cremation (see ww
have any implant
13
14
Box 2.10). Under the proposed reforms, this responsibility will transfer
to the Medical Examiners. If you are required to view the body, check
the notes, ECGs, and X-​rays for possible implants, but also examine the
patient for scars or palpable implants (pacemakers are usually, but not
always, on the anterior chest wall). If you believe there is an implant, talk
to the mortuary staff who will be able to remove it.
Remuneration Under prior arrangements junior doctors were paid around
£70 for completing the form (E p. 40); this fee is under review as part
of the new reforms. Any fee comes from the patient’s relatives via the
funeral director who keeps the money if you fail to take it. The reason
you are paid is because this is not a standard NHS service and you are
taking responsibility for the fact the body will not be able to be exhumed
for evidence if there is any doubt in the future as to the cause of death.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
.n
kX
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kX
et
.n
kX
o
o
w.B
.n
kX
o
o
w.B
ww
ww
ww
Box 2.10 Problematic implants for the cremation
of human remains
t
t
e
X.n
ok
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e
X.n
ok
ok
o
w.B
ww
ww
t
ok
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e
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e
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• Pacemakers; implantable cardioverter defibrillators; cardiac
resynchronization therapy devices; implantable loop recorder
• Ventricular assist devices
• Implantable drug pumps including intrathecal pumps
• Neurostimulators and bone growth stimulators
•Hydrocephalus programmable shunts
• Any other battery-​powered implant
• Fixion nails (intramedullary nails for fixing long bone fractures)
• Brachytherapy implants
o
w.B
e
X.n
ok
o
B
.
w
ww
t
e
X.n
ok
o
B
.
w
In Scotland, the information previously contained on the cremation form will be included on the
revised MCCD. Arrangements in the rest of the UK are under review.
14
Eg For England and Wales: Mwww.justice.gov.uk/​downloads/​burials-​and-​coroners/​cremations/​
cremation-​doctors-​guidance.pdf
13
ww
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ww
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.B
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w
w
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Death
w
101
t
t
et
.ne
.ne
Completing
Cremation X
4 .n
X
X
k explanatory:
ok
oself-​
ok
of the questions are
o
o
Bo Most
B
B
• Details of the deceased:
name,
address,
occupation
.
wdeath,
w.
• Date and time
of
place of death
w
w
• Are you aw
relative of the deceased?
w
ww
• Have you, so far as you are aware, any pecuniary interest in the death
of the
deceased?
et you
et practitioner? Generally it .isnthe
et
n
n
• .Were
the deceased’s usual medical
.
X
Xas the usual medical practitioner
GP who is regarded
kXlast
ok • patient’s
oyouk attended
otheir
Please state for how long
the deceased during
o
o
o
B
illness? eg 5 days .B
wthe.Bdeceased’s death w
• Please state w
thew
number of days and hours before
w
w saw them alive? eg 1 day, 12 hours
w
w
that you last
• Please state the date and time that you saw the body of the deceased
and
that you made of
tthe body? eg date, time, external
etthe examination
echeck
et
n
n
n
examination
to confirm identify.and
for implantable devices
.
.
X your medical notes, andkX
X
the observations of yourself andkothers
ok • From
oplease
immediately before andoatothe time of the deceased’s death,
o
o
B
B and other conditions whichw
Byour conclusions
describe the symptoms
led.to
wof .death.
about the cause
Outline the symptoms
in the period leading
w
w
ww
up to thew
patient’s death; include the datew
of admission to hospital
B
• Has a post-​mortem examination been made? Usually the answer to
this is no, but if it has, tick yes and give details
• Please give the cause of death. Copy what appears on the MCCD
• Did the deceased undergo any operation in the year before their death?
If yes, give brief details
• Do you have any reasons to believe that the operation(s) shortened the
life of the deceased? If yes, the case should be discussed with your
seniors/​Medical Examiner/​coroner’s office/​procurator fiscal
• Please give the name and address of any person who nursed the deceased
during their last illness. Usually enter the name of the sister responsible
for the ward where the patient died, eg Sister Jayne Smith, Ward 26
• Were there any persons present at the moment of death? If yes, give
details, as above
• If there were persons present at the moment of death, did those persons
have any concerns regarding the cause of death? If yes, give details
• In view of your knowledge of the deceased’s habits and constitution
do you have any doubts whether about the character of the disease or
condition which led to the death? Yes or no
• Have you any reason to suspect the death of the deceased was: violent
(yes or no) or unnatural (yes or no)?
• Have you any reason at all to suppose a further examination of the
body is desirable? If yes, give details
• Has the coroner been informed about the death? If yes, give details
• Has there been any discussion with a coroner’s office about the death
of the deceased? If yes, give details
• Have you given the certificate required for the registration of death? If
no, give the details of who has completed the MCCD
• Was any hazardous implant placed in the body? See Box 2.10.
• If yes, has it been removed? Yes or no
• Sign, date, and enter your contact details.
t
.ne
X
k
oo
et
oo
B
.
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.n
kX
oo
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.
ww
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o
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et
n
.
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et
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.
X
ww
t
o
o
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.
w
ww
ww
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ok
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w.B
t
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X
k
w
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X
ok
.Bo
ww
B
.B
w
ww
102
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
Death
coroner
.ne certification, registrars,
.neexaminers, and the X
.ne
X
X
in registering a death
k If a medical practitioner ocompletes
k the
ok Steps involved
onext
o
o
this is given to the
of kin, usually by the bereavement
office;
Bo MCCD,
B
B
.complete a MCCD, the coroner
. sends the relevant
if the doctor cannot
w
w
paperwork directly
w to the registrar after establishing
w a cause of death to the w
best of his/​w
her satisfaction, through a post-​w
mortem and/​or investigation w
and/​or inquest. Only once the registrar has the relevant paperwork can the
t entered into the register andneatdeath certificate issued to thennext
deathebe
et
n
.
.
of.kin,
permitting a burial or cremation
to take place.
X Certification Reforms Inkresponse
X to the Shipman InquirykX
more
ok Death
o
o
o
oo AllandMCCDs
recently the Francis Inquiry,
a new system is being introduced.
B
B
B
.
.
will be scrutinizedw
by a Medical Examiner, who will
wbe able to make cer- w
wcase
tain changesw
tow
the MCCD after examiningw
the
notes or talking to w
staff involved in the patients care and to the individual who initially completed tthe MCCD, if the cause of deatht is inaccurate. Junior doctors may
eto their local Medical Examiner
ebefore completing the MCCD
efort
speak
n
n
n
.
.
.
guidance.
Any
case
which
would
normally
have
been
referred
to
the
corX
X
kXcoroner, but if not accepted
ok oner will still be referredotoothe
okby the coro
o
oner will then be subsequently
scrutinized by the Medical
Examiner. The
B
w.BExaminer system is to:wensure
w.Bmore accurate re- w
purpose of the Medical
w
porting of disease
w processes; to better identify
w unusual patterns of death w
B
which may have public health or local clinical governance implications; to
ensure the individual completing the MCCD understands the cause of
death; and to provide an opportunity to raise other matters which might
require the death to be reported to the coroner.
Medical Examiner These are medical practitioners from any speciality
background who are licensed to practise by the GMC and with at least
5 years’ experience. As well as scrutinizing MCCD and guiding doctors
to complete these, they will also discuss the cause of death with the
family and act on any additional information the family provides. They
will work closely with the coroner’s service and registrations services,
and feed information back to clinical governance structures to aid in future healthcare planning and provision.
The Coroner The coroner15 is a government official and is usually a lawyer
but may have joint degrees in law and medicine; their job is to investigate
a death when the cause of death is unknown or cannot readily be certified as being due to natural causes (see E ‘A death should be referred
to HM Coroner if:’ p. 103).
The Coroner’s Office This is staffed by Coroner’s Officers. They are not
usually medically or legally qualified and are often serving, or ex-​police
officers. They take the majority of enquiries, and will filter which cases
are escalated to the coroner.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
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t
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X
k
o
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X
k
oo
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.
w
.n
kX
t
ww
et
n
.
X
ww
o
w.B
The term ‘coroner’ as used here applies to the coronial service in use in England and Wales and
Northern Ireland, as well as the role of the Procurator Fiscal in Scotland. Although these are all
covered by different legislation, the same basic roles and rules apply. Likewise the new role of
‘Medical Examiner’ in England and Wales is equivalent to ‘Medical Reviewer’ in Scotland.
15
Bo
o
et
n
.
kX
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
ok
o
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et
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e
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ok
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w
t
o
w.B
t
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k
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Death
w
103
t
et
nethet
Making
Any.ncase which meets the criteria.in
.ne a referral to the coroner X
X
X
be referred to the
coroner’s office for their consideration;
ok box should
okcoroner’s
okit is approdiscussing the case,othe
officer may suggest
o
Bo after
B
B
priate for the referring
w. doctor to complete the MCCD.
w. Occasionally the w
coroner’s officer
will either take over the case,w
or wish to discuss it dirw
wcoroner first, and in these situations
w the MCCD should not w
ectly with the
be completed by the referring doctor unless instructed to do so.
et or not to refer? If you are.inneanyt doubt about whether to.nrefer
et
To .refer,
n
Xto the coroner or not, speak first to your seniors, or the local
XMedical
ok Examiner for advice. ookX
ok
o
o
B
.B
wbe
w.Bif:
A death should
referred to HM Coroner
w
w
w
w
ww
• the cause of death is unknown
• it cannot
certified as beingt due to natural causes
t be readily
edeceased
et
• the
was not attended n
byethe doctor during his/​her last
n
n
.
.
.
illness
or
was
not
seen
within
the
last
14
days
or
viewed
after
death
X
X
kX
or history of violence
ok • there are any suspicious
ocircumstances
ok
o
o
o
• the death may be .linked
to an accident (whenever.B
it occurred)
B
w Bof self-​neglect or neglect
w
• there is any question
by others
w
w
• the deathw
has occurred or the illness arisen
w during or shortly
ww
B
after detention in police or prison custody (including voluntary
attendance at a police station)
the deceased was detained under the Mental Health Act
the death is linked with an abortion
the death might have been contributed to by the actions of the
deceased (such as a history of drug or solvent abuse, self-​injury, or
overdose)
the death could be due to industrial disease or related in any way
to the deceased’s employment
the death occurred during an operation or before full recovery
from the effects of an anaesthetic or was in any way related to the
anaesthetic (in any event a death within 24 hours should normally
be referred)
the death may be related to a medical procedure or treatment
whether invasive or not
the death may be due to lack of medical care
there are any other unusual or disturbing features to the case
the death occurred within 24 hours of admission to hospital (unless
the admission was purely for terminal care)
it may be wise to report any death where there is an allegation of
medical mismanagement.16
t
• .ne
•
X
k
oo •
•
o
oo
B
.
w
•
•
•
•
o
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o
w.B
t
t
.ne
X
k
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t
e
X• .n
ok
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oo
B
.
ww
ww
t
.ne
X
k
•
Bo
et
.n
kX
et
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X
k
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B
.
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.n
kX
ww
.ne
X
k
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ww
et
n
.
X
ww
k
oo
oo
B
B
.
.
This note is for guidancew
only, it is not exhaustive and in part may represent
w desired local practice
rather than the statutory
requirements. If in any doubt, contact the
coroner’s office for further
w
w
w
w
ww
advice.
et
etot Law and Practice
et
n
n
n
Coroners’ Courts: A .Guide
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Taken from: Dorries, C.
University Press, 2014.
16
, 3rd edition, Oxford
B
104
.B
w
ww
Chapter 2
o
oo
B
.
w
ww
w
Life on the wards
t
.ne
Nutrition
X
k
Bo
.B
w
w
t
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X
k
et
o
w.B
.n
kX
o
A patient’s nutritional state has a huge effect on their well-​being, mood,
compliance with treatment, and ability to heal. You should consider
­alternative nutrition for all patients without a normal oral diet for over
48h. IV fluids are only for hydration, they are not nutrition. See Table 2.8
(E p. 105) for nutritional requirements.
ww
ww
ww
et
et
et
n
n
n
.
.
.
XOral Most patients manage to consume sufficient quantitieskofXhospital
ok food to stay healthy. If onotok(egXdue to inability to feedoself,
o increased
o
demand due to malnutrition)
­
consider simple remedies,
eg assisted
B
B
B
.
.
feeding, favouritew
foods from home, medicationswfor reflux/​heartburn
w
w
w
(E p. 300)w
or nausea (E p. 188). If theyw
are still not consuming ad- w
equate nutrition then discuss with the dietician who can advise on nutritional supplements
and high-​energy drinks.
t
e
et procedure) This is a good.nshort-​
et
n
n
.
.
Nasogastric (NG) (E p. 563 for insertion
X measure, however placing
X may be uncomfortablekX
some
ok term
okthethetubetubeuncomfortable
o
o
ooit is and
people
find
the
sensation
of
once
in. Liquid
B
B
B
.
.
foods and most oral
medicines (except slow-​release
w and enteric-​coated w
ww
preparations) can
be given via NG tube; advicew
regarding medications via
w
w
this route may be required from a pharmacist. Tubes can also be endo- w
scopically placed naso-​jejunally if required, eg gastric outlet obstruction.
Gastrostomy
endoscopic gastrostomy),
net Often called ‘PEGs’X(percutaneous
net
net
.
.
.
X
X
are a good long-​term k
of feeding for patients k
cannot
ok theseorally.
o method
o who
They are typically
sited endoscopically, though
surgical and
o
o
Bo feed
B
B
radiological approaches
possible (a radiologically inserted
w. Itareis also
w. gastrostomy
is referred to asw
a RIG).
possible to placew
a jejunostomy
if required.
w
w
ww
Enteral feeding (via the gut)
Parenteral feeding (via the blood)
o
Bo
Parenteral nutrition (PN) or total parenteral nutrition (TPN) requires central access because extravasation of the feed causes severe skin irritation.
Central access can be via a long-​line (eg peripherally inserted central catheter) or central line (eg Hickman). It is used when the patient cannot tolerate
sufficient enteral feeds (eg short gut syndrome) or when gut rest is required.
t
.ne
X
k
t
o
ww
o
w.B
et
.ne
X
k
oo
B
.
w
.n
kX
ww
There is significant risk associated with PN use including line insertion,
line infection, embolism/​thrombosis, and electrolyte abnormalities. It is
essential to monitor blood electrolytes regularly including Ca2+, PO43–​,
Mg2+, zinc, and trace elements, particularly in those starting PN after a
period of malnutrition (see next paragraph).
t
e
X.n
.ne
X
k
t
et
n
.
X
ww
k
ok Refeeding syndromeoo
oo feeds must
Bo After a prolonged w
B of malnutrition or parenteral
B
period
nutrition,
.
.
welectrolyte imbalance,
be reintroduced slowly (over a few days) to prevent
particularly dPO
ww . It can be fatal but is entirely
wwavoidable if blood tests ww
are checked daily during the at-​risk period (for 3–​5d, until full feeding rate
­established)
et and any electrolyte abnormalities
et are corrected promptly..net
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
3–​
4
B
.B
w
ww
.B
w
w
w
w
Nutritional requirements
w
105
t
t
t
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.ne
.ne
Nutritional
requirements
X
X
X
ok
ok
ok
o
o
requirements
Bo Table 2.8 Nutritional
B
B
w.
w. Deficiency
w
w
Name
Sources
Daily requirement
w
w
ww
Carbohydrate Almost all foods
300g
Malnutrition
Proteint
dairy, vegetables, 50g
Kwashiorkor t
e Meat,
et
grain
n
n
.
.
.ne
X
X
X
Fat
Nuts,
meat,
dairy,
oily
56g
Malnutrition
k
ok
ok
foods
oo
o
Bo Calcium Dairy,wleafy
B
.Bvegetables
.
1g
Osteoporosis
w seafood, enriched 150micrograms
ww Hypothyroid ww
Iodine
wFish,
w
salt
Iron
Meat, vegetables, grains 15mg
Anaemia
t
t
et Dairy, leafy vegetables,.ne420mg
Magnesium
Cramps ne
n
.
.
meat
X
X
X
ok Potassium Fruits, vegetables
ok 3.5g
ok
Hypokalaemia
o
o
o
B
Selenium
Meat, fish,
vegetables
55micrograms .B Keshan disease
w.Bfoods,
w Hyponatraemia
Sodium
Processed
salt
2.4g
w
w
ww
ww
B
Zinc
Cereals, meat
t
Vitamin
.ne A
(retinoid)
X
k
B
oo Vitamin
(thiamine)
1
o
Bo
11mg
et
.n
kX
Dairy, yellow or green
900micrograms
leafy vegetables, liver, fish
Bread, cereals
1.2mg
oo
B
.
Meat,w
dairy, bread
ww
o
ww
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o
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Neurological
problems,
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Anaemia
ww
Dermatitis
et
n
.
X
Anaemia
ok
oAnaemia
B
.
w Scurvy
o
o
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.
w
ww
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oo
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.
ww Ariboflavinosis
Vitamin B2
1.3mg
(riboflavin)
Vitamin B3
Meat, fish, bread
16mg
(niacin)
Vitamin B5
Meat, egg, grains, potato, 5mg
(pantothenic vegetables
acid)
Vitamin B6
Meat, fortified cereals
1.7mg
(pyridoxine)
Vitamin B7
Liver, fruit, meat
30micrograms
(biotin)
Vitamin B9
Bread, leafy vegetables, 400micrograms
(folate)
cereals
Vitamin B12
Meat, fish, fortified
2.4micrograms
(cobalamin) cereals
Vitamin C
Citrus fruits, tomato,
200mg
(ascorbic acid) green vegetables
Vitamin D
Fish, liver, fortified
5–​15micrograms
cereals
Vitamin E
Vegetables, nuts, fruits, 15mg
cereals
Vitamin K
Green vegetables, cereals 120micrograms
t
.ne
X
k
Hair/​skin
problems
Night
blindness
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Rickets/​
osteomalacia
None
ww
t
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ok
iPT
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ww
B
106
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne
.ne
.ne
Difficult
patients
X
X
X
ok
okexcessive alcohol consumption
okcan present
o
o
PatientsBwith
Bo Alcoholism
B
.
with a range of problems,
either directly related tow
their alcohol abuse or
w. dependency
w
w
to unmasking
of
alcohol
during
enforced
abstinence during ww
w
w
their admission for unrelated medical problems. The assessment and management of these patients is discussed on E p. 372.
et patients They often take.nmany
et medications, making interactions
et
n
n
Elderly
.
.
X side effects more common.kX
X doses
Declining renal function meansk
ok and
oexcreted
o lower
may be needed for renally
drugs. Likewise, elderly
patients are
o
o
o
B
B IV fluids. Other
more prone to heart.B
w failure from fluid boluses/​wexcessive
w.higher
problems include:
increased susceptibility to infections;
pain threshold
w
w
w or other acute pathology);
w atypical disease
(can mask fractures
presenta- w
tions; poor thermoregulation (easily develop hypothermia); malnourishmente(ift unable to obtain/​prepare food);
history taking can be difficult
et with
etif
n
n
n
.
hard
of hearing. Elderly patients can.suffer
­depression and other.psychiX illness (E p. 380) and social
X
X
ok atric
ok circumstances must alwaysobekconsidered
o
prior to discharge—​liaise o
with OT, physiotherapy, and socialoservices.
B
w.B
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w
w
w
w
Aggression and violence
w
107
t
t
t
.ne
.ne
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Aggression
and
violence
X
X
X
ok majority of patientsohave
ok respect for NHS staff; however,
ok under
o
Bo The
B
B
certain circumstances. anyone can become aggressive:.
w
• Pain (E pp. 88–91)
ww
ww (E pp. 374–5)
ww
• Reversiblew
confusion or delirium, eg hypoglycaemia
• Dementia (E pp. 376–7)
• Inadequate
fear/​frustration
et communication/​
et (E p. 20)
et
n
n
n
• .Intoxication
(medications, alcohol,
recreational drugs)
.
.
XMental illness or personalitykdisorder
X (E pp. 378–81). kX
ok •The
o Ask a nurse
o when aso
o
oyou
aggressive
patient
to accompany
B sessing aggressive w
B
.B Position yourselves
.
patients.
between
the
exit and the
w that other staff know where
wyouware. The majority of ww
patient and ensure
w
w
patients can be calmed simply by talking; try to elicit why they are angry
and ask specifically about pain and worry. Be calm but firm and do not
t make threats. If this does not
t offer an oral sedative orngive
shouteor
ehelp,
et
n
n
.
.
.
emergency
IV
sedation
(E
p.
370)
or
call
hospital
security.
X
X
kX fear,
ok The aggressive relative
okRelatives may be aggressiveoothrough
o
o
They usually respond.B
to talking, though
B frustration, and/​orwintoxication.
.B
w discussing their w
make sure you obtain consent from the patient before
w
w
medical details.
w Consider offering to arrange
w a meeting with a senior w
B
doctor. If the relative continues to be aggressive, remember that your
duty of care to patients does not extend to their relatives; you do not
have to tell them anything or listen to threats/​abuse. In extreme cases you
can ask security or police to remove the relative from the hospital.
Violence Assault (the attempt or threat of causing harm) and battery
(physical contact without consent) by a patient or relative is a criminal offence. If you witness an assault or are assaulted yourself, inform your seniors
and fill in an incident form including the name and contact details of any witnesses. If no action is taken on your behalf, inform the police yourself.
Abuse Abuse is a violation of an individual’s human and civil rights and
may consist of a single act or repeated actions. It may be physical, sexual,
financial, psychological, or through neglect. Patients of any age can be
abused. Do not be afraid of asking patients how they sustained injuries or
asking directly if someone caused them. Inform a senior if you suspect a
patient has been abused (see Box 2.11).
t
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.
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oo
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.
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o
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ww
K Box 2.11 Safeguarding and protection
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et
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X
As a doctor you will often meet your patients at their most vulnerable
moments. In most instances, the forces of nature will have conspired to
weaken the individual to bring them to this point. But in sad and rare cases,
vulnerable individuals are not afforded the protection they need, and a
presentation to acute healthcare services may be a manifestation of abuse.
Two groups are particularly at risk: vulnerable adults (those in need of
community services because of mental or other illness, disability or age)
and children. While government policy on protecting these groups continues to evolve, and new statutory regulations are likely to be introduced,
your local healthcare organization should have clear policies on child
protection and adult safeguarding. In all instances, your first and most important action if you believe a patient may be subject to any form of abuse
is to bring your concerns to the attention of your consultant.
et
n
.
kX
o
Bo
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X
k
ww
w
ww
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X
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.Bo
ww
B
108
.B
w
ww
Chapter 2
Life on the wards
.B
w
w
ww
w
t
t
t
.ne stick injuries
.ne
.ne
Needle-​
X
X
X
k conok
okneedle-​stick injuries without
oserious
doctors have received
o
o
Bo Many
B
B
sequences (see Table. 2.9). However, if you have just. been exposed, get
advice as soonw
as w
possible.
ww
w
w
ww
Immediately
Stop what
t you are doing. If it is urgent,
t phone your senior/​colleague
tto
e
e
do.n
it.eYour future health is your top
priority.
n
n
X.sharp) Squeeze around thekwound
X. so
exposure (needlekor
kXPercutaneous
o
o
o
that
blood
comes
out
and
wash
with
soap
and
water;
avoid
scrubbing
or
o
Bo pressing the woundwdirectly.
B
.Bo
.
w
Mucocutaneous w
exposure (eyes, nose, mouth) Rinse
ww with water (or 1L of ww
0.9% saline w
through a giving set for eyes/​nose).
Within
hour
et anshould:
et
et
A .colleague
n
n
n
.
.
X• Talk to the patient alone, explain
X what has happened and ask
Xabout
ok risk factors:
ok
ok
o
o
o
B
injecting drugs, blood
transfusions, tattoos or piercings
in
w.Bunprotected
w.inBlast 3mth,
foreign countries,
sex (particularly
in
w
w
a developing
w country or, if male, with awman), prior testing for
ww
•
hepatitis B+C or HIV and the results
• Ask to take a blood sample for testing for hepatitis B+C and HIV.
t
t
et
.nshould:
.ne
.ne
You
X
X
X
health
ok • Phone occupational
okif during office hours or go tooothek ED and
o
their advice exactly
Bo • follow
B
. in the patient’s notes and complete
.B an
Document the event
w
w
incident form.
ww
ww
ww
Post-​exposure prophylaxis
t be prescribed antiretrovirals
t(triple therapy, within 1h), nhepaYou may
et
titis
24h),
.nBeimmunoglobulin (within X
.neor hepatitis B booster (within
. 24h)
X
X
ok according to the significance
okof the exposure. There is currently
ok no post-​
o
forohepatitis C.
Bo exposure prophylaxis
B
B
.
wassociated
w.
Table 2.9 Viruses
with needle-​stickw
injuries
w
w Hepatitis B
wHepatitis C HIV
ww
UK prevalence
<0.1%
et risk <0.5%
et <0.5%
et
n
n
Transmission
1 in 3 (without vaccine)
1 in 50
1 in 300.n
.
.
X
X
Vaccines at k
None
kX
ok Vaccination
o 1, 2, +or12mth
oNone
o
o
o
Post-​
e
xposure
Immunoglobulin
booster
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Triple
therapy
B
.B
.B
w
w
ww
ww
ww
Over the next few weeks
et
n
.
kX
o
Bo
The patient’s blood tests should take <2d for HIV and hepatitis B+C results. Following high-​risk exposure you may be advised to have a blood
test in the future (2–​6mth); during this time you should practise safe sex
(condoms) and not donate blood. You cannot be forced to have an HIV
test. Discuss with occupational health about involvement in surgery.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Pre-op assessment
w
109
t
t
t
.ne op assessment
.ne
.ne
Pre-​
X
X
X
ok
ookp clinics well before their operation
ok to:
patients attend pre-​
o
o
Bo Elective
B
B
. operation?)
• Assess the patient’s. problem (ie do they still need the
w fitness for an anaesthetic w
• Gauge their medical
andw
surgery
w
wpre-​op investigations (see NICEwguidelines, Table 2.10)
ww
• Request any
• Check consent (this should only be obtained by the surgeon performing
theeprocedure
or a person competent
t
etto undertake it, E p. 128).net
n
n
• .Answer
any questions the patient
may have.
.
X
X
X
ok Pre-​op investigationsooSeekTable 2.10.
ok
o
o
B
Table 2.10 Preoperative
w.B investigations* ww.B
w
w
w
ww
Ix
Indication
FBC
All major surgery, or intermediate surgery if CVS or renal disease.
Sickle-​ect
ell All patients with a positive family
et history of sickle cell disease .net
n
n
.
.
U+E
If
at
risk
of
AKI
plus
(i)
ASA
1
X
X and major surgery, (ii) ASAk2Xand
intermediate surgery
ok
okor (iii) ASA 3/​4 and minor surgery
o
o
o
ofailure,
B
B
B
Clotting (i) intermediate/​
major surgery if ASA 3/​4 with.liver
or
.
w taking an oral anticoagulantww
(ii) in a patient
w
wpatients with diabetes and no HbA1c
w in last 3mth
ww
HbA1c
All
†
β-​hCG
ECG
Urine β-​hCG if any doubt whether a patient may be pregnant
If (i) minor surgery, ASA 3/​4 and none in last 12mth,
(ii) intermediate surgery and cardiovascular, renal or diabetic disease
and ASA 2 or (iii) major surgery, >65yr, and none in last 12mth
Echo
Any patient with a either (i) signs/​symptoms of heart failure or
(ii) a murmur with SOB, presyncope, syncope, or chest pain
PFT/​ABG Discuss with anaesthetist if intermediate or major surgery and ASA
3/​4 due to known or suspected respiratory disease.
t
.ne
et
kX
o
Bo
o
o
w.B
o
ww
et
et
ww
et
*NICE guidelines: Mguidance.nice.org.uk/​NG45
†
Surgeries are either minor (eg skin excision, breast abscess), intermediate (eg inguinal hernia,
varicose vein excision, tonsillectomy, knee arthroscopy), or major (eg hysterectomy, discectomy,
prostate resection, joint replacement, lung operations, colonic resection). American Society of
Anaesthesiologists Physical Status Classification. ASA 1 (healthy), ASA 2 (mild systemic disease),
ASA 3 (severe disease) or ASA 4 (life-​threatening severe disease).
.n
kX
o
.n
kX
o
o
w.B
.n
kX
o
o
w.B
ww
ww
Requesting blood pre-​op
Each hospital will have guidelines on the transfusion requirements for
most elective operations; become familiar with these. Blood for transfusion is in limited supply and should only be cross-​matched when necessary.
Table 2.11 shows common blood requirements for elective surgery.
t
t
e
X.n
ok
Bo
ok
o
w.B
ww
t
e
X.n
e
X.n
ok
o
w.B
Table 2.11 Summary of operations and blood requirements
ww
ww
Blood request Operation
Minor day-​case surgery (carpal tunnel, peripheral lipoma)
No request
Group and save Laparoscopy, appendicectomy, cholecystectomy, hernia,
hysterectomy, liver biopsy, mastectomy, varicosity, thyroid
X-​match 2units Colectomy, arthroplasty, laparotomy, TURP, hip replacement
X-​match 4units Abdominoperineal resection, hepatic/​pancreatic surgery
X-​match 6units Aneurysm repair (book ICU bed post-​op)
t
t
e
X.n
ok
Bo
.n
kX
o
w.B
ww
Bo
et
.n
kX
e
X.n
ok
ww
o
B
.
w
ww
t
e
X.n
ok
ww
o
B
.
w
ww
B
110
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
Patients
.ne with medical problems
.ne
.ne
X
X
X
pp. 334–6) Put the patient
on the operating list.k
ok DM (E
oifkpatientsfirsthave
o
oo pain, an unInform the anaesthetist
had recent chest
Bo CVS
B
B
.
.
diagnosed murmur,
or
symptoms
of
heart
failure.
The
anaesthetist
w an Echo or may see the patient
w personally. may w
want you to request
w
w
w the anaesthetist as these w
Rheumatoid w
arthritis/​ankylosing spondylitis Inform
patients may be difficult to intubate or have an unstable C-​spine—​the
anaesthetist
et may want to see the .patient
et or request radiological imaging.
et
n
n
n
.
.
Contacting
the
anaesthetist/​
I
CU
Find
out
the
anaesthetist
for
your
X list and tell them aboutkany
X patients who may need further
kXinvestigaok patient’s
o
o
o
o
o
tions or a review preoperatively.
an ICU bed post-​op
B
.B If your patient will need
.B
inform ICU well in w
advance (contact details available w
from the anaesthetic dew
w
partment office)
w and confirm with ICU on the day
w that the bed is still available. ww
Special circumstances
t steroids must have nextra
Steroids
(E p. 179) Patients takingeregular
et cover
etif
n
steroid
during surgery and.nbe converted to IV preparations
.
.
X Discuss each patient’skneeds
X with your team and the anaesthetist.
X
ok NBM.
o be stopped
ok with
Anticoagulants Warfarin should
at least 5d preoperatively,
o
o
o
B
.B heart valves
a target INR of <1.5.for
w B most surgery; those with420–2).
wprosthetic
may need IV/​Sw
C heparin cover instead (E pp.w
DOACs 1d
w
w risk surgery or 2d beforewhigh bleedingStop
before low bleeding
risk surgery, ex- w
B
cept in CKD patients (CrCl <50mL/​min) on dabigatran who need it holding
for 2d (low bleeding risk surgery) or 4d (high bleeding risk surgery). Seek
haematology advice if unsure. Those needing spinal/​epidural anaesthetics
may have different rules—​discuss with the anaesthetist.
Antiplatelets Clopidogrel must be stopped 7–​10d before surgery; aspirin
is usually continued unless otherwise instructed by senior surgeon (if in
doubt check with the operating surgeon/​consultant).
Oestrogens and progestogens HRT can be continued as long as DVT/​PE
prophylaxis is undertaken. Progestogen-​only contraceptives can be continued, but combined oral contraceptives should be stopped 4wk prior
to surgery and alternative means of contraception used.
Bowel preparation See Table 2.12 E p. 111.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
t
.ne
X
k
t
.ne
X
k
w
t
.ne
X
k
ww
et
.n
kX
oo
oo
B
B
.
.
w to check include: w
save yourself timew
any allergies. Things
w later. Document
Prophylactic anticoagulation
(E pp. 420–2). ww
w
w
Antibiotics Consider pre-​op antibiotics (check local guidelines).
Bowel preparation
and IV fluid (E p. 111).
etdrugs Review
etup those which should be.nconet
Regular
these and write
n
n
.
.
Xtinued in hospital (stop COCP,
Xclopidogrel as above, etc). kX
ok TED stockings Prescribe these
okfor all patients.
o
o
oo The anaesAnalgesia and antiemetics
(E pp. 88–91 and E pp. 310–11)
B
B
B
.
.
w
thetist will usuallyw
write these up during the operation.
wwfor the patient
ww
ww
Instructions
• Where and when to go for admission (write this down for them)
t usually be on clear fluidsneatt
• If they
to have bowel prep, theyeshould
et24harebefore
n
n
.
.
.
least
the
operation
(E
p.
113)
X• Tell the patient about any drains,
X
X
k
k
k
NG
tubes
or
catheters
which
may
be
o inserted during the operation
oo
oo
Bo • Tell
B
B
.
.
them if theyw
are being admitted to ICU post-​
wop.
ww
ww
ww
Bo
Writing the drug chart Try and do this at pre-​admission clinic to
B
.B
w
ww
.B
w
w
w Bowel preparation 111
ww
t
t
t
.ne preparation
.ne
.ne
Bowel
X
X
X
ok
okGI surgery procedures, patients
ok are given
endoscopy and some
o
o
Bo Before
B
B
laxatives to clear the.bowel (Table 2.12). For surgery,
aim is to rew op anastomotic leak andwinfections.
w. theAccumulating
duce the risk ofwpost-​
w that it does not improve wcomplication rates and may ww
evidence suggests
o
Bo
even be harmful,17 hence use of bowel preparation prior to surgery is
declining. Check your local policy for guidance. Where bowel preparation is required, it is vital that patients are instructed properly and the
importance of good compliance is stressed. For example, during colonoscopy inadequate bowel preparation can lead to pathology being
missed or the procedure being aborted (see Box 2.12).
et
n
.
kX
t
et
n
.
kX
oo
e
X.n
ok
o
w.B
w.B
w
w
w for bowel preparation
ww
Table 2.12wProcedures and the potential need
Boweltpreparation
Procedure
e
et
et
n
n
n
None
OGD, ERCP,
closure (reversal) ileostomy
.
.
.
X
X haemorrhoidectomy, examination
X
Anal k
enema
ok Phosphate
o fissure,
ok
under
anaesthetic (sigmoid colon/​rectum/​
o
o
o
(on
day
of
surgery)
B
area), flexible sigmoidoscopy
w.Bperianal
w.B
Full bowel prep w
Colonoscopy, rectopexy, w
right hemi-​/​left hemi-​/​
w
wanterior resection,
ww
(see Box 2.12)
sigmoid/​pancolectomy,
abdominoperineal resection, Hartmann’s reversal
t
t
t
e
.n
.ne
.ne
X
X
X
ok Box 2.12 Full bowelopreparation
ok
ok
o
Bo A variety of oralwbowel
B
B
UK. In
. cleansing products are available
. anin the
wissued
2009, the National
Patient Safety Agency (NPSA)
alert in rew
w
sponse to safety
w incidents including a reported
w death following bowel ww
o
Bo
preparation. In particular, patients at risk of renal impairment and electrolyte imbalance need careful identification and prescribing.
• Sodium picosulfate/​magnesium citrate combinations (eg Picolax®)
give excellent bowel preparation and are relatively acceptable to
patients; they are relatively contraindicated in those with stage 4 or 5
CKD or those at risk of electrolyte imbalance, cardiac or liver failure
• Polyethylene glycols/​macrogols (eg Klean-​Prep®, MoviPrep®) require
large volumes of liquid to be drunk, but are safer in at-​risk groups.
Consider admitting elderly patients and those with comorbidities
for IV fluids and monitoring during bowel preparation. Oral medications should not be taken 1h before or after administration of bowel
cleansing preparations; where reduced absorption could prove catastrophic (eg immunosuppressives post-​
transplant) consider admission for IV ­administration. Advise patients taking the OCP to take
alternative precautions during the week following taking the bowel
preparation.
Offer patients written dietary advice on low-​residue foods for the 2d
prior to their procedure (local documents should be available); those
taking insulin will require specific advice and guidance for management.
t
.ne
X
k
t
o
ww
o
w.B
ok
Bo
o
Bo
.ne
X
k
t
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
.ne
X
ok
.Bo Cochrane
Guenaga K, et al. Mechanical bowel preparation for elective colorectal surgery.
Database Syst Rev 2005;1:CD001544.
17
ww
ok
o
o
w.B
ww
et
n
.
kX
oo
B
.
w
.n
kX
ww
t
e
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et
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X
k
w
ww
ww
B
112
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne
.ne
.ne
Surgical
terminology
X
X
X
ok
ok
ok
o
o
Bo Prefix/​suffix Meaning
B
B
w. and example ww.
Angio-​
Relating to a vessel
w
w Angioplasty—​reconstruction ofwa blood vessel
ww
Chol-​
Relating to the biliary system
t
Cholecystitis—​inflammation
e
et of the gallbladder
et
n
n
n
.
.
.
Hemi-​
Meaning half of something
X
Xexcising half the colon
X
Hemicolectomy—​
ok Hystero-​
othekuterus
ok
o
o
o
Relating
to
B
B
Hysterectomy—​
removal of the uterusw.
w.B
w
w
Lapar-​
to the abdomen
w Relating
w
ww
Laparotomy—​opening the abdomen
Nephr-​
Relating to the kidney t
et
e to the kidney
et
Nephrotoxic—​damaging
n
n
n
.
.
.
X
Total/​every X
ok Pan-​
ok complete removal of the colonookX
Pancolectomy—​
o
o
B
Per-​
Going
.B
w.Bthrough agstructure
Percutaneous—​
oing through the skinw
w
w
w Near or around a structure w
ww
Peri-​
B
net
Proct-​
.
kXPyelo-​
o
o
Thoraco-​
Trans-​
o
Bo
t
-​ectomy
.ne
X
k
-​gram
-​olith
t
e
X.n
-​oscope
-​ostomy
-​otomy
-​plasty
et
n
.
kX
o
Bo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
o
w.B
t
.ne
X
k
ww
w
t
ww
-​itis
ok
Bo
Perianal—​near the anus/​around the anus
Relating to the rectum
Proctoscopy—​examination of the rectum
Relating to the renal pelvis
Pyelonephritis—​inflammation of the renal pelvis
Relating to the thorax
Thoracotomy—​opening the thorax
Going across a structure
Transoesophageal—​across the oesophagus
Surgical excision
Nephrectomy—​removal of a kidney
A radiological image often using contrast medium
Angiogram—​contrast study of arteries
Inflammation of an organ
Pyelonephritis—​inflammation of the renal pelvis
Stone-​like
Faecolith—​solid, stone-​like stool
A device for looking inside the body
Sigmoidoscope—​device for looking into the distal colon
An artificial opening between two cavities or to the outside
Colostomy—​opening of the colon to the skin
Cutting something open
Craniotomy—​opening the cranium (skull)
Reconstruction of a structure
Myringoplasty—​repair of the tympanic membrane
.ne
X
k
oo
B
.
w
et
.n
kX
ww
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X
k
t
ww
ww
o
w.B
et
n
.
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o
o
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.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
ww
t
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ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Preparing in-patients for surgery
w
113
t
t
t
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.ne for surgery X.ne
Preparing
in-​
p
atients
X
X
ok
ok
ok
o
o
Bo Checklist
B
B
.
Before your patient
goes to theatre, you have a responsibility
to check
w.
wwbeen
w
the followingw
have
done:
w
ww
• The consent form has been signed by the patient and surgeon
• The patient has been seen by the anaesthetist
t
eoperation
ebyt the surgeon (imperative if.ntheet
• The
site has been marked
n
n
.
.
operation
could
be
bilateral,
eg
inguinal
repair)
Xare in thehernia
X
kX• The preoperative blood results
k
notes
o
o
ok
o
o
o
preoperative ECG
and/​or CXR are available .B
B •• The
w.BTED stockings, and antibiotics
w have been
Prophylactic LMWH,
w
w<12h
prescribedw
where relevant (do not give heparin
pre-​op if having
w
ww
spinal/​epidural)
• The patient
received bowel preparation
necessary
t has
epatient
et (see ifnext
et
• .The
has been adequately.fasted
section)
n
n
n
.
•
Blood
has
been
crossmatched
and
is
available
if
required
(E
pp.
412–17)
X
X
X
ok • Check if the patient hasoany
oklast-​minute questions or concerns
ok and is
o
o
still happy to proceed
B
.Bwith the operation. w.B
wand
Oral fluids pre-​
post-​op
w
w
ww
ww
In general, patients should not eat for at least 6h before going to theatre
but can have clear fluids until 2h. In emergencies this rule may be overruled, but the risk of aspiration of gastric contents will be increased.
net
net
net
.
.
.
X
X
X
are having an operation
preparation,
k which requires boweloallowed
k while
ok If patients
local guidelines as o
toowhat oral intake the patient is
o
Bo check
B
B
taking the laxatives, usually
. it is either clear fluidswonly. or a low-​residue
diet (E p. 111).ww
w
w
Nil by mouth w
(NBM) Patients cannot have anyw
oral food or significant fluid w
intake; hydration must be maintained with IV fluids. However, oral medit antiarrhythmics) may be ntaken
catione(eg
a sip of water, if not taking
et with
et
.n would put the patient at more
. risk.
.nsuch
them
Non-​essential medication
X
X
X
k omitted; check with your seniors.
k
supplements mayobe
ok as vitamin
oblack
o
o
fluids Include non-​
c
arbonated
drinks
such
as
black
tea,
coffee,
Bo Clear
B
B
water, squash drinks
w.(not milk or fruit juice). ww.
w
w
w hour orally, usually given w
Sips 30mL water/​
for the first day after major w
abdominal surgery involving bowel anastomoses.
t This includes food such asnsoup
Soft diet
jelly. Once patients have
etolerating
et and
ebet
n
n
.
.
.
been
clear fluids postoperatively
for at least 24h, they may
X
X
ok allowed to start a soft diet.ookX
ok
o
o
B Most patients canwsafely
.B drink clear fluids up to 2hwbefore
.B surgery. The
following increase the risk of aspiration:
w
w
• Pregnancyw
w
ww
Being elderly
Obesity
Stomach disorders, eg hiatus hernia, reflux
Pain (+ opioids).
et
n
.
kX
o
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•
•
•
•
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
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X
ok
.Bo
ww
B
114
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne
.ne
.ne
Booking
theatre
lists
X
X
X
ok
ok
ok
o
o
Bo Box 2.13 Elective
B
B
w. lists
w.
w
w
In some centres
w this is done by the surgeon
w or their secretary, how- ww
ever in many places this task may fall to the surgical FP trainee. If you
are required
book elective lists thist will likely be electronically using
et systemtowhich
e training for (very occasionally
et
a.local
you should .receive
n
n
n
.
X systems are still in place).
X You should find out aboutkyour
X
ok paper
ok lists.
o local
procedures for bookingoelective
o
o
B
Bthe list with your consultant/​
Discuss the order of
egistrar (you may
w.operating
w.rB
need to obtain
the
list from your consultant’s
secretary or
w
w
w
ww
direct fromw
theatre).
The list usually must be submitted by the afternoon before the
operating
et day. You should include:.net
et
n
•.n
Theatre number
.
X
X
of the consultant surgeon
kX
ok •• Name
oknumber, and location of eachoopatient
Name, sex, age, hospital
o
o
B
.B
• Special patient requirements
(eg DM, blood requested,
w.B ICU bed
booked) ww
w
wand side in full (eg open repairwleft inguinal hernia)
ww
• Operation
• Sign and leave your bleep number
• If the order of the list needs to be changed, contact theatres and
inform them as soon as possible.
t
t
t
.ne
.ne
.ne
X
X
X
ok
okorder of operations ook
o
the
Bo Box 2.14 Booking
B
.
.B
w
w
In general, surgeons
tend
to
prefer
a
specific
order
of patients:
ww before younger (except children)
ww
ww
• Older patients
• Patients with comorbidities (eg DM) before healthy
• Clean
before dirty (eg bowel
t resection)
t
et operations
ebefore
n
n
•Longer,
more complex operations
shorter.
.
.
.ne
X
X
X
ok
okemergency operationsook
o
Bo 3 Box 2.15 wBooking
B
.
.B
wregistrar
•Ensure you w
discuss the case with the ST1/​2w
and
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w on the list
ww
and that w
they have agreed to put the patient
•Enter the patient’s details as previously outlined, noting the time at
which the patient last ate
• Inform the anaesthetist covering the emergency theatre about the
patient (usually the on-​call anaesthetic registrar)
• Check the patient has been consented and make sure the results
of any relevant investigations are available (including a G+S sample
and a pregnancy test in women of child-​bearing age)
•You also need to inform the theatre coordinator.
t
e
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ok
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Haemostatic forceps
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116
.B
w
ww
Chapter 2
Life on the wards
.B
w
w
ww
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t
t
t
.ne operating theatre
.ne
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The
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.
Operating theatres
an operating area, awscrubbing-​up area, a
wwainclude
w
preparationw
room,
sluice (area for dirty equipment
and dirty laundry), ww
w
and an anaesthetic room. There will also be a whiteboard (to document
date, operation, and number of swabs/​blades/​sutures used), a display
etfor viewing radiology, and an.narea
et to write up the operation.nnotes
et
system
n
.
and
histopathology
forms.
Above
the
operating
table,
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are
usually
X
X more mobile units (satellites).
X
ok main sets of lights, as welloasoksmaller,
ok
o
o
B
Theatre staff w.B
w.B
Each operatingw
theatre has a team of assistants
who clean and maintain
w
woperation to select instru- ww
the theatre.w
The ‘scrub nurse’ scrubs for each
ments as requested by the surgical team. One other trained nurse and
an auxiliary
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et nurse act as ‘runners’ .tonfetch
et andequipment
eont
n
n
.
.
and
to monitor the number of swabs
sutures used (displayed
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Xmaintains
kXdepartmental assistant (ODA)
ok the
oand
ok operation
o
o
o
the
anaesthetic
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assists
the
anaesthetist.
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surgeon,
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w.operating
w
w
patient’s consultant,
anaesthetist.
w
w
ww
Theatre clothing
Fresh scrubs
should be worn for each operating
list and should be changed
t
net lists, or between casesXif they
nebecome
net
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dirty or potentially infected
.
.
.
X
X
Theatre shoes are
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and you will
ok withbeMRSA.
ok essential
oshoes
allowed to enter o
without
them. Theatre scrubs and
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o
Bo not
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B
. outside of theatres except w
. emergency.
not be worn uncovered
in an
w
w
Scrubbingwup
ww
ww
Scrubbing up is an art and a key part of minimizing infection risk to the
patient.t If in doubt, a theatre nurse cantshow you how to do it.
t
• .Prior
ne to scrubbing, remove jewellery
.ne and put your mask andXa .ne
theatre hat on
X
X
ok • Open a gown pack and drop
ok a pair of sterile gloves on top
ok
o
Bo • When scrubbingwup.Bforothe first patient, scrub under
B
your
. nails using a
brush with iodine or chlorhexidine. Wash hands w
for a further 5min
w
w
•Unravel your
w gown; ensure that it does notwtouch the floor
ww
• Touching its inner aspects only, put it on with the end of the sleeves
covering
your hands
eont your
etoutside of your gloves with.nyour
et
• .Put
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the
n
n
.
X bare hands
X
kXand
ok • For
okCaesarean, HIV +ve) double-​
oglove
high-​risk operationso(eg
o
o
B
protect your eyes with
or safety spectacles .B
w.Btoatievisor
• Wait for an assistant
your scrub gown from
behind
w
ww
w becomes non-​sterile, changewyour
ww
• If your hand
glove. If your gown
becomes non-​sterile you need to rescrub; change your gown and
gloves.
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The operating theatre
w
117
t
t
t
Theatre
.ne etiquette
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.ne
X
X
X
are scrubbed up: k
ok • If you
o to adjust the lights for youook
o
ask someone not scrubbed
Bo
B
.
.B
do not pick upwinstruments
which fall to the ground
w
if you are handed
an instrument by someone
who is not scrubbed,
w
w
w you can touch it before accepting
w it
ww
check that
• In operations involving the abdomen and the perineum, if you are asked
t from the perineum to thenabdomen
t you must rescrub. Thisneist
to move
enecessary
eabdomen
n
.
.
.
not
when swapping from
to perineum
X leave the operation
kX• If you sustain a needle-​stickokinjury,
kX to
andoreport
o
occupational health (E
Bo • Always
.Bgoop.to108)
.toBano operating list.
eat/​drink
and
the toilet before going
w
w
w
Watchingw
an operation
ww
ww
Make sure you can see; get a stool or stand at the patient’s head if the
anaesthetist
Although you aretnot actively participating in the
et useallows.
e techniques. If you can’t .follow
et
n
n
n
operation,
the time to learn surgical
.
.
X going on, ask. As the operation
X
X forms
fill in any histology
ok what’s
ok histologyfinishes,
okaccurately.
or TTOs if appropriate. Check
samples are labelled
o
o
o
B WHO SurgicalwSafety
.B Checklist
w.B
w
w
In 2009, thewNPSA released guidance onw
the WHO Surgical Safety ww
•
•
•
Checklist, a process by which all members of the theatre team have a
discussion about the operation and the patient in advance of ­undertaking
the procedure. The aim of this is to improve patient safety and prevent
errors such as wrong-​
site surgery, retained throat-​
packs, avoidable
­delays in obtaining blood products, or senior help should an unexpected
incident arise. Most trusts have devised their own checklist so these vary
between hospitals, but are all based on the NPSA guidance.18
et
et
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kX
o
Bo
o
o
w.B
o
ww
The checklist is read out loud before the anaesthetic is given, before
the operation starts, and after the operation is completed. Before the
operation everyone in theatre introduces themselves, the patient’s
­
­details, the procedure about to take place, and the site are confirmed,
relevant equipment is checked to be present, and VTE prophylaxis
measures are declared. At the checkout after the operation, swab
counts, instrument and sharps counts are checked, the operation note is
confirmed, and specimens labelled. Plans for postoperative management
are also confirmed.
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et
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118
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne op care
.ne
.ne
Post-​
X
X
X
k after the
ok well as seeing patientsopreoperatively,
ok
othem
you should review
o
Bo As
B
B
operation. This means
can review and discharge .day cases with your
w. you
w after the operation. w
team, as well asw
making
sure the in-​patients are w
stable
w
w
w
Discharging day cases (This may be done by nursing staff.)
Before tsending day surgery patients home,
you should make sure they
e have eaten and had fluids.nwithout
et vomiting,
et
are
alert,
have passed.n
urine,
n
.
the
Xare mobilizing without fainting,kXand have adequate pain relief.kInspect
ok operation site and checkotheir
o observations. Go throughoothe X
operation
o
B
procedure, findings, and
follow-​up with the patient. .B
w.Bfollow-​
wif they need dressing w
Organize appropriate
up care and clarify
w
w removal dates, and where this
ww
changes, suture
can be done (GP surgery, w
ED, or ward). If the patient develops any post-​op temperatures, pain, or
bleeding,
et they should contact their.nGPetor come to the ED. .net
n
.
Common
questions about discharge
X
kXfor work for up to a totaloofk7dX
can self-​certify as
ok • Patients
ounfit
o
o
o time off
(including
time
spent
as
in-​
patient); if you anticipate
required
B
B
B
.
.
work will routinely
a Fitness
w be longer than this, issuew
w to Work/​Med
3 note (E
wp.w82) for the total expected time;
w this is the responsibility ww
B
of the hospital team, not the patient’s GP. Unanticipated extensions to
the recovery period can be handled by the GP
Patients requiring proof of hospital admission (for sick pay or social
security payments) should be issued with a Form Med 10 (E p. 82)
Tell the patient if their sutures are dissolvable or if they need to return
to have them removed (give dates; often GP practice nurses will do this)
Patients can shower and commence driving again 48h after minor
surgery (as long they can perform an emergency stop; E p. 619)
Advise patients not to fly for 6wk following major surgery.
t
• ne
.
X
k
oo •
•
•
et
ww
oo
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.
w
.n
kX
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t
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X
k
ww
t post-​op care net
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et
.noatient
.
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p patients are at risk of X
complications
associated with X
the.n
operX
directly (eg haemorrhage)
or indirectly (eg PE).
ok ation, either
ok document
oofkdays since
o
o
reviewing post-​
o
p
patients,
the
number
Bo When
B
B
.
.
the operation andw
the operation they underwentw
(eg 2d post left mastw
w
ectomy). ww
w
w
Ask about pain, ability to eat and drink, nausea/​vomiting, urinary output
and colour,
bowel movements/​flatus, mobilization.
et wound
et legs, drains, stoma bags,
etIV
n
n
n
Examine
site, chest, abdomen,
.
.
.
X
X site, amount drained, colour
X
catheter bag, drainkentry
ok cannulae,
o
ok of any
fluid being drained.
o
o
o
B
B (total input
Look at the observations:
pyrexia, HR, BP, RR, 24h fluid
w.B
w.balance
and output (including
drains) and net balance);w
document all findings.
w
w
w
ww
Review the drug chart for analgesia, antibiotics, fluids.
Check postoperative Hb; transfuse if necessary (E pp. 412–17).
etother members of the MDT
eiftnecessary, eg stoma nurse,.npain
et
Involve
n
n
.
.
Xteam, physiotherapists, socialkworker,
X occupational therapist.kX
ok
o
o
o
oo
B
B
B
.
.
w
w
ww
ww
ww
B
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w
ww
.B
w
w
w
w
Post-op problems
w
119
t
t
t
.ne op problemsX.ne
.ne
Post-​
X
X
ok
ok
ok
(E pp. 486–7)
o
o
Bo Hypotension
B
B
. input, epidural, drugs, pain.
Ask about Pre-​op BP,
wfluid
w.
w
w
Look for Repeat
BP,
HR,
fluid
input/​
u
rine
output,
w
w temperature, GCS, ww
orientation, skin temp, cap-​refill, signs of hypovolaemia/​sepsis, wounds,
drain, abdomen,
any signs of active bleeding.
t Hypotension
e
et post-​op and does not .always
et
n
n
n
Management
is common
.
.
X intervention. Tachycardia
X worrying feature suggesting
shock.
kXmonitor
ok ­rIfequire
ok areis apresent
oand
this or other adverse features
do 15min obs
o
o
o
B hourly urine outputw(catheterize
.B
.B flat, and give
bladder). Lie the patient
w
oxygen. Get IVwaccess, consider fluid challenge
(eg 500mL crystalloid
w
w
STAT, E p. w
490). Send bloods for FBC andw
crossmatch (blood cultures w
if you suspect sepsis). Apply pressure to any obvious bleeding points.
Call for
etsenior review early. .net
et
n
n
.
.
Pyrexia
Temp
37.5°C,
investigate
if
this
persists/​
i
ncreases
after
the
X
X
ok first 24h post-​op (E pp.o496–505;
ok see Box 2.16). ookX
o
B Ask about Cough/​SwOB,.Bwound, dysuria/​frequency,wabdo
.B pain, diarrhoea.
w
w
Look for BP, HR,
w temp, wound, catheter, IV cannulae,
w chest, abdomen. ww
Management Urine M,C+S; blds FBC, U+E, CRP, blood cultures; Imaging
CXR, consider abdominal USS or CT, echo if new-​onset murmur.
t
t
t
.ne
.ne
.ne
X
X
X
ok Box 2.16 Possible causes
ok of post-​op pyrexia ook
o
Bo • Day 1–​2 Atelectasis;
B
B and
. treat with salbutamol/​saline
.nebs
w
chest physioww
w chest physio
w
wand
ww
• Day 3–​4 Pneumonia;
treat with antibiotics
• Day 5–​6 Anastomotic leak; need to take back to theatre
• Day
8 Wound infection; treat byeopening
up wound, antibiotics,et
t
et7–​need
n
may
to return to theatre..n
.
.n
X
X
X
k
k
k
o
of breath/​
odoO sats (E pp. 277–89)
oo
Bo Shortness
B
B
.
.
Ask about Chronicwlung/​CVS disease, previous w
PE, chest pain, ankle
swelling, new-​
nset cough.
wow
ww
ww
Look for BP, HR, temp, pallor, lungs (consolidation, crackles, air entry),
signs e
oftfluid overload, leg oedema/​ce
alft swelling.
et
n
n
n
.
.
.
blds FBC, ABG; CXR, ECG. Consider
0.9%
XManagement Sit up and give Ok;X
kX
chest physiotherapy. If o
you
suspect a
ok saline nebs, antibiotics andooregular
o
o
(medical registrar
B PE (E p. 284) callwfor.Bsenior help and specialist advice
w.B
on-​call). See also Box 2.17.
w
w
w
w
ww
2
2
I Box 2.17 Post-​op problems covered elsewhere
Bo
o
et
n
.
kX
Pain
Nausea and vomiting
Low urine output
o
B
.
w
ww
o
et
n
.
kX
w
ww
t
.ne
X
ok
.Bo
E pp. 88–91
E pp. 310–11
E pp. 392–3
ww
B
120
.B
w
ww
Chapter 2
.B
w
w
ww
w
Life on the wards
t
t
t
.ne
.ne
.ne
Wound
management
X
X
X
ok
ok
ok
o
o
Bo Types of woundwhealing
B
B
.
w. wound edges are w
Primary closure This is most common in surgery, where
w
w
opposed soon
after
the
time
of
injury
and
held
in
w
w place by sutures, Steri- w
Strips™, or staples. The aim is to minimize the risk of wound infection
with minimal
tissue formation (Table
t 2.13). used in ‘dirty’ orntrauet primaryscarclosure
ecommonly
et
Delayed
This is more
n
n
.
.
.
X wounds. The wound kis Xcleaned, debrided, and thenkinitially
X left
ok matic
ocover may be given until theoowound
open for 2–​5d. Antibiotic
is reo
o
B
B
viewed for closure. .B
.
w is much less commonlywencountered
w
Secondary closure
surgery.
w
wwThisintention
wthe wound is leftinopen
Healing by secondary
happens when
and w
heals slowly by granulation. This is used in the presence of large areas of
excised
infection, or significantettrauma, where closing the wound
etbetissue,
et
n
n
.
.
would
impossible or would give.n
rise to significant complications.
X
X
X
ok Table 2.13 Abdominal owound
ok complications
ok
o
o
B
.B Examine Management
Askw
about
w.B
w
w
Superficial wPink serous
Skin and fat w Not an emergency but
ww
B
dehiscence
net
.
kXDeep
dehiscence
o
o
discharge, burst
sutures
Pink serous
discharge,
haematoma,
bowel
protrusion
oo
B
.
w
o
Bo
o
ww
t
e
X.n
ok
Bo
Bo
o
et
n
.
kX
swelling
.ne
X
k
ask for senior review—​
wound may need packing
± antibiotics
Call for senior help
urgently. Cover the
bowel with a large sterile
swab soaked in 0.9%
saline. Check analgesia
and fluid replacement,
give antibiotics
Wound swab, broad-​
spectrum antibiotics
initially (E p. 181),
discuss with your senior
oo
B
.
ww
w
t
Tenderness,
.ne
odorous
X
k discharge,
Pyrexia, pain,
erythema, white,
yellow or bloody
exudate from
wound site
o
w.B
t
.ne
kX
ww
t
Infection
.ne
X
k
cavity exposed
(rectus sheath
closed)
Separation of
wound edges
with bowel
exposed
oo
B
.
w
.n
kX
ww
ww
t
ww
et
n
.
X
ok
ww
o
w.B
et
n
.
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ww
t
o
o
B
.
w
ww
ww
et
o
o
w.B
t
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X
k
w
ww
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Common elective operations
w
121
t
t
t
.ne
.ne
.ne
Common
elective
operations
X
X
X
ok
ok
ok
o
o
cholecystectomy
Bo Laparoscopic
B
B
Operation to remove
w. the gallbladder.
w.
w
w
Indications Symptomatic
gallbladder
stones,
asymptomatic
patients at risk ww
w
w
of complications (diabetics, history of pancreatitis, immunosuppressed).
Pre-​op No
bowel prep required, 6h fasting
t pre-​anaesthetic (E p. 111).
et This
eabdomen
et
n
n
n
Procedure
involves insufflating.the
with CO , inserting
3 or
.
.
X through the anteriorkabdominal
X wall to enable laparoscopy
X
ok 4theports
o to remove
ok and
use of operating instruments
the gallbladder.
o
o
o
B Post-​op Patients canweat.Bas soon as they recover from
B anaesthetic, can
w.the
w
usually go homew
later in the day or the following morning.
Not all patients are
w in clinic
ww
followed up; w
some consultants like to review patients
after 6–​8wk.
Complications Haemorrhage, wound infections, bile leakage, bile duct stricet stones; may require conversion
et to more major open surgery.
et
ture,
retained
n
n
n
.
.
.
X
X
ok Colectomy
oorkall of the colon (Fig. 2.11). ookX
o
o
Operation to remove part
B Indications Malignancy,
B
no.longer be managed
w.Bperforation, IBD which can
w
w
w
medically.
w
w
ww
B
2
Pre-​op Full bowel prep rarely required, 6h fasting pre-​anaesthetic (E p. 111).
Procedure This involves a midline longitudinal laparotomy incision and
resection of the diseased bowel if done open, can be done laparoscopically. A stoma may or may not be formed.
Post-​op Sips of fluid orally for 24h post-​op, gradually built up to free fluids
and then light diet. Hospital stay 3–​7d (‘enhanced recovery pathways’
used to streamline post-​op recovery). All patients followed up in clinic.
Complications Haemorrhage, wound infection, wound dehiscence, anastomotic leak.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
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t
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o
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X
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.
w
ww
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ww
t
et
n
.
X
ok
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
ok
Bo
w
t
o
w.B
t
.ne
X
k
ww
o
w.B
ww
et
et
et
n
n
n
.
.
.
X 2.11 Common large bowelkresections
X (the shaded area represents
X
ok Fig.
o the operation).
ok the
o
o
o
section
of
colon
removed
during
B
w.B
w.B
w
w
w
w
ww
B
122
.B
w
ww
Chapter 2
Life on the wards
.B
w
w
ww
w
t
t
t
Anterior
.ne resection X.ne
.ne
X
X
the rectum
k 5cm) and
ok Operation totheresect
ok with a sufficient margin (usually
oSee
o
left side o
of the colon with the rectal stump.
Fig. 2.12.
Bo anastomose
B
B
.
.
Indications Rectal w
carcinoma.
w
Pre-​op Full bowel
wwprep rarely required, phosphate
ww enema 1h pre-​op, 6h ww
fasting pre-​anaesthetic (E p. 111).
Procedure
involves a midline longitudinal
incision and reetofThis
et open.laparotomy
et
section
the diseased rectum if .done
Can be done laparoscopn
n
n
.
.
Xically.
X
X
ok Post-​op Sips of fluid orallyoforok24h
otok free fluids
post-​op, gradually builtoup
o
B
and then light diet. Hospital
4–​10d. All patients followed
up in clinic.
w.B stay
w.Bdehiscence,
Complications Haemorrhage,
wound infection, w
wound
anasw
w
w
ww
tomotic leak.
Anterior resection
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
t
et Anterior resection. .net
Fig.
.n2.12
.ne
X
X
X
resection
ok Abdominoperineal
ok (AP resection) ookcolostomy.
o
to resect the
rectum/​anus and form a permanent
Bo Operation
B
.
.B
See Fig. 2.13.
w
w
Indications Low
wwrectal carcinoma where it would
wwbe impossible to resect ww
the tumour without removing the anus, can also be performed as part of
a panproctocolectomy
for ulcerative colitis.
t
et phosphate enema 1h pre-​.onp,e6ht
Pre-​
ope Full bowel prep rarely required,
n
.
.nstoma
X
X
X
fasting
pre-​
a
naesthetic
(E
p.
111),
nurses to be involved.
k longitudinal
ok Procedure This involves oa omidline
okincision and
laparotomy
o
o
B
.B
resection of the diseased
w.B rectum and anus. wwbuilt
w
Post-​op Sips of w
fluid orally for 24h post-​op, gradually
up to free fluids
wdiet. Hospital stay 4–​10d. All w
and then light
patients followed up in clinic. w
Complications Haemorrhage, wound infection, wound dehiscence, stoma
et
et
et
retraction.
n
n
n
.
.
.
X
X
X
ok
ok AP resection
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
Fig. 2.13 AP resection.
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
t
.ne
Stomas
X
k
o
w
Stomas
t
.ne
X
k
w
123
et
.n
kX
oo
oo
B
B
.
.
Common locations LIF
ww or right hypochondrium.www reversal; mucosa ww
Features Mayw
be permanent or planned for subsequent
sutured directly to skin.
t solid stool; intermittently
t
eSoft/​
epassed.
et
Output
n
n
n
.
.
.
X
X
kX enColorectal cancer,
disease, trauma,oradiation
ok Indications
okdiverticular
o
o
o
teritis,
bowel
ischaemia,
obstruction,
Crohn’s
disease.
B
.B
w.B
Ileostomy ww
w
w RIF.
w
ww
Common locations
Featurest May be permanent or plannedt for subsequent reversal; bowel
e sutured to form a ‘spout’.toneavoid skin contact with bowel.nconet
mucosa
n
.
tents
which
are
irritating
(not
flush
with
skin).
X
X
kX
ok Output Liquid stool (may obeobile-​
ok
o
o
s
tained);
passed
continuously.
B
B
.B
wcancer,
w.enteritis,
Indications GI tract
IBD, trauma, radiation
bowel isw
w
chaemia, obstruction.
w
w
ww
Bo
Colostomy
Urostomy
t
t
t
Sometimes
pelvis.
.ne referred to as a nephrostomy
.ne if originating in renal X
.ne
X
X
ok Common locations Left or oright
okflank, lower anterior abdominal
okwall.
o
Bo Features A uretericw.catheter
B may be protrudingwfrom
B
. the skin into
the stoma.
ww
ww
ww
Output Clear urine passed continuously.
Indications
Renal tract cancer, urinary tract
ethydronephrosis,
et obstruction, spinal column
edis-t
n
n
n
orders,
urinary fistulae.
.
.
.
X
X
X
ok Common complications
ok
ok
o
o
o
B •Electrolyte/​fluidwimbalance
.B (E pp. 399–403​) w.B
• Ischaemia/​necrosis shortly after formation
w
• Obstruction/​
w prolapse/​parastomal hernia ww
ww
• Skin erosion/​infection
• Psychosocial
t
et implications. .neare
ethet
n
It .isnimportant to refer patients who
likely to need stomas .to
X care nurse prior to thekoperation.
X
X need
Patients with stomas
ok stoma
oexcess flatulence
okalso
o
o
o
to alter their diet to avoid
or overly watery
stool, so
B should also be referred
.B to the dietician. Troublesome
.B ‘high-​
output’
w
w
stomas leadingw
w to fluid balance problems worwexcessive need for bag ww
emptying require specialist gastroenterologist advice.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
t
.ne
X
k
o
Bo
oo
B
.
w
et
n
.
kX
t
.ne
X
k
ok
et
n
.
X
ok
ww
t
.ne
X
k
oo
oo
B
.
w
o
o
w.B
o
ww
oo
B
.
ww
t
.ne
X
k
ww
w
et
.ne
X
k
oo
B
.
w
.n
kX
ww
t
e
X.n
Bo
o
B
.
w
ww
t
ww
et
n
.
kX
t
et
t
.ne
X
k
ok
Bo
ww
.ne
X
ok
.n
kX
ww
o
ww
.B
w
ww
o
B
.
w
o
et
n
.
kX
oo
e
X.n
o
w.B
ok
Bo
o
w.B
.n
kX
ww
ww
Bo
et
t
et
n
.
X
ww
w
ww
o
Bo
B
.B
w
w
.ne
X
k
t
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Chapter 3
w
125
t
t
t
.ne History and
.ne examination
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
Basic history 126
examination 128
t Basic
e
et
et
Recording your clerking 129
n
n
n
.
.
.
X Medicine
X
X
ok
ok
ok
Cardiovascular o
130
o
o
B
Respiratory .132
w B 133
w.B
Gastrointestinal
w
w
w
w
ww
Neurological
134
Endocrine 139
Skin 140
t
t
e
e142
et
n
n
n
Oncological/​haematological
.
.
.
X Surgery
X
X
ok
ok 143
ok
o
o
o
Breast
(male
and
female)
B
.B
Eyes 144w
w.B
w
w
Head
and
neck
146
w
w
ww
Musculoskeletal 148
Urological 156
net Other specialties
net
.
X
Female reproductiveksystem 158
Obstetric 160 oo
B
.B
Psychiatric 162
w
Neonatal
examination
165
ww 166
Paediatric
t
t
.ne
.ne
X
X
ok
ok
o
Bo
B
w.
w
w
.
kX
o
o
t
e
X.n
ok
Bo
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
ww
et
oo
B
.
w
.n
kX
ww
ww
t
ww
et
n
.
X
ok
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
w
o
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
126
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne history
.ne
.ne
Basic
X
X
X
ok
oisk an essential skill as a junior
okdoctor and
a thorough history
o
o
Bo Taking
B
B
. basic features of
something you will become
extremely practised at.The
w. of how
wexamination
a history, withw
details
to perform a basic
are dew
w
w chapter. How to refine thesewapproaches is further
scribed in this
de- w
scribed for specific situations you may encounter.
t
et a history (E OHCM10.np.e26)
et
Taking
n
n
.
.
X•Try to be in a setting that offers
X privacy and has a bed
ok • Establish the patient’s name
okand check their date of birthookX
o
o
• Introduce yourself.and
questions.
B
B begin with open-​ended w
.B
wWhy
Presenting complaint
has the patient comew
to hospital? Let them tell
w
w
their story. w
Write their main problem(s) inw
their own words along with w
duration of symptoms and who referred them; if the referral letter has a
different
this too.
et presenting complaint then.ndocument
et
et
n
n
.
.
History
of
presenting
complaint(s)
Ask
questions
aimed
at
differentiating
X
X
kX Try
ok the causes of the presenting
ok complaint and assessing oitsoseverity.
o
o
to exclude potentially
B
.Blife-​threatening causes first. Ask.Bspecifically about
previous episodeswand investigations/​treatments.wUse the SOCRATES
w
questions for
w pain (Site, Onset, Character,
wwRadiation, Associations, ww
Timing, Exacerbating/​relieving factors, Severity). Ask about the effect
on their activities of daily living (ADLs). If there are multiple problems,
ask if they come on together or are related.
t
t
t
.ne
.ne
.ne
X
X
X
ok Risk factors Document recognized
ok risk factors for important
okdifferentials.
o
o
Bo Past medical historywAsk
B
B
operations
. about previous medical
. ICU admissions,
wproblems/​
and attempt tow
gauge the severity of each (eg w
hospital/​
exercise tolerance
w (ET), treatment); use thewdrug history to prompt the ww
patient’s memory. Consider documenting specifically about asthma, DM,
angina,tiBP, MI, stroke, VTE, epilepsy, tmalignancy.
t
.nehistory Document all drugsXalong
.ne with doses, times taken,Xand
.neany
Drug
X
document
drug allergies along with
ok recent changes.OrAlways
okdrug allergies
okthe reaction
o
o
no known
(NKDA). B
Remember
to ask
Bo precipitated.
B
. Ask about compliance too.
.
about OTC medications.
w
w
w
w (eg heart problems, ww
Family historyw
Ask about relevant illness in the
wfamily
DM, cancer). What age were they at diagnosis? Are other family members well
et at the moment?
et
et
n
n
n
.
.
.
Social
history
This
is
essential:
Home
Ask
about
who
they
live
with,
the
Xresidential home), any homekhelp,
X own
kXkind of house (eg bungalow,
k
o
o
o
o (stick/​frame),
(cooking, dressing,
Bo ADLs
.Bowashing); Mobility Walking
.Baids
exercise tolerancew(how far can they walk on level
ground? Can they
w
w wk), smoking (cigar- ww
climb stairs?);
Lifestyle Occupation, alcoholw
(units/​
ww
ettes/​d and pack-​years), recreational drugs:
• Alcohol: 1 unit = ⅓ pint of beer, ½ glass of wine, 1 measure of spirits.
• Smoking: 20 cigarettes/​d for 1yr = 1 pack-​year.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Basic history
w
127
t
t
et
Systems
the.n
HPC;
.ne review Relevant systemsXreview
.ne will often be part of X
X
review iskonly necessary if you are unsure
what is
ok a thoroughor systems
o explain the symptoms. SeeoTable
ok 3.1
are strugglingoto
and
Bo relevant
B
B
.
E OHCM10 p. 28. .
w
w
w
Table 3.1 w
Key symptoms to assess on systems
review
ww
ww
pain, palpitations, SOB, ankle swelling, orthopnoea
CVS
t Chest
e
et SOB
et
Resp
Cough (?blood), sputum, wheeze,
n
n
n
.
.
.
X
X bowel habit (?blood), stool kX
pain, nausea/​vomiting,
ok Abdo Abdo
ok distension,
o
colour and consistency,
dysuria, frequency,ourgency,
o
o
haematuria .B
B
B
.
wphotophobia, neck stiffness, weakness,
w change in
Neuro
Headache,
sensation,
ww balance, fits, falls, speech, changes
wwin vision/​hearing
ww
Systemic Appetite, weight loss/​gain, fever/​night sweats, malaise, stiff/​swollen
et joints, fatigue, rashes/​itch, sleep
etpattern
et
n
n
n
.
.
.
X
X
X
Ask if there are
any other problems that have
not been
ok Summarizing
oaksummary
okpatient
o
o
o
discussed
and
repeat
back
of
the
history
to
the
to
B check that they agree
B
B
.
.
(Box 3.1). It is a good idea tow
use the ICE questions
w
(Ideas, Concerns,
ww Expectations) at this point—​
wwask the patient if they ww
have any idea or suspicion of what might be wrong with them, if there’s
anything in particular that they’re worried about (this may prompt them
to admit specific concerns, eg having cancer), and what they expect will
happen to them while they are in hospital. The art of ‘ICE’ is to ask naturally, so patients feel able to open up to you. Doing this while examining
the patient can work well for some.
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
Most patients have
w no idea about tests and investigations
ww and find being w
admitted to w
hospital a frightening event; theyw
often value the opportunity w
to talk about possible options and ask questions.
Always
specifically
if the patient has e
any
tfinish your history by asking
t
t
further
.ne questions or any otherXissues
.nethey would like to discuss,
.asnfreX
X
shy/​reticent to ask. k
ok quently they will be too embarrassed/​
ok
o
oo
Bo T Box 3.1 Should
B
B
.
.
wclerking?
ww you take noteswwhile
wwhile
ww
There is now
simple answer to this. Taking notes
the patient talks
may allow you to record important details accurately or even to write
up your
extremely useful during busyt
t allows
et clerking as you go. This can
ebe
n
n
on-​
calls. Alternatively, not taking.notes
you to give the patient
.
.ne
X
X
X
your
undivided
attention
and
the
opportunity
to
record
the
clerking
ok
okpicture. In the end it comesodown
ok to indiconsidered the whole
o
Bo having
B
B
.
.
vidual preference and workload.
w
w
ww
ww
ww
B
After the history
et
n
.
kX
o
Bo
By the end of taking the history you should have a reasonable idea of the
differential diagnosis. Try to think of specific signs that would be present
on examination to confirm or refute these differentials. A basic examination is described in the next topic (E p. 128).
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
128
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne examinationX.ne
.ne
Basic
X
X
ok is good practice to perform
oka brief CVS, RS, abdo, and neuro
okexam on all
o
o
Bo Itpatients
B
B
but focus your
examination according to their history.
w.RR,
w. Check obser- w
vations (temp, BP,
HR,
O sats):
w
w
•Ask a nurse
wto chaperone you if necessary w
w
• Get consent before touching the patient, ask where it hurts
• First tassess briefly whether the patient tlooks well or ill.
e (E p. 154)
e
et
n
n
n
Hands
.
.
.
X
kXof disease.
kX
Of the hands forosigns
ok Inspection
o
o
o
o
Palpation Check the pulse
for rate, rhythm, and character (eg
?collapsing pulse).
B
w.B
w.B
Mouth
w
w
w
w cyanosis, mucous membranes,
w
Inspection Central
stomatitis, beefy w
tongue (diron), candidiasis, ulcers, dental hygiene (risk factor for SBE).
t
Cardiovascular
system (E pp. e
130–1)
et
et
n
n
n
.
.
.
Inspection
JVP
(very
useful
if
visible),
swollen
ankles.
X
X
X
ok Palpation Temp of hands,ocapillary-​
ok refill, carotid pulse (volume
ok and charo
o
acter), apex beat, heaves/​
B
.B thrills, hepatomegaly.
w.B(timing, volume, w
Auscultation Heartwsounds, added sounds/​
murmurs
w
w
­radiation), carotid
w bruits, basal crackles. w
w
2
Respiratory system (E p. 132)
t
t
Inspection
(flap), stridor, JVP,eRR
effort (accessory muscles,
n t andoedema.
.ne Asterixis
.peripheral
.ne
recession),
chest wall movement,
X
X
X
k
expansion. ok
ok Palpation Trachea, cervicalhyperresonant,
olymphadenopathy,
o
dull,
stony
dull.
Bo Percussion Symmetrical,
B
. crackles, wheeze, bronchialwbreath
.Bosounds, rub.
w
Auscultation Air entry,
w
ww
ww
Abdomenw
(E p. 133)
Inspection Jaundice, scars, distension, hernias, oedema.
t
t patient’s face: tenderness,
t
Palpation
away from pain and
.ne Start
.newatch
.ne
peritonism
(guarding, rebound,X
rigidity,
percussion tenderness),
masses,
X
X
ok liver, spleen, kidneys andoAAA
ok (expansile mass), hernias,o±okgenitalia, PR
Bo (masses, stool, tenderness,
B
. prostate, blood/​mucus/​
.mBelaena).
w
wspleen.
Percussion Ascites
(shifting dullness, fluid thrill), w
liver,
w
ww
Auscultation w
Bowel sounds (absent, reduced,w
increased, tinkling).
Peripheral nerves (E pp. 136–8)
et Posture, movement of limbs.
et
et
Inspection
n
n
n
.
.
.
X
Tone; power (5 normal,
2X
not even
kX4 weak, 3 against gravity only,
ok Palpation
oksensation.
against gravity, 1 twitch, o
0o
none); reflexes (tendons, plantars);
o
o
B
Coordination Finger–​n.ose,
slide heel down opposite leg.
w(EBp. 135)
w.B
w
w
Cranial nerves
w
w
ww
et
n
.
kX
o
Bo
Inspection GCS, mental state (E pp. 163–4), facial symmetry, scars,
­obvious gaze palsies, speech, posture.
Eyes (II, III, IV, VI) Acuity, pupil reactivity, fields, movements, fundi.
Face (V, VII) Sensation and power.
Mouth (IX, X, XII) Tongue movements, uvula position, cough.
Other (VIII) Hearing, balance, gait (XI), shrug, head movements.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
Recording your clerking
w
w
129
t
t
t
.ne
.ne
.ne
Recording
your
clerking
X
X
X
ok initial clerking of a opatient
ok is one of the most important
ok steps in
o
Bo The
B
B
their journey through. the hospital. It will be reread .by every team that
w and used as a benchmarkwfor
w measuring the pro- w
looks after the w
patient
w gives
gress of thew
patient’s condition. A good clerking
the patient the w
best opportunity to receive the correct investigations and treatment.
et Your name, position, location,
et date, time; state clearly why
ethet
Heading
n
n
n
.
.
.
patient
is
being
clerked
(eg
referred
from
ED
with
chest
pain).
X
X
X
ok Format Follow a logicaloorder
ok setting out each section under
ok the heado
o
B ings shown in this w
.BIf a piece of information from
topic.
w.Ba different section w
is really important
then write it in the historyw
of presenting complaint
w
wthe social history.
w
w
and/​or under
Sources
State where you got important
information from (eg patient,
et(with
etnotes,
et
relative
name and relationship),
computer records).
This
n
n
n
.
.
.
makes
it
easy
to
check
if
the
information
is
of
critical
importance.
X
X
X
ok Use the notes Don’t rely
oonk a patient’s account of theiroprevious
ok medo
o
B ical history, especially
.B
.B to find the offifor investigations and results.
winvestigations
wonTry
w
w
cial record of key
rather than relying
another doctor’s
w
w
ww
comments.
et
cord
least.
nalletof the information described
nonetthese pages at the very X
nUse
.
.
.
X
X
‘nothing abnormal
by all means, but
be
ok ‘NAD’ totorecord
ok youdetected’
okdo not(‘not
write it for aosystem
have not examinedoproperly
Bo tempted
B
B
actually done’)—​this .is inaccurate and dishonest and.even if the system
w
seems unrelatedwtowthe presenting complaint, may
lead to problems later
ww problem with that ww
if the patientwsubsequently develops an unexpected
system causing colleagues to refer back to the admission clerking.
t obvious What appears
t
t
State
now may not be
.ne the
.nenextobvious
.neto
someone
reading the notes or on
the
shift, eg below-​knee prosthetic
X
X
X
ok leg, crying constantly. ook
ok
o
Bo Differential diagnosis
B
B
. to explain the
What diseases are likely
w.What serious
w
patient’s symptoms?
diseases need
to be excluded? Make
w
w
wafter the examination. Considerwrecording the most critical ww
a list of these
evidence for and against each diagnosis.
t
et
ewillt
Management
plan This should.n
beea detailed list of the steps you
n
n
.
.
written in
Xtake to diagnose and treat thekdifferential
X diagnosis. It should bekX
ok order of priority. Alongside
oinvestigations and treatment consider
o nursing
o
o
o
B measures, frequency
Bevent of deteriin the
.ofBobservations, what to doward,
.HDU).
w
w
oration, referrals,
best location (eg respiratory w
If you have
w
referred the w
patient to another specialty, record
w the name, bleep, and time ww
Be thorough These pages represent a basic clerking; you should re-
patient was accepted. Likewise if you have handed the patient over to a
colleague at a shift change.
et
et
et
n
n
n
.
.
.
X
X
X
ok are not telling the patient oabout
ok a serious illness then stateowhy.
ok
o
B E p. 76 for otherwtips.Babout writing in the notes.w.B
ww
ww
ww
State what the patient was told This prevents confusion. If you
B
130
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne
.ne
.ne
Cardiovascular
X
X
X
ok
ok
ok
o
o
Bo History
B
B
w.or heaviness, dyspnoea (exertional,
w. orthopnoea, par- w
Symptoms Chest pain
w
w
oxysmal nocturnal)
(see
Table
3.2),
ankle/​
l
imb
swelling,
w
w palpitations, syncope w
or presyncope, limb pain (at rest or on exertion), fatigue, numbness, ulcers.
Past medical
IHD, MI, hypertension,
palpitations, syncope, clotet history
etsurgery,
et
ting
problems,
rheumatic fever, cardiac
recent dental work,
liver
n
n
n
.
.
.
X
X
kX disease.
ok problems, renal problems,oothyroid
ok
o
o
Table 3.2 Functional
B
.Bclassification of heart failurew(NYHA)
.B
wpresent
Class I
Disease
but no symptoms duringw
ordinary activity
w
w
w
ww
Class II
Angina or dyspnoea during ordinary activity (eg walking to shops)
Class III Angina or dyspnoea during minimal activity (eg making cup of tea)
eIVt Angina or dyspnoea at rest.net
et
Class
n
n
.
.
X data from Dolgin M, et al. Nomenclature
Xof the
and criteria for diagnosis of diseases
kX Williams
ok Source:
oLippincott
oMA),k 1994,
heart and great vessels, 9th edition,
and Wilkins (Boston:
and
o
o
o
B
B
B
Criteria Committee, New.York
Heart Association, Inc. Diseases of the
heart and blood vessels.
.
wfor diagnosis, 6th edition, Little, BrownwandwCo. (Boston: MA), 1964.
Nomenclature and criteria
ww
w
ww
B
Drug history Cardiac medications (and compliance), allergies (and reaction).
Social history Tobacco, alcohol, and caffeine consumption, illicit drug use
(?IV, cocaine), occupation, exercise tolerance on flat and stairs.
Family history IHD, ilipids, cardiomyopathy, congenital heart disease,
sudden cardiac death.
Coronary artery disease risk factors Previous IHD, smoking, iBP, ilipids,
family history of IHD, DM, obesity and physical inactivity, male sex.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
K Box 3.2 Palpation of central and peripheral pulses
ww
t
t
t
Central
.ne
.ne
.nande
• Carotid Two fingers, medial X
to the sternocleidomastoid muscle
X
X
ok lateral to the thyroid ocartilage
ok (do not palpate both sides
oktogether)
o
of
both
hands,
applied
halfway
between
Bo • Abdominal aortawFingertips
B
B
.
w.
umbilicus and xiphisternum.
w
w
w
w
ww
Arms
• Radial Two fingers pressed on the radial aspect of the inner wrist
t aspect of the inner wristnet
• Ulnar
ulnar
et Two fingers pressed on the
ethe
n
.
.
•.n
Brachial Two fingers pressed into
medial
X antecubital fossa, justkX
kX to the biceps tendon (ask
k
patient to flex arm against resistance
to
o
o
o
o
find the tendon). Bo
Bo
B
.
.
w
w
Legs
• Femoral Two
middle of the crease in
wwfingers pressed firmly into the
ww
ww
the groin, halfway between the symphysis pubis and the anterior
superior
spine
et Askiliacpatient
etput both your thumbs either.side
et
•.n
Popliteal
to flex their knee,
n
n
.
X the patella and press firmly
X fossa
your fingertips into the popliteal
kXwith1cm
ok • ofPosterior
opressed
ok malleolus
tibial Two fingers
posterior to the medial
o
o
o
B
.B2nd metatarsals.
• Dorsalis pedis Two fingers
w.B pressed between thew1stwand
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Cardiovascular
w
131
t
t
et
Examination
(lying at 45°) .n
.ne
.ne
X
X
X
cyanosis, pallor, facial flushing,
ok General inspection Dyspnoeaooatkrest,
ok Marfan’s,
o
rheumatological disorders, acromegaly.
Bo Turner’s, Down’s syndromes,
B
B
.
w. Box 3.2), clubbing, w
Hands Radial pulsesw
(right and left, collapsing pulse) (see
w
w
splinter haemorrhages,
Osler’s
nodes,
peripheral
cyanosis,
xanthomata.
w
w
w
Face Eyes (pallor, jaundice, xanthelasma), malar flush, mouth (cyanosis,
t palate, dentition). net
high-​aerched
et
n
n
.
.
.
Neck
JVP,
carotids
(pulse
character)
(see
Box
3.2).
X
X
X
ok Precordium Inspection (scars,
ok deformity, apex beat), opalpate
ok (apex
o
o
B beat, thrills, heavew(Table
.B 3.3)), auscultate (heartwsounds
.B (Table 3.4),
murmurs—​alsow
auscultate with the patient in both
left lateral and sitting
w
w
w
ww
forward positions).
Back Scars, sacral oedema, pleural effusions, pulmonary oedema.
t kidneys, percuss for ascites,
et Palpate liver, spleen, aorta,
eballot
et
Abdomen
n
n
n
.
.
.
X and renal artery bruits,
X
kXradiofemoral delay.
ok femoral
oBox
ok oedema,
o
o
o
Legs
Peripheral
pulses
(see
3.2),
temperature,
ulceration,
B calf tenderness, venous
.Bof hair, gangrene,
loss
w.Bguttering, thin shiny skin,
w
w
varicose veins, w
eczema, haemosiderin pigmentation
of the skin (particuw
w
ww
B
larly above the medial malleolus), lipodermatosclerosis (‘inverted champagne bottle leg’).
Blood pressure Lying and standing, consider also left and right arms separately.
Other Urine analysis, fundoscopy, temperature chart.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
Table 3.3 Characteristics of valve defects
oo
B
.
ww
t
.ne
X
k
w diastolic rumbling murmur, loud
wMid-​
w 1st HS, opening snap,
ww
malar flush, AF, tapping apex, left parasternal heave
murmur radiating
to the axilla, soft 1st HS, 3rd HS t
et Pansystolic
etparastenal
present, thrusting apex,nleft
heave
n
.
.
.ne
X
X
X
Ejection
systolic
murmur
radiating
to
the
neck,
4th
HS,
ok
ok slow rising pulse, systolic thrill
ok
reversed HSosplitting,
o
Bo
B
B
. murmur (best heard in expiration),
. collapsing
Early diastolic
wwide
wCorrigan’s
pulse,
BP, pistol-​shot femoral pulse,
sign,
w
w
wQuincke’s sign, de Musset’s sign w
ww
et3.4 Heart sounds
et
et
Table
n
n
n
.
.
.
X
X
X
blockingkof blood flow after closing of the mitral
ok 1st (S ) Physiological;
o
ok (M )
o
o
and tricuspid (T )o
valves
B
2nd (S ) Physiological;
blocking of blood flow after closing
w.B
w.ofBthe aortic (A )
w
and pulmonary
(P ) valves; aortic precedesw
pulmonary and splitting
w
w
ww
Mitral
stenosis
Mitral
regurgitation
Aortic
stenosis
Aortic
regurgitation
1
1
1
2
2
2
et
n
.
kX
o
Bo
can be heard during inspiration
3rd (S3) Sometimes pathological; caused by blood rushing into the ventricles
after S2; suggests increased volume of blood in athletes, pregnancy
or heart failure
4th (S4) Pathological; blood pushing open a stiff ventricle before S1; suggests
LVF, aortic stenosis, cardiomyopathy
et
n
.
kX
o
o
B
.
w
ww
w
ww
t
.ne
X
ok
.Bo
ww
B
132
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne
.ne
.ne
Respiratory
X
X
X
ok
ok
ok
o
o
Bo History
B
B
.
.
Symptoms Cough,w
sputum, shortness of breath,wwheeze, chest pain,
w
w
fevers and sweats,
weight
loss,
hoarseness,
snoring,
w
w day sleepiness (ob- ww
structive sleep apnoea).
t
t
Past medical
history Chest infections/​
(as child or adult),etuet HIV
epneumonias
n
n
n
.
.
.
berculosis,
status and risk factors,
allergy, rheumatoid disease.
X
X
X
ok Drug history Respiratory drugs
ok(inhalers, steroids, etc), vaccination
ok history
o
o
o
(especially BCG, Hib,.B
drugs known .toBcause respiratory
B
w pneumococcus),
problems (bleomycin,
methotrexate, amiodarone,w
etc), allergies.
w
w
ww
Social historyw
Tobacco use (expressed in pack-​
years—​ie 20 cigarettes/​d w
for 1yr = 1pack-​year) and social exposure to tobacco smoke if non-​
smoker,
exposure to other family
e(TBt pets,
et members with respiratory.nprobet
n
n
.
.
lems
etc), illicit drug use (crack
cocaine, cannabis).
X
X
X
ok Occupational history Past oandokpresent
okabout dust
jobs, asking specifically
o
o
B
exposure, asbestos, .animal
w Batopy,dander.
w.B
w
w
Family history Asthma/​
cystic fibrosis, emphysema.
w
w
ww
Examination (lying at 45°)
t
t
t
.ne
.ne
.ne
X
X
X
k
peripheralocyanosis,
tar staining, wasting/​
ok Hands Clubbing,
owkeakness of
o
o
muscles, HR, B
fine
tremor of β-​agonists, flapping
tremor of CO
Bo intrinsic
B
retention.
w.
w.
w
w
w syndrome, anaemia), mouth
w (central cyanosis), voice. ww
Face Eyes (Horner’s
Neck Trachea position (± scars), JVP.
t
et
net radiotherapy marks),Xpalpate
Chest
Inspect (shape, .scars,
.neanteriorly nodes,
.napex
X
X
(supraclavicular
axillary
nodes,
expansion,
vocal
fremitus,
ok parasternal heave),opercuss,
ok auscultate.
ok
o
Bo beat,
B
B
Chest posteriorly Inspect,
w. palpate (including cervical
w. nodes), percuss, w
w
auscultate. ww
w
w
Other Peripheral oedema, calf erythema/​tenderness, temperature chart,
breast texamination (if suspect malignancy),
abdominal examination,
e(see Box 3.3), sputum pot. .net
et
n
n
PEFR
.
.
X
X
X
ok K Box 3.3 Recording
okPEFR
ok
o
o
o
B
wis.B
w.B mouthpiece. w
Ensure the meter
set to zero and fit a neww
disposable
w
Stand the patient
w up (or sit up if unable towstand) and give them clear w
General inspection O2 requirements, cough, audible wheeze or stridor,
rate and depth of respiration, use of accessory muscles, body habitus.
2
et
n
.
kX
o
Bo
instructions. They should take as deep a breath as possible, before placing the meter in their mouth and closing their lips around the mouthpiece. Encourage them to blow out as hard and as fast as possible.
Record the reading obtained, then document the best of 3 efforts.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
w
.B
w
w
Gastrointestinal
w
w
133
t
t
t
.ne
.ne
.ne
Gastrointestinal
X
X
X
ok
ok
ok
o
o
Bo History
B
B
.
w. association with eating,ww
Symptoms Abdo pain,
vomiting, or opening
w
bowels, weight
loss,
appetite,
bruising,
bleeding,
nausea, vomiting ww
w
w
(­appearance), dysphagia, odynophagia. dysuria, urinary frequency and
­urgency,t possibility of pregnancy. Stool Change
habit, frequency,
e colour, pain on passing,
etrecurrentin bowel
eort
consistency,
urge, blood (bowl
n
n
n
.
.
.
Xpaper), offensive smell, mucus.kX
X
ok Past medical history GI bleeds,
o GORD, varices, gallstones,oliver
okproblems,
o
o
B jaundice, IBD, haemorrhoids,
w.B polyps, blood transfusions.
w.B
w
w
Drug history w
NSAIDs, anticoagulants, hepatotoxic
w drugs (E p. 174), ww
­opioids, laxatives, recent antibiotics (Clostridium difficile).
t Foreign travel, illicit drugneuset (?IV), sexual history. net
Socialehistory
n
.
XAlcohol Intake per day (in units,kEXp.. 126), CAGE questions (EkXp. .372).
k
o
o
oo
liver disease,
Bo Family history IBD, w
Bo cancer.
B
.
.
w
Examinationw(lying flat on back)
General inspection
w Oedema, wasting, jaundice,
wwanaemia, lymphadenop- ww
athy, breath odour, mouth ulcers, gynaecomastia, spider naevi, bruises.
HandseClubbing,
nail colour, palm colour,
nt
net flap, Dupuytren’s. X.net
.
.
X
X
Distension (fat, faeces,
flatus, fluid, foetus), prominent
tenok Abdomen(guarding,
okmasses,
okveins,
rebound),
organomegaly (seeoTables
3.5 and
o
Bo derness
B
B
3.6), ascites, hernial orifices
(inguinal, femoral, incisional),
w. fissures
w. bowel sounds. w
w
PR Visible haemorrhoids,
and skin tags, w
anal tone, prostate, rectal
w
w
w
masses, appearance of faeces ± blood.
t3.5 Common abdominal masses—​
t if in doubt, check with USSnet
Table
.ne RUQ, extends to RLQ, X
.ne
Liver
unable to get above, dull to percussion
X
X.
k Spleen LUQ extends to RLQ,
k
k
o
o
o
unable
to
get
above,
notch
o
o
Bo Kidney RUQ and/​
Bsmooth
o.rB
LUQ, ballotable, able to get above.it,
outline
w
w
w
w
Faeces
Indentable
mass away from umbilicus
w
w
ww
Tablet3.6 Common causes of enlargedt liver and spleen
e
e
et
n
n
n
.
.
.
Hepatomegaly
Alcohol, hepatitis,
EBV, CMV, thin patient, autoimmune
X
X metastases, lymphoma, leukaemia,
X
hepatitis, toxins,
ok
ok liveramyloidosis,
ok chest,
haemochromatosis,
hyperexpanded
o
o
o
B
.B
weg.BCOPD, heart failure wwdisease,
Splenomegaly w Chronic liver disease, autoimmune
w thrombocytopenia, EBV, CMV,
w hepatitis, HIV,
ww
haemolytic anaemia, leukaemia, lymphoma,
endocarditis, thalassaemia,
cell, myelofibrosis,
t sickle
et
emalaria,
et
sarcoid, amyloidosis,
leishmaniasis
n
n
n
.
.
.
X
XCMV, chronic liver disease, leukaemia,
kX
ok Hepatosplenomegaly Hepatitis,
okEBV,
lymphoma,
myelofibrosis, amyloidosis oo
o
o
B
w.B
w.B
w
w
w
w
ww
B
134
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne
.ne
.ne
Neurological
X
X
X
ok
ok
ok
o
o
Bo History
B
B
w.Onset, duration, coursew(improving,
w.
Presenting complaint
worsening,
w
relapsing–​remitting),
aggravating
or
alleviating
factors,
change with time ww
w
w
of day, trauma.
t weakness, tremor, twitching,
Symptoms
pain, numbness, e
tingling,
et Headache,
et
n
n
n
.
.
abnormal
movements, loss of consciousness,
seizures, ­abnormal .smells,
X (loss, diplopia, flashing klights),
X hearing, swallowing, speech,
Xbalance,
ok vision
o
oork retention,
o
o
vertigo, nausea, vomiting,ocoordination, urinary incontinence
B
.B
impotence, faecalw
incontinence,
constipation, personality,
w.B memory, lan- w
w
w
guage, visuospatial
skills, change in intellect.
w
w
w
Collateral history In many neurological conditions the patient may not be
able totdescribe all the symptoms, eg seizure;
e or family member. .net try to get a history.from
eta
witness
n
n
.
X medical history Similar episodes,
X meningitis, migraines, strokes,
X
ok Past
ok DM,
ok seizo
o
o
ures,
heart
problems,
hypertension,
psychiatric
problems.
B
.B
w.B drugs (eg antiepileptics,
wParkinson’s
Drug history Neurological
medicaw
w
tions), psychiatric
w drugs (eg antipsychotics,wantidepressants), all others ww
(especially cardiac and hypoglycaemic drugs).
t Draw a family tree with
t grandparents and allntheir
t
Familyehistory
.n and grandchildren,
.neall four
. edischildren
askX
specifically
about learning difficulties,
X
X
k psychiatric problems. ok
ok ability, epilepsy, dementia,ooCVAs,
Bo Social history Alcohol,
B
. smoking, illicit drugs, occupation,
.Botravel abroad,
w
w
dominant hand.w
w
ww
ww
Examination
Obs GCS, BP (lying and standing), HR, RR, glucose.
t
et mobility aids. .net
General
.ne appearance Posture, neglect,
.nnutrition,
X
X
kMini-​Mental State Exam (Eokp.X377) or
Tested using the
ok Cognition
o
o
o
10-​point Abbreviated.B
Mental State Exam (E p. 375).
B
.Bo
w
w
Meningism Photophobia,
neck stiffness, Brudzinski’s
sign (involuntary
wwand knees when neck flexed
wwdue to neck stiffness), ww
flexion of hips
Kernig’s sign (unable to straighten leg when hip fully flexed in supine
­patient),
t on passively flexing thenhip).
et straight leg raise (hamstring
espasm
et
n
n
.
.
.
Skin
Birthmarks,
vitiligo,
café-​
a
u-​
l
ait
spots,
ash
leaf
macules,
lumps,
tufts
X
X
X
ok of hair/​dimples at the base
oofk the spine.
ok
o
o
o
B
B
See Table 3.7 for cranial
w.B nerve examination, andwFig.
w.3.1.
w
w
w
ww
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Neurological
w
135
t
t
t
.ne 3.7 Cranial nerve examination
.ne
.ne
Table
X
X
X
ok
ok
ok
Function
Tests
o
o
Bo Nerve
B
B
.
I w
Olfactory
Smell
Rarely tested
w.
w
IIw Vision
Optic
Visual
acuity,
visual fields,
w
w
ww
(Fig. 3.1)
pupil reflexes, fundoscopy
Oculomotor III Eye movements, lift the
movements, pupil
t
t Eye
e
e
et
eyelid, pupil constriction
reflexes
n
n
n
.
.
.
Move eye down and out
XTrochlear IV Superior oblique
X
X
ok Trigeminal V Sensation
otokface,
okpower,
Facial sensation,ojaw
o
o
B
corneal reflex
.B of jaw
wmovement
w.B
muscles
w
w
w eye laterally
ww
Abducens wVI Lateral rectus muscle
Move
VII Facial muscle movement, Facial power
Facial
t
taste (anterior ⅔), et
e
et
n
n
n
salivary and lacrimal
.
.
.
X
X
X
stapedius
ok Vestibulo-​ VIII glands,
ok muscle Whispering numbers,
okWeber’s
o
o
Hearingoand balance
B
.B
cochlear
(forehead),.Rinne’s
wTaste
w B (behind ear)
IX
w
w
Glosso-​
(posterior ⅓),
Saying
‘Ahh’, swallow, gag
w
ww
pharyngeal w
parotid gland, sensation
reflex
of pharynx, nasopharynx,
middle ear
t
t
t
e
X Sensation of pharynx
.n
.ne Saying ‘Ahh’ (uvula deviates
.ne
Vagus
X
X
X
and larynx, k
of away from defect), cough,
ok
omovement
ogagkreflex
pharynx,
larynx
swallow, speech,
o
o
Bo Accessory XI wpalate,
B
B
. of
Movement
Shrug shoulders,
w. turn head
sternomastoid and
w
w
w trapezius
w
ww
XII Movement of tongue
Hypoglossal
o
Bo
t
.ne
X
k
ok
ww
Visual field
Left
t
.ne
o
w.B
4
2
5
6
Bo
o
et
n
.
kX
3
w
ww
ww
et
.n
kX
ww
Left Right
e
X.n
Optick
chiasma
o
.BoLateral geniculate
Optic nerve
X
ok
Bo
oo
B
.
w
Normal
Right
1
Stick Tongue out (deviates
Towards defect), speech
et
X.n
t1
nucleus
Optic radiation
et
n
.
kX
Visual cortex
Bitemporal hemianopia
ok
3
5
6
et
n
.
X
Unilateral vision loss
2
4
Normal fields
o
w.B
Homonymous hemianopia
ww
Upper quadrantanopia
Lower quadrantanopia
Homonymous hemianopia
(with central sparing)
ww
t
.ne
X
ok
.Bo
Fig. 3.1 Optic pathways and effect of a lesion on the visual fields at various
locations.
o
o
B
.
w
ww
w
ww
ww
B
136
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
Peripheral
.ne nerve examination
.ne
.ne
X
X
X
tremor,k muscle wasting, fasciculation,k abnormal
ok Appearance Posture,
oo and symmetry, neglect..Boo
facial expression
Bo movements,
B
.
Hold out hands With
palms up and eyes closed; look
drift (pyramidal
w forof position
worwinvoluntary
w(loss
defect), tremor,
finger movement
sense). ww
w
w
Tone Tone at wrist, elbow, knee, and ankle (increased, decreased, clasp
knife, cog-​
beats is abnormal).
t wheeling), clonus at the nankle
eIsolate
esot (≥5
eyout
n
n
Power
each joint with one hand
that only the muscle group
.
.
.
X testing can be used for thekmovement;
X
X 3.8).
compare each sidek(Table
ok are
o of main limb movements.
o
o
o
o
See
Table
3.9
for
root
levels
B
B
w.Research
wof.Bmuscle power
Table 3.8 Medical
Council (MRC) grading
w
w
w No movement
w
ww
Grade 0
Grade 1
Flicker of movement
et2
etgravity
et
Grade
Movement but not against
n
n
n
.
.
.
Weakness but movement
XGrade 3
X against gravity
ok Grade 4
okmovement against resistance ookX
Weaknesso
but
o
B
B
Grade 5
Normal
w.Bpower
w.Nervous
w
w
© Crown Copyright.
The Aids to the Examination of the Peripheral
System
w
w
ww
(Memorandum No. 45) is licensed under the Open Government Licence 3.0. Used with the
permission of the Medical Research Council.
t
t
et
Table
.ne 3.9 Root levels of mainXlimb.nmovements
.ne
X
X
ok Joint Movement ookRoot Joint Movement
ok Root
o
Bo Shoulder Abduction
B
B
C5
Hip
Flexion
L1–​2
w.
w.
Adduction
C5–​7
Adduction
3
w
w
w
w Extension L2–​
ww
Elbow
Flexion
C5–​6
L5–​S1
C7
L5–​S1
tKnee Flexion
t
et Extension
Wrist
Flexion
C7–​8.ne
Extension
L3–​.4ne
n
.
X
X
X
Extension
Ankle
Dorsiflexion k L4
ok
okC7
o
oo S1–​2
Plantarflexion
C8
Bo Fingers Flexion
B
B
.
.
Extension
C7
Big toe Extension
L5
w
ww
Abduction
T1
w
ww
ww
Reflexes Deep tendon reflexes comparing each side (Table 3.10)—​if ­absent
asknthe
plantar reflexes.
etpatient to clench their teeth.n(reinforcement);
et
et
n
.
.
X
X
X
ok Table 3.10 Tendon reflexes
ok
ok
o
o
o
B
Grading of tendon reflexes
Root levels of tendon
w.B
w.B reflexes
0
Absentw
Reflex
Root Reflex Root
w
w
w
ww
et
n
.
kX
o
Bo
±
+
++
+++
++++
Present with reinforcement
Reduced
Normal
Increased
Increased with clonus
Bicep
Supinator
Tricep
et
n
.
kX
C5–​6
C5–​6
C7–​8
o
o
B
.
w
ww
w
ww
Knee
Ankle
L3–​4
S1–​2
t
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Neurological
w
137
t
t
et
Coordination
tapping, heel–​shin. .n
.ne Finger–​nose, dysdiadochokinesia,
.ne
X
X
X
is tested withopatient
k standing with eyes openothen
k closed,
ok Romberg’sif This
o
o
more unbalanced
with eyes closed; suggests sensory
Bo positive
B
B
. touch, vibration, joint position;
. the spinalataxia.
Sensation Pinprick, w
light
dermat­
w
wand back are shown in Fig.w
omes of thew
front
3.2.w
For spinal tract anatomy ww
and function, see Table 3.11 and Fig. 3.3.
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
ww
o
Bo
t
o
ww
o
w.B
ww
w
Fig. 3.2 Dermatomes of the front (L) and back (R).
t
.ne
X
k
oo
B
.
ww
t
.ne
X
k
et
.ne
X
k
ww
oo
B
.
w
.n
kX
ww
et
et
et
n
n
n
.
.
.
XFig. 3.3 Cross-​section of the spinal
Xcord showing spinal tracts. kX
ok
ok
o
o
oo
Table 3.11 Spinal tracts
and anatomy
B
B
B
.
.
w
ww
w
Tract
Modality
Crosses (decussates) at
w
w
ww
Lateral corticospinal (pyramidal) Motor
Medulla
Anterior
Motor t
Level of exit of the cord t
et corticospinal
e
n
n
Posterior
columns (dorsal)
Light.touch,
Medulla
.
.ne
X
X
X
vibration,
position
k
ok
ok touch, pain, Level of entry
ooto the cord
Bo Spinothalamic w.Bo Hard
B
.
temperature
w
ww
ww
ww
B
138
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
neFig.
Nerves
3.4.
.ne of the hand See Table 3.12
.and
.ne
X
X
X
k movements
ok Table 3.12 Innervation ofohand
ok
o
Bo Movement w.Bo
B
w. Nerve
w
w
Finger abduction
and
adduction
Ulnar
w
w
ww
Thumb opposition and abduction
Median
Finger textension
Radial
t
e
e
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Fig. 3.4 Sensation of the hand.
et
et
et
n
n
n
.
.
.
X This forms an essentiallykand
X highly informative part of ktheXexaminok Gait
o peripheral
o Table 3.13.
ation of both the centralo
and
nervous systems;osee
o
B
B
B
.
.
wexamination
w
Table 3.13 Gait
ww
ww
ww
B
Gait
Antalgic
Description
Painful gait, limping, short weight-​bearing
on painful side
Apraxic
Unable to lift legs despite normal power,
magnetic steps/​stuck to floor
Ataxic
Uncoordinated, wide based, unsteady (as
if drunk), worse with eyes shut if sensory
Festinating
A shuffling gait with accelerating steps
Hemiparetic Knee extended, hip circumducts and drags
leg; elbow may be flexed up
Myopathic
Waddling, leaning back, abdomen sticking
out
Shuffling
Short, shuffled steps, stooped, no arm
swing
Spastic
Restricted knee and hip movements, slow,
shuffling, ‘wading through water’
Steppage
High steps with foot slapping, ‘foot drop’
.
kX
o
o
net
oo
B
.
w
t
.ne
kX
ww
o
Bo
t
.ne
X
k
o
ww
Bo
o
et
n
.
kX
w
.ne
X
k
.ne
X
k
t
ww
ww
et
.n
kX
Proximal myopathy
Parkinson’s
ww
Pyramidal tract
lesion, eg MS
Peripheral
neuropathy
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
t
.ne
X
k
Parkinson’s
Hemiplegia, eg CVA
oo
B
.
w
ww
t
e
X.n
ok
Bo
oo
B
.
ww
t
o
w.B
Cause
Mechanical injury,
sciatica
Hydrocephalus,
frontal lesions
Cerebellar, sensory
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
t
.ne
Endocrine
X
k
o
w
Endocrine
t
.ne
X
k
w
139
et
.n
kX
oo
oo
B
B
.
.
Symptoms Weight w
loss, weight gain, appetite, sweating,
heat/​cold intol­
wweakness,
ww
erance, tremor,
tiredness, dizziness,
hirsutism, joint pain/​ ww
w
w
swelling, change in appearance (skin, hair, nails, face, eyes), change in
clothes/​
size, altered sensation,
t ulcers, visual problems. net
et shoe/​hatfeatures
ebreathlessness,
n
n
.
.
Cardiorespiratory
Chest pain,
palpitations,. sleep
X
X
kXapnoea.
k
o
o
ok
o
o
o
Diarrhoea,
B GI/​urinary features w
.B constipation, nausea,wvomiting,
.B abdominal
pain, thirst, polyuria.
w
w
winfertility, gynaecomastia, ww
Reproductive w
features Menstrual irregularities,
galactorrhoea, impotence.
et features Anxiety, mood changes,
et memory problems. .net
Psychiatric
n
n
.
.
X
kXfield defects, bulging eyes.okX
ok Eye features Blurred vision,oovisual
o
o affects lipid
(thyroid function
B Past medical historywHypercholesterolaemia
B
B
.
.
levels), thyroid surgery, stroke, heart failure, liver
w adrenal surgery, brainwsurgery.
wwfailure, renal artery ww
stenosis, renal
wfailure,
Bo
History
Drug history Steroids, diuretics, OCP, HRT, levothyroxine, insulin.
t
t
Family
net tumours.
.nehistory DM, thyroid disease,
.pituitary
.ne
X
X
X
k
ok Examination (lying atoo45°)
ok
o
habitus,
‘buffalo
hump’,
facial
appearance
Bo General inspectionwBody
B
B
.
.hyperpigmentation,
w
(‘moon face’), striae, bruising, muscle wasting,
w jaw and brow ridge,wgoitre,
w gynaecomastia, hir- ww
coarse skin, w
prominent
sutism, acanthosis nigricans, vitiligo, acne, necrobiosis lipoidica, pre-​tibial
myxoedema.
t
t
et
.neTemperature, sweating, size,
.ntremor.
.ne
Hands
X
X
X
ok Eyes Lid lag, proptosis, exophthalmos,
ok
ok cranial
bitemporal hemianopia,
o
o
palsy,
fundoscopy.
Bo nerve III, IV, or VI w
B
B
.
w.
Neck Goitre, thyroid
lumps.
w
w
w
w
ww
Cardiorespiratory idHR, idBP, postural hypotension, irregular pulse, peripheral toedema, bibasal crackles (LVF).t
e Cranial nerve III/​IV/​V.nI palsy,
e peripheral neuropathy,.nslow
et
n
.
Neurological
X
X
kX
ok relaxing reflexes, weaknessoo(myopathy).
ok
o
o
B Other Joints, skin,wgenitalia,
.B fundoscopy, urine analysis,
.B U+E, early
morning cortisol, TFTs, short Synacthen test (Ew
p. 585), GTT—​more
w
w
specialist tests
won advice from an endocrinologist.
w
ww
®
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
140
.B
w
ww
Chapter 3
ww
w
History and examination
t
.ne
Skin
X
k
o
.B
w
w
t
.ne
X
k
et
.n
kX
oo
oo
B
B
.
.
Presenting skin complaint
Timing How long present w
or gradual
ww or worse;
wsitefor,andsudden
onset, getting
better
Location Original
subsequent sites ww
w
w
affected; Symptoms Itch (localized or generalized), pain, burning, bleeding,
weeping;
factors Dietary components,
drugs, sunlight (seat Exacerbating
evariability),
et water; Relieving
et
sonal
pet dander, night-​
time,
factors Emollient
n
n
n
.
.
.
Xcream, topical/​systemic steroids.
X
X
ok Current health Anorexia, odiarrhoea,
ok fever, headache, fatigue,
okweight loss,
o
o
B
depression, sore throat,
w.B joint pain.
w.B
w
w
Past medical w
history Previous skin disease, DM,
w IBD, asthma/​atopy, vari- ww
cose veins, peripheral arterial disease, cardiac problems, endocrine
disease, coeliac disease, neurological problems, ulcers, trauma, sarcoid,
et SLE, malignancy, sensitivity
etof skin to sun exposure, .lifelong
et
porphyria,
n
n
n
.
.
history
of
sun
exposure
or
use
of
sun
beds.
X
X
kXtheir efok Drug history Dermatological
okagents being used at present
oand
o
o
o
B
Btopical steroids,
fects, previous drugs.B
and their effects, oral and
wtaken,usedimmunosuppressants,
w.allergies.
other drugs being
drug
w
w
w
w
ww
Bo
B
History
Allergy Hayfever, pet dander, dust mite, etc.
Occupational history Current and previous jobs and effect of work upon
skin, exposure to chemicals; hobbies and recreational activities.
Family history Anyone else in the family affected; need to differentiate
inherited pathology versus infectious pathology.
Travel history Recent foreign travel and relationship of any travel to skin
disease—​vaccinations/​prophylaxis taken for foreign travel.
Function Restricted actions, effect on life, mobility, occupation, dominant
hand, hobbies/​sports, smoking, social support.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
t
t
.ne
.ne
.ne
Examination
X
X
X
k
k combody should beoexamined
in good natural light;o
patients
ok The whole
o arm may well
otale
of a rash on.B
their
have other.B
tell-​
signs elseBo plaining
where on the body.
w Ask patients to fully undress
wto enable a full skin w
w
w
inspection. w
Remember the importance of gaining
w consent and having a w
chaperone present.
Distribution
Solitary lesion, flexor aspects
of limbs/​
trunk, extensor
et of limbs/​
et gutters
et
n
n
n
aspects
trunk, scalp/​eyebrows/​
of nose, sun-​exposed
.
.
.
X tip of nose, helix of ear,kwebspaces
X
X
of hands or feet, periumbilical.
ok sites,
o the appearance
ok using the
o
o
o
Morphology
Noting
or
describing
of
the
rash
B
.B diagnoses.
terms defined in Boxes
of w
differential
w.B3.4–​3.7 refines the list w
w
Hair Alopecia
w(hair loss) may be generalized orwlocalized and scarring/​non ww
scarring. Hirsutism (hair in the typical male distribution), hypertrichosis
(excessive
t hair growth).
eClubbing,
et nail loss, thinning of nail.nplate,
et
n
n
.
.
Nails
pitting, ridging, onycholysis,
X
X
X
ok discolouration.
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Skin
w
141
t
t
net
.nelesions
.ne
K. Box 3.4 Non-​palpableXskin
X
X
ok
ok from blood leaking intoothe
okskin.
Bruising; discolouration
o
Bo Ecchymosis
B
B
. area of altered skin pigmentation.
Macule Flat, well-​dw
efined
w.
w
w
Petechia Non-​
b
lanching,
pinpoint-​
s
ized
purple
macule.
w
w
ww
Purpura Purple lesion resulting from free red blood cells in the skin,
non-​blanching.
et Abnormal visible dilatation
et of blood vessels (spider naevi).
et
n
n
n
.
.
.
Telangiectasia
X
X
X
ok
ok
ok
o
o
o
B
K Box 3.5 Palpable
w.B skin lesions ww.B
w
Nodule Solid,
wmostly subcutaneous lesion (>0.5cm
w diameter).
ww
Papule Raised, well-​defined lesion (<0.5cm diameter).
Plaque
etRaised, flat-​topped lesion, usually
et >2cm diameter.
et
n
n
n
.
.
.
Weal
Transient,
raised
lesion
with
pink
margin.
X
X
X
ok Urticaria Weals with paleocentres
ok and well-​defined pink margins.
ok
o
o
B
w.B
w.B
w
w
K Box 3.6
w Blisters
w
ww
B
Abscess Fluctuant swelling containing pus beneath the epidermis.
Bulla Fluid-​filled blister larger than a vesicle (>0.5cm diameter).
Pustule Well-​defined pus-​filled lesion.
Vesicle Fluid-​filled blister (<0.5cm diameter).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Abrasion Scraping off superficial layers of the skin (a graze).
Atrophy Thinning and loss of skin substance.
Crust Dried brownish/​yellow exudates.
Erosion Superficial break in the continuity of the epidermis.
Excoriation Linear break in the skin surface (a scratch).
Fissure Crack, often through keratin.
Incisional wound Break to the skin by sharp object.
Laceration Break to the skin caused by blunt trauma/​tearing injury.
Lichenification Skin thickening with exaggerated skin markings.
Scale Fragment of dry skin.
Ulcer Loss of epidermis and dermis resulting in scar.
t
.ne
X
k
t
o
ww
o
w.B
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
w
et
.n
kX
ww
t
e
X.n
ok
Bo
ww
w
K Box 3.7 Skin defects
Bo
t
.ne
X
k
.ne
X
k
t
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
142
.B
w
ww
Chapter 3
.B
w
w
w
History and examination
ww
t
t
t
.ne
.ne
.ne
Oncological/​
h
aematological
X
X
X
ok
ok
ok
o
o
Bo History
B
B
.
w. fatigue, cough, w
Symptoms Weightwloss, anorexia, weakness, lethargy,
w
w
haemoptysis,
shortness
of
breath,
postural
dizziness,
nausea, vomiting, w
w
w
diarrhoea, constipation, PR bleeding, lumps, swelling, pain, fractures, tbone pain, polyuria, prostatism,
bruising, recurrent epistaxis,
e
etrecurrent
et
haemarthrosis,
heavy menstrual .loss,
miscarriage, recurrent
n
n
n
.
.
XVTE, fevers, infections, focalkneurology.
X
kX
ok Past medical history DM, oasthma,
o iBP, IHD, liver disease,oojaundice,
o
thyB
.B malignancy (and radiotherapy),
.B epilepsy, gastric
roid problems, anaemia,
w
w
or small bowelw
surgery, malabsorption, chronic
wwdisease (eg RA), blood ww
transfusions,w
splenectomy.
Drug history
(regimen, tdate of last dose, response, side
et iron,Chemotherapy
e anticoagulants, vaccinations
et
effects),
vitamin B /​
folate,.naspirin,
n
n
.
.
X splenectomy, long-​termkantibiotics,
X
X
OCP, allergies.
ok post-​
o family support,
ok home
o
o
o
Social
history
Smoking,
alcohol,
living
circumstances,
B
.B exposure to dyes/​asbestos/​
.B coal tar, racial
help, occupation,w
previous
w
w
w
origin, diet (vegan,
vegetarian), recreational drug
use.
w
w
ww
12
Family history Malignancy, thalassaemia, sickle-​
cell anaemia, haemophilia, von Willebrand’s disease, pernicious anaemia, spherocytosis,
thrombophilia.
t
t
t
.ne
.ne
.ne
X
X
X
ok Examination
ok pigmentation, rashes oand
ok nodules,
o
inspection Bruising,
Bo General
B
B
ulceration, cyanosis,
­
w. plethora, jaundice, excoriations,
w. racial origin w
w
w
(haemoglobinopathies
and
thalassaemias).
w
w
w
Hands Nails (koilonychias, pallor, clubbing), palmar crease pallor,
arthropathy.
et
et
et
.nEyes
.n(gum
.nulcerFace
(jaundice, pallor), mouth
hypertrophy or bleeding,
X
X
X
ok ation, candida, atrophic glossitis,
ok angular stomatitis, gingivitis).
ok
o
o
Bo Lymph nodes Cervical,
B
B
. axillary, epitrochlear (elbow),winguinal.
.
winwsternum, spine, clavicles,wscapulae.
w
Bones Bony w
pain
ww
Abdomen Hepatomegaly, splenomegaly, para-​aortic nodes, ascites.
et
et
et
n
n
n
.
.
.
X Fundi (haemorrhages, engorged
X veins, papilloedema), temperature
X
ok Other
ok
ok
chart, urinalysis.
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Legs Vasculitis, bruising, pigmentation, ulceration, neurological signs.
B
.B
w
ww
.B
w
w
w
w
Breast (male and female)
w
143
t
t
t
.ne (male andXfemale)
.ne
.ne
Breast
X
X
ok
ok
ok
o
o
Bo History
B
B
.
w.bleeding/​inversion, w
Lump Size, duration,
pain, nipple discharge/​
wwmobility,
w
skin changes,w
previous
breast lumps.
w
w
Past obs/​gynae history Number of pregnancies, age of first pregnancy,
breastfeeding,
et menarche, menopause.
et
et
n
n
n
.
.
.
IHD, clotting problems,
XPast medical history DM, asthma,
X liver
kX iBP,epilepsy.
ok disease, anaemia, previousoomalignancy,
ok
o
o
B FH Breast cancer (male/​
aw
ge.B
of relative at their
w.B female), gynae cancer—​
diagnosis.
w
w
w
w
ww
DH HRT, COC use.
Examination
(lying at 45°)
eta chaperone
et
et
n
n
n
.
.
.
Ensure
is
present
and
document
their
details
in
the
notes
X job title).
X
X
ok (name,
okside first):
ok
o
o
o
Examine
both
breasts
(normal
B
.B
w.Bscars, skin changes, nipple
wdischarge/​
Inspection Asymmetry,
inversion,
w
w
skin tethering,
w erythema, oedema. Ask thewpatient to tense pectoral ww
wall by putting their hands on hips and tensing. Ask the patient to lean
forward. Look for any skin tethering.
t
t
et
.ne Ask the patient to showXyou
.newhere the lump is, palpateXall.nfour
Palpation
X
k tail, assess any palpableomasses.
k
ok quadrants (see Fig. 3.5) and
oaxillary
o
o
Bo Lymphadenopathy Axilla,
B
B
cervical, supraclavicular. The
must be
w.to adequately
w. patient
fully relaxed forwyou
palpate thew
axillary
nodes. Take the
w arm in yours as you palpate.w
ww
weight of their
Other Liver, spine.
t
t
net
.n(a)e
.ne(b)
Supraclavicular X.
X
X
lymph nodes
ok
ok
ok
o
o
Bo
B
B
upper
w. 15%
w.
50% upper w
inner quadrant
w
w
ww
outerw
18% nipple
quadrant
Axillary
t
t
lymph
nodes
e
e
et
n
n
n
.
.
.
11%
lower
X outer
X
X
klower
ok quadrant
o6%
ok
inner quadrant
o
o
o
B
.B
w.Bshowing proportion w
Fig. 3.5 Anatomy ofw
the breast. (a) Quadrants of the breast
w
w
of breast cancer
wby location. (b) Glands and lymphatics
w of the right breast.
w
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
144
.B
w
ww
Chapter 3
o
ww
w
History and examination
t
.ne
Eyes
X
k
.B
w
w
t
.ne
X
k
et
.n
kX
oo
oo
B
B
.
.
wred eye, discomfort w
Symptoms Reduced/​
vision or visual loss,
wwimpaired
wtissues
(gritty or FBwsensation),
pain of the eye orw
soft
around the eye, w
dry eyes or excessive watering, itch, swelling, photophobia or haloes
aroundtlights, floaters or flashing lights,tdiplopia, discharge.
e
e
et
n
n
.
.
Past
ophthalmic history Glaucoma,.n
myopia, cataracts, previous surgery,
X
X
X
ok glasses/​contact lens prescription
ok and last optometry check-​
oukp.
o
o
o
Past medical history .Numerous
systemic diseases can
affect the eye,
B
B
wvascular
w.Bdisease,
including DM, iBP,
disease, RA, SLE, thyroid
MS.
w
w
w anticholinergics, medica- ww
Drug history w
Ophthalmic medications, steroids,
tions for coexisting disease; allergies.
t Glaucoma, retinoblastoma.
ehistory
et
et
Family
n
n
n
.
.
.
X history Ability to self-​care,
X
X
ok Social
ok impact eye disease has oupon
okADLs and
o
o
home support received/​
needed.
B
w.B
w.B
Upper eye
lid
w
w
w
w Limbus
ww
Bo
Bo
History
Pupil
ok
et
X.n
oo
B
.
w
Lateral canthus
wwLower eye lid
Conjunctiva over
sclera
t
.ne
t
.ne
X
Medial canthus
ok
o
B
w.
kX
ww
Iris with lens
beneath
ww
t
t
Fig. 3.6
net
.ne Surface anatomy of the right
.eye.
.ne
X
X
X
ok Examination
ok
ok
o
o
Bo Inspection Exophthalmos,
B
B
proptosis,
jaundice,
pallor,
xanthelasma,
w.red eye, corneal arcus, periorbital
w. cellulitis (Fig.eyelids
(cysts, inflammation),
3.6).
w
w
w
ww
Visual acuity w
This must be tested in all patients:
• Use a Snellen chart at 6m to test visual acuity
• Make
patient is using the correct
glasses for the test (reading
et sureifthein doubt,
eint a piece
etvs
n
n
n
distance);
use a pin-​h.ole
of card
.
.
X visual acuity is very bad, kassess
X ability to count fingers, awareness
X
ok • Ifmovement
oor perception
ok of
(waving hand),
of light (pen torch).
o
o
o
B
B Check the pupils arewequal,
.B reacting to light
Pupillary response and
w.reflexes
w
w
and accommodation
w (PERLA) and for a relative
w afferent papillary defect. ww
Look for the red reflex (absent in dense cataracts). An absent red reflex at
the 6wk baby check is a red flag (treat this as a same-​day urgent referral).
t Confrontation testing toneidentify
t any visual field loss and
efields
etto
Visual
n
n
.
.
.
X
if the defect is unilateral
kX or bilateral (E p. 135). okX
ok establish
odiplopia,
o
o
o or nystagmus.
Ocular
movements
Look
for
loss of conjugate B
gaze
B
B
.
.
w
w
ww
ww
ww
B
.B
w
ww
.B
w
w
w
w
Eyes
w
145
t
t
t
Ophthalmoscopy
.ne
.ne
.ne
X
X
X
ophthalmoscope set
+10 the cornea and anteriorkchambers
ok • Withbetheexamined.
ok onof fluorescein
oo ulcers,
1 or 2odrops
highlights corneal
Bo can
B
B
.
.
abrasions, and foreign
bodies,
especially
under
the
blue
light
w
w
• With the ophthalmoscope
set on 0 the user w
can visualize the retina. It
wtowdilate the pupil
ww
is important
with 1 or 2w
drops of a weak mydriatic
(Box 3.8) (eg 0.5% or 1% tropicamide) to allow full visualization of the
retina.
et The risk of causing acute.glaucoma
et with mydriatics is small.
et
n
n
n
.
.
X
X
X
ok K Box 3.8 Descriptive
okterms in ophthalmology
ok
o
o
o
B
Accommodation Alteration
near/​far objects.
w.B in lens and pupil to focus
won.B
w
w
Acuity Abilityw
of the eye to discriminate fine detail.
w
ww
Anterior chamber Between cornea and iris, containing aqueous.
t of the eye.
Aqueous
et Fluid-​like jelly in the anterior
echamber
et
n
n
n
.
.
.
Blepharitis
Inflammation/​
i
nfection
of
eyelids.
X
X
X
ok Canthus Medial or lateralojunction
ok of the upper and loweroeyelids.
ok
o
B
Chemosis Conjunctival.B
w oedema.
w.B
Choroid Layer sandwiched
between retina and sclera.
w
w
w
w
ww
B
Conjunctiva Mucous membrane covering sclera and cornea anteriorly.
Cycloplegia Ciliary muscle paralysis preventing accommodation.
Dacryocystitis Inflammation of the lacrimal sac.
Ectropion Eyelids evert outwards (away from the cornea).
Entropion Eyelids invert towards the cornea (lashes irritate cornea).
Fovea Highly cone-​rich area of the macula (yellow-​spot).
Fundus Area of the retina visible with the ophthalmoscope.
Hyphaema Blood in the anterior chamber seen as a red fluid level.
Hypopyon Pus in the anterior chamber seen as a white fluid level.
Limbus Border between cornea and sclera.
Macula Rim around the fovea, rich in cone cells.
Miotic Agent resulting in pupillary constriction (eg pilocarpine).
Mydriatic Agent resulting in pupillary dilatation (eg tropicamide).
Optic cup Depression in the centre of the optic disc.
Optic disc Optic nerve head seen as white opacity on fundoscopy.
Posterior chamber Chamber between the iris and lens.
Presbyopia Age-​related reduction in near acuity (long-​sightedness).
Ptosis Drooping eyelid(s).
Sclera The visible white fibrous layer of the eye.
Scotoma Defect resulting in loss of a specific area of vision.
Strabismus Squint, loss of conjugate gaze.
Tonometer Apparatus for indirectly measuring intraocular pressure.
Vitreous Jelly-​like matter which occupies the globe behind the lens.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
ok
Bo
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
w
et
.n
kX
ww
t
e
X.n
ww
w
t
o
w.B
t
.ne
X
k
.ne
X
k
t
ww
ww
o
w.B
et
n
.
kX
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
ww
t
.ne
X
ok
.Bo
ww
B
146
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne and neck X.ne
.ne
Head
X
X
ok
ok
ok
o
o
Bo History
B
B
.
As well as a good w
general history, specific symptoms
w.to note include:
w
w
w ears, wax, discharge, tinnitus,
w deafness, unilateral/​ ww
Ears Pain, blocked
­bilateral features, vertigo, trauma, itching, FBs, noise exposure, occupation.
t
t
eBlocked
esneezing,
et
n
n
n
Nose
nose, watery discharge,
itching, coughing, .change
.
.
X voice, altered sensation kofXsmell/​taste, external deformity/​
X recent
ok intrauma,
o ask about daytime variation
oink symptom
epistaxis, sinusitis;
o
o
o
B
­severity, pattern of obstruction,
effects on speech and
w.B
w.Bsleep. Are symp- w
toms uni/​bilateral?
w
w
w
w
w
Throat Dysphagia, pain on swallowing, hoarseness, difficulty opening jaw
(trismus), stridor, sleep apnoea/​snoring; ask about neck lumps, vomiting,
heartburn, waterbrash (acid regurgitation or filling of mouth with saliva).
et
n
.
X
et
n
.
X
t
.ne
X
ok
k
ok Examination
oo
o pinna or masB
B
.
Ears Inspect The pinna,
auditory meatus, tenderness.over
w all four quadrants of the
w
toid; Otoscopy w
Examine
eardrum (see Fig. 3.7)
w retraction, perforation, exudate);
ww Test hearing See fol- ww
(colour, bulging/​
lowing ‘Hearing tests’ text.
t
et
Nose
deformities, tilt the head
net Rhinoscopy
.neLook for Obvious scars, deviations/​
.3.8);
.nback
and look down each nostril (Fig.
(AdministerX
lidocaine
X
X
k
ok spray first), look for polyps,
ooinflamed turbinates, pus..Book
Bo Throat Inspect Thewlips,.Baround
and inside the mouth;
w Examine The tongue
and tonsils using
wwa torch and tongue depressor,
wwcheck palate movements ww
Bo
by asking the patient to say ‘ah’ (Fig. 3.9).
t Swellings, asymmetry,nescars;
t Ask The patient to swallow,
NeckeLook
net
.n thefor tongue;
protrude
Palpate The.neck from behind and ask the .patient
X
X
X
kfor Tracheal deviation, lymphadenopathy,
ok to take a sip of water;ForoFeeloa bruit;
opp.k472–3).
o
Examine Any lumpsB
(E
Bo tenderness; Auscultate
B
w.
w.
w
w
Hearing tests
(E OHCS10 p. 540)
w
w
ww
Whisper Whisper a different number into each ear, standing 30cm away
while blocking the other ear. Ask the patient to repeat it in turn.
et
et
et
n
n
n
.
.
.
XTuning fork tests
X
kXon the patient’s mastoid bone
ok Rinne’s test Place the tuning
ofork
ok until it is
o
o
o
B
no longer heard; then
place the fork near the external
meatus
w.B
w.earBauditory
where it is still heard
in a normal ear, but not in an
with conductive
w
w
deafness. Normally
w air conduction >bonewconduction. Confusingly, a ww
normal result is called Rinne positive.
et test Place the tuning fork .innthe
et middle of the forehead and
easkt
Weber’s
n
n
.
.
which
side
the
sound
is
loudest;
in
sensorineural
deafness
the
sound
is
X in the normal ear, in kconductive
X deafness the sound kis X
loudest in
ok loudest
o
o
o
o
o
the abnormal ear. .B
B
w
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Head and neck
w
147
t
.ne
X
k
t
t
membrane
.neTympanic
.ne
X
X
(pars
flaccida)
o
ok
ok
o
o
Handle
of
malleus
Bo
B
B
w.
w.
w
w
w
w Antero-superior
ww
quadrant
t
t
e
e
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
Tympanic
membrane
B
.B
(pars
w.B
wtensa)
w
w
w
wAntero-inferior
ww
Postero-superior
quadrant
quadrant
t
t
e
e
et
Postero-inferior
Cone
of
light
n
n
n
.
.
.
quadrant
X
X
kX as
ok Fig. 3.7 Structures and quadrants
okof the right tympanic membrane
o(eardrum)
o
o
o
B seen on otoscopy. w.B
w.B
w
w
w
w
ww
tFrontal sinus
t
t
.ne
.ne
.ne
X
X
X
Superior k
ok Middle turbinate ook
oturbinate
o
Sphenoid
sinus
Bo
B
B
.
.
w
w
Inferior turbinate
ww
ww Eustachian tube
ww
Nasopharynx
et Nostril
et
n
n
net
.
.
Soft palate X.
X
X
Hard
k palate
ok
ok
oo
o
Bo Fig. 3.8 Anatomy ofwthe.Bnose.
B
w.
w
w
w
w
ww
Central incisor First premolar
t wall
Posterior
e
et
Hard palate et
Second
n
n
n
.
.
of .oropharynx
Lateral
Palatine
premolar
X PalatoX
kX incisor
ok pharyngeal
oraphe
ok First molar
o
o
o
Soft
B
arch
w.B palate Canine ww.B Second
w
molar
Uvula
Palatow
w
ww
et
n
.
kX
o
Bo
glossal
arch
Dorsum
of tongue
Third
molar
(wisdom
tooth)
Palatine
tonsil
et
n
.
kX
o
o
B
.
w
ww
Fig. 3.9 Anatomy of the mouth and oropharynx.
w
ww
t
.ne
X
ok
.Bo
ww
B
148
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne
.ne
.ne
Musculoskeletal
X
X
X
ok
ok
ok
o
o
Bo History
B
B
w. swelling, deformity, morning
w.stiffness, instability, w
Symptoms Joint pain,
w
w
sensory changes,
back
pain,
limb
pain,
muscle/​
w
w soft tissue aches, cold w
fingers and toes, dry eyes and mouth, red eyes, systemic symptoms
(fatigue,
loss, tight skin, fever,t rash, diarrhoea), injury/​trauma
et weight
e since), bleeding tendency..net
(mechanism,
timing, change in symptoms
n
n
.
.
X medical history Previous ktrauma/​
X surgery, recent infections
kX(streptook Past
o
odisease
o
o
coccal, gonorrhoeal, TB,oetc), insect/​tick bites, IBD, skin
(psorB
.B haemophilia.
.B
iasis), childhood arthritis,
w
w
w antiarthritic agents (NSAIDs,
Drug history w
Previous
ww steroids (oral/​intra-​ ww
articular), DMARDs) with beneficial/​side effects, long-​standing steroids,
Ca supplements,
vitamin D analogues,
other concurt bisphosphonates,
et
eetc),
et
rent
medications
(antihypertensives
allergies.
n
n
n
.
.
.
X of daily living Ability kto:Xbathe, dress (and undress), eat,
kXtransfer
ok Activities
ouse of the toilet; ?change with
osymptoms.
from bed to chair and back,
o
o
o
B
Social history Domestic
w.Barrangements (who elsewiswat.Bhome, location of w
w
bathroom inw
relation to bed), smoking history,
w drug and alcohol use. w
2+
Family history Rheumatoid, gout, osteoarthritis, haemochromatosis, IBD,
haemophilia.
t
t
t
.ne
.ne
.ne
Examination
X
X
X
k
routine, though the
ok Each joint has a specificooexamination
okunderlying
ojoint
similar. Always examine .the
above and
Bo principles for eachware.Bvery
B
w
below too.
w and their gait.
wwOverall appearance of thewpatient
ww
General inspection
Look Close inspection of the joint, comparing left to right if possible.
t
t
et
Feel
of warmth, tenderness,
.nAssessment
.ne crepitus, effusions, etc.X.ne
X
X
kthe joint) and passive (examiner
ok Move Active (patient moving
ojoint
ok moving
o
where appropriate. Bo
Bo joint) movements;wstressing
B
.
w. of joint laxity.
Measure Rangew
of movements (in degrees) andw
degree
w
w
ww
Ilium
t
t
e
e
et
n
n
n
Anterior superior
.
.
.
X
X
X
iliac spine
Pubis
ok
ok
ok
o
o
o
B
Femoral head in
Pubic tubercle
w.B
w.B
acetabulum
w
w
w
w
ww
Obturator foramen
Bo
o
et Ischium
n
.
kX Lesser trochanter
Greater
trochanter
et
n
.
kX
o
o
B
.
w
ww
Fig. 3.10 Anatomy of the left hip joint.
t
.ne
Femur kX
oo
B
.
w
ww
ww
B
.B
w
ww
.B
w
w
w
w
Musculoskeletal
w
149
t
et Fig. 3.10; E OHCS10 p..682)
net
Hip
.n(See
.ne
X
X
X
k rointernal
ok Inspection Leg shortening,
ok rotation (hip dislocation),
oexternal
o
of o
femur), scars, sinuses, cellulitis,
bruising.
Bo tation (fractured neck
B
B
w. landmarks (greater trochanter,
w. anterior superior w
Palpation Check bony
w
w
iliac crest) are
symmetrical,
warmth,
crepitus
and
w
w clicks on movement. w
Supine Active and passive range of movement; flexion (straight leg flexion
tflexion with knee bent 0–​135°),
0–​90°,
e(0–​
etabduction (0–​50°), adduction,(with
ein-t
n
.
ternal
45°) and external (0–​45°).n
rotation, fixed flexion deformity.n
X in lumbar lordosis, checkkthe
X popliteal fossa can touch thekXcouch).
ok hand
o
o
o
o(0–​o20°).
range of movement; extension
B Prone Active and passive
B
B
.
.
wgait (E p. 138), walking aids.
Gait Trendelenburg
ww
ww(Fig. 3.11) and lower spine/​wsacroiliac
ww
Other joints Knee
(E p. 151).
Kneee(E
t OHCS10 p. 688) net
et
n
n
.
.
Inspection
Swelling, erythema, resting
position, varus (bow-​legs) or.valgus
X knees) deformity, scars,
X cellulitis, muscle wasting
X
ok (knock-​
ok sinuses,
ok of thigh
o
o
o
muscles
compared
to
the
other
side
(especially
vastus
medialis).
B
.B medial and latw.Bbony landmarks (head wof wfibula,
Palpation Temperature,
w
eral joint lines,
wpatella), effusion (if large infra-​
wpatella sulci will be bulging ww
B
outwards with a positive patella tap, if small try milking fluid down from
thigh and stroking fluid from one side to the other), crepitus, clunks or
clicks on movement, patella position, tenderness, and mobility.
Supine Active and passive movement; flexion (0–​135°), extension (0°).
Prone Popliteal fossa cysts or aneurysms.
Stressing Cruciates Flex knee to 90°, immobilize the patient’s foot by sitting
on it and check the integrity of the anterior and posterior cruciate ligaments by pulling and pushing the lower leg, respectively; Collaterals Flex
knee to 30°, fix the thigh with your left hand and test medial collateral (pull lower leg laterally) and then lateral collateral (push lower leg
medially).
Gait Limp, walking aids.
Other joints Hip (see previous section) and ankle (E p. 150).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
t
ok
Bo
e
X.n
w
t
o
w.B
Lateral
Femur
t
.ne
X
k
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
t
ww
Medial
et
n
.
X
ww
k
oo
oo
B
B
.
.
Lateral collateral
Medial
ww
wwcollateral ligament
wligament
w
ww
Articular cartilage
Medial meniscus
Lateral meniscus
t
t
Head of fibula
e
e
et
n
n
n
.
.
.
X
X
X
Tibia
ok
ok
ok
o
o
o
B Fig. 3.11 Anatomy w
.Bright knee joint.
of the
w.B
w
w
w
w
ww
Patella
B
.B
w
ww
150
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
Ankle
.ne (See Fig. 3.12; E OHCS10
.np.e694)
.ne
X
X
X
erythema,
resting position (consider
fracture–​
ok Inspection Swelling,
oksenior
okdeviation
o
o
and get immediate
help if there is marked
of
Bo dislocation
B
B
. (E pp. 448–51). w.
the foot followingw
trauma
w and lateral malle- ww
Palpation Temperature,
bony landmarks w
(medial
ww
olus, tibiotalar joint), crepitus, pain, swelling, effusion, crepitus. After
trauma Palpate proximal fibula head to exclude its fracture, check foot
et(E p. 130), distal sensation.nand
etcap-​refill.
et
pulses
n
n
.
.
plantarflexion (0–​50°), dorsiXMovement Active and passivekmovement;
X
ok flexion (0–​15°), inversiono(0–​
o 30°), eversion (0–​15°). ookX
o
B
Gait Limp, walking aids,
ability to walk 2 paces unaided.
.B
w.B
w150).
Other joints Knee
(E
pp. 149–150) and foot (E
p.
w
w
w
w
ww
$ Ottawa ankle rules Ankle X-​ray only required in adults and children >6
if any pain in malleolar area and bony tenderness over any of: distal 6cm
of posterior edge of tibia or fibula, or tip of medial or lateral malleolus
or if unable to bear weight both immediately and in the ED for 4 steps.
et
n
.
X
ok
Bo
Bo
et
n
.
X
k
oo
B
.
Fibula
w
Lateral malleolus
Calcaneus
ok
oo
B
.
w
Cuboid
ww
Talus
t
.ne
Navicular
kX
Fig. 3.12 Anatomy of the right ankle joint.
Foot (See Fig. 3.13)
o
B
.
w
wwMedial malleolus
Tibia
ww
et
X.n
t
.ne
X
ok
w
oo
B
.
ww
ww
t
.ne
X
k
ww
t Swelling, erythema, restingneposition,
t
Inspection
high arch, bunions. et
.ne Temperature,
.n and
Palpation
pain X
or .crepitus along each metatarsal
X
X
k
k
k
forefoot bones (navicular,
and medial, intermediate
and
o phalanx,cuneiform),
oo (E p.cuboid
ooand cap-​refill.
foot
pulses
130), distal sensation,
Bo lateral
B
B
.
.
Movement As for w
examination but also adduction
w ankle and
ww and abduction ww
across the talonavicular
calcaneocuboidw
joints.
w
Gait Limp, walking aids, ability to walk 2 paces unaided.
Other joints
Ankle (E p. 150).
et Proximal
et
et
n
n
n
.
.
.
phalanx
First metatarsal
Cuneiforms
X
X
X
Medial phalanx
ok
ok(of great toe) (lateral, middle,omedial)
ok
o
o
Distal phalanx
B
Navicular
.B Talus
w.B
w
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
Cuboid Calcaneus
o
o
o
B
B Metatarsals
Tarsals
wof .thePhalanges
w.B
Fig. 3.13 Anatomy
left foot.
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Musculoskeletal
w
151
t
t
et
Back
.ne(See Fig. 3.14; E OHCS10
.p.n672)
.ne
X
X
X
k
Deformity, loss oroexaggeration
of thoracic kyphosis
ok Inspectionlateral
okor lumbar
o
deviation
from the midline (scoliosis). Bo
Bo lordosis,
B
. standing in front, palpate each
Palpation With patient
w. vertebra for pain; w
wwpalpate
w
with patient w
prone
each side of pelvis
for
w sacroiliac tenderness. w
Movement Active Flexion (touch toes with knees together and legs
straight;t most people can touch theirtshins), extension (leaning backe lateral bending (lateral flexion)
e and rotation (best assessed.nwith
et
wards),
n
n
.
.
X seated so pelvis is fixed);
X Passive With patient supine,
kXperform
ok patient
okeach leg
straight leg raise by elevating
in turn (0–​85°). oo
o
o
B Measure Schober’swtest
.Bfor lumbar flexion (markwthe.Blevel of the posterior iliac spine
in the midline; make a further
marks, one 5cm
w
w
w one 10cm above this; the distance
ww twobetween
below this and
these two w
new marks measured when the patient is standing and then in full
flexion—​
an increase of <5cm suggests
et spondylitis).
et limited lumbar flexion) (eg
ean-t
n
n
n
kylosing
.
.
.
X
X
kXknee (E p. 149).
ok Other joints Hip (E p. 149)ooand
ok
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
et
X.n
ok
Cervical
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww Thoracic
o
Bo
t
.ne
X
k
ok
ww
t
e
X.n
o
w.B
ww
wThoracic
et
X.n
Lumbar
Sacrum
t
.ne
X
k
kyphosis
oo
B
.
w
et
.n
kX
w
lordosis
w
ww
Lumbar
.ne
X
k
t
et
n
.
X
k
Coccyx o
ok
o
oo
Bo Fig. 3.14 Anatomy w
B
B
.
.
of the spine.
w
ww
ww
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
152
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
Pelvis
.ne
.ne
.ne
X
X
X
joints in the pelvis are kfixed, however the sacroiliac joint
be
ok The
o
ok acan
o
alpated for tenderness o
from behind; in a trauma emergency,
senior
Bo ­pmember
B
B
. See Fig. 3.15.
of the trauma
forw
instability.
w. team may test the pelvis w
w
Sacrum
wSacroiliac joint
w
ww
promontory
Ilium
t Sacral
t
Anterior superior
e
e
et
n
n
n
.
.
.
iliac
spine
X
X
X
ok
ok
ok
o
o
o
Pubis
B
Obturator
w.B
w.B
w
w
foramen
Ischium
w
w
ww
Symphysis
t
tpubis
e
e
et
n
n
n
.
.
.
Fig.
3.15 Anatomy
of
the
pelvis.
X
X
X
ok
ok
ok
o
o
o
B
B E OHCS10 p. 664) w.B
Shoulder (See Fig. .3.16;
werythema,
Inspection Swelling,
deformity, resting
w
w
ww position, (check from ww
B
the front, side and back), scars, sinuses, cellulitis, swelling, muscle wasting
(deltoid, supraspinatus, infraspinatus).
Palpation Temperature, bony landmarks (acromion, clavicle, spine of
scapula, cervical and upper thoracic vertebrae), crepitus, clicks.
Movement Active and passive movement; abduction (0–​90° with elbow
flexed, 0–​180° with elbow extended), adduction, internal (0–​90°) and
external (0–​
65°) rotation, flexion (0–​
180°) and extension (0–​
65°),
passive abduction should be undertaken carefully if painful.
Stressing Impingement test Arm held at 90° abduction and internally
­rotated, if pain detected it is a positive test; Scarf test Patient’s left hand
placed over their right shoulder and vice versa, if pain detected it is a
positive test (acromioclavicular joint pathology).
Other joints Elbow (E p. 153) and back (E p. 151).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
w
t
o
o
w.B
ok
Bo
ww
et
n
.
X
Acromion
ok
o
w.B
ok
ww
o
w.B
et
n
.
kX
ww
t
Scapula
o
o
B
.
w
ww
ww
Acromioclavicular joint
et
n
.
X
Spine of scapula
ww
Humerus
et
n
.
kX
o
Bo
Greater
tuberosity
Lesser
tuberosity
oo
B
.
w
.n
kX
Posterior view
Clavicle
ww
et
.ne
X
k
Anterior view
ww
et
n
Acromion
.
X
t
.ne
X
k
Fig. 3.16 Anatomy of the right shoulder joint.
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Musculoskeletal
w
153
t
t
t
Elbow
.ne (See Fig. 3.17; E OHCS10
.np.e668)
.ne
X
X
X
Swelling, erythema,
ok Inspectionplaques
okinflamed bursae, rheumatoid
oknodules or
o
overB
theoolecranon, scars.
Bo psoriatic
B
. bony landmarks (medial and
Palpation Temperature,
w.lateral epicondyles, w
ww clicks,
w
olecranon), w
crepitus,
instability.
w
w
Movement Active and passive movement; flexion (0–​150°) and extension
(0°); pronation,
supination.
t Shoulder
ejoints
et
et
n
n
n
Other
(Fig. 3.16) and
wrist (Fig. 3.18).
.
.
.
X
X
X
Anterior view k Medial
ok
o supracondylar Posterior view
ok
o
o
o
B
B
.B
crest
w.Olecranon
Medial condylew
Coronoid fossa w
w
Lateral w
condyle
w Olecranon fossa
ww
Medial
Lateral epicondyle
epicondyle
Lateral epicondyle
t
e
et
et
Capitulum
n
n
n
.
.
Head of radius.
X
X
X
of radius
Trochlea
Neck of
ok Head
okCoronoid
okradius
Neck of radius
o
o
o
process
B
w.B
w.B
w
w
Fig. 3.17 Anatomy
w of the right elbow.
w
ww
Wrist (See Fig. 3.18; E OHCS10 p. 670)
t
t
t
.ne Swelling, erythema, deformity
.ne (eg Colles’ fracture), features
.neof
Inspection
X
X
X
disease (E p. 468),
scars.
k
ok rheumatoid
oklandmarks
oradius,
o
o
Temperature,
bony
(styloid
process
of
head
Bo Palpation
B
B
.
.
and styloid processw
of ulna), scaphoid (base of thew
anatomical snuff-​box).
w (0–​75°), extension ww
Movement Active
ww and passive movement; wflexion
(0–​75°), radial (0–​20°), ulnar deviation (0–​20°), pronation, supination.
t Elbow (E p. 153) and hand
t (E p. 154).
t
Otherejoints
.n
.ne
.ne
X
X
X
ok
ok
ok
o
Capitate Bo
Bo
B
Trapezoid
w.
w. Metacarpals
Hamate
w
w
w
wPisiform
ww
Trapezium
Triquetrum Carpals
Scaphoid
Lunate
t
t
e
e
et
Radial styloid process
n
n
n
.
.
.
Ulnar styloid
X
X
X
process
Radius
ok
ok
ok
Ulna
o
o
o
B
.B
w
w.B
Fig. 3.18 Anatomy
of the wrist and hand.
w
w
w
w
ww
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
154
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
Hand
.ne (See Fig. 3.19; E OHCS10
.np.e670)
.ne
X
X
X
swelling,
features of
ok Inspection(EErythema,
okbreaks to(Ethep. skin,
okrheumatoid
o
o
p. 468) orB
osteoarthritis
468), deformity,
dislocation,
Bo disease
B
.
.
muscle wasting, nail
pitting.
w
w
Palpation Temperature,
ww palpate each metacarpal
wwand phalanx for pain or ww
crepitus, distal cap-​refill and sensation.
Movement
and passive movement;
t flexion and extension of nevery
etPIPJ,Active
eadduction
et
n
n
MTPJ,
and DIPJ, abduction and
of every MTPJ, .oppos.
.
X and circumduction of the
X
to: hold a
kXthumb MTPJ; ask the patient
ok ition
okthumb
pencil and write, pick upoa o
mug, undo a button, oppose o
their
o
B
.B of this against your own);
.Bcheck strengthandof
little finger (check strength
w
w
extension and w
or w
lacerating trauma to idenwflexion following penetrating w
ww
tify tendon injury.
Stressing Collateral ligaments of the digits following trauma or dislocation
by attempting
et to deviate the phalanges
etmedially or laterally. .net
n
n
.
.
XOther joints Wrist (E p. 153)kand
X inspect the elbow.
X
ok
o
ok
o
o
o
B
w.B
w.B
Distal phalanx
w
w
w
w
ww
B
.
kX
o
o
net
Middle phalanx
Proximal phalanx
ww
oo
B
.
w
et
Phalanges
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
Metacarpal bones
t
t
t
e
e
n
n
. First metacarpal
.
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
. bones
w.
wCarpal
w
w
w
w
ww
Radius
Ulna
t
t
e
e
et
n
n
n
Fig.
3.19 Anatomy of the hand, thumb
and fingers.
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
t
.ne
X
k
o
Bo
w
oo
B
.
w
et
n
.
kX
ok
ok
et
n
.
X
ok
ww
t
.ne
X
k
oo
o
oo
B
.
w
o
o
w.B
o
ww
oo
B
.
ww
t
.ne
X
k
ww
w
et
.ne
X
k
oo
B
.
w
.n
kX
ww
t
e
X.n
Bo
o
B
.
w
ww
t
ww
et
n
.
kX
t
et
t
.ne
X
k
ok
Bo
ww
.ne
X
ok
.n
kX
ww
Bo
ww
.B
w
ww
o
B
.
w
o
et
n
.
kX
oo
e
X.n
ww
Bo
o
w.B
.n
kX
ww
o
w.B
.ne
X
k
ww
et
n
.
X
ok
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
t
o
o
w.B
w
155
et
t
et
n
.
X
w
Musculoskeletal
t
.ne
X
k
ww
o
Bo
B
.B
w
w
w
ww
.ne
X
ok
.Bo
ww
B
156
.B
w
ww
Chapter 3
ww
w
History and examination
t
.ne
Urological
X
k
o
.B
w
w
t
.ne
X
k
et
.n
kX
oo
oo
B
B
.
.
Symptoms Polyuria,wanuria, prostatism (urgency, hesitancy,
poor stream,
wnocturia, straining), haematuria,
ww
terminal dribble,
dysuria, oedema, renal
w
w
colic, incontinence, malaise, lethargy, N+V, anorexia, weight loss, itching,
passingtstones in the urine, incontinence,
infertility, bone pain,
e discharge, genital/​perineal.lesion,
et impotence,
et
genital
scrotal pain, dyspareunia
(pain
n
n
n
.
.
Xon intercourse), FB (vaginal, urethral,
X anal), anal/​perianal problems.
kX myeok Past medical history DM, iBP,
okrecurrent UTIs, renal/​ureteric
ostones,
o
o
o
B
loma, known renal impairment/​
failure, previous vesicoureteric
w.B (steroids,
w.B disease,reflux,
gout, immunosuppression
HIV), neurological
long-​
w
w
w Male Tight foreskin,
term urinarywcatheter, STIs, spinal cord pathology;
Bo
recurrent balanitis, testicular pain/​swelling; Female Number of children,
mode of delivery and any complications, last cervical smear and result.
Drug history Nephrotoxics (including NSAIDs, ACEi, aminoglycosides),
bladder neck relaxants, infertility or impotence drugs, antiandrogens;
allergies.
Social history Foreign travel, ability to cope with ADLs, sex abroad, illicit
drug use (smoke, oral, IV).
Sexual history
• Last sexual intercourse (LSI)—​date, gender, type of intercourse
(vaginal, anal, oral), protected, relationship of partner (casual, long
term), problems or symptoms in partner, high-​risk area, sex worker
• Repeat the above for all partners in the last 3mth
•All men should also be asked if they have ever had sex with another
man in the past as this affects risk and types of STI to consider.
Occupational history Past and present jobs, exposure to dyes.
Family history Polycystic kidney disease, DM, iBP.
et
n
.
X
ok
Bo
B
History
et
n
.
X
ok
o
B
.
w
ww
t
.ne
X
k
oo
ww
ww
t
.ne
X
ok
o
B
.
w
ww
et
oo
B
.
w
ww
.n
kX
w
oo
B
.
ww
ww
t
.ne
X
k
ww
t
t
t
Examination
(lying flat, supine)
.ne
.ne (See Fig. 3.20)
.ne
X
X
X
Mental state,
ok General inspection
ok RR (?Kussmaul breathingoofk metabolic
hiccups, pallor,ohydration (dehydrated: sunkenoeyes, dry lips/​
Bo acidosis),
B
tongue; fluid-​overload:
w. peripheral oedema, pulmonary
w.Boedema).
w
w
Hands Leuconychia,
w brown nails, pale nail beds.
w
ww
Arms Bruising (purpura), pigmentation, scratch marks, fistula, BP (lying
and standing).
t
et
e(dehydration,
et
n
n
.
.
Face
Eyes (anaemia, jaundice), mouth
ulcers, fetor),.n
rash.
X
X
X
ok Neck JVP.
ok
ok
o
o
o
B
B kidney, dialysis
Abdomen Inspect (distended
scars, transplanted
w.Bkidneys,bladder,
w.lymph
port), palpate w
(ballot
bladder, liver, spleen,
nodes), perw
cuss (enlarged
w bladder, ascites), auscultatew(renal artery bruits), PR for ww
prostate.
t Size, surface, consistency nand
t symmetry of prostate innmen,
Rectum
eimpaction
eretention).
et
n
.
.
.
faecal
(will worsen urinary
X
X
X
ok Back Oedema, loin tenderness
ok on percussion.
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Urological
w
157
t
t
t
Chest
.neCVS and RS examination (pericarditis,
.ne heart failure, fluid overload).
.ne
X
X
X
Oedema, bruising, pigmentation,
scratch marks, neuropathy,
k
ok Legs weakness
oaltered
ok proxo
o
(myopathy),
reflexes, muscle wasting.
Bo imal
B
B
.
Urinalysis Glucose,w
blood, protein, nitrites, leucocytes.
w.
w
w
Other Fundoscopy
w (DM and iBP changes), blood
w glucose, weight.
ww
Bladder
Uterus
Fallopian
t
t
e
ebone
et
tube
Pubic
Seminal
n
n
n
.
.
.
Cervix
vesicles
X Ovary
X
kX Urethra
Shaft
ok Bladder
oRectum
okRectum
o
o
o
Glans
Prostate
B
Pubic bone
w.B Anus Foreskin ww.B Anus
Clitoris
w
Vagina
Urethral w
w
ww
Vas deferens
meatus
Outer labia
(sperm duct)
Urethral Scrotum
Inner labia
meatus
Epididymis t
Testis
t
t
e
e
(testicles)
n
n
.
.
.ne
X
X
X
Fig.
3.20 Anatomy
of
the
female
(L)
and
male
(R)
urogenital
systems.
k
ok
ok
oo
Bo Examination ofwmale
B
.Bogenitalia (ensure chaperone
.
present)
w
Inspection Lookwfor any ulceration (includingw
w
w retracting foreskin and ww
B
checking the glans), warts, scars, or sinuses, urethral discharge, tight
foreskin (phimosis) or retracted foreskin which is stuck leaving the glans
exposed (paraphimosis). Inspect the scrotum for skin changes or oedema and, while the patient is standing, the lie of the testes (the left testis
usually hangs lower than the right and both testes lie longitudinally—​a
high testis with a transverse lie may indicate torsion, though a torted
testis may also appear normal).
Palpate each testis in turn between the fingers and the thumb feeling for
texture, tenderness, nodules, and to compare left to right. An absent
testis may be maldescended and trapped in the inguinal canal. Examine
epididymis and follow it up superiorly to the spermatic cord and up into
the inguinal ring. Palpate inguinal lymph nodes or maldescended testis.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
oo
B
.
w
ok
Bo
o
et
n
.
kX
.n
kX
ww
t
e
X.n
.ne
X
k
ww
et
n
.
X
ok
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
t
o
o
w.B
ww
et
.ne
X
k
Examination of female genitalia See E pp. 158–9.
ww
Bo
w
t
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
158
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
t
.ne
.nesystem
.ne
Female
reproductive
X
X
X
ok
ok
ok
o
o
Bo History
B
B
w. of last period, length of menstrual
w. cycle (regular or w
Menstrual history Date
w
w
irregular), length
of
period,
associated
pain/​
s
ymptoms
w
w (Box 3.9), age when w
periods started/​stopped; bleeding/​discharge severity of periods (number
of pads/​
tampons, clots, flooding), bleeding
periods, after interet(vaginal,
et between
et
course
anal, oral), or after
menopause,
rectal/​urinary bleeding,
n
n
n
.
.
.
Xeffect on lifestyle, other vaginalkdischarge
X (colour, consistency and
Xsmell).
ok Sexual history Pain on superficial
o or deep penetration (dyspareunia),
ok type
o
o
o
B
of intercourse (vaginal,
in
.Banal, oral), use of contraception,
wprevious
w.B intercourse
foreign countries,
sexually transmitted
infections;
contraception
w
w
w
ww
current andw
previous types, problems/​benefits.
Cervical smear Date of last test and result, previous results and any treatt smears, colposcopy clinic,
mente(repeat
laser ablation).
etand/​
eandt
n
n
n
.
.
.
Past
gynae
history
Previous
problems
o
r
operations
(where
X of surgeon), breast orkthyroid
X problems, use of HRT, kprolapse.
X
ok name
o of pregnancies,
o type of
o
o
o
Past
obstetric
history
Number
number
of
births,
B
.B
delivery, complications,
forw
obstetric history).
w.Bsubfertility (E p. 160 w
w
Past medical history
w Clotting problems, thyroid problems,
w anaemia, malignancy. ww
B
Urinary problems Incontinence (on laughing/​coughing/​exercising or spontaneous), dysuria, urgency, frequency, haematuria, if symptomatic ask
about fluid intake, leg weakness, faecal incontinence, back pain and previous spinal problems/​surgery, effect on lifestyle.
Other Vaginal lumps, weight loss, other concerns.
t
.ne
X
k
oo
et
Examination
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
o
ww
o
w.B
o
et
n
.
kX
.ne
X
k
oo
B
.
w
.n
kX
t
ww
ww
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
Bo
w
Always have a chaperone who can reassure the patient and also guard the
door. Document name and role in notes. Ask friends and family members
to leave, unless the patient wants them to stay (this also provides an opportunity to ask questions which the patient may not have answered fully
with others present). As with any examination it is essential to keep the
patient informed about what you are going to do. Start with the patient
lying flat on her back with arms by her sides. It is important the patient is
relaxed and that you have a good examination lamp. See Fig. 3.21.
Abdominal Assess for scars, striae, hernias, body hair distribution, everted
umbilicus, distension, tenderness including loins (± guarding, rebound),
masses, organomegaly, percuss (masses, shifting dullness).
Ask the patient to move her feet apart, bend her knees, and let her
legs flop outwards. Have a strong light source directed at the vulva and
gloves on both hands.
Vulval Look for rashes, ulcers, warts, lumps or other lesions; spread the
labia majora using your non-​dominant thumb and index finger and look
for lesions, lumps, discharge (urethral/​vaginal), bleeding; ask the patient
to push down (look for prolapse) and cough.
Vaginal Insert a well-​lubricated index and middle finger (dominant hand) into the
vagina and feel for the cervix, noting the size, shape, consistency, and whether
it is mobile or tender. Feel above, below, and to the sides (adnexae) for masses
or tenderness. Finally, palpate the uterus by placing your other hand above
the pubic symphysis and press down with the fingers at the cervix; pressing
up feel for uterine position (anteverted/​retroverted), size, shape, consistency,
mobility, and tenderness. Inspect the finger afterwards for blood or discharge.
t
.ne
X
k
ok
Bo
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Female reproductive system
w
159
t
t
t
Cusco’s
.nespeculum While the patient
.isninethe same position insertXa well
.neluX
X
and warmed speculum
the vagina. Look at the cervix.
If you
ok bricated
ok into
ok forward
unable to visualize theocervix,
ask the patient to tilt heropelvis
Bo are
B
B
by placing her fists under
ulceration,
bleeding, cysts
w. her bottom. Look for w
wtake. swabs
or other lesions
and the cervical os. If required
and/​or a
w
w
w
ww
cervical smear.
Consider Sims’ speculum (for examining prolapses), rectal examination.
et
et
et
n
n
n
.
.
.
X
X
X
Pubic bone
ok
ok
ok
o
o
o
B
w.B
w.BClitoris
w
w
w
w
ww
Bladder
et Uterus
et
et
n
n
n
.
.
.
X
X
X
Rectum
ok
ok
ok
o
o
o
B
w.B
w.BCervix
w
w
w of the female reproductivewsystem.
ww
Fig. 3.21 Examination
t
t
et
.nBox
.nein gynaecology X.ne
X
X
K
3.9
Descriptive
terms
ok
ok
ok
o
o
Bo Anatomy
B
B
.
.
wlateral
Adnexae The areas
to the cervix wherew
thew
ovaries are located.
w
wentrance to the vagina. w
ww
Introitus The
Abnormal
t
et bleeding
Climacteric
Phase of irregular periods
n
net
.
.ne and associated symptoms
.prior
X
X
X
to
menopause.
ok
ok periods.
ok
Bleeding between
o
o
Bo Intermenstrual
B
B
Menopause The end
a woman’s menstrual cycles.
w.ofblood
w. (>80mL/​cycle).
w
w
Menorrhagia Excessive
loss during menstruation
w
w
ww
Oligomenorrhoea Infrequent menstruation, >42d menstrual cycle.
Postcoital
after sexual intercourse.
t menopause.
et BleedingBleeding
ethe
et
n
n
n
Postmenopausal
>6mth after
.
.
.
X amenorrhoea Failure ktoXstart menstruating by 16yr. kX
ok Primary
o of menstruation foro>6mth
o after
o
Secondary amenorrhoea
B
B
.BoAbsence
.
­menstruation hasw
started
and not due to pregnancy.
w
ww
ww
ww
Pain
et
n
.
kX
o
Bo
Dysmenorrhoea Pain associated with menstruation.
Dyspareunia Pain associated with sexual intercourse, can be superficial
(eg vulval or entrance to vagina) or deep (only on deep penetration).
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
wHistory and examinationw
ww
t
t
t
.ne
.ne
.ne
Obstetric
X
X
X
ok
ok
ok
o
o
Bo History
B
B
.
w. last menstrual w
Current pregnancy w
Estimated due date (EDD), gestation,
w
w
period (LMP),
method
of
conception,
scan
results,
site of placenta, w
w
w
rhesus status, concerns, attitude to pregnancy. Current symptoms Bleeding,
other vaginal
discharge, headache, visual
dysuria, urinary
et or urgency,
et disturbance,
et
frequency
constipation,
vomiting,
GORD.
n
n
n
.
.
.
XPrevious pregnancies Number kofXpregnancies (gravidity), number
Xof delivok eries
o
ok gestation,
o
o
≥24/​40wk (parity),omiscarriages, terminations (reason,
B
B
method), stillbirths,
vomiting, anaemia,
w.complications:
w.B bleeding, group w
w
B strep, BP, proteinuria,
gestational DM, poor w
foetal growth, admission.
w
w
w
160
Chapter 3
Delivery history Method of delivery and reason (vaginal, ventouse, forceps,
elective/​emergency Caesarean), gestation, birthweight, sex, complications (fever, prolonged rupture of membranes, CTG trace), postnatal
baby problems (feeding, infection, jaundice), admission to SCBU/​NNU,
outcome (how is the child now), postnatal maternal problems (pain,
fever, bleeding, depression).
t
t
e
X.n
ok
Bo
t
e
X.n
ok
o
B
.
w
e
X.n
ok
o
B
.
w
ww
ww
Past gynae history Previous problems, operations, STIs.
Past medical history DVT, PE, DM, admissions, psychiatric problems.
ww
t DM, iBP, pre-​eclampsia,
t
t
Familyehistory
.n pregnancies.
.necongenital abnormalities,XDVT,
.nePE,
multiple
X
X
k partner, type of housing,oemployment,
k
ok Social history Support fromoofamily/​
o
Bo financial problems,wsmoking,
B
B
alcohol, substance abuse.
.
w.
w
w
ww
pregnancies)
Table 3.14wAntenatal care (uncomplicated w
Gestation
et Standard antenatal care:
etpurpose of each visit* .net
(wk)
n
n
.
.
XBooking FBC, G+S, red cellkantibodies,
X rubella, syphilis, hepatitiskB,XHIV
ok
serology, sickle-​co
ell disease, thalassaemia, BMI, BP, urine
o
o
oo dipstick
and culture
B
B
B
.
.
w (combined test)
11–​14
USS for
assessment and nuchal screening
wwBP,gestational
wUrine,
wwand neural tube defects; ww
16
serum screening (for Down’s
triple/​quadruple test)
t and placental position net
20 et
USS for foetal anomalies andegrowth
n
n
.
.
red cell antibodies, anti-​D ifX.
28
Fundal
height,
BP,
urine,
FBC,
kX
kX vaccine
k
rhesus –ve. Offer
pertussis
o
o
oo
Bo 25 , 31 Fundalwheight,
BoBP, urine
B
.
.
34
Fundal height, BP, urine, anti-​D if rhesus –​vw
w
w eECV if breech at 36/​40 ww
woffer
36, 38, 40 w
Foetal position, fundal height, BP, urine,
†
†
†
41
t
.ne
Discuss induction, foetal position, fundal height, BP, urine, offer
membrane sweep
t
kX
o
Bo
e
X.n
ok
*For further information, see Mwww.nice.org.uk/​guidance/​cg62
†
For the first pregnancy only.
ww
o
B
.
w
ok
o
B
.
w
ww
t
e
X.n
ww
B
.B
w
ww
.B
w
w
w
w
Obstetric
w
161
t
t
t
Examination
.ne
.ne
.ne
X
X
X
Audible from 12wk
using a Doppler ultrasoundkand 24wk
ok Foetal aheart
oitkis faster
o
o
Pinard stethoscope;
than the mother’s o
(110–​160bpm).
Bo using
B
B
.
.
Weight Plot mother’s
618)
w weight and BMI (E p. w
wat the booking visit w
(Table 3.14). ww
w
w
Inspection Striae, linea nigra (line of pigmentation from the pubic symphysis to
navel that darkens during tthe 1st trimester), venous distent theoedema.
escars,
e
et
sion,
n
n
n
.
.
.
X height The fundus (topkofXthe uterus) is palpable from about
kX 12wkto
ok Fundal
o from the top of the pubicoosymphysis
gestation; it should be measured
o
o
B the top of the fundus
.B16 and 36wk the
tape measure. Between
w.Bwith ashould
wthe
fundal height inw
centimetres
be the same
as
gestation ±2cm,
w
w
w after 36wk.
eg 23–​27cmw
at 25wk. Fundal height is unreliable
See Fig. 3.22. w
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
36 weeks o
B
.B
w.B
40 w
weeks
w
w
w
w
ww
Bo
et
X.n
et
X.n
ok
ww
ok
o
B
w.
22 weeks
16 weeks
oo
B
.
ww
12 weeks
w
Fig. 3.22 Location of the fundus as pregnancy progresses.
t
.ne
X
k
ww
t 32wk it is possible tonassess
t
t
Foetal
position of the foetus
.nelie After
.theefoetalthehead:
.neby
palpating
across the abdomen for
X
X
X
Head palpable
midline
ok • Longitudinal
oinkfossa
ok
o
o
Head palpable
in
iliac
Bo •• Oblique
B
B
.
.
Transverse Headw
palpable in lateral abdomen. w
w
w
w after 32wk can also assess
w the presentation though ww
Presentation Palpation
this is liable to change until about 36wk. By palpating both ends of the
foetusethe
t position of the head cannbeetdetermined:
et
n
n
• .Cephalic
Head is at the bottom .
.
XBreech Head is at the top. kX
kX
ok •Engagement
o by palpating the base of theoouterus
o
o
This
is
assessed
above
B the pubic symphysis
B two hands to assess
.between
.B
how much of the
w
w
presenting part
wwis palpable. If only the top 1/​w5thwof the presenting part is ww
palpable the foetus has ‘engaged’.
Blood pressure
This must be monitored tregularly to assess for pregnancy-​
et iBP; consider
eand fundoscopy too.
et
n
n
n
induced
urine dipstick
.
.
.
X
X
X
ok Urine dipstick For proteino(pre-​
okeclampsia) and glucose (DM).
ok
o
o
B USS Lie, presentation,
confirmed
w.Band engagement can be w
w.B on USS.
w
w
w
ww
B
162
.B
w
ww
Chapter 3
ww
w
History and examination
t
.ne
Psychiatric
X
k
o
.B
w
w
t
.ne
X
k
et
.n
kX
oo
oo
B
B
.
.
Are you safe? Sit sow
patient is not between youw
and the door, remove
w the be
walarm,
all potentialw
weapons,
familiar with the panic
check notes/​ask ww
w
staff about previous violence, have a low threshold for a chaperone.
t
Set the
comfortable, ensure privacy e
and
etscene Make sure you are both
etthe
n
n
n
.
.
that
you will not be disturbed, eg.give
bleep to someone else,
have
X
X
kX
ok tissues available, emphasize
oconfidentiality.
ok
o
o
o
Basics Full name, age,.marital
were they referred
B
B status, occupation, who
w.B
by, current status w
under Mental Health Act.
w
w
w history Previous psychiatricwdiagnoses, in-​patient/​day ww
Past psychiatric
patient/​out-​patient care, do they have a community psychiatric nurse
(CPN),
previous deliberate self-​harm
etever
et(DSH), previous treatments
eandt
n
n
effects,
been admitted under.n
the Mental Health Act.
.
.
X
X medications, effects, kdidXthey/​do
history Current and
ok Medication
okprevious
o
o
oo
they
take
it,
allergies/​
r
eactions,
alternative/​herbal remedies.
B
B
B
.
.
w
Personal history ww
wwp. 166), associated
ww
• Childhood w
Pregnancy, birth, development (E
Bo
B
History
memories, names of schools attended, reason if changed schools,
types of school (mainstream/​specialist), age of leaving school,
qualifications
• Employment loss of jobs, which did they enjoy, why did they change, ask
about unemployment and why
• Relationships Current relationship(s) and sexual orientation, list of
major relationships and reasons for ending, any children and who they
live with and relationship to patient.
Forensic Contact with police, convictions or charges, sentences, outstanding charges.
Personality How would they describe their personality now and before
the illness? How would others describe it?
Social history Occupation and duration of employment/​unemployment,
where they live, concerns over money, friends and relationships, hobbies.
Drug and alcohol Smoking, alcohol, illicit drugs.
Family history Family tree with parents and siblings, ages, occupations, relationships, illnesses.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
w
.n
kX
t
ww
ww
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
ok
Bo
w
t
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Psychiatric
w
163
t
t
t
Examination
.ne
.ne
.ne
X
X
X
examine the mind
k 3.10
ok Psychiatrists
okthrough talking to the patient
o(Boxes
o
3.11). Much of the o
information is gleaned while taking
history
Bo and
B
B
. under the following headings.
. This isthecalled
and should be organized
the
w
w
Mental State Examination
(MSE).
w
w
w
w
ww
Appearance Racial origin, age, dress, make-​up, hairstyle, jewellery, tattoos, cleanliness, neglect, physical condition.
et Appropriateness, posture,
et movement (excessive, .nslow,
et
Behaviour
n
n
.
.
expression, eye contact, anxiety, suspiciousX­exaggerated), gestures, tics, facialkX
X
ok ness, rapport, abnormal movements,
o aggression, distraction,oconcentration.
ok
o
o
B Mood The patient’swsubjective
.B assessment of theirwmood.
.B
w
w
Affect Interviewer’s
objective assessment of mood
and appropriateness
w
w
ww
of patient’s response, eg flat, reactive, blunted.
Speech tform Accent, volume, rate, tone,
hesitations, stuttering;
e Associations (derailment, changing
et quantity,
et
Content
between subjects), puns.
n
n
n
.
.
.
X form Rate, flow (eg blocked),
X derailconnection (eg flight of ideas,
kXbeliefs
ok Thought
oself,
okinsertion/​
ment); Content Beliefs about
about others, thought
o
o
o
B withdrawal/​control/​
B beliefs about the world/​
future, delusions,
wb.roadcast,
w.Brituals,
overvalued ideas,
obsessions, compulsions, ruminations,
phobias.
w
w
w
w
ww
B
Perception Illusions, hallucinations (visual, auditory, tactile, olfactory), unusual experiences, depersonalization, derealization.
Cognition This can be tested formally using the Mini-​
Mental State
Examination (MMSE) on E p. 377; often the Abbreviated Mental Test
Score (AMTS) is used instead (E p. 375).
Risk Thoughts of deliberate self-​harm, suicide, harming others, plans, acquiring equipment, writing notes, previous suicide attempts. Can ‘protective factors’ be identified? Document these if so. Consider risk both
to self and to others.
Insight Awareness of illness and need for treatment.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
oo
B
.
w
ww
t
ok
Bo
.ne
X
k
t
ww
et
n
.
X
ok
o
o
w.B
ww
et
n
.
kX
o
.n
kX
What constitutes abnormal behaviour to the extent of constituting a
mental illness can be a controversial and difficult area, subject to allegations of cultural and political bias and even suggestions of undue
pharmaceutical industry influence. Two main classification systems are
accepted:
•The Diagnostic and Statistical Manual of Mental Disorders, produced
by the American Psychiatric Association; the 5th edition (2013) is
currently in use: DSM-​5
•The International Classification of Diseases, published by the World
Health Organization (covers all of medicine); 10th edition (1992) is
currently in use: ICD-​10. ICD-​11 is due to be published (2018).
e
X.n
ww
et
.ne
X
k
K Box 3.10 Defining ‘mental illness’
ww
Bo
w
t
o
w.B
t
.ne
X
k
ww
o
w.B
et
n
.
kX
ww
t
Each classification carries a slightly different emphasis and diagnostic
criteria; in rare instances, this results in an abnormal condition recognized in one, but not the other.
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
164
.B
w
ww
Chapter 3
.B
w
w
ww
w
History and examination
t
t
et
.nBox
.nein psychiatry
.ne
K
3.11 Common terms
X
X
X
ok
ok behaviours which reflects
ok emotions
Pattern of observable
o
o
Bo Affect
B
B
experienced.
w.
wof. perceived danger. w
Anxiety Feeling w
of apprehension
caused by anticipation
w
w A doctor entitled to recommend
w compulsory admis- w
Approved clinician
sion for treatment under the 2007 Mental Health Act.
Cognition
et The process of thinking,.reasoning,
et and remembering. .net
n
n
.
Compulsion
Repetitive
behaviours
in
to obsessions; X
often to
X egresponse
kX­relieve the distress causedobykthem,
k
washing hands.
o
o
Acute onset.B
ofodisordered cognition with .attentional
Bo Delirium
Bo deficits;
typically involveswchanges in arousal and maywbe associated with
hallucinations.
ww
ww
ww
Delusion A fixed, false belief that goes against available evidence and is
not explained
by the person’s religioustor cultural background.
et Global
e of cognition with preserved
et
Dementia
organic deterioration
n
n
n
.
.
.
X
X
X
ok consciousness.
ok of self as if detached or outside
okthe body.
Depersonalization Alteredosense
o
o
B
B of reality as if detachedwfrom
.Bsurroundings.
Derealization Altered.sense
w state
Emotion A complex
of feeling that results
in physical and psychow
w
w
w
ww
B
logical changes that influence thought and behaviour.
Euphoria Pathologically exaggerated feeling of well-​being.
Flight of ideas Rapid switching of topics where the thread of connection
can be determined (eg sound, content).
Formal admission Admission under a section of the Mental Health Act.
Hallucination A false sensory perception in absence of a real stimulus, eg
hearing voices; feature of psychosis if the subject lacks recognition of the
false nature.
Illusion False interpretation of a real external stimulus, eg seeing a
shadow and thinking it is a person.
Informal admission Voluntary admission as a psychiatric in-​patient.
Insight The ability of a person to recognize their mental illness.
Mania Abnormal elevation of mood with grandiose ideas, increased energy and agitation, pressure of speech, distractibility, and pleasure seeking.
Mood Emotional state that colours the person’s perception of the world.
Obsession Recurrent unwanted thoughts or images, eg my hands are dirty.
Passivity Delusional belief in external control of a person’s actions or
thoughts.
Personality disorder Enduring and inflexible behavioural patterns that
markedly differ to societal norms.
Phobia Persistent, irrational fear of an activity, object, or situation, leading
to the desire to avoid the feared stimulus; beyond voluntary control.
Psychosis Disordered thinking and perception without insight, often
­accompanied by delusions or hallucinations.
Ruminations A compulsion to consider an idea or phrase.
Stereotype Repeated pattern of movement or speech without any goal.
Thought insertion Delusional belief by a person that an external agency is
putting thoughts into his/​her mind (a passivity phenomenon).
t
.ne
X
k
oo
et
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kX
oo
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.
ww
ww
o
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t
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et
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et
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et
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et
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e
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ok
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t
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
Neonatal examination
w
w
165
t
t
t
.ne
.ne
.ne
Neonatal
examination
X
X
X
ok baby check is a keyocomponent
ok of life in paediatrics.ooAllk neonates
Bo The
B
. 72h of birth with the aim
should be examined within
wbabies
w.of:B
• Identifying unwell
(tone and respiratory
rate
w
w
w ones).very important) ww
• Identifyingw
abnormalities (especially reversible
Preparation Prior to the examination you should check the maternal
t significant maternal illness,negestation
t at birth, birthweight,ntype
efor:
et
notes
n
.
.
.
of
delivery,
problems
at
delivery
(meconium,
premature
rupture
of
memX (PROM), group B strep,
kXlow APGAR scores: appearance,
kX pulse,
ok branes
o
o
o
o
o
B grimace, activity, respiration).
w.B
w.B
Introductionw
Introduce yourself to the mother/​
parents, offer congratuw
w
w
lations and explanation.
Has the baby passed w
faeces and urine? Feeding w
well? Any parental concerns? Ask them to undress the baby to the nappy.
et baby Consider doing
ethet following first as they are.ndifet
n
n
.
.
$
Settled
X if the baby is crying: listening
X
kX to the heart and feeling
the apex
ok ficult
ofemoral
okeyes.
o
o
o
beat,
count
RR,
feeling
the
pulse,
and
looking
in
the
B
.Bgetting the baby to suck (pacifier,
wTry
w.B breast, bottle, w
$ Crying baby
w
w
parent’s little
wfinger, your little finger); if thiswfails, swaddle the baby and w
ask the parents to give the baby a feed then return in 30min.
t
t
et
Overall
.ne Take a few momentsXjust.ntoelook; is the baby: jaundiced,
.nblue,
X
X
moving normally,kbreathing normally?
ok dysmorphic,
o
ok limb
o
Tone (DegreeB
ofohead support, spontaneousB
symmetrical
Bo Neuro
. is not routinely performed.
movements), Moro
wreflex
w.
w
w
Head Anterior
w and posterior fontanelle (bulging,
w sunken), head circum- ww
ference, eyes red reflex (red flag if absent), face (dysmorphic?), ear shape
and position
(tags, pits, top of insertiontof pinna should be at the level of
t
et palate
the.n
eyes),
(with your little finger),
.ne suck reflex.
.ne
X
X
X
(single
ok Hands/​arms Fingers (number,
ok shape, colour), palms
ok crease in
o
arm
movement.
Bo 60% of Down’s andw1%.Bofonon-​Down’s), symmetrical
B
w. to the heart, apex w
Chest Respiratory
rate (RR >60 is abnormal),w
listen
w
w the clavicles for fractures. w
w
beat, gently feel
Abdo tPalpate (to exclude hepatomegaly,
splenomegaly, masses), dese testes, patent anus, enlarged.nclitoris,
et femoral pulses.
et
cended
n
n
.
.
X feet Anterior hip creases
X(symmetrical?), Barlow test k(flex
X hip to
ok Hips/​
oka click/​
o Ortolani
o
o
90°, press posteriorly, feelofor
clunk if the hip dislocates),
B test (after Barlow’swabduct
.B the hips one at a timewwhile
.B pressing on the
greater trochanter
with your middle finger, feel for
a click/​clunk as the hip
w
w
w
w
ww
relocates), note repetition of these tests can cause hip instability, ankles
(talipes, correctable or not), toes (number, shape, colour).
et
et
et
n
n
n
.
.
.
make a note), posterior hip creases.
Xdefects), buttocks (blue spots—​
X
X
ok Plot In the red book: weight,
okhead circumference, examination.
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Turn baby over Spine (straight), sacrum (lumps, dimples, hair tufts, skin
B
166
.B
w
ww
Chapter 3
ww
w
History and examination
t
.ne
Paediatric
X
k
o
.B
w
w
t
.ne
X
k
et
.n
kX
oo
oo
B
B
.
.
Basics Age in days w
1mth), weeks (until 2mth),w
months (until 2yr), or
w (until
years, gender,
gave the history, who was
present.
wwho
ww
ww
Current state Feeding and drinking, weight gain, wetting nappies/​passing
urine, tfever, bowels, crying, runny nose,
e ears, drawing up legs, rash..net cough, breathing problems,
et
pulling
n
n
.
.
X Pregnancy problems andkmedications,
X
X 2/​40
at birthk(37–​
ok Birth
o (NVD, induced,gestation
o if4LSCS
is normal), type of delivery
ventouse, o
forceps,
o
o
B
.Bspecial care, birthweight,wPROM,
.B group B strep
ask why), resuscitation,
wmaternal
(GBS), meconium,
pyrexia during labour,
vitamin K (IM or oral),
w
w
w bottle, type of milk). w
ww
feeding (breast,
Immunizations Check the child is up to date with vaccinations (Table 3.15);
t or febrile beforehandneandt
jabs will
be postponed if the child iseunwell
et often
n
n
.
.
.
children
get
a
slight
fever
for
<24h
afterwards.
X
X
X
k
k
k
o
o
o
vaccination
Bo Table 3.15 UK w
Bo schedule (from Augustw2017)
Bo
.
.
Birth
May get tuberculosis (BCG) and/​or hepatitis B if at risk
w tetanus, pertussis, poliowand
w Haemophilus
wDiphtheria,
ww
2mth
Bo
B
History
influenzae type b (DTaP/​IPV/​Hib), hepatitis B, pneumococcal
disease (PCV), Rotavirus, meningococcal group B (MenB)
3mth
Diphtheria, tetanus, pertussis, polio and Haemophilus
influenzae type b (DTaP/​IPV/​Hib), hepatitis B, and rotavirus
4mth
Diphtheria, tetanus, pertussis, polio and Haemophilus
influenzae type b (DTaP/​IPV/​Hib), hepatitis B, pneumococcal
disease (PCV) and MenB
12–​13mth
Measles, mumps, rubella (MMR), Haemophilus influenzae type B
(Hib), pneumococcal (PCV), meningococcal group C disease
(MenC), MenB
2yr to 8yr
Influenza
3yr4mth–​5yr Diphtheria, tetanus, pertussis and polio (DTaP/​IPV), MMR
12–​13yr
Human papilloma virus (girls only)
14yr
Tetanus, diphtheria, and polio (Td/​IPV) and meningococcal
groups A, C, W, and Y disease
.
kX
o
o
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et
oo
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.n
kX
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.
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et
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.
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ww
Source: data from Mhttps://​www.gov.uk/​government/​uploads/​system/​uploads/​attachment_​
data/​file/​633693/​Complete_​imm_​schedule_​2017.pdf. Contains public sector information
licensed under the Open Government Licence v3.0.
t
e
X.n
.ne
X
k
t
ww
et
n
.
X
ww
k
ok
See Table 3.16
ooand ask about school performance.
oo
Bo Development
B
B
.
.
Social history Whowthe child lives with, parental w
responsibility, parental
wof school (mainstream, ww
jobs, smoking, w
nursery/​school attendance, type
w
w
special needs), academic ability, sporting ability, friends, enjoyment of
school, foreign travel.
t Family tree with parents
ehistory
etand siblings, consanguinity .ifnreleet
Family
n
n
.
.
vant,
illnesses
in
the
family,
how
are
their
parents
and
siblings
at
the
moX asthma, eczema, hayfever,
X
X
ok ment,
ok DM, epilepsy, other diseases
okspecific to
o
o
o
presenting
complaint.
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Paediatric
w
167
t
t
t
Examination
.ne
.ne
.ne
X
X
X
of the examination can k
by simply observing
k the child;
ok Muchusually
o beofperformed
oyounger
o
o
has the advantage
limiting tears. Approach
chilBo this
B
B
. are sitting on a parent’s knee
. and feeling secure.
dren gently while w
they
w
Examination is much
ww the same as for adult patients,
wwbut include the following: ww
2 If unwell ABC and resuscitate, E pp. 238–40. Always records obs—​
for normal
ranges by age, see Box 6.11t(E p. 240).
et Ask
eyou if a child of either sex is.nover
et
n
n
.
.
Chaperone
a nurse to accompany
X
X
X
ok 10yr, if there is a child protection
ok issue, or whenever you feelooit isknecessary.
o
o
B Hydration Fontanelle,
mucous
.Bcapillary-​refill (≤2s), warmwperipheries,
.B
membranes, tears w
if crying, skin turgor, sunken eyes,
tachycardia, lethargy.
w
w
w head bobbing, nasal flaring,
w tracheal tug, cervical ww
Respiratory Grunting,
lymphadenopathy, recession (sternal, subcostal, intercostal).
et Cyanosis (check mouth),
etclubbing, mottled skin, murmurs
et
Cardiovascular
n
n
n
.
.
.
Xmay radiate to the back, femoral
X pulses (coarctation), radiofemoral
ok delay, dextrocardia, hepatomegaly
ok (heart failure). ookX
o
o
B Abdominal Check the
B genitalia if young, relevant,
w.external
w.B or boys with w
w
abdominal painw
(torsion); never do a PR (though
seniors might).
w
w
w
Neurological AVPU (Alert, responds to Voice, responds to Pain,
Unresponsive), fontanelles, tone, reflexes (including Moro and grasp reflex
if young), head circumference (growth chart), development (Table 3.16).
t
t
t
.ne
.ne
.ne
X
X
X
k development
ok Table 3.16 Key stages inoochildhood
ok
o
Bo Age Gross motor
B
B
w. Fine motor Speechww. Social
w
6wk
Holds
head
Eyes follow 90°
Startles
w
w to Smiles
ww
in line
sound
3mth t Lifts head up Eyes follow 180° t Coos
Laughs
e Sits
e Babbles
et
n
n
6mth
Transfers objects
Objects to .n
.
.
X
X
X
unsupported
mouth
ok
okthumb grip ‘Mama, dada’ Waves
okgoodbye
Pulls to stand Finger–​
o
o
Bo 9mth
B
B
12mth Walks
First wordsw. Finger foods
w. Points
unsupported
w
w
ww
ww
18mth Running
2yr
Lumps
net
Scribbles
Copies line
Asks for ‘wants’ Feeds alone
Uses fork
2–​3-​word
net sentences
et
n
.
.
X
X
tricycle Copies circle
and age Dry by day
ok 4yr Uses
okcross Name
obyknight
Hops
Copies
Counts to 10 Dry
o
o
o
B
.B
wthe.Bears and throat if there iswawsuspicion
ENT Always check
infection;
w
w or pus is ofpresent.
ww
describe thew
colour, appearance, and if an effusion
Weight, height These should be plotted on a sex-​specific growth chart.
t
ecircumference
etimportant in infants and .nthose
et
Head
This is especially
n
n
.
.
X neurological disease; thekXmeasurement should be plotted
X
ok with
o
ok on a
sex-​specific chart.
o
o
o
B
w.B
w.B
w
w
w
w
ww
X3yr.
B
.B
w
ww
t
.ne
X
k
o
Bo
oo
B
.
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et
n
.
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ok
et
n
.
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k
oo
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.
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o
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o
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et
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k
ok
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ww
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.
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o
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e
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o
w.B
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kX
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et
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.
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o
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w
ww
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w
w
w
w
Chapter 4
w
169
t
t
t
.ne Prescribing
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
Prescribing—​general considerations 170
to prescribe—​best practice 171
t How
e
et
Drug interactions 173 net
n
n
.
.
.
Reporting
adverse
drug
reactions
173
X Special considerationskX174
kX
ok
o
o
o
o
o
Controlled drugs
175
B
Enzyme inducers
w.B and inhibitors 176 ww.B
w
Endocarditis
w prophylaxis 177 w
ww
Night sedation 178
therapy 179
et Steroid
et
et
Topical corticosteroids 180
n
n
n
.
.
.
Empirical
antibiotic
treatment
181
X Clostridium difficile (C.kdiff)
X
X
ok
o 182
ok
o
o
o
B
w.B
w.B
w
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w
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oo
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.
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170
.B
w
ww
Chapter 4
.B
w
w
ww
w
Prescribing
t
t
t
.ne
.ne considerations
.ne
Prescribing—​
g
eneral
X
X
X
ok
okis increasing in medical schools,
okyet it is only
to safe prescribing
o
o
Bo Exposure
B
B
really when you are .faced daily with drug charts and. decisions that you
w will only know w
get the hang ofw
it.w
Even the most experienced w
w of doctors
by heart thew
dose and frequency of a maximum
of 30–​40 drugs, so do w
not worry if you cannot remember everything. Start basic: paracetamol
for adults
et is 1g/​4–​6h PO, max 4g/​.2n4hetin divided doses (E p. 213)..net
n
.
Many
errors in hospital
involve drugs, so it is important
Xyou want
X to
kXconsidermedical
k
k
a few things everyo
time
to prescribe a drug,
rather than
o
o
Bo just writing a prescription
.Boas a knee-​jerk reaction. w.Bo
w
Indication Isw
a valid indication for the drug?
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w
w there
wwas move
method to solve
the problem in question (such
the patient to a w
quiet area of the ward rather than prescribe night-​time sedation)?
et
et
et
Contraindications
What contraindications
are there to the.ndrug?
n
n
.
.
Does
the
patient
have
asthma
or
Raynaud’s
syndrome,
in
which
case
X
X
ok β-​blockers may create more
okproblems than they solve. ookX
o
o
B
B If a patient is nil by mouth
Route of administration
then it is
w.oral
wor.Bask(NBM),
w
w
pointless prescribing
medications; use the BNF
the pharmacist
w
w
ww
to help you use alternative routes of administration. Remember IM and
SC injections can be painful, so avoid these if possible.
t
et
Drug
when physically.n
mixed
netinteractions Some drugs
nareeincompatible
.
.
X
X
X
IV furosemide and
and other
ok togethercause(egphysiological
ok IV(egmetoclopramide),
ok combinproblems
ACEi with K -​sparingodiuretics).
Look
o
Bo ations
B
B
through the patient’s drug
(E p. 173).
. chart to spot potential drugwinteractions
.
w
Adverse effects
ww All drugs have side effects.
ww Ensure the benefits of ww
treatment outweigh the risk of side effects and remember some patients
are more prone to some side effects than others (eg Reye’s syndrome
et with aspirin, or oculogyric
et crises in young females.nwith
et
in n
. children
.nshould
metoclopramide).
Some side effects
prompt urgent action
(such as
X
X
X
statin drugs in patients
ok stopping
ok who complain of muscle pains,
okor patients
o
get wheezy with.B
β-​bolockers), but others can be advantageous
if they
Bo who
B
do not expose the
wpatient to unnecessary risksw(such
w. as slight sedation w
w
with some antihistamines).
w
w
w
Administering drugs Always double check the drug prescription and
the drug
with another member of staff
eat sign
et (qualified nurse or doctor)..nThis
ewillt
n
is .not
of uncertainty, this is .ansign that you are meticulous and
X limit the chance of a drug
X
X
ok greatly
ok error occurring, which would
ok make you
o
look careless. Equally, if o
you are asked to check a drug o
calculation then
B
B attention (often this meanswperforming
.B
take it seriously and
the drug
w.pay
w
calculation againwyourself ).
w
w
ww
+
2 If in doubt Never prescribe or administer a drug you are unsure
Bo
o
et
n
.
kX
et
n
.
kX
t
.ne
X
ok
.Bo
about, even if it is a dire emergency—​seek senior help or consult the
BNF or a pharmacist.
o
o
B
.
w
ww
w
ww
ww
B
.B
w
ww
.B
w
w
w
w
How to prescribe—best practice
w
171
t
t
t
.ne to prescribe—​
.nbeest practice X.ne
How
X
X
ok drug card Thereoareokusually at least four drug sections
ok (Figs 4.1–​
o
Bo The
B
B
.
4.3); once-​
only/​
tat
regular medications,wPRN (‘as required’)
w.doses,fluids
wsinfusions/​
w
medications,w
and
(E pp. 394–7).
Other
sections include ww
w
O , anticoagulants, insulin, blood products (often a separate card), medications prior to admission, and nurse prescriptions.
t
et the drug card As with
ethe
et
n
n
n
Labelling
patient’s notes, the drug
card
.
.
.
X have at least three identifying
X
features: name, DoB, and NHS
kXnumber
ok should
oNHS
ok number
(the NPSA advice is that the
should be usedowhenever
poso
o
B sible). There are usually
.Bspaces to document the ward,
.B
consultant, date of
w
w
admission, and number
2, 2 of 2, etc.).
ww of drug cards in use (1wof w
ww
The allergy box Ask the patient about allergies; check old drug cards if
available.
any allergies in this tbox and the reaction precipitated;
et Document
e drug allergies then record
ethist
eg.penicillin
l rash. If there are no.n
known
n
n
.
too.
Nurses
are
unable
to
give
any
drugs
unless
the
allergy
box
is
complete.
X
X
X
ok Writing a prescription
okUse black pen and write clearly,
ok ideally in
o
o
o
B capitals. Use the generic
B Voltarol ) and
w.B drug name (eg diclofenac,
w.not
w
clearly indicate w
the dose, route, frequency of administration,
date started,
w
w
ww
2
®
and circle the times the drug should be given (Figs 4.2 and 4.3). Note that
some drugs do require generic names in addition to brand names—​often
the case with medications used in Parkinson’s disease. Record any specific
instructions (such as ‘with food’) and sign the entry, writing your name and
bleep number clearly on the first prescription. See Box 4.1 for verbal prescriptions and Box 4.2 for self-​prescribing.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
t
.ne
X
k
oo
B
.
w electronic services
Electronic prescribing
Many hospitals now w
employ
w
w system so try to become ww
to help withw
prescribing. There is no universal
familiar with your system as quickly as possible—​check with your ward
pharmacist
t
et or colleagues if you need.na refresher.
et
n
.
.ne
Common abbreviations X
X
X
k
ok
ok
STAT—​
immediately
bd—​twiceo
ao
day/​12h
o
Bo IVPO—​—​intravenous
B
B
tds—​t.hree times a day/​8h
. gram
by mouth
wg—​
w four times a day/​6h
microgram—​avoid mcg or µg w
qds—​
IM—​intramuscular
w
,
—​
o
ne
dose,
two
doses
w od—​once a day/​24h w units—​avoid ‘IU’ or ‘U’
ww
SC—​subcutaneous
PRN—​as required
PR—​by rectum
om—​every morning
mg—​milligram
t
INHe
—​tinhaled
on—​every night
e
et
mL—​millilitre
n
n
n
.
.
.
NEB
—​nebulized
X
X
X
ok Changes to prescriptions
okIf a prescription is to change,oodoknot
o
o
B the original; cross itwout.Bclearly and write a new prescription
.B (Fig. 4.1).amend
Initial
w
w prescriptions. It is essential
and date anyw
cancelled
that you record the reason ww
ww
B
(eg β-​blocker stopped in wheezy asthmatic patient), otherwise someone else
might not realize why it was stopped and re-​prescribe it.
et
et
et
n
n
n
.
.
.
X doses, and original startkdates
X carried over and that the
X
ok drugs,
oand filedare
ok old drug
card(s) are crossed through
in the notes.
o
o
o
B
w.B
w.B
w
w
w
w
ww
Rewriting drug cards When rewriting drug cards, ensure the correct
B
172
Chapter 4
.B
w
w
o
oo
B
.
w
t
.ne
X
k
ww
o
Bo
et
n
.
kX
ww
w
Prescribing
t
.ne
X
k
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et
o
w.B
.n
kX
o
ww
t
ok
o
w.B
ww
et
n
.
kX
oo
e
X.n
.B
w
ww
ww
ww
Fig. 4.1 Example of cancelled drug prescription for a regular medication.
et
n
.
X
ok
Bo
B
.B
w
ww
et
n
.
X
ok
o
B
.
w
ww
t
.ne
X
k
oo
o
B
.
w
ww
ww
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
t
.ne
X
ok
t
.ne
X
k
ww
w
Fig. 4.2 Example of drug prescription for a PRN medication.
o
Bo
t
.ne
X
k
t
o
o
w.B
.ne
X
k
ww
Box 4.1 Verbal prescriptions
t
ok
Bo
t
.ne
X
k
et
n
.
X
ok
o
o
w.B
ww
Box 4.2 Self-​prescribing
ww
o
w.B
ww
F1s can only prescribe on in-​patient drug cards and TTOs. The GMC’s
‘Good Medical Practice’ guidance (2013 Mwww.gmc-​uk.org/​guidance/​
good_​medical_​practice.asp) states you should ‘avoid providing medical care to yourself or anyone with whom you have a close personal
relationship’. Do not get tempted or pressured to ignore this.
et
n
.
kX
o
ww
Verbal prescriptions are only generally acceptable for emergency situations, and the drug(s) should be written up at the first opportunity. If a
verbal prescription is to be used, say the prescription to two nurses to
minimize the risk of the wrong drug or dose being given. Check your
local prescribing policy first.
e
X.n
Bo
oo
B
.
w
Fig. 4.3 Example of a once-​only (STAT) medication.
ww
et
.n
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Reporting adverse drug reactions
w
173
t
t
t
.ne interactionsX.ne
.ne
Drug
X
X
ok list of specific drug interactions
ok are shown in Appendixo1oofkthe BNF.
o
Bo APharmacokinetic
B
.interactions Occur whenwone.Bdrug alters the abwmetabolism,
w
w
sorption, distribution,
of w
another drug which alters
wactive drug, causingoranexcretion
w
the fraction of
aberrant
response to a standardized w
dose. See the following examples:
et Metal ions (Ca , Fe .)nform
et complexes with tetracyclines
et
Absorption
n
n
.
.
which
decreases
their
absorption
and
bioavailability.
X
X
X
ok Distribution Warfarin is ohighly
ok bound to albumin, so odrugs
ok such as
o
B sulfonamides whichwcompete
.B for binding sites onandalbumin
.B cause displacewanticoagulant
ment of warfarin,
increasing its free fraction w
effect.
w
There are many
w drugs which influence the binding
w of warfarin like this. ww
Metabolism Rifampicin is a potent enzyme inducer (E p. 176) and increases
of the OCP, reducing
its clinical effectiveness; other
eoftmetabolism
etin such
et
n
n
forms
contraception should be.used
circumstances. .n
.
X
Xrenal clearance of digoxin, kresulting
X
Quinidine reducesok
the
ok Excretion
o the risk ofin
o
o
o
higher than anticipated levels
of serum digoxin and increasing
B digoxin side effectswand/​
.Bor toxicity.
w.B
w
w
Pharmacodynamic
interactions
Describe
w
w the effect that drugs ww
2+
have on the body and their mechanism of action. Interactions occur when
2 or more agents have affinity for the same site of drug action, eg:
• Salbutamol and propranolol (a non-​specific β-​blocker) have opposing
effects at the β-​adrenergic receptor; clinical effect is determined by the
relative concentrations of the two agents and their receptor affinity.
et
.n
kX
et
.n
kX
et
.n
kX
oo
oo
B
B
.
.
2 Drugs which commonly
w have interactions are worth
wkeeping an eye out for. w
wdigoxin,
wantibiotics,
These include
warfarin, antiepileptics,
antidepresw
w
w
sants, antipsychotics, theophylline, and amiodarone.
t
t
net
.ne
.drug
.ne
X
X
X
Reporting
adverse
reactions
ok
ok
ok
o
o
Bo The Yellow Card
B
B
. Scheme This has been running
. since 1964 and
wproducts
is coordinated w
byw
the Medicines and Healthcare
Regulatory
w
w During drug development,wside effects with a frequency ww
Agency (MHRA).
of 1:1000 or greater (more common) are likely to be identified, so the
Yellow tCard Scheme is important in detecting
side effects once ta
eatduty to rarer
n
n
ne
drug
isein general use. All doctors have
contribute to this. .Yellow
.
.
X
X
X
tear-​
o
ut
slips
in
the
back
of
the
BNF
can
be
sent
off
or
go
online
ok Mhttps://​yellowcard.mhra.gov.uk/​
ok . The forms can be completed
ok by anyto
o
o
o
B healthcare workerw
and.B
even by patients.
w.B
w
w
New drugs These
are marked with an inverted
triangle (▼) in the BNF.
w
w
ww
Bo
o
3+
Any suspected reaction caused by a new drug must be reported.
2 Sinister drug effects Such as anaphylaxis, haemorrhage, severe
skin reactions etc., must be reported via the Yellow Card Scheme, irrespective of how well documented they already are.
t
e
X.n
t
e
X.n
t
e
X.n
k
k
ok Common drug reactions
oo Such as constipation.B
ooopioids, indifrom
B
.
gestion from NSAIDs,
w and dry mouth with anticholinergics,
w are well recog- w
nized and considered
notw
need reporting.
ww minor effects which dow
w
Bo
B
174
.B
w
ww
Chapter 4
.B
w
w
ww
w
Prescribing
t
t
t
.ne considerations
.ne
.ne
Special
X
X
X
ok
okcarefully considered with specific
ok reflection
prescription shouldobe
o
Bo Every
B
B
of the patient in question.
If in doubt, consult the BNF
or speak to the
w. There
wof .patients
pharmacist or w
a senior.
are some groups
for whom
w
wmust be even more carefully considered.
w
ww
prescriptions
Patients with liver disease The liver has tremendous capacity and
et so liver disease is often severe
etby the time the handling of.nmost
et
reserve
n
n
.
.
drugs
is
altered.
The
liver
clears
some
drugs
directly
into
bile
(such
as
X cautiously if at all. The liverkalso
X manu-rikXfampicin) so these should beokused
o
o
oand hypoproteinaemia can.Bresult
o in increased
plasma proteins
Bo factures
.Bagents
free fractions of some
(phenytoin, warfarin,w
prednisolone) and rew
sult in exaggerated
ww pharmacodynamic responses.
wwHepatic encephalopathy ww
can be made worse by sedative drugs (night sedation, opioids, etc), and
fluid overload
by NSAIDs and corticosteroids
documented in liver
etHepatotoxic
et is well
et
failure.
drugs (such as n
methotrexate
and isotretinoin) should
n
n
.
.
.
only
be
used
by
experts
as
they
may
precipitate
fulminant
hepatic
failure
X
X
X
ok and death. Patients with established
ok liver failure have an increased
ok bleeding
o
o
o
tendency so avoid IM.injections
and employ caution if .using
any anticoaguB
w Bcan be used in liver disease,
w Bbut consider a re- w
lant drugs. Paracetamol
w
w
duced dose;w
consult the BNF/​pharmacist. Special
w considerations for patients w
with liver disease are listed under each drug monograph in the BNF.
t
Patients
renal disease Patients
et with impaired renal function
et
.ne onlywith
should
be given nephrotoxic.n
drugs with extreme caution as.nthese
X
X
X
fulminant renal
failure; these include NSAIDs,
gentamicin,
ok may precipitate
okAny
ok(impairment
o
o
ACEi, and IV contrast.
patient with renal disease
Bo lithium,
B
B
. will have altered drugwhandling
. (metabolism,
or end-​stage renalwfailure)
w
w
clearance, volume
of distribution, etc) and more
careful thought must
w prescribing for the patientswwith GFR <60mL/​min, and ww
be given when
senior input sought when GFR <30mL/​min (BNF, pharmacist or senior);
t dosing frequency, andnchoice
the amount,
et of drug needs careful thought.
net
.ne that
.normal
Remember
a creatinine in X
the. ‘normal’ range does not mean
X
X
k considerations for patients
387.oSpecial
ok renal function, E p. each
ok with renal
o
drug monograph in the BNF. Bo
Bo disease are listed under
B
w. Many drugs can cross thewplacenta
w. and have effects w
Pregnant patients
w
w In the first trimester (weeksw1–​12), this usually results in w
upon the foetus.
congenital malformations, and in the second (weeks 13–​26) and third trimesters
growth retardation or has direct
t (weeks 27–​42) usually results
eeffects
eint are
euset
n
n
n
toxic
upon foetal tissues. There
no totally ‘safe’ drugs.to
.
.
X
X known to be particularly troublesome.
X
but there are drugs
ok inThepregnancy,
okshortest
ok be used
minimum dose andothe
duration possible o
should
o
B
when prescribing in pregnancy
w.B and all drugs avoided
wif.Bpossible in the first w
trimester.
w
w
w
w
w
et
n
.
kX
o
Bo
Drugs considered acceptable Penicillins, cephalosporins, heparin, ranitidine,
paracetamol, codeine.
2 Drugs to avoid Tetracyclines, streptomycin, quinolones, warfarin, thiazides, ACEi, lithium, NSAIDs, alcohol, retinoids, barbiturates, opioids,
cytotoxic drugs, and phenytoin.
et
n
.
kX
t
o
o
B
.
w
ww
w
.ne
X
ok
.Bo
Special considerations for pregnant patients are listed under each drug monograph in the BNF.
ww
ww
B
.B
w
ww
.B
w
w
w
w
Controlled drugs
w
175
t
et patients, drugs given.tonethet
Breastfeeding
patient As with
.ne
.npregnant
X
X
X baby.
can get into breast milk
on to the feeding
k and be passed
ok mother
oconcentrated
ok maternal
Some drugs become more
in breast milkothan
o
o
B plasma (such as iodides)
.BOther drugs can
child.
w.B and can be toxic to theorw
stunt the child’sw
suckling reflex (eg barbiturates),w
act to stop breast milk
w
w to a pharmacist before ww
production altogether
(eg bromocriptine). Speak
prescribing any drug to a mother who is feeding a child breast milk. Special
considerations
for patients who are breastfeeding
are listed under each drug
et in the
et
et
n
n
n
.
.
.
monograph
BNF.
X
kX Formulary for Children. oNeonates
kX are
ok Children See the BritishooNational
o
o
B more unpredictablewin.B
B
terms of pharmacokinetics and.pharmacodynamics
wshould
than older children;
prescriptions for this age group
be undertaken
w
w
by experienced
w neonatal staff and drugs double-​
w checked prior to adminis- ww
tration. After the first month or two, the gut, renal system, and metabolic
pathways
more predictable. Almost
t all drug doses still need
et become
etot
be.calculated
by weight (eg mg/​kg).n
oreby body surface area (BSA)..There
n
n
X a few drugs which shouldknever
X prescribed in childrenkbyX a non-​
ok are
o (causesbeirreversible
specialist, including tetracycline
staining
o
o
ooof bones and
B teeth) and aspirinw(predisposes
B
to Reye’s syndrome);
others should be
.B
.
w
used with caution
such as prochlorperazine and isotretinoin.
2 Always
wwfor Children when prescribingwforwpaediatric patients.
ww
consult the BNF
t
t
t
.ne
.ne
.ne
Controlled
drugs
X
X
X
k
k
ok
oo CDs are those drugs .which
ooare addictive
drugs.B
(CDs)
Bo Controlled
B
and most often abused
and are subject to
and
ww oforthestolen,
wwthe prescription
storage requirements
Misuse of Drugs
Regulations
2001; they in- ww
w
w
clude the strong opioids (morphine, diamorphine, pethidine, fentanyl,
alfentanil, remifentanil, methadone), amphetamine-​
like agents (methylt (Ritalin )), and cocaine (anlocal
t anaesthetic).
t
e
e
phenidate
agents
n
. in a locked cabinet and X
. of their use onThese
.neare
stored
a record
a named
patient
X
X
is required to be keptobyklaw. Some other drugs may be
the
ok basiscupboard
okkept in and
o
o
such as.B
concentrated
KCl, ketamine, benzodiazepines,
Bo CD
B
.
anabolic steroids, but
w this is not a legal requirement
wand will depend upon
w
local policy. w
Thewweaker opioids (codeine) are
not treated as controlled ww
w
drugs though they are still often misused.
t
Prescribing
drugs Prescribing
patients is just e
like
et any controlled
et shouldforbein-​
n
n
n
.
.
prescribing
other drug and the .benefits
balanced against
poX side effects for each individual
X patient. Morphine, diamorphine,
X
ok tential
ok prescribed
ok and
o
o
tramadol are the most commonly
CDs on theoward. As with
B all prescriptions, write
.Ba maximum dose
details clearly and makew
sure
w.Bthe
w
w
and a minimal interval
between doses is documented
(E pp. 88–91 for
w
w
ww
®
management of pain).
Controlled drugs for TTOs E pp. 80–1.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
176
.B
w
ww
Chapter 4
.B
w
w
ww
w
Prescribing
t
t
t
.ne
.ne inhibitors X.ne
Enzyme
inducers
and
X
X
ok term enzyme inducersooiskused to describe agents (usually
okdrugs, but
o
Bo The
B
B
. the activity of the cytochrome
. P450 enzymes
not always) which alter
wphase
(mostly found w
in w
the liver) which are involved
in
metabolism
w
w
w reduction, and hydrolysis
w reactions). 1Agents
(typically oxidation,
which w
induce cytochrome P450 activity result in increased metabolism of the
affected
and subsequently reduce
etofdrugs
et the systemic drug response;
ein-t
n
hibitors
cytochrome P450 have.n
the reverse effect and result in.n
exag.
X drug responses as more
X of the affected drug remains
X
ok gerated
ok inducers
oklistedavailable
to exert its effect. Common
and inhibitors o
are
here.
o
o
B
You’ll see warfarinw
is .aB
frequent culprit (Table 4.1).w.B
w
w Appendix 1 of BNF ww
Table 4.1 w
Drugs interacting with warfarin—​
wconsult
Alcohol, amiodarone, cimetidine, simvastatin, NSAIDs
Drugs which iINR
etwhich dINR Carbamazepine,.nphenytoin,
et rifampicin, oestrogens .net
Drugs
n
.
X
X
X
ok Inducers
ok
ok
o
o
o
B
.BEach of the drugs
Table 4.2 shows drugs
induce metabolic enzymes.
w.Bthat
on the left canw
induce
the enzymes so that allw
of w
the drugs on the right
w
(and any of w
the other drugs on the left) will w
have reduced plasma levels: w
Table 4.2 Enzyme inducers
t
t
t
.ne inducers
.ne levels reduced
.ne
Enzyme
Plasma
X
X
X
ok Phenobarbital/​barbituratesook Warfarin
ok
o
Bo Rifampicin
B
B
Oral contraceptives .
w.
Phenytoin
Corticosteroids ww
w
w
ww
Ethanol (chronic use)
Ciclosporin w
Carbamazepine
(All drugs on left)
t
t
t
e
n
.
.ne
.ne
Inhibitors
X
X
X
ok
okwhich inhibit enzymes. Each
oofk the drugs
4.3 shows some drugs
o
o
Bo Table
B
B
on the left can influence
the
metabolic
enzymes
responsible
for breaking
.
w
w. of increasing
down the specific
drug on the right; this has the
effect
the
w
w
plasma levelw
of this latter drug, exaggeratingw
its biological effect.
ww
Tablet 4.3 Enzyme inhibitors
e inhibitors
etlevels increased
et
n
n
n
.
.
.
Enzyme
Plasma
X
X
X
ok Disulfiram
ok Warfarin
ok
o
o
o
Chloramphenicol
B
.B Phenytoin
w.B
Corticosteroidsww
Tricyclic antidepressants
w
w
w
ww
et
n
.
kX
o
Bo
Cimetidine
MAO inhibitors
Erythromycin
Ciprofloxacin
et
n
.
kX
o
o
B
.
w
ww
Amiodarone, phenytoin, pethidine
Pethidine
Theophylline
Theophylline
w
ww
t
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Endocarditis prophylaxis
w
177
t
t
t
.ne
.ne
.ne
Endocarditis
prophylaxis
X
X
X
ok
ok
ok
o
o
and children
with structural cardiacB
conditions
Bo Adults
B
. following cardiac conditions
Regard people with
wthe
w. as being at risk of w
w
w
developing infective
endocarditis
:
w
w
w
•Acquired valvular heart disease with stenosis or regurgitation
• Valve replacement
et congenital heart disease,.nincluding
et surgically corrected or.net
• Structural
n
.
palliated
structural
conditions,
but
excluding
atrial septal
Xdefect,
kXfully repaired ventricular septal
kXdefect or fullyisolated
kductus
repaired patent
o
o
o
Bo arteriosus, and closure
Bo
.Bodevices that are judged towbe.endothelialized
w
• Hypertrophic cardiomyopathy
• Previous infective
ww endocarditis.
ww
ww
Advice
t at risk of infective endocarditis
Offer e
people
et clear and consistent.ninforet
n
n
.
.
mation
about prevention, including:
X benefits and risks of antibiotic
X prophylaxis, and an explanation
X
ok • The
okis no longer
ok of
o
o
o
why
antibiotic
prophylaxis
routinely
recommended
B • The importancew
B
B
of .maintaining good oral health w.
w
w
• Symptoms that
may indicate infective endocarditis
and when to seek
w
w
ww
1
expert advice
• The risks of undergoing invasive procedures, including non-​medical
procedures such as body piercing or tattooing.
net
net
net
.
.
.
X
X
X
we offer prophylaxis?
ok Should
ok against infective endocarditis:
ok
not offer antibiotic prophylaxis
o
o
Bo Do
B
B
.
• To people undergoing
procedures
w. dental
• To people undergoing
non-​dental proceduresw
atw
the following sites:
w
w lower gastrointestinal tract w
ww
upper and
genitourinary tract; this includes urological, gynaecological, and
t procedures, and childbirth
obstetric
net this includes ear, nose,Xand.net
.neupper and lower respiratory
.tract;
X
X
k
ok throat procedures and
obronchoscopy.
ok
o
o
not offer chlorhexidine
mouthwash
as
prophylaxis
against
infective
Bo Do
B
B
endocarditis to people
w. at risk undergoing dentalwprocedures.
w.
w
w
ww
Managing w
infection
• Investigate and treat promptly any episodes of infection in people at risk of
infective
endocarditis to reduce the risk
developing et
etan antibiotic
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NICE clinical guidelines available at Mguidance.nice.org.uk/​CG64
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178
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Chapter 4
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w
w
w
w
Causes of insomnia Anxiety, stress, depression, mania, alcohol, pain,
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et aminophylline, SSRIs, benzodiazepine/​
et
et
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sleep
n
n
.
.
.
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ok Try to dose regular medications
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o
o
o
B
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ww
op pain, noisy ward) then it is appropriate to prescribe a one-​off or short
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are stopped, the dose should be weaned to minimize withdrawal.
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t
t
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X
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ok
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oralohypnotics
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w
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w
w
ww
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t and risk of withdrawal than t
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X
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et
et
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n
n
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.
.
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Xshould not be on hypnotics when
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ok patients with supplies of addictive
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oo
B
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E
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ww should only be prescribed
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w
w
anaesthetist and is rarely offered these days. Diazepam and temazepam
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w
w
w
w
Steroid therapy
w
179
t
t
t
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Steroid
X
X
ok
ok never be abruptly discontinued
ok as this
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o
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can precipitate an Addisonian
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w. and
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this must be
w
w
wdose if they are
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an appropriate IV corticosteroid
unable to w
take regular PO doses (Table 4.5, Box 4.3). Long-​term steroid use should
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t
etconsideration of osteoporosis
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et
n
n
n
.
.
.
X 4.5 Conversion of oralkprednisolone
X
to IV hydrocortisonekX
ok Table
o
o
o
oo dose
Normal
prednisolone
dose
Suggested
hydrocortisone
B
B
B
.
.
≥60mg/​24h PO w
100mg/​6h IV w
w
20–​50mg/​24h
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ww
≤20mg/​24h PO
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et
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n
n
n
.
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o
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w.conversion
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Box 4.3 Steroid
w
w
w
w
ww
*
*If patients with known adrenal insufficiency, or those who have been on any dose of oral corticosteroids for >3wk present unwell, consider an initial dose of 100–​200mg hydrocortisone IV
STAT, then d/​w senior as to regular steroid dose. If unable to tolerate PO administration, ensure
equivalent IV steroids given, as per Box 4.3.
These are equivalent corticosteroid doses compared to 5mg prednisolone, but do not take into account dosing frequencies or mineralocorticoid effects:
• Hydrocortisone 20mg; usually given IV 6–​8h
• Methylprednisolone 4mg; usually given once daily
• Dexamethasone 750micrograms; usually given once daily.
t
.ne
X
k
oo
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t
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X
k
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kX
oo
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w must be performed w
wsteroid therapy This is anwartwand
Withdrawing
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w
gradually if steroids have been used for >3wks. Large doses (>20mg prednisolone or equivalent) can be reduced by 5–​10mg/​wk until dose is 10mg
t be reduced more slowly,
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prednisolone/​
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oSynacthen
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w
w
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endocrinology.
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w
w
See Table 4.6 for side effects of steroids and treatment and monitoring
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e
et
et
n
n
n
.
.
.
and treatment and monitoring options
XTable 4.6 Steroid side effectskX
X
ok GI ulceration
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o
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B
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o
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.
kX
o
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w
ww
Osteoporosis (E p. 451)
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w
ww
t
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X
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.Bo
ww
B
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w
ww
180
Chapter 4
.B
w
w
ww
w
Prescribing
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t
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Topical
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X
X
X
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oarek used in the treatment of omany
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steroids These
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.
tory skin diseases.w
As with corticosteroids given w
orally or intravenously,
w
w
the mechanism
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offer symptom- ww
w
w
atic relief but are seldom curative. The least potent preparation (see
Table 5.20 E p. 221) possible should be used to control symptoms.
et of topical steroids often
etcauses a rebound worsening
etof
Withdrawal
n
n
n
.
.
.
symptoms
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kXsteroid needed to cover various
k
o
o
otopical steroids.
oo
Bo wash hands after applying
B
B
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.
w thinning of the skin, worsening
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Side effectsw
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w Localacne,
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et can precipitate an Addisonian
et crisis).
et
n
n
n
.
.
.
Potency
E
p.
221
for
a
list
of
the
common
topical
steroids
used
X
X arok ranged by potency. ookX
ok
o
o
B
w.B
w.B
w
w
w
w
ww
2
t
t
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w
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w units (FTUs)
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e &Leg
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1–2 years
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2
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w
w
3–5 years
1
2
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w
w
ww
2
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6–10 years
Fig. 4.4 Amount
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t unit of(FTU)
efingertip
et to treat various body parts. *One
ea t
n
n
adult
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.
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o
o
Reproduced with permission
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Experimental Dermatology,
w.B16: 444–​7. Blackwell Publishing.
w.B
w
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w
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See these NICE Clinical Knowledge Summaries for an excellent resource in prescribing topical
corticosteroids for different ages and body areas: Mhttps://​cks.nice.org.uk/​corticosteroids-​
topical-​skin-​nose-​and-​eyes#!scenariobasis:5/​-​468112
o
o
B
.
w
ww
w
ww
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B
.B
w
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.B
w
w
w
w
Empirical antibiotic treatment
w
181
t
t
t
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.netreatment X.ne
Empirical
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X
X
k
ok
ok These will be your keyooresource
o
antibiotic guidelines
for
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B
B
.They are written to ensure wthe. most appropriate
antibiotic treatment.
w
w
w
antibiotics are
wused prior to knowing the pathogen
w and its antimicrobial ww
sensitivities. Always seek advice from the microbiologists if deviating from
the guidelines; their choice of suitable antibiotic will depend upon likely
t
t
et and its usual antimicrobial
esensitivity,
pathogen
patient factors (agene
and
n
n
.
.
.
coexisting
disease),
and
drug
availability.
Some
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infections
and
X
kareXlisted in Tables 4.7–​4.9 (suitable
kX for an
antibiotic regimens
ok suggested
o
o
o
o
o
healthy 70kg
adult); more detailed options, including
B otherwise
.B choices for
patients with penicillin
allergies, are listed E p649. w
w.B
w
w
w prior to commencing antibiotic
w therapy is important as ww
Taking cultures
they allow subsequent therapy to be more specifically tailored. However,
culturestshould not delay treatment in the
e
et septic patient.
et
n
n
n
.
.
.
XTable 4.7 Common exampleskX
X
ok Lower UTI Nitrofurantoin
o or trimethoprim
ok
o
o
o
B
B or ciprofloxacin w.B
Pyelonephritis
Co-​
wa.moxiclav
w
Cellulitis
w Flucloxacillin 1g/​6h PO/IV ww
ww
B
Wound
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net
et
Meningitis
.
kX
o
o
Encephalitis
As for cellulitis if after ‘clean’ surgery; for ‘dirty’ surgery or
trauma, use co-​amoxiclav 1.2g/​8h IV
Ceftriaxone 2g/​12h IV. Consider adding amoxicillin 2g/​
4h IV if patient >50yr, pregnant or immunocompromised
and/​or vancomycin 1g/​12h IV if penicillin-​resistant
pneumococcal meningitis is suspected
As for meningitis + aciclovir 10mg/​kg/​8h IV (to cover
herpes simplex virus encephalitis)
Flucloxacillin. Base therapy on Gram stain of joint aspirate
oo
B
.
w
.n
kX
oo
B
.
ww
ww
Septic arthritis
w
t
.ne
X
k
ww
t
t
t
.ne 4.8 Pneumonia
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.ne
X
X
X
Table
ok
ok 500mg–​1g/​8h PO
ok
o
o
acquired
Amoxicillin
Bo Community-​
B
B
(CAP), CURB65=0–​1 .
w Amoxicillin 1g/​8h PO/​IV +wclarithromycin
w. 500mg/​
CAP, CURB65=2w
w
w
ww
12h PO/​IV
CAP, CURB65≥3
amoxiclav 1.2g/​8h IV + clarithromycin 500mg/​12h IV
t acquired Co-​
e
et variation between hospitals.nsoet
Hospital-​
There
is considerable
n
n
.
.
consult
Xaspiration pneumonia always
X local guidelines. Gram-​negative
Xcover
is important
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
Table 4.9 Septicaemia
w
w
ww
Urinary tract sepsis
Co-​amoxiclav 1.2g/​8h + gentamicin 5mg/​kg IV STAT
Intra-​abdominal
sepsis Tazocin 4.5g/​8h IV
et sepsis
et
et
n
n
.
.
Neutropenic
Tazocin 4.5g/​
8h IV + gentamicin 5mg/​kg/​24h IV.n
X
X
X
ok Skin/​bone source Flucloxacillin
ok 2g/​6h
ok
o
o
o
Severe
sepsis/​
s
eptic
Tazocin
4.5g/​
8
h
IV
+
gentamicin
5mg/​
k
g
STAT
B
shock, no clear focus
w.B
w.B
w
w
w
w
ww
IV
®
®
IV
®
B
.B
w
w
.B
w
w
wPrescribing
182
ww
w
Chapter 4
t
t
t
.ne
.ne(C. diff)
.ne
Clostridium
difficile
X
X
X
k
ok
ok
obacillus,
o
o
A Gram-​
positive spore-​forming anaerobic
which
Bo Bacteriology
B
B
. colonize the gut. Exposure w
.
can asymptomatically
to antibiotics alters the
w
w
w
balance of gut
wflora, promoting C. diff overgrowth,
w production of toxins that ww
damage colonic mucosa, and subsequent symptomatic C. diff infection (CDI).
Transmission
Via the faeco–​oral route,
after direct or indirect conet patients,
eoft spores
een-t
tact
between
or ingestion
lying dormant in the
n
n
n
.
.
.
X
X
X
C. diff is now regarded
ok vironment.
ok as a major cause of hospital-​
ok acquired
infections (HAI), E pp. o
502–3.
o
o
B
.B
Clinical features
abdominal pain are
w.ofB CDI Watery diarrhoeawand
wsevere
common; feverwand leucocytosis are also seen;
disease causes
w
w
w
pseudomembranous colitis and toxic megacolon. Consider CDI in the dif- w
ferential of unexplained fever and raised inflammatory markers in hospitalized
Elderly and frail patients
etolder adults.
et are at especially high.risk
etof
n
n
n
.
.
dehydration,
recurrent disease, and
mortality from CDI.
X
X arises.
kX as soon as suspicion ofokCDI
Through stoolosamples
ok Detection
o
o
o
Currently
this
involves
a
2-​
s
tage
process,
with
a
rapid,
screening
test for a
B
.B
.B by a more
C. diff protein (or w
PCR for the C. diff toxin gene), followed
spew
cific immunoassay
ww for the C. diff toxin. Speakwtowthe laboratory if there is ww
3
any doubt. Consider an urgent AXR to rule out toxic megacolon.
Treatment See Box 4.4. Starts with metronidazole 400mg/​8h PO or
vancomycin 125mg/​6h PO. Pay attention to fluid and electrolyte balance.
Other regimens including higher doses of PO or PR vancomycin, IV
metronidazole, or PO fidaxomicin may be required in patients who fail to
respond or who relapse after initial treatment—​always consult local guidelines and the microbiologist. Faecal microbiota transplantation (FMT) is an
effective treatment for refractory cases, offered in a few UK centres.4
Infection prevention and surveillance Barrier nursing, good hand hygiene, and cleaning of equipment is key to preventing transmission to other
patients (the spores are resistant to alcohol hand gels so hand washing with
soap is essential). Local infection prevention teams should be made aware of
suspected and confirmed cases, for advice on how to prevent transmission.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
.n
kX
o
w.B
ww
Bo
et
.n
kX
et
.n
kX
o
o
w.B
.n
kX
o
o
w.B
ww
ww
K Box 4.4 Ecology, Clostridium difficile, and antibiotics
Intestinal carriage of C. diff does not equate with disease—​what matters
is when it outgrows other colonic commensal bacteria. Hence just controlling transmission is not entirely sufficient. Instead, we need to avoid
disturbing the healthy colonic flora through indiscriminate use of broad-​
spectrum antibiotics. As part of this approach, most hospitals limit the
use of cephalosporins, quinolones, and clindamycin. The national toolkit
on antibiotic stewardship5 aids clinicians in reducing CDI rates as well as
antimicrobial resistance. Always prescribe using local antibiotic guidelines,
and regularly review whether prescriptions are needed.
t
t
e
X.n
ok
Bo
ok
ok
4
5
ww
t
t
e
X.n
ok
Bo
e
X.n
o
w.B
ww
3
ok
ww
ww
t
e
X.n
e
X.n
Bristol Stool Chart types 5–​7 not attributable to an underlying condition (or therapy) from: hospital
patients aged >2 years and community patients aged if >65 years or wherever clinically indicated.
Mhttps://​www.gov.uk/​government/​publications/​updated-​guidance-​on-​the-​diagnosis-​and-​reporting-​of​clostridium-​difficile
NICE clinical guidelines available at: Mguidance.nice.org.uk/​ipg485
Start smart then focus: Mhttps://​www.gov.uk/​government/​publications/​antimicrobial-​
stewardship-​start-​smart-​then-​focus
o
B
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w
w
w
w
Chapter 5
w
183
t
t
t
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w.
w
w
w
w
ww
Pharmacopoeia 184
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184
Chapter 5
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Pharmacopoeia
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.
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w converting enzyme inhibitor.
wDose
w
w
ACEi $ Angiotensin-​
See Tables 5.1
w
w
and 5.2 on how to commence a patient on an ACEi Indications Heart
failure, hypertension, diabetic nephropathy, prophylaxis of cardioet events Caution Pregnancy.nand
et breastfeeding, patients already
et
vascular
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n
.
.
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X to ACEi. May not be keffective
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ok osis,
o
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o
o
African-​Caribbean patients
SE Postural hypotension,
B
B cough,
.Brenal impairment
and hyperkalaemia,
taste disturbance,
and angio-​
w.dry
wurticaria
w
w
oedema. If cough
w is problematic for the patient,
w consider AT II receptor
antagonist (E p. 190), or other antihypertensive agent.
ww
ww
et
n
.
XEnalapril
et
et
n
n
.
.
X
X
Initially 5mg/​
ok Fosinopril Dose
ok 24h PO up to max 40mg/​24h4hPO
oPOk
Dose Initially
10mg/​24h PO up to max 40mg/​2o
o
o
B
.B 5–​10mg/​24h PO up to maxw80mg/​
.B 24h PO
Lisinopril
Dose
wInitially
w
w
Perindopril w Dose Initially 4mg/​24h PO up to w
max 8mg/​24h PO
ww
erbumine
Perindopril
et Dose Initially 5mg/​24h.nPOeupt to max 10mg/​24h PO .net
arginine
n
.
X
X
X
ok Ramipril Dose Initiallyo1.25–​
ok 2.5mg/​24h PO up to max 10mg/​
ok24h PO
o
o
B
.anBACEi
.B
Table 5.2 Starting
w
w
w
w antihypertensive
Patients withw
significant comorbidity and/​or taking
wother
ww
medications, as well as the frail and elderly, may need more cautious
management when starting an ACEi and when increasing the dose
t
t BP, identify target BP net
Before
U+E, document
nestarting
.Firstnedosestarting Check
.
X
X
Xto.
Start with lowest
dose and consider giving at bedtime
k
k
k
o
o
o
limit
any
problems
with
first-​
d
ose
hypotension
Bo In hospital Increase
Bo monitor
.Bodose daily/​alternate days asw
BP .allows,
w
wwU+E daily/​alternate days ww
ww
Table 5.1 ACEi
In community
net
Check U+E and BP at 7–​10d after starting therapy or increasing
dose. Increase dose every 14d until target BP reached
X.
ok
Bo
Bo
o
et
n
.
kX
.ne
X
k
t
ok
o
o
w.B
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
185
t
t
t
Acetylcysteine
(eg Parvolex
.ne
.ne) $ Acetylcysteine helpsXreplace
.ne
X
X
necessary to k
the toxic products formed
ok the substrates
oofeliminate
ok when
hepatic metabolism
paracetamol is overwhelmed.
o
o
Bo normal
B
B
. is preferred):
Dose In adults, 3 doses
w.of acetylcysteine are givenorw(5%
wglucose
• 150mg/​kgw
IVw
infusion in 200mL 5% glucose
0.9%
saline over 1h
w
ww
• 50mg/​kg IV infusion in 500mL 5% glucose or 0.9% saline over 4h
• 100mg/​kg IV infusion in 1000mL 5% glucose or 0.9% saline over 16h.
t
et Mainly used in known .noresuspected
et
Indication
paracetamol overdose
n
n
.
.
X p. 509). It should be commenced
X
X
in all patients
ok (E
okkg, thoseimmediately
ok calculated to have ingested >75mg/​
with a staggeredooverdose,
or a
o
o
B blood paracetamolwlevel
B
on the nomogram
.Babove the treatment threshold
.
in Fig. 5.1. Startw
treatment within 8h of ingestion—​
do not wait for level if
ww
w
w close to or after this time aswefficacy
patient presents
of acetylcysteine will w
decline rapidly after 8h. Discontinue treatment if the plasma concentration is
later reported
as below the treatment line
and patient is asymptomatic with
etLFTs, creatinine,
etpatients
et
n
n
n
normal
and PT. Discuss
with acidosis, encephalop.
.
.
X worsening renal function,korXPT prolongation with hepatologist
X
ok athy,
o available locally).
ok on call
(or at nearest liver centre o
if not
o
o
B SE Flushing, rash, pruritus,
nausea, and vomiting
all relatively
w.B urticaria,
w.B are
w
w
common during
treatment.
More
severe
anaphylactoid
reactions (dBP, ww
w
w
iHR, bronchospasm) should be managed as per E pp. 484–5 with infusion slowed or stopped.
o
Bo
Plasma-paracetamol concentration (mg/litre)
t
.ne
X
k
120
oo
110
100
oo
B
.
w line
Treatment
ww
90
t
.ne 80
X
k
70
60
50
40
ww
20
et
n
.
kX
oo
B
.
ww
w
.ne
X
k
ww
2 4
0.7
oo
B
.
w
0.5
0.4
0.3
t
ok0.1
o
w.B
et
n
.
kX
et
ww
et
n
.
X
0.2
ww
ww
.n
kX
8 10 12 14 16 18 20 22 24
Time (hours)
6
0.8
0.6
et
X.n
o
0
t
.ne
X
k
ww
o
w.B
10
0
o
ok
o
w.B
t
.ne 30
X
ok
Bo
Bo
et
.n
kX
Plasma-paracetamol concentration (mmol/litre)
B
®
0
ww
t
.ne
X
ok
.Bo
Fig. 5.1 Paracetamol overdose treatment nomogram.
Reproduced from M https://​www.gov.uk/​drug-​safety-​update/​treating-​
paracetamol-​overdose-​with-​intravenous-​acetylcysteine-​new-​guidance. Contains
public sector information licensed under the Open Government Licence v3.0.
o
o
B
.
w
ww
w
ww
ww
B
186
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Actrapid
.ne $ Insulin. See insulin.
.ne
.ne
X
X
X
k IV bolus;
$ Nucleoside
ok Adenosine
ok(antiarrhythmic). Dose 6mgorapid
orapid
o
needs repeated dose
12mg rapid IV bolus, then 12mg
IV bolus
Bo ifIndication
B
B
. tachycardia CI 2nd/​3rd-​dwegree
. heart block,
Supraventricular
sick
w
sinus syndromew(unless pacemaker fitted), longwQT syndrome, COPD/​
w
w
asthma Caution Pregnancy, recent MI, pericarditis, heart block, bundle branch
block, accessory pathway, hypovolaemia, valvular lesions SE Nausea, sinus
pause,
etbradycardia/​asystole, flushing,.nangina,
et dizziness.
et
n
n
.
.
XAdrenaline (epinephrine);
X anaphylaxis $ Catecholamine.
kXif inadok Dose 0.5mg/​STAT IM (0.5mL
ok of 1:1000); repeat afteroo5min
o
o
equate response Indication
B
B Suspected anaphylaxis;
.Bif in doubt give
w.and
it Caution Cerebro-​
cardiovascular disease w
SE iHR, iBP, anxiety,
w
w
sweats, tremor,
w arrhythmias.
w
®
Adrenaline (epinephrine); cardiac arrest $ Catecholamine.
et
n
.
X
et
n
.
X
ww
ww
t
Dose 1mg/​STAT IV (10mL of 1:10,000); repeat as per ALS algorithm
Indication Cardiac arrest Caution As for ‘Adrenaline (epinephrine); anaphylaxis’ SE As for ‘Adrenaline (epinephrine); anaphylaxis’.
ok Aggrastat
Bo
.ne
X
ok
ok
o
B
.
w
o
B
.
w
Alteplase $w
Plasminogen activator. See fibrinolytics.
w
ww
®
$ Glycoprotein IIb/​IIIa inhibitor. See tirofiban.
Amiloride $ Potassium-​sparing diuretic. Dose 5–​10mg/​24h PO (max
ww
20mg/​24h PO) Indication Oedema, potassium conservation when used
as an adjunct to thiazide or loop diuretics for hypertension, congestive
cardiac failure, hepatic cirrhosis with ascites CI Hyperkalaemia, anuria,
Addison’s disease Caution Renal impairment, DM, pregnancy, and breastfeeding SE Abdominal pain, GI disturbances including bleeding.
t
.ne
X
k
oo
et
t
.ne
X
k
.n
kX
oo
oo
B
B
.
.
Aminophylline;
IV $ Theophylline/​methylxanthine.
wonwideal
ww Dose Loading w
5mg/​kg (based
body weight) in w
100mL 0.9% saline IVI over w
w
20min; Maintenance 0.5mg/​kg/​h, make up 500mg in 500mL 0.9% saline (concentration
mL) IVI Indication
airways disease,
t Reversible
t
etacute asthma= 1mg/​
eloading
severe
Caution Avoid
dose if patient taking
n
n
.
.
.neoral
X
X
X
theophylline;
cardiac
disease,
hypertension,
epilepsy
SE
Tachycardia,
k
ok palpitations, arrhythmia,oconvulsions
ok
Info Theophylline o
is o
only available
Bo as an oral preparation;
B
B
aminophylline
consists
of
theophylline
and ethyl.
wsimply
w.
enediamine which
improves the drug’s solubility.
w
w
w
w
w
w
Monitoring
Stop infusion 15min prior to sampling, take sample 4–​6h after
aminophylline
commencing an infusion 10–​20mg/​L (55–​110micromol/​L)
t
e
et
et
(theophylline)
2 Toxic >20mg/​L (>110micromol/​
L)
n
n
n
.
.
.
2
Signs
of
toxicity
Arrhythmia,
anxiety,
tremor,
convulsions
X
X
X
(E OHAM3
ok
okp. 731)
ok
o
o
o
B
.B
.B
wcardiac
Amiodarone;
arrest $ ClasswIIIwantiarrhythmic. Dose
w
300mg IV/​Sw
TAT after third shock if patient
w remains in VF/​pulseless ww
B
VT Indication VF/​pulseless VT.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
187
t
t
et
Amiodarone;
arrhythmias $
Dose
.ne
.neClass III antiarrhythmic. X
.nOral
X
X
8h PO for 1wk,kthen 200mg/​12h PO for 1wk, then
ok loadingPO200mg/​
o IV loading. Initially 5mg/​kg over
ok20–​200mg/​
as maintenance dose;
o
o
Bo 24h
B
B
. then further infusion if necessary
. of up 1to20min
IVI (with ECG monitoring)
1.2g
w
w
over 24h IVI Indication
SVT, nodal and ventricular
tachycardias, atrial fibrilw
w
w VF (see above) CI Bradycardia,
w sinoatrial heart block, ww
lation and flutter,
thyroid dysfunction, iodine sensitivity Caution Pregnancy, breastfeeding, thyroid disease,
hypokalaemia, heart failure,
bradycardia SE N+V, taste
et raised
etelderly,
et
n
n
n
.
.
.
disturbance,
transaminases, jaundice,
bradycardia, hypotension,
pulX toxicity, corneal deposits,
X
X
ok monary
ok skin discolouration Info Monitor
ok LFTs and
o
o
o
TFTs every 6mth.
B
.B
.B
Amlodipine w
Seew
calcium-​channel blockers. ww
w $ Beta-​lactam. Dose 500mg–​
w 1g PO/​IV 8h Indication ww
Amoxicillin
Infection CI Penicillin allergy Caution Glandular fever, CMV infection,
ALL/​e
CtLL SE N+V, diarrhoea, rash. et
et
n
n
n
.
.
.
X
XDose 500mg–​1g PO/​IV 6hkXIndication
$ Beta-​lactam.
ok Ampicillin
okCaution
o infection,
Infection CI Penicillin allergy
Glandular fever, o
CMV
o
o
B ALL/​CLL SE N+V,wdiarrhoea,
B
.B rash.
.
w
Antacids/​alginates
ww Dose See Table 5.3
wwIndications Acid reflux ww
B
disease Caution Hepatic and renal impairment; if symptoms are severe
or persist seek expert opinion SE Depends upon preparation used, see
Table 5.3 Info The sodium load in these preparations can be significant
and they should be used with caution in patients with hepatic impairment. The alginates increase the viscosity of the stomach contents and
can protect the oesophageal mucosa from acid attack; the raft-​forming
alginates float on the surface of the stomach contents and may further
reduce the symptoms of reflux.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
Table 5.3 Antacids and alginates
o
Bo
t
Classification
.ne hydroxide
X
Aluminium
k
ww
t
e
X.n
ok
Bo
Magnesium trisilicate
ww
Other alginate
preparations
Bo
o
et
n
.
kX
o
t
.ne
X
k
oo
B
.
w
.n
kX
t
ww
et
n
.
X
ok
o
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
et
.ne
X
k
ww
o
w.B
Alginate raft-​forming
suspensions
w
eg Alu-​Cap®
Dose 1 capsule 4 times daily and at bedtime
CI hypophosphataemia, neonates
SE constipation
Dose 10mL 3 times daily in water
CI Hypophosphataemia
SE diarrhoea, belching (due to CO2 liberation)
Dose depends upon preparation, see BNF
CI and SE See magnesium carbonate
eg Peptac®
Dose 10–​20mL after meals and at bedtime
SE usually none
eg Gastrocote®
Dose 5–​15mL 4 times daily (after meals and at bedtime)
SE usually none
o
w.B
Magnesium carbonate
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
188
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Antiemetics
Dose See Table 5.4
.ne
.neIndications N+V see TableX5.5;
.nenot
X
X
effective k
all causes of N+V Caution kand SE See
ok all antiemetics areimportant
o toforestablish
the cause of N+V.
o
oo
Bo Table 5.4 Info It is w
B
B
.
.
w
w classification
Table 5.4 w
Antiemetic
ww
ww
Antihistamines
Cinnarizine, cyclizine, promethazine
t
t IM
Cyclizine
Dose 50mg/​8h PO/​eIV/​
e
et
n
n
CI Heart failure .n
.
.
X
X
SE Drowsiness,
pain on injection, urinary retention,
kX vision
ok
oblurred
ok dry
mouth,
o
o
o
B
.B
Phenothiazines
droperidol, perphenazine,
wChlorpromazine,
w.B
prochlorperazine, trifluoperazine
w
w
w Dose Consult BNF; 10mg/​8w
ww
Prochlorperazine
h PO, 12.5mg/​24h IM, 3–​
6mg/​12h buccal
CI Parkinson’s, epilepsy
t
e
et hypotension, drowsiness, agitation
et
SE Extrapyramidal
effects,
n
n
n
.
.
.
X
X
X
Domperidone,
ok Dopamine
ok metoclopramide
ok
antagonists
o
o
o
B
.B 10mg/​8h PO/​IV/​IM w.B
Metoclopramide wDose
CI Avoid in patients <21yr (especially
w
w obstruction
ww ♀) and in bowel
ww
B
SE Extrapyramidal effects
net
et
5HT3 antagonists
.
Ondansetron
kX
o
o
Miscellaneous
oo
B
.
w
ww
t
.ne
X
k
Granisetron, ondansetron
Dose 4–​8mg/​8h PO/​IV/​IM
CI QT prolongation
SE Constipation, headache, flushing, bradycardia, hypotension
Dexamethasone, benzodiazepines, hyoscine
hydrobromide, nabilone, neurokinin receptor antagonists
.n
kX
oo
B
.
ww
w
ww
Table
net 5.5 Causes of N+V andXsuggested
net antiemetic
net
.Likely
.
.
X
X
cause
Suggestedkantiemetics
ok
o prochlorperazine, metoclopramide,
ok
o
o
Promethazine,
Bo Pregnancy
B
B
.
wondansetron
w. antihistamines
w
Postoperative w In no particular order: 5HT antagonists,
w (eg cyclizine), dexamethasone,wphenothiazines (eg
ww
prochlorperazine), metoclopramide
t
Bowel
Treat the cause. Avoid
e
etmetoclopramide
et
n
n
n
.
.
.
obstruction
X
X
kX
promethazine, cyclizine
ok Motion sickness Hyoscineoohydrobromide,
ok
o
o
Vestibular
Betahistine
(see BNF), antihistamine (eg.B
cinnarizine, see
B
.Bphenothiazine
disorders
(eg prochlorperazine)
wBNF),
w
w
w
Cytotoxic w
Pre and post treatment with w
domperidone or
ww
chemotherapy
metoclopramide; add in dexamethasone, 5HT
antagonists. See BNF
et care Depends upon cause
eEt p. 93
et
Palliative
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
3
3
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
189
t
t
t
Antihistamines
$ H -​receptor
.ne
.neantagonists. Dose See Table
.ne5.6
X
X
X
Symptomatic reliefkof allergy (eg hayfever, allergickrhinitis, urok IndicationsCaution
Avoid if possible
oo in pregnancy and breastfeeding;
oo consult
Bo ticaria)
B
B
.
.
BNF if renal or hepatic
impairment; all antihistamines
have the potenw
tial to cause sedation,
more so than others
ww(Table 5.6); the sed- w
ww alsosome
ating antihistamines
possess significantw
antimuscarinic activity and w
should be used with caution in prostatic hypertrophy, urinary retention,
and inetpatients with angle-​closure glaucoma
SE Drowsiness, headache,
eintthis section
eatt
n
n
n
.
.
.
antimuscarinic
effects Info The drugs
are all antagonists
X
X are antagonists at Hkreceptors,
X
cimetidine andkranitidine
ok Handreceptors;
o
o
o
o
are useful for gastric o
acid suppression (see ranitidine).
B
w.B
w.B
w
w
Table 5.6 w
Antihistamines
w
ww
Non-​sedating antihistamines Acrivastine, cetirizine, desloratadine, fexofenadine,
levocetirizine,
loratadine, mizolastine, rupatadine
et et
et
n
n
Cetirizine
Dose 10mg/​24h.n
PO
.
.
X
X
Caution Halve
ok Desloratadine Dose
ok dose if eGFR <30mL/​min ookX
o
o
5mg/​24h PO
B
.B 10mg/​24h PO
Loratadine wDose
w.B
w
w
Sedating antihistamines
w Alimemazine, chlorphenamine,
w clemastine,
ww
1
1
2
cyproheptadine, hydroxyzine, ketotifen, promethazine
Chlorphenamine
Dose 4mg/​4–​6h PO (max 24mg/​24h); 10mg/​8h IV/​IM
(over 1min if given IV)
t
t
t
.ne
.ne
.ne
X
X
X
ok
ok of factor Xa. Indicationooandk dose VTE
o
$ Direct inhibitor
Bo Apixaban
B
. replacement 2.5mg /​12h w
prophylaxis after hip/​
knee
PO.B
for 14d for knees,
w
35d for hips (start
12–​24h after surgery); Treatment
of DVT/​PE Initially
w
w
w
w 7d, then 5mg/​12h for 6mths;
w Prophylaxis
10mg/​
12h for
of recurrent w
PE/​DVT Continue with 2.5mg/​12h; Prophylaxis of stroke and systemic emt valvular atrial fibrillationneandt 1 risk factor (Such as previous
bolismein
et
.n ornon-​
stroke
TIA, symptomatic heart. failure, DM, HTN, or >75yr).n
5mg/​
X
X
X
dose to 2.5mg/​
2h if 2 of: >80yr, <61kg, or
creok 12h (reduce
ok1Avoid
okserum
o
o
>133mmol/​L)B
Caution
in patients with significant
bleeding
Bo atinine
B
. dose before removing epidural
risk. Wait 30h afterwlast
and wait
w. catheter
w
w
5h until next dose
SE Anaemia; bruising; haemorrhage;
nausea Info No
w
w
ww
routine anticoagulant monitoring required (INR tests are unreliable).
Arthrotec® $ NSAID. See diclofenac.
t
e
X.n
.ne
X
k
t
et
n
.
X
Asacol® $ Aminosalicylate. See mesalazine.
Aspirin; antiplatelet $ NSAID. Dose Antiplatelet 75mg/​24h PO;
ok
o
ok
oNon-​
o24h
Bo ACS/​MI 300mg/​STAT
B
B
PO;
haemorrhagic stroke 300mg/​
PO for 14d
.
.
wIndication Secondary prevention
wof thrombotic
then 75mg/​24hw
PO
cerew
brovascular w
and cardiovascular events CI Active
w bleeding, children under ww
16 (Reye’s syndrome) Caution Pregnancy, breastfeeding, asthma, peptic
ulceration,
use of other anticoagulants
SE Bronchospasm,
et concomitant
et
et
GI.irritation/​
haemorrhage.
n
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
190
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
ww
w
t
t
net
Aspirin;
.ne analgesic/​antipyretic
.ne $ NSAID. Dose 300–​X9.00mg/​
X
X
4g/​
24h Indication
pyrexia CI As for
k ‘Aspirin;
ok 4–​6h PO; max
ok‘Aspirin;Pain,
ofor
Caution As ofor
antiplatelet’ SE As
‘Aspirin;
o
Bo antiplatelet’
B
B
.
.
antiplatelet’.
w
w
AT II receptor
ww antagonists Dose See Table
ww5.7; commence therapy ww
in the same way as starting an ACEi (E p. 184) Indications Patients intolerant of ACEi; heart failure, hypertension, diabetic nephropathy,
et of cardiovascular events
et Caution Pregnancy and .breastet
prophylaxis
n
n
n
.
.
Xfeeding, renal artery stenosis/​
X renal impairment, aortickinXstenosis,
ok hyperkalaemia, known allergy
ok to ACEi. May not be effective
o
o
oo African-​
Caribbean patients .SE
Postural hypotension, renal
impairment and
B
B
B
.
w disturbance, urticaria andwangioneurotic
w
hyperkalaemia, taste
oedema;
cough can occur
wwbut is less common than with
w ACEi.
ww
Tablet 5.7 AT II receptor antagonists t
e
e
et
n
n
n
.
Candesartan
Dose Initially 4–​8mg/​.24h PO up to max 32mg/​24h PO .
X
X
50mg/​24h PO up to max 300mg/​
ok Irbesartan Dose Initiallyoo75–​k1X
ok24h PO
o
o
B
B 24h PO
Losartan
Dose Initially
.100mg/​
w.B 25–​50mg/​24h PO up towmax
w
Valsartan
Dose Initially 80mg/​24h PO up to max
320mg/​24h PO
w
w
w
ww
Atenolol See beta-​blockers.
t
t
t
.ne
.ne inhibitor. See statins. X.ne
Atorvastatin
$ HMG CoA X
reductase
X
k$ Anticholinergic. Dose 500micrograms/​
ok Atropine; bradycardia
ok
oo3mg/​
o
24h Indication Bradycardia
Bo STAT IV every 3–​5wmin;.Bmax
B
. CI Glaucoma,
myasthenia gravis, pyloric stenosis, prostatic w
enlargement Caution
Down’s syndrome,
ww GORD SE Transient bradycardia,
ww antimuscarinic ef- ww
fects (constipation, urinary urgency and retention, pupil dilatation/​loss
of accommodation,
dry mouth).
t
et cardiac
et
Atropine;
arrest .$
Dose 3mg/​
n
neAnticholinergic.
.
.nSTAT
X
X
X
IV
Indication
non-​
s
hockable
cardiopulmonary
arrest
Caution
None
ok the arrest situation SE Asofor
ok‘Atropine; bradycardia’ InfooAtropine
ok is noin
o
B
longer recommended.B
use in non-​shockable
w for routineGuidelines).
w.Bcardiopulmonary w
arrest (see 2015
Resuscitation
w
w
w $ Antibacterial. See mupirocin.w
w
Bactroban
Beclometasone
Corticosteroid.t Dose 200–​400micrograms/​12h
t Chronic$asthma
eIndication
et
n
n
n
INH
(step
2eBTS guidelines) Caution TB SE
Oral
.
.
.
X
X bronchospasm (rare) Info
XDifferent
hoarse voice, paradoxical
ok candidiasis,
okinterchangeable
obekprescribed
preparations/​devices areonot
and should
o
o
B
by brand name.
w.B
w.B
w
w
Bendroflumethiazide
$ Thiazide diuretic.
w
w Dose Oedema 5–​10mg/​ ww
®
et
n
.
kX
o
Bo
alternate days PO; Hypertension 2.5mg/​24h PO Indication Oedema,
hypertension Caution DM, gout, SLE SE Dehydration, hypotension, electrolyte imbalance (especially dK+) Interaction ilithium levels and NSAIDs
decrease effect.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
191
t
et
net$ Beta-​lactam. Dose X
Benzylpenicillin
(penicillin .G)
0.6–​
.ne
.n1.2g/​
X
X
4.8g/​
24h in k
divided doses) Indication Infection;
ok 6h IV (max
ok of skin,
endocarditis CIoo
Penicillin allergy Caution History
alo
Bo throat,
B
B
.
. contraceptive pill,
lergy SE Diarrhoea Interaction
Decrease effects of oral
w
w
allopurinol increases
ww risk of rash.
ww
ww
Beta-​blockers Dose See Table 5.8 Indications Generic indications include: hypertension, angina, myocardial infarction, arrhythmias, heart
failure,
etthyrotoxicosis, anxiety, migraine
et prophylaxis, benign .essenet
n
n
n
.
.
tial
tremor;
topically
for
glaucoma
Caution
Pregnancy,
breastfeeding,
X abrupt withdrawal especially
X in patients with IHD (risk
X of reok avoid
ok AV block,
oksymptoms
o
o
o
bound
iHR/​
i
BP),
1st-​
d
egree
DM
(may
mask
B dglucose), COPDwCI.BAsthma, uncontrolled heart
w.Bfailure, marked w
w
w
bradycardia,w
dBP, 2nd/​3rd-​degree AV block,
wsevere peripheral arterial w
disease SE Bradycardia, hypotension (especially postural), heart failure,
bronchospasm, conduction disorders, peripheral vasoconstriction,
t nightmares, insomnia),neim-t
et fatigue, sleep disturbance
e(often
headache,
n
n
.
.
.effect
potence
Info
The
cardioselective
β-​
b
lockers
(Table 5.8) have less
Xon β receptors but are not kcardiospecific
X
X
k
k
and
bronchoconstriction
can
o
o
opatients.
oo (atenolol,
occur in susceptible
Water-​soluble β-​.bB
lockers
Bo still
B
.
w excreted by the kidneys andwa dose reduction is
nadolol, sotalol) are
often necessary
wwin renal impairment; thesewarewalso less likely to cause ww
2
sleep disturbance and nightmares.
et5.8 β-​blockers. Doses show.ninitial
et dose range for treatment .net
Table
.of nhypertension,
X
X
ok Cardioselective doses varyoowithk indication; consult BNF ookX
o
B
B available IV
.B
.also
Atenolol
Dosew
25–​50mg/​24h PO (100mg/​24h max);
w
w
w
Bisoprolol wDose 5–​10mg/​24h PO (20mg/​24hw
max)
ww
Metoprolol
Dose 50–​100mg/​24h PO (400mg/​24h max); also available IV
t
Non-​e
cardioselective
net50mg/​24h in divided doses)X.net
.n
.(max
Carvedilol
Dose 12.5mg/​24h PO
X
X
ok Labetalol Dose 100mg/​o1o2hkPO (max 2.4g/​24h in divided doses);
ok also
o
available.B
IV
Bo
B
.
Propranolol Dosew
40–​80mg/​12h PO, increase weeklyw
(max 320mg/​24h in
w
w
divided
doses)
w
w
ww
Sotalol
Used only to treat arrhythmias. Only commence after seeking
expert advice
t
t
e
emaintenance
et
Dose 40mg/​12h PO (usual
dose 80–​160mg/​12h
n
n
n
.
.
.
PO); also available IV
X
X
X
ok Timolol Used predominantly
ok as eye drops for the treatment
oofk
o
o
o
B
glaucoma;
in systemic effects
w.Bcase reports exist of this resulting
w.B
w
w
w
w
ww
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
192
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
ww
w
t
t
t
Betamethasone
cream See topical
.ne
.ne corticosteroid.
.ne
X
X
X
k 200mg/​8h PO; modified-​
ok Bezafibrate $ Fibrate.ooDose
orkelease preo
BNF
Indication
Hyperlipidaemias
unresponsive
Bo parations available,wcheck
B
B
.
w.primary biliary cir- w
to diet and other measures CI Hypoalbuminaemia,
w
w
rhosis, gall bladder
w disease, nephrotic syndrome,
w pregnancy and breast- w
feeding Caution Renal impairment (see BNF for reduced dosing), hepatic
impairment,
SE GI disturbance,
anorexia, cholestasis. t
et hypothyroidism
et
n
.
.ne
Bisoprolol
See beta-​blockers. .n
X
X
X
k
k
ok Bowel cleansing preparations
Klean-Prepo, o
MoviPrep ,
oo Dose(Eg
Bo Picolax , etc)w$.BLaxative.
Consult BNF.B
or local guideline
w
Indications Prior
to surgery, colonoscopy or w
radiological
examination
CI Bowel obstruction,
ww toxic megacolon Caution
w Elderly, children, dehy- ww
dration SE N+V, abdominal pain and distension, dehydration, electrolyte
disturbance
These agents should tnot be used in the treatment of
et Info
et
constipation
(see also laxatives). .ne
n
n
.
.
X
X
X
ok Bricanyl $ β agonist.oSee
okterbutaline.
ok
o
o
B
Buccastem See antiemetics
w.B (phenothiazine).ww.B
w
Budesonide
w $ Corticosteroid. Dose 100–​
w800micrograms/​12h INH; ww
®
®
®
®
2
®
1–​2mg/​12h NEB Indication Chronic asthma (step 2 BTS guidelines) Caution
TB SE Oral candidiasis, hoarse voice, paradoxical bronchospasm (rare).
t
t
t
.ne
.ne dependence. Dose Commence
.ne
Bupropion
$ Treatment of nicotine
X
X
X
before target smoking
ok 1–​2wk
ok cessation date, initially 150mg/​
ok 24h PO
6d, then 150mg/​12hoPO (max single dose 150mg;omax total daily
Bo for
B
B
dose 300mg) Indication
Smoking cessation CI Acute
w. severe
w. alcohol or benzo- w
diazepine withdrawal,
hepatic cirrhosis,w
CNS tumour, history of
w
w Hepatic impairment, renalwimpairment, pregnancy and w
seizures Caution
breastfeeding SE Dry mouth, GI disturbances, taste disturbance, agitat
t
tion, e
et
.n anxiety. $ Antimuscarinic.XSee.nhyoscine
.ne
X
X
Buscopan
butylbromide.
ok
okD $ Calcium salt. See calcium
okcarbonate.
o
o
Bo Calcichew /​Calcichew
B
B
w. $ Calcium salt. Dose
w.See BNF Indication w
Calcium carbonate
w
w
w dCa CI iCa (urine/​serum),
w eg malignancy Caution w
Osteoporosis,
History of renal stones, sarcoid, renal impairment SE GI disturbance,
dHR,earrhythmias.
t
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
®
®
®
3
2+
Bo
o
et
n
.
kX
2+
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
193
t
t
et
Calcium-​
Dose See Table
.ne channel blockersX$.nDihydropyridines.
.ne5.9
X
X
iBP, prophylaxis k
CI Unstable angina, k
ok Indicationssignificant
o of angina
o cardiogenic
aortic ostenosis,
acute porphyria Caution
Pregnancy,
o
Bo shock,
B
B
. flushing,
breastfeeding, heart .failure SE Abdominal pain, N+V,
palpiw
w
tations, dBP, oedema,
headache, sleep disturbance,
fatigue Info The
w
w
w relax smooth muscle and dilate
w both coronary and per- ww
dihydropyridines
ipheral arteries. Nimodipine preferentially acts upon cerebral vascular
smooth
and is used in the prevention
and treatment of ischaemic
etmuscle
et subarachnoid
et
n
n
n
.
.
.
neurological
deficits following aneurysmal
haemorrhage.
X
X
ok Table 5.9 Calcium-​channel
okblockers (dihydropyridines) ookX
o
o
B
w.B5mg/​24h PO up to max 10mg/​
w2.4hBPO
Amlodipine Dose
Initially
w
w
w10–​20mg/​24h PO
ww
Felodipine w
Dose Initially 5mg/​24h PO up to max
Nifedipine Dose Depends upon preparation. Always specify specific brand
consult BNF
et for modified-​release (MR).npreparations;
et
et
n
n
.
.
Nimodipine
Dose
60mg/​
4
h
PO
starting
within
4d
of
subarachnoid
X
X
X
haemorrhage and
ok
okcontinue for 21d; IV preparationoavailable,
ok
o
o
consult
BNF
B
w.B
w.B
w
w
Calcium-​cw
hannel blockers $ Verapamil,
w diltiazem. Dose See ww
B
Table 5.10 Indications iBP, prophylaxis of angina; verapamil is also
used in the management of tachyarrhythmias CI Left ventricular
failure, bradycardia, 2nd-​or 3rd-​
degree AV dissociation, sick sinus
syndrome Caution Pregnancy, patients taking β-​blockers or other negatively chronotropic drugs, 1st-​degree AV dissociation, acute phase of
MI SE Bradycardia, dBP, heart block, dizziness, flushing, headache, oedema, GI disturbance Interactions Unlike the dihydropyridines, diltiazem
and verapamil are negatively chronotropic and inotropic and should not
generally be used in conjunction with β-​blockers or other negatively
chronotropic drugs.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
t
t
.ne 5.10 Calcium-​channel blockers
.ne(verapamil, diltiazem) X.ne
Table
X
X
ok
ok
ok
Dependsoupon preparation; consult. Always o
specify specific
Bo Diltiazem Dose
B
B
brand for.modified-​release (MR) preparations;. consult BNF
w 40–​120mg/​8h PO for SVT;
wTypically
ww
Verapamil
Dose
80–​120mg/​8h PO for
w
w
ww
angina prophylaxis; 80–​160mg/​8h PO for iBP; 5–​10mg over 5min
IV with ECG monitoring for treatment of acute SVT (seek senior
help before giving IV inotropes/​
t
e
et chronotropes)
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
194
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
neDose
Calcium
10mL of 10%; give 1mL/​
.ne chloride $ Calcium
.salt.
.nemin
X
X
X
Emergency management
of dCa CI iCa Caution
ok IV Indication
ok impairment
ok History
stones, sarcoid,orenal
SE Peripheralovasodilatation,
Bo ofdBP,renal
B
B
.
. gluconate.
injection-​site reactions;
more irritant than calcium
ww $ Calcium salt.wDose
ww10mL of 10%; give ww
Calcium w
gluconate
over 3min IV Indication Emergency management of dCa , iK CI
iCa tCaution History of renal stones,
renal impairment SE
e vasodilatation, dBP, injection-​
et sitesarcoid,
et
Peripheral
reactions.
n
n
n
.
.
.
X
X salt. Dose 15g/​6–​8h PO;
XPR preResonium $
ok Calcium
okCalcium
otokmoderate)
o
o
o
parations
also
available
(see
BNF)
Indication
iK
(mild
B
.B
.BMonitor K .
Caution Pregnancy,w
breastfeeding
SE GI disturbance
wInfo
w
w
Calpol $w
Simple analgesic. See paracetamol.
w
ww
Candesartan See AT II antagonists.
et $ Imidazole antifungal.
eSeet clotrimazole.
et
n
n
n
Canesten
.
.
.
X
X
ok Captopril See ACEi. ookX
ok
o
o
B
Carbamazepine .B
$ Antiepileptic. Dose Initially.B
100mg/​12h PO;
w
wpreparations
Increase To max
2g/​24h in divided doses; PR
w
w
w
w tonic–​clonic, available
(see BNF) w
Indication Antiepileptic; generalized
chronic w
B
2+
2+
2+
+
2+
®
+
+
®
®
pain, eg trigeminal neuralgia (see BNF for dosing) CI AV conduction abnormalities, history of bone marrow depression, acute porphyria Caution Pregnancy, breastfeeding, cardiac disease, Hong Kong
Chinese/​Thai origin, history of skin conditions SE N+V, dizziness, drowsiness, headache, ataxia, visual disturbance, cytopenias, hepatic dysfunction, skin disorders Interaction Enzyme inducer.
t
.ne
X
k
oo
et
ww
oo
B
.
w
Monitoring
carbamazepine
.n
kX
oo
B
.
ww
t
.ne
X
k
w
Random sample 20–​50micromol/​L (4–​12mg/​L)
2 Toxic >50micromol/​L (>12mg/​L)
t
t
netInitially 15–​40mg/​24h X
.ne
.Dose
.ne
Carbimazole $ Antithyroid.
PO; Once
X
X
k for 12–​
ok euthyroid 5–​15mg/​24h PO
oask maintenance dose usuallyoogiven
o
Hyperthyroidism
CI
Severe
blood
disorders
Caution
Bo 18mth Indication w
B
B
.
.
Pregnancy, breastfeeding, hepatic impairment SEwN+V, pruritus, rash,
w
w
agranulocytosis.
w
w
Carvedilol See beta-​blockers.
et See cephalosporin. .net
et
Cefaclor
n
n
.
.
X
X
X
ok Cefalexin See cephalosporin.
ok
ok
o
o
o
B
Cefotaxime See cephalosporin.
w.B
w.B
w
w
Cefradinew
See cephalosporin.
w
Ceftazidime See cephalosporin.
ww
ww
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok Cefuroxime See cephalosporin.
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Ceftriaxone See cephalosporin.
B
.B
w
ww
.B
w
w
w
Pharmacopoeia
w
w
195
t
t
et
Celecoxib
inhibitor.
PO.n
(max
.ne $ NSAID/​COX2X
.ne Dose 100–​200mg/​12hX
X
4h in divided doses)
Indication Pain and inflammation;
ok 400mg/​2rheumatoid
okand
okIHD,osteoarthritis
ankylosing spondylitisoCI
CVD,
o
Bo arthritis,
B
B
. Caution Pregnancy, breastfeeding,
.
HF, allergy to any NSAID
hepatic imw
w
pairment, renalw
impairment SE GI disturbance/​w
headache, dizziw
w Decreases
wbleeding,increases
ness Interaction
effects of antihypertensives,
toxicity w
of methotrexate, increased risk of renal impairment with ACEi, AT II
antagonists,
et or ciclosporin.
et
et
n
n
n
.
.
.
Cephalosporin
Dose
See
Table
5.11
Indications
Infections
(with
known
X
X
X surantimicrobialok
sensitivity (consult local guidelines)),
ok orgicalsuspected
okbe harmful
o
o
o
prophylaxis,
other
prophylaxis
Caution
Not
known
to
B in pregnancy, present
w.Bin breast-​milk in low concentration;
w.B 0.5–​6.5% of w
w
w
patients whoware penicillin-​allergic will display
w allergy to cephalosporins w
as cephalosporins contain a beta-​lactam ring as do the penicillins and
carbapenems SE Diarrhoea (rarely antibiotic-​associated colitis), N+V, abet discomfort, headache, allergic
etreactions Info Cephalosporins
earet
dominal
n
n
n
.
.
.
amongst
the
antibiotics
which
are
most
likely
to
result
in
Clostridium
difficile
X
kX and clindamycin. Asowith
kXall antiok diarrhoea, the others being
oquinolones
o
o
o
biotics,
it
is
important
to
consult
local
guidelines
as
infectious
B different susceptibilities
B agents have
.Bdepending upon geographical
.location.
w
w
ww
ww
ww
Table 5.11 Cephalosporins (consult local guidelines)
t
t
Firstegeneration
net
.n
.n8he PO Indications UTIs, respiratory
.tract
Cefalexin
Dose 500mg (250–​500mg)
X
X
X
k sinusitis, skin and soft tissue infections
infections, otitisomedia,
ok
ok
o
o
Bo Cefradine Dosew500mg
B
B
. (250–​500mg) 6h PO Indications
w.surgical prophylaxis
but generally not used widely now
w
w
w
w
ww
Second generation
Cefuroxime Dose 750mg (750–​1500mg) 8h IV, 500mg (250–​500mg) 12h PO;
t Indications Gram-​positivenand
t
t
.ne
. e Gram-​negative bacteria; surgical
.ne
prophylaxis
X
X
X
ok Third generation ook
ok
o
Bo Cefotaxime Dosew1g.(1–​
B2g) 12h IV Indications better Gram-​
B
negative activity,
w.bacteria
but poorer coverage against Gram-​positive
than
w
w
cefuroxime;
penetrates
the
CSF
w
w
ww
Ceftriaxone
t
.ne
Dose 1g (1–​4g) 24h IV Indications better Gram-​negative activity,
but poorer coverage against Gram-​positive bacteria than
cefuroxime; penetrates the CSF
et
et
n
n
.
.
X
Xor 2g/​12h IV; Indications better Gram-​
X
1g (1–​2g) 8hkIV
ok Ceftazidime Dose
o but poorer
opkositive
negative activity,
coverage against Gram-​
o
o
o
B
bacteria.than
w B cefuroxime; good activitywagainst
w.BPseudomonas
w
w
ww
Cetirizinew
$ H antagonist. See antihistamine.
Chloramphenicol;
drops $ tAntibiotic. Dose 1 drop 0.5%/​2th
t frequencyeye
ereduce
e
TOP;
as infection
Continue for 48h
n
.
.nisecontrolled.
.nafter
X
X
X
symptoms
resolve
Indication
Conjunctivitis,
corneal
abrasions,
post
ok surgery SE Transient stinging.
ok
ok eye
o
o
o
B
w.B
w.B
w
w
w
w
ww
1
B
196
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
et
Chlordiazepoxide
$ Benzodiazepine.
.ne
.ne Dose See Table 5.12 Indications
.nAcute
X
X
X
withdrawal treatment/​
rophylaxis Caution Pregnancy, breastfeeding,
ok alcoholdisease,
okprespiratory
okrespiratory
renal impairment,
disease (sleep apnoea,
o
o
Bo liver
B
B
failure), reduce dose in
the elderly, avoid abrupt withdrawal
w. confusion,
w. SE Respiratory w
­depression, drowsiness,
ataxia, amnesia,w
dependence Info Symptoms
w
w withdrawal tend to occur 12–​4w8h after the last alcoholic drink w
of acute alcohol
and usually subside 5–​7d after the last drink. A reducing dose of chlordiazepoxide
as a surrogate CNS depressant
ethet acts
et (which is the effect alcohol
ehastto
n
n
.
.
upon
CNS) and it is uncommon.n
for physical symptoms of withdrawal
X if patients are treated with
Xthis sort of regimen; always consider
X
ok present
ok (E
ok vitamin
o
o
o
supplementation in these patients
p. 105); consult local guidelines.
B
.B
w.B regimen for alcohol
w
Table 5.12 Chlordiazepoxide
withdrawal (local
w
w
w differ from this suggested regimen)
w
ww
guidelines may
Day 1
20mg/​6h PO
Day 5
5mg/​6h PO
e2 t
et
et
Day
20mg/​8h PO
Day 6
5mg/​8h PO
n
n
n
.
.
.
X 3
X
10mg/​6h PO kX Day 7
5mg/​12h PO
ok Day
o
ok
o
o
o
Day 4
10mg/​
8
h
PO
Day 8
STOP
B
w.B
w.B
w
w
Chlorhexidine
w $ Antiseptic. Indication Skin
w preparation prior to sur- ww
B
gery or other invasive procedures (eg vascular access, spinal/​epidural
anaesthesia), surgical hand scrub, oral hygiene, antiseptic lubricant (eg
Hibitane®) CI Avoid contact with eyes, brain, meninges, middle ear and
other body cavities SE Sensitivity, mucosal irritation.
Chlorphenamine $ H1 antagonist See antihistamine.
Cimetidine $ Antihistamine (H2 antagonist). See ranitidine.
Ciprofloxacin $ Quinolone. Dose 500–​750mg/​12h PO; 400mg/​12h IV
Indication Infections: GI, respiratory, urinary CI Pregnancy, breastfeeding,
allergy to quinolones Caution Myasthenia gravis, seizures (reduced seizure
threshold), adolescents/​
children, renal impairment SE N+V, diarrhoea,
tendonitis (including tendon rupture) Interaction NSAIDs increase risk
of seizure, increase levels of theophyllines, increase nephrotoxicity of
ciclosporin, increase effect of warfarin.
Citalopram $ Selective serotonin re-​uptake inhibitor. Dose 20mg/​
24h PO (max 40mg/​24h) Indication Depression, panic disorder CI Active
mania, QT interval prolongation Caution Pregnancy, epilepsy, cardiac
disease, DM SE GI disturbance, anorexia, weight loss, dNa+, agitation
Interaction MAOI within 2wk.
Clarithromycin $ Macrolide antibiotic. Dose 250–​500mg/​12h PO/​
IV Indication Atypical pneumonias, H. pylori CI Allergy Caution Pregnancy,
breastfeeding, hepatic or renal impairment, concomitant use with statins
SE GI upset, irritant to veins.
Clindamycin $ Antibiotic. Dose 150–​450mg/​6h PO; up to 4.8g/​24h
IV in 2–​4 doses for life-​threatening infections (consult BNF) Indication
Gram-​
positive cocci and anaerobes; osteomyelitis, intra-​
abdominal
infections, MRSA CI Diarrhoea Caution Breastfeeding, acute porphyria SE GI disturbance, antibiotic-​associated colitis (namely C. diff ),
hepatotoxicity, arthralgia; discontinue drug if patient develops new
onset diarrhoea Interaction Increases neuromuscular blockade.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
Bo
o
et
n
.
kX
.ne
X
k
oo
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.
w
.n
kX
t
ww
ww
o
w.B
et
n
.
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et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
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X
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ww
t
e
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ok
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w
t
o
w.B
t
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X
k
w
ww
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
197
t
t
t
Clobetasol
.ne propionate cream
.neSee topical corticosteroids.X.ne
X
X
k
k
Loading 300mg/​
ok Clopidogrel $ Antiplatelet.
oo IndicationDosePrevention
ooSTAT PO;
of.B
atherothrombotic
Bo Maintenance 75mg/​w2.4hBPO
events following MI/​ACS/​CVA CI Pregnancy,
acw Hepatic impairment, wincreased
ww breastfeeding,
tive bleedingwCaution
risk of bleeding, ww
recent trauma/​surgery SE GI disturbance, bleeding disorders
Interaction
Increased risk of bleeding with
and anticoagulants;
etpump
et NSAIDsof clopidogrel.
et
proton
inhibitors may reduce
effectiveness
n
n
n
.
.
.
X
X Dose 1% cream 2–​3 applications/​
X
kantifungal.
$ Imidazole
ok Clotrimazole
oinfections,
ok Avoid
o
o
o
24h
Indication
Fungal
skin
vaginal
candidiasis
Caution
B contact with eyeswand.Bmucous membranes, can w
.B condoms and
damage
w
w
diaphragms SE Local
irritation.
w
w
ww
Co-​amoxiclav $ Beta-​lactam with clavulanic acid. Dose 375–​625mg/​
8h PO;t1.2g/​8h IV Indication Infection; where
amoxicillin alone is not apt impairment,
e CI Penicillin allergy Caution
eRenal
et
propriate
glandular.n
fever,
n
n
.
.
X infection, ALL/​CLL SE kN+V,
X
X
rash.
ok CMV
o diarrhoea,
ok inhibitor
o
o
o
Co-​
b
eneldopa
$
Levodopa
and
dopa-​
d
ecarboxylase
B (benserazide). Dosew.Initially
B 50mg/​6–​8h PO, increased
w.B to 100mg/​ w
w
w
24h or 100mg/​
t
wice
a
week
according
to
response;
usual mainten- w
w
w
ance dose 400–​
800mg/​
day in divided doses Indication Parkinson’s
disease Caution Severe pulmonary or cardiovascular disease, psychiatric
illness, endocrine disorders, pregnancy and breastfeeding SE GI disturbances, taste disturbances, dry mouth, anorexia, arrhythmias and palpitations, postural hypotension, drowsiness, dystonia, dyskinesia.
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
w BNF Indication w
(carbidopa). Dose
w Depends upon preparation,
wconsult
w
w
Parkinson’s disease Caution Severe pulmonary or cardiovascular disease, w
psychiatric illness, endocrine disorders, pregnancy and breastfeeding SE
t mouth, anorexia, arrhythmias
t
GI disturbances,
taste disturbances, e
dry
et
.npalpitations,
.n drowsiness, dystonia, dyskinesia.
.ne
and
postural hypotension,
X
X
X
$ Weak opioids
with paracetamol. Dose 8/​
Two
ok Co-​codamol
oktablets/​
o5k00mg
o
o
4–​6h PO (max
eight
2
4h
in
divided
doses);
30/​500mg
Bo tablets/​
B
B
.
.
Two tablets/​4–​6hw
eight tablets/​24h in divided
w doses) Indication w
w PO (maxdepression,
wileus;
Pain CI Acute
respiratory
paralytic
codeine containing w
w
w
medicines should not be used in children under 12yr, or in any patient
under the age of 18yr who undergoes removal of tonsils or adenoids for
et of sleep apnoea Caution
et Pregnancy (especially delivery),
et
thentreatment
n
n
.
.
.
XCOPD, asthma, renal impairment,
X hepatic impairment SE N+V,
Xconstiok pation Info Co-​prescribe olaxatives
ok if using opioids for >24h.
ok
o
o
B Codeine phosphate
.B60mg/​4h PO/​IM
w.B $ Weak opioid. Dose
w30–​
(max 240mg/​2w
4h in divided doses) Indication Pain
CI Acute respiratory
w
w medicines should not be ww
depression, w
paralytic ileus; codeine containing
B
Co-​careldopa $ Levodopa and dopa-​
decarboxylase inhibitor
et
n
.
kX
o
Bo
used in children under 12yr, or in any patient under the age of 18yr who
undergoes removal of tonsils or adenoids for the treatment of sleep apnoea Caution Pregnancy (especially delivery), COPD, asthma, renal impairment, hepatic impairment; never give codeine phosphate IV SE N+V,
constipation Info Co-​prescribe laxatives if using opioids for >24h.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
198
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
netβ agonist. Dose 500micrograms
.ne
.ne
Combivent
$ Antimuscarinic.with
X
X
X
bromide with
2.5mg salbutamol/​
PRN NEB
ok ipratropium
okairway
ok Indication
o
o
and other reversible
obstruction, COPD
Caution
Bo Asthma
B
B
. SE Antimuscarinic effects (commonly
. dryProstatic
hyperplasia, glaucoma
mouth),
w
w
w headaches, arrhythmias.ww
fine tremor, tension
w
ww
Corsodyl $ Antiseptic. See chlorhexidine.
Cyclizine
et $ Antihistamine (H antagonist).
et See antiemetics. .net
n
n
.
.
Dabigatran
$
Direct
thrombin
inhibitor.
and dose VTE
X110mg 1–​4Indication
X prophy­
kXlaxis after hip/​knee replacement
k
h after surgery,ok
followed by
o
o
o If >75yr then
12h for 9 d (30B
1st B
Bo 220mg/​
. doin hips) start 12–​24h after (30d
. dose.
initial dose is 75mg,wfollowed by 150mg/​12h for 9dw
in hips). Treatment
w of recurrent PE/​DVT Initial
of DVT/​PE and
wprophylaxis
wwdose must follow at least ww
5 days treatment with a parenteral anticoagulant. 150mg/​12h. If >75yr, renal
impairment or at increased risk of bleeding: 110mg/​12h. Prophylaxis of stroke
et embolism in non-​valvular.nAFetand 1 risk factor (Such as previous
et
andnsystemic
n
.
.
stroke
or
TIA,
symptomatic
heart
failure,
DM,
HTN,
or
>75yr):
150mg/​
1
X
X
X 2h.
ok If >75yr: 110mg/​12h. SEoAbdominal
ok pain; anaemia; diarrhoea;
ok dyspepsia;
o
o
haemorrhage; nausea..B
Caution Avoid in patients with significant
B
.B bleeding risk.
w
Wait 6h after epidural
catheter removal to restartwdabigatran. Info Dose
changes if receiving
or w
verapamil. No routine anti- ww
ww concomitant amiodarone w
B
®
2
®
1
coagulant monitoring required (INR tests are unreliable).
Dalteparin $ Low-​molecular-​weight heparin. Dose Consult BNF
Indication DVT/​
PE treatment and prophylaxis, ACS CI Bleeding disorders, thrombocytopenia, severe hypertension, recent trauma
Caution Hyperkalaemia, hepatic or renal impairment SE Haemorrhage,
thrombocytopenia, hyperkalaemia Interaction NSAIDs increase bleeding
risk, effects increased by GTN.
Desloratadine $ Antihistamine (H1 antagonist). See antihistamines.
Dexamethasone $ Corticosteroid. Dose See BNF Indication Cerebral
oedema (malignancy), suppression of inflammation/​
allergic disorders, diagnosis of Cushing’s disease, chemotherapy induced N+V
CI Systemic infection Caution Adrenal suppression, may precipitate tumour lysis syndrome in patients with some haematological malignancies
SE Cushing’s syndrome, deranged blood glucose, osteoporosis, psychiatric reactions, raised WCC (specifically neutrophilia).
Diamorphine $ Opioid. Dose 2.5–​5mg/​4h SC/​IM/​IV Indication
Severe pain, ACS/​acute MI, acute pulmonary oedema, palliative care
CI Respiratory depression, paralytic ileus, raised ICP/​
head trauma,
comatose patients, phaeochromocytoma Caution Pregnancy (especially delivery), COPD, asthma, renal impairment, hepatic impairment SE N+V, constipation, respiratory depression, dry mouth
Interaction MAOI Info Co-​prescribe laxatives if using opioids for >24h.
Diazepam $ Benzodiazepine. Dose status epilepticus 5–​10mg over 10min
IV (max 20mg) or 10–​40mg PR; Other short-​term usage 2mg/​8h PO (max
30mg/​24h in divided doses) Indication Seizures, status epilepticus; Short
term Anxiety, alcohol withdrawal, muscle spasms CI Respiratory depression, sleep apnoea, unstable myasthenia gravis, hepatic impairment Caution
Pregnancy, breastfeeding, history of drug abuse, respiratory disease, muscle
weakness, renal impairment SE Drowsiness, confusion, muscle weakness.
t
.ne
X
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B
.
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kX
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.
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ww
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n
.
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X
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oo
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.
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.n
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t
ww
ww
o
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et
n
.
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et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
ok
Bo
w
t
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
199
t
t
t
Diclofenac
$ NSAID. Dose 50mg/​
.ne
.ne 8h PO/​PR (max 150mg/​
.n2e4h
X
X
X
doses) Indication kPain, inflammation CI Pregnancy,
peptic
ok in divided
o
okischaemic
disease, hepatic impairment,
congestive heart failure,
o
o
Bo ulcer
B
B
heart disease, peripheral
disease, cerebrovascular
w. renalarterial
w. GI disease,disease
Caution Breastfeeding,
impairment, asthma,
paw
w
w
w
tients with w
significant risk factors for cardiovascular
events (eg iBP, w
ilipids, DM, smoking) SE GI disturbance/​
bleeding, headache, dizzit
ness Info
Arthrotec is a preparation e
oft diclofenac with misoprostol and
e
et
n
n
n
.
.
.
may
reduce GI side effects.
X
X
Xover at
$ Cardiac glycoside.
Emergency IV loading dose 0.75–​
ok Digoxin
ok0.75–​
ok1mgdoses
o
o
o
least
2h
IV
Rapid
oral
loading
dose
1
.5mg
over
24h
in
3
divided
PO
B (typically 500micrograms
.B PO initially, followed by 250micrograms
.B
PO 6h
w
w
wtachycardic Maintenance ww
later, and furtherw
w 250micrograms PO 12h laterwif still
dose 62.5–​125micrograms/​24h PO Indications Often 2nd-​
line agent in
supraventricular tachyarrhythmias (commonly AF and atrial flutter), heart
t
t
failure
eCI 2nd-​or 3rd-​degree AV dissociation,
e accessory conducting.npathet
n
n
.
.
ways
(eg
WPW)
Caution
Pregnancy,
recent
MI,
sick
sinus
syndrome,
renal
X
X
X
elderly patients,
or iCa SE N+V,
diarrhoea,
ok impairment,
okdK , dMgdizziness,
okyellow
o
o
o
bradyarrhythmias,
tachyarrhythmias,
blurred
or
B sion Therapeutic monitoring
.B(Table 5.13) should be undertaken
.B if toxicity is con-viw
w
w is poor Info Digoxin is ww
sidered (usually
presents with N+V) or if ratew
control
ww
B
®
+
2+
2+
now rarely used for rapid rate control, with other agents often being used in
preference (E pp. 256–61) or DC cardioversion (E p. 546). Digoxin is most
often used in the chronic rate control of supraventricular tachyarrhythmias
and in heart failure. Digoxin does not restore sinus rhythm, it merely slows
conduction at the AV node, limiting the number of impulses passing from
the atria through to the ventricles thus controlling ventricular rate. It also
acts as a positive inotrope, increasing the force of ventricular contraction
If rate not adequately controlled After loading with digoxin, discuss with senior
or cardiologist.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
Monitoring
.ne
digoxin
X
k
t
.ne
X
k
w
t
.ne
X
k
et
.n
kX
Optimum sampling time 6–​12h post oral dose 1–​2.6nmol/​L (0.8–​
2microg/​L); typically takes 7d to get to steady state
2 Toxic >2.6nmol/​L (>2microg/​L). Toxicity can occur at levels
<1.3nmol/​L if patient has dK+
2 Signs of toxicity (see Table 5.13; E OHAM3 p. 708)
o
o
w.B
ww
oo
B
.
w
w
w
w
w
w
w
Table 5.13 Digoxin toxicity
Symptoms
N+V, confusion, diarrhoea,
et
et yellow and blurred vision .net
n
n
.
.
Bloods
Toxicity
precipitated
by
renal
failure, dK , dMg , dT X
X
kX
k
k
Check digoxin
level (see ‘Monitoring digoxin’); toxic
o
o
oL (>2micrograms/​L)
oo if
>2.6nmol/​
Bo ECG
B
B
.
.
Tachy-​
wave inversion
w and bradyarrhythmias. ST depression/​T-​
wwbradyarrhythmias)
Complications
wwiK , cardiac dysrhythmias (tachy-​
wand
ww
Management
Airway, breathing, and circulation
Continuous ECG monitoring
t
t
e
et
Treat arrhythmias .ne
n
n
.
.
Consider
digoxin-​
b
inding
antibody
fragments
(DigiFab
,
see
BNF)
X
X
kX digoxin overdose
if known or o
suspected
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
+
2+
4
+
®
B
200
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Dihydrocodeine
$ Weak opioid.
.ne
.neDose 30mg/​4–​6h PO (maxX240mg/​
.ne
X
X
divided doses); 50mg/​
6h IM Indication Pain CI Acute
respirak 4–​Caution
ok 24h indepression,
oileus
ok delivery),
paralytic
Pregnancy (especially
o
o
Bo tory
B
B
COPD, asthma, renal
impairment;
give
w. impairment, hepatic Co-​
wp.rescribe never
dihydrocodeinewIV SE N+V, constipation Infow
laxatives if
wfor >24h.
w
ww
using opioids
Diltiazem
channel blockers.
t
et See calcium-​
eDose
et
n
n
n
.
.
.
Dipyridamole
$ Antiplatelet.
200mg modified-​release/​
X PO (max 600mg/​24hkinXdivided doses), non-​modified-​
Xrelease
ok 12h
o (see BNF) Indication Secondary
ok preveno
o
o
preparations
also
available
B
B
.B and TIA, adjunct to oral
.anticoagulation
tion of ischaemicw
stroke
for
w
w
w
prophylaxis ofwthromboembolism associated
with prosthetic heart
w
w
valves Caution Breastfeeding, aortic stenosis, unstable angina, recent w
MI SE GI disturbance, dizziness, headache, myalgia Interaction Increases
t warfarin, decreases effectnofecholinesterase
t
effecteof
inhibitors.
et
n
n
.
.
.
X
X
X
sodium See laxatives.
ok Docusate
ok Dose 1mg/​24h PO; increase
okgradually to
o
o
o
Doxazosin
$
α
antagonist.
B
.B
.B
2–​4mg/​24h (maxw16mg/​24h) Indication Benign w
prostatic hyperplasia,
w
w
hypertension
CI
Breastfeeding,
hypotension
Caution
w
w Pregnancy, hepatic ww
B
1
impairment SE Postural hypotension, headache, dizziness, urinary incontinence Interaction Increases effects of antihypertensives.
Doxycycline $ Tetracycline. Dose 100–​200mg 12–​24h PO (consult
BNF) Indication Respiratory tract infections, GU infections, anthrax,
malaria prophylaxis CI Pregnancy, breastfeeding, renal impairment, age
<12yr (stains growing teeth and bones) Caution Myasthenia gravis may
worsen, exacerbates SLE SE GI disturbance including, dysphagia/​oesophageal irritation, photosensitivity Interaction Decreased absorption
with milk, decreases effects of oral contraceptive pill, mildly increases
effects of warfarin.
Edoxaban $ Direct factor Xa inhibitor. Dose 30mg/​24 if <60kg, 60mg/​
24 if > 61kg Indication Prophylaxis of stroke and systemic embolism in non-​
valvular AF and 1 risk factor (Such as previous stroke or TIA, symptomatic
heart failure, DM, HTN, or >75yr); Treatment of DVT/​PE and prophylaxis
of recurrent PE/​DVT Caution Mitral stenosis and prosthetic heart valves.
Avoid in patients with significant bleeding risk. SE Anaemia; epistaxis;
haemorrhage; nausea; pruritus; rash (rare = allergic oedema). Info No
routine anticoagulant monitoring required (INR tests are unreliable).
Monitor LFTs for the 1st year.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
w
t
o
ww
t
e
X.n
o
w.B
t
.ne
X
k
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
t
ww
et
n
.
X
ww
ok Enalapril See ACEi. oo
ok
Bo Enoxaparin $wLow-​
.Bmolecular-​weight heparin.wDose
.BoDVT/​PE prophyw
laxis 20–​40mg/​
4h SC (E pp. 420–1); DVT/​w
1.5mg/​kg/​
ww2treatment
w PE treatment
24h SC; ACS
1mg/​kg/​12h Indication
DVT/​PE treatment w
and prophylaxis, ACS CI Bleeding disorders, thrombocytopenia, set
t Hyperkalaemia, hepatic
vere ehypertension,
recent trauma Caution
ethrombocytopenia,
eort
n
n
n
.
.
.
renal
impairment SE Haemorrhage,
hyperkalaemia
X
X
kX risk, effects increasedobykGTN.
ok Interaction NSAIDs increase
obleeding
o
o
o
B
Epilim $ Antiepileptic.
w.B See valproate. ww.B
w
w
w
ww
®
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
201
t
t
t
Erythromycin
$ Macrolide antibiotic.
50mg/​
.ne
.ne Dose 500–​1000mg/​6h PO;
.ne
X
X
X
in divided dose (typically
1000mg/​6h IV) Indication
ok kg/​24h IVpneumonias.
ok 500–​
oktoInfection;
Commonly
used in patients allergic
penicilo
o
Bo atypical
B
B
.
. renal impairment,
lins CI Allergy Caution Pregnancy,
breastfeeding, hepatic or
w
w
concomitant usew
w with statins SE GI upset, irritantwtowveins.
ww
Esomeprazole $ Proton pump inhibitor. Dose 20–​40mg/​24h PO
Indication
GORD, H. pylori eradication
Breastfeeding Caution
t SE GICI disturbance,
et PUD,
ecancer
et
Pregnancy,
hepatic impairment, gastric
headache
n
n
n
.
.
.
XInteraction Proton pump inhibitors
kXmay reduce effectiveness ofoclopidogrel.
kX
ok Felodipine See calcium-​ocohannel
o
o
blockers.
B
w.B$ Iron supplement. DosewConsult
w.BBNF as depends w
Ferrous fumarate
w
upon formulation
anaemia SE GI disturbance, w
w Indication Iron deficiency w
dark stools.
Ferrous
et gluconate $ Iron supplement.
et Dose 600mg/​8h PO.n(see
et
n
n
.
.
BNF)
Indication
Iron
deficiency
anaemia
SE
GI
disturbance,
dark
stools.
X
X
kX Iron
ok Ferrous sulfate $ Ironosupplement.
ok
oIndication
Dose 200mg/​8h PO
o
o
B deficiency anaemiawSE.B
GI disturbance, dark stools. .B
w
w
Fibrinolytic
w drugs $ Plasminogen activator.
ww Dose and indications ww
B
Depends upon specific agent, see Table 5.14 (also E p. 551) CI Recent
haemorrhage, trauma or surgery, coagulopathies, aortic dissection, aneurysm, coma, history of cerebrovascular disease, peptic ulceration,
menorrhagia, hepatic impairment; streptokinase should not be used
again beyond 4d of first administration due to antibody formation and
risk of allergic reactions Caution Pregnancy, following external chest
compression, old age, hypertension SE N+V, bleeding, hypotension.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
w
Table 5.14 Fibrinolytic drugs
o
Bo
t
.ne
X
k
t
o
o
w.B
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
w
.n
kX
ww
t
e
X.n
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X
k
t
ww
ww
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
In acute STEMI, fibrinolytic drugs should be used where primary cutaneous
intervention (PCI) is not immediately available
Alteplase
Indications Acute MI, massive PE, acute ischaemic stroke
Dose Consult BNF; given as an IV bolus followed by an IV
infusion, followed by heparin infusion
Reteplase
Indications Acute MI
Dose Consult BNF; given as two IV boluses 30min apart,
followed by heparin infusion
Streptokinase Indications Acute MI, DVT, PE, acute arterial thromboembolism,
central retinal venous or arterial thrombosis
Dose Consult BNF; typically 1.5million units in 100mL 0.9%
saline over 1h IV. Do not repeat administration after 4d of
initial dose due to risk of allergic reaction
Tenecteplase
Indications Acute MI
Dose Consult BNF; given as an IV bolus, followed by heparin
infusion
Urokinase
Indications Thromboembolic occlusive vascular disease; DVT,
PE and peripheral vascular occlusion; occluded iv catheters and
cannulae blocked by fibrin clot Dose Consult BNF
ww
ok
Bo
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
202
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
w
ww
t
et
netBPH 5mg/​24h PO; male-​
Finasteride
$ Antiandrogen. .Dose
.ne
.pnattern
X
X
X
1mg/​24h PO Indication
BPH, male-​pattern baldnesskCI Females
ok baldnessadolescents
okProstate
o obstrucCaution
cancer, urinary otract
o
Bo and
B
B
.
.
tion SE Gynaecomastia,
testicular pain, sexual dysfunction.
ww See metronidazole. www
Flagyl $ w
Antibiotic.
ww
Flecainide $ Class Ic antiarrhythmic. Dose Initial 100mg/​12h PO;
t5d; 2mg/​kg over 10–​30min slow
reduce
etto lowest effective dose over
e3–​
et
n
.
IV.n
(max 150mg) Indication VT, SVT
CI HF, history of MI, heart.n
block,
X branch block CautionkPatients
X with pacemakers, AFkSEXGI disok bundle
o fatigue Interaction
o
o
ooof action inturbance,
dizziness,
oedema,
Duration
B
B
B
.
.
creased by amiodarone,
fluoxetine,
quinine;
myocardial
w
w depression with w
β-​blockers/​verapamil.
ww
ww
w
Flixotide $ Corticosteroid. See fluticasone.
t 500mg/​6h PO; 250–​2000mg/​
Flucloxacillin
$ Beta-​lactam. Dosee250–​
et
et
n
n
n
.
.
.
6h
IV
Indication
Penicillin
sensitive
infections,
endocarditis,
osteomyelitis
X of flucloxacillin-​relatedkXjaundice, penicillin allergy SEkDiarrhoea,
X CI
ok History
o
o
o
o
o
­abdominal pain CautionB
impairment Interaction Decrease
B
. Renal increases
.B effects of oral
contraceptive pill, allopurinol
risk of rash. w
w
ww$ Triazole antifungal. Dose
ww50–​400mg/​24h PO/​IV ww
Fluconazole
®
®
Dependent on indication Indication Fungal meningitis, candidiasis, fungal
prophylaxis CI Pregnancy, acute porphyria Caution Breastfeeding, hepatic
or renal impairment SE GI disturbance.
t
t
t
.ne
.ne
.ne
X
X
X
Dose 50–​300micrograms/​
ok Fludrocortisone $ oMineralocorticoid.
ok
ok
o
disease,
other
adrenal
insufficiency,
posBo 24h PO IndicationwAddison’s
B
B
.
. cover Caution
w
tural hypotension CI Systemic infection without antibiotic
Adrenal suppression
ww SE Sodium and water retention,
ww hypertension.
ww
Flumazenil $ Benzodiazepine antagonist. Dose 200micrograms/​STAT
t
t
t
IV, followed
100micrograms/​1min
(max 1mg) Indication
.ne by OD/​
.ne if required
.ne
Benzodiazepine
toxicity CI Conditions
dependent on benzodiazepX
X
X
k Benzodiazepine dependence,
ok ines, eg status epilepticus
oCaution
ok mixed
o
o
arrhythmias.
Bo OD SE N+V, dizziness,
B
B
.
.
w
Fluoxetine w
$w
Selective serotonin re-​
uptake
inhibitor. Dose 20mg/​
w
24h PO (max
w 60mg/​24h) Indication Depression,
w bulimia nervosa and ww
OCD CI Active mania Caution Pregnancy, epilepsy, cardiac disease, DM,
bleeding disorders, glaucoma SE GI disturbance, anorexia, weight loss,
dNa+, agitation Interaction MAOI within 2wk.
t
et
et
n
n
.
.
X Dose 100–​500micrograms/​
X INH
$ Corticosteroid.
ok Fluticasone
ok asthma
ok 12hCaution
o
o
o
(consult
BNF)
Indication
Chronic
(step
2
BTS
guidelines)
B
.B
TB SE Oral candidiasis,
bronchospasm (rare).
w.Bhoarse voice, paradoxical
w
w
w
w 24h PO before con- ww
Folic acidw
$ Vitamin B9. Dose 400micrograms/​
ception and until week 12 of pregnancy; 5mg/​wk for preventing methotrexate
effects Indication Pregnancy,
folate deficient megaloblastic
et sidelong-​
eCIt Malignancy
egivet
n
n
n
anaemia,
term methotrexate
Caution Never
.
.
.
X for pernicious anaemia;kcan
X degeneration of spinal
X
ok alone
o SEcause
ok cord, uno
o
diagnosed megaloblastico
anaemia
GI disturbance.
B
w.B
w.B
w
w
w
w
ww
e
X.n
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
203
t
t
t
Fondaparinux
$ Factor Xa inhibitor.
.ne
.neDose 2.5mg/​24h SC (2.5mgXloading
.ne
X
X
op) Indication VTE
prophylaxis and treatment, ACS
Active
ok dose 6h post-​
ok Caution
ok CIbleeding
bacterial endocarditis
Pregnancy, breastfeeding,
o
o
Bo bleeding,
B
B
disorders, active PUD,. recent surgery, epidural/​spinal .anaesthesia, hepatic
w
or renal impairment
wwSE Bleeding, purpura, anaemia,
wthrombocytopenia.
w
w
ww
Furosemide $ Loop diuretic. Dose Typically 20–​80mg/​24h PO/​
IV Indication
(LVF, pulmonary
resistant hypertenetSevereOedema
et oedema),
et
sion
CI
dK and dNa , hypovolaemia,
renal impairment Caution
n
n
n
.
.
.
XHypotension SE GI disturbance,
Xhypotension, electrolyte disturbances
X
ok (dK , dNa , dMg ) Interaction
ok Increases toxicity of gentamicin,
ok digoxin,
o
o
o
B NSAIDs Info IV doses
B min (risk of
at .<4mg/​
w.B>80mg should be infused
w
deafness).
w
w
w
w$ Antibiotic. Dose 2% topical w
Fusidic acid
cream 3–​4 applications/​24h; w
oral and IV preparations available (see BNF) Indication Staphylococcal
t
t penicillin-​resistant staphyloskin infections;
IV treatment Osteomyelitis,
einfections
ebreastfeeding,
et
n
n
coccal
Caution Pregnancy,
monitor LFTs.n
SE GI
.
.
X
X
X
reversible jaundice.
ok disturbance,
ok
ok
o
o
o
Fybogel
See
laxatives.
B
w.B
w.2B4h PO; Continued w
Gabapentin w
$ Antiepileptic. Dose day 1 300mg/​
w
w
w
w
+
+
+
+
2+
®
Increase by 300mg/​24h PO up to max 3.6g/​24h in 3 divided doses
Indication Epilepsy, neuropathic pain Caution Pregnancy, breastfeeding,
renal impairment, DM, avoid abrupt withdrawal SE GI disturbance, headache, sleep disturbance Interaction Effects decreased by antidepressants.
t
t
t
.ne
.ne
.ne
X
X
X
ok Gentamicin $ Aminoglycoside.
ok Dose Once daily 5–​7omg/​
okkg/​24h IV
o
Bo adjust to serum concentration;
B
B
dosing regimens
may be used
w. Indicationother
w. meningitis,
(consult local guidelines)
Infection; w
sepsis,
endow
carditis CI Myasthenia
gravis Caution Pregnancy,
w
w breastfeeding, renal im- ww
pairment SE Ototoxic, nephrotoxic Interaction Effects increased by loop
diuretics,
t
et increases effects of warfarin.
et
n
.
.nenext dose is due (but check
.nlocal
X
X
X
Levels
are
typically
taken
1
hr
before
ok
ok
ok
first)
o
o
Bo guidelines
B
B
. IV dose 9–​18micromol/​L (5–​10mg/​
Monitoring Peak 1hw
post
w.L)
gentamicin Trough
<4.2micromol/​L (<2mg/​L)
w
w
w
ww
2 Toxic >12mg/​L (22micromol/​L) w
t
.ne
2 Signs of toxicity tinnitus, deafness, nystagmus, vertigo, renal failure
(OHCM10 E p. 756). Will vary with once-​daily regimen, check locally.
.ne
X
X
Glibenclamide
See
sulfonylureas.
k
ok
oo
Bo Gliclazide See sulfonylureas.
B
.
w
Glipizide Seew
sulfonylureas.
w
t
et
n
.
X
ok
ww
o
w.B
Glucagon $ Peptide hormone. Dose 1mg/​PRN IM/​SC/​slow IV
Indication Hypoglycaemia, in treatment of β-​blocker overdose CI Phaeo­
chromocytoma Caution Insulinoma, glucagonoma, chronic hypoglycaemia SE GI disturbance, dK+, hypotension.
et
n
.
kX
o
Bo
ww
et
n
.
kX
t
o
o
B
.
w
ww
Glycerin suppositories See laxatives.
w
ww
.ne
X
ok
.Bo
ww
B
204
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
et
Glyceryl
See.n
GTN.
.ne $ Trinitrate nitrate. X
.ne
X
X
k $ Nitrate. Dose 1–​2osprays/​
k PRN
ok GTN sublingual/​transdermal
oo Prophylaxis
o
and treatment
of
angina, left
Bo SL; 0.3–​1mg/​PRNwSL.BIndication
B
w.
ventricular failure CI Hypotensive conditions, hypovolaemia,
aortic stenw
w
osis Cautionw
Pregnancy, breastfeeding, hypothyroidism,
recent MI, head ww
w
trauma SE Postural hypotension, tachycardia, headache Info Transdermal
patchest are available, see BNF—​patients
tolerance (tachyt may develop
e to nitrates and as such it.nis esuggested
eta
phylaxis)
to ensure patients.have
n
n
.
prevent this; it is usual to have this
Xnitrate-​free period for 4–​8h toX
kX period
ok overnight when the effectsooofknitrates
oneeded.
are least likely to be
o
o
B
.B min IVI GTN.
GTN IV infusion
Nitrate. Dose 10–​200micrograms/​
w.$Bsee
wventricular
w
w
w
For typical prescription
Fig. 5.2. Indication Left
failure, onw chest pain refractory to SL w
going ischaemic
nitrates CI Hypotensive con- w
ditions, hypovolaemia, aortic stenosis Caution Pregnancy, breastfeeding,
hypothyroidism,
recent MI, head trauma
et
et SE Postural hypotension,.tachyet
n
n
n
.
.
cardia,
headache
Info
Patients
may
develop
tolerance
(tachyphylaxis)
X and as such it is suggested
X freeto
kX to ensure patients haveoaknitrate-​
ok nitrates
o
o
o
o
period for 4–​8h to prevent
this; it is usual to have this
B
.B are
.Bperiod overnight
when the effects of
nitrates
least likely to be needed.
w
w
ww
ww
ww
B
t
.ne
X
k
oo
et
.n
kX
oo
B
.
Fig. 5.2 Example ofw
a GTN infusion.
ww
oo
B
.
ww
t
.ne
X
k
w
Haloperidol $ Antipsychotic (butyrophenone). Dose Antiemetic 0.5–​
o
Bo
t
.ne
X
k
t
et
3mg/​8h PO/​IV; Other 0.5–​10mg/​8h PO/​IM/​IV Indication Schizophrenia,
agitation, N+V, motor tics, intractable hiccups CI Comatose/​CNS depression Caution Pregnancy, breastfeeding, hepatic or renal impairment,
cardiovascular disease, Parkinson’s, epilepsy SE Extra­pyramidal symptoms, cardiac arrhythmias (QTc prolongation).
o
ww
o
w.B
.ne
X
k
oo
B
.
w
.n
kX
ww
Heparin $ Glycosaminoglycan (potentiates antithrombin III).
Dose Loading dose 5000units or 75units/​kg IV; Maintenance 18units/​kg/​
h IVI (titrate dose to keep APTT within therapeutic range); Prophylactic
dose 5000units/​12h SC (seldom used as LMWH have similar benefits
and fewer side effects) Indication Rapid anticoagulation, treatment and
prophylaxis of DVT/​
PE, ACS CI Bleeding disorders, thrombocytopenia, severe hypertension, recent trauma, history of heparin-​induced
thrombocytopenia (HIT, E p. 421) Caution iK+, hepatic or renal impairment SE Haemorrhage, thrombocytopenia, iK+ Interaction NSAIDs
increase bleeding risk, effects increased by GTN.
t
e
X.n
ok
Bo
.ne
X
k
ww
et
n
.
kX
o
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
ww
Humalog® See insulin.
Bo
t
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
205
t
t
t
Humalin
.ne See insulin.
.ne
.ne
X
X
X
ok Hydralazine $ Vasodilator
ok (arterial >> venous). oDose
ok hyperteno
5–​
1
0mg
slow
IV
titrated
to
effect
(can repeat
Bo sion 25–​50mg/​12hwPO;
B
B
.
w. Hypertension, w
after 30min); Heart failure 25–​75mg/​6h PO Indication
w
w
heart failure
w CI SLE, severe tachycardia,
w myocardial insuffi- w
ciency Caution Pregnancy, breastfeeding, hepatic or renal impairment,
ischaemic
cerebrovascular
disease SE Tachycardia, palpit heart disease,
ehypotension,
etafter
et
tation,
SLE-​like syndrome
long-​term, rebound .hypern
n
n
.
.
Xtension on stopping therapy, kfluidXretention.
ok Hydrocortisone cream
o See topical corticosteroids. ookX
o
o
B
B
w.B
w.Dose
Hydrocortisone
IV/​PO $ Corticosteroid.
Acute 100–​
w
w
250mg/​6h IV;
w Chronic 20–​30mg/​24h PO win divided doses Indication ww
Adrenocortical insufficiency, acute allergic/​
inflammatory reactions CI
Systemic
infection Caution Adrenal suppression
SE Cushing’s syndrome,
t
t
e
e
et
DM,
osteoporosis, dyspepsia.
n
n
n
.
.
.
X
X
kX B . Dose Macrocytic anaemia
$oVitamin
ok Hydroxocobalamin
okafterwithout
o
o
o
neurological
involvement
Initially
1mg
three
times
a
week
IM,
2wk
B 1mg/​3mth IM; Macrocytic
B
.B anaemia with neurological
.involvement
Initially
w
w
w
1mg on alternate
then 1mg/​ ww
ww days IM until no furtherwimprovement,
®
12
2mth IM Indication Pernicious anaemia, other macrocytic anaemias with
neurological involvement Caution Do not give before diagnosis fully established SE N+V, headache, dizziness.
t
t
t
.ne
.ne
.ne
X
X
X
butylbromidek$ Anticholinergic. Dose 20mg/​6kh PO (max
ok Hyoscine
24h in divided doses);
oo 20mg/​STAT IV/​IM repeated
ooafter 30min
Bo 80mg/​
B
.
(max 100mg/​24hw
in.B
divided doses) Indication GI/​
G
U
w smooth muscle w
spasm CI Myasthenia
gravis Caution Pregnancy,
glaucoma, GI obstrucw
w
whyperplasia, urinary retentionwSE Antimuscarinic effects, w
tion, prostatic
drowsiness.
t
t
t
Hyoscine
Dose Antiemetic
.ne hydrobromide900micrograms/​
.$neAnticholinergic.
.ne
300micrograms/​6h PO (max X
24h in dividedXdoses);
X
ok Excessive respiratory secretions
ok200–​600micrograms/​4–​8oh oSCk Indication
o
Bo Motion sickness, excessive
B
secretions CI.B
Caution
w. respiratory
w Glaucoma
Pregnancy, GI w
obstruction,
prostatic hyperplasia,
urinary retention
w
SE Antimuscarinic
w effects, sedative Interaction
w Decreases effects of ww
sublingual GTN.
t 6h PO (max 2.4g/​2n4hetin
Ibuprofen
4e00mg/​
et $ NSAID. Dose 200–​
n
n
.
.
divided
doses)
Indication
Pain,
inflammation
CI Pregnancy, peptic
X
X. ulcer
kXdisease Caution Breastfeeding,
k
k
hepatic or renal impairment,
asthma, GI
o
o
o
SE GI disturbance/​
bleeding, headache Interaction
Bo disease
.Boincreases
.BoDecreases effects of antihypertensives,
toxicity of methotrexate.
w
w
w
ww
ww
InsulatardwSee insulin.
®
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
206
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
ww
w
t
t
t
Insulin
.ne Dose When starting orXchanging
.ne SC doses, liaise withXdiabetes
.ne
X
diabetes nurse specialist);
see Table 5.15 Indications
ok team (eg ketoacidosis,
ok infusion
ok DM,in
hyperkalaemia,
maintenance of oeuglycaemia
o
Bo diabetic
B
B
critical care and post. MI CI Hypoglycaemia Caution .May need dose adw
w impairment, see w
justments in pregnancy,
renal and
whepatic
ww breastfeeding,
BNF SE Hypoglycaemia,
local reactions andw
fat hypertrophy at injection w
site, rarely allergic reactions Info Table 5.16 is not an exhaustive list of
t
insulins.
In addition to these single preparations
so-​calledebietmixtures
et are also ofusedinsulin,
n
n
n
.
.
phasic
of two different insulins
and often .consist
X a rapid-​or short-​acting insulin
X
X
ok ofproportions).
ok and a longer-​acting insulin
ok(in different
o
o
o
B
w.B
w.B
w
w
Table 5.15 IV
infusions of insulins
w
w
ww
Indication
t with 10units soluble insulinnet
Hyperkalaemia
50mL of 50% glucose
et
eover
n
n
(E
pp. 399–403) (eg Actrapid ) .IVI
.
.
10min
XSliding scale
X
X
k
k
k
50mL
of
0.9%
saline
with
50units
soluble
insulin
(eg
o
o), often infused at 0–​7mL/​h depending
oo upon the
Bo (E p. 333) wActrapid
B
.Bo blood
.
patient’s
sugar
w
ww
ww
ww
®
®
Table 5.16 Properties of common subcutaneous insulins
t
t
t
Type
.neof insulin Example XOnset
.ne Peak Max duration
.ne
X
X
ok Rapid acting
ok 15–​30min 0.5–​1.25h o4–​o6hk
o
Novorapid
Bo Aspart
B
.
.B
Lispro
Humalog
15–​30min 0.5–​1w
.25h 4–​6h
w
w Apidra
w
Glulisine w
15–​30min w
0.5–​1.25h 4–​6h
ww
Short acting
t
t 2–​3h
t
Soluble
Actrapid
30–​60min
6–​8h
.ne and long acting X.ne
.ne
Intermediate
X
X
Insulatard
6–​10h
14–​
ok Isophane
ok 2–​4h
o1k8h
o
o
Bo Glargine
B
B
3–​4h
8–​16h . 20–​24h
.
wLantus
w 720h
Detemir
Levemir
3–​4h
8h
w
w
w6–​w
ww
Ipratropium
$ Anticholinergic. Dose Chronic 20–​40micrograms/​6h
t
e
et250–​500micrograms/​4–​6.hnNEB
et
INH
(max 80micrograms/​6h); Acute
n
n
.
.
Caution Glaucoma,X
prostatic
XIndication Bronchospasm; chronic
X and acute
effects.
ok hyperplasia SE Minimal antimuscarinic
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
®
®
®
®
®
®
®
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
w
207
Pharmacopoeia
t
t
t
Iron
.neSee ferrous preparations. X.ne
.ne
X
X
k
ok ISMN $ Nitrate. See isosorbide
oo mononitrate. .Book
Bo ISMO $ Nitrate.wSee.Bisosorbide
mononitrate. w
w
w
Isoket $ Nitrate.
See
isosorbide
dinitrate.w
w
ww
Isosorbide dinitrate IV infusion $ Nitrate. Dose 2–​10mg/​h
IVI Indication
Left ventricular failure, ischaemic
chest pain CI Hypotensive
et hypovolaemia,
et Caution
et
n
n
n
.
.
.
conditions,
aortic
stenosis
Pregnancy,
breastX hypothyroidism, recent
X MI, head trauma SE Postural
X hypook feeding,
ok Info
ok tolerance
o
o
o
tension,
tachycardia,
headache
Patients
may
develop
B (tachyphylaxis) to w
.B if infused for prolongedwperiods,
.B though there
nitrates
w
w
are obvious risks
about stopping a nitrate infusion;
consult senior.
w
w
ww
Isosorbide mononitrate $ Nitrate. Dose initially 20mg breakfast and
lunchtime
then 40mg breakfast andt lunchtime PO (max 120mg/​24h
et PO
e of angina, adjunct in congestive
et
n
n
n
in .divided
doses) Indication Prophylaxis
.
.
X failure Caution As GTNkSEXPostural hypotension, tachycardia,
X headok heart
o tolerance (tachyphylaxis) toonitrates
ok and
ache Info Patients may develop
as
o
o
B such it is suggestedwto.B
B
ensure patients have a nitrate-​f.ree
period for 4–​8h
w the effects of w
to prevent this; w
is usual to have this period overnight
w itlikely
ww when
nitrates are least
to be needed, hence prescribing
them to be given at w
®
breakfast and lunchtime rather than 8am and 8pm.
t
t
t
Istin
.neSee calcium-​channel blockers.
.ne
.ne
X
X
X
ok Lactulose See laxative.ook
ok
o
Dose
Initially
25mg/​
2
4h
Bo Lamotrigine $wAntiepileptic.
B
B
.
. PO for 14d;
w
Then 50mg/​24h PO for 14d, increase by max 50–​
100mg/​24h every 7–​
w
14d until seizures
Indication Epilepsy Caution w
wwcontrolled (max 500mg/​24h)
ww
Requires close monitoring of serum levels, pregnancy, breastfeeding,
hepatictor renal impairment, avoid rapid
e
et withdrawal SE Rash/​.snevere
et
skin
reactions,
cerebellar symptoms,
cytopenias.
n
n
.
.
X
X
X
k inhibitor. Dose 30mg/​24hokPO for 4–​
$ Protonopump
ok Lansoprazole
o
15mg/​24h PO maintenance
Prophylaxis
Bo 8wk,
B
. H. pyloriIndication
.Boand treatment
of peptic ulcers, w
GORD,
eradication, Zollinger–​Ellison
syndr
w
w Caution Breastfeeding, w
w impairment, gastric
ome CI Pregnancy
hepatic
w
ww
cancer SE GI disturbance, headache Interaction Proton pump inhibitors
may reduce effectiveness of clopidogrel Info Also available as a FasTab
t
which
in the mouth and isn
useful
edissolves
et in patients who are NBM..net
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
®
®
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
208
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Laxative
.ne Dose See Table 5.17XIndications
.ne Treatment and prophylaxis
.neof
X
X
(E pp. 316–17)kCaution Confirm the patient is k
constipated
ok constipation
o
oChronic
consider causes of constipation
SE See Table 5.17 Info
use
o
o
Bo and
B
B
. electrolyte imbalances andwgut. dysmotility. Ensure
of laxatives can lead to
w
adequate water
intake and increase fibre intake
wwhere possible. Always w
wwimpaction
consider faecal
and other causesw
of obstruction before com- w
mencing oral laxatives. Combinations of laxatives from different groups
can be
etused in severe constipation.n(egetlactulose and senna). .net
n
.
X
X
ok Table 5.17 Laxatives ookX
ok
o
o
B
Classification
w.B
w.B
Bulk-​forming w Eg Fybogel , Normacol
w
w CI Difficulty in swallowing, w
ww
laxatives
intestinal obstruction, colonic
atony, faecal impaction
SE Diarrhoea, flatulence,
t
e
et abdominal distension, .net
gastrointestinal obstruction
n
n
.
.
X
X 5mL spoons in water/​12h POkX
1 sachet or
ok Fybogel
ok twodocusate,
o
o
o
Stimulant laxatives
Eg bisacodyl,
glycerol, senna o
B
B
B
.
.
CI
Intestinal obstruction, acute surgical
abdomens, active
winflammatory bowel disease, dehydration
ww pain, N+V
ww SE Diarrhoea, hypokalaemia,
wabdominal
ww
®
®
®
Info Co-​danthramer should only be used in the terminally
ill as potentially carcinogenic
t
et
Bisacodyl
5–​10mg/​nocte.PO
n
neort 10mg/​mane PR
.
.ne
X
X
X
1–​2 capsules/​
PO
ok Co-​danthramer
o1k2h POnocte
ok
o
sodium
200mg/​
(max 500mg/​24h PO ino
divided doses)
Bo Docusate
B
B
Glycerin supps
w1. suppository/​PRN PR, max 4winw24h.
w
Senna
w 2 tablets/​nocte PO or 10mL/​
w nocte PO
ww
Faecal softeners
Eg arachis oil, liquid paraffin
Info Infrequently usedt
et
CI Peanut allergy
n
ne
net
.
.
.
X
X
X
Movicol , magnesium salts, rectal k
phosphates
ok Osmotic laxatives Eg(eglactulose,
okenema),
oMicrolette
Fleet
rectal sodium citrate (eg
)
o
o
Bo
B
B
CI
Intestinal
obstruction,
colonic
atony
.
.
wSE Diarrhoea, flatulence, abdominal
wdistension and
ww discomfort, nausea; local irritation
ww with rectal preparations ww
®
®
Lactulose
Movicol®
Phosphate enemas
Microlette®
t
.ne
X
ok
Bo
10–​15mL/​12h PO
1–​3 sachets/​24h PO
1/​PRN PR, max 2 in 24h
1/​PRN PR, max 2 in 24h
.ne
X
k
t
ok
o
o
w.B
et
n
.
X
o
w.B
Levothyroxine $ Thyroid hormone (T4). Dose Typically 50–​
ww
ww
200micrograms/​24h PO at breakfast Indication Hypothyroidism CI Thyrotoxicosis Caution Pregnancy, breastfeeding, panhypopituitarism, adrenal
insufficiency, cardiovascular disorders, DM SE Hyperthyroid-​like symptoms; GI disturbance, tremors, restlessness, flushing Interaction Increases
effects of TCAs and warfarin, decreases effects of propranolol.
et
n
.
kX
o
Bo
®
et
n
.
kX
t
o
o
B
.
w
ww
ww
w
ww
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
209
t
t
t
Lidocaine
.ne $ Local anaestheticX(amide).
.ne Dose Local anaesthesiaX1/​.n2/​e4%
X
SC (max 3mg/​kg (max
dose 200mg)); Antiarrhythmic
ok solution
ok total
ok Seeto
Indication Local anaesthesia,
ventricular arrhythmiaso(alternative
o
Bo BNF
B
B
. block, sinoatrial
amiodarone) CI Myocardial
w. depression, atrioventricular
wimpairment,
node disordersw
Caution Pregnancy, hepatic or renal
epilepsy,
w
w
w hypovolaemia SE Dizziness,wdrowsiness, confusion,
severe hypoxia/​
tin- w
nitus Interaction Increased myocardial depression with β-​blockers and other
antiarrhythmics,
increased risk of arrhythmias
et
et with antipsychotics. .net
n
n
.
.
XLignocaine $ Local anaesthetic (amide). See lidocaine. kX
ok Lisinopril See ACEi. ookX
o
oo
B
B
B
.
.
wsalt (mood stabilizer). DosewSeewBNF Indication Mania, w
Lithium $ Lithium
bipolar disorder
hypothyroidism, w
wwCI Pregnancy, breastfeeding,wuntreated
Addison’s disease Caution Thyroid disease, myasthenia gravis SE GI
upset, thirst,
polyuria Interaction Diuretics,
NSAIDs Info Lithium citrate
et carbonate
et interchangeable
et
and
lithium
doses are not
simply
d/​w senior/​
n
n
n
.
.
.
X
X NPSA
on stable regimens
kXmonitor level every 3mth.okThe
ok pharmacist;
have published guidance o
onothe ‘safer use of lithium’ andothis
should be
o
B consulted before commencing
w.B lithium therapy. ww.B
w
Monitoring w
Optimum sampling time 4–​7d after w
commencing treatment 12h
ww
1
lithium
.
kX
o
o
net
post dose 0.4–​1mmol/​L
2 Early signs of toxicity (Li+ >1.5mmol/​L) tremor, agitation,
twitching, thirst, polyuria, N+V
2 Late signs of toxicity (Li+ >2mmol/​L) spasms, coma, fits,
arrhythmias, renal failure (E OHAM4 p. 716)
et
t
.ne
X
k
.n
kX
oo
oo
B
B
.
.
w (antimotility). Dose 4mg
Loperamide $Opioid
PO initially then 2mg
w
w2w
PO following
every loose stool (max 16mg/​
4h in divided doses) ww
w
w
Indication Diarrhoea, control of high output stoma CI Pregnancy, IBD, any
condition
peristalsis should nott be stopped; constipation, ileus,
t
et where
megacolon
Caution Hepatic impairment,
promote fluid and electron
.
.ne can
.ne
lyte depletion in the young SE Abdominal
cramps, constipation,X
dizziness
X
X
ok Info Loperamide should notobek used in infective diarrhoeas
oorkdiarrhoea
o
Bo associated with IBD.w.Bo
B
w.
w
w
Loratadine $
H antagonist. See antihistamine.
w
w
ww
Lorazepam $ Benzodiazepine. Dose Sedation/​anxiety 1–​4mg/​
24h PO/​
IM/​IV; Seizures 4mg slow IVt (repeated once after 10min tif
et Indication
needed)
Sedation, seizures,
status epilepticus CI Respiratory
n
.
.nemyasthenia
.ne
X
X
X
depression,
sleep
apnoea,
unstable
gravis,
severe
hepatic
k breastfeeding, history of drug
kabuse, reok
Caution Pregnancy,
ooweakness,
oSEoDrowsiness,
Bo impairment
B
B
spiratory disease, muscle
renal impairment
.
.
w
w
confusion, muscle
weakness.
ww
ww
ww
B
1
Losartan See AT II antagonists.
Bo
o
et
n
.
kX
1
et
n
.
kX
t
o
o
B
.
w
ww
Mwww.nrls.npsa.nhs.uk/​resources/​type/​alerts/​?entryid45=65426
w
ww
.ne
X
ok
.Bo
ww
B
210
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
w
ww
t
t
et
Magnesium
sulfate $ Magnesium
.ne
.ne salt. Dose 2–​4g IV overX5–​.n15min
X
X
followed by an infusion (see
BNF) Indication Arrhythmias, MI,
seok oftenasthma,
oekclampsia,
ok acute
pre-​eclampsia/​
dMg Caution Pregnancy,
monitor
o
o
Bo vere
B
B
. N+V, hypotension,
BP, RR, urinary output,
w. hepatic or renal impairment
wSEwith
thirst, flushed w
skin Interaction Risk of hypotension
calcium-​channel
w
ww
blockers Infow
Magnesium sulfate 1g equivalentw
to 74mmol.
Monitoring
Levels should be checked
et
et every 6h while on IV therapy or moreet
n
n
magnesium
urgently if indicated;
Therapeutic range 1.7–​3.5mmol/​L .n
.
.
X 1.0mmol/​L Normal plasma
X
X
ok 0.7–​
okrangerange
ok
o
o
o
1.7–​
3
.5mmol/​
L
Therapeutic
B
.B
w.B
2.5–​5.0mmol/​L w
ECG changes (QRS widens)
w
w
wL Reduction in tendon reflexesw
ww
4.0–​5.0mmol/​
>5.0mmol/​L
Loss of deep tendon reflexes
t
>7.5mmol/​
L
Heart block, respiratory
e
et paralysis, CNS depression .net
n
n
.
.
>12mmol/​
L
Cardiac
arrest
X
X
X
ok
ok
ok
o
o
o
B
Maxolon $ Antiemetic
See.B
metoclopramide.
w.B (dopamine antagonist).
w
w
w
Mannitol w
$ Polyol (osmotic diuretic). Dose
w 0.25–​2g/​kg/​4–​8h over ww
2+
®
30–​
60min IVI (max 3 doses) Indication Cerebral oedema, glaucoma
CI Pulmonary oedema, cardiac failure Caution Pregnancy, breastfeeding,
renal impairment SE hypotension, fluid and electrolyte imbalance.
t
t
t
.ne
.ne
.ne
X
X
X
k (antimuscarinic). Dose 135–​
$ Antispasmodic
ok Mebeverine
oIndication
ok150mg/​8h
o
o
(20min before food)
GI smooth muscle
cramps; IBS/​diBo PO
B
B
verticulitis CI Paralytic
w. ileus Caution Pregnancy,wacute
w. porphyria SE Very w
w
rarely rash, urticaria.
w
w
w
Meropenem $ Carbapenem antibiotic. Dose 500–​1000mg/​8h IV (dose
doubled
in severe infections) Indication
Aerobic and anaerobic Gram-​
t
et and
etCaution
n
n
positive
Gram-​negative infections
Pregnancy, breastfeeding,
.
.
.ne
X
X
X
hepatic
or
renal
impairment,
sensitivity
to
beta-​
l
actams
SE
GI
disturbance
ok
okcolitis, headache, deranged LFTs.
ok
antibiotic associated
o
o
Bo including
B
B
.
. formulation, conMesalazine $ Aminosalicylate.
Dose Depends upon
ww
ww Mild/​
sult BNF; POwand
PR preparations available w
Indication
moderate ac- ww
tive ulcerative colitis and maintenance of remission CI Salicylate allergy,
coagulopathies Caution Pregnancy, breastfeeding, hepatic or renal impairment SE GI upset, bleeding disorders.
t
et
et
n
n
.
.
X
$ Biguanide. Dose
kXInitially 500mg/​24h PO with
ok Metformin
oAfter
ok breakfast;
o
o
After 1wk 500mg/​12h PO;
further 1wk 500mg/​8hoPO if required
B
.Bpolycystic ovarian
(max 2g/​24 in divided
Indication Type 2 DM,
w.orBdoses)
w
syndrome CI Hepatic
renal impairment Caution
Ketoacidosis, potential
w
w
w of lactic acidosis, iodine-​containing
w contrast, general an- ww
increased risk
aesthesia SE GI disturbance, metallic taste.
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
e
X.n
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
211
t
t
net
Methadone
$ Opioid. Dose Usual
.ne
.nerange 60–​120mg/​24h PO;X.should
X
X
given more frequently
than 12h if on prolonged use;
ok not bepatient’s
ok usual
oktheestablish
dose fromothe
dispensing pharmacy,
o
Bo the
B
B
. information Indication Aid
.in withdrawalpatient
may not tell you accurate
from
w
w
opioid dependence,
chronic pain CI Acute respiratory
depression, paraw
w
w ICP/​head trauma, comatose
w patients, phaeochromo- ww
lytic ileus, raised
cytoma Caution Pregnancy (especially delivery), arrhythmias, hepatic
or renal
impairment SE N+V, constipation,
etInteraction
et respiratory depression,
edryt
n
n
n
.
.
.
mouth
MAOI within 2wk.
X
X
X
ok Methotrexate $ Dihydrofolate
ok reductase inhibitor. Dose
ok2.5–​10mg/​
o
o
o
B wk PO (max 25mg/​
Rheumatoid arthritis,
disease,
ww.k)BIndicationlymphoma
w.BCrohn’s
psoriasis, ALL, w
non-​Hodgkin’s
CI Pregnancy,
breastfeeding,
w
hepatic or w
renal impairment, active infection,
w immunodeficient syn- ww
dromes Caution Blood disorders, effusions (especially ascites), peptic
ulcer, ulcerative
colitis SE GI disturbance/​
ucositis, pulmonary fibrosis,
et myelosuppression
et mNSAIDs,
etri-t
pneumonitis,
Interaction
co-​trimoxazole,
n
n
n
.
.
.
X
Info Patients usually
kXalso prescribed folic acidoduring
kX treatok methoprim
ment with methotrexate.oo
o
o
B Methylprednisolone
$ Corticosteroid. Dose
0mg/​24h PO;
wI.MB(exceptionally,
w2.4h2–​B4for
10–​
500mg/​
2w
4hwIV/​
up w
tow
1g/​
up to 3d) ww
B
Indication Acute inflammatory disease, cerebral oedema (associated with
malignancy), graft rejection CI Systemic infection Caution Adrenal suppression SE Cushing’s syndrome, DM, osteoporosis Interaction Duration
decreased by rifampicin, car­bamazepine, phenytoin; duration of action
increased by erythromycin, ketoconazole, ciclosporin.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
t
.ne
X
k
Metoclopramide $ Dopamine antagonist. See antiemetic.
ww
Metoprolol See beta-​blockers.
w
Metronidazole $ Antibiotic. Dose 400mg/​8h PO; 500mg/​8h IV
ww
t Anaerobic and protozoal infections,
t
Indication
sepsis, Clostridium
et abdominal
.nediarrhoea Caution Pregnancy,
.nbreastfeeding,
.nealdifficile
hepatic impairment,
X
X
X
taste, oral mucositis Interaction
ok cohol use SE GI disturbance,
okmetallic
ok Can
o
o
levels, increases effects of warfarin.
Bo increase lithium andwphenytoin
B
B
.
wIV. titrated to effect w
Midazolam w
$ Benzodiazepine. Dose 1–​10mg
w
Indication Conscious
CI Breastfeeding, w
w sedation, sedation in anaesthesia
w
respiratory depression, sleep apnoea, unstable myasthenia gravis Caution
Pregnancy,
hepatic or renal impairment,thistory of drug abuse, respiratory
etmuscle
e confusion, muscle weakness.
et
disease,
weakness SE Drowsiness,
n
n
n
.
.
.
X
X
kXE analogue. Dose treatmentok800micro$ Prostaglandin
ok Misoprostol
odose;
o
o
o
grams/​
2
4h
PO
in
divided
prophylaxis
200micrograms/​
6
2h PO
B Indication Prophylaxis
B treatment of peptic ulcerswCI.BPregnancy,–​1breast.and
w
feeding Caution
Cardiovascular/​cerebrovascular
ww
wwdisease SE Diarrhoea. ww
Mixtard See insulin.
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
1
®
B
212
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
ww
w
t
t
net antagonist. Dose 10mg/​
Montelukast
$ Leukotriene .receptor
.ne
.ne24h
X
X
X
in evening Indication Chronic
guidelines), allergic
rhinok PO Caution
ok asthmaSE(BTS
okheadache,
Pregnancy, o
breastfeeding
Abdominal pain,
o
Bo itis
B
B
rarely Churg–​Strauss. syndrome.
w
w.
Morphinew$wOpioid. Dose 2.5–​10mg/​4w
hw
IV titrated to effect; 5–​ ww
10mg/​4h IM/​SC Indication Acute severe pain, chronic pain, acute
MI, acute
depression,
ileus, raised
t LVF CI Acute respiratory
t Cautionparalytic
e
e
et
ICP/​
head trauma, comatose patients
Pregnancy (espen
n
n
.
.
.
Xcially delivery), COPD, asthma,
X arrhythmias, renal impairment,
X hepok atic impairment SE N+V,
okconstipation, respiratory depression,
ok dry
o
o
o
mouth Info Co-​prescribe
laxatives if using opioids for.B
>24h.
B
w$.BOpioid. See oral morphine.
w
MST Continus
w
w
w
w
ww
®
Mupirocin $ Antibacterial. Dose Apply to skin up to 3 times/​24h
Indication Bacterial skin infections Caution Pregnancy, breastfeeding, renal
impairment SE Local reactions; urticarial, pruritus, burning sensation, rash.
et
n
.
X
et
n
.
X
et
n
.
X
ok N-​acetylcysteine $ Amino
ok acid derivative. See acetylcysteine.
ok
o
o
o
Naloxone
$
Opioid
receptor
antagonist.
Dose
0.4–​
2
.0mg
IV/​
IM/​SC,
B
.B
.B
repeat after 2min w
if needed (max 10mg) Indicationw
Opioid reversal during
OD/​overtreatment
ww Caution Pregnancy, physical
wwdependence on opioids, ww
cardiovascular disease SE N+V, hypotension BNF Emergency treatment
of poisoning.
t
t
t
Narcan
.ne $ Opioid receptorXantagonist.
.ne Narcan is a brandXname
.nefor
X
k See naloxone for opioid overdose
ok naloxone that is no longer oused.
ok or reo
Bo versal of narcosis.w.Bo
B
w. Dose 30–​60mg/​ w
Nefopam $ Centrally acting non-​opioid analgesic.
w
w
8h PO (maxw90mg/​8h PO) Indication Moderate
w pain CI Convulsive dis- w
orders Caution Pregnancy, breastfeeding, hepatic or renal impairment,
elderly,t urinary retention SE N+V, nervousness,
t pink. urinary retention,nedryt
e lightheadedness, may colour
eurine
mouth,
n
n
.
.
X activator. Dose 5–​10mg/​1k2hXPO. (max
kXNicorandil $ Potassiumochannel
k
o
o Indication Angina prophylaxis
oo and treat12h in divided doses)
Bo 30mg/​
B
B
.
.
ment (not 1st line)
CI
Breastfeeding,
hypotension,
LVF
with low filling
wPregnancy, hypovolaemia, acute
wpulmonary
pressures Caution
oedema,
w
w
w
w
ww
®
®
MI SE Headache, flushing, GI disturbance.
Nifedipine See calcium-​channel blockers.
Nitrofurantoin $ Antibiotic. Dose 50–​100mg/​6h PO; take with food
t
et
et
n
n
.
.
X CI Pregnancy, breastfeeding,kXrenal imUrinary tract infections
ok Indication
okinfants
o
o
oo Caution
pairment, G6PD deficiency,
<3mth, acute porphyria
B
B
B
.
.
Hepatic impairment,
anaemia,
DM,
electrolyte
imbalance,
vitamin B /​
w
folate deficiency,
lung disease SE Anorexia, GI
acute and
ww
wdisturbance,
w
w
ww
chronic pulmonary reactions.
NOAC
acronym NOAC originally
‘Novel Oral Anti­
et Thehowever
ethaverepresented
e6yrt
coagulants’,
since these drugs
now been in practice .for
n
n
n
.
.
Xthe term ‘non-​vitamin K antagonist
X oral anticoagulant’ to represent
XNOAC
ok is preferred. This distinguishes
okthem from warfarin. The ocurrent
ok NOACs
o
o
B
used in the UK include
apixaban, dabigatran, edoxaban,
.Band rivaroxaban.
w.Bindividually
winformation.
See each of these
drugs
for more detailed
w
w
w
w
ww
e
X.n
12
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
213
t
t
t
Nurofen
.ne $ NSAID. See ibuprofen.
.ne
.ne
X
X
X
ok Nystatin $ Polyene antifungal.
ok Dose 100 000 units (1mL)/​
o6kh PO; topo
o
Candidiasis;
oral,
skin
Caution
GI
absorbance
minBo ical gel PRN Indication
B
B
w. (at high doses), oral irritation,
w.rash.
imal SE GI disturbance
w
w
w
w $ Proton pump inhibitor. w
Omeprazole
Dose 10–​40mg/​24h PO; IV w
preparation available for endoscopically proven bleeding ulcers (consult
t guidelines) Indication Prophylaxis
t
BNF/​e
local
and treatment of pepticeulet Hepatic
n
n
.
cers,
GORD, H. pylori eradication .Caution
impairment (no.n
more
X 20mg/​24h), can mask gastric
X
kX cancer SE GI disturbance,
ok than
opump
okheadache,of
o
o
o
dizziness
Interaction
Proton
inhibitors
may
reduce
effectiveness
B clopidogrel. w.B
w.B
w
w
Ondansetron
w See antiemetics (5HT receptor
w antagonist).
ww
Oral morphine $ Opioid. Dose oral solution 5–​20mg/​4h PO; tablets
5–​20mg/​
et 4h PO; 12h slow release .preparations
et 10–​30mg/​12h PO,.adjust
et
n
n
n
.
to
response
(larger
dose
tablets
available;
seek
senior/​
s
pecialist
advice)
X
X CI Acute respiratory kdepression,
X
Severe pain, chronic
ok Indication
ohkeadpaintrauma,
o phaeoo
o
o
paralytic
ileus,
raised
ICP/​
comatose
patients,
B chromocytoma Caution
.BPregnancy (especially delivery),
w.BCOPD, asthma, w
wwimpairment,
w
arrhythmias,w
renal
hepatic impairment
w SE N+V, constipa- w
®
3
tion, respiratory depression, dry mouth Info Co-​prescribe laxatives if
using opioids for >24h.
t
t
net
Oramorph
$ Opioid. See oral.morphine.
.ne
.ne
X
X
X
ok Oseltamivir (Tamiflu
o)k $ Antiviral. Dose Treatment
ok of influo
o
5d;
Prevention
of
influenza
75mg/​
2
4h
PO for 10d
Bo enza 75mg/​12h POwfor
B
B
.
.
Indication Treatment of influenza if started withinw48h of the onset of
wexposure prophylaxis of w
w Caution Renal im- ww
symptoms, w
post-​
influenza
pairment, pregnancy and breastfeeding (use only if potential benefit
outweighs
(eg during a pandemic))
et riskconvulsions,
et SE GI disturbances, headache,
arrhythmias,
thrombocytopenia.
n
n
net
.
.
.
X
X
X
$ Antimuscarinic.
Dose 5mg/​8–​12h PO, increase
k if reok Oxybutynin
ok doses);
opreparations
(max 20mg/​24h inodivided
modified-​release
o
Bo quired
B
B
also available Indication. Detrusor instability; urinary frequency,
urgency and
w breastfeeding, bladderwoutflow/​
w. GI obstruction,
incontinence CI w
Pregnancy,
w
w Caution Hepatic or renal impairment,
w
myasthenia gravis
prostatic hyper- w
®
®
plasia, autonomic neuropathy SE Antimuscarinic effects, GI disturbance.
t
e
X.n
.ne
X
k
t
et
n
.
X
Oxycodone $ Opioid. Dose 5mg/​4–​6h PO (max 400mg/​24h); 1–​10mg/​
ok
Bo
4h IV/​SC titrated to effect Indication Pain; moderate to severe CI Acute respiratory depression, paralytic ileus, chronic constipation, acute abdomen,
raised ICP/​
head trauma, hepatic or renal impairment if severe, acute
porphyria, cor pulmonale, comatose patients Caution Pregnancy, COPD,
asthma, arrhythmias, renal impairment, hepatic impairment SE N+V, constipation, respiratory depression, dry mouth Info 10mg PO oxycodone is
equivalent to 20mg PO morphine. 1mg IV oxycodone is equivalent to 2mg
PO oxycodone. Info Co-​prescribe laxatives if using opioids for >24h.
ok
o
o
w.B
ww
et
n
.
kXOxyContin
ww
o
w.B
ww
et
et
n
n
.
.
X
X
$ Opioid. Modified
o
ok release form of oxycodone.
ok
o
o
o
B OxyNorm $ Opioid.
.B
w.B Immediate-acting formwofwoxycodone.
w
w
w
ww
®
®
B
214
.B
w
ww
Chapter 5
Pharmacopoeia
.B
w
w
ww
w
t
t
t
Oxytetracycline
$ Tetracycline
.ne
.ne antibiotic. Dose 250–​5X00mg/​
.ne6h
X
X
Acne vulgaris, k
Pregnancy, breastfeeding,
renal
ok PO Indicationage
o rosacea CIstains
okand bones)
<12yr o(irreversibly
growing teeth
o
Bo impairment,
B
B
. SLE SE GI disturbCaution Myasthenia gravis
w. may worsen, exacerbates
wInteraction
ance including,w
dysphagia/​oesophageal irritation
Decreased
w
w
absorption w
with dairy products, decreases w
effects of oral contraceptive w
pill, mildly increases effects of warfarin.
et See thiamine.
et
et
Pabrinex
n
n
n
.
.
.
X
$ Proton pump
kX inhibitor. Dose 20–​80mg/​
k24hXPO;(con-IV
ok Pantoprazole
oulcers
preparation available foroo
endoscopically proven bleeding
o
o
B
B
sult BNF/​local guidelines)
of peptic
w.B Indication Prophylaxiswand
w.treatment
ulcers, GORD,w
H. pylori eradication Caution Hepatic
impairment (max
w
w
w
20mg/​24h), renal impairment (max oral dose 40mg/​24h), can mask w
gastric cancer SE GI disturbance, headache, dizziness Interaction Proton
t
pumpeinhibitors
may reduce effectiveness
et of clopidogrel.
et
n
n
n
.
.
.
Paracetamol
$
Simple
analgesic.
Dose
0.5–​
1
g/​
4
–​
6
h
PO/​
I
V
(max
X
X
X
ok 4g/​24h in divided doses)
okIndication Pain; mild to omoderate,
ok pyro
o
exia Caution Alcohol dependence,
hepatic impairment .SE
Rare; rash, hypoB
w.B hepatic impairmentwInteraction
w B Prolonged use w
glycaemia, blood disorders,
w
can potentiate
wwarfarin.
w
w
®
Paroxetine $ Selective serotonin re-​uptake inhibitor. Dose 20–​40mg/​24h
t 50–​60/​24h) Indication Major
tdepression, obsessive-​compulsive
t
PO (max
.ne panic disorder, post-​traumatic
.ne stress disorder Caution Pregnancy,
.ne
disorder,
X
X
X
cardiac disease, DM
ok epilepsy,
ok SE GI disturbance, anorexia,
okweight loss,
o
o
, agitation; increased
incidence of antimuscarinic, B
extrapyramidal
and
Bo dNa
B
. with fluoxetine. w.
withdrawal effectsw
compared
Penicillin w
Gw
$ Beta-​lactam. See benzylpenicillin.
ww
ww
Penicillin V $ Beta-​lactam. See phenoxymethylpenicillin.
t
t
et
Pentasa
See.n
mesalazine.
.ne $ Aminosalicylate. X
.ne
X
X
oil $ Antispasmodic.
Dose 1–​2 capsules/​
ok Peppermint
ok colic and
ok8h POin beo
o
meals Indication Abdominal
distension especially
Bo fore
B
B
.irritation. IBS
Caution Sensitivityw
to .menthol SE Heartburn, perianal
w
w ACEi.
Perindopril
wSee
ww
ww
Pethidine $ Opioid. Dose 25–​100mg/​4h SC/​IM; 25–​50mg/​4h slow
t obstetric, post-​op CI Acutenere-t
IV Indication
Pain; moderate to severe,
et depression,
eraised
n
n
.
.
spiratory
paralytic ileus,
ICP/​head trauma, comatose
X
X. ardelivery), COPD, k
asthma,
kXpatients Caution Pregnancyok(especially
o
o
renal impairment,
impairment SE N+V,
Bo rhythmias,
.Bo hepatic
.Bo less constipation than morphine,
respiratory
depression, dry mouth.
w
w
Phenobarbital
ww $ Barbiturate. Dose Epilepsy
ww(not 1st line) 60–​180mg/​ ww
+
®
24h PO at night; Status epilepticus 10mg/​kg at max 100mg/​min (max
1g) IV (see BNF) Indication Epilepsy, status epilepticus CI Pregnancy,
breastfeeding, hepatic impairment Caution Renal impairment, acute porphyria SE Respiratory depression, hypotension, sedation.
et
n
.
kX
et
n
.
kX
t
.ne
X
k
o
oo
oo
Trough
60–​180micromol/​L (15–​40mg/​L) .B
Bo Monitoring
B
.
phenobarbital
2
wToxic >180micromol/​L (>40mg/​wL)w
ww
w
ww
B
.B
w
ww
.B
w
w
w
Pharmacopoeia
t
t
et
Phenoxymethylpenicillin
(penicillin
V) $ Beta-​lactam..nDose
.ne
.ne
X
X
X
PO Indication Oral
post-​
splenectomy
k infections,
k (prophyok 0.5–​1g/​CI6hPenicillin
oCaution
allergy
History of allergyoo
SE diarrhoea
o
Bo laxis)
B
B
Interaction Decrease .effects of oral contraceptive .pill, allopurinol increases risk of rash.
ww
ww
w
w
Phenytoin $ Antiepileptic. Dose Epilepsy 3–​4mg/​kg/​24h PO increased
gradually
Status epilepticus tloading dose = 20mg/​kg IV at no
t as necessary;
ethan
e
et
more
50mg/​
min with ECG.n
monitoring,
maintenance = 100mg/​
n
n
.
.
X6–​8h thereafter IV (see BNF);kmonitor
X level (see ‘Monitoring kphenytoin’)
X
ok Indication Epilepsy, status epilepticus
o CI Pregnancy, breastfeeding,
o sinus hypoo
o
o
B tension Caution Hepatic
Bimpairment, avoid abrupt w
withdrawal,
.B acute porw.count
phyria; monitor w
blood
SE Drowsiness, cerebellar effects, hypotension,
w
arrhythmias,w
purple glove syndrome, blood w
disorders; Chronic use coarse
facies, hirsutism, gum hypertrophy Info As drug highly protein bound, may
need to adjust monitored levels for low albumin (consult pharmacist).
w
w
215
ww
ww
et
n
.
XMonitoring
et
et
n
n
.
.
Trough 40–​80micromol/​
(10–​20mg/​L)
X
kXLL(>20mg/​
>80micromol/​
L)
ok phenytoin 22 Toxic
oAtaxia,
ok
o
o
o
Signs
of
toxicity
nystagmus,
dysarthria,
diplopia
B
w.B
w.B
w
w
Phosphatewenema See laxatives.
w
ww
Phytomenadione $ Vitamin K . Dose 1–​10mg/​STAT PO/​IV det upon indication—​consultneBNF
t and/​or d/​w haematologist
t
pending
.ne Bleeding and/​or over-​
.ne
Indication
a.nticoagulation with warfarin Caution
X
X
X
ok Pregnancy, give IV slowly.ook
ok
o
Bo Picolax See laxatives.
B
B
.
wtazobactam
wwith. tazobactam. Dose w
Piperacillin with
$ Beta-​lactam
w
w
w in neutropenic patients w
4.5g/​6–​8h IVwIndication Severe infection, infection
(in combination with aminoglycoside) CI Penicillin allergy Caution Pregnancy,
t renal impairment, history
t
breastfeeding,
allergy SE Diarrhoea.et
.ne $ Antihistamine
.neof penicillin
.n
Piriton
(H antagonist).
See chlorphenamine.X
X
X
k
k
k
o
ooclopidogrel.
oo
See
Bo Plavix $ Antiplatelet.
B
B
.
.
Potassium oralwsupplement $ Potassiumwsalt. Dose Potassium
w Potassium loss CI ww
chloride: 2–​4w
g/​w
24h PO (two tablets/​8–​12h)wIndication
1
®
®
1
®
Serum potassium >5mmol/​L Caution Renal impairment, elderly, intestinal strictures, history of peptic ulcer SE GI disturbance, upper GI ulceration Info Check serum Mg2+ as this is also likely to be low in dK+.
t
et
et
n
n
.
.
kX inhibitor. See statin. okX
ok Pravastatin $ HMG CoA
oreductase
o
o
o 24h mane
Dose Initially 10–​
B Prednisolone $w.Corticosteroid.
B
.B20mg/​
w
PO though often 30–​40mg/​24 PO in severe disease
(up to 60mg/​
w 2.5–​15mg/​24h PO Indication
wSuppression
24h); Maintenance
of inflam- ww
w
w
matory and allergic disorders (eg IBD, asthma, COPD), immunosuppression
infection withouttantibiotic cover Caution Adrenal
et CI Systemic
e
et
suppression
SE Peptic ulceration,
Cushing’s
syndrome, DM, .osteon
n
n
.
.
Xporosis Interaction Duration kofXaction decreased by rifampicin,
X carbaok mazepine, phenytoin; duration
o of action increased byoerythromycin,
ok
o
o
B ketoconazole, ciclosporin
Info Consider bone and GI
.Bprotection stratw.B
egies when using
long-​
term corticosteroids; Ew
p. w
179.
w
w
w
ww
e
X.n
B
216
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Pregabalin
$ Antiepileptic. Dose
.ne
.neEpilepsy 25mg/​12h PO Xincreased
.ne
X
X
to 100–​1k50mg/​8–​12h (max 600mg/​24h
divided
k in600mg/​
ok every 7dPain/​bya50mg
o12h increased every 3–​7d up otoomax
nxiety 75mg/​
o
Bo doses);
B
B
24h in divided doses. Indication Epilepsy, neuropathic
pain, generalized
w
w. Renal
anxiety disorder
CI Pregnancy, breastfeeding Caution
w
w
w
w heart failure, avoid abruptwwithdrawal SEimpairment,
severe congestive
GI disturb- w
ance, dry mouth, dizziness, drowsiness.
et
et See antiemetics.
et
Prochlorperazine
$ Phenothiazine.
n
n
n
.
.
.
X
X
X
$ Anticholinergic.
2.5mg/​8h PO increased
ok Procyclidine
oinkdividedDosedoses;
o5–​k10mgevery
3d up to max 30mg/​24h
Acute dystonia
IM/​
o
o
o
B
.B drug-​induced extrapyramidal
.B symptoms
IV Indication Parkinsonism;
w
w
CI Urinary retention,
glaucoma, myasthenia w
gravis Caution Pregnancy,
w
ww
breastfeeding,
hepatic or renal impairment, w
cardiovascular disease, pros- w
tatic hyperplasia, tardive dyskinesia SE Antimuscarinic effects.
t
et
et
Propranolol
See beta-​blockers. ne
n
n
.
.
.
X
X
X100units
$ Heparin antagonist.
1mg IV neutralizes k
ok Protamine
ok50mg Dose
o 80–​
o
heparin IV in last 15min o
(max
at rate <5mg/​min);o1mg
IV neutralB
.BIndication Heparin
izes 100units heparin
w.SCB(max 50mg at rate <5mg/​
wmin)
OD, bleeding inw
patient on heparin therapy Caution
Risk of allergy increased
w
w
w
ww
post-​vasectomy, or in infertile men, fish allergy SE GI disturbance, flushing,
hypotension, dyspnoea Info Protamine can also be used to help reverse the
effects of LMWH but it is much less effective at this than for heparin.
t
t
t
.ne
.ne
.ne
Prozac $ Selective serotoninX
re-​uptake inhibitor. See fluoxetine.
X
X
ok
ok See budesonide.
ok
o
o
Bo Pulmicort $ Corticosteroid.
B
B
. 200–​300mg/​
w.alkaloid. Dose Nocturnal wlegwcramps
Quinine $ Plant
w
24h (nocte)w
PO; Treatment of malaria See w
BNF Indication Nocturnal leg ww
cramps, treatment and prophylaxis of malaria CI Haemoglobinuria,
myasthenia
optic neuritis, tinnitus
Caution Pregnancy (teratot
eint 1stgravis,
et hepatic
genic
trimester), breastfeeding,
or renal impairment,
n
n
.
.
.nedecardiac disease (AF, conductionXdefects, heart block), elderly, G6PD
X
X
k nausea,
ok ficiency SE Cinchonism (tinnitus,
ok headache, hot and flushed
oskin,
o
o
Bo abdominal pain, rashes,
B
B
visual
disturbances
(including
temporary
blind.
w.
ness), confusion),w
acute kidney injury, photosensitivity.
w
w
w
w
ww
®
®
Ramipril See ACEi.
Ranitidine $ Antihistamine (H2 antagonist). Dose 150mg/​12h PO; IV
t
e
X.n
.ne
X
k
t
et
n
.
X
preparation available (see BNF) Indication Peptic ulcers, GORD Caution
Pregnancy, breastfeeding, renal impairment, acute porphyria, may mask
symptoms of gastric cancer SE GI upset, confusion, fatigue.
k
ok
oo
oo
Bo Reteplase $ Plasminogen
B
B
.
.
activator. See fibrinolytic.
w
w
w
wconsult
Rifampicin
$ Antibiotic. Dose Tuberculosis
BNF; Meningitis ww
w
w
prophylaxis 600mg/​
12h PO for 2d; Other serious infections 600mg/​
12h IVt (usually after microbiology t advice) Indication Tuberculosis,
e
e prophylaxis, serious staphyloet
N..nmeningitidis/​
H. influenza meningitis
n
n
.
.
Caution Pregnancy, hepatic or X
Xcoccal infections CI JaundicekX
k renal imok pairment, alcohol dependence,
o acute porphyria SE oGIodisturbance,
o
o
B
headache, drowsiness,
hepatotoxicity, turns body
.B secretions orw.Bp450,
ange Interactionw
Induces
decreases effectsw
ofw
warfarin.
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
217
t
t
et
Rivaroxaban
$ Direct inhibitor.n
of factor Xa. Indication and dose
.ne
.neVTE
X
X
X
after hip/​knee replacement
10mg/​24h for 14d for knees,
5wk for
ok prophylaxis
ok Treatment
ok15mg/​
(start 6–​10h after surgery);
of DVT/​PE Initially
12h
o
o
Bo hips
B
B
for 21d; For prophylaxis. of recurrent PE/​DVT 20mg/​24h;. Prophylaxis of stroke
w
w
and systemic embolism
valvular AF and 1 risk
w in non-​heart
wfactor (Such as previous w
wsymptomatic
stroke or TIA,
failure, DM,w
HTN, or >75yr.) 20mg/​24h; w
Prophylaxis of atherothrombotic events following ACS with elevated cardiac biot or aspirin and clopidogrel.)
markers
with aspirinealone
et1(In2h combination
et
n
n
n
.
.
.
2.5mg/​
for 12 months. Caution
Avoid in patients with significant
X risk. Wait 6h after last
X before removing epidural
kXcatheter
ok bleeding
okSEdose
opain;
o
o
o
and wait 5h until next dose.
Haemorrhage; abdominal
constiB pation; diarrhoea;wdizziness;
.B dyspepsia; headache;whypotension;
.B
nausea;
pain in extremities;
rash; renal impairment;
w vomiting. Info No w
ww pruritus;
routine anticoagulant
monitoring required w
(INR tests are unreliable). w
Take doses >10mg/​24h with food. Reduce dose in renal impairment.
et
et inhibitor. See statin. .net
Rosuvastatin
$ HMG CoA reductase
n
n
.
.
X
X
ok (r) tPA $ Plasminogen activator.
ok See fibrinolytic. ookX
o
o
B Salbutamol $wβ.Bagonist. Dose Chronic w
airways
.B disease 100–​
200micro­gramsw
aerosol/​200–​400micrograms w
powder INH PRN (max
wgrams/​24h in divided doses);w2.5–​5mg/​4h NEB; Status ww
400–​800micro­
B
2
asthmaticus 2.5–​
5mg/​
PRN NEB; 250micrograms/​
STAT (diluted to
50micrograms/​mL) slow IV, followed by maintenance infusion of 3–​
20micrograms/​
min (3–​
24mL/​
h of the 50micrograms/​
mL solution),
titrated to heart-​rate Indication Asthma; chronic and acute, other revers+
ible airway obstruction, eg COPD, iK Caution Cardiovascular disease,
DM, hyperthyroidism SE Fine tremor, nervous tension, headache, palpitation, muscle cramps.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
t
.ne
X
k
w
Salmeterol $ Long-​acting β2 agonist. Dose 50–​100micrograms/​12h
o
ww
INH Indication Chronic asthma, reversible airway obstruction Caution
Cardiovascular disease, DM, hyperthyroidism SE Fine tremor, nervous
tension, headache, palpitation, muscle cramps.
t
.ne
X
k
t
et
.ne
X
k
.n
kX
oo
oo
B
B
.
.
Senna See laxatives.
ww
ww
w
w
w
Seretide $ Long-​acting β agonist with corticosteroid. Dose 25–​ w
50micrograms salmeterol with 50–​
fluticasone/​
12–​
t (depends upon inhaler ndevice,
t500micrograms
24h INH
see BNF) Indication Asthma
e
e
et
n
n
.
.
.
(E
p.
279)
Caution
Cardiovascular
disease,
DM,
hyperthyroidism,
X SE Fine tremor, nervouskXtension, headache, palpitation,
X
ok TB
o voice, paradoxical bronchospasm
ok muscle
o
o
o
cramps,
oral
candidiasis,
hoarse
(rare)
B Interaction See salmeterol
.B and fluticasone.
.B
w
w
w
w Dose 50mg/​24h ww
winhibitors.
Sertralinew
$ Selective serotonin re-​uptake
Bo
Sando-​K® $ Potassium salt. See potassium oral supplement.
®
2
et
n
.
kX
o
Bo
PO increased by 50mg increments at intervals of at least 1wk until desired effect (max 200mg/​24h) Indication Depression, OCD, panic disorder CI Hepatic or renal impairment, active mania Caution Pregnancy,
epilepsy, cardiac disease, DM SE GI disturbance, anorexia, weight
loss Interaction MAOI within 2wk, inhibits p. 450 enzymes.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
218
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
t
Sevredol
.ne $ Opioid. See oralXmorphine.
.ne
.ne
X
X
ok Simvastatin $ HMG CoA
okreductase inhibitor. See statin.
ok
o
o
Bo Slow-​K $ Potassium
B
B
w. salt. See potassium oralwsupplement.
w.
w
Sodium valproate
$
Antiepileptic.
See
valproate.
w
w
ww
Sotalol See beta-​blockers.
et
et diuretic (aldosterone .nantaget
Spironolactone
$ Potassium-​
sparing
n
n
.
.
X Dose 100–​200mg/​24hkPO
X(max 400mg/​24h) IndicationkOedema/​
X
ok onist).
o nephritic
o heart
ascites in cirrhosis/​malignancy,
syndrome, congestive
o
o
o
B
failure CI Pregnancy,
.Bbreastfeeding, hyperkalaemia,
wCaution
w.B hyponatraemia,
Addison’s disease
Renal impairment, w
porphyria
SE GI disturbw
w gynaecomastia, menstrual
w irregularities Interaction ww
ance, impotence,
Increases digoxin and lithium levels; risk of iK when used with ACEi or
AT II receptor
et antagonists. .net
et
n
n
.
.
Statins
$
HMG
CoA
reductase
inhibitor.
Dose
See
Table
5.18
Indications
X
X
X ascular
primary and
prevention of cardio­
ok Dyslipidaemias,
ok secondary
ok vbreasto
o
o
disease
(irrespective
of
serum
cholesterol)
Caution
Pregnancy,
B
feeding, hypothyroidism,
w.B hepatic impairment,whigh
w.Balcohol intake, SE w
w
Myalgia, myositis
GI disturbance, w
w (in severe cases rhabdomyolysis),
w
®
®
+
pancreatitis, altered LFTs (rarely hepatitis/​jaundice) Interaction Avoid
concomitant use of macrolide antibiotics and amiodarone (possible increased risk of myopathy).
t
t
t
.ne
.ne
.ne
X
X
X
ok Table 5.18 Statins ook
ok
o
Bo Atorvastatin Dose
B
B
. 24h PO
w. Initially 10mg/​24h PO up to max
w80mg/​
w
Fluvastatin
Dose Initially 20mg/​24h PO up tow
max 80mg/​24h PO
w Dose Initially 10mg/​24h PO upwto max 40mg/​24h PO
ww
Pravastatin
Rosuvastatin
Dose Initially 5mg/​24h PO
et
et up to max 40mg/​24h PO et
n
n
Simvastatin
Dose Initially 10mg/​
24h PO up to max 80mg/​24h PO .n
.
.
X
X
X
ok Stemetil $ Phenothiazine.
okSee antiemetic.
ok
o
o
o
B
B
w$ .Plasminogen
w.B
Streptokinase
activator. Seew
fibrinolytic.
w
w
w
ww
®
Sulfasalazine
$ Aminosalicylate. Dose Maintenance 500mg/​
6h PO; Acute 1–​
2g/​
6h PO until remission; PR preparations also
available Indication Rheumatoid arthritis, ulcerative colitis, Crohn’s
disease CI Sulfonamide sensitivity Caution Pregnancy, breastfeeding, renal
impairment, G6DP deficiency SE GI disturbance, blood disorders, hepatotoxicity, discoloured bodily fluids.
t
e
X.n
ok
Bo
Bo
o
et
n
.
kX
.ne
X
k
t
ok
o
o
w.B
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
219
t
et
netIndications Type 2 DMXCI.nKeto­
Sulfonylureas
Dose See Table .5.19
.ne
X
X
Pregnancy, breastfeeding,
hepatic or renal impairment,
k agents in obese
ok acidosis Caution
oline
okencourage
should not be 1st-​
patients as
will
o
o
Bo porphyria;
B
B
further weight gain SE
w. N+V, diarrhoea, constipation,
w. hyponatraemia, w
hypoglycaemia,w
hepatic dysfunction, weight gain
Info Hypoglycaemia rew
w hours and must always w
sulting fromw
sulfonylureas can persist for many
be treated in hospital; sulfonylureas should not be given on the day of
surgery
etdue to the risk of hypoglycaemia.
et
et
n
n
n
.
.
.
X
X
X
ok Table 5.19 Sulphonylureas
ok
ok
o
o
o
Glibenclamide
Dose.B
5mg (2.5–​15mg) 24h PO mane Info.Long
acting; use
B
cautiously
w in the elderly
wB
w
w
Gliclazide w Dose 40–​80mg (40–​160mg) usually
w 24h PO mane (max
ww
320mg) Info Medium acting
Glipizide
Dose 2.5–​5mg (2.5–​15mg)
et
et usually 24h PO mane (max .net
20mg) Info Short acting
n
n
.
.
X
X g) divided throughout the daykPO
X
0.5–​1.5gk
ok Tolbutamide Dose
o (0.5–​2acting
o with
meals Info
Medium
o
o
o
B
w.B
w.B
Symbicort w
$ Long-​acting β agonist withw
corticosteroid. Dose 6–​
w
w
ww
®
2
12micrograms formoterol with 100–​
400micrograms budesonide/​
12–​24h INH (depends upon inhaler device, see BNF) Indication Asthma
(E p. 279), COPD Caution Cardiovascular disease, DM, hyperthyroidism, TB SE Fine tremor, nervous tension, headache, palpitation,
muscle cramps, oral candidiasis, hoarse voice, paradoxical bronchospasm (rare) Interaction See salmeterol and fluticasone.
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
Synacthen $
wSynthetic corticotrophin (ACTH).
wwSee tetracosactide. ww
w
w
Tamiflu $ Antiviral. See oseltamivir.
t
t
Tamoxifen
$ Oestrogen receptor antagonist.
Dose Breast cancer 20mg/​
et for other
24h
indications consult
receptor-​
.nPO;
.neBNF Indication Oestrogen X
.ne
X
X
cancer, anovulatory
k infertility CI Pregnancy oCaution
k Breas
ok positive breast
othromboembolism,
o
o
increased risk of
occasional
cystic ovarian
Bo tfeeding,
B
B
.
swellings in pre-​mw
enopausal
women SE Hot flushes,
w. vaginal discharge/​ w
bleeding, menstrual
suppression, GI disturbance
Interaction Increases efw
w
w
w
w
fects of warfarin.
Tamsulosin
antagonist. Dose 400micrograms/​
24h PO Indication
etprostatic$ αhyperplasia
et
et
Benign
CI .Breastfeeding,
hypotension, hepatic
n
n
n
.
.
Ximpairment Caution Renal impairment
X SE Postural hypotension,
X headok ache, dizziness, urinary oincontinence
ok
okeffects of
Interaction Increases
o
o
B antihypertensives.w.B
w.B
w
Tazocin $ Beta-​
lactam with tazobactam. Seew
piperacillin.
w
w
ww
B
®
®
1
®
Tegretol® $ Antiepileptic. See carbamazepine.
et
n
.
kX
et
n
.
kX
o
Bo
o
o
B
.
w
ww
w
ww
t
.ne
X
ok
.Bo
Teicoplanin $ Glycopeptide antibiotic. See vancomycin.
ww
B
220
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
t
et 10–​20mg/​24h PO at bedtime
Temazepam
$ Benzodiazepine.
.ne
.nDose
.ne
X
X
X
dependency
(max 4wk course)
Indication
ok or preoperative;
ok common
ok sleep
preoperative oanxiety
CI Respiratory depression,
apo
Bo Insomnia,
B
B
. gravis, hepatic impairment
. Caution Pregnancy,
noea, unstable myasthenia
w
w
breastfeeding, w
abuse, respiratory
muscle weakw history ofSEdrug
ww disease,
ww
ness, renal impairment
Drowsiness, confusion,
muscle weakness.
Tenecteplase
$ Plasminogen activator.
t
t See fibrinolytic.
e
e
et
n
n
Terbutaline
$
β
agonist.
Dose
500micrograms/​
6h INH; 5–​.1n
0mg/​
.
.
X 12h NEB; oral preparationskXare also available, consult BNF
XIndication
ok 6–​
o airway obstruction, uterine
ok relaxation
Asthma and other reversible
o
o
o
B
.B Cardiovascular disease,wDM,
.Bhyperthyroidism
during pregnancy w
Caution
SE Fine tremor,w
nervous tension, headache, palpitation,
muscle cramps.
w
w
w
ww
Tetanus vaccine and immunoglobulin E p. 451.
t
Tetracosactide
(Synacthen ) $
e250micrograms
etSynthetic corticotrophin (ACTH).
et
n
n
n
Dose
IV/​IM Indication
Diagnosis of Addison’s disease .Caution
.
.
X
X
breastfeeding, allergic
SE Cushing’s syndrome,
kX DM,
ok Pregnancy,
ok bedisorders
o
o
o
osteoporosis Info Blood should
sampled for cortisol pre-​
doose and again
B
at 30min post Synacthen
guidelines).
w.B dose (consultant local w
w.B
w
Tetracycline
w $ Tetracycline antibiotic.wDose 250–​500mg/​6h PO ww
2
®
®
Indication Infection, acne vulgaris CI Pregnancy, breastfeeding, renal impairment, age <12yr (irreversibly stains growing teeth and bones)
Caution Myasthenia gravis may worsen, exacerbates SLE SE GI disturbance including, dysphagia/​oesophageal irritation Interaction Decreased
absorption with milk, decreases effects of oral contraceptive pill, mildly
increases effects of warfarin.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
t
.ne
X
k
oo
B
.
Theophylline
500mg/​12h PO (dew $ Methylxanthine. Dosew200–​
ww
w
w
pending upon preparation, consult BNF) Indication Severe asthma/​ w
COPD (see BTS guidelines) CI acute porphyria Caution Cardiac disease,
t hyperthyroidism, peptic ulcer
t disease SE Tachycardia, palpitat
epilepsy,
.neGI disturbance Info Theophylline
.neis only available as an oralXprepar.ne
tion,
X
X
kof theophylline and ethylenediamine
consists
ok ation; aminophylline drug’s
osolubility
ok which
o
o
allowing IV administration.
Bo simply improves the
B
B
w.
w.
Monitoring
2 Toxic >20mg/​L (>110micromol/​w
L)
w
w
ww
theophylline w
B
net
2 Signs of toxicity Arrhythmia, anxiety, tremor, convulsions
(E OHAM4 p. 731)
et
et
n
n
.
.
X
PO depending on severity
BNF); ParenteralkX
2–​
3 pairs
ok 24h
ok ) (consult
o
o
oo Indication
of a­mpoules/​
8h IV (Pabrinex
(consult local guidelines)
B
B
B
.
.
Nutritional deficiency,
especially alcoholism Caution
Reports of anaphylaxis with parenteral
wwpreparations.
ww
w
w
ww
Thyroxine $ Thyroid hormone (T ). See levothyroxine.
t heparin. Dose Depends nupon
Tinzaparin
$ Low-​molecular-​weight
et consult
eDVT/​
et
n
n
.
.
indication,
BNF Indication
PE prophylaxis and . treatX CI Breastfeeding, bleeding
X
X severe
thrombocytopenia,
ok ment
okCautiondisorders,
okor renal
o
o
o
hypertension, recent trauma
Hyperkalaemia, hepatic
imB
.B thrombocytopenia, hyperkalaemia
.B Interaction
pairment SE Haemorrhage,
w
w
NSAIDs increase
wwbleeding risk, effects increased
wwby GTN.
ww
X.
Thiamine $ Vitamin B1. Dose Oral 25–​100mg/​24h or 200–​300mg/​
®
4
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
221
t
t
et
Tiotropium
$ Antimuscarinic.n
(anti-​M3). Dose 18micrograms/​
.ne
.n2e4h
X
X
X
for inhalation also
(see BNF) Indication Maintenance
k available
ok INH; solution
oRenal
ok hyperof COPD Caution
impairment, glaucoma, o
prostatic
o
Bo treatment
B
B
trophy, cardiac rhythm
w. disorders SE Minimal antimuscarinic
w. effects.
w
Tirofiban w
$w
Glycoprotein IIb/​
IIIa inhibitor.
Dose
Initially 400nano- ww
w
grams/​kg/​min for 30min IV; Then 100nanograms/​kg/​min IV for at least
48h (max
108h treatment) Indication Prevention
in unstable anetSTEMI
et abnormalof MIbleeding/​
et
gina/​
N
patients CI Breastfeeding,
cerebron
n
n
.
.
.
history of haemorrhagic stroke,
Xvascular accident within 30d,kX
Xsevere
ok hypertension, intracranialoodisease
ok or renal
Caution Pregnancy, hepatic
o
o
B impairment, increased
.Brisk of bleeding, surgery orwmajor
.B trauma within
w
3mth SE Bleeding,
reversible thrombocytopenia.
w
w
w
w
Topical corticosteroids
Dose Consultw
BNF; guidance on applying w
topical steroids can be found on E p. 180 Indications Inflammatory
conditions
of the skin, eg eczema,
dermatitis amongst
etCI Untreated
et orcontact
et
n
n
n
others
bacterial, fungal,
viral skin lesions, rosacea,
.
.
.
X dermatitis, widespread
X popsoriasis Caution Useklowest
kXplaque
ok perioral
o5.20)
tency agent possible (Table
for shortest duration o
ofotime to limit
o
o
B side effects SE LocalwThinning
.B of the skin, worseningwlocal
.B infection, striae
and telangiectasia,
acne, depigmentation, hypertrichosis;
Systemic Rarely
w
w
w
w
ww
B
adrenal suppression, Cushing’s syndrome Info Topical steroids should
only be commenced after seeking specialist advice (either following a
dermatology review or after consideration by registrar). The decision
to stop potent topical steroids should be taken as seriously—​always be
mindful of the potential for a patient to develop an Addison crisis after
stopping long-​term potent topical steroids.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
ww
Table 5.20 Topical corticosteroid potencies
Potency
Mild
o
Bo
t
.ne
X
k Moderately
potent
Potent
t
e
X.n
w
Examples
Hydrocortisone 0.1–​2.5%, Dioderm®, Mildison®, Synalar 1 in
10 dilution®
Betnovate-​RD®, Eumovate®, Haelan®, Modrasone®, Synalar 1
in 4 dilution®, Ultralanum Plain®
Beclometasone dipropionate 0.025%, betamethasone
valerate 0.1%, Betacap®, Betesil®, Bettamousse®, Betnovate®,
Cutivate®, Diprosone®, Elocon®, hydrocortisone butyrate,
Locoid®, Locoid Crelo®, Metosyn®, Nerisone®, Synalar®
Clarelux®, Dermovate®, Etrivex®, Nerisone Forte®
t
o
ww
Very potent
oo
B
.
ww
t
.ne
X
k
o
w.B
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
t
ww
et
n
.
X
ww
ok Tramadol $ Opioid. oDose
o 50–​100mg/​4h PO/​IM/​IVo(max
ok 600mg/​
respiratory deBo 24h in divided wdoses)
B Indication Pain CI Acute
B
.
.
pression, paralytic ileus, raised ICP/​
head trauma,
comatose paw
ww Caution
w
tients, acute
porphyria, uncon­
trolled epilepsy
Pregnancy w
w
w
(especially delivery), breastfeeding, COPD, asthma, arrhythmias, hepatic
or renalt impairment SE N+V constipation,
depression, dry
e Interaction MAOI within 2wk
eInfot Co-​respiratory
et
mouth
prescribe laxatives if.n
using
n
n
.
.
X
X
X
ok opioids for >24h.
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
222
.B
w
ww
Chapter 5
.B
w
w
ww
w
Pharmacopoeia
t
net Acute infection 200mg/​X12h.nePO;t
Trimethoprim
$ Antibiotic. .Dose
.ne
X
X
100mg/​
24h POkat night Indication Urinary k
ok Prophylaxis
oCaution Pregnancy, breastfeeding,
o tractrenalinfecCI Blood dyscrasias
o
o
Bo tions
B
B
. SE GI disturbance, rash,
. hyperkalaemiaim-In
pairment, folate deficiency
w
w
teraction Increases
w phenytoin levels, increases
wwrisk of arrhythmias with ww
amiodarone.w
Valproate
Antiepileptic. Dose 300mg/​
12h PO increasing by 200mg
e3dt (max$2.5g/​
et Indication
etCI
every
24h in divided.n
doses)
Epilepsy: all forms
n
n
.
.
acute porphyria Caution Pregnancy,
XFamily history of hepatic dysfunction,
X
kXimpairment,
ok breastfeeding, hepatic oroorenal
ok (bleeding
blood disorders
o
o
B
risk), SLE, pancreatitis
GI disturbance, sedation, headache,
cerebellar
.B decreased
w.BSEblood
wEffects
effects, hepatotoxicity,
disorders Interaction
by
w
w
antimalarials,
wantidepressants, antipsychoticswand antiepileptics.
ww
Monitoring
Trough 350–​700micromol/​
(50–​100mg/​L)
et
etLL(>180mg/​
et
valproate
2 Toxic >1260micromol/​
L)
n
n
n
.
.
.
X
X
X
ok Valsartan See $ AT II oantagonists.
ok
ok
o
o
B
.B
.B 6h PO; 1–​1.5g/​
Vancomycin $w
Glycopeptide antibiotic. Dose 125mg/​
wvancomycin
w
w
12h IV; some
centres
use
continuous
infusions
of
(consult ww
w
w
local guidelines) Indication Serious Gram +ve infections: endocarditis,
MRSA, antibiotic associated colitis Caution Pregnancy, breastfeeding,
renal impairment, avoid rapid infusion, history of deafness, inflammatory
bowel disease SE Nephrotoxicity, ototoxicity, blood disorders, rash (red
man syndrome) Interaction Increased nephrotoxicity with ciclosporin, increased ototoxicity with loop diuretics.
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
w guidelines)
wlocal
Monitoring ww
Usually before 3rd or 4th dose (check
w
ww
vancomycin
Trough 10–​15mg/​L
2 Toxicity can occur within therapeutic range
t
t
e
et
n
.
.ne
.nDose
Venlafaxine
$ Serotonin and
noradrenaline
re-​uptake inhibitor.
X
X
X
ok Initially 37.5mg/​12h, increase
ok if necessary at intervalsooofk>2wks to
o
12h (max 375mg
per
24h) Indication Major depression,
generalBo 75mg/​
B
.B
w. CI Breastfeeding, high risk
w
ized anxiety disorder
of cardiac arrhythmia,
w
w
uncontrolledwhypertension Caution Pregnancy,
w hepatic or renal impair- ww
ment, heart disease, epilepsy, history of mania, glaucoma SE GI disturbance, hypertension,
dizziness,
Interaction MAOIs
t2wk, increasedpalpitation,
t withdrowsiness
e
e
et
within
risk
of
bleeding
aspirin/​
N
SAIDs, CNS
toxn
n
n
.
.
.
Xicity with selegiline, mildly increases
X effects of warfarin. kX
ok Ventolin $ β agonist.oSee
oksalbutamol.
o
oo
B
B
B
.
.
wCalcium-​channel blockers. ww
Verapamil See
$
ww
w
ww
B
®
2
Vitamin K See $ Phytomenadione.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Pharmacopoeia
w
223
t
t
t
Warfarin
.ne $ Coumarin. DoseXLoading
.ne E p. 422; MaintenanceXTypically
.ne
X
PO dictated by the
INR (though higherkdoses and
ok 1–​5mg/​on24halternative
oareknotpatient’s
o
days
uncommon) IndicationoProphylaxis
of
o
Bo dosing
B
.
thromboembolism (atrial
fibrillation, mechanical heart.B
valves, etc), treatw
w
ment of venousw
thrombosis or pulmonary embolism
CI Pregnancy, peptic
w
whypertension,
ww Caution
ulcers, severe
bacterial endocarditis
Breastfeeding, w
hepatic or renal impairment, conditions in which risk of bleeding is increased
(eg GI bleeding, peptic ulcer,
recent ischaemic
et postpartum,
etrecent surgery,
et
n
n
n
.
.
.
stroke,
bacterial endocarditis),
uncontrolled hypertenX recent SE Haemorrhage,krash,
X alopecia Interaction Avoidkcranberry
X
ok sion
oInfo Warfarin
o of 0.5mg
o
o
o
juice (ianticoagulant effect)
is available in tablets
B (white), 1mg (brown),
w.B3mg (blue), and 5mg (pink)
wbut.Bcheck which tab- w
lets are stockedw
locally.
w
w
w
w
Zolpidem $ Non-​benzodiazepine hypnotic. Dose 10mg/​24h PO at
night Indication
Short-​term treatment of
CI Breastfeeding, set impairment,
t insomnia
ehepatic
eillness,
et
vere
psychotic
neuromuscular respiratory
n
n
n
.
.
.
X
X
X apunstable myasthenia
respiratory failure,ksleep
ok weakness,
ok orgravis,
o weakness,
noea Caution Pregnancy, o
hepatic
renal impairment, muscle
o
o
B history of drug abuse
disturbance,
.B headache.
w.SEB Taste disturbance, GI Dose
w3.75–​
w
Zopiclonew
$w
Non-​benzodiazepine hypnotic.
7.5mg/​24h PO ww
w
B
at night Indication Short-​term treatment of insomnia CI Breastfeeding,
­severe hepatic impairment, neuromuscular respiratory weakness, unstable myasthenia gravis, respiratory failure, sleep apnoea Caution
Pregnancy, hepatic or renal impairment, muscle weakness, history of
drug abuse SE Taste disturbance, GI disturbance, headache.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
t
.ne
X
k
Zoton® $ Proton pump inhibitor. See lansoprazole.
ww
ww
Zyban® $ Treatment of nicotine dependence. See bupropion.
o
Bo
t
.ne
X
k
t
o
ww
o
w.B
Bo
o
et
n
.
kX
et
.ne
X
k
oo
B
.
w
.n
kX
ww
t
e
X.n
ok
Bo
w
.ne
X
k
t
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
t
.ne
X
k
o
Bo
oo
B
.
w
et
n
.
kX
t
.ne
X
k
ok
et
n
.
X
ok
ww
t
.ne
X
k
oo
oo
B
.
w
o
o
w.B
o
ww
oo
B
.
ww
t
.ne
X
k
ww
w
et
.ne
X
k
oo
B
.
w
.n
kX
ww
t
e
X.n
Bo
o
B
.
w
ww
t
ww
et
n
.
kX
t
et
t
.ne
X
k
ok
Bo
ww
.ne
X
ok
.n
kX
ww
o
ww
.B
w
ww
o
B
.
w
o
et
n
.
kX
oo
e
X.n
o
w.B
ok
Bo
o
w.B
.n
kX
ww
ww
Bo
et
t
et
n
.
X
ww
w
ww
o
Bo
B
.B
w
w
.ne
X
k
t
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Chapter 6
w
225
t
t
t
.ne Resuscitation
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
Early warning scores 226
care 228
t Intensive
e
et
et
2 Peri-​arrest 230
n
n
n
.
.
.
2
In-​
h
ospital
resuscitation
231
X 2 Advanced Life Support
kX (ALS) 232
kX
ok
o
o
o
o
o
2 Arrest equipment
and tests 234
B
.B
2 Advanced
w.BTrauma Life Support (ATLS)
w236
w
w
2 w
Paediatric Basic Life Support 238
w
ww
2 Newborn Life Support (NLS) 242
et 2 Obstetric arrest 244 .net
et
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
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wResuscitation
226
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Chapter 6
t
t
t
.ne warning scores
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k
ok Early detection of the
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o
o
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w
w
changes in management,
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w
w
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t Relies on measurement
etphysiologicalofparameters,
egenerally
etof
n
n
n
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.
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X RR, HR, BP, O saturation,
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o
B
.BBox 6.1.
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w
w
w
w
Scoring ofwthese parameters Usuallywundertaken by nursing staff ww
and it creates a means by which staff can more quickly identify clinical
deterioration. In 2017, the Royal College of Physicians updated their
et Early Warning Score (NEWS)
et and published the NEWS2;
et
National
n
n
n
.
.
.
shown
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Fig.
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X or paediatrics. Normal
Xobservations are awarded akscore
X
ok patients
okattract
o for ofeach0,
o
o
o
while
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higher
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.B score reaches a
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w.Bare added together. If wthiswtotal
w
‘threshold’ value
w (≥5, or any individual parameter
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2
1
staff should increase the frequency of observations and alert a doctor to
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t
t
et
Trends
.ne in physiological parameters
.ne Often more usefulXthan.none-​
X
X
Some patients
k may have abnormal scoresokeven when
ok off observations.
obecause
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o
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B
Bmechanisms.
. thresholds mayofbecompensatory
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agreed w
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w
bear in mind that
w they are also likely to deteriorate
w much more quickly. w
Take care inwthe interpretation of NEWS. w
For example, a patient with w
­severe chest pain can be very unwell yet have a NEWS of 0. See Box 6.2.
t
t
t
Patients
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.ne monitored by suchXscores
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Include:
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ok • Emergency admissions,ounstable
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Bo • Patients with pre-​
B
e.xisting
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w.B DM)
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w
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w have returned from ICU/​HDU
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ww
Box 6.1
et Key updates in NEWS2
etpatients might constantly.cross
et
n
n
.
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X thresholds for low oxygen
X saturations. As with manykpersistent
X
ok alarm
okdesensitized
othis patient
o
o
o
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scores
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B
B
B for saturations
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w.2”)
w
if the patient w
has been allocated to target saturations
of 88–92% to
w
w
ww
2
ensure that they are appropriately monitored. Additionally, in the original score a patient could be confused, but still be considered as not
at risk since they were ‘alert’ on the AVPU scale. NEWS2 recognizes
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new category, ‘C’, in addition to a similar score allocated for patients
responsive to Voice or Pain only, or Unresponsive (hence CVPU).
t
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t
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Fig. 6.1 National Early Warning Score (NEWS2). A total score ≥5, or any individual parameter scoring 3 should
prompt urgent review by a doctor Ask yourself, could this be sepsis? © Royal College of Physicians 2017.
CVPU
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111–130
51–90
101–110
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ww
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ww
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t
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et
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.
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Bo
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1
2
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w
ww
Early warning scores 227
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t
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.
Calling for help isw
easily said in an exam situation,w
but actually initiating
the call is much
wharder. It feels a little embarrassing
w to have to cancel ww
w
w
the arrest call since it was just a patient fainting, but it was still right to
call for help. Remember, the cardiac arrest team can be called for peri-​
arrest
patients where you simply need
etsenior
et many more pairs of hands.nand
et
n
.
some
support. It’s better.n
to prevent a cardiac arrest! Always
X ‘Adult/​paediatric/​obstetric
X
X
ok state
ok cardiac arrest team tooWard
ok A’, even
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o
if
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rrest
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w.B
w.B
w
w
w
w
ww
2 Box 6.2 Calling for the cardiac arrest team
B
228
.B
w
ww
Chapter 6
.B
w
w
ww
w
Resuscitation
t
t
t
.ne
.ne
.ne
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X
X
X
ok section aims to provide
oakbrief introduction to the decisions
okinvolved in
o
o
Bo This
B
B
referring and accepting. a patient into ICU (Intensive Care
w
w. Unit).
w
w
What does
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ward care?
w
w
ww
• Close monitoring using non-​invasive and invasive devices (such as
arterial
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et support
erespiratory failure (some units
ecant
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or
n
n
n
.
.
X offer cardiac support too) kX
ok • 1:1 nursing care and frequent,
o intensive physiotherapy.ookX
o
o
B
.Bpatient will have
Intensivists offer organ
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weach
a parent team w
overlooking their care who should
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w
w with ICU).
ww
rounds (thisw
will most likely be your first encounter
Admitting
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t intensivists
ethat
etaccept patients,
ecer-t
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but there are
n
n
.
.
.
tain
questions
that
must
be
satisfied
in
order
to
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that
a
patient
X
X
X can
ok benefit from ICU. Patientsohave
ok frequently described post-​otraumatic
ok stress
o
disorder following prolonged
remind
B
B us that it is a
.B ICU stays; this serveswto.and
tough environmentwwith frequent exposure to painful
invasive procedw
w
ures. The decision
w to commit a patient to awrigorous treatment pathway ww
B
is a complex process. A possible referral needs to be discussed with your
consultant, as the decision to admit will be made by an ICU consultant
who will often phone your consultant for further discussion.
The information required Includes any known current/​previous wants and
wishes, details of the current illness and underlying medical conditions,
the response to treatment so far, and the general physical/​functional
baseline. This is put together to decide on likely prognosis and trajectory, and therefore whether the benefits will outweigh the risks. What
are the patient’s wishes? (Not always possible in the acute setting, but
some patients are admitted to ICU electively following planned surgical
procedures such as complex open AAA repairs.)
The most difficult aspect of the decision is deciding how likely it is that the patient
in front of you will go on to have a quality of life that they will find worthwhile. Is ICU really going to make a difference? (Eg ICU cannot entirely replace liver function, but it can support the respiratory system long enough to
enable the body to recover from an infection.) Intensive care therapies can
be aggressive and unpleasant. You need to ensure that the patient is motivated to endure this, but also has a good pre-​existing baseline to rely upon.
t
.ne
X
k
oo
et
oo
B
.
w
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oo
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o
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kX
ww
et
et
et
n
n
n
.
.
.
X
X
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considered. Is the
kXthefrequently
ok Reversibility
ohave
okaspresenting
complaint something that we
chance of reversing (such
infection)?
o
o
o
B
B
B
Or is this new presentation
just the natural sequelae of .their
existing disease
.
w neurological disease
process. For example,
ww a patient with a degenerative
ww and intensive antibiotics ww
develops an w
infection. ICU can offer organ support
while the infection is being treated, but there is little that can be offered if
the patient
et is becoming breathless because
et of diaphragmatic weakness.
et
n
n
n
.
.
.
If
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Call
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t
hey
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X
X nekXbut they can advise you on further
ok cessarily need to take overoocare
ok action.
o
o
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Intensive care
w
229
t
t
t
Indications
for intubation Not
intubated
.ne
.neall patients on ICU are X
.ne
X
X
6.3), ICU offers patients
support beyond just managing
ok (see BoxPatients
ok organ
oarek unabletheto
are only intubated
in situations where they
o
o
Bo airway.
B
B
protect their own airway,
will intubate
ventilate
w. or it may be that ICU what
wis. calledand
a patient in order
to facilitate treatment (this is w
‘an induced
w
w terms).
w
ww
coma’ in layman’s
•Respiratory problems (eg hypoxia, hypercapnia, trauma)
t cannot maintain airway, net
• Neurological
problems (eg low GCSeso
et sedation
n
n
.
mandatory
is required, .e.g.
for agitation)
X the work of breathing in cardiac
X.
kX• Physiological reasons (tooreduce
k
k
o
o
respiratory failure,
and acidosis, to prevent hypercapnic
Bo failure,
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.Binoraised
.and
cerebral vasodilation
ICP, e.g. head injury,
w
w
w
‘neuroprotective
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ww measures’, e.g. in severewencephalitis/​
ww
Respiratory wean Refers to the process of reducing ventilatory support
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ehast
tient
to
n
n
.
.
been
on
a
ventilator
for
a
long
period
time,
has
COPD,
or
who
is
weak
X
X
X
ok and malnourished, this complex
ok process may take severaloweeks
ok or even
o
o
months.
There
is
no
universal
protocol.
B
w.B
w.B
Receiving anw
‘ICU step-​down’ patient w
on your ward
w
w
ww
B
When patients no longer need ICU level care, they are ‘stepped down’
to the wards. Generally, a written handover document from ICU should
accompany the patient to the ward and sometimes a telephone handover as well. Some questions to consider:
• What are the priorities of care for this patient and the next stages?
• What happens if they deteriorate? Would ICU readmit them? ICU
patients will often be discharged with a plan for re-​escalation
• Physiotherapy plans
•Have all the central venous and arterial lines been removed?
• Are there any drugs prescribed that you are not familiar with?
•Remember that there are teams from ICU in each hospital who help
with psychological counselling after a prolonged ICU stay.
Most hospitals have an outreach team who review step-​down patients.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
t
.ne
X
k
t
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X
k
w
t
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k
ww
et
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kX
oo
oo
B
B
.
.
Box 6.3 Levels
wwof care in hospital www
w
ww
Level 0 General medical/​surgical bed.
Level 1 Patients needing outreach support from ICU for medical advice,
t
emonitoring,
et as they may need escalating
etot
close
or clinical intervention
n
n
n
.
.
.
XICU or have just come from kthere.
X
kX but
ok Level 2 Often called HDUooCare;
osupport
provision of single organ
o
o
B
maintaining own airway
w.B(e.g. vasopressors, renalwreplacement
w.B therapy).
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who are intubated or needing
more than one organ
w
w
ww
supported. w
If the ICU
feel that a patient may
from ICU but the Unitt
ettheyteam
etthebenefit
is.n
full,
will try to accommodate
patient elsewhere, such
n
.
.neas
theatre recovery until an ICU
bed becomes available, or X
in some
X
X
k
ok cases may arrange a transfer
ok to an ICU in another hospital
oo that has
Bo availability. w.Bo
B
.
w
ww
ww
ww
Bo
B
.B
w
ww
230
Chapter 6
.B
w
w
ww
w
Resuscitation
t
t
et
.nPeri-​
.ne
.ne
2
a
rrest
X
X
X
ok Call the arrest teamooif kyou are concerned about A,ooB,kor C (see
Bo 3
E Box 6.2, p. 227);.call
Do not
w B for senior help early. w
w.Bthink you have to w
manage this alone.
w
w
w
w
Check airway is patent; consider manoeuvres/​adjuncts
2 Airway
with C-​spine control int trauma
et
e CALL ARREST TEAM .net
n
If no respiratory.effort—
2.n
Breathing
X
X
ok 2 Circulation If no palpable
ok pulse—CALL ARREST TEAMookX
o
o
B
B ≤8—​CALL ANAESTHETISTw.B
2 Disability
wIf .GCS
w
ww
ww
Airway w
• Look inside the mouth, remove obvious objects/​dentures
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bore suction under direct vision
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et for
et(stridor,
et
n
n
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signs of airway impairment
snoring, gurgling, or.n
no
.
X entry)
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X
ok • air
ok
ok
o
Jaw thrust/​head tilt/​chinolift with cervical spine control inotrauma
B
.B
• Oropharyngeal w
or nasopharyngeal
airway as tolerated.
w.B
w
w
Breathingw
w
ww
B
•
•
•
•
•
•
•
Look for chest expansion (does R = L?), fogging of mask (Box 6.4)
Listen to chest for air entry (does R = L?)
Feel for expansion and percussion (does R = L?)
Non-​rebreather (trauma) mask and 15L/​min O2 initially in all patients
Bag and mask if poor or absent breathing effort
Monitor O2 sats and RR
Think tension pneumothorax (in a trauma victim).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
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.
ww
ww
w
Circulation
o
Bo
•
•
•
•
•
•
t
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X
k
Look for pallor, cyanosis, distended neck veins
Feel for a central pulse (carotid/​femoral)—​rate and rhythm
Monitor defibrillator ECG leads and BP
Venous access, send bloods and perform ABG if time allows
12-​lead ECG
Call for senior help early if patient deteriorating.
t
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X
k
t
o
ww
o
w.B
.ne
X
k
oo
B
.
w
et
.n
kX
ww
Disability—​if GCS ≤8 or falling, CALL ANAESTHETIST
• Assess GCS (E pp. 344–5) and check glucose
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t
e
X.n
.ne
X
k
t
ww
et
n
.
X
ww
k
ok Exposure
oo
oo
Bo • Remove all clothing,
B
B
check temp
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.
w including perineum and back
w
• Look all overw
body
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w with a blanket.
ww
ww
• Cover patient
2 Box
et 6.4 Signs of life .net
et
n
n
.
.
X
X
respiratory effortkX
• Purposeful movement
ok •Regular
o
ok
o
o
o
•
Coughing
•
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B
.B
• Opening eyes w
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
IN-​HOSPITAL RESUSCITATION
w
231
t
t
et
.nIn-​
.ne
.ne
2
h
ospital
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X
X
X
ok
ok
ok
o
o
Bo
B
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w. Collapsed/sick patientww.
w
w
w
ww
et
etand assess
et
Shout for HELP
n
n
n
.
.
.
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X
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ok
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o
o
o
B
w.B Signs of life? ww.B
w
w
w
ww
et
et
et
n
n
n
.
.
.
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X
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YES ok
ok
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o
o
o
B
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w.B
w
w
w
w
ww
Bo
ok
et
X.n
Call resuscitation team
ok
o
B
w.
et
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ww
t
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k
Assess ABCDE
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oo
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.
ww
w
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ww
Apply pads/monitor
t
et Attempt
et
n
defibrillation .n
.
.ne
X
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X
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ok
ok
o
o
Bo
B
B
.
wLife. Support
wover
Advanced
Hand
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w
w
w resuscitation
w
ww
when
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t
e
et2015 guidelines.
et
Fig. 6.2
In-​hospital resuscitation algorithm;
n
n
n
.
.
.
Reproduced
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the
kind
permission
of
the
Resuscitation
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(UK).
X
X
X
ok
ok
ok
o
o
o
B
w.B causes
w.B
2 Box 6.5 w
Common
w
w
w
ww
Arrhythmia E p. 254
Hypoxia E pp. 277–89
Myocardial
E p. 250
Pulmonary
et infarction
et oedema E p. 278 et
n
n
Hypovolaemia
E p. 393
Pulmonary embolism E p. 284 .n
.
.
X (UTI/​pneumonia) E p. 494
X
X
(idK ) E p. 398
ok Sepsis
ok Metabolic
oEkp. 285
o
o
o
Hypoglycaemia
E
p.
328
(Tension)
pneumothorax
B
w.B
w.B
w
w
w
w
ww
+
B
232
.B
w
ww
Chapter 6
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.B
w
w
ww
w
t
t
et
.nAdvanced
.ne
.ne
2
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X
X
X
ok
ok
ok
o
o
Check
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consider
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Bo 2 Airway
B
B
.
w
w. adjuncts
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w
w
If no respiratory effort—​CALL
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wARREST TEAM
ww
If no palpable pulse—​CALL ARREST TEAM
2 Circulation
t
e
et
et
n
.
Basic
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X
kX arrest is suspected. okX
ok called as soon as cardiac oroorespiratory
o
Advanced life support
is centred around a .‘universal
B
Bo algorithm’
.Bon a This
w
w
(Fig. 6.3) which is taught
standardized course offered
hospitals.
w ofby amost
w
wwarrest team This usuallywconsists
The cardiac
team leader w
(medical registrar), F1, anaesthetist, CCU nurse, and senior hospital nurse:
t to other members
• Team
leader—​gives clear instructions
etprovides
earterial
et
n
n
.
• .F1—​
BLS, cannulates, takes
blood, defibrillates if.n
X trained, gives drugs, performs
X
kXchest compressions (see Boxok6.6)
ok • Anaesthetist—​
obreathing,
o
o
o
airway and
they may choose to
bag-​and-​mask
B
.Binsert a laryngeal mask, or intubate
ventilate the patient,
wBLS,
w.B (E pp. 556–7) w
• Nurses—​provide
defibrillate if trained, w
give drugs, perform chest
w
w
w
w
compressions, record observations, note time points, and take ECGs.
Needle-​stick injuries (E p. 108.) Commonest in times of emer-
t the sharps box nearby nandetnever leave sharps on the bed.
gency.
neHave
net
.
.
.
X
X
X
Can be veryk
during a cardiac arrest. k
antecuok Cannulation
oto difficult
o The
fossa is the best place
look first; alternatively try feet,
hands, foreo
o
Bo bital
B
B
arms, or consider external
Take
. jugular if all else fails. w
. bloods if you are
wallow
successful, but w
don’t
this to delay the giving
of drugs.
w
w Occasionally useful in cardiacwarrests, especially K which ww
Blood tests
can often be measured by arterial blood gas machines. Use a blood gas
tto obtain a sample (the femoral
t with a green needle (21G)
syringe
etis
.neeasiest—​
.neaskartery
often
NAVY E p. 530) and
a nurse to take the sample.n
to the
X
X
X
k on the clinical scenario;oifkin doubt fill
testsodepend
ok machine. Other blood bottles
o
(E p. 531).
Bo all the common blood
B
. on specific
.Bo
w
Defibrillation Taught
courses (eg ILS,wALS) and must not be
w trained. The use of automated
undertaken w
unless
ww external defibrillators ww
or AEDs (E p. 546) is becoming routine in non-​clinical areas as rigorous
trainingtis not required.
e arrest drugs These.nareet now prepared in pre-​filled.nesyr-t
n
Cardiac
.
X adrenaline (epinephrine)kX
X
10mL (1:10,000), atropine
ok inges:
o 1mg in300mg
okgive(several
preparations available), amiodarone
in 10mL. Always
a large
o
o
o
B
.Beach dose to encourage it intowthe.Bcentral circulation
flush (20mL saline) after
.
w
E inside back cover
ww of this handbook for further
wwemergency drug doses. ww
+
Cardiac arrest trolleys Found in most areas of the hospital. Know
et
n
.
kX
o
Bo
where they are for your wards. Ask the ward sister if you can open the
trolley and have a good look at the equipment within it as they differ between hospitals. They are often arranged so the top drawer contains
Airway equipment, the second contains Breathing equipment, the third
contains Circulation equipment, and the lower drawer contains the drugs
and fluids. You’ll seldom need anything that isn’t on the trolley.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
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w
ww
t
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X
k
oo
B
.
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o
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t
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X
k
o
w.B
ww
t
okAssess rhythm
o
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et
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kX
oo
.B
w
ww
ww
.n
kX
Call resuscitation
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e
X.n
o
w.B
w
233
et
CPR 30:2
Attach defibrillator/monitor
Minimise interruptions
et
n
.
kX
w
w
ADVANCED LIFE SUPPORT (ALS)
Unresponsive and not
breathing normally
o
Bo
.B
w
w
ww
Non-shockable
Return of spontaneous
Shockable
et(VF/Pulseless
et
et
n
n
(PEA/Asystole) .n
circulation
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.
X
X
X
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o
o
o
B
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t
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t
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o
o
Bo
B
B
w.
w.
w
w
wAdvanced Life Support algorithm; w
ww
Fig. 6.3 Adult
2015 guidelines.
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t
e
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ok
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t
ok
o
o
w.B
et
n
.
X
o
w.B
When you start to attend arrest calls as a foundation doctor, you can often
feel out of your depth and a little useless. That’s not the case at all! Here
is a list of incredibly useful things to start immediately when you arrive:
• Announce that you will scribe (keep a timed record of drugs and
shocks given) and communicate the need for the next dose/​shock
loudly to your team
• Be a tourniquet for your colleague, this steadies the hand during
CPR so IV access is gained faster
• Find the notes and start looking through the background so that you
can educate the team on the patient’s clinical background which can
give significant clues on why the cardiac arrest has taken place.
et
n
.
kX
o
Bo
.ne
X
k
2 Box 6.6 What can you do?
ww
ww
et
n
.
kX
t
o
o
B
.
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ww
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X
ok
.Bo
ww
B
234
.B
w
ww
Chapter 6
.B
w
w
ww
w
Resuscitation
t
t
et
.nArrest
.neand tests
.ne
2
equipment
X
X
X
ok
ok
ok
o
o
Bo Airway
B
B
.
.
Jaw thrust Pull thewjaw forward with your indexw
and middle fingers at
w mandible. Pull hard enoughwtowmake
the angle ofw
each
your fingers ache. ww
Head tilt Gently extend the neck, avoid if C-​spine injury risk.
Chin lift
chin up with two fingers,
avoid if C-​spine injury risk. et
etPull theairway
et curved
n
n
.
.n the
Oropharyngeal
(Guedel) A .rigid,
tube; choose
Xsize that reaches the angle ofktheXmouth from theplastic
X
k
k
tragus
of
the
ear.
o
oo the tongue back, then.Brotate
oo 180° Insert
down to avoidB
pushing
when
Bo upside
.
inside the mouth (do
not insert upside down in children).
w
w
Nasopharyngeal
tube, not to be used with ww
wwairway A flexible, curved plastic
ww
significant head injury. Choose the size that will easily pass through the
nose (size 6–​7mm in most adults); insert by lubricating and pushing horit
et into the patient’s nostril (not
eupwards).
et
zontally
Use a safety pin through
n
n
n
.
.
.
the
end
to
prevent
the
tube
being
lost.
X
X
ok Suction Cover the hole onoothekXside of a wide-​bore suction
okcatheter to
o
o
B
B Secretions in the parts ofwthe
cause suction at the .tip.
.Boropharynx that
w can
can be seen directly
be cleared. A thinnerw
catheter can be used to
w
clear secretions
w in the airway of an intubatedwpatient.
ww
Breathing
t
Non-​re
mask A plastic mask with
net a floppy bag attached; used
netin
.n ebreather
acutely
ill patients to give 780%X
O. with a 15L/​min flow rate. X.
X
k to O
ok Standard mask (Hudson mask)
okA plastic mask that connectsoodirectly
o
O
with
a
15L/​
m
in
flow
rate.
Bo tubing; delivers 750%
B
B
w.connects to the O tubingwviawa. piece of coloured w
Venturi A maskw
that
plastic, delivering
w either 24%, 28%, 35%, 40%,
w or 60% O . Adjust the w
flow rate according to the instructions on the coloured plastic connector,
eg 4L/​tmin with the 28% Venturi connection.
t
e mask (Ambu bag) A self-​inflating
netto
Bag
.nand
.ne bag and valve that allows
.you
X
X
X
into an inadequatelykventilating patient. Attach the O
to
k tubing
ok forcebagO with
o rate then seal the mask over
othe
a 15L/​min o
flow
patient’s
o
Bo the
B
B
. stands at the head
nose and mouth. Easiest
person
w. with two people; onew
wsqueezes
to get a firm seal
with both hands while the other
the bag. The
w
w
wETT or LMA (E
mask can bew
removed to attach the bag to an
p. 558). w
Pulse oximeter Plastic clip with a red light that measures blood O saturt Do not rely on the reading
ations.
Clip onto the patient’s indexefinger.
etthere
et
n
n
n
.
.
.
unless
is
an
even
trace
on
the
monitor
and
the
patient
has
a
pulse;
X on the different arm fromkX
kX
the BP cuff.
ok use
o
o
o
o
o
Nebulizer This is a 3cm-​
igh cylinder that attaches beneath
a mask. The
B
.Bhhalves
cylinder is made of
that can be untwisted
wtwo
w.Bso that the fluid to w
w
w
be nebulizedw
can be inserted. The nebulizerw
can be connected to a pump w
2
2
2
2
2
2
2
2
or directly to an O2 or medical air supply.
Bo
o
et
n
.
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et
n
.
kX
t
o
o
B
.
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ww
w
ww
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X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
ARREST EQUIPMENT AND TESTS
w
235
t
t
t
Circulation
.ne
.ne
.ne
X
X
X
(E p. 546) Successful
requires ECGkmonitoring
ok Defibrillation
okand defibrillation
o
oo electrodes
identify a shockable rhythm,
delivery of current through
Bo toattached
B
B
.
.
to the chest
wall.
Previously,
monitoring
was
performed
w
w and green to using
ECG leads: red w
to right shoulder, yellow to left shoulder,
apex
w
wdeliver current. Most NHS
ww
(E p. 542). w
Separate paddles were applied to
trusts now use hands-​free adhesive defibrillation electrodes which are safer
t double as monitoring leads (E
and also
edefibrillate
etp. 543).
et
n
n
n
.
.
Only
if you have been .trained,
otherwise many defibrillators
X an automated mode (AED)
X
X
ok have
ok that can provide computerized
ok rhythm
o
o
o
analysis
and
advice.
B • Check the adhesive
are correctly applied
w.Belectrodes
w.Bto the chest
w
• Switch the defibrillator
to ‘monitor’ mode w
w rhythm is identified, select required
w defibrillation energy ww
• If a shockable
using the circular dial, then charge defibrillator using ‘charge’ button
t to stand clear and stand clear
• Tellestaff
et yourself—​strive to minimize.net
n
n
.
.
the
interruption
of
chest
compressions
Xlatest possible moment kX which should continuekXuntil the
ok • Check
o
o
oo self )
O , staff, B
andoyou are clear (O , top, middle,
bottom,
B • Check the
B
.
.
the rhythm
is
still
shockable
then
press
the
‘shock’
to
ww Resume CPR, without w
wwto checkbutton
deliver thew
charge.
pausing
rhythm.
ww
B
2
2
Blood pressure Attach the cuff to the patient’s left arm so it is out of the
way and leave in place. If it does not work or is not believable (eg irregular or tachyarrhythmia) then obtain a manual reading.
Venous access Ideally an orange/​grey venflon in each antecubital fossa;
however, get the best available (biggest and most central). Remember to
take bloods but don’t let this delay giving drugs.
t
.ne
X
k
oo
Disability
o
Bo
et
oo
B
.
w
oo
B
.
ww
ww
t
.ne
X
k
w
Glucose Use a spot of blood from the venous sample or a skin prick to
get a capillary sample; clean skin first with water to avoid false readings.
Examination GCS, pupil size and reactivity to light, posture, tone of all
four limbs, plantar reflexes.
Exposure Take all the patient’s clothes off; have a low threshold for cutting them off. Inspect the patient’s entire body for clues as to the cause
of the arrest, eg rashes, injuries. Measure temp. Remember to cover the
patient with a blanket to prevent hypothermia and for dignity.
t
.ne
X
k
t
o
ww
o
w.B
t
e
X.n
ok
Bo
oo
B
.
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kX
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o
o
w.B
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
ww
et
n
.
X
Arterial blood gas Attempts to sample radial artery blood in a patient in
extremis may be futile and waste valuable time. Instead, attach a green
(21G) needle to a blood gas syringe, feel for the femoral pulse (½ to
⅔ between superior iliac spine and pubic symphysis) and insert the
needle vertically until you get blood. Press hard after removal. Even if
the sample is venous, it can still offer useful information.
Femoral stab (E p. 530.) If no blood has been taken you can insert a
green needle into the femoral vein which is medial to the artery (NAVY).
Feel for the artery then aim about 1cm medially. If you hit the artery take
20mL of blood anyway and send for arterial blood gas and normal blood
tests, but press hard after removal.
ECG Attach the leads as shown on E p. 543.
CXR Alert the radiographer early so that they can bring the X-​ray
machine for a portable CXR.
et
n
.
kX
o
.ne
X
k
ww
et
.ne
X
k
ww
Other investigations
Bo
.n
kX
w
ww
.ne
X
ok
.Bo
ww
B
236
.B
w
ww
Chapter 6
.B
w
w
ww
w
Resuscitation
t
t
et
.nAdvanced
.neLife Support (ATLS)
.ne
2
Trauma
X
X
X
k
ok
oquickly
ok
o
This is designed
to
and safely stabilize B
theoinjured patient.
Bo ATLS
B
The purpose of ATLS
to provide definitive care
all injuries, but to
w. is notthreats
w.ofthese.
w
w
recognize the
immediate
to
life
and
to
address
Remember ww
w
w
to act immediately: 710% of trauma deaths arise from airway obstruction.
As with ALS, in ATLS the patient’s care is delivered by a team which will
etof a leader and various members.
et Details of how to undertake
eant
consist
n
n
n
.
.
.
ATLS
course
are
given
in
Box
6.7;
it
is
really
useful
if
you
are
considering
X
X a
kXcareer in the acute servicesoorksurgery.
k
o
o
Bo The primary wsurvey
.Bo This allows a rapid wassessment
.Bo and relevant management
threatening issue is found
w to be undertaken. If a life-​
w
ww
this must bewtreated before moving on to the
next step of the primary w
survey. The primary survey is as follows: Airway with cervical spine prot ventilation and oxygenation
tection
et (E OHCS10 p. 782); Breathing:
eCirculation
et
n
n
n
.
.
.
(E
OHCS10 Chest trauma, p. 788);
with haemorrhage
conX (see Box 6.8 and E OHCS10
X Management of shock inktrauma,
X
ok trol
ok examination;
oEnvironment;p.
o
o
o
784); Disability: brief neurological
Exposure/​
B
.B Reassess patient’s ABCDE
Adjuncts to primary
wsurvey;
w.Band consider need w
w
w
for patient transfer.
w
w
w
B
The secondary survey This follows once all life-​threatening issues
t
.ne
X
k
oo
et
t
.ne
X
k
have been identified and dealt with; the secondary survey is a top-​to-​toe
examination looking for secondary injuries which are unlikely to be immediately life-​threatening. See Table 6.1 for a mnemonic to make sure
you don’t miss anything. The secondary survey is as follows: AMPLE history (Allergies, Medications, Past medical history, Last meal, Events
leading to presentation) and mechanism of injury; Head and maxillofacial;
Cervical spine and neck; Chest; Abdomen; Perineum/​
rectum/​
vagina;
Musculoskeletal; Neurologic; Adjuncts to the secondary survey.
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
ww
t
t
t
.ne 6.1 Secondary survey mnemonic
.ne
.ne
Table
X
X
X
k
ok
oSecondary
ok
o
o
survey
Bo Mnemonic
B
B
Has
w. Head/​skull
w.
w
w
My
Maxillofacial
w
w
ww
Critical
Cervical spine
Care t
Chest
e
et
et
n
n
n
.
.
.
Assessed
Abdomen
X
X
kX
ok Patient’s
oPelvis
ok
o
o
o
Priorities
Perineum
B
w.B Orifices (PR/​PV) ww.B
Or
w
w
w
ww
Next
Neurological
Management
Musculoskeletal
et
et definitive care
et
Decision?
Diagnostic
tests/​
n
n
n
.
.
.
X
X
kX Journal, Hughes S.C.A, 23:661–​
from Emergency o
Medicine
ok Reproduced
ok 2, 2006,
o
o
o
with
permission
from
BMJ
Publishing
Group
Ltd.
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w.B
w.B
w
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
ADVANCED TRAUMA LIFE SUPPORT (ATLS)
w
237
t
et It is highly unlikely the.nfounet
Trauma
.ne and the foundation
.ndoctor
X
X
X
will be the first k
to attend to a major trauma
patient,
ok dation doctor
oinperson
ohask sustained
ATLS can be applied
principle to any patient who
o
o
Bo though
B
B
an injury. Having a logical,
wise approach to injured
patients minimw. life-​tstep-​
wor. injuries
izes the risk of missing
hreatening complications
which subw
w
w
wbecome debilitating if left unrecognized
w
sequently may
and untreated. If w
you are working in the ED you will likely be involved in gaining IV access or
t conducting parts of the primary
tsurvey under supervision. Get
perhaps
ewith
esurvey;
ein-t
n
n
n
.
.
.
volved
conducting the secondary
it is often poorly performed
X the adrenaline of performing
Xoff. This
kX life-​saving interventions wears
ok asbitallis essential
ounconscious
okto report
o
o
o
though, as the
patient will be unable
a
B finger fracture, or damaged
.B genitalia.
.B
w
w
ww
ww
ww
2 Box 6.7 ATLS course
In thetUK, ATLS courses are coordinated
Royal College oft
e The course is currently.3ndays
et long,byandthedetails
e
n
Surgeons.
of where
.
.nand
X
X
X
when
courses
are
run
can
be
obtained
from
the
College
(E
p.
615
for
ok
ok a long waiting list for places
okas this is a
details). There isousually
o£600.
Bo contact
B
B
.
popular course; the .cost
for the 3-​day course is around
w
w
The ATLS principles
ww provide a structured
wwapproach to managing ww
B
complex trauma patients by identifying the life-​threatening priorities
and treating quickly. Keep an eye out for new research though as some
of the ATLS teachings are not always what are done in practice (eg
the ATLS approach to fluid management does not include hypotensive
fluid resuscitation now used in many departments). Check with your
local protocol over how trauma is best managed.
For those who are especially interested in trauma management after sitting
the ATLS, then consider the European Trauma or ATACC (Anaesthesia
Trauma and Critical Care) courses when you are more senior.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
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X
k
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t
et
et more?
.nfour
.ne
2.nBox 6.8 On the floor X
and
X
X
k is hypovolaemia and theoway
k to think
ok The main cause of shockoinotrauma
o
Bo about blood loss w
B
B
is that
it
can
accumulate
on
the
floor
and
in
.
w. fracturefourcanother
places. Long bones
can harbour up to 0.75L andw
a pelvic
hide
w
several litresw
of blood loss. Abdominal and chest
w wounds can hold nearly ww
your whole blood volume and will required immediate surgical intervention if suspected.
See Fig. 6.4 for where tto look for occult blood loss.
et
e
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X 6.4 Where to look for occultkX
blood loss
kXwith
ok Fig.
o Handbook
o2016,
Reproduced from Baldwin, Oxford
of Clinical Specialties,
o
o
o
B permission from Oxford
University Press.
w.B
w.B
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ww
B
.B
w
ww
238
Chapter 6
.B
w
w
ww
w
Resuscitation
t
et
et
.nPaediatric
.nLife
.ne
2
Basic
Support
X
X
X
k
ok
okis patent; consider manoeuvres/​oaodjuncts
o
CheckB
airway
Bo 22 Airway
B
.
If w
poor respiratory effort—​PAEDIATRIC
w.ARREST TEAM
Breathing
w
w
ARREST TEAM
2 Circulation
w If HR <60bpm—​PAEDIATRIC w
ww
If unresponsive to voice—​PAEDIATRIC ARREST TEAM
2 Disability
t
e
etif severely unwell; call for.nsenior
et
n
n
.
3
Call the PAEDIATRIC arrest .team
X
X
X
ok help early (Fig. 6.5). (SeeoBox
ok6.9 for life-​threatening causes.)
ok
o
o
B
B
Airway
w.B(head tilt), chin lift, jaw w
w.(Box
• Airway manoeuvres:
thrust
6.10)
w
w or nasopharyngeal airway w
ww
• Oropharyngeal
if responding only to pain
• If still impaired, CALL ARREST TEAM.
et
etdrooling, septic), do not look
eint
n
n
.
.
2.nIf you suspect epiglottitis (stridor,
X mouth, but give O , call kyour
X
X
ok the
o senior help urgently, andooankanaestheo
tist and ENT surgeon. o
B
w.B
w.B
Breathing w
w
w
w
ww
B
2
•
•
•
•
Bag and mask with 15L/​min O2 if poor or absent breathing effort
Non-​rebreather mask and 15L/​min O2 in all other patients
Monitor pulse oximeter
Effort stridor, wheeze, RR, intercostal recession, grunting, accessory
muscle use (head bobbing in infants), nasal flaring
• Efficacy chest expansion, air entry (does R=L?), O2 sats
• Effects HR, pallor, cyanosis (late sign), agitation, drowsiness.
t
.ne
X
k
oo
et
o
Bo
oo
B
.
ww
ww
Circulation
•
•
•
•
•
•
•
oo
B
.
w
.n
kX
t
.ne
X
k
w
Start CPR if HR absent or <60bpm and unresponsive
Monitor defibrillator ECG leads
Status HR + rhythm, pulse volume, cap refill (≤2s normal), BP (see Box 6.11)
Effects RR, mottled/​pale/​cold skin, urine output, agitation, drowsiness
Venous access (consider intraosseous) check glucose and send blds
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240
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242
Chapter 6
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244
Chapter 6
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E OHCM10 p. 693
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p. 89
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ww
t
et
n
.
X
o Ask about Site of onset,oradiation,
ok quality (heavy, aching,osharp,
ok tearing),
o
B intensity (scale of w1–​.1B
.B
0), time of onset, duration,w
associated symptoms
w
w
(sweating, nausea,
w palpitations, breathless, cough,
w fever), exacerbating/​ ww
relieving factors (breathing, position, exertion, eating), recent trauma/​
exertion/​
similarity to previous pain; PMH Cardiac/​respiratory
t stress,
t
eDM,
eCardiac/​
et
issues,
GORD, icholesterol; DH
respiratory medications,
n
n
n
.
.
.
antacids;
FH
IHD,
early
cardiac
death;
SH
Smoking,
exercise
tolerance.
X
X
X
ok Risk factors
ok
ok
o
o
o
B IHD iBP, icholesterol,
.B IHD.
w.BFH, smoking, obesity, DM,
wprevious
w
w
PE/​DVT Previous
PE/​
D
VT,
immobility,
ioestrogens,
w
w recent surgery, FH, ww
pregnancy, hypercoagulable states, smoking, long-​distance travel.
GI Known
(E p. 300), known peptic
eHR,t BPGORD
et ulcer, alcohol binge. .net
n
.
Obs
(both arms), RR, sats,.n
temp, GCS, pain, cardiac monitor.
X
X
kXrhythm/​
ok Look for Sweating, pallor,
okdyspnoea, cyanosis, pulseoorate/​
o
o
iJVP, mediastinal shift,
tug, chest
B volume, cool peripheries,
.Bclammy,
.Btracheal
w
w
wall tenderness, asymmetric
chest expansion/​percussion/​
breath sounds,
w
w swelling/​erythema. ww
crepitations, w
pericardial rub, heart murmurs, calf
wpain/​
musculoskeletal, pneumonia, pneumothorax (tension or simple), myocarditis, pericarditis, reflux, peptic ulcer disease; Uncommon Aortic dissection,
cardiac tamponade, sickle-​cell crisis, Takotsubo cardiomyopathy (Table 7.1).
e
X.n
Investigations ECG (E p. 542, pp. 586–8 for procedure/​interpret-
ation);eBloods
t VBG, FBC, U+E, LFT, D-​edtimer, troponin, lactate; ABG Taken
t
on.n
O if patient acutely unwell (E.n
pp. 536–7, pp. 598–9 for procedure/​
.ne
X
X
X
CXR If you suspect
pneumothorax clinically
ok interpretation);
ok a tension
ok requestper-a
immediate needle decompression
(E p. 285), otherwise
o
o
Bo form
B
B
portable CXR if the patient
is severely ill (poorer image.quality) or standard
w.for interpretation);
w suspected large w
CXR (E pp. 596–7
Bedsidew
w
w PEechoorFor
w
PE, acute MI,w
or aortic dissection; CT To rule out
aortic dissection.
Treatment
15L/​
m
in
O
if
SOB
or
sats
<94%.
Consider
IV
opioids
(and
et if pain is severe. .net
et
an antiemetic)
n
n
.
.
X
X are unable to confirm a diagnosis
X
to exclude Ifkyou
ok Diagnoses
o causes
ok imo
o
mediately, consider life-​threatening
and investigate o
until excluded:
B Cardiac ischaemia Abnormal
w.B ECG, typical history,witroponin(s)
w.B echo.
w
PE dsats, abnormal
284), iD-​dimer, CTPA.
w ECG, clinical risk (E p. w
ww
Pneumothorax Mediastinal shift, dbreath sounds, review CXR.
Aorticedissection
Evidence of shock, e
left
t
t and right systolic BP differebyt
n
n
>15mmHg,
mediastinal widening on
CXR, abnormal CT/​echo. .n
.
.
X
X
X
ok Contact cardiology/​medical
okregistrar on-​call for advice ifonecessary.
ok
o
o
B
w.B
w.B
w
w
w
w
ww
2
2
B
248
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
t
.ne 7.1 Common causes ofXchest
.nepain
.ne
Table
X
X
ok
ok Examination Investigations
ok
o
o
Bo 3ACS History
B
B
.
Sudden-​
o.nset
Dyspnoea,
ST
new
w
welevation/​
pain/​
tightness,
±arrhythmia, wLBBB, itroponin(s).
(STEMI)
w
wradiating to left pale, clammy,w Troponin(s) are not
ww
arm/​jaw, >15min, non-​tender chest needed to make the
breathlessness,
wall t
diagnosis of STEMI
t
e
e
et
sweating, nausea
n
n
n
.
.
.
X ACS Sudden-​onset kXDyspnoea,
X
depression,
T-​wave
ok 3
o ±arrhythmia, STinversion,
okwaves,
pain or tightness,
Q
ECG
(NSTEMI)
o
o
o
radiating.to
left
pale, clammy,
can .be
normal, itrop,
B
B
B
arm/​w
tender chest echo
regional wall
w shows
w jaw, >15min, non-​
wmotion
wall
abnormalities
wbreathlessness,
w
ww
sweating, nausea
pain at rest Dyspnoea,
depression, T-​wave
3ACS
et Anginal
et pale, STinversion,
et
or with ifrequency/​ ±arrhythmia,
ECG can be
(unstable
n
n
n
.
.
.
severity/​
d
uration,
clammy,
non-​
normal,
troponin
not
angina)
X
X chest wall elevated kX
ok Angina >15min
ok tender
o changes,
o
o
oECG
Exertional
pain
Dyspnoea,
Transient
B
B
B
.
.
(stable)
or tightness,
tachycardia,
troponin
not
elevated,
w
ww to left non-​tender, may
wradiating
ww+ve cardiac stress
ww
B
arm/​jaw, <15min,
breathlessness, dby
rest/​GTN
Myocarditis/​ Recent viral illness,
pericarditis pleurisy, ion lying,
dsitting forwards
test, +ve CT/​invasive
coronary angiogram,
responds to anti-​anginals
Pericardial rub,
Saddle-​shaped ST on most
otherwise normal ECG leads, iCRP/​ESR,
CVS and RS exam itroponin if myocardial
involvement, echo, MRI
Widened mediastinum
3Aortic Severe tearing
iHR, dBP,
interscapular pain, difference in
on CXR, iD-dimer,
dissection
breathlessness,
dissection flap/​aortic
brachial pulses
neurology
dilation on echo/​CT
and pressures,
iRR, neurology
Pulmonary Breathlessness, PE Often normal,
ABG: PaO2n/​d, CO2d,
embolism
risk factors (E
swollen/​red
clear CXR, iD-​dimer,
p. 284), pleurisy,
leg, tachycardia, sinus tachy, S1Q3T3, new
collapse
dyspnoea, dBP
RBBB, thrombus/​dilated
RV on echo, CTPA
Pneumo­
Sudden-​onset
Mediastinal
Pleura separated from
thorax
pleurisy ±trauma;
shift, unequal air ribs on CXR, other
tall and thin patient; entry/​expansion, investigations often
COPD, smoker
hyper-​resonance normal, CT if unsure
Pneumonia Productive cough, Febrile, coarse
iWCC/​iNØ/​iCRP,
pleurisy, feels unwell creps, dull to
consolidation on CXR
percussion
(E pp. 596–7)
Musculo­
Mechanical, may be Tender (though ECG to exclude cardiac
skeletal chest pleuritic, worse on doesn’t exclude cause, normal bloods,
pain
palpation/​movement other causes),
normal CXR
normal RS exam
Reflux or
Previous indigestion, May have upper ECG to exclude cardiac
spasm
reflux, known hiatus abdo tenderness, cause, normal bloods/​
hernia, dby antacids normal CVS and CXR, trial PPI/antacids
RS examinations
t
.ne
X
k
oo
oo
B
.
w
be normal after
pain resolves
et
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
Bo
o
et
n
.
kX
.ne
X
k
oo
B
.
w
.n
kX
t
ww
ww
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
ok
Bo
w
t
o
w.B
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
w
.B
w
w
w
Chest pain
w
249
t
et coronary syndromes.(ACS)
net
3
.nAcute
.ne
X
X
X
is a general term referring
ok K ACS
ok to presentations of varying
ok severities
myocardial ischaemia o
(Tables 7.2 and 7.3). The aim isoto allow a proBo ofspective
B
B
rather than
diagnosis tow
be. made to improve
wand.a retrospective
acute management
patient outcomes (E OHCM10
p. 118).
w
w
w
w
ww
Table 7.2 Acute coronary syndrome (ACS) classification in patients
with typical
et cardiac-​sounding chest .pain
etlasting >15min
et
n
n
n
.
.
ECG
findings
Troponin
(6–​
1
2h
post-​
p
ain)
Diagnosis
X
X
kX to make a diagnosis, STEMI
ok ST elevation or new Not
oneeded
ok
o
o
o
LBBB
but will be i
(E p. 250)
B
w.BTroponin T above 99th percentile
w.BNSTEMI
T-​wave inversion/​
w
w
flattening, ST w
depression, of the upper referencew
limit
(E pp. 251–2)
ww
absence of ST elevation. Troponin T below 99th percentile Unstable angina
ECG may still be normal of the upper reference limit
(E p. 252)
et
et
et
n
n
n
.
.
.
X
X
kX
ok Table 7.3 Interpreting troponin
ok measurements in suspected
oACS
o
o
o
B
Raised troponin can be .detected
3–​12h after myocardial necrosis.
w B troponins.
w.B Consider
the following when interpreting
w
w
w should not be interpreted in isolation.
w Use the ‘pre-​test
ww
Time
Troponins
course probability’ of acute MI (history, ECG, and echo findings) both at
presentation and over time to help interpret troponin levels
t
et pain, a raised troponin is usually
nchest
net
History
patients with cardiac-​sounding
.ne Indiagnostic
.
.
X
X
X
of ACS. Remember
that diabetics, the elderly, and females
ok
ok confusion,
othek chest)can
atypically (weakness,
nausea, pain outside
o
o
Bo Levels present
B
B
While cardiac-​
chest pain and a markedly.raised troponin
w.sounding
should w
be treated
as MI until proven otherwise,
and
wwmyocarditis
w cardiomyopathy can also causewboth.
ww
Takotsubo
There are many
causes of moderately raised troponins
Trend t Acute MI causes a sharp rise in troponin
1–​2 days, falling again over t
t overhelp
e 3–​5 days. The value over time.can
etherefore
determine the cause
n
n
.
.ne
X
X
X
is excreted renally
and during times of haemodynamic
ok PMH Troponin
okdemand
ok‘leak’stressfrom
(ie when cardiac oxygen
outstrips supply). It cano
also
o
Bo
B
B
the myocardium,
overt cardiac necrosis. Causes
of a raised
. withoutcritical
wtherefore
w. cardiac
troponin
are
illness, renal (AKI,
CKD),
(acute MI,
w
w
heart
failure,
arrhythmias,
myocarditis),
respiratory
(hypoxia,
pulmonary
w
w
ww
embolism), haematological (anaemia), neurological (ischaemic stroke,
and trauma (cardiac contusion, electrical cardioversion).
t haemorrhage),
The PMH is therefore vital in interpreting
e
et a troponin level in context.net
n
n
.
.
who may present
atypically (females, elderly, diabetics)
XECGs Inor patients
X
kX
who cannot provide
history (agitated, comatose, lowoGCS,
ok
oandkatroponin
o
o
o
dementia),
the
ECG
levels
become
more
important.
B
.B for evidence of MI (pathological
Inspect serial
wECGs
w.BQ waves),
ischaemia
(T-​wave inversion/​flattening, ST w
depression), and coronary
w
w (T-​wave normalization/​flipping,wchanging ST segments)
ww
instability
An echo can show features in keeping with acute MI (new loss of viable
new regional wall motion
et myocardium,
et abnormalities, though there.net
n
n
are other causes of these) and
other differential diagnoses (eg aortic
.
.
X
X cardiomyopathy)
X
pulmonary embolism,
ok Bleeding dissection,
obekbalanced against
oin ksuspected
o
o
o
Bleeding risk should
thrombosis risk
B
.Bwhere there is diagnostic uncertainty.
ACS, especially
w
w.BExclude aortic
dissection
and talk to seniors before startingw
ACS treatment
w
w
w
ww
Echo
B
.B
w
w
.B
w
w
wCardiovascular
250
ww
w
Chapter 7
t
t
et (ST elevation MI) (E
3
.nSTEMI
.neOHCM10 E p. 120.) X.ne
X
X
k failure, AV block, cardiac dysrhythmia.
signs Features ofoLV
ok 2 WorryingCentral,
ok to left
o
o
crushing,
heavy chest pain/​tightness,
±radiating
Bo Symptoms
B
B
arm/​jaw, shortness
anxiety.
wof. breath, nausea, sweating,wpalpitations,
w.
w
Risk factors Smoking,
obesity,
DM,
iBP,
icholesterol,
FH, previous IHD. ww
w
w
Signs Tachycardia, cool and sweaty (‘clammy’), ±LV failure or hypotension.
Investigations
ECG ST elevation (>1mm int2 or more contiguous limb leads or
etin chest
e
et
>2mm
leads) or new LBBB;
subsequent
Q waves ±T-​wave.n
invern
n
.
.
LV failure; Troponin WillX
be raised
Xsion (Fig. 7.1); CXR Cardiomegaly,
kXsignsasofECG
ok but treatment should not obeowithheld
ok alone are
findings and o
history
o
B
sufficient to make the.diagnosis
and early treatment is vital.
wforBreperfusion
w.B
Acute treatmentw
Aim
by percutaneous
coronary intervenw
tion (PCI; angiography
with stenting or balloon
w
w angioplasty) within 12h ww
of onset and 2h of first presentation to ED so seek senior help. Give O
(15L/​mtin), aspirin (300mg), a P2Y inhibitor
ticagrelor, 60mg
e or 600mg clopidogrel—​
eseet local (180mg
et
prasugrel,
protocol), diamorphine
n
n
n
.
.
.
X 5mg IV), antiemetic (Ekp.X188), and GTN (two puffs SL/​
Xmin until
ok (2.5–​
o pain after three SL doses and
onotk 5hypotenpain free; infusion if ongoing
o
o
o
B
sive E p. 203). Consider
if PCI cannot.B
occur within 2h of
w(E.Bpp. thrombolysis
wbisoprolol
first presentation
550–1). β-​blockadew
(eg
5–​10mg/​
w
w infarct size and mortalitywbut avoid in COPD, asthma, ww
PO STAT) reduces
1
2
12
hypotension, AV block, and heart failure. See Box 7.1.
Secondary prophylaxis dmodifiable risk factors (smoking, obesity, DM,
iBP, ichol), β-​blocker, statin, anti-​platelets (aspirin indefinitely, P2Y12
inhibitor usually for at least 1yr), ACEi, and anti-​anginals (β-​blockers,
amlodipine, nitrates, nicorandil, ranolazine, revascularization).
Complications Dysrhythmias (AV block, bradycardia, VF/​VT), LVF, valve
prolapse, ventricular septal/​free wall rupture, ventricular aneurysm, pericarditis, Dressler’s syndrome (E OHAM4 p. 154), and recurrent pain.
et
et
.n
kX
o
Bo
o
o
w.B
et
.n
kX
.n
kX
o
o
w.B
ww
ww
et
.n
kX
ww
et
.n
kX
Hours
oo Days Weeks .BooMonths
B
.
Fig. 7.1 Typical sequential
w STEMI.
ww ECG changes followingwanwacute
w
ww
Box 7.1 Care after myocardial infarction
• Bedtrest for 48h with continuous ECG
symptom monitoring
t
e 12-​lead ECG and thorough.nclinical
et andexamination
•.n
Daily
of CVS/​RS.ne
X• Thromboembolism prophylaxis
X (E pp. 420–2)
X
ok • β-​blockade unless contraindicated,
ok with uptitration ook
o
o
B
• ACEi/​angiotensin .IIB
receptor antagonist, with uptitration
.B
• High dose statinw
(eg atorvastatin 80mg PO OD)w
w
w
• Discuss modifiable
w risk factors and arrangewcardiac rehabilitation
ww
•Primary PCI patients are at lower risk of complications and have
shorter
patients twill require risk stratification andt
et stays; thrombolysis
consideration
for inpatient angiography
n
.
.ne in those with new dysrhythmias
.ne
X
X
X
•
Consider
electrophysiological
studies
k
ok
okand 3mth to review symptoms,
in OP clinic at o
5wk
oo lipids+BP,
Bo •Review
B
B
and optimize cardiovascular
risk (E OHCM10 p. 114).
.
.
w
w
ww
ww
ww
Bo
o
et
.n
kX
Normal
NICE guidelines available at Mguidance.nice.org.uk/​CG167
1
B
.B
w
w
.B
w
w
w
w
w
w
251
Chest pain
t
t
t
3NSTEMI
(non-​ST elevation
.ne
.ne MI)
.ne
X
X
X
and interventionkare often less ‘dramatic’ thankfor STEMI,
ok K Diagnosis
o
ooas markedly
1yr survival is poorer.oHigh TIMI/​GRACE scores, as well
Bo but
B
B
.
.
raised troponins, ongoing
pain,
dynamic
ECG
changes,
and
a large area
w all suggest higher risk w
w
of affected myocardium
(Box 7.2); ask cardiology
w
w patients needing emergencywPCI (E OHAM4 p. 44). ww
early to identify
2 Worrying signs LV failure, AV block, cardiac dysrhythmia, ongoing pain.
Symptoms,
et risk factors, and signs Overlap
et with STEMI; patients are.older,
et
n
n
n
.
.
more
comorbid,
and
present
more
atypically.
X
X
X
ok Investigations ECG Can beonormal
ok or show ST depression,ooT-​kwave invero
of changes; CXR
B sion/flattening/​normalization,
.B or complete resolution
w.Bfrom UA by raised w
Cardiomegaly, signsw
of LV failure; Troponin K Differentiate
w
w
troponin (Tables
to local protocols, typically on w
w 7.2 and 7.3); taken according w
presentation and 6–​12h after maximum symptom onset. Echo To assess for
loss of viable
myocardium, regional wall motion
structural comt
et of MI,
et(eg PE,a­ bnormalities,
plications
and differential diagnoses
aortic dissection). .ne
n
n
.
.
X treatment O (15L/​min), aspirin
X
clopidogrel (300mg),
diamorkX
ok Acute
ok(E p.(300mg),
oSL/​
phine (2.5–​5mg IV), antiemetic
188), GTN (two puffs
5min until
o
o
o
B pain free; infusion ifwongoing
B not hypo.B pain after three SL doses,
w.provided
tensive E p. 203),
and anticoagulation (2.5mg w
fondaparinux
E p. 420).
w
w
wbisoprolol 5–​10mg STAT) butw
β-​blockade (eg
beware patients with COPD, w
2
2
3
asthma, hypotension, AV block, or heart failure. Consider glycoprotein IIb/​
IIIa inhibitors and urgent PCI if high risk/​chest pain despite GTN infusion.
Secondary prophylaxis and complications These are broadly the same as in
STEMI, though complications are less common.
et
et
.n
kX
.n
kX
oo
oo
B
B
.
.
K Box 7.2 Risk
in ACS w
ww stratification
Estimation of
in ACS allows assessment
wmortality
wwof the risks and benefits ww
of interventions and careful targeting of resources to those patients who
stand to
the most. Many validated
been developedt
t benefit
emajor
et scoresInhave
e
from
trial data, including the
Thrombolysis
Myocardial Infarction
n
n
.
.
.nThe
X
X
X
(TIMI)
score.
However,
many
such
trials
had
restricted
entry
criteria.
k develok Global Registry of Acute Coronary
ok Events (GRACE) algorithms
owere
o
o
Bo oped
B
B
from a large registry
. (94 hospitals, 14 countries,
. 22,645 patients)
w
wNSTEMI,
involving patients
with all subtypes of ACS (STEMI,
and UA).
w
w
ww
Risk scoresw
can be calculated on admissionw
(to predict in hospital and
6mth mortality) and on discharge (to predict 6mth mortality).
t and a cardiology opinion for
2 High-​
Will need a CCUebed
et risk patients
et
n
n
.
.
consideration
of glycoprotein IIb/​
IIIa inhibitors and urgent PCI. .n
X intermediate-​risk patients Require
X observation to ensure painkXfree and
ok Low/​
okrisk stratification
o or CT
o
o
oimaging
clinically
stable,
then
further
stress
B
B
.B to determine need forwithelective
.
coronary calcium w
scoring,
PCI.
w
ww
ww
ww
Bo
o
et
.n
kX
4
5
t
e
X.n
3
ok
Bo
t
t
NICE guidelines available at Mguidance.nice.org.uk/​CG94
Use unfractionated heparin infusion if angiography is planned within 24h, or if significant bleeding
risk (consider in frail elderly, active/​recent bleeding complications, significant renal impairment or
those with extreme low body mass).
4
Antman EM, et al. JAMA 2000;284:835 available free online at Mjama.ama-​assn.org/​cgi/​content/​
full/​284/​7/​835 See also the excellent collection of resources available free at Mwww.timi.org
5
Granger CB, et al. Arch Intern Med 2003;163:2345 available free online at Marchinte.ama-​assn.
org/​cgi/​content/​full/​163/​19/​2345
2
e
X.n
ok
ww
o
B
.
w
e
X.n
ok
ww
o
B
.
w
ww
B
.B
w
w
.B
w
w
wCardiovascular
252
ww
w
Chapter 7
t
t
et angina
3
.nUnstable
.ne
.ne
X
X
X
based on typical history
ok K Diagnosis
ok without raised troponin (EoOHAM4
ok p. 44).
Worrying signs Featuresoof LV failure, cardiac dysrhythmia.
Bo 2Symptoms,
B
B
. and signs These overlap withwother
. forms of ACS;
risk factors,
w
w
w
typically episodes
of angina occurring on minimal
provocation or at rest,
w to GTN; more frequent and
w more severe than patient’s ww
with poor response
‘usual’ angina; few symptoms or signs between episodes of pain.
t
Investigations
inversion/​flipping, dynamic
et ECG ST depression, T-​w.ave
eflattening/​
et
n
n
n
.
.
ST/​
T
-​
w
ave
changes
over
time,
signs
of
previous
MI;
Troponins
−ve.
X treatment As for NSTEMI
X(E pp. 251–2); analgesiak(morphine,
X
ok Acute
ok(aspirin,
o
o
o
o
GTN),
antiplatelet
agents
clopidogrel),
limit
ischaemia
(β-​
B
.Bthrombus (fondaparinux).wRisk
.B stratify, further
blockade), and disrupt
w
w secondary prophylaxis as w
management
forw
NSTEMI (E pp. 251–2). ww
wand
Stable angina (E OHCM10 p. 116.)
K Frequently
encountered in primaryecare,
t retrosternal chest discomfort
et predictably
et
n
occurring
upon exertion.n
and relieved by rest and nitrates..n
.
X
X
X
Central, heavy chest
ok Symptoms
ok pain (lasting <15min) radiating
okto left arm
o
and jaw, precipitated by o
exertion and relieved by rest oro
rapidly by GTN
B
.B
(<5min), shortness
nausea, sweating, palpitations.
wof.forBbreath,
wsevere
w
w
Risk factors Common
IHD; see ACS (E p. 249);
aortic stenosis.
w
w
ww
6
Signs Tachycardia, cool and sweaty (‘clammy’), pallor. Normal after episode. See Box 7.3.
Investigations ECG Transient ST depression during pain; flat or inverted T
waves; signs of previous MI; Troponin Not elevated (if elevated, diagnosis
is NSTEMI). CT coronary angiogram if first presentation of typical chest
pain or atypical symptoms with ECG findings (ST changes or Q waves).
Functional testing if positive CTCA or previous CAD (eg myocardial perfusion scan, SPECT imaging, stress echo, or cardiac MRI). Invasive coronary
angiogram if inconclusive functional test.7
Acute treatment Pain relief with rest and GTN is characteristic. If pain
lasting >15min, investigate and treat as for NSTEMI/​UA.
Prophylaxis Assessment/​
reduction of modifiable risk factors (smoking,
obesity, DM, BP, cholesterol), statin, aspirin, ACEi, anti-​anginals (β-​blockade,
calcium channel blockers, nitrates, nicorandil, ranolazine, revascularization).
et
et
.n
kX
o
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o
o
w.B
o
ww
et
et
.n
kX
o
.n
kX
o
w.B
ww
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et
.n
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et
.n
kX
o
o
w.B
.n
kX
o
o
w.B
ww
ww
ww
K Box 7.3 Angina with normal coronaries?
Throughout your career, you will encounter numerous patients with atypical chest pain who require basic investigations to exclude serious pathology and subsequent reassurance. However, some patients experience
convincing ischaemic heart pain despite angiographically normal coronary
arteries. In this situation, considerations include coronary artery spasm
(Prinzmetal’s angina), cocaine-​induced vasospasm, microvascular angina
(post-​menopausal women with perfusion defects on functional imaging),
hypertrophic cardiomyopathy, hypertension, and aortic stenosis.
t
t
e
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ok
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ok
ok
ww
t
t
e
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e
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o
w.B
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e
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ok
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.
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e
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NICE guidelines available at Mguidance.nice.org.uk/​CG126
7
See NICE guidelines at Mguidance.nice.org.uk/​CG95
6
ww
ok
o
B
.
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e
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ww
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w
ww
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w
w
w
w
Chest pain
w
253
t
t
et dissection
3
.nAortic
.ne
.ne
X
X
X
you suspect aortic dissection,
k get help and arrange an urgent
ok K If OHCM10
oOHAM4
ok CT aorta
o
o
p. 654, or E
p. 142.)
Bo (E
B
B
. severe chest pain, anterior
. or interscapular,
Symptoms Sudden-​
wonset
wneurological
w
w
tearing in nature,
dizziness, breathlessness, sweating,
deficits.
w
w
ww
Risk factors Smoking, obesity, DM, iBP, icholesterol, FH, previous IHD.
Signs Unequal radial pulses, tachycardia, hypotension/​hypertension, difetin brachial pressures of ≥15mmHg,
et aortic regurgitation, pleural
et
ference
n
n
n
.
.
.
effusion
(L>R),
neurological
deficits
from
carotid
artery
dissection.
X
X
X
ischaemia
ok Investigations ECG Normal
okor may show LV strain/​
ok (E
o
o
o
mediastinum >8cm (rarely
irregularity
B pp. 586–8); CXR Widened
.Bseen),from
w.B
wdevelop
of aortic knuckle and
small left pleural effusion can
blood
w
w
tracking down;
Echo May show aortic root leak,
aortic valve regurgitation, ww
w
w
or pericardial effusion. Urgent CT/​
MR angiography/​
transoesophageal echo.
Acute treatment
Seek senior help. Hypotensive
Treat as shock (E pp. 490–
t
t
e X-​match 6 units, analgesia
e(IVt
5)..n
Oe(15L/​min), two large-​bore cannulae,
n
n
.
.
Xopioids). Hypertensive Aim to keep
Xsystolic BP <100mmHg (Ekpp.X272–3).
ok Further treatment Surgeryo(for
oktype A: involves the ascending
or
o
ooaortaaorta)
B conservative management
B
B
(for type B: involves descending
only).
.
.
w
w
Musculoskeletal
ww chest pain
ww
ww
B
2
Symptoms Localized chest wall pain, worse on movement and/​
or
breathing, recent trauma or exertion (eg lifting).
Signs Focal tenderness, erythema, absence of other signs in CVS or RS.
Investigations ECG Normal (no ischaemia/​MI); CXR Normal (no pneumothorax); D-​dimer Normal and low probability PE (E p. 284).
Acute treatment Reassurance and simple analgesia (E pp. 88–91).
Chronic treatment Should settle in 2wk, avoid further injury (eg heavy
lifting), regular analgesia to permit ADLs, deep breathing and coughing
(to prevent chest infection). Stop smoking.
Pericarditis (E OHAM4 p. 150.)
Symptoms Pleuritic chest pain, worse on lying flat and deep inspiration,
relieved by sitting forwards, fever, recent viral illnesses.
Signs May be no abnormalities, ±pericardial rub. Exclude tamponade.
Investigations ECG Saddle-​shaped ST in most leads (Fig. 7.2); blds iWCC
and inflammatory markers, ±iviral titres, troponin; Echo bright pericardium ± pericardial effusion; exclude tamponade and purulent pericarditis.
Acute treatment Reassurance and analgesia; paracetamol, NSAIDs. High
troponin suggests myopericarditis, but treat as ACS until proven otherwise.
Chronic treatment Usually settles in 2–​4wk. If recurrent, discuss with cardiology and consider cardiac MRI/​colchicine/​steroids.
t
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k
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et
oo
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o
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.Bo
oo
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.
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Fig. 7.2 Typical saddle-​
ww
ww shaped ST segment seen inwpericarditis.
ww
B
254
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
et
et
.nTachyarrhythmia
.nemergency
.ne
2
X
X
X
ok
ok
oakdjuncts
o
o
Check
airway is patent; consider manoeuvres/​
Bo 22 Airway
B
B
wIf no. respiratory effort—​CALL ARREST
w. TEAM
Breathing
w
w
ARREST TEAM
2 Circulation
w If no palpable pulse—​CALL w
ww
22Call
et for senior help early if patient
et‘unstable’ (Fig. 7.3): .net
n
n
.
.
X
X
X
of an unstable patient
ok 2• Signs
ok
ok
o
o
o
Reduced
conscious
level
•
Chest
pain
B
• Systolic BP <90mmHg
• Heart
w.B
w.Bfailure.
w
w
w
w
ww
• Sit patient up unless hypotensive, then lay flat with legs elevated
• 15L/​
O if SOB or sats <94% t
etminpulse
e pads if unwell
et
• .n
Monitor
oximeter, BP, defibrillator
n
n
.
.
X• Request full set of observations
X and ECG
ok • Take brief history if possible/​
ok check notes/​ask ward staffookX
o
o
B
• Examine patient: condensed
RS, ±abdo exam.B
w.Band ruleCVS,
w
• Establish likely
causes
out serious causes
w
• Initiate further
w treatment E p. 255 ww
ww
B
2
• Venous access, take bloods:
• VBG, FBC, U+E, D-​dimer, troponin, TFT, lactate, magnesium, calcium
• Consider requesting urgent CXR, portable if too unwell
• Call for senior help
• Reassess, starting with A, B, C . . .
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
2 Life-​threatening causes
o
Bo
•
•
•
•
•
t
.ne
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k
•
t
o
o
w.B
t
e
X.n
ok
Bo
et
n
.
kX
o
.ne
X
k
secondary to shock, including PE
iatrogenic (drugs).
ww
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k
oo
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.
w
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et
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.
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ok
ww
o
w.B
et
n
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t
o
o
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.
w
ww
et
.n
kX
ww
o
o
w.B
ww
w
Ventricular tachycardia (VT) or ventricular fibrillation (VF)
Torsades de pointes
Supraventricular tachycardia with haemodynamic compromise
Fast atrial fibrillation/​flutter with haemodynamic compromise
Sinus tachycardia:
•
Bo
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
e
X.n
Up to 3 attempts
t
.ne
kX
• Amiodarone 300 mg IV over 10–20 min
• Repeat shock
• Then give amiodarone 900 mg over 24 h
X.n
k
o
o
w.B
ww
• Shock
• Syncope
net
X.
k
ww
t
et
e
X.n
k
Irregular
ww
Possibilities include:
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treat as for narrow complex
• Pre-excited AF
consider amiodarone
t
.ne
No - Stable
et
n
.
X
ok
If VT (or uncertain rhythm):
• Amiodarone 300 mg IV over 20–
60 min then 900 mg over 24 h
w
ww
If known to be SVT with bundle
branch block:
• Treat as for regular narrowcomplex tachycardia
o
w.B
.Bo
w
w
Narrow QRS
Is rhythm regular?
Regular
• Vagal manoeuvres
• Adenosine 6 mg rapid IV bolus
if no effect give 12 mg
if no effect give further 12 mg
• Monitor/record ECG continuously
et
n
.
X
ok
o
.B
t
e
X.n
t
et
n
.
X
ok
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o
w.B
ok
!o
B
.
w
Seek expert help
ww
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w
ww
ww
• Myocardial ischaemia
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Is QRS regular?
o
o
w.B
ww
et
n
.
X
ww
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o
B
.
w
Seek expert help
Possible atrial flutter:
!
et
n
.
X
k
ok
No
• Record 12-lead ECG in sinus rhythm
• If SVT recurs treat again and consider
anti-arrhythmic prophylaxis
w
Probable AF:
• Control rate with beta-blocker or
diltiazem
• If in heart failure consider digoxin or
amiodarone
• Assess thromboembolic risk and
consider anticoagulation
Sinus rhythm achieved?
Yes
Irregular
ok
ww
oo
B
.
w
e
X.n
TACHYARRHYTHMIA EMERGENCY
oo
B
.
w
Adverse features?
et
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k
o
.Bo
.n
kX
Is QRS narrow (< 0.12 s)?
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w
ww
ww
!
Seek expert help
Assess using the ABCDE approach
Monitor SpO2 and give oxygen if hypoxic
Monitor ECG and BP, and record 12-lead ECG
Obtain IV access
Identify and treat reversible causes (e.g. electrolyte abnormalities)
Yes - Unstable
Synchronised DC Shock*
o
.Bo
oo
B
.
w
o
w.B
ww
ww
et
et
ok
ok
o
w.B
•
•
•
•
et
et
et
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t
et
ww
ww
ww
ww
ww
• Control rate (e.g. with beta-blocker)
255
t
t
t
t
.ne
.ne
.ne
.ne
Fig. 7.3 Adult tachycardia (with
a pulse) algorithm; 2015 guidelines.
X
X
X
X
X
k of the Resuscitation Council
ok Reproduced with the kindoopermission
ok (UK).
ok
ok
o
o
o
o
B
B
B
B
B
w.
w.
w.
w.
w.
w
w
w
w
w
w
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w
w
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* Conscious patients require sedation or general anaesthesia for cardioversion
B
.B
w
ww
256
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
t
.ne
.ne
.ne
Tachyarrhythmias
X
X
X
ok Worrying featuresodGCS,
ok dBP (systolic <90mmHg),
okchest pain,
o
Bo 2heart
B
B
failure, broad
w.QRS complexes.
w.
w
w
w Common Sinus tachycardia,wAF or flutter with fast venThink about
tricular response, AV nodal re-​entrant tachycardia. Uncommon Ventricular
tachycardia
re-​entrant tachycardia
(eg accessory pathway/​
et (VT), WAVhite),
et Non-​
et
n
n
n
.
.
.
Wolff–​Parkinson–​
atrial tachycardia.
cardiac causes Beware
X
X shock, pain, anxiety, PE.kX
ok appropriate tachycardia oin oegksepsis,
o
oofobreath, dizziAsk about Onset, .associated
Sx (chest pain, shortness
B
B
B
.
w Cardiac problems
ness, palpitations, w
collapse), previous episodes; PMH
(IHD, valvular
lesions, hypertension), thyroid
disease, DM; DH Cardiac
ww
ww
drugs, levothyroxine, salbutamol, anticholinergics, caffeine, nicotine, allergies; SH Smoking, alcohol, recreational drug use.
AF risk factors iBP, coronary artery and valvular heart disease, pulmonary
embolism, pneumonia, thyrotoxicosis, alcohol, sepsis.
Sinus tachycardia risk factors Shock (hypovolaemic, cardiogenic, septic, anaphylactic, spinal), pain/​anxiety, fever, drugs (levothyroxine, salbutamol, anticholinergics, caffeine, nicotine, cocaine).
et
n
.
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ok
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n
.
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o
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.
w
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t
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ok
o
B
.
w
ww
Obs Pulse (check apical pulse as radial can underestimate), BP, cap refill,
ww
RR, O2 sats, GCS, temp, cardiac monitor.
t
t
t
Look
‘unstable’;
.ne for Any ‘worrying features’
.ne classify arrhythmia as X
.ne
X
X
k
ok E Fig. 7.3, p. 255.ECG Powaves
ok before each QRS implyoosinus
rhythm,
Bo Investigations
B
B
. clear P waves implies AF, w
. tooth baseline
­irregular QRS without
saw-​
imw
wrate of ≥140 (narrow complexes)
w suggests SVT (including
plies atrial flutter,
w
w
ww
flutter with 2:1 block), broad regular complexes suggests VT (always check
for a pulse) (Fig. 7.4 and Tables 7.4 and 7.5); blds FBC, U+E, TFT, CRP,
t suspected), troponin,nMget , Ca , others as indicated bynesus-t
D-​dnimer
. e(eg(ifX-​PEmatch
picion
if haemorrhage);
X
X. ABG and CXR Only once treatment
X. has
k been initiated or if results
k
k
are
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o
o
o
Bo large PE, acute valvewlesion,
.Bo poor LV or pericardial effusion.
.Bo
w
Treatment w
w
ww
ww
2+
In all patients
• Airway, Breathing (with O2), Circulation (HR, BP and capillary refill)
• IV access (two large-​bore cannula in both antecubital fossa)
• Obtain ECG or view trace on defibrillator to decide on rhythm
• If hypotensive or dizzy lay flat with legs up—​call for senior help
• If semi-​conscious lay in recovery position—​call senior/​2 ARREST TEAM.
t
e
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ok
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2+
.ne
X
k
t
et
n
.
X
k
oo
oo
B
B
.
.
w
Specific arrhythmias
ww
w
wwEstablish and treat cause, egw
Sinus tachycardia
shock, sepsis (E pp. 490–5). w
AF Old or new AF? Consider urgent rate/​rhythm control (E p. 258).
SVT Usually
et time to call for help and
egett drugs ready (E p. 259)..net
n
VT.n
no pulse 3Call ARREST TEAM
and start BLS/​ALS (E p. 230).
.
X with pulse If haemodynamically
X
X
attempt chemical cardioversion
ok VT
ok Estable,
ok will need
(eg amiodarone or beta-​bolocker
p. 186); if fails or if unstable,
o
o
B
.B low GCS.
DC cardioversion (E
w.Bp. 546), with sedation orwGAwunless
w
w
w
ww
B
.B
w
ww
.B
w
w
w
w
Tachyarrhythmias
w
257
t
t
t
.ne 7.4 ECG features of tachyarrhythmias
.ne
.ne
Table
X
X
X
ok
ok P waves Broad/​narrow
ok
Rate o
Regular
o
Bo Sinus tachycardia w
B
B
.
>100
Narrow
BBB)*
✓
✓
w. (unless
w
w
Fast AF
>100
Narrow
(unless BBB)*
✘
✘
w ≥140
w
ww
SVT
✓
✓or ✘ Narrow (unless BBB)*
VT (with
✓
t ✘ Wide, not typical BBB QRS*
et pulse) ≥150
ealways
et
n
n
.
.
VT
(pulseless)
As for ‘VT with pulse’;
perform a pulse-​check .n
X
X
(carotid) kX
ok VF
o
ok
o
o
Chaotico
irregular electrical activity; never has
a pulse
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
.B strip)
ECG, lead II view
w.B
w(rhythm
w
w
w
w
ww
Sinus tachycardia
B
*80% of wide complex tachycardias (WCT) are ventricular (VT) and 20% are supraventricular
(90% VT if previous CAD). Supraventricular rhythms can produce a WCT if there is bundle
branch block (BBB; ‘aberrancy’) or an accessory pathway (‘pre-​excitation’), as part of the heart
is depolarized from outside the conduction system, and therefore more slowly. Because 1) it is
difficult to distinguish VT from SVT with aberrancy/​pre-​excitation on the ECG, 2) treatments are
similar, and 3) VT is a more unstable rhythm, if there is any doubt at all a WCT should be treated
as VT until proven otherwise.
t
.ne
X
k Fast AF
oo
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o
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et
oo
B
.
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.n
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.
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o
o
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ww
t
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et
n
.
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et
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k
VT with or without a
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et
n
.
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ww
w
t
o
w.B
t
.ne
X
k
Fig. 7.4 Typical appearance of various tachyarrhythmias.
w
ww
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X
ok
.Bo
ww
B
.B
w
w
.B
w
w
wCardiovascular
258
ww
w
Chapter 7
t
t
t
Atrial
.ne fibrillation (AF) (EXOHAM4
.ne p. 72.)
.ne
X
X
signs Heart failure,
hypotension, dGCS or chest pain.
ok 2 WorryingPalpitations,
okheart
ok malaise.
o
o
SOB,
failure, chest pains,B
dizziness,
Bo Symptoms
B
.
.
Risk factors/​cause Previous
age, acutew
illness, valvular disease,
ww AF, increasing
w
heart failure,wcardiomyopathy,
IHD, acute MI,
cardiac
surgery, HTN, PE, ww
w
pneumonia, COPD, thyrotoxicosis, alcohol, caffeine, and any acute illness.
Signs Irreg irreg pulse, hypotension if compromised, signs of a cause/​risk factors.
et ECG Absent P waves,.nirreg
et irreg QRS complexes; blds.nFBC
et
Investigations
n
.
, Ca , ±D-​dimer (PE), troponin
X(iWCC), U+E, TFT, alcohol,kXMg
X (if
Heart size, oedema, pneumonia;
ok possible ischaemic cause);ooCXR
ok Echo LV
o
o
dilatation/​impairment,
LA volume, valvular lesion. CTCA
to exclude CAD.
B
w.B
w.B
Treatment
w
w
w compromise Seek immediate
w help. Treat with shock ww
2 Haemodynamic
(E p. 546); O , IV access, DC cardioversion; if unsuccessful, amiodarone IV
±further
et cardioversion. Chronic AF.nvery
et unlikely to cause compromise:
edot
n
n
not
shock, but consider other causes
of compromise, eg sepsis.
.
.
X
X
X
stable Treatment
include:
ok •Haemodynamically
ok newoptions
ok
o
o
Conservative: if AF is probably
and the precipitant o
is obvious then
B
.Bclose monitoring may suffice.
.B
treating the cause
wand
w
• Rate control:w
if not, rate (<110bpm) over rhythm
control (cardioverting
w
w
w
ww
8
2+
2+
2
to SR) is first line because symptoms are usually rate-​related,
rate-​controlling medications are safer more successful drugs, and
anticoagulation usually continues regardless. Beta-​blockers (E p. 191) or
non-​dihydropyridine calcium channel blockers (E p. 193) are first line,
adding digoxin if needed (E p. 199). Consider pacemaker ±ablation if
flipping from sinus bradycardia to fast pAF (tachy-brady).
• Rhythm control: reverting to and staying in SR is less likely in old age,
established AF, LA dilatation, and mitral valve disease, but younger patients
with new AF and normal hearts may achieve and maintain SR, so could be
spared the risks of AF cardiomyopathy and long-​term anticoagulation. Also,
if there are disabling symptoms or AF-​induced heart failure, rhythm control
should be tried with DC/​chemical cardioversion (flecainide/​sotalol if no
structural heart disease, or amiodarone) first, and AF ablation second.
Anticoagulation Almost all patients with AF need lifelong anticoagulation,
including the 4wk prior to DC cardioversion (unless TOE excludes LA
thrombus)/​4wk afterwards (due to atrial stunning). Exceptions are patients
with strong preferences, excessive bleeding risk (eg HASBLED score),9
contraindications, very low stroke risk (CHA2DS2VASc score of 0 in men,
1 in women)10 or in sustained SR (discuss with cardiology). Options include non-​vitamin K oral anticoagulants (NOACs, eg apixaban, dabigatran,
edoxaban, and rivaroxaban), warfarin, or dalteparin (E pp. 420–2). Aspirin
should not be used as monotherapy for stroke prevention.
Complications Thromboembolic disease (eg ischaemic stroke). Drug side
effects (amiodarone, warfarin, NOACs, β-​blockers, digoxin, etc).
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
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o
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t
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e
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e
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e
X.n
NICE guidelines available at Mguidance.nice.org.uk/​CG180
HASBLED score: 1 point for each of uncontrolled HTN >160mmHg, abnormal renal/​liver
function, stroke, bleeding predisposition/​anaemia, labile INRs, elderly >65yr and drugs (alcohol, anti-​platelets, NSAIDs). Aim to reduce bleeding risk than avoid anticoagulation.
10
CHA2DS2VASc score: 1 point for each of CCF, HTN, DM, vascular disease, age 65–​74yr and female sex category. 2 points for each of age >75yr and stroke/​TIA. After assessing and reducing
the bleeding risk, the stroke risk outweighs the anticoagulation risks for patients with AF and a
CHA2DS2VASc score of 2 or more (‘consider’ anticoagulation in men with 1 point).
8
ww
t
e
X.n
ww
Bo
.n
kX
ww
t
e
X.n
ww
et
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o
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ww
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et
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ok
ww
o
B
.
w
ww
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.B
w
ww
.B
w
w
w
w
Tachyarrhythmias
w
259
t
t
t
Atrial
.ne flutter
.ne
.ne
X
X
X
tooth’ flutter waves reflecting
activity, with ventricular
k response
ok K ‘Saw 150bpm.
oksimilar atrial
osuccessful
o
o
Management
to AF, except drugs less
and
Bo around
B
B
.
. p. 78).
electrical and ablative
cardioversion
more so (E OHAM4
w
w
Supraventricular
ww tachycardia (SVT)ww
ww
2 Worrying signs Heart failure, hypotension, dGCS, or chest pain
(E OHAM4
p. 68).
et Palpitations,
et
et
n
n
Symptoms
shortness of.nbreath, dizziness, ±chest pains.
.
.
X factors Previous SVT, structural
X
X
ok Risk
ok cardiac anomaly, alcohol,
okiT .
o
Signs Tachycardia, anxiety,ohypotension if haemodynamicocompromise.
B Investigations ECG Narrow
.B complex tachycardia (unless
wmay
w.Bconcurrent BBB) w
w
w
with P waves (which
merge into QRST so be
difficult to see), regular
w rate usually ≥140; Further investigations
w
QRS complexes,
Only required if w
diagnosis in question, otherwise initiate treatment as follows.
t
Acute etreatment
O , large-​bore IV access
et (antecubital fossa). Monitor
et
n
n
n
.
.
.
rhythm
on
defibrillator:
X manoeuvres (E p. 545)kX
X
ok •• Vagal
o
ok
o
o
o
Chemical
(E
p.
545).
B Chronic treatment Ifwrecurrent,
.B seek cardiology advicewas.Bmay require elecw
w
trophysiological
testing
of cardiac conduction
ablation.
w
wpathways/​
ww
4
2
Complications Hypotension, ischaemia, heart failure in individuals with existing cardiac disease, deterioration into more sinister arrhythmia.
t
t
et
Wolff–​
.ne Parkinson–​White syndrome
.ne (WPW) (E OHAM4
.p.n80.)
X
X
X
This is a re-​
entrant
ok Aetiologywhich
ok tachyok
o
o
results from
an accessory
Bo cardia
B
B
.
conduction pathway
between
the atria
w(bundle
w.
w
w
and the ventricles
of Kent).
w
w
ww
It classically appears as a short PR
interval and a δ/​delta wave (shown by
t
t
t
arrowein
.n Fig. 7.5).
.ne
.ne
Treatment Avoid digoxin and verapamil.
X
X
X
ok Refer to a cardiologist oforokconsiderok
o
studies
and
Bo ation of electrophysiology
B
B
Fig. 7.5 δ wave
w.pathway.
w. in WPW.
ablation of accessory
w
w
w
w
w
w
Table 7.5 Anti-​dysrhythmics commonly used in tachyarrhythmias
t discussion with a senior.net
3These
et drugs should only be used
eafter
n
n
.
.
(should
LoadingX
dose 300mg/​over 60min IVI via central
Xline. line
kXAmiodarone
k
k
be given via a central
followed
by 900mg/​over 24h IVI via central
o
o
o
o12h PO forOR
but can be given Bo
200mg/​8h PO for 1wk then 200mg/​
Bo vein,
B
.
.
peripherally in an w
1wk then Maintenance dose 200mg/​
w 24h PO
emergency)
ww
ww
ww
Verapamil (avoid if patient 5mg/​over 2min IV; further 0.5–​1mg doses every
on β-​blockers)
5min until target rate achieved (total maximum
20mg) OR 40–​120mg/​8h PO
et
n
.
kX
et
n
.
kX
t
.ne
X
k
o
obedoduring IV administration of these.agents.
oo
Bo Patient must be in a monitored
B
B
.
w
w
ww
ww
Flecainide (not if patient
has IHD)
2mg/​kg/​over 10min IV (maximum 150mg) OR
100–​200mg/​12h PO
ww
B
260
.B
w
ww
Chapter 7
Cardiovascular
.B
w
w
ww
w
t
t
et OHAM4 p. 62.)
Ventricular
tachycardia (VT)
.ne
.n(E
.ne
X
X
X
(>30s),
k symptomatic, heart failure,
ok 2 Worrying signs Sustainedorooabsent
ok hypotenpulse (pulseless VT). o
Bo sion, dGCS, chestwpain,
B
B
.
w.±chest pain, arrest. w
Symptoms Palpitations, dizziness, shortness of breath,
w
w
w trauma, hypoxia, acidosis, longwQT, electrolyte disturbances. w
Risk factors IHD,
Signs Tachycardia, anxiety, pallor, hypotension, dGCS, shock.
et ECG Broad complex .tachycardia,
et P waves not before.nevery
et
n
n
Investigations
.
X rate usually >150; bldskX
X K ),
urgent TSH, U+E (especially
ok QRS,
o Check
ok situation
and Mg ; Other investigations
Should be directed by o
clinical
o
o
B
though cardioversion.B
w is main priority at this stage.
w.B
w
w
Acute treatment
w 2 Call senior help.
w
ww
3 Pulseless VT Call ARREST TEAM. Commence BLS/​ALS (E pp. 232–3).
VT with
eta pulse O , large-​bore IV cannula
et in antecubital fossa; restoration
eort
n
n
of.n
sinus rhythm with either drugs
(eg sotalol, amiodarone loading)
.
.
X cardioversion (under sedation
X
X
low GCS).
ok DC
oekxcitationunless
ok
o
o
o
Either
SVT
with
aberrancy/​
p
re-​
or
VT
Treat
as
VT.
B
.B
w.Bmay need drug therapy w
Chronic treatment This
to w
maintain sinus rhythm,
w
electrophysiological
w studies/​ablation or implantable
w cardioverter/​defib- ww
+
2+
2
rillator (E OHAM4 p. 62). Try to keep Mg >0.9 and K >4.0.
t VF (or other dysrhythmia),
t tachycardia cardiomyopathy.
t
Complications
.ne
.ne
.ne
Torsades de pointes
X
X
X
k axis (E p. 257). Develops
ok This looks like VF but hasoaorotating
ok on backo
Bo ground of iQT interval
B
B
7.6). Give Mg sulphate
2g/​IV (8mmol)
win.small(Table
w. saline)
over 15min (dilute
volume, eg 50mL ofw0.9%
±overdrive
w
pacing (E OHAM4
w p. 64).
w
ww
t
t
t
.ne
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
2+
Bo
o
et
n
.
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et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Tachyarrhythmias
w
261
t
t
et
.ne 7.6 Causes of prolongedXQT.ninterval
.ne
Table
X
X
k rate
ok QTc = QT/​√(RR interval)—​thisoallows
ok correction of the QT interval forooheart
on
an
ECG
trace.
Bo and is usually calculatedwautomatically
B
B
.
. <450ms (♀) are
wand
Normal QTc Values are gender specific: values <430ms (♂)
w
w
considered normal;
values
>450ms
(♂)
and
>470ms
(♀)
are
abnormal; values
w
w
ww
in between these are borderline. There is a dose–​response relationship between
risk of cardiac death and prolongation of QTc.*
et
etsyndrome (autosomal dominant),
et
Congenital
Romano–​W
ard
n
n
n
.
.
.
Jervell,X
Lange–​Nielsen syndrome (autosomal
X
recessive
ok
ok associated with deafness) ookX
o
o
B
Drugs
dysrhythmics (amiodarone,
w.B Anti-​
w.Bsotalol,haloperidol,
quinidine), psychoactives (thioridazine,
w
w
fluoxetine), antihistamines
w
w (terfenadine, loratadine), ww
antimicrobials (erythromycin, clarithromycin,
fluconazole)
t
e
et
et
Electrolyte
disturbance
dK , dMg n
, dCa
n
n
.
.
.
Complete
XSevere bradycardia
X heart block, sinus bradycardiakX
ok IHD
ok myocarditis
o
Ischaemia,
o
o
B
B Subarachnoid haemorrhagew.Bo
iintracranial bleed w.
et al. J Am
wwColl Cardiol
ww
ww
B
+
*Straus, M.
2+
2+
. 2006;47:362 available free online.
t
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X
k
oo
et
oo
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.
w
.n
kX
oo
B
.
ww
ww
o
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t
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o
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ok
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o
et
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.
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k
oo
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.
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e
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ww
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o
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t
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X
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t
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ww
o
w.B
et
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.
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ww
t
o
o
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.
w
ww
et
n
.
X
ok
o
o
w.B
ww
w
ww
.ne
X
ok
.Bo
ww
B
262
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
et
.nBradyarrhythmia
.neemergency X.ne
2
X
X
ok
ok
ok
o
o
Bo 2 Airway
B
B
Check
. airway is patent; consider manoeuvres/​
w
w. TEAMadjuncts
2 Breathing w If no respiratory effort—​CALL ARREST
w
w If no palpable pulse—​CALL ARREST
w TEAM
ww
2 Circulation
et for senior help early if patient
ethas ‘adverse features’ (Fig..7.6):
et
3Call
n
n
n
.
.
X
X
X
ok 2 Adverse features/features
ok
ok
o
o
o
B
• Systolic BP <90mmHg
• Ischaemic chest.B
w.B
w pain
• Syncope w
• Heart failure.
w
ww
ww
• Sit patient
hypotensive/​dizzy,
t then lay flat with legs elevated
emt in Oupif unless
et
• 15L/​
SOB or sats <94% ne
n
n
.
.
.
•
Monitor
pulse
oximeter,
BP,
defibrillator’s
ECG
leads
if
very
unwell
X
X
kX
ok •Request full set of observations
ok and ECG with long rhythm
ostrip
o
o
o
• Take brief history if.B
possible/​check notes/​ask ward.B
staff
B
• Examine patientw
: condensed CVS, RS, abdo examw
w
w
•Establish likely
w causes and rule out serious causes
w
ww
B
2
• Consider IV atropine, 500micrograms, repeat at 2–​3min intervals
(max 3mg)
• Initiate further treatment, including transcutaneous pacing, see following
sections
• Venous access, take bloods:
• VBG, FBC, U+E, LFT, troponin, TFT, lactate, calcium, magnesium
• Consider requesting urgent CXR, portable if too unwell
• Call for senior help.
• Reassess, starting with A, B, C . . .
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
t
et
.ne
.ne
2.n
Life-​threatening causes
X
X
X
k block (±following MI) ok
ok • Complete (3rd-​degree)ooheart
• Möbitz type II
Bo •Pauses
B
.
.Bo
w
>3s on w
ECG
w
• Hypoxia w
in children.
ww
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
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w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
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w.B
w.B
w
w
w
w
ww
B
.B
w
ww
t
.ne
X
k
•
•
•
•
o
Bo
Yes
Bo
o
w.B
t
ok
Satisfactory response ?
•
ok
•
•
•
o
B
.
w
Consider interim measures
:
Atropine 500 mcg IV repeat to
maximum of 3 mg
OR
Transcutaneous pacing
OR
Isoprenaline 5 mcg min–1 IV
Adrenaline 2–10 mcg min–1 IV
Alternative drugs*
ww
t
•
Yes •
•
o!k
o
B
w.
et
X.n
Seek expert help
Arrange transvenous pacing
ww
ww
.ne
X
ok
ok
•
et
X.n
et
n
.
X
Yes
ww
.B
w
ww
ww
No
o
et
n
.
kX
oo
No
Atropine 500 mcg IV
et
n
.
X
.n
kX
ww
e
X.n
w
263
et
Adverse features ?
• Myocardial ischaemia
• Heart failure
o
w.B
ok
Bo
t
.ne
X
k
Assess using the ABCDE approach
Monitor SpO2 and give oxygen if hypoxic
Monitor ECG and BP, and record 12-lead ECG
Obtain IV access
Identify and treat reversible causes (e.g.
electrolyte abnormalities)
• Shock
• Syncope
et
n
.
kX
w
w
BRADYARRHYTHMIA EMERGENCY
oo
B
.
w
ww
o
Bo
.B
w
w
•
o
B
.
w
ww
Risk of asystole?
Recent asystole
Mobitz II AV block
Complete heart block with
broad QRS
Ventricular pause > 3 s
No
oo
B
.
ww
ww
t
.ne
X
k
Continue observation
w
* Alternatives include:
• Aminophylline
• Dopamine
• Glucagon (if bradycardia is caused by beta-blocker or calcium channel blocker)
• Glycopyrronium bromide (may be used instead of atropine)
ww
t
t
netguidelines.
.ne
.2015
.ne
Fig. 7.6 Adult bradycardia algorithm;
X
X
X
k
ok Reproduced with the kind permission
ok of the Resuscitation Counciloo(UK).
o
Bo
B
B
w.
w.
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
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X
X
ok
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o
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w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
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ok
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o
o
o
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w.B
w.B
w
w
w
w
ww
B
264
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
t
.ne
.ne
.ne
Bradyarrhythmias
X
X
X
ok
ok BP <90mmHg, symptomatic
okhypoteno
o
featuresBSystolic
Bo 2sion,Worrying
B
. QRS, heart failure, VT/​wV.F.
HR <40bpm,
wbroad
w
w
w
w Sinus bradycardia MI (typicallywinferior
Think about
MI) drugs (including w
digoxin toxicity), vasovagal (Box 7.4), dT , hypothermia, Cushing’s r­ eflex
(bradycardia
et and hypertension 2°.ntoetiICP), sleep, anorexia nervosa,
et
n
n
.
.
physical
fitness;
complete
or
3rd-​
d
egree
AV
heart
block.
X
X
kX visual
ok Ask about Dizziness, postural
ok dizziness, fits/​faints, weight
ochange,
o
o
o
B
disturbance, nausea, .vomiting;
PMH Cardiac disease.B
(IHD/​AF), thyroid
w Bhead injury
wpathology,
disease/​surgery,
DM,
or intracranial
glaucoma,
w
w
eating disorder;
w DH Cardiac medications (β-​wblockers, Ca antagonists, ww
amiodarone, digoxin), eye drops (β-​blockers), anticoagulants, and antiplatelets
t SH Exercise tolerance, ADLs.
et (may need pacemaker) (Boxe7.5);
et
n
n
.
.
IHD
risk factors iBP, icholesterol,.nFH, smoking, obesity, DM, previous
X
X
X
ok angina/​MI.
ok
ok
o
o
o
Obs HR, BP, postural.B
BP, RR, sats, temp, GCS, cardiac.B
monitor.
B
wrate/​rhythm/​volume, pallor,
wshortness of breath, w
Look for Pulse
w
w
w
w
w
B
4
2+
dGCS, drowsy, iJVP (cannon waves in 3rd-​degree AV block), signs of cardiac failure (iJVP, pulmonary oedema, swollen ankles), features of iICP
(papilloedema, focal neurology E p. 364).
Investigations ECG Sinus bradycardia or complete heart block (see
Table 7.7 and Fig. 7.7), evidence of ischaemia or infarction (E pp. 586–8)
or of digoxin toxicity (see Table 7.7 and Fig. 7.7); blds FBC, U+E, glucose,
Ca2+, Mg2+, TFT, cardiac markers, digoxin level, troponin, coagulation (if
considering transvenous pacing); CXR Unlikely to be helpful in the immediate setting, but may reveal heart size and evidence of pulmonary oedema; Head CT Useful if you suspect raised intracranial pressure, though
patient will be in extremis (about to cone E p. 345) if iICP causing
bradycardia (speak to on-​call neurosurgeon). Echo for structural defects
and cardiac function (eg need for ICD/​CRT device).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
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k
o
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o
w.B
et
n
.
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o
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oo
B
.
w
.n
kX
ww
t
.ne
X
k
t
ww
ww
o
w.B
et
n
.
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et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
.ne
X
k
• Airway, Breathing (with O2) and monitor Circulation
• If either dGCS or dBP (<90mmHg systolic), 3call for senior help/​
ARREST TEAM
• IV cannula and take bloods
• Bed rest and cardiac monitoring
• Consider giving IV atropine if systolic BP <90mmHg (500micrograms at
2–​3min intervals to a maximum of 3mg)
• Check ECG to exclude myocardial infarction and to identify heart
block, extreme sinus bradycardia, or very slow atrial fibrillation.
e
X.n
ok
Bo
w
t
Treatment
t
.ne
X
k
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Bradyarrhythmias
w
265
t
t
t
.ne 7.7 ECG features of bradyarrhythmias
.ne and types of heartXblock
.ne
Table
X
X
k each QRS, rate <60 ok
ok Sinus bradycardia P waves
oprecede
o
Bo 1st-​degree AV blockwP–​R
B
. interval >5 small squares (>0.2s)
.Bo
w
w to beat, until failure of ww
Möbitz I
interval lengthens from beat
ww P–​R
wrestarts.
(Wenckebach)
AV conduction, then pattern
A usually benign
and asymptomatic disease of the AVN that improves
with exercise and rarely
pacemaker insertion t
et
etfail requires
n
.
.ne
M.ön
bitz II
Intermittent P waves
to conduct to ventricles, but
X
X
X
P–​R interval
I;
k does not lengthen, unlike Möbitz
ok
oktype
typically
of 3:1
oo2:1 (P waves:QRS complexes):BRatios
oblock.
Bo
B
and
above are considered high-​grade.AV
A less
.
wbenign and more symptomaticwinfranodal
w disease that
worsened by exercise and
more commonly requires
ww ispacemaker
w
ww
implantation
3rd-​degree
Complete dissociation
P waves and QRS
t
et AV
emayt between
block
complexes, which
be narrow or broad. A malignne
n
n
.
.
.
and
usually
symptomatic
disease
that
invariably
requires
X
kX pacemaker implantationokX
urgent o
permanent
ok
o
o
o
Digoxin
Down-​
sloping ST segment (reversed.B
tick), inverted T
B
B
.
wwaves; often present even when
w
effect/​toxicity
drug is at non-​toxic
ww levels
ww
ww
B
Rate-​controlled AF
.
kX
o
o
No P waves; irregularly irregular rhythm
net
et
oo
B
.
w
.n
kX
oo
B
.
ww
ECG, lead II (rhythm strip) view; arrows indicate P wave
Sinus
bradycardia
ww
1st-degree
AV block
o
Bo
et
.nMöbitz
type I
X
k
ww
Möbitz II with
3:1 AV block
o
o
w.B
Digoxin
effect/
toxicity
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
ww
o
Bo
ww
o
w.B
et
n
.
kX
o
o
B
.
w
ww
et
n
.
X
ok
o
o
w.B
ww
t
Fig. 7.7 Typical appearances of various bradyarrhythmias and types of
heart block.
et
n
.
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ww
w
t
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et
n
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X AV block
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ww
B
266
.B
w
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w
ww
w
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t
t
t
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X
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o
o
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.oedema, symptoms of iICP,whypothermia,
.
shortness of breath,
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of iICP (E p. 364).
w
w by a P wave, rate <60, ww
Investigationsw
ECG QRS complex will be preceded
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n
n
n
.
.
.
transvenous
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X
ok Acute
o layor flat
o (as long as
o
o
o
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w
w
w
w
signs present,
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etpacing-​wire via central line/​.pnermanent
et pacemaker (E pp. 548–9);
et
pacing/​
n
n
.
.
a
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X
X
ok when an external pacing machine
ok is not immediately available.
ok
o
o
o
Chronic treatment Consider
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B
w.Bare sign of sick sinus syndrome
w.B(E p. 267) and w
bradycardia or pauses
w
w
may need a w
permanent pacemaker system (E
w OHCM10 p. 132).
w
4
2+
2+
2
Complications Severe bradycardia and high vagal tone can deteriorate into
asystole so prompt treatment is required. Remember to talk continually
to the patient and/​or check for a pulse since pulseless electrical activity
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t
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X
k
oo
et
oo
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t
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X
k
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w bradycardia from unopposed
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ition upon heart rate is common. Often brief loss of consciousness
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t consider other diagnoses
t
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o
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w
w
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ww
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n
.
.
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X
X
X
k
ok
ok
oo
Bo Box 7.5 Drugswwhich
Bo can precipitate bradycardia
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.
.
β-​blockersReports
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ww
ww
ww
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et
n
.
kX
o
Bo
Ca2+ antagonists Verapamil and diltiazem slow heart rate
Amiodarone
Can cause conduction defects and bradycardia
α-​agonistsPhenylephrine is mainly used by anaesthetists and can cause
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Ivabradine
Used for prognosis in heart failure to slow the sinus node.
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n
.
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o
o
B
.
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ww
w
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w
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w
Bradyarrhythmias
w
267
t
t
t
Complete
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X
X
signs Features of heart
ok 2 WorryingAsymptomatic,
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ok shorto
o
dizziness (±on standing), palpitations,
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B
B
ness of breath, ±chest
w. pain.
w.
w
w
Causes Frequently
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damage
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after inferior ww
w
w
MI); also post-​cardiac surgery, drug-​induced (β-​blockers, Ca channel
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et (and potentially dGCS),.often
et iBP, cannon waves in iJVP.n(due
et
Signs
dBP
n
n
.
X asynchronous contractionkofXthe right atria against a closed
X
ok tovalve),
ofeatures of underlying disease.
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signs of heart failure,
o
o
o
B Investigations ECG w
.B dissociation of P waves
.Bfrom QRS comComplete
wrespond
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QRS implies proximal rhythm (may
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w
wto respond toto atropine);
ww
broad QRS w
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look for evidence of myocardial infarction; blds FBC, U+E, Ca , Mg ,
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cardiac
t markers, coagulation n(ifetconsidering transvenous pacing);
et
n
n
CXR
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.
.
.
X treatment If symptomatick(dizzy
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X
ok Acute
o lay flat
o supplemeno
o
o
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B tation, secure IV access
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w.Band takeatropine
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w
w
TEAM. Titrate 500micrograms
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w
w
ww
B
2+
2+
2+
2
of 3mg), followed by a large flush, until HR improves. Identify and correct precipitant. Consider external pacing/​pacing-​wire via central line (E
pp. 548–9); a rhythmical precordial thump (percussion pacing) can be used
in extremis when an external pacing machine is not immediately available.
Chronic treatment Likely to need permanent pacemaker (E OHCM10
p. 132) and/​or correction of precipitant.
Complications Severe bradycardia and high vagal tone can deteriorate into
asystole so prompt treatment is required. Remember to talk continually
to the patient and/​or check for a pulse since PEA is common and the
ECG trace may not change.
t
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X
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oo
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.
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t
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o
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.
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bw
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ww
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t
ettypes of heart block (E
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et
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n
n
n
.
.
.
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ok 1st-​
oor there
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the patient is symptomatic
is a reversible cause o
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o
o
B Möbitz II and high-​w
.BAV block These may deteriorate
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w.Bpacing,
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especially
w
w
w
w
w
when associated with an ACS or general anaesthesia—​seek cardiology w
advice.
et
et
et
n
n
n
.
.
.
X
X
X
ok
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ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
268
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
et
.nHypertension
.ne
.ne
2
emergency
X
X
X
k
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okis patent; consider manoeuvres/​
oadjuncts
o
o
Check
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Bo 22 Airway
B
B
.
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no respiratory effort—​CALL ARREST
w.TEAM
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w
w
2 Circulation
w If no palpable pulse—​CALL ARREST
w TEAM
ww
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2 Disability
t
e
etdeteriorating.
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n
n
n
.
.
.
3Call
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X
X
kX
ok If systolic >200 or diastolic
o>120:
ok
o
o
o
B
• Sit patient up
w.orBsats <94%
w.B
• 15L/​min O if SOB
w
w
• Monitor pulse
w oximeter, BP, defibrillator ECG
w leads if unwell
ww
•Request full set of observations and ECG
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e patient: condensed RS,.CVS,
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n
n
X out serious causes andkestablish
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ok new?
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o
o
B
• Do not give STAT dose
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w.B ofEantihypertensive
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• Initiate further
treatment
p. 271
w
w
• Venous access
w , take bloods:
w
ww
B
2
•
• FBC, U+E, cardiac markers, TFT, glucose, cortisol
• Consider requesting urgent CXR, portable if too unwell
• Urinalysis and β-​hCG (in women of child-​bearing age)
• Call for senior help for advice
•Re-​assess, starting with A, B, C . . .
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
2 Life-​threatening causes
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o
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t
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o
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o
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ok
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o
et
n
.
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t
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• Phaeochromocytoma
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269
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et
n
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w
w
HYPERTENSION EMERGENCY
ww
o
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ww
B
270
.B
w
ww
Chapter 7
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w
w
ww
w
Cardiovascular
t
t
t
.ne
.ne
.ne
Hypertension
X
X
X
k
ok
ok
oo mentation, seizures, retinal
o
features.B
Altered
haemorrhages,
Bo 2AKI,Worrying
B
w arterial aneurysms. ww.
chest pain, pregnancy,
w
2 Is this a hypertensive
crisis? If any of above,
w
wor acute iBP >200 systolic ww
or >120 diastolic (E p. 268).
et about Life-​threatening Hypertensive
et crisis (acute iBP, typically
et
Think
n
n
n
.
.
.
pre-​eclampsia; Other
X>200 systolic or >120 diastolic;XE p. 271),
XAnxiety,
hypertension (including
ok pain, primary (essential)ooroksecondary
ok thyroid
o
o
storm and phaeochromocytoma).
B
.B
w
w.B but consider w
Ask about The
majority of patients will be asymptomatic,
w
w
w headache, chest/​back w
possibility ofw
end-​organ damage (visual symptoms,
pains, haematuria) or secondary causes (Table 7.8) PMH Previous hypertension,
syndrome, acromegaly,
syndrome, phaeot Conn’s
et Cushing’scoarctation,
edisease,
et
n
n
n
chromocytoma,
thyroid
DM, renal artery stenosis;
.
.
.
X Cardiac and antihypertensive
X medications, steroids, contraceptive
X
ok DH
ok MAOI,
okrecreational
pill, levothyroxine/​carbimazole,
antipsychotics,
o
o
o
B
.B
drugs (cocaine, amphetamines);
FH Hypertension, .endocrine
disease,
w
wB
polycystic kidney
disease; SH Exercise tolerance,
smoking.
w
w
w
w
ww
B
Obs HR, BP (both arms with correct sized cuff ), sats, temp, GCS, repeat
BP after a period of prone relaxation.
Look for Signs of precipitating disease Radiofemoral delay, striae, central obesity, large hands/​feet/​face, tremor, exophthalmos, proximal myopathy, gravid uterus, renal bruits/​polycystic kidneys; Signs of end-​organ
damage Fundoscopy (papilloedema, hypertensive retinopathy), displaced
apex beat or S4 (suggest left ventricular hypertrophy), haematuria.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
ww
w
oo
B
.
ww
Table 7.8 Key secondary causes of hypertension
t
.nedisease or
Renal
X
k renal artery stenosis
t
.ne
X
k
ww
tInvestigations Ref net
.ne Urine microscopy, E X
.
p. 387
X
k
renal Doppler USS, ok
o
o
autoantibodies ±renal
Bo
.Bo
.Bo
biopsy
w
w
Phaeochromo­ w
Plasma metanephrines;
E p. 339
w
ww
ww
cytoma
24h urinary
catecholamines +VMA
t
t
Thyroid
dysfunction
TFTs
E pp. 340–1
e
e
et
n
n
n
.
.
.
X
X
X
ok Acromegaly
ok
oEk p. 337
o
o
o
IGF-​
1
and
pituitary
B
hormone levels
w.B
w.B
w
w
w
w
ww
Cushing’s
Urinary free cortisol; E pp. 338–9
syndrome
dexamethasone
t
t
suppression test
e
e
et
n
n
n
.
.
.
Other
causes
include
pregnancy
(gestational,
pre-​
e
clampsia/​
e
clampsia),
Conn’s
syndrome
X p. 339), hyperparathyroidism (Ekp.X403), scleroderma, coarctation of thekaorta,
X
ok (E
o sleep apnoea.
o drugs
o
o
o
(steroids, MAOI, OCP) and obstructive
B
w.B
w.B
w
w
w
w
ww
Features
Renal failure,
abnormal urine
dipstick, FH may be
relevant, renal bruit
Sweating, labile
hypertension,
palpitations
Cold/​heat
intolerance, sweating,
lack of energy
Headache, visual field
disturbance, change in
facial features
Centripetal obesity,
skin thinning,
weakness
B
.B
w
w
.B
w
w
w
w
w
Hypertension
w
271
t
t
t
Investigations
BP Ensure correct
.ne
.nesized cuff and repeat manually;
.ne a
X
X
X
of hypertension
be confirmed with blood
pressure
ok new diagnosis(BPM)
okbeshould
okmeasuring
whichocan
ambulatory (a 24h monitor
o
Bo monitoring
B
B
every 30m) or at home
ECG Features of
w. (self-​monitoring BD forw1w);
w. TFT;
LVH (E p. 587);
blds FBC, U+E, glucose, cholesterol,
Urine Blood,
w
w
protein, β-​hw
CG; CXR Unhelpful in immediatew
setting, but will show heart w
size and aortic contours. If <40yr with BP 140/​90 and BPM >135/​85 but
t damage, cardiovascular disease,
no organ
renal disease or diabetes, conespecialist
efort secondary
et
n
n
n
.
.
sider
opinion to investigate
causes (Table .7.8).
X
X cessation, regular exercise,
Xreduce
Lifestyle advice
ok Treatment
ok(smoking
okmodifiable
o
o
o
alcohol
and
caffeine,
balanced
low-​
s
alt
diet).
Identify
and
treat
B risk factors (DM and
dyslipidaemia). Pharmacological
therapy if approwBP.B
wFig..B7.8).
w
w
priate, based upon
and risk factors (Box 7.6 and
w
w
ww
Box 7.6 Hypertension: who and how to treat
eBPt in patients with HTN can be confusing
et and the evidence is always evolving.
et
Target
n
n
n
.
.
.
The
following
is
adapted
from
the
NICE
guidelines
which
themselves
can
be
conflicting:
X patient with a clinic BP >160/​
X subsequent BPM results ofkX
>150/​
ok •Any
ok 100 andtherapy.
o
o
oofor patients
95
should
be
started
on
pharmacological
This is also
true
B
B
B
.
.
who are under 80yr
with a clinic BP of >140/​90, BPM w
results of >135/​85,
w
and one or more
of (i) cardiovascular disease, (ii) renal
disease, (iii) a 10yr
w
w
w
w
ww
cardiovascular risk of >20%, or (iv) end-​organ damage (eg LVH, eGFR<60mL/​
11
min, hypertensive retinopathy or microalbuminuria)11
• The target BP then depends on age and comorbidities. If they are <80yr aim
for a clinic BP <140/​90 (or 135/​85 on BPM). If ≥80yr aim for a clinic BP
<150/​90 (or 145/​85 on BPM)
•Patients with diabetes and CKD have lower targets due to the higher risk of
complications. In T1DM aim for a clinic BP <135/​80, or <130/​80 if they also
have CKD, albuminuria or 2 or more features of the metabolic syndrome (eg
high cholesterol and central obesity).12 In T2DM aim for a clinic BP <140/​80, or
<130/​80 if they also have CKD, retinopathy, or a previous CVA/​TIA.13 In CKD
and an albumin:creatinine ratio of >70mg/​mmol, aim for <130/​8014
• The choice of antihypertensive should be guided by Fig. 7.8 and patient tolerance.
Calcium channel blockers (C) (or thiazide-​
Age <55
Age >55 or black
type diuretics, D, if C not suitable) are the
best first choice drug for most patients.
A
C (or D)
Limited data from younger patients suggest
that ACEi or ARBs (A) have better BP-​
lowering effects. ACEi or ARBs are also
A & C (or A & D)
first line for patients with (i) CKD and an
albumin:creatinine ratio >30mg/​mmol, or
(ii) diabetes mellitus (if T2DM rather than
A&C&D
T1DM, C or D should be added to ACEi or
Fig.
7.8
Treating
hypertension.
ARB as dual 1st-​line therapies)
• β-​blockers are less effective than other
classes at reducing CVS events, especially stroke. They are used as an additive
treatment or to avoid polypharmacy in patients with other indications (eg angina).
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
o
w.B
ok
.n
kX
o
o
w.B
ww
t
t
e
X.n
ok
e
X.n
ok
o
w.B
ww
ww
Follow-​up If treatment is initiated or altered in hospital, ensure GP
t
e
X.n
ok
ww
knows what investigations have been undertaken, their results, and what
the therapeutic plan is. Once BP control is acceptable, patients should
have annual GP follow-​up to review BP, lifestyle, and medication.
Complications End-​organ damage, malignant HTN, CV disease.
t
Bo
ww
t
e
X.n
o
w.B
ww
et
.n
kX
ww
Bo
.n
kX
o
w.B
ww
Bo
et
.n
kX
t
e
X.n
ok
o
B
.
w
ok
NICE guidelines available at Mguidance.nice.org.uk/​CG127
12
NICE guidelines available at Mguidance.nice.org.uk/​NG17
13
NICE guidelines available at Mguidance.nice.org.uk/​NG28
14
NICE guidelines available at Mguidance.nice.org.uk/​CG182
11
ww
e
X.n
ww
o
B
.
w
ww
B
272
.B
w
ww
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
t
Hypertensive
crises
.ne
.ne
.ne
X
X
X
>200/​1k
a 2 hypertensive emergency
ok K Elevation ofbyBPevidence
o of20 isend-​
ok7.9) orwhen2
o
o
organ damage (Table
Bo accompanied
B
B
hypertensive urgency
end-​
w. in the absence of w
wo.rgan damage (E w
OHAM4 p132).
w
w
w
w
Symptoms and signs iBP, often acute, in presence of end-​organ damage
(Table 7.9).
et
et
et
n
n
n
.
.
.
Table
7.9
End-​
o
rgan
damage
in
hypertension
X
X
ok Organ Symptoms/​signsookXInvestigations
ok
o
o
B
.B
CNS
CT head may show subarachnoid
or
dGCS, headache,
wvomiting,
w.Bhypertensive
w
w
intracranial haemorrhage;
confusion,
w
w
ww
new motor weakness, encephalopathy occurs with cerebral oedema
following loss of vascular autoregulation
seizures, coma
Eyeset Headache, visual
Fundoscopy
haemorrhages et
et showsoftenretinal
n
n
.
.
.n
disturbance
±papilloedema;
coexists with damage
X
X
X
elsewhere
k
k
k
o
oo ECG changes, elevated .cardiac
oomarkers.
pain,
Bo Heart Chest
B
B
.
orthopnoea
pulmonary
oedema
on
CXR
w
w
Aorta
Sudden
wwtearing chest Echo or CT may
wwreveal aortic dissection
ww
pain radiating to back;
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Kidneys Haematuria, lethargy,
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t
tworsening renal function; proteinuria,
t
Rapidly
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.ncellecasts
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red
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X
X
X
k
ok
okAlways confirm BP yourself,oousing
o
See Table
7.9.
Bo Investigations
B
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.secondary causes (Table 7.8).wRequest
. formalcorrect
sized cuff. Consider
ophw
thalmic assessment
ww if suspect retinal disease.ww
ww
Diagnosis This relies on a compatible history, often with previously comparatively
t normal BP, and presencenoretabsence of end-​organ damage.
etreatment
et
n
nwith
Acute
In the absence of.end-​organ damage, oral therapy
.
.
X
X
X
channel blocker or
should be instigated. Ifkend-​organ
ok a calciumis present,
ok ACEi
admitopatient
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oo ICU), with
Bo damage
B
B
.
close monitoring of . BP (Box 7.7), ECG, neurological
and fluid
warterial line, central line, catheterization).
w state, Rapid
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rew
w
wcan be dangerous, resulting inwcerebral hypoperfusion and
ww
duction in BP
is only necessary in an acute MI or aortic dissection. Otherwise, aim to
reduce diastolic BP to 100mmHg or by 25% (whichever value is higher)
over 24h (see Tables 7.10 and 7.11 for treatment options). Patients
with early features of end-​organ damage may be commenced on oral
therapy, though more severe organ damage may require treatment with
IV agents. If no evidence of LVF use labetalol; if LVF present commence
furosemide (20–​50mg IV) ±hydralazine. Consider ACEi to counteract
high circulating levels of renin. Nitroprusside and hydralazine are still
used as adjuncts in severe crises under expert guidance.
Chronic treatment BP needs checking regularly once discharged from hospital. Ensure GP knows what investigations have been undertaken, their
results, and what the therapeutic plan/​target BP is.
t
e
X.n
ok
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o
et
n
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t
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o
o
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et
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w
ww
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w
w
w
w
Hypertension
w
273
t
t
et
.ne CVA
.ne
K.nBox 7.7 BP control inX
acute
X
X
k autoregulation is impaired
ok acute ischaemic stroke,
ocerebral
ok and ago
o
Bo Ingressive
B
B
lowering of .BP results in hypoperfusion and. poor outcomes.
3Seek expert
help. Generally, only treat ifw
BPw>220/​120 or clear
ww
w include IV labetalol.
ww
evidence ofw
end-​organ damage. Suitable agents
Table
et7.10 Oral antihypertensives foretacute management of hypertenet
n
n
.
.
sive
crises (E OHAM4 p. 137) .n
X
X
X
ok Drug Dose ookComment
ok
o
o
B
Atenolol
50–​100mg/​
β-​blockers available.
Contraindicated
w.B Many
w.B
24h
PO
in asthma, peripheral
vascular disease, DM
w
w
w
w
ww
Amlodipine 5–​10mg/​24 PO Ca channel blocker; 1st line in elderly and
when β-​blocker contraindicated
et 25–​50mg/​
et Safe in pregnancy
et
Hydralazine
Vasodilator.
n
n
n
.
.
.
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X
X
kX
ok Nifedipine 10–​20mg/​8hoPOokAvoid
sublingual as rapidly dropso
BP. OK
o
o
to
use
in
conjunction
with
β-​
b
locker
B
.B verapamil or diltiazem w
.B (avoid
with β-​blockers)
w
ww
ww
ww
2+
Table 7.11 IV antihypertensives for acute management of hypertensive
crises (E OHAM4 p. 136)
t
t
t
.ne
.ne
.ne
K Patient must be in HDU/​ICU, ideally
with invasive BP monitoring. Intravenous
X
X
X
ok therapy can result in rapid fallsoinoBPkso drugs must be titrated cautiously.
ok
o
Bo Drug
B
B
Dose.
Comment
w
w.
Isoket 0.05%* w
2–​10mL/​h IVI
Venodilates. w
Useful in LVF/​angina. Easy
ww
(0.5mg/​mL) w (1–​5mg/​h)
for nursesw
to set up infusion. Drug of
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t
GTNet
1–​10mg/​h IVI
et Useful in LVF and angina
n
n
.
. Venodilates.
.ne
Hydralazine
5–​10mg/​20min IVI
Vasodilates, can cause compensatory
X
X
X
ok
ok rise in heart rate; use withooa kβ-​blocker
o
1
0min
IVI Used in eg aortic dissection.
Avoid in
Bo Labetalol 20–​w80mg/​
B
.
LVF
w.B
w
w
Nitroprussidew 0.25–​8micrograms/​ Rapid onset.
wUseful in LVF or hypertensive ww
kg/​min IVI
encephalopathy. Rarely used now: toxic
cyanide metabolites may accumulate
t
e
et sweating, iHR, iRR, and dpH.net
causing
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
®
*Isosorbide dinitrate: available as 25mL 0.1% solution (25mg in 25mL).
Bo
o
et
n
.
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et
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.
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t
o
o
B
.
w
ww
w
ww
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X
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.Bo
ww
B
.B
w
ww
274
Chapter 7
.B
w
w
ww
w
Cardiovascular
t
t
t
.ne failure
.ne
.ne
Heart
X
X
X
ok Heart failure has high morbidity/​
ok mortality and is increasingly
okcommon.
o
o
Bo KSymptoms
B
B
Breathlessness,
PND, wheeze,
w. orthopnoea,
w. oedema, fatigue. w
Causes Often multifactorial.
Assess the history, w
exam, and echo carefully.
w
w Non-​ischaemic often secondary
w to eg HTN, DM, valve w
Usually ischaemic.
disease and toxins eg chemotherapy, stimulants and alcohol, but can be
t
primary
eg HCM, ARVC, DCM,
or acquired eg peripartumeor
et (inherited
et causes
n
n
n
.
.
.
Takotsubo).
Rarer non-​ischaemic secondary
are infiltrative (amyloid,
X overload, Fabry), inflammatory
X (sarcoid, giant cell), infectious
X (viral
ok iron
ok (muscular
ok ataxia),
o
o
o
myocarditis, HIV), neuromuscular
dystrophy, Friedrich’s
B
and electrical (AF, tachycardia,
w.B pacemaker syndrome).
w.B
w
w
Signs Cachexia,w
iRR, iHR, iJVP, murmur (if valvular
disease), 3rd heart
w creps, pitting oedema (typically
w ankles but
sound, bibasal
check sacrum). w
Investigations ECG No specific features, look for arrhythmias, conduction disease
et or broad QRS (?device.ntherapy);
et blds FBC (?anaemia),.nU+E
et
n
.
(?renal
hypoperfusion),
TFTs,
fasting
lipids,
glucose,
iron,
BNP
(secreted
X failing ventricle—​normal
Xlevels unlikely in untreated heart
kXfailure);
ok byCXRtheCardiomegaly,
ok oedema,
oupper
o
o
o
pulmonary
pleural
effusions,
lobe diB
.B
.Bmotion abnormalversion, Kerley B w
lines; Echo Valvular pathology, wall
w
ities, left ventricular
ww ejection fraction (LVEF).
wwHF with preserved LVEF ww
B
15
(Box 7.8) may show ventricular hypertrophy and altered filling pressures.
Acute treatment Treat pulmonary oedema in acute decompensation (E p. 288).
Chronic treatment Conservative measures includes treating the cause, smoking
cessation and cardiac rehab. β-​blockers16 and ACEi improve prognosis and
symptoms if reduced LVEF so are 1st-​line therapy (ARB if ACEi not tolerated). An aldosterone antagonist is cautiously added as 2nd line if EF <35%
and still symptomatic. 3rd-​line therapies to be considered by specialist heart
failure teams are ivabradine (if SR and HR >70), cardiac resynchronization
therapy (if QRS >130ms, more so if LBBB, QRS >150ms, or other pacing
indication) and valsartan/​sacubitril (in place of ACEi). Advanced heart failure
therapies (transplant/​assist devices) or palliation may follow. If prognosis
>1yr an ICD is considered at any stage if EF remains <35% to prevent death.
Furosemide/​bumetanide provide symptom relief from congestion with thiazides/​inotropes if resistant.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
w
t
o
ww
o
w.B
t
.ne
X
k
et
.ne
X
k
oo
B
.
w
.n
kX
ww
K Box 7.8 Heart failure with preserved ejection fraction
Much understanding in heart failure comes from the study of patients with clear
echocardiographic evidence of inadequate left ventricular contraction. However,
the signs and symptoms of heart failure frequently manifest in those with ‘preserved
LVEF’. Many of these patients will have raised left ventricular filling pressures with
ventricular stiffening, reducing filling efficiency in diastole. This population is more
likely to be older, female, and hypertensive (a demographic rapidly increasing in size)
but poorly represented in clinical trials. Despite good theoretical backing, little or no
evidence of mortality benefit exists for ACEi, ARBs, β-​blockers, or calcium channel
blockers, while diuretics should be used with caution (since acute reductions in filling
pressures may worsen failure). Management should involve close attention to correction of dysrhythmias and comorbid conditions, as well as control of blood pressure,
and careful fluid balance.
t
e
X.n
ok
Bo
t
ww
o
w.B
et
n
.
kX
16
ww
t
o
o
B
.
w
ww
et
n
.
X
.ne
X
ok
.Bo
NICE guidelines available at Mguidance.nice.org.uk/​CG108
Avoid β-​blockers in COPD. Few β-​blockers are licensed for heart failure (eg bisoprolol, carvedilol,
and nebivolol): Patients already on a β-​blocker for another indication may need to switch.
15
ww
ok
o
o
w.B
ww
et
n
.
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o
Bo
.ne
X
k
ww
w
ww
ww
B
.B
w
ww
.B
w
w
w
w
Chapter 8
w
275
t
t
t
.ne Respiratory
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
2 Breathlessness and low sats emergency 276
and low sats 277
t Breathlessness
e
etpatient 290
et
2 Stridor in a conscious adult
n
n
n
.
.
.
Cough
291
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
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ok
ok
ok
o
o
o
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w
w
w
w
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B
t
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oo
et
oo
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.
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oo
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.
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o
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t
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ok
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o
et
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e
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o
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et
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t
o
o
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et
n
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o
o
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w
ww
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X
ok
.Bo
ww
B
276
.B
w
ww
Chapter 8
.B
w
w
ww
w
Respiratory
t
t
et
.nBreathlessness
.ne low sats X.ne
2
and
X
X
ok
ok
ok
o
Bo emergencyw.Bo
B
w.
w
manoeuvres/​
adjuncts
2 Airway ww Check airway is patent; consider
w
ww
If no respiratory effort—​CALL ARREST TEAM
2 Breathing
t
t ARREST TEAM
If no palpable pulse—​C
2 Circulation
e
eALL
et
n
n
n
.
.
.
X
X
X
ok 3 Call for senior help oearly
okif patient is deteriorating.oUse
okemergency
o
call bell to summon help
B
.B quickly—​don’t leave thewpatient.
.B
• Sit patient up w
w
w
• 15L/​min Owin all patients if acutely unwellw
ww
• Monitor pulse oximeter, BP, defibrillator’s ECG leads if unwell
• Obtain
a full set of observations including
eta brief
etnotestemp
et
•Take
history if possible/​check
/​ask ward staff
n
n
n
.
.
.
•
Examine
patient
:
condensed
RS,
CVS,
±abdo
exam
X
X
kXout serious causes
ok •Establish likely causes and
orule
ok
o
o
o
• Initiate further treatment
, see E pp. 277–8
B
w.B
w.B
• Venous access, take
bloods:
w
w
FBC, U+E,
w LFT, CRP, bld cultures, D-​dwimer, cardiac markers
ww
B
2
•
• Arterial blood gas, but don’t leave the patient alone
• ECG to exclude arrhythmias and acute MI
•Request urgent CXR, portable if too unwell
• Call for senior help
•Reassess, starting with A, B, C . . .
• In COPD/​known CO2 retention, rapidly titrate down O2 to lowest
flow to maintain normal sats for this patient (usually 88–​92%). Beware
of CO2 retention and have a low threshold for repeat ABG.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
t
t
2 Life-​
.ne threatening causesX.ne
.ne
X
X
ok •Asthma/​COPD
ok •Pneumonia
ok
o
o
oedemaB(LVF)
•Pulmonary embolism
(PE)
Bo •Pulmonary
B
• (Tension) pneumothorax
•Pleural effusion
w.
w.
w
w
• MI/​arrhythmia
•Anaphylaxis/​
w
w airway obstruction. ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
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ok
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o
o
o
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w.B
w.B
w
w
w
w
ww
B
.B
w
w
.B
w
w
w
w
w
w
277
Breathlessness and low sats
t
t
et
.ne
.nlow
.ne
Breathlessness
and
sats
X
X
X
ok Worrying featuresoRRok>30, sats <92%, systolic BPo<100mmHg,
ok
Bo 2chest
B
B
. inability to complete sentences,
pain, confusion,
wsilent
w. exhaustion, w
w
w
tachy/​bradycardia,
chest.
w
w
w
Think about 2 Life-​threatening causes of respiratory failure See Table 8.1;
t
Most likely
oedema (LVF), PE,
et COPD/​asthma, pneumonia,
epulmonary
eMI;t
n
n
n
.
.
.
Others
Pneumothorax,
pleural
effusion,
arrhythmia,
acute
respiratory
X syndrome (ARDS), ksepsis,
X metabolic acidosis, anaemia,
X pain,
ok distress
o Chronic
okbronchieco
o
o
panic,
foreign
body/​
a
spiration;
COPD,
lung
cancer,
B tasis, interstitial lungwdisease,
.B TB.
w.B
w
w
w
Ask aboutw
Speed of onset, cough, changew
in sputum (quantity, colour), w
haemoptysis, wheeze, chest pain (related to movement, pleuritic), chest
trauma,
lying
tpalpitations, dizziness, difficulty
t flat, recent travel, weightnloss;
eCardiac
emalignancy,
et
n
n
PMH
or respiratory problems,
old or exposure .to TB;
.
.
X Inhalers, home nebulizers,kXhome O , cardiac medication,kXallergies;
ok DH
o occupaSH Smoking (pack-​years), pets,
o
oo exercise tolerance, previous/​
ocurrent
B tion
B
B
.
.
(asbestos exposure).
w surgery/​immobility/​fracture/​
PE risk factors w
ww travel/​hospitaliza- w
w Recent
tion, oestrogen
(pregnancy, HRT, the pill),wmalignancy, previous PE/​ w
2
DVT, thrombophilia, varicose veins, obesity, central lines.
t
t
t
Obs
.neTemp, RR (11–​20 is normal),
.nBP,e HR, sats (should be >94%
.n),eO
­requirements (improving or worsening?).
X
X
X
ok
ofullk sentences, confusion, cyanosis,
ok CO flap,
for Ability to speak
o
o
Bo Look
B
B
. itching, swollen lips/​eyes,w.raised JVP, tracheal
tremor, clubbing, w
rashes,
shift and tug, use
of accessory muscles, abnormal
unequal air
w
w
w stridor, wheeze, bronchial breathing,
wwpercussion,
entry, crackles,
swollen/​red/​hot/​ w
tender legs, swelling of ankles, cold peripheries.
et
et
Investigations
PEFR If asthma suspected
(may be too ill); blds FBC, n
netWells
.nCRP,
.and
. U+E,
LFT,
D-​dimer (if PE suspected
score <4 E p. 284),
cardiac
X
X
X
k (May need physio or salineonebs
k to help)
cultures; Sputum
ok markers,andblood
oAFBs
o
o
send for M,C+S;
if
TB
risk;
ABG
(E
pp.
598–9),
keep on
Bo inspect
B
B
.
.
O if acutely SOB;w
ECG (E pp. 586–8); CXR (E w
pp. 596–7); portable if
w
w
unwell, though
wimage quality may be poor; Spirometry
w Should be done once ww
the patient has been stabilized to help confirm the diagnosis (E p. 600).
Treatment
et Sit all patients up and
egivet 15L/​min O – this saves.nlives.
etot
n
n
This
can be reduced later since CO
retention in COPD takes a while
.
.
X Check sats and ECGkinXall patients:
X
ok •develop.
o (E p. 291)
ok
o
o
o
Stridor—​call an anaesthetist
B • Wheeze—​give nebulizer
.B (E p. 279), eg salbutamolw5mg
.B ±ipratropium
w
500micrograms
STAT (drive by oxygen or air w
as appropriate)
w
w
w
ww
1
2
2
2
2​
2
• Unilateral resonance, reduced air entry ±tracheal deviation and shock—​
consider tension pneumothorax and treat urgently (E p. 285)
• Asymmetrical coarse crackles, dair entry, bronchial breathing—​consider
pneumonia (E p. 282)
• Symmetrical fine crackles, dair entry, iJVP—​consider LVF (E p. 288)
• Normal exam—​consider PE, asthma, cardiac, and systemic causes.
t
ok
Bo
t
e
X.n
e
X.n
ok
ww
o
B
.
w
ok
ww
o
B
.
w
Patients with chronic lung disease may normally have sats <92%. 88–​92% is a better target. See
BTS guidelines on emergency use of oxygen in adults at Mwww.brit-​thoracic.org.uk
1
t
e
X.n
ww
B
278
.B
w
ww
Chapter 8
.B
w
w
ww
w
Respiratory
t
t
t
.ne 8.1 Common causes ofXbreathlessness
.ne
.ne
Table
X
X
k Examination Investigations
ok
ok
History oo
o
Bo COPD
B
B
Usually
crackles,
hyperexpanded,
w. smoker, ±wheeze/​
w.CXR
change in
±cyanosed/​pursed-​
flat diaphragms;
w
w
w productive
wlook exclude pneumonia ww
lip breathing,
cough, worsening for infection and
and pneumothorax
wheeze
pneumothorax
ABG; sputum
t
t
e
e
et
n
n
Asthma
Known asthma,
Wheeze
±crackles, dPEFR; CXR; .n
.
.
X
X
recent exposurektoX look for signs
ok
o or of infection or exclude
okpneumonia
cold air, allergens
ando
pneumothorax
o
o
B
B eosinophil
drugs .(NSAIDs,
w Bvirusesβ-​ pneumothoraxww.ABG;
blockers),
count
w
w iWCC/​NØ/​CRP, ww
Pneumonia w Productive cough, Febrile, asymmetrical
green sputum,
air entry, crackles,
consolidation or
feels unwell
bronchial
breath
blunted angles on t
t
t
e
e
±pleuritic pain
sounds
±dpercussion CXR (E pp. 596–7);
n
n
.
.
.ne
sputum MCX
and S
X
X
k
ok
ok±hypoxia
PE risk factors,
iHR (may be
dPaCO
oo leg iJVP,
oABGs,
Bo Pulmonary
B
B
embolism
pain, .±pleuritic
only sign); may have .on
w pain and evidence of DVT;wcan
w dimer, CXRiD-​often
chest
w
shocked normal
w haemoptysis be severely w
ww
B
2
Pulmonary
oedema
.
kX
o
o
net
Pneumo​thorax
o
Bo
t
.ne
X
k
Pleural
effusion
ARDS
o
Bo
et
n
.
Anaemia/
kX​MI/​
arrhythmias
3
Anaphylaxis
Bo
o
et
n
.
kX
Known cardiac
problems,
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swollen legs
oo
B
.
Sudden
w onset
wwpleuritic chest
o
ww
o
w.B
t
.ne
kX
pain ±trauma.
Underlying lung
disease and
previous episodes
or tall, thin, male
Gradual onset
breathlessness,
±pleuritic chest
pain
Concurrent
severe illness
Chest pain,
palpitations,
dizziness, tiredness
iJVP, symmetrical
fine inspiratory
crackles, pink frothy
sputum, dependent
oedema, cold
peripheries
Unequal air entry
and expansion,
hyper-​resonant
±displaced trachea
(late)
t
.ne
X
k
o
onset,
wwSudden
itching, swelling,
urticarial rash,
new drugs/​food
of tension
pneumothorax;
CXR shows pleura
separated from ribs
ww
et
oo
B
.
w
.n
kX
Reduced expansion, Effusion on CXR
stony dull base
ww
ww
Hypoxic, very unwell New bilateral
infiltrates on CXR
Irregular or fast
Abnormal ECG
pulse, shocked, pale (E pp. 586–8),
dHb, icardiac
markers
Stridor, ±wheeze,
IM adrenaline,
shock, swollen lips
IV steroids
and eyes, blanching (E pp. 484–5);
rash
acute and
convalescent serum
tryptase
t
et
n
.
X
ok
ww
o
w.B
et
n
.
kX
o
o
B
.
w
ww
t
.ne
X
k
oo
B
.
ww Needle
decompression
w
.ne
X
k
o
w.B
Cardiomegaly + fluid
overload on CXR
(E pp. 596–7), ECG
may show ischaemia
or previous MI
ww
t
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Breathlessness and low sats
w
279
t
t
t
Asthma
.ne
.ne
.ne
X
X
X
A common chronic disease k
ok Kinflammation,
o characterized by variable airflow
okobstruction,
o
and hyper-​ro
esponsiveness that results in wheeze,
chest tightBo ness,
B
B
.
.
dyspnoea, andw
cough.
w
w breathlessness, wheeze and
Symptoms Episodic
wwchest tightness; family or ww
personal Hxw
of atopy (hayfever, eczema, asthma).
Signs Wheeze, tachypnoea, silent chest, hyperinflated chest.
et PEFR Reduced in acute .setting
et compared with best or predicted
et
Investigations
n
n
n
.
.
based
upon
age/​
h
eight,
or
diurnal
variation
on
self-​
m
onitoring
as
out-​
X
X
X
ok patient; ABG Normal or odPaO
ok with a dPaCO due to hyperventilation.
ok
o
o
3 Beware normal/​.rB
ising CO ?Patient tiring; CXR Hyperexpanded,
exB clude
w pneumothorax; Spirometryw
w.,BdFEV :FVC ratio.
pneumonia and
dFEV
w
Acute exacerbation
w Sit up and give 15L/​minwO . Salbutamol 5mg NEB ww
±ipratropium 500micrograms NEB and prednisolone 40mg PO (or
hydrocortisone
200mg IV). Drive the nebulizer
from O supply, not
et salbutamol
et 10–​1mask
et
air..n
Repeat
2.5mg NEB
every
5min and reassess.n
PEFR
n
.
X sats frequently. AntibioticskX
X
of infection.
ok and
o if evidence
ok RR >25.
o
o
o
3
Severe
Incomplete
sentences,
PEFR
<50%
of
best,
HR
>110,
B
.B <33% of best, silent chest,
.Bsats <92%, PaO
3 Life-​threatening
wPEFR
w
w
<8kPa, normalwPaCO , poor respiratory effort,
exhaustion, cyanosis,
w
w
ww
2
2
2
1
1
2
2
2
2
altered GCS, arrhythmia. 2Call ICU.
3 Near-​fatal CO2 retention. 2Call ICU.
2 Beware those with previous ICU admissions.
No improvement Call for senior help. Consider:
• Early ICU input/​assessment
• Aminophylline 0.5–​0.7mg/​kg/​h, discontinue any oral theophylline and
monitor levels (under senior guidance)
• Mg2+ sulfate 2g (8mmol) IV over 20min.
Improving Admit those in whom PEFR<75% predicted after 1h therapy;
gradually reduce supplemental O2 and step from nebs to inhalers over
several days; always check inhaler technique and ensure patient books
follow-​up with GP 48h post discharge.
Chronic treatment (E OHCM10 p. 182.) See Table 8.2, aiming for
minimum treatment resulting in symptom control; monitor PEFR; always
check inhaler technique before escalation; ensure allergen avoidance,
smoking cessation and co-​morbidities (GORD, nasal polyposis, OSA,
breathing pattern disorder) identified and controlled.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
.n
kX
o
w.B
ww
Bo
et
.n
kX
et
.n
kX
o
o
w.B
.n
kX
o
o
w.B
ww
ww
t
t
e
X.n
e
X.n
ok
ok
o
w.B
ww
ww
Low-​dose ICS and LABA (combination)
t
ok
e✓✓t
n
.
X
✓ ✓
e
X.n
Additional treatment (high-​dose ICS/​long-​acting muscarinic
agonist/​leukotriene receptor antagonist/​theophylline)
Oral steroids
ok
o
B
.
w
ww
✓
t
e
X.n
5
✓
✓
Medium-​dose ICS and LABA (combination)
Bo
t
k
1 o
o 2 3* 4*
B
✓ ✓ ✓ ✓
.
w
STEP
Salbutamol/​terbutaline
Low-​dose inhaled corticosteroid (ICS)
ok
o
B
.
w
✓
✓
* If no response to LABA, stop LABA use medium–​high-​dose ICS alone. BTS guidelines include
tables to predict PEFR where unknown. Source: data from Mhttps://​www.brit-​thoracic.org.uk/​
document-​library/​clinical-​information/​asthma/​btssign-​asthma-​guideline-​quick-​reference-​guide-​2016
ww
ww
e
X.n
Table 8.2 Simplified stepwise management of asthma (2016)
Bo
ww
ww
ww
B
.B
w
w
.B
w
w
wRespiratory
280
ww
w
Chapter 8
t
t
t
COPD
.ne (E OHAM4 p. 186.) X.ne
.ne
X
X
fixed airflow k
due to loss of elastic recoil
k in alveoli
ok K Predominantly
oofobstruction
o(bronchitis).
o
o
and narrowing
airways with excess secretions
Bo (emphysema)
B
B
2 Worrying signs dGCS,
CO .
w. risingcough,
w.
w
Symptoms Breathlessness,
isputum,wtight chest, confusion,
w NB iindex of suspicionwin (ex-​)smoker.
ww
dexercise tolerance.
Signs Wheeze, cyanosis, barrel-​chested, poor expansion, tachypnoea.
t with type 2 RF common.
et ABG Often deranged.nineCOPD,
et
Investigations
n
n
.
.
Compare
with
previous
samples
and
pay
close
attention
to
FiO
;
repeat
X
X
X
ok after 30min in seriously illopatients;
ok CXR Hyperexpanded,oflat
okdiaphragm
o
(look for evidence of
B
.Binfection, pneumothorax,wor.Bbullae); Spirometry
(E p. 600) dFEVw
, dFEV :FVC ratio (<70%).
w
Acute exacerbation
w Sit the patient up and give
wwthe minimum amount of ww
O to maintain sats ≥88% (aim for PaO 78kPa). Give salbutamol 2.5mg
±ipratropium
NEB (drive
leaving nasal O cannulae
et mask500micrograms
et by air,
et
on.n
under
if necessary) and prednisolone
30mg PO (or hydrocortisone
n
n
.
.
X200mg IV). Sputum for M,C+S.kX
X
Get an ABG and CXR (portable
ok Use
oobservations
ok if unwell).
ABG results and clinical
to guide further o
management:
o
o
B
Bregular nebs
• Normal ABG (for them)
Continue current O and give
w.BiFiO
w.watch
• Worsening hypoxaemia
, repeat ABG <30min,
for confusion
w
w
w prompt a repeat ABG sooner;wconsider NIV
ww
which should
2
2
2
1
1
2
2
2
2
2
• i CO2 retention or d GCS Request senior help 2 urgently; consider:
• ICU input/​assessment
• Aminophylline 0.5–​0.7mg/​kg/​h, discontinue any oral theophylline
and monitor levels (under senior guidance)
• NIV (Box 8.1).
Antibiotics Consider prescribing antibiotics (eg PO doxycycline or amoxicillin) if the patient has iSOB, fevers, worsening cough, purulent sputum,
or focal changes on CXR.
Chronic treatment (E OHCM10 p. 184) Smoking cessation is paramount.
Stepwise therapy with inhalers can reduce symptoms, reduce the frequency
and severity of exacerbations, and improve health status and exercise tolerance (Table 8.3). If still breathless despite maximal inhaler therapy, give
home nebulizers. If PaO2 consistently ≤7.3kPa (or ≤8kPa with additional
risk factors), long-​term O2 therapy aiming for a minimum of 15h/​d confers
survival advantage. Annual influenza and pneumococcal vaccines decrease
incidence of LRTI.3 Consider prescribing rescue packs (abx/​steroids) to
patients for acute (infective) exacerbation. Pulmonary rehab (see Box 8.2).
Complications Exacerbations, infection, cor pulmonale, pneumothorax,
respiratory failure, lung cancer (beware haemoptysis and weight loss).
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
o
w.B
t
.n
kX
o
o
w.B
ww
t
e
X.n
ww
et
.n
kX
ww
e
X.n
ww
t
e
X.n
k
k
oo
oo
B
B
.
.
w
Machines assist
through a tightly fitting
Bi-​level posiwventilation
wwmask.
w
tive airwayw
pressure (BiPAP) used in COPD
with a pH ≤7.35 w
wpatients
and CO ≥6.0kPa who have failed to respond to initial medical therapy
reduces
and length of admission.
t Patients who need NIVnusuestayt mortality
et
ally
on the respiratory ward.nore HDU/​ICU. Continuous positive
n
.
.
Xairway pressure (CPAP) is not
kXNIV since it does not helpowith
kXmechok anics
of ventilation (Eo
p.o288).
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
ok
.n
kX
o
w.B
ww
Bo
et
.n
kX
K Box 8.1 Non-​invasive ventilation (NIV)
2
NICE guidelines available at Mguidance.nice.org.uk/​CG101
Global Initiative for Chronic Obstructive Lung Disease. 2017 report. Mhttp://​goldcopd.org/​
wp-​content/​uploads/​2016/​12/​wms-​GOLD-​2017-​Pocket-​Guide.pdf
2
3
B
.B
w
w
.B
w
w
w
w
w
Breathlessness and low sats
w
281
t
t
et
.ne 8.3 Simplified COPD severity
.nassessment
.ne
Table
and treatment (GOLD
X
X
X
k
ok guidelines)
ok
oo
o
Bo GOLD Yearly w.BDyspnoea
B
Treatment .Severity of airflow
w limitation (FEV % w
stage exacerbations
w
w
ww predicted)
w
A
1 or less
Breathless only SABA or
≥80—​GOLD 1
on strenuous tSAMA
(Mild)
et
e
et
exercise
n
n
n
.
.
.
X
X
Having
or/​+ 50–​79—​k
ktoXstop LAMA
ok B 1 or less
owalking
o GOLD 2
(Moderate)
on
LABA
o
o
o
B
B 49—​GOLD 3
C
2 or more .BBreathless only LAMA +
30–​
w on strenuous LABA orww.(Severe)
(or 1 hospital
w
exercise
admission)
LABA
w
w+ ICS
ww
D
2 or more
Having to stop ICS + LABA + <30—​GOLD 4
(or 1 hospital
on walking
(triple (Very severe)
t
e
etLAMA
et
admission)
therapy)
n
n
n
.
.
.
X data from Global Initiative forkChronic
X
X
Lung Disease, 2017k
ok Source:
ouploads/​2016/​Obstructive
o Greport,
Mhttp://​goldcopd.org/​wp-​content/​
12/​wms-​GOLD-​2017-​Pocket-​
uide.pdf
o
o
o
B
.B
.B
wcommon
wCOPD
Table 8.4 Some
inhalers for asthma and
w
w
w
w
ww
1
Drug type
Short-​acting
β agonist
Medication
Salbutamol
Terbutaline
Inhaled steroids Beclometasone
Budesonide
Fluticasone
Ciclesonide
Inhaled steroids Beclomethasone/​formoterol
and long-​acting Budesonide/​formoterol
β agonist
(combination) Fluticasone/​salmeterol
Fluticasone/​vilanterol
Long-​acting
Tiotropium
anticholinergic Umeclidinium
Glycopyrronium
Aclidinium
Vilanterol and umeclidinium
Long-​acting
β agonist and
Indacaterol and glycopyrronium
long-​acting
anticholinergic Oldaterol and tiotropium
(combination) Formoterol and aclidinium
net
net
.
kX
o
Bo
.
kX
o
o
w.B
ww
o
Bo
et
.n
kX
o
o
w.B
ww
ok
Bo
et
.n
kX
o
o
w.B
t
e
X.n
ok
o
w.B
ww
et
o
o
w.B
t
ok
o
w.B
ww
t
t
ww
t
e
X.n
e
X.n
Patients with chronic lung disease who take part in a structured 8–​12wk pulmonary
rehabilitation programme with a graduated exercise regimen see increased exercise
tolerance and improved well-​being,4 although this does not reverse pathological processes or improve spirometry. Diet and other lifestyle advice are also covered.
ok
Bo
ww
e
X.n
Box 8.2 Pulmonary rehabilitation
e
X.n
ww
.n
kX
ww
t
e
X.n
Colour
Blue
Blue
Brown
Brown
Orange
Red
Pink
Red
Purple
Yellow
Grey
Green
Orange
Green
Red
Yellow
Green
Orange
ww
et
.n
kX
Trade name eg
Ventolin®
Bricanyl®
Qvar®
Pulmicort®
Flixotide®
Alvesco®
Fostair®
Symbicort®
Seretide®
Relvar®
Spiriva®
Incruse®
Seebri®
Eklira (Genuair)®
Anoro®
Ultibro®
Spiolto®
Duaklir®
4
ok
ww
o
B
.
w
ok
ww
o
B
.
w
Summarized at Mhttps://​www.brit-​thoracic.org.uk/​document-​library/​clinical-​information/​
pulmonary-​rehabilitation/​bts-​quality-​standards-​for-​pulmonary-​rehabilitation-​in-​adults/​
ww
B
.B
w
w
.B
w
w
wRespiratory
282
ww
w
Chapter 8
t
t
t
Pneumonia
(E OHAM4 p. 166.)
.ne
.ne
.ne
X
X
X
signs CURB-​65 score
≥3 (see ‘Severity’, E p. 282).
ok 2 WorryingCough,
oksputum,
okbreathless,
o
o
purulent
pleuritic chestBpain,
Bo Symptoms
B
. confusion, anorexia. w.
haemoptysis, fever,
unwell,
wwiHR,
Signs itemp,w
iRR,
dsats, unequal air entry,
wwreduced expansion, dull
percussion, bronchial breathing.
Severityt The CURB-​65 criteria (see Fig.
8.1) are a validated set of variethat support (but do not replace)
etclinical
et
ables
judgement in community-​
n
n
n
.
.
.
X
pneumonia on whether
kX to admit. In the out-​poatient
kXsetting,
ok acquired
omit urea to get a CRB-​o
65oscore; patients scoring 0 (and
possibly 1–​2)
o
o
B
are suitable for home.B
treatment.
.B
wiWCC;
w
Investigations blds
i neutrophils; iCRP;
bld cultures. If CURB-​
w
w
w cultures If CURB-​65 ≥3 (or CURB-​
w 65=2 and not had anti65 ≥2; Sputum
5
ww
6
biotics); Urine If CURB-​65 ≥2 test for pneumococcal antigen; if CURB-​65
≥3 or clinical suspicion, test for legionella antigen; ABG dPaO2 (±dPaCO2
due to hyperventilation but not if tiring or COPD); CXR MAY show focal
consolidation; repeat at 6wk if ongoing symptoms or high risk for malignancy/​empyema.
Treatment Sit up and give O2 as required. Give antibiotics according to
local policy or E p. 181 for empirical treatment. Look for dehydration
and consider IV fluids. Most patients who require IV antibiotics can safely
be switched to PO therapy by day 3.7 Offer a 5d course of antibiotic
therapy for patients with low-​severity CAP; consider a 7–​10d course
of antibiotic therapy for patients with moderate and high severity CAP.
If symptoms not resolving by day 3, repeat CRP and CXR to exclude
pleural effusion/​empyema.
Complications Empyema, respiratory failure, sepsis, confusion.
Hospital-​acquired pneumonia K Pneumonia developing ≥48h after admission
and not felt to have been incubating at time of admission. Causative organisms will include Gram –​ve bacilli (eg Pseudomonas or Klebsiella species,
E. coli.) as well as S. pneumoniae and S. aureus (including MRSA). Symptoms
and signs can be severe, particularly in frail patients with other comorbidities,
and lung necrosis and cavitation may develop. Empirical antibiotic selection
should be guided by local policy ±discussion with a microbiologist.
Aspiration pneumonia K Aspiration of gastric contents refluxing up the
oesophagus and down the trachea may lead to a sterile chemical pneumonitis. Alternatively, oropharyngeal bacteria may be aspirated causing
a bacterial pneumonia. Risk factors include dGCS (eg sepsis, anaesthesia,
seizures), oesophageal pathology (eg strictures, neoplasia), neurological
disability (eg dementia, MS, Parkinson’s disease), or iatrogenic interventions (eg NG tube, OGD, bronchoscopy). At-​risk patients can be identified by bedside swallow evaluation (E p. 356). Care is supportive, with
O2 supplementation, suctioning of secretions, and attention to prevention of further aspiration (involve SALT and chest physio). Empirical antibiotics can be of benefit if bacterial pneumonia suspected (eg persistent
fever, purulent sputum)—​eg co-​amoxiclav 625mg/​8h PO or 1.2g/​8h IV
with metronidazole 400mg/​8h PO or 500mg/​8h IV.
t
t
e
X.n
ok
Bo
ok
ok
ww
et
et
.n
kX
o
o
o
w.B
o
o
o
w.B
et
o
o
w.B
ok
o
o
w.B
t
ok
o
w.B
ok
e
X.n
ok
o
w.B
ww
t
t
e
X.n
ok
o
B
.
w
6
ww
ww
t
e
X.n
e
X.n
ok
o
B
.
w
NICE guidelines available at Mguidance.nice.org.uk/​CG191
Lim WS, et al. Thorax 2003;58:377 full-​text available free at: Mwww.ncbi.nlm.nih.gov/​pmc/​
articles/​PMC1746657
7
Oosterheert JJ, et al. BMJ 2006;333:1193 full-​text available free at: Mwww.ncbi.nlm.nih.gov/​pmc/​
articles/​PMC1693658
5
ww
t
e
X.n
ww
Bo
.n
kX
ww
t
e
X.n
ww
et
.n
kX
ww
Bo
.n
kX
ww
et
.n
kX
ww
et
.n
kX
ww
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e
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o
B
.
w
ww
Bo
t
e
X.n
o
B
.
w
ww
ww
ww
B
.B
w
ww
t
.ne
X
k
oo
B
.
w
o
Bo
t
.ne
X
k
et
n
.
kX
t
ok
ok
Bo
ww
Yes
et
X.n
t
.ne
X
k
oo
B
.
w
ww
Give antibiotics
eg amoxicillin
500mg/8h PO
o
Bo
3–5
High severity
(risk of
Hospital
t
o
B
.
w
ww
Hospital
Supportive care
Supportive care
Give antibiotics eg
amo
PO plus clarithromycin
Consider transfer to
critical care unit (especially
if CURB-65 = 4 or 5)
t
.ne
Send pleural fluid
(if present) for culture
and pneumococcal
antigen testing
o
o
w.B
ww
Give antibiotics eg coamoxicla
clarithromyc
Send sputum and blood
for culture
oo
B
.
ww
t
.ne
X
k
Send urine for legionella
and pneumococcal antigen
testing
w
Send pleural fluid (if
present) for culture and
pneumococcal antigen
testing
t
Give antibiotics
eg amoxicillin
500mg/8h PO
ww
kX
Send sputum for culture
if no recent antibiotics
Send urine for
pneumococcal
antigen testing
and consider legionella
and mycoplasma testing
Hospital
ww
)
.ne
X
ok
Send blood cultures
ok
Home
ok
o
B
.
w
Other reasons for
admission (unstable
co-morbidity, social)
No
et
n
.
X
ww
.B
w
ww
2
Moderate severity
(risk of death 9%)
ww
Bo
o
et
n
.
kX
oo
e
X.n
Low severity
(risk of death <3%)
et
n
.
X
o
w.B
.n
kX
ww
o
w.B
.ne
X
k
ww
et
.n
kX
Consider atypical and viral
pathogen serology (baseline
and follow-up samples)
oo
B
.
w
ww
ww
Fig. 8.1 Severity assessment and investigations in community-​acquired
­pneumonia. Adapted by permission from BMJ Publishing Group Limited.
British Thoracic Society guidelines for the management of community acquired
­pneumonia in adults: update 2009, Lim, W.S. et al. Thorax 2009 64 (Suppl 3):iii1.
t
e
X.n
ok
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Bo
o
et
n
.
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.ne
X
k
t
ww
ww
o
w.B
et
n
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t
o
o
B
.
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ww
et
n
.
X
ok
o
o
w.B
w
283
et
• Confusion
• Urea >7mmol/l
• Respiratory rate ≥30/min
• Blood pressure
(SBP <90 or DBP ≤60mmHg)
• Age ≥65 years
ww
w
w
Breathlessness and low sats
CURB-65 severity score:
or each feature present:
o
Bo
.B
w
w
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
wRespiratory
284
ww
w
Chapter 8
t
t
t
Pulmonary
embolism (E OHAM4
.ne
.ne p. 120.)
.ne
X
X
X
Often none except
may have pleuritic
ok Symptoms
oklegbreathlessness;
oinkTable chest
o
o
haemoptysis, dizziness,
pain; consider risk factors
Bo pain,
B
B
.
. pleural 8.5.
Signs iJVP, iRR,wiHR, dBP, RV heave, hypotension,
w
w and tachypnoea maywbewthe only clinical signs.rub, ww
±pyrexia. Tachycardia
w
Investigations D-​dimer Will be raised in many situations (infection, malignancy,
MI, CVA
name a few) while a normal
D-​dimer must be interpreted tin
et tocontext
et tachycardia
e
the
clinical
(Box 8.3); ECG.n
(sinus
commonest finding),
n
.
.ndO
X
X
X
RBBB,
inverted
T
waves
V1–​
V
4
or
S
Q
T
;
ABG
type
1
RF
(dCO
,
±
ok (if large PE); CT-​PA Is the definitive
ok imaging modality, thoughoV/​oQkscan may be)
o
o
B
B failure, pregnancy. w.B
used, eg in those with.renal
Acute treatment w
Sit w
up (unless dBP) and give 15L/​
O . If life-​threatening
w
wwminarrange
(hypotensionw
+shock) seek immediate senior support,
an urgent CT-​ w
PA + echo and consider thrombolysis. Otherwise parenteral anticoagulation
(E pp.
eg enoxaparin 1.5mg/​kg/​
and pain relief; IV fluids if dBP.
et420–2),
et2pp.4h SC
et
n
n
n
Chronic
treatment Anticoagulation .(E
420–2) eg warfarin/​DOAC.
.
.
X
X
X
ok Length of treatment willodepend
ok on risk factors/​context.ook
o
B
K Box 8.3 Clinical
PE.B
w.B risk assessment for
w
w
w
PEs are common
and potentially fatal, but associated
with non-​specific clinical
w
w
ww
8
1
3 3
2
2
2
9
signs. The CT-​PA offers excellent diagnostic accuracy but exposes your patient
to 3.6yr of background radiation, along with nephrotoxic IV contrast medium,
while taking up significant resources. So can D-​dimer testing help? Remember,
the negative predictive value of any test is determined by the prevalence of
whatever disease you are testing for: the value of D-​dimer testing lies in the excellent negative predictive value when the risk of a PE is low. In those at high risk,
negative D-​dimer levels do not provide sufficient reassurance.
The Wells score for PE (Table 8.5) is a clinically reliable method of identifying the
risk of PE, and hence deciding on further testing.
•Those scoring ≤4 are low risk: test for D-​dimers.10 If elevated, proceed to
CT-​PA; if negative, then consider alternative diagnoses
•Those scoring >4 are high risk: proceed to CT-​PA testing and start treatment
dose of LMWH.
et
et
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kX
o
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et
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et
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oo
oo
B
B
.
.
w
Clinical feature w
Points
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wwvein palpation) 3
ww
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3
t
t
HR >100
1.5 et
e
e
n
n
.
.
X>3d immobilization or surgery inkpast
X 4wk
X1.5.n
k
k
o
DVT/​PE
oo
oo 1.5
Bo Previous
B
B
.
.
Haemoptysis
1
w
wwtreatment or treatment in past
w
Malignancy (current
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ww
Source: data from Wells et al. Thromb Haemost 2000;83:358.
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et
n
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.
.
.
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ok
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o
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w
w
w
ww
Bo
o
et
.n
kX
Table 8.5 Wells score for pulmonary embolism
NICE guidelines available at Mguidance.nice.org.uk/​CG144
3mth may suffice if low risk (eg 1st PE with identified risk factor now removed); if higher risk
(recurrent or unprovoked PEs, or thrombophilia) treatment may need to be long term.
10
In pregnancy, D-​dimer testing is uninterpretable. If clinical suspicion, then a Doppler U/​S of leg
veins is the safest initial investigation—​treat if DVT seen. If this is negative, a half-​dose V/​Q scan
provides an acceptable balance of diagnostic utility with radiation exposure. The risk of CT-​PA is
not to the foetus (which can be shielded) but to proliferating maternal breast tissue.
8
9
B
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w
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w
w
w
w
Breathlessness and low sats
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285
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t
et E p. 204)
Spontaneous
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.n(OHAM4
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X
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X
spontaneously
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ok K May occurlungapparently
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ok
o
disease oroinjury (secondary).
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B
. thin, male; Marfan’s; recent
Risk factors Primaryw
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w
w
aspiration or chest
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w
ww
mechanical ventilation.
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t resonant and reducednairet entry on affected side, tachypeHyper-​
et
Signs
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n
.
.
.
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X fractured ribs.
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ok line of
Investigations CXR Lung markings
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o
o
o
B pleura seen away from
w.Bthe periphery.
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Treatment Sit up w
and give 15L/​min O . Chest drain/​
aspiration as directed by
w
w(E p. 286). In essence, primary
w pneumothoraces can po- ww
BTS guidelines
tentially be discharged, while secondary pneumothoraces require admission
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et aspiration (E p. 552) or,.more
et usually, drainage (E pp. 554–5).
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.
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X Tension pneumothorax
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w
w with unilateral hyper-​ ww
may be hypotensive,
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11
2
resonance and reduced air entry; iJVP and may have tracheal deviation
away from the side of the pneumothorax. 2 This is an emergency, it will
rapidly worsen if not treated. Sit up and give 15L/​min O2. Treat prior to
CXR. Insert a large cannula (orange/​grey) into the 2nd intercostal space,
midclavicular line. Listen for a hiss and leave it in situ; insert a chest drain
on the same side. If there is no hiss, leave the cannula in situ and consider
placing a 2nd cannula or consider alternative diagnoses; a chest drain is
usually still required to prevent a tension pneumothorax accumulating.
et
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et reflects an imbalance between
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Bo disruption
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. transudates
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w nephrotic syndrome, hypothyroidism,
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et malignancy, infection, vasculitides,
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et
n
.
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pleural
w.B
w
w
upper limit of normal
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w
w
ww
Symptoms The patient may be breathless with pleuritic chest pain.
Signs Stony
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t with
et dull
eangle
et
Investigations
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a meniscus E pp. .596–7.
n
n
n
.
.
XTreatment Sit up and give 15L/​mkinXO . Investigate the cause; if thekX
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oaideffusion
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diagnosis
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o
o
B (draining >1.5L/​24hwmay
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w
w
w
ww
Pleural effusion (E OHAM4 p. 216.)11
2
British Thoracic Society guidelines available at Mhttps ://​www.brit-​thoracic.org.uk/​standards-​of-​
care/​guidelines/​bts-​pleural-​disease-​guideline/​
11
B
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Chapter 8
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Respiratory
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t
t
Algorithms
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et
et YES
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.
.
.
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X see Fig 8.3
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w NO
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w
ww
Bo
If Bilateral/Haemodynamically unstable
proceed to Chest drain
Age >50 and significant
smoking history
Evidence of underlying
lung disease on exam or
CXR?
Primary
Pneumothorax
Aspirate
16–18G cannula
Aspirate <2.5I
Size>2cm
and/or
Breathless
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Consider discharge
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o
t
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*In some patients with a large
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ww
et
.n
kX
oo
oo
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B
.
.
Fig. 8.2 Treating spontaneous
pneumothorax in patients
w or evidence
wover 50 with no
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of underlying w
lung disease. Adapted
w
w
ww
by permission from BMJ Publishing Group Ltd, Management of spontaneous
pneumothorax: British Thoracic Society pleural disease guideline 2010, MacDuff,
A. et al.
etThorax 2010 65 (Suppl 2):ii18. .net
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Breathlessness and low sats
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w
ww
B
If Bilateral/Haemodynamically unstable
proceed to Chest drain
Age >50 and significant
smoking history
Evidence of underlying
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CXR?
Secondary
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Breathless
.
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o
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Fig. 8.3 Treating pneumothorax in patients over 50 with significant smoking
history or evidence of underlying lung disease. Adapted by permission from
BMJ Publishing Group Ltd, Management of spontaneous pneumothorax: British
Thoracic Society pleural disease guideline 2010, MacDuff, A. et al. Thorax 2010 65
(Suppl 2):ii18.
et
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Chapter 8
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X
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X
kdyspnoea,
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oheart
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o
sputum; coexistent
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B
B
. fine inspiratory basal crackles,
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Signs iJVP, tachypnoea,
cold
w
w
w
w
hands and feet;
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suggests right heart failure. ww
w
w
Investigations blds (Look specifically for anaemia, infection or MI): FBC,
U+E, tCRP, cardiac markers; BNP (normal
unlikely in cardiac
e ABG May show hypoxia;.nECG
et Excludelevels
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n
.
X may show old infarcts,kX
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o
o
B
B LV function/​ejection fraction.
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Sitw
up and give 15L/​min O . If the
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w
w early as CPAP and ICU may
w be required. Otherwise w
call an intensivist
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X guided by blood pressure:kX
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o
o
B
B h every
infusion (eg GTN starting
w.B at 4mg/​h and increasing
wby.2mg/​
10min, aimingw
to keep systolic >100; usual range
4–​10mg/​h; E p. 203)
w
w
w
ww
B
2
2
• Systolic <100 The patient is in shock, probably cardiogenic. Get senior
help as inotropes are often required. Do not give nitrates
• Wheezing Treat as for COPD alongside above-​mentioned treatment
• No improvement Give furosemide up to 120mg total (more if chronic
renal failure) and consider CPAP (see Box 8.4). Insert a urinary
catheter to monitor urine output, ±CVP monitoring. Request senior
help. Consider HDU/​ICU.
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w
Once stabilized, the patient will need daily weights ±fluid restriction. Document LV function with an echo and optimize treatment of
heart failure (E p. 274). Oral bumetanide may be preferred to oral
furosemide for diuresis since absorption is said to be more predictable
in the presence of bowel oedema, though evidence for this is lacking.
Always monitor U+E during diuresis: The heart-​sink patients are those
with simultaneously failing hearts and kidneys who seem fated to spend
their last days alternating between fluid overload and AKI—​close liaison
with the patient’s GP and palliative care teams is as essential as ever here.
t
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t
o
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o
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n
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o
o
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B
B power to
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w
w
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w
w
the acute treatment of pulmonary oedema or the chronic treatment
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et apnoea (may use nasal CPAP).
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et
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K Box 8.4 Continuous positive airway pressure (CPAP)
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w
w
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Breathlessness and low sats
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289
t
t
t
SVC
.neobstruction (E OHCM10
.np.e528.)
.ne
X
X
X
k
facial/​arm swelling,o
headache.
ok Symptoms Breathlessness,oorthopnoea,
ok facial oedema,
o
engorged
veins,
stridor.
Bo Signs Facial plethoraw(redness),
B
B
.
.
Pemberton’s test Elevating the arms over the headw
for 1min results in inw
w
creased facial
wplethora and iJVP.
w
ww
Investigations CXR/​CT Mediastinal mass, tracheal deviation, venous congestiontdistal to lesion; Other Sputum cytology
atypical cells.
e Seek senior input early.
etSit up for
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n
n
n
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.
.
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B
B
.
.
treatment
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ww distress syndrome (ARDS)
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w
w
K Acute-​onset respiratory failure due to diffuse alveolar injury following
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eoft
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.
.
.
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B Symptoms Breathlessness,
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w
w
w underlying condition. ww
B
2
Investigations CXR Bilateral infiltrates.
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treat underlying cause. Often requires ventilation.
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Chapter 8
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ENT
Bo 2 Airway Acute
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w. TEAM URGENTLY
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ARREST
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w If no palpable pulse—​CALL ARREST
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2 Circulation
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t forattempt
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n
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xamine the neck
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.
X If choking, follow algorithmkinXFig. 8.4
ok ••Avoid
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disturbing/​upsetting
o
o
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w Owhatever
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• Offer supplemental
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ww
ww
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senior anaesthetist
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n
n
• .Monitor
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.
X Check temp
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X
ok ••Take
ok ward staff or check notes
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brief history fromorelatives/​
o
o
B
.B itching (?anaphylaxis) w.B
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w
w
w causes’)
ww
2
2
•Await anaesthetic and ENT input
•Request urgent portable CXR
• Call for senior help
• Reassess, starting with A, B, C . . .
t
t
t
.ne
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X
X
X
ok Life-​threatening causes
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ok
o
o
Bo 2• Infection
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w
•Tumour w
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ww
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t
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e
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et
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.
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o
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Fig. 8.4 Adult choking treatment algorithm, 2015 guidelines. Reproduced with
the kind permission of the Resuscitation Council (UK).
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o
et
n
.
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et
n
.
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o
o
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.
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Usually, the cause of coughing is obvious (Box 8.5). Chronic (>8wk), unexplained coughing with a normal CXR and the absence of infective features requires a considered approach. Is there diurnal or seasonal variation
in coughing (cough-​variant asthma; do PEFR diary, lung function testing, and a
trial of inhaled steroids)? Is there a history suggestive of gastro-​oesophageal
reflux (trial of PPI)? Does the onset of a dry cough follow the introduction
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ok imo
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w
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et Liver
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pp.
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Bo 2 Worrying features
B
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w. expansile
w.vomiting,
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w E p. 294.
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temesis, massive
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et about Pain
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n
n
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ok
okmesenteric
o
o
bowel syndrome (IBS),odiverticular disease, adhesions,
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w
w pregnancy, ovarian cyst, w
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t porphyria. See Tablen9.1
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w loss, breath- w
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w inlumps,
ww lastweight
lessness, rashes,
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et
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B
B
.
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w
w
tension, ascites,
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peritonitis
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w
w
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t
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ternal
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B
B
.
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w
w
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of reproductive
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etECG To exclude MI; Erect.nCXR
et To exclude perforation;.nPlain
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n
.
AXR
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X
X
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ok if hepatobiliary cause suspected;
ok CT abdo Discuss with senior.
ok
o
o
o
B Treatment Givewall.B
patients O , analgesia ±antiemetics;
w.B insert a urinary w
w
w
catheter if unwell.
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w
w
w
2+
2
Shocked IV fluids 3urgent senior review
Peritonitic With IV fluids, IV antibiotics 3urgent senior review
>50yr in severe pain ?AAA, IV fluids 3urgent senior review
Abdo pain and vomiting Consider obstruction, IV fluids, NG tube, AXR
(E pp. 602–3) 3urgent senior review
• GI bleed Resuscitate with IV fluids (E p. 304) 3urgent senior review.
et
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Chapter 9
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t
t
t
.ne 9.1 Common causes ofXabdominal
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Table
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X
ok
ok
ok
History
Examination Investigations
o
o
Bo 3Perforation w
B
B
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under
. onset, severe Peritonitis,
w. Gas
abdominal pain
±bowel sounds
diaphragm, acidotic
w
w
w
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Pain, distension,
Distension,
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w
w
w
obstruction
nausea, vomiting,
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constipation
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t
t
e
e
et
sounds
n
n
n
.
.
.
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Sudden
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X
X
X or
pain, previous
acidotic,
ok infarction
ok arterial generalized
ok±AF
o
o
o
disease,
±AF
tenderness
previous
MI
B
.B
.BECG on
w
w
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w periumbilical),
wwRIF iWCC, iCRP
ww
tenderness,
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t
e
e
et
n
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.
X
previous hernia
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ok hernia
oheartburn,
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o
o
oo need for
B
B
B
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.
.
w iWCC, iCRP
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itemp, epigastric
w vomiting, diarrhoea tenderness,
wwno
ww
peritonitis
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tTender ±mass
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oo
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.
w
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t
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X
k
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iglucose, dCa2+
oo
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w
ww
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n
n epigastric
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pain radiating to back,
pancreatitis
.
.
.
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X
X
vomiting, anorexia,
ok
okgallstones tenderness,
ok
ialcoholoor
dbowel sounds
o
Bo 3Abdominal w
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B
Abdominal
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back pain, collapse,
unwell, oftenw (bedside if
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w
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e
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n
n
.
.
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ok
o
oo CTnon-​
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w
ww RUQ pain, gallstone tenderness,
w
ww
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ettenderness,
n
exam abnormal USS
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t
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.
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o
w.B
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o
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ww
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musculoskeletal
t
e
X.n
Caecum, appendix,
right ovary and
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w
297
et
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ww
et
n
.
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w
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ww
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n
.
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oo
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k
oo
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.
w.B
Fig. 9.1 Abdominalw
organs and pain, by region.
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w
w
w
ww
I Box 9.1 Causes of abdominal pain in this chapter and
elsewhere
et
et
et
n
n
n
.
.
.
Bowel
X
ok Adhesions/​ischaemia E p.o299okX Appendicitis E p. 299ookX
o
B
Diverticular disease E.p.
Dyspepsia/​peptic
w B301
w.Bulcers E p. 300
Gastroenteritis E
p. 313
Hernias E
p. 298
w
w
w
w
ww
Inflammatory bowel disease E p. 315
Irritable bowel syndrome E p. 314
Obstruction E p. 298
E p. 297
t
t
et
ePerforation
n
n
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.
.
.ne
X
X
X
ok Biliary colic/​cholecystitis Eopp.ok301–2 Hepatitis E p. 321 ook
chronic)
Bo Pancreatitis (acute/​w
.B E p. 302
.B
w
Genitourinaryw
w
ww
ww
o
Bo
Ectopic pregnancy E p. 512
Ovarian cyst E p. 514
Testicular torsion E p. 476
o
Bo
t
.ne
X
k Other
Endometriosis E p. 514
Pelvic inflammatory disease E p. 514
t
o
o
w.B
Abdominal aortic aneurysm E p. 487
ww
et
n
.
kX
o
Renal colic E p296
ww
t
Bo
oo
B
.
w
.n
kX
3 Perforation (E OHCM10 p. 606.)
Causes Peptic ulcer, appendicitis, diverticulitis, inflammatory bowel
disease, bowel obstruction, GI cancer, gallbladder.
Symptoms Acute abdominal pain worse on coughing or moving;
PMH Peptic ulcer, cancer, IBD; DH NSAIDs; SH Alcohol.
Signs iHR, ±dBP, iRR, peritonism (abdo tenderness, guarding, rebound,
rigidity), reduced or absent bowel sounds.
Investigations blds iWCC, dHb, iamylase, ilactate; CXR Erect film shows
air under the diaphragm, ±obstruction on AXR; ABG Acidosis.
Management 2 Seek senior review; resuscitate with IV fluids, 15L/​min O2,
good IV access (large ×2), analgesia (eg morphine 5–​10mg IV with cyclizine
50mg/​8h IV), NBM, and urgent X-​match 4 units; IV antibiotics (eg co-​
amoxiclav 1.2g/​8h IV), insert NG tube and urinary catheter, consider emergency CT once stable, prepare for emergency laparotomy (E p. 114).
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et
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w
ww
w
Gastroenterology
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t
t
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X
X
X
ok
ok
ok
o
of
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Bo Box 9.2 Causes
B
w.
w.
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w
w
w wall Tumours, IBD, diverticular
w disease, infarction, con- ww
Within the bowel
genital atresia, Hirschsprung’s disease.
etthe bowel lumen Impacted .faeces,
et FB, intussusception, strictures,
et
Inside
n
n
n
.
.
polyps,
gallstones.
X
X
X
ok Paralytic ileus (pseudo-​obstruction)
ok Post-​op, electrolyte imbalance,
ok uraemia,
o
o
o
B
DM, anticholinergic .drugs.
wB
w.B
w
w
w
w
ww
Symptoms Vomiting (may be faeculant), colicky abdo pain, pain may
improve with vomiting, constipation (±absolute—​no flatus or stool),
et anorexia, recent surgery..net
et
bloating,
n
n
.
.
Signs
iHR
±dBP,
iRR,
distended
abdomen,
absent
or
tinkling
bowel
X
X
ok sounds, peritonitis, scarsofrom
ok previous surgery, hernias.ookX
o
B
B Look for dilated
Investigations blds Mild .iWCC
and iamylase ±acidosis; .AXR
w Bor volvulus
w
bowel (?small or
large)
(E pp. 602–3);
erect CXR ?free air.
w
w
w
Managementw
Bowel obstruction may need w
fluid resuscitation and anal- w
B
gesia, treat according to the type and location of the obstruction:
• Strangulated Constant severe pain in an ill patient with peritonitis
(acute abdomen); can be small or large bowel. This will require urgent
surgery especially if caused by a hernia
• Small bowel Early vomiting with late constipation, usually caused by
hernias, adhesions, or Crohn’s. Treat conservatively with NBM, a NG
tube, and IV fluids (E pp. 394–7)—​often referred to as drip and suck—​
until the obstruction resolves; surgery if patient deteriorates. K+ is often
lost into the bowel and needs to be replaced in fluids (eg 20mmol/​L)
• Large bowel Early absolute constipation with late vomiting, usually
caused by tumours, diverticulitis, volvulus (sigmoid or caecal) or faeces.
IV fluids, NBM and refer to a senior surgeon. Urgent surgery may
be required if the caecum is >10cm across on AXR otherwise a CT,
colonoscopy, or water-​soluble contrast enema may be requested to
investigate the cause. Surgery is usually required except for:
• sigmoid volvulus—​sigmoidoscopy and flatus tube insertion
• faecal obstruction—​laxative enemas (E p. 207)
• colonic stenting—​may be offered for tumour palliation
• Paralytic ileus Loss of bowel motility can mimic the signs and symptoms of a
mechanical blockage. It is a response of the bowel to inflammation locally
(eg surgery) or adjacently (eg pancreatitis). The main distinguishing feature
is the relative lack of abdo pain, although the pathology responsible for the
ileus may cause abdo pain itself. USS abdo, contrast enema, or CT may
be required to exclude mechanical obstruction. Treat conservatively with
NBM, NG tube, IV fluids (E pp. 394–7) until the underlying pathology
improves. Check and correct electrolyte abnormalities, including K+ and
Mg2+ both of which may need to be replaced.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
et
n
.
kX
.ne
X
k
oo
B
.
w
.n
kX
t
ww
ww
et
n
.
kX
ww
et
n
.
X
ok
o
o
w.B
ww
et
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X
k
ww
t
e
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ok
Bo
w
t
o
w.B
t
.ne
X
k
o
w.B
ww
et
n
.
X
o Complications Strangulation,
o bowel infarction, bowel perforation,
ok dK ,
o
o
o
B
hypovolaemia.
w.B
w.B
w
w
w
w
ww
+
B
.B
w
w
.B
w
w
w
w
w
Abdominal pain
w
299
t
t
t
Adhesions
.ne
.ne
.ne
X
X
X
Previous surgery, abdominal
k sepsis, IBD, cancer, endometriosis.
ok Causes
ointermittent
oktenderness,
o
o
Symptoms and signs Chronic
abdominal pain
and
Bo may
B
B
.
develop bowel
(distension, vomiting,
w. constipation).
wwobstruction
Managementw
Analgesia
and stool softeners; w
maywneed operative division ww
of adhesions, but this may lead to new adhesions forming.
Bowel
infarction (EeOHCM10
p. 620.)
t
etischaemia/​
ePRt
n
n
n
.
.
.
Symptoms
Unwell,
sudden-​
o
nset
severe
constant
abdominal
pain,
X PMH AF, MI, polycythaemia.
kX
kX
ok blood;
o
o
o
o
o
Signs iHR (?irregular),
iRR, itemp, cold extremities,
generalized
B tenderness
.B±dBP,signs.
but few
wspecific
w.B
w
w
Investigationswblds iWCC, iamylase, w
metabolic/​
lactic acidosis; ww
Sigmoidoscopy ±biopsy may show pale, ulcerated mucosa.
Management
resuscitate with IV
fluids; analgesia, IV ABx (eg
et NBM,
et anticoagulation
et
n
n
co-​
amoxiclav
1.2g/​
8h IV), consider
with IV.nhep.
.
X (E pp. 420–2), surgicalkX
X poor
resection is often necessary.kVery
ok arin
o state
prognosis—​clarify premorbid
and consider ICU careoasoappropriate.
o
o
B Appendicitis (EwOHCM10
.B p. 608.)
w.B
w
w
$ A common
diagnostic
challenge
—​
c
omplications
w
w can be severe if left ww
1
untreated, but 15–​40% of appendicectomy specimens are normal. Can
occur in any age group; classical cases are easy enough to spot, variable
anatomy and extremes of age can make presentation atypical.
Differential UTI, diverticulitis, gastroenteritis, mesenteric adenitis, perforated ulcer, IBD, diverticulitis; Gynae Ectopic pregnancy, ovarian torsion,
ruptured ovarian cyst, salpingitis.
Symptoms Central, abdominal colicky pain worsening over 1–​2d then
developing into constant RIF pain (sensitivity and specificity of 780%2),
worse on moving, anorexia, nausea, vomiting, may have constipation,
diarrhoea, dysuria, oliguria (all non-​specific and common).
Signs itemp, iHR, ±dBP, RIF tenderness ±guarding/​rebound/​rigidity,
RIF pain on palpating LIF (Rovsing’s sign), PR tender on right (there is no
evidence that this has diagnostic utility in adults, but failure to perform
PR still considered negligent).
Investigations iWCC, neutrophilia>75%, iCRP (a useful triad with negative predictive value >97% in adults, but beware children and elderly);
bld cultures (if pyrexial), G+S; US and contrast-​enhanced CT reduce
laparotomy rates, but this must be balanced against risks of radiation
exposure and local resources.
Management Surgery—​NBM, IV fluids, analgesia, IV ABx (eg co-​amoxiclav
1.2g/​8h IV). Laparoscopic approaches reduce scarring, postoperative
pain, recovery time, and incidence of wound infections, but require
more operative time and higher skill levels than open appendicectomy.
If peritonitic, send for immediate surgery, otherwise reassess regularly
while awaiting surgery. If diagnostic uncertainty, a short period of safe
observation ±imaging can be informative.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
o
w.B
ok
o
o
w.B
t
ok
o
w.B
k
1
2
e
X.n
ok
o
w.B
ww
t
t
e
X.n
ok
ww
ww
t
e
X.n
e
X.n
ok
And hence an all too common source of tension between ED staff and junior surgical doctors—​
try to avoid becoming part of this seemingly perpetual cliché when your turn comes.
See Yeh B. Ann Emerg Med 2008;52:301 for an excellent review of the clinical utility of signs
and symptoms in adult appendicitis; available free at: Mwww.annemergmed.com/​article/​S0196-​
0644(07)01732-​5/​fulltext
o
B
.
w
ww
t
e
X.n
ww
o
Bo
.n
kX
ww
t
e
X.n
ww
et
.n
kX
ww
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kX
o
w.B
ww
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et
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kX
ww
o
B
.
w
ww
B
.B
w
w
.B
w
w
wGastroenterology
300
ww
w
Chapter 9
t
t
t
Dyspepsia
.ne (E OHCM10 p. 252.)
.ne
.ne
X
X
X
persistent symptom referable
to the upper GI tract.k
ink
ok $ Anypatients
oulcer
o Thisandwillrare
o
o
with peptic
disease, GORD, oesophagitis,
Bo clude
B
B
.
upper GI malignancies,
endoscopic
w. as well as those without
wsignificant
changes. Aim to
identify those at risk of significant
pathology, and conw
w
w in those without.
w
ww
trol symptoms
Symptoms Burning retrosternal or epigastric pain, worse on bending and
t
t nausea, vomiting, nocturnal
lying,ewaterbrash
(excess saliva), acidereflux,
et
n
n
n
.
.
cough,
symptoms improved by antacids;
symptom patterns are .poorly
Xpredictive of endoscopic findings.
X
kX
ok Signs
o(nok peritonitis), rarely epigastric
omass.
o
o
o
Epigastric
tenderness
B
B hernia, medica.B alcohol, obesity, pregnancy,
Common risk factors w
Smoking,
w.hiatus
w
w
tions (bisphosphonates,
calcium antagonists, nitrates,
corticosteroids, NSAIDs).
w
w
ww
Investigations Urgent endoscopy if ‘red flag’ symptoms (chronic GI bleeding/​
iron deficiency anaemia, unintentional weight loss, progressive dysphagia,
persistent
et vomiting, epigastric mass).noret≥55yr and persistent/​unexplained
et
n
n
.
.
dyspepsia.
Else
test
and
treat
for
H.
pylori
(Box
9.3).
Some
reserve
testing
X those who fail empirical treatment
X
kXConsider
full-​dose o
PPI.
ok for
orkequired PPIwithfor1mth
o
o
o
low-​
d
ose
maintenance
or
as-​
those
who
respond.
If sympB
.Bendoscopy or 24h ambulatorywpH
.Bmonitoring.
toms persist, consider
w
w advice Weight loss, smoking
Managementw
Lifestyle
wwcessation, alcohol reduc- ww
3
tion, avoid foods/​drugs which exacerbate symptoms, especially NSAIDs.
• GORD Antacids (E p. 187) PRN if mild; full-​dose PPI for 1–​2mth,
then low-​dose or PRN PPI; H2 receptor blockers (eg ranitidine) less
effective than PPI, but individual patients may respond better; surgical
fundoplication (rarely) if severe
• Oesophagitis As for GORD; frequency of surveillance if Barrett’s
oesophagus detected requires specialist guidance
• Peptic ulcer 1–​2mth full-​dose PPI. 95% of duodenal and 80% of gastric ulcers
are related to H. pylori, therefore ensure eradication (see Box 9.3). Gastric
ulcers are also associated with malignancy, therefore repeat endoscopy at
6wk to confirm healing. If symptom recurrence, retest, since eradication
may require different or prolonged antibiotics, and re-​infection can occur
• Gastric/​oesophageal malignancy Urgent multidisciplinary team referral
for surgery/​palliation.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
ww
o
w.B
ww
et
.n
kX
.n
kX
o
ww
o
w.B
K Box 9.3 H. pylori infection and eradication
•
.n
kX
o
w.B
ww
Bo
et
.n
kX
ww
C-​urea breath testing reliably detects infection or confirms
et
et
eradication
and is widely used innsecondary
care; faecal antigennet
n
.
.
.
tests
are
used
in
primary
care
kX• CLO tests require a biopsy
kX
kpHX
taken at OGD and rely upon
o
o
o
changes.Bo
Bo • Aindicator
.Bo
‘wash-​out’ period
of 2wk off PPI is needed for
these tests;
w
w
w are less reliable, but can w
serological
be w
used in a patient on a PPI
wtests
ww
•Treatment is with triple therapy for 1wk, eg lansoprazole 30mg/​
12htPO, amoxicillin 1g/​12h PO, clarithromycin
12h PO t
e containing metronidazole
etmay increase500mg/​
•Regimens
resistance andne
n
n
.
.
.
may be better reserved forX
2nd-​line therapy
X• 2wk
X
k
k
k
courses increase eradication
o
o effective.
oo rates by 10%, but are.Bnotocost-​
Bo
B
.
w
w
ww
ww
ww
3
13
NICE guidelines available at Mguidance.nice.org.uk/​CG184
B
.B
w
ww
.B
w
w
w
w
Abdominal pain
w
301
t
t
t
Diverticular
disease (E OHCM10
.ne
.ne p. 628.)
.ne
X
X
X
= diverticulaek(out pouchings) in the large bowel.
ok $ Diverticulosis
o of diverticulae; acutely symptomatic.
ok
o
o
Diverticulitis = inflammation
Bo $Symptoms
B
B
. improves with
Abdominal
sided,
w. pain/​cramps (usually leftww
bowel opening),wirregular bowel habit, flatus, bloating,
PR bleeding.
w
w
ww
Signs itemp, iHR, ±dBP, LIF tenderness, ±peritonitis, distension.
Investigations
blds iWCC, iCRP; CT/​colonoscopy
direct visut
et (necessary
et causesForof indirect/​
alization
only to exclude
other
symptoms). .ne
n
n
.
.
X
X fibre diet, antispasmodics
Diverticulosis kHigh-​
(eg
kX analok Management
osenna, E
oNBM,
mebeverine), laxatives (eg
p. 207); Diverticulitis
o
o
o
B gesia, fluids and ABx
amoxiclav 1.2g/​8h IV). .B
w.(egB co-​perforation,
w
Complications Obstruction,
w
w (usually painless). abscess,
ww adhesions, strictures, ww
­fistula, PR bleeding
Renaltcolic (E OHCM10 p. 638.) t
e consider other causes.nofe abdominal pain, including.nAAA,
et
$ .n
Always
X­especially if no previous renalkstone
X disease.
kX loin to
ok Symptoms Acute-​onset severe
o unilateral colicky pain radiating
ofrom
o
o
o
B groin, nausea and vomiting,
B strangury (fresweating, haematuria, dysuria,
w.B
w.sensation
quent, painful passage
of small volumes of urinew
with
of incomw
w iliac fossa or suprapubic painwsuggests another pathology. ww
plete emptying);
B
Signs iHR, sweating, patient restless and in severe pain, usually no tenderness on palpation unless superimposed infection.
Investigations Urine Hb on dipstick (790% cases), nitrates suggest UTI,
β-​hCG if ♀; blds FBC, U+E, Ca2+, urate; CT-​KUB Detects >99% stones.
Management Analgesia (NSAID first, then opioids), if <5mm should pass
spontaneously; larger stone will require urology opinion. If evidence of
infection give IV ABx (check local policy). If evidence of infection or
hydronephrosis refer urgently to urologist for nephrostomy or stent.
Complications Pyelonephritis, renal dysfunction.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
w
oo
B
.
ww
t
.ne
X
k
ww
t
t
t
.ne colic
.ne
.ne
Biliary
X
X
X
ok $ Contraction of the gallbladder
ok or cystic duct around gallstones.
ok
o
o
or
constant
RUQ/​
e
pigastric
pain
(especially
Bo Symptoms Recurrentwcolicky
B
B
.
.
on eating fatty foods), nausea, vomiting, bloating. w
w
w
Signs RUQ tenderness,
non-​peritonitic, not w
jaundiced.
w
ww
Results blds Normal; USS Gallstones.
t elective cholecystectomy.net
Management
et Analgesia, dietary advice,
eand
n
n
.
.
Complications
Passage
of
stone
into
bile duct may
Xor acutecommon
X.cause
kXcholestatic jaundice, cholangitis,
k
k
pancreatitis.
o
o
o
Bo Acute cholecystitis
.Bo
.Bo
w
w
$ Gallbladder inflammation
2° to cystic ductw
occlusion by gallstone.
ww RUQ/​egepigastric
ww
Symptoms Continuous
pain,w
unwell, vomiting.
Signs itemp, RUQ tenderness and peritonitis, Murphy’s sign (pain and cest deep inspiration during palpation
sationeof
et in RUQ, not present in LUQ).
et
n
n
n
.
.
.
Results
blds
iWCC,
iCRP;
USS
Gallstones
and
thickened
gallbladder.
X
X
kXconsider
ok Management NBM, analgesia,
okABx (eg co-​amoxiclav 1.2g/​o8hoIV);
o
o
B urgent cholecystectomy
w.Bvs interval procedure. ERCP
w.ifBdistal CBD stone. w
w
w
w
w
w
B
.B
w
w
.B
w
w
wGastroenterology
302
ww
w
Chapter 9
t
t
t
3Acute
OHCM10
.ne pancreatitis (E X
.ne p. 636.)
.ne
X
X
from a mild self-​limiting
k illness to severe and life-​tohreatening.
k
ok $ Varies‘I GET
oIdiopathic,
o
SMASHED’:
Gallstones (50%),oEthanol (25%),
Bo Causes
B
B
.Mumps, Autoimmune, Scorpion
. bites (rare),
Trauma, Steroids,
w
wERCP,
w
w
Hyperlipi­daemia,
Hypercalcaemia, Hypothermia,
Drugs (eg thiaw
w
ww
zide diuretics).
Symptoms Constant severe epigastric pain radiating to the back, i­mproved
t forward, nausea, vomiting,
esitting
etanorexia.
et
with
n
n
n
.
.
.
XSigns iHR, ±dBP, itemp, cold
Xextremities, epigastric tenderness
X with
ok peritonitis, abdominal distension,
ok dbowel sounds, mild jaundice,
ok Cullen’s
o
o
o
(bruised umbilicus) or
sign.
B
.BGrey–​Turner’s (bruised flanks)
wiWCC,
w.Biglucose, dCa , w
Results blds dHb,
iiilipase (or amylase),
w
w
w (±DIC), LFT; USS ?gallstones;
w CT If diagnosis in doubt. w
deranged clotting
Management IV fluid resuscitation, O , analgesia, urinary catheter, NBM,
NG tube.
If severe (Table 9.2) involve
ICU and plan ERCP if gallstone
et Monitor
etglucose.
et
n
n
aetiology.
fluid balance, .obs,
Daily U+E, FBC,.nCRP;
.
X
X
LMWH (E pp.k420–2).
kX
ok prophylactic
ofailure, respiratory failure,oohaemorrhage,
o
o
Complications
DIC,
renal
B
.B necrosis), pseudocysts,
thrombosis, sepsis
w(infected
w.Babscess, chronic w
w
pancreatitis. w
w
w
w
4
5
6
2+
2
Table 9.2 Modified Glasgow score for predicting acute pancreatitis severity
et
In 1974
developed a scoring system,
netRanson
net
.
.
validated
for use in alcohol-​inducedX
acute
X
>55yr
k pancreatitis; this remains widelyokused. The
o
<8.0kPa oo
modified Ranson criteria (1979)
have been
Bo PaO
B
Bo disease.
WCC
>15 .× 10 /​L
validated for gallstone-​r.elated
In
w
w
1984, Blamey et w
al.* at the Royal Infirmary
Ca (uncorr) w<2mmol/​L
w >10mmol/​L in Glasgow modified
w 8 of the 11 Ranson
ww
Glucose
criteria
and
validated
these
for
prognostic
ALT
>100u/​L
use in both
t alcohol and gallstone inducednet
LDHet
>600u/​L
epancreatitis.
acute
n
n
.
.
.
Urea
>16mmol/​L
X
kXAlbumin
kX
<32g/​L ok
o
o
Bo Score 1 point for eachwparameter
Bo present on admission or withinwthe.Bfirsto48h. A score
.
of ≥3 predicts an episode of severe pancreatitis and should prompt ICU/​HDU referral.
Reproduced from
Gut, Blamey S. L., et al., 25, 1340–​6, 1984,
ww
wwwith permission from BMJ
ww
Publishing Group Ltd.
et
et
et
n
n
n
.
.
.
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X
ok
ok
ok
o
o
o
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w.B
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w
w
w
w
ww
.n
kXAge
Variable
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2
9
2+
*Original article available free at Mwww.ncbi.nlm.nih.gov/​pmc/​articles/​PMC1420197
t
k
o
Bo
t
e
X.n
4
5
6
t
e
X.n
e
X.n
British Society of Gastroenterology guidelines at Mgut.bmj.com/​content/​54/​suppl_​3/​iii1.full
Case series available free at Mwww.ncbi.nlm.nih.gov/​pmc/​articles/​PMC1700547
Lipase slightly more specific. Overall trend in relation to pain is more important than absolute
values.
ok
ww
o
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.
w
ok
ww
o
B
.
w
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.B
w
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.B
w
w
w
w
Abdominal pain
w
303
t
t
t
Chronic
.ne pancreatitis (E OHCM10
.ne p. 270.)
.ne
X
X
X
k can be due to gallstones
alcohol, obut
ok CausesalsoUsually
ok (which
o
cause recurrent
pancreatitis), familial,Bo
cystic fibrosis,
Bo may
B
hyperparathyroidism,
w. iCa .
w.
w
w
Symptoms General
w malaise, anorexia, weightwloss, recurrent epigastric ww
pain radiating to back, steatorrhoea, bloating, DM.
Signs Cachexia,
epigastric tenderness.et
et
et
n
n
n
.
.
.
XInvestigations blds Glucose (?DM, E pp. 334–6); Stoolkdelastase;
X
ok USS (±endoscopic), CT/​oMoRCPkXmay show characteristicoochanges,
eg
o
B microcalcification.w.B
B
.
w Diet Refer to w
Management Analgesia,
advise to stop drinking
ww
wwwithalcohol;
dietician: low
fat, high calorie, high protein
fat-​
soluble vitamin w
­supplements; Pancreatic enzymes eg Creon before eating; Surgery Coeliac-​
t stenting of the pancreatic
plexuseblock,
etduct, pancreatectomy. .net
n
n
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
2+
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t
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oo
et
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.
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o
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e
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et
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.Bo
ww
B
304
.B
w
ww
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
et
.nGI
.ne
.ne
2
bleeding
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X
X
X
ok
ok
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o
o
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. airway is patent; consider manoeuvres/​
wCheck
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w
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ww
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2 Circulation
t
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3Call
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X the patient on their sidekX
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if vomiting
ok •• Lay
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o
o
o
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w bloods:
ww
•Two goodw
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• 0.9%
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.
.
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o
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.
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w
w
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ww
ww
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• Seniors may consider giving terlipressin 2mg IV over 5min if gastro-​
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If bleeding is severe and the patient haemodynamically unstable:
• Call for senior help
• Give O–​ve blood, request X-​matched units
• Contact the on-​call endoscopist and alert surgeons
• 2 Reassess, starting with A, B, C . . .
t
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.n Life-​threateningXcauses
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ok •• Gastro-​
ok
o
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Upper GI malignancy.
Bo • Vascular malformations
B
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w.
w.
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et
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w
w
wAcute upper GI bleeds 305
ww
t
t
t
.ne upper GI bleeds
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X
X
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ok
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o
o
Bo (E OHAM4 p. 224.)
B
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.
w. dGCS, iHR, dBP, posturalwBPwdrop,
2 Worrying features
durine output,
w
w frank PR blood, chest pain, w
ww
frank haematemesis,
coagulopathy, liver disease.
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H. pylori), Mallory–​Weiss
egastro-​oesophageal varices, oesophagitis,
et swallowed
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n
n
n
.
.
.
X Other Oesophageal korXgastric cancer, vascular malformations,
X
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o 9.4).
ok
underlying coagulopathy (Table
o
o
o
B Ask about Colour,wquantity,
vomit,
frequency, onset,
.B mixed in or throughoutblack
.Bstool
stool colour and consistency (those on iron may have w
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w
w
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w dizziness, fainting, sweating, ww
7
et
n
.
X
ok
Bo
B
SOB, weight loss; PMH Coagulopathy, liver problems (?varices), peptic ulcers;
DH NSAIDs, anticoagulants, steroids; SH Alcohol.
Obs Pay special attention for iHR, dBP; check postural BP, GCS.
Look for Continued bleeding, colour of vomit, cold extremities, sweating, pulse
volume, bruises, other bleeding (nose, mouth), abdominal tenderness ±peritonitis,
masses, signs of chronic liver disease (E pp. 319–23); PR Fresh blood/​melaena.
Investigations blds FBC, U+E, LFT, clotting, G+S or 2–​4 unit X-​match; low
platelets may indicate hypersplenism (?2° to portal hypertension/​chronic liver
disease); iiurea (out of proportion to icreatinine); check for coagulopathy;
ECG ?ischaemia; OGD Allows diagnosis and definitive treatment only after adequate
resuscitation; timing guided by clinical assessment of severity: Risk scoring can be
useful in this regard (Table 9.3), but does not replace clinical judgement. Discuss all
potential major bleeds with seniors and an endoscopist at an early stage.
et
n
.
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ok
o
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.
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Table 9.3 Rockall risk scoring system for GI bleeds
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X
Reproduced from Gut, Rockall T. A., et al., 38, 316–​21, 1996, with permission from BMJ
Publishing Group Ltd.
The Rockall score was developed to predict risk of death or rebleeding based upon the
complete score calculated after endoscopy (eg will occur in 11% of those with Rockall=3).
3Suspicion of rebleeding requires urgent discussion with the endoscopist and surgeon on call
± interventional radiology. As an alternative, the Blatchford score was developed to predict those
not requiring intervention based upon admission parameters, marginally outperforming the Rockall
score in this regard. It is somewhat more complex and less widely used (online calculators available
eg Mwww.mdcalc.com). NICE has managed to end up recommending the use of both scores.
ok
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X
k
ww
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k
ww
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e
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w
Clinical information allows initial risk stratification, to which endoscopic
findings (in italics) are added for complete assessment. ≤2 = low risk
Feature
0
1
2
3
Age
<60yr
60–​79yr
≥80yr
Shock: systolic BP >100mmHg
and HR
<100/​min
>100/​min <100mmHg
Comorbidity
Nil major
Heart
Renal/​liver Metastatic
failure, IHD failure
disease
Diagnosis
Mallory–​Weiss/​none All other
Upper GI
malignancy
Bleeding on OGD Nil recent
Recent
t
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X
k
ww
NICE guidelines available at Mguidance.nice.org.uk/​CG141
w
ww
ww
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ww
B
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w
ww
306
Chapter 9
.B
w
w
ww
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Gastroenterology
t
t
t
.ne 9.4 Common causes ofXupper
.neGI bleeding
.ne
Table
X
X
k Examination Investigation
ok
ok
History oo
o
Bo Peptic ulcers Epigastric/​
B
B
hest pain, Epigastric
on OGD,
w. cmelaena,
w. Ulcer
heartburn,
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may
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w
ulcers,
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w previous
w if be +ve
ww
NSAIDs, alcohol
perforated
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t
et Heartburn,
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alcohol, hiatus hernia.ne
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erosions on OGD
n
.
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X
X
X
Gastro-​
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haematemesis
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iPT, deranged
k
k
ok oesophageal previous liver
signs of LFT,
oodisease, tenderness,
oovarices on
Bo varices
B
alcohol.B
chronic liver disease
OGD
.
w
w Tear seen on OGD w
Mallory–​
Forceful vomiting
Epigastric w
w
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w
w
if not resolving
t large-​bore cannulae. IVnfluids
Management
NBM until OGD, O , e
two
et regular
et
n
n
±blood,
obs (HR, BP, postural
BP, urine output); consider
cath.
.
.
X
X (see also Box 9.5): kX
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ok eterization,
okvitalICU
o
ooover-​
• Blood transfusion This is o
often
and lifesaving. However,
B
B
B
.
.
transfusion is also
associated
with
increased
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and
w
w rebleeding.
Assess each patient
ww carefully and discuss transfusion
ww targets with a senior ww
B
2
8
8
• PPIs Reduce rebleeding, surgery and transfusion, only when given after
endoscopy to patients requiring endoscopic therapy (high-​dose PO/​IV eg
omeprazole 40mg BD as effective as more cumbersome bolus/​72h infusion)
• Mallory–​Weiss tears (E OHAM4 p. 234.) These occur after repeated
forceful vomiting, often after alcohol excess. Bright red blood appears as
streaks or mixed with vomit. Bleeding often resolves spontaneously
• Clotting abnormalities (E p. 418.) Consider: platelet transfusion if active bleeding
and plts <50 × 109/​L; FFP if PT/​APTT >1.5 × control; prothrombin complex
concentrate or recombinant clotting factors if on warfarin/​DOAC
•H. pylori (E p. 300.) Test and eradicate if positive.
3Gastro-​oesophageal varices (E OHAM4 p. 232.)
Symptoms Symptoms of chronic liver failure (E pp. 319–23); known liver
disease, excess alcohol; varices are asymptomatic until they bleed. Signs Signs
of chronic liver failure (E pp. 319–23). Investigations Varices seen on OGD.
Acute bleed Resuscitate according to E p. 304 then:
• Terlipressin 2mg/​over 5min IV if not already given
• Antibiotics Cirrhotic patients have dimmune function; spontaneous bacterial
infections are associated with imortality (eg Tazocin® 4.5g/​8h IV)
• OGD (urgent) For banding (oesophageal) or sclerotherapy (gastric)
• Bleeding still uncontrolled Consider a Sengstaken–​Blakemore tube and
transjugular intrahepatic portosystemic shunting (TIPS).
Once bleeding controlled Terlipressin 1–​2mg/​6h over 5min IV, for up to 5d; treat
cause of liver failure; drisk of recurrent bleeding by dportal pressure (by TIPS
or propranolol 40–​80mg/​12h PO) or further banding.
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T Box 9.5 What about other drugs?
et
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kX
ww
t
Once haemostasis is achieved, continuation of aspirin where previously indicated (under PPI cover) is associated with reduced mortality (albeit at a higher
risk of rebleeding).9 NSAIDs should be stopped and alternative analgesics prescribed. Data for other antiplatelet drugs and anticoagulants are more complex
and each case will need careful discussion between the relevant specialists.
o
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Villanueva C,
.
2013;368:11 free at Mwww.nejm.org/​doi/​full/​10.1056/​NEJMoa1211801
Sung JJY, et al. Ann Intern Med 2010;152:1 (subscription required—​check ATHENS).
ww
B
.B
w
ww
.B
w
w
wAcute lower GI bleeds 307
ww
t
t
t
.ne lower GI bleeds
.ne
.ne
Acute
X
X
X
ok
ok
ok
o
o
Worrying features
Continuous
bright-​
r
ed
PR
bleeding,
iHR, dBP,
Bo 2postural
B
B
.
w. dGCS, abdominal pain,
w
drop, dizziness,
weight loss, vomiting.
w
w
w Common Polyps, diverticular disease,
w angiodysplasia, haem- ww
Think about
orrhoids, IBD, colon cancer, upper GI bleed (E pp. 305–6); Other Aorto-​
enteric
etfistulae, ischaemic colitis, radiation
et proctitis, Meckel’s diverticulum.
et
n
n
n
.
.
.
X about Onset, quantity,kX
(red, black, clots), type
blood
kXofvomiting
ok Ask
o colour
opain,
(fresh, mixed with stool, streaks
on toilet paper), abdominal
o
o
o
B (colour), pain on w
opening
.B bowels, straining, change
.inBbowel habit, anwbleeding,
orexia, weight loss,
dizziness, SOB; PMH Previous
diverticular
w
w
w DH NSAIDs, anticoagu- ww
disease, IBD,wpeptic ulcer, liver disease, AAA;
lants, steroids, iron; FH IBD, bowel cancer; SH Alcohol. See also Box 9.6.
et
n
.
X
et
n
.
X
et
n
.
Xbruises,
for Pale and cold extremities,
sweating, pulse volume,
ok Look
ok (nose, mouth),
oktenderness
other sources of bleeding
abdominal
o
o
o
B ±peritonism, masses,
.Bsigns of chronic liver disease
.B(E pp. 319–23);
wpalpable
w
PR Blood, melaena,
mass, haemorrhoids.
See Table 9.5.
w
w
w blds FBC, clotting, U+E, LFT,
w G+S or X-​match 2 units; ww
Investigations
ABG Only if unwell; OGD To exclude upper GI bleed, urgent if shocked;
t
et For investigation, biopsy,
et
ECGnIfeage >50yr; Sigmoidoscopy/​colonoscopy
.
.nangiography
.nand
treatment;
may require mesenteric
or capsule enteroscopy
if
X
X
X
k
ok bleeding source cannot beooidentified.
ok
o
o
B Management Lower
.B by surgeons
managed
w.BGI bleeding is traditionally
w
while upper GI w
bleeding is usually a medical condition.
w Although 785% of w
w will settle with conservative w
lower GI bleeds
management, always beware w
the brisk upper GI bleed presenting as PR bleeding.
t rarely possible to tellnethe
t
t
Diagnosis
of significant lowereGI
.nefromIt ishistory
. alone,cause
.n
bleeds
and examination
investigations are essential.
X
X
X
ok Fresh blood on toilet paper oFresh
ok blood or streaking stool only
okand patient
o
a
nal
fissure,
but
arrange
follow-​
up flexible
Bo well: treat as haemorrhoids/​
B
B
.
w.
sigmoidoscopy to w
rule out bowel cancer.
w
w
Mild bleedingw
(no evidence of shock) Bleeding
wshould usually settle with ww
Obs HR, BP, postural BP, GCS, RR, sats.
conservative management. Consider early discharge and follow-​up.
Moderate bleeding (Postural drop, iHR.) Secure IV access and fluid resuscitate ± blood until haemodynamically stable, catheterize, hourly fluid
balance, senior review, may need urgent OGD if possibility of upper
GI source
3Severe bleeding (Fresh bleeding/​clots, dBP.) Resuscitate according to
E p. 304, transfuse, call senior, on-​call endoscopist, and surgical registrar.
• 715% of patients with acute, severe PR bleeding will have an upper
GI bleeding source identified on OGD. For the remainder, options
include colonoscopic haemostasis, radiological embolization, or surgical
resection.
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e
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o
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.
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.
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w
ww
308
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
t
.ne 9.5 Common causes ofXlower
.neGI bleeding
.ne
Table
X
X
ok
ok Examination Investigation
ok
o
o
Bo Upper GI bleed History
B
B
Haematemesis,
Liver disease, w.dHb, iurea, lesion
w.
fresh PR bleeding, epigastric
w
w clots or melaena, tenderness,wPRw on OGD
ww
epigastric pain
blood or melaena
t
t or
GI cancer
or
Change in bowel
PReblood
dHb ±dMCV, et
e
n
n
polyps
habit, weight loss, .melaena,
mucus,
lesion on
.
.nor
X
X
abdominal painkX palpable mass
sigmoidoscopy
k
k
o
colonoscopy
oo
oo
Bo Inflammatory Abdominal
B
B
.
pain,
itemp, abdo tender.dHb,
w weight ±peritonitic, PRww iCRP,iWCC,
bowel disease w
lesions on
w diarrhoea,
w sigmoidoscopy
ww
loss, mouth ulcers blood, mucus,
or
melaena
colonoscopy
Diverticular
Abdominal pain,
Tenderness,
diverticulaeet
et
et PR dHb,
n
n
disease
fever, change in
±peritonism,
on colonoscopy
.
.
.n
X
X
bowel habit kX blood, mucus
k
k
o
Abdo pain,
generalized iWCC,
acidotic,
oo Shock,
ooroprevious
Bo Bowel
B
B
.
.
ischaemia
previous
arterial
tenderness
±AF
w
w MI on ECG
disease
wwRecurrent fresh PR blood orww dHb, lesions on
ww
Angiodysplasia
Bo
or radiation
proctitis
PR blood, old age,
previous pelvic
radiotherapy
Haemorrhoids Painless, fresh red
blood on toilet
paper, perianal itch,
constipation
Anal fissure
Pain on defecating,
fresh blood on
toilet paper,
constipation
et
X.n
ok
oo
B
.
w
ww
o
t
.ne
X
k
melaena
colonoscopy,
consider argon
plasma coagulation
Often not palpable Lesions seen on
on PR, perianal tags, proctoscopy
may have rectal
prolapse
Posterior/​anterior Proctoscopy to
PR tear, perianal
visualize lesions
tags, tenderness
kX
t
.ne
oo
B
.
ww
t
.ne
X
k
w
t
ww
et
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X
k
.n
kX
oo
oo
B
B
.
.
Causes Oesophagitis,
w gastric erosions, gastritis, peptic
w
ww ulcer, gastric/​bowel ww
cancer, polyps,
IBD, angiodysplasia, GI lymphoma.
w
w
Symptoms Anorexia, weight loss, tired, change in bowel habit, melaena,
vague intermittent
pain.
t anaemic,abdo
e
et tenderness; PR Blood, mass.
et
Signs
Pale/​
cachexic,
mild.n
abdo
n
n
.
.
X
X
X
Stool Faecal occult
ok Investigations
ok blood (FOB), ova, cysts,oandokparasites;
o
blds FBC (dHb, dMCV o), iron, ferritin, vitamin B , folate,
U+E, LFT;
B
.Bneed a video capsule endoscopy
OGD±colonoscopy May
or small bowel CT/​
wdisease
w.B
MRI if small bowel
suspected.
w
w
w
w
ww
Treatment Investigate and treat the cause, treat anaemia with ferrous sulfate 200mg/​8h PO, consider admission for transfusion if Hb <80g/​L or
if symptomatic
with anaemia.
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
Chronic gastrointestinal blood loss
10
12
Those with a simultaneous iron deficiency and vitamin B12 and/​or folate deficiency may have a
normal or raised MCV; in this instance, significant variation in red cell size will be reflected in an
increased red cell distribUTIon width (RDW).
10
B
.B
w
w
.B
w
w
wAcute lower GI bleeds 309
ww
t
t
t
Colorectal
.ne polyps (E OHCM10
.nep. 616.)
.ne
X
X
X
finding at colonoscopy;
their importance klies in the
ok $ A commonpotential
ok
oo
ofoadenomatous polyps.
Bo premalignant
B
B
.
.
Causes Vast majority
sporadic;
rare
familial
syndromes.
w
Symptoms Oftenw
ww bowel habit, blood ww
w none; intermittent abdo pain,waltered
w
or melaena in stool, tenesmus, weight loss.
Signs PR Palpable mass if very distal, blood, mucus.
Investigations dHb, lesion on colonoscopy.
Treatment Polypectomy (send for histology), multiple polyps may need
colonic resection or regular colonoscopy follow-​up.11
t
t
e
X.n
ok
Bo
ok
o
w.B
ok
$ Dilated and displaced perianal vascular tissue (anal cushions).
Symptoms Recurrent fresh red blood on toilet paper or streaking stools
±pain or pruritus ani (anal itch), constipation.
Risk factors Constipation with straining, multiple vaginal deliveries.
Signs Not palpable unless prolapsed; PR Blood, otherwise normal.
Investigations Proctoscopy To visualize haemorrhoids, Sigmoidoscopy To
identify other pathology (eg malignancy).
Treatment High-​fibre diet, topical Anusol®, injection of sclerosants, band
ligation, coagulation, cryotherapy, may need haemorrhoidectomy.
Strangulated haemorrhoids Painful, tender mass, unable to sit down, treat
with ice packs, stool softeners, regular analgesia, and bed rest. Once
stable, inject piles and consider elective haemorrhoidectomy.
ww
t
t
e
X.n
ok
e
X.n
o
w.B
Haemorrhoids (E OHCM10 p. 632.)
ww
Bo
t
e
X.n
t
e
X.n
ok
o
B
.
w
ww
e
X.n
ok
o
B
.
w
ww
ww
ww
t
t
t
.nefissure (E OHCM10 p.X630.)
.ne
.ne
Anal
X
X
ok Symptoms New-​onset extreme
okpain ±fresh red blood on opening
ok bowels,
o
o
Bo history of constipation
B
B
and straining (beware Crohn’s. and cancer).
w.posteriorly
w(10% anterior), peri- w
Signs Anal tear visible
on the anal margin
w
w PR May be impossible duewtowpain.
w
anal ulcers, fistulae;
Investigations Sigmoidoscopy If suspicious of pathology once pain controlled.
t conservative High-​fibre diet;
t lidocaine ointment, 0.2–​n0.3%
Treatment
e5%
et
.neointment,
.ninjection
. than
GTN
botulinum toxin
all marginally better
X
X
X
k
rate 95%.
ok ­placebo; ­internal sphincterotomy
ok
oo p.cure
o
Bo Angiodysplasiaw(E.BOHCM10
B
628.)
.
wascending
$ Submucosal w
arteriovenous malformation, often
colon.
w
w recurrent blood in the stool,
w abdo pain is rare.
ww
Symptoms Elderly,
Signs May be normal, pallor; PR Blood or melaena.
Investigations
Faecal occult blood, colonoscopy
angiography. t
et Angiographic
eif tactive, mesenteric
n
n
Treatment
embolization
bleeding; argon plasma
.
.
.necoX
X
X
agulation
(endoscopic);
rarely
resection;
treat
anaemia,
eg
ferrous
sulfate.
k
k
ok
oo
oo
Bo I Box 9.6 Causes
B
B
.
.
covered
w of rectal bleeding w
w elsewhere
w
w
w
ww
Inflammatory bowel disease E p. 315 Upper GI bleed E pp. 305–6
12
Bowel ischaemia E p. 299
kX
o
Bo
Diverticular disease E p. 301
Infective diarrhoea E p. 313
t
.ne
t
e
X.n
ok
o
B
.
w
t
e
X.n
ok
o
B
.
w
The British Society of Gastroenterology guidelines for colonoscopic follow-​up are at Mwww.bsg.
org.uk/​images/​stories/​docs/​clinical/​guidelines/​endoscopy/​ccs_​10.pdf
12
For a useful meta-​analysis, see Mwww.cochrane.org/​CD003431
11
ww
ww
ww
B
310
.B
w
ww
Chapter 9
Gastroenterology
.B
w
w
ww
w
t
t
t
.ne
.ne
.ne
Nausea
and
vomiting
X
X
X
ok
ok
ok
o
o
iHR,
i/​
d
BP,
dGCS,
severe
pain
Bo 2 Worrying features
B
B
. (head, chest,
w. constipation, blood/​coffee
w
abdomen), head injury,
grounds, purpuric rash.
w
w
w
w
ww
Think about 2 Life-​threatening Raised intracranial pressure (ICP), meningitis, tMI, bowel obstruction, acute abdomen,
DKA; Common Post-​otp,
edrug induced (opioids), gastroenteritis,
et
pain,
other ­infection, alcohol;
n
n
.
.
.ne
X
X
X
Other
Gastroparesis,
paralytic
ileus,
pregnancy,
electrolyte
imbalance
k
k
ok , Na ), migraine, labyrinthitis,
oo Ménière’s, chemotherapy,
oo Addison’s,
Bo (Ca
B
B
eating disorder (Table
9.6).
.
.
ww timing, relation to wfoodww
Ask about
Frequency,
or medications, colour, ww
w
blood, coffee grounds, melaena, dizziness, diarrhoea, constipation, flatus,
pain, headaches, head trauma, visual problems, pregnancy; PMH Previous
t
et migraines, DM; DH Opioids,
echemotherapy,
et
surgery,
digoxin; SH Alcohol.
n
n
n
.
.
.
X
X
kX
ok Obs Temp, fluid balance,oHR,
okBP, blood glucose, GCS, stool
ochart.
o
o
Look
for
and
assess
volume
status
(E
p.
394),
SOB,
distended/​
B
B bowel sounds, hernias,wsurgical
.tinkling
.B scars,tender/​
w
peritonitic abdomen,
mouth
w rash, photophobia, papilloedema.
ulcers, neck w
stiffness,
ww
ww
2+
+
Investigations Vomiting without the worrying features usually does not
turgent investigation. If recurrent,
t check U+E for dehydration
t
require
or
.ne imbalance and AXR ifXbowel
.ne obstruction suspected. Otherwise
.ne
electrolyte
X
X
according to related
ok investigateamylase,
ok symptoms. Consider: blds FBC,
okU+E, LFT,
Ca , oMg ; CXR Aspiration; ABG If oacutely unwell;
Bo glucose,
B
B
CT brain If head trauma
w. (E p. 452); gastric emptying
w. studies if suspect w
w
gastroparesis. w
w
w
w
Treatment Investigate and treat underlying disease; vomiting is
distressing—​
t
et so E p. 188 for pharmacology
et and selection of appropriate
antiemetics.
n
n
.
.
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
2+
Bo
o
et
n
.
kX
2+
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
wNausea and vomiting 311
ww
t
t
t
.ne 9.6 Common causes of X
.neand vomiting
.ne
Table
nausea
X
X
ok
ok Examination Investigations
ok
o
o
Bo Raised ICP/​ History
B
B
. blurred Febrile, stiff neck, wiWCC/​
. NØ/​CRP,
Headache,
wdizzy,
meningitis
vision,
feels ill, photophobia, rash,
abnormal CT brain or
w
w
wdrowsy
ww
low GCS w
CSF results
Bowel
Colicky pain,
Distended tender Distended bowel
t tinkling loops on AXR net
obstruction
abdomen,
et absolute
esounds
n
or.n
ileus
constipation, brown bowel
(E pp. 602–3) .
.
X
X
X
vomit
k
k
o Acute
o Tender, rigid, Pneumoperitoneum
ok
o
o
Severe abdo o
pain
B
B
abdomen
guarding, rebound on.B
wc.offee-​
w CXR
w
Upper GI
Blood/​
Tender abdomen,
w
ww dHb, iurea
ww
ground vomit
PR melaena
Diarrhoea, feels
Febrile, epigastric
better after vomiting tenderness, not
peritonitic
Labyrinthitis Dizziness
Unable to stand
predominant,
tinnitus
Migraine
Visual aura,
Photophobia,
headache
visual field defects
Hyperemesis ♀ usually between Normal; palpable
gravidarum
uterus
7–​12/​40
bleed
Gastro-​
enteritis
et
n
.
X
ok
Bo
et
n
.
X
ok
o
B
.
w
ww
iWBC, iLØor NØ,
positive stool culture
t
.ne
X
Acute investigations
ok
normalo(E p. 367)
B
.
w
ww Acute investigations
normal
ww
β-​hCG+ TFTs often i,t
et
et
iurea if dehydrated
n
n
.
.
.ne
XDrug induced Many medicationskcanXinduce vomiting, particularly opioids,
X
k
k
o
chemotherapy
ooand digoxin toxicity
oo
Bo
B
B
.
.
w
w
ww
ww
ww
t
t
t
.ne
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
312
.B
w
ww
Chapter 9
o
oo
B
.
w
ww
w
Gastroenterology
t
.ne
Diarrhoea
X
k
Bo
.B
w
w
t
.ne
X
k
et
o
w.B
.n
kX
o
2 Worrying features iHR, dBP, low urine output, PR blood,
weight loss, abdo pain.
ww
ww
Think about Acute Gastroenteritis, antibiotics, laxatives, drugs, pseudo-
membranous colitis (E p. 314), overflow diarrhoea (2° to constipation),
post-​chemotherapy, bowel ischaemia; Chronic IBD, IBS, colorectal cancer,
diverticular disease, alcoholism, malabsorption disorders (eg coeliac,
chronic pancreatitis), thyrotoxicosis, bowel resection, parasitic/​fungal infections, autonomic neuropathy, carcinoid, Addison’s disease (Table 9.7).
et
n
.
kX
t
ww
et
n
.
kX
oo
e
X.n
k
oo
B
B
.
w E. coli, Salmonella, Shigella,
w.Campylobacter
Traveller’s diarrhoea
spp.,
w
w
­giardiasis, amoebic
w dysentery, cholera, tropical
w sprue.
ww
Ask about Normal bowel habit and frequency, onset/​frequency of
t
et recent constipation, stool
echaracter
et
diarrhoea,
(floating, greasy, bloody,
n
n
n
.
.
.
mucus),
colour,
abdominal
pain,
pain
relief
on
opening
bowels,
nausea,
X
X
X
flatus, fluid intake,
mouth ulcers; PMH
ok vomiting,
okweightIBS,loss,
okColorectal
o
o
o
cancer,
IBD,
diverticular
disease,
surgery;
DH
Recent
ABx,
immunoB
.Babroad, other household members
.B affected/​
suppression; SH Travel
sick
w
w
contacts, occupation
ww (food, healthcare), alcohol.
ww
ww
Medications causing diarrhoea Antibiotics, laxatives, colchicine,
t
t
digoxin,
net diuretics, propranolol,XPPIs.
.ne iron, NSAIDs, ranitidine,
.thiazide
.ne
X
X
HR, BP, postural k
sats, fluid balance, stool chart.
ok Obs Temp,
o(EBP,p.RR,394),
ok
o
o
for Volume status
cachexia, mouth
ulcers, clubbing,
Bo Look
B
B
. conjunctiva, thyroid mass,wabdomen
.
jaundice, rashes, w
pale
tenderness
w
±peritonitis, masses,
distension, surgical scars;wPR Pain, masses, stool
w
w
ww
o
Bo
o
Bo
colour, consistency; may reveal a rectum loaded with faeces suggesting
overflow diarrhoea, particularly in the elderly, immobile patient with poor
diet and recent constipation—​treat as constipation (E pp. 316–17).
Investigations Stool M,C+S x3, C. difficile toxin, ova, cysts, and parasites;
blds FBC, U+E, glucose, LFT, Ca2+, TFT, CRP, vitamin B12, folate, iron studies,
anti-​tissue transglutaminase (TTG) antibodies, bld cultures; AXR Obstruction, mucosal oedema, faecal impaction; Sigmoidoscopy If not improving (or
within 24h if suspected IBD/​likely flare); Colonoscopy If cancer suspected.
Management See Box 9.7.
t
.ne
X
k
t
o
ww
t
o
w.B
et
.ne
X
k
oo
B
.
w
ww
.n
kX
ww
et
et
n
n
.
.
X review drugs (consider kX
Increase fluidkintake,
ok • Conservative
oside effects);
alternatives without GI
start stool chart—​
o
o
oothis will
B
B
B
.
often be kept more
accurately on a busy ward if .you
w it themselves
w educate
patients to complete
w
w
w
w
ww
• Infective Isolation and barrier nurse if infective source thought
possible, ABx if systemically unwell
• Medical
in infective
et Anti-​motility agents should
etbe avoided
et
n
n
n
.
.
.
diarrhoea, IBD, or pseudomembranous
colitis.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
e
X.n
K Box 9.7 General management of diarrhoea
B
.B
w
ww
.B
w
w
w
w
Diarrhoea
w
313
t
t
t
.ne 9.7 Common causes of X
.ne
.ne
Table
diarrhoea
X
X
ok
ok Examination Investigation
ok
o
o
Bo Gastroenteritis History
B
B
. iCRP, +ve
Sudden
sweating,wiWCC,
w. onset, itemp,
±vomiting,
abdo tenderness
microbiology on
w
w
w abdominal cramps
w stool sample
ww
Inflammatory Crampy abdo pain, Abdo tenderness, iWCC, iCRP;
t
boweledisease
weight loss, blood in ±peritonitis,
oedema et
et mucus,PR mucosal
n
n
stool, mouth ulcers .blood/​
or megacolon on
.
.n
X
X
X
eye/​skin/​joint
AXR; lesions
seen on
k
k
k
o
oo manifestations sigmoidoscopy
oo
Bo Irritable bowel Bloating,
B
B
.
.
abdominal Abdo tenderness, Diagnosis
w relieved by non-​peritoniticwwexclusion; ofnormal
syndrome
cramps,
defecation
ww
w investigations
ww
Malabsorption Weight loss, pale
Pale, abdo
dHb, dalbumin,
disorders
greasy stools, tired, tenderness,
dCa ±anti-​TTG t
t
t
e
e
anaemia
oedema,
bloating, or endomysial .ne
n
n
.
.
X
X PR pale stool antibodieskX
ok Bowel cancer Abdo pain,oweight
ok PR blood or dHb,odMCV,
o lesion
o
B
B
B
loss, fresh
blood or melaena, mucus/​ on
colonoscopy
.
.
w
melaena
palpable mass w
w
ww iWCC, iCRP,
ww
Diverticular w LIF pain, PR bleeding LIF tenderness,
2+
±peritonitis
disease
net
diverticulae on
et abdo colonoscopy
n
ndiffet
Pseudo-​
Recent antibiotics .itemp,
iWCC, iCRP, C.
.
.
X
X
X
weeks), k
tenderness,
toxin +ve;k
may
ok membranous (days/​
o AXR
crampy abdo
PR green, foul
showo
toxic
dilatation
oopain,
Bo colitis
B
green .watery
stool smelling, ±blood .B
w poor Abdo distension
Overflow
Constipation,
may show
w
wwAXR
diarrhoea w mobility, abdominal and tenderness,
faecal loading
w
ww
pain
PR palpable stool
t
t
net p. 428.)
.ne gastroenteritis (E
.OHCM10
.ne
Infective
X
X
X
k in most
ok $ Diarrhoea, accompaniedoobyknausea, vomiting, ±abdominal
opain;
o
(including
norovirus)
but
other
infectious
agents
important.
Bo cases due to virusesw
B
B
.
w. patient may w
Symptoms Rapidwonset, recent vomiting and/​ow
r diarrhoea,
implicate a w
certain food, feels unwell, crampy
w abdominal pain, flu-​like w
symptoms, pyrexia; other members of household/​contacts affected.
Appearance
of stool Blood 2° colonic ulceration
et spp.);
et (typical for Campylobacter
et
n
n
or .Shigella
watery ‘rice’ stool.n
suggests cholera.
.
X itemp, iHR, dehydrated,
X
X
ok Signs
ok flushing, sweating, abdominal
ok tendero
o
ness, general malaise; PR o
tender, peri-​anal erythema.
B Investigations Stool w
.B
.B
culture Result may take ≥48h; C.wdiff. toxin assays and
w
w
norovirus PCR
w where clinical suspicion; bldswiWCC, iCRP, iurea; if ww
et
n
.
kX
o
Bo
prolonged, consider sigmoidoscopy and discuss with microbiology.
Treatment Admit if clinical concern or not meeting fluid needs orally; isolation/​
barrier nursing with rigorous hand-​
washing by nurses, doctors,
and visitors; push oral fluids ±oral rehydration solutions, antiemetics
(E p. 188); IV fluids if not tolerating oral fluids. Surprisingly few indications
for antibiotics, even after identification of a causative bacterium—​always
discuss with microbiology. Some causes are notifiable (E p. 501).
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
314
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
et
Pseudomembranous
colitis.n
.ne
.ne
X
X
X
of Clostridium k
often following antibiotic k
ok $ Overgrowth
o difficile,
o use. Difficult
o
treat, with a high mortality
in vulnerable groups, alwaysoremember this
Bo tocondition
B
B
. to start antibiotics on scanty
.
when tempted
w
wevidence.
w
Symptoms Usually
3–​9d after antibiotic therapyw
(can be 24h–​6wk), rapid
w
w
ww
onset of high-​quantity green, foul-​smelling stool, crampy abdo pain.
Investigations blds iiWCC, dK ; Stool C. difficile toxin, M,C+S.
Treatment
et 2 Stop unnecessary antibiotics;
et isolate and barrier nurse,.nrehyet
n
n
.
.
drate
with
PO/​
I
V
fluids
and
correct
electrolyte
abnormalities,
metronidaX 400mg/​8h PO and/​or vancomycin
kX 125mg/​6h PO (oraloroute
kX targets
ok zole
orelapsing
o
o
o
GI
tract).
For
persistent
or
disease,
consider
IV
metronidazole,
B
.B
PR vancomycin, PO
or stool transplantation
wfidaxomicin,
w.Bas per ID advice. w
w
w
Complicationsw
Toxic megacolon, perforation,w
high risk of spread to other w
patients via hands of healthcare workers; spores not killed by alcohol gels.
Irritable
syndrome (IBS)
t(E OHCM10 p. 266.) net
et bowel
epain,
n
n
$.Consider
in those with >6mth abdo
bloating, or altered bowel.habit.
.
XDiagnostic criteria Central/​lower
X
X 3 mths
k
k
abdo
pain
at least 1d/​wk for
o associated with 2 or more
oof: (1) pain related
okpast
o
o
o
to
defecation,
(2)
altered
B
B
.B
bowel frequency, w
(3).altered stool form.
w
Red flags Thesew
w should prompt urgent consideration
ww of other diagnoses ww
B
+
13
include unintentional weight loss, rectal bleeding, age >60yr, family history of bowel or ovarian cancer.
Signs Often normal or generalized abdo tenderness; exclude a pelvic mass.
Investigations If fits diagnostic criteria and no red flags, exclude other pathology by checking for normal FBC, ESR, CRP, coeliac serology; CA125 if
♀ with persistent bloating/​pain; further tests only if suspicion this is not
IBS (eg TFT, faecal calprotectin, colonoscopy, OGD, parasites).
Treatment Reassure and explain; basic lifestyle, exercise, and dietary advice
including attention to regular meals and non-​caffeinated drinks, with limited
intake of foods high in insoluble fibre (eg bran); consider dietician and/​or
psychology referral; mebeverine 135mg/​8h PO, loperamide, or Fybogel®
according to symptoms. Treat refractory constipation (E pp. 316–17).
Amitriptyline 10mg nocte or SSRIs (2nd line) have visceral analgesic effects.14
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
oo
B
.
w
.n
kX
ww
$ Impaired absorption of nutrients due to a wide range of GI pathology.
Causes Coeliac disease, chronic pancreatitis, tropical sprue, cystic fibrosis, small bowel/​gastric resection, bacterial overgrowth, IBD.
Symptoms Diarrhoea ±steatorrhoea, weight loss, tiredness, SOB, dizziness, bruising, swelling, vomiting, gluten intolerance, abdo pain.
Signs Cachexia, pale, dehydrated, mouth ulcers, sore tongue, abdo tenderness, oedema, bruises.
Investigations blds dHb, dMCV, dCa2+, dalbumin, diron, dfolate, iPT;
+ve anti-​endomysial or anti-​tissue transglutaminase antibodies sensitive
for coeliac disease; duodenal biopsy gold standard for coeliac diagnosis;
Stool Elastase for assessment of pancreatic function; Hydrogen breath
test For small bowel bacterial overgrowth.
Treatment Refer to dietician and gastroenterologist, may need nutrient
±pancreatic supplements, gluten-​free diet (coeliac).
t
e
X.n
ok
Bo
t
13
14
ww
o
w.B
et
n
.
kX
et
n
.
X
ww
t
o
o
B
.
w
ww
ww
ok
o
o
w.B
ww
et
n
.
kX
o
.ne
X
k
ww
et
.ne
X
k
Malabsorption disorders (E OHCM10 p. 266.)
ww
Bo
w
t
o
w.B
t
.ne
X
k
See Mwww.romecriteria.org for diagnostic resources.
NICE guidelines available at Mguidance.nice.org.uk/​CG61
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Diarrhoea
w
315
t
t
et
Inflammatory
bowel disease
.ne
.n(IBD)
.ne
X
X
X
colitis ($ OHCM10kp. 262), Crohn’s disease ($ OHCM10
p. 264).
ok $ UlcerativeRecurrent
o ±blood ±mucus associatedowith
okabdo
o
diarrhoea
pain,
Bo Symptoms
B
B
. and weight loss.
.
malaise, tiredness, anorexia,
w
w
Signs itemp, iHRw
±dBP, pale, abdo pain ±peritonism,
abdo mass, abdo
wwpalpable
ww
swelling (toxicw
megacolon), malnourished; fistulae ±fissures
in Crohn’s (Table 9.8).
Extra-​intestinal
manifestations Mouth tulcers, erythema nodosum, t
et gangrenosum,
e episcleritis, iritis, .acute
e
pyoderma
conjunctivitis,
n
npri.
.nankylosing
X
X
X
arthropathy,
clubbing,
sacroiliitis,
spondylitis,
fatty
liver,
k
ok mary sclerosing cholangitis,
oocholangiocarcinoma. .Book
Bo Investigations blds iWCC,
B
.
dalbumin (as a marKer
of inflammation, not
ww iCRP,
wwdvitamin
nutrition), dKw(diarrhoeal
losses), dCa , diron,w
dfolate,
B (terminal ww
ileal disease), bld cultures; Faecal calprotectin sensitive but non-​specific screen
for colonic inflammation—​if negative may avoid endoscopy Stool cultures Vital
t including C. difficile; AXR Mucosal
in ruling
causes of exacerbation
etouttoxicinfective
eresidue
et
n
n
n
.
.
.
oedema,
megacolon >6cm, faecal
suggests uninvolved mucosa;
X
X
kX and
± colonoscopy Shows
appearances/​
lceration
ok Sigmoidoscopy
okof characteristic
ouconsidered.
o
o
o
allows biopsy; CT/​MRI If concern
abscess and if surgery being
B Complications Toxic wmegacolon,
.B bowel obstruction, perforation,
w.B malabsorp- w
tion, fistulae, fissures,
strictures, malignancy.
w
w
w
w
w
B
15
16
16
16
16
16
16
16
+
2+
12
Table 9.8 Differentiating between ulcerative colitis and Crohn’s
t
Feature
.ne
Symptoms
X
k
oo
et
.n
kX
oo
B
.
w
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
o
w.B
oo
B
.
w
.n
kX
ww
t
.ne
X
k
t
ww
16
o
w.B
et
n
.
kX
o
o
B
.
w
ww
et
n
.
X
ww
t
w
ww
See Mwww.ecco-​ibd.eu for a range of European guidelines.
Related to disease activity.
15
ww
ok
o
o
w.B
ww
et
n
.
kX
o
et
.ne
X
k
Treatment This depends upon disease severity. Rehydrate and correct electrolyte imbalances; avoid antimotility/​antispasmodic agents. Systemically well
patients with mild–​moderate UC (<6 stools/​day) should start oral ±rectal
mesalazine (eg Pentasa® 2g/​24h PO). For mesalazine-​refractory disease or for
Crohn’s, give oral ±rectal steroids (eg prednisolone 40mg/​24h PO tapering by
5mg/​wk for total of 8wk). More severe disease requires IV steroids (eg hydrocortisone 100mg/​6h IV). Consider antibiotics until infectious causes ruled out
(eg co-​amoxiclav 1.2g/​8h IV). Monitor the patient closely (daily abdo exam,
bloods ±AXR) and involve surgeons early. Elemental diet, immunosuppressive
drugs (eg azathioprine), and biological agents (eg infliximab) may also be used.
Surgery This is indicated as an emergency procedure in cases of perforation or massive haemorrhage. Urgent surgery is performed in UC for toxic
megacolon or failure to respond to maximal medical therapy after 5–​7d;
delaying beyond this risks poor operative results. Surgery in Crohn’s is never
curative and associated with high recurrence and complication rates, but is
indicated for obstruction, abscesses, and fistulae.
e
X.n
ok
Bo
ww
w
t
ww
Bo
t
.ne
X
k
Ulcerative colitis (UC)
Crohn’s
Diarrhoea and PR blood/​
Diarrhoea, abdo pain and
mucus prominent
weight loss prominent
GI involvement Colon only, extending
Anywhere along GI tract, most
proximally from rectum to
commonly terminal ileum
variable extent
Endoscopy
Continuous inflamed mucosa Inflamed, thickened mucosa;
from rectum proximally
aphthous ulcers; skip lesions
Histology
Mucosal and submucosal
Inflammation extends beyond
inflammation, crypt abscesses, the submucosa, granulomas
reduced goblet cells
present
.ne
X
ok
.Bo
ww
B
316
.B
w
ww
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
t
.ne
.ne
.ne
Constipation
X
X
X
ok
ok
ok
o
o
Worrying features
Abdominal
pain,
distension,
nausea/​
vomiting,
Bo 2iHR,
B
B
. PR bleeding.
wt.inkling bowel sounds, weight
wloss,
dBP, absent/​
w
w
w Serious Bowel obstruction,
w bowel/​ovarian cancer; ww
Think about
Common Medications, poor diet, paralytic ileus, dehydration, functional
disorders;
et Other Anal fissure/​stricture,
et pelvic mass, spinal injury,.nhypoet
n
n
.
.
thyroid
(Table
9.9).
X
kX vomiting, date bowelsolast
kXopened,
ok Ask about Abdo pain,oonausea,
o
o
B
B frequency, stool consistency
normal bowel habit .and
and colour, blood
w.Bflatus,
in stools, pain w
on w
opening bowels, straining, bloating,
fluid intake,
w
w discharge; PMH IBS, ww
weight loss,w
tenesmus, recent surgery; ♀: periods,
IBD, diverticulosis, hernias, previous surgery, colon cancer, hypothyroidism;
et DH (see ‘Medications causing
etconstipation’) SH Mobility, .diet.
et
n
n
n
.
.
X
X
causing constipation
Opioids, iron supplements,
kX channel blockers,
ok Medications
ocalcium-​
ok drugs,
non-​magnesium antacids,
psychotropic
o
o
o
B
anticholinergics, chronic
w.B laxative use (may leadwtowthe.Bdevelopment of a w
dilated atonic w
colon).
w
w
w
Obs Temp, HR, BP, fluid balance.
Look
distennetfor Volume status (EXp..394),
net tenderness ±peritonism,
net
.
.
X
X
absent/​tinklingkbowel sounds, hernias, scars; k
ok sion, masses,
oimpaction, melaena/​blood. oo PR Anal fisrectal masses, faecal
o
Bo sures,
B
B obstruction
. FBC, U+E, TFT, Ca ; AXR w
Investigations blds
To .exclude
w
Sigmoidoscopy ±biopsy
ww if sub-​acute onset; Colonoscopy
ww If cancer suspected. ww
Management See Boxes 9.8–​9.10.
t
t
et 9.8 General management
.nBox
.ne of constipationX.ne
K
X
X
k
ok • Conservative Increaseofluid
okintake, high-​fibre diet, review
odrugs:
o
consider alternatives
without
GI
side
effects;
start
stool
chart—​
Bo
B
B
.
w. patients to
this will often be
wwkept more accurately ifwyouweducate
w
completew
it themselves.
w
• Medical E p. 207 for detailed first-​line laxative prescribing information;
begin
with a bulk-​forming laxative
(eg Fybogel ); if necessary t
etintreatment
et(eg Movicol
add
or switch to an osmotic laxative
); if stools soft .ne
n
n
.
.
X
X
but
still
difficult
to
pass,
add
a
stimulant
laxative
(eg
senna).
k will help soften impactedGlycerol
kX while
ok suppositories or arachisooiloenemas
ostool,
o
o
B
phosphate enemas.should
reserved for when other
fail.
w BNewerbe medications
wbe.Bmeasures
• Refractory symptoms
thatw
may
initiated under
w
specialistw
advice include prucalopride, linaclotide,
w and lubiprostone. ww
2+
®
®
et
n
.
kX
o
Bo
• Opioid-​induced constipation Avoid bulk-​forming agents; use osmotic
and/​or stimulant laxatives. Naloxegol or methylnaltrexone bromide
may be added for refractory symptoms.
• Surgical disimpaction Scooping hard faeces from the rectum is a
seriously unpleasant point of last resort for everyone concerned.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Constipation
w
317
t
t
t
.ne 9.9 Common causes of X
.ne
.ne
Table
constipation
X
X
ok
ok Examination Investigation
ok
o
o
Bo Bowel History
B
B
.
. loops of
Pain, distension,
Distension,
wvomiting,
wDilated
obstruction nausea,
tenderness, absent/​
bowel on AXR
w
w
wconstipation
ww
tinkling bowelw
sounds
Paralytic ileus Absence of flatus, Distended abdomen, Distended bowel
t recent operation absent
t sounds loops on AXR, dKnet
ecancer
ebowel
n
n
.
Bowel
Abdo pain, weight PR.blood
or melaena, dHb, lesion on .
Xmucus/​palpable
X
loss, fresh blood or
mass sigmoidoscopy/​
kX
k
o
o
ok
melaena
colonoscopy
o
o
o
B
B
.B or
Ano-​rectal Freshw
red. blood on Perianal tags, may wProctoscopy
pathology
toilet
paper, ±pain have a tear or w sigmoidoscopy
w
w
ww
tenderness w
Poor diet
Anorexia (eg post-​ Cachexia
dHb, dMCV, dCa
t
t
op), low-​fibre diet
e
e
et
n
n
n
.
.
.
Drugs
See
‘Medications
causing
constipation’
X
X
X
ok
ok
ok
o
o
o
B Poor diet w.B
w.Badequate nutri- w
$ A surprisingw
number of in-​patients fail tow
achieve
tion, with major
w impacts on wound healing,wrecovery, and physical con- w
B
+
2+
dition. Try to recognize this and involve dieticians where appropriate,
while avoiding prolonged NBM periods where possible. Markers for
nutritional adequacy are problematic, but end-​of-​the-​bed assessment
is useful. Where constipation is a feature, encourage to aim for regular
high-​fibre meals, with good fluid intake and regular physical activity.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
K Box 9.9 Hints and tips
o
Bo
ww
w
•Prescribe prophylactic laxatives for patients at risk of developing
constipation (eg when prescribing opioids, post-​op)
•Exclude obstruction before prescribing a laxative
• Lactulose is poorly tolerated by many patients and is associated
with abdominal pain and bloating
•Reassess regularly for resolUTIon of constipation—​do not put off
doing a rectal examination
• Consider malignancy in all patients >40yr presenting with altered
bowel habit.
t
.ne
X
k
t
o
ww
o
w.B
ok
Bo
oo
B
.
w
.n
kX
.ne
X
k
t
ww
et
n
.
X
I Box 9.10 Causes of constipation covered elsewhere
o
o
w.B
Anal fissures/​haemorrhoids E p. 309
Inflammatory bowel disease E p. 315
Irritable bowel syndrome E p. 314
et
n
.
kX
o
et
.ne
X
k
ww
t
e
X.n
Bo
t
.ne
X
k
ww
ok
o
w.B
Bowel obstruction E p. 298
Polyps E p. 309
ww
et
n
.
kX
t
o
o
B
.
w
ww
ww
w
ww
.ne
X
ok
.Bo
ww
B
318
.B
w
ww
.B
w
w
ww
w
Gastroenterology
Chapter 9
t
t
et
.nLiver
.ne
.ne
2
failure
emergency
X
X
X
ok
ok
ok
o
o
Bo 2 Airway
B
B
. airway is patent; consider manoeuvres/​
wCheck
w. adjuncts
ARREST TEAM
2 Breathing w If no respiratory effort—​CALL w
w If no palpable pulse—​CALL w
ww
ARREST TEAM
2 Circulation
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
et
et
et
n
n
n
.
.
.
X Altered mental state or coagulopathy
X
kX
in the presence ofojaundice.
ok $3Call
okif patient deteriorating.
o
o
o
for
senior
help
early
B
w.B
w.B
Airway
w
w
wthe mouth, wide-​bore suctionwif secretions present
ww
• Look inside
• Jaw thrust/​head tilt/​chin lift; oro/​nasopharyngeal airway if tolerated.
et
et
et
Breathing
n
n
n
.
.
.
•
15L/​
m
in
O
if
SOB
or
sats
<94%
X
X
ok • Monitor O sats and RR.ookX
ok
o
o
B
Circulation w.B
w.B
w
w
• Venous access
, take bloods:
w
w
ww
B
2
2
FBC, U+E, LFT, PT/​APTT, CRP, glucose, amylase, Ca2+, Mg2+,
PO43–​, bld cultures, paracetamol levels, viral serology
• Start IV fluids 1L of 5% glucose over 4–​6h
• Monitor HR, ECG, BP.
•
t
.ne
X
k
oo Disability
et
oo
B
.
w
.n
kX
oo
B
.
ww
t
.ne
X
k
• Check blood glucose treat if <3.5mmol/​L (E p. 328)
• Check GCS, pupil reflexes, limb tone, plantar responses.
ww
o
Bo
• Check temp
• Ask ward staff for a brief history or check notes:
• previous liver disease, likely causes (Box 9.11)
• Examine patient brief RS, CVS, abdo, and neuro exam:
• signs of chronic liver disease
• ECG, ABG, and urgent portable CXR
• Stabilize and treat E pp. 319–23
• Call for senior help and arrange transfer to HDU/​ICU
• Reassess, starting with A, B, C . . .
t
.ne
X
k
t
o
ww
t
o
w.B
ww
w
Exposure
.ne
X
k
ww
oo
B
.
w
et
.n
kX
ww
et
et
n
n
.
.
X failure
X
ok 2 Box 9.11 Causesoofokliver
ok
o
o
B
B
Acute liver failure
overdose, drugs, toxins,.B
alcoholic hepatitis,
w.Paracetamol
w ischaemic
viral hepatitis, autoimmune hepatitis,
hepatitis
w
w
Budd–​Chiari
w (heart failure and shock), w
ww
Decompensated
Alcohol excess, malignancy, GI bleeds, metabolic
chronictliver disease
disturbances, sedatives,
vein thrombosis, acute t
e
et portal
illness, surgery,.n
infection
(eg spontaneous bacterial.ne
n
.
peritonitis)
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
e
X.n
B
.B
w
ww
.B
w
w
w
w
Liver failure
w
319
t
t
t
.ne failure
.ne
.ne
Liver
X
X
X
ok
ok
ok
o
o
Bo 2 Worrying features
B
B
Ascites, hepatic flap, altered. mental state, and
w. features
jaundice are cardinal
of decompensation
w
wwin liver disease; also ww
w bleeding, renal failure, iHR, w
beware active
dBP.
Thinktabout 2 Emergencies Acute liver
decompensated chronic
t failure,
e hepatic encephalopathy;
eAcute
et
liver
disease,
liver failure Paracetamol.n
overn
n
.
.
X (E p. 509), alcoholic hepatitis,
X hepatitis (A, B, C, E, CMV,
X
ok dose
ok‘Drug-​viral
oktoxinsEMV),
pregnancy, medications (see
induced hepatotoxicity’),
(eg
o
o
o
B poisonous mushrooms),
B
B
vascular (eg Budd–​Chiari), sepsis,
Weil’s disease,
.
.
w‘Drug-​induced hepatoabscess; Chronic w
liverw
failure Alcohol, medications (see
toxicity’), obesity,
w idiopathic, autoimmune, hepatitis
ww (B±D, C), malignancy, ww
Wilson’s disease, haemochromatosis, α -​antitrypsin deficiency.
et induced hepatotoxicity.nThisetmay result in response to a.nlarge
et
$n
Drug-​
.
number
of
drugs,
ranging
from
mild
elevations
in
LFTs
to
fulminant
hepatic
X
X
X
ok failure. Paracetamol, NSAIDs,
okACEi, erythromycin, fluconazole,
okand statins
o
o
o
commonly cause hepatocellular
limit normal with
B
.B injury (ALT >2× upper
w.Bciprofloxacin, iso- w
normal/​minimally w
iALP). Chlorpromazine, oestrogens,
w
w
niazid, phenytoin,
w erythromycin, and co-​amoxiclav
w can all cause cholestasis w
1
(iALP, with or without associated hepatocellular damage). Always ask about
recreational drugs (eg cocaine, mushrooms) and OTC or herbal medications.17
t
t
t
.neabout Tiredness, jaundiceX(+onset),
.ne abdo pain, drowsinessX±confu.ne
Ask
X
k bowel, urine), distension, oankle
k swelling,
ok sion, bruising, bleeding (skin,
onose,
o
o
infections
(sore
throat),
weight
loss,
hair loss,
Bo vomiting, rashes, recent
B
B
.Previous jaundice, gallstones,w.blood transfusions;
w
darkening skin; PMH
DH See ‘Drug-​
nduced hepatotoxicity’; FH Liver
wiw
wwdisease, recent jaundice; ww
SH Alcohol, IVDU, tattoos, piercings, foreign travel, sexual activity.
Obs Temp,
HR, BP, RR, O sats, GCS, blood
glucose, urine output.
t liver
etfor Volume
eAcute
et
n
n
Look
status E p. 394;
failure Drowsiness,
.
.
.nconX
X
X
fusion,
slurred
speech,
jaundice,
flapping
tremor
(asterixis),
poor
co-​
ok ordination, bruising, foetor
okhepaticus (sweet, faecal smelling
ok breath),
o
o
o
B abdominal t­ enderness,
.Bhepatomegaly, ascites; Chronicwliver
.Bdisease Cachexia,
w
palmar erythema,
clubbing, xanthelasma, spiderw
naevi, caput medusa, gyw
w
naecomastia,w
muscle wasting, splenomegaly,w
genital atrophy, track marks w
(IVDU), pneumonia/​chronic lung disease, darkened skin.
Investigations
These are aimedeatt establishing the extent and poset of liver$damage,
et
n
n
n
.
.
.
sible
cause
and
finding
a
possible
cause
of
any
decomX
X
kXclotting,
especially intercurrent
Urine MSU; blds o
FBC,
ok pensation,
ok infection.
o
o
o
iron,
ferritin,
U+E,
LFT,
hepatitis
serology
(A,
B+C),
EBV
and
CMV serB ology, caeruloplasmin
.B
.B
(if <50yr), autoimmune screen
(antimitochondrial,
w
w
antinuclear andwanti-​smooth muscle antibodies,
w
ww E p. 607), bld cul- ww
2
et
n
.
kX
o
Bo
tures; Urgent USS abdo Looking for parenchymal mass(es), dilated ducts
or portal vein thrombosis; Urgent ascitic tap (E pp. 564–5) and white
cell count to check for spontaneous bacterial peritonitis (E p. 322).
OGD may help assess for varices and check for upper GI bleed as cause of
decompensation.
17
et
n
.
kX
t
o
o
B
.
w
ww
w
.ne
X
ok
.Bo
Useful review article available free at Mwww.ncbi.nlm.nih.gov/​pmc/​articles/​PMC2773872
ww
ww
B
.B
w
ww
320
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
t
3Acute
.ne liver failure (E OHAM4
.ne p. 268.)
.ne
X
X
X
and jaundice without
k
ok $ Acute encephalopathy,oocoagulopathy
ok previous
o
Bo cirrhosis (Table 9.10).
B
B
wof. acute liver failure
w.
Table 9.10 Types
w
w
w
w
ww
Liver failure <7d of disease onset
Hyperacute fulminant hepatic failure
Liver failure
t 1–​4wk of disease onset neAcute
t fulminant hepatic failure net
efailure
n
Liver
4–​12wk of disease onset . Subacute fulminant hepatic failure
.
X Late-​onset hepatic failure kX.
kXLiver failure 12–​26wk of diseaseokonset
o
oo
Bo Symptoms Bruising/​wb.leeding,
Bo drowsy ±confusion, w
.Bpain.
abdo
Signs Drowsiness,
confusion, slurred speech, w
flapping tremor
wwcoordination,
w jaundice,ascites.
ww
(asterixis), poor
bruising, hepatomegaly,
Investigations Initiate liver screen as detailed (E p. 313) blds iPT/​
APTT,
etiiALT, iALP, ibilirubin, .iammonia,
et iWCC, dglucose, .dMg
et ,
n
n
n
.
dPO
;
ABG
Respiratory
alkalosis,
metabolic
acidosis
(poor
prognosis);
X Masses, echogenicity, portal
Xvein flow.
X
ok USS
ok early,
ok with invao
o
o
Treatment
Discuss
with
a
senior
often
needs
ICU/​HDU
B
B need transfer to a specialist
sive monitoring, and
liver centre, where
wfor.may
w.B
w
w
may be considered
transplantation.
Monitor
blood
glucose every 2h; ww
w
w
B
2+
3–​
4
insert a catheter and monitor fluid balance.
• i PT Give one-​off dose of vitamin K 10mg IV. PT prolongation is used
to monitor disease progress; FFP and/​or platelets may be indicated if
the patient is bleeding or needs an invasive procedure
• Stop Aspirin, NSAIDs, and hepatotoxic drugs (E p. 319); check all drugs in BNF
• Antibiotic Prophylaxis in all patients (eg cefotaxime) ±antifungals
• Daily bloods FBC, U+E, LFT, PT18
• Steroids May improve survival in more severe alcoholic hepatitis
• Lactulose 10–​20mL/​8h PO in all patients (helps remove ammonia)
• Close monitoring of cardiovascular status and blood glucose; if need IV
fluids, avoid Na+ if cHRonic liver disease/​ascites.
Complications Renal failure (hepatorenal syndrome), respiratory failure
(ARDS), cerebral oedema, bleeding, sepsis, dglucose, iNa+, dK+.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
w
t
o
o
w.B
oo
B
.
w
.n
kX
ww
$ Acute liver inflammation on a background of chronic alcohol excess.
Symptoms and signs Jaundice, anorexia, fever, and RUQ pain.
Investigations blds iWCC, ibilirubin, iALT ±iPT. −ve hepatitis/​autoimmune serology; Ascitic tap to exclude spontaneous bacterial peritonitis.
Treatment As for acute liver failure. Transplantation may have a role in
highly selected patients.
t
e
X.n
.ne
X
k
t
ww
et
.ne
X
k
Alcoholic hepatitis
ww
t
.ne
X
k
et
n
.
X
ww
ok
o
ok
o
o
Bo Vascular liver w
B
B
.
.
disease
w hepatic jaundice or w
$ Diagnosed by
Doppler uss; these diseases canw
w
w
w orcause
acute liver failure, often treated by anticoagulation
endovascular methods. w
• Budd–​Chiari hepatic vein obstruction
• Portal
(pain and deranged
etveinof obstruction
et LFTs; jaundice only if other
et
n
n
causes
liver disease coexist) .n
.
.
X ischaemia due to hypotension
kXrise. and/​or hepatic arteryostenosis.
kX
ok • Liver
oALT
Typically causes massive
o
o
o
B
w.B
w.B
w
w
w
w
ww
Strictly, the INR is specific for warfarin therapy; the pattern abnormal clotting in liver disease is
different and more reliably reported as PT and APTT prolongation.
18
B
.B
w
ww
.B
w
w
w
w
Liver failure
w
321
t
t
t
Glandular
Epstein–​Barr virus, EBV.)
.ne fever (Infectious mononucleosis,
.ne
.ne
X
X
X
Usually young (10–​
k30yr), sore throat >1wk, fever,
ok Symptomsrash,
oneck,
ok lethargy,
o
o
lumps in the
anorexia.
Bo malaise,
B
B
Signs Red tonsils ±white
w. exudate, tender lymphadenopathy,
w. splenomegaly,
rash (especially w
with amoxicillin/​ampicillin), palatal
petechiae, jaundice.
w
Investigationsw
blds ilymphocytes (atypical on w
film), iALT, +ve Monospot/​
Paul Bunnell, +ve IgM for EBV.
Management
rehydration, analgesia,
etavoid Rest,
et gargle with warm saline/­​
et
n
n
n
.
.
.
­aspirin,
amoxicillin/​ampicillin,
avoid alcohol, consider short course
X oral steroids if very severek(eg
X
X
encephalopathy).ok
ok ofComplications
ofailure,hepatic
o
o
o
Hepatitis,
liver
thrombocytopenia,
splenic
rupture,
B haemolysis, encephalitis.
.B
.B
w
w
w
Acute viral
(E OHCM10 p. 278.)
whepatitis
ww
Causes Hepatitis A,B,C and E, cytomegalovirus (CMV) and EBV.
Symptoms Jaundice, rash, diarrhoea, abdo pain, flu-​like symptoms (eg
fever, malaise, anorexia, fatigue, nausea, vomiting, arthralgia, sore throat).
Signs Patient may have no signs, itemp, urticarial rash, jaundice, hepatomegaly, splenomegaly, lymphadenopathy.
Investigations blds iWCC, ibilirubin, iALT ±iPT, +ve hepatitis serology (eg
check anti-​hepatitis A, B, C, ±E, see Table 9.11 for hepatitis B interpretation).
Management Avoid alcohol, supportive treatment, monitor for progression to acute liver failure (E p. 320) which may need interferon-​α.
Complications Natural history varies widely depending upon virus and
host; risks include acute liver failure or chronic disease.
et
n
.
X
ok
Bo
et
n
.
X
ok
o
B
.
w
ww
ww
ww
t
.ne
X
ok
o
B
.
w
ww
ww
t
t
t
.ne
.ne
.ne
X
X
X
k
ok
o(E
ok
o
viral hepatitis
OHCM10 p. 406) Bo
Bo Chronic
B
. by hepatitis B(±D) andw
$ Hepatitis >6mth,w
caused
C. .
w
w
Symptoms and
signs
Usually
asymptomatic,
signs
of
w
w chronic liver disease. ww
Investigations blds Deranged LFT ±iPT; abnormal viral serology (check
anti-​hepatitis
antibody then PCR for viral
if positive; see Table 9.11
t
et BCserology);
et beload
for.n
hepatitis
USS Liver.n
may
suggestive of cirrhosis..ne
X
X
X
referkto a hepatologist for antiviral treatment.
ok Treatment Avoid alcohol;(20%),
o hepatocellular carcinoma (esp
okHBV).
o
o
Bo Complications Cirrhosis
B
B
w. in hepatitis B
w.
Table 9.11 Serology
w
w
w
w
ww
19
Surface antigen (HBsAg)
Anti-​core (anti-​HBc) IgM
Anti-​core (anti-​HBc) IgG
‘e’ antigen (HBeAg)
Anti-​e (Anti-​HBe)
net
X.
ok
Bo
Active virus replication—​acute or cHRonic disease
Acute infection
Chronic infection (or previous infection if HBsAg –​ve)
High infectivity
Low infectivity
.ne
X
k
t
ok
o
o
w.B
ww
et
n
.
X
ww
o
w.B
$ In chronic hepatitis B infection, HBeAg negativity is associated with immune
control of the virus and low/​undetectable viral DNA. Beware, however, the
subset of patients in whom the virus develops a precore mutation leading to
absent production of HBeAg, despite loss of immune control and rising viral
DNA titres. These patients are at high risk for disease complications.
Bo
o
et
n
.
kX
et
n
.
kX
t
o
o
B
.
w
ww
.ne
X
ok
.Bo
A rapidly evolving area with huge progress in the treatment options for hepatitis C. For a range
of current European guidelines, see Mwww.easl.eu
19
ww
w
ww
ww
B
322
.B
w
ww
Chapter 9
.B
w
w
ww
w
Gastroenterology
t
t
t
Decompensated
chronic liver
.ne
.nefailure (E OHCM10 p.X276.)
.ne
X
X
is the final common
ok $ Cirrhosis
ok histological pathway foroka variety of
diseases; problemso relate to synthetic functiono(coagulopathy,
Bo liver
B
­ascites 2° to hypoalbuminaemia),
decreased detoxification
w.
w.B (encephalop- w
athy), or portalw
hypertension (variceal bleeding).
w
w
w
w
Symptoms and signs As for acute liver failure (E p. 320) but look for stigmata
of chronic liver disease: spider angioma, palmar erythema, gynaecomastia.
t and clotting profile; Establish
Investigations
et Measure severity LFTs,.neU+E
et
n
n
.
.
underlying
cause
Hepatitis
serology,
immunoglobulins,
liver
autoantibodies,
X α -​antitrypsin, caeruloplasmin,
X
kX precipiliver biopsy; o
Identify
ok ferritin,
obldk cultures,USS,
o
o
o
tant
of
decompensation
FBC,
ascitic
tap,
OGD.
Treatment
This
B
B and transplant assessment;
.input
.Bdeal with upper
requires hepatology
w
w
wpp. 305–6), treat sepsis, support
GI bleeding w
(E
ww alcohol cessation, lac- ww
tulose (to reduce ammonia levels). Ascites Low-​salt diet, daily weights,
spironolactone 100mg/​24h PO increasing dose every 48h to 400mg/​24h
et ascitic tap for diagnosis
e(Et pp. 564–5) and to exclude.nsponet
±furosemide;
n
n
.
.
taneous
bacterial
peritonitis;
may
need
long-​
t
erm
antibiotics,
therapeutic
X
X
X
ok paracentesis, or TIPS if orecurrent.
ok Complications High mortality,
ok portal
o
o
hypertension,
bleeding
varices,
e
­
ncephalopathy,
hepatocellular
carcinoma.
B
w.B
w.B
Spontaneous
bacterial peritonitis
w
w
w
w
ww
1
Symptoms Abdominal pain in the presence of ascites, associated
with fever. Signs Fever, iHR ±dBP, abdo tenderness ±peritonitis.
Investigations blds iWCC, iCRP; Ascitic tap >250 white cells/​mm3 or
identification of organisms (E pp. 564–5). Treatment Prompt IV antibiotics: (eg Tazocin® 4.5g/​8h IV).
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
w sclerosing cholan- w
Causes Primaryw
biliary cholangitis (E p. 325), primary
ww
gitis (E p. w
325), autoimmune hepatitis (type
I and II—​see Table 9.12); w
primary biliary cirrhosis and type I autoimmune hepatitis may overlap.
t fever, malaise, rash, jointnpain,
t
Symptoms
have
et Often asymptomatic, may
or.n
symptoms of chronic liver disease.
.neSigns Signs of chronic liverXdisease.
. e
X
X
blds Deranged LFT
±iPT, +ve autoantibodies (Table
9.12);
ok Investigations
ok Autoimmune
ok 30mg/​
And liver biopsy. Treatment
hepatitis Prednisolone
o
o
Bo USS
B
B
.azathioprine; Other diseases Ew.p. 325. Complications
24h PO initially then
wcirrhosis,
Acute liver failure,
hepatocellular carcinoma.
w
w
ww
ww
Table 9.12 Autoantibodies in autoimmune liver disease
et biliary cholangitis Anti-​m.nitochondrial
et (AMA) present in 95%.nandet
Primary
n
.
98%
X(780% ♀)
Xspecific
X
ok Primary sclerosing cholangitisookAnti-​
ok (ANA),
smooth muscle (SMA), antinuclear
o
o
(770% ♀, 780% IBD) .B
p-​ANCA
B
w
w.Bantinuclear (ANA)
Autoimmune hepatitis
Anti-​smooth musclew
(SMA),
w
type I (80% ♀)
w
w
ww
B
Autoimmune liver disease (E OHCM10 p268.)
Autoimmune hepatitis type II Anti-​liver/​kidney microsomal type 1 (LKM1)
(mainly children; 90% ♀)
Bo
o
et
n
.
kX
et
n
.
kX
o
o
B
.
w
ww
w
ww
t
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w
w
w
Liver failure
w
323
net
net p. 288.)
net
Haemochromatosis
(E OHCM10
.
.
.
X
X
X
recessive diseasekcausing excess iron accumulation.k
ok $ Autosomal-​
o hyperpigmentation, DM.ooSigns HepatoFatigue, lethargy,oarthralgia,
Bo Symptoms
B
megaly, signs of chronic
liver disease, cardiac failure, or.B
conduction defects,
.
w tanned skin. Investigationswbldswitransferrin
saturation
hypogonadism ±impotence,
w
w
false-​negatives esp. in younger w
(>60% in ♂ w
and >50% in ♀ highly specific, butw
♀),iALT, iglucose, genetic testing (2 common mutations account for 70% of
ECG Cardiomyopathy ort conduction delays; Liver biopsy (DiagCaucasian
t patients);
eseverity).
et
Treatment Venesection n
(1eunit/​wk) until ferritin normalizes
then
nosis,
n
n
.
.
.
Xevery 3–​6mth; transferrin saturation
Xor genetic screening of relatives.kX
ok Non-​alcoholic fatty liver
okdisease (E OHCM10 p.o285.)
o
o
o
B $ Spectrum of damage
B
from fat deposition in absence of.B
other causes.
.
w failure. Investigations
Symptoms and signs
Obesity, hypertension, diabetes,
liver
ww
blds Full liver w
screen to rule out other causes; HbA
ww; USS ± elastography may ww
show fat deposition and evidence of cirrhosis; liver biopsy. Treatment Weight
loss; manage
et cardiovascular risk; monitor
etfor transplantation.
et
n
α .-​n
antitrypsin deficiency (E.n
OHCM10 p. 290.)
.
X Genetic disease with complexkinheritance
X
X
causing liver and lung k
ok $Symptoms
o liver failure,
o damage.
and signs Breathlessness,
family history.
Investigations
o
o
o
B blds dα -​antitrypsinwlevels,
.Bgenetic testing; liver biopsy. Treatment
w.B Stop smoking, w
COPD treatment.
may need liver transplant,
w
w
w
w
w
1C
1
1
Wilson’s disease (E OHCM10 p. 285.)
$ Autosomal-​recessive disease; copper accumulates in the liver and CNS.
Symptoms Tremor, slurred speech, abnormal movements, clumsiness, depression, personality change, psychosis, liver failure, family history. Signs Kaiser–​
Fleischer rings in eyes, signs of liver failure. Investigations blds dcaeruloplasmin,
dtotal serum copper, iserum free copper, genetic testing; Urine i24h copper
excretion (especially if a dose of penicillamine is given); copper on liver biopsy.
Treatment Lifelong penicillamine, may need liver transplant, screen relatives.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
ww
$ Bacterial infection typically transmitted via exposure of skin cuts or mucous membranes to water contaminated with rat urine.
Symptoms Recent contact with dirty water, high fever, malaise, anorexia, fatigue, nausea, vomiting, arthralgia, pharyngitis, conjunctival oedema, neck
stiffness, photophobia, jaundice, bleeding and kidney failure. Signs Acute liver
failure, meningism, bruising, tender RUQ, myocarditis. Investigations Urine Dipstick haematuria, culture; blds dHb (haemolytic), iurea, icreatinine, ibilirubin,
iALT, serology. Treatment Doxycycline 100mg/​12h PO or benzylpenicillin
600mg/​6h IV and supportive care of renal/​liver failure.
et
et
.n
kX
o
o
o
w.B
ok
Bo
o
o
w.B
t
ok
o
w.B
e
X.n
ok
o
w.B
ww
t
t
e
X.n
ww
ww
t
e
X.n
ok
o
B
.
w
ww
t
e
X.n
$Predicting outcomes in chronic liver disease This is of considerable importance, not least
in prioritizing use of organs for transplantation. The ‘Child’ scoring system originated in
1964 from attempts by Child and Turcotte to assess operative risks for cirrhotic patients
undergoing porto-​systemic shunt surgery. Later modifications to include albumin and
INR led to the ‘Child–​Turcotte–​Pugh’ score which is still widely used. With the advent
of liver transplantation, more precise stratification of patients with advanced disease
was needed: for the NHS transplantation programme, the UKELD (UK end-​stage liver
disease) score is calculated from serum Na+, creatinine, bilirubin, and INR.
The original description of the UKELD score (Neuberger J, et al., Gut
2008;57:252) is available online at Mgut.bmj.com/​content/​57/​2/​252.abstract
(subscription required, but many NHS trusts provide access through ATHENS).
Online calculators for the Child score are widely available (eg Mwww.mdcalc.
com). Information on the NHS transplantation programme, including liver transplants and a UKELD calculator is available at Mwww.organdonation.nhs.uk
ww
ok
.n
kX
ww
t
e
X.n
ww
et
.n
kX
ww
Bo
.n
kX
o
w.B
Weil’s disease (leptospirosis)
Bo
et
.n
kX
e
X.n
ok
ww
o
B
.
w
ww
B
324
.B
w
ww
Chapter 9
o
oo
B
.
w
t
.ne
X
k
et
o
w.B
.n
kX
o
2 Worrying features iHR, dBP, drowsiness, dGCS, bleeding, slurred
speech, poor coordination, tremor/​flap, renal failure, weight loss.
ww
ww
Think about
o
Bo
ww
w
Gastroenterology
t
.ne
Jaundice
X
k
Bo
.B
w
w
et
n
.
kX
t
ok
.B
w
ww
ww
et
n
.
X
ok
Bo
et
n
.
kX
oo
e
X.n
Pre-​hepatic Haemolysis, malaria.
Hepatic Paracetamol overdose, viral hepatitis, alcohol, chronic liver
disease, Gilbert’s syndrome, pregnancy, medications (E p. 325), toxins
(eg poisonous fungi), vascular disease (eg ischaemia, Budd–​Chiari), sepsis.
Cholestatic Choledocholithiasis, ascending cholangitis, pancreatic cancer,
cholangiocarcinoma, primary biliary cirrhosis, 1° sclerosing cholangitis.
Ask about Tiredness, jaundice (+onset), abdo pain, itching, dark urine,
pale stools, drowsiness, confusion, bruising, bleeding (skin, nose, bowel,
urine), bloating, vomiting, rashes, recent infections (sore throat), weight loss,
generalized aching, hair loss, darkening skin, joint pain; PMH Previous jaundice, gallstones, breathing problems, blood transfusions; DH Paracetamol
and medications (E p. 325); FH Liver disease, recent jaundice; SH Alcohol,
IVDU, tattoos, piercings, foreign travel, sexual activity (?abroad).
o
w.B
et
n
.
X
ok
o
B
.
w
ww
ww
ww
t
.ne
X
ok
o
B
.
w
ww
Obs Temp, RR, HR, BP, urine output, O2 sats, glucose, GCS.
Look for Volume status (E p. 394), bruising, evidence of bleeding,
ww
t
t
t
drowsiness,
.ne confusion:
.ne
.ne
Pre-​hepatic Splenomegaly, pale X
conjunctiva, breathlessness.
X
X
ok Hepatic Signs of acute orochronic
ok liver failure (E pp. 319–23).
ok
o
tenderness
±peritonism,
Charcot’s
triad (fever,
Bo Cholestatic Abdominal
B
B
.
. cachexia.
w
jaundice and RUQw
pain = cholangitis), palpable gallbladder,
ww
wwurobilinogen; blds FBC, ww
Initial investigations
Urine MSU, bilirubin,
reticulocytes and LDH (both elevated in haemolysis), blood film, clott LFT (total and conjugatedet bilirubin), amylase, lipase, nparating, e
U+E,
et
cetamol
serology, bld cultures;.Urgent
.n levels, hepatitis, EBVXand.nCMV
X
X
ducts,
k
ok USS Abdo (?dilated bile 9.12.
ok cirrhosis, pancreatic mass,
ometastases).
o
o
Bo See Table 9.13 andwBox
B
B
.
w.
Table 9.13 Laboratory
investigation of jaundice
w
w
w
w
w
w
Urine
Liver tests
Other tests
Pre-​hepatic
Urobilinogen iunconjugated t
dHb, nMCV, dhaptoglobin, t
t
e
e
jaundice
bilirubin .n
ireticulocytes
n
.
.ne
X
X
X
May have positive hepatitis
k
ok Hepatic Urobilinogen oimixed
ok Abilirubin,
serology or iparacetamol
iALT/​
ST
oo levels
Bo jaundice
B
B
.
.
Cholestasis Bilirubin,
dark iconjugated bilirubin, Dilated
wducts on USS
urine
ww iALP, iγGT
w
ww
ww
Cholangitis Bilirubin, dark iconjugated bilirubin, iWCC, iCRP, dilated biliary
urine
iALP, iγGT
ducts
Bo
o
et
n
.
kX
et
n
.
kX
t
.ne
X
k
oo
Liver failure E pp. 319–23
B
.
w
ww
I Box 9.12 Causes of jaundice covered elsewhere
o
o
B
.
w
ww
Haemolysis E p. 408
ww
B
.B
w
ww
.B
w
w
w
w
Jaundice
w
325
t
t
t
Gilbert’s
.ne syndrome X.ne
.ne
X
X
disease causing mild, self-​
ok $ Benign autosomal recessive
ok typically
ok resolving
o
o
during acute illness.
Bo unconjugated hyperbilirubinaemia
B
B
w.
w.
Choledocholithiasis
w
w
$ Gallstonew
in common bile duct, causing obstructive
jaundice.
w
ww
Risk factors ♀, pregnancy, DM, obesity, age. Symptoms Often none, preceding tbiliary colic, dark urine, pale tstool. Signs Jaundice, mild RUQ
e Investigations blds iALP,
eibilirubin; USS Dilated bile .ducts.
et
tenderness.
n
n
n
.
.
X
Xexclude pancreatitis and kcholangitis,
X
Maintain hydration,
ok Treatment
oco-​kamoxiclav
opermits diagprophylactic antibiotics (eg
1.2g/​8h IV); ERCP
o
o
o
B nosis and stone removal;
cholecystectomy usually deferred
until jaundice
w.BPancreatitis,
w.Bclotting
resolved. Complications
cholangitis, w
hepatitis,
defects.
w
w
w
ww
Cholangitis
$ Infection of the bile duct with Charcot’s triad: fever, jaundice, RUQ pain.
t Signs itemp, iHR ±dBP,
et Unwell, abdo pain, rigors,
ejaundice.
et
Symptoms
n
n
n
.
.
.
RUQ
tenderness
(Murphy’s
+ve).
Investigations
blds
iWCC,
iCRP,
X
X
X
ok ibilirubin; USS ?duct dilatation,
ok stones. Treatment eg co-​aomoxiclav
ok 1.2g/​
o
o
8h
IV;
may
need
an
urgent
ERCP
if
gallstones
are
in
the
common
B
.B
.B bile duct.
w
w
Primary biliary
ww cholangitis (E OHCM10
wwp. 282.)
ww
B
$ Chronic, progressive autoimmune destruction of interlobular bile
ducts. Previously known as primary biliary cirrhosis.
Symptoms and signs Fatigue, pruritus, cholestatic jaundice, cirrhosis. Investigations blds iALP, iγGT ±ibilirubin, iIgM, anti-​mitochondrial antibodies (E
p. 322); USS ±liver biopsy for staging. Treatment Ursodeoxycholic acid (helps
symptoms and delays progression); colestyramine 4–​8g/​24h PO for itching;
monitor for signs of decompensation and screen for osteoporosis (DEXA);
in advanced disease immunosuppression (eg methotrexate, steroids); replace
fat-​soluble vitamins (A, D, E, K); refer for liver transplant assessment.
t
.ne
X
k
oo
et
ww
oo
B
.
w
.n
kX
oo
B
.
ww
w
Primary sclerosing cholangitis (E OHCM10 p. 282.)
t
.ne
X
k
ww
t
t
$ .Inflammation
and fibrosis of intra-​
net
.neand extrahepatic bile ducts.X.ne
X
X
signs Chronic biliary
obstruction leading to cirrhosis;
IBD
k UC,
ok Symptomsinand780%,
o790%
oknot related
of which
but course of IBD
o
o
Bo present
B
B
to PSC. Investigations. blds iALP, ±ibilirubin, iimmunoglobulin
levels,
w antibodies (SMA), antinuclear
w.antibodies (ANA),
anti-​smooth muscle
w
w
w A1, B8 or DR3; ERCP Multiple
w strictures; fibrosis on ww
p-​ANCA, HLA-​
liver biopsy. Treatment Trials of immunosuppressive agents have proven
disappointing;
acid can
screen for osteoet(DEXA)ursodeoxycholic
ethelp symptoms;(71%
et
n
n
n
.
.
porosis
and monitor for .cholangiocarcinoma
per annum);
X
X
X
ok transplantation key, but disease
ok recurs in 15% post transplant.
ok
o
o
o
B Cholangiocarcinoma
B (OHCM10 E p. 286.) w.B
w.(90%)
$ Adenocarcinoma
or squamous cell carcinoma of intra-​and
w
extrahepaticw
biliary epithelium; strong relationship
ww with IBD and PSC. ww
Symptoms and signs Jaundice, pruritus, weight loss, dull RUQ ache. Courvoisier’s
law An tenlarged gallbladder in the presence
of jaundice is not caused by
e (suggests pancreatic or .biliary
et cancer).
et
gallstones
Investigations blds.iALP,
n
n
n
.
X
X ± biopsy. Treatment ­Surgeryk(10–​
X
CA19.9; USS, MRCP,kERCP
ok ibilirubin,
oERCP + stenting.
o 40%);
else palliate: chemotherapy,
o
o
o
B
w.B
w.B
w
w
w
w
ww
B
.B
w
ww
t
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k
o
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oo
B
.
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et
n
.
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k
ok
et
n
.
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.
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o
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o
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o
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ww
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w
ww
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w
w
w
w
Chapter 10
w
327
t
t
t
.ne Endocrinology
.ne
.ne
X
X
X
ok
ok
ok
o
o
Bo
B
B
w.
w.
w
w
w
w
ww
2 Hypoglycaemia emergency 328
329
t Hypoglycaemia
e
et 330
et
2 Hyperglycaemia emergency
n
n
n
.
.
.
Hyperglycaemia
331
X Sliding scales 333 kX
kX
ok
o
o
o
o
o
Diabetes mellitus
334
B
Pituitary axis
w.B337
w.B
w
w
Adrenal
w disease 338
w
ww
Thyroid disease 340
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
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.
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o
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ww
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328
.B
w
ww
Chapter 10
.B
w
w
ww
w
Endocrinology
t
t
et
.nHypoglycaemia
.ne
.ne
2
emergency
X
X
X
ok
ok
oakdjuncts
o
o
Check
airway is patent; consider manoeuvres/​
Bo 22 Airway
B
B
ARREST
wIf .no respiratory effort—​CALLw
w. TEAM
Breathing
w
2 Circulation
w If no palpable pulse—​CALLwARREST TEAM
ww
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
t
t
e
edeteriorating.
et
n
n
n
.
.
.
3Call
for senior help early if patient
X glucose is normally >3.5mmol/​
X L
X
ok •• Blood
okcan have symptoms
ok
o
o
o
Poorly controlled diabetics
of hypoglycaemia
B
with a glucose >3.5mmol/​
w.B L.
w.B
w
w
Coma or w
low GCS with low glucosew
ww
• Protect airway
• 15L/​m
if SOB or sats <94%
et in Ovenous
etpresent
et
•Establish
access unless already
n
n
n
.
.
.
X IV glucose STAT (75–​1k00mL
X
or 200mL of 10%)kX
ok •• Give
o or offor20%
If unable to establish IVoaccess,
large insulin overdoses
o
oo give 1mg
B
B
glucagon SC/​IM .B
.
w
• Begin to follow
emergency
protocol E pp. 344–5
GCS)
ww(low
ww is responsible, GCS shouldwreturn
ww
• If hypoglycaemia
to 15 in <10min
B
2
• Start 1L 10% glucose/​4–​8h IV, adjust rate to keep glucose >5mmol/​L
• Monitor finger-​prick glucose every 30min–​1h until patient stable
• Attempt to determine the cause of the hypoglycaemia and review
diabetes treatment if appropriate
• Call for senior help
• Reassess, starting with A, B, C; if no improvement E pp. 344–5.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
GCS 15/​15 with low glucose
o
Bo
t
.ne
X
k
t
o
o
w.B
ok
Bo
oo
B
.
w
.ne
X
k
et
.n
kX
t
2 Box 10.1 Causes of hypoglycaemia
o
o
w.B
• Insulin overdose
• Medication (eg sulphonylurea)
• Fasting/​starvation
• Sepsis
•Renal failure
et
n
.
kX
o
.ne
X
k
ww
t
e
X.n
ww
w
• Give 15–​20g of quick-​acting carbohydrate (eg. 170–​225mL
Lucozade®) or one glucose gel (eg GlucoGel®) orally
• Monitor finger-​prick glucose 1–​2h until stable, aim for >5mmol/​L
• If CBG remains <4.0 mmol/​L despite 3× oral glucose, consider
glucagon or IV glucose as above mentioned
• Once the patient has recovered, give a long-​acting carbohydrate
(eg toast, biscuits)
• Attempt to determine the cause of the hypoglycaemia (Box 10.1)
and adjust diabetes treatment as appropriate.
ww
Bo
t
.ne
X
k
ww
et
n
.
kX
•
•
•
•
•
et
n
.
X
ok
o
w.B
Alcohol excess
Acute liver failure
Insulinoma
Glucocorticoid deficiency
Neoplasm.
ww
o
o
B
.
w
ww
ww
w
ww
ww
t
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Hypoglycaemia
w
329
t
t
t
.ne
.ne
.ne
Hypoglycaemia
X
X
X
k
ok Worrying featuresodGCS,
ok recurrent episodes, lossoofoawareness,
Bo 2non-​
B
B
diabetic, lacking
w.insight, or unable to communicate
w. symptoms.
w
w
w Most likely Excess insulin or oralwhypoglycaemics in a diabetic ww
Think about
or accidental dose in non-​diabetic, alcohol; Other Dumping syndrome (DM
or post-​
surgery), liver failure, adrenal
(Addison’s), pituitaryeint
etgastric
et failure
n
n
n
sufficiency,
sepsis, insulinoma, other.neoplasia,
malaria.
.
.
X about Sweating, hunger,
X
X
recent food, previous
ok Ask
ok exercise,
okloss, hypos
o
o
o
and
awareness,
usual
blood
sugars,
seizures,
weight
tiredB ness, anxiety, palpitations;
.B PMH DM, gastric surgery,
.B liver or endow
w
crine disease; DH
ww Insulin dose, oral hypoglycaemic
ww dose, compliance; ww
SH Alcohol, Occupation (eg commercial driver).
Obs HR,
temp, GCS, recent and
blood glucose.
t BP,Pale,RR,sweating,
efor
et current
ebet
Look
tremor, .slurred
speech, focal neurology (can
n
n
n
.
.
X eg hemiplegia), dGCS,kabdo
X
(injection sites, lipodystrophy),
kX
ok severe,
o naevi,scars
pigmented scars, jaundice,ospider
hepatomegaly. oo
o
B Investigations Finger-​
.Bprick glucose If the result is unexpected
ask for a rewmachine
w.inBa fluoride
peat on a different
and send a blood sample
oxalate
w
w
w
w
ww
B
1
1
(E p. 531) tube for a laboratory glucose result. If not known to be diabetic
send samples for FBC, U+E, LFT, glucose, insulin, C-​peptide, and cortisol,
prior to correcting hypoglycaemia; do not let this delay treatment. Further
investigations Hypoglycaemia is very rare in an otherwise healthy non-​diabetic
patient in the absence of alcohol. Consider ‘other’ causes listed previously
(also see Box 10.2). For suspected insulinoma, the investigation of choice is
glucose, insulin, and C-​peptide levels at the time of hypoglycaemia or after a
72h observed fast. See E OHCM10 p. 214.
Treatment Follow treatment for ‘Hypoglycaemia emergency’ (E p. 328).
DM A single episode of mild hypoglycaemia should not prompt a change
of medication. If the patient is having regular hypos then consider a
dose reduction, especially if lack of awareness of hypoglycaemic episodes. Try to establish any diurnal pattern of hypos, then reduce appropriate insulin dose by 20%; consult BNF to reduce the doses of
oral hypoglycaemics. Ensure the patient is aware of the sick day rules
(E Box 10.7 p. 335). Alcohol Hypoglycaemia following alcohol will not
reoccur after correction in the absence of further alcohol consumption. Once the patient’s blood sugars are stable they can be discharged.
Dumping syndrome Fast passage of food into the small intestine (following
gastric surgery or in severe diabetic autonomic neuropathy) can cause
fluid shifts and rapid glucose absorption. Excessive insulin secretion results in rebound hypoglycaemia 1–​3h after a meal. A diet low in glucose
and high in fibre will improve the symptoms. Aim for frequent, smaller
meals. Neoplasia If suspected, arrange appropriate imaging and referral
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
o
ww
.ne
X
k
oo
B
.
w
ww
ww
o
Bo
et
n
.
kX
Addison’s/​pituitary failure E p. 337, p. 338
Acute liver failure E p. 320
1
et
n
.
X
w
ww
ww
t
.ne
X
ok
.Bo
Sepsis E p. 494
o
o
B
.
w
ww
ww
ok
o
w.B
I Box 10.2 Hypoglycaemia covered elsewhere
et
n
.
kX
.n
kX
t
o
o
w.B
ww
et
.ne
X
k
ww
t
e
X.n
ok
Bo
w
t
o
w.B
t
.ne
X
k
Loss of early autonomic symptoms warning of mild hypoglycaemia (eg tremor, sweating) seen in
those with longstanding DM and frequent hypoglycaemic episodes.
ww
B
330
.B
w
ww
Chapter 10
.B
w
w
ww
w
Endocrinology
t
et
net
.nHyperglycaemia
.emergency
.ne
2
X
X
X
ok
ok
ok
o
o
Check
airway
is
patent;
consider
manoeuvres/​
adjuncts
Bo 2 Airway
B
B
.
w. TEAM
ARREST
2 Breathing wwIf no respiratory effort—​CALLw
w If no palpable pulse—​CALLwARREST TEAM
ww
2 Circulation
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
t
e
etdeteriorating.
et
n
n
n
.
.
.
3Call
for senior help early if patient
X
X
X
ketoacidosis (DKA)
ok Diabetic
ok<94%(E p. 332.)
ok
o
o
o
•
15L/​
m
in
O
if
SOB
or
sats
B
.B
.B
• Call for senior help
w
w
w
w
•Establish venous
w access, take bloods: w
ww
FBC, U+E, glucose, osmolality, HCO , bld cultures
• Check BP:
eif tSBP<90mmHg, give 500mL.n0.9et% saline IV over 10–​15min .then
et
n
n
.
recheck;
if
SBP
<90,
give
further
500mL
0.9
%
saline
IV
over
10–​
X
X
kXcare teams.
and call ICU/​co
ritical
ok 15min
ok
o
o
o
if
SBP
≥90,
give
1L
0.9
%
saline
IV
over
60min
B
.B and ketones (dipstick urine
• Check finger-​prick
wglucose
w.Bfor ketones if
w
w
capillary testing
w unavailable)
w
ww
B
2
−
3
•
•
•
• Start a fixed rate insulin infusion of 0.1unit/​kg/​h IV (use 50units human
soluble insulin eg Actrapid® in 50mL 0.9% saline; max. rate 15unit/​h)
• Venous blood gas; if pH <7.1 call ICU/​critical care team
• Monitor glucose and ketones hourly, and venous HCO−3 and K+ at 60min
and 2hrly thereafter (Box 10.3); remember K+ will fall unless replaced
• Further management E p. 332; ECG, CXR, MSU to determine cause
• Reassess, starting with A, B, C . . .
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
ww
oo
B
.
ww
w
t
.ne
X
k
2 Box 10.3 Consider HDU admission in DKA for:
ww
t
et or kidney failure •Young .people,
et elderly, comorbidities, or pregnant
• n
n>6mmol/​
. Heart
.ne
• GCS <12, sats <92%
• Ketones
L, HCO <5mmol/​L,X
pH <7.1
X
X
k
k
•oK <3.5mmol/​L, anion gap >16 Eop. 599
ok • SBP <90
o
o
Bo
B
B
w.
w(E. p. 332.)
Hyperosmolar
hyperglycaemic
state (HHS)
w
w
w
ww
• 15L/​min Owif SOB or sats <94%
• Call for senior help
•Establish
venous access, take bloods: t
t U+E,
eFBC,
ebld cultures
et
n
n
n
glucose, osmolality,
.
.
.
X 1L 0.9% saline IV overk60min
X
X
ok •• Give
oat 0.05units/​kg/​h) ONLY if plasma
ok ketones
Start IV insulin (fixed rate
o
o
o
B
.B ketones).
>1mmol/​L or 2+ urinary
wglucose
w.B
• Monitor U+Ew
and
w
w
wMSU to determine cause ww
• Further management
E p. 332; ECG, CXR,
(Box 10.4)
• Reassess
et , starting with A, B, C ... n. et
et
n
n
.
.
X
X
X
ok 2 Box 10.4 Life-​threatening
ok precipitants of oDKA/​
ok HHS
o
o
B
• Sepsis
• Trauma/​surgery .B
w.B
w
• MI
• Other acute w
illness.
w
w
w
ww
+
2
•
−
3
B
.B
w
ww
.B
w
w
w
w
Hyperglycaemia
w
331
t
t
t
.ne
.ne
.ne
Hyperglycaemia
X
X
X
ok
ok
ok
o
o
dGCS, ketonuria, acidosis, vomiting.
Bo 2 Worrying features
B
B
w.
w.(DKA E p. 332), w
Think aboutw
2 Emergencies Diabetic ketoacidosis
w
whyperglycaemic state (HHS Ew
hyperosmolar
p. 332); Common After sugary w
food, steroids, non-​compliance with diabetic treatment, infection, or acute
t diabetics or severely unwellnnon-​
illnesse(in
et diabetics), new diagnosis of.nDM.
et
n
.
.
Ask
about
‘Osmotic
symptoms’
(thirst,
polyuria,
frequency,
urgency),
X
Xrashes, breathlessness, cough,
Xsputum,
weight loss, vomiting,
ok tiredness,
ok PMH
ooralk hypoglyo
o
o
chest
pain,
abdo
pain,
dysuria;
DM;
DH
Insulin
dose,
B caemic dose, medication
.B SH Alcohol.
w.B changes and compliance,
wsteroids;
w
w
w
Obs Temp, w
RR, GCS, urine dip, BM, recentw
and current blood glucose, w
fluid balance.
t Volume status (E p. 394),nsweet-​
Lookefor
smelling breath (ketones). Signs
et perineum
et
n
n
.
.
.
of infection
Check skin thoroughly (including
and feet) for abscesses
X
X
kX look in mouth for dental
and injection site o
problems,
ok orchestrashes
ok infection,
o
o
o
for
poor
air
entry
or
creps,
abdominal
tenderness.
B Investigations wFinger-​
B and sus.Bprick glucose (±ketones wif .available
w if result
w dipstick Ketones,
pect DKA) w
repeat
unexpected; w
Urine
evi- ww
dence of infection (E pp. 604–5); blds Send if patient is unwell, has
persistent hyperglycaemia (over 48h), or has urinary ketones (type 1
DM), request FBC, U+E, LFT, osmolality, pH/​HCO−3 (venous), blood
cultures; ABG Unnecessary unless concerns regarding respiratory status
(venous pH adequate for DKA); ECG/​CXR If treatment has been required.
t
.ne
X
k
oo
et
oo
B
.
w
t
.ne
X
k
.n
kX
oo
B
.
w takes hours to days w
tient is unlikely w
suggest underlying pathology.w
DKA
wtoHHS
w
to develop while
takes days to weeks. w
Type 1 diabetes Check finger-​prick glucose (±ketones if available) and
t
t be transiently normalnsoon
urine.eGlucose
usually high in DKA but
et
.n a dose ofis insulin.
.ne may
. dipafter
AssessX
volume
status (E p. 394), check
X
X
ketonuria and check
(normal
ok stick forpH
oka venous blood gas for pH/​oHoCOkIf hyperglyor absenceBofo urinary ketones excludes DKA).
Bo venous
B
caemia persistent,w
try. to establish any diurnal pattern
and i appropriate
w.glucose.
w
insulin doses byw
20% with close monitoring of blood
w
w
ww
Type 2 diabetes Check finger-​prick glucose and urine. The glucose must
be raised
for a diagnosis of HHS. If unwell,
the treatment plan
t initially.
tglucosefollow
e
e
et
for n
HHS
Otherwise monitor
levels every 6h forn48h,
n
.
.
.
and
Xincrease oral/​IV fluid intake,kbut
X reassess. DKA can occur in type 2
ok diabetics who require insulin
o it is very unusual (evenoolowkXlevels of
o
o
For.B
persistent hyperB residual insulin production
.B inhibit ketogenesis). w
glycaemia increasewthe dose of hypoglycaemic medication
or consider
w
w
starting/​increasing
w insulin with frequent finger-​
wprick glucose checks.
ww
B
Treatment A single episode of hyperglycaemia in an otherwise well pa-
−
3
et
n
.
kX
o
Bo
Non-​diabetic patients New diabetics often present with DKA/​HHS; have
a low threshold for starting treatment plans later in this section. Other
triggers These can include steroids, pregnancy, and stress, eg severe
illness or surgery.
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
w
.B
w
w
w Endocrinology
332
ww
w
Chapter 10
t
t
et OHAM4 p. 516.)
Diabetic
.ne ketoacidosis (DKA)
.n(E
.ne
X
X
X
resulting k
in ketosis l acidosis and hyperglycaemia
l
k
ok K Insulin deficiency
odiuresis.
omissed
o
o
due to osmotic
Typically seen following
insulin
Bo dehydration
B
B
. of T1DM.
treatments or infection
w. in T1DM, or as a first presentation
w(≥11mmol/​
Diagnose basedw
upon presence of hyperglycaemia
L), acidosis
w
w
(venous pH w
<7.3 or HCO <15mmol/​L), andw
blood ketones ≥3mmol/​L or w
ketonuria (≥2+). Stabilize the patient as shown E p. 330, then:
trehydration (see ‘DKA fluids’)
• Continue
IV insulin infusion and fluid
et venous
eafter
eat
n
n
n
.
.
• .Monitor
K , pH, and HCO
1h, 2h, and then 2hrly using
X venous sample on a gas analyser
X for rapid testing
X
ok • Monitor
okketones
ok ketones
o
o
o
venous
glucose
and
hourly
aiming
for
blood
B
to fall by >0.5 mmol/​
/​h
w.BL/​h and glucose by >3mmol/​
w.LB
w
w
w
• If patient uses
long-​acting insulin continue at normal
dose/​time
w
w
• Continue fixed rate insulin infusion until ketones <0.6mmol/​L and pH w
>7.3. At this point, convert to regular SC insulin if eating and drinking
normally,
et otherwise use a sliding.nscale
et (E p. 333). See Box 10.5..net
n
.
XDKA fluids 0.9% saline is the mostkappropriate
X
X
replacement. A guide
ok would
o1h, 1L over 2h,fluid
ooverk 4h.in Ifadults
be to prescribe 1L over
1L over 2h, and 1L
syso
o
o
B
B
tolic BP <90mmHg on.B
admission an initial 500–​1000mL bolus
must be carefully
.
w can lead to ceregiven under senior w
Since excess fluid replacement
w supervision.
bral oedema,w
reassess
frequently for signs of overload
ww(E p. 394), and tailor to ww
2
−
3
+
−
3
volume status and patient weight. Add 40mmol/​L KCl after the first litre of fluid if
the plasma K+ is 3.5–​5.5mmol/​L. Omit additional KCl if K+ >5.5; if K+ <3.5 seek
senior review. Add a 10% glucose infusion at 125mL/​h if glucose <14mmol/​L but
do not stop saline.
et
et
.n
kX
.n
kX
oo
oo
B
B
.
.
These patients require
close monitoring. If severely w
ill, catheterize, consider
wwor ICU,
admission tow
HDU
and an arterial and/​
worwcentral line. If obtunded or ww
persistent vomiting, keep NBM and pass NG tube. Dehydration and dGCS
predispose to thromboembolism: give prophylactic LMWH (E pp. 420–1).
t
Consider
precipitants: poor compliance/​
insulin dose, alcohol,
et
netbloodincorrect
.ne likely
.nlow
infections
(may be asymptomatic—​c.heck
cultures, MSU and CXR;
X
X
X
ok threshold for starting antibiotics),
ok MI (check an ECG), CVA, surgery,
okpregnancy.
o
o
Bo Hyperosmolar hyperglycaemic
B
B
state (HHS) (E
w. hyperglycaemia
w. OHAM4 p. 524.) w
K Severe, uncorrected
leads to
dehydration, but in the
w
w
presence ofwresidual insulin production inwT2DM, ketoacidosis does w
not develop. Previously referred to as hyperosmolar non-​ketotic state
t Diagnose based upon nraised
t plasma osmolality (typically
(HONK).
emOsmol/​
e(typically
et
n
n
.
.
.
>340
kg) with high glucose
>30mmol/​L).
X
Xon the treatment plan E p.k330,
X
the patient as shown
ok •• Stabilize
ok based
o then:
o
o
o
Continue
IV
fluid
replacement
on
clinical
state
and
comorbidities
B
.Bfailure)
(eg elderly with w
heart
w.B
w
w
• Monitor U+E,
glucose and osmolality every 2h.
Be aware that
w
w
ww
Bo
o
et
.n
kX
T Box 10.5 Management tips in DKA/​HHS
3
hyperglycaemia will drive redistribution of water into the extracellular
fluid, lowering serum Na+ concentrations (‘spurious hyponatraemia’)
• Commence IV insulin (fixed rate 0.05 units/​kg/​hr) only once glucose has
stopped falling with IV fluids alone (unless i blood ketones at diagnosis)
t
ok
Bo
t
e
X.n
2
3
t
e
X.n
ok
o
B
.
w
e
X.n
ok
o
B
.
w
Joint British Diabetes Societies guidelines at Mhttp://​www.diabetologists-​abcd.org.uk/​JBDS/​
JBDS_​IP_​DKA_​Adults_​Revised.pdf
Plasma osmolality may be estimated as 2×([Na+] + [K+])+ urea + glucose while awaiting a formal
lab measurement.
ww
ww
ww
B
.B
w
ww
.B
w
w
w
w
Sliding scales
w
333
t
t
t
.ne scales
.ne
.ne
Sliding
X
X
X
k They
ok
okand control of blood glucose
olevels.
allow strict monitoring
o
o
Bo These
B
B
. insulin whose
are used in the treatment
of diabetic patients requiring
w. disrupted
wvomiting,
oral intake is significantly
(eg NBM, severe
or serious
w
w
w
illness), and w
in critical illness, where good w
glycaemic control improves w
outcomes, eg post MI or on ICU, but are no longer used in the management
et of DKA or HHS where fixed-​
ertate insulin infusions are advised.
et
n
n
n
.
.
.
Both
the
insulin
infusion
and
appropriate
IV
maintenance
fluids
are
preX on the infusions section
X the drug card (Fig. 10.1).kX
ok scribed
okas ofnecessary),
o Use 0.9%
o
o
saline
or
5%
glucose
(with
KCl
accordingBtoothe blood gluB cose (use 0.9% saline
B
.
.
w if the glucose is running >11mmol/​
w L).
w
w
w
w
ww
Date
Route Fluid
Additives
Vol Rate
Signature
18.8.18 IV
0.9% saline 50units Actrapid 50mL Sliding Scale
P Roluos
et IV 5% glucose 20mmol.nKClet 1L 8h
et
18.8.18
P Roluos
n
n
.
.
X
X for a sliding scale.
X
ok Fig. 10.1 Prescribing insulinoandokfluids
ok
o
o
B
Insulin
Date
glucose
w.B Start time Blood
w.B Rate (mL/h)
w
w
(mmol/L)
w
w
ww
B
Actrapid
Dose
1unit/mL
.
kX
o
o
net
18.8.18
13:45
Route
IV
Signature
S Dixon
oo
B
.
w
t
.ne
kX
<4
4–7
7.1–11
11.1–20
>20
Stop – call doctor
1
2
4
7 – call doctor
oo
B
.
ww
t
.ne
X
k
Fig. 10.2 Example of sliding scale regimen (check local guidelines).
ww
o
Bo
w
If the patient remains hyperglycaemic despite the sliding scale (Fig. 10.2)
then check the infusion pump and cannula; if no problems found, then
increase infusion rates by 1.5–​2-​fold, and check venous pH (T1DM) or
osmolality (T2DM). If the capillary blood glucose is <4mmol/​L check
that there is 5% glucose running, increase the fluid rate and/​or glucose
concentration (up to 10%); recheck glucose in 30min. If persistently
<4mmol/​L stop the sliding scale, and restart the infusion at half the
doses once blood glucose >6mmol/​L. If glucose <2 E p. 328.
Stop a sliding scale once a patient is eating normally and able to resume
normal diabetes medication. Give normal dose of SC insulin 30min before stopping the scale, unless rapid acting (eg Novorapid®, Humalog®) in
which case give at same time as stopping the scale.
t
.ne
X
k
t
o
ww
t
e
X.n
o
w.B
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
t
ww
et
n
.
X
ww
k
insulin o
ok Prescribing
o drug cards for prescribing.insulin.
ooAlways spehospitals have separate
Bo Most
B
B
.
cify the insulin formulation,
‘U’ for units
w and avoid using thewabbreviation
w
(since this canw
bew
misread as a zero). See Fig. 10.3
w for an example.
ww
Breakfast
Insulin
Dose (units)
Route
Start t
et
et
n
n
18
SC
18.8.18
.
.
.ne
X
X
X
k Start
Insulin ok Dose (units)
Route
ok Night
o
oo 18.8.18
Bo
B
10
SC .B
.
w
w
Fig. 10.3 Prescribing
ww subcutaneous insulins. ww
ww
B
.B
w
ww
334
Chapter 10
.B
w
w
ww
w
Endocrinology
t
t
t
.ne
.ne
.ne
Diabetes
mellitus
X
X
X
k
ok
o≥7.0mmol/​
oLk2h after a
plasma glucose
L, or ≥11.1mmol/​
o
o
Bo K75gFasting
B
B
. or HbA >48 mmol/​mol (on
. one occasion if
oral glucose load
symptomatic orw2w
occasions in no symptoms). ww
w
w resulting in dependence ww
• Type 1 Autoimmune
pancreatic β-​cell destruction,
on exogenous insulin; typically presents in children or young adults
• Type
insulin hyposecretion
t or resistance to effects, net
et 2 Relative
esecretion
n
n
requiring
drugs to potentiate insulin
or effects, or exogenous
.
.
.
X insulin; typically occurs in adults,
X
especially if overweight kX
k
k
o
o
o
glucose o
(IGT) HbA 42–​4o
mol or
Bo • Impaired
.Btolerance
.B 7mmol/​
plasma glucose ≥7.8mmol/
L after OGTT, but <11.1mmol/
L; 20–50%
w
w
progress to T2DM
w in 10yr
w
w
wfasting
wglucose
• Impaired
glucose (IFG) Plasma
≥6.1mmol/​L after w
an overnight fast, but <7.0mmol/​L; lower risk of developing T2DM
tintolerance first detected during
• Gestational
degree of glucose
et (E Any
ewill
et
n
n
.
.
pregnancy
p. 519); around 30%
progress to T2DM within.n
5yr.
X
X
X
ok Type 1 DM (E OHCM10
okp. 206.)
ok
o
o
o
B
B loss, thirst, polyuria, abdo
Symptoms Tiredness, .weight
w breath,
w.Bpain, vomiting.
Signs Sweet-​smelling
shock, abdominal w
pain (all suggest DKA).
w
w
w
ww
B
4
1c
1c
Investigations Glucose testing as previously mentioned. Check venous HCO−3
and pH and urine (ketones) to exclude DKA. If uncertainty about type of
diabetes, positive islet cell or glutamic acid decarboxylase antibodies, or low
C-​peptide levels all suggest T1DM. Check HbA1C (see Box 10.6).
Treatment Resuscitate and investigate for DKA; in the absence of DKA, a
new diagnosis of T1DM does not necessitate admission, but the patient
should be started on a suitable insulin regimen by an appropriately experienced individual (eg endocrine registrar or diabetes nurse specialist)
with regular finger-​prick glucose monitoring and prompt out-​patient
follow-​up. For properties of some commonly used insulins E p. 205.
Chronic management E p. 336. Involve diabetes team ASAP.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
t
.ne
X
k
t
.ne
X
k
w
t
ww
et
.ne
X
k
.n
kX
oo
oo
B
B
.
.
HbA reflects non-​
nzymatic glycosylation of haemoglobin
w at a rate prowweglucose.
w
portional tow
plasma
Since erythrocytes
(and hence haemoglobin) ww
w
undergo slow but constant turnover, HbA reflects plasma glucose control over the preceding 1–​3 months and is a reliable predictor of diabetes
et
et be set with patient involvement,
et
complications.
Target HbA levels should
n
n
n
.
.
.
taking
into
account
an
individual’s
risk
profile,
as
well
as
tolerability
X and T2DM are 48mmol/​kmolX(looserof
kXtherapy. Initial targets in bothokT1DM
o
o or treatment refractory),.Bwithootreatment inapplied if frail.B
elderly
Bo targets
tensification in T2DM
w if levels rise to 58mmol/​mwol.w
ww
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
Bo
K Box 10.6 HbA1c
1c
1c
1c
5
4
5
In the presence of diabetes symptoms, a random plasma glucose ≥11.1mmol/​L may be considered
diagnostic; in the absence of symptoms, all tests should be repeated on a separate occasion.
Ie 86.5% (48mmol/​mol) and 87.5% (58mmol/​mol). Since 2009 HbA1c levels have been reported
by NHS labs as mmol per mol (of haemoglobin without glucose attached) but previous units of %
were reported in key trials, used in guidelines and still permeate the consciousness of some older
patients and clinicians.
B
.B
w
ww
.B
w
w
w
w
Diabetes mellitus
w
335
t
t
t
Type
206.)
.ne2 DM (E OHCM10 p. X
.ne
.ne
X
X
k also present with diabetic complications,
As for type 1, butocan
ok Symptomsproblems,
ok
o
neuropathy,
MI, CVA, claudication.Bo
Bo egSignsvisual
B
.
Foot ulcers, w
infections, peripheral neuropathy,
w. poor visual acuity w
w
w
and retinopathy,
evidence
of
cardiovascular
disease.
w
w
w
Investigations blds Confirm diagnosis based upon plasma glucose testing
±OGTT (E pp. 334–6), HbA (Box 10.6), U+E, lipid profile; ECG.
et T2DM may initially be controlled
et by a healthy diet with.nminet
Treatment
n
n
.
.
Ximal rapid-​release carbohydrates
X (as found in sugary drinkskorXsweets)
ok and weight loss. If medication
okrequired, uptitrate pharmacological
o
o
oo(Table agents
before adding in insulin therapy
10.1).
B (usually to triple therapy)
B
B
.
.
w E p. 336. See Box 10.7.ww
Chronic management
w
w
w
ww
Table 10.1 Medications for glycaemic control in T2DM
Classet
Examples Comment
et
et
n
n
n
.
.
.
Biguanides
Metformin
1st
line
for
obese;
iglucose
uptake
and
X
X
X
ok
okdappetite; avoid if any renal failure
ok
o
o
o
Sulphonylureas
Gliclazide
Add to metformin (1st line if.B
metformin not
B
iinsulin secretion,
w.B suitable);
w but causes weight
w
gain. Cautious use inw
the elderly due to risks of
w
w
ww
B
1c
*
hypoglycaemia
Thiazolidinediones Pioglitazone 2nd line if other drugs not tolerated or effective;
dinsulin resistance; avoid in heart failure
DPP-​4 inhibitors Sitagliptin
2nd line if other drugs not tolerated or
effective; iinsulin and dglucagon secretion
SGLT2 inhibitor Dapagliflozin 2nd line if other drugs not tolerated or effective;
blocks renal reabsorption of glucose and
promotes urinary excretion of excess glucose
GLP-​1 activators Exenatide, 2nd line if other drugs not tolerated or effective,
(given SC)
liraglutide
especially if iBMI; iinsulin and dglucagon secretion
Insulin
Isophane
Added eg if triple oral therapy insufficient (or
(given SC) if metformin not tolerated and dual therapy
insufficient)
Acarbose
Rarely used in current practice; dcarbohydrate
α-​glucosidase
absorption; causes flatulence
inhibitors
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
.ne
X
k
w
t
o
ww
o
w.B
t
.ne
X
k
et
.ne
X
k
ww
oo
B
.
w
.n
kX
*For more information, NICE guidelines are available at Mguidance.nice.org.uk/CG87
t
ww
ww
et
et
n
n
.
.
X
X
diabetic patients about
ok Educate
okwhat to do if they are feeling unwell:
ok
o
o
o
•
Drink
plenty
of
fluids
B
Bsoup, fruit juice, or fizzy drinks w
.B
• If not eating, try milk,
instead
wof.blood
• Increase frequency
glucose monitoring to atw
least 4 times/​day
w
wattention if you cannot keep fluids down,
w becoming drowsy or
ww
• Seek medical
confused, blood glucose <4mmol/​L or persistently >20mmol/​L
• If on tinsulin 3 This should never be stopped;
can arise from
t
e illness, regardless of calorie.nintake.
et hyperglycaemia
intercurrent
Consider increasing insulin dose
ife
n
n
.
.
blood
glucose
>13mmol/​
L
even
if
unable
to
eat.
Dipstick
urine
for
ketones
at
least
X and seek medical attentionkif X
X
+ve
ok • daily
o diabetic
ok intake
o
o
o
If
on
tablets
Continue
regular
medications
providing
calorie
B
continues. Metformin
w.Bmay need to be stopped if becoming
w.Bdehydrated: seek
w
w
medical advice.
w
w
ww
e
X.n
K Box 10.7 Sick day rules
B
.B
w
w
.B
w
w
w Endocrinology
336
ww
w
Chapter 10
t
t
et mellitus
Long-​
.ne term managementXof.ndiabetes
.ne
X
X
mellitus is associated
macrovascular (IHD, k
PVD)
ok K Diabetes
ok with
o CVA,
o
o
microvascular (nephropathy,
neuropathy, retinopathy)
complicaBo and
B
B
. studies show reductionswin.complications with
tions. Large, long-​
wterm
control of riskw
factors; these should be assessed
w
ww at least annually in a ww
formal review.
Education and lifestyle Ensure understanding and motivation for glycaemic
control
compliance, and dietetas
et (including self-​monitoring,.nmedication
et
n
n
.
well
as
assessing
risk
of
hypoglycaemic
unawareness).
risk
Xfor complications (physical activity,
X smoking cessation,Modify
X.factors
k
k
k
foot
care).
o
oo
oo Refer
Bo for education classes.
B
B
.
.
w and adjust therapy
Glycaemic control w
Measure HbA (every 3–​6mth)
wBox
w
accordingly w
(see
10.6); consider revising
target if tight control un- ww
w
acceptable to patient based upon individual risk profile.
BP Aimtfor BP <140/​80 (uncomplicated
or <135/​85 (uncomplieT1DM); if end-​organ damage.naim
et forT2DM)
et
cated
BP <130/​80 (E pp. 270–3).
n
n
.
.
X an ACEi as 1st line (pluskdiuretic
X or Ca channel blockerkX
ok Use
o
o if African-​
Caribbean descent).
o
o
o
B
.B and consider cardiovascular
Lipids Measure lipid profile
risk factors; in all
w
wlow.Brisk)
T2DM age >40yr
(except those judged to be very
initiate statin
w
w
w
w
ww
6,7
1c
2+
therapy (primary prevention—​atorvastatin 20mg) and assess response;
in T1DM consider statin therapy in those with microalbuminuria, family
history, age >35yr, or other high-​risk features.
Nephropathy Test early morning urine albumin:creatinine ratio; if ≥2 repeated
measurements show microalbuminuria (♂: >2.5mg/​mmol, ♀: >3.5mg/​
mmol), tighten BP control, initiate ACEi and consider renal referral.
Retinopathy Arrange annual retinal screening; sudden loss of vision, rubeosis
iridis, pre-​retinal or vitreous haemorrhage, or retinal detachment require
emergency ophthalmology review; new vessel formation requires urgent referral; pre-​proliferative retinopathy, significant maculopathy, or unexplained
change in visual acuity require routine referral.
Footcare Assess annually for ulcers, peripheral pulses, sensory function,
and foot deformity. If ulcers present, refer urgently to a specialist diabetic footcare team. Those with previous ulcers, absent pulses or impaired sensation require referral to a footcare team for frequent review.8
Neuropathy Assess for autonomic neuropathy in the form of unexplained vomiting (gastroparesis—​
consider trial of prokinetic agents,
eg metoclopramide), erectile dysfunction (offer phosphodiesterase-​5
inhibitor, eg sildenafil), nocturnal diarrhoea, bladder voiding problems,
or orthostatic hypotension. Neuropathic pain9 requires oral neuropathic
agent (eg gabapentin, amitriptyline, duloextine). Refractory or severe
pain may require opioid analgesia and specialist pain service referral.
Pneumovax® and yearly flu vaccines These should be offered to all patients.
et
et
.n
kX
o
Bo
o
o
w.B
o
ww
et
et
.n
kX
o
o
o
w.B
ok
o
o
w.B
t
ok
o
w.B
k
o
Bo
7
8
9
e
X.n
ok
o
w.B
ww
t
t
e
X.n
ok
ww
ww
t
e
X.n
For NICE guidelines on management of T1DM see Mguidance.nice.org.uk/​NG17
For NICE guidelines on management of T2DM, see Mguidance.nice.org.uk/​NG28
For NICE guidelines on footcare in T2DM, see Mguidance.nice.org.uk/​NG19
For NICE guidelines on neuropathic pain, see Mguidance.nice.org.uk/​CG173
o
B
.
w
ww
t
e
X.n
ww
6
.n
kX
ww
t
e
X.n
ww
et
.n
kX
ww
Bo
.n
kX
o
w.B
ww
Bo
et
.n
kX
e
X.n
ok
ww
o
B
.
w
ww
B
.B
w
ww
.B
w
w
w
w
Pituitary axis
w
337
t
t
t
.ne
.ne
.ne
Pituitary
axis
X
X
X
ok
ok
ok
o
o
Bo Hypopituitarism
B
B
.may affect one or more anterior
K Failure of secretion
hormones.
w
w.pituitary
w
w
Causes Damage
to
the
hypothalamic–​
p
ituitary
axis
after
surgery, irradiation, ww
w
w
tumours, ischaemia, infection (eg meningitis), or infiltration (eg amyloidosis).
Symptoms and signs These are specific to each hormone lost, eg growth
et (GH) loss: weakness, malaise,
etdcardiac output, hypoglycaemia;
et
hormone
n
n
n
.
.
.
Xgonadotrophin (LH, FSH) loss:
Xamenorrhoea, dlibido, erectile
kXdysfuncglucook tion; TSH loss: hypothyroidism
ok (E pp. 340–1); ACTH
oloss:
o
o
o
(E p. 338).
B corticoid insufficiency
B
B
.
.
Investigations Testsw
of pituitary function include LH,
TSH, paired
w hormones:
ww FSH,
with target w
organ
testosterone/​
oestradiol,
T , cortisol and ww
w
insulin-​like growth factor-​1 (IGF-​1, a marker of growth hormone secretion). Dynamic
testing (eg short Synacthen
test E p. 585) is also inet Generally,
et function
et
formative.
testing of pituitary
should be undertaken
n
n
n
.
.
.
Xand interpreted with specialistkadvice.
X
X
ok Treatment Identify and treat underlying
o cause; appropriate hormone
okreplacement
o
o
o
B may be required eg w
hydrocortisone
(E p. 205) or thyroxine
p. 207).
.B
w.B(E
3 On the ward,
the most important point is to
ensure
any patient with
w
w
w gets regular steroids (increased
w in acute illness and given ww
panhypopituitarism
4
®
IV if necessary) with early endocrinologist involvement (E p. 332).
Diabetes
et insipidus
et due to loss of either.nADH
et
.nurine
K .n
Inability to form concentrated
X
X
X
(neurogenic) or renal
response (nephrogenic). ok
ok secretionNeurogenic
okbrain
o
idiopathic,
tumour or metastases,
Bo Causes
B
.
.Bo head trauma,
cranial surgery; Nephrogenic
drugs (eg lithium), w
CRF, post-​obstructive
w
uropathy, iCa
ww, dK .
ww
ww
Symptoms Polyuria, thirst (may be extreme).
Signs Dilute
clinically dehydratedt(E pp. 394–7).
t
et urine,
e
Investigations
durine osmolality (<400mOsmol/​
kg), iplasma osmolality,
n
.
.ntest
.neand
and iNa . In the water deprivation
(fluid balance, weight, urine,
X
X
X
k 8h without fluids)—​failureokto concenok plasma osmolality recorded
oover
o
o(an ADH anaBo trate urine (>600mOsmol/​
B
k
g)
confirms DI. Desmopressin
.the production
.Burine
w
w
logue) is then given—​
of a concentrated
at this point
w
implies neurogenic
implies nephrogenic DI.
ww DI; failure to concentratew
ww
Treatment Identify and treat the cause. In neurogenic DI, intranasal
desmopressin
may be used regularly. In
t nephrogenic DI, bendroflume­
etor NSAIDs
et
thiazide
may be used. .ne
n
n
.
.
X Omission of desmopressinkinXa patient with DI who is unablektoXdrink (eg
ok 3
dGCS) is life-​threatening.
in
o
ooPay attention to fluid balance
oothese patients.
B NBM,
B
.
Acromegaly w.B
w
K Hypersecretion
ww of GH from a pituitary tumour
ww drives soft-​tissue and ww
2+
+
+
et
n
.
kX
o
Bo
skeletal growth resulting in characteristic facial and body features.
Symptoms and signs Enlarged hands and feet, coarse facial features, prognathism, macroglossia; headache ±bitemporal hemianopia. Sweating,
hypertension, and hyperglycaemia are markers of disease activity.
Investigations IGF-​1 levels reflect GH secretion; OGTT and other tests of
pituitary function under specialist guidance; pituitary MRI.
Treatment Transsphenoidal resection of pituitary tumour where possible;
medical therapy includes somatostatin analogues (eg octreotide).
et
n
.
kX
t
o
o
B
.
w
ww
w
ww
.ne
X
ok
.Bo
ww
B
338
.B
w
ww
Chapter 10
.B
w
w
ww
w
Endocrinology
t
t
t
.ne
.ne
.ne
Adrenal
disease
X
X
X
ok
ok
ok
o
o
syndrome
(E OHCM10 p. 224.)
Bo Cushing’s
B
B
K Excess of glucocorticoids
(eg cortisol); ‘Cushing’s
w.
w. disease’ when due w
w
w
to an ACTH-​
p
roducing
pituitary
tumour.
ACTH
w
w may also be pro- w
duced ectopically, eg by small-​cell lung cancers. Adrenal adenomas or
carcinomas
ACTH-​independent causes
t onaresteroids
t (and will suppress ACTH).
e
e
et
A patient
may becomen
‘Cushingoid’.
n
n
.
.
.
X
Weight gain, depression,
tiredness, weakness,
kX psychosis,
kX oligo-​
ok Symptoms
oimpotence,
or amenorrhoea, hirsutism,
infections, DM. oo
o
o
B
Signs Central obesity.B
hump), moon-​face, water
w (buffalo
w.B retention,onlyiBP,in w
thin skin, striae,
bruising,
peripheral wasting; hyperpigmentation
w
w
w or ectopic ACTH production.
w
w
Cushing’s disease
Investigations iglucose, i24h urinary cortisol, plasma ACTH and 8am cort
t OHCM10 p. 225); imagingntests
tisol, e
dexamethasone
suppression testse(E
et
n
.
.
are
problematic due to high rates of.n
‘incidentalomas’ on adrenal CT or
pituX MRI and are only done after
Xbiochemical confirmation of the
X
ok itary
oksource
ok diagnosis.
o
o
o
Treatment
Localize
and
remove
of
cortisol,
eg
transsphenoidal
resecB
B If surgical
.B adrenalectomy for adrenal
.adenoma.
tion of pituitary adenoma,
w
w
w metastatic lung cancer), ww
treatment fails
worwunsuitable (eg ectopic ACTHwfrom
suppress steroidogenesis, eg with ketoconazole or metyrapone. If iatrogenic
cause, try to taper steroid dose (E p. 179). Consider bone protection with
bisphosphonate and vitamin D; monitor for iglucose.
Complications Osteoporosis, DM, infection, poor healing, infertility.
t
t
t
.ne
.ne
.ne
X
X
X
ok
o(Ek OHCM10 p. 226.) ook
o
insufficiency
Bo Adrenal
B
. typically seen upon abrupt withdrawal
.B of long-​term
K Adrenal deficiency,
w
w
w autoimmune (com- w
steroid therapy;w
1° adrenal (Addison’s) disease includes
w TB
monest in UK),
(commonest worldwide),w
metastases (eg lung, breast), w
Waterhouse–​Friderichsen syndrome (sepsis and adrenal haemorrhage).
t
t weakness, dizziness, depresSymptoms
lethargy, weight
net
.neabdoTiredness,
.neloss, vomiting,
sion,
pain, diarrhoea or constipation,
myalgia. X.
X
X
k scars,
ok Signs Vitiligo, postural hypotension,
ok hyperpigmentation ofoocreases,
o
Bo and mouth (buccal).
B
B
.
.
w
wFBC
Investigations dNa
, iK , iurea, may have abnormal
and LFT. If susw
w
w short Synacthen test: orderw250micrograms Synacthen ww
pected perform
+
+
®
t
e
X.n
ok
Bo
et
n
.
kX
o
Bo
®
from pharmacy, once this arrives send a blood sample for cortisol and
ACTH levels, give the Synacthen® IM/​IV (E p. 585); repeat cortisol levels
in 30min. Addison’s is excluded if initial, or 30min cortisol is >550nmol/​L.
Treatment Hydrocortisone 20–​30 mg/​day in divided doses to mimic normal
circadian rhythm. May also need fludrocortisone (50–​
200micrograms
PO OD) if electrolytes deranged or postural hypotension. 2If unwell,
double dose of oral steroids for during of illness. If vomiting, needs IV/​IM
hydrocortisone—​100mg stat and seek medical attention.
2Addisonian crisis Shock, dGCS, or hypoglycaemia in a patient with
Addison’s disease or stopping long-​term steroid therapy. Resuscitate according to E pp. 488–9, send bloods for cortisol levels, and give hydrocortisone (200mg IV STAT, then 100mg IV/​8h) and broad-​spectrum
antibiotics (eg Tazocin® 4.5g IV); seek urgent endocrinologist advice.
.ne
X
k
t
ok
o
o
w.B
ww
ww
o
w.B
et
n
.
kX
ww
t
o
o
B
.
w
ww
et
n
.
X
w
ww
.ne
X
ok
.Bo
ww
B
.B
w
ww
.B
w
w
w
w
Adrenal disease
w
339
t
t
t
Hyperaldosteronism
(E OHCM10
.ne
.ne p. 228.)
.ne
X
X
X
aldosterone secretion,
resulting in Na and water retention;
k typok K Excess
ok(Conn’s
ohyperplasia.
o
o
from an adrenal adenoma
syndrome), or adrenal
Bo ically
B
B
Symptoms Thirst, polyuria,
w. weakness, muscle spasms,
w.headaches.
w
w
Signs Hypertension
(especially
if
refractory
to
multiple
antihypertensive ww
w
w
agents or young age of onset).
Investigations
dK , normal or iNa , metabolic
alkalosis; measure plasma
t supine
eandt aldosterone
e30min
eaf-t
renin
together after
(postural changes
n
n
n
.
.
.
X renin secretion). Ideally thekX
X
should be off all antihypertensives
ok fect
o patientwith
othekdiagnosis;
apart from α-​blockers. iAldosterone
drenin supports
o
o
o
B consider CT abdow(but
abnormal
.Bbeware ‘incidentalomas’: w
.B CT findings,
such as a small w
adrenal mass of no clinical significance).
w
w
w resection may be at- ww
Treatment Spironolactone;
if adenoma, surgical
tempted after 4wk medical therapy once electrolytes and BP controlled.
t
Secondary
hyperaldosteronism This occurs
when renal perfusion is e
deet leading
et Common
n
n
.
.
creased,
to high renin secretion.
causes include.ndiurX heart failure, liver failure,
Xand renal artery stenosis. Features
X are
ok etics,
okratio
okwith spiro
o
o
similar,
but
aldosterone:renin
will
not
be
high.
Manage
B onolactone or ACEi.
w.B
w.B
w
w
Phaeochromocytoma
(E OHCM10 p.w
228.)
w
ww
B
+
+
+
K Catecholamine (eg noradrenaline) production from tumours within the
adrenal medulla, or more rarely extra-​adrenal source. Consider in those
with drug-​resistant or young-​onset hypertension, or typical symptoms.
Symptoms Episodic anxiety, sweating, facial flushing, chest tightness,
breathlessness, tremor, palpitations, headaches, abdo pain, vomiting, or
diarrhoea.
Signs Episodic hypertension.
Investigations Plasma and urine (24h collection) metanephrines. Imaging if
biochemistry positive.
Treatment Surgical resection of tumour can safely be performed only
after adrenoreceptor blockade. α-​blockers (eg phenoxybenzamine) are
given prior to β-​blockers (eg propranolol) to avoid hypertensive crisis of
unopposed α-​adrenoreceptor stimulation. See Box 10.8.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
o
Bo
t
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.
w
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kX
ww
ww
2 Box 10.8 Cautious prescribing needed
Many drugs can precipitate a crisis in a patient with phaeochromocytoma.
Think before prescribing and if in doubt, seek advice. Put a warning
on the patient’s drug charts to alert prescribers. Common culprits are
­opioids, β-​blockers, dopamine-​receptor antagonists, and steroids.
t
e
X.n
ok
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et
n
.
kX
o
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et
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t
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o
B
.
w
ww
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n
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w
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.ne
X
ok
.Bo
ww
B
340
.B
w
ww
Chapter 10
.B
w
w
ww
w
Endocrinology
t
t
t
.ne
.ne
.ne
Thyroid
disease
X
X
X
ok
ok
ok
o
o
Bo Hyperthyroidism
B
B
. driven by excess thyroxine.
K Hypermetabolic
wstate
w.
w
w
Causes Graves’
disease
(50–​
6
0%;
agonistic
autoantibodies
to TSH re- ww
w
w
ceptor), toxic multinodular goitre (15–​20%), subacute thyroiditis (15%;
self-​
limiting,
painful granulomatous
as de Quervain’s
t infiltrates
et orwithpainless
einfiltrates),
et
thyroiditis,
lymphocytic
toxic adenoma.n(5%),
n
n
.
.
Xamiodarone (either due to kexcess
X iodine or drug induced kthyroiditis),
X
ok excess exogenous replacement.
o
o
o
o
o
B
Symptoms Weight loss,
agitation, anxiety, psychosis,.B
w.B
w sweating, heat in- w
tolerance, diarrhoea,
tremor, oligomenorrhoea.
w
w
w irregular pulse, warm hands,
w tremor, goitre ±nodules, w
Signs Thin, iHR,
lid lag, lid retraction, muscle weakness; Specific to Graves’ disease Exophthalmos,
pretibial myxoedema,
acropachy.et
et ophthalmoplegia,
et if d thenthyroid
n
n
.
.
.nthyInvestigations
TSH
used
as
screening
test—​
measure
(free
Xroxine, ie active, not bound ktoXplasma proteins); antithyroidfTkperoxidase
X
k
o
o
oino Graves’ and other forms.B
antibodies positive
of o
thyroiditis (TSH
Bo (TPO)
B
.
receptor antibodies
more
specific
for
Graves’
but
not
routinely
measw
ww AF; USS Thyroid, or nuclear
ured); ECG to
wexclude
ww scintigraphy may help ww
B
4
localize lesion and assess uptake.
Treatment Symptom relief with propranolol 40mg/​6h (or rate limiting calcium
channel blocker if asthmatic); suppress thyroid function using carbimazole in
dose titrated to TFTs, or with thyroxine in ‘block and replace’ approach.
Other options include radioiodine ablation or surgical resection.
Complications CCF, AF, ophthalmopathy, osteoporosis.
3Thyrotoxic storm This is caused by infection, severe illness, recent thyroid surgery or radioiodine. Tachycardia, ±AF, fever, agitation, confusion, or coma with ifT4 or iT3. Resuscitate as required (E pp. 488–9)
and get senior help. Propranolol (suppresses sympathetic response,
blocks T4 to T3 conversion and alleviates symptoms), propylthiouracil
(inhibits T3/​T4 production and T4 to T3 conversion and hydrocortisone
(reduces iodine uptake and inhibits T4 to T3 conversion) are the main
treatments. Carbimazole (inhibits T3/​T4 production) has a slower onset
of action but may be preferred to propylthiouracil since it has a longer
duration of action and is less hepatotoxic.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
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.
ww
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o
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t
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o
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o
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.
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t
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et
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et
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w
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ok
.Bo
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.B
w
ww
.B
w
w
w
w
Thyroid disease
w
341
t
t
t
Hypothyroidism
.ne
.ne
.ne
X
X
X
and insidious; characterized
by insufficient thyroxine
ok K Common
ok
ok release
o
o
Box 10.9).
Bo (see
B
B
.thyroiditis (autoimmune destruction),
Causes Hashimoto’s
w
w.lithium), resolution
w
w
stage of subacute
thyroiditis, drugs (eg amiodarone,
iatrogenic
w
w
ww
(post surgery or radioiodine), iodine deficiency (commonest worldwide). See also Box 10.10.
et Fatigue, lethargy, weight.ngain,
et hair loss, depression, confusion,
et
Symptoms
n
n
.
.
menorrhagia, infertility.
Xdementia, cold intolerance, constipation,
X
X
ok Signs Obese, bradycardia,odtemp,
ok cold/​dry hands, macroglossia,
ok jaundice,
o
o
B pitting oedema, goitre,
peripheral neuropathy, slow relaxing
.B
wdfT
w.B reflexes.
Investigations iTSH,
; +ve thyroid autoantibodies.
w
w
w
w24h PO, gradually titrated ww
Treatment Levothyroxine
(T ): 50micrograms/​
up into range 50–​150micrograms/​24h based upon monthly TFTs until
TSH e
int normal range; yearly TFT once
et stable. Beware of worsening
et
n
n
.
.
underlying
ischaemic heart disease:
consider propranolol 40mg/​.6n
h PO
X prevent iHR.
X
ok toComplications
ok myxoedema coma.ookX
o
o
Angina
from
treatment,
B
w.B
w.B
w
w
K Box 10.9
w Subclinical thyroid disease
w
ww
B
4
4
Patients with normal fT4 and T3 but i or dTSH have subclinical (hypo/​
hyper) thyroid disease. Although some will progress to frank hypo/​
hyperthyroidism, there is no management consensus. Positive autoantibodies increase likelihood of progression to overt thyroid dysfunction. Threshold for treatment lower if patient symptomatic. Recheck
TFTs after 3mth; if TSH grossly i or d (eg >10 or <0.1mU/​L) then
consider levothyroxine/​carbimazole or surveillance.
dTSH and dfT4 suggests ‘sick euthyroidism’ in systemic illness—​
recheck after recovery.
t
.ne
X
k
oo
et
ww
oo
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.
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kX
w
oo
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.
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t
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k
ww
t
t
et
.nBox
.necovered elsewhere X.ne
I
10.10
Thyroid
disease
X
X
ok
ok
ok
o
Eo
p. 403
Bo Parathyroid disease
B
B
w.
w.
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
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ok
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o
B
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et
et
et
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ww
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w
w
w
w
Chapter 11
w
343
t
t
t
.ne Neurology
.ne
.ne
X
X
X
ok
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ok
o
o
Bo
B
B
w.
w.
w
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ww
2 Coma and reduced GCS emergency 344
and reduced GCS 346
t Coma
t
e
e348
et
2 Adult seizures emergency
n
n
n
.
.
.
2
Paediatric
seizures
emergency
349
X Seizures 350 kX
kX
ok
o
o
o
o
o
Neurodegenerative
353
B
B TIAdisorders
.B
2 Stroke/​
emergency 354 w
wC.VA/​
w
w
Stroke
w 355
w
ww
Focal neurology 357
pain 360
et Back
et
et
Headache 362
n
n
n
.
.
.
Dizziness
366
X
X
X
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B
w.B
w.B
w
w
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ww
B
344
.B
w
ww
Chapter 11
.B
w
w
ww
w
Neurology
t
t
et
.nComa
.ne GCS emergency
.ne
2
and
reduced
X
X
X
k
ok
okis patent; consider manoeuvres/​
oadjuncts
o
o
Check
airway
Bo 22 Airway
B
B
.
.
If no respiratory effort—​CALL ARREST
w
wTEAM
Breathing
w
w
2 Circulation
w If no palpable pulse—​CALL ARREST
w TEAM
ww
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
t
e
etunwell or deteriorating. .net
n
n
.
.
3
Call for senior help early if patient
X
X
ok Airway and C-​spineookX
ok
o
o
B
• Stabilize cervical spine
.Bif there is any risk of injuryw(eg.Bfall)
w
• Look inside the
mouth, remove obvious objects/​
dentures
w
wwstridor, snoring)
ww
• Listen for w
upper airway compromise (gurgling,
• Wide-​bore suction under direct vision if secretions present
• Jaw thrust
et /​chin lift; oro/​nasopharyngeal
et airway if tolerated. .net
n
n
.
.
Breathing
X
X
X
ok • 15L/​min O if SOB/​satso<94%;
ok beware if previous COPD/​
oCkO retainer
o
o
•
If
hypoxic
E
p.
276
B
.B
w.B
• Monitor O satsw
and RR
w
w
• Bag and mask
w ventilation if poor/​absent respiratory
w effort.
ww
2
2
2
Circulation
t
• Venous
, take bloods:
et , troponin, clotting, G+S,.nbldet
.neVBG,access
.nCa
FBC, U+E, LFT, glucose,
X
X
X
k
paracetamol,osalicylate
and alcohol levels ok
ok • ECGcultures,
o
o
o
and treat arrhythmias
B
B p. 262)
.B (tachy E p. 254; brady
.E
• Start IV fluids if w
shocked
w
• Monitor HR,w
w cardiac trace and BP.
ww
ww
Disability
• Check
glucose
et blood
n
net
net
• .Check
for sedatives:
.
.
X
X
X
benzodiazepines,
ok Opioids,
ok antihistamines, TCAs, baclofen,
ok alcohol
seizures (E p.o348)
o
Bo •• Control
B
B
Check GCS (Box 11.1),
reflexes, limb tone, plantar .responses, neuro obs:
w. pupil
w (see Table 11.1) w
look for brainstem,
lateralizing or meningeal
w
w for airway support if GCSw≤8worsigns
w
• Call anaesthetist
airway concerns.
Exposure
et temperature
et
et
• .Check
n
n
n
.
.
X• Look over whole body for kevidence
X of injury or rashes kX
ok • Ask ward staff for a briefoohistory
and check medical notes
o
oo
B
B
B
• Examine patient brief
RS, CVS, abdo, and neuro exam
.
.
w
• ABG, but don’t w
leave the patient alone
•Request urgent
ww portable CXR
ww
ww
2+
•
•
•
• Stabilize and treat, see following sections
• Call for senior help
• Reassess, starting with A, B, C . . .
Bo
o
et
n
.
kX
et
n
.
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t
o
o
B
.
w
ww
w
ww
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X
ok
.Bo
ww
B
.B
w
ww
t
Stabilization
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X
k • Get senior help
o
Bo
o
Bo
•
•
•
•
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w
w
w
w
COMA AND REDUCED GCS EMERGENCY
oo
B
.
w
t
.ne
X
k
et
o
w.B
.n
kX
o
Treat hypoxia with O2, airway aids, ±ventilation
Treat arrhythmias and hypotension urgently
Start broad-​spectrum antibiotics if sepsis suspected (?meningitis)
Treat simple metabolic/​intoxication abnormalities:
• glucose <3.5mmol/​L, give 100mL of 20% glucose STAT
• glucose >20mmol/​L, 0.9% saline 1L IV STAT (consider DKA/​HHS)
• opioids (pinpoint pupils and dRR), naloxone 0.4mg IV/​IM STAT
®
• history of chronic alcohol excess, Pabrinex 2 pairs IV over 10min
• benzodiazepine overdose alone, flumazenil 200micrograms IV.
ww
et
n
.
kX
ww
t
ok
.B
w
I Box 11.1
wwdGCS covered elsewhere
ww
ww
Hypoxia E pp. 277–89
Bradyarrhythmia E pp. 264–7
Liver failure E pp. 319–23
Hypotension E pp. 486–7
Meningitis E p. 364
Metabolic E pp. 399–403
Hypoglycaemia E p. 329
Pyrexia E pp. 496–505
et
n
.
Hypertension
E pp. 270–3
X
t
.ne
ww
et
n
.
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oo
e
X.n
o
w.B
w
345
et
n
.
X E pp. 331–2 Overdose Ekpp.X507–9
ok Tachyarrhythmia E pp. 256–61 oHyperglycaemia
ok
o
oo
B
B
B
.
.
w
w
Further management
ww function (see Table 11.1):ww
ww
• Check brainstem
normal stabilize the patient and get an urgent CT head
gradual-​
mannitol
and urgent CT head et
t onset dysfunction consider
t
e
.nrapid-​onset dysfunction giveXmannitol,
.ne normalize PaCO withXventi.n
X
and contact a neurosurgeon
urgently; the patient’skbrain is
k lator
k
o
o
o
herniatingo
to iintracranial pressure o
Bo • If CTprobably
.BLPdue
.B
normal consider
to test for meningitis or encephalitis
w
w
• If CT and LP normal
the
cause
is
probably
metabolic
or
ww
ww intoxication.
ww
Table 11.1 Common causes of reduced GCS
Cause
Signs
net
net
net
.Intoxication
.
.
X
X
X
May have shallow,
slow breathing, pinpoint pupils suggests
ok
oksuggests
ok
iiRR
salicylates
o
o
Bo Brainstem opioids,
B
B
Eyes dilated
w. or slow reacting pupil (unilateral
w. or bilateral), absent
dysfunction
corneal reflex, eyes looking in different
directions (III, IV, VI
w
w
w lesion), eyes fixed: doll’s head movements
w (not drifting back to ww
•
•
•
t
.ne
X
ok
Bo
Lateralizing
(cerebral
dysfunction)
Meningism
Bo
o
et
n
.
kX
2
forwards gaze when neck rotated)
Swallow water not swallowed spontaneously/​no gag reflex
Respiration apnoeas, gasping, irregular, or Cheyne–​Stokes
breathing (alternating rapid breathing and apnoeas)
Body increased tone and upgoing plantars unilaterally/​
bilaterally/​crossed
Facial asymmetry, asymmetrical tone, and plantar responses
.ne
X
k
t
ok
o
o
w.B
ww
et
n
.
X
ww
o
w.B
Neck stiffness, photophobia, Kernig’s sign, Brudzinski’s sign,
straight leg raise (E p. 134)
et
n
.
kX
o
o
B
.
w
ww
w
ww
ww
t
.ne
X
ok
.Bo
ww
B
346
.B
w
ww
Chapter 11
.B
w
w
ww
w
Neurology
t
t
et
.ne and reduced
.nGCS
.ne
Coma
X
X
X
ok
ok
ok
o
Bo Think about w.Bo
B
wd.glucose, Na , Ca , w
No focal neurology dO , iCO , low BP, metabolic (i/​
w
w
K ; acidosis/​
a
lkalosis,
renal/​
l
iver
failure/​
d
ecompensation,
constipation), w
w
w
overdose (alcohol, opioids, TCAs, benzodiazepines), epilepsy/​post-​ictal,
hypothermia,
itemp, hypothyroid, malignant
et dysfunction
et CVA,HTN.
et
Brainstem
or lateralizing.n
signs
tumour, abscess, haeman
n
.
.
X hypoglycaemia or rarelykXother metabolic abnormalities.kX
ok toma,
Meningism Meningitis, encephalitis,
o
oo subarachnoid haemorrhage.
oo
B
B
B
.
.
Ask about (notes,
relatives, contacts, nurses)
Baseline, speed of
ww
wwseizures,
onset, headache,
chest pain, palpitations, vomiting,
weight loss; ww
w
w
PMH Cardiac, respiratory, DM, kidney, liver, psychiatric, stroke/​TIA,
seizures,
DH Elicit PMH from DH, consider the possibility of
et dementia;
et (overdose or withdrawal).
et
overdose;
SH Alcohol, recreationalndrugs
n
n
.
.
.
X GCS (Table 11.2), temp,
X
X
ok Obs
ok BP, HR, O sats, O requirements,
ok RR,
o
o
o
pupil size.
B
B
w.limb
w.B
Neuro obs w
GCS,
movements, pupil size
and
reactivity, HR, BP,
w
w
ww
RR, temp. w
+
+
2
2+
2
2
2
Look tfor Respiration Rate, depth, distress,
added sounds, air entry on
nesides; Pulse Rate/​rhythm;XAbdomen
net Rigidity, pulsatile mass,Xorgano­
net
both
.
.
.
X
distension; Neuro Pupil
papilloedema (late
k responses,
ok megaly;plantars;
oinjection
oksign), limb
Skin Rashes,
marks, trauma; DREoconstipation.
o
Bo tone,
B
B
. FBC, U+E, LFT, Ca , glucose,
Investigations w
blds
CRP,
w. troponin,
clotting, bld cultures,
toxicology screen (paracetamol,
salicylate, alw
w
w
w
cohol); ABGw
pH, dO or diCO ; ECG Arrhythmias;
CXR Evidence of w
aspiration; CT if the patient has focal neurology or there is no clear diagt an urgent CT head is required,
t the patient may need ntoebet
nosisethen
.n first; AXR Faecal impaction;
.neLP After a CT scan if CTXnormal.
.
intubated
X
X
k
k
k
o
o
o
Bo
.Bo
.Bo
w
w
ww
ww
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
2+
2
Bo
o
et
n
.
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et
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Coma and reduced GCS
w
347
t
t
t
.ne 11.2 GCS scoring (3/​15Xminimum)
.ne
.ne
Table
X
X
ok
ok4 Motor Obeys commandsook 6
spontaneously
o
Bo Eyes Open
B
.
.B
Open to command
3
Localizes pain
5
w
w
w
w
w
Open to pain
2
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w
w
w
No response
1
Abnormal flexion to pain
3
Voice tTalking and orientated 5
Extension to pain
2et
t
e
e
n
n
n
.
.
.
Confused/​
4
No
movement
X
X 1
kX disorientated
k
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o
o
o
Inappropriate words
Bo
.Bo 32
.Bo
w
w
Incomprehensible
sounds
ww
ww
ww
No vocalizations
1
t
t 304:81–​4.
Source:
data
from Teasdale G, Jennett B. Lancet e
1974
e
et
n
n
n
.
.
.
Originally
described in 1974 as a 14-​point scale
(omitting ‘abnormal flexion’) by
X
X use in patients with head injuries,kX
at the University of Glasgow
ok neurosurgeons
ok andfortrauma.
o this revised
scale is now widely used in acuteomedicine
o
o
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348
.B
w
ww
Chapter 11
.B
w
w
ww
w
Neurology
t
t
et
.nAdult
.ne
.ne
2
seizures
emergency
X
X
X
ok
okconsequences are dangerous
okfor patients
seizures and their
o
o
Bo $andWhile
B
B
anxiety provoking
doctors, they are often self-​
imiting and over-​
w. Toforbegin
w. lthe
treatment has w
risks.
with stay calm,
keep
safe,
w
w
w CBG, andpatient
start timing,w
observe, gather information, check
plan ahead. w
Afterwards, document exactly what you saw.
et
et
et
n
.
Check airway is.n
patent; consider manoeuvres/​adjuncts
2.n
Airway
X
X
X
If no respiratory
ok 2 Breathing
ok effort—​CALL ARRESToTEAM
ok
o
o
TEAM
2 Circulation
B
.IfBno palpable pulse—​CALL ARREST
w.B
2 Disability ww If GCS ≤8—​CALL ANAESTHETIST
w
w
w
ww
3 Call for senior help if seizure >5min. All timings are from the start
of the tfirst fit; the clock only restarts tonce the patient has been fit-​free
e
e
et
forn
>30min.
n
n
.
.
.
X 5min
X
ok 0–​
ok and easy to forget ookX
o
o
•
Start
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;
this
is
very
important
B
.B
.B
• 15L/​min O in allw
patients
w
w
• Keep patientw
safe and put into recovery position
if possible
w
w
ww
2
• Monitor HR, O2 sats, BP, cardiac trace, temp
• Venous access (after 3–​4min). Take bloods:
2+
• FBC, U+E, LFT, CK, Ca , glucose, bld cultures, AED levels
• Check GLUCOSE: if <3.5mmol/​L give 100mL of 20% glucose STAT
(Box 11.2).
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
t
.ne
X
k
oo
B
.
• Call for senior
whelp and attach a cardiac monitor
wwapart
wteeth
ww
• Consider w
an airway adjunct but do not force
• If IV access: lorazepam 4mg IV/​2min, repeat at 10min if no effect
• If no
access: diazepam 10mg PR e
ort5–​10mg buccal midazolam, et
netIVevery
10min if no effect up
.repeat
.nto 3 doses
.n
X
X
X
• Ask ward staff about history
/​check notes
k
k
k
o
malnourished,
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oo Pabrinex 2 pairs IV if not
oo
Bo •20–​If alcoholism/​
B
B
.
.
40min
ww and senior help www
w
• Call for anaesthetist
w
w
• If not taking phenytoin: phenytoin 20mg/​kg IV at <50mg/​min
• If taking
phenobarbital 10mg/​
t kg IV over 10min (max 1g)net
et phenytoin:
• .Monitor
ECG, BP, and temp. .ne
n
X
X.
kX>40min
k
k
o
o
o
Thiopental or propofol
Bo •• Transfer
Boon ICU/​HDU
Bomonitoring.
.EEG
to ICUw
for. general anaesthetic, intubation,
w
ww
ww
ww
B
5–​20min
®
2 Box 11.2 Life-​threatening causes
et cardiac disease • .Meningitis,
et encephalitis, malaria .net
Hypoxia/​
n
n
.
X Hypoglycaemia
X• iICP and CVA
X
ok Metabolic (dCa , idNa
o)k • Drug overdose
ok
o
o
o
B
Trauma
clampsia
.B (pregnancy).
w.B • Hypertension/​wew
w
w
w
ww
•
•
•
•
2+
+
B
.B
w
ww
.B
w
w
w
w
PAEDIATRIC SEIZURES EMERGENCY
w
349
t
t
et
.nPaediatric
.ne emergency X.ne
2
seizures
X
X
ok
ok
ok
o
o
Bo 2 Airway
B
B
Check
airway
is
patent;
consider
manoeuvres/​
w.
w.TEAMadjuncts
2 Breathing wIf no respiratory effort—​CALL ARREST
w
w If no palpable pulse—​CALL ARREST
w TEAM
ww
2 Circulation
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
t
e
et
et
n
n
n
.
.
.
children having a seizure. All timings
X3 Call for senior help in allkX
X are
ok from the start of the firstofit;othe
okfree period
clock only restarts with o
a fit-​
o
B of >30min. w.B
w.B
w
w
Step 1
w
w
ww
• Start timing; this is very important and easy to forget
• Maintain airway, assess ABC, check pupil size, posture, neck stiffness,
fontanelle,
et temp, and for rashes .net
et
n
n
.
.
•
15L/​
m
in
O
in
all
patients
X GLUCOSE: if <3.5mmol/​
X
X
ok • Check
ok L give 2mL/​kg of 10%oglucose
ok STAT
o
o
(Box
11.3):
B
.B blood and one fluoridewbottle
.B (E pp. 534–5)
take 10mL ofw
w clotted
w treatment
prior towgiving
glucose, but don’t let thiswdelay
ww
B
2
•
• Keep patient safe, be alert for vomit occluding the airway
• Monitor HR, O2 sats, BP, cardiac trace, temp
• Venous access, take bloods:
2+
2+
• FBC, U+E, LFT, CRP, Ca , Mg , glucose, bld cultures, anticonvulsant levels (if on anticonvulsants), venous blood gas
• If IV access: further lorazepam 0.1mg/​kg IV (max 4mg)
• If no IV access: diazepam 0.5mg/​kg PR (max 10mg)
• Ask parents or ward staff about history/​check notes.
t
.ne
X
k
oo
et
oo
B
.
w
ww
.n
kX
w
oo
B
.
ww
t
.ne
X
k
Step 2 (10min after either lorazepam/​diazepam)
ww
t further lorazepam 0.1mg/​
t g IV (max 4mg)
• If IVeaccess:
et
.nekgkPR
• .Ifnno IV access: paraldehyde 0.4mL/​
with 0.4mL/​kg olive oil.n
or
X
X
X
k
ok 0.8mL/​kg of a pre-​prepared
ok50:50 solution (max 20mLoofomixture).
o
Bo Step 3 (10min w
B
B
after
either
lorazepam/​
p
araldehyde)
.
w.
• Call for anaesthetist
and senior help
w
w
w0.4mL/​kg PR as above unless already
w given
ww
• Paraldehyde
• If not on phenytoin: phenytoin 20mg/​kg IV/​IO at <50mg/​min
• If on tphenytoin: phenobarbital 20mg/​tkg IV/​IO over 20min.
e
e
et
n
n
n
.
.
.
Step
4
(20min
after
either
phenytoin/​
p
henobarbital)
X
X
X
ok •Rapid sequence intubation
ok
ok
o
o
o
pyridoxine, paracetamol, diclofenac.
B • Consider mannitol,
w.B
w.B
w
w
w Life-​threatening causesw
ww
2 Box 11.3
• Meningitis,
et encephalitis, malaria .net •• Hypoxia
et
• .Hypoglycaemia
iICP and CVA
n
n
.
X
(dCa , idNa )kX
• Drug overdose kX
ok •• Metabolic
oinjury
Trauma/​non-​accidental
• Hypertension.
o
o
oo
B
B
B
.
.
w
w
ww
ww
ww
2+
+
B
350
.B
w
ww
Chapter 11
o
oo
B
.
w
ww
w
Neurology
t
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Seizures
X
k
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.B
w
w
t
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X
k
et
o
w.B
.n
kX
o
2 Worrying features Preceding headache or head injury, duration
>5min, prolonged post-​ictal phase, adult onset, recent depression
(overdose).
ww
ww
ww
Think about 2 Life-​threatening See Box 11.2; Most likely Idiopathic
o
Bo
et
n
.
kX
t
ok
o
w.B
.B
w
ww
ww
et
n
.
X
ok
et
n
.
kX
oo
e
X.n
(>50%), epilepsy, alcohol withdrawal, hypoglycaemia, hypoxia, trauma;
Other Kidney or liver failure, pseudoseizures, overdose (tricyclics, phe­
nothiazines, amphetamines); Non-​seizure Brief limb jerking during a faint,
rigors, syncope, arrhythmias. See Table 11.3.
Ask about Get a detailed description of the fit from anyone who witnessed the episode (see Boxes 11.4 and 11.5); headache, antecedent
head trauma, chest pain, palpitations, SOB, alcohol withdrawal; PMH previous seizures, cerebrovascular/​cardiac/​respiratory/​hepatic/​renal/​psychiatric disease, DM, alcohol, pregnancy, surgeries; DH Anticonvulsants,
hypoglycaemics, benzodiazepines; SH Occupation, driving, hobbies, social
support, alcohol intake, last drink, illicit drugs, recent travel; FH Epilepsy.
et
n
.
X
ww
t
.ne
X
ok
k
oo
o
B
B
.
.
Obs GCS, temp, w
CBG (recheck), BP, O sats, alcohol
withdrawal
score.
w
ww
w
Look for w
Sweating, tremor, head injury, w
tongue biting, neck stiffness, w
papilloedema, focal neurology, urinary or faecal incontinence, pregnancy,
infection,
t limb trauma (eg posteriorndislocation
et of shoulder).
et
.ne
Investigations
blds VBG, FBC,.U+E, LFT, glucose, Ca , Mg ,.n
blood
X
X
X
levels;
If hypoxia or metabolic
ok cultures, anticonvulsant
okdrugABGscreen,
ok upset
o
Urine Consider
β-​hCG ifBo
pre-​menopausal
Bo suspected;
B
♀; ECG To exclude
lesion, iICP,
w.dysrhythmia; CT May showif wthea. focal
w
w
haemorrhage or
infarction, perform as urgentw
patient has a perw
w
sistent GCS <15 post-​fit, focal neurology or if the seizure was <4d post-​ w
trauma; MRI Is the neuroimaging of choice in suspected epilepsy; LP If
t May help to exclude encephalt
meningitis
net or encephalitis suspected;
neEEG
.for
.ne
itis. or as out-​patient investigation
epilepsy.
X
X
X
k treatment outlined on E p.o348.
k Correct
ok
ousing
Stop seizure
o
o
Bo Treatment
B
B
metabolic upset (glucose,
Mg , Ca , Na ) and exclude
threatening
wto. establish
w.Securelife-​airway
causes while trying
the cause (Box w
11.6).
if still
w
w≤8. Consider specialist opinion,wmoving ward, and ITU.
ww
fitting or GCS
Bo
2
2+
2+
2+
2+
+
et
et
et
n
n
n
.
.
.
X witnessing or describing seizures,
X
document exactly whatk
kX starting
ok IfOnset
owarning,
oall happened:
Position, activity, any
in one limb or
over, preso
o
o
B
.B
ence of tonic phase .(arched
w B back, muscle spasm).
wmovements,
w
During Loss ofw
awareness, limb movements, eye
jaw and
w breathing, peripheral or central
w cyanosis, incontinence
ww
lip movements,
(urinary and faecal), duration, HR, and rhythm.
t (Todd’s paresis E p. n352).
et Tongue trauma, sleepy, limb
eweakness
et
Afterwards
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
K Box 11.4 Describing a seizure
B
.B
w
ww
.B
w
w
w
w
Seizures
w
351
t
t
t
.ne 11.3 Common causes ofXtransient
.ne loss of consciousness X.ne
Table
X
ok
ok Examination Investigations
ok
o
o
Bo Epileptic History
B
B
. may Often normal, may
Known
waura,epilepsy,
w. Often normal,
seizure
have
post-​ictal
have tonguew
or limb may have
w
ww
(E p. 352) wconfusion/​weakness
trauma w
focal lesion or
metabolic cause
t
t
Alcohol
Usually >50units/​wk
Anxious,
sweaty,
iMCV and γGT;
e
e
et
n
n
withdrawal
alcohol consumption, .ntachycardic, tremor dplatelets, .mild
.
X p. 352) last drink >24h agokX ±chronic liver failure anaemia
X
ok (E
o short Responsive to pain, Normal
ok
o
o
o
Pseudo-​
Unusual
features,
B
seizures/​
duration,
respiration,
w.Bmemory of normal
w.Binvestigations
w
psychogenic event
no injuries w
wFeels cold/​hot, no LOC, Febrile, source
w of iWBC, NØ or ww
Rigors
coarse shaking, infective infection (eg UTI,
LØ and CRP, +ve
pneumonia),
no injury urine dipstick et
et symptoms
et
n
n
.
.
.n
Pregnant, may be X iBP, palpable uterus, Proteinuria,
XEclampsia
X
k
k
k
(E
p.
518)
unaware
foetal
heart
peripheral
oedema
o
oo
oo on
Doppler
Bo Transient Palpitations,
B
B
.
.
of cardiac
w pale, sudden Evidenceinjury
ww Arrhythmia
arrhythmia/​ LOC
or heart block
ww ±limb jerking; rapid disease, w
ww
B
Stokes–​Adams recovery with flushing
t
.ne
Narcolepsy
X
k
oo
Vasovagal
syncope
(E p. 266)
o
t
.ne
X
k
following fall,
irregular/​absent
pulse during attack
Excessive daytime
Often normal; loss of
sleepiness, collapse,
postural muscle tone
sleep paralysis
and tendon reflexes
±hallucinations
during attacks
Feels light-​headed ±hot, Bradycardia and
then collapse while
hypotension during
standing, ±fine limb
episode, GCS 15/​15
jerking, ±urinary inconti­ within min, no focal
nence, rapid recovery,
neurology
no post-​ictal phase
et
oo
B
.
w
.n
kX
on ECG, 24h
ECG and BP
monitoring, echo
HLA typing,
sleep studies
t
.ne
X
k
oo
B
.
ww ±postural drop
ww
w
t
.ne
X
k
(systolic drop
of 20mmHg or
more)
ww
et
.n
kX
oo
oo
B
B
.
.
Box 11.5 Assessing
‘first fit’
w
ww fromafirst-​
History Detailed
hand witness, documented
waccount
ww carefully.
ww
Investigations FBC, U+E, LFT, glucose, Ca , Mg , PO , clotting, medication levels,
urine and
serum toxicology screen (including
paracetamol and salicylate); CT tot
etstructural
etrecent
exclude
causes (non-​urgent, unless
trauma or altered neurology);
n
n
.
.
.neof
consider
LP
after
CT
only
if
infection
suspected;
MRI is the neurologists’ imaging
X
X
X
k
epilepsy, but
ok choice in suspected
okcan be arranged from their clinic.
oosenior doctor
Admit onlyBifoGCS <15 or drowsy; discuss B
with
Bo Management
.
.
­regarding suspicion of
(E p. 619, 1yr
wseizures and need to advise towstopwdriving
ban); do not start
antiepileptic medication—​this decision
should be made by a
w
w
w
ww
neurologist in an urgent out-​patient clinic (‘first fit’ clinic).
I Box
et 11.6 Causes of seizures
et elsewhere in this book
et
n
n
n
.
.
.
Raised
ICP
E
p.
364
Hypertensive
emergency
E
p.
268
X
ok Hypoglycaemia E p. 329 ookX Hypoxia E p. 276ookX
o
B
.B E p. 364
Hypocalcaemia E p. 402
encephalitis
w.EBpp. 400–1 Meningitis/​
w
w
w
Hyper/​hyponatraemia
Eclampsia
E p. 518
w
w
ww
Bo
2+
2+
3−
4
B
.B
w
w
.B
w
w
w Neurology
352
ww
w
Chapter 11
t
t
t
Epilepsy
.ne (E OHCM10 p. 490.)
.ne
.ne
X
X
X
and unprovoked
of a group of neurons
ok $ Abnormal
ok discharge
ok causes a
o
Epilepsy is the recurrence
of ≥2 such seizures. o
Bo seizure.
B
B
. which neurons are misfiring
Symptoms Depends
won
w.and when. Classify w
w
seizures basedw
on a careful history and close
observation. The 2017
w
w
w
system uses simpler language but you should still know the old terms:
Onset and evolution
etStart unilaterally in a focal area
eoft brain giving stereotyped motor,
et
• Focal
n
n
n
.
.
.
X sensory, or autonomic symptoms
X (previously ‘partial’) kX result
ok • Generalized Start bilaterally
okin both cerebral hemispheres.ooAlways
o
o
in reduced awareness
(previously ‘primary generalized’)
B
w.BPreviously ‘secondary generalized’
w.B seizures.
• Focal into generalized
w
w
Awareness This
w is important as conscious levelwimpacts on their safety. ww
• Focal aware Focal symptoms but awareness remains completely intact.
Previously
referred to as a ‘simple partial’
seizures
t always
t
etimpaired
enot
• .Focal
awareness Awareness
present (including.n
ae
n
n
.
X vague lack of awareness). Previously
X ‘complex partial’ seizures.
X
ok Motor
ok
ok
involvement
o
o
o
B
.B with movement (eg twitching,
• Focal motor Focal seizure
w
w.Bor jerking)
• Focal non-​motor
Affects sensation, emotion, thinking,
experience
w
w
w
w
ww
•
1
Generalized motor Either ‘other motor’ or a tonic–​clonic seizure (ie
initial tonic whole body spasm followed by a clonic jerking phase)
• Generalized non-​motor Absence seizures; the stopping of activity with
staring/​eye-​rolling and sometimes lipsmacking; usually <45s.
Signs dGCS, tongue trauma, limb weakness, incontinence, Todd’s paresis
(transient weakness following a seizure; mimics a TIA), post-​ictal state.
Investigations Often normal; MRI and EEG (±provocation) may aid diagnosis and seizure classification. Consider EEG/​video telemetry.
Treatment Changing AEDs should be by specialists. Beware some drugs
lower seizure thresholds (fluoroquinolones, cephalosporins, penicillins,
pethidine, tricyclics, clozapine). Consider NG/​IV AEDs if they are NBM.
et
o
Bo
et
.n
kX
et
.n
kX
o
ww
o
w.B
.n
kX
o
o
w.B
ww
ww
t
t
t
.ne
.ne
.ne
X
X
X
withdrawal ok
ok Alcoholconsider
ok
o
the possibility
of alcohol withdrawal B
aso
a cause or proBo Always
B
voking factor for seizures
w. (E p. 372).
w.
w
w
w seizures Seen in morewsevere traumatic brain injury, ww
Post-​traumatic
where AEDs are often used prophylactically. Arrange an urgent CT scan
if not already
t done; if haematoma nseen
eotherwise
et (E p. 452), contact a neurosuret
n
n
geon,
hourly neuro obs .and reassess if dGCS.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
et
et
et
n
n
n
.
.
.
X
X
X
ok
ok
ok
o
o
o
B
w.B
w.B
w
w
w
w
ww
1
Guidelines available at Mguidance.nice.org.uk/​CG137 and Mhttp://​www.ilae.org/​
B
.B
w
ww
.B
w
w
w
w
Neurodegenerative disorders
w
353
t
t
et
.ne
.ndisorders
.ne
Neurodegenerative
X
X
X
k
ok
oOHCM10
ok
o
o
disease
(E
p. 494.)
Bo Parkinson’s
B
B
$ Common neurological
w. disorder (affects $1%
wof. >60yr). Cardinal w
w
w
features include
resting
tremor,
rigidity,
and
bradykinesia.
w
w
w
Symptoms and signs Coarse resting tremor (‘pill rolling’, unilateral at
onset);trigidity (‘cog-​wheeling’); falls, tfestinant gait; small handwriting,
e impulsivity, speech/​swallow
e problems; sensation normal.
et
depression,
n
n
n
.
.
.
XInvestigations Clinical diagnosis;ksingle-​
X photon emission CT if indistinguishable
X
ok from benign essential tremor;
o exclude other causes of ‘Parkinsonism’,
ok
eg
o
o
o
B drug induced (haloperidol).
B
B
Refer to specialist early if suspected.
.
.
Management MDT
ww(PD doctors, specialist nurses,
wwPT, OT, SALT). Anti-​ w
parkinsonianw
medications should be started,wtitrated, and amended by w
specialists. Levodopa enhances dopamine transmission but effectiveness reduces after
years. First line is eithert levodopa with a peripheral dopa-​
et someinhibitor
eif symptoms interfere with lifestyle,
et
decarboxylase
(eg carbidopa)
n
n
n
.
.
.
X a choice of levodopa, dopamine
X
(eg ropinirole), or monoamine-​
kXoff ’ and
ok oroxidase
ok if agonists
o‘on-​
inhibitors (eg selegiline)
they do not. Problematic
o
o
o
B ‘end-​of-​dose’ phenomena
.B with levodopa may require
of a
w
w.Bthe(egaddition
MAO-​B inhibitor,
dopamine agonist, or COMT-​
inhibitor
tolcapone).
w
w
wis at strict times, so drug chart w
ww
Administration
timings may need changing.
B
2
Complications Depression, dementia (late stage): Parkinson’s disease may have
pathological overlap with Lewy body dementia (E p. 377) with movement and
cognitive dysfunction coming at contrasting stages in each disease.
Parkinson’s-​plus syndromes These share some features of Parkinson’s
(eg multisystem atrophy: Parkinson’s plus autonomic and cerebellar dysfunction; progressive supranuclear palsy: Parkinson’s plus impaired upwards gaze). These tend to be refractory to standard therapy.
t
.ne
X
k
oo
et
oo
B
.
w
.n
kX
oo
B
.
ww
ww
w
Motor neuron disease
o
Bo
t
.ne
X
k
$ Degenerative disease affecting upper and lower motor neurons.3
Diagnosis Primarily clinical but EMG can help. Progressive motor weakness
(UMN and LMN E p. 353) and behavioural change; sensation unaffected.
Fasciculations progress to spasticity, poor swallow, and dementia.
Management Supportive. Early referral to neurology-​
led MDT care
including MND nurse, PT, OT, SALT, palliative care, and dietetics is vital.4
Quinine and baclofen for cramps. Exercise programmes. Prognosis 3–​5yr.
Complications Aspiration, respiratory failure, frontotemporal dementia.
t
.ne
X
k
t
o
ww
t
ok
Bo
e
X.n
o
w.B
Huntington’s disease
et
.ne
X
k
oo
B
.
w
.n
kX
ww
.ne
X
k
ww
t
et
n
.
X
$ Incurable inherited (autosomal dominant) disorder characterized
by involuntary limb movements (chorea), dementia, and behavioural
disturbance (depression, psychoses). Onset at 30–​50yr.
ww
k
oo
oo
B
B
.
.
w
Friedreich’s ataxia
ww
w
$ Inherited w
(autosomal recessive) disorder characterized
by progressive w
ww
limb and gait ataxia, dysarthria, loss of proprioception, absent tendon
reflexest in the legs, and extensor plantar
Inability to walk oce after disease onset. May.nalso
et responses.
et
curs
715yr
develop heart failure and
DM.
n
n
.
.
X
X
ok Supportive management.ookX
ok
o
o
B
w.B
w.B
w
w
w
w
ww
2
3
4
NICE guidelines available at Mguidance.nice.org.uk/​NG71
Resources for patients, carers, and doctors at Mwww.mndassociation.org
NICE guidelines available at Mguidance.nice.org.uk/​NG42
B
354
.B
w
ww
Chapter 11
.B
w
w
ww
w
Neurology
t
t
et
.nStroke/​
.ne
.ne
2
C
VA/​
T
IA
emergency
X
X
X
ok
ok
oakdjuncts
o
o
Check
airway is patent; consider manoeuvres/​
Bo 22 Airway
B
B
wIf no. respiratory effort—​CALL ARREST
w. TEAM
Breathing
w
w
2 Circulation
w If no palpable pulse—​CALL ARREST
w TEAM
ww
If GCS ≤8—​CALL ANAESTHETIST
2 Disability
t
t
e
emay
et
n
n
n
.
.
.
3
Call for senior help early. Patient
need urgent aspirin, thrombX thrombectomy, or transfer
X
kX to Hype