Oxford Handbook of Emergency Medicine ( PDFDrive.com ).pdf

OXFORD MEDICAL PUBLICATIONS

Oxford Handbook of

Emergency

Medicine

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Oxford Handbook of

Emergency

Medicine

Fourth edition

Jonathan P. Wyatt

Consultant in Emergency Medicine and

Forensic Physician

Royal Cornwall Hospital, Truro, UK

Robin N. Illingworth

Consultant in Emergency Medicine

St James’s University Hospital, Leeds, UK

Colin A. Graham

Professor of Emergency Medicine

Chinese University of Hong Kong,

Hong Kong SAR, China

Kerstin Hogg

Clinical Research Fellow,

The Ottawa Hospital, Ottawa, Canada

with senior international advisors:

Michael J. Clancy

Consultant in Emergency Medicine

Southampton General Hospital,

Southampton, UK

Colin E. Robertson

Professor of Emergency Medicine

Royal Inﬁ rmary, Edinburgh, UK

Great Clarendon Street, Oxford OX2 6DP

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First edition published 1999

Second edition published 2005

Third edition published 2006

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ISBN 978–0–19–958956–2

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Oxford University Press makes no representation, express or implied, that the

drug dosages in this book are correct. Readers must therefore always check the

product information and clinical procedures with the most up-to-date published

product information and data sheets provided by the manufacturers and the most

recent codes of conduct and safety regulations. The authors and publishers do not

accept responsibility or legal liability for any errors in the text or for the misuse or

misapplication of material in this work. Except where otherwise stated, drug dosages

and recommendations are for the non-pregnant adult who is not breastfeeding.

Dedicated to Dr Robin Mitchell (1964–2010)

Emergency Physician in Christchurch, Edinburgh and Auckland.

Outstanding clinician and teacher, tremendous colleague and friend.

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vii

Abbreviations and symbols

Normal values xvii

Acknowledgements xix

1 General approach

2 Life-threatening emergencies

3 Medicine

4 Toxicology

179

5 Infectious diseases

219

6 Environmental emergencies

253

7 Analgesia and anaesthesia

271

8 Major trauma

319

9 Wounds, fractures, orthopaedics

401

10 Surgery

503

11 Ophthalmology

533

12 Ear, nose and throat

545

13 Obstetrics and gynaecology

563

14 Psychiatry

601

15 Paediatric emergencies

630

Index

737

Contents

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° degrees

8 approximately

+ve positive

–ve negative

± plus or minus

i increase(d)

d decrease(d)

ABC airway, breathing, circulation

ABG arterial blood gas

AC acromio-clavicular

ACE angiotensin-converting enzyme

ACTH adrenocorticotropic hormone

ACS acute coronary syndrome

AF atrial ﬁ brillation

AIDS acquired immune deﬁ ciency syndrome

AIO Ambulance incident ofﬁ cer

AIS abbreviated injury scale

ALS advanced life support

ALT alanine aminotransferase

ALTE apparently life-threatening event

AP antero-posterior

APLS Advanced Paediatric Life Support

APTT activated partial thromboplastin time

ARDS adult respiratory distress syndrome

ARF acute renal failure

AST aspartate transaminase

ATLS advanced trauma life support

AV atrio-ventricular

bd twice daily

BKPOP below knee Plaster of Paris

BKWPOP below knee walking Plaster of Paris

BLS basic life support

BMG bedside strip measurement of venous/capillary blood glucose

BNF British National Formulary

BNFC British National Formulary for Children

Abbreviations and symbols

ABBREVIATIONS AND SYMBOLS

BP blood pressure

BTS British Thoracic Society

BZP benzylpiperazine

CBRN chemical, biological, radiological, nuclear

CCU critical care unit

CK creatine kinase

cm centimetre(s)

CMV cytomegalovirus

CN chloroacetophenone

CNS central nervous system

CO carbon monoxide

carbon dioxide

COHb carboxyhaemoglobin

COPD chronic obstructive pulmonary disease

CPAP continuous positive airways pressure

CPR cardiopulmonary resuscitation

CRF chronic renal failure

CRP C-reactive protein

CSF cerebrospinal ﬂ uid

CT computed tomography

CTPA computed tomography pulmonary angiography

CVP central venous pressure

CVS cardiovascular system

CXR chest X-ray

DIC disseminated intravascular coagulation

DIPJ distal interphalangeal joint

DKA diabetic ketoacidosis

dL decilitre

DPL diagnostic peritoneal lavage

DPT diphtheria, pertussis, and tetanus

DSH deliberate self-harm

DVT deep venous thrombosis

EBV Epstein–Barr virus

ECG electrocardiogram

ECT electroconvulsive therapy

ED emergency department

EEG electroencephalogram

EMLA eutectic mixture of local anaesthetics

ENT ear, nose and throat

EPAP expiratory positive airway pressure

ABBREVIATIONS AND SYMBOLS

ESR erythrocyte sedimentation rate

ET endotracheal

ETCO

end-tidal carbon dioxide

FAST focused assessment with sonography for trauma

FB foreign body

FBC full blood count

FFP fresh frozen plasma

FG French Gauge

FiO

inspired oxygen concentration

FOB faecal occult blood

G6-PD glucose 6-phosphate dehydrogenase

g gram(s)

G gauge

GA general anaesthetic

GCS Glasgow Coma Score

GFR glomerular ﬁ ltration rate

GI gastrointestinal

GHB gammahydroxybutyrate

GMC General Medical Council

GP general practitioner

GTN glyceryl trinitrate

GU genitourinary

5HT 5-hydroxytryptamine

HATI human anti-tetanus immunoglobulin

Hb haemoglobin

HCG human chorionic gonadotrophin

HCM hypertrophic cardiomyopathy

Hct haematocrit

HDU high dependency unit

HHS hyperosmolar hyperglycaemic state

HIV human immunodeﬁ ciency virus

HONK hyperosmolar non-ketotic hyperglycaemia

hr hour/s

HTLV human T-cell lymphotropic virus

ICP intracranial pressure

ICU intensive care unit

IDDM insulin dependent diabetes mellitus

IHD ischaemic heart disease

IM intramuscular

INR international normalized ratio (of prothrombin time)

xii

ABBREVIATIONS AND SYMBOLS

IO intra-osseous

IPAP inspiratory positive airway pressure

IPg interphalangeal

IPPV intermittent positive pressure ventilation

ISS injury severity score

ITP idiopathic thrombocytopenic purpura

IUCD intrauterine contraceptive device

IV intravenous

IVI intravenous infusion

IVRA intravenous regional anaesthesia

IVU intravenous urography

JVP jugular venous pressure

KE kinetic energy

kPa kiloPascal(s) pressure

KUB X-ray covering the area of kidneys, ureters and bladder

L litre(s)

LA local anaesthetic

LAD left axis deviation

LBBB left bundle branch block

LDH lactate dehydrogenase

LET lidocaine epinephrine tetracaine

LFTs liver function tests

LMA laryngeal mask airway

LMP last menstrual period

LMWH low molecular weight heparin

LP lumbar puncture

LSD lysergic acid diethylamide

LV left ventricular

LVF left ventricular failure

LVH left venticular hypertrophy

m metre(s)

MAOI monoamine oxidase inhibitor

MAST military anti-shock trousers

max maximum

MC metacarpal

MCA Mental Capacity Act

MCPJ metacarpophalangeal joint

MDU Medical Defence Union

MI myocardial infarction

min minute/s

xiii

ABBREVIATIONS AND SYMBOLS

MIO medical incident ofﬁ cer

mL millilitre(s)

mmHg millimetres of mercury pressure

mmol millimoles

MMR mumps, measles, and rubella

MRI magnetic resonance imaging

MRSA meticillin resistant Staphylococcus aureus

MS multiple sclerosis

MSU mid-stream specimen of urine

MT metatarsal

MTPJ metatarsophalangeal joint

MUA manipulation under anaesthetic

NAC N -acetyl cysteine

NAI non-accidental injury

ND notiﬁ able disease

NG nasogastric

NHS National Health Service

NIV non-invasive ventilation

NO nitrous oxide

NSAID non-steroidal anti-inﬂ ammatory drug

NSTEMI non-ST segment elevation myocardial infarction

NWBPOP non-weight-bearing Plaster of Paris

oxygen

OA osteoarthritis

OCP oral contraceptive pill

od once daily

OPG orthopantomogram

ORIF open reduction and internal ﬁ xation

ORT oral replacement therapy

PA postero-anterior

PACS picture archiving and communication system

PAN polyarteritis nodosa

PCI percutaneous coronary intervention

pCO

arterial partial pressure of carbon dioxide

PCR polymerase chain reaction

PE pulmonary embolus

PEA pulseless electrical activity

PEEP positive end-expiratory pressure

PEFR peak expiratory ﬂ ow rate

PGL persistent generalized lymphadenopathy

xiv

ABBREVIATIONS AND SYMBOLS

PICU paediatric intensive care unit

PID pelvic inﬂ ammatory disease

PIPJ proximal interphalangeal joint

PO per os (orally/by mouth)

arterial partial pressure of oxygen

POP plaster of Paris

PPE personal protective equipment

PPI proton pump inhibitor

PR per rectum

PRF patient report form

PRN pro re nata (as required)

PSP primary spontaneous pneumothorax

PV per vaginam

qds four times a day

RA rheumatoid arthritis

RAD right axis deviation

RBBB right bundle branch block

RBC red blood cells

Rh Rhesus

ROSC restoration of spontaneous circulation

RR respiratory rate

RSI rapid sequence induction/intubation

RSV respiratory syncytial virus

rtPA recombinant tissue plasminogen activator

RTS revised trauma score

RV right ventricular

SA sino-atrial

SARS severe acute respiratory syndrome

SC subcutaneous

SCIWORA spinal cord injury without radiographic abnormality

sec second(s)

SIDS sudden infant death syndrome

SIGN Scottish Intercollegiate Guidelines Network

SIRS systemic inﬂ ammatory response syndrome

SL sublingual

SLE systemic lupus erythematosus

SpO

arterial oxygen saturation

SSP secondary spontaneous pneumothorax

SSRI selective serotonin re-uptake inhibitor

STD sexually transmitted disease

ABBREVIATIONS AND SYMBOLS

STEMI ST segment elevation myocardial infarction

SVT supraventricular tachycardia

T ° temperature

tri-iodothyronine

thyroxine

TAC tetracaine, adrenaline and cocaine

TB tuberculosis

tds three times a day

TFTs thyroid function tests

TIA transient ischaemic attack

TIMI thrombolysis in myocardial infarction

tPA tissue plasminogen actvator

TSH thyroid stimulating hormone

u/U unit(s)

U&E urea and electrolytes

URTI upper respiratory tract infection

USS ultrasound scan

UTI urinary tract infection

V volts

VA visual acuity

VF ventricular ﬁ brillation

VHF viral hemorrhagic fever

V/Q ventilation/perfusion (scan)

VT ventricular tachycardia

WB weight-bear(ing)

WBC white blood cells

WCC white cell count

WHO World Health Organization

WPW Wolff Parkinson White (syndrome)

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xvii

Note that ‘normal’ values in adults may vary slightly between labs.

Normal values in pregnancy are shown in b The pregnant patient, p.576.

Arterial blood gas analysis

Biochemistry

Normal values

35–45 nanomol/L

pH 7.35–7.45

(on air) >10.6 kPa, 75–100 mmHg

pCO

4.5–6.0 kPa, 35–45 mmHg

bicarbonate 24–28 mmol/L

base excess

± 2 mmol/L

alanine aminotransferase (ALT) 5–35 iu/L

albumin 35–50 g/L

alkaline phosphatase 30–300 iu/L

amylase 0–180 Somogyi U/dL

aspartate transaminase (AST) 5–35 iu/L

bicarbonate 24–30 mmol/L

bilirubin 3–17 micromol/L

calcium (total) 2.12–2.65 mmol/L

calcium (ionized) 1–1.25 mmol/L

chloride 95–105 mmol/L

creatine kinase (CK) 25–195 iu/L

creatinine 70–150 micromol/L

C-reactive protein (CRP) <10 mg/L

glucose (fasting) 3.5–5.5 mmol/L

G glutamyl transpeptidase (4)

11–51 IU/L

(5)

7–33 IU/L

magnesium 0.75–1.05 mmol/L

osmolality 278–305 mosmol/kg

potassium 3.5–5.0 mmol/L

sodium 135–145 mmol/L

urea 2.5–6.7 mmol/L

urate (5)

150–390 micromol/L

(4)

210–480 micromol/L

xviii

NORMAL VALUES

Haematology

Metric conversion

Length

Weight

Volume

1 L = 1.76 UK pints = 2.11 US liquid pints

1 UK pint = 20 ﬂ uid ounces = 0.568 L

1 US liquid pint = 16 ﬂ uid ounces = 0.473 L

1 teaspoon 8 5mL

1 tablespoon 8 15mL

Temperature

T ° in °C = ( T ° in Fahrenheit – 32) ×

–

Pressure

1kPa = 7.5mmHg

RBC (women)

3.9–5.6 × 10

(men)

4.5–6.5 × 10

Hb (women) 11.5–16.0g/dL

(men) 13.5–18.0g/dL

Hct (women) 0.37–0.47

(men) 0.40–0.54

MCV 76–96 femtoL

WCC

4.0–11.0 × 10

neutrophils

2.0–7.5 × 10

/L (40–75 % of WCC)

lymphocytes

1.5–4.0 × 10

/L (20–40 % of WCC)

monocytes

0.2–0.8 × 10

/L (2–10 % of WCC)

eosinophils

0.04–0.40 × 10

/L (1–6 % of WCC)

basophils

<0.1 × 10

/L (<1 % of WCC)

platelets

150–400 × 10

prothrombin time

(factors I, II, VII, X) 12–15sec

APTT (factors VII,

IX, XI, XII) 23–42sec

International Normalized Ratio (INR) therapeutic targets

2.0–3.0 (for treating DVT, pulmonary embolism)

2.5–3.5 (embolism prophylaxis for AF)

3.0–4.5 (recurrent thrombo-embolic disease,

arterial grafts & prosthetic valves)

ESR (women) <

(age in years+10)

mm/hr

(men) <

(age in years)

mm/hr

1m = 3 feet 3.4 inches 1 foot = 0.3048m

1cm = 0.394 inch 1 inch = 25.4mm

1kg = 2.20 pounds 1 stone = 6.35kg

1g = 15.4 grains 1 pound = 0.454kg

1 ounce = 28.4g

xix

A number of people provided comments, help and moral support. Special

thanks are due to Dr Phil Munro. We also wish to thank:

Miss Sehlah Abassi, Mr David Alao, Dr Matt Baker, Dr Joan Barber, Dr Ruth

Beach, Mr Dewald Behrens, Dr Ash Bhatia, Dr Angela Bonnar, Dr Rachel

Broadley, Dr Chris Brown, Mrs Debra Clayton, Mr Jon Davies, Dr Kate

Evans, Dr James Falconer, Miss Paula Fitzpatrick, Mrs Jennifer Flemen,

Dr Adrian Flynn, Dr Debbie Galbraith, Mr Blair Graham, Dr Catherine

Guly, Mr Chris Hadﬁ eld, Dr Steve Halford, Mr Andrew Harrower, Miss

Emily Hotton, Mr Jim Huntley, Mrs Eileen Hutchison, Mr Nicholas Hyatt,

Dr Karen Illingworth, Mr Ian Kelly, Mr Jacques Kerr, Dr Alastair Kidd,

Dr Paul Leonard, Mr Malcolm Lewis, Mr AF Mabrook, Dr Simon Mardel,

Dr Nick Mathiew, Ms Carolyn Meikle, Dr Louisa Mitchell, Dr Claudia

Murton, Dr Louisa Pieterse, Dr Stephanie Prince, Dr Laura Robertson, Miss

Katharine Robinson, Dr Andrew Sampson, Mr Tom Scott, Dr Simon Scott-

Hayward, Ms Karen Sim, Mr Toby Slade, Dr Timothy Squires, Mr Ashleigh

Stone, Dr Luke Summers, Dr Rob Taylor, Dr Ross Vanstone, Ms Fiona

Wardlaw, Dr Mike Wells, Mr Ken Woodburn, Mrs Polly Wyatt.

Acknowledgements

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The emergency department 2

Note keeping 4

Radiological requests 6

Triage 7

Discharge, referral, and handover 8

Liaising with GPs 10

Telephone advice 11

Liaising with the ambulance crew 12

Coping as a junior doctor 14

Inappropriate attenders 16

The patient with a label 17

The patient you dislike 18

Special patient groups 19

Discharging the elderly patient 20

The patient with learning difﬁ culties 21

Patient transfer 22

Breaking bad news 24

What to do after a death 26

Medicolegal aspects: avoiding trouble 28

Medicolegal aspects: the law 30

Infection control and prevention 32

What to carry in your car 34

At the roadside 36

Major incidents 38

General approach

Chapter 1

2 CHAPTER 1 General approach

The emergency department

The role of the emergency department

The emergency department (ED) occupies a key position in terms of the

interface between primary and secondary care. It has a high public proﬁ le.

Many patients attend without referral, but some are referred by NHS

Direct, minor injury units, general practitioners (GPs), and other medical

practitioners. The ED manages patients with a huge variety of medical

problems. Many of the patients who attend have painful and/or distressing

disorders of recent origin.

Priorities are:

• To make life-saving interventions.

• To provide analgesia.

• To identify relevant issues, investigations, and commence treatment.

• To decide upon need for admission or discharge.

ED staff work as a team. Traditional roles are often blurred, with the

important issue being what clinical skills a member of staff is capable of.

ED staff include:

• Nurses (including nurse practitioners, nurse consultants, health care

assistants).

• Doctors (permanent and ﬁ xed-term).

• Reception and administrative staff (receptionists, secretaries,

managers).

• Radiographers, including reporting radiographers.

• Other specialist staff (eg psychiatric liaison nurses, plaster technicians,

physiotherapists, paramedic practitioners, physician assistants,

occupational therapists, clinic/ED ward staff).

• Supporting staff (security, porters, cleaners, police).

Physical resources

A principal focus of the ED is to provide immediate resuscitation for

patients who present with emergency conditions. In terms of sheer

numbers, more patients attend with minor conditions and injuries, often

presenting quite a challenge for them to be seen and treated in a timely

fashion. Different departments have systems to suit their own particular

needs, but most have a resuscitation room, an area for patients on trolleys,

and an area for ambulant patients with less serious problems or injuries.

Paediatric patients are seen in a separate area from adults. In addition,

every ED requires facilities for applying casts, exploring and suturing

wounds, obtaining X-rays, and examining patients with eye problems.

Discharge from the ED

To work efﬁ ciently, the overall hospital system needs to enable easy ﬂ ow

of patients out of the ED. Options available for continuing care of patients

who leave the ED, include:

• Discharge home with no follow-up.

• Discharge home with GP and/or other community support/follow-up.

• Discharge with hospital clinic follow-up arranged.

• Admission to hospital for further investigation and treatment.

• Transfer to another hospital with more specialist facilities.

THE EMERGENCY DEPARTMENT

Emergency department staff beyond the emergency

department

In addition to their roles in providing direct clinical care in their

departments, many ED staff provide related clinical care in other settings

and ways:

• Short stay wards (sometimes called clinical decision units) where

emergency care can be continued by ED staff. The intention is for

admissions to these units to be short: most of the patients admitted

to such wards are observed for relatively short periods (<24hr) and

undergo assessments at an early stage to decide about the need for

discharge or longer-term admission.

• Outpatient clinics enable patients with a variety of clinical problems (eg

burns, soft tissue injuries, and infections) to be followed up by ED staff.

• Planned theatre lists run by ED specialists are used by some hospitals to

manage some simple fractures (eg angulated distal radial fractures).

• Telemedicine advice to satellite and minor injury units.

Emergency medicine in other settings

As the delivery of emergency care continues to develop, patients with

emergency problems are now receiving assessment and treatment in a

variety of settings. These include minor injury units, acute medical assessment

units and walk-in centres. Traditional distinctions between emergency

medicine, acute medicine, and primary care have become blurred.

4 CHAPTER 1 General approach

Note keeping

General aspects

It is impossible to over-emphasize the importance of note keeping.

Doctors and nurse practitioners each treat hundreds of patients every

month. With the passage of time, it is impossible to remember all aspects

relating to these cases, yet it may be necessary to give evidence in court

about them years after the event. The only reference will be the notes

made much earlier. Medicolegally, the ED record is the prime source

of evidence in negligence cases. If the notes are deﬁ cient, it may not be

feasible to defend a claim even if negligence has not occurred. A court

may consider that the standard of the notes reﬂ ects the general standard

of care. Sloppy, illegible, or incomplete notes reﬂ ect badly on the

individual. In contrast, if notes are neat, legible, appropriate, and detailed,

those reviewing the case will naturally expect the general standards of

care, in terms of history taking, examination, and level of knowledge, to

be competent.

The Data Protection and Access to Medical Records Acts give patients right

of access to their medical notes. Remember, whenever writing notes, that

the patient may in the future read exactly what has been written. Follow

the basic general rules listed below.

Layout

Follow a standard outline:

Presenting complaint Indicate from whom the history has been obtained

(eg the patient, a relative, or ambulance personnel). Avoid attributing

events to certain individuals (eg patient was struck by ‘Joe Bloggs’).

Previous relevant history Note recent ED attendances. Include family and

social history. An elderly woman with a Colles’ fracture of her dominant

hand may be able to manage at home with routine follow-up provided

she is normally in good health, and has good family or other support, but

if she lives alone in precarious social conditions without such support,

then admission on ‘social grounds’ may be required.

Current medications Remember to ask about non-prescribed drugs

(including recreational, herbal, and homeopathic). Women may not

volunteer the oral contraceptive pill (OCP) as ‘medication’ unless

speciﬁ cally asked. Enquire about allergies to medications and document

the nature of this reaction.

Examination ﬁ ndings As well as + ve features, document relevant –ve

ﬁ ndings (eg the absence of neck stiffness in a patient with headache and

pyrexia). Always document the side of the patient which has been injured.

For upper limb injuries, note whether the patient is left or right handed.

Use ‘left’ and ‘right’, not ‘L’ and ‘R’. Document if a patient is abusive or

aggressive, but avoid non-medical, judgemental terms (eg ‘drunk’).

Investigation ﬁ ndings Record clearly.

Working diagnosis For patients being admitted, this may be a differential

diagnostic list. Sometimes a problem list can help.

NOTE KEEPING

Treatment given Document drugs, including dose, time, and route of

administration (see current British National Formulary ( BNF ) for guidance).

Include medications given in the ED, as well as therapy to be continued

(eg course of antibiotics). Note the number and type of sutures or staples

used for wound closure (eg ‘5 × 6/0 nylon sutures’).

Advice and follow-up arrangements Document if the patient and/or

relative is given preprinted instructions (eg ‘POP care’). Indicate when/

if the patient needs to be reviewed (eg ‘see GP in 5 days for suture

removal’) or other arrangement (eg ‘Fracture clinic in one week’).

Record advice about when/why the patient should return for review,

especially if there is a risk of a rare but serious complication (eg for low

back pain ‘see GP if not better in 1 week. Return to the ED at once if

bladder/bowel problem or numb groin/bottom’ that might be features of

cauda equina syndrome).

Basic rules

• Write legibly in ballpoint pen, ideally black, which photocopies well.

• Always date and time the notes.

• Sign the notes, and print your name and status below.

• Make your notes concise and to the point.

• Use simple line drawings or preprinted sheets for wound/injury

descriptions.

• Avoid idiosyncratic abbreviations.

• Never make rude or judgemental comments .

• Always document the name, grade, and specialty of any doctor from

whom you have received advice.

• When referring or handing a patient over, always document the time of

referral/handover, together with the name, grade, and specialty of the

receiving doctor.

• Inform the GP by letter ( b Liaising with GPs, p.10), even if the patient

is admitted. Most EDs have computerized systems that generate such

letters. In complex cases, send also a copy of ED notes, with results of

investigations.

Pro formas

Increasing emphasis on evidence-based guidelines and protocols has

been associated with the introduction of protocols for many patient

presentations and conditions. Bear in mind the fact that, for some patients,

satisfactory completion of a pro forma may not adequately capture all of

the information required.

Electronic records

In an electronic age, there has been an understandable move towards

trying to introduce electronic patient records. The potential advantages

are obvious, particularly in relation to rapidly ascertaining past medical

history. When completing electronic records, practitioners need to follow

the same principles as those outlined above for written records.

Access to old records can make a huge contribution to decision making.

One potential advantage of electronic records is that they can be accessed

rapidly (compared with older systems requiring a porter to search through

the medical records store and retrieve paper-based notes).

6 CHAPTER 1 General approach

Radiological requests

‘I am glad to say that in this country there is no need to carry out

unnecessary tests as a form of insurance. It is not in this country desirable,

or indeed necessary, that over protective and over examination work

should be done, merely and purely and simply as I say to protect oneself

against possible litigation’ — Judge Fallon, quoted by Oscar Craig, Chairman

Cases Committee, Medical Protection Society.

Requesting investigations

The Royal College of Radiologists’ booklet ‘ Making the Best Use of a

Department of Clinical Radiology: Guidelines for Doctors ’ (6th edn, London,

RCR, 2007) contains very useful information and is strongly recommended.

General aspects

• An X-ray is no substitute for careful, thorough clinical examination. It is

usually unnecessary to request X-rays to conﬁ rm the clinical diagnosis

of uncomplicated fractures of the nose, coccyx, a single rib, or toes

(other than the big toe).

• If in doubt about the need for X-rays or the speciﬁ c test required,

consider relevant guidelines (eg Ottawa rules for ankle injuries,

b p.484) and/or discuss with senior ED staff or radiologist.

• When requesting X-rays, describe the indication/mechanism of injury,

clinical ﬁ ndings, including the side involved (right or left — spelt out

in full, not abbreviated) and the suspected clinical diagnosis. This is

important for the radiologist reporting the ﬁ lms without the advantage

of being able to examine the patient.

• Do not worry about specifying exactly which X-ray views are required.

The radiographer will know the standard views that are needed, based

on the information provided (eg AP + simpliﬁ ed apical oblique views for

a patient with suspected anterior shoulder dislocation). In unusual cases,

discuss with senior ED staff, radiographer, or radiologist.

• Always consider the possibility of pregnancy in women of child-bearing

age before requesting an X-ray of the abdomen, pelvis, lumbar spine,

hips, or thighs. If the clinical indication for X-ray is overriding, tell the

radiographer, who will attempt to shield the foetus/gonads. If the risks/

beneﬁ ts of X-rays in pregnant or possibly pregnant women are not

obvious, consult senior ED or radiology staff.

X-ray reporting system

Many hospitals have systems so that all ED X-rays are reported by a

specialist within 24hr. Reports of any missed abnormalities are returned

with the X-rays to the ED for the attention of senior staff, so that

appropriate action can be taken.

System for identifying abnormalities

In addition to the formal reporting system described above, a system is

commonly used whereby the radiographer taking the ﬁ lms applies a sticky

‘red dot’ to hard copy X-ray ﬁ lms and/or request card or to the equivalent

electronic image if they identify an abnormality. This alerts other clinical

staff to the possibility of abnormal ﬁ ndings.

TRIAGE

Triage

The nature of ED work means that a sorting system is required to ensure

that patients with the most immediately life-threatening conditions are seen

ﬁ rst. A triage process aims to categorize patients based on their medical

need and the available departmental resources. One most commonly used

process in the UK is the National Triage Scale (Table 1.1 ).

As soon as a patient arrives in the ED he/she should be assessed by a

dedicated triage nurse (a senior, experienced individual with considerable

common sense). This nurse should provide any immediate interventions

needed (eg elevating injured limbs, applying ice packs or splints, and giving

analgesia) and initiate investigations to speed the patient’s journey through

the department (eg ordering appropriate X-rays). Patients should not

have to wait to be triaged. It is a brief assessment which should take no

more than a few minutes.

Three points require emphasis:

• Triage is a dynamic process. The urgency (and hence triage category)

with which a patient requires to be seen may change with time. For

example a middle-aged man who hobbles in with an inversion ankle

injury is likely to be placed in triage category 4 (green). If in the waiting

room he becomes pale, sweaty, and complains of chest discomfort, he

would require prompt re-triage into category 2 (orange).

• Placement in a triage category does not imply a diagnosis, or even the

lethality of a condition (eg an elderly patient with colicky abdominal

discomfort, vomiting, and absolute constipation would normally

be placed in category 3 (yellow) and a possible diagnosis would be

bowel obstruction). The cause may be a neoplasm which has already

metastasized and is hence likely to be ultimately fatal.

• Triage has its own problems. In particular, patients in non-urgent

categories may wait inordinately long periods of time, whilst patients

who have presented later, but with conditions perceived to be more

urgent, are seen before them. Patients need to be aware of this and to

be informed of likely waiting times. Uncomplaining elderly patients can

often be poorly served by the process.

Table 1.1

National Triage Scale Colour Time to be seen by doctor

1 Immediate Red Immediately

2 Very urgent Orange Within 5–10 min

3 Urgent Yellow Within 1 hr

4 Standard Green Within 2 hr

5 Non-urgent Blue Within 4 hr

8 CHAPTER 1 General approach

Discharge, referral, and handover

Most patients seen in the ED are examined, investigated, treated, and

discharged home, either with no follow-up, or advice to see their GP (for

suture removal, wound checks, etc.). Give these patients (and/or attending

relative/friend) clear instructions on when to attend the GP’s surgery and

an indication of the likely course of events, as well as any features that

they should look out for to prompt them to seek medical help prior to

this. Formal written instructions are particularly useful for patients with

minor head injury ( b p.367) and those with limbs in POP or other forms

of cast immobilization ( b Casts and their problems, p.424).

The referral of patients to an inpatient team can cause considerable

anxiety, misunderstanding, and potential conﬂ ict between ED staff and

other disciplines. Before making the referral the following should be

considered.

Is it appropriate to refer this patient to the inpatient team?

Usually, this will be obvious. For example, a middle-aged man with a

history of crushing chest pain and an ECG showing an acute MI clearly

requires urgent management in the ED, and rapid admission for further

investigation and treatment. Similarly, an elderly lady who has fallen, is

unable to weight-bear and has a fractured neck of femur will require

analgesia, inpatient care and surgery.

However, difﬁ cult situations occur where the clinical situation is less clear;

for example, if a man experienced 4–5min of atypical chest pain, has a

normal ECG and chest X-ray (CXR), and is anxious to go home. Or a lady

has no apparent fracture on X-ray, but cannot weight-bear.

Is there appropriate information to make this decision?

This requires a balance between availability, time, and appropriateness.

In general, simple investigations which rapidly give the diagnosis, or clues

to it, are all that are needed. These include electrocardiogram (ECGs),

arterial blood gas (ABG), and plain X-rays. It is relatively unusual to have

to wait for the results of investigations such as full blood count (FBC), urea

& electrolytes (U&E), and liver function tests (LFTs) before referring a

patient, since these rarely alter the immediate management. Simple trolley-

side investigations are often of great value, for example, stix estimations

of blood glucose (BMG) and urinalysis. If complicated investigations are

needed, then referral for inpatient or outpatient specialist care is often

required.

Has the patient had appropriate treatment pending the admission?

Do not forget, or delay, analgesia. Treat every patient in pain appropriately

as soon as possible. A patient does not have to ‘earn’ analgesia. Never

delay analgesia to allow further examination or investigation. Concern

regarding masking of signs or symptoms (for example, in a patient with an

acute abdomen) is inhumane and incorrect.

DISCHARGE, REFERRAL, AND HANDOVER

How to refer patients

Referral is often by telephone, and this can create problems:

• Introduce yourself and ask for the name and grade of the specialist.

• Give a clear, concise summary of the history, investigations, and

treatment that you have already undertaken.

• Early in the discussion say clearly whether you are making a referral for

admission or a request for a specialist opinion. With ever increasing

pressure on hospital beds, inpatient teams can be reluctant to come

and see patients, and may appear to be happier to give advice over

the phone to avoid admission. If, in your view, the patient needs to

be admitted, then clearly indicate this. If, for whatever reason, this is

declined, do not get cross, rude, or aggressive, but contact senior ED

medical staff to speak to the specialist team.

• When the specialist team comes to see the patient, or the patient is

admitted directly to a ward, the ED notes need to be complete and

legible. Make sure that there is a list of the investigations already

performed, together with the available results and crucially, a list of

investigations whose results remain outstanding. The latter is essential

to ensure continuity of care and to prevent an important result ‘falling

through the net’. Similarly, summarize treatment already given and the

response. In an emergency, do not delay referral or treatment merely

to complete the notes, but complete them at the earliest opportunity.

• Encourage inpatient specialists who attend patients to write their

ﬁ ndings and management plan in the notes, adding a signature and the

time/date.

Handing over patients

Dangers of handing over

Handing over a patient to a colleague, because your shift has ended and

you are going home, is fraught with danger. It is easy for patients to be

neglected, or receive sub-optimal or delayed treatment. It is safest

to complete to the point of discharge or referral to an inpatient team

every patient that you are seeing at the end of a shift. Occasionally this

may not be possible (eg if there is a delay in obtaining an X-ray or other

investigation). In these situations, hand over the patient carefully to the

doctor who is taking over and inform the nursing staff of this.

How to hand over

Include in the handover relevant aspects of history and examination

performed, the investigation results, and the treatment undertaken. Sign

and aim to complete records on the patient as soon as possible. Note the

time of hand over, and the name of the doctor or nurse handed over to.

When accepting a ‘handed-over patient’ at the start of a shift, spend time

establishing exactly what has happened so far. Finally, it is courteous (and

will prevent problems) to tell the patient that their further care will be

performed by another doctor or nurse.

10 CHAPTER 1 General approach

Liaising with GPs

Despite changes in the way that care (particularly out of hours) is delivered,

GPs still have a pivotal role in co-ordinating medical care. Often the GP will

know more than anyone about the past history, social and family situation,

and recent events of their patient’s management. Therefore, contact the

GP when these aspects are relevant to the patient’s ED attendance, or

where considerations of admission or discharge are concerned.

Every attendance is followed routinely by a letter to the GP detailing the

reason(s) for presentation, clinical ﬁ ndings and relevant investigations,

treatment given, and follow-up arrangements.

If a patient dies, contact the GP without delay — to provide a medical

contact and assistance to the bereaved family, to prevent embarrassing

experiences (eg letters requesting clinic attendances), and out of courtesy,

because the GP is the patient’s primary medical attendant. Finally, the GP

may be asked to issue a death certiﬁ cate by the Coroner (in Scotland, the

Procurator Fiscal) following further enquiries.

Always contact the GP prior to the discharge of a patient where early

follow-up (ie within the next 24–72hr) is required. This may occur with

elderly patients where there is uncertainty about the home situation and

their ability to manage. A typical example is an elderly lady with a Colles’

fracture of her dominant wrist who lives alone. The ED management of

this patient is relatively simple ( b p.444). However, merely manipulating

a Colles’ fracture into a good position, supporting it in an adequate

cast, and providing analgesia, is only one facet of care. The GP may know

that the lady has supportive relatives or neighbours who will help with

shopping and cooking, and will help her to bath and dress. The GP and

the primary care team may be able to supplement existing support and

check that the patient is coping. Equally, the GP may indicate that with

additional home support (eg home helps, meals, district nurses), the

patient could manage. Alternatively, the GP may indicate that the Colles’

fracture merely represents the ﬁ nal event in an increasingly fragile home

situation and that the patient will require hospital admission, at least in the

short-term.

For the same reasons, a GP who refers a patient to the ED and indicates

that the patient requires admission does so in the full knowledge of that

patient’s circumstances. Always contact the GP if it is contemplated

that the patient is to be discharged — preferably after senior medical

consultation.

Finally, remember that GPs are also under considerable pressure.

Some situations may appear to reﬂ ect the fact that a patient has been

referred inappropriately or the patient may report that they have tried

to contact their GP unsuccessfully. Rather than irately ringing the practice

and antagonizing them, inform the ED consultant who can raise this

constructively and appropriately in a suitable environment.

TELEPHONE ADVICE

Telephone advice

Many departments receive calls from patients, parents, and other carers

for advice. Approach these calls in exactly the same way as a face-to-face

consultation. Formally document details of the call, including:

• Date and time of the call.

• The caller’s telephone number.

• The caller’s relationship to the patient.

• The patient’s name, age, and sex.

• The nature of the problem.

• The advice given.

As with all notes, date, time, and sign these notes.

NHS Direct

In England and Wales NHS Direct provides a 24-hr, 7-day a week telephone

service providing information and advice on health matters. It is staffed by

nurses who respond according to protocols.

The telephone number for NHS Direct is 0845 4647.

The equivalent service in Scotland is NHS24 tel. 08454 242424.

These services have internet websites at www.nhsdirect.nhs.uk and

www.nhs24.com

Telephone advice calls from other health professionals

Occasionally, other health professionals request advice regarding the

management of patients in their care. Such advice should be given by

experienced ED staff.

Telemedicine

Increasingly, emergency health care is provided by integrated networks,

which include EDs, minor injuries units, radiology departments, and GP

surgeries connected by telemedicine links. This has advantages in remote

or rural settings, enabling a wide range of injuries and other emergencies

to be diagnosed and treated locally. The combination of video and

teleradiology may allow a decision to be made and explained directly

to the patient. A typical example is whether a patient with an isolated

Colles’ fracture needs to have a manipulation of the fracture. Expertise

is required to undertake telemedicine consultations safely. This specialist

advice should be given by senior ED staff, and careful documentation is

crucial.

12 CHAPTER 1 General approach

Liaising with the ambulance crew

Paramedics and ED staff have a close professional relationship. Paramedics

and ambulance staff are professionals who work in conditions that are

often difﬁ cult and sometimes dangerous. It is worth taking an off-duty day

to accompany a crew during their shift to see the problems they face.

A beneﬁ t of paramedic training has been to bring ambulance staff into the

ED to work with medical and nursing staff, and to foster the communication

and rapport essential for good patient management.

In the UK, a patient brought to an ED by ambulance will routinely have a

patient report form (PRF) (see Fig. 1.1 ). This is completed by the crew at

the scene and in transit, and given to reception or nursing staff on arrival.

The information on these forms can be invaluable. In particular, the time

intervals between the receipt of the 999 call, and arrival at the scene and

at hospital, provide a time framework within which changes in the patient’s

clinical condition can be placed and interpreted.

The initial at-scene assessment will include details of the use of seat belts,

airbags, crash helmets, etc., and is particularly valuable when ampliﬁ ed by

speciﬁ cally asking the crew about their interpretation of the event, likely

speeds involved, types of vehicle, etc.

The clinical features of the Glasgow Coma Score (GCS) , pulse rate, blood

pressure (BP), and respiratory rate form baseline values from which trends

and response to treatment can be judged. Useful aspects in the history/

comments section include previous complaints, current medications, etc.,

which the crew may have obtained from the patient, relatives, or friends.

The PRF will also contain important information about oxygen, drugs, IV

ﬂ uids administered, and the response to these interventions. Before the

crew leave the department, conﬁ rm that they have provided all relevant

information.

Do not be judgemental about the crew’s performance. Remember the

constraints under which they operate. Without the beneﬁ ts of a warm

environment, good lighting, and sophisticated equipment, it can be

exceedingly difﬁ cult to make accurate assessments of illness or injury

severity, or to perform otherwise simple tasks (eg airway management

and intravenous (IV) cannulation).

Do not dismiss the overall assessment of a patient made by an experienced

crew. While the ultimate diagnosis may not be clear (a situation which

pertains equally in the ED), their evaluation of the potential for life-

threatening events is often extremely perceptive. Equally, take heed of

their description of crash scenes. They will have seen far more than most

ED staff, so accept their greater experience.

Most ambulance staff are keen to obtain feedback, both about speciﬁ c cases

and general aspects of medical care. Like everyone, they are interested

in their patients. A few words as to what happened to Mrs Smith who

was brought in last week and her subsequent clinical course is a friendly

and easy way of providing informal feedback, and helps to cement the

professional relationship between the ambulance service and the ED.

LIAISING WITH THE AMBULANCE CREW

Fig. 1.1 An example of a patient reporting form. Reproduced with kind permission

from the Scottish Ambulance Service.

14 CHAPTER 1 General approach

Coping as a junior doctor

Although many junior doctors coming to the ED have completed more

than 12 months of work since qualiﬁ cation, the prospect of working at the

‘sharp end’ can be accompanied by trepidation. As with many potentially

worrying situations in life, reality is not as terrifying as its anticipation. The

number of hours worked may not appear long in comparison with other

posts, but do not assume that this makes an ED job ‘easy’. Being on duty

inevitably involves much time standing, walking, working, thinking, and making

decisions. It is unusual to come off-shift without feeling physically tired.

Active young doctors can usually cope with these physical demands, but a

demanding professional life and demanding social life are rarely compatible.

Make the most of time off and try to relax from the pressures of the job.

One function of relaxation is to enable you to face work refreshed and

invigorated. You are mistaken if you believe that you can stay out all night

and then work unimpaired the next day. Tired doctors make mistakes.

They also tend to have less patience and, as a consequence, interpersonal

conﬂ icts are more likely.

A greater problem is the mental aspect of the job. Doctors often ﬁ nd that

the ED is the ﬁ rst time in their careers when they have to make unequiv-

ocal decisions based on their own assessment and investigations. This is

one of the great challenges and excitements of emergency medicine. It is

also a worry. Decision-making is central to ED practice and, with experi-

ence, the process becomes easier. Developing a structured approach can

pre-empt many problems and simplify your life. After taking an appropriate

history and completing the relevant clinical examination of a patient, ask

yourself a series of questions such as:

• Do I know what is likely to be wrong with this patient?

• What investigations are required to conﬁ rm the diagnosis?

• Do I know what treatment is needed and have I got the skills needed?

• Does this patient require referral to an inpatient team ( b p.8)?

• If not, do they need to be reviewed in the ED or another specialist clinic?

The wide spectrum of problems with which ED patients can present

means that no individual can be expert in every possible condition. It

is therefore as important to recognize and accept when you are out of

your depth as it is to make decisions and treat patients whom you know

you can manage. Seek help appropriately and do not just try to muddle

through. Help may be readily available from senior ED staff, but in some

departments direct contact with a specialist team is required. One of

the most difﬁ cult situations is where a specialist either refuses to come

to see the patient or gives telephone advice that is clearly inappropriate.

You must always act as the patient’s advocate. If you refer a patient with

a fractured neck of femur, and the telephone message from the inpatient

team is ‘bring him back to the Fracture Clinic in one week’, it is clearly

wrong to carry this out. First, check that the doctor has understood the

details of the patient’s condition and your concerns. More conﬂ ict and

aggravation is caused by communication errors (usually involving second-

hand telephone messages) than by anything else. If the situation remains

unresolved, consult senior ED staff. Whatever happens, never lose your

cool in public and always put your patient’s interests ﬁ rst.

COPING AS A JUNIOR DOCTOR

Learning in the ED

Try to learn something new every day. Keep a note of patients with

interesting or unusual problems, and later check what happened to them.

Ask senior staff for advice. Use the ED reference books. Try to note all

new conditions seen during a shift and read about them later.

Staff interaction

The nature of the job, the patients, and the diversity of staff involved

means that a considerable degree of camaraderie exists. For an outsider,

this can initially be daunting. Junior medical staff are likely to work for

4 − 12 months in the department. Other staff may have spent a lifetime

there with long-established friendships (or sometimes animosities).

Respect their position and experience, learn from them.

The nub of this is an understanding that the role of one individual and that

of other individuals in the department are inextricably linked. Any junior

(or senior) doctor who feels that they are the most important individual

in their working environment will have an extremely uncomfortable

professional existence. In the ED, every member of staff has a role. Your

professionalism should dictate that you respect this. Only in this way will

you gain reciprocal respect from other staff members.

Never consider any job ‘beneath you’ or someone else’s responsibility.

Patients come before pride. So, if portering staff are rushed off their

feet and you are unoccupied, wheel a patient to X-ray yourself — it will

improve your standing with your colleagues and help the patient.

Shifts

Rule 1 Never be late for your shift.

Rule 2 If, for whatever reason, you are unable to work a shift, let the

senior staff in the ED know as soon as possible.

Ensure that you take a break. Two or three short breaks in an 8-hr shift

are better than one long one. Remember to eat and maintain your ﬂ uid

intake. Shift working may mean that you will work sometimes with familiar

faces and perhaps occasionally with individuals with whom you ﬁ nd social

contact uncomfortable. Put these considerations aside while you are at

work, for the sake of the patients and your peace of mind.

If you can’t cope

Finally, if you feel that you are unable to manage or that the pressure

of the job is too great — tell someone . Don’t bottle it up, try to ignore it,

or assume that it reﬂ ects inadequacy. It doesn’t. Everyone, at some time,

has feelings of inability to cope. Trying to disguise or deny the situation

is unfair to yourself, your colleagues, and your patients. You need to tell

someone and discuss things. Do it now. Talk to your consultant. If you

cannot face him or her, talk to your GP or another senior member of

staff — but talk to someone who can help you.

The BMA Counselling Service for Doctors (tel: 08459 200169) provides a

conﬁ dential counselling service 24 hr a day, 365 days of the year to discuss

personal, emotional, and work-related problems. The Doctors’ Support

Network ( www.dsn.org.uk ) and Doctors’ Support Line (tel: 0844 395

3010) are also useful resources.

16 CHAPTER 1 General approach

Inappropriate attenders

This is an emotive and ill-deﬁ ned term. Depending upon the department,

such patients could comprise 4–20 % of attendances.

The perception as to whether it is appropriate to go to an ED or attend a

GP will vary between the patient, GP, and ED staff. Appropriateness is not

simply related to the symptoms, diagnosis, or the time interval involved. It

may not necessarily be related to the need for investigation. For example,

not all patients who require an X-ray necessarily have to attend an ED.

Further blurring of ‘appropriate’ and ‘inappropriate’ groups relates to the

geographical location of the ED. In rural areas, GPs frequently perform

procedures such as suturing. In urban areas, these arrangements are less

common. For ill-deﬁ ned reasons, patients often perceive that they should

only contact their GP during ‘ofﬁ ce’ hours, and outside these times may

attend an ED with primary care complaints.

It is clearly inappropriate to come to an ED simply because of a real or

perceived difﬁ culty in accessing primary care. Nevertheless, the term

‘inappropriate attendance’ is a pejorative one — it is better to use the

phrase ‘primary care patients’. It must be recognized that primary care

problems are best dealt with by GPs. Many departments try to prevent

this primary care workload presenting to the ED. Some departments

tackle the problem by having GPs working alongside ED staff.

Managing inappropriate attenders

Only through a continual process of patient education will these problems

be resolved. Initiatives include nurse practitioner minor injury units and

hospital-based primary care services. Evaluations are underway but, to

function effectively, such services require adequate funding and stafﬁ ng.

It can sometimes be difﬁ cult to deal with primary care problems in the

ED. After an appropriate history and examination, it may be necessary to

explain to patients that they will have to attend their own GP. This may

need direct contact between the ED and the practice to facilitate this.

Inappropriate referrals

Sometimes, it may appear that another health professional (eg GP,

emergency nurse practitioner, nurse at NHS Direct) has referred a patient

to the ED inappropriately. Avoid making such judgements. Treat patients

on their merits, but mention the issue to your consultant. Remember

that the information available to the referring clinician at the time of the

prehospital consultation is likely to have been different to that available at

the time of ED attendance.

THE PATIENT WITH A LABEL

The patient with a label

Some patients will have been referred by another medical practitioner,

usually a GP. The accompanying letter may include a presumptive diagnosis.

The details in the letter are often extremely helpful, but do not assume

the diagnosis is necessarily correct. Take particular care with patients who

re-attend following an earlier attendance. The situation may have changed

since the previous doctor saw the patient. Clinical signs may have developed

or regressed. The patient may have not given the referring doctor and

ED staff the same history. Do not pre-judge the problem: start with an

open mind. Apply common sense, however. Keep any previous history in

mind. For example, assume that a patient with a known abdominal aortic

aneurysm who collapses with sudden, severe, abdominal pain, signs of

hypovolaemic shock, and a tender pulsatile mass in the abdomen, to have a

ruptured abdominal aortic aneurysm, rather than intestinal obstruction. The

patient’s

previous ED and hospital case notes are invaluable and will often

give useful information and allow, for example, ECG comparisons, aiding

the diagnostic process. A call to the GP can also provide useful background,

which they may not have had time to include in their referral letter or may

have excluded for conﬁ dentiality or other reasons.

Self-labelled patients

Take care with patients who label themselves. Those with chronic or

unusual diseases often know signiﬁ cantly more about their conditions than

ED staff! In such situations, take special notice of comments and advice

from the patient and/or their relatives. Do not resent this or see it as a

professional affront — rapport with the patient will increase markedly and

management will usually be easier.

Regular attenders

Every ED has a group of ‘regular’ patients who , with time, become physically

and sometimes emotionally attached to the department. Some have

underlying psychiatric illnesses, often with ‘inadequate’ personalities. Some

are homeless. Regular attenders frequently use the ED as a source

of primary care. As outlined above, make attempts to direct them to

appropriate facilities, because the ED is unsuited to the management of

chronic illness, and is unable to provide the continuing medical and nursing

support that these patients require.

Repeated presentations with apparently trivial complaints or with the

same complaint often tax the patience of ED staff. This is heightened if the

presentations are provoked or aggravated by alcohol intake. Remember,

however, that these patients can and do suffer from the same acute events

as everyone else. Keep an open mind, diagnostically and in attitude to the

patient. Just because he/she has returned for the third time in as many

days complaining of chest pain, does not mean that on this occasion he

does not have an acute MI! Maintain adequate documentation for each

attendance. Occasionally, especially with intractable re-attenders, a joint

meeting between the social work team, GP, ED consultant and psychiatric

services is required to provide a deﬁ nitive framework for both the patient

and the medical services. For some patients, it will be possible to follow a

plan of action for ED presentations with a particular complaint.

18 CHAPTER 1 General approach

The patient you dislike

General approach

Accept the patient as he or she is, regardless of behaviour, class, religion,

social lifestyle, or colour. Given human nature, there will inevitably be

some patients whom you immediately dislike or ﬁ nd difﬁ cult. The feeling

is often mutual. Many factors that cause patients to present to the ED may

aggravate the situation. These include their current medical condition, their

past experiences in hospitals, their social situation, and any concurrent use

of alcohol and/or other drugs. Your approach and state of mind during

the consultation play a major role. This will be inﬂ uenced by whether the

department is busy, how much sleep you have had recently, and when you

last had a break for coffee or food.

Given the nature of ED workload and turnover, conﬂ ict slows down

the process and makes it more likely that you will make clinical errors.

Many potential conﬂ icts can be avoided by an open, pleasant approach.

Introduce yourself politely to the patient. Use body language to reduce a

potentially aggressive response.

The patient’s perspective

Put yourself in the patient’s position. Any patient marched up to by a

doctor who has their hands on hips, a glaring expression, and the demand

‘Well, what’s wrong with you now?’ will retort aggressively.

Defusing a volatile situation

Most complaints and aggression occur when the department is busy and

waiting times are long. Patients understand the pressures medical and

nursing staff have to work under, and a simple, ‘I am sorry you have had to

wait so long, but we have had a number of emergencies elsewhere in the

department’, does much to diffuse potential conﬂ ict and will often mean

that the patient starts to sympathize with you as a young, overworked

practitioner!

There is never any excuse for rude, abusive, or aggressive behaviour

to a patient. If you are rude, complaints will invariably follow and more

importantly, the patient will not have received the appropriate treatment

for their condition. It may be necessary to hand care of a patient to a

colleague if an unresolvable conﬂ ict has arisen.

Management of the violent patient is considered in detail on b p.610.

SPECIAL PATIENT GROUPS

Special patient groups

Attending the ED is difﬁ cult enough, but can be even more so for certain

‘special’ patient groups. It is important that ED staff are sensitive to the

needs of these groups and that there are systems in place to help them

in what may be regarded as an intimidating atmosphere. The following list

is far from exhaustive, but includes some important groups who require

particular consideration:

• Children : they are such an ‘obvious’ and large ‘minority’ group that they

receive special attention to suit their particular needs (see b Paediatric

emergencies, p.630).

• Pregnant women : see b Obstetrics and gynaecology, p.563.

• Those with mental health problems : see b Psychiatry, p.601.

• The elderly : who often have multiple medical problems and live in

socially precarious circumstances.

• Patients with Alzheimer’s disease and other states associated with

chronic confusion.

• Those with learning difﬁ culties : b p.21.

• Patients with hearing problems.

• The visually impaired.

• Those who do not speak or understand English : arrangements should be in

place to enable the use of interpreters.

• Patients with certain cultural or religious beliefs (particularly amongst

‘minority groups’) : these can impact signiﬁ cantly upon a variety of

situations (eg after unsuccessful resuscitation for cardiac arrest—

b Breaking bad news, p.24).

• Those who are homeless or are away from home, friends, and family

(eg holiday makers).

• Those who have drug/alcohol dependency.

Isn’t everyone special?

Taken at face value, the concept that certain groups of patients are

‘special’ and so require special attention does not meet with universal

approval. There is a good argument that every patient deserves the best

possible care. Whilst this is true, it is also obvious that certain patients

do have additional needs that need to be considered. Many of these

additional needs relate to effective communication. There are some

tremendous resources available that can help practitioners to overcome

communication difﬁ culties (eg www.communicationpeople.co.uk ).

20 CHAPTER 1 General approach

Discharging the elderly patient

There are no set predisposing factors that determine patients most at risk

following discharge. Those that affect the chance of difﬁ culties at home

include the current medical problem, underlying functional and social factors.

Risk indicators

Multiple pathologies and atypical symptoms render this group more vulnerable

to the physical, functional, and social effects of acute illness. Past medical

history and pre-admission status are especially important determinants

for patients with dementia or psychiatric illness. There may be evidence of

recently changed circumstances, a recent bereavement, a change in medical or

physical condition, increasing confusion, or unusual behaviour. The patient may

not be able to afford adequate food or heating. Community services may not

be aware that support is needed or help may have been offered, but refused.

Other important indicators are:

• Those living alone.

• Absence of close family support or community services.

• Unsuitable home circumstances (eg external or internal stairs).

• Difﬁ culty with mobility.

Determining those unable to cope

Look for evidence of self-neglect that suggests that the elderly person

is having difﬁ culty coping at home (eg poor personal hygiene, unclean or

unsuitable clothing). Evidence of recent weight loss may suggest difﬁ culties

with food preparation or eating, unavailability of food, or may be due to

serious pathology, such as a malignancy or tuberculosis. Signs of old bruising

or other minor injuries may be consistent with frequent falls. Shortness of

breath and any condition producing impaired mobility are important factors.

Falls are a common problem of old age and require careful analysis, perhaps

at a special ‘Falls’ clinic. Correctable factors include damaged walking aids,

loose rugs, poor lighting, or unsuitable footwear or glasses. Common medical

causes include cerebrovascular disease, arthritis, and side-effects of drugs.

Many elderly people claim that they can cope at home when they are unable

to do so. If in doubt, ask relatives, the GP, and community support agencies.

They may give helpful insight into the patient’s mental state, which can be

investigated/assessed further, whether it be a cognitive or reactive condition.

The decision to discharge

Hospital admission for an elderly person is a frightening experience and

can lead to confusion and disorientation. If circumstances allow, discharge

home is often a more appropriate outcome. If there are concerns regarding

their functional ability and mobility, ask for an occupational therapy and/

or physiotherapy assessment with, if appropriate, a home assessment.

The elderly person is best seen in their home environment with familiar

surroundings, especially if there is evidence of cognitive deﬁ cit. The provision

of equipment and recommendations for adaptations can be made at this

point if required. A wide range of community services including district

nurse, health visitor, home help, crisis care, social work, hospital discharge,

and rapid response therapy teams can be contacted to provide immediate

follow-up and support and play a crucial role in preventing later breakdowns

in home circumstances and unnecessary admissions for social reasons.

THE PATIENT WITH LEARNING DIFFICULTIES

The patient with learning difﬁ culties

Patients with learning difﬁ culties use the healthcare system more than the

general population. Unfortunately, many healthcare professionals have

little experience with these patients. However, understanding common

illness patterns and using different techniques in communication can result

in a successful consultation. Patients with learning difﬁ culties often have

complex health needs. There are many barriers to assessing health care,

which may lead to later presentations of illness. Patients may have a high

tolerance of pain — take this into consideration when examining them.

Associated health problems

Patients with learning difﬁ culties have a higher incidence of certain problems:

• Visual and hearing impairment.

• Poor dental health.

• Swallowing problems.

• Gastro-oesophageal reﬂ ux disease.

• Constipation.

• Urinary tract and other infections.

• Epilepsy.

• Mental health problems ( i incidence of depression, anxiety disorders,

schizophrenia, delirium, and dementia), with speciﬁ c syndromes

having their own particular associations (eg Down’s is associated with

depression and dementia; Prader–Willi with affective psychosis).

• Behavioural problems (eg Prader–Willi, Angelman syndrome).

Leading causes of death

These include pneumonia (relating to reﬂ ux, aspiration, swallowing, and

feeding problems) and congenital heart disease.

The patient’s perspective

Past experiences of hospital are likely to have a big impact on the patient’s

reaction to his/her current situation. Most patients have problems with

expression, comprehension, and social communication. They ﬁ nd it difﬁ cult

to describe symptoms — behavioural change may the best indication that

something is wrong.

Tips for communication

• Explain the consultation process before starting.

• Speak ﬁ rst to the patient, then to the carer.

• Use open questions, then re-phrase to check again.

• Aim to use language that the patient understands, modifying this

according to comprehension.

• Patients may have difﬁ culties with time, so try to relate symptoms to

real life temporal events (eg ‘did the pain start before lunch?’)

• They may not make a connection between something that they have

done and feeling ill (eg several questions may be required in order to

establish that they have ingested something).

• Take particular note of what the carer has to say — information from

someone who knows the patient well is invaluable.

22 CHAPTER 1 General approach

Patient transfer

The need to transfer

When patients have problems that exceed the capabilities of a hospital

and/or its personnel, transfer to another hospital may be needed.

Timing the transfer

Do not commence any transfer until life-threatening problems have been

identiﬁ ed and managed, and a secondary survey has been completed.

Once the decision to transfer has been made, do not waste time

performing non-essential diagnostic procedures that do not change the

immediate plan of care. First, secure the airway (with tracheal intubation

if necessary). Ensure that patients with pneumothoraces and chest injuries

likely to be associated with pneumothoraces have intercostal drains

inserted prior to transfer. This is particularly important before sending a

patient by helicopter or ﬁ xed wing transfer. Consider the need to insert a

urinary catheter and a gastric tube.

Arranging the transfer

Speak directly to the doctor at the receiving hospital. Provide the following

details by telephone or telemedicine link:

• Details of the patient (full name, age, and date of birth).

• A brief history of the onset of symptoms/injury.

• The pre-hospital ﬁ ndings and treatment.

• The initial ﬁ ndings, diagnosis, and treatment in the ED and the response

to treatment.

Write down the name of the doctor responsible for the initial reception

of the patient after transfer. Establish precisely where within the receiving

hospital the patient is to be taken. Where possible, prepare the receiving

unit by sending details ahead by fax/email. Pre-printed forms can help in

structuring the relevant details and avoiding omissions.

Preparing for transfer

Transfer team

If the patient to be transferred may require advanced airway care, ensure

they are accompanied by a doctor who can provide this. The accompanying

nurse should be trained in resuscitation with a good knowledge of the

equipment used during transfer.

Equipment

‘Transfer cases’ containing a standardized list of equipment must be

immediately available and regularly checked. Take all the emergency

equipment and drugs that might prove necessary to maintain the ‘Airway’,

‘Breathing’ and ‘Circulation’ (ABC) during transfer. In particular, take at

least twice the amount of O

estimated to be necessary (a standard ‘F’

cylinder contains 1360 L of O

and will therefore last <3hr running at 10L/

min). Before leaving, ensure that the patient and stretcher are well-secured

within the ambulance. Send all cross-matched blood (in a suitably insulated

container) with the patient.

PATIENT TRANSFER

Monitoring during transfer

Minimum monitoring during transfer includes ECG monitoring, pulse

oximetry, and non-invasive BP measurement. If the patient is intubated

and ventilated, end-tidal carbon dioxide (CO

) monitoring is mandatory.

An intra-arterial line is recommended, to monitor BP during the journey.

Make allowances for limited battery life on long transfers: spare batteries

may be needed. Plug monitors and other equipment into the mains supply

whenever possible.

Accompanying documentation

Include the following:

• Patient details : name, date of birth, address, next of kin, telephone

numbers, hospital number, GP.

• History, examination ﬁ ndings, and results of investigations (including

X-ray ﬁ lms).

• Type and volume of all ﬂ uids infused (including pre-hospital).

• Management including drugs given (type, route, and time of

administration), practical procedures performed.

• Response to treatment, including serial measurements of vital signs.

• Name of referring and receiving doctors, their hospitals, and telephone

numbers.

Some departments use standard forms to ensure that important

information is complete.

The relatives

Keep the patient’s relatives informed throughout. Explain where and why

the patient is going. Document what they have been told. Arrange transport

for relatives to the receiving hospital.

Before leaving

Prior to transfer, re-examine the patient. Check that the airway is

protected, ventilation is satisfactory, chest drains are working, IV cannulae

patent and well secured, and that the spine is appropriately immobilized,

but pressure areas protected. Ensure that the patient is well-covered to

prevent heat loss. Inform the receiving hospital when the patient has left

and give an estimated time of arrival.

After leaving

Communicate to the receiving hospital the results of any investigations

that become available after the patient has left. Contact the receiving

doctor afterwards to conﬁ rm that the transfer was completed satisfactorily

and to obtain feedback.

Intra-hospital transfers

In many respects, the only difference between intra- and inter-hospital

transfers is the distance. The principles involved in organizing a transfer

are the same, whether the patient is to be conveyed to the computed

tomography (CT) scanner down the corridor, or to the regional

neurosurgical unit miles away.

24 CHAPTER 1 General approach

Breaking bad news

A proportion of patients presenting to the ED have life-threatening

conditions and some will die in the department. Often, the event will be

sudden and unexpected by family and friends. It may already involve other

family members (eg in the context of a road trafﬁ c collision). In contrast to

hospital inpatients or those in general practice, an opportunity to forewarn

relatives as to what has happened or the eventual outcome is unlikely.

The relatives may already be distressed after witnessing the incident or

collapse, and may have been directly involved in providing ﬁ rst aid.

It is inappropriate for junior hospital staff without suitable experience to

speak with distressed or bereaved relatives. The task must be undertaken

by someone with sufﬁ cient seniority and authority, who also has the skills

of communication and empathy. The most important component is time.

Reception

Relatives usually arrive separately and after the patient. Anticipate

this by designating a member of staff to meet them and show them to

a relatives’ room, which should afford privacy, comfortable seating, an

outside telephone line, tea, coffee, and toilet facilities. Paper tissues, some

magazines, and toys for small children are useful.

While the relatives are waiting, a designated nurse should stay with them

to act as a link with the department and the team caring for the patient.

This nurse can pre-warn relatives of the life-threatening nature of the

patient’s condition and assist in building (an albeit short) relationship

between staff and relatives. The link nurse should also check that

important details have been recorded correctly, eg the patient’s name,

address, date of birth, religion (in case last rites are required), next of kin

(name, relationship to patient, address and phone no.), and the patient’s

GP. This information should be collected as soon as possible, since later

the relatives may be too upset to remember all these details or it may be

difﬁ cult to ask for them.

Breaking the news

Irrespective of who performs this task, remember a number of points. If

you are the person who informs the relatives, ensure the link nurse is with

you. After leaving the resuscitation room or clinical area, allow a minute

or two of preparation to make yourself presentable, checking clothing for

bloodstains, etc. Conﬁ rm that you know the patient’s name. Enter the

room, introduce yourself, and sit or kneel by the relatives so that you are

at their physical level. Ensure that you speak with the correct relatives and

identify who is who. Speak slowly, keep your sentences short and non-

technical. Do not hedge around the subject. In their emotional turmoil,

relatives very often misconstrue information. Therefore, you may need to

re-emphasize the important aspects.

For many critically ill patients, their ultimate prognosis cannot be deter-

mined in the ED. In these situations, do not raise unrealistic expectations

or false hopes, but be honest and direct with the relatives and the patients.

BREAKING BAD NEWS

If the patient has died, then use the words ‘death’ or ‘dead’. Do not use

euphemisms such as ‘passed away’, or ‘gone to a better place’.

After giving the news, allow relatives a few minutes to collect their

thoughts and ask questions. In some cases, these may be unanswerable. It is

better to say ‘we don’t yet know’, rather than confuse or give platitudinous

answers.

Common responses to bad news or bereavement include emotional

distress, denial, guilt, and aggression. The feelings of guilt and anger can

be particularly difﬁ cult to come to terms with, and relatives may torture

themselves with the idea that if only their actions had been different, the

situation would never have arisen, or the clinical outcome would have been

different.

Relatives seeing patients

Many relatives wish to see or touch their loved ones, however brieﬂ y.

Television and cinema have prepared much of the population for the sights

and sounds in the ED. In some departments, relatives are encouraged to

be present in the resuscitation room. In selected situations the stratagem

has beneﬁ ts. If the relatives are present during resuscitation, it is essential

that the link nurse is present with the relatives to provide support, explain

what is happening, and accompany them if they wish to leave.

More frequently, the relatives can see the patient in the resuscitation room

brieﬂ y or while they are leaving the ED (eg to go to CT scan room or

theatre). Even a few seconds, a few words, and a cuddle can be immensely

rewarding for both relative and patient. The link nurse can give guidance

beforehand as to the presence of injuries (especially those involving the

face), monitors, drips, and equipment, to diminish any threatening impact

that these may have.

When death occurs

Even before death has occurred, involvement of religious leaders is valuable.

As early as possible, inform the hospital chaplain, who can provide

invaluable help to relatives and staff.

When a patient has died, offer the relatives the opportunity to see the

body. This contact, which should be in a private quiet room, can greatly

assist in the grieving process. With careful preparation, most patients who

have died from multiple injuries can be seen by relatives in this fashion.

Remember that followers of some faiths, such as Muslims and Hindus,

have important procedures and rituals to be followed after death,

although these may not always be feasible after a sudden death, especially

from trauma. In such situations, discuss the matter with the Coroner’s or

Procurator Fiscal’s ofﬁ cer, and obtain help from an appropriate religious

leader to look after the bereaved relatives.

26 CHAPTER 1 General approach

What to do after a death

Who to contact

Any suspicious death must be immediately reported to the Police who

will liaise directly with the Coroner or Procurator Fiscal (in Scotland).

Following all deaths in the ED, a number of important contacts must be

made as soon as possible:

• Informing the next of kin : if the relatives are not already present in ED, it

may be necessary to ask the Police for assistance.

• Notifying the Coroner (Procurator Fiscal in Scotland).

• Informing the patient’s GP.

• Cancelling hospital outpatient appointments.

• Informing social work and health visitor teams as appropriate.

Ensure deceased’s relatives are given information about the process

for death certiﬁ cation and registration, and how to organize funeral

arrangements. Most EDs have useful leaﬂ ets that cover these matters and

can answer many questions. Some departments have formal arrangements

for counselling after bereavement. Often the GP is the best individual

to co-ordinate bereavement care, but in any event, give the relatives a

telephone number for the ED so they can speak to a senior nurse or

doctor if they need further information or help.

Information for the Coroner or Procurator Fiscal

Report sudden deaths as soon as possible to the Coroner (in Scotland

the Procurator Fiscal). It is helpful to give the following information if it

is available:

• Patient’s name, address, date of birth.

• Next of kin (name, relationship, address, phone no.).

• Patient’s GP.

• Date and time of patient’s arrival in the ED.

• Date and time of patient’s death.

• Name and job title of doctor who pronounced death.

• Details of the incident, injuries, or illness.

• Relevant past medical history.

• When the patient last saw a doctor (the Coroner may be happy for a

GP or hospital doctor to write a death certiﬁ cate if they saw the patient

recently for the condition that caused death, eg a patient with known

terminal cancer).

• The patient’s religion : some faiths may wish to arrange burial before the

next sunset, but this may not be feasible after a sudden death.

• Anything else that is important, eg difﬁ culties in communication with

the next of kin due to language or deafness.

WHAT TO DO AFTER A DEATH

Looking after the staff

The death of a patient or the management of patients with critical illness

inevitably affects the ED staff. This is particularly so when some aspect of

the event reminds staff of their own situation or relatives. These episodes

often occur at the busiest times and when everyone in the ED is working

under pressure.

One of the most difﬁ cult situations is to have to inform parents of the

death of their child and help them in the initial grieving process, and then

return to the busy department where many people are waiting with

increasingly strident demands. It would be easy to respond that such

individuals, with injuries or illnesses that are minor or present for days or

weeks, are time-wasting. However, this approach will lead to conﬂ ict and

is unfair to all concerned. Instead, take 5 − 10min for a break in the staff

room before returning to the fray. Remember that in these circumstances

you too are a patient. Even senior and experienced staff may be distressed

after difﬁ cult resuscitation situations and may require support.

Organ donation

There is considerable potential to assist with the process of organ/tissue

donation in the ED. However, the possibility of organ donation is sadly

often overlooked in the ED. Many patients who die after unexpected

cardiac arrest are potential donors of corneal tissue and heart valves.

Kidneys may also be retrieved from some patients who have died in the

ED, if a protocol for this has been arranged with the transplant team and

the local Coroner or Procurator Fiscal. Many other patients who are

moribund, intubated and ventilated (eg following massive subarachnoid

haemorrhage) may be identiﬁ ed as potential donors of other tissues

also. Consider the possibility of organ donation in patients who die in the

ED or who are moribund with no hope of survival. Most hospitals have

specialist organ donation nurses (previously known as ‘donor transplant

coordinators’) who will educate, advise and assist with the process of

organ donation. Useful information about organ/tissue transplantation is

available on the website of the British Transplantation Society (www.bts.

org.uk).

28 CHAPTER 1 General approach

Medicolegal aspects: avoiding trouble

Medicolegal problems are relatively common in the ED. Many of these

problems may be avoided by adopting the correct approach.

Attitude

Be polite and open with patients. Try to establish a good rapport. Be as

honest as possible in explaining delays/errors.

Consent (see General Medical Council guidance)

Use the consent form liberally for anything that is complex, risky, or

involves sedation or general anaesthetic (GA). Ensure that the patient

understands what is involved in the procedure, together with its potential

beneﬁ ts and risks. Whenever possible, attempt to obtain consent from

parent/guardian in minors, but do not delay life-saving treatment in order

to obtain consent.

Documentation ( b Note keeping, p.4)

Good notes imply good practice. Keep careful notes, using simple, clear,

unambiguous language. Write your name legibly and document the time

that you saw the patient. Remember that successful defence of a medical

negligence claim may depend upon accurate, legible, comprehensive,

contemporaneous notes. Try to avoid abbreviations, particularly where

there is room for confusion. In particular, name the digits of the hand

(thumb, index, middle, ring, and little ﬁ ngers) and specify right or left by

writing it in full.

Be meticulous in documenting the nature, size, and position of any wounds

( b p.402). Write down a diagnosis, together with a full interpretation

of any investigations. Ensure that all attached documents (nursing

observations, blood results, ECG) are labelled. Document all instructions

and advice given to the patient, together with any follow-up arrangements

made.

Referral ( b Discharge, referral, and handover, p.8)

Always seek senior help or refer those patients with problems beyond

your knowledge or expertise. Record any referral made, together with

the name and grade of the doctor referred to, the time it was made, and

a summary of the facts communicated. After referral, be cautious about

accepting telephone advice alone — an expert cannot usually provide an

accurate opinion without seeing the patient.

Return visits

Take special care with any patient who returns to ED with the same

presenting complaint, because it is no better, has deteriorated, or the

patient is simply dissatisﬁ ed. Do not automatically rely upon previous

diagnosis and X-ray interpretations as being correct — treat the patient as

if they were attending for the ﬁ rst time. Try to involve the consultant in

these cases.

MEDICOLEGAL ASPECTS: AVOIDING TROUBLE

Discharge against advice

Always attempt to persuade the patient to accept the treatment offered,

but if this is refused, or the patient leaves before being seen, ask the patient

to sign an appropriate form. Patients not deemed competent (see Mental

Capacity Act below) to make this decision may need to be held against

their wishes — seek senior help with this. Write full notes explaining what

happened.

Mental Capacity Act (b p.629)

The Mental Capacity Act 2005 outlines how a person is unable to make a

decision for himself if he/she is unable to:

• Understand the information relevant to the decision.

• Retain the information.

• Use or weight that information as part of the process of making the

decision.

• Communicate his/her decision.

A patient lacks capacity if at the time he/she is unable to make a decision

for himself/herself in relation to the matter because of an impairment or a

disturbance in the functioning of the mind or brain.

Access to records

All ED staff should bear in mind that patients may gain access to their

medical records and read what has been written about them. Patients in

the UK have a statutory right of access to information about themselves

(set out in the Data Protection Act 1998) and this includes medical

records. Competent patients may apply for access to, and copies of, their

own records. Applications are usually made in writing via the hospital’s

legal department.

Medical defence organization

Join a medical defence organization. The Medical Defence Union (MDU),

MDDUS, and Medical Protection Society provide professional indemnity

cover for emergencies outside hospital, and advice and support for all

sorts of medicolegal matters that are not necessarily covered by NHS

trusts, eg statements to the Coroner or Procurator Fiscal, support at

inquests or fatal accident inquiries, allegations of negligence, legal actions,

and problems with the GMC. They also provide members with useful

information and booklets about consent, conﬁ dentiality and other issues.

Further information

www.the-mdu.com/hospital

www.mddus.com

www.medicalprotection.org

30 CHAPTER 1 General approach

Medicolegal aspects: the law

Conﬁ dentiality

Medical information about every patient is conﬁ dential and should not

be disclosed without the patient’s consent. In the UK the police do not

have routine access to clinical information, but some information may be

divulged in certain speciﬁ c circumstances:

• The Road Trafﬁ c Act (1972) places a duty on any person to provide

the police, if requested, with information that might lead to the

identiﬁ cation of a vehicle driver who is suspected of an offence under

the Act. The doctor is obliged to supply the person’s name and address,

but not clinical information.

• Suspicion of terrorist activity.

• Gunshot wounds (see www.gmc-uk.org ).

• Disclosure in the public interest. The General Medical Council advises

that this might include situations where someone may be exposed to

death or serious injury (eg murder, rape, armed robbery, child abuse).

Although this may provide ethical permission for the doctor to reveal

details without consent, it does not place him/her under any legal

duty to do so. Discuss these cases with your consultant and/or your

medical defence organization. (General Medical Council (GMC) advice:

www.gmc-uk.org ).

Ability to drive

A patient’s ability to drive may be impaired by injury (especially limb or

eye), by drugs (eg after GA, opiates, alcohol) or medical conditions (eg

TIAs, epilepsy, arrhythmias). In each case, warn the patient not to drive and

ensure that this warning is documented in the notes. It may be prudent to

provide this warning in the presence of a close relative.

For further information on medical aspects of ﬁ tness to drive see:

www.dft.gov.uk/dvla/medical/ataglance.aspx

Police requests for blood alcohol

In the UK, the police may request a blood or urine sample under

Section 5 of the Road Trafﬁ c Act (1988) from a patient they suspect to

have been in charge of a motor vehicle with an illegal blood alcohol level

( > 80mg/100mL). In such circumstances, specimens should only be taken

if they do not prejudice the proper care and treatment of the patient.

The relevant specimens should only be taken by a police surgeon (clinical

forensic physician) and with the patient’s consent.

A change in the law (Police Reform Act 2002) also allows a police surgeon

to take a blood sample from an unconscious patient who is suspected

of having been the driver of a motor vehicle while under the inﬂ uence

of alcohol and/or drugs. The blood sample is retained and tested later,

depending upon the patient later giving consent. Again, only permit the

police surgeon access to the patient if this will not delay or prejudice

proper care and treatment of the patient.

MEDICOLEGAL ASPECTS: THE LAW

Reporting deaths to the Coroner (or Procurator Fiscal)

Many deaths that occur in (or in transit to) the ED are sudden and

unexpected, and/or follow trauma. The exact cause of death is seldom

immediately apparent. Accordingly, do not be tempted to sign death

certiﬁ cates. Instead, report all deaths to the Coroner (the Procurator

Fiscal in Scotland). See b p.26 for details of the information required.

Police statements

Do not provide information to the police until patient consent has been

obtained. Writing a police statement requires thought and care. Write

the statement yourself. Keep statements brief and try to avoid hearsay,

conjecture, or opinion on the likely outcome. List injuries using both

medical and non-medical language, explaining terminology in detail as

necessary. State the investigations and treatment provided as accurately

as possible (eg what sutures and how many were used). Having written

the statement, ask your consultant to read it and comment on it. Get

the statement typed (a friendly ED secretary may help if you cannot

type yourself, and will also know how you can claim the relevant fee).

Having checked it, sign and date the statement, and give it to the ofﬁ cer

concerned. Always keep a copy of the statement and the ED notes, so

that they are easily available if you are called to court.

Court appearances

In advance Discuss the case with your consultant, and review the notes,

the questions that you might be asked, and the likely court procedures.

Get a good copy of the notes and any investigations. Ask whether you

should take the original records to court.

On the day Dress smartly, arrive early, and behave professionally. Be

prepared for a long wait, so take a book to read. Turn off your mobile

phone. Once in court, you have the option of taking an oath before God

or afﬁ rming without religious connotation. You are equally bound to tell

the truth whichever you choose. Use the same form of address that others

have already used (eg ‘My Lord’, ‘Your Honour’). Answer directly and

simply. Use comprehensible language, free of medical jargon. Remember

that you are a professional witness, not an expert. Therefore, conﬁ ne

the expression of opinion to within the limits of your knowledge and

experience — if asked something outside this, say so!

Inquest/fatal accident inquiry If you are called to give evidence at an inquest

(in Scotland, a fatal accident inquiry), discuss the case with your consultant

and also with your medical defence society.

Further information and advice about reports and appearing in court

The medical defence organizations ( b p.29) have useful advice sheets for

their members about writing reports and appearing in court.

32 CHAPTER 1 General approach

Infection control and prevention

Staff in the ED have an important role in preventing and controlling

infection, which can be a serious risk to patients, relatives, and staff.

Organisms such as Staph. aureus , including MRSA ( b p.235), can readily

be transmitted by contaminated hands or equipment, causing infection of

wounds, fractures, and in-dwelling devices (eg catheters or chest drains).

Infected blood can transmit many infections, including hepatitis B and C

( b p.239) and human immunodeﬁ ciency virus (HIV; b p.242). Viral gas-

troenteritis is usually spread by the faecal-oral route, but vomiting may

cause widespread viral contamination of the surroundings and equipment,

with a risk of transmission to other patients and staff.

Coughing and sneezing produces small droplets of infected secretions,

which could involve viruses such as inﬂ uenza ( b Inﬂ uenza pandemics,

avian ﬂ u, and swine ﬂ u, p.252), severe acute respiratory syndrome (SARS;

b p.251), and respiratory syncytial virus (RSV; b p.682). A nebulizer

used on an infected patient may spread respiratory viruses widely, as

occurred in the outbreak of SARS in Hong Kong in 2003 which involved

many ED staff.

Standard precautions for preventing infection

Standard precautions (also known as ‘universal precautions’) should be

used at all times and with all patients to reduce the risks of infection.

Blood and body ﬂ uids from all patients should be treated as infected.

These standard precautions include:

• Hand hygiene Essential, but often neglected. Decontaminate your hands

before and after every patient contact, and after any activity that might

contaminate hands, including removing gloves. Hands that are visibly

dirty or possibly grossly contaminated must be washed with soap and

water, and dried thoroughly. Alcohol hand gel can be used if the hands

look clean. Cover broken skin with a waterproof dressing.

• Personal protective equipment (PPE) Wear suitable disposable gloves

for any contact with blood, body ﬂ uids, mucous membranes, or non-

intact skin. Latex gloves are widely used, but cause allergic reactions in

some patients and staff, who need special nitrile gloves. Use a disposable

plastic apron if there is a risk of blood or body ﬂ uids contaminating

clothing. After use, dispose of it and wash your hands. Impervious

gowns are needed if there is a high risk of contamination. Use a mask ,

face shield, and eye protection if blood or body ﬂ uids might splash in

your eyes or mouth. Protection against respiratory viruses, eg SARS

or inﬂ uenza requires special masks or respirators (eg FFP3), which must

be ﬁ tted and used properly. Powered air-purifying respirators should be

used for high-risk procedures such as intubating patients with serious

viral infections.

• Safe handling and disposal of sharps Avoid handling needles directly or

using hand-held needles. Never re-sheathe needles. Place used needles

and blades immediately into a ‘sharps bin’. If possible, use safety needles

and cannulae, which reduce the risk of needlestick injury. If, despite

all precautions, a needlestick injury does occur follow local approved

INFECTION CONTROL AND PREVENTION

procedures to minimize the risk of infection and look after the people

involved (see b Needlestick injury, p.418).

• Managing blood and bodily ﬂ uids Samples of blood or other body ﬂ uids

must be handled safely, with care not to contaminate request forms

or the outside of the container. Follow local approved procedures

for dealing with spillages of blood or body ﬂ uids: wear suitable PPE

(usually a disposable apron and gloves) and disinfect the spillage with an

appropriate agent such as diluted bleach.

Planning for outbreaks of infectious diseases

Planning to cope with an outbreak of a serious infectious disease such

as SARS or pandemic ﬂ u ( b p.252) is a considerable challenge for ED

staff and for the whole community. The ED must be organized so that

patients can be assessed properly with a minimum risk of infecting staff or

other patients. If possible, patients with serious airborne diseases should

be treated in negative pressure isolation rooms by staff in appropriate PPE

who are fully trained to minimize the risks of spreading and acquiring the

infection. In high risk situations a ‘buddy’ system for staff may be helpful,

with each doctor or nurse being watched closely by another person to

check that full safety precautions are maintained.

Assessment of febrile patients

Hospitals in Hong Kong with experience of SARS use the FTOCC criteria

when assessing febrile patients for potentially serious infectious diseases:

• F — fever ( > 38 ° C).

• T — travel history.

• O — occupational history.

• C — clustering of cases.

• C — contact history (eg someone with SARS or avian ﬂ u).

Similar criteria are used in the UK Health Protection Agency’s algorithm:

www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/AvianInﬂ uenza/

Further information

Standard precautions

www.rcn.org.uk/downloads/publications/public_pub/002725.pdf

Masks and respirators

www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/SevereAcute

RespiratorySyndrome/Guidelines/sars040Facemasksand respiratorsFAQ/

Pandemic inﬂ uenza/avian ﬂ u

b Inﬂ uenza pandemic, avian ﬂ u, and swine ﬂ u, p.252.

SARS

b SARS, p.251.

34 CHAPTER 1 General approach

What to carry in your car

If you are interested in out of hospital work, join the British Association for

Immediate Care (BASICS: www.basics.org.uk ), which is a valuable source

of information and expertise. It can give advice on clothing, medical and

protective equipment and their suppliers, and Immediate Care courses.

The equipment that could be carried is extensive. In the UK, except in

the most remote situations, it is likely that an ambulance will be on scene

quickly. Emergency ambulances carry many items of equipment, eg for

intubation, volume infusion and splintage, and also some drugs. There is a

risk of carrying too much equipment in your car and getting diverted from

the primary aims of pre-hospital care, which are to perform only relevant

life-saving techniques, and to transfer the patient rapidly and safely to the

nearest appropriate hospital.

The equipment listed below is a personal choice based on experience

attending out-of-hospital calls over the past 20 years:

Personal equipment

• High quality wind/waterproof reﬂ ective jacket and over-trousers. If your

ﬁ nances do not run to this, at least have a reﬂ ective ‘Doctor’ tabard.

• Protective helmet.

• Protective footwear — leather boots with steel toecaps are ideal.

• 2 pairs of latex gloves.

• 1 pair of protective gloves (eg leather gardening gloves).

General equipment

• Reﬂ ective warning triangle.

• Fire extinguisher.

• Heavy-duty waterproof torch.

• Clothes-cutting scissors.

• Mobile phone.

WHAT TO CARRY IN YOUR CAR

Medical equipment

The equipment listed is only of value if you know how to use it, it is secure

(ie locked in a case in a locked vehicle), and it is in date:

• Stethoscope.

• Hand-held suction device + Yankauer and soft ﬂ exible suckers.

• Laryngoscope, adult curved blade, spare batteries, and bulb.

• Selection of tracheal tubes of varying sizes + syringe to inﬂ ate cuff.

• Magill’s forceps.

• Selection of oropharyngeal and nasopharyngeal airways.

• Laerdal pocket mask.

• Venous tourniquet.

• Selection of IV cannulae (2 each of 14G and 16G) and syringes.

• 2 × IV-giving sets.

• 2 × 1000mL 0.9 % saline bags.

• 1 roll of 1-inch zinc oxide tape.

• 1 roll of 3-inch Elastoplast.

• Small selection of dressings and bandages.

• Cervical collar.

• Cricothyrotomy kit.

• Intercostal chest drain set.

• 2 × 0/0 silk suture on a hand-held cutting needle.

• Local anaesthetic, eg lidocaine 1 % (for nerve blocks).

• Splints for IV cannulation sites.

36 CHAPTER 1 General approach

At the roadside

Priorities

It is easy in an emergency to forget the simplest, most life-saving

procedures. At worst, an individual trying to help can aggravate the

situation, slow the process of care, and even become a casualty

themselves.

If you arrive ﬁ rst at the scene of a collision, the initial priority is to ensure your

own safety and that of other rescuers.

• Park safely so your car will not obstruct other vehicles (including

emergency vehicles), preferably where its presence will alert other road

users to the collision. Put your hazard warning lights on. If you have a

warning beacon, put it on the roof of the car and switch it on.

• If you have a mobile phone, dial ‘999’ and request ambulance, ﬁ re, and

police to attend. Remember to give the exact location, a brief description

of the incident, and number of casualties. Tell the emergency service

operator who you are, as well as the number of your mobile phone.

• Switch off the engine of your car and of any other vehicles.

• Ensure that no-one is smoking or displays a naked ﬂ ame.

• Events involving electricity or chemicals have speciﬁ c hazards.

Involvement of overhead or underground electric cables poses risks,

compounded if water is involved or sparks produced. The risk from high

tension cables extends for several metres. Phone the power company

to ensure that the source is turned off before approaching. Electriﬁ ed

rail lines may be short-circuited by a trained individual using a special

bar carried in the guard’s compartment.

Chemical incidents

Do not approach a chemical incident until declared safe by the Fire

Service. Lorries carrying hazardous chemicals must display a ‘Hazchem’

board (see Fig. 1.2 ). This has:

• Information on whether the area should be evacuated, what protective

equipment should be worn, aspects relating to ﬁ re-ﬁ ghting, and if the

chemical can be safely washed down storm drains (top left). A white

plate means that the load is non-toxic.

• A 4-digit UN product identiﬁ cation number (middle left).

• A pictorial hazard diamond warning (top right).

• An emergency contact number (bottom).

The European ‘Kemler’ plate contains only the UN product number

(bottom) and a numerical hazard code (top) — a repeated number means

intensiﬁ ed hazard. Mixed loads <500kg may only be identiﬁ ed by a plain

orange square at the front and rear of the vehicle.

The transport emergency card (TREM card) carried in the driver’s cab

gives information about the chemical for use at the scene of a crash. The

ﬁ re tender may be equipped with CHEMDATA — a direct link with the

National Chemical Information Centre at Harwell. Alternatively, contact

a Poisons Information Centre or the transport company.

Helicopters

If helicopters are used for transport/evacuation, remember:

• Communications in or near helicopters are difﬁ cult because of the noise.

• Ensure any loose objects are secured to prevent them being blown away.

AT THE ROADSIDE

• Never enter the landing space area during landing or take-off.

• Never enter or leave the rotor disc area without the pilot’s permission.

• Duck down in the rotor disc area and only approach in full view of the pilot.

• If the helicopter cannot land and the winch is used, do not touch the cable

before it has touched the ground to earth any static electrical charge.

Hazchem advice for the control of the chemical

Specialist advice

and telephone number

Suppliers name

(optional)

0705 826435

Danger labels

Specialist advice

Bromoacetyl bromide

Corrosive

2513

4WE

Pace

transport

Hazard symbol and

description in a

diamond on white

square background

(rest of label is black

lettering on an

orange backround)

Substance

identification

number and

name

Multiload

Marine pollutant

Other dangerous

substance

Green

Compressed

gas

Red/white

stripes

4.1

Red

Yellow

Organic

peroxide

5.2

6.1

stow a way

from

foodstuffs

Harmful

White White

Toxic

6.1

Corrosive

Black

Yellow

5.1

BlueWhite

White Red

Compressed

gas

Red

Flammable

liquid

Poision

gas

Flammable

gas

Oxidising agent

4.1

Spont aneously

combustible

Flammable

solid

Fig. 1.2 Hazchem advice and danger labels.

38 CHAPTER 1 General approach

Major incidents

A major incident involves a lot of people. The casualties may have multiple

injuries, minor injuries/burns, or other emergencies such as food poisoning

or chemical inhalation. Every hospital accepting emergencies has a Major

Incident plan to use when the normal resources are unable to cope and

special arrangements are needed. There will be action cards for key staff

detailing their duties. All staff need to familiarize themselves with their

roles in advance.

Call-in lists must be up to date and available at all times.

Major incident practices must be held regularly to check arrangements and

contact details and to remind staff what they should do.

Alert

The ambulance service or the police should warn the hospital of a possible

or deﬁ nite major incident. Initial messages are often inaccurate because

they are based on confused and incomplete information from the scene.

Occasionally, patients arrive without warning from a major incident near

the hospital.

Ensure that the ED consultant on duty is informed immediately of any

suspected major incident, enabling them to participate in the decision

to start the major incident procedure. Senior medical, nursing, and

administrative staff will set up the hospital’s Control Centre and prepare

for action. If the major incident is conﬁ rmed, the full hospital response is

initiated, following the procedures in the plan.

Communications are vital, but switchboards rapidly become overloaded.

Staff should therefore be called in using non-switchboard phones if

possible. All staff should wear their identiﬁ cation badges.

Action in the ED

• Check that the ED consultant and hospital switchboard know about the

incident and that the major incident procedure has been started.

• Inform all ED staff on duty (doctors, nurses, receptionists, porters).

• Call in other ED staff in accordance with the Major Incident plan.

• Clear the ED of any patients who are not seriously ill or injured. Prepare

the department to receive patients from the incident.

• Doctors and nurses arriving to help should be given appropriate action

cards. Staff should have labels or tabards so that ED staff and other

specialties (eg anaesthetists) can be identiﬁ ed easily.

• Prepare a triage point at the ambulance entrance. This should be

staffed by a senior doctor and nurse who direct patients to the most

appropriate area of the department. If possible, a nurse should stay with

each patient until he/she is discharged or admitted to a ward.

• All patients should be labelled immediately with a unique Major Incident

number, which is used on all notes, forms, blood samples, property

bags, and lists of patients. Collect names, addresses, and other details as

soon as possible, but this must not delay triage or emergency treatment.

Keep lists of anyone leaving the ED.

• Ensure that the hospital Control Centre is regularly updated regarding

the situation in the ED.

MAJOR INCIDENTS

Wards and theatres

Beds must be cleared to receive patients, preferably on 1 or 2 wards,

rather than many different wards. A senior surgeon should triage patients

needing operations and co-ordinate theatre work.

Relatives and friends

Relatives and friends of casualties should be looked after by social workers

and chaplaincy staff in an area near to, but separate from, the ED, perhaps

in the outpatient department. Keep relatives informed as soon and as

much as possible. Security staff at each entrance to the ED should direct

relatives and friends of casualties to the appropriate area and not allow

them into the ED.

Press

Journalists and television crews will arrive rapidly after a major incident.

Keep them out of the ED — direct them to a pre-arranged room to be

briefed by a press ofﬁ cer and senior staff.

Arrangements at the site of a major incident

The police are in overall command. The ﬁ re service take control of the

immediate area if there is a ﬁ re or chemical risk. The police, ﬁ re, and

ambulance services will each have a control vehicle, with an Incident

Ofﬁ cer to co-ordinate their staff and the rescue work.

There may be a Medical Incident Ofﬁ cer (MIO) and also a Mobile Medical

Team of doctors and nurses, who should if possible be sent from a

supporting hospital, rather than the hospital receiving the ﬁ rst casualties.

These staff must be properly clothed (yellow and green high-visibility

jacket marked ‘Doctor’ or ‘Nurse’, over trousers, green helmet with visor

and chin strap, safety boots, gloves, knee pads, torch, ID badge), and must

be trained and equipped with suitable medical supplies and action cards.

The mobile medical team must report to the MIO, who is in charge of all

medical and nursing staff on site and works closely with the Ambulance

Incident Ofﬁ cer (AIO). The MIO should record the names of the mobile

medical team and brief them about their duties and the site hazards and

safety arrangements. The MIO is responsible for supervising the team,

arranging any necessary equipment and supplies, and making sure that the

team are relieved when necessary. The MIO and AIO relay information to

the hospitals and distribute casualties appropriately.

Debrieﬁ ng staff

Debrieﬁ ng is important after a major incident, so that staff can discuss

what happened and express their feelings. Mutual support of the team

is essential. Counselling may be required. Senior staff should prepare a

report on the incident and review the major incident plan.

Further information

NHS Emergency Planning guidance

www.dh.gov.uk/en/Managingyourorganisation/Emergencyplanning/index.htm

CBRN (Chemical, Biological, Radiological and Nuclear) incidents

b Decontamination of patients, p.211.

This page intentionally left blank

Anaphylaxis 42

Treatment algorithm for adults with anaphylaxis 44

Choking 45

Cardiac arrest 46

In-hospital resuscitation algorithm 47

Adult basic life support 48

Cardiac arrest management 50

Advanced life support algorithm 52

Notes on using the advanced life support algorithm 53

Post-resuscitation care 54

Central venous access 56

Severe sepsis and septic shock 59

Shock 60

Life-threatening

emergencies

Chapter 2

Life-threatening emergencies in children are considered in

Chapter 15, Paediatric emergencies

631

b Paediatric basic life support 646

b Choking from a foreign body 648

b Anaphylaxis in children 650

b Paediatric advanced life support 652

42 CHAPTER 2 Life-threatening emergencies

Anaphylaxis

( Anaphylaxis in children is covered in b p.650)

Anaphylaxis is a generalized immunological condition of sudden onset,

which develops after exposure to a foreign substance. The mechanism may:

• Involve an IgE-mediated reaction to a foreign protein (stings, foods,

streptokinase), or to a protein–hapten conjugate (antibiotics) to which

the patient has previously been exposed.

• Be complement mediated (human proteins eg G -globulin, blood

products).

• Be unknown (aspirin, ‘idiopathic’).

Irrespective of the mechanism, mast cells and basophils release mediators

(eg histamine, prostaglandins, thromboxanes, platelet activating factors,

leukotrienes) producing clinical manifestations. Angio-oedema caused by

ACE inhibitors and hereditary angio-oedema may present in a similar way

to anaphylaxis. Hereditary angio-oedema is not usually accompanied by

urticaria and is treated with C1 esterase inhibitor.

Common causes

• Drugs and vaccines (eg antibiotics, streptokinase, suxamethonium,

aspirin, non-steroidal anti-inﬂ ammatory drugs (NSAIDs), intravenous

(IV) contrast agents).

• Hymenoptera (bee/wasp) stings.

• Foods (nuts, shellﬁ sh, strawberries, wheat).

• Latex.

Clinical features

The speed of onset and severity vary with the nature and amount of the

stimulus, but the onset is usually in minutes/hours. A prodromal aura or a

feeling of impending death may be present. Patients on B -blockers or with

a history of ischaemic heart disease (IHD) or asthma may have especially

severe features. Usually two or more systems are involved:

Respiratory Swelling of lips, tongue, pharynx, and epiglottis may lead to

complete upper airway occlusion. Lower airway involvement is similar to

acute severe asthma — dyspnoea, wheeze, chest tightness, hypoxia, and

hypercapnia.

Skin Pruritus, erythema, urticarial, and angio-oedema.

Cardiovascular Peripheral vasodilation and i vascular permeability cause

plasma leakage from the circulation, with d intravascular volume, hypoten-

sion, and shock. Arrhythmias, ischaemic chest pain, and electrocardiogram

(ECG) changes may be present.

GI tract Nausea, vomiting, diarrhoea, abdominal cramps.

ANAPHYLAXIS

Treatment

• Discontinue further administration of suspected factor (eg drug).

Remove stings by scraping them carefully away from skin.

• Give 100 % oxygen (O

• Open and maintain airway. If upper airway oedema is present, get

specialist senior help immediately. Emergency intubation or a surgical

airway and ventilation may be required.

• In patients with shock, airway swelling, or respiratory difﬁ culty give 0.5mg

(0.5mL of 1:1000 solution) adrenaline intramuscular (IM). Repeat after

5min if there is no improvement. In adults treated with an adrenaline auto-

injector (eg EpiPen

) the 300mcg dose is usually sufﬁ cient, but additional

doses may be required. Give only 50 % of the usual dose of adrenaline to

patients taking tricyclic antidepressants, MAOIs, or B –blockers.

• In profound shock or immediately life-threatening situations, give CPR/

ALS as necessary, and consider slow IV adrenaline 1:10,000 or 1:100,000

solution. This is recommended only for experienced clinicians who can

also obtain immediate IV access. Note the different strength of adrenaline

required for IV use. If there is no response to adrenaline, consider glucagon

1–2mg IM/IV every 5min (especially in patients taking B -blockers).

• Give a B

-agonist (eg salbutamol 5mg) nebulized with O

for

bronchospasm, possibly with the addition of nebulized ipratropium

bromide 500mcg.

• Give IV ﬂ uid if hypotension does not rapidly respond to adrenaline.

Rapid infusion of 1–2L IV 0.9 % saline may be required, with further

infusion according to the clinical state.

• Antihistamine H

blockers (eg chlorphenamine 10–20mg slow IV) and

blockers (eg ranitidine 50mg IV) are commonly given. They are

second line drugs that, with hydrocortisone 100–200mg slow IV, may

reduce the severity/duration of symptoms.

• Admit/observe after initial treatment: prolonged reactions and biphasic

responses may occur. Observe for at least 4–6hr after all symptoms

have settled.

Report anaphylactic reactions related to drugs/vaccines to the Committee

on Safety of Medicines. Further investigation of the cause (and possibly

desensitization) may be indicated. Where identiﬁ ed, the patient and

GP must be informed and the hospital records appropriately labelled.

Medic-Alert bracelets are useful.

Notes on treatment algorithm on b p.44

1 An inhaled B

-agonist such as salbutamol may be used as an adjunctive

measure if bronchospasm is severe and does not respond rapidly to

other treatment.

2 If profound shock judged immediately life-threatening give CPR/ALS if

necessary. Consider slow IV adrenaline (epinephrine) 1:10,000 solution.

This is hazardous and is recommended only for an experienced practitioner

who can also obtain IV access without delay. Note the different strength of

adrenaline (epinephrine) that may be required for IV use.

3 If adults are treated with an EpiPen

the 300mcg will usually be sufﬁ cient.

A second dose may be required. Half doses of adrenaline (epinephrine)

may be safer for patients on amitriptyline, imipramine, or B -blocker.

4 A crystalloid may be safer than a colloid.

44 CHAPTER 2 Life-threatening emergencies

Treatment algorithm for adults with

anaphylaxis

1 Resuscitation Council (UK) guidelines , 2008 . See: www.resus.org.uk

Fig. 2.1 Anaphylaxis algorithm.

When skills and equipment available:

• Establish airway

• High flow oxygen

• IV fluid challenge

• Chlorphenamine

• Hydrocortisone

Monitor:

• Pulse oximetry

• ECG

• Blood pressure

1 Life-threatening problems:

Airway: Swelling, hoarseness, stridor

Breathing: Rapid breathing, wheeze, fatigue, cyanosis, SpO

< 92%, confusion

Circulation: Pale, clammy, low blood pressure, faintness, drowsy/coma

3 IV fluid challenge:

Adult - 500–1000 mL

Child - crystalloid 20 mL/kg

Stop IV colloid

if this might be the cause

of anaphylaxis

4 Chlorphenamine 5 Hydrocortisone

200 mg

100 mg

50 mg

10 mg

5 mg

2.5 mg

Child less than 6 months

250 micrograms/kg 25 mg

2 Adrenaline (give IM unless experienced with IV adrenaline)

IM doses of 1:1000 adrenaline (repeat after 5 min if no better)

• Adult: 500 micrograms IM (0.5 mL)

• Child more than 12 years: 500 micrograms IM (0.5 mL)

• Child 6–12 years: 300 micrograms IM (0.3 mL)

• Child less than 6 years: 150 micrograms IM (0.15 mL)

Adrenaline IV to be given only by experienced specialists

Titrate: Adults 50 micrograms; Children 1 microgram/kg

Adrenaline

Call for help

• Lie patient flat

• Raise patient’s legs

Diagnosis - look for:

• Acute onset of illness

• Life-threatening airway and/or breathing

and/or circulation problems

• And usually skin changes

Airway, Breathing, Circulation, Disability, Exposure

Anaphylactic reaction?

See also: Anaphylactic reactions – Initial treatment

Adult or child more than 12 years

Child 6–12 years

Child 6 months to 6 years

(IM or slow IV) (IM or slow IV)

CHOKING

Choking

The management of choking is rightly taught as part of ﬁ rst aid. Recognition

of the problem is the key to success. Clues include a person experiencing

a sudden airway problem whilst eating, possibly combined with them

clutching their neck.

Severity of airway obstruction

Victims with severe airway obstruction may be unable to speak or breathe

and become unconscious (see Fig. 2.2 ).

1 Resuscitation Council (UK) guidelines, 2010 ( www.resus.org.uk )

Fig. 2.2 Adult choking algorithm.

Unconscious

Start CPR

Conscious

5 back blows

5 abdominal

thrusts

Encourage cough

Continue to check for

deterioration to ineffective

cough or until obstruction

relieved

Assess severity

Mild

Airway obstruction

(effective cough)

Severe

Airway obstruction

(ineffective cough)

46 CHAPTER 2 Life-threatening emergencies

Cardiac arrest

Clinical features and recognition

Follow resuscitation algorithm ( www.resus.org.uk ) shown opposite.

Cardiac arrest is a clinical diagnosis:

• Suspect cardiac arrest in any patient who is unconscious and who

does not have signs of life. If you check a pulse, examine only for a

major (carotid or femoral) one and take no longer than 10sec. Other

‘conﬁ rmatory’ clinical features (eg colour, pupil size/response) waste

time and do not help. Note that some respiratory efforts, such as

gasping, may persist for several minutes after the onset of cardiac arrest.

Occasionally, an arrest may present as a grand mal ﬁ t of short duration.

• Most patients have had a sudden and unexpected out-of-hospital event.

Prior warning to the department is usually relayed by radio or direct

telephone link from the Ambulance Service. While resuscitation is

continued, ensure that accompanying relatives/friends are met and taken

to an appropriate room, which has a telephone, facilities for making tea

and coffee, and where privacy is possible. Arrange for a member of staff to

stay with the relatives to act as a link with the Resuscitation Team.

Information to obtain from ambulance crew/relatives

• Patient details : including age, past medical history, current medication,

chest pain before event

• Times of : collapse (often an approximation), 999 (or 112) call, arrival on

scene, start of cardiopulmonary resuscitation (CPR), ﬁ rst deﬁ brillating

shock (if appropriate), other interventions (eg advanced airway

management, drugs), restoration of spontaneous circulation (ROSC)

• Was there any bystander CPR ?

Where a patient in cardiac arrest is brought to hospital by ambulance, the

cardiac arrest team (ED staff, the hospital team, or a combination of both)

should already be present in the resuscitation room with all equipment

ready to receive the patient.

The team leader

The team leader controls, co-ordinates, organizes the team and makes

treatment decisions. 4–6 team members are optimal. Each should know

their role. Perform resuscitation in a calm, quiet, conﬁ dent manner with

minimal interruption to the performance of basic life support (BLS) or

deﬁ brillation.

Start the following procedures simultaneously:

• Continue BLS.

• Remove/cut clothing from the upper body to allow deﬁ brillation,

ECG monitoring, chest compression, and IV access.

• Obtain the ECG trace (through deﬁ brillator pads or monitor leads).

If already attached to an ECG monitor, note (print out if possible) the

rhythm. Beware movement artefact, disconnected leads, electrical

interference, etc.

• Follow the ALS algorithm ( b p.52).

• Do not interrupt CPR except to perform deﬁ brillation.

IN-HOSPITAL RESUSCITATION ALGORITHM

In-hospital resuscitation algorithm

1 Resuscitation Council (UK) guidelines , 2010 ( www.resus.org.uk ).

Fig. 2.3

Advanced life support

when resuscitation team arrives

Shout for HELP and assess patient

Collapsed/sick patient

Handover

to resuscitation team

Signs

of life?

YES

Call resuscitation team

CPR 30:2

with oxygen and airway adjuncts

Apply pads/monitor

Attempt defibrillation

if appropriate

Assess ABCDE

Recognise and treat

Oxygen, monitoring,

IV access

Call resuscitation team

if appropriate

48 CHAPTER 2 Life-threatening emergencies

Adult basic life support

Airway and ventilation

Usually in the ED, advanced airway techniques will be used from the

outset. If basic techniques are used (Fig. 2.4 ):

• With the patient on his/her back, open the airway by tilting the head

and lifting the chin. (Use jaw thrust instead if neck trauma suspected.)

• Remove any visible obstructions from the mouth, but leave well-ﬁ tting

dentures in place.

• Aim for each breath to last 8 1sec and make the chest rise. After each

breath, maintain the head tilt/chin lift, take your mouth away from the

patient’s and watch for the chest to fall as the air comes out.

1 Colquhoun MC et al . (1999). ABC of Resuscitation , 4th edition. BMJ Books, London.

Fig. 2.4 Mouth to mouth ventilation.

ADULT BASIC LIFE SUPPORT

Technique for chest compression (Fig. 2.5 )

• Place the heel of one hand over the middle of the lower half of the

patient’s sternum, with the other hand on top. Extend or interlock

the ﬁ ngers of both hands and lift them to avoid applying pressure to the

patient’s ribs.

• Positioned above the patient’s chest and with arms straight, press down

to depress the sternum 5–6cm.

• Release all the pressure and repeat at a rate of 100–120/min.

• Compression and release phases should take the same time.

• Use a ratio of 30 chest compressions to 2 ventilations (30:2).

• Aim to change the person providing chest compressions every 2 min,

but ensure that this is achieved without causing signiﬁ cant pauses.

1 Colquhoun MC et al . (1999). ABC of Resuscitation , 4th edition. BMJ Books, London.

Fig. 2.5 Chest compressions.

50 CHAPTER 2 Life-threatening emergencies

Cardiac arrest management

Deﬁ brillation

• Most survivors have an initial rhythm of VF/VT. The treatment for this

is deﬁ brillation. With time, the chances of successful deﬁ brillation and

survival d dramatically. Adhesive deﬁ brillator pads have replaced manual

paddles in most hospitals. Place one pad to the right of the upper

sternum below the clavicle, the other in mid-axillary line level with V

ECG electrode position. Avoid placement over the female breast. To

avoid problems with pacemakers, keep pads > 15cm away from them.

• With biphasic deﬁ brillators, use shock energy of 150J, for (mostly older)

monophasic deﬁ brillators, select 360J energy.

• Plan for chest compressions to be as continuous as possible, with

minimal delays. Having paused brieﬂ y to assess the rhythm, recommence

compressions until the deﬁ brillator is charged. Pause brieﬂ y to deliver

a shock (removing O

sources and transdermal glycerol trinitrate

(GTN) patches), then immediately restart CPR with 30:2 compressions:

ventilation, and continue for 2min before reassessing the rhythm or

feeling for a pulse.

• In monitored patients with pulseless ventricular tachycardia/ﬁ brillation

(VT/VF) where deﬁ brillation is not immediately available, give a single

precordial thump . With a tightly clenched ﬁ st, deliver one direct blow

from a height of 820cm to the lower half of the sternum.

Airway management

Techniques for securing the airway, providing oxygenation and ventilation

are covered in b Airway obstruction: basic measures, p.324. Although

tracheal intubation has long been considered to be the gold standard

deﬁ nitive airway, only attempt this if suitably experienced. Laryngeal

mask airway is a readily available, rapid alternative, which is easy to insert.

Whatever method is used, aim to ventilate (preferably with 100 % O

) using

an inspiratory time of 1sec, a volume sufﬁ cient to produce a normal rise of the

chest, at a rate of 10/min. For patients with tracheal tubes or laryngeal mask

airways, ventilate without interrupting chest compressions, which should be

continuous (except for deﬁ brillation or pulse checks as appropriate).

End-tidal CO

monitoring is very useful to conﬁ rm correct tracheal tube

placement and indirectly measure cardiac output during CPR.

Drugs

There is little evidence that any drug improves outcome. Central venous

cannulation is difﬁ cult, has risks and interrupts CPR. Peripheral access

is easy and quick. Having given a peripheral IV drug, give a 20mL saline

bolus and elevate the limb for 10–20sec. If IV access is impossible, consider

intraosseous route ( b p.640). It is no longer recommended for any

drugs to be given by tracheal tube. Similarly, do not attempt intracardiac

injections.

The ﬁ rst drug used in cardiac arrest (after oxygen) is adrenaline. In

the case of VF/VT, administer adrenaline after three shocks, whereas

in asystole/PEA, give it as soon as possible (see b Adult life support

algorithm, p.52).

CARDIAC ARREST MANAGEMENT

Non-shockable rhythms: PEA and asystole

Pulseless electrical activity ( PEA ) is the clinical situation of cardiac arrest with

an ECG trace compatible with cardiac output. PEA may be caused by:

• Failure of the normal cardiac pumping mechanism (eg massive MI,

drugs such as B -blockers, Ca

2 +

antagonists or electrolyte disturbance,

eg hypokalaemia, hyperkalaemia).

• Obstruction to cardiac ﬁ lling or output (eg tension pneumothorax,

pericardial tamponade, myocardial rupture, pulmonary embolism (PE),

prosthetic heart valve occlusion, and hypovolaemia).

Prompt and appropriate correction of these can result in survival. Remember

potentially reversible causes as the 4H’s and 4T’s (see Table 2.1 ).

Asystole is the absence of cardiac (particularly ventricular) electrical activity.

If unsure if the rhythm is asystole or ﬁ ne VF, continue chest compressions

and ventilation in an attempt to increase the amplitude and frequency of

VF, and make it more susceptible to deﬁ brillation.

Length of resuscitation

The duration of the resuscitation attempt depends upon the nature of

the event, the time since the onset, and the estimated prospects for a

successful outcome. In general, continue resuscitation while VF/pulseless

VT persists, always provided that it was initially appropriate to commence

resuscitation. If VF persists despite repeated deﬁ brillation, try changing

pad position or deﬁ brillator.

Asystole unresponsive to treatment and arrests which last > 1hr are rarely

associated with survival. However, exceptions occur — particularly in

younger patients, hypothermia, near drowning, and drug overdose.

Mechanical CPR

There are several devices available that can provide mechanical CPR.

These include the ‘AutoPulse’ circumferential load-distributing band chest

compression device (comprising a pneumatically actuated constricting band

and backboard) and the ‘LUCAS’ gas-driven sternal compression device (with

accompanying suction cup to provide active decompression). Widespread

use of these devices may develop if early encouraging results are conﬁ rmed

by larger studies. Mechanical CPR is potentially very useful in situations where

the resuscitation attempt is prolonged (eg cardiac arrest associated with

hypothermia, poisoning or following ﬁ brinolytic treatment for PE), ensuring

consistent CPR over a long period of time and freeing up an additional

member of the team.

Table 2.1

4H’s 4T’s

Hypoxia Tension pneumothorax

Hypovolaemia Tamponade (cardiac)

Hyper/hypokalaemia/metabolic

disorders

Toxic substances (eg overdose)

Hypothermia Thromboembolic/mechanical obstruction

52 CHAPTER 2 Life-threatening emergencies

Advanced life support algorithm

1 Resuscitation Council (UK) guidelines , 2010 ( www.resus.org.uk ).

Fig. 2.6

CPR 30:2

Attach defibrillator/monitor

Minimise interruptions

Shockable

(VF/Pulseless VT)

1 Shock

During CPR

• Ensure high-quality CPR: rate, depth, recoil

• Plan actions before interrupting CPR

• Give oxygen

• Consider advanced airway and capnography

• Continuous chest compressions when advanced

airway in place

• Vascular access (intravenous, intraosseous)

• Give adrenaline every 3–5 min

• Correct reversible causes

Reversible causes

• Hypoxia

• Hypovolaemia

• Hypo-/hyperkalaemia/metabolic

• Hypothermia

• Thrombosis - coronary or pulmonary

• Tamponade - cardiac

• Toxins

• Tension pneumothorax

Non-Shockable

(PEA/Asystole)

Call

resuscitation team

Unresponsive?

Not breathing or

only occasional gasps

Return of

spontaneous

circulation

Immediately resume

CPR for 2 min

Minimise interruptions

Immediately resume

CPR for 2 min

Minimise interruptions

Immediate post cardiac

arrest treatment

• Use ABCDE approach

• Controlled oxygenation and

ventilation

• 12-lead ECG

• Treat precipitating cause

• Temperature control/

therapeutic hypothermia

Assess

rhythm

NOTES ON USING THE ADVANCED LIFE SUPPORT ALGORITHM

Notes on using the advanced life

support algorithm

• Establish the underlying cardiac rhythm as quickly as possible in order to

determine which ‘loop’ to follow to provide appropriate treatment —

for VF/pulseless VT, the initial focus is deﬁ brillation and good CPR; for

asystole/PEA, the initial focus is good CPR, IV adrenaline, and searching

for potentially reversible causes.

• Do not interrupt CPR except to perform deﬁ brillation.

• Search for and correct potentially reversible causes of the arrest.

• Give IV adrenaline 1mg and amiodarone 300mg for VF/pulseless VT

refractory to three shocks, followed by 1mg adrenaline every 3–5min.

A further dose of 150mg IV amiodarone may be given for recurrent or

refractory VF/VT. Lidocaine (1mg/kg) IV is an alternative to amiodarone,

but do not give it if amiodarone has already been given.

• For torsade de pointes, and refractory VF in patients with suspected

digoxin toxicity or hypomagnesaemia (eg on K

losing diuretics), give IV

magnesium sulphate 2g (= 8mmol = 4mL of 50 % solution).

• In asystole and PEA, give IV 1mg adrenaline as soon as possible and

thereafter every 3–5min.

• Exercise caution before using adrenaline in arrests associated with

cocaine or other sympathomimetic drugs.

• Atropine is no longer routinely recommended in asystole or slow PEA.

• In PEA arrests associated with hyperkalaemia, hypocalcaemia, or Ca

2 +

channel blocking drug or magnesium overdose, give 10mL 10 % IV

calcium chloride (6.8mmol).

• With good quality CPR, acidosis develops slowly. Do not ‘routinely’ give

an alkali. Give 50mL of sodium bicarbonate 8.4 % solution (50mmol) if

arrest is associated with tricyclic overdose ( b p.194) or hyperkalaemia

and consider it in patients with severe acidosis (arterial pH<7.1, base

excess less than –10). Allow further administration to be guided by

repeated arterial blood gas (ABG) results.

• Follow loops of the algorithm for as long as it is considered appropriate

for the resuscitation to continue. Provided that the attempt was

commenced appropriately, it should not normally be stopped if the

rhythm is still VF.

Pacing and external cardiac percussion

Pacing may be of value in patients with extreme bradyarrhythmias, but its

value in asystole is unproven (except for rare cases of trifascicular block

with P waves present). If there is a delay before pacing can be performed,

external cardiac percussion can provide a cardiac output and ‘buy time’.

Perform external cardiac percussion using a clenched ﬁ st:

• Over the heart at a rate of 100/min.

• With a blow more gentle than a precordial thump.

• Each blow should generate a QRS complex. If this, and a detectable

output, is not achieved restart conventional CPR.

54 CHAPTER 2 Life-threatening emergencies

Post-resuscitation care

Features such as coma or pupil reﬂ exes are unreliable prognostic

indicators in the early post-resuscitation phase. Accurate prognostication

in an individual patient is rarely possible before 24–72hr. Involve the

intensive care unit/critical care unit (ICU/CCU) team early.

Pending this and following ROSC

• Ensure that the airway is protected ( b p.324).

• Maintain oxygenation and ventilation. Correct hypoxia and prevent

hypercapnoea under ABG guidance (may require IPPV). Use pulse

oximetry to monitor SpO

non-invasively, titrating inspired oxygen

concentration to achieve SpO

of 94–98 % .

• In intubated patients, insert an oro- or nasogastric tube to decompress

the stomach.

• Obtain a 12-lead ECG and a CXR (check position of tracheal tube,

central lines and presence of pneumothorax etc.).

• Optimize cardiac output: inotropes, vasodilators, ﬂ uids and/or diuretics

may be needed under haemodynamic monitoring guidance. If the arrest

is associated with an acute coronary syndrome, consider immediate

thrombolysis and/or coronary revascularization.

• Cerebral blood ﬂ ow autoregulation is deﬁ cient post-arrest. Maintaining

arterial pressures ‘normal’ for the patient may prevent hypotensive

hypoperfusion. i BP above the normal for the patient may worsen

cerebral oedema.

• Seizures aggravate brain injury by i ICP and cerebral metabolic

requirements. Treat with appropriate anticonvulsants (as b p.149) and

ensure adequate oxygenation and ventilation.

• Measure U&E, Ca

2 +

, Mg

2 +

, and correct abnormalities appropriately.

• Obtain full blood count (FBC) to exclude anaemia contributing to

myocardial ischaemia and to provide an admission baseline.

• Both hypo- and hyperglycaemia compromise neurological outcome.

Monitor plasma glucose concentration regularly and aim to avoid both

hypo- and hyperglycaemia (keep the level d 10mmol/L).

• No drug has been shown to improve cerebral outcome following

cardiac arrest. The routine use of steroids, mannitol, Ca

2 +

channel

blockers, etc., is unwarranted.

• When any drug is used, remember that pharmacokinetic proﬁ les

are often impaired post-resuscitation. Dose adjustment and careful

monitoring are needed.

• Avoid/treat hyperthermia with antipyretic or active cooling.

• There is compelling data to support the early induction of mild

therapeutic hypothermia (32–34 ° C) in patients who are comatose

following out of hospital VF arrest. Mild hypothermia is believed to be

neuroprotective in this situation (and pending more data, may be of

beneﬁ t in other situations as well, eg other arrest rhythms, in-hospital

arrests, paediatric patients). Cooling may be initiated by external

techniques (cooling blankets, water or air circulating blankets) or

internally by an infusion of 30mL/kg of 4 ° C 0.9 % saline — liaise with ICU.

Mild hypothermia is typically maintained for 12–24hr.

POST-RESUSCITATION CARE

Training

Theoretical knowledge is important, but many of the skills required during

the management of a cardiac arrest need expert teaching and supervised

practice. Attend an approved Resuscitation Council (UK) Advanced Life

Support course (see www.resus.org.uk ) — preferably before starting in

the ED.

56 CHAPTER 2 Life-threatening emergencies

Central venous access

Indications

Central venous access may be required for:

• Administration of emergency drugs.

• Central venous pressure measurement.

• Administration of IV ﬂ uids, especially when peripheral veins are

collapsed or thrombosed. Note : other routes (eg femoral vein) are

generally preferable for giving large volumes rapidly.

• Transvenous cardiac pacing.

Choice of vein

The external jugular vein is often readily visible and can be cannulated

easily with a standard IV cannula.

The internal jugular and subclavian veins are generally used for central

venous access in the ED. Subclavian vein cannulation has a relatively high

risk of pneumothorax, so the internal jugular vein is usually preferable, via

a ‘high’ approach. When possible, use ultrasound (USS) guidance and the

right side of the neck ( d risk of thoracic duct damage). If, however, a chest

drain is already in situ, use the same side for central venous cannulation.

The femoral vein is useful for temporary access in severe trauma, burns,

and in drug addicts with many thrombosed veins.

Seldinger technique for central venous access

The method of choice, because the relatively ﬁ ne needle d risk of

complications such as pneumothorax. The technique involves inserting

a hollow metal needle into the vein. A ﬂ exible guidewire is threaded

through the needle, which is then removed. A tapered dilator and plastic

cannula are inserted over the guidewire and advanced into the vein. The

guidewire and dilator are removed, and the cannula secured. Once the

cannula is in place, check that venous blood can be freely aspirated and

secure the cannula.

Precautions and problems

Central venous access is a specialized technique with potentially life-

threatening complications, including: pneumothorax, haemothorax, arterial

puncture, thoracic duct damage, air embolism, and infection.

• Expert supervision is essential. Cannulation is particularly difﬁ cult

and hazardous in hypovolaemic, shocked, or agitated patients. In such

situations, consider whether it is possible to defer the procedure.

• USS has become widely available and is increasingly used by suitably

trained ED specialists. It d complications and failure rates by clarifying

the relative positions of needle, vein, and surrounding structures.

Variant anatomy and vein patency can also be assessed by USS.

• Bleeding dyscrasias and anticoagulant treatment are contraindications

to internal jugular and subclavian vein access.

• Severe pulmonary disease is a relative contraindication to central venous

access, especially by the subclavian route, because a pneumothorax

would be particularly dangerous.

CENTRAL VENOUS ACCESS

Methods

Use aseptic technique. If possible, tilt the trolley 10 ° head down to ﬁ ll

the internal jugular and subclavian veins and d risk of air embolus. After

successful or attempted subclavian or internal jugular cannulation, take a

chest X-ray (CXR) to check for pneumothorax and the position of the

cannula.

External jugular vein

The vein can be seen and felt as it crosses superﬁ cially over the

sternomastoid muscle and runs obliquely towards the clavicle. Gentle

pressure on the lower end of the vein will distend it. A standard IV cannula

can easily be inserted into the external jugular vein, but passing a catheter

centrally may be difﬁ cult because of valves and the angle at which the vein

joins the subclavian vein.

Internal jugular vein

The internal jugular vein runs antero-laterally in the carotid sheath, parallel

to the carotid artery, and deep to the sternocleidomastoid muscle. The

high approach described has less risk of pneumothorax than lower

approaches (Fig. 2.7 ).

• Turn the patient’s head away from the side to be cannulated.

• Identify the carotid pulse at the level of the thyroid cartilage.

• Insert the needle 0.5cm lateral to the artery, at the medial border of

sternomastoid muscle.

• Advance the needle at an angle of 45 ° parallel to the sagittal plane,

pointing towards the ipsilateral nipple. The vein should be entered at a

depth of 2–4cm and blood aspirated freely. If it is not, try again slightly

more laterally.

Subclavian vein (infraclavicular approach)

• Turn the patient’s head away from the side of cannulation.

• Identify the mid-clavicular point and the sternal notch.

• Insert the needle 1cm below the mid-clavicular point and advance it

horizontally below and behind the clavicle, aiming at a ﬁ nger in the

suprasternal notch. The vein is usually entered at a depth of 4–6cm

(Fig. 2.8 ).

Femoral vein

Insert the needle 81cm medial to the femoral artery and just below the

inguinal ligament, pointing slightly medially and with the needle at 20–30 °

to the skin.

58 CHAPTER 2 Life-threatening emergencies

1 Rosen M et al . Handbook of Percutaneous Central Venous Catheterization. W.B. Saunders,

London.

2 Cosgriff JH. An Atlas of Diagnostic and Therapeutic Procedures for Emergency Personnel .

J.B. Lippincott, Philadelphia.

Fig. 2.7 Internal jugular cannulation.

Carotid artery

Sternomastoid

muscle

Fig. 2.8 Subclavian vein cannulation.

Clavicle

First rib

Superior vena cava

Finger in

suprasternal

notch

Subclavian vein

SEVERE SEPSIS AND SEPTIC SHOCK

Severe sepsis and septic shock

Septic patients have a systemic inﬂ ammatory response syndrome (SIRS)

as a consequence of infection. Severe sepsis refers to septic patients with

evidence of organ hypoperfusion. Septic shock is present when septic

patients exhibit hypotension unresponsive to intravenous ﬂ uid resuscitation.

Systemic inﬂ ammatory response syndrome

This requires 2 or more of:

• Body temperature of > 38 ° C or <36 ° C

• Heart rate > 90/min

• Respiratory rate > 20 breaths/min or PaCO

< 4.3kPa

• WCC > 12 × 10

/L or <4 × 10

/L or > 10 % immature (band) forms

Management

Severely septic patients have SIRS with evidence of hypoperfusion (eg

systolic BP <90mmHg and/or lactate > 3mmol/L). Obtain senior/ICU help

early. Intensive therapy of severely septic patients focuses upon certain

therapeutic goals :

• CVP of 8–12mmHg.

• mean arterial pressure > 65mmHg.

• urine output > 0.5mL/kg/hr.

• central venous saturation > 65 % .

Adopt the following approach:

• Obtain senior/ICU assistance now.

• Assess and manage airway, breathing, circulation (ABC) — in particular,

provide high ﬂ ow oxygen, secure good IV access and give an initial IV

ﬂ uid bolus of 20mL/kg of 0.9 % saline. Some patients may require early

tracheal intubation and IPPV.

• Look for obvious sources of infection.

• Check BMG (and treat if hypoglycaemic).

• Take blood cultures before starting antibiotics (the choice of antibiotics

will depend upon the likely cause and is considered on b p.60).

• Patients who remain hypotensive and/or have a lactate > 3mmol/L

require central venous and arterial catheterization in an intensive care/

resuscitation setting, with IVI noradrenaline to maintain mean arterial

pressure > 65mmHg and IV 0.9 % saline 500mL boluses every 20mins

to achieve CVP 8–12mmHg (12–15mmHg in mechanically ventilated

patients).

60 CHAPTER 2 Life-threatening emergencies

Shock

Shock is a clinical condition characterized by failure to adequately perfuse

and oxygenate vital organs. Clinically, shock is recognized by:

• Hypotension Generally considered to be systolic BP <90mmHg (in

adults), but values may be higher in young, ﬁ t or previously hypertensive

patients. Associated tachycardia ( > 100/min) is common, but may not be

present in patients with cardiac or neurological causes or in those taking

B-blockers. A few patients with haemorrhagic shock have a paradoxical

bradycardia.

• Altered consciousness and/or fainting (especially on standing or sitting

up) may result from d cerebral perfusion.

• Poor peripheral perfusion Cool peripheries, clammy/sweaty skin, pallor,

d capillary return, but note that in the early phase of endotoxic septic

shock there may be vasodilatation with warm peripheries.

• Oliguria d renal perfusion with urine output <50mL/hr (in adults).

• Tachypnoea.

Classiﬁ cation of shock

Traditional classiﬁ cation of types of shock is artiﬁ cial — mixed aetiologies

are common.

Hypovolaemic shock

• Blood loss: trauma, gastrointestinal (GI) bleed (haematemesis, melaena),

ruptured abdominal aortic aneurysm, ruptured ectopic pregnancy.

• Fluid loss/redistribution (‘third spacing’) : burns, GI losses (vomiting,

diarrhoea), pancreatitis, sepsis.

Cardiogenic shock

• Primary : myocardial infarction (MI), arrhythmias, valve dysfunction,

myocarditis.

• Secondary : cardiac tamponade, massive pulmonary embolus, tension

pneumothorax.

Septic shock (see b p.59)

More common at the extremes of age, in patients with diabetes mellitus,

renal/hepatic failure and the immunocompromised (eg HIV infection,

underlying malignancy, post-splenectomy, steroid therapy). Note that

fever, rigors and i white cell count (WCC) may not be present.

• Organisms responsible include Gram + ve and –ve, especially Staph. aureus,

Strep . pneumoniae , N meningitidis , coliforms including enterococci and

Bacteroides (especially in patients with intra-abdominal emergencies,

such as ruptured diverticular abscess). In the immunocompromised,

Pseudomonas, viruses, and fungi may cause septic shock.

Anaphylactic shock: see b p.42.

Neurogenic shock: see b p.382.

Other causes

These include poisoning ( b p.183) and Addison’s disease ( b p.155).

SHOCK

Management of shock

Investigation and treatment should occur simultaneously. Get senior help

immediately.

• Address the priorities — ABC.

• Give high ﬂ ow O

by mask.

• Secure adequate venous access and take blood for FBC, U&E, glucose,

liver function tests (LFTs), lactate, coagulation screen, and if appropriate,

blood cultures.

• Monitor vital signs, including pulse, BP, SpO

, respiratory rate.

• Check ABG.

• Monitor ECG and obtain 12 lead ECG and CXR.

• Insert a urinary catheter and monitor urine output hourly.

• For shock associated with d effective circulating blood volume, give

IV crystalloid (0.9 % saline) 20mL/kg as bolus. Give further IV ﬂ uids

including colloid 9 blood (aim for haematocrit (Hct) > 30 % ) according

to aetiology and clinical response (and in particular, pulse, BP, central

venous pressure (CVP), and urine output). Use caution with IV ﬂ uid

infusion in shock related to cardiogenic causes, and in ruptured or

dissecting aortic aneurysm.

• Look for, and treat speciﬁ cally, the cause(s) of the shock. Echocardiography,

USS, CT, and/or surgical intervention may be required. Speciﬁ c treatments

include:

• Laparotomy : ruptured abdominal aortic aneurysm, splenic and/or

liver trauma, ruptured ectopic pregnancy, intra-abdominal sepsis.

• Thrombolysis/angioplasty : MI.

• Thrombolysis : PE.

• Pericardiocentesis/cardiac surgery : cardiac tamponade, aortic valve

dysfunction.

• Antidotes : for certain poisons.

• Antibiotics : sepsis. The choice of antibiotic will depend upon the

perceived cause and local policies (eg ceftriaxone for meningococcal

disease). Where there is no obvious source, empirical combination

therapy is advised (eg co-amoxiclav + gentamicin + metronidazole).

Obtain specialist microbiological advice early, especially in

neutropaenic/immunocompromised patients.

• Inotropic and vasoactive therapy, assisted ventilation, and invasive

monitoring (including arterial and CVP lines) are often needed as part

of goal directed therapy. Get specialist ICU help early.

Chapter 00

Electrocardiogram interpretation 64

Chest pain 66

Angina 67

Acute coronary syndromes 68

ST segment elevation MI 70

Myocardial infarction: electrocardiogram changes 72

STEMI: treatment 76

Pericarditis 78

Bradyarrhythmias 80

Treatment of bradyarrhythmias 82

Tachycardia algorithm–with pulse 84

Tachyarrhythmias 86

Broad complex tachyarrhythmias 87

Narrow complex tachyarrhythmias 88

Atrial ﬁ brillation 89

Hypertensive problems 90

Aortic dissection 92

Haemoptysis 94

Oxygen 95

The dyspnoeic patient 96

Hyperventilation 97

Arterial blood gases 98

Cardiogenic pulmonary oedema 100

Non-cardiogenic pulmonary oedema 102

Pleural effusion 103

Acute asthma: assessment 104

Acute asthma: management 106

COPD 108

Pneumonia 110

Pulmonary aspiration 112

Medicine

Chapter 3

Spontaneous pneumothorax 114

Deep venous thrombosis 118

Pulmonary embolism 120

Upper gastrointestinal bleeding 122

Lower gastrointestinal bleeding 124

Headache 126

Subarachnoid haemorrhage 128

Migraine 130

Other causes of headache 132

Acute confusional state (delirium) 134

Dementia 135

The unconscious patient 136

Collapse and syncope 140

Acute generalized weakness 142

Stroke 144

Transient ischaemic attacks 146

Seizures and status epilepticus 148

Hypoglycaemia 150

Hyperglycaemic crises 152

Sodium derangements 154

Addisonian crisis 155

Thyrotoxic crisis 156

Urinary tract infection 158

Chronic renal failure 160

Hyperkalaemia 162

Hypokalaemia 164

Porphyria 165

Bleeding disorders 166

Patients on anticoagulants 170

Blood transfusion 172

Sickle cell disease 176

Medicine

64 CHAPTER 3 Medicine

Electrocardiogram interpretation

The electrocardiogram (ECG) is normally recorded so that a deﬂ ection

of 10mm = 1mV. The recording rate is 25mm/sec, 1mm = 0.04sec, 1 large

square = 0.2sec. There is an ECG ruler on the inside back cover. Follow a

systematic approach.

Rate Calculate the rate by dividing 300 by the number of large squares in

one R–R interval.

Frontal plane axis Normally lies between –30 * and + 90 * (see Fig. 3.1 ).

With a normal axis, QRS complexes in I and II are both + ve. An axis

more –ve than –30 * (I + ve, aVF and II –ve) is left axis deviation (causes:

left anterior hemiblock, inferior myocardial infarction (MI), ventricular

tachycardia (VT), Wolf Parkinson White (WPW) syndrome). An axis more

+ ve than + 90 * (I –ve, aVF + ve) is right axis deviation (causes: pulmonary

embolism (PE), cor pulmonale, lateral MI, left posterior hemiblock).

P wave Normally <0.12sec wide and <2.5mm tall. They are best seen in

leads II and V

which are chosen for rhythm strips or monitoring. A tall

peaked P wave in II may reﬂ ect right atrial hypertrophy; a widened biﬁ d P

wave left atrial hypertrophy. P waves are absent in atrial ﬁ brillation (AF).

PR interval Normally 0.12–0.2sec (<5 small squares). A short PR interval

(abnormally fast conduction between atria and ventricles) implies an

accessory pathway (eg Wolf Parkinson White syndrome).

A prolonged PR interval occurs in heart block (ﬁ rst, second or third

degree, see b Bradyarrhythmias, p.80).

QRS width Normally 0.05–0.11sec (<3 small squares). Prolonged QRS

complexes may be due to: right bundle branch block (RBBB) (RsR' or

M shape in V

), left bundle branch block (LBBB) (QS or W shape

in V

with RsR' or M shape in V

), tricyclic antidepressant poisoning

( b p.194), hypothermia, ventricular rhythms, and ectopics.

Head

–90°

aVL–30°

aVR–150°

Left

Feet

Right

I 0°

II+60°

+120° III

±180°

aVF

+90°

Fig. 3.1 Diagram of the ECG frontal axis.

ELECTROCARDIOGRAM INTERPRETATION

QRS amplitude The QRS amplitude can indicate left ventricular

hypertrophy (LVH). Signs of LVH are: (S in V

+ R in V

) > 35mm; R in I >

15mm; R in aV

> 11mm.

Q waves May be normal in III, aV

, and V

, but are abnormal in other

leads if > 0.04sec or > ½ of the height of the subsequent R wave.

ST segment elevation is caused by: acute MI, pericarditis (concave up),

ventricular aneurysm, Prinzmetal’s angina, LVH, Brugada syndrome,

hypertrophic cardiomyopathy, benign early repolarization.

ST segment depression is caused by: ischaemia, digoxin, LVH with strain.

QT interval = start of Q wave to end of T wave.

= QT⁄√R–R (Bazett’s formula). Normal QT

is <440msec.

At rates of 60–100/min, QT should be <1/2 R–R interval.

prolonged QT

predisposes to ‘torsades de pointes’ ( b Broad

complex tachyarrhythmias, p.87) and is caused by acute MI, hypothermia,

hypocalcaemia, drugs (quinidine, tricyclic antidepressants), certain

congenital diseases (eg Romano–Ward syndrome).

T waves Abnormal if inverted in V

4–6

. Peaked T waves are seen in early

acute MI and hyperkalaemia ( b p.162). Flattened T waves (sometimes with

prominent U waves) occur in hypokalaemia.

1.0

0.5

QRS interval

Isoelectric line

PR segment

ST segment

0.04

0.0

P–R interval

0.2 0.4 0.6 0.8

Seconds

Voltage

(mV)

1 mm 10 mm

Q–T interval

Fig. 3.2

66 CHAPTER 3 Medicine

Chest pain

Always take chest pain seriously. It may reﬂ ect life-threatening illness.

Triage patients with chest pain as ‘urgent’ and ensure that they are seen

within a few minutes. Ischaemic heart disease is understandably the ﬁ rst

diagnosis to spring to mind in the middle-aged or elderly, but chest pain

may have a variety of other disease processes, many of which are also

potentially life-threatening (Table 3.1 ).

Reaching the correct conclusion requires accurate interpretation of the

history, examination and investigations, bearing in mind recognized patterns

of disease presentations.

History

Characterize the pain

• Site (eg central, bilateral or unilateral).

• Severity.

• Time of onset and duration.

• Character (eg ‘stabbing’, ‘tight/gripping’, or ‘dull/aching’).

• Radiation (eg to arms and neck in myocardial ischaemia).

• Precipitating and relieving factors (eg exercise/rest/GTN spray).

• Previous similar pains.

Enquire about associated symptoms Breathlessness, nausea, and vomiting,

sweating, cough, haemoptysis, palpitations, dizziness, loss of consciousness.

Document past history, drug history, and allergies. Old notes and old

ECGs are invaluable — request them at an early stage.

Quickly consider contacting cardiologists if acute coronary syndrome

(ACS) is likely ( b ST segment elevation MI: treatment, p.76).

Examination and resuscitation

Evaluate Airway, Breathing, Circulation (ABC) and resuscitate (O

, venous access,

IV analgesia) as appropriate. Listen to both lung ﬁ elds and check for tension pneu-

mothorax and severe left ventricular failure (LVF). Complete full examination.

Investigations

These depend upon the presentation and likely diagnosis, but an ECG and

CXR are usually required. Remember that these may initially be normal

in MI, PE and aortic dissection. Ensure that all patients receive ECG moni-

toring in an area where a deﬁ brillator is readily available.

Table 3.1 The differential diagnosis of chest pain

Common causes Less common causes

Musculoskeletal (eg costochondritis) Aortic dissection

Acute coronary syndrome

Cholecystitis

Pneumothorax

Herpes zoster

Oesophagitis Oesophageal rupture

Pneumonia Pancreatitis

Pulmonary embolism

Vertebral collapse

Obscure origin (eg precordial catch) Tabes dorsalis (very rare)

Potentially rapidly fatal.

ANGINA

Angina

Angina is deﬁ ned as discomfort in the chest, arm, neck, or adjacent areas

due to myocardial ischaemia. It can be brought on by exertion, cold weather

and emotion. It occurs when coronary artery blood ﬂ ow fails to meet the

demand of the myocardium (eg during exercise, coronary artery spasm

or anaemia). Ischaemia may produce ST depression or inversion, which

resolves on recovery.

First presentation of angina

Patients may come to the ED with angina as a ﬁ rst presentation of

ischaemic heart disease (IHD). Always consider the possibility of MI. In

particular, suspect myocardial cell death with any pain lasting > 10min (even

if relieved by glyceryl trinitrate (GTN)). A normal examination, normal ECG

and normal baseline cardiac markers do not exclude MI. If in any doubt, admit

the patient . If considering discharge, discuss with senior ED/medical staff.

Atypical cardiac chest pain

Patients with acute MI are occasionally sent home from the ED

inadvertently. Cardiac chest pain may be poorly localized, and may present

with musculoskeletal features or gastrointestinal (GI) upset. In particular,

patients with acute coronary syndromes commonly have chest wall

tenderness. Some patients understandably play down symptoms in order

to avoid admission to hospital. If the clinical history is suspicious of cardiac

pain (especially in a patient with risk factors, such as family history of IHD,

hypertension, smoking), then refer for admission. Do not be fooled by a

normal ECG, normal examination, or the fact that the patient is <30 years

old. Remember that oesophageal pain may improve with GTN and true

cardiac pain may appear to improve with antacids. The decision whether

or not to refer the patient for admission and investigation depends upon

an assessment of the risk of MI. In general, exclude an MI where chest pain

lasting > 15min has some features of IHD. Also refer patients who look

unwell, even if the chest pain lasts <15min.

68 CHAPTER 3 Medicine

Acute coronary syndromes

Coronary artery plaque rupture can result in a variety of ischaemic

conditions which fall under the overall term of ‘acute coronary syndrome’

and include unstable angina, non-ST segment elevation MI (NSTEMI)

and ST segment elevation MI (STEMI). Patients labelled as having acute

coronary syndrome, but without initial ST elevation, comprise a relatively

heterogenous group — some later proving (on the basis of elevated blood

troponin levels) to have suffered an NSTEMI.

The patient presenting with unstable angina or NSTEMI

Unstable angina can occur as worsening angina or a single episode of

‘crescendo’ angina, with a high risk of infarction. Features include angina

at rest, i frequency, i duration, and severity of pain (including response

to GTN). It may be difﬁ cult to distinguish between unstable angina and

NSTEMI in the ED.

• Provide O

to maintain SpO

94–98 % and attach cardiac monitor.

• Administer IV opioid analgesia ( ± antiemetic) as required.

• Give aspirin 300mg PO and clopidogrel 300mg PO.

• Start low molecular weight heparin (LMWH), eg dalteparin 120units/

kg SC every 12hr (max 10,000U) or enoxaparin 1mg/kg SC every 12hr.

Synthetic pentasaccharide fondaparinux 2.5mg SC may be used instead.

Follow local guidelines.

• If pain is unrelieved, commence GTN intravenous infusion (IVI; start at

0.6mg/hr and i as necessary), provided systolic BP is > 90mmHg.

• Glycoprotein IIb/IIIa inhibitors (eg eptiﬁ batide and tiroﬁ ban) are going

out of favour for patients at risk of NSTEMI or high TIMI risk score (see

Table 3.2 ).

• If high risk of NSTEMI, haemodynamically stable and no contraindications,

consider atenolol (5mg IV slowly over 5mins repeated once after 15mins),

according to local policy. Contraindications include: hypotension,

bradycardia, second or third degree heart block, heart failure and severe

reactive airways disease.

• Refer for admission, repeat ECGs and blood troponin testing 12hr after

pain onset.

• Discuss with cardiology all patients at high risk of NSTEMI or with TIMI

score > 3. They may beneﬁ t from early revascularization procedures.

ACUTE CORONARY SYNDROMES

Normal lead II (Fig. 3.3 )

Ischaemic changes in lead II (Fig. 3.4 )

Prinzmetal’s or ‘variant’ angina

Angina associated with ST elevation may be due to coronary artery vasos-

pasm. This may occur with or without a ﬁ xed coronary abnormality and

may be indistinguishable from an acute MI until changes resolve rapidly

with GTN as pain is relieved.

Table 3.2 TIMI risk score: increasing score predicts mortality or

adverse event

Risk factor Points

Age > 65 1

3 + risk factors for coronary artery disease

Family history of IHD, hypertension, hypercholesterolemia, diabetes,

or smoker

Known coronary artery disease with stenosis ≥50 %

Aspirin use in last 7 days 1

Recent episode of angina prior to this event 1

Raised troponin levels (or other cardiac marker) 1

ST segment deviation ≥0.5mm on ECG

Fig. 3.3

Fig. 3.4

70 CHAPTER 3 Medicine

ST segment elevation MI

IHD is the leading cause of death in the Western world. Mortality from

acute MI is believed to be 45 % , with 70 % of these deaths occurring before

reaching medical care. Contributory risk factors for MI include smoking,

hypertension, age, male sex, diabetes, hyperlipidaemia, and family history.

MI pathology

MI mostly affects the left ventricle. It usually results from sudden occlusion

of a coronary artery or one of its branches by thrombosis over a pre-

existing atheromatous plaque. Patients with IHD are at risk of sustaining

an MI if additional stresses are placed upon their already critically impaired

myocardial circulation (eg a high level of carboxyhaemoglobin (COHb)

following smoke inhalation). MI may also occur in vasculitic processes,

eg cranial arteritis ( b p.132) and Kawasaki disease.

MI diagnosis

The diagnosis of acute MI requires 2 out of the following 3 features:

• A history of cardiac-type ischaemic chest pain.

• Evolutionary changes on serial ECGs.

• A rise in serum cardiac markers.

Note that 50–60 % of patients will not have a diagnostic ECG on arrival

and up to 17 % will have an entirely normal initial ECG. Late presentation

does not improve diagnostic accuracy of the ECG.

History

The classic presentation is of sudden onset, severe, constant central

chest pain, which radiates to the arms, neck, or jaw. This may be similar

to previous angina pectoris, but is much more severe and unrelieved

by GTN. The pain is usually accompanied by one or more associated

symptoms: sweating, nausea, vomiting, breathlessness.

Atypical presentation is common. Have a high level of suspicion. Many

patients describe atypical pain, some attributing it to indigestion (be wary

of new onset ‘dyspeptic’ pain). Up to a third of patients with acute MI

do not report any chest pain. These patients tend to be older, are more

likely to be female, have a history of diabetes or heart failure, and have a

higher mortality.

These patients may present with:

• LVF.

• Collapse or syncope (often with associated injuries eg head injury).

• Confusion.

• Stroke.

• An incidental ECG ﬁ nding at a later date.

In a patient who presents with possible MI, enquire about past

medical history (IHD, hypertension, diabetes, hyperlipidaemia) and

contraindications to thrombolysis. Ask about drug history, including drugs

of abuse (particularly cocaine b p.215).

ST SEGMENT ELEVATION MI

Examination

Examination and initial resuscitation (maintain SpO

in normal range, IV

cannula, analgesia) go hand in hand. The patient may be pale, sweaty, and

distressed. Examination is usually normal unless complications have super-

vened (eg arrhythmias, LVF). Direct initial examination towards searching

for these complications and excluding alternative diagnoses:

• Check pulse, BP and monitor trace (?arrhythmia or cardiogenic shock).

• Listen to the heart (?murmurs or 3rd heart sound).

• Listen to the lung ﬁ elds (?LVF, pneumonia, pneumothorax).

• Check peripheral pulses (?aortic dissection).

• Check legs for evidence of deep vein thrombosis (?PE).

• Palpate for abdominal tenderness or masses (?cholecystitis, pancreatitis,

perforated peptic ulcer, ruptured aortic aneurysm).

Investigations

The diagnosis of ST segment elevation myocardial infarction within the

ﬁ rst few hours is based upon history and ECG changes (serum cardiac

markers may take several hours to rise — see below).

• Record an ECG as soon as possible, ideally within a few minutes of

arrival at hospital. Sometimes patients arrive at hospital with ECGs of

diagnostic quality already recorded by paramedics. If the initial ECG is

normal, but symptoms are suspicious, repeat the ECG every 15min and

re-evaluate.

• Request old notes (these may contain previous ECGs for comparison).

• Ensure continuous cardiac monitoring and pulse oximetry.

• Monitor BP and respiratory rate.

• Obtain venous access and send blood for cardiac markers, U&E, glucose,

FBC, lipids.

• Obtain a CXR if there is suspicion of LVF or aortic dissection.

Cardiac markers

Troponins are now universally used. Troponin T (cTnT) and Troponin

I (cTnI) are proteins virtually exclusive to cardiac myocytes. They are

highly speciﬁ c and sensitive, but are only maximally accurate after 12hr.

Troponin T and I cannot be used to rule out MI in the ﬁ rst few hours. In

addition, cardiac cells may release troponin into the blood when cardiac

muscle is damaged by pericarditis, pulmonary embolism with a large clot

burden, or sepsis. Renal failure reduces excretion of troponin.

Chest pain assessment units

These units are becoming established in some EDs. A combination of

ECGs, ST segment monitoring, cardiac markers, and exercise testing is

used to allow discharge of low to moderate risk patients within 6–12hr.

However, simply excluding an acute coronary syndrome is only part of

the assessment of chest pain.

72 CHAPTER 3 Medicine

Myocardial infarction: ECG changes 1

Infarction of cardiac muscle results in ECG changes that evolve over

hours, days, and weeks in a relatively predictable fashion.

Hyperacute changes

Frequently ignored, although often subtle, some or all of the following

may be observed within minutes of infarction:

• i Ventricular activation time , since the infarcting myocardium is slower to

conduct electrical impulses. The interval between the start of the QRS

and apex of the R wave may be prolonged > 0.045sec.

• i Height of R wave may be seen initially in inferior leads in inferior MI.

• Upward-sloping ST segment — having lost normal upward concavity, the

ST segment straightens, then slopes upwards, before becoming ele-

vated.

• Tall, widened T waves.

Evolving acute changes

In isolation, none of these changes are speciﬁ c to MI. In combination, and

with an appropriate history, they can diagnose MI:

• ST elevation : the most important ECG change. ST segments become

concave down and are signiﬁ cant if elevated > 1mm in 2 limb leads, or

> 2mm in 2 adjacent chest leads.

• Reciprocal ST depression may occur on the ‘opposite side’ of the heart.

• Pathological Q waves (deﬁ ned on b p.65) reﬂ ect electrically inert

necrotic myocardium. ECG leads over a large transmural infarct show

deep QS waves. Leads directed towards the periphery of a large infarct

or over a smaller infarct may show a QR complex or a loss of R wave

amplitude .

• T wave inversion : typically deeply inverted, symmetrical and pointed.

• Conduction problems may develop. LBBB in a patient with acute cardiac

chest pain makes interpretation of the ECG very difﬁ cult. LBBB does not

have to be new to be signiﬁ cant. Do not delay intervention in patients

with a good clinical history of MI in order to obtain old ECGs.

Sgarbossa criteria for diagnosing ACS in the presence of LBBB

• ST segment elevation > 1mm in leads with positive QRS complexes.

• ST segment depression in leads V1, V2, or V3.

• ST segment elevation > 5mm in lead with negative QRS complexes.

If all 3 are present, MI is likely.

Chronic changes

In the months following an MI, ECG changes resolve to a variable extent.

ST segments become isoelectric, unless a ventricular aneurysm develops.

T waves gradually become + ve again. Q waves usually remain, indicating

MI at some time in the past.

MYOCARDIAL INFARCTION: ECG CHANGES 1

Electrocardiogram changes following myocardial infarction

(Fig. 3.5 )

Electrocardiograms after myocardial infarction (Figs 3.6 and 3.7 )

Normal Hours Days Weeks

Months

Fig. 3.5

aVL

III

aVF

aVRI

Fig. 3.6 Acute inferolateral infarction with ‘reciprocal’ ST changes in I, aVL, and V

–V

IaVR

II aVL

III V

aVF

Fig. 3.7 Acute anteroseptal infarction with minimal ‘reciprocal’ STchanges in III and aVF.

74 CHAPTER 3 Medicine

Myocardial infarction: ECG changes 2

Localization of myocardial infarction

MI usually affects the left ventricle (LV), occasionally the right ventricle

(RV), but virtually never the atria. The part of myocardium affected is

implied by which leads show changes (Table 3.3 ).

Posterior myocardial infarction

Posterior MI nearly always occurs as part of inferior (postero-inferior) or

lateral (postero-lateral) MI. No conventional electrode views the poste-

rior heart, since intervening tissues result in an attenuated signal. ECG

diagnosis of true posterior MI may be made from the use of V

7–9

and from

reciprocal changes seen in leads V

1–3

: tall, slightly widened R (reciprocal

of Q), concave up ST depression (reciprocal of ST elevation), upright tall

widened T (reciprocal of inverted T).

Right ventricular infarct

This occurs most often as part of an inferior MI. In the presence of

changes of acute MI in the inferior leads, ST elevation in V

suggests right

ventricular involvement. In this case, record an ECG trace from lead V

The diagnosis of RV infarct helps determine treatment of ensuing cardiac

failure. Treat RV failure with IV ﬂ uids to maintain adequate ﬁ lling pressure

and exercise caution if considering use of nitrates.

Blood supply to the heart and coronary artery dominance

The left anterior descending artery supplies the anterior and septal cardiac

areas (Fig. 3.9). The circumﬂ ex branch supplies the anterolateral aspect of

the heart. The right coronary artery supplies the right ventricle. In most

people the right coronary artery also supplies the sino-atrial node, the

inferior wall of the left ventricle and the ventricular septum. In 15 % of

individuals, the inferior wall is supplied by the circumﬂ ex branch of the left

coronary artery (left dominance).

Table 3.3

ECG leads Location of MI

1–3

Anteroseptal

5–6

, aV

Anterolateral

2–4

1–6

Extensive anterior

I, II, aV

, V

Lateral

II, III, aV

Inferior

, V

R Right ventricle

MYOCARDIAL INFARCTION: ECG CHANGES 2

IIIIII

Fig. 3.8 ECG of subendocardial infarct.

Ascending aorta

Right coronary

artery

Left main stem

Left anterior

descending artery

Posterior

descending artery

Septal branches

(

of the LAD

)

Circumflex coronary

artery

Diagonal branches

(of the LAD)

Fig. 3.9

76 CHAPTER 3 Medicine

STEMI: treatment

Speed is crucial — time is muscle. Ambulance control may alert the ED in

advance of a patient with cardiac-type chest pain. Work efﬁ ciently as a

team to ensure treatment is not delayed.

• Give O

to maintain SpO

94–98 % and attach cardiac monitor.

• Obtain IV access and take samples for U&E, glucose, FBC, cardiac

markers.

• Provide small increments of IV opioid analgesia titrated to effect.

• Ensure the patient has had 300mg aspirin and 300mg clopidogrel PO.

• Contact cardiology for primary percutaneous coronary intervention

(PCI). Arrange transport to the cath lab.

• For patients undergoing PCI, consider IV glycoprotein IIb/IIIa receptor

antagonist as an adjuvant. Be guided by local protocol.

• If PCI is not available, consider thrombolysis and monitor carefully. Start

LMWH, heparin, or fondaparinux, according to local protocols.

• If pain continues, give IVI GTN (start at 0.6mg/hr and i as necessary),

provided systolic BP is > 90mmHg.

• Consider atenolol (5mg slowly IV over 5min, repeated once after

15min), or metoprolol, unless contraindicated (eg uncontrolled heart

failure, hypotension, bradyarrhythmias, COPD).

Indications for PCI or thrombolysis

• ST elevation of > 1mm in 2 limb leads, or

• ST elevation of 2mm in 2 or more contiguous chest leads, or

• LBBB in the presence of a typical history of acute MI (NB: LBBB does

not have to be new).

Primary angioplasty for ST segment elevation MI

Primary percutaneous coronary intervention (coronary angioplasty and

stenting) is the treatment of choice for STEMI. Compared with throm-

bolysis, PCI administered within 12hr of symptom onset results in lower

mortality and re-infarction rates. The sooner it is performed, the greater

the beneﬁ ts.

Thrombolysis

If PCI cannot be performed within 90min of diagnosis, thrombolytic

therapy is an alternative. The beneﬁ ts reduce markedly with time delay,

so if PCI is not available, do not delay the administration of a thrombolytic

agent. Rural areas with long hospital transfers may have a protocol for

ambulance administered thrombolysis, aided by telemedicine advice from

the ED or cardiology. Patients presenting > 12hr after symptom onset will

not beneﬁ t from thrombolysis.

Strokes, intracranial haemorrhage and major bleeds are more common

in patients given thrombolysis. Intracranial bleeding is more common in

older patients, those with hypertension on admission and those given tPA.

Prior to administering thrombolysis, always explain the beneﬁ ts and risks

to the patient. Obtain verbal consent to give the medication and record

this in the notes.

STEMI: TREATMENT

Contraindications to thrombolysis

Most are relative, but discuss any contraindications with the patient and

cardiology:

• Head injury, recent stroke, previous neurosurgery or cerebral tumour.

• Recent GI or GU bleeding, menstruation, or coagulopathy/warfarin.

• Severe hypertension (eg systolic BP > 200mmHg, diastolic BP > 120mmHg),

aortic dissection or pericarditis.

• Puncture of non-compressible vessel (eg subclavian vein), traumatic

CPR, d GCS post-arrest.

• Major surgery within recent weeks.

• Pregnancy.

Choice of thrombolytic agents

Tissue plasminogen activator (tPA), rather than streptokinase, is the agent

of choice. Always use tPA if streptokinase was given > 5 days ago or in

anterior MI in a patient <75 years old and <4hr of onset of symptoms, or

if hypotensive (systolic BP <90mmHg).

Alteplase (recombinant tPA (rtPA)) is most effective given by an

accelerated regimen, eg 15mg IV bolus, followed by 0.75mg/kg (max 50mg)

IVI for 30min, then 0.5mg/kg (max 35mg) IVI over 60min. Give LMWH (eg

enoxaparin 1mg/kg stat) or heparin concomitantly through a separate IV

line (5000unit IV bolus, then 1000units/hr IV), according to local protocols.

Reteplase (modiﬁ ed tPA) can be given as two IV boluses of 10units each

exactly 30min apart. Give LMWH/heparin as for alteplase.

Tenecteplase (modiﬁ ed tPA) is given as a single IV bolus over 10sec. Dose

according to weight (<60kg = 30mg; 60–69kg = 35mg; 70–79kg = 40mg;

80–89kg = 45mg; > 90kg = 50mg). Give LMWH/heparin as for alteplase.

Streptokinase Given as 1.5mega-units by continuous IVI over 1hr. Strepto-

kinase is allergenic (may require slow IV chlorphenamine 10mg and IV

hydrocortisone 100mg) and frequently causes hypotension ( d IVI rate

and tilt the bed head down — treatment rarely needs to be discontinued).

After a recent streptococcal infection, streptokinase may be ineffective

due to the antibodies produced.

Further management

Arrhythmias Occur commonly after MI. Occasional ventricular ectopics

or transient AF (lasting <30sec) require no treatment. Watch for sudden

VT/VF and treat as in b Cardiac arrest, p.46.

Hypokalaemia Treat if K

<4mmol/L.

Pulmonary oedema Treat as described on b p.101.

Cardiogenic shock d cardiac output with tissue hypoxia, which does not

improve with correction of intravascular volume. Mortality is 50–80 % .

Contact ICU and cardiologist. Echocardiography may be required to

exclude conditions requiring urgent surgical repair (mitral regurgitation

from papillary muscle rupture, aortic dissection, ventricular septum rupture,

cardiac tamponade from ventricular wall rupture) or massive PE. If these

are excluded, emergency coronary intervention may i survival.

78 CHAPTER 3 Medicine

Pericarditis

Acute inﬂ ammation of the pericardium characteristically produces chest

pain, low grade fever, and a pericardial friction rub. Pericarditis and

myocarditis commonly co-exist.

Causes

• Myocardial infarction (including Dressler’s syndrome — see b p.79).

• Viral (Coxsackie A9, B1-4, Echo 8, mumps, EBV, CMV, varicella, HIV,

rubella, Parvo B19).

• Bacterial (pneumococcus, meningococcus, Chlamydia , gonorrhoea,

Haemophilus ).

• Tuberculosis (TB; especially in patients with HIV) — see b p.232.

• Locally invasive carcinoma (eg bronchus or breast).

• Rheumatic fever — see b Acute arthritis, p.497.

• Uraemia.

• Collagen vascular disease (SLE, polyarteritis nodosa, rheumatoid

arthritis).

• After cardiac surgery or radiotherapy.

• Drugs (hydralazine, procainamide, methyldopa, minoxidil).

Diagnosis

Classical features of acute pericarditis are pericardial pain, a friction rub

and concordant ST elevation on ECG. The characteristic combination of

clinical presentation and ECG changes often results in a deﬁ nite diagnosis.

Chest pain is typically sharp, central, retrosternal, and worse on deep

inspiration, change in position, exercise, and swallowing. A large pericardial

effusion may cause dysphagia by compressing the oesophagus.

A pericardial friction rub is often intermittent, positional, and elusive. It

tends to be louder during inspiration, and may be heard in both systole

and diastole. Low grade fever is common.

Appropriate investigations include: ECG, chest X-ray, FBC, erythrocyte

sedimentation rate (ESR), C-reactive protein (CRP), U&E, and troponin.

Obtain blood cultures if there is evidence of sepsis or suspicion of a

bacterial cause (eg spread of intrathoracic infection). A pericardial effusion

is most quickly and easily demonstrated by echocardiography or FAST

scanning: clinical evidence of cardiac tamponade is rare.

ECG changes

In acute pericarditis ECG changes result from associated epicardial inﬂ am-

mation (see Fig. 3.10 ). Sinus tachycardia is usual, but AF, atrial ﬂ utter or

atrial ectopics may occur. ST elevation is concave up (unlike MI, b p.72),

and present in at least 2 limb leads and all chest leads (most marked

in V

3–6

). T waves are initially prominent, upright, and peaked, becoming

ﬂ attened or inverted over several days. PR depression (reﬂ ecting atrial

inﬂ ammation) may occur in the same leads as ST elevation (this PR–ST

discordance is characteristic). Pathological Q waves are not present.

Pericardial effusion causes d QRS amplitude in all leads. Electrical alternans

is diagnostic, but rare.

PERICARDITIS

Management

Refer to the medical team for echocardiography and treatment.

The appropriate treatment depends on the underlying cause.

Idiopathic pericarditis or viral pericarditis in young patients is usually

benign and self-limiting, responding to symptomatic treatment (high dose

NSAID ± PPI cover). Occasionally, it follows a relapsing course before

‘burning itself out’.

Dressler’s syndrome (autoimmune pericarditis ± effusion 2–14 weeks

after 3 % of MIs) requires cardiology specialist care.

Pericardial effusion may occur with any type of pericarditis. It is relatively

common in acute bacterial, tuberculous, and malignant pericarditis.

Acute tamponade may occur following cardiac rupture with MI, aortic

dissection, or after cardiac surgery. Summon senior help and arrange

immediate echocardiography for patients with signs of tamponade, with

pericardiocentesis under ultrasound guidance, and then a deﬁ nitive

drainage procedure. Emergency ‘blind’ pericardiocentesis is described on

b p.343.

II IIII

Fig. 3.10 ECG of pericarditis.

80 CHAPTER 3 Medicine

Bradyarrhythmias

Bradycardia is a ventricular rate of <60/min in the adult. It usually reﬂ ects

inﬂ uences on or disease of the sino-atrial (SA) node, or atrioventricular

(AV) block. Intraventricular conduction disturbances may progress to AV

block. Sinus bradycardia may be physiological (eg athletes), due to drugs

( B -blockers), or pathological (hypothyroidism, hypothermia, hypoxia, iICP,

sick sinus syndrome, MI, myocardial ischaemia). Bradycardia also occurs in

up to 1/3 of patients with hypovolaemia (eg GI bleed, ectopic pregnancy).

Sick sinus syndrome (or ‘sinus node disease’) is usually the result of

ischaemia or degeneration of SA node. It is characterized by sinus pauses

( > 2sec) or sinus arrest. Junctional or other escape beats may occur and

occasionally a tachyarrhythmia may emerge (‘tachy-brady’ syndrome).

Patients may present with dizziness, collapse, loss of consciousness or

palpitations. A continuous 24hr ECG tape may demonstrate arrhythmias.

AV block may be caused by IHD, drugs (eg excess digoxin) or cardiac

surgery.

First degree AV block Conduction from atria to ventricles occurs every

time, but is delayed. The PR interval is > 0.2sec (5 small squares on

standard ECG) (Fig. 3.11 ).

Second degree AV block Only a proportion of P waves are conducted to

the ventricles. There are two types:

• Mobitz type I block (Wenckebach) : the PR interval becomes increasingly

lengthened until a P wave fails to conduct (Fig. 3.12 ).

• Mobitz type II block : failure to conduct P waves may occur regularly

(eg 3:1) or irregularly, but the PR interval remains constant (Fig. 3.13 ).

Third degree (complete) heart block Atrial activity is not conducted to

ventricles. With a proximal block (eg at the AV node), a proximal escape

pacemaker in the AV node or bundle of His may take over, producing

narrow QRS complexes at a rate of 8 50/min. With distal AV block, a

more distal escape pacemaker results in broad bizarre complexes at a

rate of 8 30/min. Ventricular asystole may occur if the escape pacemaker

stops discharging, unless a subsidiary pacemaker takes over (Fig. 3.14 ).

Intraventricular conduction disturbances

The intraventricular conducting system commences as the bundle of His

and divides into right and left bundle branches — the latter subdivides

further into antero-superior and postero-superior divisions. These two

divisions and the right bundle branch are referred to as the ‘fascicles’.

Blockage of 2 out of 3 fascicles = bifascicular block .

• RBBB + left anterior hemiblock causes left axis deviation and RBBB

pattern on ECG.

• RBBB + left posterior hemiblock causes right axis deviation and RBBB

pattern on ECG.

Trifascicular block is present when bifasciular block is accompanied by

a prolonged PR interval. Note that true blockage of all 3 fascicles would

cause complete heart block, so ‘trifascicular block’ represents impending

progression to complete heart block.

BRADYARRHYTHMIAS

Fig. 3.11 ECG of ﬁ rst degree heart block.

Fig. 3.12 ECG of Mobitz type I AV block.

Fig. 3.13 ECG of Mobitz type II AV block.

Fig. 3.14 ECG of complete AV block.

82 CHAPTER 3 Medicine

Treatment of bradyarrhythmias

The emergency treatment of bradycardia depends upon two important

factors: the clinical condition of the patient and the risk of asystole. Give

, insert an IV cannula and follow the 2010 European Resuscitation

Council Guidelines shown opposite ( www.resus.org.uk ).

Atropine is the ﬁ rst-line drug. The standard dose is 500mcg IV, which may

be repeated to a total of 3mg. Further doses are not effective and may

result in toxic effects (eg psychosis, urinary retention).

Adrenaline (epinephrine) can be used as a temporizing measure prior

to transvenous pacing if an external pacemaker is not available. Give by

controlled infusion at 2–10mcg/min, titrating up according to response

(6mg adrenaline in 500mL 0.9 % saline infused at 10–50mL/hr).

External transcutaneous pacing is available on most deﬁ brillators. It

allows a pacing current to be passed between 2 adhesive electrodes

placed over the front of the chest and the back. Select external demand

pacing mode at a rate of 70/min, then gradually i the pacing current from

zero until capture is shown on the monitor. Clinically, capture results in

a palpable peripheral pulse at the paced rate and clinical improvement in

the patient’s condition. Provide small doses of IV opioid ± sedation if the

patient ﬁ nds external pacing very uncomfortable.

Transvenous cardiac pacing is the treatment of choice for bradycardic

patients who are at risk of asystole. The technique should only be

performed by an experienced doctor. The preferred route of access is the

internal jugular or subclavian vein. However, if thrombolysis has recently

been given or is contemplated, or if the patient is taking anticoagulants,

use the right femoral vein instead. Obtain a CXR to exclude complications.

A correctly functioning ventricular pacemaker results in a pacing spike

followed by a widened and bizarre QRS (Fig. 3.15 ).

Permanent pacemakers and implantable deﬁ brillators

Increasingly sophisticated implantable devices are being used to manage

arrhythmias. Occasionally, a patient will present to the ED with a

malfunctioning pacemaker. Get urgent specialist advice. External trans-

cutaneous pacing will provide temporary support whilst the problem is

resolved. A special magnet may be needed to inactivate an implantable

deﬁ brillator which ﬁ res repeatedly.

Fig. 3.15 Paced rhythm.

TREATMENT OF BRADYARRHYTHMIAS

Algorithm for the management of bradycardia (Fig. 3.16 )

See www.resus.org.uk

Seek expert help

Arrange transvenous pacing

*Alternatives include:

• Aminophylline

• Dopamine

• Glucagon (if beta-blocker or calcium channel blocker overdose)

• Glycopyrronium bromide can be used instead of atropine

YES

Adverse features?

• Shock

• Syncope

• Myocardial ischaemia

• Heart failure

Atropine

500 mcg IV

YES

• Assess using the ABCDE approach

• Give oxygen if appropriate and obtain IV access

• Monitor ECG, BP, SpO

, record 12-lead ECG

• Identify and treat reversible causes

(e.g. electrolyte abnormalities)

Observe

Satisfactory

response?

Interim measures:

• Atropine 500 mcg IV

repeat to maximum of 3 mg

• Isoprenaline 5 mcg min

–1

• Adrenaline 2–10 mcg min

–1

• Alternative drugs*

• Transcutaneous pacing

Risk of asystole?

• Recent asystole

• Mobitz II AV block

• Complete heart block

with broad QRS

• Ventricular pause >3s

Fig. 3.16 Algorithm for the management of bradycardia.

84 CHAPTER 3 Medicine

Tachycardia algorithm–with pulse

Yes/Unstable

• Amiodarone 300 mg IV over 10–20 min

and repeat shock; followed by:

No/Stable

NarrowBroad

Is QRS narrow (< 0.12s)?

Irregula

Narrow QRS

Is rhythm regular?

Regular

Irregular Regular

Adverse features?

• Shock

• Syncope

• Myocardial ischaemia

• Heart failure

Synchronised DC Shock

Up to 3 attempts

Broad QRS

Is rhythm regular?

• Assess using the ABCDE approach

• Give oxygen if appropriate and obtain IV access

• Monitor ECG, BP, SpO

, record 12-lead ECG

• Identify and treat reversible causes (e.g. electrolyte abnormalities)

• Amiodarone 900 mg over 24 h

TACHYCARDIA ALGORITHM

Irregular narrow complex

tachycardia

Probable atrial fibrillation

Control rate with:

• β-Blocker or diltiazem

• Consider digoxin or amiodarone

if evidence of heart failure

Possibilities include:

• AF with bundle branch block

treat as for narrow complex

• Pre-excited AF

consider amiodarone

• Polymorphic VT

(e.g. torsade de pointes -

give magnesium 2 g over 10 min)

If ventricular tachycardia

(or uncertain rhythm):

• Amiodarone 300 mg IV

over 20–60 min;

then 900 mg over 24 h

If previously confirmed

SVT with bundle branch block:

• Give adenosine as for regular

narrow complex tachycardia

• Use vagal manoeuvres

• Adenosine 6 mg rapid IV bolus;

if unsuccessful give 12 mg;

if unsuccessful give further 12 mg

• Monitor ECG continuously

Probable re-entry paroxysmal SVT:

• Record 12-lead ECG in sinus

rhythm

• If recurs, give adenosine again and

consider choice of anti-arrhythmic

prophylaxis

Yes

Sinus rhythm restored?

Possible atrial flutter

• Control rate (e.g. β-Blocker)

Seek expert help

Fig. 3.17 Tachycardia algorithm with pulse (www.resus.org.uk).

86 CHAPTER 3 Medicine

Tachyarrhythmias

The single Resuscitation Council 2010 tachycardia algorithm (Fig. 3.17 )

(see www.resus.org.uk ) is based on the fact that, irrespective of the exact

underlying cardiac rhythm, many of the initial management principles in

the peri-arrest setting are the same:

• Rapidly assess ABC.

• Monitor cardiac rhythm and record a 12-lead ECG.

• Provide O

• Identify and treat reversible causes.

• Assess for evidence of instability (signs of shock, syncope, signs of heart

failure, or myocardial ischaemia) — these indicate the need for urgent

intervention, initially in the form of synchronized cardioversion.

The unstable patient with tachyarrhythmia

Synchronized cardioversion

This requires two doctors — one to perform cardioversion, the other

(experienced in anaesthesia) to provide sedation/anaesthesia and manage

the airway. The patient will not be fasted and is therefore at particular risk

of aspiration. The arrhythmia may d cardiac output and i circulation times,

so IV drugs take much longer to work than usual. If the ‘sedation doctor’

does not appreciate this and gives additional doses of anaesthetic drugs,

hypotension and prolonged anaesthesia may result.

Electrical cardioversion is synchronized to occur with the R wave to

minimize the risk of inducing VF. Synchronized cardioversion is effective

in treating patients who exhibit evidence of instability with underlying

rhythms of SVT, atrial ﬂ utter, atrial ﬁ brillation, and VT — choose an initial

level of energy according to the rhythm:

• For broad complex tachycardia or AF, start with 200J monophasic or

120–150J biphasic. If unsuccessful, i in increments to 360J monophasic

or 150J biphasic.

• Start with a lower energy for atrial ﬂ utter and paroxysmal SVT — use

100J monophasic or 70–120J biphasic. If this is unsuccessful, increase in

increments to 360J monophasic or 150J biphasic.

Amiodarone

If cardioversion is unsuccessful after 3 synchronized shocks, give amio-

darone 300mg IV over 10–20min and repeat shock. Give amiodarone

by central vein when possible as it causes thrombophlebitis when given

peripherally. However, in an emergency, it can be given into a large

peripheral vein.

BROAD COMPLEX TACHYARRHYTHMIAS

Broad complex tachyarrhythmias

May be caused by VT, or rarely by SVT with aberrant conduction. The

default position should be that broad complex tachycardia is VT. Provide

as appropriate, insert an IV cannula and follow the Resuscitation

Council guidelines (Fig. 3.17 ) and (www.resus.org.uk ).

The priorities in broad complex arrhythmias associated with tricyclic

overdose are airway management, oxygenation, ventilation and correction

of metabolic disorders: give IV bicarbonate, but avoid anti-arrhythmic

drugs (b Tricyclic antidepressant poisoning, p.194).

Evaluating ECGs: is it VT or SVT with aberrant conduction?

VT is much more likely as a cause of the broad complex tachycardia if:

• The patient is > 60 years.

• The patient has a history of IHD or cardiomyopathy.

• There is clinical evidence of AV dissociation (intermittent cannon ‘a’

waves seen on jugular venous pressure (JVP), ﬁ rst heart sound of vari-

able intensity).

• Inverted P waves in lead II.

• The frontal plane axis is bizarre (–90 ° to –180 ° ).

• The QRS is > 0.13sec.

• There are ‘capture’ or ‘fusion’ beats.

• The QRS is bizarre, not resembling a bundle branch block pattern

• All chest leads (V

1–6

) are concordant (QRS complexes point the same

way).

• R > R´ (or r´) in V

• There is a deep S wave (either QS, rS or RS) in V

Torsades de pointes

This is a rare form of polymorphic VT, associated with hypomagnesaemia,

hypokalaemia, long QT interval (congenital or drug related, eg sotalol,

antipsychotics, antihistamines, antidepressants). A constantly changing

electrical axis results in QRS complexes of undulating amplitude. Usually

paroxysmal, it may degenerate to VF. Get expert help and treat with IV

magnesium sulphate (2g over 10min = 8mmol or 4mL 50 % magnesium).

Refractory cases may require overdrive pacing.

Fig. 3.18

Fig. 3.19

88 CHAPTER 3 Medicine

Narrow complex tachyarrhythmias

These are almost always of supraventricular origin. Underlying rhythms

include:

• Sinus tachycardia.

• Paroxysmal AV re-entrant tachycardia (often referred to as ‘SVT’).

• AF with fast ventricular response.

• Atrial ﬂ utter.

• Atrial tachycardia.

• Junctional tachycardia.

Give O

, insert an IV cannula, and follow the algorithm in Fig. 3.17 ( www.

resus.org.uk ). Determine if the rhythm is regular. Treat irregular rhythms

(AF) as outlined in Fig. 3.17 . If the ventricular rate is exactly 150/min, atrial

ﬂ utter with 2:1 block is likely (Fig. 3.20 ).

The compromised patient with shock, syncope, acute cardiac failure, or

cardiac ischaemia should be treated with emergency electrical cardioversion.

It is reasonable to give IV adenosine while arranging the cardioversion, as

long as this does not delay the procedure.

For stable patients consider

Vagal stimulation The most effective way is a Valsalva manoeuvre while

supine or tilted head down. Instruct the patient to attempt to blow the

plunger out of a 50mL bladder tip syringe. If unsuccessful, in the young

patient, massage the carotid sinus for 15sec (1 side only), by gently

rubbing in a circular action lateral to the upper border of the thyroid

cartilage. Carotid sinus massage may be dangerous (especially if there is a

carotid bruit or previous stroke/TIA).

Adenosine This temporarily blocks conduction through the AV node. It

has a very short half-life (10–15sec). Adenosine can successfully terminate

re-entrant tachycardias and may ‘unmask’ other conditions (eg atrial

ﬂ utter) by temporarily producing a conduction block. It is contraindicated

in 2 * or 3 * AV block, patients with WPW and asthmatics. The effects

are blocked by theophylline and potentiated markedly (and dangerously)

in the presence of dipyridamole, carbamazepine or in a denervated

heart — seek advice. Warn the patient about transient ﬂ ushing and chest

discomfort. Give adenosine by fast bolus 6mg IV injection into an IV

cannula in the antecubital fossa and ﬂ ush with 0.9 % saline (Fig. 3.17 ) while

recording a rhythm strip. If unsuccessful, repeat with 12mg, then 12mg.

If adenosine is contra-indicated, consider IV verapamil 2.5–5mg over 2min.

Avoid verapamil in patients with cardiac failure, hypotension, concomitant

B -blocker therapy, or WPW.

Fig. 3.20 Narrow complex tachycardia.

ATRIAL FIBRILLATION

Atrial ﬁ brillation

Atrial ﬁ brillation is rapid, irregular, uncoordinated atrial activity, and is

associated with an irregular ventricular response.

Causes

Acute AF may be associated with: IHD (33 % ), heart failure (24 % ), hyperten-

sion (26 % ), and valvular heart disease (7 % ). Other cardiac causes are sick

sinus syndrome, pericarditis, inﬁ ltrative heart disease, cardiomyopathy,

myocardititis, congenital heart disease, and post-cardiac surgery.

Non-cardiac causes include: sepsis, PE, thyrotoxicosis, electrocution,

lung or pleural disease, chest trauma, hypokalaemia, hypovolaemia,

hypothermia, drug abuse (eg cocaine). Paroxysmal AF sometimes occurs

in ﬁ t athletes.

Holiday heart: binge drinking or occasionally alcohol withdrawal may

cause acute AF in patients with no other predisposing factors. AF usually

resolves spontaneously within 48hr. The diagnosis of ‘holiday heart’ is one

of exclusion after cardiac disease and other causes have been ruled out.

Clinical features

AF d cardiac output by 10–20 % , irrespective of underlying ventricular

rate. Clinical presentation varies according to the cause and effect of

the AF. Some patients are asymptomatic; others suffer life-threatening

complications (heart failure, angina). Patients with underlying IHD may

develop ischaemia during periods of rapid ventricular rate.

Treatment

Patients in AF can be treated with cardioversion or rate control. If signs of

shock, syncope, acute cardiac failure, or ischaemia are present, consider

electrical cardioversion under sedation. Patients may also be chemically

cardioverted with ﬂ ecainide 50–150mg IV (contraindicated in patients with

cardiac disease) or amiodarone 300mg IV (safer in patients with cardiac

disease). Both drugs may cause hypotension. If the patient has had symp-

toms for longer than 48hr, they are at risk of cardiac thromboembolism

and stroke when cardioverted, so instead, give rate control medications

and commence IV or low molecular weight heparin. Rate control drugs

include metoprolol 5mg IV and diltiazem (IV form not available in UK).

Digoxin 500mcg IV is the drug of choice in patients with CCF. See 2006

NICE guidelines ( www.nice.org.uk ).

Atrial ﬁ brillation in Wolff Parkinson White syndrome

This may result in an irregular, broad complex tachycardia. Impulses are

conducted from the atria via the AV node and an accessory pathway.

Do not give AV-blocking drugs (digoxin, verapamil, or adenosine) as this

can result in acceleration of conduction through the accessory pathway,

leading to cardiovascular collapse or VF. Seek expert help.

Atrial ﬂ utter

The typical atrial rate is 300/min, so a regular 2:1 block will give a QRS

rate of 150/min. Variable block may result in an irregular rate. Consult

with an expert to discuss treatment.

90 CHAPTER 3 Medicine

Hypertensive problems

Bear the following points in mind when managing a hypertensive patient

in the ED:

• Most patients with hypertension are asymptomatic.

• Hypertension is an important risk factor for cardiovascular disease and

stroke.

• Most patients found to be hypertensive in the ED do not require any

immediate intervention or treatment, but do require careful follow-

up — usually by their GP.

• Never intervene on the basis of a single raised BP measurement in the

absence of any associated symptoms and signs.

Approach

Approach patients found to be hypertensive as follows:

• Those with no previous history of hypertension, and no other concerns

or history of other conditions (eg diabetes, peripheral vascular disease,

IHD, or stroke) — arrange follow-up and monitoring with GP.

• Those known to be hypertensive already on treatment — arrange

follow-up and monitoring with GP.

• Those displaying evidence of end organ damage (eg LV hypertrophy,

retinal changes, renal impairment) — refer to the medical team.

• Those with hypertension associated with pain, vasoconstriction (eg acute

pulmonary oedema) or stroke — treat underlying cause where possible.

Do not intervene in stroke associated hypertension except under the

direction of a neurologist or stroke specialist.

• Those with hypertension directly associated with symptoms or

signs — contact the medical team and consider whether intervention

is appropriate (see below).

Mild/moderate hypertension (diastolic 100–125mmHg)

Ascertain if the patient has a past history of hypertension and is taking drug

therapy for this. Examine for retinal changes and evidence of hypertensive

encephalopathy. Investigate as appropriate (U&E, urinalysis, CXR, ECG).

Further management will depend upon the BP and the exact circum-

stances. If the BP is moderately elevated (ie diastolic BP: 110–125mmHg)

and the patient is symptomatic, refer to the medical team. If the patient is

asymptomatic with normal examination and renal function, he/she may be

suitable for GP follow up.

HYPERTENSIVE PROBLEMS

Severe hypertension (diastolic > 125mmHg)

Patients with a diastolic BP > 125mmHg require urgent assessment. Search

for evidence of hypertensive encephalopathy : headache, nausea, vomiting,

confusion, retinal changes (haemorrhages, exudates, papilloedema), ﬁ ts,

focal neurological signs, d conscious level. Ask about recent drug ingestion

(eg ecstasy or cocaine — b pp. 214 & 215).

Investigations

Insert an IV cannula and send blood for U&E, creatinine, and glucose. Obtain

a CXR and ECG, and perform urinalysis. If there is d conscious level, focal

signs, or other clinical suspicion that the hypertension may be secondary to

stroke or intracranial haemorrhage, arrange an emergency CT scan.

Management

• Refer patients with a diastolic pressure > 125mmHg or evidence of

hypertensive encephalopathy to the medical team. Resist commencing

emergency treatment until consultation with an expert. There is a sig-

niﬁ cant risk of complications (stroke or MI) if the BP is reduced rapidly.

It may be appropriate to commence oral antihypertensive therapy using

a B-blocker (eg atenolol or labetalol) or calcium channel blocker (eg

nifedipine).

• If treatment is appropriate, commence an IVI of sodium nitroprusside,

labetalol or GTN with continuous BP monitoring via an arterial line and

admit to high dependency unit (HDU) or ICU. Sodium nitroprusside

has a very short half-life ( 8 1–2min) and acts as a vasodilator of both

arterioles and veins. IV labetolol may be preferred if aortic dissection

( b p.92) or phaeochromocytoma are suspected.

• Beta-blockers are contraindicated in hypertension caused by cocaine,

amphetamine or related sympathomimetic drugs ( b p.215), since

B-blockade may cause unopposed A-adrenergic activity with paradox-

ical hypertension and d coronary blood ﬂ ow.

Hypertension in pregnancy

Hypertension may be part of pre-eclampsia or eclampsia (see b p.592).

Pre-eclampsia is diagnosed with 2 or more of: hypertension ( > 140/90),

proteinuria and oedema. This can be associated with haemolysis,

elevated liver function tests (LFTs), low platelets (HELLP syndrome).

Check urine for protein and check blood for FBC, LFT, platelets, and

coagulation screen. Call for senior obstetric help. Eclampsia is diagnosed

with the onset of grand mal seizures after 20 weeks gestation, and carries

a signiﬁ cant mortality rate.

92 CHAPTER 3 Medicine

Aortic dissection

Remember: hypertensive patients with sudden, severe chest, and/or back

pain may have acute aortic dissection.

Pathology

Aortic dissection is longitudinal splitting of the muscular aortic media

by a column of blood. The dissection may spread proximally (possibly

resulting in aortic incompetence, coronary artery blockage, cardiac

tamponade), distally (possibly involving the origin of various arteries), or

rupture internally back into the aortic lumen, or externally (eg into the

mediastinum, resulting in rapid exsanguination).

More than 70 % of patients have a history of hypertension. It occurs

more frequently in those with bicuspid aortic valve, Marfan’s syndrome

or Ehlers–Danlos syndrome. Up to 20 % follow recent cardiac surgery or

recent angiography/angioplasty.

Dissection may be classiﬁ ed Stanford type ‘A’ or ‘B’, according to whether

the ascending aorta is involved or not, respectively. Overall mortality is

30 % (35 % type A and 15 % type B).

Type A Type B

Fig. 3.21

AORTIC DISSECTION

History

Aortic dissection may mimic the presentation of an MI, requiring a high

index of suspicion. It typically presents with abrupt onset sharp, tearing or

ripping pain (maximal at onset) in anterior or posterior chest. Migration of

the pain may reﬂ ect extension of the dissection. Syncope occurs in 8 10 %

of patients, sometimes in the absence of any pain. Occasionally, patients

can present with neurological deﬁ cit associated with chest pain.

Examination

The patient is usually apprehensive and distressed, with pain which is dif-

ﬁ cult to alleviate, even using IV opioid. Clues to the diagnosis include:

• An aortic regurgitation murmur (30 % ).

• Asymmetry or absence of peripheral pulses or a pulse deﬁ cit (15–20 % ).

• Hypertension.

• Hypotension with features of tamponade or neurological signs in asso-

ciation with pain (eg secondary to spinal/carotid artery involvement).

Investigations

• Send blood for U&E, glucose, FBC, coagulation, and cross-matching.

• Obtain an ECG and CXR.

Thoracic aortic dissection usually results in an abnormal CXR. One or

more of the following changes may be seen:

• A widened or abnormal mediastinum (present in 875 % ).

• A ‘double knuckle’ aorta.

• Left pleural effusion ( 8 20 % ).

• Deviation of the trachea or nasogastric (NG) tube to the right.

• Separation of two parts of the wall of a calciﬁ ed aorta by > 5mm (the

‘calcium sign’).

The ECG may demonstrate MI, LVH. or ischaemia.

Note thatu 8 12 % of patients with aortic dissection have a normal CXR

and 8 30 % have a normal ECG.

CT angiography or formal angiography will provide the deﬁ nitive diagnosis.

In a haemodynamically unstable patient, trans-oesophageal echo in theatre

may be the investigation of choice.

Management

On suspicion of aortic dissection:

• Provide O

by face mask as appropriate.

• Insert 2 large-bore (14G) IV cannulae and cross-match for 6U (inform

blood bank of suspected diagnosis).

• Give IV morphine and titrate according to response ( ± anti-emetic).

• Call cardiothoracic team and cardiologist at an early stage.

• Insert an arterial line (preferably right radial artery) and discuss with

specialist teams how to control the BP (eg labetalol infusion).

• Arrange further investigation based upon specialist advice and available

resources (eg aortography, echocardiography, CT scan, MRI).

Type A dissections are usually treated surgically; type B lesions are usually

treated medically.

94 CHAPTER 3 Medicine

Haemoptysis

Haemoptysis may be the chief or sole complaint of patients presenting to

the ED. It always warrants investigation.

Causes of haemoptysis

Presentation

Ascertain the exact nature and volume (eg ‘bright red streaks’ or

‘dark brown granules’). Patients sometimes have surprising difﬁ culty

distinguishing vomited blood from that coughed up. Enquire about weight

loss, and take a drug history and smoking history.

Investigation

• Send blood for FBC, coagulation screen, U&E, LFTs.

• Request Group and Save if evidence of signiﬁ cant haemorrhage.

• If SpO

<94 % on air, or the patient has COPD, check ABG.

• Obtain CXR and ECG.

• Perform urinalysis — if shocked, insert catheter and monitor output.

• Collect sputum samples. Send for microscopy, culture, and sensitivity.

• Initiate further investigations according to the likely diagnosis.

Treatment

• Airway : clear and secure (coughing/suction). Put on a face mask and

shield if maintaining the airway or intubating. Ensure nearby high ﬂ ow

suction. Massive haemorrhage may require tracheal intubation. Whilst

preparing for this, tilt trolley so that the patient is head-down.

• Breathing : provide O

to maintain saturations at 94–98 % . If ventilation is

inadequate, assist with bag and mask or tracheal tube.

• Circulation : insert a large bore (14G) IV cannula (use 2 if hypovolaemic).

Give IV ﬂ uids/blood/clotting factors as clinically indicated ( b p.172).

Further treatment

Commence speciﬁ c treatment measures aimed at life-threatening

underlying cause (eg LVF, PE, infection, coagulopathy). In cases of large

haemoptysis, it is appropriate to admit for further investigation and treat-

ment. If the patient is stable and has only had a small amount of blood

stained sputum, urgent outpatient investigation may be appropriate.

Respiratory

• Infection (URTI, pneumonia, TB, lung abscess)

• Carcinoma (bronchial or laryngeal)

• Bronchiectasis

Cardiovascular

• Pulmonary oedema

• PE

• Ruptured aortic aneurysm (aorto-bronchial ﬁ stula)

Coagulation

disorder

• Drugs (eg warfarin, heparin)

• Inherited (eg Haemophilia, Christmas disease)

Trauma

• Penetrating or blunt

Other

• Goodpasture’s, Wegener’s granulomatosis

OXYGEN

Oxygen

Oxygen is the most commonly administered hospital therapy. In recent

years, high ﬂ ow oxygen was widely used in the treatment of medical

and surgical emergencies, and initial resuscitation. There is now a move

towards safer treatment with controlled oxygen therapy.

Common problems

• Failure to prescribe oxygen.

• Failure to check ABG in patients requiring oxygen therapy.

• Failure to monitor or review patients on oxygen therapy.

• Inadvertent administration of another gas other than oxygen.

• Inadvertent disconnection from the oxygen supply.

• Depletion of an oxygen tank during transfer ( www.nrls.npsa.nhs.uk ).

Oxygen cylinders

When administering oxygen in the ED, always use piped oxygen from the

wall outlet. Only use an oxygen cylinder when transporting the patient

to the radiology department or ward. Oxygen is highly ﬂ ammable. Do

not take a cylinder out of its support cage and never let it fall. In the UK,

oxygen cylinders are colour-coded white. The commonest small cylinder

is B (or M-6), which holds 170L oxygen. The commonest large cylinder is

E (or M-24), holding 680L. Before a patient leaves the ED, always check

that the cylinder is full. If the patient is being transferred to another hos-

pital, check there is enough oxygen for the journey. The formula is:

Volume of cylinder in L/ﬂ ow rate

minutes cylinder will last

Oxygen requirements

The aim of oxygen therapy is to optimize tissue oxygen delivery. Use pulse

oximetry to guide whether the patient requires supplemental oxygen. In

previously healthy patients, aim for SpO

94–98 % , but in patients with

known COPD or type II respiratory failure, aim for SpO

88–92 % . Always

take an ABG in patients with chronic lung disease, to assess their optimal

oxygen treatment (see b p.98 on ABG interpretation). Repeat the ABG

within 30 min after changing the inspired oxygen concentration. When

assessing a critically ill patient, it is appropriate to give high ﬂ ow oxygen

and to titrate the inspired oxygen concentration (FiO

) down according

to the ABG results.

Oxygen delivery

• Use a high concentration oxygen reservoir mask (non-rebreathing

mask) in hypoxic patients without chronic lung disease.

• Use a simple face mask for patients with a mild hypoxia, without chronic

lung disease.

• Use a 28 % Venturi mask for patients with COPD or known type II respi-

ratory failure.

• Use a tracheostomy mask for patients with tracheostomy.

Prescribing oxygen

The oxygen prescription should include the target SpO

, the oxygen mask

type and oxygen ﬂ ow rate. In an emergency, it is appropriate to administer

oxygen prior to prescribing, but do not forget to prescribe the oxygen

after resuscitation. See www.brit-thoracic.org.uk.

96 CHAPTER 3 Medicine

The dyspnoeic patient

The normal adult respiratory rate is 11–18/min, with a tidal volume of

400–800mL. Acute dyspnoea is a common presenting symptom.

Common causes of acute dyspnoea

Cardiac

• Cardiogenic pulmonary oedema ( b p.100).

• MI ( b p.68).

• PE ( b p.120).

• Arrhythmias ( b p.80).

Respiratory

• Asthma ( b p.104) or exacerbation of COPD ( b p.108).

• Pneumonia ( b p.110).

• Pleural effusion ( b p.103).

• Pneumothorax ( b p.114).

Trauma

• Aspiration of FB or vomit ( b p.112).

• Pneumothorax/haemothorax ( b p.334).

• Flail chest ( b p.332).

• Drowning incident ( b p.258).

Other

• Hypovolaemia or fever from any cause.

• Hyperventilation syndrome ( b p.97).

• Respiratory compensation for metabolic acidosis (DKA, salicylate over-

dose).

Approach

Follow the ABC approach and resuscitate as necessary. The main aim of

treatment is to correct life-threatening hypoxia. Enquire about speed of

onset of dyspnoea, past medical history and associated symptoms (cough,

haemoptysis, fever, wheezing, chest pain). Examine carefully, paying atten-

tion to the respiratory rate, depth, and pattern. Apply a pulse oximeter.

Pulse oximetry

This is simple, rapid, safe, and non-invasive, but it does not provide infor-

mation about ventilation or arterial partial pressure of carbon dioxide

(pCO

). A normal oxygen saturation does not exclude signiﬁ cant lung

pathology (eg PE). Pulse oximetry may be inaccurate or misleading in:

• Poor peripheral perfusion/shock.

• Methaemoglobinaemia.

• Hypothermia.

• CO poisoning (see b p.208). SpO

values may be falsely high as COHb

reads as oxyhaemoglobin. COHb can be measured on venous blood

gas testing or COHb pulse oximeter.

• Nail varnish/synthetic ﬁ ngernails (if a ﬁ nger probe is used).

• Excessive movement.

Correlate readings with clinical ﬁ ndings: a non-pulsatile trace (or heart

rate different from that on cardiac monitor) suggests the saturation

reading is probably inaccurate.

HYPERVENTILATION

Hyperventilation

Hyperventilation is breathing which occurs more deeply and/or more

rapidly than normal. CO

is ‘blown off ’, so that pCO

d . Hyperventilation

may be primary (‘psychogenic’) or secondary. A classical secondary cause

is DKA — Kussmaul’s respiration represents respiratory compensation for

a metabolic acidosis.

Secondary causes of hyperventilation

• Metabolic acidosis (eg DKA, uraemia, sepsis, hepatic failure).

• Poisoning (eg aspirin, methanol, CO, cyanide, ethylene glycol).

• Pain/hypoxia.

• Hypovolaemia.

• Respiratory disorders (eg PE, asthma, pneumothorax).

Primary (psychogenic or inappropriate) hyperventilation

Typically, the patient is agitated and distressed with a past history of panic

attacks or episodes of hyperventilation. They may complain of dizziness,

circumoral paraesthesia, carpopedal spasm, and occasionally sharp or

stabbing chest pain. Initial examination reveals tachypnoea with equal

air entry over both lung ﬁ elds, and no wheeze or evidence of airway

obstruction. It is important to consider secondary causes (such as PE or

DKA). Therefore, perform the following investigations:

• SpO

• ECG.

• ABG if SpO

d , or if symptoms do not completely settle in a few

minutes.

• BMG.

If symptoms do not completely settle in a few minutes, obtain:

• CXR.

• U&E, blood glucose, FBC.

Treatment

Do not sedate a patient who is hyperventilating. Once serious diagnoses

have been excluded, use this information to help reassure the patient with

primary hyperventilation. Often this is all that is required, but it may be

helpful to try simple breathing exercises (breathe in through nose — count

of 8, out through mouth — count of 8, hold for count of 4 and repeat).

Discharge the patient with arrangements for GP follow-up. If these simple

measures fail, reconsider the diagnosis and refer the patient to the medical

team for subsequent observation and treatment.

98 CHAPTER 3 Medicine

Arterial blood gases

Blood gas sampling is useful in assessing breathless patients, septic patients,

diabetic patients in ketoacidosis, those who are critically ill and patients

who have ingested poisons. This enables rapid measurement of blood pH,

bicarbonate, O

and CO

. Most ED blood gas analysers will also measure

blood glucose, K

, Hb, and lactate, so arterial or venous blood gas sampling

will also test for anaemia, hyperkalaemia, and hypoglycaemia.

Assessing respiratory function

Arterial sampling helps in the assessment of a patient with low SpO

or in patients with known lung disease (especially if they are receiving

supplemental oxygen). If possible (caution required), take the ﬁ rst sample

with the patient breathing room air. If this is not possible, document the

inspired oxygen concentration. Look speciﬁ cally for:

• Hypoxia, (pO

<10.6kPa on air).

• Hypercarbia, (pCO

> 6.0kPa).

• Bicarbonate retention (HCO

–

> 28mmol/L).

• Acidosis (pH <7.35).

Differentiating between type I and type II respiratory failure

In type I failure there is hypoxia with normal or d pCO

. In type II failure,

there is hypoxia with i pCO

, and frequently an i HCO

–

. In type II failure,

the patient may develop life-threatening respiratory failure if administered

high concentrations of oxygen. Aim to maintain SpO

at 88–92 % , and

recheck ABGs in 30min.

Differentiating between acute and chronic type II respiratory failure

Patients who normally have a slightly i pCO

will also show i HCO

–

on ABG. The kidneys adapt over a period of days to retain bicarbonate,

in attempt to buffer the respiratory acidosis (see nomogram inside front

cover). Respiratory acidosis in a patient with chronic type II respira-

tory failure ( i pCO

, i HCO

–

and pH <7.35) indicates life-threatening

impairment of lung function.

In acute respiratory failure, the lungs are unable to eliminate CO

(caused

by d GCS or hypoventilation from any cause), which results in i pCO

and

a respiratory acidosis. Patients may require ventilatory support.

A venous blood sample will give accurate readings for K

, lactate, glucose,

HCO

–

, Hb and COHb. In addition, a normal venous pCO

will exclude

hypercarbia.

Other blood gas results

Blood gas analysers calculate the base excess from the HCO

–

concentra-

tion and pH. Levels <–2mmol/L indicate that the patient has a metabolic

acidosis. Levels > 2mmol/L indicate a metabolic alkalosis (for example, as a

result of chronic bicarbonate retention in type II respiratory failure).

ARTERIAL BLOOD GASES

Metabolic acidosis

The usual pattern of results in metabolic acidosis is pH<7.35, HCO

–

<24mmol/L and BE <–2mmol/L. There may be compensatory hypocarbia

(pCO

<4.5kPa). Metabolic acidosis has many possible causes:

• i Acid load (lactic acidosis, ketoacidosis, or ingestion of salicylates,

methanol, ethylene glycol, or metformin).

• d Removal of acid (renal failure or renal tubular acidosis types 1 and 4).

• Loss of bicarbonate from the body (diarrhoea, pancreatic, or intestinal

ﬁ stulas, acetazolamide, or renal tubular acidosis type 2).

The anion gap

The anion gap is the quantity of anions not balanced out by cations,

(a measurement of negatively charged plasma proteins). The normal value

is 12–16mmol/L. It is measured by:

(Na

+ K

) – (Cl

–

+ HCO

–

) all measured in mmol/L

Measuring the anion gap helps distinguish the cause of a metabolic acidosis.

A high anion gap indicates that there is excess H

in the body. The

commonest cause of a high anion gap metabolic acidosis is lactic acidosis.

Most blood gas analysers will measure lactate (normal <2.0mmol/L).

Causes of a lactic acidosis

• Tissue hypoperfusion (trauma with major haemorrhage, septic shock).

• Tissue hypoxia (hypoxaemia, carbon monoxide or cyanide poisoning).

• Hepatic failure.

• Renal failure.

• Ethylene glycol or methanol poisoning ( b p.203; b p.202).

• Cocaine or amphetamines ( b p.215).

• Salicylate poisoning ( b p.189) or iron poisoning ( b p.201).

• Biguanides (metformin).

• Isoniazid.

• Strenuous exercise.

The other causes of a high anion gap metabolic acidosis are ketoacidosis

(diabetic or alcohol induced) and renal failure.

Causes of a normal anion gap metabolic acidosis are chronic diarrhoea,

pancreatic or intestinal ﬁ stulas, acetazolamide, or renal tubular acidosis.

The osmolal gap

This is the difference between calculated serum osmolarity and laboratory

measured serum osmolality. Serum osmolarity can be calculated by:

(2 × Na

) + urea + glucose (all measured in mmol/L)

Subtract the calculated result from the laboratory measured osmolality to

give the osmolal gap. Normally this is <10mOsm/kg.

An elevated osmolal gap can be caused by alcohol, methanol, ethylene

glycol or acetone ingestion, mannitol, or sorbitol.

100 CHAPTER 3 Medicine

Cardiogenic pulmonary oedema

Left heart failure results ine i left ventricular end-diastolic pressure, causing

i pulmonary capillary hydrostatic pressure. Fluid collects in extravascular

pulmonary tissues faster than the lymphatics clear it.

Causes of cardiogenic pulmonary oedema

Often an acute complication of MI and IHD, or exacerbation of pre-ex-

isting cardiac disease (eg hypertension, aortic/mitral valve disease). Other

causes are:

• Arrhythmias.

• Failure of prosthetic heart valve.

• Ventricular septal defect.

• Cardiomyopathy.

• Negatively inotropic drugs (eg B -blockers).

• Acute myocarditis.

• Left atrial (LA) myxoma (may produce syncope, fever, i ESR, but is very

rare).

• Pericardial disease.

The history is frequently dramatic. Dyspnoea and distress may prevent

a full history from being taken. Find out the length of the history and

whether there is any chest pain. Check current drug therapy/allergies and

establish what emergency prehospital treatment has been administered.

Examination usually reveals a tachypnoeic, tachycardic, and anxious

patient. If the pulmonary oedema is severe, the patient may be cyanosed,

coughing up frothy pink sputum and unable to talk. Check pulse and BP,

auscultate the heart for murmurs, and 3rd/4th heart sounds of gallop

rhythm. Look for i JVP (also a feature of PE and cardiac tamponade). Listen

to the lung ﬁ elds — ﬁ ne inspiratory crepitations (crackles) may be limited

to the bases or be widespread. Wheeze may be more prominent than

crepitations. Cardiogenic pulmonary oedema is associated with evidence

of d cardiac output (sweaty, peripherally cool, and pale). Consider other

diagnoses (eg sepsis) in patients with warm, ﬂ ushed extremities.

Investigation

Commence treatment before completing investigations:

• Attach a cardiac monitor and check SpO

with pulse oximeter.

• Obtain ECG. Check for arrhythmias, LAD, LVH, LBBB, recent or

evolving MI.

• Send blood for U&E, glucose, FBC, troponin.

• If severely ill or SpO

<94 % in air obtain ABG.

• Request old hospital notes/ECGs.

• Obtain a CXR and look for features of cardiogenic pulmonary oedema:

• upper lobe diversion (distension of upper pulmonary veins)

• cardiomegaly (LV and/or LA dilatation)

• Kerley A, B, or C septal lines

• ﬂ uid in interlobar ﬁ ssures

• peribronchial/perivascular cufﬁ ng and micronodules

• pleural effusions

• bat’s wing hilar shadows.

101

CARDIOGENIC PULMONARY OEDEMA

Treat urgently. Provide the following within the ﬁ rst few minutes:

• Check that the airway is clear.

• Raise the back of the trolley to sit the patient up and support with

pillows if necessary.

• Provide high ﬂ ow O

by tight-ﬁ tting face mask.

• If systolic BP > 90mmHg, give 2 puffs of GTN SL (800mcg) and com-

mence GTN IVI, starting at 10mcg/min, i every few minutes according

to clinical response (monitor BP closely; take special care to avoid

hypotension). Alternatively try buccal GTN (3–5mg).

• Give IV furosemide 50mg. Larger doses may be needed in patients

already taking oral furosemide.

• If the patient has chest pain or is distressed, give very small titrated

increments of IV opioid (with anti-emetic). Do not give opioids to

patients who are drowsy, confused. or exhausted as this may precipi-

tate respiratory arrest.

• Consider inserting a urinary catheter and monitor urine output.

• Treat underlying cause and associated problems (arrhythmias, MI,

cardiogenic shock, acute prosthetic valve failure).

Monitor the SpO

and the clinical response to this initial treatment. Rapid

improvement may occur, due to venodilatation and reduction of preload.

If the patient does not improve, recheck ABG and consider:

• Non-invasive ventilation (continuous positive airway pressure (CPAP)

or bilevel positive airway pressure (BiPAP). Non-invasive ventilation

(NIV) appears safe in acute cardiogenic pulmonary oedema and may

avoid the need for intubation.

• If hypotensive refer to ICU for treatment of cardiogenic shock ( b

p.77). An intra- arterial line, Swan–Ganz catheter and inotropic support

(dobutamine) are likely to be required. Echocardiography may help to

exclude valve or septal rupture and guide treatment.

• Rapid sequence intubation in the presence of cardiogenic pulmonary

oedema may be associated with cardiovascular collapse. Stop nitrates

prior to administering anaesthesia and be ready to give pressors

± ﬂ uids immediately post-induction.

Prosthetic valve failure

Always consider valve failure in patients with prosthetic valves, of which

a large variety are in common use. All are associated with some risks

(eg embolism, failure, obstruction, infection, haemorrhage from associated

anticoagulation), which vary according to design. Acute failure of a pros-

thetic aortic or mitral valve results in dramatic acute onset pulmonary

oedema with loud murmurs. The patient may deteriorate rapidly and not

respond to standard drug treatment. Resuscitate as described above. CXR

will show a prosthetic heart valve ± pulmonary oedema. Call urgently

for expert help (ICU team, cardiologist, and cardiothoracic surgeon).

Emergency transthoracic or transoesphageal echocardiography conﬁ rms

the diagnosis. Immediate valve replacement is required.

102 CHAPTER 3 Medicine

Non-cardiogenic pulmonary oedema

Pulmonary oedema may occur in the absence of i pulmonary venous

pressure. The following mechanisms may be responsible:

• i Capillary permeability.

• d Plasma oncotic pressure.

• i Lymphatic pressure.

Changes in capillary permeability, secondary to a variety of triggers, is

the mechanism most frequently implicated in non-cardiogenic pulmonary

oedema, when it occurs as the Adult Respiratory Distress Syndrome

(ARDS). Since the mechanisms producing cardiogenic and non-cardiogenic

pulmonary oedema differ, so the approach to treatment differs.

Causes of non-cardiogenic pulmonary oedema

• ARDS (sequel to sepsis, trauma, pancreatitis).

• Intracranial (especially subarachnoid) haemorrhage.

• IV ﬂ uid overload.

• Hypoalbuminaemia (liver failure, nephrotic syndrome).

• Drugs/poisons/chemical inhalation.

• Lymphangitis carcinomatosis.

• Smoke inhalation.

• Near drowning incidents.

• High altitude mountain sickness.

Approach

Distinguishing non-cardiogenic from cardiogenic pulmonary oedema is

usually apparent from the history. Evaluate the patient and resuscitate

according to ABCs. Direct treatment towards the underlying cause and

according to the physiological disturbance. To estimate the latter, invasive

monitoring may be required (urinary, intra-arterial, central venous and

pulmonary artery catheters). Involve ICU early and provide appropriate

IV ﬂ uids, inotropes, tracheal intubation, IPPV and positive end expiratory

pressure (PEEP) as required.

103

PLEURAL EFFUSION

Pleural effusion

Under normal circumstances, each pleural cavity contains <20mL ﬂ uid.

Causes

An exudate is diagnosed if the pleural ﬂ uid:serum protein > 0.5,

ﬂ uid:serum LDH > 0.6, or ﬂ uid LDH > 2/3 the upper limits of laboratory

normal value for serum LDH.

Exudates

• Pneumonia (bacterial, viral, mycoplasma).

• Malignancy (bronchial carcinoma, mesothelioma, lymphoma).

• TB.

• PE with pulmonary infarction.

• Collagen vascular disease (SLE, rheumatoid arthritis).

• Subphrenic abscess.

• Amoebic liver abscess.

• Pancreatitis.

• Chylothorax (thoracic duct injury — rare).

Transudates

• Cardiac failure.

• Nephrotic syndrome.

• Hepatic failure.

• Ovarian hyperstimulation.

• Ovarian ﬁ broma (Meig’s syndrome — rare).

• Peritoneal dialysis.

Clinical presentation

Symptoms are usually due to the underlying disease process. A mild dull

ache and dyspnoea (initially on exercise, later at rest) may occur if the

effusion is large. A history of vomiting followed by chest pain points to a

ruptured oesophagus — a surgical emergency.

Signs of an effusion are not apparent until > 500mL are present. Dyspnoea,

stony dullness to percussion, with absent breath sounds over the effusion are

characteristic. Bronchial breathing may be heard just above the effusion.

Very large unilateral effusions may produce evidence of mediastinal shift

(away from the collection of ﬂ uid).

Investigations

CXR can demonstrate pleural effusions as small as 250mL, as blunting of

the costophrenic angle. Other investigations depend on likely cause.

Treatment

Provide O

and resuscitate as necessary, according to the underlying

pathology. Emergency therapeutic pleural aspiration is rarely required in

the ED, except where haemothorax is suspected. Refer to the medical

team for further investigation (including ultrasound guided diagnostic

pleural aspiration).

104 CHAPTER 3 Medicine

Acute asthma: assessment

Follow the British Thoracic Society guidelines ( www.brit-thoracic.org.

uk ) to assess and manage adults presenting with asthma, b p.106. The

guidelines reﬂ ect continuing concern over asthma deaths. Patients with

severe asthma and one or more adverse psychosocial factors (psychiatric

illness, alcohol or drug abuse, unemployment) have i mortality. Measure

the peak expiratory ﬂ ow rate and compare it against that expected (see

Fig. 3.22 ). The peak ﬂ ow acts as an immediate triage tool: remember that

patients with life-threatening asthma may be too dyspnoeic to do this.

Make an initial assessment of the severity of acute asthma based upon

a combination of clinical features, peak ﬂ ow measurement and pulse

oximetry as outlined below.

Moderate exacerbation of asthma

• Increasing symptoms.

• Peak ﬂ ow 50–75 % best or predicted.

• No features of acute severe asthma (below).

Acute severe asthma

Any 1 of:

• Inability to complete sentences in 1 breath.

• Respiratory rate ≥25/min.

• Heart rate ≥110/min.

• Peak ﬂ ow 33–50 % best or predicted.

Life-threatening asthma

A patient with severe asthma with any 1 of:

• Cyanosis.

• Exhaustion, confusion, coma.

• Feeble respiratory effort.

• SpO

<92 % .

• Silent chest.

• Bradycardia, arrhythmia, hypotension.

• pO

<8kPa.

• Normal pCO

(4.6–6.0kPa).

• Peak ﬂ ow <33 % best or predicted.

Near fatal asthma

• i pCO

and/or requiring mechanical ventilation with i inﬂ ation

pressures.

Other investigations

Obtain ABG if SpO

<92 % or if there are other features of life-threatening

asthma.

Obtain a CXR (without delaying treatment) if there is:

• Suspected pneumomediastinum or pneumothorax.

• Suspected consolidation.

• Life-threatening asthma.

• Failure to respond to treatment satisfactorily.

• Requirement for ventilation.

105

ACUTE ASTHMA: ASSESSMENT

PEF L/min

660

650

640

630

620

610

600

590

580

570

560

550

540

530

520

510

500

490

480

470

460

450

440

430

420

410

400

390

380

Ht.

(ins)

190

Ht.

(cms)

183

175

MEN

167

160

145

152

160

167

175

Ht.

(cms)

Ht.

(ins)

IN MEN, VALUES OF PEF UP TO 100 LITRES/MIN, LESS THAN

PREDICTED, AND IN WOMEN LESS THAN 85 LITRES/MIN, LESS

THAN PREDICTED, ARE WITHIN NORMAL LIMITS.

15 20 25 30 35 40 45 50 55 60 65

AGE IN YEARS

STANDARD DEVIATION MEN

STANDARD DEVIATION WOMEN

48 = litres/min

42 = litres/min

660

650

640

630

620

610

600

590

580

570

560

550

540

530

520

510

500

490

480

470

460

450

440

430

420

410

400

390

380

WOMEN

Fig. 3.22 Peak expiratory ﬂ ow rates in normal adults.

Nunn AJ, Gregg I. (1989). New regression equations for predicting peak expiratory ﬂ ow in adults.

Br Med J 298 : 1068–70.

106 CHAPTER 3 Medicine

Acute asthma: management

Initial treatment

Follow BTS/SIGN guidelines ( www.brit-thoracic.org.uk ) summarized as

follows:

• Provide high ﬂ ow O

• Put the trolley back and side rails up so the patient is sitting up and

holding on to the side rails (to use pectoral muscles as accessory

muscles of respiration).

• If the patient cannot talk, start treatment, but get senior ED and ICU

help in case intubation and ventilation are required.

• Check trachea and chest signs for pneumothorax.

• Ask about previous admissions to ICU.

• Administer high dose nebulized B

agonist (eg salbutamol 5mg or terbu-

taline 10mg), or 10 puffs of salbutamol into spacer device and face mask.

For severe asthma or asthma that reponds poorly to the initial neb-

ulizer, consider continuous nebulization.

• Give a corticosteroid: either prednisolone 40–50mg PO or hydrocorti-

sone (preferably as sodium succinate) 100mg IV.

• Add nebulized ipratropium bromide (500mcg) to B

agonist treatment

for patients with acute severe or life-threatening asthma or those with a

poor initial response to B

agonist therapy.

• Consider a single dose of IV magnesium sulphate (1.2–2g IVI over 20min)

after consultation with senior medical staff, for patients with acute

severe asthma without a good initial response to inhaled bronchodi-

lator therapy or for those with life-threatening or near-fatal asthma.

• Use IV aminophylline only after consultation with senior medical staff.

Some individual patients with near-fatal or life-threatening asthma with a

poor response to initial therapy may gain additional beneﬁ t. The loading

dose of IVI aminophylline is 5mg/kg over 20min unless on maintenance

therapy, in which case check blood theophylline level and start IVI of

aminophylline at 0.5–0.7mg/kg/hr.

• IV salbutamol is an alternative in severe asthma, after consultation with

senior staff. Draw up 5mg salbutamol into 500mL 5 % dextrose and run

at a rate of 30–60mL/hr.

• A patient who cannot talk will be unable to drink ﬂ uids and may be

dehydrated.

• Avoid ‘routine’ antibiotics.

• Repeat ABG within an hour.

• Hypokalaemia may be caused or exacerbated by B

agonist and/or

steroid therapy.

107

ACUTE ASTHMA: MANAGEMENT

Criteria for admission

Admit patients with any features of

• A life-threatening or near-fatal attack.

• Severe attack persisting after initial treatment.

Management of discharge

Consider for discharge those patients whose peak ﬂ ow is > 75 % best or

predicted 1hr after initial treatment. Prescribe a short course of oral pred-

nisolone (eg 40–50mg for 5 days) if initial peak expiratory ﬂ ow rate (PEFR)

<50 % , and ensure adequate supply of inhalers. If possible arrange for

review by an asthma liaison nurse before discharge. At a minimum, inhaler

technique and peak expiratory ﬂ ow monitoring should be reviewed.

Arrange/advise GP/asthma liaison nurse follow-up within 2 days. Fax or email

the discharge summary to GP. Advise to return to hospital if symptoms

worsen/recur.

Referral to intensive care unit

Refer any patient requiring ventilatory support or with acute severe or

life-threatening asthma failing to respond to therapy, evidenced by:

• Drowsiness, confusion.

• Exhaustion, feeble respiration.

• Coma or respiratory arrest.

• Persisting or worsening hypoxia.

• Hypercapnoea.

• ABG showing d pH.

• Deteriorating peak ﬂ ow.

Cardiac arrest in acute asthma

The underlying rhythm is usually PEA. This may reﬂ ect one or more

of the following: prolonged severe hypoxia (secondary to severe

bronchospasm and mucous plugging), hypoxia-related arrhythmias or

tension pneumothorax (may be bilateral). Give advanced life support

according to the guidelines in b Cardiac arrest, p.46 and treat tension

pneumothorax if present ( b p.328). Aim to achieve tracheal intubation

early in view of the higher than normal required lung inﬂ ation pressures

and the attendant risk of gastric inﬂ ation in the absence of a tracheal tube.

108 CHAPTER 3 Medicine

COPD

Chronic obstructive pulmonary disease (COPD) is characterized by

chronic airﬂ ow limitation due to impedance to expiratory airﬂ ow, mucosal

oedema, infection, bronchospasm and bronchoconstriction due to d lung

elasticity. Smoking is the main cause, but others are chronic asthma, α-1

antitrypsin deﬁ ciency and chronic infection (eg bronchiectasis).

History

Exertional dyspnoea, cough, and sputum are usual complaints. Ask about:

• Present treatment including inhalers, steroids, antibiotics, theophyllines,

nebulizers, opiate analgesia, and home O

treatment.

• Past history: enquire about previous admissions and co-morbidity.

• Exercise tolerance: how far can they walk on the ﬂ at without stopping?

How many stairs can they climb? Do they get out of the house?

• Recent history: ask about wheeze and dyspnoea, sputum volume and

colour. Chest injuries, abdominal problems and other infections may

cause respiratory decompensation.

• Read the hospital notes: have there been prior ICU assessments? Has the

respiratory consultant advised whether ICU would be appropriate?

Examination

Examine for dyspnoea, tachypnoea, accessory muscle use, and lip-pursing.

Look for hyperinﬂ ation (‘barrel chest’) and listen for wheeze or coarse

crackles (large airway secretions). Cyanosis, plethora (due to secondary

polycythaemia) and right heart failure (cor pulmonale) suggest advanced

disease. Look for evidence of hypercarbia: tremor, bounding pulses,

peripheral vasodilatation, drowsiness, or confusion.

Check for evidence of other causes of acute dyspnoea, particularly: asthma

( b p.104), pulmonary oedema ( b p.100), pneumothorax ( b p.114), PE

( b p.120). Remember that these conditions may co-exist with COPD.

Investigations

• SpO

, respiratory rate, pulse rate, BP, T

, and peak ﬂ ow (if possible).

• CXR (look for pneumothorax, hyperinﬂ ation, bullae, and pneumonia).

• ECG.

• ABG (or capillary blood gas), documenting the FiO

. Use pCO

to guide

therapy.

• FBC, U&E, glucose, theophylline levels and, if pneumonia is suspected

and/or pyrexial, blood cultures, CRP, and pneumococcal antigen.

• Send sputum for microscopy and culture if purulent.

Treatment

Give O

— remember that hypercapnoea with O

is multifactorial. The aim

is to maintain SpO

88–92 % without precipitating respiratory acidosis or

worsening hypercapnoea (see b Oxygen, p.95 and b Arterial blood

gases, p.98). If the patient is known to have COPD and is drowsy or has

a documented history of previous hypercapnoeic respiratory failure, give

FiO

of 28 % via a Venturi mask and obtain ABG. Titrate up the FiO

with

serial ABG sampling until the minimum FiO

that achieves SpO

88–92 % .

Reduce inhaled oxygen concentration if SpO

> 92 % .

109

COPD

Give bronchodilators and steroids

• Give nebulized salbutamol 5mg or terbutaline 5–10mg.

• Consider adding nebulized ipratropium 0.5mg.

• Use O

driven nebulizers unless the patient has hypercapnoeic, acidotic

COPD, in which case use nebulizers driven by compressed air, supple-

mented by O

via nasal prongs at 1–4L/min.

• Give steroids (eg prednisolone 30mg PO stat or IV hydrocortisone

100mg).

Other drug treatments

• Give antibiotics (eg amoxicillin, tetracycline, or clarithromycin) if the

patient reports i purulent sputum, or there is clinical evidence of pneu-

monia and/or consolidation on CXR.

• Consider IV aminophylline or salbutamol if there is an inadequate

response to nebulized bronchodilators.

• Consider naloxone if the patient is taking an opioid analgesic that may

cause respiratory depression.

See NICE guideline on COPD, 2010 ( www.nice.org.uk ).

Non-invasive ventilation (NIV)

NIV is recommended as standard early therapy for hypercapnoeic ventila-

tory failure during exacerbations of COPD. NIV will improve the blood

gas measurements in the ED, d intubation rates, d mortality, and length

of hospital stay.

NIV takes two forms — CPAP and BiPAP, (which may be more suitable for

treating type II respiratory failure in COPD). Both CPAP and BiPAP have

been used to treat acute cardiogenic pulmonary oedema. Patients with

sleep apnoea use CPAP at night. The positive airway pressure is delivered

by a tightly adhered face mask, which is sized to ﬁ t the patient. The patient

is awake, and must be compliant with wearing the mask.

Unlike tracheal intubation, NIV does not protect the airway. Therefore,

contraindications include coma and vomiting. Absolute contraindications

include apnoea and cardiac arrest. A pneumothorax will be converted into

a tension pneuomthorax with NIV. Severe agitation may make effective

NIV impossible.

The patient should always be cared for by staff who are familiar with the

ventilator and mask, in the resuscitation room.

Start BiPAP at 10cmH

O inspiratory positive airway pressure (IPAP)/

5cmH

O expiratory positive airway pressure (EPAP), and titrate upwards:

• To treat persistent hypercapnoea, increase IPAP by 2cm at a time.

• To treat persistent hypoxia, increase IPAP and EPAP by 2cm at a time.

• The maximum IPAP/EPAP is 25/15cmH

• For CPAP, commence treatment at 5–8cmH

110 CHAPTER 3 Medicine

Pneumonia

Pneumonia involves symptoms and signs of lower respiratory tract

infection (breathlessness, productive cough, and fever) usually associated

with CXR abnormalities. Pneumocystis pneumonia may occur with minimal

or no CXR changes. Consider pneumonia in patients with septicaemia or

acute confusional states.

Causes

Bacterial (80–90 % ) Streptococcus pneumoniae is the commonest cause of

community-acquired pneumonia. Others include Mycoplasma pneumoniae ,

Haemophilus inﬂ uenzae , Legionella , Chlamydia psittaci , Staphylococcus

aureus (can cause fulminant pneumonia in patients with inﬂ uenza). Gram

–ve and anaerobic infections are rare. Always consider TB, particularly

in chronic alcoholism, poor social circumstances, immigrants and those

travelling to developing countries, or individuals not BCG vaccinated.

Immunosuppressed patients (eg HIV, steroid therapy) are at i risk of TB

and Pneumocystis jirovecii pneumonia.

Viral (10–20 % ) Predominantly inﬂ uenza A&B, respiratory synctal virus

(RSV), rarely varicella and severe acute respiratory syndrome (SARS).

Rickettsial (1 % ) Rarely, Coxiella burnetti .

Signs and symptoms

Fever, cough, and production of sputum are common complaints.

Breathlessness, pleuritic chest pain, myalgia, rigors, or haemoptysis may

occur. Pneumonia can present without obvious chest signs: Mycoplasma

pneumonia may present in children and young adults with sore throat,

headache, nausea, abdominal pain and diarrhoea. Legionella can present

with constitutional upset, diarrhoea or confusion, particularly in the

elderly. Pneumocystis pneumonia in immunosuppressed patients may

present with cough, dyspnoea, and marked hypoxia, with relatively few

other ﬁ ndings.

Examination and investigation

• Check respiratory rate, pulse, and BP.

• Auscultation may reveal a patch of inspiratory crackles, signs of consoli-

dation are present in <25 % .

• Check BMG, SpO

(obtain ABG if <94 % , or known to have COPD).

• Assess for signs of SIRS (2 or more of RR > 20, HR > 90, temp > 38.3

or <36.0

C, WCC<4 or > 12 × 10

/L, confusion, glucose > 8.3mmol/L),

which in combination with signs of pneumonia signify sepsis.

• Assess for signs of severe sepsis (sepsis + signs of organ dysfunction

b p.59). Oxygen dependence, poor urine output, systolic BP<90mmHg,

blood lactate > 3mmol/L. Commence ﬂ uid resuscitation immediately if

present, take blood cultures and give IV antibiotics.

• Obtain CXR. Look for patchy or lobar opaciﬁ cation, mass lesions, or an

air bronchogram. In early pneumonia the CXR may be normal.

• Obtain blood cultures, sputum cultures, and consider urinary pneumo-

coccal and Legionella antigen testing.

111

PNEUMONIA

Assessment: admit or discharge

Some patients with ‘mild’ illness, good social circumstances, and no signiﬁ -

cant co-morbidity may be safely discharged with appropriate antibiotics

(eg amoxicillin 0.5–1g PO tds), simple analgesia for pleuritic pain to aid

deep breathing/coughing and GP follow-up.

Patients with CURB-65 score ≥3 have severe pneumonia with a high risk of

death; those who score 2 are at i risk of death and should be considered

for inpatient treatment or hospital-supervised outpatient care; patients

with CURB-65 score 0 or 1 are at low risk of death and may be suitable

for home treatment ( www.brit-thoracic.org.uk ; see Table 3.4 ).

Treatment

Patients deemed suitable for discharge

Provide simple analgesia, oral antibiotics, and GP follow-up.

Patients admitted, but not severely unwell

Start either oral or IV antibiotics, as follows:

• Either amoxicillin 0.5–1g PO tds + erythromycin 500mg PO qds (or

clarithromycin 500mg bd).

• Or if IV therapy is needed: ampicillin 500mg IV qds + erythromycin

500mg IV qds (or clarithromycin 500mg bd). Local guidelines will apply.

• Monitor SpO

and provide O

accordingly.

• Provide simple analgesia.

Patients with sepsis or severe sepsis (see b p.59)

Commence IV crystalloid ﬂ uids, take blood cultures and administer IV

antibiotics (eg co-amoxiclav 1.2g IV tds + clarithromycin 500mg IV bd)

immediately. Contact ICU and make preparations for arterial line, central

line and urinary catheter insertion. Aim for CVP > 8mmHg, MAP > 65mmHg

and urine output > 0.5mg/kg/hr. See severe sepsis guidelines ( www.

surviving sepsis.org ).

Differential diagnosis

Pneumonia-like presentations can occur with pulmonary oedema,

pulmonary infarction, pulmonary vasculitis (eg SLE, PAN, Churg–Strauss

and Wegener’s), aspergillosis, allergic alveolitis, bronchial or alveolar cell

carcinoma, acute pancreatitis, and subphrenic abscess.

Table 3.4

CURB-65 score for pneumonia Score

Confusion 1

Urea > 7mmol/L 1

Respiratory rate ≥30/min

Low BP (systolic <90mmHg or diastolic ≤60mmHg)

Age ≥65 years

112 CHAPTER 3 Medicine

Pulmonary aspiration

Aspiration of solid or liquid material into the upper and lower airways is

likely when one or more of the following features are present:

• d GCS : head injury, stroke, overdose, seizures, sedation, anaesthesia.

• d Cough and/or gag reﬂ exes : related to above factors and/or bulbar

dysfunction, intubation/extubation, Guillain–Barré syndrome, multiple

sclerosis, myasthenia gravis.

• Tendency to regurgitate/vomit: alcohol, full stomach, upper GI tract

pathology (including hiatus hernia, oesophageal obstruction, pregnancy).

• May occur in inﬁ rm or elderly fed via nasogastric tube.

Clinical features

Large food particles sufﬁ cient to cause complete airway obstruction

cause choking, inability to speak, i respiratory effort, cyanosis, loss of

consciousness, and death. Smaller particles may pass through the vocal

cords causing coughing, stridor, tachypnoea, and wheeze. 80 % of patients

are aged <4 years, with peanuts being the classic inhaled objects. Delayed

presentation with cough, wheeze, haemoptysis, unresolved pneumonia,

abscess formation, or empyema occurs in 830 % often days or weeks later.

Vomiting/regurgitation is often witnessed and pulmonary aspiration

conﬁ rmed by seeing gastric contents in the oropharynx or trachea during

intubation or following suction. Gastric content is a mixture of semi-

solid and liquid material — aspiration leads to a sudden onset of severe

dypsnoea, wheeze, and cyanosis. Its acid nature causes severe damage

to the alveolar-capillary membrane, with denaturation of pulmonary

surfactant, i pulmonary permeability with oedema and atelectasis.

Hydrocarbons (eg petrol, parafﬁ n) cause severe pulmonary toxicity if

aspiration occurs during ingestion or following regurgitation/vomiting.

Investigations

ABG

These show hypoxaemia within minutes of acid aspiration. Initially, patients

may hyperventilate with d pCO

until pulmonary compliance i work of

breathing sufﬁ cient to result in hypoventilation.

CXR

Abnormalities develop in > 90 % of patients, but may take hours/days.

Appearances depend on the nature of the aspirated material and the

patient’s position at the time of the episode (right lower lobe is most

frequently and severely affected, followed by left lower lobe and right middle

lobe). In severe aspiration, diffuse bilateral inﬁ ltrates and pulmonary

oedema similar to ARDS appearances are present. Less severe episodes

produce atelectasis followed by alveolar inﬁ ltration.

Intrapulmonary foreign body (including peanuts)

Rarely radio-opaque. Resulting collapse, hyperinﬂ ation, or consolidation

is usually obvious and depends on whether obstruction is complete or

partial and if supervening infection is present. If the history strongly sug-

gests an inhaled FB, but CXR is normal, consider an expiratory CXR,

which may show evidence of air trapping distal to the obstruction.

113

PULMONARY ASPIRATION

Prevention

Prevention is everything. Pay meticulous attention to airway protection.

This may involve positioning (tilt head down on the right hand side),

suction to the oropharynx (Yankauer catheter avoiding stimulation of the

gag reﬂ ex) and if necessary, tracheal intubation. Tracheal intubation does

not completely protect against aspiration of ﬂ uid into the lungs, but it is

the best preventative measure. In at-risk patients, pass an NG tube to

empty the stomach. However, NG tubes can also predispose to aspiration

by preventing closure of the oesophageal sphincters and interfering with

coughing and clearing the pharynx.

Treatment

Correct hypoxia and give nebulized salbutamol for associated bronchospasm.

If particulate aspiration is present, refer for urgent bronchoscopy. Although

secondary infection is common, the use of antibiotics or steroids is not

routinely indicated.

114 CHAPTER 3 Medicine

Spontaneous pneumothorax

Primary spontaneous pneumothorax (PSP) may occur in previously

healthy individuals. Secondary spontaneous pneumothorax (SSP) occurs

in older patients with pre-existing chronic lung disease (like COPD or TB)

and may also occur with asthma, bronchial carcinoma, Marfan’s syndrome,

infection, cystic ﬁ brosis, and oesophageal rupture.

Presentation

Most patients present with unilateral pleuritic chest pain and dyspnoea.

Classical physical signs may not be present (depending upon the size of

the pneumothorax): tachypnoea, tachycardia, normal/hyper-resonant per-

cussion note withe d air entry on the affected side. Rarely, there may be a

clicking sound at the cardiac apex.

Severe symptoms (inability to speak, gasping, low SpO

) should prompt

rapid assessment for tension pneumothorax: tracheal deviation,

tachypnoea, tachycardia, and hypotension. Treat tension with immediate

decompression using a needle in the second intercostal space (just above

the third rib) in the mid-clavicular line ( b p.328). Severe symptoms are

also found in patients with SSP (disproportionate to the pneumothorax

size). In the absence of signs of tension pneumothorax, obtain an

emergency portable CXR and involve an experienced doctor.

Investigation and treatment

• Monitor pulse, SpO

, and BP. Ensure IV access.

• Administer high ﬂ ow oxygen (aim SpO

90–92 % in patients with

COPD).

• When there are no signs of tension, an ABG will help assess patients

with chronic lung disease, and guide oxygen therapy.

Erect CXR

• When using digital images, always use a picture archiving and communi-

cation system (PACS) workstation. The signs of pneumothorax may be

subtle and difﬁ cult to spot.

• Look for a displacement of the pleural line.

• Do not mistake the scapular edge for the lung edge.

• Some patients with COPD have emphysematous bullae, which can

mimic pneumothorax. If in doubt, ask for senior review prior to treating

for pneumothorax.

• An air ﬂ uid level at the costophrenic angle may be present.

CT scan

Can be of use in the sub-acute setting for assessing bullous lung disease in

a stable patient. CT is not a primary diagnostic modality.

Intervention

• Should be guided primarily by the patient’s symptoms. If the patient is

breathless, they should undergo an intervention.

• The size of the pneumothorax can be estimated on CXR by measuring

from the chest wall to the lung edge at the level of the hilum. This is

115

SPONTANEOUS PNEUMOTHORAX

only an estimate and assumes symmetrical lung collapse. The cut-off of

2cm is used to determine treatment.

• Intervention for PSP is needle aspiration. If unsuccessful, do not repeat

aspiration. Instead insert a Seldinger chest drain.

• Treatment for symptomatic SSP is chest drain insertion and admission.

• Treatment for SSP without breathlessness is admission. Aspiration

should be performed by an experienced doctor and may require CT.

• Always insert chest drains for bilateral pneumothoraces.

• Always insert a chest drain immediately following emergency needle

decompression.

• Pleural aspiration and drain insertion should be performed by a doctor

who has prior training and experience.

• Ensure the patient has IV access. Perform in a monitored environment

with an assistant and appropriate supervision. Use aseptic technique.

• Always discuss the procedure with the patient and document that they

have given their consent.

• If the patient is on anticoagulation or has a known coagulopathy dis-

order, discuss with a haemotologist ﬁ rst.

Aspiration technique

Conﬁ rm the side of the pneumothorax. Sit the patient upright. Inﬁ ltrate 1 %

lidocaine, then insert a 16G IV cannula just above the 3rd rib (in the 2nd

intercostal space) in the mid-clavicular line. Alternatively, lay the patient on

their side with the pneumothorax side upwards. Insert cannula in the 5

intercostal space, in the anterior axillary line. Remove the needle, attach a

three-way tap, then aspirate air with a 50mL syringe. Continue aspiration

until the patient coughs excessively, or until 2.5L of air is removed.

Seldinger chest drain insertion

Conﬁ rm the side of the pneumothorax. Keep the patient comfortable,

ensure adequate analgesia (this may require 1mg increments of morphine IV),

but avoid sedation. Sit the patient upright and rest their hand behind their

head. Inﬁ ltrate 10mL 1 % lidocaine at the anterior axillary line in the 5th inter-

costal space. Aspirate a small amount of pleural air during inﬁ ltration and

note the depth of the pleural space. Locate the pleural space with the intro-

ducer needle (aspirate while advancing through chest wall), then advance the

guidewire through the needle. Remove the introducer needle, make a small

skin incision and gently pass the dilator over the guidewire using a twisting

action. Do not push the dilator more than 1cm past the depth of the pleural

space. Pass the chest drain over the guide wire to a depth of 10–12cm.

Remove the guide wire, connect to an underwater seal drain and suture in

pace. Check the drain is bubbling and swinging, and organize a CXR.

Discharge

Patients without breathlessness, with small PSP may be considered for

discharge. Give the patient verbal and written instructions to return if

their symptoms worsen and warn them not to ﬂ y. Ensure they have an

appointment with a respiratory physician in the next week.

See http://www.brit-thoracic.org.uk

116 CHAPTER 3 Medicine

YES

YES*

YES

Spontaneous pneumothorax

If bilateral/haemodynamically unstable

proceed to chest drain

Age >50 and significant

smoking history

evidence of underlying

lung disease on exam or

CXR?

Secondary

pneumothorax

>2 cm or

breathless

Size

1–2 cm

Admit

high flow oxygen (unless suspected

oxygen sensitive)

observe for 24 hours

Primary

pneumothorax

Size >2 cm

and/or

breathless

Aspirate

16–18G cannula

aspirate <2.5L

Consider discharge

review in OPD in 2–4

weeks

Success

(<2 cm and

breathing

improved)

*In some patients with a large

pneumothorax but minimal

symptoms conservative

management may be

appropriate

Chest drain

Size 8–14Fr

admit

Aspirate

16–18G cannula

aspirate <2.5L

Success

size

now <1 cm

Fig. 3.23 Management of pneumothorax.

1 Thorax 2010; 65 (Suppl 2): ii18eii31. doi:10.1136/thx.2010.136986.

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118 CHAPTER 3 Medicine

Deep venous thrombosis

DVT and PE are manifestations of the same disease process whereby

abnormal clotting occurs in the veins of the legs or pelvis. The clots may

break from the vein wall and embolize to the lungs. Untreated DVTs are

associated with a 1–2 % mortality from PE. Around half of those with DVT

will go on to develop post-thrombotic syndrome, with lifelong pain and

swelling of the leg.

Risk factors

• Recent surgery (where a general anaesthetic was administered, espe-

cially orthopaedic, abdominal, spinal and obstetric).

• Recent admission to hospital.

• Current malignancy.

• Being bedbound.

• Sepsis.

• IV drug use (where patient injects in the femoral vein).

• Pregnancy/pelvic masses.

• Immobility such as recent fracture with crutches and plaster cast.

• Previous DVT/PE.

• Thrombophilia or family history of venous thromboembolism.

Clinical features

DVT classically produces leg pain with swelling, warmth, tenderness, and

dilated superﬁ cial veins in the affected leg. These signs are non-speciﬁ c

and often not present. A small or partially occluding thrombus may be

completely asymptomatic. History and clinical examination alone cannot

safely exclude DVT — if a DVT is suspected, investigate further. Investigate

for PE, rather than DVT if the patient has tachycardia, hypoxia, increased

respiratory rate, or breathlessness ( b Pulmonary embolus, p.120).

Differential diagnosis

• Muscular tear: typically acute onset.

• Rupture of a Baker’s cyst: again, typically acute onset.

• Cellulitis or other infection.

Investigation and management

• Record pulse rate, RR, BP, SpO

, and T ° in all patients.

• Take a full history including concurrent illness, past history, recent

operations, travel, and family history.

• Examine the affected leg for signs of plethora, deep vein tenderness,

swelling (measure both legs, 10cm distal to tibial tuberosity), oedema

and dilation of the skin veins.

• Perform full examination checking for signs of PE or occult carcinoma.

• Calculate the clinical probability assessment score. The Wells score

(Table 3.5 ) is the most widely used clinical prediction score.

• Take FBC, U&E, CRP, glucose.

• Take D-dimer if Wells score indicates DVT is ‘unlikely’ (<3 points).

• If D-dimer normal and DVT ‘unlikely’, DVT has been ruled out.

119

DEEP VENOUS THROMBOSIS

The Wells score was not developed with injecting drug users or pregnant

women, both of whom are at higher risk of DVT. These patients should

always undergo ultrasound scanning.

All patients investigated for DVT with a ‘likely’ Wells score ( ≥ 3) or an

elevated D-dimer level require ultrasound scanning. A normal whole leg

ultrasound scan (femoral, popliteal, and calf vein scan) will exclude DVT. If

a thigh scan is performed (the femoral and popliteal veins), DVT can only

be excluded by two normal thigh ultrasound scans, one week apart.

All patients with a ‘likely’ score should be anticoagulated with LMWH

while awaiting an outpatient ultrasound scan.

Patients diagnosed with calf or thigh DVT should be treated with

LMWH and discharged with a week’s supply, an appointment for the

anticoagulation services, and medical outpatient follow-up. Advise them

to return immediately if they become breathless or have chest pain.

Upper limb DVT

Seen almost exclusively in patients with in-dwelling central or long lines,

often for chemotherapy. May be associated with plethora and swelling of

the arm or face. If suspected, request an ultrasound of the arm and neck

veins, or a CT scan with contrast.

Superﬁ cial thrombophlebitis

Patients present with a painful, tender area of skin. The diagnosis is made

clinically with a ﬁ rm, tender superﬁ cial vein, and overlying erythema. This

may co-exist with DVT and superﬁ cial thrombus may propagate into

deep veins. If there is any doubt as to the presence of a DVT, investigate

using the DVT protocol. Otherwise, treat with NSAID. Arrange follow up

either in the ED, a medical clinic or with the GP.

Table 3.5 Wells clinical probability assessment score for DVT

Clinical feature Score

Active cancer (treatment within 6 months or palliative care) 1

Paralysis, paresis, or recent POP immobilization of a leg 1

Recently bedridden for > 3 days or major surgery <12 weeks 1

Localized tenderness along the distribution of the deep venous system 1

Entire leg swelling 1

Calf swelling > 3cm compared with asymptomatic leg 1

Pitting oedema (greater in the symptomatic leg) 1

Dilated superﬁ cial veins (non-varicose) 1

Previously documented DVT 1

Another diagnosis more likely than DVT -2

Total score < 3 means DVT is ‘unlikely’. Score of 3 or more signiﬁ es DVT is ‘likely’.

120 CHAPTER 3 Medicine

Pulmonary embolism

The mortality of diagnosed and treated pulmonary embolism is 7 % . Many

more people die from undiagnosed PE. Venous thromboembolism develops

in patients already suffering from sepsis, cancer, or COPD or in patients

recovering from stroke, MI, surgery, and joint replacement. Pulmonary

embolic disease can result in a variety of symptoms often misdiagnosed as

asthma, anxiety, pneumonia and ACS.

History

Most patients with PE experience dyspnoea, commonly without other

symptoms. Syncope with cyanosis, cardiac arrest or angina are signs

of massive PE. A minority present with pleuritic chest pain, some with

additional haemoptysis. Always consider PE in patients with unexplained

hypoxia or breathlessness. Take a full history of concurrent illness, surgical

procedures, recent hospital admission, past history including DVT and PE,

travel and family history.

Examination

Examination may be normal.

• Tachycardia and tachypnoea are common.

• Pyrexia following lung infarction is common.

• 30 % of all patients with PE have normal SpO

• Always record BP. Hypotension indicates massive PE.

• Perform a full respiratory and cardiovascular examination.

• Always examine the legs for signs of DVT.

Any patient scoring 2.0 or more on the Wells score, OR who has an

elevated D-dimer, requires pulmonary imaging. Note that a normal

D-dimer will not exclude PE in a patient with moderate or high probability

of PE. Only a normal D-dimer and a low clinical probability will safely

exclude PE.

Table 3.6 Modiﬁ ed Wells clinical probability assessment score for PE

Clinical feature Score

Signs of DVT (minimum of objective leg swelling and tenderness) 3.0

IV drug use 3.0

PE is the most likely diagnosis 3.0

HR > 100 1.5

Prior PE or DVT diagnosis 1.5

Bed ridden for > 3 days or surgery, within the past 4 weeks 1.5

Cancer (treated actively or with palliation within last 6 months) 1.0

Haemoptysis 1.0

Total score <2.0 = low risk PE, 2.0–6.0 = moderate risk PE, > 6.0 = high risk PE.

121

PULMONARY EMBOLISM

Investigations for suspected pulmonary embolus

• If hypoxic, tachycardic, or hypotensive, insert an IV cannula.

• All patients should have blood taken for FBC and U&Es.

• Take a D-dimer test on any patient who scores <2.0 on the Wells score

(Table 3.6 ). Normal D-dimer in a patient scoring <2.0 excludes PE.

• Arrange ECG (to look for MI or pericarditis) and CXR (to look for

pneumothorax, pneumonia). Many patients with PE have a normal ECG

and CXR.

Diagnostic imaging for pulmonary embolus

There are two forms of imaging for PE: CT pulmonary angiography

(CTPA) and ventilation-perfusion (V/Q) scanning. CTPA uses a higher

dose of radiation (not good for young patients or pregnant patients), but

will give a deﬁ nitive answer, as well as diagnose other conditions often

confused with PE (like aortic dissection).

V/Q scanning uses a low dose of radiation (good for the young and

pregnant), but may not give a deﬁ nitive answer. V/Q scans are reported

as low, intermediate and high probability of PE. The V/Q scan probability

must concord with the clinical probability to diagnose or exclude PE (both

low probability or both high probability). All other combinations are

non-diagnostic and the patient must have a CTPA.

Pitfalls in diagnosis

• Investigating for PE because the patient has an elevated D-dimer. The

D-dimer is irrelevant if there are no clinical symptoms or signs of PE.

• Deciding not to take the D-dimer because the patient is post-surgery,

elderly, or has had recent trauma. If the Wells score is <2.0, a D-dimer

test is rapid and may avoid admission for diagnostic imaging if normal.

Treatment of pulmonary embolus

Anticoagulate with LMWH and arrange to commence the patient on

warfarin therapy. If the patient is ambulant, not hypoxic with a normal

pulse rate and RR, many hospitals commence warfarin and follow-up as

an outpatient. Admit patients who are hypoxic, hypotensive, tachycardic,

tachypnoeic, or elderly for further management.

Suspected massive PE

• In patients with marked hypoxia and/or cardiovascular compromise, call

for urgent ICU expert help.

• If available, an emergency echo will demonstrate a dilated right ventricle

and right heart failure.

• Do not take unstable patients for a CT or V/Q.

• If suspicion of PE is high and the patient is haemodynamically unstable,

administer thrombolytic therapy. Do not delay. Administer alteplase

(rTPA) 100mg over 2 hr or 0.6mg/kg (max 50mg) over 15min as per

European Cardiology guidelines ( www.escardio.org ).

122 CHAPTER 3 Medicine

Upper gastrointestinal bleeding

Causes of upper gastrointestinal bleeding

Common

• Peptic ulceration.

• Mucosal inﬂ ammation (oesophagitis, gastritis, or duodenitis).

• Oesophageal varices.

• Mallory–Weiss tear.

• Gastric carcinoma.

• Coagulation disorders (thrombocytopenia, warfarin).

Rare

• Aorto-enteric ﬁ stula (especially after aortic surgery).

• Benign tumours (eg leiomyomas, carcinoid tumours, angiomas).

• Congenital (eg Ehlers–Danlos, Osler–Weber–Rendu, pseudoxanthoma

elasticum).

History

Take a detailed history, whilst resuscitating as necessary. Upper GI

bleeding usually presents with haematemesis and/or melaena. Major upper

GI bleeding may present with fresh PR bleeding.

Ask about the amount and duration of bleeding, any past history of GI

bleeding or liver problems, and associated symptoms (abdominal pain,

weight loss, anorexia). Syncope usually infers a signiﬁ cant bleed. Take a

full drug history (ask about aspirin, NSAIDs, warfarin, iron) and enquire

about alcohol consumption.

Examination

Check ABCs. Rapidly assess for evidence of hypovolaemic shock (pulse

and respiratory rates, BP, GCS, skin colour/temperature, capillary reﬁ ll).

Look at any available vomit or faeces. Check for abdominal masses,

tenderness or surgical scars (including aortic grafting). Look for stigmata

of liver disease. Perform a PR examination and check for faecal occult

blood (FOB).

Investigation and diagnosis

Request old hospital notes and send blood for FBC, clotting screen, U&E,

blood glucose, Group and Save or cross-matching (according to clinical

features). Urea may be i , but creatinine will be normal unless renal

function is impaired. Check SpO

(obtain ABG if <94 % ) and consider CXR

and ECG. Endoscopy is the investigation of choice to identify the source

of the bleeding.

Risk of further bleeding and death

The risk of mortality and further complications increases with increasing age,

co-morbidities (especially cancer and heart failure), liver disease, continued

bleeding, elevated urea, and passage of PR blood.

123

UPPER GASTROINTESTINAL BLEEDING

Only consider patients scoring 0 on the initial Rockall score (Table 3.7 ),

with no further evidence of bleeding, for discharge home from the ED

with follow-up. Any patient scoring > 0 requires urgent endoscopy.

Treatment of moderate/severe haemorrhage

• Check airway and breathing. Provide O

to maintain SpO

94–98 % .

Insert 2 large (14G) IV cannulae, send FBC, U&E, clotting, cross-match.

• Start IV ﬂ uids followed by blood as necessary.

• Avoid omeprazole acutely unless the patient has known peptic ulcer

disease (give 40mg diluted in 100mL saline as IVI over 30min).

• If the patient is anticoagulated, or has a clotting disorder (eg due to

liver disease), discuss with a haematologist and give vitamin K/clotting

factors/fresh frozen plasma (FFP) accordingly.

• Insert a urinary catheter and monitor the urine output.

• Ensure that patients with severe uncontrolled variceal bleeding, severe

encephalopathy, hypoxia, acute agitation, or evidence of aspiration have

their airways secured, if necessary by tracheal intubation.

Managing severe haemorrhage possibly due to varices

For unstable patients with a past history of varices or clinical features of

hepatic failure, arrange emergency endoscopic treatment:

• Commence ﬂ uid rescucitation.

• Give terlipressin (2mg IV repeated every 4–6hr).

• Check International Normalized Ratio (INR) and give IV vitamin K if

prolonged.

• Give prophylactic antibiotics eg ciproﬂ oxacin or second/third generation

cephalosporin which may d mortality in severe haemorrhage.

• Consider ballon tamponade as a salvage procedure in a patient with

massive haemorrhage, at risk of death. If experienced in the technique,

insert a 4 lumen Sengstaken/Minnesota tube. Inﬂ ate the gastric balloon

then the oesophageal balloon to a pressure of 30–40mmHg in order to

tamponade the bleeding varices. Regularly aspirate both ports.

See http://www.sign.ac.uk

Table 3.7 Initial Rockall Score for risk of death in upper GI bleeding

Points 0 1 2 3

Age <60 60–79 > 80

Shock HR<100

Systolic

BP > 100mmHg

HR > 100

Systolic

BP > 100mmHg

Systolic

BP<100mmHg

Comorbidity Cardiac failure,

ischaemic heart

disease or

any major

co-morbidity

Renal failure

Liver failure

Disseminated

malignancy

Any score > 0 signiﬁ es increased risk of mortality.

124 CHAPTER 3 Medicine

Lower gastrointestinal bleeding

The commonest cause of apparent lower GI bleeding is upper GI haem-

orrhage. 820 % of acute GI haemorrhage is from the colon or rectum.

Angiodysplasia and bleeding from diverticulae are the most frequent

causes, but inﬂ ammatory bowel disease or, very rarely, aorto-enteric ﬁ stulae

may be responsible. Lower GI haemorrhage often settles spontaneously:

localization of the bleeding source may be difﬁ cult.

History

Nature of bleeding Melaena may occur following small bowel or proximal

colon bleeding, as well as upper GI haemorrhage. Conversely, large

volumes of fresh or ‘plum-coloured’ rectal bleeding may follow upper GI

haemorrhage. Bloody diarrhoea suggests inﬂ ammatory bowel disease or

infective colitis.

Associated symptoms Weight loss, anorexia, or a change in bowel habit

raise suspicion of colonic carcinoma. Abdominal pain may be a feature

of ischaemic colitis, inﬂ ammatory bowel disease, or carcinoma. Anal pain

commonly occurs with anal ﬁ ssure or complication of haemorrhoids.

Syncope or postural dizziness May indicate signiﬁ cant haemorrhage.

Past medical history Ask about inﬂ ammatory bowel disease, peptic

ulceration, or other illnesses. Previous aortic surgery with graft insertion

can rarely result in formation of an aorto-enteric ﬁ stula (symptoms

include sporadic or fulminant bleeding, often with syncope).

Drug history Ask about salicylates, NSAIDs, corticosteroids, and

anticoagulants.

Family and social history Note any family history of peptic ulcers,

inﬂ ammatory bowel disease. Enquire about alcohol consumption.

Examination

First assess for signs of hypovolaemia and commence resuscitation if nec-

essary. Document pulse, BP (comparing erect and supine, noting any pos-

tural drop), T ° and SpO

. Examine the abdomen and PR in all cases.

Investigations

Obtain blood for cross-matching (ask for 4–6U of type speciﬁ c if urgent),

FBC, U&E, glucose, and coagulation studies. Perform an ECG on any

patient > 50 years.

Risk of further bleeding and death

The risk of mortality and further complications increases with increasing

age, co-morbidities, haemodynamic disturbance, and the use of NSAIDs or

aspirin. Only consider discharge if the patient is young, otherwise healthy,

has passed only a small amount of blood PR, and does not take NSAIDs

or anticoagulants. Always arrange follow up for these patients.

125

LOWER GASTROINTESTINAL BLEEDING

Treatment

Patients with signs of hypovolaemia require immediate resuscitation:

• Give O

• Attach monitoring (cardiac monitor, S pO

, BP monitoring).

• Insert two large bore IV cannulae.

• Give 1L of 0.9 % saline or Hartmann’s solution IV stat and give further

ﬂ uids according to response.

• Insert a NG tube.

• Insert a urinary catheter.

• Correct any coagulopathy.

• Consider the need for a central venous line.

• Contact the surgical team and ICU.

See http://www.sign.ac.uk

126 CHAPTER 3 Medicine

Headache

Headaches of non-traumatic origin account for 8 0.5 % of ED attendances;

10–15 % have serious underlying pathology. Patients typically present in

one of three ways:

• Severe headache, unlike any previous one (‘ﬁ rst severe’ or ‘worst

ever’).

• Headache with associated worrying features (altered mental status,

fever, focal neurology).

• Chronic severe headache unresponsive to treatment.

Causes

Primary headaches

• Migraine.

• Tension headaches.

• Cluster headaches.

• Miscellaneous (benign cough headache, benign exertional headache,

headache associated with sexual activity).

Secondary headaches

• Head injury.

• Vascular (stroke, intracranial haematoma, subarachnoid haemorrhage,

unruptured arterio-venous malformation, venous thrombosis, hyper-

tension).

• Non-vascular intracranial disorder ( i cerebrospinal ﬂ uid (CSF) pres-

sure, post-LP, intracranial tumour).

• Substance misuse or withdrawal (including analgesia withdrawal or

rebound).

• Infection (encephalitis or meningitis).

• Metabolic (hypoxia, hypercapnoea, hypoglycaemia, carbon monoxide

(CO) poisoning, dialysis).

• Craniofacial disorder (pathology of skull, neck, eyes, nose, ears, sinuses,

teeth, mouth, temporomandibular joint dysfunction).

• Neuralgias (trigeminal, occipital and other cranial nerves).

Approach

Use a detailed history and examination (including vital signs and neurolog-

ical examination) to search for potentially serious causes. Look particularly

for the following (some typical features in brackets):

• Subarachnoid haemorrhage (sudden, severe onset, syncope) —

b p.128.

• Meningitis or encephalitis (fever, neck rigidity) — b p.224.

• Head injury (history or signs of trauma) — b p.354.

• i intracranial pressure (papilloedema, loss of retinal vein pulsation).

• Stroke (focal neurological signs) — b p.144.

• Acute glaucoma (painful red eye, d VA, irregular semi-dilated pupil) —

b p.542.

• Cranial arteritis (jaw pain, temporal artery tenderness) — b p.132.

127

HEADACHE

History

Features suggesting possible serious pathology are:

• Sudden onset headache.

• Worst headache ever.

• Dramatic change in pattern of headache.

• Known HIV or malignancy.

• The presence of a ventriculo-peritoneal shunt.

• Headache coming on during exertion.

• New onset headache in those aged > 50 years.

Ask about drugs and the possibility of toxins (eg CO).

Examination

Check GCS, pulse rate, respiratory rate, BP, T ° and SpO

• Feel the head for muscular tenderness, arterial tenderness, trigger

points for neuralgia, and look for evidence of head injury.

• Examine the eyes for VA, pupil reactions, eye movements. Look at the

fundi for papilloedema.

• Palpate the sinuses for tenderness.

• Look in the ears for haemotympanum or infection.

• Check the oral cavity for infection.

• Look for evidence of purpura/rash of meningococcal infection.

• Complete a full neurological examination (include cranial nerves, limb

tone, power, sensation, co-ordination and reﬂ exes).

Check for Kernig’s sign : straightening the knee whilst the hip is ﬂ exed

produces discomfort in the presence of meningeal irritation.

Management

Investigation and emergency treatment will be tailored according to the

presentation of the patient, based upon the likely diagnosis.

• Check FBC, ESR, CRP, U&E, blood glucose.

• If pyrexial and no other obvious source of infection found, take blood

cultures and consider IV cefotaxime 2g. Start IV ﬂ uids and admit.

• Give paracetamol (oral or IV if vomiting) and an NSAID.

• An effective treatment for headache is IV metoclopramide 10mg with IV

ﬂ uids.

• Arrange an emergency CT brain for any patient with an acute severe

headache, or with a history of seizure, or an abnormal neurological

exam. Arrange a CT for any patient with HIV.

• If subarachnoid haemorrhage is suspected and CT normal, admit for

lumbar puncture.

It may be safe to discharge home a patient with slow onset headache that

has resolved following treatment, with normal examination and blood

tests. Arrange GP follow up. Always advise to reattend if symptoms

worsen.

128 CHAPTER 3 Medicine

Subarachnoid haemorrhage

Consider subarachnoid haemorrhage in any ‘worst ever’

or sudden onset headache

Atraumatic subarachnoid haemorrhage can occur at any age and is an

important cause of sudden collapse and death. Most bleeds follow rupture

of saccular (‘berry’) aneurysms in the circle of Willis. Other bleeds may

be due to arteriovenous malformations, tumours, or connective tissue

disorders.

History

Up to 70 % of patients with subarachnoid haemorrhage report rapid onset

or ‘worst ever’ headache. This is classically described as ‘like a blow to the

back of the head’, accompanied by neck pain, photophobia, and vomiting.

In 25 % , exertional activities precede the event. The patient may present

after syncope or ﬁ ts. Drowsiness and confusion are common. ‘Warning

headaches’ may precede subarachnoid haemorrhage. Unilateral eye pain

may occur.

Examination

Document pulse rate, BP, T

, and GCS. An unconscious patient with signs

of Cushing’s response signiﬁ es i intracranial pressure. Perform full cranial

and peripheral nerve examination. There may be focal motor and sensory

signs due to intracerebral extension of the haemorrhage or vasospasm,

subhyaloid haemorrhages (blotchy haemorrhages seen in the fundi) or

cranial nerve palsies. Oculomotor nerve palsy is characteristic of a berry

aneurysm involving the posterior communicating artery. Neck stiffness is

often absent in ED presentations, either because meningeal irritation has

not yet occurred or because the patient is deeply unconscious.

Investigation

This may need to proceed alongside resuscitation in seriously ill patients:

• Assess airway and breathing. If the patient is unconscious, open the

airway and contact ICU. Consider urgent RSI, tracheal intubation and

ventilation.

• Obtain venous access and check BMG, FBC, clotting screen, U&E.

• CXR may show changes of neurogenic pulmonary oedema.

• ECG may demonstrate ischaemic changes.

• Arrange emergency CT scan for all suspected cases (maximally sensitive

within 12hr). Admit for lumbar puncture (LP) (done > 12hr after head-

ache onset) even if CT scan is normal.

• Involve the neurosurgical team early. It may be useful to use the Hunt

and Hess score (see Table 3.8 ) when communicating severity by phone.

129

SUBARACHNOID HAEMORRHAGE

Treatment

Tailor this according to the presentation and the need for resuscitation:

• Maintain SpO

94–98 % .

• Provide adequate analgesia and antiemetic. Codeine (30–60mg PO),

paracetamol (1g PO) and/or NSAID may sufﬁ ce. Some patients require

more potent analgesics (eg morphine titrated in 1mg increments IV

according to response) — proceed slowly to avoid drowsiness.

• If unconscious (GCS < 8), severely agitated or combative, tracheal intu-

bation (with general anaesthetic (GA)) will allow IPPV and control of

pCO

to within normal levels. Insert a urinary catheter and arterial line.

Contact neurosurgical team — further treatment options include:

• Nimodipine (60mg PO every 4hr or 1mg/hr IVI) to prevent and treat

ischaemic neurological deﬁ cits secondary to vasospasm.

• Mannitol IV (eg 200mL of 10 % ) if there is evidence of i ICP.

Table 3.8 Hunt and Hess scale for subarachnoid haemorrahage

Grade

1 Asymptomatic, mild headache, slight nuchal rigidity

2 Moderate to severe headache, nuchal rigidity, no neurologic deﬁ cit

other than cranial nerve palsy

3 Drowsiness/confusion, mild focal neurological deﬁ cit

4 Stupor, moderate-severe hemiparesis

5 Coma, decerebrate posturing

130 CHAPTER 3 Medicine

Migraine

Patients with recurrent migraine rarely attend the ED unless symptoms

are different from usual — take care to avoid missing more serious condi-

tions. The pathogenesis of migraine is not entirely clear, but there is initial

vasoconstriction and subsequent vasodilatation of both intracranial and

extracranial blood vessels.

Presentation

Precipitants include fatigue, alcohol, menstruation, oral contraceptive pill

(OCP), hunger, chocolate, cheese, shellﬁ sh, and red wine.

A prodrome lasting 5–30min occurs in a third of patients, with blurred

vision, photophobia, or scintillating scotomata (an area of blurred or

absent vision surrounded by moving zig-zag lines), malaise, anorexia, and

vomiting. A few experience hemiparaesthesiae, mild unilateral weakness,

ataxia, or dysphasia. The following headache may last 4–72hr, and is

usually ‘throbbing’ and unilateral, but may be generalized. Photophobia,

nausea, or phonophobia is common.

Rare forms of migraine

Hemiplegic migraine Profound hemiplegia precedes the development of

the headache by 30–60min. The weakness and other focal deﬁ cits usually

resolve quickly. Occasionally, they may be slow or fail to resolve.

Basilar migraine Brainstem disturbances, with impaired consciousness,

vertigo, dysarthria, diplopia, and limb weakness.

Ophthalmoplegic migraine Transient unilateral ophthalmoplegia and

ptosis, which may last several days.

Acephalgic migraine Very occasionally, neurological defects may be

present without headache.

Examination

Look for evidence of other serious diagnoses.

Treatment of acute attacks

• Give simple analgesia (eg paracetamol 1g PO PRN qds or NSAID) in

combination with an anti-emetic (eg metoclopramide 10mg PO, or IV).

• Refer for admission patients who have neurological signs, altered mental

status, or where there is diagnostic uncertainty (including change in

severe headache pattern).

• Acute attacks that fail to respond to simple measures may respond to

other drugs, but these are associated with signiﬁ cant adverse effects.

5HT

agonist sumatriptan (6mg SC or 50mg PO or 20mg intranasally) is

effective, but discuss with a senior ﬁ rst.

Sumatriptan causes vasoconstriction and is therefore contraindicated

in IHD, uncontrolled hypertension, basilar, and hemiplegic migraine.

Rebound headache may occur in up to 45 % .

Ergotamine is best avoided (see BNF ). It causes nausea, vomiting,

abdominal pain, and muscular cramps. It is contraindicated in peripheral

vascular disease, IHD, pregnancy, breast feeding, hemiplegic migraine,

Raynaud’s disease, liver and renal impairment, and hypertension.

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132 CHAPTER 3 Medicine

Other causes of headache

Cluster headache

These are more common in men. Often there is a family history. Headache

usually occurs at night, waking the patient. Sometimes alcohol may act as a

precipitant. Headaches are typically ‘clustered’ into up to eight attacks per

day each lasting between 15 and 180min. Pain is usually severe, centred

upon the eye. Associated symptoms, often unilateral, include conjunctival

injection, lacrimation, nasal congestion, rhinorrhoea, forehead, and facial

sweating, miosis, ptosis.

Treatment High ﬂ ow O

(12L/min via reservoir mask) for 15min

sometimes provides relief. Otherwise, use paracetamol/NSAID. Consult

before contemplating starting ergotamine or sumatriptan.

Trigeminal neuralgia

Characterized by stabbing unilateral pain within the distribution of the

trigeminal nerves. Stimulation of the ‘trigger area’ (eg by touching, hair

brushing, or even chewing) induces very severe pain. Treat with car-

bamezepine and oral analgesia. Admit if the pain is severe and unrelieved.

Tension headache

The diagnosis is only made after exclusion of more serious pathology.

The history may be described in a dramatic manner. The headache is

usually continuous, pressing, or tight (‘band-like’) in nature. It is usually

bitemporal or occipital. Usual features of migraine are absent and the

headache does not worsen with exertion.

Examination often reveals pericranial muscle tenderness, but is otherwise

normal.

Treat with simple analgesia (eg paracetamol 1g PO qds PRN) and

advise GP follow-up. Reassure the patient that a thorough history and

examination have not revealed any worrying features.

Cranial (‘temporal’ or ‘giant cell’) arteritis (see b p.541)

Consider this in all patients > 50 years with recent onset of headache or

change in headache pattern. There may be weight loss, night sweats, low

grade fever, jaw claudication, ande d vision (up to 10 % present with acute

visual loss), shoulder girdle stiffness, and muscular aches (polymyalgia).

Involvement of carotid or vertebral arteries may lead to TIAs or stroke.

Examination: the temporal arteries may be tender, reddened, pulseless,

or thickened. Fundoscopy is usually normal, but papilloedema can occur

later in the disease.

Investigation: i ESR > > 40mm/hr, often with a low grade anaemia and

leucocytosis. A normal ESR does not exclude temporal arteritis.

Treatment: in view of the serious risk of rapidly progressive visual loss,

if suspected give 200mg IV hydrocortisone (or 40mg prednisolone

PO) immediately. Refer to the neurologist or ophthalmologist as an

emergency — the diagnosis may be conﬁ rmed by temporal artery biopsy.

133

OTHER CAUSES OF HEADACHE

Space-occupying lesions

If the headache is always located on the same side, consider space

occupying lesions and arteriovenous malformations. Headaches that are

dull, aching, and made worse by lying down or straining are typical of

space occupying lesions.

Malignant hypertension

Hypertension is an unusual cause of headaches, but is seen in patients with

malignant hypertension and diastolic BP > 130mmHg ( b p.90).

Ventricular shunts

Assume that any patient who presents with headaches associated with

a ventricular shunt has infection/blockage and refer as an emergency.

Associated drowsiness is a particular pointer to blockage.

Analgesic headache

Chronic use of simple analgesics, sympathomimetics, ergotamine,

or cocaine is associated with headaches. Stopping or starting certain

medications (eg OCP) can also cause headache, as can withdrawal from

caffeine. Exclude serious causes and advise GP follow-up with advice on

medication use.

Cerebral venous thrombosis

This is more common than was previously realized. It presents in similar

fashion to subarachnoid or subdural haemorrhage: sudden onset head-

ache with nausea and vomiting. It may be associated with sinus infections,

pregnancy and the post-partum period. The diagnosis may be missed on

CT, but a clue includes i ICP at LP.

Meningitis (see b p.224)

Encephalitis

Miscellaneous causes

Headaches may also result from:

• Hypoxia and hypercapnoea.

• Poisons: eg CO and solvents ( b p.208).

• Drugs: eg nitrates, sildenaﬁ l.

• Post-traumatic ( b p.368).

134 CHAPTER 3 Medicine

Acute confusional state (delirium)

Deﬁ nition of delirium

Delirium is a form of organic brain syndrome characterized by:

• Disturbed conscious level and mood (overactivity, excitement, drowsi-

ness or stupor).

• Global disturbance of cognition (memory, orientation, attention,

speech, motor function).

• Rapid onset with ﬂ uctuating course (often worse at night, with reversal

of usual sleep–wake cycle) and brief duration.

• Perceptual distortions and hallucinations (especially visual).

Causes of acute confusion

One or more of the following may be the underlying cause of an acute

confusional state (several causes frequently co-exist):

• Prescribed medication: digoxin, cimetidine, steroids, analgesics, diuretics,

anticholinergics, antiparkinsonian drugs.

• Drugs of abuse: opioids, benzodiazepines, ecstasy, amphetamines, hal-

lucinogens.

• Withdrawal: from alcohol, opioids, hypnotics or anxiolytics.

• Infection: pneumonia, UTI, septicaemia, meningitis, encephalitis.

• Metabolic: hypoxia, hypercapnia, hypoglycaemia, acidosis, hyponat-

raemia, hypercalcaemia.

• Cardiac: acute MI, cardiac failure, endocarditis.

• Neurological: head injury, chronic subdural haematoma, meningitis, post-

ictal state.

• Organ failure: respiratory, renal and hepatic failure.

• Endocrine: myxoedema, thyrotoxicosis, diabetes, Addison’s disease.

Differential diagnosis

Delirium can occur at any age, but is much more common in the elderly.

It is often misdiagnosed as schizophrenia, depression, or dementia (see

opposite). Differentiation can be difﬁ cult, but the following are more

suggestive of physical illness:

• Non-auditory hallucinations.

• Dysarthria.

• Ataxia.

• Gait disturbance.

• Incontinence.

• Focal neurological signs.

Approach

Search systematically for (and exclude) the physical causes of acute confu-

sion outlined above.

135

DEMENTIA

Investigation of acute confusion

Perform a thorough, careful physical and mental state examination (see

b Mental state examination, p.606) on acutely confused patients. It may

be impossible to obtain an accurate history from the patient, so actively

seek other sources of information: relatives, carers, GP, and previous

medical records.

Look carefully for evidence of alcohol/drug intoxication or evidence of

withdrawal states. Examine for focal neurological signs and signs of acute

cardiac, respiratory, or abdominal abnormalities (including acute urinary

retention). Document basic vital signs (GCS, pulse, BP, respiratory rate

and T * ) in all cases.

Mandatory basic investigations

• BMG.

• U&E, FBC, and blood glucose.

• Urinalysis.

• SpO

and ABG.

• ECG.

• CXR.

Adopt a low threshold for additional investigations based on clinical

suspicion — blood cultures, serum paracetamol and salicylate, CT brain

scan, and even LP may be indicated.

Be careful not to miss: hypoglycaemia, head injury, Wernicke’s encephalopathy,

opioid intoxication, acute alcohol withdrawal, CO poisoning.

Dementia

Dementia is an acquired, progressive decline in intellect, behaviour, and

personality. It is irreversible and typically occurs with a normal level of

consciousness. Note that patients with dementia are at risk of delirium

resulting from an acute infective or metabolic origin — a clue to this may

be an acute deterioration in mental state.

The commonest causes of dementia are Alzheimer’s disease, vascular

dementia, and Lewy body dementia.

136 CHAPTER 3 Medicine

The unconscious patient: 1

Treatment may be needed before any diagnosis is made. Remember:

• Airway.

• Breathing.

• Circulation.

Initial resuscitation

Airway and cervical spine Whatever the cause of coma, a patient may die

or suffer brain damage due to airway obstruction, respiratory depression.

or circulatory failure. Clear and protect the airway immediately, and

immobilize the cervical spine if trauma is suspected.

Breathing If breathing appears inadequate ventilate with O

using a self-

inﬂ ating bag with an O

reservoir. An uninjured patient who seems to be

breathing adequately can be examined supine, but nurse him/her in the

recovery position toe d risk of airway obstruction. Record RR.

Circulation Measure pulse and BP. Observe and feel the skin for colour,

sweating and T ° . Obtain reliable venous access. Monitor ECG. Replace IV

ﬂ uid if indicated.

Conscious level Assess level of consciousness using GCS ( b Head injury:

examination, p.360). Check the blood glucose (initially by BMG) and treat

hypoglycaemia immediately ( b p.150). Record pupil size. Give slow IV

thiamine (ie 2 pairs of Pabrinex

ampoules in 100mL 5 % glucose over

30min — see BNF ) to patients with a history of alcoholism or who appear

malnourished.

Common causes

• Hypoglycaemia

• Drug overdose

• Head injury

• Stroke

• Subarachnoid haemorrhage

• Convulsions

• Alcohol intoxication

Uncommon causes

• Type 2 respiratory failure

• Cardiac failure

• Arrhythmias

• Hypovolaemic shock

• Anaphylaxis

• Hepatic/renal failure

• Hypothermia/hyperthermia

• Meningitis/encephalitis

• Malaria

• DKA/HHS

• Non-convulsive status epilepticus

• Wernicke’s encephalopathy

137

THE UNCONSCIOUS PATIENT: 1

History

Obtain a history from the ambulance crew and the patient’s relatives and

friends. Ask:

• How was the patient found?

• When was he/she last seen?

• Is there any suggestion of trauma?

• Is there any history of ﬁ ts?

• Has there been recent foreign travel?

• Previous symptoms and medical history (including depression).

• Note any drugs available.

Check previous ED records and hospital notes.

Examination

Examine thoroughly for illness and injury. Check clothes and possessions

for tablets and cards/bracelets warning of pre-existing disease.

i Respiratory rate may reﬂ ect obstructed airway, aspiration, pneumonia,

DKA, liver/renal failure, salicylate poisoning, methanol, or ethylene glycol.

Respiratory depression may be due to poisoning (eg barbiturates, opioids,

tricyclics) or i ICP. Brainstem compression or damage by stroke may

cause rapid, irregular or intermittent (Cheyne–Stokes) breathing.

If bradycardic consider: hypoxia, complete heart block, i ICP, digoxin or

B-blocker poisoning ( b p.198).

If tachycardic consider: airway obstruction, hypoxia, hypovolaemia, SVT,

VT, or anticholinergic overdose.

AF may be associated with cerebral emboli.

Hypotension suggests hypoxia, shock (hypovolaemic, anaphylactic, septic),

or poisoning.

Hypertension may be due to i ICP.

Skin: look for pallor, cyanosis, jaundice, spider naevi, skin crease/scar

pigmentation (Addison’s disease), rashes (eg purpura in meningococcal

infection or DIC), injection marks (drug addiction or medical treatment),

and signs of trauma. Erythema or blistering over pressure points indicate

the patient has been unconscious for some hours.

Measure rectal T° with a low-reading thermometer if the skin feels cold.

Coma is common at <30 ° C ( b Hypothermia: presentation, p.254).

138 CHAPTER 3 Medicine

The unconscious patient: 2

Neurological examination include GCS, limb strength, muscle tone and

reﬂ exes, optic fundi, ear drums, neck stiffness (except in neck injury), and

palpation of the fontanelle in babies. Lateralizing signs, such as facial or

limb weakness, may be caused by a stroke, intracranial bleeding or pre-

existing problems (eg previous stroke or Bell’s palsy). Ocular nerve palsy

or divergent squint with coma can indicate Wernicke’s encephalopathy,

requiring IV thiamine or tricyclic poisoning. Look for subtle signs of

seizure activity (eg twitching of ocular muscles or eyelids, unusual limb

movements), which may indicate non-convulsive status epilepticus. Look

at the fundi — spontaneous central retinal venous pulsations are rare with

i ICP. Subhyaloid haemorrhages (blotchy fundal haemorrhages) suggest

subarachnoid haemorrhage.

Hypoglycaemia can cause localized weakness/coma and mimic stroke.

Coma without lateralizing signs is usually due to poisoning, a post-ictal

state, brainstem stroke, or hepatic failure: extensor plantar reﬂ exes are

common in these conditions.

Tricyclic antidepressants often cause coma with dilated pupils, a divergent

squint, i muscle tone, jerky limb movements, and extensor plantars.

In severe poisoning, there may be muscle ﬂ accidity with respiratory

depression ande d reﬂ exes ( b p.194).

Coma with small pupils and respiratory depression suggests opioid

poisoning ( b p.188). In unexplained coma, give a therapeutic trial

of naloxone (0.4–0.8mg IV), observing for changes in conscious level,

respiratory rate, and pupil size.

Investigations

• BMG and blood glucose. If BMG is low, do not wait for the laboratory

result to conﬁ rm this before starting treatment.

• ABG (record FiO

and whether breathing spontaneously or IPPV).

• FBC, prothrombin time, U&E.

• Check paracetamol and salicylate levels if poisoning is suspected: para-

cetamol alone does not cause coma (except in late cases with liver

failure), but a mixture of drugs may have been taken. Drug screening for

sedatives/hypnotics is not needed, but in unexplained coma keep blood

for later analysis if necessary.

• ECG may show arrhythmias ( b Tricyclic antidepressant poisoning,

p.194).

• CXR may show pneumonia, aspiration, trauma, or tumour.

• CT scan may be needed to diagnose subarachnoid haemorrhage, stroke,

or head injury.

Psychogenic coma

Patients sometimes pretend to be unconscious. It can be difﬁ cult to be

certain of this — exclude other causes ﬁ rst. Suspect psychogenic coma if

serious pathology has been excluded and when the eyes are opened, only

the sclera show as the eyes deviate upwards (Bell’s phenomenon).

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140 CHAPTER 3 Medicine

Collapse and syncope

Syncope is a sudden, transient loss of consciousness, with spontaneous

recovery.

Priorities

• Identify serious or life-threatening problems and institute treatment.

• Decide which patients require admission.

• Decide which patients require follow-up.

History of syncopal episode

Was it a simple faint? Vasovagal or neurally-mediated syncope is a

common response to an overwarm environment or prolonged standing,

and can be precipitated by sudden fright or visual stimuli (eg the sight

of blood). Other contributors are large meals, prolonged starvation

or alcohol. There are usually premonitory symptoms of feeling unwell,

nauseated, dizzy, or tired, with yawning, blurred or ‘tunnel’ vision, or

altered hearing. If the fainter cannot get supine (eg bystanders keeping

them upright), seizure-like twitching may occur ( convulsive syncope ).

Vomiting and incontinence may occur and do not reliably discriminate

seizures from faints.

Was it a seizure? Look at the ambulance records. An eyewitness account

is crucial. Ask what the witnesses actually saw (do not assume they know

what a ‘ﬁ t’ looks like). There should typically be no prodrome, there is

often a cry followed by tonic/clonic movements. Cyanosis, saliva frothing

from the mouth, heavy breathing, tongue biting, or incontinence suggest

a generalized seizure. Post-ictal drowsiness or confusion is normal — very

rapid recovery questions the diagnosis.

Was it a cardiac event? Cardiac syncopal events are also abrupt in

onset (eg collapse due to hypertrophic cardiomyopathy) and may be

accompanied by pallor and sweating. Recovery may be rapid with ﬂ ushing

and deep/sighing respiration in some cases (eg Stokes–Adams attacks).

Nausea and vomiting are not usually associated with syncope from

arrhythmias. Ask about previous episodes and chest pain, palpitations,

history of cardiac disease, and family history of sudden death. Syncope

associated with exertion is a worrying feature: possible causes include

aortic or mitral stenosis, pulmonary hypertension, cardiomyopathy, or

coronary artery disease.

Other causes Carotid sinus syncope is neurally mediated, and often occurs

with shaving or turning the head. Syncope may be secondary to effects of

medication (eg GTN, B-blockers, anti-hypertensive drugs). Syncope may

also be the presenting feature of subarachnoid haemorrhage, ruptured

ectopic pregnancy, aortic or carotid dissection, PE, or GI bleed. Syncope

is rarely caused by a TIA.

141

COLLAPSE AND SYNCOPE

Assessment and treatment

If a patient suddenly loses consciousness in the ED, assess responsiveness

and check for a pulse. Keep the airway clear, give O

, and monitor pulse

and ECG. Note any neurological signs during the episode and obtain BP,

SpO

, and BMG.

Patients seen following syncope Obtain a detailed account from the patient

and witnesses. Look for signs of tongue biting, incontinence, or other

injuries, examine the CVS for murmurs, arrhythmias or abnormalities.

Perform a neurological examination and look for focal signs. Do postural

tests (supine and standing or sitting pulse and BP). A degree of postural

hypotension is common, but postural symptoms (eg dizziness, weakness,

etc.) are always signiﬁ cant (look for causes of hypovolaemia eg GI bleed,

ectopic pregnancy). Check BMG to exclude hypoglycaemia and an ECG

looking for arrhythmias, LVH, ischaemia, previous or acute MI, and QT

prolongation. An abnormal ECG may be the only clue to an underlying

hypertrophic cardiomyopathy (HCM) or Brugada syndrome.

Disposal

Admit patients for cardiology review within 24 hr if they present with:

• An ECG abnormality.

• Heart failure.

• Loss of consciousness on exertion.

• Family history of sudden death <40 year or inherited cardiac condition.

• Age > 65 year with no prodromal symptoms.

• A heart murmur.

Refer patients for assessment by a specialist in epilepsy if they present

with one or more of:

• A bitten tongue.

• Amnesia, unresponsiveness, unusual posturing, or prolonged limb

jerking, head turning to one side.

• History of a prodrome.

• Post-ictal confusion.

It may be appropriate to discharge patients with full recovery, appropriate

history for vasovagal syncope and a normal examination.

See www.nice.org.uk

Diagnoses not to be missed

• GI bleed: syncope ( ± postural symptoms) indicate signiﬁ cant blood

loss and hypovolaemia. Perform PR examination to check for blood/

melaena.

• Ectopic pregnancy: suspect this in women with syncope and abdominal

pain or gynaecological symptoms. Do a pregnancy test.

• Ruptured abdominal aortic aneurysm.

• PE ( b Pulmonary embolism, p.120). A witness may give a history of

cyanosis. Indicative of massive thrombus.

142 CHAPTER 3 Medicine

Acute generalized weakness

Weakness may be a feature of common neurological problems (eg TIA/

stroke), or accompany many of the causes of collapse (see b Collapse

and syncope, p.140). Less commonly, generalized muscle weakness may

be the presentation of a number of other diseases.

Guillain–Barré syndrome

Guillain–Barré follows a respiratory or GI viral infection and is character-

ized by progressive symmetrical weakness, spreading from distal muscles

to involve proximal muscles. Symptoms and signs include muscle tender-

ness, back pain, loss of muscle reﬂ exes, sensory symptoms (paraesthesiae

of ﬁ ngers and toes) and disturbance of the autonomic nervous system

(hyper- or hypotension, tachy- or bradycardia, bladder atony). Beware

respiratory failure, which can rapidly progress to respiratory arrest. Serial

vital capacity measurements are advised. Refer to the medical team/ICU.

Multiple sclerosis

Multiple sclerosis (MS) is a demylinating disease of the CNS. It is more

common in females and usually presents between ages 20–50. The disease

follows a relapsing and remitting course with sensory loss, stiffness, and

weakness of legs, ataxia, autonomic impairment (bladder dysfunction),

and diplopia. Patients may present with these symptoms during their ﬁ rst

exacerbation or with optic neuritis (pain in one eye with visual blurring).

Arrange admission under neurology. If patient has eye symptoms, arrange

urgent ophthalmology review.

Polymyositis

Polymyositis is an inﬂ ammatory myopathy that presents with symmetrical

proximal muscle weakness, arthritis and sometimes muscular tenderness.

Patients report difﬁ culty climbing stairs, standing from a low chair, or

lifting arms to brush hair. Creatine kinase (CK) levels are raised. Refer to a

rheumatologist for treatment.

Myasthenia gravis

This is a rare autoimmune disease, which results in painless weakness in

which the muscles are fatiguable, but tendon reﬂ exes and pupil responses

are normal. Ptosis, diplopia, and blurred vision are the commonest pres-

entations. Usually, cranial nerves are involved to a greater extent than

limb muscles and the distribution is asymmetrical. Crises may present with

severe muscle weakness in which the major concern relates to respiratory

compromise — the patient may require emergency temporary ventilatory

support.

If the diagnosis is suspected in a patient not known to have myasthenia

gravis, refer to a specialist who may wish to perform an edrophonium test .

Patients with known myasthenia gravis may present with weakness due

to under-treatment, over-treatment (cholinergic crisis), or an adverse

reaction to an unrelated drug. Refer to the medical team for investigation.

143

ACUTE GENERALIZED WEAKNESS

Periodic paralysis

This encompasses a family of hereditary diseases associated with defects

in muscle ion channels. Episodes of weakness can be associated with

ﬂ uctuations in serum potassium levels lasting a few hours to a week.

Patients may develop myotonia between attacks and ﬁ xed proximal

muscle weakness. Treatment tends only to be required for hypokalaemic

periodic paralysis with oral potassium supplementation.

Wound botulism

Botulism has made a recent come back in the IV drug injecting community.

Botulinum toxin inhibits the release of acetylcholine at neuromuscular

junctions, sympathetic and parasympathetic synapses. Wound infection

with Clostridium botulinum presents with diplopia, blurred vision, ptosis,

and neck weakness, which can progress to respiratory failure. Treatment is

with antitoxin, benzylpenicillin, and metronidazole, along with respiratory

support.

It is worth remembering that generalized weakness may also be caused by:

• Spinal cord compression.

• Tetanus.

• Alcoholic myopathy.

• Diphtheria.

• Lead poisoning.

144 CHAPTER 3 Medicine

Stroke

A stroke is an acute onset of focal neurological deﬁ cit of vascular origin

which lasts > 24hr. The blood supply to the brain has two sources — the

internal carotid and the basilar arteries. The internal carotids supply the

anterior and middle cerebral arteries, known as the anterior circulation.

The basilar artery supplies the posterior cerebral artery in 70 % of people

(the posterior circulation). Anterior and posterior communicating arteries

in the circle of Willis provide collateral circulation in cases of carotid

artery stenosis.

Pathogenesis

70 % of strokes occur in those aged > 70yrs, but they can occur at any age.

Cerebral infarction (80 % )

Results from:

• Thrombosis secondary to atherosclerosis, hypertension and rarely

arteritis.

• Cerebral embolism from AF, valve disease/replacement, post-MI, ven-

tricular aneurysm, myxoma, endocarditis or cardiomyopathy.

• An episode of hypoperfusion.

Cerebral haemorrhage (20 % )

Associated with:

• Hypertension (rupture of small arteries in the brain).

• Subarachnoid haemorrhage (see b p.128).

• Bleeding disorders (including anticoagulants) and intracranial tumours.

Presentation

Stroke preceded by neck pain may indicate carotid/vertebral artery dissec-

tion or subarachnoid haemorrhage. Headache is an unusual presentation

of stroke and may indicate cerebral haemorrhage. Be alert to the possi-

bility of different pathology requiring urgent treatment (eg hypoglycaemia,

Todd’s paresis, hemiplegic migraine, meningitis, encephalitis, brain abscess,

head injury, Bell’s palsy, ‘Saturday night palsy’, tumours).

Undertake a thorough examination including:

• Assessment of mental status/GCS and signs of meningeal irritation.

• Evidence of head or neck injury.

• Examination of pupils, fundi, and cranial nerves.

• Assessment of motor function (tone, power, and reﬂ exes).

• Assessment of sensory function (including speech and comprehension).

• Examination for cerebellar signs (co-ordination, speech).

• Check for sources of embolism (AF, murmurs, carotid bruits).

Localization on clinical grounds alone can be difﬁ cult, and differentiation

between infarction and haemorrhage requires CT/MRI. NICE recommend

the use of the ROSIER score to identify patients presenting with acute

stroke (see Table 3.9 ). The ROSIER score will pick up the majority of

patients who are having a stroke, but may not identify patients with

posterior circulation infarcts.

145

STROKE

Investigation

Examine and investigate ﬁ rstly to exclude other conditions and secondly

to conﬁ rm the diagnosis of stroke. As a minimum requirement: BMG,

FBC, ESR, U&E, blood glucose, ECG, CXR. Monitor with pulse oximeter

(if SpO

<94 % obtain ABG) and cardiac monitor.

Emergency CT

Arrange emergency CT scan where:

• The patient presents with symptoms under 4hr of duration. They may be

eligible for emergency thrombolysis treatment. Time is of the essence.

• The patient is on warfarin, heparin, or other anticoagulant.

• There is a known bleeding disorder.

• GCS <13.

• Unexplained progressive or ﬂ uctuating symptoms.

• Papilloedema, neck stiffness or fever.

• There was a severe headache at onset of symptoms.

Management

• Immediately correct hypoglycaemia if present (see b p.150).

• Hypertension and labile BP are common in the early post-stroke period.

Do not attempt to reduce the BP on presentation.

• Give supplemental oxygen only if SpO

<95 % .

• Screen the patient’s ability to swallow (try a teaspoon of water).

• If intracranial haemorrhage has been excluded, all patients should

receive aspirin 300mg as soon as possible. Give this rectally if unable to

swallow. Give PPI if there is a history of dyspepsia. If allergic to aspirin,

give alternative antiplatelet drug such as clopidogrel.

• Wherever possible, admit patients directly to units where they can be

cared for by staff specializing in stroke treatment and rehabilitation.

Thrombolysis

If intracranial haemorrhage has been excluded within 4hr of onset of

symptoms, alteplase may be administered by a trained and supported

emergency physician, only where the patient is managed within a specialist

acute stroke service. See local guidelines and http://www.nice.org.uk

Table 3.9 ROSIER score for stroke recognition

Criteria Points

Facial weakness (asymmetrical) 1

Arm weakness (asymmetrical) 1

Leg weakness (asymmetrical) 1

Speech disturbance 1

Visual ﬁ eld defect 1

Loss of consciousness or syncope –1

Seizure –1

Stroke unlikely if score 0 or less.

146 CHAPTER 3 Medicine

Transient ischaemic attacks

A TIA is an episode of transient focal neurological deﬁ cit of vascular origin

lasting <24hr. A TIA gives major warning for the development of stroke

(5 % within 48hr, up to 50 % in 5 years). Even in patients with resolution of

symptoms/signs, most have evidence of infarction on CT/MRI.

Presentation

Carotid territory involvement produces unilateral weakness or sensory

changes, dysphasia, homonymous hemianopia, or amaurosis fugax.

Vertebrobasilar territory involvement produces blackouts, bilateral motor

or sensory changes, vertigo, and ataxia.

Causes

Most TIAs result from thrombo-embolic disease involving either the

heart (AF, mitral stenosis, artiﬁ cial valves, post-MI) or extracranial vessels

(carotid artery stenosis). Other causes include:

• Hypertension.

• Polycythaemia/anaemia.

• Vasculitis (temporal arteritis, polyarteritis nodosa, SLE).

• Sickle cell disease.

• Hypoglycaemia.

• Any cause of hypoperfusion (eg arrhythmia, hypovolaemia).

• Syphilis.

Assessment

To diagnose a TIA, the symptoms must have resolved within 24hr.

Document vital signs and perform a thorough neurological examination.

Look for possible sources of emboli eg arrhythmias (especially AF), heart

murmurs, carotid bruits, MI (mural thrombus).

Investigations

• Check BMG.

• Send blood for FBC, ESR, U&E, blood glucose, lipids (INR if on anti-

coagulants).

• Record an ECG to search for MI, arrhythmia.

Management

• Calculate the ABCD

score (Table 3.10 ).

• Admit to a stroke unit patients scoring 4 or more points, or anyone

with more than one TIA in the previous week.

• Patients scoring 3 or less points, or who present one week after symp-

toms have resolved, may be suitable for discharge with stroke team

follow-up in the next week.

• Start the patient on daily aspirin 300mg immediately.

• Admit patients with continuing symptoms or residual deﬁ cit (by deﬁ ni-

tion, not a TIA).

See http://www.nice.org.uk

147

TRANSIENT ISCHAEMIC ATTACKS

Table 3.10 ABCD

score for TIAs

Criteria Points

Age Age 60 or over 1

BP at assessment Systolic > 140mmHg or diastolic > 90mmHg

at assessment

Clinical features Speech disturbance 1

Unilateral weakness 2

Duration of symptoms 10–59min 1

60 min or more 2

Diabetes 1

Patients scoring > 4 points are at increased risk.

148 CHAPTER 3 Medicine

Seizures and status epilepticus

First ﬁ t

A ﬁ rst ﬁ t has enormous consequences — do not diagnose without good

evidence

A detailed history from both the patient and any witnesses is crucial to the

diagnosis. The presence of jerking movements or incontinence does not

necessarily reﬂ ect epilepsy. Carefully document what was seen, in order

to avoid confusion with vasovagal syncope or other types of collapse. Full

rapid recovery suggests a syncopal event. Always consider alcohol/drug

use, withdrawal states, hypoglycaemia, arrhythmia, head injury, subarach-

noid haemorrhage, stroke/TIA, infection (including meningitis) or metabolic

disturbance.

As part of the general examination, carefully examine the CNS, documenting:

GCS, confusion, focal abnormalities, ﬁ ndings on fundoscopy. Examine the

cardiovascular system and check for signs of aspiration.

Todd’s paresis may follow seizures — focal deﬁ cit or hemiparesis may

persist for up to 24hr and indicates a high chance of structural lesion.

Investigations BMG, glucose, FBC, U&E, blood cultures if pyrexial, ECG,

and if there are chest signs, a CXR. Check urine pregnancy test if of child-

bearing age. All patients with new onset seizures need brain imaging at

some stage: a signiﬁ cant number have structural CNS abnormalities.

Arrange emergency CT scan for patients with focal signs, head injury,

known HIV, suspected intracranial infection, bleeding disorder (including

anticoagulants), or where conscious level fails to improve as expected.

Disposal A patient presenting with a ﬁ rst seizure may be discharged

home, accompanied by an adult, if they have normal neurological and

cardiovascular examinations, the ECG and electrolytes are normal,

and there is an appointment with an epilepsy specialist in the coming

week. Admit any patient with more than one seizure that day or who

does not ﬁ t the above criteria. Ensure clear documentation of follow-up

arrangements, including booked clinic appointment. Meantime, advise the

patient not to drive or use machinery and to take sensible precautions,

with supervision when performing activities, such as swimming/bathing

until reviewed.

Document this advice in the notes.

Seizures in known epileptics

Ask about any change from the patient’s normal seizure pattern. Possible

causes of poor seizure control include: poor compliance with medica-

tion, intercurrent illness/infection, alcohol, or drug ingestion. Examine to

exclude any injury occurring from the ﬁ t, especially to the head. Occult

dislocations (eg shoulder) may occur. Check vital signs, BMG and anticon-

vulsant levels if toxicity or poor compliance is suspected. Refer patients

with a signiﬁ cant change in seizure pattern to the medical team. Discharge

to the care of a responsible adult those patients who are fully recovered

with no injuries, symptoms or other concerns.

149

SEIZURES AND STATUS EPILEPTICUS

Status epilepticus

This is continuous generalized seizures lasting > 30min or without inter-

vening recovery. Cerebral damage i with duration. Precipitants include

cerebral infection, trauma, cerebrovascular disease, toxic/metabolic dis-

turbances, childhood febrile seizures. Mortality is 8 10 % (due to underlying

pathology). Although seizures typically start as generalized, tonic/clonic,

these features may gradually diminish, making diagnosis difﬁ cult (coma

with virtually no motor evidence of seizure, eg minimal twitching of ocular

muscles only). Complications include hypoglycaemia, pulmonary hyper-

tension, pulmonary oedema and precipitous i ICP can also occur.

Treatment of status epilepticus

• Establish a clear airway (a nasopharyngeal airway may help).

• Give high ﬂ ow O

• Monitor ECG, SpO

, T ° , pulse rate, and BP.

• Obtain IV access, check BMG and correct hypoglycaemia if present

(50mL of 20 % glucose IV).

• Give IV lorazepam 4mg slowly into a large vein (diazepam 10mg is an

alternative). Repeat IV lorazepam 4mg slowly after 10min if seizures

continue.

• Buccal midazolam 10mg (can be repeated once) or rectal diazepam

solution 10–20mg (can be repeated up to total 30mg) are alternatives if

there is no venous access.

• If alcohol abuse or malnutrition is suspected, give slow IVI thiamine in

the form of Pabrinex

2 pairs of ampoules in 100mL of 0.9 % saline (this

occasionally causes anaphylaxis; be prepared to treat — see BNF ).

• Consider the possibility of pregnancy-related ﬁ ts (eclampsia) in women

of childbearing age and treat accordingly (with IV magnesium sulphate—

— as outlined on b p.592).

• Check ABG and save blood for cultures, FBC, U&E, glucose, calcium,

magnesium, LFTs, clotting, drug levels (and toxicology screen if poi-

soning/overdose is suspected).

• Search for features of injury (especially head injury) and infection (look

for a rash).

• If seizures continue despite above therapy, call ICU and consider the

use of phenytoin (18mg/kg IV, 50mg/min) with ECG monitoring, or

fosphenytoin (20mg/kg phenytoin equivalent IV, <150mg/min). A 70kg

patient would require 1400mg phenytoin equivalent of fosphenytoin

(28mL Pro-Epanutin

) diluted in 100mL 0.9 % saline or 5 % glucose, given

over 10–15min.

• After 30min, contact ICU and proceed without delay to rapid sequence

induction (ideally with thiopental), tracheal intubation, and continue

anticonvulsant medication.

150 CHAPTER 3 Medicine

Hypoglycaemia

Hypoglycaemia can mimic any neurological presentation including coma,

seizures, acute confusion, or isolated hemiparesis.

Always exclude hypoglycaemia in any patient with coma,

altered behaviour, neurological symptoms, or signs

Plasma glucose is normally maintained at 3.6–5.8mmol/L. Cognitive func-

tion deteriorates at levels <3.0mmol/L, but symptoms are uncommon

> 2.5mmol/L. In diabetics, however, the threshold for symptoms can be

very variable. Hypoglycaemia is potentially fatal, and accounts for 2.4 % of

deaths in diabetics on insulin. Even mild episodes aggravate pre-existing

microvascular complications and lead to cumulative brain damage.

Causes

In diabetics, the commonest cause is a relative imbalance of administered

versus required insulin or oral hypoglycaemic drug. This may result

from undue or unforeseen exertion, insufﬁ cient or delayed food intake,

excessive insulin administration (due to time, dose or type of insulin).

Other causes are:

• Alcohol (in addition to alcohol directly causing hypoglycaemia, the

features of hypoglycaemia may be mistaken for alcohol intoxication or

withdrawal).

• Addison’s disease.

• Pituitary insufﬁ ciency.

• Post-gastric surgery.

• Liver failure.

• Malaria.

• Insulinomas.

• Extra-pancreatic tumours.

• Attempted suicide or homicide with large doses of insulin or oral

hypoglycaemic drug.

Symptoms and signs

Common features: sweating, pallor, tachycardia, hunger, trembling, altered

or loss of consciousness, irritability, irrational or violent behaviour, ﬁ tting,

focal neurological deﬁ cit (eg hemiplegia). Look for Medic-Alert bracelet/

chain.

Diagnosis

Check venous or capillary blood with glucose oxidase strip (BMG). If

<3.0mmol/L, take a venous sample for a formal blood glucose level,

but give treatment without waiting for the result. Take appropriate

samples if overdose of insulin, oral hypoglycaemic agent, or other drugs

is suspected.

151

HYPOGLYCAEMIA

Treatment

This depends upon the conscious state and degree of co-operation of the

patient. Choose the appropriate option from the following:

• 5–15g of fast-acting oral carbohydrate (eg Lucozade

, sugar lumps,

Dextrosol

, followed by biscuits and milk).

• Glucagon 1mg: SC, IM, or IV. Can be administered by relatives, ambu-

lance crew and when venous access is difﬁ cult. Glucagon is not suitable

for treatment of hypoglycaemia due to sulphonylurea drugs, liver failure

or in chronic alcoholism (as there may be little liver glycogen available

for mobilization).

• Glucose 10 % solution 50mL IV, repeated at 1–2min intervals until the

patient is fully conscious or 250mL (25 g) has been given.

• Glucose 50 % solution (25–50mL IV) is hypertonic, liable to damage

veins and no more effective than glucose 10 % . If glucose 50 % is used,

give it into a large vein and follow with a saline ﬂ ush.

• The time taken for return of consciousness and the incidence of

nausea, vomiting and other adverse effects are similar for IV glucagon

and glucose.

The persistence of an altered conscious level suggests another underlying

pathology (eg stroke), or may reﬂ ect the development of cerebral

oedema due to hypoglycaemia, which has a high mortality. Maintain

plasma glucose at 7–11mmol/L, contact ICU and consider mannitol and/

or dexamethasone. Arrange urgent investigation (eg CT scan) and search

for other causes of altered consciousness.

Overdose Glucose infusions may be needed for 24hr or longer after

poisoning with insulin or oral hypoglycaemic drug, depending upon

exactly what and how much has been taken. Hypokalaemia may be a

problem. Block excision of the injection site has been used as successful

treatment for insulin overdose. Octreotide may be helpful in recurrent

hypoglycaemia due to overdose of a sulphonylurea drug ( b p.197).

Discharge

90 % of patients fully recover in 20min. Provided that the cause for

the episode has been identiﬁ ed and fully corrected, it is reasonable

to discharge the patient after observation in the ED, with appropriate

follow-up.

Arrange follow up having considered the following:

• Why did this episode occur?

• Has there been a recent change of regimen, other drugs, alcohol, etc.?

• Is the patient developing hypoglycaemic unawareness or autonomic

dysfunction?

152 CHAPTER 3 Medicine

Hyperglycaemic crises

Diabetic keto-acidosis (DKA) is caused by absolute or relative d insulin

levels. Plasma glucose i causes an osmotic diuresis, with Na

and water

loss (up to 8–10L), hypotension, hypoperfusion, and shock. Normal

compensatory hormonal mechanisms are overwhelmed and lead to

i lipolysis. In the absence of insulin this results in the production of non-

esteriﬁ ed fatty acids, which are oxidized in the liver to ketones.

Younger undiagnosed diabetics often present with DKA developing

over 1–3 days. Plasma glucose levels may not be grossly i ; euglycaemic

ketoacidosis can occur. Urinalysis demonstrates ketonuria.

Hyperosmolar hyperglycaemic state (HHS) is caused by intercurrent

illness, inadequate diabetic therapy and dehydration. It develops over

days/weeks, and is more common in the elderly. HHS is characterized by

i glucose levels ( > 30mmol/L), i blood osmolality, and a lack of urinary

ketones. Mortality is 85–10 % , but may be even higher in the elderly.

Causes

Think of the four ‘I’s separately or (often) in combination:

• Infection: common primary foci are urinary tract, respiratory tract, skin.

• Infarction: myocardial, stroke, GI tract, peripheral vasculature.

• Insufﬁ cient insulin.

• Intercurrent illness: many underlying conditions precipitate or aggravate

DKA and HHS.

Clinical features

Hyperglycaemic crisis may present in various ways. Some of the following

are usually present:

Signs of dehydration thirst, polydipsia, polyuria, d skin turgor, dry mouth,

hypotension, tachycardia.

GI symptoms are common in DKA with nausea, vomiting, and abdominal

pain. This can be severe and mimic an ‘acute surgical abdomen’.

Hyperventilation (respiratory compensation for the metabolic acidosis)

with deep rapid breathing (Kussmaul respiration) and the smell of acetone

on the breath, is pathognomonic of DKA.

True coma is uncommon, but altered conscious states and/or focal

neurological deﬁ cits (which may correct with treatment) are seen

particularly in older patients with HHS.

Diagnosis and investigations

Aim to conﬁ rm the diagnosis and search for possible underlying cause(s):

• Check BMG and test the urine for glucose and ketones.

• Send blood for U&E, blood glucose, creatinine, osmolality (or calculate

it): mOsm/L= (2 × Na

) + glucose (mmol/L) + urea (mmol/L).

• Check ABG (look for metabolic acidosis ± respiratory compensation).

• FBC and CXR (to search for pneumonia).

• ECG and cardiac monitoring (look for evidence of hyper/hypokalaemia).

• Blood cultures and if appropriate, throat or wound swabs.

• Urine/sputum microscopy and culture.

153

HYPERGLYCAEMIC CRISES

Treatment

• If altered consciousness/coma is present, provide and maintain a patent

airway.

• Give high FiO

by mask. Consider the possible need for GA and IPPV

for coma ± severe shock.

• Commence IV infusion with 0.9 % saline (if the lab result subsequently

shows initial plasma Na

to be > 150mmol/L, give 0.45 % saline). Give

1000mL of 0.9 % saline over 0.5–1hr, then 500mL/hr for next 2–3hr.

Persistent hypotension may require i in infusion rate and/or colloid

administration. Avoid over-rapid infusion with the risks of pulmonary

oedema and ARDS, especially in the elderly and patients with IHD.

• Insulin: start an infusion of soluble insulin using an IV pump or paediatric

burette at 6U/hr. No loading dose is required. Check plasma glucose

levels every hour initially. When plasma glucose <14mmol/L, d insulin

infusion rate to 4U/hr and replace the saline solution with 10 % dextrose

to help ketone clearance and acid-base state.

• Electrolyte balance: although total body K

is low, plasma K

may be

normal, i or d . With treatment, K

enters cells and plasma levels d :

therefore unless initial K

levels are > 5.5mmol/L, give 20mmol/hr of

KCl, monitor ECG, and check K

levels hourly. Despite the presence of

metabolic acidosis, do not give sodium bicarbonate. Other electrolytes

such as Ca

2 +

, Mg

2 +

, and PO

2 –

are commonly disturbed, but rarely need

emergency correction.

• Consider an NG tube to d risk of gastric dilation and aspiration.

• Monitor urine output (most accurate with urinary catheter).

• Consider a central venous catheter to monitor CVP to guide treatment

in the elderly or severe illness.

• Arrange admission to ICU, HDU, or acute medical admissions unit.

Other aspects of treatment

Signs of infection are often masked. T ° is rarely i , and i WCC may only

reﬂ ect ketonaemia. If in doubt, treat with a broad-spectrum antibiotic.

Over-rapid ﬂ uid replacement can cause cardiac failure, cerebral oedema,

and ARDS, especially in patients with underlying cardiac disease or the

elderly. CVP monitoring may be needed.

Clotting Hyperglycaemia causes a hypercoagulable state: DVT or PE may

occur. Administer prophylactic anticoagulation with LMWH in DKA or

hyperosmolar states.

154 CHAPTER 3 Medicine

Sodium derangements

Abnormal sodium states can occur with hypervolaemia, euvolaemia, or

hypovolaemia, depending on the underlying pathophysiological process.

Hypernatraemia

Causes include diabetes insipidus (lack of ADH or lack of renal response

to ADH), diarrhoea, vomiting, diuretics, hypertonic saline, sodium

bicarbonate administration, or Cushing’s syndrome.

Treatment should not correct the Na concentration faster than 1mmol/L/hr.

Use 0.9 % saline to correct hypovolaemia (patients who have tachycardia,

hypotension, or postural hypotension). Once the patient is euvolaemic,

use an infusion of 0.45 % saline, or 5 % dextrose. The free water deﬁ cit can

be calculated using the formula:

Free water deﬁ cit (in litres) = 0.6 × weight (kg) × (serum Na/140–1)

and should be replaced over 48hr (in addition to normal maintenance ﬂ uids).

Check serum Na

after 2–3hr to monitor correction rate.

Complications of hypernatraemia include seizures, subdural and intra-

cerebral haemorrhages, ischaemic stroke, and dural sinus thrombosis.

Rapid correction of sodium levels (particularly in chronic hypernatraemia)

can cause cerebral oedema and further neurological complications.

Hyponatraemia

Causes include excessive ﬂ uid loss replaced by hypotonic ﬂ uids (diarrhoea,

burns, prolonged exercise, such as marathon running), polydypsia,

ecstasy ingestion, syndrome of inappropriate ADH secretion, nephrotic

syndrome, renal impairment, hepatic cirrhosis, cardiac failure, and many

prescription drugs (including diuretics, heparin, and ACE inhibitors).

Treatment of acute hyponatraemia (<24hr duration) Those with mild

symptoms can be effectively treated by ﬂ uid restriction. Patients who

present with seizures or signs of raised intracranial pressure are at risk of

death and should be treated more aggressively. Serum Na

<120mmol/L

is associated with risk of brain herniation. Give up to 200mL of 2.7 % saline

IV over 30min and recheck serum Na

levels.

Treatment of chronic hyponatraemia ( > 24hr duration) is associated with

central pontine myelinolysis, particularly in patients with low K

levels or

alcoholic patients. Chronic hyponatraemia should be corrected no faster

than 10mmol/L in 24hr. Treat the underlying cause. This may be as simple

as discontinuing a diuretic. Patients with cardiac failure, cirrhosis, or

nephrotic syndrome (hypervolaemic patients) should be ﬂ uid restricted.

Severe hyponatraemia in association with seizures or d GCS may be

cautiously treated with hypertonic saline (2.7 % saline 200mL over 30min

and recheck serum Na

). Aim to increase serum Na

by no more than

5mmol/L using this method.

See www.gain-ni.org

155

ADDISONIAN CRISIS

Addisonian crisis

Acute adrenocortical insufﬁ ciency is rare and easily missed. The most

common cause is sudden withdrawal of chronic steroid therapy (delib-

erately or inadvertently). An Addisonian crisis may also be precipitated

in these patients by intercurrent injury, infection or stress — increasing

steroid requirement. 80 % of Addison’s disease in the UK is idiopathic

(autoimmune), and may be associated with Graves’ disease, Hashimoto’s

thyroiditis, insulin dependent diabetes mellitus (IDDM), pernicious

anaemia, hypoparathyroidism, and ovarian failure. Other causes include

TB, fungal infections, metastatic disease, congenital adrenal hyperplasia,

drugs (eg metyrapone or cytotoxic agents), haemorrhage into the adrenal

glands occurring as a complication of anticoagulation or meningococcal

septicaemia (Waterhouse–Friderichsen syndrome). Look for a Medic–

Alert bracelet indicating that the patient is taking steroids.

Precipitating factors

Infection, trauma, MI, cerebral infarction, asthma, hypothermia, alcohol,

pregnancy, exogenous steroid withdrawal or reduction.

Clinical features

Addison’s disease frequently has an insidious onset with weakness, apathy,

anorexia, weight loss, abdominal pain (which may be severe enough to

mimic an acute abdomen), and oligomenorrhoea. In crisis, the main fea-

tures may be shock (tachycardia, peripheral vasoconstriction, severe pos-

tural hypotension occasionally with syncope, oliguria, profound muscle

weakness, confusion, altered consciousness leading to coma), and hypogly-

caemia. Chronic features of Addison’s disease are: areas of vitiligo and

hyperpigmentation in the palmar creases, buccal mucosa, areolae, scars,

and in the axillae.

Investigations

Hyperkalaemia, hyponatraemia, hypoglycaemia, uraemia, mild acidosis,

hypercalcaemia, and eosinophilia may be present. If Addisonian crisis is

suspected, take appropriate blood samples, but start treatment without

waiting for results.

Management

• Obtain IV access.

• Take blood for cortisol (10mL in a heparinized tube) and ACTH if pos-

sible. Contact the biochemistry lab to warn them that these tests will be

required.

• If features of haemodynamic compromise are present, commence

volume replacement with IV 0.9 % saline if shocked.

• Give hydrocortisone sodium succinate 100mg IV stat.

• Take blood, urine, and sputum for culture and sensitivity.

• Check BMG and blood glucose, and treat hypoglycaemia with 50mL of

10 % glucose IV (repeated if necessary).

• If infection is suspected as a precipitating cause, consider giving broad

spectrum antibiotics.

• Refer for admission.

156 CHAPTER 3 Medicine

Thyrotoxic crisis

A rare condition, occurring in 1–2 % of patients with established

hyperthyroidism (usually toxic diffuse goitre ‘Graves’ disease’). Mortality

is signiﬁ cant (810 % ).

Causes

It is often precipitated by a physiological stressor:

• Premature or inappropriate cessation of anti-thyroid therapy.

• Recent surgery or radio-iodine treatment.

• Intercurrent infection (especially chest infection).

• Trauma.

• Emotional stress.

• DKA, hyperosmolar diabetic crisis, insulin-induced hypoglycaemia.

• Thyroid hormone overdose.

• Pre-eclampsia.

Clinical features

Onset may be sudden with features of hyperthyroidism and adrenergic

overactivity. Fever, cardiovascular, and neurological symptoms are common.

Weight loss, i appetite, tremor, irritability, emotional lability, heat

intolerance, sweating, itch, oligomenorrhoea, agitation, anxiety, confusion,

coma, palpitations, tachycardia, AF (rarely, complete heart block). It may

mimic an ‘acute abdomen’, with abdominal pain, diarrhea, and vomiting.

Differential diagnosis

Includes acute pulmonary oedema, neuroleptic malignant syndrome, septic

shock, anticholinergic or sympathomimetic overdose, drug withdrawal, or

acute anxiety states.

Investigations

• U&E, BMG, and blood glucose, Ca

2 +

(hypercalcaemia occurs in 810 % ).

• FBC, differential WCC, coagulation screen.

• Screen for infection: MSU, blood cultures, sputum.

• T

and T

(for later analysis), TSH.

• CXR (searching for pulmonary infection or congestive heart failure).

• ECG (looking for arrhythmias).

Treatment

• Manage the airway and give O

if indicated.

• Obtain IV access and commence IVI 0.9 % saline (initially 500mL 4-hourly).

• Pass NG tube if vomiting.

• If sedation is required, give small titrated amounts of benzodiazepine

(eg diazepam 5–20mg PO/IV) or haloperidol.

• Commence dexamethasone 4mg 6 hourly PO or give hydrocortisone

100mg IV.

• Give broad spectrum antibiotic if infection is suspected.

• Consider cooling measures in hyperthermia.

• Refer for admission (consider admission to ICU).

• Once admitted, propranolol (or esmolol) and carbimazole will normally

be given together with iodine.

• Do not give aspirin (this can exacerbate the clinical problem by dis-

placing thyroxine from thyroid binding globulin).

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158 CHAPTER 3 Medicine

Urinary tract infection

The urinary tract is normally bacteriologically sterile. Urine infection is

present if > 10

colony-forming units are present per mL of urine. Except

at the extremes of age, urinary tract infections (UTIs) are much more

common in females due to the shorter urethral length. Most UTIs occur

because of organisms invading the bladder via the urethra. Proximal

invasion via the ureter may result in acute or chronic pyelonephritis,

particularly if anatomical derangement exists with impaired ureteric

or bladder emptying. In both sexes, underlying structural abnormality i

UTI risk. Blood-borne spread of infection to the urinary tract can occur,

(eg in bacterial endocarditis or systemic Gram –ve infection). UTI is

usually caused by a single organism. The commonest organism (90 % ) at all

ages is E. coli. Proteus, Klebsiella, and saprophytic staphylococci account for

most of the remainder in adults. Other organisms (eg Pseudomonas ) more

commonly cause UTI in hospitalized patients or following instrumentation.

Urinary tract infection: presentation

UTIs usually present to the ED in one of two ways

Lower UTI (cystitis) Dysuria, frequency, haematuria, suprapubic discomfort,

urgency, burning, cloudy urine with an offensive smell. Patients with acute

urethral syndrome have identical symptoms, but –ve urine culture.

Upper UTI (acute pyelonephritis) Often systemically unwell with malaise,

fever, loin and/or back pain, vomiting, rigors and occasionally Gram –ve

septicaemia.

Investigations

Reagent strip (dipstix) urinalysis may show haematuria, proteinuria, + ve

nitrite, and leucocyte esterase tests. A patient with clear urine, –ve on

dipstix testing, is extremely unlikely to have a UTI. False + ve results may

be secondary to urinary tract tumours or excessive exercise. A false –ve

nitrite test may reﬂ ect pathogens that do not convert dietary nitrates to

nitrites.

Urine microscopy may show leucocytes ( > 100/mL correlates well with

infection, but may be due to contamination or other urinary tract

pathology). RBCs are commonly seen on microscopy, but in isolation

have a low degree of sensitivity or speciﬁ city for UTI. Underlying renal

pathology is suggested by ﬁ nding urinary crystals, RBC, or granular casts.

MSU for culture and sensitivity. Transport the sample to the laboratory

without delay to ensure that bacterial overgrowth does not artiﬁ cially i

the count. Dipslides dipped into freshly passed urine and transported in a

plastic container to the laboratory are an alternative.

159

URINARY TRACT INFECTION

Treatment

• It is usually reasonable to discharge female patients with uncomplicated

lower UTIs with antibiotics . Commence a 3–6 day course of trimetho-

prim or nitrofurantoin. Provide advice regarding ﬂ uid intake, no ‘holding

on’, and voiding after intercourse. Drinking barley water is as effective

as attempts at urinary alkalinization with sodium bicarbonate. ( Note:

urinary alkalinization renders nitrofurantoin ineffective). Advise the

patient to see her GP for review, MSU result, and repeat MSU.

• Elderly men and women with asymptomatic bacteriuria should not

receive antibiotic treatment unless they show signs of being unwell.

• In pregnancy, both symptomatic and asymptomatic bacteriuria should

be treated with an antibiotic such as amoxicillin.

• Given the difﬁ culty in distinguishing prostatitis from simple UTI in men,

they should receive a 2-week course of ciproﬂ oxacin, trimethoprim, or

co-amoxiclav. Arrange GP follow-up.

• Treat catheterized patients with symptoms or signs of UTI for 7 days

with ciproﬂ oxacin or co-amoxiclav. Treatment is more effective if the

catheter is changed in the ED prior to commencing antibiotics.

• Do not treat catheterized patients with asymptomatic bacteriuria with

antibiotics.

Refer for investigation and treatment all male patients and females with

recurrent infections, pregnancy, GU malformation, immunosuppression,

or renal impairment.

Patients with acute pyelonephritis usually require admission for parenteral

antibiotics, ﬂ uid replacement, and analgesia. Assess and treat for severe

sepsis ( b Shock, p.60).

See http://www.sign.ac.uk

160 CHAPTER 3 Medicine

Chronic renal failure

Patients with established chronic renal failure (CRF) are likely to be very

well known to the hospital. Obtain old notes and recent blood results,

and liaise early with in-patient specialist teams.

Established chronic renal failure (not on dialysis)

Patients with mild CRF (glomerular inﬁ ltration rate (GFR) > 40mL/min —

100mL/min) are unlikely to have speciﬁ c problems related to their

underlying renal failure. With GFR <40mL/min, and especially if GFR

<10mL/min, complications may inﬂ uence presentation and treatment.

These patients are prone to pathological fractures.

Secondary hyperparathyroidism and osteomalacia (lack of active vitamin D)

occur in moderate GFR. In severe CRF, aluminium bone disease, and B

microglobulin related amyloidosis may be associated with pathological

fractures.

‘Pseudo-gout’ due to high Ca

2 +

/PO

–

production and twitching/tetany due

to hypocalcaemia may occur.