Clinical Surgery in General - part 1 ppsx

Amlot MB BS FRCP Senior Lecturer, Department of Immunology, Royal Free and University College Medical School, London, UK J.. Atkins MSc FRCS Registrar in Plastic Surgery, Royal Free Hosp

Surgery in General

RCS Course Manual

Commissioning Editor: Laurence Hunter Project Development Manager: Janice Urquhart Project Manager: Frances Affleck

Designer: Erik Bigland

Illustration Manager: Bruce Hogarth

Illustrator: Ethan Danielson

CHURCHILL LIVINGSTONE

An imprint of Elsevier Science Limited

© Royal College of Surgeons 1993

© Royal College of Surgeons 1996

© Royal College of Surgeons 1999

© R M Kirk, W J Ribbans 2004 All rights reserved

The right of R M Kirk and W J Ribbans to be identified as

authors of this work has been asserted by them in

accordance with the Copyright, Designs and Patents Act

1988

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Note

Medical knowledge is constantly changing Standard safetyprecautions must be followed, but as new research andclinical experience broaden our knowledge, changes intreatment and drug therapy may become necessary orappropriate Readers are advised to check the most currentproduct information provided by the manufacturer of eachdrug to be administered to verify the recommended dose,the method and duration of administration, and

contraindications It is the responsibility of the practitioner,relying on experience and knowledge of the patient, todetermine dosages and the best treatment for eachindividual patient Neither the Publisher nor the editorsand contributors assumes any liability for any injuryand/or damage to persons or property arising from thispublication

paper manufactured from sustainable forests

What is the book about? Basic science texts deal with

anatomy, physiology and pathology Clinical textbooks

deal in a systematic manner with guidance on managing

individual patients We have attempted to create a bridge

between the basic sciences and their incorporation into

clinical practice In the past general surgery dominated

teaching and postgraduate surgical examinations, but

many of the included subjects have successively been

separated into specialities In order to offer the best

management to our patients, we may need to know about

specialities outside of surgery, such as imaging

tech-niques, radiotherapy, cancer chemotherapy, and terminal

care We have tried to identify and demonstrate some of

those subjects

The chapters fall into three types Some are intended to

be revelatory; not intended to cover the subject in detail

but offering a simply presented, comprehensible account,

which can be expanded by further reading, for example,

Pathogenesis of cancer Some are for reference, because

apart from the principles, the specific details cannot be

retained in full and need to be looked up, for example

Fluid, electrolyte and acid/base balance The third type are

intended to emphasize that becoming a surgeon is

more than acquiring facts; even more important is the

acquisition of professional attitudes of common sense,

competence, commitment, and compassion Books cannot

transmit attitude, they can merely set out for young

surgeons the high personal and professional standards

that are crucial, for example in Good surgical practice.

Experts often find it difficult to write 'down' for

trainees, and especially for those whose first language is

not English and those taught medicine in languages other

than English Teachers often feel, quite reasonably, that

aspiring experts should learn the basic specialist terms,

but too often the trainees learn the words without fully

understanding their clear meaning Consequently, the

contributors have been exhorted to use simple, direct

language, define complex terms and acronyms, and,

when in doubt, to prefer comprehensibility over

compre-hensiveness Most have been very tolerant

A minority of readers studied Latin or Greek at schooland even those who have done so, do not always recognizethe words when they encounter them in medical texts One

of us, deprived of such an education, vividly remembersencountering the word 'parotid' in a dictionary; it was arevelation to discover that the parotid gland is simply the

'beside the ear gland' (G para = beside + otis - ear) In

con-sequence of this the contributors have been encouraged todefine interesting or difficult terms Although it is often

frowned upon, the eponymous (G epi - upon + onyma = a

name; a distinguishing name) titles of diseases, ments, clinical features, incisions and manoeuvres honourthose who described or recognized them They could beinserted as footnotes, or in a glossary at the end of thebook They do not get overlooked within the text and theyoffer struggling readers moments of relaxation

instru-Surgery was traditionally taught within the master/apprentice relationship The master is often not con-sciously aware of the tacit skills he or she has acquired andpasses on to the apprentice by example, rather than byexplicit teaching The trainee is similarly unaware of assim-ilating it The transfer of this unrecognized wisdom is oftendisparaged as mere skill but is described and extolled by

Michael Polanyi in his book Personal knowledge 1 Wordsalone and this book alone, cannot contain the whole ofknowledge In the present day obsession with objectivity,information that defies statistical analysis is often ignored,when in reality it is only our ignorance of it that prevents

us from utilizing it The really important truths defy tive description Bernard Levin2 stated, 'Most things thatare fundamentally important are not susceptible to logicalanalysis I would go so far as to state that that is how weknow they are fundamentally important.' Because of theneed for trainees to rotate through the sub-specialities,long-term master/apprentice relationships are truncated

objec-As a trainee, assimilate as much as possible by reading but

Michael Polanyi Personal knowledge, Routledge & KeeganPaul, London, 1958

2Times, London, 13th February 1989

Preface

be receptive to the lessons you can acquire through your

contact with experienced senior colleagues In the longer

term, when you become a senior, be receptive to the fresh

lessons to be learned from your juniors

Apology

There is no epicene (G epi = upon + koinos = common;

common to both genders) word for he and she, him and

her, his and hers Most of the older textbooks recognizedonly male surgeons but this must no longer be so.However, there are times when specifying both sexesseveral times in a sentence becomes tedious; repeatedcutting from singular to plural is clumsy Some sexuallyattributable words have acquired special meanings, such

as Master, with the connotation of teacher or leader;Mistress has a quite different connotation!

W.J R

Acknowledgements

We are grateful for the expert and experienced advice of

Laurence Hunter, the pleasure of working once again

with Janice Urquhart and with a newly encountered and

expert copy editor, Rosaline Crum The contributors have

generously agreed to forego any payment in order that

the royalties can be donated to the Royal College of

Surgeons of England towards funding the very successful

Research Fellowships

Professor Marc Winslet, Head of the Academic partment of Surgery at the Royal Free Hospital, has notonly contributed to the book, but he has also generouslyallowed the organization and editing of the book to becentred within the Department

Tushar Agarwal MB BS MRCS(Ed)

Specialist Registrar, Academic Surgical Unit, St Mary's

Hospital, London, UK

Peter L Amlot MB BS FRCP

Senior Lecturer, Department of Immunology, Royal Free

and University College Medical School, London, UK

J L Atkins MSc FRCS

Registrar in Plastic Surgery, Royal Free Hospital,

London, UK

Wynne Aveling MA MB BChir FRCA

Consultant Anaesthetist, University College London

Hospitals, London, UK

Daryll M Baker PhD FRCS(Gen)

Consultant Vascular Surgeon, Royal Free Hospital,

London, UK

Tom Bates MB BS MRCS LRCP FRCS

Consultant Surgeon in General Surgery, The William

Harvey Hospital, Ashford, Kent, UK

T J Beale FRCS(Eng) FRCR

Consultant Radiologist, Central Middlesex Hospital,

London, UK

Satyajit Bhattacharya MS MPhil FRCS

Consultant Surgeon, Hepatic and Pancreatic Surgery

Unit, The Royal London Hospital, London, UK

Peter E M Butler FRCSI FRCS FRCS(Plast)

Consultant Plastic Surgeon, Royal Free Hospital,London, UK

N J W Cheshire MD FRCS FRCS(gen)

Consultant Vascular Surgeon, Regional Vascular Unit,

St Mary's Hospital, London, UK

John P S Cochrane MS FRCS

Consultant Surgeon, Whittington Hospital, London, UK

Richard E C Collins FRCS(Eng) FRCS(Ed)

Chairman Intercollegiate Board in General Surgery1998-2001; Consultant General and Endocrine Surgeon,Kent and Canterbury Hospital, Canterbury, UK

Carmel Coulter FRCR FRCP

Consultant Clinical Oncologist, St Mary's Hospital,London, UK

K Cox MB MS MA FRCS FRACS FACS

Emeritus Professor of Surgery, University of New SouthWales, New South Wales, Australia; Formerly Director

of the World Health Organization Regional TrainingCentre for Health Development

M K H Crumplin MB FRCS

Honorary Consultant Surgeon, Maelor Hospital, NorthEast Wales Trust, UK

Professor Sir Ara Darzi KBE

Professor of Surgery and Head of Department ofSurgical Oncology and Technology, Imperial College ofScience, Technology and Medicine, St Mary's Hospital,London, UK

Andrew Davenport MA MD FRCP

Director, International Society of Hemodialysis;Consultant Renal Physician and Honorary SeniorLecturer, Royal Free Hospital, London, UK

VII

Brian Davidson MB ChB MD FRCS

Professor of Surgery, Royal Free and University College

School of Medicine, London, UK

J L Dawson (deceased)

Ahmet Dogan MD PhD MRCPath

Senior Lecturer and Consultant, Department of

Histopathology, Royal Free and University College

Medical School, UCL Hospitals, London, UK

Glenn Douglas BA(Hons) IPFA MIHSM

Chief Executive, Ashford and St Peter's Hospitals NHS

Trust, Eastbourne, UK

Len Doyal BA MSc

Professor of Medical Ethics, Barts and the London

School of Medicine, Queen Mary, University of London,

London, UK

Peter A Driscoll BSc MD FRCS FFAEM

Consultant in Emergency Medicine, Hope Hospital,

Salford, UK

Roshan Fernando MB ChB FRCA

Consultant Anaesthetist and Honorary Senior Lecturer,

Department of Anaesthesia, Royal Free Hospital,

London, UK

F Kate Gould MB BS FRCPath

Consultant Microbiologist, Freeman Hospital,

Newcastle upon Tyne, UK

Stuart W T Gould FRCS

Senior Lecturer in Surgery, Imperial College of Science,

Technology and Medicine, London, UK

Clair S Cricks BSc PhD

Post Doctoral Research Fellow, Dana Farber Cancer

Institute, Harvard Medical School, Boston, USA

Pierre J Guillou BSc MD FRCS FRCPS(Glas) FMedSci

Professor of Surgery, St James's University Hospital,

School of Medicine, Leeds, UK

Chris G Hargreaves BSc MRCP FRCA

Consultant in Intensive Care Medicine and Anaesthesia,Whittington Hospital, London, UK

John A Henry FRCP FFAEM

Honorary Consultant, Head of Academic Department ofAccident and Emergency Medicine, Imperial CollegeFaculty of Medicine, St Mary's Hospital, London, UK

Barrie Higgs MB BS MSc FRCA

Consultant and Honorary Senior Lecturer, Departments

of Anaesthesia and Physiology, Royal Free Hospital andRoyal Free and University College School of Medicine,London, UK

Daniel Hochhauser MRCP DPhil

Kathleen Ferrier Reader in Medical Oncology, RoyalFree and University College Medical School, London,UK

R W Hoile MS FRCS(Eng)

Consultant General Surgeon, Medway MaritimeHospital, Gillingham, Kent, UK; Principal SurgicalCoordinator of National Confidential Enquiry intoPerioperative Deaths (NCEPOD)

Robert A Huddart MA MB BS MRCP FRCR PhDSenior Lecturer and Honorary Consultant, Institute ofCancer Research and Royal Marsden Hospital, Surrey,UK

Iain A Hunter BMedSci BM BS FRCS(Eng)

Clinical Research Fellow, St James's University Hospital,School of Medicine, Leeds, UK

Donald J Jeffries BSc MB BS FRCP FRCPath

Professor of Virology and Head of Department ofMedical Microbiology, St Bartholomew's and the RoyalLondon School of Medicine and Dentistry, London, UK

Jennifer Jones BSc MB BS FRCP FRCA

Consultant Anaesthetist, St Mary's Hospital, London,UK

Anna C Kurowska BSc BA FRCP

Consultant in Palliative Medicine, Whittington Hospital

and Edenhall Marie Curie Centre, London, UK

Sunil R Lakhani BSc MB BS MD FRCPath

Professor of Breast Cancer Pathology, The Breakthrough

Toby Robins Breast Cancer Research Centre, Institute of

Cancer Research and The Royal Marsden Hospital,

London, UK

David Leaper MD ChM FRCS FRCSEd FRCSGlas FACS

Professor of Surgery, University Hospital of North Tees,

Stockton-on-Tees, UK

Richard C Leonard BA MRCP FRCA FANZCA FFICANZCA

Consultant Intensivist, St Mary's Hospital, London, UK

Liang Low FRCSI

Specialist Registrar in Surgery, University Hospital of

North Tees, Stockton-on-Tees, UK

Valentine M Macaulay MD PhD MRCP

Cancer Research UK Senior Clinical Research Fellow and

Honorary Consultant in Medical Oncology, Molecular

Oncology Laboratories, Weatherall Institute of Molecular

Medicine and Oxford Radcliff Trust, Oxford, UK

John W McClenahan MA MS DipllndMgt PhD FOR

Fellow in Leadership Development, King's Fund,

London, UK

Paul McMaster MA MB ChM FRCS

Professor of Hepatobiliary Surgery and Transplantation,

Queen Elizabeth Hospital, University of Birmingham,

Birmingham, UK

Caroline A Marshall MB BS MRCP FRCA

Consultant Anaesthetist, Southampton University

Hospitals Trust, Southampton, UK

Atul B Mehta MA MB BChir MD FRCP FRCPath

Consultant Haematologist, Royal Free Hospital,

London, UK

Richard W Morris BSc MSc PhD

Senior Lecturer in Medical Statistics, Department of

Primary Care and Population Sciences, Royal Free and

University College London, London, UK

Paul D Nathan PhD MRCP

Specialist Registrar Medical Oncology, Department of

Oncology, Royal Free Hospital, London, UK

Katherine E Orr MB ChB FRCPath

Consultant Microbiologist and Honorary SeniorLecturer, Freeman Hospital, Newcastle upon Tyne, UK

Jason Payne-James LLM FRCS (Ed & Eng) DFM

Honorary Senior Research Fellow, Central MiddlesexHospital, London; Director, Forensic HealthcareServices, London

Anthony L G Peel MA MChir FRCS

Consultant Surgeon, North Tees Hospital, Tees, UK

Stockton-on-Michael W Platt MB BS FRCA

Consultant and Honorary Senior Lecturer inAnaesthetics and Pain Management, St Mary's HospitalNHS Trust, London, UK

William J Ribbans FRCS FRCSEdOrth

Consultant Surgeon, Northampton General Hospital,Northampton, UK

Michael Saleh MB ChB MSc Bioeng FRCSEd FRCSEng

Professor of Orthopaedic and Traumatic Surgery,University of Sheffield; Honorary Consultant, NorthernGeneral Hospital, Sheffield; Honorary Consultant,Sheffield Children's Hospital, Sheffield, UK

Hank J Schneider FRCS

Consultant General and Paediatric Surgeon, The JamesPaget Hospital, Great Yarmouth, UK

J A R Smith PhD FRCS(Ed) FRCS(Eng)

Consultant Surgeon, Northern General Hospital,Sheffield, UK

Martin Smith MB ChB FRCSEd(A&E) FFAEM

Specialist Registrar in Emergency Medicine, HopeHospital, Salford UK

Vinnie Sodhi MB BS BSc FRCA

Portex Research Fellow in Obstetric Anaesthesia,Department of Anaesthesia, Royal Free Hospital,London, UK

Jeremy J T Tate MS FRCS

Consultant Surgeon, Royal United Hospital, Bath, UK

Clare P F Taylor MB BS PhD MRCP MRCPath

Consultant in Haematology and Transfusion Medicine,

Royal Free Hospital and National Blood Service,

London, UK

Adrian Tookman MB BS FRCP

Medical Director, Edenhall Marie Curie Centre, London;

Consultant in Palliative Medicine, Royal Free Hospital,

London, UK

Robin Touquet RD FRCS FFAEM

Consultant in Accident and Emergency Medicine,

St Mary's Hospital, London, UK

Ines Ushiro-Lumb MB BS MSc MRCPath

Consultant Virologist, Department of Virology, Barts

and The London NHS Trust, London, UK

Patricia A Ward MB BS MRCP FRCSEd(A&E) FFAEMDirector of Resuscitation, Accident and EmergencyDepartment, St Mary's Hospital, London, UK

Denis Wilkins MB ChB MD FRCS ILTConsultant General and Vascular Surgeon, DerrifordHospital, Plymouth; Chairman, Court of Examiners,Royal College of Surgeons of England; Chairman of theSpecialist Advisory Committee in Training in GeneralSurgery for Great Britain and Ireland

M C Winslet MS FRCSProfessor of Surgery and Head of Department,University Department of Surgery, Royal Free Hospital,London, UK

Gillian M H Wray MB BS FRCAConsultant in Anaesthesia and Intensive Care Medicine,

St Bartholomew's Hospital, London, UK

x

S W T Gould, T Agarwal, T J Beale

6 Influence of co-existing disease 64

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SECTION 1

EMERGENCY

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1 Resuscitation

R Touquet, P A Ward, M I/I/ Platt, J A Henry

Objectives

Recognize the variety of presentations to

an accident and emergency (A & E)

department; these are often

multidisciplinary, complex, and neither

solely medical nor solely surgical.

Understand the rationale for prioritizing

resuscitation sequences and basing

decisions on the patient's responses to

interventions.

Follow protocols to avoid errors of omission.

Understand arterial blood gases, both in

terms of acid-base balance and gas

exchange.

Understand the difference between

oxygen tension (Pao 2 , partial pressure) and

oxygen saturation (Sao 2 ).

Recognize that the doctor in A & E may be

the last generalist to manage the patient

before admission under a specialist team.

'Scientia vincit timorem'(Knowledge conquers fear)

INTRODUCTION

Collapse (Latin col = together + lapsare = to slip; extreme

prostration, depression and circulatory failure) or coma

(Greek koma = deep sleep; unrousable loss of

conscious-ness) are features of diverse life-threatening conditions

depressing or injuring the central nervous system The cause

is often unknown when the patient arrives in the

resuscita-tion room Furthermore, there may be more than one

cause, for example a hypoglycaemic patient may fall and

sustain a head injury

When a patient with an altered level of consciousness

arrives in the accident and emergency department, apply

the resuscitation sequence described in the American

College of Surgeons' Advanced Trauma Life Support

Course, whether the cause appears medical or surgical.The initial sequence is the primary survey (ABCDE, seebelow), a systematic assessment that can be performedwhile undertaking any resuscitative procedures Instituteongoing monitoring of vital signs while observing theirresponse to any procedure undertaken, such as immedi-

ately infusing 2 litres of crystalloid into an adult with

hypovolaemic shock

When the patient is stable, with clinically acceptablevital signs, carry out the secondary survey, a thoroughexamination from head to toe to avoid missing any patho-logical condition You are often the last doctor to carry out

a complete examination If the patient needs to be ferred immediately to the operating theatre, the second-ary survey must be carried out later, on the ward, bymembers of the admitting team

trans-PART 1: PRIMARY SURVEY WITH INITIAL RESUSCITATION

Greet and talk reassuringly to a conscious patient Do nottreat the patient as an inanimate object Take notice of thehistory from the ambulance crew Involve them in theinitial resuscitation and have them immediately available

to give any further details of the history Ensure that theambulance transfer form is signed by a member of theaccident and emergency department staff

The standard sequence of the initial primary survey is:Airway, with cervical spine control

BreathingCirculationDisability - a brief neurological assessmentExposure - undress the patient completely, but briefly, toavoid hypothermia

Key points

Apply an appropriately sized cervical collar to steady the head In-line cervical spine

3

1 EMERGENCY

immobilization prevents iatrogenic (Greek iatros

= physician + gennaein = produce) spinal cord

damage in those with unsuspected neck injury.

• Be particularly careful if you pass an

orotracheal tube.

Airway

/Assess

Talk to the patient; look for signs of confusion or agitation

which may indicate cerebral hypoxia Listen for stridor or

gurgling sounds from a compromised airway Detect

expired warm air with your hand in a patient who is

breathing Check if chest movements are adequate and

equal

If the patient has inhaled smoke, look for carbon

deposits in the mouth or nostrils, which raise the

possi-bility of upper airway burns and associated carbon

monoxide poisoning If so, call an anaesthetist to pass an

endotracheal tube

Manage

Keep the airway open and clear it Remove any foreign

bodies, such as sweets; suck out vomit Lift the chin

for-wards to bring the tongue off the back of the

naso-pharynx If the gag reflex is diminished, insert an oral

(Guedel) airway; if this is not tolerated, but obstruction is

still present, consider gently inserting a well-lubricated

nasopharyngeal airway Do not insert a nasopharyngeal

airway if basal skull fracture is a possibility Once the

airway is secured, deliver 10-15 1 min'1 oxygen through a

face mask with a reservoir device, which provides about

85% inspired oxygen

None of these basic airway manoeuvres protects the

lungs from aspiration of gastric contents or blood If the

patient has an absent gag reflex, insert a cuffed tracheal

tube by the oral or nasal route to facilitate efficient

venti-lation and protect the lungs

If you cannot provide an airway in any other way,

urgently carry out a needle cricothyroidotomy followed,

if necessary, by a surgical cricothyroidotomy

Breathing

/Assess

Assess any cyanosis If the neck veins are engorged,

con-sider the possibility of a tension pneumothorax, cardiac

tamponade, air embolus, pulmonary embolus or

myo-cardial contusion Check the position of the trachea; if it is

deviated to one side, has it been pushed over by a tension

pneumothorax on the opposite side? Count the

respir-atory rate (normally 12-20 per minute) and expose, inspect

4

and palpate the anterior chest wall Assess breath sounds

or their absence by auscultation A severe asthmatic maypresent with collapse and have a silent chest because withextreme airway narrowing no air can move in or out ofthe lungs If three or more consecutive ribs are fractured

in two or more places, with a segment of paradoxicalchest wall motion, this is a flail chest The underlying pul-monary contusion may cause acute respiratory failure Ifthere is any doubt about the adequacy of the patient'sairway or breathing, urgently obtain expert help fromphysicians and anaesthetists

Manage

Prevent hypoventilation, hypercapnia (Greek kapnos =

smoke, vapour - carbon dioxide) and cerebral latation They produce increased intracerebral pressurewhich is extremely dangerous in traumatized patients,especially if they have suffered a head injury Both adultsand children have a normal tidal volume of 7 ml kg-1 Apatient with rapid, shallow breathing and signs of fatigueand distress is unable to sustain a normal tidal volume.Hypercapnia is likely, with a resultant increase in cerebralperfusion and oedema Institute assisted respiration,initially by bag-valve-mask positive pressure ventilation

vasodi-An arterial blood sample demonstrates a high arterialcarbon dioxide tension (PaCO2) level if breathing is inad-equate If possible, ventilate and oxygenate the hypoxic orapnoeic patient for at least 3 min before attempting intu-bation Do not prolong any attempt for more than 30 sbefore returning to bag-valve-mask ventilation Anapnoeic patient needs urgent ventilatory support.With assisted ventilation, aim to keep the arterial bloodoxygen above 10 kPa (80 mmHg) and the carbon dioxidebelow 5.5 kPa (40 mmHg), but above 4 kPa (30 mmHg) toprevent brain ischaemia In a patient with head injury anddecreased consciousness, a reduction of the Paco2 to justabove 4 kPa (30 mmHg) reduces cerebral oedema and intra-cerebral acidosis

Key points

• Assume that a spontaneously breathing patient who is agitated, aggressive or with a

depressed level of consciousness, is hypoxic.

• Remember, though, that restlessness is also caused by, for example, a full bladder or a tight plaster of Paris splint.

Urgently take arterial blood samples from all collapsedpatients who are not likely to recover immediately, formeasurement of oxygen, carbon dioxide and acid-base

RESUSCITATION I

balance Aspirate arterial blood from the radial artery or,

failing this, from the femoral artery, into a heparinized

syringe (a 2 ml syringe whose dead space has been filled

with heparin 1000 units ml-1)

Maintain arterial oxygen tension (Pao2) above 10 kPa

(80 mmHg), with added inspired oxygen, to preserve

tissue viability The exception is the patient with chronic

obstructive airways disease (COAD), who depends on

hypoxic drive rather than Paco2 to breathe and will tend

to hypoventilate when given added oxygen of more than

35% Diagnose this from the arterial blood gas, which

shows a high Paco2 with a normal pH Give all collapsed

patients high-flow oxygen initially, as patients whose

res-piration is dependent on hypoxic drive are uncommonly

encountered in A & E

You may need to administer oxygen to produce a

higher than normal Pao2 In, for example, carbon

monox-ide poisoning, elevated pulmonary vascular resistance,

sickle cell crisis and anaerobic infections the treatment is

to produce an elevated Pao2

Circulation

Assess

Assess the patient for shock

Early signs of shock

• Anxiety, tachycardia of 100-120 mirr- 1 ,

tachypnoea of 20-30 mirr- 1 , skin mottling,

capillary refill time of more than 2 s, and

postural hypotension.

Initially assume hypovolaemia from occult bleeding if

there is postural hypotension with a fall of systolic blood

pressure of 20 mmHg, a fall of diastolic blood pressure

of 10 mmHg and a rise of pulse of 20 beats per minute

(20:10:20 rule) Supine systolic blood pressure does not

drop until an adult has lost around 1500-2000 ml of

blood, or 30-40% of the blood volume of 70 ml kg-1

body-weight; by this time the patient is ashen in colour because

of blood-drained extremities

The level of consciousness is also decreased because of

inadequate cerebral circulation, particularly if blood loss

was rapid As a guide, a palpable carotid pulse indicates

a systemic blood pressure of at least 60 mmHg

Key point

If the carotid pulse is absent, initiate

immediate basic cardiopulmonary resuscitation

(CPR, see below).

Manage

Control haemorrhage from any external bleedingpoints by direct pressure, with limb elevation whereappropriate

1 Intravenous access The Parisian scientist Jean Poiseuille

(1797-1869) calculated that the rate of flow of fluidthrough a pipe is proportional to the fourth power of theradius, and inversely proportional to the length In aseverely traumatized or hypovolaemic patient, never fail

to insert two short, wide-bore cannulae of 14 gauge orlarger, sited in peripheral veins, whether introduced per-cutaneously or by surgical cutdown

2 Venous cutdown Acquire skill in this safe, simple and

quick technique for intravenous access Prefer the nous vein anterior to the medial malleolus or the basilicvein in the elbow crease Make a transverse, 2 cm incisionanterior to the medial malleolus or to the medial epi-condyle of the humerus Delineate, by blunt dissection,the long saphenous or basilic vein Ligate the vein distallywith 2/0 black silk Control the vein proximally with asimilar loose ligature Make a transverse incision acrossone-third of the circumference of the vein to enable theinsertion of a 14- to 12-gauge cannula Secure the cannula

saphe-in place by tightensaphe-ing the proximal suture This technique

is applicable for collapsed infants

3 Intraosseous infusion is an even simpler technique for

children under 7 years In order to avoid the potential risk

of osteomyelitis, thoroughly clean the area around thesite of insertion, two fingers' breadth distal to the tibialtuberosity, on the anteromedial tibial surface Insert a spe-cially designed intraosseous trocar and cannula throughthe cortex of the bone into the marrow cavity You mayslowly infuse crystalloid and colloid solutions into themarrow (20 ml kg-1 initially for the collapsed child),together with drugs used in resuscitation, with the excep-tion of sodium bicarbonate and bretylium The circulationtime from here to the heart is only 20 s

4 Central venous cannulation, even in experienced

hands, may be dangerous for the trauma patient, who isoften restless Such patients may not survive an iatrogenicpneumothorax or a cervical spinal cord injury caused byturning in the presence of an unsuspected neck injury; asthe above routes of access avoid the possibility of thesecomplications, they are to be preferred Central venouspressure monitoring is useful in the stabilized patient, butthese lines are not for resuscitation other than in patientswith cardiac arrest, when drugs should be administeredcentrally Carry out central vein cannulation after clean-ing the area with antiseptic surgical solution

a Unless the patient has a head injury, apply a 20°head-down tilt to fill the vein and reduce the risk of airembolus The easiest route for an anaesthetist is via theright internal jugular vein, which provides the most direct

1 EMERGENCY

access to the right atrium Turn the patient's head towards

the opposite side and you can feel the vein as the softest

part of the neck, usually lateral to the carotid artery in a

line from the mastoid process to the suprasternal notch

The easiest route for you, or an accident and emergency

clinician, is probably through the right subclavian vein

Pull the right arm caudally, to place the vein in the most

convenient relation to the clavicle for cannulation Unless

there is a possibility of spinal injury, to improve access

place a sandbag beneath the upper thoracic spine so that

the shoulders lie more posteriorly

b For jugular vein cannulation, introduce the needle

through the skin at approximately the midpoint of a line

running from the mastoid process to the suprasternal

notch, aiming laterally at 30° to the skin, towards the right

big toe or right nipple, or towards the previously

pal-pated jugular vein For subclavian vein access, introduce

the needle through the skin 2 cm inferior to the junction

of the lateral and middle thirds of the clavicle Advance

the needle, aspirating continuously and snugging the

inferior bony surface of the clavicle, aiming at the

supe-rior aspect of the right sternoclavicular joint for not more

than 6 cm

c Aspirate until blood freely appears; ensure the bevel

of the needle is now directed caudally; remove the

syringe and immediately insert the Seldinger wire,

flexi-ble end first, through the needle Remove the needle;

rail-road the plastic cannula over the Seldinger wire, then

remove the wire Check that the cannula is in the central

vein by briefly allowing retrograde blood flow into the

attached intravenous giving set

d Aftercare: secure the line with a suture through the

skin and dress the wound with a sterile dressing Return

the patient to the horizontal position and obtain a chest

X-ray to check the position of the central venous cannula

and to exclude a pneumothorax

5 Correct hypovolaemia by rapid intravenous infusion

of warmed crystalloid or colloid solutions followed byblood Rapid loss of more than 40% of a patient's bloodvolume produces pulseless electrical activity, leading tocirculatory standstill unless you carry out immediateresuscitation You cannot measure the blood volume orblood loss in the resuscitation room Therefore monitorthe vital signs (delineated in Part 2), especially inresponse to treatment such as fluid replacement, adjust-ing your treatment accordingly

6 If the carotid pulse is impalpable, the heart hasbecome an ineffective pump and irreversible braindamage results unless you take immediate action tocorrect the specific causes of electromechanical dissoci-ation, such as massive blood loss, tension pneumothorax

or cardiac tamponade If there is no improvement or ifthese conditions are not present, commence cardiacmassage for cardiac arrest (Fig 1.1) Check the heart'selectrical rhythm on the monitor Place the leads in thecorrect positions as quickly as possible If no rhythm isvisible, turn up the gain knob on the monitor and checkfor a rhythm in two different ECG leads Alternatively,monitor through the paddles of a defibrillator, one placedjust to the left of the expected position of the apex beatand one inferior to the right clavicle

7 External chest compression If you cannot feel the

carotid pulse after you have controlled ventilation, placeone hand over the other on the sternum, the lower border

of the hands being two fingers breadth above thexiphisternal-sternal junction If the hands are lower yourisk damaging the liver Keep your arms straight, with theshoulders in a direct line over the hands so that you donot tire Depress the sternum smoothly for 4-5 cm, at arate of 100 per minute, with a ratio of two ventilations tofifteen compressions

Key point

• The absence of a pneumothorax on this film

does not exclude the possibility of one

developing subsequently, possibly under

tension.

If direct venous access is not obtained during CPR, for

immediate drug therapy to the heart muscle give

drugs via a peripheral venous line, infusing 5%

dex-trose solution after injecting each drug, to flush it into

the central circulation You may give certain drugs,

such as adrenaline (epinephrine), atropine, lidocaine

(lignocaine) and naloxone via the tracheal tube route,

in double the intravenous dosage.

pres-of the vena cava, further facilitating the driving pres-of blood

up the carotid arteries; this is the thoracic pump effect.Feel for the carotid or femoral pulse every 2 min

8 Diagnose the correct cardiac rhythm quickly Therhythm is ventricular fibrillation in 70% of patients withnon-traumatic cardiac arrest and the chance of successful

Fig 1.1 Adult advanced life support The Resuscitation Council (UK) Reproduced with permission.

resuscitation is directly proportional to the speed of

applying a DC shock in the correct manner and sequence

(Fig 1.1) There must be no delay following arrest, and

this is why ambulance crews are being trained to use, and

are issued with, defibrillators

9 Internal cardiac massage External chest compression

does not effectively resuscitate an empty heart that is incardiac arrest from hypovolaemic shock; however inter-nal cardiac massage is indicated in the A & E department

for direct penetrating trauma only It is not for blunt

7

1

trauma, when the patient, at the very least, just has a

palpable pulse on arrival When there is no appropriate

response to prompt rapid transfusion, consider internal

cardiac massage for penetrating trauma This is the only

indication for an emergency thoracotomy for internal

cardiac massage by trained personnel in the A & E

depart-ment If you have had appropriate training, it is both

safe and haemodynamically superior to external cardiac

massage, although the latter can be initiated without

delay and performed by non-surgeons Open-chest

cardio-pulmonary resuscitation (CPR) enables you to feel and

see the heart, and direct electric defibrillation

10 Create a left-sided thoracotomy through the fourth or

fifth intercostal space once the patient is receiving

intermit-tent positive pressure ventilation through a tracheal tube

Immediately compress the heart using your left hand,

without at first opening the pericardial sac, by placing your

thumb over the left ventricle posteriorly and fingers

anteri-orly in front of the heart Compress the heart at the rate of

100 times per minute, adjusting the force and rate to the

filling of the heart Open the pericardium, avoiding the

phrenic and vagus nerves You may inject adrenaline

(epinephrine), atropine and lidocaine (lignocaine), but

not sodium bicarbonate, directly into the left ventricle,

avoiding the coronary arteries For internal defibrillation use

internal 6 cm paddle electrodes with saline-soaked gauze

pads and insulated handles Place one paddle posteriorly

over the left ventricle and one over the anterior surface of the

heart (10-20 J)

11 Drugs In a patient with cardiac arrest, if possible

give drugs such as adrenaline (epinephrine) centrally, and

for this reason become proficient in at least one method

of central venous cannulation Use the approach with

which you are most familiar The infraclavicular approach

is often the most convenient and practicable means of

access

Disability

This term signifies a brief neurological assessment you

must carry out at this stage of the initial examination The

mnemonic used in the Advanced Trauma Life Support

Course is useful:

A = Alert

V = responds to Verbal stimuli

P = responds to Painful stimuli

U = Unresponsive

Now assess the presence or absence of orientation in time

(does the patient know the day and month?), space

(knows where he or she is?) and person (knows who he

or she is?) These perceptions are usually lost in this

sequence with lessening of consciousness Alternatively

use the Glasgow coma scale at the outset

Record the pupil size and response to light (Table 1.1).Bilateral small pupils denote opiate poisoning unless dis-proved by failure of naloxone to reverse the constriction

If necessary, give up to 2 mg of naloxone (i.e five vials of0.4 mg) If there is a response, you may need to give more,because naloxone has a short half-life You may give it via

an endotracheal tube if you do not have intravenousaccess The other common cause of bilateral small pupils

is a pontine haemorrhage, for which there is no specifictreatment

Expose

In a severely traumatized patient always carry out acomplete examination of the entire skin surface Removeevery article of clothing Carefully protect the spine.Complete examination demands log-rolling by a mini-mum of four trained people so that you can examine theback Perform this early if there is a specific indication,such as injury to the posterior chest wall, or at the latest

at the end of the secondary survey Protect all patients,particularly children, from hypothermia

Consider inserting a nasogastric tube or, if you suspect

a cribriform plate fracture, an orogastric tube Insert aurinary catheter after inspecting the perineum for bruis-ing and bleeding, and carrying out a rectal examination

in an injured patient (see Ch 2)

PART 2: MONITORING

Key point

• Throughout the initial assessment, resuscitate, monitor and react to changing clinical and vital measurements (see also Ch 9).

• Pulse Remember that in an elderly or even a

middle-aged person a rate of more than 140 beats per minute

is very unlikely to be sinus tachycardia as this is too fastfor someone of that age Atrial flutter runs at around

300 beats per minute, and therefore if there is 2-1 ventricular block the ventricular rate is 150 beats perminute The rate of supraventricular tachycardia isusually 160-220 beats per minute

atrio-• Respiratory rate is important Do not forget it The

normal range is 12-20 breaths per minute It rises earlywith blood loss or hypoxia, and, as well as being a veryuseful indication of the patient's clinical state, it is one

of the physiological parameters that is mandatory forthe calculation of the revised trauma score

• Blood pressure drops in hypovolaemia when the blood

loss is greater than 3040% of the total blood volume 8

-1

RESUSCITATION I

Table 1.1 Pupil size and response to light in comatose patients

Dilated Atropine in eye

3rd nerve lesion normal consensual light

reflex, e.g posterior communicating

artery aneurysm

Enlarging mass lesion above the tentorium,

causing a pressure cone

Optic nerve lesion:

Old: pale disc and afferent pupil

New: afferent pupil with normal disc, loss of direct

light reflex, loss of consensual reflex in other

eye - both constrict with light in other eye

Cerebral anoxiaVery poor outlook if increasing supratentorialpressure - if dilated pupils preceded by unilateraldilatation or if due to diffuse cerebral damageOverdose: e.g amphetamines (including MDMA

"Ecstasy")carbon monoxidephenothiazinescocaineglutethimideantidepressantsHypothermia

Constricted Pilocarpine in eye

Horner's, e.g brachial plexus lesion

Acute stroke uncommonly (brainstem

occlusion or carotid artery ischaemia: small

pupil opposite side to weakness)

Pilocarpine in both eyes (glaucoma treatment)Opiates, organophosphate insecticides andtrichloroethanol (chloral)

Pontine haemorrhage or ischaemia (brisk tendonreflexes, and raised temperature: poor

prognostic sign)Alcohol poisoning (dilatation shaking)(Macewan's pupil))

If pupils normal in size, and reacting to light, consider metabolic, systemic non-cerebral causes

(N.B Normal pupils do not exclude a drug overdose)

about 2000 ml in an adult Fit young adults, and

especially children, maintain their blood pressure

resiliently, but then it falls precipitously when

com-pensatory mechanisms are overwhelmed

Pulse pressure is the difference between systolic and

diastolic pressures Diastolic pressure rises initially

fol-lowing haemorrhage, because of vasoconstriction from

circulating catecholamines Systolic pressure stays

con-stant, therefore the pulse pressure decreases This is

fol-lowed by a greater decrease in the pulse pressure as the

systolic blood pressure falls once 30% of the patient's

blood volume has been lost

Capillary refill time is the period it takes for blood to

return to a compressed nailbed on release of pressure

It may be lengthened by hypothermia, peripheral

microvascular disease and collagen diseases, in

addi-tion to hypovolaemia The normal value is 2 s, but this

increases early in shock, following a 15% loss of blood

volume

Temperature fall indicates the degree of blood loss in a

hypovolaemic patient, quite apart from primary

hypothermia Restore blood volume adequately

because simple warming of a hypovolaemic patientproduces vasodilatation with resulting further fall inblood pressure A patient with primary hypothermia isusually also hypovolaemic, so rapid rewarming results

in a drop in blood pressure unless blood volume isreplaced Ensure your resuscitation room has awarming device, ideally as part of a rapid transfuser, sothat intravenous fluid at 37-38°C can be immediatelyinfused to the hypovolaemic or hypothermic patient

• Urinary output The minimum normal obligatory

output is 30 ml h-1 In a child it is easily remembered as

1 ml kg-1 h-1 Suspect renal pathology if you find morethan a trace of +protein on stick testing

• Central venous pressure (CVP) is measured in

centime-tres of water by positioning the manometer on a standsuch that the zero point is level with the patient's rightatrium The normal pressure is around 5 cmH2O fromthe angle of Louis, with the patient at 45° to thehorizontal

The CVP is a measure of the filling pressure (preload) tothe right atrium It reflects the volume of blood in the

9

1 73 EMERGENCY

central veins relative to the venous tone It is not a

measure of left heart function, until right ventricular

func-tion is compromised as a result of poor left heart funcfunc-tion

It may be low if the patient is hypovolaemic, and rises to

normal with correction If it rises slowly with a fluid

chal-lenge, this usually indicates hypovolaemia Particularly in

the young, peripheral vasoconstriction to conserve central

blood volume occurs in the presence of hypovolaemic

shock, maintaining central venous pressure to a limited

degree It is raised if the circulating volume is too large,

as might happen with renal failure or with

overtransfu-sion Overtransfusion not only precipitates heart failure,

due to dilatation of the heart, but in a patient with a head

injury the resultant rise in intracranial pressure may cause

irreversible damage to the already bruised brain

Therefore assiduously monitor the CVP in these

circum-stances

The CVP also rises with malfunctioning of the right

side of the heart It cannot then be used as an indicator of

systemic circulatory filling, except as a measure of

chang-ing cardiac function It may be raised for mechanical

reasons, such as tension pneumothorax or cardiac

tam-ponade It is also raised in the presence of pulmonary

embolism, or when the heart is failing for lack of

muscu-lar power due to contusion or infarction

Arterial blood gases

pH (normal range 7.35-7.45)

Does the patient have an acidosis, alkalosis or neither

(Table 1.2)? The lower the pH, the more acidic is the blood

sample, the opposite being the case for alkalosis Acid (as

hydrogen ions) is produced continually from

metaboliz-ing cells, mostly as carbon dioxide More is generated by

lactic acid production during conditions of hypoxia, for

example in shock, or in cardiac or respiratory arrest

Inadequate tissue perfusion results in acid buildup Most

acid-base abnormalities result from an imbalance

between production and removal of H+ ions (Table 1.3).

Hydrogen is adsorbed by buffers, the largest being teins, both intra- and extracellularly In the extracellularfluid, the largest buffer is haemoglobin However, bicar-bonate is a highly dynamic buffer, enabling an exchange

pro-to occur between hydrogen and carbon dioxide Thisenables hydrogen to be excreted rapidly via the lungs ascarbon dioxide:

Hydrogen ions are also excreted via the kidneys, but overhours or days, leaving respiratory compensation to be themost rapid method the body has for correction

The complex proteins of the body are optimally formed at ideal pH When the pH of tissues changes, itinduces conformational changes in proteins, affectingtheir function, especially enzymes and cell membranechannels This is why it is crucial to maintain normal pH.Carbon dioxide is the largest generator of H+ ions, tentimes more than the production of lactic or other

con-metabolic acids (Table 1.3).

Pco 2 (normal range 35-45 mmHg, 4.5-5.5 kPa)

• Pco2 is high: suggests a respiratory acidosis (if pH islow); or a compensated metabolic alkalosis (see below)

• Pco2 is low: suggests a respiratory alkalosis (if pH ishigh); or a compensated metabolic acidosis (see below).The partial pressure of carbon dioxide is related to thedegree of lung ventilation Hyperventilation reducesPco2 and vice versa If the patient is not breathing ade-quately, carbon dioxide is not adequately excreted andhydrogen ions build up, leading to acidosis caused byinadequate ventilation, that is, a respiratory acidosis pHfalls, indicating acidosis Anxious patients and those inearly hypovolaemic shock have a tachypnoea, resulting inoverexcretion of carbon dioxide, with loss of hydrogenand a resulting respiratory alkalosis

When the patient is ventilated mechanically or ally, an end-tidal carbon dioxide measuring device gives

manu-Table 1.2 Reading of arterial blood gases for acid-base balance

If Pco2 > 5.5 kPa, suggests respiratory acidosis (pH < 7.35), or attempted

compensation of a metabolic alkalosis (pH > 7AS and BE > +3)

Base excess (BE) is always affected by metabolic acid-base changes:

Metabolic acidosis causes BE < -3 Metabolic alkalosis causes BE > +3

10