SIMPSON’S FORENSIC

MEDICINE
Professor CEDRIC KEITH SIMPSON CBE (1907–1985) MD (Lond), FRCP,
FRCPath, MD (Gent), MA (Oxon), LLD (Edin), DMJ. Keith Simpson was the first
Professor of Forensic Medicine at the University of London and undoubtedly
one of the most eminent forensic pathologists of the twentieth century. He spent
all his professional life at Guy’s Hospital, and he became a household name
through his involvement in many notorious murder trials in Britain and over-
seas. He was made a Commander of the British Empire in 1975. He was a superb
teacher, through both the spoken and the printed word. The first edition of this
book appeared in 1947 and in 1958 won the Swiney Prize of the Royal Society of
Arts for being the best work on medical jurisprudence to appear in the preceding
ten years.
Professor Simpson updated this book for seven further editions. Professor
Bernard Knight worked with him on the ninth edition and, after Professor
Simpson’s death in 1985, updated the text for the tenth and eleventh editions.
Richard Shepherd updated Simpson’s Forensic Medicine for its twelfth edition
in 2003. Jason Payne-James and Richard Jones have updated the 13th and this
edition.
 SIMPSON’S FORENSIC
MEDICINE
14th Edition

Edited by
Professor Jason Payne-James, LLM, MSc, FFFLM, FRCS,
FRCP, FCSFS, RCPathME, FFCFM(RCPA), DFM, LBIPP, Mediator
Specialist in Forensic & Legal Medicine & Consultant Forensic Physician
Honorary Clinical Professor, William Harvey Research Institute
Queen Mary University of London
Consultant Editor-in-Chief, Journal of Forensic & Legal Medicine
Lead Medical Examiner, Norfolk & Norwich University
Hospital NHS Foundation Trust, Norwich
Director, Forensic Health Services Ltd, Southminster, United Kingdom

Richard Jones, BSc(Hons), MBBS, PgCUTL, FRCPath, FHEA,

MCIEH, MFFLM, MRSPH
Clinical Senior Lecturer in Forensic Pathology
Wales Institute of Forensic Medicine
Cardiff University School of Medicine
College of Biomedical and Life Sciences, Cardiff
Home Office-Registered Forensic Pathologist,
Honorary Consultant Forensic Pathologist
Cardiff and Vale University Health Board, Cardiff, United Kingdom
iv 

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Library of Congress Cataloging-in-Publication Data

Names: Payne-James, Jason (Forensic physician), editor. | Jones, Richard (Forensic pathologist), editor.
Title: Simpson’s forensic medicine / edited by Professor Jason Payne-James and Dr. Richard Jones.
Other titles: Forensic medicine
Description: 14e. | Boca Raton : CRC Press, 2019. | Preceded by Simpson’s forensic medicine / Jason Payne-James
… [et al.]. 13th ed. c2011. |
Includes bibliographical references and index.
Identifiers: LCCN 2019014218| ISBN 9781498704298 (pbk. : alk. paper) | ISBN 9780367333195 (hardback : alk.
paper) | ISBN 9781315157054 (ebook)
Subjects: | MESH: Forensic Medicine
Classification: LCC RA1051 | NLM W 700 | DDC 614/.1--dc23
LC record available at https://lccn.loc.gov/2019014218

Visit the Taylor & Francis Web site at

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 Contents
About the authors vii 14 Identification of the living and the dead 198
Contributors viii
15 Restraint and control techniques 208
Preface ix
Acknowledgements x 16 Police custodial healthcare 217

17 Sexual assault, genitoanal injury and

1 Principles of forensic practice 1 female genital mutilation 229

2 The ethics of medical practice 13 18 Safeguarding and protection

of children and vulnerable adults 244
3 Medicolegal aspects of death 30
19 Transportation medicine 257
4 Violence in society, medicolegal ­
investigation of death and the autopsy 40 20 Torture and cruel, inhuman and degrading
t­ reatment 271
5 The appearance of the body after death 55
21 Principles of forensic science and crime
6 Death from natural causes 69 scene investigation 276
7 Deaths and injury in infancy 83 22 Principles of toxicology 295
8 Assessment, classification and 23 Alcohol 302
d
­ ocumentation of injury 105
24 Licit and illicit drugs 307
9 Ballistic injuries 133
25 Medicinal poisons 321
10 Regional injuries and patterns of injury 149
26 Miscellaneous poisons 325
11 Pressure to the neck and asphyxia deaths 162

12 Heat, cold and ­electrical trauma 177 Index333

13 Immersion and drowning 191

v
 About the authors
Jason Payne-James
is an independent
Specialist in Forensic
and Legal Medicine
with a range of
research and clini-
cal interests. From
a clinical perspec-
tive, Jason has been
a forensic physician
for almost three
decades. Previously,
he worked in hospital
medicine, predomi-
nantly in surgical,
trauma and gastroenterological specialties. He taught
anatomy at the London Hospital Medical College. His
interests include injury, wound and scar documenta-
tion and interpretation, imaging of injury and scars,
clinical and ethical aspects of healthcare in custody,
complaints against healthcare professionals, forensic
evidence collection, restraint and less-lethal systems,
miscarriages of justice, harm and death in custody and
torture.
He has published on a wide range of subjects includ-
ing healthcare in custody, torture, death in custody,
use-of-force, TASER photo-documentation and irri-
tant spray. He acts an expert witness in these areas in
the UK and overseas. Jason was President of the Faculty
of Forensic & Legal Medicine of the Royal College of
Physicians (2015–2017); Present of the World Police
Medical Officers (2011–2014); he is Honorary Clinical
Professor at the William Harvey Research Institute,
Queen Mary University of London; external Consultant
to the UK National Crime Agency and National Injuries
Database; Consultant Editor-in-Chief of the ‘Journal of
Forensic & Legal Medicine’; Member of the Executive
Committee of the European Council of Legal Medicine;
Visiting Professor at the University of Belgrade, Serbia.
He is an independent member of the Scientific Advisory
Committee on the Medical Implications of Less-Lethal
Weapons. He is a member of the International Forensic
Expert Group of the International Rehabilitation
Council for Torture Victims.
In addition to this, and the 13th Edition of
Simpson’s Forensic Medicine, Jason has co-authored
and co-edited a large number of internationally
recognised publications including the first and
second editions of the Encyclopaedia of Forensic
and Legal Medicine; Forensic Medicine: Clinical
and Pathological Aspects; Symptoms and Signs of
Substance Misuse (1st, 2nd and 3rd editions); he co-
authored the Oxford Handbook of Forensic Medicine
and co-edited Age Estimation in the Living and Current
Practice in Forensic Medicine (1st and Volumes);
and Monitoring Detention, Custody, Torture and
Ill-treatment. He designed the ForensiGraph  and the
ForensiDoc  App.
Richard Jones is a
forensic pathologist
w ith a particular
interest in education,
and is a Fellow of the
Higher Educat ion
Academy. He is com-
mitted to providing
educational materi-
als in forensic sci-
ence, medicine and
pathology to a broad
aud ience on l i ne,
including via a web-
site ‘Forensic Medicine for Medical Students’ www.
forensicmed.co.uk. In addition to co-authoring the
13th Edition of Simpson’s Forensic Medicine he has
published peer-reviewed articles in the forensic med-
ical literature, including on the development of teach-
ing for medical students on safeguarding vulnerable
patients at risk of abuse or neglect, and complexity in
forensic pathology. As a UK Home Office-accredited
forensic pathologist, he attends scenes of suspicious
deaths, and performs medico-legal autopsies for
police authorities and ­c oroners. He is a member of the
Training and Education Subcommittee of the Faculty
of Forensic & Legal Medicine of the Royal College
of Physicians, and was a UK Consulting Editor/
Editorial Board Member of Medicine, Science and the
Law (2011–2017). He was a Specialist Reviewer for the
Welsh Child Protection Systematic Review Group
(2006–2013).
vii
 Contributors

Soren Blau PhD Andrew Parry BSc (Hons)

Senior Forensic Anthropologist Senior Reporting Forensic Scientist
Victorian Institute of Forensic Medicine Cellmark Forensic Services
Melbourne, Australia Abingdon, UK

Romina Carabott Sabine Maguire

Forensic Odontologist Honorary Lecturer
Formerly of Expert Forensics Ltd Division of Population Medicine
Cardiff Medicentre School of Medicine
Heath Park Cardiff University
Cardiff, UK Cardiff, UK

Sam Evans Denise Syndercombe-Court

Chief Photographer Professor of Forensic Genetics
School of Dentistry Department of Analytical, Environmental and
College of Biomedical & Life Sciences Forensic Sciences
Cardiff University King’s College London
Heath Park Franklin-Wilkins Building
Cardiff, UK London, UK

Tina Lovelock CChem FRSC MCSFS

Interpretation Lead, Chemistry Lead
& Senior Reporting Forensic Scientist
Cellmark Forensic Services
Abingdon, UK

viii
 Preface
The broad range of subjects embraced by the terms
‘forensic medicine’ since the first edition of Keith
Simpson’s eponymous Forensic Medicine was published
in 1947 has expanded considerably. Most forensic prac-
titioners from any background will, at some stage, be
asked ‘have you cut up any dead bodies recently?’ as
there remains a belief that this is the main function of
those working in forensic medicine. In practice, how-
ever, the pathological side of forensic medicine is small
compared to the number and workload of those work-
ing in the clinical (living) aspects of forensic medicine.
The fields of safeguarding, insurance medicine, and
refugee medicine, for example, could be considered
to be aspects of ‘forensic medicine’. There is a general
move to capture this trend by referring to either ‘foren-
sic & legal medicine’ or ‘legal & forensic medicine’. The
terms are interchangeable but reflect the general view
that this is a defined and extensive area of medicine
that warrants its own specialty status, on a par with all
other mainstream specialties. Whatever the specialty
is called, doctors and other healthcare professionals
working in these areas need to have a basic knowledge
and understanding of medical ethical principles, of rel-
evant law and the many aspects of forensic science. This
we hope to provide.
Earlier editions of Simpson’s have been directed
predominantly at a medical readership. This has now
changed as forensic disciplines have expanded and
the role of forensic medicine and sciences has grown.
Much of this growth is related to a greater public aware-
ness of the essential roles that these disciplines play in
a fair justice system. Although forensic medicine has
a long history of involvement with the criminal justice
systems, this role has also been extended into many
parts of the civil justice system including family law.
This has been accompanied by a dramatic growth in
undergraduate and postgraduate courses with a foren-
sic element. It is crucial that students and practitioners
in such settings are able to understand how their area
of work or study interrelates and interacts with others
in different settings. Whether one is a budding foren-
sic practitioner, law enforcement officer, healthcare
professional, lawyer, or someone who, by the nature
of their work, will at some stage (like it or not) become
involved in forensic matters, there is an increasing need
to be aware of, and understand, the basics of forensic
medicine and how it relates to the other specialties.
This, the 14th edition of Simpson’s Forensic Medicine,
has been revised to assist all those groups; not merely
doctors and other healthcare professionals. We hope
it provides a solid introduction and background to the
principles of practice for those embarking on careers in
forensic settings, for those in practice and for those who
may not be from a forensic background but whose daily
workload brings them into contact with situations that
require an awareness of such matters. This probably
applies to most healthcare professionals.
Within this edition, each chapter provides recom-
mendations to access more detailed information about
a subject, whether online, as peer-reviewed journal
articles, or substantive publications. We hope this
edition of Simpson’s will encourage readers to further
explore the world of forensic medicine and its many fac-
ets. We all work within multiprofessional settings, and
in forensic terms, each of us provides a small piece of
the jigsaw in the investigation and resolution of a case.
It is, therefore, essential to have a good awareness of
the roles and limitations of our knowledge base, and
when and where we should defer to other colleagues.
Although the perspective provided in this book is gen-
erally from the point of view of a doctor, we hope we
have identified common issues for all practitioners. We
know our readership originates from a variety of differ-
ent countries and contrasting legal systems. Examples
that we provide of relevant regulations, law, codes and
practice will, of necessity, predominantly be derived
from the England & Wales jurisdictions. However, every
reader must make themselves familiar with those that
apply within their own professional setting, their own
country and their own jurisdiction. We also strongly
advise, in an age when many guidance documents are
kept online as evolving and developing resources, to
check always that you are using the most up-to-date
version.
Any mistakes or misinterpretations are those of the
authors who will happily receive comment and criti-
cism on any aspect of the content. We hope that readers
will find that this new edition of Keith Simpson’s classic
text addresses your needs.
Jason Payne-James
Richard Jones
September 2019
ix
 Acknowledgements
Jason Payne-James thanks his colleagues from law,
police, medicine and science for collaborating on the
great variety of cases on which he has worked. He
would also like to thank his long-suffering family for
their continued support and encouragement both day
and night. The Taylor & Francis team led by Miranda
Bromage must be thanked for their professionalism and
forbearance as this edition developed, and our thanks
must also go to Nora Naughton for all her hard work.
x
Richard Jones also thanks his colleagues from those
many organisations with which he works, and espe-
cially for their continued support and mentoring, often
in very difficult circumstances. He also thanks his
enthusiastic students who, over the years, have inspired
him to reflect on the knowledge base underpinning
forensic medicine and pathology.
1 Principles of forensic practice
▪▪ Introduction
▪▪ Legal systems
▪▪ Doctors and other healthcare professionals and the law
▪▪ Evidence for courts
Introduction
Different countries have different legal systems, which
broadly divide into two areas of law – ­c riminal and
civil. The various systems have generally evolved over
many years or centuries and are influenced by a wide
variety of factors including culture, religion and poli-
tics. By and large, the rule of law has been established
over many hundreds of years and is generally accepted
because it is for the mutual benefit of the population –
it is the framework that prevents anarchy. Although
there are some common rules (e.g., concerning mur-
der) that are to be found in every country, there are also
considerable variations from country to country in
many of the other codes or rules. The laws of a country
are usually established by an elected political institu-
tion, the population accepts those laws and they are
enforced by the imposition of penalties (such as fines,
prison sentences, or community service) on those who
are found guilty of breaking them.
Those working within the medical, healthcare and
scientific professions are bound by the same general
laws as the population as a whole, but they may also
be bound by additional laws, rules, standards or regu-
lations specific to their area of practice. Standards of
practice may be described to which all should aspire,
although deviation from best practice may be allowable
depending on the nature of the standard. Each profes-
sion may, in addition to standard-setting bodies, also
have its own regulatory body, which may also have the
ability to sanction inappropriate professional behav-
iour, irrespective of whether laws have been broken.
The training, qualification and registration of doctors,
scientists and related professions is of great relevance
at the current time, in light of the recognised need to
ensure that evidence, both medical and scientific, that
is placed before the court, is established and recog-
nised. In the United Kingdom, the independent Forensic
Science Regulator is tasked with establishing and
enforcing quality standards for forensic science used in
the investigation and prosecution of crime. Fraudulent
professional and ‘hired guns’ risk undermining their
own professions, in addition to causing miscarriages
of justice where the innocent may be convicted and the
▪▪ Healthcare professionals as witnesses in court
▪▪ Bibliography and information sources
▪▪ Further general resources
guilty acquitted. It is crucial that medical and scientific
professionals understand that the evidence they provide
in any case, is only one part of the overall body of evi-
dence and that, in contrast to how broadcast media rep-
resent us, the solving of crimes is generally the result of
meticulous painstaking and often tedious effort as part
of a multiprofessional team. The final arbiter of how that
evidence is interpreted in the context of the case is the
role of the judge (and in relevant jurisdictions, the jury).
The great diversity of the legal systems around the
world poses a number of problems for authors when pro-
viding details or examples of the law in a book such as
this. Laws on the same aspect often differ widely from
country to country, and some medical procedures (e.g.,
abortion) that are routine practice (subject to appropri-
ate legal controls) in some countries are considered to be
a crime in others. Within the United Kingdom, England
& Wales has its own legal system, and Scotland and
Northern Ireland have their own legal traditions which,
although distinct from that of England & Wales, share
many values. There are also smaller jurisdictions with
their own individual variations in the Isle of Man and
the Channel Islands. Overarching this is European leg-
islation and with it the possibility of final appeals to the
European Court, although the nature of this may change
dependent on the outcome of negotiations of the United
Kingdom in leaving Europe. That body of law will how-
ever, still remain. Other bodies (e.g., the International
Criminal Court) may also influence regional issues and
particular types of cases, such as war crimes.
Where relevant, this book will utilise the England &
Wales legal system for most examples, making refer-
ence to other legal systems if necessary. However, it is
down to the individual professional who is working in,
or exposed to, forensic matters to be aware of those cur-
rent laws, statutes, codes and regulations that not only
apply generally but also specifically to their own area of
practice and in their own jurisdiction.
Legal systems
Laws are rules that govern orderly behaviour in a col-
lective society and the system referred to as ‘the Law’
is an expression of the formal institutionalisation of the
2 Principles of forensic practice
promulgation, adjudication and enforcement of rules.
There are many national variations but the basic pat-
tern is often similar. The exact structure is frequently
developed from, and thus determined by, the political
system, culture and religious attitudes of the country in
question. In England & Wales, the principal sources of
these laws are Parliament and the decisions of judges in
courts of law. Criminal courts generally deal predomi-
nantly with disputes between the State and individual,
and the civil courts with disputes between individuals.
Most jurisdictions will have a range of other legal bod-
ies that are part of these systems or part of the overall
justice system (e.g., employment tribunals, asylum tri-
bunals, mental health review tribunals and other spe-
cialist dispute panels) and such bodies may deal with
conflicts that arise between citizens and administrative
bodies, or make judgements in other disputes. All such
courts, tribunals or bodies may, at some stage, require
input from medical and scientific professionals.
In England & Wales, decisions made by judges in the
courts have evolved over time and this body of decisions
is referred to as ‘common law’ or ‘case law’. The ‘doc-
trine of precedent’ ensures that principles determined
in one court will normally be binding on judges in infe-
rior courts. The Supreme Court of the United Kingdom is
the highest court in all matters under English and Welsh
law, Northern Irish law and Scottish civil law. It is the
court of last resort and highest appeal court in the United
Kingdom; however, the High Court of Justiciary remains
the highest court for criminal cases in Scotland. The
Constitutional Reform Act 2005 established (amongst
other functions) a Supreme Court which assumed the
judicial functions of the House of Lords, which were pre-
viously undertaken by the Lords of Appeal in Ordinary
(commonly called Law Lords). The ‘long title’ of the Act
further detailed the changes it enacted – ‘An Act to make
provision for modifying the office of Lord Chancellor,
and to make provision relating to the functions of
that office; to establish a Supreme Court of the United
Kingdom, and to abolish the appellate jurisdiction of the
House of Lords; to make provision about the jurisdic-
tion of the Judicial Committee of the Privy Council and
the judicial functions of the President of the Council; to
make other provisions about the judiciary, their appoint-
ment and discipline; and for connected purposes’. Along
with the concept of Parliamentary Sovereignty is that the
judiciary (the judges) are independent of state control,
although the courts will still be bound by statutory law.
This separation is one that is frequently and increasingly
tested by politicians and the media in particular.
Criminal law
Criminal law is that law which addresses the relation-
ship between the state and the individual and as such
is probably the area in which medical and scientific
knowledge requiring expertise within a legal setting
(forensic medicine and forensic science) is most com-
monly required. Criminal trials involve offences that
are ‘against the public interest’; these include offences
against the person (e.g., murder, assault, grievous bodily
harm, rape), property (e.g., burglary, theft, robbery), and
public safety and security of the state (terrorism). In
these matters, the state acts as the voice or the agent of
the people. In continental Europe, a form of law derived
from the Napoleonic era applies. Napoleonic law is an
‘inquisitorial’ system and both the prosecution and the
defence have to make their cases to the court, which
then chooses which is the more credible. Evidence is
often taken in written form as depositions, sometimes
referred to as ‘documentary evidence’. The Anglo-
Saxon model applies in England & Wales and in many
of the countries that it has influenced in the past. This
system is termed the ‘adversarial’ system. If an act is
considered of sufficient importance or gravity, the state
‘prosecutes’ the individual. Prosecutions for crime in
England & Wales are made by the Crown Prosecution
Service (CPS), who assess the evidence provided to them
by the police. They must consider two main questions:
(1) Is there enough evidence against the defendant?
When deciding whether there is enough evidence to
charge, Crown Prosecutors must consider whether evi-
dence can be used in court and is reliable and credible.
Crown Prosecutors must be satisfied there is enough
evidence to provide a ‘realistic prospect of conviction’
against each defendant; and (2) Is it in the public inter-
est for the CPS to bring the case to court? A prosecution
will usually take place unless the prosecutor is sure that
the public interest factors tending against prosecution
outweigh those tending in favour. Thus, even when there
is sufficient evidence to justify a prosecution or to offer
an out-of-court disposal, prosecutors must go on to con-
sider whether a prosecution is required in the public
interest. The more serious the offence or the offender’s
record of criminal behaviour, the more likely it is that a
prosecution will be required in the public interest.
In a criminal trial, it is for the prosecution to prove
their case to the jury or the magistrates ‘beyond reason-
able doubt’. This standard of proof was outlined in the
case of Woolmington v Director of Public Prosecutions
[1935] AC 462 when Viscount Sankey, the then Lord
Chancellor, stated:
Throughout the web of the English Criminal Law one
golden thread is always to be seen that it is the duty of
the prosecution to prove the prisoner’s guilt subject to
what I have already said as to the defence of insanity
and subject also to any statutory exception. If, at the
end of and on the whole of the case, there is a reason-
able doubt, created by the evidence given by either the
prosecution or the prisoner, as to whether the prisoner
killed the deceased with a malicious intention, the
prosecution has not made out the case and the prisoner

is entitled to an acquittal. No matter what the charge or
where the trial, the principle that the prosecution must
prove the guilt of the prisoner is part of the common
law of England and no attempt to whittle it down can
be entertained.
Nowadays, the burden of proof is often simplified to
being ‘sure’. If that level cannot be achieved, then the
prosecution fails and the individual is acquitted. If the
level is achieved then the individual is convicted and
a punitive sentence is applied. The defence does not
have to prove innocence because any individual is pre-
sumed innocent until found guilty. Defence lawyers aim
to identify inconsistencies and inaccuracies or weak-
nesses of the prosecution’s case and can also present
their own evidence.
The penalties that can be imposed in the criminal
system commonly include financial (fines) and loss of
liberty (imprisonment) and community-based sen-
tences. A number of countries still permit corporal
punishment (beatings), mutilation (amputation of parts
of the body) and capital punishment (execution). The
World Medical Association has published a number of
documents related to the involvement of healthcare pro-
fessionals in such occurrences, including the Medical
Ethics Manual.
In England & Wales, the lowest tier of court (in both
civil and criminal cases) is the Magistrates’ Court. These
courts tend to deal with less serious crime and are lim-
ited in the punishments they can administer to those
found guilty. Lay (non-legal) magistrates (Justices of
the Peace) sit in the majority of these courts advised by
a legally qualified justice’s clerk. In some magistrates’
courts a district judge will sit alone. The majority of
criminal cases appear in magistrates’ courts. The Crown
Court sits in a number of centres throughout England
& Wales and is the court that deals with more seri-
ous offences, and considers appeals from magistrates’
courts. Cases are heard before a judge and a jury of 12
people. Appeals from the Crown Court are heard in the
Court of Appeal Criminal Division. Special youth courts
are utilised for those under 18 years of age (Figure 1.1).
Civil law
Civil law is concerned with the resolution of disputes
between individuals. The aggrieved party undertakes
the legal action. Most remedies are financial. All kinds
of dispute may be encountered, including those of
alleged negligence, contractual failure, debt, and libel
or slander. The civil courts can be viewed as a mecha-
nism set up by the state that allows for the fair resolu-
tion of disputes in a structured way. In England & Wales,
the County Court is where trials for most civil cases are
held. The Family Court (and Family Division of the High
Court) deal with all kinds of legal disputes to do with
children and the breakdown of relationships. Most
Legal systems 3
seriously, the Family Court will deal with cases where
the government (local councils, in practice) intervenes
in a family to protect children from harm. That can lead
to the children being taken into care and eventually
adopted or placed with extended family. These cases
are ones where forensic practitioners are most likely to
be involved.
The Family Court also deals with the majority of
orders designed to protect people against domestic vio-
lence. The court may issue a ‘non-molestation order’
instructing an individual not to contact, harass, threaten
or be violent to another person or it can make an ‘occu-
pation order’ preventing someone from, for example,
living in or returning to the family home. More complex
family cases may be dealt with the Family Division of
the High Court which also deals with specific issues
such as forced marriage and female genital mutilation.
The standard of proof in the civil setting is lower than
that in the criminal setting. In civil proceedings, the stan-
dard of proof is proof on the balance of probabilities – a
fact will be established if it is more likely than not to have
happened.
In a decision of the Court of Appeal in Re (N) v Mental
Health Review Tribunal [2006] QB 468 it was stated that
there is only one single standard of proof in the civil sys-
tem but that the standard was flexible in its application:
Although there is a single standard of proof on the bal-
ance of probabilities, it is flexible in its application. In
particular, the more serious the allegation or the more
serious the consequences if the allegation is proved,
the stronger must be the evidence before the court will
find the allegation proved on the balance of probabili-
ties. Thus, the flexibility of the standard lies not in any
adjustment to the degree of probability required for
an allegation to be proved (such that a more serious
allegation has to be proved to a higher degree of prob-
ability), but in the strength or quality of the evidence
that will in practice be required for an allegation to be
proved on the balance of probabilities.
If the standard of proof is met, the penalty that can be
imposed by these courts is designed to restore the posi-
tion of the successful claimant to that which they had
before the event, and is generally financial compensa-
tion (damages). In certain circumstances, there may be
a punitive element to the judgement.
The Magistrates’ Court is used for some cases, but
the majority of civil disputes are dealt with within the
County Court in the presence of a circuit judge. The
High Court has unlimited jurisdiction in civil cases
and has three divisions:
• Chancery – specialising in matters such as com-
pany law;
• Family – specialising in matrimonial issues and
child issues and others as described above; and
• Queen’s Bench – dealing with general issues.
4 Principles of forensic practice

UK Supreme Court
Appeal only, on points of law. Employment Appeal Tribunal
Justices of the supreme court Appeals from the employment
tribunals.
Employment appeal judges and
members
Court of Appeal
Appeal only, on points of law to either the
criminal or civil divisions.
Lord Chief Justice, heads of division and Employment Tribunal (England &
court of appeal judges Wales; Scotland)
Claims about matters to do with
employment.
Employment judges and members
High Court
Chancery, queen’s bench and family divisions. All three
divisions hear appeals from other courts, as well as Upper Tribunal
‘first instance’ cases. Appeals from the first-tier tribunal.
High court and deputy high court judges Upper tribunal judges

Crown Court
Jury trial for all indictable and some either-way criminal First-tier Tribunal
offences. Appeals against conviction and sentence from Appeals from executive agency
the magistrates’ court. decisions.
Circuit judges, recorders and juries Tribunal judges and members

There are a number of other

Magistrates’ Court tribunals outside of this structure
County Court Family Court
Trial for most criminal offences. (for example, School exclusion
Trial for most civil cases. Trial for most family cases.
Some civil matters. panels) - their supporting
Circuit judges, recorders, High court judges, circuit judges,
Magistrates, district judges legislation explains their individual
district judges, deputy recorders, district judges, deputy
(magistrates’ courts), appeal routes.
district judge district judge and magistrates
deputy DJ (MC)s

Figure 1.1 The structure of the court system in England & Wales.

In both civil and criminal trials, the person against
whom the action is being taken is called the defendant;
the accuser in criminal trials is the state and in civil tri-
als it is the plaintiff.
Doctors and other healthcare
­professionals and the law
Doctors and other healthcare professionals may become
involved with the law in the same way as any other pri-
vate individual: they may be charged with a criminal
offence or they may be sued through the civil court.
A doctor may also be witness to a criminal act and may
be required to give evidence about it in court.
However, these examples will only apply to the
minority of professionals reading this book. For the
majority, it is the nature of their work which may result
in that individual providing evidence that may subse-
quently be tested in court. Doctors (or other healthcare
professionals) may have one of two roles in relation to
the court, either as a professional witness or as an expert
witness. The distinction between these roles may be
blurred.
Professional witness
In 1924, Dr Graham Grant, a police surgeon (forensic
physician) in the East End of London, differentiated pro-
fessional from expert witnesses in his book ‘Practical
Forensic Medicine’ (Figure 1.2a and 1.2b).
Little has changed. A professional witness is one
who gives factual evidence. This role is equivalent to a
simple witness of an event, but occurs when the doc-
tor is providing factual medical evidence. For example,
an emergency medicine physician may confirm that a
leg was broken or that a laceration was present and may
report on the presentation and treatment given. A pri-
mary care physician may confirm that an individual
has been diagnosed as having epilepsy or angina. No
comment or opinion is generally given and any report
or statement deals solely with the relevant medical find-
ings on a factual basis.
Expert witness
An expert witness is one who expresses an opinion about
medical or scientific matters in which they may not ini-
tially have had direct involvement, but by virtue of their
 Doctors and other healthcare ­professionals and the law
(a)
(b)
Figure 1.2 (a) Practice Forensic Medicine: A Police-Surgeon’s
Emergency Guide, 3rd edition. (b) The difference between
professional and expert evidence: a view from the early
20th Century.
knowledge are permitted to express their opinion in
order to assist the court. Their expertise may be estab-
lished by virtue of education, training, certification,
skills or experience, and their acceptability is generally
determined by the judge. The judge may consider the wit-
ness’s specialised (scientific, technical or other) opinion
about evidence or about facts before the court within the
expert’s area of expertise, referred to as an ‘expert opin-
ion’. Expert witnesses may also deliver ‘expert evidence’
within the area of their expertise. Their testimony may
be rebutted by testimony from other experts or by other
5
evidence or facts. An expert may form an opinion, for
example, about how the fractured leg or the laceration
was caused, and if there are conflicting accounts may
give opinion on which account is most likely. An expert
will express an opinion about the cause of the epilepsy
or the ability of an individual with angina to drive a pas-
senger service vehicle. Before forming an opinion, an
expert witness will ensure that the relevant facts about
a case are made available to them. Dependent on the
nature of their instructions they may need to examine
the patient, for example if the defence is that the defen-
dant was too physically incapacitated by a medical con-
dition to carry out what was alleged. Most professional
bodies will provide guidelines for their members about
these roles. In the United Kingdom, the General Medical
Council publishes guidance for doctors acting as expert
witnesses (https://www.gmc-uk.org/ethical-guidance/
ethical-guidance-for-doctors/acting-as-a-witness).
There are often situations of overlap between these
professional and expert witness roles. For example,
a forensic physician may have documented a series
of injuries having been asked to assess a victim of
crime by the police and then subsequently be asked
to express an opinion about causation. A forensic
pathologist will produce a report on their post mor-
tem examination (professional aspect) and then form
conclusions and interpretation based upon their find-
ings (expert aspect).
The role of an expert witness should be to give an
impartial and unbiased assessment or interpretation of
the evidence that they have been asked to consider. The
admissibility of expert evidence is in itself a substantial
area of law. Those practising in the USA will be aware
that within US jurisdictions admissibility is based on two
tests: the Frye test and the Daubert test. The Frye test (also
known as the general acceptance test) was stated (Frye v
United States, 293 F. 1013 (D.C.Cir. 1923)) as:
Just when a scientific principle or discovery crosses
the line between the experimental and demonstrable
stages is difficult to define. Somewhere in the twilight
zone the evidential force of the principle must be rec-
ognized, and while courts will go a long way in admit-
ting expert testimony deduced from a well-recognized
scientific principle or discovery, the thing from which
the deduction is made must be sufficiently established
to have gained general acceptance in the particular
field in which it belongs.
Subsequently in 1975, the Federal Rules of Evidence
– Rule 702 provided:
If scientific, technical, or other specialized knowledge
will assist the trier of fact to understand the evidence
or to determine a fact in issue, a witness qualified as an
expert by knowledge, skill, experience, or training, or
education may testify thereto in the form of an opinion
or otherwise.
6 Principles of forensic practice
It appeared that Rule 702 superseded Frye and in
1993 this was confirmed in Daubert v Merrell Dow
Pharmaceuticals, Inc. 509 US 579 [1993]. This decision
held that proof that establishes scientific reliability of
expert testimony must be produced before it can be
admitted. Factors that judges may consider were:
• Whether the proposition is testable.
• Whether the proposition has been tested.
• Whether the proposition has been subjected to
peer review and publication.
• Whether the methodology technique has a known
or potential error rate.
• Whether there are standards for using the tech-
nique.
• Whether the methodology is generally accepted.
The question as to whether these principles applied
to all experts and not just scientific experts was explored
in cases and in 2000 Rule 702 was revised to:
If scientific, technical, or other specialized knowledge
will assist the trier of fact to understand the evidence
or to determine a fact in issue, a witness qualified as
an expert by knowledge, skill, experience, or train-
ing, or education may testify thereto in the form of an
opinion or otherwise, provided that (1) the testimony is
sufficiently based upon reliable facts or data, (2) the tes-
timony is the product of reliable principles and meth-
ods, and (3) the witness has applied the principles and
methods to the facts of the case.
Committee Notes of the Federal Rules also empha-
sise that if a witness is relying primarily on experience
to reach an opinion, then that witness must explain
how that specific experience leads to that particular
opinion.
In England & Wales, His Honour Judge Cresswell
reviewed the duties of an expert in National Justice
Compania Naviera SA v Prudential Assurance Co Ltd
[1993 2 Lloyd’s Rep 68] (commonly known as ‘the Ikarian
Reefer’ case) and identified the following key duties of
expert witnesses and their evidence:
• Expert evidence presented to the court should be,
and should be seen to be, the independent product
of the expert uninfluenced as to form or content by
the exigencies of litigation.
• An expert witness should provide independent
assistance to the Court by way of objective, unbi-
ased opinion in relation to matters within his
expertise.
• An expert witness in the High Court should never
assume the role of an advocate.
• An expert should state facts or assumptions upon
which his opinion is based.
• An expert should not omit to consider material
facts which could detract from his concluded
opinion.
• An expert witness should make it clear when a
particular question or issue falls outside his area
of expertise.
• If an expert’s opinion is not properly researched
because he considers that insufficient data is
available, then this must be stated with an indica-
tion that the opinion is no more than a provisional
one.
• In cases where an expert witness, who has prepared
a report, could not assert that the report contained
the truth, the whole truth and nothing but the
truth without some qualification, that qualification
should be stated in the report.
• If, after exchange of reports, an expert witness
changes his views on a material matter having
read the other side’s report or for any other reason,
such change of view should be communicated
(through legal representatives) to the other side
without delay and when appropriate to the court.
• Where expert evidence refers to photographs,
plans, calculations, analyses, measurements,
survey reports or other similar documents, these
must be provided to the opposite party at the same
time as the exchange of reports.
Another case further clarified the role of the expert
witness (Toulmin HHJ in Anglo Group plc v Winther
Brown & Co. Ltd. [2000])
• An expert witness should at all stages in the pro-
cedure, on the basis of the evidence as he under-
stands it, provide independent assistance to the
court and the parties by way of objective unbiased
opinion in relation to matters within his exper-
tise. This applies as much to the initial meetings
of experts as to evidence at trial. An expert witness
should never assume the role of an advocate.
• The expert’s evidence should normally be con-
fined to technical matters on which the court
will be assisted by receiving an explanation, or to
evidence of common professional practice. The
expert witness should not give evidence or opin-
ions as to what the expert himself would have
done in similar circumstances or otherwise seek
to usurp the role of the judge.
• The expert should cooperate with the expert(s) of
the other party or parties in attempting to narrow
the technical issues in dispute at the earliest pos-
sible stage of the procedure and to eliminate or
place in context any peripheral issues. He should
cooperate with the other expert(s) in attending,
without prejudice, meetings as necessary and in
seeking to find areas of agreement and to define
precisely areas of disagreement to be set out in the
joint statement of experts ordered by the court.
• The expert evidence presented to the court should
be, and should be seen to be, the independent

product of the expert uninfluenced as to form or
content by the exigencies of the litigation.
• An expert witness should state the facts or assump-
tions upon which his opinion is based. He should not
omit to consider material facts which could detract
from his concluded opinion.
• An expert witness should make it clear when a par-
ticular question or issue falls outside his expertise.
• Where an expert is of the opinion that his conclu-
sions are based on inadequate factual information
he should say so explicitly.
• An expert should be ready to reconsider his opin-
ion, and if appropriate, to change his mind when
he has received new information or has consid-
ered the opinion of the other expert. He should do
so at the earliest opportunity.
These points remain the essence of the duties of an
expert within the English and Welsh jurisdiction.
Further guidance is given in Kennedy v Cordia [2016]
UKSC 6 para 48 adopting Coopers (S Africa) v Deutsche
Gesellschaft [1976] 352 at 371 which states
…expert’s opinion represents his reasoned conclusion
based on certain facts or data, which are either com-
mon cause, or established by his own evidence or that of
some other competent witness. Except possibly where
it is not controverted, an expert’s bald statement of his
opinion is not of any real assistance. Proper evaluation
of the opinion can only be undertaken if the process of
reasoning which led to the conclusion, including the
premises from which the reasoning proceeds, are dis-
closed by the expert.
In other words, the expert cannot just state his opin-
ion, the expert has to justify it.
When an expert has been identified, it is appropriate
that the expert is aware of relevant court decisions that
relate to the expert’s role within their own jurisdiction.
All experts should be aware of the preceding cases, and
if not, should not be considered eligible to perform the
expert role.
Civil court procedure in England & Wales also now
allows that, ‘where two or more parties wish to submit
expert evidence on a particular issue, the court may
direct that the evidence on that issue is to be given by
a single joint expert, and where the parties who wish to
submit the evidence (‘the relevant parties’) cannot agree
who should be the single joint expert, the court may (a)
select the expert from a list prepared or identified by the
relevant parties; or (b) direct that the expert be selected
in such other manner as the court may direct’.
The aims of these rules are to enable the court to
identify and deal more speedily and fairly with the
relevant points at issue in a case. Where both parties
in criminal and civil trials appoint experts, courts
encourage the experts to meet in advance of court
hearings in order to define areas of agreement and
disagreement.
Evidence for courts 7
Recent cases within the United Kingdom emphasise
the increasing scrutiny that experts are being subjected
to, which have sometimes resulted in suspension or
criticism. In Pool v GMC [2014] EWHC 3791 a psychia-
trist was found to have failed to restrict his opinion to
areas in which he had expert knowledge and experience
and had neither requisite qualifications or experience
to act as an expert. In Squier v GMC [2016] EWHC 2739
(Admin) the decision of a professional regulatory panel
was subject to rigorous review by the High Court. The
court overturned the factual findings of the regulatory
panel in a ‘shaken baby’ case and also laid down guid-
ance regarding the use of expert evidence. This guid-
ance set out the core duties of an expert when citing the
works of others which are:
• The duty to explain that a hypothesis is controver-
sial.
• The duty to provide to the court all material con-
tradicting a controversial hypothesis.
• The duty to make all material available to other
experts in the case when advancing a controver-
sial hypothesis.
• The duty to take all reasonable steps to verify
information provided.
• The duty not to leave out relevant information.
• The duty to take into account all material facts
before them.
• The duty to set out all material and literature relied
upon in forming an opinion.
This area of law will continue to evolve.
Evidence for courts
Court structure in other jurisdictions will have similar
complexity to that in England & Wales and, although
the exact process doctors and other professionals may
experience when attending court will depend to some
extent upon which court in which jurisdiction they
attend, there are a number of general rules that can be
made about giving evidence. In recent years, courts
have developed better, but far from ideal, communica-
tion systems, informing witnesses who are required to
give evidence in court of their role and the procedures in
place, prior to attendance. In England & Wales all courts
have witness services that can respond to questions and
those who have never been to court before can have the
opportunity of being shown the layout and structure of
a court.
Statements and reports
A statement in a criminal case is a report that has a stan-
dard wording so that it can be used as evidence. There is
an initial declaration that ensures that the person pre-
paring the statement is aware that they must not only
tell the truth but must also ensure that there is nothing
8 Principles of forensic practice
within the report that they know to be false. The state-
ment makes reference to the relevant legislation. The
effect of this declaration is to render the individual liable
for criminal prosecution if they have lied. A statement
provided when acting as a professional witness will be
based on the contemporaneous notes or records made
at the time of examination), and it is important that the
statement accurately reflects what was seen or done at
the time.
A statement may be agreed by both defence and pros-
ecution, negating the need for court attendance. If, for
example, the defence do not accept the findings or facts
expressed, the doctor will be called to court to give live
(oral) evidence and be subject to examination, cross-
examination and re-examination.
In civil proceedings a different official style may be
adopted. In these cases, a sworn statement (an affida-
vit) is made before a lawyer who administers an oath or
other formal declaration at the time of signing.
In many countries, a statement in official form or a
sworn affidavit is commonly acceptable alone and per-
sonal appearances in court are unusual. However, in
the system of law based on Anglo-Saxon principles, per-
sonal appearances are common in the criminal justice
system and it is the testing by the defence and prosecu-
tion of the live evidence given in court (together with
written reports/statements made by that witness) that
may be particularly significant.
If a case comes to trial, any statement or relevant evi-
dence in the prosecution case must be disclosed to all
interested parties at the court; at present, the same prin-
ciple of disclosure does not apply to all reports prepared
for the defence in a criminal trial. Thus, a defence team
may commission a report that is not helpful to the client’s
defence. This does not have to be disclosed to the pros-
ecution team. Failure to disclose evidence by the police
or prosecution may fatally undermine the prosecution
case, and this subject is one that is of continuing rele-
vance. The format for reports in civil trials is different. In
England & Wales, the Ministry of Justice publishes and
updates a civil, criminal and family procedure rules and
practice directions, and these are accessible online. It is
important to understand that, although these are pub-
lished, practice sometimes varies from the published
rules and directions and is updated regularly.
Attending court
If requested to appear as a witness for the court, it is the
duty of all to comply. Attendance at court by profession-
als is generally presumed without the need to resort to a
formal summons from the court. Most courts now have
some form of witness liaison units that liaise with all
witnesses in a case, attempting (often unsuccessfully)
to ensure that the dates of any trial are convenient for all
witnesses. Court listing offices try to take into account
‘dates to avoid’ (e.g., clinics or operating sessions,
pre-booked holidays or other court commitments), but
this is not always successful. When notified that a court
case in which you are a witness is going to take place, it is
generally possible to agree a specific day on which your
attendance is required. However, the court does have
the power to compel attendance even when you have
other commitments. In this case, a witness summons
may be issued. This is a court order signed by a judge or
other court official that must be obeyed or the individual
will be in contempt of court and a fine or imprisonment
may result. Most courts and judges are reasonable, but
it requires flexibility and as much notice as possible on
both sides.
Waiting to give evidence inevitably involves possible
delays and frustration, so it is sensible to take work to court
so that some of the time is not wasted. Examples of reasons
for last-minute changes in the need for court attendance
include factors such as a guilty plea being entered on the
first day of the trial, or acceptance of a lesser charge, or the
case being dropped because of disclosure failures.
Evidence in court
When called into court, each witness will undergo
some process in which they commit to telling the truth.
‘Taking the oath’ or ‘swearing- in’ requires, for those with
religious beliefs, swearing on their respective holy book
(e.g., the New Testament, the Old Testament, the Quran)
or a public declaration or affirmation that they will tell
the truth. Regardless of how it is done, the effect of the
words is the same: once the oath has been taken, the wit-
ness is liable for the penalties of perjury.
Whether called as a witness of fact, a professional
witness of fact or an expert witness, the process of giv-
ing evidence is the same.
In a criminal trial, whichever of the defence or pros-
ecution has called the witness will be the first to examine
them under oath. This is the ‘examination in chief’ and
the witness will be asked to confirm the truth of the facts
in their statement(s). This examination may take the form
of one catch-all question as to whether the whole of the
statement is true, or the truth of individual facts may be
dealt with one at a time. If the witness is not an expert,
there may be questions to ascertain how the facts were
obtained and the results of any examinations or ancillary
tests performed. If the witness is an expert, the question-
ing may be expanded into the opinions that have been
expressed and other opinions may be sought.
When this questioning is completed, the other law-
yers will have the opportunity to question the witness;
this is ‘cross-examination’. This questioning will test
the evidence that has been given and will concentrate
on those parts of the evidence that are damaging to the
lawyer’s case. It is likely that both the facts and any opin-
ions given will be tested.
The final part of giving evidence is the ‘re-examina-
tion’. The original lawyer has the opportunity to clarify

anything that has been raised in cross-examination but
generally cannot introduce new topics. The rules of evi-
dence (what is and isn’t admissible in front of a jury) are
hugely complex and frequently trials are interrupted to
discuss these and other legal points.
The judge may ask questions at any time if he feels
that by doing so it may clarify a point or clear a point of
contention, or if he thinks counsel are missing a point.
The judge may allow the jury to ask questions. However,
most judges will try to refrain from asking questions
until the end of the re-examination.
Healthcare professionals as
witnesses in court
Any medicolegal report must be prepared and written
with care because it will either constitute the medical
evidence on that aspect of a case or it will be the basis of
any oral evidence that may be given in the future. Any
healthcare professional who does not, or cannot, sustain
the facts or opinions made in the original report while
giving live evidence may, unless there are reasons for
the specific alteration in fact or opinion, find themselves
professionally embarrassed. Any medical report or state-
ment submitted to courts should always be reviewed by
the author prior to signing and submitting it to avoid fac-
tual errors (e.g., identifying the wrong site of an injury or
sloppy typographical errors) and it is advisable to have it
peer-reviewed by a colleague. However, any comments
or conclusions within the report are based upon a set of
facts that surround that particular case. If other facts or
hypotheses are suggested by the lawyers in court dur-
ing their examination, any witness must be prepared
to reconsider the medical evidence in the light of these
new facts or hypotheses and, if necessary, should accept
that, in view of the different basis, the conclusions may
be different. Prior to giving live evidence the doctor must
refresh their memory of the case by reviewing the report
and materials supplied. If, whilst giving evidence, the
doctor does not know the answer to a question posed, or
it is outside their range of experience, they should make
this clear and, if necessary ask the judge for guidance in
the face of particularly persistent counsel.
Anyone appearing before any court in either role
should ensure that their dress and demeanour are com-
patible with the role of an authoritative professional and
respectful to the court. It is imperative that doctors and
others providing professional or expert witness evidence
give their evidence in a clear, unbiased and dispassion-
ate manner.
The oath or affirmation should be taken in a clear
voice. Most courts are audio-recorded and microphones
are placed for that purpose, not for amplifying speech.
In some courts, witnesses may be invited to sit, whereas
in others they will be required to stand. Many expert
witnesses prefer to stand as they feel that it adds to their
Healthcare professionals as witnesses in court 9
professionalism, but this decision must be a matter of
personal preference.
Evidence should also be given in a clear voice that is
loud enough to reach across the court room. Take time in
responding and be aware that judges (and lawyers) will
be writing the responses on paper or a laptop. Most wit-
nesses will at some time have been requested to ‘Pause,
please’ to give time for the judge to complete notes.
The witness should always answer the question
posed, not the one the witness believes should or
would have liked to have been asked. Questions should
be answered fully and then the witness should stop
and wait for the next question. Do not feel the need to
fill the silence with an explanation or expansion of the
answer. If the lawyers want an explanation or expan-
sion of any answer, they will ask for it. Clear, concise
and complete should be the watchwords when answer-
ing questions.
A witness should also expect to have qualifications,
experience and opinions challenged. However, becom-
ing hostile, angry, flippant or rude as a witness does not
impress the court or the jury and is easily exploited by
counsel. Part of the role of the lawyers questioning is to
try and elicit such responses. The lawyers are in control
in the courtroom and they will very quickly take advan-
tage of any witness who shows such emotions. A judge
will normally intervene if he feels that the questioning
is unreasonable or unfair.
A witness must be alert to attempts by lawyers to
circumscribe answers unreasonably: ‘yes’ or ‘no’ may
be adequate for simple questions but they are simply
not sufficient for most questions and, if told to answer
a complex question ‘with a simple “yes” or “no” doctor’,
he should decline to do so and, if necessary, explain to
the judge that it is not possible to answer such a complex
question in that way.
The old adage of ‘dress up, stand up, speak up and
shut up’ is still entirely applicable and it is unwise to
ignore such simple, appropriate and easy to follow
advice.
Box 1.1 summarises key elements of how to be best
prepared for court attendance.
Preparation of medicolegal reports
The diversity of uses of a report is reflected in the indi-
viduals or groups that may request one: a report may be
requested by the police, prosecutors, Coroners, judges,
medical administrators, government departments, city
authorities or lawyers of all types. The nature and the
format of the report may vary in each setting. If unfamil-
iar with the process always ask for a sample report in the
correct style. Many courts will have standard proforma
or procedural rules that will assist. Before agreeing to
write a report, it is essential to be sure that the author
(1) has the expertise to write such a report and (2) also
has the authority, permissions and consent to write such
10 Principles of forensic practice
Box 1.1 T
 ips on preparing for court
appearance
Before court
• Prepare.
• Be clear about instructions.
• Have all relevant paperwork.
• Familiarise yourself with your report/state­ments.
• Read through in advance copies of literature
referred to.
At court
• Dress smartly and conservatively.
• Arrive early.
• Identify yourself to court staff.
• Tell the usher whether you wish to affirm or give
an oath on your respective holy book.
• Meet with lawyer/counsel before giving evi-
dence if possible.
Giving live (oral) evidence
• Turn phones/tablets off.
• Summarise your background/position/role.
• Speak to the jury (or judge) when answering
questions.
• Watch the speed of notetaking of counsel and
judge.
• If referred to bundles or exhibits, take your time.
• Listen to question, digest and give a considered
response (to the question).
• Be prepared to say ‘I don’t know’.
• Be prepared to say ‘that’s not my area of
expertise’.
After court
• Seek feedback.
a report. If consent has not been sought, advice should
be sought from the relevant court or body for permis-
sion to proceed. The fact of a request, even from a court,
does not mean that a doctor can necessarily ignore the
rules of medical confidentiality; however, a direct order
from a court is a different matter and should, if valid,
be obeyed. Any concerns about such matters should be
raised with the appropriate medical defence organisa-
tion or standard setting body.
In general terms, release of medical records requires
the consent of the patient and, if at all possible, this
should be given in writing to the doctor. There are
exceptions, particularly where serious crime is involved
(see also Chapter 2). Different jurisdictions or legal sys-
tems may be subject to different rules that allow reports
to be written without consent or medical records to be
released without consent. In the absence of consent
from the patient, this should be explained in the report
and the reasons why commented upon, as should on
whose directions the report was written.
In general, in most countries, it is considered inap-
propriate for non-judicial state agencies to order a doctor
to provide confidential information against the wishes
of the patient, although where a serious crime has
been committed the doctor may have a public duty to
assist the law-enforcement system. Complainants of an
assault are normally entirely happy to give permission
for the release of medical facts so that the perpetrator
can be brought to justice, however some may limit that
consent to the matters relevant to the case. However,
consent cannot be assumed, especially if the alleged
perpetrator is the husband, wife, partner or other mem-
ber of the family. It is also important to remember that
consent to disclose the details of the injuries sustained
in an alleged assault does not imply consent to disclose
all the medical details of the complainant, and a doc-
tor must limit his report to relevant details only. A court
may, in certain circumstances, order disclosure of med-
ical records if it is believed that details contained within
may have relevance to the case in hand.
Mandatory reporting of healthcare and related
issues may be relevant in some countries; often these
relate to terrorism, child abuse, use of a weapon and
other violent crime. Such reporting for suspected cases
of child abuse and neglect to government authorities
is required by parliaments in all Australian states and
territories. However, the laws are not the same across
all jurisdictions. The main differences often relate to
who has to report and what types of abuse and neglect
have to be reported. There are also other differences,
such as the ‘state of mind’ that activates the report-
ing duty (i.e., having a concern, suspicion or belief on
reasonable grounds) and who the report is made to.
One recent example is that in the United Kingdom of
a mandatory reporting duty for female genital mutila-
tion (FGM) requiring regulated health and social care
professionals and teachers in England & Wales to report
known cases of FGM in under 18-year-olds to the police.
The FGM duty came into force on 31 October 2015 and
the first successful prosecution of a case of FGM was
in 2019.
Content of a statement or report
The basis of most reports and statements lies in the con-
temporaneous notes made at the time of an examina-
tion and it is essential to remember that copies of these
notes will be required in court if you are called to give
live evidence. Do not use handwritten statements as
they may be open to misinterpretation.
Most court or tribunal settings have specific proto-
cols for evidence production but in general most will
include the information and details referred to below.
When instructed to prepare an expert report always

clarify whether or not a specific structure is required
and if so, follow it assiduously. For example, in the
civil justice ­s ystem in England & Wales the process,
and how the evidence is dealt with, is described in
Part 35 of the Civil Procedure Rules which refers to
experts and assessors and their roles.
A professional witness statement (one that simply
reports facts found at examination) will be headed by
specific legal wording. The statement should include the
full name of the practitioner, their age and their profes-
sional address. The reason for the examination should be
stated, and then the relevant history as recounted (e.g.,
‘he told me he was hit twice on the right forearm with a
baseball bat’), the medical findings (e.g., two tramline
bruises, both 6 × 4 cm in size, purple in colour with asso-
ciated swelling in the middle 1/3 of the ulnar bone with
a possible fracture), and what treatment was given (e.g.,
pain relief and referral for X-ray). The statement sum-
marises the personal involvement of the practitioner. A
professional witness statement simply reports facts.
Clarity and simplicity of expression make the whole
process simpler. Statements can be constructed along
the same lines as the clinical notes; they should be
structured, detailed (but not overelaborate – avoid com-
plex medical and scientific terms unless absolutely nec-
essary, and where possible explain them) and accurate.
Do not include every single aspect of a medical history
unless it is relevant and consent has been given for its
disclosure. A court does not need to know every detail,
but it does need to know every relevant detail, and a good
report will give the relevant facts clearly, concisely and
completely, and in a way that someone without medical
training can understand.
The contemporaneous clinical notes may be required
to support the statement and it is essential to ensure that
all handwriting within such medical notes has been
reviewed (and interpreted) prior to entering the witness
Box 1.2 Some Standards Which May Apply to Autopsy Examinations in the UK
• Council of Europe Group of Ministers.
Recommendation R (99) 3 of the Group of Ministers
to Member States on Harmonisation of Medico-
Legal Autopsy Rules.
• Codes of Practice and Performance Standards
for Forensic Pathologists in England, Wales and
Northern Ireland. Royal College of Pathologists,
2012.
• Post mortem cross sectional imaging guid-
ance from the Royal Colleges of Radiology and
Pathology, 2012.
• Chief Coroner guidance on post mortem scanning,
2013.
Healthcare professionals as witnesses in court 11
box. It is always embarrassing trying (and failing) to
interpret your own handwriting in a witness box in front
of a judge and jury.
Autopsy reports are a specialist type of report and
may be commissioned by the Coroner, the police or any
other appropriate person or body. Again, as with expert
reports, there are standardised protocols or proformas
(Box 1.2).
The authority to perform the autopsy will replace the
consent given by a live patient, and is equally impor-
tant. The history and background to the death will be
obtained by the police or the Coroner’s officer, but the
doctor should seek any additional details that appear
to be relevant, including speaking to any clinicians
involved in the care of the deceased and reviewing the
hospital notes. A visit to the scene of death in non-sus-
picious deaths, especially if there are any unusual or
unexplained aspects, is advisable.
An autopsy report is confidential and should only be
disclosed to the legal authority who commissioned the
examination. Disclosure to others, who must be inter-
ested parties, may only be made with the specific per-
mission of the commissioning authority and, in general
terms, it would be sensible to allow that authority to deal
with any requests for copies of the report.
Doctors must resist any attempt to change or delete
any parts of their report by lawyers who may feel those
parts are detrimental to their case; any requests to
rewrite and resubmit a report with alterations for these
reasons should be refused. Persistent and inappropri-
ate pressure may require referral to the regulatory body.
At times, lawyers, but more often police personnel, may
sometimes need to be reminded or informed of the
duties of a healthcare professional which is to assist the
court, not the relevant instructing body. Always seek the
advice of the judge on matters arising that may result in
potential breaches of these important duties.
• Standards for Coroners’s pathologist in post mor-
tem examinations of deaths that appear not to be
suspicious. Royal College of Pathologists, 2014.
• Information to be included in the ‘history’ section
of a forensic pathologist’s report. Forensic Science
Regulator, 2014.
• The use of time of death estimates based on heat
loss from the body. Forensic Science Regulator,
2014.
• Legal issues in Forensic Pathology and tissue
retention: issue 3 guidance. Forensic Science
Regulator 2014.
12 Principles of forensic practice
Bibliography and information
sources
Anglo Group plc v Winther Brown & Co Ltd and others. [2000] All
ER (D) 294.
Boccaccini MT, Brodsky SL. Believability of expert and lay wit-
nesses: implications for trial consultation. Prof Psychol Res Pr
2002;33:384–388.
Burton JL, Rutty GN (eds). The Hospital Autopsy: A Manual of
Fundamental Autopsy Practice, 3rd edn. London: Hodder
Arnold; 2010.
Cooper J, Neuhaus IM. The ‘hired gun’ effect: assessing the effect
of pay, frequency of testifying and credentials on the percep-
tion of expert testimony. Law Hum Behav 2000;24:149–171.
Court of Appeal in Re (N) v Mental Health Review Tribunal [2006]
QB 468.
Cramer RJ, Brodsky SL, DeCoster J. Expert witness confidence and
juror personality: their impact on credibility and persuasion
in the courtroom. J Am Acad Psychiatry Law 2009;37(1):63–74.
Crown Prosecution Service. Code for Crown Prosecutors. https://
www.cps.gov.uk/publication/code-crown-prosecutors
(Accessed 29 March 2019).
Daubert v Merrell Dow Pharmaceuticals, Inc. [1993] 509 US 579.
http://www.law.cornell.edu/supct/html/92-102.ZS.​html
(Accessed 29 March 2019).
Federal Rules of Evidence Article I. General provisions, Rule 702.
https://www.law.cornell.edu/rules/fre/rule_702 (Accessed 29
March 2019).
Freckelton I. A guide to the provision of forensic medical evi-
dence. In: Gall J, Payne-James JJ (eds) Current Practice in
Forensic Medicine. London: Wiley; 2011.
Freckelton I, Selby H. Expert Evidence: Law, Practice, Procedure and
Advocacy, 6th edn. Sydney: Lawbook Co; 2016.
Frye v United States, 293 F. 1013 (D.C.Cir. 1923). https://www.law.ufl.
edu/_pdf/faculty/little/topic8.pdf (Accessed 29 March 2019).
House of Commons Debates, Volume 483, 29 January 1951
(quote of Hartley Shawcross).
National Justice Compania Naviera SA v Prudential Life Assurance
Co (‘The Ikarian Reefer’) [1993] 2 LILR 68, 81–82.
Lynch J. Clinical Responsibility. Oxford: Radcliffe Publishing; 2009.
Ministry of Justice (England and Wales). Civil procedure rules.
ht tp: //w w w.justice.gov.uk /cour ts/procedure -rules/
civil (Accessed 29 March 2019).
Ministry of Justice (England and Wales). Criminal procedure
rules. http://www.justice.gov.uk/courts/procedure-rules/
criminal (Accessed 29 March 2019).
Ministry of Justice (England and Wales). Family procedure rules.
ht tp: //w w w.justice.gov.uk /cour ts/procedure -rules/
family (Accessed 5 April 2019).
Ministry of Justice. Practice Direction 32: evidence https://www.
justice.gov.uk/courts/procedure-rules/civil/rules/part32/
pd_part32#evidence (Accessed 6 April 2019).
Payne-James JJ, Bloomer JA. Court skills. In: Dalton M (ed). Forensic
Gynaecology. Cambridge: Cambridge University Press; 2015.
Payne-James JJ, Newton MA, Bassindale C. Forensic sci-
ence, forensic medicine and sexual crime. In: Radcliffe P,
Gudjonsson G, Heaton-Armstrong A (eds). Witness Testimony
in Sexual Cases. Oxford: Oxford University Press; 2016.
Re (N) v Mental Health Review Tribunal [2006] QB468.
Stark MM. Clinical Forensic Medicine: A Physician’s Guide, 3rd edn.
New York: Humana Press; 2011.
Toulmin HHJ in Anglo Group plc v Winther Brown & Co. Ltd.
[2000]. http://www.bailii.org/ew/cases/EWHC/TCC ​ /​
2000/127.html (Accessed 23 July 2019).
Woolmington v Director of Public Prosecutions [1935] AC 462.
Further general resources
Acting as a witness in legal proceedings. http://www.gmc-uk.
org/guidance/ethical_guidance/21193.asp (Accessed 6 April
2019).
Crown & Procurator Fiscal. Our role in investigating deaths.
http://www.copfs.gov.uk/investigating-deaths/our-role-in-
investigating-deaths (Accessed 6 April 2019).
Crown Prosecution Service. Disclosure manual. https://www.cps.
gov.uk/legal-guidance/disclosure-manual (Accessed 6 April
2019).
Female Genital Mutilation: A guide for healthcare professionals.
https://www.england.nhs.uk/north/wp-content/uploads/
sites/5/2016/01/fgm-hp-guide.pdf (Accessed 6 April 2019).
Guide to Coroner Services. Ministry of Justice. https://assets.
publishing.service.gov.uk/government/uploads/system/
uploads/attachment_data/file/363879/guide-to-coroner-
service.pdf (Accessed 6 April 2019).
Mandatory reporting of child abuse and neglect. https://aifs.
gov.au/cfca/publications/mandatory-reporting-child-abuse-
and-neglect (Accessed 6 April 2019).
Mandatory reporting of female genital mutilation: procedural
information. https://www.gov.uk/government/publications/
mandatory-reporting-of-female-genital-mutilation-proce-
dural-information (Accessed 6 April 2019).
Part 35 of the Civil Procedure Rules. https://www.justice.gov.uk/
courts/procedure-rules/civil/rules/part35 (Accessed 6 April
2019).
The Forensic Science Regulator. https://www.gov.uk/govern-
ment/organisations/forensic-science-regulator (Accessed 6
April 2019).
The judicial system of England & Wales: a visitor’s guide.
h t t p s : // w w w. j u d i c i a r y. u k / w p - c o n t e n t /u p l o a d s /
2016/05/international-visitors-guide-10a.pdf (Accessed 6
April 2019).
2 The ethics of medical
practice
▪▪ Introduction
▪▪ Basis of medical ethics
▪▪ International codes of medical ethics
▪▪ Duties of doctors and other healthcare professionals:
UK perspective
▪▪ Medical ethics in practice
Introduction
Medical and healthcare practice has many forms and
can embrace many backgrounds and disciplines.
Examples include the predominantly science-based
Western medicine, traditional Chinese medicine,
Ayurvedic medicine in India, and the many local sys-
tems from Africa and Asia. In some cases, two forms
may work together such as Chinese and Western medi-
cine in parts of China. Other alternative and comple-
mentary forms of medicine may be applied with varying
degrees of evidence and science on which they are
based. Alternative forms of medicine may have their
own traditions, conventions and codes of conduct. This
chapter focuses on the relatively easily defined science-
based Western medicine. It is important to recognise
that although often described as modern, the origins of
science-based medicine as ‘Western medicine’ can be
traced through ancient Greece to a synthesis of Asian,
North African and European medicine.
Basis of medical ethics
The Greek tradition of medical practice was epitomised
by the Hippocratic School on the island of Kos around
400 BC and there the foundations of both modern medi-
cine and the ethical facets of the practice of that medi-
cine were laid. What is now known as the Hippocratic
Oath was developed at and for those times, yet it remains
the basis of ethical medical behaviour today, even
though some of the detail is now obsolete. Its endur-
ing nature is a testament to its simple common sense
and universal acceptance. The following is a g­ enerally
accepted translation:
I swear by Apollo the physician and Aesculapius and
Health and All-heal and all the gods and goddesses,
that according to my ability and judgement, I will keep
this Oath and this ­stipulation – to hold him who taught
me this art, equally dear to me as my own parents, to
make him partner in my livelihood: when he is in need
of money, to share mine with him; to consider his fam-
ily as my own brothers and to teach them this art, if they
▪▪ Confidentiality
▪▪ Consent
▪▪ Regulation of doctors and other professionals
▪▪ Bibliography and information resources
▪▪ Further general resources
want to learn it, without fee or indenture. To impart
precept, oral instruction and all other instruction to my
own sons, the sons of my teacher and to those who have
taken the disciple’s oath, but to no-one else. I will use
treatment to help the sick according to my ability and
judgement, but never with a view to injury or wrong-
doing. Neither will I administer a poison to anybody
when asked to do so nor will I suggest such a course.
Similarly, I will not give a woman a pessary to produce
abortion. But I will keep pure and holy both my life
and my art. I will not use the knife, not even sufferers
with the stone, but leave this to be done by men who
are practitioners of this work. Into whatsoever houses I
enter, I will go into them for the benefit of the sick and
will abstain from every voluntary act of mischief or cor-
ruption: and further, from the seduction of females or
males, of freeman or slaves. And whatever I shall see
or hear in the course of my profession or not in connec-
tion with it, which ought not to be spoken of abroad, I
will not divulge, reckoning that all such should be kept
secret. While I carry out this oath, and not break it, may
it be granted to me to enjoy life and the practice of the
art, respected by all men: but if I should transgress it,
may the reverse be my lot.
It is commonly believed that all doctors (in the
United Kingdom defined as a medical practitioner reg-
istered by the General Medical Council) have taken the
Hippocratic Oath. This is in fact not the case, although
some do, depending on where they trained, but the key
principles espoused within the Oath lay the foundation
for what is broadly called ‘medical ethics’. The principles
of medical ethics have developed over several thousand
years and continue to evolve and change, influenced by
society, the legal profession and the medical profession
itself. Most days in the media there will be a headline
news story with its basis in the interpretation of aspects
of medical ethics, such as euthanasia, the death pen-
alty, torture and abortion. The laws governing the prac-
tice of medicine vary from country to country, but the
broad principles of medical ethics are universal and are
formulated not only by national medical associations,
but by international organisations such as the World
Medical Association (WMA).
14 The ethics of medical practice
International codes of
medical ethics
Since its foundation in 1947, a central objective of the
World Medical Association (WMA) was to establish
and promote the highest possible standards of ethical
behaviour and care by physicians. To try and achieve
this the WMA adopted global policy statements on
a range of ethical issues related to medical profes-
sionalism, patient care, research on human subjects
and public health. The WMA Council and its standing
committees regularly review and update existing poli-
cies and continually develop new policy on emerging
ethical issues. The WMA serves as a resource of ethics
information by cooperating with academic institu-
tions, global organisations, and individual experts in
the field of medical ethics. As a result of the horrific
violations of medical ethics during the Second World
War (1939–1945), the international medical community
restated the Hippocratic Oath in a modern form in the
Declaration of Geneva in 1948 most recently amended
and revised in 2006 to state:
At the time of being admitted as a member of the
medical profession:
• I solemnly pledge to consecrate my life to the service
of humanity.
• I will give to my teachers the respect and gratitude
that is their due.
• I will practise my profession with conscience and
dignity.
• The health of my patient will be my first consider-
ation.
• I will respect the secrets that are confided in me,
even after the patient has died.
• I will maintain by all the means in my power, the
honour and the noble traditions of the medical pro-
fession.
• My colleagues will be my sisters and brothers.
• I will not permit considerations of age, disease or
disability, creed, ethnic origin, gender, nationality,
political affiliation, race, sexual orientation, social
standing or any other factor to intervene between
my duty and my patient.
• I will maintain the utmost respect for human life.
• I will not use my medical knowledge to violate
human rights and civil liberties, even under threat.
• I make these promises solemnly, freely and upon my
honour.
The WMA has also amended the ‘Duties of a Physician
in General’ on a number of occasions, most recently in
2006. Box 2.1 shows the WMA duties of physicians, in
general, to patients and to colleagues.
The principles espoused by these duties and the
pledges are embraced in one form or another by most
medical bodies representing medical practitioners
around the world. Table 2.1 identifies some key WMA
Declarations in recent years, and shows the breadth of
subject matter that requires consideration. Often these
amend or revise previous declarations (the Declaration
of Geneva of 1948 being most recently amended in
2006).
Duties of doctors and other
healthcare professionals:
UK perspective
Increasingly, regulatory bodies are defining how pro-
fessionals should work in relatively unambiguous
terms. The General Medical Council (GMC) in the
UK issues publications on how a registered medical
practitioner (a doctor) should undertake good medi-
cal practice. Good Medical Practice advises doctors on
their duties. Key points from that document are pro-
vided in Box 2.2.
The GMC publishes advice and guidance for
doctors in the UK in a number of specific areas,
for example, concerning the use of chaperones
when undertaking intimate examinations. Box 2.3
shows the advice given by the GMC on this sub-
ject in November 2013. This was updated in 2014 to
include a paragraph on doctors’ knowledge of the
English language.
It is the responsibility of the medical practitioner
to ensure for each patient seen, in whatever clinical
setting (including places of detention such as police
and prison custody, and mental health facilities) that
they are following such guidance. Visual assessment or
physical examination that involves touching, by hand,
of an intimate area will constitute an intimate exami-
nation. An intimate examination is likely to include
examinations of breasts, genitalia and rectum, but
could also include any examination where it is neces-
sary to touch or even be close to the patient. For such
an examination, it is appropriate for the relevant prin-
ciples described in Box 2.3 to be put into practice. It
is essential to record all such information within con-
temporaneous medical records, including any reason
why a patient declines to have a chaperone present. A
medical practitioner should always be mindful of how
any actions might be perceived at a later date by any-
one reviewing their conduct, and to ensure they can
justify whatever action they took.
Other healthcare professionals have expanded roles
in healthcare. For example, in the UK, nurses and para-
medics may assess detainees in police custody. Sexual
Assault Nurse Examiners are increasingly in prac-
tice around the world. All have their own professional
standards and accountability, and the duties that they
have to their patients may be very explicit (similar to
 Duties of doctors and other healthcare professionals: UK perspective 15

Box 2.1 Duties of a physician as defined by the World Medical Association

A. Duties of a physician in general • Owe his/her patients complete loyalty and all the
A physician shall: scientific resources available to him/her: when-
ever an examination or treatment is beyond the
• Always exercise his/her independent professional
­physician’s capacity, he/she should consult with or
judgement and maintain the highest standards of
refer to another physician who has the necessary
professional conduct.
ability.
• Respect a competent patient’s right to accept or
• Respect a patient’s right to confidentiality: it is
refuse treatment.
ethical to disclose confidential information when
• Not allow his/her judgement to be influenced by
the patient consents to it or when there is a real
personal profit or unfair discrimination.
and imminent threat of harm to the patient or to
• Be dedicated to providing competent medical ser-
others and this threat can be only removed by a
vice in full professional and moral independence,
breach of confidentiality.
with compassion and respect for human dignity. • Give emergency care as a humanitarian duty
• Deal honestly with patients and colleagues, and
unless he/she is assured that others are willing and
report to the appropriate authorities those physi-
able to give such care.
cians who practise unethically or incompetently or • In situations when he/she is acting for a third
who engage in fraud or deception.
party, ensure that the patient has full knowledge
• Not receive any financial benefits or other incen-
of that situation.
tives solely for referring patients or prescribing • Not enter into a sexual relationship with his/
specific products.
her current patient or into any other abusive or
• Respect the rights and preferences of patients, col-
exploitative relationship.
leagues, and other health professionals.
• Recognise his/her important role in educating the
C. Duties of physicians to colleagues
public but use due caution in divulging discoveries
A physician shall:
or new techniques or treatment through non-pro-
fessional channels. • Behave towards colleagues as he/she would have
• Certify only that which he/she has personally them behave towards him/her.
verified. • Not undermine the patient–physician relationship
• Strive to use healthcare resources in the best way to of colleagues in order to attract patients.
benefit patients and their community. • When medically necessary, communicate with
• Seek appropriate care and attention if he/she suf- colleagues who are involved in the care of the
fers from mental or physical illness. same patient. This communication should respect
• Respect the local and national codes of ethics. patient confidentiality and be confined to neces-
sary information.
B. Duties of physicians to patients
A physician shall:
• Always bear in mind the obligation to respect
Source: From WMA International Code of Medical Ethics. Latest
human life.
amendment: WMA General Assembly, Pilanesberg,
• Act in the patient’s best interest when providing
South Africa, October 2006. Copyright World Medical
medical care. Association. All rights reserved.

GMC guidelines) or more generalised. The Nursing and Failure to comply with the Code may bring their fit-
Midwifery Council (NMC) in the UK, which is the pro- ness to practise into question. Box 2.4 gives a summary
fessional body for nurses, has its own Code. The Code of the main components of the NMC Code of perfor-
presents the professional standards that nurses and mance standards and behaviours expected of registered
midwives must uphold in order to be registered to prac- nurses and midwives.
tise in the UK. It is structured around four themes: The Health & Care Professions Council (HCPC) is
a body created by statute in England & Wales, which
1. Prioritise people regulates healthcare professionals (e.g., arts therapists,
2. Practise effectively biomedical scientists, chiropodists/podiatrists, clinical
3. Preserve safety scientists, dietitians, hearing aid dispensers, occupa-
4. Promote professionalism and trust tional therapists, operating department practitioners,
16 The ethics of medical practice

Table 2.1 Example Declarations of the World Medical Association (many have been revised and amended
in subsequent years)
1948 The Declaration of Geneva Humanitarian goals of medicine
1964 The Declaration of Helsinki Human experimentation and clinical trials
1970 The Declaration of Oslo Therapeutic abortion
1973 The Declaration of Munich Racial, political discrimination in medicine
1975 The Declaration of Tokyo Torture and other cruel and degrading treatment
or punishment
1981 The Declaration of Lisbon Rights of the patient
1983 The Declaration of Venice Terminal illness
1983 The Declaration of Oslo Therapeutic abortion
1984 The Declaration of Sao Paolo Pollution
1987 The Declaration of Madrid Professional autonomy and self-regulation
2006 The Declaration of Ottawa Child health
2009 The Declaration of Delhi Health and climate change
2016 The Declaration of Taipei (adopted by the 3rd WMA Research on Health Databases, Big Data and
General Assembly, Washington, DC, USA, October Biobanks
2002 and revised by the 67th WMA General Assembly,
Taipei, Taiwan, October 2016)

orthoptists, paramedics, physiotherapists, practitio-
ner psychologists, prosthetists/orthotists, radiogra-
phers, and speech and language therapists). The HCPC
was set up to protect the public and keeps a register of
health professionals who meet its standards for train-
ing, professional skills, behaviours and health. All of
these professions have at least one professional title
that is protected by law, including those shown above.
This means, for example, that anyone using the titles
‘physiotherapist’ or ‘dietitian’ must be registered with
the HCPC.
It is a criminal offence for someone to claim that they
are registered with the HCPC when they are not, or to
use a protected title they are not entitled to use.
Medical ethics in practice
The formal role of ethics in contemporary health and
social care has become much more clearly defined. One
example of its practical application in the UK is the NHS
Health Research Authority who has its own Research
Ethics Service whose role is
to enable and support ethical research in the NHS. It
protects the rights, safety, dignity and wellbeing of
research participants and has a duty to provide an effi-
cient and robust ethics review service that maximises
UK competitiveness for health research and maxi-
mises the return from investment in the UK, while
protecting participants and researchers. It protects
the rights, safety, dignity and wellbeing of research
participants and to facilitate and promote ethical
research that is of potential benefit to participants, sci-
ence and society.
The NHS Health Research Authority provides gover-
nance arrangements for research ethics committees,
most recently updated in 2018.
Medical ethics as a subject is incorporated into
medical school curricula as the need for knowledge
of such matters becomes increasingly important with
high-technology medicine creating clinical scenarios
that may need to be assessed and interpreted by the
courts. However medical ethics, like forensic medicine,
although essential to safe and proper practice, is allot-
ted too little time in most medical schools and other
healthcare professions training.
Examples of the type of subject that may be embraced
in discussions on medical ethics might include:
• Patient autonomy and their right to refuse or
choose treatment.
• Non-maleficence – do no harm.
• Beneficence – acting in the patient’s best interests.
• Dignity.
• Honesty – providing informed consent.
• Justice – how healthcare is apportioned when
health and financial resources may be limited.
It is important for doctors and other healthcare
professionals to be aware of these issues, even if
they do not provide immediate answers to clinical

Box 2.2 Duties of a doctor
1. Patients need good doctors. Good doctors make
the care of their patients their first concern: they
are competent, keep their knowledge and skills up
to date, establish and maintain good relationships
with patients and colleagues, are honest and trust-
worthy, and act with integrity and within the law.
2. Good doctors work in partnership with patients
and respect their rights to privacy and dignity.
They treat each patient as an individual. They do
their best to make sure all patients receive good
care and treatment that will support them to live as
well as possible, whatever their illness or disability.
3. Good medical practice describes what is expected
of all doctors registered with the General Medical
Council (GMC). It is your responsibility to be famil-
iar with Good Medical Practice and the explana-
tory guidance which supports it, and to follow the
guidance they contain.
4. You must use your judgement in applying the
principles to the various situations you will face
as a doctor, whether or not you hold a licence to
practise, whatever field of medicine you work in,
and whether or not you routinely see patients. You
must be prepared to explain and justify your deci-
sions and actions.
5. In Good Medical Practice we use the terms
‘you must’ and ‘you should’ in the following ways:
• ‘You must’ is used for an overriding duty or
principle.
• ‘You should’ is used when we are providing an
explanation of how you will meet the overrid-
ing duty.
• ‘You should’ is also used where the duty or prin-
ciple will not apply in all situations or circum-
stances, or where there are factors outside your
control that affect whether or how you can fol-
low the guidance.
6. To maintain your licence to practise, you must
demonstrate, through the revalidation process,
that you work in line with the principles and val-
ues set out in this guidance. Serious or persistent
failure to follow this guidance will put your regis-
tration at risk.
Patients must be able to trust doctors with their lives
and health. To justify that trust you must show respect
dilemmas. Sometimes these factors conflict, for exam-
ple, a Jehovah’s witness declining a blood transfusion
even though the doctor knows that death will ensue.
There are very few medical or healthcare activities
that do not have some ethical considerations, varying
from research on patients to medical confidentiality,
Medical ethics in practice 17
for human life and make sure your practice meets the
standards expected of you in four domains.
A. Knowledge, skills and performance
• Make the care of your patient your first concern.
• Provide a good standard of practice and care.
• Keep your professional knowledge and skills up to
date.
• Recognise and work within the limits of your
competence.
B. Safety and quality
• Take prompt action if you think that patient safety,
dignity or comfort is being compromised.
• Protect and promote the health of patients and
the public.
C. Communication, partnership and teamwork
• Treat patients as individuals and respect their
dignity.
• Treat patients politely and considerately.
• Respect patients’ right to confidentiality.
• Work in partnership with patients.
• Listen to, and respond to, their concerns and
preferences.
• Give patients the information they want or need in
a way they can understand.
• Respect patients’ right to reach decisions with you
about their treatment and care.
• Support patients in caring for themselves to
improve and maintain their health.
• Work with colleagues in the ways that best serve
patients’ interests.
D. Maintaining trust
• Be honest and open and act with integrity.
• Never discriminate unfairly against patients or
colleagues.
• Never abuse your patients’ trust in you or the pub-
lic’s trust in the profession.
You are personally accountable for your profes-
sional practice and must always be prepared to justify
your decisions and actions.
Source: Taken from Good Medical Practice. https://www.gmc-uk.
org/ethical-guidance/ethical-guidance-for-doctors/
good-medical-practice/professionalism-in-action.
from informed consent to doctor–doctor relationships.
Often, law develops as a result of public and political
debate on such issues. Breaches of medical ethical val-
ues (e.g., dishonesty, fraud, sexual assault) may result
in disciplinary processes and the sanctions that can
be applied by regulatory bodies are wide from giving
18 The ethics of medical practice
Box 2.3 Guidelines for intimate examinations
The GMC regularly receives complaints from patients
who feel that doctors have behaved inappropriately
during an intimate examination. Intimate examina-
tions, that is examinations of the breasts, genitalia or
rectum, can be stressful and embarrassing for patients.
When conducting intimate examinations you should:
• Explain to the patient why an examination is nec-
essary and give the patient an opportunity to ask
questions.
• Explain what the examination will involve, in a way
the patient can understand, so that the patient
has a clear idea of what to expect, including any
potential pain or discomfort.
• Get the patient’s permission before the examina-
tion (and assess their capacity to consent to the
examination).
• Record that permission has been given for the
examination.
• Offer the patient a chaperone (an impartial
observer who should usually be a health profes-
sional, rather than a relative or friend, although
Box 2.4 Summary of professional conduct standards for nurses and midwives
You must put the interests of people using or needing
nursing or midwifery first and uphold the standards set
out in the Nursing & Midwifery Council Code. Action
can be taken – including removal from the register – if
you fail to do so.
You must:
Prioritise people: make their care and safety your
first concern and make sure that their dignity
is preserved and their needs are recognised,
assessed and responded to; make sure that those
receiving care are treated with respect, that their
rights are upheld, and that any discriminatory
attitudes and behaviours towards those receiving
care are challenged.
Practise effectively: assess need and deliver or
advise on treatment, or give help without too
much delay, and to the best of your abilities, on
the basis of the best evidence available and best
practice; communicate effectively, keeping clear
advice or warnings to erasure from the relevant regis-
ter and withdrawal of the licence to practice against the
doctor found guilty of unethical practices.
Although the spectrum of unethical conduct is wide,
certain universally relevant subjects are recognised. The
you should comply with a reasonable request to
have such a person present as well as a chaperone).
• You should record any discussion about chaper-
ones and the outcome in the patient’s medical
record; if a chaperone is present you should record
their identity, and if the patient did not want a
chaperone, you should record that the offer was
made and declined.
• Keep discussion relevant and avoid unnecessary
personal comments.
• Give the patient privacy to undress and dress and
use drapes to maintain the patient’s dignity. Do
not assist the patient in removing clothing unless
they have asked you to, or you have checked with
them that they want you to help.
• Stop the examination if the patient asks
you to.
Source: From Intimate examinations and chaperones. General
Medical Council, 2013. (https://www.gmc-uk.org/-/
media/documents/maintaining-boundaries-intimate-
examinations-and-chaperones_pdf-58835231.pdf).
and accurate records; reflect and act on feedback
you receive to improve your practice.
Preserve safety: make sure that patient and public
safety is protected; work within the limits of your
competence, exercising your professional ‘duty
of candour’ and raising concerns immediately
whenever you come across situations that put
patients or public safety at risk.
Promote professionalism and trust: be a model of
integrity and leadership for others to aspire to;
uphold the reputation of your profession at all
times and display a personal commitment to the
standards of practice and behavior set out in this
Code.
Source: Adapted from The Code: Performance standards of
practice and behavior for nurses and midwives. Nursing
and Midwifery Council, 2015. (https://www.nmc.org.uk/
standards/code/).
seriousness with which each is viewed may vary in dif-
ferent parts of the world, as will the sanctions applied.
However, the World Medical Association defines quite
clearly, from a medical perspective, standards that
should be followed (see Box 2.1).

Confidentiality
Confidentiality and consent are the two primary duties
of doctors and other healthcare professionals. They
are key to medical practice. Within the UK, the GMC
has published guidance on both confidentiality and
consent, which gives explicit background and practi-
cal guidance to UK medical practitioners. Many other
countries will provide similar information orientated to
the local jurisdiction and statute. Practitioners must be
aware of requirements in their own jurisdiction.
The UK guidance emphasises that patients have a right
to expect that information about them will be held in con-
fidence by their doctors. Confidentiality is a primary, but
not an absolute duty. Doctors must use their own judge-
ment, and sometimes seek additional advice on applying
the principles of confidentiality and always anticipate
having to later explain and justify any decisions or actions
taken if there is an alleged breach of confidentiality.
A key element of the doctor–patient relationship is
trust. If patients do not trust that confidentiality will be
maintained they may fail to seek medical attention or
may provide incomplete information to obtain appropri-
ate care. A typical example may be a person with drug
or alcohol dependence in a detention setting, who may
believe that full disclosure of problems may have adverse
consequences on their impending court case. A balance
is needed in providing appropriate information to others
to ensure safe, effective care for the patients themselves
and the wider community. Communication must take
place with the patient about relevant information so that
they are aware of why medical information may be dis-
closed to other healthcare professionals. In the course of
this disclosure non-medical healthcare professionals may
also have access to personal information.
There are, however, a number of permissible situa-
tions when confidentiality may not apply. Box 2.5 identi-
fies those circumstances where confidential information
may be allowably disclosed by medical practitioners.
In England & Wales there is a system by which a senior
personnel member within the National Health Service
Box 2.5 W
 hen confidentiality may not
apply
• If required by law (e.g., mandatory reporting of
female genital mutilation).
• If the patient consents – implicitly or expressly.
• If justified in the public interest.
• Reporting concerns about driving capabilities.
• Reporting firearm and knife wounds.
• Reporting serious communicable diseases.
• Reporting in relation to insurance or employ­ment
purposes.
Confidentiality 19
(NHS) acts as a ‘Caldicott Guardian’ and is responsible
for protecting the confidentiality of patient and service-
user information and enables appropriate information-
sharing. Each NHS organisation is required to have a
Caldicott Guardian. The mandate covers all organisa-
tions that have access to patient records, so it includes
acute trusts, ambulance trusts, mental health trusts,
primary care trusts, strategic health authorities and
special health authorities.
It is essential if a healthcare professional holds per-
sonal data about patients that they are familiar with
assorted regulations and legislation that may apply to
their possession of those data. Personal data is informa-
tion that relates to an identified or identifiable individ-
ual. In 2018, the General Data Protection Regulations,
along with the Data Protection Act 2018 (DPA 2018)
was introduced. These, along with the European Data
Protection Board (EDPB), have substantially altered the
regime by which personal data is stored. In addition, the
UK health departments provide guidance on how that
data must be held, for what period of time and how it
must be disposed of. Protection of computers, includ-
ing passwords, and paper-based records is expected.
Sanctions have been taken against doctors and health-
care organisations who have allowed medical records to
be left where the public or other unauthorised personnel
have access to them.
Disclosure of personal information
Personal information can be disclosed without breaching
duties of confidentiality in a number of scenarios. These
are: when the patient consents, whether implicitly or
explicitly for the sake of their own care or for local clinical
audit, or explicitly for other purposes; when the disclosure
is of overall benefit to a patient who lacks the capacity to
consent; disclosure is required by law; the disclosure is
permitted or has been approved under a statutory process
that sets aside the common law duty of confidentiality;
and disclosure can be justified in the public interest. The
GMC advises that if information about a patient is being
disclosed, information must be anonymised if it is prac-
ticable to do so, and that the patient has ready access to
information explaining how their personal information
will be used for their own care or local clinical audit, and
that they have the right to object. Disclosures should be
the minimum necessary for the purpose and follow all rel-
evant legal requirements, including the common law and
data protection law. Records should be kept of all decisions
and actions.
Disclosures required by law
Disclosure may be required because of statute, for exam-
ple, notification of known or suspected types of commu-
nicable disease. Figure 2.1 shows an example of a Public
20 The ethics of medical practice

NOIDs WEEKLY REPORT

STATUTORY NOTIFICATIONS OF INFECTIOUS DISEASES

in ENGLAND and WALES

WEEK 2019/36 week ending 08/09/2019

CONTENTS

Table 1 Statutory notifications of infectious diseases in the past 6 weeks with totals for the
current year compared with corresponding periods of the two preceding years

Table 2 Statutory notifications of infectious diseases for diseases for WEEK 2019/36 by PHE
Region, county, local and unitary authority including additional diseases notifiable from
6th April 2010

Registered Medical Practioner in England and Wales have a statutory duty to notify a Proper Officer of
the local authority, often the CCDC (Consultant in Communicable Disease Control), of suspected cases
of certain infectious diseases:

Acute encephalitis Haemolytic uraemic syndrome * Rubella

Acute infectious hepatitis Infectious bloody diarrhoea * SARS *
Acute meningitis Invasive group A Streptococcal Scarlet fever
disease
Acute poliomyelitis Legionnaires disease * Smallpox
Anthrax Leprosy Tetanus
Botulism * Malaria Tuberculosis
Brucellosis * Measles Typhus
Cholera Meningococcal septicaemia Viral haemorrhagic fever
Diphtheria Mumps Whooping cough
Enteric fever (typhoid or paratyphoid) Plague Yellow fever

Food poisoning Rabies

* Notifiable from 6th April 2010

Notifications of infectious diseases, some of which are later microbiologically confirmed, prompt local
investigation and action to control the diseases. Proper officers are required every week to inform the
PHE (formerly the Registrar General) anonymised details of each case of each disease that has been
notified. PHE has responsibilty of collating the weekly returns from proper officers and publishing
analyses of local and national trends.

All weekly data are Provisional

© Public Health England - Information Management Department

Figure 2.1 An example front page of the Public Health England weekly Notification of Infectious Disease
Report (https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/830662/
NOIDS-weekly-report-week36-2019.pdf)

Health England weekly ‘Notification of Infectious
Diseases Report’ illustrating a wide range of condi-
tions that registered medical practitioners in England
& Wales have a statutory duty to notify a ‘Proper Officers
of the local authority’ (who may be the Consultant in
Communicable Disease Control).
Certain government agencies or bodies may have
statutory power to access patients’ records. Patients’
medical records and related personal information
may be required by regulatory bodies if there has
been a complaint against a healthcare professional.
Courts may require access to medical records when
there is a concern that medical issues or conditions
might materially be relevant in a case. Information
must be disclosed if it is required by statute, or if
ordered by a judge or presiding officer of a court. It
is important to ensure that disclosure is required by
law and information should only be disclosed that is
relevant to the request. Patients should be informed
about such disclosures, unless the purpose would be
undermined, for example, by prejudicing the preven-
tion, identification or prosecution of serious crime.
If there is some ambiguity about the lawfulness of a
request and if disclosure is not consented to, then legal
advice and advice from a medical defence organisa-
tion or Caldicott guardian should be sought. The GMC
provides a framework about disclosing patients’ per-
sonal information.
Disclosing information with consent
Certain patients may wish to withhold particular
aspects of personal information, and unless other rea-
sons for disclosure apply this wish must be respected. If
such a request might influence aspects of medical care,
it should be ensured that the patient is fully aware that
withholding information may compromise that care.
Those who are provided with such information must
be reminded of their own duty of confidence. Clinical
situations such as medical emergencies may mean that
information is passed without consent, and an explana-
tion should later be given to the patient advising them
of the reasons for that disclosure. Disclosure may also
be permitted for audit if the patient is aware of that pos-
sibility and they have not objected to it.
Disclosure requiring express consent
Consent to disclose personal information must always
be sought for any reason beyond clinical care and
audit. Many important uses of patient information
contribute to the overall delivery of health and social
care. Examples include health services management,
research, epidemiology, public health surveillance, and
education and training. There are also important uses
of patient information that are not connected to the
delivery of health or social care, but which serve wider
Confidentiality 21
purposes. These include disclosures for the administra-
tion of justice, and for purposes such as financial audit
and insurance or benefits claims. Anonymised infor-
mation will usually be sufficient for purposes other
than the direct care of the patient and you must use it
in preference to identifiable information wherever pos-
sible. If you disclose identifiable information, you must
be satisfied that there is a legal basis for breaching con-
fidentiality. The patient must always be made aware of
the nature and extent of information being disclosed.
The information disclosed must be unbiased, relevant
and limited to the needs expressed. The patient should
generally be offered the opportunity to see any report
or disclosure prior to it being disclosed, unless poten-
tially non-disclosable confidential information about
another person is contained within it.
Disclosure in the public interest
Confidential medical care is recognised in law as being
in the public interest. There may be a public interest in
disclosing information if the benefits to an individual or
society outweigh both the public and the patient’s inter-
est in keeping the information confidential. In particu-
lar, in the forensic context, disclosure may be justified to
protect individuals or society from risks of serious harm,
such as from serious communicable diseases or serious
crime.
In some circumstances, disclosing personal infor-
mation without consent is justified in the public inter-
est for important public benefits, other than to prevent
death or serious harm, if there is no reasonably prac-
ticable alternative to using personal information. It
is always appropriate to seek advice in such circum-
stances, for example from a Caldicott Guardian or a
medicolegal adviser from a medical defence organisa-
tion. In addition to risks of harm, there are more gen-
eral areas where disclosure may be permissible in the
public interest and these can relate to areas such as
research, education and public health. The opportunity
to anonymise such information should always be taken
if appropriate, although in many settings it may be pos-
sible to obtain consent. A decision to disclose must also
take into account the practicalities of obtaining con-
sent in relation to the need for disclosure.
Disclosures to protect the patient
or others
Disclosure of information may be required for the
patient’s own protection, but if they have capacity then
a refusal to consent to disclosure should be respected.
It is important that the reasons why a disclosure is con-
sidered in their interests is made clearly and unam-
biguously. In the criminal justice setting, issues of
domestic violence are examples of where disclosure
22 The ethics of medical practice
may be relevant (e.g., evidence of previous assaults in
medical records) but disclosure is refused by the patient.
Disclosure without consent may be justified when oth-
ers are at risk of serious harm or death that may be
reduced by such disclosure. Some circumstances, which
often may relate to serious crime (e.g., murder, sexual
assault and child abuse) require the prompt disclosure
of information to appropriate bodies (e.g., police). Such
an approach may also be appropriate if there is a belief
that the patient (adult or child) is a victim of neglect
or physical, sexual or emotional abuse. If appropriate,
the patient should be informed of a decision to disclose
before doing so.
Disclosure concerning patients without
the capacity to consent
A number of factors may be relevant in the setting where a
patient lacks the capacity to consent. Is the lack of capac-
ity temporary or permanent? If temporary, is there any
immediate necessity for disclosure, and can disclosure
be deferred until the patient regains capacity to consent?
If the patient has someone who has a lawful role in mak-
ing decisions for them, they should be consulted. In all
settings it is expected that the doctor is seen to act in the
patient’s best interests, and this should take into account
views of others, including family and other healthcare
professionals.
Disclosure after death
A duty of confidentiality continues after a patient has
died, although there may be situations when relevant
information must be disclosed, for example, when
the patient has died in the UK, to help a Coroner or
Procurator Fiscal with an inquest or fatal accident
inquiry, and on death certificates, and when a person
has a statutory right of access to records. There are other
circumstances (for example, when reviewing someone’s
testamentary capacity before death) where personal
information may be disclosed after a patient’s death. The
decision for disclosure will depend on the facts of the
case. When making the decision to disclose consider-
ation must be given to factors such as whether such dis-
closure is likely to cause distress to the patient’s partner
or family, and whether the information is already in the
public domain or can be anonymised or de-identified,
and the reason for the disclosure. Examples of when
medical information may be disclosable include: when
the disclosure is permitted or has been approved under
a statutory process that sets aside the common law duty
of confidentiality; when there is a public interest to pro-
tect others from a risk of death or serious harm; and
when it is necessary to support the reporting or inves-
tigation of adverse incidents, or complaints, for clinical
audit, and clinical outcome review programmes.
Consent
In order to give consent to a treatment, an investiga-
tion or a process, an individual must have sufficient
capacity, they must possess sufficient understanding
or knowledge of the proposed intervention and their
agreement to undergo the proposed treatment, inves-
tigation or process must be voluntary, that is, it must be
freely given and not tainted by any degree of coercion
or undue influence from others. The GMC emphasises
that (in selected extracts taken from current guidance):
Whatever the context in which medical decisions are
made, you must work in partnership with your patients to
ensure good care. In so doing, you must:
• Listen to patients and respect their views about
their health.
• Discuss with patients what their diagnosis, progno-
sis, treatment and care involve.
• Share with patients the information they want or
need in order to make decisions.
• Maximise patients’ opportunities, and their ability,
to make decisions for themselves.
• Respect patients’ decisions.
It further states:
Ensuring that decisions are voluntary
• Patients may be put under pressure by employers,
insurers, relatives or others, to accept a particular
investigation or treatment. You should be aware of
this and of other situations in which patients may
be vulnerable. Such situations may be, for example,
if they are resident in a care home, subject to mental
health legislation, detained by the police or immi-
gration services, or in prison.
• You should do your best to make sure that such
patients have considered the available options and
reached their own decision. If they have a right to
refuse treatment, you should make sure that they
know this and are able to refuse if they want to.
Respecting a patient’s decisions
• You must respect a patient’s decision to refuse an
investigation or treatment, even if you think their deci-
sion is wrong or irrational. You should explain your
concerns clearly to the patient and outline the possible
consequences of their decision. You must not, how-
ever, put pressure on a patient to accept your advice.
Expressions of consent
• Before accepting a patient’s consent, you must con-
sider whether they have been given the information
they want or need, and how well they understand

the details and implications of what is proposed.
This is more important than how their consent is
expressed or recorded.
• Patients can give consent orally or in writing, or
they may imply consent by complying with the pro-
posed examination or treatment, for example, by
rolling up their sleeve to have their blood pressure
taken.
• In the case of minor or routine investigations or
treatments, if you are satisfied that the patient
understands what you propose to do and why, it is
usually enough to have oral or implied consent.
• In cases that involve higher risk, it is important
that you get the patient’s written consent. This is
so that everyone involved understands what was
explained and agreed.
• By law you must get written consent for certain
treatments, such as fertility treatment. You must
follow the laws and codes of practice that govern
these situations.
You should also get written consent from a patient if:
• The investigation or treatment is complex or
involves significant risks.
• There may be significant consequences for the
patient’s employment, or social or personal life.
• Providing clinical care is not the primary purpose
of the investigation or treatment.
• The treatment is part of a research programme or
is an innovative treatment designed specifically for
their benefit.
• If it is not possible to get written consent, for exam-
ple, in an emergency or if the patient needs the
treatment to relieve serious pain or distress, you
can rely on oral consent. But you must still give the
patient the information they want or need to make
a decision. You must record the fact that they have
given consent, in their medical records.
Recording decisions
• You must use the patient’s medical records or a
consent form to record the key elements of your dis-
cussion with the patient. This should include the
information you discussed, any specific requests by
the patient, any written, visual or audio informa-
tion given to the patient, and details of any deci-
sions that were made.
Patients with capacity to make decisions
Consent is a key concept of healthcare and it is expected
that all decisions about treatment and healthcare come
about as a result of collaboration between doctors and
patients. Consent should be based on trust, openness and
good communication. In the UK, doctors are expected
to work in partnership with their patients in order to
Consent 23
optimise care. Previously the standard test to measure
whether there has been a breach in their duty of care was
known as the Bolam test, which was introduced following
the landmark clinical negligence claim Bolam v Friern
Hospital Management Committee 1957. The test expects
that standards of care have been followed in accordance
with a responsible body of opinion, that is, the medical
professional must demonstrate that they acted in a way
that a responsible body of medical professionals in the
same field would regard as acceptable or reasonable.
However, in the UK the law on informed consent has
changed following a Supreme Court judgement. Doctors
must now ensure that patients are aware of any ‘material
risks’ involved in a proposed treatment, and of reason-
able alternatives, following the judgement in the case
Montgomery v Lanarkshire Health Board. This is a marked
change to the Bolam test. This test will no longer apply to
the issue of consent, although it will continue to be used
more widely in cases involving other alleged acts of neg-
ligence. In a move away from the ‘reasonable doctor’ to
the ‘reasonable patient’, the Supreme Court’s ruling has
outlined the new test: ‘The test of materiality is whether,
in the circumstances of the particular case, a reasonable
person in the patient’s position would be likely to attach
significance to the risk, or the doctor is or should reason-
ably be aware that the particular patient would be likely
to attach significance to it.’ This decision enshrines in
law principles that are already in the GMC’s guidance
on consent. Consent may be given orally or in writing –
this is express or explicit consent. Consent may also be
given implicitly, for example, by allowing blood pressure
to be taken by removing clothing to give access to the
arm. It is generally accepted that for higher risk or more
complex procedures, if there is a risk to life or lifestyle,
for research or in the criminal setting (e.g., the taking of
intimate samples such as penile or vaginal swabs) that
written consent is appropriate. In some settings written
consent is mandatory.
The responsibility for seeking consent is that of the
doctor undertaking the investigation or treatment.
Such a duty can be delegated if the person to whom it is
delegated is appropriately trained and has appropriate
knowledge of the treatment or investigation proposed.
Young people, children and consent
Age is not necessarily a determining factor in the ability
to consent, although it is generally accepted that those
aged 16 years and older have the capacity to make deci-
sions about treatment or care. Many children below the
age of 16 years may also have the capacity to understand
and consider options. In the UK the GMC publishes guid-
ance on making decisions in those aged under 18 years
and how capacity and best interests may be assessed. The
capacity of children below the age of 16 years to consent
to medical treatment depends on whether the child has
24 The ethics of medical practice
achieved a sufficient understanding and intelligence to
appreciate the purpose, nature, consequences and risks
of a particular treatment (including no treatment) and
has the ability to appraise the medical advice. Reference
is made in England & Wales to Gillick competency and
the Fraser guidelines. Gillick competency and the Fraser
guidelines refer to a legal case which looked specifically
at whether doctors should be able to give contraceptive
advice or treatment to under 16-year-olds without paren-
tal consent. They are now widely used to help assess
whether a child has the maturity to make their own deci-
sions and to understand the implications of those deci-
sions. Following an initial court case and then an appeal,
the case went to the House of Lords and the Law Lords
(Lord Scarman, Lord Fraser and Lord Bridge) ruled in
favour of the judgement delivered by Mr. Justice Woolf
in the original case (Gillick v West Norfolk 1984):
…whether or not a child is capable of giving the neces-
sary consent will depend on the child’s maturity and
understanding and the nature of the consent required.
The child must be capable of making a reasonable
assessment of the advantages and disadvantages of the
treatment proposed, so the consent, if given, can be
properly and fairly described as true consent.
The Fraser guidelines refer to the guidelines set out
by Lord Fraser in his judgement of the Gillick case in
the House of Lords (1985), which apply specifically to
contraceptive advice. Lord Fraser stated that a doctor
could proceed to give advice and treatment:
‘provided he is satisfied in the following criteria:
• that the girl (although under the age of 16 years of age)
will understand his advice.
• that he cannot persuade her to inform her parents or
to allow him to inform the parents that she is seeking
contraceptive advice.
• that she is very likely to continue having sexual inter-
course with or without contraceptive treatment.
• that unless she receives contraceptive advice or treat-
ment her physical or mental health or both are likely
to suffer.
• that her best interests require him to give her contra-
ceptive advice, treatment or both without the parental
consent.’
In the same case Lord Scarman commented:
…it is not enough that she should understand the nature
of the advice which is being given: she must also have a
sufficient maturity to understand what is involved
and more generally on parents’ versus children’s
rights:
…parental right yields to the child’s right to make his
own decisions when he reaches a sufficient under-
standing and intelligence to be capable of making up
his own mind on the matter requiring decision.
This test of competence is utilised in a number of
other jurisdictions.
Patients without capacity to make
decisions
If patients are unable to make decisions for themselves,
the doctor must engage with those who are close to the
patient and with colleagues involved in the healthcare.
In England & Wales decisions about those who lack
capacity is governed by the Mental Capacity Act 2005
(MCA). The MCA is intended to protect and empower
people who may lack the mental capacity to make their
own decisions about their care and treatment. It applies
to people aged 16 and over. It covers a range of decisions
about everyday living (e.g., what to wear) and more seri-
ous potentially life-changing decisions (e.g., having
major surgery). There is no specific group that lacks
capacity but examples of conditions which may have an
effect include:
• Dementia
• Severe learning disability
• Brain injury
• Mental health illness
• Cerebrovascular accident
• Unconsciousness caused by an anaesthetic or
sudden accident
The presence of these or other health conditions
does not automatically mean that the individual lacks
the capacity to make a specific decision, and the nature
of capacity may vary dependent on the task (e.g., they
may lack the ability to make financial decisions, but be
able to manage day-to-day tasks). The MCA assumed
that every person has the capacity to make a decision
themselves, unless it is proved otherwise; that wherever
possible, people should be assisted in making decisions;
an unwise decision does not necessarily mean a per-
son lacks capacity; and if decision making on behalf of
someone who lacks capacity you must act in their best
interests. Additionally, treatment and care provided to
someone who lacks capacity should be the least restric-
tive of their basic rights and freedoms.
The Act sets out a 2-stage test of capacity:
1. Does the person have an impairment of their
mind or brain, whether as a result of an illness,
or external factors such as alcohol or drug use?
2. Does the impairment mean the person is unable
to make a specific decision when they need to?
Mental capacity can also fluctuate with time – some-
one may lack capacity at one point in time, but may be
able to make the same decision at a later point in time.
Whenever possible people should be allowed the time

to make a decision themselves. The determination of
capacity is made by determining whether the person is
able to:
• Understand the decision to be made and the infor-
mation provided about the decision: the conse-
quences of making a decision must be included in
the information given.
• Retain the information: a person should be able
to retain the information given for long enough
to make the decision – information can only be
retained for short periods of time, it should not
automatically be assumed that the person lacks
capacity, for example, written information could
be used to assist a person’s ability to retain it.
• Use that information in making the decision: a
person should be able to weigh up the advantages
and disadvantages of making the decision.
• Communicate their decision: if a person cannot
communicate their decision, for example, if they
are unconscious, the Act specifies that they should
be treated as if they lack capacity. All efforts should
be made to help the person communicate their
decision before deciding they are not able to do so.
Regulation of doctors and other
professionals
The General Medical Council
Regulation of the work of healthcare professionals is
governed in many countries around the world by regula-
tory bodies that may have powers to assess the individ-
ual’s performance and work. In the UK, the regulatory
body for registered medical practitioners (doctors) is the
General Medical Council (GMC). The Medical Act 1858
established the General Council of Medical Education
and Registration of the United Kingdom as a statutory
body. Subsequent Acts have refined this. Currently all
the GMC’s functions derive from a statutory require-
ment for the establishment and maintenance of a
register, which is the definitive list of doctors as provi-
sionally or fully ‘registered medical practitioners’. The
GMC controls entry to the List of Registered Medical
Practitioners (‘the medical register’). The Medical Act
1983 (amended) notes that, ‘The main objective of the
General Council in exercising their functions is to pro-
tect, promote and maintain the health and safety of the
public.’ The GMC also regulates and sets the standards
for medical schools in the UK, and liaises with other
nations’ medical and university regulatory bodies over
medical schools overseas, leading to some qualifica-
tions being mutually recognised. It also regulates post-
graduate medical education. Most recently the GMC is
responsible for a licensing and revalidation system for
Regulation of doctors and other professionals 25
all practising doctors in the UK, separate from the reg-
istration system. The GMC has legal powers designed to
maintain the standards the public have a right to expect
of doctors. If a doctor fails to meet those standards, the
GMC acts to protect patients from harm – if necessary,
by seeking to remove the doctor from the register and
removing their right to practise medicine.
Before the GMC can stop or limit a doctor’s right to prac-
tise medicine, it needs evidence of impaired fitness to prac-
tise. Examples of such evidence include doctors who have
not kept their medical knowledge and skills up to date and
are not competent, have taken advantage of their role as a
doctor or have done something wrong, are too ill, or have
not adequately managed a health problem to enable them
to work safely. The GMC can also issue a warning to a doc-
tor where the doctor’s fitness to practise is not impaired but
there has been a significant departure from the principles
set out in the GMC’s guidance for doctors, Good Medical
Practice. A number of sanctions are available. For example,
a warning will be disclosed to a doctor’s employer and to
any other enquirer during a 5-year period. A warning will
not be appropriate where the concerns relate exclusively to
a doctor’s physical or mental health.
Doctors (and other healthcare professionals) in the
UK have a ‘professional duty of candour’, and detailed
guidance as to how this ought to be achieved in practice
has been issued by the GMC. In essence, it is a duty to be
honest with patients when things go wrong, and builds
on the recommendations made by Sir Robert Francis in
the wake of the significant failures in the provision of
basic healthcare in Mid Staffordshire NHS Foundation
Trust hospital.
Legal framework for GMC fitness
to practise procedures
The legal framework for the Fitness to Practise proce-
dures is set out in the Medical Act 1983 and the Fitness
to Practise Rules 2004. These are updated at frequent
intervals. In particular these rules set timelines and
structure to the procedures.
The Medical Act gives the GMC powers and respon-
sibilities for taking action when questions arise about
doctors’ fitness to practise. The detailed arrangements
for how these matters are investigated and adjudicated
upon are set out in rules which have the force of law.
Procedures are divided into two separate stages:
‘Investigation’ and ‘Adjudication’. In the investigation
stage cases are assessed to determine whether they need
referral to the Medical Practitioners Tribunal Service
(MPTS) for adjudication. The adjudication stage consists
of a hearing by a medical practitioner’s tribunal.
Where the complaint raises questions about the doc-
tor’s fitness to practise, an investigation will commence
and the complaint will be disclosed to the doctor and
26 The ethics of medical practice
his/her employer/sponsoring body. This is intended to
ensure that there is a complete overview of the doctor’s
practice and makes the information available to those
responsible for local clinical governance. Further infor-
mation may be sought from the complainant, whose
consent will be needed to disclose the complaint to the
doctor.
The doctor is given an opportunity to comment on
the complaint. An investigation may need further doc-
umentary evidence from employers, the complainant
or other parties, witness statements, expert reports on
clinical matters, an assessment of the doctor’s perfor-
mance and an assessment of the doctor’s health.
At the end of the investigation of allegations against
a doctor, the case will be considered by two senior
GMC staff known as case examiners (one medical and
one non-medical) who can conclude the case with no
further action, issue a warning, refer the case to the
Panel or agree undertakings. They must have in mind
the GMC’s overarching objective of public protection
(including the protection of patients and maintaining
public confidence in the ­profession) in considering
whether there is a realistic prospect of establishing that
a doctor’s fitness to practise is impaired to a degree jus-
tifying action on registration. Cases can only be con-
cluded or referred to a Fitness to Practise Panel with
the agreement of both a medical and non-medical case
examiner. If they fail to agree, the matter will be con-
sidered by the Investigation Committee, a statutory
committee of the GMC. A warning will be appropriate
if there is evidence to suggest that the practitioner’s
behaviour or performance has fallen below acceptable
standards to a degree warranting formal censure by
the GMC, but does not w ­ arrant referral to a tribunal,
and action on registration is not necessary. A decision
may be made that, despite there being evidence that the
practitioner’s practice is impaired, no further action
will be taken if that practitioner accepts undertakings
restricting future practice or behaviour, or to undergo
medical supervision or retraining, for example.
At any stage of the investigation a doctor may be
referred to an interim orders tribunal of the MPTS which
can suspend or impose conditions on a doctor’s practice
while the investigation continues. Cases referred to an
interim order tribunal are those where the doctor faces
allegations of such a nature that it may be necessary
for the protection of patients, or it may be in the public
interest or in the interests of the doctor for the doctor’s
registration to be restricted whilst the allegations are
resolved. An interim orders tribunal may make an order
suspending a doctor’s registration or imposing condi-
tions upon a doctor’s registration for a maximum period
of 18 months. An interim orders tribunal must review
the order within 6 months of the order being imposed,
and thereafter, at intervals of no more than 6 months.
If an interim orders tribunal wishes to extend an order
beyond the period initially set, the GMC will apply to
the High Court (or the Court of Session in Scotland) for
permission to do so.
The Fitness to Practise Panel hears evidence and
decides whether a doctor’s fitness to practise is impaired.
Fitness to Practise hearings are the final stage of proce-
dures following a complaint about a doctor.
A Fitness to Practise Panel is composed of medi-
cal and non-medical persons and normally comprises
three to five panelists. In addition to the chairman, who
may be medical or non-medical, there must be at least
one medical and one non-medical panelist on each
panel. A legal assessor sits with each panel and advises
on points of law and of mixed law and fact, including the
procedure and powers of the panel. One or more spe-
cialist advisers may also be present to provide advice to
the panel in relation to medical issues regarding a doc-
tor’s health or performance. The GMC is normally repre-
sented at the hearing by a barrister. The doctor is invited
to attend and is usually present and legally represented.
Both parties may call witnesses to give evidence and if
they do so the witness may be cross-examined by the
other party. The panel may also put questions to the
witnesses. The panels meet in public, except where they
are considering confidential information concerning
the doctor’s health or they are considering making an
interim order.
Once the panel has heard the evidence, it must decide
whether the facts alleged have been found proved and
whether, on the basis of the facts found proved, the doc-
tor’s fitness to practise is impaired and, if so, whether
any action should be taken against the doctor’s registra-
tion. If the panel concludes that the doctor’s fitness to
practise is impaired, the following sanctions are avail-
able: to take no action; to accept undertakings offered
by the doctor provided that the panel is satisfied that
such undertakings protect patients and the wider pub-
lic interest; to place conditions on the doctor’s registra-
tion; to suspend the doctor’s registration; or to erase the
doctor’s name from the Medical Register, so that they
can no longer practise. The process is summarised in
Figure 2.2.
Doctors have a right of appeal to the High Court (Court
of Session in Scotland) against any decision by a panel to
restrict or remove their registration. The GMC, and the
Professional Standards Authority (which oversees and
scrutinises nine healthcare regulatory bodies in the UK),
may also appeal against certain decisions if they consider
the decision was too lenient. Any doctor whose name has
been erased from the Medical Register (‘the Register’)
by a Fitness to Practise Panel can apply for their name to
be restored to the Register. Doctors cannot apply to have
their name restored to the Register until after a period
of 5 years has elapsed since the date their name was
erased. These processes were brought into sharp focus
in 2018 by the case of Dr Hadiza Bawa-Garba who had
Dealing with concerns about a doctor
Referral to the GMC
It is often better for patients to raise
their concerns through local complaints
procedures in the first instance with the
NHS Hospital Trust, Primary Care Trust
(or equivalent) or private healthcare body.
NHS
Local Procedures
• Internal review
• No action required
• Internal/Local action
• Information exchange
• Referral to the GMC
Private Health
Local Procedures
• Internal review
• No action required
• Internal/Local action
• Information exchange
• Referral to the GMC
GMC
GMC Procedures
• Internal review
• Information exchange
• Further investigation
by the GMC
• Conviction or decisions
from another regulatory body
• Inappropriate complaints
would be closed at this stage
Figure 2.2 The GMC’s Fitness to Practise procedures. (From https://www.gmc-uk.org/-/media/documents/
DC4541_The_GMC_s_Fitness_to_Practise_procedures.pdf_25416512.pdf.)
Stage one
Further investigation
Where a matter raises serious concerns
about a doctor’s practice, the GMC will
undertake an investigation. This may
include an assessment of the doctor’s
health or performance, where appropriate.
GMC case examiners will then decide
what action to take, for example referral
to a fitness to practise panel. If the case
examiners cannot agree or a warning is
offered and the doctor refuses to accept
the warning, the case will be referred to
the Investigation Committee.
GMC
• Further Investigation
The case examiners may decide to:
• Take no action
• Issue a warning
• Refer to a FTP Panel
• Agree undertakings
• Referral to the Interim
Orders Panel (IOP)
Stage two
Investigation Committee MPTS
and interim orders Fitness to Practise Panels comprise the final
If both case examiners decide that a warning stage of the fitness to practise procedures.
is appropriate, the doctor may exercise All aspects of the doctor’s fitness to
his/her right to an oral hearing before the practise will be considered and there are no
Investigation Committee. If the two case longer separate streams for conduct, health
examiners do not agree on the appropriate
and performance.
outcome, the case will be decided by a
meeting of the Investigation Committee. MPTS
• Fitness to practise panel
GMC
The panel may decide to:
• Investigation Committee
• Issue a warning to the doctor
• No action required
• Put conditions on the doctor’s
• Warning issued
registration
• Referral to a FTP Panel
• Suspend the docter’s name
• Undertakings agreed
from the medical register
• Referral to the IOP
• Erase the doctor’s name from
the medical register
GMC
• Interim Orders Panel
• IOP directs interim conditions
(restricting practice)
• IOP directs suspension with
immediate effect
Regulation of doctors and other professionals
27
28 The ethics of medical practice
been erased from the Register, despite recognised institu-
tional failings at the time. Dr Bawa-Garba was convicted
of gross negligence manslaughter following the death of
six-year-old Jack Adcock from sepsis. The MPTS decided
she should be allowed to return to train and practise as a
doctor after a year’s suspension. The GMC had appealed
that MPTS decision. The GMC argued suspension was
not sufficient and appealed the MPTS’s sanction to the
Divisional Court of the Queen’s Bench Division of the
High Court. The Divisional Court held that the MPTS’s
decision was not consistent with, and did not respect,
the verdict of the jury that Dr Bawa-Garba’s conduct was
‘truly exceptionally bad’. The Divisional Court considered
that the MPTS had been wrong to take into account that
there were systemic failings of the Hospital and that Dr
Bawa-Garba shared with others the responsibility for
failings in the care and treatment of Jack. The Divisional
Court concluded that, in view of the decision of the jury as
to Dr Bawa-Garba’s personal culpability, the MPTS was
wrong to think that public confidence in the profession
could be maintained by any sanction short of erasure
from the Medical Register. The Divisional Court, there-
fore, quashed the order of suspension of the MPTS and
substituted an order of erasure. Subsequently the Court
of Appeal unanimously held that the Divisional Court
was wrong to interfere with the decision of the MPTS. The
Court of Appeal set aside the order of the Divisional Court
that Dr Bawa-Garba should be erased from the Medical
Register and restored the order of the Tribunal that she be
suspended from practice for 12 months subject to review.
On 13 August 2018, the Court of Appeal overturned the
High Court’s decision to remove Dr Bawa-Garba from the
medical register following the successful outcome of her
appeal.
Regulatory bodies for other healthcare professionals
in the UK follow a process similar to that of the GMC
when assessing the performance of practitioners. All
publish regular updates of their fitness to practise find-
ings and the outcomes.
Bibliography and information
resources
Access to Health Records Act (1990). https://www.legislation.gov.
uk/ukpga/1990/23/contents (Accessed 1 April 2019).
Bawa-Garba (Appellant) v General Medical Council (Respondent)
[2018] EWCA Civ 1879. On appeal from: [2018] EWHC 76
(Admin).
Biggs H. Healthcare Research Ethics and Law: Regulation, Review
and Responsibility. London: Routledge Cavendish; 2010.
Bolam v Friern Hospital Management Committee [1957] 1 WLR 583.
British Medical Association (BMA) Medical ethics toolkits. https://
www.bma.org.uk/ethics (Accessed 17 April 2019).
Dhai A, Payne-James J. Problems of capacity, consent
and ­confidentiality. Best Pract Res Clin Obstet Gynaecol
2013;27(1):59–75.
Francis R. Report of the Mid Staffordshire NHS Foundation Trust
Public Inquiry, 2013. https://www.gov.uk/government/pub-
lications/report-of-the-mid-staffordshire-nhs-foundation-
trust-public-inquiry (Accessed 1 April 2019).
General Medical Council. Confidentiality: guidance for doctors.
Manchester: GMC, 2009. http://www.gmc-uk.org/guidance/
ethical_guidance/confidentiality.asp (Accessed 1 April 2019).
General Medical Council. Consent: patients and d ­ octors mak-
ing decisions together. Guidance for doctors. https://www.
gmc-uk.org/ethical-guidance/ethical-guidance-for-doctors/
consent (Accessed 1 April 2019).
General Medical Council. 0–18 years: Guidance for all doctors.
https://www.gmc-uk.org/ethical-guidance/ethical-guidance-
for-doctors/0-18-years (Accessed 1 April 2019).
General Medical Council. Guidance to the GMC’s Fitness to
Practise Rules 2004 (as amended) (2016). https://www.gmc-
uk.org/-/media/documents/DC4483_Guidance_to_the_FTP_
Rules_28626691.pdf (Accessed 1 April 2019).
General Medical Council. Fitness to practise statistics 2016.
https://www.gmc-uk.org/-/media/documents/2016-fitness-
to-practise-annual-statistics_pdf-71779372.pdf (Accessed 1
April 2019).
General Medical Council. Good medical practice. https://www.
gmc-uk.org/ethical-guidance/ethical-guidance-for-doctors/
good-medical-practice (Accessed 1 April 2019).
General Medical Council. Openness and honesty when
things go wrong: the professional duty of candour.
ht tps: //w w w.gmc-uk .org/ethical- guidance/ethical-
guidance-for-doctors/candour---openness-and-honesty-
when-things-go-wrong (Accessed 1 April 2019).
General Medical Council. Disclosing personal information: a
framework. https://www.gmc-uk.org/ethical-guidance/ethi-
cal-guidance-for-doctors/confidentiality/disclosing-patients-
personal-information-a-framework (Accessed 1 April 2019).
General Medical Council. Managing and protecting personal
information. https://www.gmc-uk.org/ethical-guidance/
ethical-guidance-for-doctors/confidentiality/managing-and-
protecting-personal-information (Accessed 1 April 2019).
General Medical Council. Intimate examinations and chaperones,
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boundaries-intimate-examinations-and-chaperones_pdf-
58835231.pdf (Accessed 20 May 2019).
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bailii.org/uk/cases/UKHL/1985/7.html (Accessed 1 April 2019).
Health & Care Professionals Council. Fitness to Practice
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reports/2018/fitness-to-practise-annual-report-2018/
(Accessed 3 June 2019).
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guide-to-the-general-data-protection-regulation-gdpr/
(Accessed 1 April 2019).
Lynch J. Health Records in Court. Oxford: Radcliffe Publishing; 2009.
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McLean S. Autonomy, Consent and the Law. London: Routledge
Cavendish; 2010.
Mental Capacity Act 2005. https://www.legislation.gov.uk/
ukpga/2005/9/contents (Accessed 1 April 2019).
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org/ (Accessed 1 April 2019).
Montgomery v Lanarkshire Health Board [2015] UKSC 11.

NHS England. Confidentiality policy, 2018. https://www.england.
nhs.uk/wp-content/uploads/2016/12/confidentiality-policy-
v4.pdf (Accessed 6 April 2019).
NHS Health Research Authority. Research Ethics Service and
Research Ethics Committees. https://www.hra.nhs.uk/about-us/
committees-and-services/res-and-recs/ (Accessed 1 April 2019).
NHS Health Research Authority. Governance arrangements for
Research Ethics Committees. https://www.hra.nhs.uk/plan-
ning-and-improving-research/policies-standards-legislation/
governance-arrangement-research-ethics-committees/
(Accessed 1 April 2019).
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things go wrong: the professional duty of candour. https://
www.nmc.org.uk/globalassets/site​documents/nmc-publica-
tions/openness-and-honesty-professional-duty-of-candour.
pdf (Accessed 2 April 2019).
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2016–2017. https://www.nmc.org.uk/globalassets/sitedocu-
ments/annual_reports_and_accounts/ftpannualreports/
annual-fitness-to-practise-report-2016-2017.pdf (Accessed 2
April 2019).
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Maxwell; 2014.
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general principles. J Forensic Leg Med 2018;57:66–72.
Further general resources 29
UK Caldicott Guardian Manual. A manual for Caldicott
Guardians. 2017. https://assets.publishing.service.gov.uk/
government/uploads/system/uploads/attachment_data/
file/581213/cgmanual.pdf (Accessed 2 April 2019).
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(Accessed 2 April 2019).
Health & Care Professions Council (HCPC). http://hpc-uk.org/
(Accessed 6 April 2019).
Medical Act 1858. http://www.legislation.gov.uk/ukpga/Vict/21-
22/90/enacted (Accessed 2 April 2019).
Medical Act 1983. http://www.legislation.gov.uk/ukpga/
1983/54/contents (Accessed 2 April 2019).
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(Accessed 2 April 2019).
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(Accessed 2 April 2019).
3 Medicolegal aspects of death
▪▪ Introduction
▪▪ Prolonged disorders of consciousness
▪▪ Tissue and organ transplantation
Introduction
All doctors and most healthcare professionals encoun-
ter death, and the dying, at some time in their career. It
is important to have an understanding of the medical
and legal aspects of these phenomena.
Definition of death
Only organisms that have experienced life can die, as
death represents the cessation of life in a previously liv-
ing organism. Medically and scientifically, death is not an
event; it is a process in which cellular metabolic processes
in different tissues and organs cease to function at differ-
ent rates.
This differential rate of cellular death results in sub-
stantial debate – from ethical, cultural, religious and
moral perspectives – as to when ‘death’ actually occurs.
One pragmatic solution to this argument is to consider
the death of a single cell (cellular death) and the ces-
sation of the integrated functioning of an individual
(somatic death) as two separate aspects.
Cellular death
Cellular death implies the cessation of respiration (the
utilisation of oxygen) and the normal metabolic activ-
ity in the body tissues and cells. Cessation of respira-
tion is soon followed by autolysis and decay, which, if
it affects the whole body, is unchallengeable evidence
of true death. The differences in cellular metabolism
determine the rate at which cells die and are not all
simultaneous – with the exception of an event such as
synchronous death of all of the cells following a nuclear
explosion.
Skin and bone can remain metabolically active
and thus ‘living’ for many hours and their cells can be
successfully cultured days after somatic death. White
blood cells are capable of movement for up to 12 hours
after cardiac arrest – a fact that makes the concept of
microscopic identification of a ‘vital reaction’ to injury
of doubtful reliability. The cortical neuron, on the other
hand, dies after only 3–7 minutes of complete oxygen
deprivation. A body dies cell by cell and the complete
▪▪ Cause of death determination and certification
▪▪ Bibliography and information sources
▪▪ Further general resources
process may take many hours, although this will not be
evident to observers.
Somatic death and resuscitation
Somatic death means that the individual will never
again communicate or deliberately interact with the
environment. The individual is irreversibly unconscious
and unaware of both the world and their own existence.
The key element in this definition is ‘irreversible’, as lack
of communication and interaction with the environ-
ment may occur in a variety of settings such as when in
a deep sleep, under anaesthesia, under the influence of
drugs or alcohol or as a result of a temporary coma from
head injury.
There is no statutory definition of death in the United
Kingdom but, following proposed ‘brain death criteria’
by the Conference of Medical Royal Colleges in 1976, the
courts in England and Northern Ireland have adopted
these criteria as part of the law for the diagnosis of death.
In 2008, the Academy of Medical Royal Colleges
published a ‘Code of Practice for the Diagnosis and
Confirmation of Death’, stating that
Death entails the irreversible loss of those essential
characteristics which are necessary to the existence
of a living human person and, thus, the definition of
death should be regarded as the irreversible loss of the
capacity for consciousness, combined with irreversible
loss of the capacity to breathe. This may be secondary
to a wide range of underlying problems in the body, for
example, cardiac arrest… The irreversible cessation of
brain-stem function whether induced by intracranial
events or the result of extracranial phenomena, such
as hypoxia, will produce this clinical state and there-
fore irreversible cessation of the integrative function of
the brain-stem equates with the death of the individual
and allows the medical practitioner to diagnose death.
Criteria for the diagnosis and confirmation of death
are specified following cardiorespiratory arrest, in a
primary care setting and in hospital, and following
irreversible cessation of brain-stem function, where
specified conditions have been fulfilled (see Boxes
3.1–3.3).

Box 3.1 C  riteria for the diagnosis and confirmation of death following
c­ ardiorespiratory arrest
Simultaneous and irreversible onset of apnoea and
unconsciousness in the absence of the circulation, fol-
lowing ‘full and extensive attempts’ at reversal of any
contributing causes of cardiorespiratory arrest.
One of the following applies:
• Criteria for not attempting cardiopulmonary
resuscitation (CPR) are fulfilled, or
• CPR attempts have failed, or
• Life-sustaining treatment has been withdrawn,
where a decision has been made that such treat-
ment is not in the patient’s best interest, or where
there is an ‘advance decision’ from the patient to
refuse such treatment.
The person responsible for confirming death
observes the individual for a minimum of 5 ­minutes,
Advances in resuscitation techniques in recent
decades, for example in technologies such as ventila-
tion, and in the pharmacological support of the uncon-
scious patient, result in the survival of patients who
would otherwise have died as a result of direct cerebral
trauma or of cerebral hypoxia from whatever cause.
Previously, brain-stem death would eventu-
ally result in respiratory arrest causing myocardial
hypoxia and cardiac arrest. Artificial ventilation
interrupts that process and while ventilation is con-
tinued, myocardial hypoxia and cardiac arrest are
prevented.
Box 3.2 C riteria for the diagnosis of death following irreversible cessation of
­brain-stem function (adults and children over the age of 2 months)
Absence of brain-stem reflexes:
• Pupils are fixed and do not respond to changes in
light intensity.
• Corneal reflex is absent.
• Oculovestibular reflexes are absent when ice-cold
water is introduced into the ear canals.
• No motor responses within the cranial nerve dis-
tribution can be elicited by stimulation of any
somatic area.
• No cough reflex response to bronchial stimulation
by a suction catheter placed in the trachea down
to the carina.
• No gag response to stimulation of the posterior
pharynx with a spatula.
• No spontaneous respiratory response following
disconnection from the ventilator (‘apnoea test’),
Prolonged disorders of consciousness 31
ensuring an absence of a central pulse on palpation
and an absence of heart sounds on auscultation.
In a hospital setting, supplementary ‘evidence’ of
death may be provided in the form of asystole on a
continuous electrocardiogram (ECG) display, absence
of contractile activity using echocardiography or
absence of pulsatile flow using direct intra-arterial
pressure monitoring.
Confirmation of the absence of pupillary responses
to light, of the corneal reflexes and any motor response
to supra-orbital pressure.
The time of death is recorded when these criteria
have been fulfilled.
S ource: Adapted from Academy of Medical Royal Colleges.
(2008). A Code of Practice for the Diagnosis and
Confirmation of Death. London.
There is a spectrum of survival: some patients will
recover both spontaneous respiration and conscious-
ness, others will not regain consciousness but will regain
the ability to breathe on their own and some will regain
neither consciousness nor the ability to breathe and will
require permanent artificial ventilation to remain ‘alive’.
Prolonged disorders of
consciousness
Disorders of consciousness (DOC) include: coma,
vegetative state (VS), and minimally conscious state
where arterial blood gas sampling confirms an
increase in PaCO2 by more than 0.5 kPa above the
starting level.
Brain-stem testing should be made by at least
two medical practitioners, registered for more than 5
years, and who are competent in the interpretation of
such tests; at least one of these individuals must be a
consultant.
Ancillary investigations – cerebral angiography, per-
fusion and neurophysiological – may be appropriate in
some circumstances; brain-stem tests cannot be per-
formed, for example, where there are extensive maxil-
lofacial injuries.
Source: Adapted from Academy of Medical Royal Colleges.
(2008). A Code of Practice for the Diagnosis and
Confirmation of Death. London.
32 Medicolegal aspects of death

Box 3.3 C
 onditions necessary for the diagnosis and confirmation of death f­ ollowing
irreversible cessation of brain-stem function
Irreversible brain damage resulting from damage of
known aetiology or, following continuing clinical obser-
vation and investigation, there is no possibility of a
reversible or treatable underlying cause being present.
Potentially reversible causes of coma have been
excluded.
There is no evidence that the state is caused by
depressant drugs, for example narcotics, hypnotics or
tranquillizers; specific antagonists may need to be used.
Hypothermia as the cause of unconsciousness has
been excluded.
Potentially reversible circulatory, metabolic and
endocrine disturbances have been excluded as the
cause of the continuation of unconsciousness, includ-
ing hyperglycaemia or hypoglycaemia.
Potentially reversible causes of apnoea have been
excluded, for example the effects of neuromuscular
blocking agents.
Source: Adapted from Academy of Medical Royal Colleges.
(2008). A Code of Practice for the Diagnosis and
Confirmation of Death. London.

(MCS). Following severe brain injury, many patients
progress through stages of coma, VS and MCS as they
emerge into a state of full awareness. However, some
will remain in a vegetative or minimally conscious
state for the rest of their lives. The diagnosis, manage-
ment and lifelong (including end-of-life [EOL]) care
of adults who have prolonged disorders of conscious-
ness (PDOC), persisting for more than 4 weeks fol-
lowing sudden onset profound acquired brain injury
is a sensitive and complex area. In 2013, The Royal
College of Physicians published ‘Prolonged Disorders
of Consciousness: National Clinical Guidelines, which
advise clinical and ethical standards of care for peo-
ple with PDOC.’ For the purposes of the guidelines,
the definitions in Table 3.1 are used to differentiate
between these states.
Based on a large cohort analysis the American
Academy of Neurology practice guideline recom-
mended that VS may be judged to be ‘permanent’
12 months after traumatic brain injury or 3 months
after non-traumatic brain injury. The UK RCP guide-
lines recommended a more cautious period of 6
months for non-traumatic brain injury. In light of the
documented late recoveries, it is important to view
the temporal definitions as probabilities. The US Task
Force emphasised that permanent VS refers to progno-
sis and identifies the point after which recovery of con-
sciousness is ‘highly improbable’ but not impossible.
In such circumstances, the withdrawal of hydration
and assisted nutrition may be considered in the ‘best
interests’ of the patient.
The first, and most significant case regarding the
legality of such withdrawal of ‘life sustaining’ treatment
concerned Tony Bland, in ‘persistent vegetative state’
following an accident at a football ground (Airedale
NHS Trust v Bland). Since that case, in which permis-
sion to remove assisted feeding was granted, additional
cases have sought to clarify the position following the

Table 3.1 Definitions of disorders of consciousness

Coma A state of unrousable unresponsiveness, lasting more than 6 hours in which a person:
(Absent wakefulness and • cannot be awakened
absent awareness) • fails to respond normally to painful stimuli, light or sound
• lacks a normal sleep–wake cycle, and
• does not initiate voluntary actions.
Vegetative state (VS) A state of wakefulness without awareness in which there is preserved capacity for
(Wakefulness with spontaneous or stimulus-induced arousal, evidenced by sleep–wake cycles and a range of
absent awareness) reflexive and spontaneous behaviours.
VS is characterised by complete absence of behavioural evidence for self- or environmental
awareness.
Minimally conscious A state of severely altered consciousness in which minimal but clearly discernible
state (MCS) behavioural evidence of self- or environmental awareness is demonstrated.
(Wakefulness with MCS is characterised by inconsistent, but reproducible, responses above the level of
minimal awareness) spontaneous or reflexive behaviour, which indicate some degree of interaction with their
surroundings.
 Tissue and organ transplantation 33

enactment of the Human Rights Act 1998, the ‘right to
life’ and the right not to be subjected to inhuman and
degrading treatment.
A recent judgement in the UK Supreme Court, the
UK’s highest court, has determined that legal permis-
sion from the Court of Protection will no longer be
needed to end life support for patients in a permanent
VS when relatives and doctors agree it should be turned
off (An NHS Trust and others v Y and another 2018). The
case related to a the 52-year-old financial analyst – Mr Y
who was in a PDOC. After suffering a cardiac arrest as a
result of coronary artery disease, experts agreed it was
highly improbable that Mr Y would re-emerge into con-
sciousness and, even if he did, he would have profound
cognitive and physical disability and would always be
dependent on others.
Tissue and organ transplantation
The laws relating to tissue and organ donation and
transplantation are dependent upon the religious and
ethical views of the country in which they apply. The
laws vary in both extent and detail around the world,
but there are very few countries where transplanta-
tion is expressly forbidden and few religions that for-
bid it – Jehovah’s Witnesses are one such group; they
also reject transfusion of donated blood. In the UK, the
Human Tissue Authority has issued guidance regarding
the issues of consent for removal of organs for either
research or transplantation under the Human Tissue
Act where donors are deceased. It applies in England,
Wales and Northern Ireland, and is not affected by the
Human Transplantation (Wales) Act 2013. The guidance
is summarised in Figure 3.1.
The organs and tissues to be transplanted may derive
from one of several sources, which are outlined below.
Homologous transplantation
Homologous transplantation is the process by which
tissue is moved between sites on the same body. For
example, skin grafts may be taken from the thigh to
place on a burn site or bone chips from the pelvis may be
taken to assist in the healing of a fracture of a long bone.
Homologous blood transfusion can be used in certain
situations such as when there is a religious objection to
the use of anonymously donated blood.
Live donation
In this process, tissue is taken from a living donor
whose tissues have been matched to, or are compat-
ible with, those of the recipient. The most common
example is blood transfusion but marrow transplan-
tation is now very common. Other live donations
frequently involve the kidneys as these are paired

Removal
of organ
from
deceased
The donor
Consent from the The Consent from the
deceased donor* is primary purpose
primary purpose deceased donor* is
required to remove/ for the removed organ
for the removed organ is required to remove/
store/use the organ is for research - the organ
for transplantation use the organ for
for research is not going to be
transplantation
transplanted

Organ Organ
transplantation is transplanted
occurs and treatment (no planned research
is combined with intervention)
research
Organ
* Consent in this case cannot be Recipient
means either the consent Treatment interventions being
transplanted consent is
of the donor, their researched can take place before or
required for
nominated representative after implantation of the removed
transplantation
or - in the absence of organ. The organ can be
either of these - the sent for disposal or,
consent of a person in Health research involving patients is with valid consent
the most appropriate subject to approvals from relevant from the deceased
‘qualifying relationship’ bodies. donor*, stored and/
to the donor immediately or used for research
before they died. More Note: Recipients of organs subjected to
guidance on this is research interventions must have given
available from the HTA. their consent to receive the organs.

Figure 3.1 Consent requirements for removal of organs for research or transplantation. (Adapted from HTA. Guidance
on consent for transplantation research where donors are deceased.)
34 Medicolegal aspects of death
organs and live donors will, if the remaining kidney is
healthy, maintain their electrolyte and water balance
without problem.
Most kidneys for transplant are derived from cadav-
eric donation, but live donation is also possible and the
long-term clinical results are better. The removal of
kidneys from cadavers must follow legal requirements,
including the definition of death and consent. Kidney
donation by well selected living donors with good
health coverage carries negligible risks. This can only
be ensured through rigorous selection procedures,
careful surgical nephrectomy and follow up of the
donor to ensure the optimal management of untoward
consequences. The Transplantation Society adopted
a consensus statement on the care of the live kidney
donor, prepared by a forum involving over 100 experts
from more than 40 countries from around the world.
This consensus statement addressed the responsibil-
ity of communities for living donors. In particular, it
defined the responsibilities of the transplant centre
which is charged, amongst other duties, with facili-
tating the long-term follow up of living kidney donors
and, if need be, their treatment, with identifying and
tracking complications that may be important in defin-
ing risks for informed consent disclosure (on the care
of the live kidney donor). The care of the live kidney
donor is often neglected in schemes where vulner-
able individuals are exploited and encouraged to sell
their kidneys by unscrupulous practitioners. Forced
organ harvesting is a form of organ trafficking. On
June 17th 2019, The China Tribunal Report concluded
‘Forced organ harvesting has been committed for years
throughout China on a significant scale and that Falun
Gong practitioners have been one – and probably the
main – source of organ supply. The concerted persecu-
tion and medical testing of the Uyghurs is more recent
and it may be that evidence of forced organ harvesting
of this group may emerge in due course. The Tribunal
has had no evidence that the significant infrastructure
associated with China’s transplantation industry has
been dismantled and in the absence of a satisfactory
explanation as to the source of readily available organs,
concludes that forced organ harvesting continues
until today (https://chinatribunal.com/final-judge-
ment-report/). It is also alleged that in some countries
prisoners of conscience are killed for the purpose of
removing one or more of their organs. The recipients
of these harvested organs are citizens of that country
or international transplant tourists who travel and pay
substantial sums to receive trafficked organs.
A World Health Assembly Resolution acknowledged
the risk of exploitation of live kidney donors and urged
Member States to
protect the poorest and vulnerable groups from trans-
plant tourism and the sale of tissue and organs.
Cadaveric donation
In many countries, cadaveric donation is the major
source of all tissues for transplantation. The surgical
techniques to harvest the organs are improving, as
are the storage and transportation techniques, but the
best results are still obtained if the organs are obtained
while circulation is present or immediately after cessa-
tion of the circulation. The aim is to minimise the ‘warm
ischaemic time’. Some organs (e.g., kidneys) are more
resilient to anoxia than others and can survive up to 30
minutes after cessation of cardiac activity.
Cadaveric donation is now so well established that
most developed countries have sophisticated laws to
regulate it. However, these laws vary greatly: some
countries allow the removal of organs regardless of the
wishes of the relatives, whereas other countries allow
for an ‘opting-out’ process in which organs can be taken
for transplantation unless there is an objection from
relatives. In the United Kingdom, Wales has enacted (in
2015) legislation – the Human Transplantation (Wales)
Act 2013 which permits an opt-out system of organ
donation, known as presumed consent. The act permits
hospitals to presume that people aged 18 or over, who
have been resident in Wales for over 12 months, want
to donate their organs at their death, unless they have
objected specifically. That Act is in contrast to the law
still applicable in England, which relies on an opt-in
system; only those who sign the NHS Organ Donation
Register, or whose families agreed, are considered to
have consented to be organ donors. In the latter system,
the transplant team must ensure that the donor either
gave active permission during life or at least did not
object and that no close relative objects after death.
The statutory framework governing organ dona-
tion from the living and the dead for transplantation
in England and Northern Ireland is embodied in the
Human Tissue Act 2004 (with a similar framework in
Scotland) – and the Human Tissue Authority has Codes
of Practice to be followed in such circumstances. Code
F, ‘Donation of solid organs and tissue for transplanta-
tion’ is the relevant one and emphasises that
… donated organs and tissue must be used in accordance
with the expressed wishes of donors, their nominated
representatives, or their relatives, that donors and their
relatives must be given the information they need to be
able to make a decision that is right for them and that
those seeking consent should do so with sensitivity and
an appreciation of the particular circumstances in each
case. It also means that the dignity of the donor must be
respected at all times and that practitioners should work
with proper skill, care and training, in accordance with
good practice and other relevant professional guidance.
If an autopsy will be required by law for any reason, the
permission of the Coroner, Procurator Fiscal or other legal
officer investigating the death must be obtained before

harvesting of tissue or organs is undertaken. In general,
there is seldom any reason for the legal officer investigat-
ing the death to object to organ or tissue donation because
it is self-evident that injured, diseased or damaged organs
are unlikely to be harvested and certainly will not be
transplanted and so will be available for examination.
Description of intraoperative findings by transplant
surgeons will suffice in many cases, although it may
sometimes be desirable for the pathologist who will sub-
sequently perform the autopsy to be present at the organ
retrieval procedure in order to see the extent of exter-
nal and internal trauma ‘first-hand’. In what is almost
always a tragic unexpected death, the donation of organs
may be the one positive feature and can often be of great
assistance to the relatives in knowing that the death of a
loved one has resulted in a good outcome for someone.
Xenografts
Xenotransplantation is the transplantation of living cells,
tissues or organs from one species to another. Such cells,
tissues or organs are called xenografts or xenotransplants.
Advances in xenotransplantation have the potential to
resolve the issue of organ shortages. Organs or tissue
such as heart valves, corneas, hearts and kidneys have
been explored for potential as xenografts. However, such
procedures may meet with a degree of concern from the
public. Grafting of animal tissue into humans has always
seemed tempting and clinical trials have been performed
with some success. But there is, for example, considerable
difficulty with cross-matching the tissues and consider-
able concern about the possibility of transfer of animal
viruses to an immunocompromised human host. Strains
of donor animals, usually pigs, are being bred in clini-
cally clean conditions to prevent viral contamination, but
there is still no guarantee of a close or ideal tissue match.
There has also been an increasing interest in the devel-
opment of patient-derived xenograft (PDX) models where
human tumours are xenotransplanted into immunocom-
promised mice and such models act as translational tools
in preclinical studies of cancer treatments. It is essential
that clear protocols are in place for the study of the many
aspects of xenotransplantation and for the introduction
of such xenografts into the clinical setting. Such protocols
must take into account the variable religious and cultural
sensitivities which will influence individuals’ perception
of such practices.
Cloning
A potentially cheaper solution involves the cloning of
animals for use as transplant donors. This research took
a step forward with the successful cloning of Dolly the
sheep in 1996. However, other advances have been slow
to appear and although cloning remains a theoretical
course of action, much research is still to be done, with
its attendant moral and ethical considerations.
Cause of death determination and certification 35
Cause of death determination and
certification
When deciding on what to ascribe an individual’s death
to, the doctor is making a judgement about causation,
which may be relatively straightforward in an individual
who has a documented history of ischaemic heart disease
and who experiences a cardiac arrest in hospital while on
a cardiac monitor. Difficulties arise, for example, where an
individual suffers a traumatic event, but has severe under-
lying natural disease, or where there are many potentially
fatal conditions, each capable of providing an explanation
for death at that time.
The degree of certainty with which the doctor is
required to decide the cause of death may vary between
jurisdictions, and it may be more ‘intellectually honest’
to provide the cause of death determination in a more
‘narrative’ style, such as is increasingly seen in coroners’
conclusions at inquests in England & Wales.
The law relating to causation is complex, varies
between jurisdictions and is a vast subject of law beyond
the scope of this book. However, common themes in
this area of law are that ‘the cause’ is something that is
‘substantial and significant’ (i.e., it is sufficient to have
caused death), and that the outcome would not have
occurred ‘but for’ the occurrence of the illness, dis-
ease or alleged action/omission of another person (i.e.,
it was necessary for such illness or other factor to have
occurred for the outcome to be fatal).
In general, if a doctor knows the cause of death, and
that cause of death is ‘natural’ (without any suspicious or
unusual features), they may issue a medical certificate of
cause of death (MCCD – commonly called a ‘death cer-
tificate’ [Figure 3.2]). Which doctor may do this varies: in
some countries the doctor must have seen and treated the
patient before death, whereas in other countries any doctor
who has seen the body after death may issue a certificate.
The format for certifying the cause of death was
defined by the World Health Organisation (WHO) in
1979 and is an international standard that is used in
most countries. The system divides the cause of death
into two parts: the first part (Part I) describes the
condition(s) that led directly to death; Part II is for other
conditions, not related to those listed in Part I, that have
also contributed to death.
Part I is divided into subsections and generally three:
(a), (b) and (c), are printed on the certificate. These sub-
sections are for disease processes that have led directly
to death and that are causally related to one another, (a)
being caused by or is a consequence of (b), which in turn
is caused by or is a consequence of (c), etc. It is impor-
tant to realise that, in this system of death certification,
it is the disease lowest in the Part I list that is the most
important, as it is the primary pathological condition in
the ‘chain of events’ leading to death. It is this disease
 36
Medicolegal aspects of death

Figure 3.2 Sample of a Medical Certificate of Cause of Death (doctor’s counterfoil omitted).

that is most important statistically and that is used to
compile national and international mortality statistics.
Doctors should not record the mode of death (e.g.,
coma, heart failure) in isolation on the death certificate
but, if a mode is specified, it should be qualified by indi-
cating the underlying pathological abnormality leading
to that mode of death. For example:
Ia Congestive cardiac failure
Ib Essential hypertension
or
Ia Coma
Ib Subarachnoid haemorrhage
Ic Ruptured congenital aneurysm
Some jurisdictions will allow specific causes of death
that would not be allowed elsewhere. In the UK, it is
acceptable in certain situations, i.e., if the patient is over
80 years of age, to record ‘Ia: Old age’. The term ‘frailty’
may also be included.
At the other end of the age range, the diagnosis of
sudden infant death syndrome (SIDS) is now well estab-
lished; unfortunately, the diagnostic criteria are seldom
as well known and even less frequently are they applied
to the letter.
The utility of the second part of the death certifi-
cate is perhaps questionable and has a tendency to be
used as something of a ‘dustbin’ to record all, many
or some of the diseases afflicting the patient at the
time of death, regardless of their causative role in
that death. Guidance for doctors completing Medical
Certificates of Cause of Death in England & Wales has
been updated by the Office for National Statistics in
2018. Similarly, the Scottish Government produced
such guidance in 2014.
In the UK, it has long been recognised that existing
arrangements for death certification are confusing,
provide inadequate safeguards, with no mechanism to
identify patterns, take action and learn from them.
Dr Harold Shipman, a general practitioner, was able
to kill many patients because he relied on others hav-
ing no reason to question or suspect malpractice when
he certified the causes of death. The system depends
on the integrity of a doctor and there is no independent
oversight.
Inquiries into deaths and practices at Mid
Staffordshire and Southern Health NHS Foundation
Trusts showed that improved reporting and investiga-
tions could have prevented many unnecessary deaths.
A new system was proposed following a number of
reviews (starting with that of Harold Shipman in 2003),
intended to introduce independent safeguards and
checks to highlight patterns, both through a review
Cause of death determination and certification 37
of relevant medical records and by making sure that
the family has the chance to raise any concerns. This
independent review will make identifying malpractice
easier, provide opportunities for the NHS to learn and
address system failures earlier.
One of the recommendations was the introduc-
tion of the new role of Medical Examiners (Medical
Reviewers in Scotland) in England & Wales. These are
seniors who will scrutinise and confirm the cause of all
deaths that do not need to be investigated by a coroner
before a medical certificate of cause of death (MCCD)
is issued (Figure 3.2). Reforms enabled in the Coroners
and Justice Act 2009, introduced Medical Examiners. In
April 2019 all acute hospitals in England & Wales began
to establish Medical Examiner (ME) services. MEs are
involved after a death. In all cases not investigated by a
coroner, the ME needs to address the following issues:
• What did the person die from? (ensuring accuracy
of cause of death on the medical certificate)
• Does this case need to be reported to a coroner?
(ensuring timely, accurate referral)
• Are there any clinical governance concerns?
(ensuring the relevant authority is notified)
The ME addresses these issues by:
• Carrying out a proportionate review of medical
records (focusing on the last hospital admission,
selected investigation results, correspondence,
and interventions) – this is recorded on a form.
• Discussing the case with the Qualified Attending
Practitioner (QAPs) who will complete the MCCD
(the QAP will have completed a form which sum-
marises the QAP’s planned wording for the MCCD
– which will be discussed and agreed prior to com-
pletion of the MCCD with the ME).
• Interacting with bereaved relatives to clarify
whether they have any concerns or questions
regarding the cause or circumstances of death,
and review the MCCD.
Currently this is a non-statutory process but it is
anticipated that a statutory service which will addi-
tionally include oversight of all community and out-of-
hospital deaths will be in place by 2021. International
classifications of disease are now well established and
the WHO produced, with the full official name, the
International Statistical Classification of Diseases and
Related Health Problems. The short form, International
Classification of Diseases (ICD) is the international ‘stan-
dard diagnostic tool for epidemiology, health manage-
ment and clinical purposes’. ICD is the foundation for
the identification of health trends and statistics glob-
ally, and the international standard for reporting dis-
eases and health conditions. ICD defines the universe
of diseases, disorders, injuries and other related health
38 Medicolegal aspects of death
conditions, listed in a comprehensive, hierarchical fash-
ion that allows for:
• Easy storage, retrieval and analysis of health infor-
mation for evidenced-based decision making.
• Sharing and comparing health information
between hospitals, regions, settings and countries.
• Data comparisons in the same location across dif-
ferent time periods.
Uses include monitoring of the incidence and prev-
alence of diseases, observing reimbursements and
resource allocation trends and keeping track of safety
and quality guidelines. They also include the counting
of deaths as well as diseases, injuries, symptoms, rea-
sons for encounter, factors that influence health status
and external causes of disease. ICD can be used for both
clinical diagnoses and death certificates. In this clas-
sification, each condition is given a four-digit ICD code,
which simplifies both data recording and data analysis
and allows information from many national and inter-
national sources to be compared. The current version
is ICD 10 and this will be superseded by ICD 11 in 2020.
A version of ICD 11 has been released in 2018 to allow
preparations to be made prior to formal launch.
In some countries, doctors also have to record
the manner of death (e.g., homicide, suicide) on the
death certificate, as advocated by the World Health
Organisation; however, in most Western countries
with an efficient medicolegal investigative system,
the conclusion about the manner of death may be to
a legal officer, for example, the Coroner in England &
Wales, the Procurator Fiscal in Scotland or the Medical
Examiner in some of the states of the USA. Chapter 4
expands on the role of the coroner in medicolegal
death investigation.
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Maxwell; 2014.
Practice parameters: Assessment and management of patients
in the persistent vegetative state. St Paul: American Academy
of Neurology: Quality Standards Subcommittee. www.aan.
com/Guidelines/Home/Get​GuidelineContent/83 (Accessed
4 April 2019).
Royal College of Pathologists. Medical examiners. https://www.
rcpath.org/profession/committees/medical-examiners.html
(Accessed 4 April 2019).

Royal College of Physicians. Prolonged disorders of conscious-
ness: National clinical guidelines: Report of a Working Party.
https://www.rcplondon.ac.uk/guidelines-policy/prolonged-
disorders-consciousness-national-clinical-guidelines
(Accessed 4 April 2019).
Shipman Inquiry: Archived at The National Archives. http://
webarchive.nationalarchives.gov.uk/20090808154959/http://
www.the-shipman-inquiry.org.uk/home.asp (Accessed 4
April 2019).
Sia D, Moeini A, Labgaa I, Villanueva A. The future of
patient-derived tumor xenografts in cancer treatment.
Pharmacogenomics 2015;16(14):1671–1683.
Skene L, Wilkinson D, Kahane G, Savulescu J. Neuroimaging and
the withdrawal of life-sustaining treatment from patients in
vegetative state. Med Law Rev 2009;17:​245–261.
The Human Transplantation (Wales) Act 2013 (Consequential Pro-
vision) Order. http://www.legislation.gov.uk/uksi/2015/865/
article/3/made (Accessed 4 April 2019).
The Task Force. The Multisociety Taskforce report on PVS: medical
aspects of the persistent vegetative state, Part 1 and 2. New
Eng J Med 1994;330:1499–1508, 572–579.
United Nations. Manual on the effective prevention and inves-
tigation of extra-legal, arbitrary and summary e­ xecutions.
http://www.ohchr.org/Documents/Professional​Interest/
executions.pdf (Accessed 4 April 2019).
Further general resources 39
World Health Assembly. 2004. Transplantation. http://www.
who.int/transplantation/publications/en/ (Accessed 4 April
2019).
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of death. https://apps.who.int/iris/handle/​10665/40557
(Accessed 8 April 2019).
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(10th Revision). http://apps.who.int/classifications/icd10/
browse/2016/en (Accessed 8 April 2019).
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http://apps.who.int/iris/handle/10665/40557?locale=fr&mo
de=full (Accessed 4 April 2019).
Further general resources
Academy of Medical Royal Colleges (AMRC). http://www.aomrc.
org.uk (Accessed 4 April 2019).
World Health Organisation (WHO). ICD-10. http://apps.who.
int/classifications/icd10/browse/2016/en (Accessed 4 April
2019).
4 Violence in society,
medicolegal ­investigation of
death and the autopsy
▪▪ Introduction
▪▪ Homicide and interpersonal violence
▪▪ Medicolegal investigation of death
▪▪ The autopsy
Introduction
Both the clinical and pathological aspects of forensic
medicine have substantial involvement in the investi-
gation and management of interpersonal violence, the
volume of which is a matter of public health concern
internationally.
Homicide and interpersonal
violence
The United Nations ‘Global Study on Homicide 2013’
provides the most comprehensive, and most recent,
international data on ‘intentional homicide’ (excluding
killings directly related to war and other conflicts, due
to legal interventions, ‘justifiable killings’ such as those
in self defence, and ‘non-intentional homicide’, such as
those involving recklessness or negligence).
In 2012, there were 437,000 homicides, giving an
average rate of 6.2 per 100,000 people; there were
marked regional and sub-regional variations, the high-
est rates occurring in Central America (just over 25 per
100,000 people), and Southern Africa (just over 30 per
10,000 people), and the lowest rate occurring in Western
Europe (at around 1 per 100,000 people).
The rate in Europe appears to remain relatively stable,
and at low levels, reflecting improvements in socioeco-
nomic conditions in many Eastern European countries,
although geopolitical upheaval and forced migration
can substantially influence this. There are national dif-
ferences. Often the data is several years behind, but in
2011 Japan had one of the lowest rates in the world (at 0.3
per 100,000 people, representing 442 homicides) whilst
the UK had a rate of 1 per 100,000. There were differences
between the component countries:
• England & Wales 1.1 per 100,000 (551 homicides
2012–2013);
• Scotland 1.74 per 100,000; and
• Northern Ireland 1.42 per 100,000
This compares with rates in the USA (4.7 per 100,000),
the Russian Federation (9.2 per 100,000), and Honduras
▪▪ The ‘Minnesota protocol’
▪▪ Exhumation
▪▪ Bibliography and information sources
▪▪ Further general resources
(90.4 per 100,000). Box 4.1 explores the inequalities that
exist in violent death, as in life. The overall trend glob-
ally appears to be one of a decreasing homicide burden.
However, in the UK, the number of homicides (in the UK
the term embraces the offences of murder, manslaugh-
ter and infanticide) has been increasing from its low
point in 2015–2016 to 726 in 2018.
Global homicide data by age
The UN ‘Global Study’ data from 2013 shows that most
victims were less than 44 years of age (15–29 years 43%;
30–44 years 30%). Thirty six thousand were children
under 15 years (8% of the total).
In England & Wales in 2012–2013 there were 67 homi-
cides under the age of 16 years (12% of the total), with
some differences between genders (10% of male victims
compared with 16% of female victims).
Fifteen per cent of victims were young men, aged
between 15 to 29 years, living in the Americas. In
England & Wales, 7% of the population is between 20–24
years of age, but they account for 11% of homicide vic-
tims (188 deaths); this probably reflects the increased
numbers of young male victims (140 deaths).
The highest rate of homicide in England & Wales
was in children under 1 year of age (at 3 per 100,000,
representing 22 deaths). The majority of victims under
16 years were acquainted with their principal suspect
(69%, 46 offences), and in 40 cases they were killed by a
parent or step-parent.
Global homicide data by gender
The UN ‘Global study on Homocide’ data show that
males account for 79% of all homicide victims, and 95%
of all perpetrators. The average homicide rate for males
was 9.7 per 100,000.
The rate for females was 2.7 per 100,000; 47% were
killed by an intimate partner or family member (com-
pared with 6% of all male victims).
In Europe, males aged 30–44, and 45–59 years had
a higher risk of being a homicide victim than their
younger counterparts, probably due to the relative

Box 4.1 Inequalities in death – violence and homicide as a public health problem
Analysis of age-adjusted homicide rates in the USA
shows a marked difference between white and black
males (8.7 per 100,000, compared with 66.2 per 100,000,
respectively). Age was the strongest predictor of homi-
cide rate, followed by the level of urbanisation. Rates
were significantly higher for both black and white men
living in areas of low educational levels, or high levels of
income inequality, and rates were significantly lower in
areas with a low prevalence of crowded housing.
In England & Wales, of the homicides recorded in
the three-year period ending in March 2013, 77% of
victims were white, and 11% were black. Census data
reported the relative proportions of white and black
individuals to be 86%, and 3%, respectively. Black
victims were therefore over-represented, and white
under-represented. Black males were over four times
more likely to be a victim of homicide than white males
(5.5 per 100,000 compared with 1.2 per 100,000). Black
victims were also younger than white victims (average
increased importance of interpersonal violence in this
region compared with violence related to other criminal
activities (including gang-related violence).
In England & Wales, 96% of male homicide victims,
and 87% of female victims, over 16 years of age were
killed by a man.
Global intimate partner and domestic
violence-related homicide
Fourteen per cent of all homicide victims were killed
by an intimate partner or a family member, with a
global rate of 0.9 per 100,000. The rates were quite stable
between regions, and over time, although the propor-
tions of this type of homicide compared with the total
homicides within a region varied (e.g. 28% of all homi-
cides in Europe, compared with 8.6% of homicides in the
Americas). When the homicide rate was high in a region,
the proportion of deaths related to, for example, other
criminal activities was more prevalent than in regions
with low homicide rates.
Female victims were consistently higher in this type
of homicide. Of the 93,000 women killed in 2012, 47%
were killed by an intimate partner or family member.
Regional variations included: 3300 deaths in Europe,
200 in Oceania, and 19,700 in Africa.
Seventy-nine per cent of those homicide victims
killed by intimate partners were women.
Female homicide victims in England & Wales were
more likely than male victims to have been killed by a
partner or ex-partner (45% compared with 4%). Global
studies report comparable data of between 40%–70%.
Homicide and interpersonal violence 41
age 28 years, compared with 40 years, respectively),
and were more likely to be stabbed or shot (compared
with homicide by hitting, kicking etc.). Twenty-five per
cent of black victims were shot, compared with 6% of
white victims.
In the UK, analysis of the socioeconomic characteris-
tics of homicide victims between 1981 and 2000 reveals
that people living in the poorest 10% of areas were 4.5
times more likely to be murdered than those living in
the least poor 10% of areas between 1981 and 1985,
and 5.7 times more likely to be murdered between
1996 and 2000.
A study in Scotland showed a marked inequality in
death from assault; between 2000 and 2002; a man
under 65 years living in one of the most deprived areas
was nearly 32 times more likely to die due to an assault
than if he had been living in one of the most affluent
areas, and a woman of the same age was 35 times more
likely to die due to an assault.
Female victims in this category of homicide were
younger than other female homicide victims (41 years
compared with 51 years).
Male victims of this sort of homicide in England &
Wales were more likely to be killed with a sharp instru-
ment than other male victims (60% compared with 38%),
whilst female victims of partner/ex-partner homicide
were more likely to be killed by strangulation than other
female homicide victims (27% compared with 16%).
Fifty-two per cent of all homicides in England &
Wales resulted from a quarrel, a revenge attack or a loss
of temper (rising to 61% where the principal suspect
was known to the victim). Box 4.2 describes the extent
of non-fatal intimate partner violence in the UK and
globally.
Homicide mechanism
Weapons played a significant role in homicide glob-
ally (Box 4.3); firearms were involved in 177,000 (41%)
of homicides, ‘other means’ (including physical force/
blunt objects) accounted for just over one third of
deaths, whilst sharp objects accounted for 24% of
deaths.
Firearms were involved in 66% of deaths in the
Americas, whilst ‘other means’ predominated in Europe
(54%), and Asia (47%).
Sharp objects were most commonly used in the UK
accounting for 35% of deaths in 2012–2013 in England
& Wales, and 38% in Scotland between 2003 and 2013.
There was no significant difference in the proportion
of deaths from this mechanism between the genders
in England & Wales.
42 Violence in society, medicolegal i­nvestigation of death and the autopsy

Box 4.2 Non-fatal intimate partner violence

Even in countries with very low homicide rates, a signif-
icant proportion of women experienced physical and/
or sexual violence. In the UK in 2005, for example, 5.9%
of women reported having experienced physical and/
or sexual violence from an intimate partner in the pre-
ceding 12 months, and 28.4% reported having experi-
enced such violence in their lifetime.
The World Health Organisation stated that between
10 and 69 per cent of women globally reported being
physically assaulted by an intimate partner during their
lifetime, and most women who are targets of physi-
cal aggression generally experience multiple acts of
aggression over time.
There are differences in the nature and incidence of
violence between non-heterosexual intimate relation-
ships, and these may highlight other vulnerabilities
within those groups.

The second most common method of killing in England
& Wales was ‘kicking or hitting without a weapon’ (20% of
the total), although there were gender differences present;
25% of male homicide victims were killed by this method,
whilst the second most common method of homicide in
female victims was strangulation or asphyxiation (at 16%);
29 people were killed by a firearm.
Alcohol consumption was highly associated with
homicide; it preceded nearly 50% of homicides in
Australia between 2008 and 2010 (that consumption
being by victim, perpetrator, or both).
This data gives a broad overview of the incidence,
demographics and means of homicide. As with much
of the published data, it may be up to a decade behind
the times and, when considering the current position, it
is always important to recognise that social trends and
geopolitical change can often dramatically influence
these factors.

Box 4.3 Homicide mechanism by geographical region

Africa Americas Asia
(54 countries) (36 countries) (50 countries)

17%

28% 47% 28%

42% 17%

66%
30% 25%

Europe Oceania Global

(42 countries) (10 countries) (192 countries)

13% 10%

35% 35%

54% 41%

33%
24%
55%

Firearms Sharp objects Others

Adapted from Office on Drugs and Crime (UNODC). Global Study on Homicide 2013.

Medicolegal investigation of death
If a death is natural and a doctor can sign a death cer-
tificate, this allows the relatives to continue with the
process of disposal of the body, whether by burial or
cremation. If the death is not natural or if no doctor can
complete an MCCD, some other method of investigating
and certifying the death must be in place. In England
& Wales there are approximately 500,000 deaths each
year, of which, more than half are certified by doctors
without referral to coroners. In 2018, 220,600 deaths
were reported to coroners. This is a decrease on previ-
ous years predominantly because there was a decrease
in the number of deaths under Deprivation of Liberty
Safeguard (DoLs) authorisations reported to Coroners.
DoLS was an amendment to the Mental Capacity Act
2005 and it ensures people who cannot consent to
their care arrangements in a care home or hospital are
protected if those arrangements deprive them of their
liberty. Arrangements are assessed to check they are
necessary as well as being in the person’s best interests.
Representation and the right to challenge a deprivation
are other safeguards that are part of DoLS. Following
amendment to the Coroners and Justice Act 2009, as
of 3 April 2017, an individual under a DoLS is no lon-
ger considered to be ‘otherwise in state detention’. As a
result, the number of DoLS deaths reported to Coroners
fell 66% to 3900 in 2017 compared to the previous year.
Of deaths reported to the coroner, approximately
39% required a post mortem examination to deter-
mine the cause of death, compared with 60% in 1995.
There were 85,600 post mortem examinations ordered
by coroners in 2018, a decrease of 1% on 2016. Eight per
cent fewer inquests were opened in 2018, driven by a fall
in DoLS deaths. Twenty nine thousand one hundred
inquests were opened in 2018, down 8% compared to
2017, driven by fewer DoLS deaths reported to coroners,
which prior to the 2009 Act amendment required an
inquest, as all state detention deaths do. Inquest con-
clusions were down 9%, driven by a fall in natural cause
Box 4.4 P
 roposed circumstances in which doctors in England & Wales would
be required to refer deaths to a coroner
• There is no attending practitioner or the attending
practitioner(s) is unavailable within a prescribed
period.
• The death may have been caused by violence,
trauma or physical injury, whether intentional or
otherwise.
• The death may have been caused by poisoning.
• The death may be the result of intentional
self-harm.
• The death may be a result of neglect or failure of
care.
Medicolegal investigation of death 43
conclusions. In 2018, 30,700 inquest conclusions were
recorded, down 9% on 2017, reflecting the decrease in
the number of inquests opened and fewer DoLS deaths
(almost all had a natural cause conclusion).
The role of the coroner in England & Wales was
reformed by the coroners and Justice Act 2009, which
created a new nationwide post of Chief Coroner, over-
seeing local Coroners (now called Senior Coroners, Area
Coroners and Deputy Coroners, depending on their
seniority).
The types of deaths that cannot be certified by a doc-
tor are examined by a variety of legal officers in other
countries: Coroners, Procurators Fiscals, Medical
Examiners, Magistrates, Judges and even Police
Officers. The exact systems of referral, responsibility and
investigation differ widely, but the general framework
is much the same. The systems are arranged to identify
and investigate deaths that are, or might be, unnatu-
ral, overtly criminal, suspicious, traumatic or caused
by poisoning, or that might simply be deaths that are
unexpected or unexplained (Box 4.4).
There is currently no legal duty for a doctor to report
an unnatural death to the coroner, but legislative
changes are imminent in England & Wales, and will
place a statutory duty on all doctors to report certain
categories of death to the coroner (see Box 4.4). The
Registrar of Deaths currently has such a duty to inform
the Coroner about any death that appears to be unnat-
ural or where the rules about completion of the death
certificate have not been complied with, although their
responsibilities are likely to change as the proposed
new ‘Medical Examiner’ system comes into effect (Box
4.5). Deaths are also usually reported to the coroner by
members of the public, the police and, in the future in
England & Wales, will also be reported to the ‘Medical
Examiner’.
Following the death of a person who has not been
receiving medical supervision, and where no doctor
was in attendance, the fact of death can be confirmed by
nurses, paramedics and other healthcare professionals
• The death may be related to a medical procedure
or treatment.
• The death may be due to an injury or disease
received in the course of employment, or indus-
trial poisoning.
• The death occurred whilst the deceased was in cus-
tody or state-detention, whatever the cause.
• The cause of death is unknown.
Source: Department of Health. Death Certification Reforms. Draft
guidance for registered medical practitioners, March 2016.
44 Violence in society, medicolegal i­nvestigation of death and the autopsy
Box 4.5 T
 ypes of deaths that need to be
reported to the Coroner by the
Registrar of Deaths
The circumstances in which the Registrar of Deaths
currently must refer a death to the Coroner are
contained in the Registration of Births and Deaths
Regulations 1987:
• The deceased was not attended in his last illness
by the doctor completing the certificate.
• The deceased had not been seen by a doctor
either after death or within 14 days prior to
death.
• Where the cause of death is unknown.
• Where death appears to be due to poisoning or
to industrial disease.
• Where death may have been unnatural or where
it may have been caused by violence or neglect
or abortion or where it is associated with suspi-
cious circumstances.
• Where death occurred during a surgical opera-
tion or before recovery from an anaesthetic.
as well as by doctors. The police will usually investigate
the scene and the circumstances of the death and report
their findings to the coroner or other legal authority.
The coroner, through his officers, will attempt to find a
family practitioner to obtain medical details. That fam-
ily practitioner, if found, may be able to complete the
death certificate if he is aware of sufficient natural dis-
ease and if the scene and circumstances of the death are
not suspicious.
If no family practitioner can be found, or if the practi-
tioner is unwilling to issue a death certificate, the cause
of death will presumably be unknown, and the coroner
must initiate an investigation into the death. Such an
investigation must also be initiated when the death was
violent or unnatural, or where it occurred in custody or
state detention according to the Coroners and Justice
Act 2009.
The purpose of the coroner’s investigation is to
­ascertain who the deceased was, how, when and where
they came by their death, and any other details required
by registration of death legislation.
In order to enable the Coroner to decide whether
or not an investigation into the death is required, they
may request that a ‘suitable practitioner’ – who may not
necessarily be a registered medical practitioner – makes
a post mortem examination of the body, the extent of
which is not prescribed.
A post mortem examination for the coroner may now
be limited to an external examination (as is possible
in the Scottish ‘View and Grant’ examinations), or a
‘minimally invasive’ radiological examination (such
as a post mortem CT-based examination), or involve an
invasive internal examination, depending on the cir-
cumstances, the wishes of the family of the deceased,
and the ability of the proposed examination to provide
the coroner with answers sufficient for them to fulfil
their investigatory responsibilities. The ability to make
a limited post mortem examination of the body in the
appropriate circumstances is more humane for the
family of the deceased, and in line with human rights
responsibilities of the State to not only ensure an effec-
tive investigation into the death, but to ensure that the
rights of the family are not unnecessarily infringed
upon.
Given the differences in the powers available to
medicolegal authorities throughout the world, it is not
surprising that the autopsy rate varies widely from juris-
diction to jurisdiction; in some cases, it is nearly 100 per
cent but it may fall as low as 5–10 per cent. Some jurisdic-
tions with low autopsy rates insist on the external exami-
nation of the body by a doctor with medicolegal training.
Autopsy examinations are not the complete and final
answer to every death, but without an internal exami-
nation it can often be impossible to be able to address
the questions raised by a death to the satisfaction of the
family of the deceased, and the medicolegal authority.
An invasive post mortem examination is still consid-
ered to represent the ‘gold standard’ when it comes to
deciding what the most likely cause (and mechanism) of
death is, despite the recent interest in the use of cross-
sectional imaging techniques as an adjunct to invasive
examinations, and in the absence of any post mortem
examination it is well known that a significant propor-
tion of causes of death given by doctors are subsequently
shown to be incorrect following an invasive autopsy.
The coroner can discontinue their investigation if
the post mortem examination identifies the cause of
death, and the coroner no longer believes it necessary
to continue the investigation. If they need to continue
their investigation they must hold an inquest (a pub-
lic inquiry into the death) which, in the case of a death
occurring in custody or detention, for example, must be
held with a jury.
At the conclusion of the inquest, the coroner (or jury)
makes a ‘determination’ in relation to the ‘who, how,
when and where’ questions that are to be addressed by
the coroner’s investigation, and a ‘conclusion’ (rather
than the previous term – a verdict) which cannot be
framed in such a way as to determine criminal or civil
blame for the death. The ‘conclusions’ options are:
• Accident or misadventure
• Alcohol/drug related
• Industrial disease
• Lawful killing (e.g., the legal use of lethal force by
a police officer)
 The autopsy 45

• Unlawful killing (which includes murder, man-
slaughter, infanticide)
• Natural causes
• Open (i.e., there is insufficient evidence for any
other conclusion)
• Road traffic collision
• Stillbirth
• Suicide
There is an increasing trend, however, for the
c­ oroner to deliver a ‘narrative conclusion’ which is a
factual record of how, and in what circumstances, the
death occurred, and this is often used in those cases in
which the cause of death does not fit easily into any of
the ‘short-form’ conclusions. Within the narrative con-
clusion, the coroner may request an inquest jury (if the
inquest is held before a jury) to address specific ques-
tions perceived to be of concern.
The autopsy
The words autopsy, necropsy and post mortem exami-
nation are synonymous, although post mortem exami-
nation can have a broader meaning encompassing any
examination made after death, including an external
examination. In general terms, autopsies are performed
for two reasons: clinical clarification and medicolegal
purposes.
The clinical autopsy is performed in a hospital mor-
tuary after consent for the examination has been sought
from, and granted by, the relatives of the deceased. The
doctors treating the patient should know why their
patient has died and be able to complete a death cer-
tificate even in the absence of an autopsy. These exami-
nations have been used in the past for the teaching of
medical students and others, and for research, but have
been in decline worldwide for several decades.
The medicolegal autopsy is performed on behalf of
the State. The aims of these examinations are much
broader than those of the clinical autopsy; they aim to:
• Identify the body.
• Estimate the time of death.
• Identify and document the nature and number of
injuries.
• Interpret the significance and effect of the inju-
ries.
• Identify the presence of any natural disease.
• Interpret the significance and effect of the ­natural
disease present.
• Identify the presence of poisons.
• Interpret the effect of any medical or surgical
treatment.
Autopsies can, in theory, be performed by any doctor
but, ideally, they should be performed by a pathologist

Box 4.6 The diagnostic approach to the autopsy mirrors that familiar to clinicians

Clinical medicine Forensic pathology

Take a history from the patient (sometimes a
collateral history from relatives etc.)
Ask specific questions relating to body sys-
tems (functional enquiry)
Physical examination
Make a provisional diagnosis (an impression/
opinion)
Decide whether investigations are necessary
to confirm or refute the provisional diagnosis
Consider whether literature search/expert
consultation is required
Initiate a management plan/treatment plan
Review results of investigations and refine
­diagnosis/treatment plan
Take a history (of the circumstances leading to death/the dis-
covery of the body) – from police/coroner or other relevant
witnesses.
Interrogate the medical records of the deceased to identify
specific relevant medical history
Consider the issues/questions raised by the death
Consider the need for imaging or other investigations before
the post mortem examination
External and internal post mortem examinations
Make a provisional diagnosis (if there is enough evidence from
the objective pathological findings to support an opinion of
the cause of death)
Decide whether further investigations are necessary to refine
the diagnosis
Consider whether literature search/expert consultation is
required
Carry out microscopic examination/brain dissection (or
observe that dissection if being made by another expert)
Review findings from all post mortem investigations and
refine cause (and manner) of death diagnosis
46 Violence in society, medicolegal i­nvestigation of death and the autopsy
Box 4.7 The autopsy examination
A short summary of basic techniques is given below.
• An incision is made from the larynx or suprasternal
notch to the pubis. An incision to the suprasternal
notch may be extended on each side of the neck to
form a ‘Y’ incision. The extra exposure this brings is
useful in cases of neck injury or in children.
• The skin on the front of the chest and abdomen
is reflected laterally and the anterior abdominal
wall is opened, with care taken not to damage
the intestines. The intestines are removed by cut-
ting through the third part of the duodenum as
it emerges from the retroperitoneum and then
dissecting the small and large bowel from the
mesentery.
• The ribs are sawn through, or cut with shears, in
a line from the lateral costal margin to the inner
clavicle and the front of the chest is removed.
• The tongue and pharynx are mobilised by passing
a knife around the floor of the mouth close to the
mandible. These are then removed downward as
the neck structures are dissected off the cervical
spine.
• The axillary vessels are divided at the clavicles, and
the oesophagus and the aorta are dissected from
the thoracic spine as the tongue continues to be
pulled forwards and downwards.
• The lateral and posterior attachments of the dia-
phragm are cut through close to the chest cavity
wall and then the aorta is dissected off the lower
thoracic and lumbar spine.
• Finally, the iliac vessels and the ureters can be
bisected at the level of the pelvic rim and the
organs will then be free of the body and can be
taken to a table for dissection.
• The pelvic organs are examined in situ or they can
be removed from the pelvis for examination.
• The scalp is incised coronally and the flaps reflected
forwards and backwards. The skull-cap is carefully
specifically trained to undertake such an examination.
The diagnostic process underpinning an autopsy mir-
rors that utilised in clinical medicine (Box 4.6).
Medicolegal autopsies are a specialised version of
the standard autopsy (described in detail in Box 4.7)
and should be performed by pathologists who have
had the necessary training and experience in foren-
sic pathology, and who are aware of the need to guard
against making the ‘classic mistakes’ and falling foul of
the ‘common medicolegal misconceptions’ described in
Box 4.8. Box 4.9 lists the ‘basic principles for best prac-
tice’ in forensic pathology identified by the Honorable
Stephen Goudge who conducted an Inquiry into paedi-
atric forensic pathology in Ontario, Canada in 2007.
sawn through and removed, leaving the dura
intact. This is then incised and the brain removed
by gentle traction of the frontal lobes while cut-
ting through the internal carotid arteries, cranial
nerves, the tentorium and the upper spinal cord.
• The organs are dissected in a good light with ade-
quate water to maintain an essentially blood-free
area. Although every pathologist has his or her
own order of dissection, a novice would do well
to stick to the following order so that nothing is
omitted: tongue, carotid arteries, oesophagus,
larynx, trachea, thyroid, lungs, great vessels, heart,
stomach, intestines, adrenals, kidneys, spleen,
pancreas, gall bladder and bile ducts, liver, blad-
der, uterus and ovaries or testes and finally the
brain.
• Samples should be taken for toxicology and his-
tology as necessary.
• Detailed notes should be made at the time of your
examination and the report (or protocol) should
be written as soon as possible, even if you can-
not complete it because further tests are being
performed.
• All reports should include all of the positive find-
ings and all of the relevant negative findings,
because in court the absence of a comment may
be taken to mean that it was not examined or
specifically looked for and, if a hearing or trial is
delayed for many months or years, it would not be
credible to state that specific details of this exami-
nation can be remembered with clarity.
• The conclusions should be concise and address all
of the relevant issues concerning the death of the
individual. A conclusion about the cause of death
will be reached in most cases, but in some it is
acceptable to give a differential list of causes from
which the court may choose.
The autopsy should be performed in a mortuary with
adequate facilities (Figure 4.1).
However, where there are no trained staff or no ade-
quate facilities, which can occur not only in some devel-
oping countries but also in some so-called developed
countries that do not adequately fund their medicolegal
systems, non-specialist doctors may occasionally have
to perform autopsies and histopathologists may have
to perform medicolegal autopsies. A poorly performed
autopsy may be considerably worse than no autopsy at
all; it is certainly worse than an autopsy delayed for a
short while to await the arrival of a specialist. The qual-
ity of medicolegal autopsies for coroners in England &
Wales has previously been criticised in a report from

Box 4.8 M
 oritz’s ‘classic mistakes in forensic pathology’ and Petty’s ‘devil’s dozen’
medicolegal misconceptions
The ‘classic mistakes’ to be avoided wherever possible:
• Not examining the body at the scene of the crime
(wherever possible).
• Misinterpreting post mortem changes.
• Being unaware of the objective of the medicolegal
autopsy.
• Performing an incomplete autopsy.
• Failure to make an adequate examination and
description of external abnormalities.
• Not taking adequate photographs of the evidence.
• Not exercising good judgement in the taking or
handling of specimens for toxicologic examination.
• Permitting the body to be embalmed before per-
forming a medicolegal autopsy.
• Confusing the objective with the subjective sec-
tions of the written autopsy report.
• Permitting the value of the autopsy report to be
jeopardised by minor errors.
The ‘devil’s dozen’ of medicolegal misconceptions
to be aware of:
• All physicians are good death investigators.
• The time of death can be precisely determined by
the examination of the body.
Box 4.9 T
 he role of the forensic pathologist: Basic principles for best practice:
The Goudge Inquiry into paediatric forensic pathology in Ontario
1. To ‘think truth’ rather than ‘think dirty’. To do so
requires:
• An independent and evidence-based approach
emphasising the importance of thinking
objectively.
• Pathology evidence to be observed accurately
and followed wherever it leads.
• Guarding against confirmation bias (where evi-
dence is sought or interpreted in order to sup-
port a preconceived theory).
2. Remain independent of the coroner, police, pros-
ecutors, and defence teams in order to discharge
responsibilities objectively, and in an impartial
manner (independence).
3. Autopsy findings must be independently review-
able and transparent. This requires:
The autopsy 47
• Only true and suspected homicide victims need
examination.
• The autopsy can properly be carried out without
a ‘history’.
• Any pathologist is qualified (to perform a medico-
legal autopsy).
• The autopsy always yields the cause of death.
• Poison is always detected by toxicologists.
• The autopsy must be immediate.
• The autopsy is over when the body leaves the
autopsy room.
• Embalming will not obscure the effects of trauma
and disease.
• The cause and manner of death are the only results
of the autopsy.
• The medicolegal autopsy is criminally or prosecu-
tion oriented.
Source: Adapted from Petty CS. The devil’s dozen. Popular
medicolegal misconceptions. South Med J 1971;64:819–823
and Moritz AR. Classical mistakes in forensic pathology.
Am J Clin Pathol 1956;26:1383–1397.
• Care in recording and preserving information
received pre-autopsy, steps taken at autopsy,
and materials preserved after autopsy.
• This transparency is necessary to ensure that
the pathologist’s opinions can be properly
reviewed and confirmed or challenged.
4. The work of the forensic pathologist work at
autopsy must be understandable to the criminal
justice system. The autopsy must be performed so
that it can be described in clear and unambiguous
language to lay people.
5. Teamwork is fundamental to sound autopsy prac-
tice. Teamwork promotes excellence.
6. The forensic pathologist’s practices at autopsy
must be founded on a commitment to quality.
48 Violence in society, medicolegal i­nvestigation of death and the autopsy

Figure 4.1 Modern forensic autopsy facilities, including directional overhead lighting – with inbuilt video projection
and recording capability – to facilitate optimal forensic pathological examinations. (Courtesy of Richard Jones.)

Box 4.10 Q
 uality and the medicolegal autopsy: The main findings of the NCEPOD
report ‘The Coroner’s autopsy: do we deserve better?’ (2006)
• 1 in 4 autopsy reports was poor/unacceptable • The following types of case were poorly examined:
(26% of 1691 reports reviewed). • decomposed bodies
• Failure to do an external examination of the body • epilepsy cases
before evisceration by technicians occurred in one • deaths in the very elderly
third of mortuaries. • The presence or absence of injury was not
• No examination of the brain was made in 1 in 7 well-recorded.
cases. • There was poor communication between patholo-
• A questionable cause of death was given in 1 in 5 gist and coroner in many cases.
cases. • Microscopy was only performed in 19% of cases.
• The heart was poorly examined in cases in which a
cardiomyopathy might have been present.

2016 undertaken by the National Confidential Enquiry

into Patient Outcome and Death (NCEPOD) (Box 4.10).
The first crucial part of any autopsy is observation
and documentation and these skills should lie within
the competence of almost every ­doctor. All documenta-
tion should be in writing, and diagrams, drawings and
annotations must be signed and dated at the end of the
examination. Photographs are extremely useful in all
medicolegal autopsies, but are essential in suspicious
deaths. Photographic documentation of injuries should
include a scale and some anatomical reference point for
ease of review.
Many autopsies will require ancillary investigations,
such as radiological, toxicological, biochemical and micro- Figure 4.2 Operative microscopy in the forensic autopsy
scopic analyses (Figures 4.2 and 4.3). These will all have suite facilitates detailed examination and documentation
financial implications. Such matters and unwillingness of pathological findings. (Courtesy of Richard Jones.)

Figure 4.3 Post mortem radiology is important in many
cases in forensic pathology. Note the body is enclosed
in a body bag to prevent contamination of the body and
loss of ‘trace evidence’ from the surface of the body,
prior to autopsy. Hands (and usually feet) are similarly
protected by paper or plastic bags before recovery of a
body from a scene. (Courtesy of Richard Jones.)
of some individuals to allow autopsy on relatives have
been active drivers in exploring other means of undertak-
ing appropriate examinations to establish cause of death.
There is substantial interest in many countries into the util-
ity of more modern radiological modalities, such as com-
puted tomography (CT) and MRI, in a post mortem setting,
and results of studies suggest that there is potential for vir-
tual autopsy (‘virtopsy’) techniques playing a significant
role, where such facilities are available, in reducing the
requirement for a full autopsy examination (Figure 4.4).
The use of imaging techniques in forensic medicine also
has potential for wider application in the clinical setting
for survivors of, for example, manual strangulation or stab-
bing, where injury characteristics can be better defined.
The ‘Minnesota protocol’
The Minnesota Protocol on the Investigation of
Potentially Unlawful Deaths (The Revised United Nations
Manual on the Effective Prevention and Investigation of
Extra-legal, Arbitrary and Summary Executions) aims to
protect the right to life and advance justice, accountabil-
ity and the right to a remedy, by promoting the effective
investigation of potentially unlawful death or suspected
enforced disappearance. The Protocol sets a common
standard of performance in investigating potentially
unlawful death or suspected enforced disappearance
and a shared set of principles and guidelines for States,
as well as for institutions and individuals who play a
role in the investigation. Its full scope is summarised
in Box 4.11. The protocol, which covers all stages of the
pathological death investigation process, from scene
examination to ancillary tests, recognises the need for
The ‘Minnesota protocol’ 49
such cases to be dealt with by objective, experienced,
well-equipped and well-trained pathologists, and much
of the detail contained within the protocol codifies the
standards already followed by forensic pathologists
when performing suspicious death autopsies in many
countries. Forensic pathologists in England & Wales, for
example, agree to follow the quality standards set out
in a Code of Practice and Performance Standards (see
Box 4.12).
Where the death is definitely due to crime or if there
is a possibility of crime (a suspicious death), the doctor
should attend the scene (locus) before the body is moved
in order to gain an understanding of the surround-
ings, blood distribution in relation to the body and any
other relevant factors (e.g., the presence of weapons)
(Figure 4.5). Precise documentation of attendance, of
people present and of the observations should be made.
Formal photography (and also video recording where
appropriate) should be taken of the scene in general, of
the body in particular and of any other significant fea-
tures; these should be taken by someone with training
in forensic photography.
The identity of the body should be confirmed to the
doctor by a relative or by a police officer or other legal
officer who either knows the deceased personally or
who has had the body positively identified to them by a
relative or by some other means (e.g., fingerprints).
If the remains are mummified, skeletalised, decom-
posed, burnt or otherwise disfigured to a point at which
visual identification is impossible or uncertain, or if the
identity is unknown, other methods of establishing the
identity of the remains must be used, but the autopsy
cannot be delayed while this is done.
If there can be no direct identification of the body, a
police officer must confirm directly to the doctor that
the body or the remains presented for autopsy are those
that are the focus of the police inquiry.
The body should be examined with the clothing in
place so that material defects caused by trauma that may
have damaged the body (e.g., stab wounds, gunshot inju-
ries) can be identified and linked to wound sites. When
removed, the clothing must be retained and exhibited in
a formal ‘chain of custody’ prior to review and analysis.
In suspicious deaths, or if there are any unusual fea-
tures, the body should be photographed clothed and
then unclothed and then any injuries or other abnor-
malities should be photographed in closer detail.
X-rays and other radiological imaging techniques
may be ­advisable in victims of gunshot wounds and
explosions and where there is a possibility of retained
metal fragments, and are mandatory in all suspicious
deaths in children.
The surface of the body should be examined for the
presence of trace evidence. This includes from items (e.g.,
fibre and paint) and biological samples (e.g., fibres, hair,
blood, saliva, semen). This examination and subsequent
50 Violence in society, medicolegal i­nvestigation of death and the autopsy

C
B D

D
C C

A
B
A A

Bone gsr Blood

vrt density density density

Figure 4.4 Suicidal pistol contact head shot. Post mortem CT of head showing CT-dense deposits in subcutaneous tis-
sues around entrance (A, see also photo with ample soot in a contact head shot). Skull defect of exit (B). Blood-dense
shapes in brain show hemorrhage along bullet track (C, straight/linear constellation) and blood inside ventricles (D).
(VRT, syngo via [Siemens Germany], segmented anatomy visualizer images. Images courtesy of the Virtopsy Team.)

Box 4.11 T
 he scope of The Minnesota Protocol on the investigation of potentially
unlawful deaths
1. The Minnesota Protocol aims to protect the right
to life and advance justice, accountability and
the right to a remedy, by promoting the effec-
tive investigation of potentially unlawful death or
suspected enforced disappearance. The Protocol
sets a common standard of performance in inves-
tigating potentially unlawful death or suspected
enforced disappearance and a shared set of prin-
ciples and guidelines for States, as well as for
institutions and individuals who play a role in the
investigation.
2. The Minnesota Protocol applies to the investiga-
tion of all ‘potentially unlawful death’ and, mutatis
mutandis, suspected enforced disappearance. For
the purpose of the Protocol, this primarily includes
situations where:
a. The death may have been caused by acts or
omissions of the State, its organs or agents, or
may otherwise be attributable to the State, in
violation of its duty to respect the right to life.
This includes, for example, all deaths possibly
caused by law enforcement personnel or other
agents of the state; deaths caused by para-
military groups, militias or ‘death squads’ sus-
pected of acting under the direction or with the
permission or acquiescence of the State; and
deaths caused by private military or security
forces exercising State functions.
b. The death occurred when a person was
detained by, or was in the custody of, the State,
its organs, or agents. This includes, for exam-
ple, all deaths of persons detained in prisons,
in other places of detention (official and oth-
erwise) and in other facilities where the State
exercises heightened control over their life.
c. The death occurred where the State may have
failed to meet its obligations to protect life. This
includes, for example, any situation where a
state fails to exercise due diligence to protect
an individual or individuals from foreseeable
external threats or violence by non-State actors.
d. There is also a general duty on the state to inves-
tigate any suspicious death, even where it is not
alleged or suspected that the state caused the
death or unlawfully failed to prevent it.
3. The Protocol outlines States’ legal obligations
and common standards and guidelines relating
to the investigation of potentially unlawful death
(Section II). It sets out the duty of any individual
involved in an investigation to observe the highest
The ‘Minnesota protocol’ 51
standards of professional ethics (Section III). It
provides guidance and describes good practices
applicable to those involved in the investigative
process, including police and other investigators,
medical and legal professionals and members of
fact-finding mechanisms and procedures (Section
IV). While the Protocol is neither a comprehen-
sive manual of all aspects of investigations, nor a
step-by-step handbook for practitioners, it does
contain detailed guidelines on key aspects of the
investigation (Section V). A glossary is included
(Section VI). Annexes (Section VII) contain anatom-
ical sketches and forms for use during autopsies.
4. States should take all appropriate steps to incor-
porate Protocol standards into their domestic
legal systems and to promote its use by relevant
departments and personnel, including, but not
limited to, prosecutors, defence lawyers, judges,
law enforcement, prison and military personnel,
and forensic and health professionals.
5. With respect to armed groups, see Report of the
UN Fact-Finding Mission on the Gaza Conflict,
UN doc. A/HRC/12/48, 25 September 2009, para.
1836. OHCHR, Guiding Principles on Business and
Human Rights, UN doc. HR/PUB/11/04 (2011). 2005
UN Basic Principles and Guidelines on the Right
to a Remedy and Reparation for Victims of Gross
Violations of International Human Rights Law and
Serious Violations of International Humanitarian
Law (hereafter, UN Basic Principles and Guidelines
on the Right to Remedy and Reparation).
6. The Protocol is also relevant to cases where the
United Nations, armed non-State groups exer-
cising State or quasi-State authority, or business
entities have a responsibility to respect the right
to life and to remedy any abuses they cause or
to which they contribute. The Protocol can also
guide the monitoring of investigations by the UN,
regional organizations and institutions, civil soci-
ety and victims’ families, and can aid teaching and
training on death investigations. States’ Parties
to relevant treaties may have specific obligations
that go beyond the guidance set out in the pres-
ent Protocol. Although some States may not yet
be in a position to follow all of the guidance set
out within it, nothing in the Protocol should be
interpreted in such a way as to relieve or excuse
any State from full compliance with its obligations
under international human rights law.
52 Violence in society, medicolegal i­nvestigation of death and the autopsy
Box 4.12 Q
 uality assurance and the
forensic pathologist
Forensic pathologists in England, Wales and Northern
Ireland have agreed to standards set out in the ‘Code
of Practice and Performance Standards’ document
produced by the Forensic Science Regulator, the
Royal College of Pathologists, UK Government Home
Office, and the Department of Justice for Northern
Ireland (a separate set of standards also applies in
Scotland).
The quality standards to be met cover all stages
of a death investigation in which the pathologist is
involved including:
• The initial contact made with the pathologist.
• The briefing (of the circumstances relevant to
the death) given to the pathologist.
• Attendance and examination of scenes of the
discovery of the body.
• The autopsy.
• The autopsy report.
• Legal conferences.
• Interaction with defence pathologists (includ-
ing at so-called ‘second post mortem examina-
tions’ or ‘defence autopsies’).
• Attendance at court and giving expert opinion.
sampling should be performed by appropriately trained
individuals which may include police officers, Crime
Scene Investigators (CSIs)/Scenes of Crime Officers
(SOCOs), forensic scientists, forensic pathologists and
sometimes forensic physicians. Where samples are to be
taken from the body itself as opposed to the surface of the
body – fingernail clippings, head and pubic hair, anal and
genital swabs – these should be taken by the pathologist.
Forensic scientists may also wish to examine the
body using specialist techniques, and the pathologist
must be aware of their needs and allow them access at
appropriate times.
Accurate documentation of the external features
of injuries or abnormalities, their position, size, shape
and type, is often the most important aspect of a forensic
examination and often has much greater value in under-
standing and in reconstructing the circumstances of
injury than the internal dissection of any wound tracks
or of damaged internal organs.
The internal examination must fulfil two require-
ments: to identify and document injuries and to identify
and document natural disease. The former may involve
the examination of wound tracks caused by knives, bullets
or other penetrating objects. It may also involve determin-
ing the extent and depth of bruising on the body by reflect-
ing the skin from all of the body surfaces and identifying
and describing areas of trauma to the internal organs.
Figure 4.5 Examination of the skeletal remains at a
wooded ‘scene’. The forensic pathologist wears appropri-
ate protective equipment in order to prevent contamina-
tion of the remains. The attendance at the ‘scene’ follows
discussion with the crime scene manager regarding
the health and safety implications of the ‘scene’, the
approach to the body/remains and a forensic strategy
for the recovery of ‘trace evidence’, including swabs and
‘tape lifts’ from sites such as exposed skin surfaces and
body orifices. (Courtesy of Richard Jones.)
A complete internal examination of all three body
cavities (cranium, thorax and abdomen), with dissection
of all of the body organs, must be performed to identify
any underlying natural disease.
Samples of blood (for blood grouping, DNA analysis,
toxicology) and urine (for toxicology) will be routinely
requested by the police. Blood should be collected from
a large limb vein, preferably the femoral vein, and urine
should be collected through the fundus of the bladder.
All samples should be collected into appropriate quality
assured containers, which are sealed and labelled in the
presence of the pathologist. For quality assurance and
preservation of evidence, standardised sampling kits
should be used for all these processes.
When poisoning is suspected, other samples, includ-
ing stomach contents, intestinal contents, samples of
organs including liver, kidney, lung and brain, may be
requested. The storage, preservation and handling of
these specimens will depend upon the suspected poi-
son. Specialist advice must be obtained or the samples
may be useless. Specific precautions may be required for
certain suspected toxic substances and infectious dis-
eases to protect the pathologist and other investigators.
Tissue samples should be retained in formalin for
microscopic examination. If there is any doubt, whole
organs, brain and heart in particular, should be retained
for specialist examination.
In all of these aspects of the examination, care-
ful notes must be kept with appropriate diagrams and
images where necessary. This information will form the
basis for the post mortem report.

Exhumation
It is rare for a body to be removed from its grave for fur-
ther examination; the most common reasons for exhu-
mation are personal, for example, if a family chooses to
move the body or if a cemetery is to be closed or altered.
In England & Wales a licence from the Ministry of Justice
must be applied for before exhumation can be done. Once
a licence is granted the correct site of the grave must be
determined from plans and records of the cemetery, as
well as inscriptions on headstones.
In some countries with a low autopsy rate, for exam-
ple Belgium, exhumations are more common, as legal
arguments about an accident or an insurance claim, for
example, require an examination of the body to estab-
lish the medical facts.
Logistics need to ensure that the body or human
remains are examined as quickly as possible. Thus, a
clear multiprofessional approach is required involving
amongst others the mortuary, the coroner, the patholo-
gist, the police and everyone else with a legitimate
interest in the exhumation. Depending on the reason
and state of the burial or cremation site, there may be
additional needs for other disciplines such as forensic
anthropologists and forensic archaeologists.
An examination of a body after exhumation is seldom
as good as the examination of a fresh body, but it is sur-
prising how well preserved a body may remain and how
useful such an examination often is. It is almost impos-
sible to predict how well preserved a body might be, as
there are so many confounding factors (Figure 4.6). The
autopsy that follows an exhumation should be the same
as that performed at any other time, and should be per-
formed by a trained forensic pathologist. All relevant
local protocols should be observed, and dependent on
the reason for the exhumation, relevant samples (e.g.,
for histology, toxicology) must be taken.
In cases of possible poisoning, advice must be taken
on the collection of other samples, such as soil from
Figure 4.6 Removal of a coffin lid following an exhu-
mation. Liquid mud covers the upper body following
leakage of the coffin lid as indicated by the arrow.
(Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
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taken of any fluid or solid material within the coffin;
these control samples may prove useful if any sugges-
tion of contamination is raised at a later date. The pro-
cess must be as rigorous and meticulous as a forensic
post mortem.
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Shaw M, Tunstall H, Dorling D. Increasing inequalities in risk of
murder in Britain: trends in the demographic and spatial dis-
tribution of murder, 1981–2000. Health Place 2005;11:45–54.
United Nations. Manual on the effective presentation and inves-
tigation of extra-legal, arbitrary and summary executions,
1991 (The ‘Minnesota Protocol’). http://www.ohchr.org/
Documents/Issues/Executions/UN​M anual​2015/Annex1_
The_UN_Manual.pdf (Accessed 5 April 2019).
UN Office on Drugs and Crime (UNODC). Global study on
homicide 2013. United Nations publication, Sales No.
14.IV.1. http://www.unodc.org/documents/gsh/pdfs/
2014_GLOBAL_HOMICIDE_BOOK_web.pdf (Accessed 5 April
2019).
UN Women. Violence against women prevalence data: sur-
veys by country. http://www.unwomen.org/en/what-
we-do/ending-violence-against-women/facts-and-figures
(Accessed 5 April 2019).
Wheeler J, Anfinson K, Valvert D, et al. Is violence associated with
increased risk behavior among MSM? Evidence from a pop-
ulation-based survey conducted across nine cities in Central
America. Glob Health Action 2014;7:​24814.
World Health Organisation. Global status report on violence pre-
vention. http://www.who.int/violence_injury_prevention/vio-
lence/status_report/2014/en/ (Accessed 5 April 2019).
Further general resources
Burton JL, Saunders S, Hamilton S. Atlas of Adult Autopsy Pathology.
Boca Raton: CRC Press; 2015.
Burton JL, Rutty GN. The Hospital Autopsy: A Manual of Fundamental
Autopsy Practice, 3rd ed. London: Hodder Arnold; 2010.
Office for National Statistics. https://www.ons.gov.uk/ (Accessed
5 April 2019).
The Coroners’ Society of England and Wales. http://www.coro-
nersociety.org.uk/ (Accessed 5 April 2019).
United Nations. The Minnesota Protocol on the Investigation of
Potentially Unlawful Deaths (The Revised United Nations Manual
on the Effective Prevention and Investigation of Extra-legal,
Arbitrary and Summary Executions) 2017.
UN Women. http://www.unwomen.org/en/about-us
(Accessed 5 April 2019).
5 The appearance of the body
after death
▪▪ Introduction
▪▪ The early post mortem interval
▪▪ Other post mortem changes
Introduction
If irreversible cardiac arrest has occurred, the indi-
vidual has died and eventually all the cells of the body
will cease their normal metabolic functions. From
this point, the changes of decomposition begin. Death
results in extensive biochemical changes in all body
tissues due to lack of circulating oxygen, altered enzy-
matic reactions, cellular degradation, and cessation of
anabolic production of metabolites. These biochemical
changes may provide chemical markers for helping to
more accurately determine the time since death (post
mortem interval, or PMI), but as yet no validated studies
exist, although this is a fruitful area for research.
Eventually the changes become visible to the naked
eye. An understanding of the nature and variability of
these visible changes is important for three reasons:
first, because it is important to know the normal prog-
ress of decomposition so that normal changes are not
misinterpreted for signs of an unnatural death; second,
that signs of unnatural death are not misinterpreted as
signs of a natural death; and third, as the changes may
be relevant in estimating how long the individual has
been dead.
The appearance of the body after death reflects PMI-
dependent changes, but the reliability and accuracy
of supposed traditional markers of the PMI have often
been shown to be false, given their dependence on the
wide variability of biological and environmental factors.
The early post mortem interval
Rapid changes after death
When the heart stops and breathing ceases, there is an
immediate fall in blood pressure and the supply of oxy-
gen to the cells of the body ceases. Initially, the cells
that can use anoxic pathways will do so until their met-
abolic reserves are exhausted, and then their metabo-
lism will begin to fail. With loss of neuronal activity,
all nervous activity ceases, the reflexes are lost and
breathing stops. In the eye, the corneal reflex ceases
and the pupils stop reacting to light. The retinal vessels,
viewed with an ophthalmoscope, show the break-up
▪▪ Estimation of the post mortem interval
▪▪ Biblography and information sources
▪▪ Further general resources
or fragmentation of the columns of blood, sometimes
referred to as ‘trucking’ or ‘shunting’ as the appear-
ance has suggested the movement of railway carriages.
The eyes themselves lose their intraocular tension.
The muscles rapidly become flaccid (primary flaccid-
ity), with complete loss of tone, but they may retain their
reactivity and may respond to touch or taps and other
forms of stimulation for some hours after cardiac arrest.
Discharges of the dying motor neurons may stimulate
small groups of muscle cells and lead to focal twitching,
although these decrease with time.
The fall in blood pressure and cessation of circulation
of the blood usually render the skin, conjunctivae and
mucous membranes pale. The skin of the face and the
lips may remain red or blue in colour in hypoxic/conges-
tive deaths. The hair follicles die at the same time as the
rest of the skin. Neither hair nor nails grow after death,
as is sometimes said, although both may appear more
prominent in the post mortem setting.
Loss of muscle tone after death may result in voiding
of urine and faeces. These findings are sometimes said
to be pathognomonic of conditions such as deaths from
epilepsy or asphyxia but may be present in many other
causes of death. Post mortem leakage of semen from
the penile urethra may occur but the presence of semen
cannot be used as a definite indicator of sexual activity
before death.
Regurgitation of gastric contents is a common fea-
ture of terminal collapse and it is a common feature
after cardiopulmonary resuscitation (CPR). Gastric
contents are identified in the mouth or airways in a sig-
nificant proportion of all autopsies. The presence of such
material cannot be used to indicate that gastric content
aspiration was the cause of death unless it is supported
by eyewitness accounts or by microscopic identification
of food debris in peripheral airways in association with
an inflammatory response.
Rigor mortis
Rigor mortis is, at its simplest, a temperature-dependent
physicochemical change that occurs within muscle
cells as a result of lack of oxygen. The lack of oxygen
means that energy cannot be obtained from glycogen
56 The appearance of the body after death
via glucose using oxidative phosphorylation and so ade-
nosine triphosphate (ATP) production from this process
ceases and the secondary anoxic process takes over for
a short time but, as lactic acid is a by-product of anoxic
respiration, the cell cytoplasm becomes increasingly
acidic. In the presence of low ATP and high acidity, the
actin and myosin fibres bind together and form a gel.
The outward result of these complex cellular metabolic
changes is that the muscles become stiff. However, they
do not shorten unless they are under tension.
It is clear from the short discussion above that if mus-
cle glycogen levels are low, or if the muscle cells are acidic
at the time of death as a result of exercise, the process of
rigor will develop faster. Electrocution is also associated
with rapidly developing rigor and this may be caused
by the repeated stimulation of the muscles. Conversely,
in the young, the old or the emaciated, rigor may be
extremely hard to detect because of the low muscle bulk.
Rigor develops uniformly throughout the body but it
is generally first detectable in the smaller muscle groups
such as those around the eyes and mouth, the jaw and
the fingers. It appears to advance down the body from
the head to the legs as larger and larger muscle groups
become stiffened. The only use of assessing the presence
or absence of rigor lies in the estimation of the time of
death. The key word here is ‘estimation’, as rigor is such
a variable process that it can never provide an accurate
assessment of the time of death. Extreme caution should
be exercised in trying to assign a time of death based on
the very subjective assessment of the degree and extent
of rigor. Charts or tables that assign times since death
based on the assessment of rigor should be viewed with
great scepticism. On its own, rigor mortis has very little
utility as a marker of the PMI because of the large num-
ber of factors that influence it.
The chemical processes that result in the stiffening
of the muscles, in common with all chemical processes,
are affected by temperature: the colder the temperature
the slower the reactions and vice versa. In a cold body,
the onset of rigor will be delayed and the length of time
that its effects on the muscles can be detected will be
prolonged, whereas in a body lying in a warm environ-
ment, the onset of rigor and its duration will be short.
It is also important to be aware of the micro-envi-
ronment around the body when assessing rigor: a
body lying in front of a fire or in a bath of hot water will
develop rigor more rapidly than if it were lying outside
in winter. When the post mortem cooling of a body is
extreme, the stiffening of the body may result from the
physical effects of cooling or freezing rather than rigor.
This will become apparent when the body is moved to
a warmer environment (usually the mortuary) and the
stiffening caused by cold is seen to disappear as the
body warms. Continued observation may reveal that
true rigor then develops as the cellular chemical pro-
cesses recommence.
In temperate conditions rigor can commonly be
detected in the face between approximately 1 and 4
hours after death and in the limbs between approxi-
mately 3 and 6 hours after death, with the strength of
rigor increasing to a maximum by approximately 18
hours after death. Once established, rigor can remain
for up to 2 days or so after death until autolysis and
decomposition of muscle cells intervene and muscles
become flaccid again. These times are only very rough
guidelines and can never be absolute.
It is best to test for rigor across a joint using very
gentle pressure from one or two fingers only; the aim is
to detect the presence and extent of the stiffness, not to
‘break’ it. If rigor is broken by applying too much force,
those muscle groups cannot reliably be tested again.
However, re-establishment of rigor mortis following
mechanical loosening also occurs with muscular rigid-
ity at re-establishment equalling, or even exceeding the
degree observed before breaking.
Cadaveric rigidity
‘Cadaveric rigidity’ (also known as ‘instantaneous rigor’,
‘kataleptische Totenstarre’, and ‘spasme cadvérique’) is
said to represent the instantaneous post mortem onset
of rigor mortis, the basis for which is the very occa-
sional discovery of a body in an unusual position, or of
items gripped firmly in the hand of the deceased before
the ‘expected’ onset of rigor. Most cases are said to be
related to individuals who are at high levels of emotional
or physical stress immediately before death and many
historic reports relate to battlefield casualties, but there
are many reports of individuals recovered from rivers
with weeds or twigs grasped firmly in their hand (Figure
5.1) or the finger of a suicidal shooting found tightly
gripping the trigger. It has been argued, however, that
the majority of historical accounts do not stand up to
critical scrutiny, and that a more likely explanation is
the onset of rigor in an individual positioned such that
gravity does not cause the gripped object to fall, or con-
strained in some way such as their unusual position is
maintained.
Post mortem hypostasis
Cessation of the circulation and the relaxation of the
muscular tone of the vascular bed allow simple fluid
movement to occur within the blood vessels. Post mor-
tem hypostasis or post mortem lividity (also known
as livor mortis or suggillation) are the terms used to
describe the visual manifestation of this phenomenon.
There is also filling of the dependent blood vessels.
The passive settling of red blood cells under the influ-
ence of gravity to blood vessels in the lowest areas of the
body is of forensic interest. This results in a pink, pur-
plish or bluish colour to these lowest areas and it is this
colour change that is called post mortem hypostasis or

Figure 5.1 ‘Cadaveric rigidity’ (also known as ‘instan-
taneous rigor’). This example represents post mortem
finding is present in a body recovered from water, where
vegetation is seen tightly ‘gripped’ in the hand.
lividity. Hypostasis is not always seen in a body and it
may be absent in the young, the old and the clinically
anaemic or in those who have died from severe blood
loss. It may be masked by those with darker skin tones
and other conditions such as jaundice.
Post mortem hypostasis occurs where superficial
blood vessels can be distended by blood. Compression
of skin in contact with a firm surface, for example, pre-
vents such distension, and results in areas of relative or
complete pallor within hypostasis (Figure 5.2). Relative
pallor within hypostasis may also be caused by pressure
of clothing or by contact of one area of the body with
another. It is generally considered to develop in the first
30 minutes after death, becoming very obvious up to
about 12 hours after death.
Figure 5.2 Post mortem hypostasis in a posterior distri-
bution. The body has been rolled to the right side. Areas
of pallor can be seen as a result of pressure of the body
on a firm surface, whereas parts of the body that had
not been in direct contact with that surface are purple/
pink because of the ‘settling of blood under gravity’. This
body had been lying on its back since death.
The early post mortem interval 57
Figure 5.3 Post mortem hypostasis distribution f­ ollowing
hanging. Note the skin discoloration is in the legs and
hands because of their dependent position in relation to
the vertical body after death.
The site and distribution of the hypostasis must be
considered in the light of the position of the body after
death. A body left suspended by the neck after hanging
may develop deep hypostasis of the lower legs and arms,
with none visible on the torso (Figure 5.3), whereas a
body that has partially fallen head first out of bed will
have the most prominent hypostatic changes of the head
and upper chest.
If a body has lain face downwards, or with the head
in a position lower than the rest of the body, hyposta-
sis can cause significant problems for interpretation.
Hypostasis in the relatively lax soft tissues of the face
can lead to intense congestion and the formation of
petechial haemorrhages in the skin of the face, and in
the conjunctivae, raising concerns about the possibil-
ity of pressure having been applied to the neck. Areas
of pallor around the mouth and nose may also add to
the impression of pressure having been applied to those
areas implying ‘suffocation’ (Figure 5.4a–c). In such cir-
cumstances, the pathologist must attempt to exclude
pressure to the mouth, nose and neck as having a role
in the death by careful examination and dissection of
those structures following removal of the brain and
heart, and looking for bruising and skeletal injury.
The colour of hypostasis is variable and may extend
variously from a pinkish hue to dark pink to red to deep
purple and, in some congestive hypoxic states, to blue.
The original skin colour will influence all these apparent
colour changes. It is the positioning of the hypostasis
rather than the colour that has significance and in gen-
eral, no attempt should be made to form any conclusions
about the cause of death from these variations of colour.
There are few colour changes that may act as indicators
of possible causes of death: the cherry pink colour of
carbon monoxide poisoning, the dark red or brick red
colour associated with cyanide poisoning and infection
by Clostridium perfringens, which is said to result in
58 The appearance of the body after death

(a) (b) (c)

Figure 5.4 (a) Post mortem hypostasis pattern on the front of a body found face down on a bed. The linear marks are
formed by pressure from creases in a blanket. Pallor around the mouth and nose are caused by pressure against the
bed and do not necessarily indicate marks of suffocation. (b) Post mortem hypostasis in male who died face down
obliquely across an open drawer - causing the linear pallor across the upper right chest and neck. (c) ‘Cherry red’
hypostasis on the back of the trunk in a case of fatal carbon monoxide poisoning.

bronze hypostasis. Again, these colour changes should
be treated with caution, not overinterpreted, and taken
into account with all other findings at post mortem.
The presence of hypostasis can give an indication that
a body has been moved after death. For example, if a body
is found lying prone, but the hypostasis pattern is pres-
ent on the deceased’s back, it is a reasonable assumption
that the body was originally positioned supine. Moving a
body several times after death will also have an effect on
hypostasis. Even after the normal post mortem coagu-
lation of the blood has occurred, movement of the red
blood cells, although severely reduced, still continues.
This continued ability of the red blood cells to move is
important because changes in the position of a body
after the initial development of hypostasis will result in
redistribution of the hypostasis and examination of the
body may reveal two overlapping patterns.
diurnal variation), exercise, infection and the
menstrual cycle.
• The second assumption is that it is possible to take
post mortem body temperature readings and,
using mathematical formulae, to extrapolate that
data and generate a reliable estimate of the time
taken by that body to cool to that measured tem-
perature.
• The third assumption is that the body has lain in
a thermally static environment; this is generally
not the case and even bodies lying in a confined
domestic environment may be s­ubject to the
daily variations of the central heating system,
while the variations imposed on a body lying
outside are potentially so great that no sensible
‘average’ can be achieved.

Cooling of the body after death

Plateau of variable
The cooling of the body after death cannot be viewed duration
solely as a simple physical property of a warm object in 36.9°C
a cooler environment. If it could, then the estimation of (98.4°F) Temperature° Decomposition
the time since death (the post mortem interval – PMI),
would be a simple process. Newton’s Law of Cooling
Rigor
states that heat will pass from the warmer body to the
cooler environment and the temperature of the body
will fall. However, a human body is not a uniform struc-
ture: its temperature does not fall evenly and, because
each body will be present in its own unique environ-
ment, each will cool at a different speed, depending
upon the many factors surrounding it (Figure 5.5). feels
In order to use body temperature as an indicator cold
of the time of death the following three basic forensic 0 6 12 18 24 30 36 42 48 54
assumptions must be made: Hours after death

• The first assumption is that the body temperature Figure 5.5 The sequence of major changes after death
was 37°C at the time of death. However, many in a temperate environment. Note that the core body
factors affect body temperature in life, including temperature does not show a fall for the first hour or so.
variation throughout any 24-hour period (i.e., The times are only rough estimates.

Many other variables and factors also affect the rate
of cooling of a body (Box 5.1) and together they show
why any trained forensic practitioner will be reluctant
to make any pronouncement on a specific time of death
based on the body temperature alone.
Other post mortem changes
As the PMI increases, the body undergoes ­additional
changes that reflect tissue ‘breakdown’, autolysis and
progressive decomposition/putrefaction.
Decomposition/putrefaction
In the cycle of life, dead bodies are usually returned,
through reduction into their various components, to
the chemical pool that is the earth. Some components
will do this by entering the food chain at almost any
level – from ant to tiger – whereas others will be reduced
to simple chemicals by autolytic enzymatic processes
built into the lysosomes of each cell.
The early changes of decomposition are important
because they may be mistaken for signs of violence or
trauma.
Decomposition results in liquefaction of the soft tis-
sues over a period of time, the appearance of which, and
the rate of progress of which, is a function of the ambient
temperature: the warmer the temperature, the earlier the
process starts and the faster it progresses. In temperate
climates the process is usually first visible to the naked
eye at about 3–4 days as an area of green discoloration of
the right iliac fossa of the anterior abdominal wall. This
‘greening’ is the result of the extension of the commensal
gut bacteria through the bowel wall and into the skin,
where they decompose haemoglobin, resulting in the
green colour. The right iliac fossa is the usual ­origin as
the caecum lies close to the abdominal wall at this site,
but then can extend throughout the body (Figure 5.6a).
Box 5.1 E xamples of factors affecting
the rate of cooling of a body
• No reliable ‘timetable’ for decomposition can be
Mass of the body.
• constructed because environmental factors may favour
Mass/surface area.
• enhanced or delayed decomposition, and such factors
Body temperature at the time of death.
• will generally be unknown to those investigating the
Site of reading of body temperature(s).
• death.
Posture of the body: extended or curled into a
fetal position.
• decomposition rates.
Clothing: type of material, position on the
body – or lack of it.
• Obesity: fat is a good insulator.
• Emaciation – lack of muscle bulk allows a body
to cool faster.
• Environmental temperature.
• Winds, draughts, rain, humidity.
Other post mortem changes 59
This green colour is but an external marker of the pro-
found changes that are occurring in the body as the gut
bacteria find their way out of the bowel lumen into the
abdominal cavity and the blood vessels.
The blood vessels provide an excellent channel
through which the bacteria can spread with some ease
throughout the body. Their passage is marked by the
decomposition of haemoglobin which, when present in
the superficial vessels, results in linear branching pat-
terns of variable discoloration of the skin that is called
‘marbling’ (Figure 5.6b). Over time, generalised skin
discolouration occurs and, as the superficial layers of
the skin lose cohesion, blisters or large bullae contain-
ing red or brown putrefaction fluid form (sometimes
gas filled) in many areas (Figure 5.6c and d). When
these burst, the contents are released and the skin
sloughs off.
In temperate climates particularly, considerable
gas formation in soft tissues and body cavities is com-
mon and the body begins to swell, with bloating of the
face, abdomen, breasts and genitals (Figure 5.7). The
body rapidly becomes unidentifiable. The increased
internal pressure causes the eyes and tongue to pro-
trude and forces blood-stained fluid up from the lungs
which often ‘leaks out’ of the mouth and nose as ‘purge
fluid’. Such fluid is frequently misinterpreted by those
inexperienced with decomposition-related changes as
representing injury-associated haemorrhage. The post
mortem appearance can be misleading in many cases,
with wrong assumptions being made, for example
about body habitus and ethnic origin.
The role of insects and other animals may be signifi-
cant in accelerating the decomposition process; domes-
tic animals and other predators are not excluded from
this process. As decomposition continues, soft tissues
liquefy; however, some organs are relatively resistant to
putrefaction and may be identifiable for many months.
These include the prostate and the uterus and the ten-
dons and ligaments. Eventually, skeletalisation will be
complete and, unless the bones and teeth are destroyed
by larger animals, they may remain for years.
Box 5.2 identifies some of the factors that influence
Immersion and burial
Immersion in water or burial will slow the process of
decomposition. Casper’s Law (or Ratio) states that: if all
other factors are equal, then, when there is free access
of air, a body decomposes twice as fast than if immersed
in water and eight times faster than if buried in earth.
60 The appearance of the body after death

(a) (b)

(c) (d)

Figure 5.6 (a) Greening of upper chest wall. (b) Marbling seen in blood vessels in the chest wall. The marbling
­represents decomposition changes within the blood vessels. (c) Skin slippage and fluid collection following decompo-
sition. (d) Blisters and bullae evident – early decomposition.

Box 5.2 E xamples of factors which can

affects rate and manner of
decomposition
• Temperature.
• The availability of oxygen.
Figure 5.7 Putrefaction/decomposition of approximately • Prior embalming.
1 week in temperate summer conditions. Note the ‘bloat- • Cause of death.
ing’ of soft tissues, distortion of facial features and ‘purge • Burial, and depth of burial.
fluid’ emanating from the mouth and nose. • Access by scavengers (insect and animal
predation).
Water temperatures are usually lower than those on • Trauma, including wounds and crushing blows.
land. A body in water may adopt a number of positions, • Humidity, or wetness.
but the most common in the early stage is face down • Rainfall.
with the air-containing chest nearest the surface and • Body size and weight.
the head and limbs hanging dependently lower in the • Clothing.
water. Hypostasis follows the usual pattern and affects • The surface on which the body rests.
the head and limbs, and these areas may also be dam- • Contents of the gastrointestinal tract.
aged by contact with the bottom if the water is shallow

Figure 5.8 Disposition of a body floating in water.
Typically, the head and limbs hang down, resulting in
superficial injuries to the head/face, back of the arms and
hands, knees and top of the feet.
and the river, lake or sea bed uneven (Figure 5.8). Often
such damage must be distinguished from pre-death,
pre-immersion trauma. Figure 5.9 shows the forehead
of a male immersed for 7 days in a tidal river. Most of the
appearance relates to contact with the river bed. Trauma
was excluded as this was a witnessed immersion.
The first change that affects the body in water is the loss
of epidermis. Gaseous decomposition progresses and the
bloated body is often, but not always, lifted to the surface
by these gases, most commonly at about 1 week but this
time is extremely variable. Marine predators are often as
active as animals found on land and they can cause exten-
sive damage (Figure 5.10). Exposure to water can, in some
cases, predispose to the formation of adipocere, but this
is unusual unless a body lies underwater for many weeks.
The effects and the timescale of the changes following
burial are so variable that little can be said other than bur-
ied bodies generally decay more slowly, especially if they
are buried deep within the ground. Many factors including
the level of moisture in the surrounding soil and acidity of
the soil will significantly alter the speed of decomposition.
Figure 5.9 Forehead of male immersed for 7 days in a
tidal river – appearance due to movement of body across
river bed, not assault.
Other post mortem changes 61
Adipocere
Adipocere is a chemical change in the body fat, which is
hydrolysed to a waxy substance with a texture similar
to soap. The need for water means that this process is
most commonly seen in bodies found in wet conditions
(i.e., submerged in water or buried in wet ground) but
this is not always the case and some bodies from dry
vaults have been found to have adipocere formation,
presumably the original body water being sufficient to
allow for the hydrolysis of the fat (Figure 5.11a and b).
In the early stages of formation, adipocere is a pale,
rancid, greasy semi-fluid material with a most unpleas-
ant smell. As the hydrolysis progresses, the mate-
rial becomes more brittle and whiter and, when fully
formed, adipocere is a grey, firm, waxy compound that
maintains the shape of the body. The speed with which
adipocere can develop is variable; it would usually be
expected to take weeks or months, but it is reported to
have occurred in as little as 3 weeks. All three stages of
adipocere formation can coexist and they can also be
found with areas of mummification and putrefaction if
the conditions are correct.
Mummification
A body lying in dry conditions, either climatic or in a
microenvironment, may desiccate instead of putrefy –
a process known as mummification (Figure 5.12a and
b). Mummified tissue is dry and leathery and generally
brown in colour. It generally occurs in the absence of
bacterial or insect influence. It is most commonly seen
in warm or hot environments such as desert and leads
to the spontaneous mummification of bodies buried
in the sand in Egypt. However, it is not only bodies
from hot dry climates that can be mummified, as the
Figure 5.10 Marine creature predation in a body recovered
from the North Sea after 3 months. Much of the skin has
been removed by crustaceans, and the arm muscles by
larger fish who have cleaned out most of the body cavity.
(Reproduced with permission from Saukko P and Knight B.
Knight’s Pathology 4E, London, CRC Press, 2016.)
62 The appearance of the body after death

(a) (b)

Figure 5.11 (a) Adipocere formation. Following burial for 3 years, waxy adipocere forms a shell around the skeleton of
this infant. (b) Advanced adipocere formation after 2.5 years in a grave. Exhumation due to exclusion of an acciden-
tal death (fall) in a bathtub. ([a] Adapted from Simpson’s 13th ed Fig. 5.11b; [b] From Saukko P and Knight B, Knight’s
Forensic Pathology, 4th ed., Chapter 2. CRC Press. London. 2015.)

microenvironment necessary for mummification may Skeletalisation

exist anywhere.
The speed of skeletalisation will depend on many factors,
Mummification of newborn infants whose bodies
including the climate and the microenvironment around
are placed in cool dry environments (e.g., below floor
the body. It will occur much more quickly in a body on the
boards) is common, but adults may also be mummi-
surface of the ground than in one that is buried (Figure
fied if they lie in dry places, preferably with a draught.
5.13). Generally speaking, in a body subject to burial, soft
Mummification is, however, much more likely in the
tissues will be absent by 2 years. Tendons, ligaments, hair
thin individual whose body will cool and desiccate
and nails may be identifiable for some time after that.
quickly.
At about 5 years, the bones will be bare and disartic-
Mummification need not affect the whole body, and
ulated, although fragments of articular cartilage may be
some parts may show the normal soft tissue decomposi-
identified for many years and for several years the bones
tion changes, skeletalisation or formation of adipocere,
will feel slightly greasy and, in a situation where they are
depending on the conditions. Mummified tissues are
cut with a saw, a wisp of smoke and a smell of burning
not immune to degradation and invasion by rodents,
organic material may be present. There are a number of
beetles and moths, especially the brown house moth,
techniques for extracting DNA from bone.
in temperate climates.

(a) (b)

Figure 5.12 (a) Mummification. The skin is dry and leathery following recovery from a locked room for 10 weeks.
(b) Mummification of the hand. ([a] Reproduced with permission from Saukko P and Knight B. Knight’s Pathology 4E,
London, CRC Press, 2016.)

Figure 5.13 Skeletisation.
Dating bones, as with all post mortem dating, is
fraught with difficulty. The microenvironment in which
the bone has lain is of crucial importance and the exam-
ination and dating of bones is now a specialist subject. It
is the forensic anthropologist, along with a forensic sci-
entist who will have the relevant skills and techniques
to manage this type of material.
In the UK, the medicolegal interest in bones fades rap-
idly if a bone from a body is considered to be more than
70–80 years of age, because even if it was from a crimi-
nal death, it is most unlikely that the killer would still
be alive. However, with longer survival rates, and crimi-
nal charges being brought against people in their 10th
decade for non-recent sexual abuse, it seems reason-
able to assume that this timeframe could be extended.
Carbon-14 dating is of no use in this short timescale,
but examination of the bones for levels of strontium-90,
which was released into the atmosphere in high levels
only after the detonation of the nuclear bombs in the
1940s, may allow for the differentiation of bones from
before and after that time. Work has been undertaken
on another radioisotope - 210Pb – but at present there is
no reliable means of accurately dating bones.
Post mortem injuries
Dead bodies are not immune to sustaining injuries and
can be exposed to a wide range of trauma. It is impor-
tant to bear this possibility in mind when examining
any body so that pre- and post mortem injuries are not
confused.
Predation by animals and insects can cause serious
damage. If there is any doubt about the nature of bite or
other marks, an odontologist or veterinarian should be
consulted (Figure 5.14). In water, fish, crustaceans and
larger animals can also cause severe damage, but there
is additional damage caused by the waterlogging of the
skin and the contact movement of the body across the
bottom or against the banks. Contact with boats and pro-
pellers can lead to patterns of injuries that in the absence
Estimation of the post mortem interval 63
Figure 5.14 Post mortem animal predation. The wound
margins of these rat bites are free from haemorrhage or
reddening. Such injuries are commonly present around
the eyes, ears and nose. (Reproduced with permission
from Saukko P and Knight B. Knight’s Pathology 4E,
London, CRC Press, 2016.)
of witnesses may not be easily recognisable and may be
confused with injury sustained in an assault.
Post mortem injuries do not actively bleed but many
do leak blood, especially those on the scalp and in
bodies recovered from water. The confirmation that a
wound is post mortem in origin may be extremely dif-
ficult because injuries inflicted in the last few minutes of
life and those that were caused after death may appear
exactly the same. In general, post mortem injuries do
not have a rim of an early inflammatory response in
the wound edges, but the lack of this response does not
exclude an injury inflicted in the last moments of life.
Estimation of the post mortem
interval
Opinions on the post mortem interval (PMI) are fre-
quently sought from forensic practitioners. For a foren-
sic pathologist an estimation of PMI is based on the
pathological findings. While none of the changes after
death is capable of providing a precise ‘marker’ of PMI,
the most reliable would appear to be related to the cool-
ing of the body after death, where appropriate measure-
ments have been recorded.
Body temperature
When considering temperature, it is the core tempera-
ture which is relevant (as opposed to that of the digits or
skin surface). Historically, the temperature of the body
was taken rectally using a long, low-reading thermom-
eter (0–50°C was considered to be adequate). However,
rectal temperature recording can potentially interfere
with the forensic assessment of the area particularly
64 The appearance of the body after death
with regard to determining the location and presence
of biological materials such as semen, blood or hair.
Electronic temperature probes allow the use of other
orifices, including the nose and ear, for temperature
taking, although it must be accepted that these loca-
tions are unlikely to register the same temperature as
the deep rectum or the liver.
The most widely recognised means of estimating the
time of death with temperature is Henssge’s nomogram
(see Box 5.3). Crucially, the 95 per cent accuracy claimed
for this method is, at best, only 2.8 hours on either side
of the most likely time (a total spread of over 5.5 hours).
Henssge’s nomogram relies on three measurements
– body temperature, ambient temperature and body
weight – and lack of accuracy in any one of these will
substantially degrade the final result. Corrective factors
can be applied to allow for clothing, air movement and/
or water (Table 5.1). Whilst the use of the nomogram is
advocated by forensic pathologists in some jurisdictions,
it has enjoyed limited acceptance in the UK, and realisti-
cally it should be accepted that the results it provides are
an indicator of a range of time of death and actual time of
death may still lie outside the range provided.
Indeed, the need to record the ambient temperature
poses one of the major problems because of fluctuating
temperatures at the scene. The first police officers or
scientists at the scene should always be encouraged to
take the ambient temperature adjacent to the body and
to record the time that they made their measurement.
This, however, may give rise to concerns about inter-
pretation of physical findings (dependent on how and
by what route the temperature is taken). Occasionally
meteorological data sources can assist in providing such
information.
In the past various ‘rules of thumb’ have been used to
calculate the time of death from the body temperature
but like most ‘rules of thumb’ they are not derived from
any evidence base and should be considered as simple
guesswork, and not to be used in forensic practice.
Additionally, the perceived temperature of the body
to touch is mentioned in court as an indicator of the time
of death; this assessment is so unreliable as to be useless
and is even more so if the pathologist is asked to com-
ment upon the reported observations of another person.
The UK Forensic Science Regulator, which sets quality
standards for the provision of forensic science services,
has issued guidance on the application of post mortem
cooling methods to the estimation of time since death
and unambiguously states that the pathologist must
make clear to the investigator that the accuracy of the
estimate cannot be determined, and that it should not
be used to define the period in which death occurred.
Various other methods have been researched in as
yet unsuccessful attempts to find a technique to deter-
mine time of death. Biochemical methods, includ-
ing vitreous humour potassium levels and changes in
enzyme and electrolyte levels elsewhere in the body,
remain as interesting research tools but none has been
widely accepted in routine case work as they have not
yet been proved to be valid.
Other techniques used in estimating or
corroborating PMI
Forensic entomology has an important role in estab-
lishing time of death, but as with other methods the
accuracy and limitation of such determinations must
be understood. Forensic entomologists can deter-
mine a probable time of death – in the region of days
to months – from examination of the populations and
stages of development of the various insects that invade
a body. The use of insects to estimate PMI requires
knowledge of the insect’s life cycle, the relationship of
the insect to the remains, and the relationship of the
remains to the habitat in which they are discovered.
Insects pass through a number of distinct stages dur-
ing their life cycle. For example, a female blowfly in the
family Calliphoridae arrives at the body and deposits
eggs in body openings associated with the head, anus,
and genitals, or in wounds. Following hatching, larvae
or maggots feed on the decomposing tissues. There are
three larval stages, with a moult (an instar) in between
each stage. Once the maggot is fully developed, it
ceases to feed and moves away from the remains before
pupariation. The puparium is an inactive stage during
which the larval tissues are reorganised to produce the
adult winged fly (Figure 5.15a and b). The time from
egg laying through the instars to pupation varies from
species to species and the ambient temperature, but
with the relevant expertise a PMI can be determined
from these data.
Other animals, both large and small, will arrive to
feed on the body, with the species and the rapidity of
their arrival depending on the time of year and the envi-
ronment. The examination of buried bodies or skeletal
remains may require the combined specialist skills of
the forensic pathologist, an anthropologist, an odon-
tologist and an entomologist.
Analysis of gastric contents – other than for toxicolog-
ical purposes – may assist in an investigation, but cannot
reliably be used to accurately determine time of death
although it may provide an indicator within a 6 hour or
so timeframe (see Box 5.4). The presence or absence, and
nature (if present), of gastric contents may be very useful
in terms of corroborating accounts of witnesses. Review
of such evidence generally requires full retention of gas-
tric contents, analysis by a forensic scientist, interpreta-
tion by a forensic physician or gastroenterologist, and
review of pre-death medical records and post mortem
findings. In some cases, plant analysis can provide a reli-
able estimation for skeletal remains dating, when tradi-
tional techniques are not applicable. Forensic botany is a
 Estimation of the post mortem interval 65

Box 5.3 The rectal temperature: Time of death relating nomogram

ve factors
correcti
Using ak ed–still air)
(n 2,8
dard
Stan 20 24 28
32 2,8
15
10 20 24
35 5 15 28 36
10
14 16 18 20 22 200
5
10
12
14 16 18
24 180 40
2
6 10
12 20 160 34
6 10 12 14 16 140
2 8 44
30 6 10 12 14 120 24 30
2
6
8
10 12 110 20 38
8 100 26
2 18 48
6 10 33
2
4
6
8 90 14
16 22
28
10 20 42
4 8 12
25 2 6
8 16
18 24 36 52
4 10
2 6 14 22 31
4 8 12 20 46
80 2 6
10 18
26
56
4 6 8 24 40
70 2 16

4,5
4 6 28
20 14 22 A

3,2
60 2 4 12 50 60
10 20 35
4 8 26 M
50 2 6
16
18
24 30 B
3 45
40 2 3 5
14 22 28 55 65 I
2 12
10 30 1 2 4 10 20 26 40
E
2 8 18 24 34 N
20 1 6 16 50 60 70 T
22
5 14 32
15 1 12
20
30 45 75 °C
4 18 55 65
10 10 10 28 35
6 16
26 40 80 10
8 14 50 60 70
24 35

7,0
4,5
7 12 22 40 45
30 55
6 20 35 80
5 10
18 25 40 45 50 60 70 5
30
16 35 40
10 25 30 50
80
10 15 20 25 30
40 50 60 70
40 50 60
0 30 40 50 80
60 70 0
°C
10 20 40 60 80 100 120 160 200
R 15 30 50 70 90 110 140 180
E 5
C KILOGRAM
T
U
M
10

15

20

This nomogram is for ambient temperatures up to proportionally adjusted by corrective factors of the
25°C. Permissible variation of 95% (+/− h). The Henssge real body weight, giving the corrected body weight by
nomogram expresses the death-time (t) as follows: which, the death-time is to be read off. Factors above
1.0 may correct thermal isolation conditions and fac-
Trecturm − Tambient tors below 1.0 may correct conditions accelerating the
= 1.25 exp (Bt) − .25 exp (5Bt);
37.2 − Tambient heat loss of a body.
B = −1.2815 (kg−.625 ) + .0284
How to read off the time of death
The nomogram is related to the chosen standard; Connect the points of the scales by a straight line accord-
that is, a naked body extended lying in still air. Cooling ing to the rectal and the ambient temperature. It crosses
conditions differing from the chosen standard may be the diagonal of the nomogram at a specific point.
(Continued)
66 The appearance of the body after death

Box 5.3 (Continued) The rectal temperature: Time of death relating nomogram
Draw a second straight line going through the
centre of the circle, below left of the nomogram, and
the intersection of the first line and the diagonal. The
second line crosses the semicircle of the body weight
and the time of death can be read off. The second line
touches a segment of the outermost semicircle. Here
can be seen the permissible variation of 95%.
Example: temperature of the rectum 26.4°C; ambient
temperature 12°C; body weight 90 kg.
Result: time of death 16 ± 1.8 hours. Statement: the
death occurred within 13.2 hours and 18.8 hours (13
hours and 19 hours) before the time of measurement
(with a reliability of 95%).
Note: if the values of the ambient temperature and/
or the body weight are called into question, repeat
the procedure with other values which might be pos-
sible (see Table 5.1 for ‘corrective factors’). The range of
death-time can be seen in this way.
Requirements for use
• No strong radiation (e.g. sun, heater, cooling
system).
• No strong fever or general hypothermia.
• No uncertaina severe changes of the cooling con-
ditions during the period between the time of
death and examination (e.g., the place of death
must be the same as where the body was found).
• No high thermal conductivity of the surface
beneath the bodyb.
a Known changes can be taken into account: a change of the
ambient temperature can often be evaluated (e.g., contact the
weather station); use the mean ambient temperature of the
period in question. Changes by the actions of the investigators
(e.g., taking any cover off) since finding the body are negligible:
take the conditions before into account.
b  Measure the temperature of the surface beneath the body too.
If there is a significant difference between the temperature
of the air and the surface temperature, use the mean. This
representation of the nomogram should not be used for
actual cases, as distortion of the scales in reproductions can
cause error. The original form can be downloaded from http://
www.rechtsmedizin.uni-bon.de/dienstleistungen/for_Med/
todeszeit. A detailed analysis of the use of the nomogram can
be found in ‘Estimation of time since death’.

Table 5.1 Empirical corrective factors of body weight

Corrective Wet-through clothing/covering
Dry clothing/covering In air factor wet body surface In air/water
3.5 Naked Flowing
0.5 Naked Still
0.7 Naked Moving
0.7 1–2 thin layers Moving
Naked Moving 0.75
1–2 thin layers Moving 0.9 2 or more thicker Moving
Naked Still 1.0
1–2 thin layers Still 1.1 2 thicker layers Still
2–3 thin layers 1.2 More than 2 thicker layers Still
1–2 thicker layers Moving or still 1.2
3–4 thin layers 1.3
More thin/thicker layers Without influence 1.45
Thick bedspread + clothing 1.8
Combined 2.4
Note: For the selection of the corrective factor of any case, only the clothing or covering of the lower trunk is relevant!
Personal experience is needed, nevertheless this is quickly achieved by the consistent use of the method.

(a)
Figure 5.15 (a) Maggot infestation of a body recovered from heated premises approximately 2 weeks after death.
Forensic entomology may assist in estimating post mortem interval (PMI) in such cases. (b) Maggot infestation below
skin surface – note also mummification of fingertips.
Box 5.4 Gastric contents and the post mortem interval: The ‘Truscott Case’
In 1959, a 12-year-old girl, Lynne Harper, was found
dead in woodland in Ontario, Canada. She had been
strangled and sexually assaulted. A 14-year-old boy,
Steven Truscott, was convicted of her murder and sen-
tenced to death, although this was later commuted to
life imprisonment. His conviction was quashed in 2007,
following a second ‘Reference’ to the Court of Appeal.
Whilst there appeared to be agreement amongst
the expert witnesses at trial, and at subsequent appeal
hearings, that Lynne had died as a result of strangula-
tion (a ligature fashioned out of her blouse), there was
intense controversy regarding the pathological assess-
ment of the post mortem interval.
The Crown case was that, due to the presence of
recognisable food particles (vegetable matter and
possibly meat) within the stomach contents, Lynne
newer discipline that includes many subdisciplines such
as palynology (including mycology), anatomy, dendro-
chronology, limnology and ecology and its role is likely
to continue to develop in the future.
In all cases of determination of PMI, it is for the foren-
sic practitioner to advise the justice system of the limits
of each technique.
Biblography and information
sources
Alberti F, Gonzalez J, Paijmans JLA, et al. Optimized DNA sam-
pling of ancient bones using Computed Tomography scans.
Mol Ecol Resour. 2018;18(6):1196–1208.
Amendt J, Richards CS, Campobasso CP, et al. Forensic ento-
mology: applications and limitations. Forensic Sci Med Path
2011;7:379–392.
Biblography and information sources 67
(b)
must have died between 1½ and 2 hours after her last
meal had finished, a time period in which Steven was
thought to have had ‘exclusive opportunity’ to kill her.
Her body was found two days after her disappear-
ance, and the environmental conditions in the area had
been hot and damp. Evidence of decomposition, how-
ever, was lacking raising the possibility that she had
been killed at a later time than was suggested by the
crown.
It was recognised on appeal that gastric empty-
ing times were subject to variation precluding its use
as a reliable factor in the assessment of time of death,
although it might assist an investigation in other ways,
such as confirming that death occurred after a particu-
lar meal was eaten.
Belsey SL, Flanagan RJ. Post mortem biochemistry: ­current appli-
cations. J Forensic Leg Med 2016;41:49–57.
Brown A, Marshall TK. Body temperature as a means of estimat-
ing time of death. Forensic Sci 1974;4:125–133.
Burger E, Dempers J, Steiner S, Shepherd R. Henssge nomogram
typesetting error. Forensic Sci Med Path 2013;​9:​615–617.
Cartozzo C, Singh B, Boone E, Simmons T. Evaluation of DNA
extraction methods from waterlogged bones: a pilot study.
Forensic Sci 2018;63(6):1830–1835.
Cook GT, MacKenzie AB. Radioactive isotope analyses of skeletal
materials in forensic science: a review of uses and potential
uses. Int J Legal Med 2014;128(4):685–698.
Crostack C, Sehner S, Raupach T, Anders S. Re-establishment of
rigor mortis: evidence for a considerably longer post mortem
time span. Int J Legal Med 2017;131(4):1039–1042.
Donaldson AE, Lamont IL. Biochemistry changes that occur after
death: potential markers for determining post-mortem inter-
val. PLOS ONE 2013;8(11):e82011.
68 The appearance of the body after death
Faris AM, Wang HH, Tarone AM, Grant WE. Forensic entomology:
evaluating uncertainty associated with postmortem interval
(PMI) estimates with ecological models. J Med Entomol 2016;​
53:​1117–1130.
Forensic Science Regulator/Royal College of Pathologists. The
use of time of death estimates based on heat loss from the
body. FSR-G-211 Issue 1 2014 https://www.gov.uk/govern-
ment/publications/time-of-death-estimations (Accessed 5
April 2019).
Goff L. Forensic entomology. In: Resh VH, Cardé RT (eds).
Encyclopedia of Insects, 2nd ed. Burlington, MA: Elsevier; 2009,
381–386.
Gondek AT, Boessenkool S, Star B. A stainless-steel mortar, pestle
and sleeve design for the efficient fragmentation of ancient
bone. Biotechniques 2018;64(6):266–269.
Haglund WD, Sorg MH (eds). Forensic Taphonomy: The Post-
mortem Fate of Human Remains. Boca Raton, FL: CRC Press;
1997.
Hawksworth DL, Wiltshire PE. Forensic mycology: the use of fungi
in criminal investigations. Forensic Sci Int 2011;​206:1.
Henssge C. Death time estimation in case work. I. The rec-
tal temperature time of death nomogram. Forensic Sci Int
1988;38:209–236.
Lancia M, Conforti F, Aleffi M, et al. The use of Leptodyctium
riparium (Hedw.) Warnst in the estimation of minimum post-
mortem interval. J Forensic Sci 2013;58(Suppl 1):S239–S242.
Legge CM, Payne-James JJ, Puntis JWL, Short SL. Post mortem
gastric content analysis: its role in determining time since
death. In: Gall JAM, Payne-James JJ (eds). Current Practice in
Forensic Medicine, Volume 2. Chichester: Oxford Editorial
Office; 2016.
Madea B. Estimation of the Time Since Death, 3rd ed. London: CRC
Press; 2016.
Marshall TK. The use of body temperature in estimating the time
of death and its limitations. Med Sci Law 1969;3:178–182.
Marshall TK, Hoare FE. Estimating the time of death. J Forensic Sci
1962;7:56–81, 189–210, 211–221.
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evidence to aid in forensic death investigation. Croat Med J
2005;46(4):606–612.
Pirch J, Schulz Y, Klintschar M. A case of instantaneous rigor? Int J
Legal Med 2013;127:971–974.
Schrag B, Uldin T, Mangin P, et al. Dating human skeletal
remains using 90Sr and 210Pb: case studies. Forensic Sci Int
2014;234:190.e1–190.e6.
Sher J. ‘Until you are dead’: Steven Truscott’s Long Ride into History.
Toronto: Vintage Canada; 2002.
Shirley NR, Wilson RJ, Jantz LM. Cadaver use at the University
of Tennessee’s Anthropological Research Facility. Clin Anat
2011;24:373–380.
Shkrum MJ, Ramsay DA. Forensic Pathology of Trauma. Totowa:
Humana Press, Inc.; 2007.
Simpson K. The case against Steven Truscott in Canada. Medico-
Legal J 1968;36:58–71.
Truscott (Re), 2007 ONCA 575 Court of Appeal for Ontario tran-
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Further general resources
Payne-James JJ, Byard RW. Encyclopedia of Forensic & Legal
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Saukko P, Knight B. Knight’s Forensic Pathology, 4th ed. London:
CRC Press; 2015.
6 Death from natural causes
▪▪ Introduction
▪▪ Cardiovascular system
▪▪ Respiratory system
▪▪ Gastrointestinal system
Introduction
In those countries where death is certified, the respon-
sibility for certification falls either to the doctor who
attended the patient during life or a doctor who has suf-
ficient knowledge of the clinical history to give a reason-
able assessment of the cause of death. Many studies have
shown that there is a large error rate in death certificates
and that in 25–60 per cent of deaths there are significant
differences between the clinician’s presumption of the
cause of death and the lesions or conditions identified
at autopsy.
Thus, raw epidemiological data must be treated
with some caution. All doctors should take the task of
certifying the cause of death very seriously but, often
it is a job usually delegated to junior staff with least
­experience.
In England and Wales following a number of reviews
and introduction of legislation, it was intended that all
deaths would be scrutinised by independent, senior
­doctors (referred to as a Medical Examiner) who would
consult with attending doctors on the wording of the
cause of death given on the Medical Certificate of Cause
of Death (MCCD), and to discuss any concerns with the
bereaved relatives. From April, 2019 a non-statutory
Medical Examiner system has been rolled out in England
& Wales with the intention of it becoming a statutory
system extending into primary care in the future. In
Scotland, however, the Death Certification Review
Service, which is run by Healthcare Improvement
Scotland and checks on the accuracy of a sample of
MCCDs, was established in 2015. The reviews are
designed to: improve the accuracy of MCCDs; provide
better quality information about causes of death so that
health services can be better prepared for the future; and
ensure that the processes around death certification are
robust and have appropriate safeguards in place.
There is a different approach to sudden and unex-
pected deaths, as these deaths are usually reportable
to the authorities for medicolegal investigation. In
England & Wales, doctors should only issue a death cer-
tificate if they are satisfied that they know the cause of
death and that it is from natural causes.
▪▪ Gynaecological conditions
▪▪ Deaths from asthma and epilepsy
▪▪ Bibliography and information sources
The World Health Organisation (WHO)’s defini-
tion of a sudden death is death within 24 hours of the
onset of symptoms, but in forensic practice most sud-
den deaths occur within minutes or even seconds of
the onset of symptoms. Indeed, it is very likely that a
death that is delayed by hours will not be referred to the
Coroner or other medicolegal authority, as a diagnosis
may well have been made, and a death certificate can be
­completed by the attending doctors.
It is crucial to remember that a sudden death is not
necessarily unexpected and an unexpected death is
not necessarily sudden, but these two factors are often
­combined.
Cardiovascular system
Disease of the heart
When a natural death is very rapid, the most common
cause of irreversible cardiac arrest is a cardiovascular
abnormality. While some degree of geographical varia-
tion is to be expected, the following lesions are the most
significant as causes of sudden unexpected death.
Coronary artery disease
Narrowing of the lumen of a coronary artery (stenosis)
by atheroma may lead to chronic ischaemia of the mus-
cle supplied by that artery. If the myocardium becomes
ischaemic, it may also become electrically unstable,
predisposing to the development of an abnormal heart
rhythm – an arrhythmia. The oxygen requirement of
the myocardium is related to the heart rate; an increase
in heart rate, for example during exercise, following a
large meal or as a consequence of a sudden adrenaline
response to stress, anger, fear or other such emotion will
lead to an increase in myocardial oxygen demand. If
that increased oxygen demand cannot be met, because
of limitation of blood flow through the stenotic ves-
sel, the myocardium distal to the stenosis will become
ischaemic. Ischaemia does not invariably lead to myo-
cardial infarction, it just needs to be enough to initiate
a potentially fatal arrhythmia and, particularly if that
70 Death from natural causes

part of the heart rendered ischaemic includes one of the (a)

pace-making nodes or a major branch of the conducting
system, the risk that rhythm abnormalities will develop
is substantially increased.
Complications related to atheromatous plaques may
worsen the coronary stenosis and the subsequent myo-
cardial ischaemia by a number of mechanisms. Bleeding
may occur into a plaque. This may be seen as sub-inti-
mal haemorrhage at autopsy. Sudden expansion of the
plaque may lead to rupture, which may also occur if the
plaque ulcerates. When a plaque ruptures, the extruded
cholesterol, fat and fibrous debris which will flow down
the coronary artery and impact distally, often causing
multiple small areas of infarction. The endothelial cap (b)
of a ruptured plaque may act as a flap valve within the
vessel and cause a complete obstruction.
An atheromatous plaque is also a typical site for the
development of thrombus, which will further reduce the
cross-sectional area of the vessel lumen without neces-
sarily fully blocking the vessel.
Coronary thrombosis underlies most of the compli-
cations of coronary artery atherosclerosis, including
unstable angina, acute myocardial infarction and sud-
den cardiac death (SCD) but such thrombi are found
with variable frequency at autopsy of between 13 and
98 per cent (Figure 6.1a and b).
Myocardial infarction occurs when there is severe
stenosis or complete occlusion of a coronary artery so
Figure 6.1 Significant coronary artery atherosclerosis
that the blood supply is insufficient to maintain oxy-
and acute thrombosis. (a) Macroscopic and
genation of the myocardium. If there is adequate collat-
(b) microscopic appearance. (Courtesy of Richard Jones.)
eral circulation, blood can still supply the myocardium
by other routes. The fatal effects of an infarction may in relation to sudden death. SCD is defined as the unex-
develop at any time after the muscle has become isch- pected death without an obvious noncardiac cause that
aemic (Figure 6.2a–d). occurs within 1 hour of witnessed symptom onset (estab-
The area of muscle damaged by a myocardial infarc- lished SCD) or within 24 hours of unwitnessed symptom
tion is further weakened by the process of cellular onset (probable SCD). In the United States, its incidence
death and the generalised inflammatory response to is 69/100,000 per year. Dysfunctions of the cardiac con-
these necrotic cells. The area of the myocardial infarct duction and autonomic nervous systems are known to
is most at risk between 3 days and 1 week after the clini- contribute to SCD pathogenesis. Many different abnor-
cal onset of the infarction and it is at this time that the malities have been found; it may be difficult to deter-
compromised area of myocardium may rupture, lead- mine if conduction system lesions are the cause of a fatal
ing to sudden death from a haemopericardium and car- arrhythmia or merely an incidental finding but, in the
diac tamponade (Figure 6.3a). The rupture occasionally absence of any other abnormality, it may be reasonable
occurs through the interventricular septum, resulting to conclude that they were a significant factor in causing
in a left–right shunt. If a papillary muscle is infarcted, the death. The Swiss Society of Legal Medicine has made
it may rupture, which may cause mitral valve prolapse, recommendations to combine forensic post mortem
which itself may be associated with sudden death or cardiac examination and clinical recommendations for
may present as a sudden onset of valve insufficiency genetic testing of inherited cardiac diseases to optimise
with heart failure (Figure 6.3b). the diagnostic procedures and preventive measures for
An area of infarction heals by fibrosis, and fibrotic living family members. The key points of the recommen-
plaques in the wall of the ventricle or septum may also dations are:
interfere with physical or electrical cardiac function.
Cardiac aneurysms may form at sites of infarction, • A forensic autopsy for all SCD victims under 40
which have the potential to calcify and rupture. years of age.
Physical lesions in the cardiac conducting system • The collection and storage of adequate samples for
have been studied intensively in recent years, especially genetic testing.

(a)
(c)
Figure 6.2 Myocardial infarction. (a) Macroscopic appearance of acute left-ventricular myocardial infarction.
(b–d) Microscopic appearance of myocardial infarction with early necrosis (b), organisation including residual haemo-
siderin-laden macrophages and fibroblasts (c), and extensive replacement fibrosis (d). (Courtesy of Richard Jones.)
• Communication with the families.
• A multidisciplinary approach including cardioge-
netic counselling.
Hypertensive heart disease
Long-standing hypertension can result in cardiac
remodelling, manifested by left ventricular hypertrophy
(and cardiomegaly). Although the ‘normal heart weight’
(approximately 400 g for the average male) is dependent
on body size/weight, an enlarged heart predisposes an
individual to chronic myocardial hypoxia and electri-
cal instability which, when combined with a trigger, can
result in a fatal arrhythmia. Some authors consider a
heart weight of greater than 500 g to represent an inher-
ently unstable heart. Hypertensive heart disease fre-
quently coexists with coronary artery atherosclerosis,
increasing the potential for the development of fatal
arrhythmias at times of cardiovascular ‘stress’. There are
regional and ethnic variations in the incidence of such
diseases but in general the global burden of hyperten-
sion is rising and accounts for substantial morbidity
and mortality. Lifestyle factors such as diet and physical
inactivity contribute to this burden, further highlighting
the need for prevention efforts to curb this public health
Cardiovascular system 71
(b)
(d)
epidemic. Regular physical activity is associated with
lower blood pressure, reduced cardiovascular risk, and
cardiac remodelling. While exercise and hypertension
can both be associated with the development of left ven-
tricular hypertrophy (LVH), the cardiac remodelling from
hypertension is pathological with an associated increase
in myocyte hypertrophy, fibrosis, and risk of heart failure
and mortality, whereas LVH in athletes is generally non-
pathological and lacks the fibrosis seen in hypertension.
Aortic stenosis
Aortic stenosis is a disease that classically affects older
individuals with calcified tricuspid aortic valves, but
may also be seen in younger people who have a congen-
ital bicuspid aortic valve. It is the most common form
of valvular heart disease. Angina, exertional syncope
and heart failure are key symptoms indicating a need
for intervention. The accompanying myocardial hyper-
trophy is similar to that caused by hypertension – lead-
ing to LVH – which may, in some cases, produce heart
weights of over 700 g.
In aortic stenosis, myocardial perfusion is worsened
by the narrow valve, which results in a lower pressure at
the coronary ostia and hence in the coronary arteries.
72 Death from natural causes
(a)
(b)
Figure 6.3 Complication of myocardial infarction: hae-
mopericardium. (a) The pericardial sac has been opened
to reveal a heart surrounded by blood clot. During the
healing process, an area of infarcted myocardium has
weakened to such an extent that it has ruptured. The
accumulation of blood within the intact pericardial sac
leads to compression of the heart, interfering with its
ability to pump blood effectively (cardiac tamponade),
and to cardiac arrest. (b) Typical appearance of pitting
ankle oedema (caused by compression from socks) in
patients with heart failure. ([a] From Burton J, Saunders S,
Hamilton S. Atlas of Adult Autopsy Pathology. Boca Raton:
CRC Press 2015; Fig. 3.5b page 55.)
Sudden death is common in these patients. The devel-
opment of symptoms in patients with severe aortic
stenosis predicts a high likelihood of mortality. Aortic
valve replacement is needed in such cases. In asymp-
tomatic patients, the risk of sudden death is perceived to
be low varying among studies from 0.25 to 1.7 per cent
per year. Many advocate conservative management of
these patients until symptoms develop.
Senile myocardial degeneration
Senescence is a well-accepted concept in all animals,
and an increasing number of humans are surviving into
their 10th and 11th decades. The cause of a sudden death
in these elderly individuals can often be very difficult
to determine. In very general terms the senile heart is
small, the surface vessels are tortuous and the myocar-
dium is soft and brown owing to accumulated lipofus-
cin in the cells, but otherwise potentially fatal changes
are similar to those in the younger population.
Primary myocardial disease
Primary diseases of the myocardium are much less com-
mon than the degenerative conditions described above
and they commonly affect a significantly younger age
group. They include conditions where there is a struc-
tural abnormality of the heart that is visible to the naked
eye and/or under the microscope (myocarditis and the
cardiomyopathies) and those conditions having no rec-
ognisable morphological/structural abnormality (the
channelopathies).
Myocarditis has multifactorial aetiology and occurs
in many infective diseases, such as diphtheria and viral
infection, including influenza. Complications, includ-
ing sudden death, associated with the infection may
occur some days or even weeks after the main clinical
symptoms. Myocarditis may sometimes be suspected
from visual inspection because of the presence of pale
or haemorrhagic foci in the myocardium (having a ‘mot-
tled’ appearance), although histological confirmation of
multifocal inflammatory cell infiltrates and associated
myocyte necrosis requires extensive sampling at post
mortem examination (Figure 6.4). Inflammation of the
pericardium may occur for many reasons, for example
after myocardial infarction or following viral infection.
Figure 6.5 shows the effects of chronic pericardial
inflammation with the formation of fibrous adhesion
bands between the inner aspect of the pericardium and
the epicardium of the heart.
Most cardiomyopathies are familial diseases.
Cascade family screening identifies asymptomatic
*
*
*
Figure 6.4 Myocardial inflammation – an ­inflammatory
cell infiltrate (arrows) between myocytes showing
­contraction band necrosis (*).
(Courtesy of Richard Jones.)

Figure 6.5 Fibrinous pericarditis (arrow points to
­fibrinous deposits on the epicardial surface of the heart).
patients and family members with early traits of disease.
The inheritance is autosomal dominant in a majority of
cases, and recessive, X-linked or matrilinear. There are
a number of disorders including:
• Hypertrophic cardiomyopathy (HCM), which is
an inherited disease of cardiac muscle sarcomeric
proteins, characterised by symmetrical or asym-
metrical hypertrophy, a sub-aortic mitral ‘impact
lesion’ and myocyte disarray. This is an autosomal
dominant cardiac disorder, with interstitial fibro-
sis and small vessel disease, with or without mac-
roscopic hypertrophy. More than 100 mutations in
ten genes, all encoding sarcomeric proteins, have
been identified as responsible for this disease.
• Dilated cardiomyopathy (DCM), which may be a
primary disorder, or a secondary phenomenon (for
example following chronic alcohol misuse).
• Arrhythmogenic right ventricular cardiomy-
opathy (ARVCM), an inherited cardiomyopa-
thy characterised by fibro-fatty replacement of
predominantly the right ventricle (RV). Patients
are predisposed to life-threatening ventricular
arrhythmias and generally slowly progressive
ventricular dysfunction. The disease is inherited
as an autosomal dominant trait with incomplete
penetrance and variable expressivity.
The cardiomyopathies are an important group of condi-
tions linked to sudden death in the young, and are of par-
ticular importance in deaths occurring during exercise,
or on the athletic field.
The channelopathies are a group of disorders rep-
resenting a proportion of sudden deaths, presumed
to be of cardiac origin. SCD following ventricular
tachyarrhythmias constitutes an important clinical
cause of mortality; 4 per cent of cases may involve ion
­channel-mediated cellular excitation in structurally
normal hearts. Changes in these mechanisms may
Cardiovascular system 73
disturb action potential conduction, depolarisation/
repolarisation gradients, or Ca 2+ homeostasis with
potential arrhythmogenic consequences. Defects in
genes encoding myocyte contractile units have been
characterised and these affect the function of sodium,
potassium and calcium channels. Patients may pres-
ent with symptoms of palpitations or haemodynamic
compromise, including dizziness, seizure or syncope,
particularly following exertion. In all inherited car-
diac death syndromes, first-degree relatives should be
referred to a cardiologist and should undergo testing
appropriate for the condition.
The main syndromes currently recognised include
Wolff–Parkinson–White, long QT syndrome, Brugada
syndrome, short QT syndrome, and catecholaminergic
polymorphic ventricular tachycardia.
Pathologically, there are no macroscopic (visible to
the naked eye) or microscopic abnormalities in the heart
as the defects are at a molecular level (at the ryanodine
receptor, for example). Molecular investigations must be
key elements in the post mortem investigation of such
presumed SCDs with a structurally normal heart.
Diseases of the arteries
The most common lesion of (extracardiac) arteries
associated with sudden death is the aneurysm. Several
varieties must be considered as they are very commonly
found in sudden unexpected death autopsies.
Atheromatous aneurysm of the aorta
These aneurysms are most commonly found in elderly
individuals in the abdominal region of the aorta (Figure
6.6a and b). In 2014, the prevalence of abdominal aortic
aneurysm (AAA) was reported to be between 1 and 12.7
per cent (mean 5.7%, median 5%).
They are formed when the elastic component of the
aortic wall underlying an atheromatous plaque is dam-
aged and the aortic wall balloons due to blood pressure.
The aneurysms may be saccular (expanding to one side)
or fusiform (cylindrical). The wall of the aneurysm is
commonly calcified and the lumen is commonly lined
by old laminated thrombus.
Many aneurysms remain intact and are found as
an incidental finding at autopsy, but others eventually
rupture. The rupture may be repaired by either endovas-
cular or open surgical techniques if diagnosed in time,
but many individuals die too quickly for any help to be
given. The endovascular repair has a lower 30-day mor-
tality rate, but in both cases a mortality of around 20 per
cent if the patient was haemodynamically unstable, and
nearer 40 per cent if stable. The aorta lies in the retro-
peritoneal space and that is often where the bleeding is
found; it may lie to one side and envelop a kidney. Rarely,
the aneurysm itself, or the retroperitoneal haematoma,
74 Death from natural causes
(a)
(b)
Figure 6.6 (a) A saccular aneurysm of the abdominal
aorta. (b) A perforated abdominal aortic aneurysm:
forceps have been passed through the perforation.
(Courtesy of Richard Jones.)
ruptures through the retroperitoneal tissues to cause
haemoperitoneum.
Dissecting aneurysm of the aorta
The damage caused by an atheromatous plaque can also
result in an intimal defect and weakening of the media,
allowing blood from the lumen to dissect into this weak-
ened arterial wall. Once the dissection has started, the
passage of blood under pressure extends the dissection
along the aortic wall. The most common origin of a dis-
secting aneurysm is in the thoracic aorta and the dissec-
tion usually tracks distally towards the abdominal region,
sometimes reaching the iliac and the femoral arteries. In
fatal cases, the track may rupture at any point, resulting in
haemorrhage into the thorax or abdomen. Alternatively, it
can dissect proximally around the arch and into the peri-
cardial sac, where it can produce a haemopericardium,
cardiac tamponade and sudden death. Involvement of the
renal arteries can result in renal failure.
Dissecting aneurysms (Figure 6.7a and b) are princi-
pally found in individuals with hypertension, but may
also be seen in younger individuals with connective tis-
sue defects, such as Marfan syndrome, where there may
(a)
(b)
Figure 6.7 Thoracic aortic dissection. The origin of the
dissection is in the aortic root, just above the tricuspid
aortic valve (a) with a plane of dissection in the aortic
media (b). (Courtesy of Richard Jones.)
be medial degeneration. In such patients who survive
the initial dissection, there is a further risk of re-dissec-
tion in the future.
Syphilitic aneurysms
Syphilitic aneurysms are rare since the introduction of
antibiotics but should always be considered as an aetio-
logical factor in patients with aortic aneurysms. The rar-
ity reflects effective treatment of primary and secondary
syphilis, but they are still encountered in routine autop-
sies on old people and in individuals from areas without
an established healthcare system. The aneurysms are
thin walled; they are most common in the thoracic aorta
and especially in the arch. It is assumed Treponema
pallidum invades the aortic wall and the inflammatory
response progresses towards obliterative endarteritis
and necrosis of the muscular and elastic fibres in the
aortic media. This results in weakening of the aortic
 Cardiovascular system 75

wall and can lead to severe complications, represented (a)

by aortic aneurysm, aortic valvular insufficiency, aortic
root dilation and coronary ostial stenosis. The aneu-
rysms can rupture, causing massive haemorrhage.

Intracranial vascular lesions

Several types of intracranial vascular lesion are impor-
tant in sudden or unexpected death.

Ruptured berry (saccular) aneurysm

A relatively common cause of sudden collapse and often
rapid death of young to middle-aged men and women
is subarachnoid haemorrhage as a consequence of rup- (b) Aneurysm
ture of a berry (saccular) aneurysm of the basal cerebral
arteries, either in the circle of Willis itself (on the under Anterior
cerebral
surface of the brain) or in the arteries that supply it.
These are often described as congenital, but it may more
Anterior
appropriate to consider them as acquired, often shortly Middle
communicating
after birth. The aneurysms may be a few millimetres cerebral
in diameter or may extend to several centimetres; they
may be single or multiple and they may be found on
one or more arteries in about 1%–2% of the population Internal
(Figure 6.8a) and Figure 6.8b shows common sites for carotids
aneurysms related to the cerebral arteries. Posterior
The aneurysms may be clinically silent or they may communicating
leak, producing a severe headache, neck stiffness, Posterior
unconsciousness and sometimes paralysis or other neu- cerebral
rological symptoms. The rupture of a berry aneurysm on
Posterior
the arterial circle of Willis allows blood to flood over the cerebral
base of the brain or, if the aneurysm is embedded in the
brain, into the brain tissue itself. The precise mechanism Superior
cerebellar Basilar
of sudden death following subarachnoid haemorrhage
is not understood: bathing the brain-stem in blood may
invoke vascular spasm resulting in critical ischaemia
of cardiorespiratory control centres or the presence of Posterior
inferior Vertebral
subarachnoid blood under pressure may directly affect
cerebellar
such brain-stem cardiorespiratory control.
An area of controversy in forensic medicine is
the role of assault in the development of subarach- Figure 6.8 (a) Berry aneurysm of the proximal middle
noid haemorrhage from a ruptured berry aneurysm. cerebral artery and associated subarachnoid haemor-
Particular difficulties arise when rupture of an intra- rhage. (b) Common sites for aneurysms related to the
cerebral aneurysm follows an altercation not attended assorted cerebral and cerebellar arteries.
by any physical evidence of blunt force head injury; a
causative role for a transient elevation of blood pres-
sure, owing to the emotional ‘stress’ of the altercation, The individual collapses rapidly following such a blow –
is controversial and may be further complicated by and suffers a cardiac arrest – and is subsequently found
alcohol or drug intoxication. The causation of either to have a basal subarachnoid haemorrhage associated
death or, in those that survive, the life-changing effects with a ‘tear’ in an intracranial blood vessel, often a ver-
is often a matter of long debate in criminal cases. tebral artery. Microscopy of the relevant artery reveals
An additional entity frequently encountered in foren- no evidence of an intrinsic vascular abnormality and
sic pathology practice is that of ‘traumatic basal sub- toxicological analysis reveals no evidence of stimulant
arachnoid haemorrhage’. The common scenario in such drugs, such as cocaine or amphetamine. Issues that may
cases is of an individual, often intoxicated by alcohol or become relevant in court relate to whether the death was
drugs, sustaining a blow to the head or neck which results caused by, for example, a punch or by the impact of the
in a rapid extension and rotation of the head on the neck. head on the ground after the punch. Often it is impossible
76 Death from natural causes

to know. Criteria for ascribing such basal subarachnoid

haemorrhage to trauma have been proposed, but such
cases are often complicated by a lack of independent wit-
ness evidence to the incident, although the wider usage
of CCTV and mobile phone recordings has in some cases
enabled clear links between mechanisms and pathologi-
cal outcome to be confirmed. The post mortem demon-
stration of such intracranial vascular injury requires
careful in situ dissection techniques, preferably under
operating microscopy, in order to exclude artefactual
vascular disruption.

Cerebral haemorrhage, thrombosis and

infarction
Sudden bleeding into brain tissue is common, usually in
old age and in those with significant hypertension and,
together with cerebral thrombosis and resulting brain
infarction, is the commonest cause of the well-recog-
nised cluster of neurological signs colloquially termed a
‘stroke’.
The term cerebrovascular accident (CVA) is in com-
mon usage in such circumstances, both as a clinical
diagnosis and as a cause of death. If the exact cause
is known it is useful to apply the specific term that
describes the aetiology (cerebral haemorrhage or cere-
bral infarction) or, if the aetiology is unknown, to use
the generic term cerebrovascular lesion (Figure 6.9).
Spontaneous intracerebral haemorrhage is most
often found in the external capsule/basal ganglia of one
cranial hemisphere and arises from rupture of a micro-
aneurysm of the lenticulo-striate artery, often referred
to in the past as a Charcot–Bouchard aneurysm. This
nomenclature is probably inappropriate, but irrespec-
tive of the name arterial rupture causes sudden expan-
sion of a haematoma which compresses the internal
capsule and may destroy some of it, leading to hemiple-
gia (Figure 6.10).
Figure 6.9 Acute cerebral infarction (­ predominantly
middle cerebral artery territory).
(Courtesy of Richard Jones.)
*
Figure 6.10 Recent intracerebral haemorrhage
in a hypertensive individual (*), the dark areas showing
blood clot.
Death in such circumstances is not usually sudden,
although there is a complex interaction between the
brain and the heart, and thus a stroke affecting a region
of the brain important in such control can precipitate a
cardiac arrest.
Respiratory system
The major cause of sudden death within the respiratory
organs is vascular. Pulmonary embolism (PE) is very
common and is the most clinically under-diagnosed
cause of death. It is the third most common life-threaten-
ing condition after myocardial infarction and stroke. In
almost every case, the source of the emboli is in the deep
leg or pelvic veins (Figure 6.11a and b). PE is a manifesta-
tion of venous thromboembolism (VTE). PE shares risk
factors with deep vein thrombosis (DVT) and is regarded
as a consequence of DVT rather than a separate clinical
entity. Risk factors for VTE include major surgery, major
trauma, high age, myocardial infarction, chronic heart
failure, prolonged immobility, malignancy, thrombo-
philia and prior VTE. Tissue trauma, especially where it
is associated with immobility or bed rest, is a very com-
mon predisposing factor in the development of DVT. Most
thromboses remain silent and cause no problems, but a
proportion embolise and block pulmonary arteries of
varying size. Large thromboemboli can occlude the ori-
gin of the pulmonary arteries (saddle emboli), resulting in
massive acute right-heart strain and failure as a result of
mechanical blockage, whereas smaller thromboemboli

(a)
(b)
Figure 6.11 Fatal pulmonary thromboembolism.
(a) Thrombus which has formed in life has broken away
from the peripheral circulation to be transported in the
bloodstream to this lung, where it has lodged in, and
occluded, a pulmonary vein. Note how the thromboem-
bolus protrudes from the cut end of the occluded blood
vessel (*). (b) Microscopic appearance. ([a] From Burton J,
Saunders S, Hamilton S. Atlas of Adult Autopsy P
­ athology.
Boca Raton: CRC Press 2015 (Fig 4.37b, page 96)
with p
­ ermission.)
become lodged in smaller-calibre pulmonary blood ves-
sels where they interfere with pulmonary function and
lead to myocardial ischaemia and cardiac arrest.
Even without any risk factors some PEs occur unex-
pectedly in normal, ambulant people who have reported
no clinical symptoms. This sometimes makes establish-
ing the causal relationship between death and an injuri-
ous event difficult. For the purposes of civil law (where
the standard of proof for causation is ‘on the balance of
probabilities’) the embolism can often be linked to the
trauma, but in a criminal trial in which a higher stan-
dard of proof (‘beyond reasonable doubt’) is required,
it may be much harder to demonstrate a causal link
between the two events.
Other rare causes of sudden death in the respiratory
system (excluding bronchial asthma which is covered
Gynaecological conditions 77
Figure 6.12 Disseminated pulmonary tuberculosis (TB).
Note also the cavitating (secondary TB) lesion.
separately below) include massive haemoptysis from
cavitating pulmonary tuberculosis or from an invasive
tumour (Figure 6.12). Rapid (but not sudden) deaths can
also occur from fulminating chest infections, especially
severe forms of influenza.
Gastrointestinal system
The main causes of sudden death in the gastrointesti-
nal system are predominantly vascular in nature; severe
bleeding from a gastric or duodenal peptic ulcer can be
fatal in a short time, although less catastrophic bleed-
ing may be amenable to emergency medical/surgical/
endoscopic intervention (Figure 6.13a). Bleeding from
oesophageal varices as a result of portal hypertension
from any cause has a significant mortality that increases
after a first event (Figure 6.13b).
Mesenteric thrombosis and embolism, often related
to aortic or more generalised atherosclerosis, may result
in infarction of part of the small or large intestine. The
diagnosis may be unclear and a rapid but not sudden
death is likely if the infarction remains undiagnosed.
Intestinal infarction owing to a strangulated hernia,
or obstruction owing to torsion of the bowel as a con-
sequence of adhesions, can also be rapidly fatal (Figure
6.14a and b).
Peritonitis, following perforation of a peptic ulcer,
diverticulitis or perforation at the site of a colonic
tumour for example, can be fatal if not treated (Figure
6.15) and even when treated has a significant mortality.
Often these conditions present as sudden death
because of failure to seek medical assistance early after
symptom onset, by which time the effects of sepsis are
overwhelming.
Gynaecological conditions
When a female of childbearing age is found deceased,
a complication of pregnancy must be considered to be
the most likely cause of death until other causes have
78 Death from natural causes

(a) (a)

(b) (b)

Figure 6.13 (a) A perforated duodenal ulcer.

(b) Oesophageal varices seen as longitudinal darker lines Figure 6.14 (a) Intestinal infarction following volvulus
in the lining of the oesophagus which in this case has of the sigmoid colon. (b) Small bowel infarction showing
been turned inside out at autopsy. infarcted loops of small intestine.

been excluded. Abortion is a particular risk in countries in high-income countries is 1 in 3300, compared to 1 in 41
where legal abortion is not available. in low-income countries. UK evidence suggests a mortal-
A ruptured ectopic pregnancy, usually in a Fallopian ity rate of ∼8.5/100,000 during pregnancy or shortly after
tube, is another serious obstetric emergency that can childbirth of which heart disease was the most significant
result in death from intraperitoneal bleeding unless figure, contributing to 2/100,000. There is an international
rapidly treated by surgical intervention (Figure 6.16).
Maternal deaths (occurring during pregnancy or
within 12 months of parturition in the UK) can be clas-
sified into ‘direct’ deaths (caused by diseases specifically
related to pregnancy, such as pulmonary thromboem-
bolism, pre-eclampsia, obstetric haemorrhage, amniotic
fluid embolism, acute fatty liver of pregnancy or ectopic
gestation), ‘indirect’ deaths (from pre-existing disease
exacerbated by pregnancy such as congenital heart dis-
ease or a cardiomyopathy) or ‘coincidental’ deaths.
From 1990 to 2015, the global maternal mortality
ratio declined by 44 per cent – from 385 deaths to 216
deaths per 100,000 live births, according to UN data. This
gives an average annual rate of reduction of 2.3 per cent.
Almost all maternal deaths can be prevented, as evi- Figure 6.15 Peritonitis. Note the fibrinous d
­ eposits on
denced by the huge disparities found between the richest the surface of loops of intestines.
and poorest countries. The lifetime risk of maternal death (Courtesy of Richard Jones.)
 Deaths from asthma and epilepsy 79

(a)

(b)

Figure 6.16 Ectopic pregnancy leading to rupture

of the Fallopian tube and massive intra-abdominal
­haemorrhage.

strategy aimed at reducing the global maternal mortality

ratio (MMR) to less than 70 per 100,000 live births by 2030.
There are also country-level targets: The primary national
target is that by 2030, every country should reduce its
MMR by at least two-thirds from its 2010 baseline. The
secondary target, which applies to countries with the
highest maternal mortality burdens, is that no country
should have an MMR greater than 140 deaths per 100,000
live births by 2030. (c)

Deaths from asthma and epilepsy

Deaths from acute asthma occur even with increasingly
effective pharmacological control of this chronic condi-
tion. ‘Acute asthma’ may be triggered by a number of
common and household allergens, as well as commonly
abused drugs such as heroin and crack cocaine (particu-
larly when it is smoked). In hospital, mortality may be in
the order of 10 per cent if the patient requires mechani- *
cal ventilation. Studies suggest that deaths in people
with asthma may relate substantially to co-morbidities,
of which the pathologist must be aware. Visual autopsy
Figure 6.17 Bronchial asthma. (a,b) Microscopy dem-
findings include hyper-inflated lungs and plugging of
onstrating airway ‘remodelling’, mucus distension and
the airways by tenacious, viscous mucus. Microscopy
inflammatory cell infiltration, including neutrophils and
of the lungs commonly reveals chronic airway remod-
eosinophils. (c) Acute bronchial asthma: the lungs are
elling, with basement membrane thickening, goblet cell
hyperinflated, cover the pericardium in the midline (the
and smooth muscle hyperplasia, and super-imposed
heart can only just be seen in this photograph – asterisk),
airway inflammation with eosinophils (Figure 6.17a–c).
and do not collapse when removed from the chest cavity
An anaphylactic component may be responsible for
at autopsy. Such an appearance is similar to the classic
a fatal outcome, and post mortem blood sampling for
appearance of ‘emphysema aquosum’ seen in drowning,
mast cell tryptase is often rewarding.
and can usually be distinguished from drowning by the
Epilepsy is a condition in which a person has recur-
circumstances of the death, and by microscopy. (From
rent seizures. Epilepsy is common and more than 2 per
Burton J, Saunders S, Hamilton S. Atlas of Adult Autopsy
cent of the population will have two or more seizures
Pathology. Boca Raton: CRC Press 2015; Fig. 4.31 page 93.)
during their lives. A seizure is defined as an abnor-
mal, disorderly discharging of the brain’s nerve cells,
80 Death from natural causes

resulting in a temporary disturbance of motor, sen-
sory or mental function. There are many types of sei-
zures, depending primarily on what part of the brain
is involved. The term epilepsy says nothing about the
type of seizure or cause of the seizure, only that the
seizures happen again and again. Seizures that have
no known underlying cause may be called primary or
idiopathic epilepsy. A seizure may start as a partial,
or focal, seizure, involving the face or arm. Then the
muscular activity spreads to other areas of the body.
Healthy people may have seizures under certain cir-
cumstances. If the seizures have a known cause, the
condition is referred to as secondary or symptomatic
epilepsy. Some of the more common causes include
the following: head injuries; toxic chemicals or drugs
of abuse; alcohol or benzodiazepine withdrawal; and
stroke. There may be specific reasons why a person
with epilepsy may die (e.g., drowning as a result of a
seizure while swimming), but there are approximately
500 sudden and unexpected deaths in epileptics each
year in the UK where the precise cause of death is not
identified. Such deaths have been classified as Sudden
Unexpected Death in Epilepsy (SUDEP), defined as a
‘sudden unexpected, witnessed or unwitnessed, non-
traumatic and non-drowning death in epilepsy, with
or without evidence of a seizure, and excluding docu-
mented status epilepticus, where post mortem exami-
nation does not reveal a toxicological or anatomic
cause of death’ (Figure 6.18). The rate of sudden death
in epilepsy may be >20 times the incidence rate of sud-
den death in the total population of the same age.
The mechanism of death in such cases is uncertain,
but may be related to a seizure-induced arrhythmia,
seizure-mediated inhibition of respiratory centres or a
complication of anti-epileptic treatment. Post mortem
findings in SUDEP are non-specific (e.g., pulmonary
oedema and congestion) and the utility of the presence of
a tongue injury in diagnosing a seizure is c­ ontroversial.

Generalised tonic-clonic seizure

Spread to respiratory Spread to cardiovascular

Spread to midbrain
centres in medulla centres in medulla

Ascending arousal Respiratory Serotonin neuron

system inhibition nuclei inhibition inhibition

Loss of
arousal
? ?
PGES Hypoventilation/
Apnoea

Predisposing
factors Cardiac autonomic
neuron dysfunction
Prone/face
down Congenital
Sleep/Sleep Arrhythmias/ LQTS
apnoea Asystole
Intrinsic cardiac
Intrinsic
dysfunction
pulmonary
dysfunction SUDEP/death

Figure 6.18 Pathophysiological mechanisms underlying sudden unexpected death in epilepsy (SUDEP). SUDEP often
results from a generalised tonic-clonic seizure, which leads to inhibition of specific midbrain and medulla-mediated
effects via an unknown pathway. Other factors shown may predispose these patients to SUDEP. (Abbreviations:
LQTS, long QT syndrome; PGES, postictal generalised EEG suppression). (From Dlouhy BJ, Gehlbach BK, Richerson GB.
Sudden unexpected death in epilepsy: basic mechanisms and clinical implications for prevention. J Neuro Neurosurg
Psych 2016; 87:402–413; Fig. 3 page 408.)

Neuropathological examination of the brain is
important in order to exclude the presence of a lesion
capable of providing an explanation for seizure activity,
(e.g., non-recent brain injury; arteriovenous malforma-
tion; tumour). At present, the pathogenesis is considered
to be multifactorial. Potential neuroimaging biomarkers
have been identified but as yet these remain as research,
rather than clinicopathological tools.
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7 Deaths and injury in infancy
▪▪ Introduction
▪▪ Stillbirths
▪▪ Infanticide
▪▪ The estimation of maturity of a newborn baby or fetus
Introduction
The outcomes of disease and trauma may be expected
to be the same in individuals of all ages but, in practice,
the anatomical and physical differences between chil-
dren, younger adults and older adults may vary. This
may be due to different body proportions, structural
differences and metabolic changes. Specific features
of injuries to infants and children require their own
particular consideration. Some of these considerations
relate to the law, and some to medical and pathological
factors. Newborns, infants, toddlers, younger children
and adolescents have their own unique problems, such
as stillbirth and sudden infant death syndrome, which
are different from those of fully developed adults. They
may also be dependent on others, have a range of vul-
nerabilities and be at risk of abuse, whether emotional,
physical or sexual.
Stillbirths
The Births and Deaths Registration Act 1953, as
amended by the Stillbirth Definition Act 1992, provides
for the registration of all babies born after 24 or more
weeks completed gestation that did not, at any time,
breathe or show signs of life, as stillbirths in England &
Wales. Similar definitions apply in Scotland & Northern
Ireland. There are no provisions to allow the registra-
tion of stillbirths before the 24th week of pregnancy.
Prior to 1992, only babies born showing no sign of life
after the 28th week of gestation were counted as hav-
ing been stillborn. Registrations for stillbirths began
on 1 July 1927 in England & Wales when the annual
­estimated number of stillbirths was calculated as 26,021
(14,519 males and 11,502 females). The numbers steadily
decreased during the 20th century and in 2017 the num-
ber stood at 3284. The ratio of male stillbirths to female
stillbirths was 1:1 in 2013. The causes of many stillbirths
remain unknown, but may include maternal infections
in pregnancy, maternal disorders (especially hyperten-
sion and diabetes), intrauterine infections, birth trauma
or congenital abnormalities.
▪▪ Child abuse
▪▪ Child sexual abuse
▪▪ Bibliography and information sources
▪▪ Further general resources
If death occurs more than a couple of days before
birth, the fetus is commonly macerated because of the
effects of early decomposition combined with exposure
to fluid (Figure 7.1). The infant is discoloured, usually
a pinkish-brown or red, with extensive desquamation
of the skin; the tissues have a soft, slimy translucence
and there may be partial collapse of the head with over-
riding of the skull plates. The appearance of the child is
quite different from that seen in an infant that has died
following a live birth and then begun to putrefy. Because
many, if not most, of these deaths occur after the onset of
labour and during the process of birth itself, no evidence
of maceration will be present.
The Infant Life (Preservation) Act 1929 made it an
offence to destroy a baby during birth; however, an
exception was made in the Act for doctors acting ‘in
good faith’ who, to save the life of the mother, have to
destroy a baby that becomes impacted in the pelvis dur-
ing birth.
As babies that are stillborn have never ‘lived’ in the
legal sense, they cannot ‘die’ and so a death certificate
cannot be issued. Currently, in England & Wales, a
­special ‘stillbirth certificate’ may be completed either
by a doctor or a midwife if either was present at the birth
or by either one of them if they have examined the body
of the child after birth.
The causes of stillbirth are varied and may be unde-
terminable, even after a full autopsy. Indeed, it may be
impossible to determine on the pathological features
alone if the death occurred before, during or after birth.
Infanticide
The term infanticide has a very specific meaning in
the many countries that have introduced legislation
designed to circumvent the criminal charge of murder
when a mother kills her child during its first year of life.
In England & Wales, Section 1 of the Infanticide Act
1938 states that:
Where a woman by any wilful act or omission causes the
death of her child … under the age of twelve months, but
at the time … the balance of her mind was disturbed by
84 Deaths and injury in infancy
Figure 7.1 Maceration following intrauterine death. Note
the widespread skin slippage and the umbilical cord
around the neck.
reason of her not having fully recovered from the effect
of giving birth to the child or by reason of the effect of
lactation consequent upon the birth of the child, then
… she shall be guilty of … infanticide, and may … be
dealt with and punished as if she had been guilty of the
offence of manslaughter of the child.
Because manslaughter is a less serious charge than
murder and does not result in the mandatory penalty
of life imprisonment that is attached to murder, a ver-
dict of infanticide allows the court to make an appro-
priate sentence for the mother, which is more likely to
be probation and psychiatric supervision than custody.
The Infanticide Act indicates that the law recognises the
special nature of infanticide.
In England & Wales, there is a legal presumption
that all deceased babies are stillborn and so the onus
is on the prosecution, and hence the pathologist, to
prove that the child was born alive and had a separate
existence. In order to do this, it must be shown that the
infant breathed or showed other signs of life, such as
movement or pulsation of the umbilical cord, after hav-
ing been completely expelled from the mother.
In the absence of eyewitness accounts, pathologists
can make no comment about the viability or otherwise
of a baby at the moment of complete expulsion from the
mother. They may be able to give an opinion on the pos-
sibility of separate existence if they can establish that the
child had breathed. However, establishing that breath-
ing had taken place is not incontrovertible evidence of
(a)
(b)
Figure 7.2 (a) Thoracic organs from a stillbirth. The lungs
are firm and heavy with no crepitation when squeezed. (b)
Microscopy of lungs from stillbirths showing partial expan-
sion of terminal air spaces as a consequence of hypoxia-
induced inspiratory efforts. Note also meconium aspiration.
([a] Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
a ‘separate existence’, as a baby in a vertex delivery can
breathe after the head and thorax have been delivered but
before delivery of the lower body.
The ‘lung flotation test’, used as the definitive test
for breathing, and hence a separate existence, and
depended upon for years, came to be considered unre-
liable. A study recently explored this, however, and
suggested that the test was reliable in 98 per cent of
cases. The authors concluded that although there was
not a single false-positive result (where the lungs of a
stillborn individual floated) there were cases where a
live born child’s lungs did not float. Nevertheless, lungs
that don’t float cannot be taken as proof that a newborn
never breathed at all (Figure 7.2a and b).
To complicate matters further, deceased newborn
babies may be concealed shortly after birth and may
not be discovered until decomposition has begun,
which precludes any reliable assessment of the state of
 The estimation of maturity of a newborn baby or fetus
Figure 7.3 Newborn infant disposal with
­ ecompositional/putrefactive skin changes.
d
(Reproduced with p ­ ermission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
expansion of the lungs. Even with fresh bodies, the prob-
lems are immense and any prior attempt at ventilation or
chest compression during cardiopulmonary resuscita-
tion (CPR) negates any reliable opinion being given on
their having been spontaneous breathing after birth.
There are other indicators of life, for example, if
there is confirmed milk in the stomach (which must
have been consumed) or if the umbilical cord remnant
is shrivelled or shows an inflammatory ring of impend-
ing separation, the child must have lived for some time
after delivery.
Establishing the identity of the infant and the iden-
tity of the mother can be problematic, as the deceased
child may often be hidden or abandoned (Figure 7.3).
Often the standard detective work of establishing facts,
taking statements, and reviewing CCTV footage may
provide clues. Ultimately, DNA will be used to confirm
identity and parentage if it is unclear.
In those cases where the mother is traced, further legal
action depends on whether the pathologist can definitely
decide if the baby was born alive or was stillborn. If live-
born, no charge of infanticide can be brought in English
law unless a wilful act of omission or commission can be
proved to have caused the death. Omission means the
deliberate failure to provide normal care at birth, such
as tying and cutting the cord, clearing the air passages
of mucus and keeping the baby warm and fed. The wil-
ful or deliberate withholding of these acts, as opposed to
simple ignorance and inexperience, may be hard to prove
to the criminal standard. Acts of commission are more
straightforward for the ­doctor to demonstrate as they
may include a range of trauma, including head injuries,
stabbing, drowning and strangulation.
The maturity of the infant is rarely an issue as most
infants found deceased after birth are at or near full
term of 38–40 weeks. The Human Embryology and
Human Fertilisation Act 1990 lowered the legal limit
85
from the 28 weeks previously set under the Abortion
Act 1967. Before that, abortions were illegal in England
& Wales. Abortion after 24 weeks can be carried out
after that time if there is grave risk to the life of the
woman or severe fetal abnormality. An abortion must
be agreed by two doctors (or one in an emergency) and
carried out by a doctor in a ­government-approved hos-
pital or clinic. The limit of 24 weeks broadly represents
the point at which a fetus is said to become ‘viable’.
However, babies born this early do have some chance
of survival, and some born even earlier have survived.
In infanticide, the maturity is not legally material as it
is the deliberate killing of any baby that has attained a
separate existence, and this does not depend directly
upon the gestational age.
The estimation of maturity of a
newborn baby or fetus
An estimation of gestational age of the body of a baby or
fetus in relation to an abortion, stillbirth or alleged infan-
ticide may be required for police investigation and crimi-
nal proceedings. A rough estimate may be provided by
Haase’s Formula (described by the German obstetrician
Carl Friedrich Haase in the first half of the 19th century):
fetal length in centimeters during the first 3 to 5
months of pregnancy correlates to the square of the age
in months, and during the second half of pregnancy the
age in months is multiplied by 5
The accuracy of this formula does not appear to have
been assessed in published studies.
There is considerable variation in any of the mea-
sured parameters owing to sex, race, nutrition and indi-
vidual variation, but it is possible to form an estimate of
the maturity of a fetus by using the brief notes in Box 7.1.
In living (from extremely premature to all newborn
infants) the New Ballard Score can be used. The New
Ballard Score is a set of procedures developed by Dr.
Jeanne L Ballard to determine gestational age through
neuromuscular and physical assessment of a newborn
infant. Some elements of this may be adaptable to assist
in the maturity of the deceased, although more research
in this area is required. A systematic review in 2017 by
Lee and colleagues identified limitations in such gesta-
tional age estimation techniques.
Post mortem maturity may also be assessed using
anthropological, histological, and radiological tech-
niques, reviewing, for example, the femur length, ossi-
fication centres and the histological appearances of the
major organs. Gestational age determination (in the
same way as post mortem age determination and age
determination in the living) should always now be con-
sidered a multiprofessional exercise, but there are few
recent peer-reviewed studies in this field.
86 Deaths and injury in infancy

Box 7.1 Estimation of fetal maturity

4 weeks 1.25 cm, showing limb buds, enveloped in villous chorion.
12 weeks 9 cm long, nails formed on digits, placenta well-formed, lanugo all over body.
20 weeks 18–25 cm, weight 350–450 g, hair on head.
24 weeks 30 cm crown–heel, vernix on skin.
28 weeks 35 cm crown–heel, 25 cm crown–rump, weight 900–1400 g.
32 weeks 40 cm crown–heel, weight 1500–2000 g.
36 weeks 45 cm crown–heel, weight 2200 g.
40 weeks 48–52 cm crown–heel, 28–32 cm crown–rump, 33–38 cm head circumference, lanugo now absent or
(full term) present only over shoulders, head hair up to 2–3 cm long, testes palpable in scrotum/vulval labia close
the vaginal opening, dark meconium in large intestine.

Unexplained deaths in infancy • The incidence is markedly greater in multiple

The reported figures for unexplained deaths in England
& Wales represent infant deaths (deaths under one
year of age) that occurred in the calendar year referred
to. Unexplained infant deaths include sudden infant
deaths (SIDS – ‘cot deaths’) coded to the International
Classification of Diseases Tenth Revision (ICD-10) code
R95 and unascertained deaths (ICD-10 code R99). The
latter are infant deaths where no medical cause was
recorded.
There were 219 unexplained infant deaths in England
& Wales in 2016, an increase compared with 2015 (195),
but still lower than in 2006 (285). In 2016, the unex-
plained infant mortality rate rose to 0.31 deaths per 1000
live births. Unexplained infant deaths accounted for 8.3
per cent of all infant deaths occurring in 2016. In 2016,
the unexplained infant mortality rate remained the
highest amongst mothers aged less than 20 years (0.98
deaths per 1000 live births). These numbers, however,
have substantially reduced over recent decades gener-
ally coinciding with social and housing improvements,
and campaigns such as the ‘Back to Sleep’ campaign
in the early 1990s, which encouraged mothers to place
babies on their back to sleep rather than face down or
on their side. Advice to mothers to refrain from smoking
during pregnancy or near to their babies after birth, and
to avoid overheating babies by wrapping them up too
closely, have all impacted infant mortality rates.
Sudden infant death syndrome (SIDS) is defined as
the sudden death of an infant less than 1 year of age
that remains unexplained after a complete autopsy and
death scene investigation, and remains the most com-
mon cause of death in the post-perinatal period in coun-
tries with a relatively low infant mortality rate.
The following are the main features of the syndrome.
• Most deaths take place between 1 month and
6 months, with a peak at 2 months.
• There is little sex difference, although there is a
slight preponderance of males similar to that seen
in many types of death.
births, whether identical or not. This can partly be
explained by the greater incidence of premature
and low birth-weight infants in multiple births.
• There is a marked seasonal variation in temperate
zones: SIDS is far more common in the colder and
wetter months, in both the northern and southern
hemispheres.
• There are apparent social, racial and ethnic dif-
ferences, but these are explained by fundamental
underlying socio-economic factors, which show
that there is a higher incidence in any disadvan-
taged families such as those with poor housing,
lower occupational status, one-parent families,
etc. However, no class, race or creed is exempt from
these devastating deaths.
The essence of SIDS is that the deaths are unexpected
and autopsy reveals no adequate cause of death. The his-
tory is usually typical: a perfectly well child – or one with
trivial symptoms – is put in the sleeping place at night
only to be found dead in the morning. At autopsy, noth-
ing specific is found in the true SIDS death, although in
about 70 per cent of cases the autopsy reveals intratho-
racic petechiae on the pleura, epicardium and thymus,
which formerly gave rise to the misapprehension that
SIDS was caused by mechanical suffocation. These pete-
chiae are now believed to be agonal phenomena and not
an indicator of the cause of death (Figure 7.4).
The aetiology of SIDS is unknown, but it is believed
to be multifactorial. A large variety of possible causes
have been suggested, including allergy to cow’s milk or
house-mites, botulism, prolonged sleep apnoea, spinal
haemorrhages, deficiencies of liver enzymes, selenium
or vitamin E, various metabolic defects, vaccinations,
hyperthermia, hypothermia, carbon monoxide or diox-
ide poisoning, viral bronchiolitis, muscle hypotonia and
abnormal development of key cardiorespiratory control
areas in the brainstem. As yet, none of these has been
substantiated. Changes in the ways in which unex-
pected infant deaths are categorised by pathologists and

Figure 7.4 Multiple petechiae on the surface of the thy-
mus and right lung in a sudden infant death. (Reproduced
from Keeling J and Busuttil A. Paediatric Forensic Medicine
and Pathology. London: Hodder Arnold, 2008.)
death investigators, and increasing caution in applying
the term ‘sudden infant death syndrome’, make assess-
ment of nationally and internationally collected data on
incidence potentially inaccurate and confusing.
As with sudden unexplained death in the adult, it is
likely that causes not detectable by macroscopic or
microscopic means, but by molecular biological tech-
niques, may be found to be relevant in at least some
cases. Recent studies, however, indicate that it appears
only a small proportion will be due to cardiac genetic
predisposition, and it appears that it is the same for
other genetic causes.
All healthcare professionals must certainly be vigi-
lant when involved in the assessment of any infant
death. A key concern in the management of SIDS is
to support the parents and family by keeping them
informed of any developments and ensuring that the
appropriate bereavement counselling services estab-
lished in many developed countries are made available.
Child abuse
Child abuse is a generic term that includes all forms
of physical and emotional ill-treatment, sexual abuse,
neglect and exploitation that results in actual or poten-
tial harm to the child’s health, development or dignity.
In 1946, Caffey and colleagues described multiple frac-
tures in the long bones of infants suffering from chronic
subdural haematomas (SDH). Previously in the 19th
century, Tardieu described similar phenomena. Over
50 years have passed since Kempe and colleagues pub-
lished ‘The Battered Child Syndrome’, describing harm
Child abuse 87
from inflicted injury mechanisms derived from parents
and caregivers. From this emerged a rapidly expand-
ing literature on paediatric forensic medicine and child
protection and safeguarding, which has offered new
insights into the extent of the problem, injury mecha-
nisms, and the sequelae of abuse and neglect, informing
diagnosis and guiding clinical practice in the treatment
and management of children who become involved in
the child protection system.
After many inquiries, in many jurisdictions, and with
medical professionals often uncomfortably subject to
media and regulatory scrutiny, there have been improve-
ments in child protection and forensic practices result-
ing in recognition of the need for specialised forensic
training, improved funding, development of resources
and development of professional standards that sup-
port accountable, objective, safe and robust practice.
However, child abuse remains a major social problem,
and few medical specialties are excluded from involve-
ment. The assessment of living and deceased potentially
abused children involves not only forensic physicians
and forensic pathologists, but paediatricians, primary
care physicians, general practitioners, psychiatrists
and safeguarding teams. Many others may be involved
including social workers and school teachers.
In England & Wales familial homicide, as laid out
by the Domestic Violence, Crime and Victims Act 2004,
carries a prison sentence of up to 14 years. The Act closed
a legal loophole that allowed those jointly accused of the
murder of a child or vulnerable adult to avoid prosecu-
tion by remaining silent or blaming each other. The Act
placed a clear legal responsibility on adults who have
frequent contact with a child or vulnerable adult to take
reasonable steps of protection if they knew or should
have known the child or vulnerable adult was at signifi-
cant risk of serious physical harm from members of that
household.
Epidemiology
Physical abuse of children occurs in males and females
of any age. The spectrum of injury may vary. Fatalities
are more common in children under the age of 2 years
and the most common mode of death is head injury. The
upper age limit is very difficult to define: physical abuse
is more likely to stop at a younger age, whereas sexual
abuse may continue into the teens and even older.
When injuries (or cutaneous marks and scars) are
evident in infants and children, the most common
issues of contention are whether they are caused by
accident or abuse (non-accidental injury [NAI]). In both
the living and deceased child, the distinctions may be
impossible to determine. There has been an increasing
availability of good quality evidence relating to the clin-
ical assessment of paediatric injury, marks and scars,
and knowledge of this evidence-base is crucial in the
proper interpretation of such cases.
88 Deaths and injury in infancy
Injuries in the deceased child
Post mortem in children
The post mortem examination of a child is a specialised
procedure that must be carried out by a pathologist with
specific training and experience in paediatric autopsy
pathology. In many jurisdictions, dedicated perinatal
and paediatric pathologists make these examinations
in regional specialist centres.
Full radiological skeletal surveys precede the physi-
cal examination of the body, and evidence of old or
recent fractures usually results in a medicolegal autopsy
to exclude assault. The need for detailed documenta-
tion during the autopsy is similar to that involved in
adult autopsies, and the procedure progresses from
an inspection of the surface of the body to the internal
organs in a similar manner.
The procedure is adapted to take account of develop-
ment-specific differences between children and adults;
the presence of incomplete skull bone fusion, and rem-
nants of the fetal circulation, for example. A detailed
description of the perinatal and paediatric autopsy
is beyond the scope of this book, and the interested
reader is directed to specialist texts listed at the end of
this chapter.
It is essential that as much information (including
accounts of all witnesses, pre-existing medical records,
and school records) be reviewed. When a child dies or
is seriously harmed as a result of abuse or neglect, a
review is conducted to identify ways that profession-
als and organisations can improve the way they work
together to safeguard children and prevent similar inci-
dents from occurring again. Each UK nation has its own
terminology and guidance for carrying out and sharing
the learning from the reviews. Cases that meet the cri-
teria set out in the relevant guidance are reviewed by
multi-agency panels.
In England, Child Death Overview Panels (CDOP)
are tasked with collecting and reviewing information
about each child death with a view to identifying: any
case giving rise to the need for a review mentioned in
Regulation 5(1)(e) of the Local Safeguarding Children
Board Regulations 2006; any matters of concern affect-
ing the safety and welfare of children; and any wider
public health or safety concerns arising from a particu-
lar death or from a pattern of deaths. The Government
publishes a series of standardised forms recording data
about child deaths. Figures 7.5 and 7.6 show examples.
Form A is used for notification of a child death and Form
B4 for Sudden Unexpected Death in Infancy.
Bruising
The features of bruises that are important can be summed
up as site, age and pattern. Bruising of the arms and legs,
especially around the upper arms, forearms, wrists,
ankles and knees, may be evidence of gripping by an
adult. Bruises on the face, ears, lips, neck, lateral thorax,
anterior abdomen, buttocks and thighs require an expla-
nation, as these sites are less likely to be injured in child-
hood falls (Figures 7.7–7.9). In very general terms, bruises
over soft tissue areas in non-mobile infants, bruises that
carry an imprint of an implement and multiple bruises of
uniform shape are suggestive of some forms of physical
abuse.
The explanation given by the carers of how each
bruise came to be present on the child must be docu-
mented with great care. This is because frequently an
interpretation may be required comparing the injuries
documented with a ­variety of explanations in cases of
possible NAI.
Skeletal injury
Currently in the UK the Royal College of Radiologists
recommends that imaging should always include skel-
etal survey in children under two years of age and skele-
tal survey and CT head scan in children under one year.
Figure 7.10 shows the recommended images to be taken
in suspected physical abuse of children.
Children who are older than one year and have exter-
nal evidence of head trauma and/or abnormal neuro-
logical symptoms or signs should also have a CT head
scan. Skeletal surveys may occasionally be indicated in
older children and may include those with communi-
cation or learning difficulties who are unable to give a
full history or those where there is clinical suspicion of
bony injury.
Healing fractures (representing previous traumatic
episodes) can be visualised by radiological means
although histological assessment post mortem is more
precise.
Rib fractures are rarely accidental in children. They
may occasionally be associated with birth trauma, but
in general they are a feature of the application of sub-
stantial force. One particular pattern that may be seen
on X-ray or at autopsy comprises areas of callus on the
posterior ribs, often lying in a line adjacent to the verte-
brae, and giving a ‘string-of-beads’ appearance. This pat-
tern is interpreted as indicating an episode or episodes of
forceful squeezing of the chest by adult hands. The pos-
sibility that such posterior rib fractures can be caused by
cardiopulmonary resuscitation (CPR) is thought unlikely
on biomechanical grounds, as such fractures occur as a
result of anterior–posterior compression during ‘squeez-
ing’ of the chest. Anterolateral rib fractures as a conse-
quence of CPR are rare. The discovery of rib fractures in
an infant who has undergone CPR without underlying
bone disease or major trauma warrants a full child pro-
tection investigation (Figure 7.11a and b).
A skull fracture is a marker of significant force
applied to the head, and skull fractures are common in
 Child abuse 89

Notification of Child Death Form

CDOP Identifier (Unique identifying number assigned by CDOP administrator)

………………………………………….

Notification of Child Death

Notification to be reported to CDOP administrator at:
Secure email:
Tel:
The information on these forms and the security for transferring it to the CDOP
administrator should be clarified and agreed with your local Caldicott guardian.
Please remember it is a statutory requirement to notify CDOP of all child deaths from birth up
to their 18th birthday. If there are a number of agencies involved, liaison should take place to
agree which agency will submit the Notification. However, unless you know someone else has
done so, please notify CDOP with as much information as possible,

Child’s Details

Full Name of Child

Any aliases Male / Female

DOB / Age / / NHS No.

days/months/years

Address

Postcode

Name of school/nursery

Other significant household and family members (parents, siblings,

other relevant adults)

Name DOB Relaonship Address

Figure 7.5 Form A: Child death notification. (Continued)

90 Deaths and injury in infancy

Death details:

Date of death / /

Where was the child

when they died? 1

Suspected cause of
death

Case Management:

Y / N / NK
Is there to be a Joint Agency Response?

Y / N / NK
Death discussed with the medical examiner?
Y / N / NK
Death to be investigated by Coroner?
Y / N / NK
Post mortem examination?

Notification Details:
Please outline the circumstances leading to notification. Also include if any other
review is being undertaken (e.g. internal agency review); and whether any immediate
action is being taken as a result of this death.

1 The place where the child is believed to have died regardless of where death was confirmed. Where a child is
brought in dead from the community and no signs of life were recorded during the resuscitation, the place of death
should be recorded as the community location; where a child is brought in to hospital following an event in the
community and is successfully resuscitated, but resuscitation or other treatment is subsequently withdrawn, the place
of death should be recorded as the location within the hospital where this occurs

Figure 7.5 (Continued) Form A: Child death notification.  (Continued)

 Child abuse 91

Details of relevant agency contacts (please give as much information as you

have easily available to you):

√ Lead
Agency Name and contact details Professional
(only one
ck is
required)
Community
Paediatrician
Local Paediatrician/
Neonatologist
Terary Paediatrician/
Neonatologist
Other local or terary
specialists
GP

Midwife

Health Visitor

School Nurse

Obstetrician

Police – Collision
Invesgaon Unit or
Child Protecon
Children’s Social Care

Nursery/School
College/Or Local
Educaon Authority
Others (list all agencies
known to be involved)

Referral details

Date of referral / /

Name of referrer

Agency

Address

Tel Number

Email

Figure 7.5 (Continued) Form A: Child death notification.

92 Deaths and injury in infancy

Form B4 – Sudden unexpected death in infancy

CDOP Identifier (Unique identifying number) ………………………………………….

Form B4– Sudden unexpected death in infancy

(For unexpected deaths of infants and young children from birth to age 2 years)
Form B4 is to be completed by the SUDI paediatrician or designated
deputy, and will almost always be completed at or immediately after the
local case review meeting. In those rare instances where there is no
local case review meeting the SUDI paediatrician or designated deputy
should complete this form at the conclusion of the investigation.
Please answer all questions or circle or tick the “not known” option.
A. Predisposing or risk factors.
Please circle or tick your responses

Family:

Previous SUDI in first or second degree relative?

(i.e. sibling, half sibling, parent’s sibling or half sibling) Y N Not Known

Apparent life-threatening events in first or second degree relative?

(i.e. sibling, half sibling, parent’s sibling or half sibling) Y N Not Known

Mother smokes? Y N Not Known

Father smokes? Y N Not Known

Other smoking in household? Y N Not Known

Illicit substance use in household? Y N Not Known

This baby:

delivery at less than 37 weeks gestation? Y N Not Known

birthweight less than 2500g? Y N Not Known

twin, triplet or higher order birth? Y N Not Known

previous apparent life-threatening event? Y N Not Known

under medical or HV attention for poor growth? Y N Not Known

breast fed? (more than 1 day) Y N Not Known

immunisations up to date? Y N Not Known

regular pacifier (dummy) user? Y N Not Known

B. Circumstances of Death:

Had any signs of illness been identified in the baby in last 24 hours by the family,
carers or professionals? Y N Not Known

Figure 7.6 Form B4: Sudden death. (Continued)

 Child abuse 93

Time from when the baby was last seen/heard to be alive and being found dead:
10 minutes
10 minutes–1 hour
1–2 hours
2–4 hours
4–6 hours
Not known
Time of day found dead:
24.00–06.00
06.00–12.00
12.00–18.00
18.00–24.00
Not known
Immediately before being found dead or collapsed was the child thought to be:
Awake
Asleep
Not known

If asleep, what position was child put down in?

Prone
Supine
Side
Other
Not known
When found what position was child in?
Prone
Supine
Side
Other
Not known

If thought to be asleep, where was the child sleeping?

Cot, crib, carry cot, Moses basket
Car seat
Adult bed (alone)
Adult bed (with another person)
Sofa (alone)
Sofa (with another person)
Floor
Other place (please specify)
Not known

Figure 7.6 (Continued) Form B4: Sudden death. (Continued)

94 Deaths and injury in infancy

If sharing a sleep surface with another person who was that person?
Mother
Father
Both parents
Sibling
Other (please specify)
Not known
If sharing a bed/other sleeping place with another person had that person taken
the following in the past 8 hours:

Alcohol (2 or more units) Y N Not Known

Cannabis Y N Not Known

Sedative drugs (prescribed or not) Y N Not Known

Opiates Y N Not Known

Other prescribed drugs (specify) Y N Not Known

Other illicit drugs/substances (specify) Y N Not Known

Did the child have a dummy when put down for last sleep? Y N Not Known

If sharing a sleep environment with another person was there any evidence of
overlying? Y N Not Known

If yes, please specify what this evidence was.

Was the sleeping place thought by those conducting the scene examination to be
hazardous? Y N Not Known

If so please specify what was thought to be hazardous.

Was resuscitation attempted when the child was found? Y N Not Known

Was a spontaneous circulation and/or breathing re-established?

Y N Not Known
How long after initial presentation to medical attention was the child declared
dead?
<1 hour
1–2 hours
2–6 hours
6–24 hours
>24 hours
Not known

Figure 7.6 (Continued) Form B4: Sudden death. (Continued)

 Child abuse 95

What samples/investigations were taken at time of presentation/resuscitation

or after death identified but before transfer to mortuary?
Blood culture Y N Not Known
CSF Y N Not Known
Blood for metabolic investigations Y N Not Known
Blood for toxicology Y N Not Known
Skin biopsy for fibroblast culture Y N Not Known
X-ray skeletal survey Y N Not Known
Other (specify)
Was an initial multi- agency discussion meeting held (telephone or face to face) in
the first 24 hours after the death? Y N Not Known

Which agencies were involved in the initial discussion meeting?

Secondary (hospital) paediatrics Y N Not Known

General practitioner Y N Not Known
Health visitor Y N Not Known
Community Paediatrics Y N Not Known
Other health professionals (specify) Y N Not Known
Police Child Abuse Investigation Team Y N Not Known
Other police (specify) Y N Not Known
Children’s services (Social care) Y N Not Known

Other Social Care (specify) Y N Not Known

Other professional agencies (specify) Y N Not Known

Was a home/scene visit carried out by professionals after the death?

Y N Not Known
If a visit was carried out, how long after the death was this?
<4 hours
4–12 hours
12–24 hours
24–48 hours
48–72 hours
>72 hours
Not known
If a visit was conducted, who attended?
Police Y N Not Known
Paediatrician Y N Not Known
Social care Y N Not Known
GP Y N Not Known
Specialist HV Y N Not Known
Child’s own HV Y N Not Known
Other (specify) Y N Not Known

Figure 7.6 (Continued) Form B4: Sudden death. (Continued)

96 Deaths and injury in infancy

Was the death reported to the coroner? Y N Not Known

If not – please specify why not.
Who conducted the postmortem examination?
Specialist paediatric pathologist Y N Not Known
Adult pathologist Y N Not Known
Forensic pathologist Y N Not Known
Other (please specify) Y N Not Known
What was the cause of death as given by the pathologist?
1a
1b
1c
2
Were there any significant additional pathological findings noted by the
pathologist? Y N Not Known
If so, please specify

Final Case Review

For final completion by the CDOP Chair

Was a final case review meeting held? Y N Not Known

if so how long after the death was this meeting?
<2 months
2–3 months
3–4 months
4–6 months
>6 months

Who attended?
Police Y N Not Known

Paediatrician Y N Not Known

Social care Y N Not Known

Pathologist Y N Not Known

Coroner or coroner’s officer Y N Not Known

GP Y N Not Known

Specialist HV Y N Not Known

Child’s own HV Y N Not Known

Other (specify) Y N Not Known

What was the cause of death as ascribed by the local case review meeting?
1a
1b
1c
2

Figure 7.6 (Continued) Form B4: Sudden death. (Continued)

 Child abuse 97

Were any significant contributory or causal factors identified at this meeting?

Y N Not Known

Was the postmortem report available to this meeting? Y N Not Known

Was the Avon Clinicopathological classification scheme used?

Y N Not Known
If so please give final classification of the death:

Was a report from this meeting sent to the relevant professionals?

Police Y N Not Known

Paediatrician Y N Not Known

Social care Y N Not Known

Pathologist Y N Not Known

Coroner or coroner’s officer Y N Not Known

GP Y N Not Known

Specialist HV Y N Not Known

Child’s own HV Y N Not Known

Other (specify) Y N Not Known

Were the parents/family offered the opportunity to meet with one or more of the
professionals after the case review meeting?
Police Y N Not Known

Paediatrician Y N Not Known

Social care Y N Not Known

Pathologist Y N Not Known

Coroner or coroner’s officer Y N Not Known

GP Y N Not Known

Specialist HV Y N Not Known

Child’s own HV Y N Not Known

Other (specify) Y N Not Known

Please provide any additional information that you think is relevant.

Figure 7.6 (Continued) Form B4: Sudden death.

fatal cases of physical child abuse. They are not always
associated with brain injury although up to one-third
may be. Abusive skull fractures are more likely to be
multiple, comminuted, bilateral or cross sutures. Less
often, fractures of the occipital or frontal bones are
present and basal fractures are uncommon (Figure 7.12)
and some fractures may be caused in settings other
than assault, such as birth trauma (Figure 7.13).
Skull fractures from falls may occur from relatively
low heights, with studies suggesting that a head-first fall
98 Deaths and injury in infancy
Figure 7.7 Multiple ‘fingertip’ bruises on the front
of the trunk in an abused infant. (Reproduced with
­permission from Saukko P and Knight B. Knight’s
Pathology 4E, London, CRC Press, 2016.)
from 0.9 m onto a concrete surface had a high likelihood
of fracture. Even a fall from that height onto a carpeted
surface has a significant risk of fracture. Skull fractures
in dead children can be caused by a fall from a height
that is below 0.9 m, from a seat, a chair or a mattress,
for example, but the incidence of a fracture decreases
with decreasing height and is, therefore, dependent on
the nature of the impacting surface and of the fall. Falls
from furniture onto the floor can cause skull fractures
in children and low-height falls can occasionally cause
fatal head injury.
Figure 7.8 Fingertip grip marks to left buttock and lower
back of infant. It is rare for grip marks and finger marks to
show distinct patterns of four fingers and a thumb.
Figure 7.9 Ear bruising in an infant raises the possibility
of NAI. Radiology revealed multiple rib fractures.
Head injuries
Head injuries are the most frequent cause of death in
child abuse and, even when they are non-fatal, they may
result in severe and permanent neurological disability.
‘Shaken Baby syndrome’ (SBS) has been the sub-
ject of intense controversy; the diagnosis has in the
past depended on the triad of subdural haemorrhage
(SDH), retinal haemorrhage (RT) and encephalopathy.
The hypothesis correlating the triad with shaking as the
injurious mechanism has been hotly contested, and has
been extensively reviewed in pathological, clinical and
legal communities. There is no doubt that infants do suf-
fer abusive injury at the hands of their carers, and that
impact and shaking can cause physical effects, but it is
now generally agreed that the finding of the ‘triad’ alone
should not lead to an automatic assumption that it was
caused by NAI. Thus, as for all forensic cases, it is essen-
tial to be aware of all the evidence and relevant factors
before coming to any opinions about the causation.
Whether from direct blows or from ‘shaking’, it is
clear that if sufficient force is applied to the head of a
child, brain injury can occur, and that injury carries
with it a substantial risk of disability or death. The
terms ‘Abusive Head Trauma’ (AHT) and ‘Inflicted
Head Injury’ (IHI) have gained wider appeal, and allow
the c­ linico-pathological and radiological findings to
be emphasised. In summary, the diagnosis of IHI or
accidental trauma (AT) in infants is based on clinical,
radiological and/or ophthalmological findings such as
 Child abuse 99

Head, chest, spine and pelvis:

anterior posterior (AP) and lateral skull
AP chest (to include the shoulders) and both obliques (obliques to include all ribs, left and right, 1–12)
AP abdomen and pelvis
lateral views to include the whole spine (For children under one year, this may be possible with one
view, for larger children and those over one year, separate views will probably be required.)

Upper limbs (where possible):

AP of the whole arm (centred at the elbow, if possible)
Coned lateral elbow
Coned lateral wrist
Posterior anterior (PA) hand and wrist
In larger children where a single whole arm view is not possible:
AP humerus (including the shoulder and elbow)
AP forearm (including the elbow and wrist)
Coned lateral elbow
Coned lateral wrist
DP hand and wrist
Lower limbs, where possible:
Whole AP lower limb, hip to ankle
Coned lateral knee and ankle
Coned AP ankle (mortise view)
DP foot
For larger children:
AP femur
AP tibia and fibula
AP knee
AP ankle
Coned lateral knee
Coned lateral ankle
DP foot
Follow-up imaging: 11–14 days, no later than 28 days after initial skeletal survey.
Follow-up radiographs should be performed of any abnormal or suspicious areas on the initial skeletal
survey plus the following views:
Chest AP and both obliques (to include the shoulders and all ribs, left and right, 1–12).

Figure 7.10 Skeletal survey: standard views, including follow-up, to be obtained.

SDH, encephalopathy, RH, and signs of impact. Each
case must be considered in its own context before con-
clusions are reached.
Ocular injuries
The significance of ocular lesions – such as RH, reti-
noschisis and orbital content haemorrhage – is a fur-
ther area of controversy in the medical and scientific
community. All children suspected of being physically
abused should have their eyes examined by an oph-
thalmologist, and the eyes should be examined as an
integral component of the post mortem examination
following the death of a child suspected of being
abused. A recent study has described the presence
of ‘cherry hemorrhages’ (isolated, elevated circular
bleeds, typically in the equatorial retina), and ‘peri-
macular ridges’ (elevated, circular retinal folds with a
canopy of internal limiting membrane [ILM]) in asso-
ciation with ILM tears in AHT. Survivors had optic
nerve atrophy and macular ganglion cell loss, and the
study authors thought that infants under 16 months
of age were particularly susceptible to damage from
vitreomacular traction by rotational and/or acceler-
ation-deceleration forces. It is essential that a multi-
professional team review all aspects of findings in the
100 Deaths and injury in infancy

(a)

(b)

Figure 7.12 Multiple skull fractures following blunt

Figure 7.11 Rib fractures in infancy. (a) X-ray of ribs and
part of the thoracic spine removed at autopsy. Note the
right-sided posterior rib fractures showing evidence
of healing (callus formation). NAI should be suspected
in such cases, and thoroughly investigated by a multi-
disciplinary team. (b) A posterior rib fracture, with callus,
following post mortem removal and fixation. Microscopy
of fractures assists in their ‘ageing’. (Reproduced from
Keeling J and Busuttil A. Paediatric Forensic Medicine and
Pathology. London: Hodder Arnold, 2008.)
force impacts against the floor. (Reproduced with
­permission from Saukko P and Knight B. Knight’s
Pathology 4E, London, CRC Press, 2016.)
Visceral injuries
Visceral injuries are the second most frequent cause of
death and it is the organs of the ­abdomen – the intestine,
mesentery and liver – that are most commonly injured
(Figure 7.16a). The anterior abdominal wall of a child
offers little or no protection against direct trauma from

context of the known facts of the case and of the current

state of the medical evidence base (Figure 7.14a and b).

Oral injuries
Lips may be bruised or abraded by impacts or pressure to
the face and, if the child is old enough to have teeth, the
inner side of the lips may be bruised, abraded or lacerated
by contact with the tooth edges. Tooth patterned marks
may be seen. A torn frenulum (frenum) inside the lip is
an occasional finding and this may be caused by a tan-
gential blow across the mouth or by an object, typically
a feeding bottle, being rammed forcibly into the mouth
between lip and gum (Figure 7.15a and b). The current
evidence indicates that a child with a torn frenum should
undergo a full child protection evaluation but, if no other
injuries nor any social concerns are identified, this find-
ing alone is not diagnostic of physical abuse. The intraoral Figure 7.13 Depressed skull fracture. Not all infant skull
hard and soft tissue should be examined in all suspected fractures are non-accidental in origin; instrumentation
abuse cases, and a dental opinion sought where abnor- and manual dis-impaction from the birth canal led to this
malities are found. fracture.
 Child abuse 101

(a) (b)
(i)

(ii)

Figure 7.14 Retinal haemorrhages. (a) Macroscopic post mortem appearance and (b) microscopy showing widespread
haemorrhage within multiple layers of the retina. (i) Vitreous body; (ii) retinal pigment epithelium. ([b] Reproduced
from Keeling J and Busuttil A. Paediatric Forensic Medicine and Pathology. London: Hodder Arnold, 2008.)

fist or foot, and blows from the front can compress the
duodenum, the jejunum or the mesentery between the
skin of the abdominal wall and lumbar spine. This com-
pression crushes the soft tissues and may even result in
transection or perforation of the bowel, resulting in peri-
tonitis and shock (Figure 7.16b). Crushing or rupturing of
the mesentery may lead to intra-abdominal bruising or
to frank intraperitoneal or retroperitoneal haemorrhage.
The liver is relatively large in a child and the liver
edge is palpable below the costal margin. It can be rup-
tured by direct blows to the abdomen. Splenic injuries
are rare in physical child abuse because of its relatively
protected anatomical site (Figure 7.17).
Other injuries
Other injuries in physical child abuse include burns
and human bites. There are a range of means of caus-
ing burns/thermal injury including the application of
heated metal objects or lighted cigarettes to the skin,
forced immersion in hot water, and contact with some
chemicals (e.g., from acid). Some thermal injuries can
be accidentally sustained, but others reflect a degree
of neglect (e.g., a child pulling a saucepan full of boil-
ing water from the top of a cooker or from an oven).
Different burns have different patterns and character-
istics. Cigarette burns from firm contact with the skin
are commonly depigmented, circular or oval deep
partial thickness burns, 5–10 mm in diameter, with a
pigmented rim. The differential diagnosis of such burn
scars includes dermatological conditions such as impe-
tigo, and vaccination scars.
Human bites are common in child abuse and can be
multiple. They must be differentiated from bites from sib-
lings, other children or even domestic pets. Swabs from a
new possible bite site should be taken as soon as possible,
as DNA of the perpetrator may be recovered. If there is
doubt about whether a mark or injury does represent
a bite, a forensic odontologist should be asked to pro-
vide an opinion. The forensic odontologist may be able
to compare the bite with a suspected biter’s dentition,
although this aspect of their practice is controversial,

(a) (b)

Figure 7.15 (a) Torn frenum due to forced bottle feed to mouth; (b) Bruising to upper lip (with intact frenum) caused
by same mechanism. ([a] Reproduced from Keeling J and Busuttil A. Paediatric Forensic Medicine and Pathology.
London: Hodder Arnold, 2008.)
102 Deaths and injury in infancy

(a)

Liver

Stomach
Pancreas
Duodenum Transverse
colon
Small
intestine
Urinary
bladder
Urethra

(b) Heavy blow Anterior abdominal

wall

Intestine

Spine Figure 7.17 Non-accidental, blunt force, intra-­abdominal

Figure 7.16 (a) Diagrammatic representation of sagittal sec-
tion showing relative positions of intra-abdominal organs in
female. (b) Transection or perforation of the bowel.
visceral injury (same infant as in Figure 7.7). Note the
liver laceration leading to an intra-abdominal haemor-
rhage. (Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)

and has suffered from severe criticism in the USA, where
conclusive matches have been shown to be erroneous,
leading to several high-profile exonerations.
Accidental injury in children occurs far more often
than acts of child physical abuse. However, it can be
extremely difficult to distinguish between them. All
healthcare professionals who work with or assess children
must always bear in mind the possibility of child abuse.
Child sexual abuse
Despite increased awareness of the nature and extent of
sexual abuse in children it remains a worldwide prob-
lem. Data as to its extent is difficult to interpret as it is
likely that there is increased reporting. In the UK it is
believed that up to 1 in 20 may have experienced some
form of sexual abuse as a child according to current defi-
nitions (Box 7.2).

Box 7.2 Child sexual abuse classification

Child Sexual Abuse is divided into contact and non-
contact abuse
Contact abuse involves touching activities where
an abuser makes physical contact with a child, includ-
ing penetration. It includes:
• Sexual touching of any part of the body whether
the child’s wearing clothes or not.
• Rape or penetration by putting an object or body
part inside a child’s mouth, vagina or anus.
• Forcing or encouraging a child to take part in sex-
ual activity.
• Making a child take their clothes off, touch some-
one else’s genitals or masturbate.
Non-contact abuse involves non-touching activi-
ties, such as grooming, exploitation, persuading
children to perform sexual acts over the internet and
flashing. It includes:
• Encouraging a child to watch or hear sexual acts.
• Not taking proper measures to prevent a child
being exposed to sexual activities by others.
• Meeting a child following sexual grooming with
the intent of abusing them.
• Online abuse including making, viewing or distrib-
uting child abuse images.
• Allowing someone else to make, view or distribute
child abuse images.
• Showing pornography to a child.
• Sexually exploiting a child for money, power or
status (child exploitation).
Source: From the NSPCC - https://www.nspcc.org.uk/preventing-
abuse/child-abuse-and-neglect/child-sexual-abuse/

Complaints of non-recent and current abuse con-
tinue to emerge at individual and institutional level.
It is essential that the assessment, diagnosis and
management of child sexual abuse is undertaken with
a multidisciplinary approach involving healthcare pro-
fessionals, families, social care agencies and where rel-
evant, law enforcement agencies.
Bibliography and information
sources
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8 Assessment, classification
and documentation of injury
▪▪ Introduction ▪▪ Mechanisms of death following trauma
▪▪ Terminology of injury ▪▪ Self-inflicted injury
▪▪ Injury and the law ▪▪ Torture
▪▪ Non-fatal violence-related injury ▪▪ Documentation of injury or marks of injury
in England and Wales ▪▪ Bibliography and information sources
▪▪ Types of injury ▪▪ Further general resources
▪▪ Survival after injury

Introduction determining the nature of and degree of seriousness of

The assessment, classification and documentation
of injury are key elements of forensic medicine. Any
healthcare professional working in any aspect of foren-
sic medicine must be able to appropriately document
injury in a way that can be understood and interpreted
by others. Most non-forensic healthcare profession-
als will not be trained in the interpretation of injuries
and wound causation, but accurate documentation can
greatly assist the legal process at a later stage.
There are a variety of criminal offences of physical
assault against individuals, not all of which cause visible
evidence of injury (e.g., some poisoning, some infec-
tion). The role of the forensic pathologist and forensic
physician is to ensure that the medical relevance of
findings, or absence of them, is understood by a court
or tribunal in the context of the particular case at issue.
Terminology of injury
Words to describe injury or harm are used non-spe-
cifically by lay persons and non-forensic healthcare
professionals. In a legal setting, the use of a particular
word may have a specific meaning that can influence
the nature of the charge and the penalties or sentence
related to an offence.
One frequent error in English-speaking jurisdictions
is the use of the word ‘laceration’ in the context of a cut
to the skin. In the forensic setting, as discussed below,
a laceration is a split or tear in the skin caused by blunt
impact. If the word laceration is used wrongly in court
or in written evidence to describe a cut caused by a knife
(an incised wound) this may have implications with
regard to the credibility of the witness.
Each jurisdiction will have its own specific legal
classification of injury or wounding, and again the use
of such terms may have its own particular relevance.
Forensic practitioners must be familiar with such clas-
sifications in their own jurisdiction (and others if they
also practise elsewhere) in order to assist the courts in
an injury.
Most harm or injury can be embraced by one of the
following broad groups, (using terms used within the
England & Wales jurisdiction).
Those with a fatal outcome:
• Murder (homicide)
• Manslaughter (homicide)
Those without a fatal outcome:
• Assault, assault occasioning actual bodily harm
• Common assault
• Battery, or common battery
• Wounding or wounding with intent
• Poisoning
• Inflicting grievous bodily harm or causing griev-
ous bodily harm with intent
Sexual offences:
• Penetrative
• Non-penetrative (both with or without extra-gen-
ital injury)
Injury and the law
In England & Wales, murder and manslaughter are two
of the offences that constitute homicide. Manslaughter
can be committed in one of three ways:
1. Killing with the intent for murder but where a
partial defence applies, namely loss of control,
diminished responsibility or killing pursuant to
a suicide pact.
2. Conduct that was grossly negligent given the risk
of death, and did kill, is manslaughter (‘gross
negligence manslaughter’).
3. Conduct taking the form of an unlawful act
involving a danger of some harm, that resulted
in death, is manslaughter (‘unlawful and danger-
ous act manslaughter’).
106 Assessment, classification and documentation of injury
The term ‘involuntary manslaughter’ is commonly
used to describe a manslaughter falling within (2) and
(3) while (1) is referred to as ‘voluntary manslaughter’.
The crime of murder is committed, where a person: of
sound mind and discretion (i.e., sane); unlawfully kills
(i.e., not self-defence or other justified killing); any rea-
sonable creature (human being); in being (born alive
and breathing through its own lungs - Rance v Mid-
Downs Health Authority (1991) 1 All ER 801 and AG Ref
No 3 of 1994 (1997) 3 All ER 936; under the Queen’s Peace;
with intent to kill or cause grievous bodily harm (GBH).
In the England & Wales jurisdiction a ‘wound’ (used
in the colloquial setting interchangeably with ‘injury’)
has a specific legal meaning: a wound is an injury that
breaks the continuity of the skin. There must be a divi-
sion of the whole skin structure and not merely a division
of the cuticle or upper layer. A bruise (or subcutaneous
rupture of blood vessels) is not a wound as the skin is not
broken. A broken bone is not (legally) a wound, unless it
is a comminuted fracture.
The Offences Against the Person Act 1861 which has
been amended over the years, sets out a range of offences
for which an individual, in England & Wales, can be
prosecuted when that individual is alleged to have
caused injury to another person. This statute excludes
homicide and sexual offences (which are ­covered by the
Sexual Offences Act 2003).
The language used in a law whose origins go back
almost one and half centuries can sometimes be difficult
to understand. The main offences relevant to injury assess-
ment by forensic practitioners are found in the follow-
ing sections of the Offences Against the Person Act 1861.
Section 18
Section 18 of the Offences Against the Person Act 1861
created the offences of wounding and causing grievous
bodily harm, with intent to cause grievous bodily harm,
or to resist arrest. It is punishable with life imprison-
ment. The specific wording of the offence is:
Whosoever shall unlawfully and maliciously by
any means whatsoever wound or cause any griev-
ous bodily harm to any person … with intent … to do
some … grievous bodily harm to any person, or with
intent to resist or prevent the lawful apprehension or
detainer of any person, shall be guilty of felony, and
being convicted thereof shall be liable … to be kept in
penal servitude for life … .
The key element of this offence is the intent to cause
grievous bodily harm. Types of injury would include
stabbings or shootings, but may also include trying to
poison or infect a person.
Section 20
This section creates the offences of wounding and
inflicting grievous bodily harm. They are less serious
than the offences created by Section 18 and carry a
maximum prison sentence of 5 years. The key element
of this offence is the causing of grievous bodily harm or
wounding but without having had the intent to do so.
Section 47
This section of the Act creates the offence of assault
occasioning actual bodily harm. It encompasses those
assaults that result in substantial injuries, typically
requiring a degree of medical treatment for the victim
and provides the penalty to which a person is liable on
conviction of that offence on indictment. A periorbital
haematoma with a superficial laceration after a punch,
or a broken tooth, are the types of injury that could be
considered a Section 47 assault.
Non-fatal violence-related injury in
England and Wales
A variety of sources is available for information on non-
fatal (and fatal) violence-related injury. The Violence
and Society Research Group based at Cardiff University
in Wales reports on Emergency Department atten-
dances for ­v iolence-related injuries each year via the
National Violence Surveillance Network. These data
are available online and are continuously updated, as
are the Office for National Statistics data for crime in
England & Wales which include data for all types of
violent crime. Figures published in 2018 showed a rise
in the number of offences (n = 40,147) involving knives
or sharp instruments (a 16% increase compared with
2017) and provisional NHS data showed admissions for
assaults involving a sharp instrument increasing by 14
per cent for England. There had been a rise of 2 per cent
in recorded offences involving firearms (n = 6492). The
number of homicides recorded by the police showed a
fourth consecutive rise, increasing by 12 per cent com-
pared with 2017 after a long-term decline (n = 736).
How does the body respond to injury?
When an injury is sustained, tissue damage is accompa-
nied by a disturbance of cellular function, and the host
inflammatory response is initiated, resulting in cascade
of tightly regulated physiological and behavioural pro-
cesses which have evolved to rapidly destroy or isolate
the cause of the disturbance, remove damaged or dead
tissue, and restore normal function.
Damaged or dead cells express molecules
(Damage-Associated Molecular Patterns (DAMPs),
and ‘Alarmins’) that are recognised by cells of the immune
system – principally neutrophils and monocytes/macro-
phages – which produce chemicals (cytokines and che-
mokines) which recruit more immune cells to the injured
area, and thereby create a cytotoxic environment which
aims to kill invading pathogens. However, this process
also causes further cellular/tissue damage. The blood
clotting system is also activated to stop bleeding at the site
 Non-fatal violence-related injury in England and Wales
of injury, and vascular alterations take place to facilitate
the delivery of immune cells to the injury location.
The outcome of the host response to trauma depends
on the nature and the severity of the injurious insult,
the presence of pathogens and the extent of the body’s
physiological response(s). An efficient and effective
coordinated localised response leads to resolution of the
inflammatory environment, healing/repair of damaged
tissue, and restoration of normal function.
These processes assist in the microscopic ‘ageing’
of injuries which is reliant on the recognition of, and
subjective assessment of, the nature and extent of the
inflammatory response to trauma, and of the healing
processes that may have followed.
Severe (or multiple) insults, lead to an exaggerated,
systemic (throughout the body) inflammatory response,
which can set the scene for major organ dysfunction,
organ failure and death.
Modern pre-hospital trauma care, advanced trauma
life support-based resuscitation, and ‘damage-control
surgery’ aim to minimise the adverse physiological con-
sequences of trauma, and sustain life for long enough
to enable that injured person to receive artificial organ
support in an intensive care unit and definitive surgi-
cal repair. Trauma management has traditionally been
aimed at preventing the so-called ‘triad of death’: meta-
bolic acidosis, hypothermia and coagulopathy (abnor-
mal blood clotting), thought to be caused by a complex
interaction between the physiological responses to
trauma and haemorrhage, environmental factors, and
resuscitation/surgical interventions.
The following factors may all influence whether the
trauma sustained is likely to have a fatal outcome:
Box 8.1 Physiological complexity and the body’s response to injury
The physiological response to injury is not only com-
plicated (it involves multiple individual components),
but complex (it represents the orchestrated response
of multiple interacting components), and the ‘behav-
iour’ of the response is non-linear; the behaviour of
the whole is something other than that which can be
predicted by analysing the individual components.
This leads to difficulties in treating severely injured
patients – and preventing their death – as well as a rec-
ognition that a ‘systems approach’ needs to be taken
if our understanding of medicine and science is to be
advanced. Such an approach has been influenced by
the mathematics of ‘chaos theory’ and complexity sci-
ence, and has been taken forward by the emerging dis-
ciplines of Systems Biology and Network Medicine.
The key properties of so-called ‘complex non-linear
systems’ are:
• The relationships between highly inter-­connected
system components are not linear.
107
• The nature and severity of the injury(s) (the
‘trauma load’): some injuries (such as decapita-
tion) are obviously incompatible with life, and
severe injury to vital organs such as the brain and
heart can be rapidly (but not invariably) fatal.
• The mechanism of injury: the nature of the transfer
of energy to a vital organ can influence survivabil-
ity (a low-energy penetration by a knife might be
survivable, for example, if emergency medical and
surgical care is provided rapidly, whilst a higher
energy gunshot wound to the same organ might
lead to a rapid death).
• The rapidity with which emergency medical care is
provided, and the availability of modern trauma
care/intensive care facilities: if the injury is sus-
tained in a rural location – poorly served by pre-
hospital personnel – or the injurious event is
unwitnessed, potentially survivable injuries can
become fatal.
• The age and health status of the injured p ­ erson:
increasing age influences the survivability of
individuals sustaining multiple rib fractures fol-
lowing blunt force chest impact in a road traffic
collision, for example, and pre-existing cardiac or
respiratory disease tends to reduce the ability of
the body to maintain vital functions in the face of
a traumatic insult.
• The body’s physiological response to injury:
­medical/surgical intervention, and infection/
sepsis.
The significance of physiological complexity and the
host response to injury is considered in Box 8.1.
• Components exhibit a variety of properties or
behaviours, ranging from the stable to chaotic,
with some demonstrating complex, self-similar-
ity at multiple scales in space and time (so-called
fractals).
• Small alterations in components can lead to expo-
nential changes in the behaviour of the system
(there is extreme ‘sensitive dependence on initial
conditions’).
• Even though the behaviour of the system is com-
plex, simple rules govern the behaviour of the indi-
vidual components (the system is ‘deterministic’).
• The interactions between those individual com-
ponents is capable of producing unexpected
behaviour (so-called ‘emergence’).
In the context of trauma patients, the undesired
‘emergent properties’ of the host response to injury
include multiple organ dysfunction and failure, and
death.
108 Assessment, classification and documentation of injury
Types of injury
Injury caused by the application of physical force can
be divided into two main groups: blunt force and sharp
force. These make up the predominance of injury seen by
forensic pathologists and forensic physicians but there
are a number of other means of causing injury which
may be significant. These include ballistic, ­thermal,
chemical, and electrical injury.
Figure 8.1 Reddening (erythema) from having been
struck to the upper arm with a flat piece of wood. The red
colour disappeared after a few hours and blanched on
pressure distinguishing it from bruising.
(a) (b)
Figure 8.2 (a) Visible swelling to the right side of face and eyelids after repeated punches. (b) Periorbital haematoma
(black eye) caused by direct impact from fist. (c) Diagrammatic representation of potential bleeding and tracking sites
after direct impact to nose or orbital region (1) around globe, (2) beneath skin and scalp anatomical planes, (3) intra-
cranial. Each can result in visible bruising if tracked via tissue planes or via bone fractures.
Blunt force injury
Blunt force injury (trauma) refers predominantly to
injury that is not caused by instruments, objects or
implements with cutting edges. The nature of the force
applied may include direct blows (impacts), traction,
torsion and oblique or shearing forces. Blunt force
trauma may have a number of outcomes:
• No injury
• Tenderness
• Pain
• Reddening (erythema; Figure 8.1)
• Swelling (oedema; Figure 8.2)
• Bruising (contusion; Figure 8.3)
• Abrasions (grazes; Figure 8.4)
• Lacerations (Figure 8.5)
• Fractures (Figure 8.6)
The amount of force applied in blunt force injuries
can be described as weak (for example a ‘gentle’ slap on
the face), weak/moderate, moderate, moderate/severe
or severe (for example, a full punch as hard as possible).
The more forceful the impact, the more likely that visible
marks will be evident.
The term ‘tenderness’ is used to describe pain or
discomfort experienced on palpation by the examining
clinician of an area of injury. Both pain and tenderness
are subjective findings and are thus dependent on (1)
the pain threshold of the individual and (2) their truth-
fulness. Other features of blunt force injury are visible
effects of contact. Reddening (sometimes referred to as
erythema) describes increased blood flow to areas that
have been subject to trauma, but not to the extent that
the underlying blood vessels are disrupted. Reddening
can be distinguished from bruises by its ability to blanch
from finger pressure and its usual resolution within 6
hours or so.
(c)
2
3
1

(a)
(b)
(c)
Figure 8.3 (a) Bruising (contusion) to thigh (a) following
direct blunt force (fall between iron girders); (b) shows
resolution of bruising 5 days after injury as seen in 8.3a;
(c) bruising to scrotum and penis after direct kicks with
shod foot. (Courtesy of Jason Payne-James.)
Types of injury 109
(a)
(b)
(c)
Figure 8.4 (a) Variable depth abrasions (grazes) caused
by impact against concrete surface. (b) Superficial
­fingernail abrasions to the right lower thigh and knee. (c)
Superficial fingernail abrasions to the right and left back.
([a] Courtesy of Jason Payne-James.)
Bruises
Bruises are discolouration of the skin surface caused
by leakage of blood from damaged blood vessels, often
small-diameter vessels such as venules or arterioles,
into underlying tissues. The degree, nature and colour
of the bruise is, in part, related to the colour of the over-
lying skin. Bruising is most commonly seen in the skin,
but it can also occur in the deeper tissues, including
110 Assessment, classification and documentation of injury

now be used as it does not assist in understanding the

type or mechanism of injury. The word bruising is best
used to describe visible external marks caused by leak-
age of blood into skin and subcutaneous tissues, while
‘contusion’ can be used to describe leakage of blood into
tissues in body cavities, (using the word bruise in this
context is also acceptable). The term ‘haematoma’ can
be used to refer to a palpable collection of liquid blood
under the skin (and one which, could be aspirated by a
needle or surgically incised and drained).
‘Petechiae’ are small bruises, often described as ‘pin-
point haemorrhages’, and, in the past, have been said
to be <2 mm in size. However, that is an arbitrary fig-
Figure 8.5 Laceration, with irregular edges, maceration
ure and, like all bruises, petechiae can develop, evolve
and skin bridging caused by direct impact to forehead
and coalesce, and the use of a rigid size measurement is
with wooden pole. (Courtesy of Jason Payne-James.)
inappropriate (Figure 8.7a and b).
Direct blunt force, in addition to unambiguous
impacts such as strikes with fists, kicks or weapons,
also includes mechanisms such as poking, squeezing
and gripping. Indirect blunt force may be represented
by suction (as in ‘love bites’; Figure 8.8a and b) or fol-
lowing compression.

(a)

Figure 8.6 Hand with abrasions, swelling, redden-

ing and underlying fracture of 5th metacarpal caused
by repeated punching of cell door. (b)
(Courtesy of Jason Payne-James.)

muscle and internal organs (and may not be evident

until surgical intervention or post mortem). The extent
of damage to the blood vessels is generally proportion-
ate to the force applied: the greater the force, the more
blood vessels are damaged, the greater the leakage of
blood and the larger the bruise.
Once outside the confines of the blood vessel, blood
is broken down, resulting in the various colour changes
seen. Eventually, all of the blood is removed and the
overlying skin returns to its normal colour. Figure 8.7 (a) Close up of cheek after manual
A number of terms have been used in the past to s­ trangulation – multiple petechiae present 2 hours
describe bruises, which unnecessarily complicates the after event. (b) Scleral blood, caused by coalescence of
understanding of their nature. The term ‘ecchymosis’ multiple petechiae, 36 hours after manual strangulation.
has been used for specific types of bruise but should not ([b] Courtesy of Jason Payne-James.)

(a)
(b)
Figure 8.8 (a) Classical love or ‘hickey’ bite - bruising
to neck caused by suction. (b) Circumferential suction
bruise to nipple. (Courtesy of Jason Payne-James.)
Compression may produce petechiae at the level of,
or above, the compressing force (e.g., in ligature stran-
gulation, or by crushing/chest compression in a crowd).
Bruises evolve and can ‘migrate’. The effects of grav-
ity and anatomical tissue planes are two of the factors
that may determine how the position of a bruise might
change (Figure 8.9). Thus, the presence of a bruise in one
place does not always imply that the blunt impact was
applied at that particular site. Some superficial bruises
(often called intradermal bruises), caused by leak-
age of blood confined to the epidermis and the upper
strata of the dermis, can remain in the position in which
the impact occurred, and ‘patterned’ bruises, which
reproduce the nature of the object that caused them,
often have such an ‘intradermal’ element. Intradermal
bruises are often associated with diffuse compression
forces such as pressure from a car tyre or from a shoe
Types of injury 111
(a)
(b)
Figure 8.9 Extensive bruising following tissue planes and
contours, one week after multiple blunt force impacts
to (a) head and (b) face (neck was spared impacts).
(Courtesy of Jason Payne-James.)
during a stamp or a kick (Figure 8.10a–c). The depth
of such bruises can only be confirmed at post mortem
examination.
Certain types of blunt injury commonly cause evi-
dentially useful patterns. Single patterned bruises may
indicate the nature of the impacting object. ‘Tramline’
(or ‘tram-track’ or ‘railtrack’) bruises (Figure 8.11) are
those caused by impacts from longitudinal, generally
cylindrical or rod-like, objects (where blood is forced
laterally from the point of impact, rupturing blood ves-
sels either side of the impacting object) and shoeprint
bruises may be seen from stamp injuries (Figure 8.12).
112 Assessment, classification and documentation of injury
(a)
(b)
(c)
Figure 8.10 (a) Patterned bruise to right forearm –
pattern matched to trainer of assailant. (b) Patterned
bruise caused by impact of dog chain. (c) Patterned
bruise (bruise obliquely towards midline) caused by
impac of 2 × 2 inch length of wood.
(Courtesy of Jason Payne-James.)
The distribution (pattern) of a number of bruises may
also help corroborate the nature of the causative force.
A row of four 1–2 cm oval or roundish bruises may be
caused by the impact of knuckles in a punch; groups of
small oval or roundish bruises could also be caused by
fingertip pressure, as in gripping, and there is some-
times a single, larger, thumb bruise on the opposite
side of the limb (Figure 8.13). In clinical practice this
so-called typical appearance is rarely seen, because
of movement of the victim and assailant and re-siting
of the gripping hand during a struggle, repeated pok-
ing with a single finger may also create such a pattern
of bruising. Fingertip bruises on the neck or along the
jaw line are commonly seen in manual strangulation.
Often they may appear as single long, linear bruises as
the bruising from the individual fingertips coalesces.
Examination of injuries must always be undertaken
in the best available light and, in the case of bruises,
such is required in order to ensure that small or subtle
skin colour changes are not missed. Particularly with
darker skin tones, good lighting is essential to identify
all areas of bruising.
Age estimation based on the colour of bruising is
not now considered appropriate, with one e­ xception –
the appearance of yellow is indicative of early healing
change in the injury occurring over a timeframe of some
hours. A study that followed colour changes of multiple
bruises, of known age, over a couple of weeks found that
yellow colouration in a bruise did not appear before 18
hours after the blunt contact. However, the colour of a
bruise must not be assessed from photographic images
– where colour reproduction may be inaccurate – and
it must also be understood that the perception of yel-
low colour may be influenced by the visual capability
of the viewer, interobserver variation and underlying
skin tone. In addition, bruises known to be older than
18 hours may be associated with no yellow colouration.
Studies in children suggest that estimation of ageing of
bruising cannot be reliably achieved by colour interpre-
tation alone, and this principle also generally applies to
adults.
Estimating the age of a bruise (and other injuries) at
post mortem examination is enhanced by microscopy,
in which inflammatory and healing changes are sought,
although this technique can still only allow a patholo-
gist to give a broad timeframe for when that injury was
likely to have been sustained.
Bruising can appear after death: blood vessels are
just as easily damaged by the application of force and,
provided that there is blood with some pressure within
those vessels, bruising can occur. Such pressure may
exist at the lowermost vessels because of the static
weight of the column of blood. Post mortem bruises
are generally small and lie on the dependent parts of
the body. Bruising may also be found in areas of post
mortem dissection and extreme care must be taken in
 Types of injury 113

(a) (b)

(c)

Stretching Tramline bruises

Compression

Figure 8.11 (a) Tramline bruise caused by impact from cylindrical firm object (in this case, a police baton). (b) Tramline
bruise to right hip region caused by impact from broom handle. (c) Creation of parallel bruises with central sparing by
impact from cylindrical object – ‘tramline’, ‘tramtrack’ or ‘railtrack’ bruises. ([a & b] Courtesy of Jason Payne-James.)

interpreting ‘new’ bruises when a post mortem exami-
nation has been performed.
Abrasions
An abrasion (or graze) is a superficial injury involving
(generally) outer layers of skin without penetration of
the full thickness of the epidermis. They are caused
when there is contact between a rough surface and
the skin, often involving a tangential ‘shearing’ force
(Figure 8.14). They can also be caused by crushing of the
skin when the force is applied vertically down onto the
skin. Bites and the grooved, often parchmented, abra-
sion found in hanging, can cause typical ‘crush’ abra-
sions (Figure 8.15).
The appearance of abrasions always represents the
exact contact area (unlike bruises) and the nature of the
abrasion itself may assist in determining the direction of
the contact from the blunt, abrasive object, or the direc-
tion of the body when making contact. A variety of abra-
sions have been described including scratches (linear
abrasions, e.g., caused by fingernails; Figure 8.16a–c),
scuff (brush) abrasions (very superficial abrasions, with
no bleeding, Figure 8.17) and point or gouge abrasions
(deeper linear abrasions caused by objects such as metal
nails, often with bleeding; Figure 8.18).
As the epidermis does not contain blood vessels,
superficial abrasions might not bleed, but the folded
nature of the junction between the dermis and the epi-
dermis, and the presence of loops of blood vessels in the
dermal folds, will mean that deep abrasions have a typi-
cal punctate or spotty appearance. Deeper abrasions
may therefore bleed, resulting in subsequent scabbing
and possible scarring.
The size, shape and type of abrasion depends upon
the nature of the surface of the object which contacts the
skin, its shape and the angle at which contact is made.
Contact with the squared corner of an object (e.g., a
brick) could result in a linear abrasion, whereas contact
with one face of the same object will cause a larger area
of ‘brush’ abrasion.
Contact with a rough surface, such as a road, espe-
cially when associated with the higher levels of force
114 Assessment, classification and documentation of injury
Figure 8.12 Shoeprint bruise following stamping injury
to face. It may be possible to match the footwear pat-
tern and assist in the identification of the shoe owner.
(Courtesy of Jason Payne-James.)
Figure 8.13 Grip marks from fingers of assailant: bruises
from grip and abrasions from fingernails seen on upper
inner arm. (Courtesy of Jason Payne-James.)
Figure 8.14 Abrasion to right face and cheek caused
by kick from shod foot. Linearity of abrasion assists
in determining direction of movement.
(Courtesy of Jason Payne-James.)
Figure 8.15 Ligature mark with parchmented abrasion
posterior part of the neck.
(Courtesy of Jason Payne-James.)
found in traffic accidents, can result in deep areas
of often discoloured areas of ­abrasion – ‘gravel rash’
(Figure 8.19).
Tangential contact with a relatively smooth surface
can also result in such fine, closely associated, linear
abrasions that the skin may simply appear reddened
and roughened. This may be termed a ‘friction burn’;
close examination will usually reveal the true nature
of the wound. A closely woven carpet will cause such a
lesion, although the term ‘carpet-burn’ may be applied
in that setting.
The direction of the causative force can be identi-
fied by close inspection of the injury; (magnification
of a high-resolution digital image can be useful when
changes are subtle) and for identifying the elevated frag-
ments of the epidermis which are pushed towards the
furthest (distal) end of the abrasion (Figure 8.20).
Crush abrasions – often associated with ‘intrader-
mal’ bruising – are important because they may retain
 Types of injury 115

(a) (c)

(b)

Figure 8.16 (a) Multiple fingernail scratches with wheal reaction and superficial abrasions. (b) Deeper abrasions
caused by fingernails. (c) Large abrasions caused when climbing over brick wall whilst being pursued by police dog.
([a & b] Courtesy of Jason Payne-James.)

Figure 8.17 A very superficial abrasion. (Courtesy of

Jason Payne-James.)
the pattern of the causative object. As for all marks, inju-
ries and scars in the forensic setting, written descrip-
tions accompanied by body diagrams and images (both
still and moving) enhance and clarify the evidence for
the courts.
Figure 8.18 Deep linear point or gouge abrasions to
forehead. (Courtesy of Jason Payne-James.)
Photographs of injuries should be taken from a dis-
tance (to locate the site of the lesion), close up (to see
the detail of the lesion) and then close up with a ruler or
scale (to ensure the accuracy of the description). Scales
116 Assessment, classification and documentation of injury

Figure 8.19 Deep and extensive abrasion (’gravel rash’)
caused by contact with road surface after motorcycle
accident.
that include colour standards are also available (e.g.,
Forensigraph).
Scaled photographs of injuries are also essential
to allow subsequent comparison to be made between
those injuries and scaled photographs of ‘suspected
injury causing implements or surfaces’. Many differ-
ent injury causing objects have been identified in this
way, such as car radiator grills, the tread of escalator
steps, plaited whips (see Box 8.2) and the lines from
floor tiles.
Lacerations
A laceration is a ‘split or tear’ in the skin caused by blunt
force compressing or stretching the skin, or applying
a shear force to it. Lacerations often extend through
the full thickness of the skin and, depending on the
anatomical site, can bleed profusely (e.g., the scalp).
Because the skin is composed of many different tis-
sue types, some of the more resilient tissues will not
be damaged by the forces that split the weaker tissues.
This is what enables a distinction to be made between
an open wound apparently made by a blunt object and
one made by a sharp object. Those most resilient tis-
sues are often nerves, fibrous bands of fascial planes
and, sometimes, at the base of the laceration, an occa-
sional medium-sized elastic blood vessel. These struc-
tures are seen to extend across the defect in the skin
and are often referred to as ‘bridging fibres’. The same
blunt force causing such a laceration may also cause
irregular splits, bruising and abrasion at the margins
of the wound (Figure 8.21). These features are generally
absent in sharp force injuries.
Lacerations are most common where the skin can
be compressed between the applied force and underly-
ing bone (e.g., over the scalp, face, elbows, knees, and

(a)

(b) Terminal
Direction Tags epidermal tag
of impact

Figure 8.20 (a) Directional scuff – note raised skin layers on left side of abrasion: yellow arrow indicates direction
of abrasive movement; red arrow indicates line of terminal epidermal tags. (b) Direction of tangential force can be
determined by position of raised epidermal skin layers. ([a] Courtesy of Jason Payne-James.)
 Types of injury 117

Box 8.2 Patterned injuries and the forensic pathologist – R v V Neville Heath 1946
The body of Marjorie Gardiner was discovered in bed
in a hotel in London, England, in June 1946. Her ankles
were bound by a handkerchief and her left arm lay
diagonally under her back to lie close to the right wrist,
and the wrists appeared to have been tied, although no
restraint was present. Heavy bloodstaining was pres-
ent at the scene and, on releasing the ankle bindings, a
large amount of blood issued from her vagina.
At autopsy, blunt force injuries were present on
the face and lower jaw, and there were 17 patterned
injuries to the trunk and breasts which appeared as
stippled intradermal bruises with abrasion, having
parallel linear components and diamond-shaped
intervening components, and a rounded ‘end’; they
had the appearance of having been caused by a flex-
ible cane or whip, having a patterned surface. There
were bite marks to the breasts, and the vagina was
lacerated.
A search of Heath’s belongings revealed a leather
riding whip with a hard tip; human blood, insufficient
for grouping, was found on the whip. When the pathol-
ogist, Keith Simpson, examined that whip, he thought
that the pattern of the weave ‘corresponded in fine
detail’ with the marks on the body, saying ‘it is identical,
in my view, and the mark of the tip corresponds with
the projecting metallic tip’.
Heath was charged with murder (and that of a simi-
lar murder in Bournemouth), and found guilty. He was
executed in October 1946.
Comparisons and overlays of scaled photographs of
the patterned injuries with scaled photographs of the
implement would be made in modern investigations,
in order to see whether the whip could be excluded
as having caused the patterned injury, and the whip
would also be examined by forensic scientists for fin-
gerprints and DNA (of the assailant and victim) in order
to allow the jury to decide whether or not the whip has
caused the injuries, and who had wielded it. The bite
marks would have been examined and compared with
Neville Heath’s own dentition.

(b)

(a)

Skin
Bone

Figure 8.21 (a) Laceration to ear following impact with baseball bat – note irregularity of laceration and associated
swelling bruising masked by dry blood. (b) Mechanism of causation of laceration. (Courtesy of Jason Payne-James.)
118 Assessment, classification and documentation of injury

shins). They are very rare (unless severe force has been (a)
applied) over the soft, fleshy areas of the body such as
the buttocks, breasts and abdomen.
The margins of a laceration are usually ragged; how-
ever, if a thin, regular, object inflicts an injury over a
bony area of the body, the wound caused may look very
sharply defined and can be mistaken for an incised
injury. Careful inspection of the margins will reveal
some crushing or tearing and bruising, and examina-
tion of the inner surfaces of the wound will reveal the
presence of bridging fibres.
The shape of the laceration (e.g., linear, curvilinear
or stellate) rarely reflects the nature of the impacting
object (unless accompanied by other patterned blunt
force injury).
When significant tangential blunt force is applied to
the skin, for example owing to the rolling or grinding
action of a vehicle wheel, the laceration may be hori- (b)
zontal and result in a large area of separation of skin
from the underlying tissues (often called ‘flaying’ or
‘degloving’).

Sharp force injury

Injuries caused by sharp force need to be distinguished
(but are sometimes indistinguishable) from blunt force
injuries such as lacerations or gouge and point abra-
sions. In general, sharp force injuries have cleanly
divided, distinct wound edges, which may span irregu- Figure 8.22 (a) Sutured incised wound caused by razor
lar surfaces, and penetrate different types of tissue with blade – note how wound follows contours. (b) Incised
the same contact. There are no bridging fibres (Figure wound caused by knife drawn across surface of
8.22). They are referred to as ‘incised’ wounds. ­fingers. In this case contours are spared.
(Courtesy of Jason Payne-James.)

Incised, slash and stab wounds
Incised wounds are caused by objects with a sharp or
cutting edge, often a knife but other examples include
shards of glass, broken glass and bottles, the edges of
pieces of broken pottery or ceramics, or the edge of a
broken tin can (Figure 8.23). The edges of the wound will
give some indication as to the sharpness of the weapon
causing it. A sharp-edged object/implement will leave
no bruising or abrasion of the wound margins. Careful
inspection of the depths of the wound will reveal that
no bridging fibres are present because the cutting edge
divides everything in its passage through the skin and
underlying tissues.
Incised wounds, by their nature, are only life-threat-
ening if they penetrate deeply enough to damage a blood
vessel of significant size. Thus, incised wounds over the
wrist or neck, where major arteries lie in more superfi-
cial tissues, can prove fatal. An incised wound caused
by an object sweeping or moving across the skin surface
is sometimes referred to as a ‘slash’ wound or a ‘slice’
wound (Figure 8.24). In contrast, a stab wound is caused
by a motion down through (rather than across) the skin
surface. A surgical operation wound is an example of an
incised wound. There is an artificial distinction between
a stab and slash wound in forensic terms.
A stab wound is (like a slash wound) caused by a sharp
implement and is generally said to have penetrated the
body deeper than its length on the skin surface. A stab
wound can, however, be quite shallow if its progress
into the body is impeded, for example by the presence
of bone or cartilage, in which case its depth may not
exceed its length on the skin surface. Classifying such
a wound as a stab is relatively straightforward in the
deceased, but in the living (1) the depth of the wound
may not be accessible and (2) if it has been recorded at
all, the measurement of the skin surface wound may be
inaccurate.
Forensic pathologists may also have the advan-
tage of being able to determine the direction of such
wounds. The direction or depth of a wound in the liv-
ing may not be clear (or indeed recorded at all) when
interpreting medical or operative notes in survivors of
stab injuries. This lack of detail may be aggravated by
the move from open to laparoscopic surgery. However,
 Types of injury 119

(a) (c)

(d)

(b)

Figure 8.23 (a) Sutured incised wound across right side of head and face. (b) Incised wound to neck caused by use of
knife. (c) Irregular incised wounds after broken bottle slashed twice across back of head and neck. (d) Glass broken on
impact near upper left nose. Sutured. Multiple satellite superficial shard cuts. (Courtesy of Jason Payne-James.)

imaging techniques (CT, US and MRI) may all provide
detailed wound track length information, and if such
information is not recorded in the clinical notes, it
may be determinable by further review of the imaging.
The depth of the injury and its direction are of great
importance when considering different accounts of
causation of stab wounds and so the more information
recorded at the time of treatment, the more helpful it
can be to the justice system.
Any weapon with a point or tip can cause a stab
wound; the edge of the blade does not need to be
sharp. For example, a ballpoint pen or a screwdriver
can cause stab injuries. Stab-like wounds may also
be caused by other (relatively) blunt objects such as
car keys. For penetration of the skin to occur, a vari-
ety of factors determine how much force is required,
including:
• The sharpness of the tip of the weapon: this is often
the most important factor and the sharper the tip,
the easier it is to penetrate the body.
• The geometry of the knife, including the radius of
the blunt edge at the tip.
• The sharpness of the ‘cutting edge’ of the imple-
ment.
• The nature of the force applied: stabbing incidents
are usually dynamic, involving complex relative
movements between victim and assailant.
• Whether clothing has been penetrated: some
items of clothing, such as thick leather jackets,
may offer significant resistance to penetration.
• Whether bone has been injured: skin offers little
resistance to penetration by a sharp knife, but
injury to bone tends to suggest that a greater
force has been used to inf lict the wound.
Significant penetration of bone may also dam-
age the knife.
Once a knife or other sharp implement has pen-
etrated the skin, subcutaneous tissues (except bone)
offer little further resistance to deeper penetration and,
to an assailant, it may appear that the rest of the weapon
120 Assessment, classification and documentation of injury
(a)
(b)
Figure 8.24 (a) Slash wound across left forearm from
knife, penetrating skin, muscle and tendon. (b) Slash-
type wound to forearm; wound is wider than it is deep.
(Courtesy of Jason Payne-James.)
‘follows through’ with almost no additional effort or
force being applied. The insertion of a sharp knife into
the body, especially through the skin stretched across
ribs, requires only moderate force and can be easily
achieved, and pressure from a single finger may be suf-
ficient to push a very sharp implement through the chest
wall at this site.
The nature of a stab entrance wound on the skin sur-
face can assist in determining the size and the cross-
sectional shape of the weapon used (Figure 8.25). If a
blade of some sort is used, the general comments in Box
8.3 apply.
Chop injury
Chop injuries may be caused by a variety of implements
that are generally heavy, and relatively blunt, bladed
instruments. These include some machetes, Samurai
swords and axes. Because of the variability of the ‘blade’,
injuries sustained may be a mixture of sharp and blunt
force wounds, typically involving bruised, crushed and
abraded wound margins. These are often referred to as
‘chop’ wounds. Fractures and amputations may also
result from the use of such implements and substantial
scarring may ensue (Figure 8.26). It is with implements
such as these that interpretation of the nature of wounds
(sharp vs blunt, slash vs stab) may be particularly chal-
lenging.
Other types of injury pattern
Documentation of the site, orientation and pattern(s) of
the wounds will often reveal useful indications about
the causation of the wound. Particular actions such as
Figure 8.25 Knife wound with knife tip in the bottom
right of figure. (Courtesy of Jason Payne-James.)
punches, kicks, bites, scratching, holding or gripping
injuries and defence injuries can sometimes be identi-
fied by their patterns (Figure 8.27).
Punching
A punch is a blow delivered by the clenched fist. The
blow can be directed anywhere, and the effects are,
in part, dependent on force of delivery. Visible injury
is more likely to be seen over those areas of the body
where the skin is closely applied to bone, as in the face
and skull. The entire range of blunt force injuries can
be caused, including reddening, swelling, bruises,
abrasions, lacerations and fractures. These findings
may also be present on the hand delivering the punch.
On the face, the lips may be compressed against the
teeth, resulting in bruising, abrasion and lacerations
inside the lips. An imprint bruise or abrasion of the
teeth may be present. Any examination following a
blow to the face or mouth always requires intraoral
examination. A single punch to the nose or forehead
can cause bilateral periorbital bruising (black eyes).
Severe force punches can break ribs. Intra-abdominal
injury, including mesenteric laceration, intestinal
rupture and injury to the major abdominal organs,
may result, particularly if punches of adequate force
are delivered to a vulnerable (i.e., untensed) abdomen.
Kicking and stamping
Kicking and stamping injuries from shod or unshod
feet may also exhibit the entire gamut of blunt force
injury. However, kicks and stamps can be more pow-
erful than punches, and more so if delivered to an
individual already vulnerable (e.g., lying on the floor
or unconscious). Stamping to the chest, head, thorax,
abdomen and limbs can cause substantial bony and

Box 8.3 E xamples of features to consider which can influence the appearance of a
possible stab wound
A slit-like wound will distort, after removal of the
weapon, because of the action of elastic fibres present
in the skin. If the fibres are orientated at right angles to
the skin surface wound, it will be pulled outwards and
get shorter and wider; if they run parallel to the skin sur-
face wound, it will be pulled lengthways and the edges
will tend to close and the wound elongate slightly.
Even if the edges of the wound are gently pushed
together, the resulting defect is rarely the exact size as
the knife.
The dimensions of the wound on the skin surface
and depth of the wound also depend on the shape/con-
figuration of the blade and how deeply it was inserted.
Movement of the knife in the wound, as a conse-
quence of relative movement between the assailant
and victim, may cause the wound to be enlarged. If the
knife is twisted or rotated within the body, an irregu-
larly-shaped, or even triangular, skin surface wound
may be result.
Many knives have only one cutting edge; the other
being blunt. This design may be reproduced in the
wound where one wound apex is sharp or ‘V’-shaped,
while the other is blunt, or rounded. The blunt wound
apex may ‘split’ at each side, an appearance commonly
referred to as a ‘fishtail’.
Figure 8.26 Multiple hypergrophic scars to left
arm and shoulder caused by machete.
(Courtesy of Jason Payne-James.)
Types of injury 121
Provided that clothing has not intervened, skin
adjacent to the stab wound may be bruised and/
or abraded as a consequence of forcible contact
between the skin and, for example, the hilt/blade
guard of a knife, or the ‘knife-wielding’ hand of the
assailant.
The depth of a wound within the body may be
greater than the length of the blade if a forceful stab is
inflicted. This is because the abdomen and, to a lesser
extent, the chest, and other soft tissues can be com-
pressed by the force of the knife hilt or knife-wielding
hand against the skin.
A blunt object such as a screwdriver or ‘spike’ will
tend to indent, split and bruise the skin on penetra-
tion. Different types of screwdriver can cause different
patterns of injury, for example ‘cross-head’ or ‘Phillips’
screwdrivers can cause very distinctive cruciate skin
surface wounds.
Unusually shaped stab wounds may be caused by
implements less commonly encountered in stabbing
assaults; scissors, for example, may cause a ‘Z-shaped’
skin surface injury, while chisels may cause rectangular-
shaped stab wounds. When such injuries are encoun-
tered, it is important to consider unusual causative
implements.
Figure 8.27 Typical severe fingernail scratching injuries
to the face. (Courtesy of Jason Payne-James.)
organ damage, and can result in life-changing or fatal
injury. Stamps to the abdomen, for example, can result
in liver, spleen, pancreas and intestinal rupture, leading
to internal haemorrhage and peritonitis. Kicking and
stamping may leave areas of intradermal bruising that
122 Assessment, classification and documentation of injury

reflect the pattern of the sole of the shoe which may lead (a)
to identification of the assailant.

Bite injuries
A bite mark can be described as a mark caused by
teeth alone, or by teeth in combination with other
mouth parts. Biting is a dynamic process and bite
marks can be complex injuries. Bites can be human
or animal.
Bite damage can be caused by a mixture of ­c utting –
predominantly from the incisor teeth – and tearing
when teeth clamp down on skin and other tissue.
The appearance of bite marks made by human teeth/
mouths can vary significantly from there being little
to no visible injury, to reddening, swelling, bruising,
abrasions/cuts and substantial skin and tissue loss. (b)
In some cases, the pattern of individual teeth marks
is very clear as these leave an imprint or impression
at the site of injury.
Bite marks may be seen in all crimes of violence
including sexual assaults, child and elder abuse, and
also on the sports field.
Bite marks may be found on almost any surface of
the body; specific sites are associated with specific
forms of assault (Figure 8.28a–c). The neck, breasts and
shoulders are often bitten in a sexually motivated attack,
while in child abuse bites to the arms and the buttocks
are ­common.
A forensic odontologist should review any possible
bite marks when confirmation of identity of the biter is
required. There have, however, been many judicial con-
cerns about the practice of bite mark-suspect dentition
comparisons by forensic odontologists, and even the
ability of forensic practitioners to reliably recognise that
an injury is, in fact, a human bite mark. (c)
Despite these concerns, it is essential that forensic
practitioners, and all healthcare professionals caring for
the vulnerable, consider whether the injury that they are
examining could be a bite mark so that the injured area
can be swabbed for DNA recovery, and so that it may be
photographed with a scale by a trained forensic photog-
rapher.

Defence injuries
In situations of assault and attack it is a normal reflex to
protect oneself. In many instances, that reflex inevita-
bly results in the individual being assaulted sustaining
injury, albeit whilst potentially reducing the extent of
injury that might otherwise have been sustained.
When a knife or a stabbing implement is directed at Figure 8.28 (a) Human bite with tissue loss to the right
an individual, the head and face may be protected by ear. (b) Bite mark with bruising, skin lifts and teeth
raising the hands and arms to cover the head and face. marks to chest. (c) Bite causing tissue loss to chin – no
The hand may attempt to grab or deflect a weapon. The identifiable teeth marks are evident.
arms and hands sustain injuries but the head, face and (Courtesy of Jason Payne-James.)

(a)
(b)
Figure 8.29 (a) Defence injuries to right hand causing
by knife. (b) Example of how trying to fend off a knife –
or grasp it – may result in defensive injuries to palm.
(Courtesy of Jason Payne-James.)
eyes are protected. In addition, in incidents involving
knives where a knife may be thrust towards an indi-
vidual, he may try and defend himself by grabbing the
knife blade and deflecting it away from, for example,
the chest and abdomen. Grabbing of the cutting edge
of the blade can result (if the knife is sharp enough)
in cuts to the part of the hand that seizes that blade
(generally the palm or gripping side of the hand and
fingers; Figure 8.29). Both the assailant and victim
can sustain incised wounds if there has been a strug-
gle. It is generally suggested that the dominant hand
may automatically be used to defend onself but, if the
dominant hand (most commonly the right) is other-
wise engaged, the non-dominant hand may be used.
Multiple defence wounds may be sustained during an
assault, and such wounds to the hands may be of vari-
able depth, or discontinuous, as the hand is not a flat
surface. Distinguishing between defence wounds to
the palm of the hand from fending of an attack, and
wounds to the hands caused by the assailant’s own
hands slipping down to blade when undertaking the
assault may be very difficult to distinguish.
Defence-type injury after blunt weapon assault
will be seen in the same regions, namely the extensor
Survival after injury 123
Figure 8.30 Bruising to extensor aspect of left arm –
raised to ward off impact from baseball bat.
(Courtesy of Jason Payne-James.)
surfaces of arm and upper arm (Figure 8.30) which may
be raised to protect against blows, and on the back,
or the back of the legs, if an individual is taken to the
ground and, for example, kicked. The victim will tend to
curl up in a ball with hands and arms over the head and
legs tucked up towards the chest.
Defence injuries may also be absent following an
assault. This may be for a number of reasons including
unconsciousness from assault, or incapacity through
drugs or alcohol or restraint by another person or
­persons.
Survival after injury
The length of survival following infliction of an injury
is difficult to determine: every human being is different
and this variability in survival and post-injury activity
is to be expected. It is, however, a subject on which any
forensic pathologist or forensic physician should expect
to be asked. Any expression of either survival time or of
the ability to move and react must be given on the basis
of the ‘most likely’ scenario, accepting that many dif-
ferent versions are possible. The court must be advised
of the difficulties of this assessment based on medical
findings alone. The medical evidence should be taken
in context with all other evidence including eyewitness
accounts, CCTV and body worn video.
It must be remembered that survival for a time after
injury and long-term survival are not one and the same
thing. The initial response of the body to haemorrhage
is ‘compensatible shock’, shutting down peripheral
124 Assessment, classification and documentation of injury
circulation; if blood loss continues, the homeostatic
mechanisms may be overwhelmed and the individual
enters the phase of ‘uncompensated shock’, which leads
inexorably to death.
Many examples exist of individuals with apparently
potentially immediately fatal wounds who have per-
formed purposeful movements/actions for some time
after what subsequently turns out to be a ‘fatal’ injury.
Forensic practitioners should always be very wary about
allotting fixed times after which somebody could not have
survived, as they will almost invariably be confronted
with other evidence showing that they clearly did do so.
Mechanisms of death
following trauma
Given the complexity of the physiological responses to
injurious insults, evaluating why an individual died at a
particular time is extremely difficult, unless, for exam-
ple, their physiological status was being monitored in an
intensive care unit.
All injurious insults lead to a disturbance of function
at varying levels/scales (i.e., sub-cellular, cellular, tis-
sue, organ and whole organism), and to varying degrees,
and a fatal outcome depends on the interaction between
the disturbance in function and the physiological resil-
ience of the injured person. Systems biologists refer to
complex physiological systems – the central nervous
system, or cardiovascular system, for example – as being
‘robust yet fragile’, meaning that healthy physiologi-
cal function can withstand remarkably diverse insults
and disturbances up to a threshold beyond which they
fail. When viewed in this light, death following trauma
occurs when the degree of injury is such that it over-
whelms the physiological limit of the organ(s)/systems
disturbed by the traumatic insult.
The common final pathways of fatal injuries are usu-
ally mediated by disturbances in the electrical activity
in the brain, leading to impaired cardiovascular and
respiratory function, and heart, leading to abnormal
heart rhythms (arrhythmias); both of which can termi-
nate in cardiac arrest. See Box 8.4 for some examples of
mechanisms of death following trauma.
Self-inflicted injury
All types of injury can be self-inflicted, accidentally
inflicted or deliberately inflicted by another. Many self-
inflicted injuries are caused by those with psychiatric or
mental health issues, or in association with stressful life
situations and anxiety. Patterns of injury are well docu-
mented in such individuals. In the forensic setting there
is a small, but important, group of individuals who self-
injure for other reasons, such as staging an assault for
attention-seeking and similar motives, or to deliberately
implicate others in criminal acts or for financial gain
Box 8.4 E xamples of mechanisms
of death following trauma
• Pulseless electrical activity (PEA) cardiac arrest
due to massive haemorrhage (internal and
external).
• Ventricular arrhythmias following brain swell-
ing and internal herniation due to blunt force
head injury.
• Ventricular arrhythmias following traumatic
basal subarachnoid haemorrhage (caused by
blunt impact to head, usually at the level of the
skull base).
• Ventricular fibrillation following alternating cur-
rent electrocution.
• Ventricular fibrillation following blunt impact to
the front of the chest.
(e.g., insurance fraud). Such injuries may not always fol-
low the pattern of ‘typical’ self-harm injury. Cases have
been described of single self-stab wounds to the heart
and head.
Fatal self-inflicted blunt force injuries may be
inflicted following, for example, jumping from a height
or under a train. In the absence of witnesses, or CCTV
evidence, consideration must be given to a question
such as ‘were they pushed?’ or other alternative sce-
narios. There may be no specific features to the injuries
that identify them as self-inflicted. Self-inflicted bite
marks may occasionally be seen on the arms of an indi-
vidual who claims to have been assaulted or blunt force
injuries to the head or other parts of the body. Abrasions
might be created by using objects such as abrasive pads
to fabricate injury.
Self-inflicted incised or stabbing injuries, however,
often show specific patterns that vary depending on the
intention of the individual. In suicidal individuals, self-
inflicted sharp force injuries are often found at specific
sites on the body referred to as ‘elective sites’; for slash
type wounds these are most commonly on the front of
the wrists and neck, whereas stab wounds are often
inflicted over the precordium and the abdomen. In indi-
viduals who are not intending to commit suicide, the site
can be anywhere on the body that can be reached by the
individual (Figure 8.31a and b). Generally, the eyes, lips,
nipples and genitalia tend to be spared.
The other features of self-inflicted injuries lie in
the multiple, predominantly parallel, nature of the
wounds and, in suicidal acts, the more superficial inju-
ries are referred to as ‘hesitation’ or ‘tentative’ injuries
(Figure 8.32).
The forensic practitioner has an important role in
the evaluation of the nature and pattern of injuries that
might be self-inflicted. In the absence of an admission of

(a)
(b)
Figure 8.31 (a) Multiple linear burn marks (caused by
heated knife blade applied to the skin) – note healed
lesions between acute lesions. (b) Multiple incised
wounds to forearm caused by a male with a psychotic
episode harming himself with a knife blade.
(Courtesy of Jason Payne-James.)
Figure 8.32 Multiple new incised wounds with smaller
and more superficial tentative injuries (arrowed).
(Courtesy of Jason Payne-James.)
Torture 125
self-harm from an individual, it may be possible to come
to a view as to whether injuries are likely to have been
self-inflicted if the characteristics listed in Table 8.1 are
considered. Some or all of these characteristics, com-
monly inflicted by some form of implement such as a
knife or a nail, may be present, but it is important to note
that only some, and rarely all, may be present in an indi-
vidual case. The absence of a particular feature listed
does not preclude self-injury; neither does its presence
necessarily imply self-injury.
For some cases, it may not be possible to exclude
assault, and evidence of self-harm, rather than assault,
must come from alternative sources, such as other wit-
ness evidence.
The staging of assault or injury may also involve other
individuals complicit in the process. In such a setting,
injuries that are unusual (although not unknown) as
‘self-harm’ injuries (e.g., black eyes or deep abrasions)
may have been inflicted by an accomplice. In such
cases, the detail of the accounts given (or not given) can
be crucial in determining the actual course of events.
Torture
Article 3 of the European Convention on Human Rights
states that no-one shall be subjected to torture or to
inhumane or degrading treatment or punishment.
Unfortunately, such treatment and punishment is still
widely found throughout the world.
The International Committee of the Red Cross uses
definitions for torture and other forms of ill-treatment
which are: torture consists of severe pain or suffering,
whether physical or mental, inflicted for such purposes
as obtaining information or a confession, exerting pres-
sure, intimidation or humiliation; cruel or inhumane
(synonymous terms) treatment consists of acts which
cause serious pain or suffering, whether physical or
mental, or which constitute a serious outrage upon indi-
vidual dignity. Unlike torture, these acts do not need to
be committed for a specific purpose; and humiliating
or degrading (synonymous terms) treatment consists of
acts which cause real and serious humiliation or a seri-
ous outrage upon human dignity, and whose intensity is
such that any reasonable person would feel outraged; ill-
treatment is not a legal term, but it covers all the above-
mentioned acts.
Forensic physicians and pathologists may be asked
to assess individuals claiming torture or other forms
of ill-treatment and human rights abuse. Such assess-
ments can be complex and it may be necessary to assess
and interpret physical findings for which there may be
a number of explanations. The doctor’s role is to assess
these findings impartially. In order to make an assess-
ment for physical evidence of torture a structured exam-
ination must take place, which involves the history, the
medical history and then the physical examination.
126 Assessment, classification and documentation of injury
Table 8.1 Some characteristics that may be associated with self-inflicted injury
Characteristic
On an area of the body that the individual can access
themselves
Superficial or minor injury
If there is more than one cut they are of similar
appearance, style and orientation
If there are other types of injury (e.g., scratches, cigarette
burns) they are of similar appearance, style and
orientation
Multiple similar injuries
Parallel injuries
Injuries grouped in a single anatomical region
Injuries are grouped on the contralateral side to the
patient’s handedness
Tentative injuries
Old healed scars in similar sites
Scars or healing wounds of different ages in similar sites
Slow-healing injuries
Psychiatric and related issues – such as eating disorders,
drug and alcohol misuse
The physical examination must involve systematic
examination of the skin, face, chest and abdomen, mus-
culoskeletal system, genitourinary system and the central
and peripheral nervous systems. Specific examination
and evaluation are required following specific forms of
torture which include: beatings and other blunt trauma;
beatings of the feet; suspension; other positional torture;
electric shock torture; dental torture; asphyxiation; and
sexual torture, including rape. Specialised diagnostic
tests can be used to assess damage (e.g., radiological
imaging, nerve conduction studies).
The history taking should include direct quotes
from the victim, establishment of a chronology, where
possible backing it up, for example, with old medical
records and photos. A summary of detention settings
and abuses, must be obtained with details of the condi-
tions within those settings and methods of torture and
ill-treatment. Attention must also be paid to, and may
require specialist assessment of, the psychological sta-
tus of the victim. Specific torture techniques that may
be described include:
Additional Comments
Sites less accessible to reach (e.g., the middle of the
back) are less likely
Although more severe injury can be caused – particularly
in those with psychiatric disorder or suicidal intent
Typically self-inflicted cutting injuries are more
superficial, numerous and similar than those sustained in
an assault by another person – where the natural
reaction of the injured person is to avoid repeated injury,
and both assailant and victim will be moving
As above – more than one similar injury should raise an
index of suspicion as to the possibility of self-infliction
Raise a high index of suspicion as to the possibility of
self-infliction
As above
As above
A right-handed person is more likely to create injury on
the left-hand side of the body
Smaller or lesser injuries grouped with the main injuries
suggest the initial ‘tentative’ attempts at self-harm
May indicate previous attempts at self-harm
May indicate repeated previous attempts at self-harm
Persistence of wounds that would otherwise have been
expected to heal – in the absence of any other factors.
• Beating of the soles of the feet (falanga, falaka or
bastinado; Figure 8.33).
• Amputation (Figure 8.34).
• Positional torture – e.g., cheera (legs stretched
apart) or Parrot’s Perch (wrists tied over knees –
a pole placed under the knees).
• Suspension – e.g., Palestinian hanging (arms and
wrists tied and elevated behind the back; Figure
8.35), which can result in disruption of shoulder
joint complexes and subsequent deformity.
• Electrical burns (Figure 8.36).
• Wet submarino – immersing the victim’s head in
a container full of water until the person almost
drowns.
• Dry submarino – placing the victim’s head inside
a plastic bag until nearly suffocated.
Each of these may have short- and long-term sequelae.
It is extremely important to recognise that there
may be no physical evidence of torture. Where scars or
marks are present it is important, for the credibility of

Figure 8.33 Bruising to feet caused by repeated
blunt impact to feet – falanga.
(Courtesy of Jason Payne-James.)
Figure 8.34 Amputation of right thumb as a form of
­torture. (Courtesy of Jason Payne-James.)
Figure 8.35 Visible abnormality subsequent to
joint d
­ isruption after Palestinian hanging.
(Courtesy of Jason Payne-James.)
the examination, to distinguish between alleged torture
scars and injuries and non-torture scars and injuries.
Istanbul Protocol
In order to address the issues of torture and human
rights abuses it is important that there are effective ways
of documenting and comparing findings. The Istanbul
Protocol is the shortened term to describe the Manual
on Effective Investigation and Documentation of Torture
Documentation of injury or marks of injury 127
Figure 8.36 Electrical burns – scarring to scrotum
as a result of application of electrodes.
(Courtesy of Jason Payne-James.)
and Other Cruel, Inhuman or Degrading Treatment or
Punishment, a set of international guidelines for docu-
mentation of torture and its consequences. It became a
United Nations official document in 1999 and provides
a set of guidelines for the assessment of persons who
allege torture and ill-treatment, for investigating cases
of alleged torture, and for reporting such findings to the
judiciary and any other investigative body. It is the most
appropriate means by which robust evidence can be pre-
sented in a standardised manner to the relevant authori-
ties. It is in the process of revision and the new version is
likely to be available in 2020.
Interpretation of findings regarding scars or marks is
undertaken using the following scale (this scale is also
useful in criminal and other trial settings):
• Not consistent: could not have been caused by the
trauma described.
• Consistent with: the lesion could have been caused
by the trauma described but it is non-specific and
there are many other possible causes.
• Highly consistent: the lesion could have been
caused by the trauma described, and there are few
other possible causes.
• Typical of: this is an appearance that is usually
found with this type of trauma.
• Diagnostic of: this appearance could not have
been caused in any way other than that described.
Documentation of injury or marks
of injury
Doctors and other healthcare professionals outside the
forensic setting tend to use medical terminology within
reports and statements. This approach is generally not
helpful, either to colleagues attempting to interpret
their meaning or to courts, (including non-medically
qualified judges and juries), unless a concurrent expla-
nation in lay terms is provided.
128 Assessment, classification and documentation of injury
Forensic pathologists may be dependent on avail-
able information, from police, from witnesses, from
medical records, from family and many other sources
to determine what may or may not have caused fatal
injury. Forensic physicians dealing with the injured
living person may be able to get a history directly from
that person, but may not have access to other materi-
als. If it is possible to take a history, then the relevance
of each factor listed below should be considered:
• When did the injury or injuries happen?
• Have they been treated (e.g., at hospital or at home)?
• Are there any pre-existing illnesses (e.g., skin
disease)?
• Are there any pre-existing (but unrelated) sites of
injury?
• Does the individual take any regular physical
activity which puts them at risk of injury (e.g., at
work, or whilst participating in contact sports)?
• Is the person taking regular medication (e.g., anti-
coagulants, steroids)?
• What is the handedness of the complainant and
suspect?
• Were drugs and/or alcohol used?
• What weapon or weapons was/were used (if still
available)?
• What clothing was worn?
Most of this information should be easily obtainable
from the history and documented in the contemporane-
ous medical notes.
The following characteristics should be recorded
wherever possible for each injury identified:
• Location (anatomical – measure distance from
landmarks)
• Presence of pain or tenderness
• Reduced mobility/altered function
• Nature of injury (e.g., bruise, laceration, abrasion)
• Size (measure, do not estimate. Use a ruler or a
scale – which could include a colour standard e.g.,
Forensigraph®)
• Shape
• Colour
• Orientation
• Possible age (is it consistent with account?)
• Causation (is it consistent with account?)
• Handedness (of complainant and suspect)
• Time (that injury was caused)
• Transientness (has it changed in appearance?)
The recording of such information in the clinical set-
ting should ideally be in three forms: first in a written
form, appropriately describing the injury; second as a
hand-drawn body diagram; and third, ideally, to sup-
plement the first two, in digital image form. There are
some Apps which can record all this type of information
and data (via tablet or smartphone) which can generate
immediate reports summarising all such information
(e.g., ForensiDoc ®). Such documentation will ensure
that the opportunity for proper interpretation is max-
imised. Thus, any clinical notes should: record the
appropriate history; record accurately and clearly all
findings – positive and negative; record legibly; sum-
marise findings with clarity; use consistent terminol-
ogy; and interpret within the limits of your experience.
If the healthcare professional is not able to interpret
findings then this should be stated clearly in any report.
There is frequently an ‘evidence gap’ for those who
are seriously injured, and who require immediate
resuscitation and immediate surgery or ventilation,
when compared with those with relatively minor inter-
personal assaults, where the complainant can give a
full account and injuries can be documented, and the
deceased, who will have a full post mortem examina-
tion carried out by a forensic pathologist. The need to
save life and stabilise the critically injured is the prior-
ity, rather than the need to document injury accurately,
or to retrieve crucial evidence, and lack of forensic skills
mean that often hugely important evidence (e.g., nature
of injury or important trace materials) is lost. There is
a clear argument for those involved in the care of the
severely or critically injured to have access to forensic
physicians who can (with the consent of the clinical
teams) gather evidence at the earliest opportunity.
Forensic pathologists must document and record
all injuries identified at post mortem examination in
detail, sufficient to enable subsequent review of their
findings, and to demonstrate the reliability of their con-
clusions in any legal forum.
Forensic photography
Forensic photography is a specialised area embracing a
range of imaging techniques that allow best presentation
of visually relevant evidence in an appropriate format. The
principles are straightforward, and ensure that interpre-
table images are retained. Photographic techniques have
included the use of ultraviolet, infrared and polarised light
photography, which have been said to enhance or identify
items or injuries of interest. Data are somewhat lacking as
to the utility of these techniques which in general enhance
or show features which may not ordinarily be visible to the
naked eye. Caution should be used when reviewing such
images. An essential element of forensic photography is
data management of images and how these are appropri-
ately stored, reproduced and shared. Forensic practitio-
ners need to work closely with forensic photographers to
ensure that the relevance of images taken is best suited
to the requirements of the evidential and court process.
All forensic practitioners should consider undertaking
training in forensic photography. Poor-quality imaging
is now unacceptable and it is appropriate that those most
skilled in producing robust evidence are used to provide it
for courts and other agencies. Guidelines are available on
best practice. Boxes 8.5 and 8.6 describe 2D and 3D pho-
tography of patterned injuries in more detail.

Box 8.5 2D photography of patterned injuries
The utilisation of conventional 2D photography for the
image-capture of a patterned injury often results in
some form of visual distortion which can change the
appearance of the patterned injury in the image. Further
error is introduced by the use of inappropriate measur-
ing scales and poor placement of the correct scale next
to the injury.
The following method is recommended for obtain-
ing photographic evidence of patterned injuries to
a sufficient standard for analysis and presentation to
court.
A. Equipment
For best practice in obtaining sufficient images, there
are basic equipment requirements:
• Digital Single Lens Reflex (DSLR) camera. DSLRs
are advisable as smartphones in general produce
Images that are of poor quality.
• Prime (macro) lens e.g. 60 mm or 105 mm. A
shorter focal length than 60 mm will cause barrel
distortion.
• Use of a suitable single flashgun or ringflash,
properly positioned so as not to cause unwanted
shadows.
• A rigid L shaped scale (ABFO No.2), and a lon-
ger straight scale if required for large patterns.
Without this scale being placed correctly, and
photographed with the injury, further analysis is
affected, and the photograph being inadmissible
in court. The use of tape or adhesive scales should
be avoided.
B. Correct positioning of the camera to the injury
Forensic analysis of patterned injuries is severely
affected by distortion. Photographic distortion is one
of the few controllable variables in this process. There
are three main types of photographic distortion:
• Type 1. When taking the photographs, the film
plane (CCD or CMOS sensor) of the camera must
be perpendicular to the plane of the injury. If the
Box 8.6 3D imaging in bite-mark photography
Bite marks are frequently discovered on curved parts
of the body which creates a problem for their accurate
documentation by forensic practitioners. A 3D anatom-
ical structure has to be recorded in a 2D image which
is free of visual distortion. Current best photographic
Documentation of injury or marks of injury 129
photographer fails to do this correctly, angular dis-
tortion occurs.
• Type 2. The scale must be placed on the surface
of the skin to ensure that the scale is on the same
plane as the injury.
• Types 3 and 4. Applying too much pressure on the
scale when it is placed next to the injury can warp
a portion of the scale. Tilting the scale will cause
distortion.
The scale should be close to the injury, but not so
close as to obscure any less obvious peripheral marks.
C. The sequence of images of an injury
1. Image of the person’s means of identification (e.g.
patient label, consent form, etc.).
2. A locator shot, showing the injury an identifiable
anatomical area, without a scale (e.g. the whole
arm, full face, or leg).
3. Close-up shots of the injury, including the whole
of the scale (e.g. all 3 circles of an ABFO No. 2 scale
must be shown, helping to identify any angular
distortion).
4. If an injury is on a curved surface, then multiple
views (at least 3) will be needed.
5. If an injury is on an area such as the chest, the posi-
tion of the body should be taken into account.
6. Detailed shots of specific features of an injury, if
required.
7. An image of the person’s means of identification
again, to ‘close the sequence’.
D. Photography of a suspected implement
In some situations, it is relevant to the investigation to
examine the implement suspected to have caused the
patterned injury. In this case the striking edge of the
implement should be photographed employing the
same technique used to photograph the injury. This
will enable the trained professional to compare scaled
photographs of the suspect implement and patterned
injury using photographic ‘overlay’ techniques.
practice utilises a digital single lens reflex (DSLR) cam-
era, and requires strict adherence to protocols devised
to minimise distortion, as described above. It is inevi-
table, however, that some distortion to the bite mark
will be introduced in the image, and this may lead to
(Continued)
130 Assessment, classification and documentation of injury
Box 8.6 (Continued) 3D imaging in bite-mark photography
inaccurate measurements being made in the subse-
quent image analysis. This error is introduced in two
ways:
• Camera operator error – caused by not adhering
to protocol (angular distortion) and poor choice of
camera lens (a short focal length will cause barrel
distortion).
• Incorrect placement of the scale in relation to the
bite mark.
These errors are common in forensic imaging. To
reduce error, it has been proposed that practitioners
employ 3D image capture. Stereo-photography, and
laser scanning, have been shown to be more precise,
robust and accurate forms of recording bite marks than
2D photography. 3D image capture, however, is still in
its infancy. Complete 3D bite-mark analysis requires 3D
capture of both the injury and the dental cast of the sus-
pected biter(s). To date, no one system has been shown
to perform the task for both applications adequately.
There are two methods of 3D image capture: active
and passive. Active methods use laser scanning to gather
the data for reconstruction, and involve reasonably
expensive equipment. Most of these systems employ a
red laser light to scan the object’s surface, which then
reflects back to a digital sensor. As the sensor and the
laser are calibrated to capture the object at a known
distance, the scanner’s software can interpret the data
using trigonometry to create a 3D model of the object.
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Currently, a laser scanner creates the most precise
3D model of a dental cast. However, the lack of por-
tability of most of these systems makes them difficult
to use in capturing the actual bite mark, particularly in
children who are unable to stay still for a long time.
Passive stereo-photogrammetry devices are more
portable, and often use a DSLR camera with a specif-
ically-designed stereo lens attached. Two strategi-
cally placed mirrors collect two images from slightly
different angles on to one sensor (CCD or CMOS). The
scanner’s software compares the different points of ref-
erence to apply the principles of triangulation, and cre-
ate a 3D model. While the portability and relatively low
cost of this device makes it a viable option for capturing
bite marks, to date, such devices provided inadequate
3D models of a dental cast.
2D imaging, and the subsequent analysis, requires
correct scale placement for consistent measurements
of the bite mark. 3D imaging devices are calibrated to
fixed distances and do not require any scale placement.
In addition, poor camera positioning does not have a
significant effect on the data set.
There is a lack of published data as to what consti-
tutes the true shape and extent of a patterned injury
which might provide a credible baseline against which
to compare the accuracy of patterned injury imaging
measurements; 3D imaging has the potential to control
at least the measurement variable in the process of bite
mark analysis.
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9 Ballistic injuries
▪▪ Introduction
▪▪ Types of firearms
▪▪ Firearms injuries
▪▪ Air weapons, unusual projectiles and other weapons
▪▪ Determination of accident, suicide or murder
Introduction
The unlawful use of firearms as weapons of assault
continues to increase. Firearms are relatively easy to
obtain, whether in jurisdictions where their possession
is controlled and use is permitted or not. Legislation
intended to reduce availability often seems to have
an impact only on those with a lawful need or reason
for possession, rather than on those intent on using
firearms for criminal purposes. In whichever jurisdic-
tion the forensic practitioner practices, he or she will
encounter injury and death caused by a wide variety of
firearms. Often the availability and control of firearms
is a focus of intense political debate. The nature of the
firearm is often dependent on the jurisdiction. Firearm
injury may be deliberate (as in conflict or assault) or
accidental or unintentional (e.g., hunting injuries).
Types of firearms
Within England & Wales a firearm is ‘a lethal barreled
weapon of any description from which any shot, bullet or
other missile can be discharged’ (section 57 (1) Firearms
Act 1968). It includes:
• Any prohibited weapon (see below in this guid-
ance section 5 Firearms Act 1968), whether it is
such a lethal weapon as aforesaid or not.
• Any component part of such a lethal or prohibited
weapon.
• Any accessory to any such weapon designed or
adapted to diminish the noise or flash caused by
firing the weapon.
The term ‘lethality’ itself is a complex issue and
although case law exists (Moore v Gooderham [1960] 3
All E.R. 575), only a court can decide whether any par-
ticular weapon is a ‘firearm’ for the purposes of the Acts.
There are two main types of firearm: those with
smooth barrels, which fire groups of pellets or shot, and
those with grooved or rifled barrels, which fire single pro-
jectiles or bullets. Both of these types of weapon rely upon
the detonation of a solid propellant to produce the gases
▪▪ Evidence recovery
▪▪ Blast injuries
▪▪ Mass disasters
▪▪ Bibliography and information sources
▪▪ Further general resources
that propel the projectile(s). Airguns and air rifles form
a separate group of weapons that rely upon compressed
gas to propel the projectiles. These weapons, and more
unusual forms of projectile or firearm, such as the rub-
ber bullet, stud (also known as power-actuated or nail)
guns and humane killers, are considered at the end of this
section.
Modern propellants consist of nitrocellulose or
other synthetic compounds prepared as small coloured
flakes, discs or balls. During the process of firing a bullet
or shotgun cartridge the following sequence of events
occurs: the firing pin strikes the primer cup and the
primer compound explodes; small vents between the
primer cup and the base of the cartridge case allow the
flame of this detonation to spread to the propellant; the
propellant burns rapidly, producing large volumes of
gas, which are further expanded by the very high tem-
peratures of the ignition; and the pressure of this gas
propels the shot or bullet from the barrel.
The speed with which the projectile leaves the end of
the barrel (the muzzle velocity) varies from a few hun-
dred metres per second in a shotgun to a thousand or
more in a high-velocity military weapon. The energy of
the projectile is proportional to the speed at which it
travels and is calculated from the kinetic energy (½MV2)
of the bullet. Higher muzzle velocities are considerably
more effective at delivering energy to the target than
larger bullets. The extent of injury, and wound pattern,
created by a firearm is, in part, directly related to the
muzzle velocity.
Shotguns
Shotguns, commonly used in the sport, hunting and
farming sectors, are long-barrelled, smooth-bore fire-
arms that are used to discharge cartridges that usually
contain a number of shot. These guns may have single
or double barrels, commonly 26–30 inches (66–76 cm)
in length; the double-barrelled weapons are arranged
either ‘side by side’ or ‘over and under’. The length of the
barrel makes handling and concealing shotguns dif-
ficult and so it is not uncommon for the barrels to be
134 Ballistic injuries
(a) (b)
Case
Shot
Wad
Powder
charge
Brass head
Primer
Figure 9.1 Shotgun cartridge structure: (a), image of a
shotgun cartridge; (b), diagram of structure of typical
cartridge.
shortened for criminal activities. This shortening of the
barrel has little impact on the effectiveness of the gun,
especially over short to middle distances. A shotgun
generally has an effective range of about 30–50 m.
The cartridges for shotguns (Figure 9.1) consist of a
metal base, or head, containing a central primer cap,
supporting a cardboard or plastic tube containing the
propellant charge and the shot, which is closed by a thin
disc or a crimp at the end of the tube. The shot may be
contained within a plastic wad or there may be discs of
felt, cork or cardboard, acting as wads above and below
the shot. The plastic wads open into a petal-shape
in flight and may themselves contribute to an injury,
especially at close range.
Shotgun cartridges are designated according to the
size of the individual shot contained within and can
vary significantly in number depending on the shot
size (typically 6–850 in number for a 12-bore cartridge).
There are also cartridges that contain a single heavy
projectile, commonly referred to as a ‘slug’. The types of
wound produced by a shotgun will be dependent on the
(a)
Figure 9.2 Revolvers and pistols. (a) Heckler & Koch USP (Universal Service Pistol), Germany, 1993. Calibre 9 mm para-
bellum. (b) Ruger GP–100, USA, 1987. Calibre .357 Magnum.
calibre, shot size and distance at which the shotgun was
discharged from the target (see below).
Rifled firearms
This group of firearms usually fire one bullet at a time
through a barrel that has had a number of spiral grooves
cut into the bore. The resultant projections, referred to
as ‘lands’, engage with the bullet and impart gyroscopic
spin that produces a more stable and accurate trajec-
tory. Rifled weapons fall into two main groups: hand
guns and rifles.
Revolvers and pistols are short-barrelled hand guns.
Revolvers contain a rotating cylinder into which car-
tridges are manually loaded. Pistols, or semi-automatic
hand guns, usually contain a magazine enclosing the
cartridges located within the grip. The firearm is dis-
charged when the cocked firing pin, or striker, impacts
on to the primer cup in the base of the cartridge by pull-
ing the trigger. The main difference in the two types of
firearm is the method of operation (Figure 9.2).
In the revolver, the cylinder rotates to align a new
cartridge with the firing pin and the barrel, which is
achieved by either pulling the trigger (double action)
or by manually cocking the hammer and subsequently
pulling the trigger (single action). The fired cartridge
cases remain in the gun until they are manually
unloaded.
In a pistol, the forces generated each time a cartridge is
discharged are used to recycle the weapon, which involves
extracting and ejecting the fired cartridge case, resetting
the firing mechanism and loading a new cartridge from
the magazine into the chamber. For semi-automatic
weapons this occurs each time the trigger is pulled.
Rifles are long-barrelled weapons that are designed to
accurately fire projectiles at targets at a much greater dis-
tance than revolvers or pistols. Rifles have been designed
to use many different types of operating mechanism,
ranging from single shot bolt-action rifles to fully auto-
matic gas-operated assault rifles, some of which are
capable of firing in excess of 700 cartridges per minute.
(b)
 Firearms injuries 135

Firearms injuries
Injuries sustained from discharge of firearms can origi-
nate from the smoke, flame and gases of combustion
(as well as the projectile). These exit the barrel, together
with portions of unburned, burning and burnt pro-
pellant and other items such as wadding and plastic
containers for the pellets. These items and particles
will usually follow the projectile(s), but in some guns
they may also precede them. The distance they will
travel from the end of the muzzle is extremely variable,
depending mainly on the type of weapon and the type
of propellant. They can also escape from small gaps
around the breech and will soil hands or clothing close
to the breech at the time of discharge. The presence,
location and distribution of such items and particles
may have substantial evidential value in the forensic
investigation of a shooting incident, and determining
who fired or handled the weapon (see Box 9.1).

Injuries from smooth-bore guns

Discharge from a cartridge forces pellets along the
barrel by the gases of detonation. The pellets leave the
muzzle in a compact mass, the components of which
spread out as it travels away from the gun. The shot pat-
Figure 9.3 A 9 × 19 mm Luger semi-automatic pistol
tern expands as a long, shallow cone with its apex close
cartridge (left), and a NATO 5.56 × 45 mm automatic rifle
to the muzzle of the shotgun. The further away from the
cartridge (right).
gun the victim is situated, the larger the pellet spread,
and the larger the area of potential damage (Figure 9.4).
The cartridges for rifled weapons consist of a metal
cartridge case, usually constructed of brass, steel or alu-
minium, a primer cup located in the base, propellant
contained within the cartridge case and a single bullet Box 9.1 The forensic investigation of
fitted into the mouth of the case. The size and design of shooting incidents
the cartridge is dependent on the weapon in which it is The forensic recovery of evidence generated at
to be used and the desired ballistic performance of the the scene of the discharge of a firearm assists with
projectile. Rifle cartridges usually have a larger case to reconstruction of the incident, and in particular, the
bullet ratio, thus a larger propellant load, than hand gun assessment of projectile trajectory and range-of-fire.
cartridges. This is due to the fact that rifle cartridges are The examination of fired bullets and cartridge cases
required to be effective over a much greater distance (up recovered from the shooting scene can be used to
to 2 km) (Figure 9.3). compare the marks observed with those produced
Bullet size (or calibre) and design vary and are pri- from the discharge of a firearm suspected to have
marily concerned with ballistic performance and the been used in the crime. This information can then
ability of the projectile to transfer its kinetic energy to be entered into a firearms database that allows the
the target on impact. The formation of wounds is related determination of links between scenes at which the
to the transfer of the energy of the bullet to the body tis- same firearm may have been used and to establish
sues, and many types of ammunition are specifically gun crime trends, both nationally and internationally.
designed to result in specific wound patterns. In addition, forensic scientists can use specialist
Expanding bullets, also known as Dum-Dum bullets, equipment to determine the velocity and kinetic
are projectiles designed to expand on impact, increasing energy of a projectile in flight, which can be used to
in diameter to limit penetration and/or produce a larger establish the ballistic performance of a projectile and
diameter wound for faster incapacitation. Two typical the lethality of a weapon/ammunition combination.
designs are the hollow-point bullet and the soft-point In the UK, this is routinely used to determine if air
bullet. The Hague Convention of 1899, Declaration III weapons have lethal potential or are especially dan-
prohibits the use of expanding bullets in international gerous according to current UK firearms legislation.
warfare.
136 Ballistic injuries
(a)
(b)
4 3 2 1(a)
6 5
1(b)
Figure 9.4 Variation in appearance of a shotgun wound at
increasing range of discharge: (a)/1(a), split wound from
contact over bone; (b)/1(b), usual round contact wound;
2, close but not contact range up to approximately 30 cm
(variable); 3, ‘rat hole’ (scalloped) wound from 20 cm
to approximately 1 m (variable); 4, satellite pellet holes
appearing over approximately 2 m; 5, spread of shot
increases, central hole diminishes; 6, uniform spread with
no central hole over approximately 10 m. All these ranges
vary greatly with barrel choke, weapon and ammuni-
tion. (Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
Contact wounds are created when the gun muzzle
abuts the skin and usually results in a circular entrance
wound that approximates the size of the muzzle (Figures
9.5 and 9.6). The wound edge will be regular and often
has a clean-cut appearance with no individual pellet
marks apparent. Often there will be smoke soiling of at
least some of the margin of the wound. There may be a
narrow, circular rim of abrasion around some or all of
the entrance wound, caused when the gases of the dis-
charge enter through the wound and balloon the tissues
upwards so that the skin is pressed against the muzzle.
If the discharge was over an area supported by bone,
the gases cannot disperse as readily as they would in
soft, unsupported areas such as the abdomen, and the
greater ballooning of the skin results in splits (lacera-
tions) of the skin, which often have a radial pattern. In
contact wounds, any wadding or plastic shot containers
Figure 9.5 Suicidal twelve-bore shotgun entrance wound,
with soot soiling. The wound shows the outline of the
non-fired muzzle, indicating that the weapon was a
double-barrelled shotgun pressed against the skin at dis-
charge. (Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
Figure 9.6 Firm contact entrance wound just above the
umbilicus from a twelve-bore shotgun. Clothing pre-
vented soot soiling, but minor peripheral abrasions were
caused by impact of a belt. Gas expansion in the disten-
sible abdomen has prevented skin splitting at the wound
edges. (Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
may usually be recovered from the wound track. The tis-
sues along the wound track may be blackened and the
surrounding tissues are said to be pinker than normal
supposedly as a result of the carbon monoxide contained
within the discharge gases creating carboxyhaemoglo-
bin. As with most colour descriptions in forensic medi-
cine, the theory is not always clearly backed up by the
findings.
A close discharge, within a few centimetres of the
skin surface, will also produce a wound with a similar
appearance, but as for the muzzle gases can escape,
there will be no muzzle mark (Figure 9.7). More smoke
soiling can occur, and burning of skin, with singe-
ing and clubbing of melted hairs, may be seen around
the wound (Figure 9.8). Powder ‘tattooing’ of the skin
around the entry wound may be evident. This tattoo-
ing results from burnt and burning flakes of propellant
causing tiny burns on the skin and cannot be washed
off. As with contact discharges, wads will often be found
in the wound track.
At intermediate ranges (between 20 cm and 1 m),
there will be diminishing smoke soiling and burning of
Figure 9.7 A close-range shotgun entrance wound with
minimal scalloping of the edges, some soot staining,
and peripheral stippling. (From Burton J, Saunders S,
Hamilton S. Atlas of Adult Autopsy Pathology. Boca Raton:
CRC Press; 2015 (Fig. 2.38a page 47), with permission.)

Figure 9.8 Suicidal close range discharge of a twelve-
bore shotgun wound to the chest. This wound has torn
a large ragged defect in the chest wall and there is soot
discolouration at the medial wound edge because of the
tangential orientation of the discharge.
the skin, but powder tattooing may persist. The spread
of shot will begin, first causing an irregular rim to the
wound. This is called a ‘rat-hole’ because of the appear-
ance of the wound edge; the term ‘scalloping’ may also
be used. Additional injuries, sometimes remote from
the entrance wound, caused by the wads or plastic shot
containers may be seen (Figure 9.9). Substantial tissue
damage may occur when both barrels are fired simul-
taneously (Figure 9.10).
At a range of over 1 m, smoke damage and tattooing
are generally absent and the nature of such longer
range injuries will depend upon the spread of the shot,
which in turn is ­dependent upon the construction of
the barrel. With a normal length barrel shotgun, satel-
lite pellet holes begin to be seen around the main cen-
tral wound at a range of about 2–3 m. It is important to
­document the spread of the shot so that if the weapon
is recovered, test firings using identical ammunition
can be performed to establish the range at which a
particular spread of shot will occur. Estimates based
Figure 9.9 Abraded bruise surrounding an intermediate-
range homicidal shotgun entrance wound, caused by
impact against the skin from the opening up of the plas-
tic wadding. Note the scalloping of the wound edges.
Firearms injuries 137
Figure 9.10 Upper left thigh injury caused by interme-
diate discharge of both barrels of sawn-off shotgun
to outer leg – bruising, swelling, massive soft tissue
­disruption caused by discharge.
on generalisations about the ratio of the diameter of
this spread to the range are unreliable. At long ranges
(>20–50 m), there is a uniform peppering of shot, and
this is rarely fatal although lifechanging injuries can
occur, such as loss of eyes (Figure 9.11a–c).
Shotguns rarely produce an exit wound when fired
into the chest or abdomen, although single-pellet exit
wounds can occasionally be seen. Exit wounds can
be seen when a shotgun is fired into the head, neck or
mouth. The exit wound in these cases may be a huge
ragged aperture, especially in the head, where the skull
may virtually explode with the gas pressure from a con-
tact wound, ejecting part or even all of the brain from
the cranial cavity (Figure 9.12).
Wounds from rifled weapons
Bullets fired from rifled weapons, generally at a higher
velocity than pellets from a smooth-bore weapon, will
commonly cause both an entry and an exit wound.
However, many bullets are retained within the body
because they did not possess enough energy to com-
plete the passage through it, or energy was dissipated
on contact with other structures (e.g., bone). A bullet
has an upper limit of wounding potential derived from
its mass and velocity. Wound severity is related to the
bullet construction and its trajectory, as well as the
properties of the body tissues traversed.
Entrance and exit wounds
Contact wounds from a rifled weapon are generally cir-
cular, unless over a bony area such as the head, where
splitting caused by the propellant gas is common (Figure
9.13). There may be a muzzle mark on the skin surface if
the gun is pressed hard against the skin, and a pattern
may be imprinted from a foresight or self-loading mech-
anism. There may be slight escape of smoke, with some
local burning of skin and hair, if the gun is not pressed
138 Ballistic injuries

(a)

Figure 9.12 Suicidal twelve-bore shotgun entrance

(b) wound in a ‘site of election’ under the chin. The cir-
cular soot discoloration on the skin surface indicates
a very close (or even ‘loose’ contact) discharge. Note
the extensive destruction reflecting the explosive
effect of shotgun discharges to the head. (Reproduced
­ ermission from Saukko P and Knight B. Knight’s
with p
Pathology 4E, London, CRC Press, 2016.)

tightly. Bruising around the entry wound is not uncom-

mon (Figures 9.14 and 9.15).
At close range (up to about 20 cm), there will be some
smoke soiling and powder burns, and skin and hair may
(c) be burnt, although this is variable and depends upon
both the gun and the ammunition used. The shape of
the entry wound gives a guide to the angle that the gun
made with that area of skin: a circular hole indicates that
the discharge was at a right angle to the skin, whereas an

Bone

Figure 9.11 (a) Distant-range shotgun entrance wound,

with a central hole surrounded by peripheral satellite
pellet holes. This wound was caused by discharge from
Cratered on
approximately 4 m; measurement of shot-spread can be inner surface
compared with that created from test-firing the suspect
weapon and ammunition to provide a more accurate
assessment of range of fire. (b) Pellet injuries from a
medium range twelve-bore shotgun discharge (approxi-
mately 7–9 m, excluding the possibility of a suicidal dis-
charge). (c) Shotgun pellet injury to skin from discharge Figure 9.13 A firm contact discharge of a fired weapon
about 12 m away. ([b] From Saukko P, Knight B. Knight’s against tissue overlying bone (e.g., the skull) causes
Forensic Pathology, 4th ed. Boca Raton: CRC Press; 2016, expanding hot gases to be forced backwards towards the
Figure 8.20 with permission.) barrel, raising a dome under the skin, causing it to split.
This can give rise to a ragged entrance wound. (From
Saukko P, Knight B. Knight’s Forensic Pathology, 4th ed.
Boca Raton: CRC Press; 2016 [Fig 8.38 page 256].)
 Firearms injuries 139

Figure 9.16 Circular distant gunshot entrance wound

from a rifle bullet. There is no associated soot soiling
or burning of the wound edges, with only minimal
­marginal abrasion and bruising. (Reproduced with
Figure 9.14 Close-range gunshot entrance wound from
­permission from Saukko P and Knight B. Knight’s
a pistol, with powder tattooing on the adjacent skin.
Pathology 4E, London, CRC Press, 2016.)
The eye is blackened as a result of bleeding ‘tracking’
down from fracturing of the anterior cranial fossa in the
(Figure 9.17). No burning, smoke or powder soiling will
skull base. (Courtesy of Richard Jones.)
be evident. If the bullet has been distorted or fragmented,
or if it has fractured bone, the exit wound may be consid-
oval hole, perhaps with visible undercutting, indicates
erably larger and more irregular, and those fragments of
a more acute angle.
bullet or bone may cause multiple exit wounds, poten-
Examination of the entry wound will show that
tially leading to difficulties in interpretation.
the skin is inverted; the defect is commonly slightly
Where skin is firmly supported, as by a belt, tight
smaller than the diameter of the missile because of the
clothing or even a person leaning against a partition
elasticity of the skin. Very commonly, there is an ‘abra-
wall, the exit wound may be as small as the entrance and
sion collar’ or ‘abrasion rim’ around the hole, which is
may fail to show the typical eversion. To increase the
caused by the friction, heating and dirt effect of the mis-
confusion, it may also show a rim of abrasion, although
sile when it indents the skin during penetration. Bruising
this is commonly broader than that of an entry wound.
may or may not be associated with the wound.
The internal effects of bullets depend upon their
When the discharge was from >1 m or so, there may
kinetic energy. Low-velocity, low-energy missiles, such
be no smoke soiling, burning or powder tattooing. At
as shotgun pellets and some revolver bullets, cause
longer ranges (which may be up to several kilometres
simple mechanical disruption of the tissues in their
with a high-powered rifle), the entrance wound will
path. High-velocity bullets, however, cause far more
have the same features of a round or oval defect with an
damage to the tissues as they transfer large amounts of
abrasion collar (Figure 9.16). At extreme ranges, or fol-
energy, which results in the formation of a temporary
lowing a ricochet, the gyroscopic stability of the bullet
cavity in the tissues. This cavitation effect is especially
may be lost and the missile begins to wobble and even
pronounced in dense organs, such as liver and brain,
tumble, and this instability may well result in larger,
but occurs in all tissues if the energy transfer is large
more irregular wounds.
enough and can result in extensive tissue destruction
The exit wound of a bullet is usually everted with
split flaps, often resulting in a stellate appearance

Figure 9.17 Typical exit wound with everted, split edges,

Figure 9.15 Suicidal contact gunshot entrance wound
to the temple. The skin is burnt and split because
of the effects of the discharge products.
(Courtesy of Richard Jones.)
with no soiling of the surrounding skin. (Reproduced
from Saukko P, Knight B. Knight’s Forensic Pathology,
4th ed. Boca Raton: CRC Press; 2016, Figure 8.31,
with p
­ ermission.)
140 Ballistic injuries
Box 9.2 The death of President J.F. Kennedy
At approximately 1230 hours on Friday, 22nd November
1963, the President of the United States of America,
John F. Kennedy, was shot whilst travelling in an open-
top car being driven through Dallas, Texas. He was
taken to the nearby Parkland Hospital where he was
pronounced dead at 1300 hours. Medicolegal investi-
gation into his death has been the subject of intense
controversy ever since; his body was taken out of the
jurisdiction of Dr. Earl Rose, the Dallas County Medical
Examiner, without his agreement, and an autopsy was
performed by two Navy Pathologists and one Forensic
Pathologist with limited practical experience in a mili-
tary hospital in Bethesda, between 2000 and 2300
hours on the same day of his death.
The autopsy documentation has been heavily criti-
cised – few photographs were taken, blood-stained
contemporaneous notes were destroyed, and there
was confusion as to the interpretation of the wounds
found. The main source of dispute is in relation to the
number of gunshot wounds, their tracks within the
head and neck, and whether they represent entrance
or exit wounds.
The absence of detailed dissection contributed to
the confusion regarding a set of wounds to the back and
front of the neck (altered by emergency surgical inter-
vention to create a tracheostomy) and the p ­ recise loca-
tion of an entrance wound at the back of the head. The
ballistic and forensic pathological evidence has been
recently scrutinised on behalf of PBS America (the p
­ ublic
broadcasting service, and broadcasted via the NOVA
away from the wound track itself. The cavitation effect
may be exacerbated by the radial stretching of tissues
creating a temporary wound cavity.
The importance of an adequate description of gun-
shot wounds at autopsy is illustrated very well by the
ongoing controversy surrounding the death of US
President John F Kennedy in 1963 (Box 9.2), and sub-
stantial tissue damage and loss, and unknown other
factors (e.g., d
­ irection of wound track, distance from
weapon) all impact on the extent to which reliability
can be placed on the conclusions drawn. This, how-
ever, does not appear to prevent people coming up with
their own theories, in which speculation and general
assumptions play a large part.
Air weapons, unusual ­projectiles
and other weapons
Air guns and rifles
Air weapons rely upon the force of compressed air to pro-
pel the projectile, usually a lead or steel pellet although
darts and other projectiles may be used. There are three
Series); Dr. Peter Cummings, a Forensic Pathologist,
examined the original autopsy photographs and X-rays,
and clothing worn by JFK (the brain has not been found)
and considered the skull f­racture pattern – linear frac-
tures radiating forwards and upwards from the back of
the right side of the head, with perpendicular curved
fractures connecting them – to ­represent the effects of
a shot to the back of the right side of the head, and not
from the front of the head as many commentators have
claimed. The ballistics examination of the rifle, and full
metal jacket ammunition used, showed convincingly
that wounds to JFK and Governor John Connelly could
be explicable on the basis of two ­gunshots from the
Texas Book Depository.
The consequences of an inadequate foren-
sic autopsy in such a high-profile death have been
immense and, following the publication of the Warren
Commission Report in 1964, and that of the House
Select Committee on assassinations in 1979, there is
continued speculation about the exact nature of events
leading to JFK’s death, which is likely to continue indefi-
nitely due to the absence of key evidence and trusted
documentation. This is the case for many historically
important but historically remote deaths, and provides
much opportunity for documentary makers, authors
and amateur sleuths.
Source: Wilber CG. Medicolegal Investigation of the President
John F. Kennedy Murder. Springfield: Charles C Thomas
Publisher; 1978.
common ways in which the gas is compressed. The sim-
plest method employs the compression of a spring which,
when released, moves a piston along a cylinder; more
powerful weapons use repeated movements of a lever
to pressurise an internal cylinder. The third type has an
internal cylinder which is ‘charged’ by connecting it to a
pressurised external source. The barrel of an air weapon
may or may not be rifled; the more powerful examples
have similar rifling to ordinary handguns and rifles.
The energy of the projectile will depend mainly on
the way in which the gas is compressed: the simple
spring-driven weapon is low powered, while the more
complex systems can propel projectiles with the same
energy, and hence at approximately the same speed, as
many ordinary handguns.
The injuries caused by the projectiles from air weap-
ons will depend upon their design, but entry wounds
from standard pellets are often indistinguishable from
those caused by standard bullets in that they have a
defect with an abrasion rim. The relatively low power of
these weapons means that the pellet will seldom exit,
but if it does do so, a typical exit wound with everted
margins will result.
 Air weapons, unusual ­projectiles and other weapons
Miscellaneous firearms and weapons
A number of other implements may fulfil the criteria
for firearms while others may mimic their effects. It is
appropriate to have an understanding of the nature and
mechanics of such implements to take their possible
effects into consideration when determining injury cau-
sation. In public disorder situations, a variety of Kinetic
Energy Devices (KED) are available to law-enforcement
or security organisations. These ‘impact devices’ are
intended to deliver an impact of sufficient force to dis-
suade or prevent an acutely behaviourally disturbed
person from harming others (or themselves). A wide
range of KEDs are available around the world. They
are not intended to cause serious, life-changing or life-
threatening injury, although serious injury and fatalities
do occur. KEDs are known by a variety of names, includ-
ing plastic bullets, rubber bullets, baton rounds, impact
rounds and attenuating energy projectiles (AEP). The
names are not used consistently in the literature. Impact
rounds are made from materials of lower density than
standard bullets, are larger, and fired at lower velocities.
Impact rounds have a complex balance between effec-
tiveness and unintended consequences. Many rounds
may be safe and effective when they strike one part of
the body, but may cause serious injury or even death if
they strike a vulnerable area of the body.
Accuracy of targeting is thus a key attribute of these
types of round if unintended injuries are to be mini-
mised. The projectiles are often cylinders made of rub-
ber, plastic, wood, or foam, and can be as large as the
full-bore diameter of the launcher. Another type of KED,
is the ‘beanbag projectile’ which consists of a tough fab-
ric bag filled with compliant material. The beanbag flat-
tens on impact maximizing the area of surface contact.
Since 2005, the UK Home Office currently permits the
police the use of a bespoke blunt impact round referred
to as the Attenuating Energy Projectile (AEP) as a less
lethal support to firearms operations (see Figure 9.18).
The approved AEP (designated as L60A2) is fired from a
37 mm breech loaded weapon. The approved launcher
is the Heckler and Koch L104A2, equipped with an
approved L18A2 optical sight. The projectile has been
designed with a nose cap that encloses a void. This
design feature is intended to attenuate the delivery of the
impact energy by extending the duration of the impact
and minimising the peak forces. It thereby delivers a
high amount of energy to maximise its effectiveness,
while reducing the potential for life-threatening inju-
ries. Operational use of the AEP in the UK police service
is limited to authorised officers who have been specifi-
cally trained in use of the system. They are rarely fired
in mainland UK; perhaps 10–20 occasions per annum
although the most recent (2018) date indicate they were
deployed on 530 occasions in the preceding year. These
data are published regularly by the UK government. A
typical impact round is about 100 mm long, 35 mm in
141
Figure 9.18 Attenuated energy projectile (AEP).
diameter and when discharged has a muzzle velocity of
~69 ms -1. Marks left on the skin surface by KEDs may
be patterned and distinctive to that particular device.
The most vulnerable areas in terms of potential for seri-
ous or life-threatening injury from KEDs are: the head,
facial skeleton, brain, eyes: the thorax, rib fractures,
lung contusion/laceration, heart injury; the abdomen
and all intra-abdominal organs (solid and hollow) are
vulnerable to some forms of non-penetrating impact.
Injuries and deaths from stud guns (or power-acti-
vated or nail-guns) are well recorded. Stud guns are
devices used in the building industry to fire steel pins
into masonry or timber by means of a small explosive
charge. They have been used for suicide and even homi-
cide, but accidental injuries are more common often to
the eye and head. The skin wound often appears similar
to many small-calibre entry wounds, although the find-
ing of a nail on exploration or from imaging techniques
will usually solve the diagnostic problem.
Humane killers are devices used in abattoirs, and by
veterinary surgeons, to stun animals before slaughter.
They may fire either a small-calibre bullet or a ‘captive
bolt’, where a sliding steel pin is fired out for about 5 cm
by an explosive charge. The skin injury will depend on
the type of weapon used. These weapons have been used
for both homicide and suicide, but accidental discharges
are also recorded and may cause serious injury or death.
Bows and crossbows are used recreationally but
may also be used as weapons of assault and cause both
fatal and non-fatal injuries. These weapons fire arrows
or bolts, which are shafts of wood or metal with a set of
flights at the rear to maintain the trajectory of the projec-
tile. The tips of these projectiles may have many shapes
from the simple point to complex, often triangular,
forms. The shape of the entrance wound depends on the
type of arrowhead: broadheads produced star-shaped
142 Ballistic injuries
Serving
String Arrow retention
spring
Flight groove
Riser
Cocking Barrel
stirrup
Figure 9.19 A typical crossbow.
to triangular wounds, field-tips caused circular, oval or
slit-like injuries (Figure 9.19).
The energy produced is extremely variable, depend-
ing on the construction of the weapon. The injuries
caused depend on the energy of the projectile as well
as on its construction. However, if the projectile has a
simple pointed tip, and if it has been removed from the
body, the entry wounds can appear very similar to those
caused by standard bullets, with a central defect and
surrounding abrasion rim.
Determination of accident, s­ uicide
or murder
The determination of the circumstances in which an
individual has died from a firearm injury is crucial.
Where a firearms-related death occurs in circum-
stances in which the police or security service personnel
may be involved, an effective investigation by the State –
including an adequate autopsy – is a requirement under
human rights law (Box 9.3).
Those who investigate deaths and those who contrib-
ute to the investigation, including forensic pathologists
and forensic physicians, must always consider the possi-
bility of ‘staging’ of homicide in order to give the appear-
ance of death having occurred as a result of accident or
suicide. For those who have killed themselves, it should
be expected that the wounds are both in an accessible
site and range of the deceased’s arm, unless some other
device has been used to reach and depress the trigger. The
Sight
(style varies)
Latch
Stock
Sight
bridge
Trigger
Foregrip
Limb
Box 9.3 Human Rights law and a
­firearms-related death
Abdulmenaf Kaya was shot dead in 1993. His brother
alleged that he was deliberately killed by security
forces, but the government stated he had been
killed in a gun battle between security forces and a
group of terrorists.
A case was brought to the European Court of
Human Rights against the Turkish government
under Article 2 (‘Right to Life’) alleging unlawful kill-
ing but the Court found no violation. The govern-
ment did, however, fail to comply with an obligation
to make an effective investigation into the death, in
violation of procedural obligations inherent in the
article.
Specific deficiencies in the medicolegal investiga-
tion of this death were: performing a hasty autopsy
‘in the field’; failure to record the number of bullets
striking the deceased, and a failure to determine
range of fire; and failure to test for gunpowder traces
on the deceased’s clothing or body; failure to con-
sider any scenario other than ‘lawful killing’ by secu-
rity forces, rather than an arbitrary killing by agents
of the State.
Source: Kaya vs Turkey, 158/1996/777/978 Judgement of
19th February 1998.

Box 9.4 Activity capability following gunshot wounds
Activity capability following a gunshot wound to the
head*
An elderly man with financial and domestic difficulties,
who erroneously thought he had cancer, left his private
hotel, on a winter’s night, returning the next morning
with blood on his face. He told the maid that he was
going upstairs to the bathroom, where he collapsed and
lost consciousness. He died a few hours later, and was
found to have a gunshot wound under his chin; powder
was found in the wound (but not on the skin) and the
wound track passed upwards through the mouth and
into the skull just behind the roof of the left orbit, where
it continued through the left cerebral cortex to exit the
skull through the left frontal bone, causing extensive lac-
eration to his brain.
On retracing his steps, the man’s 45 Colt revolver was
found on a seat in a shelter in nearby gardens, at the site
of a large pool of blood, and there was a bullet hole and
fragments of bone and brain on the roof of the shelter
above the seat.
weapon must be present at the scene, although it may be
at a distance from the body because it may have been cat-
apulted away from the body by the gun recoil, or by move-
ment of the individual if death was not instantaneous.
The deceased’s DNA or fingerprints should be present
on the weapon (unless gloves were worn). Suicidal gun-
shot i­ njuries are most commonly in the ‘sites of e­ lection’,
which vary with the length of the weapon used.
Both long-barrelled and short-barrelled weapons
can be used in the mouth, below the chin, on the front
of the neck, the centre of the forehead or, more rarely,
the front of the chest over the heart. Discharges into the
temples are almost unique to handguns and are usu-
ally on the side of the dominant hand, but this is not an
absolute rule. People rarely shoot themselves in the eye
or abdomen or in inaccessible sites such as the back. It
is unusual for females to commit suicide with guns and
females are rarely involved in firearms accidents.
If suicide can be ruled out by the range of discharge,
by absence of a weapon or by other features of the injury
or the scene, a single gunshot injury could be either
accident or homicide. Multiple firearm wounds strongly
suggest homicide. However, there have been a number
of published reports of suicidal individuals who have
fired repeatedly into themselves even when each wound
is potentially fatal. The distinction between homicide,
suicide and accident can sometimes be extremely dif-
ficult and a final conclusion can only be reached after a
full medicolegal investigation.
It is as unwise to state that a gunshot wound, as with
any other sort of injury, must have been immediately
Evidence recovery 143
It had started to snow about an hour and a half before
the man returned to his accommodation, and footprints
were present in snow, as well as blood spots around the
shelter and to the private hotel. Letters written by him
the day before indicated his intention to kill himself.
Activity capability following a shotgun wound to the
chest**
Forensic pathologist DiMaio recounted a case involv-
ing substantial injury to the heart of a young man
shot in the chest with a 12-gauge shotgun, at a range
of 3–4 feet, which ‘literally shredded’ the heart; he
was capable of running 65 feet (20 metres) before
collapsing.
* Smith S. Voluntary acts after a gunshot wound of the brain.
Police J 1943;16:108–110.
** D iMaio VJM. Bloody bodies and bloody scenes. In: DiMaio
VJM. Gunshot Wounds: Practical Aspects of Firearms, Ballistics
and Forensic Techniques, 2nd ed. Boca Raton: CRC Press; 1999,
254.
fatal, as is demonstrated by the cases described in
Box 9.4. It is most likely that severe damage to the brain,
heart, aorta and any number of other vital internal
organs will lead to rapid collapse and death; however,
many forensic practitioners will have seen cases of sur-
vival (sometimes long-term) following a contact dis-
charge of a firearm into the head.
Evidence recovery
In the living, all efforts must be directed to saving life but,
if at all possible, the emergency medicine specialist, and
surgeon, should make good notes of the original appear-
ances of the injuries and preferably take good-quality
images of any entry or exit wounds before any surgical
cleaning or operative procedures are performed. Intra-
operatively it is useful to record the nature and direction
of possible wound tracks, and their length. Any foreign
objects such as wads, bullets or shot, and any skin removed
from the margin of a firearm wound during treatment,
should be carefully preserved for the police. The presence
of a forensic physician at the time can be helpful in ensur-
ing that appropriate documentation is made, for presenta-
tion at a later stage in court. Ideally, the police should be
contacted (with the individual’s consent) should surgical
intervention be required so that a ‘chain of custody’ for
evidence can be established.
Those arrested for possible involvement in firearms
offences will need detailed examination and taking of
samples, including skin and hand swabs, and nasal
samples, to identify any firearms residue. Standardised
144 Ballistic injuries
and approved processes should be applied to all these
forms of trace evidence collection.
The same general rules apply to the post mortem
recovery of exhibits. The skin around the wounds may
be swabbed for powder residue if this is necessary, but
the retention of wounds themselves is no longer consid-
ered to be essential. Swabs of the hands of the victim
should be taken. The pathologist must ensure that accu-
rate drawings and measurements of the site, size and
appearance of the wound are obtained and that distant
and close-up photographs are taken of each injury with
an appropriate scale in view.
In many countries, all firearm wounds, whether or
not they are fatal, must be reported to the police, irre-
spective of the consent of the injured individual. The
UK General Medical Council advises, having reiterated
the duty of confidentiality, ‘the police should usually be
informed whenever a person presents with a gunshot
wound. Even accidental shootings involving lawfully
held guns raise serious issues for the police about, for
example, firearms licensing’.
Blast injuries
Armed conflict and terrorist activity lead to many deaths
from explosive devices. Domestic and international
terrorist activity is now present in many countries and
therefore there has been an increase in the experience
of medical personnel in the assessment and treatment of
blast (explosive) injuries. They may derive from a number
of sources including improvised explosive devices (IEDs),
car bombs and suicide bombers. The nature of the explo-
sive device may alter the nature of injury, and the position
or activity of the individual (e.g., in a vehicle, on foot) at
the relevant time may also have substantial influence on
injury and outcome. Experience with IEDs has resulted
in substantial research and drivers for revised coding of
injury such as the Military Combat Injury Scale.
In military bomb, shell and missile explosions, the
release of energy may be so great that death and disrup-
tion from blast effects occur over a wide area. In con-
trast, terrorist devices, unless they contain very large
amounts of explosive, are generally of less power and
the pure blast effects are far more limited. However,
the locations in which such devices are often detonated
may be within relatively confined spaces (e.g., subways
and buses), influencing the subsequent pattern of injury
caused. The energy generated by an explosion decreases
rapidly as the distance from the epicentre increases.
When an explosion occurs, a chemical interaction
results in the generation of huge volumes of gas, which
are further expanded by the great heat that is also gener-
ated. This sudden generation of gas causes a compres-
sion wave to sweep outwards; at the origin, this is at
many times the speed of sound.
The pure blast effects can cause either physical frag-
mentation or disruption of those within the immediate
vicinity solely from the effects of the wave of high pres-
sure and hot gases striking the body. A minimum pres-
sure of about 700 kPa (100 lb/inch 2) is needed for tissue
damage in humans. There will also be pressure effects
upon the viscera and these effects are far more damag-
ing where there is an air–fluid interface, such as in the air
passages, the lungs and the gut. Rupture and haemor-
rhage of these areas represent the classical blast lesion.
Blast injuries can be categorised as primary to qua-
ternary injuries. Primary injuries result from the effect
of transmitted blast waves on gas-containing structure
(e.g., thorax); secondary injuries result from the impact
of airborne debris; tertiary injury results from transpo-
sition of the entire body due to blast wind or structural
collapse, and quaternary injuries make up the remain-
der, including burns. Quinary blast injuries have also
been proposed: the clinical consequences of post-deto-
nation environmental contamination such as bacteria.
Although the primary effect of blast is large, in
most cases many more casualties, fatal and otherwise,
are caused by secondary and tertiary effects of explo-
sive devices, especially in the lower-powered terrorist
bombs. These effects include:
• Burns – directly from the near effects of the explo-
sion and secondarily from fires started by the
bomb.
• Missile injuries from parts of the bomb casing,
contents or shrapnel or from adjacent objects.
• Peppering by small fragments of debris and dust
propelled by the explosion (Figure 9.20).
• Various types of injury owing to collapse of struc-
tures as a result of the explosion.
• The body impacting against other structures or
objects.
• Injuries and death from vehicular damage or
destruction, such as decompression, intrusion
of occupant space, fire and ground impact of
bombed aircraft and crash damage to cars, trucks,
and buses.
Figure 9.20 Multiple abrasions and lacerations caused
by flying debris projected in a bomb blast. (Courtesy of
Professor T K Marshall, Queens University, Belfast.)

Figure 9.21 Massive disruption of the body of an
individual who had constructed an explosive device.
(Courtesy of Richard Jones.)
The investigation of the scene of an explosion is a
huge and technically complex exercise with a number
of factors to be considered, including triaging to pre-
serve life and evacuating casualties, whilst concurrently
attempting to establish and maintain a crime scene (or
scenes) for the identification, sampling and preserva-
tion of evidence.
Full assessment of both the living and the dead
following an explosion is essential, with careful
documentation of the sites and sizes of all injuries.
Multiprofessional teams including forensic patholo-
gists, forensic physicians, forensic scientists, forensic
anthropologists, forensic odontologists and crime
scene investigators are required to ensure the integ-
rity and proper interpretation of evidence. For the
deceased, post mortem radiology is essential, in order
to identify unexploded ordinance, and items com-
prising components of the explosive device, which
may assist in determining its source. Identification
of deceased individuals is important, not only from a
moral and ethical standpoint for families, but also to
enable the relevant medicolegal authority to discharge
their responsibilities. The identification of suicide
bombers, whose bodies are frequently extensively dis-
rupted following the explosion, can be extremely chal-
lenging, particularly if previously unknown to security
services (Figure 9.21).
Box 9.5 Triage Levels and Colour Coding to categorise disaster victims in the field
• Red Triage Tag (‘Immediate’ or T1 or Priority 1):
Patients whose lives are in immediate danger and
who require immediate treatment.
• Yellow Triage Tag (‘Delayed’ or T2 or Priority 2):
Patients whose lives are not in immediate danger
and who will require urgent, not immediate, medi-
cal care.
• Green Triage Tag (‘Minimal’ or T3 or Priority 3):
Patients with minor injuries who will eventually
require treatment.
Mass disasters 145
Mass disasters
Most mass disasters are now either natural disasters
or terrorist and criminal events. For the non-specialist
doctor at the scene of a mass disaster of any kind, the
first consideration is the treatment of casualties, for
which the first, and often most testing, role is on triage.
Those faced with triaging patients in mass disasters are
faced with a number of practical and ethical decisions.
Box 9.5 illustrates the widely accepted colour-code sys-
tem used to categorise disaster victims in the field. The
‘expectant’ category can be the most challenging for
caregivers from an ethical and emotional standpoint.
In 2017, the World Medical Association (WMA) revised
its Statement on Medical Ethics in the Event of Disasters.
The key points are summarised in Box 9.6.
The International Committee of the Red Cross and
other bodies have provided advice on the appropriate
and dignified management of the dead which is con-
sidered to be one of the three key pillars of humani-
tarian response to disaster. The investigation of the
causes of death, the causes of the incident (such as a
bomb), and the identification of the dead, are specialist
operations involving individuals from a wide variety of
professional backgrounds, including those with exper-
tise in the provision of emergency mortuary accom-
modation, pathologists, dentists, the police and the
usual state agencies responsible for sudden death; in
England & Wales this is the Coroner. A team of patholo-
gists, assisted by police officers and mortuary staff, and
backed up by dental and radiological facilities, inspects
each body and records all clothing, jewellery and per-
sonal belongings still attached to the bodies. The body,
or body part, is then carefully examined for every aspect
of identity, including sex, race, height, age and personal
characteristics. All these details are recorded on stan-
dard forms and charts and the information is sent back
to the identification teams, who can compare this post
mortem information with ante mortem information
obtained from others including relatives, friends and
work colleagues. A post mortem examination is usually
performed to determine the cause of death, retrieve any
• Black Triage Tag (‘Expectant’ or No Priority):
Patients who are either dead or who have such
extensive injuries that they cannot be saved with
the limited resources available.
Adapted from Kennedy K, Aghababian RV, Gans
Source: 
L, Lewis CP. Triage: techniques and applications in
decision making. Ann Emerg Med 1996;28(2):136–144.
146 Ballistic injuries
Box 9.6 Recommendations from the WMA Statement on Medical Ethics
in the Event of Disasters (2017)
The medical profession is at the service of the patients
and society at all times and in all circumstances.
Therefore, the physicians should be firmly committed
to addressing the health consequences of disasters,
without excuse or delay.
• The WMA reaffirms its Declaration of Montevideo
on Disaster Preparedness and Medical Response
(2011) recommending the development of ade-
quate training of physicians, accurate mapping of
information on health system assets and advocacy
towards governments to ensure planning for clini-
cal care.
• The WMA recalls the primary necessity to
ensure the personal safety of physicians and
other responders during the event of disasters
(Declaration on the Protection of Health Care
Workers in situation of Violence, 2014). Physicians
and other responders must have access to appro-
priate and functional equipment, both medical
and protective.
• Furthermore, the WMA recommends the following
ethical principles and procedures with regard to the
physician’s role in disaster situations:
• A system of triage may be necessary to deter-
mine treatment priorities. Despite triage often
leading to some of the most seriously injured
receiving only symptom control such as anal-
gesia, such systems are ethical provided they
adhere to normative standards. Demonstrating
care and compassion despite the need to allo-
cate limited resources is an essential aspect of
triage. Ideally, triage should be entrusted to
authorised, experienced physicians or to physi-
cian teams, assisted by a competent staff. Since
cases may evolve and thus change category, it
is essential that the official in charge of the tri-
age regularly assesses the situation.
The following statements apply to treatment beyond
emergency care:
• It is ethical for a physician not to persist, at all
costs, in treating individuals ‘beyond emergency
care’, thereby wasting scarce resources needed
elsewhere. The decision not to treat an injured
person on account of priorities dictated by the
disaster situation cannot be considered an ethi-
cal or medical failure to come to the assistance of
a person in mortal danger. It is justified when it is
intended to save the maximum number of indi-
viduals. However, the physician must show such
patients compassion and respect for their dignity,
for example, by separating them from others and
administering appropriate pain relief and seda-
tives, and if possible, ask somebody to stay with
the patient and not to leave him/her alone.
• The physician must act according to the needs
of patients and the resources available. He/she
should attempt to set an order of priorities for
treatment that will save the greatest number of
lives and restrict morbidity to a minimum.
Relation with the patients
• In selecting the patients who may be saved, the
physician should consider only their medical sta-
tus and predicted response to the treatment, and
should exclude any other consideration based on
non-medical criteria.
• Survivors of a disaster are entitled to the same
respect as other patients, and the most appropri-
ate treatment available should be administered
with the patient’s consent.
Aftermath of disaster
• In the post-disaster period, the needs of survivors
must be considered. Many may have lost fam-
ily members and may be suffering psychological
distress. The dignity of survivors and their families
must be respected.
• The physician must make every effort to respect
the customs, rites and religions of the patients and
act in impartiality.
• As far as possible, detailed records should be kept,
including details of any difficulties encountered.
Identification of patients, including the deceased,
should be recorded.
Media and other third parties
• Physicians should take into consideration that
in any disaster media is present. The work of
the media should be respected and facilitated
as appropriate in the circumstances. If needed,
physicians should be empowered to restrict the
entrance of reporters and other media represen-
tatives to the medical premises. Appropriately
trained personnel should handle media relations.
• The physician has a duty to each patient to exer-
cise discretion and to seek to ensure confidential-
ity when dealing with third parties. The physician
must also exercise caution and objectivity and
(Continued)

Box 9.6 (Continued) Recommendations from the WMA Statement on Medical Ethics
in the Event of Disasters (2017)
respect the often emotional and politicised atmo-
sphere surrounding disaster situations. Any and all
media, especially filming, must only occur with the
explicit consent of each patient who is filmed. With
regard to social media use, p
­ hysicians must adhere
to these same standards of discretion and respect
for patient privacy.
Duties of paramedical personnel
• The ethical principles that apply to physicians
in disaster situations should also apply to other
healthcare workers.
Training
• The WMA recommends that disaster medicine
training be included in the curricula of university
and post-graduate courses in medicine.
Responsibility
• The WMA calls upon governments and insurance
companies to cover both civil liability and any
foreign objects that, for example, may be related to an
explosive device, and to seek any further identifying fea-
tures, such as operation scars and prostheses.
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personal damages to which physicians might be
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the line of duty.
The WMA requests that governments
• Ensure the preparedness of healthcare system to
serve in disaster settings.
• Share all information related to public health
timely and accurately.
• Accept the participation of demonstrably quali-
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• Give priority to the rendering of medical services
over anything else that might delay necessary
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ukpga/1968/27/contents (Accessed 8 April 2019).
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(Accessed 8 April 2019).
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ters/ (Accessed 8 April 2019).
10 Regional injuries and
­patterns of injury
▪▪ Introduction
▪▪ Head injuries
▪▪ Neck injuries
▪▪ Spinal injuries
Introduction
Specific regions of the body may be particularly suscep-
tible to types of trauma that may not cause serious or
fatal injury elsewhere. One example of this is the single
stab wound. If this penetrates the limbs then a serious
or fatal outcome is very unlikely, unless a large artery is
penetrated. If a single stab wound penetrates the heart or
the abdominal aorta a fatal outcome is much more likely.
Consideration of patterns of injuries according to the body
region, and the potential complications of those injuries,
is therefore a relevant component in both the clinical and
pathological evaluation of trauma.
Head injuries
Any trauma to the head or face that has the potential
for damaging the brain can have devastating conse-
quences. Normally the brain is protected within the
bony skull, but it is not well restrained within this
compartment and injuries to the brain result from dif-
ferences between the motion of the solid skull and the
relatively ‘fluid’ brain. There are three main compo-
nents of the head: the scalp, the skull and the brain.
Scalp
The scalp is vascular, hair-bearing skin; at its base is a
thick fibrous membrane – the galea aponeurotica. Lying
between the galea and the skull is a very thin sheet of
connective tissue penetrated by blood vessels (emissary
veins) emerging through the skull. Beneath this con-
nective tissue is the periosteum of the outer table of the
skull. Injury to the vascular scalp can lead to seemingly
dramatic haemorrhage which can usually be stopped by
local application of pressure but, in some circumstances
(e.g., acute alcohol or drug intoxication), can lead to
physiological shock and death. Bleeding scalp injuries
can continue to ooze after death, particularly when the
head is in a dependent position.
The scalp is easily injured by blunt trauma as it can be
crushed between the weapon or object and the under-
lying skull. Bruises of the scalp are associated with
▪▪ Chest injuries
▪▪ Abdomen
▪▪ Bibliography and information sources
▪▪ Further general resources
prominent oedema because this normal tissue response
cannot spread and dissipate as easily as in other areas
of the body. The easiest way to detect scalp injuries is
by finger palpation, but shaving is often required for
optimal visual assessment, documentation and pho-
tography of injury in the deceased, and sometimes in
the living. In the living, a good history from the consent-
ing, cooperative individual, examined in good lighting,
can normally localise any injury. It is surprisingly dif-
ficult to identify the site of profuse bleeding from the
scalp in an individual with abundant head hair. In the
living, if there is evidence of stamping or assault by an
implement it may also be necessary to shave the hair so
that potential ‘patterned injury’ can be identified and
recorded for overlay comparison.
Lacerations of the scalp can usually be distinguished
from incised wounds; careful examination often reveals
crushed, abraded or macerated wound edges and tissue
bridging in the wound depths (Figure 10.1).
Occasionally such a distinction is more difficult, and
it may be that the nature and properties of the scalp, its
relative ‘thinness’ and tethering to the skull, contributes
to the appearance of an incised wound following blunt
impact.
Tangential forces or glancing blows, either from an
implement or from a rotating tyre (e.g., in a road traf-
fic incident), may tear large flaps of tissue, exposing the
underlying skull. If hair becomes entangled in rotating
machinery, portions of the scalp may be avulsed. These
are referred to as ‘scalping’ injuries.
Skull fractures
The skeleton of the human head is divided into three main
parts: the mandible, the facial skeleton and the closed
container that contains the brain – the calvarium. The cal-
varium is made up of eight plates of bone, each of varying
thickness, with buttresses passing through and across the
bony margins. The skull is designed in part to protect the
brain and in part to provide a mobile but secure platform
for the receptor organs of the special senses.
The complexity of the skull structure means that
mechanisms of skull fracture can be extremely complex
150 Regional injuries and p
­ atterns of injury
Figure 10.1 Scalp laceration caused by a heavy torch.
Following shaving of hair from around the injury, the
crushed and abraded wound edges can clearly be
seen. (Reproduced with permission from Saukko P and
Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
as a result of both direct force (e.g., direct impact to the
parietal bone causing a linear fracture) and indirect
force (e.g., an orbital blowout fracture caused by impact
to the eyeball). These mechanisms have been studied
extensively and much is known about the way the skull
behaves when forces are applied to the head. The skull,
although rigid, is capable of some distortion and if the
forces applied exceed the ability of the skull to distort,
fractures will occur. The site of fracture therefore rep-
resents that point at which the delivered energy has
exceeded the capability of the skull to distort, which
may not necessarily be at the site of impact, unless that
applied force has resulted in a localised depressed frac-
ture. The skull’s capability to distort before fracturing
varies with age, and an infant skull may permit signifi-
cant distortion following impact without fracturing.
Apart from depressed fractures underlying major,
localised areas of trauma, skull fractures alone are not
necessarily life threatening. The presence of a skull frac-
ture indicates the application of blunt force to the head,
and it is the transmission of such force to the intracranial
contents – i­ ncluding the brain – that has the potential
to cause life-threatening injury. Fatal brain injury can
occur in the absence of externally visible scalp injury,
or skull fracture and, conversely, scalp injury overly-
ing skull fracture may be associated with minimal (or
no recognisable) brain injury or neurological deficit. In
clinical practice, however, intracranial injury should
always be suspected in the presence of skull fracture.
A pathologist can only make broad comments about
the possible effect upon an individual of a blow to the
head. As with all injuries, a wide spectrum of effects is to
be expected in a population sustaining the same injury
in exactly the same way.
Scalp abrasions, bruises or lacerations represent
contact injuries, and their presence may assist in the
(a)
(b)
(c)
(d)
Secondary fracture
in anterior fossa floor
Transverse
‘hinge’ fracture
Ring fracture
around foramen
magnum
Figure 10.2 Types of skull fracture. (a) Linear fracture; (b)
‘spiders web’ fracture; (c) depressed fracture; and (d) base
fractures.
identification of the point of contact/impact. Bruises,
however, may develop and move across tissues planes,
and may not precisely represent the site of contact/
impact by the time the scalp is examined. Abrasions do
identify sites of impact. A direct blow to the nose can
cause blunt force injuries to the nose itself, but may also
cause bilateral periorbital bruising, as may impacts
to the central forehead, even though no impact was
applied to the eyes or orbital region.
There are a variety of fracture types to the skull, often
dependent on the nature of the impacting force (Figure
10.2). Blows to the top of the head commonly result in long,
linear fractures that pass down the parietal bones and may,
if the force was severe enough, pass inwards across the
floor of the skull, usually just anterior to the petrous tem-
poral bone in the middle cranial fossa. If the vault fractures
extend through the skull base from both sides, they may
 Head injuries 151

meet in the midline, at the pituitary fossa, and produce

a complete fracture across the skull base, referred to as a
hinge fracture (Figure 10.3). This type of fracture indicates
the application of very severe force and may be seen, for
example, in traffic accidents or falls from high buildings.
Falls from a height onto the top of the skull or onto
the feet, where the force is transmitted to the base of the
skull through the spine, may result in ring fracture of the
base of the skull around the foramen magnum, whereas
significant ‘broad surface’ blows to the skull vault, par-
ticularly the parietal bones, may result in a ‘spider’s web’
type of fracture composed of radiating lines transected
by concentric circles.
Depressed fractures result in fragments of skull
being forced inwards and, because of the bilayer con-
struction of the skull, the degree of inner table fragmen-
tation may be much greater than that of the outer table
and fragments of bone can be driven into the underlying
meninges, blood vessels and brain tissue. Blows to the
head by implements such as round-headed hammers Figure 10.3 A ‘hinge fracture’ of the skull base caused
may cause depressed vault fractures that have a curved by impact to the left side of the head after the v­ ictim
outline with dimensions and a profile similar to that of was thrown to the ground, having been hit by a car.
the impacting surface of the implement (Figure 10.4). (Reproduced with permission from Saukko P and
The orbital plates, the upper surfaces of the orbits Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)
within the skull, are composed of extremely thin sheets
of bone which are easily fractured, and these ‘blow-out’ The anatomy of the blood vessels within the skull
fractures may be the only indication of the application has a major influence on the type of bleeding that will
of significant force to the skull. They may be seen as a occur following trauma (Figure 10.5). The meningeal
consequence of a fall onto the back of the head. arteries run in grooves in the inner table of the skull and
Skull fractures in children and infants have great lie outside the dura. They are generally protected from
significance in the forensic setting and their interpre- the shearing effect of sudden movement but are dam-
tation can be extremely difficult. It is self-evident that aged by fracture lines that cross their path. The venous
skull fractures may be the result of either deliberate or sinuses lie within the dura and the connecting veins
accidental acts and differentiation will depend on the pass between the sinuses and the cortical veins; these
consideration of as much relevant information as possi- vessels are at particular risk of ‘shearing’ injury when
ble. The assessment of such injury is now seen as essen- there is differential movement between the brain and
tially multiprofessional and may require the expertise the skull. The effective blood supply to the brain (the
of others such as radiologists, paediatricians and endo- cerebral arteries and veins), lies beneath the arachnoid
crinologists. membrane and is generally protected from all but pen-
etrating injuries.

Intracranial haemorrhage
The clinical significance of any space-occupying lesion
within the cranial cavity is the effect that the resultant
raised intracranial pressure has on brain structure and
function.
Intracranial bleeding, which in effect creates a
space-occupying lesion, is the cause of many deaths
and disability following head injury, often as a result of
delayed or missed diagnosis. Bleeding can compress the
brain and, if it ­continues for sufficient time, and in suffi-
cient quantity, can raise the pressure within the cranial
cavity. As the intracranial pressure increases, blood flow Figure 10.4 Depressed skull fracture, with rounded
to the brain decreases and, if the intracranial pressure contours in the centre of the image, closely replicating
reaches a point where it equals or exceeds arterial blood the dimensions of a round-headed hammer. Additional
pressure, the blood flow to the brain will cease. fracture lines also seen. (Courtesy of Richard Jones.)
152 Regional injuries and p
­ atterns of injury
Scalp
Emissary vein
Dura
Cortical vein
Cerebral
artery
Arachnoid
granulation
Subarachnoid
space
Falx
Figure 10.5 Anatomy of the blood vessels and structures related to cranial bones in diagrammatic form.
Two main types of haemorrhage within the skull
cavity, each resulting in haemorrhage in different tis-
sue planes, are extradural and subdural haemorrhage.
Extradural haemorrhage is associated with damage to
the meningeal artery, particularly the middle menin-
geal artery, in its course in the temporal bone (Figure
10.6a and b). Damage to this vessel leads to arterial
bleeding into the extradural space. As the blood
accumulates, it separates the dura from the overlying
skull and forms a haematoma (a collection of blood).
Arterial bleeding is generally rapid, and the develop-
ment of the haematoma will result in a rapid displace-
ment of the brain and the rapid onset of symptoms.
Extradural haemorrhages may present in the clinical
setting with head trauma followed by a ‘lucid period’
of half an hour or more, before sudden, rapid dete-
rioration occurs. Rarely, extradural haemorrhage can
develop as a result of venous bleeding from damaged
perforating veins or dural sinuses, in which case the
development of symptoms will be slower.
The second most important cause of traumatic intra-
cranial haemorrhage is damage to the communicating
veins as they cross the (potential) ‘subdural space’, caus-
ing subdural haemorrhage (Figure 10.7). This venous
damage is not necessarily associated with fractures of
the skull. In many instances, particularly in the very
young and the very old, there may be no apparent pre-
vious history or evidence of any trauma to the head.
These venous injuries are associated with rotational or
shearing forces that cause the brain to move relative to
the inner surface of the skull; this motion is thought to
stretch the thin-walled veins, causing them to rupture.
The venous bleeding lies in the subdural space. Recent
subdural haemorrhages are dark red in colour and shiny,
Periosteum
Thicker
outer table
Diploe
Thinner inner
table
Meningeal
artery
Venous sinus
Pia mater
Arachnoid
mater
Brain
but begin to turn brown after several days; microscopi-
cally, haemosiderin can be identified with Perls’ stain
(Figure 10.8). Older subdural collections (chronic sub-
dural haematoma) may be enclosed in gelatinous ‘mem-
branes’, which can harden into a firm rubbery capsule
in extreme cases. Such old collections of subdural blood
are most commonly seen in the elderly, whose cerebral
atrophy allows space for the formation of the haematoma
without apparent significant clinical effect. Chronic
subdural haematomas are also seen in those prone to
frequent falls, such as those with alcohol dependencies.
Occasionally, subdural haemorrhages may be present for
many months or even years before diagnosis, which can
be difficult because of the often non-specific neurologi-
cal changes. Spontaneous subdural haemorrhages can
occur without trauma (although there may be underly-
ing pathology such as sepsis, bleeding diathesis or vas-
cular malformation).
The effects of both extradural and subdural haem-
orrhages are essentially the same: they can act as
space-occupying lesions compressing the brain and,
as discussed below, and at their most severe, can cause
internal herniation (e.g., through the tentorium cer-
ebelli, or the foramen magnum – ‘coning’). There may
also be resultant traumatic brain contusion and swell-
ing, which compounds the clinical deterioration and
can hasten a fatal outcome in the absence of medical
and neurosurgical intervention.
Traumatic subarachnoid haemorrhage
Small areas of subarachnoid haemorrhage are common
where there has been direct trauma to the brain, either
from an intrusive injury, such as a depressed skull frac-
ture, or from movement of the brain against the inner

(a)
Fracture line
Skull
Dura
Meningeal artery
Haematoma
(b)
Figure 10.6 Extradural haemorrhage. Schematic repre-
sentation (a) of the formation of an extradural haemor-
rhage and autopsy appearance (b) of a large right-sided,
temporoparietal, extradural haemorrhage associated
with deep scalp bruising at the site of impact. There
was a linear skull fracture on the right passing through
the middle meningeal artery. (Reproduced with permis-
sion from Saukko P and Knight B. Knight’s Pathology 4E,
London, CRC Press, 2016.)
surface of the skull as a result of acceleration or decel-
eration injuries. These small injuries are usually asso-
ciated with areas of underlying cortical contusion and
sometimes laceration.
Large basal subarachnoid haemorrhages can be
of traumatic origin and follow direct blows or kicks to
the neck, particularly to the upper neck adjacent to the
ear. However, any blow, or even movement to avoid an
impact which results in rapid rotation and flexion of the
head on the neck can cause such damage. The vertebral
arteries are confined within foraminae in the lateral
margins of the upper six cervical vertebrae and are sus-
ceptible to trauma either with or without fracture of the
foramina. It is considered that arterial injury leading
to basal subarachnoid haemorrhage most likely occurs
in the intracranial portions of the vertebral arteries
(Figure 10.9a and b).
Head injuries 153
(a)
Skull
Dura
Arachnoid
Pia and brain
surface
Dura sinus
Ruptured bridging vein
Haematoma
(b)
Figure 10.7 Subdural haemorrhage. Schematic repre-
sentation of the formation of a subdural haematoma (a)
and autopsy appearance of an acute right-sided subdural
haemorrhage (b). (Courtesy of Richard Jones.)
Most basal subarachnoid haemorrhages are non-
traumatic in origin and arise from the spontaneous
rupture of a berry aneurysm of one of the arteries in the
circle of Willis. In the deceased, particular care must be
taken to exclude this natural cause, and special autopsy
dissection techniques are required to evaluate the
integrity of the vertebral arteries.
Figure 10.8 Microscopy of a ‘healing’ acute subdural
haemorrhage, of approximately 4 days’ duration, with
iron-pigment-laden macrophages demonstrated by
Perls’ staining. (Courtesy of Richard Jones.)
154 Regional injuries and p
­ atterns of injury

(a) Traumatic brain injury

(b)
Figure 10.9 Traumatic basal subarachnoid haemorrhage.
(a) Autopsy appearance of basal subarachnoid haemor-
rhage, covering the brain-stem, visualized following
removal of the cerebral hemispheres and tentorium cer-
ebelli. The basilar artery has been ligated. (b) The source
of the bleeding is a tear in a vertebral artery, confirmed
following visualisation of fluid leakage from the cannu-
lated injured vessel. (Courtesy of Richard Jones.)
Injuries that have resulted in skull fractures or intra-
cranial haemorrhage are clear macroscopic markers of
significant force having been applied to the head and
therefore to the brain. Sometimes, however, these mark-
ers are absent but, as a result of acceleration or decelera-
tion forces, the brain has been significantly traumatised.
Whatever the precise cause of the trauma, the effects on
the brain of traumatic brain injury (TBI) are the same
and, as a consequence of the body’s response to primary
TBI, cerebral oedema develops the effects of which give
rise to secondary brain injury. The mechanism of cere-
bral oedema is complex, but is in part caused by transu-
dation of fluid into the extracellular space.
As oedema develops, the brain swells and, because it
cannot expand beyond the confines of the cranial cavity
to compensate for this swelling, the intracranial pres-
sure rises and the brain is ‘squeezed’ around meningeal
folds (under the tentorium cerebelli, causing injury to
the temporal lobe unci and exerting pressure on the
brain-stem, for example), and downwards through the
foramen magnum. This type of internal herniation is
known as coning and exerts pressure on the brain-stem
(Figure 10.10).
The oedema increases the brain weight and the sur-
face of the brain becomes markedly flattened, often with
haemorrhage and necrosis of the unci and the cerebellar
tonsils; sectioning reveals compression of the ventricles,
sometimes into thin slits.
Direct injuries to the brain from depressed or com-
minuted skull fractures can result in areas of bruising
and laceration of the cortex, often associated with larger
sites of haemorrhage. These injuries can occur at any

(a) Normal Oedematous (b)

Normal weight
(<1500 g) Increased weight
(>1500 g)
Palpable sulci
Flattened gyri
Filled sulci
Rounded gyri

Normal hippocampal Grooved uncus,

gyrus and uncus swollen hipocampal
gyrus

Normal cerebellar Herniated cerebellar

tonsil tonsil

Midliner shift if
oedema is unilateral

Figure 10.10 (a) Schematic representation of the effects of brain swelling and ‘internal herniation’ caused by raised
intracranial pressure. (b) Transtentorial herniation in brain trauma. Compression of the medial temporal lobes against
the tentorium edges has caused bilateral haemorrhagic necrosis (arrows). Haemorrhagic infarcts in the left temporal
lobe (asterix) followed compression of the left posterior cerebral artery, and there is slight midline shift to the right (of
the vertical white line).

site, above or below the tentorium. Penetrating injuries
from gunshots or from stab wounds can cause injuries
deep within the white matter, and the tissue adjacent to
the wound tracks will often be contused and lacerated.
Axonal injury
The terminology of axonal injury is in flux. However, dif-
fuse axonal injury (DAI) is one of the most common and
important pathological features of TBI. Neuronal axons
in the white matter of the brain appear to be particu-
larly vulnerable to injury due to mechanical loading of
the brain during, for example, blunt impact head injury.
Traumatic DAI has been found in all severities of TBI
and is even thought to underlie concussion associated
with mild head injury. The transmission of mechani-
cal energy following blunt impact head injury, which
may be accompanied by rotational head movement
and acceleration/deceleration forces, damages axonal
processes. Traumatic DAI encompasses mechanical
disruption of axonal cytoskeletal components as well
as subsequent physiological abnormalities that follow
disturbances of function. The clinical manifestation of
DAI ranges from confusion and concussion to cognitive
dysfunction and persistent coma. Recent research has
highlighted links between TBI and the development of
neurodegenerative disorders – such as Alzheimer’s dis-
ease – later in life.
When the brain is subjected to the forces described
above, traumatic injury to axons within the brain sub-
stance can occur as a consequence of ‘shearing’ effects
because of the differential movement of the various com-
ponents of the brain which move in different ways, or at
different speeds, relative to each other. This shearing can
cause contusions and lacerations deep within the sub-
stance of the brain, and differential movement of com-
ponents of the brain results in damage at the interface
between those structures.
The shearing effects are also identifiable on micros-
copy, where damage to axons can be visualised with the
aid of special staining techniques. These changes have
been termed traumatic axonal injury which, when pres-
ent at multiple sites throughout vulnerable areas of the
cerebral hemispheres and brain-stem, may be described
as diffuse traumatic axonal injury. Axonal injury takes
a variable time to develop, or at least to become appar-
ent under the microscope, and in cases of immediate or
very rapid death following brain injury the microscopic
changes may not be identifiable. β-amyloid precursor
protein (β-APP) takes part in the axoplasmic transport
system and accumulates at sites of interruption of axo-
plasmic flow. Where there has been survival for sev-
eral hours, immunohistochemical staining for β-APP
may identify injured axons, although interpretation of
such staining may be problematic, given that this stain
also highlights axonal injury caused by non-traumatic
Head injuries 155
Figure 10.11 Microscopy of axonal injury. The immunohis-
tochemical staining of β-amyloid precursor protein (β-APP)
demonstrates axonal injury in white matter (corpus cal-
losum). Discrete axonal swellings and ‘axonal retraction
bulbs’ can be visualised following traumatic brain injury if
the injured person survived for some hours after sustain-
ing their head injury. (Courtesy of Richard Jones.)
phenomena including hypoxia-ischaemia (Figure 10.11).
Progressive axonal injury, resulting in the formation of
axonal retraction ‘bulbs’, can easily be recognised by
silver staining techniques after some 12 hours following
axonal injury, and subsequently on routine haematoxylin
and eosin (H&E) staining.
It has been recognised for many decades that some
boxers developed the disabling progressive neurode-
generative ‘punch drunk syndrome’ (called dementia
pugilistica). Repetitive mild TBI led to the abnormal
accumulation of another protein in the brain – tau – and
recent research has identified neurofibrillary tangles
and neuropil threads containing this protein in distri-
butions different to those seen in other neurodegen-
erative diseases, prompting the description of a new
entity – Chronic Traumatic Encephalopathy (CTE). CTE
has been described in the brains of American Football
players, military personnel exposed to explosive blasts
and, most recently, soccer players (from ‘heading the
­football’).
Coup and contrecoup injuries
A coup injury to the brain is one that occurs at the site of
primary impact, when deformation of the skull contacts
the underlying brain. The site of scalp injury will gener-
ally approximate the site of brain injury. Such a coup
injury to the brain is often represented by localised sub-
arachnoid haemorrhage and cortical surface contusion
with, or without, laceration.
In a ‘moving head injury’, such as might be expe-
rienced following a fall onto the back of the head, for
example, impact causes the skull to stop moving sud-
denly, while movement of the brain continues momen-
tarily before also stopping. As a consequence of such
relative movement, and the effects of deceleration
forces acting on the skull and the cranial contents, a
distinctive pattern of head/brain injury can be recog-
nised (Figure 10.12a and b).
156 Regional injuries and p
­ atterns of injury
(a)
Scalp injury
(fracture)
brain damage
(b)
May suffer
secondary fracture
Temporal and
frontal contusion
Scalp injury
(fracture)
Figure 10.12 Example of schematic representation of the
formation of coup and contrecoup brain injury. (a) Impact
to the non-moving head causing coup injuries, and (b) a
fall onto the back of the head – a ‘moving head injury’ –
causing contrecoup injuries.
The site of impact is characterised by contact inju-
ries to the scalp (bruising, abrasion and laceration,
for example), skull (linear or depressed fractures) and
sometimes cerebral contusion, although these are less
commonly seen when the impact site is on the back of
the head. Intracranial bleeding, particularly subdural
and subarachnoid haemorrhage may be present and, of
particular significance in interpreting the nature of the
head injury, there are frequently cerebral contusions at
sites remote from the primary impact. These are referred
to as contrecoup injuries and may be, for example, on
the under-surfaces of the frontal and temporal lobes fol-
lowing a fall onto the back of the head (Figure 10.13). The
precise mechanism by which they are caused remains
controversial, suggestions being that they represent the
effects of contact against the irregular surfaces of the
anterior and middle cranial fossae (of the skull base),
or perhaps the effect of differential pressures within the
brain following deceleration. The ability to distinguish
between coup and contrecoup injuries is often impor-
tant in the criminal setting, for example when attempt-
ing to determine sites of weapon impact, as opposed to
impact caused by a subsequent fall.
Figure 10.13 Contrecoup contusions on the inferior-­
surface of the brain. (Courtesy of Richard Jones.)
A definitive opinion regarding the nature of head
and brain injuries in a difficult case will require close
clinico-pathological correlation, a neuropathological
­
assessment (if deceased) and an evaluation of witness
and other evidence. Examples of causes of death following
head injury are listed in Table 10.1.
Neck injuries
The neck is the site of many different types of injury,
some minor, some completely incapacitating and result-
ing in death. These can be blunt (direct and indirect)
and sharp force/penetrating in nature. Their relevance
in forensic medicine results from the presence of a large
number of vital structures – the upper respiratory and
gastrointestinal tracts, major blood vessels, major nerve
trunks, the vertebral column and the spinal cord. It is
particularly prone to injury as a consequence of assault
or accidents as it can be grasped easily and the weight
of the head means that rapid movement of the head on
the neck (e.g., sudden deceleration in a road traffic colli-
sion) can result in substantial trauma. Protection of the
integrity of the neck in the living, following severe trau-
matic insults, likely to have caused skeletal damage, is
imperative prior to clinical and radiological assessment.
Layered dissection of the anterior (and often posterior)
neck structures is an integral part of the forensic post
mortem examination.
Penetrating trauma – sharp force or ballistic –
to the neck has the potential to injure a variety of com-
plex structures and requires careful evaluation in the
living as well as at post mortem examination. Of partic-
ular forensic significance in incised wounds to the neck
is the pattern of injury (self-inflicted versus assault), the
 Spinal injuries 157

Table 10.1 Examples of causes of death following head injury

Timing after head injury Cause of death
Immediate • decapitation
• brainstem disruption
Very rapid • diffuse cerebral vascular injury
• traumatic basal subarachnoid haemorrhage
• severe diffuse traumatic axonal injury
Rapid • diffuse traumatic axonal injury
• cerebral substance disruption
• haemorrhage: e.g., external from scalp wounds; internal via injured cerebral
vessels (including into nose/throat/lungs)
Delayed • mass effect of intracerebral haemorrhage with internal cerebral herniation
• global brain swelling (oedema) with raised intracranial pressure and internal
herniation
• hypoxic-ischaemic encephalopathy
• cerebral infarction
• infection: meningitis; pneumonia (aspiration or hypostatic following
intubation/mechanical ventilation)
• post-traumatic epilepsy
Remote (long delay post injury) • post-traumatic epilepsy
• post-traumatic dementia (pugilistica)/chronic traumatic encephalopathy (cte)
• infection as a complication of persistent vegetative (or minimally conscious)
state: ‘bed sores’, pneumonia, renal tract infection etc.

presence of arterial injury capable of explaining blood
patterns such as ‘arterial spray’ or ‘arterial rain’ at the
scene of a suspicious death and venous injury raising
the possibility of death having been caused by cardiac
air embolism.
The application of pressure to the neck, whether it
be manual or by means of a ligature, and the pattern of
injury seen in such a scenario, is considered separately
in Chapter 11.
Spinal injuries
The spine is a complex structure with interlocking but
mobile components often described as having anterior,
middle and posterior ‘sub-columns’. Damage to one of
the sub-columns is unlikely to result in instability: if
the middle column is damaged then the likelihood of
instability, neural damage is increased, and if all three
columns are involved then fracture-dislocations and
spinal cord damage is expected. The spine is designed to
flex to a great extent but lateral movement and extension
are more limited. The spine is very commonly injured
in major trauma such as road traffic collisions or falls
from a height, and severe injury with discontinuity is
easily identified. The history of the event (e.g., the height
fall distance) is often very important in predicting the
potential injury patterns, but distances may be poorly
estimated by bystanders. Sometimes the spinal injuries
are more subtle and at post mortem it is only after care-
ful dissection that damage to the upper cervical spine
and, in particular, disruption of the atlanto-occipital
joint will be revealed.
For the survivors of trauma, spinal injuries may have
some of the most crucial long-term effects because the
spinal cord is contained within the spinal canal and
there is little, if any, room for movement of the canal
before the cord is damaged. The sequelae of spinal
damage will depend upon the exact anatomical site and
mechanism of injury.
The type of injury to the spine will depend upon
the degree of force and the angle at which the spine is
struck. A column is extremely strong in compression
and, unless the force applied is so severe that the base
of the skull is fractured, vertically applied forces will
generally result in little damage if the spine is straight.
Angulation of the spine will alter the transmission of
force and will make the spine much more susceptible to
injury, particularly at the site of the angulation.
Force applied to the spine may result in damage to
the discs or to the vertebral bodies. The other major
components of the vertebrae – the neural arches and the
transverse processes – are more likely to be injured if the
direction of the force of the trauma is not aligned with the
spine.
158 Regional injuries and p
­ atterns of injury
Figure 10.14 Crushed vertebral body as a result of a
hyperflexion injury.
Whiplash injuries associated with road traffic fatali-
ties are very common and are caused by hyperextension
of the neck; hyperflexion is less likely to cause damage.
Hyperflexion injuries can be caused if heavy weights are
dropped onto the back of a crouching individual; this
scenario may be seen in roof falls in the mining industry.
Hyperflexion injuries are also seen in sports – particu-
larly rugby scrums and diving. Such injuries can cause
fatalities or substantial disability such as quadriplegia.
Forceful extension of the spine can be seen, although
rarely now, in the cervical injuries associated with judi-
cial hanging where there is a long drop before the sud-
den arrest and forceful extension of the neck. Forceful
flexion of the spine will commonly lead to the ‘wedge’
fracture or compression of the anterior aspect of a ver-
tebral body (Figure 10.14). Lateral forces will lead to frac-
ture dislocations where one vertebral body passes across
its neighbour; this displacement will seriously compro-
mise the integrity of the vertebral canal. Damage to the
intervertebral discs can occur as a solitary lesion or it
may be part of a more complex spinal injury.
Chest injuries
The chest can be subject to all kinds of injury and is
particularly susceptible to both blunt and penetrating
injuries.
Adequate respiration requires freedom of movement
of the chest, functioning musculature and integrity of the
chest wall. Any injury that impairs or prevents any of these
activities will result in a reduction in the ability to breathe,
which may result in asphyxiation. External pressure on
the chest may result in traumatic asphyxia by restricting
movement; this may occur during road traffic collisions
or following collapse of structures such as mine tun-
nels, or buildings in earthquakes. Pressure on the chest
that restricts movement may also occur if the individual
simply gets into, or is placed into, a position in which the
free movement of the chest is restricted. This positional
asphyxia occurs most commonly in individuals that are
rendered immobile through alcohol or drugs and may be
seen following restraint in custodial settings; it may also
be seen in the healthy, for example, attempting to climb
through a small window to gain access to a property.
Blunt injury may result in fractures of the ribs. The
fracture of a few ribs is unlikely to have much effect,
other than causing pain, in a fit adult. In an individual
with respiratory disease (e.g., chronic obstructive pul-
monary disease) there are greater risks for the develop-
ment of respiratory compromise or infection. If there are
numerous rib fractures, and particularly if they are in
adjacent ribs, the functional integrity of the chest wall
may be compromised, limiting respiratory capabili-
ties even in fit individuals. Two fractures to a number
of adjacent ribs may result in the so-called ‘flail’ chest
where, clinically, the area between the fractures may
be seen to move inwards on inspiration – paradoxical
respiration (Figure 10.15). The clinical effects of such
injuries depend on their extent and on the respiratory
reserve of the individual: an elderly man with chronic
lung disease may be tipped into terminal respiratory
failure by injuries that would only be a painful irritant
to a fit young man. Trauma that has fractured left sided
10th, 11th and 12th ribs may be substantial enough to
cause injury to the underlying spleen.
Rib fractures may have other more serious conse-
quences. If the irregular ends of the fractured bones are
driven inwards, they may penetrate the underlying pleu-
ral lining of the chest wall cavity, or even the underlying
lung itself, resulting in a pneumothorax (an abnormal col-
lection of air in a chest cavity). If subcostal, or pulmonary,
blood vessels are also injured, the resulting haemorrhage
associated with the leakage of air will produce a haemo-
pneumothorax (an abnormal collection of air and blood in
a chest cavity). Pneumothoraces may also develop if frac-
tured rib margins are forced outwards through the skin.
Children are, in general, more resilient and better
able to cope with rib fractures. However, rib fractures
in children have a particular place in forensic medicine,
as they can be a marker for non-accidental injury.
Rib (and sternal) fractures in adults are frequently
identified at post mortem examination following car-
diopulmonary resuscitation (CPR) or cardiac massage.
They are usually located anteriorly, or laterally, and
involve those ribs underlying the regions that experience
most compression during CPR. They are frequently sym-
metrical and, if there has been no survival following CPR
attempts, they lack associated haemorrhage. Posterior
rib fractures, or fractures of the first rib, for example,
would be unusual as a consequence of CPR. The nature
of rib fractures thought to be related to CPR may become
the subject of argument in court and, in an individual
with a history of chest trauma who subsequently receives
CPR attempts, microscopic examination of rib fractures
identified at post mortem examination – for evidence of
‘healing changes’ – may be of assistance.

(a)
(b)
Rib fractures
Costal
cartilage
Flail
Sternum
segment
Rib
Fracture
separation
(c)
Figure 10.15 Multiple rib fractures (a) following a road
traffic collision. There were many ’flail’ segments (b)
and fractures rib ends pierced the underlying lung (c).
([a & c] Courtesy of Richard Jones.)
Penetrating injuries of the chest, whether caused by
sharp-force trauma (stab wounds) or gunshot wounds,
may result in damage to any of the organs or vessels
within the thoracic cavities. The effect of the penetra-
tion will depend mainly upon which organ(s) or vessel(s)
are injured. Penetration of the chest wall can lead to the
development of pneumothorax, haemothorax or a com-
bination (haemopneumothorax).
Damage to the lungs can also result in the develop-
ment of pneumothoraces, and damage to the intratho-
racic blood vessels will result in haemorrhage, which
Abdomen 159
may be confined to the soft tissues of the mediastinum or
enter the pleural cavities. Haemorrhage from penetrat-
ing injuries to the chest may remain concealed with little
external evidence of bleeding and it is not unusual to find
several litres of blood within the chest cavity at post mor-
tem examination. It is possible to exsanguinate into the
thoracic cavity. Following penetrating chest injury, and
when an injured person is capable of purposeful move-
ments following infliction of such an injury, external
blood loss may not be apparent at the locus of infliction of
that injury, resulting in potential difficulties in the inter-
pretation of the scene of an alleged assault. It follows that
the lack of any evidence of external bleeding at such a
scene does not imply that infliction of the – subsequently
fatal – injury could not have occurred at that locus. The
answer to the question commonly asked in court, ‘Would
you not have expected immediate bleeding from such a
serious injury’, must be ‘Not necessarily’.
Abdomen
The anatomy of the abdominal cavity plays a major
role in determining the type of injuries that are found.
The vertebral column forms a strong, midline, verti-
cal structure posteriorly, and blunt trauma, especially
in the anterior/posterior direction, may result in com-
pression of the organs lying in the midline against the
vertebral column. This compressive injury may result
in substantial blunt force injury to intra-abdominal
organs, including bruising (or even transection) of the
duodenum or jejunum, rupture of the pancreas, rupture
of the liver, and disruption of omentum and mesentery
(Figures 10.16 and 10.17).
The forces generally required to cause these inju-
ries in an adult are severe and they are commonly
encountered in road traffic collisions. In an otherwise
healthy adult, it would be unusual but not impossible
for a simple punch to the abdomen to cause significant
intra-abdominal injuries, but kicks and stamps are
commonly the cause of major trauma. The kidneys and
the spleen are attached only by their hila and are sus-
ceptible not only to direct trauma but also to rotational
and shearing forces that may result in avulsion from
their vascular pedicles. Blunt trauma to the spleen is
sometimes associated with delayed rupture leading to
Figure 10.16 Mesenteric bruising and laceration follow-
ing blunt force trauma in a road traffic collision.
160 Regional injuries and p
­ atterns of injury
Figure 10.17 Multiple lacerations of the liver following
blunt force abdominal trauma in a road traffic collision.
(Courtesy of Richard Jones.)
haemorrhage and possibly death some hours or even
days after the injury. Pancreatic trauma can cause fatal
pancreatitis or peritonitis, although sometimes may
lead to the development of a pseudocyst, with little or
no short-term or long-term sequelae. Once diagnosed
the successful treatment of these conditions may be
conservative or surgical. The best opportunity of sur-
vival for many of these conditions is immediate assess-
ment, diagnosis and resuscitation.
Abdominal injuries in children may have the same
causes, but the forces required to cause them will be
considerably reduced, and the slower compressive forces
associated with squeezing of the abdomen during abuse
may also result in the injuries described above. The pos-
sibility of intra-abdominal injuries being caused by CPR
is also one that is raised in court, but such instances of
injury to either solid or hollow intra-abdominal organs
in adults or children are very rare.
Penetrating injuries to the abdomen can be the result
of either gunshots or sharp-force trauma. The effects of
these injuries will depend almost entirely on the organs
and vessels involved in the wound track. A penetrat-
ing injury to the aorta, or inferior vena cava, can result
in severe haemorrhage and may produce rapid death.
Peritonitis from a ruptured bowel or stomach may not be
recognised until too late, by which time overwhelming
sepsis will have developed. The presence of peritonitis,
and blood clots at post mortem are both factors which
may give indications of how long before death intra-
abdominal trauma had occurred.
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11 Pressure to the neck
and asphyxia deaths
▪▪ Introduction
▪▪ Classification of asphyxia
▪▪ Phases and signs of ‘asphyxia’
▪▪ Types of mechanical asphyxial mechanisms
Introduction
The translation of the word ‘asphyxia’ from the Greek
means ‘absence or lack of pulsation’. It is now a word
commonly used to describe an interference in the trans-
fer of oxygen from the air to cells, tissues and organs by a
variety of mechanisms. That interference might be par-
tial (leading to hypoxia) or complete (leading to anoxia)
(Table 11.1).
In forensic medicine, asphyxia often describes a
situation where there has been a physical obstruction
between the mouth and nose to the alveoli, although
other asphyxial mechanisms exist, in which there is an
inability to utilise oxygen at the cellular level without
there being a physical airway obstruction. The term
asphyxia is a term frequently misunderstood in non-
forensic medicine and attempts have been made to stan-
dardise the classification of ‘asphyxia-related deaths’
seen in forensic practice.
Classification of asphyxia
There are almost as many classification schemes
for the forensic aspects of asphyxia-related deaths
as there are textbooks, and definitions for types of
asphyxia deaths are equally varied, with attempts
made to correlate post mortem findings with the
known circumstances of death. No single system has
been formally adopted.
Two examples of proposed classification schemes
are shown in Figures 11.1 and 11.2, the latter of which
is based on pathophysiological criteria. As with all clas-
sifications, the key element is that those using them, and
those interpreting them, are clear about the clinical and
pathological relevance of each, and how a particular
case fits into a particular classification scheme.
This chapter focusses on those circumstances in
which there has been a physical interference with the
oxygenation of blood, by occlusion of the airways or
the application of pressure to the neck or chest. Any
compromise of oxygenation due to immersion in water
(drowning) or toxins (e.g., carbon monoxide) will be
explored elsewhere. Gases, liquids or solids (and their
▪▪ Obstruction or occlusion of the airways
▪▪ Pressure to the chest or abdomen
▪▪ Bibliography and information sources
▪▪ Further general resources
metabolites) which deprive the body of oxygen by sim-
ple displacement of oxygen from the lungs, or more
systemically where the transport of oxygen by haemo-
globin or mitochondrial oxidative phosphorylation is
interfered with, can be termed asphyxiants.
A simple classification of asphyxial mechanisms is
described below.
Mechanical: Figure 11.3:
• Strangulation (pressure applied to the neck by
means of a ligature, or by hands etc.) (Figure
11.3b–d).
• Hanging (pressure applied to the neck by means of
a ligature combined with the weight of the body)
(Figure 11.3e).
• Choking (physical obstruction within the airways).
• Compression asphyxia (pressure applied to the
chest or abdomen, resulting in a physical interfer-
ence with the ability to breathe effectively).
• Smothering (physical obstruction of the mouth/
nose preventing effective breathing).
Non-mechanical:
• Carbon monoxide poisoning (chemical interfer-
ence with respiration at a cellular level.
• Cyanide poisoning (Table 11.1).
• Other asphyxiants.
Miscellaneous:
• Drowning (physical interference with effective
respiration by a liquid).
Phases and signs of ‘asphyxia’
Forensic medicine textbooks have traditionally described
a stereotypical sequence of events following obstruction
of the airways leading to fatal asphyxia (see Box 11.1). The
origins of this description are unclear and it is best con-
sidered to be of historical interest, as such a sequence is
not relevant to all obstructive asphyxia events, or specific
to a particular event, and the pathophysiology of airway
obstruction remains incompletely understood.
 Phases and signs of ‘asphyxia’ 163

Table 11.1 Examples of asphyxia conditions and some terminology applied

Underlying cause of death Name
Lack of oxygen in the inspired air Suffocation
Blockage of the external orifices (nose/mouth) Suffocation/smothering
Blockage of the internal airways by physical obstruction Gagging/choking
Compression of the internal airways by external pressure Strangulation/hanging
Limitation of chest movement Traumatic asphyxia
Failure of oxygen transportation (For example, carbon monoxide poisoning)
Failure of oxygen utilisation (For example, cyanide poisoning)

Asphyxia (forensic situations where a body does not

receive or utilise adequate amounts of oxygen)

Suffocation (a broad term encompassing Strangulation (asphyxia by closure Mechanical asphyxia (asphyxia by Drowning (asphyxia by
asphyxia due to vitiated atmosphere and of the blood vessels and/or air restriction of respiratory movements immersion in a liquid)
smothering associated with deprivation passages of the neck as a result of either by position of the body or external
of oxygen) external pressure on the neck) chest compression)

Smothering Choking Confined Positional (or postural) Traumatic asphyxia

(obstruction of (obstruction spaces/ asphyxia (the position of the (caused by external
the air of the air entrapment individual compromises the chest compression
passages passages vitiated ability to breathe) by a heavy object)
above the below the atmosphere
epiglottis, epiglottis)
including the
nose, mouth
and pharynx)
Ligature strangulation (pressure Hanging (pressure on Manual strangulation
on the neck is applied by a the neck is applied by a (external pressure on neck
constricting band tightened by a constricting band structure by hands, forearms
force other than the body tightened by or other limbs)
weight) gravitational weight of
the body or part of the
body)

Figure 11.1 Classification of asphyxia in forensic contexts. (Adapted from Sauvageau A, Boghossian E. 2010,
Classification of asphyxia: the need for standardisation.)

Asphyxia

Failure in supply of
adequate amounts of
oxygen (e.g., due to
displacement of
environmental oxygen by
other gases; consumption
of oxygen without
replacement; confinement
in sewers etc.)
Failure to transfer oxygen
from the environment into
the blood (e.g., external/
internal obstruction in
smothering, choking and
hanging; extrinsic/intrinsic
compromise of thoracic cage
function in mechanical/
traumatic asphyxia or chest
wall trauma; and reduced
oxygen binding capacity of
the blood in carbon monoxide
toxicity)
Failure of transport of oxygen
due to a breakdown in supply
or uptake, or a problem with
blood flow due to local vascular
compression reducing cerebral
blood flow (e.g., hanging and
strangulation)
Failure of cells to take up
oxygen (e.g., cyanide
impeding cellular utilisation
of oxygen by damaging
enzyme systems - chemical
asphyxia)
Complex cases/
combined mechanisms
(e.g., drowning and
hanging: combined
venoarterial occlusion,
upper airway
obstruction from lifting
of the tongue, and
tracheal compression
etc.)

Figure 11.2 Classification of asphyxia by pathophysiological mechanism. (Adapted from Byard 2011, Commentary on
Sauvageau.)
164 Pressure to the neck and asphyxia deaths

(a)
Impermeable plastic
(b)
Irrespirable atmosphere
Blocked
Smothering pad
pharynx or glottis
Manual strangulation
Ligature
strangulation Blocked trachea

Inverted
posture

Pressure on chest

(c) (d)

(e)

Figure 11.3 (a) Examples of the causes of

mechanical asphyxia. (b) Grip marks to the
neck and (c) jaw following attempted manual
strangulation. (d) Ligature mark after attempted
garrotting – note congestion (‘tide mark’)
above double ligature. (e) Male suspended from
ligature.

Research into the pathophysiology of asphyxia con-
tinues, and has been assisted by attempts to analyse
the sequence of events depicted in documented filmed
recordings made by individuals who have hung them-
selves. Agonal sequences of movements have been
described, together with timings of their appearance
(see Table 11.2).
The ‘classic signs of asphyxia’ were traditionally
described as:
• Petechial haemorrhages in the skin of the face and
in the lining of the eyelids.
• Congestion and oedema of the face.
• Cyanosis (blue discolouration) of the skin of the
face.
• Right heart congestion and abnormal fluidity of
the blood.
However, none of these signs is specific to ‘asphyxia’
(however defined). Ambroise Tardieu was convinced that
petechiae (Tardieu spots) were pathognomonic of suffo-
cation, but they are not. They may be frequently seen, for
example, in those dying from congestive cardiac failure
deaths. Raised intravascular pressure in blood vessels
 Phases and signs of ‘asphyxia’ 165

Box 11.1 Sequence of events that may

be seen in asphyxia episodes
Dyspnoea phase: Increased respiratory rate and
effort, cyanosis, and increased heart rate and blood
pressure.
Convulsive phase: Loss of consciousness, laboured
respiratory movements, facial congestion/petechiae,
altered heart rate and blood pressure (variable), and
involuntary micturition/defecation.
Pre-terminal respiratory phase: Irregular respirations,
alternating apnoea and gasps, failure of respiratory
and circulation centres in the brain, and transient
tachycardia.
Figure 11.4 Petechial (and more confluent) haemor-
Terminal phase: Respiratory arrest, hypotension, fee- rhages in the facial skin and conjunctivae following
ble, irregular heart rate, then asystole; pupils dilate manual strangulation.
and reflexes are lost.

after 10–30 seconds of compression. In the absence of

in the head/neck explains the first three signs, and right
heart congestion and fluidity of blood can be considered
irrelevant to ascribing death to ‘asphyxia’. Of these clas-
sic signs, the finding of petechiae in the face/neck is of
most importance to the forensic pathologist; it is a finding
that requires an explanation, and a careful search for any
evidence capable of supporting a diagnosis of ‘pressure
having been applied to the neck or chest’ (Figure 11.4).
Additional non-specific findings in asphyxial deaths
include congestion of the viscera and the presence of
petechiae (Figure 11.5).
The length of time that pressure to the neck/chest
must be maintained to produce congestion and pete-
chiae in a living victim is a matter of continued con-
troversy, but it is generally accepted, from experience
with the living victim, that it may be rapid, perhaps
petechiae (caused by the leakage of blood from vessels),
it follows that if death resulted from the application of
pressure to the neck, death must have supervened before
petechiae could be produced. The absence of petechiae
does not exclude compression, often an important factor
in criminal trials.
Where the event or assault has resulted in death,
examination by a forensic pathologist is required to iden-
tify potentially subtle evidence of assault. Determining
the nature of an asphyxial death can be very challeng-
ing and requires a detailed review of known pre-mortem
events, death scene findings, autopsy findings, and the
results of other post mortem investigations including
toxicological analysis.
Asphyxial insults are not necessarily fatal, the out-
come being largely dependent on the nature of the

Table 11.2 Sequences of events in filmed hangings

Feature observed Average time after hanging
Rapid loss of consciousness 10 +/− 3 s
Mild generalised (tonic-clonic) convulsions 10 +/− 3 s
Decerebrate rigidity (limb extension/extensor rigidity) 19 +/− 5 s
Deep rhythmic abdominal respiratory movements 19 +/− 5 s
Decorticate rigidity (upper limb flexion/lower limb extension) 38 +/− 15 s
Loss of muscle tone 1 min 17 s +/− 25 s
End of deep abdominal respiratory movements 1 min 51 s +/− 30 s
Last muscle movement 4 mins 12 s +/− 2 mins 29 s
Source: Sauvageau et al. Agonal sequences in 14 filmed hangings with comments on the role
of the type of suspension, ischaemic habituation, and ethanol intoxication on the
timing of agonal responses. Am J Forensic Med Path 2011;32:104–107.
166 Pressure to the neck and asphyxia deaths
Figure 11.5 Tardieu spots (subpleural petechial haemor-
rhages) following manual strangulation. These are no
longer considered to be specific for asphyxia.
insult, its degree and its length of time. It is possible for
some survivors to suffer no significant adverse long-term
health effects, although others (if oxygen deprivation is
prolonged) may survive but with neurological sequelae.
A persistent vegetative state may develop following irre-
versible hypoxic–ischaemic brain injury, depending on
the length of time inadequate oxygenation was experi-
enced. In the living survivor, appropriate examination,
documentation, sampling (e.g., for DNA at the site of
compression) and investigations (which may include
radiological imaging) will optimise the recovery of foren-
sically useful evidence in order to assist subsequent legal
proceedings. If such an individual presents to hospital,
it is appropriate for such an examination to be made by
a suitably experienced forensic physician at the earliest
opportunity. It is important to remember that there may
be additional injuries unrelated to the asphyxia mech-
anism that may have forensic significance. They may
require review by an o ­ torhinolaryngologist (an ear, nose
and throat [ENT] specialist). Cervical arterial injuries
may also be documented resulting in stroke.
In survivors of an ‘asphyxial episode’, a thorough
history and clinical examination may exhibit a range of
signs and symptoms including some or all of:
• Hoarseness.
• Stridor (noisy breathing due to obstructed airflow
in the upper airway).
• Pain and tenderness around the neck and struc-
tures within the neck.
• Damage to the larynx and associated cartilages.
• Fracture to the hyoid bone.
• Dried saliva around the mouth.
• Cyanosis (in the immediate period after the
attack).
• Congestion (manifest as discolouration) and
oedema of the structures above any level of com-
pression.
• Petechiae above the level of the compressive force
that has caused the asphyxia.
• Haemorrhage from the mouth, nose and ears.
• Incontinence of faeces and urine.
Types of mechanical asphyxial
mechanisms
Pressure to the neck
Three types of the application of direct pressure to the
neck are of particular importance in forensic medi-
cine: manual strangulation, ligature strangulation and
hanging. In each of these it is not possible to predict how
rapidly death will occur; in some cases, death will be
relatively ‘slow’, allowing time for the development of
the classic signs of asphyxia (although such signs may
be evident following the application of pressure to the
neck for a matter of seconds), while in other cases such
signs will be entirely absent.
The application of circumferential pressure to the
neck or direct pressure to the sides of the neck may lead
to any of the following, the precise nature of which is
dependent upon the type, site, force and time period of
the pressure applied:
• Obstruction of the jugular veins, causing impaired
venous return of blood from the head to the heart
(leading to cyanosis, congestion, petechiae).
• Obstruction of the carotid arteries which, if severe,
causes cerebral hypoxia and collapse.
• Stimulation of carotid sinus baroreceptors at the
bifurcation of the common carotid arteries result-
ing in a neurologically mediated cardiac arrest
(see Box 11.2 and Figure 11.6).
• Elevation of the larynx and tongue, closing the air-
way at the level of the pharynx (the cartilaginous
trachea is more resistant to compression, unless
severe force is applied to the neck).
Following mechanical pressure to the neck, loss of
consciousness can occur rapidly, perhaps by 10 sec-
onds, and such a timeframe would generally seem to
be confirmed by analysis of filmed hangings. The use
of a sleeper hold (vascular neck restraint) has suggested
that loss of consciousness can occur in just under 10
seconds. The time taken to produce a fatal outcome,
however, has never been satisfactorily established, and
is hugely variable although filmed hanging analysis sug-
gests a lack of recognisable respiratory movements after
about 2 minutes and a lack of muscle movements after
about 7.5 minutes. These effects must relate in part to
the physical application of pressure, as free divers, in
 Types of mechanical asphyxial mechanisms 167

Box 11.2 ‘Vagal inhibition’ or reflex cardiac arrest

It has been recognised for some time that the mechani- system, and possibly inherited genetic susceptibilities
cal stimulation of the carotid sinus baroreceptors in to cardiac arrhythmias during stressful events (such as
the neck can result in an unpredictable, and some- channelopathies).
times fatal, outcome. Fatalities have been described,
for example, following apparently minimal pressure
being applied to the neck, and such events have been (a)
attributed to vagal inhibition or reflex cardiac arrest
(Figure 11.6). Therapeutic carotid sinus pressure is car- Internal
ried out on individuals with an arrhythmia, while being jugular vein
Hyoid bone
closely monitored, and is considered to be generally
safe. The clinical response, however, has also been
described as being unpredictable, and deaths have
occurred because of ventricular arrhythmias/asystole.
Stimulation of the carotid sinus baroreceptors
results in impulses being transmitted via the carotid Carotid
bifurcation
sinus nerve (a branch of the glossopharyngeal nerve)
to the nucleus of the tractus solitarius, and vagal nuclei, Common
in the medulla. Parasympathetic impulses descend to carotid artery
the heart via the vagus nerve leading to a profound
(b)
bradycardia and potentially asystole.
Death may supervene at any time following the
application of pressure to the neck, and it is thought
that such ‘vagal inhibition’ may explain why many indi-
viduals found hanging show none of the classic signs
of asphyxia.
Whether or not such a mechanism can explain some
cases of sudden death following neck compression on
its own remains a matter of debate. There is substan-
tial (unevidenced) support for the possibility of such
an explanation for death, although a systematic review
of reported fatalities purporting to be explicable on
the basis of reflex cardiac arrhythmia following carotid
bifurcation stimulation found no support for such an
explanation in the vast majority of cases. Figure 11.6 The carotid sinus baroreceptor and pres-
It is likely that the pathophysiology of fatal neck sure to the neck: (a) the location of the carotid sinus
compression is multifactorial, incorporating com- at the bifurcation of the common carotid artery in the
plex heart–brain interactions, emotional stress/ neck, and (b) pressure to the neck causing compres-
adrenaline-mediated effects on the cardiovascular sion of the carotid sinus.

the absence of pressure applied to the neck, can breath-
hold in static apnoea settings for more than 10 minutes.
Historic animal experiments indicated the potential for
their survival up to 14 minutes following obstructive
asphyxiation.
Strangulation
Manual strangulation is used to describe the applica-
tion of pressure to the neck using the hands (although
some would add forearms/limbs), and is a relatively
common mode of homicide, particularly where there is
disparity between the sizes of the assailant and victim.
The external signs of manual strangulation (Figure 11.7)
can include bruises and abrasions on the front and sides
of the neck, and the lower jaw; the pattern of skin sur-
face injuries is often difficult to interpret because of the
dynamic nature of an assault, and the possibility of the
repeated re-application of pressure during strangula-
tion. These signs are often florid in the survivor and may
be more pronounced in the fatality where death has not
been immediate. It is generally not possible to reliably
determine which of an assailant’s hands caused a par-
ticular set of injuries or how much pressure must have
been exerted by an assailant during the process of stran-
gulation based on the injury pattern (as was illustrated
168 Pressure to the neck and asphyxia deaths
Ear bleed
Nose bleed
Ligature mark
Figure 11.7 Potential signs of strangulation when cardiac arrest is delayed and circulation persists.
in the ‘Barleycorn Public House Murder’, described in
Box 11.3). Bruises caused by fingertip pressure (rounded
or oval-shaped bruises up to approximately 2 cm in size)
and fingernail scratches (linear or crescent-shaped
abrasions, imprints or skin breaches) may be seen, the
latter being made either by the assailant or the victim
(Figure 11.8).
Ligature strangulation may be homicidal, suicidal
or accidental and involves the application of pressure
to the neck by an item capable of constricting the neck,
for example, a scarf, a neck-tie, a belt, a pair of tights, or
cable tie (Figure 11.9). There is frequently a clear demar-
cation of congestion, cyanosis and petechiae above the
Box 11.3 Manual strangulation: ‘The Barleycorn Public House Murder’
The Licensee of a public house was found dead on the
floor of her bedroom. At autopsy, a bruise was present
on the right side of the neck just below the angle of
the jaw, with a curved scratch at its upper border, and
three bruises lay in a group (and in a line with each
other) on the left side of the neck over the thyroid car-
tilage. Two scratches were on the mid-line of the neck.
On dissection, there was a fracture of the right
superior horn of the thyroid cartilage and bruising
behind the larynx. Bruising was present at the back of
the head, over the shoulder blades, and the back of
the trunk and the crest of the left hip.
Petechiae
Congestion
Petechiae
Bruises, abrasions
and fingernail marks
Paler skin below neck
level of the constricting ligature, and there is usually a
ligature mark on the neck at the site of constriction. This
mark may be formed by a combination of compression
and abrasion of the skin, and often reflects the nature
of the ligature itself, sometimes replicating the pattern
of the ligature. Precise documentation (including mea-
surement and scaled photography) of any pattern visible
within a ligature mark, may enable comparison to be
made with putative ligature in that case at a future date.
Ligatures that are wide, or of a soft, non-abrasive mate-
rial, however, may leave very little evidence of compres-
sion on the skin of the neck, or even injury to underlying
structures, because of pressure dispersal.
A man was subsequently arrested, confessing to the
murder by strangling her with his right hand. He had a
deformed right hand; he had lost the greater part of the
distal two phalanges of each finger, although his thumb
was intact. The defence called Sir Bernard Spilsbury,
who did not consider that the defendant could have
strangled her with that hand. He was acquitted of mur-
der but subsequently was arrested and convicted for a
separate burglary. Many years later, he confessed to the
murder to ‘The People’ newspaper.

­i nvestigation.
Figure 11.8 Surface injuries on the neck and jaw in man-
ual strangulation. Note multiple bruises and abrasions;
some of these injuries are caused by the victim trying to
release the grip of the assailant.
Marks on the neck in ligature strangulation may
encircle the neck horizontally, although clothing, or
hair, may be interposed between the ligature and skin,
resulting in discontinuities in the mark. There may be
marks suggestive of crossover of the ligature, or knots,
but there will be no pattern suggestive of a suspen-
sion point, distinguishing ligature strangulation from
Figure 11.9 Ligature mark from a nylon scarf. Although
the fabric was broad, tight stretching of the fabric
resulted in a well-defined linear ‘band’ that could be
mistaken for that made by a cord or wire.
Types of mechanical asphyxial mechanisms 169
hanging, in which the individual’s body weight against
a ligature leads to pressure being exerted on the neck.
At post mortem examination, ligature marks are fre-
quently seen as brown parchmented bands, reflecting
post mortem drying of the abraded skin. While acci-
dental and suicidal ligature strangulation does occur, it
is recommended that such cases are treated with great
caution until homicide can be excluded by thorough
Pressure can be applied to the neck by means other
than the hands or a ligature. A variety of restraint tech-
niques are described that involve applying force to the
neck. These are often by means of the neck being placed
in the crook of the arm, when substantial pressure can
be applied. Such techniques have a variety of descrip-
tive names (e.g., vascular neck restraint; choke-hold;
sleeper hold; arm-lock). Each has the potential for fatal-
ity and investigations into deaths following police/secu-
rity service contact frequently involve the evaluation of
potential effects of restraint techniques used prior to
death. Such techniques may or may not result in the
production of asphyxial signs or neck injury. Many law-
enforcement bodies prohibit these techniques.
The ‘choking game’ is a relatively new phenomenon
of non-suicidal, non-autoerotic self-strangulation often
undertaken by young adolescents in order to experience
fleeting euphoric sensations. This activity has attracted
many participants worldwide, with images and videos
being posted on assorted social media. As with all neck
compression, there is an unquantifiable risk of fatality.
The extent of injury to soft tissues, muscles and the
skeleton of the neck (hyoid bone and thyroid cartilage)
following strangulation varies depending upon the
nature of the pressure applied to the neck. Post mortem
dissection of neck structures should always be carried
out following ‘drainage’ of the vasculature of the neck,
which can be achieved by carrying out the dissection
after removal of the brain and heart. Such a technique
avoids the production of artefactual haemorrhage at the
back of the larynx (Figure 11.10). Box 11.4 describes a
controversial historic case in which artefact may have
been erroneously attributed to trauma caused by neck
compression. There may be bruising within the ‘strap
muscles’ in the neck and injury to the superior horns
of the thyroid cartilage, which are particularly vulner-
able to compressive injury (Figure 11.11). Suspected
fractures should be confirmed under the microscope as
triticeous cartilage mobility at the tips of the horns may
simulate fractures. The greater horns of the hyoid bone
may also be injured, albeit less frequently than the thy-
roid cartilage. Radiological techniques are effective at
identifying such injuries in the deceased. Calcification
and ossification of the hyoid bone and thyroid cartilage
occurs with increasing age, and such change is associ-
ated with less flexible structures that are more prone
to injury following neck compression. Internal neck
170 Pressure to the neck and asphyxia deaths
Figure 11.10 Layered in situ dissection of the anterior neck
structures is essential in order to evaluate injuries follow-
ing pressure to the neck. Such dissection must be carried
out following ‘drainage’ or ‘decompression’ of the blood
vessels in the neck to avoid artefactual haemorrhage.
Box 11.4 The disappearing bruise
In 1929 Sidney Fox’s mother, Rosaline, died in a fire in
her room in a Margate hotel. An inquest recorded acci-
dental death verdicts, but suspicion was raised when
Sidney claimed on insurance policies entered into by
his mother. He was arrested and forensic pathologist Sir
Bernard Spilsbury examined her exhumed body, find-
ing evidence of significant cardiac disease but no soot in
the air passages and no carbon monoxide in the blood.
There were no petechiae or injuries on the surface of the
neck. Spilsbury discovered bruising of the left edge of
the tongue, a pinpoint haemorrhage in the lining of the
epiglottis, ‘bruising’ of the congested left thyroid lobe,
and a recent ‘bruise’ in loose soft tissue at the back of
the larynx, and ascribed these findings to pressure to
the neck, giving the cause of death as ‘asphyxia due
to manual strangulation’. There was no bruising in the
strap muscles of the neck, and there were no laryngeal
fractures, save for post mortem fractures of the hyoid
bone that Spilsbury admitted to making. Sydney Fox
was charged with the murder of his mother.
Defence pathologists Sir Sidney Smith and
Dr. Robert Bronte were alarmed to find no evidence of
Figure 11.11 Fracture of the left superior horn of the
thyroid cartilage following strangulation.
injuries are commonly less extensive in ligature stran-
gulation, with haemorrhage often being more localised
to the site of ligature application.
Hanging
Hanging describes suspension of the body by the neck.
Any material capable of forming a ligature can be used
for hanging. The pressure of the ligature on the neck is
produced by the weight of the body; it is not necessary
for the body to be completely suspended, with the feet
bruising to the formalin-fixed larynx, and thought that
Spilsbury may have misinterpreted post mortem disco-
louration. In addition, no microscopic sampling of this
‘bruise’ had taken place. At trial, Spilsbury insisted he
had seen a bruise but had probably cut it away during
the dissection process.
The defence view was that Mrs. Fox had died of
heart failure and fright during an accidental fire, and
that anyone, even Spilsbury, could mistake post mor-
tem discolouration for a bruise to the naked eye. Fox,
however, was convicted and hanged.
This case highlights the need for photographic doc-
umentation of findings at post mortem examinations,
and the need for confirmatory microscopy of critical
injuries. This disputed bruise in this case could repre-
sent an example of what is now called the ‘Prinsloo-
Gordon’ artefact – apparent bleeding from congested
vasculature in loose soft tissue at the back of the lar-
ynx – and pathologists now take active steps to drain
blood as far as possible from the neck, by removing the
brain and chest organs/heart, prior to neck dissection
in case there is suspected neck compression.

Figure 11.12 Suicidal hanging: the rope rises to a point,
leaving a gap in the ligature mark – the suspension point
– on the neck.
off the ground and the body hanging free under grav-
ity, as death may result from hanging where the body
is slumped in a sitting, kneeling or half-lying position,
with the point of suspension occurring at the level of, for
example, a door-handle. As with ligature strangulation,
a ligature mark is commonly present – often accompa-
nied by a deep indentation or furrow in the skin – but
discontinuous at some point around the neck. This dis-
continuity reflects the suspension point, which may be
at the sides or back of the neck, or even at the front of the
neck. If the ligature mark is seen to rise at the sides of the
neck, for example, to form an inverted V-shaped mark
at the back of the head, the suspension point was at the
back of the head (Figures 11.12 and 11.13).
The precise mechanism of death in hanging is prob-
ably multifactorial, involving venoarterial occlusion,
upper airway occlusion due to lifting of the tongue and
adjacent soft tissues, and tracheal compression. In the
absence of classical signs of asphyxia, even in hangings
in which there is complete suspension, the inference
must be that death has occurred more rapidly than it
Figure 11.13 Partial parchmented ligature mark with
sparing to left side of neck at site of suspension.
Types of mechanical asphyxial mechanisms 171
takes for such signs to appear, raising the possibility that
carotid sinus pressure and neurogenic cardiac arrest
has played an important role.
Hanging by judicial execution involves a drop, for
example through a trapdoor, calculated to result in
cervical spinal cord injury and fracture-dislocation of
the cervical spine, but without decapitation. However,
excluding judicial execution hangings, internal injury
to neck structures in hangings is frequently inconspicu-
ous, and may be entirely absent.
Non-judicial hanging is frequently a suicidal act of
males. Some cases are accidental and entanglement
with cords and ropes can occur, for example with
restraint harnesses or window-blind cords in children.
Occasionally, a homicide is staged to resemble a suicidal
hanging, and the investigators and pathologist must be
alert to the presence of injuries not capable of being
explained by hanging, or being atypical for hanging.
Post mortem toxicological analysis should be performed
in all hangings in order to determine whether the indi-
vidual was capable of self-suspension. A controversial
hanging death, said to have been a staged homicide, is
described in Box 11.5.
In survivors of accidental or suicidal hanging there
may be no adverse sequelae. For some there may be
residual hypoxic brain damage that may be profound,
or only detectable by neuropsychological assessment.
Others have motor and/sensory loss as a result of brain
damage. In addition, attempts to breathe when the
upper airway is blocked by an elevated tongue, due to
ligature pressure to the neck, raises intrathoracic pres-
sure and can lead to the escape of air into the medias-
tinum (pneumomediastinum) and the tracking of air in
the soft tissues of the neck (cervical emphysema).
Autoerotic asphyxia
Autoerotic asphyxia is the term used to describe those
fatalities occurring during some form of solitary sexual
activity. Many other terms have been used to describe
deaths such as these including sexual asphyxia, sex
hanging, asphyxiophilia, Kotzwarrism, autoasphyxio-
philia and hypoxyphilia. The recurrent feature tends to
be the use of a device, appliance or restraint that causes
neck compression, leading to cerebral hypoxia, with the
aim of heightening the sexual response. Such deaths,
which generally but not exclusively involve men, occur
predominantly as a result of failure of safety devices,
or their judgement/belief that they can terminate the
activity before losing consciousness.
The presence of some or all of the following features
should be considered when concluding that death
occurred as a result of autoerotic asphyxia:
• Evidence of solo sexual activity.
• Private or secure location.
172 Pressure to the neck and asphyxia deaths
Box 11.5 A forensic controversy: A suicidal
hanging or a staged homicide?
In 1992, Mr. Gilfoyle’s heavily-pregnant wife was
found hanging in the garage of their home. He was
convicted of her murder and lost his first appeal.
His case was referred to the Court of Appeal by the
Criminal Cases Review Commission. The case for the
Crown was that Mr. Gilfoyle had murdered his wife
and ‘staged’ the scene to simulate suicide. A steplad-
der was next to the body; one foot was resting on the
bottom rung of the ladder. No suspicion was aroused
initially, and the body was cut down without photo-
graphs being taken. At autopsy, a single ligature mark
was present and two small scratches immediately
above it.
A disputed ‘suicide letter’ had been found.
Defence pathologists giving evidence at the sec-
ond appeal indicated that there was nothing in the
pathology that was inconsistent with suicide – it was
neutral – and the Crown admitted that the patho-
logical evidence could not prove murder. The pros-
ecution evidence, however, suggested that it would
have been impossible for her to have physically tied
the rope to the beam from which she was found
hanging and other circumstantial evidence raised
suspicion of Mr. Gilfoyle’s involvement in the death.
The original verdict was considered safe, and the
2000 appeal dismissed.
In 2010, Mr. Gilfoyle’s solicitor gained access to
unused exhibits and found diaries of the deceased
indicating attempts at suicide. He was released from
prison on licence in 2010, but the CCRC declined to
refer his case to the Court of Appeal.
• Evidence of previous similar activity in the past.
• No apparent suicidal intent.
• Unusual props including ligatures, clothing, and
pornography.
• Failure of a device or set-up integral to the activity
causing death, or their judgement.
Death often results from the application of pres-
sure to the neck, and as with other ligature-related
deaths, the presence of classic asphyxial signs is vari-
able. The presence of gags or other means of occluding
the airways may lead to a death more akin to upper
airway occlusion than pressure to the neck, and the
addition of an asphyxiant substance (such as nitrous
oxide gas) within coverings over the head may lead
to suffocation. The presence of injuries suggestive of
assault must be looked for carefully, and the possibil-
ity of third-party involvement must always be consid-
ered in such cases.
Obstruction or occlusion of the
airways
Choking, suffocation and smothering
Accidental ingestion of objects or food can cause chok-
ing with internal obstruction of the upper air passages
by an object or substance impacted in the pharynx or
larynx below the epiglottis. This is referred to as bolus
obstruction. Choking is, most commonly, acciden-
tal and common causes include misplaced dentures
in adults and inhaled objects such as small toys, and
marbles in children. In medical practice there are risks
associated with individuals who are sedated or anaes-
thetised, when objects such as extracted teeth or blood
from dental or ear, nose and throat (ENT) operations
may occlude the airway without provoking the normal
protective reflex of coughing. In the law-enforcement
setting, deaths may occur when individuals attempt to
swallow wraps or packages of illicit drugs. Obstruction
commonly leads to respiratory distress with congestion
and cyanosis of the head and face.
Café coronary
Café coronary is a term used to describe complete and
abrupt upper airway obstruction by a bolus of food, often
meat, which occludes the oesophagus and larynx. It is so
named as the sudden onset of symptoms simulates acute
myocardial infarction. If food enters the larynx during
swallowing, it usually causes gross choking symptoms
of coughing, distress and cyanosis, which can be fatal
unless the obstruction is cleared by coughing or some
rapid treatment is offered. However, if the piece of food
is large enough to occlude the larynx completely, it will
prevent not only breathing but also speech and coughing.
The individual may die silently and quickly, the cause of
death remaining hidden until the autopsy (Figure 11.14).
Suffocation and smothering
Suffocation is a term usually used to describe a fatal
reduction of the concentration of oxygen in the respired
atmosphere, and often incorporates smothering. A
reduction in atmospheric oxygen can occur, for exam-
ple, in a decompressed aircraft cabin, or in a grain silo.
Mechanical obstruction of the upper airways can lead
to suffocation, as is seen when plastic bags are acciden-
tally, h
­ omicidally, or suicidally placed over the head
(Figure 11.15). Post mortem examination in such cases
rarely reveals any of the classic asphyxial signs.
Similarly, smothering, the physical occlusion of the
nose and mouth, may leave no asphyxial signs in sur-
vivors or the deceased. If the individuals are unable to
struggle, owing to extremes of age or intoxication, for
example, they may have no evidence of injury, including
around the mouth or nose. Occasionally, examination

Figure 11.14 Impaction of food in the larynx – a café
coronary.
will reveal intraoral injury (including bruising, abrasion
or laceration to the lips and inside the mouth or bruising
of the gums in an edentulous individual) and soft tissue
dissection of the face may reveal subcutaneous bruising
around the mouth and nose. As with manual strangling,
smothering may be very difficult to diagnose at post mor-
tem examination.
Retention of items/objects alleged to have been used
to smother individuals that survive, for example, may
have evidential value. Saliva, for example, may be iden-
tified on a pillow used in an attack and DNA matching
may corroborate the account given.
Figure 11.15 Suicidal plastic bag asphyxia. Suffocation by
plastic bag often leaves no autopsy asphyxial signs, and
removal of the bag by another individual prior to autopsy
would cause significant interpretation problems.
Pressure to the chest or abdomen 173
Pressure to the chest or abdomen
Compressional and positional asphyxia
Pressure on the trunk (chest and/or abdomen) can
result in an inability to breathe effectively and result in
death. Workmen trapped in collapsed earth trenches,
or buried in grain silos, for example, can find that they
are unable to expand their chests, leading to marked
‘asphyxial signs’ (Figure 11.16). Similarly, individuals
trapped under heavy machinery experience an inabil-
ity to breathe effectively. Sometimes, individuals are
crushed by the weight of many other people fleeing
danger, such as during a fire in a sports stadium, or
compressed against walls and fences whilst still stand-
ing. These examples of ‘compression asphyxia’ are
commonly referred to as traumatic or crush asphyxia
(Box 11.6).
A less dramatic presentation of asphyxial signs is
commonly seen in individuals who find themselves
in such an awkward body position that they too are
unable to breathe effectively. They may, for example,
attempt to squeeze through small gaps in railings, or
small open windows, and become wedged preventing
expansion of the chest (Figure 11.17). Others may find
themselves hanging head first over the side of a bed,
with their head flexed into their chest, restricting air
(a)
(b)
Figure 11.16 Traumatic asphyxiation in the workplace: (a)
there is gross congestion of the head and face, with pete-
chiae following burial, up to the axillae, in an avalanche
of iron ore, and (b) gross conjunctival haemorrhages
following chest compression by ash.
174 Pressure to the neck and asphyxia deaths
Box 11.6 Traumatic (‘crush’) asphyxia
The Bethnal Green Tube Disaster
During World War Two, the East End of London was a
frequent target for aircraft bombing raids, and civilians
sought shelter in deep-level underground train sta-
tions like that at Bethnal Green.
Warning sirens sounded during the night-time on
3rd March 1943, and a large crowd of people started
to make their way down a dimly-lit dark staircase at
the station entrance. Panic set in when a nearby anti-
aircraft battery fired, and a man tripped over a woman
who fell holding a small child. One hundred and sev-
enty-three men, women and children died, and autop-
sies of the bodies of four individuals, representing the
age groups of the victims, were performed.
Whilst the cause of death in each was attributed to
‘asphyxia due to suffocation by compression’, three of
the four ‘showed changes quite out of keeping with
prolonged asphyxia’, such that the pathologist, Keith
Simpson, thought that ‘death could have occurred very
quickly, perhaps within 30 seconds of being crushed’.
Figure 11.17 This male slipped through some attic stairs
and became wedged and unable to breathe. Note the post
mortem-dependent hypostasis visible on the exposed
lower torso.
The Hillsborough Stadium Disaster
On 15th April 1989, Liverpool and Nottingham Forest
football teams played the semi-final of the Football
Association Cup (FA Cup) in Hillsborough Stadium,
Sheffield.
Six minutes into the match, it was stopped because
it became apparent that fans were being crushed in
one of the stands, and were being pulled onto the
pitch. Ninety-six men, women and children died (one
dying two days later and one dying four years later).
‘Traumatic asphyxia’ or ‘crush asphyxia’ was causal in
94 of the deaths. The time of death in these cases was
the subject of controversy, as was the management of
the access to the ground by fans. Verdicts of accidental
death were given at the conclusion of the first inquest
in 1991, but this verdict was quashed in 2012 and a sec-
ond inquest was opened into the deaths in March 2014.
On 26th April 2016, the jury in that inquest concluded
that all 96 people had been unlawfully killed.
entry. Others (e.g., in law-enforcement settings) may
be restrained in positions that prevent them from
breathing adequately. Such scenarios are referred to
as positional or postural asphyxia, and those involved
are usually unable to extricate themselves from the
position in which they find themselves because of
impaired cognition or consciousness as a result of
intoxication, or those restraining them misinterpret
their struggle to breathe as resistance. Controversy
exists in the forensic community regarding the poten-
tial role of restraint techniques by police, in particu-
lar, where arms are being secured behind the back and
the subject is being placed in a face-down position.
Deaths in such a scenario rarely involve restraint in
isolation but occur on a background of intense exer-
tion, substance misuse and mental health problems;
it is likely that such deaths represent the culmina-
tion of a number of adverse physiological factors, and
determining cause of death is often complex and chal-
lenging. For some cases, the relevant contribution of
position vs other factors is impossible to determine.
Nevertheless, restraint techniques used by police/
security forces and others must minimise the risk of
positional asphyxia.
Individuals with impaired neurological function
owing to neurological disease may also succumb to
positional asphyxia, for example, by attempting to
get out of a hospital bed with cot sides, and becoming
trapped between the bed and a wall. Diagnostic criteria
for positional asphyxia can be seen in Box 11.7.

Box 11.7 Criteria for diagnosing ­positional asphyxia
1. The deceased is discovered in a position that pre-
vents adequate breathing/respiration (including
confined positions, flexion of the head on the
chest, partial or complete external airway com-
pression, and neck compression).
2. An examination of the scene, and a review of the
circumstances suggest that the deceased placed
her/himself in that position, and that there is no
evidence of the involvement of another individual.
3. The deceased could not remove her/himself from
the position in which they were found (due to, for
example, the effects of alcohol/drug intoxication,
or a neurodegenerative disorder).
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Further general resources
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Medicine, 2nd ed. Oxford: Elsevier; 2016.
12 Heat, cold and ­electrical
trauma
▪▪ Introduction
▪▪ Injury caused by heat
▪▪ Cold injury (hypothermia)
Introduction
Heat, cold and electricity are examples of some the
physical agents that can cause non-kinetic injuries to
the body.
Injury caused by heat
Burns are caused by the transfer of energy from a physi-
cal (e.g., hot water, an iron) or chemical (e.g., bleach or
acid) source into living tissues that causes disruption of
their normal metabolic processes and commonly leads
to irreversible changes that end in tissue death. Burns
may be superficial or cause deep charring of ­tissue
including muscle and bone. The skin can tolerate a high
surface temperature as it is able to dissipate heat rap-
idly. If the rate of absorption of heat exceeds dissipation
rate then burn injury will occur when the temperature
rises high enough to disrupt cellular processes. Little
local cellular damage occurs with a surface skin tem-
perature below 44°C unless exposed for >6 minutes.
Skin surfaces exposed to temperatures in the range
44°C–51°C can suffer increased damage with limited
exposure time, the rate of cellular destruction doubling
with each degree rise in temperature. The epidermis is
rapidly destroyed above 51°C and full-thickness skin
destruction above 70°C. The degree of damage is there-
fore related to temperature and how long the heat source
is applied to the skin.
The heat source may be dry or wet; where the heat is
dry, the resultant injury is called a ‘burn’, whereas with
moist heat from hot water, steam and other hot liquids it
is generally known as ‘scalding’. Certain settings, such
as war zones or terrorist attacks result in particular types
of thermal injury, from improvised explosive devices,
which may be associated with all other features of blast
injury, posing particular management problems.
Burns
Dry burns may be conveniently classified by their sever-
ity (degree of burn injury and depth of tissue burned)
and extent (burn area).
▪▪ Electrical injury
▪▪ Bibliography and information sources
▪▪ Further general resources
Severity of burn
Several systems of classification of burn severity exist,
which can sometimes lead to confusion as there may be
some overlap of terms (Figure 12.1). Perhaps the most
widely used historically is:
• First degree – erythema and blistering (vesicula-
tion).
• Second degree – burning of the full-thickness of
the epidermis and exposure of the dermis.
• Third degree – destruction down to subdermal tis-
sues, sometimes with carbonisation and exposure
of muscle and bone.
Some classifications extend this classification to 4th,
5th and 6th degree burns which simply reflect more
extensive tissue damage.
In recent years another classification has been used
to reflect potential treatment options and this describes
three main categories of burn, full thickness (destroying
the full thickness of skin) and partial thickness which
divide into superficial and deep (see Box 12.1).
Extent of burn
The size of the area of burning may be more important
in the assessment of the dangers of the burn than the
depth. Mapping the area of skin burned on body charts
may be helpful, although body surface area affected by
burns may be conveniently expressed as a percentage
of the total body surface area (TBSA) using the ‘Rule of
Nines’. The Rule of Nines (also known as the Wallace
Rule of Nines) is a tool used to assess the TBSA involved
in burn patients, which is essential in estimating fluid
resuscitation requirements and aids the clinician in
rapidly assessing the severity of burns and intravenous
fluid needs. Alterations to the Rule of Nines may be made
based on body mass index (BMI) and age. The Rule of
Nines estimation of body surface area burned is based on
assigning percentages to different body areas. The entire
head is estimated as 9% (4.5% for anterior and posterior).
The entire trunk is estimated at 36% and can be further
178 Heat, cold and e
­ lectrical trauma
Figure 12.1 The extensiveness of burns on a body recov-
ered from a fire may be varied. This individual had sec-
ond and third degree burns after dousing himself with
petrol before setting himself on fire ­(self-immolation).
Note the molten and singed hair, carboxyhaemoglobin
levels may be low in rapid flash petrol fires leading to dif-
ficulties in assessing vitality at the time of the fire.
broken down into 18% for anterior components and 18%
for the back. The anterior aspect of the trunk can further
be divided into chest (9%) and abdomen (9%). The upper
extremities total 18% and thus 9% for each upper extrem-
ity. Each upper extremity can further be divided into
anterior (4.5%) and posterior (4.5%). The lower extremities
Box 12.1 A practical classification of burns related to extent of tissue damage
Very superficial burns, for example, those caused by
sunburn, may simply cause reddening with mild
blistering that may occur after 12–18 hours. After
5–10 days the damaged layers of cells peel off
without residual scarring.
Partial-thickness burns destroy the whole of the epi-
dermis and possibly part of the next cellular layer:
the dermis.
Superficial partial-thickness burns result in fluid pro-
duction which lifts off the dead epidermis forming
blisters and subsequently scabs. Sensory nerves
are estimated at 36%, 18% for each limb. An alternative
is the Lund and Browder Chart published in 1944, cre-
ated by Dr. Charles Lund, Senior Surgeon at Boston City
Hospital, and Dr. Newton Browder. Both these and other
estimates may overestimate the TBSA and apps have
been created to ensure a more accurate assessment to
refine resuscitation measures (Figure 12.2a and b).
Factors influencing mortality risk include burn area,
increasing age and the presence of inhalation airway
injury; the presence of multiple risk factors substantially
increases the risk of death from burns. There is consid-
erable individual variation and the speed and extent of
emergency treatment will play a significant part in the
morbidity and mortality from burns. Improved thera-
pies in recent years mean that there are improved mor-
tality figures for those even with >75% TBSA. In dry
burns, any clothing can offer some protection against
heat, unless it ignites. Scars or burns from such injury
may reflect the pattern or style of clothing worn at the
time of burn (Figure 12.3).
Scalds
The general features of scalds are similar to those of
burns, with erythema and blistering, but charring
of the skin is only found when the liquid applied is
extremely hot, for example, with molten metal. The
pattern of scalding will depend upon the way in which
the body has been exposed to the fluid: immersion
into hot liquid results in an upper ‘fluid level’, whereas
poured, splashed or scattered droplets of liquid result
in scattered punctate areas of scalding. Runs or streams
of hot fluid will leave characteristic areas of scalding.
These will generally flow under the influence of grav-
ity and this can provide a marker to the orientation or
position of the victim at the time the fluid was moving
(Figure 12.4). This may be useful for corroboration when
two different accounts of how the injury was sustained
are given.
If only small quantities of hot liquid hit the skin,
cooling will be rapid, which will reduce the amount of
are damaged and the burn is very painful. New
epithelium grows quickly and the burn heals in
10–14 days with little or no scarring.
Deep partial-thickness burns are often less painful as
nerve endings are destroyed and scarring is likely
to be marked if the wound is allowed to heal spon-
taneously without skin grafting.
Full-thickness burns destroy all skin elements and may
require substantial reconstructive surgery because
of the potential for incapacitating scarring.
 Injury caused by heat 179

(a) (b) Lund and Browder Chart

9% xxxx
A A Simple erythema

1
1
Partial thickness loss
Front 18% (PTL)
13 13 Full thickness loss
Back 18% (FTL)
2 2 2 2

%
1½ 1½ 1½ 1½
Region PTL FTL
9% 9% Head
1 2½ 2½
1½ 1½ 1½ 1½
Neck
B B B B Ant. trunk
Post. trunk
1% Right arm
Left arm
C
Buttocks
C C C
18% 18% Genitalia
Right leg
1¾ 1¾
Left leg
1¾ 1¾
Total burn

Relative percentage of body surface area

affected by growth
Area Age 0 1 5 10 15 Adult
A – ½ of head 9½ 8½ 6½ 5½ 4½ 3½
B – ½ of one thigh 2¼ 3¼ 4 4½ 4¼
C – ½ of one leg 2½ 2½ 2¼ 3 3¼ 3½

Figure 12.2 (a) The ‘Rule of Nines’. (b) Lund and Browder Burns Chart.

damage done to the skin. However, if clothing is soaked
by hot fluid, the underlying skin may be badly affected,
as the fabric will retain the hot liquid against the skin
surface. Scalding is seen typically in industrial settings
where steam pipes or boilers burst. It may also be seen
in toddlers who pull kettles and saucepans down upon
themselves by grabbing the handle of the vessel.
Scalds are also seen in child physical abuse and are
the most common intentional thermal injury in chil-
dren. In a systematic review of the medical literature,
several characteristics of the history and burn injury
were associated with a significantly higher perceived
likelihood of abuse, including children with reported
inflicted injury, absent or inadequate explanation,
hot water as agent, immersion scald, a bilateral/sym-
metric burn pattern, TBSA ≥10%, full thickness burns,
and concurrent injuries. Accidental scalds (e.g., from
hot beverages/liquids being pulled off a cooker) are
predominantly spill injuries from flowing liquid, char-
acterised by scalds with irregular margins and burn

Figure 12.3 Dark areas represent burn from

water, pale areas spared by clothing. Figure 12.4 Pattern of scalding from running water
(Courtesy of Richard Jones.) poured over head and back.
180 Heat, cold and e
­ lectrical trauma
(a)
(b)
(c)
Figure 12.5 (a) Pattern of scalding from forced
­immersion in a hot bath. Note the clear demarcation
between scalded and uninjured skin representing the
fluid level of the bath. (b) Sparing of skin on the but-
tocks reflects firm contact between those parts and the
base of the bath. (c) Scarring on a 4-year-old placed in a
scalding bath.
depth, and lacking a ‘glove and stocking’ distribution.
Intentional scalds are predominantly those caused by
forced immersion in hot water, giving rise to symmetri-
cal glove and stocking injuries to the limbs, sparing skin
folds (and buttocks in those forced to sit in hot water),
which are of uniform depth (Figure 12.5).
Pathophysiological consequences
of thermal injury
Tissue exposed to burn or scald trauma elicits an acute
inflammatory response, leading to increased capillary
permeability at the injured site; tissue fluid loss associ-
ated with thermal injury can be severe enough to cause
dehydration, electrolyte disturbance and hypovolaemic
shock and, if the burn area exceeds 20% of the TBSA, the
release of systemic inflammatory mediators which may
lead to acute lung injury and multiple organ dysfunc-
tion/failure. Burned skin provides no protection against
infection, increasing the risk of sepsis in survivors.
Exposure to heat/hyperthermia
Hyperthermia, a condition where the core body tem-
perature is greater than 40°C (100°F), occurs when heat
is no longer effectively dissipated, leading to exces-
sive heat retention. Its development may be associated
with those who have taken prescribed drugs including
some anti-psychotics and those who have taken illicit
stimulants including cocaine and amphetamine and
some novel psychoactive substances. These appear to
elevate metabolic rate/heat production or reduce sweat-
ing. It may also occur in those with medical conditions
(e.g., hyperthyroidism), or in those who are resisting
restraint. It may occur in those exposed to high ambi-
ent temperatures (heat stroke) and has a high risk of
mortality or morbidity, which can occur in the young
and fit (exertional heat stroke) as well as the elderly and
infirm (non-exertional heat stroke). Other examples
may include children trapped in hot cars. Exertional
heat illness is recognised within military training pro-
grammes. Autopsy findings in such cases are non-spe-
cific but can include diffuse petechial haemorrhages of
serosal membranes and lung congestion as well as fea-
tures in keeping with ‘shock’ and multiple organ failure
in those who survive for a short period, if resuscitative
measures are ineffective.
Pathological investigation of bodies
recovered from fires
When a fire results in a fatality, there must be a low
threshold for treating the death with caution, in view of
the potential for there to have been an attempt made to
conceal a homicide. The need for safety of investigators
after events such as gas explosions, is a very important
consideration in the examination of fire scenes.
The fire scene must be examined by specialist inves-
tigators with expertise in the interpretation of the causes
and identification of the point of origin or seat of the
fire. They will have expertise in the use of accelerants,
such as petrol (see Box 12.2). Attendance at the scene
by a pathologist is important and assists subsequent
interpretation of post mortem findings (Figures 12.6

Box 12.2 Fire scene investigation
Fires are investigated by a wide range of professionals
with a range of objectives, including the identification
of any ‘defect, act or omission’ that led to the fire, in
order to inform fire protection and prevention methods,
the detection of a criminal act (arson), or to establish lia-
bility for the purposes of an insurance policy. Two prin-
cipal factors will be considered during the investigation:
what/where was the origin (seat) of the fire, and how did
it start? If the seat of the fire can be identified with preci-
sion, the list of potential causes can be narrowed down.
All fires require a combination of oxygen, fuel and
heat. Oxygen is normally freely available in air and fuel
is provided by almost any material given the right con-
ditions. The heat, initially, is provided by a source of
ignition, such as from a lit match, cigarette or heating
appliance. Thereafter, the fire provides its own source of
heat in a chain reaction.
Once ignited, a fire spreads through a number of
mechanisms. These include radiation (or direct flame
impingement), convection (the movement of hot air
currents) and conduction (the transfer of heat energy
through a material). Two types of fire are recognised:
smouldering combustion and flaming combustion.
Typical examples of smouldering combustion include
a lit cigarette or a barbeque; a garden bonfire would be
described as an example of flaming combustion.
Smouldering is a form of flameless combustion.
Certain materials are prone to this when ignited. These
are principally natural materials that produce a rigid
char on combustion, such as ­cotton and cellulose-based
materials (e.g., wood). Smouldering combustion can also
be produced when the oxygen levels are reduced during
burning, such as in a sealed room. Smouldering fires can,
however, transform into flaming fires and vice versa. The
rate of smouldering will vary depending on the nature of
the materials involved. Due to the nature of smouldering
fires, they can produce intense but quite localised burn-
ing patterns. This assists in distinguishing the burning
patterns produced by flaming and smouldering fires.
Smouldering fires spread by direct contact and
hence result in severe yet localised damage. In con-
trast, flaming fires spread by a variety of mechanisms
including direct flame impingement, radiation and con-
vection. Flames and radiated heat can therefore ignite
materials such as paper several feet away from the origi-
nal fire. Hot gases rise from the flaming fire to ceiling
height and then spread throughout a room or rooms.
This layer of hot air and gases can reach temperatures of
several hundred degrees centigrade. The heat from this
layer radiates down from the ceiling and can ignite items
well away from the original fire. By this mechanism, light
shades and the tops of curtains can be ignited.
Injury caused by heat 181
An understanding of these fundamental mecha-
nisms is essential to correctly identify the origin of the
fire and not be misled by false indications. For example,
a fire in a typical domestic lounge will spread across the
ceiling and may ignite the tops of the curtains. If these
then fall to the floor, the casual observer might mistak-
enly infer a second seat of fire.
Although a fire may damage or destroy items of
interest this is not inevitably the case. It may be pos-
sible, by careful observation and the use of excavating
and reconstruction techniques, to determine the cause
of a fire despite severe damage.
Several complementary methods are used to deter-
mine the origin of the fire. As a general rule, fires will
tend to spread upwards and outwards. A good place to
start, therefore, is by finding the lowest area of severe
damage. Heat and flames are quite directional and
will leave patterns of charring in some places and pro-
tected areas in others. All of these will assist in deter-
mining the origin of the fire.
The area of origin can be determined by scorch or
char patterns, comparing the relative damage of simi-
lar items, the distortion or melting of metals and other
heat- and time-related observations. It may sometimes
be necessary to determine the cause, or probable
cause, by a process of elimination.
Exposed surfaces can become charred during a fire
or smoke may be deposited. Other surfaces may be
protected from the effects of heat and smoke leaving
‘cleaner’, less damaged areas. These ‘protected’ areas
enable the investigator to reconstruct items and estab-
lish their position and condition at the time of the fire.
Having established, with reasonable accuracy, the
origin of the fire, it is then necessary to consider the
potential causes. The presence of electrical or heating
items needs to be established and may require further
laboratory examination and testing for appliance mal-
function or misuse. Consideration would also be given
to the possible involvement of a discarded lit cigarette
or a naked flame, such as from a match, lighter or can-
dle. The presence of a severe, yet localised pattern of
damage may be indicative of a smouldering fire, such
as initiated by a lit cigarette.
There are some typical indications of a deliberate
fire, such as multiple points of ignition, the use of a
flammable liquid, a modified fuel load (e.g., the arm-
chairs stacked on top of the sofa!) the presence of an
incendiary device or timing mechanism. A deliberate
act may also be inferred by indirect forensic evidence.
The presence of a broken window at a point of entry,
footwear or tool marks, a drop of blood or snagged
fibres could all indicate a suspicious event.
182 Heat, cold and e
­ lectrical trauma
Figure 12.6 Charred body at the scene of a fire showing
the ‘pugilist attitude’ and post mortem skin splits on the
chest. Extreme care must be taken to preserve the teeth in
such cases, in order to assist identification of the deceased.
(Reproduced with permission from Saukko P and Knight B.
Knight’s Pathology 4E, London, CRC Press, 2016.)
and 12.7). The site of the deceased when discovered is
important because sometimes, when flames or smoke
are advancing, the victim will retreat into a corner,
a cupboard or other hiding place, or they may simply
move to a place furthest away from the fire or to a door-
way or window, all of which may indicate that the vic-
tim was probably still alive and capable of movement for
some time after the start of the fire.
Figure 12.7 The finding of a body or apparent human
remains in a burnt-out car always requires full investiga-
tion which may involve pathologists, anthropologists,
scientists and specialists including odontologists and
police. Carboxyhaemoglobin levels may be low in rapid
flash petrol fires leading to difficulties in assessing vitality
at the time of the fire. (Courtesy of Richard Jones.)
The pathological investigation of bodies recovered
from fires should attempt to:
• Confirm the identity of the deceased.
• Determine whether the deceased was alive at
some time during the fire (or was dead before it
started).
• Determine why the deceased was in the fire (and
why they could not get out of it).
• Determine the cause of death.
• Determine (or give an opinion as to) the manner
of death.
Visual identification from facial features may be pos-
sible if there has been limited fire damage to the body,
but heat damage can cause major distortion of such fea-
tures even in the absence of direct burns.
Personal effects may assist identification, as will
unique medical features and factors such as the pres-
ence of scars and tattoos, but where there is severe
charring of the body more robust means of identifica-
tion must be relied on such as dental examination and
comparison of the dentition with available ante mortem
records or DNA analysis.
Post mortem radiography should usually be per-
formed before dissection, with particular emphasis on
radiographs to assist identification (e.g., dentition, sur-
gical prostheses), to identify fractures (including heal-
ing fractures with callus) and to exclude projectiles such
as bullets and shrapnel (Figure 12.8).
Determining whether a person was alive during the
fire at post mortem examination may be possible by
the finding of soot in the airways, oesophagus and/
or stomach; the implication being that active respira-
tion was required to inhale the soot. The presence of
soot below the level of the vocal cords, often accom-
panied by thermal injury of the epithelial lining of the
airways, is particularly useful, and may be confirmed
Figure 12.8 Radiography of charred remains is
always recommended. The X-ray of remains shown
here i­dentifies part of a disposable lighter.
(Courtesy of Richard Jones.)
 Injury caused by heat 183

under the microscope (Figures 12.9–12.11). Blood

samples can be taken for a rapid assessment of car-
boxyhaemoglobin levels, as a convenient marker of
the inhalation of the combustion products of fire, that
is, the inhalation of carbon monoxide, a product of
incomplete combustion.
While carboxyhaemoglobin levels are commonly
elevated in fire deaths (a level of >50% often being con-
sidered reliable evidence of death having occurred as a
consequence of breathing in the combustion products
of fire), lower levels do not necessarily mean that the Figure 12.10 Soot staining can be seen in the oesopha-
deceased was not alive at some time during the fire. In gus in this body recovered from a house fire. Such stain-
some circumstances, such as flash-over fires and petrol ing indicates that the deceased was alive – and able to
conflagrations in vehicles, for example, it is not uncom- swallow – at the time of the fire.
mon to find low post mortem carboxyhaemoglobin lev-
els. Other factors may raise carboxyhaemoglobin levels.
Cigarette smokers, for example, may ‘tolerate’ an elevated
background carboxyhaemoglobin saturation level which
although <5% in the majority of smokers may be as high
as 20% in heavy cigar smokers, whereas individuals with
chronic heart and/or lung disease may not tolerate even
very low levels before succumbing in a fire (Box 12.3).

(a)

Figure 12.11 Thermal injury to the back of the throat

provides evidence of the inhalation of hot gases ­during
a fire, and provides a useful sign of vitality at the time
of a fire.

Box 12.3 Examples of reasons for

(b)
Figure 12.9 Pathological evidence of vitality at the
time of the fire. Soot staining following inhalation of
the combustion products of fire is clearly visible to the
‘naked eye’ in this trachea (a), and such a finding can be
confirmed under the microscope (b).
­failure to escape from a fire
• Deceased was already dead before the start of
the fire.
• Deceased was intoxicated (alcohol and/or
drugs).
• Deceased was elderly and/or disabled.
• Deceased was immobile.
• Deceased was rapidly overcome by fumes/
smoke because of ‘poor physiological reserve’
(e.g., ischaemic heart disease or chronic obstruc-
tive airways disease).
• Deceased had insufficient time to escape the
fire owing to the nature of the fire itself (an
explosion or ‘flash fire’).
• There was panic/confusion.
• Escape routes were obstructed (deliberately or
accidentally).
• Deceased was in an unfamiliar environment (and
did not know where the escape route was).
184 Heat, cold and e
­ lectrical trauma

Deaths occurring during a fire

Most bodies recovered from fires with burns will not
have died from the direct effect of burns, but from
exposure to the many products of combustion (smoke,
carbon monoxide, cyanide and a cocktail of toxic com-
bustion by-products) and/or the inhalation of hot air/
gases (Box 12.4).
For those who survive the initial burn trauma and
exposure to products of combustion, death may occur
because of the large variety of potential complications
of thermal injury such as hypovolaemic shock follow-
ing fluid loss, overwhelming infection, the inhalation Figure 12.12 ‘Pugilistic positioning’ post mortem caused
of combustion products (causing acute lung injury and by heat having more effect on flexor muscles than
respiratory failure), renal failure or bleeding diatheses. ­extensors.
While the determination of ‘manner of death’ usu-
ally rests with the appropriate medicolegal authority,
an opinion from the forensic pathologist is frequently Careful consideration of all apparently traumatic
sought. The interpretation of injury in bodies recovered lesions must be made in order to determine the true
from fire is complicated by artefacts related to exposure nature of such post mortem lesions; the lack of naked
to fire: eye or microscopic evidence of vitality (such as ery-
thema, blistering, tissue swelling, bruising or an acute
• The so-called ‘pugilist attitude’ of the body reflects inflammatory reaction) will frequently distinguish
differential heat-related contraction of muscle, artefact from trauma inflicted before death, unless they
leading to flexion of the forearms, hands and were inflicted at, or around, the time of death. In cases
thighs (Figure 12.12). where there is doubt, an evaluation of the overall pat-
• Post mortem splitting of fragile burnt skin (Figure tern and distribution of such lesions may assist in the
12.13). interpretation of artefact versus ante mortem trauma.
• Fire- and heat-related fractures. The manner of death may be homicide (following
• Heat-related ‘extradural haemorrhage’, caused arson or where death was caused by violence before the
when severe heat has been applied to the scalp, fire being set), accident (e.g., an intoxicated individual
resulting in expansion of the blood in the skull
diploë and the intracranial venous sinuses, which
rupture, resulting in the formation of a collection
of brown and spongy blood outside the meninges
(Figure 12.14).
These artefacts may cause concern to non-forensic
professionals attending the scene, and may be misin-
terpreted as signs of ante mortem violence.

Box 12.4 Examples of mechanisms

of death in fires
• Interference with respiration (owing to a reduc-
tion in environmental oxygen and/or the pro-
duction of carbon monoxide and other toxic
substances).
• Inhalation heat injury leading to laryngospasm,
bronchospasm and so-called ‘vagal inhibition’
and cardiac arrest.
• Exposure to extreme heat and shock. Figure 12.13 Post mortem artefactual skin splitting is
• Trauma. seen on the left-hand side of the face and scalp. No
• Exacerbation of pre-existing natural disease or haemorrhage is apparent in these splits and care must
burns. be taken not to interpret these inappropriately as ante
mortem injuries.

Figure 12.14 Post mortem fire-related skull fractures in
a severely charred body. There is a reddish-brown heat
haematoma/extradural haemorrhage on the inner sur-
face of the carbonised cranial vault.
attempting to cook, or from a discarded cigarette) or,
rarely, suicide (self-immolation).
Cold injury (hypothermia)
Cold injury (hypothermia) has both clinical and foren-
sic aspects; death from hypothermia occurs even in
temperate climates in winter. In marine disasters or
water immersion, hypothermia may be as common a
cause of death as drowning. In cold seas and oceans,
and lakes in high latitudes, death from immersion may
occur within a few minutes from sheer heat loss and
before true drowning can occur.
Deaths from exposure occur through heat loss from
a mixture of radiation, convection, conduction, respi-
ration and evaporation. Environmental temperatures
below 10°C are probably sufficient to cause harmful
hypothermia in vulnerable individuals.
Hypothermia occurs when a person’s normal body
core temperature of around 37°C (98.6°F) drops below
35°C (95°F). Core temperature is best measured by an
oesophageal probe. If core temperature cannot be mea-
sured, the degree should be estimated using clinical signs.
Treatment is to protect from further heat loss, minimise
afterdrop – the continued fall of deep body temperatures
during rewarming – and prevent cardiovascular collapse
during rescue and resuscitation. It is usually caused by
being in a cold environment, and can be triggered by a
combination of factors, including prolonged exposure to
cold (such as staying outdoors in cold conditions or in a
poorly heated room for a long time), inadequate cloth-
ing, rain, wind, sweat, low BMI, inactivity or being in cold
water.
If a body gets cold, the normal response is to warm up
by becoming more active, putting on more clothing lay-
ers or moving indoors. If exposure to the cold continues,
Cold injury (hypothermia) 185
other physiological processes will attempt to prevent
any further heat loss. These processes include shivering
(which keeps the major organs at normal temperature),
restricting blood flow to the skin and releasing hor-
mones to generate heat. After prolonged exposure to the
cold, these responses are not enough to maintain body
temperature. At this point, shivering stops and heart
rate decreases. This can happen quickly. Alcohol con-
sumption enhances hypothermia as it causes peripheral
vascular dilatation and increased heat radiation. Wind
and rainfall exacerbate the drop in body temperature.
The body may rapidly lose temperature when immersed
in cold water, as water has a cooling effect that is 20–30
times that of dry air. Hypothermia may confer a protec-
tive effect on survival following cold water immersion,
but survival may be accompanied by severe hypoxic
brain injury.
In some patients, there may be an underlying medi-
cal cause (such as thyroid or pituitary dysfunction), or it
may be associated with immobile or demented patients
or conditions such as pneumonia. Hypothermia is char-
acterised by depression of the cardiovascular and ner-
vous systems, the latter causing cognitive impairment.
Generally, the elderly, children and trauma patients
are susceptible to hypothermia. Hypothermia can be
classified into mild (core temperature 32°C–35°C com-
pared with a normal of 37.5°C), moderate (30°C–32°C),
or severe (<30°C). Below a core temperature of 32°C,
shivering ceases and thus this extra muscle activity
will no longer generate heat, worsening the situation.
Unconsciousness may occur between core tempera-
tures of 27°C and 30°C, while ventricular fibrillation and
apnoea occur at core temperatures below 27°C. Those
who may be prone to developing hypothermia are those
in extreme weather conditions (e.g., climbers, walkers,
skiers, sailors), homeless people who are unable to find
shelter, heavy drug and/or alcohol users (collapsing in
the open) and those who have been immersed in cold
water. Those who have been subject to severe trauma
(e.g., trapped in a motor vehicle requiring extrica-
tion) are prone to hypothermia whilst they are being
­recovered.
Hypothermia is usually diagnosed on the basis of
typical symptoms and environment, and can be divided
into mild, moderate and severe cases (Box 12.5). When
unconscious, a person’s pulse may be difficult to iden-
tify or locate and they may not appear to be breathing.
Treatment of severe hypothermia may not be success-
ful. The key to treatment is a controlled rewarming that
must be under medical supervision with full resuscita-
tion facilities, and may require other therapeutic inter-
ventions such as dialysis.
It is important to remember that the weather does not
have to be unusually cold for hypothermia to develop
and, even in moderately cold winter weather, many
elderly individuals will become hypothermic.
186 Heat, cold and e
­ lectrical trauma

Box 12.5 Features of mild, moderate and severe hypothermia

Mild cases • Drowsiness
• Shivering • Slurred speech
• Feeling cold • Apathy
• Lethargy • Slow, shallow breathing
• Cold, pale skin • Weak pulse
Moderate cases Severe cases
• Violent, uncontrollable shivering • Loss of control of hands, feet and limbs
• Cognitive impairment • Uncontrollable shivering that suddenly stops
• Confusion • Unconsciousness
• Loss of judgement and reasoning • Shallow or no breathing
• Loss of coordination, including difficulty moving • Weak, irregular or no pulse
around or stumbling • Stiff muscles
• Memory loss • Dilated pupils

Children have a high body surface-to-weight ratio necrosis following microvascular injury and thrombo-
and lose heat rapidly. In some cases of deliberate neglect sis (Figure 12.17).
or careless family circumstances, infants may be left in Hypothermia may cause behavioural abnormali-
unheated rooms in winter and suffer hypothermia. ties that can lead to death-scene findings that appear
In an unrefrigerated body, the finding of indistinct suspicious. Paradoxical undressing is a phenomenon
red or purple skin discolouration over large joints, that describes the finding of partially clothed, or naked,
such as the elbows, hips or knees (and in areas of skin individuals in a setting of lethal hypothermia. The
in which such discolouration cannot be hypostasis)
raises the possibility of hypothermia and is found in
approximately 50 per cent of presumed hypothermia (a)
deaths (Figure 12.15). The nature of such discoloura-
tion (‘frost erythema’) is not completely understood,
but may reflect capillary damage and plasma leakage;
microscopy reveals no red blood cell extravasation, dis-
tinguishing it from bruising.
Classically, haemorrhagic gastric lesions (Wisch­
newsky spots) may be seen in hypothermia deaths. It
has been hypothesised that cooling of the body in the
setting of cold ambient temperatures primarily leads
to circumscribed haemorrhages of the gastric glands
in vivo or in the agonal period. Subsequently, due to
autolysis, erythrocytes are destroyed and haemoglobin
is released. Following exposure to gastric acid, haemo- (b)
globin is hematinised, leading to the typical blackish-
brownish appearance of Wischnewsky spots seen at
gross examination (Figure 12.16). Like Tardieu spots
and asphyxia, Wischnewsky spots are not specific to
hypothermia as they are identical to those lesions seen
in some deaths following sepsis and shock, as well as in
cases of alcohol misuse.
Other gastrointestinal lesions sometimes found in
deaths caused by hypothermia include haemorrhagic
erosions and infarction in the small bowel (because of Figure 12.15 (a) Pinkish discolouration over the large
red blood cell ‘sludging’ and submucosal thrombosis), joints in fatal hypothermia. (b) When a partially-clothed
and haemorrhagic pancreatitis with fat necrosis. body is found outdoors, caution is needed in order
Cold injury to the extremities may be severe enough to exclude foul play. This scene, however, illustrates
to cause frostbite, which reflects tissue injury that hypothermia-related disrobing (‘paradoxical undressing’)
varies in severity from erythema to infarction and and the so-called ‘hide and die’ phenomenon.

Figure 12.16 The black lesions seen in the stomach are
superficial haemorrhagic gastric ‘erosions’ often seen
in hypothermia. These are sometimes referred to as
‘Wischnewski’ spots.
Figure 12.17 Frostbite of the knuckles. (Reproduced
with permission from Saukko P and Knight B. Knight’s
Pathology 4E, London, CRC Press, 2016.)
pathophysiology of this is uncertain but it may reflect cog-
nitive dysfunction and abnormal processing of periph-
eral cutaneous stimuli in a cold environment, leading the
individual to perceive warmth and thus to shed clothing.
The phenomenon of ‘hide and die syndrome’
describes the finding of a body that appears to be hid-
den, for example, under furniture or in the corner of a
room, often surrounded by disturbed furniture, clothes
or other artefacts. In these cases, the individual has
placed themselves in the location. It is thought that this
phenomenon reflects a terminal primitive ‘self-protec-
tive’ behaviour and may be more commonly observed
where there is a slow decrease in core body temperature.
It may be difficult to differentiate between ‘hide and die’
and deliberate concealment by another.
Electrical injury
Injury and death from the passage of an electric cur-
rent through the body is common in both industrial and
Electrical injury 187
domestic circumstances. The essential factor which
causes harm is the current (electron flow) measured in
milliamperes (mA). This current is determined by the
resistance of the tissues in ohms (Ω) and the voltage of
the power supply in volts (V). According to Ohm’s Law,
to increase the current (and hence the damage), either
the resistance must fall or the voltage must increase,
or both.
Most cases of electrocution, fatal or otherwise, origi-
nate from public power supplies, which is delivered
throughout the world at either 110 V or 240 V. It is rare
for death to occur at less than 100 V. The current needed
to produce death varies according to the time during
which it passes and the part of the body across which it
flows. Usually, the entry point is a hand that touches an
electrical appliance or live conductor, and the exit is to
earth (or ‘ground’), often via the other hand or the feet.
In either case, the current will cross the thorax, which is
the most dangerous area for a shock because of the risks
of cardiac arrest or respiratory paralysis.
When a live metal conductor is gripped by the hand,
pain and muscle twitching will occur if the current
reaches about 10 mA. If the current in the arm exceeds
about 30 mA, the muscles will go into spasm, which
cannot be voluntarily released because the flexor mus-
cles are stronger than the extensors: the result is for the
hand to grip or to hold on. This ‘hold-on’ effect is very
dangerous as it may allow the circuit to be maintained
for long enough to cause cardiac arrhythmia, whereas
the normal response would have been to let go so as to
stop the pain.
If the current across the chest is 50 mA or more, even
for only a few seconds, fatal ventricular fibrillation is
likely to occur, and alternating current (AC, common in
domestic supplies) is much more dangerous than direct
current (DC) at precipitating cardiac arrhythmias.
The tissue resistance is important. Thick dry skin,
such as the palm of the hand or sole of the foot, may
have a resistance of 1 million ohms, but when wet, this
may fall to a few hundred ohms and the current, given a
fixed supply voltage, will be markedly increased. This is
relevant in wet conditions such as bathrooms, exterior
building sites or when sweating.
The mode of death in most cases of electrocution is
ventricular fibrillation caused by the direct effects of
the current on the myocardium and cardiac conduct-
ing system. These changes can be reversed when the
current ceases, which may explain some of the remark-
able recoveries following prolonged cardiac massage
after receipt of an electric shock. The victims of such
an arrhythmia will be pale, whereas those who die as
a result of peripheral respiratory paralysis are usually
cyanosed. Even rarer are the instances in which the
current has entered the head and caused primary brain-
stem paralysis, which has resulted in failure of respira-
tion. This may occur when workers on overhead power
188 Heat, cold and e
­ lectrical trauma

supply lines or electric railway wires touch their heads

against high-tension conductors, usually 660 V.
The scene of a suspected electrical death should
be reviewed to try and identify causative agents and
ensure that no risk persists. Health and safety legisla-
tion may require that an electrical death (e.g., in the
work setting) should be fully reviewed to prevent fur-
ther electrical exposure.

The electrical lesion

Unless the circumstances are accurately known, it can
be difficult to know whether a dead victim has been
in contact with electricity. When high voltages or pro-
longed contact have occurred, extensive and severe
burns can be seen, but a few seconds of contact with a
faulty appliance may leave minimal signs. Where the
skin is wet or where the body is immersed, as in a bath,
there may be no signs at all, as the entrance and exit of
the current may be spread over such a wide area that no
focal lesion exists.
Usually, however, there is a discrete focal point of
entry and, as the electrical current is concentrated at
that point, enough energy can be released to cause a
thermal lesion. The entry points may be multiple and
obvious, or they may be single and very inconspicuous.
As the most common place is on the hands, these should
always be examined with particular care (Figures 12.18
and 12.19).
The focal electrical lesion is usually a blister, which
occurs when the conductor is in firm contact with the
skin and which usually collapses soon after inflic-
tion, forming a raised rim with a concave centre.
Characteristically, the skin is pale, often white, and there
is an areola of pallor (owing to local vasoconstriction),
(a)
Figure 12.19 Multiple electrical marks/burns on the
hand, associated with scorching and blistering.
sometimes accompanied by a hyperaemic rim. The blis-
ter may vary from a few millimetres to several centime-
tres. The skin often peels off the large blisters leaving
a red base. The other type of electrical mark is a ‘spark
burn’, where there is an air gap between metal and skin.
Here, a central nodule of fused keratin, brown or yel-
low in colour, is surrounded by the typical areola of pale
skin. Both types of lesion often lie adjacent to each other.
In high-voltage burns, multiple sparks may crackle
onto the victim and cause large areas of damage, some-
times called ‘crocodile skin’ because of its appearance
(Figure 12.20).
Internally, there are no characteristic findings in
fatal electrocution. Deaths from electricity, gener-
ally, do not have specific findings at the autopsy. The
diagnosis is commonly based on the circumstances of
the death and the morphologic findings, above all the
current mark. The skin lesions are mainly thermal in
nature, but opinions vary as to whether histological
appearances are specific to electricity. It has been said
that the cell nuclei line up in parallel rows because of

Pale zone
Metal Collapsed blister
with raised edge
and pale areola
240 V

(b)

Pale areola
Fused nodule
Spark of keratin
240 V
Figure 12.20 Thigh of a victim showing high-voltage
Figure 12.18 Electrical mark on the skin: collapsed blister burns. The appearance is sometimes called ‘crocodile
formation following firm contact (a) and a ‘spark burn’ skin’ and is caused by arcing of the current over a consid-
across an air gap (b). erable distance.

the electric field, but similar appearances can occur in
purely thermal burns. Metallisation of the skin may be a
marker of electrocution. The use of a scanning electron
microscope equipped with an Energy Dispersive X-Ray
Spectroscopy (EDS) probe may allow the detection and
the identification of the metals embedded in the skin
and their evaluation in the context of the ultrastructural
morphology, and assist in diagnosis.
Death from lightning
Hundreds of deaths occur each year from atmospheric
lightning, especially in tropical countries. A lightning
strike from cloud to earth may involve property, animals
or humans. Huge electrical forces are involved, produc-
ing millions of amperes and phenomenal voltages. Some
of the lesions caused to those who are struck directly
or simply caught close to the lightning strike are purely
electrical, but other injuries will be from burns or from
the explosive effects of a compression wave of heated air
leading to ruptured tympanic membranes, pulmonary
blast injury and muscle necrosis/myoglobinuria. Many
bizarre appearances may be found, especially the par-
tial or complete stripping of clothing from the victim,
which may arouse suspicions of foul play. Severe burns,
fractures and gross lacerations can occur, along with the
well-known magnetisation or even fusion of metallic
objects in the clothing. The usual textbook description is
of ‘fern- or branch-like’ patterns on the skin, the so-called
Lichtenberg figure (Figure 12.21) but others claim that
such marks are not seen, although if they have seen the
image in Figure 12.21, it is unlikely they would disagree.
Red streaks following skin creases or sweat-damped
tracks are more likely, although many bodies are com-
pletely unmarked.
Figure 12.21 The ‘Lichtenberg figure’ and lightening
fatalities. Note the fern-like branching pattern of skin
discolouration particularly on the upper right chest.
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Yankelson L, Sadeh B, Gershovitz L, et al. Life-threatening events
during endurance sports: is heat stroke more prevalent than
arrhythmic death? J Am Coll Cardiol 2014;​64(5):463–469.
Further general resources
Payne-James JJ, Byard RW (eds). Encyclopedia of Forensic and Legal
Medicine, 2nd ed. Oxford: Elsevier; 2016.
13 Immersion and drowning
▪▪ Introduction
▪▪ Evidence of immersion
▪▪ Post mortem artefact and immersion
▪▪ Pathological diagnosis of drowning
▪▪ Alternative mechanisms of death in immersion
Introduction
Drowning has been defined as ‘…the process of expe-
riencing respiratory impairment from submersion/
immersion in liquid’. There are over 400,000 drown-
ing deaths worldwide per annum. The finding of a
body in water does not necessarily mean that they
have drowned. The majority of bodies found in water
are there as a result of an accident (e.g., slipping from
a river bank, or falling in when intoxicated) or suicide.
When investigating it is important that all features and
known history are taken into account when a body is
recovered. For example, ligatures to the hands or feet,
or weights within clothing may be the responsibility of
the person themselves, or may indicate a criminal act.
Obvious questions to be addressed include: was the
individual dead before they entered the water; do they
have any physical health problems (e.g., epilepsy); is
there any history of self-harm or mental health issues?
Fatal drowning can occur in water only a few centime-
tres deep. Unintentional bathtub drowning deaths are
well-recognised in the elderly population. When inves-
tigating a possible drowning death as much knowledge
as possible of the circumstances and locus is needed to
make a proper and accurate determination of the cause
of death. Jumping or diving into water may result in
limb, neck or head injuries that render a person inca-
pable of swimming and extracting themselves from the
water. Bodies are frequently retrieved from water; this
process in itself may be hazardous for those in recovery
teams and may, because of its complexity, result in loss
of important evidence. Accurate documentation and
photographic and video evidence may assist in ensur-
ing as much relevant evidence as possible is available.
The medicolegal investigation of deaths following
the recovery of a body from water is complex, given that
a wide range of scenarios for death exist; some exam-
ples are given in Box 13.1. The potential role of inherited
cardiac disease in drowning is described in Box 13.2.
The pathologists and other investigators must attempt
to address all of these potential explanations for death
and determine whether there is any pathological
▪▪ The role of alcohol and drugs in drowning
▪▪ Other investigations in bodies recovered from water
▪▪ Bibliography and information sources
▪▪ Further general resources
evidence capable of supporting a diagnosis of drown-
ing. The death investigation must also address other
questions such as: how did the individual get into the
water; and what prevented survival? Other important
factors such as post mortem drug and alcohol levels
in the drowning victim may have considerable sig-
nificance in determining what happened. Local poli-
cies (e.g., education of children about water hazards)
may influence the demographics of unintentional fatal
drowning deaths of children. Similarly, if risks of drug
and alcohol intoxication whilst in or near water are rec-
ognised, incidences may be reduced in the adult popu-
lation. The Royal College of Pathologists has published
guidelines on autopsy for bodies recovered from water.
Evidence of immersion
Water immersion results in a number of changes to the
body, and these changes are dependent on a variety of
factors including: water temperature, the nature of the
water (i.e., salt vs fresh), bacterial contamination, tidal
flow, the nature of the sea or river bed, the presence of
marine life, the habits of the individual, and clothing
worn.
Generally, if immersed for long enough, the skin
of the hands and feet will become irregular and mac-
erated. The fingertips become opaque and wrinkled
(‘washerwoman’s fingers’; Figure 13.1) within a few
hours of immersion. The speed of these changes is deter-
mined by the nature of the immersant water. As immer-
sion time increases, macerated skin begins to separate
from underlying tissues, leading to skin and nail peeling
and apparent ‘degloving’ of the skin of the hands and
feet (Figure 13.2). Loss of pigment layers may be appar-
ent, causing colour change in skin, which often misleads
as to the ethnic origin of the deceased.
It is not possible to estimate the post mortem interval
from signs of immersion and decomposition in a body
recovered from water, as there are so many factors that
may influence the appearance. There is an oft-quoted
(but not evidence-based) ‘rule of thumb’ recognising
that decomposition in water in temperate climates
192 Immersion and drowning

Box 13.1 Examples of reasons for death

in a body recovered from
water
• Died of natural causes before falling and enter-
ing the water (e.g., myocardial infarction or
stroke).
• Died of natural causes whilst swimming (e.g.,
myocardial infarction or stroke).
• Died of natural causes while in the water, having
entered the water either voluntarily or acciden-
tally (e.g., under the influence of drugs and/or
alcohol and micturating into a canal and losing Figure 13.1 ‘Washer woman’s hands’. Typical appearance
balance). after a few days in water.
• Died from exposure and hypothermia in the
water (particularly those with low BMIs, the
young and the elderly). occurs at roughly half the rate of a body left in air. This
• Died of injuries or other unnatural cause before does not assist in providing appropriately reliable evi-
entering the water (e.g., physical assault). dence. Henssge’s temperature-time of death nomogram
• Died of injuries following entering the water method may be useful (within the limitations already
(e.g., diving into unrecognised shallow water, discussed), with the application of the required ‘correc-
causing cranial or cervical fracture). tive factor’.
• Died of injuries whilst in the water (e.g., being Bloating of the body (face, abdomen and genitals)
hit by a boat or jet ski, shark attack). owing to gas formation in soft tissues and body cavities
• Died from submersion, but not drowning. is often evident after approximately a few days’ immer-
• Died from true drowning as a result of aspira- sion in temperate conditions, after which skin and hair
tion of water into the lungs. loosening leads to their detachment. However, the
skin and hair can be found in place many weeks after
immersion.
Gaseous decomposition and bloating often causes
the body to float to the surface of the water in which it is
Box 13.2 Drowning and inherited submerged after a few days, leading to its discovery. If
c­ ardiac disease the body is obese with much adipose tissue it may sink
Post mortem genetic testing (‘molecular autopsy’) for only a short period, even in the absence of bloating.
for the inherited cardiac channelopathies congenital
Long QT Syndrome (LQTS), and Catecholaminergic
Polymorphic Ventricular Tachycardia (CPVT), by
researchers at the Mayo Clinic in 35 unexplained
cases of drowning in the USA revealed that almost
29% of those drowning whilst swimming were
mutation positive. Women were disproportionately
affected, and none had previously been diagnosed
with a channelopathy in life. This study highlights
the need to consider inherited cardiac diseases in
the medicolegal investigation of immersion/ sub-
mersion deaths, and for material to be retained at
autopsy that will facilitate genetic mutation analysis
relevant to the death investigation and to the future
health of surviving family members. Mapping an
individual’s genome will be of great relevance, but
in terms of cause of death in medicolegal investiga-
tion, it must be recognised that it adds additional
pieces of evidence, but does not necessarily solve
the problem. Figure 13.2 Peeling of the epidermis from the foot
(degloving) following a few weeks of immersion.

Post mortem artefact and
immersion
Bodies immersed in water may be subject to movement
from tidal flow, wind and waves and come into con-
tact with sand/silt, rocks, piers and other underwater
objects, all of which cause injury to the skin and under-
lying structures (Figure 13.3). Specific injury patterns
may be identified. For example, contact of a body with
moving propeller blades classically leads to deep ‘chop’
wounds and/or lacerations and sometimes traumatic
amputation. Artefactual post mortem injuries produced
in such circumstances must be differentiated from ante
mortem injuries suggestive of assault.
Other artefactual injuries characterised by immer-
sion include damage to the body by marine life (e.g.,
shark, alligators, fish, crustaceans, molluscs and insects;
Figure 13.4). As the post mortem interval increases,
Figure 13.3 Post mortem injuries predominantly to the
back of the hand of a body recovered from a shallow
river. Such injuries are likely to have been caused by
contact against the river bed.
Figure 13.4 Post mortem injuries caused by marine
creature predation. This body was recovered from the
sea and the circular skin defects are likely to have been
caused by crustaceans such as crabs.
Pathological diagnosis of drowning 193
fragments/limbs may become detached and lost due to
decomposition and movement of the body in water.
Pathological diagnosis of drowning
Pathophysiology of drowning
Drowning is a complex phenomenon embracing a range
of psychological, physical, clinical and pathological
mechanisms. Some of these relate to the upper airway
being out of the water, and others relate to the upper
airway being underwater. Immersion in water causes
an interplay between cardiorespiratory responses to
skin and deep body temperature, including cold shock,
physical incapacitation, and hypovolaemia, as precur-
sors of collapse and submersion. These are combined
with the diving response, autonomic processes, fear of
drowning, upper airway reflexes, water aspiration and
swallowing, emesis, and electrolyte disorders. The out-
come is determined by a mixture of cardiac, pulmonary,
and neurological insults. Regardless of the composition
of water/fluid, drowning, the process of experiencing
respiratory impairment from submersion in a liquid,
may also result in pulmonary surfactant insufficiency/
damage, pulmonary oedema, alveolitis, hypoxaemia
and metabolic acidosis. In addition, as the popularity of
water-based sports advances, specific conditions such
as swimming-induced pulmonary oedema are being
recognised.
As time in cold water continues, so does the likelihood
of hypothermia (core body temperature <35°C). As hypo-
thermia develops, cognitive function becomes impaired
increasing the risks of (1) poor decision-making and (2)
aspiration of water.
Drowning reflects a combination of the physical
presence of water within the respiratory system (caus-
ing a mechanical asphyxia) and fluid and electrolyte
changes which vary according to the medium (sea vs
fresh water) in which immersion has occurred.
Fresh water is hypotonic compared with blood plasma
and, when inhaled, is rapidly absorbed into the blood-
stream, causing transient (but probably clinically irrel-
evant) electrolyte dilution and hypervolaemia. It results
in alveolar collapse/atelectasis because of changes in
the surface tension properties of pulmonary surfactant,
resulting in intrapulmonary (left to right) shunts.
Seawater is generally three times more hyperosmolar
than blood plasma, and following inhalation the hyper-
osmotic seawater can result in serious effects to the
lung and alveoli. These effects may be predominantly
categorised into insufficiency of pulmonary surfactant,
blood–air barrier disruption, inflammation, oxidative
stress, autophagy and apoptosis. Aspiration of fresh or
sea water therefore leads to systemic hypoxaemia caus-
ing myocardial depression, reflex pulmonary vasocon-
striction and altered pulmonary capillary permeability,
194 Immersion and drowning

contributing to pulmonary oedema. There is an inverse Alternative mechanisms of death in

relationship between survival and the volume of aspi-
rated fluid but even small quantities (i.e., as little as immersion
30 mL) can cause arterial hypoxaemia. Explanations for the death of individuals recovered from
water without autopsy signs of aspiration of water led
Signs of drowning to the concept of ‘dry drowning’, although alternative
explanations for such deaths include trauma, the effects
Post mortem findings ascribed to drowning reflect the
of intoxication, arrhythmia, laryngospasm or some other
pathophysiology of submersion, immersion and aspira-
neurologically mediated mechanism. The need for this
tion of the drowning medium (Box 13.3). It is important
terminology has been questioned and the use of the term
to be aware that none of these findings are diagnostic of
‘dry drowning’ is obsolete and confusing.
drowning or present in all verified drownings, and so
Stimulation of trigeminal nerve receptors by immers-
the autopsy diagnosis of drowning is one that requires
ing the face (and pharyngeal/laryngeal mucosa) in water
considerable reflection and a definitive answer may not
has been shown to elicit reflex apnoea, bradycardia
always be established. Boxes 13.4 and 13.5 give exam-
and peripheral vasoconstriction in humans, the ‘diving
ples of how deaths initially ascribed to drowning can be
response’, which is augmented by anxiety/fear, a water
the subject of ongoing controversy, and prompt reviews
temperature of less than 20°C and possibly alcohol,
many years after the death.

Box 13.3 Findings that may be associated with drowning

External foam/froth and frothy fluid in the airways
reflects an admixture of bronchial secretion/mucus,
proteinaceous material and pulmonary surfactant with
aspirated fluid (Figure 13.5). This froth/foam has been
likened to ‘whisked egg white’ in texture and consis-
tency, with a different quality to that seen in, for exam-
ple, cardiac failure.
Emphysema aquosum/heavy lungs describes hyper-
expanded and ‘water-logged’ lungs, whose medial
margins meet in the midline and which do not collapse
on removal from the body. There may be rib imprints
on the surface of the lungs, and copious frothy fluid
may exude from their cut surfaces. Combined lung Figure 13.5 Frothy fluid exuding from the mouth
weights of over 1 kg has been said to indicate fresh- following drowning.
water drowning (Figure 13.6).
Pleural fluid accumulation has been associated with
drowning, the volume of which controversially being
said to reflect the post mortem interval.
Subpleural haemorrhages Paltauf’s spots, named
after Arnold Paltauf (1860–1893) an Austrian medi-
cal examiner who described petechial haemorrhages
located beneath the pulmonary pleura, probably
reflect haemolysis within intra-alveolar haemorrhages,
and have been described in 5%–60% of drownings).
Miscellaneous signs including middle ear conges-
tion/haemorrhage, bloody/watery fluid in the intra-
cranial sinuses, engorgement of solid organs, reduced
weight of the spleen and muscular haemorrhages in
the neck and back have all been proposed as additional
physical signs of drowning. Figure 13.6 Emphysema aquosum following drown-
Microscopy of the lungs revealing alveolar distension, ing. The lungs are hyperinflated, crossing the midline
haemorrhage and rupture, and narrowed capillaries, and obscuring the pericardial sac. There are sub-
has been proposed as a sign of drowning but remains pleural haemorrhages in the right lung middle lobe
open to debate. (Paltauf’s spots).

Box 13.4 The death of Natalie Wood Wagner
The body of actress Natalie Wood was found floating
face-down in the ocean at Catalina Island, near Los
Angeles, on 29th November 1981. She had been with
her actor husband, Robert Wagner, on their boat, to
which they had returned after a meal the night before.
She was last seen alive at 2245 hours by Mr. Wagner,
who noticed that she was missing at around midnight.
A dinghy was missing, and subsequently found nearby
with the key in the ignition, but in the ‘off position’ and
appeared not to have been used.
Life was pronounced extinct at 0744 hours, and
a scene examiner found rigor mortis to be present,
with very slight blanching hypostasis on the back of
the trunk. Core body temperature was almost at water
temperature. She was clothed in a ‘down jacket’, night-
gown and socks.
At autopsy, the presence of white froth in the mouth
and nostrils, filling the airways and exuding from the
increasing the likelihood of the development of a fatal
arrhythmia. Cardiac arrest has also been documented
following entry of water into the nose.
The cold shock response, which is initiated by periph-
eral subcutaneous receptors, causes respiratory effects
(inspiratory gasp and uncontrolled hyperventilation,
respiratory alkalosis and cerebral hypoxia) and cardio-
vascular effects (tachycardia, increased cardiac output,
hypertension and ‘heart strain’ potentially leading to
cardiac irritability and ventricular fibrillation), which
appear temperature dependent.
Box 13.5 Death in a bathtub
Henry Keogh was convicted of murdering his fian-
cée, Anna-Jane Cheney, in August 1985, in Adelaide,
South Australia. She had been found by Mr. Keogh
slumped in the bath, with her face submerged in water.
Resuscitation efforts were unsuccessful. The death was
not treated as suspicious and an initial autopsy revealed
a bruise on the top of the head. A further examination
of the body revealed two further bruises at the back of
the head/neck.
Following cremation of the body, the pathologist’s
report described bruising on the lower left leg, and
that this was ‘an important part of the examination
as to cause of death; which was drowning’. Mr. Keogh
was arrested and stood trial in March 1995; the jury was
unable to agree a verdict, and a second trial took place
in August 1995.
The Prosecution argued that the bruising on the
lower left leg represented a ‘grip mark’ and death was
The role of alcohol and drugs in drowning 195
cut surfaces of the voluminous and heavy lungs was in
keeping with drowning, and post mortem toxicology
showed an alcohol level of 0.14 gms% (140 mg/dL).
The death was thought to have been accidental but a
review of the autopsy findings was undertaken in 2012,
in view of conflicting statements regarding the circum-
stances leading up to the discovery of the body, and
concerns that death might have occurred earlier than
when the alarm had been raised.
That review concluded that, in the presence of
bruising to the arms and a scratch on the neck, a non-
accidental mechanism could not be excluded for these
injuries prior to entry into the water. The manner of
death was considered undetermined, and the cause
of death was changed to drowning and other unde-
termined factors. This case intermittently comes under
further review, most recently in 2018 and as a subject
for broadcast documentaries.
Co-stimulation of both diving and cold shock
responses may precipitate arrhythmias including atrial
fibrillation and those associated with drug-induced pro-
longed QT intervals.
The role of alcohol and drugs in
drowning
Alcohol and drugs are often frequently found in the
blood of drowning victims and their contribution to the
death may be difficult to determine. but there is a strong
due to forcible drowning. There were three bruises on
the outside of the leg and a single bruise on the inside
– a combination said to be classic for grip. The patholo-
gist hypothesised that the legs had been forced over
the head and the head pushed under the water.
Autopsy photographs, which were in black and
white, had no identifying features and did not show
the whole body. The presence of bruising in the photo-
graphs was later disputed. Some of the bruising to the
scalp could also have been an artefact of the initial post
mortem examination.
Histological sampling was limited, and a review of a
sample of bruise from the inside left ankle suggested
that bruising to the ankle was some days old and that
death may have been caused by anaphylactic reaction
to the antihistamine drug Hismanal. His conviction was
overturned in 2014 and Mr. Keogh was released from
prison in 2015.
196 Immersion and drowning
association between substance use and ‘fall-related’
cases; concussive head injuries may be exacerbated by
alcohol, with immersion/submersion contributing to a
fatal outcome. Vasodilation from alcohol and other sub-
stances may initiate and worsen hypothermia. The use
of alcohol and drugs may encourage risk-taking behav-
iour. Additionally, a person intoxicated through alcohol
(or other drugs) has a reduced ability to respond appro-
priately and may be hampered by confusion, ataxia and
incoordination as a direct result of the substance use.
Other investigations in bodies
recovered from water
Strontium (Sr) concentration in tooth samples has
been used for the diagnosis of seawater drowning, and
research continues on this. Although there are no other
specific reliable biochemical markers for drowning,
there has been some promising research into utilising
lung-body weight (LB) ratio with post mortem vitreous
humor sodium and chloride (PMVSC) to diagnose salt-
water drowning when the immersion time is less than 1
hour. Additionally, the use of real-time polymerase chain
reaction (PCR) assays with TaqMan probes to differenti-
ate freshwater from marine bacterioplankton have been
shown to assist in the diagnosis of drowning. This will
continue to be an area of important research but inter-
pretation may be complicated by uncertainties about the
nature of drinking water/human microbiomes.
Diatoms
Diatoms are microscopic organisms present in sea and
fresh water, and have a siliceous capsule that survives
acid digestion in the laboratory (Figure 13.7). The pres-
ence of diatoms in the lung tissues, internal organs
and bone marrow is considered by some to be sup-
portive evidence in the diagnosis of death by drown-
ing. Quantitative diatom analysis in the lung tissues,
combined with the diatom analysis of the drown-
ing medium, may provide supportive evidence in
Figure 13.7 Diatoms from lake water.
determining if a body recovered in water was due to
drowning or not. In particular, a diatom database of the
rivers, seas, and lakes is essential as is collection of a
water sample from the putative site of drowning to allow
a rigorous comparison of the diatom species in water
and biological samples. It must be emphasised however
that the interpretation of diatom testing remains con-
troversial, as diatoms have been found to be ubiquitous
in food and the environment, have been found in non-
drowning deaths and have been absent in confirmed
cases of drowning. The use of diatomology in the foren-
sic diagnosis of drowning must currently be used with
caution and in the light of available evidence, but may
be useful to corroborate other findings.
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Further general resources
Payne-James JJ, Byard RW. Encyclopedia of Forensic and Legal
Medicine. Oxford: Elsevier; 2016.
14 Identification of the living
and the dead
▪▪ Introduction
▪▪ Methods of identification
▪▪ Identity of decomposed or skeletalised remains
▪▪ Mass disasters
Introduction
Loss of identity and proof of identity is a common prob-
lem in the medicolegal setting. Such loss of identity
might be deliberate, for example, if someone wishes to
conceal their own identity or that of another for criminal
or other personal reasons, or it might be unintentional,
for example, due to natural disaster (e.g., tsunami, wild-
fire, volcanic eruption) or terrorist or accidental events
(e.g., 9/11). Individuals (themselves or relatives) or legal
and national authorities may require that identity to be
established. This may apply to living or deceased indi-
viduals.
Formal, correct identification of a body is a key ques-
tion to be answered when a body is found in any medi-
colegal investigation of death. In England & Wales, it
represents the first question to be answered at the
Coroner’s inquest. Often visual identification by an
appropriate person may not be possible due to factors
such as facial trauma, decomposition, loss of body parts
or deliberate mutilation and other techniques must be
employed to confirm identity.
All governments require systems to be in place for
the rapid implementation of mass disaster responses
in situations of multiple deaths so that casualties and
deceased can be identified expeditiously. This is for
legal process, reassurance and support for relatives of
the injured and deceased.
Assessment of the deceased to establish identity is
a specialised task for a multiprofessional team which
may include forensic pathologists, forensic odontolo-
gists, forensic anthropologists, forensic physicians and
radiologists. Their work will be often set in challenging
and difficult conditions, in the midst of humanitarian
work and investigations for possible criminal cases. All
those working in the forensic setting should be aware of
the general principles to establish identity in the living
and deceased.
This same group of practitioners may be called
upon (individually or together) to assist in establishing
a person’s age. The two main settings where this may
be relevant is in criminal cases and asylum applica-
tions. Reasons to know age are manifold, and frequently
▪▪ Age estimation in the living
▪▪ Bibliography and information sources
▪▪ Further general resources
individuals have no records with them, and the estima-
tion is required to determine, for example, if they have
achieved the age of criminal responsibility in the rel-
evant jurisdiction or if are they classed by age as chil-
dren, in which case different legal principles may apply
to their situation. Estimation of age is simpler in children
and young people where developmental milestones may
be relevant and is more difficult and far less precise in
mature adults. However, recent advances in DNA analy-
sis and in particular the recognition that the epigenetic
signature of DNA methylation changes during an indi-
vidual’s lifespan means that DNA methylation age-cor-
related changes have the potential to act as a (relatively)
accurate means of age estimation.
There are additional means of identification such as
fingerprint or DNA databases, but these will only be of
relevance where the databases are well established and
where the individual has been convicted of, or is being
investigated for criminal offences. For these reasons, the
person or body with no previous criminal record may
prove to be more difficult to identify than those with such
a record with, or exposure to, a justice system. The pro-
liferation of genealogical databases has however created
an additional potential source of DNA profiles that can
be accessed by police and other bodies, and is likely to
result in complex human and civil rights concerns over
the coming years.
Methods of identification
Identification criteria
Identification criteria used are referred to as primary or
secondary. Primary identification criteria are 1) finger-
prints, 2) DNA, and 3) dental.
It must be recognised that in recent years the speci-
ficity of some aspects of fingerprint and dental assess-
ments have been brought into question. Secondary
criteria include features such as unique medical char-
acteristics, deformity, marks and scars, radiological
evidence, personal effects and distinctive clothing.
Examples of other features that may also provide
some assistance in identification include clothing,

photographs and location. Additional techniques such
as gait analysis or facial profiling from CCTV can be use-
ful when other features cannot be used, although their
accuracy is less consistent.
DNA profiling
The specificity of individual DNA profiles means that
from a statistical point of view it can be considered spe-
cific to any given individual.
The molecule of DNA has two strands of sugar and
phosphate molecules that are linked by combinations
of four bases, adenine, thymine, cytosine and gua-
nine, forming a double helix structure. Only about 10
per cent of the molecule is used for genetic coding (the
active genes), the remainder being ‘silent’. In these
silent zones, there are between 200 and 14,000 repeats
of identical sequences of the four bases. Sir Alec Jeffreys
found that adjacent sequences were constant for a
given individual and that they were transmitted, like
blood groups, from the DNA of each parent. The statis-
tical analysis of DNA identification is extremely com-
plex and it is important that any calculations are based
upon the DNA characteristics of a relevant population
and not upon the characteristics of a ‘standard’ popu-
lation somewhere else in the world. Forensic genetics
developed from protein-based techniques and brought
with it the term ‘DNA fingerprinting’, this being based
on restriction fragment length polymorphisms (RFLPs)
of high-­molecular-weight DNA. Development of ana-
lytical techniques resulted such as the amplification
of much smaller short tandem repeat (STR) sequences
using the polymerase chain reaction (PCR) which soon
replaced RFLP analysis and became standard in genetic
identification. STR multiplexes are now available which
simultaneously amplify up to 30 STR loci from as little as
15 cells or fewer. The huge volume of information asso-
ciated with the great range of observed STR genotypes
allows for genetic individualisation (with the exception
of identical twins).
Unlike before, there is now no need to match blood
with blood, and semen with semen, as all the DNA in
one individual’s body must of necessity be identical.
Buccal swabbing permits simple sampling of a sus-
pect. A suspect in any crime leaving cells or biological
fluids at a scene leaves proof of their presence at the
scene. The continued ability to analyse smaller and
smaller amounts of DNA and to recover and analyse
historical samples means that many old crimes can
be investigated (or reinvestigated) and there is now a
considerable number of individuals being found guilty
of a crime decades later as a result of DNA advances.
Additionally, and some might argue more impor-
tantly, there is a considerable body of those who were
incorrectly convicted, being exonerated, as a result of
these newer techniques. It is important (as with most
Methods of identification 199
elements of forensic science) that the use of DNA should
be considered as another piece of the jigsaw in the over-
all puzzle of solving crime and identifying unknown
individuals.
Comparison of DNA profiles with assumed or known
family members or against known databases can ensure
a person’s identity is established. If these comparisons
cannot be done, other tests must be used.
As forensic DNA analysis continues to progress,
identifying, extracting and amplifying smaller and
smaller amounts of genetic material, so the risks of
contamination from other sources increase. Crime
and mass disaster scenes have great potential for cross
contamination and standard operating procedures to
avoid contamination must always be in place to mini-
mise this risk. Appropriate protective clothing must be
worn to prevent the investigators obscuring any rel-
evant DNA by their own material being inadvertently
shed from exposed skin, or by sneezing, or perhaps
even by touching. In many jurisdictions, it is now a
requirement for all those involved in the identification,
collection and analysis of samples to provide exclusion
DNA samples in the same way as exclusion fingerprints
were once provided.
Examination of dental structures
Forensic odontology is one of the most important
specialties available to establish or confirm identity
of unknown bodies whether in isolation, after terror-
ist events, in mass graves or after natural disasters.
The success of such identification is very dependent
on access to ante mortem records from general den-
tal practitioners. Pre-existing (ante mortem) dental
records and charts and radiographic images can be
compared with examination of the dentition of the
deceased (Figure 14.1). If these are not immediately
available an odontologist will construct dental charts
of bodies whose identity remains unknown or uncon-
firmed despite a police investigation, so that, should
dental information become available at a later date,
the two sets of records may be then be compared. The
essence of the identification by dentition is compari-
son. This implies that the dental chart has to be com-
pared with, and found to match, a chart whose origins
are known (Figure 14.2). Unfortunately, studies suggest
that the recording of accurate dental charts by general
dental practitioners is sometimes inadequate.
The forensic odontologist is of prime importance in
mass disasters where trauma is likely to make visual
identification impossible. The great advantage of den-
tal identification is that the teeth are the hardest and
most resistant tissues in the body and can survive total
decomposition and even severe fire, short of actual cre-
mation and thus DNA samples (e.g., from teeth pulp)
which can be collected by the forensic odontologist can
be stored for future analysis (Figure 14.3).
200 Identification of the living and the dead
Figure 14.1 Identification from the teeth: post mortem X-rays (outlined in red) are compared with ante m­ ortem radi-
ography which, in this case shows a good match. (From Saukko P, Knight B. Knight’s Forensic Pathology. 4th ed. Boca
Raton: CRC Press, 2016 [Fig. 26.8].)
Figure 14.2 Example of completed dental chart.
Figure 14.3 Despite soft tissue destruction, dentition
is retained after fire.
Where no previous records are available, exami-
nation of the mouth and the teeth can still give some
general information on age, sex, diet and ethnic origin,
and some dentures may have the name or initials of the
individual printed on them.
Dental identification of a burnt body
The discovery of a body involved in a fire is one of two
types of scenarios; the first being when it is useful for
the forensic odontologist to attend the scene before the
body is moved, the other being when fetal or newborn
remains are suspected to be present.
Teeth are in fact very well protected by the hard and
soft tissues of the oral cavity. It is not uncommon for
a body to show signs of incineration, while the molar
teeth have only slight damage, if any, from fire. As the
temperature of the environment and, hence, the body
in question, rises the tongue will swell protecting the
surfaces of the teeth facing the inside of the mouth. The
ramus of the mandible will also offer some protection
to the outer surfaces of the molar teeth, as will the soft
tissue of the cheek.
The anterior teeth (upper and lower incisors and
canines) are the most susceptible to fire damage. Again,
as the temperature of the environment rises, soft tissues
will start losing moisture, and the lips being only soft
tissue will therefore shrink away, leaving the front teeth
unprotected. In cases where the fire has been fierce or
prolonged these teeth will be calcined, in other words,
turned into ash.
These teeth will maintain their shape for as long as
they remain undisturbed but the slightest force will
cause them to crumble and disintegrate. While the
posterior teeth anatomy and restorations often provide
most of the information for identifying a deceased indi-
vidual, in a time when people may have less dental treat-
ment due to better dental care, the shape and position of
anterior teeth could be vital for facial comparison with a
smiling photograph of the presumed deceased.
The forensic odontologist attending the scene would
stabilise the incinerated teeth using transparent cold
cure acrylic (Figure 14.4a and b). This material is found
in most surgeries and comes in a liquid monomer and
powder which will solidify within minutes of being
mixed together. Thus, powder and liquid can be mixed,
at the scene, to a runny consistency and then dripped
gently over the incinerated teeth and allowed to seep
through and set. This only takes a few minutes. The teeth
can then be examined properly at the mortuary once the
body has been moved. It is still worth covering the head
with a plastic bag tied at the neck to ensure any frag-
ments that fall off during transit are not lost.
 Methods of identification 201

(a)

(b)

Figure 14.4 Preserving fire-damaged teeth at the scene. A forensic odontologist applies cold cure acrylic liquid to
teeth (a), which sets and helps protect the teeth during transportation to the mortuary (b).

Fingerprints can only be established by matching the parameters that

The recovery of the fingerprints from decomposing and
damaged bodies requires the use of specialised tech-
niques which are the province of the fingerprint experts.
Prints may often be obtained from desquamated skin
or from the underlying epidermis after shedding of the
stratum corneum following prolonged submersion.
Their accuracy has been called into question recently
but they retain their usefulness in many cases where
identification is required, such as air disasters, in partic-
ular with intact trauma victims with few burn injuries.
Morphological characteristics
Identity cannot be established by the simple measure-
ment of a set of parameters of an individual or a body. It
can be measured or seen on an individual with the same
parameters that were known to apply to, or to be present
on, a named individual. Identification is established by
matching a range of general observations made about
the body to a range of general information known to be
true about that particular individual. The finding of a
unique medical feature (e.g., a previous uncommon sur-
gical procedure), or a combination of specific features,
that is known to be possessed by that individual alone
will add considerable weight to the conclusions.
In both the living and dead, the height, weight,
Body Mass Index (BMI) and general physique must
be recorded and compared. Hair colour and length,
including bleaching or dyeing, the presence of a beard
or moustache and the amount and distribution of other
202 Identification of the living and the dead
body hair, including genitalia and other sites that are
commonly shaved, all need to be established. Skin pig-
mentation should also be recorded as far as possible. All
clothing, jewellery and other ornaments on the person
must be recorded and photographed as they may pro-
vide useful information about the sex, race and even
occupation and social status of the body, even if they
are not sufficient for identification. Surgical scars, old
injuries, congenital deformities, striae from childbirth
or rapid weight changes, cultural or tribal scars or
markings, circumcision, female genital mutilation, pig-
mented lesions, papillomata and other skin marks or
abnormalities must all be recorded. Appropriate pho-
tography of such features should always be done so that
others (e.g., a relative, friend or doctor) may be able to
confirm an identity from these features.
In a living person or recently deceased intact body,
the facial appearance may be of great significance from
ethnic and racial aspects and from individual appear-
ances. High-quality frontal and profile photographs
should be taken for comparison.
Tattoos and body piercings
Tattoos and piercings that have been individualised
(e.g., by site, design, or specific personal information)
may provide unique features for identification. The
main use of tattoos and piercings in forensic medicine is
in the identification of the bodies of unknown persons.
Once again, the simple presence of a tattoo does not gen-
erally confirm identification and ideally there has to be
a comparison with, for example, images of that person
where the tattoos are visible. Good quality ante mortem
images can be very helpful when compared with images
of the deceased, and can be used if a visual identifica-
tion is not possible or so that they can be circulated
when the identity is not known.
Worldwide there is a vast range of tattoos. Some
designs have specific meaning or significance within
certain subgroups of society. Others may, for example,
indicate previous or current military service, or street
gang membership. Others are personalised to that indi-
vidual. However, nowadays designs originating from
throughout the world are purely used as body decora-
tion, and they provide little assistance in assessing the
region or nationality or cultural group of origin of the
individual. Names and dates of birth within tattoos
may be useful. Decomposing bodies should be exam-
ined carefully for tattoos, which may be rendered more
visible when the superficial desquamated stratum cor-
neum is removed. Prior to current techniques of identi-
fication the discovery of a tattoo on a body part provided
a means of identification (Box 14.1).
Body piercing is widespread, and the site and type
of piercing should be noted and piercings can be used
as part of visual identification or can be recovered for
Box 14.1 The ‘Sydney Shark Case’ (1935)
A shark in a Sydney, Australia aquarium vomited
a human arm, severed at the shoulder, with rope
around the wrist. It was well preserved despite hav-
ing been in the shark’s digestive tract for the week in
which it had been in the aquarium. The arm bore a
tattoo of two boxers in fighting poses on it, enabling
police to identify a man who had gone missing some
nine days before the shark’s capture. Examination of
the arm revealed that it had been cut off the body
rather than being bitten off by a shark. A man was
arrested and subsequently acquitted.
identification by relatives if visual identification is not
possible.
Identity of decomposed
or skeletalised remains
When apparent human skeletal remains are discovered,
a number of questions need to be asked. The answers to
these questions may require the expertise of patholo-
gists, anthropologists, odontologists, radiologists, anat-
omists and scientists. Box 14.2 shows the questions and
answers that may arise.
Where pre mortem clinical radiological images are
available comparison of these with the post mortem
films may give a definite identity.
Mass disasters
Mass disasters require systematic collection of foren-
sic evidential samples; a chain of custody ensuring
continuity and integrity of the sample trail; and once
analysed, the application of appropriate evidential and
interpretative standards. At the time of the disaster it
may initially be unclear whether an event has happened
by accident, natural disaster or following a crime. Ante
mortem data from potential decedents, including den-
tal, fingerprint and DNA samples should be sought at the
earliest opportunity for later comparison. Comparator
fingerprints can be obtained from personal items, in
the home, workplace or crime databases. DNA samples
can be obtained from items such as toothbrushes, hair-
brushes and razors. Possible family members may be
asked to provide samples for DNA analysis. General
dental practitioners should be approached to provide
dental charts, radiographs and dental impressions
where available. Matching of the ante mortem data with
the post mortem samples may be done using specialised
software systems when available so that identities can
be confirmed.

Box 14.2 Issues arising following the discovery of apparently human remains
Are the remains actually bones?
Sometimes objects such as stones, plastic models or
even pieces of wood are mistaken by the public or
police for bones: the anatomical shape, character and
texture may not always be obvious to someone who is
medically trained, but in most cases will be.
Are the remains human?
This is a more difficult question to answer. Differentiating
human from animal bones is not always easy. A foren-
sic pathologist or forensic physician should be able to
identify almost all of the human skeleton, although
phalanges, carpal and tarsal bones can be extremely
difficult to positively identify as human because some
animals have extremity bones with features similar
to the human hand and wrist. Identifying the source
of fragmented or burned/cremated bones generally
requires the skill of a forensic anthropologist or com-
parative anatomist.
Do the remains represent one or more bodies (is there
co-mingling of body parts)?
Clearly, if there are two intact skulls or two intact left
femurs then specific expertise is not required. If there
is no obvious duplication, it is important to examine
each bone carefully to assess whether the sizes and
appearances match. Excluding the possibility of co-
mingling of skeletal remains is the realm of the forensic
anthropologist.
What is the biological sex?
There is a vast anthropological literature on these
matters with norms established for a range of popu-
lations. The skull and the pelvis offer the best informa-
tion on sexing; although the femur and sternum can
provide assistance. There are, however, many studies
which explore these and other structures including
the maxillary sinus volume, and the nature of teeth
and the size of the patella. It is important to attempt
to determine the sex of each of these structures and
not to rely on the assessment of just one. Examination
by a forensic anthropologist or anatomist is vital.
An emergency or major incident may result in fatali-
ties. Disaster victim identification (DVI) is the interna-
tionally accepted term for the processes and procedures
for recovering and identifying deceased people and
human remains in multiple fatality incidents. The
Mass disasters 203
What was the age of the person at death?
This will require a multiprofessional approach utilising
the skills of the forensic pathologist, anthropologist,
odontologist and radiologist, each contributing to the
overall picture.
What was the height (stature) of the person?
The head to heel measurement of even the newly
deceased is rarely the same as the person’s standing
height in life, owing to a combination of factors, including
muscle relaxation and shrinkage of intervertebral discs.
If a whole skeleton is present, an approximate height
can be obtained by direct measurement but, because of
a range of factors (e.g., changes in joint spaces, articu-
lar cartilage) this can only be an approximation. If only
some bones are available, calculations can be made
from established tables, of which there are many. Height
can be estimated from a range of long bones including
the humerus, ulnar and femur. Other bones such as the
sternum have also been used in this setting.
What is the ancestry of the deceased?
This is a very complex area of much controversy and sits
firmly within the realm of anthropologists whose main
focus lies within the field of craniometrics.
Can a personal identity be discovered?
The previous criteria can assign bones broadly to vari-
ous groups of age and sex but putting a name to the
individual depends, as does all identification, upon hav-
ing reliable, corroborative ante mortem data. There are
occasions when foreign bodies such as bullets or other
metallic fragments may be found embedded in the skel-
eton; these may either relate to the cause of death or
may simply be an incidental finding. Sometimes these
can assist in identification. Surgical or other implant
procedures (e.g., pacemakers, arthroplasty implants,
implantable defibrillators) have a unique reference
number which may identify the maker; these and other
unique medical data are often useful in establishing
identity, and can frequently be seen after radiological
imaging and tracked, following referral to the implant
manufacturer, to the named patient.
process involves bringing together ante mortem and
post mortem information to make a positive identi-
fication by scientific means in a dignified manner,
taking into account the needs of the investigation pro-
cess, the needs of the bereaved and the needs of the
204 Identification of the living and the dead
community. Within the UK, the National Disaster Victim
Identification Unit coordinates the national capability
of the police service to respond to mass fatality inci-
dents in the UK. The team works with police services,
government departments, local authorities and other
agencies to do this. The Coroner in England & Wales (or
Procurator Fiscal in Scotland), is responsible for chair-
ing the Identification Commission, where the identity of
the deceased is confirmed. It is the Coroner’s responsi-
bility to establish the deceased’s identity and how, when
and where the death occurred. They have the power to:
take lawful possession and control of deceased persons
or human remains from when the death is reported
until all enquiries are complete; authorise removing the
deceased from their place of death to a mortuary; and
authorise a post mortem examination. Body recovery
teams will identify the deceased wherever they may be
found. They will then be photographed before they are
moved to assist any criminal investigation and to assist
the Coroner in establishing cause of death. At the mor-
tuary, any personal items will be retrieved. These will be
used as indicators of the potential identity of the person.
Investigators will then go with a family liaison officer to
recover items that could assist the identification, such as
personal items from the deceased’s home that may yield
fingerprints or DNA, or their dental records from their
dentist. Once identification evidence has been collected
this will be presented to the Identification Commission
which will decide if it meets the standards required to
confirm identity. Further evidence may need to be col-
lected. If identity reaches the standard of proof required
then the evidence will then inform an inquest into the
death.
Age estimation in the living
For the deceased, investigation of identity and age is
generally undertaken by order of, and with the con-
sent of, legal authorities, for example, the Coroner in
England & Wales.
In the living, other constraints apply. The essential
element of any age estimation procedure is to ensure
that it complies with, and fulfils, all local and/or
national legal and ethical requirements. All practitio-
ners, clinical or forensic, must take full responsibility
for their actions in relation to the human rights of the
subject undergoing investigation. It is essential that the
practitioner, clinical or forensic, undertaking the esti-
mation is experienced in the interpretation and presen-
tation of data emanating from the investigation. They
must have a current and extensive understanding of the
limitations of their investigation both in relation to the
physical technology available to them and to the nature
of the database to which they will refer, for comparison
purposes. This also requires that the practitioner has a
realistic understanding of the variation expressed by
the human form and the extrinsic and intrinsic factors
that may affect any age estimation process.
Four main means of age estimation are available,
and the more of these that are used the more likely
it is that the result of the examination will correlate
well with the chronological age of the individual.
Underestimation of age is unlikely to raise any issue in
relation to an infringement of human rights (as younger
persons tend to be treated more advantageously in the
legal process) but an over-estimation of age can have
adverse effects. It is essential that the final estimation
is robust and conveys a realistic range within which
the chronological age is most likely to occur. As yet,
the use of DNA for age estimation is not a feature of the
legal process. Any element of doubt must result in an
increased range of possibilities. It is not possible in any
circumstance to ascertain with certainty whether an
individual is 20 or 21 years of age. An assessment of 20
years ranges from a specific calendar date (birthday) to
a date that is 364 days beyond that date and only one
day short of the assessment of an age of 21 years. The
means of assessment that should be used now to esti-
mate age in the living are:
• Social and psychological evaluation: This
requires evaluation by a highly trained clinician
or social work practitioner.
• External estimation of age: This evaluation must
be undertaken by a qualified clinician (a forensic
physician, or a paediatrician for the child and geri-
atrician for the elderly; examination by more than
one practitioner may be appropriate).
• Skeletal estimation of age: This investigation can-
not be undertaken visually and therefore relies
on technology to assist the process (exposure to
much of the relevant technology has risk from ion-
ising radiation and can only be undertaken with
informed consent).
• Dental estimation of age.
Certain aspects of each of these means of assessment
are well recognised. External estimation of age should
use Tanner staging to assess child maturity (Figure
14.5). Skeletal estimation will assess hand/wrist radio-
graphs in the first instance, which are compared against
standards previously published. A visual intraoral
inspection will inform the practitioner as to the stage
of emergence and loss of the dentition and is particu-
larly useful for age evaluation in the pre-pubertal years.
Pubertal and post-pubertal individuals will, however,
require a radiographic investigation subject to their
local regulatory guidelines and statute.
 Bibliography and information sources 205

Stage G = genitals (boys) B = breasts (girls) P = pubic hair (girls)

1 Pre-adolescent Pre-adolescent No hair

2 Scrotum pink and Breast bud Few fine

texture change, slight hairs
enlargement
of the penis

3 Longer penis Larger, but no Darkens,

larger testes nipple contour coarsens,
separation starts to
curl

4 Penis increases Areola and pailla Adult type,

in breadth, dark from secondary smaller
scrotum mound. area
Menarche usually
commeneces at
this stage

5 Adult size Mature (pailla Adult type

projects, areola
follows breast
contour)

Figure 14.5 Tanner staging for the assessment of child maturity.

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15 Restraint and control
techniques
▪▪ Use of force
▪▪ Conflict resolution
▪▪ ‘Empty hands’: unarmed restraint
▪▪ Handcuffs
▪▪ Batons
Use of force
Law enforcement personnel and others are required on
some occasions to use restraint techniques to control
individuals who may be violent or suffering from some
form of acute behavioural disturbance. A key element of
such force is that it requires a sensitive balance between
the duty of care to the individual being restrained, pay-
ing due attention to their safety and security, and those
who may be harmed, including the behaviourly dis-
turbed person requiring restraint, the general public
and the law enforcement personnel. A general principle
is that the least possible effective force should be used.
The determination of the level of force used to restrain
an individual often becomes a crucial element in a
criminal trial or an employment tribunal. Additionally,
such determinations may be required in civil justice and
coronial justice settings, where either the detained per-
son or the law enforcement officer has sustained harm,
or the events have resulted in a fatality. Close analysis
will be undertaken of the type and means of restraint
that was used to secure that control.
The phrase ‘use of force continuum’ is sometimes
used to indicate the level of force appropriate for use
against a non-compliant person by law enforcement,
or security personnel, and under which circumstances.
Police and other law enforcement agencies will gener-
ally have a published policy which will vary in nature
but embraces the appropriate use of restraint tech-
niques and personal protection strategies for personnel.
Such policies can provide guidance about appropriate
actions in response to actual or perceived threats, bal-
ancing factors such as the safety of others, the presence
of weapons, and the size of the non-compliant indi-
vidual, with the level of force used by law enforcement/
security personnel. There is a risk of unintended harm
with all restraint techniques, and there is a risk of death
with some of them. It is important to understand the
intended effects, and risks to health, of each of these
techniques and devices. The term less-lethal weapon
is used to differentiate such devices from firearms used
by law enforcement personnel, which are generally
▪▪ Irritant sprays
▪▪ Impact rounds
▪▪ Dogs
▪▪ Conducted energy devices
▪▪ Bibliography and information sources
used with the intention of killing. Table 15.1 lists the
techniques and devices generally available to police
personnel in the UK.
Conflict resolution
All law enforcement personnel involved in restraint con-
trol or public order settings should have an understand-
ing of conflict resolution and the factors that will affect
how individuals respond to certain threats or actions. It
is important that any progression or escalation of force
is reasonable in order that any adverse outcome may be
justified at a later date. All law enforcement personnel
should be taught de-escalation techniques to reduce
the need for physical means of restraint. The offender
behaviour is characterised in a number of ways rang-
ing from that of compliance, to verbal and gestured
responses, passive resistance, active resistance, assault
and aggression to the most serious category, aggravated
aggression (which may involve the use of a weapon).
Many factors may affect the subsequent behaviour of an
individual and how an officer responds (Box 15.1).
Around the world there are a wide variety of tech-
niques, implements and weapons which may be used
for control and restraint. Many are techniques used for
crowd control including the use of tear gas, water can-
non, horses, and ‘kettling’. The use of these techniques
will vary from country to country. Some may cause
injury and some, either through inappropriate use or
some other circumstance, may result in physical com-
plications. Doctors, particularly forensic physicians and
emergency medicine specialists, may become involved
in the assessment of the medical consequences of con-
trolling or restraining people. Forensic pathologists may
be involved in determining the cause of death. This often
becomes a major issue at inquest where other factors
(apart from the use of the restraint technique) such as
drug or alcohol intoxication, associated self-harm and
mental health issues commonly feature. When assess-
ing a non-fatal restraint case, a full clinical assessment
with documentation of injuries and, if necessary, appro-
priate referral to specialists is crucial. The history from

Table 15.1 Techniques and devices used by police
services in the UK for personal restraint and control
• Use of force
• Conflict resolution
• ‘Empty hand’: unarmed restraint
• Handcuffs
• Batons
• Irritant sprays
• Impact rounds
• Dogs
• Conducted electrical energy devices/weapons
• Spit guards (or spit hoods, or bite guards)
the injured person may need further clarification by
direct communication with the restraining personnel
concerned. Review of available CCTV, body worn video
or video recordings recorded on phones and broadcast
on social media by members of the public may all assist
in the proper determination of the facts in these cases.
‘Empty hands’: unarmed restraint
A variety of arm locks and holds, pressure-point control
and knee and elbow strikes may be used. If excessive
force is used, either directly by the officer or as a result
of the restrained person moving, joints such as the wrist,
elbow or shoulder can be strained to varying degrees.
Other soft tissue injuries may be found.
Neck hold and neck restraints (sometimes known
as vascular neck restraint or sleeper holds) are avoided
by many law enforcement agencies, as there is a real,
unpredictable risk of serious injury or fatality from
neck compression. If an individual is restrained in such
a hold the neck and head should be examined carefully
Box 15.1 C
 onflict resolution: Factors
affecting the behaviour of an
individual and how an officer
responds
• Presence of an imminent danger
• Comparative ages
• Sex and size
• Strength
• Skills
• Specialist knowledge
• Presence of drugs or alcohol
• Mental state
• Relative position of disadvantage
• Injury
• Number of individual’s involved
• Whether weapons are present
• Officer’s overall perception of the situation
Handcuffs 209
Figure 15.1 Scleral haemorrhage 2 hours after
neck compression in a restraint setting.
(Courtesy of Jason Payne-James.)
for signs of injury. Examination for petechiae is manda-
tory in the skin of the head, neck, face, ears and scalp,
the intraoral mucosa and the eyes (Figure 15.1). Clothing
can be grabbed in a scuffle and the tightening, ligature
effect of this can cause linear or patchy type bruising
around the neck.
Positional asphyxia is a term that describes respi-
ratory impairment as a consequence of the position
in which a person finds themselves, including whilst
being restrained. It can occur as a result of the indi-
vidual being held down and being unable to maintain
adequate respiratory movement either because of the
chest and/or the diaphragm being splinted, for exam-
ple, because law enforcement/security personnel are
kneeling on the chest and thorax. The risk of death is
further heightened by lying prone (face down), being
handcuffed behind the back, being unable to change
position, obesity, respiratory or cardiac disease, and
struggling against restraint.
Handcuffs
Three main means of handcuffing individuals exist: tra-
ditional handcuffs with two wrist pieces connected by a
short chain; rigid cuffs whereby the two wrist pieces are
connected by a bar and cannot move in relation to each
other; and plasticuffs, in effect, larger-size cable ties
which are easy to store and easy to apply but less secure
than the first two types. The fixed connecting bar of the
rigid handcuffs allows controlled application of force
across the wrist to gain control. Once applied, simple
pressure against the wrist allows the single bar of the
cuffs to release over the top of the wrist and close with
a ratchet mechanism. If the individual is noncompliant
and continues moving, the handcuffs can progressively
tighten causing increasing pain and potentially increas-
ing the risk of neurological and skin damage. A num-
ber of injuries may be caused by handcuff application.
Soft tissue injuries may be produced by movement of
the wrist within the handcuff, movement of the hand-
cuff on the wrist or by the handcuff being too tight. The
commonest injuries are blunt force injuries of redden-
ing, abrasions and bruising, particularly to the radial
210 Restraint and control techniques
and ulnar borders of the wrists. Superficial cuts, from
the edge of the cuff, may be present in the same loca-
tions. Numbness or hyperaesthesia in the distribution
of the cutaneous nerves distal to the applied cuff are
not uncommon. Specific handcuff neuropathies may be
caused and single or multiple nerves may be affected,
the extent being determined by a number of factors
including the tightness of compression, the length of
time compression has occurred and the degree of resis-
tance by the detainee.
In most cases, the damaged nerves fully recover
within a few weeks. Persistence of symptoms will
require nerve conduction studies.
It is rare for handcuffs to cause fractures of the wrists
secondary to the use of handcuffs. However, they should
be considered when there is marked tenderness, loss of
movement or extensive bruising. The most vulnerable
parts of the wrist are the styloid processes, particularly
on the ulna. Sometimes simple imprints will be seen,
and at other times, substantial and obvious blunt force
injury is present (Figure 15.2a and b).
(a)
(b)
Figure 15.2 Handcuff injuries. (a) Imprint of handcuff
­following tight, prolonged application; (b) bruise,
­abrasion, laceration and underlying ulnar styloid
­fracture following struggle after handcuff applied.
(Courtesy of Jason Payne-James.)
Batons
Law enforcement and security agencies commonly use
batons to gain control. In the UK, two baton types are in
general issue: the three-part gravity friction lock baton
made of steel (an expandable baton with two telescopic
tubes that extend to a locked format with the flick of the
user’s wrists [e.g., ASP]) (Figure 15.3), and an acrylic
patrol baton (APB), which is available in three lengths:
22, 24 and 26 inches (approximately 56, 61 and 66 cm).
In the past, a 15-inch (38 cm) wooden patrol baton was
available. Such batons can be used for defensive and
offensive activities: the long portion can be used for a
direct strike, the baton can be held at both grip and long
end and used to push back an individual and both ends
can be used to the front and back to jab against someone
else. The potential for injury will vary with the amount
of energy transferred in a baton strike. The heavier,
expandable baton will potentially cause more injury
than the lighter standard patrol baton. All batons have
the capability of causing significant injury including
skull fracture and death. If batons are deployed, ana-
tomical areas targeted are classified into low, medium
and high risk of injury areas. Areas of low injury poten-
tial (and thus intended primary targets causing control
predominantly by pain infliction) are the lower limbs
(in the areas of the common peroneal, femoral and tib-
ial nerves) and upper limbs (in the areas of the radial
and median nerves) avoiding joints. Potential medical
complications of strikes in these areas include bruising
(a)
(b)
Figure 15.3 ASP baton. (a) Fully extended and (b) non-
extended. (Courtesy of Jason Payne-James.)

Figure 15.4 Baton strike ‘imprint’ injury.
(Courtesy of Jason Payne-James.)
of the target area, occasional cortical fractures and
transitory motor dysfunction of the affected limb. The
medium injury potential areas (and therefore not pri-
mary targets) are knees and ankles, wrist, elbow, hands,
upper arms and the clavicles. Predictable medical com-
plications include bone fractures, joint dislocation and
soft tissue damage. Higher injury potential areas (which
should not be targeted) are the head, neck/throat, spine,
loins (kidneys) and abdomen (small bowel, stomach,
liver, pancreas). Complications include damage to solid
and hollow organs, which could lead to serious injury
(e.g., liver laceration, gastrointestinal perforation) and
death. Injuries from a baton strike can embrace the
full spectrum of blunt force injury. Tramline bruising
is a patterned bruise typical of having been struck by
a baton. Circular patterned bruising can occur as a
result of someone being struck by the end of the baton
(Figure 15.4). Lacerations may be caused by baton blows
over bony surfaces. Fractures are rare but can occur, for
example from direct impact to the ulna.
Irritant sprays
Irritant sprays (formerly referred to as incapacitant
sprays) use a variety of agents to render individuals or
groups of individuals temporarily incapable of purpose-
ful action. In the UK, two main irritant sprays are used
by police services – CS and PAVA.
The active ingredient of CS irritant spray,
o-­chlorobenzylidine malonitrile, is a solid at room tem-
perature but is dissolved in an organic s­ olvent – methyl
iso-butyl ketone (MIBK) – to be used as a liquid aero-
sol. This is used to spray the face of a person from up to
3–4 m away, delivering CS to the eyes, nose and mouth
and causing immediate irritation to the eyes, upper
respiratory tract and skin (Figure 15.5). The effects on
the eyes and the skin many last up to 2.5 hours, whilst
those to the throat and respiratory tract usually last up
to 30 minutes. Table 15.2 lists the potential effects of
exposure to irritant sprays.
Impact rounds 211
Figure 15.5 Example of CS spray containers.
(Courtesy of Jason Payne-James.)
About 10% of people sprayed are not incapacitated by
exposure. It is not possible to predict who will respond
and who will not.
PAVA (pelargonic acid vanillylamide) is the synthetic
equivalent of capsaicin (the active ingredient of natural
pepper). It is intended to be directed towards the eyes
as it is generally utilised as a jet rather than a spray,
and causes extreme discomfort and eye closure. Less
research has been done on PAVA, but the broad effects,
treatment and management are similar to those of CS
spray. Effects on eyes, respiratory system, mouth or skin
that last for >6 hours should generally be referred for
specialist assessment to the relevant department. The
most important action is to stop continued exposure by
removal of the affected individual from the contami-
nated environment to a well-ventilated area, preferably
with a free flow of air and removal of contaminated
clothing. Each exposed individual should have a full
clinical assessment with particular reference to eyes,
oral and nasal cavity, respiratory system and skin.
Impact rounds
A number of firearms are adapted to fire impact rounds
(known by a variety of names, including plastic bullets,
rubber bullets, and baton rounds). The names are not
used consistently. A variety of projectiles of different
types are available. In the UK, the ‘Attenuating Energy
Projectile’ is used. Figure 15.6 illustrates examples of the
range of shapes and materials that may be used. Impact
rounds are made from materials of lower density than
‘normal’ bullets, are larger, and fired at lower velocities.
The design, relatively large in size, low in weight, and low
velocity, is intended to reduce the risk of skin penetration
while exerting severe pain on impact. This is intended
to minimise severe or fatal injury. As with police
batons, the intended usage and effect may be achieved,
but often, because of the dynamics of the situation,
the wrong area of the body may be hit or unintended
increased force of impact is sustained and significant
injury can result. Fatalities have been recorded. Some
212 Restraint and control techniques

Table 15.2 Effects of exposure to irritant sprays

Eyes: Clinical efects – generally expected duration of most intense effects
• Lachrymation (tears) (<15 mins)
• Pain (<30 mins)
• Blepharospasm (eyelids closed) (<30 mins)
• Conjunctival erythema (redness) (<30 mins)
• Reduced visual acuity (blurred vision) (<30 mins)
• Photophobia (sensitivity to light) (<60 mins)
• Periorbital oedema (swelling around the eye)
• Damage to the ocular surface from the direct trauma of a high-pressure jet
• Iritis may develop as a non-specific response
• Conjunctivitis
• Corneal abrasions due to rubbing the eyes
Mouth: Clinical effects
• Stinging or burning sensation
• Possible nausea and vomiting (rare)
Respiratory tract: Clinical effects
• Nose discomfort, pain and rhinorrhoea (<30 mins)
• Sneezing and coughing
• Sore throat
• Shortness of breath
• Bronchospasm (rare)
• Laryngospasm (rare)
• Tracheitis
• Bronchitis (rare)
• Pulmonary oedema may develop 12 to 24 hours after excessive exposure (rare)
NB: Patients with pre-existing respiratory disease, such as asthma or bronchitis, are more at risk of severe effects.
Skin: Clinical effects
• Burning sensation and erythema (<24 hrs)
• Chemical burns, blistering
• Allergic contact dermatitis (rare: but if law enforcement personnel are regularly exposed to irritant spray they may
require changes in work practice and referral to Occupational Health teams should be made)
• Leukoderma (rare)
• Initiation or exacerbation of seborrhoeic dermatitis (rare)
• Aggravation of rosacea (rare)
Cardiovascular: Clinical effects
• Pre-existing cardiac problems can be worsened and hypertension exacerbated after exposure. For example, angina
attacks may develop.
Other: Psychological effects
• In one study, one quarter of those exposed to CS spray were diagnosed with Post Traumatic Stress Disorder; a past
psychiatric history and a more external locus of control was associated with post-traumatic morbidity.
Source: Adapted from McGorrigan J, Payne-James JJ. Irritant sprays: clinical effects and management Recommendations
for Healthcare Professionals (Forensic Physicians, Custody Nurses and Paramedics). Faculty of Forensic & Legal
Medicine, 2017.

projectiles are intended to impact on the ground prior
to hitting the subject, dissipating the energy in advance.
The projectiles are frequently irregular cylinders made
from rubber, plastic, wood or foam, and can be as large
as the full-bore diameter of the launcher. Projectiles may
consist of a single, long round, or several shorter ones
fired concurrently. One additional group is the ‘beanbag
projectile’ which consists of a tough fabric bag filled with
compliant material (Figure 15.7). Baton rounds have two
roles: public order and as another alternative to the use

Figure 15.6 Examples of baton rounds.
(Courtesy of Jason Payne-James.)
of conventional firearms against individuals armed with
bladed weapons. For use in a public order role, the nor-
mal operating range is 20–40 m. For use as a less-lethal
alternative to firearms, it may be used at 1 m range.
Because of their size and profile, they are only accurate
at short distances and the projectiles are prone to tumble
after discharge, decreasing their accuracy. Deaths from
baton rounds are very uncommon and principally result
from head and chest trauma. Impact to the lower torso
and limbs results in bruising, abrasions and occasionally
skin lacerations. There is a very low reported frequency
of intra-abdominal trauma. Fractures to limbs do occur
occasionally. The chest is regarded as a vulnerable area
and although the system has been designed to avoid
impact to this region, these may occasionally occur in
operational practice; rib fracture and pulmonary contu-
sion may occur.
Dogs
Trained dogs from law enforcement agencies are capa-
ble of restraining and detaining individuals who need to
be controlled. In some cases, dogs bite. Bites all require
medical assessment as there may be, dependent on the
site and degree of injury, a risk of infection, neurological
Figure 15.7 Bean bag round.
(Courtesy of Jason Payne-James.)
Conducted energy devices 213
or vascular injury. In some circumstances, bites may of
such a degree that soft tissue defects requiring surgi-
cal intervention may be created. There are cases where
limbs have been lost from necrotising fasciitis following
infection after police dog bites. All those who sustain
such injuries must be advised to seek medical assis-
tance should apparent infection develop. Many health-
care professionals provide prophylactic antibiotics for
any penetrating injury. On occasions, the origin of the
bite injury may be disputed and a forensic odontologist
or forensic veterinarian may be required to provide a
definitive opinion.
Conducted energy devices
Conducted energy devices have been developed and are
part of the use of force continuum with the specific aim
of providing a less-lethal option of incapacitation of the
acutely behaviourly disturbed, or violent, non-compli-
ant individual. The most widely used by law enforce-
ment agencies is the TASER (named after the fictional
Thomas A Swift’s Electrical Rifle). The TASER comes
in a variety of models. Currently, the two most widely
used models are the X26 and X2, but newer versions are
continually developed. (Figure 15.8a and b). TASER
conducted energy devices are battery-operated, pistol-
like devices which exert their effects by delivering brief
pulses of electricity into the body, and can be used in
two main ways: probe mode and drive-stun mode.
(a)
(b)
Figure 15.8 (a) TASER® X2 and (b) barbs.
(Courtesy of Jason Payne-James.)
214 Restraint and control techniques
Table 15.3 Potential effects of TASER® discharge
Localised superficial burns and erythema at the
probe sites
Probe penetration of organs or body cavities (all the
following have been documented):
• Pleura
• Brain
• Eye
• Nasolacrimal duct
• Testis
• Urethra
• Digital tendon
• Pharynx
Musculoskeletal injury from the induced muscle
contraction
• Spinal compression fractures
• Ethmoid bone fracture
Secondary injury (from TASER-induced falls)
• Non-fatal and fatal head injury
Epileptic seizures
Source: Adapted from Sheridan RD, Payne-James JJ.
TASER: Clinical effects and management of
those subjected to TASER discharge. Faculty of
Forensic & Legal Medicine, 2017.
Probe mode is when darts are fired at the subject from a
cartridge fixed to the front of the TASER. These darts,
which travel at 40–50 metres per second, are designed
to embed in clothing or skin while remaining electri-
cally connected to the TASER by fine insulated wires.
Drive-stun mode is when the electrodes at the front of
the TASER are directly applied to clothing or to the
skin. The effect of the discharge depends on the mode
of use. Because of the small separation of the electrodes
in drive-stun mode, the principal action of the TASER
is to induce pain. When the barbs are propelled, the
greater barb separation allows the discharge to induce
involuntary (and painful) contraction of skeletal muscle
that results in temporary neuromuscular incapacita-
tion Such effects are almost instantaneous with only a
slightly slower recovery. Table 15.3 summarises some of
the clinical effects associated with TASER discharge.
There is some evidence that inspiratory activity may
be severely compromised. TASER  devices are used
in physically and emotionally charged settings. These
factors in isolation have the potential to precipitate
adverse cardiac or cerebrovascular events in individu-
als suffering from clinically diagnosed or subclinical
cardiovascular disease. Frequently alcohol, illicit drugs
or prescribed drug intoxication may be present in asso-
ciation with acute mental health crises. All have the
potential to increase the risk of cardiopulmonary arrest,
even in the absence of TASER use. The UK govern-
ment’s independent advisory committee on the medical
implications of less-lethal weapons took the view that it
would be prudent to assume that there is a possibility
that, in some situations, it would be possible for rapid
ventricular capture to be induced. This may be less of an
issue for a young, healthy individual, but could be sig-
nificant in those with diseased hearts or who have taken
illicit or prescription drugs which have intrinsic effects
on cardiac electrophysiology or coronary perfusion.
Such devices can assist in the safe and proper enforce-
ment of law. However, it is important that any current
and new technologies being introduced as less-lethal
options are appropriately and robustly tested and scru-
tinised in a scientifically credible manner to reassure a
sometimes appropriately cynical and sceptical general
public. Unfortunately, some devices are deployed with-
out appropriate review.
Spit guards/hoods/masks
Spit guards (also known as spit hoods or spit masks) are
devices intended to cover the mouth, face and head of a
restrained person in order to prevent them spitting at,
or biting others. These devices generally comprise of a
synthetic mesh, placed over the head, with a reinforced
panel at the front which is used to cover the mouth and
nose area. There is substantial controversy about their
role, and whether they represent a type of restraint
device, with views polarised between human rights
campaigners who express concerns about their utility,
their safety, and their encroachment on human rights,
in contrast with (predominantly) law enforcement cam-
paigners who believe they reduce the possible risks of
transmission of infection and subsequent need for pro-
phylaxis by law enforcement professionals so exposed.
Parallels have been drawn to their resemblance to
hoods used in detention settings, as the practice of
hooding has been recognised as a form of torture and/
or cruel, inhuman and degrading treatment or punish-
ment (CID) by a number of international and regional
human rights bodies.
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16 Police custodial healthcare
▪▪ Introduction
▪▪ Principles of care
▪▪ Healthcare in police custody
▪▪ Risk assessment, risk identification and diversion
Introduction
The care of detainees in short-term police custody is a
complex area and important in terms of forensic medi-
cine. The term ‘police custody’ is used here to mean that
time in which an individual is in the care of a police
service investigating an allegation of crime. This time
is generally limited (in England & Wales to 24 hours)
unless judicial permission is given to extend it, or for
certain offences (such as those that are terrorist-related)
where custody time limits may not apply. Longer term
custody (in prison or other detention centres) is not con-
sidered here, although the patient profiles may be simi-
lar. In England & Wales, the Police & Criminal Evidence
Act 1984 (a law that determines how a detainee in police
custody is dealt with and managed) attempts to identify
such risk factors at the earliest opportunity. All those
who are arrested are asked a series of questions about
their health and wellbeing. Such risk assessment tools
are administered by the police officers tasked with
ensuring the care of detainees. Positive responses to any
questions result in the seeking of advice from a health-
care professional (usually a doctor or a nurse). A num-
ber of studies from different countries identify a high
proportion of drug, alcohol and mental health issues, in
addition to the more general physical problems that a
population will have.
Principles of care
The studies show that whilst ‘forensic’ healthcare issues
(drugs, alcohol and mental health) are over-represented
in the police custody patient group – which may change
subject to jurisdiction – the associated chaotic lifestyles
may also result in poor management and compliance
with treatment in what might be termed ‘general’
healthcare issues. Such inadequate or absent treatment
may increase risks of harm to all those detainees with
chronic conditions such as cardiovascular disease,
asthma, diabetes, epilepsy, thromboembolic disorder,
and schizophrenia which have their own increased risks
to an individual’s well-being. Such vulnerabilities and
poor care can result in morbidity and mortality. Deaths
and harm in custody are frequently avoidable but are
▪▪ Deaths and harm in police custody
▪▪ Prevention of death and harm in police custody
▪▪ Bibliography and information sources
▪▪ Further general resources
dependent on an awareness of the police personnel of
the significant risk factors and a high­-quality healthcare
professional team.
Healthcare in police custody
Delivery of healthcare to detainees in police custody var-
ies across the world. Healthcare services in this context
may include general medical services, and also more
forensic and police-related processes such as forensic
sampling of assault suspects and complainants, assess-
ment of drivers suspected of driving under the influence
of drugs and alcohol, documentation and management of
injuries, review of restraint-related injury, determination
of ‘fitness to interview’ and ‘fitness to be charged’. In the
UK, doctors, nurses and paramedics may provide some of
these functions. Irrespective of the reason for assessment
of the detainee the duties of consent and confidentiality
apply, with few exceptions. Any breach of these duties
must be documented and the reasons for such a breach
recorded. Doctors in this setting are referred to as foren-
sic physicians (sometimes forensic medical examiners
or forensic medical officers), nurses as custody nurses
(sometimes custody or forensic nurse practitioners), and
paramedics as custody paramedics (sometimes forensic
paramedics). The term ‘clinical forensic medicine’ (foren-
sic medicine in the living) is used to differentiate it from
forensic pathology. In the UK, the Faculty of Forensic
Legal Medicine of the Royal College of Physicians has
been tasked with, and has established, quality standards
for relevant healthcare professionals and provided guid-
ance for the management of conditions and forensic
assessments required in custody.
Nature of health problems of detainees
In general, health problems in custody may be divided
into ‘forensic healthcare’ issues which may directly
relate to the reason for that person’s arrest and deten-
tion and embraces mental health, drug and alcohol
problems, and ‘general’ healthcare issues (e.g., diabe-
tes, asthma, epilepsy) that are not related to the reason
for arrest but which may require management whilst in
custody. Additionally, specific harm or injury related to
218 Police custodial healthcare
Table 16.1 Typical profile and health issues of those in
police custody in UK*
• ~85% male
• Mean age was ~34 years
• 29% English not first language
• ~14% no fixed abode
• ~30% not registered with primary care physician
• ~7% previously detained under the Mental Health
Act 1983
• ~17% had previously self-injured
• ~34% dependent on heroin
• ~34% dependent on crack cocaine
• ~25% dependent on alcohol
• ~17% dependent on benzodiazepines
* Adapted from Payne-James JJ, Green PG, Green N, et al.
Healthcare issues of detainees in police custody in
London, UK. J Forensic Leg Med 2010;Jan;​17(1):​11–17.
specific methods of restraint may be sustained as dis-
cussed in the previous chapter. There are many studies
that identify the unique and extensive vulnerabilities
of this patient group. Table 16.1 illustrates some typical
findings for detainees in police custody. With ageing
populations, it is likely that chronic medical conditions
and mental health issues such as dementia will have
increasing relevance in these populations.
Alcohol and all illicit (and some licit) drugs may
present as some form of intoxication. The clinical skill
of the healthcare professional is required to determine
whether the current (or future) degree of intoxica-
tion presents a risk to that individual whilst in, or after
release from, police custody. The main risk is one of car-
diorespiratory arrest. Alcohol and some drugs (notably
heroin and benzodiazepines) all present potential risks
from withdrawal. Alcohol, in particular, poses a risk of
death from alcohol withdrawal syndrome. Figure 16.1a
and b show scoring systems that identify the degree of
withdrawal from respective substances and indicate
when intervention is required.
In one study ∼55% police detainees had active medi-
cal conditions, 7% of whom were prescribed medication
for those medical conditions but only 4% had access to
the medication, and of those, 40% were not taking their
medication regularly and many were not taking it at all.
A wide range of diseases, including asthma, epilepsy,
diabetes, deep vein thrombosis, pulmonary embolism,
hepatitis, and hypertension, and poor concordance with
medication, can all increase the risk of death and harm
to those in custody. It has also been shown that sev-
eral other health-risk measures, including body mass
index, smoking and healthcare use were worse for police
detainees when compared with the general population.
Finally, those who have been restrained by police or
others, may have been harmed and may die in custody.
There is a paucity of medical data on the outcome of the
use of restraint and control techniques. Deaths or inju-
ries inflicted using any restraint technique or weapon
always result in much public scrutiny, and systems for
recording the use, and adverse outcomes, of such tech-
niques are needed to inform the public and medical
professionals.
Because those exposed to restraint techniques –
but not arrested – may be reluctant to identify them-
selves, it is possible that exposure to these and others
forms of control and restraint cause more harm than is
documented. The use of assorted tear gas bombs and
other compounds, and water-cannon in crowd control,
also needs prospective research to identify risk for med-
ical complications. Often more information is available
in the media than in peer-reviewed medical literature.
Risk assessment, risk identification
and diversion
Any individual detained in police custody in England &
Wales will have a risk assessment undertaken as soon
as possible after arrival in police custody. Figure 16.2a
and b shows a typical risk assessment form, the first part
of which comprises direct questioning of the detainee,
and the second the custody officer’s assessment. This
risk assessment should be reviewed throughout the
detainee’s time in custody. The purpose of screening is
to detect issues or risk factors for physical or mental ill-
health at an early stage so that an appropriate health-
care professional’s opinion can be sought. Injuries
should be documented, and any use of force identified,
including the application of handcuffs. One of the aims
of any subsequent healthcare assessment should also be
to identify conditions and brief interventions that may
be appropriate for the detainee’s health and welfare.
This may include screening for addictive behaviours in
police custody and mental health conditions, and refer-
ral to relevant teams.
Often contact is via a single, relatively brief, consul-
tation, but opportunities should be sought to identify
opportunities to intervene, and offer those interven-
tions if available. For identifying alcohol issues, screen-
ing processes such as the Fast Alcohol Screening Test
(FAST) and the Alcohol Use Disorders Identification Test
(AUDIT) may be appropriate.
Deaths and harm in police custody
Death and harm in police custody are consistently
caused in five main ways: alcohol and drug intoxication,
alcohol withdrawal, self-harm, restraint-related injuries
and natural disease. The first three are the most common
preventable causes of harm or death in custody in most
settings and it is essential that appropriate techniques
are used to identify those at risk and to put in place
 Deaths and harm in police custody 219

mechanisms for reducing and avoiding unwanted out-
comes. All countries should collect robust data regard-
ing deaths and harm related to police custody but this is
not currently the case. Any death in state custody should
be investigated independently and thoroughly and any
acts of commission or omission that contributed to the
death should be identified and dealt with appropriately
(which may include regulatory, employment and crimi-
nal courts or tribunals). The Independent Office for
Police Conduct (IOPC) publishes data on deaths related
to police contact in England & Wales. In 2017–2018 in
England & Wales, there were the following number of
fatalities in each category of police related death: 29 road
traffic fatalities; four fatal police shootings; 23 deaths in

(a)

Clinical Opiate Withdrawal Scale (COWS)

Flowsheet for measuring symptoms over a period of time during buprenorphine induction.

For each item, write in the number that best describes the patient’s signs or symptom. Rate on just the apparent relationship to opiate withdrawal.
For example: If heart rate is increased because the patient was jogging just prior to assessment, the increased pulse rate would not add to the score.

Patient Name: Date:

Buprenorphine Induction:
Enter scores at time zero, 30 minutes after first dose, 2 hours after first dose, etc. Times of Observation:
Resting Pulse Rate: Record Beats per Minute
Measured after patient is sitting or lying for one minute
0 = pulse rate 80 or below • 2 = pulse rate 101–120
1 = pulse rate 81–100 • 4 = pulse rate greater than 120
Sweating: Over Past 1/2 Hour not Accounted for by Room Temperature or Patient Activity
0 = no report of chills or flushing • 3 = beads of sweat on brow or face
1 = subjective report of chills or flushing • 4 = sweat streaming off face
2 = flushed or observable moistness on face
Restlessness Observation During Assessment
0 = able to sit still • 3 = frequent shifting or extraneous movements of legs/arms
1 = reports difficulty sitting still, but is able to do so • 5 = Unable to sit still for more than a few seconds
Pupil Size
0 = pupils pinned or normal size for room light • 2 = pupils moderately dilated
1 = pupils possibly larger than normal for room light • 5 = pupils so dilated that only the rim of the iris is visible
Bone or Joint Aches if Patient was Having Pain Previously,
only the Additional Component Attributed to Opiate Withdrawal is Scored
0 = not present • 2 = patient reports severe diffuse aching of joints/muscles
1 = mild diffuse discomfort • 4 = patient is rubbing joints or muscles and is unable to sit still because of discomfort
Runny Nose or Tearing Not Accounted for by Cold Symptoms or Allergies
0 = not present • 2 = nose running or tearing
1 = nasal stuffiness or unusually moist eyes • 4 = nose constantly running or tears streaming down cheeks

GI Upset: Over Last 1/2 Hour

0 = no GI symptoms • 3 = vomiting or diarrhea
1 = stomach cramps • 5 = multiple episodes of diarrhea or vomiting
2 = nausea or loose stool
Tremor Observation of Outstretched Hands
0 = no tremor • 2 = slight tremor observable
1 = tremor can be felt, but not observed • 4 = gross tremor or muscle twitching
Yawning Observation During Assessment
0 = no yawning • 2 = yawning three or more times during assessment
1 = yawning once or twice during assessment • 4 = yawning several times/minute
Anxiety or Irritability
0 = none • 2 = patient obviously irritable/anxious
1 = patient reports increasing irritability or • 4 = patient so irritable or anxious that participation
anxiousness in the assessment is difficult
Gooseflesh Skin
0 = skin is smooth • 5 = prominent piloerection
3 = piloerection of skin can be felt or hairs standing up on arms
Score: 5–12 = Mild
Total score
13–24 = Moderate
25–36 = Moderately Severe
Observer’s initials
More than 36 = Severe Withdrawal

Figure 16.1 (a) Clinical Opiate Withdrawal Scale.  (Continued)

220 Police custodial healthcare

(b)

Figure 16.1 (Continued) (b) Assessment of alcohol withdrawal. (Reproduced from Sullivan JT et al. Assessment of
alcohol withdrawal: the revised Clinical Institute Withdrawal Assessment for alcohol scale [CIWA-Ar]. Br J Addict
1989;84:1353–1357.)
 Deaths and harm in police custody 221

(a)

Figure 16.2 Example Risk Assessment Proforma for Detainees in Police Custody.
(Continued)
222 Police custodial healthcare
Figure 16.2 (Continued) Example Risk Assessment Proforma for Detainees in Police Custody.
(Continued)
or following police custody; 57 apparent suicides follow-
ing police custody; and 170 other deaths following police
contact that were independently investigated. Figure
16.3 illustrates the number of fatalities following deaths
in police custody and following police contact from
2004 to 2018 in England & Wales. Figure 16.4 shows the
primary cause of death in custody – England & Wales –
1998/9 to 2008/9.
Work has been done worldwide by those involved in
healthcare in custody settings to look at the nature and
causes of deaths in custody and there are similarities
between many of these studies, irrespective of juris-
diction. Sometimes the studies focus on all deaths in
custody (e.g., in police custody, prison custody, secure
mental health units) and others solely on police settings.
Detainees may be arrested for drink/drug driving
offences after road traffic collisions (RTCs) and are taken
to a police station. It is crucial that proper medical assess-
ment is undertaken of such individuals, being aware of
all the factors of any collision (e.g., type of impact, use
of seat belts, deployment of airbags, whether extraction
of the detainee was required, what the speed at impact
was, etc.) so that serious underlying injury is not missed
whilst the police procedures are being undertaken. This
ensures that risk factors over and above the use of alco-
hol and/or drugs are taken into account, and in particu-
lar the risk that substance misuse is masking significant
clinical conditions; a full clinical examination remains
essential. Particular attention should be paid to drink-
drivers who have refused, or were not able to complete,
a breath alcohol measurement. Missing a serious injury
can result in a fatal outcome. This principle, however,
is a key issue in care and requires not only an initial
awareness, but the need for appropriate monitoring
(e.g., rousing to ensure there has been no deterioration
in conscious level) so that treatable, potentially fatal
injuries are not missed. Failure to recognise high-risk
patients remains a common problem, in particular for
healthcare professionals who have little experience in
custodial medicine, and deaths or harm outcomes that
could have been avoided may result in severe penalties
to those who have failed in their duties. Complaints
about healthcare professionals to their respective regu-
latory bodies appear to be increasing.
Specific issues may arise which require an aware-
ness of local trends and behaviours. Often these relate
to drug use (either due to the nature of the drug taken
or the means by which it was administered). Anthrax
(caused by Bacillus anthracis) is rare in the UK but was
identified in injecting drugs misusers. Ultra-potent
opioids (e.g., fentanyl and carfentanil) are now widely
available, and detainees (and police and healthcare
professionals caring for them) may be at risk of expo-
sure to these potent narcotics necessitating guidance
for scene safety and force protection from medical
directors. The availability of novel psychoactive sub-
stances (NPS) with many different modes of action and
clinical effects often makes assessment difficult. Rare
medical conditions may also be responsible for deaths
in police custody.

(b)
Figure 16.2 (Continued) Example Risk Assessment Proforma for Detainees in Police Custody.
Cruel, inhuman and degrading
­treatment and torture
The healthcare professional working in custodial set-
tings should be aware that this is often an opportunity
to identify and assist those who have – either during the
current period of detention, or previously – been subject
Deaths and harm in police custody 223
to cruel, inhuman and degrading treatment or torture.
Such issues may be disclosed by the detainee, or may be
established during the clinical assessment. Often those
who have fled oppressive regimes may come into con-
tact with criminal justice or immigration systems. The
healthcare professional should always be in a position
to ask appropriate questions and refer to appropriate
224 Police custodial healthcare

Deaths in or following police custody

40
35
30
25
20
15
10
5
0
20 5

20 6

20 7

20 8

20 9

20 0

20 1

20 2

20 13

20 4

20 5

20 6

8
/0

/0

/0

/0

/0

/1

/1

/1

/1

/1

/1

/1

/1
/
04

05

06

07

08

09

10

11

12

13

14

15

16

17
20

20
Figure 16.3 Total number of deaths in police custody or following police custody in the UK from 2004 to 2018.

agencies or personnel if such issues are identified. The
Istanbul Protocol (described in Chapter 8) provides the
means to ensure that such allegations can be properly
investigated. Appropriate enquiry or awareness may
identify individuals who have been trafficked or sub-
ject to forced marriage or female genital mutilation
(FGM – described in Chapter 17). The relevance of such
issues will be dependent on the jurisdiction in which the
healthcare professional is working.
Excited delirium syndrome
Unexpected deaths periodically occur in individuals
held in police custody. These decedents have usually
had significant physical exertion associated with vio-
lent and/or bizarre behaviour, have been restrained by
the police, and often have drug intoxication. An autopsy
in such cases may not provide a satisfactory explana-
tion for the cause of death, and these deaths may then

35

30

25
Percentage

20

15

10

0
nt ed
e

siv sc te /

ed

ia

ow ty
s

de

or Al ntio ior

n
ay tat d/
lu na ela nd
se

r
os

io

kn ali
he
rw t s ne

te in
at
ici

te pr
dr o n

ob ed

n
e e d

n
au

ct
rd

nc U s r l a

er

un on
io
de ta

Ot
el
Ai /no rtai
Su

ru
de ed
lc

ve

th
ug ho

tr

g sus

i
st

nt
ra

to iv

po
lo

in

te
e
tu

rin es
ra
ta

Hy
ec

in
Na

st
en

du juri
sr

Re

se
cid

rie

In

do
Ac

ju

er
In

Ov
co
in

Figure 16.4 Primary cause of death in custody in England & Wales from 1998/9 to 2008/9. (Adapted from the
Independent Police Complaints Commission. Death in or following police custody: an examination of the cases 1998/99–
2008/09. IPCC, London, 2010.)

be attributed to the excited delirium syndrome (ExDS),
or an ‘acute behavioural disturbance’. The pathogen-
esis of excited delirium syndrome/acute behavioural
disturbance-associated deaths is likely to be multifac-
torial and includes a variety of factors such as positional
asphyxia, hyperthermia, drug toxicity, and/or catechol-
amine-induced fatal arrhythmias.
Generally, the forensic medical community has clas-
sified patients who presented with altered sensorium and
aggressive agitated behaviour, and a combination of other
symptoms including ‘superhuman’ strength, diaphore-
sis, hyperthermia, propensity to break glass, attraction
to light or lack of willingness to yield to overwhelm-
ing force, who then died with a positive drug screen for
sympathomimetic agent, and no other anatomical cause
of death, as an ‘Excited Delirium’ (or acute behavioural
disturbance-associated) death. In recent years, it has
become increasingly clear that many patients with this
constellation of symptoms and signs have been man-
aged in emergency departments for decades and in only
a minority of cases is the outcome fatal. Law enforcement
and emergency medical services (EMS) in the USA have
many years of experience of dealing with ExDS patients.
Individuals with ExDS (or acute behavioural disturbance)
most frequently come to the attention of police, forensic
physicians and emergency departments because of the
associated violent, agitated, and erratic behaviour. These
out-of-hospital ExDS (or acute behavioural disturbance)
subjects have traditionally been transported to custody
and survived, transported to the hospital and survived,
or have a sudden cardiac arrest with death ensuing. If
death occurs, a forensic autopsy is required. When the
outcome is fatal, forensic pathologists may, in the absence
of other apparent causes of death, typically rule that death
is a consequence of excited delirium, although the use of
this diagnostic ‘label’ is not currently preferred in the UK.
Instead, a ‘narrative’ style cause of death is given, iden-
tifying those factors thought to be most important. The
concept of excited delirium remains controversial, but has
become a matter of increasing concern for forensic and
emergency physicians and other primary care health pro-
fessionals as many work with policing agencies respon-
sible for the policy and procedures used in the field.
Forensic physicians and healthcare practitioners who
encounter such individuals are generally supportive of
this diagnosis as a means to identify the at-risk patient.
The key practical element in care of the detained
(or about to be detained) individual is to differentiate
between an aggressive individual who is trying to avoid
arrest, and an individual with ExDS (or an acute behav-
ioural disturbance). Such an individual represents a
medical emergency and requires immediate trans-
port to a medical facility with full resuscitation and life
support capability. A Special Panel Review of Excited
Delirium produced a simple ‘aide memoire’ to assist
in making this crucial diagnosis (Figure 16.5). The UK
Prevention of death and harm in police custody 225
Faculty of Forensic and Legal Medicine and the Royal
College of Emergency Medicine have produced guide-
lines on management in police custody of acute behav-
ioural disturbance.
Prevention of death and harm in
police custody
Any episode of death or harm in police custody is a trag-
edy. It is a tragedy for families of the deceased, but it can
also be hugely disruptive and traumatic for any of those
who have been involved in the arrest, care and health-
care assessment of that person. Adequate training of
law-enforcement personnel in relation to restraint plays
a vital role in preventing deaths in custody. Concepts
such as ExDS (or acute behavioural disturbance),
and the potential dangers of vascular restraint holds,
assist officers in making appropriate restraint deci-
sions. Understanding the broad principles of positional
asphyxia, such as how some positions and some indi-
viduals are more prone to respiratory compromise, and
that kneeling on someone’s back may increase the risk of
death, means that some potentially fatal situations are
avoided. Such training in ‘use of force’ tactics needs to
include an understanding of the effects, and complica-
tions, of less-lethal weapons and personal protection
systems including batons, irritant sprays and conducted
energy devices. Different means of providing healthcare
for detainees exist across the world. Some are compa-
rable (or aim to be comparable) to healthcare for the
non-detainee (e.g., UK, France, Netherlands) whilst
others have lower, or less consistent, standards of pro-
viding healthcare for detainees. The standards of the
healthcare professionals are key, as certain skills may
be needed in general medical problems, but with a great
emphasis on mental health and substance misuse. All
countries should have minimum standards of training
and qualification for healthcare professionals working
with detainees in police custody. Over recent years sub-
stantial advances have been made in setting standards
for short-term custodial healthcare in a variety of ways
in different countries. It is essential that any practitioner
has knowledge of, and is trained in, aspects of mental
health, drug and alcohol misuse, medical law and eth-
ics, forensic sampling and police process in addition to
basic training. Police or law-enforcement officers tasked
with the care of detainees must also have training in
order to identify those patients at risk. Non-medical
factors, such as the use of CCTV to monitor those iden-
tified as being at risk of self-harm, and the availability
of ligature knives, should an individual gain access to a
ligature, are common-sense ideas that should be widely
disseminated (see Figure 16.6). Life signs monitoring
devices are available for use in police cells but are not
substitutes for appropriate staffing with appropriately
trained and qualified healthcare professionals. Training
226 Police custodial healthcare

Figure 16.5 Excited delirium syndrome pocket card (front and back) for law enforcement and EMS providers created
by the work of the National Institute of Justice Technology Working Group (TWG) on Less-Lethal Devices (Reproduced
by permission of NIJ).

(a) (b)

(c) Figure 16.6 (a) A custody suite with CCTV monitoring facilities.
(b) Suspension point in a cell where detainee had torn a strip of
a blanket and attached it to a lighting frame. (c) A ligature knife:
this should be in the possession of all gaolers or detention officers
responsible for prisoners, so that they can immediately respond to
and deal with incidents of self-hanging or ligature application.

of all those who come into contact with or are respon-
sible for, the care of detainees in basic or immediate life
support or cardiopulmonary resuscitation should be
compulsory. Continuous professional development and
update training is essential so that lessons learnt can
be applied to day-to-day practice, in order to maximise
recognition of healthcare issues and minimise the risks
of death or harm as an outcome.
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Torture and Ill-treatment: A Practical Approach to Prevention and
Documentation. Boca Raton: CRC Press, 2017.
Payne-James JJ, Green PG, Green N, et al. Healthcare issues of
detainees in police custody in London, UK. J Forensic Leg Med
2010;17(1):11–17.
Payne-James JJ, Rivers E, Green P, Johnston A. Trends in less-lethal
use of force techniques by police services within England and
Wales: 2007–2011. Forensic Sci Med Pathol 2014;10(1):50–5.
Payne-James JJ, Smith G, Rivers E, et al. Effects of incapacitant
spray deployed in the restraint and arrest of detainees in the
Metropolitan Police Service area, London, UK: a prospective
study. Forensic Sci Med Pathol 2014;​10(1):62–8.
Payne-James JJ, Stark MM, Butler B, Seymour C. So you want a
career in forensic and legal medicine? Br J Hosp Med (Lond).
2018;79(3):C38–C41.
Rekrut-Lapa T, Lapa A. Health needs of detainees in police cus-
tody in England and Wales; literature review. J Forensic Leg
Med 2014;27:69–75.
Sondhi A, Williams E. Health needs and co-morbidity among
detainees in contact with healthcare professionals within
police custody across the London Metropolitan Police
Service area. J Forensic Leg Med 2018;57:96–100.
Southall P, Grant J, Fowler D. Police custody deaths in Maryland, USA:
an examination of 45 cases. J Forensic Leg Med 2008;15:227–230.
Stark MM, Payne-James JJ. Provision of clinical forensic medical
services in Australia: a qualitative survey 2011/12. J Forensic
Leg Med 2014;21:31–7.
Stark MM, Payne-James JJ. People can die from opiate with-
drawal. Med Sci Law 2017;57(2):103.
Sturgiss EA, Parekh V. The work forensic physicians with police
detainees in the Canberra City Watchhouse. J Forensic Leg
Med 2011;18:57–61.
Ünal V, Özgün Ünal E, Çetinkaya Z, İmalı M, et al. Custody and
prison deaths autopsied in Istanbul between 2010 and 2012.
J Forensic Leg Med 2016;39:16–21.
Vilke G, Payne-James JJ, Karch SB. Excited Delirium Syndrome:
redefining an old diagnosis. J Forensic Leg Med 2012;19:7–11.
Vilke GM, Payne-James JJ. Excited Delirium syndrome: aetiology,
identification and treatment. In: Gall JAM, Payne-James JJ (eds).
Current Practice in Forensic Medicine, Vol 2. Chichester: Wiley, 2016,
97–114.
Further general resources
Faculty of Forensic & Legal Medicine. Resources https://fflm.
ac.uk/resources/publications/ (Accessed 13 August 2019).
Payne-James JJ, Byard RW. Encyclopedia of Forensic and Legal
Medicine, 2nd ed. Oxford: Elsevier, 2016.
Payne-James JJ, Beynon J, Nuno Vieira D. Monitoring Detention,
Custody, Torture and Ill-treatment. A Practical Approach to
Prevention and Documentation. Boca Raton: CRC Press, 2017.
Stark MM, Payne-James JJ, Scott-Ham M. Symptoms and Signs of
Substance Misuse, 3rd Ed. Boca Raton: CRC Press, 2014.
17 Sexual assault, genitoanal
injury and female genital
mutilation
▪▪ Introduction
▪▪ Examination requirements
▪▪ Definitions and the law
▪▪ Intimate partner violence
▪▪ Medical assessment
▪▪ Evidential samples and documentation of findings
Introduction
Adults and children, of any sex (and by whichever
gender they may identify themselves) may all be com-
plainants of sexual assault, but the incidence may
vary, including by geographical location and cultural
background. In many studies a significant propor-
tion of the population may have been subject to sex-
ual assault (which may include sexualised touching,
attempted penetration [oral, anal, vaginal, other], or
completed penetration). It is important to understand
that all groups may be subject to sexual assault. One
study showed that compared to cisgender (i.e., non-
transgender) men, cisgender women and transgender
people had higher odds of sexual assault. Among cis-
gender people, gays/lesbians had higher odds of sexual
assault than heterosexuals for men but not for women.
People unsure of their sexual identity had higher odds
of sexual assault than heterosexuals, but effects were
larger among cisgender men than cisgender women.
Bisexuals had higher odds of sexual assault than het-
erosexuals with similar magnitude among cisgender
men. Sexual assault occurs within families, or may
be by strangers, and may be associated with crimes
against humanity, war crimes and genocide. The 2017
data regarding sexual offences in England & Wales esti-
mated that 20% of women, and 4% of men, have expe-
rienced some type of sexual assault since the age of 16
years, equivalent to an estimated 3.4 million female
victims and 631,000 male victims. An estimated 3.1% of
women (510,000) and 0.8% of men (138,000) aged 16 to
59 years experienced sexual assault in the year ending
March 2017. The data showed that around 5 in 6 victims
(83%) did not report their experiences to the police.
The increase in sexual offences recorded by the police
is thought to be driven by improvements in recording
practices and a greater willingness of victims to come
forward to report such crimes, including non-recent
victims.
▪▪ Medical findings after sexual contact
▪▪ Care after sexual assault
▪▪ Female genital mutilation
▪▪ Bibliography and information sources
▪▪ Further general resources
Examination requirements
It is important the complainants of sexual assault are
examined by those who are trained and competent in
sexual offences medicine. They are often forensic phy-
sicians but may come from many other backgrounds
include genitourinary medicine, gynaecology, and
primary care. Their role is to provide independent,
unbiassed evidence to courts, but also to manage the
medical aspects of any assault and provide support
in the future. Complainants (and suspects of sexual
assault) should be offered, where possible, the choice of
a doctor of their own sex/gender. Sexual Assault Referral
Centres (SARCs) – specialist centres for assessment of
complainants of rape and other forms of sexual assault
– have been established in most countries to provide an
effective and sensitive setting to optimise the identifica-
tion and recovery of evidence. They provide appropriate
assessment and sampling following the initial assault,
and post-assault care with regard to issues such as gen-
itourinary health, contraception, prophylaxis against
acquired infections and counselling. Emergency con-
traception may involve use of the oral contraceptive or
insertion of an intrauterine device. Prevention of sexu-
ally transmitted infection, for which there is a huge
range of potential risk, will require appropriate pre-
scribed medication for which standard prophylactic/
therapeutic regimens will apply. These regimens change
from time to time, and it is important that the most up to
date information is utilised. Human immunodeficiency
virus (HIV) and hepatitis B infection in particular are
of great concern to patients and specialist advice must
be sought regarding post-exposure prophylaxis. Risks
of infection are dependent on many additional factors
including multiple assailants, associated injury, intra-
venous (IV) drug use, and high prevalence areas for cer-
tain infections.
Most SARCs now aim to provide complainants who
do not wish to involve the authorities immediately an
230 Sexual assault, genitoanal injury and female genital mutilation
anonymised assessment and collection of samples, so
that a complainant may later proceed with police inves-
tigation if they change their mind.
Definitions and the law
Each jurisdiction has its own laws or statutes relating to
sexual assault. In England & Wales, the Sexual Offences
Act 2003 applies. Key definitions and offences from this
Act are listed in Box 17.1. The Act defines numerous other
specific offences including, for e­ xample, ‘rape and other
offences against a child under 13’.
Intimate partner violence
A significant proportion of women experience physical
and/or sexual violence from partners.
The World Health Organisation stated that between
10% and 69% of women globally reported being physi-
cally assaulted by an intimate partner during their
lifetime, and most women who are targets of physical
aggression generally experience multiple acts of aggres-
sion over time.
In the UK, factors associated with a man’s risk for
abusing his partner are:
• Individual factors: young age, heavy drinking,
depression, personality disorders, low academic
achievement, low income, and witnessing/expe-
riencing violence as a child.
Box 17.1 Key elements of offences under the Sexual Offences Act 2003
(England & Wales)
Section 1: Definition of the act of ‘rape’
A person (A) commits an offence [of rape] if:
• He intentionally penetrates the vagina, anus or
mouth of another person (B) with his penis
• (B) does not consent to the penetration, and
• (A) does not reasonably believe that (B) consents.
• A person found guilty of rape under this section
is liable, on conviction on indictment, to imprison-
ment for life.
Section 2: Definition of the offence of ‘assault
by penetration’
A person (A) commits an offence if:
• He intentionally penetrates the vagina or anus of
another person (B) with a part of his body or any-
thing else
• The penetration is sexual
• (B) does not consent to the penetration and
• Relationship factors: marital conflict/instability,
male dominance in the family, economic stress,
and poor family functioning.
• Community factors: weak community sanctions
against domestic violence, poverty, and low social
capital.
• Societal factors: traditional gender norms, and
social norms supportive of violence.
Medical assessment
The purpose of a medical assessments for complainants
and suspects of sexual assault is to identify and collect
evidence that may assist the courts to establish the facts
of the case and to identify and treat injury or other risk
issues (e.g., infection). Appropriate consent must be
sought. Figure 17.1 shows a sample consent form.
The medical needs should always take priority over
the evidential needs. The medical and scientific evi-
dence may help confirm, or corroborate, the account
of either the complainant or suspect. In many cases the
medical evidence is neutral with regard to contrasting
accounts given, and the determination of the facts in
the case (e.g., was there valid consent, was there penile
penetration of the vagina?) is a matter for the court.
To avoid cross-contamination, different examiners
should assess the complainant and suspect from the
same incident, in separate facilities. Disposable barrier
clothing should be worn to minimise the risk of con-
tamination. Appropriate cleaning of the area/facility
• (A) does not reasonably believe that (B) consents.
• A person guilty of an offence under this section is
liable, on conviction on indictment, to imprison-
ment for life.
Section 3: Definition of ‘sexual assault’
A person (A) commits an offence if:
• He intentionally touches another person (B)
• The touching is sexual
• (B) does not consent to the touching and
• (A) does not reasonably believe that (B) consents.
A person guilty of an offence under this section is liable:
a. On summary conviction, to imprisonment for a
term not exceeding 6 months or a fine not exceed-
ing the statutory maximum, or both
b. On conviction or indictment, to imprisonment for
a term not exceeding 10 years.
 Medical assessment 231

Name of Complainant Date

8. Consent to History, Examination and Report

I, _____________________________________________ consent to a forensic examination, as explained to

me by _____________________________________________________________________________________

I understand that the forensic examination will include (delete if not applicable)

a) A full medical history and complete examination;

b) Collection of forensic and/or medical specimens;

c) Taking of notes, photographs/videos/digital images for recording and evidential purposes (including
second opinions from medical experts and peer review). I have been told that any sensitive photographs,
videos and/or digital images will be stored securely and only be made available to other non-medical
persons on the order of a judge;

d) I understand and agree that the doctor/nurse may provide a statement/report for the police;

e) I understand and agree that a copy of the medical notes may be given to professionals involved in the
case (eg police or lawyers) and may be used in a court;

f) I agree to the use of my anonymised photographs/videos/digital images/medical notes for teaching;

g) I agree to the use of my anonymised photographs/videos/digital images/medical notes for audit and
research;

h) I have been advised that I may halt the examination at any time.

Signed _______________________________________ Date ___________________________________

If verbal consent Signature & Name of Witness ________________________________________

________________________________________

Figure 17.1 Consent to history, examination and report. (From the Faculty of Forensic & Legal Medicine pro forma
for adult female and male forensic sexual assault examination. [https://fflm.ac.uk/wp-content/uploads/2014/04/
Proforma-for-ADULT-female-and-male-forensic-sexual-assault-examination-JULY-2010.pdf].)

and equipment to be used for the examination should
be carried out using suitable cleaning agents, pre- and
post-­examination.
In some cases, the need for urgent medical care
because of injury overrides the immediate need for a
sexual assault examination. Healthcare aspects have
priority. Wherever possible, examinations should be
undertaken at the earliest opportunity in order to ensure
best opportunities for evidential sampling. For example,
if an examination under anaesthetic for vaginal or anal
injuries is necessary, the sexual offence examiner or
forensic physician should be present at that examina-
tion with the treating doctors to take relevant samples.
The sexual offence examiner must explain the
nature, purpose and process of the assessment, in order
that consent is fully informed and that chaperones
are used when appropriate. An assessment for sexual
assault requires a detailed history and examination. The
232 Sexual assault, genitoanal injury and female genital mutilation
history of the alleged assault from the complainant is an
extremely important part of the assessment, as it assists
in ensuring the best opportunities for evidence recovery.
For example, apart from genito-anal assault or penetra-
tion, sites where there has been licking, kissing or biting
may allow DNA recovery. The examiner should ensure
that they record the briefing details from the referring
police team, and then compare those details with the
account of the complainant themselves confirming or
amending it as necessary. Discrepancies may become
very significant at a later stage of any legal proceed-
ings. Apart from a general medical history, detail of the
full history of events and any specific physical contacts
must be identified (e.g., penis to mouth, mouth to geni-
talia, penis to anus, penis to vulva/vagina, ejaculation,
object/implement penetration of mouth/vulva/vagina/
anus, kissing/licking/biting/sucking/spitting). Recent
drug and alcohol intake must be recorded in as much
detail as possible, and this may be relevant in terms of
ability to recall events appropriately or if there is a pos-
sibility of drugs or alcohol having been administered in
possible cases of drug-facilitated sexual assault. Specific
questions are also asked about events after the assault
as these may affect subsequent findings or recovery of
evidence. Such questions include ‘Since the assault have
you… noted pain… noted bleeding… brushed teeth…
passed urine… defaecated… douched?’ A full medical
history must include past medical history, past surgical
history, past gynaecological history, menstrual history
and past psychiatric history so that, if necessary, any
influence of these on examination findings can be con-
sidered. Previous sexual history should not generally be
relevant, but it is important to enquire sensitively about
recent sexual activity before the alleged assault and
sexual activity after the assault. The appropriateness
of the need for this information is still subject to some
debate. Based on this history, an appropriate examina-
tion can be undertaken to collect appropriate evidential
samples. Figure 17.2a–d shows the specifics of informa-
tion that should be sought from the complainant.
The nature of the examination of the adult in sexual
assault cases is determined in part by the history elic-
ited, in that certain points may direct an examiner to
areas of particular interest. The following should always
be documented: weight, height (and Body Mass Index),
general appearance, skin abnormalities of changes (e.g.,
scars, tattoos, piercing) and appearance of the hair (e.g.,
dyed, shaved).
A standard general physical examination will be car-
ried out and a detailed physical, external examination
which identifies injury or abnormality. The absence of
injury and abnormality is also recorded. This examina-
tion will be documented on body diagrams and images
of abnormalities should be taken. The external exami-
nation will focus on those areas likely to have been in
physical contact with an alleged assailant and which
might yield trace evidence including the DNA of that
alleged assailant.
The genito-anal examination may be undertaken
by naked eye or, depending on the available facilities,
with the assistance of specialist lighting, magnification
or colposcopes. Examination of a female complainant
(dependent in part on the history) will record the pres-
ence of any abnormalities or the absence of any findings
in the following anatomical sites: thighs, buttocks and
perineum; pubic area; pubic hair; labia majora; labia
minora; clitoris; posterior fourchette; fossa navicularis;
vestibule; hymen; urethral opening; vagina and cervix.
For the male (suspect or complainant) the buttocks,
thighs, perineum, anus, perianal area, testes, scrotum
and penis (including shaft, glans and coronal sulcus)
will be examined.
Evidential samples and
documentation of findings
Appropriate samples in sexual assault will assist in
determining the nature of sexual contact, the gender
and possibly identity of the assailant and possible links
with other offences. Samples that may be required
include buccal swabs (for DNA), blood (for drugs and
alcohol), urine, hair (head and pubic), nails and swab
samples from body orifices, mouth, ears, nose and geni-
talia, including vulva, vagina, cervix, penis, anal canal
and rectum. Appropriate sample kits, assembled with
appropriate quality control, for particular areas of the
body should be used wherever possible (Figure 17.3)
Sampling must conform to agreed protocols and a clear
chain of custody established. The Faculty of Forensic &
Legal Medicine provides guidance as to sampling and
an example of guidance for some samples is shown
in Figure 17.4. This guidance is updated regularly and
as with all published guidance, practitioners should
ensure that they are using the most recent version.
Table 17.1 summarises the type of sample and what
may be achieved from analysis of such a sample. In all
cases if uncertain, confirm with forensic science labo-
ratories (1) the type of specimen required and (2) how
it should be stored to ensure optimum preservation.
Samples should be taken in the light of the known his-
tory and accounts of events. If there is any doubt whether
a particular sample may be relevant it is better to take
a sample and retain it for later analysis. In the case of
a suspect the doctor should advise the police investiga-
tors regarding samples as legal requirements will need
to be observed in order to appropriately request samples.
Control swabs may be required, depending on local lab-
oratory protocols and standard operating procedures.
The persistence of evidentially relevant materials is
variable and advice should be sought from a forensic
scientist or forensic toxicologist if uncertain whether
it is appropriate to take a sample. In general, foreign
 Evidential samples and documentation of findings 233

(a)

12. Details of the Assault from Complainant

Asked to direct forensic sampling and determine risk of STIs and pregnancy (see Medical Aftercare)

Confirmation / additions from complainant (verbatim & recorded contemporaneously) _____________________

___________________________________________________________________________________________

___________________________________________________________________________________________

Kissing/licking/biting/ (details, including sites)

NOT KNOWN / NO / YES
sucking/spitting?

Mouth to (details)
NOT KNOWN / NO / YES
genitalia/anus?

Digit to (details)
NOT KNOWN / NO / YES
vulva/vagina/anus?

Penis into (details)

NOT KNOWN / NO / YES
vulva/vagina?

(details)
Penis into mouth? NOT KNOWN / NO / YES

(details)
Penis into anus? NOT KNOWN / NO / YES

(details, including sites)

Ejaculation? NOT KNOWN / NO / YES

Object to (details)
NOT KNOWN / NO / YES
vulva/vagina/anus?

Other sexual/physical (details)

NOT KNOWN / NO / YES
act(s)

(details)
Injuries? NO / YES

(details)
Ano-genital bleeding? NO / YES

(details)
Weapon used? NOT KNOWN / NO / YES

(details)
Damage to clothing? NO / YES

Figure 17.2 (a) Details of Assault from the Complainant. (From the Faculty of Forensic & Legal Medicine pro forma for
adult female and male forensic sexual assault examination [https://fflm.ac.uk/wp-content/uploads/2014/04/Proforma-
for-ADULT-female-and-male-forensic-sexual-assault-examination-JULY-2010.pdf].)
(Continued)
234 Sexual assault, genitoanal injury and female genital mutilation

(b)

13. Details of Assailant(s)

Asked to determine risk of STIs (see Medical Aftercare)

Confirmation / additions from complainant (verbatim & recorded contemporaneously)

___________________________________________________________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

14. Post Assault ask if relevant

Eaten NOT KNOWN/ NO / YES

Drank NOT KNOWN/ NO / YES

Passed urine NOT KNOWN/ NO / YES (note time)

Bowels open NOT KNOWN/ NO / YES

Wiped/ washed NOT KNOWN/ NO / YES (specify site and disposal of eg cloth/tissue)

(specify)
Changed clothes

(sites)
Self harm

Brushed: teeth / gums / dentures

Mouth wash / spray used

Circle:

Washed / bathed / showered / douched

Changed tampon / pad / sponge / diaphragm

Figure 17.2 (Continued) (b) Details of Assailant(s) and Post Assault events. (From the Faculty of Forensic & Legal
Medicine pro forma for adult female and male forensic sexual assault examination [https://fflm.ac.uk/wp-content/
uploads/2014/04/Proforma-for-ADULT-female-and-male-forensic-sexual-assault-examination-JULY-2010.pdf].)
(Continued)
 Evidential samples and documentation of findings 235

(c)

15. Direct Questions ask if relevant

If yes, note if previously experienced

Since assault Details
the problem described

Abdominal pain

Urinary symptoms

eg dysuria, frequency,
haematuria, incontinence, UTI

Genital symptoms

eg soreness, discharge, bleeding,

dyspaerunia, pruritis,injuries

Bowel symptoms

eg soreness, pain on
defaecation, discharge, bleeding,
change in bowel habit,
incontinence, pruritis, injuries

Figure 17.2 (Continued) (c) Direct Questions to be asked of complainant. (From the Faculty of Forensic & Legal
Medicine pro forma for adult female and male forensic sexual assault examination [https://fflm.ac.uk/wp-content/
uploads/2014/04/Proforma-for-ADULT-female-and-male-forensic-sexual-assault-examination-JULY-2010.pdf].)
(Continued)
236 Sexual assault, genitoanal injury and female genital mutilation

(d)

16. Sexual History

(note who was present when taken) Asked to assist with interpretation of forensic evidence and medical aftercare – for the latter the time
frame may need to be extended to ‘since last normal menstrual period’

Dates and times of other relevant sexual activity within the previous 10 days ____________________________

___________________________________________________________________________________________

Items used in previous intercourse

Condom NOT KNOWN / NO / YES Spermicide NOT KNOWN / NO / YES

Lubricant NOT KNOWN / NO / YES Other (specify) ____________________________________

If relevant, clarify types of intercourse in last 10 days only: ____________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

17. Drug and Alcohol Use In Relation To Assault

Was alcohol consumed? NOT KNOWN / NO / YES

If yes, please specify Prior / During / After Offence

Start of drinking __________________________ End of drinking ___________________________

Quantity and type of beverage consumed __________________________________________________

Time last ate ________________________________________________________________________

Have any illicit drugs been used by/administered to the subject within 4 days of the examination?

NOT KNOWN / NO / YES

If yes, please specify Prior / During / After Offence

Give details __________________________________________________________________________

___________________________________________________________________________________________

Are any other substances suspected of having been used by/administered that could be relevant to the offence?

If yes, please specify Prior / During / After Offence

Give details __________________________________________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

If applicable – drugs/alcohol history _____________________________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

___________________________________________________________________________________________

Figure 17.2 (Continued) (d) Sexual History: Drug and Alcohol Use in Relation to Assault. (From the Faculty of Forensic
& Legal Medicine pro forma for adult female and male forensic sexual assault examination [https://fflm.ac.uk/wp-con-
tent/uploads/2014/04/Proforma-for-ADULT-female-and-male-forensic-sexual-assault-examination-JULY-2010.pdf].)

Figure 17.3 Example of pre-packed quality controlled
sample kit. (Courtesy of Jason Payne-James.)
biological fluids (e.g., semen) can be detected in the
mouth up to about 48 hours after contact, in the anus or
rectum up to about 3 days and in the vagina or endocer-
vix up to about 7 days.
As with all forensic assessments, documentation
of genito-anal injuries must be thorough, legible and
meticulous, recording relevant positive and nega-
tive findings. Documentation of findings should be in
written form (ideally using standardised proforma),
with body diagrams accompanying all written notes.
Nowadays, photographic images should be taken of all
abnormalities, with colour bars and scales in all images.
If colposcopy has been used for genito-anal assessment,
photographic or video recordings (e.g., DVD) should,
wherever possible, be used. Most jurisdictions will have
guidelines for the safe custody and viewing of such sen-
sitive images.
Medical findings after sexual
contact
The interpretation of findings after sexual assault,
unlike the assessment and documentation of findings,
should only be undertaken by a practitioner experi-
enced in such assessments and fully aware of current
published medical literature concerning physical find-
ings after sexual assault. It is incorrectly assumed by
many that sexual assaults will always result in injury
to the victim whether adult or child. In the majority of
cases medical abnormalities (in both adults and chil-
dren) will be absent. If present, they may heal within
a few days. Conversely, consensual sexual activity can
result in injury to the body and genitalia. The presence
or absence of injuries in association with allegations of
sexual assault do not by themselves indicate whether
the particular activity was consensual or non-consen-
sual, and it is essential that these facts are understood
when reporting and interpreting findings.
Medical findings after sexual contact 237
Many factors may affect the severity of injury in
sexual assault cases. Similar injuries may be seen in
both consensual and non-consensual sexual contact.
Some of the factors that may influence the possibility
of genital injury are age of the complainant, type of
sexual activity, relative positions of the participants
and degree of intoxication of either or both of the par-
ticipants. Consensual insertion or attempts at insertion
of a finger or fingers, penis or any other object into the
vagina may result in bruises, abrasions and lacerations
of the labia majora, labia minora, hymen and posterior
fourchette. Consensual digital vaginal penetration may
result in accidental fingernail damage or injury to parts
of the female genital tract that may not be noticed at
the time.
Non-genital injury of even a minor nature can often
be very significant evidentially, particularly in the
absence of genital injury, and corroborate accounts of
assault. Marks of blunt contact (e.g., punches, kicks),
restraint (e.g., ties around wrists or ankles, grip marks)
and bite marks are all examples of non-genital inju-
ries seen in sexual assault complainants (Figure 17.5).
Occasionally, false allegations do occur and analysis of
the character and nature of the injury in the light of the
accounts given is crucial in determining whether there
may be any suggestion of deliberate self harm.
Anal penetrative intercourse is part of the normal
sexual repertoire of many couples of all sexual orien-
tations. Consensual anal intercourse can (in the same
way as vaginal sex) be pain and discomfort free and
generally does not leave any residual visible injury.
Non-consensual anal intercourse if done without force,
with or without lubrication and without physical resis-
tance on the part of the person being penetrated may
also leave no residual injury and may be pain free. The
effects of drugs and alcohol may make penetration eas-
ier. The likelihood of pain or injury in non-consensual
anal intercourse may be increased:
• In someone who has not experienced anal inter-
course.
• In the absence of lubrication.
• If force is used.
• If there is great disparity between the size of the
anus (which varies little in the adult) and the penis
(which may vary a lot).
The types of injury include bruises, fissures or tears.
In the absence of repeated trauma, any fissures, tears or
lacerations would be expected to heal within 2 weeks or
so and leave no residual marks. It is important for any
practitioner to be aware of, or to be able to distinguish,
abnormalities caused by medical conditions that may
mimic, or be mimicked by injury after sexual contact.
Common conditions include anal fissure caused by
 238
Sexual assault, genitoanal injury and female genital mutilation

Figure 17.4 Recommendations for the collection of forensic specimens from complainants and suspects, 2019. (From Faculty of Forensic & Legal Medicine.)
 Female genital mutilation 239

Table 17.1 Type of sample taken and what may identified by analysis
Sample type What may be identified by analysis
Blood Presence and amount of alcohol and drugs; identify DNA
Urine Presence and amount of alcohol and drugs
Hair (head), cut and Identify biological fluids (wet and dry); foreign material (e.g., vegetation, glass, paint, fibres);
combed comparison with other hairs found on body; past history of drug use
Hair (pubic), cut and Identify biological fluids (wet and dry); foreign material (e.g., vegetation, glass, fibres);
combed comparison with other hairs found on body; past history of drug use (prescribed; licit and illicit)
Buccal scrape DNA profiling
Skin swabs (at sites of Identify biological fluids (e.g. semen, saliva – wet and dry); cellular material; lubricant
contact) (e.g., KY, Vaseline)
Mouth swabs Identify semen
Mouth rinse Identify semen
Vulval swab Identify biological fluids (e.g., semen, saliva); foreign material (e.g., hairs, vegetation, fibres)
Low vaginal swab Identify body fluids (e.g. semen, saliva); foreign material (e.g., hairs, vegetation, fibres);
identify biological fluids (e.g., semen, saliva); foreign material (e.g., hairs, vegetation, fibres)
High vaginal swab Body fluids (e.g., semen, saliva); foreign material (e.g., hairs, vegetation, glass, fibres); identify
biological fluids (e.g., semen, saliva); foreign material (e.g., hairs, vegetation, fibres)
Endocervical swab Identify biological fluids (e.g., semen)
Penile swabs (shaft, glans, Identify biological fluids (e.g., semen)
coronal sulcus)
Perianal swabs Identify biological fluids (e.g., semen)
Anal swabs Identify biological fluids (e.g., semen)
Rectal swabs Identify biological fluids (e.g., semen)
Fingernail swabs, cuttings Identify foreign material (e.g., skin cells), matching of broken nails
or scraping

constipation, threadworm, poor hygiene and inflam-

matory bowel conditions.
Care after sexual assault
Care of those who have been sexually assaulted is most
appropriately managed in SARCs by those with special-
ist skills or access to others such as genitourinary medi-
cine specialists who can provide the most appropriate
and up to date post-assault treatment and advice. It
should be the responsibility of the examining doctor or
healthcare professional to ensure that appropriate post-
assault prophylaxis against pregnancy, or HIV or other
genitourinary conditions are anticipated. Counselling or
psychological support should also be offered to support
complainants. Proactive support should be offered and
follow-up should be provided so that vulnerable individ-
uals do not have the problems associated with the initial
assault compounded by poor or absent care later.
Female genital mutilation
Female genital mutilation (FGM) includes procedures
that intentionally alter or cause injury to the female gen-
ital organs for non-medical reasons. The World Health
Organisation states that
The procedure has no health benefits for girls and
women. Procedures can cause severe bleeding and
problems urinating, and later cysts, infections, as
well as complications in childbirth and increased risk
of newborn deaths. More than 200 million girls and
women alive today have been cut in 30 countries in
Africa, the Middle East and Asia where FGM is con-
centrated. FGM is mostly carried out on young girls
between infancy and age 15.
FGM is a violation of the human rights of girls and
women. It is known to be harmful to girls and women in
many ways. It is painful and traumatic. FGM can cause
several immediate and long-term health consequences.
240 Sexual assault, genitoanal injury and female genital mutilation
(a)
(b)
Figure 17.5 (a) Fingertip/hand bruising seen on inner
aspect of thigh; (b) Scleral haemorrhages with some
facial petechiae due to strangulation. These both rep-
resent typical extra-genital injuries that may be seen in
cases of sexual assault.
Dependent on the nature of FGM it can cause excessive
bleeding, swelling of genital tissue and problems urinat-
ing, and severe infection that can lead to shock and in
some cases, death, as well as complications in childbirth
and increased risk of perinatal deaths. Communities
that practise FGM report a variety of sociocultural rea-
sons for continuing with it. From a human rights per-
spective, the practice reflects deep-rooted inequality
between the sexes, and constitutes an extreme form of
discrimination against women. FGM is generally car-
ried out on minors and is therefore a violation of the
rights of the child. The practice also violates the rights
to health, security and physical integrity of the person,
the right to be free from torture and cruel, inhuman or
degrading treatment, and the right to life when the pro-
cedure results in death. FGM comprises all procedures
involving partial or total removal of the external female
genitalia or other injury to the female genital organs for
non-medical reasons.
The WHO/UNICEF/UNFPA Joint Statement classi-
fied FGM into four main types. Experience with using
this classification has revealed the need to subdivide
these categories to capture more closely the variety of
procedures. Although the extent of genital tissue cutting
generally increases from Type I to III, there are excep-
tions. Severity and risk are closely related to the ana-
tomical extent of the cutting, including both the type
of FGM performed and the amount of tissue that is cut,
which may vary between the types. Type IV comprises a
variety of practices that do not involve removal of tissue
from the genitals. Though limited research has been car-
ried out on Type IV FGM, in general, these forms appear
to be less associated with harm or risk than the types I, II
and III, that all involve removal of genital tissue.
The Types of FGM are:
Type I: Partial or total removal of the clitoris and/or
the prepuce (clitoridectomy). When it is important to
distinguish between the major variations of Type I muti-
lation, the following subdivisions are proposed:
• Type Ia, removal of the clitoral hood or prepuce
only
• Type Ib, removal of the clitoris with the prepuce
Type II: Partial or total removal of the clitoris and
the labia minora, with or without excision of the labia
majora (excision). When it is important to distinguish
between the major variations that have been docu-
mented, the following subdivisions are proposed:
• Type IIa, removal of the labia minora only
• Type IIb, partial or total removal of the clitoris and
the labia minora
• Type IIc, partial or total removal of the clitoris, the
labia minora and the labia majora
Type III: Narrowing of the vaginal orifice with cre-
ation of a covering seal by cutting and appositioning the
labia minora and/or the labia majora, with or without
excision of the clitoris (infibulation). When it is impor-
tant to distinguish between variations in infibulations,
the following subdivisions are proposed:
• Type IIIa, removal and apposition of the labia
minora
• Type IIIb, removal and apposition of the labia
majora
Type IV: All other harmful procedures to the female
genitalia for non-medical purposes, for example: prick-
ing, piercing, incising, scraping and cauterisation.
In England & Wales, the FGM mandatory reporting
duty is a legal duty provided for in the FGM Act 2003 (as
amended by the Serious Crime Act 2015). The legislation
requires regulated health and social care professionals
and teachers in England & Wales to make a report to the
police where, in the course of their professional duties,
they either: are informed by a girl under 18 that an act
of FGM has been carried out on her; or observe physical
signs which appear to show that an act of FGM has been
carried out on a girl under 18 and they have no reason to
believe that the act was necessary for the girl’s physical
or mental health or for purposes connected with labour
or birth. For the purposes of the duty, the relevant age is
the girl’s age at the time of the disclosure/identification

of FGM (i.e., it does not apply where a woman aged 18
or over discloses she had FGM when she was under 18).
Complying with the duty does not breach any confiden-
tiality requirement or other restriction on disclosure
which might otherwise apply. The duty is a personal duty
which requires the individual professional who becomes
aware of the case to make a report; the responsibility
cannot be transferred. The only exception to this is if the
professional is aware that another individual from the
same profession has already made a report; there is no
requirement to make a second report. The first success-
ful prosecution for FGM was achieved in the UK in 2019.
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18 Safeguarding and protection
of children and vulnerable
adults
▪▪ Introduction
▪▪ Child abuse and neglect
▪▪ Definitions
▪▪ Legislation in England & Wales
▪▪ Safeguarding children and young people
▪▪ Physical abuse
▪▪ Sexual abuse
Introduction
It is now well recognised that children and adults world-
wide can be vulnerable and at risk of neglect or assault,
due to the circumstances in which they find themselves,
and their vulnerability might fluctuate over time as
those circumstances change. Article 19 of the United
Nations Convention on Rights of the Child (UNCRC)
states that:
Children have the right to be protected from being hurt
and mistreated, physically or mentally. Governments
have a duty to ensure that children are properly cared
for and to protect them from violence, abuse and
neglect by their parents or anyone else who looks after
them.
Governments and other agencies seek to protect
children and adults who might be vulnerable through
a process known as ‘safeguarding’ – a concept based
on consent, balancing autonomy with protection from
a risk of harm. Child safeguarding is not defined in
law but has been described as: ‘Arrangements to take
all reasonable measures to ensure that risks of harm to
children’s welfare are minimised.’ The key e­lements are:
• Protecting children from maltreatment.
• Preventing impairment of children’s health or
development.
• Ensuring that children are growing up in circum-
stances in which care is safe and effective.
• Enabling children to have optimum life chances
and to enter adulthood successfully.
‘Child protection’ is the term used to refer to the activ-
ity taken to protect children who are suffering or at risk
of suffering significant harm. Such harm is defined in
England under Section 31 of the Children Act 1989 as: ‘ill
treatment or the impairment of health or development’. To
▪▪ Neglect and emotional abuse
▪▪ Fabricated or induced illness in children
▪▪ Management of child abuse
▪▪ Safeguarding vulnerable adults
▪▪ Elder abuse
▪▪ Bibliography and information sources
▪▪ Further general resources
decide whether harm is significant, the health and devel-
opment of the child is ‘compared with that which could
reasonably be expected of a similar child’. Other jurisdic-
tions will utilise their own definitions and terminology.
Thresholds for determining what constitutes significant
harm will also vary. Safeguarding children and young
people is a responsibility for all of society and in health-
care is an essential element of child health provision. The
roles and responsibilities of those in contact with or treat-
ing children and potentially vulnerable adults, and their
duties of care, are much better defined in many countries
now, with a more proactive approach to intervening at
early stages when concerns about wellbeing are raised.
Recognition of child (and elder) abuse is not a new prob-
lem, and can occur in many forms, and can be interpreted
in various ways in different cultures. Child sexual abuse
may be universally condemned, but use of children as
cheap labour, for example, may not be seen as abuse by
every society or culture.
Child abuse and neglect
Child abuse can result in adverse physical outcomes
(death, injury), psychiatric, psychological and behav-
ioural disorders (persisting into adulthood) may ensue,
together with developmental delay, growth retarda-
tion and failure to thrive. Increased drug and alcohol
misuse and self-injurious behaviour are also observed.
There is also a clear increased risk of children who have
been abused, becoming abusers themselves as adults.
The risk factors for abuse can be classified according to
the children themselves (e.g., behavioural issues, being
adopted), parents (e.g. drug, alcohol or mental health
issues, domestic violence) and environmental and
social factors (e.g., poverty, unemployment, single par-
ent). For many children, multiple predisposing factors
for increased risks of abuse are present.

Definitions
Article 1 of the United Nations Convention on the Rights
of the Child (UNCRC) defined children as persons under
18 years of age. This age limit may be applied variably
in different cultures, and jurisdictions may vary in how
that age limit is applied. The UNCRC places a duty on the
state to promote the wellbeing of all children in its juris-
diction. Article 3 of the Convention states that any deci-
sion or action affecting children, either as individuals
or as a group should be focused on their best interests.
Child abuse can be defined in a number of ways and
many governments have systems in place to ensure that
health professionals recognise that they have an overrid-
ing duty to report concerns if they believe that the child
may be at risk of harm. Some jurisdictions have man-
datory reporting of all suspected child abuse whereas
others may focus on single issues such as female genital
mutilation (FGM). There are advantages and disadvan-
tages to mandatory reporting of child maltreatment and
it remains a matter of substantial debate. Physical abuse
of a child is defined by the World Health Organisation
(WHO) as ‘that which results in actual or potential physi-
cal harm from an interaction or lack of interaction which
is reasonable within the control of a parent or person in a
position of responsibility, power or trust’. In 1962, Henry
Kempe identified ‘the battered child syndrome’. The
term ‘Non-Accidental Injury’ (NAI) generally describes
injury that was considered to be inflicted by another and
by inference as a deliberate assault.
Within the UK, child abuse is classified as physical
abuse, emotional abuse, sexual abuse and neglect. All
can occur concurrently.
Examples of physical abuse include hitting, shak-
ing, throwing, poisoning, burning or scalding, drown-
ing, or when a parent or carer feigns the symptoms of,
or deliberately causes, ill-health to a child whom they
are looking after.
Emotional abuse is the persistent emotional ill-
treatment or neglect of a child such as to cause severe
persistent adverse effects on the child’s emotional devel-
opment. For example, it may involve seeing or hearing
the ill-treatment of another. It may involve serious bul-
lying, causing children frequently to feel frightened or
in danger, or the exploitation or corruption of children.
Emotional abuse to a greater or lesser degree is involved
in all types of ill-treatment of a child, although it may
occur alone.
Sexual abuse involves forcing or enticing a child
or young person to take part in sexual activities. Such
activities may include physical contact, including pen-
etrative or non-penetrative sexual acts; non-contact
activities, such as involving children in looking at, or
being involved in the production of, pornographic mate-
rial or watching sexual activities, or encouraging chil-
dren to behave in sexually inappropriate ways.
Legislation in England & Wales 245
Neglect is the persistent failure to meet a child’s basic
physical or psychological needs, likely to result in the
serious impairment of the child’s health or develop-
ment. It may involve a parent or carer failing to provide
adequate food, shelter and clothing, failing to protect a
child from physical harm or danger, or failing to ensure
access to appropriate medical care or treatment.
Most jurisdictions now have laws, statutes or codes
in place aimed at protecting children and identifying
those children at risk.
Legislation in England & Wales
Legislation in England & Wales provides a structure to
the management of such cases. The Children Acts of
1989 and 2004 set out specific duties: Section 17 of the
Children Act 1989 puts a duty on the local authority to
provide services to children in need in their area, regard-
less of where they are found; Section 47 of the same Act
requires local authorities to undertake enquiries if they
believe a child has suffered or is likely to suffer signifi-
cant harm. The Director of Children’s Services, and Lead
Member for Children’s Services in local authorities, are
the key points of professional and political accountabil-
ity, with responsibility for the effective delivery of these
functions.
The Children Act 1989 identified a number of prin-
ciples including:
• The child’s welfare being the court’s paramount
consideration (‘the paramountcy principle’).
• Parents have prime responsibility for bringing up
children.
• Local authorities should provide supportive ser-
vices to help parents in bringing up children.
• Local authorities should take reasonable steps to
identify children and families in need.
• Every local authority should have a register of chil-
dren in need.
• Sensitivity to ethnic considerations in assessing a
child’s needs and providing services.
The 1989 Act created protection orders for children
‘at-risk’ including:
• Emergency Protection Orders: for which any per-
son may apply to court and then has parental
responsibility for the child.
• Police Protection Provision: by which a police offi-
cer can take a child into police protection without
assuming parental responsibility.
• Child Assessment Orders: which allow proper
assessment of a child up to 7 days.
• Care and Supervision Orders: which allow the
child to be placed in the care of, or under supervi-
sion of, the local authority for up to 8 weeks.
246 Safeguarding and protection of children and vulnerable adults
The Act used the term ‘harm’ to describe the effects
of ill-treatment and poor care leading to injury, impair-
ment of health or development of a child. The term ‘sig-
nificant harm’ was used to determine the severity of the
ill-treatment and is the threshold for compulsory inter-
vention in child protection cases. All police services
within the UK should now have specialist Child Abuse
Investigation Units tasked with investigating suspected
cases of child abuse.
Safeguarding children and young
people
In response to a number of high-profile deaths of chil-
dren, the Children Act 2004 imposed a duty on local
authorities to establish Local Safeguarding Children
Boards, which have overall responsibility for deciding
how relevant organisations work together to safeguard
and promote the welfare of children in their areas.
Where statutory child protection proceedings have
been initiated, then a local authority social care worker
is tasked with taking the lead in supporting and safe-
guarding the child. Serious case reviews are undertaken
when a child dies or is seriously injured, and abuse or
neglect are known or suspected to be factors in the
death. They are carried out under the auspices of Local
Safeguarding Children Boards so that lessons can be
learned locally. Children in care are children who are
‘looked after’ by a local authority under the Children
Act 1989 and Social Services and Wellbeing Act 2014.
The term ‘looked-after children’ is utilised in both stat-
ute and guidelines. Looked-after children are those
that are given accommodation away from their families
at the request of their parent and those in care as the
result of a Care Order. The Looked-after Children ser-
vice is responsible for children who cannot, for what-
ever reason, live with their families. The service aims
Box 18.1 Systematic review of evidence relating to physical child abuse
With increasing health professional, legal and public
expectations that child abuse should operate from
a clear scientific evidence base, The Cardiff Child
PrOtection Systematic REviews project (CORE INFO),
was established in 2002. As the first of its kind world-
wide, it established a robust methodology for system-
atically reviewing the predominantly observational
literature in the field. These 15 systematic reviews are
now held under the umbrella of the Royal College
of Paediatrics & Child Health under the title of Child
Protection Evidence. Drawing on a pool of profession-
als, across all medical disciplines including radiology,
pathology, surgery, paediatrics and dentistry, a panel
to support children living with relatives, family, friends
and foster families, or sometimes, especially for older
young people, in children’s homes and units. The quality
of life of such children is of major concern and should
be assessed. In the UK, the Children’s Commissioner
publishes the ‘Stability Index’ which provides an annual
measure of the stability of the lives of children in care.
Physical abuse
Physical abuse takes many forms. Children are prone to
injury as a result of accident and play and sports, and the
type and site of injury will relate to those factors as well
as their age and mobility. Deciding whether an injury
represents an accident or physical abuse can be chal-
lenging. A number of systematic reviews provide practi-
tioners with a reliable evidence base to assist in making
diagnoses of physical abuse. (See Boxes 18.1–18.6 which
summarise some of these findings.)
The prevalence, number and location of bruising
relates to motor development. Non-abusive bruises tend
to be small, sustained over bony prominences, and found
on the front of the body (Figure 18.1a and b). In children
alleged to have been subject to abuse, bruising is com-
mon. Certain parts of the body are particularly vulner-
able. Significantly more children with physical abuse
had bruises, and had significantly more sites affected.
The odds of a physically abused child having bruising to:
buttocks/genitalia, left ear, cheeks, neck, trunk, front of
thighs and upper arms were significantly greater than
in children where abuse was excluded. Petechiae, lin-
ear or bruises with distinct pattern, bruises in clusters,
additional injuries or a child known to social services for
previous child abuse concerns were significantly more
likely in physical abuse. Figure 18.2 shows areas on the
body where bruises were significantly more likely to
occur in a child with confirmed physical abuse than in
one where physical abuse was excluded.
of trained critical appraisal reviewers was created. The
15 systematic reviews address all aspects of physical
abuse and are predominantly aimed at
• Addressing the recognition of abusive injuries.
• Identifying characteristics that may distinguish
them from unintentional injuries.
• The dating of such injuries.
• Optimal investigation strategies to detect occult
injury.
The systematic reviews are updated as new e
­ vidence
becomes available.

Box 18.2 The main systematic review findings relating to thermal injury in
infants and children
 hanging trends indicate that scalds and non-scald
C samples. Notably, there is no evidence to support
burns are equally common among children now, partly
contributed to by a rise in contact burns due to hair
styling devices, such as hair straighteners.
• High-quality comparative data of scalds suggests
that those due to abuse are more likely to be caused
by hot water (rather than beverages), immersion
rather than pull-over or spill injuries, and to involve
the lower limbs, buttocks or perineum.
• They may also involve the hands and forearms
(‘glove and stocking’ injuries), are usually bilateral
but may involve a single limb. Characteristically,
they will have clear upper margins, and equal
depth of burn, as opposed to accidental injuries
which usually have an irregular margin and typi-
cally involve the deepest burn at initial point of
contact (e.g., hand/arm), becoming more super-
ficial as the cooling liquid travels down the body.
• Co-existent injuries can include fractures, other
cutaneous injuries, prior burns and research sug-
gests these children may show toxicology evi-
dence of exposure to illicit substances on hair
Box 18.3 The main systematic review findings relating to abdominal injuries
in infancy and childhood
• Abusive abdominal injuries are predominantly
blunt trauma (the exception being the insertion
of long embroidery needles into the liver/caecum/
rectum, also described as being inserted into the
brain of infants).
• Solid and hollow organ injuries appear equally
common, but hepatic injury may be underes-
timated due to children’s capacity to compen-
sate for subcapsular haematomas and the lack
of explicit sensitivity and specificity of screening
with liver enzymes.
• Key characteristics distinguishing abusive abdom-
inal injuries is the young age of the patients, with
mean age of 3 years in contrast to the mean age
of unintentional injuries being 7 years, although
abusive duodenal injury may occur throughout
childhood.
• No child less than two years of age has been
described with a duodenal injury from acciden-
tal mechanisms. Both duodenal and pancreatic
Physical abuse 247
the lack of splash marks as an indicator of abusive
scalds, which may be due to newer taps producing
aerated water, where individual droplets are not
sufficiently hot to cause a scald.
• Abusive non-scald burns lack high-quality com-
parative studies, thus precise distinguishing fea-
tures are harder to define. Contact burns are the
most common intentional and unintentional burn,
although children have been subject to caustic,
flame and irradiation burns.
• Characteristics of abusive contact burns include
a clearly demarcated edge, present on the back,
shoulders or buttocks, may be multiple and occur-
ring across the age span. The pattern of the burn
may facilitate matching to the object that was the
source of the heat.
• Identification of burns due to being microwaved
include characteristic sparing of the subcutane-
ous fat beneath burned epidermis and dermis, and
below the fat layer, significantly burned muscle
with no nuclear streaming.
injuries are extremely rare in childhood, predomi-
nantly resulting from high-impact collisions or
crush injury. Duodenal injuries sustained include
intramural haematomas, perforation or transec-
tions, the latter being more common in abuse
than other causes; typically, trauma was between
the 3rd and 4th part of the duodenum.
• The range of pancreatic injuries are similar, with a
high fatality rate among abused children. Further
intrabdominal injuries include hepatic, splenic,
renal, adrenal trauma, or gastric/colonic or blad-
der rupture, or chylous ascites many, but not all,
of whom had associated injuries including rib frac-
tures or head injury.
• It is notable that abdominal bruising was fre-
quently absent, even in the presence of liver tran-
section, the reason for which is postulated to be
that the impact is absorbed by the viscera, thus no
bruise is evident externally.
248 Safeguarding and protection of children and vulnerable adults
Box 18.4 The main systematic review findings relating to infant and childhood
­abusive head trauma (AHT)
• The spectrum of injuries seen in AHT includes
intracranial, cutaneous and possibly cervical liga-
mentous injury.
• There may be associated fractures, such as rib or
metaphyseal, although the presence of skull frac-
tures is more commonly associated with non-abu-
sive head trauma.
• The predominant intracranial association is sub-
dural haemorrhage (SDH), typically multiple, bilat-
eral, and which may be interhemispheric, over the
convexities or in the posterior fossa. SDH may be
accompanied by subarachnoid haemorrhage,
Box 18.5 The main systematic review findings relating to spinal injuries in
infancy and childhood
• Some of the most exciting new research evidence
relates to the pattern of ligamentous cervical
injury seen in association with AHT.
• In the live child, these will only be identified if
magnetic resonance imaging (MRI) includes short
T1 inversion recovery (STIR) sequences, which are
not routinely performed.
• The presence of nuchal, interspinous, posterior
atlanto-axial, posterior atlanto-occipital and cap-
sule ligamentous injury was seen only in infants
with spinal trauma, not in those undergoing spi-
nal imaging for medical reasons, and were sig-
nificantly more common amongst those with AHT
than those with direct trauma to the cervical spine.
• Spinal cord injury per se is rare, although spinal
SDH extending throughout the spine to the lum-
bosacral area is now well recognised in association
Box 18.6 Types of injury in physical abuse
Head injury of all types: the assessment of possible non-
accidental (inflicted) infant head injury (which used
to be called ‘shaken-baby’ syndrome) is an extremely
complex, and controversial area requiring multiprofes-
sional evaluation to determine the relevance of clinical
and radiological findings.
Skin injury: in particular it is important to recognise
possible slap marks, punch marks, grip marks, pinching
and poking marks; certain injuries (e.g., cigarette burns)
are readily identifiable.
although both types of intracranial haemorrhage
are equally likely to be present in non-abusive
head trauma.
• Extradural haemorrhage (EDH) is strongly associ-
ated with non-abusive head trauma.
• With increasing sophistication in neuro-imaging,
it is apparent that hypoxic ischaemic injuries in
association with SDH are strongly associated with
AHT.
• Cerebral oedema and shear injury are also asso-
ciated with AHT, but intra-parenchymal injury is
equally likely in abusive or non-abusive injury.
with posterior fossa SDH. It is not yet clear whether
these are due to tracking of blood through the
subdural space, or are the result of trauma to the
spine itself in association with AHT. Children who
exhibit significant cervical trauma, including frac-
tures or anterolisthesis, tend to be young infants
with co-existent AHT. In contrast, those children
sustaining thoraco-lumbar injuries, including
vertebral compression fractures (often multiple),
dislocations, subluxations or ligamentous injury,
tend to be older, with a mean age of 16 months,
and may present with or without symptoms.
• Co-existent AHT is more common in the youngest
infants, but may still be present in the toddlers,
and rib and limb fractures are also common co-
existent injuries.
Abdominal injury: all intra-abdominal organs can be
damaged by direct impact (e.g., punches or stamps).
Chest injury: squeezing or crushing can result in sub-
stantial injury including rib fractures, ruptured great
vessels and cardiac bruising.
Skeletal injury: a range of injuries may be seen, from
frank fractures, via metaphyseal fracture to subperios-
teal new bone formation.

(a)
(b)
Figure 18.1 (a) Bruises to left lower leg – typical site of
accidental bruising. (b) Bruising and swelling to left outer
eye in a 7-year-old female – running into a door.
Figure 18.3a–c shows examples of non-accidental
bruising. All bruising, as with other findings in sus-
pected child abuse, must be assessed in the context of
medical, social and developmental history, the expla-
nation given and the patterns of non-abusive bruising.
Examples of patterns of bruising that should raise the
possibility of physical abuse include multiple bruises
in a non-mobile infant, multiple facial bruising to the
neck or abdomen, or patterned bruises. Multiple scars,
cigarette burns, bite marks or a torn frenulum should
also raise concerns for physical abuse.
Intentional scalds or burns may take many forms
including application of lighted cigarettes, heated
implements, (Figure 18.4) or immersion injuries with
symmetrical, well-defined clear upper margins (tide
marks). Unintentional scald injuries more commonly
Physical abuse 249
Right Left Left Right
Figure 18.2 Sites in children where bruising is signifi-
cantly more likely to occur following physical abuse.
(From Kemp A, Maguire SA, Nuttall D, et al. Bruising in
children who are examined or suspected child abuse.
Arch Dis Child 2014;2:108–113.)
result from spill injuries of other hot liquids; they usu-
ally affect the upper body with irregular margins and
variable depth of burn (Figure 18.5). Box 18.2 details
the main systematic review findings relating to thermal
injury in infants and children.
In infants (under 18 months) physical abuse must
be considered in the differential diagnosis when they
present with a fracture in the absence of clear history
of trauma. Multiple fractures are more common after
physical abuse than after accidental injury.
As with all suspected child abuse, it is essential to
know how the injury was disclosed, and the history
given to account for the injury. Frequently, there may be
conflicting accounts. Examples of features that should
raise concerns of possible abuse include discrepancies
in the history, a changing account, different accounts
by different carers and delays in presentation, and
inconsistency of the injury when compared with the
account(s). Specific enquiry should be made regarding
pre-existing conditions, which may cause excessive or
easy bruising (e.g., haemophilia or other bleeding dia-
theses), or known dermatological conditions, which
may mimic, or be mimicked by, physical abuse (such as
psoriasis, or eczema). Other aspects that are essential
are the emotional, behavioural and developmental his-
tory, the nutritional history, family history (e.g., genetic
or inherited disorders), social history and environmen-
tal history.
250 Safeguarding and protection of children and vulnerable adults
(a)
(b)
(c)
Figure 18.3 Bruises caused by non-accidental trauma. (a)
Inflicted injury-finger marks to neck from slap from hand
by non-accidental injury (NAI). (b) Bilateral buttock bruis-
ing in 6-year-old repeatedly struck with kitchen spatula.
(c) Periorbital bruising to 7 year old who sustained a
punch to the left eye (note also scleral haemorrhage).
Figure 18.4 Scar caused by application of heated cutlery
handle to lower limb and then moved across surface.
Figure 18.5 Accidental scald injury.
Physical examination requires a comprehensive
head to toe examination with appropriate consent. In
addition to a full general examination all scars, healing
injuries and new injuries must be noted.
Each injury, scar or mark must be examined and
documented in appropriate detail (preferably in writ-
ten form, on body diagrams, and photodocumented
with appropriate scaled rulers) so that they are capable
of proper independent, external review and interpreta-
tion. If injury is noted, consideration should be given to
repeat examination and serial photography to note the
evolution of injury or scars.
If physical abuse is suspected then consideration
must be given to a full radiographic skeletal survey,
which must subsequently be reviewed by a paediatric
radiologist, and perhaps bone scintigraphy. Most juris-
dictions will have standard NAI screening protocols.
In addition, laboratory-based investigations may also
be required and include blood count, urinalysis, liver
function, amylase, calcium, phosphorus, vitamin D,
screen for metabolic bone disease; coagulation stud-
ies. Endocrinological or other conditions which may

Table 18.1 Example of typical skeletal survey*
Radiographs should include:
• Skull: AP & lateral & Townes if clinically indicated
• Chest: AP & 2 oblique views for ribs
• Abdomen AP including pelvis & hips
• Spine lateral - cervical, thoracic and lumbar regions
• Humerus AP (L & R)
• Forearm AP (L & R)
• Femur, AP (L & R)
• Tibia/Fibula, AP (L & R)
• Hands, PA (L & R)
• Feet, DP (L & R)
Source: Adapted from Royal College of Radiologists. Standards for
Radiological Investigations of Suspected Non-accidental
Injury
* Joint document produced in collaboration with the Royal College
of Paediatrics and Child Health. London: RCR, 2008. BFCR(08)1.
2016.
affect bone strength may requires specialist referral.
Table 18.1 identifies a typical skeletal survey protocol.
Supplementary views may be required such as AP
and lateral coned views of joints if not well seen on full
length views. Lateral views are required of any sus-
pected shaft fracture. Follow-up radiographs may be
required and are ideally performed 2 weeks after initial
survey.
Interpretation of physical findings in physical abuse
cases requires a full understanding of mechanisms of
injury and how those mechanisms apply with respect
to the accounts of causation (of which there may be sev-
eral) given (Box 18.6).
Sexual abuse
There are many ways in which a child may disclose
abuse; for example, it may be to a teacher, a friend or a
sibling. The sexual abuse may be chronic and long term
or it may be an acute or single episode. Reporting of
non-recent abuse has dramatically increased in recent
years. Such disclosure may have been delayed for many
decades, or for a few days in acute episodes, which may
result in loss of forensically supportive evidence. The
use of video interviews is widely accepted as a means of
getting accounts of children and in the UK all aspects of
criminal investigations. ‘Achieving Best Evidence’ is a
strategy to ensure that the justice system is fair, acces-
sible, and delivers the justice victims and witnesses
need, deserve and demand. In particular, it ensures
that support is available to vulnerable and intimidated
witnesses, including children. Pubertal and pre-puber-
tal girls are more likely to have significant genital signs
if they are examined within 7 days of the last episode of
sexual abuse, although the majority are likely to have
Sexual abuse 251
none. Anal signs in particular are more likely to be
present in the acute phase (within the first 72 hours).
Speed is of the essence when disclosure of recent sexual
contact is made. Symptoms of longer-term abuse may
be non-specific and include sleep disturbance, enure-
sis and encopresis. Injuries may be acute or old and
include abrasion and bruising of the genitalia, acute
or healed tears of the hymen, anal bruising or lacera-
tions. Frequently there will be no abnormalities on
­examination.
The principles of examination and documentation of
the sexually abused child are in many respects similar
to those of an adult but a joint examination by a paedia-
trician and a forensic physician is often recommended.
There are increased complexities added by virtue of
consent issues and authority for documentation, for
example, with looked-after children. The need for pres-
ervation and security of items such as medical records
images, and colposcope recordings often creates sub-
stantial logistical problems. Most jurisdictions will have
specific guidelines and protocols.
It is essential for a permanent record of the genital or
anal findings to be obtained whenever a child is exam-
ined for possible sexual abuse. A colposcope or camera
may be used. The images must be of adequate quality
to demonstrate the clinical findings to other indepen-
dent reviewers of the case. Further examinations may
be required after initial assessments to determine
whether abnormalities or features evolve or change.
Examinations for acute or recent child sexual abuse
are similar to those for adult sexual assault. Emphasis
must be on as much detail of alleged events as possi-
ble to ensure proper consideration of body sites to be
examined and forensic samples to be taken. Genito-
anal examination may be particularly stressful for a
child and is done at the end of the general assessment
and examination. Genital examination can be done in
the supine ‘frog-leg’ position with hips flexed and the
soles of the feet touching, and if, for example, a hymenal
abnormality is seen, the prone knee–chest position can
additionally be used. A lateral position may be appro-
priate for some children, while others may be comfort-
able held on a carer’s lap. Examiners must be aware of
a potential risk that an examination may further trau-
matise an already traumatised child. Therapeutic needs
(e.g., for genital injury) may have priority over forensic
examination, but if treatment is required under general
anaesthesia, thought should be given to forensic assess-
ment, with appropriate consent at the time of therapeu-
tic intervention.
The need for examination following disclosure of
chronic or non-recent sexual abuse will need to take
into account its relevance. A physical examination of a
female alleging penetrative sexual assault pre-puber-
tally but disclosing in her thirties after vaginal delivery
252 Safeguarding and protection of children and vulnerable adults
of children will provide no information. Examination
of a pre-pubertal girl alleging vaginal penetration some
months earlier may have value. A male alleging historic
anal penetration with immediate pain and bleeding at
the time may have persistent scarring. Review of medi-
cal records of the individual at the time of the allega-
tions may provide helpful supportive evidence.
The interpretation of physical signs found after
genito-anal assessment is a very difficult and complex
area. Most complainants of child sexual abuse have no
genito-anal abnormalities when examined after alleged
sexual abuse. It is essential that precise and consistent
terminology is used in the description of abnormality
and injury so that abnormal findings are clearly under-
stood (Box 18.7). The presence of certain infections may
have relevance in sexual abuse enquiries. The impli-
cations of these findings must be determined with an
understanding of the context of presentation and a
detailed awareness of current research findings, and
may require additional expertise, for example, from
genitourinary medicine or virology specialists.
Neglect and emotional abuse
Childhood experiences, both positive and negative,
have a tremendous impact on future violence victimi-
sation and perpetration, and lifelong health and oppor-
tunity. As such, early experiences are an important
public health issue. Much of the foundational research
in this area has been referred to as Adverse Childhood
Experiences (ACEs). As the implications of ACEs are
better recognised, research is identifying associations
with features later in life such as non-suicidal injuri-
ous behavior. Additionally, a number of behavioural
Box 18.7 Features that may be seen in
sexual abuse
Genital erythema/redness/inflammation
Oedema
Genital bruising
Genital abrasions
Hymenal transections
Hymenal clefts and notches
Labial fusion
Vaginal discharge in pre-pubertal girls
Anal/perianal erythema
Perianal venous congestion
Anal/perianal bruising
Anal fissures, lacerations, scars and tags
Reflex anal dilatation
characteristics may indicate both neglect and emo-
tional abuse, for example, age-­inappropriate social
skills (e.g., inability to use knife and fork), bedwet-
ting and soiling, inability to self-dress, smoking, drug
and alcohol misuse, sexual precocity and absenting
from school. Certain features associated with possible
neglect may be evident during assessment and physi-
cal examination and include unkempt child, ill-fitting
or absent items of clothes, dirty or uncut nails, local skin
infections/excoriations and low centiles for weight and
height. However, some of these features may be seen in
normal, non-abused children. There may be a failure
to thrive. There may be considerable geographical and
cultural differences in the manifestation of such abuse.
Certain groups of children are at particular risk of
emotional abuse such as unplanned or unwanted chil-
dren, looked-after children, children of the ‘wrong’
sex, children with behavioural issues and children in
unstable or chaotic family settings. In the UK, emotional
abuse is most prevalent in 5 to 15-year-olds. Every prac-
titioner should be aware of the particular risks and how
to identify matters of concern.
Fabricated or induced illness in
children
Fabricated or induced illness (previously known as
Munchausen syndrome by proxy or factitious disorder
by proxy) takes place when a caregiver elicits healthcare
on the child’s behalf in an unjustified way. It is a term
used to describe a relatively rare behavioural disor-
der affecting a child’s primary caregiver, typically the
mother. The carer presents a false history or appear-
ance of illness for their child to healthcare profession-
als. Examples of how illness can be claimed, fabricated
or induced include manipulation of required drug regi-
mens (e.g., in diabetics), suffocation and administration
of noxious substances (e.g., salt). Injury may be caused
to ears and eyes initiating otorhinolaryngological and
ophthalmological repeat referral. Such approaches
may result in the child presenting, or being presented
repeatedly to healthcare professionals with a range of
often inexplicable or puzzling symptoms. The motives
behind such behaviour are unclear, but psychiatric,
mental health or attention-seeking problems may be
associated with such behaviour. Management of the
perpetrator is largely dependent on their capacity to
acknowledge the abusive behaviour and collaborate
with helping agencies.
Management of child abuse
The management of child abuse will depend on the
type of abuse or abuses experienced and many other
factors such as their health, and where they are living.
Every jurisdiction will have its own legal requirements,

policies, protocols and procedures. Every episode of
child abuse that is missed has the potential for a fatal
outcome or long-term harm to a child which is why
practitioners in contact with children must be ever
vigilant.
Safeguarding vulnerable adults
Ageing populations mean that more individuals will be
vulnerable by virtue of age and frailty. Other particularly
vulnerable adult groups include those with mental health
or learning difficulties. States must provide effective pro-
tection of vulnerable people against torture or inhuman/
degrading treatment (Article 3 European Convention on
Human Rights 1950) and, in England & Wales, multi-
agency Safeguarding Boards for the protection of vul-
nerable adults at risk of abuse or neglect are required
by virtue of the Care Act 2014 in England, and the Social
Services and Well-being (Wales) Act 2014 in Wales. The
Domestic Violence, Crime and Victims Act 2004 intro-
duced the criminal offence of ‘causing or allowing the
death of a child or vulnerable adult, in England & Wales.
A person could be convicted of this offence if they were,
or ought to have been, aware of the risk of serious physi-
cal harm to a child or vulnerable adult, and failed to
take reasonable steps to protect them from that harm.
Figure 18.6 shows the torso of a vulnerable 19-year-old
male who died suffering from severe malnutrition due
to familial neglect and Figure 18.7 shows the posterior
thighs and buttocks of an immobile female with mental
health conditions when found at home.
Elder abuse
Elder mistreatment is now recognised internationally
as a pervasive and growing problem. The age at which
Figure 18.6 The torso of a vulnerable 19-year-old
male suffering from severe malnutrition due to familial
neglect. Note the prominence of the skeletal anatomy
with the absence of muscle bulk.
Elder abuse 253
Figure 18.7 A large sacral pressure sore extending
deeply into soft tissues and exposing bone in a woman in
her mid-forties with chronic mental health illness, living
with her family. Additional pressure areas with faecal
contamination must raise the possibility of neglect of
vulnerable individuals and inadequate care nursing and
medical care.
the term ‘elder’ is applied varies between jurisdictions
and in some settings may be applied to all those over 60
years of age.
The UK’s ‘Action on Elder Abuse’ definition states:
‘Elder abuse is a single, or repeated act, or lack of appro-
priate action, occurring within any relationship where
there is an expectation of trust which causes harm or dis-
tress to an older person.’ Types of abuse include, but are
not limited to, psychological/emotional, physical, sexual
abuse, and financial exploitation. There are concerns
that deaths that may have been attributed to natural
causes may have missed instances of abuse. Proper scru-
tiny of circumstances leading to death is crucial if crimes
or episodes of abuse and neglect are not to be missed.
The US National Academy of Sciences defined elder
abuse/mistreatment as: (a) intentional actions that
cause harm or create a serious risk of harm (whether or
not harm is intended), to a vulnerable elder by a care-
giver or other person who stands in a trust relationship
to the elder, or (b) failure by a caregiver to satisfy the
elder’s basic needs or to protect the elder from harm.
Elder abuse has received increasing global attention
in the last few decades. It takes many forms, includ-
ing physical, emotional/psychological, financial and
sexual abuse, as well as neglect. Screening for such
events should be standard practice for any healthcare
professional who is asked to assess injuries in such an
individual.
The WHO reported on the abuse of the elderly and
referred to studies showing a rate of abuse of 4–6%, in
domestic settings, if physical, psychological and finan-
cial abuse and neglect were included.
Some surveys of staff working in institutional set-
tings revealed that 10% admitted to committing at least
one act of physical abuse themselves, and 36% reported
254 Safeguarding and protection of children and vulnerable adults
Box 18.8 Risk factors for elder abuse/maltreatment
Individual (victim):
• Older than 74 years
• Woman
• High levels of physical dependence or intellectual
disability
• Dementia
• Depression
• Aggression/challenging behaviour
Individual (perpetrator):
• Male (physical aggression); female (neglect)
• Depression
• Alcohol and substance abuse
• Hostility/aggression
• Financial problems
• Stress/caregiver ‘burnout’
Relationship:
• Dependence of perpetrator on the victim
­(financial, emotional, accommodation)
• Long-term history of difficulties in the relationship
having witnessed an incident of physical abuse by other
members of staff.
The WHO estimates that at least 4 million people over
60 years of age experience elder abuse in Europe in any
one year, with 2500 homicides due to maltreatment. The
estimated prevalence of elder maltreatment in Europe is
3% (0.4% for the UK), although it may be as high as 25% for
‘vulnerable adults requiring care’, and ‘even higher’ for
nursing and residential home residents. Risk factors for
elder abuse and maltreatment can be seen in Box 18.8.
As with child abuse, extreme vigilance is required so
that episodes of abuse in the elder population are not
missed or ignored.
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safeguarding-ethics-toolkit (Accessed 1 May 2019).
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Testimony in Sexual Cases. Oxford: Oxford University Press;
2016.
Royal College of Radiologists. Standards for radiological inves-
tigations of suspected non-accidental injury: joint docu-
ment produced in collaboration with the Royal College of
Paediatrics and Child Health. London: RCR; 2008. https://
www.rcr.ac.uk/audit/skeletal-surveys-non​-accidental-injury
(Accessed 1 May 2019).
World Health Organisation (WHO) International Network for the
Prevention of Elder Abuse (INPEA). Missing voices: views of
older persons on elder abuse. Geneva: WHO; 2002. http://
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NMH_VIP_02.1.pdf?sequence​=1 (Accessed 1 May 2019).
19 Transportation medicine
▪▪ Introduction
▪▪ Transportation law
▪▪ Transportation ‘under the influence’
▪▪ Personal transport and road traffic injuries
Introduction
All forms of transport on (air, water or land) may be
associated with a risk of harm or injury to vehicle occu-
pants and others. Particular environments render indi-
viduals at risk of specific types of injury. The incidence
of those risks may be well-established but are often
substantially increased when other human factors are
taken into account, including lack of experience, expo-
sure, risk-taking behaviour, fatigue and the effects of
drugs and alcohol.
Transportation law
Virtually every jurisdiction has laws which limit the
speed at which vehicles can move, and the amount of
alcohol and/or drugs under which an individual is law-
fully deemed to be capable of safely controlling, or being
in charge of, a means of transportation.
The underlying principle of such laws is to increase
public safety, and the safety of the individual. The
faster a person is moving in a vehicle (whether in con-
trol of a vehicle or as a passenger), the greater the risk
of loss of control and collision, and the greater the
extent and seriousness of injury. The greater the degree
of intoxication, whether through drugs or alcohol,
the greater the risk of loss of control. Legal limits are
established in most countries for maximum acceptable
levels of alcohol in blood, breath or urine. Currently,
in England & Wales, the maximum legal permissible
blood alcohol concentration is 80 mg alcohol/100 mL
of blood. Many consider this too high and believe that
it should be reduced to 50 mg alcohol/100 mL of blood
to bring it (and the equivalent breath and urine levels)
into line with many countries in the rest of the world
and, indeed in other parts of the UK where, for exam-
ple in Scotland, it is 50 mg alcohol/100 mL of blood. In
2012, the UK government announced a new offence
of driving with a specific controlled drug in the body
above that drug’s accepted limit. The aim was to reduce
expense, effort and time wasted from prosecutions that
fail because of difficulties proving a particular drug
impaired a driver. On 2nd March 2015, eight generally
▪▪ Train and railway injuries
▪▪ Aviation incident-related injury and fatalities
▪▪ Marine fatalities
▪▪ Bibliography and information sources
prescribed, and eight illicit, drugs were added into new
regulations that came into force in England & Wales.
Regulations on amphetamine came into force on 14th
April 2015. Table 19.1 shows the current UK levels for
these drugs permitted by law.
The assessment of the effects of drugs and alcohol on
a person’s ability to drive (in addition to a simple legal
limit) is very important because of the variable response
to the effects of alcohol and other substances. In many
cases, ‘driving under the influence’ may be confirmed
by the ability, or failure, to pass standardised tests of
sobriety, or by a medical examination to determine
whether the ability to drive may be impaired, follow-
ing preliminary impairment tests undertaken by police
personnel.
Such laws apply at the personal level (e.g., the indi-
vidual driving a car or a bicycle), at a management level
(e.g., the individual in charge of a subway station) and
at a corporate level (e.g., the senior officers in transport
companies such as sea ferries). In all cases, it is per-
ceived that such individuals, or corporate bodies, may
have a duty of care to those around them, whether as
private individuals (e.g., friends being given a ride to a
party) or as paying clients (e.g., customers paying for
transport across the sea).
In England & Wales, The Transport and Works Act
1992 defines specific offences related to the use of alco-
hol and drugs in transport systems, and defines the
powers that police have to investigate such matters,
including the power to take evidential breath, blood
and urine tests.
This area of law is vast, and varies from jurisdiction
to jurisdiction but, increasingly, legal action is being
taken at a higher corporate level such that accountabil-
ity is required throughout all levels of an organisation.
The Corporate Manslaughter and Corporate Homicide
Act 2007 came into force in 2008 and introduced a new
offence across the UK: corporate entities (companies
and organisations) may now be prosecuted when there
has been a gross failing, throughout the organisation,
in the management of health and safety, where such a
failure has fatal consequences.
258 Transportation medicine
Table 19.1 Drug levels permitted by law when driving a motor vehicle in the UK
‘Illegal’ drugs (‘accidental exposure’ – zero
tolerance approach)
benzoylecgonine
cocaine
delta-9-tetrahydrocannabinol (cannabis)
ketamine
lysergic acid diethylamide
methylamphetamine
methylenedioxymethamphetamine (MDMA)
6-monoacetylmorphine (heroin)
‘Medicinal’ drugs (risk based approach)
clonazepam
diazepam
flunitrazepam
lorazepam
methadone
morphine
oxazepam
temazepam
Separate approach (to balance its risk)
amphetamine
Transportation ‘under the influence’
In general, two types of offence are committed when
under the influence of alcohol or drugs. The first is where
relevant maximum permissible alcohol concentrations
have been prescribed and an individual is found to
exceed that prescribed concentration. Secondly, in many
jurisdictions, it is the effect that alcohol (or drugs) has
on the ability to drive properly that is assessed. Initial
screening may be carried out by law-enforcement offi-
cers at the scene of an alleged offence or accident, using
‘field impairment tests’.
Evidential breath alcohol machines are used to take
breath samples and, if for some medical reason (e.g.,
asthma, oral trauma) it is not possible for an individual
to provide a sample, a blood or urine sample must be
sought. The experience in all jurisdictions is that indi-
viduals (who might suspect they exceed the relevant
legal limit) may provide a variety of reasons for not pro-
viding relevant samples (e.g., previously undiagnosed
asthma, needle phobia) and, although some of those
reasons may be valid, many have been tested in court
and found wanting.
Threshold limit in microgrammes
per litre of blood (µg/L)
50
10
2
20
1
10
10
5
Threshold limit in blood (µg/L)
50
550
300
100
500
80
300
1,000
Threshold limit in blood (µg/L)
250
The nature and purpose of medical assessments of
the intoxicated driver varies in detail from jurisdiction
to jurisdiction. Generally, however, the medical assess-
ment of an individual’s ability to drive a motor vehicle is
established by undertaking a full history and examina-
tion and reviewing certain physical and eye signs (see
Figure 19.1). Previously used tests to assess intoxication
have been shown to have no solid evidence-base.
The aim of the physical medical examination is pri-
marily to determine whether there is any medical con-
dition (either longstanding or temporary) which might
account for the individual’s actions and behaviour. The
examination may then determine: (1) whether the indi-
vidual’s ability to drive a motor vehicle is impaired; and
(2) which drug/substance is causing this impairment;
and (3) whether there is a medical reason for the indi-
vidual’s apparently impaired status (e.g., neurological
disorder, psychiatric disorder). Increasingly, certain
procedures that measure psychomotor function and
‘divided attention tests’ are used.
Previously, ‘Divided attention tests’, which assess
an individual’s balance and coordination, as well as the
ability to follow simple instructions, include the ‘walk
 Transportation ‘under the influence’ 259

(a)

Figure 19.1  (a) and (b) Impairment tests for ‘driving under the influence’ cases. (Taken from Faculty of Forensic & Legal
Medicine. Proforma – Section 4 RTA Assessment [England, NI and Wales], 2016.) (Continued)
260 Transportation medicine

(b)

Figure 19.1 (Continued) (a) and (b) Partial proforma for assessments (alcohol & drugs) under England & Wales
road ­traffic legislation. These pages identify the relevant medical consultation and examination details.
(Taken from the Faculty of Forensic & Legal Medicine ‘Assessments (alcohol & drugs) under the RTA – 2019’
[https://fflm.ac.uk/wp-content/uploads/2019/08/Section4_RTAform_Jun19.pdf].)

and turn test’, ‘one-leg stand test’, ‘horizontal gaze
nystagmus test’ and Romberg tests have been used.
If such tests are used, it is important they are repro-
duced and scored in identical ways. It is also essential
to understand that initial studies, which suggested
high sensitivities and specificities in results for Drug
Recognition Programs within the USA, have not been
confirmed in controlled laboratory studies. The results
of the few studies that have been performed suggest
that the accuracy of such assessments, in general, is
not be sufficiently robust for evidential purposes (in
terms of determining the culpable drug/substance),
but when used they can help corroborate other witness
and toxicological evidence. The majority of individuals
will have used a mixture of drugs and alcohol, which
often renders tests for specific drugs groups inappro-
priate or wrong.
It is important to recognise that the results of ‘field
impairment tests’ (‘preliminary impairment tests’ in the
UK) do not necessarily establish impairment of driving
through drugs other than alcohol, but may be useful in
screening for individuals suspected of being impaired
as a consequence of drug use, and provide supportive
evidence of impairment. They cannot be used with cer-
tainty to confirm that drugs have been used, or the par-
ticular drug or drugs that may have consumed.
Anyone using these tests, in association with a medi-
cal examination, must be able to interpret them in the
context of that medical examination, the circumstances
in which field tests were undertaken, and the limitations
of the evidence base on which such screening tests are
established. They also need to be aware of what medi-
cal conditions may mimic the effects of drugs and alco-
hol, and vice-versa, as these issues may often be raised
sometime after the examination when the case gets
to court.
Personal transport and road
traffic injuries
Those injured by collisions on the road or off-road, using
personal transport can be divided into three broad
groups: pedestrians, cyclists (pedal or motor) and the
drivers or passengers of vehicles. Of these three broad
groups, it is pedestrians who are most often injured,
although the proportion of pedestrian victims in the
overall road traffic-injured population varies greatly
between countries depending on patterns of transport
use. It is perhaps self-evident that where there is greater
mingling of motor transport, cycles and pedestrians
there is also a greater risk of injury to the pedestrian and
to the cyclist. Cyclists have been involved in fatal inci-
dents with pedestrians. Most road deaths in the world
occur in countries where driving laws and regulations
are less developed and may include not only issues with
the driver, but issues with poorly maintained vehicles.
Personal transport and road traffic injuries 261
Pedestrians
Pedestrians struck by motor vehicles sustain injuries
from the initial impact with the vehicle (the primary
injuries) and also from contact with other objects, or the
ground, following the primary contact with the vehicle
(the secondary injuries). The class of vehicle impacting
has been shown to significantly affect the risk of fatal-
ity and serious injury. Advances in safer vehicle design,
and legislation to reduce vehicle speeds, have been suc-
cessful in reducing the effects of such contact but do not
eradicate them completely.
Primary injuries often form recognisable patterns,
although a variety of factors may alter the totality of
injuries sustained. When an adult is hit by the front of
a standard car, for example, the front bumper (fender)
will generally make contact at about knee level. The
exact point of primary contact will be determined
by a large number of factors, including orientation of
the victim (which will determine whether impact is
anterior, posterior or lateral), the nature of the front
of the car, the size of the car (which can be very vari-
able in height profile), and the height of the individual.
Comparison of measurements of lower limb injuries
(from the heel), with measurements of relevant parts
of the car (from the ground) may assist in the recon-
struction of pedestrian versus car collisions (Figure
19.2) and is one of the many factors taken into account
by accident investigators.
Other typical primary injury sites include the thigh,
hip or pelvis caused by contact with other parts of the
car, such as the bonnet (the hood). At relatively low
speeds (e.g., 20 kph/12 mph), the victim may be thrown
off the bonnet either forwards or to one side. Between 20
and 60 kph (12–36 mph), the pedestrian may strike the
bonnet (hood) and the head may strike the windscreen
or the surrounding metal body work. At higher speeds
(60–100 kph/36–60 mph), pedestrians may be projected
up into the air; sometimes they will pass completely over
the vehicle and will avoid hitting the windscreen and
other points on the vehicle (Figure 19.3). Such impacts,
however, will generally cause major injury, including
complex fractures or traumatic amputations. The elderly
is over-represented in pedestrian fatalities and serious
injuries.
Secondary injuries are often more serious, and
potentially lethal, than the primary injuries. Such sec-
ondary injuries vary from simple ‘brush abrasions’,
caused by ‘skidding’ across the surface of the road,
to fractures of the skull or axial skeleton, caused by
direct contact with a hard surface, to hyperextension
or hyperflexion fractures of the spine. Ground contact is
often the major source of injury and the majority relate
to severe head injury. It is important to remember that
the visible external injuries may not be those associated
with fatality; it is often internal injuries that are more
significant.
262 Transportation medicine

(a) (b)

Figure 19.2 (a) A pedestrian struck by the front of a car may be projected forwards or lifted onto the vehicle; (b) ‘bum-
per injuries’ including a compound fracture of the right lower leg, and laceration of the left shin probably ­following
primary impact to this pedestrian’s right leg. ([b] Reproduced with permission from Saukko P and Knight B. Knight’s
Pathology 4E, London, CRC Press, 2016.)

Figure 19.3 At speeds of over 23 kph (15 mph) a pedestrian can be ‘scooped up’ onto a car, suffering head injuries on
impacting the windscreen. They may then fall off sideways or, at higher speeds, be thrown over the roof. (Reproduced
with permission from Saukko P and Knight B. Knight’s Pathology 4E, London, CRC Press, 2016.)

Even in the absence of skull fracture, traumatic externalised, internal organs may be ruptured and
brain damage, including traumatic axonal injury, is there may be fractures of the spine. Compression of the
frequently observed in fatally injured pedestrians. This chest may result in multiple rib fractures, causing a ‘flail
occurs as a consequence of the rotational, deceleration chest’. The rotation of the wheel may strip off large areas
forces produced when the rapidly moving head is sud- of skin and subcutaneous tissue; this is called a ‘flaying
denly stopped at impact, leading to ‘shearing’ injuries injury’ (Figure 19.4). On occasion, patterned injuries are
to the brain and its coverings. Fractures of the spine, recognised on the skin surface bearing the characteris-
especially in the cervical and thoracic segments, may tics of tyre-treads (Figure 19.5).
lead to cord damage. Fractures of the limbs are common
but, apart from those of the legs that are associated with
the primary impact sites, they are somewhat unpredict-
able because of random ‘flailing’ of the limbs following
primary impact.
When an adult is struck by a larger vehicle, for exam-
ple a van, a 4 × 4, a sport utility vehicle (SUV), truck or
lorry, or when a small child is struck by any vehicle, the
typical lower limb primary contact injury site tends to
be ‘higher up’ (pelvis, abdomen, chest or head). It is
likely that the victim will make contact with more of
the front of the vehicle or be projected along the line of
travel of the vehicle and ‘run-over’.
‘Run-over’ injuries are relatively unusual and the Figure 19.4 Pedestrian leg injury from a rotating
effects are variable, depending on the area of the body wheel resulting in ‘flaying’ of the skin. (Reproduced
involved, the weight of the vehicle and the surface area ­ ermission from Saukko P and Knight B. Knight’s
with p
of the contact. The skull may be disrupted and the brain Pathology 4E, London, CRC Press, 2016.)

Figure 19.5 Intradermal bruising reflecting the pattern of
a vehicle tyre tread. Note that the bruising is in the ‘val-
leys’ and not the ‘hills’ in the tread. Scaled photographic
documentation of such a patterned injury will allow
future comparisons to be made between it and the tread
pattern of a suspect vehicle. (Courtesy of Richard Jones.)
Where the risk of pedestrian and other road-related
fatalities and serious injuries has been treated as a pub-
lic health and social issue, educating the public, par-
ticularly children and young people, has resulted in a
significant reduction in pedestrian and other fatalities.
Seat Belt Legislation
Seat belt law exists and applies to all
occupants
Seat belt law exists and applies to front
seat occupants only
No law
No data
Figure 19.6 The State of Seat belt Legislation Worldwide. (Courtesy of the World Health Organisation.)
Personal transport and road traffic injuries 263
Vehicle occupants
Most road traffic collisions involve the front, or the front
corners, of the vehicle and a high percentage of impacts
are against either another vehicle or a stationary object.
This type of impact rapidly decelerates the vehicle. Less
commonly, the vehicle is hit from behind, causing an
‘acceleration’ impact. The least common impacts are
side impacts and ‘roll-overs’.
Many countries have legislation regarding the
requirement to wear seat belts, both in the front and
back of moving vehicles.
Figure 19.6 shows 2011 data which identify those
countries with seat belt legislation.
Substantial evidence of seat belt efficacy has been
shown by several studies, and it is widely recommended
that motor vehicle occupants use properly-fitted seat
belts. However, some countries with national seat belt
laws permit various exemptions which may lower use
rates. Unrestrained front-seat occupants in a vehicle
subjected to rapid deceleration during a collision will
continue to move forwards as the vehicle decelerates
around them, and will impact those parts of the vehi-
cle that are in front of them. The degree of injury sus-
tained by the occupant is very much dependent on the
vehicle’s speed at the moment of impact, its deforma-
tion properties and the structure of the part (or parts)
of the vehicle being impacted by the occupant (Box 19.1,
Figures 19.7–19.9).
The unrestrained rear-seat passenger is also liable to
injury through either deceleration or acceleration. The
injuries, in general, may not be as severe as those caused
to the front-seat occupants. In a deceleration impact, the
rear-seat passengers will be thrown against the backs of
264 Transportation medicine
Box 19.1 Injuries that may be expected to occur in an unrestrained impact/collision
• The face and head hit the windscreen glass, frame
or side-pillars, causing skull and facial fractures,
injury to the brain and its coverings, and cervical
spine injury.
• The chest and abdomen contact the fascia or the
steering wheel, causing rib, sternal, heart and liver
injuries.
• The momentum of the heart within the thorax,
perhaps aided by hyperflexion, may tear the
aorta at the termination of the descending part of
the arch, at the point where the vessel becomes
attached to the vertebral column.
• The legs of the passenger are thrown forwards
and the knees may strike the parcel shelf, causing
fractures.
Cervical spine
injury
Face and
head injury
Steering wheel
impact
Braced leg fracture Pelvic fracture
Figure 19.7 Major points of injury to an unrestrained
driver of a vehicle in deceleration impact.
the front seats and may impact the front-seat occupants.
They may be projected over the front seat to hit the wind-
screen and even be thrown out through the windscreen.
The function of seat belts
The mandatory use of seat belts has had a profound
effect on road traffic fatality rates in the UK and other
countries where similar legislation has been enacted.
The combination of a horizontal lap strap and diagonal
shoulder strap was introduced as a satisfactory compro-
mise between effectiveness and social acceptability. To
be effective, a seat belt must (1) be worn and (2) worn
correctly and any alteration in their fixing or structure
can compromise their efficacy (Box 19.2).
Seat belts correctly worn can also cause injuries, the
nature and severity of which is dependent on the force
and nature of the impact. Any individual involved in a
collision in which intrusion into the vehicle cabin has
occurred, or where they have been trapped within the
• The legs of the driver, which are commonly braced
on the brake and clutch pedals, may transmit the
force of impact along the tibia and femur to the
pelvis. All of these bones may be fractured or
dislocated.
• On the rebound from these impacts, the heavy
head may swing violently backwards and cause
injury to the cervical or thoracic spine.
• The occupants of the car may be ejected out of
the vehicle through the windscreen, increasing
the risks of secondary injuries or being run over by
another vehicle.
Figure 19.8 Facial injuries from shattered windscreen
glass in an unrestrained driver. The toughened glass
breaks into small fragments, which produce character-
istic ‘sparrow foot’ marks. The forehead laceration was
made by the windscreen rim.
vehicle, or who has had to be extracted from the vehi-
cle by emergency services, should have a full medical
assessment, as should anyone under the influence of
drugs or alcohol at the time of a collision, or who has or
has appeared to lose consciousness, as all these have the
capability of being associated with, or masking severe
injury. Such an assessment should always include, in
addition to basic physiological observations, palpation
and testing of range of movement of all limbs, palpation
of the clavicle, lateral and anteroposterior compres-
sion of the chest, and a full abdominal examination, in

Figure 19.9 Deceleration-related thoracic aortic transec-
tion following a road traffic collision (arrow indicates one
edge of the torn aorta). The typical site for deceleration
aortic injury is just distal to the origin of the left subcla-
vian artery. (Courtesy of Richard Jones.)
Box 19.2 The role of a seat belt
A seat belt that is correctly installed, and worn, acts
in the following ways:
• It spreads the deceleration forces at impact over
the whole area of contact between the straps
and the body surface so that the force delivered
to the body per unit area is reduced.
• It is designed to stretch during deceleration
and some belts have a specific area for this to
occur. This stretching slightly extends the time
of deceleration and reduces the force per unit
time.
• It restrains the body during deceleration, keep-
ing it away from the windscreen, steering wheel
and other obstructions at the front of the vehi-
cle, thus reducing injury potential.
• It prevents ejection into the road through burst
doors or windows, which used to be a common
cause of severe injury and death.
order that occult fracture or internal organ injury is not
missed. Repeat observations may be useful in identi-
fying a deterioration in condition and an indicator for
urgent transfer and treatment.
Air bags and other injury reduction systems
Air bags were developed in an attempt to aid the protec-
tion of all car occupants following a collision by rapidly
deploying a ‘soft method of restraint’ that is only present
when required. Most modern cars now have sophisti-
cated air-bag systems, many providing protection not
only from front impacts but also from the sides or cor-
ners of the vehicle.
Personal transport and road traffic injuries 265
The deployment of an air bag relies upon the explo-
sive production of gas, usually from the detonation
of a pellet commonly made of sodium azide. For the
deployment to be timed correctly, the deceleration of
the vehicle following impact needs to be sensed and the
detonation of the pellet completed in microseconds so
that the bag is correctly inflated at the time the occupant
of the car is beginning to move towards the framework
of the vehicle.
Air bags are designed to provide protection to the
‘average-sized adult’ in the front of the car and this pro-
tection depends upon the occupant responding to the
impact in an ‘average’ fashion. Air bags can cause inju-
ries, most frequently abrasions or burns, and guidelines
exist as to the minimum size that a person should be
when sitting in an air-bag protected seat. Most cars have
the option of disabling air bags if those of short stature
(generally children) are occupying such seats. Air bags,
in general, should never be used in the presence of baby
seats. At particular risk, are babies who are placed on
the front passenger seat in a rear-facing baby seat that is
held in place by the seat belt. The back of the baby seat
may lie within the range of the bag when it is maximally
expanded, and fatalities have been recorded following
relatively minor vehicle impacts when the air bag has
struck the back of the baby seat.
Newer technologies such as automatic emergency
braking (AEB) and forward collision warning (FCW)
systems separately, and together, have the potential
to further reduce fatality and serious injury but, in all
cases, the systems are not applicable to every crash or
vehicle impact environment. The enforcement of cur-
rent systems, introduction of new systems, appropriate
legislation and public education is likely to significantly
decrease the number of fatalities and serious injury in
the future.
Motorcycle and pedal cycle injuries
Most injuries to motorcyclists are caused by falling from
the machine onto the roadway. Many of the injuries can
be reduced or prevented by the wearing of suitable pro-
tective clothing and a crash helmet. Severe abrasions –
often with substantial tissues loss caused by contact with
the road surface – are almost universal following an acci-
dent at speed, and injuries to the limbs and to the chest
and spine occur very commonly because of contact with
other objects or vehicles, entanglement with the motor
bike or direct contact with the road (Figure 19.10). Despite
the introduction of the mandatory wearing of crash hel-
mets in the UK, head injuries are still a common cause
of morbidity and mortality. In countries where there is
no mandatory requirement for motorcycle helmets, the
incidence is substantially increased. Figure 19.11 shows
which countries had motorcycle helmet laws and helmet
standards in 2013.
266 Transportation medicine
Figure 19.10 Extensive ‘brush’ abrasion of the left flank in
a motor cyclist thrown across a rough surface.
A less common injury occurs from ‘tail-gating’,
where the motorcyclist travels under the rear of a truck,
causing severe head injuries or even decapitation. This
scenario can also occur with an approach from the side,
although these mechanisms of injury have been some-
what reduced in some countries by legislation intro-
ducing bars at the sides and rear of trucks to prevent
motorcycles and cars passing under the vehicle. This
does not prevent injury but modifies the nature of the
most serious ones, and should reduce fatalities.
Injuries associated with pedal cycles are very com-
mon because of the large numbers of cycles in use.
Frequently, the injuries are run-over injuries, caused
by cyclists under-taking a lorry to the left or right, for
example, and where the lorry driver does not see that
cyclist. Most injuries associated with cycles tend to be of
mild or moderate severity because of their low speeds.
However, impact, by or run-over, by large vehicles can
Comprehensive
Comprehensive/no standard
Not comprehensive/no law
Data not available
Not applicable
Figure 19.11 Map showing which countries have motorcycle helmet laws and helmet standards in 2013. (Courtesy of
the World Health Organisation. The State of Seatbelt Legislation Worldwide https://www.who.int/gho/road_safety/
leg­islation/seat_belt/en/)
result in severe and fatal injuries which are often crush-
ing and compressive in nature. Other injuries, espe-
cially to the head and chest, are common when cyclists
fall from their relatively high riding position on such an
inherently unstable machine.
Other transportation methods (e.g., the Segway
Personal Transporter) have their own types and range
of risk of injury or fatality. The Segway has been asso-
ciated with a wide range of injuries including ortho-
paedic, maxillofacial, neurological and thoracic cases.
Tragically, the owner of Segway Inc, died having lost
control of the Segway he was using, falling over a cliff.
Newer devices such as hoverboards present new
ways of being injured. In 2015–2016 there were almost
25,000 hoverboard injuries in the US. Although many
were upper extremity limb fractures, almost 6% sus-
tained critical injuries.
Train and railway injuries
Railway injuries are most commonly seen in countries
with a large railway network, such as India and China,
and in any country where rail crossings are unprotected
or unmanned. Although mass disasters, such as the
derailment of a train, occasionally lead to large num-
bers of casualties, most deaths and injuries occur as
an aggregation of numerous individual incidents, most
of which are accidents, such as at rail crossings, or as a
result of children playing on the railway line. Criminal
acts may occur where individuals are deliberately
pushed into the path of oncoming trains. Railway lines

and bridges crossing them are a common site for suicide
attempts and there have been many initiatives to try and
reduce the incidence of this type of suicidal behaviour.
It is important to remember that railway employees may
be considerably affected by rail deaths and they should
be provided with appropriate support and counselling.
Medically, there is nothing specific about railway
injuries except the frequency of very severe mutila-
tion. The body may be in many pieces and soiled by axle
grease and dirt from the wheels and track, and local
vegetation. Where passengers fall from a train at speed,
multiple injuries caused by repeated impacts and roll-
ing may be seen, often with multiple abrasions from
contact with the coarse gravel of the railway line bal-
last. It is generally very difficult to be able to determine
the sequence of events because of the severe damage to
the body.
Suicides on railways fall into two main groups: those
who lie on the track (sometimes placing their neck
across a rail so that they are decapitated) and those
who jump in front of a moving train from a platform,
bridge or other structure near to the track. Jumping from
a moving train is much less common. The injuries pres-
ent will depend on the exact events, but they are usually
extensive and severe when there has been contact with a
moving train, although they may be localised with black
soiling at the crushed decapitation or amputation site if
the individual has lain across the track (Figure 19.12).
There is a risk of secondary injury if survival occurs
where other factors such as electrified lines are pres-
ent. On electrified lines, an additional cause of suicidal
or accidental injury or death is present in the form of
electric shock from either a live rail or overhead power
lines. The voltage in these circuits is high, often in the
region of 600 V. Death is rapid and often associated with
severe burns at the points of contact or earthing (see
also Chapter 12).
Figure 19.12 Traumatic amputation of the right arm and
bruising of the face and chest in a pedestrian struck by a
passing train.
Aviation incident-related injury and fatalities 267
A careful search for unusual injuries inconsistent
with the setting, and examination for a vital response
to the severe blunt force injuries, should be made, as
homicides may be concealed by staging the scene, with
the deceased being placed on the rail track in an attempt
to conceal the true cause of death.
Railway workers may be injured or killed by falling
under, or by being struck by, moving rolling stock or by
being trapped between the buffers of two trucks while
uncoupling or coupling the rolling stock. The injuries
associated with the squeezing between rolling stock are
often those of a flail chest, with or without evidence of
traumatic asphyxia (See also Chapter 11).
Aviation incident-related injury and
fatalities
Aviation incidents can be divided into two main
groups: those which involve the crew and the large num-
bers of passengers of a modern, commercial aircraft,
and those which involve the occupants of small, rela-
tively slow, light aircraft. Additional, but much smaller,
groups include those involving ultralight aircraft and
paragliders. More recently consideration has been given
to injuries sustained by impact from unmanned aircraft
systems (drones). Skull fractures and ocular globe rup-
tures have been reported.
Large aircraft are pressurised and, if the integrity of
the cabin is breached, there can be rapid decompression
and the passengers may suffer barotrauma. If the defect
in the cabin is large enough, victims may exit through
the defect and fall to their death. When an aircraft hits
the ground, the results will depend on the rapidity of
transfer of the forces, and this is dependent on the speed
of the aircraft and the angle of impact. If the forces are
very severe, all passengers may be killed by deceleration
injuries and by multiple trauma owing to loss of integ-
rity of the fuselage.
In lesser impacts, the results may be similar to those
of motor vehicle crashes, although the forces are usually
greater and the injuries sustained are proportionately
more severe. The usual lap-strap seat belt offers little
protection in anything but the most minor accident. Fire
is one of the greatest hazards in air crashes and accounts
for many deaths.
In light and ultralight aircraft crashes, the velocity,
and hence the forces, may be less than in large com-
mercial aircraft, but they are still often fatal. In some
cases, the pilot may be separated from the aircraft and
without a parachute the injuries are those that would
be expected with a fall from a substantial height. The
investigation of air accidents is a task for specialist
medical personnel, who are often available from the
national air force or from a civil authority. There should
always be a full autopsy on the pilot or suspected pilot,
with full microscopic and toxicological examination to
268 Transportation medicine
exclude natural disease, intoxication by drugs and alco-
hol, and carbon monoxide toxicity. These findings will
be included in the overall assessment of the incident
which will include consideration of the activities prior
to the incident and the condition and performance of
the aircraft.
Marine fatalities
Fatalities in the marine setting embrace a range of
marine-specific and general injury types. The range of
activities include commercial diving, recreational div-
ing, use of powered water sport bikes, sailing, motor
cruising and commercial marine transport (e.g., oil
tankers, container ships, passenger vessels). The likeli-
hood of dying in a marine environment is enhanced by
not wearing appropriate safety gear. In the recreational
setting, fatalities occur when individuals fall from ves-
sels and drown, or succumb to hypothermia, or cannot
be recovered back on board.
Physical injuries in recreational sailing are wide-
spread and examples include those of suffering direct
trauma (e.g., to the head or neck following uncontrolled
gybe; Figure 19.13), loss of digits or limbs when caught up
in winches or anchor cable, limb or skull fractures from
direct impact from flailing blocks, and friction burn
injury from uncontrolled rope movement. Drowning
may occur from being trapped after inversion of the
vessel (see also Chapter 13). Between 2000 and 2011, the
US Coastguard reported 271 sailing-related fatalities
and 841 injuries. Falls overboard and capsizing were
the most common fatal accidents. Operator inattention,
inexperience, and alcohol use were common prevent-
able factors contributing to fatal and non-fatal injury.
Changes in the way in which established sports are
undertaken or the introduction of new sports, may
introduce new or different patterns of injury. Rowing
has had a growth in popularity, particularly open-
water and coastal rowing. This may affect the pattern of
Figure 19.13 Abrasion of neck caused by mainsheet dur-
ing uncontrolled gybe whilst sailing.
musculoskeletal and back injuries recorded. Kitesurfing
is a relatively new sport and kite surfers are at risk of
injury in a number of ways. Research has shown that
the injury rates may be influenced by the nature of the
kitesurf equipment used.
Motor-powered vessels may cause injury from explo-
sion or fire, and those in the water may sustain injury
from rotating propellers.
Commercial vessels may cause their own specific
problems, such as asphyxiation in storage tanks or falls
from heights. Most of these scenarios are of an indus-
trial/occupational nature and may involve potential
breaches of health and safety legislation. In the UK, the
Marine Accident Investigation Branch (MAIB) examines
and investigates all types of marine accidents, involving
UK ships worldwide, and other ships in UK territorial
waters, and publishes regular reports on its findings.
Marine life may also cause injury. In the US since
the 1900s, there have been ∼5000 shark attacks of
which ∼1200 were fatal. Fatalities were associated with
swimming, boating, three or more bites, limb loss or
tiger shark attack. The most common attacks involved
bites to the legs or arms with limb loss occurring in 7%
of attacks.
The majority of transportation injuries and fatalities,
whether related to air, sea or land would be reduced if
appropriate public health and education messages were
given and reinforced to the public. Many are avoidable,
and many are predictable.
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way fatalities, injuries and close calls on railway employees. J
Occup Rehabil 2015;25(3):557–568.
Baumbach SF, Stawinski T, Schmitz D, et al. Influence of kite-
surf equipment on injury rates. J Sports Med Phys Fitness
2018;58(10):1482–1489.
Bhatti JA, Razzak JA. Railway associated injuries in Pakistan. Int J
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20 Torture and cruel, inhuman
and degrading treatment
▪▪ Introduction
▪▪ Definitions
▪▪ Investigation
Introduction
Torture is one of the most serious violations of funda-
mental human rights and is prohibited in international
human rights and humanitarian law in all circum-
stances. Despite the absolute prohibition of torture in
international law, it is still believed to be practiced in
more than 100 countries around the world. Torture and
other forms of ill-treatment not only have physical and
psychological effects on individuals and their com-
munities, but they also undermine the rule of law and
democratic institutions in civil societies. All forensic
practitioners should be aware of the prevalence of such
behaviours and actions and be prepared to raise con-
cerns when it is believed any form of ill-treatment or tor-
ture has occurred.
Definitions
The International Committee of the Red Cross provides
definitions for torture and other forms of ill-treatment
which are shown in Table 20.1.
Investigation
The investigation of possible ill-treatment and torture,
once initiated, may be undertaken in a number of ways.
This will depend on whether the incidents appear to be
single events (perhaps a single gaoler being violent to
detainees or withholding food and water) or apparent
systematic abuses, at the behest of state institutions
or the state itself. Such behaviours may occur in any
site of detention. Who to raise such issues with will
depend on the nature of the detention, and whether
any independent body or organisation has oversight
for complaints. In England & Wales, complaints about
police custody may be referred to the Independent
Office for Police Conduct (IOPC) and for prisons, to the
Prison & Probation Ombudsman. Such bodies work in
an open and transparent manner, publishing reports
of their findings in the public domain. Not all jurisdic-
tions have independent investigatory bodies, and non-
governmental organisations such as the International
Committee of the Red Cross, Amnesty International
or Reprieve may become involved (Table 20.1). Many
▪▪ The Istanbul Protocol
▪▪ Bibliography and information sources
▪▪ Further general resources
countries have independent human rights organisa-
tions who will address concerns, often at substantial
personal risk to the members of those organisations.
The Istanbul Protocol
The Manual on Effective Investigation and
Documentation of Torture and Other Cruel, Inhuman
or Degrading Treatment or Punishment (commonly
known as the Istanbul Protocol) outlines international,
legal standards on protection against torture and sets
out specific guidelines on how effective legal and medi-
cal investigations into allegations of torture should be
conducted. It was adopted by the United Nations in 1999
and has been revised with an updated version being
published in 2020. It is authoritative but non-binding,
and identifies existing obligations of states under inter-
national treaties and international law, and assists
states in properly implementing relevant standards.
The Istanbul Protocol provides common, international
guidelines for the assessment of persons who allege tor-
ture and ill-treatment, for investigating cases of alleged
torture, and for reporting such findings to the relevant
court or investigating body.
The Protocol covers a range of topics including:
• Relevant international legal standards
• Relevant Ethical Codes
• Legal Investigation of Torture
• General Considerations for Interviews
• Physical Evidence of Torture
• Psychological Evidence of Torture
It is the assessment of physical evidence of torture (and
to a lesser degree, the psychological evidence) which is of
key relevance to forensic medicine. The Protocol identi-
fies procedures for a torture investigation including how
to interview the alleged victim and other witnesses, selec-
tion of the investigator, how to secure and obtain physical
evidence, and detailed guidelines on how to establish a
special independent commission of inquiry to investi-
gate alleged torture and ill-treatment. The manual also
includes comprehensive guidelines for clinical exami-
nations to detect physical and psychological evidence of
torture and ill-treatment.
272 Torture and cruel, inhuman and degrading treatment

Chapter V of the Istanbul Protocol describes the key

Table 20.1 International Committee of the Red Cross
features and the order in which they should be carried
definitions of torture and other forms of ill-treatment
out. These are shown in Table 20.3.
• Torture consists of severe pain or suffering, whether Only those relevant elements of the assessment need
physical or mental, inflicted for such purposes as to be undertaken but it is essential that any practitioner
obtaining information or a confession, exerting undertaking the assessment is familiar with the nature,
pressure, intimidation or humiliation.
• Cruel or inhuman (synonymous terms) treatment
consists of acts which cause serious pain or Table 20.3 Istanbul Protocol: Medical Evaluation
suffering, whether physical or mental, or which for the Physical Evidence of Torture
constitute a serious outrage upon individual dignity.
A. Interview structure
Unlike torture, these acts do not need to be
B. Medical history
committed for a specific purpose.
1. Acute symptoms
• Humiliating or degrading (synonymous terms)
2. Chronic symptoms
treatment consists of acts which cause real and serious
3. Summary of interview
humiliation or a serious outrage upon human dignity,
C. Physical examination
and whose intensity is such that any reasonable
1. Skin
person would feel outraged; Ill-treatment is not a legal
2. Face
term, but it covers all the above-mentioned acts.
3. Chest and abdomen
4. Musculoskeletal system
Clinical examination 5. Genitourinary system
6. Central & peripheral nervous systems
The clinical examination to detect physical evidence of
D. Examination and evaluation following specific
torture follows a systematic pattern broadly recogni-
forms of torture
sable to most healthcare professionals, namely history,
1. Beatings and other forms of blunt trauma
examination, diagnosis, interpretation and manage-
• Skin damage
ment. Table 20.2 lists the elements to consider in a medi-
• Fractures
cal evaluation under the Protocol.
• Head trauma
• Chest and abdominal trauma
Table 20.2 Istanbul Protocol: Guidelines for the 2. Beatings of the feet
medical evaluation of torture and ill-treatment • Closed compartment syndrome
• Crushed heel and anterior footpads
Possible considerations for evaluations
• Rigid and irregular scars
I Case information • Rupture of the plantar aponeurosis
II Clinician’s qualifications and tendons
• Plantar fasciitis
III Statement regarding veracity of testimony 3. Suspension
IV Background information • Cross suspension
V Allegations of torture and ill-treatment • Butchery suspension
VI Physical symptoms and disabilities • Reverse butchery suspension
VII Physical examination • ‘Palestinian’ suspension
• ‘Parrot perch’ suspension
VIII Psychological history/examination
4. Other positional torture
IX Photographs 5. Electric shock torture
X Diagnostic test results 6. Dental torture
XI Consultations 7. Asphyxiation
XII Interpretation of findings 8. Sexual torture including rape
XIII Conclusions and recommendations • Review of symptoms
• Examination following a recent assault
XIV Statement of truthfulness
• Examination after the immediate phase
XV Statement of restrictions on the medical • Follow-up
evaluation/investigation (for subjects in custody) • Genital examination of women
XVI Clinician’s signature, date, place • Genital examination of men
XVII Relevant annexes (e.g., clinician’s CV, images, • Examination of the anal region
body diagrams, test results) E. Specialised diagnostic tests
 The Istanbul Protocol 273

and effects, of different types of torture. Interpretation of so (see also Chapter 17). It is also essential to distinguish
findings must be balanced and non-biased, and requires between acute (recent) injury and old injury which may
appropriate knowledge of published information which be manifest as marks or scars, and to distinguish between
should be interpreted critically in the light of documented injury, marks and scars that are due to ill-treatment,
findings. Numerous publications have explored the and those that are caused by other factors (e.g., culture,
nature and patterns of ill-treatment and torture, allow- employment, sports and accident). The phrase ‘absence
ing regional and geographical differences to be reviewed. of visible evidence of maltreatment is not evidence of
Many m ­ ethods of ill-treatment and torture methods absence of maltreatment’ is appropriate, which is why
(including sensory deprivation – isolation/blindfolding, the assessment must be as thorough and complete as the
beating – fists, sticks, truncheons, whipping – electric circumstances allow. Figures 20.1–20.5 provides some
cords, rape, suspension, falaka, electric shocks, sharp example of visible evidence of maltreatment or torture
force injury, burning) are used. The objective interpreta- (see also Chapter 8).
tion of findings is crucial, to best assist the complainant
of ill-treatment, so that the evidence is accepted as being
accurate by whichever body (e.g., prison, court, tribunal,
judge) is going to rely on it in their deliberations. This is
important because, although the accounts for marks or
scars given by victims may be true, they can sometimes
be false. If false, this may be as a result of an intention to
mislead the examiner and courts, poor recall, or misin-
terpretation due a variety of causes (e.g., mental health
issues). The body adjudicating on the medical assessment
will find it easier to accept findings and conclusions if the
examiner is clearly seen to be independent and unbiased.
The methods used may leave minimal or no evidence, Figure 20.2 Amputation of digit (right thumb). Note neat
and any injuries that are produced may heal without scars ­suggesting involvement of someone with medical
visible evidence. This has particular relevance to sexual skills.
assault, where penetrative sexual contact only has vis-
ible evidence in a minority of cases, and that acute injury
(whether to anus or vagina) often heals within 72 hours or

Figure 20.3 Disruption of shoulder joint complex

­secondary to prolonged suspension by arms.

Figure 20.1 Multiple tramline bruises from whipping Figure 20.4 Scarring to penile shaft from cigarette
with an electrical cable. burns.
274 Torture and cruel, inhuman and degrading treatment
Figure 20.5 Deformity of left elbow following fracture
dislocation during restraint.
Table 20.4 Level of Consistency of Injuries, Marks
or Scars with the Trauma Described (each individual
injury, mark or scar needs to be considered in the
context of each of these levels of consistency)
Not consistent Could not have been caused by
the trauma described.
Consistent with The lesion could have been
caused by the trauma describe
but it is non-specific and there
are many other possible causes.
Highly consistent The lesion could have been
caused by the trauma described,
and there are few other possible
causes.
Typical of This is an appearance that is
usually found with this type of
trauma.
Diagnostic of This appearance could not have
been caused in any way other
than that described.
Interpretation
The Istanbul Protocol provides guidance to describe
injuries and findings and their relationship to the physi-
cal trauma(s) described (see Table 20.4).
Cruel, inhuman and degrading treatment and tor-
ture occur to a greater or lesser degree in countries
around the world. Few, if any, countries are spared.
The differences may be that in some countries the
treatment or torture is state-sanctioned. The role of
the forensic practitioner is to identify and document
such events, and raise the issues with those in a posi-
tion to take action, so that sanctions can be appropri-
ately applied. Additionally, the practitioner should be
aware of where to refer the victim of such treatment, in
order to assist their physical and psychological reha-
bilitation as required. The Faculty of Forensic & Legal
Medicine has published Quality Standards for health-
care professionals working with victims of torture in
detention.
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Thomsen AB, Eriksen J, Smidt-Nielsen K. Chronic pain in torture
survivors. Forensic Sci Int 2000;108:155–163.
Torp-Pedersen S, Matteoli S, Wilhjelm J, et al. Diagnostic accuracy
of heel pad palpation: a phantom study. J Forensic Leg Med
2008;15:437–442.
Tsai AC, Eisa MA, Crosby S, et al. Medical evidence of torture
and other human rights violations in Darfur. PLoS Med
2012;9(4):e1001198.
United Nations. Istanbul Protocol: Manual of the effective investiga-
tion and documentation of torture and other cruel, inhuman or
degrading treatment or punishment, 2004. https://www.ohchr.
org/Documents/Publications/training8Rev1en.pdf
Unuvar U, Ulas H, Fincanci SK. Diagnosis of torture after 32 years:
assessment of three alleged torture victims during the 1980
military coup in Turkey. Forensic Sci Int 2014;244:e42–47.
Wenzel T, Mirzaei S, Nowak M. Assessment of sequelae of torture
for refugees in host countries. Lancet 2016;387(10020):746.
Williams A de, Pena CR, Rice ASC. Persistent pain in survivors
of torture: a cohort study. J Pain Symptom Manage 2010;40:
715–722.
Further general resources
Payne-James JJ, Beynon J, Nuno Vieira D. Monitoring Detention,
Custody, Torture and Ill-treatment: A Practical Approach to
Prevention and Documentation. Boca Raton: CRC Press; 2017.
21 Principles of forensic
­science and crime scene
investigation
▪▪ What is forensic science?
▪▪ Locard’s exchange principle
▪▪ Scene examination
▪▪ Evidence recovery
▪▪ Chain of custody
▪▪ Sample analysis
What is forensic science?
‘Forensic science’ is a description of the application of
any science to matters of legal interest, which Professor
Jim Fraser of Strathclyde University views as ‘the investi-
gation, explanation, and evaluation of events of legal rel-
evance including the identity, origin, and life of humans,
materials (e.g., paints, plastics), substances (e.g., drugs
and poisons), and artefacts (e.g., clothing, shoes). This is
done using scientific techniques or methodologies which
allow us to describe, infer, and reconstruct events.’ It has
also been described as the science of associating people,
places and things involved in criminal activities.
Whether forensic science is a science at all has been
debated for many years, with some commentators
arguing that it is a science founded on two fundamen-
tal principles (or laws): the principle of individuality, or
uniqueness, named after the American criminalist Paul
Kirk (1902–1970), and Locard’s ‘exchange principle’.
Locard’s exchange principle
Much of the work of forensic practitioners is based on the
principle described by Edmond Locard (1877–1966) who
was director of the crime laboratory in Lyon, France.
This principle (also known as Locard’s theory) – in sim-
ple form ‘every contact leaves a trace’ – provides a basis
for the recovery and interpretation of evidence (see Box
21.1). When applied to a criminal setting it states that if
a perpetrator of a crime comes into contact with a scene
(or someone within that scene), then something will be
brought into the scene, and something will be taken
away. It is for the forensic practitioner to identify what
those types of contact were by identifying the contact
and putting it into an evidentially-sound format.
The principle can be applied in all settings, for exam-
ple, by linking a suspect’s DNA to seminal fluid obtained
from a complainant’s vagina, by identifying paint from
a car that has hit an object, or by identifying hair from a
balaclava used in an armed robbery.
▪▪ Blood pattern analysis
▪▪ Damage assessment
▪▪ Fingerprints
▪▪ Footwear
▪▪ Trace evidence
▪▪ Bibliography and information sources
The public appetite for forensic science-orientated
entertainment, and general interest in ‘all things foren-
sic’ has raised awareness of the role of forensic science in
the criminal justice system, but there is increasing con-
cern among its practitioners that broadcast series and
dramas have raised unrealistic expectations about what
can and cannot be achieved in real life (see Box 21.2).
Scene examination
The principles of establishing, managing and investigat-
ing a crime scene should be similar worldwide. The aim
is to secure, identify and preserve evidence that may
have value in a subsequent court setting.
A crime scene is an entity which is created when
police cordon off an area of interest in relation to an
actual or a suspected offence (Figure 21.1). A zone is
cordoned off, within which all people accessing or leav-
ing are entered into (and have to sign) a ‘scene log’. As
such, this provides information as to who has had access
to evidence that could have a bearing on the outcome
of a case. The scene will be guarded by police or other
security personnel. This can be a significant commit-
ment of staff when areas are extensive and the manage-
ment of personnel is crucial to ensure expeditious and
cost-effective progress.
In the UK, a crime scene manager (CSM) is in over-
all charge of the scene and controls the personnel that
assist in the examination. The CSM acts as liaison with
the Senior Investigating Officer (SIO) as to examination
strategy depending on the demands of the enquiry. The
CSM and their staff are most often civilian across UK
police forces but there are some areas where the Scene
of Crime Officers (SOCOs), or Crime Scene Investigators
(CISs), are still serving police officers. It is usually the
CSM who is the point of contact for all those examining
the scene as the SIO has overall management responsi-
bility for the case to be taken forward.
At larger incidents, it is likely that a CSM, SOCOs/CSIs,
exhibits officer and photographers would be present. If

Box 21.1 Locard’s exchange principle
‘The truth is that none can act with the inten-
sity induced by criminal activities without
leaving multiple traces of his passing. […] The
clues I want to speak of here are of two kinds:
Sometimes the perpetrator leaves traces at
a scene by his actions; sometimes, alterna-
tively, he picked up on his clothes or his body
traces of his location or presence.’*
‘Wherever he steps, wherever he touches,
whatever he leaves, even without conscious-
ness, will serve as a silent witness against him.
Not only his fingerprints or his footprints, but
his hair, the fibers from his clothes, the glass
he breaks, the tool mark he leaves, the paint
he scratches, the blood or semen he deposits
or collects. All of these and more, bear mute
witness against him. This is evidence that does
not forget. It is not confused by the excite-
ment of the moment. It is not absent because
human witnesses are. It is factual evidence.
Physical evidence cannot be wrong, it cannot
perjure itself, it cannot be wholly absent. Only
human failure to find it, study and understand
it, can diminish its value.’†
* Translated from Locard E. L’enquête criminelle et les
methods scientifiques. Paris: Flammarion, 1920, in Crispino
F, Ribaux O, Houck M, Margot P. Forensic science: A true
science? Aus J Forensic Sci 2011; 43:157–176.
†    K irk P.L. Crime Investigation: physical evidence and the police
laboratory. New York: Interscience Publishers Inc, 1953.
it is deemed necessary, other specialists such as foren-
sic pathologists or forensic physicians and various other
forensic specialists (e.g., a blood pattern interpretation
expert) may also be in attendance.
Before entering the crime scene, a briefing is usu-
ally conducted when the facts, as they are known, are
presented to parties who will be conducting the initial
examinations. Once an examination strategy is decided,
the evidence collection can commence. The importance
of these briefings cannot be overstated as they ensure an
efficient approach with evidence maximised.
Within a crime scene, certain precautions need to be
taken to ensure that contamination is not introduced
(either from investigator-to-scene or scene-to-investi-
gator). Wearing overalls, gloves, overshoes and masks
ensures that the minimum, if any, cross-contamination
will occur. It is best to avoid touching anything if at
all possible, as all surfaces can harbour evidence. For
example, light switches or door handles may be of inter-
est for DNA or fingerprints. Wall or door jambs may be
useful for fingerprints so should not be leant on. Staff
Scene examination 277
Box 21.2 Does the ‘CSI effect’ exist?
The American TV crime drama ‘CSI: Crime Scene
Investigation’ aired in the USA for the first time in
2000, and became popular worldwide. The portrayal
of forensic science and forensic scientists was highly
stylised for dramatic effect; forensic science was the
‘star of the show’. Soon after its appearance, how-
ever, the media started to refer to the ‘CSI effect’ to
describe the alleged adverse effects of the portrayal
of forensic science in the drama on the expecta-
tions of jurors in the criminal justice system, which
favoured defendants in cases where forensic evi-
dence was absent, or where there were uncertainties
or ambiguities in the forensic evidence presented
to them. Although some commentators question
whether the ‘CSI effect’ is real, the potential effect of
misrepresentation of forensic science in the popu-
lar media has important implications for the way in
which the forensic science community in general,
and forensic practitioners individually, communicate
the utility, reliability and limitations of forensic evi-
dence in legal proceedings.
Figure 21.1 Crime scene cordon. Deceased found by
motorway, in vegetation. Tape represents police line
beyond which entry, exit and activity is controlled and
maintained in detail. (Courtesy of Manlove Forensics Ltd.)
examining scenes may have to move across the floor on
stepping plates as there may be footwear (or other) evi-
dence that still needs to be recovered.
Generally speaking, if there are human remains at
crime scenes, examinations are focused on the immedi-
ate area around the remains so that they can be removed
for a post mortem examination. The reason for this is
simple; remains are prone to rapid changes, especially
during the first few weeks of decomposition, making evi-
dence recovery by both scientists and pathologists more
challenging. Careful observation at a scene is required
in order to recognise human remains altered by fire or
deliberate modification (including by chemicals, as illus-
trated by the case of the ‘acid bath murders’ in Box 21.3).
278 Principles of forensic ­science and crime scene investigation

Once evidence gathering by SOCOs/CSIs and scien-

tists is complete, other searches can take place. These
are the ‘fingertip’ searches carried out by Police Search
Advisory (POLSA) staff. Following this examination, the
scene can be closed down. In the case of premises, they
may remain in police possession but be made secure
and alarmed, or in the case of external areas, the cordon
is removed and normal life resumes.

Evidence recovery
At a scene, however large or small, once items of forensic
interest are found, they are recorded appropriately and
assigned an affidavit or exhibit number. They are usually
given the initials of the person responsible for the item
being ‘seized’ (very often an exhibits officer) followed by
a sequential number, for example ‘JDM.1’. The item is
usually photographed before being removed carefully,
so as not to disturb the relevant evidence, and pack-
aged. There are a number of different types of packag-
Figure 21.2 Sealed and labelled weapon tube
ing that can be used for different items. Paper sacks are
­containing a bloodstained knife.
used for clothing because, if the item is slightly damp,
(Courtesy of Manlove Forensics Ltd.)
this allows moisture to pass through. Plastic bags can be
used for items such as cigarette ends. Plastic tubes that
item and the time and date of seizure. The label is then
screw together are used for sharp items such as knives or
signed by the person who seized the item (Figure 21.3).
screwdrivers; these are known as weapons tubes (Figure
See Box 21.4 to learn more about what the work of a
21.2). Cardboard boxes can also be used for such items
forensic scientist entails.
with plastic ties to secure the item in place.
If there is no exhibit label integral with the bag, a
separate label will need to be filled out and secured to Chain of custody
the packaging containing the item. This contains details Once an exhibit has been created, each time it is trans-
describing the item, its origin, the person seizing the ferred from one place to another the details need to be

Box 21.3 The discovery of modified human remains at a scene: The ‘acid bath
murders’
The complete disposal of a dead body, leaving no trace
for forensic experts to effect an identification of the
remains, has proved elusive for many murderers; Haigh
planned to evade justice for the murder of Olive Durand-
Deacon in 1949 by dissolving her body in sulphuric acid.
Examination of yellow, greasy sludge-soaked earth
from his workshop in Crawley, West Sussex, England,
revealed dentures, human gallstones, most of a left
foot, fragments of human bone, part of a plastic hand-
bag, and a lipstick case top.
At trial, the forensic pathologist, Keith Simpson,
stated that he considered that the human remains
belonged to a single person, and that a pelvic bone frag-
ment had female characteristics, the better-preserved
bones showed ‘senile change’, and that the bones were
of an ‘elderly woman’. The damage to the remains could
have been caused by immersion in sulphuric acid. He
could not determine cause of death. Mrs. Durand-
Deacon’s dentist confirmed that the dentures were hers.
Haigh told police ‘Mrs. Durand-Deacon no lon-
ger exists. She has disappeared completely, and no
trace of her can ever be found. I have destroyed her
with acid … how can you prove murder if there is no
body?’. He describes having shot her through the back
of the head – there were blood stains on a wall in the
workshop in keeping with the scenario – and putting
her body in a 40-gallon drum, returning over the fol-
lowing day to empty the drum’s contents outside the
workshop before adding more acid. He pleaded guilty
to murder but his defence was that he was insane at the
time of the killing. A psychiatrist called for the Defence
admitted that Haigh knew that what he did was pun-
ishable by law, and he was convicted and executed.**
Source: Simpson K. The acid-bath murder(s). R v John George
Haigh. The Police Journal 1950;23:190–202; Lord
Dunboyne. The trial of John George Haigh (The acid bath
murder). Notable British Trials Series. William Hodge & Co.
Ltd., London UK 1939 (138–140).

Figure 21.3 A typical exhibit label detailing the unique
item number, the item description, the details of where
the item was recovered, the time and date on which the
item was recovered and the details of the person who
recovered the item. (Courtesy of Manlove Forensics Ltd.)
Box 21.4 A typical day in the life of a senior forensic scientist in the UK
As a senior ‘reporting’ forensic biologist I manage
between 10 and 20 cases on a typical day, including
sexual assaults, homicide, assaults, and often a ‘cold
case’ where new techniques can be employed on
original exhibits/samples in order to detect a histori-
cal, unsolved crime. At any time during the day routine
work can be interrupted by requests to deliver urgent
reports, give advice or attend a scene or a court.
On any given day, the cases I am dealing with are
likely to be at different stages and require different
tasks to be undertaken at any time. One of the first
tasks of the day I undertake as a priority is to set a strat-
egy for any new case I am allocated. I receive a submis-
sion form from the police that gives a summary of the
circumstances surrounding an incident, a list of the
exhibits submitted and a request detailing what the
police aim to prove by the examination of the items
submitted. I review the information and the examina-
tion request and, if necessary, contact the police for
any further information or for additional exhibits that
I believe are necessary to undertake the examination
Sample analysis 279
recorded. This is the ‘chain of custody’. This is achieved by
using continuity forms which demonstrate that the exhibit
has been passed from one person to another. When an
exhibit is placed in a secure store, this fact is logged along
with the location of the exhibit so it can easily be relocated
when required. Each person who has examined the item
as part of their work signs the exhibit label to demonstrate
they have seen the item.
Once examinations of an exhibit have been con-
cluded, it is retained for a period of time before it is
destroyed or, on occasion, returned. This can be 3
months in more routine cases or at least 30 years in seri-
ous cases. Often, items are not destroyed as personnel
may realise that advances in technology could reveal
evidence that is not at that time apparent.
Sample analysis
DNA analysis
What is DNA profiling?
Within most cells in the body, there is a nucleus contain-
ing 23 pairs of chromosomes which package the double
helical structure of the DNA molecule. Normally, the
nucleus will consist of 22 autosomes and two sex chro-
mosomes; two Xs in females, and an X and a Y in males.
The DNA molecule is made up of a sugar-phosphate
backbone with four different attached nucleic acids
appropriately, and to ensure that a full interpretation
and evaluation of the findings can be undertaken in
due course.
Once the examination of the exhibits in a case has
begun, I view the items in question in conjunction
with the forensic examiner making the initial examina-
tion under my supervision. In a suspected homicide
this may require the examination of an exhibit, such
as a weapon or items of clothing, for the presence of
bloodstaining. A visual examination of the item is made
using varied light sources and, if necessary, low-power
microscopy in order to detect microscopic traces of
blood, supplemented by presumptive chemical testing
of stains of interest.
Depending on the case, some exhibits may require
an examination for the presence of hairs, saliva, fae-
ces or urine, and joint examinations may be necessary
where the presence of other types of trace evidence
requires consideration by another forensic specialist.
When the initial examinations have been under-
taken, I examine the items myself, and review and
(Continued)
280 Principles of forensic ­science and crime scene investigation
Box 21.4 (Continued) A typical day in the life of a senior forensic scientist in the UK
confirm the initial findings made by the forensic exam-
iner. I will then make key decisions to progress the
case, such as the selection of relevant blood/body fluid
stains for DNA profiling analysis, or the interpretation
of the nature and distribution of any blood present in
order to comment as to how the blood was deposited
on the item. For example, in a case where it is alleged a
person was kicked or stamped upon, I may be able to
comment as to whether the nature and distribution of
bloodstaining on an assailant’s footwear is indicative of
the wearer having kicked or stamped on an individual. I
may need to assess the presence of any textile damage
to a garment, for example, to determine if a garment
had been cut or torn, and I may have to establish if any
stab cuts are present and establish if a particular imple-
ment could have caused damage to a garment.
A great deal of time is spent reviewing analytical
results and compiling reports or statements for court,
as well as reviewing other scientists’ strategies, reports
and statements. Such peer review is essential for qual-
ity assurance purposes, and forms part of the formal
quality assurance system in which forensic scientists in
my organisation operate (including the accreditation
standards for laboratories – ISO 17025 – and for crime
scene ­investigation – ISO 17020).
Once all the examinations and analyses are com-
pleted in a case, I write an evidential statement or a
report detailing the findings and offer any interpreta-
tion if possible. Reports are initially sent to the police
informing them of the results obtained, however, if
the case proceeds to trial an evidential statement will
need to be provided, providing a full evaluation of the
findings, documenting the continuity of exhibits, and
containing explanations of the techniques employed in
the case. In some cases, the version of events given by
the victim and suspect may differ, and I may be able to
offer an opinion in my statement as to whether or not
the scientific findings offer scientific support in favour
of one of the versions of events over the other.
Every six weeks I will be on call 24 hours a day for
one week in order to respond immediately to any
request to attend a crime scene, which may be indoors
or outdoors. The request will usually require the inter-
pretation of bloodstain patterns at the scene in order
to shed light on the events that led to the death of
the individual(s) and to offer advice on the recovery of
trace evidence at the scene. Prior to entering the crime
scene, I will usually attend the police station where the
investigation is being run, and will be ‘briefed’ by the
police crime scene manager or the ­investigating officer
regarding the circumstances of the incident as known
at that time. Often the information provided at the
early stage of the investigation will be limited, and that
from witnesses may be incorrect, so keeping an open
mind when interpreting the scene is essential.
At many scenes involving the discovery of a body, I
will initially work closely with a Home Office Pathologist
and Crime Scene Investigators to ensure that relevant
trace evidence is recovered from the body, and that
any blood patterns are observed and documented
with the body in situ. Depending on the type of scene,
I may work closely with other experts. For instance, in
cases where an attempt has been made to conceal a
murder by setting fire to the scene, I will work closely
with the expert in fire investigation in order to examine
the scene in a coordinated, sequential manner so that
no potential evidence is compromised or overlooked.
On completion of the scene examination, I ‘debrief’
the crime scene manager and/or the investigating offi-
cer on my interpretation of the bloodstain patterns at
the scene, and offer advice as to which exhibits ought
to be submitted to the forensic science laboratory as a
priority to assist the investigation.
The police will normally submit key exhibits in rela-
tion to the scene to be examined immediately in order
to assist in the charging of a suspect or to identify an
assailant if the case is undetected. This will require the
examinations and any DNA profiling tests undertaken
to be completed within 48 hours of submission to the
laboratory. One of the most satisfying aspects of my job
is obtaining a DNA profile from a sample and obtain-
ing a match on the National DNA Database, allowing
the police to apprehend an assailant for a violent crime
who until then was unknown to the investigation.
Periodically, I am required to attend court to
give evidence in a trial, which involves travelling to
a court which is usually in the region in which the
crime occurred. When giving expert forensic science
evidence, I will be expected to explain complex scien-
tific methods and evidence in ‘layman’s terms’ to the
court, and I can expect to be subjected to cross exami-
nation by the defence in which I may have to consider
alternative hypotheses for my findings or robustly
defend my interpretation and conclusions.
Andrew Parry BSc (Hons)
Senior Reporting Forensic Scientist
Cellmark Forensic Services
Abingdon, UK
(http://www.cellmarkforensics.co.uk/)

that pair with a complementary chain to produce the
double helix. One chromosome of each pair is inherited
from the mother and the other from the father. DNA
is also present in mitochondria, which are organelles
located in the cell cytoplasm; this latter DNA is inherited
through the maternal lineage.
Currently, the most common type of DNA profiling
utilises the fact that there are short regions, normally
consisting of between three to five nucleotides in length,
repeated a variable number of times along a chromo-
some. These are called short-tandem repeats (STRs).
They are generally believed to be non-coding and are
conserved from generation to generation. The number of
repeats gives the name to the STR variant (the allele) on
the chromosome and varies between individuals. The
range of variation is relatively low and, individually,
each allele occurs quite commonly (generally between
5 per cent and 40 per cent of the population). A person
can have the same (homozygous) or different STR alleles
(heterozygous) at each region (locus) that is analysed.
The power of DNA analysis is realised when one con-
siders that currently sixteen different loci are analysed,
giving a total of 32 alleles plus an indication of the sex
of the individual in a collection referred to as DNA17.
How is a DNA profile obtained?
A sample that is taken for analysis undergoes several
steps before a DNA profile can be obtained. The first is
to extract the DNA from the cellular matrix. Different
chemical processes may need to be used in order to
recover the DNA: for example, a ground tooth would
receive very different treatment from that of a cigarette
end.
Following this, the amount of DNA within the sample
is estimated. In forensic samples, the concentration of
DNA is often very low and measured in nanograms per
microlitre (ng/µl). This stage is necessary so that the cor-
rect amount of the extracted sample is used for the next
stage (amplification) to ensure an optimum chemical
concentration for maximum sensitivity. The scientist
will normally amplify around 0.5 to 1 ng of the DNA
(aiming for a minimum of 0.2 ng, roughly the rough
equivalent of around 30 cells).
Amplification is carried out using the polymerase
chain reaction (PCR), which uses a thermostable enzyme-
catalysed reaction over a number of cycles in which the
double strands are separated to allow a complementary
strand to be produced and annealed. Each PCR cycle, if
it were 100 per cent efficient, would double the amount
of DNA present within each sample. Around 28 cycles
are used in a standard DNA17 analysis. A short comple-
mentary ‘primer’ labelled with an attached fluorescent
dye starts the process by annealing to the flanking region
of the STR and enables labelled copies of the STR to be
detected and its size measured.
Sample analysis 281
The loci that are amplified vary in the number of
repeats that are commonly encountered and so a range
in size and thus molecular weight exists. The sample is
subjected to capillary electrophoresis in a genetic analy-
ser across a high potential difference. This means that
the low molecular weight alleles pass through the cap-
illaries and are detected more rapidly than those of a
higher molecular weight. As each of the STR alleles have
been tagged with a fluorescent dye, they are detected
as they pass a laser detector. The time of detection,
calibrated against a molecular weight standard, and
the particular dye label enables a range of STRs to be
analysed in the same sample. As each allele passes the
laser, it registers as a peak in intensity of the fluorescent
dye. This is translated into an electropherogram (EPG)
which represents a DNA profile as a series of peaks along
a graphical line (Figure 21.4).
If a profile has been obtained from a crime scene
sample such as a blood stain, it can then be compared
with a reference sample, often a mouth (buccal) swab,
from an individual believed to be connected to the case,
or a match searched for on a DNA database. If DNA pro-
files do not match then they could not have come from
the same person. Conversely, if the crime scene profile
matches at every locus then the DNA could have come
from the reference person. Only identical twins would
share the same profile. If a large number of loci have one
or more alleles in common, however, then the analyst
may suspect that the profile comes from a close relative
of the identified individual instead.
Once a matching profile has been identified a statistic
can be provided as to the likelihood of the match in com-
parison with a hypothesised unrelated person. The more
incomplete a s­ ample profile is (a partial profile) the more
people may be expected to match by chance. The way in
which the statistics are calculated relies on an assump-
tion of independence between loci; most STRs are on dif-
ferent chromosomes or far enough apart to assume this.
This independence allows the frequency of the alleles
at each locus to be multiplied across all the loci. Even
if many of the individual matching alleles are common
in the population, the likelihood of some other person
providing the same profile decreases rapidly with each
added locus. It is estimated that the probability of any
other person unrelated to an identified person sharing
the same profile will be less than one in one ­billion.
Box 21.5 illustrates some significant historic cases in
which the use of DNA evidence was crucial.
DNA Statistics and Bayes Theorem
Discussion of DNA profiling inevitably involves terms such
as ‘likelihood of a match’, or ‘match probability’. These are
used in the expression of the strength of the evidence and
the methodology used relies on the use of Bayesian statis-
tics, methods that use the theories developed by Thomas
Bayes, an 18th-century clergyman. These differ from the
282 Principles of forensic ­science and crime scene investigation

Figure 21.4 DNA profile. (Courtesy of Professor Denise Syndercombe-Court.)

Box 21.5 Historic legal cases in which DNA evidence was significant

First UK criminal conviction utilising DNA evidence
In November 1987, Robert Melias was convicted in
Bristol, England for rape following comparison of his
DNA profile with that contained in a semen sample
recovered from the victim. He pleaded guilty and was
sentenced to eight years in prison.
First UK murder conviction utilising DNA evidence:
Colin Pitchfork
Following the rape and murder of a 15-year-old school-
girl, Dawn Ashworth, in Leicestershire in 1986 – less
than a mile from the discovery of the body of Linda
Mann, another 15-year-old schoolgirl in 1983 – a local
youth was arrested and charged with Dawn’s murder.
DNA analysis, however, showed that he could not
have been her assailant, and he was released. Police
invited all young men in the area to give blood sam-
ples for profiling, but screening of some 5 000 samples
failed to reveal a ‘match’.
A man was subsequently overheard in a public
house saying that he had ‘taken the place’ of a friend
during the screening; that man, Colin Pitchfork, was
arrested and a DNA profile of his blood matched that
of Dawn’s killer. He confessed to her murder and that of
Linda Mann, and was convicted in 1987.
First UK post-conviction exoneration utilising DNA
evidence
In 1988, Michael Shirley was convicted of the rape and
murder of Linda Cook; a semen sample was recovered
but was of insufficient volume to permit DNA profiling.
Low copy number DNA analysis was performed in
1999, the results of which were inconclusive. Further
work in 2001 revealed ‘foreign’ DNA bands that did not
match Shirley or Cook, and the Court of Appeal ruled
that his original conviction was unsafe. He was released
in 2003.

frequentist approach often encountered in scientific anal-
yses as they include a measure of subjectivity to assist in
determining the probability of an outcome. For example,
when undertaking a long series of experiments tossing a
coin, we expect that the frequency of getting a head would
be 50% (probability 0.5). If, however, the coin has a small
weight attached to one side this would tend to bias the out-
come. Bayes theorem offers a way to condition the prob-
ability to account for additional information. In its odds
form Bayes Theorem is more simply stated as:
Posterior odds = Likelihood ratio × Prior odds
in which the prior odds (belief that the frequency of get-
ting a head when tossing a coin is 50%) is multiplied by
the likelihood ratio. In terms of the coin throwing, the
likelihood ratio can be defined as:
Probability that the coin
is fair
Likelihood ratio =
Probability that the coin
is not fair
Bayesian inference is useful in forensic investiga-
tions because the likelihood ratio, which represents the
probability of the evidence under two propositions, is
provided as part of the investigation and we can use it
to update the prior odds at the time. In relation to DNA
evidence, if a single DNA profile from a crime scene
matches a given individual, one can assess the prob-
ability of the evidence given two hypotheses:
A. The DNA originated from that person
B. The DNA originated from another, random, unre-
lated person.
The probability of the outcome being true in regards to
hypothesis (A) is 1.0. Looking at the alternative hypoth-
esis (B), one has to consider a number of factors such as
the rarity of each allele and any potential knowledge of
Box 21.6 How do forensic scientists interpret forensic evidence?
The interpretation of forensic evidence is a broad and
sometimes complex subject, which usually relies upon
some form of expert opinion permissible in the adver-
sarial legal system in the UK.
Following several miscarriages of justice over the last
40 years or so, there has been a drive by forensic practi-
tioners and statisticians to introduce methods of inter-
pretation of evidence that are less subjective and more
objective. This is gradually being achieved by encour-
aging the use of databases, data from studies and sur-
veys, soft data (via the experience of the scientist) and
by using a framework from which the interpretation
Sample analysis 283
the ethnicity of the subject will be extremely low for a
full profile but will increase when the profile is incom-
plete (contains fewer loci available to match). The ratio
of the two probabilities, A and B, provides the likelihood
ratio. In Bayesian inference, this could be restated as:
Posterior odds
(of guilt after considering all the evidence)
= Genetic odds
(of getting a full matching profile)
× Non-genetic odds
(prior odds of guilt after considering
all the other evidence)
It is very important when considering DNA evidence
(and indeed other forensic evidence), that it is expressed
as the probability of the scientific evidence (E) given
two hypotheses put forward by the prosecution and the
defence (Hp or Hd) under consideration of the scientific evi-
dence. This is distinct from the probability of the hypoth-
esis given the evidence, which is the question addressed
by the jury, which considers all of the evidence. This high-
lights the danger of a jury considering the scientific evi-
dence alone, such as a piece of very strong DNA evidence,
without considering reasons for the DNA being present
that may not be associated with the crime. Presenting the
sometimes very persuasive scientific evidence in isolation
is called the ‘prosecutor’s fallacy’ or ‘transposing the con-
ditional’ where the relative positions of the conditional (|)
probability are more easily seen when the above equation
is represented in the formula:
p(Hp |E) p(E | Hp ) p(Hp )
= ×
p(Hd | E) p(E | Hd ) p(Hd )
See Box 21.6 for an exploration of how forensic scien-
tists interpret forensic evidence.
of evidence can be based. One such approach is via
the use of Case Assessment and Interpretation (CAI), a
phrase coined in the 1990s by Dr Ian Evett and co-work-
ers in the Forensic Science Service (FSS). CAI provides
a framework and methodical approach that can be
used for all evidence types by scientists in their chosen
fields of expertise. It incorporates the use of compet-
ing propositions and the evaluation of a likelihood ratio
(via the odds form of Bayes theorem) and, in addition,
the key process of case pre-assessment. In the labora-
tory environment, the scientist reviews the information
from the case circumstances and, items submitted and
(Continued)
284 Principles of forensic ­science and crime scene investigation
Box 21.6 (Continued) How do forensic scientists interpret forensic evidence?
makes an assessment as to the potential evidence that
may be recovered and, if so, what this may mean in the
context of the case scenario. It also prompts the scien-
tist to ask for further information or raise questions. It
is also at this stage that the scientist will identify one of
three routes the case may follow: factual (or technical),
investigative or evaluative.
Factual route: This is regarded as being a findings-
led process with mainly facts being communicated to
the courts and the police. There is only limited inter-
pretation which may involve calibration and frequen-
tist statistics. Typically, questions such as ‘how much
alcohol is present in the blood sample?’ or ‘how many
glass particles are there on the surface of the coat?’ fall
into this category.
Investigative route: There is some level of interpreta-
tion, which is based upon one or more scenarios and
questions posed by the police or courts. This route
tends to be followed by scientists in the laboratory and
scientists attending scenes when details about the case
circumstances are often scant. Generally, the interpre-
tation will involve generating one or more explanations
for the presence or absence of evidence based upon
what is known and found. For example: ‘one explana-
tion could be that the suspect smashed the window at
the scene’ or ‘another explanation is that the blood pat-
tern suggests that an offender attacked the victim with
a knife in the hallway of the premises’. Note: there are
no probabilities associated with explanations.
Evaluative route: This route can use both hard and
soft data and the evaluation of a likelihood ratio in
light of two competing (mutually exclusive) proposi-
tions, usually one for the prosecution and another for
the defence, which are formulated at the pre-assess-
ment stage of the case. Depending upon the evidence
involved and the case circumstances, a case that can be
evaluated falls into one of the following levels:
• Sub-source & Source: The evaluation is based upon
observations, measurements and analyses, includ-
ing reference to databases, such as the interpre-
tation of a DNA profile (sub-source). The finding
of saliva matching a particular individual may be
reported at source level as: ‘the findings provide
strong support for the proposition that the saliva
stain on the clothing originated from the suspect
rather than some unrelated individual’.
• Activity: This evaluation is based upon observa-
tions, measurements and analyses, and in addition
to source level, aspects of transfer and persistence,
distribution, numbers recovered and reference
to forensic studies. Typically, evidence has been
transferred following some activity. If the scientist
is able to address propositions at this level this will
provide more assistance to the police and to the
courts. Following on from the saliva evaluation at
source level, there may have been an allegation
that the suspect bit an individual’s arm. Assume
that a DNA profile matching the suspect has been
obtained from the stain on the arm and the sus-
pect has said he met the person in a night club,
then the scientist may evaluate the evidence as:
‘the findings provide strong support for the prop-
osition that the suspect bit the arm of the jacket
rather than via casual contact’.
• There is a third ‘offence’ level which should not be
addressed by the forensic scientist as this consid-
ers the nature of the offence itself and is for the
courts to consider.
The general benefits of CAI are well established and
documented. In essence it provides:
• Logic by using a framework of pre and post assess-
ment of the relevant circumstances.
• Balance via addressing competing propositions.
• Transparency by detailing how and why a conclu-
sion has been reached and what data have been
used.
• Robustness where the process allows for indepen-
dent scrutiny and challenge.
The evaluation of the findings is generally commu-
nicated on a scale of evidence. The most recognised is
that listed by European Network of Forensic Science
Institutes (ENFSI) and the Association of Forensic
Science Providers and has been used by most areas
of the UK forensic community for many years. The
scale runs from ‘no support for either proposition’ to
‘extremely strong support’ in favour of one or other of
the hypothesis considered.
Over the last few years, the topic of cognitive bias
in forensic science has become increasingly important,
and ways and means to minimise such effects are being
introduced. Cognitive bias is another broad subject
that can be sub-categorised in a number of other biases
and effects which can influence the expert (either con-
sciously or unconsciously) in arriving at an opinion or
conclusion. However, there are measures in place for
the practitioner based in the laboratory to follow so as
to minimise any potential risk. A guidance publication
by the Forensic Science Regulator (FSR-G-217 Cognitive
Bias Effects – relevant to forensic science examinations)
provides an important and useful resource.
Typically, the pre-assessment stage of a case, prior
to establishing if findings are present, can overcome
the temptation to tailor a conclusion to fit evidence
(Continued)

Box 21.6 (Continued) How do forensic scientists interpret forensic evidence?
recovered or not, but also what findings, if any, are
expected in light of the case scenario.
Other key measures highlighted in FSR-G-217 which
should be followed to minimise bias include:
• The communication of results should be clear and
unambiguous.
• The interpretation of the evidence should be
based upon a methodical approach and built on
principles that have been tested, validated and
transparent (such as CAI).
• Practitioners must be appropriately trained, expe-
rienced and continuously meet acceptable stan-
dards of competence in their field of expertise and
in interpretation of pertinent findings.
• All cases must undergo a full independent and
peer review of the findings and reinterpretation
by another competent scientist.
Mixed DNA results
A DNA profile can often be a mixture of DNA from more
than one person. This is very common, especially in
cases of sexual assault, and can lead to significant com-
plications in interpretation. If a case involves people
who are closely related this can also complicate analysis
as they are more likely to share alleles than unrelated
people. Different methods of looking at DNA mixtures
have come under significant scrutiny but guidance on
the use of probabilistic statistical approaches will assist
in removing interpretation bias.
Other forms of DNA analysis
The ability to get a DNA profile from very small
amounts (low-template DNA) of biological material
emphasises the need to reduce contamination risks
as far as possible and the laboratory environment and
procedures need to be designed and monitored with
this in mind. Historically, methods were employed to
increase the num­ber of amplification cycles – low copy
num­ber (LCN) – but these have been subject to legal
challenge and today the chemistries provided have
overcome most of these problems and full profiles can
be obtained from amounts as low as 0.125 ng (approxi-
mately 20 cells).
DNA profiling is often used to identify potential
individuals who have handled an item, depositing skin
cells or cell-free DNA (cfDNA), such as on a door handle,
for example. It can also be used to assist in the identi-
fication of wearers of garments such as gloves or hats
and shoes. In some instances, skin cells may be visible
Sample analysis 285
Whilst the scientist attending a scene does not
always have the same safeguards in place as work-
ing in the laboratory, it is recognised that the scien-
tist will only make a provisional interpretation in the
field and make it clear that any opinion or conclusion
may change as more information arises or changes.
The scientist will undergo a debriefing with another
competent scientist at the laboratory to discuss tests
performed, initial opinions, exhibits collected, etc. In
the majority of cases where a scientist has attended a
scene, the case will be followed up in the laboratory
and further examinations and test will be conducted
and one of the routes discussed followed accordingly.
Dr Tina Lovelock CChem FRSC MCSFS
Interpretation Lead, Chemistry Lead & Senior
Reporting Forensic Scientist at
Cellmark Forensic Services
Abingdon, UK
(http://www.cellmarkforensics.co.uk/)
microscopically, and sampling appropriately directed.
In other instances, a whole area may need to be specu-
latively swabbed.
The Y-STR DNA technique uses the same STR-based
technology as standard DNA profiling but looks at a
number of STRs on the Y-chromosome (i.e., only from
males). This can be extremely useful in cases of sexual
assault when amounts of male DNA are very low com-
pared with female within a sample and it is difficult to
separate the two. Results would be expected to be the
same in related males.
Mitochondrial DNA analysis can be used where
nuclear cellular material is low, for example, from hair
shafts or in cases where decomposition has meant that
much of the DNA that would have been used has degraded.
Mitochondrial DNA is in the form of a small circular mol-
ecule and, typically, there may be 1000 or more mitochon-
dria in the cytoplasm of a single cell. The analysis normally
involves sequencing the polymorphic control region. As
mitochondrial DNA is inherited from the mother (mater-
nal mitochondria in the egg outnumbers that present in
the fertilising sperm cell by at least 200 times), female
relatives and children from the same mother would be
expected to have the same mitochondrial DNA profile.
Single nucleotide polymorphisms (SNPs) are areas
where single base-pair variation occurs. As it looks at
such small areas, this can be used in cases where DNA
is severely degraded (e.g., by heat). This type of DNA
analysis was used to identify individuals from the World
Trade Centre in 2001. It has more recent forensic uses in
inferring visible traits (e.g., hair eye and skin colour) and
biogeographical ancestry.
286 Principles of forensic ­science and crime scene investigation
National DNA Database
The UK National DNA Database (NDNAD) is the oldest
DNA database in the world. It holds the details of people
arrested in connection with an arrestable offence under
the Police and Criminal Evidence Act 1984 as well as
data relating to crime stains for which there are no refer-
ence profiles. Crime scene samples are searched against
the database and compared with each other, nightly, in
order to identify whether or not there could be a match
to someone on the database, or a link to another crime.
It is highly efficient as around 10% of the population
(mostly young to middle-aged men) have their profiles
recorded on the database. Over 60% of cases in which a
DNA profile is obtained from the crime scene provides
a name to police. The power of the database also means
that there is a strong possibility that a familial link
would be uncovered but such searches require special
authorisation for privacy reasons and are limited to seri-
ous cases. Typically, there are under 20 such compari-
sons made annually.
There have been considerable concerns raised about
the NDNAD by many, including those with an interest
in civil liberties, about the appropriateness of retention
and the delay or absence of destruction of profiles. This
is especially with regards to those who never go to trial
for the allegation for which they were arrested, those
who are acquitted and the vulnerable, such as children.
The judgement in the case of S and Marper v UK (2008)
before the European Court of Human Rights, in which
the petitioners had requested that their DNA profiles
were removed from the NDNAD but were refused by
UK courts, led to the Protection of Freedoms Act (PoFA)
2012. This law ensures that samples are destroyed
within six months, and profiles from those who are
not convicted are held for a maximum of three years,
although there is special consideration in exceptional
circumstances, or if the individual is a minor.
Body fluid analysis
Forensic scientists will often be requested to conduct
searches for a number of biological fluids, including
blood, semen, saliva, urine, faeces and others in attempts
to identify individuals (and in some instances species)
who may have left the stains (using DNA analysis) as well
as interpreting them in the context of their location. Most
identifications are done through chemical tests but these
are done on samples that are distinct from the material
used for DNA and the link between body fluid and indi-
vidual cannot be made. Methods to co-extract DNA and
RNA from such samples can be used to provide a more
robust body fluid source identification and person associ-
ation: techniques include use of messenger RNA (mRNA),
micro RNA (miRNA), and epigenetic approaches, are
most commonly described and these techniques have
also been used to differentiate venous and menstrual
blood, for example.
Blood
The presence of blood is normally suggested by its colour
and the chemical reaction it gives when a presumptive
test is applied. Blood, however, does not always appear
as red/brown in colour and may have been diluted. This
can make it very challenging to locate stains, particu-
larly on a darker surface.
Stains that are to be tested are scraped with the edge
of a piece of folded sterile filter paper. The presumptive
tests used are generally leuco-malachite green (LMG)
or Kastle–Meyer (K-M). Both involve the addition of the
reduced form (colourless) of each reagent to the filter
paper followed a few seconds later by hydrogen perox-
ide. If a rapid colour change occurs after the addition of
both chemicals, and the colour of the scraping is typical
(green for LMG, pink for K-M) of a bloodstain, then the
presence of blood is indicated. The colour change occurs
as blood has a peroxidase-like activity due to haemoglo-
bin, which catalyses the oxidation of each chemical to
its coloured form.
When bloodstains cannot be seen, different methods
of detection can be used. For example, luminol, in solu-
tion, provides a blue chemiluminescent signal in the
presence of iron (present in haemoglobin) and provides
a very sensitive technique for latent bloodstains.
Semen
Human semen is made up of both a liquid and a cellu-
lar fraction in non-vasectomised post-pubescent males.
Semen is detected by forensic scientists using the acid
phosphatase (AP) test, as AP occurs in high levels in
human semen. When testing clothing or other larger
items, a press-test of filter paper onto a dampened item
suspected of bearing semen staining is used. The filter
paper is then removed and sprayed with the AP reagent.
If a purple colour develops, the presence of semen is
indicated (Figure 21.5). Bacterial infections can give
false reactions with AP reagent (a pinkish colour). False
positives can also occur from vaginal AP; however, gen-
erally only AP from semen produces the quick change to
a strong purple colour.
Semen is confirmed by locating the stained area on
the garment and extracting some of the stain before
making up a microscope slide containing some of the
extract. If spermatozoa are seen, the presence of semen
is confirmed.
If swabs are to be tested, they can also be pressed
onto a piece of filter paper before AP is applied or, alter-
natively, the swab can be extracted, the cellular frac-
tion spun down and a fraction of the liquid supernatant
tested instead to conserve cellular material. In a similar

Figure 21.5 A positive reaction result for acid
­ hosphatase (AP), indicating that semen could
p quantities of liquid supernatant can be added to a solu-
be ­present, after application of the AP reagent
­(photographed at two m ­ inutes after application).
(Courtesy of Manlove Forensics Ltd.)
manner, a microscope slide is made to search for sper-
matozoa.
It is important to note how much semen is found
on different swabs from different areas of the body, by
quantifying the number of sperm cells, as this can have
a bearing as to how recently semen was deposited.
It should be noted that in homes where adult male
clothing is washed with the rest of the laundry, sperm
cells found normally on underwear may be expected to
be transferred to other items within the wash. Washing
items will not remove all sperm cells from an area of
staining but will remove the chemical that will react with
AP reagent. Therefore, if looking for older stains, it can
be worthwhile examining significant exploratory areas
to look for sperm cells despite a negative AP reaction. In
such instances, it is best practice to analyse control areas
to demonstrate the absence of sperm cells elsewhere.
If a male has been vasectomised successfully, no
sperm cells should be present within an ejaculate. In
these cases, a second chemical test can be used for con-
firmation. Prostate specific antigen (PSA) found in semen
uses an antibody-based technique. The Florence Iodine
test to detect choline in seminal fluid can also be used in
which a small amount of the reagent is introduced to a
slide carrying some of the extracted stain. The iodine in
a potassium iodide solution is precipitated by the chemi-
cally basic choline forming characteristic brown crys-
tals, suggesting the presence of semen. However, this
method is not considered to be very sensitive and cau-
tion should be taken in the interpretation of the results.
Saliva
As saliva stains are usually translucent, a test used to
locate and identify such stains is very important. The
Blood pattern analysis 287
locator test detects the presence of amylase, an enzyme
found in high levels in human saliva. The most com-
monly used method for amylase is the Phadebas test
which can be used in two ways. It can be used in a press-
test whereby Phadebas paper is placed against the item
under test and wetted. If a uniform blue colour devel-
ops, the presence of amylase is confirmed. Depending
on the location and strength of the reaction, an opinion
can be given as to the presence of saliva. The areas giv-
ing positive chemical reactions can then be isolated and
submitted for DNA analysis. In cases where allegations
of kissing/licking/biting/sucking different parts of the
body have been made, this can be a very useful test to
employ.
The Phadebas test can also be used as a tube test
whereby stains/swabs are extracted and measured
tion of the test reagent. This method can be extremely
useful in cases where staining is suspected to be very
light as it is highly sensitive and easier to interpret than
the press-test method.
Care needs to be taken in the interpretation of
Phadebas results as other human body fluids such as
vaginal secretions, sweat and faeces can also contain
amylase, albeit usually at lower levels. It should also be
borne in mind that not all people secrete salivary amy-
lase; therefore, its absence does not mean that saliva was
not present.
Urine and faeces
On occasion, the presence of urine or faeces needs to be
confirmed, for example, from cases of alleged anal rape
or deliberate soiling of items. There is the simple method
of dampening and warming items with regard to each
body fluid, with the characteristic odour developing, or
one can use chemical tests, which are available for both
urine and faeces.
In the case of urine, tests such as the dimethy­
laminocinnamaldehyde (DMAC) test can be employed
to detect the presence of urea, a chemical constituent of
urine. Other tests can also be employed, for example, for
the chemical creatinine, another constituent of urine.
Both of these tests rely on colour changes to provide
positive results.
Stains suspected to be faecal in nature can be tested
using Edelman’s test, which detects the presence of uro-
bilinogen, a chemical constituent of faeces.
Blood pattern analysis
If an individual sustains an injury that bleeds, that
blood can be transferred to clothing, footwear and
surrounding objects and surfaces. Bloodstain pattern
analysis (BPA) can be used to assist the investigator
in a variety of ways. It may be possible to determine
288 Principles of forensic ­science and crime scene investigation

a sequence of events, the movement of people in the

course of an assault, a minimum number of blows, and
to comment on a possible weapon used to inflict injury.
It may also be possible to determine the location of an
attack site(s) using simple mathematics to determine
the point of origin of bloodstains.
The nature and distribution of the staining can vary
greatly, depending on several factors including:

• The type of blood vessel damaged

(a)
• The location of the damage (exposed or under
clothing)
• The mobility and actions of the injured individual
after receiving the injury

Bloodstain patterns are divided into a number of cat-

egories, from those that result in blood falling with grav-
ity, to contact stains, and those distributions that result
from forces being applied to the source of the blood (e.g.,
impact spatter or cast-off).

Downward drips
Downward drips are formed when blood falls from a
surface (such as the end of a finger) under the force of (b)
gravity. If they land on a flat surface, they will make a
characteristic circular stain, although if the surface is not
smooth (e.g., pavement) the stain can be quite distorted
(Figure 21.6).
If blood is dropped onto an absorbent surface such as
carpet, the stain can be much smaller while still being of
the same volume. If a number of drops fall onto the same
location, a distribution which could be confused with
a more active event is created as the blood makes con-
tact with other wet staining already present. The force of
the blood drops falling into wet blood that has already
fallen results in a number of smaller, satellite drops (c)
being projected away from the area of impact. Such sat- Figure 21.6 Blood dripped onto (a) painted metal,
ellite droplets can be projected for quite some distance (b) wood and (c) concrete.
from the centre of the distribution; this is dependent on (Courtesy of Manlove Forensics Ltd.)
the height from which the blood is falling, the texture
and absorbance of the surface and the amount of blood
already present.

Contact blood staining

Contact bloodstains are formed when a blood-stained
item comes into contact with another, non-stained
item (Figure 21.7). If a surface is moving when it comes
into contact with another surface, and one is blood-
stained, a blood smear will result. Contact smears
are divided into wipes and swipes. If a surface is con-
tacted, for example, by a bloodstained hand, the result-
ing stain is a swipe. Conversely, if a clean hand moves
through blood staining on a surface, the resulting stain
is termed a wipe. Figure 21.7 A contact bloodstain created by a
Other types of contact staining commonly encoun- ­bloodstained hand touching a wall.
tered are footwear marks and fingerprints left in blood. (Courtesy of Manlove Forensics Ltd.)

It can be a matter of great contention as to whether or not
a fingerprint was left by a bloodstained finger or whether
an impression was made by a finger into an existing wet
bloodstain. Scientifically, it can be very difficult to dis-
tinguish between the two alternatives.
In cases involving marks, there may be areas of the
mark that are so faint that they cannot be resolved by
the eye, or indeed the camera lens. Such marks require
enhancement and there are a variety of chemicals avail-
able that will effectively enhance marks in blood.
Impact spatter
When someone is struck in an area that bears wet blood
staining, the stains can be broken up and projected
away from the area of impact. The staining that results is
termed impact spatter and is characterised by a number
of different-sized blood stains on surrounding surfaces.
The greater the force that is applied the smaller the stains
tend to appear. If stains are projected in a perpendicu-
lar direction onto a surface, they will appear circular. If
there is an angle less than 90°, the stains become ellipti-
cal in shape and may have a characteristic tail, having
the appearance of an exclamation mark (Figure 21.8). By
careful measurement and the application of some simple
mathematics, it is possible to determine the angle of inci-
dence with the surface and thus the trajectory that the
drop of blood would have made. By measuring a num-
ber of different stains, it can be possible to locate an area
where the impact occurred.
The force made by the discharge of a firearm can
create bloodstains so small they are termed misting.
Such staining will travel forwards as well as backwards
towards the weapon if it is in close enough proximity to
the wound.
Coughing or sneezing may create patterns similar to
impact spatter if an individual has blood within their
airways. It may be possible to see some alteration of the
staining because of the mucus content of such stains but
care needs to be taken in interpretation.
Figure 21.8 A typical impact spatter pattern. The
source of wet blood was located at the centre
of the b
­ ottom edge of the picture.
(Courtesy of Manlove Forensics Ltd.)
Blood pattern analysis 289
Cast-off
Cast-off is formed when an item bearing blood staining is
moved through the air with sufficient force to drive blood
from its surface. For example, if an individual is repeat-
edly beaten with a baseball bat, blood may gather on the
face of the bat each time it is raised and lowered, and this
blood may be driven off by centrifugal forces. Such stain-
ing is often in a line, hence the common term ‘in-line’ cast-
off (Figure 21.9). Owing to the movement of the end of such
a weapon, the staining can form a figure of eight pattern.
Items such as knives and fists can also produce cast-off.
Arterial spurting
When an artery is damaged (e.g., by a knife or blunt
impact), blood is projected under high pressure, which
does not happen with venous bleeding (the venous
system being a low-pressure system). If the injury is
exposed, blood can be projected over some distance,
landing on adjacent surfaces. As a result of the quantity
of blood being expelled from the body, such staining can
be very heavy and will form a very characteristic pattern
of large stains and runs. There may also be a wave-like
pattern to the stains because the pressure with which
the blood is forced from the body reflects the pumping
action of the heart (Figure 21.10).
Physically altered blood stains
Bloodstains can be physically altered over time or by the
addition of other body fluids. This may mean that the
blood/admixture does not have the expected appear-
ance, or have the same physical properties as whole
blood. On occasion, injuries can be inflicted following
a gap in time after an initial assault and blood may have
begun to clot. Subsequent blows can result in unusual
stains being observed. These may be an admixture of
blood and mucus/saliva if injuries are to the facial area,
or other body fluids such as urine may affect the appear-
ance of blood staining (Figure 21.11).
Figure 21.9 Cast-off blood patterns created when a
baseball bat wet with blood was swung through the air.
(Courtesy of Manlove Forensics Ltd.)
290 Principles of forensic ­science and crime scene investigation
Figure 21.10 Projected blood pattern: arterial
spurt/gush. (Image copyright Forensic Science Service
[FSS]. Reproduced with permission.)
Figure 21.11 Blood mixed with another body fluid
­projected onto a wall. Note the dilute appearance.
(a)
Figure 21.12 (a) A section of carpet with no blood staining visible. (b) The same section treated with luminol,
­revealing superimposed hand and footwear marks.
Someone who has bled into their stomach may vomit
so-called ‘coffee grounds’, the appearance of such
‘altered blood’ being caused by the mixing of blood with
the acidic stomach contents.
Other body fluids may mimic blood; decomposition
fluid is often mistaken for evidence of a violent assault
where none has occurred.
Luminol
If attempts have been made to clean away blood staining,
the scientist can use chemical means to visualise stain-
ing that may have been present prior to those efforts.
The use of luminol, a highly sensitive chemiluminescent
compound, can help the scientist visualise where blood
staining had been present before any such cleaning
efforts. It should be noted that the carrier for this chemi-
cal is primarily water so its use should be one of the final
actions at a scene (Figure 21.12).
Damage assessment
When items are broken, it can be possible, by visual and
microscopic examination, to tell whether or not two or
more items are fragments of one original item; for exam-
ple, the two broken halves of a plate. This is achieved
by comparing gross features as well as finer details. The
more points of comparison that can be made, the stron-
ger the opinion that can be offered.
By examining the edges of, and fibre damage to,
clothing items that have been torn or cut, it may be
possible to comment on what type of damage actually
occurred, as in many cases where allegation of tearing
occurs, a cut has been used to start a tear. It is also pos-
sible to comment on how recently damage may have
occurred.
Using controlled tests and reconstructions, it is also
possible to comment on whether or not a specific item
or action caused an area of damage.
(b)

Fingerprints
Fingerprints are formed within the womb at approxi-
mately 12 weeks of gestation and, apart from damage
by environmental factors do not alter during one’s life-
time. There is some debate as to the purpose of these
ridges, with support for the notion that the presence
of fingerprints leads to an increase in grip, and/or
enhances the sensitivity for the perception of texture.
The overall nature of a fingerprint can be described in
terms of loops, whorls or arches, describing the overall
appearance of the pattern of ridges. On a smaller scale
the ridges themselves form the next level of detail within
the fingerprint; they can terminate or can divide into
two. These characteristics enable particular patterns
to be formed that are termed ridge ending, bifurcation,
short ridge, spur, dot, bridge, lake or delta. Furthermore,
the sweat glands on the ridges themselves give an addi-
tional area for comparison should this be required.
As there are sweat glands within the ridges, an
impression of these secretions can be left as a fingerprint
on a surface (latent marks). Such marks usually com-
prise a mixture of water-soluble and fat-soluble com-
pounds. As the fingerprint is made up of compounds
from the body, their chemical composition can reveal,
for example, that someone is a smoker or drug user. It
is often necessary to use specialised light, or chemical
enhancement, on fingerprints so that all available parts
of the mark can be seen. Different wavelengths of light,
and specialised chemicals, are used to enhance the dif-
ferent compounds within a fingerprint (Figure 21.13).
Fingerprints may also be left (patent marks) if
there is a contaminant such as ink, blood or paint – for
example, on the finger before it makes contact with a
surface. Another way of leaving a fingerprint is to make
(a) (b)
Figure 21.13 A fired shotgun cartridge: (a) untreated,
and (b) treated with cyanoacrylate (superglue) fumes,
revealing finger marks.
Footwear 291
Figure 21.14 A finger mark in blood left on the blade of
a knife. The finger was wet with blood prior to touching
the blade.
an impression into a surface, such as one coated with
grease or blood (Figure 21.14).
It is the theory that fingerprints are unique to each
person which enabled them to become one of the pri-
mary methods by which identifications of suspected
offenders were made. Fingerprints have been used for
many years to identify individuals and, for example,
have been known to confirm identity by the Chinese in
the 3rd century be.
Fingerprints were traditionally recorded from an
individual by coating their fingers with black ink and
rolling them onto a card form. A record of the palmprint
is now also taken. This ensures that all available detail
is recorded. While this method is still the main way by
which fingerprints are recorded, scanning machin-
ery is more commonly being used and, as technology
improves, will supersede the ink-based method.
Databases of fingerprints are held on a card-based
system using the ‘Tenprint’ forms used to take inked fin-
gerprints (Figure 21.15). In recent years, each individ-
ual’s ridge detail characteristics have also been loaded
onto computer-based searchable databases. In the
UK, this was initially NAFIS (the National Automated
Fingerprint Identification System) but this only held
data from England & Wales. IDENT1 now combines data
from England, Scotland and Wales allowing the search
of around 7 million records against marks (including
palm marks).
Footwear
Footwear marks
When people wearing footwear come into contact with
a surface, they often leave an impression. The extent to
which this occurs may depend on many factors, such as
how dirty the sole of the shoe is or the floor surface itself.
The resulting footwear impression can be photographed,
lifted using a variety of media, or it can be recovered
whole (marks on paper, for example) and submitted to a
laboratory for a suitable method of ­enhancement.
292 Principles of forensic ­science and crime scene investigation
Figure 21.15 Inked fingerprints used as exemplars for comparison.
There are many different methods of enhancing foot-
wear marks, some of which are used in the enhancement
of fingerprints. Often photographing under controlled-
lighting conditions, or the addition of specialist light
sources, can improve the detail within a mark. When
a mark warrants a more intensive examination (e.g., in
a serious assault) the enhancement may be carried out
using chemicals. For soil deposits, potassium or ammo-
nium thiocyanate can be used, which reacts with metal-
lic ions in the soil. Marks in blood may be enhanced
using Amido Black solution, which reacts with the pro-
teins in the blood. There are many other methods of
chemically enhancing marks.
To carry out a comparison of the recovered footwear
marks with a suspect shoe, a test impression of the sole
pattern is required. This can be prepared by brushing
the sole with aluminium or black powder, and then plac-
ing the shoe, sole-side down, onto adhesive plastic. The
plastic is then placed onto an acetate sheet and labelled
to identify the shoe and ensure the correct orientation
of the impression. This can then be laid over the photo-
graph of the mark recovered from the crime scene and a
comparison made between them.
When shoes are compared, various details are con-
sidered. As the footwear is worn, general wear charac-
teristics develop in the areas of the sole that come into
Figure 21.16 Recovered footwear mark showing d ­ amage
features. (Image copyright Napier Associates Ltd.
Reproduced with permission.)
contact with the ground. Damage detail in the form of
cuts and nicks may also be formed in a random fashion
on the sole of the footwear (Figure 21.16). Examination
of footwear involves comparing the sole pattern, size
and degree of wear in the mark found at a scene, with
a test mark made from an item of footwear. If damage
detail is present in the scene mark, and it corresponds
with damage in the test mark, it is sometimes possible to
state conclusively that a mark left at the scene was made
by a particular shoe, and by no other.
When determining the size of a sole pattern, it is not
usually possible to establish the exact shoesize, because
of the many variations in sole patterns of a particular
model distributed throughout the population. It is pref-
erable to estimate the size of a shoe from its sole pattern
by giving a range of sizes that the shoe could be. This
allows for variation in sole pattern between different
moulds, and manufacturers.
Footwear marks and skin
When contact is made with a person with sufficient
force, by kicking or stamping, skin deposits may be
transferred to the inner surface of clothing while next
to the skin. Such deposits may require specialist light
sources, and chemical treatment, to increase the con-
trast between the mark and the background, and allow
effective photographic recording.
When forceful contact is made directly to the surface
of the skin, it is possible for a patterned injury to be left
on the skin, forming a mark which may be characteris-
tic of the surface that made the contact. In the case of
shoe marks, the surface is often made up of regularly-
spaced components that may leave a patterned injury
which corresponds with the pattern of sole components.
The pressure exerted during such a forceful contact
may force blood in the surface of the skin into the gaps
between the sole pattern components, leaving what is
often referred to as a negative impression. Forceful con-
tact with skin that is close to a bone often results in a

patterned injury which bears a greater degree of detail.
However, as the surfaces (of the body and the patterned
surface of interest) are not flat, distortion can interfere
with visual comparison techniques, including those
relying on photographic ‘overlays’ between scaled pho-
tographs of the patterned injury and patterned surfaces
of interest. Photographic overlay techniques can be
used to determine comparisons.
Trace evidence
This type of evidence can include anything that has
been transferred by means such as contact with a sur-
face or a person and this is the practical application of
Locard’s exchange principle. Often the material is very
small and requires microscopic examination. Organic
material such as pollen can be considered as trace evi-
dence but more often it involves man-made materials
such as glass, paint and fibres.
Glass
Glass is manufactured for use in construction by float-
ing it on the surface of molten tin. This produces a glass
that is very flat and can be mass-produced. A mixture of
silicon and various other minerals is added to a furnace
and then poured onto the molten tin. Glass can also be
moulded into containers or pressed into sheets with pat-
terns. When glass is broken, small fragments are show-
ered into the surrounding area. If a person were near
to the breaking glass it would be expected that some of
these fragments would transfer to the individual. These
fragments will remain on the individual’s clothing until
such time that they fall off. The length of time that these
glass fragments remain on clothing depends on many
factors, such as the type of clothing, and the activity of
the individual.
Glass fragments recovered in the laboratory, or from
assault victims and suspects, can be compared with
another source of glass by various means, including the
measurement of their refractive index and their chemi-
cal composition.
Paint
There are many varieties of paint for many different
uses. If damage is caused to a painted surface, small
flakes can be transferred. In road traffic collisions, for
example, there may be a two-way transfer of material.
Once recovered, paint evidence is examined microscop-
ically to identify it, and determine whether it is made up
from different layers of paint. Each type of paint may be
discriminated by its colour, texture and composition.
Various light sources may be used to distinguish differ-
ent types of paint, or the components can be identified
using chemical tests and analytical techniques, such as
chromatography and spectrophotometry.
Bibliography and information sources 293
In cases where there are multiple layers of paint in
a sample, it may be possible to state that the evidential
sample came from a suspect car; however, it is often
used as corroborative evidence in a case. In graffiti cases
it is possible to recover microscopic particles of aero-
solised paints in colours that match the colours used in
a specific incident of vandalism.
Fibres
Clothing and soft-furnishings are made in a wide array
of fabrics that come from all manner of sources. Natural
fibres, such as wool, cotton and linen have been used for
centuries and they are often combined with man-made
fibres to improve their versatility. Within the types of
fibre used there may be many different dyes and other
materials incorporated into them which give different
properties to the finished garment. All of these charac-
teristics enable the forensic fibre examiner to identify
sources of fibres and compare them with fibres that
have been transferred to other garments or furnish-
ings. Identification of the fibres involves microscopic
and analytical techniques, and it is possible to use the
results in tandem with the number and location of the
recovered fibres to give an interpretation of the circum-
stances that caused the transfer to occur. For example,
it may be possible to state in which seat of a car a sus-
pect was sitting, so that their version of events of the
incident can be evaluated. It is sometimes possible to
find an original source of a fibre that is prevalent in a
case by going to manufacturers and obtaining details of
the amount and geographic distribution of a particular
product.
Bibliography and information
sources
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Bandelt H-J, Richards M, Macaulay V (eds). Human Mitochondrial
DNA and the Evolution of Homo Sapiens. Berlin-Heidelberg:
Springer-Verlag Press; 2006.
Barbasin M, Shewale JG. Assessment of DNA extracted from
forensic samples prior to genotyping. Forensic Sci Rev
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Butler JM. Fundamental of DNA separation and detection. In:
Butler J (ed). Fundamentals of Forensic DNA Typing. San Diego:
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Butler JM. Short tandem repeat typing technologies used
in human identification testing. BioTechniques 2007;43(4):
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analysis (Accessed 21 May 2019).
Crown Prosecution Service. DNA 17 profiling: legal guidance. Gov
UK. https://www.cps.gov.uk/legal-guidance/dna-17-profiling
(Accessed 21 May 2019).
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EuroForGen. Network of Excellence. Making Sense of Forensic
Genetics, 2017. https://www.euroforgen.eu/dissemination-
activities/making-sense-of-forensic-genetics/ (Accessed 21
May 2019).
Forensic Science Regulator. Guidance: DNA Mixture
Interpretation. FSR-G-222, Issue 2, 2018. https://www.gov.uk/
government/publications/dna-mixture-interpretation-fsr-
g-222 (Accessed 21 May 2019).
Forensic Science Regulator. Guidance: The Control and Avoidance
of Contamination in Crime Scene Examination involving
DNA Evidence Recovery FSR-G-206. Issue 1. https://www.
gov.uk/government/publications/­c rime-scene-dna-anti-
contamination-guidance (Accessed 21 May 2019).
Gelman A, Carlin JB, Stern HS, et al. Bayesian Data Analysis, 3rd ed.
London: Chapman and Hall/CRC; 2013.
Gill P. Application of low copy number DNA profiling. Croat Med
J 2001;52:229–232.
Green RL, Lagacé RE, Oldroyd NH, et al. Developmental validation
of the AmpFlSTR NGM Select PCR Amplification Kit: a next-
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Harbison S, Fleming R. Forensic body fluid identification: state of
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a state laboratory. J Forensic Sci 2009;54:95–102.
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1997;110:118–124.
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Sciences; 2018, 153–208.
22 Principles of toxicology
▪▪ Introduction
▪▪ Principles
▪▪ Definitions
▪▪ Testing matrices
Introduction
Drugs and alcohol influence lives in many ways. The
heroin- and crack-dependent intravenous drug user
arrested for robbery, the recreational cocaine user sus-
pended following drug screening at work, the student
arrested for driving under the influence of drugs and
alcohol, and the chronic alcoholic dying in police cus-
tody because of untreated alcohol withdrawal are all
examples of how drug abuse can have a huge impact
on individuals, and the people with whom they are
involved. In contrast, this impact may be low compared
with the number of cancer patients dying without
adequate pain relief because they have been adminis-
tered inadequate doses of analgesics as a result of their
physicians fearing legal proceedings against them.
Doctors treating patients dying of severe pain risk being
accused of illegal prescribing or, even more tragically,
being charged with euthanasia because post mortem
drug testing demonstrates blood concentrations said to
exceed the ‘therapeutic range’.
One of the key tasks faced by forensic practitioners
is to determine the role that a specific drug (or drugs)
played in instances of impairment and death. This
task is made complicated by a series of issues, many of
which arise simply because physicians, toxicologists
and lawmakers fail to understand the basic issues of
forensic science and the way these issues may interplay
in complex legal, clinical and pathological matters. As a
consequence, the interpretation of forensic evidence is
often based more on anecdote and intuition than on
controlled scientific studies. Inadequate or bad science
or the misinterpretation of established sciences can lead
to wrong legal decisions. The risk of faulty and unjust
verdicts or conclusions can only be reduced if the limita-
tions of the science are understood.
Stories of exotic poisonings give rise to plots that
fascinate television viewers but which, more often than
not, can pose vexing problems for forensic scientists.
Fortunately, they are uncommon. Detailed knowledge
of exotic poisons is a skill not much in demand today.
What is required is the ability to recognise (and man-
age) the common complications of commonly abused
▪▪ Specific testing matrices
▪▪ Interpretation
▪▪ Bibliography and information sources
drugs, such as stimulants, opiates, cannabinoids, hal-
lucinogens, solvents, some anaesthetics and some
prescription medications. The ability to measure drug
concentrations in any tissue has become ever more pre-
cise. The problem is to determine what those measure-
ments signify, and whether they are mainly of academic
rather than clinical or practical interest.
Principles
The term ‘toxic’ may be used in different ways. Some
use the term synonymously with ‘poisonous’, meaning
to imply that ingestion of a particular substance will
cause death. Others mean only to imply that some sort
of illness will result if the substance is ingested. The defi-
nition of ‘lethal dose’ is more precise, but now that the
molecular mechanisms of many poisons are known, the
relevance of this concept is not as important as it once
was. Drug sensitivity and resistance vary from indi-
vidual to individual (if for no reason other than their
size). Thus ‘lethal dose’ is said to represent the dose of
that drug at which all subjects given it will die, and that
dosage will be expressed in grams, micrograms or mil-
ligrams per kilogram.
The abbreviation LD50 specifies the dose at which
50% of those who take a particular dose will die. The
LD50 depends partly on the mode of drug administra-
tion, because the route of ingestion determines exactly
how much drug is ultimately absorbed into the system,
that is, the route of ingestion determines bioavailabil-
ity. A drug injected intravenously is 100% bioavailable
because the entire dose of drug enters the circulation.
The amount absorbed after oral ingestion is variable.
A 10 mg dose of morphine given intravenously would
be expected to result in a peak plasma concentration
of between 100 and 200 nanograms per mililitre. But if
that same amount were given by mouth the peak plasma
concentration would be only a fraction of that seen after
intravenous injection. Because of anatomic and meta-
bolic differences, the LD50 for any particular drug var-
ies from experimental animal to experimental animal,
and the results obtained from the study of experimen-
tal animals cannot be directly extrapolated to humans.
296 Principles of toxicology
The process of extrapolation from animals to humans
is so unreliable that courts in many different countries
have held that animal studies alone do not suffice to
prove causation in humans.
The issue of receptor physiology is extremely impor-
tant. Drugs exert their effects by binding with receptors.
How well a particular drug will bind to a receptor deter-
mines how effectively it will act (or how toxic it will be). It
does not help much to know that opiates bind to the mu
(µ) receptor. What matters is how effectively any partic-
ular opiate binds to the receptor, and receptor-binding
ability is altered by many factors. On a weight for weight
basis, oxycodone is many times more powerful than
morphine, simply because it is a better fit for the bind-
ing site on the µ receptor than is morphine. Receptors
are subject to mutation. More than 140 different muta-
tions have been identified within the µ receptor itself.
Mutations cause receptors to change shape. Structural
distortions of the receptor make some drugs fit better
while others fit worse. The actual result cannot be pre-
dicted without knowledge of the mutation and the struc-
ture of the receptor, but this knowledge is rarely, if ever,
available to forensic pathologists or forensic toxicolo-
gists as they have neither the facilities nor the budget
to study receptor or enzyme genetic composition. How
may this be important in clinical practice? An exam-
ple could be the patient who asks for a ‘stronger’ pain
medication not because he or she is a drug seeker, but
because they carry a mutation that prevents the current
pain reliever from binding normally to the µ receptor.
Definitions
Drug tolerance
Tolerance occurs after chronic exposure to a specific
drug. An individual is said to be tolerant when increas-
ingly large doses of the drug produce less and less effect.
One might suppose that the classic mechanisms of
receptor down-regulation and desensitisation explain
these phenomena, but they do not, and the reason why
tolerance occurs is not really understood. Extraordinary
degrees of tolerance can be attained. During the course
of drug administration, the effective dose of any par-
ticular drug can increase 100- to 1000-fold, and the
process may occur very rapidly: for example, cocaine
tolerance begins to emerge after the first dose of drug
is ­administered.
Substance dependence
Dependence is said to exist when an individual can-
not function normally in the absence of a specific drug.
Dependence goes hand in hand with tolerance as it
too is controlled, at least partly, by receptor distribu-
tion, density and genetic make-up. The Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition
Table 22.1 The DSM-V establishes nine types of
substance-related disorders
1. Alcohol
2. Caffeine
3. Cannabis (e.g., marijuana)
4. Hallucinogens
5. Inhalants
6. Opioid (e.g., heroin)
7. Sedatives, hypnotics, or anxiolytics (e.g., diazepam,
‘Quaaludes’)
8. Stimulants (cocaine, methamphetamine)
9. Tobacco
(DSM-V) is the most recent version of the American
Psychiatric Association’s standard text on the names,
symptoms and diagnostic features of every recognised
mental illness, including addictions. The DSM-V recog-
nises substance dependancies, and substance-related
disorders resulting from the use of different classes of
drugs (Table 22.1).
Although major grouping of psychoactive substances
are specifically identified, use of other or unknown sub-
stances additionally may form the basis of a substance
related or addictive disorder.
The DSM-V describes two types of disorders.
‘Substance use disorders’ are patterns of symptoms
resulting from use of a substance which the individual
continues to take, despite experiencing problems as a
result. The second type, ‘substance-induced disorders’,
are symptoms that may be caused directly by the drug
during or immediately after individual episodes of use.
Irrespective of the particular substance, the diagnosis
of a substance use disorder is based upon a pathological
set of behaviours related to the use of that substance.
These behaviours fall into four main categories:
1. Impaired control
2. Social impairment
3. Risky use
4. Pharmacological indicators (tolerance and with-
drawal)
The DSM-V allows clinicians to specify how severe
the substance use disorder is, depending on how many
symptoms are identified. ‘Mild’ severity – in the presence
of two or three symptoms; ‘moderate’ in the presence
of four or five symptoms and ‘severe’ with six or more
symptoms. These can further be classified as ‘in early
remission,’ ‘in sustained remission’, ‘on maintenance
therapy’ and ‘in a controlled environment’ (Table 22.2).
Social impairment may appear as individuals con-
tinue to use despite problems with work, school or
meeting family/social obligations. This may mani-
fest as repeated work absences, poor school perfor-
mance, neglect of children or failure to meet household

Table 22.2 The DSM-V: 11 different criteria for
substance misuse disorders
1. Taking the substance in larger amounts or for longer
than you meant to.
2. Wanting to cut down or stop using the substance
but not managing to.
3. Spending a lot of time getting, using, or recovering
from use of the substance.
4. Cravings and urges to use the substance.
5. Not managing to do what you should at work,
home or school, because of substance use.
6. Continuing to use, even when it causes problems in
relationships.
7. Giving up important social, occupational or
recreational activities because of substance use.
8. Using substances again and again, even when it
puts you in danger.
9. Continuing to use, even when you know you have a
physical or psychological problem that could have
been caused or made worse by the substance.
10. Needing more of the substance to get the effect
you want (tolerance).
11. Development of withdrawal symptoms, which can
be relieved by taking more of the substance.
responsibilities. Addiction may also be indicated when
someone continues substance use despite having inter-
personal problems because of it. Important and mean-
ingful social and recreational activities may be given up
or reduced because of substance use.
Risky use implies a failure to refrain from using the
substance despite the harm it causes, or repeatedly uses
substances in physically dangerous situations such as
while operating machinery or driving a car. Some will
continue to use addictive substances even though they
are aware it is causing or worsening physical and psy-
chological problems.
The presence of pharmacological indicators of tol-
erance refers to the adjustment the body makes as it
attempts to adapt to the continued and frequent use
of a substance. Tolerance occurs when people need to
increase the amount of a substance to achieve the same
desired effect. Specific drugs will vary in terms of how
quickly tolerance develops and the dose needed for tol-
erance to develop. Withdrawal is the body’s response
to the abrupt cessation of a drug, once the body has
developed a tolerance to it. The resulting cluster of (very
unpleasant and occasionally fatal) symptoms is specific
to each drug.
Drug idiosyncrasies
This term is used to describe unanticipated drug reac-
tions. For the most part these reactions are allergic in
nature. They fall into the category of hypersensitivity
Definitions 297
reactions, where an inappropriate and excessive reac-
tion to an allergen (such as pollen, dust, animal hair or
certain foods) causes symptoms. These symptoms may
range in severity from those of a mild allergic reaction
to anaphylactic shock. Pathologists have been debating
for more than half a century whether the pulmonary
oedema associated with heroin abuse might be a type
of hypersensitivity reaction, although this hypothesis
has never been convincingly proven.
Drug interactions
This term describes unanticipated symptoms and signs
that result after two or more different drugs have been
given. Interactions may be good or bad, depending on
which types of drugs are involved. Many permutations
are possible: a drug could interact with other drugs,
endogenous chemical agents, dietary components, or
chemicals used in, or resulting from, diagnostic tests
(such as a contrast medium used for angiography).
In recent years, the term drug interaction has come
to take on a completely new meaning for clinicians and
forensic scientists. If two drugs are both metabolised
by the same enzyme system, one may interfere with
the metabolism of the other. For example, two different
P450 hepatic enzymes (CYP3A and CYP2B6) metabolise
methadone. Methadone induces production of CYP3A,
so that abnormally low concentrations of carbamaze-
pine, which is also metabolised by that enzyme, might
unexpectedly result. However, if methadone is taken
with a drug that inhibits CYP3A, such as diltiazem (also
metabolised by CYP3A), methadone will not be metabo-
lised and concentrations will be unexpectedly high.
Until fairly recently, it was not generally recognised
that drugs could interact with the channels that control
electrical conduction in the myocardium. The shape of
the cardiac action potential is determined by the sequen-
tial opening and closing of dedicated channels within
the cell membrane of cardiomyocytes. These channels
conduct potassium, sodium and calcium. There are sev-
eral varieties of each channel, as well as many genetic
variations (genetic polymorphism). Some polymor-
phisms are harmless but others are not. If the channel
is sufficiently altered it may not function properly, pre-
venting normal ion conductance. The channel respon-
sible for most unexpected drug reactions (arrhythmias
and sudden death) is the one that conducts potassium
back into the cell after depolarisation (known as hERG,
or ‘slow repolarising potassium conductance channel’).
Drugs that combine with this channel can disrupt the
normal cycle of cardiac repolarisation, causing fatal
cardiac arrhythmias. Recently, it was discovered that
arsenic is an hERG channel poison, and it may well be
that an arsenic–hERG interaction was responsible for the
death of Emperor Napoleon. Unanticipated drug–hERG
interactions are the main reason for drug recalls in the
United States and Europe.
298 Principles of toxicology
Testing matrices
General principles
Drugs can reliably be detected and quantitated in any
tissue of the body. It is the interpretation of those quanti-
ties that is critical. Interpreting the significance of any
drug found is the major issue facing forensic practitio-
ners on a daily basis. Detection proves that ingestion,
or at least exposure, has taken place, but the mere pres-
ence of a drug, even in seemingly large quantities, says
nothing about toxicity and even less about intention
or motivation. Does it really matter whether urinary
cocaine metabolite concentrations exceed some speci-
fied range? It does not, unless the individual’s state of
hydration is known, as well as the specific gravity and
acidity of their urine, and usually this information is
rarely available in the forensic setting. No matter how
many decimal points are added to the results, specific
measurements have inherent limitations.
The effect of media stories regarding techniques for
forensic measurement and analysis (what can be termed
the ‘CSI effect’) can be pernicious. Many practitioners
believe (wrongly) that precise laboratory measurements
can supply information that could not have been gath-
ered by accurate history and scene investigation alone.
Each investigative modality has its contribution to make
to a forensic investigation. There are a number of mis-
understandings concerning toxicology, and failure to
consider them can lead to needless effort and expense,
not to mention an incorrect conclusion.
Suppose a left-handed heroin user is found dead with
a needle mark in his left antecubital fossa. Some might
take that as proof that another person administered the
injection, which would be likely. It would be an unnec-
essary waste of laboratory resources to measure drug
concentrations in the skin adjacent to an injection site
because, once a drug is injected into the blood stream,
it circulates throughout the body. Skin measurement
of drug concentrations would have meaning only if
concentration measurements were made of skin taken
from both sides of the body, and were found to be dif-
ferent. The same might be said for the value of vaginal,
rectal or nasal swabs. The route of administration can-
not be determined by measuring the drug concentra-
tion in those areas. The recovery of cocaine from the
vagina does not necessarily mean it was absorbed via
that route. It just means that the circulation persisted for
some time after drug use. That being the case, distribu-
tion of drug to nasal, rectal and vaginal mucosa would
be anticipated.
Analysis of drug paraphernalia may also be a poor use
of resources; unless the decedent was participating in a
needle-exchange programme, they may have reused the
syringe many times. Drugs will, no doubt, be detected in
the syringe, but whether their presence has anything to
do with the death being investigated is an open question.
It is not generally appreciated that the site where the
blood sample is collected at autopsy may well determine
the final analytical result. After death, concentrations of
weakly basic drugs (such as cocaine) are higher on the
left side of the heart than on the right, and concentra-
tions in the heart are higher than those in the leg. Drug
concentrations in blood collected from any tissue taken
at autopsy may, or may not, bear a reliable relationship
to concentrations that existed in life.
Regardless of whether the specimen is from the heart
or the leg, there is ample proof that post mortem drug
concentrations almost always exceed those measured
in the immediate ante mortem period. It follows that
autopsy blood measurements, taken in isolation, cannot
implicate any drug as a cause of death. Quantification
can only prove exposure or ingestion. The concept of
‘normal’ or ‘therapeutic’ drug concentration measure-
ments made in the living does not have any relevance
to the dead. It makes no sense to discuss therapeutic
drug concentration in cadavers: blood is a living tissue
and cadavers cannot be said to have blood, only reddish
clumped liquid that was once living blood.
Whether or not an individual dies from taking a
drug, often depends on the phenomenon of tolerance
(decreasing effect with increasing dose), but for all
intents and purposes, there is no effective way to mea-
sure tolerance after death. Thus, a laboratory result that
might seem to indicate a massive drug overdose could
merely be an incidental finding. The highest blood
cocaine level ever reported in a human was measured in
a man (>35,000 ng/mL) who had no physical complaint
other than the 45-calibre bullet that traversed his brain!
Often, it is sufficient just to demonstrate that a drug is
present. For example, was the rape complainant really a
victim of drug-facilitated assault, or was he/she a pro-
miscuous chronic drug abuser? Was the individual with
an unconfirmed urine test positive for opiates really a
drug abuser, or was he/she taking a cough medication
containing codeine? A simple way to help answer the
question is to take a hair sample. Drugs are stable in
hair for perpetuity. Prior drug use in an alleged rape
victim is easy enough to establish, simply by hair test-
ing. In the instance of the individual with the urine test
positive for opiates, the presence of other components
of cough syrup in their hair would probably yield a cor-
rect interpretation of the findings. There is not always
a need to test hair, but there is often a reason to collect
and store a sample, even if it is never analysed.
Specific testing matrices
Blood and urine
Blood is still the preferred testing matrix for drug
detection. It is always collected into a sodium fluoride-
containing tube (which prevents further drug degra-
dation). There are differences between pre- and post

mortem blood specimens. When blood is drawn in the
hospital, either for therapeutic drug monitoring or drug
detection, only the plasma is analysed. In death, con-
centrations in whole blood are measured. Drug con-
centrations, especially the concentration of alcohol, are
different in plasma and whole blood. Serum and plasma
contain 10–15% more water than whole blood. It follows
that plasma ethanol concentrations are 10–15% higher
than corresponding whole-blood concentrations. The
difference may seem small, but it is more than enough
to convict or exonerate a driver accused of driving under
the influence.
Urine was once the preferred specimen for post mor-
tem drug screening but, increasingly, blood samples are
considered a better testing matrix. Advances in technol-
ogy have substantially reduced the costs of gas chroma-
tography/mass spectrometry (GC/MS), and screening
whole blood involves not much more expense than the
cost of screening urine, but provides greatly enhanced
sensitivity. After death, drug concentrations tend to
increase faster in cardiac blood, for example, than else-
where in the body, making such samples more sensitive
indicators of drug use, although they are less specific.
The routine screening of cardiac blood also helps avoid
another problem: at autopsy, there is often no urine in
the bladder. Some centres have dispensed with urine
testing entirely; they first screen cardiac blood with
GC/MS and then confirm their findings in a peripheral
blood sample.
Vitreous humour
Vitreous humour is a useful testing medium, especially
for the diagnosis of electrolyte disorders, renal failure,
hyperglycaemia and ethyl alcohol ingestion. The vitre-
ous humour is, in many ways, protected from the exter-
nal environment, and it may be the only reliable testing
matrix available when individuals have drowned or
when bodies are found after an extended period of
environmental exposure. Measurement of alcohol con-
centrations in the vitreous humour may even help dis-
tinguish between post mortem alcohol formation and
ante mortem ingestion. There is an emerging tendency
to also measure the concentrations of abused drugs in
the vitreous humour, although for the present, too few
measurements have been reported to allow accurate
extrapolation from vitreous humour concentrations to
concentrations in other tissues.
Hair testing
Measurement of abused drug concentrations in hair can
yield valuable information about drug exposure and
drug compliance, and sometimes hair testing can reveal
the presence of drugs that were completely unexpected.
Once deposited in hair, drugs and their metabolites are
stable indefinitely. It requires very little effort to collect
Interpretation 299
hair at autopsy, place it in a sealed envelope and file the
sample. For reasons that are not entirely clear, the par-
ent drug is often found in higher concentrations within
the hair than is the metabolite. Should questions about
drug use arise some time in the distant future, they will
be easily answered if a hair sample has been retained.
Liver
Liver analysis can be especially valuable in cases where
the drug sought (such as a tricyclic anti-depressant) is
highly bound to protein. Liver analysis is also valuable
if the drug undergoes enterohepatic circulation. Some
drugs, such as morphine, may be detectable in the liver
long after they have been cleared from the blood, only
because they remain in the enterohepatic circulation for
so long. There is, however, one important caveat: most
drugs readily diffuse from the stomach into the right
lobe of the liver so, as a rule, only the left lobe of the liver
should be used for analytical testing.
Stomach
The testing of stomach contents is only worthwhile if
(1) the volume of the gastric contents is recorded, (2) a
homogeneous specimen is analysed and (3) the total
drug content within the stomach is computed. It does
no good to know the drug concentration in gastric fluid
if the total volume of the gastric contents is not also
known. It may also be possible to identify small pill
fragments by microscopic examination of the gastric
fluid. Very little should be made of low-level drug con-
centrations found in stomach, as ion trapping may cause
small amounts of some charged drugs, such as cocaine
and morphine, to appear in the gastric contents, even if
the drug has been injected intravenously. However, the
detection of high concentrations of some drugs in the
stomach (such as morphine) does not necessarily prove
oral ingestion; it may just be an artefact produced by
enterohepatic circulation.
Interpretation
Post mortem drug concentration measurements can-
not be interpreted in isolation, if for no other reason
than that tolerance eventually emerges to most abused
drugs. A living heroin addict may very well have a higher
morphine concentration than an occasional heroin user
lying in the mortuary, but both might have much lower
morphine concentrations than a hospice patient treated
with a diamorphine syringe driver. Tolerance is not the
only issue.
Drugs taken previously are likely to be stored in
deep body compartments, only to be released as the
body decomposes (a process that begins immediately
after death). Drug measurements made under these
circumstances might give the false impression that the
300 Principles of toxicology
drugs were, in fact, circulating in the blood at the time
of death. This phenomenon was strikingly illustrated in
a study of post mortem blood fentanyl concentrations.
Fentanyl concentrations were measured in post mor-
tem specimens collected in 20 medical examiner cases
from femoral blood, heart blood, heart tissue, liver tissue
and skeletal muscle. In a subset of seven cases femoral
blood was obtained shortly after death and then again
at autopsy. The mean collection times of between the
two post mortem samples were 4.0 hours and 21.6 hours,
respectively. In four of the cases fentanyl concentrations
rose from ‘none detectable’ in the samples taken shortly
after death, to concentration as high as 52.5 µg/L. If only
the toxicology results were considered in isolation, a
pathologist confronted with a case of unexpected sud-
den death might very well make the mistake of classify-
ing fentanyl as the cause of death, even though none was
present in the blood at the time of death.
Finally, there is the issue of genetic polymorphism.
Not only does post mortem redistribution (Figure 22.1)
ensure that concentration measured at autopsy will be
higher than in life, there is always the possibility that
high drug concentrations, even those measured in life,
do not always reflect drug overdose: the individual
simply may not have been able to metabolise the cor-
rect dose of drug they had been given. This possibility
was only realised a few years ago when a newborn died
of morphine poisoning that originated in the mother’s
breast milk. As is often the case, she had been pre-
scribed codeine for post-labour pain. When the infant
died unexpectedly it was discovered that the mother
was an ultra-rapid metaboliser of cytochrome P450
Nasal cavity
Oeosophagus
Right Left
lung lung
Heart
Liver
Stomach
Figure 22.1 Post mortem redistribution. Blood values
measured after death have little or no relationship
between levels that existed in life. Aspiration of stomach
contents into the lungs often occurs at the time of death,
and drugs that were in the lungs diffuse into the heart.
Blood from the illiofemoral vessels is generally consid-
ered preferable for testing.
2D6, causing her to produce much more morphine
when taking codeine than would normally be expected.
Individuals with a normal genetic compliment convert
roughly 10% of codeine into morphine, accounting for
codeine’s modest pain-relieving effects, but because of
the mother’s genetic make-up, much higher concentra-
tions of morphine were found in the infant than would
normally be predicted, even though the mother was not
taking excessive doses of codeine.
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sources
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Manual of Mental Disorders (DSM-V). Arlington: American
Psychiatric Association; 2013. https://www.psychiatry.org/
psychiatrists/practice/dsm/about-dsm (Accessed 13 May
2019).
Arora B, Velpandian T, Saxena R, et al. Development and valida-
tion of an ESI-LC-MS/MS method for simultaneous identifica-
tion and quantification of 24 analytes of forensic relevance
in vitreous humour, whole blood and plasma. Drug Test Anal
2016;8(1):86–97.
Cook DS, Braithwaite RA, Hale KA. Estimating antemortem drug
concentrations from postmortem blood samples: the influ-
ence of postmortem redistribution. J Clin Pathol 2000;53:
282–285.
Cooper GA, Kronstrand R, Kintz P. Society of Hair Testing guide-
lines for drug testing in hair. Forensic Sci Int 2012;218(1–3):
20–24.
Drummer OH. Forensic toxicology. EXS 2010;100:579–603.
Fernández P, Seoane S, Vázquez C, et al. Chromatographic deter-
mination of drugs of abuse in vitreous humor using solid-
phase extraction. J Appl Toxicol 2013;33(8):740–745.
Ferner RE. Post-mortem clinical pharmacology. Br J Clin Pharmacol
2008;66:430–443.
Jung BF, Reidenberg MM. Interpretation of opioid levels: com-
parison of levels during chronic pain therapy to levels from
forensic autopsies. Clin Pharmacol Ther 2005;​77:324–334.
Karch SB, Drummer O. Karch’s Pathology of Drug Abuse, 5th ed.
Boca Raton: CRC Press; 2015.
Karch SB, Goldberger BA, Druid H. Karch’s Drug Abuse Handbook,
3rd ed. Boca Raton: CRC Press; 2019.
Karch SB, Stephens BG, Ho CH. Methamphetamine-related
deaths in San Francisco: demographic, pathologic, and toxi-
cologic profiles. J Forensic Sci 1999;44:359–368.
Kintz P, Villain M, Cirimele V. Hair analysis for drug detection. Ther
Drug Monit 2006;28:442–446.
Koren G, Cairns J, Chitayat D, et al. Pharmacogenetics of mor-
phine poisoning in a breastfed neonate of a codeine-pre-
scribed mother. Lancet 2006;368:704.
Kuwayama K, Miyaguchi H, Iwata YT, et al. Time-course measure-
ments of drug concentrations in hair and toenails after single
administrations of pharmaceutical products. Drug Test Anal
2017;9(4):571–577.
LeBeau M, Moyazani A. Drug-Facilitated Sexual Assault, A Forensic
Handbook. London: Academic Press; 2001.
Leung KW, Wong ZCF, Ho JYM, et al. Surveillance of drug abuse
in Hong Kong by hair analysis using LC-MS/MS. Drug Test Anal
2018;10(6):977–983.

Levine B. Principles of Forensic Toxicology, 3rd ed. Washington:
American Association for Clinical Chemistry; 2010.
Metushi IG, Fitzgerald RL, McIntyre IM. Assessment and compari-
son of vitreous humor as an alternative matrix for forensic toxi-
cology screening by GC-MS. J Anal Toxicol 2016;40(4):243–247.
Moriya F, Hashimoto Y. Redistribution of basic drugs into cardiac
blood from surrounding tissues during early-stages postmor-
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tion of fentanyl in blood. Am J Clin Pathol 2010;133:447–453.
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Pélissier-Alicot AL, Gaulier JM, Champsaur P, Marquet P.
Mechanisms underlying postmortem redistribution of drugs:
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Forensic Sci Rev 2017;29(1):23–55. Review.
23 Alcohol
▪▪ Ethanol sources and concentrations
▪▪ Ethanol metabolism
▪▪ Elimination of alcohol
▪▪ Ethanol measurement
Ethanol sources and concentrations
Alcohol (ethanol) may be ingested or it may be pres-
ent in the body by virtue of bacterial action occurring
after death. Depending on local practice, blood alcohol
concentrations (BAC) can be expressed in many differ-
ent units and notations, but they are all similar in their
meaning. The definition of what constitutes a standard
unit of alcohol also varies from country to country. In
the USA it is 14 g (17.74 mL) ethanol, in the UK one unit
is 8 g (10 mL). The number of units in a drink is based on
the size of the drink, as well as its alcohol strength. For
example, a pint of strong lager contains 3 units of alcohol,
whereas the same volume of low-strength lager has just
over 2 units.
In most countries, there are tables listing the alcohol
content of common beverages by brand name, and there
are standard formulae (such as the Widmark formula)
for calculating the amount of alcohol ingested and the
time of ingestion (Box 23.1). As an alternative to the com-
plex equations used by toxicologists, a simple formula,
first introduced by American toxicologist Charles Winek
(Box 23.2), is often used by practitioners in the USA. It
must be remembered, however, that Winek’s formula is
intended only to provide a rough working estimate. If a
trial and court proceedings are to ensue, the Widmark
formula must be employed although it is important to
be aware BAC calculations by Widmark’s equation in
certain groups, for example, elderly individuals, may
be complicated by a high variation of Widmark factors.
There is a tendency to an elevation of the actual BAC
with increasing age.
Ethanol metabolism
When considering the pathways and factors that modu-
late blood alcohol levels and how the body disposes of
alcohol, it is important to understand how alcohol is
distributed within the body, and what can influence
the absorption of alcohol and contribute to its first-pass
metabolism. Most alcohol is oxidised in the liver, but the
kinetics of alcohol elimination can be modified by vari-
ous factors (including genetic and environmental).
▪▪ Clinical effects of alcohol
▪▪ Post mortem considerations
▪▪ Bibliography and information sources
Absorption
Alcohol is absorbed from the stomach and small intes-
tine by diffusion, with most of the absorption occurring
in the small intestine. The rate of absorption varies with
the emptying time of the stomach but, generally, the
higher the alcohol concentration of the beverage, the
faster the rate of absorption. Gastric absorption accounts
for 30 per cent and 10 per cent of ethanol administered
with food and water, respectively, and only a small per-
centage of the ethanol undergoes first-pass metabo-
lism in the liver. The more rapid absorption of ethanol
administered with water compared with food can lead to
higher BACs. The maximum absorption rate occurs after
consuming an alcoholic beverage containing approxi-
mately 20%–25% (by volume or v/v) alcohol solution on
an empty stomach. The absorption rate may be less when
alcohol is consumed with food or when a 40% (v/v) alco-
hol solution is consumed on an empty stomach. The rate
may also decrease when high fluid volume/low alcohol
content beverages, such as beer, have been consumed.
In contrast, pre-mixed cocktails with relatively low
fluid volume but high alcohol content may cause rapid
absorption. The BAC is higher after drinking vodka/tonic
than beer or wine after fasting. A binge pattern is sig-
nificantly more likely to result in a BAC above 80 mg/dL
after drinking vodka/tonic than beer or wine. The effect
of carbonation of the drink consumed may also vary the
absorption rate.
Elimination of alcohol
Ethanol is converted into acetaldehyde via the actions
of alcohol dehydrogenase resulting in the production
of acetic acid and then acetaldehyde. Acetaldehyde is
responsible for most of the clinically observed side-
effects produced by alcohol. The measured alcohol
concentration depends on both weight and sex because
these two factors determine the total volume of body
water and consequently the BAC. In general terms, the
more a person weighs, the larger the volume of water
their body will contain. After consuming equal amounts
of alcohol, someone who is obese or has a greater

Box 23.1 Widmark’s formula
During the early part of this century, E.M.P. Widmark,
a Swedish physician did much of the foundational
research regarding alcohol pharmacokinetics in the
human body. In addition, he developed an algebraic
equation allowing one to estimate any one of six vari-
ables given the other five. Typically, we are interested
in determining either the amount of alcohol consumed
by an individual or the associated BAC given the values
of the other variables. According to Widmark’s equa-
tion, the amount of alcohol consumed (A) is a function
of these several variables:
From Equation 1
N = f(W, r, Ct, ß, t z)
where:
N = amount consumed
W = body weight
r = the volume of distribution (a constant)
Ct = BAC
ß = the alcohol elimination rate
t = time since the first drink
z = the fluid ounces of alcohol per drink
Widmark’s equation relates these variables accord-
ing to:
Equation 2
Wr(C t + ßt )
N=
0.8z
Box 23.2 Winek’s formula
Winek’s formula is based on the simple observation
that, on average, a 150-pound (68 kg) man will have a
BAC of 0.025% after drinking 1 ounce (29.5 mL) of 100-
proof (50%) alcohol. It follows that:
BAC = (150 / body weight in pounds)
   (% ethanol / 50)
   (ounces consumed) (0.025)
Thus, if a 200-pound (90.7 kg) man drank five
12-ounce (354.9 mL) cans of beer, and the beer
contained 4% ethanol, then the BAC would be
approximately:
BAC = (150 / 200) (4 / 50) (60) (0.025)
  = 0.090% (90 mg%)
Elimination of alcohol 303
where:
N = the number of drinks consumed
W = body weight in ounces
r = volume of distribution (a constant relating the
distribution of water in the body in L/kg)
Ct = BAC in kg/L
ß = the alcohol elimination rate in kg/L/h
t = time since the first drink in hours
z = the fluid ounce of alcohol per drink
0.8 = the density of ethanol (0.8 oz per fluid ounce)
Worked example
Assume we are interested in determining the amount
of alcohol consumed (number of drinks) given certain
information. The information we are given includes: a
male weighing 185 lb, r = 0.68 L/kg, Ct = 0.15 g/100 mL,
ß = 0.015 g/100 mL/h, t = 5 h, and drinking 12 fl oz
beers with 3% alcohol by volume. We introduce this
information into Equation 2 according to:
(180 lb)(16 oz/lb)(0.68 L/kg)(0.0015 kg/L
 
 + (0.00015 kg/L/h)(5 h)) 
N=
(0.8)(0.48 floz/drink )
Note that we had to convert the 0.15 g/100 mL and
the 0.015 g/100 mL/h to kg/L which simply amounts
to moving the decimal point two places to the left.
Solving for A we find:
1958.4(0.00225)
N=
0.384
proportion of body fat will have a lower BAC than a thin
person. Females have more fat tissue than males of the
same weight and, therefore, a smaller volume of body
water. As a result, the BAC will be slightly higher in
women than in men after consuming an equal amount
of alcohol.
Alcohol elimination occurs at a constant rate in each
individual. Ethanol is eliminated from the body mainly
by oxidative metabolism in the liver by Class I isoen-
zymes of alcohol dehydrogenase (ADH). After drinking
on an empty stomach, the elimination rate of ethanol
from blood falls within the range 10–15 mg/100 mL/h.
In non-fasted subjects the rate of elimination tends to
be in the range 15–20 mg/100 mL/h. In alcoholics dur-
ing detoxification, because the activity of microsomal
enzyme (CYP2E1) is enhanced, the ethanol elimination
rate might be 25–35 mg/100 mL/h. Current data suggests
that the physiological range of ethanol elimination rates
from blood is from 10 to 35 mg/100 mL/h. In moderate
drinkers 15 mg/100 mL/h remains a reasonable value
to apply to the general population whereas for alcohol
304 Alcohol
dependent and other binge drinkers 19 mg/100 mL/h
may be more appropriate. Studies have also shown that
females eliminate alcohol at a faster rate than males
which may relate to relative liver/weight ratio.
Ethanol measurement
Evidential breath testing is used by most law enforce-
ment agencies in most countries with respect to road
traffic (driving) offences. A wide variety of devices are
available for measuring the ethanol content of expired
air, and the mode of operation of most devices caused
ethanol contained in the sample to be oxidised with an
electrochemical sensor. The value provided is directly
proportional to the concentration of the ethanol pres-
ent in the body. Quality control and standardisation of
such evidential machines is important to ensure accu-
rate analysis. In the presence of factors such as use of
alcohol-containing mouthwash or regurgitation of
stomach contents, different jurisdictions may apply dif-
ferent protocols, to overcome risks of false elevations,
by repeating evidential breath tests after a period of
time or replacement by either blood or urine analysis.
Alcohol-based or ­a lcohol-containing hand-washes or
swabs should be avoided in the vicinity of evidential
breath devices because of the possibility of affecting
the result of analysis.
Clinical effects of alcohol
Ethanol is a central nervous system depressant, and
the degree of apparent intoxication generally correlates
with the amount consumed. As blood concentrations
rise, initial feelings of relaxation and disinhibition give
way to blurred vision, loss of coordination and behav-
ioural issues, including risk-taking behaviour. As alco-
hol levels continue to rise, unconsciousness can occur.
The highest levels of consumption can lead to death as
a result of cardiorespiratory arrest. There is substantial
inter-subject variation with tolerance in the alcohol-
dependent that may allow the consumption of massive
amounts of alcohol and result in BACs that result in
death in the non-alcohol dependent. Thus, single BACs
have very little meaning when taken in isolation except
that, of course, a large amount of alcohol has been con-
sumed. A BAC exceeding 0.40 per cent (400 mg%) may
be lethal in a non-drinker but might produce few, if
any, symptoms in a chronic alcoholic. If an individual
is severely intoxicated, aspiration of vomit may lead to
asphyxiation and death. Chronic alcohol dependence
is associated with a wide range of medical conditions
including the development of hepatitis, liver cirrhosis,
portal hypertension and oesophageal varices, liver fail-
ure and heart failure with potentially fatal outcomes.
Prior to being closed down as part of austerity measures
by the UK government, the Forensic Science Service in
the UK produced a leaflet Blood Alcohol Concentration
and General Effects (Figure 23.1) but the majority of cli-
nicians would be uncomfortable classifying the effects
(even in general terms) within quite such narrow spe-
cific quantified ranges, as described in this publication,
because of the huge variability in response to consum-
ing alcoholic drinks. It does, however, give a reasonable
indication of the progression of alcohol intoxication.
It is also important to understand that there are
substantial risks for those who are dependent on alco-
hol and suffer alcohol withdrawal. Untreated alcohol
withdrawal can be fatal and those involved in clinical
assessment and management must understand how
to diagnose and treat such individuals. The degree of
alcohol withdrawal can be quantified using the Clinical
Institute Withdrawal of Alcohol Assessment Scale –
revised (see Chapter 16, Figure 16.1b).
Post mortem considerations
The situation is much more complicated after death.
Bacterial enzymes (predominantly alcohol dehydro-
genase and acetaldehyde dehydrogenase) act upon
carbohydrates within the cadaver. Glycogen or lactate
is converted to pyruvate and then ethanol. The amount
of alcohol produced depends on the amount of glyco-
gen or substrate available. Accordingly, post mortem
ethanol production will be greater in some tissues than
in others. For example, the glycogen content of liver is
8 g/100 g wet tissue weight, whereas that of vitreous
humour is only 90 mg/100 g.
Other factors also help determine how much alcohol
will be produced. Terminal hyperthermia, such as might
be seen in a patient with sepsis, or storage of the body at
high ambient temperatures, will accelerate alcohol pro-
duction, as will bowel trauma or disruption of the bowel
owing to surgery or malignancy. Aircraft accidents or
other causes of severe body disruption almost always
cause the production of ethanol in large quantities.
Whether any alcohol detected was formed before or
after death is fairly easy to determine. The easiest way
is to compare the ethanol content of urine (UAC) which,
unless the decedent was diabetic, contains no carbo-
hydrates, and vitreous humour (which only contains
very small amounts of carbohydrate) with the amount
measured in blood. If the ethanol was definitely con-
sumed and not formed post mortem, then determina-
tion of the ratio between vitreous humour and blood
alcohol concentrations can be very useful. If the UAC:
BAC ratio is less than 1:2, this is generally considered
confirmation that ethanol concentrations were rising
at time of death. A ratio of greater than 1:3 suggests that
the decedent was in the post-absorptive stage. Ratios
much greater than 1:3 indicate heavy consumption over
a long period of time.

Figure 23.1 Blood alcohol concentrations and general effects.
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24 Licit and illicit drugs
▪▪ Harm reduction
▪▪ Legal status of drugs
▪▪ Commonly misused drugs
Harm reduction
When considering the use of licit or illicit (legal or ille-
gal) drugs it is important to recognise that an essential
part of the treatment of substance misuse is the prin-
ciple of harm reduction. There are certain common fea-
tures to be considered (see Table 24.1).
Harm reduction (or harm minimisation) refers to a
range of public health policies designed to reduce the
harmful consequences associated with drug use and
other high-risk activities. This may embrace a number
of areas, but perhaps the area where complications of
substance misuse (of which there are many) have been
substantially reduced is with regard to intravenous
drug misusers. Skin infections from unsafe injection
practices are the most common, even when free needle
exchanges are available. Some countries (including
the UK) proactively encourage needle exchange even
within prisons to reduce the physical and infective risks.
Stigmata of intravenous drug use are commonly seen
in association with injection site ulcers, abscesses, deep
vein thrombosis, venous ulcers and ‘post-phlebitic limb’
(Figures 24.1–24.4). Severe complications, such as nec-
rotizing fasciitis requiring hospitalisation, may occur.
Injectors may be very adept at gaining vascular access
for the administration of drugs, and any clinician should
be aware of the wide variety of sites that may be used for
injection (Figure 24.5). Infectious systemic complica-
tions occur less often, such as transmission of human
immunodeficiency virus (HIV) and hepatitis, but in
some areas of the world essentially all injection drug
users are infected with the hepatitis C virus. Studies
have shown that of the non-viral ­i njecting-related inju-
ries and diseases (IRID), skin and soft tissue infections
at injection sites were the most commonly reported.
Other IRID included: infective endocarditis (lifetime
prevalence ranging from 0.5%–12%); sepsis (2%–10%);
bone and joint infections (0.5%–2%); and thrombo-
sis and emboli (3%–27%). In the case of anthrax, the
source of infection is believed by some to be the ani-
mal skins used to transport heroin into Europe, but
person-to-person spread occurs via the exchange of
saliva or blood. Heart valve infection (endocarditis),
secondary to the injection of non-sterile material, can
▪▪ Drug facilitated sexual assault
▪▪ Bibliography and information sources
lead to valve destruction and some confusing medical
symptoms, such as when bacterial vegetations sepa-
rate from the valve and circulate through the body. At
the same time that the incidence of this complication
seems to be decreasing, the rate for valvular infection
with mixed organisms, many of which are drug resis-
tant, seems to be increasing. Other complications are
so rare as to merit little attention, but occasionally,
as with the anthrax outbreak amongst injecting drug
users in Scotland in 2009, even rare complications can
become clinically significant. Botulism and tetanus as a
result of wound infections due to Clostridium botulinum
and Clostridium tetani among users of injected drugs
occurred in the UK during 2003 and 2004.
Legal status of drugs
The legal status of drugs varies widely around the world
and different jurisdictions have different ways of clas-
sifying drugs in relation to their perceived harm to
society. The penalties associated with crimes such as
possession, possession with intent to supply, and impor-
tation may reflect the political, religious, cultural or
social environment of the country in question.
Table 24.2 shows the 2018 classification of drugs and
associated penalties in England & Wales. These classi-
fications are subject to regular review and in April 2019
prescription drugs pregabalin and gabapentin were
reclassified as class C controlled substances following
an increasing number of fatalities linked to these drugs.
Re-classification of drugs occurs fairly regularly,
often as knee-jerk political responses to perceived con-
cerns of the general public. Drugs are available through-
out the world and their cost and availability is influenced
by demand and effect. Increasingly ‘legal highs’ are
being developed; these are often synthetic drugs that
mimic the effects of some illegal drugs, and which may
then be sold via the Internet. They are referred to broadly
as novel psychoactive substances (NPS).
Commonly misused drugs
There are many different types of drugs of misuse. The
use of any particular drug varies, depending on geog-
raphy, social setting, fashion, availability, cost, legal
308 Licit and illicit drugs

Table 24.1 Aspects of harm reduction

• The number of people who inject drugs and the number of people imprisoned for drug use (where data is available).
• Needle and syringe programmes (NSP), opioid substitution therapy (OST), HIV and hepatitis C and TB testing and
treatment for people who use drugs, in both the community and in prisons.
• The harm reduction response for people who use amphetamine-type stimulants, cocaine and its derivatives,
and new psychoactive substances.
• Drug-checking in nightlife settings.
• Harm reduction for women who use drugs.
• Drug consumption rooms.
• Drug-related mortality and morbidity and the overdose response, as well as naloxone peer distribution in the
community and naloxone provision in prisons.
• Developments and regressions in funding for harm reduction.
Source: From ‘The Global State of Harm Reduction 2018’, Harm Reduction International.

Figure 24.1 Multiple drug injection sites.

(Courtesy of Jason Payne-James.)

Figure 24.3 A venous ulcer following deep vein throm-

bosis secondary to intravenous drug administered into
the femoral vein. (Courtesy of Jason Payne-James.)

located within certain vital areas of the hind-brain.

Figure 24.2 An abscess at site of drug injection.
(Courtesy of Jason Payne-James.)
status, and effects. Seemingly disparate agents may
exert their effects via similar final common pathways
(e.g., khat and methamphetamine). Drugs can be clas-
sified into eight main groups according to their mode of
action (Table 24.3).
Stimulants
All drugs in this group act by increasing concentrations
of a neurotransmitter called dopamine. Dopamine is
Dopamine has many different actions, but perhaps
the best known involves mediating the sense of plea-
sure. Some drugs, such as cocaine (Figure 24.6), simply
prevent the reuptake of dopamine, allowing it to accu-
mulate in the space between nerve endings (synaptic
cleft), while others, such as the amphetamines (khat has
nearly the same structure as amphetamine, as does the
drug called fenethylline or Captagon in the Middle East),
have a similar action to cocaine but, in addition, cause
presynaptic neurons to release additional dopamine
stored within their endings. The net result is that even
more dopamine accumulates within the synapses lead-
ing, in turn, to an enhanced dopamine effect. However,
like many of the newer antidepressants, cocaine also
blocks the reuptake of serotonin (sometimes causing
a disorder known as serotonin syndrome) and blocks
the reuptake of all catecholamines, especially nor-
epinephrine. It is this last action that explains most of
 Commonly misused drugs 309

(a)

(b)

Figure 24.4 ‘Post-phlebitic limb’ of the left leg following

repeated injection into femoral vein. Note the increased
size of the left calf compared with the right, and the red-
dened (inflamed) skin. (Courtesy of Jason Payne-James.)
(c)
the vascular disease associated with stimulant abuse.
Excessive concentrations of catecholamines within the
heart cause fibrosis (Figure 24.7) or even micro-infarc-
tion of the myocardium (Figure 24.8). This process dis-
rupts the normal electrical flow of the heart, causing an
irregular heartbeat (arrhythmia). The result can be fatal.
When moderate doses of stimulants are ingested, the
main effect is a profound state of euphoria, which rapidly
dissipates in the case of cocaine, which has a half-life of
one hour, but persists for much longer in the case of other
drugs, such as methamphetamine, which has a half-life Figure 24.5 Sites of intravenous (IV) injection.
closer to 12 hours. The half-lives of other amphetamines, (a) Forearm; (b) dorsum (top) of the foot; (c) neck.
and khat, fall somewhere in between. All stimulants, (Courtesy of Jason Payne-James.)
except for khat, can be injected, insufflated (snorted)
or smoked. Khat (Figure 24.9) is chewed. The onset of smokers, but the effects produced are no different than
effects after smoking or injecting occurs much more with uncrystallised methamphetamine.
rapidly than when the drug is taken orally because the Physical effects of stimulant use generally include
drug reaches the brain more quickly. Rapid onset usu- dilation of pupils, increased heart rates and raised
ally implies that a drug’s effects will be more rapidly ter- blood pressure. The problem for a clinician involved
minated. Blood levels after smoking free-base cocaine in attempting to assess or determine the type of drug
are comparable to those seen after injecting cocaine used in an intoxicated individual is that few users (either
intravenously. The term ‘crystal meth’ (Figure 24.10) is dependent on, or using drugs recreationally) use a single
reserved for methamphetamine that has been allowed to drug, and thus drugs from different groups may produce
crystallise slowly – the less volatile the solvent, the larger a wide variety of clinical states. Heavy cocaine users
the crystals that form – but it is also smoked, resulting often manifest some paranoid symptoms. If psychosis
quickly in high plasma concentrations. Chemically, does occur, it can include formication (the sensation of
crystal meth and methamphetamine are identical: having insects crawling on or under the skin), and self-
both can be dissolved, injected, insufflated or smoked. injury. Extreme forms of this syndrome are manifest by
Large crystals are highly prized by methamphetamine self-injury. Methamphetamine abusers not infrequently
310 Licit and illicit drugs

Table 24.2 Drug classification and penalties in England & Wales 2018
Supply and
Class Drug Possession production
A Crack cocaine, ecstasy (MDMA), heroin, LSD, magic Up to 7 years in prison, an unlimited Up to life in
mushrooms, methadone, methamphetamine fine, or both prison, an
(crystal meth) unlimited fine,
or both
B Amphetamines, barbiturates, cannabis, codeine, Up to 5 years in prison, an unlimited Up to 14 years
ketamine, methylphenidate (Ritalin), synthetic fine, or both in prison, an
cannabinoids, synthetic cathinones (e.g., unlimited fine,
mephedrone, methoxetamine) or both
C Anabolic steroids, benzodiazepines (diazepam), Up to 2 years in prison, an unlimited Up to 14 years
gamma hydroxybutyrate (GHB) gamma- fine, or both (except anabolic in prison, an
butyrolactone (GBL), piperazines (BZP), khat steroids – it’s not an offence to unlimited fine,
possess them for personal use) or both
Temporary Some methylphenidate substances None, but police can take away a Up to 14 years
class (ethylphenidate, 3,4-dichloromethylphenidate suspected temporary class drug in prison, an
drugsa (3,4-DCMP), methylnaphthidate (HDMP-28), unlimited fine
isoproplyphenidate (IPP or IPPD), or both
4-methylmethylphenidate, ethylnaphthidate,
propylphenidate), and their simple derivatives
Source: https://www.gov.uk/penalties-drug-possession-dealing.
a The government can ban new drugs for one year under a ‘temporary banning order’ while they decide to the drugs should be classified.

Table 24.3 Drugs classified into eight main groups according to their mode of action
Drug group Examples
Stimulants Amphetamines (fenethylline, captagon), cocaine, ephedra, khat
Opiates and opioids Naturally occurring opiates, synthetic opioids
Sedative hypnotics Zolpidem
Hallucinogens LSD (lysergic acid diethylamide), mescaline
Dissociative anaesthetics GHB (γ-hydroxybutyrate), PCP (phencyclidine), Salvia divinorium
Cannabinoids ‘Spice’, THC (tetrahydrocannabinol)
Solvents Toluene, glue, lighter fuel
New synthetic agents Piperazines

manifest symptoms of florid paranoid psychosis. The
unique feature of methamphetamine psychosis is that it
may reoccur years after drug usage has been discontin-
ued. Its occurrence seems to be related to methamphet-
amine-induced damage to cortical white matter. These
pathological changes can be visualised with magnetic
resonance imaging (MRI) scanning. This ability is not
shared by cocaine or other stimulants.
The most feared consequence of any type of stim-
ulant abuse is the syndrome referred to as ‘excited
delirium’. Although not recognised as a specific
International Classification of Diseases entity, the exis-
tence of this disorder is accepted by forensic patholo-
gists, forensic physicians, forensic toxicologists and
by many authoritative bodies, including the American
Medical Association and the American Academy of
Emergency Physicians. The syndrome, which is some-
times lethal, is notable for the acute onset of hyper-
thermia and agitated violent behaviour that often
culminates in a sudden unexplained death. The contri-
bution of restraint, struggle and the use of conducted
energy devices (CEDs) to the cause of death in these

Figure 24.6 Cocaine. (Photograph by DJ Young, courtesy
of the US DEA.)
Figure 24.7 Fibrosis of the heart secondary to stimulant
abuse. (Courtesy of Steven B Karch.)
Figure 24.8 Zone of micro-infarction in the
heart ­secondary to stimulant abuse.
(Courtesy of Steven B Karch.)
cases is the subject of considerable controversy; there
is good evidence that a central nervous system (CNS)
dysfunction of dopamine signalling underlies the
delirium and produces fatal autonomic dysfunction
(see also Chapter 16).
Commonly misused drugs 311
(a)
(b)
Figure 24.9 (a) Khat; (b) Green residue on tongue
after chewing Khat. ([a] Photo by DJ Young,
courtesy of the US DEA.)
Figure 24.10 ‘Crystal meth’. (Photo by DJ Young, courtesy
of the US DEA.)
The vascular complications of stimulant abuse are
numerous. Mostly, but not entirely, they relate to cate-
cholamine excess. Excessive amounts of norepinephrine
(noradrenaline) damage the walls of blood vessels, and
can cause vascular wall dissection, stroke and coronary
artery spasm. The presence of excess norepinephrine also
312 Licit and illicit drugs
50
1 initial depolarisation
2 plateau phase
0
repolarisation
mV
0 rapid 3
depolarisation
50
resting membrane
potential
4 4
100
Figure 24.11 Identifiable stages of the cardiac action
potential. (Courtesy of Steven B Karch.)
accelerates the onset of coronary artery disease, induces
cardiac enlargement and produces scarring (referred to
as interstitial fibrosis of the myocardium). The combi-
nation of myocardial fibrosis and cardiac enlargement
is referred to as myocardial remodelling. Remodelling
greatly favours the occurrence of sudden cardiac death.
Both cocaine and methamphetamine interact with the
ion pores controlling the normal electrical cycling of
the heart (the action potential) but react with different
channels. Cocaine blocks the sodium channel (a prop-
erty shared by all local anaesthetics) and the hERG potas-
sium channel. Methamphetamine does not share either
of those properties, but does interact with L-type calcium
channels, which provides another reason for how meth-
amphetamine can cause arrhythmias. Together, these
interactions lead to prolonged repolarisation of the heart
cells, another abnormality that is arrhythmogenic mech-
anism associated with a greatly increased risk of sudden
death (Figure 24.11).
The World Drug Report 2018, published by the United
Nations Office of Drug and Crime Control (UNODC),
notes that the range of drugs and drug markets are
expanding and diversifying as never before. There is
a potential supply-driven expansion of drug markets,
with production of opium and manufacture of cocaine
at the highest levels ever recorded. Figure 24.12 shows
the usage of some groups of drugs worldwide.
Markets for cocaine and methamphetamine are
extending beyond their usual regions and, while drug
trafficking online using the ‘darknet’ (i.e. that part of the
Internet hidden from public view) continues to repre-
sent only a fraction of drug trafficking as a whole, it con-
tinues to grow rapidly. Non-medical use of prescription
drugs has reached epidemic proportions in parts of the
world. The opioid crisis in North America has resulted
in the Commission on Narcotic Drugs scheduling six
analogues of fentanyl, including carfentanil, which
Figure 24.12 Global use of groups of drugs. (From the
World Drug Report 2018.)
are contributing to the high number of fatalities. This
builds on the decision by the Commission at its 60th
session, in 2017, to place two precursor chemicals used
in the manufacture of fentanyl and an analogue under
international control. The Report also makes reference
to addiction to tramadol, rates of which are soaring in
parts of Africa. Non-medical use of this opioid pain-
killer, which is not under international control, is also
expanding in Asia. The impact on vulnerable popula-
tions is a cause for serious concern, putting pressure on
already strained healthcare systems. At the same time,
more new psychoactive substances are being synthe-
sised, and more are available than ever, with increasing
reports of associated harm and fatalities. In the UK, the
prescribed drugs gabapentin and pregabalin are con-
sidered at substantial risk for misuse.
Opiates and opioids
The term ‘opiates’ refers to morphine, other contents
of the opium poppy (such as codeine), and compounds
made by modification of the morphine molecule. Box
24.1 lists commonly abused opioids. Opioids are syn-
thetic molecules. Opiates and opioids both exert their
effects by binding to the µ1 opiate receptor located on
neurons throughout the brain. Similar receptors are also
found in the intestine, explaining why opiate users are
almost always constipated. Stimulation of the µ1 recep-
tor relieves pain, depresses respiration and reduces gut
motility. The only important difference between heroin,
morphine and all the other synthetic opioids is their rel-
ative affinity for the µ1 receptor. Some opioids conform
to the shape of the µ1 receptor better than others and,
accordingly, produce greater or lesser effect, with some
synthetic opioids being more than 1 000 times as potent
as morphine itself.
Opiate use can be accompanied by numerous
medical complications often related to the process of

Box 24.1 Common opiates and opioids
• Buprenorphine
• Codeine
• Fentanyl
• Hydrocodone
• Kratom
• Methadone
• Meperidine (pethidine)
• Figure 24.13 Pinpoint (pinhole) pupils.
Oxycodone
• (Courtesy of Jason Payne-James.)
Oxymorphone
• Propoxyphene
• receptor than morphine. The molecular structure of the
Tramadol
injecting itself. However, there are some complications
that are specific to opiates and opioids. Heroin smokers,
for example, can develop a specific type of brain degen-
eration that is not very different from ‘mad cow’ disease
(bovine spongiform encephalopathy [BSE]); however,
these cases remain very uncommon.
Several features of opiate abuse do merit special con-
sideration. Tolerance is one of these. With chronic use,
the user becomes less and less responsive to the drug’s
effects and must increase the dosage to achieve the same
effect. This phenomenon is just as much a problem for
hospital patients as it is for addicts. Tolerance to different
opiate effects emerges at different rates. Tolerance to the
pain-relieving effects of morphine emerges quickly, but
tolerance to morphine-induced respiratory depression
emerges very slowly. This differential effect often leads
to potentially life-threatening situations. Clinicians
need to be aware of the physical effects of intoxication
with these drugs, and the symptoms produced by their
withdrawal. Perhaps the best-known sign of acute use of
opiates is the presence of pinpoint pupils (Figure 24.13).
Withdrawal from opiates (‘clucking’, ‘rattling’) leads to
a number of different symptoms, the severity of which
is mostly dependent on how severely addicted the indi-
vidual is: symptoms may include the presence of goose-
flesh, rhinorrhoea, lacrimation, yawning, abdominal
pain, muscle pain and diarrhoea and vomiting.
Some opioids are much more potent than oth-
ers. Novel synthetic opioids have recently emerged
on the recreational drug market. They include fen-
tanyl (a potent narcotic analgesic) and its analogues
(e.g., acetylfentanyl, acryloylfentanyl, carfentanil,
α-methylfentanyl, 3-methylfentanyl, furanylfentanyl,
4-fluorobutyrylfentanyl, 4-methoxybutyrylfentanyl,
4-chloroisobutyrylfentanyl, 4-f luoroisobutyrylfen-
tanyl, tetrahydrofuranylfentanyl, cyclopentylfentanyl
and ocfentanil) and compounds with different chemi-
cal structures, such as AH-7921, MT-45 and U-47700.
Fentanyl, for example, is more than 100 times more pow-
erful than morphine, because it is a better fit for the µ1
Commonly misused drugs 313
opiate can also have an effect on routine drug screening
tests. Routine drug screening tests (including the vari-
ous test kits used in most casualty wards) are antibody
based. The antibodies used have usually been designed
to attach to morphine and will not react at all in the
presence of synthetic opioids such as fentanyl. More
worryingly, carfentanil – a synthetic fentanyl analogue
approved for veterinary use, with an estimated anal-
gesic potency approximately 10,000 times that of mor-
phine and 20–30 times that of fentanyl, based on animal
studies – has become available. Since 2016, an increas-
ing number of reports describe detection of carfentanil
in the illicit drug supply. Little is known about the phar-
macology of carfentanil in humans. Its high potency
and presumed high lipophilicity, large volume of dis-
tribution, and potential active metabolites have raised
concerns about the management of people exposed to
carfentanil as well as the safety of first responders. It has
been associated with a number of deaths in association
with other illicitly used drugs.
The non-narcotic materials used to adulterate
heroin (and other drugs) by street dealers are called
excipients. They are used to increase drug volume in
hopes of increasing revenue. The compounds added
to enhance drug effects (called adulterants) are rela-
tively insoluble. This lack of solubility causes veins to
become sclerotic, explaining the track marks seen in
repeated injection users (Figure 24.14). The adulterants
used in cocaine production tend to be more soluble and
cause far less damage to peripheral veins, even though
they can occasionally be quite toxic in their own right.
Much of the cocaine sold on the streets in the USA has
been adulterated with levamisole, an anti-helminthic
­piperazine-type drug with the ability to cause bone
marrow suppression. Occasional clusters of multiple
deaths have been reported as a result of the adulteration
of street heroin with illicitly produced α-methyl fentanyl
(as opposed to the unsubstituted, medicinal fentanyl).
This can be problematic for toxicologists because the
presence of fentanyl is not detected by routine screen-
ing assays and will not be detected even when routine
screening is performed of whole blood using gas chro-
matography/mass spectrometry.
314 Licit and illicit drugs
Figure 24.14 Track marks from intravenous drug admin-
istration. Note also gooseflesh (piloerection) caused by
opiate withdrawal. (Courtesy of Jason Payne-James.)
Finally, there is the problem of genetic polymorphism,
which refers to mutations that occur in all opiate recep-
tors, and in almost all liver enzymes, including those
that metabolise the opiates. Depending on the type of
mutation affecting the receptor, drug effects can be mini-
mised, exaggerated or not altered at all. Individuals may
be classified as poor, normal, rapid or super-metabolis-
ers, depending on which mutation is present in which
gene. Tests are available that can differentiate between
different kinds of metabolisers in the living, but they
are not generally available for use in autopsy material.
Undiagnosed polymorphisms often explain why patients
fail to respond to what appear to be adequate doses of
drug. Genetic polymorphism can also explain the occur-
rence of unexpected deaths.
Sedative hypnotics
A very long list of prescription medications is available
for the treatment of insomnia. The drugs most frequently
prescribed for insomnia (which may also have an anxio-
lytic action) include benzodiazepines (BZs), non-benzo-
diazepines (nonBZs) and antidepressants. Older drugs,
such as long-acting barbiturates and chloral hydrate
have fallen out of favour. BZs increase the effect of the
neuro-transmitter called GABA (γ-amino butyric acid).
In the absence of drugs, the GABA A receptor
(GABA A R) binds to GABA, which is the major inhibitory
neurotransmitter within the CNS. When it is activated,
the GABA A receptor selectively conducts chloride ion
through its central pore into the cell. As a consequence,
the neuron becomes hyperpolarised. When a cell is
hyperpolarised, action potentials are less likely to occur
and neurotransmission is slowed. The active site on
the GABA A receptor is, of course, GABA. However, the
receptor also contains a number of other different bind-
ing sites, including areas where BZs, non-BZs, barbitu-
rates, ethanol and even inhaled anaesthetics can bind.
Box 24.2 Some common sedative
­hypnotic drugs
Benzodiazepines
Triazolam
Estazolam
Temazepam
Non-diazepines
Eszopiclone
Zaleplon
Antidepressants
Trazodone
Amitryptiline
Melatonin receptor agonist
Ramelteon (Rozerem)
Any drug that can bind to the GABA A receptor is likely
to exert sedative, anticonvulsant and anxiolytic effects.
Some drugs may produce muscle relaxation while oth-
ers may produce euphoria. In general, these are very safe
drugs. Death from overdose is rare. However, combina-
tions of high doses of BZs with other drugs, such as alco-
hol, barbiturates, opiates and tricyclic antidepressants
may lead to coma and death, mediated primarily by respi-
ratory depression. Flumazenil is an appropriate reversal
agent, which should be used with caution because its
effects are short-lived and somewhat unpredictable, and
re-sedation may occur later. Supportive care in an appro-
priately monitored setting is usually sufficient treatment
for those who have ingested drugs in this category.
The BZs have long been the drug of choice for the
treatment of insomnia, but long-term use leads to
dependence and abrupt discontinuation can even lead
to the occurrence of seizures. The nonBZ hypnotics
are more effective at speeding the onset of sleep than
BZs and are thought to have fewer side effects and drug
interactions. Antidepressants are considered third-
line drugs for the treatment of insomnia and, in most
countries, have not been approved for the treatment
of insomnia. Nonetheless, they are widely prescribed,
despite the fact that any antidepressant may precipitate
serotonin syndrome. A list of the most popular agents
is shown in Box 24.2. A notorious historic case of fatal
sedative toxicity is summarised in Box 24.3.
Hallucinogens
Criteria for membership in this group are difficult to
define. All members are said to share five common
properties:
• Changes in mood and perception dominate in
­proportion to any other effects the drug may exert.
 Commonly misused drugs 315

• There is minimal impairment of intellect or

­memory.
• Use is not associated with agitation.
• There are minimal side effects.
• Craving and addiction do not occur.
Hallucinogens have traditionally been divided into
two groups depending on their chemical structure – the
phenylalkylamines and indolealkylamines. Mescaline
is the best known of the former group while psilocybin
(magic mushrooms), bufotenine (also known as bufo-
tenin or cebilcin-derived from the skin of cer­tain toads)
and LSD (lysergic acid diethylamide, Figure 24.15) are
the three best-known indolealkylamines.
In recent years, these distinctions have become
blurred, as both dissociative anaesthetics and designer
amphetamines such as MDMA (3,4-methylenedioxy-
methamphetamine, commonly known as ecstasy)
(Figure 24.16), share some properties with the halluci-
nogens. The most important distinction appears to be
that, at worst, use of hallucinogens leads only to behav- Figure 24.15 LSD (lysergic acid diethylamide) blotter,
ioural toxicity. However, the hallucinatory ‘designer’ complete sheet. (Photo by DJ Young, courtesy of the
amphetamines have been responsible for many deaths, US DEA.)
often a result of hyperthermia and multiorgan failure.
PMA (paramethoxyamphetamine) appears to be the also confirms the existence of MDMA-associated
most dangerous member of this latter group. neuro-toxicity. High doses of MDMA given to rats pro-
The most notorious of the designer amphetamines, duce dramatic decreases in brain serotonin concentra-
by far, is MDMA. Shortly after MDMA was introduced tions, although animals fully recover after one week.
into England, reports of MDMA-induced hepatic fail- In controlled human studies, the spinal fluid of MDMA
ure began to appear in major medical journals. MDMA users has been found to contain reduced concentra-
seized by police in the UK is primarily manufactured tions of 5-hydroxyindoleacetic acid, the major serotonin
in clandestine laboratories located in the Netherlands metabolite.
and Belgium. Most reported deaths from MDMA have
involved heat-related illness, usually associated with Dissociative anaesthetics
rhabdomyolysis. Substantial experimental evidence Five drugs fall into this category: phencyclidine
(PCP), ketamine, γ-hydroxybutyrate (GHB), dextro-
methorphan and Salvia divinorum (Figure 24.17). All
Box 24.3 Fatal sedative toxicity are hallucinogens, and the first four share the same
and Marilyn Monroe mechanism of action: they block the NMDA receptor,
Norma Jean Baker – better known as Marilyn Monroe, the predominant molecular mechanism involved in
a famous Hollywood actress – was found dead in memory function and learning. Salvia has no effect on
bed in August 1962; bottles of pills – including the the NMDA channel. Instead, it specifically blocks the κ
‘sleeping pills’ Nembutal, and chloral hydrate – being
found on a table next to her bed.
At autopsy, there were no fresh needle puncture
marks, or injuries suggestive of assault – a dark red-
dish-blue bruise was present on the lower left back,
just above the hip. No pill residue was noted in the
stomach or small intestine. Post mortem toxicology
revealed pentobarbital and chloral hydrate ‘well
above fatal dosages’. Despite samples of blood, liver,
kidney, stomach contents, urine and intestine being
saved for toxicology, only blood and liver were ana-
lysed, fuelling suspicions in some circles about the Figure 24.16 MDMA (3,4-methylenedioxymethamphet-
method in which the drugs had been administered. amine) tablets. (Photo by DJ Young, courtesy of the
US DEA.)
316 Licit and illicit drugs
Figure 24.17 Salvia divinorum. (Photo by DJ Young,
­courtesy of the US DEA.)
receptor. Drugs that bind to the κ receptor usually pro-
duce intense feelings of unhappiness and depression
and all have hallucinogenic (psychotomimetic) effects.
Salvinorin A, the active ingredient in Salvia divino-
rum, is the exception. The only reason for taking Salvia
is to produce hallucinogenic effects, but many poten-
tially useful drugs also stimulate κ-receptors and the
psychological side effects that result from this stimula-
tion can be so strong that the drug cannot be used for
its intended clinical purpose (the reason phencyclidine
was withdrawn from the human market).
The effects produced by salvinorin A are qualitatively
different than those produced by the other hallucino-
gens such as LSD or mescaline, and the mechanism of
action is not understood. It is known that κ-opioid recep-
tors also play a key role in the human stress response.
Because κ stimulation tends to neutralise the effects of
µ1 stimulation, some feel the presence of the κ receptor
may diminish the possibility of drug overdose. There is
also evidence that stimulation of κ receptors in some
way protects the neuron from damage; in particular,
damage produced by hypoxia/ischaemia is minimised
in the presence of κ receptor agonists but, again, the
mechanisms involved remain totally unknown.
Marijuana (Cannabis)
Marijuana (Figure 24.18), derived from the Cannabis
plant, and which has multiple street names (e.g.,
weed, hash, skunk), is a drug that interacts with many
different receptors. The body itself produces mari-
juana-like drugs called endocannabinoids. These are
compounds with structures similar to that of THC
(tetrahydrocannabinol), the active ingredient in mari-
juana. Endogenously produced endocannabinoids bind
with specific endocannabinoid receptors known as C1
and C2. Surprisingly, there is evidence that, in addition
Figure 24.18 Cannabis leaf (marijuana).
to binding C1 and C2, THC also interacts with the BZ
receptor and opioid receptors. THC increases pulse rate
in direct proportion to the dose administered. It may
decrease cardiac output, and can sometimes cause
syncope, particularly in those with pre-existing heart
disease.
Whether or not THC relieves pain is still debated,
but there is little doubt that, once within the body, THC
remains in the body fat stores for a very long time (>1
month). It is then slowly released back into the circu-
lation by an assortment of different stimuli, including
dieting and stress. Both of the latter conditions lead to
increased secretion of ACTH and cortisol which, in turn,
can also cause THC stored in fat to be released. If stress
can cause the release of THC stored in fat cells, what is
to be made of the driver suspected of driving under the
influence who is found to have low concentrations of
THC in his blood, even if he had not smoked marijuana
for weeks prior to the event? In this case THC stored
weeks earlier would have been released. Should he be
charged with driving under the influence? It is essential
that an appropriate clinical examination be undertaken
to determine whether or not there is clear evidence of
any drug having been consumed and, if so, whether that
drug has an effect on that individual’s ability to drive
properly. As is also the case with phencyclidine, so much
marijuana is stored in fat tissue that the interpretation
of post mortem blood levels is almost impossible. After
death, as individual’s cells die, they release their drug
content and there is no way to differentiate between THC
that was ingested just before death from drug that was
ingested one month earlier.
Multiple new drugs are increasingly becoming avail-
able as governments limit the availability and legality of
so-called ‘legal highs’. For example, ‘Spice’ has recently
become popular. It is sold mostly over the Internet and
at ‘head shops’. Spice is the popular name for a mol-
ecule named JWH-018 (1-pentyl-3-[1-napthoyl]indole).
It exerts many of the same effects as the cannabinoids

but has a completely different structure. Although the
structure of Spice is very different from THC, it none-
theless avidly binds at the same C1 and C2 receptor, at
exactly the same sites where THC is active. The effects
produced are said to be the same as smoking marijuana,
but are believed to last much longer. The potential use of
this compound as a transdermal pain reliever is under
investigation, but if it ever does come to market there
will, no doubt, be a thriving black-market trade.
Solvents
Solvents such as toluene volatize at room temperature,
allowing users to inhale the fumes, a practice referred to
as ‘huffing’. Use of these agents and others such as glue,
or gas fuel for cigarette lighters is much less common
now than previously. Glue-sniffing was more frequent
in the 1980s but still occurs. Clinical examination may
reveal traces of the inhalant, such as glue, around an
individual’s mouth and face, with the persistent odour
of the relevant inhalant. Some individuals may have
evidence of singeing of beard or hair, or evidence of old
burn injury to the face, as many of the agents used for
such practices are highly flammable and do not asso-
ciate well with lighted cigarettes. Toluene, as opposed
to the solvents found in hair spray, dry-cleaning fluid
and gasoline, is the agent most often responsible for fatal
intoxication. The mechanism seems to be the disruption
of normal cardiac electrical activity. Inhalation of any
solvent will result in transient euphoria, headache and
ataxia. Members of this group selectively destroy brain
white matter, and a distinctive pattern can be identi-
fied in the MRI scans of chronic abusers. Solvents share
some properties with other depressants such as barbi-
turates, benzodiazepines and even alcohol. However,
the solvents, as a group, interact with so many different
receptor subtypes that their actual mechanism of action
remains unclear.
Novel psychoactive substances
(legal highs)
These drugs first emerged in New Zealand during
the early 2000s, but use has quickly spread to involve
Europe and the USA. By the end of 2015, more than 560
NPS had been reported to the European Monitoring
Centre for Drugs and Drug Addiction. The most popu-
lar compounds are synthetic cannabinoids and psy-
chostimulatory derivatives of cathinone (so-called
β-keto-amphetamines). These drugs are commonly (and
sometime incorrectly) known as ‘legal highs’. Their legal
status is generally an evolving one, and what was legal
one day may, by virtue of new legislation, become illegal
almost overnight. Governments are concerned by the
proliferation of such substances, many of which may
be sold in corner shops or over the Internet, and they
Commonly misused drugs 317
appear to be taking rapid action to address these prob-
lems. They are frequently referred to in the media, and
by users, by the umbrella name ‘Spice’.
Governments and authorities face an uphill struggle
as ways to develop substances that avoid legal sanc-
tion are used to get around the inevitable clamp down
as some legal highs become fashionable. In 2016, the
Psychoactive Substances Act 2016 was introduced in
the UK with the intent of restricting the production, sale
and supply of a new class of psychoactive substances.
Table 24.4 summarises the main effects and intentions
of the Act.
Many of these newly abused drugs belong to the
chemical class known as piperazines, derived from
piperazine and benzyl chloride. Piperazines were origi-
nally used as worming agents in humans and in veteri-
nary medicine, particularly in the treatment of round
worms (especially Ascaris); they paralyse the worms
so they are flushed out by peristalsis. However, the
medicinal use of piperazines is banned in many coun-
tries. Ironically, more than half of the cocaine sold in
the USA is contaminated with levamisole, a piperazine
anti-­helminthic drug, which was initially withdrawn
from the US market because it is known to induce bone
marrow suppression. Several piperazines derivatives
are now in circulation.
1-Benzylpiperazine (BZP) is a stimulant. It is sold as
an alternative to amphetamine, methamphetamine and
MDMA and, on occasion, is misrepresented as MDMA.
It interacts with numerous different receptors, but the
net effect produced more or less resembles that of an
amphetamine-type drug. Consequently, the adverse
effects associated with BZP use are likely to include
confusion, agitation, vomiting, anxiety and palpita-
tions. There is strong evidence that higher plasma levels
of BZP are associated with an increased incidence of
seizures. Co-ingestion of ethanol increases the likeli-
hood of adverse BZP-induced symptoms, but reduces
the incidence of BZP seizures.
When taken in small doses the piperazine com-
monly abbreviated as TFMPP (trif luoromethyl­
phenylpiperazine) is said to produce effects like those
of MDMA. However, in large doses, or when combined
with BZP, or alcohol or both, it may be toxic. A recent
clinical trial employing a fixed dose of TFMPP and BZP
had to be discontinued early because so many of the par-
ticipants experienced agitation, anxiety, hallucinations,
vomiting, insomnia and migraine. As with BZP, many of
the effects resemble those produced by amphetamines,
including increased heart rate and blood pressure and
insomnia.
Meta-chlorophenylpiperazine (MCPP) is also a piper-
azine and a non-selective serotonin receptor agonist. It
is sold as legal alternative to illicit stimulants, mostly in
New Zealand. Like the other piperazines, MCPP is some-
times sold as faux MDMA. MCPP causes headaches in
318 Licit and illicit drugs

Table 24.4 Main Effects & Intentions of the Psychoactive Substances Act 2016
• Makes it an offence to produce, supply, offer to supply, possess with intent to supply, possess on custodial premises,
import or export psychoactive substances; that is, any substance intended for human consumption that is capable
of producing a psychoactive effect. The maximum sentence will be 7 years’ imprisonment
• Excludes legitimate substances, such as food, alcohol, tobacco, nicotine, caffeine and medical products from the
scope of the offence, as well as controlled drugs, which continue to be regulated by the Misuse of Drugs Act 1971
• Exempts healthcare activities and approved scientific research from the offences under the act on the basis that
persons engaged in such activities have a legitimate need to use psychoactive substances in their work
• Includes provision for civil sanctions – prohibition notices, premises notices, prohibition orders and premises orders
(breach of the 2 orders will be a criminal offence) – to enable the police and local authorities to adopt a graded
response to the supply of psychoactive substances in appropriate cases
• Provides powers to stop and search persons, vehicles and vessels, enter and search premises in accordance with a
warrant, and to seize and destroy psychoactive substances.
Source: https://www.gov.uk/government/collections/psychoactive-substances-bill-2015.

humans, and has been used as a challenge agent for test-
ing potential anti-migraine medications. Up to 10 per
cent of those who take MCPP will develop a migraine
headache, and 90 per cent of individuals who commonly
suffer from migraines will have an attack if challenged
with MCPP. This has tended to limit the use of MCPP as a
recreational drug, and may explain why no deaths have
been reported after its use. There are also reports that
MCPP has been used as a cocaine adulterant.
Harm reduction measures on the club and rave scene
have included on-the-spot analysis of drugs to ensure
that what has been bought (even though illegal) is what
it is purported to be rather than something more dan-
gerous.
As these drugs are relatively new, with little expo-
sure experienced by humans, there are many concerns
for possible ill-health effects that remain unknown. It
should be noted that some amphetamine analogues
containing paramethoxy group are known to cause
severe hyperthermia and even death owing to concur-
rent monoamine oxidase inhibitor (MAOI) and mono-
amine releasing action. The deaths of two young men
in Sweden in 2009 were attributed to methadrone over-
dose.
As time progresses, and the usage of specific NPS
increases, neuropharmacological and clinical knowl-
edge has progressed for a number of these substances
such as mitragynine (‘Kratom’), synthetic cannabinoids
(e.g., ‘Spice’), dimethyltryptamine and novel serotoner-
gic hallucinogens, the cathinones mephedrone and
methylone, ketamine and novel dissociative drugs,
γ-hydroxybutyrate, γ-butyrolactone, and 1,4-butane-
diol. Mephedrone, for example, had blood concen-
trations in cases of fatal intoxications higher than in
non-fatal cases. However, in both circumstances there
is great variability in mephedrone concentration mea-
sured, potentially attributable to interindividual differ-
ences in pharmacokinetics-pharmacodynamics and
poly-drug use complicates the interpretation of the
forensic toxicological analysis.
NPSs are also associated with injection use and the
accompanying risks (e.g., hepatitis C).
Drug facilitated sexual assault
Drug facilitated sexual assault (DFSA) is a matter of
substantial public concern. All published data indicates
that alcohol intoxication combined with voluntary drug
consumption presents the greatest risk factor for DFSA,
despite populist perceptions that covert drink-spiking
is a common occurrence. There is a need to develop
policies that encourage early responders to suspected
DFSA (e.g., law enforcement agencies, medical staff,
support agencies), to collect detailed information about
the individual’s licit and illicit drug consumption his-
tory, in order to assist in providing appropriate and more
thorough contextual information.
Certain drugs have been identified as having par-
ticular potential for use in DFSA and these include,
ethanol, chloral hydrate, BZs, non-BZ sedative-hyp-
notics, GHB, ketamine, opioids, dextromethorphan,
barbiturates, anticholinergics and antihistamines.
Clinical examination, and early collection of blood,
urine and hair samples as soon as possible after an
alleged incident may assist in determining the possi-
ble drug group involved (if any), and the time at which
it was administered. Such information may assist the
toxicology laboratory in directing appropriate investi-
gation techniques. Possibly the most important future
need is for education to ensure that children and young
people understand the implications of drug-induced
risky decisions, reduced inhibitions and reduced abil-
ity to resist.
GHB is produced as a post mortem artefact, both in
the urine and the blood, and post mortem GHB blood
measurements are particularly difficult to interpret.

Different laboratories have different ‘cutoffs’ for reporting
GHB results, and these values may vary from country to
country and from laboratory to laboratory. GHB is widely
used in club scenes as a ‘party drug’ and consumed with
alcohol, benzodiazepines, opiates, stimulants and ket-
amine. There is an unpredictable risk of fatality which is
increased in the presence of other substances.
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solvent abuse. J Toxicol Clin Toxicol 2002;40:21–34.
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25 Medicinal poisons
▪▪ Introduction
▪▪ Serotonin syndrome
▪▪ QT interval prolongation (long QT syndrome)
Introduction
Large doses of any medicine may cause cardiotoxicity,
or neurotoxicity, but when toxicity occurs it usually does
so as a result of the drug’s shared ability to stimulate
the same set of receptors as are stimulated by abused
drugs. Analgesics such as oxycodone and hydroco-
done bind to the same set of µ receptors as morphine.
Antitussives, such as dextromethorphan, bind the same
set of N-methyl-d-aspartate (NMDA) receptors as any
other dissociative anaesthetic. Barbiturate drugs are
rarely the cause of death except, perhaps, in epileptics,
where death is more likely to be caused by the absence
of the drug rather than any excess (sudden unexpected
deaths in epileptics – SUDEP). Members of the benzo-
diazepine family (alprazolam, clonazepam, diazepam,
zolpidem) bind the benzodiazepine receptor located on
the γ-aminobutyric acid A (GABA A) receptor acting syn-
ergistically with opiates to depress respiration. Second-
and third-generation antidepressants cause ‘serotonin
syndrome’, but the underlying mechanism is just the
same as that of cocaine – the antidepressants prevent
the reuptake of serotonin, leading to the accumulation
of excess serotonin in the synaptic cleft between nerve
endings. When prescription medications are consid-
ered, two disorders have come to predominate most
discussion: serotonin syndrome and QT interval pro-
longation.
Serotonin syndrome
Serotonin syndrome (SS) was first recognised in 1991
by psychiatrist Harvey Sternbach. Over time, mild
cases have been increasingly recognised, making it
difficult to determine the true frequency. Symptoms
are due to excessive serotonin activity throughout
the nervous system as a result of medication expo-
sure. It is generally described as a clinical triad of
mental status changes, autonomic instability, and
neuromuscular abnormalities (primarily rigidity
and clonus), but may be manifest in a wide variety
of presentations which include tachycardia, tremor,
hyperref lexia, diarrhoea, diaphoresis, shivering
or mydriasis, and progress to moderate cases with
▪▪ Drugs with unique modes of action
▪▪ Bibliography and information sources
hypertension, hyperthermia up to 40°C, hyperactive
bowel sounds, diffuse and ocular clonus, mania and
agitation. Severe cases are life-threatening and are
identified by delirium, severe hypertension, tachy-
cardia, rigidity, and hyperthermia greater than 41°C.
These may be complicated by seizures, renal failure,
disseminated intravascular coagulation and death.
Subacute or chronic cases may occur, though moder-
ate to severe cases typically present within 12 hours
of onset. A huge variety of drug combinations, or a
single drug, can induce SS as can withdrawal from
medication. Such drugs include selective serotonin
reuptake inhibitors (SSRIs), tricyclic antidepressants
(TCAs), monoamine oxidase inhibitors (MAOIs), sero-
tonin norepinephine reuptake inhibitors (SNRIs),
triptans, trazodone, opioids, buspirone, linezolid,
L-tr yptophan, and methylenediox ymethamphet-
amine (MDMA), and others. The combination of
MAOIs with other serotonergic drugs (in particular
meperidine, dextromethorphan, SSRIs or MDMA)
is associated with severe symptoms. SS can present
with non-specific laboratory abnormalities including
metabolic acidosis, rhabdomyolysis, elevated creati-
nine, myoglobinuria, leukocytosis and elevated cre-
atine kinase. The mainstay of treatment is supportive
care, namely hydration, control of autonomic distur-
bances, treatment of rigidity and hyperthermia, and
agitation control. Additional treatment, including
agents to reverse or block the effects of excess sero-
tonin agonism may be appropriate. Table 25.1 shows
the range of presentation of SS.
SS is a clinical diagnosis, and there are two clini-
cal tools for diagnosing the syndrome. The first are the
Hunter Criteria. The patient must have taken a seroten-
ergic agent and have one of the following: spontaneous
clonus; inducible clonus plus agitation or diaphoresis;
ocular clonus plus agitation or diaphoresis; inducible
clonus or ocular clonus, plus hypertonia and hyperther-
mia; tremor plus hyperreflexia. The second diagnostic
tool uses the Sternbach Criteria. The patient must be
using a serotonergic agent, must have no other causes
of symptoms, must not have recently used a neurolep-
tic agent and must have three of the following: mental
322 Medicinal poisons

Table 25.1 Presentation of serotonin syndrome–spectrum of symptoms of serotonergic toxicity

Severity Neuromuscular excitation Altered mental status Autonomic dysfunction
Mild Hyperreflexia Anxiety Diaphoresis
Tremor Restlessness Mydriasis
Myoclonus Insomnia Tachycardia
Moderate Opsoclonus Agitation Hypertension
Spontaneous or inducible Hyperthermia
clonus (<40°C, <104°F)
Hyperactive bowel sounds
Diarrhoea, nausea, vomiting
Severe Rigidity Coma Severe hyperthermia
Respiratory failure Delirium (≥40°C, ≥104°F)
Tonic-clonic seizure Confusion Dynamic blood pressure
Source: Wang RZ et al. Cleveland Clinic J Med 2016;83(11):810–817.

status changes; agitation; hyperreflexia; myoclonus;
diaphoresis; shivering; tremor; diarrhoea; incoordina-
tion; fever. Generally, the Hunter Criteria are considered
more specific and more sensitive than the Sternbach
Criteria. A list of drugs known to cause SS is given in
Box 25.1.
QT interval prolongation (long QT
syndrome)
Since the 1990s, the concept of primary ‘inherited’
arrhythmia syndromes, or ion channelopathies,
has developed from advances in molecular genet-
ics. Alterations in genes coding for membrane pro-
teins, such as ion channels or their associated proteins
responsible for the generation of cardiac action poten-
tials (AP), cause specific malfunctions which eventu-
ally lead to cardiac arrhythmias. These arrhythmic
disorders include a wide variety of conditions. Among
these, long QT, and Brugada, syndromes are the most
extensively studied, and drugs cause a phenocopy of
these two diseases. More than 10 different genes have
been reported to be responsible for each syndrome.
Individuals with long QT syndrome (LQTS) experience
abnormal prolongation of the QT interval – the portion
of the electrocardiogram (ECG) that represents repolari-
sation of cardiomyocytes (Figure 25.1). The QT interval
extends from the onset of the Q wave to the end of the
T wave. The normal rate-adjusted length for the QT
interval is less than 440 milliseconds. A prolonged QT
interval favours the occurrence of a lethal form of ven-
tricular tachycardia known as torsades des pointes. The
QT prolongation may be caused by genetic aberration
or it may be acquired. Even those with the genetic form
of the disease may have a perfectly normal-appearing
electrocardiogram until some event causes the QT
interval to lengthen, become pathologically long and
produce an arrhythmia. The diagnosis is made by DNA
resequencing.
An acquired form of this disorder also exists and is,
in fact, much more common than the heritable form
of the syndrome. Acquired LQTS is the result of a drug
interaction between a drug and one of the channels
which controls the orderly sequence of depolarisa-
tion within the heart’s individual cardiomyocytes. The
structure in question is called the ‘rapid delayed repo-
larising channel’, abbreviated as hERG. The molecular
structure of the hERG channel is shown in Figure 25.2.
Some individuals carry mutations that make them
more subject to hERG interactions. The end result
is the same as with any hereditary cause of the dis-
ease: QT prolongation, arrhythmia and sudden death.
Methadone is perhaps the most notorious of the drugs
that produces this syndrome but, as indicated in Box
25.2, the list of drugs is a long one and is growing con-
tinuously. Routine toxicology screening will not reveal
whether this interaction has occurred, and there will be
no detectable changes at autopsy, making a thorough
review of the medical history mandatory; even then the
diagnosis may be impossible to make at autopsy.
Drugs with unique modes of action
Some drugs have unique modes of action. Examples
include lithium, which though itself is devoid of any
psychoactive effects except as a mood stabiliser, has a
very complex mode of action. In fact, its mode of action
is not known with certainty. There is some evidence that
an excitatory neurotransmitter could be involved. It has
also been proposed that lithium alters gene expression.
Chronic lithium poisoning is characteristically asso-
ciated with greater toxicity than acute ingestion, and
 Drugs with unique modes of action 323

Box 25.1 Drugs known to cause sero- QRS

complex

tonin syndrome R
Antidepressants
Monoamine oxidase inhibitors
Selective serotonin reuptake inhibitors
Tricyclic antidepressants
Bupropion ST
segment
Trazadone PR
segment T
P
Narcotic analgesics
Buprenorphine
Fentanyl
PR interval Q
Hydrocodone
S
Merperidine
QT interval
Oxycodone
Pentazocine
Figure 25.1 Electrocardiogram (ECG) showing QT interval
Tramadol which can be prolonged in the repolarisation of cardio-
Stimulant drugs myocytes. (Courtesy of Steven B Karch.)
Cocaine
All amphetamines No discussion of forensic toxicology would be com-
plete without some mention of insulin poisoning via the
Methylphenidate
exogenous administration of insulin. Insulin poisoning
Migraine treatments was once a popular means of homicide; now it is rare.
All triptans (agents that bind type 1 serotonin Insulin overdose can cause fatal brain damage, but if
receptors overdose is suspected it can be confirmed by several dif-
ferent methods. Analysis of homicidal insulin overdose
Psychedelics
LSD (lysergic acid diethylamide)
MDMA (3,4-methylenedioxymethampheta­mine,
commonly known as ecstasy)
MDA (3,4-methylenedioxyamphetamine)
Miscellaneous agents (many different types of
drugs fall into this category)
Chlorpheniramine
Dextromethorphan
Lithium
Olanzapine
Risperidone
Ritonavir

is usually manifested by neurotoxicity of rapid onset.

Another feature of lithium poisoning is delayed cardio- Figure 25.2 Rapid delayed repolarising (hERG) channel:
toxicity, usually manifesting as bradycardia. Diagnosis a computer rendering showing an experimental anti-
of poisoning is by measurement of blood lithium con- arrhythmic drug docking in within the central cavity of
centrations. the hERG potassium channel.
324 Medicinal poisons

Bibliography and information

Box 25.2 Drugs causing QT
prolongation sources
Baird-Gunning J, Lea-Henry T, Hoegberg LCG, et al. Lithium poi-
All of the drugs listed below have been shown to soning. J Intensive Care Med 2017;32(4):249–263.
cause ventricular tachycardia (torasades des pointes). Barile FA. Clinical Toxicology: Principles and Mechanisms. Boca
Note that many, though far from all, are either drugs Raton: CRC Press; 2004.
intended to treat cardiac arrhythmias or are macro- Beakley BD, Kaye AM, Kaye AD. Tramadol, pharmacology, side
lide antibiotics. effects, and serotonin syndrome: a review. Pain Physician
2015;18(4):395–400.
• Amiodarone • Ibutilide Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med
• Arsenic trioxide • Levomethadyl 2005;352:1112–1120.
• Astemizole • Mesoridazine Byard RW. A review of the potential forensic significance of tradi-
• Bepridil • Methadone tional herbal medicines. J Forensic Sci 2010;55:89–92.
• Chloroquine • Pentamidine Drummer O. The Forensic Pharmacology of Drugs of Abuse. London:
• Cisapride • Pimozide Hodder Arnold; 2001.
• Clarithromycin • Procainamide Dvir Y, Smallwood P. Serotonin syndrome: a complex but easily
• • avoidable condition. Gen Hosp Psychiatry 2008;30(3):​284–287.
Disopyramide Quinidine
Ferner RE. Forensic Pharmacology: Medicines, Mayhem and
• Dofetilide • Sotalol Malpractice. New York: Oxford University Press; 1996.
• Droperidol • Sparfloxicin Flanagan RJ, Taylor AA, Watson ID, Whelpton R. Fundamentals of
• Erythromycin • Terfenadine Analytical Toxicology. London: Wiley-Interscience; 2008.
• Halofantrine • Thioridazine Glaister J. A Text-Book of Medical Jurisprudence, Toxicology and
• Haloperidol Public Health. Edinburgh: Livingstone; 1902.
Johansen NJ, Christensen MB. A systematic review on insulin
overdose cases: clinical course, complications and treatment
options. Basic Clin Pharmacol Toxicol 2018;122(6):650–659.
is always a challenging task in forensic practice because
Karch SB, Drummer O. Karch’s Pathology of Drug Abuse,
of the difficulties in toxicological analysis as well as
5th ed. Boca Raton: CRC Press; 2015.
the elusive pathologic changes. C-peptide is a peptide Luff AP. Text-Book of Forensic Medicine & Toxicology, Volumes I and
that is made when proinsulin is split into insulin and II. London: Longmans, Green and Co; 1895.
its C-peptide fragment. This event occurs just before Ramalho D, Freitas J. Drug-induced life-threatening arrhyth-
release of insulin from the pancreas. If concentrations of mias and sudden cardiac death: a clinical perspective of
the peptide are very low and insulin very high, the dis- long QT, short QT and Brugada syndromes. Rev Port Cardiol
parity would suggest that exogenous insulin had been 2018;37(5):435–446.
administered. However, unless the blood specimen is Sunderland N, Wong S, Lee CK. Fatal insulin overdoses: case
frozen, levels of C-peptide may degrade rapidly. DNA report and update on testing methodology. J Forensic Sci
2016;61(Suppl 1):S281–S284.
analysis offers another possible approach. Biosynthetic
Thorpe EL, Pizon AF, Lynch MJ, Boyer J. Bupropion induced sero-
insulin is now produced by genetic engineering. Some of
tonin syndrome: a case report. J Med Toxicol 2010;6:​168–171.
the bioengineered insulin has a slightly different struc- Tong F, Wu R, Huang W, et al. Forensic aspects of homicides by
ture than human insulin and these differences can be insulin overdose. Forensic Sci Int 2017;278:9–15.
detected. A friend, relative or care-giver may be the one Turker I, Ai T, Itoh H, Horie M. Drug-induced fatal arrhythmias:
who carries out homicide by insulin injection. Suicide acquired long QT and Brugada syndromes. Pharmacol Ther
by insulin overdose is well recognised. 2017;176:48–59.
26 Miscellaneous poisons
▪▪ Arsenic
▪▪ Carbon monoxide
▪▪ Cyanide
Arsenic
When arsenic is detected in a post mortem tissue sam-
ple the significance of its presence is often difficult to
determine. The presence of arsenic may indicate acute
poisoning or it may indicate nothing at all. This pre-
dicament arises because arsenic exists in two forms:
organic and inorganic. The term ‘organic’ indicates that
the arsenic is bound to another organic molecule and
unable to exert toxicity (the resultant compounds are
called arsenosugars and arsenobetaine). In contrast,
the term inorganic arsenic indicates that the arsenic
atom exists as a salt bound to another cation; this salt
may disassociate and then cause poisoning. The arsenic
found in oysters from contaminated oyster beds is an
example of organic arsenic, whereas the arsenic found
in coal deposits is an example of the inorganic form. The
standard method used to detect arsenic in post mortem
materials does not differentiate organic from inorganic
arsenic, so the mere detection of this compound has
little significance, at least not without a very suggestive
clinical history.
In its free form, arsenic is highly toxic. This is unfor-
tunate as arsenic is found in the drinking water of mil-
lions of people all around the world. Estimates suggest
that more than 13 million Americans, mainly those who
use well water, are exposed to toxic levels of free arsenic
every day. The entire aquifer of the Indian subcontinent
is also contaminated with arsenic, which explains why
many Indian herbal remedies are contaminated with
arsenic. Mere exposure to arsenic does not guarantee
illness because the liver is capable of rapidly detoxifying
free arsenic and excreting it from the body. This protec-
tive mechanism does have its limits though, and in the
presence of massive amounts of arsenic, the liver’s abil-
ity to detoxify arsenic is overwhelmed.
Arsenic poisoning was once a popular type of homi-
cide, but no longer. Chronic arsenic poisoning is now
most likely to be seen in children who have ingested
arsenic pigments found in old lead-based paints (the
two elements are often commingled). Such paint still
exists on the walls of some Victorian-era homes and
constitutes a health menace.
▪▪ Lead
▪▪ Methanol
▪▪ Bibliography and information sources
Three forms of arsenic poisoning are recognised:
acute, subacute and chronic. At any stage of the disease
the breath may have garlic-like odour (as will a cadaver’s
tissues at autopsy). In acute poisoning, when 1 g or more
of inorganic arsenic has been administered, gastroin-
testinal symptoms predominate with bloody vomiting
and severe diarrhoea. The diarrhoea can be sufficiently
copious to cause shock and cardiorespiratory failure.
If the victim dies very quickly, no abnormalities
will be evident at autopsy. However, if a few hours
pass before death occurs, inspection of the upper gas-
trointestinal (GI) tract will show that the oesophagus
has become red and inflamed. In some instances, the
inflammation can be so intense that the bowel is said to
have a ‘red velvet’ appearance. The only other reliable
post mortem change produced by arsenic poisoning is
bleeding from the muscle that lines the inner surface
of the left side of the heart (an area known as the left
ventricular subendocardium). Unfortunately, this is a
relatively non-specific abnormality seen in conditions
where the blood pressure suddenly collapses; the car-
diac changes can be especially prominent when there
has been massive blood loss from arsenic-induced
bloody diarrhoea.
Chronic arsenic poisoning presents a very different
picture and may be difficult or even impossible to prove
with certainty. It is sometimes diagnosed as gastroen-
teritis or, occasionally, neuropathy. Victims may present
with vague symptoms of leg and arm pain secondary to
arsenic-induced nerve damage. In chronic poisoning
the skin may become overly dry and pigmented, espe-
cially within the lines of the forehead and neck. Hair loss
is common, and there may be swelling of the legs. In the
early stages of chronic poisoning, the stomach looks
normal, but eventually haemorrhagic gastroenteritis
will develop. The liver will contain excessive amounts
of fat, but usually only around the edges. The kidney and
heart will be damaged, but the damage is only apparent
if the tissues are examined with a microscope. The nails
may show ‘Mee’s lines’ – transverse white bands across
the fingernails. It has been proposed that a chronic
arsenic intoxication diagnostic score (CAsIDS) be used
to establish chronic poisoning. A distinctive feature of
326 Miscellaneous poisons
CAsIDS is the use of bone arsenic load as an essential
criterion for the individual risk assessment of chronic
arsenic intoxication, combined with a systemic clini-
cal assessment. Such cases (fatal and non-fatal) provide
complex clinical conundra.
Carbon monoxide
Intoxication from carbon monoxide (CO) is a phenom-
enon that occurs in a wide variety of settings worldwide.
CO is a major environmental toxin whose effects were
described over a century ago by Haldane. It is consid-
ered a public health issue in many countries. It is a
colourless, odourless and non-irritant gas produced by
the incomplete combustion of hydrocarbons and found
whenever organic matter is burned in the presence of
insufficient oxygen. The highest concentrations to be
found in the modern urban environment are generated
by motor vehicles, petrol-powered tools, heaters and
barbecues. Ambient air concentrations of more than
100 ppm are considered dangerous to human health.
The effects observed include a variety of physical and
neurological signs and symptoms ranging from none
to death. Exposure occurs in two main ways: (1) acute
exposure for varying lengths of time where the effects
are generally immediately obvious, and (2) delayed or
chronic exposure where the effects may be unrecog-
nised for days, months or years. The diagnosis of CO
exposure may be one of exclusion. Figure 26.1 shows
Public Health England’s guidelines for diagnosing CO
poisoning.
The problems of recognising low-grade exposure to
CO may result in a considerable underestimation of the
problem. Between 1995 and 2018, a total of 697 deaths
from unintentional CO poisoning occurred in the UK,
with a male to female ratio of 2:1. The number of deaths
each year has reduced dramatically from 65 deaths in
1995/96 to 3 deaths in 2017/18.
CO dissolves in plasma and binds to oxygen-trans-
porting proteins haemoglobin (in plasma) and myoglo-
bin, and the cytochrome system in tissues. The most
significant affinity is for haemoglobin. CO is absorbed
through the lungs and binds to haemoglobin (Hb) form-
ing carboxyhaemoglobin (COHb). This a reversible reac-
tion that can be described as follows:
HbO2 + CO → COHb + O2
The affinity of Hb for CO is up to 250 times greater
than that for oxygen and the presence of CO results in
a shift of the oxygen–haemoglobin dissociation curve
to the left, causing decreased oxygen-carrying capacity
and impaired delivery of oxygen to the tissues. Cellular
hypoxia results and cardiac function is diminished
because of hypoxia. The link between levels of CO and
effects is not direct. The amount of uptake is governed
by a number of variables, all of which are interrelated
and include: relative concentrations of CO and oxygen,
alveolar ventilation, duration and intensity of exposure.
However, chronic exposure to high levels of CO leads
to CO binding to proteins with less affinity than hae-
moglobin, such as myoglobin and cytochromes of the
P450 system, particularly a3. Differential affinity may
also account for some of the variations in response to
exposure. Hypoxic stress caused by CO exposure alone
would not seem to account for some of the longer-term
effects and it is believed that CO also initiates a cascade
of events culminating in oxidative stress.
The World Health Organisation has issued guide-
lines for the level of CO in the air that will prevent blood
COHb levels from rising above 2.5 per cent. Exposure to
CO may be difficult to detect. Work, domestic and lei-
sure settings may all account for exposure. If exposure
is suspected, it is appropriate to use a system such as
the CH2OPD2 mnemonic to try to explore the source of
environmental exposure (enquiring about Community,
Home, Hobbies, Occupation, Personal, Diet and Drug
issues). Systematic enquiry is the most efficient way of
establishing a cause and a source.
Poisoning by CO is described as a ‘disease with a
thousand faces’ because of its many different clinical
presentations. Classic acute CO intoxication is said to
cause the triad of cherry-red lips, cyanosis and reti-
nal haemorrhages, but this type is rare. In many cases
a more insidious presentation develops and the only
indicator may be a general malaise or suspicion of a
viral-type illness. Specific symptoms include headache,
dizziness, nausea, shortness of breath, altered vision,
altered hearing, chest pain, palpitations, poor concen-
tration, muscle aches and cramps and abdominal pain.
Sometimes these may occur in clusters and sometimes
in isolation. More serious effects include loss of con-
sciousness, myocardial ischaemia, hypotension, con-
gestive cardiac failure, arrhythmias, mental confusion
and mood variation. These symptoms and signs may be
present during acute exposure at higher level in non-
fatal cases, but also in the more chronic or prolonged
exposures.
In addition to the symptoms and signs discussed
there are a variety of neurological, psychiatric and psy-
chological sequelae that may develop days, months and
years after initial exposure.
Diagnosis is made by measurement of venous COHb
levels; however, there is no absolute level that can confirm
the presence or absence of poisoning. A level above 10 per
cent is considered to confirm the diagnosis, unless the
individual is a heavy smoker (Box 26.1). Concentrations
of COHb in arterial blood are not significantly different
from venous concentrations and so an arterial sample
is not required for diagnosis. Arterial blood gas mea-
surements can show a mixed picture of normal partial
pressure of o­ xygen, variable partial pressure of carbon
dioxide, and decreased oxygen saturation, all in the
 Carbon monoxide 327

Figure 26.1 Diagnosing CO poisoning. (From Public Health England, 2015.) (Continued)

presence of a metabolic acidosis. Problems arise, par-
ticularly in chronic, lower-dose exposures, because the
COHb concentration will revert to ‘normal’ values once
the source of exposure has been removed; however, the
removal process is dependent on the half-life of COHb in
the particular setting. Normal COHb levels do not neces-
sarily rule out CO poisoning.
Table 26.1 shows the symptoms produced by increas-
ing concentrations of CO within the body.
CO was once a frequent means of suicide, but changes
in technology have led to a marked decrease in the num-
ber of deaths. In the 1950s, inhaling coal gas accounted
for nearly half of all suicides in the UK, but the rate
markedly declined after natural gas replaced coal gas
328 Miscellaneous poisons

Figure 26.1 (Continued) Diagnosing CO poisoning. (From Public Health England, 2015.)

in the 1960s. The introduction of catalytic converters for
automobiles has reduced, but not quite eliminated, sui-
cides committed by inhaling the exhaust fumes from a
car engine operating in an enclosed space. The catalytic
converters found in cars today eliminate over 99 per
cent of the CO produced but, even then, very substantial
amounts of CO may be generated if a car is left with
its engine running in a closed garage. The majority of
accidental poisonings and suicides by CO occur as a
result of burning charcoal in a confined space. In the
most frequent scenario, a charcoal barbecue is lit in a
closed room. If death was solitary and intended, then
 Methanol 329

most of the time the increase is asymptomatic and blood

Box 26.1 Haemoglobin concentrations
of carbon monoxide (CO)
and guideline symptoms
• In non-smokers less than 3% total haemoglobin
contains CO
• In smokers 2–10% of haemoglobin contains CO
• 20–30% of haemoglobin causes headache, nau-
sea, vomiting and confusion
• 30–40% of haemoglobin causes dizziness, mus-
cle weakness, confusion, rapid heart beat
• 50–60% of haemoglobin causes loss of
consciousness
• Over 60% of haemoglobin causes seizures,
coma, death
concentrations are modest. In non-smokers, the average
blood cyanide concentration is less than 0.01 micromol
µ mol/L, rising fourfold after smoking. In chronic smok-
ers, concentrations may be 10 times higher.
Large infusions of sodium nitroprusside, used to
treat hypertensive emergencies, can lead to serious cya-
nide poisoning, but more commonly cyanide poisoning
is encountered in fire survivors, as many contemporary
fabrics and building materials contain plastics that
can liberate cyanide during combustion. Cyanide is
said to have the smell of bitter almonds, but approxi-
mately 10 per cent of the general population are con-
genitally unable to perceive this smell. This rarely leads
to exposure in the autopsy suite because, in the course
of normal circumstance, multiple staff members will be
present and at least one is like to perceive the odour.

the windows and doors are likely to have been sealed off.
If not, it may be difficult to determine whether or not the
Lead
cause of death was accident or suicide. Routes of lead exposure include contaminated air,
water, soil, food and certain lead-containing consumer
products, particularly those made in China. It has been
Cyanide associated with the use of Ayurvedic medicines and
Cyanide ions prevent cells from utilising oxygen; they food contamination. In adults, the most common cause
inhibit the enzyme cytochrome c oxidase. High concen- of lead poisoning is occupational exposure, whereas in
trations of cyanide lead to cardiac arrest within minutes children it is the lead paint that exists in older homes.
of exposure. Exposure to lower levels of cyanide over a Aged lead paint is likely to peel off walls and may look
long period (e.g., after use of cassava roots as a primary like an attractive item of food to children. Lead is toxic
food source, which is a relatively common occurrence in because it can substitute for calcium in many funda-
tropical Africa) results in increased blood cyanide lev- mental cellular processes, although how it does so is
els, which can cause weakness and a variety of symp- not entirely clear: neither the electronic structures nor
toms including permanent paralysis. Cigarette smoking the ionic radii of the two elements bear any particular
also increases blood cyanide concentrations, although resemblance. Nonetheless, lead can cross red blood cell
membranes as well as the blood–brain barrier and enter
the neuroglia cells which support brain function. This
Table 26.1 Symptoms produced by carbon monoxide explains why exposed children may develop permanent
learning and behavioural disorders.
Concentration
Symptoms of lead poisoning include abdominal pain,
(ppm) Symptom
headache, anaemia, irritability and, in severe cases, sei-
35 Headache, dizziness zures, coma and death. X-rays will expose dense lines
100 Headache, dizziness in the long bones of children, and red cells undergo a
change known as basophilic stippling, where blue-stain-
200 Headache, loss of judgement ing remnants of destroyed DNA are seen lining the mar-
400 Frontal headache gins of the red cells. This change is diagnostic for lead
800 Dizziness, nausea, convulsions poisoning. The main tool for diagnosis is measurement
of the blood lead level. Treatment depends on the blood
1600 Tachycardia, nausea, death in less level and is designed to remove the lead from the body
than 1 hour (chelation therapy).
3200 Tachycardia, nausea, death in less
than 20 minutes
6400 Convulsions, respiratory arrest,
Methanol
death in 1–2 minutes Like ethanol, methanol can cause fatal central nervous
system (CNS) depression. Methanol intoxication is an
12,800 Unconsciousness after two breaths, uncommon but serious poisoning. Its adverse effects are
death in 3 minutes due primarily to the impact of its major metabolite formic
330 Miscellaneous poisons
acid and lactic acid resulting from cellular hypoxia. All of
these processes occur in the liver. Formic acid (formate)
is toxic because it inhibits mitochondrial cytochrome c
oxidase, causing hypoxia at the cellular level. Symptoms
including abdominal pain and loss of vision can appear
a few hours to a few days after exposure, reflecting the
time necessary for accumulation of the toxic byprod-
uct. Methanol also causes metabolic acidosis. Methanol
poisoning most often occurs after drinking windscreen-
washer fluid, but methanol is also used in copy machines
and can be found in many other products, even embalm-
ing fluid. Methanol poisoning still remains a well-known
consequence of ‘moonshine’ liquor ingestion, although
this practice is increasingly uncommon. When paedi-
atric poisoning occurs, it is usually the result of having
ingested methanol-containing household products.
Ingestion of even small amounts of methanol, in addi-
tion to causing profound metabolic acidosis, may lead to
blindness or even multiorgan failure and death.
The initial symptoms of methanol intoxication
include CNS depression, with headache, dizziness,
nausea, lack of coordination and confusion. Large doses
quickly lead to unconsciousness and death. Once the
initial symptoms have passed, a second set of symptoms
can be observed 10–30 hours after the ingestion. These
include blindness and worsening acidosis. These sec-
ondary symptoms are caused by accumulating levels of
formate in the bloodstream. The process may progress
to death by respiratory failure.
Methanol poisoning treatment can include admin-
istration of ethanol or fomepizole, both inhibitors of the
enzyme alcohol dehydrogenase to prevent formation
of its metabolites, and hemodialysis to remove metha-
nol and formate. Supplemental treatment with sodium
bicarbonate for metabolic acidosis and haemodialysis
or even haemodiafiltration can be used to remove meth-
anol and formate from the blood.
Because of its toxic properties, methanol is frequently
used as a denaturant additive for ethanol manufactured
for industrial uses as this addition of methanol exempts
industrial ethanol from liquor excise taxation. Methanol
is often referred to as ‘wood alcohol’ because it was once
produced chiefly as a by-product of the destructive dis-
tillation of wood.
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 Index
A aneurysm phases and signs, 162–166
atheromatous, of the aorta, 73–74 restraint, 171–172, 209
abdomen
Charcot-Bouchard, 76 aspiration of water, 193–194
asphyxia due to pressure on,
circle of Willis, 75 assault
173–174
dissecting, of the aorta, 74 child, see children
injury, 159–160 intracranial, 75–76 occasioning actual bodily harm,
child, 160, 248 ruptured berry, 75–76 offence of, 106
organs, see organs syphilitic, 74–75 sexual, see sexual assault
abortion, 78 animals subarachnoid haemorrhage and,
abrasion, 113–116 decomposition, predation and, 75, 152–153
abuse, child, see child abuse 60, 63–64, 67–68 asthma, 77, 79–81
Abusive Head Trauma (AHT), 98 transplanted material from, 35 atheromatous aortic aneurysm,
accident anthropology, forensic, 53, 63, 68, 73–74
children, 102 145, 198, 203 atheromatous plaque, 70
fire death, 184–185 antidepressants, 308, 314 Attenuating Energy Projectile
firearms death due to, serotonin syndrome, 308, 323 (AEP), 141
142–143 anus (in sexual assault) autoerotic asphyxia, 171–172
accidental trauma in infants, 98 examination, 237 autopsy (post mortem
acid bath murders, 278 child, 252 examination;
acid phosphatase test, 286 penetration/intercourse, 237 necropsy), 45–49
actual bodily harm, offence of aorta clinical, 45
assault occasioning, 106 aneurysms, 73–74 Coronary commissioning/
adipocere, 62 stenosis (incl. aortic valve), requiring, 11
adjudication (fitness to practice 71–72 diagnostic approach, 45
procedures), 25 appeal (doctor’s right of) against drowning, 194
affidavit, 8 decision on fitness-to- examination, 46
affirmation, 8, 9 practice, 26–28 facilities, 46, 48
age determination appearance after death medicolegal, 45, 46, 47, 48
bruising, 112 early post mortem interval, Minnesota protocol, 49–52
decomposed remains, 203 55–58 permission for organ/
fetal, 85 facial, 57, 202 tissue harvesting for
gestational, 85 arms, defence injuries, 122–123 transplantation, 34
living, 204, 205 arrhythmias, 69, 71 quality, 48
air bags, 265 drowning, 194–195 rate variations between
air rifles, 133, 140 drug-induced, 322 jurisdictions, 44
aircraft fatalities, 267–268 arrhythmogenic right ventricular reports, 11
airgun, 133, 140 cardiomyopathy, 73 aviation incidents, 267–268
airway in drowning, 194 arsenic, 325–326 axonal injury, traumatic, 155
alcohol, see ethanol; methanol hERG channel and, 297
Alcohol Use Disorders Identification artefactual injuries, immersed
B
Test (AUDIT), 218 body, 193
allergic drug reactions, 297 arterial disease bacteria and decomposition, 59
amphetamines, 308, 309–310 coronary, 69–71 ballistic injuries, 133–147
designer, 315 extracardiac, 73–76 Barleycorn Public House
amputation arterial spurting, 289 Murder’, 169
in torture, 273 asphyxia, 162–175 baroreceptors, carotid sinus,
by train, 267 classification/types, 162, 163, 166, 167
amylase test, 287 166–172 baton(s), 210–211

333
334 Index

baton (plastic) rounds, 133, 211–213 neuropathological haemoglobin concentrations

Bayes theorem, 281–283 examination, 81 in, 329
beanbag projectile, 141 vascular lesions, 75–76 poisoning, 162, 326–329
behavioural abnormalities in brain-stem death/cessation of symptoms, 329
hypothermia, 186–187 function, 31, 32 carboxyhaemoglobin (COHb),
benzodiazepines, 314 breastfeeding and morphine 326–327
1-benzylpiperazine (BZP), 317 poisoning, 300 fire victims, 182, 183
berry aneurysm, ruptured, 75–76 breath tests, alcohol, 258, 304 cardiac problems, see heart
best practice, forensic pathologist, 47 bruising, 109–113 cardiomyopathy, 73
bicycle (pedal cycle) injuries, 266 child/infant, 245–249 cardiorespiratory arrest, criteria
bite wounds/marks, 122; see also deceased, 88 for diagnosis and
‘love’ bites feet, due to torture, 126, 127 confirmation of death
infant, 101 from footwear/shoewear, 111, 114, following, 31
photography, 129–130 121–122, 292 cardiovascular disease, 69–76
self-inflicted, 124 patterned, 112 carotid sinus baroreceptors,
from trained dogs, 213 pedestrians, 263 166, 167
Bland case, 32–33 brush abrasion, 113 case law, 2
blast (explosions), 144–145 bullets, 137, 139, 140, 141; see also Casper’s Law (or Ratio), 59
bleeding, see haemorrhage plastic rounds cast-off, 289
blisters, electrical causing, 188 Dum-Dum, 135 cellular death, 30
blood, 279–280 burial, 43, 53 central nervous system stimulants,
alcohol concentrations, and buried remain, 60–62 see stimulants
clinical effects, 304 burns, 177–178 cerebral haemorrhage, 76
as drug testing matrix, 298–299 classification, 178 cerebral infarction, 76
post mortem, 57–58 electrical, see electrical trauma cerebral oedema, 154
bloodstains, 279–280 infant, 101 cerebral thrombosis, 76
pattern analysis, 287–290 self-inflicted, 125 cerebrovascular accident (CVA), 76
blowflies, 67 severity and extent, 177–178 certification of death, 35–38
blowout fracture of orbit, 150 BZP (1-benzylpiperazine), 317 cervical spinal injury, 158
blunt-force injury, 107, 108–118 chain of custody, 278–279
abdomen, 159 Chancery, 4
C
chest, 158 channelopathies, 72
Body Mass Index (BMI), 202 cadaver (dead body; the deceased) chaperones in intimate
body appearance, see appearance examination, 14
dead, see cadaver donation from, 34 Charcot-Bouchard aneurysm, 76
fluids, see fluids identification, see identification chest
piercings, 202 infant, injuries, 88–102 asphyxia due to pressure on,
body temperature, after death, cadaveric rigidity, 56 173–174
58–59 café coronary, 172 injury, 158–159
bombing (explosions), 144–145 cannabis (marijuana), 316–317 child, 248
bone capacity (mental) child abuse, 87–102, 244–253
dating, 63 to consent, disclosure accidental injury, 102
determination of remains as, concerning patients bites, 101
202, 203 without, 21–22 bruising, 88, 98
fractures, infants, 88–98 to make decisions burns, 101
sex determination from, 203 consent of patients with, 23 definitions, 245
bow(s), 141–142 consent of patients without, epidemiology, 67, 87
bowel, see intestine 24–25 law, 245–246
bows, 141 Captagon (fenethylline), 308 management, 252–253
brain; see also entries under car(s) physical, 88–102, 244, 245–251
cerebral occupant injuries, 263–265 regional injuries
injury, 132, 154–155 pedestrian injuries, 261–263 skeletal, 88–98, 100
child, 98 carbon monoxide, 326–329 skull fractures, 97–98, 100, 151
pedestrians, 262 diagnosis, 326, 327–328 head injuries, 98–99
with skull fractures, 150 fire victims inhaling, 183 ocular, 99–199

oral, 100
visceral, 100–101
scalds, 179, 247
sexual, 102–103, 244, 251–252
child death notification, 89–91
Child Death Overview Panels
(CDOP), 88
children (and young people); see also
child abuse; infants
post mortem in, 88
hypothermia, 185, 186
safeguarding, 246, 252–253
consent, 23–24
Children Act (1989), 244, 245, 246
choking, 172
choking game, 169
chop injury, 120
chronic arsenic intoxication
diagnostic score (CAsIDS),
325–326
circle of Willis aneurysm, 75
civil law, 3–4
Clinical Institute Withdrawal
Assessment of
Alcohol Scale, Revised
(CIWA-Ar), 220
cloning, 35
clothing
fibres, 293
in hypothermia, paradoxical
undressing, 186–187
cocaine, 308, 309–310, 312, 317
codeine and morphine poisoning in
breastfed neonate, 300
cold injury, see hypothermia
cold shock response, 195
colleagues, duty of physician to, 15
coma, 31, 32
common law, 2
complex non-linear systems’, 107
compression (pressure)
asphyxia due to, 162, 166–172,
173–175
handcuff, neuropathy due to, 210
consciousness
prolonged disorders of, 31–33
definitions of, 32
conducted electrical weapons,
213–214
spit guards/hoods, 214
conduction, cardiac, and sudden
death, 70
confidentiality, 10, 17, 19–22
not applying, see disclosure
conflict resolution, 208–209
consent (to disclose), 10, 15, 17, 19,
20–21
consent form to history
examination and report
(sexual assault), 231
contact blood staining, 287, 288
contact wounds
rifled weapons, 137–139
shotgun, 136
contrecoup injury to brain, 155–156
convulsions, see seizures and
convulsions
cooling, body, after death, 58–59
coronary artery disease, 69–71
Coroner
Commissioning/requiring
autopsy, 11
referral of deaths to, 43, 44
Coroners and Justice Act
(Amended) 2017
coughing blood, 289
County Court, 3
coup injury to brain, 155–156
courts, 1, 2
civil law, 3–4
criminal law, 1–3
evidence for, see evidence
witness in, see witnesses
cranial fractures, see skull fractures
crash helmets, motorcycle, 265
crime scene
evidence recovery, 278
examination, 276–278
Crime Scene Investigation effect, 277
criminal law, 1–3
statements and reports, 7–8
crocodile skin, 188
crossbows, 141–142
Crown Prosecution Service, 2
crush abrasions, 113, 114–115
crush asphyxia, 174
crystal meth (methamphetamine),
309
CS irritant spray, 211
CSI effect, 277
cuffs, 209–210
cyanide, 329
cytochrome P450 enzymes, 297, 300
D
damage (to items) assessment, 290
Damage-Associated Molecular
Patterns (DAMPs), and
’Alarmins, 106
Index 335
dating of bones, 63
death (mortality; fatality), 30–103;
see also cadaver;
homicide, infanticide;
lethal dose; suicide;
survival
alcohol detection after, 232
appearance after, 55–58
asphyxia, 162–175
bruising after, 112–113
burns-related, factors influencing
risk of, 178
certification, 35–38
definitions, 30–31
determination of cause of, 35–38
disclosure after, 22
drug redistribution after, 300
electrocution, 187, 188–189
fire, see fire
firearms, determination of
circumstances, 142–143
immersion
example causes, 192
mechanisms, 194–195
infants and children, 83–103
lightning, 189
medicolegal investigation, 43–45
multiple, see mass disasters
natural causes, 69–81
in police custody, 218–219
rapid changes after, 55
sudden and unexpected (from
natural causes), 69–81
suspicious, 48, 49, 157
time of, see time of death
transportation
aircraft, 267–268
marine, 268
railway, 266–267
deceased, see cadaver
deceleration injuries with car
occupants, 263
seatbelts and, 263–264
decisions and capacity to consent,
see capacity
Declarations of World Medical
Association (WMA), 14, 16
decomposition/putrefaction,
59–60
Identification of remains with,
202, 203
defence injuries, 122–123
degloving of immersed body,
191, 192
delirium, excited, 310
336 Index
dental structures, identification
from, 199–201
dependence, drug, 296–297
Deprivation of Liberty Safeguards
(DoLS), 43
dextromethorphan, 315
Diagnostic and Statistical Manual
of Mental Disorders
(DSM-IV), substance
abuse, 296–297
diatoms, 196
dilated cardiomyopathy, 73
dimethylaminocinnamaldehyde
(DMAC) test, 287
disclosure, 19–22
consent to, 10, 15, 17, 19, 20–21
disorders of consciousness,
prolonged, 31–33
dissecting aortic aneurysm, 74
dissociative anaesthetics, 315–316
divided attention tests, 258–261
diving response, 194
DNA analysis, 279–281
historic legal cases, 282
mixed DNA results, 283–286
of handled items, 285
profiling, 199, 279–281
DNA database, National, 285–286
DNA profiling, 199, 279–281
doctors/physicians, 4–7
in court
as witnesses, 4–7, 9–11
ethics and, see ethics
mass disasters and, 145–147
regulation, 25–28
doctrine of precedent, 2
documentation and records; see also
statements and reports
autopsy, 48, 49
evidence in, 2
injury, 127–130
child, 251
sexual assault, 232–236
dogs (law enforcement), 213
domestic violence
homicide, 41–42
non-fatal, 41
dopamine and stimulants, 308
downward drips of blood, 288
driving under influence of drugs,
257, 258–261
alcohol, 257, 258, 304
drowning, 162, 191–196
alcohol and, 195–196
diatoms, 196
pathophysiology, 193–194
signs of, 194
drugs, 295–324; see also ethanol;
toxicology
classification, 310
dependence, 296–297
driving under influence of, 257,
261
harm reduction, 307, 308, 318
idiosyncrasies, 297
interactions, 297
interpretation of measurements,
299–300
legal status, 307
licit and illicit, 307–318
common agents, 307–318
legal highs, 316, 317–318
medicinal, 321–324
in police custody, 218, 222
principles, 295–296
receptors, 296
redistribution (post mortem), 300
sexual assault using, 318–319
testing matrices, 298–299
tolerance, see tolerance
with unique mode of action,
322–323
withdrawal, see withdrawal
dry drowning, 194
dry submarino, 126
DSM-IV, substance abuse, 296–297
Dum-Dum bullets, 135
duties
physicians, 14–16, 17
UK perspectives, 14–16
of witnesses, 7
World Medical Association’s
amendments, 14, 15
expert witness, 6, 7
dyspnoea phase of asphyxia, 165
E
ear
bruising, 98
laceration, 117
ectopic pregnancy, 78
Edelman’s test, 287
eggs, insect, 67
elder abuse, 253
elderly, hypothermia, 185
electrical restraint devices, 213–214
electrical trauma (including burns),
187–189
torture, 273
electropherogram (EPG), 281
embolism
mesenteric, 77
pulmonary, 76–77
emergence, 107
emotional abuse of children,
245, 252
emphysema aquosum, 79, 194
empty hand restraint, 209
endocannabinoids, 316
end-of-life care, 32
entomology, see insects
entrance wounds
crossbows, 142
rifled weapons, 137–140
epidermal effects of immersion,
191, 192
epidural haemorrhage, see
extradural haemorrhage
epilepsy, 79–81
ethanol (alcohol), 302–305
absorption, 302
clinical effects, 304
driving and, 257, 258, 304
drowning and, 195–196
elimination of, 302–304
measurement, 304
metabolism, 302
methanol added to (for industrial
use), 330
pharmacokinetics, 303
absorption, 302, 304
elimination, 303–304
police custody and, 218, 220, 222
post mortem considerations, 304
screening, 218
sources and concentrations, 302
ethics (medical), 13–28
international codes, 14, 15, 16
mass disasters, 145, 146–147
practical aspects, 16–18
evidence, 7–9
for courts, 7–9
criminal law, 2, 3
documentary, 2
immersion, 191–192
recovery; see also samples
crime scene, 277, 278
firearms incident, 143–144
trace, 292–293
examination (human)
asphyxia survivors, 165–166
exhumed body, 53
intimate, guidance, 14
post mortem, see autopsy

in professional witness
statement, 11
scene of crime, 276–278
sexual assault, 229–230, 230–232
child, 251–252
torture, 272–273
examination (questioning in court),
8–9, 10
exchange principle, Locard’s, 276
excited delirium syndrome,
224–225, 226, 310
execution by hanging, 170–172
exhibit label, 278–279
exhumation, 53
exit wounds
crossbows, 142
rifled weapons, 137–140
expert witness, 4–7
explosions, 144–145
express consent, disclosure
requiring, 21
extension injury to neck, 158
extradural (epidural) haemorrhage,
152, 153
heat-related, 184
eye injury, see ocular injury
F
fabricated illness by proxy, 252
face
appearance/features
after death, 57, 200, 202
fire victim identification, 182
immersion in water, response to,
194–195
factitious disorder by proxy, 252
faeces, 287
falls
child, 98
from height, skull fracture, 151
familial homicide, 87
Family Court, 3
Fast Alcohol Screening Test
(FAST), 218
fat, body, chemical changes, 62
fatality, see death
Federal Evidence Rule 702 on
expert testimony, 5–6
female genital mutilation, 239–241
females; see also sexual assault
gynaecological conditions, 77–79
fenethylline, 308
fentanyl, 312
post mortem measurements, 300
fetus
deaths, 83
maturity estimation, 85
fibres, 293
field impairment tests, 261
fire(s), 180–185
cyanide poisoning in
survivors, 329
deaths during, 184–185
pathological investigation of,
180–183
escape failure, reasons, 183
investigations, 181
firearms, 133–140
bloodstains with, 289
determining circumstances of
death due to, 142–143
evidence recovery, 143–144
impact rounds, 212–213
injuries, 135–140
types, 133–135
fitness to interview’ and ‘fitness to
be charged’, 217
fitness to practice procedures, 25–28
flaming combustion, 181
flexion injury to neck, 158
fluids, body
analysis, 286–287
blood mixed with or mimicked
by, 289–290
food, choking on, 172
footwear, 291–292
marks left on skin, 114, 121–122,
292
force (use in law enforcement), 208
fractures
child/infant, 88–98, 247, 248
rib, see rib fractures
skull, see skull
sternal, 158–159
freshwater drowning, 193, 194, 196
frostbite, 186, 187
Frye test, 5
G
gamma-amino butyric acid type A
receptors (GABAA), 314
receptors, 314
gamma-hydroxybutyrate (GHB),
315, 318–319
gas formation, 59, 60
immersed body, 61
gastric contents
blood in, 290
Index 337
as drug testing matrix, 299
regurgitation after death, 55
time of death estimation, 67, 68
gastric haemorrhagic lesions in
hypothermia, 186, 187
gastrointestinal tract
disorders, 77
hypothermia and, 186
infant injuries, 100–101
general acceptance test, 5
General Medical Council
on duties of doctors, 14–16
regulations, 25
fitness to practice procedures,
25–28
genetic polymorphisms
and mutations (in
toxicology), 300; see
also single nucleotide
polymorphisms
ion channels, 297
and long QT syndrome, 322
opiate receptors, 296, 312
Geneva Declaration (of World
Medical Association), 14
genital (in sexual assault)
examination, 232
child, 251–252
injuries, 232
GHB (γ-hydroxybutyrate), 315,
318–319
Gilllick competence, 23–24
glass, 292–293
glue-sniffing, 317
graze, 113–116
grievous bodily harm, 106
gunshot injuries, 137–140; see also
firearms
gynaecological conditions, 77–79
H
haematoma, 110
haemoglobin, CO binding to, see
carboxyhaemoglobin
haemoptysis, massive, 77
haemorrhage/bleeding
cerebral, 76
extradural (epidural), 152, 153, 184
gastric, in hypothermia, 186
intracranial, 151–152, 184
retinal, 98, 101
subarachnoid, 75–76, 152–153, 154
subdural, 98, 152, 153
subpleural, 194
338 Index
hair as drug testing matrix, 299
hallucinogens (psychedelics)
serotonin syndrome, 323
hallucinogens, 314–315
hand guns, 134–135
hand(s); see also empty hand restraint
defence injuries, 122–123
strangulation using, 168–169
handcuffs, 209–210
hanging, 162, 170–171, 172
harm reduction with drugs, 307,
308, 318
head injuries, 149–156
child/infant, 88–98, 248
Health & Care Professions Council
(HCPC), 15–16
heart; see also arrhythmias
disease/disorders, 69–73
drowning and, 192
stimulant-related, 309
reflex cardiac arrest, 167
heat injury, 177–185
height determination from
decomposed/skeletalised
remains, 203
helmets, motorcycles, 265
Henssge’s nomogram, 64, 65
hepatic, see liver
hepatitis, viral, 229, 307
hERG potassium channel, 297, 322,
323
heroin, 297, 298, 299, 307, 312–313
adulterants, 313
hesitation’ or ‘tentative’
injuries, 124
‘hickey’ bites, 111
hide and die syndrome, 186–187
High Court, 3–4
Appeal against Fitness to Practice
decision, 26–28
Hippocratic Oath, 13, 14
HIV, 229, 239, 307
homicide (incl. murder), 40–42
domestic violence-related, 41–42
familial, 87
fire, 184–185
firearms, 142
global data
by age, 40, 41
by gender, 40–41
incidence, global, 40
infant, 83–85
mechanism, 42
as public health problem, 41
homologous transplantation, 33
human immunodeficiency virus,
229, 239, 307
Human Rights Act 1998, 33
human, identifying remains as, 203
humane killers, 141
hyperextension injury (neck), 158
hyperflexion injury (neck), 158
hypersensitivity reactions, drug, 297
hypertensive heart disease, 71
hyperthermia, 180
hypertrophic cardiomyopathy, 73
hypnotics, 314
hypostasis, post mortem, 56–58
hypothermia, 185–187
cold water, 185–187, 193, 196
I
ICD (International Statistical
Classification of Diseases
and Related Health
Problems), 37–38
IDENT1, 291
identification (of the dead or living),
198–205
dental, 122, 199–201
fingerprints, 201, 290–291
fire victims, 182
infant (dead) and mother, 85
methods, 198–202
criteria, 198–199
DNA profiling, 199
morphological characteristics,
201–202
tattoos and body piercings, 202
idiosyncratic drug reactions, 297
imaging (radiology), post mortem,
44, 48–49
fire victims, 182
immersion (in water), 60–2, 191–196;
see also drowning
diagnosis, 191, 193–194
evidence of, 191–192
hypothermia, 185–187, 193, 196
torture, 126
immersion and, 60–62
impact rounds, 211–213
impact spatter (blood), 288–289
incised wounds, 118
self-inflicted, 125
infant(s); see also child abuse
deaths, 83–85
non-accidental, 83–85, 249, 250
skull fractures, 88–98, 151
newborn, see neonates
infanticide, 83–85
infection
intravenous drug users, 307
sexually-transmitted, 229
‘Inflicted Head Injury’ (IHI), 98
inhalant abuse, 317
injection of illicit drugs, 307
injuries (trauma)
ballistic, 133–147
body response to, 106–107
cold, see hypothermia
documentation, 127–130
electrical, see electrical trauma
from force or restraint, 209–214
head, 149–156
heat, 177–185
immersed body, artefactual, 193
law, 105–106
non-accidental, see non-accidental
injury
non-fatal violence-related injury,
106–107
post mortem, 63–64
regional, 149–160
infants and children, 83–103, 151
self-inflicted, 124–126
in sexual assault, 237
subarachnoid haemorrhage due
to, 75, 152–153
survival after, 123–124
terminology, 105
transportation, 257–268
types of, 108–123
inquest, 43, 44
insects (and entomology),
decomposition, predation
and, 60, 63, 67–68
insulin poisoning, 323–324
interactions, drug, 297
interim orders tribunal, 26
International Committee of the Red
Cross, 271, 272
international dimensions
legal systems, 1
medical ethics, 14, 15, 16
International Statistical
Classification of Diseases
and Related Health
Problems (ICD), 37–38
interpersonal violence, 40–42
intervertebral disc injury, 158
intestine (bowel)
infant injuries, 100–101
infarction, 77
intimate examination, guidance, 14

intimate partner violence, 230
intracranial haemorrhage, 151–152
heat-related, 184
intracranial vascular lesion, 75–76
intrauterine death, 83, 84
intravenous drug misuse, 307
investigations (fitness to practise
procedures), 25–26
ion channels
cardiac/myocardial, drug
reactions and, 297
stimulants, 312
genetic disorders
(channelopathies), 73
genetic polymorphisms, see
genetic polymorphisms
irritant sprays, 211
exposure to, 212
ischaemic (coronary) heart disease,
69–71
Istanbul protocol, 127, 271–274
J
judicial hanging, 171
jury, inquest, 44, 45
JWH-018 (Spice), 316–317
K
Kastle–Meyer (K-M) test, 286
ketamine, 315, 318
khat, 309
kicking, 120–122, 292
kidney
injury, 159
transplant, live donor, 33–34
Kinetic Energy Devices (KED), 141
knife wounds, 118, 119, 120, 121,
122–123
L
lacerations, 105, 116–118
scalp, 149
larvae, insect, 67
law
disclosure required by, 19–21
drugs and the, 307
criminal, 1–3
civil, 3–4
doctors/healthcare professionals
and, 4–7
enforcement, force and restraint
in, 208–214
injuries, 105–106
sexual offences, 230
systems, 1–4
international comparisons, 1
lead, 329
legal highs, 316, 317–318
legal issues, see law
lethal dose (LD) and LD50, 295
Leuco-malachite Green (LMG) test,
286–287
levamisole as drug adulterant,
313, 317
Lichtenburg figure, 189
ligature strangulation, 168–169
lightning deaths, 189
lip injury, infant, 100, 101
lithium, 322–323
live donation, 33–34
liver
as drug testing matrix, 299
injury, 159, 160
infant, 101
lividity, post mortem, 56–58
Locard’s exchange principle, 276
long QT syndrome, 322
‘love’ bites, 110, 111
low copy number DNA
analysis, 285
low-template DNA analysis, 285
luminol, 290
Lund and Browder chart, 178, 179
lung flotation test in
infanticide, 84
lungs
in drowning, 194
injury, 159
tuberculosis, 77
M
maggots, 67
Magistrates’ Court, 3–4
major disasters, see mass disasters
males
sexual assault of, examination, 232
suicide by hanging, 171
manual strangulation, 168–169
marijuana, 316–317
marine fatalities, see sea
mass disasters, 202–204
doctors and, 145–147
maternal deaths, 78–79; see also
mother
m-chlorophenylpiperazine (MCPP),
317–318
Index 339
MCPP (meta-chlorophenylpiperazine),
317–318
MDMA (3,4-methylenedioxy­
methamphetamine),
315, 317
mechanical asphyxia, 162, 166–172
Medical Act 1983, 25
Medical Examiners (Medical
Reviewers in Scotland) in
England & Wales, 37
medicinal poisons, 321–324
Mee’s lines, 325
men, see males
Mental Capacity Act 2005, 43
mental capacity, see capacity
meow, see mephedrone
mephedrone, 318
mesenteric injury, 159
mesenteric thrombosis and
embolism, 77
meta-chlorophenylpiperazine
(MCPP), 317–318
methadrone, 318
methamphetamine, 309–310
methanol, 329–330
3,4-methylenedioxymethamphet-
amine (MDMA), 315, 317
methylone, 318
midwives, code of conduct/
performance/ ethics, 15
minimally conscious state, 31–32
Minnesota protocol, 49–52
mistakes, medicolegal, 47
misting, 289
mitochondrial DNA analysis, 285
mitragynine (‘Kratom’), 318
morphine poisoning, neonatal
breastfeeding, 300
morphological characteristics,
201–202
mortality, see death
mortuary, 46
mother of dead baby, identification,
85; see also maternal
deaths
motorcycle injuries, 265–266
mouth injury, infant, 100, 101
multiple deaths, see mass disasters
mummification, 62–63
Munchausen syndrome by
proxy, 252
murder, see homicide
muscles, cardiac, see myocardium
mutations, see genetic
polymorphisms
340 Index

mycology, 68 opiates and opioids, 312–314 petechiae, 110

myocardium
infarction, 69–70
ion channels, see ion channels
primary disease, 72–73
senile degeneration, 72
N
National Confidential Enquiry into
Patient Outcome and
Death (NCEPOD), 48
National DNA database, 285–286
National Violence Surveillance
Network, 106
natural causes of sudden death, 69–81
neck
hold and restraint, 209
injury, 156–157
pressure causing asphyxia, 162,
166–172
necropsy, see autopsy
neglect, child, 245, 252
neonates (newborns)
breastfeeding and morphine
poisoning, 300
maturity estimation, 85
nerve injury with handcuffs, 210
neurological disease, asphyxia, 174,
175
neuropathological examination of
brain, 81
neuropathy, handcuff, 210
newborns, see neonates
non-accidental injury
of children/infants, see child abuse
to self, 124–125
nurses, code of conduct/
performance/ ethics, 14–16
Nursing and Midwifery Council, 15
O
oath
Hippocratic, 13, 14
taking the, 8, 9
ocular injury
infant, 99–100
odontology, 199–201
oedema, cerebral, 154
Offences against the Person
Act (1861) and
amendments, 106
ophthalmological injury, see ocular
injury
receptors, 296, 312
mutations, 295, 314
oral injury, infant, 100, 101
orbital fractures, 151
organs/viscera
injury, 159–160
infants, 100–101
punching, 120
stamping, 121–122
transplantation, 33–35
P
P450 enzymes, 297, 300
paint, 293
arsenic in, 325
lead in, 329
palynology, forensic, 68
pancreatic trauma, 159, 160
papillary muscle infarction and
rupture, 70
pathologist, forensic
best practice, 47
quality assurance, 52
patient
capacity of, see capacity
confidentiality, 10, 15, 17, 19
consent, 10, 19
disclosure to protect the, 21
duty of physician to, 15
Paultauf’s spots, 194
PAVA (pelargonic acid vanillylamide)
spray, 211
pedal cycle injuries, 266
pedestrian injuries, 261–263
penalties incl. sentences (criminal
offence), 1, 3
deliberate injury to another,
105, 106
drug misuse, 310
infanticide, 84
penetrating injury
abdomen, 160
brain, 155
chest, 158, 159
neck, 156–157
sharp objects, see sharp-force
injury
penetrative sexual offence, 232
child, 245, 251–252
definition, 230
peritonitis, 77, 160
persistent vegetative state,
32–33
asphyxia, 164
Phadebas test, 287
phencyclidine, 315, 316
photography, forensic, 128–130
bite-mark, 129–130
medicolegal autopsies, 48
patterned injury, 129
suspicious deaths, 48
physical examination, see
examination
physicians, see doctors
piercings, body, 202
pink hypostasis, 57
piperazines, 317
as adulterants, 313, 317
pistol, 134, 135
plaque, atheromatous, 70
plastic bags/containers for
evidence, 278
plastic rounds, 211–213
pledges, 14
pleural fluid accumulation in
drowning, 194
pneumothorax, traumatic, 158
poisoning, see toxicology
Police & Criminal Evidence Act 1984,
217
police custodial healthcare
deaths and harm in, 218–222,
224–225
prevention, 225–227
health problems of detainees,
217–218
principles of care, 217
risk assessment, 218, 221–222
risk identificaiton, 218
torture, identification in, 223–224
pollen, 292
polymerase chain reaction (PCR), 281
positional asphyxia, 174, 175
positional torture, 126
post mortem examination, see
autopsy
post mortem hypostasis, 56–58
post mortem interval, see time of
death
postural asphyxia, 174
potassium channel, hERG, 297, 323
powder burns/tattooing, 138, 139
precedent, doctrine of, 2
predation by animals incl. insects, 60,
63–64, 67–68
pregnancy-related deaths, 77–79
preliminary impairment tests, 261

pressure, see compression
professional colleagues, duty of
physician to, 15
professional witness, 4
statement, 11
promises, 14
proof (standards of) in criminal law,
2–3
protection, child, 244, 252–253
psychedelics, see hallucinogens
Psychoactive Substances Act 2016,
317, 318
psychological evaluation in age
determination, 204
public interest, disclose in, 21
pugilist attitude, 182, 184
pulmonary embolism, 76–77
pulmonary non-vascular problems,
see lungs
pulmonary thromboembolism,
causation, 77
punching, 120
putrefaction, see decomposition
Q
QT interval prolongation, 322
quality assurance, forensic
pathologist, 52
Queen’s Bench, 3–4
questioning (examination) in court,
8–9, 10
R
radiological investigations, see
imaging
railway injuries, 266–267
rape, definition, 230
records, see documentation
re-examination, 8, 9
reflex cardiac arrest, 167
Registrar of deaths, 43
regulation of doctors and other
professionals, 25–28
renal, see kidney
reports, see statements and reports
respiration, cessation of (cellular
death), 30
respiratory disease, 76–77
respiratory phase of asphyxia, pre
terminal, 165
restraint (use in law enforcement),
208–214
asphyxia, 174, 209
Index 341
resuscitation, 30–31 sexual assault, 229–239
retinal haemorrhage, 98, 101 care after, 239
revolvers, 134 child, 102–103, 244, 251–252
rib fractures, 158–159 definitions, 230
infants, 88, 100 documentation, 232–236
rifle, 134 drug-facilitated, 318–319
air, 133 examination, 229–230, 230–232
rifled firearms, 134–135; see also law, 230
bullets medical findings after, 236–239
cartridges, 135 nurse examiners, 14
wounds, 137–140 samples, 232–236, 239
rigidity, cadaveric, 56 Sexual Offences Act 2003, 106, 230
rigor mortis, 55–56 sexually-transmitted infection, 229
road traffic accidents, 261–266; Shaken Baby syndrome (SBS), 98
see also driving sharp-force injury, 118–120; see also
assessment, 259–260 penetrating injury
rubber bullets (plastic rounds), 133, abdomen, 159
212–213 self-inflicted, 124
Rule 702 (Federal Evidence) on shearing effects causing axonal
expert Testimony, 5–6 injury, 155
Rule of Nines, 179 shoewear see footwear
run-over injuries, 262 short tandem repeats (STRs), 281
Y chromosome (Y-STR), 285
shotgun (smooth-bore firearms),
S
133–134
saliva, 287 cartridges, 134
Salvia divinorum and Salvinorin A, injuries, 135–137
315–316 single nucleotide
samples, evidential (and their polymorphisms, 285
analysis), 279–287 skeletal estimation of age in the
in sexual assault, 232–236, 239 living, 204
scalds, 178–180 skeletal injury, see fractures
child, 179, 247 skeletalisation, 60, 63, 202, 203
scalp injuries, 149 skin; see also bruising; burns
scene of crime, see crime scene electrical lesions, 187, 188–189
sea, fatalities at, 268 immersion effects, 193
drowning, 268 injury, child, 248
seatbelts, 263, 264–265 tattoos and piercings, 202
sedatives, 314 skull fractures, 100–102
seizures and convulsions infants/children, 88–98, 151
in asphyxia, 165 road traffic accident, 261
epileptic, 79–81 slash wounds, 118–120
self-inflicted injuries, 124–126 smoke soiling, 136, 138
semen analysis, 286–287 smooth-bore firearms, see
senile myocardial degeneration, 72 shotgun
sentences, see penalties smothering, 162, 172–173
serotonin syndrome, 314, smouldering fire, 181
321–322 sneezing blood, 289
antidepressants, 314 social evaluation in age
drugs causing, 323 determination, 204
stimulants, 308–309 soft furnishing fibres, 293
symptoms, 322 solvents, 317
sex determination of remains, 203 somatic death, 30–31
sexual abuse, child, 87 sperm cells, 287
sexual asphyxia, 171–172 Spice (JWH-018), 316–317
342 Index
spinal injury, 157–158
pedestrians, 261, 262
spit guards/hoods, 214
splenic injury, 158
stab wounds, 118–120
self-inflicted, 124
stamping, 111, 114, 120–122, 292
standards of proof, see proof
statements and reports, 7–8;
see also documentation
content of, 10–11
medicolegal, preparation of, 9–10
preparation, 9–10
stature determination from
decomposed/skeletonised
remains, 203
sternal fracture, 158–159
stillbirths, 83
stimulants, 308–12
serotonin syndrome, 308–309, 323
stomach, see entries under gastric
strangulation, 162, 167–170
signs of, 168
stroke (cerebrovascular
accident), 76
strontium-90
blood, drowning, 196
bone dating, 63
stud guns, 141
subarachnoid haemorrhage, 75–76
traumatic basal, 75, 152–153, 154
subdural haemorrhage, 98, 152, 153
subpleural haemorrhage, 194
substance misuse, see drugs;
toxicology
sudden and unexpected death
diagnosis, 37
Form B4, 92–97
infants (SIDS), 86–87
from natural causes, 69–81
suffocation (deliberate/intentional),
86, 172–173
suicide
carbon monoxide inhalation,
327–329
fire, 185
firearms, 142–143
hanging, 172
railway, 267
suffocation, 172
Supreme Court, 2
survival
asphyxial episode, 166
hanging, 171
fires, cyanide poisoning, 329 toxicology (poisoning), 295–330;
hypothermia, 185 see also drugs
spectrum of, 31 definitions, 296–297
trauma, 123–124 interpretation of measurements,
spinal, 157 299–300
suspension (torture), 273 testing matrices, 298
suspicious deaths trace evidence, 144, 232, 279–280,
autopsies, 49 292–293
blood patterns, 157 train injuries, 266–267
photographs, 48, 49 tramadol, 323
swearing in (taking the oath), 8, 9 tramline bruises, 111, 113
sworn statement, 8 transplantation, 33–35
Sydney Shark Case’ (1935), 202 transportation, 257–268
syphilitic aneurysm, 74–75 trauma load, 107
trauma, see injuries
traumatic asphyxia, 174
T
traumatic brain injury, 32
Tardieu spots, 164 triage, mass disasters, 145
Taser®, 213–214 trifluoromethylphenylpiperazine
tattooing, 138, 139, 202 (TFMPP), 317
tattoos, 202 trunk, asphyxia die to pressure on,
teeth and associated structures, 173–174
identification from, trust (doctor–patient), 17, 19
199–201 tuberculosis, pulmonary, 77
temperature; see also heat injury; tyre-tread bruising, 262, 263
hypothermia
body, and time of death, 57–58,
U
64–67
environmental, 57 unarmed restraint, 209
and rigor mortis, 56 undressing in hypothermia,
tetrahydrocannabinol (THC), 316 paradoxical, 186–187
TFMPP (trifluoromethyl- urine, 287
phenylpiperazine), 317 as drug testing matrix, 298–299
THC (tetrahydrocannabinol), 316
thermal injury, see heat injury;
V
hypothermia
thorax, see chest vagal inhibition, 167
thromboembolism, pulmonary, vascular disorders and lesions,
76–77 stimulant-related,
thrombosis 308–309, 311; see also
cerebral, 76 aneurysm
mesenteric, 77 vegetative state (VS), 31–33
time of death (post-mortem vehicle accidents, see driving; road
interval) traffic accidents
early, 55–59 ventricular cardiomyopathy,
estimation, 64–68 arrhythmogenic right, 73
body temperature, 58–59 ventricular tachycardia
tissue transplantation, 33–35 with QT interval
tolerance (drug), 296 prolongation, 322
opiates, 313 vertebrae, injury, 158
torsades des pointes, 322 vertebral artery trauma, 75, 153
torture, 271–274 violent crime, data on, 106
identification in police custody, virtual autopsy, 49
223–224 viscera, see organs/viscera
 Index 343

‘vitality’ of fire victims, determination, WHO women, see females

182, 183, 184 elder abuse, 253–254 World Health Organization
vitreous humour sudden death, definition, 69 definition of sudden
alcohol, 304 Widmark formula, 303 death, 69
as drug testing matrix, 299 Willis’ circle aneurysm, 75 World Medical Association (WMA),
vulnerable adults, safeguarding, 253 Winek’s formula, 303 14, 15, 16
Wischnewsky spots, 186
withdrawal (drug), 297
W X
alcohol, 304
water opiates, 219, 313 xenografts, 35
diatoms, 196 witnesses, 4–7 X-ray radiography, fire
immersion in, see immersion attending court, 8 victims, 182
weapons tubes, 278 giving evidence, 8–9
weight, body, in time of death healthcare professionals as,
Y
estimation, 64, 66 9–11
wet submarino, 126 professional, see professional young people, see children
whiplash injury, 158 witness Y-STR, 285