March 2007

Vol. 2 No.
1 March 2007
The Malaysian Journal

of Forensic Pathology
and Science
A peer reviewed journal dedicated

to the promotion of Forensic
Pathology and Science
Mal J For Path Sci (2007); Vol. 2 No. 1
The Malaysian Journal of

Forensic Pathology and Science
____________________________________________________
EDITORIAL BOARD
Editor-In-Chief
Assoc. Prof. Dr. Shahrom Abd. Wahid.
Forensic Unit, Department of Pathology,
Medical Faculty UKM.
Members
Dr. Shahidan Md. Noor (Kuala Lumpur)
Dr. Zahari Noor (Kuantan)
Dato’ Dr. Bhupinder Singh (Penang)
Dr. Nurliza Abdullah (Sabah)
Dr. Jessie Hiu (Sabah)
Dr. Mohd. Suhani Mohd. Noor (Kedah)
Dr. Azaini Ibrahim (Melaka)
INTERNATIONAL EDITORIAL BOARD
Members
Prof. Dr. Emmanuel N. Michalodimitrakis (Greece)
Prof. Dr. Amri Amir (Indonesia)
Additional Prof. Dr. OP Murty (India)
Assoc. Prof. Dr. Gilbert Lau (Singapore)
PUBLISHER
Westgate Publisher, Blk. D-7-3A (Level 9), Menara Uncang Emas, No. 85 Jalan Loke Yew, 55200
Kuala Lumpur.
FORENSIC COORDINATOR
ForenSci Center, No. 85 Jalan Loke Yew, 55200 Kuala Lumpur.
PRINTER
DS Business Form Sdn Bhd, 40 Jln TPK 2/5 Tmn Perindustrian Kinrara, 58200 Kuala Lumpur.
(KKDN PQ1780/2182)
CONTENTS
INVITED ARTICLE
1-8
Forensic Medicine in Greece: Modernizing and updating the
specialty
Michalodimitrakis M, Kranioti EF, Mylonakis PP, Mavroforou
AJ.
ORIGINAL ARTICLES
9-19
Female deaths due to cardiac causes in Malaysia : 10 years
autopsy review
OP Murty, Seng LK, Nuraeiniza I, Chee AS, Syahir BM
20-26
Aggravated suicidal responses to police arrest
Michalodimitrakis M, Kranioti EF, Mylonakis PP, Mavroforou
AJ.
27-36
Forensic facial reconstruction by clay sculpting-composite
technique at Forensic Identification Center, Hospital UKM
Noorazma S, Shahrom AW
37-52
Lesson learned by the forensic investigators: An accomplice
must be corroborated by independent evidence.
Shahrom AW, Zarida H, Anisah, Md Rizal AR
53-83
Organ weights of Malay, Chinese, Indian, and Indonesian
ethnic groups in Malaysia
OP Murty, Ling CS, Suhashni G, Mohd Fahmee AR, Nurasma Z,
Khalsom S
84-90
Cardiac Troponin I in suspected sudden cardiac deaths at
Forensic Unit, UKM Hospital : A preliminary observation
i
Shahrom AW, Swarhib MS, Azuriah AA, Zarida H, Aznool HA
CASE REPORTS
91-96
Fatal latent interstitial pneumonia complicating chloral
hydrate and midazolam pre-procedural sedation
Faridah MN, Zarida H, Shahrom AW
97-119
Partially cooked brain surface in fatal electrocution
Rohayu, Zarida H, Siew SF, Shahrom AW
120-126
An accidental group death (3 victims) due to solvent abuse
Shahrom AW, Zarida H, Mohd Azaini I
127-136
Determination of the manner of death in a drowning case of a
teenage boy
Swarhib MS, Zarida H, Shahrom AW, Aznool HA
137-144
Accidental fatal fall of a psychiatric patient from a psychiatric
ward
Faridah MN, Zarida H, Shahrom AW
ii
INVITED ARTICLE
Forensic Medicine in Greece: Modernizing and updating the

specialty
Michalodimitrakis M, Kranioti EF, Mylonakis PP, Mavroforou AJ.
Department of Forensic Sciences, University of Crete Medical School, Heraklion,

Crete, Greece.
Abstract
Development of Forensic Medicine in order to cover all aspects of forensic

sciences is essential in our era. Collaboration and harmonization of the forensic
systems as well as the training schemes in the European and international arena
are of paramount importance. In Greece there has been a great deal of discussion
and debate on the ways to update the training and to improve the quality of daily
service provided by the forensic departments.The scopes of the current article are
to review the existing model of forensic service in Greece as well as the training
schemes in this specialty and to offer a critical insight in those topics that require
revision.
Keywords: Forensic Medicine, forensic systems, Greece, forensic training,

harmonization.
Address for correspondence and reprint request: M. Michalodimitrakis MD, JD
Head of the Department of Forensic Sciences, University of Crete-Medical School
71110 Heraklion, Crete, Greece; E-mail:michalom@uoc.gr ; Fax: +30-2810-392521
Introduction
European System
The characteristic feature of forensic medicine in Europe is that the investigation

takes place only after issuance of a pertinent order by the investigative authorities
(prosecutor, police, and investigative judge). The philosophy of the European
violent death investigation procedure is similar to Continental European process
as it was developed in 1215: when the takeover of trials by the clergy was
1
initiated and marked a common point of abandonment of the continental European

and Anglo-Saxon systems of criminal justice1.
Unlike the Anglo-Saxons, the Europeans did not use laymen in the criminal
investigation procedures as was suggested by the fourth Lutheran Council. The
process was then, and has developed as, an inquisitorial system, placing the judge
as the central authority to whom the accusation, inquiry and trial have been
entrusted. Over the course of time, the system presented many inadequacies that
led to widespread dissatisfaction. The vesting of all power in the judge,
connecting the judge to the gentry and to the executive branch, all generally
proved ruinous to the defendant’s right. As Montesquieu stated, power has the
inherent property of being abused, and this has been proved true many times.
The ideas of Voltaire, Montenieu, Rousseau, Lock, Montesquieu, Thomasius,

Beccaria and other representatives of the Age of Enlightment had already
prepared the way for the reformation in criminal justice imposed by the French
Revolution. The French Revolution, for that reason, can be also considered a
revolution in criminal procedure and human rights protection. The new criminal
procedure, as reformed by the Napoleonic Code in the following decades, is the
basis of current European criminal procedure 2.
In general the system aims mainly to scrutinize deaths that are suspicious and may
possibly have a homicidal or criminal element. In addition, the autopsy rate is
lower than in England because the system does not tend to investigate natural or
innocently accidental deaths. However, changes occurring in medicine, and the
need of the state to establish accurate death statistics for epidemiological and legal
purposes, have led several European countries to expand the scope of medico-
legal investigation. Deaths unattended medically during life are not permitted to
be certified by a medical practitioner and are referred to the police. Police
authority in most cases decides whether or not an autopsy is required, without the
benefit of a forensic pathologist advise3.
Under the continental European system there is no identifiable medico-legal

officer. In most cases, an autopsy can be ordered only on permission given by the
judge of the first instance. In some countries, the local public prosecutor can
authorize autopsy but only in a few countries the police officers are so authorized.
Furthermore, the judge may be required to be present at the autopsy. The delay
inherent in obtaining permission for the medico-legal autopsy seriously
compromises the forensic evidence4.
2
The Greek Legal System
In Greece the law pertaining to criminal investigation procedures has always

relied on the principles of the continental European system since its formulation in
1834, shortly after the liberation of Greece in 1821.
The same concepts are found in the last codified legislation of January 1st, 1951,
which is currently in effect. Thus, judicial authorities, which are authorized with
the constitutionally-established guarantee of life tenure and independence of
opinion and are therefore considered as effective guardians of the constitutional
rights of the accused, carry out the investigative process. All the other officials
participating in the process (police, forensic pathologists and others) are under the
control and direction of these authorities. For that reason medico-legal
investigation typically, can take place only after an order by a judicial authority.
This causes a lack of autonomous jurisdictional powers on the part of the forensic
pathologist and the subordination of his office to the judicial investigators. Thus,
the Greek forensic pathologist is not empowered with the full and independent
authority of his American colleagues.
In reality upon the report of any death without medical certification the police
officer automatically shifts the case to the pathologist filling the name of the
deceased in a pre-typed form for autopsy. Thus the pathologist can accept or
decide on his/her own judgment. Additionally, all those cases of apparent violent
or suspicious deaths traditionally are transferred immediately to the forensic
pathologist. This is the procedural framework within which forensic pathology
and legal medicine are practiced in Greece5.
Organization of Forensic Medicine
Because of the absence of forensic pathologists in the rural areas, their duties are
passed to specifically authorized doctors, who of course are not qualified in
forensic pathology. This has occasionally resulted in poor medico-legal
investigation, according to a number of studies. In the majority of criminal cases,
the prosecutor or district attorney can issue an order-invitation to any licensed
forensic pathologist or forensic expert who serves in another jurisdiction.
Alternatively, a body can be transferred to an established university, hospital, or
state medico-legal unit or department for examination.
The formal operation of forensic medicine in Greece is encountered mainly in

large cities including the capital and involves the Hospital, State and Universities
based service. There are two hospital based medico-legal units in Greece, one at
3
the Department of Forensic Sciences of the University of Crete in Heraklion and

the other in Serres, both functioning independently. The hospital services come
under the aegis of the Ministry of Health. There are also two organized State
Medico-legal Services: one in Athens and one in Piraeus, employing eight local
forensic experts in distant places from the capital.
The Departments of Forensic Medicine at the Universities of Athens and

Thessaloniki, are under the aegis of the Ministry of Education while those at the
other Universities, which are based in Crete, Alexandroupolis and Ioannina
belong to the Ministry of Education but the Ministry of Health reviews their
medical standards. In the near future, two more additional university departments
are expected to be established, one in Larissa and the other in Patras. The
Department of Crete has the most modern instrumentation and in its 10 years of
operation has developed forensic pathology, anthropology, toxicology and
genetics at the level that is recommended by the standards of European Union.
Particularly, the Forensic Pathology is practiced in a competitive way to that
followed by the Medical Examiner Offices in USA. The Forensic Department in
Athens is the oldest in Greece, existing for more than 170 years and it is well
equipped specializing more in toxicology since the autopsies are performed by the
Athens State Service. Similarly the University Department of Thessaloniki has a
history that dates back to more than 60 years ago with good records mostly in
clinical cases.
Teaching and Specialization
The University Departments are involved with the teaching of Forensic Sciences
(pathology, anthropology, genetics, toxicology, clinical forensic medicine and
medical law-medical ethics), which is mandatory to all medical students in
Greece. The seven universities include in their curricula one or two semesters of
instruction in forensic medicine, mainly forensic pathology. Postgraduate
education in the field of Forensic Medicine leading to master or doctorate degree
has not yet been formulated. Nevertheless, almost all departments of forensic
medicine have established an independent process of training the young
physicians and other scientists in forensic theory and practice. The postgraduate
student is eligible for a master degree after one year, or a doctorate degree after
three years. The programs, tests, practice, and final defence are described by the
medical school, which offers the degree according to the regulations existing in
the university.
The specialization in forensic pathology leads to an official license after taking

exams at the end of the training scheme and the physician becomes qualified as
medico-legal expert. This responsibility belongs exclusively to the university
departments. Forensic medicine has been recognized by an enactment of the
4
Ministry of Health and Education as a separate field of medical specialization

since 1955.
Training involves three years of postgraduate study in the Departments of

Forensic Medicine at the universities of Crete, Athens, and Thessaloniki. The
trainee spends the first year in anatomic pathology and the remaining two years in
forensic pathology. Over the past years there has been discussion and proposals
have been made for revision aiming to increase the training from three to five
years. Eventually, the authorities of the Ministry of Health approaching the
concept of European Union on the specialty approved a course of four years
training in the speciality. Thus the training scheme has been changed including
one year in anatomic pathology and three in forensics. Nevertheless, the
experience acquired by the trainees in microscopic analysis of the findings is
poor, a common characteristic in most European countries compared to the
American standards. Another problem is that Forensic Medicine is not a popular
one among medical graduates and therefore the number of qualified forensic
pathologists is disappointingly small reflecting the universal problem of this
branch of medicine6.
Practice of Forensic Medicine
Unlike the teaching and specialization in forensic medicine, which follow a rather
uniform style and are an exclusive responsibility of the University Departments,
the daily practice and application of forensic medicine lacks of uniformity. In
some Departments like in Crete the daily practice is solely forensic pathology
with emphasis in detailed autopsy with radiology and microscopic examination by
the same pathologist, which is at the expense of clinical forensic medicine being
abolished. In other places emphasis is given mainly in clinical forensic medicine
whereas pathology is served less and almost solely macroscopically. We believe
that further and more in depth development of Forensic Pathology can be
achieved by harmonizing the standards of forensic medicine in Greece with those
of other countries of the European Union and the USA, something that already has
happened in the jurisdiction of the University Department of Forensic Medicine
which serves the entire island Crete7,8. The Department of Crete accepts also the
cases from the rest of Greece upon the often request from the judicial or police
authorities engaged in the detailed examination of difficult or complicated fatal
events.
Athens is served simultaneously in the same territorial jurisdiction by two

different systems (one university service in Athens and State Service in Athens
and Piraeus). The previous legislation (Law 1910, article 6, par 1 of law
1649/1986, article 5, par 4) did not clearly allow the university departments to
perform autopsies and conduct medico-legal investigations in these parts of
5
Greece, leaving this responsibility to the State Services. The factors which led to
modification of the law included: difficulties in teaching of undergraduate
students, training and specialization, and inadequacies in the daily medico-legal
practice, which demands updated laboratories, tools and good methodology in the
investigations.
In almost all Forensic Medicine Departments of Universities and State Services

the forensic pathologists and experts (experts overview only autopsies not
performed by themselves or analyze microscopically the autopsy findings) are
responsible for the medical examinations in case of rape or any other sexual
offence assisted usually by a gynaecologist. However, in times of emergency or if
no forensic expert is available the police, the prosecutor, or the judge may request
from a general practitioner or any medical doctor to assist in these matters. The
same practice is applied in drug cases where the participation of a psychiatrist and
a chemist is mandatory to determine the state of dependence in a person under
custody. Drug addiction may receive special detoxification treatment according to
the law (law 1729/1987, law 2161/1993). The report of the forensic expert in any
drug case usually contains data about the existence and extent of dependence
(physical and psychological) on certain substances of abuse. Information such as
the daily dose required to avoid withdrawal syndrome, influence of the drug on
the behaviour, and conscience of the addict, and the recommended suitable
treatment should be included in the report. The inability of the addict to terminate
the drug abuse on his/her own should also be identified. Nevertheless, this type of
clinical forensic medicine practice gradually is being transferred to the
psychiatrists (general or forensic where available) as it falls to their specialty.
Generally speaking there is an underlying tendency in practice of forensic

medicine in Greece to abandon the old fashioned practice and to adopt an updated
international model of pathology-oriented specialty, which is the model of
Forensic Medicine applied in Crete.
New Legislation
The last law governing the application of Forensic Medicine in Greece (law
2071/1992, article 123, par. 4) ratified in 1992, allows that wherever exist both
University and State Services, the investigating law officer can order either
Service or Department to investigate any case. Relevant to this is a regulation by
the Supreme Court, which equalizes the case load (Supreme Court enactment No
3065/11-5-1996). Nevertheless, in the meantime a natural resolution of preference
occurred in favor of University Departments over State Services.
The Department of Forensic Sciences at the University of Crete has successfully

functioning with the Medical, Police and Judicial Authorities of Crete and the rest
6
of Greece. With the assistance and cooperation of the two local forensic
pathologists in the western part of Crete (employees of Ministry of Justice and
Ministry of Health) integrates jurisdiction, cases and scientific duties in teaching
and research and being lastly the Center of Training in Forensic Pathology for the
trainees of the Balkan countries accredited by the Balkan Academy of Forensic
Sciences. The Toxicology Unit of the Department analyzes also specimens and
samples from other jurisdictions apart from the cases of Crete with 1100-1200
autopsies per year. Anthropology Section of the Department is collaborated with
prominent scientists like Prof.M.Yasar Iscan and Sema Aka in forensic
Odontology and apart from the forensic anthropology it has been developed the
topic of forensic archaeology. The last section is recently granted with a
prestigious project to examine anthropologically and genetically numerous
collections of skeletons and bones of Minoan and Mycenean populations lived
4000 years ago in Knossos, Troizine and Olympia.
Death investigations in Greece consist mainly of sudden natural deaths, traffic

accidents, homicides (less than 10%), drownings, drug abuse deaths, occupational
accidents, SIDS, suicides (hanging, gunshots and shotguns, pesticides etc) and
every unattended by physician death.
Proposal for updating
Because of the inadequacy of training and practice in forensic pathology in

Greece compared with the other more experienced European and American
countries, considerable discussion has been raised during the past five years on
reforming the entire postgraduate curriculum in duration and quality. Along these
lines the following propositions have been made9:
1. The training period should last 5 years: 2 years in anatomic pathology and
3 years in forensic pathology.
2. The training should take place in the universities with appropriate staffing
and equipments according to the established international standards after
having awarded an official accreditation.
3. A state body should establish the curriculum of the postgraduate training
in forensic pathology as well as in forensic sciences in a way to be similar
in all training centers.
4. Accreditation of all the departments and the trainers to be eligible to offer
training in forensic pathology or medicine should be given by the Ministry
of Health after advice given by a scientific committee.
5. Cooperation among various disciplines such as forensic toxicology,
forensic genetics, forensic dentistry, criminalistics, questioned documents,
and forensic anthropology is necessary. An ideal training center should
7
develop at least units of forensic toxicology, forensic genetics and forensic

anthropology supplementary to the main forensic pathology department.
6. A number of 250 autopsies per year per trainee and 50 of them should be
cases of homicide.
7. A forensic department in order to be accredited must have at least 300
autopsy cases per year.
8. An important issue is the establishment of a National Forensic Pathology
Society acting as an official organization. Its responsibilities should be:
• The establishment of guidelines for training and professional
practice.
• Supervision of the quality of the training provided by each
department,
• The establishment of rules for the relationship between the
pathologists and the State.
• Regulation of ethics and deontology in forensic sciences.
• Creation of a central library and publication of a journal devoted to
Forensic Sciences.
9. Organization of educational courses to offer similar training to
professionals in specialties related to the field of forensic sciences, such as
medical practitioners, lawyers, judges and police officers.
10. Encouragement by the state of a continuous educational program and
collaboration among national and international institutions and
organizations, by the provision of scholarships and grants.
References
1. Muller G, Le Pool-Griffiths F. Comparative Criminal Procedure NYU

Press, New York, 1969: 7-10
2. Patouris N. The accusatorial and inquisitorial models of criminal process,
PhD Thesis, New York State University, New York, 1981: 80-97
3. Knight B. The international practice of forensic sciences. In Eckert WG.
Introduction to Forensic Sciences. St Louis, Mosby,1981: 80-97
4. Harvard J. An International Survey of Medico-legal Systems of
Investigation of Sudden and Unexplained Deaths. Proceedings of the 3rd
International Meeting in Forensic Medicine, Pathology and Toxicology,
1963: 6-8
5. Michalodimitrakis M. The practice of forensic medicine in Greece and its
problems, Med Sci Law 1984; 24(2): 119-121
6. Sexton J, Hennigar G. Forensic pathology-the hidden specialty, J Forensic
Sci, 1979; 24(1): 275-282
7. Brinkman B. Harmonization of medico-legal autopsy rules. Int J Legal
Med 1999;113:1-14
8
8. Michalodimitrakis M, Tsakalof A: The practice of forensic medicine in

Greece. In Proc Ann Meet TIAFT, Fuknoka, Japan, 1992; 30: 544-547
9. Mavroforou A, Michalodimitrakis M: Forensic Pathology on the
Threshold of the 21st Century and the need of Harmonization of Current
Practice and Training. The Greek Concept, Am J Forensic Med Pathol
2002; 23(1): 19-25
9
ORIGINAL ARTICLE
Female deaths due to cardiac causes in Malaysia : 10

years autopsy review
OP Murty, Seng LK, Nuraeiniza I, Chee AS, Syahir BM
Forensic Pathology Unit, Department of Pathology , Faculty of Medicine,

University of Malaya, Kuala Lumpur 59100, Malaysia
Abstract
This study was aimed to find out deaths of females due to cardiac causes in the
last 10 years. The study was also designed to find out the prevalence and
common causes of cardiac death and associated factors relating to cardiac causes
of death among females. All cases were retrospectively reviewed from autopsy
records of patients who were autopsied at University Malaya Medical centre,
Kuala Lumpur from 1996 to 2005. The reports were analyzed from age, body
weight, sex, ethnicity, work, educational, menopausal, and cardiac risk factors.
Out of 5579 autopsy conducted during this period, 83 females out of the total
936 females had died due to cardiac reasons. Out of these 83 cases, These deaths
were due to diseases and injuries of the heart; majority (66.3%) were married;
30.1% were housewives; 31.3% were between 41-50 years old; 44.6% were
Chinese and 25.3% weighed between 61-70kg. The three main causes found were
advanced coronary artery disease (14.5%), hypertensive heart disease (13.3%),
and coronary atherosclerosis (12.0%) Most of the coronary arteries were
narrowed due to arteriosclerosis. Incidence of atherosclerosis was found in left
anterior descending artery (57.8%) and right coronary artery (44.6%) cases. In
majority of the cases structural or functional abnormality could be associated.
All of the cardiac risk factors examined were associated with sudden cardiac
deaths; however, hypertension, diabetes, pre-menopausal age had strongest
relationships. In conclusion, most of the females dying due to cardiac causes in
this study were married. Most were Chinese housewives of age group 41 to 50
years and died due to advanced coronary artery disease, coronary atherosclerosis
or hypertensive heart disease
Keywords: Cardiac deaths in females; sudden death in females; heart ; coronary

artery disease in females; CAD
9
Address for correspondence and reprint request: Dr.O.P.Murty, Additional Professor,

Forensic Medicine and Toxicology, All India Institute of Medical Sciences, New Delhi 110029.
Email : opmurthy 2006 @hotmail.com, dropmurty@yahoo.co.in
Phone 009111 26593274, 0091 9868397155 ( Office )
Introduction
Cardiac causes of death in this study are referred to the diseases and injuries of
the heart that causes severe abnormal heart rhythm by stopping blood flow from
the heart, resulting from a ventricular fibrillation or ventricular tachycardia.
Causes were categorized into heart-related conditions and other medical
conditions. Heart-related conditions are hypertension, coronary artery disease,
atherosclerosis, ischemic heart disease, right ventricular dysplasia, heart valve
disease, cardiomyopathy, tumors, and infections. Other medical conditions
include thyroid disease, some lung diseases, genetic factors, electrolyte imbalance,
and alcohol and drug abuse.
Primary cardiac causes also include congenital heart diseases such as tetralogy
of Fallot, aortic stenosis, Marfan syndrome. Primary electrophysiologic
abnormalities, e.g. long QT syndrome, Wolff-Parkinson-White syndrome, primary
ventricular fibrillation, right ventricular outflow tract ventricular tachycardia can
cause sudden death. Other causes of sudden death are pulmonary embolism and
aortic dissection or aneurysm dilatation. Normally these are due to genetic
abnormalities. 1
Risk factors for cardiac causes of death are mainly from underlying heart diseases
such as atherosclerotic heart disease. Therefore, the predisposing factors of
atherosclerotic heart disease also become the risk factors of cardiac death. Scarred
or enlarged heart is prone to develop life-threatening ventricular arrhythmias.1
Hypertrophy of myocardium with or without congestive heart failure also
contribute to the high incidences of cardiac death.
Diabetic females are more prone to cardiac diseases because most of them tend
to be overweight and physically inactive, with high cholesterol levels, and high
blood pressure. Anatomical factors such as smaller vessels with slower onset
make them more vulnerable than males. They may have more advanced disease or
more associated medical problems once diagnosed. Females have higher chances
to have congenital disease such as long Q-T syndrome, hypertrophic
cardiomyopathy, and non-ischemic cardiomyopathy.2 These are other prominent
predisposing factors associated cardiac deaths are smoking, hypertension,
diabetes and excessive alcohol intake.3
10
Different patients may give different kinds of histories. Some describe

palpitations, sudden breathlessness or chest pain. A large percentage of the
women who experienced cardiac arrest in one study had no specific documented
history of heart disease, heart attacks, or chest pain as clinical features.2
Materials and Methods
This is a retrospective study of last 10 years at University Malaya Medical Centre,

Kuala Lumpur. All female deaths in last 10 years were studied and cases where
cause of death was cardiac due to any reason were selected. A designed Proforma
was filled up and data were analyzed in different possible parameters.
Results
Out of 83 cases, the highest cases of cardiac causes of death in females were
among the age group of 41-50 years old with 26 cases (31.3%), all others are
depicted in figure 1.
Out of 83 cases, majority were Chinese with 37 cases (44.6%), followed by

Malaysian-Indian with 22 cases (26.5%). Both Malay and Indonesian consist of 8
cases (9.6%). Indian-Sikh and other ethnic group consist of 2 cases (2.4%) and 6
cases (7.2%) respectively (Fig. 2).
From 83 cases, 55 of them were married women (66.3%). This is followed by 19

(22.9%) cases who were single women. Only 6.0% or 5 of them were widower
and finally 4.8% or 4 of them had an unknown status (Fig. 3).
Out of 83 cases, 25 cases (30.1%) were housewives, followed by skilled workers

with 15 cases (18.1%), unskilled workers with 14 cases (16.9%) and unemployed
with 8 cases (9.6%).There were 21 cases (25.3%) with unknown occupation (Fig.
4).
Out of 83 cases, the commonest group of body weight that had cardiac death was
between 61-70 kg with 21 cases (25.3%), followed by weight between 51-60 kg
with 20 cases (24.1%), all other groups are also depicted in figure 5.
Major causes of cardiac deaths in females in this study are depicted in figure 6.
Out of 83 cases, 16.9% were normal, 6.0% had diabetes, 13.3% had hypertension,
2.4% had liver disease, 1.2 % had diabetic nephropathy, 4.85 had hypertension
with diabetes. In 37 cases (44.6%) underlying disease(s) were not mentioned like
arthritis, obesity, dental caries etc.
11
Table 1 shows that most of the coronary arteries were in normal condition.
However, the narrowing of coronaries commonly occurred in left anterior
descending artery (57.8%) and right coronary artery (44.6%)
Discussion
Females are quite safe till their menopausal phase as hormonal status does not
encourage atherosclerosis until unless some metabolic disorder is present in the
person. Estrogen is believed to be cardioprotective4 and when estrogen levels
drop, the rates of cardiac death increase. Age group of 41-50 years old falls in the
pre-menopausal to menopausal period where the hormonal change in the body
starts.. Therefore the post-menopausal women showed high mortality rate if we
added all the cases above the 50 years old (Fig. 1).
Chinese and Malaysian continental Indian have the highest number of cases) of
cardiac diseases (Fig. 2. This may also be contributed by severe alcohol
consumption which is the predisposing factor for cardiovascular disease.5
Besides, majority residents in Petaling Jaya are Chinese (55%)6.
AGE
30
31.3%
20 22.9 %
10 10.8 % 10.8 %
9.6%
Frequency
6.0%
4.8%
3.6%
0
0-10 11-20 21-30 31-40 41-50 51-60 61-70 71-80
AGE IN DECADES
12
N/B: Mean Age = 39.6 years old, S.D = 1.656 years old, n = 83
Fig. 1 : Age distribution of the cases
In Malaysia, most of the women were married by the age of 30 years old and
above this number of marriages among ladies is much less.7 This could have
contributed to the highest number of married women who died from cardiac death
(Fig. 3). It is well established fact that exercises reduce the risk of cardiovascular
disease8 . It appears that married women tend to stay in the house most of the
time due to their preoccupation in house-hold affairs and there could be the lack
of exercise which also predisposed them to cardiovascular disease.
Housewives had the highest number of cardiac death (30.1%). Besides, cardiac
death among employed female were much higher than unemployed female (Fig.
4). This may be due to the fact that more stress of work increases the risk of
getting cardiovascular disease and associated underlying diseases.9 Employed
worker were divided into skilled workers and unskilled workers. However, there
was not much different of cardiac death between skilled and unskilled workers.
Muslim cases were less as the community does not encourage postmortem
examination in natural and unsuspected deaths.
13
ETHNIC
Others
7.2% Malay
Indonesian 9.6%
9.6%
Indian-Sikh
2.4%
Malaysian-Indian Chinese
26.5% 44.6%
N/B: Others = Singaporean, Philippines, Iraqi, Thai American.
Fig. 2 : Ethnic distribution of deceased female due to cardiac death
Cardiac death mainly occurs in females with normal weight , is consistent with
our study also (Fig. 5), but there were 6 cases (7.2%) involving females with
extremely high weight (91–110 kg) because obesity was probably one of the
underlying factor in cardiac death.10
Most of the cardiac deaths (Fig. 6) that we found were due to advanced coronary
disease (14.5%), hypertensive heart diseases (13.3%) and coronary atherosclerosis
(12.0%). This is quite similar with the worldwide distribution where
arteriosclerosis overwhelmingly contributes to more mortality, approximately half
of all deaths.11
More than half of the cases (55.4%) had underlying diseases (Fig. 7). There was
no significant finding of relationship between underlying disease and cardiac
death, in female of other cases.
14
STATUS
unknow n
4.8%
w idow
single
6.0%
22.9%
married
66.3%
Fig. 3 : Marital status of the deceased female due to cardiac death
An obstruction of more than 75% of blood vessel lumen in coronaries arteries is

considered significant to cause uncompensated ischemia of heart.11 Obstructions
of the vessels were most frequently occurred at the left anterior descending artery
(Fig. 8). This artery is the major artery for the blood supply to apex of the heart.
This is followed by right coronary artery, which supplies the right and posterior
part of the heart.11
15
OCCUPATIONS
30
30.1%
25.3%
20
18.1%
16.9%
10 9.6%
Frequency
0
unemployed housew ife skilled unskilled unknow n
occupation
Fig. 4 : Occupation status before death
Conclusion
In conclusion, most of the cardiac deaths in females in this study were near
menopause (31.3%) and postmenopausal (38.5%) women. Chinese females were
the most affected group (44.6%) and most of the cases were married women
(66.3%). Most of them were employed, with 18.1% were skilled workers and
16.9% were unskilled workers. Most of the cases had normal body weight ranges.
Furthermore, the common causes were advanced coronary heart disease (14.5%),
hypertensive heart disease (13.3%) and coronary atherosclerosis (12.0%) and most
of the obstruction occurred in left anterior descending artery (57.8%) and right
coronary artery (44.6%). The incidence of sudden cardiac death increases near or
after menopause in all ethnic groups.
16
BODY WEIGHT
30
25.3 %
24.1%
20 21.7%
14.5%
10
Frequency
4.8%
3.6% 2.4% 2.4%
1.2%
0
0-10 41-50 61-70 81-90 101-110
31-40 51-60 71-80 91-100
BODY WEIGHT (KG)
Fig. 5 : Body Weight distribution of the cases
This study can help to plan some preventive measures and treatment planning for
this group. A periodical medical check-up near menopause is recommended to
all females. A regime of good exercises, balanced diet and hormonal supplement
can reduce the morbidity.
17
cause of death
Advanced coronary ar 12 14.5%
Coronary Atheroscler 10 12.0%
hypertensive heart d 11
13.3%
myocardiac infarctio 6 7.2%
ischemic heart disea 5 6.0%
7 8.4%
cardiomyopathy
cardiac tamponade 8 9.6%
chronic rheumatic he 2 2.4%
coronary thrombosis 4
4.8%
right ventricular dy 3
congenital heart dis 3 3.6%
cause of death
congestive heart fai 3

Laceration of heart 2
rupture of aorta 2 2.4%
stab w ound to heart 2
others 3 3.6%
0 2 4 6 8 10 12 14
Frequency
N/B: Others = Hemorrhage with contusion of heart, Bacterial Endocarditis, Acute Myocarditis,
Myocardial Abscess.
Fig. 6 : Causes of death and their incidence in this study
Table 1 : Narrowing in % of coronary arteries due to atherosclerosis in the

cases is shown
Lumen size Right Left anterior Left Aorta

coronary descending circumflex
artery artery coronary
artery
Normal 46 (55.4%) 35 (42.2%) 57 (68.7%) 54 (65.1%)
<50%
narrowing 16 (19.3%) 14 (16.9%) 9 (10.8%) 10 (12.0%)
50%-75%
narrowing 2 (2.4%) 9 (10.8%) 2 (2.4%) 0 (0.0%)
18
>75%
narrowing 10 (12.0%) 10 (12.0%) 6 (7.2%) 4 (4.8%)
Fully
obstructed 2 (2.4%) 4 (4.8%) 0 (0.0%) 0 (0.0%)
Narrowing
of unknown 7 (8.4%) 11 (13.3%) 9 (10.8%) 15 (18.1%)
percentage
Total 83 (100.0%) 83 (100.0%) 83 (100.0%) 83 (100.0%)
References
1. Malineni KC, (2004, November 11). Sudden Cardiac Death, Retrieved April
23, 2006, from http://www.emedicine.com/med/topic276.htm
2. C Albert, (2003, July 31). Circulation: Journal of the American Heart
Association, Retrieved May 26, 2006, from
http://www.ynhh.org/healthlink/womens/womens_7_03.html
3. Kannel WB, Plehn JF, Cupples LA. Cardiac failure and sudden death in the
Framingham Study. Am Heart J. 1988 Apr; 115(4): 869-75.
4. Johnson RR, Sweeney ME. Debate: The potential role of estrogen in the
prevention of heart disease in women after menopause. Current Control
Trials Cardiovascular Med. 2000; 1(3): 139–142.
5. Tolstrup J, Jensen MK, Tjønneland A, et al. Prospective study of alcohol
drinking patterns and coronary heart disease in women and men. BMJ 2006;
332: 1244-1248.
6. Wikipedia, the Free Encyclopedia (April 15 2006.). Petaling Jaya. Retrieved
May 31, 2006 from http://en.wikipedia.org/wiki/Petaling_Jaya.
7. Rabieyah Mat, Roszaini Omar. Demographic trends in Malaysia with special
focus on women. Retrieved May 31, 2006 from
http://www.ancsdaap.org/cencon2002/papers/Malaysia/Malaysia--
REVISED.PDF.
8. Thompson PD. Exercise and Physical Activity in the Prevention and
Treatment of Atherosclerotic Cardiovascular Disease. Arteriosclerosis,
Thrombosis, and Vascular Biology. 2003; 23: 1319.
9. Smith M. (October 17, 2002). Job Stress Can Kill Your Heart. Retrieved
May 31, 2006 from http://www.webmd.com/content/article/52/50210.htm.
19
10. Divitiis OD, Fazio S, Petitto M, et al. Obesity and cardiac function.
Circulation. 1981; 64: 477-482.
11. Kumar V, Cotran RS, Robbins SL. The blood vessels. In: Schmitt W,
Hacker H, eds. Robbins Basic Pathology. Philadelphia, Pa: Saunders. 2005:
511
20
ORIGINAL ARTICLE
Aggravated suicidal responses to police arrest

Michalodimitrakis M, Kranioti EF, Mylonakis PP, Mavroforou AJ.
Department of Forensic Sciences, University of Crete Medical School, Heraklion,

Crete, Greece.
Abstract
Suicide during confrontation with the law enforcement officers may occur and in
this report we present three cases of suicide after confrontation with police among
180 suicides investigated by the Department of Forensic Sciences in the region of
Crete over a 5-year period, accounting for a prevalence of 1.67%. All subjects
were male and all incidents occurred after police pursued or arrested them for a
previous criminal action in felony degree. The actions of an emotionally disturbed
individual who is suddenly confronted with police officers or the prospect of
incarceration are extremely unpredictable, and suicide is only one of the potential
actions that such an individual may choose. Although public perception and media
remained biased in most of the cases, careful attention and comprehensive death
investigation is the best way to preserve the public trust.
Keywords: Pathology, forensic science, suicide, autopsy, police confrontation,

death in custody.
Address for correspondence and reprint request: M. Michalodimitrakis MD, JD
Head of the Department of Forensic Sciences, University of Crete-Medical School
71110 Heraklion, Crete, Greece; E-mail:michalom@uoc.gr ; Fax: +30-2810-392521
Introduction
Deaths that occur in association with law enforcement activities represent a
particular topic in the forensic literature. Studies have examined fatalities caused
by firearms1, neck holds2, and acute drug reactions3 occurring in police pursuits or
apprehensions. Deaths occurring in police custody have also received much
attention4-10. Suicides in custody are especially important because the prison or
jail environment is reasonably controlled and the safety of prisoners is the legal
responsibility of the institution9,11,12.
20
One aspect of police–associated deaths that has not received attention is the
incidence of suicides that occur during confrontation with law enforcement
officers. Occasionally an armed suspect being pursued, apprehended, or otherwise
confronted by police officers suddenly turns his gun on himself. While there is a
temptation to assume that these deaths are straightforward suicides, witnessed by
police agents willing to testify to the exact circumstances, they pose a special
investigative challenge for the forensic pathologist13 because of the likelihood the
testimony given by the law enforcement officers involved in the incident to be
rejected by the suspect’s family, the media, and occasionally by the police
administration.
Although all suicides require attention in detail, in those occurring when police is
involved comprehensive investigation is necessary. A retrospective analysis of the
suicides occurred during police confrontations in our region was carried out
recognizing the need to address this issue.
Methods and Results

The population base for this study is the inhabitants of island Crete, in Greece,
which is 750,000 and increase up to 5 million during the summer tourist period.
For this study, we reviewed the circumstantial suicides to identify cases in which
law enforcement officers were present in the context of pursuit, confrontation, or
apprehension of the person who committed suicide.
All together there were a total of 3,022 records of death investigations from 1999
to 2003. A total of 180 cases were classified as suicides and three cases of
suicides were identified in which on-duty police officers were confronting,
pursuing, apprehending, or arresting the subject of the death investigation
representing approximately 1.67 % of all suicides. The case histories, along with
autopsy findings and toxicology results of these three cases are summarized:
Case No 1.
A 48-year old male was wanted and arrested for smuggling of antiquities. He was
transferred to police headquarters after apprehension for further inquisition by the
examining judge who conducted the procedure. He was finally charged in felony
degree and a confinement in jail was ordered. When the policemen tried to have
the accused handcuffed for transportation to the local jail he suddenly escaped the
detention, run across the room and he jumped out through the window landing on
to the ground from a height of 12 meters approximately. He was pronounced dead
at the scene and the following autopsy revealed multiple skull and rib fractures
with extensive craniocerebral and lung injuries. Toxicological analysis disclosed
traces of ethanol but no abuse of drugs.
21
Case No 2.
A 39-year old male was arguing with his wife in their apartment when the
neighbors called the police. Before the arrival of the policemen the man shot his
wife twice to death. When the policemen arrived at the scene and approached the
flat in an attempt to speak with the husband through the closed door they heard
another shot fired. They entered the house and found the woman dead in the
bedroom and the man in the living room floor with a 9mm semiautomatic pistol,
three fired cartridge cases, and two bullets were recovered from the scene.
The autopsy revealed two distant gunshot wounds on the body of the woman one
through and through on the head and one on the left side of the chest. A deformed
bullet was found wedged inside the body of the 6th thoracic vertebra. In the man it
was revealed a tight contact gunshot wound of the right temporal scalp and an exit
wound of the left posterior parietal scalp. Toxicology was positive for traces of
ethanol in blood samples taken from the man.
Case No 3.
A 58-year old male started a quarrel with some kids playing in his courtyard for
making noise. The argument continued with the father of one of the kids who
prompted to protect his son. The subject returned to his house and came back with
a two-barrel shotgun firing at the kid’s father from a distance of approximately 10
meters with a shell loaded with small size pellets. The victim suffered a large
shotgun wound in his back transported to the local hospital and after several days
treatment he finally survived from the injuries. When the police officers arrived
right after the incident, the man tried to escape using a van. They chased him to
his residence where he ran to the back of his house. Over the noise of the sirens,
officers yelled for him to drop the shotgun, then saw him sited on the top of a
ladder and having the gun under the his chin. He shot himself and then fell down.
The autopsy revealed a large contact shotgun wound with heavy deposits of
fouling at the site of the entrance wound and imprint of the unfired barrel.
Massive destruction of the face, forehead and the scalp with portions of brain
scattered in the near proximity was apparent. Toxicology showed blood ethanol
levels of 0.7 g/l but no drugs were detected.
Discussion
The three cases represented herein indicate that suicides during police
confrontation represent 1.67 % of all suicides in our region. All victims were male
at different ages and were pursued for crimes committed in felony degree. Alcohol
consumption was detected in all cases but in low levels, whereas no evidence of
drug use was found in any case.
22
The motives of these suicides varied. In the first case there were no indications
that the subject was considering suicide until the policemen were ordered to
incarcerate him. In the second case there were clear indications that the subject
was contemplating suicide before police confronted him. In the third case the
victim’s behavior indicated that he was emotionally distraught but not necessarily
suicidal, and the police confrontation may have precipitated the suicide. The
contribution of police pursuing and confrontation to unexpected and irrational
behavior in fleeing or cornered suspects has been reported14,15. The most striking
feature of this type of suicides is that the deaths occur within the course of the
capture and shortly before the arrest and confinement. This is better understood
when one considers the feelings of helplessness, confusion, isolation, and panic
that are commonly experienced by the pursued and entrapped individuals because
of the accusations of recently committed criminal actions16. Sometimes this
situation is further aggravated psychologically from the feelings of guilty when
the perpetrators realize the consequences from their unfair and criminal behavior.
It is also well known that some acutely excited, agitated and violent people, in
states of so called “excited delirium” are at risk of dying unexpectedly when they
are restrained by law enforcement officers or hospital security personnel6.
There have been several studies of deaths in custody showing that suicide is one
of the most common causes of death in jail or prison17-19. Furthermore, the rate of
suicide among prisoners is much higher than in the general population20 and
various risk factors have been identified21,22. The rate of violent deaths among
people on probation was reported as being 10-fold higher than in the general
population23 and particularly for those aged 35 to 54 it was 35-fold24.
In a report from Australia it was shown that half of the deaths in custody were
attributed to self-harmful behavior8 and illicit drugs and alcohol abuse problems
are detected very often in such cases25-27. Most consistently, the suicides usually
occur within the first few hours or days of incarceration28. In a study conducted in
Canada it was found that the rates of suicide among inmates in federal (long-term)
were higher than in provincial (short-term) settings29, which contradicts with other
reports30. This difference in suicide rates between the federal and provincial
inmate populations was attributed to the loss of preventive efforts in the national
correction system.
Less consistent is the type of prisoner at risk to commit suicide. Although it is not
known whether suicide is more common among prisoners charged with non-
violent crimes or in violent offenders there is general agreement that suicides in
custody are preventable and changing the system may result in the reduction of
suicide rates31-33. However, in another report it was found that most of the suicides
in federal penitentiaries in Canada were not preventable34. Nevertheless, the
Correctional Service in Canada has introduced in the last years a new policy to
ensure a comprehensive strategy for prevention, management and response
23
regarding suicides, which includes awareness and prevention workshops available

to all inmates35. Also such preventive policy in Denmark resulted in no police
custody deaths over a five-year period36.
Suicides during police confrontation carry the potential for public controversy,
adverse media attention, accusations of police brutality, and allegations of cover-
up. The actions of an emotionally disturbed individual who is suddenly confronted
by the police officers or the prospect of incarceration are extremely unpredictable,
and the suicide is only one of the actions that such individual may choose. In
certain cases the presence of police may precipitate a suicidal action because
police officers do not always react in a preventive manner 37. Additionally, on
several occasions individuals attempt or commit suicide by intentionally
provoking the law enforcement officers to shoot them. Although these cases
technically are classified as homicides one can consider them as assisted
suicides38. Most of these victims may have previous suicide attempts or medically
documented psychiatric disorder39.
In all these cases it is of paramount importance the forensic pathologist and the
other investigators to document the injuries and collect evidence in an objective
manner, recognizing the potential for public controversy. Despite the fact that the
public perception and the media remain biased in most of the cases, careful
attention and comprehensive death investigation remain the best way to preserve
the public trust.
References
1. Stone I, Holt J, Gillett M. Coordination of Resources in Officer-Involved

Shootings. J Forensic Sci 1991; 36: 40-46.
2. Reay D, Eisele J. Death from Law Enforcement Neck Holds. Am J
Forensic Med Pathol 1982; 3: 253 – 258.
3. Mirchandani H, Rorke L, Sekula-Perlman A, Hood I: Cocaine-Induced
Agitated Delirium, Forceful Struggle, and Minor Head Injury. Am J
Forensic Med Pathol 1994; 15: 95 – 99.
4. Cox B, Skegg K. Contagious suicide in prisons and police cells. J
Epidemiol Community health 1993; 47: 69 – 72.
5. Smith R. Deaths in Prison. BMJ 1984; 288: 208-212.
6. Pollanen M, Chiasson D, Cairns J, Young J. Unexpected death related to
restraint from excited delirium: a retrospective study of deaths in police
custody and in the community. CMAJ 1998; 158: 1603-1607.
7. Lawlor D, Kosky R. Serious suicide attempts among adolescents in
custody. Aust N Z J Psychiatry 1992;26:474-8.
8. McDonald D, Thomson NJ. Australian deaths in custody, 1980-1989. 2.
Causes. Med J Aust 1993;159:581-5.
24
9. Blaauw E, Vermunt R, Kerkhof A. Deaths and medical attention in police

custody. Med Law 1997; 16: 593-606.
10. Bhana B. Custody-related deaths in Durban, South Africa 1998-2000. Am
J Forensic Med Pathol 2003; 24: 202-7.
11. Fruhwald S, Frottier P. Death behind bars. CMAJ 2002; 167: 1127-1128.
12. Reay D. Death in Custody. Clin Lab Med 1998; 18: 1-22.
13. Danto B. Medical Problems and Criteria Regarding the Use of Tear Gas by
Police, Am J Forensic Med Pathol 1987; 8: 317-322.
14. Copeland A. Deaths Resulting from Police Pursuit. Am J Forensic Med
Pathol 1988; 9: 228-232.
15. Wilber CG. Deadly force: some human and ethical considerations. Am J
Forensic Med Pathol 1982; 3: 165-77.
16. Granzow B, Puschel K. Fatalities During Imprisonment in Hamburg 1962-
1995. Arch Kriminol 1998; 201: 1-10.
17. Dooley E. Prison Suicide in England and Wales 1972-87. Br J Psychiatry
1990; 156: 40-45.
18. Blaaw E, Kerkhof A,Vermunt R. Suicides and other deaths in police
custody. Suicide Life Threat Behav 1997; 27: 153-163.
19. Markus P, Alcabes P. Characteristics of suicides by inmates in an urban
jail. Hosp Community Psychiatry 1993; 44: 256-261.
20. Fruhwald S, Frottier P,Eher R, Benda N,Ritter K. Did suicidal behavior
have relevance for prison suicide? Psychiatr Praxis 2001; 28: 326-329.
21. Copeland A. Deaths in Custody, Revisited. Am J Forensic Med Pathol
1984; 5: 121-124.
22. Frost R, Hanzlick R. Deaths in Custody: Atlanta City Jail and Foulton
County Jail, 1974-1985. Am J Forensic Med Pathol 1988; 9: 207-211.
23. Pritchard C, Cox M, Dawson A.Suicide and violent death in a six-year
cohort of male probationers compared with pattern of mortality in the
general population: Evidence of accumulative socio-psychiatric
vulnerability. J R Soc Health 1997;117:180-185.
24. Daigle M. Death in our prisons. CMAJ 2003;168:830.
25. Jordan F, Schmeckpeper K, Strope M. Jail suicides by hanging: An
epidemiological review and recommendations for prevention. Am J
Forensic Med Pathol 1987;8:27-31.
26. Fruhwald S, Frottier P, Benda N, Eher R, Konig F, Matsching T.
Psychosoziale Charakteristika von Suidopfen in Gefagnissen. Wien Klein
Wochenschr 2002; 114:691-696.
27. Giles H, Sandrin S. Alcohol and deaths in police custody. Alcohol Clin
Exp Res 1992;16:670 – 672.
28. Smialek J, Spitz W. Death Behind Bars. JAMA 1978;240(23):2563-2564.
29. Wobeser W, Datema J, Bechard B, Ford P. Causes of death among people
in custody in Ontario,1990-1999. CMAJ 2002;167:1109-1113.
30. Hayes L, Blaauw E. Prison suicide : a special issue. Crisis 1997;18:146-
147.
25
31. Donahue D, Chavern H. Suicide Prevention at the County Jail. FBI Law
Enforcement Bull, 22-24, 1981.
32. Wooldredge J, Winfree L. An aggregate-level study of inmate suicide and
deaths due to natural causes in US jails. J Res Crime Delinquency 1992;
29: 466-479.
33. Joukamaa M. Prison Suicide in Finland,1969-1992. Forensic Sci Int 1997;
89: 167-174.
34. Laishes J. Inmate Suicides in the Correctional Service of Canada. Crisis
1997; 18: 157- 162.
35. Bouchard F, Laishes, Moloughney B. Death in our prisons. CMAJ 2003;
168: 829-830.
36. Segest E.Police Custody: Deaths and Medical Attention. J Forensic Sci
1987; 32: 1696-1703.
37. Hutson H, Anglin D, Yarbrough J, Hardaway K, Russell M, Strote J,
Canter M, Blum B. Suicide by cop. Ann Emerg Med 1998; 32: 665-669.
38. Harruff R, Llewellyn A, Clark M, Hawley D, Pless J. Firearm Suicides
During Confrontations with Police. J Forensic Sci 1994; 39: 402-411.
39. Wilson E, Davis J, Bloom J, Batten P, Kamara S. Homicide or suicide: the
killing of suicidal persons by law enforcement officers. J Forensic Sci
1998; 43: 46-52.
26
ORIGINAL ARTICLE
Forensic facial reconstruction by clay sculpting-composite

technique at Forensic Identification Center, Hospital
UKM
Noorazma S, Shahrom AW
Forensic Identification Center, Hospital UKM, Bandar Tun Razak, Cheras,

Malaysia.
Abstract
Facial reconstruction has been developed as part of the identification procedure at

the Forensic Identification Center, HUKM. The facial reconstructions is used as a
tool to ‘jog’ people’s memory and thus help in successful identifications of
unknown skeletal remains / missing person. In this work we discuss the procedure
of a solid model three-dimensional facial reconstruction by clay sculpting of an
unknown skull. A selected photograph of head hair is then added compositely to
the reconstructed clay model to give more human look of the finished face. The
advantages of this technique is discussed.
Keywords: Facial reconstruction, clay sculpting, identification, unknown,

skeletalised remains.
Address for correspondence and reprint requests: Dr Noor Azma Sohari. Forensic
Odontologist, Forensic Unit, Hospital UKM, Jalan Yaacob Latif, Bandar Tun Razak, Cheras,
56000 Kuala Lumpur, Malaysia.
Tel: 03 – 91702571, Fax: 03 -91711673 e-mail: noorazma_s@yahoo.com
Introduction
Facial reconstruction or facial approximation is the process of recreating the face
of an unidentified person. It is also called facial approximation and it can be done
either on the skull of the skeletal remains itself or from the duplication of the
individual’s skull. This reconstructed face is then used to aid in the process of
identification although it cannot be taken as confirmation of an identification. It
27
can be used in cases of finding missing person, in criminal investigations and

created for remains believed to be of historical significance.
There are two types of facial reconstruction and they are two-dimensional and
three-dimensional approximation. The two-dimensional facial reconstructions are
drawings based on radiographs, ante-mortem photographs and the skull.
Professor MM Gerasimov did a lot of two-dimensional reconstruction drawings
prior to sculpting the skull.1 However, these types of two-dimensional technique
take quite some time to do. Currently there are computer software programs that
can quickly produce facial approximation in two-dimensional which are called
F.A.C.E and C.A.R.E.S. The current program being used by the police in
Malaysia is the F.A.C.E program where it can edit and manipulate facial features
rather easily and giving a quick result.
Generally, three-dimensional facial reconstruction could either be solid model

sculptures or high resolution three-dimensional computer images in the form of
surface representation. Solid model sculptures are usually created with modeling
clays or plasticine2 and can represent internal structures and mechanical properties
but they are static and quite difficult to duplicate. However, it has been used as a
good tool to ‘jog’ people’s memory and thus help in successful identifications of
missing person. This can be confirmed further with other verified methods for
positive identification such as DNA, fingerprint or dental data comparison.
High resolution three-dimensional computer images produced surface

representation that is a hollow shell with no internal surface although they can
have size, shape, texture and colour. It can be done either with laser scanners and
three-dimensional digitizers although they are most accurate and comprehensive
when using laser scanner.2 The computer is programmed to ‘manipulate’ the
scanned photographs of the unknown skeletal remains as well as ante-mortem
photographs from family album, magazines or publishers. The resultant
reconstructed product will then be used to for initial identification.
Materials and Method

An unknown skull which was referred to our center by the police for facial
reconstruction photographed. It was cleaned from debris and remnants and
rephotographed. The anthropological ethnicity, gender and age of the skull is
determined the forensic pathologist, forensic anthropologist and forensic
odontologist of our center. This is important as to determine which soft tissue
thickness to be used later in the process of sculpting. The maxilla with the rest of
the upper part of the skull was fixed together with the mandible at their respective
condylar fossa. Eye sockets, nasal aperture and dental area were covered with
28
wax. Sculpting clay and tools were used to reconstruct the face using anatomical
landmarks and established soft tissue thickness as guidelines.
Soft tissue thickness for the skull were reconstructed based on anatomical
landmarks of an average male from established soft tissue thickness studies by
Suzuki (1948). We also use soft tissue thickness established by O’Grady and
Taylor 1990 which was described by Clement & Taylor3 for caucasian skull.
These anatomical landmarks were marked on the skull and then coloured matches
were fixed on them. The length of the matches represented the appropriate soft
tissue thickness and the coloured end is useful as it is visible through the thin
layer of clay.
Following this, muscles and soft tissues were built onto the skull in an anatomical
manner so that the shape, origin and insertion of muscles are as found in nature.
Combination Method,4 whereby both anatomical and tissue depth method are
being used in this technique.
First, the temporalis, masseter, buccinator and occipito-frontalis muscles were

built followed by obicularis oculi and obicularis oris. After this stage, the nose
and lips were reconstructed.
The forehead was made to extend from the hair margin to the eyebrows and it is
relatively featureless. Between the eyebrows a small elevation called glabella was
reconstructed and it is where vertical wrinkle produced when frowning.
29
Fig. 1: The cleaned skull was placed in anatomical position. It was given
landmarks followed by clay sculpting of the underlying facial muscles and glands.
Coloured matches are used to mark anatomical landmarks on the skull.
Next, the temporal region was sculpted. The region is situated on the lateral side
of the face, in front of the external ear and above the zygomatis arch of the cheek.
Superiorly it is demarcated by the temporal crest which indicates the upper limit
of the temporalis muscle. In real life, this muscle usually contracts when we
clench our teeth.
The orbital region is bounded by the bony rim of the orbit. The eyes are usually
near the midpoint of the vertical height of the face. Two eyelids, superior and
inferior palpebrae were reconstructed in front of both eyes. The two palpebrae are
separated by palpebral fissures. Extending from the margins of the eyelids are
eyelashes. In real life, these palpebrae are movable and have the purpose of
protecting the eyeballs. The lateral and medial angles of the eyelids are called
lateral and medial canthi. Lateral canthi has no feature. The medial canthus is
separated from the eyeball by lacrimal lake and here also lies the lacrimal
caruncle.
The profile of the nose was reconstructed from an arbitrary line. This external
nose is pyramidal in shape. Superiorly it is confluent with the forehead at the root
of the nose and supported by nasal bones and is immobile. Inferiorly, the tip of
the nose is called the apex. The ridge that connects the root and apex is called
dorsum of the nose. Both apex and dorsum of the nose are supported by cartilage
and so in real life, they are mobile. The nostrils are separated by nasal septum and
bounded laterally by ala. The width between the alae should be about the same
width as one eye or the space between the eyes. The nasolabial grooves of the
upper lip are continuous with alae (flared lateral margins) of the nose to form ala
grooves.
The lips were reconstructed as wide as the interpupillary distance. In the upper lip
the vermilion (red zone of the lip) protrude in the midline to form a tubercle. The
lower lip was made to show a slight depression in the midline to correspond to the
tubercle. From the midline to the corners of the mouth, the lips widen and then
narrows laterally which then are separated from the cheek by the nasolabial
grooves. The corners of the mouth are located at the level of maxillary canines
and first premolars. The philtrum separate the septum of the nose to the upper lip
and this form the midline. The labiomental groove separates the lower lip from
the chin.
The chin is the most prominent feature in the mental area. The prominence in this
region is called mental protuberance and above it is a groove called labiomental
groove which separate it from lower lip. This groove should be approximately
30
midway between apex of the nose and the chin. It should also about the same
level as angle of the mandible.
The cheek is an extensive area of the face below the temporal region. It can be
divided into two. The first one is the upper and anterior region overlying the
zygomatic arch (cheek bone) and body of maxilla while the second one is the
lateral and posterior region overlying the buccinator muscle, ramus of mandible,
parotid gland, masseter muscle, parotid duct and mandibular condyle. The
muscles have been built earlier therefore, at this stage we were merely ‘fleshing
out’ the cheek according to soft tissue depth thickness up to the level of the
coloured matches tip.
The parietal and occipital region of the head are covered by scalp which consist of
tissues therefore they were made to emulate layers of soft tissues. The muscles of
facial expression were then reconstructed and the eyes were completed. The
medial palpepral ligament were extended 3 mm over the medial rim of the orbit
while the lateral palpebral ligament extended 5 mm from the lateral rim of the
orbit. The eyelids were extended from this and covered part of the iris.
Fig. 2: The figure of process of clay sculpting (left) and the “finished sculpted
face” (right).
31
The ‘fleshing out’ of the brows and scalp to within 1 mm of the depth marker
were done at this stage. The neck was built-up and the ears were reconstructed.
The ears were positioned so that the top of tragus is positioned at the external
acoustic meatus and set obliquely with a 15º posterior inclination. There could be
a number of variations in the appearance of the ears.3
Final ‘fleshing’ of the face were carried out to the tips of the depth markers and
characterization might be added such as facial features for certain ethnic groups.
Fig. 3 : The “finished reconstructed human face”. This composite photograph was
relayed to the police for furtehr action by them
The “finished sculpted face” (Fig. 2) is then photographed. The 2D photographed

is uploaded into Photoshop™ software. A small programme which has been
developed by our center is used to select variuos hair styles of various era/decade
to suit the “finished sculpted face”. The selected head hair is then added to the
“finished sculpted face” after some finer adjustment.
The “finished reconstructed human face” (Fig. 3) was then relayed to the police,
who published it in the local newspaper.
In our experience, we found the combined clay sculpting-composite technique to

have more human looking finished product compared to the clay scuplting
technique alone. Other advantages are that, the various facial components in our
data bank can be added or modified onto the sculpted facial contour (the “finished
32
sculpted face”) very quickly (within minutes) when the request arise along the
time of police investigation.
Discussion
Facial reconstruction may either be three-dimensional (3D) from a skull or skull
model or two-dimensional (2D) from radiographs and photographs of skull.2
Reconstruction technique was first developed by German anatomists in the late
1800s for historical purposes and this was followed by the work of Russian
anthropologist Gerasimov who developed the clay three-dimensional method and
used it in forensic cases.1 It was then the landmark work of Dr Clyde Snow5 who
was assisted by Betty Gatliff that forensic facial reconstruction rapidly began to
be recognized worldwide.
The purpose of forensic facial reconstruction is to produce an image from a skull

which offers a sufficient likeness of the living individual that will facilitate in
identification of skeletal remains when there are no other means available. A
skull may tell of age, sex and the ethnic groups and thus partly contribute to the
cranial identification.4 Sex determination is a key analysis that forensic
anthropologists perform in order to construct a biological profile of human
remains.6
Stephan7 suggested that in the English literature, facial approximation methods

have been commonly classified into three types: "Russian," "American," or
"Combination." These categorizations are based on the protocols used, for
example, whether methods use average soft-tissue depths (American methods) or
require face muscle construction (Russian methods). However, he said that in
reality a combination of both method of face anatomy and average soft-tissue
depths have been used.
Facial reconstruction has been widely criticized. Evaluation of the reliability of

the clay dimensional method is rarely reported on.8 Author such as Stephan and
Henneberg 9 claimed that high resemblance of a facial approximation to the target
individual does not indicate recognizability, as the facial approximation was
poorly recognized even though it bore good resemblance to the target individual.
Another authors (Nelson and Michael)10 suggested that the lack of accuracy of the
soft tissue depth data and the sparsely placed anatomical landmarks as well as the
lack of understanding how soft tissue changes between the landmarks contributed
to errors and become subjective in nature in the manual reconstructions and
computer-aided facial reconstruction. The use of facial soft tissue thickness
measured at selected anatomical landmarks being used for 2D and 3D facial
reconstruction has been criticized because they were mainly taken from cadavers.8
Smith and Throckmorton11 looked at two-dimensional (2D) ultrasound scanning
33
of facial tissues in living orthodontic patients but was against converting this
result to 3D scanning for forensic reconstruction due to variation in their
comparability.
The shape of the lips varies with age, gender, ethnic origin, occlusion and loss of
vertical dimension. In young adults the upper lip usually does not cover all of the
upper incisors but the teeth could be completely covered with age. When the teeth
are highly attrited or due to inadequate dentures, position of the lips will also vary.
Similarly, certain occlusions are associated with lip features such as short upper
lip in Class II Division II occlusions. The philtrum of the lip will be affected by
the length of the lip, the lip support of the teeth and shape of base of the nose.3
The size of the mouth has been studied and debated by a number of authors. After
studying 96 subjects by measuring mouth width and lip thickness from their
photographs. Wilkinson12 concluded that the most reliable indicator of the mouth
width is the interlimbus distance. However, the lip thickness was related to the
height of the teeth. Another author (Stephan)13 who measured living Australians
using photogrammetric methods insisted mouth width as canine width plus 57%
of the cumulative distance between the lateral canine borders and the pupil centres
on each side.
However, facial reconstruction has also been shown to be successful by several

authors. Phillips14 reported three cases of successful recognition following facial
reconstruction which lead to the identification of six unknown bodies. The well
known Betty Gatliff 4 has produced a number of facial reconstructions whereby
they were successfully identified.
A recent study by Shahrom et.al (2005)15 looked at another way of finding a face
and this was done even without the availability of the skull. It was a two-
dimensional facial reconstruction using mitochondrial DNA phylogeny tree and
image morphing technique. It was found that the accuracy of the resulted
morphed face (Mandelian Morphing) is between 60-70%.
A group of authors raised the subject of missing persons and that it is of great
concern to the community with numerous associated emotional, financial, and
health costs.16 Therefore, they proposed that it is important for odontological
input being included in the investigation of missing persons and so forensic
odontologist must be employed to assist in missing person inquiries. They also
suggested that a national missing persons dental records database be established
for future missing persons investigations.
34
References
1) Taylor KT. Two-Dimensional Facial Reconstruction from the Skull. In:
Forensic Art and Illustration. CRC Press LLC, Florida 2001: 361 – 417.
2) Shahrom AW, Venezis P, Chapman RC, Gonzales A, Blenkinsop C and
Rossi ML. Techniques in facial reconstruction: computer-aided facial
reconstruction using a laser scanner and video superimposition.
International Journal of Legal Medicine 1996, 108(4) 194-200.
3) Clement J and Taylor R. Reconstruction of facial features of the deceased
by sculpting. Continuing Dental Education, School of Dental Science,
University of Melbourne. 2000
4) Taylor KT. Three-Dimensional Facial Reconstruction on the Skull -
Gatliff BP with Taylor K. In: Forensic Art and Illustration. CRC Press
LLC, Florida. 2001: 419-475.
5) Snow CC, Gatliff BP and Mc Williams KR. Reconstruction of facial
features from the skull: An evaluation of its usefulness in forensic
anthropology. Am J Physic Anthropol 1970; 33: 221-228
6) Williams BA and Rogers TL.. Evaluating the Accuracy and Precision of
Cranial Morphological Traits for Sex Determination Journal of Forensic
SciencesVolume 2006; 51(4): 729
7) Stephan CN. Beyond the Sphere of the English Facial Approximation
Literature: Ramifications of German Papers on Western Method Concepts
Journal of Forensic Sciences 2006; 51(4): 736-739
8) Quatrehomme G, Cotin S, Subsol G, Delingette H, Garidel Y, Grévin G
et.al. A Fully Three-Dimensional Method for Facial Reconstruction Based
on Deformable Models. J Forensic Sci 1997;42(4):649-652
9) Stephan CN and Henneberg M.. Recognition by forensic facial
approximation: Case specific examples and empirical tests. Forensic
Science International, 2005; 156(2-3): 182-191.
10) Nelson L.A and Michael SD. The application of volume deformation to
three-dimensional facial reconstruction: A comparison with previous
techniques. Forensic Science International 1998; 94(3): 167-181.
11) Smith SL and Throckmorton GS.. Comparability of Radiographic and 3D-
Ultrasound Measurements of Facial Midline Tissue Depths. Journal of
Forensic Sciences 2006; 51(2): 244-247
12) Wilkinson CM, Motwani M, and Chiang E. The relationship between the
soft tissues and the skeletal detail of the mouth. J Forensic Sci. 2003;
48(4):728-32
13) Stephan CN. Facial approximation: An evaluation of mouth-width
determination Am J Phys Anthropol 2003; 121(1): 148 – 57
35
14) Phillips VM. Skeletal Remains Identification by Facial Reconstruction

Forensic Science Communications Jan 2001; 3
15) Shahrom AW, Lim LS, Md-Zain BM & Noorazma S. 2-D Facial
Reconstruction (When Skull is not Available) Using Mitochondrial DNA
(MTDNA) Phylogeny Tree and Image Morphing Techniques: A
Preliminary Study. Int J Medical Toxicology & Legal Medicine. 2005
July-December, VIII(1): 1-5.
16) Blau S, Hill A, Briggs CA. and Cordner SM., Missing Persons–Missing
Data: The Need to Collect Antemortem Dental Records of Missing
Persons. Journal of Forensic Science 2006; 51(2): 386
36
ORIGINAL PAPER
Lesson learned by the forensic investigators: “An accomplice must

be corroborated by independent evidence”.
Shahrom AW, Zarida H*, Anisah CN**,Md Rizal AR**
Forensic Unit, Department of Pathology, Medical Faculty UKM, Malaysia.

Department of Pathology, Faculty of Medicine and Health Sciences, UPM,
Malaysia.*
Law Faculty, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.**
Abstract
Any forensic investigation requires teamwork approach. Sometimes each

component of the team has contributed to the optimum effort in a forensic
investigation. However, the basic principle of proving a crime is sometimes ‘over
looked’. We present a case of murder trial to illustrate this phenomenon, i.e. “It is
an established rule of practice that an accomplice must be corroborated by
independent evidence as to the identity of every person whom he impeaches”. The
basis of the law on evidence is discussed.
Keywords: Strangulation, ligature, cause of death, accomplice, decomposed body
Address for correspondence and reprint request: Assoc. Prof. Dr. Shahrom bin Abd. Wahid,
Forensic Unit, Department of Pathology, Medical Faculty, Universiti Kebangsaan Malaysia, Jalan
Yaacob Latif, Bandar Tun Razak, Cheras, 56000 Kuala Lumpur, Malaysia.
Tel: 03 – 91702444, Fax: 03 -91711673 e-mail: shahromwahid@gmail.com
Introduction
In any of death investigation, a multidicplinary approach is adopted. The various

forensic components such as forensic pathology, forensic biology, forensic
chemistry, forensic toxicology, forensic odontology, ballistics, etc. are involved.
The investigating officer from the police department lead or decide on the
direction of the crime investigation. He is guided by the Deputy Public Prosecutor
(DPP) who determines on the strength of evidence available whether to charge
and prosecute a suspect in court.
However, most of the forensic practitioners are only concern with his/her own
area of expertise. They only work as compartmentalized segments without the
37
benefit of looking at the “big picture” of the case. We believe this should not be
the case. Every forensic practitioner of all expertise need to be aware of the
“summarized big picture” of a case investigated. Therefore, they may contribute
their expertise more effectively and to avoid any deficiency to the case
investigated.
Furthermore, through this case study the authors wish to show that every forensic
practitioner of all expertise need to have exposure to the final outcome of each
case investigated to ensure no miscarriage of justice. Any discrepancy may be
improved in the future case investigation as part of the “continuous improvement
acitivity” exercise.
Here we present a case of murder trial to illustrate this phenomenon. In our case
study, the status of the prosecution witness as an accomplice requires
independent corroborative evidence which determine the outcome of this case.
The basis of the law on evidence is presented in the discussion segment.
Case Study
On the 20th of October 2004, in the Court of Appeal, Malaysia which was presided
by the Honourable Judge MOKHTAR SIDIN, JCA; the Honourable Judge
GHAZALI MOHD YUSOFF, JCA; and the Honourable Judge AUGUSTINE
PAUL, JCA for the case of Harcharan Singh - vs - Public Prosecutor , the
Honourable Judge Augustine Paul JCA delivered following judgment of the court.
The charge preferred against the accused persons in this case is as follows
[translation]:
That both of you, on 1 March 1996 at about 10:30 p.m. in a house at 306, Desa
Aman, Sungai Buloh in the District of Gombak, State of Selangor, with common
intent, carried out the murder of Shaikh Abdul Rub Samdani Siddiqi. Hence, the
both of you have committed an offence which is punishable under section 302 of
the Penal Code read together with section 34 of the same Code.
Both the accused persons claimed trial to the charge. Briefly stated the facts of the
case are that on 15 March 1996 Ulang Sipang (PW1) came across a big parcel
when he was walking to his Kampong at Batu 16, Batu Caves, Gombak. He
informed Corporal Ramli Tawil (PW2) about it. They found a dead body (“the
deceased”) in the parcel. Inspector Mohamad Maizan (PW6) was then informed.
Upon further investigation a handphone was found at the scene. It was found to be
registered in the name of one Jasbir Kaur (PW8) for the use of her business
partner Shaikh Abdul Rub, a Pakistani national who was later identified as the
deceased. The police took possession of PW8’s car. It was examined by the police
38
Polilight expert. Samples of earth found on the seats and rubber mats were taken
for Polilight examination. Two strands of hair were also found on one of the
rubber mats in the boot of the car. Later the exhibits were sent to the Chemistry
Department for analysis together with a sample of hair taken from the deceased.
In dealing with the events that led to the death of the deceased we can do no better
than reproduce the able summary of the facts as found by the learned trial Judge in
his Grounds of Judgment. It reads as follows:
SP8 Jasbir Kaur Pritam Singh is the wife of the 1st Accused. In 1996, she was a
business woman. As stated above, the deceased was her business partner. She has
been managing a bed and breakfast villa and selling cloth and Punjabi costumes
since 1994. Previously, she was working for the deceased who was also known to
her as Khan whose wife was originally with him in Malaysia but has since
returned to Pakistan. Jasbir Kaur was invited by the deceased to become his
business partner. This business partnership very soon developed to an extent and
dimension beyond the frontiers of purely business partnership.
After the deceased had been missing for 3 to 4 days, Jasbir Kaur made Dang
Wangi police report No 4759/96. She was subsequently informed by the police of
the deceased’s death. The last occasion Jasbir Kaur saw the deceased was at noon
on 1 March 1996 at Georgetown Pharmacy, Tuanku Abdul Rahman Road, where
she bought some medicine. In 1996, Jasbir Kaur was staying near Tuanku Abdul
Rahman Road. On that date, the deceased had telephoned Jasbir Kaur to inform
her that he was going to Singapore and that he was giving his house key to his
servant.
On 2 March 1996, at the invitation of her mother-in-law, Jasbir Kaur together with
the 1st Accused and 2 brothers-in-law went to Taiping, to attend the birthday
party of a grandchild of her mother-in-law, and returned to Selayang on 3 March
1996.
On 1 March 1996, Jasbir Kaur’s husband i.e. the 1st Accused took her car to
work. After 6.00 p.m. when she left her house, she did not see her car there; even
until 10.00 p.m., her car was still not there. She knew the 1st Accused was then
using her car. Jasbir Kaur said the deceased knew the 1st Accused and that the 1st
Accused and the deceased had no arguments. Jasbir Kaur had given the deceased
her handphone for the deceased to use. Whenever the handphone was turned on,
Jasbir Kaur’s name would appear on the screen thereof.
Jasbir Kaur remembered the visits by some police officers such as DSP Gan and
Insp. Mohamed to her house. At first she did not know of the reason for these
visits, but was later told that the police wanted to take her car for inspection. For
the remote control, ignition key and car which she handed to the police, she was
given a search list which she refused to sign.
Initially, Jasbir Kaur testified that she had no misunderstanding with the deceased
who also never used force on her and that apart from the business partnership, she
had nothing to do with the deceased who also had no quarrel with her family.
Jasbir Kaur described the deceased as a person of good personality, although the
39
deceased was sometimes drunk and had engaged himself in senseless talk, and
occasionally was hot tempered. However, later in her evidence, she admitted that
the deceased had assaulted her and pushed her aside when she opened a door. She
knew the deceased had an intense liking for women, but she did not interfere.
Between 7.00 p.m. and 11.00 p.m. on 1 March 1996, she was in her mother’s
house at No. 306, Desa Aman, which she and the 1st Accused frequently visited.
Under cross-examination, Jasbir Kaur admitted that the deceased had assaulted
her 3 to 4 times in order to have sex with her. The deceased had brought women
to Jasbir Kaur’s place of business, to view blue films or pornography and to have
sex. The deceased had forced her to have sex with him. Besides, the deceased
made numerous attempts to have sex with her, in December 1995, January and
February 1996. She added that in December 1995, the deceased had made several
attempts to molest her at the lodging house, Villa Exclusive, where the deceased
had been a lodger. In the fourth attempt, the deceased pulled her hair, brought her
to her room and assaulted her. The deceased broke a glass bottle and threatened to
kill her. He assaulted her by pushing her against the wall, while she pulled his
hair, assaulted him and then escaped. Jasbir Kaur told her husband, the 1st
Accused, her cousin, the 2nd Accused that the deceased did not succeed in having
sex with her, but her head and body were swollen. Be that as it may, she did not
make a police report on the above episodes because she was ashamed, being a
married woman. The 1st Accused was furious and told his wife Jasbir Kaur to
cease the business partnership with the deceased. After the 4th attempt by the
deceased, Jasbir Kaur stopped working at the lodging house for a while but
continued subsequently. Jasbir Kaur then described the deceased as a fierce
person who had assaulted her and her workers.
SP9 (Gurmit Singh Sarup Singh) was a police constable in Sitiawan. In March
1996, he stayed at No 1371, Batu 11, Sg Buloh. He is married to Nachatra Kor S
Pritam Singh. He knew the deceased who always visited Jasbir Kaur who is
Gurmit Singh’s sister-in-law, i.e. the wife of the 1st Accused who is Gurmit
Singh’s brother.
On 1 March 1996, Gurmit Singh went to house No 306, Desa Aman, Sg Buloh. At
about 9.30 p.m., he was sitting outside the house when Jasber Singh, the 2nd
Accused, was also there. Subsequently, the 1st Accused and the deceased were
walking towards the house. On arrival, the deceased went straight into the house,
followed by the 1st Accused. They were both engaged in altercations and
accusations. The 2nd Accused then entered the house. The two Accused and the
deceased quarrelled for about half an hour. Gurmit Singh then heard a loud bang,
apparently caused by a falling object to the floor. On entering the house
subsequently, Gurmit Singh saw the deceased had already collapsed on the floor,
face downwards or prostrate. At that time, the 1st Accused, holding a stick, swore
at the deceased in the following Punjabi words:
Tu Ney Mere Zindagi Bardad Karte.
Tu Ney Mere Ghar Barbad Kardid Ta.
40
Tu Ney Meray Aufar Nu Makiah.

These Punjabi words were translated by the certified Punjabi Interpreter in open
Court as:
You have destroyed my life.
You have destroyed my family.
You have hurt my wife.
The 1st Accused then climbed on top of the deceased’s body, cursing and
swearing at the deceased. The 2nd Accused ran to a room in the house, then
returned with a rope to tie the deceased’s neck, with the 1st Accused pulling one
end of the rope and 2nd Accused the other end. Within 5 to 6 seconds, the 1st
Accused requested Gurmit Singh to hold and pull the rope. At this stage, it is
necessary to note that there was absolutely no evidence whatsoever that Gurmit
Singh had ever participated in the 1st and 2nd Accuseds’ act of pulling the rope
around the deceased’s neck. Gurmit Singh noticed that the deceased’s neck was
red and that the deceased was already dead. Gurmit Singh and the 2nd Accused
then loosened the rope on the deceased’s neck. The 2nd Accused then took a bed
sheet from a room, walked past Gurmit Singh and wrapped the deceased’s body
with the bed sheet. Meanwhile, the 1st Accused reversed Jasbir Kaur’s car in
order to carry the deceased’s body into the boot thereof. The 1st Accused opened
the boot and held it, lest it might close back, while the 2nd Accused and Gurmit
Singh carried the deceased’s body into the boot, after which the 1st Accused
drove the car, with Gurmit Singh as the passenger in the front seat while the 2nd
Accused took a back seat. They left Sg Buloh for Kepong, and stopped at Jinjang
Petronas Station where the 1st Accused refilled RM10.00 of petrol, since the car
was running out of petrol. They proceeded towards Genting Lama Road, which
was dark. After travelling for about 40 minutes, the 1st Accused stopped the car
and opened the boot. Gurmit Singh and the 2nd Accused carried the deceased’s
body and dumped it, but Gurmit Singh was not too sure of the place. Thereafter
they returned home.
The deceased was already motionless when Gurmit Singh entered the house
subsequently where he saw the 1st and 2nd Accused in the house. Gurmit Singh
testified that 3 days before the incident, the 1st Accused had personally hatched a
plan to assault or cause injury to the deceased, because the 1st Accused suspected
SP8 Jasbir Kaur, the 1st Accused’s wife, was having a clandestine extra-marital
relationship with the deceased. Pursuant to the plan, two pieces of stick, one of
which was longer than the other, were used by the 1st and 2nd Accused
respectively to beat the deceased, in addition to the use of the rope tied around the
deceased’s neck and pulled by the 1st Accused and the 2nd Accused at both ends
of the rope respectively. Gurmit Singh found the deceased lying prostrate, spotted
some blood on the deceased’s face and rear right ear.
SP9 admitted under cross-examination that he had been arrested and detained by
the police for 15 days. He agreed to be a prosecution witness and he was not
charged in Court. As will be seen later, DSP Gan who took a statement from
41
Gurmit Singh, testified that no agreement or promise was made to Gurmit Singh
for co-operating with the police. Gurmit Singh had known the deceased for more
than 2 years before the incident, but was not on talking terms with him as they had
quarrelled before, over the deceased’s clandestine extra-marital relationship with
Gurmit Singh’s two sisters-in-law, viz Hasbinder Kaur and SP8 Jasbir Kaur with
whom the deceased had been intensely intimate. Further, the deceased also
frequented the shop of SP9’s wife at Semua House, Masjid Road, Kuala Lumpur.
These state of affairs had caused and enhanced Gurmit Singh’s mistrust and
distrust in the deceased. The deceased had indeed seduced all these women. Prior
to this ill-fated incident, Gurmit Singh has had an altercation with the deceased in
Jasbir Kaur’s house in Selayang.
It is to be observed that so far there has been no attempt by the defence to impeach
Gurmit Singh’s credit and there was therefore no question of impeaching the
credit of SP9 at this stage. Gurmit Singh has undergone incisive cross-
examination by the defence and his evidence in my considered view remains
unscathed so far. His evidence is clear, concise and consistent and there is nothing
in his demeanour or testimony which can lead me to conclude otherwise. He has
given his evidence with all fairness and truthfulness. I therefore accept him as a
credible and reliable witness whose evidence must be considered and accepted as
an integral, essential and cogent part of the case for the prosecution after a
maximum evaluation thereof.
Dr Shahrom Abdul Wahid (PW10) conducted the post-mortem examination on
the deceased. It was his finding that the cause of death was ligature strangulation
which was not accidental. He said that the injuries could have been caused by
more than one person. The defence made an attempt to impeach the credit of
PW9. The learned trial Judge accepted the explanation given by PW9 and held
that his credit has been re-established.
It was submitted by the defence at the close of the case for the prosecution that
PW9 is an accomplice. In dealing with this submission the learned trial Judge said
in his Grounds of Judgment:
On the defence submission that Gurmit Singh is an accomplice and so is not a
credible witness, I hold that SP9 has not participated in the commission of the
offence stated in the charge. There is not an iota evidence that SP9 was a
participes crimines, i.e. a participant in the commission of the offence in question.
42
Fig. 1: The deceased was wrapped with bed sheets like a ‘parcel’ before
being dumped at a secluded area.
Fig.2: The partially decomposed deceased person showing a tight ligature

around his neck.
43
Fig. 3: The secluded area where the body had been found (arrow).
When SP9 subsequently entered the house, the deceased’s body was sprawling
prostrate on the floor and was motionless. SP9 cannot be treated as an accomplice
unless he has had a conscious hand in the commission of the murder of the
deceased or he makes admission of facts showing that he has participated in the
commission of the murder of the deceased herein. Gurmit Singh’s participation, if
at all, was clearly after the deceased was already dead. He did not participate in
causing the death of the deceased. In the instant case, I therefore hold that SP9’s
evidence shall be treated as that of an ordinary evidence and not the evidence of
an accomplice and so the question of corroboration does not arise at all.
The learned trial Judge then called for the defence of both the accused persons. At
the conclusion of the defence case he convicted both of them and sentenced them
to death. This appeal is by both the accused persons against their conviction and
sentence.
Before us it was strenuously argued by learned counsel that PW9 is an
accomplice. There is no evidence to suggest that PW9 had ever participated in the
first and second accuseds’ act of pulling the rope around the deceased’s neck.
However, he was a witness to the final moments of their attack on the deceased
and he assisted them in disposing off the body and did not inform anyone of
whatever he had seen and the assistance that he had rendered. He is therefore an
accessory after the fact. The question that requires to be determined is whether
44
such a witness is an accomplice. In Davies v Director of Public Prosecutions

(1954) 1 All ER 507 the House of Lords held that persons who are particeps
criminis in respect of the actual crime charged, whether as principals or
accessories before or after the fact in felonies or persons committing, procuring or
aiding and abetting in the case of misdemeanours are accomplices. In England
section 1 of the Criminal Law Act 1967 has abolished the distinction between
felonies and misdemeanours. There is no such distinction in this country.
However, it has been accepted that an accomplice is a person who is particeps
criminis in respect of the actual crime charged (see Re Soo Leat (1956) MLJ 54;
Kuan Ted Fatt v PP (1985) 1 MLJ 211; Namasiyiam v PP (1987) 2 MLJ 336).
There is some controversy as to whether an accessory after the fact is an
accomplice in the strict sense as he is not concerned in the original offence for
which the accused has been charged. As Sarkar on Evidence 14th Ed Vol 2 says at
pp 1912 – 1913:
In the penal laws of this country ordinarily two classes have been recognised:
Persons who are principals (i.e. directly or indirectly concerned in the offence)
and abettors or instigators (i.e. privy to the offence). The term ‘accomplice’
obviously includes principals in the first and second degrees as also abettors. An
accessory after the fact is one who knowing a felony to have been committed
receives, relieves, comforts, assists, harbours or maintains a felon. In a case it was
doubted whether an accessory after the fact is an accomplice (R v
Chutterdharee, 5 WR Cr 59: see also Nga Pauk v R, A 1937 R 513) but the
Judicial Committee has held that he is (Mahilikilili v R, A 1943, PC 4; 44 Cr LJ
1; Mahadeo v R, A 1936 PC 242: 40 CWN 1164; see Ismail v R, A 1947 L 220).
An accessory after the fact being not concerned in the original offence for which
the accused is tried, may not in the strict sense come within ‘accomplice’, but
even in such cases there are exceptions, e.g., the possessor of stolen property soon
after theft may be presumed to be the thief (v. ill (a) to s 114) and he is an
accomplice in the case against the thief. All accessories after the fact are not of the
same degree of criminality, as so much depends on the particular facts of each
case. In many cases the question whether an accessory after the fact is or is not an
accomplice in law may assume an academic form, the principal point to which
consideration is applied being whether corroboration of his evidence is required.
Whether an accessory after the fact does or does not come technically within the
category of ‘accomplice’, he is on the same footing as an accomplice and his
evidence is no better. The presumption of untrustworthiness equally attaches to
his evidence and on the same principle as that of an accomplice, the sounder rule
would be to require corroboration (see Alimuddin v R, 23 C 361 post; R v Kalu,
A 1937 O 259; Shyan Kumar v R, A 1941 0130; Brijpal v R, A 1936 O 413;
Turab v R, A 1935 0 1; Sundor Lal v R, A 1934 O 315; Nawab v R, A 1923 L
391; Bahawala v R, A 1925 L 432; Hayatu v R, A 1929 L 540; Ismail v R, A
1947 L 220; Ashutosh v S, A 1959 Or 159 and cases post), except when it can be
dispensed with in the special circumstances of a case. In such cases the real
question is the degree of credit to be attached to the evidence of these witnesses
45
who as accessories are concerned with the accused in some other offence arising
out of the original offence.
Strictly speaking an accessory after the fact cannot be an accomplice as he is not

concerned in the commission of the original offence. In Kuan Ted Fatt v PP
(1985) 1 MLJ 211 the Federal Court did not treat a witness who was present at the
time of the commission of the offence as an accomplice as he had no prior
knowledge that the offender intended to commit the offence charged. However, it
can be safely stated that the question of whether an accessory after the fact is an
accomplice is academic as his evidence must be considered on the same principles
as that of an accomplice. Where he has played an active role his evidence must be
corroborated. On the other hand if his role has been passive his evidence may be
accepted with the usual corroboration warning.
What remains to be considered is whether the role played by PW9 requires his
evidence to be corroborated. He helped to loosen the rope around the deceased’s
neck. He helped to carry the body of the deceased to the boot of the car. When the
car was driven off he sat as a passenger in the front seat. When the car later
stopped PW9 and the second accused carried the deceased’s body and dumped it.
After that he did not mention what he knew to anyone. It is clear that the role
played by PW9 is not passive. He was an active accessory after the fact. Where a
witness plays such an active role his evidence is no better than that of an
accomplice (see Alimuddin v R 23 C 361). A similar view has been expressed in
the case of a witness who admits that he is cognisant of the crime to which he
testifies and took no steps to prevent or disclose it (see R v Chando 24 WR Cr
55; Bihari v State AIR 1957 Or 260). The need to treat PW9’s evidence with
caution is made stronger by the fact that he said that he was not charged as he had
agreed to become a witness for the prosecution. In support we refer to cases such
as Amar v R AIR 1931 L 406 and Indar v R AIR 1931 L 408 where it was held
that the testimony of a person who has thrown to the wolves his erstwhile
associates and friends in order to save his own skin must be received with great
caution. In the circumstances it was our view that the evidence of PW9 requires to
be corroborated.
The learned trial Judge did consider the evidence in corroboration of the
testimony of PW9 in his alternative finding of PW9 being an accomplice. As he
said in his Grounds of Judgment:
In the event that I have erred in my aforesaid finding that Gurmit Singh is not an
accomplice, I shall now consider the finding in the alternative that he is an
accomplice and treat him as such. It is trite law that this alternative finding that
Gurmit Singh is an accomplice is permissible and there is nothing objectionable.
In Teja Singh v PP (1950) MLJ 71, at pp 73-74, Spenser Wilkinson, J said:
46
I can see nothing wrong in a Court finding, as a matter of law, that a witness is not
an accomplice and then going on to indicate what its finding would be in case it
should be held that this matter of law has been wrongly decided.
This principle was followed and applied in Ismail Mat Saat v PP (1955) 1 MLJ
(CA); Chua Sin Teng v PP (1963) MLJ 150 (HC); and Lee Poh Chet v PP (No
2) 1 MLJ 187(CA).
Therefore, even by treating Gurmit Singh as an accomplice, it is my specific
finding that Gurmit Singh’s evidence that the deceased’s death was jointly caused
by 1st and 2nd Accused has been corroborated by the evidence of SP10 Dr
Shahrom Abdul Wahid, in particular the extent of the injuries established in the
post-mortem report and also the cause of these injuries, culminating in the
deceased’s death. SP7 the Polilight expert’s evidence has also corroborated the
evidence of Gurmit Singh to the extent that the 1st and 2nd Accused had jointly
transported and carted the deceased’s body which they threw into a ravine. The
detailed analysis of the evidence given by SP6 Insp Mohamed and SP13 the
chemist Mr. Lim Kong Boon, as given above, have in my view cumulatively
corroborated Gurmit Singh’s evidence.
We are unable to comprehend how the extent of the injuries and the cause of death
as stated in the post-mortem report can corroborate PW9’s evidence that the
deceased’s death was jointly caused by the first and second accused. PW10 did
say that the ligature mark on the neck of the deceased was consistent with the
pattern of the red nylon ligature which was tied around the deceased’s neck. He
said in evidence that the ligature around the deceased’s neck could have been
caused by one or more persons. In cross-examination he said that the death of the
deceased could have been caused by one person if the deceased had been rendered
unconscious as a result of the beating of his head. This evidence does not in any
way corroborate PW9’s testimony that the deceased’s death was jointly caused by
the first and second accused. The learned trial Judge also said that the evidence of
the Polilight expert’s evidence has also corroborated the evidence of PW9 to the
extent that the first and second accused had jointly transported and carted the
deceased’s body which they threw into a ravine. It will be observed that the
Polilight expert collected some earth and hair samples from the boot of the car of
PW8. Lim Kong Boon (PW13) analysed the samples of hair taken from the car
and the deceased and said that they could have come from the same source though
he is unable to state the percentage of similarity. He ought to have stated the
percentage of similarity found and the minimum that is required to support his
conclusion which he did not. In the absence of such evidence his conclusion is not
supported by reasons as required by section 51 of the Evidence Act 1950. That
deprives the testimony of PW13 of its evidential value on the principles explained
in Sim Ah Song v R (1951) MLJ 150. In any event the similarity in the hair found
in the car and that of the deceased means little. It only shows that the deceased
47
was placed in the boot of the car as described by PW9. However, that does not
connect the accused persons with the crime. As Lord Reading CJ said in R v
Baskerville (1916) 2 KB 658 at p 667:
We hold that evidence in corroboration must be independent testimony which

affects the accused by connecting or tending to connect him with the crime. In
other words, it must be evidence which implicates him, that is, which confirms in
some material particular not only the evidence that the crime has been committed,
but also that the prisoner committed it.
In commenting on the significance of the need for corroboration with regard to the
identity of the accused Sarkar on Evidence 15th Ed Vol 2 says at p 2105:
It is an established rule of practice that an accomplice must be corroborated by
independent evidence as to the identity of every person whom he impeaches. The
accomplice may know every circumstances of the crime, and while relating all the
other facts truly, may in order to save a friend, or gratify an animosity, name some
person as one of the criminals who was innocent of the crime (R v Krishna Bhat,
10 B 319; see also R v Malapa, 11 BHC 196; R v Budhu Nanku, 1 B 475).
Thus the similarity of the hair sample of the deceased with that of the sample
found in the boot of the car does not amount to corroboration as it does not show
that both the accused persons had committed the crime. We also fail to see how
the evidence of PW6 and PW13 can cumulatively corroborate the evidence of
PW9 as found by the learned trial Judge. In the circumstances it is our view that
evidence which has been found to be corroborative by the learned trial Judge does
not qualify to be described as such in law.
The only evidence in this case to connect the two accused persons to the crime is
that of PW9. As we have found that his evidence requires to be corroborated and
of which there was none there was no evidence on which the defence could have
been called. In the upshot we allowed the appeal and quashed the conviction and
sentence imposed on the accused persons.
Discussion
The extract from the judgement shows the exercise of discretionary power under
section 114 of the Evidence Act 1950 (Part III - Production And Effect Of
Evidence, Chapter VII - Burden Of Proof) which reads as follow:
“Section 114. Court may presume existence of certain fact
The court may presume the existence of any fact which it thinks likely to have
happened, regard being had to the common course of natural events, human
48
conduct, and public and private business, in their relation to the facts of the
particular case.”
It can be understood from the case that heavy reliance have been put by the
Lordships on Illustration (b) of the section:
“The court may presume—

…………………
(b) that an accomplice is unworthy of credit unless he is corroborated in material
particulars;”
Presumption of fact of this nature is a short-cut to the proof process, as presumed

fact, if not disputed, becomes proof. Failure on the part of the prosecution to
tender independent evidence to corroborate the accomplice’s testimony renders
the latter to be of no value.
The reason why the law is drafted in such a way is simply to avoid incidents of
accomplice, either he is a co-accused (Section 10 read with section 114 (b)) or a
(interested) witness, from using the court’s platform to escape liability and put the
blame on others. The same standard was also adopted in the high-profilic murder
case of Hazleza Ishak (SABARUDIN BIN NON & ORS V PUBLIC
PROSECUTOR [2005] 4 MLJ 37), where the court cautiously considered the
evidence of the accomplice-turned-prosecution witness to see whether there were
any discrepancies of testimony by the accomplice and whether the evidence was
sufficiently corroborated by way of circumstantial evidence.
The principles governing evidence that requires corroboration whether as a matter

of practice or as a matter of written law were set out in Lim Guan Eng v Public
Prosecutor [1998] 3 MLJ 14:
"So far as the law governing corroboration is concerned, we accept the following
propositions to be well settled and beyond controversy:
(1) As a general rule, the conviction of an accused may proceed upon the
uncorroborated evidence of one witness.
(2) There are cases where either common law -- as a matter of practice which
has, through passage of time, acquired the force of law -- or statute, creates an
exception to the general rule in respect of certain categories of witnesses by
calling for, or indeed demanding, that their evidence may not to be acted upon in
the absence of independent corroboration. Accomplices illustrate the common law
exception, while s 6(1) Evidence Act 1950 illustrates the statutory exception.
(3) Evidence that requires corroboration, whether as a matter of practice having
the force of law or by direction of statute:
49
(a) must first be capable of belief before any question of corroboration may arise,
for evidence that falls of its own inanition cannot be saved by the presence of
abundant corroboration; (b) cannot corroborate itself, for tainted evidence does
not remove its taint by repetition, notwithstanding s 157 of the Evidence Act
1950; and (c) cannot be corroborated by evidence that itself requires
corroboration.
(4) To constitute true corroboration in the eyes of the law, the corroborative
evidencemust: (a) be capable of belief; (b) be independent in the sense
mentioned in proposition (3)(c) above; (c) be in respect of the fact or facts that
lie at the axis of the dispute, that is to say, upon the fact in issue and not upon
some collateral matter or upon a fact in respect of which there is no quarrel. In
other words, it must be corroboration upon a material particular but need not be
identically repetitive of the evidence that requires corroboration.
(5) At common law, a trial court is entitled to act upon uncorroborated evidence
which in itself requires corroboration provided that it warns itself of the danger of
so acting. The warning must not amount to mere lip-service. Good reasons must
be furnished for departing from the accepted rule. Departure from the normal rule
may be justified where the evidence requiring corroboration emanates from a
witness who is a person of high character and the offence is one that does not
carry with it any serious moral stigma."
According to S.133 Evidence Act 1950, an accomplice competent witness against
an accused person, and a conviction is not illegal merely because it proceeds upon
the uncorroborated testimony of and accomplice. As such, an accomplice may still
be a credible witness without any corroboration. However it depends on the court
after assessing the factual evidence that was presented before it. From the facts of
this case, it is fair that the Appeal court has treated SP9 as an accomplice because
he is not an innocent party in the whole setup. At the very least he is a tainted
witness which has his own interest to serve. As such his evidence has to be
scrutinized with caution. Hence, the imperative need that his evidence be
corroborated.
S.114(b) Evidence Act has been used by the court to show that we are only
humans. Due to this the court may presume that an accomplice is unworthy of
credit unless he is corroborated in material particulars after considering the
existence of any fact which it thinks likely to have happened especially when it
relates to human conduct. It is conceded that the court has made a fair assessment
with regard to the testimony of SP9.
The main issue in this case is corroboration. To what extent should the DPP prove
the corroborative evidence up to the standard required by law. As the learned
judge says “it is our view that evidence which has been found to be corroborative
by the learned trial Judge does not qualify to be described as such in law”. It is
submitted that there are 2 points here worth considering.
50
(i) Corroborative evidence which affects the accused by connecting or

tending to connect him with the crime.
(ii) Corroborative evidence which would implicate the accused that is
which confirms in some material particular not only that the crime has
been committed, but also that the accused committed it.
The law on corroboration has been clearly stated by Sharma J in Atan bin Abdul
Gani. (1970) 2 MLJ143, namely,
(a) It is not necessary that there should be independent confirmation of every

material circumstance in the sense that the independent evidence in the case
should in itself be sufficient to sustain conviction. All that is required is that there
must be some additional evidence rendering it probable that the story of the
accomplice is true and that it is reasonably safe to act upon it.
(b) The independent evidence must not only make it safe to believe that the crime
was committed but it must in some way reasonably connect or tend to connect the
accused with it by confirming in some material particular the testimony of the
accomplice the accused committed the crime.
It is submitted that the story tendered by SP9 is most probably true because
the corroborative evidence of the forensic team (led by SP10) testify as to
this, that the cause of death was due to strangulation and that both the
accused had been seen doing it.
(c) The corroboration need not be direct evidence that the accused committed the
crime. It is sufficient if it is merely circumstantial evidence of his connection with
the crime.
(d) Corroborative evidence required for accepting the testimony of an accomplice

need not by itself conclusively establish the guilt of the accused. It is sufficient if
it is a piece of circumstantial evidence which tends to connect the accused with
the crime with which he is charged.
As such, with due respect to the learned judges , it is humbly submitted that, the
degree that the law requires for corroboration is only reasonable in nature, the
objective is to support or confirm the evidence of the accomplice in at least one
material fact pointing to the guilt of the accused. In this case, it is submitted that
the cumulative effect of the independent corroborative evidence (medical report),
chemist report, etc.) tends to show that there were no other persons except the two
accused who have committed the murder.
51
Hence, it is further submitted that the learned judges in the appeal court have
given a narrow and strict interpretation of the corroborative evidence needed for
accomplice testimony. This would in a way affect the whole system of justice
which at the end of the day might cause miscarriage of justice to the parties
concerned.
Conclusion
Whatever the opinion of this case in the eye of a “reasonable man” for the proof
of “beyond reasonable doubt”, the forensic investigators should always have in
their mind that “An accomplice must be corroborated by independent evidence” in
their forensic quest to pursue justice.
References
1. Alimuddin v R 23 C 361;
2. Amar v R AIR 1931 L 406 and Indar v R AIR 1931 L 408;
3. Bihari v State AIR 1957 Or 260;

4. Criminal Law Act 1967 [England]: s.1
5. Davies v Director of Public Prosecutions (1954) 1 All ER 507;
6. Evidence Act 1950: s.51
7. http://www.kehakiman.gov.my/jugdment/coa/archive/B-05-81-00.htm
8. Kuan Ted Fatt v PP (1985) 1 MLJ 211;
9. Kuan Ted Fatt v PP (1985) 1 MLJ 211;
10. Namasiyiam v PP (1987) 2 MLJ 336;
11. R v Baskerville (1916) 2 KB 658
12. R v Chando 24 WR Cr 55;
13. Re Soo Leat (1956) MLJ 54;

14. Sarkar on Evidence 14th Ed Vol 2
52
15. Sim Ah Song v R (1951) MLJ 150;
53
ORIGINAL ARTICLE
Organ weights of Malay, Chinese, Indian, and Indonesian

ethnic groups in Malaysia
OP Murty, Ling CS, Suhashni G, Mohd Fahmee AR, Nurasma Z, Khalsom S
Forensic Pathology Unit, Department of Pathology , Faculty of Medicine,

University of Malaya, Kuala Lumpur 59100, Malaysia
Abstract
This is a retrospective study on organ weights of different ethnic groups in

Malaysia based on materials of 1773 medico-legal autopsies in healthy people.
The study was aimed to find an average range of organ weights for
Malaysian/South East Asia and compare it with other ethnic groups around the
world. Non availability of normal range of weights of local people made these
comparisons a little difficult for local comparisons. The study included only
subjects which were above 12 years of age and were healthy. Case materials were
collected from 1773 autopsy cases which were normal and healthy from every
angle, for the past five years (2000-2004) at the Forensic Pathology Unit
University Malaya Medical Centre. The main organs that were analyzed included
the heart, lung, liver, pancreas, spleen, adrenal, kidney and brain. It was found that
weights of different organs were positively correlated to height and body
weight. Females generally had lower organ weights as compared to males. There
were differences in mean organ weight between the different ethnic groups
present in Malaysia. The weights were found quite different as mentioned in the
standard scientific literature. The organ weights of local dominant Malay groups
were quite similar to Indonesian people. Western population generally had a
higher organ weight compared to this study.
Keywords: Normal organ weight; autopsy; organ weight; medico-legal deaths.
Address for correspondence and reprint request: Dr.O.P.Murty, Additional Professor ,

Forensic Medicine and Toxicology, All India Institute of Medical Sciences , New Delhi 110029.
Email : opmurthy 2006 @hotmail.com, dropmurty@yahoo.co.in Phone 009111 26593274, 0091
9868397155 ( Office )
53
Introduction
Human organ weights are important to forensic pathologist in cases of sudden
deaths, and establishing the relationship between disease and trauma. As any
deviation in weights from the normal range suggests some pathological change in
the organ and thus helps in giving the opinion regarding to the cause of death in
various pathological conditions and also in finding out the relationship between
trauma and disease in routine forensic practice. Organ weight also plays a
significant role in estimation of body height and weight of an individual.
The relationship of the specific size of organ to actual body weight is a dynamic
process throughout growth and development, the onset of disease, and changes in
nutritional status. It has been known that the liver, heart, kidney and brain make
up 7% of the actual body weight. Human organ weight was reported to be
dependant on races, gender, environmental and socioeconomic condition that are
quite different in various part of Malaysia.
As literature available on the subject for the Malaysian population is scanty, hence
the present study is an attempt to project standardized normal range of various
organ weights (with no pathological lesions) among the Malaysian population and
to find differences and similarities among the different races in Malaysia
regarding organ weight.
Materials and Methods

The study was a retrospective examination of autopsy reports. The organs are
weighed using an electronic weighing scale measuring in gram unit. Main vital
organ weighed were heart, right and left lungs, liver, spleen, pancreas, right and
left adrenal glands, right and left kidneys and brain. Other organs, namely thymus
and reproductive organs were weighed if there was a requirement in the case.
The histopathology was done in organs if pathological changes were found or
suspected.
All autopsy reports for the past five years (2000-2004) were examined and the
information regarding the patient’s ethnicity, gender, body weight, height as well
the various organ weight and cause of death were manually copied to a form
(enclosed in appendix) which had been subdivided earlier to different categories
of ethnic groups i.e. Malay, Chinese, Indian, Indonesian, miscellaneous and
gender.
54
Cases with age less than 12 years or diseases and conditions known to influence
the weight of the organs (Table 1) were excluded.
Table 1: The exclusion criteria
pancreas
kidneys
spleen
brain
heart
lungs
Cause of death
liver
Septicaemia x x x x x x x
Peritonitis x x x x x x x
Aspiration x
Cranio-cerebral injury x
Ischemic heart disease x
Myocardial infarction x
Pulmonary tuberculosis x
Hypertensive heart disease x x
Stab wound to chest x
Asphyxia x
Paraquat poisoning x
Ruptured heart x
Ruptured spleen x
Drowning x
Cardiac tamponade x
Liver cirrhosis x
Laceration of heart x
Laceration of lung x
Diabetes nephropathy x x x
**All organ weight in autopsy cases with uncertain cause of death were not taken
into consideration. Inclusion criterias for cases were normal deaths, accidents,
homicide, suicide etc without any pathology. All weights in this mortuary are
recorded by electronic machine which is calibrated from time to time. All
pathologists who take up job here are given training in the beginning for
dissection and organ separation so inter-personal variations are less.
Statistical analysis
Statistical analysis of data was carried out using a statistical software package
(SPSS version 11.5). The data on organ weight were used for comparison with
other variables i.e. body weight and height. Data on various organ weights
55
showed Gaussian distribution. This distribution was used for the comparison with
other variables (height, body weight and race). The distribution limits of various
organ weight versus height and body weight groups in Fig. 1 – Fig. 25 were
calculated using standard deviation derived from the distribution of all organ
weights. Cases with 5 groups of races were tested with ANOVA (F-test) and
corrected for multiple comparisons with Scheffe’s post-hoc test. Other statistical
test (Student’s t-test were unpaired and two-sided).For all cases p value of less
than 0.05 were considered statistically significant.
Results
400
300
200
HEART
100
N= 283 231 286 177 100
MALAY INDIAN MISCHELLENOUS

CHINESE INDONESIAN
RACEPT
Fig.1 : Heart weight (g) versus ethnic groups
56
1800
461
1600
1400
1200
1000
BRAIN
1507
800
N= 233 324 302 140 124

CHINESE INDONESIAN
RACEPT
Fig. 2 : Brain weight (g) versus ethnic groups

700
600
500
400
300
RLUNG
200
N= 209 261 263 125 91

CHINESE INDONESIAN
RACEPT
Fig. 3 : Right lung weight (g) versus ethnic groups
57
600
500
400
300
LLUNG
200
N= 181 277 244 114 88

CHINESE INDONESIAN
RACEPT
Fig. 4 : Left lung weight (g) versus ethnic groups

220
200 1066
180
160
140
120
SPLEEN
100
80
N= 187 236 249 111 89

CHINESE INDONESIAN
RACEPT
Fig. 5 : Spleen weight (g) versus ethnic groups
58
130
120
110
100
90
80
PANCREAS
70
60
N= 232 247 226 143 80

CHINESE INDONESIAN
RACEPT
Fig. 6 : Pancreas weight (g) versus ethnic groups
2000
1111
1800
1064
1471
1386
1153
1600
1400
1200
LIVER
1000
N= 226 318 263 135 111

CHINESE INDONESIAN
RACEPT
Fig. 8 : Liver weight (g) versus ethnic groups
59
220
200
87
4
50
102
165
178
200
231
56
151
241
1515 1059
180 1125
1054
160
140
120
LKIDNEY
100
80
N= 300 368 337 155 134

CHINESE INDONESIAN
RACEPT
Fig . 7 Kidney (left and right) weight (g) versus ethnic groups
400
300
200
HEART
100
N= 29 120 454 316 42
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 9 : Heart weight (g) versus height
60
1800
461
376
1406
1600
1400
1200
1000
1649
BRAIN
1689
1680
800
N= 40 118 429 325 74
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 10 : Brain weight (g) versus height
600
1461
500
400
300
LLUNG
200
N= 14 82 371 292 47
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 11 : Left lung weight (g) versus height
61
700
600 1358
500
400
300
RLUNG
200
N= 20 96 371 307 53
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 12 : Right lung weight (g) versus height
220
200 1683
180
514
160
140
120
SPLEEN
100
80
N= 17 75 334 294 54
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. : 13 Spleen weight (g) versus height
62
130
120
110
100
90
80
PANCREAS
70
60
N= 25 113 377 261 39
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 14 : Pancreas weight (g) versus height
220
200
180 1358
160
140
120
LKIDNEY
100
80
N= 34 117 508 418 72
<150 150-159 160-169 170-179 180-189
HEIGHTGP
63
220
200
180 1696
1701
1511
1574
1144
1197
1551
1358 1078
160 493
140
120
RKIDNEY
100
80
N= 30 101 441 382 65
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 15 : Kidney (left and right) weight (g) versus height

2000
1800 962
493
1164
1635
1740
1600
1400
1200
LIVER
1000
N= 31 105 431 327 52
<150 150-159 160-169 170-179 180-189
HEIGHTGP
Fig. 16 : Liver weight (g) versus height
64
400
937
300
1682
892 285
200
HEART
100
N= 97 280 356 187 78 23 8
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 17 : Heart weight (g) versus weight (kg)

1800
461
1600
1400
1200 968
556
990
841
1000
1649
BRAIN
1680
1660
800
N= 103 218 332 215 115 48 29
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 18 : Brain weight (g) versus weight (kg)
65
700
600
500
400
300
RLUNG
200
N= 64 187 292 191 107 36 25
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 19 : Right lung weight (g) versus weight (kg)

600
500
400
300
LLUNG
200
N= 50 164 283 198 107 36 22
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig.20 : Left lung weight (g) versus weight (kg)
66
220
200 868
1066 440
731
1761
180
160
140
120
SPLEEN
100
80
N= 60 142 277 176 110 42 23
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 21 : Spleen weight (g) versus weight (kg)

130
120
110
100
90
80
PANCREAS
70
60
N= 83 211 323 159 68 24 13
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 22 : Pancreas weight (g) versus weight (kg)
67
220
200
730
588 1598
1366
180 492
975 862
160
140
120
LKIDNEY
100
80
N= 89 238 400 275 145 56 26
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 23 : Left kidney weight (g) versus weight (kg)

220
200
730
180 1533
1366 1696
937
1373
1598
972 552
168
1147
1197
342
1695
160 206
440
720
1501
140
120
RKIDNEY
100
80
N= 79 200 351 243 136 52 24
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 24 : Right kidney weight (g) versus weight
68
2000
1800 492 1373

730
912
1386 1153
1462
1104
868 1123
1038
1279
1600 328
1460
862
1614
588
711
1400
1200
LIVER
1000
N= 66 193 350 242 116 33 17
<45 45-54 55-64 65-74 75-84 85-94 >95
WEIGHTGP
Fig. 25 : Liver weight (g) versus weight (kg)
Table 2: Descriptive Statistics - All (male and female)
Std.
N Min Max Mean Deviation
HEART 1083 195.00 360.00 278.266 41.114
RLUNG 952 300.00 600.00 437.757 94.055
LLUNG 908 270.00 555.00 412.215 77.731
LIVER 1061 1100.00 1895.00 1421.656 195.275
PANCREAS 935 70.00 125.00 95.448 15.748
SPLEEN 877 100.00 200.00 133.973 28.010
R ADRENAL 1028 3.00 10.00 6.1804 2.111
L ADRENAL 985 3.00 12.00 6.453 2.247
THYROID 65 20.00 35.00 23.492 3.985
R KIDNEY 1151 100.00 195.00 131.745 21.795
L KIDNEY 1303 100.00 195.00 131.109 24.847
BRAIN 1141 900.00 1695.00 1307.871 130.679
69
Table 3: Descriptive Statistics - Male
Std.
HEART 914 195.00 360.00 281.862 40.147
RLUNG 841 300.00 600.00 442.365 94.935
LLUNG 810 270.00 555.00 416.737 78.309
LIVER 894 1100.00 1895.00 1440.332 196.564
PANCREAS 786 70.00 125.00 96.103 15.742
SPLEEN 764 100.00 200.00 134.568 27.941
R ADRENAL 872 3.00 10.00 6.283 2.170
L ADRENAL 837 3.00 12.00 6.537 2.281
THYROID 56 20.00 35.00 23.607 4.057
R KIDNEY 999 100.00 195.00 132.341 21.601
L KIDNEY 1135 100.00 195.00 131.954 25.064
BRAIN 964 1000.00 1695.00 1328.838 123.210
Table 4: Descriptive Statistics - Female
Std.
HEART 169 195.00 350.00 258.823 40.951
RLUNG 111 300.00 600.00 402.847 79.151
LLUNG 98 280.00 550.00 374.847 61.416
LIVER 167 1200.00 1800.00 1321.677 153.979
PANCREAS 149 70.00 120.00 91.993 15.373
70
SPLEEN 113 100.00 200.00 129.956 28.272
R ADRENAL 156 5.00 10.00 5.609 1.641
L ADRENAL 148 3.00 10.00 5.980 1.988
THYROID 9 20.00 30.00 22.778 3.632
RKIDNEY 152 100.00 180.00 127.829 22.721
LKIDNEY 168 100.00 190.00 125.399 22.587
BRAIN 166 900.00 1475.00 1193.440 107.410
Many conditions are known to influence the size and weight of the organs. Some
diseases enlarge the organ and some may diminish the organ weight. Even the
normal organ weights show a great variation.
Multiple comparisons
Dependent Variable: HEART
Scheffe
Mean
Difference Std. 95% Confidence
(I) RACEPT (J) RACEPT (I-J) Error Sig. Interval
Lower Upper
Bound Bound
MALAY CHINESE
-11.756(*) 3.625 .033 -22.942 -0.571
INDIAN
-1.361 3.428 .997 -11.938 9.215
INDONESIAN
-3.174 3.918 .957 -15.263 8.914
MISC
-7.262 4.756 .675 -21.938 7.412
CHINESE MALAY
11.756(*) 3.625 .033 0.571 22.942
71
INDIAN
10.394 3.616 .083 -0.764 21.554
INDONESIAN
8.582 4.084 .353 -4.019 21.183
MISC
4.493 4.894 .932 -10.606 19.594
INDIAN MALAY
1.361 3.428 .997 -9.215 11.938
CHINESE
-10.394 3.616 .083 -21.554 0.764
INDONESIAN
-1.812 3.910 .995 -13.877 10.251
MISC
-5.901 4.749 .819 -20.556 8.754
INDONESIAN MALAY
3.174 3.918 .957 -8.914 15.263
CHINESE
-8.582 4.084 .353 -21.183 4.019
INDIAN
1.812 3.910 .995 -10.251 13.877
MISC
-4.088 5.114 .959 -19.869 11.692
MISC MALAY
7.262 4.756 .675 -7.412 21.938
CHINESE
-4.493 4.894 .932 -19.594 10.606
INDIAN
5.901 4.749 .819 -8.754 20.556
INDONESIAN
4.088 5.114 .959 -11.692 19.869
* The mean difference is significant at the .05 level.
Multiple Comparisons
Dependent Variable: RIGHT LUNG
Scheffe
Mean
Lower Upper
Bound Bound
MALAY CHINESE
-32.189(*) 8.613 .008 -58.773 -5.606
INDIAN
-26.209 8.5988 .055 -52.747 .3296
INDONESIAN
-24.050 10.492 .263 -56.432 8.331
MISC -
-63.052(*) 11.654 .000 -99.021
27.083
72
CHINESE MALAY
32.189(*) 8.613 .008 5.606 58.773
INDIAN
5.980 8.107 .969 -19.041 31.003
INDONESIAN
8.139 10.093 .957 -23.012 39.290
MISC
-30.862 11.296 .114 -65.727 4.002
INDIAN MALAY
26.209 8.598 .055 -0.329 52.747
CHINESE
-5.980 8.107 .969 -31.003 19.041
INDONESIAN
2.158 10.080 1.000 -28.954 33.271
MISC
-36.843(*) 11.285 .031 -71.673 -2.012
INDONESIAN MALAY
24.050 10.492 .263 -8.331 56.432
CHINESE
-8.139 10.093 .957 -39.290 23.012
INDIAN
-2.158 10.080 1.000 -33.271 28.954
MISC
-39.001 12.787 .055 -78.466 .463
MISC MALAY
63.052(*) 11.654 .000 27.083 99.021
CHINESE
30.862 11.296 .114 -4.002 65.727
INDIAN
36.843(*) 11.285 .031 2.012 71.673
INDONESIAN
39.001 12.787 .055 -0.463 78.466
Dependent Variable: LEFT LUNG
Scheffe
Mean
Lower Upper
Bound Bound
MALAY CHINESE
8.939 7.345 .830 -13.733 31.611
INDIAN
21.079 7.539 .099 -2.191 44.350
INDONESIAN
4.132 9.189 .995 -24.231 32.496
73
MISC
-28.533 9.987 .087 -59.361 2.294
CHINESE MALAY
-8.939 7.345 .830 -31.611 13.733
INDIAN
12.140 6.747 .519 -8.687 32.967
INDONESIAN
-4.806 8.551 .989 -31.203 21.589
MISC
-37.472(*) 9.404 .003 -66.500 -8.446
INDIAN MALAY
-21.079 7.539 .099 -44.350 2.191
CHINESE
-12.140 6.747 .519 -32.967 8.687
INDONESIAN
-16.947 8.718 .437 -43.858 9.964
MISC
-49.613(*) 9.556 .000 -79.110 -20.116
INDONESIAN MALAY
-4.132 9.189 .995 -32.496 24.231
CHINESE
4.806 8.551 .989 -21.589 31.203
INDIAN
16.947 8.718 .437 -9.964 43.858
MISC
-32.666 10.905 .063 -66.327 0.995
MISC MALAY
28.533 9.987 .087 -2.294 59.361
CHINESE
37.472(*) 9.404 .003 8.446 66.500
INDIAN
49.613(*) 9.556 .000 20.116 79.110
INDONESIAN
32.666 10.905 .063 -0.995 66.327
Dependent Variable: LIVER
Scheffe
Mean
Lower Upper
Bound Bound
MALAY CHINESE
-47.029 16.755 .097 -98.732 4.672
INDIAN
-39.601 17.468 .274 -93.502 14.300
74
INDONESIAN
48.086 20.948 .262 -16.554 112.727
MISC
-55.319 22.321 .190 -124.196 13.558
CHINESE MALAY
47.029 16.755 .097 -4.672 98.732
INDIAN
7.428 16.051 .995 -42.102 56.959
INDONESIAN
95.116(*) 19.783 .000 34.072 156.160
MISC
-8.289 21.231 .997 -73.802 57.224
INDIAN MALAY
39.601 17.468 .274 -14.300 93.502
CHINESE
-7.428 16.051 .995 -56.959 42.102
INDONESIAN
87.687(*) 20.390 .001 24.770 150.605
MISC
-15.717 21.798 .971 -82.980 51.544
INDONESIAN MALAY
-48.086 20.948 .262 -112.727 16.554
CHINESE
-95.116(*) 19.783 .000 -156.160 -34.072
INDIAN
-87.687(*) 20.390 .001 -150.605 -24.770
MISC
-103.405(*) 24.675 .002 -179.546 -27.266
MISC MALAY
55.319 22.321 .190 -13.558 124.196
CHINESE
8.289 21.231 .997 -57.224 73.802
INDIAN
15.717 21.798 .971 -51.544 82.980
INDONESIAN
103.405(*) 24.675 .002 27.266 179.546
Dependent Variable: PANCREAS
Scheffe
Mean
Differen Std. 95% Confidence
(I) RACEPT (J) RACEPT ce (I-J) Error Sig. Interval
Lower Upper
Bound Bound
MALAY CHINESE
-0.341 1.435 1.000 -4.7705 4.0877
75
INDIAN
-3.096 1.467 .348 -7.6245 1.4309
INDONESIAN
2.321 1.669 .748 -2.8294 7.4716
MISC
0.103 2.035 1.000 -6.1776 6.3845
CHINESE MALAY
0.341 1.435 1.000 -4.0877 4.7705
INDIAN
-2.755 1.445 .458 -7.2147 1.7040
INDONESIAN
2.662 1.649 .626 -2.4280 7.7530
MISC
0.444 2.019 1.000 -5.7871 6.6768
INDIAN MALAY
3.096 1.467 .348 -1.4309 7.6245
CHINESE
2.755 1.445 .458 -1.7040 7.2147
INDONESIAN
5.417(*) 1.677 .034 .2414 10.5943
MISC
3.200 2.042 .653 -3.1021 9.5026
INDONESIAN MALAY
-2.321 1.669 .748 -7.4716 2.8294
CHINESE
-2.662 1.649 .626 -7.7530 2.4280
INDIAN
-5.41(*) 1.677 .034 -10.5943 -.2414
MISC
-2.217 2.191 .906 -8.9813 4.5460
MISC MALAY
-0.103 2.035 1.000 -6.3845 6.1776
CHINESE
-0.4448 2.019 1.000 -6.6768 5.7871
INDIAN
-3.2002 2.042 .653 -9.5026 3.1021
INDONESIAN
2.217 2.191 .906 -4.5460 8.9813
Dependent Variable: SPLEEN
Scheffe
Mean
Lower Upper
Bound Bound
76
MALAY CHINESE -1.899 2.739 0.975 -10.354 6.556

INDIAN -1.625 2.707 0.986 -9.982 6.732
INDONESIAN 5.434 3.352 0.622 -4.914 15.782
MISC -5.065 3.603 0.740 -16.187 6.056
CHINESE MALAY 1.899 2.739 0.975 -6.556 10.354
INDIAN 0.273 2.542 1.000 -7.573 8.119
INDONESIAN 7.333 3.220 0.270 -2.607 17.272
MISC -3.167 3.480 0.935 -13.909 7.576
INDIAN MALAY 1.625 2.707 0.986 -6.732 9.982
CHINESE -0.273 2.542 1.000 -8.119 7.573
INDONESIAN 7.060 3.193 0.300 -2.797 16.916
MISC -3.440 3.455 0.911 -14.106 7.226
INDONESIAN MALAY -5.434 3.352 0.622 -15.782 4.914
CHINESE -7.333 3.220 0.270 -17.272 2.607
INDIAN -7.060 3.193 0.300 -16.916 2.797
MISC -10.499 3.981 0.139 -22.787 1.789
MISC MALAY 5.065 3.603 0.740 -6.056 16.187
CHINESE 3.167 3.480 0.935 -7.576 13.909
INDIAN 3.440 3.455 0.911 -7.226 14.106
INDONESIAN 10.499 3.981 0.139 -1.789 22.787
Dependent Variable: RIGHT KIDNEY
Scheffe
Mean
Lower Upper
77
Bound Bound
MALAY CHINESE -8.948(*) 1.768 0.000 -14.403 -3.493

INDIAN -3.697 1.837 0.400 -9.365 1.971
INDONESIAN 3.521 2.257 0.657 -3.443 10.486
MISC -7.171(*) 2.285 0.044 -14.222 -0.122
CHINESE MALAY 8.948(*) 1.768 0.000 3.493 14.403
INDIAN 5.251 1.733 0.057 -0.094 10.596
INDONESIAN 12.469(*) 2.173 0.000 5.765 19.174
MISC 1.776 2.202 0.957 -5.017 8.570
INDIAN MALAY 3.697 1.837 0.400 -1.971 9.365
CHINESE -5.251 1.733 0.057 -10.596 0.094
INDONESIAN 7.218(*) 2.230 0.034 0.340 14.097
MISC -3.474 2.258 0.668 -10.441 3.491
CHINESE -12.469(*) 2.173 0.000 -19.174 -5.765
INDIAN -7.218(*) 2.230 0.034 -14.097 -0.340
MISC -10.693(*) 2.611 0.002 -18.749 -2.637
MISC MALAY 7.171(*) 2.285 0.044 0.122 14.222
CHINESE -1.776 2.202 0.957 -8.570 5.017
INDIAN 3.474 2.258 0.668 -3.491 10.441
INDONESIAN 10.693(*) 2.611 0.002 2.637 18.749
Dependent Variable: LEFT KIDNEY
Scheffe
Mean Std. 95% Confidence
(I) RACEPT (J) RACEPT Difference Error Sig. Interval
78
(I-J)
Lower Upper
Bound Bound
MALAY CHINESE -10.401(*) 1.890 0.000 -16.231 -4.571
INDIAN -2.388 1.929 0.821 -8.338 3.561
INDONESIAN 6.320 2.403 0.141 -1.094 13.734
MISC -6.846 2.525 0.119 -14.634 0.941
CHINESE MALAY 10.401(*) 1.890 0.000 4.571 16.231
INDIAN 8.012(*) 1.832 0.001 2.362 13.664
INDONESIAN 16.721(*) 2.327 0.000 9.545 23.898
MISC 3.554 2.452 0.717 -4.008 11.116
INDIAN MALAY 2.388 1.929 0.821 -3.561 8.338
CHINESE -8.012(*) 1.832 0.001 -13.664 -2.362
INDONESIAN 8.708(*) 2.358 0.009 1.435 15.983
MISC -4.458 2.481 0.521 -12.113 3.196
CHINESE -16.721(*) 2.327 0.000 -23.898 -9.545
INDIAN -8.708(*) 2.358 0.009 -15.983 -1.435
MISC -13.166(*) 2.866 0.000 -22.008 -4.326
MISC MALAY 6.846 2.525 0.119 -0.941 14.634
CHINESE -3.554 2.452 0.717 -11.116 4.008
INDIAN 4.458 2.481 0.521 -3.196 12.113
INDONESIAN 13.166(*) 2.866 0.000 4.326 22.008
Dependent Variable: BRAIN
Scheffe
79
Mean
Lower Upper
Bound Bound
MALAY CHINESE -2.652 10.608 1.000 -35.384 30.078
INDIAN 89.585(*) 10.769 0.000 56.360 122.811
INDONESIAN -5.066 13.206 0.997 -45.813 35.680
MISC 2.627 13.728 1.000 -39.730 44.984
CHINESE MALAY 2.652 10.608 1.000 -30.078 35.384
INDIAN 92.238(*) 9.878 0.000 61.761 122.717
INDONESIAN -2.413 12.491 1.000 -40.953 36.125
MISC 5.280 13.041 0.997 -34.958 45.518
INDIAN MALAY -89.585(*) 10.769 0.000 -122.811 -56.360
CHINESE -92.238(*) 9.878 0.000 -122.717 -61.761
INDONESIAN -94.652(*) 12.627 0.000 -133.613 -55.692
MISC -86.958(*) 13.172 0.000 -127.600 -46.318
INDONESIAN MALAY 5.066 13.206 0.997 -35.680 45.813
CHINESE 2.413 12.491 1.000 -36.125 40.953
INDIAN 94.652(*) 12.627 0.000 55.692 133.613
MISC 7.693 15.230 0.993 -39.296 54.683
MISC MALAY -2.627 13.728 1.000 -44.984 39.730
CHINESE -5.280 13.041 0.997 -45.518 34.958
INDIAN 86.958(*) 13.172 0.000 46.318 127.600
INDONESIAN -7.693 15.230 0.993 -54.683 39.296
Table 5: Normal organ weight (g) for males from various sources
Organ Snell Gray Grewal Bernard Reddy

knight
80
Heart 283- 283-339.6 311.3 240 300

339.6
Right 650.9 622.6 360-570
lung 1188.6 6735.3
Left lung 537.7 566 325-480
Liver 1415- 1415-1698 1273.5- 1245 1400-
1698 1688 1500
Right 127.25 127.35-169.89 141.5 170
kidney 120-220
Left 127.25 127.35-169.89 141.5 170
kidney
Brain 1400.35 1245.8 1400
Pancreas 56.699(may>169.8) 84.9
Spleen 198.1 141.5-198 138.2 150-200
Table 6: Normal organ weight (g) for females from various sources
Organ Snell Gray Grewal Bernard Reddy

knight
Heart 226.4-283 226.4-283 253.7 211.3 250
Right lung 650.9 622.6 668.7 360-570
Left lung 537.7 1188.6 566 668.7 360-570
Liver 1132- 1132-1415 1273.5- 1312.7 1400-
1415 1688 1500
Right 113.2- 113.2-155.6 141.5 158.7
kidney 115.65 120-175
Left 113.2- 113.2-155.6 141.5 158.7
kidney 115.65
Brain 1132 1132.7 1275
Spleen 198.1 141.5-198 132 150-200
Pancreas 56.699(may>169.8) 84.9
Discussion
Many conditions are known to influence the size and weight of the organs. Some
diseases enlarge the organ and some may diminish the organ weight. Even the
normal organ weights show a great variation. Most commonly used literature by
Forensic Pathologists in relation to normal organ weights are compared with the
findings in this study.2,11,,12,13,16
81
According to one study15 conducted on organ weights for 2025 autopsies

performed , the mean organ weight as observed in the their study in general were
more than that reported from other parts of India and were comparable with the
western population. Exclusion criteria included septicaemia and gross organ
pathology
In the literature there does seem to be a certain agreement that all the organ
weights for females are generally lower than that of males.8 Some authors have
commented on the relationship between the organ weight and height and body
weight.10
On the basis of the results of this study, it was concluded that for the male
population, mean organ weight for heart, right lung, left lung and spleen was
lower than the western population.2,12 However, mean organ weight for liver,
right kidney and left kidney fell within the range of normal organ weight for
western population. Mean organ weight for heart, right lung, left lung, left kidney,
brain, spleen and pancreas was lower than Indian population.16 However, mean
weight for right kidney was higher than in Indian. The mean weight for the liver,
left and right adrenal fell within the normal organ weight for the India population.
For the female population, right lung, left lung and spleen was lower than the
western population. Mean organ weight for heart, liver, right kidney and left
kidney fell within the normal range. The mean weight for right lung, left lung,
brain and spleen showed lower than India population. However, the mean organ
weights that showed higher than India population were heart, right kidney and
pancreas. The mean weight of liver, right adrenal and left adrenal fell within the
normal organ weight for the India population. Western population generally had a
heavier organ weight because of their bigger frame. Hence, they are taller and
heavier.
In our study, mean organ weight for heart, right lung, right kidney and left kidney
showed significant difference (p<0.05) between Malay and Chinese. This is
mainly due to differences in dietary habits, nutritional status, cultural and
socioeconomic status. Mean organ weight for liver, pancreas, right kidney and
brain showed significant difference between Indian and Indonesian. Malay and
Indian showed significant differences in the organ weight of the brain. Besides
that there was significant difference between Chinese and Indian for weight of left
kidney and brain. Mean organ weight for kidney and liver showed significant
difference between Chinese and Indonesian but there no significant difference
(p>0.05) in any organ weight between Malay and Indonesian. This may be
because the Malays and Indonesians have been known to have similar dietary
habits, culture and lifestyle.
82
Mean organ weight for male is generally higher than female. This is because
females are generally smaller in size and their nutritional profile is different
compared to males.
On the basis of the results of this study, it was concluded that weight of heart, left
lung, spleen and right kidney is positively correlated to human body height in cm.
For right lung the correlation to the height of the 4 height groups were positively
correlated except group 180-189 cm. Besides that, the weight of the brain
correlated positively with height except for the group <150cm.
For the body weight, there was positive correlation for the weight of heart, brain
and right lung. For the right kidney, left kidney and liver, there was positive
correlation to the body weight of the 6 groups except >95kg group.
Conclusion
On the basis of this study, it was found that weight of heart, left lung, spleen and
right kidney were positively correlated to human body height in cm. For the
body weight also positive correlation for the weight of heart, brain and right lung.
Females generally had a lower organ weight compared to males. For males, mean
organ weight for heart, right lung, left lung and spleen was lower than the western
population. For the female population, right lung, left lung and spleen was lower
than the western population. In this study, mean organ weight for heart, right
lung, right kidney and left kidney showed significant difference (p<0.05) between
Malay and Chinese. Mean organ weight for kidney and liver showed significant
difference between Chinese and Indonesian but there no significant difference
(p>0.05) in any organ weight between Malay and Indonesian
References:
1. Kumar V, Cotran RM, Robbins SL. In: Robbins Basic Pathology, 7th Ed,
WB Saunders Company, Philadelphia, 2003.
2. H Pan, TJ Cole: A Comparison of Goodness of Fit Test for Age-related
Reference Ranges. Statistics in Medicine Vol 23; p 1749 – 1765.
3. Basant K Puri: SPSS in Practice An Illustrated Guide, 2nd Ed, Arnold,
London 2002.
4. Kohli A, Agarwal BBL: Study of Normal adult Organ Weight in The
North Indian Population, JFMT, 1996; 12: 21-22
5. Gharpure PV, Jhala HI 91958) : Normal Standard for Body weight and
Organ Weight in India; IMG 92, 93 : 445-447
83
6. Rental Edgar, Hamilton Smith. In: Glaister’s Medical Jurisprudence and

Toxicology, 13th Ed. Churchill Livingstone, Edinburgh, 1973, 755
7. Tanaka GI. Japanese Man-Mass of Organs and other characteristics of
Normal Japanese, Health Physics, 1979; 36(3): 336-46
8. E Boyd, Normal variability in weight of the adult human liver and spleen,
Arch.Patho. 16 (1933), 350-372
9. AS David –wesy, spleen weight distribution in Ibadan and its relationship
to disease, Afr.J.Med Sci. 11(1982) 53-59
10. L Garby,O Lammert, KF Kock, B Thobo-Carlsen.Weights of brain,heart,
liver kidneys and spleen in healthy and apparently healthy adult Danish
subjects, Am .J.Hum.Biol. 1993; 5: 291-296
11. Knight Bernard. In: Forensic Pathology, 2nd edition, Arnold, 1996, p.599
12. Gray Henry. In: Gray’s Anatomy, 15th edition, Chancellor Press, 1994.
13. Reddy KS Narayan. In: The Essentials of Forensic Medicine and
Toxicology, 13th edition Suguna Devi,1992, p.477
14. Susan Sprogoe-Jakobsen, Ulrik Sprogoe-Jakobsen: the weight of the
normal spleen, Forensic Science International, 1997; 88 215-223.
15. Dalbir Singh, YS Bansal, Sreenivas M, A.N. Pandey, Seema Tyagi:
Weights of human organs at autopsy in Chandigarh zone of North-West
India 2003. ( personal communication )
16. Grewal S Rajinder. In: Medical Jurisprudence and toxicology, Calcutta
:Scientific book Agency(1993).
17. British National Formulary Number 48 (Sept 2004)
18. Snell RS. In: Clinical Anatomy for Medical Students, 6th Ed. Lippincott
Williams and Wilkins, Pennsylvania, 2000.
84
ORIGINAL ARTICLE
Cardiac Troponin I in suspected sudden cardiac deaths at

Forensic Unit, UKM Hospital: A preliminary observation
Shahrom AW, Swarhib MS, Azuriah AA, Zarida H*, Aznool HA**

Malaysia*
Department of forensic Pathology, Hospital Sultanah Aminah, Johor Baru,
Malaysia**
Abstract
Seven cases of suspected sudden cardiac deaths were tested with cardiac Troponin
I (cTnI) test and nitro-blue tetrazolium test for the presence of myocardial
necrosis/infarction. Our preliminary observation shows all the selected cases
which were reactive with the cTnI test were also positive with the NBT test. The
positive NBT test reflects the presence of myocardial necrosis myofibrils. This
may be present in the cases of acute myocardial infarction, myocarditis and
cardiomyopathy as has been shown by the final diagnosis of all seven cases in our
study.
Keywords: Troponin I, sudden death, acute myocardial infarction, coronary

occlusion,
Address for correspondence and reprint requests: Assoc. Prof. Dr. Shahrom bin Abd. Wahid,
Introduction
Troponin-I (TnI) is one of the thin filament-associated regulatory protein of

muscle.1 It is encoded by three different genes that are differentiatially expressed
by the various muscle tissues, resulting in slow and fast twitch skeletal and
cardiac TnI isoforms.2
84
The unique amino acid sequence of cTnI makes it an ideal candidate for the
laboratory detection of acute myocardial infarction (AMI) and has facilitated the
development of monoclonal antibodies that do not cross react with skeletal muscle
troponins (3). Published studies from various groups have demonstrated the utility
of cTnI measurement for detection of AMI.3,4
CKMB and cTnI both elevated beyond normal reference limits within 4-6 hours
after infarction. Typical reference limits were, as reported by Bodor et al,3 6.7
ng/ml for CKMB and 3.1 ng/ml for cTnI.
Likewise, each report sites similar time frames for the peak values of CKMB and
cTnI : CKMB peaked in 13-15 hours, cTnI in 11-15 hours. Typical ranges were
39-185 ng/ml for CKMB and 18.5-188 ng/ml for cTnI.5
However, CKMB level returns to normal after 36-48 hours, while levels of cTnI
remains elevated for up to 6-10 days. The level of cTnI is very low in normal
healthy people, and not detected in patients with skeletal muscle injury. Therefore,
cTnI is considered as a specific marker for diagnosis of AMI.
Hence, in this preliminary observation we are trying to correlate between the

reactivity of the cTnI and the positivity of the NBT and the diagnosis of the
cardiac condition.
Materials and method
The forensic cases which were suspected by pathologists to be of cardiac origin

for the cause of death were selected for Troponin I rapid test. The inclusion
criteria include history of chest pain prior to the death, dark purplish hue of the
congested face together with distended neck veins, and past history heart attack. A
total of seven cases were selected.
Assay procedure
Troponin I-Check 1 is a rapid immunochromatographic test. The test device is
allowed to reach to room temperature. The deceased’s forensic number is
recorded on the device. 6 drops (200 µl) of serum is dispense into the sample well.
The result is read between 15 – 20 minutes (Fig. 1). (Troponin I Check-1 test is
performed on human serum or plasma. Heparinized samples should not be used).
Nitro-blue tetrazolium test

Myocardial tissues were sampled from 5 areas (i.e. (1) the interventricular septum,
(2) the anterior wall of left ventricle, (3) the lateral wall of left ventricle, (4) the
posterior wall of left ventricle, and (5) the apex) for Nitro-blue tetrazolium (NBT)
85
test. The NBT reagent and procedure was done as described by Lie JT (1979).6
The NBT stain of vital and infarcted myocardium is shown in fig. 4.
Results
All the seven cases selected showed reactivity with the Troponin I-Check 1 test.
The NBT test were positive in all seven cases. Five of the seven cases were given
final diagnosis as “Coronary occlusion by atheroma”, i.e. the coronary artery
showed luminal occlusion by atheroma of at least 75%. One of the seven cases
died of myocarditis and the last decedent died of cardiomyopathy. The summary
of the results are presented in table 1.
Table 1: The results of Troponin I rapid test in relation to the diagnosis of

the case and the results of Nitro blue tetrazolium.
Troponin I Nitro blue

Autopsy No. Diagnosis
rapid test tetrazolium
Coronary occlusion
1. Reactive Positive (1,4,5)
by atheroma
2. Reactive Positive (2,3,4,5) Myocarditis
3. Reactive Positive (2,3,4,5) Cardiomyopathy
Coronary occlusion
4. Reactive Positive (4,5)
by atheroma
Coronary occlusion
5. Reactive Positive (4,5)
by atheroma
Coronary occlusion
6. Reactive Positive (all 5)
by atheroma
Coronary occlusion
7. Reactive Positive (all 5)
by atheroma
86
Fig. 1: Troponin I-Check 1 test showed reactivity lines in the test well (left) and
control well (right).
Fig. 2: The cut surface of the left anterior descending coronary artery showing at
least 75% luminal occlusion.
87
Fig. 3: Cut surface of the left ventricle showing patchy areas of infarction.
Fig. 4: Nitro BT stain of interventricular septum. The vital tissue stained dark
blue (light arrow) and the infarcted area pale brown (no dye uptake).
88
Discussion
The Troponin I-Check_1 is a rapid qualitative assay for the detection of cardiac
Troponin I in serum. The method employs a unique combination of a monoclonal
dye conjugate and polyclonal solid phase antibodies to identify Troponin in the
test samples with a high degree of sentivity.
Stat cTnI is an established test used for the diagnosis of AMI in patients with
severe chest pain.
However, the cTnI test is recommended for blood from living patient instead of
postmortem blood. Our preliminary observation shows all the selected cases
which were reactive with the cTnI test were also positive with the NBT test. The
positive NBT test reflects the presence of myocardial necrosis myofibrils. This
may be present in the cases of acute myocardial infarction, myocarditis and
cardiomyopathy as has been shown by the final diagnosis of all seven cases.
This preliminary observation warrants further study with regards to the specificity
and sensitivity of cTnI test in the diagnosis of myocardial necrosis in postmortem
cases. If this test is specific and sensitive in the detection of the myocardial
necrosis it may be used as the front line screening test for the sudden death cases.
Those with reactive cTnI test may be exempted from further postmortem
examination if the history of the chest pain and other myocardial infarction
precipitating factors are present. Thus, the diagnosis of AMI may be made in line
with the WHO recommendation, i.e. 2 out of 3 criteria (chest pain, myocardial
biomarkers and ECG changes).
References
1. Bucher EA, Maisonpierre PC, Konieczny SF, Emerson CP Jr. Expression

of the troponin complex genes : transcriptional coactivation during
myoblast differentiation and independent control in heart and skeletal
muscles. Mol Cell Biol 1988; 8: 4134-42
2. Bodor GS, Porter S, Landt Y, Ladenson JH. Development of monoclonal
antibodies for an assay of cardiac troponin I and preliminary results in
suspected cases of myocardial infarction. Clin Chem 1992; 38: 2203-14
3. Cummins B, Auckland ML, Cummins P. Cardiac specific troponin I radio-
immunoassay in the diagnosis of acute myocardial infarction. Am Heart J
1987; 113: 1333-44
89
4. Bodor G, Porter S, Ladenson J. Human cardiac troponin I measurement in

suspected myocardial infarction with a double monoclonal antibody
sandwich ELISA. Clin Chem 1990; 36(6): 1103
5. The joint European Society of Cardiology/American College of cardiology
committee. Myocardial infarction redefined. J Am College of Cardiology
2000; 36(3): 959-69
6. Lie JT. Heart and cardiovascular system, In: Ludwig J (ed). Current
methods of autopsy practice. 2nd ed. 1979, Philadelphia, WB Saunders,
p21-50.
90
CASE REPORT
Fatal latent interstitial pneumonia complicating chloral hydrate
and midazolam pre-procedural sedation
Faridah MN*, Zarida H,** Shahrom AW*
Forensic Unit, Department of Pathology, Faculty of Medicine, UKM, Malaysia*

Malaysia**
Abstract
This unusual case is concerned of a child who had an undiagnosed infiltrative lung
disease, and he was given pre-procedural sedation (chloral hydrate and
midazolam) before undergoing a radiologic procedure. The sedation had had been
blamed to cause the unexpected death of the child. Postmortem examination
revealed the presence of latent interstitial pneumonia which might have
complicated the pre-procedural sedation. This incident has changed the screening
procedure, i.e. forced expiratory volume (FEV1) has been included before such a
procedure is implemented. Discussion of the case and further suggestion for a pre-
procedural respiratory test are discussed in this paper.
Keywords: Infiltrative lung disease, pre-procedural sedation, radiologic

procedure, interstitial pneumonia, midazolam
Address for correspondence and reprint requests: Assoc. Prof. Dr. Shahrom bin Abd. Wahid,
Introduction
Deaths due to pre-procedural sedation has been documented in previous paper.9
For instance, the use of intravenous drugs for sedation in 95 cases has produced
some adverse effects in 85 cases, some of which resulted in 51 deaths, 9
permanent neurological injuries, 21 prolonged hospitalisations, and only 14 had
no harm (ibid.). The adverse effects were mainly due to drug overdosages, and
drug interactions in multi-drug usages.
91
The standard practice proposed by the Scottish Intercollegiate Guidelines Network

produced some guidelines for pre-procedural sedation.8 Among the standard
practice for pre-procedural sedation are to check the patients’ respiratory rate and
pattern, pulse rate and colour, body temperature, ECG, blood pressure, arterial
haemoglobin oxygenation by pulse oxymetry and end-tidal carbon dioxide. Some
guidelines were also proposed for discharge just after sedation in paediatric
patients. The airway must be patent and the patient is easily rousable. Oxygen
saturation is more than 95% breathing air, and they are haemodynamically stable.
Hydration must be adequate, urine output adequate, and normal responsiveness
and orientation for age and mental status and walk is unaided. No nausea and
vomiting noted and the pain is controlled (ibid.).
Literature search has shown that there were no documented deaths in infiltrative
lung disease after a pre-procedural sedation. This unusual case is presented to
describe the occurrence of an undiagnosed lung disease in a child, which had
caused an unexpected death in a child after a pre-procedural sedation. Some
discussion of the lung disease and its pathology, and how it could affect the
sedation in the child is discussed. Further, a suggestion to include a respiratory
test is brought forth, which might help to screen such diseases in a paediatric
patient.
Case Report
A two-year old girl with a body weight of 7.5 kg was sedated at 1215 hours with
750 mg chloral hydrate orally for the procedure of CT scan at the Radiology
Department. She was still active until 1315 hours despite the sedation. 1 mg of
midazolam (0.13 mg/kg) was given to the child at about 1320 hours later. The CT
scan was performed about 35 minutes after the intravenous sedation. After the
procedure, the child was brought to the Surgery Clinic. She appeared drowsy and
lethargic. The child was discharged at 1510 hours and brought by her mother to a
bus stop about half km away from the hospital. At the bus stop, the child turned
blue and stopped breathing. She was rushed to the Emergency Department and
resuscitation was done. She was pronounced dead at 1545 hours. Postmortem
examination revealed a healthy girl with cyanosis of the fingernails. Internal
organs appeared congested. The right and left lungs were firm, rubbery and
contained moderate amount of oedema fluid. Whitish mucus was present in the
distal bronchioles. The stomach mucosa appeared mildly inflamed. Other organs
appeared unremarkable. Histological examination of the lung revealed thickened
alveolar membrane with some fibrosis. The interstitial spaces were filled with
plenty of mononuclear cells, haemosiderin-laden macrophages, and occasional
polymorphs.
92
A diagnosis of interstitial pneumonia complicating the pre-procedural sedation

(chloral hydrate and dormicum) with fatal outcome was made.
Fig. 1: The lung revealed thickened alveolar membrane with some fibrosis. The
interstitial spaces were filled with plenty of mononuclear cells, haemosiderin-
laden macrophages, and occasional polymorphs.
Fig. 2: The haemosiderin-laden macrophages found within the interstitial space.

(Perl’s stain x 400)
93
Discussion
The interstitial lung disorders (ILD) are chronic, non-malignant, non-infectious
diseases of the lower respiratory tract characterised by inflammation and
derangement of the alveolar walls.1 The major consequence of ILD is loss of
functional alveolar-capillary units and thus, limitation in the transfer of oxygen
from air to blood. This may complicate patient’s condition who undergone
surgical procedure with general anaesthesia. Affected individuals have dyspnoea,
particularly with exercise and are restricted in their activities. If the disease
progresses, death usually results from oxygen deprivation of vital organs (ibid.).
The ILD derive their name from the fact that all are characterised, to a variable
extent, by derangement of the alveolar interstitium, the connective tissue matrix
that forms the structural backbone of the alveolar walls. Because these
derangements usually include the deposition of scar tissue, they are also called
“fibrotic lung diseases”.1 Alternatively, because the widespread inflammation and
fibrosis of the alveolar walls are reflected in the chest x-ray as “inflitration” of the
lung parenchyma, the ILD are often grouped with the “diffuse infiltrative
diseases” of the lung, a term that also includes infectious and neoplastic disorders.
Since they are inflammatory disorders of the lower respiratory tract, the interstitial
lung diseases are also called the “interstitial pneumonias” or “chronic
pneumonitides” (ibid.).
Latent interstitial pneumonia may be present unnoticed. However, the condition

may be detected when it complicates certain surgical procedure such as pre-
procedural sedation with chloral hydrate and midazolam such as in this case. It is
often chronic, and affects a wide span of age from infancy to old age, although in
the majority of cases, it affects elderly patients of 50 years of age.2 There is no
family history of any lung disease in this case, although there have been reports of
interstitial lung disease in several family clusters (ibid.). Postmortem examination
showed presence of cyanosis of the fingernails however, no clubbing of the
fingers and toes were noted. Literature has shown that physical examination may
not be revealing however, there may be cyanosis, clubbing of the fingers and toes
present (ibid.).
Postmortem examination also revealed firm and rubbery lungs which contained
moderate amount of oedema fluid. Whitish mucus was present in the distal
bronchioles. The stomach mucosa appeared mildly inflamed. Other organs
appeared unremarkable. Histologically, the lung revealed thickened alveolar
membrane with some fibrosis. The interstitial spaces were filled with plenty of
mononuclear cells, haemosiderin-laden macrophages, and occasional polymorphs.
Kobzik L. and Schoen F.J. (1994)5 documented that in early cases, the lungs are
firm in consistency and microscopically, the lung parenchyma shows pulmonary
oedema, intra-alveolar exudation, hyaline membrane, and infiltration of
94
mononuclear cells in the interstitium. These findings are consistent with those of
idiopathic pulmonary fibrosis or interstitial pnuemonitis (ibid). The presence of
macrophages indicated that it is a latent histological process at repairing the lung
parenchymal tissue. Also, the presence of haemosiderin-laden macrophages
indicated that there were haemorrhages in the pulmonary parenchyma, which was
about three days in duration.3 The presence of polymorphs showed the occurrence
of pneumonia, and attempt at repairing the lung tissues are indicated by the influx
of mononuclear cells mainly, macrophages and lymphocytes.
From the literature, the chest radiographs may show a pattern of diffuse
reticulonodular markings in the lower zones.5 Lung function tests in patients may
indicate reduction of the total lung capacity, vital capacity and residual volume.
Evidence of airway obstruction can be determined by either an increase or normal
FEV1/FVC ratio.7 A restrictive respiratory functional pattern is usually present,
which reflects the stiff, non-compliant lungs characteristics of interstitial
pulmonary fibrosis (ibid.). In the investigation of this case, however, chest
radiograph, and lung function test were not done.
Midazolam is commonly used to provide sedation and it is considered the safest

agent to be used in a child. It has a rapid onset and could last for one hour.6
Chloral hydrate is similarly, quite safe for sedation and can be given alone or
together with midazolam. However, adverse effects may occur in patients with
renal or hepatic dysfunction (ibid.). There was no mention, however, of any lung
diseases in causing adverse effects in patients who were given sedation. The fact
that this child has died a few hours after a mild sedation in a hospital setting is not
to be taken lightly. This case has clearly shown that it is not uncommon to have an
undiagnosed pulmonary disease in a paediatric patient. In order that this condition
not to be missed in future is to implement a respiratory test, FEV1. This test is
essential to assess the lung capacity in particular the oxygenation of the functional
alveolar-capillary units. According to a study by Javadpour et al. (2005)4 patients
with cystic fibrosis with an FEV1 less than 60% are more likely to retain carbon
dioxide. Carbon dioxide is a marker of mechanical impairment, increase dead
space, ventilation perfusion abnormalities. The inability to defend carbon dioxide
during exercise is associated with a rapid decline in lung function (ibid.). Latent
interstitial pneumonia, which has some development of interstitial fibrosis, may
show some carbon dioxide retention, and a reduction in FEV1.
The question still remains, is whether misadventure or negligence has occurred in

this case. By definition, misadventure is an occurrence of mishap when all
precautions have been adequately taken. The informed consent should be taken
from the family concerned, where some advice has been given on the benefits
versus risks involved in the procedure. Negligence, on the other hand, is an
occurrence of mishap when some precautions have been missed deliberately. In
this case, it may be considered a misadventure, when all the necessary precautions
95
had been taken, as to the standard procedure taken by the hospital concerned. The
suggestion now, is to include FEV1, a simple respiratory test so that condition such
as latent interstitial pneumonia could now be practically screened beforehand.
This is thought to help avoid unexpected deaths in children with such conditions
in future.
References
1. Crystal RG (1987), Interstitial lung disorders. In: Braunwald E, Isselbacher
KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS (eds.) Harrison’s
Principles of Internal Medicine. New York: Mc-Graw Hill: 1095-1103.
2. Doyle E. (2002) Review: Emergency analgesic in the paediatric population.
Part IV. Paediatric sedation in the accident and emergency department: pros
and cons. Emergency Medicine Journal, 19: 284-287.
3. Janssen W (1984) Forensic Histopathology. Springer Verlag: Berlin.
4. Javadpour SM, Selvadurai H, Wilkes DL, Schneiderman-Walker J and Coates
AL (2005) Does carbon dioxide retention during exercise predict a more rapid
decline in FEV1 in cystic fibrosis? Archives of Disease in Childhood, 90: 792-
795.
5. Kobzik L, Shoen FJ (1994) The lung. In: Cotran RS, Kumar V, Robbins SL
and Schoen FJ (eds.) Pathologics Basis of Disease (5th ed.). WB Saunders:
Philadelphia. 714-715.
6. Nordt SP and Clark RF (1997) Midazolam: A review of therapeutic uses and
toxicity. Journal Emergency Medicine, 15(3): 357-365.
7. Reynolds HY (1994) Interstitial lung diseases. In: Isselbacher KJ, Braunwald
E, Wilson JD, Martin JB, Fauci AS, Kasper DL(eds.) Harrison’s Principles of
Internal Medicine, Vol.2 (13th ed.) Mc-Graw Hill: New York: 1206-1209.
8. Website: http://www.sign.ac.uk. Revised edition-May, 2004. Scottish
Intercollegiate Guidelines Network: Safe sedation of children undergoing
diagnostic and therapeutic procedures- A national clinical guideline.
9. Website: http://www.emedicine.com/emerg/topic403.htm. Last updated in
January 29, 2007: Hom J. Paediatrics- Sedation.
96
CASE REPORT
Partially cooked brain surface in fatal electrocution
Rohayu SA, Zarida H*, Siew SF, Shahrom AW**
Department of Forensic Medicine, General Hospital Kuala Lumpur

Forensic Unit, Department of Pathology, Medical Faculty, Universiti Kebangsaan
Malaysia**
Department of Pathology, Faculty of Medicine and Health Sciences, Universiti
Putra Malaysia*
Abstract
A 45 year old Chinese male was found dead in a bathroom. He was lying naked
and still holding to a shower head in his right hand. Severe electrical burnt marks
were present on the right hand, upper part of the chest and left thigh. The Brain
was congested with the under surface of right frontal lobe showed “a tanned
cooked lesion” measuring 6cm x 4cm. Cut surfaces of the brain were
unremarkable. The cause of death was given as “fatal accidental electrocution in a
bathroom”. We believe that the electric entry point was through the head, chest
and right hand before exiting through the left thigh. The investigation of the
National Electrical Board’s expert concluded the faulty of electrical appliance and
not the aberrant electrical supply lead to the fatal accident.
Keywords: Electrocution, current, voltage, resistance, bathroom.

Address for correspondence and reprint request: Dr Rohayu Shahar Adnan, Department of
Forensic Medicine, Hospital Kuala Lumpur, Jalan Pahang, 50586, Kuala Lumpur, Malaysia.
email: adnanmiss@gmail.com
Introduction
There is widespread use of electricity for domestic and industrial purposes in the
modern world. Electricity not only beneficial in daily activities but it can also
cause injury and death. Electrocution is one of the categories of injuries
produced by physical agents, others being injuries from heat, cold, radiation and
changes in pressure.
97
Electrocution may occur following the passage of a substantial electrical current

through the tissues, which can cause skin lesions, organ damage and death
(Knight 1996).11 The possibility of electrocution exists whenever there is
electrical power or lighting (Cohen 1993).5 Beside electricity derived from a
power source, natural electricity in the form of lightning can also give rise to
morbidity and mortality (Lifschultz & Donoghue 1993; Wetli 1996; Lewis
1997).14,27,13
Given its universal distribution, electricity, as opposed to motor vehicles, causes

remarkably few deaths. The incidence of fatal electrocution in the United States
is about 1500 per year, inclusive of 100 to 200 cases of lightning fatalities
(Mellen et al. 1992).16
The vast majority of electrical fatalities are accidental (Wright & Davis 1980).28
Most are due to contact with current of low voltage, usually 210 to 250 V, which
is the domestic supply (Polson 1985).21 Accidents can occur at home and at the
workplace, indoors and outdoors, wherever there is electrical supply. Several
factors lead to electrical accidents, which may be human factor or factors related
to the electrical appliances or the electrical supply.
Carelessness and ignorance are important human factor leading to electrocution

both at home and in industry. Most electrical accidents in industry are due to
carelessness (Somogyi &Tedeschi 1977).25 Fatal carelessness can occur not only
at industrial set-up but may also occur at home such as in our case.
CASE REPORT
History
A 45 year old Chinese male was found dead, in a bathroom of his house. The
deceased’s daughter who woke up at about 10.00 a.m., found her father lying
naked in the shared bathroom grabbing a shower head in his right hand. She
phoned her mother for help. Her mother came back straight from office to help
her husband. On arrival, she asked her daughter to switch off the main switch
board. However before the main switch board was put off, she already tried to
help her husband by grabbing his feet. Her daughter who was downstairs heard a
loud thud. When she went up she saw her mother lying on the floor breathless.
Neighbours came to help but nothing could be done further. The police had
requested a postmortem examination to determine the cause of death.
98
Postmortem examination
External examination revealed an adult Chinese male, 178 in height and 87 kg in

weight with a patterned skin mark in an irregular dumbbell shape noted on the
right side front of chest measuring 19cm x 9cm. The skin mark was charred and
blackened in the centre with multiple collapsed blisters. The margins were
erythematous. His right upper limb was deformed in a fixed flexion position at
both the elbow and the wrist. All the fingers of his right hand were in a gripping
position. Extensive collapsed skin blisters noted in the right arm and forearm
including the armpit, of which some were ruptured and peeled off exposing the
underlying raw tissues. Fluid filled blister noted on the back of right hand and all
the fingers were blackened and charred due to thermal heat proximally and on the
flexor surfaces. Extensive collapsed skin blisters and peeling skin were present on
the extensor surfaces of all the fingers. A small abrasion appreciated on the right
elbow. A cluster of three irregular skin marks were seen on the posterolateral
aspect of left thigh. Two of the skin marks were tanned and flat (the exit point of
the electrical current), whereby one skin mark in the centre had skin peeled off
exposing the reddish raw surface of underneath tissue. There was bruising of the
right upper eyelid measured with right subconjunctival haemorrhage.
Internal examination revealed occipital subgaleal haematoma, non-fractured skull

and normal dura mater. The Brain weighed 1520 grams with congested surface
vessels. On the under surface of right frontal lobe was “a tanned cooked lesion”
measuring 6cm x 4cm. Cut surfaces of the brain were unremarkable. The mouth,
tongue, throat and neck structures were unremarkable. Both right and left lungs
were congested. The heart and coronary arteries were normal. The stomach, liver,
spleen, pancreas, kidneys and intestines were unremarkable.
Laboratory analysis of the blood revealed no alcohol or drugs.
Histological sections from the skin mark, showed some cap of epidermis which
was detached and raised into a blister with a large space underneath. The cells of
epidermis were elongated with horizontally oriented and stretched nuclei of the
lower zone. The underlying dermis was more eosinophilic.
Histological sections from the “tanned cooked lesion” of the brain did not show
any evidence of reactive gliosis such as gemistocytic astrocytes or chronic
inflammatory exudates (healing of old infarct in the brain). The histological
sections confirm that the above lesion was due to electrocution and not due to old
cerebral infarction.
99
Cause of death
The cause of death was given as “fatal accidental electrocution in a bathroom”.
Review of the case
This case is an example of tragic ends due to the faulty electrical appliances.
The shower appliance cord connecting to the shower head was frayed but still
being used by the family which may be due to ignorance and carelessness of
both parents.
The post mortem examination revealed possibility of two routes for the current
path which are right side of head to the left thigh and right hand to the left thigh.
The entry marks for the head is evidenced by the cooked appearance of the right
frontal lobe undersurface.
The right hand which was holding firmly to the faulty shower apparatus showed
extensive burn and collapsed blister. We believe the deceased fell down with
condition of tetanic spasm induced by the electrocution, resulted in hold-on
effect leading to charring of the flexor surfaces of the right hand fingers.
Moreover, as the right upper limb was in flexion position due to muscle
contraction in the bicep groups which has bigger mass than the triceps during the
electrocution process, the shower head rested on the chest. Prolonged contact
lead to charring of the chest burn marking. This burn mark also has spark lesion
appearance which can be explained by the irregular contour and shape of the
shower head. The presence of hyperaemic border around the chest burn mark
also showed that the electrical injury was sustained ante mortem. He fell onto
the back of his head which was revealed by the occipital subgaleal haematoma
and supine position of the body when he was found by his daughter.
The mechanism of death can be due to extrinsic chest muscle paralysis resulted
from prolonged exposure to the electrical current via the faulty shower
appliances evidenced by the facial congestion and cyanotic appearance of his lip
leading to respiratory collapse. In addition, the electrocution may also lead to
concurrent ventricular fibrillation. These events superimposed on each other
leading to his demise.
A group of experts from the National Electrical Board (NEB) came to the
deceased house and mortuary to investigate the death. From their inspection and
investigation, the NEB concluded that the faulty electrical appliance and not the
aberrant electrical supply lead to the fatal accident.
100
Fig. 1: The deceased found in a fixed flexion deformity of the right elbow and
wrist due to the electrical burn (point of entry). His face and neck were
congested.
Fig. 2: The electric current passed through the brain evidenced by the burnt and
cooked appearance of the right frontal lobe under surface.
101
Fig. 3: Section taken from the lesion in Fig.2 did not show any evidence of
reactive gliosis such as gemistocytic astrocytes or chronic inflammatory exudates.
It excludes diagnosis of old infarct in the brain.
(b)
Fig. 4: The exit point of the electrical current on the lateral aspect of the left
thigh.
102
Fig. 5: The deceased’s bathroom with faulty electrical shower heater where the
fatal incident occur.
(a)
103
(b)
(c)
Fig. 6 (a), (b), (c): Close up view of the faulty shower apparatus leading to the
fatal incident.
Discussion
Ignorance may lead to electrocution because of the immaturity of the victim.

Rabban et al (1997)22 noted that the incidence of pediatric electrical injuries is
highest among toddlers and in the pre-school age. Infants and toddlers, by nature,
are inquisitive and tend to have hand or oral contact with various objects in their
environment. Most low voltage electrocutions among young children occur from
oral contact with electrical cord, while some result from inserting objects into wall
sockets (Rabban et al. 1997).22
Ignorance among adults leading to electrocution may be due to low socio-

economic status. Ignorance of safety regulations among workers may lead to
fatal electrocution at the workplace due to lack of understanding, or failure of the
employer to provide adequate training on safety.
104
Intoxication may be another causal factor. Mellen et al.(1992)16 noted significant

blood alcohol in 31% of the cases in their series, that might impair judgment or
motor function, leading to an accident.
Natural diseases that may impair function such as vertigo, or those that
incapacitate such as coronary heart disease or cerebro-vascular catastrophe, may
lead to accidental contact with a live conductor. A person rendered unconscious
by intoxication or natural disease may fall onto a live conductor.
Risk-taking behaviour may be a factor among adolescents and adults leading to

high-voltage electrocution. As opposed to young children, older children are at
higher risk for high-voltage contact as they may climb trees, telephone poles,
transformer towers and rooftops with high-tension cables strung overhead
(Rabban et al.1997).22
There are a number of possible hazards in the domestic and industrial settings
such as defective wiring of the sockets or frayed/broken electrical cord (Polson
1985).21
Poor housing may also be a factor leading to electrocution (Al-Alousi 1985) as
in overcrowded low-cost homes with inadequate wiring resulting in overloading
of the few wall sockets available.
Deaths due to electrocution can be classified as accidental (domestic, industrial

or auto-erotic cases), suicidal and homicidal depending on circumstances
surrounding the fatal incident.
Electrocution
Electrocution is literally defined as execution/kill by electric shock. Electrical
current can only travel along conductors therefore no electrical injury occurs
unless some part of the body completes the circuit between two conductors
(Hirsch & Zumwalt 1985).9 In other words, the body must be incorporated into
the electrical circuit to enable electrons to pass through the tissues. Considering
the fact that the body becomes part of the electrical circuit during electrocution,
there has to be a point where the electrical current enters the body from a
conductor, and another from which it leaves to body to another conductor.
However, it is not invariable that entry and exit marks should be present in every
cases of electrocution (Al-Alousi 1990).1
It has been noted that among the injuries produced by physical agents, probably
none is governed by the law of physics more strictly than that induced by
electricity (Somogyi & Tedeschi 1977).25 The passage of electricity through a
conductor, including the human body is governed by Ohm’s law.
105
An electrical injury and its extent and severity if it does occur, depend on several
well-defined electrical and physical factors with regard to the agent (electricity)
and the host (victim).
Type of current
There are two types of current in both domestic and industrial use; direct current
(DC) and alternating current (AC). AC is the type of current supplied for public
utility, and is used to power most domestic electrical gadgets. DC is broadly
applied in industry where electrolytic activity is required, such as in plating and
in purification of metals (Somogyi & Tedeschi 1977).25
In general, the human body is more sensitive to AC compared to DC, where AC

is four to six times more likely to cause death (Knight 1996).11 The greater
incidence of fatality from AC is due to the ‘tetanoid’ effect elicited by AC,
giving rise to the ‘hold-on’ effect that prevents the victim from taking his hands
off the live conductor (Somogyi & Tedeschi 1977; Knight 1996).25,11 This hold-
on effect will continue until the circuit is broken (Hirsch & Zumwalt 1985).9 It
has been noted that an AC of 70 to 80 mA may be lethal, while a DC of 250 mA
may be tolerated without damage.
AC is also more likely to be arrhythmogenic than DC, where the passage of AC

at 100 mA for only 0.2 seconds may cause ventricular fibrillation and arrest. On
the other hand, DC at high amperage is used medically for terminating
arrhythmia (Knight 1996).11
An important aspect of AC is its alternating frequencies with some frequencies

more disturbing than others. The usual frequency of AC is 50 to 60
cycles/seconds (cps). This frequency lies in the range that is particularly
disturbing to the brain and heart should they lie in the current path, and accounts
for the arrhythmogenic tendency of AC by interacting with vulnerable phase of
the cardiac cycle. The risk of disrupting the vulnerable phase increases as the
duration of current flow increased (Hirsch & Zumwalt 1985).9 The ‘danger
range’ for AC frequencies in relation to ventricular fibrillation is 40 to 150 cps,
and the danger decreases with the increasing number of cycles. It has been noted
that the heart is 20 times less likely to fibrillate at 1720 cps compared to 150 cps
(Somogyi & Tedeschi 1977; Knight 1996).25,11
The amount of current necessary to cause the hold-on effect may be less than
that required to cause fibrillation, the victim may succumb to a current that
would otherwise have not been lethal (Hirsch & Zumwalt 1985).9 A current of
50 mA or so is needed to cause ventricular fibrillation. Skeletal muscles will go
into spasm when the current reaches 10 to 40 mA at 50 cps. When the entry
point is at the hand, the stronger flexor muscles will go into spasm, giving rise to
106
the hold-on effect. Knight (1996) noted that hold-on can appear with current as
low as 9 to 10 mA.
Electromotive force
The electromotive force of electricity is its voltage. The usual domestic voltage
is 220 to 240 V. The conventional demarcation between low-voltage (low-
tension) and high-voltage (high-tension) is 1000 V or 1 kV.
Certain amount of electricity or current must pass through the body to cause
fatality. Therefore, according to Ohm’s law, minimum amount of voltage must
be applied to the skin to overcome resistance to produce the potentially fatal
current. The domestic voltage of 240 V, and 110 V for some countries, is
sufficient to cause deaths, and they account for most fatalities. (Somogyi &
Tedeschi 1977 ; Knight 1996).25,11 For domestic appliances, 42 V is considered
safe, while children’s electric toys are considered safe at 24 V, although fatality
have been reported even at 24 V (Polson 1985).21
In contrast to the above mentioned electrocution from a discharge of extremely

high voltage, such as 10 kV may be survived, as the shock may give rise to the
‘throw-off’ effect by physically flinging the victim off the conductor, at times in
an explosive manner. It has been noted that deaths following low-voltage
electrocution are primarily due to ventricular fibrillation, while those following
high-voltage electrocution are due to the ensuing electrothermal injuries
(Somogyi & Tedeschi 1977).25
Resistance
Ohm’s law dictate that the current produced is inversely proportional to the
resistance of the conductor. As the usual currents available for domestic use have
a fixed voltage, resistance then becomes the major variable in determining the
flow of current in a domestic electrical accident. Different tissues in the human
body vary in their resistance to the passage of electricity, depending on their
respective water content.
The most resistant part of the body to an electrical current is the skin, which
often forms the major barrier when it is dry. Internal tissues have much lower
resistance compared to skin. After skin, the degree of resistance in decreasing
order is as follows: bone; fat; nerve; muscle; blood; and body fluids (Somogyi &
Tedeschi 1977).25 It follows that once epidermal barrier has been breached, with
the aid of intracellular fluids and the vascular system, the current will pass
through the body quite easily (Knight 1996).11
The resistance of the skin varies depending on the thickness of the keratin-
covered epidermis, and also the relative number of hair follicles and sweat and
sebaceous glands. Therefore, thick callous skin on the soles and finger pads are
107
more resistant than thin delicate skin. Knight (1996)11 noted that dry, thick
callous skin may offer a resistance of up to 1,000,000 Ω compared to the average
500 to 10,000 Ω of other skin. For a healthy individual in general, resistance is
highest in the skin of the back, and lower in the forearm, followed by the palms,
arm, and scalp (Somogyi & Tedeschi 1977).25
More important than the thickness of the skin is the dryness or the dampness of
the skin. The skin may be damped by sweat or external source of water or fluid.
A dry palm skin with a resistance of 1000,000 Ω may be able to offer a
resistance of only 1200 Ω when wet. Thus, the net effect of a fixed voltage with
a wet skin is the passage of greater amount of current into the body and higher
risk of electrical injury.
In view of the resistance offered by the skin, there will be energy transfer from
the electron flow to the skin. The heating effect of a current can be
demonstrated below (Somogyi & Tedeschi 1977)25:
H = C2R
4.187
where 4.187 is a constant and:
H – heat in gram calories/second.

C- current in amperes.
R – resistance in ohms.
As can be seen, heat produced is directly proportional to the resistance offered

by the skin. The higher the skin resistance the more likely it is for cutaneous
electrical burns. It is also one of the reasons why immersed skin may not show
electrical burns.
Broad surface area and good contact also reduces skin resistance by about a
hundred-fold (Polson 1985).21 It has been noted that when current begins to pass
through the skin, associated electrolytic changes will cause the resistance to drop
further, even down to 380 Ω (Knight 1996).11
Arc current
It is important to understand that electrical injury to the body may occur without
direct contact with the conductor of the electric current. In this situation there is
an ‘air gap’ between the skin and the conductor, as would occur when a body
approaches a high-voltage line, and the current will ‘jump’ the gap as a spark.
The electric arc may pass through the body, resulting in electrocution. The
relationship between the voltage and the distance at which arcing can occur in
dry air to produce injury is as demonstrated (Somogyi & Tedeschi 1977)25:
108
Voltage Distance between skin and conductor

1000 V Few mm
5000 V 1 cm
20,000 V 6 cm
40,000 V 13 cm
100,000 V 35 cm
While arcing most often occurs following exposure to high voltage current, it may
also occur with low-voltage current whenever the body resistance is low. Arcing
generates temperature as high as 4000° C, and the effects are similar to those of a
flame from other sources.
Aside from arcing, there may also be direct flow of current in an ‘indirect’ manner
which can lead to electrocution. An example would be a person who is
electrocuted when he urinates on a high-tension conductor, where the current will
ascend the stream of urine (Polson 1985).21
Amount of current
The amount of electricity flowing through a conductor is expressed by the number
of electrons per unit time, and Amperes is an acceptable index of the current flow
(Knight 1996).11 In accordance with Ohm’s law, the current is directly
proportional to the applied voltage, and inversely proportional to the resistance of
the tissue. For tissue damage to occur, the time for which the current is flowing is
also important.
The amount of current is the most important electrical parameter for electrical
injury to occur. The degree of tissue damage is proportional to the quantity of
electricity flowing through them. Somogyi and Tedeschi (1977)25 noted that as
body resistance can only be estimated the retrospective determination of the
amount of current flow may be based primarily on the response to the electrical
contact by the victim.
The amount of current that may cause fatal electrocution is those that will lead to
cardiac arrhythmia. It is generally agreed that the passage of 50 to 80 mA for only
a few seconds is likely to cause fatality. A current of 30 mA may cause painful
muscular contraction and consciousness is likely to be loss at about 40 mA
(Somogyi & Tedeschi 1977; Knight 1996).25,11 Ventricular fibrillation
predominantly occur following exposure to currents between 80 mA to 3 A for at
least one second.
Polson (1985)21 noted that an electrical current exceeding 4 A would not be

accompanied by ventricular fibrillation. This is in fact the principle of the
treatment with a defibrillator. He described a case of a man who survived contact
109
with a 20 kV circuit which he attributed to the high amperage, which is possible

with a skin resistance of 30,000 Ω or less. This, together with the ‘throw-off’
effect may explain the apparent survivability following contact with high-tension
conductors.
Duration of contact
In general, the severity of the disturbance caused by the flow of a given amount
of current is proportional to the duration of the flow (Hirsch & Zumwalt 1985).9
It follows that the longer is the duration of contact, the more current will pass
through the body and the greater will the amount of body damage be.
The hold-on effect associated with AC as described above increases the risk of
fatality by prolonging the duration of contact with the live conductor while the
victim is unable to let go. The duration determines the amount of damage
following such contacts.
Somogyi and Tedeschi (1977)25 noted that it is difficult to determine the duration
of contact retrospectively. In general, should the victim survive, the contact must
have been very short if he did not loose consciousness and was able to interrupt
the circuit voluntarily. In fatal cases involving low voltage electrocution, one can
infer that the duration of contact was not short because of the severity of the
burns (Peng & Shikui 1995).19
Surface area of contact

This factor modifies the external appearances of electrical injury (Polson
1985).21 As mentioned, cutaneous electrical injury is the result of heat generated
as the electrical current overcomes the skin resistance. With a small contact area,
such as during contact with the end of a rod or wire, the thermal energy
generated will be concentrated at the small surface area, giving rise to a small
circular electrical burn.
Conversely, a broad conductor applied closely may electrocute without

producing any external mark. In a large contact area, less current will pass
through per square area of the skin. The flow of the current is almost unimpeded,
and occurs without significant generation of heat. This explains the absence of
external marks following electrocution in the bath or swimming pool, where the
wet state of the skin also markedly reduces resistance (Goodson 1993).8
Site of contact
This is related to resistance. Polson (1985)21 noted that if the contact was to the
dry, thickened palm of a manual worker, the resistance offered may prevent
electrocution, as opposed to contact with the arm or face.
110
Transitional resistance
Transitional resistance or insulation refers to the resistance provided by any
material situated between the live conductor and the skin, or between the skin
and the earth (Somogyi & Tedeschi 1977).25 The use of rubber boots or glove
will prevent or minimize the earthing of the current to complete the circuit, thus
avoiding fatal electrocution.
Similarly, if the person is barefooted, the nature of conductivity of the floor is

important. Thick carpeted floor, unless it is damp, will provide adequate
insulation.
However electrocution may still occur in spite of protective gears. The use of
rubber gloves may not protect the wrist, and the boots or shoes may have worn
soles or tears that allow water to enter. The soles may also be compromised by
the presence of nails or metal studs.
Path of the current

The actual path of the current in the body between the sites of contact is a very
important factor in determining the outcome of electrocution. Fatal electrocution
will occur if the path taken contains vital structures (Knight 1996).11 The current
will enter at one point and then leaves the body at the exit point, either to the
earth or to a neutral conductor of the electricity supply.
An electrical current will pass through the body in the shortest route between the
entry and the best exit rather than along the areas of weakest resistance
(Somogyi & Tedeschi 1977).25 Therefore, irrespective of tissue dispersion, the
greatest density of current will develop on the shortest path.
As a general rule, the sites of entrance and exit of the current will determine its
path in the body (Somogyi & Tedeschi 1977).25 Contact is most often with a
hand, often being used to hold, touch or manipulate some electrical device.
There are several paths that a current may take in the body:
Hand-to-hand path - both hands comes into contact with the live conductor, or
one hand touches a live conductor while another touches a neutral conductor of
the supply or an adequately grounded object. Here the current will enter through
the left hand and travel across the thorax, including the heart, and will exit
through the right hand to the tap to pass to earth.
Hand-to-foot path - hand comes in contact with a live conductor while the foot is
well grounded. Here the current will enter through the hand and again pass
through the thorax to exit through the foot that is grounded.
Head-to-hand path - the head comes in contact with a live conductor while the
hand is in contact with an adequately grounded object. Here the current will travel
111
through the head and neck, including the brain, to exit via the hand to be
grounded.
Head-to-foot path - when the foot, instead of the hand is grounded. The current
will still pass through the head and neck, and probably also through the heart.
The most common passage is for the current to pass through the heart, which can
be achieved either with the hand-to-hand or hand-to-foot paths. It has been noted
that the most dangerous scenario is having the current enter through the right
hand and exit through the feet, as the current will then pass obliquely along the
axis of the heart, giving rise to fatal arrhythmia. This route increases the current
flow across the heart by a factor of 1.5 to 2.5 compared with left-hand entry
(Knight 1996).11 Entry through the head is uncommon both in industrial and
domestic settings (Polson 1985).21
Other factors
Pre-existing cardiac disease may predispose to death from low tension
electrocution (Somogyi & Tedeschi 1977; Polson 1985).25,21 However, it has
been found that those with cardiac disease appeared better able to withstand
severe shocks than healthy persons.
It has been said that tolerance may be gained to electric shock, as in among
professional electricians (Knight 1996).11 This may be due to decreased
sensitivity that would accompany the expectation of a shock, as a person who is
taken by surprise may succumb to shocks that ordinarily would not produce any
ill-effects (Polson 1985).21 However this is only for brief contacts, where the
duration is less than that required to produce physiological or structural damage.
The physical condition of the victim may also be a factor that will influence the
effect of an electrical shock (Polson 1985)21 such as fatigue resulting in slow
reaction time. A shock may cause injury and fatality to someone who was not in
good physical state because he was too tired to immediately detach himself from
the electrical contact (Peng & Shikui 1995).19
Mode of death in electrocution

Death due to electricity does not necessarily occur immediately, it may be
delayed death or late death. Nevertheless, death often occurs immediately.
(Somogyi & Tedeschi 1977; Polson 1985).25,21
Most deaths from electricity are from cardiac arrhythmias, mainly ventricular
fibrillation that will terminate in cardiac arrest (Knight 1996). In fact, as a rule,
immediate deaths from exposure to low-voltage currents are caused by
ventricular fibrillation with exceptions (Somogyi & Tedeschi 1977).25
112
Arrhythmia is caused by the passage of electricity through the myocardium,

especially in the epicardial layers, and probably across the endocardium as well,
with possible dislocation of the conducting systems. The most vulnerable stage
of the cardiac cycle is the end of systole (Somogyi & Tedeschi 1977).25
Following this mode of death the body either remains pale or only slightly
congested on autopsy (Knight 1996).11 Polson (1985)21 noted that this mode of
death is not invariably associated with immediate loss of consciousness or
respiratory arrest; some can walk about before they die.
Electricity supplied for domestic and industrial use is most dangerous in terms of
ventricular fibrillation. Although current of less than 50 mA is not likely to be
fatal, far less current, even in the microampere range can cause fibrillation if
applied directly to the heart. Such ‘microshocks’ may occur in those with
indwelling catheters hooked to monitors or implanted cardioverters (Hirsch &
Zumwalt 1985; Hutse et al.1997).9,10
The passage of a current across the chest and abdomen may cause spasm of the
intercostal muscles and diaphragm, leading to respiratory paralysis. This is less
common than ventricular fibrillation as a mode of death (Knight 1996).11 This
‘tetanic’ asphyxia occurs with the passage of low or medium current of 20 to 30
mA that can induce tetanic contraction of the extrinsic muscles of respiration,
causing death through mechanical asphyxia (Polson 1985).21 In view of the very
low voltage involved, the duration of contact must be prolonged (Peng & Shikui
1995).19 The victims are likely to be cyanosed, as opposed to the pallor
associated with ventricular fibrillation. Prolonged contact may lead to the
formation of endogenous burn at the point of contact, causing the resistance to
be lowered, thus increasing the amperage above the critical level at which
ventricular fibrillation may occur (Polson 1985).21
Rarely, the current passes through the brainstem as in head-to-hand or head-to-

foot paths. This will cause paralysis of the cardiac or respiratory centers, leading
to death (Knight 1996).11 The effect may be induced by the electrical force itself
or by hyperthermic effect (Al-Alousi 1990).1
Finally in fatal electrical accidents, the death is not invariably cause by the
electric energy itself, but may also be caused by non-electrical trauma, that is,
mechanical injury. This is often seen with high-voltage accidents where the
explosive ‘throw-off’ effect may cause the victim to fall from height. Serious
fractures and other injuries may also result from electrically induced violent
muscle spasms (Somogyi & Tedeschi 1977; Knight 1996).25,11 In these cases it
may be difficult to decide on the immediate cause of death. Careful assessment
of the severity of the mechanical injury will help solve this problem (Al-Alousi
1990).1 In the presence of water and electricity, the cause of death may not be
113
electrocution, but drowning caused by muscle paralysis from the electric shock
(Goodson 1993).
Cutaneous electrical mark

Skin electrical mark provides the most valuable ‘diagnostic’ information in the
investigation of an electrical death, although it is not, by itself, absolute proof of
an electrocution (Al-Alousi 1990).1
These ‘electrical marks’ or ‘electrical burns’ may be seen at the point of contact
of the body surface through which the current enters (entry mark), and may also
appear at the part of the body that was earthed or grounded (exit mark), through
which the current passes out of the body to complete the circuit (Knight 1996).11
However when the contact surface area is large and skin resistance is low,
electrocution can occur without any cutaneous mark. In these situations, the
circumstances of the death will provide a clue to the actual cause of death.
The basis of a cutaneous electrical mark is heat as part of the electrical energy is
converted to thermal energy in the presence of skin resistance. Therefore, the
mark is in fact thermal burn from heating of the epidermis and dermis as the
current passes through which is sometimes difficult to differentiate from a burn
produced by other causes.
The only difference between the two is the origin of the forces that produces
them; in an ordinary burn it is of an extrinsic nature, while in an electrothermic
burn it is of an intrinsic nature or endogenous, having been produced within the
tissue itself (Somogyi & Tedeschi 1977; Polson 1985).25,21 Some have indicated
that when low amounts of electrical energy are applied on the skin, local
electrolysis becomes an important factor for causing injury (Al-Alousi 1990).1
In situations where the contact area is large and/or the resistance is low, the
thermal energy generated in terms of calories per square centimeter of surface
area per second may be too low to produce a burn, although the current that
passes through is sufficient to cause fatality (Hirsch & Zumwalt 1985).9 The
tissue temperature at the contact point can easily reach 95° to 100° C, and tissue
damage can occur even at a temperature of 50° C within 25 seconds (Shahrom
1993; Knight 1996).24,11
Generally, the appearance of the cutaneous electrical mark depends on whether it

is the result of direct, firm contact with the live conductor, or from arcing, and
this broadly depends whether the current was low or high voltage (below or
above 1000 V respectively) (Polson 1985).21
During firm contact, the passage of the current through the high skin resistance
gives rise to thermal energy that heats up the tissue fluids and steam is produced.
114
This steam may split the epidermis or the epidermo-dermal junction, giving rise
to a raised blister at the site of contact. The blister may rupture should the
duration of contact be prolonged or the area is relatively large.
When the current flow ceases, the blister will cool and collapses. The appearance
of the collapsed blister or ‘umbilicated nodule’ is the typical low-voltage current
mark. The mark is often a small, circumscribed or elliptical, crater-like with
raised edge, indurated lesion and has a greyish or darkened umbilicated center of
charring (Al-Alousi 1990; Knight 1996).1,11 There is commonly a pale zone
immediately surrounding the lesion, which may be due to arteriolar spasm.
Knight (1996)11 claimed that this zone of pallor survives death and is virtually
pathognomonic of electrical damage. Outside the pale zone there is often a
hyperemic border which is the outermost rim of the heated burn area. The
hyperemic border often indicates that the electrical mark was ante mortem in
nature (Shahrom 1993).24
The entry and exit marks generally have the characteristics noted above although
the exit mark may be less severe (Knight 1996).11 Indeed, their appearances are
often similar that it may not be possible to determine from external examination
alone (Pepper & Wecht 1980).20
Generally the mark will be the same size as the conductor with which the victim
comes into contact (Somogyi & Tedeschi 1977).25 Sometimes the mark will
reproduce the shape of the conductor, especially when it is a linear wire or a
shaped metal object (Knight 1996).11 The medico-legal value of these patterned
electrical marks is that they may be useful in determining the causative object
and for reconstructing the events of death. They may also indicate for the first
time that the un-witnessed death was caused by electrocution.
In the absence of direct contact or when the contact is not firm, arcing will occur,
especially with high-voltage electrocution (Polson 1985).21 As mentioned, the
current will jump the gap as a spark. The spark is at an extremely high
temperature, between 3000° - 4000° C and will cause the outer layer of the
keratin to melt over a small area. When the keratin cools it will fuse into a hard
brownish nodule that is usually raised above the surrounding surface. This mark
is called a ‘spark lesion’. The nodule will be surrounded by a pale zone. Should
the keratin burn, there will be a blackened carbonized center while the margin of
the nodule appear brownish (Shahrom 1993; Knight 1996).24,11 It has been noted
that in many electrical burns a combination of collapsed blister and spark lesion
may be seen, due to the movement of the hand or body against the conductor, or
because irregularity of the shape of the conductor prohibits uniform firm contact
(Knight 1996).11
115
During low-voltage electrocution, if the contact is more prolonged the skin will
burn and even become charred, producing a Joule burn. This burn is endogenous,
as opposed to changes caused by exogenous thermal energy, i.e. spark lesion
from arcing (Polson 1985).21
At times the marks may be minimal so as to be inconspicuous, and may be

missed following external examination done only superficially during autopsy.
These lesions may be seen as tiny white discs 1 to 3 mm in diameter, with no
obvious hyperemic border (Shahrom 1993; Knight 1996)24,11 and are often
present on the palmar aspect of the hands and may be obscured by ‘flexion’ of
the fingers from rigor. These lesions can be mistaken for warts or callused
nodules on gross examination. Knight (1996)11 noted that exit marks are not
often seen, and should be looked for on the contra-lateral hand or feet. In
addition, electrical mark can also occur under intact clothing or hair and may
remain undetected (Somogyi & Tedeschi 1977).25 The recognition of
electrocution is important because it draws attention to wiring or appliance that
is dangerous to others (Polson 1985).21
The spark from a high-voltage electrical source, such a grid transmission cable,
can arc over a considerable distance, the victim may be ‘showered’ with sparks
giving rise to multiple spark lesions, the so-called ‘crocodile skin’ effect (Knight
1996).11 With arcing there is the risk of severe thermal burns because of the
considerable heat generated in the sparks. These burns may be aggravated by
burns from ignited clothing. Gross soft tissue destruction and charring of the
bone or fusion of bone into pearl-like bodies would imply direct contact with the
supply (Polson 1985).21 Accompanying mechanical injuries may be present, but
they are not specific (Al-Alousi 1990).
Electrical marks may be induced postmortem (Somogyi & Tedeschi 1977).25 The
detection of vital reaction (hyperemic border) will decide whether the exposure
to the current occurred before or after death. Moreover, electrical mark resist
putrefaction, should exhumation become necessary (Al-Alousi 1990).1
If death occur early from ventricular fibrillation, and supply has not been cut or
the victim’s body has not been removed from the live conductor, severe burning
with charring may occur postmortem (Knight 1996).11
Metallisation
‘Metallisation’ is a specific feature of electrical injury and lightning stroke,
although it is likely to be prominent only in lightning stroke (Polson 1985).21
This phenomenon occurs when the passage of a current from a metal conductor
into the body give rise to a form of electrolysis, so that metallic ions are
embedded into the skin, and even into the subcutaneous tissue. There will be
darkening of the skin, the color varying with the composition of the conductor. It
116
may be brown or black if the conductor is of iron, or yellow-brown if of copper,

and copper salts may also leave a blue mark on the skin.
Metallisation occurs with both AC and DC. It has been claimed that
metallisation will distinguish between a true electrical mark and a thermal burn
(Polson 1985),21 where metallisation provides decisive evidence that the burn
was produced by electrothermic force (Somogyi & Tedeschi 1977).25
Metallisation may also distinguish between exit and entrance marks that are
similar on gross appearance (Perper & Wecht 1980).20
Histology of cutaneous electrical mark

Examination of the skin mark will demonstrate a very sharp demarcation from
normal to damaged skin, without the usual progressive gradation seen in burns
from other sources (Perper & Wecht 1980).20 There are vacuolations in the
epidermis and sometimes in the dermis from splitting of the tissue by steam from
the heated tissue fluids. These vacuoles may coalesce to form a large blister that
separates the dermis from the epidermis (Shahrom 1993).24 Separation of the
cells in the lower epidermis may form sharp slits, called ‘electrical channel’. The
affected tissue will appear more eosinophilic from transcutaneous coagulation.
There is pyknosis of the epidermal nuclei. Characteristically, these nuclei will
appear elongated, and are aligned in a parallel fasciculate or palisading fashion,
called ‘nuclear streaming’ (Al-Alousi 1985),1 and are prominent among the
nuclei of the basal cells and keratinocytes of the lower layer of the epidermis
(Shahrom 1993).24
These features may also be observed in burns from other sources, hypothermia,
cauterisation, and in ‘barbiturate blisters’ (Shahrom 1993).24
Changes in other organs from electrocution

The changes are predominantly physiological and functional rather than
morphological (Knight 1996),11 and all internal appearances on autopsy depend
on the cause of death, although they are non-specific (Al-Alousi 1990).1
Non-specific organ congestions are common in all cases (Hirsch & Zumwalt
1985).9 However in those who die from respiratory paralysis the congestion will
be more pronounced with petechial hemorrhages of the serous membranes, and
the dark blue-red hypostasis of cyanosis (Knight 1996).11 Tetanic contraction of
the diaphragm may lead to regurgitation of gastric content into the airways
(Shahrom 1996).24
In high-voltage deaths there may be injuries related to mechanical trauma such

as fractures and internal organ injuries (Somogyi & Tedeschi 1977).25 The
thermal energy may lead to melting of the bones and formation of ‘oseous-
pearls’ of calcium phosphate. These are pea-sized, greyish-white hollow
117
particles usually found on the surface of the injured bones. Muscles may be
cooked, or torn by spasm during the shock (Al-Alousi 1990).1
References
1. Al-Alousi L. 1990. Homicide by electrocution. Med. Sci. Law. 30(3): 239-

246.
2. Bancroft J. and Cook H. 1984. Manual of Histological Techniques.
Edinburgh: Churchill Livingstone. pp. 151-157.
3. Byard R. 1991. Autoerotic death. Am. J. For. Med. Pathol. 12(1): 74-76.
4. Chandrasiri N. 1988. Electrocution by dielectric breakdown (Arcing) from
overhead high tension cable. Med. Sci. Law. 28(3): 237-240.
5. Cohen R. 1993. Electric shock. In: Current Medical Diagnosis and
Treatment. Tierney et al. East Norwalk: Appleton and Lange. pp. 1232-
1233.
6. Danielsen L. et al. 1991. Diagnosis of electrical skin injuries. Am. J. For.
Med. Pathol. 12(3): 222-226.
7. Ghosh D. et al. 1997. Electrical injury on removal of implantable
defibrillator after death. Heart. 77(5): 484-485.
8. Goodson M. 1993. Electrically induced deaths involving water
immersions. Am. J. For. Med. Pathol. 14(4): 330-333.
9. Hirsch C. and Zumwalt R. 1985. Electrical injury. In: Anderson’s
Pathology. 9th Ed. Vol. 1. Kissane J. St. Louis: Mosby. pp. 140-144.
10. Hutse W. et al. 1997. Inappropriate shocks in a patient treated with a
cardioverter defibrillator. Heart. 77(4): 386-387.
11. Knight B. 1996. Forensic Pathology. 2nd Ed. London: Arnold. pp. 319-330.
12. Lechleuthner A. 1995. Electric shock to paramedic during
cardiopulmonary resuscitation of patients with implanted
cardiodefibrillator. Lancet. 345(8944): 253.
13. Lewis A. 1997. Understanding the principles of lightning injuries. J.
Emerg. Nurs. 23(6): 535-541.
14. Lifschultz B. and Donoghue E. 1993. Deaths caused by lightning. J. For.
Sci. 38(2): 353-358.
15. Marc B. et al. 2000. Suicide by electrocution with low-voltage current. J.
For. Sci. 45(1): 216-222.
16. Mellen P. et al. 1992. Electrocution: a review of 155 cases with emphasis
on human factors. J. For. Sci. 37(4): 1016-1022.
17. Mitchell E. and Davis J. 1984. Electrocution from street lighting. J. For.
Sci. 29(3): 836-842.
18. Odesanmi W. 1987. Things are not always what they seem! Joule burns in
electrocution – a report of four cases. Med. Sci. Law. 27(1): 63-67.
19. Peng Z. and Shikui C. 1995. Study of electrocution death by low-voltage.
For. Sci. Int. 76: 115-119.
118
20. Pepper J. and Wecht C. 1980. Electrical injuries. In: Microscopic

Diagnosis in Forensic Pathology. Springfield: Charles C. Thomas. pp. 258-
267.
21. Polson C. 1985. Electrical injuries and lightning stroke. In: The Essentials
of Forensic Medicine. 4th Ed. Polson et al. Oxford: Pergamon. pp. 271-
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22. Rabban J. et al. 1997. Mechanisms of pediatric electrical injury: new
implications for product safety and injury. Arch. Pediatr. Adolesc. Med.
15(7): 696-700.
23. Romero B. et al. 1997. Myocardial necrosis by electrocution: evaluation of
non-invasive methods. J. Nucl. Med. 38: 250-251.
24. Shahrom A.W. 1993. Patologi Forensik. Kuala Lumpur: Dewan Bahasa
dan Pustaka. pp. 474-484.
25. Somogyi E. and Tedeschi C. 1977. Injury by electrical force. In: Forensic
Medicine. Vol. 1. Tedeschi C. et al. Philadelphia: Saunders. pp. 645-674.
26. Suruda A. et al. 1999. Fatal injuries in the United States construction
industry involving cranes 1984-1994. J. Occup. Environ. Med. 41(12):
1052-1058.
27. Wetli C. 1996. Keraunopathology. Am. J. For. Med. Pathol. 17(2): 89-98.
28. Wright R. and Davis J. 1980. The investigation of electrical deaths: a
report of 220 fatalities. J. For. Sci. 25(3): 514-521.
29. Yamazaki M. et al. 1997. An electrocution death of an infant who had
received an electric shock from an uncovered oval shaped lamp switch in
his mouth while in a hospital. J. For. Sci. 42(1): 151-154.
119
CASE REPORT
An accidental group death (3 victims) due to solvent

abuse
Shahrom AW, Zarida H,* Mohd Azaini I**

Malaysia.*
Department of Forensic Medicine, Hospital Melaka, Malaysia.**
Abstract
Three teenagers (2 Malays and 1 Indian) were found dead under a tree near. Some
“glue-sniffing paraphernalia” were found scattered under the tree. Postmortem
examination on all three victims revealed nonspecific congestion of organs but
otherwise there was no significant natural disease found in their body that could
have caused or contributed to his death at that particular moment in time. The
blood, kidney, lung and brain tissues were found to contain toluene. Quantitative
analysis showed 18.0, 18.2 and 7.5 microgram per milliliter toluene in their blood
respectively. The latter victim had 59 milligrams ethyl alcohol per 100 millilitres
blood. Their death was associated with organic solvent (toluene) intoxication
which resulted from glue sniffing activity. The police investigation revealed that
they died of accidental death.
Keywords: Solvent abuse, glue sniffing, accidental death, toluene
Address for correspondence and reprint request: Assoc. Prof. Dr. Shahrom bin Abd. Wahid,
Introduction
“Glue sniffing” or solvent abuse as a habit was recognized in the United States
round 1960. A decade later attention was drawn in the United Kingdom to this
problem. Commonly used solvents and their toxic constituents are shown in
120
table1. Kupperstein and Susman (1968)¹ stated that “a number of communities in

widely separated parts of the United States began reporting a high incidence of
‘glue sniffing’ around 1960.”
Table 1: Common solvents and their toxic constituents.
Common solvents Toxic constituents*
Lighter fluid Carbon tetrachloride, Naptha (Petroleum

origin), Perchlorethylene, Trichlorethylene
Fingernails polish remover Acetone, Alcohol, Aliphatic acetate, Benzene
Lacquer thinner Aliphatic acetate, Methyl, ethyl, propyl

alcohol, Toluene
Cleaning fluid-spot removal Carbon tetrachlorides, Trichlorethylene,

Trichlorethanol
Household cements Acetone, Isopropanol, Methyl ethyl ketone,

Methyl Isobutyl ketone, Toluene
Model cements Acetone, Naptha (Petroleum origin), Toluene
Plastic cements Acetone, Aliphatic acetate, Cyclohexane,

Hexane, Toluene
*Non-volatile and non-lethal constituents not listed.
Press and Done (1967),²,³ in a study of twelve fatalities, eight deaths were due to
suffocation by a plastic bag, and in two cases death was presumed to be caused by
intotoxication although not confirmed by analysis.
The first report of a case addiction to glue sniffing in Great Britain was given by
Meny and Zachariadis in 1962.
Zabedah et. al (2001)4 reported the profile of solvent abusers in East Malaysia. In
their study, 27 of the 37 children, age ranging between 8 and 20 years, willingly
admitted to sniffing glue for a period between a few months to 2 years.
Haematuria and proteinuria were found in 21 children (78%). 16 blood samples
with toluene levels ranging from 0.3 to 41 microg/ml and 10 urine samples have
elevated urinary hippuric acid levels ranging from 1.2 to 7.4 mg/ml. Strong
121
positive correlation was noted between mean blood toluene levels and duration of
abuse.
However, we have not yet seen any report in the literature on accidental group
deaths in Malaysia as a result of solvent abuse.
Fig. 1: Three teenagers lying dead under a tree with some “glue-sniffing
paraphernalia” found nearby.
Fig. 2: Close-up photographs of all the three dead teenagers.
122
Case Report
Three teenagers (2 Malays and 1 Indian) were found dead at about 8.00 a.m. under
a tree near the Sri Sabah Flats in Cheras. Some “glue-sniffing paraphernalia” were
found scattered under the tree (Fig. 1 and Fig. 2). The police requested post
mortem examination to determine the cause of death.
Deceased A
The deceased was clad in a yellow T-shirt and had no mark of suspicious external
injury. There was no injection mark of intra-venous drug abuser. Internal
examination revealed nonspecific congestion of organs but otherwise there was no
significant natural disease found in his body that could have caused or contributed
to his death at that particular moment in time. The blood, kidney, lung and brain
tissues were found to contain toluene. Quantitative analysis showed 18.0
microgram per milliliter toluene in the blood. (Note: The fatal level for toluene
in blood is 10-20 microgram per milliliter - Randall C. Baselt: Analytical
Procedures for Therapeutic Drug Monitoring and Emergency Toxicology). The
cause of death was given as organic solvent intoxication.
Deceased B
The deceased was clad in a blue T-shirt and had no mark of suspicious external
injury. There was no injection mark of intra-venous drug abuser. Some dried
blood was found at the nostrils amd mouth region. The face, shins and forearms
were soiled with sand. A yellowish sticky material (hardened glue) was found
adhered on the skin of the right forearm. Internal examination revealed
nonspecific congestion of organs but otherwise there was no significant natural
disease found in his body that could have caused or contributed to his death at that
particular moment in time. The blood, kidney, lung and brain tissues contained
toluene. Quantitative analysis showed 7.5 microgram per milliliter toluene in
the blood. Alcohol content was 59 milligrams ethyl alcohol per 100 millilitres.
The cause of death was given as alcohol and organic solvent intoxication.
Deceased C
The deceased was clad in a white T-shirt and had no mark of suspicious external
injury. There was no injection mark of intra-venous drug abuser. Some dried
blood was found at the nostrils amd mouth region. The face, shins and forearms
were soiled with sand. A yellowish sticky material (hardened glue) was found
adhered on the skin of the right forearm. Internal examination revealed
nonspecific congestion of organs but otherwise there was no significant natural
123
disease found in his body that could have caused or contributed to his death at that
particular moment in time. The blood, kidney, lung and brain tissues contained
toluene. Quantitative analysis showed 18.2 microgram per milliliter toluene in
the blood. The cause of death was given as organic solvent intoxication.
Discussion
The volatile organic solvents contained in glues used by “sniffers” can be toxic to
organ systems such as the heart, liver, kidney, brain and bone marrow.
Cardiac deaths in solvent abuse include fatal arrhythmias, believed to be due

directly to the solvent affecting the myocardium, and myocardial infarction and
dilated cardiomyopathy. Baerg and Kimberg5 have noted the occurrence of
centrilobular hepatic necrosis and acute renal failure in “solvent sniffers”. Luric
also comment on hepatic and renal damage following acute toluene poisoning. No
histological confirmation was possible in our case as the tissues were autolysed.
Baker and Tichy6 studied the effects of toluene on the nervous system in acute and
chronic exposure. Under acute condition, scattered abnormalities of neurons were
seen in brain and spinal cord. An experient with chronic exposure revealed more
definitive nervous abnormalities consisting of increased pigmentation and
neuronal shrinkage. Patchy loss of myelin, particularly in perivascular areas, was
also seen. The cerebellar folia were considered to be abnormal with a decrease in
the number of Purkinje cells as well as degenerative changes.
The effects on the ECG, of inhalation of vapourized lacquer thinner – a mixture of

butylacetate, toluene and ethyl alcohol – was studied on rabbits, normal human
subjects and epileptics. Slight slowing of the normal waves was recorded from the
brains of rabbits only on exposure to doses approaching lethal levels and was
always preceded by other signs of intoxication. No ECG changes were noted in
the human subjects.
There is little evidence in the literature that a single acute exposure of toluene
intoxication alters the blood picture in any way, and even a small exposure over a
short period produces nothing more alarming than a relative lymphocytosis. Bone
marrow depression and hepatic enlargement have been reported. Workers exposed
to high concentrations of toluene may develop bone marrow depression and
associated anaemia and leucopenia. Anaemia and macrocytosis without
luekopenia was noted by Greenberg et al.7 One “sniffers” death had been
attributed to aplastic anaemia.
Acute intoxication is characterized by complaints of headache and feeling of

fatigue and confusion. Some patients may act drunk. In addition, there may be
124
nausea and vomiting as well as disturbances of equilibrium and co-ordination. Co-

ordination may be sufficiently impaired to be potentially injurious.
Unconsciousness have also been observed.
Specific post-mortem features have not as yet been identified either

macroscopically or microscopically in volatile substance abuse deaths.
Toxicological analysis for volatile substances is hence necessary for the
identification of the cause of death. Four pathophysiological mechanisms for acute
volatile solvent abuse deaths have been postulated – anoxia, vagal inhibition,
respiratory depression and cardiac arrhythmia. Of these, cardiac arrhythmia due to
“sensitization” of the heart to adrenaline is probably the most common. The triad
od hypoxia, a volatile substance and adrenaline was found to be more toxic than
the combination of volatile substance and adrenaline. There is a case of successful
resuscitation from ventricular fibrillation after toluene inhalation in a 16-year-old
boy.
A particularly dangerous practice is the use of a plastic bag in the administration

of the agent. Rebreathing of air contained in a bag will sharply decreased pO2 and
increased pCO2 of arterial blood and aggravate any tendency towards cardiac
arrhythmia caused by hydrocarbons, thus inducing anoxia in a sensitized
myocardium. Furthermore, the “sniffer” may become unconscious while sniffing
and the plastic bag can cause suffocation.
Two of deceaseds in our cases showed 18.0 and 18.2 microgram per milliliter
toluene in their blood which is within the fatal level. The fatal level for toluene is
between 10-20 microgram per milliliter. One of the deceased showed 7.5
microgram per milliliter toluene in the blood. Alcohol content was 59 milligrams
ethyl alcohol per 100 millilitres. The latter deceased person died of mixed alcohol
and organic solvent intoxication.
We believed the victims were having some glue sniffing sessions secludedly
under the tree that night. All three had been intoxicated with the toluene and died
‘accidentally’ (without involvement of any other party) in view of the absence of
any suspicious mark of injury on their body. The police did not find any evidence
of foul play in their investigation.
References
1. Kupperstein LR, Susman RM, A bibliography of the inhalation of glue
fumes nd other toxic vapors – A substance abuse practice among
adolescents. Int J Addict 1968; 3 (1): 177-97.
125
2. Press E, Done AK. Physiological effects and community control measures

for intoxication from the intentional inhalation of organic solvents. J
Paediat 1967; 39: 451-61.
3. Press E, Done AK. Physiological effects and community control measures
for intoxication from the intentional inhalation of organic solvents. J
Paediat 1967; 39: 611-22.
4. Meny J, Zachariadis N. Addiction to glue sniffing. Br Med J 1962; 2:
1448.
5. Baerg RD, Kimberg DV. Centrilobular necrosis and acute renal failure in
“Solvent Sniffers”. Ann Int Med 1970; 73: 713-20.
6. Baker AB, Tichy FY. Effects of organic solvents and industrial poisonings
on central nervous system. A Res Neuro and Mental Dis Proc 1953; 32:
475-505.
7. Greenberg L, Myers MR, Heimann H, Moskowitz S. Effects of exposure
to toluene in industry. JAMA 1942, 118: 573-8.
8. Zabedah MY, Razak M, Zakiah I, Zuraidah AB. Profile of solvent abusers
(glue sniffers) in East Malaysia Malays J Pathol. 2001 Dec;23(2):105-9.
126
CASE REPORT
Determination of the manner of death in a drowning case of a
teenage boy
Swarhib MS, Zarida H*, Shahrom AW, Aznool HA**
Forensic Unit, Department of Pathology, Medical Faculty, University

Kebangsaan Malaysia.
Department of Forensic Medicine, Hospital Sultana Aminah, Johor bahru,
Malaysia.**
Malaysia.*
Abstract
A Chinese teenager was allegedly found in a ‘near-drowning’ condition in the

swimming pool at his house. He was rushed to a specialist medical center but
pronounced dead on arrival. The deceased was sent to Hospital UKM for
postmortem examination. The external examination revealed some “restraint
marks” on the wrists and ankles, “tram line bruises” over the arm and back,
bruises over the face and lips and abraded bruises over both legs. Internal
examination revealed evidence of drowning and no other injury contributed to the
death. The toxicology results from chemistry department were normal. The
history, visit to the scene and postmortem findings were suggestive of death
consistent with homicidal drowning.
Keywords: Drowning, homicide, misadventure, restraint marks, tram line bruise
Address for correspondence and reprint request: Dr. Mohamed Swarhib, Forensic Unit,
Department of Pathology, Medical Faculty, University Kebangsaan Malaysia, Jalan Yaacob Latif,
Bandar Tun Razak, Cheras, 56000 Kuala Lumpur, Malaysia. Tel: 03-91702444, Fax: 03-
91711673, email: dr_aungthuya@yahoo.com
Introduction
Many bodies are recovered from water, but not all have drowned. Of those that
have drowned, pathological proof is often difficult or even impossible to obtain.
The autopsy diagnosis of drowning presents one of the major problems in forensic
practice, especially when there is delay in recovering the victim.1 The
determination of the cause of death of a person whose body is found in the water
requires careful collaborative investigations by forensic pathologists and police
officers. The autopsy examination is an essential element but represents only a
127
part of the totality of the investigations. The investigation of such death should
take into account not only the autopsy examination but also biochemical and
histological analysis, background of the circumstances preceding death and body
recovery.2
Case Report
A 15 years old Chinese male was allegedly found in the swimming pool at 03:40
a.m. in his house. He was ‘nearly drowned’. He was rushed to a specialist medical
center near to their house where death was pronounced on arrival and the body
was sent to mortuary of Hospital University Kebangsaan Malaysia at about 06:30
a.m. He was later said to have drown in the swimming pool and no other history
was forthcoming.
A medico-legal autopsy was performed on the following morning about 08:30

a.m. The body was in a good state of preservation, upper half of the body was
naked, wearing a brown colored shorts and dark green brief, which were soaked
with water.
The deceased’s left leg was tied with a rope in multiple loops at the ankle. Both
legs showed multiple patterned abrasions around both ankles. Circumferential and
patterned abrasions were present around both wrists. Both hands and feet distal to
the abrasions were somewhat swollen and oedematous. Closer inspection on the
abrasions around the wrists revealed that epidermal layers which were peeled off
in the direction towards the fingers. (Fig.1) Washer women skin appearances were
more marked on the hands than feet.
A B
Fig.1: Restraint marks present on both wrist and ankles with abraded bruises over
both shins.
128
Fig. 2: Bruises over the left temporal and lip (note: no whitish froth at the nostrils
and mouth after compression of the chest)
There were bruises 2x1.5cm and 2x0.6cm over the forehead, bruise 5x4cm over
the left temporal just beside the left eye, (Fig.2) bruise 5x4cm over the high
occiput, bruise 2.5x1.5cm over the upper lip with laceration of the inner mucosa
of the upper lip against the upper left incisors,(Fig.2) multiple parallel tram line
bruises 7x0.5cm, 5x0.6cm, 5x1cm and 5x0.5cm were found over the lateral aspect
of left arm, (Fig.3) bruises 1.5x1.5cm over the posterior aspect of right forearm
and right elbow
Fig.3: Tram line bruises over the left arm and back
area, tram line bruises 5x0.5cm and 5x0.4cm, scratches 5cm and 4cm over the
right half of the back, bruise 5x4cm over the left pectoral area, abraded bruises
3x2.5cm and 1.5x0.4cm over the right knee, abraded bruises 5x3.5cm, 3x2cm,
11x7cm over the right shin and 11x7cm and 6x5cm over the left shin. (Fig.1B)
The external injuries found on the deceased body were consistent with the age of
between 24 hours to five days based on the gross appearance and histo-
pathological examination.
129
Internally, sub-galeal haematoma 8x8cm was noted over the occipital area, the
skull was intact, the meninges and brain were intact. The neck muscle were intact,
the thyroid cartilage and hyoid bones were not fractured, the ribs were also intact,
the deep contusions were noted over the left pectoral muscle and right half of the
back muscles, that were coincide with the superficial bruises.
The trachea and bronchus were filled with fine white froth, the lungs were over
inflated covering the anterior mediastinum and filling the whole chest cavity, the
ribs marking were prominent, the texture was crepitant, (Fig.5) the stomach was
empty with thin film of fluid, the heart, liver, kidneys were unremarkable, the
bladder contained 80-100cc of straw colored urine.
Fig. 5: Over inflated lung and some amount of fine froth in the trachea
The blood and urine samples were sent to chemistry department to exclude the
alcohol and toxicology, the results were returned as normal.
Follow-up of the case
It was evident from the autopsy that the cause of death was consistent with
drowning. However the police want to know whether the manner of death can be
interpreted according to any of the Section 300 of the Penal Code10 i.e.:
Except in the cases hereinafter excepted, culpable homicide is murder –
(a) if the act by which the death is caused is done with the intention of causing
death;
(b) if it is done with intention of causing such bodily injury as the offender
knows to be likely to cause the death of the person to whom the harm is
caused;
(c) if it is done with the intention of causing bodily injury to any person, and
the bodily injury intended to be inflicted is sufficient in the ordinary
course of nature to cause death; or
130
(d) if the person committing the act knows that it is so imminently dangerous
that it must in all probability cause death, or such bodily injury as is likely
to cause death, and commits such act without any excuse for incurring the
risk of causing death, or such injury as aforesaid.
The injuries like tram line bruises over the left arm and back, mucosal contusion
of the lips, bruises on the face, head and chest, the abraded bruises on the shins,
are consistent with non accidental injuries which means that the victim had been
tortured prior to the drowning. The injuries were inflicted to the deceased between
24 hours to five days based on the gross appearance and histopathological
examination.
The history provided by the police revealed that there was a dispute between the
assailants and the deceased with regard to money. The deceased was accused of
stealing his rich uncle’s money by his uncle’s bodyguards but he denied this
accusation. He was tied and hanged by the wrists and ankles for a few days. He
was starved and beaten to get confession to the accusation.
One night, his uncle asked him about the accusation. He denied of the accusation
despite the beating and torture that he had received. According to the police, one
of the bodyguard testified that the uncle instructed them to give the deceased ‘a
bath’, i.e. to throw him into the swimming pool and fish him out repeatedly to
teach him a lesson. They did just that a few times and suddenly realized the
deceased was not breathing. They then rushed the deceased to the nearest medical
center but the deceased was pronounced dead on arrival.
The police requested opinion whether the postmortem findings support the above
said information. We are in the opinion that, the injuries found on the deceased
body were in concordance to the history, i.e. signs of being tortured within a few
days.
There was no question about the cause of death, i.e. drowning. However, whether
the deceased was repeatedly thrown into and fished out from the pool, prior to his
drowning is very difficult to be established. We compare the signs found in the
deceased in this case with other cases. We found the deceased had very much less
persistent whitish froth coming out from the nostrils and mouth compared to other
cases of fresh water drowning (fig. 6 and fig. 7). Furthermore, the deceased had
only thin film of fluid in his stomach (almost empty). The deceased had no natural
disease that could have caused or accelerate his death at that particular moment in
time.
Assuming the deceased was still strong while being tied at wrists and ankles, and
accidentally fell into the pool while trying to escape from the assailants, the
deceased will struggle vigorously to avoid drowning. This will lead to plenty of
131
fresh water entering the lungs and the stomach. The deceased will show
significant amount of persistent whitish froth coming out from the nostrils and
mouth as the victims in fig. 6 and 7. Furthermore, the deceased will have
significant amount of the pool water in his stomach at the time of death.
Fig. 6: Persistent whitish froth coming out from the nostrils and mouth of a victim
of fresh water drowning.
Fig. 7. Persistent whitish froth coming out from the nostrils of another victim of
fresh water drowning.
However, if the deceased was repeatedly thrown into and fished out from the pool
with both wrists and ankles tied, he will be in sheer exhaustion prior to drowning.
There will be small amount of fresh water entering the lungs and stomach but the
water will be entering the circulation repeatedly which lead to fluid and
132
electrolytes derangement as well as interstitial space disruption and oedema.

When this is done repeatedly, it will mimicked the changes of near drowning in
the deceased person. However, the deceased can be fully drowned if the repeated
immersion was not stopped, i.e. when he was found not breathing by the
bodyguard as in this case.
From these findings we made the conclusion that the postmortem findings were in
concordance to the history given by the bodyguard. We believe the assailants
know that their action is likely to cause death to the deceased and/or is sufficient
in the ordinary course of nature to cause death to the deceased as for the
interpretation of the Section 300 of the Penal Code. Therefore we concluded that
the cause and manner of death as: “Homicidal drowning”.
According to the police, there were independent witnesses to this tragedy. They
were the driver and a maid who live in the house.
Discussion
The investigation of drowning by the pathologist can be difficult. His role is to

determine whether the findings are consistent with accident, suicide or homicide.
That can be complicated if the drowned bodies have decomposition changes.
However in many instances evidence from other sources helps to resolve the
matter.
Peter Pullar stated that in our forensic practice it is helpful to consider the
possibilities under two main heading3. (1). Cases with signs of drowning. (2).
Cases with no signs of drowning. These two groups can be conveniently divided
into (a).cases without injury and (b) cases with injuries.
Cases with signs of drowning without injury can be – the deceased entered the
water voluntarily, or involuntarily while under the influence of alcohol or drugs,
or because of natural diseases such as ischaemic heart disease, epilepsy, etc…
Cases with signs of drowning with injuries can be – the deceased was injured by
another person or persons and put into the water while unable to save himself
there by drowning or the injury did not involve another person and were caused
when the deceased struck some projection or object while entering or in the water.
Cases without signs of drowning without injury can be – possibility of death

occurring in the course of immersion rather than classical drowning.
Cases without signs of drowning with injuries can be – the deceased may have
fallen into the water after a collapse from natural causes, the injuries being
sustained at that time. Alternatively death may be due to violence and the body
was disposed of by immersion.
133
It will be clear from this that the pathological investigation of such cases is
difficult and it must be agreed that this is an area of forensic practice in which the
pathologist is unable to give an opinion which is sufficiently positive as to satisfy
the requirements usually demanded in medico-legal investigation.
Again in the vision of law enforcement personnel, the first thought as respond to a
drowning incident is probably that there has been a tragic accident. Even though
all drowning cases should be considered possible homicides until proven
differently, very often the responding officer is already in the mindset of
accidental death. Ever since we were children we have thought of drowning as
accidental; we were trained to automatically think of drowning as accidents.
Everyone has heard of someone who died in a drowning accident. We read about
drowning accidents in newspapers and books, we watched them on television and
in movies, and we were trained how to manage and prevent them in water safety
and rescue courses. Part of the reason we think about drowning as accidental is
because we tend to think of water for recreational activities. That was not always
the case.
We are perhaps quick to perceive homicide when victims recovered from water
have a gun shot wound in their head, have a stab wound on the body, bricks tied
to their body, or when the obvious, available witness information is not making
sense. For the most part autopsies generally do not look for much more than to
prove that the victim did die of drowning. We have to look deeper into the
situation surrounding suspicious death or accidents. When asked, the average
police officer does not think of a drowning as suspicious unless there are other
visible circumstances. The FBI has made statements as long as ten years ago that
they believed that not all drowning were accidental. However in basic law
enforcement this concept has not been well shared or expanded upon.4
Unintentional injury is the number one leading cause of death in children and
adolescents in United States5. One adolescent dies every hour as the direct result
of injury.5 In Wisconsin, the number of deaths due to unintentional injury for
those age 15 to 24 years exceeds the number of deaths from all other causes
combined.6 Drowning is a significant injury problem among adolescents. From
1993 to 1995, more than 3100 teens and young adults drowned in the United
States, which makes drowning the second leading cause of unintentional death in
those under age 20 years.6 Water submersion is a lethal injury for teens. 30% to
50% of pediatric victims die following a submersion injury.7
Several risk factors are associated with adolescent drowning. One factor is the
increase in risk-taking behavior that occurs during adolescence. Teens dare each
other to swim further, dive deeper, stand up in a canoe or indulge in other
behaviors that increase the risk of drowning.8 Failure to use life vests while
134
swimming and boating contributes to adolescent drowning. Only 13% adolescents

routinely wear a life vest.7
Some teen drowning deaths are associated with hyperventilating before attempting
to swim long distances under water. This practice is extremely dangerous because
this hyperventilation causes an increase in arterial oxygen, a rapid fall in carbon
dioxide level that can result lack of stimulus to breath, in a reduced cerebral blood
flow leading to loss of consciousness in water which usually leads to death.3
Alcohol contributes significantly to teen drowning. Adolescents frequently

combine water activities with alcohol. Up to 50% of adolescents who drown have
a positive blood alcohol level.7 males are a high-risk population for drowning.
Male adolescents are 6 times more likely to drown than female adolescents.7 For
unknown reasons, African American males have a much higher risk of drowning
than white males.9
Teen with epilepsy constitute a high risk for drowning. Children and adolescents
with seizure disorders have a 13-fold increase in risk of drowning.7 All teens
should be warned never to swim alone, but this point should be strongly
emphasized to patients with epilepsy and their parents.
Conclusion
The investigation of the drowning by the pathologist can be difficult. Our role is
to determine whether the findings are consistent with accident, suicide or
homicide. That can be complicated however every effort must be made to reach
the correct conclusion. However the solution to an unnatural or suspicious death is
seldom reached by one discipline working in isolation. The drowning cases
exemplify the importance of objective cooperation between the pathologist and
the law enforcement authorities in achieving the end.
135
References
1. Pekka S, Bernard N. Immersion Death: Knight’s Forensic Pathology; 3rd

ed. London: Arnold. 2004; Chap16: 395.
2. Davis J. Bodies found in the water: an investigative approach. Am J
Forensic Med Pathol: 7; 281-7.
3. Peter P. Mechanical asphyxia: Taylor’s principles and practice of medical
jurisprudence; editor AK Mant. Churchill Livingstone, 1984. 13th ed;
Chap13: P 300-2.
4. Hendrick W. Drowning continues to hold it’s unprecedented position in
the top two causes of accidental death to children in the United States.
Sortie Publication Inc.2003.
5. Runyan CW, Gerken EA. Epidemiology and prevention of adolescent
injury: A review and research agenda. JAMA, 1989; 262: 2273-79.
6. Center for disease control and prevention: Ten leading causes of death in
United States 1993-95. National Center for Injury Prevention and Control,
Atlanta GA; 2000.
7. Quan L. Near drowning. Peds in Review. 1999; 20: 255-59.
8. Rivara FP. Where Do We Go From Here?: Pediatric Injury Control in
1999. Pediatrics 1999; 103: 883-88.
9. Gwen M. Fatal injuries in adolescents. Wisconsin Med J: Dec 2000;
99(9):34-8.
10. Section 300, Chapter XVI, Penal Code (Act 574). International Law Book
Services (May 2000), Kuala Lumpur. p13
136
CASE REPORT
Accidental fatal fall of a psychiatric patient from a psychiatric
ward
Faridah MN, Zarida H,* Shahrom AW
Forensic Unit, Department of Pathology, Faculty of Medicine, UKM, Malaysia.

Malaysia.*
Abstract
This is a case report of a 23-year old female patient, who had escaped from a
psychiatric ward, and fell from the hospital building. The pattern of injury is
described in relation to the impact of the fall. Some other injuries are also
described in relation to her acts of escape through a window in the toilet to the
exterior part of the building. The manner of death is discussed with regards to the
postmortem findings, as well as, investigations at the scene of death.
Keywords: psychiatric ward, hospital building, impact, manner of death.
Address for correspondence and reprint request: Dr Faridah bt Mohd Nor, Forensic Unit,
Department of Pathology, Medical Faculty, Universiti Kebangsaan Malaysia, Bandar Tun Razak
56000 Kuala Lumpur, Malaysia.
Tel:03-91702354, Fax:03-91711673, e-mail:mnfaridah@yahoo.com
Introduction
Falls from a considerable height of a building, are more common in suicide and in
accidents than in homicide.4 These falls have been reported to be high in
incidence in children (ibid). However, Goonetilleke (1980) documented that the
incidence of suicidal falls involved females is higher in the second and third
decades, while the incidence of suicidal falls involved males is higher in the sixth
and seventh decades.2 Goren et al. (2003) reported that females had a higher
suicidal rate than males, and the majority of accidental falls occurred at home
rather than at workplace.3
Older age group was found to be significantly associated with self-destructive

acts, which are more determined, and usually involve less violent methods. They
have less warnings of suicidal intent.5 Perret et al. (2006) found that the incidence
137
in suicidal rate among young people of less than 25 years of age from 1993 to
2002 in Geneva, Switzerland, was on the average of 11/100,000 per annum.
Seventy-seven percent were male, and 23% were female.7 The youngest victim
was 14 years old, and most victims were 18 years old and over (89%). For men,
the use of firearms was the most common method (38%), followed by fall from
height (16%) and drowning (10%). For women, fall from height was the most
frequent (40%), followed by firearms and medication overdoses (20% each),
hanging (13%) and drowning (7%) (ibid).
The impact may occur due to primary or secondary impact on landing. The
primary impact is usually the most severe injury.4 The mechanism of impact
however, varies in different scenarios. It depends on whether the person falls or
jumps from a height. The trajectory is usually downwards and outwards, and the
distance that the body strikes the ground from the jumping point is variable. The
body may turns and twists in an unpredictable manner, which depends on the
height of the fall and the time available for turning (ibid).
We report this case to share our experience in investigation of such a case, i.e. fall
from a height. The determination of the manner of death requires a detail
postmortem examination and thorough investigation of the scene, before
conclusion of the manner of death can be made.
Case Report
A 23-year old female was found dead on a patio behind a hospital. She was
thought to be a psychiatric patient who has fallen from the Psychiatric Ward on
the third floor of the hospital. According to the ward staff, she was last seen in the
toilet at about 5.00 a.m., after which she was completely missing from the ward
for the next two hours.
Follow-up of the case

The investigation of this case, requires two scene visits, i.e. the scene of death and
the suspected site of the fall (the toilet in the ward on the third floor of the
building). These visits were essential to ascertain the manner of death of the
deceased.
a. Visit to the scene of death

We were shown to the scene of death by the police. At the scene we found an
adult female body, fully clad in a pair of long pants and a blouse. She was lying
face down on the patio, near a small gutter. Her face was covered with blood.
Both arms and right leg were in flexed position. There was no intermediate
138
structure present along the pathway of the fall. The patio was covered with big
square tiles next to a small gutter, near the building.
The body was transferred to the mortuary after being examined and photographed
by the police.
b. Visit to the suspected site of fall

On inspection of the toilet on the third floor of the building, we found windows
were located high above the head level, which were covered with metal grills. The
grill hole measures 27.5cm by 19cm. There were some dirt wiping marks on the
surface of the window grill. These marks were consistent with those caused by the
deceased squeezing herself through the window grill.
Fig. 1: The toilet windows opening where the deceased was believed to have
fallen from.
Postmortem examination
Postmortem examination revealed that she sustained a severe head injury, fracture
of the distal left radio-ulna, fracture of the right patella and multiple abrasive-
contusions on the abdomen, anterior aspect of the arms and legs bilaterally. There
were some abrasive-contusions on the upper back, lateral aspect of bilateral
shoulders, central back and bilateral gluteal regions.
139
Internal examination showed comminuted fracture of the frontal, left parietal,

right temporal and right occipital bones, with contusion-laceration of the frontal
lobes and a generalised subarachnoid haemorrhage. There were also lacerations of
the right lobe of the liver and the hilum of the right kidney.
Fig. 2: The deceased with head injury and fracture of the distal left radio-ulna,
fracture of the right patella and multiple abrasive-contusions on the abdomen,
anterior aspect of the arms and legs bilaterally.
Fig. 3: The downward direction (arrow) of the graze on the abdomen.
140
Opinion and conclusion
On external examination, there were two patterns of injury noted i.e. injuries on
impact with the ground, and injuries due to squeezing through the window grill.
She had a severe head injury, fracture of the distal left radio-ulna, fracture of the
right patella, and abrasive-contusions on the anterior aspect of the arms and legs
bilaterally, as a result of an impact with the ground surface. The head fracture was
caused by an impact on the left supero-lateral side of her body onto the ground
surface.
She also sustained fracture of the right patella, which indicated an evidence of
flexion of the right knee. She had fracture of the distal left radio-ulna, which
indicated an evidence of hyperextension of the left forearm during her attempt “to
brake” the fall. The injuries due to squeezing through the window grill were
shown by the abrasive-contusions on the upper back, lateral aspect of bilateral
shoulders, central back and bilateral gluteal regions.
From the measurements of the window grill, which measures 27.5 by 19 cm, it
was shown to be large enough to accommodate the deceased body. By
comparison, the deceased were measured over the head, shoulder and hip, the
bony landmarks thought to be relevant to explain her body passage through the
window grill. Her head measured 19 by 16 cm, her shoulder measured 34 by 17
cm, and her hip measured 28 by 17 cm. From these measurements, it was
concluded that it was possible for the deceased to pass through the window grill
with some difficulty, as shown by the abrasive-contusions on her body especially
the abrasion on her abdomen with the downward direction of the graze (Fig. 3).
Internal examination showed laceration of the right lobe of the liver and laceration
of the hilum of the right kidney caused by the deceleration impact from the fall.
From the suspected site of fall to the site of death, the fact that she was found
about 4 metres away from the site of fall gave some indications to the manner of
death. The evidence indicated that she had climbed up the toilet window,
squeezed herself through the window grill (wiping marks were evident), and
traveled about 4 metres away from the window grill to the right side of the
building. While clinging and trying to climb to the other ledge, she had slipped
and fell down.
In conclusion, both the scene examination and postmortem findings had clearly
indicated that she was trying to escape from the ward through the toilets window
and accidentally fell to her death. We concluded that the cause and manner of
death was due to severe head injury consistent with an accidental fall from a
height.
141
Discussion
Fatal falls can occur in many ways depending on the height from where the body
falls. If the body falls on to the head, a massive fracture along with a scalp
laceration may result, and sometimes, extrusion of the brain matter.4 Fracture of
both the vault and base of skull can occur. The base of skull may be compressed
against the cervical spine, and the cervical spine may be driven into the base of
skull. The latter injury is more common with high rise falls onto the feet, which
causes the classic ‘ring fracture’ of the occipital bone. This happens when the
impact is transmitted up the spinal column, and the upper vertebrae along with a
ring of bone around the foramen magnum are forced into the skull. In this case,
she sustained severe head injury with comminuted fracture of the frontal, left
parietal, right temporal and right occipital bones, and contusion-laceration of the
frontal lobes and generalised subarachnoid haemorrhage. These injuries were
consistent with those of impact on her left supero-lateral side of the head onto the
ground surface, resulting in the head fracture.
Where falls occur onto the feet, this can cause a deceleration force to be exerted
on the axial skeleton. The latter may break at several points. Tibial or femoral
bones may be broken, often bilaterally. The pelvis, hip joints and femoral necks
may fracture and dislocate. The sacroiliac joints are most vulnerable, and an
upward force may force the sacrum into the pelvis (ibid). The transmitted force
may also fracture the spine, at mid or upper thoracic level. If the falls occurs onto
the side of the body, several combinations of injury may occur. Shoulder girdle,
arm and rib fractures may occur. Lacerations of the back and buttocks may also
occur. Severe abdominal injuries with rupture of the liver, lungs, heart or spleen
may sometimes occur (ibid.) In this case, superficial and multiple abrasive-
contusions were found on the anterior aspect of the arms and legs bilaterally.
Fracture of the distal left radio-ulna and fracture of the right patella were also
present. Additionally, there were laceration of the right lobe of the liver and
laceration of the hilum of the right kidney.
The manner of death in this case was ‘thought to be quite straightforward’ in the
first instance. It was quite usual to consider the manner of death in this case as a
suicide; particularly that she was a psychiatric patient and had escaped from a
psychiatric ward. However, further investigation revealed no evidence to indicate
suicide. For instance, no suicidal note was left behind, no signs or history of
frustrations, no signs of preparation beforehand, no other methods of suicide used,
and finally, no other fatal self-infliction injuries (other than due to the fall) were
present.
142
Homicidal death was quite remote in this case as there were no sign of struggle in
the toilet. There were no sign of blood stain in the toilet either to indicate if there
was any involvement of a second or a third person, leading to the person’s death.
Accidental death was suitably considered in this case. The fact that she had
slipped and fell from the building was a clear indication of an accidental death.
The escape mechanism, as shown by the wipe marks on the window grill
(deliberate action by the deceased), was a corroborative finding of this case.
In brief, this case has shown that a correct conclusion can only be reached if all
the experts (the forensic pathologist, crime scene investigator and the police
personnel) work as a team, and discussion of the case is vital to come to a correct
diagnosis.
Jumping from a general hospital has been the most common means of suicide. In
a study done by White et al. (1995)8 in 12 subjects between January 1980 and
January 1992, who jumped from a large general teaching hospital, eight of them
succumbed, which gave a suicide rate of 1.7 per 100,000 admissions. There were
three clinical subgroups in these jumpers: those admitted for suicide attempts, the
acutely delirious and the chronically medically ill patients. The predominant
factors appearing in the third subgroup were pain, dyspnoea, confusion, poor
prognosis, and recent adverse news. It was also found that the proximity and ease
of access to balconies and windows appeared to be highly relevant to the
prevention of hospital jumping.8
The cause for prevention of such circumstances happening again is important to

raise here, as patients are increasingly being admitted to the wards for various
illnesses, and those who are admitted on temporary basis, may undergo temporary
depression.6 The medical staff should be sensitive to the possibility of suicide in
their patients, as the social difficulties, and the sense of helplessness and
uselessness can be over-whelming, and a good doctor-patient relationships is
essential to overcome any difficulties encountered by the patients.1 Measures for
the psychological support and rehabilitation of such patients should be
emphasised. Perhaps, a special committee should be set up to cover several
aspects of care of patients such as to review cases of psychiatric patients,
considers improvements in the hospital design, and facilitates communication
between nursing staff and physicians sponsor educational programs for the staff.6
143
References
1. Brown W and Pisetsky JE. Suicidal behavior in a general hospital. American
Journal Medicine 1960; 29 (2): 307-315.
2. Goonetilleke UKDA. Injuries caused by falls from heights. Med Sci Law
1980, 20 (4): 262-275.
3. Goren S, Subasi M, Tyrasci Y and Gurkan F (). Fatal falls from heights in and
around Diyarbakir, Turkey. Forens Sci Int 2003, 137(1): 37-40.
4. Knight B (1991) Forensic Pathology. Edward Arnold: London: 162-163.
5. Conwell Y, Duberstein PR, Cox C, Herrmann J, Forbes N and Caine ED. Age
differences in behaviors leading to completed suicide. American Journal
Geriatric Psychiatry 1998; 6: 122-126.
6. Litman RE and Farberow NL. Suicide prevention in hospitals. Humanities,
Social Sciences and Law and Medicine 1965; 10 (1): 488-498.
7. Perret G, Abudureheman A, Perret-Catipovic M, Flomenbaum M and La
Harpe R. Suicides in the young people of Geneva, Switzerland, from 1993 to
2002. Journal Forensic Science 2006; 51(5): 1169.
8. White RT, Gribble RJ, Corr MJ and Large MM. Jumping from a general
hospital. General Hospital Psychiatry 1995; 17(3): 208-215.
144
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Vol. 2 No.

The Malaysian Journal

A peer reviewed journal dedicated

The Malaysian Journal of

INTERNATIONAL EDITORIAL BOARD

Shahrom AW, Swarhib MS, Azuriah AA, Zarida H, Aznool HA

Forensic Medicine in Greece: Modernizing and updating the

Michalodimitrakis M, Kranioti EF, Mylonakis PP, Mavroforou AJ.

Department of Forensic Sciences, University of Crete Medical School, Heraklion,

Development of Forensic Medicine in order to cover all aspects of forensic

Keywords: Forensic Medicine, forensic systems, Greece, forensic training,

The characteristic feature of forensic medicine in Europe is that the investigation

initiated and marked a common point of abandonment of the continental European

The ideas of Voltaire, Montenieu, Rousseau, Lock, Montesquieu, Thomasius,

Under the continental European system there is no identifiable medico-legal

The Greek Legal System

In Greece the law pertaining to criminal investigation procedures has always

Organization of Forensic Medicine

The formal operation of forensic medicine in Greece is encountered mainly in

the Department of Forensic Sciences of the University of Crete in Heraklion and

The Departments of Forensic Medicine at the Universities of Athens and

Teaching and Specialization

The specialization in forensic pathology leads to an official license after taking

Ministry of Health and Education as a separate field of medical specialization

Training involves three years of postgraduate study in the Departments of

Practice of Forensic Medicine

Athens is served simultaneously in the same territorial jurisdiction by two

In almost all Forensic Medicine Departments of Universities and State Services

Generally speaking there is an underlying tendency in practice of forensic

The Department of Forensic Sciences at the University of Crete has successfully

Death investigations in Greece consist mainly of sudden natural deaths, traffic

Proposal for updating

Because of the inadequacy of training and practice in forensic pathology in

develop at least units of forensic toxicology, forensic genetics and forensic

1. Muller G, Le Pool-Griffiths F. Comparative Criminal Procedure NYU

8. Michalodimitrakis M, Tsakalof A: The practice of forensic medicine in

Female deaths due to cardiac causes in Malaysia : 10

OP Murty, Seng LK, Nuraeiniza I, Chee AS, Syahir BM

Forensic Pathology Unit, Department of Pathology , Faculty of Medicine,

Keywords: Cardiac deaths in females; sudden death in females; heart ; coronary

Address for correspondence and reprint request: Dr.O.P.Murty, Additional Professor,

Different patients may give different kinds of histories. Some describe

Materials and Methods

This is a retrospective study of last 10 years at University Malaya Medical Centre,

Out of 83 cases, majority were Chinese with 37 cases (44.6%), followed by

From 83 cases, 55 of them were married women (66.3%). This is followed by 19

Out of 83 cases, 25 cases (30.1%) were housewives, followed by skilled workers

Fig. 1 : Age distribution of the cases

N/B: Others = Singaporean, Philippines, Iraqi, Thai American.

Fig. 2 : Ethnic distribution of deceased female due to cardiac death

Fig. 3 : Marital status of the deceased female due to cardiac death

An obstruction of more than 75% of blood vessel lumen in coronaries arteries is

Fig. 4 : Occupation status before death

BODY WEIGHT (KG)

Fig. 5 : Body Weight distribution of the cases

congestive heart fai 3

Fig. 6 : Causes of death and their incidence in this study

Table 1 : Narrowing in % of coronary arteries due to atherosclerosis in the

Lumen size Right Left anterior Left Aorta

Normal 46 (55.4%) 35 (42.2%) 57 (68.7%) 54 (65.1%)

Total 83 (100.0%) 83 (100.0%) 83 (100.0%) 83 (100.0%)

Aggravated suicidal responses to police arrest

Shahrom AW, Zarida H*, Anisah CN,Md Rizal AR