Parikh 's

Textbook of

Toxicology
for Classrooms and Courtrooms
Seventh Edition

PubathenftCxsMtHJton
36. Introduction and Law Relating to Poisons
37. Toxicological Evidence
38. Common Household Poisons
39. Mineral Acids and Caustic Alkalis
40. Organic Acids
41. Vegetable Acid Poisons
 Introduction and
Law Relating to Poisons
INTRODUCTION_________________________
Many Western textbooks devote only a
smallpart of their text to clinical and forensic
toxicology. In some parts of the world, such
asSouth East Asia, Africa, and the Indian
subcontinent, many poisons, such as acids,
alkalis, phenols, arsenic, antimony, madar,
powdered glass, dhatura, oleander, strych­
nine, aconite, etc., that produce obvious
lesions, are still being used. They are easy
todetect, both clinically and at autopsy. In
the West, pharmaceutical substances,
agrichemical substances, and medicinal
preparations, active in low dosage, are now
being used as poisons. Most of these sub­
stances do not produce any gross or even
histological changes in the body, and are,
therefore, difficult to detect. This section
includes commonly used substances both
intheWest and in other parts of the world.
Accordingly, it would appear long to the
reader. However, the use of this book on
aninternational basis has necessitated such
indulgence. Study of poisons helps the
practitioner to manage poisoning cases
brought to him in day-to-day practice. The
natureof poisons varies from place to place
and depends on availability, accessibility,
occupation, etc. Common poisons are of
plants, animals or chemical origin. Their
actions vary depending on the dose, route
andhealth of the person consuming.
Q. 36.1. Define toxicology. Give the legal
definition of poison.
Toxicology deals with the effect of toxic
substances on the body when administered
by any route. Poisons are substances which
are deleterious or injurious to the body
leading to disease, deformity or death or
illness, infirmity or death.
Toxicology is the science which deals
with poisons with reference to their sources,
properties, mode of action, symptoms
which they produce, lethal dose, nature of
the fatal results, treatment, methods of their
detection and estimation, and autopsy
findings. It is also concerned with law
regarding their sale and prescription.
Forensic toxicology deals with the medical
and legal aspects of the harmful effects of
poisonous substances on the human body.
Sections 284, 299, 300, 304A, 324, 326, and
328 IPC deal with offenses relating to
administration of poisons.
A poison is a substance which, when
administered, inhaled or ingested, is
capable of acting deleteriously on the
human body. Thus, almost anything is a
poison. There is really no boundary
between a medicine and a poison, for a
medicine in a toxic dose is a poison and a
poison in a small dose may be a medicine.
In law, the real difference between a
medicine and a poison is the intent with
which it is given. If the substance is given
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
with the intention to save life, it is a
medicine but if it is given with the intention
to cause bodily harm, it is a poison.
Toxinology is the science which deals with
toxins produced by plants, animals,
bacteria, and fungi, which are harmful to
man.
Q. 36.2. Briefly discuss the important provi­
sions regulating the control of drugs in
your country.
In India, these are: (1) the Drugs and
Cosmetics Act, 1940 and the rules made
thereunder, and (2) Narcotic Dugs and
Psychotropic Substances Act, 1985.
1. Under the Drugs and Cosmetics Act,
1940, a cosmetic means any article
intended to be rubbed, poured, sprinkled
or sprayed on, or introduced into, or
otherwise applied to, the human body
or any part thereof for cleansing,
beautifying, promoting attractiveness or
altering the appearance, and includes
any article intended for use as a
component of cosmetic but does not
include soap. The Act has been further
amended by Drugs (Amendment) Act,
1964 (13 of 1964) to include Ayurvedic
and Unani drugs. The main aim is to
control quality, purity, and strength of
drugs. The label or container of medicine
should display the formula or a list of
ingredients contained in the drug. The
Act provides stringent punishment in
respect of offenses concerned with drug
adulteration.
Under the Drugs and Cosmetics Rules,
1945, the drugs are classified in certain
schedules, and regulations are laid
down for their storage, display, sale,
dispensing, labelling, prescribing, etc.
Schedule H and L drugs are required to
be labelled with the words "SCHEDULE
H DRUG" and "SCHEDULE L DRUG",
Warning — To be sold by retail on the
prescription of a registered medical
practitioner only. The prescription shall
mention the name and address of the
person for whose treatment it is given.
Any such prescription must be com­
pounded in the authorised premises
(chemist's shop) only by or under the
supervision of a qualified pharmacist
and must not be dispensed more than
once unless specifically asked for. At the
time of dispensing, a note should be
made of the name and address of the
patient, the date on which the prescrip­
tion is dispensed, the serial number
under which it is entered in the register
(in case of poisons), the batch number,
and the date of expiry of potency. In
addition, the poisons are subject to the
following regulations:
a. A person must possess a license to
stock, sell or distribute poisons listed
in the rules.
b. The supply of listed poisons must be
entered in a register which must be
maintained for this purpose.
c. These poisons must be kept in autho­
rised premises only in a cupboard or
drawer reserved solely for this
purpose and to which customers are
not permitted to have access.
d. They must be kept in leakproof
containers labelled with the word
"poison" in red letters.
e. Certain poisons are not allowed to be
kept in more than the given concentra­
tion while others have to be coloured.
2. The Narcotic Drugs and Psychotropic
Substances Act, 1985, prohibits cultiva­
tion, manufacture, possession, sale,
purchase, transport, import, export, etc.,
of these drugs and substances except for
m edical and scientific purposes as
provided in the Act.
Narcotic drugs covered under the Act are:
(a) cannabis (hemp), (b) coca leaf, (c) opium,
and (d) any other narcotic substance or
preparation which the Central Government
may declare to be a manufactured drug.
 Introduction and Law Relating to Poisons
A psychotropic substance, according to the
Act, means any s u b s ta n ce , n a tu ra l or
synthetic, or any natural m aterial or any
salt or preparation of such substance or
material, specified in the scheduled list of
77 psychotropic substances, w hich include
substances, like cannabis, am phetamines,
tranquillisers, LSD, etc. The Act views the
addict with sym pathy, and m akes some
special provisions in this regard.
Narcotic drugs and psychotropic sub­
stances are also subject to stringent national
and international control in all countries.
The Convention on N a rc o tic D ru gs is
applicable to drugs, such as opium, opium
alkaloids, coca and coca alkaloids, cannabis
and its products, and synthetic drugs, such
as pethidine, etc. T h e c o n v e n tio n on
Psychotropic Substances is applicable to
substances, such as h allu cin og en s, like
LSD; stim u lan ts, lik e a m p h e ta m in es;
hypnotics, like secobarbital, methaqualone;
and tran q u illisers, lik e m ep rob a m a te,
diazepam, etc.
The aim of all these regulations and acts
is to: (a) control manufacture, storage, distri­
bution, sale, dispensing, and im port-export
of drugs, (b) penalise people for possession
and use of certain d ru gs, (c) m aintain
quality of drugs, (d) com pel the manufac­
turers to list d ang ero us in gred ien ts in
patent medicines, and (e) prevent cases of
addiction and poisoning,
Q. 36.3. W rite short n o te s on : (1 ) h u m a n
poisoning, (2 ) c a ttle p o is o n in g .
Human p oison in g: The circum stances may
be suicidal, h o m ic id a l, stu p e fy in g , or
accidental.
The poisons used for suicidal purposes
are: potassium cyanide, hydrocyanic acid,
opium, barbiturates, organophosphorus
compounds, and oleander, etc., according
to availability and use in the particular
place. A suicidal poison o f choice m ust be
cheap, easily available, and capable of
being administered in any food or drink. It
509
must have a pleasant taste and no repulsive
smell. The lethal dose should be small, and
the lethal period short and preferably
painless.
The poisons used for homicidal purposes
are: arsenic, antimony, aconite, thallium,
organophosphorus compounds, oleander,
madar, strychnine, powdered glass, rarely
insulin and other drugs, and very rarely
cultures of disease germs. Opium is some­
times used to kill children. An ideal homicidal
poison should be cheap, easily available,
colourless, odourless, and tasteless. It must
be capable of being administered in any
food, drink, or drug without arousing any
suspicion. The symptoms should resemble
any natural disease or serious illness. The
lethal dose should be small and the lethal
p eriod su fficiently lo ng to p erm it the
poisoner to escape safely and not to arouse
any suspicion thereafter. There should be
no an tid ote and no p o ssib ility o f its
detection either at autopsy or by laboratory
m ethods. In som e countries, death by
homicidal poisoning is more common than
violence because bloodshed is considered
to be a more brutal crime than poisoning.
The poisons used for stupefying purposes
are: alcohol, dhatura, cannabis indica, and
cigarettes containing arsenic, dhatura or
cannabis. In the West, and occasionally in
India, chloral hydrate mixed with alcoholic
beverage is sim ilarly used. The latest
addition to this is Rohypnol (Roche).
Accidental poisoning commonly takes
place as a result of: (1) carelessness in
sto ring p oisonous and non -p oison ou s
m aterials together, (2) quack rem edies,
(3) bites by poisonous anim als, such as
snakes and scorpions, (4) greater use of
chemicals in industry and for household
purposes, and (5) putting poisonous sub­
stances in food containers.
C a t t le p o is o n in g : C a ttle p o iso nin g is
generally resorted to by cobblers for the
 510 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

sake of hides. Rarely, cattle are destroyed capsicum, semicarpus anacardium (marking
by owners when they are useless. The nut), calotropis (madar), and plumbago
poisons used to destroy cattle are: abrus rosea (lal chitra) and plumbago zeylanica
precatorius, arsenic, yellow oleander, and (chitra). The animal poisons include cantha-
parathion. Sometimes, aconite, madar, nux rides, snakes, scorpions, spiders, and
vomica seeds and snake venomare also used. poisonous insects.
Mechanical: The mechanical subgroup
Q. 36.4. Classify poisons according to their
includes coarsely powdered glass, chopped
mode of action. Add a brief note on each
hair, dried sponge, and diamond dust.
group.
Neurotics: Neurotic poisons act chiefly on
According to their mode of action, poisons
are classified in six groups, viz: (1) corro­ the nervous system though some neurotics
sives, (2) irritants, (3) neurotics, (4) cardiac, have a local irritant action. All alkaloidal
(5) asphyxiants, and (6) miscellaneous. poisons fall into this group. The chief
symptoms in general are usually headache,
Corrosives: A corrosive poison is simply a drowsiness, giddiness, delirium, stupor,
highly active irritant and not only produces coma, and sometimes convulsions or
inflammation but also actual ulceration of paralysis, though individual poisons may
the tissues. This group consists of strong have characteristic effects. Postmortem
acids and strong alkalis. These include examination usually does not show any
mineral acids, such as sulphuric acid, nitric marked changes on naked eye examination
acid, hydrochloric acid; organic acids, such and the cause of poisoning has to be
as oxalic acid, carbolic acid, acetic acid, inferred from the history and symptoms or
salicylic acid; vegetable acid, as for example, from the result of analysis of the viscera.
hydrocyanic acid; and concentrated alkalis,
This group consists of poisons which
such as caustic soda, caustic potash, and
have specific action on the cerebrum, spinal
carbonates of ammonium, sodium and
cord, and peripheral nerves, the poisons
potassium.
being known as cerebral, spinal, and
Irritants: Irritant poisons produce symp­ peripheral, respectively.
toms of pain in the abdomen, vomiting and Cerebral: The poisons acting on the
purging. The postmortem appearances are cerebrum may have a somniferous, inebriant
usually evident to the naked eye, and show or deliriant effect. The somniferous poisons
redness or ulceration of the gastrointestinal include opioids; the inebriant ones include
tract. This group consists of inorganic, alcohols, anaesthetics, sedatives and hyp­
organic, and mechanical substances. Corro­ notics, fuels, and agrochemical compounds;
sives in dilute solutions act as irritants. while the deliriant ones include dhatura,
Inorganic: The inorganic subgroup belladonna, hyoscyamus, and cannabis indica.
consists of non-metallic and metallic Spinal: The poisons acting on the spinal
poisons. The non-metallic poisons include cord include nux vomica and its alkaloids,
phosphorus, chlorine, bromine, and iodine. and gelsemium.
The metallic poisons include arsenic,
Peripheral:The poisons acting on the peri­
antimony, mercury, lead, copper, thallium,
pheral nerves include curare, and conium.
zinc, manganese, barium and radioactive
substances. Cardiac: These are poisons acting on the
Organic: The organic subgroup consists heart and include digitalis, oleander,
of vegetable and animal poisons. The aconite and nicotine.
vegetable poisons include castor seeds, croton Asphyxiants: These are poisons acting on
seeds, abrus precatorius, colocynth, ergot, the lungs and include irrespirable gases,
 Introduction and Law Relating to Poisons
such as carbon monoxide, carbon dioxide,
sewer gas, and some war gases.
Miscellaneous: As the name suggests,
poisons having widely different pharmaco­
logical actions are put together in this group.
It includes analgesics and antipyretics; anti-
histaminics; tranquillisers; antidepressants;
stimulants; hallucinogens; street drugs; and
designer drugs.
Q. 36.5. Write short notes on: (1) routes of
administration of poisons, (2) action of
poisons.
Routes of Administration
Poisons m ay gain entry into the body by
enteral route, e.g. by mouth or by.rectum,
to be absorbed across the enteral mucous
membrane; parenteral route, e.g. by injection
either in trad e rm al, subcutaneous, intra­
muscular, intravenous, intra-arterial, intra-
peritoneal, intrathecal or into the bone
m arrow; b y inhalation through the air
passages; by external application on wounds,
unbroken skin; introduction into natural
orifices, such as rectum, vagina, urethra,
nose, eyes, subsynovial, intracardiac, etc.
and by sublingual route.
Action of Poisons
The action of poisons may be— (1) local,
(2) remote, (3) local and remote combined,
and (4) general.
The local action results from its direct
action on the part and may cause corrosion
as in the case of strong mineral acids; or
congestion and inflammation as in the case
of irritants. Such poisons generally produce
gross n a k e d eye changes seen at the
postmortem examination.
The remote action is due to absorption of
the poison into the system. It may be either
specific or non-specific. The specific action
depends o n the effect of the poison on
certain o rg an s with which it has special
affinity, e.g. opioids on the cerebral cortex;
strychnine o n the spinal cord; and digitalis
on the heart muscle. Remote action may be
511
localised to a definite organ, e.g. the liver
during detoxication, or kidney during excre­
tion. Certain poisons, such as corrosives, are
capable of producing a remote non-specific
action, such as shock, similar to that which
often results from severe mechanical injury.
Certain poisons, e.g. oxalic acid, carbolic
acid, produce both local and remote actions.
General action results when the absorbed
poison evokes response from a wide variety
of tissues beyond the limits of one or two
systems, e.g. arsenic, mercury, lead, barbi­
turates, paraquat, etc.
Q. 36.6. Discuss the factors which modify
the action of poisons.
These are: (1) dose, (2) form of poison,
(3) method of administration, and (4) condi­
tion of the body.
Dose
As a general rule, small doses produce
therapeutic action; large doses produce
toxic effects. However, there are certain
exceptions to this general rule:
1. Some individuals have an idiosyncrasy
(inherent intolerance) towards certain
drugs and foods resulting in intense
symptoms. This is seen with drugs, such
as morphine, cocaine, quinine, aspirin, and
many others, and certain articles of food,
e.g. mushrooms, eggs, milk, and shell-fish.
2. Some individuals are allergic towards
certain drugs. Allergy means hypersensi­
tivity acquired as a result of previous
administration of the toxic agent or
induced by the simultaneous presence of
another poison. Penicillin is the most
important modern example of acquired
hypersensitivity. Many protective sera
are other examples.
3. Habit diminishes the effects of certain
poisons, since a tolerance toward them is
gradually developed. Such tolerance is
common in the case of alcohol, opioids,
pethidine, and tobacco. It should not be
confused with addiction.
512 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

4. Two poisons, as for example, alcohol and sufficiently soluble by the hydrochl
barbiturates in non-toxic doses, when acid in the stomach, to make the-
administered simultaneously may cause poisonous effects felt. Some substan^
toxic symptoms due to synergism which such as alcohol and barbiturate, in^
means that the final response is greater toxic doses may prove toxic due to
than the sum of their individual actions. synergism.
The effect is called additive, if the final 3. M echanical combination: The action of
response is equal to the sum of their indi­ a poison is considerably altered when
vidual actions. combined mechanically with inert
5. If a poison exerts an emetic effect, a large substances. Alkaloids when taken with
dose may induce violent vomiting and animal charcoal fail to act. Corrosive acids
mitigate the evil effects of a poison. or concentrated alkalis, when sufficiently
Occasionally, a large dose acts differently diluted with-water, act as irritants.
from a small dose of the same poison.
As for example, a large dose of arsenic M e th o d of Adm inistration
may produce death by shock while a
A poison acts most rapidly when inhaled
small dose results in gastrointestinal
in gaseous or vaporous form or when
irritation.
injected intravenously; next, when injected
6. Some poisons, such as arsenic, mercury, intramuscularly or subcutaneously; and
lead, barbiturates, digitalis and carbonleast rapidly when swallowed. There is
monoxide, are eliminated slowly and further slowing of action, if the substance
may accumulate in the body (cumulative ingested is partly soluble, or the stomach
poisons).. Their repeated administrationis full. There is still further slowing ofaction
even in small doses may result in chronic
if the poison is applied to unbroken skin.
poisoning. Certain poisons act differently when they
Form of Poison are introduced through different routes.
Snake venom is highly toxic when injected
Under this heading, the important factors
but is harmless when ingested. Cocaine acts
to be considered are: (1) physical state,
as a local anaesthetic when injected andas
(2) chemical combination, and (3) mecha­
a deliriant and convulsant when ingested.
nical combination.
1. P hysical state: G ases and vapours act C on dition of the Body
more rapidly than fluid poisons. Fluid Under this head, the important factors tobe
poisons act more rapidly than solid ones, considered are: (1) age, (2) state of health,
of which fine powders act more quickly and (3) sleep and intoxication. •V.
than coarse ones. Synthetically coated
pills soluble in the alkaline contents of 1. Age: Poisons have greater effect at the
the small intestine might have their two extremes of age.
action delayed for several hours. 2. State o f health: Persons in poor health
2. Chem ical combination,.-The toxic effects are more susceptible to poisons, e.g. a
of substances may vary greatly from 30% concentration of carbon monoxide
chemical combination. Some substances in blood may kill a person sufferingfrom
become inert, e.g. acids with alkalis; and coronary heart disease. In certaindiseases,
strychnine with tannic acid. Some sub­ the tolerance of the body to certaindrugs
stances become poisonous, such as lead is increased, e.g. hypnotics and opiates
carbonate and copper arsenite which are in mania or delirium tremens, and
insoluble in water but are rendered strychnine in paralysis.
 Introduction and Law Relating to Poisons 513
kcp and intoxication:The bodily func- to ordinary illness. Other persons who have
3< are at low metabolic level during taken similar food, medicine or fluid, are
sleep and intoxication. The action of a also affected similarly and simultaneously.
poison is, therefore, delayed if a person The symptoms rapidly increase in severity
goes to sleep after taking it or if a person and are followed by death or recovery.
is intoxicated when he takes a poison. Poison can be detected in the ingested food,
medicine, and fluid, or vomit, gastric
FAIE OF POISONS IN THE BODY lavage, blood, urine and stool of the victim.
(TOXICOKINETICS)_____________________
C h ron ic p o ison in g : Symptoms develop
Unless the poison is given in a small amount
insidiously and gradually. There is an
and in a liquid state, the greater part of it
exacerbation of symptoms after the suspec­
may be lost by vomiting or diarrhoea. Once
ted food, medicine or fluid is administered.
it is absorbed, the body may deal with it in
There is remission or even complete
one of several ways. It may be excreted
unchanged. Commonly, it will be partly or disappearance of symptoms on the removal
of the patient from his usual surroundings.
completely metabolised, or converted to
another active compound prior to further Poison can be detected in the food, medi­
metabolism (biotransformation). When not cine or fluid which is being administered
or in the vomit, urine or stool of the victim.
completely metabolised, it may be detected
in the original form or in the form of inter­ While the main symptoms in chronic
mediate products in the tissues (e.g. liver, poisoning are usually malaise, and gradual
bile) or the excreta (e.g. urine). Certain deterioration of health, repeated attacks of
tissues, such as the epi-dermis, nails, hair, undiagnosed gastrointestinal irritation should
and bones, may retain inorganic poisons, arouse suspicion of homicidal poisoning.
such as arsenic, after it is eliminated from
the rest of the body, and the bony skeleton Poisoning in the Dead
may hold such poisons as arsenic, lead, and The evidence of poisoning will depend on:
radioactive isotopes for long periods. (1) postmortem examination, (2) chemical
analysis, (3) experiments on suitable
Q 7 /. How will you diagnose a case of animals, and (4) moral and circumstantial
poisoning? evidence. Poisons retard the action of
To diagnose poisoning, it is essential that putrefactive organisms to some extent. In
one should be familiar with the outstanding a number of cases, therefore, the bodies are
symptoms and signs of poisoning in the comparatively well preserved.
living persons together with its effects as P ostm ortem exam ination: This should be
found in the examination of the dead. carried out in the manner already described
in the Chapter 5 on 'Medicolegal Autopsy'.
Poisoning in the Living
The smell from the clothes and body, froth
The evidence of poisoning depends upon at nose and mouth, stains about the lips and
whether the poisoning is acute or chronic: chin, colour of skin and postmortem lividity,
Acute poison in g: Symptoms suddenly marks of injection, and condition of natural
appear soon after the suspected food, medi­ orifices may help to diagnose poisoning.
cine or fluid has been taken, although in The alimentary system should be examined
bacterial food poisoning, the symptoms very carefully since signs of corrosives and
may be delayed. The person, previously irritant poisons are likely to be found
known to be in good health, is affected with therein. These signs may manifest as hyper-
a group of symptoms which do not conform aemia, softening, ulceration, and perforation.
 514 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Chemical analysis: The most important
proof of poisoning is the analytical detec­
tion of poison in the parenchyma of the
organs of the body. The finding of poison
in the food, medicine or fluid, alleged to
have been taken, is corroborative. However,
clinical and postmortem findings form a
clinging evidence in cases where CA is
negative.
Experiments on suitable animals: The sus­
pected food, medicine or fluid, or the poison
extracted from the viscera, can be fed to
domestic animals, such as the dog and cat.
These animals are affected by the poison in
the same way as human beings. Such proce­
dure is not acceptable in some countries. In
India, Prevention of Cruelty to Animals Act
enunciates the guidelines and punishment.
Moral and circumstantial evidence: Clues
regarding the recent purchase of poison by
the victim or accused, his behaviour, the
conduct of those looking after the victim,
suicide note, and history of quarrel or
financial problems may also provide
valuable information. The body may be
disposed of clandestinely or hastily.
Q. 36.8. Mention the duties of a doctor
when he examines a case of suspected
poisoning.
In all cases of poisoning, the doctor must
record the preliminary particulars, viz. name
in full, age, sex, occupation, address, date
and time, brought by whom, history, dying
declaration necessary or not.
The doctor's first duty is to treat his
patient. If the doctor in private practice is
certain that'his patient is suffering from
suicidal or accidental poisoning, he is not
bound to supply information of his own
accord to the police or magistrate. However,
if he is summoned by the investigating
police officer or magistrate for such
information, he should do so. In accidental
poisoning, if there is any indication of
danger to the general public, as for
example, from food poisoning from a
public eating house or contamination of
public drinking water, the doctor must
notify the public health authorities at once.
If the doctor is convinced that homicidal
poisoning has occurred, he has a duty to
protect society; he must inform the nearest
police officer or magistrate (Sec. 44 CrPC).
He should take every precaution to prevent
the possibility of further administration of
the poison to the patient.
In every case of suspected poisoning, the
doctor must keep the records of the case in
meticulous detail. He must collect and
preserve properly and in separate con­
tainers stomach washings, and samples of
vomit and urine passed in his presence
only, and blood likely to contain poison, for
transmission to the forensic science
laboratory (FSL). Any suspicious article,
such as—(1) utensils used for preparing the
poison, (2) bottles or containers of solid or
liquid medicine found at the scene,
(3) food or drink lying near the patient, or
(4) clothes or bed sheet soiled by vomit,
urine or faeces, should be preserved for
possible future examination. If the patient
is serious, arrangement for taking a dying
declaration should also be made. In the
event of death, a death certificate should not
be issued but the fact of death must be
communicated to the nearest police officer
for necessary investigation. Any opinion
about the nature of poison can be given
only after report from the forensic science
laboratory.
The doctor in charge of a government or
public hospital must report to police all cases
of poisoning, either suicidal, homicidal or
accidental, admitted to his institution.
Q. 36.9. Describe in detail the general
principles of treatment of acute poisoning.
Q. 36.10. Write short notes on: (1) household
emetics, (2) stomach tube, (3) chelating
agents.
If the poison is known, specific treatment
must be instituted. If not, treatment is given
 Introduction and Law Relating to Poisons 515
ongeneral lines. The main aim of treatment 1. If the patient is conscious and coopera­
is to help the patient to stay alive by tive, and vomiting is not contraindicated
attention to respiration and circulation (corrosives, strychnine, petroleum disti­
while he is assisted to get rid of the poison llates, coma, severe cardiac or respira­
bymetabolism or excretion. While to some tory diseases, and advanced pregnancy),
extent, the details will vary according to the it should be induced either by tickling
portal of entry of the poison (inhalation, the fauces or by the use of emetics.
injection, contact or ingestion), the main Household emetics, such as warm water,
objects include: (1) removal of unabsorbed one tablespoonful of mustard powder
poison from the body, (2) use of antidotes, (15 gm) or two tablespoonful of common
(3) elimination of the absorbed poison, salt in a tumblerful (200 ml) of tepid
(4) treatment of general symptoms, and water, readily available in every house­
(5) maintenance of the patient's general hold, may be used in an emergency.
condition. Ipecac 1-2 gm or ipecac syrup in a dose
of 30 ml does act as an emetic in about
Removal of Unabsorbed Poison 20-30 minutes. The dose may be repeated
from the Body one time.
Depending upon the route of entry, the Apomorphine, 6 mg by subcutaneous
followingprinciples should be kept in mind. injection, followed by naloxone hydro­
chloride (Narcan) 5-10 mg i.m. or i.v., to
1'ih w i poisons: If the poison, e.g. carbon counteract its narcotic effects, may be
monoxide, automobile exhaust or gas from used: (1) it produces prompt vomiting
a sewer has been inhaled, the patient within three to five minutes, (2) it
shouldbe removed to fresh air and artificial facilitates gastric lavage by removing
respiration commenced at once. The air gastric contents which may obstruct the
passages should be kept free from mucous stomach tube, and (3) it produces reflux
by postural drainage and aspiration. of upper intestinal contents (enteric
coated tablets, etc.) into the stomach.
Injected poisons: If the poison has been
When apomorphine is given by mouth,
injected, a tight tourniquet should be
about twice the hypodermic dose is
applied proximal to the point of injection.
required and vomiting is not produced
It must be released every 10 minutes for 1
for half an hour.
minute to prevent gangrene. The wound
2. Gastric lavage (stomach washing), if not
may be excised and poison removed by
contraindicated, may be life-saving, if
suction, and/or neutralised chemically. The
undertaken within four to six hours after
common examples of injected poisons are
the ingestion of poison (Fig. 36.1).
hypnotics, insulin, snake bite, insect bite, etc.
It is contraindicated mainly in corrosive
Contact poisons: If the poison be spilled poisoning except carbolic acid for fear of
or sprayed on skin, eye or wound, or be rupture of the stomach. In other cases, it
inserted into vagina, rectum or urinary can be performed after taking necessary
bladder, the best way to treat it is to wash precautions. As for example, (1) in strych­
it out with plain warm water and/or to nine poisoning, convulsions should be
neutralise it by a suitable antidote. controlled; (2) in kerosene or volatile
Ingested poisons: The object is to remove poisons or in comatose conditions, airway
from the stomach as soon and as much of should be sealed by cuffed intubation to
the poison as possible. For this purpose, avoid the high risk of aspiration into the
(1) vomiting (emesis) may be induced, and/ air passages; and (3) in hypothermia, body
or the (2) stomach washed out (gastric lavage). temperature would need careful attention.
516 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Fig. 36.1: Stomach tube. (A) A filter funnel is
attached to the upper end of the rubber tube,
(B); (C) Suction bulb; (D) Mouth gag with a
central hole. The mouth gag covers the 50 cm
mark from the lower end of the rubber tube
(E) which is rounded and perforated
Procedure: The patient should be prone
or semiprone on his side with hips higher
than his head, as this will aid respiratory
drainage and also prevent regurgitated
material from entering the respiratory tract.
The dentures, if any, must be removed. The
airway must be clear and a mouth gag with
a central hole is necessary especially in
unconscious patients to prevent the rubber
tube being bitten off by the teeth. In adults,
for gastric lavage, the stomach tube
(Fig. 36.2) is usually satisfactory. It is a
Fig. 36.2: Procedure of stomach-wash in a
child. The child is wrapped in a blanket to
avoid struggling. The stomach contents are
rem oved by means of a French rubber
catheter to which a syringe is attached
flexible rubber tube (not stiff) about 12.7
mm in external diameter and about a metre
and a half in length. A filter funnel is
provided at the upper end. A suction bulb
is also provided to suck out fluids when
siphon action fails and to push air into the
tube to force out any obstruction. The lower
end is blunt and rounded to avoid any
injury when it is being passed and is
perforated by more than one opening on
its sides to allow the administered fluid to
enter the stomach easily. The distance
between the lips and the cardiac end of the
stomach is about 45 cm in the adult.
Therefore, the tube is marked at a point
about 50 cm from the lower end. In
emergency, a soft rubber tube of suitable
length to one end of which a funnel is
attached forms an efficient stomach tube.
The lower end of the tube should be
lubricated with liquid paraffin, glycerine,
milk or some other substance, and passed
through the hole in the middle of the mouth
gag, over the tongue (depressing it, if
necessary), and down the oesophagus. At
about the mark, the tip of the tube should
be lying in the stomach in the adult, and
one must make sure of this by any one of
the following tests: If little air is forced
down the tube, one should be able to hear
bubbling sounds through the stethoscope
applied over the stomach. If the tube has
entered the trachea, a hissing noise is heard
at the funnel end; besides, if the patient is
not unconscious, reflex coughing takes
place and bubbles of air will come out of
the funnel-end dipped in water.
After testing, about quarter litre of plain
warm water (35°C) is run into the funnel,
which is held above the level of the patient's
mouth. The fluid enters the stomach by
gravity. The funnel is then lowered, below
the level of the patient's stomach, over a
receptacle, to allow the gastric contents to
siphon off. Subsequent washings are done
with half litre of fluid. Using too much fluid
for the first wash is likely to sweep the
 Introduction and Law Relating to Poisons 517
poison onwards into the duodenum. The absorbed, or (c) the poison has been adminis­
first w ashing, which is usually done with tered by route other than ingestion. They
warm w a te r, should be preserved for can be classified into four groups, in accor­
chem ical analysis. The process is then dance with their mode of action, namely:
repeated either with warm water or other (1) mechanical or physical, (2) chemical,
fluid preferably containing an appropriate (3) physiological or pharmacological, and
antidote until the returning fluid is of the (4) universal.
same colour and character as the lavage
M echanical or physical antidotes: These
fluid. Stomach washing is based on Syphon
are substances which impede the absorp­
mechanism.
tion of poisons by their presence. These are
When the poison is thus removed, some
few in number, such as demulcents, bulky
of the an tid o te or other suitable solution
food, and activated charcoal. Demulcents
may be left in the stomach to deal with the
are substances, such as fats, oils, milk, egg
effects and after-effects of whatever small
albumin, etc., which prevent the absorption
quantities may have escaped lavage or are
of the poison by forming a coating on the
later excreted in the stomach. The useful
mucous membrane of the stomach. They
solutions for this purpose are: magnesium
act in this manner both in corrosive and
sulphate or sodium sulphate to ensure
irritant poisoning. Fats, oils, and milk,
purgation of any poison that has passed the
however, should not be used for fat-soluble
intestine; sodium bicarbonate to counteract
poisons, e.g. phosphorus, organophos-
the irrita tio n of the stomach in aspirin
phates, DDT, etc. Bulky food, such as banana,
poisoning an d to accelerate salicylate excre­
acts as a mechanical antidote to glass by
tion; activated charcoal to adsorb alkaloids;
imprisoning its particles and thus prevent­
and liquid paraffin as a demulcent fluid.
ing its action. Activated charcoal is specially
Before the stomach tube is withdrawn,
useful in adsorbing alkaloidal poisons, such
it should b e pinched to prevent aspiration
as strychnine, and to a lesser degree, mineral
of m aterial into the lungs.
poisons. It is given in a dose of 30-60 gm in
In children, a Ryle's tube or a number 8 children and 60-100 gm in adults in five
to 12 French rubber catheter is usually times the quantity of water. The correct
satisfactory. About 25 cm length is nece­
dose of activated charcoal is about 5 to 10
ssary to re a ch the stomach. The catheter is times the amount of drug ingested.
passed through the nose or the mouth into
the sto m ach with the usual precautions and Chem ical antidotes: These are substances
the sto m ach wash done using a 50 ml glass which act either by direct chemical action
syringe. Many centres do not do stomach or by oxidising the poison to form a non­
wash nowadays as a matter of routine. It is toxic or an insoluble compound. Some of
more or less replaced by administration of the examples are as follows:
activated charcoal. Dilute acetic acid or vinegar neutralises
alkalis by direct chemical action. Canned
Use of Antidotes fruit juice is an useful alternative for this
Antidotes are remedies which counteract purpose. Dilute alkalis, e.g. milk of
or neutralise the effect of poisons without magnesia, will neutralise acids; however,
causing appreciable harm to the body. They bicarbonates should not be used owing to
need to be used because: (a) the poison may the risk of rupture of stomach from the
not have been com pletely removed by liberated carbon dioxide. Tannin (strong
emesis or gastric lavage or these procedures tea) produces insoluble compounds with
are contraindicated, (b) the poison is already most alkaloids, glucosides and metals.
 518 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Potassium permanganate is an oxidising
agent effective against all oxidisable poisons,
such as most of the alkaloids, amidopyrin,
antipyrine, barbiturates, phosphorus,
cyanides, etc. The usual strength of the
solution is 1:1,000 approximately (1 gm in
a litre) and even 100-150 ml of this solution
can be left in the stomach without any
harm. A weak solution of iodine, 15 drops
of the tincture to a tumblerful (200 ml) of
water, may be helpful in the absence of
permanganate.
Physiological or pharmacological antidotes:
These agents produce effects which are
opposite to that of the poison. Examples of
physiological antagonists are: atropine for
pilocarpine, diazepam for strychnine, nalo­
xone for morphine, atropine and oximes for
organophosphorus compounds, N-acetyl
cysteine for acetaminophen, and mazicon
for benzodiazepins. However, the antagonism
is usually not complete and the remedy may
itself produce most undesirable side effects.
Certain chelating agents are widely used
as specific antidotes against some heavy
metals. These are substances which pro­
duce a firm non-ionized cyclic complex
(chelate) with cations. Such compounds can
form stable, soluble, non-toxic complexes
with calcium and certain heavy metals. The
important amongst them are BAL, (British
anti-Lewisite or 2,3-Dimercapto propanol)
EDTA (ethylenediaminetetraacetate) and
versenate (calciumdiethyltetraacetate) for
arsenic; EDTA and versenate for mercury
and lead; N-penicillamine for mercury, lead
and copper; and desferrioxamine-B (DFM)
for iron.
BAL (British anti-Lewisite), also called
dimercaprol is used in the treatment of Constituents
certain types of heavy metal poisoning. It 1. Powdered charcoal
is given deep intramuscularly as a 10 per
cent solution in arachis oil with benzyl 2. Magnesium oxide
benzoate. In severe poisoning, a dose of
3. Tannic acid
3 mg/kg is administered at 4 hourly inter­
vals for the first 2 days, at 6 hourly intervals
during the third day, and at 12 hourly
intervals thereafter for about 10 days. BAL
is contraindicated, if the liver is extensively
damaged.
EDTA is a chelating agent and is effective
in lead, mercury, and copper poisoning.
The usual adult dose is 1 gram twice daily
for periods up to 5 days given by slow
intravenous infusion in isotonic glucose
saline. After an interval of 2 days, this course
of treatment may be repeated. EDTA has
been shown to be superior to BAL in some
respects for the treatment of poisoning by
arsenic and mercury. It is contraindicated
in renal damage.
Penicillamine (cuprimine) is a degrada­
tion product of penicillin and has the
advantage that it can be given orally,
continually, and that it is much less toxic
than EDTA. It is the treatment of choice in
copper, lead and mercury poisoning. A
dose of 30 mg/kg body weight up to a total
of 2 grams per day in four divided doses
given orally is satisfactory. It is specially
useful in hepatolenticular degeneration
(Wilson's disease) which is caused by a
disorder of copper metabolism.
Desferrioxamine chelates iron. It is chiefly
valuable in the treatment of acute iron
poisoning. In certain chronic diseases, such
as haemochromatosis characterised by
excessive retention of iron in the tissues,
desferrioxamine is useful in accelerating the
removal of iron from the body.
Universal antidote: It is an antidote that is
used in those cases where the nature of the
ingested poisons is unknown or where it is
suspected that a combination of two or
more poisons has been taken. It consists of
a mixture of readily available substances,
as follows:
Quantity Purpose
2 parts Adsorbs alkaloids
(burnt toast)
1 part Neutralises acids
(milk of magnesia)
1 pari Precipitates alka­
(strong tea) loids, certain gluco-
sides and many
 Introduction and Law Relating to Poisons
The mixture is administered in a dose of
a tablespoonful stirred up in a tumblerful
(200 ml) of water, and may be repeated
once or twice. Even when given soon after
the ingestion of poison, it is not very effective.
Though it is called universal antidote, it is
not a Panacea in all cases. Infact, in many
institutions, this is replaced by activated
charcoal administration. H ow ever, its
immediate household or hospital use can
not be written off.
Elimination of the Absorbed Poison
This may be achieved by accelerating its
excretion especially in the urine. Ample
amounts of fluid should be administered
to maintain adequate diuresis. Salicylates
and phenobarbitone can be easily excreted
in alkaline urine; am phetam ines and
quinine can be easily excreted in acid urine.
Elimination by catharsis (magnesium citrate
or sulphate, sorbitol) when not contra­
indicated may be encouraged.
Peritoneal dialysis has been used for
salicylate poisoning in children and may
have a place in those centres not yet
possessing artificial kidney. Haemodialysis
lias been employed for removing barbi­
turates, boric acid, glutethimide, methyl
alcohol, salicylates and thiocyanates from
the blood. Haemyerfusion is superior to
haemodialysis for removal of lipid-soluble
drugs. Exchange transfusion is only feasible
with small children and has been applied
to poisonings by salicylates, barbiturates,
iron salts, carbon monoxide, etc. All toxic
substances, including non-dialysable ones,
are removed by this technique.
A new alternative to lavage, dialysis, and
haemoperfusion is whole bowel irrigation.
The technique is promising; however, the
patient needs to be carefully monitored
throughout the procedure.
Treatment of General S ym pto m s
The treatment of symptoms should be
applied as indications arise. Morphine
519
should be given for pain, oxygen or artificial
respiration for respiratory failure, cardiac
stimulants for failing circulation, and an
anaesthetic, barbiturates, or diazepam for
convulsions. Saline infusion may be useful
to counteract dehydration as well as to
enhance diuresis to excrete toxic substances.
The addition of sodium bicarbonate to the
infusion may be of value when the alkali
reserve is diminished. Administration of
glucose will combat depletion of liver
glycogen, and the restoration of potassium
or sodium balance may be necessary.
Maintenance of the
Patient’s General Condition
The patient should be kept warm and
comfortable. Once the struggle to preserve
life has been won, one of the main dangers
to the patient is the subsequent develop­
ment of upper respiratory tract infection.
This is a special hazard in elderly people,
in those who were unconscious for an hour
or more, in those who had had a respiratory
infection before poisoning, and in those
who inhaled a very small amount of
vomitus. To avoid this risk, prophylactic
administration of antibiotics to all cases is
desirable. The importance of good nursing
care (especially for the unconscious patient)
and physiotherapy cannot be over­
emphasised.
Any patient known to have or suspected
of having attempted suicide should not be
allowed to leave the hospital without being
interviewed by a psychiatrist who can
institute further necessary supportive
psychotherapy.
Q. 36.11. Describe the salient features of
the Scandinavian method for treatment of
poisoning cases.
This is a method of intensive supportive
therapy. The regimen consists of: (1) assess­
ment of the patient, (2) emergency measures,
and (3) general care.
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Assessment of the Patient rectal temperature below 36°C is indicative
Clinical examination is made to assess the of significant hypothermia, and it would
disturbance in vital functions, e.g. central contribute to shock, acidaemia and hypoxia.
nervous system, respiratory system, cardio­ Emergency measures: This includes
vascular system, and body temperature, management of respiratory failure, cardiac
and also to detect any coincident disease failure and prevention of further absorp­
which may influence the treatmeni given. tion of poison, on usual lines.
Central nervous system: Impairment of the General care: This includes management of
level of consciousness is the most constant hypothermia, correction of water and electro­
feature of hypnotic, sedative and psycho­ lyte imbalance, treatment of infection and
tropic drug poisoning. Depending on the general nursing care, on usual lines.
response of the stimulus, the patient's state It is claimed that the intensive suppor­
of consciousness is classified into four tive therapy described here reduces the
grades: mortality rate to2%. However, the techniques
Grade 1: Drowsy but responding to vocal involved in the therapy require facilities
commands. which are generally difficult to be obtained
Grade 2: Unconscious but responding to in a majority of places where poisoned
minimally painful stimuli. patients are initially admitted for treatment.
Grade 3: Unconscious but responding only Q. 36.12. Describe Glasgow Coma Scale:
to maximum painful stimuli, e.g. (a) The toxicity rating, (b) minimum lethal
rubbing the patient's sternumwith dose, (c) usual fatal dose, (d) toxico-
the knuckles of the clenched fist. kineties, (e) poison information centre.
Grade 4: Unconscious and not responding Toxicity rating of a poison is decided based
to painful stimuli. upon the quantity of the dose required to
Respiratory system: Once a clear airway is cause fatality. If the dose is less the toxicity
established, the adequacy of ventilation is is more. The grading in order of severity to
determined by arterial puncture and least severity is:
measurement of blood pH, pC02, p02 and a. Super toxic = 6 -> usual fatal dose is
standard bicarbonate or by Wright's below 5 mg/kg body weight
spirometer which signifies the presence of b. Extremely toxic = 5 -» usual fatal dose
respiratory impairment, if the minute range is 5 mg to 50 mg/kg body weight
volume is less than four litres. If arterial c. Very toxic = 4 51 to 500 mg/kg body
blood gas analysis is not possible at short weight
notice, the pCOz is measured by the d. Moderately toxic = 3 —> 501 mg/kg to
rebreathing method. 5 g/kg
Cardiovascular system: Cardiovascular e. Slightly toxic: 2 5..1 - 15 g/kg
function is responsible for maintaining- f. Practically non-toxic - 1 —> more than
blood pressure and peripheral circulation/ 15 g/kg.
tissue perfusion. A systolic blood pressure Minimum lethal dose is the minimum dose
less than 90 mm Hg in persons above 50 level which is fatal to 50% of animal that
years and less than 80 mm Hg in young are administered that dose (LD 50).
persons is indicative of shock. Tissue Usual fatal dose is derived from animal
perfusion is best assessed by measuring the experimental data and statistics of human
urinary output. poisoning. The higher the toxicity rating,
Body temperature: Body temperature is the greater is its (toxicity) potency.
monitored by using a low reading rectal Toxicokinetics means the various changes
thermometer graduated from 0°-50°C. A the poison undergoes upon entering the
 Introduction and Law Relating to Poisons 521
Ctembeforeitcoursesmits process of meta- 3. Inappropriate w ords. (Random or
5-|jSni/catabolism, we shall be hurveldy. exclamatory articulated speech, but no
^ s0n information centre—Poison. conversational exchange).
4. Confused. (The patient responds to
questions coherently but there is some
production disorientation and confusion).
5. Oriented. (Patient responds coherently
t neurological scale which aims to give
and appropriately to questions such as
a reliable, objective way of recording the
the patient's name and age, where they
conscious state of a person for initial as
are and why, the year, month, etc.)
well as continuing assessment.
, A patient is assessed against the criteria Best Motor Response (M)
of the scale. There are 6 grades starting with the most
, The resulting points give the Glasgow severe:
Coma Score (GCS). 1. No motor response.
* Initially used to assess level of conscious­ 2. Extension to pain (decerebrate response:
ness after head injury. adduction, internal rotation of shoulder,
e The scale <was published in 1974 by pronation of forearm).
Graham Teasdale and Bryan J. Jennett, 3. Flexion in response to pain (decorticate
professors of neurosurgery at the response).
University of Glasgow. 4. Withdraws from pain (pulls part of body
* The scale comprises three tests: eye, away when pinched; normal flexion).
verbal and motor responses. 5. Localizes to pain. (Purposeful move­
- The three values separately as well as ments towards changing painful stimuli;
their sum are considered. e.g. hand crosses midline and gets above
The lowest possible GCS (the sum) is 3 clavicle when supraorbital pressure
(deep coma or death). applied).
* The highest is 15 (fully awake person). 6. Obeys commands. (The patient does
simple things as asked).
Best Eye Response
Interpretation
There are 4 grades starting with the most
severe: •
Generally, comas are classified as:
1. No eye opening. •
Severe, with GCS <8
2. Eye opening in response to pain. (Patient •
Moderate, GCS 9-12
responds to pressure on the patient's •
Minor, GCS e >13
fingernail bed; if this does not elicit aThe GCS has limited applicability to child­
response, supraorbital and sternal ren, especially below the age of 36 months.
pressure or rub may be used). The verbal performance of even a healthy
child would be expected to be poor conse­
3. Eye opening to speech. (Not to be confused
with an awaking of a sleeping person; quently the paediatric Glasgow Coma Scale,
a separate yet closely related scale, was
such patients receive a score of 4, not 3.)
4. Eyes opening spontaneously. developed for assessing younger children.
It is claimed that the intensive supportive
Best Verbal Response (V) therapy described here reduces the mortality
There are 5 grades starting with the most rate to 2 per cent. However, the techniques
severe: involved in the therapy require facilities
1. No verbal response. which are generally difficult to be obtained
2. Incomprehensible sounds. (Moaning but in a majority of places where poisoned
no words). patients are initially admitted for treatment.
 37
Toxicological Evidence

Q. 37.1. Write an essay on ‘toxicological capable of acting deleteriously on the body.

evidence’. There is really no delineation between a
In the present era, the advances of synthetic medicine and a poison because a medicine
chemistry and the fast changing conditions in a toxic dose is a poison and a poison in a
of living have placed an ever increasing small dose may be a medicine. In law, the
number of highly poisonous substances real difference between a medicine and a
within the reach of modern man. More poison is the intent with which it is given
people take (toxic) chemicals and medica­ and its intrinsic capacity to do the bodily
tions now than ever before. Such sub­ harm. If the substance is given with the
stances play a primary or secondary, direct intention to provide relief from some
or indirect, role in bringing about unnatural symptoms or to save life, it is a medicine
death. Under such circumstances, a medical but if it is given with the intention to cause
practitioner is more likely to miss a case of bodily/mental harm, it is a poison. As for
poisoning, especially of a homicidal nature, example, chloral hydrate, in a dose of
unless he is constantly aware of its possi­ 300 mg when used as a hypnotic, is a
bility. In addition, chemical analysis has medicine but when used in a higher dose,
become so complex that it needs to be say 3 gm, as knock out drops to render a
handled only by competent analysts having victim of robbery or rape helpless, it is a
proper facilities, working with all possible poison. Similarly when a barbiturate is
assistance from the medical practitioner given in a therapeutic dose for the relief of
and pathologists as regards clinical sympto­ insomnia, it is a medicine; even if it is given
matology and autopsy findings. in a higher dose for the control of
To appreciate the role and responsibili­ convulsions, it is still a medicine. However,
ties of the various concerned agencies in such a high dose if given to a normal
proper perspective, this topic is discussed healthy person would cause coma and
under the following headings: (1) toxico­ possibly death and then it is a poison.
logical evidence— forensic aspects, Though generally, the dose determines
(2) toxicological evidence— analytical the toxicity, it must be remembered that
aspects, and (3) toxicological evidence— certain factors modify the action of a sub­
interpretation. stance introduced in the body. An indivi­
dual may be adversely affected by a
FORENSIC ASPECTS____________________
nontoxic dose of a given substance. For
A poison is commonly defined as a sub­ example, individuals having idiosyncrasy,
stance which, when administered, is allergy, or suffering from some cardiac or

522
 Toxicological Evidence 523
debilitating disease are more adversely their smell, unless masked by putrefactive
affected by a nontoxic dose than a person odour, are: alcohol, camphor, carbolic acid,
in good health. Conversely, a person conium, cyanide, kerosene, nicotine, opium,
habituated or addicted to a certain drug can organophosphorus compounds, paral­
tolerate much larger doses of that drug dehyde, petroleum products, phosphorus,
without apparent harm as compared to a and oil of wintergreen, etc.), (2) when there
normal healthy person. is some other evidence, such as (a) presence
Proof that poisoning has occurred is of foreign material in the form of powder,
based mainly on the following factors, viz: capsules, tablets, or leaves in the stomach,
(1) signs and symptoms suggesting (b) irritation, ulceration or discolouration
exposure to a toxic substance, (2) autopsy of the mucous membrane of the stomach,
findings, (3) evidence of pathologic lesions (c) laryngeal oedema—common in deaths
associated with a particular toxic substance, from alcohol and barbiturates, (d) acute
and (4) conclusive evidence of absorption lung congestion and oedema provided
of a toxic substance in the tissues and body heart disease and intracranial lesions could
fluids of the deceased as determined by be excluded, (e) acute swelling of the
chemical analysis. brain with or without a pressure cone,
(f) markedly distended urinary bladder,
Symptoms and Signs and (g) intravascular sickling, (3) from
While it is not possible to catalogue all the negative evidence, such as no trauma or no
possible toxic substances within the reach signs of disease in any organ to account for
of m odem man, an attempt has been made the cause of death, or (4) when the body is
in the ensuing pages to cover the main decomposed.
d iagn ostic signs, symptoms, and other
relevant details of a number of common Evidence of Pathological Lesion
poisons. For this purpose, the material has Sometimes, in a case of fatal poisoning, no
been organized in the following manner: poison may be found on chemical analysis
A table of common household poisons especially when a large time interval
is given. A glance at the data will show between time of ingestion and death is
what poison the product probably contains. involved. However, in many of these cases,
This is followed by a detailed discussion of during the period of survival, pathological
a number of common poisons, the less changes in the organs would have occurred
common ones being discussed in small which are demonstrable by gross and/or
types. Thereafter, an alphabetical poison microscopic examination. Although such
table has been provided, containing almost changes may not be specific for that parti­
all common poisons encountered any­ cular poison it is still possible to attribute
where. The table shows at a glance the death to such a substance on circumstantial
toxicological characteristics of the various evidence, e.g. carbon tetrachloride poison­
poisons and provides a convenient ing resulting in death after about a week
summary and an integrated picture of their or 10 days after exposure. After such
differing aspects. interval, carbon tetrachloride would not be
detected by chemical analysis. However, it
Autopsy Findings is a hepatotoxic and nephrotoxic agent.
At autopsy, the medical officer suspects the When such changes are observed and there
presence of poison: (1) when he notes any is a history of exposure, it is possible to
peculiar smell on opening the body implicate carbon tetrachloride as a cause
(substances which may be detectable by of death, although these changes are not
: 524 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
specific for this poison. Similarly, in
thallium poisoning, diagnostic changes
may be found in hair roots.
ANALYTICAL ASPECTS___________________
Analytical toxicology, an important branch
of forensic science, deals with the detection
and estimation of a variety of poisons in
biological and other materials in low
concentration.
The most important proof that poisoning
has occurred depends on evidence of
absorption of a toxic substance in the body.
The most direct evidence of such absorp­
tion is the detection of a toxic substance
followed by its quantitative estimation in
tissues obtained at autopsy or occasionally
in blood, urine, and gastric material
obtained from a living patient.
The exception to the general rule
requiring evidence of absorption of a toxic
agent relates to cases involving ingestion
of corrosive mineral acids and alkalis, e.g.
concentrated sulphuric acid and sodium
hydroxide which are generally identifiable
in the gastrointestinal contents.
The common poisons met with in India
are insecticides, pesticides and the poiso­
nous plants, such as dhatura, aconite,
strychnos nux vomica, opium, oleander,
etc., which grow wild and may be collected
without suspicion on account of their
medicinal use. Sedatives, tranquillisers and
other synthetic drugs are commonly
misused in the West. In India, such misuse
is confined to bigger cities only.
Poisoning as a possible cause of death is
usually indicated by scene investigation
(prescriptions, medications, containers,
etc.), history of the case, autopsy findings,
by gross or microscopic pathologic findings
or absence thereof. Analysis is greatly
facilitated when such information is
forthcoming.
Where a specific substance is suspected
as the causative agent, direct analysis for
this substance may initially be made. This
will either confirm the suspicion or rule out
the substance as a factor concerned with
death. As a rule, general systematic toxico­
logical analysis is undertaken, even when
a particular poison is suspected.
It is beyond the scope of this chapter to
present details of the various analytical
procedures. A reference may be made to
standard textbooks on analytical toxicology
for this purpose.
Other Examinations
In addition to chemical analysis, other
examinations, such as histopathological,
indirect biochemical, biological/pharma­
cological, serological, etc., become occasio­
nally necessary in forensic toxicology.
Blood is useful for all these examinations
except histopathological.
Embalming and Toxicological Analysis
In dealing with cases of suspected poison­
ing, autopsy should be performed prior to
embalming. The embalm ing process
(though not prevalent in India) interferes
with both the qualitative identification of
the poison and its quantitation,, as shown
by the following examples:
1. Cyanide reacts chemically with formalin
in the embalming fluid so that it is no
longer identifiable as such.
2. Most embalming fluids contain methyl
or ethyl alcohol or both so that analyses
for these substances are rendered meaning­
less. So, it is extremely difficult, if not
impossible, to detect and identify most
volatile poisons in an embalmed body.
3. Fixation of the tissues by formalin makes
them more resistant to the action of
organic solvents used for extraction of
non-volatile organic compounds, e.g.
most drugs. Therefore, no or low
recoveries of such substances will result.
In the case of already embalmed dis­
interred bodies, it is desirable to furnish the
toxicologist a sample of embalming fluid,
 , for burial, as control, should any
»5 itivc chemical findings be obtained.
f°s‘ ise, tissues from those parts of the
least affected (e.g. buttock muscle,
*>° tje of liver, vitreous) by embalming
fid should be retained for analysis. In
dia also bodies are som etim es not
mbatoed and consequently such problems
n0t commonly encountered.
putrefaction and Toxicological Arccrty**
putrefaction complicates the problems of
toxicological analysis and leads to difficul­
ties in interpretation of results, as shown
by the following examples:
l Some substances that might be present
in the tissues may undergo chemical
changes and may no longer be identifi­
able, e.g. nitrite. In the case of hydrolytic
chemical changes, the breakdown pro­
duct instead of/ in addition to the original
poison may be detected, as in the case of
aconite, parathion, carbaryl, etc.
2. Putrefaction of normal tissue compo­
nents may produce substances which
yield chemical reactions similar to those
obtained from basic toxic compounds,
such as, neurine, beta-phenylethyl
amine, tyramine and other amines.
Though these can create considerable
interference problems, methods to
overcome the same are available.
3. Volatile substances may be lost as a
result of putrefaction.
4. Ethyl alcohol may be produced from
normal tissue components in advanced
putrefaction.
Despite these limitations, most toxic
substances are still identifiable, and these
include amongst others: carbon monoxide,
cyanide, fluoride, barbiturates, organo-
phosphorus compounds, endrine, hyoscine,
strychnine, yellow oleander, nicotine, etc.,
and inorganic poisons, such as arsenic,
antimony, mercury, lead, thallium, etc.
MTERPIKTATION__________________ _
The report of the chemical analyst usually
includes detection of the poison. In the case
of some poisons, like methyl alcohol, ethyl
alcohol, cyanide and drugs, the report also
includes their concentration/tissue.level.
The poison levels in the tissue, in general,
vary a lot from one fatal case to another.
The report, therefore, also includes a toxico­
logical interpretation of the quantitative
data obtained from the poison case in ques­
tion, i.e. whether or not the observed tissue
level of the poison detected is of the same
order as that found in other fatal cases
involving that poison. For this purpose, the
data bank at the institution or that from the
literature is utilised. This is a proper
modem approach than that of working out
the ingested fatal dose. The latter cannot he
evaluated with any certainty and, therefore,
has been given up in modern toxicological
practice. H ow ever, the analyst should
maintain a detailed record of his work on
quantitation, etc., including the substances
for which negative results were obtained.
The record should also include all weights
and volumes of samples taken up for
analysis, the dates of work, when started
and when completed, and the test results.
Proper interpretation of an analytical
result also requires that the analyst is know­
ledgeable about the pharmacokinetics of
the poison called as toxicokinetics and the
technique of reporting, as shown below:
1. In the absence of history or any other
clue of poisoning, such as due to insulin,
the general scheme of chemical analysis
would give negative results.
2. Despite history of exposure to a toxic
substance, no positive analytical finding
may be obtained. There are several
reasons for this apparently contradictory
result: (a) The poison may have been
vomited out, excreted, neutralised,
metabolised, detoxified, or the poison is
so obscure or present in such small
quantity that it cannot be detected in the
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
general scheme of analysis and by the
available methods of chemical analysis:
A case has been recorded where succinyl-
choline was used as an injection with
homicidal intent. It is metabolised to
succinic acid and choline, which are
normal constituent of the body tissues.
Thus, chemical detection of the drug in
the body tissues is difficult save in
exceptional circumstances, (b) Less and
less amount of poison would remain
with higher time gap between ingestion
and death, and in some instances, a long
survival period may leave the poison 3.
residues beyond the detection limit,
(c) The absorbed poison is not evenly
distributed in various organs and this
relative distribution varies substantially
with different poisons, (d) The distribu­
tion of poison may also vary with its
mode of administration. As for example,
blood levels may be higher than liver
levels when the poison is administered
by the intravenous route. The reverse
generally applies when the poison is
administered orally, (e) The analyst has
to look for all possible types of poisons
in whatever little amount of specimen he
has received. There are chances of
missing the detection of poison, when
too little of the specimen is submitted for
analysis. Sometimes, the relevant tissues
and/or the controls may not have been
submitted. As for example, in snake bite
poisoning, in the absence of tissue round
the site of bite for immunological exami­
nation, the general scheme of chemical
analysis would fail to provide any proof
of poisoning. Any unusual delay in
submission and analysis especially in
cases of in vitro labile compounds may
also fail to provide proof of poisoning.
(f) Detection of highly potent toxic
substance (very low LD) is quite difficult.
(g) The sample may not have been
properly preserved, (h) Problems posed
by putrefaction are already outlined.
(i) If the victim has been treated, the
medication itself may alter the poisonous
substance and make its detection diffi­
cult or even impossible, (j) For reasons
not clear, in deaths due to intravenous
narcotism, sometimes even when the
victim was found with the needle with
syringe attached still in the vein, no
narcotic is detected. Considering such
diverse limiting factors, non-detection of
poison in postmortem tissues need not
necessarily be interpreted as "no poison"
having been involved.
The isolated material may not be iden­
tical due to alteration by biochemical
processes. Common examples are the
findings of phenobarbitone when primi­
done has been taken and the finding of
oxazepam when diazepam has beentaken,
or morphine when heroin is involved.
There could be many instances when the
original poison and tire metabolite or even
the latter alone would be detectable.
The most commonly used narcotic among
the addict population is heroin which is
diacetyl morphine. The metabolic
processes degrade the compound to
morphine which is detected from the
liver, bile and urine. If at autopsy, a fresh
needle puncture mark is found and the
presence of heroin can be demonstrated
at this site, it would be justifiable to say
that morphine in the tissue was derived
from the usage of heroin.
Codeine is methyl morphine. The meta­
bolic processes degrade only a small part
of the absorbed codeine to morphine.
Therefore, finding of high concentration
of codeine with small amounts of mor­
phine would suggest that the origin of
the latter was probably codeine. The
finding of high concentration of morphine
and only small amount of codeine, on the
other hand, would indicate that the former
was due to the use of either morphine or
heroin along with codeine, usually also
with other prominent opium alkaloids, as
in street samples of (crude) heroin.
 Toxicological Evidence 527
A finding of quinine, caffeine, or metha- the conclusion about the lethal dose on
qualone which are commonly used as the basis of the poison level in post­
active adulterants in street samples of mortem tissue/fluid such as liver or
heroin, in suspected narcotic deaths of blood not being rational or precise is no
persons having relatively fresh as also longer held strictly valid in modern
old n e e d le marks m ay suggest the toxicological practice. Looking to the
possibility of heroin addiction even complexities involved, such an exercise
though no narcotic may be demonstrable has to be done with utmost caution.
in the postmortem tissue or fluids. 6. Every quantitative measurement has a
4. The reaction to a therapeutic dose of a certain degree of uncertainty and as a
substance may range from slight effect resu lt the figure quoted w ith ou t a
to signs of over-dosage. Therefore, the probable error can be misleading. The
so-called lethal dose cannot be fixed in reasonable range of probable erro r
any rigid sense. As such, the giving of would be around 2 standard deviations.
an ordinarily fatal dose may result in a It is, how ever, im portant that the
significant survival rate whereas high, recipient of the result understands as
yet ordinarily non-lethal doses some­ near as possible what the result signifies.
times result in death. Such results are 7. N ormal concentrations (values) are
due to personal variation in response of averages of many observations. There­
each individual. Age, weight, sex, state fore, when a substance that is normally
of health, route of administration, and not present in the body is isolated, it
the association of other synergic sub­ indicates exposure to this substance.
stances (all these) play an important part. H ow ever, when a substance that is
The lethal dose is the dose that kills in normally present is isolated it becomes
the case in question. It may be remarkably necessary to consider the order of
small in those who are seriously ill or magnitude before interpreting the result
who show idiosyncrasy or allergy to the as exposure to the toxic levels of this
poison. Such a dose may hardly have any substance. Generally, the normal levels
effect on those who are habituated or would be orders of magnitude (1 order
addicted to the particular substance. of magnitude lower means 10_1 = 1 /1 0
What is usually implied by the term times or one-tenth) lower than observed
"minimum lethal dose" is the smallest fatal levels, say, in the case of insecticidal
dose that has been recorded as fatal to a poisoning, vis-a-vis the environmental
healthy person of that age group. It is pollution levels in normal samples. The
roughly around ten times the maximum normal levels are ordinarily, i.e. under
pharmaceutical dose, in the case of similar analytical conditions and using
drugs. In the interpretation of toxico­ the usual analytical methodology, not
logical data, the pharmacologically detectable, i.e. below the detection limits
evaluated LD50 is a good guide to go by. under the ordinary course of analysis.
5. From the analytical report of the poison Determination of normal levels requires
concentration in a given body tissue/ much higher sensitive methodology.
fluid, it is possible to arrive at a proper Likewise, the average arsenic content of
interpretation by comparing the hair is about 1 /2 ppm (part per million) but
observed concentration(s) with those the range of normal values may be up to
recorded in fatal poisoning cases 4 ppm. Therefore, while an analytical result
I involving the poison in question. The of 3 ppm may look like over-exposure
earlier toxicological practice to arrive at when compared with the normal average,
523 Textbook of Medical Jurisprudence, Forensic Medicine and

such a conclusion should not be hastily

f
It is the responsibility of the medi
arrived at without considering the officer to determine the cause ofdeatijy
statistical significance of the normal data, time since death. The toxicologist as ares^
the extreme observed values and the co­ of his analysis provides the evidence thata
efficient of variation (CV = 100 x standard potentially toxic substance was taken and
deviation divided by the mean or average also indicates its residual level in thepost,
value, expressed as a percentage). It should mortem tissue/fluid, and may in certain
also be remembered that arsenic is cases be able to give a good guess of the
concentrated in hair and nails. A course of dosage taken. If the observed poison level
ordinary dose of arsenic over an extended is in the range of a toxic or lethal level and
period could lead to a concentration in hair if all other clinical and pathologic findings
of over 70 ppm, as reported by the Royal fit then it can be said that poisoning is the
Commission on Arsenical Poisoning, in cause of death. It is generally possible to
therapy of dermatological cases, while the give a rough estimate of the likely survival
concentration in other tissues would be time after exposure to fatal amounts of
comparatively low. various materials.
38 Common Household Poisons

q 36.1. Give a brief outline of com m on f. Fire extinguishing Carbon tetrachloride,

household poisons. fluids methyl bromide
g. Matches Antimony, phosphorus
The poisons in daily use m ay be conve­ sesquisulphide, pota­
n ien tly dealt w ith in three groups, viz. ssium chlorate
domestic household poisons, medicinal 4. Rat poisons:
a. Rat paste Potassium/zinc/alumi-
household poisons, and garden poisons, as nium phosphide, barium
per the following table: carbonate, thallium
acetate
b. Rodine (brown bran Yellow phosphorus
DOMESTIC HOUSEHOLD POISONS
paste)
Preparation Toxic components c. Warfarin It is a 4-hydroxy coumarin
1. Babies and children: 5. Sanitary:
a. Baby powder Boric acid a. Deodorants Formaldehyde, naphtha­
b. Crayons (chalk) Coloured with copper, lene
arsenic, lead compounds b. Drain cleaners Sodium hydroxide
c. Crayon (wax) Para-nitroaniline, azo dyes c. Lysol Phenol
d. Fireworks Arsenic, antimony, lead, 6. Miscellaneous:
thiocyanate, phosphorus a. Anti-rust products Ammonium sulphide,
e. Toys (paints) Lead, chromium, copper, naphtha, oxalic acid
etc. b. Cleaning solvents Petroleum hydrocarbons
2. Cosmetics: (inflammable)
a. Cuticle remover Potassium hydroxide, c. Cleaning solvents Carbon tetrachloride,
trisodium phosphate (non-inflammable) trichlor-ethylene
b. Depilatories arsenic Barium sulphide, thallium d. Dentifrices, mouth­ Hydrogen peroxide
c. Hair wave Thioglycolate salts, washes
bromates e. Fluorescent lamps Beryllium
d. Nail polish removers Acetone, ethylacetate f. Furniture polish Turpentine, denatured
e. Sun tan lotions Denatured alcohol, methyl spirit
salicylate g. Ink remover Sodium hypochlorite
3. Kitchen: (5%), oxalic acid
a. Baking powder Tartaric acid (mild irritant) h. Insecticide (spray) Organochloro, organo-
b. Baking soda Sodium bicarbonate phosphorus and carba­
(causes alkalosis in mate insecticides
doses over 5 gm/kg) i. Lavatory cleaners Mineral acids
c. Dish washing com­ Sodium polyphosphates, j. Marking ink Aniline
sodium carbonate k. Moth balls Naphthalene
pounds (machine)
l. Paint removers Sodium hydroxide, ace­
d. Domestic fuel Kerosene
tone, methylene chloride
e. Domestic gas LPG (Accumulated gas (carbon monoxide)
explodes with air when Aniline, nitrobenzene
flame/spark is provided) m. Shoe polish
n. Straw hat cleaner Oxalic acid
(contd.)

529
530 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

MEDICINAL HOUSEHOLD POISONS GARDEN POISONS

1. Antiseptics Iodine
2. Cough remedies Codeine
3. Headache remedies Aspirin, phenacetin,
analgin
4. Pep tablets Benzedrine
5. Sleeping preparations Barbiturates
6. Throat tablets Potassium chlorate
7. Tonic syrup Easton’s syrup
(strychnine)
8. Others Antidepressants, tranqui­
llisers, antibiotics, etc.
9. Hair dye (Vasmol) Paraphenyiene diamine’
resorcinol, etc.
1. Fungicides Lead arsenate, copper
compounds, organic
mercurials, lime, sulphur
2. Insecticides, pesticides Nicotine, tar oils, organo-
chloro and organophos-
phorus compounds,
carbamates, cyanides,
etc.
3. Weed killers (herbicides) Sodium chlorate, arse-
nious oxide and arsenites,
dinitrocresol, paraquat

Corrosives
By corrosion is meant dissolution or gradual wearing away by chemical action. The
corrosive poisons are classified as follows:
1. Mineral acids a. Sulphuric acid
b. Nitric acid
c. Hydrochloric acid
2. Organic acids a. Oxalic acid
b. Carbolic acid
c. Acetic acid
d. Salicylic acid
3. Vegetable acid a. Hydrocyanic acid
4. Alkalis a. Caustic potash and soda
b. Ammonium hydroxide
39 Mineral Acids and Caustic Alkalis

q . 39.1 . Give
the general characteristics, urine scanty, but with alkalis, there may be
symptoms a n d signs, tre a tm e n t, post­ tenesmus and frequency of stools with
modern appearances, an d m e d icolegal blood and mucus. Traces of poison may
aspects of poisoning by mineral acids and also find their way into the trachea and be
strong alkalis. A dd a note on vitriolage. followed by respiratory tract symptoms'.
Mineral Acids and Caustic Alkalis Dyspnoea is often present from oedema of
the glottis and is more marked in the
Mineral acids and strong alkalis are corro­
volatile or strong fuming fluids. Collapse
sive poisons. In dilute solutions, they act
from shock sets in, with cold clammy skin,
as irritants. The symptoms and signs of the
pale anxious face, sunken eyes, dilated
group as a whole are very similar. Their
pupils, rapid feeble pulse, and sighing
action is mainly a local one on the tissues of
respirations. Consciousness is usually
the alimentary tract and to some extent on
retained until near the end, and death may
the respiratory tract. As a rule, there is no
rem ote systemic action with the exception result from primary shock, suffocation due
of sho ck. Their action is characterised by: to oedema of the glottis, or perforation of
(1) extraction of w ater from the tissues, the stom ach. If the quantity of poison
(2) coagulation of cellular proteins, and swallowed is small, death may be delayed
(3) conversion of haemoglobin into haematin. until hypostatic pneumonia develops. The
patient may recover and death may ensue
General sy m p to m s a n d sig n s: The onset of later from complications, such as stricture
s y m p to m s is im m ed ia te . Soon after of the oesophagus with resulting emacia­
sw allo w in g the poison, there is burning tion and malnutrition. The sites likely to be
sensation in the mouth, throat, oesophagus, affected by local contact and the early, late,
sto m a c h , and ab d o m e n , fo llow ed by and delayed effects of corrosives are shown
intense thirst, difficulty in swallowing, diagrammatically in Fig. 39.1.
c o n tin u o u s retch in g , and vom itin g of
shreddy blood-stained material. The vomit Treatm ent: Stomach w ash and emetics are
may be acid ic or alk alin e in re a ction contraindicated. However, a soft stomach
depending upon the substance taken. There tube or Levine tube can be passed with care
are sign s of corrosion of m outh, lips, or within about an hour of the ingestion of
both. The tongue is swollen or shrivelled poison to prevent serious caustic burns of
according to the nature of the corroding the stomach wall followed by ulceration,
agent. With the ingestion of corrosive acids, contraction, and even stricture. If an acid
the bowels tend to be constipated and the has been taken, alkaline carbonates are

531
532 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Fig. 39.1: Diagram matic representation of the site of action and the effects of corrosives:
A. Sites likely to be affected by local contact: (1) Skin—fa ce or elsewhere, (2) mouth and
thorat, (3) upper alimentary tract, (4) respiratory tract
B. Early effects: (1) Pain and shock, (2) vomiting, (3) dyspnoea due to respiratory obstruction
from laryngeal oedem a
C. Late effects: (1) Perforation of stomach, (2) pulm onary oedem a or bronchopneumonia
D. D elayed effects: (1) O e so p h a g e a l or p ylo ric stricture, (2) laryngeal stricture,
(3) pulmonary fibrosis

contraindicated. Weak alkalis and plenty

of w ater or neutralising agents, such as
milk and egg albumin, should be given. In
the case of an alkali, a weak acid, such as
vinegar, will neutralise its effects. Morphine
by injection is necessary to relieve pain, ice
to suck to relieve thirst, intravenous fluids
to combat fluid loss, and corticosteroids for
shock and to prevent oesophageal stricture.
Tracheostomy may be necessary, if there is
acute oedema of the glottis. The other treat-
ment is along the lines indicated for general
treatm ent of poisoning. M ed ico leg a l a sp ects: Attempted suicide
P o s tm o rtem ap p eara n ces: These may be with corrosives is not seen now owing
expressed generally as signs of corrosion largely to the use of other less painful sub­
and partial destruction of the parts with stances, like barbiturates, synthetic narco­
w hich the poison has been in contact. tics, and organophosphorus compounds.
Externally, the lips may be burnt and trickle Corrosives are rarely used for homicide
marks may be found running from the owing to their painful action. They are
mouth to the chin, neck, and chest. Inter­ sometim es throw n on the face out of
nally, they vary in extent from localised jealousy or in fits of rage. This is known as
patches to extensive areas, particularly in vitriolage. They cause severe injury or even
death from accidental spilling.
stomach. Perforation of the stomach is
common with sulphuric acid. Irritation of V itriolage (Fig. 39.3): This means throwing
the respiratory tract is found in case of vola­ of any corrosive; not necessarily sulphuric
tile poisons, e.g. nitric acid, hydrochloric acid, on a person with malicious intent out
acid (Fig. 39.2). of jealousy, hatred or vengence to seek
 Mineral Acids and Caustic Alkalis
Fig. 39.3: Vitriolage. The facial disfigurement
of this person is due to throwing of sulphuric
acid by some one out of malice. The injury is
characterised by corrosive stains on the skin
and trickled marks. In this case, eyes are
spared. The permanent disfigurement of face
results in grievous hurt
revenge. These fluids are usually thrown
on the face with the object of destroying
vision or causing facial disfigurement and
this results in grievous hurt, Sulphuric acid
(oil of vitriol) is most commonly employed
for this purpose and hence it is called
vitriolage. Nitric and carbolic acids are
sometimes used. The use of caustic soda,
caustic potash, iodine and marking nut
juice has also been recorded. Sulphuric acid
produces severe chemical bums. They are
characterised by discolouration and
staining of skin and clothing (brown or
533
black in sulphuric acid and yellow in nitric
acid), trickle marks, absence of vesication
and red line of demarcation, and the
presence of the chemical substance in the
stains. Immediate treatment consists of
washing away the corrosive acid with large
amount of water and soap or dilute solution
of sodium or potassium bicarbonate. Later,
a thick paste of magnesium oxide is
applied. The raw surface may afterwards
be covered with antibiotic ointment; when
the eyes are involved, they should be
washed at once with a large amount of
w ater followed by irrigation with 1%
solution of sodium bicarbonate. A few
drops of olive oil are then instilled into the
eyes. Eyedrops containing antibiotics and
steroids are helpful. Acid attacks have been
on the increase. Consequently, in a separate
section in the law for punishment in these
cases, rigorous punishment up to seven
years is recommended acid attack.
Q. 39.2. What is acid attack? What is its
punishment?
Acid attack is throwing or attempting to
throw acid or any acid substance or with
corrosive or burning nature and which can
cause bodily injury leading to scars or
disfigurement or temporary or permanent
disability or grievous hurt to that person.
The punishment ranges from 5 to 7 or
10 years to life imprisonment and fine
depending on gravity of the case which is
paid to victim as compensation. (IPC
Section 326A and Section 326B)
 40 Organic Acids #

The important poisons amongst this group It has two distinct effects, local and
are oxalic, carbolic, acetic, and salicylic acids. remote, e.g. shock, hypocalcaemia, and
They have a powerful and rapid action. They renal damage. Even dilute solutions cause
act as strong irritants locally and also possess serious systemic effects: Oxalic acid
a powerful remote action after absorption. combines with serum calcium to form
insoluble calcium oxalate (hypocalcaemia).
Q. 40.1. Give the general characteristics, Local action: It readily corrodes the
symptoms and signs, treatm ent, post­ mucous membrane of the alimentary tract
mortem appearances, and m edicolegal
but rarely the skin.
aspects of oxalic acid poisoning.
Remote action: Large doses cause rapid
OXALIC ACID__________________________ death from shock (narcotic effect). There is
Oxalic acid is a corrosive acid. It is a a sour taste in the mouth and burning in
crystalline substance, sparingly soluble in the throat and stomach. This is followed by
water, and resembling in appearance persistent vomiting. The vomit is black in
magnesium sulphate and zinc sulphate. It colour 'coffee ground' due to altered blood.
can be differentiated from them by the If the case is of short duration, the intestinal
following features: tract is not affected, but when life is prolon­
ged, there is pain and tenderness over the
Oxalic Magnesium Zinc abdomen and purging and tenesmus may
acid sulphate sulphate
appear. After absorption, signs of collapse
1. Taste Sour and Bitter and Bitter and
acidic nauseating metallic soon appear.
2. Reaction Strongly Neutral Slightly acid Numbness and tingling indicate the
acidic effects of hypocalcaemia on the nervous
3. Heat Sublimes Not so Not so
4. Sodium Efferve- No efferve- No efferve- system. Spasmodic twitching of muscles of
carbonate scence but scence but a scence but a the face and extremities and even convul­
no precipi- white precipi- white precipi- sions may follow.
5. Ink or iron Bleaches Not so Not so Where death is not rapid, evidence of
irritation of the kidneys may be found as
oxalic acid has a nephrotoxic action. There
Symptoms and signs: The character and may be oliguria, and the urine contains
severity of the symptoms depend upon the albumin, blood, and calcium oxalate crystals.
amount and the concentration of the acid The presence of calcium oxalate crystals in
swallowed. the urine is termed oxaluria. These crystals
534
have the shape of an envelope when seen
under a microscope.
Fatal dose: The average fatal dose of the
poison is about 15 to 20 gm. The smallest
recorded fatal dose is 5 gm.
Fatal period or survive Death
usually occurs within an hour. The longest
recorded period is five days.
Treatment: Since the degree of corrosion is
not as severe as in mineral acids, a soft
stomach tube can be passed with care and
the stomach washed out using lime water.
Warm water should not be used for stomach
washas it may dissolve more acid. The antidote
for oxalate poisoning is any calcium pre­
paration which converts the poison into
insoluble calcium oxalate, the most readily
available preparation being chalk. A
suspension of 30 gm of chalk in water or
milk will neutralise about 20 gm of oxalic
acid. Alkalis, such as soda, potash or
ammonia, should not be given as their
oxalates, are soluble. Calcium gluconate
may be given by mouth or 10 ml of a 10%
solution intravenously. In severe cases,
parathyroid extract should be given.
Urinary output should be checked to detect
the possibility of renal damage and fluid
intake controlled as found necessary. The
rest of the treatment is symptomatic.
acid haematin. The mucous membrane is
corroded and detached in varying degrees
depending on the concentration of the acid.
Perforation, however, is rare. The blood
vessels in the submucous layer may be seen
distinctly as dark lines due to acid haematin.
The outer coat of the stomach may be
inflamed.
If the effects are only narcotic, there will
be congestion of lungs, liver, kidneys and
brain, without any local changes. Where
death has been delayed, inflammation will
be found in the upper portion of the small
intestine and the kidneys.
M edicolegal aspects: Oxalic acid and its
salts are used in industry as bleaching
agents, and in calico printing. Its household
use for bleaching has made it a dangerous
substance. Accidental poisoning is due to
its being mistaken for magnesium sulphate
or sodium bicarbonate. Oxalates occur in
the leaves of rhubarb and have caused
poisoning when the leaves are used as safe
vegetables. Oxalic acid is sometimes taken
with suicidal intention but rarely used for
homicide on account of its sour taste and
rapid action. Solutions containing oxalic
acid cause falling off of hair when poured
on the head. Oxalic acid is sometimes used
to erase writing in attempts at forgery.

Awoman aged 50 swallowed about 30 gm of Q. 40.2. Give the general characteristics,

oxalic acid in beer. In half an hour she com­ symptom s a n d signs, treatm ent, post­
plainedof burning pain in the stomach and was m ortem ap pearances, an d m edicolegal
foundrollingabout. Chalkandwater were freely a s p e c ts of c a rb o lic a c id (p h e n o l)
given and she recovered.
poisoning.
Postmortem appearances: If the poison is CARBOLIC ACID (PHENOL)_____________
taken in a concentrated form, the appea­ When pure, carbolic acid (phenol) consists
rances are similar to those in poisoning by of colourless, prismatic needle-like crystals
mineral acids, except that the lips and chin having a sweetish burning taste and
do not show staining. The mucous mem­ characteristic phenolic smell. Though it
brane of the tongue, mouth, throat and does not turn blue litmus red and has no
gullet is commonly white as if bleached but acid reaction, it is called an acid because it
is sometimes reddened by irritation. forms carbolates (salts) when acted upon
The stomach contains a dark brown by strong bases. It is slightly soluble in
gelatinous liquid due to the formation of water and readily soluble in glycerine and
 536 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
alcohol. It liquefies and becomes pink on
exposure to light and air. The commercial
acid is mixed with impurities, like cresol
and may be dark brown in colour. Carbolic
acid enters into the composition of most
disinfecting agents, such as Dettol and
lysol.
symptoms and signs: Poisoning by carbolic
acid is known as carbolism. It has two
actions, viz. a local action on the skin, and
alimentary tract, and a remote action after
absorption. It is rapidly absorbed from the
alimentary tract, rectum, vagina, serous
cavities, wounds, and even intact skin.
L ocal action: Skin—It is a coagulant of
protein but does not enter into any firm
combination with it, and thus it has remark­
able penetrating qualities. It, therefore,
causes necrosis and sloughing of the tissues.
Carbolic acid acts as a mild corrosive and
anaesthetic upon the skin and mucous
membranes. It causes eschar formation.
A lim en tary tract: Hot burning pain
extends from the mouth to the stomach,
followed by tingling and anaesthesia.
Swallowing and speech become painful
and difficult. Vomiting may not take place
owing to the anaesthetic action on the
stomach. The lips, mouth and tongue are
corroded. The chin and cheeks may be
burnt. These bums appear white, bleached
and hardened. They later become brown,
the dead tissue sloughing rapidly.
Rem ote action: Shock ensues, both local
(corrosive) and the more remote (central
nervous depressant) action of phenol being
rapidly established. The victim feels giddy.
The skin is cold and clammy, pulse weak
and thready, pupils contracted and
pinpoint, temperature subnormal, and
breathing stertorous and laboured. The
breath smells strongly of carbolic acid. On
account of contracted pupils and cold and
clammy skin, it is likely to be mistaken for
opium poisoning.
When death is not rapid, evidence of
irritation of kidneys may be found as
carbolic acid has a nephrotoxic action.
There may be suppression of urine or
oliguria. The urine contains albumin, blood
casts and metabolic products of carbolic
acid, viz. hydroquinone and pyrocatechol.
On standing or when exposed to air, the
metabolic products are oxidised resulting
in dark smoky green colour of the urine.
This is known as carboluria and served as a
warning of the toxic action of carbolic acid
when it was used as an antiseptic dressing
in the past. Coma usually follows rapidly
and death results from paralysis of the
respiratory or cardiac centre.
The presence of carbolic acid in the urine
is indicated by addition of a little ferric
chloride when the urine turns blue or little
bromine water when urine forms a white
precipitate of tribrom phenol. The urine
containing carbolic acid also reduces
Benedict's and Fehling's solution.
Fatal dose: Twenty drops of pure phenol
have caused death and probably twice that
quantity of most carbolic disinfectants
would be dangerous.
Fatal period: Death from carbolic acid
usually occurs in three to four hours. It has,
however, followed in three minutes and has
been delayed for as many as 60 hours.
Treatment: Since the degree of corrosion is
not as severe as mineral acids and the
tissues are also hardened by carbolic acid,
a soft stomach tube can be passed with
care. Thorough gastric lavage using a 10%
solution of glycerine in water or plain water
to which some magnesium sulphate is
added should be carried out and continued
until the washings no longer emit phenolic
odour. Then, about one ounce of magne­
sium sulphate or two ounces of medicinal
liquid paraffin may be left in the stomach.
Magnesium sulphate forms an insoluble
sulphocarbolate. Alcohol which tends to
prevent the cauterising action of phenol
 Organic Acids 537

maybe given in 10% solution but as it does viscera in poisoning with other corrosives.
n0t combine in any way, it should be M edicolegal aspects: Carbolic acid and its
removed shortly afterwards. Demulcents, derivatives are used as antiseptics, dis­
such as white of an egg or milk may be infectants, and surface anaesthetics. Some
helpful. Intravenous saline with sodium of these substances were used in the past
bicarbonate should be administered to
to commit suicide. They are now displaced
render the urine alkaline. Other treatment
by soporifics. Phenol is rarely used for
should be along general lines. The surface
homicide because of its smell and taste. It
(skin or mucous membrane) burns should
is sometimes used to procure abortion.
be washed with water, followed by a local
Accidental poisoning may occur from
application of castor oil. If this is not
indiscriminate medicinal use of this
available, bums may be mopped with soap
substance.
and water or swabbed with alcohol.
A healthy woman, aged 30, swallowed
Postmortem appearances: The grayish- nearly 15 ml of an alcoholic solution of
white stains produced by the poison may carbolic acid containing 35.8 per cent of the
be present at the angles of the mouth and poison. About half the poison was removed
on the chin, and its odour is usually by the use of stomach pump, the remaining
perceptible. The mucous membranes of the half having been absorbed. The most promi­
mouth and oesophagus are swollen, nent symptoms were insensibility within 10
hardened and discoloured and the tongue minutes and dizziness speedily passing
is usually white and swollen. into profound coma, irregular breathing
The mucous membrane of the stomach and pulse, contracted pupils, cyanosis, fall
forms projecting folds and prominent rugae. in body temperature to 94°F, and
It is thickened, more or less brownish in haemoglobinuria which appeared one hour
colour, and looks leathery. The contents after the poison was taken and lasted for
appear dark brown mucoid with chara­ seven and half hours. The urine gave
cteristic phenolic smell. The peritoneal reaction for carbolic acid for two days. The
surface of the stomach is injected. The woman recovered with energetic treatment.
duodenum and upper part of the small
intestine may show evidence of corrosion SN on Carboluria: Urinary findings of
and injection of vessels. The liver and spleen carbolic acid go by the name of carboluria.
frequently show a whitish hardened patch In this, patient's urine is clear in start but
where the stomach has been in contact with latter becomes smoky in colour. This is due
them, due to the transudation of phenol. to hydroquinone and pyrocatechol, which
The glottis may show some swelling and are the products of carbolic, acid in urine.
congestion. The lungs and brain are fre­ SN Ochronosis or phenol marasmus: In
quently congested. The kidneys may show chronic expesure to phenol, amount
parenchymal degenerative changes. surgeous, nurses, etc., who used it as dis-
The viscera to be sent to the chemical infectoment, a group of manifestations
examiner should be preserved in saturated known as ochronosis or Phenol and skin
solution of sodium chloride and not in pigmentation, vertigo, headache anorexia
rectified spirit, which is used to preserve and loss of weight.
 Vegetable Acid Poisons

Under this heading, the following poisons is commonly used in veterinary practice,
are discussed, viz. hydrocyanic acid and its contains 4 per cent.
salts, the cyanides. Hydrocyanic acid is a vegetable acid
Hydrocyanic acid is a general proto­ naturally found in many fruits, e.g. peach,
plasmic poison. It inhibits the cytochrome plum, and bitter almonds, and leaves of
oxidase system for oxygen utilisation in cherry-royal, a preparation which is used
cells. Death is due to cytotoxic or histotoxic medicinally. It exists in the form of
anoxia, although the blood may contain a glycoside amygdalin, which is harmless.
normal oxygen content. Other enzyme The enzyme emulsin hydrolyses it and
systems are also inhibited but to a lesser liberates the harmful hydrocyanic acid. It
degree. Cyanides show, in addition, a is also liberated from cyanides by reaction
corrosive effect on the mucous membrane. with acids.
Hydrocyanic acid is readily absorbed
Q. 41.1. G iv e the ge n eral ch aracters, from mucous membrane and is very toxic
sym ptom s an d signs, treatm ent, post­ when inhaled. The rapidity with which the
m ortem ap pearances, and m edicolegal
(salts) cyanides, upon ingestion, cause
aspects of poisoning by hydrocyanic acid
death will depend on the amount of
an d cyanides.
hydrochloric acid present when the salt was
HYDROCYANIC ACID AND CYANIDES swallowed and the subsequent liberation
of hydrogen cyanide which is absorbed by
Hydrocyanic acid, also known as cyanogen the gastric mucosa. Cyanides tend to
or prussic acid, is a colourless gas with a change into carbonates, if kept too long but
penetrating odour resembling that of bitter
the mixture is still poisonous.
almonds. Liquid hydrocyanic acid is a
highly volatile colourless fluid. Hydro­ Symptoms and signs: Inhalation of the gas
cyanic acid combines with bases of several results in instantaneous death. When a
metals and strong alkalis to from cyanides large dose of liquid hydrocyanic acid is
(salts). The cyanides are white powders and swallowed, symptoms usually occur at
are used in photography, electroplating, once but in some cases there is an interval
metallurgy, tanning, fumigation of ships, of about one minute. This may allow the
and in agriculture to prevent plant decay. victim to perform certain voluntary acts,
The pharmacopoeial preparation of such as corking or throwing away the bottle
hydrocyanic acid contains about 2% of the or walking some distance. If death is
anhydrous acid while Scheele's acid, which delayed for a few minutes, agonising

dyspnoea, convulsions and dilated pupils
may be noted.
With a small dose, the individual first
experiences headache, confusion, giddi­
ness, nausea and some loss of muscular
power. The characteristic smell of bitter
almonds may be noticed at the mouth and
inthebreath. There may be violent convul­
sionsbefore the patient loses consciousness
anddies. A small quantity of fine froth may
appear at the mouth. In gaseous form, it
has bitter almond odour, but 20 to 40% of
population may not be able to appreciate
the odour as this depends on a sex-linked
recessive trait inheritance.
Following ingestion of the salts, e.g.
potassium cyanide, the symptoms appear
after about 10-20 minutes as it has to be
acted upon by hydrochloric acid of the
gastric juice to liberate hydrocyanic acid.
Principal symptoms include giddiness,
dyspnoea, dilated and fixed pupils, convul­
sive seizures, and loss of muscle power.
There may be a corrosive effect on the
mouth, throat and stomach, and epigastric
pain and vomiting. The face is cyanosed,
the jaw may be tightly clenched, and froth
may be seen at the mouth. The respirations
are spasmodic, and the pulse almost
imperceptible. Death occurs from respira­
tory paralysis.
Chronic poisoning occurs from repeated
exposure to non-lethal doses of hydro­
cyanic acid or cyanides among photo­
graphers, gilders and others who handle
these preparations. Such persons suffer
from headache, vomiting, diarrhoea,
chronic cachexia, and mental disturbances.
Fatal dose: 50 to 60 mg of the pure acid, 30
drops of the pharmacopoeial preparation,
60 drops of crude oil of bitter almonds, and
200 mg of potassium cyanide have proved
fatal.
Fatal period: Death in some cases is
immediate but the average period may be
539
taken as about two to ten minutes for hydro­
cyanic acid and 30 minutes for sodium or
potassium cyanide.
Treatment: Only immediate treatment may
be of value. The aim is to reverse the
cyanide-cytochrome combination. This is
achieved by converting haemoglobin to
methaemoglobin so that the cyanide will
combine with methaemoglobin to form
cyanmethaemoglobin, which is non-toxicj
Also, cyanide can be converted to relativep
non-toxic thiocyanate. Treatment should,
therefore, be as follows. Survival for four
hours is usually followed by recovery.
Two 20 ml ampoules of 1.5% Dicobalt
tetracemate (Kelocyanor) are injected
intravenously followed by 20 ml of 50%
glucose. Intravenous administration of
50 ml of 1% sterile aqueous solution of
methylene blue (methylthionine chloride,
USP) may also be used as an antidote. It
converts haemoglobin into methaemo­
globin which combines with free cyanide
thereby removing it from the reaction.
Hydroxocobalamin: 50 mg/kg in commercial
solution (1000 |Ag/ml) as an IV infusion
works by combining with cyanide and
forming cyanocobalamin which is excreted
in urine.
In the case of potassium cyanide or dilute
hydrocyanic acid poisoning, the stomach
should be lavaged with a 5 to 10% solution
of sodium thiosulphate, 'or a mixture of
sulphates (ferrous and ferric) of iron follo­
wed by a solution of potassium carbonate
to form Prussian blue which is inert.
Emetics may be used, if a stomach tube is
not readily available.
In poisoning by inhalation with hydro­
cyanic acid gas (cyanogen), the patient
should be removed from the source of
contamination. The use of artificial respira­
tion and 100% oxygen is of the highest
value. Intravenous administration of
sodium nitrite and sodium thiosulphate
will be necessary and should be repeated
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
if symptoms reappear. In case of mercury
cyanide poisoning, injection of BAL may be
necessary.
Postmortem appearances: These are those
of asphyxia. The appearances are external
and internal.
Externally, there is smell of bitter
almonds from the body. The face, lips, and
body surface frequently show irregular
pink patches. Sometimes, the skin is livid
or cyanosed and the nails blue. There may
be fine froth at the mouth. The eyes may
be bright, glistening and prominent with
dilated pupils. The postmortem staining is
pink often incorrectly referred to as cherry
red. Rigor mortis sets in early, if there have
been convulsive seizures.
Internally, the characteristic smell of
bitter almonds is usually present in the
stomach, serous cavities and brain. The
mucous membrane of the stomach may be
pink, and the other organs together with
blood, are usually of the same shade owing
to the impeded oxygenation of the tissues
by the cyanide and the postmortem forma­
tion of cyanmethaemoglobin. Blood stained
froth may be found in the trachea and
bronchi. The brain and meninges are
hyperaemic and petechial haemorrhages
appear in the pleura and pericardium,
brain, meninges and lungs.
When potassium cyanide has been
taken, there may be slight corrosion of the
mouth and reddening of gastric mucous
membrane which may be of a brick red to
brown colour due to the formation of
alkaline haematin. The stomach may
contain frank or altered blood from the
erosions and haemorrhages in its walls.
The brain, lungs, blood, stomach contents,
urine, and vomit should be preserved for
chemical analysis taking care that the
samples present no hazard to those
packing, transporting, or unpacking them.
It is necessary that the dissector takes
precautions to prevent ill-effects from
inhalation of cyanide from stomach
contents during autopsy and the rubber
gloves worn are in perfect condition.
M edicolegal aspects: Hydrocyanic acid and
cyanides are used principally as suicidal
agents, the cyanides being about three
times as common as the acid owing to their
more common usage in the garden and in
photography. Since cyanides satisfy most
conditions of a suicidal poison of choice,
they are usually resorted to by those who
have firmly made up their mind to commit
suicide. Some suicide bombers use cyanide
to die before they are cought or after their
task is over. Hitler appears to have killed
himself by cyanide.
Accidental poisoning occasionally
occurs when it is used for fumigation or
disinfection. Chemists and laboratory
assistants are sometimes overcome by the
sudden evolution of hydrocyanic acid
following the pouring away of cyanide
solutions into sinks already containing
strong acid residue.
Homicidal poisoning is rare because of
the peculiar smell and taste of the acid.
Hydrocyanic acid is also used as a cattle
poison. The double cyanides, viz. potassium
ferrocyanide and potassium ferricyanide
are non-toxic but may produce poisonous
symptoms and cause death when taken
with acids.
In some countries, hydrocyanic acid is
used for judicial execution. The condemned
person is strapped to a chair. Cyanogen is
evolved by dropping cyanide 'eggs' into a
pan containing strong acid. The inhalation
of fumes of cyanogen causes instantaneous
death.Cult suicide by about 900 people
taking by mouth cyanide solution prepared
by Dr Schat, a doctor of the group
happened with the doctor ending himself
by shooting himself with a gun. Near
Baroda in India in a field cyanide contami­
nated water caused death of three people.
Industrical effluents should be properly
disposed, otherwise such incidents are
liable to be repeated.
 Vegetable Acid Poisons 541
Illustrative Cases

Awoman swallowed 50 ml of a solution of potassium cyanide, used for photographic purposes. The
quantity taken amounted to 300 mg. In 2 minutes, she became unconscious, the whole of the body
was slightly convulsed, and the pupils were dilated. She foamed at the mouth, the pulse was small
and feeble, and she died within 20 minutes.
Amanbought a 7 lb tin of Cymag to fumigate a small greenhouse. He sprinkled one-third over the
staging, shut the door and returned to the house. Finding he had left his keys in the greenhouse he
went back and opened the door. He was found lying with his feet on the threshold and his head in
thehouse. His keys were still on the staging. Analysis showed traces of cyanide in the lungs but no
perceptible cyanide in the stomach or other viscera.
§
42. Non-Metallic Poisons
43. Metallic Poisons
44. Vegetable Poisons
45. Animal Poisons
46. Mechanical Poisons

47. Food Poisoning and Poisonous Foods

42
Non-Metal lie Poisons
__________IRRITANT POISONS___________
The irritant poisons are classified as: (1) in­
organic poisons (non-metals and metals),
(2) organic poisons (vegetables and
animals), and (3) mechanical poisons.
Corrosives in very dilute solutions act as
irritants.
Irritant poisons cause symptoms of
gastroenteritis and also exert a marked
depressant action after absorption. Chronic
metallic poisoning leads to such a lingering
death that chronic arsenic poisoning has
been known as a 'slow-poison'.
General symptoms and signs: The onset of
symptoms and signs which is variable is
usually within half an hour to an hour.
There is burning sensation in the mouth,
throat, oesophagus, stomach and abdomen,
followed by intense thirst, difficulty in
swallowing, continuous retching, painful
vomiting and diarrhoea. The vomited
matter at first consists of normal stomach
contents, but later becomes bilious in chara­
cter and may be of dark brown appearance
due to altered blood. The diarrhoea is severe,
accompanied by tenesmus and consists at
first of loose stools and later of stools mixed
with mucus and blood. Collapse from
shock sets in with cold clammy skin, pale
anxious face, rapid feeble pulse, and
sighing respirations. Cramps may affect the
muscles of the limbs. Consciousness is
usually retained during this period.
545
Convulsions and/or coma may follow.
Death occurs within 24 hours from shock,
or in a few days from exhaustion. The
patient may recover and death may ensue
later from stricture of the oesophagus or
other sequelae.
Postmortem appearances show changes
chiefly in the stomach, and frequently in
the duodenal and rectal portions of the
intestinal tract.
NON-METALUC POISONS____________
The important poisons in this group are:
(1) phosphorus, and (2) iodine.
PHOSPHORUS___________________________
Q. 42.1. G iv e the g e n eral ch arac te rs ,
symptoms, signs, treatment, postmortem
ap pearances, and m edicolegal aspects
of phosphorus poisoning. Add a note on
necrobiosis of liver.
Phosphorus exists in two forms, viz. white
as crystalline and red as amorphous. The
white one becomes yellow on exposure to
the air. It is, therefore, also called yellow
phosphorus. It exists in the form of trans­
lucent, waxy, luminous cylinders. It is
slightly soluble in alcohol, freely soluble in
carbon disulphide, and insoluble in water.
Being easily oxidisable, it is kept sub­
merged in water to prevent ignition. When
exposed to atmosphere, it gives off dense
white fumes of phosphoric and phosphorus
 546 Textbook of Medical Jurisprudence; horensic Medicine and Toxicology
acids with a strong odour of garlic and are
luminous in the dark. The fumes glow with
pale yellow colour (phosphorescence). Red
phosphorus is inert unless contaminated
with yellow phosphorus. It is non-luminous,
amorphous, odourless, insoluble in carbon
disulphide, and does not give off fumes
when exposed to air. Mixed with powdered
glass, it is used on the side (striking surface)
of the match box. The tip of the match stick
contains a mixture of potassium chlorate
and antimony sulphide.
Phosphorus is a protoplasmic poison. It
affects cellular oxidation. Its effect on
cellular metabolism is comparable to
ischaemia. Under such anoxic condition,
the metabolism of the cells diminishes
considerably. This is known as necrobiosis,
which is classically manifested in the liver.
Deposition of glycogen in liver is inhibited
while deposition of fat is increased.
Acute Poisoning
Symptoms and signs: There are two phases
in the symptoms, primary, due to the local
irritant action on the gastrointestinal tract,
and secondary, due to the action of the
absorbed poison, and there is usually a
considerable interval between them.
The primary symptoms usually occur
within two to six hours. There is burning
pain in the throat, oesophagus and stomach
with intense thirst, frequent gaseous eruc­
tations, nausea, vomiting, and diarrhoea.
The patient may complain of a garlic taste
in the mouth and a garlic odour may be
perceived in the breath. The vomited
matter is darkened by blood, smells of
garlic, and is luminous in the dark. The
faeces may be dark, luminous and offen­
sive. The luminosity of vomit and faeces is
diagnostic. This primary irritative stage
lasts one to two days and may be so severe
that the victim dies from collapse and
cardiac failure. However, this is not the
usual course and remissions are common
after the usual bouts of vomiting and
diarrhoea. Contact of phosphorus withskin
produces slow healing burns.
In the usual clinical course, there is a
remission lasting for about two to three
days. Then, secondary symptoms occur
due to the absorbed poison damaging
mainly the liver and kidneys. The original
symptoms return, and in addition, there is
jaundice and distension of the abdomen
due to enlargement and necrosis of the
liver. In the early stages, the liver is
enlarged due to fatty degeneration
(necrobiosis) and in late stages, it is
shrunken due to necrosis (acute yellow
atrophy). Purpura and epistaxis may follow
due to hypoprothombinaemia. The faeces
are pale. The urine is scanty and concen­
trated, strongly acid in reaction, and
contains blood, albumin, bile, and some­
times sugar and crystals of tyrosine, leucine
and cystine due to disturbed metabolism.
Pregnant women abort with alarming
flooding. Nervous system involvement
manifests as frontal pains, insomnia,
ringing in the ears, impaired vision, formi­
cation, cramps, and paralysis. Priapism is
frequent. Death results from hepatic and
renal insufficiency. The clinical picture is
suggestive of acute yellow atrophy of the
liver.
Fatal dose: A dose of 60-120 mg is usually
considered a fatal dose, though as with all
gastric irritants, vomiting may permit
recovery from much larger doses.
F a tal p eriod: Death may occur from
collapse within 24 hours. In the normal
course, it may occur in six to seven days or
longer.
Treatment:Demulcents (oily and fatty sub­
stances including milk) are contraindicated
as they dissolve and promote absorption
of phosphorus. The stomach should be
lavaged with 0.5% solution of potassium
permanganate repeatedly, till no more
smell of garlic is perceptible, and the bowel
evacuated by a brisk purgative. Potassium
 vMetallic Poisons
permanganate acts as a chemical antidote.
It oxidises phosphorus to harmless
compounds, viz. phosphoric acid and
phosphates. A dilute solution of copper
sulphate (0.1%) may be used as an antidote
instead of permanganate. 200 mg of copper
sulphate may be given every five minutes
until vomiting occurs. Copper sulphate is
reduced by phosphorus and is precipitated
as metallic copper on the particles of phos­
phorus, thus rendering them inert. Liquid
paraffin may retard absorption and may be
given. Intravenous saline is useful to
combat shock, calcium gluconate, if blood
calciumis diminished, and sodium bicarbo­
nate to maintain alkali reserve. Intravenous
dextrose may be needed to protect the liver.
Peritoneal or haemodialysis may be
necessary to combat renal failure. Skin
bums should be thoroughly washed with
1%copper sulphate solution.
Postmortem A ppearances
If death takes place within the first 24
hours, the appearances generally are those
of a highly irritant poison, consisting of
inflammation or erosion of the mucous
membrane of the pharynx, oesophagus,
stomach and intestines, with cloudy
swelling of the liver and kidneys. The
contents of both stomach and bowel may
be luminous in the dark, and the body may
smell of garlic.
Where the usual course has been follo­
wed and death takes place after an interval
of a few days, characteristic external and
internal appearances are found.
Externa/: The body may be emaciated and
may smell of garlic. Jaundice and haemorr­
hages both under the skin and from various
natural orifices of the body are the special
features of external examination.
Internal: Fatty degeneration and haemorr­
hages are the special features of the internal
examination. The toxic effects are well
marked in the stomach and intestines, liver,
heart, kidneys, and blood.
547
The mucous membrane of the stomach
and intestine is yellowish or grayish white
in colour, softened, inflamed, or even corro­
ded. Patchy areas of erosion with haemorr­
hages and perforation are common. The
contents of the stomach and intestines may
have a garlicky odour and may be luminous
in the dark.
The liver undergoes necrobiosis. Its
characteristics and differentiating features
from acute yellow atrophy are as follows:
Fatty degeneration of the heart muscle,
kidneys and voluntary muscle fibres is
present. Subendocardial haemorrhages in
Necrobiosis Acuteyellowatrophy
1. Size Enlarged at Smaller with a
first but wrinkled capsule
shrunken later
2. Colour Uniformly yellow Dirty yellow
3. Consistency Soft and greasy Hard and brittle
4. Structure Fatty degenera- Necrosis of most cells
spots
5. Stage of Early Late
poisoning
the left ventricle are common. The blood
may appear tarry and its coagulability is
diminished.
In a case of suspected phosphorus
poisoning, the viscera for chemical analysis
should be preserved in saturated solution
of-common salt and not in spirit as the
luminosity is lost. Sometimes, the chemical
examiner reports the presence of phos­
phates in the viscera. This has no signifi­
cance. Finding of phosphorus in free form
only is of significance.
Medicolegal Aspects
Yellow phosphorus is an ingredient of
fireworks and certain rodent and insect
poisons. Accidental deaths in children who
have eaten fire crackers or rat pastes are
known. Occasionally, rat pastes and vermin
killers which contain yellow phosphorus
 Textbook of Medical Jurisprudence. Forensic Medicine and Toxicology
(zinc phosphide, aluminium phosphide)
are taken to commit suicide. The smell and
taste of phosphorus in the form of rat
poison can be disguised when mixed in
strong sweet tea or coffee; it can then be
used as a homicidal poison because
(a) symptoms appear after some delay and
resemble acute liver disease, and (b) death
occurs after a few days. However, it must
be remembered that phosphorus can be
detected even in putrefied bodies.
Phosphorus, concealed in moist paper, wet
cloth, or dung, is occasionally used to set
fire to postal letter boxes and huts.
Phosphorus is certainly not responsible for
the so-called spontaneous combustion in
cotton bales. It is due to heat generation
from bacterial fermentation or drying oils.
Chronic Poisoning
It results from frequent inhalation of phos­
phorus fumes over a period of years. The
gas commonly attacks the lower jaw in the
region of a decayed tooth where the
suppurative microorganisms are already
present. The first symptom is toothache,
followed by swelling of the jaw, loosening
of the teeth, necrosis of gums, and then
sequestration of bone in the mandible. This
is known as the phossy jaw. It is an osteo­
myelitis of the jaw bone with multiple
sinuses discharging foul smelling pus.
Constitutional symptoms, such as weak­
ness, weight loss, anaemia, jaundice, and
pain in the joints are common.
Illustrative Cases
A 43-year-old man was admitted to hospital
three days after ingesting 1.2 gm of yellow
phosphorus in the form of rat poison. Within a
few hours of taking the poison his skin felt hot
and flushed. He said he had such flatulence as if
he had eaten many onions. The next day there
werenosymp-toms. Onthe third day, hebecame
mildly jaundiced and vomited black syrup-like
material which contained altered blood and
mucus. Inhospital next day, vomiting continued
inspite of gastric lavage withpermanganate. He
became oliguric and had persistent diarrhoea
On the day after admission, he suffered froma
series of convulsions, followed by spastic, then
flaccid quadriplegia, and died.
In 1952 at the County of London Sessions,
Ekpeyong Eyo was sentenced to 12 months'
imprisonment for administering rat poison toa
number of students. The rat poison had been
added to tea, coffee and soup.
An airman was shot whilst navigating a plane
over enemy territory, the bullet entering the left
thighandpassing into the abdomen. Thewound
emitted a visible vapour with the characteristic
smell ofphosphorus. Themissilefragments were
removed by operation but most of the phos­
phorus estimated at 200 mg was not recovered.
For 2 days, thepatient made goodprogress, then
became semi-comatose. The skinbecame yellow,
anuria developed and death occurred on the
sixth day after the injury. The autopsy showed
fatty degeneration and necrosis of the liver and
fatty degeneration of the kidney.
Hunter records the case of a match dipper of30,
who after 12 years' employment with yellow
phosphorus developed pain in the upper jaw.
Three teeth were extracted but the socket broke
down and the jaw sloughed. Sequestra were
removed frombothsides, andeventually, 5 years
later, the whole lower jaw had to be removed.
IODINE________________________________
Iodine occurs as brown, scaly crystals with
a metallic lustre and unpleasant taste. At
all temperatures, it gives off a violet-
coloured vapour possessing a characteristic
odour.
Iodine has a direct action on the cells by
precipitating proteins. The effects are thus
similar to those produced by acid corro­
sives and the principal manifestations of
poisoning are vomiting, collapse, and
coma. The vapours of iodine are strongly
irritant to the respiratory passages.
Q. 42.2. Give symptoms, signs, treatment,
postmortem appearances, and medico­
legal aspects of iodine poisoning. Add a
note on iodism.
Symptoms and signs: When iodine is
swallowed, the symptoms are those of a
 Non-Metallic Poisons
corrosive and irritant poison. There is
burning pain extending from the mouth to
the stomach. The taste is unpleasant and
thirst intense. The lips and oral mucosa are
stained yellow or brown. Its irritant action
onstomach and bowels is characterised by
severe pain in the abdomen with vomiting
and diarrhoea, the vomit and stool being
dark, yellow, brown, or blue, and with a
peculiar smell of iodine. The micturition is
painful and the urine may be suppressed
or scanty. When voided, it is dark brown,
contains albumin, and has a strong smell
of iodine. In addition to the irritative
symptoms, it causes marked depression,
weak pulse, delirium and collapse.
Injection of iodine compounds may
cause sudden fatal collapse as a result of
hypersensitivity. Inhalation of iodine
vapours is responsible for oedema of the
glottis and death from asphyxia.
Prolonged ingestion of iodine or iodine
compounds leads to chronic poisoning
called iodism. This term is also used for
idiosyncratic reactions to iodides or to
iodine. The classical features are headache,
acute coryza, bronchial catarrh, conjuncti­
vitis, and oedema of the face and eyelids
which clear up when the drug is withheld.
Severe cases may be accompanied by
collapse.
Fatal dose: The fatal dose of iodine in the
solidform is about 2 gm. 8-10 ml of tincture
iodine may cause death. Iodides have been
given in large doses over long periods
without any ill-effect though alarming
symptoms have been recorded from a
single dose of less than 1 gram.
Fatal period: The average fatal period is 24
hours. Rapid death may occur from
anaphylaxis.
549
The stomach should be washed
out with 1% starch solution or 5% solution
of sodium thiosulphate. Demulcents, such
as starchy foods, eggs, milk, oils, etc., are
helpful. In cases of intolerance, the adminis­
tration of the drug should be stopped forth­
with and antihistamines and/or steroids
administered. In chronic poisoning, the use
of iodine or iodides should be discontinued.
High sodium chloride intake speeds up the
recovery.
Postmortem appearances: Skin rashes and
oedema of the eyes and face may be
observed. The mucous membranes and lips
may be stained yellow or brown. There may
be excoriation and corrosion of mucous
membranes of the mouth, oesophagus and
stomach. There may be oedema of the
glottis, and sometimes acute oedema of the
lungs and effusion of fluid into the pleural
and pericardial sacs. The kidneys show
glomerular and tubular necrosis. The heart
and liver may show fatty degeneration.
Medicolegal aspects: Tincture of iodine is
occasionally taken to commit suicide. Iodine
preparations cannot be used for homicidal
purposes as they colour farinaceous foods
blue. Iodine in strong solution has been
employed for vitriolage. Injection of iodine
compounds may cause sudden fatal
collapse. Children may be attracted by its
rich colour and may ingest it. A weak
solution of iodine, 15 drops of the tincture
to a tumblerful (200 ml) of water/ may be
helpful in the absence of potassium per­
manganate, as a chemical antidote against
all oxidisable poisons. During travel, water
can be made potable by addition of 5 drops
of 2% tincture of iodine per quart or litre of
suspect drinking water and waiting for 20
minutes. If water is cloudy, double or four
times the quantity of tincture of iodine
drops will be required.
 Metallic Poisons
The important poisons in this group are:
arsenic, mercury, lead, copper, thallium,
and zinc. They cause symptoms of gastro­
enteritis and also exert a marked depressant
action after absorption.
Arsenic is a grey substance which is said
to be non-poisonous as it is insoluble, in
water and, therefore, cannot be absorbed
from the alimentary canal. However, it is
continuously changing into arsenious oxide
or white arsenic which is tasteless and very
poisonous. Arsenic causes toxicity by
combining with sulphydryl enzymes, and
thus interfering with cell metabolism.
Locally, it causes irritation of the mucous
membranes and remotely depression of the
nervous system.
Sources of Arsenic
In therapeutics, arsenic is only of historical
interest, being very rarely used now. The
element or its derivatives are met with in
industry and agriculture.
Arsenious oxide (As20 3): The term arsenic
or white arsenic refers to arsenious oxide,
also known as arsenious acid and arsenic
trioxide, or Sankhya and Somalkhar in the
local language. It occurs in two forms,
either as a white crystalline powder or as
opaque, brittle mass, resembling enamel.
It has no smell or taste, and is sparingly
550
soluble in water. Arsenic powder, in spite
of its heavy weight, floats on the surface of
water and adheres to the side of the vessel.
Therefore, it is commonly given mixed with
milk, tea, or coffee in homicidal poisoning.
Sulphides o f arsenic: These are the yellow
orpiment (hartal) or arsenic trisulphide
(As2S3) and the red realgar (manseel) or
arsenic disulphide (As2S2).
C opper com p ou n ds o f arsenic: These
compounds include ScheeTs green (copper
arsenite), Paris green or emerald green
(copper acetoarsenite), etc., and go by the
name Hirwa in the local language.
O thers: The other compounds include
arsenate of lead and arsenites of sodium
and potassium and organic compounds.
Q. 43.1. Describe the symptom s, signs,
treatm ent, an d postm ortem appearances
of a ca se of a c u te arsenic poisoning.
The principal manifestations of acute arsenic
poisoning are acute gastrointestinal distur­
bances. Subacute and narcotic manifesta­
tions also occur under certain circumstances.
Symptoms and signs: Symptoms in acute
poisoning usually manifest within 15 to 30
minutes after the dose, but may be delayed,
if arsenic is taken with food. There is nausea
and burning pain in the oesophagus,
stomach and epigastrium. Severe, conti­
nuous and persistent vomiting follows.
 Metallic Poisons
Vomit initially contains stomach contents,
later bile, and finally, mucus mixed with
alteredblood. The main effect, however, is
diarrhoea accompanied by tenesmus and
anal irritation. The stools are tinged with
blood, watery like the rice water stools of
cholera, and contain shreds of mucous
membrane and fragments of the poison in
three or four hours. Intense thirst is a
constant feature but drinking water
accentuates the vomiting. Painful cramps
in the legs may develop due to dehydra­
tion, and the urine may be suppressed. Skin
eruptions may appear in late stages. In
manycases, remissions occur during which
the patient is moderately comfortable. The
symptoms then recur. Collapse sets in, with
coldclammy skin, pale anxious face, sunken
eyes, dilated pupils, rapid feeble pulse, and
sighing respirations. Convulsions or coma
may precede death.
Insome cases where the patient survives
the initial acute attack, the poisoning
becomes subacute, the symptoms persisting
in lesser degree for some time. The patient
becomes progressively weak and may die
of heart failure and weakness in 7 to 10
days.
When a large dose of arsenic is taken and
the poison is quickly absorbed, the symp­
toms of gastroenteritis may be absent, and
symptoms of narcotic poisoning, such as
vertigo, headache, spasms, followed by
stupor and vascular collapse may be
present. Death occurs in 2-3 hours.
Fatal dose: The fatal dose of arsenic in an
adult is usually stated as 120-200 mg.
Fatal period: In the narcotic form, the
average fatal period is about 2 to 3 hours.
In the gastrointestinal form, it is about 12
to 48 hours. A patient who survives the
acute attack may die 7-10 days later from
subacute poisoning and heart failure, or
some weeks later from chronic poisoning
with its attendant damage to liver and
kidney.
Though vomiting has occurred,
the stomach should be repeatedly washed
out with warm water and milk to remove
arsenic particles adherent to mucous
membrane of the stomach. Then freshly
precipitated hydrated ferric oxide (which
is rather slow to prepare) is administered
as an antidote with the object of forming
ferric arsenite, a harmless salt. The precipi­
tate is given suspended in water, in table­
spoonful dosage, at short intervals, for two
or three days. If ferric oxide cannot be
quickly prepared, calcined magnesia or
charcoal may be substituted. Treatment
must be immediate. Butter and greasy sub­
stances are useful to prevent absorption.
No alkalis should be given by mouth since
they increase the solubility of white arsenic.
A saline purgative, such as sodium
sulphate, left in the stomach, is beneficial.
The systemic effects should be treated by
intramuscular injection of dimercaprol
(BAL) in oily solution. By virtue of its two
'SH' radicals, it combines with free arsenic
and also dislodges arsenic from combina­
tion with tissue SH groups. It thus reverses
the inhibition of tissue oxidation through
sulphydryl enzymes by arsenic, and forms
a non-toxic BAL-As complex which is
excreted by the kidneys.
Parenteral fluids should be adminis­
tered to counteract dehydration, glucose to
combat liver damage, sodium bicarbonate
to regulate acid-base balance, morphine to
control pain and ice to control thirst. Blood
or plasma transfusion may be needed.
Particular attention should be given to
supporting the heart. Anuria may require
dialysis by artificial kidney treatment.
Additional symptoms should be treated
along general lines.
Postmortem appearances: The character of
the appearances depends very largely upon
the quantity taken and the period which
has elapsed before death.
Externally, in acute poisoning, the body
presents a dehydrated and cyanosed
 552 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
appearance with sunken eyeballs. The skin
is wrinkled and may be jaundiced. Rigor
mortis lasts longer than usual.
Internally, the stomach appearance is
classically described as red velvet. The
mucosa appears red, oedematous, and
swollen in patches corresponding to
deposit of arsenic particles. It is covered
with a considerable amount of tenacious
mucus tinged with blood. Small acute
ulceration or large erosions may be found
at the pyloric end. Submucous petechial
haemorrhages are common. The mucous
membrane of the small intestine is inflamed
usually in its upper part, and of the large
intestine, the rectum is most prone to
inflammation.
Petechial haemorrhages under the
endocardium of the left ventricle are
comparatively common and may be found
even when the stomach presents little sign
of irritation. Haemorrhages may be found
in the abdominal organs, and occasionally,
there may be widespread haemorrhages in
larynx, trachea and lungs.
The liver may show patchy fatty
degenerative changes and, less frequently,
necrosis with jaundice. The heart and
kidneys may show fatty degeneration.
Decomposition is not significantly retarded
by the presence of arsenic in acute
poisoning.
Q. 43.2. Describe the symptoms an d signs
of va rio u s sta g es of c h ro n ic a rs e n ic
poisoning. A dd a note on treatm ent an d
postm ortem ap pea ra nce s.
Chronic arsenic poisoning may result from:
(1) the after effects of an acute attack,
(2) accidental ingestion of repeated small
doses by those working with the poison,
(3) taking food or drink in which there are
traces of the poison, and (4) when the
excretory function is interfered with or if
the intake exceeds the excretory capacity
of the body.
Symptoms and signs: In chronic poisoning,
irrespective of the mode of administration,
a classical state of ill-health results as
represented by the following four stages:
(1) the first stage of nutritional and gastro­
intestinal disturbances, (2) the second stage
of catarrhal changes, (3) the third stage of
skin rashes, and (4) the fourth stage of
nervous disturbances.
First stage o f nutritional and gastrointestinal
disturbances: The earliest sign is gradual
emaciation. Loss of appetite, nausea, and
intermittent attacks of vomiting and
diarrhoea are common. These alimentary
disturbances may be misdiagnosed.
Second stage o f catarrhal changes: A little
later, the patient may feel as if he has a
common cold. The mucous membranes are
inflamed, resulting in conjunctivitis,
running of the eyes and nose, coughing,
hoarseness of voice, and bronchial catarrh.
Third stage o f skin rashes: At this stage,
there is irritation of the skin, often accom­
panied by a vesicular eruption and some­
times this assumes the form of a nettle rash
for which arsenical poisoning may be
mistaken. After long exposure, there may
be a patchy brown pigmentation of the skin
called 'rain drop7 type pigmentation, and
this may give rise to a mistaken diagnosis
of Addison's disease. Hyperkeratosis of the
palms and soles follow. At this stage, there
may be falling out of the hair and brittleness
of nails. White bands known as Mee's lines
crossing the nails of the fingers and toes
may be noticed; they indicate periods of
arrested growth due to interference with
normal metabolism.
Fourth stage o f nervous disturbances: At
this stage, there is tingling and numbness
of the hands and feet and tenderness of the
muscles, sometimes with paresis. Arsenical
neuritis closely resembles that associated
with chronic alcoholism. Other symptoms
include headache, drowsiness, and impair­
ment of vision and mental activity.
 Metallic Poisons 553
There may be evidence of liver damage, POiSONING|BY O RGANIC
kidney damage, and bone marrow de­ A R SEN ICAlJpU PO U NPS_______________
pression at some stage. Involvement of the These are commonly known as the arsphen-
heart is a common feature of chronic amines. They were used in the past for treat­
poisoning, and may prove fatal. The ment of syphilis, parasitic blood diseases,
diagnosis of chronic arsenical poisoning and Trichomonas vaginalis. Their chief toxic
rests entirely on a balanced assessment of manifestation from intravenous use is an
the whole symptomatology including the immediate anaphylactic reaction, known as
circumstances. No one symptom or sign is the nitritoid crisis, which may end fatally.
diagnostic. In West Bengal, many patients Administered repeatedly even in medicinal
with skin rashes started going to doctor. doses, toxic manifestations include exfolia­
Attentionwas drawn to this sudden splurge tive dermatitis (arsenical dermatitis), toxic
ofcases. On further investigation, it became jaundice, nephritis, agranulocytosis, optic
clear that people in that area are consuming atrophy and arsenical encephalopathy. Death
water containing non-acceptable doses of may ensue from convulsions and coma
arsenic contaminated water due to arsenic with cyanosis and anuria.
containing effluents. Q. 43.3. State the points in favour of and
Treatment: The treatment of chronic against arsenic as an ideal hom icid al
poisoningconsists in removal of the patient agent.
fromfurther exposure. Dimercaprol (BAL) In the past, arsenic was a popular homicidal
has greatly improved the prognosis. agent because:
Vitamin B complex and intravenous 1. It is cheap, easily available, and the lethal
sodium thiosulphate are useful. The other dose is small (120 mg for an adult).
treatment is symptomatic. Complete 2. It is practically tasteless, odourless, and
recovery may require six months to one can, therefore, be given in food, drink,
year. or 'paan' (betel leaf) without arousing
suspicion.
Postmortem a ppearan ces: In chronic 3. The symptoms in acute poisoning come
poisoning, retardation of decomposition is on within quarter to half an hour, thus
evident. The effects of long-standing providing opportunity to the poisoner
absorption of the poison are seen in pro­ to make good his escape.
gressive emaciation; anaemia; fatty degene­ 4. Acute poisoning may be confused with
rative changes in the heart muscle, liver and cholera or bacterial food poisoning.
kidneys; in addition to congestion of the 5. Chronic poisoning by small doses pro­
gastrointestinal tract. Microscopy may duces delayed death from progressive
disclose peripheral neuropathy. The skin debility resembling certain diseases.
changes have been described under The disadvantages in the use of arsenic
symptomatology. as a homicidal poison are:
Samples of hair and nail should be taken 1. It retards putrefaction. The body is,
for analysis. For this purpose, hair must be therefore, well preserved.
complete with their bulbs, and nails should 2. It does not deteriorate. Therefore, chemi­
be whole. Arsenic is also deposited at the cal analysis of viscera reveals its presence
end of long bones which may be examined even after several years.
for the presence of poison. A few centi­ 3. Heat does not destroy it. Therefore, it can
metres of the shaft of lower end of femur is be detected even from charred remains,
suitable for this purpose. if the body is burnt.
 1
554 /' Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

4. In chronic poisoning, as it is excreted inculture. Arsenious oxide is a constituent of

hair, nails, bones, skin, etc., its detection rat poisons, sheep dip, printer's ink, etc. It
is possible when any of these structures is also used for the preservation of timber
is available. and leather against white ants. Sulphides
of arsenic are used as depilatories. Copper
Q. 43.4. Write short notes on: (1) tolerance, compounds of arsenic have been in use for
(2) absorption, (3) distribution, (4) elim ina­colouring artificial flowers, children's toys,
tion, (5) uses, a n d (6) postm ortem im bibi­ and wallpapers. Arsenate of lead is used
tion of arsenic. as a fungicide and insecticide. Arsenites of
Tolerance: Certain individuals develop the sodium and potassium are used in weed
habit of arsenic eating (arsenophagia), killers, sprays for fruit trees, sheep dip, and
either as a tonic or as an aphrodisiac. They insect poisons. Various cosmetic prepara­
develop a certain amount of tolerance to tions contain arsenic in one form or the
bear it up to 250 mg or perhaps more in other. Arsenic is used by the quacks for
one dose. Chronic poisoning may occur in the cure of various diseases ranging from
due course. Those who eat arsenic are common cold to cancer.
called as arsenophagists. Suicide, homicide, accident, or other
A bsorption: Arsenicals are rapidly absor­ purposes: Arsenic used to be a popular agent
bed from the alimentary tract and skin. for homicidal purposes in the past. It was
Irritation, corrosion and systemic absorp­ then generally administered in 'paan' (betel
tion occur when pastes containing arsenicals leaf), tobacco, tea, coffee, or with some
are applied to the skin. article of food. Fly papers and weed killers
have been soaked in tea or wine and used
Distribution: After absorption, arsenic is with homicidal intent. Mass homicidal
found in the greatest quantity in the liver. poisoning has sometimes occurred when
The kidneys contain proportionately less, arsenic is mixed in some article of food or
and the other organs contain traces in drinking water from a well or tank.
according to their blood content. In cases Arsenic is sometimes applied locally inthe
in which life is prolonged, it may be found form of a paste or ointment to abortion
in the muscles for a matter of days, in the sticks to procure abortion.
bones for a matter of weeks, and in keratin
Accidental cases of poisoning by arsenic
tissues, hair, nail, and skin for months.
sometimes occur. Poisoning in children
Elimination: Arsenic is eliminated mainly may occur, if they chew paint or eat vermin
by the urine, but also in faeces bile, sweat, or bait or ant syrup containing arsenic.
and other secretions. After a single dose, it Accidental poisoning may also occur from
may be found in the urine within half an its injudicious medicinal use as an
hour and continues to be excreted for about aphrodisiac, or in the treatment of various
10 to 14 days or even longer. In chronic diseases by quacks.
intermittent poisoning, arsenic is excreted Arsenic has also been used as a cattle
in keratin tissues and bones. Hair and nails poison, with success, it is fed to the animal
will show successive deposits of arsenic. mixed with fodder.
Arsenic will probably not be found in the
In 1952 in France, a chemist Jacques Cazenive,
hair until about a week after ingestion but
59, was held responsible for the death of 73
is present in the hair for long periods even, children and injury to 270. The cause of death
after all traces have left the viscera. was "Baumol", a talcum powder made by the
Uses: The various compounds of arsenic chemist which contained arsenic which had
replaced zinc dioxide as an ingredient. An
are in use in the arts, industry and agri­
 Metallic Poisons 555
epidemic of sores and burns had arisen in the Baden records the case of one London husband
localityfromthe use of this powder. whose numerous rich wives died one after other
On the evening of 16 January 1923, one of suspected poisoning. Scotland Yard exhumed
Azimullah, aged 70, was served by a woman their bodies and found arsenic. The man went
withtwoloaves ofbread and potato curry mixed to the gallows proclaiming his innocence, and
witharsenic. Shortly after eating one loaf with years later, a curious student of toxicology tested
thevegetable, he started getting burning pain the soil where the wives were buried and found
inthe throat, to relieve which some 'ghee' that it was full of natural arsenic. The poison
(butter) was administered. Vomiting, followed could well have seeped into the coffins. The
by purging, commenced and he died next student wondered if the wives were really
morning. The chemical examiner, UP, detected poisoned. However, it was too late.
arsenic in the viscera as well as in the bread.
(Allahabad High Court Criminal Application No.
449, 1923). MERCURY (PARA) ________________ _
Adaughter-in-law who failed to bring an Metallic mercury, also known as quick­
additional doftry of ten thousand rupees for a silver, is a liquid metal with a bright silvery
carwas sought to be done away with by the son lustre. It exists in nature as the metal itself
of a landlord of Badal and his mother who and as the sulphide (cinnabar or ras sindoor).
conspiredwith a doctor to administer arsenic to Metallic mercury is not poisonous, if
her insmall doses. At the end of three months, swallowed because it is not absorbed. It
she was taken to Delhi almost dying, for
vaporises at room temperature and causes
treatment. The chemical examiner of Uttar
Pradeshfoundsufficient arsenic inher hair, nails poisoning, if vaporised mercury is inhaled,
and the scales from the soles of her feet to swallowed, or rubbed into the skin.
establish the crime. (Annual Report of FSL, UP, Mercury depresses cellular enzymatic
lor 1958). mechanisms by combining with sulphydryl
Apersonwho was living with the deceased had groups. Mercuric compounds being soluble
illegal connection with his daughter-in-law. He are more poisonous than mercurous
poisoned her with arsenic to get rid of her. The compounds which are less soluble.
policewho received the report of this suspicious
death went to the spot and found the body
burning on the pyre. They collected the ashes
Sources of Mercury
and bones in which arsenic was discovered. Mercuric chloride or corrosive sublimate:
(FSL, UP, Reportfor 1948). Also known as perchloride of mercury, it
is in the form of white crystalline powder
Postmortem im bibition o f arsenic: Certain or tablets or use as a germicide. It has an
samples of earth contain small traces of acrid metallic taste, no smell, and is
arsenic probably derived from the use of commonly the cause of acute poisoning.
arsenical weed killers in the burial ground,
M ercu rou s c h lo rid e o r c a lo m e l: Also
or on account of drainage of water contami­ known as subchlqride of mercury, it is a
nated by arsenic. It is known that when a heavy, amorphous, white tasteless powder,
dead body is buried in such earth, small insoluble in water.
quantities of arsenic may enter the dead
body. Where the soil contains arsenic, and Others: Other poisonous mercurial salts are
arsenic poisoning is suspected, samples of mercuric oxide or red precipitate (sipichand),
earth from around the dead body should mercuric ammonium chloride or white
be collected for chemical analysis at the precipitate, mercuric potassium iodide,
time of exhumation. In arsenical poisoning, mercuric nitrate, and mercuric cyanide.
the concentration of arsenic in various Organic com pounds o f mercunf: These
organs should be more than that in the were used principally as diuretics in the
earth. past, and as fungicides in seed commerce.
556 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Q. 43.5. Describe the symptoms, signs, must, therefore, be removed without delay
tif^ rrie n t, and postmortem a p p e a ra n c e s
by emetics or gastric lavage. Activated
of acute mercury poisoning. charcoal is also effective in the usual
m jm p to m s a n d s ig n s : The sym ptom s dosage; addition of magnesium sulphate
commence soon after the poison is swallo­ increases its adsorptive power and hastens
wed. The taste is metallic, with a feeling of the removal of ingested poison. BAL and
constriction in the throat, a burning sensa­ penicillamine derivatives (cuprimine) are
tion from mouth to stomach, and pain effective antidotes. Where the kidneys
radiating over the abdomen. The mouth, show signs of damage, administration of
tongue, and fauces become corroded and alkaline fluids, peritoneal dialysis or haemo­
the mucous membrane appears grayish dialysis maybe necessary. The general treat­
white. There is nausea, with frequent ment of shock and collapse will also be
vomiting of long stringy masses of white required, and symptomatic treatment
mucus, mixed with blood, followed by should be given as indications arise.
profuse purging, often bloody, with painful P ostm ortem appearances: The appearances
tenesm us. C ollapse sets in, with cold of corrosive poisoning will be present, if the
clammy skin, pale anxious face, sunken poison is taken in a concentrated form.
eyes, dilated pupils, rapid feeble pulse, and Otherwise, the signs of irritant poisoning j
sighing respirations. Syncope, convulsions will be observed.
and general insensibility usually precede The tongue is white and sodden in appea- j
death which may take place in a few hours. ranee and the mouth generally has a diffuse j
If death is not rapid, on the second or grayish white escharotic appearance. Eschar
third day, salivation may develop, the means a hard crust over a raw surface, e.g.
gums may become swollen and inflamed, material covering a deep bum. The mucous
and the breath foul. Some loosening of teeth m em brane of the alimentary tract is
and ulcerative glossitis may follow. A renal inflamed and corroded. The muscular coats
lesion soon appears due to nephrotoxicity of are so softened that it is difficult to remove
mercury. The urine contains albumin and the organ without rupture. Mercury has a
blood and death ensues from urasmia. selective action on the caecum and large
Caecum and large intestine show areas of intestine which show intense inflammation,
erosion, corrosion, and necrosis, due to re­ ulceration, and even gangrene. The kidneys
excretion of mercury. show a toxic nephritis. The liver and heart
F a t a l d o s e : The fatal dose of corrosive may show fatty degeneration, and heart
sublimate is about 1 to 2 gm. subendocardial haemorrhages also.
F a ta l p eriod: Death may occur within a few Q. 43.6. Give a brief account of chronic
hours but is usually delayed for 3 to 5 days. poisoning by mercury.
Delayed deaths are usually due to uraemia.
This may be the result of: (1) the after effects
Treatm ent: The stomach should be washed of an acute attack, (2) injudicious medical
out with 250 ml of a 5% solution of sodium administration, and (3) continuous acci­
formaldehyde sulphoxylate and about 100 dental absorption in those working with the
ml of this solution left in the stomach. This metal or its salts as in the manufacture of
substance reduces the per-chloride to a less thermometers, barometers, fur felt, mirrors,
soluble (less toxic) mercurous compound. and ultraviolet apparatus, or in police
Egg albumin which forms an insoluble officers engaged in finger print detection
albuminate of mercury may be adminis­ work where finger print powder contains
tered. It is soluble in excess of albumin and mercury.
 Metallic Poisons*
The symptoms and signs of chronic
mercurypoisoning are: excessive salivation
withmetallic taste in the mouth, loosening
of teeth with painful inflamed gums, and
occasionally a blue-black line on the gums as
with lead poisoning. Irritation of the skin
mayoccur. Nephritis is a serious complica­
tion. Abortion is common. Mercuria lentis,
i,e. discolouration of the capsule of the lens
ofthe eye due to deposition of mercury, as
observed through a slit-lamp, is one of the
early symptoms of chronic mercury
poisoning. It has no effect on visual acuity.
Nervous symptoms, such as tremors, and
mental symptoms known as erethism, are
seen in chronic mercury poisoning. The
tremor is known as the hatter's shake,
because it is common in workers of that
industry. It is coarse, intentional, and
affects the hands, arms, tongue, and later
thelegs. Erethism is a peculiar disturbance
ofthepersonality characterised by shyness,
irritability, tremors, loss of memory and
insomnia. It is common in workers in
mirror industry.
Treatment consists of removal of the
patient from exposure to mercury and
promoting elimination of the mercury by
bowels and kidneys. The rest of the treat­
ment is symptomatic.
At postmortem, the changes in the large
intestine, due partly to re-excretion, are
often very striking, with necrosis which
spreads, and may involve practically the
whole of the lower bowel. Kidney damage
consisting of tubular nephritis, and fatty
degeneration of the liver and cardiac
muscle are observed.
Indeath from mercury poisoning, in addi­
tionto routine viscera, bones, teeth, hair and
nails should also be preserved for chemical
analysis.
Q. 43.7. C o m m e n t on m e d ic o le g a l
aspects of poisoning by mercury.
Accidental poisoning may occur from:
(1) accidental ingestion of antiseptic solu­
557
tions containing the perchloride or cyanide,
or of antiseptic tablets of the perchloride oi
iodide, (2) soluble salts employed as vaginal
douches, (3) absorption of mercurial pre­
parations applied to the skin, and (4) intra­
venous administration of organic mercurials
as diuretics.
In children, accidental poisoning may
occur from: (1) the use of ammoniated
mercury in some bleaching creams, and
(2) swallowing the sulphocyanide of
mercury stick or tablet, the chief constituent
of Pharoah's serpents, which when ignited,
give out pungent smell and ash in the form
of a long tortuous figure resembling a
snake, and hence the name.
Suicidal and homicidal poisoning is rare.
After absorption, mercury passes rapidly
to the foetus in utero through the placental
circulation and causes abortion.
Chronic mercury poisoning occurs in
industrial workers from continued inhala­
tion of volatalised mercury. The effect of
chronic poisoning may be delayed for
many years. Much responsibility, therefore,
rests on the medicolegal expert to establish a
cause and effect relationship.
LEAD (SHISHA)_________________________
As with other metals, the soluble com­
pounds of lead are more poisonous than
lead itself, except when lead is in the
volatile state. Lead may obtain access to the
body by inhalation, by ingestion, or by
absorption from the skin or mucous sur­
faces. The primary effect of lead is to cause
spasm of the capillaries and arterioles. The
toxic effects result from fixation of lead in
certain tissues, such as the brain and
peripheral nervous system.
Sources o f lead: The principal salts of lead
which produce toxic effects are the acetate
(sugar of lead or salt of satum), the oxide
(litharge, mudrasang) converted into the
oleate in the form of diachylon, the carbo­
nate or white lead (safeda), the tetroxide or
558 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

the red lead (vermillion, sin&ur), the yellow

chrome or the chromate of lead, and tetra­
ethyl lead.

Q. 43.8 D escribe the symptoms, signs,

p eatm ent and postmortem appearances
of acute lead poisoning.
Acute lead poisoning is rare. Symptoms are
similar to those of acute arsenical, or
mercurial poisoning, except that diarrhoea
is replaced by constipation and the stool is
blackened and offensive. The principal
manifestations are gastrointestinal or
central nervous system disturbances.

and signs: The symptoms consist

of metallic astringent taste, dry throat,
thirst, nausea, and vomiting with colic-like
pains in abdomen, relieved by pressure.
Fig. 43.1: Paralysis d ue to chronic lead
There may be purging but more usually
poisoning. Big joints are generally affected
constipation. The faeces are offensive and while small joints escape. In this case, there is
black owing to the formation of lead wrist drop and foot drop. The right wrist joint is
sulphide and the urine is suppressed. When also getting affected. Note the manner in
the case is protracted, the patient may suffer which he writes. The knee is inflamed and
from cramps in the legs and arthralgia. hence bandaged. ( Courtesy. Dr GB Sahay)
Headache, drowsiness and paralysis of the
limbs may be observed. Finally, collapse Fatal period: Death may occur on the second
precedes death. Acute cases may survive or third day. Acute poisoning is rare, and
and develop the symptoms of chronic may be followed by chronic poisoning.
poisoning. Treatment: xhe stomach should be washed
In poisoning by tetraethyl lead, gastric out with a 1% solution of magnesium or
symptoms are absent or slight. Cerebral sodium sulphate followed by ample
symptoms, the so-called lead encephalo­ washings with plain water to remove the
pathy, predominate. It is characterised by lead sulphate formed. Morphine and
headache, sleeplessness, tremors of the eyes, atropine help to relieve painful colic. The
mouth and fingers, sometimes paralysis, or bowel should be cleared at regular intervals
loss of vision, hallucinations, excitement, to get rid of excreted lead. Calcium favours
and delirium or apathy; and convulsions the deposition of lead in the skeleton. A diet
(Fig. 434). The patient may suffer from rich in milk, and administration of calcium
permanent mental changes or insanity. salts and vitamin D are helpful. Calcium
versenate (EDTA) and penicillamine are
Fatal dose: phe fataj dose 0f absorbed lead useful antidotes. Peritoneal or haemo­
has been estimated to be 0.5 gram. Fatal dialysis may be necessary. The rest of the
dose of lead acetate is about 20 grams, and treatment is symptomatic.
lead carbonate about 4 grams. A drop or If commercial tetraethyl lead is spilled
two of pure tetraethyl lead may cause on the skin, washing the area with kerosene
serious symptoms. within 15 minutes after contact, will
remove the poison quantitatively. When
gasoline containing tetraethyl lead is
swallowed, the treatment is the same as
that for gasoline.
Postmortem appearance? These are chiefly
of gastroenteritis. The gastric mucosa is
congested. There may be eroded patches.
The large intestine may contain black-
coloured faeces.
Q. 43.9. Give a detailed account of chronic
lead poisoning (plumbism, saturnism, or
saturnine poisoning).
Lead poisoning is nearly always of the
chronic type. It is encountered in various
industries, e.g. through ingestion in type­
setting, plumbing, battery work, and
glazing pottery; through inhalation in the
manufacture of white lead, smelting, from
paint in oxyacetylene ship breaking,
diamond cutting, file making, turning, car
welding and polishing; and through
ingestion and inhalation in painting, coach
building, lacquering, tinning, vitreous
enamelling, and colour and dye manu­
facture and use. In home, chronic lead
poisoning may occur from use of 'ghee'
(butter) stored in tins or taking food cooked
intinned vessels. Formerly, it used to occur
fromdrinking water supplied through lead
pipes.
Chronic poisoning may also result from
the mobilisation of lead already stored in
the body tissues, especially the bones, e.g.
in acidosis, and symptoms of acute or
chronic poisoning may develop, even years
after the original absorption of lead.
Symptoms and signs: Although chronic
poisoning correctly describes prolonged
exposures, manifestations often are acute. The
main symptoms and signs are: facial pallor;
anaemia with punctate basophilia; lead
line; colic and constipation; paralysis;
encephalopathy; renovascular manifesta­
tions; reproductive system manifestations;
and general symptoms.
Facial palIor The facial pallor particularly
about the mouth is one of the earliest and
most consistent sign. It is supposed to be
due to vasospasm.
Anaemia with punctate basophilia: The
blood shows hypochromic anaemia, asso­
ciated with polychroma si a. punctate
basophilia, reticulocytosis poikilocytosis,
an increase in mononuclear cells and
decrease in polymorphonuclear cells.
Punctate basophilia means the presence of
many dark-blue-coloured pinhead like
spots in the cytoplasm of red blood cells.
These are stained with basic dyes and hence
the name. The condition is due to toxic
action of lead on porphyrin metabolism,
porphyrins are excreted in the urine, the
amount being as much as 500 pg/day.
Lead line: This is a stippled bluish-black
line due to subepithelial deposition of lead
sulphide granules on the gums at the junc­
tion with the teeth (not on the teeth). It is
seen on the gums of carious teeth, espe­
cially noticeable on the upper jaw. Its colour
is due to the action of hydrogen sulphide
liberated by microorganisms from de­
composing protein food around carious
teeth in the presence of circulating lead. A
somewhat similar line may be seen in cases
of mercury, copper, bismuth, iron and
silver poisoning.
Colic and constipation: The colic generally
affects intestines, ureters, uterus and blood
vessels. It is relieved by pressure on the
abdomen. It is a late manifestation but
constitutes an acute symptom of chronic
plumbism. Obstinate constipation (also
known as dry belly ache) is associated
with it.
Paralysis: This is usually a late manifes­
tation, seen in less than 10 per cent of cases.
Onset may be gradual or sudden. There is
' commonly paralysis of extensor muscles of
wrist (wrist drop) but peroneal muscles
(foot drop) or other muscle groups may
also be affected. The paralysis is associated
with degeneration of nerve and atrophy of
562 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

by its colour. Accidental poisoning occurs Thallium poisoning should normally be

when copper has been added to keep the suspected when there are gastrointestinal
green colour of vegetables. Copper sulphate symptoms, polyneuritis, and loss of hair
is rarely been used as a cattle poison. Copper from head, lateral two-thirds of the eye­
subacetate is formed by the action of brows, and axilla. An X-ray of the abdomen,
vegetable acids on improperly tinned showing a high density hepatic opacity is
copper vessels. It may cause poisoning from diagnostic.
contamination of food stored in such vessels.
In R vs Fletcher (1953), Mrs Fletcher was accused
of murdering her husband with "Thalrat" rat
THALLIUM ___________________________ poison. Mr. Fletcher suffered from depilation,
Thallium is a soft white heavy metal with polyneuritis and pain in the extremities. He was
nervous and crying. He died after 11 days, his
a lustrous colour which tarnishes on expo­
condition not being diagnosed. At postmortem,
sure to air and forms thallus oxide. The arsenic and lead were sought with negative
metal and its compounds are highly toxic, results. 100 mg of thallium was found in his
the important ones being thallium acetate
and thallium sulphate. These salts being Hausman and Wilson report the case ofawoman
soluble, colourless and nearly tasteless can who was given an unknown quantity of thallus
be easily administered by mouth in food sulphate. Initially, a burning sensation inthefeet
radiating to the knees was recorded. By the fifth
or drink. They are readily absorbed from day, she had severe leg pains and could not
the skin also. Toxic symptoms from walk. Thereafter, her condition deterio-ratedand
thallium poisoning resemble those of lead. she became lethargic and un-responsive until the
eleventh day, when she died.
Q. 43.13. G iv e a s u cc in ct a c c o u n t of
thallium pois oning. A d d a n ote on its The fatal dose is about one gram of a
m ed ic o leg a l aspects. soluble salt. Death follows a fatal dose in
Symptoms of acute thallium poisoning two days to two weeks depending upon the
appear about 12-36 hours after a toxic dose. amount ingested.
They include abdominal pain, vomiting Treatment must follow the general
and diarrhoea. Neurological symptoms procedure for heavy metal poisoning.
may predominate and these include At autopsy, if death has occurred soon
peripheral neuritis, impaired vision, ataxia after ingestion, there is gastroenteritis with
and convulsions. Loss of hair occurs two liver and kidney damage. In the central
weeks after ingestion. nervous system, chromatolysis and swelling
Chronic poisoning may occur in workers as well as degeneration of ganglion cells
engaged in the manufacture of rat and may be found. In 7 days, the hair follicles
vermin poisons, depilatory pastes, luminous begin to show oedema of epithelial cells
paints and in the glass and dye industries. with dissolution of rete layers and brittle
Besides falling of the hair, inhibition of proximal end of hair. Thallium may be
growth and sexual development, nephritis, recovered from blood, urine, liver and
peripheral neuritis and mental distur­ kidney. Diagnostic changes may be found
bances have been described. Transverse in the hair roots. Thallium resists putrefac­
lines on the finger nails, known as Mee's tion and heat. It can, therefore, be detected
lines, are also seen. This is called as Thalo- in decomposed bodies and even in the
toxicosis. The triad of thallium: 1. alopecia ashes of cremated bodies.
with skin rash, 2. Painful peripheral M edicolegal aspects: Thallium is used as
neuropathy, 3. Mental confusion with an ideal homicidal poison in some European
lethargy. countries and Australia where it is also
 Metallic Poisons 563
used as a rodenticide. Accidental intoxica­ the poison. There is no specific antidote,™
tion may result from its therapeutic use as Sodium bicarbonate in tepid water should 1
adepilatory or from its accidental ingestion be given freely. Demulcents should also be |
when used as a rodenticide. Chronic given and the case treated on general lines.
poisoning occurs from industrial exposure.
mortem appear,,;; r<: These are similar
ZINC___________________ . J H to those of other irritants in the case of the
sulphate, and corrosives in the case of the
Zinc is a bluish white, lustrous metal. The
chloride.
toxic effects are confined mainly to three
salts of the metal, namely, the sulphate Medicolegal aspects: Cases are recorded in
(white vitriol), the action bf which is which the soluble salts have been adminis­
irritant; the chloride, which pi corrosive; tered occasionally to commit suicide,
and the phosphide which is used as a homicide, or abortion. Zinc sulphate has
rodenticide. been taken in mistake for Epsom salt.
Accidental poisoning may occur through
Q. 43.14. Give a succinct acco unt of eating food cooked or stored in galvanised
poisoning by zinc. Add a note on zinc iron vessels.
phosphide.
Zinc phosphide is a steel-grey-coloured
Symptoms and signs: The symptoms from crystalline powder with garlicky odour. It j
zinc sulphate are chiefly those of gastro­ is an effective and economic rodenticide. J
intestinal irritation, and consist of metallic In human beings, its action starts imme-jj
taste in mouth, pain in gullet, stomach and diately after it comes in contact with gastricJj
abdomen, vomiting and diarrhoea. Collapse acid, when highly toxic phosphine gas is
may follow. The chloride has a stronger released.
corrosive action, destroying the mucous Following ingestion, there is metallic
membrane of the mouth, throat, oeso­ taste in the mouth, and burning in the
phagus and stomach. Vomiting is severe, throat, oesophagus and stomach, followed
there is purging with tenesmus and blood, by nausea, vomiting, diarrhoea, and abdo­
and symptoms of shock. There may be minal pain. The patient may complain of
remission of symptoms followed by garlic taste in the mouth and garlic odour
recurrences. may be perceived in the breath. Sometimes,
The symptoms and signs of chronic there may be a symptom-free period
poisoning are closely allied to those of lead followed by gastrointestinal disturbances,
and copper. evidence of liver damage, and haemorr­
Fatal dose: The smallest fatal dose of zinc hages in the skin. The liberated phosphine
sulphate is about 15 gm. The chloride is gas causes dyspnoea, pulmonary oedema,
more toxic, 400 mg having proved fatal. and bradycardia, followed by circulatory
collapse or neurological symptoms, coma,
Fatal period: Death from zinc sulphate and death. Shock, oliguria, acidosis, tetany,
poisoning, though rare, has occurred in 2 and convulsions are other features.
hours after taking 90 gm and on the fifth
The fatal dose of zinc phosphide is 5
day after taking 15 gm. In poisoning by zinc
grams. The fatal period varies from a few
chloride, death occurs within a few hours hours to 24 hours.
from shock or after several weeks from
after-effects of the poison. As for treatment, if skin or clothes are
contaminated, the clothing should be
Treatment: The stomach should be washed removed and the affected parts washed
out unless marked vomiting has removed thoroughly with soap and water. If the
564 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
poison is ingested, vomiting may be
induced by giving a tablespoon of salt in a
glass of warm water and the treatment
continued till the vomiting fluid is clear.
Gastric lavage may be undertaken with
3-5% solution of sodium bicarbonate which
minimises the conversion of zinc phosphide
to phosphine. Zinc phosphide adheres
firmly to the crypts in the mucous mem­
brane of the stomach and even if a small
quantity remains in the stomach after
vomiting or gastric lavage, it is sufficient
to cause death by slow absorption. It is,
therefore, particularly important to keep
the patient under observation for delayed
symptoms after initial recovery. General
supportive measures include administra­
tion of vitamin K, corticosteroids, and seda­
tives. Other symptomatic measures may be
taken as need arises.
Pathological findings from ingestion of
zinc phosphide include petechial haemorr­
hages in the skin, garlic odour on opening
the stomach, grayish black residues of the
poison sticking to the mucous membrane
of the stomach, and congestion of liver,
spleen, kidney, brain, and lungs. Eve^
necrobiosis of the liver and other findings
similar to phosphorus poisoning may be
seen.
Zinc phosphide is an effective rodenti*
cide and pesticide. It is easily available and
cheap. It may, therefore, be used for
suicidal purposes. It has been used with
homicidal intent in cases of dowry deaths.
Accidental poisoning amongst children and
farmers is known.
Q. 43.15. Write short note on ‘metal fume
fever’.
Metal fume fever due to expoture to zinc
fumes shows chills, fever, muscle pains,
fatigue, cough, dysproce, salivation, sweat­
ing, tachycardia, cyanosis fever resolve
36 hours after exposur to fumes ceases.
The worker is free at week end and fever
reappears on Monday hence called as
Monday fever. This is seen also on exposure
to fumes of chromium, cadmium, cobalt,
manganese, mercury, magnesium, etc.
Treatment is symptomatic and chelating
agents.
■ m%
566 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Treatment: There is no specific antidote for lines on them. The oil is brownish in colour,
ricin poisoning. Treatment must, therefore, viscid in appearance, unpleasant in smell,
be based on general principles. and bitter in taste. The active principle is
crotin, a toxalbumin, which is an irritant
Postmortem appearances: Fragments of and vesicant. A less poisonous glycoside,
seeds may be found in the stomach. The
crotonoside, is also present. jU
bowel is inflamed and there are occasional
erosions and submucous haemorrhages. Symptoms and s k These |j| similar to
There may be haemorrhages in internal poisoning by ricin. The oil causes blistering
organs. externally, and on ingestion capes severe
gastrointestinal irritation with burning !
M edicolegal, a sp ects: Accidental cases pain in the abdomen, vomiting, powerful
occur among children from eating the purging, and frequently a burning pain at
seeds. The seeds have been administered the anus. In substantial dosage, collapse
in food with homicidal intent. The powder precedes death.
of the seeds causes local irritation of the
Fatal dose and fatal period: The fatal dose
skin, and mucous membrane of the nose is 20 drops of the oil or four seeds. Death
and eyes. In the George Markov political may occur in about four to six hours or may
assassination in London, a tiny sphere be delayed for three to six days.
drilled out to carry ricin was injected from
Treatm ent: The treatment is based on
an air weapon concealed in an umbrella.
general principles.
CROTON TIGL1UM (JAMALGOTA, NEPALA) Postmortem appearances: These are similar
to those described under ricinus communis.
Q. 44.2. G ive a brief a cco unt of poisoning
M edicolegal aspects: Croton oil has been
from croton tiglium. administered in food with homicidal intent.
This plant grows all over India. The seeds Poisonous symptoms have been produced
and the oil (croton oil) extracted from the by eating the seeds or inhaling their dust.
seeds are poisonous. The seeds resemble Accidental poisoning has resulted from the
small castor seeds in size and shape (oval) use of croton oil as a purgative. It has been
but differ in their appearance (Fig. 44.2). used as an abortifacient. Wild tribes have
They are blackish-brown in colour with a used the oil as an arrow poison.
white oily kernel and have longitudinal
ABRUS PRECATORIUS (JEQUIR1TY BEAN)
Q. 44.3. G ive a brief a cco u n t of poisoning
from abrus precatorius. A dd a note on sui.
This is also known as Indian liquorice,
Rosary pea, crab's eye, gunchi or rati. The
plant is found all over India and though all
its parts are poisonous, the seeds are
commonly used as poison. They are of the
size of a small pea, about 0.85 cm long and
0.65 cm broad, and have an average weight
of 120 mg (Fig. 44.3). They are tasteless,
odourless, oval, and red in colour, with a
black spot on one pole. The active principle
Fig. 44.2: Croton seeds is abrin, a toxalbumin, and its actions
(Note the difference in appearance) resemble those of viperine snake bite.
 568 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Fig. 44.4: Fruit of colocynth, (above) and the
plant (citrullus colocynthis or bitter apple) below
Fatal dose and fa ta l period: The fatal dose
is about 1 to 2 gm. The fatal period varies
from 24 hours to a few days.
T reatm en t: General management and
symptomatic, dopamine.
Postm ortem appearances: There is irrita­
tion of the alimentary tract and occasionally
inflammation of kidneys and the urinary
bladder.
M edicolegal aspects: Colocynth is occasio­
nally taken to commit suicide. As it causes
congestion of the pelvic viscera, it has been
used to procure abortion.
ERGOT__________________________________
Q . 44 .5 . G iv e a brief a c c o u n t of ergot
poisoning. A d d a note on ergotism.
Ergot is the sclerotium (compact mycelium
or spawn) of the parasitic fungus Claviceps
purpurea, which grows on cereals, like rye,
barley, wheat, etc. It gradually replaces the
grain by forming a curved dark purple
mass, larger than the original grain. Such
mass, when dried and powdered, forms the Fatal d ose and fa ta l period: The fatal dose
ergot of the market. It has a peculiar colour of ergot may be as low as 1 gm. Death may
and disagreeable taste. It contains several occur in 24 hours or may be delayed for
active principles of which the important several days.
ones are ergotoxin, ergotamine, and ergo-
metrine. They stimulate smooth muscles of
the arterioles, intestines and uterus. Ergot
is used especially for its stimulant action
on the uterus and in the treatment of
migraine. It is in common use in veterinary
practice also.
Symptoms and signs: Acute poisoning is
rare. The main symptoms are irritation of
the throat, dryness and intense thirst,
nausea, vomiting, diarrhoea, pain in the
abdomen, tingling in the hands and feet,
muscle cramps, dizziness and a feeling of
coldness, all resulting from contractions of
the smooth muscle. Abortion and haemorr­
hages in the uterus may occur. Bleeding
from nose and other mucous membranes
is common after large doses.
Chronic poisoning (ergotism) is not
common now. It used to be caused by the
ingestion of ergot-contaminated flour. The
symptoms are those of gastrointestinal
catarrh, followed by a convulsive or
gangrenous form. Convulsive ergotism is due
to changes in the central nervous system
which cause very painful tonic contractions
of voluntary muscles, drowsiness, head­
ache, and giddiness, and lead eventually to
madness. The patient complains of itching,
a feeling of numbness, and formication, that
is, cutaneous sensation as if ants are
creeping under the skin. Severe psychiatric
disturbances are common. Gangrenous
ergotism may resemble Raynaud's disease.
It is characterised by vasomotor distur­
bances, e.g. pain and numbness leading to
gangrene of the fingers, toes, nose, and ears.
Gangrene also occurs in the intestine and
forms ulcers. Complete recovery usually
occurs, if the use of ergot derivatives is
discontinued prior to the appearance of
gangrene.
 Vegetable
569
treatment: In acute poisoning, the stomach
andbowel should be emptied of the poison.
In chronic poisoning, the use of ergot
preparations should be discontinued. The
restofthe treatment is purely symptomatic.
Vasodilators are helpful.
postmortem appearances: They are not
characteristic. The internal organs are
congested. Particles of the sclerotia may be
detected in the stomach. Gangrene of the
fingers and toes may be present.
Fig. 44.6: Section of capsicum seeds. Embryo!
Medicolegal aspects: Acute poisoning may is curved inwards
occur when ergot is taken in a large dose
to procure abortion. Chronic poisoning lachrymation, and redness. When ingested
results from ingestion of ergot contami­ in sufficient quantity, it acts as an irritant
natedbread for a long time. poison, and causes burning sensation
in the mouth, throat, oesophagus, and
CAPSICUM (CHILLIS)____________________ stomach.
Q. 44.6. Give a brief account of capsicum Treatment: When applied to the skin, it
froma medicolegal point of view. Differen­ should be washed out with water and
tiate chilli seeds from dhatura seeds. irritation treated symptomatically:' When
Capsicumfruits are powdered and univer­ ingested, the tongue should be scraped by
sally employed as a condiment, the condi­ a blunt edged instrument and ice given to
ment being known as red pepper or suck. When thrown in the eyes, they should
lalmirch. It has a pungent smell and taste be washed in saline, and antibiotics applied.
which lasts for a long time. The active Cortisone drops may be helpful.
principles are capsaicin and capsicin,
exceedingly acrid, volatile, non-alkaloidal, Medicolegal aspects: The powder is used
non-fatal substances (Figs 44.5 and 44.6). as a means of torture to extort money or a
confession of some guilt by introducing it
Symptoms and signs: Applied to the skin,
into the nostrils, eyes, urethra, vagina, or
it causes irritation and vesication. When
thrown in the eyes, it causes burning, rectum; burning it under the nose; and
rubbing it on the breasts of the females. It
may be thrown into the eyes to facilitate
robbery. The fumes from burning chillis
irritate the eyes and upper respiratory
passages. Superstitious people use them
to scare away devils and ghosts. Recently,
Indian police want to resort to chilli
bomb to facilitate clearing the mobs in
agitations.
The seeds, about 0.30 cm long and wide,
resemble dhatura seeds (Figs 44.7 and 44.8)
and may be differentiated from them as
Fig. 44.5: Chilli seeds follows:
 570 lexTDook or Meaicai jurisprudence, horensic ivieaicine

Chilli seeds Dhatura seeds

1. Size Small and thin Large and thick
2. Colour Pale yellow Brown or black
3. Appearance Smooth and Kidney-shaped,
finely pitted and
reticulated
4. Smell Pungent Odourless
5. Taste Pungent Bitter
6. Convex border Single Double edge
edge
7. On section Embryo curved Embryo curved
inward like outward
figure 44.4

Fig. 44.9: M arking nuts. 0 o u r te s y : Dr NK

V M ohanty)

by dhobis (washermen) as marking ink on

clothes. The nut is black, roughly cone-
shaped, and has a thick pericarp. The
contained juice is brown, oily, and acrid.
Its active principles are semecarpol and
- V} bhilawanol (Fig. 44.9).

%: j Sym ptom s and signs: When the juice is

■# V applied to skin, it causes irritation and
painful blisters containing acrid serum
Fig. 44.7: Dhatura seeds which causes an eczematous eruption on
any part of the skin with which it comes
into contact. The lesion resembles a bruise
which may later ulcerate and slough.
Internally administered, the juice is much
less irritant. Taken in larger doses, it causes
blisters in the mouth and throat and severe
gastroenteritis, followed in some cases by
dyspnoea, cyanosis, tachycardia, coma, and
death.
Fatal dose and fa t a l period: The fatal dose
is about 5 to 10 gm and death may result
Fig. 44.8: Section of dhatura seeds. Embryo is within 12 to 24 hours.
curved outwards T reatm ent: This is symptomatic. When
applied externally, the parts should be
SEMECARPUS ANACARDIUM washed with w arm w ater and bland
(MARKING NUT)__________________________ liniments applied.

Q. 44.7. G ive a brief a c co u n t of poisoning

P ostm ortem a p p eara n c es: The findings
from sem ecarpus an ac ard iu m . Differen­ confirm the clinical features. The blister
tiate artificial bruise from true bruise. fluid should be preserved in rectified spirit
The fruit of this plant is known as Bhilawan and sent to a forensic science laboratory for
or the marking nut because its juice is used analysis, if necessary.
 Vegetable Poisons
571
Table 44.1: Artificial bruise and true bruise-

2. Situation Accessible parts Anywhere

3. Appearance Blister No blister

4. Colour changes Characteristic

5. Ecchymosis
6. Contents Extravasated Fig. 44.10: Calotropis (mddar) plant with j
flowers and buds. (Courtesy. Dr NK Mohanty)|
7. Itching Present Not so
purple flowers and Calotropis procera which -
8. Fingers May showmarks Not so has white flowers. They yield four active
due to scratching
principles, viz. uscharin, calotoxin, calactin,
9. Analysis Chemical found Not so and calotropin. The leaves and the stem,
in the blister fluid when cut or crushed, yield an acrid milky
juice, which is acidic in reaction and bitter
Medicolegal aspects: The juice is used as in taste; when heated or allowed to stand,
an abortifacient by application to the os it forms a white clot leaving a clear straw-
uteri by means of an abortion stick. It is coloured serum. The serum contains an
applied to the genitals as a punishment for active principle, gigantin, which is highly
adultery. It is used by malingerers to toxic, while the clot contains, a less
produce an artificial bruise to support a poisonous resin.
false charge; its presence, however, can be All the parts of the plant are used in
detected by chemical analysis of the blister Indian medicine, the flowers as digestive
fluid. The juice may be instilled into the stimulants; the leaves as external poultice;
eyes to produce an irritant conjunctivitis. the powdered root as an emetic; and the
This is resorted to by personnel in army, milky juice as a vesicant, depilatory, and for
navy or air force when they wish to leave treatment of .chronic skin conditions. The
the job or by inmates of jail to avoid work. juice is used by tanners for removing hair
Accidental poisoning may occur from from the hides and for deodourising them. ]
internal administration by quacks. The
juice, like vitriol, has been thrown on the Symptoms: When the juice is applied'
face with evil intentions. externally, the skin becomes red and
Table 44.1 summarises the differentiating vesicates. When instilled into the eyes, it
features of an artificial bruise and true produces fulminating conjunctivitis which
may result in permanent impairment of
bruise.
vision. When taken internally, it acts as a
CALOTROPIS (MADAR, AKDO) gastrointestinal and cerebrospinal poison.
There is an acrid bitter taste, burning pain
Q. 44.8. Give a brief account of poisoning in the throat and stomach, and nausea,
from calotropis. vomiting and diarrhoea, followed by
This plant (Fig. 44.10) grows wild almost dilated pupils, tetanic convulsions, collapse
everywhere in India. There are two and death. When powdered madar root is
varieties, viz. Calo-tropis gigatitea which has used as snuff, death ensues immediately.
572 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Fatal dose and fa ta l period: The fatal dose crystalline glycoside. When the bruised
is uncertain. The fatal period is about 12 root or twigs are applied externally, the
hours. skin becomes red and vesicates. Taken
Treatm ent: This is on general lines, viz. internally in small doses, the plant acts as
gastric lavage with warm w ater, and a sudorific and stimulates the contraction
administration of demulcents, stimulants of the muscular tissue of the heart, intestine
and other drugs as indicated by the and uterus. Taken internally in large
symptoms. doses, the plant acts as an irritant poison
P ostm ortem appearances: These include and produces the same symptoms as
dilated pupils, froth at the nostrils, those of calotropis poisoning. The treat­
stomatitis, and acute inflammation of the ment and postmortem appearances are also
alimentary tract. The stomach may show similar.
an acute ulcer or perforation. The viscera The fatal dose is not certain. The fatal
including the brain and its meninges are period is also uncertain.
congested.
M edicolegal aspects: Madar juice has been M edicolegal aspects: The root is ingested
used— (1) sometimes for infanticide by as an abortifacient or applied to the cervix
mixing it with milk or water, (2) by inges­ directly or as a paste via the abortion stick.
tion and by local application on an abortion Malingerers use it to produce artificial bruise.
stick to procure abortion, (3) as a cattle It is rarely used as a homicidal poison.
poison by introducing a smeared cloth in
the rectum of an animal or mixing it with Illustrative Cases
fodder, (4) to produce artificial bruises, and A woman was given a quack medicine
containing plumbago root by her paramour to
(5) rarely for suicide or homicide. The root
cause miscarriage. She suffered from severe
of calotropis procera is highly poisonous
gastrointestinal irritation with vomiting and
to cobras and other poisonous snakes. diarrhoea and died after 10 days. At post­
Snake charmers use it to control the newly mortem, the foetus was found to have separated
caught snakes which cannot even stand its from the gravid uterus.
smell. The use of calotropis as an arrow Jitan Ali Mir of Murshidabad was sentenced to
poison is known. four years of imprisonment for bringing a false
charge of dacoity (robbery) and torture. He had
PLUMBAGO ROSEA (LAL CHITRA)
produced artificial bruises on his skin by
AN D PLUMBAGO ZEYLANICA (CHITRA)
application of plumbago rosea to fabricate the
Q. 44.9. G iv e a brief ac c o u n t of poisoning complaint and bring about such a charge.
from p lu m b a g o ro se a a n d p lu m b a g o A woman mixed a small quantity of the
ze y la n ic a . powdered root of Lai Chitra with milk and gave
it to her husband who started vomiting and
The roots of these plants contain an active
purging within 2 hours and died the same day.
principle, plumbagin, a highly acrid
 Animal Poisons

The important topics in this group are: difficulty in swallowing and speech,
cantharides, snakes and scorpions. The nausea, vomiting of blood-stained material,
symptoms produced by cantharides are and diarrhoea with blood and mucus. As
time ensues, nephrotoxic effects manifest
those of local irritation, and irritation of the
gastrointestinal and genitourinary tracts. by a dull pain in the loins and a constant
The symptoms produced by snakes and desire to micturate but only small amount
scorpions are mainly local, neurotoxic, of blood-stained urine is passed (strangury).
haemotoxic, and myotoxic. The inflammation extends to the urinary
bladder and urethra. In the male, persistent
CANTHARIDES (SPANISH FLY) and painful erection of the penis (priapism)
Q. 45.1. Give a brief account of symptoms, may occur with frequent seminal emissions.
signs, treatm ent, postm ortem a p p e a ­ In the female, engorgement of the vulva,
rances, and m e d ic o le g a l as p e cts of and abortion may occur. Convulsions and
poisoning by the Spanish fly. coma precede death. Blister formation may
take place in the mouth and other parts of
The Spanish fly is about 2 cm long and
the alimentary tract in contact with the
0.75 cm broad. The colour of its head, legs
poison.
and wing sheaths is shiny emerald green.
The powder of the dried body is grayish F atal doserMl .5 gin- of the powder, one
brown and contains shining green particles. ounce of the tincture, and 10 mg of the
The active principle is cantharidin which active principle, cantharidin, is regarded as
causes a blister or vesicle on the skin. a fatal dose.
Therefore, the Spanish fly is also known as
Fatal period: This varies from 24 hours to
blister beetle or cantharis vesicatoria.
a week.
Cantharis may be administered in the form
of powdered beetles, the tincture, or the Treatment: The stomach is washed out with
active principle. warm water. Fatty substances and alcohol
must be avoided but demulcents and
Symptoms and signs: When applied to
albumin may be given. The rest of the
skin, an inflammatory response results in
treatment is symptomatic.
2-3 hours, and vesicles form later. When
swallowed, symptoms appear in about an P ostm ortem ap p earan ces: The whole
hour. There is burning sensation in the alimentary tract from the mouth down­
mouth, throat, oesophagus, stomach, and wards shows intense inflammation. The
abdomen, followed by intense thirst, stomach contents are bloody, and parts of
574 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

the powdered beetle may be found as For medicolegal purposes, snakes are
shining elytra or wing cases of the insect. classified into two groups, viz, poisonous
The shining wings of the beetle resist putre­ and non-poisonous. This classification is
faction and provide a clue to the identity not quite correct as some of the non-
of the poison. The kidneys and the genito­ poisonous snakes can kill small animals by
urinary tract show severe inflammation. their poison. The differentiating features of
Pelvic viscera are congested. Pericardial the poisonous and non-poisonous snakes
and endocardial haemorrhages are are given in Table 45.1. Jfe-
common. The lungs may be oedematous The poisonous snakes are further classi­
and air passages may show blood-stained fied on the basis of poison secreted by them
mucus. into three main types, viz. (1) elapids
:v J* "tvects: Cantharis is used as (secreting neurotoxic venom), (2) vipers
(1) an aphrodisiac, (2) an abortifacient, (vasculotoxic), and (3) sea snakes (myotoxic).
(3) a counter-irritant to the skin in the E lapids: This group consists of cobra, king
blistering plaster, and (3a) in hair oils to cobra, common krait, banded krait, and the
promote hair growth. coral snake. The head is nearly of the same
Accidental poisoning may occur: (1) from width as that of the neck and the pupils are
eating fowls which have ingested cantha- round. The fangs are situated anteriorly but
rides, (2) from use of blistering plaster, and being covered w ith a fold of mucous
(3) when it is used as an aphrodisiac or membrane, they may be difficult to see.
abortifacient. They are short, fixed, and grooved.
Generally, therefore, the snake cannot bite
____ m jO P B iPIA )_____________________ _ through the clothing or inject a complete
. 3 /e o m e d ico le ga l classification dose. The tail is usually round.
Tabulate the d iffe re n tia tin g Vipers: This group consists of pit vipers and
-•res o- poisonous an d non-poisonous pitless vipers. The pit is situated between
the eye and the nostril and helps to detect

TateSe 45.1: Differentiating features of poisonous and non-poisonous snakes

Poisonous Non-poisonous
. Belly scales as seen by Large, and cover the entire breadth of the Small like those on the back or modera*
turning the snake with belly. Some harmless snakes also have tely large but do not cover the entire
belly upwards such belly scales (Fig. 45.1A) breadth of the belly (Fig. 45.1B.C)
. Head scales Small (vipers) (Fig. 45.2)
(a) Large with conspicuous pit between Large (Fig. 45.3) with the exceptions as
the eye and nostril (pit vipers) (Fig. 45.4) outlined under the poisonous snakes,
(b) Third labial touches the eye and nasal viz. pit vipers, cobra, king cobra, coral,
shields (cobra, king cobra, or coral) and kraits
(Fig. 45.5)
(c) Central row of scales on back enlarged,
and under surface of the mouth with only
four infralabials, the fourth being the
largest kraits, and perhaps bands or half
rings across the back (Figs 45.6 and 45.7)
5. Fangs Long and canalised likehypodermic needle Short and solid
(Figs 45.8 and 45.9)
Tail Compressed Not markedly compressed
5- Habits Generally nocturnal Not so
6- Bite Two fang marks with or without small A number of small teeth marks in a row
marks of other teeth
 Animal Poisons
warmblooded prey in the dark. The head
is triangular and wider than the neck and
the pupil is vertical. The fangs are long,
movable and canalised like hypodermic
needle. This snake can, therefore, bite
through clothes and give a complete dose.
The fangs are easy to see when erected but,
being too big, lie tucked up by the side of
theupper jaw. While the bites of pit vipers
are seldom fatal to human beings, those of
pitless vipers are dangerous. The tail is
usually tapering. The bamboo snakes
belong to the category of pit vipers while
575
the Russell's viper and the saw-scaled viper
belong to the category of pitless vipers.
Sea $11a They are found in the vicinity
of sea coasts. They have small heads, and
flat rudder-like tail to help in swimming.
The nostrils are situated on the top of the
snout and are valved to enable free
breathing. Their belly plates are not broad
and they have dull and tuberculated scales
on their back. Their venom apparatus is
delicate with very short fixed fangs which
are situated posteriorly. Therefore,
generally, they do not bite.

Fig. 45. V. Large belly scales covering the entire breadth of the belly as in (A) Belly scales small
like those on the back as in (B) or moderately large but not covering the entire breadth of the
belly as in (C)

Fig. 45.3: Large head scales of non-poisonous

Fig. 45.2: Small head scales of poisonous snakes. Some poisonous snakes have large
snakes, e.g. Russel viper head scales
 576 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Fig. 45.8: Elapid fangs (cobra in this case) Fig. 45.9: Viper fangs are easy to see in the
being converted by mucous membrane are erected position as in this case. (Courtesy.
difficult to see. (Courtesy. Dr HA Reid) Dr HA Reid)
 Animal Poisons
577
q . 45.3.Nam e the poisonous snakes of
India and tab u la te th e d iffe re n tia tin g
features of the different groups.
Themost poisonous snakes in India accor­
dingto their severity are the krait and cobra
among the elapids and the Russell's viper
andthe saw-scaled viper among the vipers.
The differentiating features between the
elapidsand the vipers are given in Table 45.2.

Q. 45.4. Give the main characteristics of

the important poisonous snakes of India.
The important poisonous snakes of India Fig. 45.10: Cobra. (Courtesy. Dr NK Mohanty)
are the cobra, king cobra, common krait,
banded krait, common green pit viper, its neck to form a hood only when enraged.
Russell's viper, and saw scaled viper. Their In the absence of a hood, the cobra is
characteristics are given below: identified by 2 or 3 series of very dark or
black belly scales under and below the neck
Cobra (naja tripudians, naag, or k a la
or by the divided tail shields; The cobra
samp): This snake (Fig. 45.10) grows to a
prefers populated areas and iisfdistribution
length of about 1.5 to 2 metres. Its colour is
in India is widespread.
usuallyblackbut may be variable. The head
is nearly of the same width as that of the King cobra (naja bungaru0uim adryad, raj
neck which is generally provided with a naag, or raj samp): This snake is bigger
hood bearing a spectacle mark. It expands than the common cobra. It grows to a length
of about 2.5 to 4.5 metres. The young king
Table 45.2: Differentiating features between the cobra is jet black in colour while the adult
elapids and the vipers
king cobra may be yellow, green, brown or
Elapids (cobra) Vipers
black. There are usually white or yellow
1. Body Long and cylindri- Short with narrow
cal neck cross-bars or chevrons on the body. It has
2. Head Nearly of the same Triangular and wider a hood but no spectacle mark on it. The tail
width as that of the than the neck and scales are entire proximally but divided
neck, covered by usually covered by distally. The king cobra prefers jungles or
large scales or numerous small forests and is found in their vicinity.
shields special in scales
Commorikrait (bungams caerulus, manyar,
3. Pupils Round Vertical kalotaro, chitti, or kawriya):/This snake
4. Maxillary Carries other teeth Carries only the grows to a length of 1 to 1.25 or even
bone also besides the poison fang 1.50 metres. Its colour is usually glistening
poison fang black and has single or double white arches
5. Fangs Short, fixed and Long, movable, and across the back beginning some distance
grooved, and so, canalised, and so, from the head. It has a central row of
usually cannot bite can bite through
hexagonal scales on the back and a creamy
through clothing or clothingandmay also
may give only a inject a fatal dose white belly. The head is covered with large
sub-lethal dose shields and the tail scales are entire. The
6. Tall Round Tapering common krait prefers to live in or near the
7. Venom Neurotoxic Vasculotoxic house, is widespread in India, and is
8. Other Ovo-viviparous Oviparous responsible for a number of cases of snake
characteristics bite in India.
 57# Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Banded krait (bungarusfasciatus orkoelea
krait): This snake (Fig. 45.11) is bigger and
stouter than the common krait and grows
to a length of about 2 metres. In addition
to the distinguishing features of the
common krait, the banded krait as the name
suggests, has alternate black and yellow
bands across its back. It is commonly found
in Assam, Bengal and parts of South India.
Common green pit viper (lachesis gramineus,
bamboo snake, or hara phisi): This snake
grows to a length of 30 to 100 cm. Its colour
is usually vivid green, rarely yellow or
brown. The body is flat and broad and the
head is triangular with a pit between the Fig. 45.12: Russell's viper
eye and the nostrils. The flanks have a
yellowish white line. The tail is long with sound when about to bite. It prefers plains.
divided scales. This variety usually occurs It is found throughout India but not in
in the hills and is widely distributed in dense jungles.
Saw-scaled viper (echis carinata, phoois.i,
Russell's viper (daboia, chant viper, ghonus, echis, or afai): This snake (Fig. 45.13) grows
or khadchitro): This snake (Fig. 45.12) to a length of 50 to 75 cm. Its colour is
grows to a length of about 1.5 metres. Its brown or brownish grey or greenish. It can
colour is brown or buff and has three rows be identified by (1) a triangular head with
of black diamond-shaped spots or chains a white mark on it resembling an arrow,
on the back. It is stouter than any other (2) a wavy line on each flank with diamond­
poisonous snake in India. It can be shaped areas between the upper curves of
identified by (1) a flat triangular head with the two wavy lines, (3) small head scales,
a distinct V mark, with its apex pointing (4) broad belly plates, (5) undivided tail
forward, (2) small head scales, (3) broad shields, and (6) body scales serrated like a
undivided belly plates, and (4) a narrow saw, and hence the name. The reptile makes
short tail with shields divided in two rows. a peculiar rustling sound when it moves
Its nostrils are bigger than those of other on account of the rough scales of the back.
Indian snakes. It makes a terrific hissing This snake is found throughout India.

Fig. 45.13: Saw-scaled viper

 Animal Poisons 579
q. 45.5. Discuss the characteristics of A myotoxic venom produces genera­
snake venom. lised muscular pain, followed by myoglo­
Inthe fresh state, it is a clear transparent, binuria, three to five hours later, ending in
amber tinted fluid and dries into a yellow respiratory failure in fatal cases.
granular mass which retains its activity for
many years. It contains toxalbumins and Q. r.... h detail the hallmarks of
several toxic principles, such as the a venom ... nakejhite. |j
following: The hallmark of attack by a venomous
1. Fibrinolyses snake is the presence of fang marks; these
2. Proteolysins are usually two but only one may be
3. Neurotoxins (predominant in elapid evident, if the bite is sideways on. In
contrast, bites by non-poisonous snakes
4. Cholinesterase (predominant in elapid produce a characteristic U-shaped set of
venom) teeth marks. One can get an idea about the
size of the snake from the distance between
5. Haemolysins (predominant in viper
the fang marks.
venom)
6. Thromboplastin (predominant in viper Symptoms and signs: It important to
venom) realise that poisonous snake-bite is not
7. Agglutinins necessarily the samejas snake bite
8. Cardiotoxins poisoning.
9. Coagulase, hyaluronidase, lecithinase, Poisoning may occur frombite (injection)
etc. or absorption of venom through cuts or
Elapid venom is mainly neurotoxic, scratches. In some cases, instantaneous
viper venom mainly vasculotoxic, and sea death occurs fromshock due to fright, even
snake venom myotoxic. before any symptoms commence.
A neurotoxic venom causes muscular The degree of toxicity depends upon the
weakness of the legs and paralysis of the size of the person bitten, the potency of the
muscles of the face, throat and respiration. venom, the maintoxic principles it contains,
The neurotoxins of cobra venom produce and the amount injected, which in turn
both convulsions and paralysis, whereas depends upon the age, size, sex and species
krait venom causes only muscular of the snake, whether it had recently taken
paralysis. Local symptoms at the site of the a prey, whether the bite is on bare skin or
bite are minimum as compared to those through clothing, the type of fang whether
caused by vasculotoxic venom. canalised or grooved, and the season and
A vasculotoxic venom produces enzy­ the time of bite. In the case of vipers where
matic destruction of,cell walls and coagula­ the channel is complete andlthe fangs
tiondisorders*As a result, the endothelium movable, the shake gives a complete dose.
of blood vessels is destroyed, red cells are In the case of elapids,j|.g. a icobra, the
lysed, and other tissue cells are destroyed. groove is variously formed and the fangs
Locally, there is oozing of haemolytic being rigid, the transfer of venom is rarely
blood, and a spreading cellulitis. Haemorr­ substantial. The season is also important
hages fromexternal orifices of the body are because snakes which have recently^
common. Other functional disturbances emerged from hibernation have a parti-;
are related to the involved organ, e.g. cularly potent venom. Nocturnal bites mag
convulsions from haemorrhage in the be more serious than those which occui|j
during the day.
 A bite from an elapid snake is attended
by mild local symptoms as compared to
bite by viper, but by marked neurotoxic
effects. There is slight burning at the site of
the bite which shows a triple response. This
is followed about 15 minutes to two hours
by marked neurotoxic effects such as
giddiness, lethargy, muscular weakness and
spreading paralysis. There is salivation and
even vomiting. Weakness in the legs is mani­
fested by staggering. This is followed by
difficulty in speaking and swallowing. Ptosis
and paralysis of the extraocular muscles may
occur. Breathing becomes slow and labou­
red. The patient is conscious but unable to
speak. After a couple of hours, respirations
cease with or without convulsions and the
heart stops. In the event of recovery, the skin
and cellular tissues surrounding the bite
mark undergo necrosis (Figs 45.14 to 45.16).
A bite from a viper is attended by severe patient as in Fig. 45,14 showing
local symptoms and marked vasculotoxic necrosis after cobra
effects. There is intense local pain, swellin Dr HA Reid)

Fig. 45.14: This person was bitten on the hand by Fig. 45.16: Same patient as in Fig. 45.14 showing
a elapid snake (cobra). Ptosis indicates systemic healing after necrosis from a cobra bite six
elapid poisoning. (Courtesy. Dr HA Reid) months later. (Courtesy. Dr HA Reid)
ecchymosis and severe oozing of haemo­
lytic blood. Serous and serosanguinous
blisters sometimes appear. Nausea and
vomiting occur. Intravascular haemolysis
may lead to haemoglobinuric nephritis.
Petechial haemorrhages, bleeding from the
gums, haemoptysis and bleeding from the
mucous membrane of the rectum and other
orifices of the body are common. Collapse
sets in with cold clammy skin, rapid feeble
pulse, and dilated pupils insensitive to
light, followed by coma and death. In the
event of recovery, the local lesion suppu­
rates and undergoes superficial necrosis
(Figs 45.17 to 45.20).

Fig. 45.17: This patient was bitten on

leg by a viper. Swelling of the bitten part and
spreading cellulitis of the leg are seen. The skin
of the right leg has been opened in similar
area for comparison. ( Courtesy'. Dr NK Patoria)

one or two hours, generalised muscular

Fig. 45.18: This patient was bitten by a viper
on the hand. Swelling of the hand is seen,
(iCourtesy. Dr HA Reid)
pain and stiffness develop, starting in the
neck and limb girdle. Myoglobinuria causes |
a characteristic brown discolouration of the
urine and serum transaminase becom e^
elevated. Hyperkalaemia resulting frqnv|
leakage of cellular^potassium follow ing
extensive muscle damage may become a’
problem. Respiratory failure may ensue
(Fig. 45.21).
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
fig. 45.21: This patient was bitten by a sea
snake. There were no local symptoms.
Movement of neck, trunk and limbs— leg
straightening as shown here—becam e very
painful. A few hours later, urine was brown from
myo-globinuria. Electrocardiogram showed
typical pattern of hyperkalaemia. (Courtesy.
Dr HA Reid)
FataI dose: 15 mg of the dried cobra venom,
20 mg of the viper venom, 6 mg of the krait
venom, and 8 mg of the saw-scaled viper
venom are fatal. The amount of dried cobra
venom yielded in one bite is about 200-350
mg. The viper bite yields about 150-200 mg,
the krait about 20 mg, and the saw-scaled
viper about 25 mg.
Fatal period: Death may occur instanta­
neously from shock due to fright. Generally,
death from cobra venom occurs within a
few minutes to few hours while that from
viper venom in a few days. Sea snake bite
is mostly not fatal.
Q. 45.7. Give the main principles of treat­
ment of venomous snake b?*e,
The main principles of treatment include:
(1) allaying anxiety and fright, (2) preven­
tion of the spread of venom, (3) use of
antivenin and other antitoxic therapy, and
(4) general measures.
Allaying ' The patient
should be reassured by pointing out that
(1) all snakes are not poisonous, (2) even
poisonous snakes are not fully charged
with poison, and (3) even a snake fully
charged with poison cannot always inject
a lethal dose.
Spread of
snake venom through the body is mostly
by diffusion and lymph circulation. There­
fore, efforts to reduce lymph circulation
are helpful and this can be achieved by
(1) immobilisation, (2) application of tourni­
quet, (3) cleansing the wound, and (4) incision
and suction.
/ . ■nobiUsatim Activity increases the spread
of venom. The bitten part should, therefore,
be immobilised. Besides reducing the
spread of venom, immobilisation eases the
pain of snake bite.
Tourniquet: Application of a tourniquet is
possible only when the bite is on a limb. If
the bite is on face, neck or trunk, firm pre­
ssure over the bitten area may be applied.
Material, such as a rubber tube, handker­
chief or grass, that is available on the spot
can-serve as a tourniquet. It should be
applied approximately 5 cm proximal to the
bite and tight enough to occlude the super-3
ficial venous and lymphatic circulation
without impeding the arterial or deep j
venous blood flow. Normally, an additional||
tourniquet at a distance of 5 cm proximal
to the first one is desirable. It should be
released for a minute every half an hour or
for 30 seconds every quarter hour to allow
the escape of small quantity of toxin to
enter the general circulation where it is
destroyed. It should probably be applied
up to two hours. Longer use could lead to
aggravation of the tissue damage. Nowadays,
It is felt that torniquet application is not
necessary. However, it may be applied
lightly to prevent lymphatic flow.
Cleansing the wound: The wound should be
cleaned with plain water or saline.
Incision and suction: It is said that free
incisions of the wound through the fang
marks (avoiding blood vessels, nerves and
periosteum), and thorough sucking either
with a breast pump or mouth (only if there
is no injury in the mouth, tongue or lips)
can remove up to 20% of the injected
 Animal Poisons 583
venom, if done within the first 30 minutes. within a few minutes, can help to amelio­
p0r parts of the body where a tourniquet rate local necrosis.
cannot be applied, suction is specially to A test dose prior to therapeutic dose is
ke relied upon. When the poison is sucked necessary to test for serum sensitivity.
by mouth, the sucker should spit out the Serum is available in the form of lyophilised
saliva and bloody fluid quickly and rinse powder in an ampoule. It retains its
the mouth well. It is not advised nowadays. potency for 10 years. It is dissolved in
Cryotherapy (application ice) is also not distilled water or normal saline before
allowed. injection. The initial dose of the serum is
This method appears to have some place only determined by the concentration of the
inthosefewcases ofpoisonous snake bites where serum, the size of the patient, the size of
thereis likely to be considerable delay, say more the snake, and the nature of the venom. It
than 4 hours, in reaching the hospital, and in should preferably be large enough to
those areas where antivenin is not available. combine with all the venom present in the
body. The concentration of the serum and
Antivenin: It is of two kinds, either specific
dosage data for adults and children
or polyvalent. Specific antivenin is pre­ accompany the package. Generally, for an
paredby hyperimmunising horses against adult, 60 ml of polyvalent serum is injected
thevenomof a particular snake while poly­ initially, one-third -being given subcuta­
valent antivenin is prepared by hyper­ neously or locally around the bite, the other
immunising horses against the venoms of third intramuscularly, and the remaining
four common poisonous snakes, viz. third intravenously. The intravenous dose
(1) cobra, (2) common krait, (3) Russell's can be repeated any time, if collapse appears
viper, and (4) saw-scaled viper. The or every six hours till the symptoms dis­
strengthof the polyvalent antivenin is such appear.
that 1 ml will neutralise 0.6 mg of dried If a person is sensitive to serum, desensi­
cobravenom, 0.45 mg of dried krait venom, tisation is achieved by injecting multiple
0.6mg of dried Russell's viper venom, and small doses under cover of adrenaline,
0.45 mg of dried saw-scaled viper venom. antihistamines, and corticosteroids.
Themortality from poisonous snake bite In as much as antivenin can neutralise
isnearly 40%. Antivenin treatment reduces circulating toxin only and not the toxin
it to less than 10%. It should be given as fixed in the tissues, the toxin's action at
per instructions accompanying the phial. tissue level may be antagonised by
neostigmine-atropine therapy in case of
While antivenin is very effective even
when given after a delay, it is important to elapid bite and heparin along with
supportive fibrinogen transfusion in case
establish the necessity for its use. Delayed
of viper bite.
serum sickness type of response is quite
common and fatal anaphylactic reaction While symptoms of systemic poisoning
may occur. It should, therefore, be given generally do not ensue, in bites from sea
only if signs of systemic poisoning, e.g. snakes, the principles already outlined here
ptosis or haemorrhagic signs develop after hold good in management of sea snake bite
snake bite. Its use may also be considered poisoning also. Seg snake antivenin can be
in all patients with extensive local tissue effective even when started several hours
damage because the risk of systemic after the onset of poisoning symptom^
poisoning in such cases is high. Injection When antivenin is not available ipcal
of antivenin, if done at the site of the bite infiltration ofkarbolic soap around the site
584 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

of the bite in case of elapid snakes and findings include necrosis of the renal 1
heparin in case of vipers is recommended. tubules, and cloudy swelling and granular
General measures: Stimulants are helpful changes in the cells of other organs. . .*
in paralytic cases and artificial respiration M edicolegal aspect s: Snake bite is generally
is often required. Transfusion of whole accidental, rarely homicidal and still rarely 1
blood may be helpful in haemorrhagic suicidal (Cleopatra). Cattle are sometimes !
cases. Steroids are effective in combating poisoned by chamars (cobblers) for the sake
the allergic manifestations of antivenin of hides by a peculiar method. A cobra is
therapy. Aspirin, short-acting barbiturates, placed in an earthen vessel with a banana.
and antibiotic prophylaxis to combat The cobra is irritated by applying heat to
secondary infection together with general the vessel. It bites the fruit, the pulp of
supportive measures are beneficial. A which is then smeared on a rag, and the
patient bitten by an elapid snake, if not rag thrust in the animaTs rectum with the
dead in two hours will probably recover help of a bamboo stick. Sui (abrus precato-j
rapidly and completely. A patient bitten by rius) poisoning of cattle resembles viperine
a viper is in danger for a much longer time, snake bite.
and convalescence is very protracted.
SCORPIONS____________ _______________
Q. 45.8. G ive a succinct ac co unt of post­
m ortem a p p ea ra n ce s an d m edic olega l Q. 45.9. Briefly discuss scorpion bite from
aspects of venom ous snake bite. :a m e d ic o le g a l point of view.
Scorpions have a crab-like appearance with
Postmortem appearances: One or two bite
a long, fleshy, five segmented, tail-like post­
marks about 1 cm deep in case of elapid
abdomen, ending in a broad sac and a pro­
and 2.5 cm deep in case of viper may be
minent hollow sting which communicates
found. There is some swelling and cellulitis
by means of a duct with the venom secret­
about the bitten part.
ing glands. The venom contains toxalbu-
If the venom is predominantly neuro- mins having neurotoxic and haemotoxic
toxic, there are no definite appearances
actions. Its toxicity is greater than that of
indicating the cause of death except the
snakes but only a small quantity is injected.
signs of asphyxia.
Red scorpion venom contains a potent
In case of viper bite, the local appea­ cardiotoxin (Fig. 45.22). ,
rances are more striking due to severe
oozing of blood from the puncture site. The
blood is generally fluid and haemolysed
causing early staining of the blood vessels.
There are haemorrhages in the lungs and
in the serous membranes. Endocardial
haemorrhages are seen especially in the left
ventricle. Petechiae are also found within
the kidney pelvis, and mucosa of the
urinary bladder, stomach, and intestines.
Blood fails to clot normally even after addi­
tion of thrombin because of the extremely
low level of fibrinogen. Arterioles and
capillaries are characterised by blurred
walls and swollen endothelial cells. Other Fig. 45.22: Scorpion. ( Courtesy. Dr NK Mohanty)
 Animal Poisons
Symptoms and signs: The local irritation
is characterised by redness and burning
pain radiating from the site. There may be
headache, giddiness, nausea, profuse
perspiration, priapism, excessive saliva­
tion, ventricular premature contractions
dilated pupils, urticaria and muscular
cramps followed in some cases by coma.
Although the duration of symptoms is
ordinarily 24 to 48 hours, neurologic
manifestations may persist for up to one
week. While the mortality in adults is
negligible, children may succumb to
pulmonary oedema. Pathologic findings in
cases of death are widespread haemorr­
hages. Myocardial damage is found in
deaths from red scorpion stings.
585
T reatm ent: A ligature should be tied
proximal to the site of the sting, provided
the bite is on a limb, the site incised, if nece­
ssary, and the wound washed with plain
water, ammonia or potassium permanga­
nate. A local infiltration of an anaesthetic
lessens pain and immobilisation of the
bitten part diminishes absorption of venom.
A specific antivenin is available for most
species and should be tried. Injection of
calcium gluconate, 10 ml of 10% solution
slowly intravenously relieves muscular
cramps and injection of atropine helps to
prevent pulmonary oedema. The rest of the
treatment is symptomatic.
Medicolegal aspects: Scorpion poisoning is
accidental.
 46 Mechanical Poisons
Mechanical poisons are actually not
poisons because they are not absorbed but
produce symptoms of irritant poisoning
solely in consequence of their mechanical
action, on the part with which they come
in contact. Such substances, as explained
in the definition of poison, are included in
section 328 IPC within the meaning of
poison, and include powdered glass, pins,
needles, chopped hair, etc., the most
common being powdered glass. ^
POWDERED GLASS
Q. 46.1. Give a brief account pjpoisoning
by pow dered glass.
Powdered glass merits special attention, as
this substance and similar products such
as powdered diamonds are mentioned in
the literature as poisons.
Symptoms and signs: When taken internally,
coarse particles of powdered glass produce
a sharp burning pain in the throat, stomach
and abdomen. There is nausea and vomi­
ting, the vomit being blood-stained. There
is generally constipation but sometimes
diarrhoea with tenesmus and blood. Death
may occur from shock, if stomach or intes­
tine has been perforated. Due to presence
of silica which is radio-opaque, glass pieces
may cast a faint shadow on X-ray and this
helps in diagnosis.
5?
Treatment: This consists of giving bulky
food, such as large quantity or rice or
banana, to envelop the fragments of glass
within it, and then emetics and laxatives
but no violent purgatives. The rest of the
treatment is symptomatic.
m ^ stm o rtem appearances: There is
inflammation of the stomach and intestines.
Erosions and ulcerations may also be
found. Occasionally, there may be a
perforation. Fragments of powdered glass
■ may be found adherent to tenacious mqcus
secretion of the stomach.
In a fatal case of suspected homicide,
viscera should not be preserved iri?glass
vessels. The glass recovered from viscera
and its relationship to glass seized from an
accused person can be decided by spectro­
scopic examination for unusual elements.
M edicolegal aspects: Mixed with food,
coarse particles of powdered glass have
been administered with homicidal intent.
Finely powdered glass is less destructive
in its effects; well-powdered glass bangles
administered in food by women with a
view to kill their husbands have resulted
in failure of their mission! Accidental conta­
mination of food with glass may occur from
the glass container itself. It is sometimes
used to destroy cattle.
586
 Food Poisoning and Poisonous Foods
The term 'food poisoning' may be used in
a general or special sense. When the term
is used in its general or wider sense, it
includes all illnesses resulting from
ingestion of foods containing non-bacterial
or bacterial products. When the term is
used in its special or restricted sense, it
means that the poisoning is due to bacterial
products only. The bacterial products
include bacteria and their toxins. The
poisoning resulting therefrom is, by
convention, known as bacterial food
poisoning. The non-bacterial products
include poisons derived from plants and
animals, and inorganic chemicals. Foods
containing such products are, by conven­
tion, known as poisonous foods.
The illness is characterised by: (1) simul­
taneous attack of many persons at the same
time, (2) history of ingestion of common
food by all sufferers, and (3) similarity of
signs and symptoms in a majority of cases.
Generally, diagnosis poses no problem
except when only one or two persons may
be affected, when it may be missed and a
suspicion of poisoning from other sources
may be aroused. Further, in case of
attempted poisoning, it may be alleged that
the symptoms are due to some article of
food or drink. A medical practitioner
coming across a case of food poisoning
from a public eating house must report it
to public health authorities.
BACTERIAL FOOD POISONING________
This is of three types, viz. (1) infection type,
(2) toxin type, and (3) botulism.
Infection type: This results from ingestion
of viable microorganisms that multiply in
the gastrointestinal tract and produce a true
infection, e.g. Salmonella group of organisms.
Toxin type: This results from toxins pro­
duced by multiplying organisms that have
gained access to the prepared food, e.g.
enterotoxin produced by the Staphylo­
coccus.
Botulism: This results from ingestion of
preformed botulinum toxin inthe preserved
food. The toxin is produced by Clostridium
botulinum.
Q. 47.1. Give a brief account of infection
type of food poisoning.
In this type of food poisoning, the organisms
multiply in the gut and cause gastro­
enteritis. The common organisms responsible
for the attack are the Salmonella group of
organisms, and occasionally, the Shigella
group.
The natural reservoir of Salmonella orga­
nisms is in certain birds, mammals and
reptiles. Food may be contaminated with
infected excreta of mice or rats, or infection
may be transferred by flies or by human
carriers employed in the handling of
food. Shigella infection is the result of
588 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

contamination of food or water supplies Q. 47.2. Give a brief account of toxin type
with the faeces of the individuals who of food poisoning.
either have the disease or, less often, are For this type of poisoning to occur, (1) the
asymptomatic carriers of the organism. food must be contaminated by a strain of
The outbreak of Salmonella food organism that produces enterotoxin, (2) [[
poisoning is likely to occur whenever large must be suitable for growth of this orga-
amounts of food are prepared and the
nism, and (3) the infected food must be kept
unconsumed food kept for future meals.
at a temperature suitable for bacterial
Accordingly, such food poisoning is
growth and for a sufficiently long time so
reported far more frequently from
canteens, restaurants, hospitals and other that an appreciable quantity of enterotoxin
institutions than from private houses. is formed. Food such as milk, custard, and
previously prepared meat dishes are the
Symptoms and signs: Depending on the
chief sources.
susceptibility of individuals to Salmonella
food poisoning, while some participants Most cases are due to some strains of
may remain free from symptoms, others staphylococci which produce a heat stable
may be severely affected. enterotoxin. Other toxin producing orga­
The incubation period is longer than nisms which may give rise to such food
. staphylococcal food poisoning. A delay of poisoning are Proteus vulgaris, Streptococcus
12 hours or more is usual. The onset is viridans (milk streptococci), B. coli, and
sudden. A chill maybe the initial symptom, Clostridium welchii when present in large
followed by headache, nausea and numbers.
vomiting, severe abdominal cramps, and
marked prostration. Three characteristics Sym ptom s and sign s: The toxin being
that differentiate it from staphylococcal already present in food, the symptoms
food poisoning are: (1) muscular weakness, develop rapidly within one to four hours.
(2) fever, and (3) persistent, very foul The first symptom is salivation, followed
smelling diarrhoea. The diagnosis rests on by acute gastroenteritis, and recovery in
the isolation of the causative organism from about 24 hours.
the patient and suspected articles of food.
Unlike Salmonella food poisoning, this
Treatment: The stomach should be washed condition is not an infection. But like
and the bowel emptied by a cathartic, if
botulism, it is the result of ingesting
diarrhoea is not present. For infection with
preformed toxins contained in the food.
the Salmonella group of organisms, the
The characteristics that differentiate it from
antibiotic of choice is chloramphenicol.
botulism are: (1) symptoms appear rapidly
Ampicillin or septran can also be used. For
infection with the Shigella group of and are mainly gastrointestinal, (2) they are j
organisms, ampicillin and tetracyclines are of short duration, and (3) recovery is
used. Cotrimoxazole is as good as ampicillin usually prompt and complete.
and preferred by some. The rest of the treat­ Treatment: This is largely symptomatic and
ment is symptomatic.
on the same lines as in Salmonella food
Postmortem appearances: These are those poisoning.
of gastroenteritis and general toxaemia.
The mucosa of alimentary tract is inflamed Postm ortem appearances: These are the
or even ulcerated. Internal organs are same as those found in Salmonella food ;
congested. poisoning. I
 Food Poisoning and Poisonous Foods 589
q. 47.3. Give a succinct account of botulism. central nervous system. Degenerative
The term botulism is derived from changes occur in the liver and the kidneys.
'botulismus' meaning a sausage, since large
outbreaks of the disease were first observed
Q. 47.4. Give a brief account of poisonous
foods.
following ingestion of improperly cooked
sausage. The causative agent is an anae­ By usual implication, this term excludes
robic spore forming bacillus, Clostridium conventional food poisoning by bacteria
botulinum, which produces an exotoxin. It and their toxins and is restricted to poison­
iscommonly found in the soil. The toxin is, ing by articles of food due to: (1) contained
therefore, likely to be present in such soil toxic principles, (2) metallic contamination,
contaminated undercooked or canned and (3) food allergy.
foods. The foods that are most often Containing toxic principles: The articles of
responsible are meat, fish and vegetables. food containing toxic principles are
The toxin is destroyed by heat at 80°C poisonous food grains, infected rye,
for 30 minutes and, therefore, adequate adulterated oil, and poisonous mushrooms.
cooking gives protection against it. The The most common food grain so affected
toxin paralyses the muscles by blocking is Lathyrus sativus (kesari dal), which gives
nerve impulses at the myoneural junction. rise to lathyrism, a spastic paralysis of the
It blocks the action of acetylcholine. lower limbs. The other food grains which
Symptoms and signs: The symptoms may be so affected are Lolium temulentum
commence within 12-36 hours. The initial (darnel), Stigmata maides (maize), and
symptom is usually diplopia from ocular Paspalaifi&scrobiculatum (kodra). The
muscle palsy, followed by difficulty in manifestations are usually neurological,
swallowing and speech. The picture is thus viz. spastic paraplegia and polyneuritis.
one of bulbar palsy. Respiratory paralysis The contaminated rye (Claviceps purpurea)
with extension to the breathing centre produces convulsive or gangrenous type of
closes the scene. Gastrointestinal symptoms ergotism. The mustard oil contaminated
are rare. The temperature is normal or with argemone oil (katkar oil) produces
subnormal throughout. The victim is dropsy. The poisonous mushrooms
usually conscious to the end. The fatal produce symptoms of irritant poisoning,
dose of contaminated food may be less neurotic poisoning, or both.
than 5 grams. Death may occur within Metallic contamination: This is probably
24-48 hours or may be delayed for a week. more common than dangerous. Various
The diagnosis rests on the isolation of the metallic poisons formerly occurred in food
bacillus from food, or patient's vomit, stuffs as dyes, preservatives or colouring
faeces, or viscera. matter. Such severe poisoning is not
Treatment: The stomach should be washed common nowadays.
out and the bowels emptied by saline Food allergy: This is due to sensitivity to
purges, if necessary. The administration of certain articles of diet, usually protein­
anti-botulinum serum is an urgency. aceous in nature. It is followed by an illness
Management of bulbar and respiratory characterised by nausea, vomiting,
failure is as for poliomyelitis. Mortality is diarrhoea, fleeting joint pains, and urti­
60 to 70%. caria. Oedema of the glottis and asthmatic
Postmortem appearances: The pathological seizures may follow. Many articles of
changes consist of congestion and haemorr­ food are implicated, viz. shell fish, eggs,
hages in all the organs and especially in the tomatoes, strawberries, mussels, etc. In this,
590 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

the individual factor plays a very important to 50% of cases, obtundation, seizures, and
part. The abnormality is not in the food but nuchal rigidity may develop as a result of
in the allergic individual. Diagnosis is complicating anthrax meningitis. This stage
generally not difficult. Antihistaminics and is of rapidly progressive shock, associated
steroids are of value. hypothermia, and death occurs within
1. Smallpox presents with a characteristic 24-36 hours.
rash in a centrifugal in distribution
BIOTERRORISM ______________ _____
(i.e. more abundant in the face and
extremities). Q . 47.5. What bio lo gic agents have the
2. Potentially delayed recognition of the
potential to be used as weapons of mass
destruction?
disease by health personnel because of
its rarity and presumed eradication of B a c te r ia l a g en ts: Anthrax, tularemia,
the disease. plague, Q fever, glanders and melioidosis.
3. Increased mobility and crowding of the Viral agents: Smallpox, viral hemorrhagic
population. fevers, Venezuelan equine encephalitis.
4. Virtually nonexistent immunity to small­ Biologic toxins: Botulinum, ricin, staphylo­
pox among the population at risk because coccal enterotoxin B and T-2 mycotoxins.
of the absence of naturally occurring
disease and the discontinuation of routine Q. 47.6. What epid em iologic clues should
vaccination in the early 1970s. raise suspicion that a disease outbreak is
The syndrome generally presents with due to bioterrorism?
the classic triad of—(1) symmetric, descen­ • Large epidemic with a similar disease or
ding, and progressive flaccid paralysis that syndrome, especially ima.discrete
always begins in bulbar musculature in population.
(2) an afebrile patient with, (3) a clear senso- • Unusually numerous cases of un­
rium. The bulbar palsies are prominent and explained diseases or deaths.
can be summarized in part as the 4 Ds: dip­ • Disease that is unusual to theigeographic
lopia, dysarthria, dysphonia, and dysphagia. area or transmission season.
Anticholinergic signs and symptoms, such • Multiple simultaneous or serial epide­
as dry mouth, ileus constipation, and uri­ mics of different diseases in the same
nary retention, are often present. Sensory population.
changes, how ev® |are not observed. • Disease outbreaks of the same illness in
Because the toxins do not cross the blood- noncontiguous areas.
brain barrier, central nervous system • Disease known to be transmitted by a
symptoms are absent. vector that is not present in the local area.
Anthrax: The initial phase fallows an • Single case of a disease due to an
incubation period of 1—10 days and begins uncommon agent (e.g. smallpox).
with the insidious onset of mild fever, • Unusual age distribution for common
myalgia, malaise, nonproductive cough, diseases.
some chest or abdominal pain, and in some • Unusual strains or variants of organisms
cases, nausea and vomiting. The second or antimicrobial resistance patterns
phase develops within 1-3 days and begins different from those circulating in the
abruptly with acute dyspnea, diaphoresis, local area.
further fever, and cyanosis. Stridor may • More severe disease than expected for
result from tracheal compression by known pathogen or failure to respond
enlarged mediastinal lymph nodes. In up to standard therapy.
 Food Poisoning and Poisonous Foods 591
, Similar genetic type of agents isolated treated as a national health emergency, and
from distinct sources at different times the proper authorities should be promptly
or locations. notified.
# Unusual routes of exposure for a
pathogen (e.g. inhalational route for a Q. 47.9. What is botulism?
disease that normally develops through Botulism is a clinical syndrome brought
other exposure). about by ingestion or inhalation of the
toxins produced by the spore-forming
Smallpox;The disease usually begins after bacillus Clostridium botulinum. These toxins,
a 12- to 14-day incubation period (range: which exist in seven distinct antigenic types,
7-17 days) and consists of high fever, exert their cytotoxic effect by preventing
malaise, andprostration with headache and acetylcholine release at the neuromuscular
backache. These symptoms are followed by junction, resulting in blockade of neuro­
the appearance of a maculopapular rash muscular transmission and flaccid muscle
that progresses to papules (1-2 days after paralysis.
appearance of rash), vesicles( 4th-5th day),
pustules (7th day), and finally scab lesions Q. 47.10. How is the diagnosis of botulism
(14th day). Other organs are seldom established?
involved. Death, which commonly occurs Laboratory testing is generally not critical
during the second week of illness, most to the diagnosis of botulism. The standard
likely results from the toxemia associated test is the mouse bioassay, in which type-
with circulating immune complexes and specific antitoxin protects mice against any
soluble variola antigens. botulinum toxin in the sample. Sample
specimens include serum, gastric aspirates,
Q. 47.7. What clinical features distinguish stool, and respiratory secretions. Polymerase
smallpox from other viral diseases, such chain reaction may be used to detect C.
as measles and chickenpox? botulinum genes in environmental sample.

Q.47.8. What factors make smallpox an Q. 47.11. Describe the classic appearance
extremely potent bioterrorism agent? of the cutaneous form of anthrax.
These factors give smallpox the potential Cutaneous anthrax is initiated when spores
for rapid spread and the ability to cause ill­ of B. anthracis are introduced into the skin
ness that can certainly overwhelm existing through cuts or abrasions or by biting flies.
medical and public health, system. A single The primary lesion—a painless, pruritic
suspected case of smallpox should be papule appears 1-7 days.
48. Somniferous Poisons (Opioids]
49. Drug Dependence
50. Inebriant Poisons
51. Sedatives and Hypnotics
52. Fuels
53. Agrichemical Poisons
54. Deliriant Poisons
55. Spinal Poisons
56. Peripheral Nerve Poisons
57. Cardiac Poisons
58. Asphyxiants (Irrespirable Gases]
48
Somniferous Poisons (Opioids)

The poisons in this group are known as analgesic but no narcotic properties. The
somniferous or narcotic poisons because ripe and dry poppy capsules (Fig. 48.1)
they are used to lessen pain and induce contain only a trace of opium and are used
sleep (somniferous or narcotic effect). The for their sedative and narcotic effect. The
important poison in this group is opium. poppy seeds (khas khas), creamish in colour,
Its action is characterised by two sets of are harmless as they do not contain opium.
symptoms, viz. excitement and narcosis, of They are used as food. They yield a bland
which the latter, as the group indicates, oil which is used for cooking and lighting
predominates. Heroin (Brown sugar) is a purposes.
synthetic derivative of opium. It is also Fresh crude opium is dark brown but
a potent narcotic analgesic but with a becomes black on standing. It occurs in
very high addiction potential. Pethidine rounded, irregular, flattened masses, with
(meperidine, demerol) is a synthetic a characteristic smell and a bitter taste. The
analgesic having a morphine-like action. It principal alkaloids of opium used in
causes a greater degree of euphoria as com­ medicine are morphine and codeine. These
pared to morphine. However, its potential act as narcotics or sedatives. Apomorphine,
for addiction is also high. Such addiction is prepared from morphine, is chiefly used as
difficult to treat, and carries considerable an emetic. Poisoning may occur from any
mortality. of the preparations containing opium, its
alkaloids or their derivatives.
OPIUM AND MORPHINE_______
Opium(Afim) is the dried juice obtained by
incision of the unripe capsules of the white
poppy, Papaver somniferum, a^plant which
grows in India, its activity is due to the
phenanthrene and isoquinoline group of
alkaloids. The phenanthrene group
comprises morphine (about 10%), codeine
(about 0.5%), thebaine (about 0.3%), and
their synthetic derivatives, such as dionin,
heroin, etc., and the narcotic properties
are due to them. The isoquinoline group
comprises papaverine (about 1%) and
narcotine (about 6%) which have mild
596 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Q. 48.1. Give a brief account of symptoms, minute. Pulse is imperceptible. Pupils dilate
signs, fatal dose, and fatal period in a case terminally when asphyxia ensues but still
of opium poisoning. do not react to light. "Coma deepens and
death results from asphyxia due to
Symptoms and signs: These are practically
respiratory paralysis. The breath may smell
those of morphine poisoning on account of
of opium throughout the illness.
the high morphine content of opium. They
usually appear within half an hour to an F a ta l d o se: In a person not addicted to
hour after ingestion and within about 3-5 opium, 200 mg of morphine and its
minutes after injection. The poison acts on equivalent of opium (2 gm) is fatal. 10 ml
the central nervous system causing first a of tincture of opium is regarded as a
stimulation and later a depression followed dangerous dose. The fatal dose of tincture
by narcosis. Accordingly, the effects can be of opium recorded in children varies from
described in three stages, viz (1) excitement, 1-3 drops.
(2) stupor, and (3) narcosis. Fatal period: The usual fatal period is about
Stage of excitement: This stage is absent if 9 to 12 hours.
the dose taken is large. In adults, there is a
Q.48.2. Discuss the diagnosis and
sense of wellbeing of brief duration.
differential diagnosis of a case of opium
Laughter, hallucinations, and rapid heart
poisoning.
rate occur. In children, convulsions may
occur. Diagnosis: If the crude drug or one of its
preparations is used, the breath smells of
Stage of stupor: The stage of excitement is
opium (raw flesh-like). The pin point
soon followed by weariness, headache,
immobile pupils, Cheyne-Stokes respira­
giddiness, a sense of weight in the limbs,
diminished sensibility, and a strong tions, slow pulse, cyanosis, froth at the nose
tendency to sleep from which the patient and mouth, and moist perspiring skin are
can be roused by painful stimuli. The pupils the outstanding features. Opium suspends
are contracted, face and lips cyanosed, and all body secretions except sweat so that
an itching sensation felt all over the skin. even during the comatose state, the skin,
The pulse and respiration are almost although cold, is often bathed in profuse
normal. perspiration resulting in subnormal
temperature and hypothermia (tempera­
Stage o f narcosis; The patient passes into
ture less than 35°C).
deep coma from which he cannot be
aroused. The muscles are relaxed and Differential diagnosis: Opium or morphine
reflexes are abolished. The pupils are poisoning clearly resembles (1) intracranial
contracted to pin point and do not react to lesions, such as cerebrovascular accidents
light. The blood pressure falls. The pulse is especially pontine haemorrhage, (2) meta­
rapid and feeble. The breathing is slow/ bolic conditions, such as uraemic coma
gradually diminishing in rate. The skin is and diabetic coma, (3) alcohol poisoning,
cold, with profuse perspiration, and the (4) carbolic acid poisoning (5) organophos-
temperature is subnormal (hypothermia— phorus poisoning, and (6) other comatose
body temperature less than 35°C). conditions, such as epileptic coma, hyste­
In fatal termination, there is marked rical coma and barbiturate poisoning, from
cyanosis. Froth escapes from the mouth. which it must be distinguished.
Breathing is sighing and irregular (Cheyne- Cerebrovascular accidents: These generally
Stokes type), the rate being 2 to 4 per occur in elderly hypertensive persons. The
 onset is abrupt and there is hemiplegia. The poisoning, the pupils are not pin point, but
pupils are unequal and breathing stertorous frequently show alternate contraction and
(noisy). In pontine haemorrhage, though dilatation, the respiration is shallow but the
thepupils are contracted to pin point, there rate is greater, and there is suppression of
is hyperpyrexia due to stimulation of the urine.
heat regulating centre in the third ventricle.
Metabolic conditions: In uraemic coma, the Q.48.3. Discuss briefly the treatment, post­
breath has ammoniacal smell, urinary mortem appearances, and medicolegal
findings are characteristic, there is history aspects of a case of opium poisoning.
of kidney disease, and there are cardiac Treatment: Emetics usually fail due to
manifestations. In diabetic coma, the breath depression of the vomiting centre. The
smells of acetone, breathing is of the stomach should be washed out first with
Kussmaul type; popularly known as air- tepid water (only if the patient is seen in
hunger, blood sugar is raised, and urinary early stages), the return being retained for
findings are characteristic. analysis, and then with a solution of
R Alcohol poisoning: The breath smells of potassium permanganate, 1:5000 strength,
alcohol. The pupils may be contracted but till the washed water returns with its
dilate on pinching the face or neck and original pink colour. Some solution should
I slowly return to their original size be left in the stomach to oxidise the alkaloid
(MacEwan's sign), and there is no paralysis. that might be excreted in the stomach after
I Carbolic acid poisoning: The smell of breath, ^absorption. In the absence of potassium
j the stained patches on the lips and the permanganate, the stomach should be
mouth, and the green colour of the urine washed out with an infusion of tea or tannic
are characteristic. . acid or a mixture of finely powdered animal
charcoal and water. Gastric lavage should
Organophosphorus poisoning: There is froth be carried out even after hypodermic
at the mouth and nostrils and the breath
injection of the drug as the alkaloid is re­
mayhave kerosene-like or garlic-like smell.
excreted into the stomach after absorption.
The pupils are constricted and there are
The intestines should be cleared out by
other features of muscarinic and nicotinic
enemata, or by purgatives, such as magne­
effects of the poison.
sium sulphate 15 gm orally.
Other comatose conditions: In epileptic
Nalorphine (lethidrone) is a specific
coma, there is history of previous attacks.
Inthe majority of cases, there is a fit, with antidote to morphine and related opium
or without a preliminary aura. The”patient alkaloids. It is given intravenously in a dose
loses consciousness, and the muscles are of 5 to 10 mg every 15 minutes till the pupils
convulsed for a few seconds or minutes begin to dilate, respirations become normal,
during which he may bite his tongue or the patient is aroused, or a maximum of 40
otherwise damage himself. The coma mg is administered. However, the drug of
usually clears up in about an hour. In choice nowadays is naloxone, which is a
hysterical coma, there is also a previous pure antagonist. It is given in a dose of 0.4
history of attacks. The patient is usually a to 0.8 mg intravenously or intramuscularly
female. The fit usually occurs in the and can be repeated every 10 or 15 minutes,
presence of bystanders. While the muscles up to a maximum of 10 mg with similar
are convulsed, the tongue is usually not criteria.
bittenand the patient rarely injures herself. ■ If the patient is seen in the early stages, j
Recovery is also rapid. In barbiturate he should be kept awake by making himJ
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

walk in the open air, supporting him them quiet or from overdose of a medical
during the procedure, and taking care not preparation.
to exhaust him. Depending on his condi­ Sometimes, opium is used to steady^
tion, artificial respiration and oxygen may nerves before doing some bold act, e.g
be necessary. Antibiotics are necessary in homicide. It is rarely used for doping race
cases of prolonged coma. Body warmth horses and as a cattle poison.
must be maintained. The rest of the treat­ Opium and its preparations cause addic­
ment is symptomatic. The treatment must tion, of which, heroin (diacetyl morphine),
be continued till the patient is conscious, an artificial alkaloid derived from
and even then, care must be taken that a morphine, is the most dangerous. Brown
relapse does not occur. sugar is crude heroin.
Postmortem appearances: These are those
of comatoasphyxia. The appearances are Q. 48.4. Give a brief account of opium
external and internal.
addiction (chronic poisoning).
Opium addiction (morphinomania or
Externally, the smell of opium is present.
morphinism), is the result of regular useof
The face is deeply cyanosed, almost black;
opium or its preparations either medically
the finger nails blue; and the neck veins
for relief of pain or otherwise as an
engorged and distended. The postmortem
aphrodisiac, or just to get 'high7(euphoric
lividity is almost black, and is better seen
feeling of well-being). Because of the user's
in a fair-skinned body. There is froth at the
rapid development of tolerance and the
nose and mouth, but neither so fine nor so
high physical dependence induced, larger
copious as in drowning.
and larger doses are required to get the
Internally, the stomach may show the
same effect, and later, just to remain normal
presence of small, soft, brownish lumps of
(prevent withdrawal symptoms). The
opium. The trachea, bronchi, lungs and
result is chronic poisoning characterised by
brain exhibit a marked degree of venous
physical, mental, and moral degeneration.
congestion. In addition, the trachea and
Physical degeneration manifests as emacia­
bronchi are covered with froth and the
tion, infection especially skin ulceration,
lungs are oedematous. The blood is usually
anorexia, constipation, impotence, sterility,
dark and fluid.
etc. Mental degeneration manifests as loss
In cases of suspected opium poisoning, of memory, irritability, depression, and
blood, bile and brain should be preserved gradual dementia. Moral degeneration
in addition to routine viscera. manifests itself as crimes which the addict
M edicolegal aspects: Opium is so easily commits to get the supply of the drug.
obtained everywhere in India, and death Death from loss of tolerance to the drugand
from its use is so painless that it is the infection is common and suicide far more
poison of choice for suicidal purposes. common than in the general population.
On account of its black colour, charac­
teristic odour and bitter taste, it is rarely HEROIN (BROWN SUGAR)_____________
used for homicidal purposes. It is This is a synthetic derivative of opium,
sometimes used for infanticide. Death has available in the form of white to dark brown
resulted from the breastfeeding of an infant powder. It is a potent narcotic analgesic
by a woman who had smeared her nipple with a strong euphoric effect. It is sold
with tincture of opium with evil intention. illegally on the street under the name
Accidental poisoning may occur from smack, brown sugar, junk, and dope. It can
drugging of infants and children to keep be smoked, inhaled as a snuff, or injected.
 Somniferous Poisons (Opioids) 599
Amongst all the addictive drugs, it is the liver should be collected. Lungs and brain
most dangerous. may also be preserved as heroin's concentra-
The place where heroin activities are tion in these organs in acute deaths is higher,
conducted is generally known as a shooting Q 48 5 short note on meperic|ine or
gallery. A small amount of heroin, dissolved
in water, heated and filtered through a
small piece of cotton or the filter of a Pethidine causes muscle twiching, tremors
dgarette is injected intravenously as a test convulsions. It causes dilated pupils and
dose. This process of injecting a small tachycardia. Poisoning is treated with
amount, withdrawing some blood to naloxone, diazepam and carbamazapine.
ensure that the needle is in the vein and to a4,use used to be common among
keepthe lumen open, is known as booting’ medical and paramedical people. The
or ’fooling’. It helps to assess the potency present editor (Dr Subrahmanyam) saw a
ofthedrugandtokeephighbyintermittent case of positive pethidine detected on
Ejection. chemical analysis in a case of a person
Toleranceoccurs very rapidly. If the drug found hanSed to a tree on the out skirts of
is then withheld, the patient experiences a villa8e near 4he Andhra Border of Tamil
withdrawal symptoms, such as sweating, Nadu' India-14was later found 41134he was
malaise, anxiety, depression, a general seda4ed wi4h Pethidine and then han§ed-
feeling of heaviness, and cramp-like pains Q. 48.6. Write short note on fentanyl.
in the limbs. Further and larger doses are ~ . , . - , ,. , , , . , .
then required to allay these symptoms. “ 71 18 s5mthebc substance related t0
With larger doses, a confusional state with Tf
hallucinations, illusions, and personality
changes rapidly develops. The withdrawal _ . ... _ , . . . .
symptoms are severe and include twitching ”
and convulsions. The addictiorclis quite 5 minutes
rr,ir'11 QOafter
0 IV injection.
irm
severe, difficult to treat, and canies consi­ It abolishes reflex effects of painful
derable mortality. stimuli. Heart rate decreases because of
Sometimes, the user collapses suddenly vagal stimulation. It causes marked respira-
and dies. He is found in an obscure place 4ory Naloxone is given to
counteract mental clouding and respiratory
(shooting gallery) which he has chosen to
ensure privacy. These factors and the life- dePr™ - Muscle relaxant may be requi­
r e which commonly involves the abuse led to combat mcreased tone o chest muscles,
of alcohol and other drugs result in bruises Famous pop singer Michael Jackson died
orinjuries that may simulate an assault and 3 er enany on o er rug use.
lead to a suspicion of homicide. The body Q. 48.7. Write short note on propofol,
maybe dumped to a different location with p fol * a werful anaesthetic. It is
consequent inappropriate postmortem called as ^ of amllesia It is commonly
rigidity and lividity. , . used to render patients unconscious for
Heroin is so rapidly metabolised that no surgery. Popking Michael Jackson was
detectable drug may be found in the blood found to have been administered propofol
after 30 to 60 minutes of injection. However, causing his death. Other substances found
morphine alkaloids may be detected in the are midazolam, diazepam, lidocaine an<*
urine for hours or days after a single ephidrine. His death was attributed
exposure. Atautopiy blood, urine, bile, and propofol.
49
Drug Dependence
Below is a glossary intended to supplement
the main text by providing an explanation
as well as a definition of certain important
terms commonly used in the description of
drug dependence.
Addictive drugs: Drugs which when taken
result in compulsive use, usually in
increasing amounts, on account of
tolerance. However, tolerence should not
be confused with addiction.
Drug: Any chemical that changes the way
the body works or the way one thinks, feels,
or acts. It is normally given to relieve pain
or cure disease.
Drug abuse: This term now covers (1) use
of drugs to affect the mind and body for
non-medical reasons, (2) using substances
which are illegal, (3) using chemicals that
were never intended to be put into the
body, e.g. glue sniffing, and (4) excessive
use of therapeutic drugs.
Habituatioti: The condition arrived at from
repeated consumption of a drug. Usually,
it involves a desire (not a compulsion) to
continue taking the drug, but with little or
no need to increase the dosage.
Hypnotics: These are drugs which produce
sleep, as for example, barbiturates.
Narcotics: These are drugs that relieve pain
and produce sleep or stupor, e.g. opium,
morphine, pethidine, etc.
600
Physical dependence: This means that the
body needs the drug (even in the absence
of psychological dependence) to feel
normal and function properly. The
physiology of the body is altered to such
an extent that the cells can function
satisfactorily only when such drugs with
their increasing dosage are continued. The
presence of withdrawal symptoms
(especially physical pain) is a proof of
physical dependence.
Psychological dependence: This means that
the mind needs the drug. There is a craving
for the repeated or compulsive use of a
drug to satisfy emotional or personality
needs. When the drug is discontinued,
pleasure or absence of discomfort are
involved, but not physical pain.
Psychotropic drugs: These are drugs that
alter mental functions by their action and
include stimulants, depressants, narcotics,
and hallucinogens.
Sedativesi Drugs which produce a calming
effect on the central nervous system.
Stimulants: Drugs which produce wake­
fulness, exhilaration, alertness, and such
other effects, by acting on the central
nervous system, e.g. amphetamines.
Tolerance: Development of body or tissue
resistance to the effects of a drug so that
larger doses are required to produce the
original effect.
q. 49.I. Write short notes on: (1) drug the senses, such as marihuana, LSD, and
addiction, (2) drug ha b it, (3) drug phencyclidine (PCP, angel dust).
dependence, (4) physical dependence, These drugs are taken either singly, or
(5) psychological dependence, (6) preg­ in combination, and administered either by
nancy and addiction. the oral route, by subcutaneous injection
Drug addiction is defined as a state of (skin popping), intravenous injection (main
periodic or chronic intoxication, harmful to lining), or as, snuff. A recent fashion,
theindividual and to society. It is produced probably to avoid detection by the authori­
byrepeated consumption of a drug, either ties, is to inject the drug subcutaneously
natural or synthetic. It is characterised by under a tattoo mark or intravenously into
(1) craving or actual need to continue the venous plexus under the tongue, or by
taking the drug and to obtain it by any injection in the rectum or vagina. LSD is
means, (2) a tendency to increase the dose, usually taken on a sugar cube or by putting
(3) apsychological and sometimes physicala drop on a blotter paper and licking it
dependence upon the effects of the drug, when the drug effect is desired.
and (4) withdrawal symptoms when the Drugs should normally be used for
drug is withdrawn. sound medical reasons only. With the
Drug habit is defined as a condition increasing stresses of life and the varieties
which results from the continued use of a of drugs available, they are now being used
drug, which does not cause much harm to for recreation, in an attempt to enhance
the individual or society. The common performance, to produce a change to some
habit forming drug is caffeine (coffee). The desired state, to control anger or distress,
habit is characterised by (1) a tendency (but to promote well-being, or as important tool
not craving) to take the drug and repeat it, for some unique experience in awareness,
asandwhen convenient, (2) harmful effects relationships and spiritual growth (more
mainly to the individual, and (3) psycho­ being, as with hallucinogens).
logical but not physical dependence upon The terms hard drugs and soft drugs are
the effects of the drug. sometimes used in the discussion on
WHO has coined the term drug depen­ addiction. The term hard drugs refers to
dence to replace the terms "drug addiction narcotics, such as opium, morphine, heroin,
and drug habit". It has been defined as a pethidine, etc. The term soft drugs refers
state, psychological or physical, in which a to non-narcotics which are frequently
person has the compulsion to take a drug abused, and these include: hypnotics, e.g.
ona continuous or periodic basis, either to barbiturates; stimulants, e.g. amphet­
experience its pleasurable effects or to amines; non-narcotic analgesics, e.g.
avoid the discomfort of its absence. The pentazocine; tranquillisers, e.g. diazepam,
number of drugs which are being used for and chlordiazepoxide; and hallucinogens,
addiction is increasing day by day. The e.g. LSD, phencyclidine, glue, etc.
common drugs of addiction are: (1) volatile Those who use the drugs for sound
anaesthetic solvents commonly toluene, medical reasons are not likely to become
known as glue sniffing, (2) alcohol, (3) addicts. A majority of addicts are neurotic
hypnotics, such as barbiturates, (4) individuals with personality problems. <
tranquillisers, (5) narcotic analgesics, such They use the drugs just for 'kick' or tqJ
as opium, morphine, heroin and pethidine, escape from the realities of life. Repeated!
(6) stimulants, such as amphetamine and use of the drug leads to tolerance and thdg
methylphenidate (Ritalin), (7) cocaine, and addict must have it under any circudfl
(8) drugs causing dependence distortion of stances, and by any means, including crtfae,
602 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

sexual perversions, and prostitution. When who smoke during pregnancy deliver j
under the influence of the drug, the addict infants with significantly lower birth I
appears calm and composed; when the weight than non-smoking women. Babies 1
effect wears off, he is restless, irritable, or born of alcoholic mothers often present \
depressed—generally but not always the foetal alcohol syndrome (FAS) chara- j
reverse of the drug action itself. cterised by prenatal growth deficiencies in j
Addiction is harmful to the individual length and weight, short palpebral fissures,
because it leads to mental and physical microcephaly, and CNS anomalies. Maternal
degeneration. It is also harmful to the cocaine abuse can result in premature
society as it leads to moral degeneration. delivery of an infant with serious cardio­
Mental degeneration manifests itself in vascular and CNS complications, low birth
careless behaviour. The addict disregards weight, poor feeding patterns, irritability,
conventions, customs, and feelings of tremors, and involuntary movements.
others. Physical degeneration manifests In some states in the US, criminal charges
itself in careless habits. The addict is have been brought against pregnant and
constipated, emaciated due to loss of postpartum drug addicts. Some of these
appetite, and his personal hygiene is very charges are: foetal endangerment, involun­
poor. He is likely to suffer from skin tary manslaughter, child endangerment,
diseases and infections. Impotence and assault with a deadly weapon, child abuse,
sterility are common. Moral degeneration criminal neglect, and possession and
manifests itself in crimes, which the addict distribution of a harmful (controlled) sub­
commits to get the supply of his drug. He stance to a minor.
may tell lies, cheat, steal, or resort to any DRUG ABUSE DEATHS________________
other means. Death from accidental over­
Drug deaths may occur in epidemics, e.g. fl
dosage and infection is common and suicide heroin and methyl alcohol. Epidemics of
is several times more common than in the 'khopri' deaths in India due to consump-1
general population. Addiction in pregnant tion of adulterated alcohol are common
women can lead to premature, stillborn, or in areas where alcohol is prohibited.
addicted infants. Falciparum epidemic in New York in 1933
Addiction is difficult to break. The was due to sharing the common equipment
treatment must preferably be carried out contaminated by malarial blood. Sudden
in an institution to ensure adequate death known as overdose or acute reaction
supervision so that the addict does not is not uncommon. It is probably due to
obtain secret supplies from anywhere. The some unexpected sensitivity causing
cardinal principles of treatment include cardiac arrest following arrhythmia. In
detoxification by appropriate drugs, such a case, the addict may be found with
cheerful company, plenty of exercise in the needle and syringe still in the vein.
open air, good appetising food, attention Drug administration may trigger intra­
to bowels, and psychotherapy. Those who vascular sickling in certain heamoglobino-
originally used the drug for some disease pathies resulting in sudden death. Other
and have thus acquired addiction are likely complications include sepsis, bacterial
to be cured with lesser difficulty than those endocarditis, viral hepatitis, and AIDS.
who used the drug mainly for its kick or Q. 49.2. Outline the procedure to investi­
other effect. ga te a d e a th d ue to narcotism (drug
Pregnancy and addiction: The negative abuse death).
effects of drug abuse on the developing The diagnosis of death due to narcotismis
foetus have now been identified. Women based on (1) examination of the scene where
thebody is found, (2) investigation of the meant for oral use, are injected intra­
circumstances, (3) history obtained from venously. Hepatic lymph adenopathy is
friends and relations, (4) autopsy common. Subacute bacterial endocarditis
examination, and (5) toxicological evidence. may be seen. The urinary bladder is fre­
It should be remembered that (1) drug quently distended and often this is the only
abuse victims are commonly found in clue to death from drugs.
obscureor unusual piaces where they have If any drug packets or injection equip­
sought privacy to inject the drugs, (2) they ment are recovered at the scene of death or
are often moved from the scene and from the deceased's clothing or personal
dumped to a different location a few hours effects, like shoes, wallet, etc., they should
afterdeathso that the case may at first sight be properly preserved for laboratory
appear tobe a homicide, and (3) the pattern examination, if incision through the skin
of rigor mortis or lividity may not be reveals a needle track or fresh subcuta­
consistent with the position of the body neous perivenous extravasation, the entire
when seen by the doctor. All such factors area should be excised and a corresponding
andthe lifestyle which frequently involves control sample taken from the other side.
abuseof alcohol and other drugs may result The toxicologist may be able to detect either
inbruises that may simulate assault and the narcotic or the adulterant (quinine).
misleadthe investigator as to the real cause Stomach contents may show intact tablets
of death. or capsules and suggest the type of drug
In a skin popper, a skin incision at the ingested. Liver, bile and kidneys should be
injection site may reveal (1) black debris in preserved as in any other case of poisoning.
the dermis from carbonaceous material of Urine may show the presence of either the
the sterilised needle, (2) acute or chronic drug or the metabolic products. A majority
abscesses or diffuse subcutaneous scarring, of abused drugs can be routinely detected
and (3) foreign body granulomatas (skin in the urine. Blood is required for deter­
popping). mination of the narcotic and gamma
In main liners, hyperpigmented linear globulin levels. In inhalation or solvent
needle track scars (tracers) overlying abuse cases, the whole lung shouldbe taken
sclerosed, thrombosed, subcutaneous veins with the trachea tied for analysis of
of the antecubital fossa, forearms, and bronchial air,
dorsal aspects of hands are common.
In addicts, using the inhalation method SOLVENT ABUSE/GLUE SNIFFING
irritation, congestion, and atrophy of the Q. 49.3. Give a brief account of solvent
nasal mucosa is common. Perforation of the abuse commonly known as glue sniffing.
nasal septum may be seen. The phenomenon of solvent abuse, now
The most conspicuous feature of a fatal widespread in many parts of the world,
narcotic injection is severe congestion and involves deliberate inhalation of a variety
oedema of the lungs which manifest as of substances, especially organic solvents,
shaving cream froth at the nose and mouth to achieve pleasurable distortion of the
filling the trachea and bronchi. This gives senses. The inhalation results in a state of,
rise to the suspicion of drowning, if the intoxication characterised by euphoria,J
victimis found in the bathroom, a common sometimes of an erotic nature, and distortion
place for drug administration. Foreign of perception leading to actual hallucinaj*
body granulomatas in lungs are found, if tions. As the most common sub stan *
drugs, such as barbiturates and methadone, inhaled initially was a toluene-ba^H
 50
Inebriant Poisons

This group of poisons are characterised by- strength of a liquid is obtained by dividing
two sets of symptoms, viz. excitement and the alcohol per cent (volume strength) by
narcosis, the stage of excitement being well 0.571. The percentage of alcohol in a liquid
marked in some and that of narcosis in is obtained by multiplying the proof
others. The classical inebriant is alcohol. strength by 0.571. Rectified spirit contains
The discussion in this chapter is restricted 95% by volume of alcohol. In absolute
to ethyl alcohol, Arrack (country liquor), alcohol, the remaining water content is
methyl alcohol, isopropyl alcohol, and removed by special technique, bringing it
ethylene glycol. down to not more than 0.2% water. {In the
United States, the term proof refers to twice the
I ALCOHOL (ETHYL ALCOHOL)___________ percentage of alcohol by volume. Thus the
j The term alcohol in popular use refers to common 80-proof whiskey sold in USA
■ ethyl alcohol (ethanol) which is present in contains 40% alcohol by volume). One
f various fermented and distilled beverages, drink is generally defined as a 12 oz beer, a
f Itisa transparent, colourless, volatile liquid 4 oz glass of wine, or a 1 1/4 shot of 80-
■ having a spirit-like odour and burning proof alcoholic beverage).
taste. It is the active ingredient of many
Arrack is an eastern name for any
social beverages, such as wines, beers,
country liquor, distilled from coco-palm,
whiskeys, and brandies, its approximate
rice, sugar, or jaggery. Its strength may be
percentage in such beverages being as
as high as that of whisky. It is commonly
follows, as per ISI (Indian Standards Insti­
fortified with potassium bromide, chloral
tution, now Bureau of Indian Standards)
hydrate, dhatura or bhang for a greater
specifications:
kick. Different provinces in India have
Beverages Alcohol % by Proof different names for such liquors. (In
volume (degrees) Andhra Pradesh, it is known as Gudamba
Rum 42.8 75 (derived fromgud= jaggery); inMaharashtra,
Whiskey, brandy 42.8 75 Khopri; and in Gujarat, Lattha}. Such
Gin 42.8/40.0/37.2 75/70/65
Wines 8-15.5 14-27 inferior or adulterated country liquor
Beers 2-10.0 3.5-17.5 should not be confused with country
Country liquor 11.4-45.7 20-80 liquor/country spirit manufactured
Proof spirit indicates a mixture con­ according to IS specifications.
taining 57.10% by volume or 49.28% by Country liquor, per se, while more
weight of absolute alcohol. The proof intoxicating than either imported or Indian-
605
 606 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
made foreign liquor, e.g. whisky, will have
the same clinical effects as ethyl alcohol.
Serious toxic effects are common when
(1) the liquor is adulterated by denatured
spirit which contains methyl alcohol, or
(2) the so called country liquor is prepared
from toxic preparations, like varnish and
french polish containing methyl alcohol.
Death has followed from consumption of
the so-called country liquor 'Khopri' in
Maharashtra and 'Lattha' in Gujarat.
Q. 50.1. Give a brief account of the m eta­
bolism of ethyl alcohol.
Ethyl alcohol is rapidly absorbed from the
gastrointestinal tract. The rate of absorption
depends upon (1) concentration of alcohol
in the fluid imbibed, (2) presence or absence
of food in the stomach, (3) condition of the
stomach wall (gastrectomy, chronic gastritis,
etc.), (4) rate of drinking, (5) quantity of
alcohol ingested, (6) weight of the person,
and (7) development of tolerance. The first
two factors are most important. Alcohol is
absorbed more rapidly from concentrated
than from dilute solutions; the presence of
food in the stomach, especially fats and
proteins, will retard absorption, milk being
very effective for this purpose.
Following absorption, the concentration of
alcohol in blood reaches a maximum in about
45 to 90 minutes after ingestion. The concen­
tration of alcohol in various tissues after
equilibrium is established is as follows:
With blood as 1.00, the average for brain is
1.17, plasma 1.16, urine 1.33, vitreous and
bile 1.12, liver 0.91, and blood clot 0.77.
These ratios vary a little.
Approximately, 90% of absorbed alcohol
is oxidised in the liver, the remaining 10%
is excreted mainly by the kidneys and
lungs. Normally, the body can metabolise
about 1/2 fluid ounce of absolute alcohol,
roughly equivalent to one drink (one fluid
ounce of whisky or 12 ounces of beer) every
hour. If the intake exceeds this measure, the
subject manifests signs and symptoms of
drunkenness unless he has developed
tolerance. The average fall is around 15-18
mg ethanol per 100 ml of blood per hour. It
is, therefore, possible to calculate how long
after a given dose the body will be alcohol-
free and to estim ate with reasonable
accuracy w hat the blood-alcohol
concentration was a few hours before a
blood analysis was made.
It is important to know that the concen­
tration of alcohol in blood varies conti­
nuously, first increasing during the period
of absorption, and then decreasing on
account of metabolism. Since the glomerular
filtrate has a concentration similar to that
in the plasma, a given sample of urine
will reflect the average blood alcohol |
concentration during the time the urine has ;
accumulated in the urinary bladder. As the 1
bladder may have contained urine before 1
taking alcohol, it is necessary to empty the |
bladder and use a second sample collected I
within 30-60 minutes for any such test. 1
Q. 50.2. Give a succinct account of acute
ethyl alcohol poisoning.
Ethyl alcohol depresses the central nervous
system irregularly in descending order
from cortex to medulla. It first depresses
the higher centres which control judgement
and behaviour (stage of excitement—blood C
alcohol 30-100 mg%), then the motor I
centres (stage of incoordination—blood I
alcohol 100-300 mg%), and finally the vital I
centres in the medulla (stage of narcosis— 1
blood alcohol over 300 mg%). The breath |
smells of alcohol throughout.
The effects appear early in those who are |
mentally or physically fatigued, in epi- I
leptics, in persons with head injury, and in 1
those who have taken barbiturates or other |
CNS depressants.
The statutory limit for a charge of
drunken driving in most states in USA is
0.08-0.10%; in Canada and Britain 0.08%;
in Scandinavian countries 0.05%; in Austria
0.04%; and m Czechoslovakia, Poland,
other East European countries 0.03%, and indisposition usually following recovery
India 0.15%. from drunkenness.
Stage of excitement: This is a feeling of well­ The approximate relationship between
being and pleasure resulting from inhibi­ the alcoholic content of blood and clinical
tion of the higher centres. The drinker manifestations is tabulated in Table 50.1.
converses well, laughs and smiles readily, The table is intended to provide a general
or becomes angry easily. He may disclose guideline of clinical manifestations in relation
secrets. He may behave in an obscene to blood levels in those persons who are not
manner or talk in vulgar language. Sexual regular and excessive drinkers, recovery has
desire may be aroused. been recorded after blood alcohol levels of 780
mg% and above.
Stage of incoordination: There is incoordi­
nation of thought, speech, and action, Fatal dose: This will depend on the age and
which manifest as impaired judgement, habits of the patient and the strength of the
liquor taken. Death usually occurs from
confusion, slurred speech, and staggering
gait. The drinker may suffer from hiccups large quantity taken in a short time. A
and is untidy in his appearance. He may concentration of 0.35% (350 mg%) and
become morose, euphoric, or irritable— above of alcohol in blood is generally
depending on his inherent emotions. sufficient to cause death.
Nausea and vomiting are common. The Fatal period: The usual fatal period is 12
pupils are dilated. Most offenses are to 24 hours though death may be delayed
committed in this stage. Impaired judge­ for 5 to 6 days.
mentmaylead to accidents, sexual excesses, Table 50.1: Blood alcohol level and clinical manifes-
violence, and crime. [tations
Stage of narcosis: The patient passes into % Mg% Effect ’
deep sleep and responds only to strong Less than 0.03% Less than 30
stimuli. The pulse is rapid, temperature 0.03-0.05 30-50
0:05-0.10 50-100
subnormal, breathing stertorous, and the 0.10-0.15 100-150
pupils may be contracted. However, on 0.15-0.20 150-200
pinching the neck or face, they dilate 0.20-0.30 200-300 Very drunk
initially and slowly return to their original 0.03-0.35 300-350
Over 0.35 Over 350 Comatose to death
size. This is known as MacEwan's sign and
is helpful to differentiate alcoholic coma 1. Selective impairment: Increase in reaction time;
from other comatose conditions. Th this impairment of complex skills, such as flying an
aircraft or driving a motor vehicle. Detectable only
stage lasts for more than 12 hours, death
ensues from paralysis of the cardiac or 2. Slight impairment: Flushed face; dilated pupils;
respiratory centre or later from the effects
of pulmonary oedema. However, a recent 3. Under the influence: Flushed face; dilated sluggish
opinion states that this test is not found pupils; euphoria; loss of restraint; test errors;
stagger on sudden turning.
positive. 4. Drunk: Flushedface; dilatedsluggish/inactivepupils;
Death from acute alcoholism is not clouding of intellect; incoordination of thought,
common. Recovery occurs with acute speech, andaction; staggering gait withreelingand
lurching while making sudden turns.
depression and gastrointestinal irritation 5. Very drunk: Flushed or pale face; pupils inactive,
which continue for 24 hours or longer.
Headache is also present as an hangover incoordination of thought, speech, and action;
effect and is due to cerebral oedema. A staggering, reeling gait withtendency to lurch and
fall; vomiting; amnesia.
hangover means a temporary state of
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
;f C )f (la ith: Death is due to depression
^of the respiratory centre. Alcohol may be
lethal at relatively lower blood levels when
combined with other central nervous
system depressants, such as barbiturates,
carbon monoxide, or morphine, and/or in
the presence of some natural disease of
heart or lungs.
Q. 50.3. Explain selective impairment from
alcohol intoxication with special reference
to driving a motor vehicle.
A motor vehicle is a complicated piece of
machinery, the handling of which requires
skill, dexterity, and mental acuity, all of
which are selectively reduced, even
eliminated, by alcohol. Thus, an individual
may be intoxicated to the point of being
unable to operate an automobile safely
while appearing sober.
Research shows that a driver's ability is
adversely^affected with a blood alcohol
content of .03-05% (or sometimes even
less), which means consumption of just two
beers in about an hour. Alcohol causes
faulty depth perception, poor peripheral
vision, distorted colour vision, and reduced
night vision. For example, after an impaired
driver's pupil is exposed to the glare of
oncoming headlights, it can take from two
to eight seconds to adapt to the dark condi­
tions as compared to one second required
by a non-impaired eye. In addition, an
alcohol impaired driver's ability to judge
distance may also be reduced, making it
difficult to change lanes or determine
whether a car is approaching, moving
away, or standing still.
Driving ability is generally impaired
even in the hangover phase due to the after­
effects of alcohol on judgement, perception,
reaction time, and coordination. An increase
of one-tenth of a second in reaction time
means that a car travelling at 80 km an hour
needs an additional 2.2 metres of road to
pull up.
Q. 50.4. Describe briefly the treatment and
postm ortem a p p e a ra n c e * In a case of
death from ethanol poisoning. Add a note
on m e d icole g a l aspects. 1
Treatment: The stomach should be lavaged I
with care with 5% solution of sodium I
bicarbonate in warm water. The patient I
should be kept warm. Isotonic saline with!
5% glucose (preferably fructose) may b e!
required to deal with symptoms of hypo-1
glycaemia, if present.
The increase in intracranial pressur el
which often occurs can be treated with!
saline purges and intravenous hypertonic
glucose solution. When there is respiratory^
depression, artificial respiration may be
necessary along with oxygen inhalation.
Very serious cases will require haemo­
dialysis or peritoneal dialysis.
Postmortem appearances.* The clothes are
generally in a disorderly/torn condition.
Stains due to vomit or blood may be
present. The tongue may be furred. Rigor
mortis lasts longer than usual. Bruises are
generally found on various parts of the
body. Other injuries may be present.
An odour of alcoholic beverages is often
evident on opening the body. The blood is
fluid and dark. The brain is slightly oede-
matous. Shrinkage of cerebral cortex (grey
matter) is common in chronic alcoholics. In
individuals who sustain head injury with
subdural or epidural haemorrhage and
survive for hours to days, the analysis of
the brain blood clot may reveal initial blood
alcohol level at the time of injury. Vitreous
analysis is very helpful in all cases. Oedema
of the larynx, a bolus of food obstructing
the larynx (cafe coronary), fatty liver, or
acute haemorrhagic pancreatitis are
commonly found when death has been
sudden or unexpected. The stomach
usually shows signs of alcoholic gastritis
to a varying degree. The mucous mem­
brane of the small intestine is oedematous
but not ulcerated. This finding is important
 Inebriant Poisons 609

from an insurance point of view when chronic gastroenteritis, wasting, peripheral

death occurs after consumption of alcohol neuropathies, impotence and sterility, and
and food. fatty changes in the liver and heart. Alcohol
Atraveller left Mumbai for Poona (a distance of is a hepatotoxic poison. Cirrhosis of liver
about200km) inhis car commencing his journey is common. A useful index of liver damage
at about 10.00 p.m. At about 12.00 midnight, he is the level of enzyme gamma-glutamyl
halted at a wayside restaurant where he con­ transpeptidase in the serum, the normal
sumedalcohol and ate food. At about 2.00 a.m., level being less than 36 units. Moral
heresumedhis journey reaching Poona at about degeneration manifests as crimes which the
6.00 a.m. About 10.00 a.m., he started vomiting addict commits to get his drink. He becomes
and died at about 11.00 a.m. next day. At
suspicious of his wife's fidelity and may
postmortem, extensive ulcerations were found
inthe small intestine. Laboratory examination assault her or the suspected paramour.
confirmedthat this was a case of Salmonellafood Mental degeneration results in dementia.
poisoning—a suspicion already aroused at Three common clinical syndromes which
autopsy from the finding of ulcerations of the result from chronic alcoholism are: (1) deli­
small intestine. rium tremens, (2) Korsakoff's psychosis,
and (3) acute hallucinosis.
In addition to the usual viscera, vitreous
fluid/CSF may be preserved for chemical Delirium tremens is a state of excitement
analysis. Blood should be collected from a with hallucinosis which usually lasts 3 to
peripheral vein, and precautions for its 4 days, it results from (1) an unusual bout
preservation as mentioned under collection of drinking, (2) sudden withdrawal of
of samples should be followed. alcohol, (3) acute infection, e.g. pneumonia
or influenza, (4) shock from injury, e.g.
Medicolegal aspects: Poisoning by alcohol fracture of a bone, and (5) exposure to cold.
is comparatively common, although death
It is characterised by an attack of acute
directly due to its ingestion occurs in a far
insanity in which the main symptoms are
smaller number of cases. However, there
sleeplessness, marked tremors, excitement,
is a liability to fatal complications, such as
fear and hallucinations chiefly visual and
head injuries, serious bleeding from trivial
occasionally auditory. He may seek escape
injuries, suffocation (cafe coronary),
from his terrifying new world by suicide.
drowning, and exposure. A strong relation­
He is often violent with a tendency to
ship exists between alcohol, crime, and
homicide. He is for the time being insane
violence. Chronic alcoholism is a common
and not responsible for his actions.
cause of sexual jealousy crimes, especially
those of a homicidal nature. A passenger Treatment involves sedatives, such as
who accepts a lift from the driver of a motor chlorpromazine 100 mg four times a day
vehicle whom he knows to be drunk orally, intravenous hypertonic glucose to
accepts the risk of contributory negligence relieve cerebral oedema, and withdrawal
in the event of an accident. of some CSF to reduce intracranial tension.
Infection, if present, must be treated
CHRONIC POISONING energetically.
(ALCOHOLIC ADDICTION) ^ _________ Korsakoff's psychosis is a syndrome
This results form continued use of alcohol. characterised by hallucinations, disorienta­
It is characterised by a gradual physical, tion and multiple neuritis. The patient's
moral and mental deterioration (alcoholic memory for recent events is lost and he fills
dementia). Physical degeneration manifests the gap by confabulation. This state lasts
aslack of personal hygiene, loss of appetite, about from one month to a year.
610 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Acute hallucinosis is a state of hallucina­ it is accompanied by some act of commission

tion chiefly auditory with systematised or omission which causes danger to thelife
delusions of persecution lasting from or property of the individual or to some
weeks to months. It is a psychiatric emer­ other persons. Thus, a person maybe
gency; the patient may become homicidal charged with being drunk and disorderly
or suicidal in response to his hallucinations. or being drunk and in charge of a vehicle.
These patients must be hospitalised, A doctor may be charged for operating or
sedated, observed closely, and treated as delivering a baby negligently when
for delirium tremens. intoxicated.
The drug antabuse (disulfiram) acts by
sensitising the patient to even a small dose Diagnosis
of alcohol, and is the most suitable Under section 53 (1) of the CrPC, an
treatment for almost all cases. It is examination of the accused can be carried
administered in a single daily dose of 0.5 out by a medical officer at the request of
gm and can be continued for a long time. It the police even without his consent and by
can be given in tea or any other non­ use of force, if necessary. Such examination
alcoholic beverage even without the may include taking of fluids in cases of
patient's knowledge (in some countries). suspected intoxication.
Temposil (calcium carbamide citrated),
50 mg tablet once a day also sensitises the Clinical Examination
individual to alcohol and can be used in Clinically, in the absence of head injury and
place of antabuse with lesser side effects. other pathological conditions, a person is
Hypnosis and psychotherapy are helpful. definitely under the influence of alcohol, if
Postmortem appearances in patients there is smell of alcoholic beverage in his
dying after chronic ingestion of large breath and/or in the vomited matter (if
amounts of alcohol include degenerative any), provided there is a combination of all
changes in the liver, kidneys and brain, or most of the following groups of symp­
atrophic gastritis, cirrhosis of the liver, and toms or signs, viz:
cardiomyopathy. 1. General demeanour: Excited, hilarious,
talkative, abusive.
DRUNKENNESS__________________________
2. Clothes: Disarranged, disorderly.
Q. 50.5. Define drunkenness.
3. Eyes: Suffusion of the conjunctivae.
Or
Pupils may vary from extreme dilatation
Describe insobriety. G ive a brief a cco unt to extreme contraction and maybe equal
of the clinic al tests an d the la boratory or unequal. Fine lateral nystagmus is
specim ens required to diagnose it. indicative of alcoholic intoxication.
Drunkenness is a condition which results
4. Tongue: Dry, furred, or excessive
from excessive intake of alcohol and the
salivation.
person is so much under its influence that
(1) he loses control over his mental faculties, 5. Speech: Slurred and incoherent. Certain
(2) he is unable to perform the duties on test phrases, e.g. British Constitution
which he is engaged at a particular time, may be asked.
and (3) he may be a source of danger to 6. Memory: Loss or confusion particularly
himself or to others. as regards recent events and apprecia­
In places where there is no prohibition, tion of time. Simple sums of addition or
drunkenness in itself is not a crime unless substruction may be asked.
 Inebriant Poisons 611
l Coordination: Impaired. Unable to with a syringe and 20 gauge needle. CSF,
thread a needle, button his clothes, stand vitreous, or bile can also be used when it is
withhis heels together with eyes closed, difficult to obtain blood due to decomposi­
or pick up coins dropped on the floor. tion.
Gait uncertain, reeling or falling. Stagger
Urine: The urine sample is collected in the
onsudden turning. Tremors of the hand
usual manner in a large, chemically clean,
make writing difficult. The signature can
sterilised, screw capped bottle. It is desir­
be compared with that on the driving
able to ask the patient to empty the bladder
license. Finger-nose test is impaired.
and use a second sample collected within
8. Reflexes: Delayed and sluggish. ' ; • 30 to 60 minutes. 30 mg of phenyl mercuric
nitrate is used as a preservative for every
9. Unusual actions: Hiccups, belching,
vomiting, fighting. 10 ml of urine. The bottle is screwed, sealed,
and labelled with appropriate particulars.
Thus, the important clinical signs of
drunkenness are: (1) smell of alcoholic Breath: The person is asked to blow into a
beverage in breath, (2) loss of self-control special container or directly into a breath
and disordered clothing, (3) sluggish analyser (drunkometer, intoximeter,
dilated pupils and fine lateral nystagmus, alcometer). This is a preliminary screening
(4) slurred or incoherent speech, (5) un­test based on the principle that alcohol
steady gait, and (6) confused mental state reacts with an oxidising agent and produces
or impaired memory for recent events. change in its colour, proportional to the
The common laboratory tests include amount of alcohol. The amount of alcohol
estimation of alcohol from (1) blood, in approximately 2,100 ml of alveolar air is
(2) urine, (3) breath, and at autopsy, and taken to be the same as that in 1 ml of blood.
(4) vitreous fluid, bile, and other tissues. Electronic breathalysers not necessarily
working on the principle of chemical
Collection of Samples reaction of alcohol with an oxidising agent
are also available. These give quantitative
Blood: The skin is cleaned with soap and
results. Some of these devices with print­
water or a solution of 1:1000 mercuric
out of results of analysis have been accepted
chloride. A syringe free from the slightest
for court work abroad. Even so, the
trace of alcohol and other chemicals
uncertainty arises out of the important
(preferably a fresh disposable syringe)
assumption that the absorption was
should be used. 5 mg of sodium fluoride
already complete in the given case; if not,
and15 mg of potassium oxalate can be used
as preservative for 5 ml of blood. Blood overestimates of blood-alcohol concen­
container should be tightly stoppered to tration are likely.
prevent loss of alcohol by evaporation and
Q. 50.6. Com ment on the value of labora­
labelledwith name, date, time of taking the
tory tests in the diagnosis of drunkenness.
specimen and signature of the medical
officer. It is kept in a refrigerator and sent While dealing with analytical findings on
as soon as possible to the laboratory. specimens containing alcohol, the follow­
Vitreous fluid can be taken in place of ing facts must be borne in mind:
bloodtor postmortem alcohol estimation in 1. The site of blood collection is important.
drunken individuals from whom a blood Blood for alcohol estimation should be
sample is not obtainable due to extensive collected from a peripheral vein.
trauma. Only crystal clear colourless fluid 2. Alcohol concentration may fall slightly on
should be used. It can be collected slowly storage.
612 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
3. Alcohol can be produced in the body
after death or during storage due to
fermentation. It is, therefore, essential that:
(a) blood sample is not contaminated
during collection, (b) a proper preserva­
tive is added, (c) the sample is preserved
in a refrigerator, and (d) analysis is done
as quickly as circumstances permit.
4. In dealing with embalmed bodies, the
possibility of alcohol in the embalming
fluid must be considered.
Blood tests: The blood alcohol tests prove
with reasonable accuracy the concentration
of alcohol which was present at the time of
taking the sample. The amount of alcohol
eliminated by the body over a given period
of time may also be estimated with a fair
degree of accuracy. These tests also prove
what the probable effect of alcohol was on
the person concerned. Volatile substances,
like acetone, ether, paraldehyde, may be
estimated as alcohol unless sensitive
methods are used.
Urine tests: A sample of urine collected
within 30-60 minutes after the person has
com pletely em ptied his bladder will
indicate with reasonable accuracy the
average blood-alcohol level over the time
the sample was collected, the ratio of
urinary alcohol to blood-alcohol being
approximately 4:3. Examination of urine
may be of great value in indicating if the
person is a diabetic, is suffering from
ketosis, or has recently taken barbiturates
or other drug.
Breath tests: The breath alcohol test needs
special apparatus, specially trained opera­
tor, and active cooperation of the person.
The limitations of the test have already been
outlined.
DIFFICULTIES IN DIAGNOSIS
Conditions which simulate drunkenness
must be ruled out before diagnosing
insobriety. There are other difficulties as
well.
1. The chief conditions most likely to b ^
mistaken for drunkenness are: mental
d isease, sho ck , head injury, hyp0,
glycaemia, and poisoning from carboy
monoxide, opium, atropine, dhatura
barbiturates, amphetamines, antihista-
minics, insulin, and the like. Less likely
to be m istaken for drunkenness are
uraemia, disseminated sclerosis, ataxia,
Meniere or Parkinson's disease, and
cerebellar tumour.
2. H ead injury and alcoholism may be
associated.
3. The combination of drugs of the barbi­
turate group and alcohol can enhance
the sym ptom s of intoxication due to
synergistic action. Other drugs that are
dangerous in combination with alcohol
include narcotics, tranquillisers, anti-
histaminics, and hypnotics. Therefore,
persons who are taking these prepara­
tions for medicinal reasons may be unfit
to d rive after a very small dose of
alcohol. The doctor, while prescribing
such drugs, should warn the patient
accordingly.
4. Mentally unstable subjects, epileptics,
and th ose w ho h ave suffered from
cerebral trauma at some earlier date may
show an excessive reaction to small
amounts of alcohol.
5. There is no single clinical test which by
itself would justify a medical practitioner
in coming to the conclusion of drunken­
ness in a person.
6. Laboratory tests, being objective, certainly
enhance the value of clinical tests.
7. A lcohol acts differently on different
individuals and so also on the same indi­
vidual at different times. Intoxication in
females is approximately 25% more than
in males.
Therefore, in giving evidence, the expert
witness should explain to the court the
limitations of the tests and the inferences
to be drawn from them and base his expert
 614 textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
1. Consumption Cases
The common questions raised at criminal
trials in consumption cases are: (1) Has the
person consumed liquor, and (2) if so, what
is his blood alcohol level.
Under the BPA and rules made there­
under, the prohibition officer or police
officer produces the concerned person for
medical examination and/or collection of
his blood. The medical officer examines the
person and issues a certificate in the
prescribed Form "A" containing the result
of his clinical examination as to whether the
person has or has not consumed alcohol
and is or is not under its influence. The
medical officer collects and forwards in the
manner prescribed the blood of such person
to the chemical examiner vide Form "B"
who issues a certificate in the prescribed
Form "C" as regards the percentage of
alcohol and such other particulars as may
be necessary or relevant.
The medical officer should make a
thorough clinical examination as outlined
under "diagnosis of drunkenness" and
observe all precautions as mentioned under
"collection of blood sample" to comply
with the rules under the BPA. The collected
sealed sample should be sent to the
chemical examiner by registered post or
through a special messenger with a
forwarding letter bearing his (medical
officer's) seal to avoid any possibility of
tampering.
Determination of Blood/Urine Alcohol
The chemical examiner, after checking the
sample in forensic context, may determine
the alcohol content of blood by a suitable
method including the modified versions of
Kozelka and Hine/Cavett method. The
latter involves aeration/distillation or
diffusion under low pressure. It utilises the
principle that alcohol is easily oxidised to
acetic acid by oxidising agents, such as
potassium dichromate and sulphuric acid.
Each ml of N/20 dichromate solution that
is reduced in the process is equivalent t0
0.575 mg of alcohol. Other modern
available methods may also be used.
The advantages of this method are-
(1) Distillation/diffusion and oxidation are
carried out separately but simultaneously
(2) volatile decomposition products, like
aldehydes, sulphides, and ketone bodies do
not interfere with the analysis, and (3) the
apparatus is inexpensive, its assembly
simple, and its use easy and rapid.
The specific requirements of the method
are: (1) All reagents must be of recognised
analytical quality, and (2) the apparatus
must be cleaned carefully before use.
Depending upon the type of sample,
resources available, need for accuracy, and
need for. specificity, other methods for
estimation of blood alcohol may be used.
These include: (1) gas chromatography,
(2) alcohol dehydrogenase (ADH) method,
and (3) breathalysers. The principle of the
various methods is briefly outlined below.
Gas chromatography: A measured
microlitre quantity of sample containing
alcohol is put into a previously heated
chamber. The vaporised alcohol is carried
by an inert carrier gas, usually nitrogen,
through a column packed with a suitable
adsorbent material. The various consti­
tuents of the sample are separated due to
differences in adsorption, etc./and detected
by a sensitive detector. A record on a
moving chart (chromatogram) provides the
qualitative and quantitative analysis.
The advantages of this method are:
(1) The procedure is simple, sensitive, and
reasonably specific, (2) only small quantity
of a sample is required, and (3) the analysis
is not interfered with by other ingredients,
e.g. other alcohols, aldehydes, ketones, etc.
These elute at different intervals and the
chromatogram records separate peaks for
these substances, if present.
This technique is very useful when
deaths are due to consumption of poiso­
nous liquor. Alcohol and other denaturants,
 - Inebrioni Po
especially methyl alcohol are simulta­
neously recorded, identified, and quantified.
This biochemical method is
based on the principle that the enzyme
ADH (alcohol dehydrogenase) converts
alcohol into acetaldehyde with co-enzyme
NAD (nicotinamide adenine dinucleotide,
previously called DPN, diphosphopyridine
nucleotide or co-enzyme-1). The reaction
is driven to completion by maintaining a
high pH and removing acetaldehyde with
semicarbazide. The increase in absorbance
at 340 nm (NADH) is monitored on a
spectrophotometer.
The principle of the test and
its admissibility in court work are already
described under collection of breath sample
in the diagnosis of drunkenness.
The degree of intoxication has great bearing
in cases of sudden deaths, assaults,
accidents, and when diminished responsi­
bility is claimed as a defence. Under the
BPA, a person having a blood alcohol level
of 0.05% (50 mg%) and above has legally
committed the offence of consumption. As
per recent amendment of Section 117 of the
Motor Vehicles Act, it is an offence to drive
or attempt to drive a motor vehicle with
any quantity of alcohol in blood (no
threshold limit specified).
The amount of alcohol consumed can be
estimated from the blood alcohol level.
When the blood alcohol level is 0.1%, that
is 100 mg%, the amount ingested is
approximately 0.85 ml of absolute alcohol
per kg of body weight. In a person with
70 kg body weight, this would amount to
approximately 60 ml (70 x 0.85) of absolute
alcohol or approximately 140 ml of hard
liquor, such as whisky, brandy, etc., of-75°
proof strength. Therefore, when the blood
alcohol level in such a person is 0.05% or
50 mg%, the legal lim it, the amount
ingested would be 30 ml of absolute
alcohol, or about 150 ml (five and a quarter
615
fluid ounces) of 20% alcohol, the maximum
percentage that can be.found in a medicinal
preparation, like Wincarnis. This means
that a medicinal preparation, when taken
in a prescribed dose [the prescribed dose
being about 30 ml (a fluid ounce = 28.4 ml)
or less], cannot produce blood alcohol level
above or anywhere near the prescribed legal
limit of 0.05% or 50 mg%. (These numbers
are different in other countries.)
In the interpretation of analytical
findings, it is essential to make sure that
necessary precautions in collection, pre­
servation, and storage of the sample have
been followed, the analytical method
correctly applied, and results interpreted
in proper perspective keeping in mind the
limitations already outlined under Value
of laboratory tests' in the diagnosis of
drunkenness.
The defence attorney has a right to make
certain on cross examination that the
samples were properly collected, pre-Vj
served, transported, and analysed; there
was no possibility of mix-up or tampering
with the sample; and the chain of evidence
has been maintained.
Concentration of alcohol in blood is
expressed as mg% (w/v), or as percentage
as follows:
50 mg% (w/v) = 0.05% (w /v), i.e. 50 mg
alcohol per 100 ml blood.
It is also expressed as mg% (w /w ) in
solid tissues, like viscera sent for chemical
analysis, i.e. so many mg alcohol per 100
grams tissue.
Widmark's formulae to estimate alcohol:
a=cpr, where a is the total amount of alcohol
in gm absorbed in the body; c is the
concentration of alcohol in blood (in gm/ kg);
p is the weight of the person (in kg); and r
is a constant namely 0.68 in men and 0.5 in
women. For urine analysis, the formula is
a=3/4 qpr, q being concentration of alcohol
in urine (in gm/litre).
616 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Example: 70 kg male has consumed 120 ml colourless liquid with a faint spirit-like
(around 4 fluid ounces) of 75% proof liquor. odour and a burning nauseous taste. It |s
His blood alcohol (peak) level will be ■ -! used in industry for denaturing rectified
spirit so as to render it non-drinkable.
120x0.428x0.8x1000 0/ , Q, 0/
70 xTo x 0.68 mg% w /v =86 mg%. Rectified spirit mixed with five per cent
methyl alcohol is known as methylated
(75% proof strength = 42.8% by volume;
spirit, and is used in arts and manufacture
density of alcohol has been rounded up
under the name of denatured spirit or
as 0.8).
denatured alcohol. It is found as an
2. Possession Cases antifreeze in gas lines and is also used as a
solvent in paint removers, varnish, etc.
The common questions raised in possession
cases are: (1) Whether the sample contains Q. 50.7. D escribe the m o d e of action,
ethyl alcohol, (2) Whether the sample is symptoms and signs, treatment, and post­
altered spirit, denatured spirit, medicinal m ortem ap p e a ra n ce s in a case of methyl
preparation, toilet preparation, antiseptic aico h o l poisoning.
preparation, flavouring syrup, etc., (3)
Mode o f action : Methyl alcohol is more
Whether the sample is fermented wash
toxic than ethyl alcohol. Since it is slowly
(from brewing), and (4) Whether the
excreted from the body, it acts as a cumula­
sample conforms to the specifications on
tive poison. During metabolism, it is
the label, if any.
converted into formaldehyde and formic
Under section 117, any prohibition acid. These metabolites are responsible for
officer or police officer is authorised to its toxic action. The symptoms correlate
search in the presence of panchas (public with the degree of acidosis.
persons) any person, article or premises,
Symptoms and signs: The symptoms may
believed to provide evidence of possession
appear within an hour after ingestion but
of an intoxicant, and take charge of such
are commonly delayed. Poisoning is
articles in the prescribed manner.
manifested by headache, dizziness, nausea,
Under section 121(1), he may open any
vomiting, and pain in the abdomen. There
package and examine any goods and may
is marked m uscular weakness and
stop and search any vehicle or other means
depressed cardiac action. Spirit-like odour
of conveyance for evidence of intoxicant.
is usually present in the breath. Dyspnoea
Under section 123(1), he may seize and and cyanosis are common. Acidosis results
detain any article likely to contain an from accumulation of acid metabolites. The
intoxicant and forward the article under poisonous effects are most marked in the
section 123(2) to the nearest police station. eyes, causing either temporary blindness
The article so seized is forwarded to the or, in severe cases, atrophy of the optic
chemical examiner for examination of nerves resulting in permanent blindness.
contents and opinion thereon. Other toxic effects relate to liver and
A selection of tests is carried out on the kidney. Convulsions are common as a
article to detect the various constituents, terminal event in fatal cases, and death
and the results reported by the chemical occurs from respiratory failure.
examiner in the prescribed proforma. Finding of intestinal contraction is diag­
nostic of methanol poisoning. Contraction
METHYL ALCOHOL____________________ affects either the small bowel or the large
Methyl alcohol (wood alcohol, wood spirit, bowel or both, being described as resembl­
wood naphtha, carbinol, or methanol) is a ing a thick pipe of very narrow lumen.
 Inebriant Poisons
Dr Subrahmanyam has seen a serious
caSe of 25 persons admitted in Suryapet
Civil hospital where people who consumed
illicit liquor presented with varying stages
0f loss of vision including total blindness.
fatal dose: About 60 to 240 ml would kill
most adults. 15 ml is known to cause
blindness. Serious symptoms have been
produced in children by intake of 1 ml/kg
of denatured alcohol containing methyl
alcohol.
Fatal period: Death may occur within 24
to 36 hours or may be delayed for 3 to 4
days.
Treatment consists of (1) preventing
absorption by gastric lavage (2) use of
bicarbonate to combat acidosis, and (3)
administration of ethanol as a competitive
antagonist. Whole bowel irrigation is
excellent, if facilities permit.
The stomach should be lavaged with
5%solution of sodium bicarbonate in warm
water. Acidosis will require oral adminis­
tration of sodium bicarbonate in a dose of
2 gm (1/2 teaspoonful) in 250 ml of water
every two hours to maintain neutral or
slightly alkaline urine. If oral therapy is not
possible, 50 gm of sodium bicarbonate
dissolved in one litre of 5% dextrose
solution can be given intravenously along
with 10-15 units of insulin. The plasma
bicarbonate level should be maintained at
around 20 mEq per litre. Intravenous
administration of molar sodium lactate is
helpful. Oral administration of 50% ethyl
alcohol in a dose of 0.75 to 1 ml/kg body
weight for three to four days is beneficial.
It prevents methanol oxidation to formal­
dehyde and formic acid and aids meanwhile
its excretion in urine and breath.
Indications for haemodialysis include
any ocular findings, metabolic acidosis,
renal failure and a blood methanol level
over 50 mg%.
Antidote 4-methylpyrazole is a specific
alcohol dehydrogenase inhibitor. It blocks
617
the formation of formaldehyde and formic
acid. Excretion of methanol can then occur
by renal or pulmonary routes. It has few
side effects. It should be used, if available.
Folinic acid speeds up metabolism of
formic acid and may be used. The rest of
the treatment is symptomatic. Eyes should
be kept covered to protect from strong
light.
Postm ortem appearances: Cyanosis is
marked. The blood is generally fluid and
dark. Cerebral and pulmonary oedema are
seen. The gastrointestinal mucosa is
inflamed. The liver shows necrobiosis and
kidneys show tubular degeneration.
Viscera and postmortem blood should be
preserved as outlined under ethyl alcohol
poisoning.
Medicolegal aspects: Accidental poisoning
may occur. Poisoning is generally due to
consumption of liquor containing methyl
alcohol by drinkers of cheap illicit liquor,
methanol having got into the liquor by
accident or design, the latter for economic
gain by the most unscrupulous bootleggers.
ISOPROPYL ALCOHOL________________
Isopropyl alcohol is found in rubbing
alcohol. It is a colourless liquid with a faint
alcoholic odour. It is twice as potent as
ethanol on a weight to weight basis and is
also slowly metabolised with the result that
the patient is more drunk and for a longer
time as compared to ethanol. It is consumed
by alcoholics as a cheap substitute for
ethanol or to get a greater kick. One of the
metabolic products is acetone which is a
CNS depressant.
Symptoms and signs: Poisoning is mani­
fested by headache, dizziness, nausea,
vomiting (haematemesis), and acute pain
in the abdomen, followed by marked
muscular weakness, depressed cardiac
action, and collapse. There is a chara­
cteristic fruity odour of acetone in the
breath giving the impression of diabetic
618 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

ketoacidosis. In children, hypoglycaemia source of intoxication and suicidal^

may occur. In severe cases, coma persists ^ accidental poisoning.
for more than 24 hours and death ensues Sym ptoms and signs: When ingested, the
from respiratory arrest. Isopropyl alcohol intoxicating effects resemble drunkenness,
is excreted unchanged by the kidneys and soon progressing to coma and death within
lungs. Its half-life is about 8-12 hours. 24 hours unless specific treatment can be
Fatal dose and fa ta l period: Infants have given on an emergency basis. Glycol is
been poisoned by isopropyl alcohol baths. metabolised in the body but a small amount
More than a single swallow is a toxic dose is converted to glyoxal, glycolic acid, formic
for children. The lethal dose for an adult acid, glyoxylic acid, and oxalic acid. The
(70 kg) is about 2.5 ounces of 70% isopropyl metabolites cause metabolic acidosis and
alcohol. The average fatal period is 24 may damage the kidneys. Hypoglycaemia
hours. may occur. The patient may suffer from
focal or generalised seizures. If the intoxica­
Treatment: Supportive treatment is all that
tion is acute, the patient develops pulmonary
is necessary. In severe intoxication, dialysis oedema and congestive heart failure in
is essential. Hypoglycaemia will need
12-36 hours, and kidney failure in 48-72
intravenous glucose.
hours.
P ostm o rtem a p p eara n c es: Cyanosis is F atal dose and fa t a l period: The fatal dose
marked. The blood is generally fluid and is about 100 ml and the fatal period about
dark. The gastrointestinal mucosa is 24-72 hours.
inflamed and haemorrhagic. The stomach
Treatm ent: J f the patient is promptly seen
contents may emit fruity smell of acetone.
Cerebral and pulmonary oedema are seen. after ingestion, lavage may be helpful.
The kidneys show tubular degeneration. Pyridoxirie and thiamine help conversion
of glyoxalate to non-toxic byproducts. 4-
M edicolegal aspects: Poisoning is mainly methyl pyrazole is useful as an antidote.
accidental from isopropyl baths in infants Serious cases require emergency treatment,
and ingestion by children less than six years such as dialysis, whole bowel irrigation, or
old. Drunkards may use it in place of competing ethanol. The indications for
ethanol and get poisoned thereby. emergency treatment include: (a) history of
ethylene glycol ingestion, (b) metabolic
ETHYLENEGLYCOL _____________________
acidosis, and (c) an ethylene glycol level
The glycols are easily available, being greater than 20 mg/dl.
widely used as antifreeze agents in cooling
Postmortem appearances: Autopsy appea­
systems of radiators of motor engines and
rances include cerebral oedema, chemical
solvents in industry. Their action is
meningoencephalitis, acute tubular
characterised by the intoxicating features
necrosis, and oxalate crystals in the tissues.
of alcohol and irritant features of oxalate
poisoning. The toxic compounds are M ed ico leg a l a sp e c t s : Ethylene glycol
ethylene, diethylene, and hexyl glycols, of poisoning is mostly accidental or suicidal.
which ethylene glycol is most commonly Drunkards may consume it in place of
encountered in medicolegal work as a ethanol.
 Sedatives and Hypnotics

Sedatives are drugs which produce a (physical dependence). The symptoms are
calming effect on the central nervous mainly digestive, nervous, cardiac, and
system while hypnotics are drugs which cutaneous. Pain, nausea, vomiting and
produce sleep. The important substances gastritis due to irritant action of the drug
which are considered from this group are: are very striking. In addition, erythematous
(1) chloral hydrate, and (2) barbiturates. and urticarial rashes may occur along with
tremors, convulsions, and depression.
CHLORAL HYDRATE_____________________ Delirium tremens may supervene when the
This is a colourless crystalline substance drug is withdrawn.
havinga peculiar bitter-sweet but nauseous Fatal dose: The lethal dose for an adult is
taste and aromatic smell. It is a powerful about 5 gm but varies greatly.
and reliable hypnotic. In small doses, it
Fatal period: Death usually takes place in
produces natural sleep but in larger doses
about 8 to 12 hours but may be delayed for
(5 to 6 gm), it is a depressant of the central
two to three days.
nervous system and paralyses the vital
centres. The pharmacopoeial dose is 0.3 to Treatment: The stomach should be washed
1.2 gm. out with warm water containing an alkali
which will decompose the unabsorbed
Q. 51.1. Discuss the m edicolegal aspects chloral hydrate. Haemodialysis may be
of chloral hydrate poisoning. necessary. The rest of the treatment is
symptomatic.
Symptoms and signs:lt is absorbed rapidly
from the stomach, small intestine, and Postmortem appearances: These are those
rectum. When ingested, there is retro­ of asphyxia. The peculiar odour of chloral
sternal burning sensation followed by hydrate may be perceived in the stomach
nausea and vomiting in early stages. Later, contents.
thereis drowsiness merging into coma. The There is irritation of the gastric mucosa.
blood pressure falls, respiration becomes In chronic poisoning, fatty degeneration of
slow and shallow, and death results from liver, kidney, heart, and other internal
paralysis of the respiratory and cardiac organs may be seen.
centres. Sometimes, a rash may be seen on Chloral hydrate rapidly deteriorates
the skin due to idiosyncrasy. after death. Chemical analysis of the viscera
Prolonged use of chloral hydrate pro­ should, therefore, be done as a matter of
duces tolerance and may lead to addiction urgency.
 Textbook of Medical Jurisprudence. Forensic Medicine and Toxicology

M edicolegal aspects: Accidental poisoning c. Quinal barbitone (seconal—red capsules)

may result from a large dose used as a d. Quinal with amylobarbitone (tuinak
hypnotic. It is rarely used for suicide. It is red/blue capsules)
often added to liquor for a greater kick. It
Ultrashort action 15-20 minutes — F0r
is covertly added to beer with homicidal
duration of anaesthesia — Fatal dose 1
intent. Chloral hydrate (sometimes known
a. Thiopentone sodium (pentothal—white
as dry wine) is used in alcohol to produce
powder or solution)
sleep in, say, a watchman. Its action is so
b. Methohexobarbitone (brevital—white
rapid that it has been given the name
powder or solution)
"knock out drops"; it renders a victim of
robbery or rape suddenly helpless. Long Barbiturates depress the central nervous
continued use leads to addiction. system and the effect varies from mere
tranquillity to deep coma depending on the
BARBITURATES___________________________ dose. They are cumulative, being partly
These compounds are used as sedatives, destroyed in the liver and slowly excreted
hypnotics and, when given intravenously, in the urine.
as anaesthetics. They are also useful in psy­
Q. 51.2. Discuss b a rb itu ra te poisoning.
chiatric disorders, epilepsy, and strychnine G ive its m e d ic o le g a l aspects. Add a note
poisoning.
on ch ronic poisoning (addiction).
Barbiturates are classified into four
groups as follows, depending on whether Symptoms and signs: Poisoning is mani­
their action is long, intermediate, short, or fested by giddiness, ataxia and slurred
ultrashort. speech, a short period of confusion
(incorrectly called automatism), excitement,
Long action — Effect from 1 to 8-12 hours
and delirium, followed by stupor and later
or — up to 1-2 days — Fatal dose 3-4 gm
coma. The limbs are flaccid, reflexes are
a. Barbitone (veronal—white tablets)
lost, and the pupil reacts to light by
b. Barbitone sodium (medinal—white tablets) alternate contraction and dilatation.
c. Phenobarbitone (gardenal, luminal—small As poisoning advances, the face becomes
white tablets) cyanotic; blood pressure falls; temperature
d. Methyl phenobarbitone (prominal—small is subnormal; respirations are slow, sighing
white tablets) and periodic (Cheyne-Stokes), or rapid and
Intermediate action — Effect from 1/2 to shallow; and bowel sounds are absent.
4-8 hours — Fatal dose 2-3 gm Oliguria may be present, the urine contain­
a. Allobarbitone (dial—white tablets) ing albumin and sugar. Barbiturate blisters
b. Amylobarbitone (amytal—blue capsules) are found on sites of friction or pressure,
such as interdigital clefts, axilla, and inner
c. Aprobarbitone (allonal/somnifaine—
aspects of the knees and calves. Death is
white tablets)
due to respiratory or cardiac failure in early
d. Butobarbitone (soneryl—pink tablets) stages or due to bronchopneumonia or
e. Pentobarbitone (nembutal—yellow oedema of the lungs in late stages. Some­
capsules) times, the patient may make gradual recovery.
Short action — Effect from 1/4 to 2-4 Fatal dose: The fatal dose of a long-acting
hours — Fatal dose 1-2 gm barbiturate is 3-4 gm, medium acting 2-3
a. Cyclobarbitone (phano.derm—white gm, and short acting 1-2 gm. In general,
tablets) the sedative (therapeutic) dose when
b. Hexobarbitone (evipan—white tablets) doubled becomes a hypnotic dose (induces
 Sedatives and Hypnotics 621

sleep) and the minimum lethal dose is intravenous chlorothiazide and/or mannitol
about ten times the therapeutic dose. The (500 ml of a 20% solution) results in
lethal blood levels are as follows: considerable increase in the elimination rate
* Long acting barbiturates... 10 m g /100 ml of barbiturates. The rest of the treatment is
U Intermediate acting barbitu rates ... symptomatic.
7mg/100ml P o s tm o rtem a p p ea ra n c es: These are
• Short acting barbiturates... 3 m g /100 ml mainly those of asphyxia. Fine froth is seen
Alcohol potentiates the action of barbitu­ emerging from the nose and mouth.
rates so that sublethal doses of either may Residual capsules or powder of the drug
cause death jointly with the other. in the stomach may be found. There may
Fatal period: Comm only, the patient be evidence of bronchopneumonia or of
remains in coma for 24-48 hours before oedema of the lungs. The kidneys may
death takes place. Occasionally, coma may show degeneration of the convoluted
last for several days and the patient may tubules. Other organs may be congested.
die subsequently. The brain should be preserved for chemical
Treatment: Gastric lavage should be carried analysis in addition to stomach, liver,
out with warm water using potassium spleen, kidneys, blood, and urine.
permanganate solution and suspension of Barbiturates are -chiefly excreted in the
animal charcoal. A concentrated solution urine and this affords a ready means of
ofmagnesium sulphate should be left in the detecting both acute and chronic poisoning
stomach to ensure purgation and minimise even during life. As ultrashort-acting
intestinal absorption. Body warmth must barbiturates are quickly redistributed in the
be maintained. body and usually administered intra­
To maintain a clear airway, the foot-end venously, it is more practical to detect them
of the bed should be raised and respiratory inbody fat, after death by chemical analysis.
mucus aspirated as and when necessary. The present editor (Dr Subrahmanyam)
Oxygen should be given continuously to saw a case wherein barbiturate lumps were
counter cyanosis. Artificial respiration may found in the stomach in a case brought for
be necessary. autopsy examination. Even the dead pet
For circulatory depression and shock, dogs contained the barbiturate in stomach,
intravenous doses of 2.5 mg of metaraminol when autopsied. Barbiturate blebs are seen
(Aramine) at 20 minutes intervals should on the back of the person who consumed
be given till the systolic blood pressure barbiturates.
reaches 100 mm Hg. If two or possibly three M edicolegal asp ects: Most deaths from
consecutive injections of metaraminol fail, barbiturates are either suicidal or acci­
this treatment should be abandoned. dental. The popularity of barbiturates as
If the coma is prolonged, amphetamine soothers for the harrying pace and anxieties
sulphate in a dose of 10 mg every half an of modem life has resulted in a number of
hour may be given till obvious improve­ addicts who might poison themselves from
ment occurs. Prophylactic administration an overdose taken accidentally or through
of antibiotics is necessary to prevent pulmo­ mental confusion from barbiturate automa­
nary complications. Dialysis and exchange tism or simultaneous ingestion of alcohol.
transfusion, or whole bowel irrigation, In some states in the US, judicial execution
where facilities permit, are valuable. is carried out by a lethal intravenous
The urinary bladder will require cathete­ injection of which sodium pentothal is the
risation. Forced osmotic diuresis using chief ingredient, the other ingredients being
saline, Pavulon (muscle relaxant), and
Chronic poisoning (addiction) may
occur from prolonged use of barbiturates
in epilepsy or psychotherapy. It is
characterised by apathy, loss of power of
concentration and somnolence, sometimes
accompanied by other signs, such as
vertigo, tremors, ataxia, thick speech,
delirium, hallucinations which are usually
visual, emotional instability, and general
mental deterioration. The urine may show
albumin, sugar and casts. The dependence
is both physical and psychological. ^
treatment is the same as that for other drugs
of addiction. Withdrawal convulsions have
been reported after about 4 to 5 days after
withdrawal of the drug.
B a rb itu rate au to m a tism : Barbiturate
automatism is a condition that can cause
death of a person, when the consumer
forgets to have taken the early dose and
continues to take automatically till coma
supervenes and even death may ensue.
 52 Fuels
The important fuels discussed under this
heading are all derived from petroleum,
chief amongst which are kerosene, petrol
and naphtha.
PETROLEUM (ROCK OIL)_________________
Petroleum contains gas and liquid consti­
tuents. It is an oily liquid found under the
ground in several parts of the earth. The
refined oil is known as kerosene. The other
products which are separated during the
process of purification are classified into 2
groups according to their boiling point in
relation to kerosene. Those which are
lighter and boil at a lower temperature than
kerosene are known as gasoline, and
include ether, pentane, hexane, octane,
petrol, naphtha, benzine, etc. Those which
are heavier and boil at higher temperatures
than kerosene include the lubricating oils,
vaseline and paraffin. In general, among
the petroleum distillates, the toxicity is
inversely proportional to the boiling point.
Therefore, while liquid paraffin and
vaseline are in common use in medicine as
harmless products, ether, petrol, naphtha,
benzine, etc. are highly poisonous when
swallowed or inhaled.
Petroleum distillates are irritants
because they dissolve fats. They also
depress the cells of the central nervous
system. The effect on liver, kidneys and
bone marrow may be from contaminants,
such as benzene.
623
#
Q. 52.1. Give a brief account of kerosene
poisoning.
Symptoms and signs: After ingestion of
lighter distillates, there is a kerosene taste,
a sensation of burning in the throat, nausea,
vomiting, colicky pain and diarrhoea. The
breath, vomit and urine smell of kerosene.
The respirations become slow and shallow.
Cyanosis develops. Lung complications, ,
such as bronchopneumonia, and pulmo-.
nary oedema, are common. The central
nervous system depression results in giddi­
ness, weakness and drowsiness followed by
coma and death from respiratory failure.
Inhalation of fumes causes headache,
vertigo, nausea, vomiting, and lung compli­
cations followed by intense excitement,
hallucinations and convulsions. In fatal
cases, cyanosis, unconsciousness and coma
precede death.
Chronic poisoning is known to occur
from inhalation in persons who handle
petroleum products. The principal symp­
toms are dizziness, weakness, weight loss,
anaemia, nervousness, pain in limbs, peri­
pheral numbness, and paraesthesias.
Treatment requires isolation of the patient
from exposure and symptomatic manage-
Fatal dose and fa ta l period: Ingestion of
more than 10 ml of kerosene may be fatal.
Petroleum products spread over a large
surface area, such as the lung, and cause
624 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology.

intense pulmonary irritation. Fatal period

is, therefore, a few hours.
Treatment:If ingested, the stomach should
be washed out with warm water containing
5% sodium bicarbonate. Its absorption can
be slowed by giving 250 ml of liquid
paraffin orally, followed by a saline
cathartic. If the poison has been inhaled, the
patient must be removed to the open air
and artificial respiration persisted in. The
rest of the treatment is symptomatic.
P ostm ortem appearan ces: There may be
acute gastroenteritis and kerosene odour Fig. 52.1 : Kerosene poisoning. This woman t f f l
may be observed in the contents of the
an unknown dose of kerosene and died insSteK
of treatment. In addition to cyanosis (asphm lt
stomach and lungs. Pulmonary oedema
death), froth is seen emerging from the
and bronchopneumonia are found. and nose. However, it is neither so fine nor so
Degenerative changes in the liver and copious as in drowning
kidneys and hypoplasia of the bone
marrow occur after prolonged period of taken kerosene in m istake for wapr.'
inhalation. Other signs of asphyxia may be Isolated cases of petroleum poisoning and
seen. In case of death from petroleum, the death occur among persons attempting to
lungs and the brain together with other suck petrol from car tanks through rubber
viscera should be preserved for chemical tubing.
analysis in saturated saline (Fig. 52.1).
Dr Subrahm anyam saw a case of
M edicolegal aspects: Kerosene is occasio­ kerosene poisoning in Dachur. A toddler
nally used for self-immolation. Homicidal drank water from a broken drinking glass,
attempts by pouring kerosene on clothes that turned out to be kerosene and m s
and igniting them are common in case of brought to the primary health care centre,
dowry deaths in India. However, most with respiratory manifestation. Adminis­
fatalities are accidental. The majority of tration of crystalline penicillin and constant
cases have been young children who have monitoring lead to recovery and discharge.
 Agrichemical Poisons

The potent chemicals used in agriculture commonly used alkyl phosphates include
mayharmpersons by accidental exposure, hexaethyl tetraphosphate (HETP), tetra­
either during their application to crops or ethyl pyrophosphate (TEPP), octamethyl
dueto careless storage. In Sri Lanka, many pyrophosphoramide (OMPA), and mala-
thousands of hospital admissions each year thion. The commonly used aryl phosphates
arefor agrichemical poisoning with over a include parathion (Folidol), and Diazinon
thousand deaths annually. Of these, about (Tik-20). Poisoning can occur from inhala­
three-quarters are self-administered, the tion, ingestion and absorption through
remainder being accidental and occupa­ unbroken skin. The poisonous effects may
tional. be cumulative. These compounds are^
The commonly used agricultural chemi­ powerful inhibitors of cholinesterase at the
cals are the organophosphorus compounds, myoneural junctions and synapses of the
viz. alkyl and aryl phosphates; the chlori­ ganglions; acetylcholine, therefore, accumu­
natedcompounds, such as DDT and Endrin; lates and results in hyperexcitation of the
thecarbamates, such as aprocarb (Baygon) voluntary and involuntary muscles. A drop
andCarbaryl (Sevin); the coal-tar product, in the activity of cholinesterase to 30 per
naphthalene; herbicides, such as paraquat; cent of normal or lower is associated with
and the metallic compounds, such as zinc toxic symptoms.
phosphide and aluminium phosphide. The
discussion here is restricted to: (1) organo­ Q. 53.1. Describe the action of organo­
phosphorus compounds, (2) chlorinated phosphorus compounds on the human
compound—endrin, (3) coal-tar product— body. Give a brief account of poisoning
naphthalene, (4) herbicide—paraquat, and by any one of them.
(5) the metallic compound—aluminiumThe main toxic effects are: (a) muscarine­
phosphide. Zinc phosphide is discussed like, (b) nicotine-like, and (c) on the central
under zinc. nervous system.
ORGANOPHOSPHORUS COMPOUNDS As a result of the muscarine-like effects,
the following symptoms and signs are
The development of a number of organo­ observed:
phosphorus compounds for use as pesti­
cides, vermicides, and rodenticides, has 1. Bronchial tree: Tightness in the chest
introducedseveral dangerous new poisons. with prolonged wheezing expiration is
Chemically, these organic compounds suggestive of bronchospasm and
are the alkyl and aryl phosphates. The increased secretion. Therefore, there is
 626 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
discomfort or pain in the chest, dyspnoea,
cough, pulmonary oedema, froth at the
mouth and nose, and cyanosis. The
effects simulate bronchial asthma.
2. G a stro in testin a l A norexia, nausea,
vomiting, abdominal cramps, epigastric
and substemal tightness (? cardiospasm)
with heartburn and eructations,
diarrhoea, tenesmus, and involuntary
defaecation. i;X
3. Sweat glands: Increased sweating.
4. Salivary glands: Increased salivation.
5. Lacrimal glands: Increased lacrimation.
Tears may be red due to porphyrin in
lacrimal glands.
6. Heart: Slight bradycardia.
7. P upils: Slight miosis, occasionally
unequal, and later more marked miosis.
8. Ciliary body: Blurring or dimness of
vision.
9. Urinary bladder: Frequency of micturi­
tion and involuntary micturition.
As a result of nicotine-like effects, the
following symptoms and signs are
observed:
1. S triated m uscle: Easy fatigue, mild
weakness, muscular fasciculations,
cramps, generalised weakness of
muscles of respiration with dyspnoea
and cyanosis.
2. Sympathetic ganglia: Pallor, occasional
elevation of blood pressure.
As a result of action on the central nervous
system, the following effects may appear
approximately in the following order:
1. Irritability, apprehension, restlessness.
2. Fine fibrillary tremors of hands, eye lids,
face or tongue.
3. Mental confusion progressing to stupor
and muscular weakness with tremors
and convulsions.
4. Coma with absence of reflexes and
depression of respiratory and circulatory
centres.
Symptoms and signs: Illness first affects
involuntary muscles and secretory glands,
then voluntary muscles, and finally vital
brain centres. According to the route of
entry, the respiratory or gastrointestinal
symptoms are more marked. The respira­
tory symptoms may mimic an attack of
bronchial asthma. The initial complaint is
headache, malaise and a sense of tightness
in the chest, and dimness of vision due to
pin-point pupils. In the next two to eight
hours, there may appear, approximately in
this order, nausea, abdominal cramps,
vomiting, diarrhoea, profuse sweating and
salivation, frequent urination, and mus­
cular twitching. This symptom complex is
sometimes called SLUD, the prominent
symptoms being salivation, lacrimation,
urination, and defaecation. In some cases,
chromogenic tears (red tears) may be shed
due to accumulation of porphyrin in the
lacrimal glands. If poisoning is severe,
pulmonary oedema, coma, convulsions and
possibly death may ensue. Death is
generally caused by paralysis of muscula­
ture but may result from respiratory failure,
circulatory arrest, oedema of lungs or brain.
The author has come across a case where
a doctor was charged with administering
organophosphorus compound by injection
to his wife. Her illness resembled bronchial
asthma for which she was treated with
injection of adrenaline but died. On a
complaint of suspicious death, an autopsy
was performed. Organophosphorus
compound was detected from the injection
site and viscera.
Fatal dose: The average fatal dose of HETP
is 160 mg by intravenous (i.v.) or intra­
muscular (i.m.) route and 350 mg orally;
OMPA 80 mg by i.v. or i.m. route and 175
mg orally; TEPP 45-50 mg i.m. or i.v. and
100 mg orally; malathion 1 gm orally;
 Agrichemical Poisons 627
parathion (Folidol) 80 mg by i.v. or i.m. 4. Cholinesterase reactivators: The oximej
route and 175 mg orally; and Diazinon (Tik- compounds, Protopam (pralidoxime ;
20) lgm orally. chloride), pralidoxime iodide and PAM
fatal period: In fatal doses, death may (pyridine aldoxy methiodate) are rapid
ensue within half to three hours or may cholinesterase reactivators and act by
sometimes be delayed for few more hours. dephosphorylating the inactivated
The acute effects in non-fatal cases last for cholinesterase. They act as specific anti­
6-30 hours, fading during the next 48-72 dotes and should be used to supplement
hours or sometimes persist for as long as atropine therapy. The dose is 1 to 2 gm
3 weeks. i.v. for adults and 25 to 50 mg/kg for
children, given as a 5% solution in iso­
Treatment: It should aim at (1) decontami­ tonic saline, and repeated every 12 hours,
nation, (2) care of the airway, (3) adminis­ if symptoms persist or recur.
trationof an antidote, (4) administration of
cholinesterase reactivators, and (5) other 5. Other measures: A diuretic and a brisk
measures including general measures. saline purgative may be useful. Restless­
ness may be combated by quick acting
1. Decontamination: The physician and barbiturates or diazepam. The rest of the
those who are in charge of nursing these treatment is symptomatic. In serious
cases should wear rubber gloves. The cases, an exchange transfusion may be
patient must be removed from the source necessary.
of exposure and stripped of all clothes.
The exposed areas are decontaminated The first four to six hours are most critical
by washing with tap water and soap or in acute poisoning. In delayed paralysis
some alkaline solution. If the poison is resulting from demyelination, damage is
ingested, the stomach should be washed permanent.
with tap water with or without potassium Postmortem appearances: The changes are
permanganate. suggestive of asphyxia. Externally, the face
2. Care.ofthe airway: The foot-end of the bed is cyanosed. There is froth, usually blood­
is raised to ensure drainage of respira­ stained, at the nose and mouth. A kerosene­
tory mucus. Secretions may need to be like smell may be perceived. Internally, the
aspirated, and tracheostomy may be stomach contains greenish oily substances
necessary. Artificial respiration may be used as diluents, and their kerosene-like or
required, and positive pressure oxygen garlic smell is easily perceived. The
should be given, if pulmonary oedema contents of the stomach are blood-stained,
ensues. the mucosa is congested, and submucous
3. Antidote: Atropine blocks the peripheral petechial haemorrhages are seen. The other
(muscarinic) actions of the excessive postmortem findings are: pulmonary
acetylcholine levels built up by the oedema, capillary dilatation, petechial
cholinesterase inhibitors, but the central haemorrhages, and hyperaemia of lungs,
and neuromuscular reactions are un­ brain and other organs. In delayed
affected. It is administered in a dose of paralysis of the extremities induced by
2 mg every 15 to 30 minutes i.m. or i.v., parathion, malathion, and other com­
till signs of atropinisation appear pounds, the findings are demyelination of
(flushed face, dry mouth, dilated pupils, ascending and descending spinal tracts
fast pulse and warm skin). As much as with degeneration of motor horn cells.
12 mg of atropine has been given safely Organophosphorus compounds resist
in the first two hours! putrefaction and poisoning can be detected
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
in exhumed bodies. The viscera for
chemical examination should be preserved
in saturated saline in suspected cases of
poisoning.
M edicolegal aspects: Organic phosphorus
compounds are in common use agri­
culturally and domestically as pesticides,
vermicides, and rodenticides. Being easily
available, they are used for suicide. They
are mixed with alcohol to mask the smell
and have been used for homicide. A num­
ber of non-fatal cases have been recorded
in persons handling fruits sprayed with an
organic phosphorus insecticide. A number
of accidental deaths through contamination
and leakage of these compounds to edible
commodities have also been recorded
(Kerala food poisoning cases in India).
Some of the compounds in concentrated
form are intensely poisonous to human
beings. Workers engaged in the manufac­
ture, packing, or spraying them are at
special risk of accidental poisoning.
CHLORINATED COMPOUNDS____________
Many chloro compounds have been
synthesised as insecticides from dicholoro-
propene (DD) to the very complex modern
synthetics in common use as pesticides. Of
this group, the agents which are commonly
employed are: DDT, Endrin, Gammexane,
Dieldrin, etc. Their effects on mammals are
essentially the same from the clinical stand­
point and the compounds can, therefore,
be described as a group. The chemical proto­
type for the group is chlorophenothane,
which is commonly known as DDT, and its
description applies to all the members of
the group. However, since endrin poisoning
is common in certain parts of India, it is
described here.
Endrin
Of all the chlorinated insecticides, endrin should be given in a dose of 10 ml of 10%
is the most toxic. It is a synthetic, fat-soluble solution intravenously every four to six
but water-insoluble, chemical having an hours. Atropine does not appear to have
unpleasant taste. It is stable for months to
a year or even more. It is sold in the market
as Endrin-We 16, Endox-DB-50, EndtoxEc.
20, Endrex, Tafdrin, and a variety of other
trade names. These preparations contain
endrin in 20-50% concentration mixed with
50-80% of a solvent such as aromax, a
petroleum hydrocarbon smelling like
kerosene.
Endrin is chiefiy used against insect pests
of cotton, 'paddy', sugarcane and tobacco.
It is a popular insecticide with action
against a wide variety of plant pests and,
therefore, also known as plant penicillin. It
is extensively used in India in Andhra
Pradesh where poisoning is occurring at an
alarming rate since 1959 both in urban and
rural populations.
Symptoms and signs: Toxic effects rapidly
follow ingestion, inhalation or skin
contamination. The main symptoms are
salivation, vomiting, abdominal pain,
tremors, convulsions, oozing of fine white
froth occasionally blood-stained from both
mouth and nostrils and severe dyspnoea.
Gradually, the convulsions become severe
and continuous followed by coma which
may terminate in respiratory failure and
death. Diarrhoea is not a constant feature.
In some cases, convulsions herald the onset
of symptoms.
Fatal dose:Toxic symptoms appear with a
dose of 1 gm. The lethal dose is about 6 gm.
Fatal period: The fatal period ranges from
half an hour to several hours, the majority
dying within an hour or two.
Treatment: This is largely symptomatic.
Decontamination of the body should be
carried out and the airway cared for as
outlined under poisoning by organo-
phosphorus insecticides. Barbiturates and
diazepam are useful to control convulsions.
Calcium decreases the toxicity of endrin. It
FT*
630 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Q. 53.2. Write short notes on: (a) naphtha­
lene (b) paraquat (c) aluminium phosphide.
Naphthalene
This is a solid volatile substance obtained
from the middle fraction of coal-tar distilla­
tion and has chemical properties similar to
benzene. It occurs in large, lustrous,
crystalline plates with a characteristic
odour. It is used as a deodorant in lava­
tories, as a pesticide in moth balls, and in
the dye industry for the manufacture of
indigo and certain azo dyes. Toxic effects
follow from its absorption from the skin,
and from the respiratory and gastro­
intestinal tracts. N aphthalene causes
haemolysis with subsequent blocking of
renal tubules and hepatic necrosis. Haemo­
lysis occurs only in those with hereditary
deficiency of glucose-6-phosphate de­
hydrogenase in the red cells.
When naphthalene is chlorinated, a
waxy substance is produced. Such chlori­
nated naphthalene is used in industry as
an insulating coat on electric wires and
other electric equipment.
Sym ptom s and signs: The serious effects of
poisoning are acute nephritis, jaundice,
haemolytic anaemia, and optic neuritis.
When ingested, there is gastric irritation
with nausea, vomiting and abdominal pain.
Other symptoms include burning sensation
in the urethra, pain in the bladder and loins,
and occasional strangury. The urine may
be dark-brown or black containing albumin
and haemoglobin. Severe poisoning may
damage the liver and kidneys, and result
in convulsions, cyanosis, profuse perspira­
tion, coma and death. When inhaled,
naphthalene chiefly causes headache,
malaise, nausea, vomiting, conjunctivitis,
mental confusion and visual disturbances.
Contact with naphthalene dust on bedding
has given rise to dermatitis, conjunctivitis,
vomiting, headache, jaundice, and haema-
turia.
C hlorinated naphthalene produces
varying degrees of skin irritation and acne
and appears to have a toxic effect on the
liver, and various systemic effects similar
to those of naphthalene.
F a tal d ose and fa t a l period: The fatal dose
of ingested naphthalene is approximately
2 gm. Death may take place in a few hours
or be delayed up to two to three days.
T reatm ent: The patient should be kept
warm. The stomach should be washed out
with warm water or saline. Bowels should
be cleared by magnesium sulphate. Sodium
bicarbonate should be administered to
maintain an alkaline urine to prevent the
precipitation of acid haematin crystals and
blocking of the renal tubules. Blood trans­
fusion may be necessary. Hydrocortisone ■}
is helpful in limiting naphthalene haemo­
lysis. Chronic poisoning occurs in those!
who repeatedly handle the drug. The localj
effects disappear in one to six months after
discontinuing exposure.
A case of naphthalene (moth balls)
poisoning was brought to new Civil
Hospital Surat. Dr Subrahmanyam had
seen this case of attempted suicide by an
18 yrs old student. When her mouth was
opened, the smell was clear and diagnosis
was suggested, she recovered well with
treatment.
P ostm ortem a ppearances: The skin may be
yellow. The gastric mucosa may be yellow,
congested or inflamed. Liver and kidneys
may show severe damage. The other
organs may be congested. The respiratory
tract may show signs of irritation.
M edicolegal aspects: Suicide by ingestion
of naphthalene has been reported. How­
ever, most cases are accidental, the poison
having been inhaled from bed clothes
heavily dusted with the powder or from
ingestion of moth balls by children.
Naphthalene is not soluble in water and
may remain in a garment after washing. As
 Agrichemical Poisons 631

it is soluble in oil, baby oils may act as a useful. Artificial respiration and oxygen
solvent promoting absorption through skin may be required. In serious cases, an
and this may result in accidental poisoning. exchange transfusion may be necessary.
The rest of the treatment is symptomatic.
Paraquat
Postmortem appearances: There may be
Paraquat is a herbicide that is sprayed on ulceration around the lips and chin due to
unwanted weeds and other vegetation dribbled paraquat. The mucosa of the
before planting crops. It is absorbed by the
mouth and oesophagus may be reddened
foliage and rapidly kills the plant but is
or desquamated. The stomach may show
inactivated when in contact with the soil.
- erosion and patchy haemorrhages. The
It is produced commercially as a brownish
liver may show fatty change and necro­
concentrated liquid of the dichloride salt
in 10-30% strength under the trade name biosis. The kidneys may reveal cortical
'Gramoxone' and for horticultural use, as pallor, if there is renal failure. In delayed
brown granules called 'Weedol' at about deaths, the lungs are large and stiff, keeping
5% concentration. their shape when removed from the chest.
There may be fibrinous pleurisy and
Toxicity occurs mainly through inges­
sometimes slight bloody pleural effusions.
tion and occasionally through inhalation
The main appearances are microscopic and
while spraying. Accidental deaths are
unless the history is known, thfeicondition
generally due to decanting of the concen­
trate from the original containers. may be misdiagnosed as bronchopneu­
monia.
Symptoms and signs: Concentrated para­ In addition to histological samples, the
quat is irritant to all epithelial tissues. The viscera to be preserved include the usual
lips, mouth, pharynx, and oesophagus are blood samples, urine, stomach contents,
superficially eroded. This is followed by lungs and liver. Paraquat is excreted over
blood-stained vomiting and bloody stools. along period and can be detected in the
The lungs are affected by direct aspiration, urine at autopsy many days after ingestion.
either during swallowing or vomiting. The
liver is mainly affected. It undergoes a Medicolegal aspects: Poisoning is mainly
centrilobular necrosis, with giant mito­ accidental and suicidal. Rarely, homicide
chondria and crystalline inclusion bodies is possible and the poisoning may be
seen on electron microscopy. Renal failure mistaken for viral pneumonia.
maydevelop within two or three days from
diffuse tubular damage. Myofibril fragmen­ Aluminium Phosphide
tation may occur. This is an effective pesticide and rodenti
cide. It is sold under various trade names
Fatal dose and fa ta l period: 5 ml of e.g. Celphos, Alphos, Fumigran, Phostoxin
swallowed Gramoxone or 1-2 gm of
etc. A 3 gm tablet, which resembles £
Weedol are usually fatal. Death occurs medicinal preparation, contains 56 per cen
rapidly from acute hepatorenal failure.
of the active ingredient. It is easily availabl
Delayeddeaths within about two weeks are and cheap. Therefore, it is frequentl
due to progressive lung damage, where it misused with homicidal intent in cases c
causes fibrosing alveolitis and rigid stiff dowry deaths in rural India; only a part c
lungs [Adult Respiratory Distress the tablet is usually sufficient for this pui
Syndrome (ARDS) - see Injuries to Lungs]. pose. The toxic effects are due to liberatio
Treatment:The stomach is washed with tap of phosphine gas when the tablet comes i
water; a brisk saline purgative may be contact with gastric juice. Symptoms, sign
 632 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

and other details are similar to poisoning aggressive forced diuresis, and sympto­
by zinc phosphide, discussed under zinc. matic management help in recovery. This
hair dye is a common, inexpensive and
Hair Dye Poisoning emulsion based. It consists of paraphenyl-
In southern India, Kadapa and Nellore enediamine, resorcinol, propylene glycol,
presented cases of attempting to commit EDTA (ethylenediamine tetra-acitic acid
suicide with a hair dye popularly called as sodium), liquid paraffin, cetostearyl alcohol,
Vasmol-33, among young women. Rhabdo- sodium lauryl sulphate, herbal extracts
myolysis evidenced by chocolate-colored preservative and perfumes. It is emerging
urine angioneurotic oedema with stridor as a popular suicidal agent more so in
and acute renal failure constitute an early women. Average ingested amount was 150 i
triad of manifestations. When patient arrives, ml. Prompt treatment, early arrival ands
a gastric lavage is done. Early tracheostomy, correct diagnosis show recovery.
54 .....
Deliriant Poisons
 634 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

features have already been outlined under The pupils are dilated, insensitive to lig^t
the topic "Capsicum".An average-sized and the power of accommodation for near
fruit contains 450 to 500 seeds, and weighs vision is paralysed (blind as a bat). The
about 8 grams. One hundred seeds weigh body temperature is raised. The skin is dry
about 1 gram. All parts of the plant are and hot (hot as a hare) due to inhibition of;
poisonous but the seeds and fruits more so. sweat secretion and stimulation of heat
The active principle contains the alkaloids, regulating centre. There is vomiting. These
laevohyoscyamine, hyoscine or scopola­ symptoms are soon followed by giddiness
mine, and traces of atropine. and unsteady gait, the person staggering
An alkaloid is a complex chemical like a drunken individual. The mind is
substance found in various plants. It is so affected early, the patient being at first
called because it behaves like an alkali and restless and confused, and later becoming
combines with acids to form salts. The delirious, and mutters indistinct words
distribution of alkaloids in the plant is not (mad as a wet hen). He is subject to visual
uniform; some are concentrated in the and auditory hallucinations. He appears to
roots, others in the seeds, still others in the grasp at imaginary objects, picks at his
bark, and so on. They act mainly on some clothings, and tries to pull imaginary threads
portion of the central nervous system, each from the tips of his fingers. The delirium
having its own individual action. passes off in an hour or so and the patient
becomes drowsy (Figs 54.4 and 54.5). There
Q. 54.1. Give a brief account of dhafura may be a scarlatiniform rash. The drowsi­
poisoning. ness may progress to stupor or coma and
The alkaloids of dhatura stimulate the rarely death from respiratory paralysis.
higher centres of the brain, and then the Secondary delirium may appear when the
motor centres. They inhibit secretion of patient recovers.
sweat and saliva, dilate the cutaneous The important symptoms and signs can
blood vessels, dilate the pupil and stimulate be summarized under 9 Ds, viz: (1) dryness
the heat regulating centre situated in the of the mouth and throat, (2) difficulty in$
floor of the third ventricle. The initial
stimulation is followed by depression and
paralysis of the vital centres in the medulla.
Symptoms and signs: The symptoms are
described as "dry as a bone, red as a beet,
blind as a bat, hot as a hare, and mad as a
wet hen". They appear within half an hour,
if seeds are taken, or earlier, if a decoction
(concentrated water extract) of seeds is
used, and almost immediately, if the alka­
loids are taken. In most cases, powdered
seeds are administered in food.
The earliest symptom is a bitter taste in
the mouth. Due to inhibition of salivation,
there is dryness of the mouth and throat
(dry as a bone) resulting in difficulty in
talking, dysphagia and unquenchable
thirst. The face is flushed due to dilatation Fig. 54.4: Acute dhatura poisoning. The victim
of cutaneous blood vessels (red as a beet). picks at the clothings. (Courtesy: Dr GB Sahay)

Fig. 54.5: Visual hallucination in acute dhatura
poisoning. The victim is seen, pulling out
imaginary threads from the nail bed. His pupils
are dilated. He is, therefore, wearing goggles
to avoid flash of light. (Courtesy: Dr GB Sahay)
talking, (3) dysphagia, (4) dilatation of
cutaneous blood vessels, (5) dilatation of
pupils, (6) dry hot skin, (7) drunken gait,
(8) delirium, and (9) drowsiness. And, these
may be mistaken for drunkenness, or heat
stroke.
Fatal dose and fatal period: This is about
100 to 125 seeds. The lethal dose for the
alkaloids is about 60 mg for adult and 4 mg
for children. Death usually occurs within
24 hours.
Treatment: The stomach should be evacua­
ted to remove the remnants of the crushed
seeds by a stomach wash with either a weak
solution of potassium permanganate or
4 to 5% tannic acid. Physostigmine in a
dose of 1-4 mg (repeated, if necessary, at
intervals of 1 to 2 hours) or Neostigmine
(2.5 mg i.v. every 3 hours) act as physio­
logical antidotes. Purgatives are beneficial
and the rest of the treatment is sympto­
matic. Moistening of the tongue and change
in the size of the pupils towards the normal
are valuable guides in treatment. In non-
fatal cases, recovery takes a day or two,
the effect on the pupils being the last to
disappear.
Postmortem appearances: These are those
of asphyxia. Dhatura seeds may be found
in the stomach. There is congestion of the
gastrointestinal tract. Dhatura seeds resist
putrefaction and are found even when the
body is decomposed,
Medicolegal aspects: IS India, dhatura is
employed mainly as a stupefying poison
prior to robbery, kidnapping, and rape. It
is sometimes known as a road poison as it is
commonly encountered-during a journey.
The powdered seeds are mixed with food,
tea, drink, or in 'paan' (betel leaf) and given
to an unwary traveller by an apparently
obliging person^Sm ingestion of such
material, the travellerbecomes very drowsy.
When he wakes up, he finds that his
pockets are picked, removable belongings
lost, and the apparently obliging person
vanished. If he goes to the police station to
lodge a complaint, ,he is taken to be a
drunkard on account of his drunken gait
and difficulty in talking. Generally, the
railways and pilgrim places put warning
boards asking the travellers not to accept
any food or 'prasad' from strangers to
obviate such mishaps.
A small dose either due to inhalation of
smoke, smoking, or from ingestion j
deprives the person of his reasoning ability,j
At times, he appears to be in the right statei
of mind but actually does not know withj
whom he is talking, nor remembers whatf
has happened when the alienatioj
(intoxication episode effect) is over. Such
an effect is achieved when the victimJ |
exposed to fumes from burning the seeds
mixed with resin, or by mixing dhatura
with tobacco in cigarettes. The smoker,
636 Textbook of Medical Jurisprudence. Forensic Medicine and Toxicology
during the temporary twilight phase, will
allow his pockets to be picked without any
resistance or would even give away any
valuable article, e.g. a wrist watch if asked
for! Children can be easily kidnapped by
giving them candy or sweets mixed with
dhatura. They comply with the instructions
of the poisoner to follow him! Likewise,
women have been abducted, robbed and
raped.
Accidental cases occur (1) when children
and adults eat the raw fruit or seeds mis­
taking them for edible fruits or capsicum
seeds respectively, (2) from the use of
dhatura as an aphrodisiac, and (3) when the
decoction of seeds is added to country
liquor or toddy for a greater kick.
HYOSCYAMUS NIGER________________
Also known as scopolamine or henbane
and khorasani ajwayan in the local langu­
age, this plant grows in the Himalayan
ranges at high altitudes. All parts of the
plant are poisonous. They contain the
alkaloids atropine, hyoscine and hyoscy-
amine. The symptoms and signs closely
resemble those of poisoning by dhatura.
125 mg of hyoscyamine or 15-30 mg of
hyoscine hydrobromide would lead to a
fatal outcome in 24 hours in most cases. The
treatment is similar to that for poisoning
by dhatura. Postmortem appearances are
also similar to those for dhatura.
Hyoscyamus seeds may be found in the
stomach. Hyoscine resists putrefaction.
Hyoscyamus has varied uses. In small
doses, it is used as medicine. Its calming
effect is used in controlling tremors in
Parkinson's disease, in delirium, and
psychotic conditions. It is also used to
control the spasms of asthma and
whooping cough. It has proved useful in
cases of depression. In good old days, it was
used in combination with morphine to
produce twilight sleep to facilitate painless
childbirth. In war, it is used to control shell­
shock. Poisoning is generally accidental
through an overdose or rarely homicidal
as in the Crippen case. In forensic work, it
can be used as a truth serum or lie detector.
It is said that a criminal under its influence
is half awake and half asleep. His mental
condition becomes such that he is not able
to fabricate lies or withhold truth during
interrogation, which he could do during his
normal waking state.
CANNABIS INDICA_____________________
Q. 54.2. W hat is cannabis? Describe its
preparations. Give the symptoms of acute
poisoning. Discuss the m e d ic o le g a l
significance.
Also known as cannabis sativa or Indian
hemp (Fig. 54.6) in India, Dagga in South
and Central Africa, and Hashish in Egypt,
this plant grows all over India, and all its
parts are poisonous. Its cultivation is
restricted by law. The active principle is not
an alkaloid but a fat-soluble oleoresin,
cannabinol (tetrahydrocannabinol - THC).
The poison is absorbed both from the
digestive and respiratory tract. It is a
stimulant of the central nervous system and
is used in the following four forms.
1. Bhang: Also known as siddhi, patti, or
sabji, it is prepared from the dried leaves
and fruit shoots which are used as an
infusion in the form of a beverage. It
contains the active principle in a concentra­
tion of 15% and is the least potent.
Fig. 54.6: Cannabis sativa or Indian hemp,
(Draw by Miss AC Parik)
 Deliriant Poisons
2. Majun: This is a sweetmeat made with
bhang. It produces grandiose delusions, in
addition to all the effects of bhang.
3. Ganja: This consists of the flowering tops
of the female plant, specially grown so that
there is a large amount of resinous exudate.
It contains the active principle in a concen­
tration of about 25%. The resin has a rusty
green colour and characteristic odour. It is
mixed with tobacco and smoked in a pipe.
InIndia, it is largely indulged in by sadhus
andfakirs, a class of people who dress in
scarlet-coloured loose clothes and claim to
haverenowned the worldly bonds (Fig. 54.7).
4. Charas: Also known as hashish, it is the
resinous exudate from the leaves and stems
of the plant. It is of dark green or brown
colour. It is smoked with tobacco in a pipe
or'hookah' and is the most potent of all
cannabis preparations, containing the
active principle in a concentration varying
between 25 and 40%.
The drug is commonly used for its
supposed aphrodisiac, hypnotic and
analgesic actions. It leads to psychological
Fig. 54.7: A ganja addict. A tem ple priest
smoking ganja in a pipe to get the religious
fervour. (Courtesy: Dr MN Ganapathy)
637
dependence and intense craving in children.
The active principle being fatsoluble, is
stored in fat cells of the body where it acts
like a time release capsule, the effect of a
single dose lasting for over 7 days.
The term marihuana or marijuana (pot,
grass, tea, Mary Jane) is used in America
to refer to cannabis. It is a Mexican term
meaning 'pleasurable feeling'. The form in
which it is generally used is similar to ganja.
It is eaten alone or as part of confection, or
drunk in beer or some other beverage, or
smoked in cigarettes (Reefers). These
cigarettes contain about 500 mg of Indian
hemp and are known as reefers or weed.
Their use appears to lead to heroin addic­
tion, especially in teen-agers.
Symptoms and signs: In a small dose, the
effects are somewhat similar to those of
alcohol causing euphoria at first followed
by narcosis. The patient is pleased with
himself, has a feeling of cheerfulness and
well-being, and tends to become talkative.
His appetite is increased and he eats his
food with great relish, and may seek sexual
enjoyment. In a susceptible person or with
a larger dose, there is loss of perception of
time and space. He is the subject of visual
hallucinations. He sees nude beautiful
women dancing before him, playing music,
and singing amorous songs. This stage is
followed by one of narcosis characterised
by giddiness, confusion, and ataxia.
Commonly, there is tingling and numbness
of the extremities or in severe cases genera­
lised anaesthesia. The victim may pass into
deep sleep for about six hours and wake
up fully recovered. Rarely, drowsiness may
be followed by coma and collapse, and death
may occur from respiratory paralysis.
Insanity in India is often attributed to the
chronic use (addiction) of this drug in any
form, and is known as hashish insanity. In
some cases, delusions of grandeur or
persecution develop. The addict is likely to
commit sexual jealousy crimes of a
 638 Textbook of Medical Jurisprudence Forensic Medicine and Toxicology

homicidal nature. Following the continued and charas are sometimes used as stupe­
use of cannabis or rarely after its consump­ fying poisons prior to robbery, kidnapping
tion for the first time, he may run amok. and rape.
Fatal dose and fa ta l period: The minimum Impaired judgement trom marihuana
lethal dose of charas is about 2.0 gm, of use may lead to accidents, sexual excesses,
ganja about 8.0 gm, and of bhang about violence, and crime. Rarely, the victims run
10.0 gm per kilo body weight. Death may amok. This is a condition resulting fromthe
occur in about 12 hours in acute poisoning. continued use of cannabis or even its use
for the first time. It is characterised by a
Treatment: This is on the same lines as other
frenzied desire on the part of the person to
narcotics. Broadly, it consists in washing
commit murders. A number of individuals
out the stomach with warm water; hypo­
are killed, the first ones being those against
dermic injection of strychnine; strong tea
whom the assailant has some real or
or coffee by mouth or per rectum; and
imaginary enmity, followed by others who
artificial respiration, if necessary. Saline
are in the way, until the homicidal tendency
purgatives may be helpful.
lasts. The person may then commit suicide
Postmortem appearances: There are no or surrender himself to the police.
characteristic findings. The usual appea­
Ganja is taken to steady the nerves before
rances of asphyxia are found.
performing some bold act, e.g. homicide.
Medicolegal aspects: Most cases of poisoning Charas and ganja are sometimes used to
are accidental or due to overindulgence. Its dope cigarettes. Smoking such cigarettes is
use in chocolates causes intense craving stated to improve memory recall. Sadhus
among children for its euphoric effects. The and temple poojaris (priests) use them to
'Bhola Manucca' chocolates sold near a get into a religious mood. Majun and charas
school in Bombay, India, which caused a are used by road poisoners to stupefy
mishap were found to contain THC. Majun persons to facilitate robbery.
 55 Spinal Poisons
This group of poisons act mainly on the
j spinal cord. The action may be a stimulant
one resulting in the production of spasms
or a depressant one resulting in paralysis
and loss of sensation. Strychnine is an
| example of the former variety of poison and
gelsemium of the latter.
STRYCHNOS NUX-VOMICA (KUCH1LA)
j Strychnine is a powerful alkaloid obtained
I from the seeds of strychnos nux-vomica
(Fig. 55.1) and other species of strychnos
plants which grow in India. The ripe fruits
| of the plant contain seeds which are
poisonous. The seeds are hard and flat,,
about 2 cm in diameter and cm in
thickness, and slightly convex on one side
and concave on the other. They are
[ yellowish-brown in colour and have a
shining hard pericarp (outer coat) covered
| withfine silky hair. They are intensely bitter
in taste and contain the active principles
strychnine, brucine and loganin. The bark,
wood and leaves of the plant contain
brucine but no strychnine. Brucine has the
Fig. 55.1: Seeds of strychnos nux-vomica.
(Courtesy: Dr NK Mohanty)
639
same physiological actions as strychnine
but of a much milder degree (5-10%). The
amount of loganin that is present in the
seeds is in too small a quantity to exert any
substantial toxic effects.
Strychnine stimulates all parts of the
central nervous system and particularly the
anterior horn cells of the spinal cord
causing greatly increased reflex excitability.
Normal inhibition of spread of motor cell
stimulation is lost so that any slight stimulus,
such as noise, light, or air breeze, causes
violent reflex generalised muscle spasms.
Q. 55.1. Describe the signs, symptoms,
differential diagnosis, treatment, and
autopsy appearances of a typical case
of strychnine poisoning.
Symptoms and signs: If unbroken nux-
vomica seeds are ingested, they are not
poisonous as the hard pericarp is not
soluble in the digestive juices. If broken
seeds are taken or the seeds chewed, there
is an intensely bitter taste in the mouth.
Within 15 minutes to an hour, symptoms
of poisoning appear. The patient is anxious
and restless. He may complain of stiffness
of muscles before typical convulsions
occur. These convulsions are at first clonic
(intermittent) and then tonic (sustained) in
nature. They affect simultaneously both the
flexors and extensors. During this stage, the
muscles become so stiff and rigid that the
body is arched, with only the back of the
 640 Textbook of; Medical Jurisprudence, Forensic Medicine and Toxicology

head and heels touching the ground. This 1 at at dose and fa ta l period: Ingestion of
state is known as opisthotonos. Sometimes, one crushed seed or about 15-30 mg 0f
the body is curved forward (emprosthotonos) strychnine, that is, the alkaloid content of
or sideways (pleurothotonos). The chest is one seed of nux-vomica is fatal. The usual
more or less fixed so that breathing is fatal period is 1-2 hours.
difficult and cyanosis ensues. Blood-stained
Treatment: The patient should be kept in
froth may be seen at the mouth. The facial
bed in a dark, quiet room. Quick anaes­
muscles contract into a fixed grin, the so-
thesia with chloroform, or an intravenous
called risus sardonicus and eyes appear
barbiturate, if spasms permit, should be
prominent and staring. After about a
effected. The stomach is then washed out
minute, the convulsion passes off and the
with a dilute solution of potassium per­
muscles are completely relaxed. The patient
manganate. A suspension of animal char­
looks comparatively normal, though some­
coal should be introduced to adsorb any
what exhausted, and breathing is resumed.
free strychnine and afterwards removed.
This remission is only temporary. As
Tannic acid may be used, if charcoal is not
poisoning progresses, spasms increase in
obtainable. Barbiturates, likephenobarbitone
severity, duration, and frequency. Any
sodium, sodium amytal, etc., act as anti­
sound or movement will elicit a spasm.
dotes and should be given intravenously
Death usually supervenes either during a
in doses of 500-750 mg, and repeated in
spasm and is due to asphyxia from spasm
similar or lesser dosage as often as required.
of respiratory muscles, viz. diaphragm,
The quantity should be sufficient to put the
thoracic, and abdominal muscles or from
patient to sleep or if convulsions are present,
exhaustion due to repetition of spasms. The
enough to stop them. A mild convulsion
mind remains clear till the end, the patient
experiencing extreme pain during con­ should be awaited before repeating the
vulsions. Death is incredibly painful. dose. Avertin anaesthesia per rectum in a
dose of 250 mg, repeated as required, is
Diagnosis: Strychnine poisoning may in
very helpful. Other useful drugs include
some respects resemble tetanus, epilepsy
mephenesin (mynesin), a muscle relaxant
and hysteria. Epilepsy is to be distin­
by slow intravenous drip in a dose of 3 mg/
guished by the loss of consciousness and
kg body weight, and intravenous diazepam
clonus, and hysteria by the character of the
in a dose of 2.5 mg. The former acts by
convulsions. The chief differentiating
paralysing the voluntary muscles while the
points between strychnine poisoning and
latter acts as an anticonvulsant by inhibiting
tetanus are given in Table 55.1.
the polysynaptic reflexes in the spinal cord
Table 55.f: Differentiating points between strychnine and is preferable to barbiturates as it causes
poisoning and tetanus less respiratory depression. Artificial
Strychnine Tetanus respiration, oxygen and supportive therapy
1. History of poisoning History of injury may be necessary.
2. Onset is sudden Onset is gradual
3. Generalised convulsions Lock jaw Postmortem appearances: These are those
4. Chest fixed during Not so of asphyxia. Rigor mortis sets in almost
convulsions immediately after death and passes off
5. Complete relaxation in Relaxation between the early. The remains of the seeds may be
between seizures spasms is never complete
found in the stomach. Strychnine resists
6. Ends fatally in a few hours Death rare within a few
few hours putrefaction and can be detected from
7. Chemical analysis reveals Not so viscera in exhumed putrefied bodies. In
the poison deaths from suspected strychnine
 Spinal Poisons 641

poisoning, brain and spinal cord should be rare on account of the intensely bitter taste
preserved for analysis in addition to usual and the convulsions that follow rapidly
viscera. after ingestion, but has been recorded.
M edicolegal aspects: Poisoning from Suicide with strychnine is rare because
strychnine is mostly accidental from its use death is incredibly painful. Nux vomica
as an aphrodisiac, from an overdose of a seeds are used to destroy cattle. Strychnine
medicinal preparation, or when children is used to kill stray dogs, as a rodenticide,
eat the seeds out of curiosity. Homicide is and sometimes as an arrow poison.
56
Peripheral Nerve Poisons
These act especially on the end-plates of the
motor nerve terminals. Poisoning from
them is very rare. The important poisons
in this group are curare and conium.
CURARE_________________ ____________
Curare (urare, woorara), a black resinoid
mass, almost wholly soluble in water, is
obtained from the bark and wood of the
plant strychnos curare. The active
principles are the alkaloids curarine or
curarina and curine. Curare is used in
therapeutics as a muscle relaxant and to
prevent violent convulsions. It paralyses
motor nerve endings in voluntary muscles
by interfering with the production of
acetylcholine. Like snake venom, it causes
symptoms when injected or absorbed
through an injured surface but not when
swallowed.
Sym ptom s and sign s: The voluntary
muscles become paralysed and the affected
person is unable to move. The muscles of
respiration become involved and death
follows from asphyxia. The mind remains
clear till the end.
Fatal dose and fa ta l period: 30-60 mg of
curare is fatal in about an hour or two.
T reatm ent: If the drug is applied to a
wound or introduced by an arrow, a
ligature should be applied at the proximal
end and the poison washed out with a
642
solution of potassium permanganate or
sucked out with impunity provided there
is no injury to the lips, tongue or gums.
Prostigmine is a physiological antidote
and its intravenous administration in a
dose of 2 ml of 1 in 2,000 solution has been
recommended. Artificial respiration with
oxygen may be necessary.
Postm ortem appearances: These are those
of asphyxia.
M e d ic o le g a l a s p e c t s : Poisoning from
curare is mainly accidental. Curare is used
as an adjunct in anaesthesia to bring about
muscle relaxation, and to prevent injury in
shock therapy in certain mental diseases,
and fatalities from such use are rare. Curare
may be used in strychnine poisoning. The
use of arrows poisoned by curare is well-
known.
CONIUM (HEMLOCK) ___________
Also known as spotted hemlock or conium
maculatum, this is an umbelliferous plant
and is so-called from the purple spots on
its stem. It grows in waste places. The
whole plant has a mousy odour which is
intensified by crushing the leaves or stems.
All parts of the plant are poisonous. The
toxic properties are due to the alkaloids
coniine and methyl. Coniine which causes
paralysis of the motor nerve terminals in
the muscles, gradually spreading to the
motor cells of the cord and brain. A
tincture, extract and succus are made from
the plant.
Symptoms and signs: There may be some
gastric irritation which causes pain and
vomiting. This is followed by muscular
weakness and gradually increasing
paralysis due to depression of the motor
nerves. The lower limbs are first affected
and the paralysis ascends till the muscles
of respiration are affected. Delirium,
convulsions or coma may supervene and
the patient dies of asphyxia due to respira­
tory paralysis. The breath may have a
mousy odour. The mind remains clear
almost till the end.
Fatal dose and fatal period: A piece of
plant about 1 cm in diameter may produce
fatal poisoning within a few hours.
Treatment: This is on general lines and
consists of lavage of the stomach with a dilute
solution of tannic acid, artificial respiration,
oxygen inhalations, and stimulants.
Postmortem appearances: These are those
of asphyxia. The remains of the roots or
leaves should be looked for in the stomach
contents and preserved for laboratory
analysis.
Medicolegal aspects: Symptoms may be
caused by ingestion, injection, or even
inhalation as coniine is a volatile alkaloid.
Poisoning by it is mostly accidental, chiefly
from the plant being mistaken for parsley
or some other harmless herb. One case is
recorded of a child who died of poisoning
from blowing whistles made of conium
twigs. This plant is of great historic interest.
The ancient Greeks used the juice of the
fruit or the infusion of the leaves as a state-
poison. Socrates was killed by the use of
hemlock.
57
Cardiac Poisons
These are poisons having an action mainly
on the heart, either directly or through the
nerves. Digitalis, oleander, aconite and
nicotine are important in this group.
DIGITALIS PURPUREA (DIGITALIS
OR FOXGLOVE)______________________
This is a poisonous plant. Its roots, leaves,
and seeds contain several glycosides of
which digitoxin, digitalin, digitalein, and
digitonin are the most poisonous and have
a cumulative action. The glycosides act
directly on the heart muscle and improve
the function of a failing heart. The normal
heart is affected very little unless toxic doses
are administered. Its main toxic effects are:
irritation of the stomach, slowing of heart
rate leading to heart block, extrasystoles,
and ventricular fibrillation.
Symptoms and signs: Toxic symptoms by
overdose or more insidious cumulative
action are indicated by nausea, vomiting,
abdominal pain, diarrhoea, depression,
headache and giddiness. Toxic effects on
the heart include bradycardia (the rate may
fall to 20 per minute), heart block, extra­
systoles, and fibrillation. There is a feeling
of faintness and precordial oppression. The
respirations become slow and sighing. The
patient becomes drowsy, and the condition
may deepen into coma. Convulsions may
precede death.
644
Fatal dose and fa ta l period: The usual fatal
dose is 15-30 mg of digitalin or 4 mg of
digitoxin. The fatal period varies from half
an hour to 24 hours.
Treatm ent:The stomach should be washed
with a solution of tannic acid. If parts ofj
the plant have been taken, the bowels!
should be evacuated. Atropine in a dose of
0.6 mg should be given hypodermically tq
combat bradycardia. Potassium salts may "
be given to reduce extrasystoles provided
the kidney function is normal. Specific
antidotes, such as novocaine or propranolol
for digitalis-induced arrhythmias, are
helpful. Trisodium EDTA may help to
lower serum calcium. The rest of the
treatment is symptomatic. ECG monitoring
is necessary as a guide to treatment.
Posttnortem appearances: These are not
characteristic. There may be irritation of the
gastric mucosa and digitalis leaves or seeds
may be found in the stomach. The seeds
are reddish brown, remarkably small, and
somewhat angular in shape, with peculiar
markings. These characteristics make it
easy to distinguish them from seeds of other
poisonous plants, such as hyoscyamus,
dhatura, belladonna, etc.
M edicolegal aspects: Poisoning is mainly
accidental from an overdose of a medicinal
preparation or from eating leaves by
mistake. Digitalis is a cumulative poison
 Cardiac Poisons 645

and persons taking it for a long time may

suddenly develop symptoms of poisoning.
Homicidal poisoning is recorded and it is
interesting to note that no suspicion of
poisoning may arise in such cases. Rarely, it
may be used to simulate heart disease, and
result in death.
Anoldlady ingested about 50 tablets of digoxin
forheart disease, onone afternoon, and died the
same evening.
Ayoungmanswallowedadecoction(concentrated
water extract) of foxglove by mistake for a
purgative medicine. He was seized with
vomiting, pain inthe abdomen and purging. He
becamedrowsy, his pulse became irregular, and
pupils were dilated. Convulsions preceded his
death, which occurred after 22 hours.
Anurse, employed tolookafter apatient, forged
certainwills, andpoisonedher patient withtoxic
doses of digitalis, to benefit financially from
these wills.
Mr KA, a 23-year-old student of Kanpur (India)
feignedheart disease byingestionofa toxic dose
of digitalis to frighten his fiancee. He was
admitted to the hospital for treatment of heart
disease. Diagnostic ECG changes were found.

OLEANDER (KANER)____________________
The oleander plant grows wild in India. Its
graceful flowers are used as offerings in the
temples. There are two varieties, viz. the
white (Nerium odorum), and yellow (Cerbera
thevetia). The white one bears white or pink
flowers and is known as Nerium odorum or
true oleander in contradistinction to the
yellow oleander, which bears yellow bell­
shaped flowers (Figs 57.1 to 57.3). In addi­
tion, the yellow oleander bears globular
fruits about 5 cm in diameter, containing a
single nut, triangular in shape and light
brown in colour. The nut contains pale
yellowseeds (Fig. 57.4). A plant closely allied
to Cerbera thevetia is Cerbera odollam (Dabur,
Dhakur). It also grows wild all over India.

Nerium Odorum (White Oleander. Kaner)

All the parts of the plant are poisonous. The Fig. 57.3: Cerebra thevetia. (Courtesy: Dr SV
active principle is nerin consisting of three Phanindra)
646 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
Fig. 57.4: The triangular nuts of yellow oleander
having two cells, ea ch containing a pale
yellow seed
glycosides, viz. neriodorin, neriodorein and
karabin, the last one being so-called after
the vernacular name of the plant. The
principal action of neriodorin is similar to
that of digitalis causing death from cardiac
failure. Neriodorein causes muscular
twitchings and tetanic spasms more power­
ful than those of strychnine. Karabin acts
on the heart like digitalis and on the spinal
cord like strychnine.
Sym ptoms and signs: Vomiting, pain in the
abdomen, and frothy salivation usually
occur, followed by restlessness. The pulse
is slow and weak, and respirations hurried.
There is difficulty in swallowing.and often
lock jaw. Muscular twitchings of the
extremities deepen into tetanic spasms,
frequently affecting one side more than the
other. This is followed by exhaustion,
drowsiness, coma and death from heart
failure.
F a ta l d o se and fa t a l p erio d : About 15
grams of the root can kill an adult in about
24 hours.
Treatment: This consists in washing out the
stomach and treating the symptoms.
Administratioribf an anaesthetic is usually
necessary. Morphine injection seems to be
beneficial.
P ostm ortem appearances: These are not
specific. Petechial haemorrhages on the
heart are a characteristic feature. Nerium
odorum resists heat and can, therefore, be
detected even from the burnt remains of the
dead body.
M edicolegal a sp ects: Suicide with decoc­
tion (concentrated water extract) from root,
leaves, or fruit of Nerium odorum is common
among village girls, in certain parts of India
on account of dowry problems or matri­
monial mishaps. The root is commonly
used both locally and internally for procuring
abortion. Accidental poisoning is sometimes
met with when (1) any part of the plant is
used as a lovephilter (increases attraction!
between the giver and taker), (2) the
decoction of the leaves is applied externally!
to reduce swellings, (3) the root is used -
internally as a remedy for venereal!
diseases, or (4) the root in the form of a
paste is used in treatment of cancerous!
conditions and other growths. The use of
Nerium odorum as a cattle poison has been
recorded. For this purpose, it is mixed with
the fodder or a rag smeared with the juice
of the root is thrust in the animaTs rectum.;
Yellow O le an d e r
(C e rb e ra Thevetia, Pila Kaner)
This plant (Fig. 57.3) also is highly poiso­
nous. The active principles are the three
glycosides, viz. thevetin, thevotoxin and
cerberin. Glycosides are substances found
in plants and are composed of a sugar and
a non-sugar compound, the latter having a
toxicological action. Thevetin and thevo­
toxin are isolated from the kernels of the
seeds. Thevetin and cerberin reside in the
milky juice which exudes from all the parts
of the plant. Thevetin is a powerful cardiac
poison. Thevotoxin is less toxic than
thevetin and resembles the glycosides of
digitalis in action. Cerberin has an action
like strychnine.
Sym ptom s and signs: These consist of a
burning sensation in the mouth with
 Cardiac Poisons;
tingling of the tongue, dryness of the throat,
vomiting, diarrhoea, headache, dizziness,
dilated pupils, irregular action of the heart
somewhat resembling that due to digitalis,
drowsiness, collapse, coma, and death.
Tetanic convulsions are occasionally
observed.
Fatal dose and fa ta l period: 8 to 10 seeds
or 15 to 20 gm of the root prove fatal to an
adult, death ensuing within 24 hours.
Treatment: This is the same as that of
poisoning by Nerium odorum. Good results
havebeen achieved by intravenous adminis­
tration of molar solution of sodium lactate
to combat acidosis and 5 per cent glucose
solution with 1.2 mg of atropine, 2 ml of
adrenaline 1:1000 and 2 mg of noradrena­
line (if blood pressure is low) to counteract
heart block.
Postmortem appearances: These consist of
signs of gastrointestinal irritation, conges­
tion of the various organs, generalised
engorgement of veins and subendocardial
ecchymoses. Yellow oleander resists
putrefaction and can be detected even years
after death in exhumed putrefied bodies.
Medicolegal aspects: The root and seeds of
yellow oleander are used for suicide by
women in certain parts of India, on account
of dowry problems or matrimonial mishaps.
Theyare also used for abortion. Cattle poison­
ing occurs when the seeds are crushed,
mixed with fodder, and fed to the animal.
CERBERA ODOLLAM
(DABUR, DHAKUR, PILIKIRB1R)____________
This plant grows wild all over India. The
fruits resemble unripe mangoes. A toxic
milky juice comes out of all the parts of the
plant. The active principles are a glycoside
cerberin and a weak alkaloid cerebroside
having a digitalis like action. The symp­
toms include gastrointestinal irritation and
cardiac toxicity. There is bitter taste in the
mouth with nausea, vomiting, abdominal
pain and diarrhoea. These are generally
647
followed by irregular respiration, gSieral
weakness, bradycardia, collapse, and death
from heart failure.The fatal dose is kernel
of one fruit and the fatal period 1 to 2 days.
Treatment is similar to poisoning by Cerbera
thevetia. Poisoning is common in Tamil
Nadu and Kerala in India where the kernel
of the fruit is eaten by women to commit
suicide, mostly on account of dowry prob­
lems or matrimonial mishaps. Accidental
poisoning occurs in children who eat the
fruit in mistake for an edible onegThe j
powdered kernel may be added to algdhol
with homicidal intent..'
ACONITE (MITHAZAHAR, M1THA BISH f
This plant is known as Aconitum namellus j
or monkshood. In India, it grows ia the
Himalayan ranges. All parts of the plant
are poisonous, the root being most potent.
The dry root (Fig. 57.5) is tapering, shghtly
arched, usually shrivelled, and with
longitudinal wrinkles. It is 5-10 cm long,
1-2 cm thick at the upper extremity/ and j
dark brown externally. It is white!
internally, when freshly cut, but becomes]
pink on exposure to air. It has an acrid,
sweetish taste, which gives it the name
Mitha Bish (Mitha = sweet; Bish = poison).
It is sparingly soluble in water. The chief
active principle is the alkaloid aconitine, a
very potent poison; the other active princi-]
pies are picraconitine, pseudoaconitine and
aconine. It stimulates and then depresses
the myocardium, smooth muscles, skeletal
muscles, central nervous system, and
peripheral nerves.
 648 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology - ^
Q. 57.1. Describe the symptoms, signs,
treatment, postmortem appearances, and
medicolegal aspects of aconite poisoning,
Symptoms and signs: Contact with any of
the preparations of aconite produces
immediate tingling and numbness which
extend over the whole body. There is
tingling and numbness in the lips, mouth,
tongue and pharynx, followed by saliva­
tion, nausea, vomiting, and diarrhoea. The
patient feels giddy, his vision and speech
are impaired, the limbs become weak, and
he is unable to stand or walk. Twitching of
the muscles and convulsions may occur.
The pulse is slow and irregular (vagal
stimulation) when collapse takes place. The
breathing is rapid at first but soon becomes
slow, laboured and shallow. The pupils
alternately contract and dilate but remain
fully dilated in the later stages. Mind
remains clear till the end. Death ensues
from cardiac arrhythmia or respiratory
paralysis.
Fatal dose and fa ta l period: One gram of
the root, 250 mg of the extract, 25 drops of
the tincture, or 4 mg of the alkaloid prove
fatal. The average fatal period is about six
hours.
Treatment: Gastric lavage should be affected
with a solution of tannic acid (10 gm in
2 litres of water) or strong tea or potassium
permanganate (1:1000) to precipitate any
remaining alkaloid. The heart may be
supported by hypodermic injections of
atropine 1 mg, or digitalin 0.25 mg. Cardiac
arrhythmias may require 50 ml of 0.1%
novocaine given slowly intravenously.
Artificial respiration and oxygen inhalation
may be necessary. The rest of the treatment
is symptomatic.
Postmortem appearances: The findings are
not characteristic. Remnants of the plant or
root may be found in the contents of the
stomach. The odour of chloroform may be
perceived when the liniment is swallowed.
Aconite is largely destroyed in the body
and also by alkalis. It is, therefore, difficult
to detect it after death. The alkali present
in wood ash meant to preserve the vomit
may destroy aconite. Therefore, acetic acid
is added to rectified spirit in the ratio of
1:2 and such acidified spirit is added to
preserve the vomit.
M edicolegal aspects: Aconite is one of the
most potent poisons known to mankind.
Accidental poisoning occurs from (1) eating
the root in mistake for horse-radish root,
(2) quack remedies, (3) therapeutic applica­
tion of liniment containing aconite or
drinking it, and (4) when added to liquori
for a greater kick.
Homicidal cases are not uncommon. It
is sometimes administered to the victim |
with betel leaf to disguise its tingling tasjg
Aconite is said to be useful to hunters|fo
destroy tigers and elephants (arrow poison),
to the rich to destroy troublesome relatives,
and to jealous husbands to destroy unfaith­
ful wives. It offers the following advantages
as a homicidal poison:
1. It is cheap and easily available.
2. The lethal dose is small, and the fatal I
period is also short.
3. Its colour can be disguised by mixing it
with pink-coloured drinks.
4. Its taste can be masked by mixing it with
sweets or by giving it with betel leaves.
5. It is largely destroyed in the body and,
therefore, cannot be detected by chemical
analysis.
The root of aconite is extensively used
by tribals as an arrow poison. The use of
aconite root as a cattle poison has been
recorded. Sometimes the root is used as an
abortifacient.
NICOTINE (TOBACCO)____________ _
Q. 57.2. Discuss nicotine (tobacco)
poisoning.
Tobacco is the leaf of the tobacco plant,
Nicotiana tabacum . The dried leaves
 Cardiac Poisons 649

(tambaku) are chewed or used in the form of cancer of the mouth, tongue, throat,
smoke or snuff. All parts of the plant except larynx, and lungs is common. Non­
theripe seeds contain the alkaloid nicotine, thrombocytopenic purpura has been
apyridine derivative, as the active principle. reported after smoking mentholated
Nicotine is used extensively in agricultural cigarettes.
and horticultural work as fertilisers,
Fatal dose: The fatal dose is about 60 mg
fumigants, and insecticide sprays. Poison­
of nicotine or about 2 gm of tobacco. One
ing is caused by absorption either through
cigarette contains one gram of tobacco,
intact or broken skin, by inhalation, or
about half the lethal dose! A teaspoonful
ingestion. Nicotine first stimulates, then
of insecticide is fatal.
depresses, and later paralyses autonomic
ganglia. Fatal periods: Death may occur rapidly in
a few minutes when nicotine is swallowed.
Symptoms and signs: Mild poisoning
In some, it may be delayed for a few
occurs when tobacco is chewed or smoked hours.
for the first time or when insecticide spray
has been inhaled. Dizziness, nausea, Treatment: If nicotine has contaminated the
vomiting, headache, perspiration, general skin, it should be removed by flooding the
weakness, and mild rise in blood pressure skin with water and scrubbing it vigorously
withincreased pulse rate may occur. These with soap. If it is ingested, the stomach
symptoms subside in a few hours. should be washed with warm water
containing activated charcoal, tannin ;
Acute poisoning occurs when nicotine is
(strong tea), or potassium permanganate. I
absorbed in poisonous amounts. There is
burning in the mouth, throat, and stomach, A purgative, such as sodium sulphate, I
15 gms in 100 ml of water is useful. The y
followedby rapid progression of symptoms
function of the heart will need careful
ofmild poisoning, passing into prostration,
attention; artificial respiration and oxygen
\ convulsions, respiratory slowing, cardiac
may be necessary. The rest of the treatment
irregularity and coma. Death may occur
from cardiac arrhythmia, exhaustion, or is symptomatic. Those with chronic nicotine
poisoning should be removed from the risk
respiratory failure.
of further exposure. Patients with leuko­
Chronic poisoning results from the plakia, hyperacidity, peptic ulcer, respira­
continued use of tobacco by chewing, tory problems, high blood pressure, angina,
smoking or from exposure to nicotine thromboangiitis obliterans, and tobacco
during processing, storage or insecticide amblyopia should stop smoking perma­
spray. Those who chew tobacco suffer from nently.
chronic cough, laryngitis, pharyngitis, and
bronchitis; and those who handle it suffer Postmortem appearances: These are those
from dermatitis. In all, tobacco stains on of asphyxia. There may be characteristic
teeth, bad odour in breath, angiospasms smell in the stomach with brown dis­
and muscular tremors may be found. In colouration of its wall, if nicotine has been
addition, there may be amblyopia, blind­ swallowed or of the skin, if it has been
ness, cardiac arrhythmia with extrasystole spilledJBepending on the strength of the
and chest pain suggesting angina pectoris. poison, there may be gastric irritation^
Occlusive thromboangiitis obliterans is and pulmonary oedema. Nicotine resists
common and an increase in the incidence putrefaction.
 textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

M edicolegal aspects: Nicotine is a drug of (3) absorption through skin when applied
addiction and leads to psychological depen­ as a poultice, (4) excessive smoking, or
dence. Its use leads to serious, oral, dental, (5) exposure to'fertilisers, insecticides, and
respiratory, and cardiac problems resulting fumigants. Malingerers soak tobacco leaves
in chronic disability and decreased life in water and bandage them in the arm
expectancy. In many cases, the poisoning pits to become sick with fever in the next
is mainly accidental and occurs from 6-8 hours and avoid duty. Tobacco has
(1) chewing a large dose, (2) ingestion of been used for infanticide in certain parts of
the decoction (concentrated water extract), India.
 Asphyxiants (Irrespirable Gases)
Asphyxiants mainly produce respiratory
embarrassment. The important asphyxiants
amongst others include carbon monoxide/
carbon dioxide, hydrogen sulphide and
some war gases. Carbon monoxide reduces
the oxygen carrying capacity of the blood;
carbon dioxide produces oxygen lack in the
tissues; hydrogen sulphide paralyses the
respiratory centre.
CARBON MONOXIDE
Q. 58.1. Mention the sources, clinical fea­
tures, treatment, and postmortem ap pea­
rances of carbon monoxide poisoning.
Add a note on medicolegal aspects.
This is a colourless, odourless, non-irritant
gas which cannot be perceived by the senses.
It is formed by incomplete combustion of
carbon and organic matter. The principal
sources are: water gas, and illuminating gas;
gases resulting from explosion in mines,
from dynamite and other high explosives;
fromimproperly regulated oil heaters, large
oil lamps, and gas heaters without efficient
fiues; and from gases formed in crank cases,
exhaust of vehicular engines, cycle engines,
and in burning houses.
The affinity of carbon monoxide for
haemoglobin is about 200-300 times greater
than that of oxygen. It displaces oxygen and
combines with haemoglobin to form
carboxyhaemoglobin which is a relatively
stable compound. This results in tissue
anoxia. It was formerly thought that the
toxicity of the gas is due to its anoxic action
but recently Lo Menzo and Pentelez have
shown that dissolved CO interferes with
some vital cellular enzymes.
Symptoms mid signs: These depend upon
the degree of saturation of carbon monoxide
in the blood. The approximate relationship
between carboxyhaemoglobin level and
clinical manifestations is summarised in
Table 58.1.
Saturation of haemo­
globin with CO
0- 10% No appreciable symptoms
10-20% Shortness of breath on exertion,
mild headache, lassitude and
flushed skin
20-30% Throbbing headache, buzzing in
theears. Breathlessness, muscu­
larweakness andincoordination,
30-40%
40-50% All symptoms intensified. Maybe
mistaken with drunkenness.
Incoordination, staggering, mental
confusion, loss of memory, palpi­
tation and dyspnoea
50-70% Intermittentasphyxial convulsions,
coma, Cheyne-Stokes respiration,
respiratory para-lysis and death
Above 70% Rapidly fatal due to respiratory
 652 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology
The gas being odourless and non-
irritant, the onset of symptoms is insidious.
A feeling of lassitude merges into a state of
drowsiness with a dulling of the senses
which is followed by stupor and coma. The
rapidity with which these symptoms
develop depends on the concentration of
the gas and the length of exposure. If a
person breathes carbon monoxide in a low
concentration for a considerable length of
time, especially during sleep, he will be
poisoned just as effectively as though he
were exposed to a high concentration for a
shorter period. When a low concentration
of gas is inhaled, coma may not supervene
immediately but the victim may not be able
to escape from the dangerous atmosphere
and save himself as his senses are dulled,
judgement impaired, and he does not
appreciate the danger he is exposed to. In
the event, he is able to appreciate the
danger, he cannot escape on account of
muscular weakness and incoordination. He
does not call for help due to lethargy and
mental confusion. When a high concentra­
tion of gas is inhaled, there is sudden
muscular weakness, followed by rapid
coma and death. The patient may show
reddish patches on the skin and occasio­
nally blisters. If recovery follows after
coma, its completeness varies with the
depth of anoxia and the length of time
during which the brain suffered. Confusional
states are common and disorientation or
amnesia sometimes occurs. Symmetrical
softening of the basal nuclei due to pro­
longed anoxia may cause Parkinsonism.
The patient may also show symptoms
referable to the respiratory or cardiac
systems.
Fntnl dose and fa ta l period: When a person
is at rest, 0.1% of carbon monoxide in the
atmosphere will result in stupor and coma
in two and a half to three hours, but with
exercise an hour would suffice. Al%
concentration will result in stupor and
coma in 15-20 minutes. The debilitated,
diseased or drunk may succumb to lower
saturations.
I refitment: The patient must be removed
at once to fresh air and body warmth
maintained. No further treatment may be
necessary, if the patient is conscious and
breathing. Giving oxygen speeds elimina­
tion of CO. Artificial respiration isnecessary,
if breathing is even slightly irregular.
Whole blood transfusion is useful in grave
cases. Prophylactic antibiotics against lung
infection are helpful. Even after normal
respiration has returned, the patient should
be kept at absolute rest till all acute symp­
toms disappear.
Postmortem appearances: Externally, fine
froth may be seen at the mouth and nose.
The colour of the skin, especially in areas
of postmortem staining, and in fair-skinned
persons, is bright cherry red, if saturation
of CO in biood exceeds about 30%. Below
20%, such colouration is not visible. Skin
blisters may be seen on those areas of the
body in contact with the ground or where
skin is in apposition, such as axillae and the
inner side of the thighs. The lesions are due
to hypoxia. Internally, blood, tissues and
viscera are of a bright cherry red colour, if
there is more than 5 gm COHb/lOO ml of
blood. Serous effusions are common. The
brain may be oedematous and petechial
haemorrhages may be seen on the meninges.
Necrosis and cavitation of the basal ganglia,
notably the putamen and globus pallidus,
may be found in cases of prolonged
hypoxia. The lungs may be oedematous or
show bronchopneumonia. Myocardial
degeneration, and necrotic patches in the
cardiac muscle are not uncommon.
Carboxyhaemoglobin is stable and can be
detected even in highly putrefied bodies.
In cases of suspected carbon monoxide
poisoning, a layer of 1-2 cm of liquid para­
ffin should be added immediately over the
collected blood sample to avoid exposure to
air.
654 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

is a depleted oxygen cylinder and a new Supportive treatment with stimulants is

carbon dioxide supply working through a necessary.
common union. Failure to recognise serious P ostm ortem appearances: The general
respiratory depression and cyanosis may signs of asphyxia are present. The offensive
provide cause for unexpected deaths from smell of the gas is noted on opening the
carbon dioxide under anaesthesia. body. Postmortem staining is bluish green
in colour and there is a tendency to rapid
HYDROGEN SULPHIDE___________________ putrefaction. In some cases, the colour of
Hydrogen sulphide or sulphurated hydro­ organs is darker brown than usual due to
gen is a colourless gas with a smell of rotten the postmortem combination of hydrogen
eggs. It is found where sulphur containing sulphide and methaemoglobin.
organic material is undergoing decay, as in
M ed ico leg a l a sp ects: Poisoning from
sewers, cesspools, privies, and tannery
hydrogen sulphide is always accidental,
vats. It is produced in the manufacture of
causing a number of deaths in sewer
artificial silk and other industries where
sulphur is used. It is formed in human workers.
intestine during life and in the body after
death when putrefaction sets in. WAR GASES___________________ ___
The toxicity and rapidity of action are Q .5 8 .2 . E xp lain th e term war gases.
comparable to hydrocyanic acid. It converts C las sify th e m . Briefly describe their
oxyhaemoglobin of the blood to methaemo- actions.
globin. In life, this action does not proceed The term war gases is inappropriate as all
further and there is no formation of the substances used are not gases nor used
sulphmethaemoglobin. This occurs princi­ in times of war only. The term is meant to
pally after death. signify an agent suitable for destruction or
Symptoms and signs: If pure hydrogen damage, according to need, e.g. in war, or
sulphide is inhaled, death occurs at once to disperse unruly mobs. These substances
from paralysis of the respiratory centre. If may be either true gases, smokes, vaporised
the concentration is less intense, it produces liquids, or fine powders. An ideal war gas
giddiness, nausea, pain in the abdomen, must have the following qualities:
laboured breathing and irregular heart 1. It must be capable of being manufac­
action. There maybe delirium, convulsions tured cheaply in enormous quantities,
or coma preceding death which occurs preferably as a by-product of some
from asphyxia. Pulmonary oedema and industry.
bronchopneumonia may occur. In lesser
2. It must be definitely toxic in low concen­
concentrations, there is conjunctivitis,
tration, so that it is effective against
irritation of the air passages, a feeling of
troops distributed over a wide area.
languor and sleepiness, and death may
occur during sleep without the patient 3. The substance must be heavier than air
regaining consciousness. A 0.2% concentra­ so that it will not be easily dispersed.
tion in air would be fatal in a few minutes. 4. It must be capable of enough volatilisa­
Treatment: The patient should be removed tion to pervade the terrain which is
at once to fresh air and body warmth assailed.
maintained. Artificial respiration with 5. Its chemical composition must be stable
oxygen may lead to recovery unless the and not of a type to corrode the con­
respiratory centre is very depressed. tainers in which it is stored.
 Textbook at Modlcal Jurlspfudoncu, fotonslc Modlcloe and Toxicology
arsine). Both are volatile irritant liquids,
mustard having the smell of garlic and
lewisite the smell of geraniums. Mustard
gas causes severe irritation of the eyes,
nose, throat and respiratory passages. It
penetrates the clothes, and causes intense
itching blisters, and ulcers in the moist
areas of the skin, in rare instances, the
stomach is inflamed as a result of
swallowing the chemical and this results in
nausea, vomiting and gastric pain. The
lewisite repidly blisters the skin and
inflames the mucous membranes. After
absorption, it causes haemolysis of the red
cells and may produce signs of arsenic
poisoning.
The regulation gas mask protects the
wearer from inhaling the vapour but does
not protect the skin from burns, unless
special clothes are worn. The treatment is
symptomatic—removal of contaminated
clothes, washing the body with soap and
water, and attention to eyes, respiratory
irritation, and bums. BAL is a good anti­
dote for lewisite poisoning.
Stemutators: Also known as nasal irritants
or vomiting gases, these are organic
compounds of arsenic. They are fired in
artillery shells and after explosion permeate
the air and cover the landscape. The
commonly used compounds are diphenyl-
chloroarsine (DA) diphenylamine chloro-
arsine (DM), and diphenylcyanoarsine
(DC). A person inhaling the air or
swallowing food or water contaminated by
these chemicals suffers from intense irrita­
tion of the nose and sinuses with excessive
sneezing, malaise, headache, salivation
nausea, vomiting, pain in the chest and
prostration.
The regulation gas mask will protect
against the stemutators. The treatment is
symptomatic. Sodium bicarbonate is useful
as a mouth wash.
\‘i‘rvc and blood poisons: Also known as
paralysants, the substances tried have been
carbon monoxide, hydrocyanic acid, and
hydrogen sulphide. Carbon monoxide may
be formed by the combustion of the
explosive when a large shell bursts in a
dugout and causes poisoning of soldiers
trapped in such cavities. I lydrocyanic acid
and hydrogen sulphide, despite their
toxicity, are not suitable as war gases and
have not been employed in that role to any
extent.
\< .<<< "UNis; These are chemicals related to
phosphate esters in toxicity. They are
colourless and odourless volatile liquids.
Toxic effects follow inhalation, ingestion,
or absorption through skin. The chemical
causes inactivation of cholinesterase and
consequent acetycholine poisoning, similar
to organophosphorus poisoning.
Miscellaneous: Very little is known about
this group, except that gruesome tragedies
followed from "yellow/red rain" which
struck Laotian tribesmen, and MIC (methyl
isocyanate) which struck inhabitants near
Union Carbide Factory in Bhopal (India).
Yellow/red rain: Laotian tribesmen were
struck by two gases; one coloured yellow
and the other red. They experienced the
combined effects of mustard gas, phosgene,
chlorine, and nerve poison. Both the gases
made their victims feel as if their body was
going to blow up. Coughing yielded blood.
There was burning in the throat and
swallowing was painful. These symptoms
were followed by eyes turning yellow as if
the victims had jaundice, the vision
becoming blurred, and the nose tingling as
if hot pepper had been inhaled. Breathing
caused sharp pain, teeth felt loose, and the
gums smelled rotten. Any one whose bare
skin was touched by a droplet suffered
severe necrosis of the affected area and high
fever with the skin red and turning bluish
black. It took about 2 weeks to die, the
victims being in severe agony throughout.
Methyl isocyanate (MIC): This is a fairly
stable liquid below 27°C. It is highly volatile
 Asphyxiants (Irresplrc
and reacts vigorously with moisture,
alkaloids, and many common solvents. It,
therefore, must be stored under strictly inert
conditions. It is used in the manufacture of
pesticides, adhesives, and plastics. Even if
a very small dose is ingested, inhaled, or
absorbed through the skin, it usually
proves fatal. In Bhopal, India, victims dying
within48 hours of exposure complained of
severe burning in the throat, unbearable
eye irritation, chest pain, and laboured
breathing. Death was due to pulmonary
oedema. Those who survived for 5 to 6 days
experienced the original symptoms.and
neurological effects, such as motor weak­
ness, paralysis in some cases, convulsions,
coma and cerebral oedema leading to
death. Those who survived over a week
developed delayed symptoms, such as
657
shivering, dyspnoea, jaundice, weakness of
limbs, and died due to exhaustion. Those
who survived longer suffered from
fibrosing alveolitis. In pregnant women
who survived the exposure, abortion,
premature delivery, and stillbirths have
been common. Like many other agro­
chemicals, as long-term effect, MIC may
turn out to be a cancer causing and muta­
genic substance. Chemical analysis of the
blood reveals the presence of MIC, cyanide
ions, and monomethylamine in the body.
The treatment is symptomatic. It consists
of administration of hydrocortisone against
inflammation, antibiotics (tetracycline and
ampicillin) against lung infection, eye-
drops against eye irritation, and oxygen to
combat respiratory failure. Sodium thio­
sulphate may be tried as an antidote.
# 11

59. Analgesics and Antipyretics

60. Antihistaminics
61. Tranquillisers
62. Antidepressants
63. Stimulants
64. Hallucinogens
65. Street Drugs and Designer Drugs
66. Alphabetical Poison Table
59 Analgesics and Antipyretics #

The discussion under this heading is restric­ drug which lowers the temperature in
ted to four selected topics, viz. (1) drugs in cases of pyrexia. The commonly used
common therapeutic use, (2) commonly preparations in this group are: aspirin and
abuseddrugs, (3) drugs having no medicinal paracetamol.
value, and (4) street drugs or designer
drugs. ASPIRIN_________________________________
The drugs in common therapeutic use Aspirin (acetylsalicylic acid) is a white
are: (a) analgesics and antipyretics, e.g. crystalline powder with an acid taste. It is
aspirin and paracetamol (acetaminophen), one of the most common household reme­
(b) antihistaminics, e.g. antazoline, dies for pains, aches, and pyrexias.
chlorpheniramine, diphenhydramine, and
promethazine, (c) tranquillisers, e.g. Symptoms and signs: Poisoning results
chlorpromazine, meprobamate, and from idiosyncrasy or overdose. The symp­
toms include giddiness, buzzing in the ears,
reserpine, and (d) tricyclic antidepressants,
e.g. amitriptyline and imipramine. oedema of the face and eyelids, skin rash,
cyanosis, dyspnoea, and later flushed skin
The commonly abused drugs are: (a) the
and pyrexia. Aspirin irritates the mucous
stimulants, e.g. amphetamines (speed),
membrane of the stomach. Therefore,
methyl phenidate (Ritalin), and cocaine
nausea and vomiting are common, and
(crack). The others, such as drugs of addic­
there may be haematemesis and melaena
tion, substance abuse, marihuana, etc., are
due to erosion of gastric mucosa. Fatal
already discussed.
haemorrhage may occur due to hypopro-
The drugs which have no medicinal value thrombinaemia. Hyperpnoea is an important
in the present state of knowledge mainly indication of aspirin poisoning and is due
include hallucinogens, e.g. LSD, peyote, to stimulation of the respiratory centre.
mescaline, and phencyclidine. This leads to hyperventilation which in turn
Street drugs or designer drugs are those produces a respiratory alkalosis. Complex
drugs which are not obtained from legally acid-base disturbances may follow. Aspirin
manufactured sources but from surreptitious causes severe acidosis due to reduction of
ones. alkali reserve. Ketosis, albuminuria and
glycosuria are not uncommon. Hyperpyrexia
ANALGESICS AND ANTIPYRETICS_________ and encephalopathy are seen. The mental
An analgesic is a drug which relieves pain changes are called salicylate gags restless­
without inducing sleep. An antipyretic is a ness, hallucinations and convulsions. The
661
 662 Textbook of Medical Jurisprudence. Forensic Medicine and Toxicology
breath smells of acetone and a mistaken
diagnosis of diabetic coma may be made.
Dr Subrahmanyam saw an young woman
taking a single Aspirin tablet and pre­
senting with hemarthrosis and multiple
petechial haemorrhages scattered over the
body. Death may occur due to cardiac
failure, respiratory failure and hypo-
prothrombinaemia.
Aspirin in urine can be detected by
addition of a few drops of ferric chloride
when it develops a violet colour.
Fatal dose and fa ta l period: Even a small
dose may prove fatal due to idiosyncrasy.
The minimum fatal dose is 5-10 gm. The
fatal period varies from a few minutes to
several hours.
Treatm ent: Gastric lavage is carried out
with warm water and some quantity of 5%
solution of sodium bicarbonate left in the
stomach to combat the acidosis. Forced
alkaline diuresis, peritoneal dialysis, and
haemodialysis are useful. Exchange trans­
fusion may be necessary in severe cases.
Special attention should be directed to
restoration of electrolyte balance and the
possibility of potassium loss. Intravenous
fluids are required to counter the effect of
dehydration from vomiting and sweating.
Vitamin K should be given, if there is
abnormal bleeding. Blood or platelet
transfusions are very helpful.
P ostm ortem appearances: There may be
rashes on the skin. Particles of aspirin may
be seen in the stomach. The gastric mucosa
is congested and eroded. Petechial
haemorrhages may be seen at other sites in
the body due to hypoprothrombinaemia.
Pulmonary oedema is common.
M edicolegal aspects: Poisoning is generally
accidental from idiosyncrasy or over­
dosage.
Reye's syndrome:Reye's syndrome presents
acute hepatic failure and encephalopathy.
This is precipitated in children below 15
years of age, if they are patients of influenza
or chickenpox. To start with, the patient j.s
lathargic (stage I) then he becomes
stuporous and shows conjugate deviation
of eyes and sluggish pupillary reaction
(stage 11). Then he enters coma and progre­
ssive stages of coma. First he presents a
decorticate posture, later decerebrate
rigidity and inconsistant oculocephalic
reflex. Finally pupillary reaction stops, no
response is shown to painful stimuli,
oculocephalic reflex becomes negative and
assumes a flaccid posture and the end
comes soon. In cases of recovery, perma­
nent neurological deficits may hamper the
life.
PARACETAMOL (ACETAMINOPHEN)
Paracetamol, a metabolite of phenacetin, is
now becoming a more common cause of
overdosage because of its widespread use
in place of aspirin. However, in India, this
is not common.
Symptoms and signs: In acute poisoning,
paracetamol does not behave like aspirin.
It does not affect acid-base balance. It does
not stimulate respiration. It does not
increase cellular metabolism. It has no
cardiovascular system effects. Bleeding
from mucosal at erosion may rarely occur.
The symptoms can be described under
three stages, viz. gastrointestinal, latent,
and hepatic failure. In the first stage, the
symptoms are deceptively mild. Vomiting
is seldom severe or accompanied by other
symptoms and the patient remains fully
conscious. This may lead to a false sense of
security. In the second stage, after a lapse
of about 24 hours, though the liver
undergoes damage, the patient is relatively
pain-free. He may complain of anorexia,
epigastric pain, and malaise, due to hepatic
damage. In untreated victims, the third
stage of hepatic failure is seen after about
three to five days. It is characterised by liver
failure, gastrointestinal haemorrhage,
cerebral oedema, renal tubular necrosis,
 Analgesics and Antipyretics
and cardiomyopathy. In cases where
patient survives the III stage, complete
resolution of the liver injury occurs.
fatal dose and fa ta l period. Ingestion of
20 tablets each of 500 mg of paracetamol is
usually fatal within three to five days.
Treatment: The important considerations in
management are as follows:
1. All patients who have taken an overdose
or suspected of having done so should
be admitted to the hospital since the
history and the clinical state of the
patient may be misleading. A patient
apparently well 12 hours after taking an
overdose may die of acute hepatic failure
up to 5 days later.
2. Gastric lavage should be carried out, if
thepatient is admitted within four hours
of taking an overdose.
3. While protracted vomiting needs
adequate hydration, it is important to
remember that paracetamol can cause
fluid retention. More than 2.5 litres of
intravenous fluids daily would be risky.
4. Complications of severe hepatic necrosis,
such as hypoglycaemia, metabolic
acidosis and generalised bleeding should
be treated with dextrose infusion,
bicarbonate infusion, vitamin Kj and
whole blood or plasma respectively. Oral
methionine 10 grams over 12 hours in
4 doses prevents hepatic damage, if
given within 10 hours.
5. Haemodialysis may be necessary for
acute renal failure. Its value, however,
is uncertain.
663
6. In cases of moderate or severe poisoning,
N-acetylcysteine (Mucomix) should be
given orally. It is most effective when
given within 16-24 hours of overdosage.
It prevents hepatic damage. The initial
dose is 140 mg/kg followed by 70 mg/
kg every four hours for a total of
17 doses. While it may cause skin rash,
nausea, vomiting and drowsiness which
may last for 48 hours, these side effects
are acceptable in view of the serious
dangers of paracetamol poisoning.
7. In patients with evidence or suspicion of
cerebral oedema, intravenous adminis­
tration of hypertonic glucose is useful.
Postm ortem appearances: Remains of
paracetamol tablets may be found in the
stomach. The typical findings are skin
rashes, jaundice, petechial haemorrhages,
gastrointestinal bleeding, hepatic necrosis,
renal tubular necrosis and cerebral oedema.
Medicolegal aspects: Poisoning is generally
accidental due to overdosage and indiscri­
minate use as an analgesic and antipyretic.
Patients who attempted suicide have
regretted the choice of this drug on account
of the painful interval between ingestion
and death. More common in children.
Long-term use of paracetamol for pain
relief may develop toxic hepatitis, more
commonly among patients also taking
isoniazid, rifampicin, barbiturates, and
in AIDS victims. In children, low body
temperature, oliguria and hepatomegaly
are seen. Intentional over dosage as on
at most at suicide has been in vogue in
USA and UK. In India, these are not very
common.
60
Antihistaminics
Antihistaminics are drugs which antagonise
the action of histamine. They are used in
allergic disorders and other conditions, such
as colds, motion sickness, and Parkinson's
disease. The common preparations include:
antazoline (Antistine), chlorcyclizine
(Histantin), chlorpheniramine maleate
(Piriton), diphenhydramine (Benadryl),
halopyramine hydrochloride (Synopen),
mepyramine maleate (Anthisan), and
promethazine hydrochloride (Phenergan).
Many antihistaminics have other effects,
such as anticholinergic, antiadrenaline, and
anti-serotonin effects. They are classified as
non-sedating, like cetirizine; mildly seda­
ting, like chlorpheniramine and cyclizine;
moderately sedating, like antazoline,
doxylamine; and highly sedating, like
diphenhydramine, hydroxyzine.
Symptoms ami signs: Overdosage produces
complex clinical signs resulting from initial
depression followed by excitation of the
central nervous system. In young children,
the excitatory effects are more prominent
and hyperpyrexia may occur.
There is dryness of the mouth, nausea
and vomiting. Drowsiness, headache,
664
blurred vision, urinary retention and
nervousness are common. In a large over­
dosage, fixed dilated pupils, disorientation,
ataxia, hallucinations, stupor and coma
occur. Sometimes, an excitatory effect
predominates resulting in hyperreflexia,
tremors, excitement, nystagmus, and
convulsions. Death results from respiratory
failure and cardiovascular failure.
Over dose causes excitation, muscular
incoordination, hypotension.
Fatal dose: The fatal dose is about one
gram.
Treatment: The stomach should be washed
out with warm water and a small amount
of sodium bicarbonate solution left in the
stomach. 10 mg Diazepam intravenously
will control the convulsions; short-acting
barbiturates are not quite effective. The rest
of the treatment is symptomatic.
Postmortem appearances: These are those
of asphyxia.
Medicolegal aspects: Poisoning is usually
accidental from overdosage or indis­
criminate use.
61
Tranquillisers

Tranquillisers are drugs which relieve ression, coma, and collapse. The individual
anxiety and mental tension without tranquillisers may produce some charac­
producing sedation (drowsiness) or sleep. teristic signs, such as jaundice due to
They are used in various neurotic chlorpromazine, aplastic anaemia due
conditions, anxiety states, and for the relief to meprobamate, and reactivation of peptic
of tension, so common nowadays due to ulcer due to reserpine.
the complexities of life. They are also used
Treatment: The absorption should be
in anaesthesia for their muscle-relaxant
delayed by the use of activated charcoal or
properties. A large number of tranquillisers
milk. The stomach should then be washed
are available in the market under different
out or emetics given. The rest of the treat­
trade names. The common ones include
ment is symptomatic. Flumazenil orally or
diazepam, chlorodiazepoxide, oxazepam,
TV injection of 0-3 to 1.0 mg.
lorazepam, alprazolam.
Sumytoms and signs Common; symptoms Postmortem appearances: These are non­
of poisoning are restlessness, tremors, specific.
diplopia, nightmares, hallucinations, Medicolegal aspects: Poisoning is generally
drowsiness, weakness, incoordination, accidental from overdosage or indiscrimi­
followed by cyanosis, respiratory dep­ nate use, or rarely suicidal.

665
 Antidepressants
Antidepressants are drugs used generally
in psychiatric practice to treat endogenous
depression. These drugs have an initial
sedative effect followed by an anti­
depressant effect after a week or more.
Amitriptyline and imipramine are the
tricyclic antidepressant (TCA) drugs in
common use. Prozac and Zoloft are recent
additions.
Sym ptom s am i sign s: Dryness of the
mouth, blurred vision, sweating, dizziness,
and urinary retention are prominent initial
features. Hypotension, tachycardia,
tremors, confusion and abdominal pain are
common. Allergic jaundice sometimes
occurs. Acute overdosage may result in
convulsions, cyanosis, coma, respiratory
depression, and cardiac arrhythmias
ending in death. These features appear one
to two hours after taking the dose and
seldom last longer than 18-24 hours but
sudden death from cardiac arrhythmias
may occur up to six days.
fa t a l d ose: The fatal dose varies from
1-2 gm.
7 t ea lm m t: Treatment is mainly supportive
and involves gastric lavage, management
of arrhythmias; maintenance of blood
pressure; control of convulsions; and arti­
ficial respiration, if necessary. ECG
monitoring is advisable. It is important to
avoid quinidine and procainamide to
control arrhythmias as they have action on
the heart similar to TCA. Physostigmine,
though very efficacious in reversing CNS
effects and counteracting some cardiac
effects, may precipitate a cholinergic crisis
and should not be tried till other therapy
has been used. The rest of the treatment is
symptomatic.
Postm ortem appearances: The findings
are non-specific. Liver damage may be
present.
M edicolegal aspects: Poisoning is acci­
dental or suicidal.
65
Street Drugs and Designer Drugs
As the name suggests, these are drugs to
be obtained, not from pharmacies but, from
surreptitious sources (on the street) as they
are sold in contravention of the drug rules.
This group of drugs includes stimulants,
depressants, narcotics, hallucinogens,
inhalants, and designer drugs.
It is natural that quality control of street
drugs is non-existent and many such drugs
are likely to be adulterated with substances
that look, taste, or even feel like the original
drug. Frequently, even the user himself
does not know what he has actually taken.
In the event of poisoning, the treatment
poses a major problem; forensic problems
arise in the event of death.
On account of the fear of AIDS and other
infectious diseases, addicts have now
turned to smoking, snorting, and inges­
tion of drugs and the true addict may not
have any needle mark—a cardinal sign of
the addict a little while ago. The complica­
tions from the use of such drugs mainly
pertain to the nervous, cardiac, and respira­
tory systems, with few specific symptoms
that will help the clinician to arrive at a
diagnosis and administer appropriate
treatment. Therefore, any patient, who
has agitation, delirium, confusion, coma,
hyperthermia, and cardiac or respiratory
symptoms that seem out of place should
be suspected as a possible user of street
drugs and treated accordingly.
672
If the patient is agitated, it is often
appropriate to treat as if the intoxicant is
cocaine. This treatment is appropriate for
amphetamines, phencyclidine and anti­
cholinergic intoxicants. Hyperthermia is
the worst prognostic indicator in these
patients, unless the temperature can be
effectively controlled by rapid cooling.
Patients with cardiac problems will need
continuous monitoring and attention to
rate and rhythm of the heart and mainte­
nance of blood pressure at the appropriate
level. Patients with respiratory depression
should receive naloxone until the
possibility of narcotic poisoning has been
ruled out. Mezicon should be used to treat
benzodiazepine overdosage. The rest of the
treatment is symptomatic.
Designer Drugs
The term 'designer' is used to indicate an
analog, i.e. a compound similar in its action
to another compound but different in its
structure. To circumvent legal problems in
the storage, distribution, and sale of street
drugs, clandestine laboratories
manufacture new drugs by altering the
chemical structure of a known drug, either
legal or illegal. Since substitution of the
base leads to many products, a large
number of compounds are possible. These
drugs are incredibly cheap to produce and
some of them are more toxic than the
 Street Drugs and Designer Drugs
original drug. The compounds so produced
are called designer drugs (analogs) and are
not illegal even though the parent
compound is officially restricted. These
synthetic chemicals can be safely sold till
they are brought within the purview of
drug control regulations.
Designer drugs are classified in four main
groups, viz. (1) stimulants (amphetamine
group), (2) depressants (methaqualone
group), (3) narcotics (opioid group), and
(4) hallucinogens (phencyclidine group).
Drugs based on the amphetamine
chemical structure include MDMA, MDA,
DOMand others. At moderate doses, these
drugs produce hallucinations similar to
LSD. Known on the street as ecstasy,
MDMA has been associated with sudden
death through cardiac arrhythmia. An
acutechoreoathetoid disorder may be seen.
Hyperthermia with seizures or muscular
hyperactivity leading to rhabdomyolysis
and potential acute renal failure are
relatively common. Hypertension with
673
complaints of chest pain are common but,
unlike cocaine, rarely lead to ECG changes.
Other complications include cerebral
haemorrhage and death. There are not
many analogs of drugs of the methaqualone
group. Complications from their use
include slurred speech, staggering gait,
altered perception, respiratory depression,
coma, and death. The narcotic analogs of
the opioid group include Fentanyl and
Meperidine or Pathedine: Over dose of
pethidine causes mydriasis, tremors, hyper-
reflexia, delerium, myoclonus, convulsions.
After intramuscular injection, its action is
for 2-3 hours. It is redasive and emphoriant.
Tachycardia is seen. After IM injection, also
corneal anaesthesia may be seen. Dry mouth
and beterred vision are also encountered.
They produce analgesia, euphoria, drowsi­
ness, respiratory depression, convulsion,
coma, and death. The analogs of the
phencyclidine group cause illusions,
hallucinations, impaired perception, and
bad trips with their consequences.
66
Alphabetical Poison Table

(Revised by Dr SK Singhal, Professor of Forensic Medicine and Toxicology, ACPM

Medical College, Dhule 424 005, India; Dr CK Parikh, Medicolegal Consultant, Mumbai
400 005, India; and Dr Patrick Besant-Matthews, Forensic Pathologist, Dallas, Texas,
USA).

674
 Stimulants

These are drugs which stimulate the central the relief of fatigue and elevation of mood.
nervous system and produce a false sense Profound behavioural changes may occur
of euphoria which is followed by depression. including a characteristic amphetamine
The commonly abused preparations are psychosis clinically resembling acute
amphetamines and cocaine. paranoid schizophrenia. The symptoms
usually disappear when drug use ceases.
AMPHETAMINES_____________________ Fatal dose and fa ta l period: The fatal dose
Amphetamines (pep pills, ups, speed) have is 120-200 mg. Death has followed five days
varied uses. The alpha and beta adrenergic after ingestion of 140 mg.
effects from their use appear to be due to
Treatment:The patient should be kept in a
release of neurotransmitters in a fashion
darkened room. Gastric lavage with tap
similar to cocaine. The commonly used
water and activated charcoal is recommen­
preparations are Benzedrine, dexamphet­
ded. Sedation will be necessary. The rest of
amine sulphate (Dexedrine), and methyl-
phenidate (Ritalin). They are used as the treatment is symptomatic.
appetite suppressants, mood elevators, for Postmortem appearances: Particles of
the relief of fatigue, and in the treatment of unabsorbed drug may be found in the
narcolepsy. These drugs can be taken stomach. Reddish blotches on the skin,
orally, by inhalation, and even intravenously generalised oedema of the lungs and
for 'kicks' or as sex stimulants. Tolerance is pulmonary petechial haemorrhages are
common and leads to addiction. common. The adrenals may show haemorr­
hagic reaction.
Symptoms and signs:Toxic effects manifest
as euphoria, talkativeness, restlessness, M edicolegal asp ects: Overdose is a
insomnia, tremors, dry mouth, nausea, common cause of poisoning. Amphet­
vomiting, diarrhoea, abdominal cramps, amines are drugs of addiction. Suicide is
palpitations and tachycardia. Mania and sometimes triggered by the prolonged
delirium with hallucinations, mainly audi­ depression and errors of judgement which
tory, result from larger doses. Convulsions follow intense stimulation from continued
and coma are characteristic features of high dosage.
severe poisoning.
Chronic poisoning, also known as COCAINE____________ _ _ _ _ _
addiction occurs from the continued use of Cocaine is an alkaloid derived from coca,
these drugs over a long period of time for the dried leaves of the plant Erythroxylum
667
668 Textbook of Medical Jurisprudence- Forensic Medicine and Toxicology

coca. It is a colourless crystalline substance meet to enjoy cocaine and transact illegal
having a bitter taste. It is a recreational drug activities in relation thereto.
of choice for the modem affluent class of 1 * The ordinary fatal dose is 1 gm
persons. Coke, crack, crystal, freebase are orally. The fatal dose after application to
different names given to the same prepara­ mucous membrane may be as low as 30 mg,
tion with slight modification and in different the drug being rapidly absorbed by this
stages of purity. The common routes of route.
administration are chewing, application
lo t ul p, no, j; Death usually occurs in about
to nasal mucous membrane (snorting),
two hours.
smoking, and intravenous injection.
Treat men i: If the drug is injected, absorp­
Cocaine is said to reduce appetite and
tion should be limited from the injection site
feeling of fatigue. It is commonly used as
by tourniquet. If applied locally to the nose
an aphrodisiac or pleasing intoxicant. Drug
or throat, it should be removed by washing
addicts use it as snuff, either pure or mixed
with warm water or normal saline. If
with boric acid.
swallowed, the stomach should be washed
Symptoms end signs: Cocaine first acts as with a dilute solution of potassium
a stimulant and then a depressant of the permanganate or tannic acid. Medicinal
nervous system. The psychoactive effects charcoal may also be employed. Excitement
are due to its action on the neurotransmitter should be controlled by barbiturates or
sites by production of dopamine which diazepam. Cardiorespiratory stimulants
goes to the pleasure centre of the brain. The and artificial respiration may be required.
stimulant stage is characterised by dryness Further treatment is symptomatic.
of the mouth, bitter taste, euphoria, Postmortem appearances: Death being due
increased physical and mental energy, and to asphyxia or cardiac failure, the signs of
stimulation of libido. Restlessness, excite­ such form of death are likely to be found.
ment and delirium may appear. The patient Cocaine is largely destroyed in the human
may become maniacal and may have system and it is difficult to detect it by
hallucinations. Other physical effects chemical analysis.
include flushed face, dilated pupils, blurred
vision, tachycardia, hyperthermia, and an Chronic Cocaine Poisoning
increased respiratory rate. Toxic dosage The sense of well-being experienced on
will produce incoordination, muscular administration of cocaine causes a number
twitches and convulsions. This is followed of persons to drift into addiction, also
by a stage of depression which is chara­ known as cocainism, cocainophagia or
cterised by feeble respiration and collapse, cocainomania. The tongue and teeth of
ending in death from respiratory or cardiac habitual cocaine eater are black. When
failure. Myocardial ischemia and infarction cocaine is used as a snuff, there is generally
due to coronary artery constriction is seen ulceration of the nasal septum. The
in some cases. symptoms of chronic cocaine poisoning are
In fact, cocaine is so hard on the body characterised by anorexia, loss of weight,
that it is often mixed with heroin to dampen weakness, tremors, impotence, moral
its harsh effects. This combination is called deterioration and insanity. The effects of
a speedball and can be deadly. A crack house cocaine lead to increased erotic tension in
is a euphemism for a place where crack women and nymphomania. In men, the
cocaine is sold or smoked. Like the shooting condition leads to many sexual perversions,
gallery of heroin, it is a place where people mainly homosexuality, and libidinous
 1(Deccan Chronicle 13.12.2012).

Fig. 63.'* Magnan’s symptom. The cocaine

Magnan’s symptom. The cocaine addict is disturbed by feeling of Insects
addict Is trying to squeeze out sand particles (cocaine bugs) creeping on the skin.
from under the skin. (Courtesy. Dr GB Sahay) (Courtesy. Dr GB Sahay)

Magnan’ssymptom. The cocaine addict is looking for cocaine bugs under the pillow.
(Courtesy. Dr GB Sahay)
 64
Hallucinogens
Hallucinogens (psychedelics) are drugs
which produce bizarre effects on the mind,
such as distortion of time, space, sound,
colour, and other sensations (synaesthesia).
The important hallucinogens are LSD,
peyote, mescaline, and phencyclidine. The
psychotropic effect resulting from their use
is known as 'atrip7. When the effect is a
panic reaction, it is known as 'abadtrip'.
When the trip experience recurs in a drug-
free state, it is known as a 'flash back7.
LSD, PEYOTE, MESCALINE,
PHENCYCLIDINE (PCP)_________________
LSD, chemically known as lysergic acid
diethylamide, is synthesised from rye
ergot. It is tasteless, odourless, and the most
potent, widely used hallucinogenic drug,
having a powerful effect in minute closes.
It is available in the form of clear liquid,
thin squares of gelatin window panes, and
pills of varying size and colours. It is
usually taken on a sugar cube or by putting
a drop on a blotter paper and licking it
when the drug effect is desired (microdots.)
Thin squares of gelatin and clear liquid can
be put in the eyes, and the pills can be eaten.
25-50 jug produce all the effects. It causes
central sympathetic stimulation. The
person experiences a dream-like state or
out of the body fealing. Loss of contact with
reality, swaying field of vision objects
distorted like images in a curved mirror and
670
on closing the eyes unending series of color­
ful images even nudes appear. Mydriasis,
hippus vertigo, altered time sense, and
impaired ability to concentrate, Many of
these persons get supreme relaxation, and
happy feeling. Uncontrolled laughter or
sometimes weeping is seen.
Peyote is obtained from a variety of
cactus (peyotol) plants. It is available in the
form of hard brown discs, tablets, and
capsules. It can be chewed, swallowed,
taken in tea, or smoked. It is not as potent
as LSD. It is used by tribal Indians of the
arid regions for their religious ceremonies.
Mescaline is another hallucinogen
derived from the peyotol plant. Its
availability, use, and effects are similar to
those of peyote.
Phencyclidine (PCP, angeldust, killer
weed) is available in the form of liquid,
white crystalline powder, capsules, and
pills. It can be taken orally, smoked, and
injected.
Hallucinogens do not have any valid
medicinal use at the present moment. They
are taken by youngsters in a spirit of
adventure, just for kicks. A more profound
reason is a desire to escape from the
realities of life, or to enter a world of fantasy
where they can expand their mind, feel
more creative or super-human, and can
have communion with nature, divine
spirits, or God.
679
 682 Toxtbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Main symptoms Average fatal Treatment Medicolegal

and signs dose and points and
fatal period poison sources
Salivation, vomiting, abdo- 6 grams Decontaminate Suicidal. Homicidal.
minal pain, tremors, body. Gastric Accidental. Plant
Neurotoxic dyspnoea, white fine froth 2 hours lavage, saline penicillin
Cholinergic from mouth and nostrils, cathartics. Atropine.
convulsions, coma 10 ml 10% calcium
gluconate i v. Paral­
dehyde. Oxygen.
Blood transfusion

Ergot Irritation of throat, thirst, Uncertain Stomach wash with Abortifacient.

nausea, vomiting, diarrhoea,
Vasoconstrictor. colicky pain, giddiness,
Smooth (uterine) tingling in small muscles,
muscle contractor hypoglycemia, anuria. In
chronic cases, convulsive
and gangrenous ergotism
Ether If ingested, burning pain,
vomiting, dilated pupils,
Anaesthetic absent corneal reflex,
intoxication. When
inhaled, it produces
features similar to chloro­
form. Sometimes epilepti­
form convulsions
5% tannic acid. Accidental from
Uncertain Magnesium sulphate, contaminated food
Intravenous fluids.
Amyl nitrite inhala­
tions. Sodium nicoti-
nate 140 mg i.v.
30 ml orally Gastric lavage, Accidental
More than demulcents, Suicidal
0.15% in blood stimulants. Oxygen, Addiction
artificial respiration.
Uncertain Anticonvulsants.
Maintain blood
pressure

Ethylene glycol When ingested, effects 100 ml Gastric lavage. Accidental

resemble drunkenness, Pyridoxine and Suicidal
CNS depressant progressing to nephro- 24-72 hours Use in place of ethyl
Nephrotoxic toxicity, hypoglycemia, conversion of alcohol
coma, seizures, collapse glyoxalate to non­
toxic byproducts.
Antidote 4 methyl
pyrazole. Dialysis,
whole bowel
irrigation, or
competing ethanol

Hallucinogens Unusual hilarity, emotional Uncertain Limt stimulation, Accidental

swings, hallucinations, tranquillisers, Suicidal
Mechanism of action suspiciousness, bizare Not known symptomatic Homicidal
on CNS not known behaviour, synaesthesia, measures, Habit forming
nausea, vomiting, widely psychotherapy
dilated pupils, insomnia,
tremors, vertigo,
headache, psychotic
reactions, bad trips, flash-

(contd)
 676 Textbook of Medical Jurisprudence. Forensic Medicine and Toxicology

(confd)
Name and Main symptoms Average fatal Treatment Medicolegal
and signs dose and points and
fatal period poison sources
Antihistamlnics Dry mouth, nausea, vomiting, Up to 1 gm Gastric lavage, leave Accidental. Treatment
Antiallergic drowsiness, lethargy, ataxia, dilute NaHC03 in of allergic conditions,
Anticholinergic aplastic anaemia, agranulo- Uncertain stomach. Diazepam colds, motion sick*
Antiadrenaline cytosis, fixed dilated pupils, 10-20 mg i.v. to ness, and Parkinson’s
Antiserotonin coma. Sometimes only exci­ control convulsions, disease
Sedative tation with tremors, delirium, Prostigmine 1 mg
convulsions, hyperreflexia i.m. Oxygen. Artificial
respiration
Antimony Metallic taste, burning in 750 mg of tartar Same as that of Accidental. Homicidal,
throat, vomiting, dysphagia, emetic. 100-200 arsenic poisoning for use in alloys type metal
Irritant. Inhibits profuse bloody diarrhoea, mg of butter of tartar <
sulphydryl enzymes muscle cramps, oliguria, antimony chlo- hydrochloric acid i
skin eruptions. In chronic ride poisoning for butter
cases, irritability, bleeding of antimony. Large
gums, emaciation, nephritis, 24 hours quantity of water
render antimony
chloride as insoluble
chloride
See alcohol (ethyl)

Burning pain in throat and 120-200 mg Stomach wash. Homicidal. Accidental

abdomen, severe vomiting, Demulcents. Freshly Abortifacient. Aphro-
tenesmus, bloody liquid 24 hours prepared hydrated disiac. Cattle poison,
sulphydryl enzymes purging, with shreds of ferric oxide. 10% Used in weed killers
mucus. Muscle cramps. solution of BAL i.m. and rat pastes
Mind remains clear. Acute 3 mg per kg body
poisoning resembles cholera. weight 4 times on
Chronic poisoning resem­ first day, then twice
bles certain diseases daily for 10 days. 10
mg morphine i.m. Ice
fluids. Dialysis

Aspirin Flushed face, oedema of 5-10 gm
face, skin rash, tinnitus,
Gastric irritant. deafness, hyperpnoea, Few minutes to in stomach. Restora­
Non-narcotic nausea, vomiting, hema- few hours
analgesic and temesis, melena, hypo-
antipyretic prothrombinemia, acute
renal failure, pulmonary
oedema, respiratory arrest
Gastric lavage. Leave Accidental Idiosyncrasy
some dilute NaHC03
tion of electrolyte
normality and acid
base balance. Vit Kr
Blood or platelet trans­
fusion. Forced alkaline
diuresis. Peritoneal
dialysis, hemodialysis.
General measures

125 mg See datura Accidental stupefying

24-48 hours

(contd.)
 Alphabetical Poison Table 677

<£***>
and Main symptoms Average fatal Treatment Medicolegal
and signs dose and points and
3clM fatal period poison sources
Barbiturates Nausea, confusion, drowsi- Long acting Stomach wash, Suicidal. Accidental
Cerebral ness, ataxic gait, deep barbiturates 3 enema, maintain overdose from
depressant sleep, shallow breathing, grams body warmth. 2.5 sleeping tablets or
Hypnotic fall of blood pressure. Skin mg metaraminol i.v. treatment of epilepsy,
rash, blisters, cyanosis, 24-48 hours for 2-3 doses to Automatism,
absent bowel sounds, raise BP to 100 mm Addiction problems.
alternate contraction and Hg. Coramine i.v. 5 Ingredient of lethal
dilatation of pupils. ml 25% followed by i.v. injection for
Areflexia. Cardiorespiratory 10 ml in 15 minutes, judicial execution
then 20 ml every 30
minutes till reflexes

Hemodialysis.
fusion. Stimulants.
Artificial respiration
Barium Abdominal pain, vomiting, 1 gram Give magnesium Accidental during use
purging. Cardiac arrhyth- sulphate 15 gm. of barium sulphate in
Locally irritant mia (missed beats), rise in 12 hours After some time, X-rays. Suicidal
Cardiac depressant blood pressure, areflexia stomach wash with occasionally

10 liters. 10 ml 10%
i.v. sodium sulphate.
10 mg morphine

Sodium chloride 1 Accidental

gram orally hourly.
In unconscious Idiosyncrasy
Average 6-12 patients, 1 liter
normal saline i.v.
daily for 4 days.
Oxygen, diuretics,
psychosis analeptics as
m
 Alphabetical Poison Table 685
(corf*)
Hum* ond Main symptoms Average fatal Treatment Medicolegal
action and signs dose and points and
fatal period poison sourci
Marihuana See cannabis

Marking nut See Semecarpus

anacardium

Mercury Metallic taste, salivation, Metallic mercury Emetics, or stomach wash Accidental
choking, dysphagia, not poisonous. with magnesium carbonate Abortifacient
Corrosive and corrosion of mucous Corrosive sub­ or sodium formaldehyde Suicidal
irritant. Nephrotoxic membrane of mouth and limate 1-2 gm sulphoxylate 250 ml 5%,
and 100 ml to be left in
stomach. Egg white.
Activated charcoal orally.
Magnesium sulphate. BAL
200 mg twice daily i.m.
Sodium thiosulfate i.v.
Penicillamine orally, alkaline
gums, penetrating ulcers,
uraemia, mercuria lentis,
tremors (hatter's shake),

Methyl alcohol Alcoholic smell, headache, 15 ml causes Gastric lavage with 5% Accidental from
dizziness, nausea, vomiting, blindness NaHC03. Ethyl alcohol 80° use in place of
Neurotoxic, pain in abdomen, intestinal proof (brandy) 1 ml/kg body ethyl alcohol
Respiratory contraction - bowel like 60-240 ml weight 4-6 hourly for 1-3
depressant thick rubber pipe of narrow days. Combat acidosis with
lumen, muscular weakness, Up to 4 days NaHCOa orally or 5% i.v.
cyanosis, optic neuritis, solution. Protect eyes.
acidosis, stupor, respiratory Hemodialysis. Antidote 4-
failure methylpyrazole. Folinic
acid. Whole bowel irrigation,
if possible
See aspirin 30 ml
Depending on concentra- More than Same as inhalation or Accidental
tion and exposure, symp- 250 ppm ingestion of other hydro­
toms range from light carbons. Removal of the
Narcotic, headedness, nausea, Uncertain patient from exposure,
Respiratory headache, and impairment decontamination, support
of concentration and of respiration, monitoring of
coordination to stupor, dysrhythmias, and general
irritability, and gait
disturbances. Inhalation
hemoglobin levels without
inhalation of carbon
monoxide. Its use as a
paint remover in a poorly
ventilated setting may
stress patients or workers
with underlying cardio­
pulmonary disease or
concomitant carbon
monoxide exposure
Cconfer.)
Naloxone 0.4-0.8 mg i.v.

(contd•)
 Alphabetical Poison Table 687

Main symptoms Average fatal Treatment Medicolegal

and signs dose and points and
fatal period poison sources
Burning pain, thirst, yellow 15-20 ml Stomach wash (with soft Accidental
coloration of mucous mem­ rubber tube, if possible). Suicidal
Corrosive, brane and teeth, yellow 18 hours Give milk, magnesium Abortifacient
if diluted brown vomitus, tender oxide, egg white or melted Vitriolage
and distended abdomen, butter. 10 mg morphine.
oliguria, shock. Choking, Intravenous fluids. Ice
lacrimation, dyspnoea, and sucking. Cortisone
cough are due to inhalation

Nitrous oxide Hysterical excitement, Uncertain Inhalation of oxygen and Accidental

laughter, light anaesthesia. carbon dioxide, artificial Laughing gas
Anaesthetic Uncertain respiration, stimulants

Bitter taste, twitching ol

muscles of face, risus
Spinal irritant acting sardonicus, convulsions,
mainly on anterior opisthotonos, cyanosis,
horn cells
salivation, epigastric pain.
Mind remains clear till the
end. Death is incredibly
painful
Powdered nux bital or 10 mg diazepam errors or eating
vomica 2 grams, i.v. Mephenesin i.v. 3 mg/ fruit. Suicidal.
Strychnine kg body weight. Stomach Homicidal.
15-30 mg wash with 5% tannic acid. Love-philter.
Tubocurarine. Oxygen and Aphrodisiac
artificial respiration

Oleander Dysphagia, vomiting, pain, Nerium odorum Stomach i with 5% Accidental

salivation, diarrhoea, lock-
Cardiac depressant jaw, feeble pulse, fall of
blood pressure, muscular
spasms, drowsiness,
coma
Opium See morphine
Contains alkaloids
Organophosphorus Respiratory symptoms
CNS depressant ing, contracted pupils.
vomiting. Sweating, saliva- 6 hours
tion, lacrimation (some­
times red tears), urination
and defecation, mental
confusion, stupor,
convulsions, areflexia,
coma
15 grams,\felow tannic acid. Molar sodium (drug). Suicidal.
oleander 8-10 lactate solution i.v. 5% Abortifacient.
seeds glucose with 1.2 mg Love-philter.
atropine, 2 ml 1:1000 Cattle poison
24 hours adrenaline, and 2 mg
noradrenaline i.v.
2 grams See morphine. Metha­ Near ideal suicidal
done may be used in poison. See
6-12 hours chronic poisoning as morphine
temporary substitute
1 gramofTik-20 Remove clothing. Accidental
(variable for Decontaminate body, Suicidal
other com- Stomach wash, care of Homicidal
pounds) airway. 2 mg atropine i.v.
half hourly till pupils
dilate. Oxime compound
PAM 1 gram 12 hourly.
Oxygen. Intravenous
fluids. Exchange
transfusion. Charcoal
hemoperfusion. Diuretic,
brisk purgative. Diazepam,
if necessary
 Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

Name and Main symptoms Average fatal Treatment Medicolegal

action and signs dose and points and
fatal petiod poison sources
Somecarpus External application causes 10 grams Wash the part with warm Accidental. Torture
tinacardium blister formation. Taken water. Apply bland Abortifacient.
(marking nut) orally, severe gastro­ 24 hours liniments. If taken orally, Vitriolage
intestinal irritation, wash the stomach with Malingerer’s
Irritant dyspnoea, cyanosis, warm water. Give milk, conjunctivitis and
tachycardia, coma ice to suck, and 10 mg artificial bruise

r
morphine i.m. for pain
See hydrogen sulphide

Snake bite Locally, burning at the 15 mg of cobra Apply ligature proximally. Accidental
site, teeth marks, and venom. 40 mg Wash the part and incise. Cattle poisoi
Neurotoxins in elapids. oozing. Elapid: Giddiness, of viper venom, Suck the blood by suction
vasculotoxins in vipers, lethargy, muscular weak- 6 mg of krait pump. Give specific anti-
and myotoxins in ness, ptosis, paralysis of venom venin when available or
snakes leg muscles, dimness of polyvalent antivenin 20 ml
vision, dysphagia, cyanosis, Few hours in subcutaneously around the
convulsions. Viper. Nausea, bite from cobra bite, 20 ml intramuscularly,
vomiting, hemolysis, and few days and 20 ml intravenously.
hemorrhages, dilatation of in viper. Sea Repeat i.v. dose if collapse
pupils, necrosis of renal snake bite not occurs or 6 hourly. Inject
tubules, collapse. Sea fatal atropine 0.6 mg and
snake: Locally sharp initial neostigmine 0.5 mg i.v. to
prick becoming painless. combat fixed toxins of
Generalized muscular elapids. Inject heparin and
pain, myoglobinuria, fibrinogen in viper bite
hyperkalemia cases. General measures

Sodium nitrite Headache, giddiness, nausea, 2 grams Gastric lavage. 1% Accidental,

vomiting, marked cyanosis methylene blue 1 mg/kg Used as a
Cardiac depressant due to methemoglobinemia, Few hours to body weight. Vit C. mordant by
hypotension, hemoglobinuria, some days General measures. weavers
Maintain body warmth

Spanish fly See cantharides

Strychnine See nux vomica

Sulfuric acid Burning pain, thirst, black 10-15 ml Stomach wash (with soft Accidental
vomit, detachment of rubber tube, if possible). Vitriolage
corroded mucous mem- 12 hours Give milk, magnesium Abortifacien
brane, dysphagia, chalky oxide, egg white, melted Suicidal
white teeth. Black trickle butter. 10 mg morphine
marks on lips, cheeks, i.m. for pain. Intravenous
and chin. Abdominal pain, fluids, oxygen, cortisone
collapse, coma, death

Tear gas Irritation of eyes with flow —
of tears, spasm of eyelids,
Irritant photophobia. Cough, bron- Not fatal
chial spasm, pain in chest,
and frontal headache
Remove the patient to fresh Accidental. War
air. Wash eyes with cold gas to disperse
water. Put liquid paraffin unruly mobs
drops in eyes and use dark
cortisone eyedrops. Atropine
and oxygen in threatened
pulmonary oedema. Anti­
histamines are helpful
 Alphabetical Poison Table

Average fatal Treatment

diarrhoea, peripheral
neuritis, ptosis, impaired 2 days to 2
vision, ataxia, convulsions, weeks

See organophosphcrus

Restlessness, tremors, 10 grams Gastric lavage, activated Accidental,

diplopia, drowsiness, charcoal, general measures. Suicidal.
weakness, incoordination, Uncertain Blood transfusion. Antidote Addiction
cyanosis, pulmonary oedema is Flumazenil problems
collapse, coma, skin blisters

Burning in abdomen, 200 ml Gastric lavage with 3-5% Suicidal

bicarbonate solution, Abortifacient
strangury, albuminuria, 43 hours demulcents, alkaline Counterirritant
hematuria, cyanosis. diuretics, general
measures
See methyl alcohol
Metallic taste, nausea; pain 15 gramsof No emetics. Stomach Accidental from
in oesophagus, stomach, zinc sulphate wash with warm water.
SCCC-S'-. c c:c ‘.-'gee -CC ~g z.no Give milk, egg white,
vomiting, diarrhoea, chloride black tea, EDTA. 10 mg
muscle spasms, collapse. morphine i.m. for pain
Fumes of zinc oxide 24 hours

Garlic taste in mouth, garlic 5 grams Remove clothing and

odour in breath, nausea, pain
in oesophagus, stomach, Up to 24 h (wash with water). Dowry death.
Emetics, gastric lavage Accidental,
with 3-5% NaHCOa. Supportive
Vitamin K,