Poisoning is the most frequent of all the causes of violent death (the casualties of war excepted), as is

shown by the statistics of different countries. The facility with which poisons may be procured, the
ease with which they can be administered, and the close resemblance that many of them bear to
disease in their symptoms and post-mortem lesions, will account for the fact of their extensive
employment, both for homicidal and suicidal purposes.
The science of Toxicology, which treats of the nature, symptoms, effects, doses and modes of
detection of poisons, is very properly included in a treatise on Medical Jurisprudence since, as already
remarked, so large a proportion of violent deaths is to be ascribed to poisoning, it is as important that
the medico-legal student should be properly instructed in this branch of the subject.

TOXICOLOGY
Toxicology is the area of forensic medicine that deals with the categorisation and
determination of drugs within the human body and also how they are a contributing
factor in criminal acts. There are many different kinds of drug available openly in our
society today and many have side effects that can lead to changes in an individual's
mood and behaviour. And in some cases these changes in behaviour and mood can lead
to outbursts of violence. These outbursts of violence can lead to murder - intentional or
otherwise.
Role of a Toxicologist
The role of a Toxicologist is to examine samples of blood and urine and determine
whether or not an individual has been using - or is under the influence - of an illegal
narcotic substance.
They may also be charged with examining blood and tissue samples taken from a corpse
in order to determine if they have died as a result of drugs or other illicit chemicals; illicit
chemicals can also be qualified as poisons which when introduced into the human blood
stream can cause serious illness or death.
After taking a drug either through means of injection or inhalation the individual can
become highly strung, deeply depressed, euphoric or angry and as a result these feelings
of varying emotions can lead those users of drugs to commit levels of crime that would
normally be unknown to them had they not been under the influence.
Alcohol is also considered to be a drug and is illegal in certain circumstances; such as in
the workplace or when consumed by underage drinkers.
Areas of Toxicology
There are two main areas of Toxicology:
Screening: This form of Toxicology is used as a basic means of identifying the presence of
illegal drugs in a sample of blood taken from a suspect or corpse. This test provides a
quick result and is based on adding a particular solution - or series of solutions - to blood
or urine; when mixed with a contaminated sample will change colour. This test can show
the presence of cocaine, heroin, morphine or LSD within the system.
Confirming: This particular method of toxicology is used as a means of 'growing' drug
crystals from samples taken from an individual through blood or urine. A solution is
added to the sample and left underneath a microscope. This solution assists the drug in
the sample to form crystals, which have very defined characteristics that are
representative of certain narcotics.
A toxicologist will also be responsible for testing tissue samples from the liver, kidneys,
stomach, heart and lungs of a deceased individual if there are no visible signs of death.
These tests are carried out to provide evidence of either drug abuse or the intake of
poisons administered without the deceased's knowledge.
Advances
As with all avenues of forensic medicine, Toxicology has moved on greatly in recent years
and it has become a most reliable means of identifying many different kinds of drugs both prescription and illegal - that can be administered into the body.
It has also taken on a more commercial feel and can be used by corporations and
organisations in order to test their employees for substance abuse especially in jobs
requiring the use of heavy machinery or jobs which require the employee to drive for
long periods of time.
Toxicology has also given us many insights into how poisons - both man made and those
found in nature - can react adversely with the human body and its organs.

Poisons in this category have been classifi ed as irritant poisons, because they
mainly produce infl ammation on the site of contact, especially in the
gastrointestinal tract, respiratory tract and the skin. When a poison has a
systemic eff ect and death ensues because of it, then it is classifi ed as a poison
aff ecting that system most, for example, cardiac poison or cerebral poison or a
spinal poison. Arsenic is a heavy metallic inorganic irritant poison. Metallic
arsenic is not poisonous as it is insoluble in water and cannot be absorbed from
the gastrointestinal tract. However arsenious oxide or arsenic trioxide (sankhyal
or somalkar) is poisonous. Two organic arsenic non toxic variants, mostly present
in food regularly consumed by humans are arsenobetaine and arsenocholine.
They are found in shell fi sh, cod, and haddock. Provide the list of inorganic and
organic arsenic compounds with their physical properties and uses. An extended
communication on all the Indian poisonous plants in a particular region is though
beyond the scope of this section, some important plants commonly involved in
poisonings, follows logically. It would be however relevant to mention here that a
great deal of ignorance about these poisonous plants is a fact even among many
of the clinicians routinely dealing with poisoning cases. The problem is made
more intense by the fact that there is no accurate information available in India,
since very few cases are reported or published in literature. It is also agreed that
many of the experimental works are performed on laboratory animals and
discussed in veterinary literature. The applicability of such studies in human
beings is an open challenge. It is also true that many of plant poisoning cases
the treatment is practically same, i.e. symptomatic measures and supportive
therapy. Rarely these cases have any antidote therapy. There is virtually chaos
in the areas of plant identifi cation and nomenclature. Organic animal irritant
poisons include eff ects of bites/stings of poisonous snakes and insects.
Envenomation that can occur with these bites and stings lead to toxic condition
which at times be serious enough to cause even the death of the victim. The
following discussion orbits around the more common of these toxicological
syndrome complexes.

Poisons are classified as according to the mode of action:

1. Corrosive Poisons: These are highly active irritants which produce both
inflammation and ulceration of tissues. This group consists of strong acids and
alkalis.
2. Irritant poisons : These produce symptoms of pain in the abdomen, vomiting
and purging.
A. Inorganic poisons
Metallic Arsenic, antimony, mercury, lead and copper
Non Metallic - Phosphorus, chlorine, bromine and iodine
B. Organic Poisons Vegetable Castor oil
Animal Snakes, scorpions, spiders.
C. Mechanical Poisons
Powder glass, diamond dust.
3. Neurotic Poisons : - These chiefly act on the central
nervous system. Symptoms usually consist of headache, drowsiness, giddiness,
delirium, stupor,
coma, and convulsion.
a. Cerebral Poisons Opium, alcohol, sedatives, hypnotics, Anaesthetics
Mechanisms of action of poisons are

1. Local action-Poisons act directly on the tissues and cause corrosion, irritation
and inflammation.
2. Remote action-As the poison gets absorbed systemically, it produces both
specific CNS, spinal cord, cardiac and nonspecific shock. Poisons And The Oxygen
Pathway
Most of the poisonings involve the oxygen pathway,
from the inspired air to cellular respiration. The effects and the poisons involved
are given in Table 1.
Table - 1 : Some major
causes of blockade of
the oxygen pathway due to

poisoning with mechanisms.

Cause
Mechanism
Effect

Asphyxiant gases (e.g. butane, methane, carbon dioxide, nitrogen)

Hypoxic gas mixture R
Reduced inspired oxygen fraction (FIO2)

Respiratory depression (e.g. opioids, barbiturates other sedatives and hypnotics.

Failure of ventilation (type II respiratory failure)
Reduced alveolar oxygen tension (PAO2)

Respiratory muscle disorders: paralysis (e.g.organophosphates botulinus toxin)

or spasm (e.g.strychnine,phencyclidine) Aspiration pneumonitis
Adult respiratory distress

syndrome (paraquat)
Failure of oxygen transfer (type I respiratory failure)
Reduced arterial oxygen tension (PaO2)

Carboxyhaemoglobin (carbon monoxide) Methaemoglobin

(e.g.nitrites) Haemolysis (e.g.arsine, stibine)
Loss of functioning haemoglobin
Reduced arterial oxygen content(CaO2)

Myocardial depressants (e.g.b-blockers, tricyclic antidepressants,

dextropropoxyphene)

Chemical asphyxiants (cyanide, hydrogen sulphide)

Reduced cardiac output

Block of cytochrome enzyme chain

Reduced tissue oxygen delivery(QO2)

Reduced tissue oxygen consumption (VO2) causing failure of oxidative

metabolism

Fate of poisons in the body

Greater part of a poison is lost by vomiting and diarrhea. After absorption the
poison is dealt with in one of the several ways. Most frequently the poison
undergoes biotransformation in the liver. The main route of excretion of the
poison or its end products is the urinary tract. Other routes are bile ducts, sweat
glands, saliva, mucus and lungs. Epidermis, hair and nails retain inorganic
poisons like Arsenic. Bony skeleton holds substances like lead and radioactive
metals.
2. TOXICOLOGY Toxicology is the science which deals with poisons with
reference to their sources, properties, mode of action, symptoms, lethal dose,
nature of the fatal results, treatment, method of their detection and estimation
and autopsy findings
3. POISONS Poison is a substance which when administered, inhaled or ingested
is capable of acting deleteriously on the human body
4. THE LAWS OF POISONS The drugs and cosmetic act 1940 The pharmacy act
1948 Drugs control act 1980 Narcotic drugs and psychotropic substances act
1985
5. CLASSIFICATION OF POISONS ACCORDING TO MODE OF ACTION
Corrossives Acids and alkalies
Irritants Metallic, nonmetallic, organic vegetables, animals, mechanical
Neurotics Somniferous, inebrians
6. CLASSIFICATION OF POISONS ACCORDING TO MODE OF ACTION Deleriants
Spinal Cardiac Asphyxiants Peripheral poisons
7. ROUTE OF ADMINISTRATION Enteral Parenteral Inhalaional External
application Introduction into natural orifice
8. ACTION OF POISONS Local Remote Combined remote and local General
action
9. FACTORS MODIFYING ACTION OF POISONS Dose and quantity Form of poison
Method of administration Condition of the body
10. TYPE OF POISONING Acute Chronic Sub acute Fulminant
11. FATE OF POISONS IN THE BODY
12. DIAGNOSIS OF POISONING In the Living In the Dead
13. DIAGNOSIS OF POISONING - In the Living A/c or C/c
14. DIAGNOSIS OF POISONING - In the Dead PM examination Chemical analysis
15. MEDICO-LEGAL DUTY OF DOCTOR IN SUSPECTED CASE OF POISONING
Medical Duties and Legal Duties
16. MEDICAL DUTY Care and treatment of the patient
17. LEGAL DUTY Assist the police to determine the manner of death Record the
preliminary particulars and keep the records All cases need not be informed to
the police If patient dies, death certificate should not be issued
18. TREATMENT OF POISONS Removal of unabsorbed poisons from the body
Immediate resuscitative measures Use of antidots Elimination of un absorbed
poisons Treatment of General Symptoms and General Measures Maintenance of
the patients general condition and follow up

19. ANTIDOTS Are remedies which counteract or neutralise the effect of poisons
without causing appreciable harm to the body
20. CLASSIFICATION OF ANTIDOTS Mechanical / Physical Chemical
Physiological / Pharmacological Universal
PLANT POISONS
1. Definition- A substance which & when taken or administered into body in
whatever manner or form other than therapeutic amounts, causes disturbances
of function which may result in illness or death.
2. Thevetia peruviana Yellow Oleander Kaneru Nerium oleander Pink Oleander
Kaneru White Oleander Strychnos nux vomica Bitter Nut Goda KaduruPagiantha
dichotoma Eves Apple Divi KaduruCerbera manghas Sea Mango Diya
kaduruRicinus communis Castor bean Thel / Beheth Endaru Weta EndaruDatura
stramonium Thorn Apple / Angels Kalu Aththana TrumpetAdenia palmata
HondalaGloriosa superba Glory Lily NiyangalaAbrus precatorius Black-eyed Susan
/ Rosary Olinda pea / Precatory bean
3. Gloriosa superba Glory Lily [Niyangala]
4. Scientific name: Gloriosa superbaSinhala name: NiyangalaTamil:
Karththigaikkilangu, IllangalliEnglish/common names: flame lily, glory lily, tiger
clawPlant habitat: native of tropical Africa, India, Malaya, etc found in low
country Sri LankaTraditional use: tuber bruises and sprainsPoisonous parts of
the plant: The entire plant, especially the tubers, are extremely poisonous
5. Main toxic constituents: colchicine (+ gloriosine in tubers)Constituent type:
alkaloidMode of action: Colchicine has an antimitotic effect It stops cell
division by disrupting the spindle apparatus during the metaphase Cells with
rapid turnover are affected (bone marrow, intestinal epithelium, hair-producing
cells -> hair loss) It can alter neuromuscular function (It can withstand drying,
storage and boiling - tubers not a foodsource!)Clinical features of poisoning:
Initial symptoms develop within 6-12 hours of ingestion burning pain,
numbness, itching and tingling around the mouth and throat with thirst nausea,
intense vomiting abdominal pain, severe diarrhoea with blood and mucus
These lead to electrolyte imbalance, dehydration, hypovolaemic shock
manifested hypotension and tachycardia
6. After 24 hours patients develop Muscle weakness, myoglobinuria,
bronchial constriction, leucopenia, thrombocytopenia, clotting defects with
bleeding, polyneuropathy cardiac arrhythmias, hepatic insufficiency, acute renal
failure In severe cases there may be Respiratory depression, confusion,
delirium, convulsions, coma Death occurs due to shock or respiratory
failureDiagnosis: Toxicological, biomedical, blood gas, haematological
analysesTreatment of poisoning: hospitalize the patient immediately induce
vomiting (ipecac) / gastric lavage give repeated activated charcoal
supportive care eg IV fluid, assisted ventilation may be neededReferences:
Jayaweera DMA. Medicinal plant use in Ceylon - Part 3.Colombo: The National
Science Foundation, 2006;http://www.inchem.org/documents/pims/plant
(Accessed 4 July 2008];Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka.
Colombo: SriLankan College of Paediatricians, 2006
7. Thevetia peruviana Yellow Oleander [Kaneru]
8. Thevetia peruvianaFamily: ApocyanaceaeSinhala name/s: kaneruTamil
name/s: manjal alariEnglish/common name/s: yellow oleander, lucky nutPlant
habitat: often used for hedging in Sri Lanka native of Central & S.America but

now grown throughout tropical and subtropical regionsToxic part of the plant:
seed (although all parts toxic)Lethal dose: kernel of one fruit (or 2 leaves for a
child)Main toxic constituent/s: thevetin A, thevetin BConstituent type: cardiac
glycosidesMode of action: inhibit sodium-potassium ATPase increased
intracellular sodium and serum potassium negative chronotropic, positive
inotropic effects
9. Voltage dependent Na+ channel L-type Ca2+ channel Na+/K+ ATPase 2
K+ 3 Na+ K+ channel(s) Ca2+ 3 Na+ -adrenergic receptor Na+/Ca2+
exchanger SR (Mitochondria) Heart muscle Ryanodine receptorNa+/K+
ATPaseNa+/Ca2+ Antiporter Representative Cardiac Cell
10. 2 K+Phase 2 3 Na+ Ca2+ Ca2+ 3 Na+ Ca2+ Ca2+ SR (Mitochondria)
Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ Cell Electrophysiology
11. = DigoxinDigoxin K+ 2 [K+]Phase 2 3 [Na+] Na+ Ca2+ Ca2+ 2+ Ca
Ca2+2+ Ca2+ SR (Mitochondria) Ca 2+ 2+ 2+2+ 2+ Ca Ca Ca Ca2+ 2+ Ca2+
2+ Ca Ca Ca 2+ Ca 2+ Ca Ca Ca2+ Ca2+ Ca2+2+ Ca2+ Ca2+ Ca2+ Ca 2+ 2+
Ca 2+ Ca 2+ Ca Ca2+ Ca 2+ Ca Therapeutic & Toxic MoA
12. Clinical features of poisoning: digoxin-like Early on: burning sensation
in mouth, tingling of tongue, dry throat, giddiness, nausea vomiting, diarrhoea
Cardiovascular: sinus bradycardia, first and second degree heart block, junctional
rhythms, atrial and ventricular extrasystoles, ventricular fibrillation Other:
yellow vision, anxiety, convulsions, coma Diagnosis: cardiac glycoside blood
levels seed remnants, vomitus, gastric aspirate may help identify monitor
serum potassium and electrolytes Treatment of poisoning: induce emesis at
home (ipecac) gastric lavage within 1 hour or activated charcoal atropine
0.5mg IV for bradycardia, repeated cardiac pacing for third degree heart block
anti-digoxin Fab antibodies in severe casesReferences: Lucas GN, De Silva TUN.
Poisonous plants of Sri Lanka. Colombo: Sri Lankan College ofPaediatricians,
2006; IPCS Inchem. Thevetia peruviana. Dated March 1990 [Accessed
athttp://www.inchem.org/documents/pims/plant on 29 June 2008];
www.wikitox.org
13. Nerium oleander Pink Oleander [Kaneru]
14. White Oleander
15. Strychnos nux vomica Bitter Nut [Goda Kaduru]
16. Scientific name : Strychnos nux-vomicaSinhala name : Godakaduru, Visha
kaduruTamil name : Eddi, Etti, KagodiEnglish/common name : Poison nut, Nux
vomica, bitter nutPlant habitat dry forests of Ceylon, flowers in August A
moderate sized or large tree with an erect trunk, Slide 5 Bark Wood Leaves
Flowers FruitTraditional use : Root - cures fever and bites of venomous
snakes Used for preparation of homeopathic medicineToxic part of the plant :
seed (although all parts toxics)
17. Main toxic constituents : strychnine, (brucine)Constituent type :
alkaloids.Lethal dose : plant poisoning is rare possibly due to bitter taste The
quantity of strychnine in one seed could be fatal If seeds are swallowed
uncrushed they are not poisonousMode of action : Strychnine is a potent
convulsant. It causes increased reflex excitability in the spinal cord Brucine
resembles strychnine activity but it is less potentClinical features of poisonings :
Symptoms appear within 15 - 30 min of ingestion - Initial symptoms bitter
taste in mouth, feeling of suffocation - Twitching of the muscles in neck, body
and limbs - Extreme contractions affecting all muscles in the body - The patient
is conscious and has intense pain. - Complications - lactic acidosis,
rhabdomyolysis, acute renal failure - Death is caused by asphyxia or muscular
paralysis

 18. Diagnosis : Based on history of ingestion and development of muscular

stiffness Strychnine (and brucine) can be measured chemically but there is no
time to perform this procedure before treatment Measure acidosis, serum
potassium, SGOT, LDH, CPK etcTreatment of poisonings : Activated charcoal
Support respiratory and cardiovascular functions If convulsions cannot be
controlled with diazepam (IV or rectal), or if they recur, administer
phenobarbitone or phenytoin. Intubation with suxamethonium chloride may be
necessary When convulsions and hyperactivity are completely controlled,
gastric lavage can be performed safelyReferences :
http://www.inchem.org/documents/pims/plant [accessed 29 June2008];
Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: TheNational
Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka.
Colombo: Sri Lankan College of Paediatricians, 2006
19. Pagiantha dichotoma Eves Apple [Divi Kaduru]
20. Cerbera manghas Sea Mango [Diya kaduru]
21. Ricinus communis Castor bean[Thel / Beheth Endaru]
22. Poisonus plants of Sri lanka Ricinus communis
23. Scientific name: Ricinus communis Linn.Synonyms: Ricinus africanus
Willd., Ricinus communis L. var. viridis (Willd.) Mll. Arg., Ricinus inermis Jacq.,
Ricinus lividus Jacq., Ricinus macrocarpus G. Popova, Ricinus microcarpus G.
Popova, Ricinus persicus G. Popova, Ricinus speciosus Burm., Ricinus viridis
Willd., Ricinus vulgaris Mill., Ricinus zanzibaricus G. Popova, Croton
spinosusFamily: Euphorbiaceae (spurge family)Sinhala name/s: Erandu, Telerandu, beheth endaru, thel endaruTamil name/s: Amanakku, Muttu-kottai,
AndagamEnglish/common name/s: castor bean, castor-oil plant, Palma
ChristiiPlant habitat: Cultivated as a decorative plant in village gardens in Sri
lanka Probably of African origin but now grows in tropical, subtropical and
temperate areas Commercially cultivated mainly in Brazil, India, Italy,
etc.Traditional use: In Sri lanka the root of the plant is used in pleurodynia
(muscular rheumatism) and rheumatic pains while seeds are used for lumbago
and sciatica Africans use the bark for stitching up wounds & as a dressing for
sores Local application of fresh leaves to the lactating breast is said to produce a
powerful galactogogic action. They are also used headaches The root is a remedy
for abdominal pains and diarrhoea while root bark (and seed oil) is a purgative
also used for skin diseases and sores
24. Toxic part of the plant: seeds are the most toxic part (leaves are also
poisonous)Lethal dose: 1mg/kg pure ricin in man Ingestion of a single well
chewed bean has caused death 1-3 seeds can be fatal to a child 2-4 seeds
cause severe poisoning in an adult poisoning is unlikely if seeds are swallowed
without chewingMain toxic constituent/s: RicinConstituent type: Glycoprotein or a
toxalbumin member of a class of plant toxins known as type 2 ribosome
inactivating proteins Mode of action: Ricin impairs chain elongation in protein
synthesis, causing cell death and tissue damageClinical features of poisoning:
Early on - burning sensation of the mouth and throat occurs After 3-6 hrs nausea, vomiting, severe abdominal pain and diarrhoea resulting in dehydration
electrolyte imbalance and shock Cardiovascular - hypotention, tachycardia, ECG
changes and circulatory failure Other - prostration, blurring of vision, loss of
consciousness, convulsions, haemolysis, uraemia and liver necrosis
25. Diagnosis: Blood gases and electrolytes analysis Close monitoring of
renal, hepatic hematological systems & blood clotting. Botanical &
pharmacognostical identification of a sample of the plant or vomitus
Radioimmunoassay with antiricin antibodies labeled with iodine 125 for ricin in
plasma or urineTreatment of poisoning: Induce emesis at home (ipecac)

Immediate gastric lavage or activated charcoal Correct fluid & electrolyte

imbalance immediately In case of bronchial asthma, oxygen, B2-agonist eg
salbutamol and corticosteroids may be necessary (if acute poisoning occurred by
inhalation) Antihistamines or corticosteroids may be beneficial in treating skin
lesions (if acute poisoning occurred by skin exposure) References: Jayaweera
DMA. Medicinal plants used in Ceylon. Part 2. Colombo: The National Science
Foundation, 2006 http://www.inchem.org/documents/pims/plant.htm
www.wikipedia.org Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka.
Colombo: Sri Lankan College of Paediatricians, 2006
26. Weta Endaru
27. Datura stramoniumThorn Apple / Angels Trumpet [Kalu Aththana]
28. Datura metel
29. Scientific name: Datura metelSynonyms: Datura fastuosa (L.) Datura alba
(Nees.)Family: SolanaceaeSinhala name: Ela-attanaTamil name: AyigamCommon
names: Devils trumpet, downy thorn-apple, black datura, angels trumpet
30. Plant habitat:Native to China, India and South East Asia. It is a common
weed in waste and cultivated land in Sri-lanka and now it is used in landscaping
and gardening .Plant description: Shrub-like annual herb with large flowers,
typically white or yellow with deep purple accents. Leaves are alternate and
simple.Traditional use: Leaves/dried flowers are used to relieve asthma or
wheezing like symptoms in many cultures eg Chinese herbal medicine (yng jn
hu). Leaf poultices are applied to engorged breasts to relief excess milk
production, rheumatic swelling of joints and lumbago. Powdered root is rubbed
into gums or stuffed into cavities for toothache.Toxic part of the plant : all
parts.Main toxic constituents : tropane alkaloids
31. Leaves/flowers - mainly atropine Seeds/roots - mainly hyoscyamine Fruits
scopolamineDose: Accidentally (or intentionally) ingesting even a single leaf
could lead to severe side effectsSymptoms: anticholinergic Thirst, dry mouth,
blurred vision, photophobia, urinary retention occur soon after ingestion. Skin is
hot, dry and flushed. Pupils are dilated and fixed. Cardiovascular effects are sinus
tachycarida, hypertension, supra/ventricular arrhythmias, orthostatic
hypertension. Severe poisoning causes disorientation, agitation, violent
behaviour, convulsions, delirium, visual and auditory hallucinations, ataxia,
respiratory depression, coma.
32. Mode of action: It stimulates the central nervous system and
simultaneously depresses peripheral nerves and dilates the pupils by peripheral
action. The most probable action in this case is paralysis of the occulomotor
nerve ending or its myoneural junction.Treatment of poisoning: Ipecac to induce
emesis or gastric lavage. Activated charcoal to reduce absorption of toxic
substances. Catheterization to empty bladder if necessary Diazepam for
hallucinations and delirium.References: www.wikipedia.org/wiki/Datura_metel
www.ces.ncsu.edu/depts/hort/consumer/ poison/Daturme.htm
www.people.vcu.edu/~asneden/tropane%20alkaloids. pdf
waynesword.palomar.edu/ww0703.htm DMA Jayaweera. Medicinal plants used
in Ceylon Parts 1-5. Colombo: National Science Foundation, 2006 Lucas GN, De
Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of
Paediatricians,
33. Adenia palmata [Hondala]
34. Adenia palmata Synonyms: Adenia hondala, Granadilla hondala,
Modecca palmata Family: Passifloraceae Sinhala name/s: hondala Tamil
name/s: kondala English/common name/s: ? Plant habitat: large aerial plant
climbing by tendrils attached to large trees growing in the wet and dry zones
along forest edges Traditional use: ? Toxic part of the plant: fruit (which closely
resembles passion fruit -> accidental ingestion by children) Lethal dose: ? Main

toxic constituent/s: a cyanogenic glycoside, a toxalbumin and emulsin (an

enzyme) Constituent type: cyanogenic glycoside
35. Mode of action: 1st phase hydrocyanic acid 2nd phase local
toxalbumin effects 3rd phase - hypersensitivity reaction Clinical features of
poisoning: 1st phase vomiting, fever, restlessness, dizziness, disorientation,
abdominal pain and diarrhoea within one hour 2nd phase necrotising enteritis
-> diarrhoea with blood and mucus, abdominal colic and right iliac fossa
tenderness after a variable period of time 3rd phase myocarditis with ECG
changes, tender hepatomegaly, retinopathy with papilloedema, exudates and
haemorrhages may be seen 2- 3 weeks after ingestion all transient Diagnosis:
cardiac glycoside blood levels seed remnants, vomitus, gastric aspirate may
help identify monitor serum potassium and electrolytes Treatment of
poisoning: if no vomiting occurs induce emesis with ipecac syrup or perform
gastric lavage activated charcoal will help with the absorption of toxic
substances IV fluid therapy may be needed antidotes for cyanide poisoning
not usually necessary blood transfusion may be necessary in the 2nd
phaseReference: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka.
Colombo: Sri Lankan College of Paediatricians, 2006
36. Datura metel atropine, hyoscine, hyoscyamine alkaloids seed (all)Gloriosa
superba colchicine tuberNicotiana tabacum nicotine leaf (all)Pagiantha
dichotoma ? narcotic, datura-like seed(Peganum harmala) harmaline
seedStrychnos nux vomica strychnine seedAlocasia macrorrhiza calcium oxalate
crystals leaf/stem (all) (needle-like), toxicAnthurium sp. proteinsDieffenbachia
sp.Scindapsus aureusZantedeschia aethiopicaCerbera manghas cerberine,
odollum,thevetin cardiac glycosides fruit kernelThevetia peruviana thevetin A,
theventin B fruitAdenia palmata cyanogenic glycoside, toxalbumin, cyanogenic
glycosides fruit emulsin enzymeManihot utilissima linamarin, (linase enzyme)
tuberAbrus precatorius abrin toxalbumins seedJatropha curcas curcin seed
(all)Jatropha multifida JatrophinRicinus communis ricinEucalyptus robusta oil of
eucalyptus (eugenol) volatile oils allMyristica fragrans myristicin seed
(aril)Amanita phalloides phalloidin, phalloin, phallolysin phlallatoxins aerial parts
alpha, beta, gamma amanitin amatoxins (mushroom)
37. Abrus precatoriusBlack-eyed Susan / Rosary pea / Precatory bean [Olinda]
38. Manihot utilissima Scientific name: Manihot utilissimaSynonyms:
Jatropha manihot (Kunth), Manihot manihot (Cockerell), Manihot melanobasis
(Muell)Family: EuphhorbiaceaeSinhala name: "Manyokka"Tamil names:
Maravalli AlavalliEnglish /common name: cassava, manioc, tapiocaPlant
description: shrub with a big tuberous rootPlant habitat: The sweet and bitter
cassava plants are indigenous toSouthern and Central America but have been
introduced to almostall tropical countriesTraditional use : Used as a food source.
American Indians use thebrown juice for burns By : J.S.R.Sherif
E.M.A.K.Ekanayaka
39. Toxicity of the plant : The leaves and roots contain free and bound forms
of thecyanogenic glycoside linamarin, which is converted to cyanide in the
presence oflinamarinase, a naturally occurring enzyme in cassava or via
exposure to theatmosphere. (Slide 5)Two varietiesSweet - contains as little as 20
milligrams of cyanide (CN) per kilogram of freshrootsBitter - may produce more
than 50 times as much (1 g/kg)The paralytic neurological disease caused by
long-term consumption of cassava iscalled mantakassa. Yam that is cut, washed
and boiled in an open container at72C for long enough will destroy the enzyme
and any hydrocyanic acid formed willevaporate.Lethal dose : One dose of pure
cassava cyanogenic glucoside (40mg) issufficient to kill even a cow. Hence about
300 grams of fresh root is enough to killan adult human and about 125 grams of
fresh root would be enough to kill a childMode of action :A "large" sudden dose

(HCN) is highly poisonous to all humans and animalsbecause it rapidly

inactivates cellular respiration thereby causing death. This meansthat it stops
cells from being able to use oxygen. The heart, respiratory system andcentral
nervous system are most susceptible to cyanide poisoning and cease tofunction
as a result of lack of oxygen.
40. Clinical features of poisoning : Acute: Within 3-6 hours of ingestion
burning epigastric pain, vomiting, flushing of skin, dry mouth, tachycardia, pupil
constriction, restlessness, giddiness and hallucinations occur. Chronic: initial
symptoms are described as tremor, cramps, a heavy feeling and/or weakness in
the legs, a tendency to fall down and difficulty remaining upright There is a
visible hypertonic gait when walking or running Occasionally there will be lower
back pain, blurred vision, speech difficulties and/or paresthesia of the legs, but
they disappear within a month, later some people will develop dysarthria,
abnormalities of eye movement, hypertonicity of the arms Diagnosis Acute
poisoning: signs of extreme metabolic acidosis Chronic poisoning: a visible
hypertonic gait when walking or running, bilateral brisk knee and Achilles tendon
reflexes without signs of vertebral lesions The onset of the disease takes less
than one week and then remains stable Urinary concentrations of (thiocyanate
and linamarin are elevated) (Cyanide (CN-) is normally converted thiocyanate
(SCN-) by the enzyme rhodanase) Treatment of poisoning There is no known
treatment for cyanide poisoning . Treatment with sodium thiosulphate
(Na2S2O3), a cyanide antidote, gave disappointing results. A good and varied
diet, high dose multivitamins (specially B12 ,it detoxifies the HCN) and physical
rehabilitation are advised.References Affran DK. Cassava and its economic
importance.
Forensic Toxicology is a branch of Forensic Medicine dealing with Medical and
Legal aspects of the harmful effects of chemicals on human beings. Below given
are described the general considerations of Forensic Toxicology useful for
Undergraduate and Post-Graduate Student of Forensic Medicine.
Poisoning in India:
Suicidal (KCN, HCL, Opium, Barbiturates, organophosphorus, oxalic acid oleander
etc), homicidal(arsenic, aconite, thallium, oleander, madar, carbamates,
organophosphorus etc.) and accidental poisoning are seen in India. Older poisons
like opium and arsenic are replaced by newer poisons.
Common homicidal poisons are: Arsenic, Antimony, Oleander, Nux-Vomica,
Madar, powdered glass and aconite. Cattle Poisoning is also common, the poison
used are Arsenic, Abrus precatrotius, Yellow oleander, zinc phosphide, nitrates,
aconite etc.
Important Definitions:
Toxicology: is the science dealing with properties, action, toxicity, fatal dose,
detection estimation of, interpretation of the result of toxicological analysis and
management of Poisons.
Poison: A Poison is defined as any substance which when administered in living
body through any route (Inhalation, Ingestion, surface absorption etc) will

produce ill-health or death by its action which is due to its physical chemical or
physiological properties. Eg: alphose, sulphuric acid, arsenic etc.
Drug (WHO 1996): Drug is any substance or product that is used or intended
to be used to modify or explore physiological systems or pathological states for
the benefit of the recipient. Eg: paracetamol, ciprofloxacin, salbutamol,
oestrogen, insulin etc.
Clinical Toxicology: Deals with human diseases caused by, or associated with
abnormal exposure to chemical substances.
Toxinology: refers to toxins produced by living organism which are dangerous to
man, eg: snake venom, fungal and bacterial toxins etc.
Chelating Agents: are the substances which act on absorbed metallic poisons.
They have greater affinity for metals as compared to endogenous enzymes. The
complex of agent and metal is more water soluble than metal itself, resulting in
higher renal excretion of the complex. E.g.: British anti-lewisite (B.A.L.,
dimercaprol), E.D.T.A. (ethylene diamine-acetic acid), Penicillamine (Cuprimine),
Desferroxamine etc.
Ecotoxicology: It is concerned with the toxic effects of chemical and physical
agents on living organisms, especially in population and communities within
defined population. Acute poisoning is caused by an excessive single dose, or
several dose of a poison taken over a short interval of time.
Chronic Poisoning is caused by smaller doses over a period of time, resulting in
gradual worsening. eg: arsenic, phosphorus, antimony and opium.
Subacute poisoning shows features of both acute and chronic poisoning.
Fulminant poisoning is produced by a massive dose. In this death occur rapidly,
sometimes without preceding symptoms.
Parasuicide (attempted suicide or pseudicide) is a conscious often impulsive,
manipulative act, undertaken to get rid of an intolerable situation.
Culpable Homicide: Sec 299 IPC; Causing death of a person by an act, with the
intention of causing such bodily injury and is likely to cause death, or with the
knowledge that he is likely, by such an act to cause death.
Antidote: Antidotes are substances which counteract the effect of poison. They
are divided into Mechanical, Chemical, Physiological and specific receptor
antagonists.
Laws in relation to poison and drugs: Different sections of Indian penal code
related to poisons are as follows
Sec. 272 I.P.C. - Punishment for adulterating food or drink intended for sale, so as
to make the. same noxious, may extend upto 6 months imprisonment of either
term and/or fine upto one thousand rupees.

Sec. 273 I.P.C. - Punishment for selling noxious food or drink may be
imprisonment of either description for a period of 6. months and or fine upto one
thousand rupees.
Sec. 274 I.P.C. - Punishment for adulteration of drugs in any form with anychange
in its effect knowing that it Will be sold and used as un-adulterated drug, may be
imprisonment of either description for a period-of 6 months and or fine.
Sec. 275 l.P.C. - Punishment for knowingly selling adulterated drugs with less
efficacy or altered action serving it for use as unadulterated may be
imprisonment of either description for 6 months and or fine.
Sec. 276 I.P.C. - Punishment for selling a drug as a different drug or Preparation,
may be imprisonment of either description which may extend upto 6 months and
or fine. .
Note - In the State of West Bengal, the punishment for these offences
described under sections 272 to 276 may be upto imprisonment for life
with or without fine.
Sec. 277 I.P.C. Punishment for fouling water of public spring or reservoir may be
imprisonment of either description which may extend up to a period of 3 months
and or fine.
Sec. 278 I.P.C. - Punishment for voluntarily making atmosphere noxious to health
is fine which . may extend upto five hundred rupees.
Sec. 284 I.P.C. Punishment for negligent conduct with respect to poisonous
substance may be imprisonment of either description which may extend upto 6
months and or fine which may extend upto one thousand rupees.
Sec. 328 I.P.C. :Punishment' for causing hurt by means of poison or any
stupefying, intoxicating or unwhlolesome drug or any other thing with the intent
to commit an offence shall be imprisonment of either description for a term
which may extend to ten years with or without fine.
Sources of Poison:
1. Domestic or household sources - In domestic environment poisoning may
more commonly occur from detergents, disinfectants, cleaning agents,
antiseptics, insecticides, rodenticides etc.
2. Agricultural and horticultural sources- different insecticides, pesticides,
fungicides and weed killers.
3. Industrial sources- In factories, where poisons are manufactured or poisons are
produced as by products.
4. Commercial sources- From store-houses, distribution centers and selling
shops.

5. From uses as drugs and medicines Due to wrong medication,overmedication

and abuse of drugs.
6. Food and drink contamination in way of use of preservatives of food grains or
other food material, additives like colouring and odouring agents or other ways
of accidental contamination of food and drink.
7. Miscellaneous sources- snakes bite poisoning, city smoke, sewer gas poisoning
etc.
Classification of poisons
1. According to the site and mode of action
(A). local Action
Corrosive
Strong Acid: mineral acid and organic acid
Strong alkali
Metallic: Mercuric Chloride
Irritant
Mechanical: Glass Powder
Chemical
Inorganic: weak acid, weak alkalies, Inorganic non-metals, Inorganic
Metals.
Organic: Chemical preparations, Animal and vegetable origin
(B) Remote Action
Neurotics
C.N.S. Poisons
i. Somniferous: opium and its alkaloids, Barbiturates.
ii. Inebriant (Intoxicant): Alcohol, ether, Chloroform.
iii. Stimulant
iv. Deliriant: Dhatura, Belladona, Hyocyamus, cannabia
indica.
v. Stupefaciant
vi. Hallucinogens

vii. Convulsant:

Spinal (Convulsant)
i. Strychnos Nux Vomica
Peripheral Nerves
i. Local Anaesthetics: Cocaine, Procaine.
ii. Relaxants (curare).
Cardiac Poisons
KCN, NaCN, Digitalis, Aconite, Nicotine, Quinine, Oleander
Asphyxiants: Carbon Dioxide, CO, hydrogen sulphide
Nephrotoxic: Oxalic Acid, Mercury, Cantherides
Hepatotoxic: Phosphorus, Carbon tetrachloride, Chloroform.
Miscellaneous: Food Poisons.
(C). Combined local and remotes action: Classification of Poison according to
motive or nature of use:
1. Homicidal: Arsenic, Aconite, Digitalis, Abrus Precatorius, Strychnos nuxvomica.
2. Suicidal: Opium, Barbiturate, Organophosphorus, carbolic acid, copper
sulphate.
3. Accidental: Aspirin, organophosphorus, copper sulphate, snakes bite, Ergot,
CO, CO2, H2S.
4. Abortifacient: Ergot, Quinine, Calotropis, Plumbago.
5. Stupefying agent: Dhatura, cannabis, chloral hybrate.
6. Agents used to cause bodily injury: Corrosive acids and alkalies.
7. Cattle Poison: Abrus precatorius, Calotropis, plumbago.
8. Used for malingering: semicarpus anacardium
Ideal Suicidal poison: should be easily available, No bad taste, cause No pain,
cheap, highly toxic, tasteless or pleasant taste, capable of being taken with food
or
drink.
Ideal Homicidal poison: it should be cheap, easily available, colorless tasteless

odourless, highly toxic, No residual product lest, S/S resembles natural diseases,
No antidote, Shows no post-mortem changes capable of being administered with
food or drink.
Route of Administration/absorbtion:
Oral (commonest) eg: alphos, acids,
Inhalation: gas poison
Parenteral (IM, IV, Sub-Cutaneous, Intra-Dermal)
Natural Orifices other than mouth (Nasal, Rectal, Vaginal, Urethral),
Ulcers, wounds and intact skin.
Fate of poison in body: A part of the poison taken orally gets eliminated
unabsorbed by means of defecation and vomiting. Before absorption the poison
may exert its effects in the G.I. Tract. When absorbed, the poison reaches
different
parts of the body and organs through circulation. Some poisons reach some
tissues easily. Others may not cross some tissue barrier. Cumulative poisons get
accumulated in some organs or tissues. A part of poison is eliminated as such
through different route of elimination. But major part is detoxified or metabolized
in
the body and than excreted after exerting its toxic effects on the body. Liver is
the
main organ to detoxify or metabolize most of the poisons.
Certain poisons like Chloroform, Phosphorus, Nitrates and Acetic acid disappear
by evaporation or oxidized or destroyed in the body and no trace of them can be
detected in the body of post-mortem is delayed.
Excretion of poisons: Unabsorbed poisons are excreted through faeces and
vomitus. Absorbed poisons are excreted mostly by urine. A part of volatile poison
is exhaled out. Some portion of poison is excreted through bile, saliva, milk,
sweat,
tear, hair and nails. Factors influencing the actions of a poison in the body.

1. Quantity: A high dose of poison acts quickly and often resulting in fatal
consequences. A moderate dose causes acute poisoning. A low dose may have
sub-clinical effects and causes chronic poisoning on repeated exposure. Very
large dose of Arsenic may produce death by shock without dose irritant
symptoms, While smaller dose than lethal dose produces its therapeutic effects.
2. Physical form: Gaseous or volatile poisons are very quickly absorbed and are
thus most rapidly effective. Liquid poisons are more rapid than solid poisons.
Some poisonous vegetable seeds may pass through the intestinal canal
ineffective when taken intact due to their impermeable pericarp. But when taken
crushed, they may be rapidly fatal.
3. Chemical form: Chemically pure arsenic and mercury are not poisonous
because these are insoluble and are not absorbed. But white arsenic (arsenic
oxide) and mercuric chloride are deadly poisonous. Barium sulphide is deadly
toxic but barium sulphate is non-toxic.
4. Concentration (or dilution): concentrated form of poison are absorbed more
rapidly and are also more fatal but there are some exceptions too.
5. Condition of the stomach: food content presence of food-stuff acts as diluent
of the poison and hence protects the stomach wall. Dilution also delays
absorption of poison. Empty stomach absorbs poison most rapidly. In cases of
achlorohydria, KCN and NaCN is ineffective due to lack of hydrochloric acid,
which is required foe the conversion of KCN and NaCN to HCN before absorption.
6. Route of administration: absorption rate is different for different routes.
7. Age: some poisons are better tolerated in some age groups. Opium and its
alkaloids are tolerated better by elderly subjects but badly by children and
infants. Belladonna group of drugs are better tolerated by children than by
adults.
8. State of body health: A well built person with good health can tolerate the
action of poison better than a weak person.
9. Presence of disease: In certain diseased conditions some drugs are tolerated
exceptionally well e.g.: sedatives and tranquilizers are tolerated in very high
dose by manic and deliriant patients.
10. Intoxication arid poisoning states - In certain poisoning cases some drugs are
well tolerated, like, in case of strychnine poisoning, barbiturates and sedatives
are better tolerated. Whereas in case of barbiturate poisoning any sedative or
tranquilizer will accentuate the process of death.
11. Sleep - Due to slow metabolic process and depression of other body functions
during sleep, usually the absorption and action of the poison is also slow. But
depressant drugs may cause, more harm during the state of sleep.
12. Exercise - Action of alcohol on C.N.S. is slowed during exercise because more
blood is drawn to the muscles during exercise.

13. Cumulative action of poisons: Preparations of cumulative poisons (poisons

which are not readily excreted from the body and are retained in different organs
of the body for a long time) like lead may not cause any toxic effect when enters
the body in low dose. But when such poisons enter over a long period of time,
may cause harm when their concentration in different tissue reaches high level
due to their cumulative property.
14. Tolerance may develop by individuals on long term exposue to a particular
poison.
15. Idiosyncracy: some persons may react adversely to a particular drug though
the general population tolerates the drug well.
Signs and symptoms: The signs and symptoms may be different for different
poisons and is responsible on the nature and action of the poison. They can be
local, remote or combined and
are will be taught in the individual poisons.
Diagnosis of poisoning
In the Living
1. History of the case as stated by the patient himself
and his/her relatives or friend. Full information about
time of onset of the present illness, Initial symptoms,
progress, relation with food, condition of other
persons taking same food or drink, possible source,
any previous history of poisoning, H/o depression,
quarrel. Also note down the color, smell, consistency,
taste and quantity of the possible poisonous
substance.
2. Signs and symptoms.
3. Details of examination.
4. Preservation and laboratory investigation of vomitus, excreta, stomach wash,
scraps from any stains area on the body, blood, stained part of the clothes,
contents of a doubtful container, left over ant part of food or drink.
In the Dead:
1. History of the case as stated by police or relatives. H/o 2 or more vital points
(1 how long the victim survived after initial symptoms. 2. Any treatment).

2. Post-mortem Examination (external and internal)

3. Chemical Analysis: detection of poison in the body fluids.
4. Preservation of viscera and other material for lab. Examination. Postmortem
Findings in Case Of Death Due To Suspected Poisoning
External Examination
1. Postmortem staining: Deep blue - In case of asphyxiant poisons and aniline.
Bright red or cherry red - In case of CO and HCN poisoning.
2. Deep cyanosis - With opium and cardiac poisons.
3. Early rigor mortis - With strychnine.
4. Early appearance of the sign of decomposition - With H2S gas.
5. Detectable smell - In case of volatile poisons, opium and HCN, KCN or NaCN.
6. Haemorrhagic spots under the skin and mucus membrane: Phosphorus. .
7. Ulceration on lips and near the angles of mouth - Corrosive poisons.
8. Stain near mouth and on hands - Nitric acid and copper sulphate.
9. White froth from mouth and nose Opium and its alkaloids. .
10. Blood tinged froth from mouth and nose Organophosphorus compounds.
11. Alopecia, hyperpigmentation and hyperkeratosis - Arsenic poisoning over a
long period.
12. Staining, erosion and ulceration near the female external genitalia - Use of
abortifacient agents or torturing agents.
13. Injection marks - Injection of poisons (snake bite or otherwise), sign of
treatment. Internal findings: The G.I.T. should be examined very carefully since
signs of corrosive or irritant poisons are likely to be find therein. These signs are
Hyperemia, softening, ulceration and perforation. Apart from this below given is
a brief note of internal finding in cases of poisoning.
1. Corrosion, ulceration and desquamation of inner aspects of lips, mucus
membrane of mouth and tongue - Corrosive agents.
2. Soft, swollen, sodden, translucent, bleached tongue and mucus membrane of
mouth-Corrosive alkali
3. Hardening of mucus membrane - Phenol
4. Phenol Yellowish discoloration - Nitric acid
5. Bluish discolouration - Copper sulphate

6. Carbonization and charring- Conc. Sulphuric acid

7. Chalky appearance and consistency of teeth -:Sulphuric acid
8. Blue lining in the gum - Chronic lead poisoning
9. Swollen gum, loose teeth, foetid smell - Acute mercuric chloride poisoning;
chronic phosphorus poisoning
10. Corrosion, irritation, desquamation and haemorrhage in the inner wall of the
esophagus - Corrosive and irritant poisons
11. Hardening and whitish discolouration In case of Carbolic acid poisoning
12. Discoloration and staining of inner aspects of mouth - With coloured poisons
13. Oesophageal stricture - A complication of sulphuric acid ingestion
14. Stomach
(a) Thickening and softening of the wall -Corrosive and irritant poisons
(b) Hard wall- Carbolic acid
(c) - Hard and leathery wall- Formaldehyde
(d) Hyperemia haemorrhageand desquamation of mucus membrane Irritant
poison
(e) Laceration and sloughing Corrosive poison
(f) Perforation - H2SO4 and HN3
(g) Yellowish discolouration of mucus membrane - HNO3; Bluish - CuSO4; Slaty
grey - HgCl3 .
(h) Stomach content - Blood - Corrosive and irritant; Yellowish HNO3 Bluish CuSO4 Luminous in dark - Phosphorus; Detectable tablet - soneryl; Powder oxalic
acid, white arsenic; Detectable smell - kerosene, alcohol, chloroform,
organophosphorus compounds, chlorinated hydrocarbons, opium, cyanogen,
formaldehyde, phosphorus; Detectable liquid - kerosene.
15. Small intestine - May show irruption, sometimes may show presence of
poisonous remains.
16. Large intestine - May show ulcerations, as in case of HgCI3 similar in
appearance of ulcers of bacillary dysentery. It particularly involves the ascending
and transverse colons.
17. Liver - Different degenerative changes occur in cases of poisoning with
poisons like phosphorus, carbon tetra-chloride, chloroform, tetrachlorethylene
and many other poisons. The type and extent of the degenerative changes occur

depending on the type of poison, dose, duration of the exposure and physical
condition of the patient.
18. Kidneys - Swollen, reddish, soft, sometime greasy in touch with haemorrhage
in calyces and other degenerative changes - cases of poisoning with mercury,
oxalic ad carbolic acid, phosphorus, cantherides, viper snake venom and many
others. In case oxalic acid poisoning, white powder of oxalate crystals are
present in the tubules and the calyces .
19. Urinary bladder - Haemorrhage in cases of abrus precatorius, viper snake bite
em, cantheride poisoning.
20. Larynx and trachea - Hyperaemic, inflamed -In cases of inhalation of irritating
gases leaking of corrosive agents while ingestion vomiting; froth in the lumen of
trachea and larynx in case of opium and organo:phosphorus poisoning.
21. Chest cavity -Smell of volatile poisons cyanogen, opium etc. can be detected.
22. Lungs - Voluminous, congested, presence of Tardieu's spots - In case of
asphyxiants and inhaled poisons. Cut section gives blood stained frothy-fluid in
case of opium and other asphyxiants.
23. Heart- Presence of subendocardial haemorrhagic spots in cases of arsenic,
phosphorus, mercuric chloride etc.
24. Brain and spinal cord - Congestion and edema of brain and spinal cord in
cases of cerebral and spinal poison (e.g. strychnine: respectively. Brain may be
congested. oedematous with occasional haemarrhagic points at places in cases
of asphyxiant poisons.
25. Uterus and vagina - Staining, congestion haemorthage, ulceration in cases of
attempted abortion by use of local abortifacient agents. Preservation of viscera
and other materials In all cases of poisoning
1. Stomach with its full contents.
2. Half of Liver or 500 gms whichever is more.
3. A loop of small intestine.
4. Half of each kidney.
5. Some portion of spleen In some particular poisons
1. Blood 100ml: in cases of absorbed poisons.
2. Urine 100ml in all cases where blood is preserved.
3. Part of both lungs in cases of Volatile poisons.
4. Heart in case of cardiac poisons.
5. Brain in cerebral poisons.

6. Spinal in spinal poisons.

7. Bones in arsenic and lead.
8. Hair in arsenic and copper.
9. Nails in arsenic.
10. Skin-scrap from areas stained with a suspected poison.
11. Stained areas of dress, suspected packet of poision, strips of tablets
recovered from pocket. Preservative used For Viscera: absolute alcohol or
rectified spirit. Exception: alcohol, chloroform, chloral hydrate, formaldehyde,
ether, phosphorus (alcohol prevents the luminosity of phosphorus in dark) etc.
Blood should be preserved in fluoride, oxalate, E.D.T.A., gold chloride or citrate
Urine and clothes: without any preservative. Management of a case of poisoning
Immediate resuscitative (Basic Management) measures in comatose patient
should be adopted to stabilize respiration, circulation and the correct CNS
depression.
A) Airway: opening up and cleaning the airways (oral cavity, Nostrils) of
secretions, vomit or any foreign body. Pull tongue forward
B) Breathing: Supplemental oxygen therapy should be administered
C) Circulation: I.V. fluid administration
D) Depression of CNS should be corrected
Specific Management
1. Removal of patient from source of exposure: Patient should be removed away
from the source of poison as quickly as possible.
2. Removal of the unabsorbed poison. In case of contact poison washing of
affected area with soap water with gentle rubbing will be helpful. In cases of
ingested poisons Gastric lavage is useful within 3 hours of ingestion and is done
by stomach tube ( Ewald or Boas tube) or by Ryles tube followed by emesis
(physical or by drugs like Ipecacuanha 1-2 gm, mustard oil 1 Tsf in a glass of
water, concentrated salt solution 6%, Zinc Sulfate 1-2gm in water, apomorphine
hcl 1-2ml o 3 mg /ml). In case of injected poison ligature is applied above the
wound. In cases of inhaled poison the patient should be immediately removed to
fresh air.
3. Diluting the poison and delaying the absorption by water or food.
4. Elimination of absorbed poison by increases urination (diuresis), increased
perspiration (diaphoresis), Dialysis, use of chelating agents.
5. Use of specific antidote

6. Symptomatic treatment including safeguarding respiration and maintenance

of circulation.
Counterindications of gastric lavage with stomach tube:
1. In corrosive poisons.
2. Convulsant poisons.
3. Unconscious or semi-conscious patients
4. In infants and children: Ryles tube or infant feeding tube is used.
Antidote: Antidotes are substances which counteract the effect of poison. They
are divided into Mechanical, Chemical, Physiological and specific receptor
antagonists.
Physical or mechanical antidote prevents the action of poison mechanically,
without destroying or inactivating the damaging actions of the poisons. Eg:
adsorbents like activated charcoal, Demulcents like egg albumin, starch or milk,
Diluents like water or milk, bulky food like boiled rice or vegetables. Chemical
antidotes are substances which disintegrate and inactivate poisons by
undergoing chemical reaction with them. Eg: Weak acids and alkali, common
salt,
egg albumin, KMNO4.
Physiological antidote have their own action producing signs and symptoms
opposite to that produced by the poison.
Eg: Naloxone for morphine, Neostigmine for datura or hyoscin group, Barbiturate
for strychnine.
Serological Antidote: Anti-snake venom serum for snake bites poisoning.
Universal Antidote: It is a combination of physical and chemical antidotes. When
the exact nature of poison is not known then universal antidote is used which
acts
against a wide range of poisons.
Constituents
Activated charcoal 2 parts

Magnesium oxide 1 part

Tannic acid 1 part
Dose 1TSF (15gms) in a glass water (can be repeated)
Activated charcoal for its adsorbent action, Magnesium oxide neutralizes acids
poisons, tannic acid precipitates alkaloids.
Household antidotes:
1. Strong liquid tea (contains tannic acid) precipitate alkaloid and metallic
poisons.
2. Starch for iodine.
3. Milk and raw egg for mercury, arsenic, heavy metal.
4. Flour suspension and mashed potatoes can be used in place of activated
charcoal.
5. Milk of magnesia or soap solution for acid poisoning.
6. Orange, lemon juice or vinegar for alkali poisoning.
Chelating agents are the substances which act on absorbed metallic poisons.
They have greater affinity for metals as compared to endogenous enzymes. The
complex of agent and metal is more water soluble than metal itself, resulting in
higher renal excretion of the complex. Eg: British anti-lewisite (B.A.L.,
dimercaprol), E.D.T.A. (ethylene diamine acetic acid), Penicillamine (Cuprimine),
Desferroxamine etc.
B.A.L. (British Anti-Lewisite, 2-3 dimercaptopropanol) has 2 unsaturated SH
radicals which combines with metal in circulation , thus tissue enzymes are
spared.
Usefuls in cases of Arsenic, mercury, copper, bismuth, gold etc
Dose: 3-4 mg/kg BW as a preparation of 10% with 20% Benzyl benzoate in
arachis
oil given deep intra-muscular (may cause embolism on I.V. inj.)4 hourly fo0r first
2
days followed by twice daily for 10 days
E.D.T.A. (Ethylene diamine tetra-acetic acid) it combines with sodium to form
sodium salt and then with calcium to form disodium calcium edentate which
combines with free metal and inactivates it biologically. It is best chelate for lead.
Dose for adults 1gm twice daily at 12 hour interval slow I.V. Injection mixed with
5% glucose saline. Penicillamine: It has stable SH radical which combines with
free metal. Dose
30mg/Kg BW/Day in 4 divide doses for 7 days.
Desferrioxamine: It is specific antidote for iron. Dose 8-12 gm orally. For
absorbed iron 2gm I.V. with 50% laevulose solution.
Duties of a Registered Medical Practitioner in connection with poisoning
cases :
(a) Try to save the life of the patient and give emergency necessarytreatment.
(b) If necessary, the patient should be sent to a better hospital, if possible a
government hospital, if the condition of the patients demands and permits the
shift.
(c) To take a detailed history of the case as to when and how the symptoms
started what is the progress; whether related to taking of any food or drink ;

whether the number of sufferer is more than one whether any treatment was
already given and whether there is any history of previous poisoning.
(d) The doctor should himself record full history of the case, the signs and
symptoms and progress.
(e) The doctor should collect and preserve the vomitus, stool, urine, clothes
stained with poison or vomitus, doubtful container with remaining part of the
poison, if any, and if necessary blood, for laboratory investigations.
(f) The doctor should arrange for a reliable attendant of his own choice, for
patient.
(g) The doctor should. inform the police station of the area about the case
irrespective of whether the patient survives or dies and whether it appears to be
a case of suicide or homicide or accident.
(h) If death is apprehended then arrangement for recording dying decleration
should be made.
(i) In case of death, death certificate should mention about the poisoning or
suspected poisoning with recommendation for post-mortem examination.