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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

barbiturates other sedatives and hypnotics.1. nitrogen) Hypoxic gas mixture R Reduced inspired oxygen fraction (FIO2) Respiratory depression (e.strychnine.g. butane.g. cardiac and nonspecific shock. spinal cord. 2.g. Table . opioids.g. it produces both specific CNS.organophosphates botulinus toxin) or spasm (e.1 : Some major causes of blockade of the oxygen pathway due to poisoning with mechanisms.phencyclidine) Aspiration pneumonitis Adult respiratory distress . The effects and the poisons involved are given in Table 1. methane. carbon dioxide. Poisons And The Oxygen Pathway Most of the poisonings involve the oxygen pathway. Cause Mechanism Effect Asphyxiant gases (e. Failure of ventilation (type II respiratory failure) Reduced alveolar oxygen tension (PAO2) Respiratory muscle disorders: paralysis (e. from the inspired air to cellular respiration. Local action-Poisons act directly on the tissues and cause corrosion. Remote action-As the poison gets absorbed systemically. irritation and inflammation.

dextropropoxyphene) Chemical asphyxiants (cyanide.g. tricyclic antidepressants.b-blockers.nitrites) Haemolysis (e. stibine) Loss of functioning haemoglobin Reduced arterial oxygen content(CaO2) Myocardial depressants (e.arsine.syndrome (paraquat) Failure of oxygen transfer (type I respiratory failure) Reduced arterial oxygen tension (PaO2) Carboxyhaemoglobin (carbon monoxide) Methaemoglobin (e.g.g. 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 .

mechanical  Neurotics – Somniferous. death certificate should not be issued 18. method of their detection and estimation and autopsy findings 3. symptoms. MEDICAL DUTY  Care and treatment of the patient 17. lethal dose. 2. mode of action. properties.In the Dead  PM examination  Chemical analysis 15. Most frequently the poison undergoes biotransformation in the liver. nonmetallic. hair and nails retain inorganic poisons like Arsenic. 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. ROUTE OF ADMINISTRATION  Enteral  Parenteral  Inhalaional  External application  Introduction into natural orifice 8. Epidermis. 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. inebrians 6. treatment. TOXICOLOGY  Toxicology is the science which deals with poisons with reference to their sources. After absorption the poison is dealt with in one of the several ways. sweat glands. Bony skeleton holds substances like lead and radioactive metals. DIAGNOSIS OF POISONING . mucus and lungs. saliva. 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 . DIAGNOSIS OF POISONING  In the Living  In the Dead 13. POISONS  Poison is a substance which when administered. organic vegetables. CLASSIFICATION OF POISONS ACCORDING TO MODE OF ACTION  Corrossives – Acids and alkalies  Irritants – Metallic. nature of the fatal results. The main route of excretion of the poison or its end products is the urinary tract.Fate of poisons in the body Greater part of a poison is lost by vomiting and diarrhea. TYPE OF POISONING  Acute  Chronic  Sub acute  Fulminant 11. inhaled or ingested is capable of acting deleteriously on the human body 4. FACTORS MODIFYING ACTION OF POISONS  Dose and quantity  Form of poison  Method of administration  Condition of the body 10. ACTION OF POISONS  Local  Remote  Combined remote and local  General action 9. DIAGNOSIS OF POISONING . animals. CLASSIFICATION OF POISONS ACCORDING TO MODE OF ACTION …  Deleriants  Spinal  Cardiac  Asphyxiants  Peripheral poisons 7. MEDICO-LEGAL DUTY OF DOCTOR IN SUSPECTED CASE OF POISONING  Medical Duties and Legal Duties 16. Other routes are bile ducts.In the Living  A/c or C/c 14. FATE OF POISONS IN THE BODY 12.

itching and tingling around the mouth and throat with thirst – nausea. especially the tubers. 2006  7.Lucas GN.inchem. glory lily. haematological analysesTreatment of poisoning: • hospitalize the patient immediately • induce vomiting (ipecac) / gastric lavage • give repeated activated charcoal • supportive care eg IV fluid. CLASSIFICATION OF ANTIDOTS  Mechanical / Physical  Chemical  Physiological / Pharmacological  Universal PLANT POISONS 1. coma • Death occurs due to shock or respiratory failureDiagnosis: • Toxicological. assisted ventilation may be neededReferences: Jayaweera DMA. polyneuropathy cardiac arrhythmias. 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. tiger clawPlant habitat: • native of tropical Africa.America but . bronchial constriction. ANTIDOTS  Are remedies which counteract or neutralise the effect of poisons without causing appreciable harm to the body 20. Definition. Medicinal plant use in Ceylon . Thevetia peruviana Yellow Oleander Kaneru Nerium oleander Pink Oleander Kaneru White Oleander Strychnos nux vomica Bitter Nut Goda KaduruPagiantha dichotoma Eve‟s 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. severe diarrhoea with blood and mucus • These lead to – electrolyte imbalance. Thevetia peruviana Yellow Oleander [Kaneru]  8. Gloriosa superba Glory Lily [Niyangala] 4. etc • found in low country Sri LankaTraditional use: • tuber – bruises and sprainsPoisonous parts of the plant: • The entire plant. De Silva TUN. hepatic insufficiency. Malaya. Scientific name: Gloriosa superbaSinhala name: NiyangalaTamil: Karththigaikkilangu. leucopenia. are extremely poisonous 5.org/documents/pims/plant (Accessed 4 July 2008].tubers not a foodsource!)Clinical features of poisoning: • Initial symptoms develop within 6-12 hours of ingestion – burning pain. causes disturbances of function which may result in illness or death. convulsions. 2. biomedical. • After 24 hours patients develop – Muscle weakness. Thevetia peruvianaFamily: ApocyanaceaeSinhala name/s: kaneruTamil name/s: manjal alariEnglish/common name/s: yellow oleander. hair-producing cells -> hair loss) – It can alter neuromuscular function – (It can withstand drying. India. dehydration. delirium. Poisonous plants of Sri Lanka. lucky nutPlant habitat: • often used for hedging in Sri Lanka • native of Central & S. acute renal failure • In severe cases there may be – Respiratory depression. myoglobinuria. blood gas. 2006. storage and boiling .Part 3. clotting defects with bleeding. thrombocytopenia.Colombo: The National Science Foundation. intestinal epithelium.http://www. hypovolaemic shock manifested hypotension and tachycardia  6.19. numbness. IllangalliEnglish/common names: • flame lily.A substance which & when taken or administered into body in whatever manner or form other than therapeutic amounts. Colombo: SriLankan College of Paediatricians. confusion. intense vomiting – abdominal pain.

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. acute renal failure . dry throat. Main toxic constituents : strychnine. 2 K+Phase 2 3 Na+ Ca2+ Ca2+ 3 Na+ Ca2+ Ca2+ SR (Mitochondria) Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ Cell Electrophysiology  11. Visha kaduruTamil name : Eddi. Colombo: Sri Lankan College ofPaediatricians. Etti. rhabdomyolysis. = 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. White Oleander  15. Dated March 1990 [Accessed athttp://www. Clinical features of poisoning: “digoxin-like” • Early on: burning sensation in mouth. 2006. body and limbs .5mg IV for bradycardia. Nux vomica.Twitching of the muscles in neck.Extreme contractions affecting all muscles in the body .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. Slide 5  Bark  Wood  Leaves  Flowers  FruitTraditional use : Root . Nerium oleander Pink Oleander [Kaneru]  14.org  13. IPCS Inchem. Strychnos nux vomica Bitter Nut [Goda Kaduru]  16. junctional rhythms. feeling of suffocation . nausea vomiting. thevetin BConstituent type: cardiac glycosidesMode of action: inhibit sodium-potassium ATPase • increased intracellular sodium and serum potassium • negative chronotropic. vomitus. positive inotropic effects  9. 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 . (brucine)Constituent type : alkaloids.cures fever and bites of venomous snakes Used for preparation of homeopathic medicineToxic part of the plant : seed (although all parts toxics)  17. first and second degree heart block. giddiness. tingling of tongue.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. ventricular fibrillation • Other: yellow vision.Complications . Poisonous plants of Sri Lanka. www. Thevetia peruviana.Initial symptoms – bitter taste in mouth. coma Diagnosis: • cardiac glycoside blood levels • seed remnants. diarrhoea • Cardiovascular: sinus bradycardia.30 min of ingestion .Death is caused by asphyxia or muscular paralysis . . De Silva TUN. bitter nutPlant habitat  dry forests of Ceylon. convulsions. KagodiEnglish/common name : Poison nut.The patient is conscious and has intense pain. repeated • cardiac pacing for third degree heart block • anti-digoxin Fab antibodies in severe casesReferences: Lucas GN.wikitox. anxiety.inchem. Voltage dependent Na+ channel L-type Ca2+ channel Na+/K+ ATPase 2 K+ 3 Na+ K+ channel(s) Ca2+ 3 Na+ β-adrenergic receptor Na+/Ca2+ exchanger SR (Mitochondria) Heart muscle Ryanodine receptorNa+/K+ ATPaseNa+/Ca2+ Antiporter Representative Cardiac Cell  10. Scientific name : Strychnos nux-vomicaSinhala name : Godakaduru. flowers in August  A moderate sized or large tree with an erect trunk. atrial and ventricular extrasystoles.org/documents/pims/plant on 29 June 2008].lactic acidosis.

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. Ricinus zanzibaricus G. Cerbera manghas Sea Mango [Diya kaduru]  21. gastric lavage can be performed safelyReferences : http://www. Popova. 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. viridis (Willd. Jayaweera DMA. castor-oil plant. tachycardia. Muttu-kottai. uraemia and liver necrosis  25. subtropical and temperate areas  Commercially cultivated mainly in Brazil.org/documents/pims/plant [accessed 29 June2008]. 2006.. severe abdominal pain and diarrhoea resulting in dehydration electrolyte imbalance and shock Cardiovascular . LDH..prostration..Synonyms: Ricinus africanus Willd. CPK etcTreatment of poisonings :  Activated charcoal  Support respiratory and cardiovascular functions  If convulsions cannot be controlled with diazepam (IV or rectal). 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.burning sensation of the mouth and throat occurs After 3-6 hrs nausea.inchem. Poisonus plants of Sri lanka Ricinus communis  23. Ricinus communis Castor bean[Thel / Beheth Endaru]  22. Popova.. Medicinal plant use in Ceylon . Telerandu. serum potassium. De Silva TUN. ECG changes and circulatory failure Other . Ricinus persicus G. Ricinus microcarpus G. or if they recur. Lucas GN. Poisonous plants of Sri Lanka.Part 3. beheth endaru. 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) . Pagiantha dichotoma Eve’s Apple [Divi Kaduru]  20. AndagamEnglish/common name/s: castor bean. Ricinus lividus Jacq. thel endaruTamil name/s: Amanakku. blurring of vision.hypotention. convulsions. Ricinus viridis Willd. Ricinus communis L.) Müll.. 2006  19. hepatic hematological systems & blood clotting. Arg. SGOT. Popova. Ricinus vulgaris Mill. Croton spinosusFamily: Euphorbiaceae (spurge family)Sinhala name/s: Erandu. Ricinus macrocarpus G. Scientific name: Ricinus communis Linn. haemolysis. Palma ChristiiPlant habitat:  Cultivated as a decorative plant in village gardens in Sri lanka  Probably of African origin but now grows in tropical. etc. Ricinus speciosus Burm. vomiting. Ricinus inermis Jacq.  Intubation with suxamethonium chloride may be necessary  When convulsions and hyperactivity are completely controlled. loss of consciousness.. Italy.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. Popova. var. 18. India. administer phenobarbitone or phenytoin. Colombo: TheNational Science Foundation. causing cell death and tissue damageClinical features of poisoning: Early on . Diagnosis: Blood gases and electrolytes analysis Close monitoring of renal. Colombo: Sri Lankan College of Paediatricians..

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

Ekanayaka  39. abdominal colic and right iliac fossa tenderness after a variable period of time • 3rd phase – myocarditis with ECG changes. phallolysin phlallatoxins aerial parts alpha.K. odollum. Abrus precatoriusBlack-eyed Susan / Rosary pea / Precatory bean [Olinda]  38. washed and boiled in an open container at72°C for long enough will destroy the enzyme and any hydrocyanic acid formed willevaporate. 2006  36. vomitus. datura-like seed(Peganum harmala) harmaline seedStrychnos nux vomica strychnine seedAlocasia macrorrhiza calcium oxalate crystals leaf/stem (all) (needle-like). gamma amanitin amatoxins (mushroom)  37. Manihot utilissima• Scientific name: Manihot utilissima•Synonyms: Jatropha manihot (Kunth). proteinsDieffenbachia sp.contains as little as 20 milligrams of cyanide (CN) per kilogram of freshrootsBitter .R. phalloin. beta.Scindapsus aureusZantedeschia aethiopicaCerbera manghas cerberine. (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. De Silva TUN. Manihot melanobasis (Muell)•Family: Euphhorbiaceae•Sinhala name: "Manyokka"•Tamil names: “Maravalli” “Alavalli”•English /common name: cassava.M. retinopathy with papilloedema. 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.S. toxicAnthurium sp. hyoscyamine alkaloids seed (all)Gloriosa superba colchicine tuberNicotiana tabacum nicotine leaf (all)Pagiantha dichotoma ? narcotic. which is converted to cyanide in the presence oflinamarinase.thevetin cardiac glycosides fruit kernelThevetia peruviana thevetin A.toxic constituent/s: a cyanogenic glycoside.A. Toxicity of the plant : The leaves and roots contain free and bound forms of thecyanogenic glycoside linamarin. toxalbumin.may produce more than 50 times as much (1 g/kg)The paralytic neurological disease caused by long-term consumption of cassava iscalled mantakassa. Manihot manihot (Cockerell). a naturally occurring enzyme in cassava or via exposure to theatmosphere. hyoscine.hypersensitivity reaction • Clinical features of poisoning: • 1st phase – vomiting. Poisonous plants of Sri Lanka.•Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) issufficient to kill even a cow. Yam that is cut. manioc. exudates and haemorrhages may be seen 2. restlessness. tapioca•Plant description: shrub with a big tuberous root•Plant habitat: The sweet and bitter cassava plants are indigenous toSouthern and Central America but have been introduced to almostall tropical countries•Traditional use : Used as a food source. disorientation. 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 child•Mode of action :A "large" sudden dose . dizziness. cyanogenic glycosides fruit emulsin enzymeManihot utilissima linamarin. Datura metel atropine. American Indians use thebrown juice for burns By : J.3 weeks after ingestion – all transient • Diagnosis: • cardiac glycoside blood levels • seed remnants. a toxalbumin and emulsin (an enzyme)• Constituent type: cyanogenic glycoside  35. fever. theventin B fruitAdenia palmata cyanogenic glycoside. (Slide 5)Two varietiesSweet . • Mode of action: • 1st phase – hydrocyanic acid • 2nd phase – local toxalbumin effects • 3rd phase . abdominal pain and diarrhoea within one hour • 2nd phase – necrotising enteritis -> diarrhoea with blood and mucus. Colombo: Sri Lankan College of Paediatricians. tender hepatomegaly.Sherif E.

it detoxifies the HCN) and physical rehabilitation are advised. Nux-Vomica. restlessness. oleander. Important Definitions: Toxicology: is the science dealing with properties. fatal dose. surface absorption etc) will .References Affran DK.) and accidental poisoning are seen in India.(HCN) is highly poisonous to all humans and animalsbecause it rapidly inactivates cellular respiration thereby causing death. organophosphorus. blurred vision. 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. Ingestion. toxicity. action. speech difficulties and/or paresthesia of the legs. Poisoning in India: Suicidal (KCN. the poison used are Arsenic. respiratory system andcentral nervous system are most susceptible to cyanide poisoning and cease tofunction as a result of lack of oxygen. tachycardia. aconite. Older poisons like opium and arsenic are replaced by newer poisons. Clinical features of poisoning : Acute: Within 3-6 hours of ingestion burning epigastric pain.  40. dry mouth. Opium. flushing of skin. later some people will develop dysarthria. 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. thallium. abnormalities of eye movement. powdered glass and aconite. homicidal(arsenic. detection estimation of. hypertonicity of the arms •Diagnosis Acute poisoning: signs of extreme metabolic acidosis Chronic poisoning: a visible hypertonic gait when walking or running. Antimony. A good and varied diet. oxalic acid oleander etc). Common homicidal poisons are: Arsenic. vomiting. Oleander. Yellow oleander. interpretation of the result of toxicological analysis and management of Poisons. aconite etc. a heavy feeling and/or weakness in the legs. Treatment with sodium thiosulphate (Na2S2O3). carbamates. The heart. Barbiturates. Cattle Poisoning is also common. Abrus precatrotius. This meansthat it stops cells from being able to use oxygen. cramps. 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 . nitrates. Cassava and its economic importance. Poison: A Poison is defined as any substance which when administered in living body through any route (Inhalation. a cyanide antidote. zinc phosphide. high dose multivitamins (specially B12 . but they disappear within a month. giddiness and hallucinations occur. madar. HCL. pupil constriction. Madar. Chronic: initial symptoms are described as tremor. gave disappointing results. organophosphorus etc.

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

Punishment for selling a drug as a different drug or Preparation. Sec. 273 I. 3.different insecticides.P. Sec. cleaning agents. . Sec. may be imprisonment of either description which may extend upto 6 months and or fine.Sec.From store-houses.P. 275 l. Commercial sources. 276 I. rodenticides etc. Sec. fungicides and weed killers. 278 I.P. 2. .C. insecticides. antiseptics. 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. distribution centers and selling shops. Sources of Poison: 1. .In factories.C.C.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. disinfectants. :Punishment' for causing hurt by means of poison or any stupefying. 328 I.P. Domestic or household sources . .C. Industrial sources.P.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. . pesticides.C. months and or fine upto one thousand rupees. Sec. may extend upto five hundred rupees.P. where poisons are manufactured or poisons are produced as by products. . 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. 4. 277 I.C.C. Agricultural and horticultural sources.Punishment for voluntarily making atmosphere noxious to health is fine which . – 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.Punishment for selling noxious food or drink may be imprisonment of either description for a period of 6.In domestic environment poisoning may more commonly occur from detergents. .P. may be imprisonment of either description for a period-of 6 months and or fine. the punishment for these offences described under sections 272 to 276 may be upto imprisonment for life with or without fine. Note . 284 I.In the State of West Bengal. Sec. 274 I.

ether. Belladona. Inebriant (Intoxicant): Alcohol. Hallucinogens . 6. local Action Corrosive Strong Acid: mineral acid and organic acid Strong alkali Metallic: Mercuric Chloride Irritant Mechanical: Glass Powder Chemical Inorganic: weak acid. Chloroform.snakes bite poisoning. Classification of poisons 1. Stimulant iv. Somniferous: opium and its alkaloids. iii. According to the site and mode of action (A). Miscellaneous sources. Stupefaciant vi. Deliriant: Dhatura. v. weak alkalies. Organic: Chemical preparations. Inorganic Metals. Poisons i. Hyocyamus. city smoke. 7.S. Inorganic non-metals. cannabia indica. ii. additives like colouring and odouring agents or other ways of accidental contamination of food and drink.N.overmedication and abuse of drugs. Animal and vegetable origin (B) Remote Action Neurotics • C. sewer gas poisoning etc. Food and drink – contamination in way of use of preservatives of food grains or other food material. Barbiturates. From uses as drugs and medicines – Due to wrong medication.5.

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

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

. But depressant drugs may cause. 7. State of body health: A well built person with good health can tolerate the action of poison better than a weak person. 12.1. 4.g. Exercise .: sedatives and tranquilizers are tolerated in very high dose by manic and deliriant patients. Sleep . Dilution also delays absorption of poison. more harm during the state of sleep. Physical form: Gaseous or volatile poisons are very quickly absorbed and are thus most rapidly effective. 10. Barium sulphide is deadly toxic but barium sulphate is non-toxic. in case of strychnine poisoning. A moderate dose causes acute poisoning. is slowed during exercise because more blood is drawn to the muscles during exercise. Chemical form: Chemically pure arsenic and mercury are not poisonous because these are insoluble and are not absorbed. Condition of the stomach: food content presence of food-stuff acts as diluent of the poison and hence protects the stomach wall. Belladonna group of drugs are better tolerated by children than by adults. But white arsenic (arsenic oxide) and mercuric chloride are deadly poisonous. 11. Opium and its alkaloids are tolerated better by elderly subjects but badly by children and infants. Some poisonous vegetable seeds may pass through the intestinal canal ineffective when taken intact due to their impermeable pericarp.Action of alcohol on C. 5. But when taken crushed. In cases of achlorohydria. A low dose may have sub-clinical effects and causes chronic poisoning on repeated exposure. Route of administration: absorption rate is different for different routes. usually the absorption and action of the poison is also slow. Liquid poisons are more rapid than solid poisons. 6.In certain poisoning cases some drugs are well tolerated. 3.Due to slow metabolic process and depression of other body functions during sleep. Empty stomach absorbs poison most rapidly. Very large dose of Arsenic may produce death by shock without dose irritant symptoms. While smaller dose than lethal dose produces its therapeutic effects. KCN and NaCN is ineffective due to lack of hydrochloric acid. 2. which is required foe the conversion of KCN and NaCN to HCN before absorption. Presence of disease: In certain diseased conditions some drugs are tolerated exceptionally well e. like.S. they may be rapidly fatal. 9. Whereas in case of barbiturate poisoning any sedative or tranquilizer will accentuate the process of death. Quantity: A high dose of poison acts quickly and often resulting in fatal consequences. Age: some poisons are better tolerated in some age groups. barbiturates and sedatives are better tolerated.N. 8. Concentration (or dilution): concentrated form of poison are absorbed more rapidly and are also more fatal but there are some exceptions too. Intoxication arid poisoning states .

Diagnosis of poisoning In the Living 1. contents of a doubtful container. quarrel. . 2. Also note down the color. Signs and symptoms: The signs and symptoms may be different for different poisons and is responsible on the nature and action of the poison. Initial symptoms. Details of examination. condition of other persons taking same food or drink. remote or combined and are will be taught in the individual poisons. smell.13. Full information about time of onset of the present illness. may cause harm when their concentration in different tissue reaches high level due to their cumulative property. Any treatment). In the Dead: 1. H/o 2 or more vital points (1 how long the victim survived after initial symptoms. stained part of the clothes. consistency. They can be local. 4. But when such poisons enter over a long period of time. 3. relation with food. History of the case as stated by police or relatives. 2. progress. Signs and symptoms. stomach wash. any previous history of poisoning. H/o depression. 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. left over ant part of food or drink. History of the case as stated by the patient himself and his/her relatives or friend. 14. taste and quantity of the possible poisonous substance. excreta. possible source. 15. Idiosyncracy: some persons may react adversely to a particular drug though the general population tolerates the drug well. Tolerance may develop by individuals on long term exposue to a particular poison. blood. scraps from any stains area on the body. Preservation and laboratory investigation of vomitus.

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

HNO3. chloroform. Large intestine . 16. loose teeth.HgCl3 . 15. Blue lining in the gum . Chalky appearance and consistency of teeth -:Sulphuric acid 8.Blood . chloroform. Liver . Powder oxalic acid.Carbolic acid (c) . Yellowish – HNO3 Bluish CuSO4 Luminous in dark .H2SO4 and HN3 (g) Yellowish discolouration of mucus membrane . organophosphorus compounds. Oesophageal stricture . Detectable liquid . Carbonization and charring. Slaty grey .Conc. carbon tetra-chloride. chlorinated hydrocarbons.Hard and leathery wall. white arsenic.Phosphorus.Formaldehyde (d) Hyperemia haemorrhageand desquamation of mucus membrane Irritant poison (e) Laceration and sloughing – Corrosive poison (f) Perforation . foetid smell . sometimes may show presence of poisonous remains. It particularly involves the ascending and transverse colons.With coloured poisons 13.Acute mercuric chloride poisoning. formaldehyde. The type and extent of the degenerative changes occur .kerosene. opium. Corrosion. phosphorus. Swollen gum. (h) Stomach content .May show ulcerations.Corrosive and irritant.A complication of sulphuric acid ingestion 14. irritation. Detectable tablet . Detectable smell .Different degenerative changes occur in cases of poisoning with poisons like phosphorus. tetrachlorethylene and many other poisons. Bluish .Corrosive and irritant poisons 11.soneryl. alcohol.6.kerosene.Chronic lead poisoning 9. Hardening and whitish discolouration – In case of Carbolic acid poisoning 12. desquamation and haemorrhage in the inner wall of the esophagus . Stomach (a) Thickening and softening of the wall -Corrosive and irritant poisons (b) Hard wall.May show irruption.CuSO4. Discoloration and staining of inner aspects of mouth . 17. chronic phosphorus poisoning 10. as in case of HgCI3 similar in appearance of ulcers of bacillary dysentery. cyanogen. Small intestine . Sulphuric acid 7.

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

Exception: alcohol. Removal of patient from source of exposure: Patient should be removed away from the source of poison as quickly as possible. 11. 7.A. Use of specific antidote . mustard oil 1 Tsf in a glass of water.V. strips of tablets recovered from pocket. 5. gold chloride or citrate Urine and clothes: without any preservative. Nails in arsenic. Stained areas of dress. oxalate. Hair in arsenic and copper. Removal of the unabsorbed poison. Skin-scrap from areas stained with a suspected poison. 8. Nostrils) of secretions. vomit or any foreign body. Bones in arsenic and lead. E. fluid administration D) Depression of CNS should be corrected Specific Management 1. 10. circulation and the correct CNS depression. suspected packet of poision. Pull tongue forward B) Breathing: Supplemental oxygen therapy should be administered C) Circulation: I. increased perspiration (diaphoresis). Diluting the poison and delaying the absorption by water or food. chloral hydrate. Management of a case of poisoning Immediate resuscitative (Basic Management) measures in comatose patient should be adopted to stabilize respiration. Zinc Sulfate 1-2gm in water. formaldehyde. 4. Preservative used For Viscera: absolute alcohol or rectified spirit. concentrated salt solution 6%. use of chelating agents.6. 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 Ryle’s tube followed by emesis (physical or by drugs like Ipecacuanha 1-2 gm. ether. In cases of inhaled poison the patient should be immediately removed to fresh air.. Dialysis. A) Airway: opening up and cleaning the airways (oral cavity. 2. 9.D. Blood should be preserved in fluoride.T. chloroform. 3. In case of contact poison washing of affected area with soap water with gentle rubbing will be helpful. In case of injected poison ligature is applied above the wound. Elimination of absorbed poison by increases urination (diuresis). Spinal in spinal poisons. apomorphine hcl 1-2ml o 3 mg /ml). phosphorus (alcohol prevents the luminosity of phosphorus in dark) etc.

Constituents Activated charcoal 2 parts . When the exact nature of poison is not known then universal antidote is used which acts against a wide range of poisons. Universal Antidote: It is a combination of physical and chemical antidotes. Counterindications of gastric lavage with stomach tube: 1.6. Physiological and specific receptor antagonists. Unconscious or semi-conscious patients 4. Demulcents like egg albumin. In infants and children: Ryle’s tube or infant feeding tube is used. Convulsant poisons. Physiological antidote have their own action producing signs and symptoms opposite to that produced by the poison. Eg: Naloxone for morphine. 3. Eg: Weak acids and alkali. Eg: adsorbents like activated charcoal. 2. Antidote: Antidotes are substances which counteract the effect of poison. Symptomatic treatment including safeguarding respiration and maintenance of circulation. KMNO4. Chemical antidotes are substances which disintegrate and inactivate poisons by undergoing chemical reaction with them. common salt. egg albumin. Barbiturate for strychnine. Diluents like water or milk. Physical or mechanical antidote prevents the action of poison mechanically. Neostigmine for datura or hyoscin group. Serological Antidote: Anti-snake venom serum for snake bites poisoning. In corrosive poisons. They are divided into Mechanical. bulky food like boiled rice or vegetables. starch or milk. Chemical. without destroying or inactivating the damaging actions of the poisons.

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

clothes stained with poison or vomitus. (g) The doctor should.whether the number of sufferer is more than one whether any treatment was already given and whether there is any history of previous poisoning. urine. the signs and symptoms and progress. for laboratory investigations. doubtful container with remaining part of the poison. (e) The doctor should collect and preserve the vomitus. (f) The doctor should arrange for a reliable attendant of his own choice. death certificate should mention about the poisoning or suspected poisoning with recommendation for post-mortem examination. (i) In case of death. (d) The doctor should himself record full history of the case. if any. for patient. stool. and if necessary blood. 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. .