Toxicology

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 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. 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+ β-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 Eve’s 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.) Müll. 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 (yáng jīn huā). 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 utilissima•Synonyms: Jatropha manihot (Kunth), Manihot manihot (Cockerell), Manihot melanobasis (Muell)•Family: Euphhorbiaceae•Sinhala name: "Manyokka"•Tamil names: “Maravalli” “Alavalli”•English /common name: cassava, manioc, 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. 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 at72°C 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 child•Mode 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 Ryle’s 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: Ryle’s 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.