Dr . SALINI CHANDRAN PROFESSOR,DEPT.OF FORENSIC MEDICINE & TOXICOLOGY - PowerPoint Presentation

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Dr . SALINI CHANDRANPROFESSOR,DEPT.OF FORENSIC MEDICINE & TOXICOLOGYSKHMC

Toxicology

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Toxicology is the science dealing with properties, actions, toxicity, fatal dose, detection of, interpretation of the result of toxicological analysis and treatment of poisons 

 Forensic toxicology deals with the medico-legal aspects of the harmful effects of chemicals on human beings

Clinical toxicology deals with diagnosis and treatment of human poisoning

Toxicology

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Poison is a substance (solid, liquid or gas), which if introduced in the living body, or brought into contact with any part thereof, will produce ill health or death, by its constitutional or local effects or both

poison

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should be cheap and easily available Should be colorless, odorless and tasteless Capable of being administered with food materials without being detected Should be highly toxic

Signs & symptoms should resemble a natural disease

Least Postmortem changes and not to be detected by any chemical tests e.g.

Fluorine and Thallium

, but

commonly used are Arsenic and Aconite

Ideal Homicidal Poison

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Should be cheap and easily available Should be tasteless or be of pleasant taste Capable of being administered with food materials Should be highly toxic

Should be capable of producing painless death

e.g. Opium and Barbiturates, but commonly used are

Organophosphorus

compounds and

Endri

n

Ideal Suicidal Poison

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Stupefying Poisons: Datura

, Cannabis

indica, Chloral Hydrate.

Abortificient

Poisons:

Calotropis

, Oleanders, Aconite, Croton,

Semecarpus

, Cantharides, Ergot, Lead, Arsenic, Mercury, and Potassium permanganate.

Cattle Poisons:

Abrus

precatorius

, Oleanders,

Calotropis

,

Organophosphorus

, Arsenic, Aconite, Strychnine, etc

Arrow Poisons:

Abrus

, Croton, Aconite, Strychnine, Curare and Snake venom etc

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Types of Poisoning

Acute Poisoning – large single dose – frequent smaller - produces signs and symptoms fast

Chronic Poisoning – small doses over a period of timeSub-acute Poisoning – between acute and chronic

Fulminant

Poisoning- massive dose-death sudden due to shock ,peripheral vascular failure

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Inhalation - FastestParenteralInjectionsApplication on mucous

memranes

Natural orificesIntact skin

Routes of Absorption

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Sudden onset of abdominal pain, nausea, vomiting, diarrhea and collapse (Arsenic)

Sudden onset of coma with constriction of pupils (Organophosphates)

Sudden onset of convulsions (Strychnine)

Sudden onset of delirium with dilated pupils. (

Datura

)

Diagnosis of Poisoning

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 COLOR CHANGES on affected skin and mucous membrane. (black color in H2SO4 &

HCl

, brown in Nitric acid) PM STAINING may be Dark brown/yellow in Phosphorus,

Cherry red in CO,

Chocolate color in Nitrates, Nitrobenzene et

c.

Cyanide – Brick Red

Diagnosis of Poisoning in the Dead

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GARLIC like (P, Arsine gas, Arsenic, organophosphates)

SWEETISH (Ethanol, Chloroform

)ACRID (Paraldehyde, Chloral hydrate)

BITTER ALMONDS – cyanide

HOSPITAL ODOUR- Phenol(carbolic acid

)

BURNT ROPE – Cannabis(marijuana)

MUSTY (fishy

) – zinc

phosphide

,

Aluminium

phosphide

ROTTEN EGG (H2S,

Mercaptans

)

ODOUR from nose and mout

h

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1. Phosphorus 2. Arsenic 3. Antimony 4. Hyoscine

5.

Strychinne 6. Nicotine

POISONS RESISTING PUTREFACTION

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274 – adulteration of drugs284 – Negligent conduct with respect to poisons

324 – Causing hurt (including poisoning)

326 – Causing grievous hurt by dangerous weapons or means (including poisoning) 328 – causing hurt to commit an offence

IPC sections

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Miosis

Mydriasis

Nystagmus

Barbiturates

Caffine

Nicotine

Opiates

Organophosphates

Alcohol

CO

Cocaine

Cyanide

Datura

Alcohol

Barbiturates

D

rugs causing pupillary changes

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AlcoholDatura

Nicotine

Bradycardia

Aconite

Digitalis

Opiates

Organophophates

Drugs causing tachycardia

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Private practitioners are bound to inform the police in case of homicidal poisoning

In suicidal and accidental-If the person dies

If private practitioner is summoned by the investigative police officer, he is bound to divulge all information

Govt

: medical practitioner – Has duty to inform all cases

Duty to arrange for Dying Declaration

Duties of Medical Practitio

ner

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Airway , Breathing,

C

irculation, Depression of CNS(correction) Decontamination/Dextrose/Drugs

Removal of unabsorbed poisons:

Inhaled poisons: Fresh air

Injected poisons: Ligature application

Contact poisons: Immediate removal of clothing and washing thoroughly

Ingested poisons: Gastric

Lavag

e

General Lines of Treatment

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Gastric Lavage

(stomach wash)

It is useful within 3 hrs of ingestion salicylates,phenothiazymes,tricyclic antidepressants – (14 -16 hrs)

Ewald’s

or Boas tube

Children – Ryle’s tu

be

Emesis

Gastrointestinal decontamination

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 1cm diameter & 1 ½ meter long Has got lateral openings or 30-40 French tube.

Middle portion has got a suction bulb

Other features are Mouth gag, 50 cm mark, etc. 250 ml of Warm water is put over funnel of the tube and is taken out by the suction pump.

This washing is preserved for analysis

1:5000 KmNO4 sol., 5% NaHCO3 sol. Or 4% Tannic acid 1 % sodium or potassium iodide is used for the

lavage

Gastric Lavage

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Patient position – left lateral ,head dependentAbsolute CI is

Corrosive poisoning due to danger of perforation of stomach. (Exception: Carbolic Acid poisoning)

Convulsant

poisons

Comatose patients

Volatile poisons

Esophageal

varices

Hypothermia

Gastric Lavage

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 It is useful within 3 hrs of ingestion Done with ipecac syrup(30 ml)

Contraindications

As in gastric

lavage

Severe heart disease

Advanced Pregnancy

 

Emesis:

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Activated Charcoal: Particles are small but with high absorptive capacity and it acts mechanically by

adsorbing

and retaining within its pores organic and some mineral poisonsDemulcents: These are substances which form a protective coating on the gastric mucous membrane and thus do not permit the poison to cause any damage

Examples include

Milk, Starch, Egg white, Mineral oil, Milk of Magnesia,

Fats and oils should not be used

for

fat soluble poisons like,

Kerosene, Phosphorus, OP compounds, DDT, Phenol, Acetone

Bulky Foods

: They act as mechanical antidote to

glass powder

ADMINISTRATION OF ANTIDOTE

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They counteract the action of poison by forming harmless or insoluble compounds by oxidizing poisons Common Salt

: Decomposes

Silver Nitrate by direct chemical action Albumen: Precipitates

Mercuric Chl

oride

Dialyzed Iron

: Neutralize

Arsenic

poison

Chemical Antidotes

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 These are substances which produce exactly the opposite actions to that of poison e.g. atropine – PHYSOSTIGMINEStrychnine - BARBITURATES

Physiological Antidotes:

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These agents act by forming stable and soluble complexes by the inner ring structure which can combine with the METALLIC POISONS e.g. British Anti Lewisite (BAL) and

Ethylene

diamine tetra-acetic acid (EDTA)superior to BAL in Ars and MercuryPenicillamine

– maximum efficiency

Dmsa

(

succimer)superior in lead

DMPS

Desferroxamine- Acute iron poisoning

Chelating agents

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two parts activated charcoal, one part tannic acid, and one part magnesium oxide 

Universal Antidote

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URINARY ALKALIZATION: Aim for a Urinary pH of 7.5-8.5 Indications: poisoning with chlorpropamide,

phenobarbitone

, salicylates, phenoxy acetate herbicides

WHOLE BOWEL IRRIGA

TION

Magnesium citrate

Sodium

sulphate

30 gm. Sorbitol

50 ml 0f 70% solution

polyethyleneglycol

Extracorporeal techniques: HEMODIALYSIS:

Multiple-dose activated charcoal: This can increase elimination of some drugs by interrupting their

enteroenteric

&

enterohepatic

circulation

PERITONEAL DIALYSIS

CHARCOAL HAAEMOPERFUSION

ELIMINATION OF POISONS

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LiverKidneyStomach

Small intestine

Blood Urine

R

outine viscera to be preserve

d

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Dextrose – 100ml of 50% solutionThiamine – 100mgNaloxone - 2mg

UNIVERSAL ANTIDOTE

COMA COCKTAIL

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Corrosives are the poisons that fixes, destroys and corrodes tissuesConcentrated acids: • Mineral acids, eg.

Sulphuric

acid, Hcl, HNo3 • Organic acids,

eg

. Carbolic acid, Oxalic acid

Concentrated

alkalies •

eg

. Caustic potash, NaOH

, KOH etc.

sulphuric

acid - (oil of vitriol)

CORROSIVES

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Teeth chalky white – sulphuric acidPerforation of stomach common – sulphuric

acid

Stomach has consistency of wet blotting paper – sulphuric acid

Crowns of teeth yellow – nitric acid

xanthoproteic

reaction – nitric acid

Pupils dilatedFatal dose 10-15ml

HCl

15-20ml

Give nothing by mouth

CORROSIVES

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Can give demulsantsDo not neutralise with strong

alkalies

Do not give bicarbonate - CO2 gas - risk of perforationCorroded areas brown or

black,HCl

- gray

VITRIOLAGE

Throwing of

sulphuric

acid to face – jealousy or revenge

Grievous hurt

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OXALIC ACID

acid of sugar, salt of sorrel

Colourless, transparent prismatic crystals, Natural constituent of plants eg

spinach

FATAL DOSE : 15‐20 gm

FATAL PERIOD: 1‐2 Hrs

Do not loose poisonous property even when diluted

VOMIT

usually contains altered blood with mucous and

HAS A COFFEE GROUND APPEARANCE

Hypocalcaemia

Signs of TETANY

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OXALIC ACID

Fulminant

poisoningUraemia-oxalate crystals in renal tubules

Metabolic acidosis, VF

TREATMENT • Stomach wash– Ca lactate, Ca

gluconate

( antidote is any prep of Ca • Ca

gluconate

10%, 10ml

i.v

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CARBOLIC ACID ( phenol) • Colourless, prismatic, needle like crystals, with burning sweet taste with carbolic/

phenolic

smellFATAL DOSE : 10‐15 gm FATAL PERIOD:

03 TO 04 H

rs

S/S Poisoning is called

CARBOLISM

Corroded mucosa appears whitish, lips , mouth and tongue corroded

WHITE AND HARDENE

D

CARBOLURIA -

Urine is

colourless

to slight green at first but turns green or even black on exposure to air.

Phenol is partly

oxidised

TO HYDROQUINONE AND PYROCATECHOL,

The further oxidation of Hydroquinone and

pyrocatechol in the urine is the cause of green coloration

CARBOLIC ACID

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CHRONIC POISONING ( Phenol marasmus

)

OOCHRONOSIS pigmentation of skin and cornea and cartilages

CAUSTIC ALKALIES

Effect esophagus> gastric mucosa

So

STRICTURE FORMATION MUCH MORE COMMON

with

alkalies

then with acids

OH‐ ion cause

saponification

of fats

LIQUIFACTIVE NECROSIS

CARBOLIC ACID

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FATAL DOSE: • NaOH, KOH: 5 gm Potassium carbonate: 18 gm • Sodium carbonate: 30 gm

Ammonia: 5‐10 ml •

FATAL PERIOD: Usually 24 Hrs

CAUSTIC ALKALIES

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Active principle: – ABRIN ( toxic protein that disables

ribosomes

, inhibits protein synthesis, antigenic properties, hemolytic properties)ABRINE- an amino acid; haemagglutinin

,

ABRALIN

- a glycoside

 

F.D. :

1 SEED

F.P.

: 3- 5 DAYS

SUI’S –

Needles –

cattle poisoning

, rarely for homicide.

Resembles

VIPERINE SNAKE BITE.

TREATMENT :Anti

abrin 

Abrus Precatorius Indian Liquorice

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Active principle: • Toxalbumin RICIN

, a water soluble glycoprotein

F.D. : 10- 20 seeds F.P. :

3-5 days

Treatment: • Gastric

lavage

• Emetics and

demulscents

• symptomatic

RICINUS COMMUNIS (CASTOR, ARANDI) 

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Active principle: uscharin, calotoxin, calactin

,

calotropin (cardiac glycoside) and gigantin (contained in serum)Medico- legal importance •

Madar

juice is commonly used as an

ABORTIFACIENT,

• May be used for homicide , suicide or infanticide •

ANIMAL POISON

ARTIFICIAL BRUISE

ARROW POISON

Calotropis gigantea/ calotropis procera madar or akdo

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Datura Atropa

belladonna

Hyoscyamus

niger

Cannabis

indica

Cocaine

DELIRIANT POISONS

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Active principle contains alkaloids: hyoscyamine

hyoscine

or scopolamine Traces of atropineDatura

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Earliest symptom: Bitter taste in mouth  Inhibition of salivation: Dryness of mouth and throat (dry as a bone)  Difficulty in talking



Dysphagia  Unquenchable thirst  Dilatation of cutaneous blood vessels

 Face is flushed (red as a beet)

 

 Pupils: Dilated

 Insensitive to light  Power of accommodation near vision paralyzed (Blind as a bat)

 

 Inhibition of sweat secretion & stimulation of heat regulating center:  Body temp. raised

 Skin dry and hot (hot as a hare) Vomiting , Giddiness, unsteady gait (drunken individual)

Initially restless and confused Later delirious, mutters indistinct words (mad as a wet hen)

Datura

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FATAL DOSE & FATAL PERIOD Seeds: 100 to 125 Alkaloids: 60 mg (Adult) 4 mg (Children) Death occurs within 24 hours

ML IMPORTANCE

ROAD POISON – stupefying persons for robbery, rape etcAntidote -

physostigmine

Datura

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a colorless ,odorless, crystalline ALKALOID with better taste prepared from the

LEAVES

of THE ERYTHROXYLON COCA PLANTCrack. White lady, snowRoute of Administration Cocaine can be administered as a drug of abuse in the following ways

Cocaine hydrochloride Snorting (intranasal) Intravenous injection

ingestion

coccaine

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Hyperthermia – cocaine feverAmotivational

syndrome

Chronic cocaine poisoningBlack tongue

COCAINE BUGS – MAGNAN’S BUGS –sensation of grains of sand under skin

SPEEDBALL

– Combination OF COCAINE AND HEROIN - injected

BROMPTONS

COCKTAIL

-mixture of cocaine + morphine (heroin) +

chlorpromazine+alcohol,earlier

used for pain management in terminal

illnes

like cancer.

 

cocaine

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Common Names :Indian hemp or cannabis sativa in India

THC

– major psychoactive ingredient in the marijuana plantcannibinol and cannbidiol also components but less present in plants

Names: marijuana, hashish,

charas

, bhang, ganja,

sinsemilla

BHANG

Least potent

form Also called

siddhi

,

patti

,

sabji

Prepared from dried leaves & fruit shoots

Cannabis indica/sativa

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Mildest and contains 15% of active principle MAJOON

: Sweet prepared with

bhangGANJA Consists of flowering tops of the female plant

It is mixed with tobacco and smoked in pipe

Contains active principle in conc. of 25% 

MARIHUANA OR MARIJUANA

Common names are pot, grass tea, Mary Jane

Smoked

in pipe or rolled in cigarette called

REEFERS OR WEED 

Cannabis indica/sativa

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CHARAS OR HASHISH Resin

exuding from leaves and stems

Dark green or brown color Smoked with tobacco in a pipe ‘hookah’ Active principle is in con of 25- 40% It is the

most powerful

of all cannabis preparations

Cannabis indica/sativa

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RUN AMOK :It is a psychotic disturbance caused by the continued use or even first time use of cannabis

It is characterized by a frenzied desire of the person to

commit murders He first kills a person against whom he may have real or imaginary enmity and then kills anyone who comes in his way until the homicidal tendency lasts. 

Then he may commit suicide or surrender himself.

Cannabis indica/sativa

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TOLERANCE & PSYCHOLOGICAL DEPENDENCE  Develops when the drug is consumed over a prolonged period of timeMAJUN AND CHARAS

used

BY ROAD POISONers 

HASHISH INSANITY (Chronic Poisoning)

Patient suffers from hallucinations and delusions of a persecuting nature

Chronic use reduces serum testosterone and sperm count

Cannabis indica/sativa

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Nicotiana Tabacum

Nereium

Odorum

Cerebera

Thevetia

Cerebera

Odallum

Aconite

Digitalis

CARDIAC POISONS

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Alkaloids - Nicotine , NornicotineRapidly acting poisonFATAL DOSE

:-

50-100MG of Nicotine

15 TO 30GM

of crude tobacco

FATAL PERIOD

:-

5-15

minutes

Brownish froth at mouth and nostrils

Nicotiana Tabacum

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Common oleander ,pink oleander ,rose laurel

Contains

cardiac glycosides-

Oleandrin

Nerin

Rosagenin

Folinerin

FATAL DOSE

:-15-20gm of the root;

5-15 leaves

FATAL PERIOD:-20-36 hrs

NERIUM ODORUM

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Suicidal-decoction of root,leaves

and seeds or paste

Homicide rare

Abortifacient

- internally

Cattle poison-juice of the root is applied on a piece of cloth and

Inserted into the anus of the animal

NERIUM ODORUM

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Yellow oleander Cardiac glycosides

Thevetin

Thevetoxin

Nerifolin

Peruvoside

Ruvoside

CERBERA THEVETI

A

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FATAL DOSE :-8-10 seeds;15-20gms of root; 5-10 leaves

FATAL PERIOD:-Uncertain

Suicide

Abortifacient

Cattle poison

CERBERA THEVETI

A

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ACTIVE PRINCIPLES :

Cerebrin

Cerebroside

Odollin

Odolotoxin

Thevetin

Cerapain

CERBERA ODALLUM

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FATAL DOSE :-Kernel of one fruitFATAL PERIOD:-1-2 days or more

PM APPEARANCES

Those of asphyxia

Congestion of organs with

petechial

hges

TREATMENT

Stomach wash

Atropine

Correct

hyperkalaemia

CERBERA ODALLUM

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Suicide –mixed with jaggery or molasses

Homicide-powdered kernel added to alcohol

Bark leaves and milky juice as emetics and purgatives

CERBERA ODALLUM

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Monk’s

Hood,blue

rocketContains alkaloids

Aconitine

Pseudoaconitine

Mesoaconitine

Indaconitine

Bikhaconitine

Picraconitine

Aconine

Jesaconitine

ACONITE

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FATAL DOSE -1-2gm root,4-5mg of aconitineFATAL PERIOD-2-6 hrs

HIPPUS

– Alternate contraction and dilatation of pupilsMistaken for horseradish

Considered as ideal homicidal poison

With betel nut –to mask its taste-homicide

Abortifacient

Cattle poison

Arrow poison

ACONITE

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INEBRIANT – ALCOHOLFollowing absorption, the concentration of alcohol in the blood reaches a maximum in about 45-90 minutes after ingestionStage of Excitement (Blood level: 50-150 mg%) 

Stage of In-coordination (Blood level: 150-250 mg%

Stage of Coma (Blood level > 250 mg%)Pupils

are contracted

but

on stimulation

of the person, e.g. by pinching or slapping .Causes them to

dilate

with slow return (

MCEWAN’S SIGN

).

CNS DEPRESSANTS

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FATAL DOSE (non-addict) : 150-250 ml of absolute alcohol consumed in 1hour.Common clinical syndromes associated with chronic

alcoholism

DELIRIUM TREMENS : acute organic brain syndrome, usually seen within 2-4 days of complete absence from heavy alcohol drinking. There is an acute attack of insanity in which there is: Clouding of consciousness with disorientation in time and space. Coarse muscular tremors of face, tongue and hands. Insomnia with reversal of sleep-wake cycle and loss of memory. Psychomotor agitation, ataxia, uncontrollable fear and tendency to commit suicide/homicide/violent assault or cause damage to property

ETHYL ALCOHOL

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ACUTE ALCOHOLIC HALLUCINOSIS: 24 – 36 hrs after withdrawal

 

Korsakoff’s psychosis often follows Wernicks’s encephalopthy so they are referred to as

WERNICKE-KORSAKOFF SYNDROME

Cause: Severe, untreated

thiamine deficiency, secondary to chronic alcohol abuse. 

WERNICKE’S ENCEPHALOPATHY

:This is an acute reaction due

to severe thiamine deficiency

, the commonest cause being

chronic alcohol abus

e.

MALLORY WEISS SYNDROME: Tears of mucosa of lower

oesophagus

with

haemorrhaging

ETHYL ALCOHOL

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SATURDAY NIGHT PALSY : from falling asleep with one's arm hanging over the arm rest of a chair, compressing the radial nerve.

DRUNKENNESS

MICTURITION SYNCOPE

ALCOHOLIC PALIMPSETS: Automatism after taking alcohol

ETHYL ALCOHOL

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  METHANOL - alcohol dehydrogenase

-

FORMALDEHYDE - aldehyde dehydrogenase -

FORMIC ACID

methanol itself not toxic.

Formaldehyde very toxic, but very rapidly

metabolised

to formic acid.

Formic acid responsible for the toxicity related to methanol ingestions

METHYL ALCOHOL

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OPTIC NERVE BECOMES OEDEMATOUSSudden loss of vision or complete blindness due to optic neuritis may occur.Permanent loss of vision

Treatment

ETHYL ALCOHOL

METHYL ALCOHOL

Slide69

Dried juice of poppy (papaver somniferum)

morphine .

codine,thebaine,papaverine.narcotineHEROIN is a natural derivative(BROWN SUGAR)

COMA

PINPOINT PUPILS

Morphine-200mg

Codine-800mg

Antidote:

NALOXONE

BODYPACKER SYNDROME

Test :Marquis test

OPIUM

Slide70

INHIBITION OF ACETYL CHOLINESTERASEMuscarinic effects: SLUDGE

White froth

CHROMOLACHRYORRHOEA – Red tearsTreatment:

Oximes

–

Pralidoxime

Atropine

for

Muscarinic

effects

FATAL DOSE –

Malathion

- 1gm

ORGANOPHOSPHATES

Slide71

Alkaloid- STRYCHNINE

Action on anterior horn cells

- on glycine

Opisthotonus

Trismus

Risus

sardonicus

NUX VOMICA

Slide72

Resembles TETANUS

Antidotes : Barbiturates

Rigor mortis earlyPostmortem caloricity

ANTIDOTE:

BARBITURATES

FATAL DOSE: 50-100mg,one crushed seed

FP – 1-2 hrs

Test: Toad test

NUX VOMICA

Slide73

COCO2Cyanide present inbitter almonds

cherry, plum kernels .cassava(

amygdalin)apricot ,peach kernels etc

A

sphyxiant poisons

Slide74

Colourless, highly volatile liquid

Odour

of BITTER ALMONDS

Powerful protoplasmic poison

Interferes with action of

CYTOCHRME OXIDASE

Histotoxic

anoxia

HYDROCYANIC ACID( Hydrogen cyanide, Prussic Acid)

Slide75

FATAL DOSE – 50mg

pureHCN

2.5 ml dilute HCN KCN -0.2-0.5 gm

Sodium cyanide-.15gm

FATAL PERIOD-2-10 minutes

Antidotes : Amyl nitrate, sodium

thiosulphate

, sodium nitrate

BRICK/BRIGHT RED

coloured

postmortem staining

FROTH

at mouth and nostrils

Test

: LEE JONES TES

T

Slide76

Anaemic anoxiaInterferes with cytochrome oxidase

COHB is formed

Treatment - Hyperbaric oxygen

CHERRY R

ED

Postmortem staining

CO

Slide77

Snakes

COBRA & KRAIT

–venom is NEUROTOXIC

VIPE

R

– Venom is

HAEMOLYTIC

SEASNAKE

– Venom is

MYOTOXIC

COBRA & KRAIT

Cause of death –

RESPIRATORY FAILURE

VIPER

–

HAEMORRHAGE AND SHOCK

SEA SNAKE –RENAL FAILURE

A

nimal irritants

Slide78

FATAL DOSE :- COBRA-12mg

RUSSEL’S VIPER 15mg

ECHIS-8mg

KRAIT-6mg

FATAL PERIOD –

COBRA AND KRAIT-1/2 -6HRS

-VIPER-1-2 DAYS

Treatment

– POLYVALENT ANTISNAKE VENOM SERU

M

Snakes

Slide79

CantharidinRenal damageSCORPIONBoth

neurotoxic

and haemolytic venom

cantharides

Slide80

Red and yellowYellow- translucent , waxy and luminous, toxicStored in waterUsed in incendiary bombs

Fulminant

poisoningAcute: GARLICKY ODOUR OF BREATH

PHOSPHOROUS

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Chronic – PHOSSY JAW – toothache , ulcerative

stomatitis

, necrosis , osteomyelitis of jawJaundiceYellow/Brown Postmortem staining

Fatal dose:1mg/kg of body weight(60-120mg)

PHOSPHOROUS

Slide82

GI and CNSDescending bilaterally symmetrical motor paralysisAbducent

&

OcculomotorBOTULISM