Systemic Toxicology

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Corrosive poisons

Alkali is more dangerous than acids


Because alkali produces liquifactive necrosis which causes deeper penetration
whereas acids produces coagulative necrosis which produces thick eschar which protects against deep penetration

Sulphuric acid
Symptoms:
Burning pain in the mouth, throat ( pharyngeal pain is the most common presenting symptom ) , epigastrium then spreads on whole abdomen
Intense thrust, salivation
Dysphasia
Dysphonia
Vomitus = Brownish black in colour or coffee-ground coloured

Signs :
Lips, angle of mouth, tongue, oral mucosa, pharyngeal mucosa- corroded and black coloured ( teeth become chalky white )
Gastric perforation is most common with sulphuric acid

Fatal dose: 5-10 ml

Fatal period : 12-24 hrs

Don’ts :
Gastric lavage
Bicarbonates/ carbonates ( this will produce CO2 which increase chances of perforations )

Dos :
Dilute the acid with water, milk, aluminium hydroxide gel
Demulscents = milk, starch, butter, egg white
Skin = wash with water, apply MgO paste/ NaHCO2 paste
Eye = Irrigate with normal saline or solution
Rest = symptomatic treatment

PM appearance
Skin, tongue, lips, esophageal & gastric mucosa are black is colour expect teeth will be chalky white
Stomach is converted into black spongy mass which readily disintegrate on touch
Wet blotting paper consistency

Medicolegal Importance ( MLI )


Vitriolage = Throwing of any corrosive with intesion to cause disfiguration of head and face
Dealt under 326 A & 326 B of IPC

Nitric acid
All the tissues come in contact with nitric acid become yellowish or brown in colour due to formation of picric acid by xanthoprotic reaction

Lips, teeth, skin, tongue, oral and GI mucosa = Yellow/ brown


Urine = Brown in colour

Treatment is same as that of sulphuric acid

Oxalis acid ( acid of sugar )


Action local Intact skin = No / min action
mucous membrane = Bleaching / corrosion = white in colour

Systemic GIT = same as H2SO4


vomitus = coffee ground vomitus ( Acid hematus + mucus)
Renal damage = Tubular necrosis leading to uremia
Extensive hypocalcemia = Tetany and convulsions, tingling of fingertips

Treatment = Gatric lavage can be done with Calcium gluconate or calcium lactate solution
Orally : Calcium gluconate or calcium lactate solution
IV : Calcium gluconate 10% 10ml = Specific treatment
Severe cases : Parathyroid extract 100 units

Medicolegal importance: Ink removing solutions for illegal over-writings


Used to remove Vote mark on fingers
Carbolic acid or phenol
Metabolism = Hydroquinone and pyrecathecol

Phenol toxicity is also called carbolism

Signs and symptoms

GIT = same as that of H2SO4


Skin = Bleaching of skin & damage of nerve ending causing numbness
Systemic = CNS depressant of respiratory centre
Only acid to cause miosis ( constriction of pupil )
Metabolic acidosis & respiratory alkalosis
Urine = Green discolouration due to hydroquinone & pyrecathecol = Carboluria

Chronic poisoning = Phenolic marasmus


Yellow pigmentation of skin, sclera and cartilages
Anorexia, weight loss
Accumulation of hydroquinone, pyrecathecol giving yellow pigmentation called as Oochronosis.

Treatment : Gastric lavage can be given = Repeated with Luke warm water containing olive oil or caster oil.

Reasons why lavage can be given


1. It anaestheses the nerve endings
2. It hardens GI mucosa ( others soften GI mucosa = risk for perforation )

After lavage 30 gm of MgSO4 left in stomach


Methylene blue given IV if there is methamoglobinemia.

PM changes
Stomach = Leather bottle stomach due to hardening of GI mucosa

Agricultural poisons
Organophosphorus compounds
MOA : very potent cholinesterase inhibitors — Inhibit true n pseudo cholinesterase

Signs and symptoms


1. Muscarinic manifestation = salivation, lacrimation, urination, diarrhoea, GI distress, emesis, miosis
2. Nicotinic manifests = Muscle weakness, areflexia, tachycardia, cramps, hypertension
3. CNS manifestation = Generalised weakness, ataxia, slurring of speech, tremors, confusion, headache, drowsiness, depression of centres , coma , death

Chromodacryorrhea = shedding red tears due to abnormal porphyria metabolism

Diagnosis of toxicity

Latent poisoning = 10-50%


Mild poisoning = 50-80%
Moderate poisoning = 80-90%
Severe poisoning = >90%

True cholinesterase = RBC cholinesterase/ acetylcholinesterase


Found in RBC, grey matter, skeletal muscle
Most specific indication of OP poisoning
Activity less than 50% = defiantly OP poisoning

Pseudocholinesterase = Plasma/ butyrylcholinesterase


Found in plasma, white matter,smooth muscle of GIT and present in viscera
It is highly sensitive to OP
Level fall rapidly in OP poisoning

Treatment

1. Atropine sulphate = act on CNS and muscarinic receptors - given until all tracheobronchial secretions are dried & pulse should not be more than 140
2. Cholinesterase reactivators = Oximes = DAM & PAM = they specifically act on nicotinic sites

They should be used together

PM changes
Kerosine smell of gastric contents

Carbamate poisoning = signs and symptoms same as OP poisoning


Treatment = Atropine is specific treatment & Oximes are contraindicated
Endrin = plant penicillin

Pyrethrins & pyrethroids


Toxicity is very low due to rapid metabolism
Used as insect repellents

Treatment is symptomatic with antihistaminics & adrenaline but both atropine & Oximes are contraindicated

Aluminium phosphide
Garlic odour
Used as rodenticide
Available in form of white tablets such as Celfos, alfos, Quilphos

Action : AlP + HCl Release phosphine gas

inhibit respiratory centres

Treatment: No specific antidote


Dopamine infusion & IV hydrocortisone is highly effective

Tests to detect ALP


Filter paper impregnated with AgNO3 used as the face mask - turns black due to release of phosphine gas which reacts with AgNO3

Phosphorus
White / yellow phosphorus = highly toxic & highly inflammable, luminescent and has garlicky odour = so it is stored under water

Red phosphorus = non toxic

Acute phosphorus poisoning


Breath, vomitus, excreta have garlicky odour
Vomitus and excreta are luminescent = It is the diagnostic feature
Smoky stool syndrome
Hemorrhagic syndrome = comprising of hematemesis, hematuria & hemorrhage into skin, mucus membrane a& parenchyma of organs
Hepatotoxicity = characterised by foetus hepaticus , flapping tremors of hands
Hepatic encephalopathy

Treatment
0.2% CuSO4 solution as lavage solution acts as chemical antidote
Gastric lavage can be also done with 1:5000 KMnO4 - converts phosphorus into H2SO4 + Phosphates which are harmless
Vitamin K 20 mg is given IV for hypoprothrombinemia

PM features
Gastric contents have garlic odour and they are luminescent
Acute yellow atrophy of liver

Chronic poisoning = Phossy jaw = It is chronic osteomyelitis of mandible with multiple sinuses discharging foul smelling pus ( this disease is obsolete )
Lucifer matches = strike anywhere matches = not used now a days
Safety matches now used = tip of stick contains potassium perchlorate + antimony sulphide
Side of matchbox contains red phosphorus + ground glass

Medicolegal importance
Diwali poisoning = accidental phosphorus poisoning
Arson = white phosphorus is mixed with cow dunk
Heavy metal poisoning
Arsenic poisoning
r

Metallic Arsenic - Non toxic


All of the metal in their native form is non poisonous except lead which is poisonous

Action : inhibits sulphhydral group of mitochondrial enzymes thereby interfering in cellular respiration
Primary target of arsenic is vascular endothelium

Acute arsenic poisoning resembles cholera

Criteria Acute arsenic poisoning Cholera

Vomiting First, followed by diarrhoea & purging Vomiting is after purging

Vomitus Blood and mucus Watery

Purging After vomiting First then vomiting

Stool Dark due to blood and mucus No blood and mucus


Then Rice watery Only rice watery

Tenesmus & Present Absent


Anal irritation

Fetal dose = 0.1-0.2 gms Arsenic trioxide

Treatment
BAL - Chelating agent of choice
Freshly precipitated ferric oxide - oral - effective
DMSA / DMPS = better than BAL

PM findings
Arsenic causes multiple erosions in gastric mucosa, it looks like red velvet = Red velvety stomach
Sub endocardial hemorrhages of ventricles
( sub endocardial hemorrhages are produced by Arsenic , mercury, viper snake bite )

Test for arsenic


Marsh, Reirsch = both are not used now
AAS ( atomic absorption spectroscopy ) = best test

Chronic arsenic poisoning


Hyperkeratosis of palm and sole
Rain drop pigmentation = brown mottled patches on eyelids
Rashes = Resembles Measles, Addison’s disease and secondary syphillis
Aldrich-mees lines = present on 10 finger nails, 1-2 mm length & occupy entire breadth of nail
Painless perforation of nasal septum
Peripheral neuropathy = both sensory and motor but predominantly sensory ( glove and stocking distribution = difficulty in sensing pain, touch,
temperature)
Black foot disease = peripheral vascular disease which produces ulceration, gangrene, spontaneous amputation of extremities

Arsenophagistis = consume arsenic on daily basis- aphrodisiac


Mercury
Metallic mercury is non poisonous

Acute mercury poisoning


3G features
1. Glossitis
2. Gingivitis
3. Greyish white coating of tongue

Burning and metallic taste - mouth, throat, abdomen

Treatment: BAL : chelating agent of choice

Chronic mercury poisoning = Hydragyrism


Classical triad:
1. Gingivostomatitis
2. Mercurial tremors
3. Mercurial erythrism

Mercurial tremors : called as Danburry tremors


First begins with fingers of hand then progresses to lips, tongue and then arm
Advancing stage = Hatter’s stake / glassblower’s shake
Final stage = concussio mercurialis

Mercurial erythism
Neuropsychiatric condition in which person is always anxious, depressed, shy, delusions & hallucinations = hence called mad Hatter

Mercuria lentis : deposition of mercury on anterior lense capsule - this gives malt brown reflex on slit lamp examination
It is bilateral but does not affect visual acuity

Acrodynia : Hypersensitivity reaction to marcury compounds in children


Present with painful pink puffy rashes hence called pink disease.

Renal damage : It is the primary target of mercury

Medicolegal importance
Minimata disease : Organic mercurial poisoning through contaminated fish

Lead
Metallic lead is poisonous

Chronic lead poisoning = plumpism/ saturnism


Features
Facial pallor : Circumoral = earliest manifestation
Blood picture : Microchtic- hypochromic anemia later becomes normocytic normochromic anemia
Punctuate basophillia = basophilic stippling = blue dots of pin head size in cytoplasm of RBC
Eosinophilia

Burtonian blue lines : seen at junction of teeth and gum


Seen at teeth which are infected / carries
Decomposition of food, H2S + lead to produce lead sulphide = this gives blue lines

Colic and constipation : seen in 85% cases = Cry belly ache, Devon’s colic, painter’s colic

Lead palsy : seen in less than 10% cases & seen mostly in adults
Affects muscle prone for fatigue
Wrist drop and foot drop

Lead encephalopathy: seen in almost all cases & most common in children

Diagnosis
Coproporphyrin III = Blood level > 0.07 mg%
Urine level 0.15- 0.30 mg / Litre

Treatment
Chelating agent of choice = EDTA
Copper
Signs and symptoms
Vomitus = Greenish blue
Skin = Greenish blue ( due to fumes of copper )
Metallic and burning pain

Treatment
Gastric lavage with 1% Potassium ferrocynide which converts to cupric ferrocynide
Chelation : penicillamine is chelation of choice

PM changes
Froth and gastric contents are greenish blue

Chronic copper poisoning


Green lines on gums
Green discolouration of hair

Vineyard sprayer’s disease = due to chronic exposure to CuSO4 spray


Histiocytic granulomatous lungs

Chalcosis = presence of copper deposits in tissues

Chalcosis lentis = It is deposition of copper in cornea or in the lense giving greenish blue discolouration

Thallium
Triad
1. Allopecia
2. Painful peripheral neuropathy
3. Skin rashes

Metal fume fever = Monday morning fever


Inhalation of metallic fumes - mc zinc
Can also be seen with copper and iron

Influenza like syndrome = Chills, fever, myalgia, headache


Snakes
Poisonous snakes
Common cobra, common krait, king cobra, Russel’s viper, saw scalded viper

Identification of snakes
1. Cobra = Hood & bispectacle mark on hood
2. Russel’s viper = heavy flat triangular shaped head, 3 rows of diamond shaped patches on entire back
3. Saw scaled viper = diamond shaped areas in between wavy lines on back
4. Common krait = single / double white bands all over its back
5. Banded krait = jet black coloured patch with same sized yellow patch all over its back

Sea snakes = 20 types in India & all are poisonous


Poisonous glands = salivary glands of snake = 2 = 1 each on side behind eyes

Criteria Poisonous snake Non poisonous snake

Head scales Vary Always large

Belly scales Large & cover whole breadth of belly Small & doesn’t cover entire belly

Fangs Grooved / canalised Solid

Teeth 2 fangs Multiple small teeth

Habitat Nocturnal Not specific habitat

Venom = Saliva
It contains 2 components
1. Enzymatic = Responsible for local & systemic effects
It contains enzymes = Proteases, proteinase, phospholipidases, phosphatidases, esterase, lecithinase, Hyaluronidase ( It is present in all snake
venoms)

2. Non enzymatic = Responsible for fatality


Contains = Neurotoxin, cardiotoxin, haemolysin, cytolysin

Signs and symptoms


1. Dry bite : Very less or no venom is injected during bite
No feature of toxicity

2. Ophitoxemia : Snake toxicity

Features
A. Cobra and krait : Neurotoxic causing ascending paralysis with minimal or no local reaction at the site of bite.
Local features starts by 8 minutes - burning pain, oozing of blood stained fluid
Systemic : begins in 30 mins - Drowsiness, weakness, reluctant to walk, stand
1st manifestation is ptosis then paralysis of lower limb then trunk and then head falls
After this paralysis of facial muscles, jaw, muscles of deglutition, tongue complete in 2hrs

Cause of death : Respiratory failure due to paralysis of respiratory muscles & paralysis of tongue which falls back

B. Viper bite : Hematotoxic causing Intra vascular hemolysis, depression of coagulation mechanism with intense local reaction
Pain, oozing of blood, swelling, blister formation on entire limb and trunk
Delayed death : necrosis of skin, muscles

Systemic : hemorrhages: Intracranial, conjunctival, scleral, middle ear, epistaxis, hemoptosis, visceral hemorrhages, hematuria , death due to shock

C. Sea snakes : myotoxic : Pain, tenderness and weakness of muscles followed by marked polymyocytis with limb-girdle distribution
Death due to paralysis of respiratory muscles

Fatal dose /Fatal period :


krait : 6mg /18hrs
Sea saw scaled : 8 mg/ 1-2days
Cobra : 12 mg/ 30min-6hrs
Russel’s viper : 15 mg/ 1-2 days

Diagnosis
Skin and subcutaneous tissue is dissected
Radioactive immunoassay = most specific & sensitive
Enzyme immunoassay = most specific & sensitive
ELISA = detect venom
Don’t do
1. Incision and suction
2. Cryotherapy or cautery both are contraindicated

Do’s
1. Reasssurance
2. Absolute immobilisation of beaten area
3. Firm pressure on bitten area
4. Bandage / tourniquet - Sutherland wrap

Specific antidote : Polyvalent ASV : effective against Cobra, Krait, Russel’s viper & Saw scaled viper
Given within 4hrs
1 vial neutralises : 6 mg of cobra and Russel’s viper & 4.5 mg of Krait and Saw scaled viper

Preparations:
ASV : vial : lyophilised white powder
Shelf life : 5yrs
ASV is produced :
1. Haffkine institute, Mumbai
2. Serum institute, Pune
3. King’s institute, Chennai
4. Central institute, Kasauli ( HP )

Other : Antibiotics, antihistamine, hydrocortisone, neostigmine, heparin, hemodialysis in severe cases

Oral consumption of snake venom is non poisonous

Alcohol
Absolute alcohol = 99.95% of alcohol

Alcoholic beverages : Mixture of alcohol + water + congeners


Congeners : Aldehyde, ketone, propyl or octal alcohol = it gives specific flavour and hangover effect

Proof spirit = It indicated concentration of alcohol in beverage


It is the mixture containing 57.1% of absolute alcohol by volume or 42.7% of absolute alcohol by weight

Absorption of alcohol
No need of digestion
20% absorbed from stomach & 80% of small intestine

Factors increasing absorption


1. Empty stomach
2. Beverages mixed with carbonated diluents
3. Beverage Consumed in warm/ hot form
4. When alcohol concentration in beverage is in between 10-20%

Factors decreasing absorption


1. Food in stomach
2. Chilled beverage
3. Concentration of alcohol less than 10% or more than 20%
4. Chronic gastritis

Distribution

Ratio of alcohol between blood and body fluids


1. Blood : urine = 1: 1.3
2. Blood : Saliva = 1 : 1.2
3. Blood: sweat = 1 : 1.2
4. Blood : CSF = 1 : 1.2
5. Blood : vitreous = 1 : 1.2
6. Blood : plasma / serum = 1 : 1.12
7. Blood : mother’s milk = 1 : 1
8. Blood : alveolar air = 2100 : 1

If female of same weight as male consumes same beverage of same quantity will have BAC 25% more than that of male
Why - 1. Greater fat compartment and lower water compartment ( alcohol is soluble in water but not in fat )
2. Faster hepatic clearance
3. Deceased activity of gastric alcohol dehydrogenase enzyme

Metabolism
Alcohol Aldehyde Kreb’s cycle
Ethyl alcohol dehydrogenase Acetaldehyde dehydrogenase
Acetic acid Acetyl CoA CO2 + H2O
🥴

Euphoria Visual disturbance Inco-ordination


MOA :
CNS Cerebral hemispheres Frontal lobe Occipital lobe Cerebellum

Midbrain RAS ( primary target ) Thalamus Spinal cord Medulla


Respiratory centres Death

GIT Moderate quantity Increase salivation & increases gastric juice thus increasing appetite
Carminative action ( clears flatulance )

Renal Inhibits ADH Increases urination ( diuresis )

Skin Vasodilation False sense of warmth


Increases heat loss, diaphoretic action = increased sweating

Fatal dose : 150-250 ml


Fetal period : 12-24 hrs

Signs and symptoms


1. Stage of excitement = When BAC is 50-150 mg%
2. Stage of in-co-ordination = BAC = 150-250 mg%
3. Stage of coma = BAC is greater than 250 mg%

Alcohol gaze nystagmus/ lateral gaze nystagmus = elicited around BAC 80mg%
McEwan’s sign = When BAC more than 300 mg%
elicited in stage of coma ( coma due to only alcohol intoxication )
Any painful stimulus will dilate the pupil and then it slowly return back to constricted size

Treatment
Gastric lavage with alkaline solution within 2hrs of ingestion
One litre of normal saline + 10% glucose + 100mg of thiamine + 15 units of insulin
Naloxone & physostigmine
Haemodialysis

Chronic addiction
Treatment:
Disulphiram
Reflex conditioned treatment
Alcohol anonymous : International organisation

Investigations:
Living : cubital vein = don’t clean with spirit, clean with soap & water
100mg of NaF/KF & 30mg of K oxalate for 10 ml of blood
Analysis to be done within 7 days

Dead : femoral vein > iliac vein


In embalmed body it is measured from vitreous or muscle

Tests for determining blood alcohol concentration


1. Kozelka- Hine test
2. Cavette
3. Gas chromatography : best for medicolegal purposes

Calculations
Widmark formula
a= pcr for blood
a = Weight of alcohol in gms
p = Weight of body in kgs
c = concentration of alcohol in blood
r = constant = 0.68 for male & 0.55 for female

a = 3/4 prv for urine


v = alcohol concentration in urine

Breath analyser
Used to calculate BAC from a breath sample
The alcohol concentration in 1ml of blood is same as 2100-2300 ml of alveolar air = it works on Henry’s principles

BAC and terminology


< 10 mg% = sober
10-80 mg% = drinking
80-150 mg% = under the influence
150-300 mg% = Intoxicated or drunk

Drunken driving
Sec 185 of motor vehicle act
Statutory limit = 30 mg%
Punishment = 1st offence = 6months or 10,000 fine or both
For subsequent offence = 2yrs or 20,000 or both

Sec 510 IPC = Misconduct of drunken person in public = imprisonment upto 24 hrs
Specific conditions of chronic alcoholism
1. Rum fits : Grand mal — withdrawal

2. Morbid jealousy/ alcohol jealousy : Delusions of reference , persecution, infidelity

3. Munich-Beer heart : Alcoholic cardiomyopathy

4. Wernicke’s encephalopathy : Decreased absorption of thiamin

5. Korsokoff’s psychosis : confabulation, polyneuropathy

6. Mania -a- potu

7. Delirium tremen : starts after 3-4 days after withdrawal = course tremors, irrational fear, wild hallucinations, delirium of horror, disorientation
= acute attack of insanity so now dealt under sec 84 IPC

Methyl alcohol
Alcohol Aldehyde
Methyl alcohol Dehydrogenase Formaldehyde dehydrogenase Formic acid

Signs & symptoms


Optic atrophy and optic neuritis
Photophobia
Snow filed vision
Blurring of vision
Central and peripheral scotomata
Sudden blindness

Treatment
Antidote : ethyl alcohol given iv to avoid gastric irritation
Severe cases : hemodialysis

Opium
Dried juice of poppy
Extraction : unriped capsule of poppy
Poppy seeds are harmless does not contain narcotics : used for cooking purposes
Ripened / dry capsule have traces of opium

Active principles : 25 alkaloids ; classified into 2 groups

1. Phenanthrene : Morphine, codeine, thebaine

2. Isoquinolone : Papaverine, Narcotine

Classification
Natural : morphine & codeine
Semisynthetic : heroine, pholcodeine
Synthetic ( designer drug ) : methadone, tremadol, fentanyl

MOA :
It exerts its action because of its similarity to naturally occurring compounds of the body called endorphins.
It inhibits all the centres except Sweating, occulomotor, vomiting.

Fatal dose :
Opium = 2 gms
Morphine = 0.2 gm

Fatal period = 6-12 hrs

Signs and symptoms


1. Stage of excitement
2. Stage of stupor : unpleasant symptoms
3. Stage of coma : muscles flaccid & no reflexes ; pin point pupils
All secretions are suspended except sweating

Treatment
Specific antidote : naloxone 2mg IV
Nalmefene : longer duration of action

Medicolegal importance
Ideal suicidal drug
DOC active euthanasia
Ideal infanticidal
Opium withdrawal = called cold turkey
Characterised by fear, chills, goose skin

Test to detect opium = Marquis test

Heroin = Diacetyl morphine


Types
1. Hydrochloride salt = white heroin = soluble in water ; used in injection
2. Alkaloidal form Brown = brown sugar Smoked on foil
Black = black tar heroin
chasing the dragon

Terms of relevance
1. Speed ball = heroin + cocaine taken IV
2. Moon rock = heroin + cocaine smoked together
3. Hot shot = sudden death after IV administration of narcotic/ heroin with needle still in vein
Accidental = heroin + strychnine ( used for increasing the potency )
Homicidal = when intentionally large amount of heroin is injected

Treatment
Naloxone for Acute
Methadone for chronic addiction

Medicolegal importance
Among the drugs of addiction, heroin is most dangerous drug of addiction

Deliriant poisons
1. Datura = thorn appl
All the parts of plant are poisonous

Datura fruit contains about 500 seeds and they resemble chilli seeds

Active principle
1. Hyoscine / scopolamine
2. Hyoscyamine
3. Atropine

Clinical features
Delirium - associated with incoherent talks & purposeless movements ( carphologia )
Diplopia
Dimness of vision
Dilatation of pupil
Dryness of mouth -
Dysphasia
Dysphonia
Dilatation of cutaneous vessels - flushing of face
Drunken gait
Death due to respiratory failure

Carphologia is associated with pill rolling movements, pulling imaginary threads from fingertips, picking up bed
cloths, trying to thread imaginary needle

Fatal dose : 100-125 seeds

Fatal period : 24hrs

Treatment
Specific antidote : physostigmine

Medicolegal importance
Used as stupefying poison for rape, robbery, kidnap
Also called roadside poison

If datura is given involuntarily = he should not be held responsible by 85 IPC


2. Cannabis
Also called pot, weed, grass, Mary Jane
Cigarettes containing cannabis Reefes / joints

Active principle : Tetrahydrocannabinol

Odour : burnt rope odour

Preparations :
1. Bhang : Drink / beverage / decoction / cannabis tea
It contains 15% of active principles
Prepared from dried leaves and shoots

2. Majoon : It is sweet, prepared from bhang + honey + ghee

3. Ganja : It is prepared from flowers of female plant


Green rustic powder - smell
15-25% active principle
Smoking
Also referred as marijuana

4. Charas/ Hashish : Resin extract from the stem


40% of active principle = Most potent preparation
Smoking
Hash oil = highly concentrated form of hashish : contains 70-80% of active principles

5. Sinsemilla : potent form of cannabis

Signs and symptoms :


1. Euphoria
2. Emotional instability
3. Erotic feelings

Chronic poisoning
1. Amotivational syndrome

2. Run amok : It is killing spree, it is homicidal impulse


Phases= Depression Killing spree Depression Kills himself / surrender himself

3. Koro : Male : penis is retracted into abdomen


Female : Breast is retracted into chest

Medicolegal importance
World’s most widely used illicit drug

Treatment
Coma cocktail : 100ml 50% dextrose + 100mg thiamine + 2mg of naloxone

It produces only psychological dependence not physical dependence

Cocain
It is obtained from Erythroxylon coca
Slang names : White lady, coke, Cadillac
Cigarette with cocaine is called as Crack

Coca leaves contain less than 2% of cocain, so this coca leaves are treated with sulphuric acid, thereby cocain gets converted into cocain
sulphate, then cocain sulphate is treated with HCl then it gets converted into cocain hydrochloride it contains 90% cocain. Cocain
hydrochloride cannot be smoked, it is mainly used by snorting or injected. This cocain hydrochloride is treated with baking soda it gives crack,
this crack is used for smoking with crackling sound

Action : Local anaesthetic


Powerful CNS stimulant : for short time then followed by CNS depression

Signs and symptoms


1. Rush : Stage of excitement / euphoria , immediately after consumption = It is only for 30-60 min
2. Crush : Intense depression

Treatment
Amyl nitrite : specific antidote

Chronic cocain addiction = cocainism / cocainophagia / covainomania


Black discolouration of teeth and tongue
Painless perforation of nasal septum
Magnan symptoms/ cocain bugs / formication = Tactile hallucinations
Bugs / insect / sand particles crawling beneath the skin then the person goes on scratching the skin
Bruxisum : Grinding of teeth

Medicolegal importance
Cocain is second most widely elicited drug
Applied on glans penis to increase the duration of coitus
Prostitute inject — into vagina — local constriction
Spinal poisons
Strychnous nux vomica : we obtain strychnine: all the parts of plant are poisonous
Seeds are called Dog buttons
It is used to kill street dogs and seeds are buttons shaped

Active principles
1. Strychnine
2. Brucine
3. Loganin

MOA :
1. Site of action : Anterior horn cells of spinal cord
2. Action : They inhibit glycine ( post synaptic inhibitory neurotransmitter) which induces convulsions

Fatal dose : 1 crushed seed

Fatal period : 1-2 hrs

Signs and symptoms


1. Ricus Sardonicus : mocking of laughter
It is peculiar facial expression, due to contraction of facial muscles which causes corners of the mouth are drawn
backwards - looks like person is grinning

2. Convulsions :
A. Opisthotonos: Spasms affect mc anti gravity muscle
Extreme hyperextention of muscles - backward bending of body

B. Emprosthotonos : Exactly opposite to Optisthotonos


Spasm of abdominal muscles = forward bending of body

C. Pleurosthotonos : Lateral / side bending of body

Management
Isolated ( because small stimulus like cool wind or sound can stimulate / induce convulsions )
In between convulsions body is completely relaxed
The person dies after 4-5 such convulsions

Treatment
Treat the symptoms first before disease
Pentobarbital sodium & Amital sodium = Specific antidote given IV

Criteria Strychnine Tetanus


1. Action of muscles All the muscles are affected simultaneously First lock jaw & then other

2. Relaxation between convulsions Present Absent

3. Detection Can be detected in body Cannot be detected in body

Medicolegal importance
Most bitter substance
1:70000 bitterness of strychnine can be detected
Used for homicidal purpose : mixed with alcohol
Asphyxiants
1. Carbon monoxide
MOA : Carbon monoxide has 200-300 times more affinity than oxygen
It combines with hemoglobin to form carboxyhemoglobin
Carboxyhemoglobin decreases the O2 concentration in blood & tissue

Signs & symptoms


1. Less than 10% : No symptoms
2. 10-20% : Breathlessness on moderate exertion, headache & weakness
3. 20-30% : severe headache, irritability, emotional instability, defective memory
4. 30-40% : cherry red discolouration of skin & mucus membrane, diminution of vision, nausea & vomiting
5. 40-50% : symptoms resemble acute alcohol intoxication
6. 50-60% : syncope & coma
7. More than 80% : Death

Treatment
Remove from exposure & bring him into fresh air
But If CO concentration is more than 25% : treatment is needed
Specific treatment : 100% O2 at atmospheric pressure : supplied by tight fitting mask
Hyperbaric oxygen can be given

PM features
Cherry red discolouration of skin, mucous membrane, blood, PM staining
Blisters : subcutaneous blisters are seen on dependent parts of the body
In delayed deaths : bilateral symmetrical necrosis of globus pallidus & putamen = most characteristic lesion

Tests to detect CO poisoning


1. Hoppe-Seyler’s test
2. Kunkel’s test
3. Spectroscopy : best
4. 15 ml water is taken and 2 drops of blood is added from the body, if colour changes to bright pink colour then it case of CO poisoning

Medicolegal importance
Used for suicide rarely in India more common in western countries

2. Cyanide
Forms
A. Gaseous : Hydrogen cyanide gas
B. Liquid : Hydrocyanic acid
C. Solid : NaCN/ KCN salt

MOA: It inhibits the enzymes cytochrome oxidase & carbonic anhydrase


It prevent ATP formation by inhibiting last step of oxidative phosphorylation
Decreases O2 carrying capacity of blood
Causes death by histotoxic or cytotoxic anoxia

Smell of cyanide : Bitter almond smell ( 20-40% cannot smell this )


Ability to smell this is sex linked recessive trait

Absorption : Salts ( NaCN / KCN ) combine with HCl in stomach to form hydrocyanic acidl
Achlorohydric person may not suffer toxic effects of cyanide

Signs & symptoms


Most rapidly acting poison = causes cellular hypoxia
CNS : vertigo, faintness, trismus, convulsions, paralysis, coma & death
GIT : bitter taste in mouth, corrosion of mouth, throat & stomach
Respiratory system: bitter almond smell of breath

Fatal dose / Fatal period :


1. Hydrogen cyanide gas = 1:2000 / immediately fatal
2. HCN liquid = 50-60mg / 2-10 mins
3. Salts NaCN/ KCN = 200-300mg / 30 mins

Treatment

Principle of treatment :

Nitrites + Hb Methemoglobin
+
Cyanide

Cyanmethamoglobin + Thiosulphate Thiocyanates Excreted in urine

Specific antidote : 3 step antidote


Amyl nitrite = Inhalational
sodium nitrite = IV
thiosulphate = IV
Test for cyanide
Lee- jones cyanide

PM : Open head first : Bitter almond smell from cavities


Birght red colour

Medicolegal importance : Ideal suicide


It is also used for judicial execution

War gases
1. Vesicants / Blistering gases
sulphur, mustard, lewisite

2. Asphyxiants / lung irritants


Chlorine, phosgene gas

3. Tear gases
Choracetophenone ( CAP )
Bromo Benzyl Cyanides ( BBC )

4. Nasal irritants
Diphenyl chlorarsine
Diphenyl cyanarsine

5. Paralysants
Cyanides, CO

6. Nerve gases
Esters of phosphoric acid = tabun, Sarin, Soman

Vegetable poisons
1. Ricinus communis
Whole plant is poisonous particularly seeds
Active principle : Ricin

Castor oil does not contain Ricin


Castor oil is taken in large quantities resemble cholera
Ricin is potential terrorist weapon

2. Semicarpus Anacardium - Marking nut


Active principle : Semicarpol & Bhilawnol

Medicolegal importance
Used to produce artificial bruises

3. Calatropis
Active principle : Calatropin, uscharin, calatoxin, Calactin
Medicolegal importance
Used to produce artificial bruises, contusions, criminal abortions

Calotropic preocera : Poisonous to snakes ( snakes cannot tolerate the smell )


Used by snake charmers

4. Abrus precatorius
Seeds : egg shaped - black tip and red body
Traditionally used by jewellers to weigh

Active principle : when injected resembles viper snake bite

Medicolegal importance
Suis (needles ) : abrus precatorius seeds are powdered mixed with onion + datura + opium + water + spirit =
paste is made & converted into shape of needle

needle is used for homicidal Purposes


Drug dependence and abuse

Criteria Drug addiction Drug habituation

Compensation Present Absent ; only desire

Dependence Both psychological and physical Only psychological

Withdrawal symptoms Characteristically present Nill or minimal

Drug dependence = Drug addiction + habituation


Types
1. Morphine type
2. Cocaine type
3. Cannabis type
4. Barbiturates & alcohol type
5. Amphetamine type

MC abused substances
1. Legal - Caffeine, nicotine, alcohol
2. Illegally - Cannabis, cocaine

Body packer syndrome = Method of illegally transporting drugs - Heroin and cocaine

Drugs are converted into cylinders

They are wrapped & heat sealed

Again wrapped in latex like condom, balloon, glove

Then swollen Body packing

Take anti GI motility drugs like loperamide

Reaching destination take laxatives

Retrieve it

Complications
1. Intestinal obstruction
2. Severe intoxication of drug if packets get ruptured

Body stuffer’s syndrome =


Drug peddlers

If they get caught by police

Consume the drug packets to destroy the evidence

Body pusher’s
Concealing in orifices of the body like ear, nose, throat, rectum, vagina

Solvent abuse : Volatile substance abuse / glue sniffing


Volatile substances are intentionally inhaled for hallucinogenic effects
MC abused substances is toluene
Others : kerosine, petrol, benzene

Methods
1. Huffing : Inhaling substances from a cloth/ paper saturated with volatile substances
2. Bagging : Substance is smeared onto inner surface of a plastic bag which is held over mouth and nose and then inhaled
3. Sniffing : Inhaling from a mouth of a container
4. Dusting : Substance inhaled like a nasal spray
5. Glading : Substance used as aerosol spray

Main lining = IV administration of a narcotic drug


Main lining Scars : Scars produced due to frequent IV administration of a narcotic drug along needle tract
Skin popping : Subcutaneous injection of narcotic : map shaped ulcers
Psychotropic drugs
1. Amphetamines : It contains amphetamine and its derivatives like MDMA ( methylene dioxy meth amphetamine )
Clinical features
Trismus & Bruxism

MDMA is specifically used for drug facilitated sexual assault so also called as club drug or rave drug

Liquid gold : Urine in amphetamine poisoning

2. LSD : Lysergic acid diethylamide


It is most potent and most widely used hallucinogen

Signs & symptoms = also called take a trip

Synesthesia : Abnormal perception of senses like seeing a smell, hearing colours, feeling sound

Delusion of being able to fly

3. Barbiturates
Blisters are seen in areas of constant friction particularly in interdigital clefts, inner thigh, calves

Typical PM feature : Symmetrical necrosis of globus pallidus and corpus callosum

Medicolegal importance
Involuntary suicide : Accidental barbiturate poisoning seen due to barbiturate automatism

4. Chloral hydrate = also referred as dry wine


Easily soluble in water and alcohol so it is mixed with water and alcohol to make a person immediately helpless
Hence called knot out drops

Medicolegal importance
Robbery and rape ( also called date rape drug )

Chloral hydrate + alcohol = mickey Finn

Cardiac poisons
Aconite
Mitha zehar, blue rocket, monk’s hood, devil’s helmet

All parts are poisoning mostly roots


Roots resembles Horse radish root

Active principle : Aconitine

Signs and symptoms


Tingling and numbness - mc presenting symptom
Sign - Hippus : Alternate constriction and dilatation of pupils

Fatal dose : 1-2 gm

Fatal period : 2-6 hrs

COD : ventricular fibrillation

Medicolegal importance :
Ideal homicidal
Food poisoning
1. Botulism
By consuming the food contaminated with C. botulinum - sausage, canned meat, fish

This produces botulinum toxin - exotoxins - powerful neurotoxin

Fatal dose : 0.01 mg or less

Treatment
Botulinum antitoxin = Trivalent ( Type A, B, E )
BIG = Botulinum Immunoglobulin = pentavalent ( Type A,B,C,D,E )

Lathyrus satires = Keasari dal


Active principle : BOAA = Beta oxyl amino alanine

Consumption of Kesari dal as more than 30% of staple food per day for more than 6 months — Neurolathyrism

It is progressive spastic paraplegia with sparing of sensation, sphincters, mental activity

Back pain Weakness in leg Difficulty to sit & stand Difficulty to walk without stick Complete paraplagia

Steeping in hot water & par boiling - 90% toxin can be removed

3. Mushrooms
<5% Mushrooms are poisonous

Amanita muscaria = most poisonous mushroom in the world


Amanita phallodes = Death cap

treatment
No specific antidote
Benzyl penicillin & atropine are used

Magic mushrooms = mushrooms containing psilocin or psilocybin: they cause uncontrollable laughter & euphoria

4. Argemone mexicana = ( Argema = cataract )


Oil Sanguinarine
Dihydrosanguinarine

Cause abnormal permeability of blood vessles and results in epidemic dropsy

COD : Congestive Cardiac failure ( CCF )

Medicolegal importance :
Cheap adulterant for mustard oil & other edible oil
Its juice is used for treating cataract

5. Fish toxicity = Ichthyotoxicosis


Toxin is present in muscles of fish so it is also called as Ichthyosarcotoxicosis.

Cigutera
Teradon ( puffer fish )

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