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Toxicology

It is a science which deals with the properties, mechanism of action, clinical features, lethal dose
and treatment of a poison.
Difference between drug and poison
Effective dose: Dose of a substance which is therapeutically effective in 50% of individuals
receiving it.
Lethal dose (Totally depends on intention): use of substance which is sufficient to produce
death in 50 % of laboratory animals.
Drug: Any substance in effective dose is a drug.
Toxin: Any substance in lethal dose is a toxin.
Classification of poisons
1) Corrosive: These include inorganic acids, organic acids and alkalis.
 Inorganic acids include HCl, H2SO4, HNO3
 Organic acids include oxalic acid, carbolic acid, salicylic acid, hydrogen cyanide
(vegetable source)
 Alkalis include NaOH, KOH, NH4OH
2) Irritants: These are organic and non-organic
 Non organic are metallic and non-metallic
Nonmetallic which include phosphorus, chlorine, iodine, bromine
Metallic: mercury, lead, copper, lithium
 Organic can be of animal source which include snakes , insect, spiders
Vegetables include castor oil croton oil
Mechanical which include powdered glass, Diamond dust, needles and hair
3) Neurotropic
Acting on Brain: Opium, alcohol, benzodiazepine, barbiturates
Acting on spinal cord: strychnine
Acting on nerve: Curare, conium maculatum
 Somniferous: causing sleep
 Inebriants: which cause excitement, narcosis
 Deliriants: which cause delirium
4) Asphyxiants: irrespirable gases
CO, CO2, Coal gases, H2S
5) Cardiac toxins
Digitals, aconite, hydro cyanic acid
6) Miscellaneous
Paracetamol
Tricyclic Anti-depressants
Antipsychotics
Food poisoning

Medico legal types of poisons


1) homicidal poisons
2) suicidal poisons
3) stupefying poisons which include Dathura, bhang, road poisons
4) Accidental poisons
5) Abortificients which include papaya and carrot seeds
6) Infanticidals
Duties of medical officer in suspected poisoning
Medical duties: include
 Resuscitation
 General measures
 Antidote
 Forced elimination of poison from body
Legal duties: include
 Inform the police
 Note the bio data, age, name, time of arrivals clinical features, diagnosis and treatment
given
 collection of specimen which include blood urine, vomits and gastric aspirate

Ideal homicide: arsenic and aconite


Ideal suicidal: barbiturates cyanide
Resuscitation:
Means maintenance of airway, breathing and circulation
1) Maintenance of airway
Tilt the head on right or left side
Oropharyngeal Airway
Endotracheal tube
Tracheostomy
2) Maintenance of breeding
Oxygen inhalation
Nasal cannula
Positive pressure ventilation Ambu bag or ventilator
3) maintenance of circulation
Take two intravenous lines 6 gage cannula
Take sample for CBC, electrolytes, LFTs, RFTs, blood grouping and coagulation profile.
Give IV crystalloids which is normal saline or IV colloids
Blood transfusion
Inotropic support: nor-adrenaline which is drug of choice

General measures in poisoning:


1) Decontamination
 Removal of patient from source (carbon monoxide)
 Removal of clothes (liquid poisons)
 Washing skin with plenty of water (skin, vagina)
2) Forced EMESIS: for unabsorbed poison
Syrup Ipacac which induce poisoning but this should be done not after one hour
3) Gastric lavage: unabsorbed poison
Lifesaving procedure that should be performed within 4 to 6 hours of ingestion of poison.
Contraindications of gastric lavage: comatose patients
Absolute contraindication: is for corrosive intake (acids or alkalis, bleeding varices)
Relative contraindication: petroleum, strychnine poisoning (induce fits)

Procedure: First arrange dying declaration


 After a septic measure NG tube is lubricated, passed from nostrils and ask the patient to
swallow it
 After passing nasogastric tube confirm the placement in the stomach
 Then in instill 500 ml of water from distal end of tube into the stomach, wait for 2 to 3
minutes and then remove the water by suction pressure. Save the 1st gastric aspirate for
toxicological analysis.
 Repeat 20 times or10 liters of water after gastric lavage remove the nasogastric tube by
pinching its distal end.
Complications:
 can be injury to nose , esophagus and stomach
 perforation of esophagus
 Aspirational pneumonia

Antidote
Substances which are used to minimize effect of toxins.
1) Chemical antidote: Substances which bind a toxin and convert them into nontoxic
substances.
Oxalic acid + Ca will convert into calcium oxalate which is nontoxic
2) Physical antidote
 Demulcents: make protective layer on mucosa e.g. egg albumin, barley water
 Delucents: milk or water
 Bulky food: boiled rice or vegetables
3) Receptor antidote: which compete with toxins for receptors
 Atropine for organ phosphorus.
 Morphine poisoning receptor antagonist
4) Dispositional antidote: substance which produce alteration in metabolism and excretion
of toxin in body.
 Paracetamol N-Acetyl cysteine (increase glutathione in hepatocytes)
5) Functional antidote: substance which produce exactly opposite effect by acting on
different system.

Chelating agents: Used to bind metals to inhibit their deposition in organs.


 Desferroxamine → Iron
 Penicillamine → copper and lead
 Dimercaprol → arsenic and mercury
 EDTA → copper, lead, iron, magnesium, calcium, and heavy metals.

Universal antidote: Charcoal


It is a fine black powder used to absorb undigested poison made by burning animal or plant
matter.
Source:
 Animal: by burning animal bone (medico legal purposes)
 Plant: burning wood Pulp and bread
Types
 Simple Charcoal is formed by burning at 100 degree Celsius.
 Activated charcoal is formed by burning on 700 to 800 degree Celsius with increased
surface area and increased absorptive power.
 Super activated is burnt at 1000 degree Celsius which further increased absorptive
Power.
Uses:
 Universal antidote
 it does not have toxicity of its own
 can be used for hemoperfusion which is modified dialysis
Dose:
Charcoal 10mg: toxin 1 mg
In adults it can be used for one gram for one kilogram.
Advantages
 don’t alter Body metabolism
 it is easily excrete
 it is cheap and it is easily available
Disadvantages
 Mechanical absorption of gastrointestinal tract
 Aspiration pneumonia
Limitations
Don't bind with alcohol/cyanide/ Iron/potassium/ lithium
Not useful in corrosive toxics.

Forced elimination of poison


 Forced diuresis: not more than one hour
 Peritoneal dialysis (Hemodialysis which is more effective)
 Charcoal hemoperfusion
Morphine also used in severe pain

Asphyxiants:
Carbon monoxide poisoning
Carbon monoxide is colorless, tasteless, order less, non-irritating gas which is a silent killer.
Carbon monoxide is a product of incomplete combustion of carbon matter.
It is present in air about 0.001%.
Domestic gas: 6-7 % → burning will increase its level in air.
Mechanism of action
 Carbon monoxide has great affinity for hemoglobin leading to formation of
carboxyhemoglobin hemoglobin
 Hb cannot bind with oxygen
 So hypoxia to body tissue occurs

02-10% → asymptomatic
10-20 % → headache with flushing and Dizziness
20-30 % → throbbing headache with dizziness
30-40% → dizziness with confusion, nausea and vomiting
40-50% → syncope, tachypnea and tachycardia
50-60% → will cause coma
60-70 % → fits, decreased pulse decreased respiratory rate and eventually death
70-80% → feeble pulse and death within an hour
80-90% → cause death within one hour

Fatal dose:
 1% concentration in air → will cause unconsciousness in 15 to 20 minutes
 Coal gas 5-7 % in air → takes 3-5 minutes
Key to diagnosis:
PaO2: normal
O2 Saturation: decreased
Medico legal:
 Accidental → in most cases
 Suicidal → which is rare
 Homicidal → which is also rare

Treatment:
Medical duties and legal duties
Medical duties:
 Resuscitation
 decontamination which is removed patient from source that is carbon monoxide
 bring patient fresh air
 Antidote: hyperbaric oxygen O2
 Add 5 % CO2 → disassociate carboxy Hb additional
 Can be given steroids and mannitol to treat cerebral edema

Postpartum appearance:
External Internal
Congested conjunctiva Blood will be Cherry red
Fine froth at mouth Brain, stomach, lungs, Kidneys are congested
Cyanosis
Hypostatis / Cherry red post mortem lividity (PML)

Hypostasis: which is pooling of blood in tone less vessels after death in dependent part of body
color will be blue.
Hydrocyanic acid (HCN) or Cyanide poisoning
Known as Vegetable acid, colored gas or bitter almond smell
Source:
 Cherry
 Plum
 Jet berry brush
 Apple seeds
 Apricot
 bitter almond oil
Uses:
 lab workers
 metal cleaning
 Steel hardening
 Rubber Industry
 Refining/extracting of gold
 photography
Mechanism of action:

Great affinity for cytochrome oxidase



Binds with cytochrome oxidase

Inhibits O2 transformation

Histotoxic / cellular hypoxia

Cause of death → brain hypoxia (respiratory Center

Fetal dose:
60 milligrams → pure acid
60 drops → bitter almond oil
200 milligram → KCN

Medico legal:
 suicidal → mostly because cheap and easy availability
 accidental →
 homicidal → never due to bitter taste
Clinical Features:
 increase cyanide level of blood
 signs and symptoms include headache, flushing, confusion, increased pulse, increased
respiratory rate, fits, feeble pulse, death
 Clinical features also include skin flushing, breathing difficulty and palpitations.
Diagnostic:
 bitter almond smell
General measures:
 removal of patients from source
 removal of clothes
 wash with plenty of water
Antidote: cyanide antidote kit
 amyl nitrate inhalant
 sodium nitrate
 sodium thiosulphate

Mechanism of action:
Nitrates convert hemoglobin into met hemoglobin and met hemoglobin has great affinity for
cyanide. Cyanide leaves cytochrome oxidase and bind with met hemoglobin to form cyano met
hemoglobin which is non-toxic.

Post Mortem Exam:


External: Internal:
Smell of bitter almond blood → Pink
Hypostasis will be pink brain, lungs, heart, Kidneys congested due to
Conjunctiva congestion increase oxygen
Fine froth mouth

Corrosive:
They have ability to damage any surface they become in contact with.
Mineral acids include H2SO4, HCL and HNO3
Most of them have local actions except shock.
Mechanism of action is local corrosive action → binds with hemoglobin to form acid hematin +
extraction of water from body tissue.

H2SO4
 Heavy, oily, colorless Odorless, no fuming
 Fatal dose is 10-15 ml
 It turns all the body tissues brown due to increase in production of acid haematin.

HNO3
 colorless , fuming, pungent smell
 HNO3 + protein → nitric oxide + trinitro phenol (picric acid)
 Xanthoproteic reaction → turns body tissues yellow.

HCL
 Colorless, fuming, stain white sour taste
 Produce Lethal erosion

Vitriolage:
Throwing of acid on somebody for jealousy, disfigurement and Visual impairment.
In 1820 → Glasgow → industrial riots
Clinical features:
 intense burning pain from mouth to stomach
 intense vomiting
 clothes → will be perforated/stained
 lips → will be excoriated
 persistent vomiting
 Teeth → white and brittle
 oral cavity → damaged mucosa filled with froth and stain
 tongue → will be swollen and stain
 angle of mouth → will have streak of acid
 Dyspnea → due to damage of epiglottis and larynx
 Shock → dehydration and vomiting
Medico legal:
 Suicidal (rare accidental)
 Accidental (mostly)
 Homicidal (not very common)

Cause of death:
 Shock
 respiratory obstruction
 perforation of stomach → peritonitis
Treatment
Medical treatment includes
 resuscitation
 no gastric lavage → contraindicated
 No Emetics
Antidote:
 buffer solutions
 sodium hydrogen phosphate
 potassium hydrogen phosphate
Organic acids
Oxalic acid
Hypokalemic and nephropathy
White crystalline substance dissolved in water
Uses:
 cleaning brass
 removal stains
 metal cleaning
 Rubber Industry
Fatal dose: is 15 to 20 grams
Fatal period: One hour which is very important
Mechanism of Action:
 is local corrosive action
 hypokalemic/will cause tetany (formation of Ca oxalate)
 Renal damage → crystal nephropathy → oxaluria
 Shock → due to Intense vomiting leads to death
Christison’s saying
If a patient after eating a crystalline substance whose taste is strongly acidic presents with violet
vomiting, pain in stomach, feeble pulse, cold sweats, shock and dies within one hour → there is
hardly any doubt regarding oxalic acid poisoning.

 because of decreased calcium levels → ventricular fibrillation


Treatment
 medical resuscitation
 general measure is decontamination
Antidote
- Calcium gluconate IV → combine with oxalate and save calcium.
- Lime orally
- Whatever has to be done should be done quickly

Postmortem appearance
External Internal
Steak → angle of mouth whitish Mucosa of esophagus, stomach is damaged having
Lips, tongue, oral cavity is excoriated gelatinous acidic fluid
And whitish stain
Diagnosis
Oxalic acid crystals → that is present in stomach and renal tubes (Kidneys)
Medico legal:
Always suicidal

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