Insecticide Poisoning

Based on forensic Medicine

1. LECTURE ON INSECTICIDE POISONING
Insecticides are variable group of chemical substances used for killing, control or eradication of
unwanted pests, insects and worms etc.
Some of the most commonly used insecticides belong to the following groups of compounds
1. ORGANO PHOSPHORUS GROUP
2. CARBAMATES
3. CHLORINATED GROUP
4. NAPHTHALENE
1.ORGANO PHOSPHORUS GROUP OF INSECTICIDES III
organo phosphorus are a diverse widely used group of dangerous poisons used as Insecticides for
spraying crops and for fumigation(to fill the area with gaseous pesticide to suffocate pest) of ships and
go downs.
Classification of Organo phosphorus compounds lifitif
They are divided into two groups owing to their chemical structure
1. ALKYL GROUP
2. ARYL GROUP
ALKYL GROUP OF ORGANOPHOSPHATE INSECTICIDES III
commonly used alkyl group organo phosphate insecticides include
1. Hexa Ethyl Tetra Phosphate ( HETP )
2. Tetra Ethyl Pyro Phosphate ( TEPP )
3. Octa Methyl Pyro Phosphate ( OMPP )
Now next two are MD
4. Malathion
5. Dipterex
ARYL GROUP OF ORGANO PHOSPHORUS INSECTICIDES III
commonly used aryl group of organophosphorus insecticides include
1. Parathion
2. Paraoxon
3. Chlorothion
4. Diazinon
5. Eketox

2. 2.CARBAMATE GROUP OF INSECTICIDES III
These are a group of poisonous organic compounds which lack phosphate group and unlike organo
phosphorus insecticides have carbamate groups substituted instead of alkyl or aryl groups in the
hydrocarbon chain.
These insecticides are reversible inhibitors of cholinesterase unlike organo phosphates.
CARBAMATE INSECTICIDES III
Commonly used carbamate group of insecticides include
1. Aldicarb 6. Premicarb
2. Carboryl 7. Propoxur
3. Methiocarb 8. Thiofanox
4. Methomyl
5. Oxamyl
MODE OF ACTION OF BOTH ORGANO PHOSPHORUS AND CARBAMATE GROUP OF INSECTICIDES IIII
They are powerful inhibitors of Cholinesterase enzyme which is present in the synapses of
ganglions and neuromuscular junctions and responsible for degradation of acetylcholine.
The resulted accumulation of acetylcholine causes hyper excitation of voluntary and involuntary
muscles with increased secretions all together resulting in toxic symptoms.
FATAL DOSE
The fatal dose of organo phosphorus compounds varies with the type of compound
The fatal dose of carbamates ranges between 25mg to 350mg orally
FATAL PERIOD I
The fatal period for both organo phosphorus and carbamate insecticides ranges from half an
hour to three weeks
PORTAL OF ENTRY
1. Gastrointestinal Tract
2. Inhalation
3. Open wounds
4. Contact with mucous membrane
5. Eyes
6. Contact with intact skin
SYMPTOMS OF ORGANOPHOSPHORUS AND CARBAMATE POISONING II
Symptoms can be classified on the basis of
Pharmacological actions of organophosphates (Ach abundance at synapse)
a. Muscarine like effects
b. Nicotine like effects
c. CNS effects
a. Muscarine like effects ilifft
1. Bronchial Tree
a. spasm
b. increases secretions
c. chest pain

3. d. dyspnoea
e. cough
f. edema
g. cyanosis
2. Gastrointestinal Tract
a. increase salivation
b. nausea
c. anorexia
d. cramps
e. epigastric and substernal tightness/ cardio spasm
f. tenesmus
g. involuntary defecation
3. Heart
a. bradycardia
4. Eyes
a. Red tears called Chromogenic tears
due to porphyrins
b. meiosis
c. blurred vision
5. Skin
a. excessive sweating
6. Urinary bladder
a. incontinence
2. Nicotine like effects itilifft
1. Striated Muscles
a. weakness
b. twitching
c. fasciculations
d. cramps
2. Cardiovascular effect
a. increased blood pressure
3. Central Nervous System Side effects tltifft
1. Irritability, confusion, tremors, convulsions.
2. Areflexia, respiratory and circulatory depression.
3. Tremors of hands, lips, face or tongue.
Additional points to remember itilittr

4. 1.Garlic like odour
2. Skin exposed to poison is red and blistered
CAUSE OF DEATH
1. Respiratory Paralysis or failure
2. Circulatory arrest
3. Edema of lungs or brain
LAB DIAGNOSIS II
The essential finding in Lab diagnosis is depression of CHOLINESTERASE ACTIVITY. In acute
poisoning, signs and symptoms generally occur when > 50% of cholinesterase is inhibited.
1.RBC ( true) cholinesterase
Plasma (pseudo) cholinesterase
RBC cholinesterase is considered more accurate as Plasma cholinesterase declines more rapidly so
less reliable.
2. P- nitrophenol test: P- nitrophenol is a metabolite of some OPCs(organophosphates
compounds) and is excreted in the urine. Its excretion in urine can be used as a confirmation test
of OPC poisoning. This test can also be performed on vomitus or gastric Lavage contents.
3. Thin Layer Chromatography.
4. Spectrophotometry
Treatment of Organo phosphorus and carbamate poisoning ttftii
Treatment may be summarized in the following order
1. Decontamination
2. Care of Airway
3. Administration of antidote
4. Administration of cholinesterase reactivators
4. General measures
Decontamination titi
1. Remove the person from the source of poison.
2. Strip off all contaminated clothes and wash the
skin and mucous membrane thoroughly with
water.
3. Gastric lavage with water, KMnO4.
Care of Airway fi
1. Suction if necessary.
2. Oxygen and postural drainage for bronchial hyper secretion.
3. Intubation, tracheostomy or artificial respiratory support if required.
ADMINISTRATION OF ANTIDOTE IIII
1. Preservative free atropine is the drug of choice.
2. Give an initial dose of 1mg I/V and make sure that no adverse effects occur.

5. 3. Repeat a dose of 2 mg every 15 minutes until
atropinization is achieved.
4. Atropinization is manifested by drying of secretions, tachycardia, flushing, dry mouth and
dilated pupils.
5. The average patient requires approximately 40mg of atropine per day, but larger doses of
500 to 1500mg per day may be necessary.
6. Intermittent administration of atropine at 15
to 30 minute intervals has to be continued for at least 24 hours till the organophosphorus and
carbamates have completely metabolized.
7. Severe cases may require several days of therapy.
8. Atropine does not reverse the muscle weakness.
CHOLINESTERASE REACTIVATORS II
1. These are oxime compounds which reactivate the phosphorylated acetyl cholinesterase enzyme
provided they are given within 12 to 24 hours of organo phosphorus poisoning.
2. Cholinesterase reactivators are contraindicated in carbamate poisoning since they reversibly
inhibit acetyl cholinesterase and their administration worsen symptoms.
1. PAM (Pyridine 2 Aldoxime Methiodide) is given
in a dose of 1 to 2gm diluted in 5% isotonic
saline and repeated 12 hourly.
2. P2S (Pralidoxime chloride) is given as 400mg
intravenously and repeated if necessary.
3. Toxigonine (Obidoxime) 250mg I/V at 12 hour intervals.
GENERAL MEASURES
1. Barbiturates or diazepam for convulsions
2. Diuretics like lasix may be required.
3. Coramine or Dextrose Saline for collapse .
4. Bronchodilators to improve respiration.
5. Tracheostomy or Mechanical ventilation if necessary.
POSTMORTEM APPEARANCES
“signs of asphyxia are evident”

6. EXTERNAL POSTMORTEM APPEAREANCE
1. Face is cyanosed.
2. Blood stained froth at nose and mouth.
3. Garlic like odour is present.
Internal post mortem appearance tltt
1. Stomach:
a. contents are blood stained.
b. congested mucosa with petechial
hemorrhages.
c. garlicky odour.
Internal post mortem appearance tltt
2. Lungs:
a. edematous.
b. petechial hemorrhages present.
Internal post mortem appearance tltt
3. Brain:
hyperemia and petechial hemorrhages.
“Petechial hemorrhages are evident in other organs aswell.”
Medicolegal Importance illIt
1. Most commonly accidental.
2. Homicidal due to rapidity of action and easy
availability.
3. Suicidal.
3. CHLORINATED INSECTICIDES IIII
These insecticides contain chlorine in their molecular structure. Some of them include.
1. DDT ( Di Chloro Di Phenyl Tri Chloro Ethane)
2. Gammaxine
3. Hexaphane
4. Aldrin
5. Dialdrin
DDT
1. DDT is the most commonly used Chloro group of insecticide. I I I

7. 2. Powered DDT is a white crystalline solid which is readily soluble is kerosene oil.
3. It is used to kill flies, mosquitoes, lice, fleas, and bed bugs.
MODE OF ACTION I
It acts on the motor cortex and the cerebellum.
PORTAL OF ENTRY
1. Oral
2. Local
3. Inhalation
SYMPTOMS OF CHLORO GROUP INSECTICIDE POISONING IIIII
1. Nausea and Vomiting
2. Coughing
3. Excitability
4. Vertigo
5. Weakness
6. Muscular tremors
7. Convulsions
8. Tingling in arms and legs
SYMPTOMS OF CHLORO GROUP INSECTICIDE POISONING IIIII
9. Paralysis of legs
10. Pulmonary edema
11. Unconsciousness and coma
12. Death from respiratory failure
FATAL DOSE
150 to 160 mg per kilogram body weight (10.5 gm for 70 kg adult)
FATAL PERIOD I
Fatal period ranges from half to four hours
TREATMENT
1. Gastric lavage with tap water.
2. Inject atropine to prevent pulmonary edema.
3. Calcium Gluconate I/V
4. Oxygen inhalation or artificial respiration.
5. Paraldehyde or diazepam for convulsions.
6. Barbiturates for muscular twitching & tremors.
POST MORTEM APPEARANCE
Signs of asphyxia with smell of kerosene in the stomach, pulmonary edema, petechial

8. hemorrhages in the submucosa of the gastrointestinal tract can be appreciated.
MEDICOLEGAL IMPORTANCE II
1. Used for suicidal purpose
2. Accidental poisoning
4.NAPHTHALENE (two combined benzene ring structure)
It is used as moth balls as pesticides eg in cloths (phenyl ki golian :P), as deodorants in lavatories,
in dying industry and electrical equipment as an insulator.
FATAL DOSE
“fatal dose of naphthalene is 2 gms”
FATAL PERIOD I
“few hours to three days”
SIGNS AND SYMPTOMS OF NAPHTHALENE POISONING III
1. Headache, nausea and vomiting
2. Staggering gait
3. In the kidney it causes acute nephritis, painful
micturation, dark brown colored urine with
albumin and hemoglobin in it
4. Jaundice, Haemoglobinuria, hemolytic anemia,
and optic neuritis
5. Dermatitis on contact
6. Convulsions, cyanosis, perspiration, coma and death
TREATMENT OF NAPHTHALENE POISONING II
1. Keep body warm
2. Stomach wash
3. Purgatives
4. Avoid fats as they dissolve naphthalene
5. Sodium bicarbonate to alkaline the urine
6. Blood transfusion
7. Hydrocortisone for hemolysis
8. Low fat and high carbohydrate, protein and vitamin diet
9. I/V glucose
POST MORTEM APPEARANCE
1. Yellow skin.
2. Gastric mucosa is yellow, congested and
inflamed.
3. Liver and kidneys are damaged.
MEDICOLEGAL IMPORTANCE II
1. Accidental
2. Suicidal
5. ALUMINUM PHOSPHIDE
Is known as agent of sure death. What are its uses give clinical features, autopsy findings and medicolegal
aspects of its overdose
USES
1.Pesticide:- Aluminum Phosphide is used as a rodenticide, insecticide and fumigant for stored
cereal grains. It is used to kill moles and rodents the tablets and pellets typically contain
chemicals that evolve ammonia which helps to reduce the potential for spontaneous ignition or
explosion of the phosphine gas PH3.

9. 2. Evidently poisonous it has been used for suicide and homicidal purposes.
3.Semiconductor application:- Industrially it is a semiconductor that is usually alloyed with other
binary materials for applications in devices such as light emitting diodes
MECHANISM OF ACTION II
On exposure to air and moisture, Aluminum phosphide tablets release phosphine gas and this is
used for fumigation. Phosphine gas produce multi organ damage.
It is supposed to be a protoplasmic poison which inhibits protein and enzyme synthesis.
It interrupts the stages of mitochondrial electron transport by inhibiting cytochrome oxidase.
Clinical Features liilt
Following ingestion of aluminum phosphide patients have a very anxious look and present to the
emergency with profuse vomiting, upper abdominal pain and breathlessness with garlicy fishy
odour
Clinical presentation may be characterized by liilttiti
Hypotension
Marked Tachycardia
Altered Sensorium
Anemia
Pulmonary oedema
Shock
Renal and Hepatic dysfunction
Accidental ingestion may occur itliti
If patients survive the initial 6-24 hrs, adult respiratory distress syndrome may supervene
-Patient with mild toxicity recover
-If patient reaches the hospital with significant hypotension death is the probable outcome
-Workers engaged in fumigation, report with minor symptoms such as
Continue
Cough
Dyspnea
Chest tightness
Headache
Giddiness
Numbness
Lethargy
Anorexia
Epigastric pain
Ronchi and Absent ankle reflexes
Labs
Increase in blood aminotransferase and bilirubin
ECG: Atrial fibrillation, ST elevation or depression, heart block
Others: Increased TLC, Magnesium ↓ Potassium↑ (arrest)
Clinical diagnosis: Analysis of gastric aspirate or breath both of which blacken a paper
impregnated with silver nitrate

10. Autopsy t
Congestion of liver, spleen, kidneys, adrenals GIT and brain that correlate with severity of
hypotension ,Myocarditis.
Histopathology does not reveal any specific changes beyond visceral congestion and patchy
necrosis of liver
TREATMENT
Reduction of absorption from GIT
i. Gastric Lavage with KMNO4 (1:10,000) in first 30-45 minutes after ingestion( oxidizes
phosphine to phosphate), repeat 2-3 times.
ii. Activated charcoal 100 Gms orally to adsorb phosphine.
iii. Antacids reduce absorption of phosphine.
iv. Anti emetics and H2 antagonists give symptomatic relief.
REDUCTION OF TOXICITY
i. Magnesium Sulphate: It reduces organ toxicity, corrects hypomagnesaemia and arrhythmias.
Dose: 200 mg/ kg every 4-6 hours or 3 Gm bolus followed by 6 Gm as infusion over 12 hours for 5-
7 days.
ii. Enhancement of excretion: Phosphine is excreted through lungs and kidneys, so adequate
hydration and renal perfusion should be maintained by I/V fluids.
Supportive treatment tittt
●Oxygen for hypoxia.
●Fluids (3-4 Litres) given in first 3-6 hours, 50% of which is normal saline
●Hydrocortisone 400 mg 4-6 hourly for shock
●Sodium bicarbonate for metabolic acidosis
●Low dose dopamine is given for hypotension and shock ( 4-6 μg/kg/minute)
● Peritoneal or Haemodialysis may be done.
Treatment tt
Recent Research:
Various fats and oils like coconut oil when used in gastric Lavage can help to decrease absorption
of phosphine gas from stomach