Organophosphate Insecticides (OPC)

Pesticides
Mahmoud L. Sakr, M.D.

Professor of Clinical Toxicology
Director of the Poison Control Center
Ain Shams University
WHAT IS A PESTICIDE
A Pesticide is a chemical used to prevent, destroy or
repel pests.
Pests
Insects, Mice, Weeds, Fungi or Microorganisms such
as Bacteria and Viruses.
Pesticides
1. Insecticides
2. Herbicides
3. Rodenticides
4. Fungicides
Insecticides
Organophosphorous compounds
Carbamates
Organochlorines
Pyrethrins
Organophosphates and
Carbamates
Organophosphate Insecticides (OPC)
Absorption
Oral, Dermal and inhalation
Pathophysiology
Inhibition of cholinesterase enzymes 
accumulation of acetylcholine at CNS,
muscarinic and nicotinic receptors  classic
cholinergic syndrome
Pathophysiology
 Inhibits cholinesterase
 True cholinesterase
 RBC membranes
 Nervous tissue
 Skeletal muscle
 Plasma cholinesterase
 Serum
 Liver
 Pancreas
 Heart
 Brain
 Aging
 Permanent, irreversible binding to
cholinesterase.
*the enzyme is permanently destroyed,
and would take several weeks to
resynthesize
Clinical manifestations of OPC toxicity
Dependent on:
Type of agent
Quantity absorbed
Type of exposure
Variety
Systems (CNS, muscarinic, nicotinic)
Onset
 Most rapid: inhalation
 Least: transdermal absorption
A 52 y old man presents with several days of diarrhea
followed by the sudden onset of confusion, frequent
vomiting, loss of bowel and bladder control,
rhinorrhea, cough, excessive tearing, and tremors. He
had profuse sweating, but no fever or chills.
Physical examination: Temperature 35.6 c, pulse
94/min, respiration 18/min, blood pressure 144/82,
mildly constricted pupils, chest scattered rhonchi, skin
diaphoretic. Neuromuscular: alert oriented to persons
and place diffuse weakness and tremors
I- Cholinergic syndrome
A- Central (CNS) manifestations
Vertigo, confusion , convulsions and coma
Due to inhibition of brain A.Ch.E
Brain cholinesterase coincides with true
cholinesterase found in RBCs
 B- Muscarinic manifestations
1- Respiratory
 Bronchospasm and wheezes
 Bronchorrhea
 Pulmonary edema
2- CVS
 Bradycardia
 Hypotension
 Arrhythmias
3- GIT
 Salivation
 Vomiting
 Diarrhea
4- Eye
 Lacrimation
 Pin point pupils
5- Skin
 Sweating
 Subnormal temperature
6- Urination
C- Nicotinic manifestations
1- Myoneural junction
Fasciculations and twitches
Muscle cramps
Muscle weakness then paralysis
2- Sympathetic ganglia
Tachcardia and hypertension
3- Adrenal medulla
Release of catecholamines
II- Cardiotoxic effects
III- Intermediate syndrome
Manifestations
Weakness of motor cranial nerves, respiratory, neck and
proximal limb muscles with subsequent respiratory
muscle paralysis so the patient may need mechanical
ventilation.
Onset
It usually occurs within the first 2 -5 days after acute
poisoning and resolution of cholinergic syndrome
Early treatment with Ch E reactivators may prevent the
intermediate syndrome
IV- Delayed neuropathy
It usually occurs 14 - 21 days after exposure to some OP
compounds even after a skin contact.
It is mixed sensory-motor neuropathy
It usually begins in the legs, first causing burning or
tingling sensations, then weakness of the lower legs and
feet. The thighs and arms also become involved.
It is due to nerve demyelination and is usually
permanent.
Investigations
1- ECG and cardiac monitoring
2- Level of true and pseudo cholinesterase enzymes
Levels of:
50 % of normal: mild toxicity (sub clinical)
30 - 40% of normal: mild to moderate toxicity
Less than 20 to 25 % of normal: severe toxicity
3- ABGs
4- Electrolytes
Differential Diagnosis
1. Carbamates
2. Drugs causing miosis e.g. opiates,
phenothiazines
3. Pontine hemorrhage
4. Gastroenteritis
5. Mushrooms
Treatment
I- Stabilization of the patient (ABCD)
II- Decontamination
A- Dermal exposure
Removal of contaminated clothes
Wash the skin using tap water
If the hair is still smelly it may be cut to avoid relapses
from continuous absorption.
B- Oral ingestion
Induction of emesis should be avoided
Gastric lavage after endotracheal intubation with cuffed
tube
Activated charcoal
III- Antidotes
A. Atropine
Actions
It antagonizes muscarinic but not nicotinic manifestations.
It improves CNS depression
Dose
Adult: 1 - 2 mg IV
Pediatric: 0.01 mg/kg
repeated till
 Dryness of secretions
 Relief of bronchospasm and wheezes.
 Do not rely on pupil size
B. Oximes (cholinesterase reactivators)
Dose:
Pralidoxime (PAM)
Obidoxime (Toxogonin)
IV- Supportive treatment

V- Frequent observation
Carbamates
They are reversible inhibitors of cholinesterase
enzyme.
Their duration of action is relatively short.
They are commonly used for domestic uses (Baygon),
have low dermal toxicity and their toxicity is rarely
fatal.
Clinical Picture and Management
Is similar to organophosphates insecticides
poisoning with the following differences
1. Picture is milder
2. Recovery is rapid. Poisoning seldom exceeds 1-2 days.
3. Pseudo-cholinesterase enzyme is rapidly replenished
within few hours.
4. No intermediate syndrome, delayed neuropathy or
cardiotoxic effects
5. Atropine required is very limited
6. Oximes are not required
Case Study
One day prior to admission, a 7-years old
patient began to complain of abdominal pain
and vomiting the child was also unable to walk.
At the ER symptoms were consistent with GE
for which she was given treatment and was
discharged. Throughout the evening she was
extremely restless complaining of pain
wherever she was touched. Vomiting continued
and diarrhea began.
She was returned to the ER. On the
way she was incontinent of urine. At
the ER the child was flaccid with
difficulty breathing and inability to see.
She was intubated and given oxygen.
She began to have twitches and pin-
point pupils she was immediately
admitted to ICU
Questions
1- The following test is immediately
needed
A. Serum phosphorus
B. Plasma cholinesterase
C. Urine arsenic
D. Serum calcium
2- The level was 0 confirming the toxicity
by
A. Organochlorines
B. Organophosphates
C. DDT
D. Zinc phosphide
3- Toxicity from this group result in
A. Metabolic interference with
production of cholinesterase
enzyme
B. Inactivation of acetylcholine
C. Inhibition of acetylcholinesterase
D. Blocking of acetylcholine at the
action sites
4- Acetylcholine is the primary chemical
transmitter for
A. The CNS
B. The postganglionic parasympathetic
fibers
C. The postganglionic sympathetic fibers
D. The preganglionic sympathetic and
parasympathetic fibers
Thank You

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Pesticides

Mahmoud L. Sakr, M.D.

IV- Supportive treatment

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