Organophosphate POISONING

PRESENTED BY
RIMSHA NASIR
ROLL NO. 120
 Organophosphorus insecticides
Organophosphorus (OP) compounds are widely
used as pesticides, especially in developing countries
Case fatality following deliberate ingestion is high (5-
20%)
OP are also used to make nerve agents which are
developed for chemical warfare and are more toxic
Mechanism of Action

• Organophosphates bind to the active site of the

acetylcholinesterase enzymes and inactivate it. As a result
acetylcholine accumulates at sites of synapses. Patient
presents with cholinergic symptoms
.
• Initially binding of organophosphates to the enzyme is
reversible and enzyme can be recovered but after a
certain time period, loss of a chemical group from the OP
enzyme
complex results in irreversible inhibition of the
enzymes. This process is known as AGEING.
History
What toxin(s) have been taken and how much?
What time were they taken and by what route?
Has alcohol or any other substance (or substances, including drugs
of misuse) been taken as well?
Obtain details from witnesses (e.g. family, friends, ambulance
personnel)
Assess capacity to make decisions about accepting or refusing
treatment
Establish past medical history, drug history and allergies, social and
family history
Record all information carefully
Clinical Presentation

• Patients present with symptoms of cholinergic excess. Both

types of Acetylcholine receptors (Muscarinic and Nicotinic) are
affected.
• Clinically patients can present in any one of the following
forms :
1. Acute Cholinergic Syndrome
2. Intermediate syndrome
3. Organophosphate Induced Delayed Polyneuropathy
(OPIDN)
Acute Cholinergic Syndrome

• Vomiting and profuse diarrhoea after ingestion

• Severe respiratory compromise due to
brochoconstriction and salivation
• Excessive sweating
• Miosis
• Muscular fasiculations
• Generalized flaccid paralysis affecting ocular and
respiratory muscles
• Ataxia
• Coma
• Convulsions
• Cardiac repolarisation abnormalities
Confirmatory Test
Diagnosis of OP Poisoning
can be
confirmed by measuring plasma
or red
cell cholinesterase activity.
i. Less than 10% (Severe)
ii. 20-50 % (Moderate)
iii. >50 % (Sub Clinical)
General Management

• ABCs : Clear the airway of excessive secretions,

administer
high flow oxygen and obtain IV access.
• Remove contaminated clothing and contact lenses,
wash
skin with soap and water and irrigate the eyes.
• Perform gastric lavage if patient presents within 1
hour of
administration
• Monitor ECG, Oxygen Saturation, Blood gases,
Temperature, Urea and Electrolytes
Specific Management
• ATROPINE: acts as a competitive antagonist at Acetylcholine
receptors
Dosage:
Initially 2 mg IV should be administered and double the dose
every 5-10 minutes until clinical improvement occurs. Further bolus
doses should be given until secretions are controlled, the skin is dry,
blood pressure is adequate and heart rate is >80bpm

• PRALIDOXIME:
It helps regenerate Acetylcholine esterase enzymes in the reversible
stage

• Magnesium sulphate IV

• BENZODIAZEPINES used to reduce agitation, fasciculation, convulsions.

Intermediate Syndrome
• Occurs in 20% patients
•Symptoms develop within1-4 days of exposure,
often after resolution of acute cholinergic
syndrome and can last for 2-3 weeks
• Patient develops weakness that spreads from
ocular muscles, to muscles of head and neck,
proximal limbs and muscles of respiration
resulting in respiratory failure.
• No specific treatment and supportive care is
needed
Organophosphate Induced Delayed
Polyneuropathy (OPIDN)

• It is a rare complication that occurs within 2-3 weeks of

Exposure.
• It is a mixed motor/sensory polyneuropathy affecting long
myelinating neurons as result of inhibition of other
enzymes other than Acetylcholine Esterase.
• Patients may present with muscle cramps, foot drop, wrist
drop, sensory loss, paresthesia, diminished tendon reflexes.
• Treatment involves physiotherapy but recovery is usually
incomplete.
Thank you