2. INTRODUCTION
• Organophosphorus compounds or
organophosphates are commonly used in the
industrial, agricultural and home settings. They were
initially developed as insecticides but some of them
as nerve gases i.e.
• Sarin ( colorless, odorless liquid, used as chemical
weapon to its extreme patency as nerve agent),
• Soman (a nerve agent, used as chemical weapon),
3. • Tabun ( clear colorless, tasteless liquid with
faint fruity odor. Acts as nerve agent), and
• VX (as nerve agent, earlier used as pesticide
and later as weapon).
• These are used as chemical warfare and in
terrorist attacks.
4. • Some Organophosphorus compounds are
used as pesticides in agriculture. These are
highly toxic and include tetraethyl
pyrophosphate and parathion.
• Other organophosphates such as coumaphos,
chlorpyrifos and trichlorfon are used as
animal insecticides and have intermediate
toxicity.
• Low toxicity compounds are malathione,
diazinon and dichlorovos. These are used as
household insecticides.
5. • Organophosphorus compounds are easily
accessible and are often used to commit suicides.
• Accidental poisoning may also occur especially
when they are kept within the reach of children.
• Farmers could get exposed while spraying crops if
they are not well protected with masks, gloves
and other protective clothing.
6. DEFINITION
• Organophophate poisons are the group of
potent nerve agents, functioning by inhibiting
the enzyme choline esterase.
• Organophosphate Poisoning occurs after dermal,
respiratory, or oral exposure to
either organophosphate pesticides (e.g.,
chlorpyrifos, dimethoate, malathion, parathion)
or nerve agents (e.g., tabun, sarin), causing
inhibition of acetyl cholinesterase at nerve
synapses.
7. INCIDENCE
• According to the World Health Organization
(WHO), there are about 1 million people a
year admitted to hospital with accidental
poisoning and 2 million with suicidal intent. It
is estimated that there could be as many as 25
million agricultural workers in the developing
world suffering an episode of poisoning each
year.
8. EPIDEMIOLOGY
• There are no accurate figures kept about the
incidence of OP poisoning.
• The vast majority of cases are accidental from the
use of pesticides. There is a much higher incidence in
rural areas of the third world.
• Hospital admissions for intentional OP poisoning are
twice as numerous as for accidental poisoning.
Intentional self-harm tends to involve much higher
doses than accidental exposure.
• Fortunately, terrorist or warfare use of OP is rare but
the potential exists to expose a great many people at
once.
9. CLINICAL MANIFESTATION
• Depends on the route of entry i.e. Ingestion,
inhalation and eye contact.
• Depends upon whether the poisoning is mild,
moderate or severe. The symptoms are basically
those of excessive acetylcholine activity.
Mild
Small or pinpoint pupils.
Painful, blurred vision.
Runny nose and eyes.
Excess saliva.
Eyes looking 'glassy‘ (fixed
stare and wide eyed).
Headache.
Nausea.
Mild muscle weakness.
Localized muscle
twitching (jerking).
Mild agitation.
10. Moderate
Pinpoint pupils, conjunctival injection (red
conjunctiva or sclera).
Dizziness, disorientation.
Coughing, wheezing, sneezing.
Drooling (unintentional spillage of saliva from
mouth), excess phlegm (excess mucus at back of
nose or throat), bronchorrhoea (production of more
than 100 ml/day of watery sputum), bronchospasm.
Breathing difficulty.
Marked muscle twitching or tremors.
Muscle weakness, fatigue.
Vomiting, diarrhea, urination.
11. Severe
Pinpoint pupils.
Confusion and agitation.
Convulsions.
Copious excess secretions.
Cardiac arrhythmias.
Collapse, respiratory depression or respiratory arrest.
Coma.
Death.
12. PATHOPHYSIOLOGY
The nervous system is made up of a large number of nerves.
When a signal reaches the end of a nerve, it releases a substance
called neurotransmitter
that carries the signal to the adjacent nerves or organ such as
muscle or gland.
Many nerves release acetylcholine as the neurotransmitter.
Once the signal passes to the next nerve, an enzyme called choline
esterase which destroys the acetylcholine.
Organophosphorus compounds block this enzyme,
thus preventing the breakdown of acetylcholine.
Then acetylcholine acts for an excessively long time causing
symptoms like twitches and increased secretions.
After some time, the muscles gets fatigued leading to paralysis.
13. DIAGNOSTIC EVALUATION
• History collection, and physical examination.
• RBS, BUN, Electrolytes, Prothrombin time, liver function
studies, and plasma cholinesterase measurements.
• Other laboratory findings include the following:
– Leukocytosis
– Hemoconcentration
– Metabolic and/or respiratory acidosis
– Hyperglycemia
– Hypokalemia
– Hypomagnesemia
– Elevated troponin levels
– Elevated amylase levels
– Elevated liver function test results.
15. • Organophosphorus poisoning is treated using drugs
that block the action of acetylcholine i.e. atropine
and drugs that regenerate the cholinesterase enzyme
i.e. pralidoxime and obidoxime.
• Diazepam is used to control seizures caused due to
the poisoning.
16. Nursing Diagnosis:
• Risk of ineffective airway clearance related to
Neuromuscular dysfunction as evidenced by
Changes in respiratory rate and depth.
• Risk of aspiration related to drug intoxication
as evidenced by speech evaluation showing
silent aspiration and vomiting.
• Risk for infection related to absorption of the
toxic substances in body as evidenced by sign
and symptoms.
17. INTERVENTIONS:
• Check airway, breathing, and circulation. Place
patient in the left lateral position, preferably with
head lower than the feet, to reduce risk of aspiration
of stomach contents. Provide high flow oxygen, if
available. Intubate the patient if their airway or
breathing is compromised.
• Obtain I/V access and give 1–3 mg of atropine as a
bolus, depending on severity. Set up an infusion of
0·9% normal saline; aim to keep the systolic blood
pressure above 80 mm Hg and urine output above
0·5 mL/kg/h. Side by side insert foley’s catheter.
18. • Record pulse rate, blood pressure, pupil size,
presence of sweat, and auscultatory findings at time
of first atropine dose.
• Give pralidoxime chloride 2 g (or obidoxime 250 mg)
intravenously over 20–30 min into a second cannula.
• Follow with an infusion of pralidoxime 0·5–1 g/h (or
obidoxime 30 mg/hr) in 0·9% normal saline.
• Insert NG tube ……Start Gastric lavage as advised by
Doctor with activated charcoal dissolving NS.
19. • Feed the fluid and aspirate each 50 ml dose….
Record the amount of fluid…
• 5 min after giving atropine, check pulse, blood
pressure, pupil size, sweat, and chest sounds.
If no improvement has taken place, give
double the original dose of atropine.
20. • Continue to review every 5 min; give doubling
doses of atropine if response is still absent. Once
parameters have begun to improve, cease dose
doubling. Similar or smaller doses can be used.
• Give atropine boluses until the heart rate is more
than 80 beats per minute, the systolic blood
pressure is more than 80 mm Hg, and the chest is
clear (appreciating that atropine will not clear
focal areas of aspiration). Sweating stops in most
cases.
