2. DEFINITION
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
acetylcholinesterase at nerve
synapses 2
3. INCIDENCE
91.86% of cases were suicidal and remaining
cases were accidental
According to WHO report 2002, about 849,000
people die globally from self-harm yearly.
In India pesticide poisoning is a major problem
in the agricultural group.
In a study conducted in Christian Medical
College and Hospital, Vellore, OP poisoning
accounts for 12% of ICU admissions and 29% of
total poisoning admissions
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4. CAUSES
Organophosphate toxicity can result from:
Household or occupational exposure
Military or terrorist action
Iatrogenic mishap.
Intentional or unintentional contamination
of food sources
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6. PATHOPHYSIOLOGY
anticholinesterase Any substance that inhibits the
enzyme cholinesterase, which is responsible for the
breakdown of the neurotransmitter acetylcholine at
nerve synapses. Anticholinesterases, which include
certain drugs, nerve gases, and insecticides, cause a
build-up of acetylcholine within the synapses, leading
to disruption of nerve and muscle function. In
vertebrates, these agents often cause death by
paralysing the respiratory muscles.
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7. PATHOPHYSIOLOGY
Acetylcholine (ACh) is one of the main
neurotransmitters of the vertebrate nervous system. It
is released at certain (cholinergic) nerve endings and
may be excitatory or inhibitory; it initiates muscular
contraction at neuromuscular junctions. Acetylcholine
receptors (cholinoceptors) fall into two main classes:
muscarinic and nicotinic receptors. Once
acetylcholine has been released it has only a transitory
effect because it is rapidly broken down by the
enzyme cholinesterase.
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8. cholinesterase (acetylcholinesterase) An enzyme
that hydrolyses the neurotransmitter acetylcholine to
choline and acetate. Cholinesterase is secreted by
nerve cells at synapses and by muscle cells at
neuromuscular junctions. Organophosphorus
insecticides (pesticide) act as anticholinesterases by
inhibiting the action of cholinesterase.
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9. PATHOPHYSIOLOGY
The primary mechanism of action of organophosphate
pesticides is inhibition of acetylcholinesterase
(AChE).
AChE is an enzyme that degrades the
neurotransmitter acetylcholine (ACh) into choline and
acetic acid.
ACh is found in the central and peripheral nervous
system, neuromuscular junctions, and red blood cells
(RBCs).
Organophosphates inactivate AChE by
phosphorelation.
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10. PATHOPHYSIOLOGY
Once AChE has been inactivated, ACh
accumulates throughout the nervous system,
resulting in overstimulation of muscarinic and
nicotinic receptors.
Clinical effects are manifested via activation of
the autonomic and central nervous systems and
at nicotinic receptors on skeletal muscle.
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11. PATHOPHYSIOLOGY
Organophosphates can be absorbed cutaneously,
ingested, inhaled, or injected.
Although most patients rapidly become
symptomatic, the onset and severity of symptoms
depend on the specific compound, amount, route
of exposure, and rate of metabolic degradation.
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12. SIGNS AND SYMPTOMS OF
ORGANOPHOSPHATE POISONING
Can be divided into 3 broad categories, including:
(1) muscarinic effects,
(2) nicotinic effects, and
(3) CNS effects.
Mnemonic devices used to remember the muscarinic effects of
organophosphates are SLUDGE (salivation, lacrimation, urination,
diarrhea, GI upset, emesis) and DUMBELS (diaphoresis and
diarrhea; urination; miosis; bradycardia, bronchospasm, emesis;
excess lacrimation; and salivation).
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14. SIGNS AND SYMPTOMS
(i) Type-I paralysis or Acute paralysis
Develops within 24-48 hours
Features include muscle fasciculations, muscle
cramps, muscle twitching and muscle weakness.
Muscle paralysis involves the respiratory
muscles leading to respiratory failure and
requires ventilation.
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15. SIGNS AND SYMPTOMS
(ii) Type-II paralysis or Intermediate
syndrome
Develops after the acute cholinergic crisis, 24-96hrs
Presence of marked weakness of neck flexon with the
inability to lift the head.
The common cranial nerves involved are those
supplying the extraocular
Most patients survive with ventilator support
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16. SIGNS AND SYMPTOMS
(iii) Type-III paralysis or OP-Induced
delayed polyneuropathy
OP-induced delayed polyneuropathy (OPIDP) is a
sensory-motor distal axonopathy
After the ingestion of large doses of certain OP
insecticides or after chronic exposure.
After 2-3 weeks of acute poisoning episode
Distal muscle weakness with sparing of neck
muscles, cranial nerves, and proximal muscles
Recovery may extend up to one year and high-
dose methyl prednisolone is beneficial 16
17. DIAGNOSIS
The portable Test-mate ChE field test measures RBC
AChE and PChE within 4 minutes
RBC AChE represents the AChE found on RBC
membranes
Plasma cholinesterase is a liver acute-phase protein that
circulates in the blood plasma
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18. DIAGNOSIS
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 18
19. DIAGNOSIS
Chest radiograph may reveal pulmonary edema
ECG findings include
Prolonged QT interval
Elevated ST segments
Inverted T waves
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20. ORGANOPHOSPHATE (OP) POISINING
MANAGEMENT
Initial treatment goal
Optimizing oxygenation
Controlling excessive airway secretions..
Patients exposed to organophosphate (OP) should be
observed for at least 12 hours in a high acuity setting.
Hhospitalizing all symptomatic patients for at least 48
hours following resolution of symptoms is
recommended.
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21. DIFFERENT MANAGEMENT
STRATEGIES USED IN THE OP
POISONING
Gastrointestinal decontamination
Role of different Antidotes in OP poisoning
Eg:Atropine, oximes and glycopyrrolate
Benzodiazepines
Magnesium Sulphate
Sodium bicarbonate
Clonidine
Fresh frozen plasma
pralidoxime
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22. GASTROINTESTINAL
DECONTAMINATION
Gastric lavage is the first intervention
patient arrives within1 hour of ingesting
patients who substantial amount of toxic pesticide
who are intubated, or conscious and willing to
cooperate
Activated charcoal
patient presents to the hospital within 1-2 hours
of ingestion or in cases of severe toxicity
1gram/kg of activated charcoal can be given orally
via nasogastric tube at the end of the lavage
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24. ATROPINE
1. An initial loading dose of 1.8–3.6 mg rapidly IV into a
fast-flowing IV drip.
2. Three to five minutes after giving atropine, check the
markers of atropinisation .A uniform improvement in most
of the cholinergic features is required clear chest on
auscultation, increase in heart rate and blood pressure.
3. If, after 3–5 minutes, a consistent improvement across
the five parameters has not occurred, then double the dose,
and continue to double each time till the patient is
completely atropinised.
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25. ATROPINE
Maintenance dose of atropine:
After achieving complete atropinisation, an atropine infusion
should be started.
The usual dose requirement is 10 – 20% of the dose of
atropine required to load the patient every hour.
In most cases, the patient will not require more than 3-
5mg/hour of atropine.
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30. PRALIDOXIME
Inj. Pralidoxime(PAM): Current WHO
guidelines recommend 30mg/kg loading
dose of pralidoxime over 10-20 min,
followed by continuous infusion of 8-10
mg /kg per hour until clinical recovery.
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31. FRESH FROZEN PLASMA
Fresh frozen plasma therapy increases BuChE
levels
Prevent the development of intermediate
syndrome and related mortality
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32. TREATMENT
MEDICAL CARE
Airway control and adequate oxygenation are
paramount in organophosphate (OP) poisonings.
Intubation may be necessary in cases of respiratory
distress due to laryngospasm, bronchospasm,
bronchorrhea, or seizures.
Immediate aggressive use of atropine may eliminate
the need for intubation.
Succinylcholine should be avoided because it is
degraded by acetylcholinesterase (AChE) and may
result in prolonged paralysis.
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33. TREATMENT/
MEDICAL CARE
Continuous cardiac monitoring and pulse oximetry should be
established; an ECG should be performed.
The use of intravenous magnesium sulfate has been reported as
beneficial for organophosphate toxicity.
The mechanism of action may involve acetylcholine antagonism or
ventricular membrane stabilization.
Remove all clothing and gently cleanse patients suspected of
organophosphate exposure with soap and water because
organophosphates are hydrolyzed readily in aqueous solutions with
a high pH.
Consider clothing as hazardous waste and discard accordingly.
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34. TREATMENT
MEDICAL CARE
Health care providers must avoid contaminating
themselves while handling patients.
Use personal protective equipment, such as neoprene
gloves and gowns, when decontaminating patients
because hydrocarbons can penetrate nonpolar
substances such as latex and vinyl.
Use charcoal cartridge masks for respiratory
protection when decontaminating patients who are
significantly contaminated.
Irrigate the eyes of patients who have had ocular
exposure using isotonic sodium chloride solution or
lactated Ringer's solution.
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37. COUNSELLING
: Counselling to the poisoned patients will reduce
the chances of a repeat attempt at poisoning.
It also enables the health care personnel to
improve the quality of treatment, minimize the
cost of therapy and the period of hospitalization.
Family counselling is mandated; this helps the
family members to cope with the situation and
accept the patient as he is.
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38. NURSING MANAGEMENT
Ineffective airway clearance related to presence of copious
secretions secondary to OP compound effects.
Endotracheal tube was secured
Frequent suctioning was done;
Humidified oxygen, and salbutamol alternating with
nebulization.
Atropine infusion was initiated at 10 mg /hr and tapered
to 2mg on the fourth day and then discontinued.
Maintained at 45° head end elevation and was positioned
laterally.
Chest physiotherapy was given to mobilize secretions.38
39. NURSING MANAGEMENT
Risk for injury related to seizure activity.
Periodic and regular assessment of GCS score
Administration of antiepileptic drugs were done.
Additional precautions were initiated with provision of
side railed cot, and positioning of patient (left lateral with
head elevation at 45 degree.
Patient should be closely observe.
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40. NURSING MANAGEMENT
Decreased cardiac output related to cholinergic
effects of OP poisoning.
Close monitoring of hemodynamic status (blood
pressure, MAP and heart rate) . MAP was
maintained between 70-80 mmHg. Atropine was
administered to maintain the target heart rate
[ Day 1: 110/min; Day 2: 100/min; Day 3: 90/min].
Adequate intravenous fluids were administered
to prevent dehydration due to salivation &
diarrhea.
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41. NURSING MANAGEMENT
Risk of fluid volume deficit related to effects of OP
poisoning.
Intravenous fluids
Urine output monitoring
In addition to intravenous fluids, nasogastric feeds
initiate .
A cumulative fluid balance sheet should maintaine.
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42. NURSING MANAGEMENT
Ineffective coping of family: related to guilt,
negative feelings and financial crises.
Open communication encourage among the family
members
Family counselling
Arrangements made for their spiritual comfort.
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43. NURSING MANAGEMENT
Risk of complications such as pressure sores, and
ventilator associated pneumonia (VAP) related to
poisoning effects and prolonged mechanical ventilation.
Positioning
Standard precautions were follow
Assessed for signs of infection, breathing pattern &
characteristics of secretions
Tubing of the ventilator change frequently as possible
Suctioning done under aseptic techniques. Adequate
chest physiotherapy and nebulisations
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