Organophosphate poisoning occurs when a person is exposed to organophosphate pesticides or nerve agents, which inhibit the enzyme acetylcholinesterase. This causes acetylcholine to accumulate at nerve synapses, resulting in overstimulation of the nervous system. Signs and symptoms include excessive sweating, vomiting, diarrhea, increased urination, blurred vision, slow heart rate, low blood pressure, and muscle weakness or paralysis. Diagnosis involves testing for low acetylcholinesterase levels in red blood cells or plasma. Treatment focuses on atropine administration to block acetylcholine receptors, pralidoxime to reactivate acetylcholinesterase, oxygen supplementation, and supportive care. Complications can include

1. ORGANOPHOSPHA
TE (OP) POISINING
PRESENTED BY
SOPHY TC
SECOND YEAR MSC NURSING
GEVT.COLLEGE OF
NURSING
KOTTAYAM
1

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
3

4. CAUSES
Organophosphate toxicity can result from:
 Household or occupational exposure
Military or terrorist action
Iatrogenic mishap.
Intentional or unintentional contamination
of food sources
4

5. CAUSES
Insecticides – Malathion, parathion, diazinon,
fenthion, dichlorvos, chlorpyrifos, ethion
Nerve gases – Soman, sarin, tabun, VX
Ophthalmic agents – Echothiophate,
isoflurophate
Antihelmintics – Trichlorfon
Herbicides – Tribufos (DEF), merphos
Industrial chemical (plasticizer) – Tricresyl
phosphate
5

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.
6

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.
7

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.
8

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.
9

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.
10

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.
11

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).
12

13. SIGNS AND SYMPTOMS
13

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.
14

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
15

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
17

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
19

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.
20

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
21

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
22

23. ATROPINE
23

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.
24

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.
25

26. BENZODIAZEPINES
26

27. MAGNESIUM SULPHATE
27

28. SODIUM BICARBONATE
28

29. CLONIDINE
29

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.
30

31. FRESH FROZEN PLASMA
 Fresh frozen plasma therapy increases BuChE
levels
 Prevent the development of intermediate
syndrome and related mortality
31

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.
32

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.
33

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.
34

35. 35

36. COMPLICATIONS
 Complications include
 respiratory failure
 Seizures
 aspiration pneumonia
 delayed neuropathy
 death.
36

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.
37

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.
39

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.
40

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.
41

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.
42

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
43

44. 44