PESTICIDE POISONING.pdf

organophosphate

1. PESTICIDEPESTICIDE
POISONINGPOISONING
July 11, 2022
BY AMELIA AKMAR
SUPERVISED BY DR HUSNA

2. DEFINITONDEFINITON
•Type of pesticide according to;
- target organism; insecticides,
herbicides, rodenticide,
disinfectant and fungicides
- chemical structure; organic,
inorganic, synthetic and
biological
Any substance or
mixture of
substances
intended for
preventing,
destroying,
repelling, or
mitigating any
insects, rodents,
nematodes, fungi,
or weeds, or any
other forms of
life declared to
be pests
”Federal Insecticide, Fungicide, and
Rodenticide Act (US EPA)

3. EPIDEMIOLOGYEPIDEMIOLOGY
•Within the study period, a total of 11 087 pesticide poisoning cases were recorded.
Sixty per cent of these cases were intentional in nature and most were found among
male individuals (57%) of the Indian race (36.4%) aged between 20 and 29 years
(25.5%), which occurred at home (90%) through the route of ingestion (94%). The
highest number of poisoning was due to herbicides (44%) followed by agricultural
insecticides (34%), rodenticides (9.9%), household insecticides (9.5%) and fungicides
(0.5%). In addition, 93.6% of intentional pesticide poisoning cases were caused by
suicide attempts. The results of this study show that there was an increasing trend in
pesticide poisoning incidents over the 10-year duration. This indicates that pesticide
poisoning is a prevalent public health problem in Malaysia, resulting in an average
incidence rate of 3.8 per 100 000 population.
Kamaruzaman NA, Leong YH, Jaafar MH, Mohamed Khan HR, Abdul Rani NA, Razali MF, Abdul Majid MI. Epidemiology
and risk factors of pesticide poisoning in Malaysia: a retrospective analysis by the National Poison Centre (NPC) from
2006 to 2015. BMJ Open. 2020 Jun 1;10(6):e036048. doi: 10.1136/bmjopen-2019-036048. PMID: 32487578; PMCID:
PMC7265005.

4. TYPE OF ACTIVE INGREDIENT
•Organochlorines (OC)
•Organophosphate (OP)
•Carbamate
•Synthetic pyrethroid (SP)
•Sulphonylurea
•Phenoxyacetic acid
•Triazine
•Imidazolinone
•Strobilurin
•Phenylpyrazole
•Neonicotinoid
•Glycine derivative

5. swallow
do not make him vomit
if the victim starts to vomit
spontaneously, turn him to lie
on his left side

move him to fresh air immediately and open
all the doors and windows to improve
ventilation. Rescuers should take care not
to breathe in the fumes themselves, and
should leave the area as soon as possible

remove all contaminated clothing/ contact
lenses. rinse the affected eye gently under
running water for at least 15 minutes,
careful not to run-off water from entering
the unaffected eye. Advise the victim not
to rub the eye.


inhale
skin/ eye
What should be done when poisoning is
suspected in the community?

6. GENERAL MANAGEMENTGENERAL MANAGEMENT
• Resuscitation and Stabilization
• Toxic Diagnosis
• Therapeutic interventions
– Decontamination
– Enhanced elimination of absorbed toxins
– Antidotes
• Supportive care
• Psychosocial interventions

7. AIRWAY
BREATHING
CIRCULATION
•Initiate airway protection by
assessing patient’s speech
•Look for airway obstruction
and evaluate gag/cough
reflex
•Airway interventions
•Opening the airway
•Examine the oropharynx for
any foreign body
•Suctioning to clear
secretions
•Airway devices: OPA, NPA
•Endotracheal intubation
•Determine if
respirations are
adequate
•Check oxygen
saturation (SPO2)
•Give supplemental
oxygen
Gross decontamination should be done prior to patient entry into the ED.
Care providers need to protect themselves with properly PPE
Assess for blood volume
status (Blood pressure
and pulse)
IV access
Treat hypotension with
fluids before
vasopressors if still
hypotensive
Place patient on
cardiac monitor and
obtain ECG
– Treat for arrhythmias

8. DISABILITY
•Perform neurologic and mental status examination by assessing
•Orientation (GCS)
•Pupil size and reactivity
•Obtain capillary blood glucose and temperature
Altered mental status and coma are common presentations of many
intoxicants
•Supplemental oxygen
•Naloxone (0.2-2mg IV/IM/IO)
•Dextrose
•Thiamine (10-100mg IV/IO)
Convulsions: Check for and correct hypoxia/hypoglycaemia. Give lorazepam
or diazepam if fits repeated and prolonged

9. Toxicological diagnosisToxicological diagnosis

What was ingested? Name of agent and type of formulation e.g. tablets or liquid, extended release, ingredients on
combination tablets, concentration of active compounds etc.
What else was ingested? Any other co-ingestant especially medications from other physicians, alcohol, traditional
medications and health supplements.
How much exposure? To be estimated in mg / kg body weight. For cutaneous exposure: body surface area exposed.
When did poisoning occur? Exact timing of ingestion or timings of ingestion episodes.
What were the symptoms post exposure?
How was patient exposed to toxin? Pertaining to route of exposure either oral, inhalation, cutaneous, or injection. For
cutaneous and inhalational exposure: duration of exposure before decontamination or removal from toxic
environment respectively.
Why exposed? The reason for toxic exposure accidental versus intentional. Occupational exposures require
notification to the Ministry of Manpower for occupational safety measures to be looked into while deliberate self
harm requires referral for pastoral care and counselling.
AMPLE history
Fact finding mission – From patient, paramedics, family, friends, GP, circumstantial evidence such as empty packets,
vomitus with pill fragments.
• Who was exposed? Demographic information including age, sex, weight.

10. Sympathomimetic
Toxidrome

- Anxiety / Delirium
- Hypertension
- Tachycardia
- Hyperpyrexia
- Mydriasis
- Diaphoresis

- Cocaine, Amphetamines, phencyclidine
(PCP), Lysergic acid (LSD)
- Withdrawal from narcotics,
benzodiazepine, alcohol, long term beta-
blocker therapy

Cholinergic
Toxidrome

- Salivation
- Lacrimation
- Urinary incontinence
- Defaecation
- Gastric cramping,
hypermotility
- Emesis


- Organophosphate
compounds
- Carbamate insecticides

11. investigations
• Random bedside glucose
• Serum electrolytes and renal function.
• Liver function test.
• Creatine kinase.
• Full Blood Count.
• Clotting screen: PT/PTT/INR.
• Arterial blood gas.
• Specific toxin level e.g. serum paracetamol, salicylate,
phenobarbital, theophylline, digoxin, iron, and lithium

12. Inhalational
exposure

Dermal exposure

eye exposure

evacuation from toxic
environment and provision of
supplemental oxygen removal of contaminated
clothing and shower or
irrigation of affected site
(dust before shower for dry
chemical)
removal of chemicals by
copious irrigation of the
affected eye by up to 1 litre
of saline or symptomatic
improvement occurs

decontamination
oral exposure

inducing emesis, performing gastric lavage,
activated charcoal, whole bowel irrigation,
cathartics

13. Induced emesis

•Never use emetics.
Ipecacuanha syrup was
once used frequently but it
may cause prolonged
vomiting and aspiration
pneumonia

•Given within 1H
•Messy, unpleasant to take and often
cause vomiting, aspiration into lungs can
cause pneumonitis
•Adult: 50g, children: 1g/kg with max 50g
through PO or via orogastrictube

•To empty the bowel rapidly of
solid contents by giving fluid
down a NG tube (bowel
preparation solution e.g. CoLyte
at 2L/H until effluent is clear.
Stop after 4L)

Activated
charcoal

Whole bowel
irrigation

14. Only consider if the patient has taken life threatening amount of poison within
previous 1H or is unconscious
Only consider if there is strong cough reflex or airway is protected by ETT
Do not use in corrosive poisoning (risk of perforation) or with petrol/paraffin
compounds (risk of pneumonitis)
Lubricate large disposable stomach tube (36/40 Fr gauge), pass it through mouth
into stomach. Confirm by aspirate gastric contents/blowing air down the tube while
auscultate stomach
Perform lavage by pouring 300mL boluses of warm saline -> siphoning it back ->
massage over stomach to help dislodge tablet debris
While withdrawing the tube, occlude it between the fingers to prevent aspiration of
fluid from tube
Gastric lavage

15. Organophosphate poisoningOrganophosphate poisoningOrganophosphate poisoning
accounts for at least 50% of
pesticides worldwide; in the UK
mainly crop spraying and sheep
dip

16. Can be absorbed through the skin, lung and GI tract
Inhibits acetylcholinesterase, which results in excess acetylcholine
accumulating at the myoneural junctions and synapses.
Excess acetylcholine initially excites then paralyzes neurotransmission at
the motor end plate and stimulates nicotinic and muscarinic sites
The term aging describes the permanent, irreversible binding of the
organophosphorus compound to the cholinesterase. The time to aging is
highly variable among different agents and can range from minutes to a
day or more. Once aging occurs, the enzymatic activity of
cholinesterase is permanently destroyed, and new enzyme must be
resynthesized over a period of weeks before clinical symptoms resolve
and normal enzymatic function returns. Antidotes are more effective if
given before aging occurs.

17. ACUTE

18. Routine laboratory test abnormalities are
nondiagnostc include evidence of
pancreatitis, hypo- or hyperglycemia,
leukocytosis, and abnormal liver function.
In severe cases, a chest radiograph may
show pulmonary edema.
Common abnormalities include torsades de
pointes, ventricular tachycardia, and
ventricular fibrillation.
ECG changes include ST-segment changes,
peaked T waves, atrioventricular block, and
prolongation of the QT interval.
Electromyography may identify and
quantify acetylcholinesterase inhibition at
neuromuscular junctions

investigations
All staff members required to wear protective
equipment
Start detoxification by removing patient’s clothes
and washing the skin thoroughly
Maintain airway patency. Perform intubation if
patient obtunded, apneic and has no gag reflex
Frequent suctioning may be required due to
bronchorrhea
Administer supplemental oxygen
Monitoring: ECG, vital signs
Establish IV access
Administer IV fluids
supportive mx

19. •Activated charcoal via gastric lavage tube
•Dosage: 1g/kg body weight
•Atropine
•Muscarinic receptor antagonist
•Major use in the reduction of bronchorrhea/bronchospasm
•Adults: 2mg IV every 10-15mins as needed, the dosage may be doubled every 10mins until sign of
atropinisation are obvious (flushed and dry skin, tachycardia, mydriasis and dry mouth)
•Children: 0.05mg/kg every 15mins as needed
Pralidoxime
Works by reactivating AchE that has been bound to OP molecule. Effects are mainly at the skeletal –
neuromuscular junctions (nicotinic effects)
Effects will be apparent within 30mins which include disappearance of convulsion and fasciculation,
improvement in muscle power and recovery of consciousness
Adults: 1gm IV over 15-30mins. Can be repeated in 1-2H as needed
Children: 25-50mg/kg IV over 15-30mins. Can be repeated in 1-2H as needed
Diazepam
Use to reduce anxiety, restlessness and to control convulsions
Dosage: 5-10mg IV

20. possible delayed effects
The intermediate syndrome (IMS)
Clinical syndrome that starts 24-96H after onset of
OP poisoning
Characterized by muscle weakness, neck flexors,
proximal extremity musculature and respiratory
musculature
Unresponsive to atropine and pralidoxime
Management involves supportive therapy
The prognosis is good with majority recovering
between 14-28 days

21. possible delayed effects
Organophosphate induced delayed neuropathy
•Begins 1-3 weeks after exposure
•Leg cramping, symmetric lower extremity
weakness, stocking paraesthesia
•Consequences include wasting of peroneal
muscles, foot drop and wasting muscles of hand
•Management include supportive therapy
•Prognosis is variable ranging from irreversible to
slowly reversible defects over 6-15 months

22. CHRONIC TOXICITY
Seen primarily in agricultural workers with daily
exposure, manifests as symmetrical sensorimotor
axonopathy. This mixed sensorimotor syndrome may
begin with leg cramps and progress to weakness
and paralysis, mimicking features of the Guillain-
Barré syndrome.

23. It was reported during the 2013
Syrian conflict, Soman ages
within minutes; thus, there is
little time to administer
antidotes. Chemical warfare nerve agents, such as
soman, sarin, tabun, and VX, are
organophosphate compounds that
inactivate acetylcholinesterases. They
are rapid acting and extremely potent;
death can occur within minutes of
inhalation or dermal exposure,

24. carbamatecarbamate
poisoningpoisoning
The carbamate insecticides—aldicarb, carbofuran, carbaryl,
ethi- enocarb, fenobucarb, oxamyl, methomyl, pirimicarb,
propoxur, and trimethacarb—are cholinesterase inhibitors that
are structurally related to the organophosphate compounds.

25. dermal
inhalation
GI exposure
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Carbamates transiently and reversibly bind to and
inhibit the cholinesterase enzyme. Regeneration
of enzyme activity by dissociation of the
carbamate–cholinesterase bond occurs within
minutes to a few hours and involves rapid,
spontaneous hydrolysis of the carbamate–
cholinesterase bond. Therefore, aging does not
occur, and as a major difference from
organophosphate poisoning, in carbamate
poisoning, restoration of normal function does not
require generation of new enzyme.
mechanism of action

26. In adults, symptoms similar to the cholinergic
syndrome observed with organophosphate
agents with shorter duration
- do not effectively penetrate the CNS in
adults, less central toxicity is seen, and
seizures do not occur.
In children, presentation differs, with a
predominance of CNS depression and
nicotinic effects.
Carbamates can also produce the
intermediate syndrome.

27. pralidoxime - controversial
carbamate-binding half-life to cholinesterase ~30
minutes,
irreversible binding does not occur; little need for
pralidoxime.
Human case reports and some (but not all) animal
studies suggest that pralidoxime may potentiate
the toxicity of carbamates such as carbaryl
avoid in known single-agent carbaryl poisonings
should be considered in mixed poisonings with an
organophosphorus compound and a carbamate or
if the type of insecticide is unknown.
Atropine
administered for muscarinic symptoms
necessary while waiting for the
carbamylated acetylcholinesterase
complex to dissociate spontaneously
and recover function (usually within 24
hours).
Therapy is usually not needed for more
than 6 to 12 hours.
Initial treatment same as for
organophosphorus compounds.

28. PROGNOSIS
Most patients recover completely
within 24 hours.
PT with depressed levels of
consciousness have a significant
mortality.
Methomyl poisoning is associated
with a high risk of cardiac arrest at
presentation as well as subsequent
death after resuscitation.
Mild poisonings
observation suffices &
discharge with follow-up.
Moderate poisonings
necessitate 24 hours of
observation that includes
evaluation for possible
concomitant exposure to
(and toxicity from) inactive
ingredients or vehicles
such as hydrocarbons.

29. Toxic chemical that is widely used as a herbicide (plant killer)
primarily for weed and grass control mainly palm oil, paddy &
rubber trees

paraquatparaquat
poisoningpoisoning
method of exposure:
•Intestinal ingestion
•Long term skin exposure
•Inhalation

31. •After absorption paraquat is concentrated inside many cells where it
undergoes redox cycling (a process involving repetitive enzyme-mediated
cycling between paraquat and paraquat radicals) -> produces superoxide
radical, a highly reactive oxygen species -> direct cellular damage
•Lungs are the main target organs -> 60–80%, mainly due to acute lung injury
and progressive pulmonary fibrosis
•Paraquat also causes renal and liver injury
•Ingestion of large amounts of liquid concentrate results in fulminant organ
failure and death (hours to days)
•Ingestion of smaller quantities usually leads to toxicity in the two key target
organs (kidneys and lungs) developing over the next 2–6 days (still >50%
mortality)

•Gastric lavage/aspirate
and urine for paraquat
•FBC, RP, LFT, ABG
•CXR

IX
NO ANTIDOTE!

32. Contaminated clothing should be removed immediately. Contaminated skin should be washed
with soap and water
Insert nasogastric tube
Stomach washout as soon as possible
Activated charcoal 50g STAT and 25g 4Hly for several days
IV fluids 4-5L per day (NS and D5%) for the first 24H, then 3L per day orally or IV for several
days to maintain good hydration
Potassium supplement
Furosemide 40mg BD IV or oral for several days
Oxygen to be avoided unless PO2 falls <60mmHg
** In selected cases with moderate to severe poisoning there may be a role of prophylactic
immunosuppressive agent eg methylprednisolone (15mg/kg) +/- cyclophosphamide (15mg/kg)
followed by dexamethasone at high dose
managementmanagement

33. ReferenceReference
July 11, 2022 end
Tintinalli’s emergency medicine manual 7th edition
Management of Poisoning, Singapore MOH
Clinical Practice Guidelines Dec/2011,
https://www.moh.gov.sg/docs/librariesprovider4/
guidelines/management-of-poisoning---
booklet.pdf
1.
2.

34. ThankThank
You!You!