Insecticide Poisoning

GROUP 6:
CARBERO, ADRIAN BRIAN
CASAL, ANGELICA MAE
CASCO, JOANNA ROSE
 CASE # 6 : KS, a 20 year old female, was brought to the E.R.
because of seizure and altered sensorium an hour after
ingesting Cythion (Malathion) pesticide when she failed a
subject in college. Patient was noted to be:
 Drooling frothy secretion
 Diaphoretic and non responsive
 Lethargic -bilateral pinpoint pupil
 BP120/80 - diaphoretic with reduced
 HR 60 bpm movement of all extremities
 RR 14cpm - on a ventilator support
 T= 37 C - muscle fasciculation ensued
 GCS =6
 Malathion is an insecticide in the chemical family
known as organophosphates.
 Products containing malathion are used outdoors
to control a wide variety of insects in agricultural
settings and around people's homes.
 Has also been used in public health mosquito
control and fruit fly eradication programs.
 May also be found in some special shampoos for
treating lice.
 you get it on your skin
 Inhalation
 if you use a product and eat, drink, or smoke afterwards
without washing your hands.
 You could also be exposed to residues of malathion if
you ate food that had been treated with this pesticide.

X
 Signs and Symptoms
 Signs and symptoms of Organophosphate poisoning
can be divided into 3 broad categories, including:
 Muscarinic effects,
 Nicotinic effects
 CNS effects

 Muscarinic Effect:
 Cardiovascular : Bradycardia, hypotension
 Respiratory : Rhinorrhea, bronchorrhea,
bronchospasm, cough, severe respiratory distress
 Gastrointestinal : Hypersalivation, nausea and
vomiting, abdominal pain, diarrhea, fecal
incontinence
 Genitourinary : Incontinence
 Ocular : Blurred vision, miosis
 Glands : Increased lacrimation, diaphoresis
 Signs and symptoms include muscle fasciculation,
cramping, weakness, and diaphragmatic failure.
 Autonomic Nicotinic Effects
 Include muscle twitching, cramping and weakness
 CNS Effects
 Include anxiety, emotional lability, restlessness, confusion,
ataxia, tremors, seizures, and coma.


 CBC
 RBC AChE represents the AChE found on RBC
membranes, similar to that found in neuronal tissue.
 lasma cholinesterase is a liver acute-phase protein that
circulates in the blood plasma. It is found in CNS white
matter, the pancreas, and the heart.
 RBC cholinesterase is the more accurate of the 2
measurements, but plasma cholinesterase is easier to
assay and is more readily available.
 CHEST RADIOGRAPH
 ECG

 Ensure that a clear airway exists. Intubate the
patient and aspirate the secretions with a large-
bore suction device if necessary. Administer
oxygen by mechanically assisted pulmonary
ventilation if respiration is depressed. Improve
tissue oxygenation as much as possible before
administering atropine, so as to minimize the risk
of ventricular fibrillation.
 In severe poisonings, it may be necessary to
support pulmonary ventilation mechanically for
several days.
 The initial intravenous dose of atropine in adults should be
determined by the severity of symptoms: An initial Adult
dose of 1.0 to 2.0 mg or pediatric dose of 0.01 mg/kg
(minimum 0.01 mg) should be administered intravenously.
If intravenous access cannot be established, atropine may
also be given intramuscularly, subcutaneously or via
endotracheal tube.
 Doses should be repeated every 15 minutes until excessive
secretions and sweating have been controlled. Once
bronchial secretion has been controlled, atropine
administration should be repeated whenever the secretions
begin to recur
 Pralidoxime should be administered as early in poisoning as possible as its
efficacy may diminish when given more than 24 to 36 hours after exposure.
 Doses are as follows:
Adult: 1.0g;
Pediatric: 25 to 50 mg/kg.
 The drug should be administered intravenously over 30 to 60 minutes.
Treatment should begin to take effect within 40 minutes with a
reduction in symptoms and the amount of atropine necessary to control
bronchial secretion.
 The initial dose can be repeated in 1 hour and then every 8 to 12 hours until
the patient is clinically well and no longer requires atropine.
 If intravenous access cannot be established, Phralidoxime may also be given
intramuscularly.
 Early administration of diazepam in addition to the combined atropine and
 pralidoxime treatment may help prevent the onset of seizures and potential
brain and cardiac morphologic damage.
 PULMONARY VENTILATION
Particularly in poisonings by large ingested doses
of organophosphate, monitor pulmonary ventilation
carefully, even after recovery from muscarinic
symptomatology, to forestall respiratory failure. In some
cases, respiratory failure has developed several days
following organophosphate ingestion, and has persisted
for days to weeks.
 CARDIOPULMONARY MONITORING
In severely poisoned patients, monitor cardiac
status by continuous ECG recording. Some
organophosphates have significant cardiac toxicity
 SEIZURE CONTROL
Ensure that causes unrelated to pesticide toxicity
are not responsible: head trauma, cerebral anoxia, or
mixed poisoning. The benzodiazepines (diazepam or
lorazepam) are the agents of choice as initial therapy


MEDICATION Kinetics Dynamics Indications
Adverse Effects and
possible food/drug
Interactions
1. Atropine sulfate















Absorption: Body
Tissues and Fluids
Distribution:
Effector Cells
Metabolism:
hydrolysis and
glucuroconjugation
Elimination:
Kidneys (Urine)
Peak: 2-4 minutes
Duration: 4 hours
1.Decreases
action of the
parasympathetic
nervous system
increasing
conduction velocity
(dromotropy) and
heart rate
(chronotropy),
enhances
conduction through
the AV junction
2.Decrease bodily
secretions
(anticholinergic
effect)


-Symptomatic
bradycardia,
bradyarrythmias
-Asystole
-Organophospate
poisoning
-Pre-intubation in
children under 5
years of age
requiring airway
manipulation to
prevent vagotonic
bradycardia
response
-Pre
succinylcholine
administration in
children under 10
and adults getting
a second dose
Palpitations
Headache
Blurred vision
Dry mouth
Dilated pupils
Drowsiness
Anxiety

MEDICATION Kinetics Dynamics Indications
Adverse Effects and
possible food/drug
Interactions
2.Pralidoxime Absorption:
Distribution:
Extracellular Fluids
Metabolism: Liver
Elimination:
Kidneys (Urine)
Half-Life: 0.8–
2.7 h.

It acts as a
competitive
antagonist of
acetylcholine at
muscarinic
receptors, blocking
stimulation of
muscles and
glands by
parasympathetic
and cholinergic
sympathetic
nerves
used as a smooth
muscle relaxant,
as a preanesthetic
to reduce
secretions, and as
an antidote to
organophosphate
poisoning
Has been used as
a spasmolytic in
many cases of gut
hypermotility, e.g.
equine spasmodic
colic.
A An adjunct to
atropine in the
treatment of
poisoning by nerve
agents having
anticholinesterase
activity.
 blurred vision
 diplopia and
impaired
accommodatio
n
 dizziness
 headache
 drowsiness
 nausea
 tachycardia
 increased
systolic and
diastolic blood
pressure
 hyperventilatio
n
 muscular
weakness
MEDICATION Kinetics Dynamics Indications
Adverse Effects and
possible food/drug
Interactions
3. Diazepam Absorption: Due to
its high lipid solubility
diazepam passes
rapidly into the brain,
and other well
perfused organs, and
is afterwards
redistributed to
muscle and adipose
tissue.
Distribution: 95% to
98% protein bound.
Highly lipophilic.
Crosses the placenta
and is excreted in
breast milk.
Metabolism: Liver
Elimination:
Half-Life: 20 to 80 h.

Reduction in cerebral
oxygen metabolism
and blood flow.
Protect against
cerebral hypoxia and
are very effective
anticonvulsant agents
against local
anesthetic-caused
seizures.

Management of
anxiety disorders
R Relief of acute
alcohol withdrawal
symptoms
Relief of preoperative
apprehension and
anxiety and reduction
of memory recall
Tsreatment of muscle
spasms, convulsive
disorders (used
adjunctively), and
status epilepticus.

Cardiovascular
CV collapse;
bradycardia;
tachycardia;
hypertension;
palpitations; edema;
hypotension; phlebitis or
thrombosis at IV sites.
CNS
Drowsiness; confusion;
ataxia; dizziness;
lethargy; fatigue;
apathy; memory
impairment;
disorientation;
anterograde amnesia;
restlessness; headache;
slurred speech; loss of
voice; stupor; coma;
euphoria; irritability;
vivid dreams;
psychomotor
retardation; paradoxical
reactions (eg, anger,
hostility, mania,
insomnia, muscle
spasms); depression;
dysarthria; hypoactivity;
tremor; vertigo.
MEDICATION Kinetics Dynamics Indications
Adverse Effects and
possible food/drug
Interactions
Dermatologic
Urticaria; skin rash.
EENT
Visual or auditory
disturbances;
depressed hearing;
blurred vision; diplopia;
nystagmus.
GI
Constipation; diarrhea;
dry mouth; coated
tongue; nausea;
anorexia; vomiting.
Genitourinary
Incontinence; changes
in libido; urinary
retention.
MEDICATION Kinetics Dynamics Indications
Adverse Effects and
possible food/drug
Interactions
Hematologic
Blood dyscrasias
including
agranulocytosis,
anemia,
thrombocytopenia,
leukopenia,
neutropenia.
Hepatic
Hepatic dysfunction
including hepatitis
and jaundice;
abnormal LFTs.



 Continuous cardiac monitoring
 Arrange a follow-up care before discharge so that
patient may be monitored for possible long-term
sequelae.
 Obtain psychiatric evaluation if warranted before
discharge.