Transcript 5._Organophosphate_Poisoning

ORGANOPHOSPHATE (OP)
POISINING
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ORGANOPHOSPHATE (OP) POISINING
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Initial treatment goal should consist of optimizing
oxygenation and controlling excessive airway secretions.
Tachycardia is neither a contraindication nor an endpoint for
atropine administration.
 Patients exposed to organophosphate (OP) should be observed
for at least 12 hours in a high acuity setting.


Because of the risk of respiratory depression or recurrent
symptoms after resolution of an acute cholinergic crisis,
hospitalizing all symptomatic patients for at least 48
hours following resolution of symptoms is recommended.
The symptoms of OP poisoning can mimic other toxicities
and disease processes. The clinician must keep in mind
that misdiagnosis is a potential medicolegal pitfall.
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ORGANOPHOSPHATE (OP) POISINING
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Organophosphate (OP) compounds are a diverse
group of chemicals used in both domestic and
industrial settings.
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ANTICHOLINESTERASE
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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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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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ACETYLECHOLIE
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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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PATHOPHYSIOLOGY
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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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PATHOPHYSIOLOGY
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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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PATHOPHYSIOLOGY
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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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SIGNS AND SYMPTOMS OF
ORGANOPHOSPHATE POISONING
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Can be divided into 3 broad categories, including:
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(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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SIGNS AND SYMPTOMS OF
ORGANOPHOSPHATE POISONING
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Muscarinic effects by organ systems include the following:
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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
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SIGNS AND SYMPTOMS OF
ORGANOPHOSPHATE POISONING
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Nicotinic signs and symptoms include muscle
fasciculations, cramping, weakness, and
diaphragmatic failure.
Autonomic nicotinic effects include hypertension,
tachycardia, mydriasis, and pallor.
CNS effects include anxiety, emotional lability,
restlessness, confusion, ataxia, tremors, seizures,
and coma.
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PHYSICAL
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Note that clinical presentation may vary, depending
on the specific agent, exposure route, and amount.
Symptoms are due to both muscarinic and nicotinic
effects.
Vital signs: Depressed respirations, bradycardia, and
hypotension are possible symptoms.
Alternatively, tachypnea, hypertension, and
tachycardia are possible.
Hypoxia should be monitored for with continuous
pulse oximetry.
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TREATMENT
MEDICAL CARE
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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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TREATMENT/ MEDICAL CARE
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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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TREATMENT
MEDICAL CARE
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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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MEDICATION
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The mainstays of medical therapy in
organophosphate (OP) poisoning include
ATROPINE, pralidoxime , and diazepam
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Initial management must focus on adequate use
of atropine. Optimizing oxygenation prior to the
use of atropine is recommended to minimize the
potential for dysrhythmias.
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MEDICATION
Anticholinergic agents
 These agents act as competitive antagonists at
the muscarinic cholinergic receptors in both the
central and the peripheral nervous system.
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These agents do not affect nicotinic effects.
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ATROPINE (ISOPTO, ATROPAIR)
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Adult
1-2 mg IV bolus, repeat q1-5min prn for desire effects
(drying of pulmonary secretions and adequate oxygenation)
Strongly consider doubling each subsequent dose for rapid
control of patients in severe respiratory distress
An atropine drip titrated to above endpoints can be
initiated until patient's condition stabilized
Pediatric
0.05 mg/kg IV, repeat q1-5min prn for control of airway
secretions
Strongly consider doubling each subsequent dose to rapidly
stabilize patients with severe respiratory distress
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COMPLICATIONS
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Complications include respiratory failure,
seizures, aspiration pneumonia, delayed
neuropathy, and death.
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MEDICOLEGAL PITFALLS
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Initial treatment goal should consist of optimizing
oxygenation and controlling excessive airway secretions.

Tachycardia is neither a contraindication nor an endpoint for
atropine administration.

Patients exposed to organophosphate (OP) should be observed
for at least 12 hours in a high acuity setting. Toxicity after
this is unlikely.
Because of the risk of respiratory depression or recurrent
symptoms after resolution of an acute cholinergic crisis,
hospitalizing all symptomatic patients for at least 48 hours
following resolution of symptoms is recommended.
The symptoms of OP poisoning can mimic other toxicities
and disease processes. The clinician must keep in mind
that misdiagnosis is a potential medicolegal pitfall.
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