ORGANOPHOSPHATE

POISONING

RISK FACTORS
Agro-industry during spraying of
crops eg coffee
Kids
Adolescents depressed.

PATHOPHYSIOLOGY
: Organophosphates form an initially reversible bond with the enzyme
cholinesterase. The organophosphate cholinesterase bond can degrade
spontaneously re-activating the enzyme or can undergo a process called aging.
The process of aging results in irreversible enzyme inactivation.
Cholinesterase is found in 2 forms: an RBC form, which is known as true
cholinesterase, and a plasma form, which is known as pseudocholinesterase.
Cholinesterases rapidly hydrolyze the neurotransmitter acetylcholine into inactive
fragments. Acetylcholine is found in sympathetic and parasympathetic ganglia and
in the terminal nerve endings of postganglionic parasympathetic nerves at the
motor endplates of nerves in the skeletal muscle. Inactivation of the enzyme
allows acetylcholine to accumulate at the synapse, leading to overstimulation and
disruption of nerve impulses. Skeletal-muscle depolarization and fasciculations
occur secondary to nicotinic stimulation at the motor endplate.
Muscarinic effects occur at the postganglionic parasympathetic synapses, causing
smooth-muscle contractions in various organs including the GI tract, bladder, and
secretory glands. Conduction can be delayed in the sinus and atrioventricular (AV)
nodes. Dysrhythmias are frequently reported; these typically include bradycardia,
though tachycardia can also occur.
Acetylcholine receptors are widely dispersed throughout the CNS. The activation of
these receptors causes a wide range of effects, including CNS stimulation,
seizures, confusion, ataxia, coma, and respiratory or cardiovascular depression.
Organophosphates are generally highly lipid soluble and well absorbed from the
skin, mucous membranes, conjunctiva, GI system, and respiratory system.

S/S
Occur withing 30-60 minutes
Muscarinic findings may include the following:
Diaphoresis and diarrhea, urination, miosis, bradycardia, bronchorrhea, bronchospasm, emesis, lacrimation and salivation
(DUMBELS)
Wheezing and/or bronchoconstriction
Pulmonary edema
Increased pulmonary and oropharyngeal secretions
Sweating
Bradycardia
Abdominal cramping and intestinal hypermotility
Miosis

Nicotinic findings may include the following:

Muscle fasciculations (twitching)
Fatigue
Paralysis
Respiratory muscle weakness
Diminished respiratory effort
Tachycardia
Hypertension

CNS findings may include the following:

Anxiety
Restlessness
Confusion
Headache
Slurred speech
Ataxia
Seizures
Coma
Central respiratory paralysis
Altered level of consciousness and/or hypotonia

Chronic Toxicity
Inhibition of neuropathy target
esterases (NTE)
Delayed neuropathy with axonal
demyelination:
Limb weakness
Unsteady gait

1 2 weeks after exposure

No specific treatment

Intermediate Syndrome
1 - 4 days after exposure
Muscle weakness
Cholinesterase inhibition
This syndrome is characterized by
weakness in the motor cranial nerves,
proximal limb muscles, neck flexors, and
respiratory muscles.

TX

A
B- administer oxygen, reduce resp secretions thru suction
C-ensure iv access, fuids
azepenes
Decontamination including gut decontamination- gastric lavage
Administer atropine- loading dose of 0.05mg per kg , then eery 15 minutes
repeat 30mg IV till ful atropinisation is complete. The endpoint for
atropinization is dried pulmonary secretions and adequate oxygenation.
Pralidoxime 2-pam
Nucleophilic agent that reactivates the phosphorylated AChE by binding to
the OP molecule. Used as an antidote to reverse muscle paralysis resulting
from OP AChE pesticide poisoning but is not effective once the OP
compound has bound AChE irreversibly (aged). Current recommendation is
administration within 48 h of OP poisoning. Because it does not significantly
relieve depression of respiratory center or decrease muscarinic effects of
AChE poisoning, administer atropine concomitantly to block these effects of
OP poisoning. Only given twice in 24 hours. IV/IM. Obidoxime is alternative.
years: 25-50 mg/kg IV initially, then 10-20 mg/kg/h IV until muscle strength
returns
D- control convusions - benzodi
Actiated charcoal to absorb any OPP in gut.