ORGANOPHOSPHORUS POISONING

INTRODUCTION:
Organophosphates are one of the most common causes of poisoning worldwide,
and are frequently intentionally used in suicides.
Organophosphorus compounds or organophosphates are commonly used in the
industrial, agricultural and home settings. Some organophosphorus compounds are
used as pesticides in agriculture. These are highly toxic and include tetraethyl
pyrophosphate and parathione. Other organophosphates such as coumaphos,
chlorpyrifos and trichlorfon are used as animal insecticides and have intermediate
toxicity. Low toxicity compounds are malathione, diazinon and dichlorovos. These
are used as household insecticides. Nerve gases (e.g. Sarin, Soman, Tabun and VX)
are used as chemical warfare and in terrorist attacks, which disrupt the mechanism
by which nerves transfer messages to organs.
CAUSES:
Organophosphorus exposure occurs through inhalation, ingestion and dermal
contact.
Organophosphorus poisoning may be intentional or unintentional.
Organophosphorus compounds are easily accessible and are often used to
commit suicides.
Accidental poisoning may also occur especially when they are kept within
the reach of children.
Farmers could get exposed while spraying crops if they are not well
protected with masks, gloves and other protective clothing.

PATHOPHYSIOLOGY:

Organophosphorus compounds are powerful inhibitors of carboxylic esterase

enzymes including acetylcholine esterase and pseudocholine esterase

They bind firmly to esterase enzyme, inactivating it by phosphorylation at

myoneural junctions and synapses of ganglion

Acetylcholine (Ach) accumulates at parasympathetic, sympathetic and somatic

sites and transfer of nerve impulses across synapses and nerve muscle junction is
prevented.

Produces hyper excitation of voluntary and involuntary muscles (i.e. both

sympathetic and parasympathetic)

Mild poisoning: Cholinesterase activity is 20-50% of normal.

Moderate poisoning: Cholinesterase activity is 10-20% of
normal.
Severe poisoning: Cholinesterase activity is <10% of normal.
CLINICAL FEATURES:
Organophosphosrus compounds produce muscarinic, nicotinic and CNS
effects:
1) Muscarinic manifestations:
Mnemonic devicesa) SLUDGE (Salivation, lacrimation, urination, diarrhea, GI upset,
emesis)

b) DUMBELS (Diaphoresis and diarrhea; urination; miosis;

bradycardia, bronchospasm and bronchorrhea; emesis;
lacrimation; salivation)
2) Nicotinic manifestations:
a) Striated muscle: muscle weakness, muscle fasciculations,
cramps, areflexia.
b) Sympathetic ganglia: hypertension, tachycardia, pallor,
mydriasis.
3) CNS manifestations:
a) Restlessness, irritability, headache, emotional lability, slurred
speech, ataxia
b) Fine fibrillary tremors of hands, eyelids, face or tongue
c) Drowsiness, mental confusion progressing to stupor
d) Coma
e) Death due to depression of respiratory and circulatory centers.
4) Intermediate syndrome:
a) Syndrome of muscular paralysis occurring 24-96 hours after
ingestion of an organophosphate and following treatment of
acute cholinergic syndrome.
b) Muscle weakness affects predominantly neck flexors, proximal
limb muscles, those supplied by cranial nerves and respiratory
muscles.
5) Chromolachryorrhoea: Shedding of red tears d/t accumulation of
porphyrin in the lacrimal gland.

DIAGNOSIS:

 Diagnosis of organophosphorus poisoning can be confirmed by

demonstrating a reduction of cholinesterase activity in plasma or in
red blood cells, to less than 50% of normal.
A chest radiograph may reveal pulmonary edema.
ECG findings include prolonged QT interval, elevated ST
segments, and inverted T waves. Although sinus tachycardia is the
most common finding in the poisoned patient, sinus bradycardia
with PR prolongation can develop with increasing toxicity due to
excessive parasympathetic activation.
MANAGEMENT:
1) Decontamination:
Remove the patient from source of exposure.
Remove all clothes.
Wash the exposed area with tap water, soap and some
alkaline solution.
If ingested, gastric lavage should be done if the patient
presents within first one hour of ingestion.
Activated charcoal is given orally at a dose of 1-2 g/kg body
weight.
2) Care of airway:
Meticulous care of the airway along with oxygenation is
important.
Foot end of bed raised to ensure drainage of respiratory
mucus.
If there is respiratory insufficiency, patient should be
ventilated.
3) Administration of an antidote:
Atropine

 Atropine is the main antidote. Atropine is administered

at a dose of 1.8 3.0 mg intravenously. Five minutes
after giving atropine, check the five markers of
cholinergic poisoning (Miosis, excessive sweating,
bronchorrhoea and bronchospasm, bradycardia and
hypotension).
If there is no improvement across the five parameters
after 5 mins then double the dose of atropine every time
and continue to double each time there is no adequate
response.
Signs of atropinisation: Clear chest on auscultation,
heart rate >80 beats/min, pupils no longer pinpoint, dry
axillae and systolic blood pressure > 90mmHg.
Once atropinised set up an infusion of atropine at an
hourly dose of 10-20% of the total dose of atropine
given initially. Review every 15 mins to see whether the
atropine infusion rate is adequate.
4) Cholinesterase reactivators Pralidoxime (2-PAM) is effective for nicotinic as well as
muscarinic features of toxicity.
Dose: 1-2 gm IV for adult
25-50 mg/kg for children
Repeated at 6-12 hrs interval for 24-48 hours.
5) Other measures:
Diuretics and saline purgative.
Barbiturate or diazepam for convulsion
Symptomatic treatment
Hemodialysis
References:

 Mathew K., Aggarwal P., Medicine Prep Manual for

Undergraduates (2013), 4th edition, Published by Elsevier, A
division of Reed Elsevier India Private Limited, Pg. no. 647-649
http://en.wikipedia.org/wiki/Organophosphate_poisoning
http://emedicine.medscape.com/article/167726-overview#a0101
http://en.wikipedia.org/wiki/Nerve_agent