Pretilachlor poisoning: A rare case of a herbicide masquerading
as organophosphate toxicity
Olita Shilpakar1, Bipin Karki2,
Bibek Rajbhandari3
1Department of General Practice and Emergency
Medicine, NAMS, Bir Hospital, Kathmandu, Nepal, 2Department of Critical Care Medicine, Om Hospital and Research Centre,
Kathmandu, Nepal, 3Department of General Practice and
Emergency Medicine, Nepal Police Hospital, Kathmandu, Nepal.
Correspondence: Dr. Olita Shilpakar, Department of General Practice and
Emergency Medicine, NAMS, Bir Hospital, Kathmandu. E-mail:
olitashilpakar1@gmail.com, Phone: +977-9841256959.
ABSTRACT
Pretilachlor is a chloracetanilide herbicide whose acute intoxication in
humans via ingestion has been rarely reported. We report a case of
suicidal ingestion of the herbicide with similar clinical manifestations
of organophosphate toxicity. Awareness among clinicians regarding such
mimickers is the key to proper management of the patient.
Keywords: bradycardia; poisoning; vomiting.
KEY CLINICAL MESSAGE
Acute oral intoxication of pretilachlor, a chloracetanilide herbicide,
in humans can present with similar clinical manifestations of
organophosphate toxicity. Clinicians should be aware of such mimickers
for proper management of the patient.
INTRODUCTION
Chloracetanilides are a group of anilide herbicides which commonly
include alachlor, butachlor, metachlor and pretilachlor. Pretilachlor is
a broad spectrum systemic herbicide with the chemical name 2-chloro-2′,
6′-diethyl-N-(2-propoxyethyl) acetanilide. It has excellent action
against annual weeds, sedges and broadleaf weeds in rice
fields.1 The mechanism of action of these group of
drugs is still not clearly understood but is known to act by inhibiting
the biosynthesis of fatty acids, lipids, proteins, flavonoids, etc.
Chronic exposure to these group of herbicides has shown probable
carcinogenic effects, however, acute toxicity from pretilachlor in
humans has not been reported yet.2 Acute pretilachlor
intoxication via ingestion can be mistaken for commonly encountered
pesticides like organophosphates resulting in fallacious management of
the patient. We report a case of a forty-two-years male who presented to
the emergency room following suicidal ingestion of the herbicide
mimicking clinical manifestations of organophosphate toxicity like
vomiting, excessive lacrimation, bowel and bladder incontinence,
bradycardia and hypotension and complete recovery following supportive
management.
CASE REPORT
A forty-two-years male presented to the emergency room with the alleged
history of suicidal ingestion of an unknown poison two hours back
following a family dispute. The patient immediately had two episodes of
non bilious non projectile vomiting followed by excessive lacrimation,
bowel and bladder incontinence and dizziness within two hours of
ingestion of the poison. There was no history of shortness of breath,
chest pain, loss of consciousness or seizures. He did not have any past
medical or psychiatric history or similar suicidal attempts in the past.
On examination in the emergency room, the patient was drowsy but
followed verbal commands. He had a radial pulse of 50 beats per minute,
blood pressure of 90/50mm Hg, respiratory rate of 16 breaths/minute,
temperature of 98.6 degrees Fahrenheit and oxygen saturation of 94% in
room air. His pupils were 3 millimeters in size bilaterally and reacting
to light. Furthermore, the peculiar garlicky smell of organophosphate
was not detected from his breath. His chest auscultation was clear,
abdomen was soft and non tender and the remaining systemic examination
did not reveal any abnormality.
With the provisional diagnosis of a possible organophosphorus poisoning,
the patient was managed initially by administering an intravenous dose
of atropine 0.6mg following which his heart rate increased to 100 beats
per minute showing a normal sinus rhythm in the 12 lead
electrocardiogram. Dermal decontamination was done by removing the
patient’s vomitus soaked clothing. The skin was cleaned thoroughly with
soap water and gastric lavage was performed simultaneously. A bolus dose
of 500ml of intravenous 0.9% Normal Saline and an intravenous dose of
pralidoxime 2grams over 30 minutes were administered. His investigations
comprising a full blood count, arterial blood gas, renal function tests,
a random blood sugar level, liver function tests, a coagulation profile
and a serum cholinesterase level were all within normal limits. A chest
radiograph and an ultrasonogram of the abdomen and pelvis did not reveal
any abnormalities.
A bottle of the herbicide pretilachlor 50% emulsifiable concentrate
(EC) was retrieved from his room and was brought to the emergency room
by his son after two hours. The patient confirmed to have consumed the
full bottle containing 250 ml of the herbicide. Close monitoring with
continuous supportive management was done for 24 hours with intravenous
fluids and antiemetics following which he gradually became asymptomatic.
His heart rate remained within the normal range, his blood pressure
normalized and a normal urine output was maintained throughout the
hospital stay. Symptoms of lacrimation and incontinence subsided. Repeat
blood counts, renal and liver functions were within normal ranges. He
was kept under observation with strict hemodynamic monitoring for the
next two days which was uneventful. He was discharged from the hospital
on the third day after a behavioural counselling session. He was in good
health during a one-week follow up in the outpatient department.
DISCUSSION
Pretilachlor is a synthetic chloracetanilide herbicide used effectively
in annual grasses and broad-leaved weeds including Echinochloa
Beauvois, Cyperus difformis and sedges in rice and paddy fields.
Pretilachlor is generally marketed in a 50% emulsifiable concentrate
formulation. It appears as a colourless and odourless liquid. It
contains an ethoxylated vegetable oil as the emulsifying agent and alkyl
aryl sulphonate of calcium salt as the surfactant.1
Chronic exposure to chloracetanilide in vitro and vivo studies have
shown that it has a role in causing neurotoxicity, genotoxicity and
carcinogenicity.2,3 Acute oral exposure might have a
dissimilar effect on humans but such cases have been rarely reported to
date. A retrospective study of 35 patients with acute oral
chloracetanilide poisoning concluded that although it was found to be of
low toxicity in most of the patients, three patients were comatose and
one patient died 24 hours after the exposure.4 Another
study by Lo et al in 113 patients with oral exposure to
chloracetanilides like alachlor and butachlor suggested that around one
fourth of the patients were asymptomatic, the rest had vomiting and
neurological symptoms ranging from drowsiness to central nervous system
depression and three fatalities after manifesting profound hypotension
and coma.5
Misdiagnosis of pretilachlor poisoning as organophosphorus toxicity in
the emergency room could be a major drawback and may lead to faulty
management. In our case, the patient displayed several similar clinical
features that are encountered with organophosphates like vomiting,
excessive lacrimation, bowel bladder incontinence, bradycardia and
hypotension. These hypersecretory effects like salivation, lacrimation,
urination, defecation, gastrointestinal motility, emesis and miosis in
case of organophosphate poisoning are due to the overstimulation of
muscarinic acetylcholine receptors in the parasympathetic system. Acute
muscarinic effects on the heart in the form of bradycardia and
hypotension can be life threatening.6 However, there
was no miosis or the presence of the characteristic garlicky odour of
organophosphorus toxicity which hinted towards an alternative diagnosis.
His serum cholinesterase level was also within normal limit which in
case of organophosphates are seen to decrease.6
No antidote is yet known to be available for pretilachlor poisoning so
the mainstay of treatment is symptomatic with initial stabilization of
the patient, decontamination, intravenous fluid resuscitation and close
hemodynamic monitoring.7 In our case, symptomatic
bradycardia was alleviated with atropine sulphate administration and the
patient became normotensive following intravenous fluids. Therefore,
further studies are recommended which would elaborate more on the
mechanism of action of this drug on the human body and the definitive
management to combat its toxic effects.8
CONCLUSION
This case highlights that despite exhibiting similar clinical
manifestations like that of organophosphorus poisoning, initial
stabilization, close monitoring, and supportive treatment are the three
important aspects for a speedy recovery in pretilachlor poisoning.
Education and awareness among the treating physicians regarding
mimickers like organophosphates is an important point to be taken into
consideration from this case report. The importance of retrieving the
poison container wherever possible for the identification of the active
compound is emphasized. Redesigning of containers with precautionary
warning labels for the general public and restricted availability of
this herbicide over the counter are highly recommended.
ACKNOWLEDGEMENTS
The authors are grateful to the patient and his family for providing
support regarding the preparation of the report.
CONFLICT OF INTEREST:
None declared.
AUTHOR CONTRIBUTION:
OS: was involved in the patient care and management and designed the
study. OS and BK: prepared the initial draft of the manuscript. OS, BK
and BR: edited the draft and reviewed the manuscript. All authors
approved the final version of the manuscript and agreed to be
accountable for any aspects related to the accuracy or integrity of the
work.
ORCID:
Olita Shilpakar https://orcid.org/0000-0002-4437-531X
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