Therapeutic Strategies in Managing Acute Paraquat Poisoning: A Review Study

Abstract

Background: Paraquat is an extremely toxic herbicide that causes such severe adverse effects as acute lung injury, pulmonary fibrosis, metabolic acidosis, cardiogenic shock, acute renal failure, and even death. Regarding the high prevalence and mortality rate without a specific antidote in paraquat poisoning, we explored managing acute paraquat poisoning.
Methods: In this study, required articles were searched using the following keywords: “paraquat poisoning” and “treatment” on an electronic database, such as Pubmed and Google Scholar from January 2013 to December 2020.
Results: This article examined pharmacokinetic, clinical, and laboratory findings, complications, diagnosis, prognostic factors, and the treatment of paraquat poisoning. Then, the medical management and therapeutic procedures of paraquat poisoning were discussed.
Conclusion: Although there exists no antidote for paraquat poisoning, numerous therapeutic methods have been suggested for treating paraquat poisoning. However, their efficacy remains undiscovered.
An interesting finding in one study indicating that endotracheal intubation is an inappropriate procedure for managing paraquat poisoning; further studies are required in this regard. For these reasons, preventing poisoning and using other herbicides with less toxicity than paraquat are recommended.

Full text

1
Review Paper: Therapeutic Strategies in Managing Acute
Paraquat Poisoning: A Review Study
Mohammad Majidi1*
1. Department of Forensic Medicine and Clinical Toxicology, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
* Corresponding Author:
Mohammad Majidi, MD.
Address: Department of Forensic Medicine and Clinical Toxicology, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Tel: +98 (914) 3472825
E-mail: majidi_m@umsu.ac.ir
Background: Paraquat is an extremely toxic herbicide that causes such severe adverse eects
as acute lung injury, pulmonary brosis, metabolic acidosis, cardiogenic shock, acute renal
failure, and even death. Regarding the high prevalence and mortality rate without a specic
antidote in paraquat poisoning, we explored managing acute paraquat poisoning.
Methods: In this udy, required articles were searched using the following keywords:
“paraquat poisoning” and “treatment” on an electronic database, such as Pubmed and Google
Scholar from January 2013 to December 2020.
Results: This article examined pharmacokinetic, clinical, and laboratory ndings,
complications, diagnosis, prognoic factors, and the treatment of paraquat poisoning. Then,
the medical management and therapeutic procedures of paraquat poisoning were discussed.
Conclusion: Although there exis no antidote for paraquat poisoning, numerous therapeutic
methods have been suggeed for treating paraquat poisoning. However, their ecacy remains
undiscovered.
An intereing nding in one udy indicating that endotracheal intubation is an inappropriate
procedure for managing paraquat poisoning; further udies are required in this regard. For
these reasons, preventing poisoning and using other herbicides with less toxicity than paraquat
are recommended.
A B S T R A C T
Keywords:
Herbicides, Paraquat,
Poisoning, Therapeutics
Citation:
Majidi M. Therapeutic Strategies in Managing Acute Paraquat Poisoning: A Review Study. International Journal of
Medical Toxicology and Forensic Medicine. 2021; 11(3):33633. https://doi.org/10.32598/ijmtfm.v11i3.33633
:
https://doi.org/10.32598/ijmtfm.v11i3.33633
Use your device to scan
and read the arcle online
Article info:
Received: 7 Jan 2021
Fir Revision: 11 Jan 2021
Accepted: 13 Jan 2021
Published: 19 Oct 2021
1. Introduction
oisoning due to peicide usually occurs
intentionally, with suicidal ideations; in
some cases, it occurs accidentally, and
rarely occurs criminally [1]. Paraquat poi-
soning was recognized in rodents since
the early 1960s. Since then, it is consumed in numerous
agricultural countries [2]. Recent udies indicated that
the mortality rate of peicide poisoning was approxi-
mately 250000 to 370000 cases, annually. Additionally,
the annual incidence of paraquat poisoning was ≥3.8
cases/100000 inhabitants/year [3, 4]. Paraquat is a high-
ly toxic, non-selective, and dose-dependent herbicide.
P
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According to udies, suicide attempts with herbicides,
like paraquat has become highly frequent in developing
agriculture countries due to their availability and co-
eectiveness in individuals [5-8]. The main route of the
involvement of paraquat poisoning is through the mouth
[8]. Furthermore, the absorption of paraquat poisoning
has been reported through other routes, such as dermal,
mucus, and inhalation contacts [5].
Unlike some developing countries and due to high
mortality, the production and diribution of paraquat
have been opped in the United States and the European
Union since 1994 and 2007, respectively [5, 6]. Stud-
ies revealed that the minimum lethal dose of paraquat
poisoning for adults equals 20-30 mg/kg. Besides, ud-
ies suggeed that the lethal doses of paraquat poisoning
are 20 mL of a 20% solution [8-11]. Mortality is very
high in all centers, despite numerous improvements in
treatment; however, the mortality rate varies from 50%
to 90%. Especially in cases of an intentional poison-
ing with concentrated formulation, the mortality rate is
100% [5]. This review udy was conducted given the
importance of the topic and high mortality rate despite
no antidote for paraquat poisoning.
Type of study
In this article, the pharmacokinetics, such as the mech-
anism of toxicity, clinical and laboratory ndings, com-
plications, as well as the diagnosis and prognosis factors
of paraquat poisoning were udied. Then, medical man-
agement and therapeutic procedures in paraquat poison-
ing were discussed.
Evidence acquisition
In this udy, required articles using the keywords
“paraquat poisoning” and “treatment” were searched on
electrical databases, such as Pubmed and Google Schol-
ar from January 2013 to December 2020.
2. Discussion
Pharmacokinetic (the absorption, distribution,
and mechanism) of toxicity
The main routes of the absorption of paraquat poison-
ing are through the mouth, skin, mucus, and respiratory
syem [5, 8]. The absorption of paraquat is very rapid
and its maximum concentration occurs within one-hour
po-ingeion. The oral bioavailability of paraquat in
humans is <5%. Moreover, the half-life of the diri-
bution is eimated at approximately 5 hours. Paraquat
minimally binds to plasma proteins and is often rapidly
diributed in all tissues. The maximum time for diagno-
sis of plasma paraquat is about 48 hours; however, it can
be detected in urine for >30 days in surviving patients.
With normal kidneys, 90% of paraquat is eliminated in
the r 24 hours of intoxication; however, with acute
renal failure, it is prolonged to more than 48 to 80 hours
[12]. Paraquat can inhibit the reduction of NAD(P)+ to
NAD(P)H, which produces oxygen radicals and inam-
matory responses, resulting in cell damage, multiple or-
gan failures, and even death. The mechanisms of action
of paraquat poisoning are presented in Figure 1.
Clinical and laboratory ndings and complications
The main clinical symptoms and signs of paraquat poi-
soning include nausea, vomiting, epigaric pain, muco-
sal lesions, inammation of the oral cavity and pharynx,
mild to moderate loss of consciousness, and fever. More-
over, the main laboratory ndings include leukocytosis,
anemia, acute hepatitis with the rise of alanine transami-
nase and aspartate transaminase, increased serum bili-
rubin, and creatinine [5, 14]. Signicant complications
of paraquat poisoning are pulmonary, cardiovascular,
hepatic, renal, coagulation, and brinolysis dysfunctions
due to cell damage [11, 15, 16]. Additionally, progressive
lung injury and acute renal failure are the main causes of
death in paraquat poisoning [11, 16].
Diagnosis
The diagnosis of paraquat poisoning is usually based
on clinical suspicions; however, measuring blood level
concentration and urine screen tes are used to conrm
the diagnosis of paraquat poisoning [1, 11]. The evalu-
ation of urinary paraquat (the level of urinary sodium
dithionite) cannot accurately predict the outcome of
paraquat poisoning in patients. However, in one udy,
patients with paraquat poisoning who had urinary para-
quat concentration about 25-50 ppm (or especially above
50 ppm) after 24 hours of consumption experienced a
mortality rate of about 90%. Serum or plasma para-
quat levels are measured by various methods, including
high-performance liquid chromatography (HPLC), gas
chromatography-mass spectrometry (GC-MS), enzyme-
linked immunosorbent assay (ELISA), and spectropho-
tometry. Serum or plasma paraquat levels are also used
to assess the prognosis of paraquat poisoning. One udy
revealed that plasma paraquat concentrations less than
2 ppm within 10 hours of intoxication indicated a good
prognosis; however, this udy was not supported in sub-
sequent udies [15].
Majidi M. Managing Acute Paraquat Poisoning. IJMTFM. 2021; 11(3):33633.
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Prognostic factors
Laboratory proles and their eects on the prognosis of
patients with paraquat poisoning were reported in limited
udies
[11, 16, 17]
. Some udies demonrated that in-
creased leukocyte, prothrombin rate, the blood, and urine
concentration of creatinine, pancreatic enzymes, and ar-
terial lactate had a poor prognosis in paraquat poisoning
[10, 11]
. Moreover, other predictors of prognosis in para-
quat poisoning include APACHE II1 and SOFA2
[11]
.
Treatment
Paraquat poisoning has no specic antidote; however,
previous udies suggeed some treatment approaches
that can be eective in the management of paraquat
poisoning. Recent proposed treatments and procedures
of paraquat poisoning are presented in Table 1. Wu et
al. (2018) in a prospective and observational clinical
udy evaluated 68 hospitalized patients with respira-
tory failure due to paraquat poisoning in Taiwan [18].
Then, a comparison was made between the do-not-
intubate group and endotracheal intubated group; they
unexpectedly concluded that the procedure of intubation
in paraquat poisoning can be considered inappropriate
treatment [18].
3. Conclusion
There exis no antidote for paraquat poisoning;
however,numerous therapeutic rategies have been sug-
geed for managing paraquat poisoning . The mecha-
nisms of multi-organ failure, especially lung injury and
the pulmonary brosis of paraquat poisoning are cell
damage caused by oxygen radicals and inammatory
cytokines (Interleukin-1β (IL-1β), interleukin -6 (IL-6),
and tumor necrosis factor-alpha (TNF-α)). Therefore,
mo proposed treatment methods are based on anti-
inammatory and anti-oxidative therapy. In addition,
decreased absorption increased elimination of paraquat,
and using procedures, such as extracorporeal and surgi-
cal procedures remain the main management methods
of paraquat poisoning. However, their ecacy remains
uneablished . Unexpectedly, a udy suggeed that en-
dotracheal intubation is an inappropriate procedure for
the management of paraquat poisoning. Thus, the pre-
vention of poisoning and using other herbicides with less
toxicity than paraquat is recommended.
Ethical Considerations
Compliance with ethical guidelines
All ethical principles were considered in this article.
Funding
This article was supported by the Urmia University of
Medical Science.
Author's contributions
The main author contributed to preparing this article.
Figure 1. The mechanisms of action of paraquat poisoning [6, 12, 13]
failures, and even death. The mechanisms of action of paraquat poisoning are presented in Figure
1.
NADPH
Paraquat Oxygen

Infla mma t io n (cytok ine re lease
& leucocyte influx)
Lipid peroxidation
C yt ot o xic it y
NADP+ Paraquat radical
Figure 1 . The mechanisms of action of paraquat poisoning [6, 12-13]
Clinical and laboratory findings and complications
The main clinic a l symp t o ms a nd signs of paraqua t poisoning includ e na usea, v omit i ng , epigastric
pain, mucosal le s io ns, inflammatio n of the oral cavity and pharynx, mild to moderate loss of
co nsciousnes s, and fever. Moreover, the ma in laboratory findings include leukocytosis, anemia,
acute hepatitis with the rise of alanine transaminase and aspartate transaminase, increased serum
b ilir ub i n, and creatinine [5, 14]. Significant complications of paraquat poisoning are pulmonary,
cardiovascular, hepatic, renal, coagulation, and fibrino lys is dysfunctio ns due to cell damage [11,
15-16]. Additionally, progressive lung injury and acute renal failure are the main causes of death
in paraquat poisoning [11, 16].
Diagnosis
The diagnosis of paraquat poisoning is usually based on clinical suspicions ; however, mea suring
blood level concentration and urine screen tests are used to confirm the diagnosis of paraquat
poisoning [1, 11]. The evaluatio n of urinary paraquat (the level of urinar y sodium dithionite)
cannot accurately predict the outcome of paraquat poisoning in patients. However, in one study,
patients with paraquat poisoning who had urinary pa raq uat concentratio n about 25 -50 ppm (or
especially above 50 ppm) after 24 hours of consumption experienced a mortality rate of about
90%. Serum or plasma paraquat levels are measured by various methods, includ i n g HPLC [W1],
GC-M S , cap illa r y electrophoresis, ELISA, and spectrophotometry. Serum or plasma paraquat
levels are also used to assess the prognosis of paraquat poisoning. One study revealed that
Redox c ycling
Multi organ damage and lung fibrosis
Oxygen radicals and
nitrite species
Majidi M. Managing Acute Paraquat Poisoning. IJMTFM. 2021; 11(3):33633.
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Table 1. Proposed treatments and the procedures of paraquat poisoning and their mechanisms of action
Recent Treatment MethodsMechanisms of Acon
Fluid infusion and pulmonary supports [19]
Parenteral nutrion [11]
Supporve therapy [11, 19]
Gastric lavage and the ingeson of charcoal [19]
Lavage with sucralfate [20]
Milk gargle and acvated carbon retenon enema [21]
Gastric lavage with “Multani mi” (Fuller’s Earth) or (calcium montmorillonite)
and Bentonite [22]
Reduce absorpon [19-22]
Rhubarb [23]
Eliminate and reduced absorpon of paraquat
[23]
Immunosuppressive (cyclophosphamide and corcosteroids) [19]
Vitamins C, E and N‑acetylcysteine [19]
Naringin, Edaravone, Quercen [19]
Lysine acetylsalicylate (a salt of aspirin) [19]
An‑C5a anbodies such as IFX‑1 [24]
Type III procollagen pepde [25]
Rapamycin [26]
Procyanidin B2 [27]
Doxycycline [28]
Rosiglitazone [29]
Silymarin [30]
ω‑3 sh oil emulsion [31]
Ambroxol [32]
Atorvastan [33]
Alpha lipoic acid [34]
Sodium tauroursodeoxycholate [35]
1‑methylhydantoin (MH) [36]
Meormin [37]
An‑inammatory and an‑oxidave properes
[19, 24-40]:
Medicines [19, 24-37]
Herbal treatment and tradional Chinese medi-
cine [38-40]
Xuebijing injecon [38]
Danshen injecon [38]
Rheum ocinale Baill [38]
Rehmannia glunosa [39]
Monoammonium glycyrrhizinate [40]
Dandelion [40]
Procedures
Extracorporeal removal techniques (even in unknown hepas viral marker status) [41-44]
Hemodialysis
Hemoperfusion, charcoal hemoperfusion, and resin hemoperfusion
Hemodialtraon and connuous venovenous hemoltraon
Blood puricaon
Surgical procedures [45‑47]
Intervenonal strategy for pulmonary salvage such as one‑lung circumvenon
Lung transplantaon with or without extracorporeal membrane oxygenaon
Other procedures [19, 48, 49]
Lung radiotherapy
Mesenchymal stem cells
Whole lung lavage therapy
Majidi M. Managing Acute Paraquat Poisoning. IJMTFM. 2021; 11(3):33633.
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Conict of interest
The author declared no conicts of intere.
Acknowledgements
The author would like to thank the management of
Imam Khomeini Hospital, Urmia, Iran, for supporting
this udy.
1. APACHE II: Acute physiology and chronic health
evaluation score
2. SOFA: Sequential organ failure assessment
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