The Successful Treatment of High Lethal Dose ‎Paraquat Poisoning With Hemoperfusion

Abstract

Paraquat (PQ), as an herbicide, is mostly used by farmers, especially in the north-west of Iran. Easy access to PQ is the reason for PQ intoxication in farm­ers. However, poisoning with PQ is rare. Most of the PQ-poisoned patients ingest it deliberately and following a suicidal attempt. PQ poisoning treatment has a poor outcome; only a small dose of slightly more than 10 mL PQ could be harmful and damage lungs forever. Under the conditions of no specific clinical feature, proper history, and diagnostic test, diagnosis is usually difficult. The ingestion of PQ in toxic doses could be fatal, destroying the lungs, kidney, heart, gastrointestinal tract, liver, and other organs. To remove PQ from the blood and intoxicants, one of the best recommendations is Hemo­perfusion (HP), as an extracorporeal method. In this case report, according to our treatments, early management of high lethal dose PQ poisoning, especially with HP could reduce the morbidity and mortality rates.

Full text

1
Case Report: The Successful Treatment of High Lethal
Dose Paraquat Poisoning With Hemoperfusion
Ali Banagozar Mohammadi1, Maryam Zaare Nahandi1, Soraya Mohammadian1*
1. Department of Internal Medicine, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
* Corresponding Author:
Soraya Mohammadian, MD.
Address: Department of Internal Medicine, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Tel: +98 (41) 35498260
E-mail: smohammadian01@yahoo.com
Paraquat (PQ), as an herbicide, is moly used by farmers, especially in the north-we of Iran.
Easy access to PQ is the reason for PQ intoxication in farm ers. However, poisoning with PQ is
rare. Mo of the PQ-poisoned patients inge it deliberately and following a suicidal attempt.
PQ poisoning treatment has a poor outcome; only a small dose of slightly more than 10 mL
PQ could be harmful and damage lungs forever. Under the conditions of no specic clinical
feature, proper hiory, and diagnoic te, diagnosis is usually dicult. The ingeion of PQ
in toxic doses could be fatal, deroying the lungs, kidney, heart, garointeinal tract, liver, and
other organs. To remove PQ from the blood and intoxicants, one of the be recommendations
is Hemo perfusion (HP), as an extracorporeal method. In this case report, according to our
treatments, early management of high lethal dose PQ poisoning, especially with HP could
reduce the morbidity and mortality rates.
A B S T R A C T
Keywords:
Paraquat, Herbicide, Outcome,
Hemo perfusion, Poisoning
Citation:
Banagozar Mohammadi A, Zaare Nahandi M, Mohammadian S. The Successful Treatment of High Lethal
Dose Paraquat Poisoning With Hemoperfusion. International Journal of Medical Toxicology and Forensic Medicine. 2020;
10(3):26726. https://doi.org/10.32598/ijmtfm.v10i3.26726
:
https://doi.org/10.32598/ijmtfm.v10i3.26726
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Article info:
Received: 14 Augu 2019
Fir Revision: 25 Augu 2019
Accepted: 01 Jul 2020
Published: 24 Oct 2020
1. Introduction
he N, N′-dimethyl-4, 4′-bipyridinium
dichloride (paraquat), is a corrosive and
highly toxic greenish-black liquid. De-
spite being banned in numerous countries
[1], it remains the second top-selling her-
bicide in some regions [2]. Its accidental
ingeion provides a high mortality rate, and it causes
local and syemic toxicity [3]. Here, we reported a case
of high-dose Paraquat (PQ) poisoning with a highly
positive urine PQ te. The presented patient was suc-
cessfully recovered with early management using He-
moperfusion (HP) after ingeion.
2. Case Report
A 29-year-old healthy male farmer with no medical his-
tory or any medication use and drug dependence was
presented to Sina Hospital (referral center), 4 hours after
an accidental consumption of 90 mL of PQ 20% (with the
claim that he thought it was Coca-Cola). He vomited im-
mediately after taking it; within 1.5 hours before hospital
admission, he experienced 4 vomiting episodes. He was
admitted to a local hospital with the chief complaint of
several episodes of vomiting. Accordingly, he was given
activated charcoal and was managed conservatively with
intravenous uids, antiemetics, and pantoprazole infusion.
Then, the patient was referred to our center, promptly.
T
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At the time of arrival at our center, his main complaints
were a sore throat and abdominal pain. On examination,
blood pressure was 110/70 mmHg, heart rate 80/minute,
regular respiratory rate of 17 per minute, regular abdom-
inal-thoracic and oxygen saturation of 95% at room tem-
perature. The temperature was recorded as 98.8º Fahren-
heit by axilla. He was conscious and oriented. Cardiac
examination data were normal. Both lung elds were
clear on auscultation. Pathologic ndings were throat ul-
cer and severe erythema, LUQ, and epigaric tenderness
without rebound guarding. Besides, the sodium dithion-
ite urine te value was equal to +3.
Endoscopy results suggeed erythema in the whole
esophagus, the body, and the antrum of the omach,
with erosion in the lower part of the esophagus. Im-
mediately after the patient’s admission, 40g N-Acetyl
Cyeine daily infusion, 1 gr daily methylprednisolone,
1gr vitamin C ampule in a single dose, uid therapy,
pantoprazole and metoclopramide ampules, 2 eps of
5-hour hemoperfusion treatment (HA230 hemoperfu-
sion cartridge), and 4-hour hemodialysis by high ux l-
ter were adminiered. The patient also received 2.5-hour
hemoperfusion with 4-hour hemodialysis on the second
and third days of hospitalization. Furthermore, 1 gr/day
cyclophosphamide was initiated for him for 3 days. The
sodium dithionite urine te result was negative after the
second day of hemoperfusion.
N-acetyl cyeine infusion and methylprednisolone
ampule was discontinued from the 10th day. Moreover,
NAC tablets 2400 mg/d divided into 4 doses, and 50 mg
prednisolone tablets daily were replaced in the patient’s
medication orders. He was discharged with decreasing
NAC, methylprednisolone, and AlMg-S syrup after 12
days. Prednisolone and NAC 30 were discontinued 24
and 30 days after the poisoning, respectively.
He was paraclinically evaluated up to 1.5 months after
discharge, and the following items checked were as fol-
lows: Hb, Hct, WBC, Plt, MCV, MCH, MCHC, Urea,
Cr, Na, K, PT, PTT, AST, ALT, ALP, BS, PH, PCO2,
HCO3, PO2, O2Sat, qualitative sodium dithionite te
(urine paraquat te); however, during this period, the
only abnormal ndings were as follows. Creatinine was
equal to 0.9 on the r day; however, it increased from
the second day and reached 3.4 on the seventh day. Then,
it dropped over 10 days and became normal. Serum urea
arted increasing since the fourth day of poisoning and
it decreased from the tenth day. The urine PQ te was
highly positive on the r day and slightly positive on
the second day. Additionally, Po2 dropped from 82 to
46 on the second day, but rose again on the third day
to 73; in other days, it reached over 84. The patient re-
ceived regular follow-up sessions until 25 months after
poisoning and during this period he had no complication.
Considering his favorable general condition, he was re-
luctant to perform paraclinical procedures. There was no
pathologic nding on examination.
3. Discussion
PQ is commercially sold in the form of liquid concen-
trate with a concentration range of 20% to 42% w/w
[4]
.
Furthermore, products containing PQ in combination
with other herbicides, like sodium chlorate and 2,4-di-
methylamine are available in the market
[4]
. The issue
is that PQ causes critical injury in the kidney while it is
eliminated by this organ. Despite treatment, the ingeion
of a small dose of PQ could severely damage the lung
and kidney
[5]
. Being a bipyridyl compound, PQ directly
damages cells by the production of superoxide radicals
or other reactive oxygen species and nitrite radicals
[6]
.
The oral ingeion of <20 mg/kg of PQ (7.5cc 20%) may
result in the erosions of the tongue, oral mucosa, and fatal
damage to the GI tract. With the consumption of 20-50
mg/kg of PQ (7.5-18.5cc 20%), renal tubular necrosis,
hepatic necrosis, and pulmonary brosis may occur with
moderate toxicity; it usually ends in death in 2-3 weeks.
Consuming >50 mg/kg of PQ (18.5cc 20%), usually
leads to death in 1-3 days, following multi-organ dys-
function and shock [7]. Early diagnosis with prompt his-
tory taking and aggressive treatment of PQ poisoning
with HP could eliminate PQ eects and reduce mortality
[5]. The elimination of PQ is almo conducted by kid-
neys, usually within 24 h in minor poisonings. However,
the terminal elimination half-life could exceed 100 h
[8]. The referred patient presented 4 hours after the con-
sumption of the poison; therefore, the urine PQ levels
could be teed and the diagnosis was based on hiory,
clinical, and laboratory ndings, as well as the documen-
tation of the consumption of the poison.
A specic antidote of PQ does not exi and a small
amount of this poison results in a fatal outcome. The
management of this poisoning agent is supportive and gas-
tric lavage; adsorbents, such as activated charcoal (1-2
g/kg) and Fuller’s earth (1-2 g/kg) should be initiated as
early as possible to prevent the absorption of the poison
[9]
. Antioxidants, such as vitamins C and E and N-acetyl
cyeine, a free radical scavenger, have also been used in
this respect. Hemoperfusion has shown to be eective in
decreasing the PQ level if given within 4-6 h of ingeion.
Hemodialysis is only used as a supportive treatment for
patients who develop acute tubular necrosis.
Banagozar Mohammadi A, et al. Hemoperfusion in Paraquat Poisoning. IJMTFM. 2020; 10(2):26726.
Summer 2020, Volume 10, Number 3

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The role of immunosuppression is controversial and
under inveigation. Some meta-analysis concluded that
patients who received glucocorticoid with cyclophos-
phamide in addition to andard care may generate a
lower risk of death at nal follow-up, compared to those
receiving andard care alone; however, other research
failed to support that claim [10, 11].
The therapeutic outcome depends on the severity of the
poisoning and the time taken to avail of medical proce-
dures. The high mortality rates are due to the toxicity of
the compound and the lack of a specic antidote. Young
age, percutaneous or inhalational route, negative PQ
te, exposure to less PQ, and fewer degrees of leuko-
cytosis, acidosis, renal, hepatic, and pancreatic failures
on admission are good prognoic factors. PQ ingeion
may provide late complications, such as oropharyngeal
ulceration, esophageal erosions, esophagitis, renal fail-
ure, pulmonary brosis, and rictures [12, 13].
Treating such cases remains supportive; therefore, leading
to high mortality. This poison always results in respiratory
and renal damage after the consumption of an unexplained
dose. The survival of our patient could be explained by sev-
eral episodes of vomiting; the lack of any lung, pancreatic, or
hepatic failure, acidosis, or other severe End Organ damage
due to the early management of preventing the poison ab-
sorption, and prompt initiation of favorable supportive treat-
ment. The mo important of all, the rapid art of hemoper-
fusion with hemodialysis could be highly eective [6, 12].
4. Conclusion
Early diagnosis with prompt hiory taking and ag-
gressive management of PQ poisoning with hemoperfu-
sion could reduce the associated mortality rate. A small
amount of PQ poison leads to a fatal outcome. There is no
specic antidote to this poison. The late complications of
PQ ingeion are severe and disabling. Thus, the health-
care team should always think of this poison in case of
respiratory and renal damage after unexplained poison-
ing hiory. Further udies are required on the eects of
HA230 hemoperfusion cartridge in PQ poisoning.
Ethical Considerations
Compliance with ethical guidelines
All ethical principles were considered in this article. This
case report was in accordance with the ethical andards of
the initutional and/or national research committee and with
the 1964 Helsinki declaration and its later amendments.
Funding
This research did not receive any grant from funding agen-
cies in the public, commercial, or non-prot sectors.
Author's contributions
All authors contributed in preparing this article.
Conict of interest
The authors declared no conict of intere.
Acknowledgements
We would like to thank the Clinical Development Research
Unit of Sina Educational, Research and Treatment Center,
Tabriz University of Medical Sciences, Tabriz, Iran; for their
assiance in this research.
References
[1] Zaare Nahandi M, Banagozar Mohammadi A. [Ban the sale of
paraquat: General health promotion (Persian)]. Hakim Health Sys
Res. 2016; 19(2):69-71. http://hakim.hbi.ir/article-1-1677-fa.html
[2] Saravu K, Sekhar S, Pai A, Barkur AS, Rajesh V, Earla JR.
Paraquat - A deadly poison: Report of a case and review. In-
dian J Crit Care Med. 2013; 17(3):182-4. [DOI:10.4103/0972-
5229.117074] [PMID] [PMCID]
[3] Raghu K, Mahesh V, Sasidhar P, Reddy PR, Venkatarama-
niah V, Agrawal A. Paraquat poisoning: A case report and re-
view of literature. J Family Community Med. 2013; 20(3):198-
200. [DOI:10.4103/2230-8229.122023] [PMID] [PMCID]
[4] Jagadeesan M, Nithyananthan P, Banupriya M, Mahendraku-
mar K, Prasanna Karthik S, Kannan R. A study on clinical prole
of paraquat poisoning in a tertiary care hospital. Int J Adv Med.
2017; 4(4):1088-91. [DOI:10.18203/2349-3933.ijam20173237]
[5] Li H, Song L, Jian X. Efcacy of hemoperfusion therapy in
patients with paraquat poisoning: A meta-analysis. Int J Clin
Exp Med. 2017; 10(8):11371-81. http://www.ijcem.com/
les/ijcem0053106.pdf
[6] Ostadi A, Paeezi M. Hemoperfusion efciency in paraquat
toxicity. Int J Med Toxicol Forensic Med. 2018; 8(4):151-6.
[DOI:10.22037/ijmtfm.v8i4(Autumn).23089]
[7] Shi Y, Bai Y, Zou Y, Cai B, Liu F, Fu P, Wang L. The value of
plasma paraquat concentration in predicting therapeutic ef-
fects of haemoperfusion in patients with acute paraquat poi-
soning. PLoS One. 2012; 7(7):e40911 [DOI:10.1371/journal.
pone.0040911] [PMID] [PMCID]
[8] Wunnapuk K, Mohammed F, Gawarammana I, Liu X, Ver-
beeck RK, Buckley NA, et al. Prediction of paraquat expo-
sure and toxicity in clinically ill poisoned patients: A model
Banagozar Mohammadi A, et al. Hemoperfusion in Paraquat Poisoning. IJMTFM. 2020; 10(2):26726.
Summer 2020, Volume 10, Number 3

4
based approach. Br J Clin Pharmacol. 2014; 78(4):855-66.
[DOI:10.1111/bcp.12389] [PMID] [PMCID]
[9] Suntres ZE. Role of antioxidants in paraquat toxicity. Toxicol-
ogy. 2002; 180(1):65-77. [DOI:10.1016/S0300-483X(02)00382-7]
[10] Li LR, Sydenham E, Chaudhary B, Beecher D, You C. Gluco-
corticoid with cyclophosphamide for paraquat-induced lung
brosis. Cochrane Database Syst Rev. 2014; (6):CD008084.
[DOI:10.1002/14651858.CD008084.pub4] [PMID]
[11] Gawarammana I, Buckley NA, Mohamed F, Naser K,
Jeganathan K, Ariyananada PL, et al. High-dose immunosup-
pression to prevent death after paraquat self-poisoning-a ran-
domised controlled trial. Clin Toxicol (Phila). 2018; 56(7):633-
9. [DOI:10.1080/15563650.2017.1394465] [PMID]
[12] Li A, Li W, Hao F, Wang H. Early stage blood purication
for paraquat poisoning: A multicenter retrospective study.
Blood Purif. 2016; 42(2):93-9. [DOI:10.1159/000445991] [PMID]
[13] Liu XW, Ma T, Li LL, Qu B, Liu Z. Predictive values of
urine paraquat concentration, dose of poison, arterial blood
lactate and APACHE II score in the prognosis of patients with
acute paraquat poisoning. Exp Ther Med. 2017; 14(1):79-86.
[DOI:10.3892/etm.2017.4463] [PMID] [PMCID]
Banagozar Mohammadi A, et al. Hemoperfusion in Paraquat Poisoning. IJMTFM. 2020; 10(2):26726.
Summer 2020, Volume 10, Number 3