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Year : 2019  |  Volume : 17  |  Issue : 2  |  Page : 34-37

Paraquat poisoning management

1 Department of General Medicine Unit V, Christian Medical College, Vellore, Tamil Nadu, India
2 Clinical Biochemistry, Christian Medical College, Vellore, Tamil Nadu, India

Date of Submission30-Jul-2019
Date of Acceptance19-Aug-2019
Date of Web Publication29-Aug-2019

Correspondence Address:
Dr. Jambugulam Mohan
Department of General Medicine Unit V, Christian Medical College, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cmi.cmi_29_19

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Paraquat a rapidly acting, nonselective herbicide is a leading cause of fatal poisoning in many parts of Asia. After rapid absorption, paraquat is concentrated inside many cells where it undergoes redox cycling. Clinical features are largely due to intracellular effects. Paraquat is actively concentrated into lung tissue leading to pneumonitis and lung fibrosis. Paraquat also causes gastrointestinal, renal, and liver injuries. Activated charcoal and Fuller's earth can minimize further absorption. Gastric lavage is contraindicated. Hemodialysis and hemoperfusion are unlikely to change the clinical course. The use of immunosuppression with dexamethasone, cyclophosphamide, and methylprednisolone evidence for efficacy is weak. Antioxidants such as acetylcysteine and salicylate used as free radical scavenging might be beneficial. The case fatality is very high in this herbicide due to the lack of effective treatment options.

Keywords: Deliberate self-harm, management, paraquat

How to cite this article:
Iyyadurai R, Mohan J, Jose A, Das S, Johnson J, Gunasekaran K. Paraquat poisoning management. Curr Med Issues 2019;17:34-7

How to cite this URL:
Iyyadurai R, Mohan J, Jose A, Das S, Johnson J, Gunasekaran K. Paraquat poisoning management. Curr Med Issues [serial online] 2019 [cited 2023 Feb 9];17:34-7. Available from: https://www.cmijournal.org/text.asp?2019/17/2/34/265826

  Case Scenario Top

A 42-year-old male presented to the emergency department with an alleged history of consumption of around 100 ml of 24% paraquat. Following ingestion, he developed multiple episodes of nonbilious, nonprojectile vomiting and nonblood stained loose stools. On admission, the patient was found to have elevated creatinine (2.25 mg%) and decreased urine output. Over the next 24 h, renal function worsened further (creatinine: 7.74 mg%), and the patient developed metabolic acidosis and hyperkalemia. He also had liver dysfunction with progressively worsening hyperbilirubinemia and transaminitis. Gastroscopy was done which showed esophageal and gastric mucosal erosions. Myocardial involvement was ruled out with serial electrocardiography and troponin T estimation.

In the ward, he was started on broad-spectrum antibiotics in view of raised counts and due to suspicion of aspiration pneumonia. He was also started on antioxidant therapy and was given first of three doses of intravenous methylprednisolone. Subsequently, he was planned for HD. While undergoing HD, he had developed worsening respiratory distress with sudden cardiac arrest. He was intubated and managed further in high-dependency unit. In spite of continued treatment with dialysis and immunosuppressive therapy, he succumbed to his illness.

  Introduction Top

Paraquat (1,1′-Dimethyl-4,4′-bipyridinium dichloride) is a nonselective contact herbicide discovered in 1955. Poisoning due to this herbicide is a major health problem in South East Asia. It is rapid acting and kills plants by translocation into the cells on contact. It is deactivated on contact with clay in the soil. It is lethal to humans and many animals. The high lethality is due to its inherent toxicity and current lack of effective treatment. Due to its lethality, it has been withdrawn from the European Union since 2007.[1] The cause of death among humans is pulmonary fibrosis.

  Clinical Presentation Top

Lethality of paraquat depends on the dose ingested. Patients who ingest large doses (50–100 ml) present with fulminant multi-organ dysfunction syndrome (MODS), pulmonary edema, cardiac and renal hepatic failure, and central nervous system involvement with seizures.[2],[3] They are categorized as severe poisoning, and in this group, death results in a few days due to MODS. Patients who ingest smaller quantities present with predominant involvement of two organs – kidney and lung (renal failure and pulmonary fibrosis). Although classified as moderate severity, the morality in this group is still more than 50%.[4] Paraquat accumulates in the lungs with lung cell damage producing decreased gas exchange and respiratory impairment. The pulmonary lesion has two phases: an acute alveolitis over 1–3 days followed by a secondary fibrosis. Gastrointestinal toxicity is common presenting as mucosal lesions of the mouth and the tongue (“paraquat tongue”).

  Management Top

Management of this herbicide poisoning is mainly supportive as there is no effective treatment. The standard principles of resuscitation which includes assessment and management of airway, breathing, and circulation should generally be followed as per routine guidelines. Monitoring daily intake output chart, cardiac status, respiratory status, and level of consciousness can predict the occurrence of organ failure. Fluid resuscitation with 15–20 ml/kg is important as hypotension is common in paraquat poisoning due to hypovolemia.

Decontamination with activated charcoal or Fuller's earth (Multani Mitti) is recommended if the patient presents within 2–4 h. Fuller's earth is preferred as contact with clay inactivates paraquat.[1] Gastric lavage is not recommended as paraquat is corrosive. Nasogastric tube must be inserted early since paraquat is a corrosive and can cause swallowing difficulties during the hospital stay [Flow Chart 1].

  Elimination of the Toxin Top

Elimination of paraquat is possible with hemodialysis (HD) and hemofiltration (HF). The problem encountered is twofold; first, paraquat is quickly removed from circulation as endogenous clearance is very high. Second, the time of initiation of HD will have an impact on the levels of paraquat deposited in the lungs, which is very short. Hence, the window available for elimination is very short. Studies done on animal models have shown that when hemodialysis is done within 2-4 h of ingestion it is effective in reducing the plasma levels of paraquat but does not reduce the paraquat induced damage to the lungs. Hence, HD can reduce the plasma load of paraquat but not reduce the toxic effects on the target organs. A comparison of studies from various parts of the world has shown that there is no difference in outcomes in patients with paraquat poisoning who were managed with early dialysis compared to those who were managed with no dialysis or initiated on dialysis only when there was a renal failure. HD must be offered to patients who have developed renal failure, but due to lung involvement, there may not be any change in outcome with dialysis.[5],[6]

  Hemofiltration and Hemodialysis Top

Studies have shown that HF demonstrated superior clearance compared to HD.[6] However, it is important to start treatment in the initial few hours and the controversy of what method is used becomes secondary. HD and HF may not be easily available in rural centers where paraquat poisoning is common.

  Immunosuppression Top

Immunosuppressants are often used in the management of paraquat poisoning. The theory behind this practice is that paraquat elicits an acute inflammatory response which eventually leads to lung fibrosis, hence intervening at an early stage, and stopping inflammatory response may inhibit the processes leading to lung fibrosis and death.

The most widely used agents are glucocorticoids such as methylprednisolone and dexamethasone and chemotherapeutic agents such as cyclophosphamide. Animal studies have shown that dexamethasone increases the expression of glycoproteinP receptors, and this was associated with a reduction in the accumulation of paraquat in the lung and increased excretion in the urine. Further studies on Wistar rats have shown that dexamethasone can ameliorate the histological and biochemical changes in paraquat poisoning and also reduces lipid peroxidation, thereby improving survival rates in Wistar rats.[4]

There are three randomized controlled trials[7],[8],[9] in comparing dexamethasone, methylprednisolone, and cyclophosphamide versus standard treatment; all the three trials showed mortality benefit in the treatment arm compared to the standard treatment arm, but these studies are limited by lack of follow-up and lack of sample size calculation, and plasma paraquat levels were not measured.

  Antioxidants in Paraquat Poisoning Top


N-acetylcysteine (NAC) replenishes cysteine which is the rate-limiting step in the generation of glutathione. NAC increased the level of glutathione in the type 2 pneumocytes in rats. NAC reduced paraquat-induced apoptosis and inflammatory markers in vitro lung cultures. NAC suppressed malondialdehyde and superoxide production, and there was an increase in the glutathione levels in all the tissues in the study animals.[10],[11]

Vitamin C

Studies on human subjects have shown that high doses of Vitamin C and antioxidants reduced mortality in a case series of ten patients.[12] The mechanism of action is that Vitamin C can donate electrons to free radicals and hence neutralize them.[13]

Vitamin E

Animal models deficient with Vitamin E poisoned with paraquat showed a reduction in lung toxicity when treated with Vitamin E. There was a reduction in lipid peroxidation. But unfortunately, human studies have shown no benefit.[14],[15]

  Desferrioxamine Top

Studies on bacteria and rats have shown that iron enhances the toxicity of paraquat and the use of desferrioxamine is protective but does not reduce mortality. To date, there are no studies with desferrioxamine in human subjects.[16],[17]

  Salicylic Acid Top

Salicylic acid inhibits cyclooxygenase, and it can scavenge hydroxyl radicals and inhibit their production. Studies done on rats have shown that salicylic acid treated rats showed improved survival while the untreated group had 100% mortality. There are no human studies on salicylic acid till date.[18]

  Laboratory Assessment of Paraquat from the Biological Samples Top

Urine dithionite test is widely available, and it is simple to administer to qualitatively screen for the presence of paraquat in the given sample. Sodium hydroxide and sodium dithionite are easily available chemicals used in this method.

Methodology for urine dithionate test

Briefly add 1N sodium hydroxide solution, to 10 ml of urine or gastric aspirate till pH is above 9 then add a spatula blade full of sodium dithionite to the sample and mix gently. View the control and test tube against a white background. A blue or green color in the solution confirms the presence of paraquat. A positive and negative control should be included in the test for confirmation. In high paraquat concentrations, the solution may turn black, which may need a repeat test with a diluted sample. This method has a sensitivity of 2 mg/l and is very rapid and easy to perform in a low-cost setting or in a rural public health center.[19]

Paraquat levels can be quantitatively assessed by methods such as high-performance liquid chromatography (HPLC) and liquid chromatography with mass spectrometric detection analysis. These methods are available in regional toxicology and forensic science laboratories.

  Prognosis Top

Identification and quantification of paraquat will help in calculating predictive value of survival of poisoned patients. There are various analytical methods which can be used for qualitative and quantitative confirmation of the poison in the body. Urine dithionate test is used to detect urine paraquat levels qualitatively. It is a simple urine spot test when positive gives a blue color to confirm the significant paraquat ingestion. A 4 h postingestion plasma sample can be used for quantitative measurement of paraquat levels. A plasma concentration of >5 mg/l at any time from the time of paraquat ingestion indicates an invariably fatal outcome.[20] Paraquat levels can also be quantified in biological samples by sophisticated methods such as second-derivative spectrophotometry, HPLC with fluorescence detection, and liquid chromatography–electrospray ionization–mass spectrometry.[21],[22] Given the high lethality of this compound upon ingestion, it is advisable that the use of this compound should be restricted.

Declaration of patient consent aThe authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Elenga N, Merlin C, Le Guern R, Kom-Tchameni R, Ducrot YM, Pradier M, et al. Clinical features and prognosis of paraquat poisoning in French Guiana: A review of 62 cases. Medicine (Baltimore) 2018;97:e9621.  Back to cited text no. 1
Yamamoto I, Saito T, Harunari N, Sato Y, Kato H, Nakagawa Y, et al. Correlating the severity of paraquat poisoning with specific hemodynamic and oxygen metabolism variables. Crit Care Med 2000;28:1877-83.  Back to cited text no. 2
Senarathna L, Eddleston M, Wilks MF, Woollen BH, Tomenson JA, Roberts DM, et al. Prediction of outcome after paraquat poisoning by measurement of the plasma paraquat concentration. QJM 2009;102:251-9.  Back to cited text no. 3
Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol 2011;72:745-57.  Back to cited text no. 4
Hong SY, Yang JO, Lee EY, Kim SH. Effect of haemoperfusion on plasma paraquat concentration in vitro and in vivo. Toxicol Ind Health 2003;19:17-23.  Back to cited text no. 5
Van de Vyver FL, Giuliano RA, Paulus GJ, Verpooten GA, Franke JP, De Zeeuw RA, et al. Hemoperfusion-hemodialysis ineffective for paraquat removal in life-threatening poisoning? J Toxicol Clin Toxicol 1985;23:117-31.  Back to cited text no. 6
Lin JL, Leu ML, Liu YC, Chen GH. A prospective clinical trial of pulse therapy with glucocorticoid and cyclophosphamide in moderate to severe paraquat-poisoned patients. Am J Respir Crit Care Med 1999;159:357-60.  Back to cited text no. 7
Lin JL, Lin-Tan DT, Chen KH, Huang WH. Repeated pulse of methylprednisolone and cyclophosphamide with continuous dexamethasone therapy for patients with severe paraquat poisoning. Crit Care Med 2006;34:368-73.  Back to cited text no. 8
Afzali S, Gholyaf M. The effectiveness of combined treatment with methylprednisolone and cyclophosphamide in oral paraquat poisoning. Arch Iran Med 2008;11:387-91.  Back to cited text no. 9
Hoffer E, Avidor I, Benjaminov O, Shenker L, Tabak A, Tamir A, et al. N-acetylcysteine delays the infiltration of inflammatory cells into the lungs of paraquat-intoxicated rats. Toxicol Appl Pharmacol 1993;120:8-12.  Back to cited text no. 10
Hoffer E, Baum Y, Tabak A, Taitelman U. N-acetylcysteine increases the glutathione content and protects rat alveolar type II cells against paraquat-induced cytotoxicity. Toxicol Lett 1996;84:7-12.  Back to cited text no. 11
Kang SA, Jang YJ, Park H.In vivo dual effects of Vitamin C on paraquat-induced lung damage: Dependence on released metals from the damaged tissue. Free Radic Res 1998;28:93-107.  Back to cited text no. 12
Perla V, Perrin NA, Greenlee AR. Paraquat toxicity in a mouse embryonic stem cell model. Toxicol In Vitro 2008;22:515-24.  Back to cited text no. 13
Redetzki HM, Wood CD, Grafton WD. Vitamin E and paraquat poisoning. Vet Hum Toxicol 1980;22:395-7.  Back to cited text no. 14
Block ER. Potentiation of acute paraquat toxicity by Vitamin E deficiency. Lung 1979;156:195-203.  Back to cited text no. 15
Korbashi P, Kohen R, Katzhendler J, Chevion M. Iron mediates paraquat toxicity in Escherichia coli. J Biol Chem 1986;261:12472-6.  Back to cited text no. 16
Hoffer E, Zonis Z, Tabak A, Taitelman U. The administration of desferrioxamine to paraquat-intoxicated rats. Vet Hum Toxicol 1992;34:300-3.  Back to cited text no. 17
Fürst R, Blumenthal SB, Kiemer AK, Zahler S, Vollmar AM. Nuclear factor-kappa B-independent anti-inflammatory action of salicylate in human endothelial cells: Induction of heme oxygenase-1 by the c-jun N-terminal kinase/activator protein-1 pathway. J Pharmacol Exp Ther 2006;318:389-94.  Back to cited text no. 18
Berry DJ, Grove J. The determination of paraquat (I, I'-dimethyl-4,4'-bipyridylium cation) in urine. Clin Chim Acta 1971;34:5-11.  Back to cited text no. 19
Blake DK, Gallagher RT, Woollen BH. Improved methods for the analysis of paraquat in biological fluids. Chromatographia 2002;55:S183-5.  Back to cited text no. 20
Jones AL, Elton R, Flanagan R. Multiple logistic regression analysis of plasma paraquat concentrations as a predictor of outcome in 375 cases of paraquat poisoning. QJM 1999;92:573-8.  Back to cited text no. 21
Dinis-Oliveira RJ, Duarte JA, Sánchez-Navarro A, Remião F, Bastos ML, Carvalho F. Paraquat poisonings: Mechanisms of lung toxicity, clinical features, and treatment. Crit Rev Toxicol 2008;38:13-71.  Back to cited text no. 22

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