Table of Contents  
Year : 2015  |  Volume : 8  |  Issue : 3  |  Page : 370-374  

Paraquat: A fatal poison

Department of General Medicine, Vijayanagara Institute of Medical Sciences, Bellary, Karnataka, India

Date of Web Publication15-May-2015

Correspondence Address:
J Shashibhushan
Department of General Medicine, Vijayanagara Institute of Medical Sciences, Bellary - 583 104, Karnataka
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.157090

Rights and Permissions

Paraquat (1, 1'-dimethyl-4, 4'-dipyridylium) is a bipyridilium herbicide used widely in our country and is a highly toxic compound. This compound is very notorious to cause rapid development of renal, liver, and respiratory failure with very high mortality due to lack of specific antidote and dearth of high-quality evidence-based treatment. Respiratory system involvement is the most common cause of death in these people. We hereby report a fatal case of a 30-year-old male with a history of paraquat consumption. The patient developed oliguric renal failure, deterioration of liver function, and acute respiratory distress syndrome over next few days. Different treatment modalities were tried to manage patient's condition. In this case, none of the strategies worked well, and death ensued due to multi-organ dysfunction syndrome.

Keywords: Acute respiratory distress syndrome, cyclophosphamide, herbicide, methylprednisolone, N-acetyl cysteine

How to cite this article:
Shashibhushan J, Venugopal K, Lingaraja M, Patanjali C P, Suresh C, Huggi V. Paraquat: A fatal poison. Med J DY Patil Univ 2015;8:370-4

How to cite this URL:
Shashibhushan J, Venugopal K, Lingaraja M, Patanjali C P, Suresh C, Huggi V. Paraquat: A fatal poison. Med J DY Patil Univ [serial online] 2015 [cited 2023 Sep 30];8:370-4. Available from:

  Introduction Top

Paraquat is a pungent smelling, bright green corrosive liquid. It is the second highest-selling weed killer globally and is available as 20% solution that needs to be diluted before agricultural use. [1] Usually, adult cases of intoxication are suicidal. The acute systemic effects are pulmonary edema, convulsions, cardiac, renal, and hepatic failure. [2] The lethal dose (LD50) in humans is approximately 35 mg/kg (10-15 ml of a 20% solution). This paper reports a case of fulminant paraquat poisoning and detailed review of the intoxication, histopathology and management.

  Case Report Top

A 30-year-old male presented to the emergency department with alleged history of consumption of 600 ml of 24% w/w Gramoxone® (Paraquat, Syngenta India Limited, Plot No B-155/1, Bharuch, Gujarat, India) 3 days prior to admission. After ingestion, patient was taken to a nearby hospital; from there, patient was referred to our hospital. At the time of admission, patient had six episodes of vomiting. On examination, he was conscious, oriented; his vitals were normal and systemic examination revealed bilateral basal crepitation and diffused abdominal tenderness. Laboratory investigations showed raised blood urea, serum creatinine, and raised total bilirubin. Complete blood count, X-ray chest, ultrasonography abdomen, urine routine, and electrolytes were normal. Subsequent day's investigations are given in [Table 1].
Table 1: Laboratory investigations of the patient

Click here to view

Gastric lavage was done and started treatment with injection piperacillin-tazobactam 4.5 g TID, injection methylprednisolone 1 g OD for 3 days, N-acetyl cysteine (NAC) 600 mg TID, and other symptomatic treatment. On day-2, patient underwent hemodialysis for raised creatinine. On day-3, patient became restless and irritable, his saturation was 48% at room air, and patient was administered oxygen at 6 L/min through Hudson's mask. His saturation did not improve, in the view of falling saturation; he was intubated and put on synchronized intermittent mandatory ventilation. On day-5, his condition deteriorated and became hypotensive (systolic blood pressure -90 mmHg) with features of acute respiratory distress syndrome. His condition did not improve despite session of hemodialysis and ventilator support and patient expired on day-6. His body was autopsied; esophageal and gastric erosions were noted. Lung, liver, and kidney were biopsied, and histopathological findings are suggestive of diffuse alveolar hemorrhage, loss of centrilobular hepatocytes, and congestion of the renal parenchyma [Table 2]. Determination of the poison was not done in any organ.
Table 2: Histopathological findings of our patient and other studies

Click here to view

  Discussion Top

Paraquat is a contact herbicide, first synthesized in 1882 as a redox indicator. Its herbicidal property was recognized in the 1950s. It is produced commercially as a brownish concentrated liquid of the dichloride salt in 20% strength under the trade name of "Gramoxone®" and for horticultural use as brown granules called "Weedol®" (Syngenta India Limited, Plot No B-155/1, Bharuch, Gujarat, India) about 5% concentration. [10]

The most common route of poisoning is the ingestion. Dermal exposure also has been reported to result in severe paraquat poisoning, especially in the presence of preexisting skin lesions. [11] Inhalation of sprayed paraquat solution usually causes local irritation but rarely results in important systemic absorption. After ingestion, the gastrointestinal tract absorbs <20% of paraquat. The presence of ulcerated mucosa or an empty stomach increases the fraction of paraquat absorbed. Blood levels peak within a few hours after ingestion.

Paraquat is not actively metabolized in the body, and more than 90% is excreted unchanged by the kidneys. After absorption, paraquat is distributed to highly perfused organs such as the lungs, kidneys, liver, and muscles, and remains partly in the intravascular space.

Paraquat concentration in the lung parenchyma is very high because of active, energy-dependent uptake of paraquat by type 1 and type 2 alveolar epithelium, via the polyamine uptake pathway. [12]

Paraquat, during "redox-cycling-process" leads to the formation of superoxide anions from which more toxic reactive oxygen species (ROS) such as hydrogen peroxide and hydroxyl radicle are formed in the presence of NADPH and cytochrome P450 reductase. [13] If the protective mechanisms such as catalase and glutathione peroxidase are overwhelmed, the resultant oxidative stress will cause cellular damage. The hydroxyl radical, which is formed in the presence of iron, is a more potent oxidant and can induce lipid peroxidation which causes cell membrane damage and cell death[Figure 1],[Figure 2] and [Figure 3]. [14]
Figure 1: Histopathology of lung (H and E, ×10). (a) Interstitial and intra-alveolar fi brin rich oedema. (b) Diffuse infiltration of interstitium and alveoli with lymphocytes and eosinophil. (c) Proliferation of type-2 pneumocytes. (d) Distended alveoli

Click here to view
Figure 2: Arrow showing focal loss of centrilobular hepatocytes (H and E, ×20)

Click here to view
Figure 3: Renal parenchymal congestion (H and E, ×10)

Click here to view

The clinical manifestations range from local irritation to multiple-organ failure and death. Systemic manifestations depend on the amount ingested, and patients can be classified into 3 categories [Table 3]. [15]
Table 3: Clinical features of paraquat poisoning

Click here to view

The diagnosis is usually from the accurate history of exposure. This can be difficult in children and case of homicide. [16] The urine dithionite test quickly confirms the presence of paraquat in urine. A paraquat blood level of >1.6 μg/mL 12 h after ingestion is universally lethal. [17]

Initial management focuses on prevention of further absorption and gastrointestinal decontamination. Adsorbents like activated charcoal (1-2 g/kg) and Fuller's earth (1-2 g/kg); given with a cathartic such as 70% sorbitol should be given as soon as possible. Hemoperfusion has been shown to decrease paraquat levels in humans if initiated within 4 h of ingestion, but there are insufficient data to support any survival benefit in humans. [18] There is no specific antidote. Paraquat is not removed by dialysis. Hemodialysis is used only as a supportive treatment for patients who develop kidney failure. [19] In a study by Afzali et al., the therapeutic effect has been reported with high dose cyclophosphamide and glucocorticoid where survival was about 75%. [20] This was further supported by Agarwal et al. [21],[22] Since there is a lack of clear evidence-based therapy, different approaches have been tried for supportive management. Although high doses of cyclophosphamide and Dexamethasone treatments, including intravenous cyclophosphamide (5 mg/kg/d) and dexamethasone (24 mg/d) for 14 days have been correlated with 75% survival rate after poisoning, [23] a subsequent study [24] did not demonstrate the usefulness of this approach. A report [25] demonstrated that pulse therapy with cyclophosphamide and methyl prednisolone (MP) might be effective in preventing respiratory failure and reducing mortality in patients with moderate to severe poisoning. Pulse therapy with MP is known as a strong anti-inflammatory treatment in clinical practice, [26] suppressing ROS production by neutrophils and macrophages, and in the arachidonic acid cascade. [27]

It has been shown that desferrioxamine can exert its protective effects not only by iron chelating but also by blocking the uptake of paraquat by the alveolar type II cells. [28] Vitamin E (a-tocopherol) exerts its antioxidant effects by scavenging free radicals and stabilizing membranes containing polyunsaturated fatty acids, [29] which may prevent the cytotoxic effects of paraquat.

N-acetyl cysteine has also been used with success in massive paraquat poisoning. [30] It is an excellent source of sulfhydryl groups. NAC is indeed converted in the body into cysteine, the rate-limiting amino acid for glutathione synthesis, promoting detoxification, and acting directly as a free radical scavenger. [31] In addition, it delays inflammation. [32]

Other general supportive care includes fluid and electrolyte management and pain control. Oxygen supplementation should be avoided if possible because it can potentiate paraquat-induced lung injury. Oxygen is indicated when patient develops hypoxia. Limitations in the management are, not used all the treatment plans discussed above. Since there is no evidence-based standard protocol, and lack of specific antidote makes the management of paraquat poisoning difficult.

  Conclusion Top

The lack of a specific antidote makes the treatment of parquet poisoning challenging. As there is no concrete proof regarding the efficacy of various modalities of treatment, further light needs to be thrown on this issue. This case report reiterates the need for early recognition and treatment of parquet poisoning which is a harbinger for multi-organ failure and even death, in severe cases.

  Acknowledgments Top

We would like to thank Dr. Gadwalkar Srikant R, Professor and HOD, Department of Medicine for his support. The authors would like to thank Dr. Yogiraj, Professor of Forensic Medicine. Dr. Shanti, professor of pathology and Dr. Chandrashekar, Assistant Professor, Department of Pathology, Vims-Bellary, for his assistance in histopathological reporting and selecting appropriate images of the autopsied specimen of this patient.

  References Top

Arts J, Schuit G, Schipper A, van der Kleij B. A case report of paraquat poisoning. Eur J Hosp Pharm 2006;12:22-4.  Back to cited text no. 1
Chen HW, Tseng TK, Ding LW. Intravenous paraquat poisoning. J Chin Med Assoc 2009;72:547-50.  Back to cited text no. 2
Smith P, Heath D, Kay JM. The pathogenesis and structure of paraquat-induced pulmonary fibrosis in rats. J Pathol 1974;114:57-67.  Back to cited text no. 3
Smith P, Heath D. Paraquat lung: A reappraisal. Thorax 1974;29:643-53.  Back to cited text no. 4
Bullivant CM. Accidental poisoning by paraquat: Report of two cases in man. Br Med J 1966;1:1272-3.  Back to cited text no. 5
Matsumoto T, Matsumori H, Kuwabara N, Fukuda Y, Ariwa R. A histopathological study of the liver in paraquat poisoning - An analysis of fourteen autopsy cases with emphasis on bile duct injury. Acta Pathol Jpn 1980;30:859-70.  Back to cited text no. 6
Beebeejaun AR, Beevers G, Rogers WN. Paraquat poisoning-prolonged excretion. Hum Toxicol 1971;4:397-407.  Back to cited text no. 7
Vaziri ND, Ness RL, Fairshter RD, Smith WR, Rosen SM. Nephrotoxicity of paraquat in man. Arch Intern Med 1979;139:172-4.  Back to cited text no. 8
Kodagoda N, Jayewardene RP, Attygalle D. Poisoning with paraquat. Forensic Sci 1973;2:107-11.  Back to cited text no. 9
Reddy KS, editor. Agricultural poisons. In: Essentials of Forensic Medicine. 24 th ed. Hyderabad: Medical Book Company; 2005. p. 439-44.  Back to cited text no. 10
Papiris SA, Maniati MA, Kyriakidis V, Constantopoulos SH. Pulmonary damage due to paraquat poisoning through skin absorption. Respiration 1995;62:101-3.  Back to cited text no. 11
Honoré P, Hantson P, Fauville JP, Peeters A, Manieu P. Paraquat poisoning. "State of the art". Acta Clin Belg 1994;49:220-8.  Back to cited text no. 12
Suntres ZE. Role of antioxidants in paraquat toxicity. Toxicology 2002;180:65-77.  Back to cited text no. 13
Jones GM, Vale JA. Mechanisms of toxicity, clinical features, and management of diquat poisoning: A review. J Toxicol Clin Toxicol 2000;38:123-8.  Back to cited text no. 14
Vale JA, Meredith TJ, Buckley BM. Paraquat poisoning: Clinical features and immediate general management. Hum Toxicol 1987;6:41-7.  Back to cited text no. 15
Stephens BG, Moormeister SK. Homicidal poisoning by paraquat. Am J Forensic Med Pathol 1997;18:33-9.  Back to cited text no. 16
Hart TB, Nevitt A, Whitehead A. A new statistical approach to the prognostic significance of plasma paraquat concentrations. Lancet 1984;2:1222-3.  Back to cited text no. 17
Bismuth C, Scherrmann JM, Garnier R, Baud FJ, Pontal PG. Elimination of paraquat. Hum Toxicol 1987;6:63-7.  Back to cited text no. 18
Wong OF, Fung HT, Kam CW. Case series of paraquat poisoning in Tuen Mun Hospital. Hong Kong J Emerg Med 2006;13: 155-60.  Back to cited text no. 19
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. 20
Agarwal R, Srinivas R, Aggarwal AN, Gupta D. Experience with paraquat poisoning in a respiratory intensive care unit in North India. Singapore Med J 2006;47:1033-7.  Back to cited text no. 21
Agarwal R, Srinivas R, Aggarwal AN, Gupta D. Immunosuppressive therapy in lung injury due to paraquat poisoning: A meta-analysis. Singapore Med J 2007;48:1000-5.  Back to cited text no. 22
Addo E, Poon-King T. Leucocyte suppression in treatment of 72 patients with paraquat poisoning. Lancet 1986;1:1117-20.  Back to cited text no. 23
Perriëns JH, Benimadho S, Kiauw IL, Wisse J, Chee H. High-dose cyclophosphamide and dexamethasone in paraquat poisoning: A prospective study. Hum Exp Toxicol 1992;11: 129-34.  Back to cited text no. 24
Lin JL, Wei MC, Liu YC. Pulse therapy with cyclophosphamide and methylprednisolone in patients with moderate to severe paraquat poisoning: A preliminary report. Thorax 1996; 51:661-3.  Back to cited text no. 25
Yoshida T, Tanaka M, Sotomatsu A, Okamoto K. Effect of methylprednisolone-pulse therapy on superoxide production of neutrophils. Neurol Res 1999;21:509-12.  Back to cited text no. 26
Fox DA, McCune WJ. Immunosuppressive drug therapy of systemic lupus erythematosus. Rheum Dis Clin North Am 1994;20:265-99.  Back to cited text no. 27
Van der Wal NA, Smith LL, van Oirschot JF, van Asbeck BS. Effect of iron chelators on paraquat toxicity in rats and alveolar type II cells. Am Rev Respir Dis 1992;145:180-6.  Back to cited text no. 28
Burton GW. Vitamin E: Molecular and biological function. Proc Nutr Soc 1994;53:251-62.  Back to cited text no. 29
Drault JN, Baelen E, Mehdaoui H, Delord JM, Flament F. Massive paraquat poisoning. Favorable course after treatment with n-acetylcysteine and early hemodialysis. Ann Fr Anesth Reanim 1999;18:534-7.  Back to cited text no. 30
Moldéus P, Cotgreave IA, Berggren M. Lung protection by a thiol-containing antioxidant: N-acetylcysteine. Respiration 1986;50 Suppl 1:31-42.  Back to cited text no. 31
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. 32


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3]

This article has been cited by
1 Aqueous Thunbergia laurifolia leaf extract alleviates paraquat-induced lung injury in rats by inhibiting oxidative stress and inflammation
Sarawoot Palipoch, Chuchard Punsawad, Phanit Koomhin, Prasit Na-Ek, Wasinee Poonsawat, Rungruedi Kimseng, Potiga Chotipong, Kingkan Bunluepuech, Gorawit Yusakul, Prasit Suwannalert
BMC Complementary Medicine and Therapies. 2022; 22(1)
[Pubmed] | [DOI]
2 Paraquat – boon or bane? A retrospective study of paraquat poisoning and outcomes in a tertiary care center in South India
Kusugodlu Ramamoorthi, Vasudeva Acharya, MelissaGlenda Lewis
Medical Journal of Dr. D.Y. Patil Vidyapeeth. 2022; 0(0): 0
[Pubmed] | [DOI]
Bidyut Kumar Das, Arindam Bose, Nur Nabab Mollah, Ankur Dasgupta
[Pubmed] | [DOI]
4 Application of oxidative process to degrade paraquat present in the commercial herbicide
Yasmin Saegusa Tadayozzi,Felipe André dos Santos,Eduardo Festozo Vicente,Juliane Cristina Forti
Journal of Environmental Science and Health, Part B. 2021; : 1
[Pubmed] | [DOI]
5 Paraquat Poisoning Presenting as the “Daisley Barton Syndrome”
Maddani Shanmukhappa Sagar, Souvik Chaudhuri, Sunil Ravindranath, Vinod Reddy
Indian Journal of Respiratory Care. 2020; 9(1): 110
[Pubmed] | [DOI]
6 Homicidal poisoning in India: A short review
Asit Kumar Sikary
Journal of Forensic and Legal Medicine. 2019; 61: 13
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
Case Report
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded548    
    Comments [Add]    
    Cited by others 6    

Recommend this journal