Paraquat Ingestion Research Articles

Neurotoxic and behavioral deficit in Drosophila melanogaster exposed to photocatalytic products of Paraquat

The Advanced Oxidative Processes have demonstrated potential for application in the degradation of organic pollutants, such as Paraquat (PQ) from water and wastewater, due to their low price, high efficiency, and non-toxic properties. In this study, we investigated whether the photodegradation of PQ with TiO2 nanotubes reduced its toxicity in Drosophila melanogaster. However, dietary ingestion of degradation products PQ for larvae resulted in a low axial ratio (pupal volume). In the adults, products of photodegradation of PQ exposure markedly diminished climbing ability in a time-dependent manner after 10 days of feeding. In addition, exposure of D. melanogaster to photodegradation of PQ reduced acetylcholinesterase and citrate synthase activities but improved oxidative stress, as evidenced by oxide nitric, protein carbonyl, and lactate production. These results suggest that the photodegradation of PQ with TiO2 nanotubes produced PQ fragments with higher toxicity than PQ, while the precise mechanism of its action needs further investigation.

Fatal Triad: Spontaneous Pneumothorax, Pneumomediastinum, and Pneumorrhachis in a Case of Paraquat Ingestion

Objective: Dependency on agriculture and the unregulated sale of paraquat makes it an easy alternative for homicidal and suicidal use in developing nations. It kills by multiorgan failure, predominantly pulmonary fibrosis, and ARDS. We report a case of alleged paraquat ingestion with spontaneous pneumothorax, spontaneous pneumomediastinum, and pneumorrhachis. Aim is to reinforce the importance of a high index of suspicion in early diagnosis when the above findings are present with ARDS in absence of trauma and a history of alleged substance ingestion. Case Presentation: A 35-year-old male presented with loose stool occasionally bloody, oral ulcers, yellow discoloration of eyes with fever, and decreased urine output for three days after consuming some substance with his seafood. On examination, he had yellow discoloration of eyes and oral mucosa along with multiple ulcers on the buccal region as well as the dorsum of the tongue and lateral margins with generalized subcutaneous emphysema. In addition, decreased air entry in the bilateral lung field and muffled heart sounds were present. He had an acute hepatorenal failure and severe metabolic acidosis with respiratory failure. Urine tested positive for myoglobin and muscle enzymes (creatinine kinase and lactate dehydrogenase (LDH)) were raised. He was intubated and shifted to the intensive care unit. Injectable N-acetyl cysteine (NAC) for acute liver failure was started with empirical antibiotics and intravenous fluids. We supplemented thiamine and vitamin K, and hemodialysis was done in view of progressive renal failure. Radiological evaluation showed spontaneous pneumothorax, pneumomediastinum, and pneumorrhachis which were managed conservatively. His respiratory parameters worsened despite maximal ventilatory support. Renal failure and metabolic acidosis worsened in spite of hemodialysis. He succumbed to his illness on day five of admission and seven days after toxin ingestion. Conclusion: We recommend that the sale of paraquat be restricted and regulated to avoid its use for suicidal and homicidal purposes. More research is required to find measures to intervene early and prevent pulmonary fibrosis. We propose that paraquat toxicity be considered early in a patient with the triad in an atraumatic setting with acute respiratory distress syndrome (ARDS).

Pulmonary Radiological Manifestations of Paraquat Poisoning: A Pictorial Essay.

Paraquat (1,1'-dimethyl-4,4'-dipyridylium) is a liquid herbicide, linked to both accidental and intentional ingestion, which can result in severe and frequently lethal poisoning. It has been known to cause injury to the lungs, kidneys, and liver. We retrospectively reviewed five cases over the last 4 years with a history of paraquat ingestion. The time duration between ingestion and high-resolution computed tomography (HRCT) was assessed. HRCT chest scan was variable, ranging from 4 to 18 days postexposure. The follow-up of the patients was also reviewed.

A study on Clinical features and management of Paraquat poisoning

Introduction: Paraquat is a widely used herbicide and a potent toxin. Ingestion, rather than inhalation, is the typical route of exposure associated with human toxicity. There have been systemic reactions following skin exposure after direct exposure to the skin (soaking of the skin with paraquat) or when the skin integrity has been breached (preexisting skin lesions or burn).Most paraquat deaths result from suicidal intent. Although paraquat ingestion leads to acute gastrointestinal tract necrosis and multiorgan failure, the lung is the target organ for toxicity among those surviving the immediate postingestion period. Material and Methods: This is a retrospective study conducted in the Department of Critical Care at NRI Medical College & General Hospital, Guntur. The study included patients with the ages above 14 years old who were presented to the Emergency Department with paraquat poisoning. This includes patients who were self-admitted or with witness account of paraquat exposure (ingestion, inhalational, mucosal or skin contact). Results: In our study, most of the patients were belongs to 26-35 years 17(48.5) followed by 18-25 years 9 (25.7), 36-45 years 6 (17.1), 46-55 years and more than 56 years were 5.7% and 2.8% respectively. The majority were male (n=29, 82.8%) and female (n=6, 17.1%) were least. The main symptoms and signs of studied patients include nausea (94.2%); vomiting (88.5%); Abdominal pain (91.4%); Paraquat tongue (88.5%), Oliguria (45.7%); Jaundice (37.1%), Respiratory distress (2.8%). For survived and non-survived patients, the Amount of ingested paraquat (mL) the mean ± SDwas 25.6±5.6 ml and 295±28 ml respectively. The difference was statistically significant (P=0.001). Conclusion: It is important to establish the diagnosis early and to pursue aggressive decontamination and prevention of further absorption. Increased awareness of the clinician and availability of the laboratory diagnostic methods will definitely help in successful management of paraquat poisoning. Paraquat poisoning is still a concern in developing countries. It may be useful to educate public health professionals and the general population about the serious consequences of exposure to this toxic agent. Paraquat poisoning is still no cure.

A Forensic Case of Suicide Ingestion of Paraquat Herbicide: New Histological Insights and Revision of the Literature.

Paraquat (PQ) is one of the most widely used herbicides in the world, and poisoning is generally associated with accidental, suicidal, or homicidal events. Therefore, in the forensic context, PQ could be in various ways involved as a possible cause of death of a subject. However, even though its systemic toxicity is known, the biological effects exerted on individual viscera have been explored only to some extent, especially in case of victim's survival. Therefore, a case concerning a suicidal ingestion of PQ with survival of 3 days was deemed of interest. Clinical toxicological analyses confirmed acute PQ intoxication, and after the death of the victim, an autopsy was performed showing local and systemic signs of ingestion of a caustic substance. Histologic examination revealed marked cellular damage to the major viscera, particularly the gastroesophageal tract, liver, kidneys, and lungs, with initial alveolar fibrosis noted despite the patient's short survival. This finding represents a new element in the context of PQ lung injury, as it has not been previously documented in the literature. Thus, histological findings in lethal intoxications after survival can reveal specific peculiarities still unknown and, therefore, assume transversal relevance not only at forensic but also clinical level.

Occult paraquat poisoning causing pneumomediastinum and organizing pneumonia.

Pneumomediastinum is not an uncommon manifestation of lung toxicity in acute paraquat ingestion. The condition is almost invariably seen with other lung parenchymal abnormalities such as consolidations, ground-glass opacities and interlobular septal thickening. The diagnosis may be challenging in cases with no history of toxin exposure, presentation with a subacute illness and/or absence of typical local or systemic features of paraquat toxicity.

Host-Guest Formulation of Carboxylatopillar[6]arene with Ergothioneine as a New Antidote for Combinational Detoxification of Paraquat.

Paraquat (PQ) is exceptionally toxic to the human body. PQ ingestion can cause severe organ damage with a mortality rate of 50-80%, resulting from the absence of effective antidotes and detoxification solutions. Herein, a host-guest formulation is proposed, in which ergothioneine (EGT), an antioxidant drug, was encapsulated by carboxylatopillar[6]arene (CP6A) to achieve a combinational therapy for PQ poisoning. Nuclear magnetic resonance (NMR) and fluorescence titration were employed to confirm the complexation between CP6A and EGT as well as PQ with robust affinities. In vitro studies proved that EGT/CP6A significantly reduced PQ toxicity. Treatment with EGT/CP6A could effectively relieve organ damage caused by PQ ingestion and enhance the normalization of hematological and biochemical parameters. The host-guest formulation EGT/CP6A also improved the survival ratio in PQ-poisoned mice. These favorable outcomes originated from synergistic effects that PQ triggered the release of EGT to combat peroxidation damage and excess PQ was engulfed within the cavity of CP6A.

Dose ingested, vomiting, and outcome in patients ingesting a standard paraquat 20SL formulation

Background FAO specifications for liquid paraquat dichloride SL formulations require the use of an emetic agent to stimulate vomiting within 30 min of ingestion. To date, there is no high-quality evidence of efficacy, despite use of the PP796 emetic since 1979. We first examined the validity of patients’ self-reported dose of paraquat ingested by examining the relationship with blood paraquat concentration and time to death for patients ingesting the standard paraquat SL formulation in a Sri Lankan cohort. As a secondary outcome, we assessed whether ingestion resulted in vomiting within 30 min and whether vomiting was associated with good outcome. Methods Patients presenting with paraquat SL self-poisoning were prospectively studied in ten Sri Lankan hospitals in 2003–08. Data on reported dose ingested, incidence and timing of vomiting after ingestion, treatment received, plasma paraquat concentration, and outcome were collected prospectively on presentation to hospital. Time between ingestion and blood sampling was incorporated by covariate adjustment. Results 441 patients were recruited to the case series, presenting a median (IQR) of 3.0 (1.5–8.1] h post ingestion. Outcome was known for 435 patients of whom 322 (74.0%) died within 42 days, a median of 1.3 (0.6–4.4) days post ingestion. Median reported dose ingested was 15 to <30 mL. There was a highly significant linear trend between log plasma paraquat and reported dose ingested (p < .001); adjustment for the log of the time from ingestion to sampling further improved the model fit. Case fatality and median time to death also showed good agreement with estimated ingestion amount. 347/438 patients (79.2%) were stated to have vomited before reaching the study hospital with 300 (68.5%) vomiting within 30 min of ingestion; time to vomiting was unknown for a further 12 (2.7%). The proportion vomiting was strongly associated with reported dose ingested (p < .001); of note the proportion vomiting within 30 min only increased to 83.3% for the highest ingestion group. Patients vomiting within 30 min had higher plasma paraquat concentrations (p = .008), and higher hazard ratio in the adjusted Cox regression model of 2.01 (95% CI 1.45–2.77) compared to those who did not. Vomiting within 30 min was associated with a higher case fatality (241/295 [81.7%] vs 68/125 [54.4%], p < .001). Forty-three (47.3%) of the 91 patients who did not vomit before reaching hospital died (one had unknown outcome). Conclusion Importantly, we found good agreement between reported dose ingested and plasma paraquat concentration, case fatality, and time to death, suggesting that the reported dose is a valid marker for the dose ingested. Vomiting occurred within 30 min for 68.5% of patients, exceeding the characteristics for a purported effective emetic in the FAO specifications. However, vomiting within 30 min was associated with approximately double the risk of death compared to those who did not vomit, larger paraquat ingestions, and higher blood paraquat concentrations. In addition, death occurred in many patients who did not vomit, and the proportion vomiting within 30 min only reached 82.1% for the highest ingested dose group. Overall, we found no evidence of benefit resulting from incorporation of the emetic, suggesting that the current FAO specification is not effective at preventing deaths after ingestion of the paraquat SL formulation.

Paraquat-associated Severe Acute Kidney Injury—Study from India

To analyze the outcomes of severe acute kidney injury in patients with paraquat ingestion. This retrospective analysis of case records was done in our institute, a tertiary care government teaching hospital, over a period of 4 years. Of the total 1310 acute paraquat poisonings during this period, severe acute kidney injury (AKI), referred for nephrology management was observed in 60 patients. Common symptoms at presentation include vomiting, oral ulcers, and abdominal pain. Oliguric AKI was present in 26%. Need for renal replacement therapy was observed in 95% of the cases. Mortality was observed in 38 of the 60 patients (68%). Factors associated with mortality on Cox regression analysis include amount of consumption. Estimated duration of survival on analysis curves was 8 days in 50% after admission and 15 days after consumption in 50%. Paraquat poisoning is associated with grave outcomes of morbidity and mortality. Severity of AKI is significant in this poisoning. Amount of consumption, latency of referral play a major role in outcomes.

Pumpkin (Cucurbita pepo) Fruit Extract Attenuates Paraquat-induced Toxicity in Wister Rats

Introduction: Paraquat is a bipyridil herbicide commonly used in modern agriculture for weed and pest control. Paraquat poisoning usually occurs through direct ingestion for suicidal intent, causing mortality as a consequence to oxidative damage, inflammation and multi-organ failure.&#x0D; Objectives: In this study, we investigated the ameliorative potential of Cucurbita pepo fruit on paraqaut-induced oxidative damage, inflammation, hyperlipidemia, hepatotoxicity and nephrotoxicity in rats.&#x0D; Methods: Rats were orally administered paraquat (2 mg/kg b.w) with or without the fruit extract (500 mg/kg b.w) or resveratrol (3.57 mg/kg b.w) co-administration for 2 weeks.&#x0D; Results: We found C. pepo fruit extract significantly restored paraquat-induced oxidative damage, acute inflammation and hyperlipidemia. Reduced glutathione (GSH) concentration was significantly abridged in paraquat treated group, while the concentration of GSH increases substantially across groups administered fruit extract and resveratrol. Furthermore, paraquat induced concomitant reduction in the activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD), which was restored by the fruit extract and resveratrol. However, nitric oxide level demonstrated a substantial elevation in paraquat-treated group, but restored by both the fruit extract and resveratrol. Moreover, pumpkin fruit extract and resveratrol supplementation suppressed overproduction of total cholesterol, triglycerides, low density lipoproteins, high density lipoproteins and thus, alleviated paraquat-induced hyperlipidemia. In addition, administration of C. pepo fruit extract and resveratrol ameliorated the hepatotoxic and nephrotoxic effect caused by paraquat.&#x0D; Conclusion: We conclude that C. pepo fruit extract and resveratrol administration ameliorated oxidative damage, acute inflammation, hyperlipidemia, hepatotoxicity and nephrotoxicity caused by paraquat ingestion.

Paraquat Poisoning In Children – A Case Report

OBJECTIVES Accidental poisoning in children is a serious public health problem in developing countries, especially where chemicals used in agriculture are ingested. Paraquat is a herbicide which is still used in Pakistan. We report a case of fatal unintentional paraquat ingestion by 3 years old child who could not survive. Lack of care in the storage of paraquat lead to the poisoning but initial inappropriate management was also one factor in the fatal outcome. Detailed history and provision of poison containers are important in the proper management of patients with poisoning.

Prediction of mortality and morbidity following paraquat poisoning based on trend of liver and kidney injury

BackgroundParaquat is a non-selective herbicide that causes severe tissue damage in various organs including the liver and kidney. The aim of this study was to determine the trend of the liver and kidney injury in patients with paraquat poisoning.MethodsThis retrospective cross-sectional study was performed at the Khorshid Hospital referral poisoning emergency center. The medical records of all patients with acute paraquat poisoning admitted from March 2017 to October 2020 were reviewed. Demographic factors, liver and kidney function tests and outcomes were recorded. Patients were divided into two groups based on the outcome of mortality (death or survived). The two groups were compared in terms of changes in creatinine and liver enzymes during hospitalization.ResultsA significant difference in mean creatinine levels between the two groups was observed from the third day after admission. The peak median Cr was 3.5 mg/dl for deceased patients in day 6 and 1.47 mg/dl for survived patients on 4th day. Minor elevations of ALT and AST were present in those who died. Logistic regression analysis shows patients who had level of creatinine higher than normal from the 2nd to 6th day post overdose, the risk of mortality was 4.83 to 7.44 times more than patients with normal creatinine level. The mean (SD) area under the curve for outcome prediction was reported to be excellent for creatinine on the 8th day post overdose (85.7 ± 13.2). Creatinine was higher than 2 on the 8th day post ingestion and had a sensitivity 100% and specificity 85.7% for mortality prediction (P value, 0.05).ConclusionsThe risk of mortality secondary to paraquat ingestion was highly associated with a rise in creatinine. Minor elevations of ALT and AST were also present in those who died. The creatinine concentration on different days post overdose can be helpful in predicting the severity of poisoning especially when the serum paraquat levels are not available.

Phenotypic analyses, protein localization, and bacteriostatic activity of Drosophila melanogaster transferrin-1

Transferrin-1 (Tsf1) is an extracellular insect protein with a high affinity for iron. The functions of Tsf1 are still poorly understood; however, Drosophila melanogaster Tsf1 has been shown to influence iron distribution in the fly body and to protect flies against some infections. The goal of this study was to better understand the physiological functions of Tsf1 in D. melanogaster by 1) investigating Tsf1 null phenotypes, 2) determining tissue-specific localization of Tsf1, 3) measuring the concentration of Tsf1 in hemolymph, 4) testing Tsf1 for bacteriostatic activity, and 5) evaluating the effect of metal and paraquat treatments on Tsf1 abundance. Flies lacking Tsf1 had more iron than wild-type flies in specialized midgut cells that take up iron from the diet; however, the absence of Tsf1 had no effect on the iron content of whole midguts, fat body, hemolymph, or heads. Thus, as previous studies have suggested, Tsf1 appears to have a minor role in iron transport. Tsf1 was abundant in hemolymph from larvae (0.4 μM), pupae (1.4 μM), adult females (4.4 μM) and adult males (22 μM). Apo-Tsf1 at 1 μM had bacteriostatic activity whereas holo-Tsf1 did not, suggesting that Tsf1 can inhibit microbial growth by sequestering iron in hemolymph and other extracellular environments. This hypothesis was supported by detection of secreted Tsf1 in tracheae, testes and seminal vesicles. Colocalization of Tsf1 with an endosome marker in oocytes suggested that Tsf1 may provide iron to developing eggs; however, eggs from mothers lacking Tsf1 had the same amount of iron as control eggs, and they hatched at a wild-type rate. Thus, the primary function of Tsf1 uptake by oocytes may be to defend against infection rather than to provide eggs with iron. In beetles, Tsf1 plays a role in protection against oxidative stress. In contrast, we found that flies lacking Tsf1 had a typical life span and greater resistance to paraquat-induced oxidative stress. In addition, Tsf1 abundance remained unchanged in response to ingestion of iron, cadmium or paraquat or to injection of iron. These results suggest that Tsf1 has a limited role in protection against oxidative stress in D. melanogaster.

A rare cause of subcutaneous emphysema with pneumomediastinum and pneumoperitoneum in a young adult: Paraquat poisoning

Paraquat is a rapid-acting herbicide widely used in many parts of the world. Although it is considered safe when exposed to the body surface, ingestion of this substance is highly fatal. Organ damage is caused by the production of free radicals and the depletion of nicotinamide adenine dinucleotide phosphate (NADPH). Multiple organs are involved in the damage, particularly organs requiring high blood flow like lungs, heart, kidneys, and liver. There is no proven effective antidote for the poisoning, and it is nearly 100% fatal. Here, we report an 18 years old young male presenting with pneumo-mediastinum, subcutaneous emphysema with pneumo-peritoneum after paraquat ingestion, which is a rare presentation of paraquat poisoning.

Diquat Poisoning: Care Management and Medico-Legal Implications.

Acute chemical intoxication represents one of the major causes of Emergency Room admittance, and possible errors in diagnosis are extremely frequent, especially when patients present generic and non-specific symptoms. Diquat, a bipyridyl class of herbicides, exerts high intrinsic toxicity as a consequence of free oxygen radicals, leading to cellular death and organ dysfunctions. Following ingestion, with the major source of absorption for suicidal purposes, the chemical induces local irritating effects; systemic symptoms appear later, while specific symptoms can occur in the following 48 h. A smoker and hypertensive 50-year-old man arrives at the E.R., reporting that an episode of herbicide inhalation occurred few hours earlier. Physical examination evidenced alkalosis with hypoxemia, leucocytosis, mild hyperglycaemia and moderate increase in creatine kinase and myoglobin. Despite blood creatine kinase and myoglobin values that were higher than normal, he was prescribed with hydration and anti-pain therapy. During the night, the man left the hospital; he returned the next morning at 8:45 a.m., with cardiorespiratory arrest, medium fixed non-reactive mydriasis, diffused cyanosis of the skin and of the mucous membranes, as well as imperceptible pulse and peripheral pressure. Despite resuscitation attempts, the patient died at 9:30 a.m.; the body was immediately transferred to the morgue. Autopsy and toxicological analyses were carried out nine days later, evidencing paraquat ingestion for suicidal purposes. GC/MS analyses to verify the presence of diquat were performed on body fluids and gastric and colon contents; all specimens resulted positive, thus confirming the cause of death as herbicide ingestion (blood diquat concentration of 1.2 mg/L; more than twice the minimum to observe a systemic poisoning). The procedure followed for patient management resulted to be not in line with the provisions of both guidelines and good clinical practices. Staff did not perform clinical-diagnostical monitoring of the patient’s condition or ask for more specific analyses (i.e., serum creatine phosphokinase monitoring). This misconduct led to a decrease in the patient’s chances to survive.

Inflammatory Esophagogastritis and Acute Kidney Injury After Intentional Ingestion of Paraquat

Paraquat a rapidly acting, nonselective herbicide is a leading cause of fatal poisoning in many parts of Asia. 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 evidence-based treatment. We describe a clinical presentation of inflammatory esophagogastritis and acute kidney injury (AKI) in young adult male after intentional ingestion of paraquat. Dosage of paraquat is 200 ml. The patient has physical problems with swallowing, sore throat, nausea and vomiting, upper abdominal pain, and hematemesis. Intravenous fluid, immunosuppressant, and antioxidant was given to reduce the effect of toxins on target organs.

Paraquat-induced lung fibrosis and multiorgan failure

Paraquat is a herbicide which is widely used by agricultural communities worldwide. It is extremely toxic for humans and ingestion of as less as 30 mL of 20%–24% concentration is usually lethal. The lack of an effective antidote is a concern due to the fatal outcomes associated with ingestion of paraquat. Herein, we are presenting a case of fatal paraquat poisoning in a young male from a center in India. The clinical course was complicated by liver, renal, and lung injury. We also describe its mechanism of toxicity, clinical features, and newer strategies being tried for treatment.

The efficacy of hemodialysis on paraquat poisoning mortality: A systematic review and meta-analysis.

Paraquat (PQ) poisoning is a serious public health concern, especially in developing countries, due to its easy access and lack of awareness of potential harms. No effective treatment has been reported yet. Conventional hemodialysis (HD) is still used in many centers for excreting PQ or reducing acute kidney injury, but there is no consensus on its efficacy. Therefore, we aimed to review the HD efficacy in PQ poisoning mortality. We searched Web of Science, PubMed, Excerpta Medical Database, Google Scholar, Scopus, Cochrane, Web of Knowledge, Pro-Quest, ScienceDirect, Springer, Clinical Key, Scientific Information Database, Magiran, and Iran-doc, in publications before January 1, 2020. We compared patients who underwent HD (Group 1) with those who did not (Group 2). The outcome was considered mortality/survival. The data were analyzed by Comprehensive Meta-analysis Software. This systematic review and meta-analysis included five studies with a combined total of 203 patients. The patients in the Group 1 had higher mortality than Group 2 (odds ratio, 2.84; 95% confidence interval: 1.22-6.64; P = 0.02). There was no evidence of publication bias (P value for Egger's test = 0.833). Although HD did not affect the survival of patients, other variables such as the amount of ingested PQ, poisoning severity, the time between PQ ingestion and the start of HD, duration, and times of HD sessions may influence the results regarding mortality.

Glucocorticoid with cyclophosphamide for oral paraquat poisoning.

Glucocorticoid with cyclophosphamide for oral paraquat poisoning.

Survival from paraquat induced renal impairment in a 17 years old male

N, N’-dimethyl-4, 4’-bipyridinium dichloride (paraquat) is a herbicide commonly used in India that leads to fatal outcome on ingestion. Paraquat interferes in the intracellular electron transfer systems inhibiting the reduction of NADP to NADPH resulting in accumulation of superoxide radical causing lipid cell membranes destruction leading to various organ damage. Life threatening effects such as acute kidney injury as paraquat elimination is mainly by kidney, acute respiratory distress syndrome and multi-organ failure are the causes of mortality in paraquat poisoning. There is no specific antidotes for paraquat poisoning so prevention and aggressive decontamination remains the mainstay of management in case of exposure or ingestion. Paraquat poisoning presentation may vary in cases depending on the amount of paraquat consumed and thus the outcome. Here we report a case of a 17 years old male who presented with acute kidney injury following ingestion of paraquat in a suicidal attempt. In our case, induced vomiting of the stomach content readily after ingestion of the poison, early haemodialysis, use of immunosuppression such as methylprednisolone, cyclophosphamide and antioxidants such as acetylcysteine, Vitamin C and Vitamin E as free radical scavenging agent , supportive measures such as adequate hydration and antibiotics might have helped in the patient’s survival. The case fatality remains very high in paraquat poisoning till date owing to lack of effective treatment options.