Management of a patient with paraquat poisoning – A case report

Abstract

Paraquat is a widely used herbicide known for its high toxicity and limited antidotal options. Accidental or intentional ingestion can lead to multiorgan failure and death, primarily due to pulmonary fibrosis. This case report presents a young adult male admitted to our ICU with acute Paraquat poisoning.

Introduction

Paraquat (1,1’-dimethyl-4,4’-bipyridinium dichloride) is a non-selective contact herbicide commonly used in agriculture. Its ingestion, even in small amounts, can be fatal due to its ability to generate reactive oxygen species (ROS), causing oxidative damage to multiple organs, especially the lungs,
kidneys, and liver(1). The toxic dose is estimated at 10–20 mL of a 20% solution, and death may occur within hours to days depending on the dose ingested and speed of medical intervention.

Case presentation

A 21 years old male with no known comorbidities presented to our ER with alleged history of consumption of paraquat poison (approx. 2-5ml). He was initially taken to outside hospital, where stomach wash was done and he was admitted there for 48 hours. During hospital stay he developed oral ulcers and progressively worsening RFT and hence he was referred to kauvery hospital for further management. On arrival in our ER he was hemodynamically stable. Initial lab investigations revealed deranged RFT.

He was admitted in ICU for further management. Urine sodium dithionate test was done which was positive, which is shown in following picture.

Picture – 1 Positive urine sodium dithionate test

He underwent a session of hemoperfusion. Repeat urine sodium dithionate testing was done 6 hours after completion of hemoperfusion which turned out to be positive. He underwent another session of hemoperfusion. Repeat urine sodium dithionate testing was negative. ENT surgeon opinion was obtained for pharyngeal examination which sloughing of mucosa of tongue and posterior pharyngeal wall. He was on conservative management. His RFT showed improving trend and there was no hypoxia and hence he was shifted to ward. Psychiatrist was involved and he advised regular follow up. He started to take oral feeds and hemodynamically stable and hence he was discharged.

Discussion

Paraquat poisoning represents one of the most severe forms of acute chemical poisoning encountered in clinical toxicology, especially in low- and
middle-income countries where the herbicide is readily available. Despite various treatment protocols being proposed over the years, the mortality
rate remains exceedingly high, particularly in cases involving large ingestions(2).

Pathophysiology

The primary mechanism of toxicity in Paraquat poisoning involves redox cycling and the subsequent generation of reactive oxygen species (ROS), particularly superoxide anions (O₂⁻). Once absorbed, Paraquat is actively taken up by alveolar epithelial cells in the lungs through the polyamine transport system. Inside the cells, Paraquat undergoes redox cycling, producing ROS such as hydrogen peroxide and hydroxyl radicals. These free radicals initiate lipid peroxidation, damage cellular membranes, and cause mitochondrial dysfunction(3). This cascade results in acute alveolitis, cellular necrosis, and ultimately irreversible pulmonary fibrosis.

Apart from pulmonary injury, Paraquat causes systemic toxicity involving the kidneys, liver, and gastrointestinal tract. Acute tubular necrosis is common, leading to oliguric or anuric renal failure(4). Hepatic dysfunction may result from direct oxidative injury or secondary to systemic inflammation. Oral mucosal and gastrointestinal tract ulcerations often develop due to the caustic nature of Paraquat, and they serve as early clinical indicators of poisoning severity.

Clinical Course and Diagnosis

The clinical course can be broadly categorized into three stages:

1. Initial phase (0–24 hours): Characterized by corrosive injury to the oropharynx and gastrointestinal tract, with symptoms like nausea, vomiting,
   and oropharyngeal ulcers.
2. Progressive organ damage (1–5 days): During this phase, pulmonary injury and renal dysfunction become evident. Hypoxia, dyspnea, and worsening renal parameters suggest systemic progression.
3. Terminal phase (>5 days): Marked by progressive respiratory failure due to alveolar collapse and fibrosis, often unresponsive to mechanical ventilation.

Diagnosis is primarily clinical, based on history and presentation. In some centers, urine dithionite tests and plasma Paraquat concentrations
may aid in risk stratification(5).

Urine sodium dithionite test

It is performed by mixing 10ml of urine sample with 2gm of sodium bicarbonate and 1gm of sodium dithionite. Based upon the colour of precipitate paraquat concenteration in sample can identified, which is explained in following picture.

Picture 2. Color of urine sodium dithionite test and their corresponding concenteration

Therapeutic Challenges

There is no specific antidote for Paraquat. Management revolves around reducing absorption, enhancing elimination, mitigating oxidative damage, and supporting failing organs.

1. Gastrointestinal Decontamination: Activated charcoal or Fuller’s earth (a clay-based adsorbent) can bind Paraquat if given within an hour of ingestion. Gastric lavage is discouraged unless performed very early due to the risk of further mucosal damage.
2. Hemoperfusion and Hemodialysis: Hemoperfusion using activated charcoal or resins may reduce plasma Paraquat levels if urine sodium dithionite test was positive(6). Its benefit decreases substantially over time due to rapid tissue uptake of the toxin. Hemodialysis is mainly supportive for renal failure rather than enhancing Paraquat elimination.
3. Immunosuppressive Therapy: A combination of high-dose methylprednisolone and cyclophosphamide has been proposed to suppress the inflammatory response in the lungs, potentially mitigating progression to fibrosis(7). Some studies report improved survival, but evidence remains inconclusive.
4. Antioxidants: The use of antioxidants such as Nacetylcysteine, vitamin C, and vitamin E has theoretical benefits due to their ROS-scavenging properties. However, clinical efficacy remains unproven, and they are often used as adjuncts rather than core therapy(8).
5. Supportive Care: Intensive monitoring in the ICU is essential. Oxygen therapy must be used cautiously because high inspired oxygen concentrations may exacerbate lung injury by increasing oxidative stress(9). Mechanical ventilation may be required, but survival beyond the need for intubation is rare.

Prognostic Factors

1. Ingested dose: A volume over 30 mL of 20% solution is often fatal.
2. Plasma Paraquat levels: Used with Proudfoot and Hart’s nomograms to estimate survival likelihood, where available(10).
3. Early onset of hypoxia or metabolic acidosis
4. Renal impairment within 48 hours
5. Mucosal ulcers: Suggest significant ingestion and predict systemic absorption

Conclusion

Paraquat poisoning is frequently fatal, especially in cases of intentional ingestion. Early identification, decontamination, and supportive care are essential. Public health strategies to restrict Paraquat access and develop effective antidotes are urgently needed Referances

1. Dinis-Oliveira RJ et al. Paraquat poisonings: mechanisms of lung toxicity, clinical features, and treatment. Crit Rev Toxicol. 2008;38(1):13-71.
2. Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol. 2011;72(5):745-757.
3. Suntres ZE. Role of antioxidants in paraquat toxicity. Toxicology. 2002;180(1):65-77.
4. Gil HW et al. Effect of blood purification on the clinical course of paraquat poisoning. Nephrol Dial Transplant. 2010;25(3):889–894
5. Lin JL et al. Combined methylprednisolone and cyclophosphamide therapy for paraquat poisoning. J Toxicol Clin Toxicol. 1996;34(4):397-403.
6. Dinis-Oliveira RJ. Paraquat poisoning: a puzzle to be solved. Toxicol Lett. 2012;212(1):1-5.
7. Wunnapuk K et al. Modelling the toxicokinetics of paraquat in humans. Clin Toxicol (Phila). 2014;52(7):617-628.
8. Hsu CW et al. Outcome of severe paraquat poisoning with acute respiratory failure. Int J Gen Med. 2008;1:91–96.
9. Lee EY et al. A case of successful treatment in paraquat poisoning with hemoperfusion and immunosuppressive therapy. Korean J Intern Med. 2001;16(3):209–213.
10. Lee Y, et al. The role of cytokines in paraquat-induced lung injury. Toxicol Appl Pharmacol. 2010;243(1):27–35.

Dr. Dhineshraj
DrNB Critical Care Medicine
Kauvery Hospital, Chennai

Mentor

Dr. Vetriselvam P
Associate Consultant Critical Care Medicine
Kauvery Hospital, Chennai