Paraquat poisoning survival: A rare triumph over a deadly herbicide

B Deepak Kumar

Consultant – General Physician, Kauvery Hospital, Tirunelveli, Tamil Nadu

Abstract

Paraquat poisoning is a highly toxic and life-threatening condition, primarily affecting the lungs and kidneys, with a high mortality rate due to its protracted clinical course and lack of an antidote. This case report presents a unique instance of deliberate paraquat ingestion by a 16-year-old female who consumed 25 mL of 24% paraquat, followed by multiple episodes of vomiting. Despite the absence of typical symptoms, the patient was promptly managed with gastric lavage, activated charcoal, and hemoperfusion therapy on the day of admission. Laboratory results revealed acute kidney injury (non-oliguric), and arterial blood gas (ABG) analysis showed compensated metabolic acidosis. The patient was started on methylprednisolone, cyclophosphamide, N-acetylcysteine, and other supportive medications. Over time, her renal parameters improved, and a CT scan revealed subpleural ground-glass opacities indicative of pneumonitis. The patient showed symptomatic improvement with timely intervention and was discharged in stable condition. Although there is no specific cure for paraquat poisoning, timely recognition, precise diagnosis, and supportive care are essential for enhancing patient survival.

Keywords

Paraquat poisoning, acute kidney injury (AKI), hemoperfusion therapy, pulmonary fibrosis

Introduction

Paraquat is a synthetic bipyridyl salt herbicide marketed as paraquat, paraquat dichloride salt, and bismethylsulfate salt. [1] It is a toxic, bright green corrosive liquid, with a pungent smell. [2] Paraquat liquid products typically have concentrations ranging from 20% to 50% (the commonly available concentration being 24%), whereas the formulations applied in the field are diluted to concentrations between 0.07% and 0.14% [1], [3].

When consumed, paraquat is very poisonous. Concentrated solutions are known to corrode even mild steel and aluminium [3]. The lethal dose (LD50) for humans is estimated to be around 3–5 mg/kg, equivalent to ingesting approximately 10–15 mL of a 20% solution [1]. The clinical manifestation of Paraquat poisoning usually depends upon the amount ingested and can be classified into three categories: In cases of MILD poisoning (less than 20 mg per kg of body weight), patients usually remain asymptomatic with minor gastrointestinal symptoms and they have a good prognosis. A mucosal lesion in the form of ulceration and bleeding is more commonly seen in the oral cavity, pharynx and oesophagus. Strawberry tongue or Raspberry tongue is another important finding in paraquat poisoning. SEVERE poisoning (20-40 mg  per kg of body weight), in which patients develop acute kidney injury and dysfunction, acute hepatic injury with elevated bilirubin and transaminases levels, acute alveolitis leading to progressive pulmonary fibrosis, with death occurring in 4 to 5 weeks; and FULMINANT poisoning (more than 40 mg per kg of body weight), in which patients develop renal failure, cardiac arrhythmias, coma, convulsions, and oesophagal perforation leading to death within hours to a few days after ingestion. The mortality rate is around 60-90% in patients with high-dose poisoning, with the lethal dose being around 20 ml [4]

Severe and fulminant Accidental or deliberate ingestion of paraquat is associated with a high mortality rate, and it produces both local and systemic toxicity [4]. The main acute systemic effects are pulmonary edema, convulsions, cardiac, renal, and hepatic failure [2]. The clinical course of paraquat poisoning is often protracted and there is no known antidote for this toxin. [3]

The kidneys and lungs are the primary targets of paraquat toxicity [2]. While lung toxicity is the hallmark of paraquat poisoning, the toxicity from inhalation is relatively uncommon. The kidneys actively secrete paraquat, accumulating large amounts in the proximal tubular epithelial cells, which results in renal toxicity. When paraquat accumulates in the pulmonary alveoli, it triggers redox cycling and the formation of reactive oxygen species (ROS), causing oxidative stress. This oxidative stress overwhelms cellular defence mechanisms and leads to alveolitis and fibrosis [3]. The first lung damage, occurring at low doses, gradually transforms into pulmonary fibrosis. This happens due to the rapid and excessive proliferation of fibroblasts, which ultimately destroys the pulmonary architecture [3]. Pulmonary fibrosis is usually the most common cause of death.

The absence of an antidote for paraquat poisoning makes timely intervention critical. For patients presenting within one hour of ingestion, gastric lavage followed by activated charcoal administration is often recommended. However, these measures have not consistently demonstrated clinical benefit in cases of pesticide self-poisoning [3]. This case report highlights a rare and clinically significant case of paraquat poisoning, exploring the clinical features, management strategies, and outcome of the patient.

Case Presentation

A 16-year-old female presented to the emergency department with alleged history of consuming 25 mL of 24% paraquat at 7:30 a.m. on 28/08/2023. The case was deliberate self-harm by ingestion of paraquat. She reported multiple episodes of vomiting (4–5 episodes) but denied symptoms such as breathlessness, abdominal pain, giddiness, or palpitations.

On examination, her Glasgow Coma Scale (GCS) score was 15/15, their pulse rate was 116 beats/min, and her blood pressure was 154/60 mmHg. Cardiovascular examination revealed no findings of note (NFND). She was admitted to the IMCU, where a Ryle’s tube was inserted, and approximately 1500 mL of stomach contents were aspirated. A stomach wash with activated charcoal was performed.

A nephrology consultation was sought, following which the patient underwent hemoperfusion therapy for six hours. Laboratory investigations revealed normal white blood cell counts and a serum creatinine level of 0.72 mg/dL. She was initiated on a pulse dose of methylprednisolone (1 g IV per day for three days), cyclophosphamide (500 mg in 100 mL normal saline for two days), N-acetylcysteine (6 g IV in 100 mL normal saline), Edaravone, Cefoperazone-Sulbactam (1 g + 500 mg), low molecular weight heparin and high dose of antioxidants.

Arterial blood gas (ABG) analysis indicated compensated metabolic acidosis, and her renal parameters suggested acute kidney injury, creatinine being 1.23 (non-oliguric AKI). Cyclophosphamide was discontinued after two doses on day three, and treatment was switched to dexamethasone and pirfenidone. Her renal function returned to normal before discharge. Dexamethasone was tapered, and she was started on oral prednisolone with subsequent tapering of steroids done on an OPD basis. Psychiatric counselling was provided, and the patient was advised of long-term mental health follow-up to address underlying stressors and prevent a recurrence.

A CT thorax on day six revealed subpleural ground-glass opacities in the anterior segment of the left upper lobe and peripheral consolidatory changes in the bilateral lower lobes, consistent with pneumonitis. However, the patient showed no symptoms or signs of respiratory tract involvement later. The patient showed symptomatic improvement and was discharged in stable condition. The patient is now doing good with no symptoms or signs of Pulmonary fibrosis with subsequent follow ups and is in a healthy condition till now.

Discussion

Paraquat is a highly toxic bipyridyl herbicide that exerts its toxicity through redox cycling, leading to the generation of reactive oxygen species (ROS) [5]. This oxidative stress results in mitochondrial dysfunction, lipid peroxidation, and extensive cellular apoptosis, primarily affecting the lungs, kidneys, and liver [6]. In this case, the patient presented with vomiting, tachycardia, and hypertension, progressing to metabolic acidosis and AKI. These manifestations align with the known pathophysiology of paraquat toxicity, which involves both local and systemic effects. Locally, paraquat ingestion causes inflammation and ulceration of oral mucosa, the tongue, and the esophagus. Systemically, it leads to renal tubular necrosis, hepatic necrosis, and pulmonary fibrosis. [7].

The lungs are particularly vulnerable due to the active uptake of paraquat by alveolar epithelial cells, leading to progressive pulmonary fibrosis and respiratory failure [8]. Acute kidney injury is another frequent complication, often necessitating hemodialysis in severe cases [9].

The clinical course of paraquat poisoning can be insidious and often presents with nonspecific symptoms, such as nausea, abdominal pain, and vomiting. This can hinder early diagnosis, leading to delays in appropriate management and referral [3]. Misclassification in emergency settings often leads to inappropriate treatments, such as atropine administration or gastric lavage, which may worsen the patient’s condition. Studies have shown that atropinisation, a common response to presumed organophosphorus poisoning, can exacerbate toxicity and mask the signs of paraquat ingestion. Furthermore, oxygen therapy, often initiated as a precaution, has been shown to increase mortality due to free radical injury and should be avoided unless PaO₂ falls below critical levels (40–50 mm Hg). This highlights the importance of correct identification and the avoidance of unnecessary interventions [10].

Diagnostic confirmation can be achieved through urine or blood tests, with a plasma concentration exceeding 1.6 pg/ml at 12 hours post-ingestion being universally fatal [7]. In a low-cost setting, Urine dithionite test can be done to qualitatively screen the presence of Paraquat in the given sample. The chemicals used to do this test are Sodium hydroxide and Sodium dithionite which are easily available.    Add 5 to 8 ml of 4% (1N) Sodium hydroxide solution to 10 ml of Urine sample and add one teaspoonful of Sodium dithionite to the sample and mix gently. A blue or green 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

The long-term prognosis for patients with paraquat poisoning remains grim, as severe pulmonary fibrosis often leads to respiratory failure [3]. While no definitive antidote exists, various treatment approaches aim to mitigate toxicity.

  • As paraquat is a corrosive poison, early insertion of a nasogastric tube is advocated to maintain nutrition. Placing a nasogastric tube may be very challenging due to severe ulcerations and friable mucosa, which may lead to complications including perforation. If the patient is conscious with no vomiting on presentation in ER, consider gastric lavage with activated charcoal (1–2 g/kg)
  • Supplemental oxygen is not advocated as the oxygen free radical-mediated cytotoxic injury causes rapid worsening of pulmonary alveolar infiltrates leading to the cascade of acute respiratory distress syndrome and subsequent pulmonary fibrosis
  • Hemoperfusion/ Hemofiltration / Hemodialysis: Hemoperfusion with charcoal-based cartridges are initiated if the patient comes within 4 to 6 hours of ingestion, beyond which it is not useful. If the patient develops acute kidney injury, then standard indications for hemodialysis are applicable, but it is always useful to start hemofiltration at the earliest to avoid subsequent development of acute kidney injury due to paraquat.
  • Immunosuppressive agents: 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. In this case, both have been used to modulate the inflammatory response and reduce oxidative damage. However, these treatments require careful monitoring and are not universally effective [3].
  • Antioxidants: Paraquat poisoning initiates release of free radicals that cause depletion of antioxidants. This leads to renal and lung injury that leads to lactic acidosis and refractory shock. Administration of antioxidants has also been tried to overcome circulatory shock due to reactive oxygen species. N-acetyl cysteine (10-12mg/kg/hr IV infusion for 2 to 3 weeks) and Vitamin C are widely used antioxidants. Edaravone, a free radical scavenging antioxidant, is beneficial for protecting the kidneys and liver from paraquat poisoning by reducing oxidative stress and inhibiting inflammatory response but did not reduce pulmonary fibrosis
  • In severe poisoning cases, hemoperfusion, haemodialysis, and diuresis promotion can enhance paraquat clearance, though their efficacy remains variable [10].
  • Psychiatrist support and periodic psychological counselling plays a major role in treating this long stay hospitalised patient. [10]

As paraquat remains readily available in countries like India, its misuse for self-harm is a significant concern [10]. There is a need for an integrated approach to both paraquat treatment and prevention, particularly in light of India’s large agricultural sector and widespread paraquat use despite its high toxicity [10]. Additionally, classifying all pesticide-related suicides under a general “pesticide” category underrepresents the actual burden caused by herbicides like paraquat. By focusing on specific agents, such as herbicides, rodenticides, and insecticides, healthcare providers can better address the unique risks posed by these substances [11].

Finally, efforts to limit the availability of paraquat, such as selling it in diluted forms rather than concentrated solutions, could help reduce its misuse as a method of self-harm and also reduce the morbidity associated with it. Such measures, alongside more rigorous public health education and regulatory control, could mitigate the impact of paraquat poisoning. Moreover, the recognition of paraquat toxicity in medical training must be improved, as the current curriculum does not sufficiently address the clinical management of this lethal poisoning. This gap must be bridged to improve the early diagnosis and effective treatment of paraquat poisoning [11].

Despite the high fatality rate associated with paraquat poisoning, this case underscores the potential for recovery through prompt and multidisciplinary management. It highlights the importance of structured treatment protocols in navigating the complexities of this condition [3]. In this case, the patient presented with vomiting, tachycardia, and hypertension, progressing to metabolic acidosis and AKI. Timely interventions led to the mitigation of further damage and recovery of the patient.

Conclusion

In conclusion, while there is no definitive antidote for paraquat poisoning, early recognition, accurate diagnosis, and supportive management remain critical in improving patient outcomes. The ongoing challenge lies in improving awareness among both healthcare providers and the public, implementing preventive measures, and refining treatment protocols to address this potentially fatal poisoning.

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