|Year : 2020 | Volume
| Issue : 2 | Page : 142-144
Fatal paraquat poisoning: A case report and review of literature
Vijoy Kumar Jha1, Anand Shankar Kannapur2, Ravikumar Hiremath3
1 Department of Nephrology, Command Hospital Air Force, Bengaluru, Karnataka, India
2 Department of Critical Care Medicine, Command Hospital Air Force, Bengaluru, Karnataka, India
3 Department of Medicine, Command Hospital Air Force, Bengaluru, Karnataka, India
|Date of Submission||30-Nov-2019|
|Date of Decision||19-Dec-2019|
|Date of Acceptance||29-Dec-2019|
|Date of Web Publication||17-Apr-2020|
Dr. Vijoy Kumar Jha
Department of Nephrology, Command Hospital Air Force, Po- Agram, Bengaluru - 560 007, Karnataka
Source of Support: None, Conflict of Interest: None
Paraquat poisoning is almost fatal if associated with the features of systemic toxicity. In this case report, we present a case of fatal paraquat poisoning and a detailed review of its intoxication, systemic manifestations, and recent development in its management. We conclude that in a case of severe paraquat poisoning, even aggressive and invasive therapies in an intensive care unit are unlikely to improve prognosis.
Keywords: Acute kidney injury, alveolitis, dexamethasone, hemoperfusion, paraquat
|How to cite this article:|
Jha VK, Kannapur AS, Hiremath R. Fatal paraquat poisoning: A case report and review of literature. Curr Med Issues 2020;18:142-4
| Introduction|| |
Paraquat is a pungent smelling, bright green corrosive liquid, and is the second highest selling herbicide globally available as a 20% solution in many parts of Asia, Pacific nations, and the Americas. It is a rapidly acting, nonselective herbicide that is relatively inexpensive and is reasonably safe to be used in agriculture. However, accidental or deliberate ingestion has an extremely high case-fatality rate. It is a common method for intentional self-poisoning in rural areas and is rarely used by the urban population. In this case report, we report a case of fatal paraquat poisoning and a detailed review of the intoxication, its systemic manifestations, and recent development in its management.
| Case Report|| |
A 65-year-old male MK with no previous comorbidities was admitted in our hospital with an alleged history of 30 ml of 24% paraquat consumption 6 h back and had throat pain, nausea, and generalized abdominal pain. Clinically on admission, he was afebrile, vital parameters were normal, and oxygen saturation was 96% at room air. He was conscious, oriented, but restless, and his systemic examination was normal.
Investigations revealed leukocytosis, mild renal dysfunction, and mildly deranged transaminases [Table 1]. His viral parameters were normal and two-dimensional echo was normal. He was managed as a case of severe paraquat poisoning with gastric decontamination with activated charcoal, intravenous (IV) dexamethasone, IV N-acetylcysteine infusion, prophylactic antibiotics, and IV fluids. He had progressive deterioration in his clinical condition and developed multi-organ failure in the form of acute kidney injury (serum creatinine – 2.5–8.78 mg/dl) requiring renal replacement therapy, acute liver failure (serum bilirubin – 1.2–14.96 mg/dl, aspartate aminotransferase – 99–1362 IU/L, and alanine transaminase – 33–482 IU/L), acute lung injury in the form of fluid overload/acute respiratory distress syndrome (ARDS), and cardiac involvement in the form of tachyarrhythmia. In view of chest X-ray features suggestive of alveolitis [Figure 1], he was given one dose of injection cyclophosphamide 200 mg (renal modified dose). Arterial blood gas analysis was suggestive of severe hypoxemia and severe metabolic acidosis. He was put on invasive ventilation with a specific setting of ARDS – tidal volume of 350 ml, PEEP of 12 cm H2O, and respiratory rate of 20–22/min. He received three sessions of hemodialysis in view of oligoanuria, which he developed 2 days after admission. His condition deteriorated further in the form of refractory shock and worsening of sensorium. In spite of all the resuscitative measures, he succumbed to his illness after 8 days of admission.
|Table 1: Hematolgical and biochemical parameters of the patient after admission|
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|Figure 1: Chest X-Ray AP view showing bilateral fluffy opacities with nonhomogenous opacities both the lung fields.|
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| Discussion|| |
Paraquat, a bipyridyl compound, is concentrated inside many cells where after absorption undergoes redox cycling and release of superoxide radicals, which can cause direct cellular damage or react further to form other reactive oxygen species and nitrite radical. Redox cycling consumes Nicotinamide-adenine dinucleotide phosphate (NADPH), one of the cell's key antioxidant defenses. The organs most commonly affected are those with high blood flow with oxygen tension and energy requirements, particularly the lungs, heart, kidneys, and liver. The brain is unlikely to be affected, as paraquat does not readily cross the blood–brain barrier. Swallowing more than 30 mL of 20%–24% (w/v) of paraquat formulation is typically lethal. Treatment options are determined on an individual basis depending on the amount ingested and the time elapsed since the exposure. It includes activated charcoal or fuller's earth, hemodialysis or hemoperfusion, high-dose glucocorticoids and acetylcysteine. None of the current treatments has proven effective for patients with signs of severe poisoning, and prognosis is uniformly poor.
Paraquat is rapidly but incompletely absorbed from the gut after ingestion and rapidly distributes into other tissues, with maximum tissue levels reached about 6 h after ingestion resulting in relatively high concentrations in the lung, kidney, liver, and muscle tissues. Its elimination is primarily by the kidneys, and in severe poisoning, kidney function is greatly reduced, leading to much slower elimination.
Acute kidney injury indicates significant paraquat poisoning due to paraquat-induced acute tubular necrosis or volume depletion. Impaired renal function is associated with increased mortality, and the rate of increase in serum creatinine concentrations correlates with poor survival. Mixed acidosis is commonly observed due to a combination of respiratory acidosis from paraquat-induced alveolitis or aspiration pneumonitis and metabolic acidosis from diarrhea, acute kidney injury, mitochondrial toxicity, or hypotension. In the index case, the patient developed oligoanuria with rising creatinine 2 days after ingestion.
Chest infiltrates may be due to a direct effect of paraquat or aspiration and may include diffuse alveolar infiltrates or pneumomediastinum and reticulo-interstitial infiltrates several weeks or later postpoisoning from progressive fibrosis. No other poisons except paraquat can cause both severe oropharyngeal burns and systemic toxicity., Gastrointestinal decontamination is to be done to limit systemic toxicity if given within approximately 2 h of ingestion, but there is benefit from giving charcoal even after up to 12 h of ingestion in a lesser degree of poisoning. During initial resuscitation, oxygen therapy need not be administered unless there is severe hypoxemia, as it may exacerbate the oxygen-mediated cellular damage induced by redox cycling. Continuous pulse oximetry is required to monitor for deteriorating gas exchange.
Hemoperfusion or hemodialysis followed by continuous hemodiafiltration or repeated hemoperfusion may be beneficial if commenced within 4 h of poisoning., Extracorporeal therapies, such as intermittent hemodialysis or hemofiltration, should be nearly as effective in enhancing elimination at comparable blood flow rates because paraquat has low protein binding, and concomitant hemodialysis and hemoperfusion may be more beneficial. Hemoperfusion was not advised in this case, as the patient arrived 6 h after ingestion. However, in view of oligoanuria and renal dysfunction, he received three sessions of hemodialysis with minimal benefit.
Anti-inflammatory plus immunosuppressive therapy, primarily using a combination of cyclophosphamide and dexamethasone, reported no benefit; however, the results of some uncontrolled or small randomized trials suggested benefit. Modest benefits from immunosuppression regimens that included dexamethasone were noted from a large retrospective study, especially when combined with hemoperfusion. In our case, the patient received injection dexamethasone since admission and also a single dose of cyclophosphamide. The dose of dexamethasone was not tapered as there were features suggestive of alveolitis. The theory behind using imunosuppression is that as paraquat leads to an acute inflammatory response, interference with this may inhibit the processes that follow that then lead to lung fibrosis and death. The most widely studied regimen uses cyclophosphamide, MESNA, methylprednisolone, and dexamethasone. Dexamethasone, in particular, has been shown to increase the expression of P-glycoprotein and other transporters and has also been shown to possess the ability to ameliorate the histological and biochemical changes induced by paraquat.
If there is a negative urinary dithionite test on a fresh urine sample 6 h after ingestion, it suggests that exposure was minimal, and the patient can be medically cleared if asymptomatic. In our case, this test was not done, as patients' relatives had come with a definitive history of paraquat poisoning and the patient had developed overt systemic manifestations. This simple test is inexpensive and can be easily performed in a laboratory. Hundred milligrams of sodium dithionite is to be added to the 10 mL of 2 M sodium hydroxide and 200 μL of this solution is to be added to the 2 mL of urine. The presence of paraquat in urine is confirmed by a color change after the addition of a dithionite solution. In a single-center study from Korea, of 233 paraquat-poisoned patients, who were taken to the hospital within 12 h after ingestion, the plasma samples obtained on arrival were tested using the sodium dithionite reaction. The effects of aggressive treatment, including cyclophosphamide pulse and continuous venovenous hemofiltration, were evaluated retrospectively. The discharge survival rate was 41.6% (97 of 233). Ninety-seven of 142 patients with negative or equivocal plasma dithionite test survived. However, all 91 patients with positive plasma dithionite test died of multi-organ failure. Cyclophosphamide and/or continuous venovenous hemofiltration could not improve survival.
Many antioxidants such as acetylcysteine, Vitamin C, and Vitamin E are used on the basis that they have the possible benefit and low toxicity.
| Conclusion|| |
In severe paraquat poisoning, once systemic toxicity manifestations appear, aggressive and intensive therapies in an intensive care unit are unlikely to improve patients' clinical condition and mortality, and therefore, relatives should be counseled accordingly to accept the outcome.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that the patient's name and initial will not be published, and due efforts will be made to conceal patient identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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