Survival After Paraquat Ingestion: A Case Series

Navaneethan Venkatachalam, A. Saras Monika, PD. Aravindan*

Department of General Medicine, Kauvery Hospital, Hosur, India

*Correspondence: dr.aravindan.hosur@kauveryhospital.com

Background

Paraquat is a broad spectrum, bright green, pungent liquid herbicide widely used across the world in agricultural applications and general weed control. Paraquat is commercially available as dichloride salt and dimethyl sulphate [1]. It belongs to a chemical group called quaternary ammonium salts and are generally known as quats. It is registered in India with CIBRC – Central Insecticide Board And registration committee and categorized as highly toxic [2]. Paraquat consumption leads to the formation of superoxide anion, singlet oxygen with hydroxyl and peroxyl radicals in cells, especially affecting lungs, kidney and liver. These reactive oxygen species leads to destruction of cell organelles inevitably leading to cell death. Cases of paraquat intoxication usually results from suicidal attempts and accidental ingestion rather than homicides. Gramaxone and Weedol are usually available brands in India [1].

Case Presentation

Case 1

A 24-years old male presented to ER with a history of paraquat consumption (50 ml) at his residence. The patient had multiple episodes of vomiting and was brought to ER after 4 h of consumption. On arrival, the patient’s vitals were stable, saturation was 97%, oral mucosa was normal and both lung fields were clear on auscultation. Gastric lavage was done with 50 mg of activated charcoal. His initial ABG and biochemical parameters were within normal limits. The patient was started on IV N-Acetyl Cysteine (NAC) infusion, Pantoprazole, antibiotics, antiemetics, and IV vitamin C. He was monitored in ICU.

Continuous Veno-Venous Hemofiltration (CVVH) with hemoperfusion was initiated within 4 h of hospital entry. On Day 3, he developed difficulty in swallowing and icterus. On examination oral mucosa was blanched and edematous with increased secretions. Oesophago- Gastro-Duodenoscopy (OGD) showed synechiae and inflammation with ulceration of oral cavity, epiglottis and aryepiglottic fold for which xylocaine viscus and mucaine gel were advised. Elective feeding jejunostomy was planned but withheld as he was tolerating oral fluids well.

Labs: SGOT – 229, SGPT – 192, urea – 92, creatinine – 3.44 and potassium – 2.9. IV potassium correction and glycopyrrolate were initiated. For the next 5 days, RFT and LFT showed an increasing trend. Five cycles of hemoperfusion and three cycles of hemodialysis were completed. On the eighth day, creatinine and LFT started decreasing and vitals were stable; hence shifted to ward.

On the tenth day, he developed difficulty in breathing with desaturation to 90 % on room air. Chest examination revealed bilateral fine crackles. CT chest revealed pulmonary fibrosis with consolidation in the lower zones, bilaterally. He was managed with oxygen support, IV steroids, and chest physiotherapy. The patient responded well and was discharged on the fifteenth day. He was doing well on follow-up.

Case 2

A 22-year- old male presented to the ER 4 h after ingestion of 25 ml of paraquat dichloride with suicidal intent. He complained of nausea and continuous emesis of clear fluid. He had a paraquat tongue (multiple erosions and superficial ulcers over tongue covered with yellowish necrotic debris after oral ingestion of paraquat). His vitals and physical examination were normal on admission. The patient underwent gastrointestinal decontamination with 30 g of activated charcoal. He was started on NAC infusion, steroids, antibiotics, IV Vitamin C, and antiemetics. The patient was then transferred to the intensive care unit for further care. He was immediately started on continuous venovenous hemoperfusion.

Survival-After-Paraquat-Ingestion-1

Fig. 1. Paraquat Tongue. Adapted from RK. Patel [11].

His blood parameters were within normal limits on Day 1. On Day 2, the second session of hemoperfusion was done for 4hrs with regulated heparin at a blood flow rate of 300 ml/h. His LFT/RFT post hemoperfusion was urea-47, creat-2.1, SGOT-32, SGPT-28. Totally 3 cycles of hemoperfusion were done. He was then given intensive psychiatric counselling. The patient requested discharge to settle his personal issues. Hence, he was discharged and had multiple follow-ups in OPD and was doing well after that.

Discussion

Paraquat is a commonly used herbicide in India. Suicides due to paraquat (PQ) are an important cause of morbidity and mortality, especially due to the absence of a specific antidote. Metabolism of paraquat generates free radicals that damage the cellular organelles and membranes, causing damage to many organs, especially the pulmonary alveolar epithelium.

Paraquat salts being caustic, the gastrointestinal tract can be severely injured after ingestion of a concentrated solution [4]. Once the large concentration of this poison accumulates in the lungs or renal cells, it leads to the generation of toxic reactive oxygen species through redox cycling, which devastates the cellular defensive system. Renal failure can result due to direct toxicity and hemodynamic changes. Conservation of renal function is vital to reduce plasma paraquat levels and thereby reduce accumulation in lung cells [4]. Symptoms of paraquat ingestion are usually dose-dependent, and intoxication can be categorized as mild, moderate, and fulminant. Mild intoxication can happen with doses ≤20 mg/kg, which usually produces minor gastrointestinal problems like transient vomiting, diarrhea, and oro-pharyngeal burns, but usually, complete recovery is possible. Moderate intoxication can occur with doses between >20 mg/kg and <50 mg/kg of the poison. Patient may suffer lung injury, pulmonary fibrosis, acute renal failure, and in the majority of cases, death occurs within 2–3 weeks. Fulminant intoxication of ≥50 mg/kg of the poison, may lead to death within 3 days, because of multiple organ failures [3]. In patients who survive longer, fibrotic changes in the alveoli result in gas exchange interference in the lungs and may progress to ARDS [4,5]. Diagnosis of paraquat poisoning is usually made based on circumstantial evidence [3]. In our patient, the clinical history, presentation, and documentation of paraquat consumption endorse the diagnosis positive.

Conventional treatment includes nasogastric tube fixation, gastric lavage with normal saline, charcoal-sorbitol lavage, forced alkalinized diuresis, and hemodialysis or hemoperfusion. Hemoperfusion with activated charcoal is effective if initiated within 4 h of paraquat intoxication [3]. Paraquat accumulation in lung tissues exerts a destructive effect, leading to hypoxemia, requiring mechanical ventilation. Ironically, oxygen supplementation may have a deleterious effect because it increases the number of toxic radicals. Oxygen should, therefore, be given only to correct hypoxemia [6]. Subsequent management includes antibiotics for supervening infection and supporting renal function with hemodialysis or filtration. Potent analgesics such as opiates may be required to alleviate intense pain from gastrointestinal tract injury, ulceration, and inflammation. Some antioxidants like vitamins C and E have been clinically used to protect against free-radical toxicity. N-acetyl cysteine is also used as an antioxidant because of its free radical scavenging property, and it will increase intracellular glutathione levels. Thereby, it will provide a protective effect on lung parenchymal cells [4,5]. There are currently no generally accepted guidelines on the treatment of patients with paraquat poisoning. While there is a paucity of evidence for effective treatment of paraquat toxicity, early treatment to induce vomiting or with gastric lavage, charcoal, and diatomaceous piles of earth may be helpful by reducing absorption. Once absorbed, hemoperfusion, hemodialysis, and continuous venovenous hemofiltration may be useful for lowering blood levels of paraquat. The continuous Venovenous Hemofiltration (CVVH) method utilizes convection via a transmembrane pressure gradient to filter solutes. It does not require dialysate fluid; instead, a substitute fluid is used to replace the filtered fluid. Alternative therapies that could be considered in the treatment of paraquat poisoning include immunosuppressant and antioxidant therapies. In our case, the patient was able to achieve a positive outcome. A possible explanation for this includes vomiting and early gastric lavage /charcoal leading to decreased absorption of paraquat, and CVVH to decrease the paraquat level after absorption. If our patient did not improve or had higher levels of paraquat after CVVH, immunosuppressant or antioxidant therapy could have been initiated. Knowing about the clinical presentation, evaluation, and treatment options for paraquat poisoning is important to reduce morbidity and mortality in these cases [7].

In a study by Lin et al., the therapeutic effect has been reported with high dose cyclophosphamide and glucocorticoid where survival is about 75% [8]. An intensive care unit study and a meta-analysis conducted by Agarwal et al. concluded that immunosuppressive therapy with cyclophosphamide and glucocorticoids has a potential role in the management of paraquat poisoning in moderate to severe poisoning cases [9,10]. Since there is a lack of clear evidence-based therapy for paraquat intoxication, different approaches have been tried for supportive management [12].

Conclusion

The data on paraquat poisoning from our country is scanty. We report this data on the survival of paraquat poisoning. The unexplained combination of gastrointestinal symptoms, acute renal injury, and respiratory failure must be suspected of paraquat toxicity, even in the absence of ingestion history. Both urine and serum concentrations of samples at known time intervals post-ingestion are to be determined for assessing the severity of the intoxication and to predict survival chance. If a patient presents early, therapeutic interventions with hemoperfusion and dialysis are recommended to prevent pulmonary and multi-organ failure.

References

  1. Conditions of paraquat use in India – Dileep Kumar. A. D-2015.
  2. Insecticides/Pesticides Registered under section 9(3) of the Insecticides Act 1968 for use in the India (December 31, 2014. Central Insecticide Board and Registration Committee, Directorate of Plant Protection, Quarantine and Storage. Department of Agriculture and Cooperation, Ministry of Agriculture, Government of India. Downloaded from http://cibrc.nic.in/reg_products.doc on January 15, 2014.
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  8. Afzali S, Gholyaf M. The effectiveness of combined treatment with methylprednisolone and cyclophosphamide in oral paraquat poisoning. Arch Iranian Med. 2008;11:387-91.
  9. Agarwal R, Srinivas R, Aggarwal AN, et al. Experience with paraquat poisoning in a respiratory intensive care unit in North India. Singapore Med J. 2006;47:1033-7.
  10. Agarwal R, Srinivas R, Aggarwal AN, et al. Immunosuppressive therapy in lung injury due to Paraquat poisoning: A meta-analysis. Singapore Med J. 2007;48:1000-5
  11. RK. Patel, et al. A rare case of “Paraquat Tongue”. Indian J Dermatol. 2022;65(3):245-246.
  12. Madhan B, Arunprasad G, Krishnan B. Paraquat tongue. BMJ Case Rep. 2014;2014:bcr2014206581.
Dr.-Navaneethan-Venkatachalam

Dr. Navaneethan Venkatachalam

General Medicine

Dr.-A.-Saras-Monikka

Dr. A. Saras Monikka

Consultant General Medicine

Dr.-P.-D.-Aravindan

Dr. P. D. Aravindan

Consultant Physician Specialist in Diabetes & Neurology

Kauvery Hospital