Severe paraquat poisoning: a 5-year follow-up of a survivor

Paraquat (PQ) is a highly toxic bipyridyl herbicide that causes systemic toxicity through excessive production of reactive oxygen species, with selective lung injury as the hallmark of poisoning.^[1] Severe cases may manifest as acute lung injury progressing to irreversible pulmonary fibrosis and respiratory failure.^[2] Mortality remains high (50%-90%).^[3] Long-term follow-up data, serial chest computed tomography (CT) imaging, and detailed treatment experiences in severe PQ poisoning remain scarce. Here, we report a patient who developed severe PQ poisoning following the ingestion of PQ solution. After early and continuous blood purification combined with prolonged intensified immunosuppressive therapy, the patient survived and completed 5 years of serial chest CT follow-up.

An 18-year-old female (weight, 45 kg) ingested approximately 100 mL of 20% PQ solution (approximately 20 g, estimated to be approximately 10-20 times the reported lethal dose)^[4] on April 20, 2021. She underwent gastric lavage and catharsis at a local hospital before being transferred to the Second Hospital of Hebei Medical University 2 h later. Her initial vital signs and consciousness were unremarkable. The blood PQ concentration was 10.5 mg/L. Based on the exposure history, estimated dose, and toxicological findings, severe PQ poisoning was diagnosed. The initial white blood cell (WBC) count was 24×10⁹/L. Early gastrointestinal decontamination (activated charcoal and catharsis), continuous venovenous hemofiltration (CVVH), and twice-daily hemoperfusion (HP) were administered until plasma PQ levels became undetectable. Antioxidant therapy included intravenous N-acetylcysteine, vitamin C, and reduced glutathione. Long-term immunosuppressive therapy with methylprednisolone and cyclophosphamide was administered according to the protocol shown in supplementary Table 1. When the WBC count decreased to <1×10⁹/L, immunosuppressive therapy was not discontinued; the regimen was adjusted with granulocyte colony-stimulating factor support under rigorous hematologic monitoring. This approach highlights the concern that abrupt cessation of immunosuppression could lead to rebound inflammation and accelerated pulmonary fibrosis in patients with severe PQ poisoning.^[5]

Despite treatment, the pulmonary lesions progressively deteriorated (Figure 1). No supplemental oxygen was administered throughout the course, based on the treating team’s concern that oxygen-induced oxidative stress could exacerbate PQ-related lung injury. Hepatic and renal functions gradually normalized within 2 weeks without progression to organ failure. On day 50, treatment was discontinued because of financial constraints. At discharge, the ABG on room air showed arterial partial pressure of oxygen (PaO₂) 40.3 mmHg (1 mmHg=0.133 kPa) and arterial partial pressure of carbon dioxide (PaCO₂) 28.9 mmHg. The patient was discharged with a recommendation to continue methylprednisolone. Four months later (August 20, 2021), she returned for follow-up with stable vital signs. Over the subsequent 5 years, serial chest CT scans demonstrated progressive improvement in the pulmonary lesions (supplementary Figure 1). Unfortunately, quantitative pulmonary function testing and formal fibrosis scoring were unavailable at our institution during follow-up.

Figure 1. computed tomography (CT) findings and clinical manifestations during the acute phase of severe paraquat (PQ) poisoning. A: on April 20, 2021: initial CT; B: on April 25; C: on April 28; D: on May 1; E: on May 7; F: on May 11; G: on May 17; H: on May 25; I: on June 9; treatment was discontinued; J: on August 20: 4-month follow-up CT, showing survival with residual dyspnea and exercise intolerance.

PQ poisoning causes mortality through acute multi-organ dysfunction caused by oxidative stress and delayed pulmonary fibrosis.^[6] Massive ingestion can lead to acute renal failure, hepatic failure, and pulmonary fibrosis, with death occurring within 2-3 weeks.^[7] A three-grade classification system based on the ingested dose per kilogram of body weight has been widely adopted in our country.^[8] According to this classification, the patient would have been considered to have a very poor expected prognosis. However, despite severe pulmonary fibrosis with persistent respiratory failure, discontinuation of treatment because of financial constraints, and subsequent discharge, she survived and later delivered two healthy infants by cesarean section. This outcome underscores the limited predictive utility of the ingested dose alone.^[9]

Currently, no specific antidote is available for PQ poisoning. Treatment focuses on gastrointestinal decontamination, blood purification to enhance toxin elimination, and immunosuppressive therapy to attenuate inflammation and retard pulmonary fibrogenesis.^[10] However, conventional interventions often fail to arrest fibrosis progression.^[1] Despite progressive pulmonary fibrosis and respiratory failure, the patient survived. These interventions may have contributed to the favorable outcome, although causality cannot be established from this single case in the absence of a comparator. First, early and sustained blood purification may have enhanced the clearance of toxins released from tissue reservoirs, attenuated the inflammatory cytokine burden, and mitigated oxidative stress.^[9] Second, intensified and prolonged immunosuppression with high-dose glucocorticoids and cyclophosphamide may have attenuated pulmonary inflammation and retarded fibrogenesis.^[5] However, young age, the absence of comorbidities, individual variability, and other unidentified factors may also have contributed substantially. Additional favorable factors included transient hepatic and renal dysfunction that normalized within 2 weeks. Significant interindividual variability in outcomes persists even among patients with comparable serum PQ concentrations, highlighting the importance of individualized risk assessment.

Funding: None.

Ethical approval: Written informed consent was obtained from the patient for publication. This report was approved by the Ethics Committee of the Second Hospital of Hebei Medical University (2026-R634).

Conflicts of interest: None.

Contributors: ZQH and WN drafted the initial manuscript and revised subsequent versions. ZQH and WN contributed equally to this work and are co-first authors. YQA approved the final manuscript as submitted. YJW and QJ performed the literature search. MCZ prepared the figures.

All the supplementary files are available at http://wjem.com.cn.