We report a case series of four men aged 21–43, referred to the respiratory intensive care unit for paraquat (PQ) poisoning. The patients ingested 50–70mL of a 20% PQ solution and presented with symptoms within 2.5–13.5h, with plasma PQ concentrations ranging from 3.5mg/L to 11.5mg/L upon admission (Table 1). They received immediate symptomatic and supportive treatments, including gastric lavage with activated charcoal, antioxidants like vitamin E, and immunosuppressive therapy with cyclophosphamide, methylprednisolone, and dexamethasone. Precautions were taken to protect the stomach and maintain cardiovascular stability. Hemoperfusion therapy was performed until plasma PQ levels were undetectable, followed by at least 12h of continuous veno-venous hemofiltration therapy for all patients. Despite these measures, all patients developed respiratory failure requiring extracorporeal membrane oxygenation (ECMO).

Following PQ ingestion, the four patients experienced varied clinical courses (Table 1). Patient 1, with advancing pulmonary fibrosis, required intubation and invasive mechanical ventilation (IMV) on day 3, and despite ECMO on day 4, succumbed to cardiac failure on day 19 (Fig. S1). Patient 2, with stable arterial blood gas (ABG) until day 4, received ECMO on day 5, and developed systemic inflammatory response syndrome and hepatic failure, leading to death on day 16 after poisoning (Fig. S2). Patient 3, with severe ABG on day 4, underwent intubation and IMV, then ECMO on day 5, but gastrointestinal hemorrhage ensued, resulting in ECMO removal on day 8 and death on day 10 (Fig. S3). Patient 4, with worsening dyspnea and ABG on day 3, was stabilized initially with ECMO but later developed septic multiorgan dysfunction on day 12, dying from cardiac failure on day 21 (Fig. S4).

PQ poisoning induces systemic toxicity through the generation of reactive oxygen species, leading to multiorgan involvement. Conventional treatments have not been able to halt the lung fibrosis progression after PQ poisoning, death can occur anywhere between 5 and 31 days after lung injury.1 In large academic centers, ECMO has become a preferred treatment strategy for critically ill poisoned patients where standard resuscitative therapy or antidotes have not been effective, aiming to preserve organ perfusion and allow time for clearance of toxins.1,2 As lung transplantation (LT) is the only curative treatment for end-stage PQ-induced pulmonary fibrosis, ECMO has been reported to offer a temporary bridge to transplantation.3–5 However, can the routine implementation of ECMO in the management of PQ poisoning yield therapeutic benefits for patients?

While ECMO can temporarily improve oxygenation, our findings suggest that it does not prevent the progression to organ failure in PQ poisoning (Figs. S1–S4). The uniformly poor outcomes in this series indicate that ECMO may not be beneficial in the setting of progressive multiple organ failure. Overall, considering other reports,3–5 in cases where other organ failures are manageable and patients are accepted for transplant, ECMO may provide a temporary bridge to transplantation. This is particularly relevant given the resource-intensive nature of ECMO and the need for careful consideration of its use in the context of PQ poisoning.