A novel low-metabolism strategy combined with multimodal detoxification for successful management of high-dose diquat–paraquat mixed poisoning: A comprehensive therapeutic analysis

Abstract

Combined diquat and paraquat poisoning is a rare but clinically significant form of poisoning, associated with severe oxidative stress and multiorgan failure. Historical case series have reported high case fatality, particularly following high-dose exposure. The absence of specific antidotes and standardized treatment protocols for mixed poisoning necessitate innovative therapeutic approaches. We present the case of an adolescent girl in her early teens who ingested 100 mL of a commercially obtained but illegally formulated diquat–paraquat mixture (200 g/L). A novel low-metabolism strategy was implemented, comprising low-concentration oxygen therapy (fraction of inspired oxygen (21%–30%), targeted sedation/analgesia, β-blockade, temperature management, and multimodal detoxification). Plasma toxin levels decreased by >97% within 20 h. Despite complications including anuria, cerebral edema, and respiratory failure, the patient achieved complete recovery after 49 days. Low-metabolism strategy reduced cellular oxygen consumption, mitigated oxidative damage, and enabled effective elimination of toxins. Dynamic monitoring guided tailored organ support. The integration of low-metabolism strategy timely and multimodal detoxification may represent a promising, albeit resource-intensive, approach for severe bipyridinium herbicide poisoning. This strategy warrants further validation in controlled studies and offers a potential framework for cases with severe poisoning.

Keywords

Diquat–paraquat mixed poisoning low-metabolism strategy multimodal detoxification oxidative stress organ support

Introduction

Diquat (DQ) and paraquat (PQ) are bipyridinium herbicides renowned for their high toxicity and capacity to induce multiorgan dysfunction syndrome (MODS) through redox cycling and excessive reactive oxygen species (ROS) generation.^1,2 Although structurally analogous, their pharmacokinetic profiles differ significantly. PQ accumulates preferentially in the lung tissue via polyamine transporters, disrupting mitochondrial complexes I and III and leading to ROS-mediated pulmonary fibrosis and acute respiratory distress syndrome (ARDS).¹ In contrast, DQ inhibits mitochondrial complex I (nicotinamide adenine dinucleotide (NADH) dehydrogenase), resulting in systemic ROS overproduction with primary toxic effects on the kidneys, liver, and cardiovascular system.³ Mortality rates for PQ and DQ poisoning range from 50% to 70%⁴ and 25% to 40%,^5–7 respectively. Following China’s regulatory restrictions on PQ, DQ usage has surged, with a concomitant increase in severe systemic toxicity due to exposure to high doses.⁸ Despite national bans, illegally formulated or sold herbicide mixtures containing PQ remain accessible in some regions.

Although clinically rare, mixed DQ–PQ poisoning presents heightened risks due to potential synergistic additive or synergistic effects, potentially accelerating the progression to multiorgan failure.^1,3 A comprehensive systematic review of 1220 experimental mixtures⁹ revealed additive, synergistic, and antagonistic effects in equal proportions, highlighting the variability of combined toxicity. However, the molecular pathways underlying DQ–PQ interactions remain unclear, complicating clinical management strategies.^10,11 Current toxicology guidelines predominantly address individual herbicide poisoning scenarios and lack evidence-based strategies for managing combined toxicity, particularly that involving supralethal doses. No previous case reports have detailed comprehensive diagnostic or antidote strategies for mixed DQ–PQ poisoning.

In this report, we describe the implementation of a novel low-metabolism strategy (LMS) to reduce systemic oxygen consumption and mitigate ROS bursts in a case of acute herbicide poisoning. In contrast to conventional supportive care, LMS integrates low-concentration oxygen therapy, targeted sedation, β-blockade, and precise temperature management to systematically lower metabolic demands, an approach that fundamentally differs from standard intensive care unit (ICU) practices. Herein, we report the management of high-dose DQ–PQ mixed poisoning (with ingested doses exceeding typical lethal thresholds) through the early application of LMS combined with multimodal decontamination. Dynamic monitoring of toxin levels was performed using high-performance liquid chromatography with tandem mass spectrometry (HPLC-MS/MS), organ function was evaluated using serial ultrasound/computed tomography (CT) imaging, and systematic support was guided by ROS dynamics. LMS aimed to mitigate oxidative stress by blocking ROS amplification pathways, whereas multimodal decontamination (including gastrointestinal lavage and adsorbent administration) reduces the bioavailability of toxins. This integrated approach prevents irreversible organ damage despite exposure to a supralethal dose, thus supporting the potential efficacy of combining metabolic modulation with intensive monitoring. This case underscores the need to further elucidate DQ–PQ interaction mechanisms and develop evidence-based approaches for mixed herbicide poisoning.

Materials and methods

The reporting of this case conforms to the Case Report (CARE) guidelines.¹²

Patient presentation

An adolescent girl in her early teens presented to the emergency department approximately 49 min after intentional ingestion of approximately 100 mL of a commercially available herbicide (Figure 1). The product label indicated “DQ 20% soluble liquid concentrate;” however, subsequent toxicological analysis confirmed the presence of both DQ and PQ (Section 2.2). Initial clinical manifestations included notable oropharyngeal ulceration (Figure 2), persistent vomiting, and significant abdominal pain. The patient’s medical history was unremarkable, with no preexisting conditions or regular medications.

Figure 1.

Toxicant: Diquat 20% soluble liquid concentrate.

Figure 2.

Aphthous ulcer: Oral mucosal ulceration following toxic substance ingestion.

Diagnostic and monitoring protocol

Toxin quantification

HPLC-MS/MS was employed for the specific identification and precise quantification of DQ and PQ concentrations in both gastric fluid and serial blood samples, confirming the presence of both compounds based on distinct retention times and mass spectra.

Advanced imaging

Comprehensive thoracic and cranial CT scans were performed at strategic time points to assess the progression and resolution of organ damage. In addition, ultrasound examinations were conducted regularly to monitor the cardiac function, pulmonary status, and volume status.

Laboratory investigations

Serial measurements were performed for complete blood count (white blood cell (WBC) count and platelet count (PLT)), renal function (creatinine and urea), hepatic enzymes (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)), cardiac biomarkers (troponin I and B-type natriuretic peptide (BNP)), coagulation profile, and arterial blood gas analysis to assess acid–base status and oxygenation.

Therapeutic interventions

Multimodal detoxification protocol

Gastrointestinal decontamination

Immediate and thorough gastric lavage was performed on admission. This was followed by the administration of activated charcoal (30 g) and montmorillonite (30 g) to adsorb the remaining toxins, and mannitol (250 mL) was administered as a cathartic agent to enhance elimination.

Whole-bowel irrigation (WBI)

WBI was implemented to prevent continued toxin absorption from the gastrointestinal tract.

Blood purification techniques

Continuous venovenous hemodiafiltration (CVVHDF) was initiated alongside intermittent hemoperfusion (HP) at a blood flow rate of 200 mL/min with administration of 35 L/24 h of replacement fluid for rapid clearance of circulating toxins.

LMS

Low-concentration oxygen therapy

Fraction of inspired oxygen (FiO₂) was maintained at 21%–30% with a target peripheral capillary oxygen saturation (SpO₂) of 85%–90% to limit substrate availability for ROS generation.

Sedation and analgesia

Continuous infusion of propofol (2 mg/kg/h) and dexmedetomidine (0.5 µg/kg/h) was provided to minimize agitation, reduce respiratory muscle work, and lower overall oxygen consumption.

β-blockade

Esmolol was administered (initial bolus (0.5 mg/kg), followed by infusion (50–200 µg/kg/min)) to maintain the heart rate between 60 and 80 bpm, reducing the demand for myocardial oxygen.

Temperature control

Core body temperature was strictly maintained between 36.5°C and 37.5°C using environmental controls to prevent fever-induced hypermetabolism.

Adjunctive therapies

Antioxidant administration

High doses of vitamin C (3 g/day for 38 days) and glutathione (2.4 g/day for 38 days) were administered to neutralize ROS and mitigate oxidative stress.

Immunomodulation

Methylprednisolone sodium succinate(500 mg/day for 3 days, tapered) and cyclophosphamide(single dose of 15 mg/kg) were administered based on local consensus guidelines, acknowledging the limited high-quality evidence for their efficacy in bipyridinium poisoning.¹⁰

Organ-specific support

Mechanical ventilation with lung-protective strategies, vasopressor support (noradrenaline 0.05–0.3 µg/kg/min) for hemodynamic stability, diuretics for volume management, and pirfenidone administration (600 mg/day for 37 days) were initiated from day 5 of hospitalization.¹³

Ethical considerations

Written informed consent was obtained from the patient’s legal guardian before the initiation of treatment and publication of this case report. The study protocol and therapeutic interventions were reviewed and approved by the Ethics Committee of the Fifth Affiliated Hospital of Guangxi Medical University (Approval No.: LW2025-DECISION-010). All procedures adhered to the International Guidelines for Health-Related Research Involving Human Subjects (CIOMS 2016). All identifiable patient information was meticulously redacted to preserve confidentiality, and all imaging studies were anonymized to prevent patient recognition. We have deidentified all patient details, reporting age as a range and dates as months/years only.

Results

Toxin clearance kinetics

This multimodal detoxification approach achieved remarkable toxin clearance within 20 h of initiation. Blood DQ concentrations decreased from 38.42 to 0.62 µg/mL, representing 98.39% clearance. Similarly, PQ levels declined from 3.75 to 0.08 µg/mL, achieving 97.87% clearance (Table 1). These substantial reductions occurred despite the extremely high initial toxin burden, suggesting that early blood purification contributed to rapid toxin clearance, although redistribution also played a role.

Table 1.

Dynamic changes in toxicant concentrations in the gastric fluid and blood at different time points.

	Concentration (μg/mL)
Toxicant	49 min after ingestion	10 h after ingestion	20 h after ingestion	34 h after ingestion	88 h after ingestion	160 h after ingestion
DQ-GF	>100.00	N/A	N/A	N/A	N/A	N/A
PQ-GF	>100.00	N/A	N/A	N/A	N/A	N/A
DQ-B	38.42	3.04	0.62	0.2	0.05	0.04
PQ-B	3.75	0.3	0.08	0.04	0.02	<0.01

HPLC was performed to detect the toxicant concentrations.

DQ: diquat; PQ: paraquat; GF: gastric fluid; B: blood; N/A: not available.

Clinical course and organ system involvement

Days 1–2: initial stabilization phase

The patient presented with stable vital signs despite significant toxin ingestion. An immediate gastric lavage was performed, and the patient was transferred to the emergency intensive care unit (EICU) for intensive management. The LMS protocol was initiated along with multimodal detoxification. Antioxidant therapy included vitamin C, glutathione, and dexamethasone administration. Bedside ultrasound-guided fluid management was performed to prevent cardiac overload while ensuring adequate perfusion. By the end of day 2, toxin levels had decreased dramatically, although the patient remained critically ill.

Day 3: multiorgan dysfunction manifestation

The patient developed anuria, marked facial and generalized edema, and decreased consciousness. Respiratory function deteriorated significantly, with oxygen saturation fluctuating between 62% and 75%; partial pressure of arterial oxygen (PaO₂) was 52 mmHg despite supplemental oxygen. Ultrasonography of the lungs revealed increased pulmonary exudation. Laboratory findings indicated renal impairment (elevated creatinine level), myocardial injury (increased troponin I level), and hepatic dysfunction (elevated enzyme level). Serum toxin concentrations had decreased substantially (DQ = 0.20 µg/mL and PQ = 0.04 µg/mL); however, intracellular toxin effects maintained intense oxidative stress. Enhanced therapeutic interventions included mechanical ventilation with low-concentration oxygen, continued sedation and analgesia, and strict control of core body temperature and heart rate.

Day 4: progressive pulmonary involvement

Chest CT revealed bilateral multifocal pulmonary inflammation (Figure 3). The patient remained under severe oxidative stress; however, she continued to receive LMS-based organ support. Mechanical ventilation parameters were meticulously adjusted based on serial blood gas analysis. Fluid resuscitation with colloids and vasopressor adjustments, guided by bedside ultrasound, stabilized circulation before the hemodialysis sessions. Antibiotics were administered to treat the toxin-induced pulmonary damage and prevent secondary infections. These interventions resulted in gradual improvements in oxygenation and blood pressure stability.

Figure 3.

Thoracic CT (Day 4): Bilateral multifocal pulmonary inflammation. CT: computed tomography.

Day 5: neurological complications

DQ and PQ concentrations further decreased to 0.05 µg/mL and 0.02 µg/mL, respectively. With the resolution of overt oxidative stress, LMS was discontinued, and the focus was shifted completely to organ support. Ultrasound assessment revealed elevated mean cerebral blood flow velocity (96.8 cm/s), increased pulsatility index (1.25), and optic nerve sheath diameter expansion (0.46 mm), suggesting worsened cerebral edema due to excessive cerebral blood flow. Interventions included maintaining the MAP at approximately 70 mmHg, reduction of cardiac output using esmolol, and mannitol administration to lower intracranial pressure.

Days 6–8: transition to recovery phase

As the blood toxin levels significantly reduced, HP was gradually discontinued, while CVVHDF was continued. Pirfenidone was administered to prevent pulmonary fibrosis. Eight days after sedation reduction, the patient opened her eyes to verbal stimuli; however, she demonstrated poor muscle tone, flaccid paralysis, and no spontaneous limb movement (GCS 3: E1V1M1). CT revealed bilateral hypodensity in the basal ganglia, thalamus, and brainstem with associated swelling, consistent with toxic encephalopathy and cerebral edema. Bilateral lower lobe lung inflammation had resolved. Mannitol was administered to manage intracranial pressure.

Days 12–24: neurological recovery

By day 12, the patient’s oxygenation had improved sufficiently to allow extubation and discontinuation of mechanical ventilation. The endotracheal tube was removed, and oxygen therapy was initiated via a nasal cannula. On day 15, her mental status had improved significantly, and she could nod and move all limbs (GCS 15: E4V5M6). By day 17, she was able to lift her lower limbs and respond appropriately to commands, and a follow-up head CT showed reduced brainstem edema. On day 24, she spontaneously voided 200 mL of urine, her vital signs remained stable, and she was transferred to a general ward for continued rehabilitation.

Days 40–49: convalescence and discharge

After 40 days of comprehensive treatment, the patient showed remarkable improvement. Oxygen therapy was discontinued, urine output normalized, and chest CT showed significantly reduced inflammation and pulmonary edema. The patient was discharged on day 49, with normal organ function and no significant neurological deficits. Follow-up on day 78 post intoxication confirmed sustained recovery with no evidence of significant pulmonary fibrosis (Figure 4).

Figure 4.

Thoracic CT (Day 78): Resolution of pulmonary inflammation without significant fibrosis. CT: computed tomography.

Table 2 summarizes the patient’s initial clinical findings, including her general condition, history of toxin ingestion, clinical symptoms, and therapeutic regimen. The application of published DQ prognostic models¹⁴ to the patient’s early laboratory data classified her as being at high risk for mortality (predicted >90%), underscoring the unexpected nature of her survival, considering the ingested dose.

Table 2.

Clinical profile of DQ–PQ co-poisoning; summary of the patient’s initial clinical findings, including general condition, history of toxin ingestion, clinical symptoms, and therapeutic regimen.

Parameter	Value
Demographics
Age	12 years
Sex	female
Weight	48 kg
Basic diseases	none
Toxicant exposure
Toxicant	DQ + PQ
Toxicant formulation	Liquid (concentration: 200 g/L)
Route	Alimentary canal
Category	Oral, swallow
Estimated dose	100 mL
Time of first toxicant detection	49 min after ingestion
Key concentrations
DQ-GF (μg/mL)	>100.00
PQ-GF (μg/mL)	>100.00
DQ-B (μg/mL)	38.42
PQ-B (μg/mL)	3.75
Clinical symptoms
Burning sensation in oropharynx	√
Nausea/vomit	√
Abdominalgia/diarrhea	√
Hematochezia	×
Oropharyngeal/ esophageal ulcer	×
Have a fever	×
Cough	√
Short of breath	√
Chest tightness	√
Jaundice	√
Oliguria	×
Anuria	×
Dizziness	×
Headache	×
Spasm	×
Coma	√
Erythra	×
Pulmonary imaging changes	√
Treatment
Gastric lavage	√
Whole-bowel irrigation	√
Adsorbent	√
Drainage	√
Diuretic	√
Omeprazole	√
Glucocorticoid	√
Cyclophosphamide	√
Antibiotic	√
Vitamin C	√
Glutathione	√
Mecobalamin	×
Diuretic	√
Renal replacement therapy	CVVHDF + HP
Renal replacement therapy times	6 h
Interval time (h)
Poisoning and first gastric lavage	1.5 h after ingestion
Poisoning and first RRT	2.5 h after ingestion
MV	√
SPO₂ begins to decrease	30.5 h after ingestion
MV start time	31.5 h after ingestion
initial FiO₂	0.21
highest FiO₂	0.5
Weaning of MV	11 d
Hospitalized time	49 d
Discharge situation (outcome)	improved

HPLC was performed to detect the toxicant concentrations.

DQ: diquat; PQ: paraquat; GF: gastric fluid; B: blood; CVVHDF: continuous venovenous hemodiafiltration; HP: hemoperfusion; MV: mechanical ventilation; FiO₂: fraction of inspired oxygen; SPO₂: peripheral capillary oxygen saturation; RRT: renal replacement therapy.

√ stands for yes; √ stands for present; and × stands for absent.

Imaging and ultrasound findings

Serial thoracic CT scans (Supplemental Figures 1–9) demonstrated progressive resolution of the pulmonary edema and inflammation throughout the treatment course. Cranial CT images (Supplemental Figures 10–14) illustrate the development and subsequent resolution of brainstem edema. Bedside ultrasound examinations provided the following critical real-time information.

pulmonary assessment on day 3 showed B1 and B2 lines indicating interstitial edema;

cardiac ultrasound maintained normal cardiac output throughout;

volume assessment revealed inferior vena cava (IVC) diameter <1 cm (hypovolemia) on day 3, transitioning to a rounded appearance of the IVC in the short axis (volume overload) by day 6; and

cerebral blood flow assessment on day 5 indicated elevated flow velocities, suggesting cerebral edema.

Treatment-related adverse events

During treatment, the following adverse events were monitored and managed: (a) sedation-related hypotension requiring vasopressor adjustment; (b) catheter-related bloodstream infection treated using targeted antibiotics; and (c) electrolyte disturbances (hypokalemia and hypophosphatemia) during CVVHDF corrected via supplementation. No long-term complications of these events were observed.

Discussion

This comprehensive case report details the successful treatment of life-threatening, high-dose DQ–PQ mixed poisoning through the novel integration of LMS with multimodal toxin elimination. Despite the potent oxidizing properties of both toxins and their potential for combined organ damage, the patient recovered completely after early LMS intervention, comprehensive multimodal toxin removal, and systematic organ support. Our report examines the components of the treatment strategy, clinical implications, limitations, and future directions for research and clinical practice.

Treatment strategy efficacy

The therapeutic approach was strategically phased according to the progression of poisoning, although considerable overlap existed between the phases owing to the complexity of multiorgan involvement.

Initial treatment phase: toxin removal and oxygen metabolism reduction

Early toxin removal

The absence of specific antidotes for DQ and PQ poisoning necessitates timely and thorough decontamination. Because prognosis strongly correlates with the ingested dose and early toxin concentration, prompt removal and enhanced excretion of absorbed toxins are paramount during initial management.^10,11 Gastrointestinal decontamination is a key component of early management in bipyridyl herbicide poisoning primarily performed through gastric lavage, adsorption, catharsis, and WBI;^15,16 however, its routine use is not recommended in all forms of poisoning due to potential adverse effects. These methods effectively reduce gastrointestinal toxin levels, although the low lipid solubility of DQ and PQ limits the adsorption efficiency of activated charcoal, often necessitating its combined use with kaolin or WBI.^17,18 WBI, typically reserved for severe cases with large toxin doses, sustained-release formulations, or substances poorly adsorbed by charcoal, is associated with the potential risk of intestinal obstruction and requires further clinical validation for use in mixed poisoning scenarios.^17,18

Multiple studies have demonstrated that early CVVHDF combined with HP significantly reduces mortality in patients with PQ poisoning.^19,20 In this case, the patient underwent multiple high-volume gastric lavages followed by the administration of adsorption agents (activated charcoal and montmorillonite) in combination with WBI, substantially reducing gastrointestinal toxin absorption. CVVHDF with intermittent HP rapidly cleared blood toxin concentrations, with DQ levels falling from 38.42 to 0.62 µg/mL (98.39% clearance) and PQ levels reducing from 3.75 to 0.08 µg/mL (97.87% clearance) within 20 h post ingestion. This demonstrates the critical role of early blood purification in toxin elimination, suggesting that early blood purification contributed to rapid toxin clearance, with redistribution also playing a role.

Notably, the patient presented to the emergency department within 49 min of ingestion, enabling early gastric lavage and rapid initiation of blood purification. This early presentation was likely a critical determinant of survival as delayed intervention (>2–4 h) is associated with poorer outcomes in patients with bipyridyl poisoning.

Oxygen metabolism reduction (LMS)

Given the established pathogenic mechanisms of DQ and PQ, combined oral poisoning with these toxins triggers severe oxidative stress, ROS production, mitochondrial dysfunction, and apoptosis. Therefore, prompt reduction of oxygen metabolism through LMS to decrease ROS production and slow the progression of multiorgan damage is essential. In this case, LMS was systematically implemented to lower the systemic oxygen metabolism through several mechanisms.

Sedation, analgesia, and mechanical ventilation. Research indicates that combining sedation, analgesia, and mechanical ventilation significantly reduces the metabolic rate, improves oxygenation indices, and diminishes secondary organ damage in patients with poisoning.²¹ In our case, the patient received 20%–30% oxygen via mechanical ventilation with continuous sedation and analgesia to reduce agitation and respiratory muscle work, thereby lowering her overall oxygen consumption.

Temperature control. Experimental studies have demonstrated that mild hypothermia reduces apoptosis induced via oxygen–glucose deprivation/reperfusion by inhibiting ROS generation, improving mitochondrial dysfunction, and regulating DNA damage repair pathways in neuronal cells.²² In this case, the patient’s core body temperature was maintained at 36.5°C–37.5°C through environmental temperature control to prevent fever-induced increases in oxygen consumption, without active hypothermia induction.

β-blocker administration. The use of β-blockers improves myocardial oxygen supply–demand balance and reduces arrhythmia risk in toxic cardiomyopathy.²³ After the patient developed tachycardia (100 bpm), low-dose esmolol was administered to maintain her ventricular rate at 60–80 bpm, which significantly reduced her myocardial oxygen consumption.

LMS fundamentally differs from standard supportive care in its goal-directed reduction of metabolic rate to limit ROS production. Although the individual components of LMS (sedation, β-blockade, and temperature control) are employed in other critical care contexts—with evidence derived primarily from studies in non-poisoned populations—their systematic combination to induce a controlled low-metabolism state in acute poisoning represents a novel therapeutic approach. Early implementation of LMS during the critical 24–72-h post-poisoning period may have reduced cellular energy expenditure and slowed apoptosis, thereby creating a vital therapeutic window for multimodal toxin elimination and subsequent organ support.

Antioxidant and immune modulation

This case highlights the importance of balancing antioxidant therapy, immunosuppression, and anti-infection treatment. High-dose reduced vitamin C and glutathione levels likely reduced oxidative stress damage by neutralizing ROS.²⁴ Immunosuppressive therapy using methylprednisolone sodium succinate and cyclophosphamide are reported to attenuate the inflammatory cascade,²⁵ although secondary infection risks require careful monitoring and their use remains controversial, with a high-quality randomized controlled trial showing no survival benefit in PQ-poisoned patients.²⁶

Potential mechanisms of mixed toxicity

Although both DQ and PQ exert toxicity through redox cycling and ROS generation, their primary target organs differ. PQ preferentially accumulates in the lungs, whereas DQ predominantly affects the kidneys and central nervous system. Their combination may lead to a broader and more severe multiorgan insult through several hypothesized mechanisms: (a) competition for or saturation of shared detoxification pathways (e.g. NADPH depletion); (b) amplification of mitochondrial dysfunction across different cell types; and (c) systemic inflammatory cascade activation exceeding the threshold of single-agent poisoning. The clinical course in this case, with nearly simultaneous severe pulmonary, renal, and neurological involvements, supports the concept of accelerated organ injury, although definitive mechanistic synergy remains to be established.

Middle treatment phase: organ function support post detoxification

Following the initial treatment, serum concentrations of DQ and PQ declined rapidly. Given the potential for mixed poisoning to cause severe multiple organ dysfunction, the second treatment phase focused on supporting and protecting vital organ functions.

Respiratory system

PQ poisoning primarily causes apoptosis-mediated pulmonary fibrosis through mitochondrial oxidative stress and oxygen free radical production, with high-concentration oxygen potentially exacerbating pulmonary damage.¹ Although DQ is absorbed less by the lungs, high-dose exposure can cause significant pulmonary injury.³ The patient developed severe hypoxia early, and pulmonary imaging and bedside ultrasonography revealed substantial pulmonary involvement. Low-concentration oxygen ventilation (21%–30%) with appropriate positive end-expiratory pressure (PEEP) adjustments reduced pulmonary edema while avoiding oxidative stress exacerbation from high-concentration oxygen. Dynamic bedside ultrasound assessment of pulmonary edema guided ventilator parameter adjustments, proving critical for improving the prognosis. Given the risk of severe pulmonary fibrosis in later PQ poisoning stages, antifibrotic therapy with pirfenidone was initiated at an early stage (day 6).

Renal system

The pharmacokinetics and redox cycling of DQ establish the kidneys as the primary excretory organs and injury targets.³ Therefore, improving renal function and maintaining metabolic homeostasis are treatment priorities. The patient developed oliguria and anuria, exhibited elevated creatinine levels, and experienced metabolic disturbances during resuscitation; she was treated successfully with diuretics and continuous renal replacement therapy, resulting in significant improvement.

Cardiovascular system

High-dose lethal DQ poisoning can lead to acute circulatory failure.²⁷ In this case, the patient developed capillary leak syndrome (CLS), characterized by interstitial edema (generalized and pulmonary), myocardial injury (elevated cardiac troponin I and BNP levels), and hypovolemic shock. Circulatory stabilization was achieved with the use of colloidal fluids and vasopressors (noradrenaline). β-blockers controlled the heart rate to reduce oxygen consumption, whereas CVVHDF removed toxins and maintained homeostasis.

Nervous system

High-dose DQ or PQ poisoning can cause significant neurological damage, including toxic encephalopathy and pontine dissolution in severe cases.^28–30 The patient presented with coma and brainstem edema on cranial CT, which confirmed the presence of toxic encephalopathy. The treatment included diuretic dehydration and blood purification. To prevent hemodynamic instability and cerebral hypoperfusion, the arterial pressure was titrated using transcranial Doppler monitoring, maintaining an MAP of approximately 70 mmHg. Esmolol controlled her heart rate, while sedation/analgesia reduced myocardial oxygen demand and cerebral blood flow, preventing hyperperfusion and edema. This comprehensive approach facilitated gradual neurological recovery.

Post-treatment phase: rehabilitation

The patient was discharged after 49 days with normal organ function at the 78-day follow-up without significant pulmonary fibrosis or neurological deficits. Therefore, long-term follow-up and tailored rehabilitation programs are essential. Psychological support and social interventions are crucial for reducing the risk of repeat poisoning in adolescents; in our study, a psychologist was involved early to provide timely intervention.

Prognostic factors and clinical implications

Key factors contributing to survival include the following: (a) young age without comorbidities; (b) presentation within 49 min after poisoning; (c) early multimodal detoxification (gastric lavage + HP +CVVHDF); (d) implementation of LMS; and (e) comprehensive organ support (mechanical ventilation, hemodynamic management, cerebral edema monitoring).

In previous cases of high-dose DQ or PQ poisoning, conventional therapies (gastric lavage, blood purification, organ protection, and life support) were routinely administered, without LMS. Thus, LMS may be a critical determinant of success. We believe that the LMS intervention may have contributed to patient survival in this life-threatening case. Therefore, we recommend that LMS be used as an adjunct in the management of severe bipyridyl herbicide poisoning, regardless of whether exposure is to a single-agent or a mixture. Its potential utility should be further evaluated in controlled studies.

Limitations and future directions

We acknowledge that a multitude of interventions limit the attribution of success to a single modality. However, rapid toxin clearance (98% within 20 h) and the temporal association between LMS initiation and clinical stabilization suggest a potential role in metabolic control. Future studies should isolate these effects by using controlled or animal models. Oxidative stress was indirectly assessed via evaluation of lactate levels, inflammatory markers, and organ dysfunction, and the direct measurement of ROS biomarkers would strengthen future investigations. Multicenter randomized trials are needed to validate this approach and provide evidence-based guidelines. Furthermore, the total hospitalization cost was ¥280,000 (approximately US$39,000), highlighting the resource intensity of such care. Cost-effectiveness analyses and the development of simplified protocols for resource-limited settings are important considerations for future research.

Conclusion

This case suggests that LMS combined with early multimodal detoxification enables survival in severe bipyridyl herbicide poisoning, even at supralethal doses. Key elements included prompt decontamination, strict maintenance of FiO₂ at ≤30%, metabolic suppression (sedation, analgesia, ventilation, and heart rate/temperature control), and dynamic monitoring to guide organ support. Causality cannot be established from a single report; however, the temporal association between LMS initiation and clinical stabilization suggests a role of LMS in mitigating oxidative stress. This approach represents a conceptual shift from conventional care. Controlled studies and cost-effectiveness assessment are required before broader implementation.

Supplemental Material

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Supplemental material, sj-pdf-5-imr-10.1177_03000605261443923 for A novel low-metabolism strategy combined with multimodal detoxification for successful management of high-dose diquat–paraquat mixed poisoning: A comprehensive therapeutic analysis by Zhenhua Li, Zhiyuan Cen, Jing Wei, Gui Huang, Kai Mo, Huaixing Yan, Lijian Liang, Haihua Du, Xinwen Mai, Shixiong Yang, Shizhuang Wei and Wei Wang in Journal of International Medical Research

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Footnotes

Declaration of conflicting interests

All authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this manuscript.

Funding

This work was supported by the Emergency Medicine Department of the First People’s Hospital of Nanning and Guangxi Key Discipline of Medical and Health Care. The funders had no role in the study design, data collection, analysis, interpretation, or the decision to submit the manuscript for publication.

Supplemental material

Supplemental material for this article is available online.

ORCID iD

Zhenhua Li

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