Venoarterial Extracorporeal Membrane Oxygenation as a Bridge to Antidote Therapy in Severe Hydrogen Sulfide Poisoning: A Case Report

Q: What is the clinical evidence from this study?

Study design: Case Report. Population: Severe hydrogen sulfide (H₂S) poisoning with refractory cardiogenic shock (n=1). Intervention: Venoarterial extracorporeal membrane oxygenation (VA-ECMO) with intravenous sodium nitrite and methylene blue. Primary outcome: Recovery of cardiac function and neurologically intact survival to hospital discharge.

Q: What does this research mean for the field?

VA-ECMO bridging with unmodified sodium nitrite and methylene blue enables cardiac recovery and favorable neurological outcome in severe, refractory hydrogen sulfide-induced cardiogenic shock. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Murli Krishna; Tapas Kumar Sahoo; Pranay Labhashankar Oza; Kartik Munta; Jakkam Chaithanya

doi:10.5005/jp-journals-11006-0249

October 26, 2026Indian Journal of Critical Care Case ReportOpen Access

Venoarterial Extracorporeal Membrane Oxygenation as a Bridge to Antidote Therapy in Severe Hydrogen Sulfide Poisoning: A Case Report

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Why the study?

Treatment for severe hydrogen sulfide poisoning remains largely experimental, with no validated approach for patients presenting in refractory cardiogenic shock.

Key Points

To describe the application of venoarterial extracorporeal membrane oxygenation as a circulatory bridge to antidote therapy in a patient with life-threatening hydrogen sulfide poisoning.
Clinical case evaluation of a 33-year-old male industrial worker who suffered collapse, seizures, and refractory cardiogenic shock following acute occupational exposure to hydrogen sulfide gas.
Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated via right femoral cannulation at a flow of 3.5 L/minute alongside intravenous sodium nitrite (300 mg) and methylene blue (2 mg/kg/hour).
Baseline evaluation revealed a severely reduced left ventricular ejection fraction of 15%, arterial lactate of 14.9 mmol/L, troponin I of 345 ng/L, and a paradoxical rise in central venous oxygen saturation to 90%.
Unmodified dosing of 300 mg intravenous sodium nitrite was tolerated on the extracorporeal circuit, increasing methemoglobin levels to 6.7%.
Support with VA-ECMO and targeted antidotes resulted in recovery of left ventricular function and normalization of central venous oxygen saturation over subsequent days.

Study Design

Type

Case Report (n=1)

Multicenter

No

Structured PICO

P

Population

1 previously healthy 33-year-old male industrial worker in India with severe H₂S poisoning and refractory cardiogenic shock (LVEF 15%, lactate 14.9 mmol/L), followed through hospital discharge on day 11.

I

Intervention

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) via right femoral arterial (21-F) and venous (25-F) cannulae (flow 3.5 L/min) for 5 days as a hemodynamic bridge, combined with unmodified intravenous sodium nitrite (300 mg) and intravenous methylene blue (2 mg/kg/hour).

O

Outcome

Hemodynamic stabilization, recovery of left ventricular function (decannulated on day 5), and neurologically intact survival to hospital discharge on day 11.hard clinical

Limitations

Single-patient case report
Absence of established pharmacokinetic dosing data for sodium nitrite and methylene blue on extracorporeal circuits
Single-patient case report describing routine clinical care
No established pharmacokinetic data exist for sodium nitrite or methylene blue on extracorporeal circuits

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Implication

This case demonstrates that VA-ECMO can serve as a life-saving circulatory bridge in refractory H₂S-induced cardiogenic shock, allowing time for unmodified intravenous doses of hydrophilic sodium nitrite and methylene blue to reverse mitochondrial toxicity.

Abstract

care unit (ICU), becoming progressively hypotensive en route and requiring high-dose vasopressors.Point-of-care ultrasound showed a severely reduced left ventricular ejection fraction (LVEF) of 15%.Computed tomography demonstrated acute pulmonary edema and aspiration pneumonitis.Despite high positive end-expiratory pressure ventilation with 100% oxygen, mild hypoxemia persisted (SpO₂ 91%).Arterial blood gas analysis revealed metabolic acidosis BackgroundHydrogen sulfide (H₂S) poisoning remains a significant source of occupational fatalities and is the second most common cause of toxic gas-induced death worldwide.1 Besides endogenous production, H₂S is released from natural sources and from industrial sources, including sulfur mining, petroleum refining, sewage treatment, and animal feeding operations; major historical incidents in Poza Rica, Mexico, and Kaixian County, China, underline its lethality.1 The primary recognized biochemical lesion is inhibition of mitochondrial cytochrome c oxidase, blocking aerobic adenosine triphosphate (ATP) synthesis and driving anaerobic glycolysis and lactic acidosis; cardiovascular, respiratory, and central nervous system toxicity are the dominant clinical consequences.2,3 Treatment remains largely experimental, based on hyperbaric oxygen and nitrite/methylene blue antidotal therapy, with no validated approach for patients in refractory cardiogenic shock.4,5 case description A 33-year-old previously healthy male industrial worker lost consciousness while transferring chemical agents into a scrubber and was exposed to H₂S gas generated as a byproduct.A colleague who attempted rescue also collapsed.On initial on-site resuscitation, the patient was unresponsive and hyperventilating; blood pressure was 100/60 mm Hg, heart rate 140 beats/minute, and peripheral oxygen saturation 80%.Following a generalized seizure treated with midazolam, he was intubated and transferred to the intensive 1,

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Cite This Study

Krishna et al. (2026) conducted a case report in Severe hydrogen sulfide (H₂S) poisoning with refractory cardiogenic shock (n=1). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) with intravenous sodium nitrite and methylene blue was evaluated on Recovery of cardiac function and neurologically intact survival to hospital discharge.

synapsesocial.com/papers/6aee6bb371a7594806220acb https://doi.org/10.5005/jp-journals-11006-0249

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Venoarterial Extracorporeal Membrane Oxygenation as a Bridge to Antidote Therapy in Severe Hydrogen Sulfide Poisoning: A Case Report

Key Points

Study Design

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Venoarterial Extracorporeal Membrane Oxygenation as a Bridge to Antidote Therapy in Severe Hydrogen Sulfide Poisoning: A Case Report

Key Points

Study Design

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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