Awake Venoarterial Extracorporeal Membrane Oxygenation: Saving Lives in Aluminum Phosphide-induced Myocarditis

CASE DESCRIPTION

A 52-year-old female presented to the emergency room in a state of shock, having ingested two tablets of aluminum phosphide 2 hours prior. Initial evaluation revealed a reduced left ventricular ejection fraction (LVEF) and metabolic acidosis, admission ECG is shown in Figure 1. She was categorized as SCAI shock stage D and scored (−3) on the survival after venoarterial ECMO (SAVE) score, indicating a high-risk status (risk class III) with a 42% in-hospital mortality rate. The venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated within 6 hours of poisoning using a USG-guided Seldinger technique. A 25Fr drainage cannula was employed in the right femoral vein, a 19Fr return in the left femoral artery, and a 7Fr distal perfusion cannula to sustain perfusion in the left lower limb. X-rays confirmed the appropriate placement of the drainage cannula in the intrahepatic IVC (Fig. 2). Remarkably, the patient was on room air during the ECMO initiation.

Within hours, the patient experienced episodes of ventricular fibrillation and tachycardia (Fig. 3), necessitating cardioversion and amiodarone treatment. Despite these challenges, ECMO support effectively maintained tissue perfusion. Lactate levels began to stabilize within a few hours of ECMO initiation, as evidenced by serial ABG analyses indicating a progressive improvement in acidosis and decreasing lactate levels (Table 1). At the 48-hour mark, severe myocardial depression led to pulmonary edema, requiring invasive positive-pressure ventilation. Careful management of fluid balance and diuretics effectively addressed the pulmonary complications.

By the 72-hour mark, signs of cardiac function recovery were evident. Consequently, a gradual reduction in ECMO blood flow commenced to alleviate the recovering heart’s afterload. Serial echocardiography over the subsequent 3 days (Video clip on journal's website) demonstrated a progressive improvement in left ventricular function. The ECMO support was systematically withdrawn, and after 84 hours, decannulation with the assistance of a vascular surgeon was performed. The patient was liberated from the ventilator the following day. Subsequent doppler scans ruled out lower limb vessel thrombosis, and the patient was discharged without any complications by the 7th day.

DISCUSSION

Aluminum phosphide ingestion is associated with high mortality rates.¹ Typically used as a rodenticide and grain storage fumigant, it releases phosphine gas upon ingestion, inhibiting cytochrome oxidase and causing cellular respiration disruption, oxidative stress, myocardial depression, circulatory collapse, metabolic acidosis, and multiorgan dysfunction syndrome (MODS).^2,3 Unfortunately, there is no specific antidote for this compound.⁴

Recent case series have highlighted the potential efficacy of VA-ECMO in patients with specific high-risk features following aluminum phosphide poisoning. These features include severe metabolic acidosis (pH ≤ 7.0), refractory shock despite maximum vasopressor and inotrope support, and a LVEF of <35%.⁵ Our case exhibited refractory shock and a low ejection fraction, warranting the use of ECMO support.

While VA-ECMO proved instrumental in this case, it is not without complications. Early detection and management of complications, such as left ventricular distension to prevent complications like aortic root thrombus, are crucial.⁶ Options for managing LV distension include vasopressor and inotrope titration, adjusting ECMO flows, utilizing IABP, and surgical venting of the left ventricle or left atrium when conservative measures fail.

The practice of initiating VA-ECMO in conscious patients is gaining traction due to its potential to reduce hospital-acquired infections, enhance patient comfort, and minimize nosocomial infections.⁷ In our case, the patient was successfully supported on awake ECMO for the initial 36 hours before necessitating mechanical ventilation due to pulmonary edema. Surgical decannulation at the arterial site followed by doppler scans to detect thrombosis is imperative.

CONCLUSION

The VA-ECMO stands as a viable life-saving intervention for severe myocarditis with reversible causes, such as viral infections or toxins like aluminum phosphide. Key factors for successful outcomes include early initiation of extracorporeal life support (ECLS) before the onset of MODS and robust multidisciplinary team support.

SUPPLEMENTARY MATERIAL

Supplementary videos to this article are available online on the website of https://youtu.be/oFiyIVLoS8E.

ORCID

Nishanth Selvaraj https://orcid.org/0000-0001-5912-1374

REFERENCES

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