Rescue with intralipid in severe aluminium phosphide poisoning with cardiovascular collapse

Dear Editor,

Aluminium phosphide (Celphos) poisoning is associated with high mortality due to rapid development of severe metabolic acidosis, myocardial dysfunction, and refractory shock. After ingestion, aluminium phosphide reacts with gastric acid to release phosphine gas, which inhibits mitochondrial cytochrome c oxidase, disrupts oxidative phosphorylation, and leads to cellular hypoxia and oxidative stress. The cardiovascular system is particularly affected, resulting in myocardial depression, arrhythmias, and circulatory collapse.[1] Management remains largely supportive as no specific antidote is available. We report a case of severe aluminium phosphide poisoning with refractory shock and myocardial dysfunction that showed marked clinical improvement following intravenous lipid emulsion (ILE) therapy.

An 18-year-old male weighing 80 kg presented with a history of intentional ingestion of two 3 g tablets of aluminium phosphide. He had multiple episodes of vomiting and abdominal pain. On admission, he was tachycardic, tachypnoeic, hypoxic, and hypotensive (a blood pressure of 80/60 mmHg), requiring noradrenaline infusion. Arterial blood gas analysis revealed severe metabolic acidosis [Figure 1]. Point-of-care cardiac ultrasound demonstrated global left ventricular hypokinesia, reduced left ventricular outflow tract velocity time integral, increased E-point septal separation, and an ejection fraction (EF) of 30–35%, suggestive of toxic myocarditis [Figure 2]. Cardiac biomarkers were elevated. Despite aggressive conventional management, including vasopressor support and non-invasive ventilation, the patient remained haemodynamically unstable.

Figure 1.

Serial lactate and bicarbonate trends during ICU course – The upper panel shows serial arterial blood gas (ABG) measurements obtained from 03 February 2026 to 06 February 2026 (a–f). Initial assessment (a) demonstrated markedly elevated lactate (11.5 mmol/L) with low bicarbonate (12.7 mmol/L), consistent with severe metabolic acidosis. Lactate levels progressively declined across subsequent measurements (b–f), reaching 0.9 mmol/L by 06 February 2026, indicating effective lactate clearance. Bicarbonate levels showed a steady rise from 12.7 mmol/L to a peak of 29.0 mmol/L at time point (d). The lower panel illustrates graphical trends: Lactate demonstrates a consistent downward trajectory, while bicarbonate shows an upward recovery trend with transient overshoot before normalisation. These findings collectively indicate reversal of tissue hypoperfusion and metabolic recovery over time

Figure 2.

(a-d). Point-of-care echocardiographic assessment before and after intravenous lipid emulsion therapy. (a and b) Pre-intralipid images showing reduced cardiac output parameters with an LVOT velocity time integral (VTI) of 13.3 cm and an E-point septal separation (EPSS) of 1.2 cm, corresponding to severely reduced left ventricular systolic function (estimated EF ≈ 30 to 35%). (c and d) Post-intralipid images demonstrating improvement in cardiac performance with VTI increased to 14.11 cm and EPSS reduced to 0.91 cm, corresponding to improved left ventricular systolic function (estimated EF ≈ 50 to 60%) following lipid emulsion therapy. LVOT:Left ventricular outflow tract; EF:Ejection fraction

In view of refractory shock, intravenous 20% lipid emulsion was administered [120 mL (1.5 ml/kg) over 10 minutes followed by 120 mL over 20 minutes].[2] This was followed by progressive haemodynamic stabilisation, improvement in metabolic acidosis, and reduction in vasopressor requirement. Repeat echocardiography showed marked improvement in myocardial contractility with recovery of EF to >50%, along with a declining trend in troponin I and pro-brain natriuretic peptide levels. The patient subsequently recovered and was discharged under stable conditions. ILE has recently been evaluated as an adjunct in aluminium phosphide poisoning. A randomised controlled trial demonstrated improvement in mean arterial pressure, arterial blood gases, and serum lactate levels with ILE.[2,3] These findings suggest that while ILE improves physiological parameters, its impact on survival remains uncertain. Nevertheless, our case highlights its role as a rescue therapy in refractory cardiogenic shock, where a clear temporal association between ILE administration and clinical recovery was observed.

The mechanism of action of ILE in aluminium phosphide poisoning remains incompletely understood. While the “lipid sink” theory explains its role in lipophilic drug toxicity, its applicability here is uncertain as phosphine is not classically lipophilic.[4,5] Alternative mechanisms may be more relevant, including provision of free fatty acids as myocardial energy substrates, stabilisation of cardiac cell membranes, and mitigation of mitochondrial dysfunction. The rapid clinical and echocardiographic improvement observed in our case supports a metabolic and mitochondrial mechanism rather than simple toxin sequestration. Timing and clinical context may also influence outcomes. While earlier administration has been suggested to be beneficial,[6] our case demonstrates that even when used after failure of conventional therapy, ILE may provide meaningful benefits in selected patients with severe cardiovascular compromise.

A key strength of this case report is the objective documentation of myocardial recovery using bedside echocardiography. The marked improvement in ventricular function, along with declining cardiac biomarkers, suggests reversal of toxin-induced myocardial depression. This aspect has not been extensively evaluated in prior clinical studies and provides important mechanistic insight.

However, as a single case, the observed improvement remains anecdotal, and a definitive causal relationship cannot be established. Concurrent therapies, including vasopressors and supportive care, may have contributed to recovery, and spontaneous improvement cannot be entirely excluded. In conclusion, while current evidence suggests that ILE improves physiological parameters, this case highlights its potential utility as a life-saving rescue therapy in refractory cardiogenic shock due to aluminium phosphide poisoning, with documented reversal of myocardial dysfunction.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that his names and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Disclosure of use of artificial intelligence (AI)-assistive or generative tools

The AI tools or language models (LLM) have not been utilised in the manuscript, except that software has been used for grammar corrections.

Author contributions

KCD, VP, VA, AR were involved in concepts, literature search, manuscript preparation, editing, review and approval.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.