# Case report: acute phosphine inhalation poisoning in a patient with Down's syndrome

## TL;DR

A patient with Down syndrome survived severe phosphine gas poisoning through intensive supportive care, including mechanical ventilation and kidney therapy.

## Contribution

This case report highlights unique cardiac injury patterns and effective treatment strategies in phosphine poisoning with Down syndrome.

## Key findings

- Phosphine poisoning caused severe cardiac damage disproportionate to lung injury.
- Supportive treatments like PICCO-guided hemodynamic management and CRRT improved outcomes.
- Down syndrome and prior gas exposure may influence the severity of phosphine poisoning effects.

## Abstract

Phosphine, a highly potent insecticide, can cause damage to multiple physiological systems when inhaled by humans, including the nervous, circulatory, and urinary systems. Currently, there is no effective antidote for phosphine poisoning, which highlights the importance of systematic and effective supportive treatment.

This paper presents a case of a patient with Down syndrome who had a history of similar gas poisoning and was exposed to high-concentration phosphine gas within 10 min, resulting in inhalation poisoning and shock. Upon admission to our hospital, the patient’s left ventricular ejection fraction (LVEF) dropped to 34% (55%-75%), lactate dehydrogenase (LDH): 586 U/L (120–250 U/L), and creatine kinase-MB (CK-MB): 12.75 ng/ml (0–5 ng/ml), indicating severe cardiac function impairment. Treatment included mechanical ventilation and PICCO-guided hemodynamic management. During treatment, the patient’s whole-blood lactate concentration peaked at 12.5 mmol/L (nearly eight times the normal range), for which continuous renal replacement therapy (CRRT) was administered. Additionally, the comprehensive application of continuous norepinephrine infusion for circulatory maintenance, targeted correction of acidosis, and administration of metaraminol and dobutamine for inotropic support were crucial for improving the patient’s prognosis. Ultimately, the patient was successfully cured.

In this case, disproportionate myocardial injury relative to pulmonary injury was observed, which may be caused by acute exposure to high concentrations of phosphine. Furthermore, the patient’s history of similar gas poisoning and Down syndrome may also contribute to this manifestation. Given the lack of a specific antidote for phosphine poisoning, our supportive treatment emphasizes the importance of PICCO for shock management and early CRRT intervention for lactate elimination and internal environment stabilization. This report provides practical experience for the treatment of phosphine poisoning, particularly for associated cardiac function damage.