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Review
. 2023 Jun 25;11(7):555.
doi: 10.3390/toxics11070555.

Zinc Phosphide Poisoning: From A to Z

Anabell Juárez-Martínez  1 , Jesús Del Carmen Madrigal-Anaya  1 , Yessika Paola Rodríguez-Torres  1 , Ramsés Dorado-García  1 , Daphne Marisol Montes-Ventura  1 , Ahgiel Jiménez-Ruiz  2
Affiliations
Review

Zinc Phosphide Poisoning: From A to Z

Anabell Juárez-Martínez et al. Toxics. .

Abstract

Zinc phosphide is a rodenticide that is used in agricultural, urban and industrial environments in México. After ingestion, it reacts with hydrochloric acid, hydrolyzing into phosphine. It causes cellular hypoxia via mitochondrial toxicity, resulting in multiple organ dysfunction and death. There is no antidote or specific treatment for zinc phosphide toxicity. We present the case of a 45-year-old female who ingested zinc phosphide with suicidal intent. On arrival at the emergency department, she had multisystemic disorders. Supportive care, decontamination and antidotal therapy were initiated. Subsequently, she evolved to clinical improvement with a resolution of the biochemical abnormalities of tissue hypoperfusion. She was discharged on day 7 without complications. In this review, we provide updated therapeutic options and discuss their specific pathophysiological basis.

Keywords: antioxidants; coconut oil; hyperinsulinemia–euglycemia therapy; intravenous lipid emulsion; magnesium sulphate; personal protective equipment; phosphine; zinc phosphide poisoning.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Electrocardiogram with sinus tachycardia. Sinus tachycardia is the most typical electrophysiological abnormality within the first 3 to 6 h, followed by ST-segment and T-wave changes [7]. Electrocardiogram obtained from the patient on admission to the Emergency Department of the Hospital Juarez de Mexico (Source: clinical record of the Hospital Juarez de Mexico).
Figure 2
Figure 2
The direct correlation between the establishment of hyperinsulinemia–euglycemic therapy with the increase in serum pH until reaching normal ranges of serum pH. The first 58 h of treatment are graphed. The numerical scale and units of measurement of insulin, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum pH, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 3
Figure 3
The direct correlation between the establishment of hyperinsulinemia–euglycemic therapy with the increase in serum bicarbonate until reaching normal ranges of serum bicarbonate. The first 58 h of treatment are graphed. The numerical scale and units of measurement of insulin, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum bicarbonate, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 4
Figure 4
The inverse correlation between the establishment of hyperinsulinemia–euglycemic therapy with the decrease in serum lactate until reaching normal ranges of serum lactate is shown. The first 58 h of treatment are graphed. The numerical scale and units of measurement of insulin, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum lactate, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 5
Figure 5
The direct correlation between the establishment of intravenous lipid emulsion 20% with the increase in serum pH until reaching normal ranges of serum pH. The first 58 h after treatment are graphed. The numerical scale and units of measurement of ILE 20%, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum pH, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 6
Figure 6
The positive correlation between the establishment of the intravenous lipid emulsion 20% and the increase in serum bicarbonate is shown. The first 58 h after treatment are graphed. The numerical scale and units of measurement of ILE 20%, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum bicarbonate, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 7
Figure 7
The inverse correlation between the establishment of the intravenous lipid emulsion 20% and the decrease in serum lactate is shown. The first 58 h after treatment are graphed. The numerical scale and units of measurement of ILE 20%, illustrated with the orange line, are plotted on the left-hand y-axis. The numerical scale and units of measurement of serum lactate, illustrated with a blue line, are plotted on the right-hand “y”-axis.
Figure 8
Figure 8
Clinical manifestations by system.
Figure 9
Figure 9
She response of capillary glucose and intravenous glucose supply was observed, after withdrawal of hyperinsulinemia–euglycemia therapy. It was observed that the decrease in the contribution of glucose to the withdrawal of insulin produced hypoglycemia, though we managed to remove this contribution up to 22 h later. The numerical scale and units of measurement of Serum glucose, illustrated with the blue line, are plotted on the left-hand “y”-axis. The numerical scale and units of measurement of intravenous glucose supply, illustrated with a orange line, are plotted on the right-hand “y”-axis.
Figure 10
Figure 10
Therapeutic proposal for zinc phosphide poisoning.
See this image and copyright information in PMC

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