Successful management of zinc phosphide poisoning-a Hungarian case

Abstract

Background: Zinc phosphide (ZnP) is the basic component of several insecticides easily accessible worldwide. Intentional or accidental intoxication may lead to severe complications and multiple organ failure, resulting in high mortality. No known antidote is currently available. The iron-chelation and the antioxidative effects are well-known features of alpha-lipoic acid (ALA), although its use in the treatment of ZnP poisoning has not been documented previously. We describe the case of a patient with serious ZnP poisoning with multiple organ failure, where ALA was also included in the patient's supportive therapy.

Case presentation: A 65-year-old man ingested 125 g of Arvalin® (containing 5 g ZnP) and presented to the Emergency Department, with respiratory insufficiency and decreased consciousness. He developed hypokalemia, hypocalcemia, low white blood cell count, elevated C-reactive protein level, mixed acidosis, hepatic and kidney damage, thickening of the jejunal wall, and lung atelectasis, which served as a basis for the ensuing bacterial pneumonia. Antibiotics and adequate supportive therapy were provided. Laboratory tests indicated liver damage (slightly increased liver enzymes, low pseudocholinesterase levels; 706 U/L on day 2), possibly caused by the patient's chronic alcoholism or the ZnP poison itself, therefore, hepatoprotective agents, ALA (Thiogamma Turbo-Set®) with N-acetylcysteine were administered for six consecutive days. Pseudocholinesterase values increased sixfold until the end of the second week of care. Fifteen days after admission, the patient was relocated to the department of psychiatry with stable vital functions, clear consciousness, declining inflammatory markers, and improved liver function. He was discharged 1 month later, fully recovered.

Conclusions: Our case is the first documented voluntary and severe ZnP poisoning in Hungary. Our patient developed multiple organ failure and atelectasis, possibly resulting in the observed respiratory infection. The development of bacterial pneumonia highlighted the dangers of phosphine-induced atelectasis. The use of ALA in our patient's case, as an antioxidant and agent for metal chelation, suggested that this agent could be a promising tool in the prevention and treatment of ZnP-induced hepatic damage.

Keywords: Alpha-lipoic acid; Dihydrolipoic acid; N-acetylcysteine; Pneumonia; Poisoning; Pseudocholinesterase; Zinc phosphide.

Fig. 1

Anteroposterior chest X-rays of the patient on day 1 (a), 7 (b), 15 (c). a Day 1, confluent atelectasis on the day of admission. Central venous cannula and endotracheal tube in correct position. b Day 7, control examination. No signs of consolidation or atelectasis. c Day 15, control examination. No signs of consolidation or atelectasis. Tracheostomy tube in control position

Fig. 2

Chest CT-scan image of the patient on day 1. Axial, coronal, and sagittal plane CT images of the lung, with a 3-mm slice width made by Siemens Somatom Definition Device. Alveolar atelectasis from base to apex

Fig. 3

Abdominal CT-scan image of the patient on day 1. Native spiral-CT image of thorax, abdomen, and pelvis with soft tissue window and a 3-mm slice width in the axial plane. The thickened jejunal wall can be seen on the reconstructed image (marked with an arrow)

Fig. 4

Changes of inflammatory markers (days 1-14)