INTRODUCTION: Chlorfenapyr is a pyrrole insecticide metabolized to the active toxin tralopyril. Reports of poisoning have increased recently. This retrospective study analyzed clinical data to examine clinical features and describe characteristics observed in fatal outcomes. METHODS: Clinical data were collected from patients with chlorfenapyr poisoning at the First Affiliated Hospital of Zhengzhou University (2020-2024). Patients were categorized into survivors and non-survivors to describe demographic, clinical, laboratory, and imaging findings. RESULTS: Twenty-one patients were included (case fatality: 28.6%). Among oral exposures, non-survivors ingested a higher estimated dose than survivors, with median 122.5 mL (IQR 105-125 mL) versus 20.0 mL (IQR 20.0-30.0 mL). Non-survivors exhibited longer symptom latency, median 24.0 versus 1.0 h and a delay in neurological symptoms, with median of 2.5 days. Plasma concentrations of chlorfenapyr and tralopyril were numerically higher in non-survivors, median 293 versus 147 ng/mL and 946 versus 531 ng/mL, respectively, compared to survivors. Clinically, non-survivors universally (100%) exhibited fever, diaphoresis, and impaired consciousness; they also showed higher frequencies of paresthesia (50%), bowel/bladder dysfunction (50%), and muscle weakness (50%). Laboratory analysis in non-survivors revealed higher creatine kinase, median 1266.0 versus 72.0 U/L, aspartate aminotransferase, lactate dehydrogenase, myoglobin, prothrombin time, and lipase. Abnormal magnetic resonance imaging signals were observed in all non-survivors (3/3) compared to only 12.5% (1/8) of survivors. DISCUSSION: In this cohort, the observed latent period followed by a hypermetabolic state aligns with the delayed conversion of chlorfenapyr to tralopyril and its uncoupling of mitochondrial respiration. The specific pattern of elevated muscle enzymes and central nervous system lesions reflects injury primarily to tissues with high metabolic demand. Furthermore, the sustained plasma toxin concentrations despite extracorporeal clearance indicate a large total body burden and prolonged toxicity. CONCLUSION: Fatal chlorfenapyr poisoning was characterized by a latency period followed by a hypermetabolic state (fever, diaphoresis) and severe neurological/muscular injury. Fever, impaired consciousness, elevated muscle enzymes (notably CK), and specific brainstem/spinal cord MRI abnormalities were observed in fatal cases, whereas these features were largely absent in survivors.
Xu et al. (2026) studied this question.