Quan Li1, Wei Yu1, Yun Qu1, Jin-Qiu Wang2, Ning Mao3, Hai Kang4,5,6. 1. Department of Emergency, Affiliated Yantai Yuhuangding Hospital of Qingdao University, 264000, Yantai, China. 2. Department of Neurology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. 3. Department of Radiology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. 4. Department of Emergency, Affiliated Yantai Yuhuangding Hospital of Qingdao University, 264000, Yantai, China. khyt058@163.com. 5. Department of Neurology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. khyt058@163.com. 6. Department of Radiology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. khyt058@163.com.
Abstract
BACKGROUND: Clinically, bromadiolone poisoning is characterized by severe bleeding complications in various organs and tissues. Bromadiolone-induced toxic encephalopathy is extremely rare. Here, we report a special case of bromadiolone-induced reversible toxic encephalopathy in a patient who had symmetrical lesions in the deep white matter. CASE PRESENTATION: A 23-year-old woman mainly presented with dizziness, fatigue, alalia and unsteady gait after the ingestion of bromadiolone. The laboratory examinations showed normal coagulation levels. Brain magnetic resonance imaging (MRI) showed apparent diffusion restriction in the bilateral deep white matter. The clinical manifestations and MRI alterations were reversible within one month of treatment with vitamin K. The neuropsychological assessment showed no neurodegenerative changes at the 2-year follow-up. CONCLUSION: With the increased use of bromadiolone as a rodenticide, more cases of ingestion have been reported annually over the past several years. Bromadiolone-induced toxic encephalopathy has no special clinical manifestations and is potentially reversible with timely treatment. Because of the reversible restricted diffusion on diffusion-weighted images (DWI) and low apparent diffusion coefficient (ADC) values, transient intramyelinic cytotoxic oedema is thought to be the cause rather than persistent ischaemia. The underlying pathophysiological mechanism is still unknown and may be coagulant-independent. This clinical case extends the current knowledge about neurotoxicity in cases of bromadiolone poisoning and indicates that MRI is useful for the early detection of bromadiolone-induced toxic encephalopathy.
BACKGROUND: Clinically, bromadiolonepoisoning is characterized by severe bleeding complications in various organs and tissues. Bromadiolone-induced toxic encephalopathy is extremely rare. Here, we report a special case of bromadiolone-induced reversible toxic encephalopathy in a patient who had symmetrical lesions in the deep white matter. CASE PRESENTATION: A 23-year-old woman mainly presented with dizziness, fatigue, alalia and unsteady gait after the ingestion of bromadiolone. The laboratory examinations showed normal coagulation levels. Brain magnetic resonance imaging (MRI) showed apparent diffusion restriction in the bilateral deep white matter. The clinical manifestations and MRI alterations were reversible within one month of treatment with vitamin K. The neuropsychological assessment showed no neurodegenerative changes at the 2-year follow-up. CONCLUSION: With the increased use of bromadiolone as a rodenticide, more cases of ingestion have been reported annually over the past several years. Bromadiolone-induced toxic encephalopathy has no special clinical manifestations and is potentially reversible with timely treatment. Because of the reversible restricted diffusion on diffusion-weighted images (DWI) and low apparent diffusion coefficient (ADC) values, transient intramyelinic cytotoxic oedema is thought to be the cause rather than persistent ischaemia. The underlying pathophysiological mechanism is still unknown and may be coagulant-independent. This clinical case extends the current knowledge about neurotoxicity in cases of bromadiolonepoisoning and indicates that MRI is useful for the early detection of bromadiolone-induced toxic encephalopathy.
Authors: Johannes Oldenburg; Carville G Bevans; Clemens R Müller; Matthias Watzka Journal: Antioxid Redox Signal Date: 2006 Mar-Apr Impact factor: 8.401
Authors: Carlos Matute; Elena Alberdi; María Domercq; María-Victoria Sánchez-Gómez; Alberto Pérez-Samartín; Alfredo Rodríguez-Antigüedad; Fernando Pérez-Cerdá Journal: J Anat Date: 2007-05-15 Impact factor: 2.610