CASE REPORT Melissa A. Pasquale-Styles, 1 M.D.; Mark A. Sochaski, 2 Ph.D.; David C. Dorman, 2 D.V.M., Ph.D.; Willane S. Krell, 3 M.D.; Aashit K. Shah, 4 M.D.; and Carl J. Schmidt, 5 M.D. Fatal Bromethalin Poisoning ABSTRACT: Bromethalin is a neurotoxin found in some rodenticides. A delusional 21-year-old male presented to a hospital with altered mental status the day after ingesting a bromethalin-based rodenticide. He died 7 days after his self-reported exposure to c. 17 mg bromethalin (equivalent to 0.33 mg bromethalin/kg). His clinicopathologic course was characterized by altered mental status, obtundation, increased cerebrospinal fluid pressure, cerebral edema, death, and diffuse histologic vacuolization of the white matter in the central nervous system seen on microscopic examination at autopsy. The presence of a demethylated form of bromethalin in the patient’s liver and brain was confirmed by gas chromatography with mass spectrometry. Clinical signs and lesions observed in this patient are similar to those seen in animals poisoned with bromethalin. This case illustrates the potential for bromethalin ingestion to result in fatal human poisoning. KEYWORDS: forensic science, bromethalin, rodenticide, rat poison, neurotoxicity syndromes, analytical chemistry Various types of rodenticides including first- and second- generation anticoagulants, cholecalciferol, zinc phosphide, strych- nine, and bromethalin have been used to control mice and rat populations. Although bromethalin accounts for a significant number of accidental rodenticide poisonings in veterinary medi- cine, human exposures are unusual. In 2004, 643 bromethalin ex- posures were reported to 62 major poison control centers across the United States (1). In contrast, nearly 16,400 anticoagulant rodenticide exposures were reported during the same time. The bromethalin exposure doses were not reported, but the vast ma- jority of exposed people experienced no signs of toxicity. Only three people had ‘‘major’’ effects, which were described simply as either ‘‘life-threatening’’ or ‘‘associated with significant disabili- ty.’’ The clinical or pathologic findings in human poisoning have never been described in detail in the English literature, and, to our knowledge, a fatal human poisoning has not been previously reported. Case Report A 21-year-old black male was transported to the emergency room after his family found him with multiple open packages of rat poison ‘‘place packs,’’ and he displayed increasingly odd behavior consisting of repetitive speech, labile emotions, and diminished responsiveness to direct questioning. He told the trans- porting rescue personnel that he had eaten ‘‘8 packs of No Pest s (United Industries Corporation, St. Louis, MO) rat and mice killer and a box of Ex-Lax s (Novartis AG, Basel, Switzerland)’’ the night before. In the emergency room, he claimed to have taken rat poison ‘‘to kill the rats inside’’ and ‘‘to kill the ratgenes.’’ He had normal vital signs but was alert and oriented to person and place only. The rest of his physical examination was unremarkable. An electrocardiogram was essentially normal. A urine drug screen was positive for barbiturates. He experienced one episode of em- esis in the emergency room and was treated with promethazine, thiamine, folic acid, and diphenhydramine. He was said to be ‘‘medically cleared,’’ and a provisional diagnosis of major depres- sion with psychosis was made. He was transferred from the emer- gency room to an inpatient psychiatric treatment center at a different location. He was in the psychiatric hospital for 3 days and was reported to be ‘‘obtunded and catatonic’’ for the last 2 days of his stay. He was then transferred to the emergency room of a third hospital for further medical evaluation. Upon admission (day 4 postingestion), he was found to be obtunded and unresponsive to verbal or painful stimuli. He had stable vital signs and was afebrile. His pupils were anisocoric (right pupil 5 mm, left pupil 2 mm) and sluggishly re- sponsive to light. All four extremities were flaccid. The rest of his physical examination was unremarkable. He was intubated and placed on a ventilator while his workup continued. A CT scan of the head showed hypodensities affecting the white matter diffusely, suggesting brain edema that was predominantly affecting the white matter. A lumbar puncture yielded clear cere- brospinal fluid (CSF) at a high opening pressure of 33 cm of H 2 O (normal 8–20 cm of H 2 O). Subsequent CSF studies revealed an elevated CSF protein of 64 mg/dL (normal 15–45 mg/dL). CSF cell counts were within normal range, antisyphilis antibodies were not detected (i.e., negative venereal disease research laboratory test), and bacterial cultures were negative for growth. Viral studies 1 Office of the Chief Medical Examiner, 520 First Avenue, New York, NY 10016. 2 CIIT Centers for Health Research, Six Davis Drive, Research Triangle Park, NC 27709. 3 Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University, 3990 John R, Detroit, MI 48201. 4 Department of Neurology, Wayne State University, 4201 St. Antoine, De- troit, MI 48201. 5 Wayne County Medical Examiner Office, 1300 East Warren Avenue, De- troit, MI 48207. Received 21 Jan. 2006; and in revised form 15 April 2006; accepted 23 April 2006; published 31 Aug. 2006. Copyright r 2006 by American Academy of Forensic Sciences 1154 J Forensic Sci, September 2006, Vol. 51, No. 5 doi:10.1111/j.1556-4029.2006.00218.x Available online at: www.blackwell-synergy.com