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A 69-year-old woman returning from a vacation in Cuba was brought to the emergency department directly from the airport. Her medical history was unremarkable, and she had no allergies. She had been well until 2 hours before the flight home, when at the Havana airport, she developed generalized weakness, increased sweating, severe nausea, and vomiting. In flight, she had lethargy, vomiting, and urinary incontinence. On arrival to the emergency department, she was stuporous and required intubation. Initial laboratory tests showed a hemoglobin level of 10.9 g/dL (reference range, 12.0-15.2 g/dL [to convert to grams per liter, multiply by 10.0]), a creatinine level of 1.31 mg/dL (reference range, 0.51-1.08 [to convert to micromoles per liter, multiply by 88.4]), and a pH of 7.22 with a normal anion gap. Serum electrolyte levels; a white blood cell count; levels of glucose, creatine kinase, lactic acid, and thyrotropin; coagulation studies; and liver function tests had normal results. An electrocardiogram showed sinus bradycardia at 53 bpm and borderline QT interval prolongation (QTc; 465 milliseconds). A urine toxicology screen had negative results for acetaminophen, salicylates, opiates, barbiturates, benzodiazepines, cocaine, and ethanol. Cerebrospinal fluid was clear, with normal levels of glucose, total protein, and white blood cells and negative microbiology and cytology testing results. A malaria smear and antigen test, respiratory viral assay, and cultures of cerebrospinal fluid, blood, and urine had negative results. Computed tomography of the head showed bilateral hyperdensity of the globus pallidi (Figure 1). Within several hours, her level of consciousness improved spontaneously, and she was extubated. Her blood pressure was 99/61 mm Hg; pulse, 80 bpm; temperature, 37.6 °C; and oxygen saturation, 99% on room air. The patient was alert but disoriented. The pupils were 2 mm and reactive. Involuntary facial muscle twitching was noted. Her muscle tone was normal, and she had mild proximal muscle weakness with occasional bilateral upper extremity and lower extremity fasciculations and jerky movements. Deep tendon reflexes were normal, with flexor plantar responses. Her sensations to pain and vibration were normal.
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C. Organophosphate poisoning
The key to diagnosis was the constellation of signs and symptoms on examination. Depressed mental status, bradycardia, emesis, diaphoresis, urination, miosis, muscle weakness, fasciculations, twitching, and myoclonic jerks triggered consideration of acute cholinergic toxicity. Computed tomography findings indicated senile calcifications of the globus pallidus.1 There are no specific radiographic features of cholinergic toxicity.2
The patient’s plasma cholinesterase (butyrylcholinesterase [BChE]) level of 373 IU/L (reference, 600-1300 IU/L) was consistent with cholinesterase inhibition. Her serum BChE and acetylcholinesterase (AChE) activity were less than the range for healthy individuals analyzed by the same laboratory3 (Figure 2). Serum toxicological analysis using mass spectrometry revealed a trace of temephos, a cholinesterase-inhibiting organophosphate (OP) larvicide commonly used in Cuba, and 3-phenoxybenzoic acid, a common pyrethroid insecticidal metabolite.
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Corresponding Author: Yonatan Serlin, MD, Montreal Neurological Institute, 3801 Rue University, Montreal, QC H3A 2B4, Canada (firstname.lastname@example.org).
Published Online: September 8, 2020. doi:10.1001/jamaneurol.2020.3193
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank the Brain Injury Research Team of the Brain Repair Centre at Dalhousie University: Alon Friedman, MD, PhD (data analysis), Cynthia Calkin, MD (psychiatry), Jong Sung Kim, PhD (toxicology), and Janine Verge, AuD, and Greg Noel, AuD (audiology). They were not compensated. We thank the patient for granting permission to publish this information.
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