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Pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome
Jason Dietz1, Samantha S Klein1, Rana Biary1
1Division of Medical Toxicology, Ronald O. Perelman Department of Emergency Medicine, NYU Grossman School of Medicine, New York, NY, USA.
Insights
Pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome presents unique white matter changes in children. Recognizing these neuroimaging findings is crucial for diagnosing opioid exposure in pediatric cases.
Area of Science:
- Neurology
- Pediatrics
- Toxicology
Background:
- The opioid epidemic impacts children, with rare cases exhibiting neurotoxicity.
- Pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome involves white matter changes.
Observation:
- A 31-month-old child presented with unresponsiveness, neurological signs, and opioid exposure confirmed by urine toxicology.
- Initial response to naloxone was incomplete, indicating significant opioid toxicity.
Findings:
- Neuroimaging revealed T2/FLAIR hyperintensity and restricted diffusion in the cerebellar hemispheres.
- These findings, while not pathognomonic, are characteristic of POUNCE syndrome.
Implications:
- Radiologists and toxicologists should consider POUNCE syndrome in pediatric cases with suggestive neuroimaging and opioid exposure.
- Early recognition of POUNCE syndrome is vital for timely and appropriate clinical management in affected children.
Introduction:
Unfortunately, children are not spared from the devastating effects of the ongoing opioid epidemic. In rare cases, young children exposed to opioids present with unique neuroimaging findings affecting the white matter, reminiscent of what was once seen with diacetylmorphine (heroin)-associated leukoencephalopathy. This constellation of findings is termed the pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome.
Case Summary:
A 31-month-old child was found floppy and unresponsive. Upon hospital arrival, there was right gaze deviation, shaking of the arms and legs, miosis, and bradypnea. Response to naloxone was incomplete, and methadone was confirmed in the child's urine.
Images:
Magnetic resonance imaging of the brain performed 24 h after admission showed abnormal T2/FLAIR hyperintensity with associated restricted diffusion symmetrically involving the cerebellar hemispheres.
Conclusion:
The imaging findings, although far from pathognomonic, should be recognizable by radiologists and toxicologists when considering possible opioid exposure in a young child.
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