P2.211: Early Recognition and Management of Pediatric Opioid Use-Associated Neurotoxicity with Cerebellar Edema (POUNCE) Syndrome: A Case Report

Introduction: Opioids are a leading cause of accidental ingestion and intentional overdose in the United States. While CHANTER syndrome (Cerebellar, Hippocampal, and Basal Nuclei Transient Edema with Restricted Diffusion) is well-characterized in adults, its pediatric counterpart, POUNCE syndrome (Pediatric Opioid Use-Associated Neurotoxicity with Cerebellar Edema), is infrequently described in the literature. POUNCE shares similar imaging features with CHANTER, notably marked cerebellar edema following suspected or confirmed opioid exposure. Clinical manifestations include encephalopathy, aphasia or dystonia that often progress to respiratory failure or status epilepticus. Outcomes vary widely depending on the timing of recognition and intervention, and range from full recovery to severe neurological deficits, herniation, or brain death. We present two cases highlighting the critical role of early diagnosis and opioid avoidance in emergency care.

Case Description: An 18-month-old was found unresponsive outside a motel and presented in cardiopulmonary arrest with status epilepticus and multi-system organ failure. Neuro-imaging revealed symmetric cerebellar infarcts and edema, consistent with opioid-induced neurotoxicity. Fentanyl metabolites were later confirmed, implicating pre-hospital exposure. A 15-year-old was found unresponsive at home and arrived to the Emergency Department with altered mental status. She had minimal response to multiple doses of naloxone. Neuro-imaging showed cytotoxic edema of the hippocampus and cerebellum, confirming POUNCE syndrome. A toxicology screen was later positive for fentanyl, cocaine, and THC. In both cases, patients received fentanyl during rapid sequence intubation (RSI) prior to imaging due to instability.

Discussion: In the context of the ongoing opioid epidemic, clinicians must consider POUNCE syndrome in pediatric patients of all ages with suspected intoxication presenting with unexplained encephalopathy, focal neurologic deficits, or seizures, especially when unresponsive to naloxone. These cases illustrate how rapid identification can influence clinical decisions, especially regarding the use of opioids for analgesia, RSI, or sedation. Ongoing iatrogenic use of opioids may inadvertently worsen neurologic injury. Neuro-imaging plays a crucial role in confirming the diagnosis, but early clinical suspicion is paramount. Increased awareness of POUNCE syndrome can prompt rapid diagnosis and treatment as well as potentially improve neurologic outcomes in this vulnerable population.

Conclusion: POUNCE syndrome is a rare but serious complication of pediatric opioid exposure. Pediatric providers must maintain a high index of suspicion for POUNCE syndrome in patients with clinical features of intoxication or unexplained neurologic deficits. Early diagnosis through imaging and opioid avoidance during initial management are essential to prevent further neurologic injury and optimize outcomes.