Case Diagnosis: Toxic leukoencephalopathy (TLE) due to accidental methadone ingestion.
Case Description or Program Description: A previously healthy, 2-year-old female, presented to the hospital unresponsive, with respiratory failure, and constricted pupils concerning for accidental ingestion of a family member’s prescription, as her urine drug screen was positive for methadone. She was given intranasal naloxone without improvement. After intravenous naloxone she awoke, but had seizure activity requiring lorazepam. CT head in ED showed edema of bilateral cerebellar hemispheres, loss of gray-white matter differentiation concerning for cerebellar infarcts consistent with methadone-induced toxic leukoencephalopathy (TLE). Repeat imaging showed worsening edema of bilateral cerebellar hemispheres with new hydrocephalus. Neurosurgery emergently performed cerebellar decompression with craniectomy and placed right external ventricular drain. MRI brain showed evolving hypoxic-ischemic insult with hemorrhagic transformation of cerebellar infarcts. Course complicated by respiratory failure, cerebral salt wasting, dysphagia, aphasia, dysconjugate gaze with visual inattention, ataxia, tetraparesis, and impulsivity. She received multidisciplinary inpatient rehabilitation and progressed from dependent to supervision level for ambulation and age-appropriate activities of daily living.
Setting: Tertiary care pediatric hospital
Assessment/Results: Our patient had bilateral cerebellar edema and increased intracranial pressure with acute hydrocephalus due to acute TLE from methadone ingestion requiring urgent neurosurgical intervention. Delaying intervention could have resulted in worse prognosis.
Discussion (relevance): TLE from opioids is well described in adult literature but scarce within pediatrics. The opioid epidemic has increased use of methadone to treat opioid use disorder, increasing potential accessibility for the pediatric population. While the incidence of methadone-induced leukoencephalopathy is rare in this population, it is just as dangerous and life-threatening.
Conclusions: It is imperative recognizing clinical and radiologic manifestations of opioid-induced TLE and being aware of potential increased intracranial pressure to minimize secondary neurologic insults. We will review neuroanatomy, image findings of this rare form of toxic encephalopathy, methadone mechanism, opioid receptor predominance within the brain, other differential diagnoses to consider, and treatment.
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