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A Case of Delayed-Onset Posthypoxic Leukoencephalopathy in a Pediatric Patient
Kristen Smolinsky1, Ivona Sediva2
1Brown University Pediatric Program, Hasbro Children's Hospital, Providence, RI, USA.
Insights
A severe traumatic brain injury case shows delayed-onset posthypoxic leukoencephalopathy. This condition emerged after initial recovery, highlighting the importance of monitoring neurological status post-injury.
Area of Science:
- Neuroscience
- Trauma Surgery
Background:
- Severe traumatic brain injury (TBI) following motor vehicle accidents presents significant management challenges.
- Early management includes advanced life support, neuroimaging, and surgical interventions.
Purpose of the Study:
- To report a rare case of delayed-onset posthypoxic leukoencephalopathy after severe TBI.
- To discuss the clinical presentation, diagnostic findings, and potential mechanisms of this complication.
Main Methods:
- Case presentation of a 16-year-old female with severe TBI.
- Details of initial management including intubation, decompressive hemicraniectomy, and neuroprotective strategies.
- Serial neuroimaging (CT and MRI) and clinical assessments to monitor neurological status.
Main Results:
- The patient initially improved after decompressive surgery and neuroprotective care.
- On hospital day 8, she developed acute neurological deterioration with confusion and combativeness.
- MRI revealed restricted diffusion consistent with delayed-onset posthypoxic leukoencephalopathy.
Conclusions:
- Delayed-onset posthypoxic leukoencephalopathy is a rare but serious complication following severe TBI.
- This case underscores the need for vigilance and continuous neurological monitoring even after initial recovery.
- Further research is needed to elucidate the pathophysiology and optimize treatment strategies for this condition.
Abstract:
We present a 16-year-old female status post traumatic brain injury from severe motor vehicle crash with prolonged extrication. Initially with a Glasgow Coma Scale of 4 and blood pressure of 80/40, she required emergent intubation. Head computed tomography was notable for skull fracture with hematoma, diffuse axonal injury, and 6-mm midline shift with right uncal herniation. On hospital day 1, she underwent decompressive R hemicraniectomy. She received neuroprotective treatment including a hypocarbic, hypernatremic state with close blood pressure monitoring for appropriate cerebral perfusion. On hospital day 4, patient was extubated and weaned off pressors and hypertonic saline. On hospital day 6, she was able to get out of bed to a chair, was speaking some words, following commands, and tolerating bites of food. On hospital day 8, she developed sudden agitation, combativeness, confusion, and could no longer follow commands. Magnetic resonance imaging now demonstrated confluent restricted diffusion consistent with acute changes. Imaging and examination findings were consistent with delayed-onset posthypoxic leukoencephalopathy.
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