Fulminant sepsis-associated encephalopathy in two children: serial neuroimaging findings and clinical course

A Kondo1, C Sugiura, Y Fujii

  • 1Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan. holbergs@nifty.com

Neuropediatrics
|February 6, 2010
PubMed

Insights

Sepsis-associated encephalopathy can cause severe, rapid brain damage in children, leading to coma and mimicking brain death. Neuroimaging reveals extensive edema and lesions, indicating profound neurological injury.

Area of Science:

  • Pediatric Neurology
  • Critical Care Medicine
  • Neuroscience

Background:

  • Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis.
  • Early recognition and understanding of SAE's neurological impact are crucial for pediatric critical care.

Observation:

  • Two children presented with acute, severe neurological deterioration following sepsis.
  • Clinical presentation included status epilepticus, deep coma, and near brain death.
  • Initial CT scans showed diffuse brain edema, and EEG revealed severe brain dysfunction.

Findings:

  • MRI demonstrated restricted diffusion in basal ganglia and white matter, indicating cytotoxic edema.
  • Serial imaging over months showed progressive, severe lesions in cerebral white matter, cerebellum, and brainstem.
  • MR angiography revealed diminished intracranial arteries, suggesting widespread vascular compromise.

Implications:

  • SAE can lead to devastating, long-term neurological damage in children.
  • Findings suggest a mechanism of severe brain injury due to rapid intracranial pressure elevation, mimicking "respirator brain".
  • Highlights the need for advanced neuroimaging and monitoring in pediatric sepsis cases.

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