Abstracts

Neurologic complications, including seizures and encephalopathy, occur in approximately 20–50% of pediatric patients with Shiga toxin-producing Escherichia coli hemolytic uremic syndrome (STEC-HUS) [Bauer et al., 2014; Steinborn et al., 2004]. Despite this, electroencephalographic (EEG) findings are incompletely characterized in the literature, particularly during the acute illness phase. Prior studies have demonstrated variable neuroimaging patterns, but few correlate these with EEG or clinical outcomes. We present a case of a child with STEC-HUS who developed encephalopathy, multifocal seizures, and burst suppression EEG, later achieving complete neurologic and electrographic recovery.

A 12-year-old previously healthy boy presented with fever, vomiting, and bloody diarrhea, progressing to colitis, acute kidney injury, diffuse pan-colitis complicated by perforation (s/p hemicolectomy and ileostomy) and systemic toxicity. He developed multiorgan failure requiring dialysis and extracorporeal membrane oxygenation (ECMO). Early in his intensive care unit course, he exhibited worsening mental status and new-onset seizures. Continuous video EEG revealed a markedly abnormal background with alternating phases of suppression and bursts of higher-voltage activity, consistent with burst suppression. The suppression ratio exceeded 49%, with greater attenuation over the right hemisphere. Ictal recordings captured five seizures—three with left occipital onset and two with right temporal onset—as well as several subclinical right occipital seizures. EEG also demonstrated multifocal epileptiform discharges, diffuse delta slowing, and intermittent SIRPIDs associated with tactile stimulation. Seizures were managed with intravenous levetiracetam, phenobarbital and midazolam drips.
Brain MRI demonstrated restricted diffusion in the bilateral thalami, caudate nuclei, globus pallidi, and posterior brainstem (tegmentum from medulla to midbrain), suggestive of toxic-metabolic injury secondary to systemic inflammation, uremia, and potential Shiga toxin neurotoxicity. With supportive care, antiseizure treatment, and improved systemic function, the EEG background evolved from burst suppression to continuous slowing, and ultimately normalized. Repeat MRI showed radiographic resolution of prior deep gray matter abnormalities. The patient was extubated, remained seizure-free on levetiracetam, and later transitioned off antiseizure medications. Cognitive function and academic performance remained intact. Residual symptoms were limited to transient neuropathic leg pain managed with gabapentin.

This case illustrates the fulminant neurological impact of STEC-HUS and the potential reversibility of profound EEG and MRI abnormalities. Continuous EEG was essential for seizure detection and monitoring recovery. Parallel evolution of neuroimaging and EEG findings supports the use of both modalities in prognostication. Clinicians should maintain high suspicion for subclinical seizures in encephalopathic patients with HUS. Early and serial EEG may inform both acute management and long-term outcomes in pediatric neurocritical care.