Ceftriaxone-Induced Encephalopathy in a Patient With Chronic Kidney Disease

Abstract

Neurotoxicity is an acknowledged side effect of third and fourth-generation cephalosporins, but its occurrence with ceftriaxone is not widely recognized. This article presents a case involving a 56-year-old woman with multiple comorbidities who sought medical attention after experiencing lipothymia. The initial diagnosis suggested a urinary tract infection with acute kidney failure, leading to the initiation of ceftriaxone and hemodialysis. Subsequently, the patient exhibited a progressive deterioration of her neurological state, characterized by agitation and chorea. Metabolic encephalopathy, seizure/nonconvulsive status epilepticus, and acute central nervous system lesions were considered primary differential diagnoses, all of which were subsequently ruled out through thorough investigations. Days later, a remarkable recovery of the patient's neurological state was observed. A retrospective analysis revealed a correlation between the improvement and the fourth day of antimicrobial suspension. Consequently, a presumptive diagnosis of ceftriaxone-induced encephalopathy was made. This unusual case underscores the importance of recognizing the potential for pharmacological encephalopathy, particularly with ceftriaxone, and emphasizes its reversibility upon discontinuation of the implicated drug. Clinicians should remain vigilant to this uncommon adverse effect, promoting timely intervention and improved patient outcomes.

Keywords: ceftriaxone; central nervous system disorders; cephalosporins; chronic kidney disease; drug-induced encephalopathy; neurotoxicity.

Figure 1. EEG carried out at the pinnacle of the patient's most evident cognitive deterioration

This EEG was conducted on a restless patient in both wakefulness and drowsiness, incorporating intermittent photic stimulation (IPS). The patient exhibited limited cooperation during the examination, with numerous movements observed throughout the study. The recording showed numerous artifacts, with a baseline activity at 5 Hz, posterior, symmetric, reactive, irregular, and of low amplitude. The slow activity was inscribed with variable localization (arrows). No clear recording of spikes and/or sharp waves, or other focal or generalized paroxysms, was observed. No electroclinical seizures were observed. In conclusion, it shows moderate encephalopathy with inscribed slow activity of variable localization, without clear evidence of epileptiform activity. The recording is overlaid with numerous artifacts.