A Case of Ceftriaxone-Associated Encephalopathy in a Patient Undergoing Peritoneal Dialysis

Antibiotic-associated encephalopathy (AAE) is an uncommon but increasingly recognized neurological complication of antimicrobial therapy. It is classified into three clinical types based on symptoms and electroencephalographic findings: Type I is characterized by acute confusional state with triphasic waves, Type II by seizures, and Type III by psychosis. Among these, Type I is most frequently associated with β-lactam antibiotics. Ceftriaxone (CTRX), a widely used third-generation cephalosporin, has been reported to induce Type I AAE, particularly in elderly patients and those with impaired renal function. Although CTRX is mainly eliminated by both biliary and renal pathways, drug clearance is significantly reduced in patients with chronic kidney disease (CKD) or those receiving dialysis, increasing the risk of neurotoxicity. Reported clinical manifestations include altered mental status, confusion, delirium, and occasionally myoclonus or seizures. Awareness of this adverse effect remains limited, and delayed recognition can lead to unnecessary diagnostic procedures and prolonged hospitalization.

A 73-year-old woman with CKD secondary to hypertension and diabetes mellitus had been receiving peritoneal dialysis since year X–8. She was also on antiepileptic medication for symptomatic epilepsy. She was admitted in January of year X for treatment of a right cheek abscess. Incision and drainage were performed under local anesthesia, and CTRX 2.0 g/day was initiated. Although the infection improved, impaired consciousness developed on hospital day 4. Neurological examination revealed no focal deficits. Brain CT and MRI showed no acute lesions, and cerebrospinal fluid analysis was unremarkable. Electroencephalography demonstrated diffuse slowing with triphasic waves, consistent with metabolic or drug-induced encephalopathy. CTRX-associated encephalopathy was suspected, and CTRX was discontinued on day 4 and replaced with ampicillin/sulbactam. Hemodialysis was initiated on day 5 to enhance drug clearance. Her level of consciousness gradually improved, and she became fully alert by day 12.

AAE is thought to result from elevated serum and cerebrospinal fluid concentrations of neurotoxic antibiotics, often due to impaired renal excretion. In patients with CKD or on dialysis, reduced clearance leads to accumulation, allowing increased penetration across the blood–brain barrier. β-lactam antibiotics, including CTRX, may interfere with inhibitory neurotransmission by antagonizing GABA-A receptors, resulting in neuronal hyperexcitability. Previous reports have documented CTRX-induced AAE mainly in elderly patients or those with renal dysfunction, typically occurring 2–7 days after initiation and resolving within several days after discontinuation. Dialysis modalities have limited efficacy for CTRX removal because of its high protein binding; however, hemodialysis can aid in reducing unbound fractions. In this case, prompt drug discontinuation and hemodialysis contributed to clinical recovery. Special attention should be paid in patients receiving antiepileptic drugs, as pre-existing central nervous system vulnerability may exacerbate neurotoxicity. Careful dose adjustment, avoidance of unnecessary prolonged use, and close monitoring for neurological symptoms are essential, particularly in elderly patients with renal impairment.

We report a case of CTRX-associated encephalopathy in a peritoneal dialysis patient. This case highlights the importance of recognizing AAE as a potential cause of acute consciousness disturbance during antibiotic therapy. Early diagnosis, discontinuation of the offending agent, and consideration of dialysis are crucial for favorable outcomes in high-risk populations.