Cefepime Induced Neurotoxicity
Location
D.P. Culp Center Ballroom
Start Date
4-5-2024 9:00 AM
End Date
4-5-2024 11:30 AM
Poster Number
112
Name of Project's Faculty Sponsor
Jennifer Delzell
Faculty Sponsor's Department
Internal Medicine
Competition Type
Competitive
Type
Poster Presentation
Presentation Category
Health
Abstract or Artist's Statement
Neurotoxicity is well established in current literature as a known adverse effect of cefepime antibiotic therapy. This is suspected to be secondary to cefepime’s ability to penetrate into the central nervous system. In the setting of renal insults, there can be decreased clearance of cefepime leading to increased risk of adverse effects. Here we present a case of cefepime induced neurotoxicity in the setting of acute on chronic kidney disease, ultimately requiring hemodialysis, which improved the patient’s neurological symptoms. An 87-year-old male with a history of active osteomyelitis, stage 3 chronic kidney disease, and insulin-dependent type 2 diabetes mellitus presented to the emergency department (ED) with worsening global dystonic movements for one week. The patient was actively receiving treatment for foot osteomyelitis with intravenous (IV) cefepime. At the time of ED evaluation, it had been 48 hours since his last dose of IV cefepime. Initial lab work revealed elevated creatinine of 5.4 mg/dL from the patient's baseline of 1.6-1.8 mg/dL. On exam, the patient had involuntary muscle contractions of bilateral upper and lower extremities and facial contractions interfering with his speaking ability. No myoclonus, confusion, or seizure-like activity was noted. Besides the addition of cefepime for the past eight weeks, no other medication changes had been made. The patient was up to date on his tetanus vaccine. Neurology evaluated patient and recommended diphenhydramine. The following day, the patient's symptoms improved but did not fully resolve. Unfortunately, the patient's kidney function continued to worsen, and urine output declined to the oliguric stage. Hemodialysis was initiated by nephrology. He received one 4-hour session, and post dialysis, no recurrence of his dystonic movements was noted. Cefepime is a fourth generation cephalosporin with broad coverage of both gram positive and gram negative bacteria particularly for pneumonia, soft tissue and intraabdominal infections. The additional advantage of cefepime’s ability to treat pseudomonas, a common drug resistant bacteria seen in hospitalized patients, reinforces its utility as a staple of in-patient antibiotic therapy. With its widespread use, cefepime has developed notoriety for adverse events collectively described as neurotoxicity. Clinical suspicion for neurotoxicity should be high in patients receiving cefepime therapy presenting with altered mental status, reduced levels of consciousness, confusion, myoclonus, aphasia, agitation, and/or seizures. There is further concern for these patients if there is underlying renal dysfunction. Patients with reduced glomerular filtration are prone to decreased cefepime clearance and increased central nervous system penetration. Prior pharmacologic studies have demonstrated that approximately 10% of serum cefepime crosses the blood brain barrier. This transferred amount increases up to 45% in the setting of renal impairment, decreased protein binding, and acidosis (1).
Cefepime Induced Neurotoxicity
D.P. Culp Center Ballroom
Neurotoxicity is well established in current literature as a known adverse effect of cefepime antibiotic therapy. This is suspected to be secondary to cefepime’s ability to penetrate into the central nervous system. In the setting of renal insults, there can be decreased clearance of cefepime leading to increased risk of adverse effects. Here we present a case of cefepime induced neurotoxicity in the setting of acute on chronic kidney disease, ultimately requiring hemodialysis, which improved the patient’s neurological symptoms. An 87-year-old male with a history of active osteomyelitis, stage 3 chronic kidney disease, and insulin-dependent type 2 diabetes mellitus presented to the emergency department (ED) with worsening global dystonic movements for one week. The patient was actively receiving treatment for foot osteomyelitis with intravenous (IV) cefepime. At the time of ED evaluation, it had been 48 hours since his last dose of IV cefepime. Initial lab work revealed elevated creatinine of 5.4 mg/dL from the patient's baseline of 1.6-1.8 mg/dL. On exam, the patient had involuntary muscle contractions of bilateral upper and lower extremities and facial contractions interfering with his speaking ability. No myoclonus, confusion, or seizure-like activity was noted. Besides the addition of cefepime for the past eight weeks, no other medication changes had been made. The patient was up to date on his tetanus vaccine. Neurology evaluated patient and recommended diphenhydramine. The following day, the patient's symptoms improved but did not fully resolve. Unfortunately, the patient's kidney function continued to worsen, and urine output declined to the oliguric stage. Hemodialysis was initiated by nephrology. He received one 4-hour session, and post dialysis, no recurrence of his dystonic movements was noted. Cefepime is a fourth generation cephalosporin with broad coverage of both gram positive and gram negative bacteria particularly for pneumonia, soft tissue and intraabdominal infections. The additional advantage of cefepime’s ability to treat pseudomonas, a common drug resistant bacteria seen in hospitalized patients, reinforces its utility as a staple of in-patient antibiotic therapy. With its widespread use, cefepime has developed notoriety for adverse events collectively described as neurotoxicity. Clinical suspicion for neurotoxicity should be high in patients receiving cefepime therapy presenting with altered mental status, reduced levels of consciousness, confusion, myoclonus, aphasia, agitation, and/or seizures. There is further concern for these patients if there is underlying renal dysfunction. Patients with reduced glomerular filtration are prone to decreased cefepime clearance and increased central nervous system penetration. Prior pharmacologic studies have demonstrated that approximately 10% of serum cefepime crosses the blood brain barrier. This transferred amount increases up to 45% in the setting of renal impairment, decreased protein binding, and acidosis (1).