CEFEPIME NEUROTOXICITY IN THE SETTING OF NORMAL RENAL FUNCTION Abigail H. Boudreaux, MD PGY-1 Department of Medicine, Ochsner Medical Center, New Orleans, LA INTRODUCTION Antibiotics are some of the most prescribed medications in the inpatient setting. Although the profound benefits of treating infections often outweigh the potential adverse effects of antimicrobial administration, it is important to be aware of iatrogenic causes of new problems in the hospital. Beta-lactams such as penicillins and cephalosporins have been known to cause neurotoxicity. CASE: An 81-year-old man with a cerebral vascular accident without residual deficits, newly diagnosed hepatocellular carcinoma, and alcohol use disorder with last drink 2 weeks ago presented with lower back pain. MRI was suspicious for lumbar osteomyelitis/discitis. Empiric treatment for osteomyelitis with vancomycin and piperacillin-tazobactam was initiated, whichwas narrowed to vancomycin and cefepime while awaiting biopsy. The patient’s mental status on admissionwas fully alert and orientedwhich progressively changed to complete disorientation by day five. Initial workup of his encephalopathy was significant only for hyponatremia of 131 (patient had been without good food intake). Vital signs, other electrolytes, renal function, complete blood count, lactate, ammonia were all within normal limits. Computed tomography of the head was without convincing evidence of large hemorrhage or midline shift. Electroencephalogram obtained was negative for seizures, but demonstrated frequent triphasic waves, suggestive of metabolic encephalopathy. Due to growing clinical suspicion for cefepime neurotoxicity and grossly negative workup for other causes of metabolic encephalopathy, the patient was transitioned to ceftriaxone. By 48 hours, he was completely back to his baseline. DISCUSSION: Cefepime neurotoxicity is thought to be due to concentration-dependent GABA receptor antagonism. While most commonly seen among patients with renal impairment, a systemic review suggested cefepime toxicity in the setting of normal renal function may be more likely to occur in patients with pre-existing brain damage, possibly due to increased blood-brain barrier permeation. Our patient had history of substance abuse and prior stroke. It may have been interesting to obtain a serum or CSF cefepime concentration before discontinuation of the drug as toxic trough levels have been proposed in literature. One paper proposed therapeutic drug monitoring targeting troughs of <7.5 mg/L in patients with risk factors for cefepime toxicity.
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