Abstract Background Acyclovir is commonly used to treat herpes simplex and varicella-zoster infections. However, in patients with renal impairment, acyclovir and its metabolite 9-carboxymethoxymethylguanine (CMMG) can accumulate, leading to neurotoxicity. Elderly patients are particularly vulnerable due to age-related decline in renal function, polypharmacy, and comorbid conditions. Clinical presentation often mimics viral encephalitis, complicating timely recognition. Case Presentation We report the case of an 82-year-old female with chronic kidney disease (CKD), congestive heart failure, hypertension, and hypothyroidism, who presented with slurred speech, confusion, visual hallucinations, and recurrent falls for 2 days. She had been treated outpatient for herpes zoster with a ten-day course of valacyclovir 1 g three times daily, in addition to gabapentin 300 mg TID.On admission, she was disoriented, hallucinating, and bradycardic(40bpm). The patient had shingles (herpes zoster) rash involving the C7-C8 dermatomes on the upper extremity and T1-T12 dermatomes on the trunk. Laboratory evaluation revealed lactic acidosis (2.4 mmol/L), elevated creatinine (4.3 mg/dL; baseline 1.5-1.8 mg/dL), and hyperkalemia (5.9 mEq/L). Brain CT was unremarkable. Dopamine infusion was initiated for bradycardia, and nephrology started continuous renal replacement therapy (CRRT) for acute-on-chronic kidney injury. Infectious disease recommended IV acyclovir for presumed varicella-zoster reactivation, despite nephrology concerns for further nephrotoxicity. CSF analysis demonstrated lymphocytic pleocytosis and a positive cytomegalovirus (CMV) PCR, but a negative varicella-zoster PCR. Despite CRRT, her mental status failed to improve, she developed acute respiratory failure requiring intubation, and ultimately passed after goals-of-care discussions. Discussion Acyclovir-induced neurotoxicity can present as confusion, hallucinations, tremors, myoclonus, agitation, or seizures, typically within days of therapy initiation in the context of renal impairment. Pathophysiology involves the accumulation of acyclovir and CMMG crossing the blood-brain barrier. Diagnosis is challenging, as neuroimaging is often unrevealing and clinical features may mimic viral encephalitis. Measurement of CMMG in serum or CSF can support diagnosis, but it is rarely available. Conclusion Acyclovir-induced neurotoxicity is an underrecognized but potentially preventable cause of altered mental status in elderly patients with renal dysfunction. This case highlights the need for appropriate renal dosing, early hemodialysis and keeping a high clinical suspicion for neurotoxicity is crucial when suspected. Vigilant monitoring and judicious antiviral use are critical to prevent morbidity in this high-risk population. This abstract is funded by: None
Bhagavathi et al. (Fri,) studied this question.
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