Official websites use. Share sensitive information only on official, secure websites. Hester 1 ; V. Martin 1 ; S. Bansil 1 ; C. Fichtenbaum 1. Tracking ID Recognize the clinical setting of acyclovir-induced neurotoxicity. Diagnose and manage acyclovir-induced neuroxicity. Doppler ultrasounds were negative for deep venous thrombosis on two different tests.
She had been in stable health without recent opportunistic infections. Her past medical history was significant for a history of shingles, orolabial herpes simplex disease, pancreatitis secondary to nucleosides, Candida esophagitis, and asthma. A small vesicle has preceded the ulcer. Laboratory data included a white blood cell count of 8.
The Alveolar-arterial gradient was Computerized Tomography of the right lower extremity with contrast and multiplanar 3D reconstructions revealed no abscess. The next day the patient developed delirium and hypoxemia. The arterial blood gas revealed a pH 7. Chest radiography demonstrated pulmonary edema. Cultures of the peritoneal fluid, bronchoalveolar lavage, blood, and spinal fluid, were all negative.
The skin biopsy demonstrated findings consistent with calciphylaxis and pressure necrosis and the absence of viral inclusions. Acyclovir was discontinued on the sixth hospital day and a serum acyclovir level 12 hours after stopping the acyclovir was 5. Twenty-four hours after stopping the acyclovir the patient became alert and was extubated within 48 hours. Given all of these findings, the patient was diagnosed with acyclovir-induced respiratory depression. Neurotoxicities such as lethargy, confusion, and delirium have been reported with acyclovir and seem to be more prevalent in the setting of kidney dysfunction, but have been identified in otherwise healthy individuals.
To our knowledge, this is the first case report of acyclovir leading to respiratory failure in a patient with chronic renal disease. As demonstrated in this case, acyclovir should be used cautiously in those with renal failure to prevent neurotoxicities.
