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Aciclovir/immunosuppressants Infections and encephalopathy: case report

A 75-year-old man developed herpes zoster reactivation involving the L2-L3 dermatome as well as CNS and blood infection caused by Varicella zoster virus (VZV) following immunosuppressive therapy with tacrolimus, prednisone and mycophenolate mofetil. Additionally, he developed aciclovir-induced encephalopathy during treatment with aciclovir for VZV infection. His immunosuppressive therapy with tacrolimus, prednisone and mycophenolate mofetil was also considered to have played a role in the development of encephalopathy [not all dosages, routes and durations of treatments to reactions onsets stated]. The man, who presented to the hospital for urgent management of esophageal perforation and pneumomediastinum following an episode of emesis, was hospitalised. He had presented from long-term care facility, where he had recently been placed due to a profound lower extremity weakness. Following repair of his esophageal tear, he was transferred to medical team for medical management of mediastinitis and evaluation of his profound lower extremity weakness. He reported that several months prior to the admission, he had a lower back pain and a rash and had been diagnosed with herpes zoster reactivation involving the L2–L3 dermatome. Consequently, he had been treated with aciclovir and prednisone. One month later, he developed the lower extremity weakness that progressed to paralysis. At that time, he was alert, interactive and had a normal mental status. On current admission, his examination revealed severe lower extremity weakness with overt lower motor neuron findings. Additionally, he was found to have signs of atrophy in the lower extremities with fasciculations and hyporeflexia. Following a comprehensive evaluation, both his CSF and serum by PCR were found to be positive for VZV. Electromyography studies showed signs of active denervation in the lower extremities with upper extremity motor nerves, concerning for multifocal motor neuropathy or VZV polyneuritis. It was found that he had undergone renal transplant 5 years prior to the admission and had been receiving maintenance immunosuppressive therapy with tacrolimus, prednisone and mycophenolate mofetil. Consequently, his herpes zoster reactivation involving the L2–L3 dermatome as well as the CNS and blood infection caused by VZV was attributed to the immunosuppressive therapy with tacrolimus, prednisone and mycophenolate mofetil. In view of the increased risk of VZV dissemination due to his immunocompromised state, the man was initiated on IV aciclovir 10 mg/kg every 8h for 3 weeks on day 3 of the admission along with cefepime for mediastinitis. Baseline creatinine at the time of admission was 0.44 mg/dL. On day 11 of admission, he developed encephalopathy with the symptoms of mild confusion, disorientation and intermittent hallucinations. Over time, he developed a progressive confusion to the point of obtundation and was responding only minimally to noxious stimuli. The differential diagnosis