Fulminant ependymitis following intraventricular rupture of brain abscess

A 48-year-old man with a history of a penetrating brain injury was referred with a presumptive diagnosis of bacterial meningitis. Examination revealed a brain abscess in addition to meningitis. Blood and cerebrospinal fluid (CSF) cultures were negative for bacteria, and empirical IV antibiotic therapy with vancomycin (VCM) and meropenem was initiated. Despite initial improvement, however, his condition rapidly deteriorated into coma following intraventricular rupture of the abscess and hydrocephalus. Thereafter, an emergency ventriculostomy was performed and the abscess was evacuated. Bacterial cultures of the pus were negative. To manage the hydrocephalus, 150–200 ml of CSF were drained daily. Intraventricular administration of VCM (20 mg q.d.) was added to the IV antibiotic therapeutic regimen after surgery. Although the primary abscess rapidly decreased in size, ependymitis developed in the fourth ventricle. This new lesion, which resulted from CSF dissemination from the primary abscess, was refractory to treatment, and eventually disappeared after the intraventricular VCM dosage was increased from 20 to 30 mg and continued for 30 days. A possible reason for the development of fulminant ependymitis and why it was refractory to treatment despite the shrinkage of the primary lesion may be that physiological CSF flow from the lateral to the fourth ventricle was lost due to CSF drainage, and the stagnant CSF flow coupled with an insufficient VCM level in the fourth ventricle facilitated the rapid growth of pathogens. Although intraventricular antibiotic administration is efficacious for treating ruptured brain abscesses, it may be associated with the unexpected development of secondary lesions.