IntroductionPatients with neurofibromatosis type 2 (NF2) develop bilateral cochleovestibular schwannomas (CVSs) that cause binaural deafness in most individuals. Hearing loss occurs in an unpredictable manner and the underlying mechanisms are not known. To gain insight into the pathophysiologic basis for hearing loss in NF2, we performed a prospective cross-sectional study of untreated ears in NF2 patients.MethodsOne hundred consecutive NF2 patients in a prospective natural history study were included. Clinical and audiometric data were analyzed for treatment naïve ears. In addition to standard MR-imaging sequences, alterations in intralabyrinthine protein content were determined utilizing high resolution FLAIR, the presence of cochlear aperture obstruction was determined by examining 3D T2 sequences, and endolymphatic hydrops was identified on delayed post-contrast FLAIR sequences.ResultsEighty-nine ears harboring 84 untreated CVSs in 56 consecutive NF2 patients (age 30±16 years) were analyzed. Thirty-four (38%) ears had varying degrees of hearing loss. Elevated intralabyrinthine protein was identified in 70 (75%) ears by FLAIR MR-imaging and was strongly associated with the presence of hearing loss (32/34 hearing loss ears; 94%)(Fisher's exact test; P = .005). Elevated intralabyrinthine protein was associated with the presence of CVS-associated cochlear aperture obstruction (64 of 67 ears with elevated protein; 96%)(Fisher's exact test; P<0.0001) in both normal and hearing loss ears. Elevated intralabyrinthine protein was not identified in ears without CVS (5 ears). While larger tumor size was associated with hearing loss (P = 0.006), 16 hearing loss ears (47%) harbored CVSs less than 0.5 cm3, including 14 ears (88%) with block of the cochlear aperture and elevated protein.DiscussionThese findings are consistent with a model in which hearing loss develops as a result of cochlear aperture obstruction and accumulation of intralabyrinthine protein. MRI based identification of elevated intralabyrinthine protein may help identify the ear at-risk for developing hearing loss.

OBJECTIVEWound infections following spinal surgery for deformity place a high toll on patients, providers, and the health care system. The prophylactic application of intraoperative vancomycin powder has been shown to lower the infection risk after thoracolumbar decompression and fusion for deformity correction. The purpose of this study was to assess the microbiological patterns of postoperative surgical site infections (SSIs) after prophylactic use of vancomycin powder in adult patients undergoing spinal deformity surgery.METHODSAll cases involving adult patients who underwent spinal deformity reconstruction at Duke University Medical Center between 2011 and 2013 with a minimum of 3 months of clinical follow-up were retrospectively reviewed. In all cases included in the study, crystalline vancomycin powder was applied to the surgical bed for infection prophylaxis. Baseline characteristics, operative details, rates of wound infection, and microbiological data for each case were gathered by direct medical record review.RESULTSA total of 1200 consecutive spine operations were performed for deformity between 2011 and 2013. Review of the associated records demonstrated 34 cases of SSI, yielding an SSI rate of 2.83%. The patients’ mean age (± SD) was 62.08 ± 14.76 years. The patients’ mean body mass index was 30.86 ± 7.15 kg/m2, and 29.41% had a history of diabetes. The average dose of vancomycin powder was 1.41 ± 2.77 g (range 1–7 g). Subfascial drains were placed in 88% of patients. All SSIs occurred within 30 days of surgery, with deep wound infections accounting for 50%. In 74% of the SSIs cultures were positive, with about half the organisms being gram negative, such as Citrobacter freundii, Proteus mirabilis, Morganella morgani, and Pseudomonas aeruginosa. There were no adverse clinical outcomes related to the local application of vancomycin.CONCLUSIONSOur study suggests that in the setting of prophylactic vancomycin powder use, the preponderance of SSIs are caused by gram-negative organisms or are polymicrobial. Further randomized control trials of prophylactic adjunctive measures are warranted to help guide the choice of empirical antibiotic therapy while awaiting culture data.