Traumatic optic neuropathy prediction after blunt facial trauma: derivation of a risk score based on facial CT findings at admission.

PURPOSE: To determine the specific facial computed tomographic (CT) findings that can be used to predict traumatic optic neuropathy (TON) in patients with blunt craniofacial trauma and propose a scoring system to identify patients at highest risk of TON. MATERIALS AND METHODS: This study was compliant with HIPAA, and permission was obtained from the institutional review board. Facial CT examination findings in 637 consecutive patients with a history of blunt facial trauma were evaluated retrospectively. The following CT variables were evaluated: midfacial fractures, extraconal hematoma, intraconal hematoma, hematoma along the optic nerve, hematoma along the posterior globe, optic canal fracture, nerve impingement by optic canal fracture fragment, extraconal emphysema, and intraconal emphysema. A prediction model was derived by using regression analysis, followed by receiver operating characteristic analysis to assess the diagnostic performance. To examine the degree of overfitting of the prediction model, a k-fold cross-validation procedure (k = 5) was performed. The ability of the cross-validated model to allow prediction of TON was examined by comparing the mean area under the receiver operating characteristic curve (AUC) from cross-validations with that obtained from the observations used to create the model. RESULTS: The five CT variables with significance as predictors were intraconal hematoma (odds ratio, 12.73; 95% confidence interval [CI]: 5.16, 31.42; P < .001), intraconal emphysema (odds ratio, 5.21; 95% CI: 2.03, 13.36; P = .001), optic canal fracture (odds ratio, 4.45; 95% CI: 1.91, 10.35; P = .001), hematoma along the posterior globe (odds ratio, 0.326; 95% CI: 0.111, 0.958; P = .041), and extraconal hematoma (odds ratio, 2.36; 95% CI: 1.03, 5.41; P = .042). The AUC was 0.818 (95% CI: 0.734, 0.902) for the proposed model based on the observations used to create the model and 0.812 (95% CI: 0.723, 0.9) after cross-validation, excluding substantial overfitting of the model. CONCLUSION: The risk model developed may help radiologists suggest the possibility of TON and prioritize ophthalmology consults. However, future external validation of this prediction model is necessary.

Diagnosis of traumatic optic neuropathy: application of diffusion tensor magnetic resonance imaging.

BACKGROUND: Using diffusion tensor imaging, we evaluated the directional diffusivities of the optic nerve in patients with traumatic optic neuropathy (TON). METHODS: Our study consisted of 12 patients with unilateral TON, 6 patients with severe traumatic brain injury (comparison group A), and 6 patients with normal conventional brain magnetic resonance imaging (comparison group B). The contralateral optic nerve in patients with TON also was evaluated (comparison group C). Two trauma radiologists, blinded to the clinical diagnosis, independently obtained the directional diffusivities. The intraorbital optic nerve was divided into anterior and posterior segments to evaluate intersegmental differences in directional diffusivities. RESULTS: The mean axial diffusivity (AD) in both optic nerve segments and the mean diffusivity (ADC) in the posterior segment on the affected side were significantly lower and differentiated subjects with TON from those in comparison groups A and B. Area under the receiver operating characteristic curve was 0.762, 0.746, and 0.737 for posterior AD, anterior AD, and posterior ADC, respectively. The mean AD, mean diffusivity, and radial diffusivity were lower in the affected nerves in comparison to the contralateral nerve (comparison group C), but the values did not reach statistical significance. CONCLUSION: Decreased AD and mean diffusivity in the posterior segment of the optic nerve may serve as a biomarker of axonal damage in patients with TON and merits further investigation as a predictor of initial visual acuity and potential visual recovery.

Prevalence and factors predictive of intraocular fungal infection in patients with fungemia at an academic urban tertiary care center.

OBJECTIVE: To report the prevalence and to identify factors predictive of intraocular infection in patients with fungemia receiving prophylactic antifungal therapy. METHODS: A retrospective review of patients who received prophylactic antifungal therapy and a dilated fundus examination at an academic urban tertiary care center from 2000 to 2007. Basic demographic information, fungal species grown, antifungal agent(s) used, number of positive blood culture specimens, visual acuity, visual symptoms, and known risks of disseminated candidiasis were noted. Logistic regression analysis was used to determine the factors significantly associated with intraocular fungal infection. RESULTS: A total of 132 patients with positive fungemia culture were requested to have ophthalmology consults. The prevalence of ocular infection was 6.9% (N=9). All nine patients were infected with Candida species. Undergoing gastrointestinal (GI) surgery within the prior 6 months was significantly related to developing intraocular infection, with an odds ratio of 18.5 (95% confidence interval, 15.1-24.3; P=0.002). Having ≥3 positive fungal blood cultures was also a significant risk factor, with an odds ratio of 2.6 (95% confidence interval, 1.8-3.7; P=0.03). Among 40 patients having GI surgery, eight (20.0%) had intraocular fungal disease, compared with one of 92 patients (1.1%) not having GI surgery. Among 125 patients with a negative baseline examination result, two of 32 patients (6.3%), who had recent GI surgery, subsequently developed fungal ocular disease, compared with 0 of 93 patients (0%), who did not have recent GI surgery. CONCLUSION: Recent GI surgery and higher numbers of positive fungal blood culture specimens may be predictive of candida ocular infections. Normal baseline fundoscopy examination results in patients with such risks may require repeat evaluations to detect delayed manifestations.

The mammalian pannexin family is homologous to the invertebrate innexin gap junction proteins.

We have cloned the genes PANX1, PANX2 and PANX3, encoding putative gap junction proteins homologous to invertebrate innexins, which constitute a new family of mammalian proteins called pannexins. Phylogenetic analysis revealed that pannexins are highly conserved in worms, mollusks, insects and mammals, pointing to their important function. Both innexins and pannexins are predicted to have four transmembrane regions, two extracellular loops, one intracellular loop and intracellular N and C termini. Both the human and mouse genomes contain three pannexin-encoding genes. Mammalian pannexins PANX1 and PANX3 are closely related, with PANX2 more distant. The human and mouse pannexin-1 mRNAs are ubiquitously, although disproportionately, expressed in normal tissues. Human PANX2 is a brain-specific gene; its mouse orthologue, Panx2, is also expressed in certain cell types in developing brain. In silico evaluation of Panx3 expression predicts gene expression in osteoblasts and synovial fibroblasts. The apparent conservation of pannexins between species merits further investigation.