Assessment of the Accuracy and Cut-Failure Rates of Eye Bank-Cut Corneas for Use in Endothelial Keratoplasty: A Comparison of Outcomes Between 2010 and 2013.

PURPOSE: To evaluate the accuracy of eye bank-prepared precut donor corneas over time by comparing cut-failure rates and corneal thickness measurements in 2010 and 2013. METHODS: A total of 2511 human corneas cut by a technician-operated mechanical microkeratome intended for endothelial keratoplasty were evaluated prospectively at one large eye bank facility in 2010 and in 2013. The endothelium was evaluated by slit lamp, and specular microscopy both before and after cutting was performed. Graft thickness as measured by pachymetry and/or optical coherence tomography was collected to assess the accuracy of the cut tissue. Cut-failure rates were compared between normal donor tissue and tissue with significant preexisting scarring. RESULTS: The combined cut-failure rate in 2010 and 2013 was 2.3% (23/1000) and 1.6% (24/1511), respectively (P = 0.23). The cut-failure rate among normal tissue in 2010 and 2013 was 2.0% (19/927) and 1.4% (19/1400), respectively (P = 0.24). The cut-failure rate among previously scarred tissue in 2010 and 2013 was 5.5% (4/73) and 4.5% (5/111), respectively (P = 0.74). The mean surgeon-requested graft thickness was 144.7 µm (range 100-150, SD 13.6) and 127.2 µm (range 75-150, SD 25.2) in 2010 and 2013, respectively (P < 0.0001). The mean deviation from target graft thickness was 21.3 µm (SD 16.3) and 13.6 µm (SD 12.5) in 2010 and 2013, respectively (P < 0.0001). CONCLUSIONS: From 2010 to 2013, the combined cut-failure rates trended toward improvement, while the accuracy of graft thickness improved. This study suggests that the accuracy and success rates of tissue preparation for endothelial keratoplasty improve with experience and volume.

Traumatic optic neuropathy: facial CT findings affecting visual acuity.

The purpose of this study was to determine the relationship between admission visual acuity (VA) and facial computed tomographic (CT) findings of traumatic optic neuropathy (TON). We retrospectively evaluated CT findings in 44 patients with TON. Mid-facial fractures, extraconal and intraconal hematomas, hematomas along the optic nerve and the posterior globe, optic canal fracture, nerve impingement by optic canal fracture fragment, and extraconal and intraconal emphysema were evaluated. CT variables of patients with and without available VA were compared. VA was converted into logarithm of the minimum angle of resolution (logMAR) to provide a numeric scale for the purpose of statistical analysis. The risk factors related to poor VA on univariate analysis were as follows: intraconal hematoma [median logMAR -4.7 versus -1.15, p = 0.016] and hematoma along the optic nerve [median -4.7 versus -1.3, p = 0.029]. Intraconal hematoma was the best predictor of poor VA (coefficient, 1.01; SE, 0.34; and p = 0.008). Receiver operating characteristic (ROC) curve analysis showed that the presence of intraconal hematoma and hematoma along the optic nerve predicted poor VA (logMAR of -3.7 or lower) with an area under the curve of 0.8 and 0.85, respectively. TON patients at higher risk of severe visual impairment may be identified based on admission facial CT.

Management strategies for persistent epithelial defects of the cornea.

Management of patients with persistent epithelial defects of the cornea can be challenging to even the seasoned ophthalmologist. It is essential that one understands not only the pathophysiology of the failure of the epithelium to migrate and close a wound appropriately, but also the mechanism of action of the available treatment modalities at one's disposal. This article serves as a review of current standard therapies, recently introduced alternative therapies gaining in popularity, and a look into the newest developments that may change the way we manage corneal surface disease.

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.

Mechanisms for PDGF, a serum cytokine, stimulating loss of corneal keratocyte crystallins.

PURPOSE: As corneal stromal cells (keratocytes) become activated before transition to the fibroblastic repair phenotype in response to injury (in situ) or serum (in culture), the corneal crystallins, transketolase (TKT) and aldehyde dehydrogenase (ALDH1A1), are lost. The authors previously showed that the serum cytokine platelet-derived growth factor-BB (PDGF), but not transforming growth factor beta2 (TGF-beta2), stimulates TKT loss. The goal of this study was to further define the molecular mechanisms for PDGF-stimulated loss of crystallins to elucidate the pathway for keratocyte activation. METHODS: Freshly isolated rabbit corneal keratocytes were plated in serum-free medium with or without PDGF and/or specific inhibitors of the PDGF-relevant signal pathway components, PDGF receptor, PI3K/AKT, or ras-initiated MAPK proteins. Intracellular TKT protein levels were quantified by immunoblotting. Ubiquitinated TKT levels were assessed by immunoprecipitation, and TKT messenger RNA (mRNA) levels were quantified by quantitative reverse transcription-polymerase chain reaction. RESULTS: PDGF treatment at the same time as inhibition of PDGF receptor, Akt, JNK, and ubiquitin-proteasome pathway prevented PDGF-induced TKT protein loss. In contrast, treatment with PDGF did not affect TKT mRNA levels. CONCLUSIONS: The results suggest that PDGF-stimulated TKT loss is mediated through cross talk between PI3K-independent Akt and JNK. This signaling pathway leads to the degradation of existing TKT protein but does not compromise the accumulation of TKT mRNA. Therefore, cells retain the potential to reaccumulate TKT protein that is enabled by PDGF removal. These findings suggest that targeting PDGF signaling could improve repair outcomes after surgical procedures in the cornea.