South Texas orbital fracture protocol for emergency department evaluation of orbital fractures.

PURPOSE: Facial trauma and orbital fractures are common reasons for ophthalmology consultation in the emergency department (ED). The purpose of this study is to assess intervention rates and evaluate the acuity of ophthalmology consultation for orbital fractures in the ED. BASIC PROCEDURES: A retrospective chart review of orbital fractures was conducted over a 23-month period. 379 cases of orbital fractures were identified in a single-center study. All patients that received an ophthalmology consultation in the ED were included. Demographics, mechanism and location of orbital fracture, ophthalmic complications, and surgical and non-surgical ophthalmic interventions were recorded. The primary study outcome was the rate of ophthalmic consultation and intervention with and without retrospective application of our proposed South Texas Orbital Fracture Protocol (STOP). RESULTS: Immediate ophthalmic intervention was performed in 18.7% of patients. Statistically significant subjective, radiographic, and physical exam features correlating with ophthalmic intervention were identified and included globe rupture, concern for entrapment, orbital roof fractures, and retrobulbar hematoma. Retrospective application of our proposed South Texas Orbital Fracture Protocol (STOP) would have resulted in 186 of 379 patients requiring ophthalmology consultation, thus reducing consultation rate by 51% with an improved rate of intervention from 18.7% to 37.6%. CONCLUSIONS: Orbital fractures can be associated with severe ocular complications. Most cases, however, do not require emergent evaluation by an ophthalmologist. We propose the South Texas Orbital Fracture Protocol (STOP) for proper assessment and triaging of orbital fractures in the ED. While this clinical decision-making tool requires validation, it may offer improved healthcare efficiency, reduced costs, fewer unnecessary inter-facility transfers, and less burnout for ophthalmology residents.

Vulnerability of Dopaminergic Amacrine Cells to Chronic Ischemia in a Mouse Model of Oxygen-Induced Retinopathy.

PURPOSE: Retinal dopamine deficiency is a potential cause of myopia and visual deficits in retinopathy of prematurity (ROP). We investigated the cellular mechanisms responsible for lowered levels of retinal dopamine in an oxygen-induced retinopathy (OIR) mouse model of ROP. METHODS: Retinopathy was induced by exposing mice to 75% oxygen from postnatal day 7 (P7) to P12. Oxygen-induced retinopathy and age-matched control mice were euthanized at P12, P17, P25, or P42 to P50. Immunohistochemistry, electrophysiology, and biochemical approaches were used to determine the effect of OIR on the structure and function of dopaminergic amacrine cells (DACs). RESULTS: The total number of DACs was unchanged in OIR retinas at P12 despite significant capillary dropout in the central retina. However, a significant loss of DACs was observed in P17 OIR retinas (in which neovascularization was maximal), with the cell loss being more profound in the central (avascular) than in the peripheral (neovascular) regions. Cell loss was persistent in both regions at P25, at which time retinal neovascularization had regressed. At P42, the percentage of DACs lost (54%) was comparable to the percent decrease in total dopamine content (53%). Additionally, it was found that DACs recorded in OIR retinas at P42 to P50 had a complete dendritic field and exhibited relatively normal spontaneous and light-induced electrical activity. CONCLUSIONS: The results suggest that remaining DACs are structurally and functionally intact and that loss of DACs is primarily responsible for the decreased levels of retinal dopamine observed after OIR.