White-eyed blowout fracture with muscle entrapment misdiagnosed as increased intracranial pressure: An important clinical lesson.

Patients with white-eyed blowout fracture with muscle entrapment in the pediatric population may be misdiagnosed as increased intracranial pressure (ICP) due to the similarity in presenting symptoms. A delay in the correct diagnosis can lead to permanent sequelae including diplopia, permanent loss of vision, and death. In this case report we discuss the treatment of a male pediatric patient who presented in the ED with nausea, confusion, and restricted eye gaze. He was misdiagnosed with increased intracranial pressure and was admitted to the PICU. Subsequent consultation by ophthalmology allowed for the correct diagnosis of a trapdoor fracture. The patient was taken to the OR for emergent orbitotomy with reduction of the fracture and release of the entrapped muscle. Symptoms of white-eyed orbital blowout fractures with muscle entrapment easily mimic symptoms of head trauma with increased ICP. Misdiagnosis of trapdoor orbital fractures with entrapment can be avoided by ordering and critically reviewing an orbital CT and requesting an ophthalmologic consultation in the ED to evaluate extraocular movement. This report should help to increase awareness of symptoms of white-eyed orbital blowout fractures with muscle entrapment, prevent confusion with elevated ICP, and assist accurate and timely diagnosis in the ED to arrange appropriate management and surgical intervention to ensure best outcomes.

Eye injury from electrical weapon probes: Mechanisms and treatment.

PURPOSE: While generally reducing morbidity and mortality, TASER® electrical weapons have risks associated with their usage, including burn injuries and head and cervical trauma associated with uncontrolled falls. The primary non-fatal complications appear to be significant eye injury but no analysis of the mechanisms or suggested treatments has been published. METHODS: We used a biomechanical model to predict the risk of eye injury as a function of distance from the weapon muzzle to the eye. We compared our model results to recently published epidemiological findings. We also describe the typical presentation and suggest treatment options. RESULTS: The globe rupture model predicted that a globe rupture can be expected (50% risk) when the eye is within 6 m of the muzzle and decreases rapidly beyond that. This critical distance is 9 m for lens and retinal damage which is approximately the range of the most common probe cartridges. Beyond 9 m, hyphema is expected along with a perforation by the dart portion of the probe. Our prediction of globe rupture out to 6 m (out of a typical range of 9 m) is consistent with the published risk of enucleation or unilateral blindness being 69 ±â€¯18%, with an eye penetration. CONCLUSIONS: Significant eye injury is expected from a penetration by an electrical weapon probe at close range. The risk decreases rapidly at extended distances from the muzzle. Not all penetrating globe injuries from electrical weapon probes will result in blindness.

Elevated levels of Merkel cell polyoma virus in the anophthalmic conjunctiva.

The human ocular surface hosts a paucibacterial resident microbiome and virome. The factors contributing to homeostasis of this mucosal community are presently unknown. To determine the impact of ocular enucleation and prosthesis placement on the ocular surface microbiome, we sampled conjunctival swabs from 20 anophthalmic and 20 fellow-eye intact conjunctiva. DNA was extracted and subjected to quantitative 16S rDNA PCR, biome representational karyotyping (BRiSK), and quantitative PCR (qPCR) confirmation of specific organisms. 16S ribosomal qPCR revealed equivalent bacterial loads between conditions. Biome representational in silico karyotyping (BRiSK) demonstrated comparable bacterial fauna between anophthalmic and intact conjunctiva. Both torque teno virus and Merkel cell polyoma virus (MCPyV) were detected frequently in healthy and anophthalmic conjunctiva. By qPCR, MCPyV was detected in 19/20 anophthalmic samples compared with 5/20 fellow eyes. MCPyV copy number averaged 891 copies/ng in anophthalmic conjunctiva compared with 193 copies/ng in fellow eyes (p < 0.001). These results suggest that enucleation and prosthesis placement affect the ocular surface flora, particularly for the resident virome. As MCPyV has been shown to be the etiologic cause of Merkel cell carcinoma, understanding the mechanisms by which the ocular surface regulates this virus may have clinical importance.

Steroid receptor coactivator-1 from brain physically interacts differentially with steroid receptor subtypes.

In vitro studies reveal that nuclear receptor coactivators enhance the transcriptional activity of steroid receptors, including estrogen (ER) and progestin receptors (PR), through ligand-dependent interactions. Whereas work from our laboratory and others shows that steroid receptor coactivator-1 (SRC-1) is essential for efficient ER and PR action in brain, very little is known about receptor-coactivator interactions in brain. In the present studies, pull-down assays were used to test the hypotheses that SRC-1 from hypothalamic and hippocampal tissue physically associate with recombinant PR or ER in a ligand-dependent manner. SRC-1, from hypothalamus or hippocampus, interacted with PR-A and PR-B in the presence of an agonist, but not in the absence of ligand or in the presence of a selective PR modulator, RU486. Interestingly, SRC-1 from brain associated more with PR-B, the stronger transcriptional activator, than with PR-A. In addition, SRC-1 from brain, which was confirmed by mass spectrometry, interacted with ERalpha and ERbeta in the presence of agonist but not when unliganded or in the presence of the selective ER modulator, tamoxifen. Furthermore, SRC-1 from hypothalamus, but not hippocampus, interacted more with ERalpha than ERbeta, suggesting distinct expression patterns of other cofactors in these brain regions. These findings suggest that interactions of SRC-1 from brain with PR and ER are dependent on ligand, receptor subtype, and brain region to manifest the pleiotropic functional consequences that underlie steroid-regulated behaviors. The present findings reveal distinct contrasts with previous cell culture studies and emphasize the importance of studying receptor-coactivator interactions using biologically relevant tissue.

Posterior displacement of the lamina cribrosa in glaucoma: in vivo interindividual and intereye comparisons.

PURPOSE: We assessed in vivo lamina cribrosa (LC) position within the optic nerve head in glaucoma. METHODS: For interindividual comparison, glaucoma patients at various stages and normal subjects were recruited. For intraindividual, intereye comparison, glaucoma patients with visual field (VF) defects in only one eye were recruited separately. Serial horizontal and vertical enhanced depth imaging optical coherence tomography (EDI OCT) B-scans of the optic nerve head were obtained prospectively from each participant. Mean and maximum anterior LC depths were measured in 11 equally spaced horizontal B-scans, excluding the LC insertion area under the Bruch's membrane and scleral rim. RESULTS: Totals of 47 glaucomatous eyes (47 patients; VF mean deviation, -12.7±8.2 dB) and 57 normal eyes (57 subjects) were enrolled for the interindividual comparison. Mean and maximum LC depths were significantly greater in the glaucomatous than in the normal eyes in all 11 scans (all P<0.03). There were 54 glaucoma patients with VF defects in only one eye (VF mean deviation, -15.6±8.8 dB) included in the intereye comparison. Mean and maximum LC depths were significantly greater in the eyes with VF defects than in the fellow eyes with no VF defects in all 11 scans (all P<0.01). CONCLUSIONS: The central and midperipheral LC is located more posteriorly in glaucomatous than in normal eyes, as well as in eyes with VF defects compared to fellow eyes with no VF defects. These results support the concept of posterior LC displacement in glaucoma and provide the basis for future in vivo human studies.

Isoflurane anesthesia interferes with the expression of cocaine-induced sensitization in female rats.

Repeated cocaine administration results in a progressive sensitization of behavior which typically occurs more readily in female rats than in males. Our recent studies of rats undergoing surgical procedures revealed that following anesthesia, females sensitized less than males receiving identical repeated cocaine injections. Since isoflurane acts primarily by increasing the effects of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) and reducing the effects of the excitatory amino acid glutamate, these amino acids may play more prominent roles in sensitization to cocaine in females than previously understood. In order to examine the effects of isoflurane on cocaine-sensitization, we administered cocaine (15 mg/kg i.p) or saline to adult male and female Sprague-Dawley rats for 9 days; on day 10, half of the rats were subjected to isoflurane anesthesia and the other half did not receive anesthesia. On day 11, rats were given their last dose of either cocaine or saline. We recorded behaviors for 1h on days 1, 9 and 11. Locomotor activity and stereotyped behaviors were quantified using photo beam monitors and the scoring of video tapes, respectively. Results indicated that a single exposure to isoflurane significantly dampens the stereotypic behavior associated with repeated cocaine administration in females but not in males. They further suggest that either GABA or glutamate play more prominent roles in cocaine-sensitization behavior in females than in males.