Imaging the Tight Orbit: Radiologic Manifestations of Orbital Compartment Syndrome.

BACKGROUND AND PURPOSE: Orbital compartment syndrome is a sight-threatening emergency caused by rising pressure inside the orbit. It is usually diagnosed clinically, but imaging might help when clinical findings are inconclusive. This study aimed to systematically evaluate imaging features of orbital compartment syndrome. MATERIALS AND METHODS: This retrospective study included patients from 2 trauma centers. Proptosis, optic nerve length, posterior globe angle, morphology of the extraocular muscles, fracture patterns, active bleeding, and superior ophthalmic vein caliber were assessed on pretreatment CT. Etiology, clinical findings, and visual outcome were obtained from patient records. RESULTS: Twenty-nine cases of orbital compartment syndrome were included; most were secondary to traumatic hematoma. Pathologies occurred in the extraconal space in all patients, whereas intraconal abnormalities occurred in 59% (17/29), and subperiosteal hematoma in 34% (10/29). We observed proptosis (affected orbit: mean, 24.4 [SD, 3.1] mm versus contralateral: 17.7 [SD, 3.1] mm; P < .01) as well as stretching of the optic nerve (mean, 32.0 [SD, 2.5] mm versus 25.8 [SD, 3.4] mm; P < .01). The posterior globe angle was decreased (mean, 128.7° [SD, 18.9°] versus 146.9° [SD, 6.4°]; P < .01). In 69% (20/29), the superior ophthalmic was vein smaller in the affected orbit. No significant differences were detected regarding the size and shape of extraocular muscles. CONCLUSIONS: Orbital compartment syndrome is characterized by proptosis and optic nerve stretching. In some cases, the posterior globe is deformed. Orbital compartment syndrome can be caused by an expanding pathology anywhere within the orbit with or without direct contact to the optic nerve, confirming the pathophysiologic concept of a compartment mechanism.

Clinical characteristics and immunohistochemical analysis of p53, Ki-67 and cyclin D1 in 80 odontogenic keratocysts.

OBJECTIVE: The aim of this study was to evaluate clinical parameters and expression patterns of Ki-67, cyclin D1 and p53 in odontogenic keratocysts. MATERIAL AND METHODS: In this study, fifty-three patients with 80 odontogenic keratocysts were included. The medical records of these patients were reviewed retrospectively. To elucidate the molecular pathogenesis of the disease, the expression of p53, Ki-67 and cyclin D1 was analyzed using immunohistochemistry. RESULTS: A total of 53 patients (mean age 38 years) with a median follow-up of 4.2 years (ranging from 4 days to 14.4 years) were evaluated. The rates of recurrence and post-operative complications varied depending on the surgical approach: cystectomy and peripheral ostectomy led to manageable low rates of complications and recurrence frequency. Immunohistochemical evaluation revealed that all lesions were positive for Ki-67 and cyclin D1 expression. The expression of Ki-67 was associated with the degree of inflammation. Cyclin D1 was expressed significantly higher in syndrome-associated keratocystic lesions. In contrast to non-syndromal lesions, all syndromal lesions expressed p53. CONCLUSION: This investigation demonstrates that the pathogenesis of syndromal keratocysts appears to differ from sporadic odontogenic keratocysts. Additionally, the primary and recurrent non-syndromal keratocysts have a similar etiology, as no differences in the expression patterns of Ki-67, p53 and cyclin D1 were observed.