Orbital Floor Blow-Out Fracture in a Patient With Idiopathic Orbital Inflammation: Diagnostic and Reconstructive...

Idiopathic orbital inflammation (IOI) is a nonspecific inflammatory orbital disorder that may cause diplopia and extraocular motility restriction. Orbital trauma in patients with pre-existing IOI and diplopia may complicate the etiologic differentiation of post-traumatic ocular findings and the surgical decision-making process. To the best of our knowledge, no case describing the surgical management of a traumatic orbital floor blow-out fracture in a patient with pre-existing IOI has been reported in the literature. This case report aims to present the clinical approach to an orbital floor blow-out fracture in a patient with IOI, with particular emphasis on surgical timing and the selection of reconstructive material.

A 40-year-old woman presented ∼24 hours after blunt periorbital trauma. She had been receiving systemic corticosteroid and methotrexate therapy for IOI and had used prism glasses for diplopia before the trauma. On presentation, marked periorbital edema, ecchymosis, left enophthalmos, extraocular motility restriction in superior and lateral gaze, and diplopia were present. Computed tomography revealed an ∼2.8 cm² blow-out fracture of the left orbital floor. Because of the pre-existing diplopia, history of IOI, and marked post-traumatic inflammation, the contribution of mechanical restriction, post-traumatic edema, and the underlying inflammatory orbital disease to the early diplopia and motility restriction could not be clearly distinguished. After confirming that the IOI was inactive and that there was no ophthalmologic contraindication to surgery, and following resolution of the acute edema, the orbital floor was reconstructed with titanium mesh during the first week after trauma.

Postoperatively, the extraocular motility restriction resolved completely, with normal ocular movements in all directions of gaze. With prism glasses, diplopia markedly improved and was limited to extreme superolateral gaze. By the second postoperative day, this residual diplopia had also nearly completely resolved. No apparent inflammatory reactivation of IOI was observed postoperatively, and methotrexate therapy was resumed.

The evaluation of orbital blow-out fractures in patients with pre-existing IOI and diplopia may be challenging because traumatic and inflammatory processes can produce overlapping clinical findings. Surgical decision-making should be based on the combined assessment of the pretraumatic ocular status, disease activity, serial ophthalmologic examinations, enophthalmos, defect size, and other radiologic features. Surgical timing should take into account IOI activity and post-traumatic inflammatory findings, whereas the selection of reconstructive material should consider the mechanical requirements of the defect, the underlying inflammatory disease, and material biocompatibility. In this case, following confirmation of inactive IOI and resolution of the acute edema, titanium mesh reconstruction performed during the first week after trauma was not associated with IOI reactivation or an apparent implant-related inflammatory complication in the early postoperative period. However, this observation from a single case should not be interpreted as a generalizable conclusion regarding the safety of titanium mesh in patients with IOI.