A Case of Superior Orbital Fissure Syndrome Induced by Penetrating Orbital Injury

PURPOSE: We report a case of superior orbital fissure syndrome induced by penetrating orbital injury caused by a steel wire and analyzed the clinical outcomes. CASE SUMMARY: A 49-year-old female visited our clinic after a penetrating orbital injury through the right inferolateral conjunctiva caused by a steel wire. The best corrected visual acuity of the right eye was 0.8 and a fixed dilated pupil was detected. Partial ptosis and ophthalmoplegia were observed in the right eye. The computed tomography image revealed no sign of orbital wall fracture, retrobulbar hemorrhage or foreign body. Slightly increased signal intensity was observed on the magnetic resonance image but other abnormal findings of the extraocular muscle and optic nerve were not detected. Under the impression of superior orbital fissure syndrome, systemic steroid was administered orally. After 1 month, ptosis and ophthalmoplegia were partially improved. After 3 months, the pupil size and response were normalized. CONCLUSIONS: The oral steroid treatment was given to reduce the edema without orbital wall fracture after the penetrating orbital injury, which caused the superior orbital fissure syndrome. The symptom was relieved 3 months after the injury.

A Case of Orbital Apex Syndrome Induced by Penetrating Orbital Injury with Long-Term Results

PURPOSE: To report a case of orbital apex syndrome induced by penetrating orbital injury by a wire with the recovery process and clinical outcomes. CASE SUMMARY: A 40-year-old female visited our clinic after a penetrating orbital injury through the left inferomedial conjunctiva by a wire. The best corrected visual acuity of the left eye was 0.6, and ptosis and total ophthalmoplegia were observed. The patient showed a dilated pupil, swelling of the optic disc on fundus exam, and an inferior field defect on the automated perimetry. The computed tomography image revealed mild retrobulbar hemorrhage, but there was no orbital bony fracture. Enhancement of the optic nerve sheath was observed on the magnetic resonance image. The patient was admitted and received systemic antibiotics and steroid treatment. After 1 month, visual acuity, ptosis, and limitation in adduction were partly improved. After 3 months, depression and adduction were improved and the pupil size was normalized. However, further improvement was not observed after the one-year follow-up. CONCLUSIONS: The recovery from orbital apex syndrome was achieved until 3 months after injury. The final outcomes may depend on the mechanism and pathophysiology of the injury. Emergent diagnosis and proper management are essential to achieve optimal clinical results.

Two Cases of Orbital Apex Syndrome

PURPOSE: To report two cases of orbital apex syndrome: one induced by penetrating orbital injury and the other by severe optic nerve swelling associated with bacterial meningitis. METHODS: We have experienced a 40-year-old male after penetrating orbital injury who complained of loss of vision, ocular pain, ptosis, hypesthesia of forehead, and total ophthalmoplegia. The CT image of this patient showed a severe retrobulbar hemorrhage and marked enlargements of extraocular muscles. In a 62-year-old male who had a same symptom after headache and decreased mentality, a bacterial meningitis was diagnosed from CSF study and we saw a very severe swelling of the unilateral entire optic nerve and optic nerve sheath in CT. We managed these two patients with a large amount of systemic RESULTS: In 40-year-old man, there were improvements of ptosis and visual acuity from negative light perception to positive, but ophthalmoplegia was not improved. In 62-year-old man, ptosis and ophthalmo-plegia were improved after early antibiotics administration and papilledema disappeared two months after development, but visual acuity was not improved from negative light perception.