Sinonasal procedures are performed adjacent to the orbit and optic pathway, so even rare complications can be devastating. Reported mechanisms of postoperative visual loss include retrobulbar hemorrhage with OCS, central/branch retinal artery occlusion (CRAO/BRAO),1,2 anterior/posterior ischemic optic neuropathy (AION/PION), optic nerve or medial rectus injury, orbital emphysema, and orbital cellulitis/orbital apex syndrome.3,4 In OCS, outcomes worsen rapidly without urgent lateral canthotomy/cantholysis, ideally within about two hours.5

CASE

Patient: Male, 26 years.

Pre-operative diagnosis: Deviated nasal septum; bilateral inferior turbinate hypertrophy.

Postoperative diagnosis: Same.

Procedure: Septoplasty; bilateral inferior turbinate RFA.

Anesthesia:  General endotracheal.

Septoplasty

After infiltration with 1% Lidocaine with epinephrine (1:100,000), a hemitransfixion incision was made at the caudal septum. Mucoperichondrial and mucoperiosteal flaps were elevated bilaterally. Deviation of the quadrangular cartilage and bony septum (vomer/ethmoid) was corrected by scoring, reshaping, and limited resection while preserving a 1-1.5 cm dorsal/caudal L-strut. The septum was centralized; quilting sutures re-opposed the flaps, and the incision was closed with absorbable suture. Silicone splints were placed and secured.

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Bilateral Inferior Turbinate Radiofrequency Ablation (RFA)

The inferior turbinates were infiltrated submucosally with dilute epinephrine. A radiofrequency probe was passed submucosally along the turbinate (anterior, mid, posterior), avoiding mucosal perforation. Energy was delivered 4-5 s at 12 W (coagulation mode) at each site to create controlled submucosal lesions that reduce volume while preserving mucosa; the contralateral side was treated similarly. Hemostasis was obtained with brief bipolar coagulation; light packing was placed. For access, the inferior turbinate was medialized; additional submucosal ablation was performed using monopolar and bipolar electrocautery as indicated, after which the turbinate was lateralized back to its native position.

Postsurgical period

Postoperatively, the patient developed acute monocular vision loss and underwent a comprehensive ophthalmic evaluation. He was seen at two hospitals in Georgia and subsequently at a tertiary center in Israel. Laboratory testing and CT imaging were unrevealing, and no definitive etiology was identified.

Differential diagnosis of nasal-surgery vision loss

1. Vascular / ischemic:

• Retrobulbar hemorrhage → Orbital compartment syndrome (OCS): Vision-threatening emergency; prompt lateral canthotomy/cantholysis improves outcomes when performed within 2 hours. Often arises from ethmoidal vessel injury.

• CRAO/BRAO or retinal arterial vasospasm: Sudden, painless monocular loss has been reported after sinonasal surgery and rhinoplasty.

• Ischemic optic neuropathy (AION/PION): Rarely reported after rhinologic procedures: perioperative hypotension, anemia, and hemodilution increase the risk for PION.

2. Direct surgical/thermal injury:

• Optic nerve injury during ethmoid/sphenoid work.

• Extraocular muscle (medial rectus) injury causing diplopia and functional compromise.

3. Pressure/air phenomena:

• Orbital/periorbital emphysema with sight-threatening sequelae reported after FESS.

4. Infectious/inflammatory:

• Orbital cellulitis / orbital apex syndrome spreading from sinuses; requires urgent imaging and IV therapy.

5. Drug/physiology related:

• Vasoconstrictor-associated arterial spasm (e.g., epinephrine mixtures) has been reported in retinal ischemic events after ENT procedures.

• Systemic hypotension/hemodilution during anesthesia predisposes to PION.