Orbital congestion complicating treatment of cerebral vascular anomalies

The decision between conservative management and invasive treatment of juxtaorbital intracranial vascular anomalies can be challenging. Whereas arteriovenous malformations (AVMs) can lead to vision loss and are potentially life-threatening if they rupture, invasive endovascular and surgical procedures also carry risks.

Two patients developed blinding orbital congestion soon after they were treated successfully for cerebral vascular anomalies. The first patient, a 36 year-old man, underwent partial embolization followed by resection of a congenital frontal-lobe AVM. The second patient, a 62 year-old woman, underwent embolization of a periorbital/skull base dural arteriovenous malformation. After intervention, both patients developed unilateral vision loss proptosis, chemosis, complete ophthalmoplegia, and increased intraocular pressure. The first patient suffered from acute orbital compartment syndrome in the absence of any acute localized hemorrhage or thrombosis. The second patient experienced refractory acute glaucoma from orbital congestion, secondary hyphema, and angle closure caused by superior ophthalmic vein and cavernous sinus thromboses.

These cases highlight the potential for orbital congestion to worsen acutely after invasive treatment of juxtaorbital cerebral vascular anomalies and suggest diverse mechanisms of resultant visual and orbital compromise. The first case represents the first report of orbital compartment syndrome after resection of a congenital AVM.