Orbital decompression: current concepts

Abstract

The orbit in Graves disease undergoes expansion in soft tissue content as a result of the infiltration of orbital fat, extraocular muscles, and the lacrimal gland. Compression of the intraorbital contents leads to disorders of the lid-corneal interface, keratopathy, motility disturbances, exophthalmos, and optic neuropathy. Orbital decompression has traditionally been reserved for those patients with unremitting optic neuropathy. This article provides a historical review of orbital decompression, as well as a review of the evolution of surgical approaches toward both soft tissue and bony decompression. Recent trends in surgical management include fat decompression, more extensive posterior sculpting of the lateral wall, and direct approaches to the medial wall. Preoperative predictors of diplopia and hypoglobus are addressed, as are the various techniques that are employed to limit new postoperative strabismus. The roles of endoscopy and combined surgical techniques are also reviewed. Expanded indications for decompression and its effect on increased intraocular pressure are discussed as well.

Efficacy and side effects of ‘swinging eyelid’ orbital decompression in Graves' orbitopathy: a proposal for standardized evaluation of diplopia

“…Furthermore, it may be used to treat disfiguring exophthalmos in patients with noncompressive GO. 1 Postoperative diplopia is the most frequently reported side effect of orbital decompression using bone removal techniques, especially in patients with compressive optic neuropathy (CON). 1 Transantral as well as transnasal orbital decompression have been reported to induce diplopia in up to 73% of patients.…”

Endoscopic transnasal orbital decompression for visual failure due to sphenoid wing meningioma

“…Surgical relief of thyroid optic neuropathy has been practised for many years, 3,4 this requiring bone removal and opening of the apical orbital periosteumFthereby relieving high tissue pressures in the orbital apex. [1][2][3][4] As the medial orbital wall is very thin and extends in continuity to the apex, it is the most readily removed for this purpose.…”

“…[1][2][3][4] As the medial orbital wall is very thin and extends in continuity to the apex, it is the most readily removed for this purpose. The orbital floor is removable only to the back of the maxilla, about 1 cm short of the orbital apex, and although the lateral wall (greater wing of the sphenoid) can be burred away to the apex, this tends to be an awkward procedureFwith thick bone and bleeding from the vascular diploi.…”

“…The orbital floor is removable only to the back of the maxilla, about 1 cm short of the orbital apex, and although the lateral wall (greater wing of the sphenoid) can be burred away to the apex, this tends to be an awkward procedureFwith thick bone and bleeding from the vascular diploi. Many different approaches to orbital decompression have been described, 3,4 but there has been recent interest in approaches that avoid skin incisionFfor example, the transcaruncular approach to the medial orbital wall. 5,6 Intraoral (transantral) or transnasal decompression has been used for many years to remove the medial orbital wall and part of the floor, and is well described in patients with thyroid eye disease.…”

Postural visual obscurations in patients with inactive thyroid eye disease; a variant of ‘hydraulic’ disease

“…[1][2][3][4][5] Although increased apical pressure will inevitably raise episcleral venous pressure, this is only rarely manifested as episcleral vascular dilation. Some patients with inactive thyroid eye disease and mild proptosis, however, have a markedly increased orbital pressure that can be associated with deep orbital vascular congestion, persistently raised intraocular pressures and, in some cases, optic neuropathy.…”