Indications for Orbital Decompression

Orbital decompression is performed in a variety of conditions and for various indications. The most common disease process leading to orbital decompression is thyroid eye disease. In this condition, the orbital fat and extraocular muscles enlarge due to inflammation. In severe cases, the enlarged muscles result in crowding at the orbital apex, which causes compression of the optic nerve as it passes through the orbital apex into the optic canal. Clinical signs of compressive optic neuropathy include decreased visual acuity, afferent papillary defect, and dyschromatopsia. Long-standing compressive optic neuropathy may result in optic nerve pallor and permanent visual loss. Further confirmation of optic neuropathy is done with automated visual field testing and orbital imaging ( ▶ Fig. 7.1). Computed tomography (CT) without contrast is adequate to assess the orbits in cases of thyroid orbitopathy. It is important to avoid unnecessary intravenous CT contrast in patients with thyroid eye disease, as there are reported cases of severe and immediate orbitopathy exacerbation following the administration of iodine-containing intravenous contrast. ¹ Magnetic resonance imaging also nicely delineates the extraocular muscles and optic nerves. However, it is important to evaluate the bony orbital walls if orbital decompression is contemplated; hence, CT is the preferred method of imaging. Further, stereotactic image guidance systems are often employed in endoscopic orbital decompression and CT imaging is required for this.

Other indications for orbital decompression surgery in patients with thyroid eye disease are to reduce proptosis causing corneal breakdown or severe cosmetic deformity. Exposure keratopathy is common in patients with thyroid eye disease because of the underlying autoimmune disorder, as well as proptosis and eyelid retraction resulting in increased ocular surface area exposed to the environment. If untreated, patients with severe exposure keratopathy may develop corneal ulceration or perforation resulting in visual loss. In addition, many patients with thyroid orbitopathy suffer psychosocially from their disfigurement. ² Surgery to restore a more normal appearance is important.

Other conditions for which orbital decompression surgery may be indicated include orbital tumors or other space-occupying lesions such as vascular malformations that are causing compressive optic neuropathy, severe proptosis with exposure keratopathy, or extreme disfigurement. In these conditions, it is important to determine that opening the bony orbital walls is appropriate and will not lead to undesired tumor seeding of the spaces outside the orbit, as in the case of a malignancy.

7.2 Surgical Approaches to Orbital Decompression

Orbital decompression may be accomplished via bone removal from any of the orbital walls or from orbital fat removal with or without bony decompression. ^{3,​ 4} Medial wall and floor decompression may be accomplished via a variety of external approaches, including transcutaneous, transconjunctival, and transcaruncular. However, the endoscopic approach has gained favor in recent years and this technique will be covered in detail below. Lateral wall decompression may be performed by removing bone from any location between the lateral orbital rim to the sphenoid trigone via a cutaneous incision. Orbital roof decompression has been reported in intractable cases. ⁵

The decision of which wall or walls to decompress is based on surgeon preference and experience as well as a variety of variables including the presence or absence of diplopia, presence of compressive optic neuropathy, and the degree of proptosis. The risk of diplopia after orbital decompression is a significant factor in the decision to undergo this procedure. ^{6,​ 7} Surgical techniques have been described to prevent diplopia, including preservation of the inferomedial strut of bone between the medial wall and floor of the orbit in cases where both walls are being removed for maximal decompression. This will be discussed in detail below. ⁸ A number of publications also advocate the utility of the balanced decompression to avoid diplopia, where the medial and lateral walls are decompressed in an effort to maintain globe centration in the orbit and prevent postoperative diplopia. Results are mixed, with postoperative diplopia ranging from 10 to 33%. ^{9,​ 10,​ 11,​ 12} In cases of compressive optic neuropathy, it is thought that decompression of the medial orbital wall extending far posteriorly is the most effective method of relieving the compressive forces on the optic nerve in the orbital apex. This may be most safely and easily accomplished via an endoscopic endonasal approach.

Lateral wall decompression may be used alone or in combination with one or two other wall decompression. Its effectiveness in cases of compressive optic neuropathy has been debated. It may be safer and more effective in individuals with a larger bone mass in the sphenoid triangle. ^{13,​ 14}

Many experts agree that there is no best method of orbital decompression and surgeons should utilize the techniques with which they are most comfortable and deliver the desired results. Ideally the approach should be tailored for each patient, since goals of surgery vary depending on indications.

7.3 Endoscopic Medial Orbital Wall and Floor Decompression

The endoscopic orbital decompression is an elegant method to decompress the medial and inferior orbit while eliminating disruption of normal external structures and preserving mucociliary function. The transantral approach to the medial wall and floor described by Walsh and Ogura ^{1,​ 15} in 1957 has given way to modern endoscopic techniques first reported by Kennedy et al. ^{2,​ 16} The extent of sinus dissection in preparation for decompression represents a balance in the need for preservation of physiologic sinus drainage pathways while limiting instrumentation of otherwise uninvolved structures within the sinonasal labyrinth. Each procedure is therefore tailored to the patient’s site and degree of disease, anatomy, and presurgical vision status.

The endoscopic approach to decompress the medial orbital wall begins with a complete dissection of the adjacent sinus cavities. This entire dissection may be performed using a zero-degree endoscope. The uncinate process is first removed at its insertion on the maxillary line. Unlike traditional endoscopic sinus surgical approaches, the superior insertion of the uncinate is left in place in order to help protect the frontal recess from obstruction secondary to orbital fat prolapse. After removal of the uncinate, the maxillary may be visualized laterally and extended posteriorly and inferiorly. This should be performed even in cases where the orbital floor is not resected in order to avoid iatrogenic maxillary obstruction. Next the ethmoid bulla, basal lamella, and posterior ethmoid air cells are completely removed. It is critical to dissect these cells superiorly to the level of the skull base and laterally to the lamina in order to enable a maximal decompression. Residual posterior air cells, particularly those adjacent to the skull base, will tend to restrict the decompression and increase the potential for postoperative mucocele formation ( ▶ Fig. 7.2). In contradistinction, the inferior aspect of the agger nasi cell and superior rim of the ethmoid bulla may be left in place to further protect against obstruction of the frontal recess. Complete removal of the remainder of the ethmoid air cells will reveal the suture lines between the sphenoid and frontal bones and the lamina papyracea. Identification of these suture lines is critical as they represent the boundary of the medial bony decompression. Posteriorly, the sphenoid suture line may be identified as a focal thickening of the bone as it transitions from the thinner lamina. The decision to open the sphenoid sinus at this point will depend on the patient anatomy and surgical goals. If a maximal apical decompression is desired, it is often beneficial to partially resect the superior turbinate and widely open the sphenoid face to allow the orbital fat to prolapse posteriorly into the sphenoid lumen. However, if the sphenoid is left intact, the superior turbinate will typically protect the sphenoid os from fat-related obstruction. Once the sinuses have been completely resected, the mucosa may be stripped from the lamina and lateral skull base to help prevent the risk of postoperative mucocele formation. The final consideration in the preparation of the medial decompression is whether or not to resect the middle turbinate. Resection carries risks of olfactory disruption, remnant lateralization with frontal obstruction, and postoperative epistaxis. Consequently, the middle turbinate should only be removed if its presence limits the decompression.

The next step is to completely remove the lamina papyracea, which, as noted, is bounded by the sphenoid, frontal, maxillary, and lacrimal bones ( ▶ Fig. 7.3). A wide osteotomy is critical as any residual bone will limit the degree of decompression. Once the bone has been removed, the periorbital fascial layer will be encountered. One may often be able to identify the medial rectus muscle and several venous structures through the periorbita. The surgeon should take note of these structures and attempt to avoid them while incising the periorbita. The extent of the periorbital incision should take into account the goals and adjunctive procedures being performed during the decompression. If a maximal decompression is desired, regardless of concerns for the induction of postoperative diplopia, then the medial periorbita may be stripped in its entirety. Conversely, a strip of periorbita may be left over the medial rectus muscle to function as a sling, which has been shown to limit diplopia rates. ^{3,​ 17} Once the periorbita has been removed, the orbital fat may be feathered medially using blunt instrumentation and gentle tonic pressure on the globe in order to further lyse the periorbital fascial bands and enhance the degree of decompression ( ▶ Fig. 7.4).

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