36 Endoscopic Orbital Decompression
Abstract
Endoscopic medial orbital wall and floor decompression may be indicated for several reasons including thyroid eye disease, compressive or stretch optic neuropathy, and orbital tumors. Access to inferomedially based orbital tumors is also facilitated by the endoscopic approach. The greatest advantages of the endoscopic technique are the avoidance of scars, an improved visualization of certain landmarks, and the ability to address concomitant sinonasal pathology or perform optic canal decompression. In order to minimize postoperative diplopia, the inferomedial strut may be preserved.
36.1 Goals
When performing endoscopic orbital decompression for thyroid eye disease, indications may be compressive or stretch optic neuropathy requiring expansion of the orbital apex or recession of the globe. Thus, the goal is bony decompression (i.e., expansion of the bony orbit) to allow restoration of optic nerve function. In other cases, exposure keratopathy and cosmetic proptosis are the primary indications. In these cases, reduction of proptosis is the primary goal. Endoscopic decompression techniques may also be used to provide access to inferomedial tumors of the extra- and intraconal spaces.
36.2 Advantages
Advantages of endoscopic orbital decompression are the avoidance of external incisions, magnified visualization of certain landmarks, and the ability to address concomitant sinonasal pathology. To minimize postoperative diplopia, the inferomedial strut can be reliably preserved using angled drills and instrumentation. Lastly, in select cases, simultaneous optic nerve canal decompression in case of compressive optic neuropathy can be performed. 1
36.3 Expectations
These depend on the individual patient’s indication for the surgery. In patients with disfiguring proptosis or exposure keratopathy, the expectation is an improvement in exophthalmometry measurements. A mean ocular recession of 3.5 to 5.5 mm might be achieved with combined medial and inferior decompression. An additional 2 mm can be achieved through concurrent lateral decompression. 2 , 3 , 4 , 5 , 6 , 7 Additional recession can be achieved with fat removal. In a review of 45 decompressed orbits (medial + lateral or medial + lateral + floor), the mean reduction in proptosis was 3.89 mm. 8
Regarding intraocular pressure, in patients with varying degrees of thyroid eye disease, decompression has been reported to decrease pressures from 19.3 ± 4.4 mm Hg to 17.0 ± 2.9 mm Hg at 1 week and to 15.9 ± 3.7 mm Hg at 6 months. 5 , 9
Visual improvement for surgical orbital apex/optic nerve decompression can vary greatly depending on severity and duration of optic nerve compression. In series with a breadth of cases treated with surgery and with or without steroid therapy, improvement varied between 27 and 82%. 10 , 11 , 12
Diplopia is a common, yet often unavoidable, outcome following endoscopic orbital decompression surgery. Rates of new-onset diplopia range from approximately 20 to 30%, although rarely resolution of diplopia may occur. 8 Additional strabismus surgery may be necessary for improvement of diplopia and patients should be routinely counseled on the potential need for corrective strabismus surgery.
36.4 Key Principles
Provide wide endoscopic access to medial and inferior walls of the orbit through comprehensive adjacent sinus surgery.
Protection of unopened sinuses against iatrogenic obstruction from orbital fat prolapse.
Removal of the medial and inferior bony walls of the orbit ± inferomedial strut.
Incision of the periorbita in order to allow feathering of extraconal fat, which facilitates orbital fat prolapse into the ethmoid and maxillary sinus cavities.
Reduction of intraorbital pressure on the neurovascular structures caused by enlarged extraocular muscles, fat, orbital tumors, and other space-occupying lesions.
36.5 Indications
Orbital decompression is performed for several conditions and indications. The most common indication for orbital decompression is dysthyroid orbitopathy resulting from Graves’ disease.
When enlarged extraocular muscles and fat increase in size due to the thyroid eye disease, compression of the optic nerve can result. Surgical decompression of the bony orbit relieves this compression and may allow for vision recovery. Other indications in patients with thyroid eye disease include the reduction of proptosis. Proptosis can lead to exposure keratopathy, corneal ulceration, and perforation which can ultimately result in vision loss. Additionally, the cosmetic disfigurement may cause psychosocial limitations in dysthyroid orbitopathy patients.
Other indications include providing endoscopic access to orbital tumors or lesions that cannot be safely accessed otherwise. These conditions may also cause compressive optic neuropathy, proptosis, and visual dysfunction.
36.6 Contraindications
Patients undergoing endoscopic orbital surgery must be candidates for general anesthesia.
36.7 Surgical Approach
36.7.1 Preoperative Preparation
A CT scan is generally obtained preoperatively to verify the bony anatomy of the orbit and the surrounding sinonasal structures. If Graves’ orbitopathy is suspected, intravenous contrast should not be applied, as there are reported cases of orbitopathy exacerbation after the administration of iodine-containing intravenous contrast. MRI scans, particularly fat-suppression sequences, can be helpful in the identification and characterization of intraorbital pathology. Contrast enhancement may facilitate localization of the ophthalmic artery, which should be avoided during intraconal surgery due to its position adjacent the optic nerve.
36.7.2 Operative Technique
As with all sinonasal surgery, the surgery begins with decongestion and optimization of hemostasis. This can be achieved by elevating the head and topicalization using 1:1,000 fluorescein-labeled epinephrine-soaked neuropathies. Local anesthetic may also be injected into the axilla of the middle turbinate to further reduce bleeding from the anterior ethmoid arterial distribution.
The entire surgery may be performed with a 0-degree endoscope. However, angled scopes are useful in the setting of inferomedial strut preservation. 13 , 14 Septoplasty or middle turbinate resection may be performed as needed. However, middle turbinate resection should be performed only when necessary, since it carries the risk of olfactory disruption, frontal sinus obstruction, and postoperative epistaxis.
The first surgical step is the removal of the uncinate process at its insertion on the maxillary line. After the removal of the uncinate process, the maxillary sinus should be opened in all cases, even when no orbital floor decompression is needed, to avoid iatrogenic maxillary obstruction. The ethmoid bulla, basal lamella, and posterior ethmoid cells are removed entirely. It is important to extend the dissection to the entire skull base if maximal decompression is necessary. The sphenoid sinus does not have to be opened in all cases as the remaining superior turbinate will typically protect the sphenoid sinus from the obstruction by orbital fat. However, if a maximal orbital apex decompression is necessary, partial resection of the superior turbinate and wide opening of the sphenoid face are required. After complete opening of the sinuses, the mucosa may be stripped from the lamina papyracea to the lateral skull base in order to avoid postoperative mucocele formation. The removal of the lamina papyracea may be performed by first creating a micro infracture. Then upbiting Blakesley forceps and ball-tipped probe are used to carefully medially reflect and remove the bony fragments (Fig. 36‑1). Once completed, the periorbital fascial layer will be encountered (Fig. 36.2). At this point, the medial rectus muscle and several venous structures might be identified through the periorbita which should be spared during periorbital incision. Depending on the extent of decompression necessary, the degree of periorbital incision can be tailored. If a maximal decompression is desired, regardless of concerns for the induction of postoperative diplopia, the medial periorbita may be stripped completely (Fig. 36.3). To decrease diplopia rate, a strip of periorbita may be retained overlying the medial rectus muscle to function as a sling (Fig. 36.2). 15 Once the periorbita has been removed, the orbital fat may be feathered medially using blunt instrumentation (e.g., double ball probe or blunt sickle knife) as well as gentle pressure on the globe in order to disrupt the periorbital fascial bands and enhance the degree of decompression (Fig. 36.4).
The endoscopic decompression of the orbital floor requires a similar extent of adjacent sinus surgery. Though rarely performed, an isolated orbital floor decompression might be performed while preserving the basal lamella and posterior ethmoid air cells. Maximizing the vertical dimension of the maxillary antrostomy is important to ensure adequate access for orbital floor decompression. The superior maxillary sinus mucosa may be reflected laterally prior to bone removal to facilitate preservation and redraping after completion of the surgery. This procedure facilitates remucosalization, reduces postoperative crusting, and expedites postoperative healing. 16 The removal of the orbital floor is performed with a curette and is limited to the area medial to the infraorbital canal. In patients without preoperative diplopia, the inferomedial bony strut may be preserved in order to limit globe prolapse and to reduce postoperative diplopia (Fig. 36.5). 8 , 13 , 17 , 18 This requires precise drilling of the orbital floor between the inferomedial strut and infraorbital canal, as down fracture using a curette risks migration of the fracture line through the strut with consequential loss of structural support. Finally, as with the medial decompression, the exposed periorbita must be incised to release the orbital fat into the maxillary sinus while avoiding direct injury to the inferior rectus muscle. In order to increase the dissection corridor for further surgical steps e.g. for intraoperative tumor resection, the orbital process of the palatine bone (OPPB) may be resected (Fig. 36.6).19
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