landmarks, but should not be solely relied on as the orbital contents shift with decompression maneuvers.

Postoperative care

Patients typically are monitored for bleeding in the hospital overnight. They are discharged with a 10-day course of antistaphylococcal antibiotics and instructed to irrigate the nose with saline solution twice a day to clear mucus and debris. Any remaining debris is cleared from the operative site under endoscopic visualization at the first postoperative office visit 1 week after surgery.

Results

The goals of orbital decompression vary depending on the indication for the procedure. In patients with compressive optic neuropathy, restoration of visual deficits is the goal, whereas in patients with corneal exposure or severe proptosis, ocular recession may be the primary endpoint. The amount of orbital decompression that is needed depends on the clinical scenario, and will dictate the technique and approaches that are used. Endoscopic decompression alone averages an ocular recession of 3.5 mm (range 2-5.5 mm), whereas the addition of concurrent lateral decompression provides an additional 2 mm of globe recession.13

Complications

New-onset diplopia or worsening preexisting diplopia has been reported to occur in anywhere from 15% to 64% of

patients undergoing orbital decompression for Graves’ dis- ease.8,11,13-16 This finding is thought to be the result of change

in vectors of the abnormal extraocular muscles with ocular recession. All patients should be informed of the possibility of postoperative diplopia and need for strabismus surgery. Although several techniques have been described to decrease diplopia, the aforementioned orbital sling technique12 and a balanced decompression14,17-18 with a concurrent lateral external component are advocated by the authors.

Postoperative epistaxis, which occurs in less than 5% of patients, is most commonly observed along the posterior remnant of the resected middle turbinate. Bleeding is managed through the use of endoscopic identification and cauterization of the bleeding site. Packing is avoided to limit pressure on the orbital contents. Persistent bleeding is managed with ligation of the sphenopalatine artery.

The incidence of postoperative infection is reduced with the use of antistaphylococcal antibiotics. Creation of a large maxillary antrostomy and limited bone removal in the region of the frontal recess helps to prevent postoperative ostial obstruction and sinusitis.

If the maxillary antrostomy is extended too far anteriorly through the thick bone of the frontal process of the maxilla, transection of the lacrimal duct with postoperative epiphora and dacryocystitis may be seen. In this scenario, endoscopic dacryocystorhinostomy may be performed to re-establish lacrimal drainage. Cerebrospinal fluid leak and blindness are very rare complications that have been reported with endoscopic sinonasal surgery.

Conclusion

Endoscopic orbital decompression provides successful treatment for patients with Graves’ orbitopathy. Excellent visualization of the orbital apex and skull base allows for effective reduction in proptosis with minimal patient morbidity. The

expanding role for transnasal endoscopic surgery leads to a natural extension for the management of selected orbital tumors and fibro-osseous lesions with orbital extension. These advanced procedures should be performed by surgeons who have significant experience in endoscopic techniques.

References

1.Brent G: Graves’ disease. N Engl J Med 358:2594-2605, 2008

2.Kronlein R: Pathology and surgical treatment of desmoid orbital cysts. Beitr Klin Chir 4:149-163, 1889

3.Sewall E: Operative control of progressive exophthalmos. Arch Otolaryngol Head Neck Surg 24:621-624, 1936

4.Hirsch O: Surgical decompression of exophthalmos. Arch Otolaryngol Head Neck Surg 51:325-331, 1950

5.Naffziger HC: Progressive exophthalmos. Ann R Coll Surg Engl 15:1-24, 1954

6.Walsh TE, Ogura JH: Transantral orbital decompression for malignant exophthalmos. Laryngoscope 67:544-568, 1957

7.Kennedy DW, Goodstein ML, Miller NR, Zinreich SJ: Endoscopic transnasal orbital decompression. Arch Otolaryngol Head Neck Surg 116:275-282, 1990

8.Michel O, Bresgen K, Russmann W, et al: [Endoscopically-controlled endonasal orbital decompression in malignant exophthalmos]. Laryngorhinootologie 70:656-662, 1991

9.Gorman CA, Garrity JA, Fatourechi V, et al: A prospective, randomized, double-blind, placebo-controlled study of orbital radiotherapy for Graves’ ophthalmopathy. Ophthalmology 108:1523-1534, 2001

10.Mourits MP, van Kempen-Harteveld ML, Garcia MB, et al: Radiotherapy for Graves’ orbitopathy: Randomised placebo-controlled study. Lancet 355:1505-1509, 2000

11.Metson R, Shore JW, Gliklich RE, et al: Endoscopic orbital decompression under local anesthesia. Otolaryngol Head Neck Surg 113:661667, 1995

12.Metson R, Samaha M: Reduction of diplopia following endoscopic orbital decompression: The orbital sling technique. Laryngoscope 112: 1753-1757, 2002

13.Metson R, Dallow RL, Shore JW: Endoscopic orbital decompression. Laryngoscope 104:950-957, 1994

14.Shepard KG, Levin PS, Terris DJ: Balanced orbital decompression for Graves’ ophthalmopathy. Laryngoscope 108:1648-1653, 1998

15.Wright ED, Davidson J, Codere F, et al: Endoscopic orbital decompression with preservation of an inferomedial bony strut: minimization of postoperative diplopia. J Otolaryngol 28:252-256, 1999

16.Eloy P, Trussart C, Jouzdani E, et al: Transnasal endoscopic orbital decompression and Graves’ ophtalmopathy. Acta Otorhinolaryngol Belg 54:165-174, 2000

17.Unal M, Leri F, Konuk O, et al: Balanced orbital decompression combined with fat removal in Graves’ ophthalmopathy: Do we really need to remove the third wall? Ophthal Plast Reconstr Surg 19:112118, 2003

18.Graham SM, Brown CL, Carter KD, et al: Medial and lateral orbital wall surgery for balanced decompression in thyroid eye disease. Laryngoscope 113:1206-1209, 2003

Figure 1 Computed tomography of an extraconal inferomedial orbital apex lesion: Cavernous hemangioma, mucocele.

operating microscope,6 visualization in the orbital apex through a direct orbital approach is limited.

The single most critical limitation inherent to the orbit is the lack of dead space as a result of the intermuscular septations and ubiquitous fat that obscure visualization. Endoscopic approaches to the orbit through the periorbital sinuses benefit from the air-filled sinus cavities and instrumentation designed for use through the transnasal approach. The view of the lateral orbital floor through a transnasal endoscopic approach is more limited.7,8 When the same endonasal approach is used, extra-

conal lesions are accessible by means of an endoscopic approach and have been removed from the orbital apex.9,10 In-

traconal lesions are not as easily approached endoscopically because they require transit across the extraocular muscles and intermuscular septa.

A transantral approach to the posterior orbit may be more useful for inferior and medial apex lesions. This approach has been used to remove cavernous hemangiomas and for tumor debulking. The removal of a cavernous hemangioma with a transnasal approach1,9 has been described in these cases; however, the lesion was approached through an ethmoidectomy and limited sphenoidectomy. The transantral

approach provides access to more inferiorly based extraconal apex lesions.10,11 This approach can also be used to

biopsy atypical lesions and to provide visualization of the orbital floor that may be helpful in the repair of orbital floor fractures that extend posteriorly.4 In this situation, the transantral approach can help visualize posterior bone supports and proper placement of an implant across the defect.

Endoscopic surgery is a useful adjunct to standard posterior orbital approaches. It may be especially useful for extraconal processes that involve the orbital apex inferiorly or medially, as these areas have good access from the paranasal sinuses. It allows removal of extraconal large lesions that would otherwise be difficult to access even with the use of a large lateral orbitomy. It has the advantage over the intranasal and orbital approaches, when used individually, of allowing more instrumentation to be used to access and visualize the operative site.

Lesions of the orbital apex pose unique surgical problems. When the lesion is extraconal and inferomedially located, the use of the endoscopic approach—either transantrally or trans-

nasally—should be considered.12 These approaches may help in accessing lesions in the apex with improved visualization and limited manipulation within the orbit.

Radiological evaluation and surgical planning

Computed tomography scanning is the imaging mode of choice for orbital disease. It allows one to evaluate sinus anatomy as well note any displacement of orbital structures (Figure 1). Magnetic resonance imaging is more useful when one is looking for intracranial complications of orbital inflammation as well as any malignancy that extends intracranially. It may also show marrow space involvement, such as osteomyelitis, earlier than computed tomography. The surgical plan for these lesions is to perform an uncinectomy and middle meatal antrostomy, followed by an anterior ethmoidectomy. Depending on the size of the lesions, this may need to be extended into a posterior ethmoidectomy and sphenoidotomy if the lesion extends posteriorly or into the cavernous sinus.

Operative technique

Endoscopic transnasal approach to these apex lesions is performed under general anesthesia with endotracheal intubation. The patient is in a reverse Trendelenburg position, and the nasal mucosa is decongested with mixture of 10% cocaine, adrenalin, and saline-soaked pledgets. It is important to do this in a minimally traumatic way because the inflamed mucosa has a tendency to bleed. Infiltration of the lateral nasal wall above the middle turbinate insertion is performed with 2 mL of 2% lidocaine with 1;80,000 adrenaline. The first step is to perform an uncinectomy and identify and enlarge the natural ostium of the maxillary sinus (Figure 2). The maxillary sinus ostium should be maximally enlarged to ensure that obstruction of the ostium does not occur with prolapse of orbital fat once the orbital periosteum is opened. Depending on the site and size of the orbital lesion, a varying amount of lamina papyracea can be exposed. In most cases, complete exposure is preferred, because it allows space for the fat to prolapse while the lesion in the orbit is addressed.

The first step is to open the bulla ethmoidalis and expose the vertical portion of the ground lamella. This is perforated at the junction of the horizontal an vertical portions and the superior meatus entered medially. Once this meatus is clearly identified, the posterior ethmoids and sphenoid ostium can be exposed and the sphenoid opened if the lesions is in the orbital apex (Figure 2). Anterior lesions will also require dissection of the frontal recess with clearance of all cells and exposure of the frontal ostium. Once the lamina papyracea is fully exposed, it is fractured with the blunt end of the Freer elevator, with the surgeon ensuring that the orbital periosteum is kept intact. The Freer is used to establish the plane between the bone and the underlying orbital periosteum. The bone is then fractured off the periosteum keeping the periosteum intact. In most cases it is prudent to remove all the lamina papyracea thereby creating the largest

possible access into the orbit. Approximately 1 cm of lamina papyracea below the frontal sinus ostium is preserved to prevent orbital fat from prolapsing and blocking the frontal

sinus drainage pathway. The orbital periosteum is incised vertically just anterior to the sphenoid. This incision is continued anteriorly with 2 horizontal incisions; one just