While Graves’ orbitopathy (GO) may manifest in several ophthalmic conditions including proptosis, limited ocular motility, disfigurement, corneal exposure, and optic neuropathy, elevated intraocular pressure (IOP) is not a commonly discussed problem associated with GO even though it was described over 100 years ago (Ophthalmology. 2001;108:145-150). Optic nerve neuropathy and elevated IOP are part of orbital compartment syndrome and may occur when the orbital pressure increases gradually, as with orbital tumors or GO. In the case of Graves’ disease, the gradual and moderate IOP increase is due to compensation of the eyelids as allowed by the slowly progressive increase in orbital volume either by orbital fat, hyaluronic acid, and water (type I) or by enlargement of the extraocular muscles (type II). And while IOP in GO patients has been demonstrated to decrease following bone removal orbital decompression (BROD),2-4 recent studies indicate that fat removal orbital decompression (FROD) may also aid in reduction of IOP. This article explores the extent to which IOP may be reduced through orbital fat removal and discusses surgical indications for patients with Graves’ disease.
A Prospective Study
A recent study of the effects of orbital fat removal on IOP in 64 patients with Graves’ disease found that IOP decreases an average of 2 mm Hg one week after FROD (Ophthal Plast Reconstr Surg. 2006;22:92-95). This was true whether or not patients had preoperative IOPs above 21 mm Hg. Moreover, the IOP decrease was statistically significant at both 1 week and 6 months after surgery (p<0.001). A further decrease of 1 mm Hg was noted between 1 week and 6 months postoperatively (p<0.001). This may be due to the absorption of postoperative edema and hemorrhage, scar formation, or the efficiency of the surgery.
Additionally, no correlation was found between the preoperative proptosis and preoperative IOP. Specifically, there was no difference in IOP reduction between GO types I and II, and FROD was equally effective in reducing proptosis as well as IOP in patients with both types of condition. This may be due to the similar compliance of the eyelid tissues (especially the ligaments) to orbital volume increase and related to the duration of increased orbital volume and age-related elasticity of the eyelid tissues. Other factors that may play a role in elevated IOP in GO include episcleral venous pressure, genetic predisposition to glaucoma, and initial orbital volume.
Finally, the IOP reductions with FROD were lower than those demonstrated with BROD. In bone decompression, IOP is reduced by 3–5.6 mm Hg.1,3 Thus, bone decompression would be expected to have a higher rate of IOP reduction because it is usually more extensive and the procedure exposes a greater volume of the sinuses to orbital content.
Discussion and Recommendations
Judging from these early prospective studies, one cannot conclude whether fat removal through the upper or the lower eyelids is more effective, or whether or not it is the incision of the septum that causes a decrease in IOP. Additionally, the effect of FROD on IOP in patients with stable Graves’ disease should be a long-term benefit, but it is impossible to determine this from the limited follow-up.
According to suggestions from previous studies,1,3,4 patients with GO should be evaluated routinely not only to measure IOP but also to observe the optic disc for any change in cup-rim ratio. In those patients exhibiting such a change, visual field perimetry should be performed, as well. In common practice and clinical settings, however, IOP above 21 mm Hg is rare and therefore usually meaningless. Reduction in IOP by surgery is indicated only in patients with significantly high IOP, such as those in the 30th or with susceptible optic nerve head. In the noted study by Robert et al, only 1 eye out of the 64 (1.6%) had a pressure as high as 29 mm Hg. Such pressure may not cause any functional damage if the optic disc is not susceptible and the duration of the increased IOP is limited. In a patient like this, high IOP may be induced by the restriction of the inferior rectus muscle only in upgaze and may not occur in primary gaze, causing only transient increase in IOP due to compensation by increased outflow.
Patients with significantly high IOP can be treated conservatively with IOP-decreasing medications if the patients are at the active stage of GO, do not have a vision- threatening condition or disfigurement, and the elevated IOP is not an indication for orbital decompression. If the IOP is exceedingly high, optic neuropathy—not glaucoma—might be the cause for visual dysfunction as part of orbital compartment syndrome. Thus, orbital compartment syndrome is an indication for surgical intervention. Until further studies support it, surgery is probably not indicated in most Graves’ disease patients with elevated IOP.
The usual indications for BROD and FROD are functional (or sight-threatening) such as optic neuropathy and severe exposure keratopathy, aesthetic such as disfiguring proptosis, and psychological. In general, surgery is performed when medical therapy with corticosteroids or radiation has failed or is contraindicated. If performed for cosmetic reasons, procedures are usually deferred for the remission stage of the disease, about 5–7 years after onset. The spectrum of complications varies with each type of surgery. BROD is usually more complicated than FROD and may induce strabismus and diplopia, orbital hemorrhage, infection, nerve injury, or cerebrospinal fluid leak. FROD is simpler to perform but bares the same complications except for cerebrospinal fluid leak. BROD is more suitable for severe proptosis due to increased orbital content, especially in type II, while FROD is especially effective if there are festoons or in treating type I. Both procedures may be combined or BROD should precede FROD. In general, the sequence of surgical treatment of GO patients is BROD, strabismus surgery, and then eyelid surgery. If followed otherwise, the outcome might be unpredictable.
||Danesh-Meyer HV, Savino PJ, Deramo V, Sergott RC, Smith AF. Intraocular pressure changes after treatment for Graves’ orbitopathy. Ophthalmology. 2001;108:145-150. |
||Robert PR, Rivas M, Camezind P, Rulfi JY, Adenis JP. Decrease of intraocular pressure after fat-removal orbital decompression in Graves disease. Ophthal Plast Reconstr Surg. 2006;22:92-95. |
||Dev S, Damji KF, DeBacker CM, Cox TA, Dutton JJ, Allingham RR. Decrease in intraocular pressure after orbital decompression for thyroid orbitopathy.Can J Ophthalmol. 1998;33:314-319. |
||Kalmann R, Mourits MP. Prevalence and management of elevated intraocular pressure in patients with Graves’ orbitopathy. Br J Ophthalmol. 1998;82:754-757. |
The author states that he has no financial relationship with the manufacturer of any product discussed in this article or with the manufacturer of any competing product.