Primary angle closure is a mechanical block involving the structures immediately around the angles: iris, lens, pupil. IOP rise in throid orbitopathy is commonly due to orbital compression - tightness of the orbit - due to inflammation of the structures withIN the orbit, this causes swelling of the orbital tissues (making the eye bulge/proptose,  red/chemotic, sometimes even have limited eye movements) - the tight orbit leads to an increase in episcleral venous pressure causing seconday glaucoma.

Yes. I did see a patient with thyroid orbitopathy with frank angle closure glaucoma. I was just wondering if the compression of the globe could have had contributed to further pushing the eye into PACG from PACS (primary angle closure suspect). The contralateral PACS eye was normal (no glaucoma).

I see. Thyroid is inflammatory, may be the inflammatory reaction along the meshwork pushed the eye to PACG assuming cataract is not that think. 

But isn't the inflammation caused by thyroid eye disease extra ocular?

Purely speculating (as a pathologist), might thyroid orbitopathy cause ocular ischaemia, leading to iris rubeosis and angle closure?

Of the mechanisms underlying the causation of open-angle glaucomas is elevated episcleral venous pressure which stems from thyroidopathy. The modified Goldmann equation, Po = F/C + Pev (where Po = intraocular pressure, F = aqueous

production, C = outflow facility and Pev = episcleral venous pressure) shows a relationship between episcleral venous pressure and intraocular pressure. Hence, when the episcleral venous pressure, the normal value of which ranges from 9 to 10 mmHg, increases, intraocular pressure rises. Following compression of the venous drainage of the eye, especially the superior ophthalmic vein, glaucoma ensues. In much the same way, retrobulbar external compression can increase compaction of anterior chamber structures, which can conceivably bring about a decreased aqueous drainage, thereby resulting into an increased intraocular pressure, hence secondary angle closure glaucoma. Also, in all probability this external compression has some good association with rubeosis iridis following central retinal vein occlusion; thus, this rubeosis iridis causes glaucoma – open angle followed by closed angle, if unchecked- due to goniosynechiae resulting from the contracture of the neovascular membrane which is reported as a zipper-angle closure.

In thyroid orbitopathy  kind of glaucoma is open angle but , added intraocular inflammation   can cause secondarily angle closure.

Could the inflammation caused by thyroid orbitopathy be intra-ocular?

Hello!

As the occurrence of CRVO is possible, we cannot deny that the inflammation is secondary to hypoxia/ischaemia that follows the occlusion itself. In light of this, thyroid orbitopathy does have the potential for intra-ocular inflammation.

Dear colleagues,

eyes with primary angle closure suspect (and its consequences) remain frequently undectected, because gonioscopy is often not performed or not performed correctly. Hence this condition is largely underreported, except for the studies done in Asian subjects, and the occurence in a patient with thyroid orbitopathy is unlikely to be more than purely coincidental. (And if it were not, it would by definition not be 'primary' anymore.)

Thyroid orbitopathy can lead to increased IOP (be sure to perform the differential pressure test to eliminate the effect of inferior rectus muscle fibrosis), as a result of increased intra-orbital pressure, as stated above. This pressure pushes the eye outwards the orbit (in the best case), but is not expected to alter the anatomy of the anterior segment.

The event of a choroidal effusion is a well known cause of secundary angle closure. However I am unaware of such a link with Thryoid orbitopathy, in spite of a search on pubmed.

The usually impressive clinical picture of orbital congestion termed 'malignant' thyroid orbitopathy, with its potential for associated vision loss due to optical nerve compression (and/or corneal damage) will in most instances lead to therapeutic intervention, eliminating the potential for intra-ocular vasculair complications and hence the potential for neovacular glaucoma.

This being said, a recently published case report demonstrates the potential for intra-ocular vascular complications exists, hence its potential complications as well. (see: A patient with branch retinal vein occlusion accompanied by superior ophthalmic vein thrombosis due to severe superior ophthalmic vein enlargement in a patient with graves ophthalmopathy. Park HS et al., 2014)

Thank you for that answer. That definitely covered a lot of my questions particularly about the anatomy of the anterior segment not really being altered by the condition. The occurrence of the two conditions (PACG and thyroid eye disease) in the case of my patient could probably have been purely coincidental. Maybe the secondary open angle glaucoma could have also contributed to the already advanced glaucomatous optic neuropathy. best regards

pressure over the epi-scleral veins and inflammation around the globe can excite any kind of reaction leading to stagnant hypoxia inside the eye with grave consequences.

If scleral buckling operation in retinal detachment could cause the Agle-closure glaucoma due to displacement and anterior forwarding iris-lens diafragm, in my opinon the similar mechanism could cause agle-closure glaucoma in thyroid orbitopathy due to external compression of the eye ball like scleral band