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LETTER TO EDITOR
Year : 2006  |  Volume : 54  |  Issue : 2  |  Page : 139-140

Glaucoma secondary to orbital varix


Department of Ophthalmology, Hull Royal Infirmary, Hull, United Kingdom

Correspondence Address:
Indira Moorthy Madgula
Department of Ophthalmology, Hull Royal Infirmary, Hull
United Kingdom
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.25842

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How to cite this article:
Madgula IM, Lukaris A. Glaucoma secondary to orbital varix. Indian J Ophthalmol 2006;54:139-40

How to cite this URL:
Madgula IM, Lukaris A. Glaucoma secondary to orbital varix. Indian J Ophthalmol [serial online] 2006 [cited 2020 Jun 5];54:139-40. Available from: http://www.ijo.in/text.asp?2006/54/2/139/25842

Dear Editor,

Vascular lesions are an important cause of an orbital mass and have varying presentations. We report a rare case of an individual who developed secondary glaucoma following recurrent attacks of orbital varix thrombosis and hemorrhage.

A 52-year-old gentleman presented with an episode of spontaneous left subconjunctival hemorrhage, periorbital ecchymosis and a left upper eyelid mass of one-week duration. He had a similar presentation five years ago that resolved within a week. During the first episode his best corrected visual acuity was 20/20 in each eye, intraocular pressure (IOP) was 18 mmHg in either eye and optic discs were normal on ophthalmoscopic examination. Dilated episcleral veins were present. There was no relevant medical, drug or family history of ocular disease.

On this occasion, examination revealed a soft mass palpable in the left upper nasal orbit displacing the globe inferolaterally, causing 3 mm of proptosis [Figure - 1]. Extraocular movements were restricted in all directions. Anterior segment was normal. The IOP (measured by Goldmann applanation tonometer) was 32 mmHg in the left eye and 18 mmHg in the right eye and the left optic disc [Figure - 2] revealed the cup: disc ratio of 0.85 as compared to 0.5. in the right eye. Gonioscopy revealed blood in Schlemm's canal in the left eye.

Humphrey visual field [Figure - 3] test was suggestive of early superior and inferior arcuate scotoma, which correlated with the disc appearance of neuro retinal rim thinning.

Computerized tomography scan of the brain and orbit [Figure - 4] revealed three extraconal serpiginous soft tissue masses at the orbital apex consistent with an orbital varix. One of them contained a phlebolith. A diagnosis of open angle glaucoma secondary to raised episcleral venous pressure consequent to the orbital varix was made. It was decided to manage the case conservatively for orbital varix, which subsided on its own in two to three months duration. A topical beta - blocker (Timolol 0.5% eye drops twice daily) was commenced to control the IOP, which got stabilized at 18.0 mm of Hg. The patient was followed up for one year after the second episode. There was no progression of glaucoma as judged by visual fields, optic disc cupping and his IOP control.

Orbital varices may be primary congenital lesions or acquired secondary to intracranial or orbital arteriovenous malformations.[1] Some lack significant connections to the systemic venous circulation, are consequently non-distensible with stagnant circulation prone to thrombosis. These patients may present with proptosis due to hemorrhagic rupture, with pain and restricted ocular movement. Lesions that extend into the eyelid may present with lid swelling and periorbital ecchymosis.[1] Our patient had a non-distensible varix that presented with the above-mentioned features. Varices are usually managed conservatively. Surgery should only be performed when vision is threatened or there is severe deformity.[3],[2]

This case was unusual because the patient developed persistently raised IOP, which led to optic disc cupping and visual field damage. The mechanism of this secondary glaucoma is likely to be raised episcleral venous pressure evidenced by dilated episcleral veins and blood in Schlemm's canal on gonioscopy.

Glaucomatous damage must have occurred gradually, either with recurrent sub-clinical attacks causing an intermittently raised IOP or by a gradual and sustained rise over the preceding five years. Whilst one would expect episodes of raised IOP to occur at times of varix rupture or thrombosis (secondary to raised intraorbital pressure), persistence is a rare finding.

As they may be at risk, we recommend that patients with orbital varices be annually reviewed to detect the development of secondary glaucoma.


  Acknowledgement Top


Mr. Nicholas Hawksworth, FRCOphth.

 
  References Top

1.
Albert DM, Jackobiec FA. Principles and Practice of Ophthalmology, Volume 4, Glaucoma, Lids & Orbit, Ophthalmic Pathology 2nd edn. WB Saunders Co: 1994. p. 3152.  Back to cited text no. 1
    
2.
Kanski JJ. Clinical Ophthalmology 3rd ed. Butterworth Heinmann Ltd: 1994. p. 569.  Back to cited text no. 2
    
3.
Zelmer RC, Gieser DK, Wilensky JT, Noth JM, Mori MM, Odunukwe EE. A practical venomanometer: Measurement of the episcleral venous pressure and assessment of the normal range. Arch Ophthalmol 1983;101:1447-9.  Back to cited text no. 3
    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]


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