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| LETTER TO THE EDITOR |
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| Year : 2015 | Volume
: 8
| Issue : 2 | Page : 135-136 |
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A case of decompressive retinopathy
Aarti S Agrawal1, Suresh J Ramchandani2, Abhijit A Naik1, Saurabh Shrivastava1
1 Department of Ophthalmology, MGM Medical College, Navi Mumbai, Maharashtra, India
2 Shivam Eye Foundation, Navi Mumbai, Maharashtra, India
| Date of Web Publication | 24-Jun-2015 |
Correspondence Address:
Aarti S Agrawal
201, Snehal Building, Adrash Lane, Marve Road, Malad West, Mumbai - 400 064, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-620X.159277
How to cite this article:
Agrawal AS, Ramchandani SJ, Naik AA, Shrivastava S. A case of decompressive retinopathy. Oman J Ophthalmol 2015;8:135-6 |
Sir,
A 56-year-old lady underwent an uneventful left eye phacoemulsification with a + 6.50 diopters lens. On postoperative day 1, autorefractometer showed high hypermetropic error. Repeat intraocular lens (IOL) master calculation showed actual power as + 20.5 diopters. Vision was 6/12 with + 7.00 diopters (reason for refractive surprise is outside the scope of this report). Pressure measured by pneumotometry was 14 mm Hg. IOL was well centered with a normal fundus. After explanation, an IOL exchange, after enlarging the same wound, was performed. On day 1 of the second surgery, vision was 6/60 with pin-hole. Anterior chamber showed + 4 cells/flare. Patient was started on hourly prednisolone drops, 3 times atropine and was reviewed the next day. She complained of severe pain and a drop in vision. Vision was counting fingers at 2 m. She had a pupillary membrane resulting in a pupillary block with an iris bombe and pressure of 35 mm Hg. Oral acetazolamide 500 mg and 300 ml intravenous mannitol was given. Pressure dropped by just 2 mm Hg, following which Nd-Yagmembranotomy was done. This led to a prompt resolution of iris bombe and drop in the pressure to 12 mm Hg within 1 h. Topical steroids, antiglaucoma medication and cyclopegics were continued and reviewed the next day. Vision was finger counting at 1 m, pupillary membrane was broken with 3+ cells and well centered IOL. Pressure was 15 mm Hg. Fundus showed multiple retinal hemorrhages in all quadrants, optic disc hemorrhage inferiorly and macular hemorrhage [Figure 1] and [Figure 2]. Fundus fluoroscein angiography done 1 week later showed multiple areas of blocked fluorescence and normal vascular perfusion [Figure 3] and [Figure 4]. Optical coherence tomographic showed hyper reflective lesions suggestive of intra and sub retinal hemorrhages [Figure 5]. | Figure 1: Fundus showing multiple hemorrhages in all four quadrants, optic disc hemorrhage inferiorly and macular hemorrhage
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 | Figure 3: Fundus fluoroscein angiography showing multiple areas of blocked fluorescence and normal vascular perfusion at 37 s
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 | Figure 4: Fundus fluoroscein angiography showing multiple areas of blocked fluorescence at 1 min 12 s
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 | Figure 5: Optical coherence tomographic showing hyper reflective lesions suggestive of intra and sub retinal hemorrhages
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A diagnosis of decompressive retinopathy following membranotomy was reached. No active treatment done. She was followed up regularly, last follow-up being 3 months after, which showed marked resolution of the hemorrhages with 6/36 vision.
There are various theories describing the pathophysiology of decompressive retinopathy, one proposed mechanism is that an acute decrease in IOP causes mechanical changes in the shape of the globe. Sudden hypotony results in scleral deformityand subsequent shearing of fragile capillaries. [1],[2] Furthermore, it can result in an expansion of the lamina cribrosa leading to decrease in axoplasmic flow and resulting in optic nerve edema that compresses the central retinal vein, resulting in diffuse retinal hemorrhages. The vascular theory states that it may reduce retinal arterial resistance, resulting in increased flow and leakage through already fragile capillaries. [3]
Fibrin pupillary-block glaucoma is often treated by laser peripheral iridotomy or intraocular tissue plasminogen activator. Tissue plasinogen works by changing proenzyme plasminogen to activated enzyme plasmin. Triggered plasmin then melts fibrin clots into low molecular weight fibrin degradation products. [4] We resorted to yagmembranotomy over tissue plasminogen activator due to financial constraints and over a yagiridotomy, due to its technical difficulty and the risk of causing an iris bleed. [5]
When we look back, a tissue plasminogen activator injection would have probably resulted in a gradual reduction in IOP and may not have produced a decompression retinopathy.
 References | |  |
| 1. | Mukkamala SK, Patel A, Dorairaj S, McGlynn R, Sidoti PA, Weinreb RN, et al. Ocular decompression retinopathy: A review. Surv Ophthalmol 2013;58:505-12.  |
| 2. | Alwitry A, Khan K, Rotchford A, Zaman AG, Vernon SA. Severe decompression retinopathy after medical treatment of acute primary angle closure. Br J Ophthalmol 2007;91:121. [ PUBMED] |
| 3. | Tyagi P, Hashim AA. Ocular decompression retinopathy following post-trabeculectomy suture lysis and management with triamcinolone acetonide. Int Ophthalmol 2011;31:425-8. |
| 4. | Wedrich A, Menapace R, Mühlbauer-Ries E. The use of recombinant tissue plasminogen activator for intracameral fibrinolysis following cataract surgery. Int Ophthalmol 1994-1995;18:277-80. |
| 5. | Friedman DS. Who needs an iridotomy? Br J Ophthalmol 2001;85:1019-21. [ PUBMED] |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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