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• Sudden lowering of IOP may cause posterior segment bleeding by three different mechanisms
  Atul Bansal
  Published on: 22 October 2007
• Mild decompression retinopathy following medical treatment of acute primary angle closure
  Eric Denion
  Published on: 23 January 2007

• Published on: 22 October 2007

  Sudden lowering of IOP may cause posterior segment bleeding by three different mechanisms

  • Atul Bansal, Glaucoma Fellow
  • Other Contributors:
    • U.S. Ramanathan

  Dear Editor,

  We read with great interest the report by Alwitry et al [1] on severe decompression retinopathy after medical treatment of acute angle closure. The authors have speculated that the mechanism of the ‘preretinal’ haemorrhage in this case was similar to the scattered ‘intraretinal’ haemorrhages seen in ocular decompression retinopathy. Although we agree with them that the haemorrhage was caused by sudd...

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  Dear Editor,

  We read with great interest the report by Alwitry et al [1] on severe decompression retinopathy after medical treatment of acute angle closure. The authors have speculated that the mechanism of the ‘preretinal’ haemorrhage in this case was similar to the scattered ‘intraretinal’ haemorrhages seen in ocular decompression retinopathy. Although we agree with them that the haemorrhage was caused by sudden lowering of intraocular pressure (IOP), we believe that the exact pathophysiological mechanism, as well the clinical signs, in this case were different from the condition originally described by Fechtner et al [2].

  It can be hypothesised that a pupillary block caused the volume of aqueous humor in the posterior chamber to increase markedly. The vitreous gel was therefore pushed toward the posterior pole. Following medical therapy the pupillary block was reversed and the aqueous humor moved rapidly through the pupil from the posterior chamber to the anterior chamber. This coupled with decreased aqueous production due to administration of aqueous suppressants allowed the vitreous body to move forward rapidly. This induced a rapid posterior vitreous detachment (PVD), disrupting small vessels on the retinal surface or optic disc, and resulted in the subhyaloid haemorrhage. In the present case the very short duration of raised IOP makes significant impairment of autoregulation of retinal vasculature unlikely and the absence of multiple intraretinal haemorrhages rules out a general compromise of mechanical stability of retinal capillaries. Obana et al [3] were the first to demonstrate a subhyaloid haemorrhage caused by PVD induced after laser iridectomy for primary angle-closure glaucoma and it should be distinguished from ocular decompression retinopathy.

  This leads to an interesting conclusion that a sudden lowering of IOP may cause posterior segment bleeding by three different mechanisms. Ocular decompression retinopathy is caused by overwhelming of capacitance of retinal capillaries and results in multiple intraretinal haemorrhages. The second mechanism and clinical picture is similar to a central retinal vein occlusion [4,5]. A sudden change in hydrostatic equation between the posterior and anterior chambers, induces a rapid PVD and may result in subhyaloid haemorrhage, as in this case.

  Figure 1 Three different mechanisms of posterior segment bleeding after sudden lowering of intraocular pressure

  

  References

  1. Alwitry A, Khan K, Rotchford A et al. Severe decompression retinopathy after medical treatment of acute primary angle closure. Br J Ophthalmol 2007;91:121

  2. Fechtner RD, Minckler D, Weinreb RN et al. Complications of glaucoma surgery. Ocular decompression retinopathy. Arch Ophthalmol 1992;110:965-8

  3. Obana A, Gohto Y, Ueda N, Miki T, Cho A, Suzuki Y. Retinal and subhyaloid hemorrhage as a complication of laser iridectomy for primary angle-closure glaucoma. Arch Ophthalmol. 2000 Oct;118:1449-51

  4. Suzuki R, Nakayama M, Satoh N. Three types of retinal bleeding as a complication of hypotony after trabeculectomy. Ophthalmologica. 1999;213:135-8

  5. Dev S, Herndon L, Shields MB. Retinal vein occlusion after trabeculectomy with mitomycin C. Am J Ophthalmol. 1996 Oct;122:574-5

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  Conflict of Interest:
  None declared.

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• Published on: 23 January 2007

  Mild decompression retinopathy following medical treatment of acute primary angle closure

  • Eric Denion, ophthalmologist
  • Other Contributors:
    • Fabien Vincent and Pierre Labalette

  Dear Editor

  We read with great interest Alwitry and coworkers' article[1] on bilateral decompression retinopathy following medical treatment of an acute primary angle closure. We would like to report the case of a 47 year -old woman who consulted in November 2000 for a mildly painful right eye. Pain had lasted for about three days. Visual acuity was 20/20 OU with no optical correction. On slit-lamp examination, b...

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  Dear Editor

  We read with great interest Alwitry and coworkers' article[1] on bilateral decompression retinopathy following medical treatment of an acute primary angle closure. We would like to report the case of a 47 year -old woman who consulted in November 2000 for a mildly painful right eye. Pain had lasted for about three days. Visual acuity was 20/20 OU with no optical correction. On slit-lamp examination, both corneas were clear, there was an anisocoria with a round, non-reactive 7-mm right pupil. IOP was 38 mmHg OD and 14 mmHg OS. Fundus examination was normal bilaterally, the 7-mm right mydriasis allowing good visualization of peripheral retina OD. On gonioscopic examination, angle was closed OD. The patient was treated topically with timolol 0.50 bid, dorzolamide tid, pilocarpine 2% tid. Three days later, visual acuity was still 20/20 OU. IOP had dropped to 15 mmHg OD. There was a reactive semi-mydriasis OD. Gonioscopy showed a Sheie III (bottom part)/ Sheie IV (top part) angle OD. Indentation gonioscopy disclosed a plateau iris configuration OD, the central iris being pushed back with no further elements disclosure. Fundus examination showed scattered blot-shaped retinal haemorrhages with one larger white-centred (probable fibrin plug) temporal haemorrhage (figure 1). A week later the patient had a laser iridotomy OD. All haemorrhages had cleared. Two weeks later, the patient took no medication. At that time, a patent right iridotomy, a right reactive semi-mydriasis with an IOP of 30 mmHg OD and a closed angle OD were noted. The patient was diagnosed with a plateau iris syndrome OD. IOP was controlled with pilocarpine 2% bid OD. In this case as in Alwitry and coworkers'(1), decompression retinopathy occurred following exclusive medical treatment of acute primary angle closure. It is remarkable that in our case IOP elevation was relatively mild and IOP drop after treatment was only 23 mmHg. One may wonder whether or not the plateau iris syndrome played a role in the occurrence of decompression retinopathy in our patient. The case we report featured mild decompression retinopathy and, as previously reported, outcome was excellent.

  

  Figure 1 Right fundus showing blot-shaped scattered haemorrhages sparring the foveola with one larger white-centred temporal haemorrhage

  References 1 Alwitry A, Khan K, Rotchford A, Zaman AG, Vernon SA. Severe decompression retinopathy following medical treatment of acute primary angle closure. Br J Ophthalmol 2007;91:121

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  Conflict of Interest:
  None declared.

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