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Journal of Postgraduate Medicine
Medknow Publications and Staff Society of Seth GS Medical College and KEM Hospital, Mumbai, India
ISSN: 0022-3859 EISSN: 0972-2823
Vol. 53, Num. 4, 2007, pp. 270-270

Journal of Postgraduate Medicine, Vol. 53, No. 4, October-December, 2007, pp. 270

Letter

Natural history of non-ischemic central retinal vein occlusion versus iatrogenic intervention

The Retina Service, The Royal Eye Hospital Manchester, England
Correspondence Address:The Retina Service, The Royal Eye Hospital Manchester, England, doctorjsg@gmail.com

Code Number: jp07093

Related articles: jp07067 , jp07094

Sir,

I read with interest the report by Issa and Qasem on the occurrence of central retinal vein occlusion (CRVO) in association with thrombotic thrombocytopenic purpura (TTP) in a 45-year-old man. [1] Given that their patient had an absent relative afferent pupillary defect from the outset and showed visual recovery from an acuity of 6/60 to 6/12 over 12 weeks, there were sufficient grounds to diagnose a "non-ischemic" CRVO. [2] Their inference that a combination of macular laser and systemic medical therapy favorably influenced the outcome of (non-ischemic) CRVO in their patient cannot be delivered with confidence. As such, their concluding sentiments are questionable because the natural history of a "non-ischemic CRVO" is one that characteristically carries a good prognosis, such that most eyes eventually enjoy good visual acuity. [2]

To recapitulate: the visual fate of an eye that suffers a CRVO is chiefly determined by whether the insult is of an "ischemic" or "non-ischemic" nature. This dichotomous classification is helpful in predicting prognosis and applies regardless of the underlying etio-pathogenesis of a CRVO. [2] Hayreh has already made the point that since the natural history for non-ischemic CRVO is resoundingly benign, it is imprecise and misleading to congratulate ourselves on the effectiveness of any interventions undertaken in parallel with the usual timecourse for clinical improvement. [3]

In both variants of CRVO it is believed that there is a blockage of the central retinal vein, but in "non-ischemic" cases there is a relatively superior blood flow owing to a better availability of collateral venous channels. [3]

Secondly, the application of macular laser at 12 weeks is also a questionable decision in this case, bearing in mind that the resolution of macular edema (as evidenced by the improvement in visual acuity) was already progressing acceptably. Clearance of edema at such a rate signifies the survival of a macular microcirculation with healthy hemodynamics. Hence it is fallacious to commemorate any laser treatment applied towards the final phase of visual recovery, when the preamble was already very satisfactory. Indeed, it would have been preferable to wait for a further four to six weeks to observe the subsequent course of visual acuity before intervening with laser photocoagulation or another anti-edema treatment. Any supposed concerns regarding the creation of "chronic macular edema" beyond 12 weeks (and consequent permanent degeneration of macular structure) are not tenable in this instance given the prevailing behavior of this patient′s CRVO.

Rather counter-intuitively, the overriding belief at present is that thrombus-clearing or preventing strategies are seemingly ineffective in CRVO. [4] A similar opinion has been expressed regarding the efficacy of hemodilution techniques in cases where raised blood viscosity has been considered relevant to the pathogenesis of CRVO. Germane too in this regard is the observation that CRVOs can occur in patients on therapeutic levels of anticoagulant therapy. [5]

Thus the proposed effectiveness of anti-thrombotic and laser treatment in modulating this patient′s CRVO is difficult to reconcile with the observation that (even when left alone) eyes that have suffered a non-ischemic CRVO overwhelmingly tend to fare well. [2] Whether the described iatrogenic input actually improved the outcome for this single patient is therefore an eminently debatable point. And importantly, when considering therapeutic strategies we must first acknowledge the natural history of the disease process under scrutiny to introduce equilibrium into the discussion and allow a better informed interpretation.

References

1.Issa SA, Qasem Q Central retinal vein occlusion associated with thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome: Complete resolution is possible. J Postgrad Med 2007;53:183-84.  Back to cited text no. 1    
2.Zegarra H, Gutman FA, Conforto J. The natural course of central retinal vein occlusion. Ophthalmology 1979;86:1931-42.  Back to cited text no. 2  [PUBMED]  
3.Hayreh SS. Prevalent misconceptions about acute retinal vascular occlusive disorders. Prog Retin Eye Res 2005;24:493-519.   Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Mohamed Q, McIntosh RL, Saw SM, Wong TY. Interventions for central retinal vein occlusion: An evidence-based systematic review. Ophthalmology 2007;114:507-19, 524.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Koizumi H, Ferrara DC, Brue C, Spaide RF. Central retinal vein occlusion case-control study. Am J Ophthalmol 2007 [Epub ahead of print].  Back to cited text no. 5    

Copyright 2007 - Journal of Postgraduate Medicine

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