Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 3672
  • Home
  • Print this page
  • Email this page

   Table of Contents      
LETTER TO THE EDITOR
Year : 2012  |  Volume : 60  |  Issue : 6  |  Page : 583

Cilioretinal infarction as a sequel to central retinal vein occlusion in a patient exposed to thrombogenic medication


Worcester Royal Eye Unit, Charles Hastings Way, Worcester, England

Date of Web Publication26-Nov-2012

Correspondence Address:
Jagdeep Singh Gandhi
Worcester Royal Eye Unit, Charles Hastings Way, Worcester WR5 1DD
England
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.103810

Rights and Permissions

How to cite this article:
Gandhi JS. Cilioretinal infarction as a sequel to central retinal vein occlusion in a patient exposed to thrombogenic medication. Indian J Ophthalmol 2012;60:583

How to cite this URL:
Gandhi JS. Cilioretinal infarction as a sequel to central retinal vein occlusion in a patient exposed to thrombogenic medication. Indian J Ophthalmol [serial online] 2012 [cited 2020 Feb 24];60:583. Available from: http://www.ijo.in/text.asp?2012/60/6/583/103810

Dear Editor,

Kannan and colleagues reported a case in which cilioretinal arterial occlusion was ascribed to cocaine. [1] One could appreciate a lack of cogency in their analysis. The authors too confessed their perplexity on observing acute cilioretinal infarction (CRI) some 3 days after cocaine exposure. A misperception of cardinal signs led to inferences that merit further consideration. The supposition - vascular insufficiency focally in the cilioarterial tree induced by cocaine - is revisited, and the thesis expanded by providing deeper insights.

On the supplied fundus images, there are retinal hemorrhages discernible across the posterior pole, which are visibly contemporaneous with CRI. The hemorrhages are present in the upper and lower retinal hemispheres on either side of the macular raphe. The area of macular pallor denotes cilioretinal insufficiency whereas the hemorrhages in the posterior retina are consistent with central venous obstruction. Indeed, this is the quintessential signature of a retinovascular cascade: central retinal vein occlusion (CRVO) of nonischemic type with secondary evocation of CRI. Retrograde transmission of intravascular backpressure after CRVO suppresses perfusion of the cilioarterial system (which has lower pressures than the adjoining central retinal artery).

Such hypoperfusion of the cilioarterial territory is expressed as macular infarction (that is, CRI). Failure to identify this clinical constellation, acronymed here as CRVO-CRI, is a renowned pitfall. [2] For those not versed with this entity, a recourse to landmark monographs will clarify this distinctive presentation. [3] Also noteworthy is that the CRVO in a "CRVO-CRI tandem" is often nonischemic. Consequently, the CRVO signs may be subtle (expressed as "venous stasis retinopathy"), as exemplified by this typical case. This is the precise way in which I have met this combined retinal vasculopathy. Another exquisite feature is observable on the angiogram : the paradoxically rapid ingress of dye into a cilioretinal bed that should have sluggish perfusion owing to CRVO-CRI. This occurrence is elucidated when one appreciates the hemodynamics and anatomical variations of the chorioretinal tree. [4] Thus dye progression is influenced by (a) oscillatory fluxes related to the cardiac cycle, (b) the intensity of retinovenous backpressure, and (c) variations within the angioarchitecture from which emanates the cilioretinal artery. Such parameters vary from one CRVO-CRI event to another and accordingly produce variation in angiographic filling of the cilioretinal system.

The notion was also advanced in this report that the retinal hemorrhages arose as a result of systemic hypertension from cocaine exposure. Hemorrhages were described in the fundus affected by cilioretinal occlusion. Only if hemorrhages had developed in both fundi could one surmise that cocaine generated transitory malignant hypertension in this young patient.

A salient omission from the pathophysiological considerations was the detail of contraceptive use. This is a defined risk factor for retinovascular occlusion. [5] I have assessed young adults with retinovascular events in whom the only detectable risk factor was the contraceptive pill.

Both contraceptive hormones and cocaine have separately been implicated in the pathogenesis of CRVO. Hence the plausible rendition is that these two agents, singly or synergistically, were the genesis of a CRVO-CRI cascade in this young patient. As epilogue, one must emphasise that there is the potential for macular infarction (CRI) in any acute CRVO fundus with cilioretinal feeders. However, the actual likelihood of CRI is determined by the trio of factors outlined earlier. Lastly, the pharmacokinetics of cocaine (as recognized by the authors) are such that selective cilioretinal spasm is improbable 3 days after cocaine exposure. The authors were sensitive to this point in their notably ambivalent conclusions.

 
  References Top

1.
Kannan B, Balaji V, Kummararaj S, Govindarajan K. Cilioretinal artery occlusion following intranasal cocaine insufflations. Indian J Ophthalmol 2011;59:388-9.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.
McLeod D. Inappropriate investigation and management of a retinal vascular occlusion. Eye (Lond) 2006;20:865-6.   Back to cited text no. 2
    
3.
McLeod D, Ring CP. Cilio-retinal infarction after retinal vein occlusion. Br J Ophthalmol 1976;60:419-27.  Back to cited text no. 3
    
4.
McLeod D. Central retinal vein occlusion with cilioretinal infarction from branch flow exclusion and choroidal arterial steal. Retina 2009;29:1381-95.   Back to cited text no. 4
[PUBMED]    
5.
Vessey MP, Hannaford P, Mant J, Painter R, Frith P, Chappel D. Oral contraception and eye disease: Findings in two large cohort studies. Br J Ophthalmol 1998;82:538-42.  Back to cited text no. 5
[PUBMED]    




 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
References

 Article Access Statistics
    Viewed1915    
    Printed13    
    Emailed0    
    PDF Downloaded118    
    Comments [Add]    

Recommend this journal