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ORIGINAL ARTICLE
Year : 2005  |  Volume : 53  |  Issue : 2  |  Page : 128-130

Premacular haemorrhage associated with arteriovenous communications of the retina induced by a valsalva-like mechanism: An observational case report


Retina - Vitreous Service, Aravind Eye hospital and Postgraduate Institute of Ophthalmology, Madurai, India

Date of Submission21-Jan-2004
Date of Acceptance09-Mar-2004

Correspondence Address:
Vasumathy Vedantham
Retina - Vitreous Service, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, 1 Anna Nagar, Madurai - 625 020, Tamilnadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.16179

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  Abstract 

A 26-year-old woman presented with sudden defective vision in the right eye following lifting a heavy bucket of water. Examination showed a dense premacular subhyaloid haemorrhage associated with arteriovenous communications of the retina (AVCRs). Spontaneous absorption of the premacular haemorrhage with consequent improvement in the visual acuity was seen after two months. The possible aetiopathogenesis of the case is also discussed.

Keywords: Arteriovenous communications, subhyaloid haemorrhage, valsalva - like mechanism


How to cite this article:
Vedantham V, Agrawal D, Ramasamy K. Premacular haemorrhage associated with arteriovenous communications of the retina induced by a valsalva-like mechanism: An observational case report. Indian J Ophthalmol 2005;53:128-30

How to cite this URL:
Vedantham V, Agrawal D, Ramasamy K. Premacular haemorrhage associated with arteriovenous communications of the retina induced by a valsalva-like mechanism: An observational case report. Indian J Ophthalmol [serial online] 2005 [cited 2020 Nov 30];53:128-30. Available from: https://www.ijo.in/text.asp?2005/53/2/128/16179

Arteriovenous communications of the retina (AVCRs) are rare congenital anomalies that are direct communications between an artery and a vein without an intervening capillary bed. They are classified into three grades, [1] Grade I is an anastomosis between a small arteriole and a venule; Grade II is an anastomosis between a branch artery and a branch vein, and Grade III is the diffuse marked dilation of the whole vascular system. Although usually non-progressive, these anomalies can be associated with complications such as central and branch retinal vein occlusion, neovascular glaucoma, optic atrophy, retinal exudation and vitreous haemorrhage. [1],[2],[3],[4],[5],[6] Decompensation of these vascular anomalies following exercise [2] and due to variations in g-forces, such as rollercoaster rides [3] have been described but complications due to a Valsalva-like mechanism have not been described so far.




  Case Report Top




A 26-year-old woman was seen with a complaint of sudden loss of vision in the right eye after lifting a heavy bucket of water. Previous ocular and systemic history was non-contributory. The best corrected visual acuity in the right eye was 6/60 and fundus examination showed a dense subhyaloid haemorrhage overlying the macula with multiple AVCRs in the superotemporal quadrant [Figure - 1]a. Two grade II AVCRs with a few superficial retinal haemorrhages in the vicinity were seen communicating between the superotemporal branch retinal vein and the superior branch macular artery, the latter appeared narrowed between the points of origin of the AVCRs. The superior branch macular artery could not be traced beyond the AVCRs and no branches were seen to arise from it distal to the AVCRs. The superotemporal branch retinal vein itself demonstrated nicking at the first arteriovenous crossing by the corresponding branch retinal artery, sausage-like dilatations proximal to the crossing. There was another grade II AVCR between the inferior branch macular artery and the superotemporal branch retinal vein in the temporal parafoveal area. In addition, there were multiple grade I AVCRs in the superior and nasal parafoveal areas with the capillary bed in this region having a corkscrew appearance. There was also a grade II AVCR in the equatorial region in the superotemporal quadrant between the superotemporal branch retinal artery and its corresponding vein [Figure - 1]b. The left eye was within normal limits.



Fluorescein angiography showed filling of the venous side of the AVCRs immediately after the arterial phase. The classic laminar venous flow was replaced by the arterial type of laminar flow (fluorescein filling of the central lumen alone owing to the hyperdynamic circulation) in the superotemporal branch retinal vein [Figure - 2]a. There was blocked fluorescence in the macular region due to the subhyaloid haemorrhage [Figure - 2]b. The late recirculation phase showed the venous type of laminar flow in the superotemporal branch retinal vein (due to diluted and relatively hypofluorescent fluorescein of the recirculation phase flowing in the central lumen) that was characteristic of AVCRs [Figure - 2]c. Visual field examination of the affected eye showed a central scotoma.



Neurological investigations including computerised tomography with contrast and MRI did not show a co-existent arteriovenous malformation in the brain and other parts of the body. The patient was kept under follow-up and spontaneous absorption of the premacular haemorrhage and improvement of visual acuity to 6/6 was seen after two months. The nasal parafoveal AVCR, previously obscured by the subhyaloid haemorrhage was clearly seen [Figure - 1]c. The patient has remained stable over 6-month follow-up period.




  Discussion Top




Archer et al [7] after studies using suction-cup ophthalmodynamometry postulated that the AVCRs act like low-resistance pathways for the flow of blood with the resultant hyperdynamic flow patterns. Endothelial injury, venous thrombosis and breakdown of the blood-retinal barrier are occasional sequelae of this vascular stress. In order to explain the development of complications associated with AVCRs, Mansour et al [2] put forward a similar hypothesis that AVCRs are associated with localised decreased retinal arterial pressure, increased retinal venous pressure, increased turbulence of blood flow, and decreased perfusion of adjacent retinal tissues due to a steal phenomenon. Spontaneous bleeding is rare in the retina [2] although it is a common presenting sign of arteriovenous communications of the pulmonary and cerebral circulations. [8]



The possible aetiopathogenesis in this case is a Valsalva-like mechanism superimposed over the haemodynamic stresses inherent in such a high pressure system. The sausage like dilatations of the superotemporal branch retinal vein testify to the high flow it experiences. The Valsalva-like mechanism due to the lifting of a heavy weight would have resulted in an increased pressure in the retinal veins, and this when added to the inherently raised hydrostatic pressure in the arteriovenous malformations might have led to a rupture of the wall of the nasal parafoveal arteriovenous malformation causing the premacular subhyaloid haemorrhage. It is also probable that the ischaemic superficial haemorrhages were due to transmission of the increased transmural pressure to the capillaries and the resultant endothelial damage. The abnormality in the superior branch macular artery suggests a possibly congenitally regressed artery and lends credence to the hypothesis that the AVCRs are due to developmental abnormalities of the retinal vasculature in utero . [1], [7]



To the best of our knowledge, this is the first case of AVCRs associated with subhyaloid haemorrhage in the macula due to a Valsalva-like mechanism. This report also highlights the fact that patients with arteriovenous communications of the retina face an increased risk of retinal vascular decompensation when engaged in activities associated with sudden changes in retinal venous pressure and hence need appropriate counselling in this regard.



 
  References Top

1.
Mansour AM, Walsh JB, Henkind P. Arteriovenous anastomosis of the retina. Ophthalmology 1987;94:35-40.   Back to cited text no. 1
    
2.
Mansour AM, Wells CG, Jampol LM, Kalina RE. Ocular complications of arteriovenous communications of the retina. Arch Ophthalmol 1989;107:232-6.  Back to cited text no. 2
    
3.
Beatty S, Goodall K, Radford R, Lavin MJ. Decompensation of a congenital retinal macrovessel with arteriovenous communications induced by repetitive rollercoaster rides. Am J Ophthalmol 2000;130:527-8.  Back to cited text no. 3
    
4.
Tilanus MD, Hoyng C, Deutman AF, Cruysberg JR, Aandekerk AL. Congenital arteriovenous communications and the development of two types of leaking retinal macroaneurysms. Am J Ophthalmol 1991;112:31-3.  Back to cited text no. 4
    
5.
Pauleikhoff D, Wessing A. Arteriovenous communications of the retina during a 17-year follow-up. Retina 1991;11:433-6.  Back to cited text no. 5
    
6.
Schatz H, Chang LF, Ober RR, McDonald HR, Johnson RN. Central retinal vein occlusion associated with retinal arteriovenous malformation. Ophthalmology 1993;100:24-30.  Back to cited text no. 6
    
7.
Archer DB, Deutman A, Ernest T, Krill AE. Arteriovenous communications of the retina. Am J Ophthalmol 1973;75:224-41.  Back to cited text no. 7
    
8.
Perret G, Nishioka H. Report on the cooperative study of intracranial aneurysms and subarachnoid hemorrhage: Section IV. Arteriovenous malformation: An analysis of 545 cases of craniocerebral arteriovenous malformations and fistulae reported to the cooperative study. J Neurosurg 1966;25:467-90.  Back to cited text no. 8
    


    Figures

  [Figure - 1], [Figure - 2]


This article has been cited by
1 Retinal vein occlusion in retinal racemose hemangioma: a case report and literature review of ocular complications in this rare retinal vascular disorder
Xue-jiao Qin,Chao Huang,Kun Lai
BMC Ophthalmology. 2014; 14(1): 101
[Pubmed] | [DOI]



 

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