Indian Journal of Ophthalmology

BRIEF REPORT
Year
: 1999  |  Volume : 47  |  Issue : 4  |  Page : 248--250

Bilateral simultaneous retinal vein occlusion


VS Gurunadh, V Baijal, MG Palit, YS Sarma 
 Command Hospital (SC) Pune, India

Correspondence Address:
V S Gurunadh
Command Hospital (SC) Pune
India




How to cite this article:
Gurunadh V S, Baijal V, Palit M G, Sarma Y S. Bilateral simultaneous retinal vein occlusion.Indian J Ophthalmol 1999;47:248-250


How to cite this URL:
Gurunadh V S, Baijal V, Palit M G, Sarma Y S. Bilateral simultaneous retinal vein occlusion. Indian J Ophthalmol [serial online] 1999 [cited 2024 Mar 28 ];47:248-250
Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1999/47/4/248/14902


Full Text

Central retinal vein occlusion (CVO) is a common retinal vascular disorder with potentially blinding complications.[1] However, a simultaneous bilateral affection is not a common entity. One such patient is described here.

 Case Report



A 44-year-old female patient presented with complaints of sudden decrease in vision in the left eye along with complaints of dizziness, weakness and malaise. She was known to have non-insulin dependent diabetes mellitus for 5 years and had been converted to insulin 3 months prior to presentation; she was also detected to be hypertensive. The patient had also undergone chemotherapy for Hodgkin's disease LP III-B stage 4 years ago.

On ophthalmic examination, visual acuity in the right eye was 6/9 unaided and 2/60 unaided in the left eye with no further improvement. Anterior segment examination, including the iris and pupil, was within the normal limits in both eyes. Ophthalmoscopy showed clear media in both the eyes. The optic discs were choked with intense hyperemia. The retinal veins were enlarged and distended. The entire retina was splashed with intraretinal haemorrhages of various shapes and sizes. There was also retinal oedema, more in the left than in the right. There was no peripheral retinal lesion in either eye. Intraocular pressure (IOP) was 12 mmHg by applanation in both eyes. A diagnosis of bilateral simultaneous CVO was made. Intravenous fundus fluorescein angiography confirmed the clinical picture with the peak phase showing tortuous and engorged veins, haemorrhages as blocked fluorescence and a greater degree of retinal oedema in the left eye [Figure:1] and [Figure:2].

ERG was not done, as it was not available. Due to the extensive haemorrhages, the CVO was considered to be indeterminate, in accordance with the central venous occlusion study group CVOS.[2]

Clinical haematology revealed an ESR of 10 mm at 1 hour (Wintrobe's), haemoglobin of 11 gms%, PCV of 40%, RBCs 3.9xl06/mm3, WBC 5000/mm3 and WBC differential count of 59% neutrophils, 35% lymphocytes, 4% eosinophils, and 2% basophils. There were no immature cells on peripheral smear.

As bilaterality of CVO is an indicator of hyperviscosity and as lymphomas have a predilection for myelomatosis,[3] the patient's serum protein analysis was done. Serum proteins were 9.4 gms/ dl (n:6-8 gms/ dl) with albumin 2.9 gms/ dl (n:3.5-5.5 gms/ dl) and globulins 6.5 gms/ dl. Serum electophoresis showed an additional band between beta and gamma regions but not as sharp as the 'M' band.

Immunoglobulin assay showed IgG of 2800mgs% (n:800-1500), IgA>600 mgs% (n:90-325 ) and IgM 283mgs% (n:45-150). The skull radiographs showed osteolytic lesions which along with hyperproteinemia and hypergammaglobulinemia in the context of hyper-viscosity syndrome pointed to a diagnosis of multiple myeloma.[4] The fasting blood sugar at the time of admission was 434 mgs%.

The patient was subjected to plasmapheresis with symptomatic improvement. She was started on melphalan. However, the patient succumbed to an intracranial bleed due to thrombocytopenia. Postmortem examination showed lesions typical of multiple myeloma in the bone marrow and the kidneys.

 Discussion



Abnormal blood viscosity plays a role in the causation of CVO.[5],[6] This patient had a double hyperviscosity insult with severe diabetes mellitus and hypergiobulinemia.The reversal of A/G ratio and increase in the levels of IgG denoted paraproteinemia. Though a sharp 'M' component suggestive of the major criteria of multiple myeloma is missing, the diagnosis of the same was arrived at with hypergammaglobulinemia, coupled with the skull radiographs.[4]

A severe hyperviscosity state predisposes one to a bilateral affection as were all the cases suffering from myeloma reported by Carr et al.[6] However, the association of diabetes mellitus with multiple myeloma causing a CVO has probably not been reported. Any case of a simultaneous bilateral CVO calls for the work up of all the systemic causes of CVO apart from diabetes mellitus and hypertension, which constitute the major etiological factors of CVO.

CVO usually occurs as a unilateral affection. In the CVO study (August 1988 to July 1992) a total of 725 eyes were enrolled; only three cases were bilateral (0.41%).[2] However, in a 17-year study by Hayreh et al (1973 to 1990) which included all forms of vascular occlusions, there were 515 patients of CVO, of whom 88 were bilateral (7.38%).[7]

References

1Clarkson JG. Central retinal vein occlusion. In: Ryan SJ, editor. Retina. St Louis, MO, USA: Mosby; 1994; Vol 2. p.379-85
2The Central Vein in Occlusion Study Group. Baseline and early natural history report: the central vein occlusion study (CVOS). Arch Ophthalmol 1993;111:1087-95.
3Alexian R. Monoclonal gammopathy in lymphoma. Arch Intern Med 1975;35:62-66.
4Durrie BGM, Giles FJ. Myeloma and other paraproteinemias. In: Weatherall DJ, Ledingham JGG, Warrel DA, editors. Oxford Textbook of Medicine, 4th ed. New York, USA: Oxford University Press Inc; 1996; Vol 3. pp 3597-605
5Trope GE, Lowe GDO, McArdle BM, Douglas JT, Forbes CD, et al. Abnormal blood viscosity and heamostasis in long standing retinal vein occlusion. Br J Ophthalmol 1983;67:137-42.
6Carr RE, Henkind P. Retinal findings with serum hyperviscosity. Am J Ophthalmol 1963;56:23-31.
7Hayreh SS, Zimmerman MB, Podhajsky P. Incidence of various types of retinal vein occlusion and their reccurence and demographic characteristics. Am J Ophthalmol 1994;117:429-41.