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 Table of Contents    
CLINICAL QUIZ
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 66  

A case of sudden painless loss of vision with partial spontaneous recovery


Department of Ophthalmology, Goa Medical College, Bambolim, Goa, India

Date of Web Publication10-Feb-2016

Correspondence Address:
Pradnya Jayant Kamat
168, 8/2, Kamat Nursing Home, Upper Bazaar, Ponda, Goa - 403 401
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-620X.176124

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How to cite this article:
Kamat PJ, Doshi PY. A case of sudden painless loss of vision with partial spontaneous recovery. Oman J Ophthalmol 2016;9:66

How to cite this URL:
Kamat PJ, Doshi PY. A case of sudden painless loss of vision with partial spontaneous recovery. Oman J Ophthalmol [serial online] 2016 [cited 2020 Feb 24];9:66. Available from: http://www.ojoonline.org/text.asp?2016/9/1/66/176124


   Case Profile Top


A 47-year-old female came with a history of loss of vision in the right eye since 4 days. It was sudden in onset and painless. She gave history of consulting an ophthalmologist within 12 h of visual loss and was treated with ocular massage and systemic acetazolamide. Within 24 h of initiation of treatment, the temporal half of vision was spontaneously restored partially. Anterior segment examination was unremarkable in both eyes. Visual acuity by Snellen's chart at presentation to us in right eye was 6/18, N10 and intraocular pressure by applanation tonometry was 12 mmHg.

Right eye fundus picture is given below [Figure 1] and [Figure 2]. Optical coherence tomography (OCT) of the macula [Figure 3] and fundus fluorescein angiography was performed to confirm the diagnosis.
Figure 1: Dilated fundus photograph of right eye

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Figure 2: Photo of optic disc of the right eye

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Figure 3: Optical coherence tomography of right eye

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   Questions Top


  1. Describe the fundus picture in [Figure 1] and [Figure 2]. Describe OCT changes in [Figure 3]
  2. What is the most likely diagnosis? What is the most common causative factor leading to it?
  3. What could be the reason for the partial spontaneous recovery of the temporal field of vision?
  4. What systemic investigations would you like to perform in such a case?


[TAG:2]Answers[/TAG:2]

  1. [Figure 1] is a dilated fundus picture of right eye showing whitish, oedematous retina affecting the temporal quadrant with relative sparing of the papillomacular bundle and not involving retina nasal to the disc. The cherry red spot is seen at the macula

    [Figure 2] shows optic disc photo with central retina artery after entering the globe dividing into superior, inferior, and an additional nasal branch. A whitish embolus (black arrow) is seen at the trifurcation with axoplasmic stasis

    [Figure 3] OCT showing normal foveal contour with hyperreflectivity of inner retinal layers temporal to fovea
  2. Diagnosis is central retinal artery occlusion (CRAO). Most common causative factor is embolism
  3. Migration of the embolus along the central retinal artery (probably due to early institution of treatment) along with anatomical variation in the branching pattern of central retinal artery in the form of an additional nasal branch probably helped in salvaging the nasal half of retina with partial recovery of temporal visual field
  4. Systemic investigations: Blood pressure, blood sugar levels, serum lipids, bleeding and clotting times, erythrocyte sedimentation rate, C reactive protein; cardiac evaluation which includes electrocardiography, echocardiography, and carotid doppler; hematological investigations include complete hemogram with peripheral smear, protein C, lupus anticoagulant, antiphospholipid antibodies, serum and urinary homocysteine, and factor V Leiden and prothrombin.


[TAG:2]Discussion[/TAG:2]

Acute occlusive events of the retinal arterial circulation are not very uncommon in elderly individuals (beyond 60 years of age) with a slight male preponderance. In many instances, it is impossible to ascertain the exact path physiologic process responsible for it. Embolism is the most common cause and carotid artery and the heart, most common sources.[1] Hence, evaluation of both these sources of embolism in every patient of branch retinal artery occlusion (BRAO) and CRAO by echocardiography and carotid Doppler is of critical importance. Typically emboli get lodged at vessel bifurcations, and 98% of the times, they involve temporal vessels.

Migration of embolus in retinal circulation has significant practical implications, as was seen in our patient. However, by the time the eye is examined the embolus that caused the occlusion might get disintegrated, migrate and disappear causing the fundus fluorescein angiography to show a normal retinal circulation despite classical fundus findings.[1],[2],[3]

Other causes include intraluminal thrombosis, vasculitis, arterial spasm, hypertensive arterial necrosis, and dissecting aneurysm. These causes are intimately related to associated systemic abnormalities such as diabetes mellitus (25%), hypertension (66%), and cardiac valvular disease (25%). Hematological abnormalities are also associated with arterial occlusions, especially in young individuals.[1],[2],[3]

Though there is no definitive treatment for retinal artery occlusion, ocular massage is known to cause large fluctuations in intraocular pressures and dilatation of arterial tree, thus, mechanically facilitating dislodgement of embolus.[4] Along with systemic acetazolamide and anterior chamber paracenthesis, it forms the most widely used form of treatment in acute stages in the emergency room. Other miscellaneous advocated treatments include thrombolysis by administering a thrombolytic agent intravenously or local intraarterial fibrinolysis by superselective administration of thrombolytic agent directly into the ophthalmic artery; isovolumic hemodilution; hyperbaric oxygen; reduction of red blood cell rigidity by giving pentoxifylline; systemic corticosteroids given intravenously to reduce vascular endothelial edema following CRAO; Nd:YAG laser arteriotomy and embolectomy; and cannulation of the supraorbital artery and retrograde injection of antispasmodic papaverine.[5]

Hayreh's studies showed that retina suffers from almost no detectable damages up to 97 min.[5] Treatment if, successfully instituted in this golden period may improve the visual prognosis by converting CRAO into BRAO.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Hayreh SS, Zimmerman MB. Central retinal artery occlusion: Visual outcome. Am J Ophthalmol 2005;140:376-91.  Back to cited text no. 1
    
2.
Hayreh SS, Podhajsky PA, Zimmerman MB. Branch retinal artery occlusion: Natural history of visual outcome. Ophthalmology 2009;116:1188-94.e1-4.  Back to cited text no. 2
    
3.
Hayreh SS, Zimmerman MB. Fundus changes in central retinal artery occlusion. Retina 2007;27:276-89.  Back to cited text no. 3
    
4.
Beatty S, Au Eong KG. Acute occlusion of the retinal arteries: Current concepts and recent advances in diagnosis and management. J Accid Emerg Med 2000;17:324-9.  Back to cited text no. 4
    
5.
Hayreh SS, Zimmerman MB. Central retinal artery occlusion: Visual outcome. Am J Ophthalmol 2005;140:376-91.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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