Was blind but now I see

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Was blind but now I see

• Grand Ward Round
• Dr Heng Li Wei
• 5th June 2008

2
History

• 74 / Indian / F
• DM on OHGA, hypt (diet control)
• Sudden onset of LE visual loss on waking up x 1
  day
• - Painless, no eye redness, no other
  neurological symptoms.

3
Examination

• VR - 6/7.5 VL - CF 3ft pH -gt 6/60
• No RAPD.
• Anterior segment
• - Mild cataracts. Otherwise NAD
• IOP 19mmHg BE.

4
Examination

• Confrontational VF

RE
LE
HM
HM
CF
CF
HM
CF
CF
HM
HM
HM
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• Posterior segment
• RE - NAD. No DR.
• LE
• Disc pink, no disc edema, CDR 0.3
• Slight pallor edema over macula
• Rest of retina pink.

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D/dx sudden painless LOV

• Vascular CRAO, CRVO
• Neuro AION ( arteritic / non-arteritic)
• Retina
• - RD
• - Vitreous hage ( PDR, NV, retina tear)
• - Wet ARMD with breakthrough hage

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OCT
OD
OS
219 microns
189 microns
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FFA
43s
1.5min
4min
8min
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Mgmt

• Treat as for Left CRAO
• Mgmt?
• - acute
• - subsequent workup

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• Ocular massage
• Carbogen therapy
• Timolol LE stat bd
• T aspirin 100mg om famotidine 20mg bd
• Pt refused AC tap
• Pt declined adm for CVM Neuro r/v.

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The next day

• Pt was very happy, said VA improved overnight.
• VR 6/9 VL 6/12
• Left RAPD grade 1
• VF by confrontation left paracentral nasal
  field blurring.
• Ishihara - R 15/15 L 9/15
• Red desaturation - R 100 L 40
• Posterior segment ISQ.

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R/v 2 weeks later

• VR 6/7.5 VL 6/9
• Left RAPD grade 1
• Ishihara - R 15/15 L 3/15
• LE very mild retina edema over macula.
• U/S carotids 28/5/08
• Neuro TCU 13/6/08
• CVM / 2DE TCU 13/6/08
• Referred to OPD to control DM hypt.
• TCU Neuro-Oph 2 months.

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CRAO protocol
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CRAO

• Causes
• Fundus appearance
• Prognosis / visual outcome
• Treatment

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CRAO - CAUSES
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Susac syndrome 1

• Triad of retinal artery occlusion, sensorineural
  deafness, encephalopathy
• Rare
• Microangiopathy affecting pre-capillary
  arterioles of brain, retina inner ear.
• Young women in young adulthood.
• Pathogenesis unknown.
• Clinical course recurrent attacks, spont
  resolution but may have sensory neurologic
  sequelae.
• Rx steriods, immunosuppressants, immunoglobulin.

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Orbital infarction syndrome 2

• Rare
• P/w acute blindness, orbital pain, total
  ophthalmoplegia, ant post segment ischaemia.
• Proposed mechanisms
• Acute perfusion failure eg. CCA occlusion
• Systemic vasculitis eg GCA
• Orbital cellulitis with vasculitis

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Fundus changes in CRAO 3

• 248 eyes permanent CRAO (175), w cilioretinal
  artery sparing (35), transient CRAO (38).
• Initial findings in permanent CRAO
• - Cherry red spot (90)
• - Retinal opacity in posterior pole (58)
• - Arterial attenuation, disc edema pallor,
  box-carring.
• Later stage findings
• - Optic atrophy, arterial attentuation,
  cilioretinal collaterals, macular RPE changes.
• 4 of CRAO had simultaneous bilateral onset.
• Intraarterial emboli observed in 20 of pts.

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Prognosis / Visual Outcome 4

• Poor except those with cilioretinal
  artery-sparing.
• 15-20 of general population have cilioretinal
  artery.
• 25 of CRAO have cilioretinal artery.
• VA improvement primarily w/n first 7 days.
• VA improvement
• - transient NA-CRAO (82), NA-CRAO w cilioret
  artery sparing (67), NA-CRAO (22).

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Treatment

• Medical therapy ocular massage carbogen
  therapy AC paracentesis.
• Intra-arterial thrombolysis (IAT)
• Hyperbaric O2 therapy (HBO)
• Transluminal NdYag embolysis/embolectomy (TYL/E)
• Transcorneal electrical stimulation

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Intra-arterial thrombolysis (IAT) 5

• Systemic rv on literature on IAT
• 23 studies, 8 selected for analysis.
• 158 pts.
• Rx instituted w/n average of 8.4h from onset of
  symptoms.
• VA improvement in 93 pts -gt 13 (gt20/20), 25
  (gt20/40), 41 (gt20/200).
• Complication rate 4.5.

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Hyperbaric Oxygenation Therapy(HBO) 6

• Off-label use
• W/n 12 hr of onset of symptoms
• Early Rx (lt2h) may be associated with increased
  visual recovery
• Other uses
• - retinal vein occlusion with CMO
• - scleral necrosis after pterygium Sx
• - orbital rhino-cerebral mucormycosis
• - anterior segment ischaemia.

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Transluminal NdYag embolysis / embolectomy 7

• Photodisrupt emboli w/n CRA/BRA to achieve rapid
  retinal reperfusion
• Embolysis embolus fragmented w/n lumen
• Embolectomy embolus observed to pass into
  vitreous
• Cx vitreous hage, subhyaloid hage

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Transcorneal electrical stimulation (TES) 8

• Longstanding CRAO/BRAO
• Jap studies
• Bipolar contact lens electrode, once 1 mth x 3
  mths.
• Outcome measures - perimetric and/or
  electrophysiological exam
• VA improved by gt0.2 logMar units in 2/3 cases.
• Visual fields improved in all 3 cases.
• Multifocal ERG improved in 2/3 cases.

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References

• Saliba et al. Susac syndrome and ocular
  manifestation in a 14-year-old girl. J Fr
  Ophtalmol. 2007 Dec30(10)1017-22.
• Borruat et al. Orbital infarction syndrome.
  Ophthalmology. 1993 Apr100(4)562-8.
• Havreb et al. Fundus changes in central retinal
  artery occlusion. Retina. 2007 Mar27(3)276-89.
• Hayreh et al. Central retinal artery occlusion
  visual outcome. Am J Ophthalmol. 2005
  Sep140(3)376-91.
• Noble J et al. Intra-arterial thrombolysis for
  central retinal artery occlusion a systematic
  review. Br J Ophthalmol. 2008 May92(5)588-93.
• Oguz H et al. The use of hyperbaric oxygen
  therapy in ophthalmology. Surv Ophthalmol. 2008
  Mar-Apr53(2)112-20.
• Opremcak et al. Restoration of retinal blood flow
  via translumenal NdYAG embolysis/embolectomy
  (TYL/E) for central and branch retinal artery
  occlusion. Retina. 2008 Feb28(2)226-35.
• Inomata K et al. Transcorneal electrical
  stimulation of retina to treat longstanding
  retinal artery occlusion. Graefes Arch Clin Exp
  Ophthalmol. 2007 Dec245(12)1773-80. Epub 2007
  Jun 26.