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OCCULAR ISCHEMIC SYNDROME
By-
Harsh Jain
Sudhanshu
B.V.P –Optometry {Pune}
Important Points
 Ischemia is the decrease of blood supply to a tissue. It can be
local, caused locally by a thrombus or embolus, or global due to
a low perfusion pressure.
 Hypoxia is lack of oxygen to a tissue from any cause.
 Syndrome is a group of symptoms which consistently occur
together.
 Stenosis means abnormal narrowing of blood vessels.
 Perfusion pressure, refers to the pressure gradient that drives
coronary blood pressure, meaning the difference between the
diastolic aortic pressure and the right atrial end diastolic
pressure.
Aetiology
 Ocular ischaemic syndrome refers to a Rare condition
resulting from Chronic ocular hypoperfusion secondary to
carotid artery stenosis.
 It is mainly unilateral {80%}
 This is chronic insufficiency of the ophthalmic artery
leading to reduced perfusion of the entire eye. The most
common cause is Carotid Stenosis.{Pocket atlas of Ophthalmology}
Pathogenesis
• The chronic ocular Hypoperfusion is secondary to Ipsilateral
atherosclerotic carotid stenosis of more than 90 % resulting in
50% reduction of Ipsilateral perfusion pressure.
• It typically affects patients during the 7th decade and may be
associated with Diabetes,Hypertension,Ischemic heart diseases
and Cerebro-vascular diseases.
Clinical Ophthalmology –Jack J Kanski
Carotid Stenosis
• It refers to atherosclerotic occlusive carotid artery disease
often associated with ulceration at the bifurcation of
common carotid artery.
• Risk factors include Male gender, old age (60-90 years),
smoking, for carotid hypertension, diabetes mellitus and
Hyperlipidaemia.
Manifestations
• Amaurosis fugax (transient retinal ischaemic attack)
• Retinal artery occlusion (due to embolus)
• Transient cerebral ischaemic attacks (TIA) Stroke
• Asymetrical diabetic retinopathy
Comprehensive Ophthalmology –A.K Khurana
Symptoms
• Loss of vision, which usually progresses gradually over
several weeks or months.
• Transient black outs (amaurosis fugax) may be noted by
some patients.
• Pain-ocular or periorbital— may be complained by some
patients.
• Delayed dark adaptation may be noted by a few patients.
Comprehensive Ophthalmology –A.K Khurana
Signs
• Cornea may show oedema and striae.
• Anterior chamber my reveal faint aqueous flare with few, if any,
cell (ischaemic pseudoiritis).
• Pupil may be mid dilated and poorly reacting. Iris shows
rubeosis iridis (in 66% cases) and atrophic patches.
• Cataract may occur as a complication in advanced cases.
• Neovascular glaucoma is a frequent sequelae to anterior
segment neovascularization.
Comprehensive Ophthalmology –A.K Khurana
Anterior Segment
Examination
• Diffuse episcleral injection and corneal oedema.
• Aqueous flare with a few cells {Ischemic pseudo-iritis}
• Iris atrophy and a mild dilated and poorly reacting pupil.
• Rubeosis Iridis is common.
• Cataract in very advanced cases.
Fundus Examination
o Venous dilatation with irregular caliber but no or only mild
tortuosity.
o Retinal arterial narrowing is present.
o Retina show midperipheral dot and blot haemorrhages,
microaneurysms and cotton wool spots.
o Retinal neovascularization is noted in 37% cases, which may be
in the form of NVD and occasionally NVE.
o Macular oedema is a common complication.
FFA
• Early phase shows delayed choroidal filling and prolonged
artero-venous transit time.{Fig –a & b}
• Late phase shows disc and perivascular hyper fluorescence,and
leakage at the posterior pole.{Fig –c}
Carotid Imaging
• It may involve color Doppler ultra-sonography, digital
subtraction angiography and MR angiography.
Management
 Anterior segment Manifestation :- are treated with topical
steroids and mydriatics.
 Neovascular Glaucoma may be treated medically or
surgerically.
 Proliferative Retinopathy can be treated with PRP although
the outcome is considerably less certain than in PDR.
 Macular Oedema may respond to intra-vitreal steroid or
anti-VEGF agents or carotid surgery.
Clinical Ophthalmology –Jack.J.Kanski
Reference
• Clinical Ophthalmology –Jack.J.Kanski
• Comprehensive Ophthalmology –A.K Khurana
• Pocket Atlas of Ophthalmology –T.Schlote.J. Rohrbach
Occular Ischemic Syndrome

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Occular Ischemic Syndrome

  • 1. OCCULAR ISCHEMIC SYNDROME By- Harsh Jain Sudhanshu B.V.P –Optometry {Pune}
  • 2.
  • 3. Important Points  Ischemia is the decrease of blood supply to a tissue. It can be local, caused locally by a thrombus or embolus, or global due to a low perfusion pressure.  Hypoxia is lack of oxygen to a tissue from any cause.  Syndrome is a group of symptoms which consistently occur together.  Stenosis means abnormal narrowing of blood vessels.  Perfusion pressure, refers to the pressure gradient that drives coronary blood pressure, meaning the difference between the diastolic aortic pressure and the right atrial end diastolic pressure.
  • 4. Aetiology  Ocular ischaemic syndrome refers to a Rare condition resulting from Chronic ocular hypoperfusion secondary to carotid artery stenosis.  It is mainly unilateral {80%}  This is chronic insufficiency of the ophthalmic artery leading to reduced perfusion of the entire eye. The most common cause is Carotid Stenosis.{Pocket atlas of Ophthalmology}
  • 5. Pathogenesis • The chronic ocular Hypoperfusion is secondary to Ipsilateral atherosclerotic carotid stenosis of more than 90 % resulting in 50% reduction of Ipsilateral perfusion pressure. • It typically affects patients during the 7th decade and may be associated with Diabetes,Hypertension,Ischemic heart diseases and Cerebro-vascular diseases. Clinical Ophthalmology –Jack J Kanski
  • 6. Carotid Stenosis • It refers to atherosclerotic occlusive carotid artery disease often associated with ulceration at the bifurcation of common carotid artery. • Risk factors include Male gender, old age (60-90 years), smoking, for carotid hypertension, diabetes mellitus and Hyperlipidaemia.
  • 7. Manifestations • Amaurosis fugax (transient retinal ischaemic attack) • Retinal artery occlusion (due to embolus) • Transient cerebral ischaemic attacks (TIA) Stroke • Asymetrical diabetic retinopathy Comprehensive Ophthalmology –A.K Khurana
  • 8. Symptoms • Loss of vision, which usually progresses gradually over several weeks or months. • Transient black outs (amaurosis fugax) may be noted by some patients. • Pain-ocular or periorbital— may be complained by some patients. • Delayed dark adaptation may be noted by a few patients. Comprehensive Ophthalmology –A.K Khurana
  • 9. Signs • Cornea may show oedema and striae. • Anterior chamber my reveal faint aqueous flare with few, if any, cell (ischaemic pseudoiritis). • Pupil may be mid dilated and poorly reacting. Iris shows rubeosis iridis (in 66% cases) and atrophic patches. • Cataract may occur as a complication in advanced cases. • Neovascular glaucoma is a frequent sequelae to anterior segment neovascularization. Comprehensive Ophthalmology –A.K Khurana
  • 10.
  • 11. Anterior Segment Examination • Diffuse episcleral injection and corneal oedema. • Aqueous flare with a few cells {Ischemic pseudo-iritis} • Iris atrophy and a mild dilated and poorly reacting pupil. • Rubeosis Iridis is common. • Cataract in very advanced cases.
  • 12. Fundus Examination o Venous dilatation with irregular caliber but no or only mild tortuosity. o Retinal arterial narrowing is present. o Retina show midperipheral dot and blot haemorrhages, microaneurysms and cotton wool spots. o Retinal neovascularization is noted in 37% cases, which may be in the form of NVD and occasionally NVE. o Macular oedema is a common complication.
  • 13. FFA • Early phase shows delayed choroidal filling and prolonged artero-venous transit time.{Fig –a & b} • Late phase shows disc and perivascular hyper fluorescence,and leakage at the posterior pole.{Fig –c}
  • 14.
  • 15. Carotid Imaging • It may involve color Doppler ultra-sonography, digital subtraction angiography and MR angiography.
  • 16. Management  Anterior segment Manifestation :- are treated with topical steroids and mydriatics.  Neovascular Glaucoma may be treated medically or surgerically.  Proliferative Retinopathy can be treated with PRP although the outcome is considerably less certain than in PDR.  Macular Oedema may respond to intra-vitreal steroid or anti-VEGF agents or carotid surgery.
  • 17.
  • 19. Reference • Clinical Ophthalmology –Jack.J.Kanski • Comprehensive Ophthalmology –A.K Khurana • Pocket Atlas of Ophthalmology –T.Schlote.J. Rohrbach