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HYPERTENSIVE RETINOPATHY
CRAO&CRVO
Presentation by:
Rajesh Paudel
Roll No.-39
HYPERTENSIVE RETINOPATHY
 It refers to fundus changes
occurring in patients
suffering from systemic
hypertension.
 It includes :
 Retinopathy
 Choroidopathy
 Optic neuropathy
CLINICAL TYPES
 Chronic hypertensive retinopathy
 Acute or malignant hypertensive retinopathy
FUNDUS CHANGES IN CHRONIC
HYPERTENSIVE RETINOPATHY
Generalised/
Focal
narrowing/
attenuation of
arterioles
Arteriovenous crossing changes
Salu’s sign : deflection of veins at A-V
crossings
Arteriovenous crossing changes
Bonnet sign : banking of veins distal to
A-V crossings
Arteriovenous crossing changes
Gunn sign : tapering of veins on either
side of crossings
Arteriolar reflex changes
 Bright and thin ,linear blood reflex is
seen normally over the surface of the
arteriole.
 More diffuse & less bright reflex is seen
due to thickening of vessel wall
Arteriolar reflex changes
Copper wiring :
reddish brown reflex
of arterioles
Arteriolar reflex changes
• Silver wiring :
opaque white
reflex of arterioles
Silver wiring
Other changes
MALIGNANT HYPERTENSIVE
RETINOPATHY CHANGES
Acute hypertensive retinopathy
 Marked arteriolar retinopathy
 Superficial retinal hemorrhage (flame
shaped)
 Focal intraretinal periarteriolar
transudates
 Cotton wool spots
 Development of microaneurysm , shunt
vessels , collaterals
Acute hypertensive choroidopathy
Elschnig’s spots:
 Black spots
surrounded by
yellow halos
 Due to clumping and
atrophy of infarcted
pigment epithelium
Acute hypertensive choroidopathy
Siegrist streaks:
hyperpigmented flecks
arranged linearly along
choroidal vessels
Acute hypertensive choroidopathy
Acute focal retinal pigment epitheliopathy
characterized by focal white spots
Serous neurosensory retinal detachment
Acute hypertensive optic neuropathy
Disc edema &
hemorrhages on the
disc and
peripapillary retina
Disc pallor
MANAGEMENT
 Blood Pressure control
 Risk reduction therapy e.g. cholesterol
lowering drugs
 Anti hypertensive drugs
CENTRAL RETINAL ARTERY
OCCLUSION
 It is an ocular emergency
 It occurs due to obstruction at the level of
lamina cribosa
 Usually unilateral
 Male >Female
ETIOLOGY OF CRAO
 Emboli
 Atherosclerosis
 Angiospasm
 Raised IOP
 Thrombophilic disorders
 Other causes
 retinal migraine
 hypercoagulation disorders
 sickling hemoglobinopathies
 Sudden painless of vision
 There may be history of
transient visual loss
(amaurosis fugax)
SYMPTOMS
 Visual acuity reduced
 Direct pupillary light
absent
 Relative afferent pupillary
defect present
SIGNS
 Narrowing of retinal vessels
 Retina becomes milky white : in eyes with cilioretinal
artery part of macula remains normal
 Cherry red spot in the centre of macula (in absence of
cilioretinal artery)
 Cattle tracking
 Atrophic changes :
• Grossly attenuated thread like arteries
• Atrophic appearing retina
• Consecutive optic atrophy
FUNDUS CHANGES OF CRAO
TREATMENT OF CRAO
Aggressive treatment of acute episodes
should be done.
 Lower the IOP
 Vasodilators and inhalation of mixture of
5% co2 & 95% O2 or patient is asked to
breathe in a polythene bag
 Fibrinolytic therapy
 IV steroids in case of arteritis
 Laser photodisruption of embolus
CENTRAL RETINAL VEIN
OCCLUSION
 It is more common than the artery
occlusion
 Occurs over sixth or seventh decade of life
ETIOLOGY OF CRVO
 Pressure on vein by atherosclerotic retinal
artery
 HTN,DM
 Hyperviscosity of blood
 Periphlebitis retinae
 Raised IOP
 Local causes:
o Orbital cellulitis
o Orbital tumors
o Facial erysipelas
o Cavernous sinus
thrombosis
TWO TYPES OF CRVO
Ischemic & Non-ischemic
NON-ISCHEMIC CRVO
SYMPTOMS
Mild to moderate vision loss
Sudden unilateral blurred vision
SIGNS
Vision:impaired moderately to
severe degree
RAPD: absent
FUNDUS EXAMINATION OF NON-
ISCHEMIC CRVO
• Mild venous congestion
and tortuosity
• Few superficial
hemorrhages
• Mild papilloedema
• Mild or no macular
edema
ISCHEMIC CRVO
SYMPTOMS
Sudden loss of vision
Usually unilateral
SIGNS
Vision acuity: worse
RAPD : marked
 Massive venous
engorgement,congestion
& tortuosity
 Massive retinal
hemorrhage
 Cotton wool spots
 Disc edema & hyperemia
 Macular hemorrhage &
edema
 Neovascularization in
late cases
FUNDUS EXAMINATION OF ISCHEMIC CRVO
Splashed tomato
appearance of fundus
MANAGEMENT OF RETINAL VEIN
OCCLUSION
Ocular examination:
 Visual acuity
 IOP recording
 Undilated slit lamp
examination
 Gonioscopy
 Fundus examination
Ocular investigations:
 Goldmann perimetry
 Electroretinograohy
 Fundus fluorescein
angiography (FPA)
 Optical coherence
tomography (OCT)
TREATMENT
 Treatment of systemic & ocular associations
such as HTN,DM,hypelipidemias,POAG
 Observation and monitoring : more than 50%
cases of CRVO resolves with almost normal
vision
 Medical therapy:
 Intravitreal anti-VEGF (bevacizumab,
ranibizumab)
 Intravitreal triamcinolone
 Laser therapy
 Pars Plana Vitrectomy
Hepertensive retinopathy , CENTRAL RETINAL ARTERY OCCLUSION ,CENTRAL RETINAL VENOUS OCCLUSION

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Hepertensive retinopathy , CENTRAL RETINAL ARTERY OCCLUSION ,CENTRAL RETINAL VENOUS OCCLUSION

  • 2. HYPERTENSIVE RETINOPATHY  It refers to fundus changes occurring in patients suffering from systemic hypertension.  It includes :  Retinopathy  Choroidopathy  Optic neuropathy
  • 3.
  • 4. CLINICAL TYPES  Chronic hypertensive retinopathy  Acute or malignant hypertensive retinopathy
  • 5. FUNDUS CHANGES IN CHRONIC HYPERTENSIVE RETINOPATHY
  • 7. Arteriovenous crossing changes Salu’s sign : deflection of veins at A-V crossings
  • 8. Arteriovenous crossing changes Bonnet sign : banking of veins distal to A-V crossings
  • 9. Arteriovenous crossing changes Gunn sign : tapering of veins on either side of crossings
  • 10. Arteriolar reflex changes  Bright and thin ,linear blood reflex is seen normally over the surface of the arteriole.  More diffuse & less bright reflex is seen due to thickening of vessel wall
  • 11. Arteriolar reflex changes Copper wiring : reddish brown reflex of arterioles
  • 12. Arteriolar reflex changes • Silver wiring : opaque white reflex of arterioles Silver wiring
  • 15. Acute hypertensive retinopathy  Marked arteriolar retinopathy  Superficial retinal hemorrhage (flame shaped)  Focal intraretinal periarteriolar transudates  Cotton wool spots  Development of microaneurysm , shunt vessels , collaterals
  • 16. Acute hypertensive choroidopathy Elschnig’s spots:  Black spots surrounded by yellow halos  Due to clumping and atrophy of infarcted pigment epithelium
  • 17. Acute hypertensive choroidopathy Siegrist streaks: hyperpigmented flecks arranged linearly along choroidal vessels
  • 18. Acute hypertensive choroidopathy Acute focal retinal pigment epitheliopathy characterized by focal white spots Serous neurosensory retinal detachment
  • 19. Acute hypertensive optic neuropathy Disc edema & hemorrhages on the disc and peripapillary retina Disc pallor
  • 20.
  • 21. MANAGEMENT  Blood Pressure control  Risk reduction therapy e.g. cholesterol lowering drugs  Anti hypertensive drugs
  • 22. CENTRAL RETINAL ARTERY OCCLUSION  It is an ocular emergency  It occurs due to obstruction at the level of lamina cribosa  Usually unilateral  Male >Female
  • 23. ETIOLOGY OF CRAO  Emboli  Atherosclerosis  Angiospasm  Raised IOP  Thrombophilic disorders  Other causes  retinal migraine  hypercoagulation disorders  sickling hemoglobinopathies
  • 24.  Sudden painless of vision  There may be history of transient visual loss (amaurosis fugax) SYMPTOMS  Visual acuity reduced  Direct pupillary light absent  Relative afferent pupillary defect present SIGNS
  • 25.  Narrowing of retinal vessels  Retina becomes milky white : in eyes with cilioretinal artery part of macula remains normal  Cherry red spot in the centre of macula (in absence of cilioretinal artery)  Cattle tracking  Atrophic changes : • Grossly attenuated thread like arteries • Atrophic appearing retina • Consecutive optic atrophy FUNDUS CHANGES OF CRAO
  • 26.
  • 27.
  • 28. TREATMENT OF CRAO Aggressive treatment of acute episodes should be done.  Lower the IOP  Vasodilators and inhalation of mixture of 5% co2 & 95% O2 or patient is asked to breathe in a polythene bag  Fibrinolytic therapy  IV steroids in case of arteritis  Laser photodisruption of embolus
  • 29. CENTRAL RETINAL VEIN OCCLUSION  It is more common than the artery occlusion  Occurs over sixth or seventh decade of life
  • 30. ETIOLOGY OF CRVO  Pressure on vein by atherosclerotic retinal artery  HTN,DM  Hyperviscosity of blood  Periphlebitis retinae  Raised IOP  Local causes: o Orbital cellulitis o Orbital tumors o Facial erysipelas o Cavernous sinus thrombosis
  • 31. TWO TYPES OF CRVO Ischemic & Non-ischemic
  • 32. NON-ISCHEMIC CRVO SYMPTOMS Mild to moderate vision loss Sudden unilateral blurred vision SIGNS Vision:impaired moderately to severe degree RAPD: absent
  • 33. FUNDUS EXAMINATION OF NON- ISCHEMIC CRVO • Mild venous congestion and tortuosity • Few superficial hemorrhages • Mild papilloedema • Mild or no macular edema
  • 34. ISCHEMIC CRVO SYMPTOMS Sudden loss of vision Usually unilateral SIGNS Vision acuity: worse RAPD : marked
  • 35.  Massive venous engorgement,congestion & tortuosity  Massive retinal hemorrhage  Cotton wool spots  Disc edema & hyperemia  Macular hemorrhage & edema  Neovascularization in late cases FUNDUS EXAMINATION OF ISCHEMIC CRVO Splashed tomato appearance of fundus
  • 36. MANAGEMENT OF RETINAL VEIN OCCLUSION Ocular examination:  Visual acuity  IOP recording  Undilated slit lamp examination  Gonioscopy  Fundus examination Ocular investigations:  Goldmann perimetry  Electroretinograohy  Fundus fluorescein angiography (FPA)  Optical coherence tomography (OCT)
  • 37. TREATMENT  Treatment of systemic & ocular associations such as HTN,DM,hypelipidemias,POAG  Observation and monitoring : more than 50% cases of CRVO resolves with almost normal vision  Medical therapy:  Intravitreal anti-VEGF (bevacizumab, ranibizumab)  Intravitreal triamcinolone  Laser therapy  Pars Plana Vitrectomy