Retinal vascular diseases 2

1
Retinal vascular diseases 2

• Dr. Mohammad Shehadeh

2
Retinal vein occlusion

• Classification
• Branch retinal vein occlusion
• Central retinal vein occlusion

3
Pathogenesis

• Atherosclerosis of the retinal arterioles make
  them rigid and they compress the veins when they
  cross it causing it to thrombose ? causing branch
  retinal vein occlusion
• Central retinal vein and artery share a common
  adventitial sheath posterior to lamina cribrosa,
  so that atherosclerosis changes of the artery may
  compress the vein causing its thrombosis ? and
  cause central retinal vein occlusion

4
Risk factors of retinal vein occlusion

• Old age 50 over the age of 65
• Systemic conditions Hypertention,
  hyperlipidemia, diabetes, smoking and obesity.
• Raised intraocular pressure
• Inflammatory diseases such as sarcoidosis
• Thrombophilic disorders inherited or aquired

5
Branch retinal vein occlusion

• Presentation depend on the extent of macular
  involvement.
• If the macula not involved it may be asymptomatic
• Sudden onset of blurred vision
• Metamorphopsia
• Relative visual field defect

6
signs

• Visual acuity depend on the extent of macular
  involvement
• Fundus signs
• Venous dilatation and tortuousity
• Flame shaped hemorrhages
• Retinal edema
• Cotton wool spots

7
(No Transcript)
8

• FA eary hypofluorescence due to blockage by
  edema and blood and late hyperfluorescence due to
  leakage of dye
• Prognosis reasonably good
• 50 return to visual acuity of 6/12 or
  better within 6 mounths
• Vision threatenin complications of BRVO
• 1- chronic macular edema
• 2- neovascularization NVD or NVE

9
Management of BRVO

• We review the patient every 6-12 weeks
• When the hemorrhages resolve we do FA
• FA shows good macular perfusion and vision is
  good no treatment is required
• FA shows macular edema with good macular
  perfusion and vision is 6/12 or worse after 3
  months ? laser photocoagulation should be
  considered but if vision is better than 6/12 ?
  no treatment is needed
• FA shows macular non perfusion and visual acuity
  is poor ? laser treatment will not improve
  vision.
• FA shows 5 or more disc diameters of non
  perfusion the patient should be reviewed every 4
  months for 1-2 years because there is risk of
  neovascularization

10
(No Transcript)
11
Central retinal vein occlusion

• Non-ischemic CRVO 75 of cases
• Ischemic CRVO

12
Non-ischemic CRVO

• Clinical features
• Presentation with sudden blurred vision
• Visual impairment moderate to severe
• Afferent pupillary defect (APD) abscent or mild

13

• Fundus features
• Tortuousity and dilatation of all branches of
  central retinal vein
• Retinal dot-blot and flame shaped hemorrhages all
  over the four retinal quadrant
• Occasional cotton wool spots
• Mild to moderate optic disc edema and macular
  edema

14
(No Transcript)
15

• FA shows
• Delayed venous return
• Good retinal capillary perfusion
• Late leakage
• Course
• Most signs resolve over 6-12 months
• Conversion to ischemic type can occur in 34
  within 3 years

16

• Prognosis
• In cases that do not convert to ischemic type,
  prognosis is good, with return of visual acuity
  to normal or near normal in about 50
• Management
• Follow up should be for years to detect
  conversion to ischemic CRVO
• High intensity laser to create anastomosis
  between retinal vein and choroidal vein, but it
  may cause fibrosis at the laser site or
  hemorrhage from ruptured vein

17
Ischemic central retinal vein occlusion

• Clinical features
• Presentation sudden and severe visual impairment
• Visual impairent severe
• APD severe

18

• Fundus features
• Marked tortuousity and engorgement of all
  branches of central retinal vein
• Extensive dot-blot and flame shaped hemorrhages
• Cotton wool spots which may be numerous
• Macular edema
• Severe optic disc edema

19
(No Transcript)
20

• FA central masking by retinal hemorrhages and
  extensive areas of capillary non-perfusion
• Course most acute signs resolve over the next
  9-12 months
• Prognosis extremely poor due to macular
  ischemia, rubeosis iridis develop in about 50 of
  cases usually 2-4 months and there is high risk
  of neovascular glaucoma

21
Management

• Follow up monthly for 6 months in order to detect
  rubeosis iridis and with gonioscopy to detect
  angle neovascularization
• If neovascularization develops , laser PRP should
  be done without delay

22
Retinal artery occlusion

• Branch retinal artery occlusion (BRAO)
• Central retinal artery occlusion (CRAO)
• Cilioretinal artery occlusion

23

• Causes
• Atherosclerosis-related thrombosis(most common
  cause of CRAO) 80 of cases
• Carotid embolism
• Giant cell arteritis
• Cardiac embolism
• Priarteritis in cases of systemic vasculitis,
  such as SLE , BehcetEtc.
• Thrombophilic disorders such as antiphospholipid
  syndrome

24
Branch retinal artery occlusion

• BRAO is most frequently caused by embolism
• Presentation with sudden and profound sectoral
  visual field loss
• Fundus features
• retinal cloudining corresponding to the area of
  occluded artery
• narrowing and segmentation of blood column
• One or more emboli may be present

25
(No Transcript)
26

• FA
• Delay in arterial filling
• Masking of background fluorescence by retinal
  swelling which is confined to the involved sector
• Prognosis
• Poor unless the obstruction can be relieved
  within few hours

27
Central retinal artery occlusion

• CRAO is most frequently the result of
  atherosclerosis
• Presentation sudden and profound loss of vision
  except when a portion of the papillomacular
  bundle is supplied by cilioretinal artery, when
  central vision is preserved
• APD is profound or total

28

• Fundus features
• Attenuation of arteries and veins with
  segmentation of the blood column
• Extensive retinal cloudiness
• Cherry red spot which is an red-orange reflex
  from intact choroid appearing through the thin
  fovea
• In eyes with cilioretinal artery , part of the
  macula will appear normal in colour

29
(No Transcript)
30

• FA
• Shows delay in arterial filling
• Masking of background choroidal fluorescence by
  retinal swelling
• A patent cilioretinal artery will fill during the
  early phase
• Prognosis
• Is poor due to retinal infarction
• Rubeosis iridis may occur and need PRP laser

31
Cilioretinal artery occlusion

• Cilioretinal artery present in 20 of population
• It arises from posterior ciliary circulation but
  supplies the retina, in the area of the macula
  and papillomacular bundle

32

• Classification
• Isolated typically affects young patients with
  an associated systemic vasculitis
• Combined with CRVO has similar prognosis to
  non-ischemic CRVO
• Combined with anterior ischemic optic neuropathy
  affects patients with giant cell arteritis and
  carry a very poor prognosis

33
(No Transcript)
34

• Presentation with acute, severe loss of central
  vision
• Fundus cloudiness localized to that part of the
  retina normally perfused by the vessel
• FA shows corresponding filling defect

35
Treatment of acute retinal artery occlusion

• Initial treatment
• Ocular massage by 3 mirror contact lens, press
  for 10 seconds then release for 5 seconds.
• Sublingual isosorbide dinitrite to dilate
  perepheral blood vessles and decrease resistance
• Lowering of IOP with intravenous acetazolamide
  and mannitol

36

• Subsequent treatment
• If the above mentioned measures are unsuccessful
  after 20 minutes we can do the following
• Anterior chamber paracentesis
• IV streptokinase ( thrombolytic drug )
• Retrobulbar injection of tolazoline to decrease
  retrobulbar resistance to flow

37
Hypertensive retinopathy

• Hypertension is diagnosed on blood pressure
  reading on several consecutive occasions 140/90
  or over.

38

• Retinal changes
• Arterial narrowing
• May be focal or generalized
• Severe hypertention may lead to obstruction of
  precapillary arterioles and the development of
  cotton wool spots
• Vascular leakage
• Leading to flame shaped retinal hemorrhages ,
  retinal edema , hard exudates and macular star.
• Swelling of the optic disc is the hallmark of
  malignant hypertension.

39

• Arteriosclerrosis
• Involves thickenning of the vessel wall
• The most important sign is arteriovenous nipping
• Grades of arteriosclerosis
• Grade 1 subtle broadening of arteriolar light
  reflex
• Grade 2 bending of veins at arteriovenous
  crossings
• Grade 3 copper wiring
• Grade 4 silver wiring

40
(No Transcript)
41

• Choroidal changes
• Rare and developes in acute hypertensive crisis
• Elshing spots focal choroidal infarcts
• Siegrist streaks fibrinoid necrosis
• Exudative retinal detachment associated with
  toxemia of pregnancy.

42
(No Transcript)
43
Retinopathy of prematurity (ROP)

• It is aproliferative retinopathy affecting
  pre-term infants of low birth weight who have
  been exposed to high ambient oxygen concentration
• The vessles reach the nasal periphery after 8th
  month of gestation but do not reach the temporal
  perephery until 1 month after delivery
• The incompletely vascularized temporal retina is
  particularly susceptible to oxygen damage
  especially in preterm infants

44
Active ROP

• Severity determined in terms of (a)location
  (b)extent (c) stages (d) plus disease
• (a) Location
• It is determined by three zones centered on the
  optic disc

45

• (b) Extent determined by the number of clock
  hours of the retina involved
• (c) Staging
• Stage1 demarcation line
• Stage 2 ridge
• Stage 3 ridge with extraretinal fibrovascular
  proliferation
• Stage 4 subtotal retinal detachment
• Stage 5 total retinal detachment

46
(No Transcript)
47
Oher considerations

• Plus disease signifies tendency to progression.
  Characterized by
• 1- failure of pupil to dilate
• 2- development of vitreous haze
• 3- dilatated tortuous vessles
• 4- Preretinal and vitreous hemorrhage

48
Threshold disease

• It is the indication of treatment in ROP.
• It is the presence of five consequetive hours or
  8 non-consequetive hours of stage 3 in zone 1 or
  2 associated with plus disease

49
screening

• Babies born at or before 31 weeks or weighing
  1500g or less should be screened for ROP
• When to screen?
• At the gestational age 34 or 4 weeks post
  delivery which ever comes later.

50
Treatment

• Ablation of immature retina by cryotherapy or
  laser ( successful in 85 of cases only)
• Retinal surgery in cases of retinal detachment

51
(No Transcript)
52
(No Transcript)