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DISORDERS OF THE VITREOUS AND RETINAL
DETACHMENT
Dr Russell J Watkins
Vitreous Virtually acellular Viscous Collagen framework, reinforces with hyaluronate 98% water; volume = 4.5ml in emmetropic eye Condensations of vitreous
Anterior hyaloid membrane Posterior hyaloid membrane Tracts in gel Cloquet’s canal
Vitreous Attachments of vitreous
Vitreous base• Strong, 3-4mm annular attachment, extending
across ora serrata Weigert’s ligament
• 8-9mm annular attachment to posterior lens surface (anterior end of Cloquet’s)
Vitreopapillary adhesions• Posterior end of Cloquet’s canal Weiss ring
Vascular adhesions (hence bleeds with PVD) Areas of vitreoretinal degeneration
• e.g. lattice degeneration, cystic retinal tufts
Vitreous Aging changes
Dissociation of hyaluronate from fibrils Pooling of hyaluronate Fibril degeneration & elasticity Drainage of hyaluronate into retrovitreal
space ( posterior vitreous detachment [PVD])
Vitreous Opacities Muscae volitantes: remnants of hyaloid system Syneresis Weiss ring Haemorrhage Tobacco dust: pigment cells Inflammatory cells
Pars planitis Chorioretinitis AC spillover
Vitreous Opacities Synchisis scintillans (settles inferiorly with rest) Asteroid hyalosis
Seen in 1:200 eyes; more common in DM Ca2+-soaps, adherent to fibrils Does not settle at rest
Neoplastic cells Amyloid
Vitreous Vitreous degeneration
Syneresis• Vitreous liquefaction, fibril aggregation &
condensation• Associated with floaters• Caused by myopia, senescence, trauma,
inflammations, hereditary causes Posterior vitreous detachment
Posterior Vitreous Detachment
Collapse of vitreous gel Associated with photopsia & floaters Causes
Senile Myopic Post-inflammatory Post vitreous haemorrhage Diabetes mellitus
Read Chignell et al (2000) Optometry in Practice 2(1);97 et seq
Posterior Vitreous Detachment
PVD with gel collapse Without vitreous haemorrhage, 4% develop
retinal breaks With vitreous haemorrhage, 20% develop
breaks PVD without gel collapse
Associated with future retinal hole or vitreous haemorrhage
Scaffold for proliferative new vessels
Vitreous Haemorrhage Proliferative retinopathies
DM Retinal vein occlusion Sickle cell retinopathy ROP Eale’s disease
PVD Trauma
Vitreous Haemorrhage Disciform macular degeneration Blood dyscrasias Subarachnoid haemorrhage (Terson’s syndrome) Complications of vitreous haemorrhage
Syneresis; Fibrosis traction RD; Haemosiderosis; Haemolytic (ghost cell) glaucoma; Synchisis scintillans; Ochre membrane
Retinal Detachment
Retinal detachment can be: Rhegmatogenous Tractional Exudative
Rhegmatogenous RD RD occurring in association with hole formation;
incidence 1:10,000 per year Predisposing conditions
Acute PVD Myopia (esp. High myopia) Age Trauma Aphakia (1% of ICCE; 0.1% of ECCE with intact
PC) Vitreoretinal degenerations
Rhegmatogenous RD Pathogenesis
Following PVD, dynamic vitreoretinal traction occurs at abnormal adhesions• This can vitreous haemorrhage
Traction energy transmission to retina To relieve traction, a break forms RD caused by collection of subretinal fluid
Rhegmatogenous RD Pathogenesis
Sensory retina detaches from RPE• Pigment cells may be avulsed into vitreous
tobacco dust• This predisposes to proliferative
vitreoretinopathy (PVR) Retina becomes opaque due to oedema Photoreceptor degeneration
Types of Break Horseshoe or U-shaped tear Atrophic hole Operculated Dialysis
Involves splitting of vitreous base Usually inferotemporal Can be spontaneous or traumatic
Macular hole Idiopathic; myopia; Commotio retinae
Types of Break Giant retinal tear
90-360° tear; may fold back Associated with PVR Trauma; myopia; Stickler’s syndrome
Bucket handle tears Usually superonasal Avulsion of vitreous base Always traumatic
Rhegmatogenous RD Symptoms
Photopsia Floaters Shadow 60% of patients with RD have ALL symptoms
Rhegmatogenous RD Examination
VA Visual fields Peripheral retinal evaluation
• BIO + 3-mirror Tobacco dust Mild anterior uveitis Low IOP
Rhegmatogenous RD Natural history
Progression to total detachment Spontaneous reattachment (can happen) Retinal & RPE atrophy “High water mark” - RPE hyperplasia Viscous subretinal fluid Intraretinal cyst formation PVR Rubeosis iridis Phthisis bulbi
Rhegmatogenous RD Principles of treatment
Localisation & closure of breaks Relief of vitreoretinal traction
• Buckling or vitrectomy Neuroretinal-rpe adhesion
• Photocoagulation or cryotherapy Internal tamponade
• Air; longer acting gases [SF6, C3F8]; Silicone oil
Complications of RD Surgery
Anterior or posterior segment ischaemia Infection Perforation or erosion of plomb into eye Extrusion of plomb Muscle imbalance Refractive changes Macular pucker Cataract Glaucoma Redetachment
Vitreoretinal Degenerations Predisposing to RD
Lattice degeneration - present in 40% of RD Snail track degeneration “White without pressure”
Benign “White with pressure”; Pigment clumping;
Diffuse chorioretinal atrophy; Peripheral microcystoid changes; Snowflake degeneration; Pavingstone degeneration; Honeycomb degeneration; Drusen; Oral pigmentary degeneration
Tractional RD Penetrating ocular trauma Proliferative retinopathies
DM Sickle cell retinopathy ROP Retinal vein occlusion Eale’s disease
Persistent hyperplastic primary vitreous Toxocariasis Pars planitis
Exudative RD Uveitis e.g. Vogt-Koyanagi-Harada syndrome Choroidal tumours
Malignant melanoma Metastatic
Low blood protein levels Hypertension Eclampsia Hypothyroidism Choroidal effusion syndrome
Retinoschisis Splits or cysts within the neurosensory retina Retinoschisis can be
Primary• Senile (level of OPL)• Juvenile/congenital (level of RNFL)
Secondary to other conditions
Senile Retinoschisis Bilateral in 33% Usually inferotemporal Usually hypermetropic Dome elevation of inner retinal layers White dots (snowflakes) on inner limiting
membrane Inner leaf has beaten metal appearance Sheathing of peripheral vessels
Senile Retinoschisis Round holes can occur in inner leaf Larger holes can occur in outer leaf 1% progress to rhegmatogenous RD Peripheral field defect though often
asymptomatic Need periodic observation with visual fields
Juvenile Retinoschisis X-linked recessive Splits in NFL Bilateral Foveal (cystoid changes BUT not CMO) or
peripheral Associated with Favre-Goldmann & Wagner’s
diseases Poor visual prognosis Predisposes to RD, esp inferotemporally
Juvenile Retinoschisis Present with
vision (may be vitreous haemorrhage) Maybe asymptomatic Even though congenital, may not be detected
for years
Secondary Retinoschisis Proliferative retinopathies Trauma Vitreous traction
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