disorders of the vitreous and retinal detachment

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