1-9 PVD and RD Flashcards
Describe the forces that keep the retina attached to the RPE
Mechanical:
- Hydrostatic forces due to IOP. Pushes outwards so retina is pushed against RPE.
- Osmotic pressure difference. Vitreous is low in protein concentration so water wants to move out. Since water can’t move out, it causes a osmotic pressure which pushes retina against RPE.
- Mechanical resistance of vitreous gel?
- Interdigitation of RPE processes and photoreceptosr (phagocytosing area)
- Adhesive matrix between retina and RPE. This is called the Interphotoreceptor Matrix (IPM)
Metabolic:
- High metabolism uses glucose and O2 to generate H2O as a byproduct. This H2O is actively pumped out of RPE/retina and to choroid to prevent fluid building below retina to cause retinal detachment.
Describe composition of Vitreous Gel
Vitreous is a gel like structure filled mostly with water. Rest is made of hyaluronic acid and collagen fibrils. There is type 5/11 core, type 2 wrapping (most abundant), and type 9 sprinkled around with edges sticking out.
How does vitreous attach to the retina?
- Vitreous adheres to retina all across vitreous cavity.
- Strength differs and increases at vitreous base, ONH, macula, and major BVs. It can also differ pathologically e.g. new BVs, retinal scars…
Overall vitreous structure?
- Orientation?
- High conc. at ONH, macula, and lower conc. at central vitreous.
- Vitreous base is near pars plana (strong adhesion)
- Cortical vitreous is around retina (weaker)
- Central vitreous at centre of eye.
- Orientation is perpendicular at vitreous base and moves posterior where it travels perpendicular to back of eye.
Describe age-related changes to the vitreous and how that leads to PVD
Vitreous undergoes molecular changes such as
- Depolymerisation of the hyaluronic acid (HA) where enzymatic digestion of HA releases H2O
- Loss of collagen 9 which cause collagen fibril aggregation.
This causes
- increased volume of liquefied spaces (synchysis senilis)
- increase optically dense areas (vitreous syneresis).
This occurs w/ age.
Posterior Vitreous Detachment is when vitreous cortex separates from ILM of retina.
- Can be partial or total.
- Due to culmination of vitreous liquefaction and weakening of vitreoretinal adhesion.
- More likely with age. But also risk factor for longer axial length, intraocular inflammation, blunt trauma, cataract surgery.
PVD signs + symptoms
- Weiss ring – Localised PVD at ONH. Since ONH is round, vitreous detaching is also round.
- Entopic phenomena (see things in head)
- Floaters – Due to collagen fibril condensation. Opacities cast shadows onto retina that look like “hairs”, “insects”, or “cobwebs”.
- Photopsia (head movement can cause flashses in vision since it causes traction along areas at risk of vitreous detachment which stimulates photoreceptors).
PVD can lead to…
- Retinal tear (if adhesion strong, can rip off retina where detaching. Liquified vitreous can then enter sub retinal space thus retinal detachment).
- Vitreous haemorrhage (if adhesion strong on BVs, can rip it upon detachment)
- Vitreoretinal interface disorders (Incomplete PVD causes traction on macula. Can cause macular hole, macular oedema, and epiretinal membrane when remnants of vitreous can deposit onto retinal surface)
Describe Rhegmatogenous RD
- What’s required to classify RRD?
- Pathophysiology?
- Causes?
- Ways to identify RRD?
Classification must require 2 conditions.
- Retinal break present AND
- Accumulation of liquefied vitreous in subretinal space.
This is because the retinal tear allows liquefied vitreous to enter and build up in subretinal space.
- Usually secondary to PVD
- Predisposed by pre-existing peripheral retinal degenerations e.g. snail track or lattice degeneration.
- Risk factors of increasing myopia, cataract surgery, blunt ocular trauma.
- Find retinal tear. Will have a base that remains attached and an apex of the flap that’s loose.
- Find area of fluid buildup. Should be obvious.
- Ask patient to move eye up and down. Buldge of fluid should smoothly move too.
Describe tractional RD
- Link with PVD?
- Cause/pathophysiology?
- How to differentiate from RRD?
Strong adhesion of vitreous pulling retina off.
- Not associated with PVD
- Due to another retinal disease leading to direct fibrotic or fibrovascular strands of vitreous causing traction on retina e.g. proliferative retinopathy, intraocular inflammation, penetrating posterior segment trauma, etc.
- No retinal breaks.
- Moving eye will not have smooth movement of fluid.
Describe exudative RD
- Pathophysiology
- How to differentiate from other RDs?
Blood retinal barrier (BRB) is compromised so fluid leaks in and builds up.
- No break in retina, no traction, but subretinal fluid still builds up.
- Secondary to pathology that breaks down BRB.
- Lack of break separates it from rhegmatogenous RD.
- Also, due to lack of break, fluid accumulation appears to be a smooth buldge.
RD signs + symptoms?
For rhegmatogenous RD,
- New/abnormal flashes +/- floaters (due to mechanical stimulation of photoreceptors when retina detaching).
- Will appear like red dark spots “showers” (unlike cobwebs in vitreous liquefaction). This is due to pigment from RPE being released when retina detaches. Red spots are RBCs. Seen as “tobacco dust” in anterior vitreous (Shafer’s sign)
For other RDs,
- Peripheral VF defect appears as fixed curtain/shadow. Due to detachment of retina at that area and can lead to central vision defects.
- RAPD if 2 or more quadrants detached or if macula detached.
Investigation and management of RD?
Investigate:
- Retinal examination (with pupil dilation) using techniques such as slit lamp indirect biomicroscopy or BIO.
- Additionally, can use OCT and B-scan ultrasonography.
Management:
- If macula still attached (more urgent since we could still save it) or macula is detached (less urgent since most serious damage already done). Both still urgent.
- For TRD and ERD, Underlying disease is treated.
- For RRD, depending on severity and location, we need to seal the break. This can be via retinopexy (laser photocoagulation or cryotherapy) or surgically.