Part 2 > Retinal Detachment > Flashcards

Retinal Detachment Flashcards

(99 cards)

Study These Flashcards
1
Q

What is the anatomy of the pars plana

A

CB starts 1mm from limbus and extends posteriorly for 6mm. Anterior 2mm consists of pars plicata, remaining 4mm flattened pars plana. In order not to endanger either lens/ retina optimal location is 4mm phakic/ 3.5mm pseudophakic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the anatomy of the ora serrata

A

junction between retina and ciliary body. In RD fusion of sensory retina with RPE and choroid limits forward extension of SRF at the ora. No equivalent adhesions between choroid and sclera and choroidal detachments may progress anteriorly to involve ciliary body (ciliochoroidal detachment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are dentate processes

A

tapering extensions of retina onto pars plana. More marked nasally than temporally and display marked variation in contour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are ora bays

A

scalloped edges of pars plana epithelium between dentate processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are meridional folds

A

small radial folds of thickened retinal tissue in line with dentate processes most commonly in superonasal quadrant. A fold may occasionally exhibit a small retinal hole at its apex. A meridional fold is a complex configuration where a dentate process with associated meriodional fold aligned with ciliary process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are enclosed ora bays

A

small islands of pars plana surrounded by retina as a result of the meeting of 2 adjacent dentate processes. Should not be mistaken for retinal holes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the vitreous base

A

3-4mm wide zone straddling the ora serrata, throughout which cortical vitreous strongly attached. Following PVD the posterior hyaloid face remains attached at vitreous base. Pre existing retinal holes within the attached vitreous base do not lead to RD. Blunt trauma may cause avulsion of vitreous base with tearing of non pigmented epithelium of pars plana along base’s anterior border and of the retina along the base’s posterior border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some innocuous peripheral retinal degenerations

A

microcystoid (peripheral cystoid) degeneration
paving stone degeneration
reticular (honeycomb) degeneration
peripheral drusen
pars plana cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the features of microcystoid (peripheral cystoid) degeneration

A

consist of tiny vesicles with indistinct boundaries on greyish white background making retina appear thickened and less transparent. Degeneration starts adjacent to ora serrata extending circumferentially and posteriorly with smooth undulating posterior border. Present in normal eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of paving stone degeneration

A

discrete yellow white patches of focal chorioretinal atrophy may have pigmented margins. Typically found between the equator and ora and more common in inferior fundus. present to some extent in at least 25% normal eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the features of reticular (honeycomb) degeneration

A

age related change consisting of fine network of perivascular pigmentation that sometimes extends posterior to the equator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the features of peripheral drusen

A

clustered or scattered small pale discrete lesions may have hyperpigmented borders. Similar to drusen at posterior pole and in eyes of older individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are the sites of vitreous adhesion

A

vitreous base (very strong)
optic disc margin (Fairly strong)
perifoveal (Fairly weak)
peripheral blood vessels (usually weak)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some examples of pathological vitreous adhesions to the retina

A

lattice degeneration
retinal pigment clumps
cystic retinal tufts
vitreous base anomalies (extensions and posterior islands)
WWOP/ WWP
Zonular traction tufts
VMT
Preretinal new vessels eg PDR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some peripheral lesions predisposing to RD

A

Lattice degeneration
Snailtrack degeneration
Cystic retinal tuft
Degenerative retinoschisis
Zonular traction tuft
WWP
WWOP
Myopic chorioidal atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the prevalence of lattice degeneration

A

present in 8% of the population. Develops in early life seen in moderate myopes. Lifetime risk of RD in person with lattice 1%. Lattice degeneration present in 40% eyes with RD. In these patients RD is caused by premature PVD and tractional tears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the pathogenesis of lattice degeneration

A

Discontinuity of iLM with variable atrophy of underlying NSR. Vitreous overlying area of lattice is synchytic but vitreous attachments around margins exaggerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some signs of lattice degeneration

A

lattice common bilateral, temporal and superior.
Spindle shaped areas of retinal thinning commonly between equator and posterior border of vitreous base
sclerosed vessels forming a network of white lines characteristic
some lesions associated with snowflakes, remnants of degenerate muller cells
associated RPE hyperplasia
Small holes common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some complications of lattice degeneration

A

do not occur in most eyes with lattice degeneration
- tears may develop due to PVD where lattice seen on flap of tear
- atrophic holes rarely lead to RD. risk is higher in young myopes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the management of lattice degeneration

A

asymptomatic patients with lattice degeneration does not need prophylactic laser even with retinal holes. Patients warned of RD symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the clinical features of snailtrack degeneration

A

sharply demarcated bands of tightly packed snowflakes that give the peripheral retina frost white appearance. Can be a precursor to lattice degeneration. Marked vitreous traction seldom present so u tears rarely occur but round holes relatively common. Prophylactic laser unneccessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the prevalence and pathogenesis of degenerative retinoschisis

A

present in 5% population over 20 years- prevalent in hypermetropes.
RS believed to develop from microcystoid degeneration by gradual coalescence of degenerative cavities resulting in separation or splitting of NSR into outer and inner layers with severing of neurones and complete loss of visual function in affected area. Typical retinoschisis split in OPL but reticular retinoschisis at RNFL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the symptoms of degenerative retinoschisis

A

photopsia/ floaters absent as no VR traction. Rare for patients to notice VF defect even if spreads posterior to equator
Occasionally symptoms from progressive RD/ VH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the signs of degenerative retinoschisis

A

RS bilateral in 80%. Distinction between reticular and typical difficult clinically. Inner layer thinner and more elevated in reticular.
Early retinoschisis- inferotemporal periphery both fundi with smooth immobile dome shaped retinal elevation. Shown on OCT and differentiate from RD
Elevation convex/ thin/ smooth and immobile unlike RD. Thin inner leaf schisis can be mistaken for RD but demarcation lines and secondary cysts absent.
Lesion may progress circumferentially until entire periphery involved/ Typical form remains anterior to equator. Reticular type spread posteriorly. Presence of pigmented demarcation line represent associated RD. Breaks may be present in inner/ outer/ both leaves. Inner breaks small round. Outer larger with rolled edges located behind equator. VF defect absolute rather than relative.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the complications of degenerative retinoschisis
uncommon- more likely in reticular form. RD rare- even in eye with breaks in both layers incidence 1%. Detachment almost always asymptomatic, infrequently progressive rarely needs surgery. Posterior extension of RS to involve fovea very rare but can occur. Slow progression. VH rare
26
What is the management of degenerative retinoschisis
Double layer breaks leads to RD. Small peripheral RS discovered on incidental exam doesnt require routine review Large RS observed periodically if breaks are present in both layers or extension posterior to equator. Retinopexy/ surgical repair may be needed for relentless foveal progression. Recurrent VH may need PPV. Progressive symptomatic RD addressed promptly. >1 surgery may be needed. Buckle for small outer layer break RD but PPV for complex RD
27
What is white with pressure WWP
Retinal areas in which translucent white grey appearance can be induced by scleral indentation. May also be observed along posterior border of lattice degeneration islands, Snailtrack, outer layer of acquired retinoschisis. Frequently seen in normal eyes may be associated with strong VR attachment but may not indicate higher risk of retinal break formation
28
What is white without pressure WWOP
Same appearance as WWP but present without scleral indentation. WWOP corresponds to area of strong VR adhesion. On cursory exam area of normal retina surrounded by WWOP may be mistaken for flat retinal hole. But retinal breaks/ GRT develop along posterior border of WWOP. If WWOP found in fellow eye of GRT, consider prophylactic laser.
29
What is a PVD
separation of cortical vitreous + delineating posterior hyaloid membrane (PHM) from NS retina posterior to vitreous base. Occurs due to vitreous gel liquefaction with age (synchisis) to form fluid filled cavities and condensation (syneresis) with access to preretinal space allowed be dehiscence in cortical gel and or PHM. Perifoveal hyaloid detachment followed by foveal separation, then detachment from posterior retina as far as equator. Disc late to detach. Process can take many months.
30
What % of patients with symptomatic PVD will have a tear and what does it rise to if VH present
10 60
31
What are the symptoms and signs of PVD
Flashing lights/ floaters/ Weis ring (Detachment of vitreous from disc). Presence doesnt indicate complete/ incomplete PVD. Can be destroyed during PVD process. Floaters may be due to vitreous blood. Blurry vision due to significant PHM or floaters. Detached PHM can be seen as crumpled translucent membrane in mid vitreous. Haem by RBC in anterior vitreous. 40-90% have tears if haem present. Shafer sign due to retinal break. Vitreous cells may signify break.
32
What is the management of PVD
Acute PVD examined within 24-48 hours with urgency if myope/ past or FH of RD/ high risk syndrome like Stickler/ pseudophakia/ VF defect/ Reduced VA/ prominent floaters. Examine retina 360 by scleral indentation. Examine fellow eye. If 10 or more vitreous cells seen in 1x1mm slit beam, retinal break in fellow asymptomatic eye is 30%. If no suspiscious findings then discharge. If high risk features then 1-6 week review. Then further review in 6-12 months. If multiple floaters review again as high risk of retinal break. SOS patients. If fundus obscured, weekly review prudent. Fundus obscuring VH in condition with non PVD VH associated with higher risk of retinal break 60-90% and RD 40%.
33
What % of eyes with acute symptomatic PVD have retinal breaks and what % of eyes have asymptomatic retinal breaks
20% 8%
34
What are the clinical features of retinal breaks
tears associated with PVD occur in upper retina more commonly temporal than nasal. Macula breaks related to PVD rare. They may be flat or associated with cuff of SRF.If fluid extend >1DD from edge of break-> RD U tears consist of flap, apex pulled anteriorly by vitreous base remains attached operculated tears in which flap torn away leave round oval break. Separated retinal patch is operculum seen suspended over break. Haem may be seen. Retinal holes are round/ oval smaller than tears- lower risk of RD. If does then shallow RD slow progressive.
35
What is a retinal dialysis
circumferential tear along ora serrata due to blunt ocular trauma. Vitreous gel remains attached to posterior margin. Appears as large peripheral break with regular rolled edge. RD slow progressive in absence of PVD
36
What is a GRT
Variant of U tear involving 90 degrees or more of the retinal circumference. Contrast to dialysis vitreous gel remains attached to anterior margin of break. Located immediate post oral retina or less commonly at equator
37
What are the risk factors for a tear to progress to RD
History of RD in fellow eye, prior cataract surgery if vitreous loss, myopia, FH of RD, Marfan/ Stickler/ Ehlers Danlos. Prophylaxis laser considered for asymptomatic breaks before cataract surgery/ laser capsulotomy/ IVT Symptomatic breaks + PVD higher risk than asymptomatic breaks Larger breaks higher risk of progression Persistent VR traction on operculated break/ U shaped break. U tears higher risk than round holes. Superior breaks higher risk than inferior ones. Superotemporal breaks high risk of macula threat in early RD. Equatorial breaks more likely to progress than oral breaks as latter located within vitreous base. Pigmentation around break suggest chronicity and low risk. Aphakia is higher risk
38
How are operculated breaks treated
if asymptomatic- low risk RD progression can be observed eg first at 2-4 weeks, then 1-3 months, then 6-12 months. If bridging vessel over break may indicate ongoing vitreous traction which may cause vitreous haemorrhage so consider treatment
39
How are asymptomatic u tear breaks treated
risk of progression to RD is 5% similiar to that in treated symptomatic U tears and observatation as for operculated tears safe in absence of high risk factors
40
How are traumatic retinal breaks treated
always be treated- same for traumatic dialysis
41
How are asymptomatic dialysis treated
follow up without treatment. Most cases treated surgically if RD present
42
How are asymptomatic subclinical RD treated
Progression detected incidentally with 10% becoming symptomatic over 2-3 years- decision about intervention made on case- case basis. Surgery if progression indicated
43
How are asymptomatic flat round holes treated
do not require prophylaxis treatment but some guidelines recommend review every 1-2 years
44
What are the therapeutic options for treating retinal breaks
BIO Slit lamp retinopexy Cryoretinopexy for post equatorial lesions with indentation.
45
Where are the distribution of breaks in RD
60% superotemporal 15% superonasal 15% inferotemporal 10% inferonasal. 50% eyes with RD have >1 break often within 90 degrees of each other
46
What governs the spread of subretinal fluid in RD
- gravity - anatomical limits (ora and optic nerve) - location of primary retinal break if primary break superiorly, SRF first spreads inferiorly on same side of fundus as the break then superiorly on the opposite site so likely location of break can be predicted
47
What are the modified Lincoff rules
Shallow inferior RD in which SRF is slightly higher on temporal side points to primary break located inferiorly on that side Primary break at 6 o clock will cause inferior RD with equal fluid levels In bullous inferior RD primary break lies above horizontal meridian If primary break in upper nasal quadrant, SRF will revolve around optic disc and then rise on temporal side until level with primary break A subtotal RD with superior wedge of attached retina points to primary break located in periphery near its highest border When SRF crosses the vertical midline above, the primary break is near to 12 o clock, lower edge of RD corresponding to side of break
48
In RD, when is SRF absorbed so when are the symptoms worse, also which quadrant of VF loss is first noticed by the patient
overnight absorption of SRF so on waking symptoms better Lower VF defect appreciated more quicker than upper defect.
49
What are some signs of RD
RAPD- in extensive RD IOP lower by 5mmHg in eye with RD if associated choroidal detachment present. In Schwartz Matsuo syndrome IOP can be raised Iritis common- mild Tobacco dust- pigment cells in anterior vitreous Retinal breaks PVR may be present
50
What are the features of Schwartz Matsuo syndrome
Raised IOP + RD + mild anterior uveitis due to dialysis secondary to blunt trauma in a young man. Aqueous cells believed to be photoreceptor OS that may compromise trabecular outflow. Both aqueous cells and elevated IOP resolve after RD repair
51
What are some examination features of longstanding RD
Retinal thinning due to atrophy Intraretinal cysts- may develop if RD present for 1 year. Disappear after retinal reattachment Subretinal demarcation lines (tide marks) caused by RPE proliferation at junction of flat and detached retina common taking 3 months to develop. Pigmentation decrease over time. They dont limit spread of SRF
52
What is PVR
epiretinal/ subretinal membrane formation, contraction of which leads to tangential retinal traction and fixed retinal fold formation. Main features are retinal folds and rigidity so retinal mobility is decreased. Progression from one stage to next not inevitable
53
What are the features of Grade A PVR
Minimal- PVR characterized by diffuse vitreous haze and tobacco dust. May also be pigmented clumps on inferior retinal surface. Seen in eyes with early PVR
54
What are the features of Grade B PVR
Moderate- wrinkling of inner retinal surface, decreased vitreous mobility, rolled edges of retinal breaks, blood vessel tortuosity, retinal stiffness. ERM responsible cannot be identified clinically
55
What are the features of Grade C PVR
Marked- characterized by rigid full thickness retinal folds (Star shaped) with heavy vitreous condensation and strands. Can be anterior A, posterior P. Dividing line is the globe equator. Severity of proliferation expressed by number of clock hours of retina involved although proliferation need not be contigious
56
What are the features of advanced disease in PVR
Gross reduction of retinal mobility with retinal shortening and funnel like triangular conformation
57
What is the management of PVR
PPV + membrane removal + ILM peel (improves success rate). Sometimes need relaxing retinotomy. PFC used to stabilise retina, then replaced by long acting gas/ silicone oil
58
What are the causes of choroidal detachment
hypotony after glaucoma drainage surgery, sulfonamide drugs like acetazolamide, topiramate, uveitis, posterior scleritis, choroidal tumours, cyclodialysis cleft after trauma/ surgery. Due to RD. Idiopathic cases labelled as uveal effusion syndrome
59
What are the symptoms/ signs and treatment for choroidal detachment
photopsia/ floaters absent as no VR traction. A VF defect may be present if large CD Low IOP common due to ciliary body detachment Brown elevations convex and smooth relatively immobile. 4 lobes present. Temporal and nasal bullae most prominent Large kissing choroidals may obscure fundal view Elevations do not extend to posterior pole as limited by vortex veins entering scleral canals. In contrast to RD, extend anteriorly beyond ora Treat according to cause- drainage via partial thickness sclerectomies is sometimes needed
60
What is uveal effusion syndrome
rare idiopathic bilateral condition affecting middle aged hypermetropic women but can occur with nanophthalmos. Due to impaired normal fluid drainage from choroid via sclera or vortex veins
61
What are the signs of uveal effusion syndrome
absent/ mild inflammation ciliochoroidal detachment followed by exudative RD Following resolution, RPE shows characteristic leopard spot mottling caused by degenerative RPE changes with high protein concentration in SRF
62
What are the differentials of uveal effusion syndrome
choroidal haemorrhage ring melanoma of anterior choroid
63
What is the treatment for uveal effusion syndrome
full thickness sclerectomy particularly in patients with nanophthalmos
64
What are the indications for urgent surgery in RD
Acute symptomatic RD as soon as possible especially if macula on. Other factors like superior/ large break/ advanced syneresis in high myopia/ dense fresh vitreous haemorrhage with obscured fundus. Even if macula off- visual results better if operated on within 72 hours
65
What is pneumatic retinopexy and what are the success rates
outpatient procedure with intravitreal gas bubble + cryo/laser to seal retinal break- reattach retina without scleral buckling. Most frequently used gas are SF6/ C3F8. Quick, minimally invasive procedure but worse success than buckling.
66
When is pneumatic retinopexy done for RD
Uncomplicated RD Small retinal break/ cluster of breaks extending over area of less than 2 clock hours in upper 2/3rds of peripheral retina
67
What is the principle of scleral buckle surgery
material sutured onto sclera (explant) creates inward indent (buckle) to close retinal breaks by opposing RPE to sensory retina and reduce dynamic VR traction at sites of local vitreoretinal adhesion. Always use this technique in RD secondary to post traumatic dialysis
68
What are some features and principles of scleral buckle explants
made from soft or hard silicone. Entire break ideally surrounded by 2mm of buckle. Important for buckle to involve area of vitreous base anterior to tear to prevent possibility of reopening tear and anterior SRF leakage. Dimensions of break can be assessed by comparing it to diameter of optic disc
69
What are the different scleral buckle configurations
radial segmental circumferential encircling depending on size/ configuration and number of breaks
70
What is the D-ACE technqiue of SRF drainage in buckles and what are its advantages and complications
Drainage of SRF via the sclera due to more rapid retinal reattachment in presence of deep or longstanding viscous SRF. Others prefer to avoid external drainage due to retinal perforation/ incarceration in drainage site/ choroidal haemorrhage and would rather do PPV instead
71
What are the complications of scleral buckling
diplopia due to mechanical effect of buckle. Can resolve spontaneously CMO in 25% responsive to treatment. ERM/ Persistent subfoveal fluid/ foveal structural disruption in macula off RD Anterior segment ischaemia- vascular compromise especially in encircling band and sickle cell haemoglobinopathies Buckle extrusion/ intrusion/infection needs removal with intense antibiotic therapy Elevated IOP resolves but can persist. Angle closure can occur Choroidal detachment resolve spontaneously as scleral oedema settles allowing improved vortex vein function
72
What are some reasons for surgical failure of scleral buckle
Missed breaks Inadequate sizing/ incorrect positioning/ inadequate height. Explant may have to be replaced/ repositioned but drainage of SRF/ IVT gas may be enough. PPV may be an option PVR most common cause of late failure. Tractional forces may open old breaks and create new ones. Several weeks back with re-detachment. Reopening of retinal break without PVR due to inadequate cryotherapy or scleral buckling or when buckle height decreases with time/ late surgical removal
73
What is fish mouthing of a retinal tear in scleral buckling
describes the phenomenon of a tear, typically a large superior equatorial U-tear in a bullous RD, to open widely following scleral buckling, requiring further operative treatment.
74
What are the commonest causes of TRD
PDR with diabetes ROP Penetrating posterior segment trauma
75
What is the pathogenesis of TRD
Progressive contraction of fibrovascular membranes overlying large areas of vitreoretinal adhesion. PVD in diabetic eyes frequently incomplete. Thought to be due to leakage of plasma constituents into vitreous gel from fibrovascular network adherent to the posterior vitreous surface. Due to strong cortical vitreous adhesions to fibrovascular proliferations, incomplete PVD. Once PVD, new blood vessels avulsed and RD does not develop.
76
What are the 3 types of VR traction in TRD
Tangential- contraction of fibrovascular membranes with puckering of retina/ distortion of blood vessels AP- Contraction of fibrovascular membranes extending from posterior retina in association with major arcades to vitreous base anteriorly/ and or bridging (trampoline) Result of contraction of fibrovascular membranes stretching from one part of the retina to another or between vascular arcades tending to pull 2 involved points together
77
What are some signs and symptoms of TRD
Photopsia/floaters absent as VR traction insidous and no acute PVD. VF defect progress slowly RD has concave configuration and absent breaks. Retinal mobility severely reduced , shifting fluid absent, SRF shallowed than RRD and seldom extend to ora, highest elevation of retina occurs at sites of VR traction. If breaks occur, assumes RRD characteristics - progress rapidly combined TRD/RRD
78
What is an exudative RD
Accumulation of SRF in absence of retinal breaks/ traction. Can occur in variety of vascular/ inflammatory/ neoplastic diseases involving retina/ RPE/choroid in which fluid leaks outside vessels accumulates under the retina. As long as RPE is pumping fluid into choroidal circulation, RD doesnt happen.
79
What are the causes of exudative RD
Choroidal tumours- melanoma/ haemangioma/ mets. Intraocular tumour considered strongly! Inflammation eg Harada/ posterior scleritis Bullous CSCR Iatrogenic- RD surgery/ PRP CNV Hypertensive choroidopathy Uveal effusion syndrome
80
What are the symptoms and signs of exudative RD
No VR traction so no photopsia/ floaters present if vitritis/ VF defect may happen suddenly and progress rapidly. RD has convex configuration as RRD but smooth surface. Detached retina mobile and exhibits shifting fluid. Cause of RD eg choroidal tumour may be obvious/ associated systemic disease like Harada/ pregnancy toxaemia. Leopard spots which are scattered areas of pigment clumps may be seen after detachment flattened
81
What is the treatment for exudative RD
Treat cause. Some resolve spontaneously, others treated with systemic steroid (harada/ posterior scleritis). In CSCR leak in RPE can be sealed by laser photocoagulation
82
What are some gases used intraocularly and if used at 100% concentration what happens to its volume
SF6- doubles lasting 10-14 days C2F6- triples lasting 30-35 days C3F8- Quadruples lasting 55-65 days
83
What are the isovolumetric (non expansile concentrations) of the 3 VR gases
SF6- 20-30% 12-16% C3F8
84
What is the difference between 1000cs and 5000cs silicone oil
1000cs- easier to inject and remove while 5000cs more viscous but less prone to emulsification
85
What are some uses for Heavy liquids like PFC
Good visibility low viscosity, flatten the posterior retina open retina folds and improve visualisation of additional membranes. Also haemostasis by localising bleeding, expression of liquified blood from behind retina and anterior floating of dislocated lens fragments or IOL. Cases of retinal toxicity and inflammation reported.
86
What are the indications for PPV in RRD
When retinal breaks cannot be visualised due to haemorrhage, vitreous debris, PCO. IOL edge effects. Scleral buckle high risk of failure if breaks missed When retinal breaks unlikely to be closed by scleral buckling eg giant tears, large posterior breaks + PVR
87
What are the indications for PPV in TRD- Diabetic related
TRD threatening or involving the macula. PPV + Anti VEGF +/- PRP endolaser prevent post operative NV which may cause VH/ Rubeosis. Extramacular TRD may be observed without surgery as it remains stable provided PDR controlled Combined TRD/RRD treated urgently even if macula not involved as likely to spread quickly
88
What are the indications for PPV in TRD- penetrating trauma
Prevent TRD. Unlike DR where ERM proliferation occurs on posterior retina, fibrocellular proliferation after penetrating trauma occurs on pre-equatorial retina and or ciliary body. Treatment aimed at rehab/ minimizing tractional process Late TRD which may be associated with IOFB or retinal incarceration develops months after successful surgery
89
What are the goals of PPV
Separate posterior hyaloid from retinal surface remove epiretinal tissue in order to release central and/ or peripheral retinal traction to close retinal breaks if present
90
What two types of epithelial membranes are encountered during PPV
Non vascular membranes found in PVR and macula pucker Fibrovascular membranes found in patients with PDR
91
What stain is used for Epiretinal membrane vs Vitreous
Trypan blue- ERM Triamcinolone- Vitreous
92
What are the aims of PPV in PVR
Release both transvitreal traction by PPV and tangential (surface) traction by membrane dissection to restore retinal mobility and allow closure of retinal breaks Localised fixed retinal folds may be freed by removal of central plaque of ERM. Membrane surgically dissected or peeled from retinal surface.
93
When is a relieving retinotomy done
when mobility of retina believed to be insufficient for sustained reattachment
94
What are the aims of PPV in TRD
PPV releases AP and or circumferential VR traction. Because membranes vascularized and retina friable- cannot peel as result in haemorrhage and retinal tearing. 3 methods to remove fibrovascular membranes 1) Delamination 2) Segmentation 3) En-bloc dissection
95
What is delamination in TRD repair
horizontal cutting of individual vascular pegs connecting membrane to surface of retina. Allows complete removal of fibrovascular tissue from retinal surface
96
What is segmentation in TRD repair
vertical cutting of ERM into small segments. Used to relieve circumferential VR traction when delamination difficult/ impossible
97
What is en-bloc dissection in TRD repair
key step to separate posterior hyaloid from retina. Incision made into epiretinal membrane using illuminated pick. Membrane then peeled using end gripping membrane forceps
98
What are some intraoperative complications that may occur with PPV
Posterior retinal breaks Peripheral retinal breaks Rarely, choroidal haemorrhage
99
What are some postoperative complications that may occur with PPV
Retinal breaks/ RRD Retinal fold- less likely to occur if patient face down immediately post op Inflammation- esp in diabetics Raised IOP- if too high can be removed via pars plana 30G needle on 1ml syringe Silicone oil associated glaucoma- direct pupil block by oil especially in aphakic eye. Prevent by inferior iridectomy. Late glaucoma by oil causing trabecular block and scarring. Risk reduced by early removal. Tube seton may be needed. Cataract- gas/ silicone cataract. Band keratopathy with extended oil tamponade
Part 2
flashcards
Decks in class (20)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions