Disclosures From Print to Practice: PVD a common process with potential for ocular morbidity Diana Shechtman OD FAAO I am on The speaker s bureau for: Bausch & Lomb, Zeavision, Carl Zeiss Meditec & Alcon Advisory Board for: Allergan, Thrombogenics, Carl Zeiss Meditec, Alcon Nutritional Dept & Arctic Dx These affiliations will have no affect on the content of this lecture FACTS 2/3 of pts > 60yo have a PVD 1 in 6 acute PVD RB 1 in 3 symptomatic RB RRD So not all breaks need treatment Though for the day When do you send patients out for second opinion to an ophthalmologist? 1. Any break 2. A break with an associated retinal hemorrhage 3. Lattice degeneration (LD) vs LD with holes 4. Symptomatic retinal break 5. Any flap tear 6. Others PVD & RBs: when do I hold and when to refer? 54 BM No Flashes (+) floater Inferior VIEW PCIOL X 6M Why would you monitor or Why would you refer? Recently a UK study revealed that asymptomatic RB (in particular inferior) should be followed due to low risk of RRD. Current lit does not provide enough evidence to suggest tx of RB other than symptomatic FT (Wilkinson 2000) How about if last year s exam revealed that there was no serous fluid cuff? This is why even normal findings should be written in Would the chart you refer this ATROPHIC hole Temporal Asymptomatic Low myope POHx: retinal hole X 5 yrs 56 WM CC: Complaints of new onset of F/F OD particularly when looking at blue sky or a white page Pertinent Hx: S/P cataract sx 1 yr ago SLE Differences b/t acute vs chronic floater Always evaluate anterior V tobacco dust! Spalton s 1
What is likely present in the periphery? Retinoschisis Atrophic hole Flap tear Congenital hypertrophy of the RPE (CHRPE) Scleral depression view Symptomatic FTs are always treated! Based on relationship b/t RB & RD, would you Hold em or Fold em? Byer s work: symptomatic flap tears lead to RRD in >50% of cases Wilkinson Opth 2000: SYMPTOMATIC FT (flat tears) has the best supportive evidence & overall consensus with regards to treatment. 50% of Flap tears are located SN The history of RB and tx Why is superior location a possible problem? ALWAYS scrutinize SUPERIOR peripheral fundus carefully in acute PVD cases In 1920, Gonin recognized that RBs were the cause of RRDs Tx of RD requires sealing of such a BREAK The question of prophylactic treatment of retinal tears to prevent a retinal detachment was further discussed by Linder1934 Late 50 s, it was recommended to tx all breaks to prevent RD Birth of photocoagulation xenon laser (Meyer-Schwickerath) TODAY it is IMPORTANT to determine when a RB requires referral for tx and when it can be follow Complications associated with treatment can occur 61 HF CC: Flashes X few months ago but subsided OD recently had shower of floaters X 4 days OS PMHx/POHx: unremarkable Is a PVD associated with SHOWER of floaters? 61 HF SLE/90D Anterior vitreous Pigmented cells OU Posterior vitreous Large PVDs OU Inferior VH OS Numerous & small circular appearance Why no flashes currently? Additionally in OS: Multiple pigmented /non-pigmented RH Inferior VH LD with retinal break Should the OD be txed, even if asymptomatic? Follow-up 3 days later Pt had appointment THAT day to see retinology Surgery was scheduled immediately OD superior OS superior 2
At this time She is experiencing flashes OD X 2d s/p surgery Has appointment Always educate scheduled about with new retinal si/s specialist next INFERIOR week VIEW HOW WE FOLLOWED THE Pt vs HOW MD s OFFICE MANAGED THE CASE She had continuous RB repairs with development of new ones Final outcome She received laser 360 OU THE FACTS 6-11% of the general population have RB(s) 1 in 10,000 will lead to a RRD Incidence of RD is 12 in 100,000/yr (0.012%) So the important Question is: Which RB should we refer? 25 WM CC: Decreased distance vision HPI: No F/F of either eye PMHx/POHx: unremarkable 1 st eye exam Entering VAs: 20/30 OD, OS Examination P: (-) APD M: -0.50 sph OU 20/15 OD, OS SLE: no pathology DFE What are we looking at? What will this condition result in? Risk of RD is <1% (Foos 74) (Byer 81) Hold 'em or Fold 'em? Cause of RRD in sequence What about this presentation: what would you do? Based on associated risk factors you have read, would it be best to monitor or get a consult? Our presentation: There s fluid & traction Although <1% of tufts develop RRD, 10% of RD are associated with breaks near cystic tuft (Byer 81) 3
28 WF CC: Presents for routine exam No specific complaint POHx: Hx of Refractive Amblyopia Entering VA OD 20/20 OS 20/200 P : (-) APD M: OD pl 20/20 OS -8.00sph 20/80- Operculated hole: round hole with over lying free floating plug of retina Complete relief of vitreoretinal traction in this area Based on on the presentation, hold or fold? Would your management change if she was NOT MONOCULAR? AOA guidelines for operculated holes: 6-12M follow-up 59 WM: Language barrier issues Hold or Fold? 58yo routine eye exam What would you do? Note the size of the operculum Superior view AOA guidelines: Fresh operculated breaks located superior should be refer Based on what you know with regards to pigment, would it be best to hold and fold? Pigment indicates it is chronic (Morse 75) Follow yearly Scleral depressing a retinal hole RH: Using SD a retinal hole is easily differentiated from a retinal hemorrhage? Scleral depress Hemorrhage will have irregular margins (heme diffuses into the surrounding tissue). A Hole has smooth borders DDx important = management b/t the two differ Scleral depression: The questions When to use the procedure? To view a more anterior structure or manipulate view of a hidden lesion Viewing a vitreoretinal abnormality in profile DDx (retinal hemorrhage, a retinal tuft ) Is there associated traction, fluid cuff To better view a shallow RD/RB What do you use? Thimble, Q-tip, Scleral Indenter How to perform I don t do 360! 4
What are we looking? Lattice Degeneration as a Routine Finding Tear in a HIGH Myope with LD Hx 25% cases of LD in HIGH myopes have an associated break There s a strong vitreoretinal attachment along its margin Snail track = morphological observation LD has been documented in 10% of autopsy eyes Is this any cause for concern? How do you manage it? The chance of LD developing an RD is 1% How about if he had a hx of contralateral RRD and the pt was a 10D myope? Most LD are watch but problems related to How can LD lead to RRD? Lattice degeneration is a condition in which peripheral retinal thinning. May be associated with pigment or holes Remember that according to B Larry u the cable guy 42% OF ALL STATISTICS t ARE MADE UP ON THE SPOT True science teaches us to doubt Claude Bernard Although risk of developing RRD from LD is <1%, 30% of eyes with RD have Lattice Degen YET, 89% of RD s from affected LD eyes occur in areas of normal peripheral retina Prophylactic laser may not prevent tear or RD in fellow eyes with & RRD/RB will still occur (wilkinson 2000 & Chauban 06) Yet, studies (like Folks 89) show that prophylactic treatment of LD of fellow eyes (of pts w hx of RRD in contralateral eye) reduced risk of new RD from 5.1% w/o tx to 1.8% w/ tx Evidence based Prophylactic. Wilkinson C. P. Ophthalmology 1/2000 Editorial by Norman Byer, M.D. in same issue Chauhan et al. Failure of Prophylactic Retinopexy. Arch Ophth. 7/06 What about this presentation Best to hold or fold why? What is a SUBclinical RD? Subclinical RD: fluid extend >1DD from the RH but NOT > 2DD posterior to the equator (Davis 73) >30% become CLINICAL RD (Davis 74) To 1/5 typically What is a sub clincial RD vs clinical? Courtesy of Dr. B. Townsend 5
Guidelines for tx RB: AOA Guideline Symptomatic retinal breaks deserve a consultation Is it symptomatic? Symptom is the most critical prognostic criteria determining the likelihood the RB will progression towards RRD >~30% of symptomatic untxed RBs in phakic eyes lead to a RRD Colyear 56 & 60, Davis 73, Shea 74 Asymptomatic RBs do not show any significant tendency towards RD Byer 1998: 162 cases (16% FT) 1 subclinical RRD (Neumman 72: <5% progress) (Davis 74) (Byer 82 n=231 X 1yr) Yet ARE SYMPTOMS everything? -1.00 sph OU No risk factors Asymptomatic But would anyone monitor even if asymptomatic? The question the MD will ask to determine urgency vs emergency? Fovea on or off? Technically on Asymptomatic. Found this in inferior peripheral view during a routine CEE What are you looking at? Given the clinical picture refer or monitor? Schsis vs RD how can I tell? translucent folds?holes Schsis RRD Likely may be monitored REFERAL 6
18 WM Asymptomatic Mom made him come to clinic POHx: Trauma X 1 wk ago Hold or Fold? Traumatic RB commonly lead to RRD Cooling 1986, Johnson 1991 Also would he be compliant to RTC? When dealing with a RB there are modified strategies based on risk factors Is there associated trauma? As high as 80% of traumatic RBs (in one study) were associated with development of a RRD Cooling 1986, Johnson 1991 Is the pt a moderate-high myope (>6D)? ~40% of phakic RD s are seen in myopes Eye disease control grp 93 OTHER risk factors Is the pt pseudophakiaor aphakic? CE accounts for up to 40% of RDs but incidence is <1% Compare to general pop, CE increases RRD by 4x Risk is higher closer to the time after surgery, Younger age, complication during CE surgery, high myopia (>26mm axial length), absence of PVD before surgery Has the pt had a yag? Ambler 1988: increase risk <2% When dealing with a RB there are modified strategies based on risk factors History of RD in the fellow eye (contralateral eye)? 5-10% of pts with hx of RD will develop RRD in fellow eye (Combs 82, Davis 74, Tornquist 63) Same dynamics Is there a STRONG family history of a RD? Marfan s syndrome, Ehlers-Danlos syndrome, Wagner s syndrome and Stickler s syndrome Risk Factors: A Review RB & risk factors that may increase progression towards RRD Fluid Traction Symptomatic Trauma Myopia RD in contralateral eye Recent cataract surgery or others FHx of RD Size & location (Sup) & lifestyle also taken into account NOW 20/20 OU distance/near.but complaints of near blur Finding attributes to complain: relative scotoma More Q: Had a blur spot when reading Often a disrupted PIL is associated with symptoms 7
SO Clinical Courses The spectrum of the disease m o m o n i Monitor or fill out a Symptomatic VMA Spontaneous Resolution Based on the what you read regarding the evolution of the disease, do you monitor or refer? RTC q3-6m (VA 20/20) May remain stable or even resolve Resolution Before and after 3M follow up Progression Progression to FTMH (Stage 2) Courtesy of Dr. B. Suddon 1 Hikichi T, Yoshida A, Clement L. Course of vitreomacular traction syndrome. Am J Ophthalmol. 1995 Jan;119(1):55-61. Abbreviations: VMA, vitreomacular adhesion; FTMH, full-thickness macular hole. 66 OCT: Helping in the Dx of VMT Print to practice: Gallemore 2000 (8% vs 30%) Should pt get a retinal consult 1 st? Terminology today What do you call this? THE SLEEPING CONDITION Age: 64 BCVA: 20/50 Symptoms: blurred vision Patient is scheduled for Cataract surgery in two weeks MIVI-TRUST, data not acc., for AB use only 68 VMA is typically asymptomatic International VMT study developed OCT anatomical classifications Duke 2013 Terminology today What do you call this? VMT = VMA + Terminology: VMA/VMT Sub classified by size of adhesion Focal vs broad Both associated with a contralateral MH4 How does management differ? Chance of MH 10-15% No real MH chance 8
62 BF June 2008 Impending FTMH OD (the old MH stage 0 = VMA) Secondary (traumatic) FTMH OS CC: CEE POHx: Decreased VA OS longstanding (~7yrs)?traumatic macular hole PMHx: HTN & DM BCVA: 20/25 OD, 20/400 OS OD Which one are you more concerned with? OD with the impending MH The stage 4 MH will not have a good prognosis for visual improvement (s/p surgery): TRAUMATIC, LONGSTANDING, Look at adjacent sides OS Based on what you read about stage 0, what would you do? RTC 3M & Home amsler Chan 2004 Stage 0 MH has a 6-fold increase in the risk of macular hole formation, in particular given the Stage 4 MH in the contralateral eye 62 BF finally RTC June 2009 Note color difference b/t two presentation and tissue plug CC: Decreased VA OD X 3M Fell down stairs 3M ago POHx: Stage 4 macular Hole OS BCVA: 20/100 OD 20/400 OS Hx 20/25 OD OD FTMH: interruption of ALL retinal layers from ILM to RPE OS a single, round, circumscribed reddish lesion located over the fovea. What s the difference? Terminology MH Not full thickness YET Stage 0 (Impending hole = VMA) Stage 1 (VMT) Full thickness Stage 2: small Stage 3: medium Stage 4: large LH (Lamellar hole): Partial foveal defect PSH (Pseudohole): FALSE appearing FTMH presence of photor accompanying ERM The role of minimal surface traction Chan Opth 2004 Central posterior vitreous adhesion to fovea Increase risk of developing MH (10%) This is VMA Pt is asymptomatic but at risk 9
Stages of Macular Holes Gass 1988 MH stage 2 Stages of Macular Holes Gass 1988 MH stage 1 = VMT Pseudocystassociated with traction NOT Full thickness Note the outer retinal layers Loss of foveal depression Donut shaped yellow ring VA 20/20 20/70 III: Full thickness macular hole 20/80-20/200 IV: Macular hole + complete PVD >400um with partial traction What s the difference? What is the typical management if VA minimal or not affected? Old theory: focal shrinkage of vitreous in the macula led to contraction of the cortical vitreous & traction The condition is NO longer IDIOPATHIC OCT has expanded our knowledge about macular hole pathogenesis Hee 1995, Gaudrin 1999, Ito 2003 0 1 20/25 20/30- in 3M 2 Is this a FULL thickness MH? Gass Arch Ophth 1988 Lamella macular hole Pathogenesis Gass in 75 believe it was a result from CME More current term describes it as an aborted MH with partial thickness defect Typically good VA (VA 20/40 or better) Surgery is controversial Success rate is 25-75% VA improvement s/p surgery is correlated with peeling of ERM & associated tractional relieve Many remain stable (w/o photoreceptors risk of damage) & may not require surgery till later. OCT criteria (2006) Lamellar macular hole LH OCT Criteria Irregular foveal contour FTMH Break in inner retinal layer Separation inner/outer retina & Intra retinal split Absence of FTMH Photoreceptors ARE present Pseudo hole 20/30 False appearing hole with associated ERM Witkin AJO march 2006 10
OCT criteria of PSH Lets talk optometry: When to fold and when to hold? Is there a difference in management? MH 1 1. Heaped foveal edge 2. Associated ERM 3. No loss of tissue or outer retina just deform MH 2 Case 1: 65 WM CC: Decreased VA OD X 3wks BCVA: 20/30 OD P: (-) APD SLE NS +2 OS 20/50 OS 273 µm JB 6wks later 20/40-20/50 551 µm Would you Hold em or Fold em? RTC 6wks-3M Gass 1988, de Bustros S : 50% of stage 1 MH abort Discrepancy may occur b/t structure & function. Although VMT may be associated with severe traction, if only the inner retina is involved, function may remain adequate Now how would you play your hand: Hold em or Fold em? 11
Initiating treatment The variable factors that one takes into account VA & degree of visual symptoms (20/40 and waviness) Occupation (pilot) Progression Associated complications (PSH) Pt was recommended to have surgery but he had Keeping in mind that success better prognosis depends on: Onset other plans Associated complications VA JB OUTCOME... Symptoms VA = 20/20 The other side of the coin 60 WF CC: Decreased vision BCVA: 20/30- OD P: (-) APD 772447 OCT 4M Follow-up Based on what you read about stage 1 progression, what is the best management? Vision has worsen over the last 2 weeks BCVA: 20/400 P: (-) APD RTC 3M Gass 1988, de Bustros S : 50% of stage 1 MH abort but 50%... Outcome: 1M s/p surgery pt was 20/30 Based upon what you know with regards to a stage 4, fodl or hold? REFER Kelly 1991 (successful txof MH) Friedman: Vitrectomy for Treatment of Macular Hole Study Group 97 Visual benefit s/p PPV (for MH stage 2-4 ) Face down Elements For yrs we use to believe that best prognosis was w face down position from 10-14 days Recent reports state 7 days is enough OCT studies show closure w/i 48hrs <500 um MH may have good prognosis with only semi seated position The GAS may have impact on face down position Short vs long acting gas used Proper gas-air ratio 12
Is facedown position a necessity? The wine glass phenomena m o m o n i Option 1 is to REFER: Given it may progress Tornambe work proposes that complete closure can be achieve w/o face down position Outside of monitor vs PPV is there anothe option? Option 2 is to MONITOR Given it may resolve & VA adequate & PPV has a # of complications Tx Options for Symptomatic VMT POHx of CMV-R & AIDS Taking HAART medication 20/25 X 2-3yrs MILD SEVERE Clinical Monitoring But may miss therapeutic window Vitrectomy Associated complications 112 Ask to RTC in 3M Pt RTC 7M with decreased vision 20/100 Light travels faster than sound. That s why some people appear bright until you hear them speak. Pt referred for surgery Closure is USUALLY noted in 75-90% of cases But it is important to EDUCATE pt after surgery Larry the Cable Guy 13
Pt failed to follow instructions: Thought he merely had to have head position down ONE TIME following the surgery Tamponade Bubble + face down position Sealed closure of the hole Allows for better glial cell adhesion LET US NOT FORGET THE BURDEN ON THE PT. Most surgeons RISK vs BENEFITS advise pts to keep a head down ~7 days Outcome depends on: initial VA, complications, onset PPV risks: cataracts, RD, infection, no resolution The New Options Today MILD SEVERE Jetrea has been commercially available Jan 2013 to tx symptomatic VMA Truncated form of active PLASMIN recombinant protease with activity against fibronectin/lamin (components of VR interference) functions as a thrombolytic agent causing an enzyme pharmacological induced vitreolysis Nonsurgical PVD The enzymatic agents alter the biochemistry of vitreous Liquefaction of the vitreous occurs LYSIS between vitreous cortex and ILM is the final outcome Clinical Monitoring Ocriplasmin (Jetrea) Vitrectomy 121 Stalman 2012 Excluded PDR, high M, wet AMD & aphakia Included symptomatic VMA, ERM, smaller MH Primary outcome VR interface contains lamin, collagen, fibronectin, which facilitate adhesion b/t ILM & vitreous cortex N > 650 pts Inclusion: VMT w VA < 20/25 & OCT showing thickness PPV advised if: MD deemed it to be necessary s/p 1M VA worsen by 2 lines or No improvement s/p tx Among those pts that resolved s/p injection, 73% were w/i 1 st week ½ OF THE DRUG IS SHORT 14
Case Sample: MIVI-Study pt 20/32 20/32 20/20 Treatment-related Adverse Events Postinjection Day 0 to 7 Proportion of Patients with Retinal Tear or Retinal Detachment baseline 7 days 14 days 20/25 20/16 20/20 Note primary outcome was PVD w VA improvement as SECONDARY outcome Patients, % 15 10 5 0 Placebo Ocriplasmin N=187 N=465 12.9 ~10% adverse affects. Most affects noted within the 1st 7 days 10.5 10.1 due to localize injection. They were transient and after 8d the adverse effects were minimal & equal b/t tx & placebo 6.5 4.1 3.7 3.2 3.2 3.2 2.7 2.6 1.1 0.5 0.6 0.5 0.0 0.0 0.0 0.0 0.0 Abbreviations: Ant., anterior; VA, visual acuity. 128 Data on file. ThromboGenics, Inc. 2013. Patients, % Placebo Ocriplasmin 4 N=187 N=465 3 2.7 2 1.6 1.1 0.9 1 0.5 0.4 0.0 0.0 n= 0 2 1 0 3 4 5 6 0 Retinal Detachment Retinal Tear Retinal Detachment Retinal Tear Pre-vitrectomy Occurrences All Occurrences 129 There s been questions with regards to initial decrease in vision Following a pt s/p tx the ME story & may attribute to CVD/ERG abnormality (<20 pts in MIVI study & was intermittent) Resolution of VMA at Day 28 By Predictors of Response Ray 2012 20/40 20/63 20/50 20/50 20/40 20/30 4,000 for 1 injection (yet, only 1 injection require) co-payment (insurance covers the cost) Patients, % 60 40 20 p=0.008 p=0.006 p<0.001 50.0 47.5 Placebo 50% 25.5 23.3 respond rate with > 3 predictive factors 14.3 14.6 p<0.001 Ocriplasmin p<0.001 Increasing the # of (+) features 37.4 was associated with 34.7 34.2 increase odds VMA resolution Singh Ophthal 2013 12.6 0 n=10 N=38 N=12 N=53 N=17 101 N=18 N=109 N=17 N=100 <65 years FTMH No ERM 1500 μm Phakic 250-400um N=43 80 47 106 119 270 123 314 135 292 Data on file. ThromboGenics, Inc. 2013 130 * 400 μm with VMA Data on file. ThromboGenics, Inc. 2013. 132 VR conditions associated with PVD process Complications likely associated with accelerated liquefaction occurs before weakening of VR adhesion VR traction site Retinal vasculature Retinal condition Retinal or vitreous hemes Avulse retinal vessel PVD noted but No Symptoms When would you bring the pt back? I will leave you with vitreous HUMOR Macula Periphery VMT syndrome &/or MH Operculasted Holes/Breaks RRD 15
Regarding PVD disorders, which of the following increases the likelihood of a concomitant RB? A. Retinal Tuft B. Pigmented cells in the vitreous C. Syneresis in the vitreous D. Pigment on the retina CC: F/F OS X 3days BCVA: 20/20 OD SLE Cataracts OS>OD + PVD OS 56 WM 20/25 OS Anterior vitreous DFE: NO RB or RRD are found Based on what you read how would you management this case? >80% of pts with pigmented cells in the vitreous present with a RB (JAMA 09) 115 Eyes With RRD From PRINT PRACTICE Pigmented cells vitreous Br J Ophthalmol 2000;84:1264 96.5% had a PVD 96% had Pigmented cell in the vitreous When would you see her back, given the presentation? Courtesy of Dr. L Alexander 62 WM with complaints of photopsia X 2 days Also noted in the inferior periphery Based on what you read with regards to VH +PVD, what is the best management? 10% of PVD+VH cases can co-exits WITHOUT a RB Yet, 50-70% of pts w/ PVD + VH also have a RB Sharma 04 Courtesy of Dr. J sowka 16
The truth about VH associated with a retinal break CC: Numerous floaters X 3 days No flashes Pohx: Lattice OU BCVA: 20/20 OD OS Low myopic Rx DFE Is a PVD associated with numerous floaters? Go directly to MD do not stop and collect a cheeseburger Because of gravity, VH have a tendency to settle inferiorly, An associated RB is not necessary at the location of the VH This may not correlate with the break s location J Sowka NSUCO Clinical Exam of a Patient with A Symptomatic PVD FULL Dilated fundus exam (use PE/tropicamide) Look specifically at the vitreous +/- pigmented cells in the anterior vitreous +/- VH I will leave you with vitreous HUMOR 17