Due to running late, there was not panel discussion of the Medical Retina talks.
Dr Gregory-Evans sends his regrets as he was unable to attend.
Huge range in prevalence of diabetes. The Masai women walking 10km or more per day to get water are not getting diabetes. Increasing urbanization of africa leading to rise in diabetes. Estimate 35% prevalence of retinopathy with most countries in Africa not having any laser. Free screening in Kilimanjaro yet still only 29% of DIABETICS had eye exam in previous year. Working to improve screening in different communities.
Laser training is needed. Residents in Nairobi learning, courses being given and innovation in the works. They are moving a laser between six different centres to deliver the care where it’s needed. What is the most dangerous component of the laser - the counter! Hung up on need to give 1500 burns but only about 260 burns on average actually are ones that take. Many patients therefore actually think they had adequate treatment. Better to give full and adequate treatment, even if leads to macular edema, then multiple under-treatments.
Gives case history, of young lady who had lost her vision more than one year prior to getting seen and was left with tractional retinal detachments. Other cases shown where patients have been seen too late considering they have known diabetes.
Concludes talk showing a surgical video of patient with tractional retinal detachment. Talks about how the traction acts like a third hand so as long as cut upward, even if visualization not great, can cut upward.
Moved his talk to the end and skipped the pathophysiology in the interest of time. Quick run through of vascular conditions including malignant hypertension, ocular ischemia, etc. Classification based on ischmic or not and anatomic location. Then runs through some cases.
45 yo M, 6/120 vision with blood and thunder macula. Lots of blockage with late leakage on FA. Typical mountain on OCT. Ischemic.
41 yo M, less extensive heme, just a bit of leakage, milder macular edema. Non-ischemic.
Evaluation includes detailed eye exam, BP, glucose, HgA1C, etc
Complications can occur early or late.
Historically, much has been tried over many years. In past, COVS was basis of a lot of treatment and BVOS study. COVS suggested only treating ischemic and BVOS waiting 3 months for resolution before grid treatment.
Another historical failure was laser chorioretinal anastamosis. But kenalog and anti-VEGF began to appear.
Radial optic neurotomy, don’t do it! Published study 208.
Biggest advance was in 2009 with SCORE Reprot No 5. Intravtreal triamcinolone led to average 15 letter improvement on ETDRS chart.
Ozurdex also did an RCT comparing single Tx. Appearing in the April 2010 Ophthalmology.
CRUISE study looking at Lucentis for CRVO to observation in a RCT. Also did a sister study on BRVO. Both studies though excluded patients who had brisk afferent pupillary defects which may be a weakness of this study.
Another study looking at Avastin and grid laser combo, in Retina.
Study of VEFG Trap that Dr Albiani involved in showing 200X more biologic activity at 1 month post injection compared with Avastin. Presents a couple of case studies from this series. Bearing in mind potential bias as investigator cherry picking cases.
Promises this to be a whirlwind tour in 15 minutes of macular degeneration.
Incidence, prevention, and treatment of this condition. In developed countries, it’s the leading cause of irreversible legal blindness. A big problem that will increase as population increases.
Prevention: diet and vitamins
Treatment: Intravit Antif VEGF, Visudyne, steroids and variations thereof
AREDS was the major study looking at prevention with Vits C, E beta-carotene, zinc and copper. AREDS-2 investigates dietary lipids omega-3 and lutein and zeaxanthin. Have also reduced Zn and omitting beta-carotene. Results expected in 2012.
Anti VEGF: Macugen, Lucentis, Avantis
Macugen, although first out of the gate, isn’t used much as not proven to be effective.
Lucentis, penetrates all levels of the retina. A number of landmark studies related to this drug, such as the MARINA study. This is the study that showed an actual average gain of lines of vision. ANCHOR compared Lucentis to PDT and proved Lucentis to be better. FOCUS showed combination of Lucentis with PDT more effective than Lucentis alone.
Avastin, the full-length molecule, initially used systemically for GI carcinoma
Steroids, anti-inflammatory effect good, but high risk glaucoma from raising IOP
CATT Trail and others comparing the intravitreal drugs and await results.
Adverse event risk actually relatively low for the intravitreal injections.
PIER study looked at decreasing dosing by extending follow-up injections but found not good to delay the injections.
PrONTO study also looked at dosing.
SAILOR, EXCITE, SUSTAIN HORIZON all failed to maintain visual acuity, at least for lucentis, if less frequent than monthly (avastin is 6 wks).
Combination Therapy therefore looking to see if can prolong gap between visits
Combo as we know now is intravit Anti VEGF, PDT, Steroid. Benefits appears to be reduction in number/frequency of retreatments.
MONT BLANC and RADICAL studies looked at combination therapy
DENALI and EVEREST are current combo studies
Bottom line is that we will have more information on combination therapies; this is evolving.
Future treatments: VEGF-trap, Pazopaniib, Combrestastin, Bevasrianib, Complement inhibitors, PDGF inhibitors, Raditaion Thearpy, Alpha5beta-1 integrin agonists
Surgical treatments: subretinal removal of CNVM (not really being done)
Optical visual rehabilitation: cataract surgery does help these patients without worsening the macular degeneration, intraocular telescopic devices, low vision mag, vision training, and occupational training.
Some of this discussion was worked into the talks to accommodate visiting speakers flight times. Selected points are noted here.
One comment though, neurologists don’t seem to believe that intermediate uveitis can potentially be associated with multiple sclerosis. Also, those with Toxoplasmosis should get neuro-imaging as they can have neurological involvement of disease.
Abbreviated talk due to running almost 1 hour behind.
Any intraocular surgery can lead to endophthalmitis. Generally pain presenting 1-7 days post-op with AC cells/flare/hypyon. Discusses ESCRS prophylactic Tx to prevent endophthalmitis. Intracameral cefuroxime vs topical treatment no significant difference.
Glaucoma filtration risk thought to be about the same as following cataract surgery (but I don’t think he is including late onset cases that are at lifelong risk.)
Post-traumatic discussed as well with higher risk bacillus infections.
Endogenous endophthalmitis only about 5% of cases. Higher chance fungal with mortality as high as 29%
TASS Toxic Anterior Segment Syndrome usually occurs within the first day following surgery. Basically hyperacute vs typical acute endophthalmitis. Vitiritis rarer in TASS.
Preventive measures include povidone iodine, sterile speculum, pre and post op coverage with little solid evidence for any in particular this topical Tx.
Reviewed all the different treatment regimens depending on nature of organism.
Endophthalmitis Vitrectomy Study also discussed with its finding of vitrectomy if LP or worse vision or chronic endophthalmitis or post trab or endogenous endophthalmitis.
Make correct diagnosis endophthalmitis vs TASS. Tap and Inject vs vitrectomy. Identify organism and use preventive measures.
Top 10 cases of posterior uveitis and what they have taught the speaker.
26 yo WM with blurry vision x 3 days. Granulomatous KPs, conj redness, 2+ cells, vitritis. Therefore a pan-uveitis.
Tb, Sarcoid, Syphilis, Lyme and others
All tests came back negative
Additional information: friend had lit a firecracker near his eye several weeks prior to uveitis presentation that did have exposed uvea other eye. Therefore, this patient had sympathetic ophthalmia! Bilat panuveitis develops 2-8 wks after initial injury. Used to be commonly made diagnosis around US civil war time. Much less seen now, likely mis-diagnosed in past. More aggressive surgery today with surgery that can expose uvea. Dalen-Fuchs nodules are the classic finding that’s been described in the fundus.
Therapy includes topical steroids and intravitreal and other immunosupressants. Is the trauma more of a red herring?
25 yo WF poor vision OD, diagnosed by resident with macular hole. Colour photos show circular change both maculas but more diffuse retinal change is the pathology. Early hypofluorescence with later hyperfluorescence on angiogram. This is the pattern of inflammation as part of white dot syndromes including AMPPE, MEWDS, Birdshot, etc. - AMPPE
AMPPE multiple cream coloured lesions, equal prevalence male & female with good outcome. MEWDS tends to be more in myopic, female, younger and is uniocular with enlarged blindspot b/o papillitis. Birdshot, is a terrible form of uveitis that comes back and is difficult to control with strong HLA A29 correlation. Multifocal choroditis looks like Histo but has inflammation associated with it. POHS caused by an infectious agent. Serpigenous also very aggressive, starting peripillary or macular then spread.
24 yo WF shows the FA of another white dot syndrome unilateral in young female: MEWDS
16 yo F who noted large blind spot suddenly right eye, saw 2 ophthalmologists recently. Fullness to disc with margins not as distinct affected eye. Both right and left eye can tell myopic fundi based on the FA. On dilated fundus exam, can actually see lots of white dots, many near the disc. Another case of MEWDS.
15 you BF decreased VA x 2 days with VA 6/9 and 6/120. Scarred retina central burnt out area with creamy white infiltrate at all borders of the lesions. Other eye normal til dilate and look nasally were see active white fluffy border. Serpigenous Choroidopathy…a destructive, chronic condition. This does poorly. But, this seems young for serpigenous, so did limited workup done to check for Syphilis which showed +ve FTA-ABs.
37 yo hispanic male more of a vitritis, definite focii inflammation in the retina. Snowballs inferiorly in the better eye. Bad eye had a hypopyon. Systemically had penile rash. Diff Diag: Bechets’, Tb, Syph, Sarcoid, Lyme and turned out to be Syphilis. Afterwards did learn that he was knowingly HIV +ve as well.
Another case this time subtle subretinal lesion but once dilate see white dots and peripapillary atrophy more easy to appreciate. This is CNVM, young patient so consider POHS. No vitiritis with this condition. Know the organism.
6/24 vision with peripheral vasculitis with adjacent old scar. Fellow eye very healthy. This patient has toxoplasmosis treated with clindamycin and pred along with topical tx. Not all reactiviated from childhood, can be acquired.
46 yo animal control officer with swollen nerve one side. FA shows hot spot on optic disc. Sarcoid, syph, Tb, toxo. Eveolved to be more obvious as cat-scratch (Bartonella)
40 yo M worked up for PSCC and noted changes in fundus. White lesions along blood vessels; white lesions with haemmorhagic centres along blood vessels. CMV retinitis. Can treat with oral valganciclovir. Can get very bad pan-retinitis when immune system working again.
Also mentions PORN (progressive outer retinal necrosis)
Referred by optom with central serous chroid retinopathy. But, angiogram shows cystoid macular edema.
History: 3 week old hispanic male born 29.5wks gestation and seen 32.5 weeks post conception. VA LP, trace TVL, dilated post-pole vessels with some communication between the vascular arcades, ghost vessels, finger-like projections of retinal vessels.
Diagnosis: ROP? FEVR? Oxygen Toxic Retinopathy? Trauma? Something else?
Additional history: can’t really talk to mom as intubated in ICU. Has lupus and stopped all her lupus meds. Ultimately died 3 months after delivery. Found immune complexes in mom’s vessels. Feel therefore an immune related disease on top of ROP for this baby.
Treatment: did not know about this lupus vasculitis at first, otherwise might have treated for that. Based on BEAT-ROP study, did inject Avastin 0.6mg OS.
Three ROP variants: Typical ROP that responds to the study protocols, an aggressive posterior form, and a smouldering form. This last form never gets to threshold and the detachment can occur much later on, eg as a teenager.
Biphasic retinal vascular development: vasculogenesis and angiogenesis both explained.
Compared risk factors between regular ROP and the smouldering form. Odds ratio favours smouldering form if some CNS abnormality. These patients need to be followed beyond the expected 45 weeks for late development of the ROP complications.
Now in our Anti-VEGF era, many of these cases may need close follow-up for injections.Talks about the BEAT-ROP study that used avastin as a treatment for ROP.
Lessons from the BEAT-ROP study:
- laser vs avastin stage III zone I and IIIp
- prospective randomized
- FDA approved with many site visits
- primary outcome recurrence stage III plus
- vascularity goes way down within 24hrs post injection
- avastin not nearly as effective to salvage eyes that already had laser as it is primarily
- neovascularization at the ridge resolves at 1-2wks with peripheral vessels crossing the ridge
- growth of intrinsic vessels is delayed making follow-up more critical as wait for peripheral perfusion
- rate of recurrence lower with avastin and occurs at two sites: leading edge and the original fibro-vascular ridge
- advantage avastin vs laser far better zone I eyes than zone II eyes
- some eyes will vascularize to ora
- when detachments occurs after avastin, typically more dry and fibrotic which may be easier to operate
- myopia and VF loss may be reduced in Zone I cases
Original training at University of Michigan, fellowship at UBC and two others since then. Now a leader in pediatric retinal surgery. Both Drs Merkur and Albiani did additional training under his guidance after their fellowships here.
Two talks based on two patients. Juvenile retinoschisis is the first case.
This first one has to do with a 2 m.o. baby with eyes that started to wander upward. Fundus looks like has traingular areas of elevation with loops of vessels. FA helps show dome shaped elevation. This is Malignant Bullous Schisis. Usually presents before 18 m.o. with schisis that marches posteriorly to eventually often involve macula. Retina scrolls up into a fold.
Think X-linked Schisis when see vitreous heme, strabismus, amblyopia. Retinoschisin the involved protein mutation. A transmembrane protein involved in cell to cell adhesion.
Foveomacular schisis has several clinical presentations, one of which is the cartweel appearance at the fovea. If get foveal displacement, it does so nasally.
OCT often helpful to define the schisis area and also can show peripheral areas that might otherwise be missed. The areas that split correspond with the distribution of the retinoschisin protein in the eye.
Surgical indications include: vit heme, intra-schsis heme, bullous cavitty, progression to macula. Sometimes hard to tell where schisis ends and traction begins if retina detaching.
Back to the 2 m.o. patient who has lost fixation form schisis cavity extension. What are our options? Observe, intravit inj’n, laser, buckle, PPV, something else.
For management, presents a 3 week old with schisis and family history of exon 4 deletion. Shows how the retina starts to scroll off to the macular area. Quoting his mentor, Dr Ross, he opts for conservative approaches first, starting with a buckle, drainage of fluid, silicone oil. Child now stable more than 5 years and one of a series now collected who all had same exon 4 mutation and had surgery in first 2 years of life. All have 6/12-6/30 final acuity. Oil removed in 44%.
Now, back to the 2 m.o patients, management opted for was the encircling band, external drainage fluid. Careful not to create OUTER retinal hole in this process. Lens-sparing vitrectomy. Child has regained central fixation. What about the left eye for this patient? Here retina so bullous it is touching in many areas. Opted for injecting Plasmin and keeping patient in prone position.
Spontaneous reversal of schisis is felt to be something that can occur. Can see a ‘high water line’ indicative of where the fluid line was in the schisis cavity.
Has also seen some kids with thick exudates in their schisis cavitis. These have all been refractory to the standard surgical techniques already discussed. Requiring re-operations with relaxing retinal incisions and not as favourable in terms of visual prognosis.
Summary. Think of schisis in boys when see vit hem or vision changes. Many variations and may not appear in 1st year with Exons 1-3. With Exon-4 there are more malignant manifestations. There is also the Exudative variant that is particularly difficult.
Discussion held after the lunch break instead of before. Here are some notes.
Q: Any pearls from ancillary testing and also sub RPE membranes. Thoughts on Anti-VEGF
A: Dr Maberley, size and duration of macular hole important. Chronicity and macular RPE changes might lead to poorer prognosis. Still a role for removing sub RPE membranes. Pre-op avastin not good for these cases.
Q: Dr Napier, as a cataract surgeon, do you have any advice if high myope and had prior vitrectomy…how to handle this very deep anterior chamber.
A: Dr Merkur, suggests keeping bottle height as low as possible yet trying to keep stable chamber. However, that missing vitreous scaffold makes this tough. If have access to 25-G system, infuse posteriorly or put gas into vitreous cavity. Also suggests hanging a bag to infuse more fluid from behind rather than setting up a second (vitrectomy) machine.
Q: Dr Maberley, asks more about longterm data of sutureless scleral fixated IOLs.
A: Dr Merkur, don’t have more data on longterm follow-up. Says one study from a group in Germany reported no complications but limited to one study.
Dr Maberley is also local faculty from UBC.
ERM, MH, SMH our most common elective retinal surgeries. OCT has been pivotable in defining our approach to these diseases from identifying the condition to confirming the surgical goals post-op.
Caveats of OCT and Visual Acuity related to diabetes. VA does not correlate well with OCT retinal thickness.
Thickening of inner retinal layer with corrugations along stress lines. CME often a factor too. Prior vascular conditions such as macular venous occlusion may have occurred. Chronicity difficult to identify. Key to talking with patient as those presenting with metamorphopsia tend to have a better prognosis.
OCT and cataract assessment before consider surgery. Often best to do the cataract/IOL first if cataract present to avoid additional surgeries. If not convinced of peripheral retina tear, could have RPE disruption that may only be found with IVFA.
If peel ILM, need to make sure get broad area. If membrane the only problem, best to not peel the ILM off. Head positioning sometimes an issue post-op. Patient can notice horizontal line from the air/fluid level. 100% risk cataract within 2 years if >50 yo.
Macular Hole well defined by OCT to confirm the diagnosis, measure diameter and perifoveal changes, and confirm proper closure post-op. IVFA may still be needed in some patients.
Goes through Don Gass’s original description of macular hole when thought to be tangential but now know more perifoveal and more vertical.
Over 90% holes should close with overage vision improved to 6/15 or so with surgery. Goes through other stats for success rates under different macular hole causes.
Next deals with subretinal haemmhrage. Difficult to tell if subfoveal especially by angiogram but OCT able to show sub-foveal. Therefore suggests management different with need to displace the blood.
Dr Albiani introduces Dr Hall, trained in Zimbabwe then in England. Has since moved to Tanzania at the Christian Medical Centre.
What do retinal surgeons in Africa do. Patients tend to present rather late. Often see trauma cases, also presenting late. Lots of paediatric cataract surgery as well that generates retinal detachments later. Also complications of HIV to deal with.
KCMC directly serves 2.5 million people. Referrals from much broader area. Dr Hall has a program that has trained 7 others across africa. All of this just scratches the surface of all those in need of retinal care.
Almost all patients present rather late. Also, very often the only eye at time of presentation. Frequently subretinal fibrosis. Goal to try to restore some navigation vision. Huge range of very interesting patients. Everyday is a grand rounds. Deal with lots of infections and vascular problems.
Trauma also a big problem, often children presenting late after lacerations.
Case of “unusual Bests’ disease.” In fact, Cysticercosis as could be seen when examine fellow eye.
Another case of damage from VKH with serous detachment, sunset glow, and subretinal membranes. Steroids initiated but still lots of traction bands. Ultimately did remove the traction bands and has navigation vision.
Full Professor here at UBC who has run the retina fellowship program for many years.
Starts with discussion of Gonin’s Principle; recognition that retinal break was the cause of the detachment. Closure of the break cures the detachment.
Pathogenesis of detachment reviewed. Liquid vitreous getting through the tear with RP pump trying to drain it and traction of vitreous on the retina opposes this.
Pneumatic retinopexy: if superior break. Gas bubble occludes the break and the RP pump draws out the subretinal fluid. Cryo done around tear which can scar later; sometimes supplement with laser. If however too much vitreous traction, this can still pull retina off later. This technique is least invasive of all but does also require proper patient positioning. Fluid can shift and lead to new breaks however.
Scleral buckling: some people think no longer needed. However, scleral buckle has been the benchmark for RD repair. Position buckle to close the tear; rarely need to drain subretinal fluid at time of surgery as long as buckle on the tear. The explant (buckle) helps relieve the vitreous traction forces. No use of gas to cause cataracts, no travel restriction as no gas to expand, no cataract formation as eye not invaded internally.
Retinal dialysis: usually in young people from trauma. Circumferential band often needed. Usually takes 2-4 years for this to occur as vitreous liquifies. Must close the dialysis with the buckle. Unfortunately, as often such a slow progression to detach, the prognosis is guarded. However, totally preventible if caught early.
Combined scleral buckle and vitrectomy: RD with superior and inferior breaks. Dr Ross prefers encircling bands to provide additional support. Worth the extra 15 minutes; then proceed with the vitrectomy now that traction is relieved. Shows video. 360 degrees of laser to prevent future detachment. If phakic, patient will get a cataract for sure. Don’t like primary vitrectomy for people under 50 if possible.
Giant retinal tear: peripheral break extending >90 degrees. Need to infuse “heavies” to posterior pole starting at optic nerve to push the retina flat. In the end, replace with fluid then C3F8. Shows movie of this.
PVR: total RD with PVR, retina is getting foreshortened. Trouble is that membranes forming not just on top but also underneath the retina. Silicone Oil needed and stays in place for 3-4 months. Unfortunately, sometimes retina so foreshortened that you have to cut it to release the subretinal traction. Another video shown.
Quiz: 40 yo male with breaks post and inferiorly. People respond with scleral buckle.
Next quiz: massive PVR; need to cut the retinal breaks.
Another: total detachment but just one break superiorly. Definitely try pneumatic first.
Last case: toxo in the eye, macula still on, break below inferior arcade. 13 yo male. Sponge is the way to go on this one.
Dr Merkur is on faculty at UBC. His residency training was at University of Ottawa, and fellowship at UBC.
This talk is on surgical management of aphakia. We’ve come along way since the early days of couching lenses.
Starts reviewing option for lens implantation when no capsular support including aphakic glasses, AC/iris fixated IOLs, next generation foldable AC IOLs, iris-sutured PC IOL, sulcus-fixated lenses and new techniques. These were all discussed.
AC IOLs seem to be showing a trend to better vision and fewer complications than even posterior fixated IOLs. People often concerned of potential chaffing issues but not outweighing its benefits.
If have complicated case, do not put something like an SA60 into the sulcus; leave aphakic if don’t have appropriate sulcus 3-piece lens.
AC IOL (non-folding ones) less technically demanding but no sutures to erode or break. They do require large incisions and could effect the angle which is of concern with glaucoma patients. Risk pupillary block and UGH. Newer open-loop designs are quite good. Still glaucoma docs shy away from this out of glaucoma concerns.
Iris-fixated claw lenses discussed. Some potential concerns with inability to dilate patient afterwards as pinch onto iris with claws.
Iris-sutured IOL. Still better than a one-piece lens in the sulcus in terms of rubbing. These patients do end up with a cat-eye pupil (which patients not always happy with) and mydriasis is restricted. Fairly stable surgery.
Sutured sulcus IOL is commonly done here in Vancouver. Rather large incision and shows off your surgical prowess. Prolene does breakdown eventually, and those are the sutures used to fixate these lenses. When these start to break down, extra trauma to the eye to re-suture them. Also risk of chaffing with iris if too anterior and of tilting the IOL. However, can get great dilation of the pupil afterwards. Surgery is long and there can be significant light toxicity with this surgery. As this is the standard technique here, he goes into greater detail showing drawings. Scleral flaps at each end where the suture will be fixated. Tie sutures to the haptics then internalize the lens. Newer lenses now that can allow 4-point fixation instead of just 2 which can help minimize decentration or tilt.
Foldable IOLs when sutured are like gummy bears in that the suture tightening can distort the lens.
New sutureless small incision sutureless scleral IOL. Technically a bit challenging but over time will be easier. Pass the haptic through avascular tissue. Broad fixation of the haptic with this technique. Shows video starting with 24-G scleretomies 180 degrees apart after a complete vitrectomy done. With bent needle, create needle tracks. Corneal incision inject IOL and leave trailing haptic out corneal wound.With end-grasping forceps, pull each prolene haptic of the IOL into the sclerotomy then bury into the needle tracks sclerotomy incision. (The video shown during the talk was presumed to be that performed by the speaker but was in fact copied from EyeTube.net without appropriate credit. He has performed the procedure and will provide me with this to post.) Minimal incision, foldable small incision, no exposed sutures.
Updating video clip first week of May so that actually surgery the speaker has performed then will re-post.
Q: from Dr Mikelberg: ruptured globes classified as within 8hr emergency. Is there really no evidence of need to do that quickly? Do we need to change this within 8hr criteria?
A: from Dr Holland; says from literature review and would agree worth exploring literature in further detail to see if indeed within 24hrs is acceptable. Even war injuries cited as up to 3 weeks before repair.
A: from Dr Hurly, mentions war trauma often very hot and therefore more likely sterile material.
Q: Dr Cornock, often with transit delays for tertiary care, within 24hrs becomes within 36hrs, etc.
A: Dr Holland; also consider getting proper staff for the O.R.
A: Dr Albiani; had case spent along time putting multiple suture in a cornea only to have it replaced by corneal transplant the next day by cornea service. Could have just waited til then?
A: from audience; war trauma does get primary closure quickly then FB might wait til within 3 weeks…so not left with open globe all that time.
Comments: from Dr D Maberley, reiterates need to close the open globe. Asks clarification re gonioscopy.
A: Dr Hurly, yes, when possible, with minimal compression of the eye, important to do gonioscopy.
Q: Dr Gardner; asks about scleral depressed exam in kids
A: Dr Kirker: may need EUA.
Comment from Dr Godinho: would be leary about extending guidelines for repair beyond 8 hrs as this will lead to too long a delay ultimately. Also asks re antibiotic coverage…
A: Dr Albiani, 4th generation ORAL fluoroquinolones offer good intravitreal penetration.
Dr Hurley is from the University of Ottawa Eye Institute and did fellowship training at Wills Eye Hospital. Dynamic speaker who runs Power Point for physicians course at the COS each year.
(Apologies, but there is no audio feed available for this talk.)
Most of the cases for this talk were from patients seen during his fellowship at Wills Hospital. Not always easy to get photos at time of injury but has great images from then.
Starts with case from Ottawa, 38 you healthy male, felt something fly up out of the water in the ocean in Haiti. Diagnosed with conjunctivitis but vision deteriorated over 4 days. Vision CF and full thickness laceration lower eyelid which in fact went right through sclera. Also had frozen globe with IOP of 0. Posteriorly saw vitreous haem and whitish material. CT scan show intravitreal FB penetrating out posterior of eye. This is now almost a week after initial injury.
Started IV Cipro, closure scleral entrance wound, removed foreign body. Later developed nasal RD. Most recently, 7/12 post-op, VA 6/6 with correction, and subretinal fibrosis present.
Foreign Body identified by Dr Seymour Brownstein and determined to be a piece of that fish…a needle fish.
Shows another case, this one from the literature, in which almost entire jaw of the needle fish was in the orbit despite a very small entry site.
How can we avoid missing something like this in the future? Certainly with a de-gloving injury or stab, you know there is damage. When less obvious, must always maintain high level of suspicion and know when to explore. Don’t just look at the wound; know the circumstances. Don’t forget detailed complete exam.
Ancillary studies: if non-metallic FB, an MRI can help but not always easy to obtain. Ultrasound good option and more accessible. UBM high resolution but does not penetrate too deeply (trade-off.)
Sums of reviewing signs of ruptured globe. When in doubt, explore.
Dr Holland is on faculty at UBC. Thanks his current cornea fellow, Greg, for helping prepare the talk.
Discussing timing of repair of anterior segment between timing of primary repair all the way to visual rehab.
Timing of initial repair: As soon as possible, next day? We usually don’t have to repair the same night but within 24hrs.
Pre-op slit lamp exam: don’t be fooled by self-sealing leak which could lead to future epithelial ingrowth
Corneal laceration repair aiming for 90% depth and trying to avoid visual axis. If further tissue damage by burying knots then leave exposed and put on bandage lens.
Incarcerated iris: how long to leave exposed. Probably 24hr rule, excise if >72 hrs.
Tissue glue and patch grafts discussed briefly. Cyanoacrylate glue extremely useful to have. Very little glue and even store bought from hardware store if must. Dry ocular surface; quite irritating to conjunctiva so cut off if ends up dribbling there.
Patch graft useful for larger defects. Can induce a lot of astigmatism if close to visual axis.
Leave aphakic at primary repair.
Lens diaphragmatic IOL sometimes needed; gives list of 3 suppliers. Need scleral suturing.
Secondary IOL to be discussed in next talk. AC vs PC IOLs. Outcome of AC IOLs just as encouraging as posterior sutured IOLs.
Goals/expectations vary. Want 20/Happy.
Gives some clinical examples with different IOLs.
Corneal laser correction options for the future. Gives example of patient going from 1.5D to 9D astigmatism after trauma and its repair. Another case with irregular astigmatism following rust ring and how laser ablation can help.
LASIK flap disrupture example; very challenging to reposition. Also mentions subluxed IOLs from trauma and need for retina surgeon assistance for those repairs.
Dr Kirker is one of the current Retina Fellows at UBC and talks about blunt ocular trauma.
Begins with case from past wk. 65 yo WF hit by golf ball directly to right eye. CF vision, no reverse APD (dilated prior night.) Aphakic, vitreous in AC, cyrstalline lens was in vitreous cavity. No break external tissue but certainly internal damage. This is blunt trauma.
Most common in young males due to more active. Some advancements with organized sports protection.
Complete exam; kids may need EUA to complete this. Key to document other eye too. Often future medicolegal so documentation for those reasons too.
Lens: cataract acute or chronic, contusion rosette, zonular loss - may need capsular tension ring for surgery.
Retinal tears: horizontal traction of globe leads to this usually at time of injury. Can get necrotic and stretch tears too. Traumatic RD more often young men. Retinal dialyses often caused by trauma and frequently not diagnosed til much later when macula comes off. Must follow patients til get a good scleral depressed exam.
Berlins Edema (commotio retinae) retinal contusion/concussion. Show histology too. Usually good prognosis for contusion.
Traumatic macular holes: acute post vit detachment or chronic from CME. Does better than age related maculer holes.
Retinal haemmhorage could be hiding a choroidal rupture. Rupture can lead to CNVM in future.
Optic nerve: direct or indirect trauma; pallor may take 3-4 weeks. Rarely, can avluse optic nerve but this is more common with open globe injuries.
Back to the initial case presentation. PPV and secondary IOL for future and happy ending we hope.