The Education Committee carefully selects presentations from the World Glaucoma Congress 2017 in Helsinki for your benefit. This edition Prof Dr Ingrida Januleviciene gives the introductions for the sessions My worst nightmare as a glaucoma surgeon, Neuroprotection: the future of glaucoma treatment and New discoveries in exfoliation.
My worst nightmare as a glaucoma surgeon
Phaco / Small eyes
Prof Dr Eugenio J. Maul
Prof Dr E.J. Maul introduced that phaco surgery in small eyes today is considered no more a nightmare – using topical anesthesia, pre-op Mannitol if necessary, proper IOL calculation formula, etc. However, postoperatively even several years after surgery, angle closure glaucoma might develop. Clinical cases were discussed describing various problems and possible solutions.
Prof Tony Wells
Prof Wells talked about hypotony as low pressure with secondary effects attributable to low IOP as choroidal detachment, disc swelling, macular changes, corneal folds, breakdown of blood-aqueous barrier. Clinical cases were presented describing glaucoma surgery as one of the common causes of hypotony, importance of scleral flap in early postoperative period, adjustable sutures, management of aqueous hyposecretion and best wish of having nightmares before the surgery, not after.
Dr Susana Duch
Dr Duch described 3 clinical cases that still might be considered as nightmares in tube surgery.
Excessive postoperative fibrosis
Prof Dr Franz Grehn
Prof Dr Grehn talked that currently we still have no ideal glaucoma operation, though technically possible, however might be not suitable for an individual eye. Management of avascular, cystic bleb was described. Classification of filtering blebs evaluating vascularity, corkskrew vessels, microcysts, encapsulation was suggested. Prof Grehn summarized that though wound healing process is still not fully clear, customized postoperative care is mandatory.
Neuroprotection: the future of glaucoma treatment
Mitochondrial dysfunction in glaucoma
Dr Pete Williams
Dr P. Williams in his talk highlighted the important issue that at the current stage there are no neuroprotective strategies in glaucoma. Speaking about glaucoma as a metabolic optic neuropathy he emphasized that RGCs are particularly vulnerable to metabolic and physical stress. Metabolism and mitochondrial health decline with age and is also exacerbated by periods of elevated IOP. Targeting neuronal metabolic decline and mitochondria may offer safe, neuroprotective treatments for glaucoma and also other age-related neurodegenerative diseases.
Regulation of lactate transport
Prof Dr Miriam Kolko
Prof Dr Kolko described the new treatment strategy for glaucoma. Though currently we are only treating IOP – the future perspective might lead to various neuroprotective strategies. Lactate is a metabolic waste product from anaerobic glycolysis. Normally, retinal lactate levels are low, however increasing dramatically during ischemic brain injury or diabetic ketoacidose. On the other hand, prof Kolko described several beneficial roles of lactate –increasing resistance toward ischemic or traumatic brain injury, preserving long-term memory, reducing glutamate toxicity, functioning as “glucose sparing” fuel. Results from recent research studies were presented.
Should neuroprotective treatment in glaucoma target the entire brain or just the optic nerve
Dr Mitchell Lawlor
Dr Lawlor referred to recent publications describing glaucoma as the whole brain disease or complex neurological disease. Analyzing damage at the optic nerve head speaker described different types of retinal ganglion cell degeneration: anterograde – optic nerve, chiasm, tract; retrograde – retinal nerve fiber layer, ganglion cell; trans-synaptic anterograde – involving lateral geniculate nucleus, cortex. Results from various studies evaluating brain changes following RGC loss and also before RGC death were provided.
Prof Keith Martin
Prof Martin talked about exciting time coming to medicine allowing the process of replacing, repairing or regenerating human cells, tissues or organs to restore or establish normal function. Results from various studies and attempts of retinal pigment epithelium, photoreceptor replacement were presented as well as retinal ganglion cell regeneration possibilities that are feasible and evidence shows that visual function can be restored after acute injury.
Present and Future of OCTA in glaucoma management
Dr Harsha Rao
Dr Rao summarized the current status of OCTA in the diagnosis of glaucoma, confounders of measurements, and in the detection of progression. In terms of disease diagnosis, he showed that whilst OCTA can differentiate glaucomatous eyes from normal, however it was not superior to traditional structural measurements. In terms of the future of OCTA, Dr Rao emphasized on the need for advancements in technology before it can become a part of routine glaucoma workup in the clinics. He also stated that in the future, it is likely that glaucoma phenotype may be defined based on OCTA features.
Projection-resolve reflectance compensated OCTA in glaucoma
Professor David Huang
Prof Huang talked about the technological improvements in OCTA that would help improve the evaluation of glaucoma. He explained about the effects of projection artifacts in OCTA images and the processes to eliminate them resulting in Projection-resolved (PR) images. Based on the evaluation of PR-OCTA images, Prof Huang showed that the superior vascular complex (SVC) in the macula region was primarily affected in glaucoma, whereas the radial peripapillary capillary plexus (RPCP) was primarily involved in the parapapillary region. Furthermore, reflectance compensated measurements of vessel density improved the diagnostic accuracy of OCTA in glaucoma.
New discoveries in exfoliation (Lindberg symposium)
Fibrillinopathy in the eye
Prof Dieter Reinhardt
Prof Reinhardt made an introduction on extracellular matrix fibers in particular microfibrils that constitute to ciliary zonules, trabecular meshwork and other structures in the eye. He talked about exfoliation syndrome as a form of fibrillinopathy. He also explained how human mutations in fibrillin 1 may cause various syndromes as Marfan’s, Weill-Marchesani, acromicric and geleophysic dysplasias and stiff skin syndrome followed by clinical interpretations.
Cell biology, autophagy and mitochondrial dysfunction in exfoliation syndrome
Dr Audrey Bernstein
Dr Bernstein covered a viewpoint on neurodegenerative diseases that typically starts with gene mutation leading to protein aggregation and with age we see declining proteostasis capacity and oxidative stress that is evaluated as pathology or the disease. Several hypothesis were raised and studies evaluating LOXL1, misfolded proteins, dysfunctional autophagy were described.
Growth factors, clusterin and complementary-biomarkers in exfoliation syndrome
Prof Colm O’Brien
Prof O’Brien talked about pseudoexfolliation syndrome as age related generalized disorder of the extracellular matrix characterized by production and progressive accumulation of fibrillar material. Protein components include fibronectin, fibrillin, collagen and laminin. Pseudoexfolliation glaucoma was discussed as more difficult to follow-up and more resistant to medical therapy highlighting the role of oxidative stress. Results of in vitro analysis of therapeutic application of fully human therapeutic antibody against connective tissue growth factor were presented.
Cardiovascular and cerebrovascular associations
Prof Dr Murat Irkec
Prof Dr Irkec made an overview on systemic findings in exfoliation syndrome. Vascular diseases are known as the major cause of death worldwide. In exfoliation syndrome systemic associations include coronary artery disease, hypertension, myocardial infarction, stroke and aortic aneurysm. Cerebrovascular and chronic cerebral diseases were found more common in patients with exfoliative than primary open angle glaucoma. Prof Irkec also presented data of systematic review and meta-analysis on ocular pseudo exfoliation syndrome and vascular disease.
Other systemic disorders associated with exfoliation syndrome
Prof Dr Barbara Wirostko
Prof Dr Wirostko described the project carried out in Utah in terms of unique genetic resource using data from patient database evaluating exfoliation as a genetic disease and a systemic disorder. Prof Wirostko raised the question could there be systemic associations that are related to elastin abnormalities providing data from cross-sectional and also longitudinal studies.
True exfoliation syndrome reawakened
Dr Chaiwat Teekhasaenee
True exfoliation or capsular delamination was initially described in workers affected by high heat. Dr Teekhasaenee describes this uncommonly reported and also benign condition.