Returning for its fourth year, the 2019 Ophthalmology Updates! Conference was the series’ biggest event yet. In the first of a two-part series, LEWIS WILLIAMS looks at the cutting-edge presentations on show.
Ophthalmology Updates! held its fourth annual event at Sydney’s Westin Hotel in late August. Delegate numbers matched or exceed previous conferences and the event’s convenor, Associate Professor Adrian Fung, should be congratulated for introducing a meeting that seems to fill a gap in the market.
The 2019 event followed the style set at previous meetings whereby each presenter covers a common condition, ‘frontier cases’ that proved challenging or required a novel approach, and illustrative case reports.
Oculoplastics: Entropion, tumours, surgical approaches
Sydney Eye and Royal North Shore Hospitals-based oculoplastics surgeon Dr Brett O’Donnell opened the academic programme with a presentation on entropion, particularly lower lid entropion. He attributed the condition to the instability of the anterior lamella (the skin and the orbicularis oculi) resulting in lid laxity with both vertical and horizontal aspects.
He dated the great innovations in relevant surgery as starting in 1954, with little further progress made after 1972. The 1954 procedure pioneered by Weiss, and revised as recently as 1972 by Quickert (basically a Weiss procedure with a resection/shortening step), involves an incision and some tissue removal from the central one-third of the lid, followed by a suturing together of the gap’s opposing sides.
This is a procedure that O’Donnell now counsels against. Despite progress in methodology, recurrence remains an issue. However, he did commend Quickert’s 1971 suturing procedure for consideration as it is good, quick, and easy to perform.
Bick’s (1966) repair for entropion and ectropion, a wedge-shaped resection at the lateral canthus, and Anderson’s (1979) replacement for that procedure, which involves the creation of a lateral tarsal strip from the posterior lamellae (after separating the lamellae from the tarsus) that is sutured to the periosteum inside the lateral orbital wall, were also detailed.
He also detailed the Jones (1960) retractor repair (by plication, a procedure that folds, sutures, and tucks excess tissue) in which the lower eyelid retractors are dissected from the tarsus and palpebral conjunctiva. Excess retractor might also be excised.
His overview of current thinking revealed a large number of procedures, each specialised for particular variations of entropion and/or lid laxity.
Looking into the future O’Donnell saw the Jones retractor repair alone, or the Jones repair with a lateral tarsal strip procedure, as the method of choice for mainstream cases. He noted that too many of the simple methods are the ones most likely to recur.
In the Jones technique, problems include difficulties finding the retractors (the Quickert technique does not need the retractors to be identified) and fibrous tissue formation post-surgery. He also noted some inter-racial anatomical differences that need to be accommodated for, particularly in Asian eyes.
Moving to his ‘frontier’ topic, O’Donnell chose to talk about orbital diseases – tumours and cysts, Graves’ Disease, and trauma. The possible approaches include those with or without bone removal, removal of the sphenoid wing, and accessing the inferior, lateral, and medial aspects of the orbit.
Whereas in the past tumours usually required bone removal, modern approaches involve the creation of a swing eyelid flap (an infero-lateral approach) and no bone removal. Access and post-surgical closure are much faster, recovery is faster, and no manipulation of the lateral rectus muscle is required. Interestingly, he noted that ophthalmologists, neurosurgeons, and ENT specialist often took different surgical approaches and paths to essentially similar problems.
He detailed cases of a cavernous haemangioma, trauma, recurrent dermoid, lateral orbital thyroid decompression, BCC, an enlarged lacrimal gland, a pleomorphic adenoma, and a sebaceous cell carcinoma. He noted that tumours are mostly lateral.
The cornea: Microbial keratitis and the neurotrophic cornea
Sydney ophthalmologist Clinical Associate Professor Chameen Samarawickrama delivered a presentation on microbial keratitis (MK) for his common condition and neurotrophic cornea for his frontier topic.
He described MK as a common cause of visual morbidity whose treatment needed to be appropriate and timely. For a country the size of Australia there are regional and seasonal changes in causative organisms that should be noted.
Significantly, CL wear has become an increasing risk factor that has a strong association with Gram –ve isolates to such an extent that he believes it is reasonable to assume that any CL-related MK cases involve Pseudomonas aeruginosa until proved otherwise.
He also argued that CL wear has introduced ‘new’ pathogens, nominating Microsporidia spp. (unicellular, spore-forming fungi), Fusarium spp. (a fungus that can penetrate Descemet’s membrane leading to possible anterior chamber effects), and Acanthamoeba spp. as candidates. However, those involved with CLs would argue that ‘newish’ would be a more appropriate description, as the history of some of those nominees goes back at least 30 years.
He also described the features of MK as being unreliable due to similarities of diseased corneal appearances attributable to disparate organisms. Furthermore, appearances can be altered by steroids, meaning that clinical suspicion often has to be relied upon. Aiding those suspicions are time frames of infections.
For example: bacteria: 1-2 days, with acute presentations, fungi: exhibiting variable time frames, protozoa: sub-acute – 1-7 days, and HSV: subacute – 1-7 days.
To maintain suspicions, Samarawickrama reported that up to one in twenty cases are atypical. To avoid confounding such cases by contamination, he advised wearing a mask while taking corneal scrapes and taking precautions to decrease the likelihood of contaminating the agar plate used with organisms not related to the patient.
He gave the aims of MK treatment as:
- Elimination of infection
- Control of inflammation
- Reduction of pain
- Avoidance of toxicity
- Predict and/or identify complications
- Restore vision
MK involves both sterilisation and healing phases. His routine is to follow a complex algorithm (flowchart/decision path) that includes lists of possibilities, the latter being required due to the significant scope of what is now possible in each case.
No investigation is required in about 95% of cases because they are usually bacterial, the associated infiltrate small (<1 mm), have a sudden onset, and typically have CLs, trauma, or ocular surface disease (OSD) as risk factors.
However, no treatment should commence in the other 5% of cases without investigating the aetiology first because the cause is probably a fungus, Acanthamoeba spp., or an unknown micro-organism. Usually, there is a specific risk factor (CL, trauma, OSD) or no identifiable risk factor and none of the presentation fits clinically with bacterial disease. Investigations include culturing, PCR, and confocal microscopy, especially in possible Acanthamoeba cases.
Treatment can also be empirical in selected cases based on probability and organisms known to be endemic in the local environment. In that context, ongoing local microbial surveillance is useful. Initial therapy should be for bacterial keratitis unless there is strong evidence of an alternative. If there are other additional factors such as corneal exposure, trichiasis, and so on, they should also be treated. Regardless of the foregoing, the audience was advised to treat all diagnoses as being provisional, and if there is no improvement after 5 days a deeper investigation is necessary.
In various comparisons between Ofloxacin (fluoroquinolone) monotherapy and gentamicin-cefazolin dual therapy, there were few differences in performance overall, such as success, rapidity of results, and complications. However, Ofloxacin reduced the risk of ocular discomfort by 68 – 78% and the risk of chemical conjunctivitis by 80%. Additionally, Ciprofloxacin (a quinolone) demonstrated a 24x increased risk of white anterior eye precipitates.
Samarawickrama also detailed the Herxheimer effect (or the Jarisch-Herxheimer effect); an acute inflammatory response that follows microbial death due to the use of appropriate antibiotics. The effect, which can be local or systemic, is due to the release of endotoxins or endotoxin-like products from lysed bacterial cells.
It is common in Gram –ve bacterial keratitis and Acanthamoeba keratitis. The appearance can be paradoxical; the eye can look worse (Herxheimer effect) despite the patient feeling better (the treatment is working).
His 2-week Ofloxacin 0.3% treatment regimen is:
- First 2 days: Hourly day and night
- Days 3 and 4: Hourly by day
- Days 5 to 7: 2 hourly by day
- Days 8 to 14: 4x day (QID)
Resistance to fluoroquinolones was given as 4%, mostly from coagulase-negative Staphylococci and some Pseudomonas aeruginosa variants. If fluoroquinolone resistance is found, cefazolin was recommended for Streptococci and ancomycin for Staphylococci. While vancomycin can be used for all Gram +ve organisms, it is known to be very toxic to the ocular surface and can result in pain, redness, and non-healing ulcers.
On the use of steroids in bacterial keratitis, the results were generally beneficial. Special care is required to avoid their use in cases of Acanthamoeba, fungal infections, HSV, those at risk of perforation, and those who already have had a penetrating keratoplasty.
In one recent Australian study, the use of high-dose steroids (prednisolone/dexamethasone) increased the likelihood of a better outcome by about 5.5%. Samarawickrama summarised his presentation by suggesting that practitioners arm themselves with a knowledge of the locally prevalent organisms, risk factors, and presenting features.
He recommended creating a management algorithm and appropriate cheat sheets, and suggested fluoroquinolone monotherapy for the majority of cases, remembering that about one in twenty will either be Acanthamoeba or a fungus. Of those few cases, about 10% will be found to be polymicrobial. If no improvement is confirmed by 5 days, the case must be investigated further.
Vitreo-retinal surgery – Peripheral retinal degeneration
Canberra-based ophthalmologist Associate Professor Rohan Essex fills various roles including vitreo-retinal specialist, paediatric ophthalmologist, and biostatistician. His presentation was on changes in the peripheral retina, particularly pre-detachment changes.
He commenced with a brief overview of the eye’s normal anatomy with a focus on the vitreous and the ora serrata and adjacent retina. Among the peripheral retinal “curiosities” as he called them were retinal tufts, ‘snowflake’ degeneration, cystic degenerations (reticular peripheral cystoid degeneration), paving stone degeneration (areas of choroidal hypoperfusion – a vascular problem), and areas that turn white when external pressure is applied via a scleral indenter (WWP – white with pressure).
In cases of retinoschisis his advice, based on current literature, is not to operate on the eye unless the condition is acute with symptomatic retinal detachment (RD). The latter has been estimated to occur in only about 0.05% of schisis cases.
In differentiating retinoschisis from RD he offered the following – a schisis is: often infero-nasal, often bilateral, almost always asymptomatic, looks different to a RD in that the retina appears thinner, not wrinkled with clear choroidal detail, it tends to quiver with eye movement rather than wafting seen in RD, outer leaf-like breaks in the retina might be seen, no evidence of changes or reaction on the part of the RPE, and an OCT image will help to visualise.
However, he warned the audience to beware of a schisis in a myope, especially a high myope (defined currently as ≥5 D). Paving stone degeneration has to be differentiated from the non-retinal problem of peripheral reticular pigment degeneration.
Moving on to lattice degeneration, Essex described a condition with criss-crossed white lines that are actually blood vessels exhibiting vessel whitening with a pigment backdrop/background. A loss of the retina’s inner limiting membrane (ILM) or more of its inner layers leads to the appearance of atrophic, round retinal holes. Complicating the appearance can be pockets of liquefied vitreous and/or vitreous condensations and adhesions at the margins. Lattice degeneration can also appear as a series of snail tracks in the retina.
When lattice degeneration and retinal tears occur together the number can vary from several to many. Traditional breaks in the retina have a 30 to 50% chance of progressing to a RD and should therefore be treated. However, operculated tears (previously referred to as horseshoe tears) can be observed rather than treated immediately.
Lattice degeneration in a phakic eye is unlikely to result in a RD in the contralateral eye either (about 1% according to the literature, 2% get round holes, and many fewer than 1% experience horseshoe tears) but if there is a lattice retinal detachment, the fellow eye is more likely to develop tears and/or detachment requiring treatment.
When cataract surgery is performed on a lattice degeneration case, about 3% experience a RD within 5 years of surgery. When there is no lattice degeneration that figure falls to <1%. A posterior vitreous detachment (PVD) occurs in about 79% of cases on average following cataract surgery but that figure is based on 87% if lattice is present and 76% if there is no lattice degeneration.
Tellingly, if lattice is present before cataract surgery, there is 21.3% chance of a RD within 5 years whereas those without lattice have a 0.7% chance of a RD. Essex also noted in passing that laser treatment ‘weakens’ the retina and can cause breaks to form. Partly because of that fact, along with the finding that often retinal breaks form in apparently normal retinal areas, there is no evidence supporting prophylaxis.