This Week in Ophthalmology — Sep 27, 2026

This AudioScholar briefing is generated by artificial intelligence for healthcare professionals and trainees. It is not medical advice.

Welcome to This Week in Ophthalmology. This week we're covering 10 notable papers spanning prevention of blinding retinal disease in children and inherited syndromes, the medical retina evidence base for vein occlusion and diabetic retinopathy, corneal and anterior segment safety, and the systemic-ocular interface, from drug ototoxicity to nutritional deficiency after bariatric surgery. Let's dive in.

We start with prevention, where the strongest paper of the week comes from Ophthalmology. Stickler syndrome is the commonest cause of retinal detachment in children, and while prophylactic cryotherapy is well established in type 1 disease, type 2 has never had a comparably large evaluation. Fleet and colleagues report a national retrospective comparative series of 197 patients with genetically confirmed type 2 Stickler syndrome, comparing time to retinal detachment in those who received the Cambridge prophylactic cryotherapy protocol against untreated controls [1]. Among bilaterally treated patients, the risk of detachment in controls was almost six times higher, and even after patient matching the untreated group still carried roughly three times the risk. The most striking signal was in second eyes: among patients who had already detached one retina, those who did not receive prophylaxis in the fellow eye had around a tenfold higher risk of losing that eye to detachment as well. No patient suffered a serious long-term adverse effect from the prophylaxis itself. This is retrospective, non-randomised evidence from a single national protocol, and the matched estimate is less emphatic than the unmatched one, but it is the largest dataset that exists in this population and it supports extending prophylaxis beyond type 1 disease.

Staying with paediatric prevention, Progress in Retinal and Eye Research carries a broad review from Zhang and colleagues on retinopathy of prematurity in the anti-VEGF era [2]. The authors emphasise that the disease now looks different depending on where you practise: in high-income settings severe disease clusters in extremely preterm infants, whereas in many low- and middle-income countries neonatal survival has outpaced screening capacity, so larger and more mature babies are affected too. On treatment, their reading of the evidence is that anti-VEGF is best supported for Zone I, posterior Zone II and aggressive disease, where it can produce rapid regression and allow continued peripheral vascularisation, while laser retains a role for anterior disease, for residual avascular retina, and in settings where reliable follow-up cannot be guaranteed. Surgery remains necessary for advanced tractional disease. They note that ranibizumab and aflibercept appear to have more reassuring systemic profiles than bevacizumab, though long-term comparative data are limited, and that faricimab and topical dexamethasone remain investigational. The recurring caution is that late reactivation and persistent avascular retina make short-term regression an inadequate definition of success.

Turning to medical retina, two papers address how far our pharmacology can be pushed. In the British Journal of Ophthalmology, Wei and colleagues report the BRAVE trial, a randomised study of 255 patients with macular oedema secondary to branch retinal vein occlusion treated with intravitreal conbercept [3]. At six months, the conbercept group gained about 17 letters compared with about 9 letters in the control group, a clear and statistically significant separation, accompanied by greater reduction in central retinal thickness. By twelve months, after the control group had also received conbercept followed by as-needed dosing, the gap narrowed to roughly 17 letters versus 14, and the anatomical advantage actually reversed in favour of the control arm. Rates of ocular and non-ocular safety events were low. The honest reading is that early treatment buys earlier visual gain, with the twelve-month differences much smaller.

Alongside that, Survey of Ophthalmology publishes a careful meta-analysis from Yaldo and colleagues on systemic fibrates in diabetic retinopathy, and the value here is that they separate prevention from progression [4]. Pooling two randomised trials, they found no evidence that fenofibrate reduces incident diabetic retinopathy in patients who do not yet have it, and they are explicit that this estimate is imprecise and cannot exclude a modest benefit or harm, at low certainty. In patients with established disease, however, five randomised trials showed progression reduced by roughly forty percent, and progression to diabetic macular oedema cut by about half, at moderate certainty. Non-randomised data pointed the same way. So the evidence supports a stage-specific role, strongest in eyes that already have retinopathy, and remains inconclusive for primary prevention.

On the anterior segment, the American Journal of Ophthalmology reports a systematic review and meta-analysis by Sadek and colleagues comparing de novo glaucoma and ocular hypertension after Descemet membrane endothelial keratoplasty versus Descemet stripping automated endothelial keratoplasty, drawing on 33 studies and more than five thousand glaucoma-naive eyes [5]. Pooled incidence of new glaucoma was about 3 percent after DMEK against 11 percent after DSAEK, with ocular hypertension at 9 percent versus 34 percent, and the DSAEK cohorts were followed roughly twice as long, yet rate-based analyses still favoured DMEK. Two important caveats temper this. When glaucoma was restricted to optic nerve or visual field criteria, the difference narrowed to about 5 versus 8 percent and was no longer statistically significant, and the head-to-head comparison also favoured DMEK but did not reach significance. Greater steroid exposure was independently associated with ocular hypertension, and overall certainty was graded low to very low. The authors conclude the pattern is consistent but the magnitude attributable to technique itself remains genuinely uncertain.

Cornea is also served by a review in the British Journal of Ophthalmology from Rousseau and colleagues on refractory herpes simplex keratitis [6]. Their framework is to re-interrogate the mix of viral replication, immune inflammation and neurotrophic dysfunction whenever a patient fails to improve, and to revisit adherence and drug exposure before escalating. They discuss steroid-sparing immunomodulators, growth factor–based therapies, autologous serum, recombinant nerve growth factor and scleral lenses for the neurotrophic component, and flag aciclovir-resistant HSV-1 as a growing problem in immunocompromised and long-treated patients, where trifluridine, foscarnet and helicase-primase inhibitors such as amenamevir have shown clinical efficacy. This is narrative synthesis rather than trial evidence, but it maps the options well.

Two papers this week sit at the systemic-ocular interface. In Survey of Ophthalmology, Lee and colleagues pooled 22 studies and 856 teprotumumab-treated patients with thyroid eye disease to quantify ototoxicity [7]. Any otologic adverse event occurred in about 27 percent of patients, clinically significant ototoxicity in around 8 percent, and among those undergoing serial audiometry, objective changes in about a fifth. Compared with placebo, teprotumumab raised the risk of otologic events nearly four-fold, and among affected patients close to four in ten still had impairment at last follow-up. Crucially, ascertainment drove the heterogeneity: active surveillance detected events at roughly twice the rate of passive reporting, at 42 percent versus 20 percent. Pre-existing hearing loss, older age and diabetes were associated with higher risk. The authors conclude these figures support baseline audiometric assessment, active symptom surveillance and explicit counselling about the possibility of persistent hearing loss.

The second, in the American Journal of Ophthalmology, is a systematic review from Abdel-Sayyed and colleagues on vitamin A deficiency after bariatric surgery [8]. Biochemical deficiency was procedure-specific: about 18 percent after Roux-en-Y gastric bypass, rising to 59 percent after biliopancreatic diversion, and reaching roughly 63 percent in pregnancy after gastric bypass. Night blindness was reported in about 60 percent of symptom-assessed cohorts. Median latency to ocular presentation was five years after gastric bypass but between 14 and 27 years after biliopancreatic diversion, jejunoileal bypass or revisional procedures. Encouragingly, 13 of 14 patients with assessable ocular outcomes improved or resolved with repletion. Certainty was limited by heterogeneity and small subgroups, but the authors argue that nyctalopia or unexplained visual decline in a post-bariatric patient warrants serum retinol testing regardless of how long ago the surgery was.

Finally, two cohort studies on ocular surface tumours and severe intraocular infection. In Ophthalmology, Mastrogiuseppe and colleagues describe a sequential multimodal protocol for conjunctival melanocytic lesions in 165 eyes at a single ocular oncology centre, combining excision or biopsy, topical chemotherapy, and adjuvant brachytherapy or proton beam therapy [9]. High-grade intraepithelial lesions recurred most often, in about a quarter of eyes and earliest, at a median of about eight months, while low-grade lesions recurred in roughly one in nine. Metastasis occurred only in invasive melanoma, in about 11 percent. Non-bulbar involvement and residual pigmentation after primary therapy independently predicted local recurrence, while ulceration, non-bulbar location and greater tumour thickness predicted metastatic spread. And in the American Journal of Ophthalmology, Kelly and colleagues report 305 eyes with culture-positive endogenous endophthalmitis across nine academic centres over twelve years [10]. Staphylococcus aureus accounted for nearly four in ten cases and fungal infection about a fifth. Blood cultures were positive in about two thirds of eyes but vitreous in only about a third, and paired blood and eye cultures grew the same organism in only about 62 percent of cases, which complicates pathogen-directed therapy. Worse presenting acuity was the dominant prognostic factor throughout, and enucleation was most frequent with gram-negative organisms, at about 28 percent overall and reaching 86 percent with Serratia.

If you only have time for one paper this week, make it the Stickler syndrome study in Ophthalmology [1]. It answers a question that has sat open for years — whether the prophylaxis benefit demonstrated in type 1 disease extends to type 2 — and it does so in the largest genetically confirmed cohort assembled, with a particularly hard-to-ignore signal in fellow eyes.

Here is what this week's evidence adds up to in Ophthalmology. First, prophylaxis against retinal detachment in genetically confirmed type 2 Stickler syndrome now has substantial, though retrospective, support, with the strongest effect in second eyes. Second, for diabetic retinopathy, the fibrate evidence is stage-specific: reasonably firm for slowing progression and reducing progression to macular oedema in established disease, and genuinely inconclusive for primary prevention. Third, DMEK is consistently associated with fewer new glaucoma and ocular hypertension events than DSAEK, but the certainty is low, steroid exposure confounds the comparison, and strict optic-nerve definitions blunt the difference. Fourth, teprotumumab ototoxicity is considerably more common than passive reporting suggests, and persists in a substantial minority, which the authors take as support for baseline audiometry and structured counselling. And finally, in endogenous endophthalmitis, presenting acuity remains the dominant predictor of outcome, while gram-negative infection, especially Serratia, carries a markedly higher risk of globe loss — and low intraocular culture yield remains an unsolved diagnostic problem.

That's your roundup for This Week in Ophthalmology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

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