Retinal capillary plexus in Parkinson's disease using optical coherence tomography angiography.

AIM: To evaluate the alterations of the retinal microvasculature and foveal avascular zone in patients with Parkinson's disease (PD) using optical coherence tomography angiography (OCT-A). METHODS: A retrospective study of PD patients examined in the Ophthalmology Department of the General Hospital of Athens, "Georgios Gennimatas" from March 2021 to March 2022 was conducted. Totally 44 patients with PD were included and 18 healthy controls were examined, hence a total of 124 eyes were enrolled in the study. The foveal and parafoveal superficial and deep capillary plexus vascular density (fSCP-VD, fDCP-VD, pSCP-VD, pDCP-CD) and foveal avascular zone (FAZ) were quantified with OCTA. Optical coherence tomography (OCT) was used to measure macular thickness. Our statistical analysis was conducted by using a mixed effect linear regression model. RESULTS: After adjustment for age and gender, the mean parafoveal superficial capillary plexus vascular density (pSCP-VD) and mean parafoveal deep capillary plexus vascular density (pDCP-VD) were significantly decreased in individuals with PD (P<0.001 in both) by -2.35 (95%CI -3.3, -1.45) and -7.5 (95%CI -10.4, -4.6) respectively. fSCP-VD and fDCP-VD didn't approach statistical significance. The FAZ area and perimeter were significantly decreased (P<0.001 in both) by -0.1 mm2 (95%CI -0.13, -0.07) and -0.49 mm2 (95%CI -0.66, -0.32) respectively. Circularity didn't approach statistical significance. Central retinal thickness (CRT) was significantly decreased in individuals with PD (P<0.001) by -23.1 µm (95%CI -30.2, -16) and temporal retinal thickness (TRT) was decreased (P=0.025) by -11 µm (95%CI -22, -1.5) while nasal retinal thickness (NRT) only approached statistical significance (P=0.066). CONCLUSION: The mean pSCP-VD, pDCP-VD, CRT and TRT are significantly decreased and FAZ is altered in individuals with PD. These findings can be potentially used as biomarkers for the diagnosis and evaluation of early PD.

A 30-Year-Old Man with a Recent History of COVID-19 Requiring Treatment with Corticosteroids Who Developed Bilateral Central Serous Chorioretinopathy During 7-Month Follow-Up.

BACKGROUND Central serous chorioretinopathy (CSCR) involves a localized serous macular detachment, secondary to retinal pigment epithelial and choroidal vascular changes, which can be an adverse effect of corticosteroid use. Most CSCR cases resolve spontaneously, and normal vision returns, while some chronic cases can result in blindness. This report is of a 30-year-old man with a recent history of Corona virus disease (COVID)-19 requiring corticosteroid treatment who developed bilateral CSCR with unilateral fibrin and a 7-month follow-up. CASE REPORT A 30-year-old male patient presented with malaise and high fever. The patient tested positive for COVID-19, caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus and was admitted. During hospitalization, he received intravenous (IV) corticosteroids for 1 week (6 mg dexamethasone IV once daily). Following hospitalization, the patient received per os methylprednisolone 16 mg (16 mg once daily for 3 days, 8 mg once daily for 3 days, 4 mg once daily for 3 days, and 2 mg once daily for 3 days). One month later, the patient presented with bilateral visual acuity (VA) deterioration and acute CSCR. The diagnosis and follow-up were performed by optical coherence tomography (OCT) and fundus fluorescein angiography (FFA). The patient was followed-up for a period of 7 months, during which, although the VA improved and remained stable, the OCT findings were changing. CONCLUSIONS This report highlights the importance of timely ophthalmological examination in patients with sudden vision loss and identification of the association between corticosteroid use and CSCR, as well as the importance of a longer follow-up period.

Alström's Syndrome, Leber's Hereditary Optic Neuropathy, or Retinitis Pigmentosa? A Case of Misdiagnosis.

A case of a patient with the Alström syndrome (AS) that was misdiagnosed as Leber's hereditary optic neuropathy or retinitis pigmentosa for 13 years is presented. AS is a rare genetic disorder caused by mutations in the ALMS1 gene. AS may lead to abnormal ciliary formation and function. AS affects metabolism, and symptomatology includes type 2 diabetes mellitus (T2DM), obesity, hypogonadism and gynecomastia in males, progressive bilateral sensorineural hearing loss, cardiomyopathy, nonalcoholic fatty liver disease (NAFLD), cirrhosis, and chronic progressive kidney disease. The onset of the above symptoms may vary significantly. The ophthalmic manifestation is early onset cone-rod dystrophy that starts as progressive vision loss, photophobia, and nystagmus in the first months of life. An accurate diagnosis may enable specialists to facilitate a significantly positive effect in the everyday life of a patient. Genetic counseling may also be recommended for these patients. Diagnosis was confirmed by DNA testing, thus highlighting its necessity in everyday practice.

Peripapillary Pachychoroid Syndrome (PPS): Diagnosing and Treating a Rare Entity.

Two cases with peripapillary pachychoroid syndrome (PPS) along with the challenges concerning correct diagnosis and treatment are presented. In the first case, the patient presented with painless unilateral gradual visual loss. Fundoscopy and optical coherence tomography (OCT) revealed cystoid macular edema (CME) in the left eye (LE), extending from the temporal optic disc margin towards the fovea, with no additional findings. Enhanced-depth imaging- (EDI-) OCT provided additional information and increased choroidal thickness nasally to the macula and pachyvessels in the outer choroidal layer, findings supportive of PPS. Photodynamic therapy (PDT) was applied at the leakage sites. Two months later, CME and subretinal fluid (SRF) had resolved, and VA had significantly improved. In the second case, a patient presented with reduced vision and metamorphopsia bilaterally over the previous 5 days. Fundoscopy revealed CME in both eyes. OCT confirmed the presence of CME in the papillomacular area in the right eye; similarly, CME was recorded in the macula of the LE with SRF located subfoveally. EDI-OCT showed increased choroidal thickness in both eyes. Treatment was administered, originally with dorzolamide eye drops along with eplerenone tablets, and then dexamethasone eye drops that eventually led to significant anatomic and functional improvement. It is important for ophthalmologists to be able to recognize the unique clinical entity of PPS, as its resemblance to disorders with similar features may lead to misdiagnoses and unnecessary, or even incorrect, interventions.

Wolfram Syndrome: A case report of two sisters Wolfram Syndrome: Case report of two sisters.

PURPOSE: To present a case of two siblings with optic atrophy associated with Wolfram Syndrome. OBSERVATIONS: Two young adult siblings presented with serious bilateral loss of vision and dyschromatopsia established in early adolescence. They were referred with a presumed diagnosis of Leber's Hereditary Optic Neuropathy. At baseline, visual acuity was 20/400 in the right eye and 20/200 in the left eye in patient A and 20/200 in both eyes in patient B, color perception tested with pseudo-isochromatic plates was 0/17 in each eye, optic discs were pale, visual field testing revealed diffuse scotomas bilaterally while electrophysiology showed delayed prominent positive deflection (P100) values in both patients. Personal history revealed Type 1 diabetes mellitus since early childhood. Patients were lost to follow-up and presented 4 years later with significant VA decrease (<20/400) and suspected hearing loss. At that point, genetic testing revealed a pathogenic variation in the WFS1 gene thus confirming the diagnosis of Wolfram syndrome. Treatment with idebenone was proposed, to which only one of the siblings agreed. The other patient remained under observation, as no known treatment for optic atrophy in Wolfram syndrome exists to date. CONCLUSIONS AND IMPORTANCE: Wolfram syndrome is a rare neurodegenerative genetic disease associated with diabetes mellitus, optic atrophy and deafness. Careful and detailed medical and family history led to appropriate testing that confirmed the diagnosis of Wolfram syndrome. To this day, there is no definite treatment for this disease, but the experimental use of idebenone has been suggested to improve visual function. Genetic testing of family members and offspring of patients is strongly recommended.

Development of Macular Atrophy in Patients with Wet Age-Related Macular Degeneration Receiving Anti-VEGF Treatment.

Age-related macular degeneration (AMD) is a leading cause of blindness. Late AMD can be classified into exudative (commonly known as wet AMD [wAMD]) or dry AMD, both of which may progress to macular atrophy (MA). MA causes irreversible vision loss and currently has no approved pharmacological treatment. The standard of care for wAMD is treatment with anti-vascular endothelial growth factors (VEGFs). However, recent evidence suggests that anti-VEGF treatment may play a role in the development of MA. Therefore, it is important to identify risk factors for the development of MA in patients with wAMD. For example, excessive blockade of VEGF through intense use of anti-VEGF agents may accelerate the development of MA. Patients with type III macular neovascularization (retinal angiomatous proliferation) have a particularly high risk of MA. These patients are characterized as having a pre-existing thin choroid (age-related choroidopathy), suggesting that the choroidal circulation is unable to respond to increased VEGF expression. Evidence suggests that subretinal fluid (possibly indicative of residual VEGF activity) may play a protective role. Patients receiving anti-VEGF agents must be assessed for overall risk of MA, and there is an unmet medical need to prevent the development of MA without undertreating wAMD.

Multifocal Pattern Dystrophy Simulating Fundus Flavimaculatus: Multimodal Imaging for Early Diagnosis.

Multifocal pattern dystrophy simulating fundus flavimaculatus (MPDSFF) is a clinical entity characterized by several clinicopathological, angiographic, tomographic, and electrophysiological findings. A 58-year-old caucasian female patient presented with bilateral floaters and metamorphopsia. Best-corrected visual acuity (VA) was 6/6 in both eyes and intraocular pressure was 14 and 15 mm Hg, respectively. Fundus examination, optical coherence tomography (OCT), autofluoresence (AF), fluorescein angiography (FA) and pattern Electroretinogram were employed for the diagnosis of this case. Clinical and imaging findings were consistent with MPDSFF. Noticeable progression was observed in OCT scans 6 months following the baseline visit, while no significant changes were observed over the following 12 months. Prognosis of VA in MPDSFF patients may remain relatively good even in the presence of considerable anatomic changes. Disease progression may be slow and significant reduction in VA may present only secondary to a choroidal neovascular membrane. Patient follow-up should include OCT scans, PERG, and AF in addition to VA and dilated fundus examination every 6-12 months. As relevant literature is limited and no effective treatment modality has been employed for this clinical entity, the identification of the cellular death pathway in pattern dystrophies may lead to an applicable management approach.

Paramacular Acute Middle Maculopathy Associated with Glyceryl Trinitrate.

An unusual case of nitroglycerin-induced Paracentral Acute Middle Maculopathy (PAMM) is presented. A 50-year-old patient with sudden vision loss and scotoma was followed up with swept-source optical coherence tomography (SS-OCT), optical coherence tomography-angiography (OCT-A), and fluorescein angiography (FA). An anal fissure treated with glyceryl trinitrate (GTN) 0.2% ointment with headache and dizziness after application was reported. Fundoscopy OS revealed mild retinal venous dilatation and tortuosity with scattered blot hemorrhages and subtle, parafoveal, whitish lesions in the outer retina. SS-OCT revealed diffuse, hyperreflective lesions in the inner plexiform (IPL), inner nuclear (INL), and outer plexiform layers (OPL). OCT-A revealed focal dropout in the deep capillary plexus. FA showed masking due to blot hemorrhages and early punctuate leakage in the inner retina. This entity was identified as nitroglycerin-induced PAMM. Over the following 8 months, after discontinuation of the ointment application, the patient was symptom-free with stable visual acuity. OCT revealed INL/OPL thinning and confirmed complete lesion resolution. This first report of retinal vascular abnormalities due to nitrite ointment provides an insight into an unknown side effect of nitroglycerin ointment use. A dose-dependent correlation between GTN application and retinal vascular abnormalities remains to be confirmed.

Epiretinal membrane-induced intraretinal neovascularization.

PURPOSE: To report a 71-year-old male patient diagnosed with epiretinal membrane-induced intraretinal neovascularization. OBSERVATIONS: The presence of an epiretinal membrane (ERM) was confirmed by Optical Coherence Tomography (OCT), fluorescein and indocyanine angiography. Optical coherence tomography angiography (OCT-A) revealed a neovascular membrane within the ERM. Intravitreal ranibizumab injections were administered three times at four-week intervals. Imaging revealed a stable membrane with no leakage. Five months after the third injection, OCT revealed intraretinal fluid. OCT-A showed a new branch of the neo-vascular membrane at the superficial capillary plexus. Following an additional ranibizumab injection, the membrane stabilized. CONCLUSIONS AND IMPORTANCE: It is conceivable that neovascularization developed due to, or in close conjunction with an epiretinal membranes already in place.

A fingerprint hidden inside the eye. A unique pattern of outer retina splitting as seen on en-face OCT and OCT-angiography.

A splitting of the outer plexiform retinal layer in a saw-like hyporeflective pattern in addition to partially formed concentric circles centred at the foveola were observed using en-face OCT and OCT-angiography in a 27-year-old female patient with rhegmatogenous retinal detachment and a 50-year-old female patient with Vogt-Koyanagi-Harada chorioretinopathy.

Peripapillary Choroidal Neovascular Membrane Secondary to Sarcoidosis-Related Panuveitis: Treatment with Aflibercept and Ranibizumab with a 50-month Follow-Up.

A case of peripapillary choroidal neovascular membrane (PCNM) secondary to sarcoidosis-related panuveitis successfully treated with anti-vascular endothelial growth factor (anti-VEGF) agents and systemic immunomodulatory therapy is reported. Diagnosis and follow-up were based on fundoscopic, optical coherence tomography as well as fluorescein angiography findings. A 45-year-old female patient presented with sudden onset bilateral blurring of vision. Fundoscopy revealed bilateral granulomatous panuveitis with solitary peripheral granuloma in the right eye and PCNM in the left eye. Diagnostic work-up including conjunctival biopsy confirmed the diagnosis of sarcoidosis. Topical and systemic corticosteroids controlled the inflammation. Within 4 weeks, PCNM showed rapid enlargement (best-corrected visual acuity [BCVA]: 6/60) with foveal involvement. Monthly intravitreal aflibercept injections and systemic methotrexate were administered. After 5 aflibercept injections, anatomical and functional improvement was noted (BCVA: 6/6). Due to aflibercept unavailability, further treatment included ranibizumab injections. During a 50-month follow-up period, every anti-VEGF injection was followed by total NV regression and 6/6 BCVA. Both aflibercept and ranibizumab appear to be effective in the treatment of PCNM secondary to sarcoidosis.

Extending the phenotypic spectrum of PRPF8, PRPH2, RP1 and RPGR, and the genotypic spectrum of early-onset severe retinal dystrophy.

PURPOSE: To present the detailed retinal phenotype of patients with Leber Congenital Amaurosis/Early-Onset Severe Retinal Dystrophy (LCA/EOSRD) caused by sequence variants in four genes, either not (n = 1) or very rarely (n = 3) previously associated with the disease. METHODS: Retrospective case series of LCA/EOSRD from four pedigrees. Chart review of clinical notes, multimodal retinal imaging, electrophysiology, and molecular genetic testing at a single tertiary referral center (Moorfields Eye Hospital, London, UK). RESULTS: The mean age of presentation was 3 months of age, with disease onset in the first year of life in all cases. Molecular genetic testing revealed the following disease-causing variants: PRPF8 (heterozygous c.5804G > A), PRPH2 (homozygous c.620_627delinsTA, novel variant), RP1 (homozygous c.4147_4151delGGATT, novel variant) and RPGR (heterozygous c.1894_1897delGACA). PRPF8, PRPH2, and RP1 variants have very rarely been reported, either as unique cases or case reports, with limited clinical data presented. RPGR variants have not previously been associated with LCA/EOSRD. Clinical history and detailed retinal imaging are presented. CONCLUSIONS: The reported cases extend the phenotypic spectrum of PRPF8-, PRPH2-, RP1-, and RPGR-associated disease, and the genotypic spectrum of LCA/EOSRD. The study highlights the importance of retinal and functional phenotyping, and the importance of specific genetic diagnosis to potential future therapy.

Comparison of Chemokine CXCL-1 and Interleukin-6 Concentrations in the Subretinal Fluid and Vitreous in Rhegmatogenous Retinal Detachment.

Purpose: Comparison of IL-6 and CXCL-1 concentrations and CXCL-1/IL-6 ratio correlations with clinical parameters (RRD extent, duration, and proliferative vitreoretinopathy - PVR-grade) between subretinal fluid (SRF) and vitreous during rhegmatogenous retinal detachment (RRD) complicated with PVR.Methods: A total of 71 eyes of 71 patients with primary RRD possibly complicated with PVR were included; 36 eyes treated with scleral buckling and 35 eyes with pars-plana vitrectomy. Enzyme-Linked Immuno-sorbent Assay was employed for CXCL-1/IL-6 measurement (ng/ml).Results: Correlation analysis between mean CXCL-1/IL-6 ratio and clinical parameters revealed non-significant results. CXCL-1/IL-6 ratio was significantly elevated in phakic eye vitreous. Optimum circumstances for elevated chemokine levels during RRD were considerable extent (2-3-quadrant) and duration (29-60-day) complicated with PVR C.Conclusions: SRF appears to be characterized by greater chemokine concentrations while vitreous retains several structural characteristics that may assist in investigating inflammation and improving understanding of underlying pathophysiological mechanisms during RRD complicated with PVR.

Acute Visual Loss Secondary to Arnold Chiari Type I Malformation Completely Resolving After Decompressive Posterior Fossa Surgery.

We describe the case of a 22-year-old woman of southeast-Asian origin, presenting with unilateral sudden visual loss after a self-healing hearing loss a week before. Ophthalmological examination showed visual acuity of light perception in the left eye, mild RAPD, normal ocular motility and an elevated optic disc with indistinct margins. Neurological examination showed no acute pathology and brain CT-MRI imaging revealed a small-almost subclinical-herniation of the cerebellar tonsils. As investigation eliminated every other infectious or inflammatory cause of papillitis, neurosurgical intervention was proposed. The patient underwent an uncomplicated occipital craniotomy with posterior fossa decompression and had a favorable revolution with regression of papilledema and a fully recovering visual acuity that reached 20/20. Chiari malformation type I refers to an abnormality of the posterior fossa that has a smaller volume than normal, leading to the herniation of cerebellar tonsils, at least 5 mm below the foramen magnum. The occurrence of papilledema associated with Chiari malformation type 1 is rare. Chiari malformation has, until today, mainly been studied among children populations, usually with a poor visual acuity recovery. The originality of our case report consists in the description of an adult patient case showing unilateral, unusual ophthalmological findings and complete recovery after surgical treatment.

An Unusual Case of Perineural Infiltration and Orbital Invasion of Squamous Cell Carcinoma Associated with Actinic Keratosis.

Actinic keratosis is considered a precancerous lesion, constituting a precursor to squamous cell carcinoma (SCC) formation. Perineural invasion has been observed in patients with cutaneous carcinoma due to local subcutaneous tissue destruction and primarily involves the trigeminal nerve due to rich innervation provided by the supraorbital nerve in addition to the facial nerve. An unusual case of perineural infiltration and orbital invasion of squamous cell carcinoma associated with actinic keratosis is presented. A 70-year-old Caucasian woman presented with complete left eye ophthalmoplegia, total left upper-eyelid ptosis, and facial pain with paresthesia. Computed tomography revealed a process of the soft tissues in the left cheek infiltrating the infraorbital canal, pterygopalatine fossa, inferior orbital fissure, and left cavernous sinus with periosteal adherence. Magnetic resonance imaging revealed pathological extension via the left infraorbital canal with a considerable area of necrosis. Treatment of facial actinic keratosis may not prevent malignant transformation and can delay diagnosis and treatment of SCC. A deep biopsy appears to be essential for a correct diagnosis. Perineural spread of cutaneous SCC may be characterized by insidious progression in the cranial trigeminal nerve, abnormal ocular motility, diplopia, or external ophthalmoplegia.

GUCY2D-Associated Leber Congenital Amaurosis: A Retrospective Natural History Study in Preparation for Trials of Novel Therapies.

PURPOSE: To describe the natural history of Leber congenital amaurosis (LCA) associated with GUCY2D variants (GUCY2D-LCA) in a cohort of children and adults, in preparation for trials of novel therapies. DESIGN: Retrospective case series. METHODS: Participants: Patients with GUCY2D-LCA at a single referral center. PROCEDURES: Review of clinical notes, retinal imaging including fundus autofluorescence (FAF) and optical coherence tomography (OCT), electroretinography (ERG), and molecular genetic testing. MAIN OUTCOME MEASURES: Demographic data, symptoms at presentation, visual acuity, evidence of progression, OCT and FAF findings, ERG assessment, and molecular genetics. RESULTS: Twenty-one subjects with GUCY2D-LCA were included, with a mean follow-up ± standard deviation (SD) of 10 ± 11.85 years. Marked reduction in visual acuity (VA) and nystagmus was documented in all patients within the first 3 years of life. Fifty-seven percent (n = 12) exhibited photophobia and 38% (n = 8) had nyctalopia. VA was worse than hand motion in 71% of the patients (n = 15). Longitudinal assessment of VA showed stability in all patients, except 1 patient who experienced deterioration over a follow-up of 44 years. Hyperopia was reported in 13 of the 17 subjects (71%) with available refraction data. Eighteen subjects had either normal fundus appearance (n = 14) or a blond fundus (n = 3), while only 4 of the eldest subjects had mild retinal pigment epithelium (RPE) atrophy (mean, 49 years; range 40-54 years). OCT data were available for 11 subjects and 4 different grades of ellipsoid zone (EZ) integrity were identified: (1) continuous/intact EZ (n = 6), (2) focally disrupted EZ (n = 2), (3) focally disrupted with RPE changes (n = 2), and (4) diffuse EZ disruption with RPE changes (n = 1). All examined subjects had stable OCT findings over the long follow-up period. Full-field ERGs showed evidence of a severe cone-rod dystrophy in 5 of 6 patients and undetectable ERGs in 1 subject. Novel genotype-phenotype correlations are also reported. CONCLUSION: GUCY2D-LCA is a severe early-onset retinal dystrophy associated with very poor VA from birth. Despite the severely affected photoreceptor function, the relatively preserved photoreceptor structure based on EZ integrity until late in the disease in the majority of subjects suggests a wide therapeutic window for gene therapy trials.

Deep Phenotyping of PDE6C-Associated Achromatopsia.

Purpose: To perform deep phenotyping of subjects with PDE6C achromatopsia and examine disease natural history. Methods: Eight subjects with disease-causing variants in PDE6C were assessed in detail, including clinical phenotype, best-corrected visual acuity, fundus autofluorescence, and optical coherence tomography. Six subjects also had confocal and nonconfocal adaptive optics scanning light ophthalmoscopy, axial length, international standard pattern and full-field electroretinography (ERG), short-wavelength flash (S-cone) ERGs, and color vision testing. Results: All subjects presented with early-onset nystagmus, decreased best-corrected visual acuity, light sensitivity, and severe color vision loss, and five of them had high myopia. We identified three novel disease-causing variants and provide phenotype data associated with nine variants for the first time. No subjects had foveal hypoplasia or residual ellipsoid zone (EZ) at the foveal center; one had an absent EZ, three had a hyporeflective zone, and four had outer retinal atrophy. The mean width of the central EZ lesion on optical coherence tomography at baseline was 1923 µm. The mean annual increase in EZ lesion size was 48.3 µm. Fundus autofluorescence revealed a central hypoautofluorescence with a surrounding ring of increased signal (n = 5). The mean hypoautofluorescent area at baseline was 3.33 mm2 and increased in size by a mean of 0.13 mm2/year. Nonconfocal adaptive optics scanning light ophthalmoscopy revealed residual foveal cones in only one of two cases. Full-field ERGs were consistent with severe generalized cone system dysfunction but with relative preservation of S-cone sensitivity. Conclusions: PDE6C retinopathy is a severe cone dysfunction syndrome often presenting as typical achromatopsia but without foveal hypoplasia. Myopia and slowly progressive maculopathy are common features. There are few (if any) residual foveal cones for intervention in older adults.

Optical Coherence Tomography Angiography of Foveal Neovascularization in Diabetic Retinopathy.

PURPOSE: To report a case of foveal neovascularization in a patient with proliferative diabetic retinopathy as seen on optical coherence tomography angiography (OCT-A). METHODS: Multimodal imaging was used for diagnostic investigation. PATIENT: A 61-year-old male with a 16-year history of insulin-dependent diabetes mellitus was referred to our medical retina department for examination and management. Meticulous fundus examination and multimodal imaging revealed proliferative diabetic retinopathy lesions, including neovascularization located in the foveal area. RESULTS: OCT-A allowed us to detect the neovascular lesion, confirm that it originated from perifoveal capillaries, estimate its retinal depth, and evaluate the vessel blood flow in multiple layers. CONCLUSION: To the best of our knowledge this is the first report of OCT-A imaging of foveal neovascularization in diabetic retinopathy. OCT-A is a very useful examination for the diagnostic investigation of patients with diabetic retinopathy.

Managing high risk glaucoma with the Ahmed valve implant: 20 years of experience.

AIM: To estimate the efficacy and safety of the Ahmed implant in patients with high risk for failure after glaucoma surgery. METHODS: In 342 eyes of 342 patients with refractory glaucoma, even with application of medical treatment, the Ahmed valve was introduced for intraocular pressure (IOP) control, in the period of the last 20y. The nature of glaucoma was neovascular in 162 eyes, pseudophakic or aphakic in 49 eyes, inflammatory in 29 eyes and non working previous antiglaucomatic surgical interventions in 102 eyes. RESULTS: Follow-up ranged from 18 to 120mo with a mean follow-up of 63.2mo. IOP before the operation decreased from 31.6±10.4 mm Hg to 18.3±5.4 mm Hg (no systemic treatment) at the end of follow up period. When we compared the IOP values before the operation using ANOVA showed statistically significant difference (P<0.001). The success rate was 85.2% during the first semester, 76.8% at 12mo and 50.3% at the end of follow up period (18 to 120mo after implantation). Success rate was 25.7% in neovascular glaucoma, 63.2% in aphakic glaucoma and 73.8% in non working previous antiglaucomatic surgical interventions. Complications due to the implant were: serous choroidal detachment in 14.8%, blockage of the tube in 2.8%, malposition of the tube in 4.9%, suprachoroidal hemorrhage in 2.1%, cataract progression in 39.6% (phakic eyes), shallow anterior chamber in 9.2%, hyphaema in 28.9%, exposure of valve in 2.6%, exposure of tube in 9.3%, hypotony in 4.9% and conjunctival fibrosis in 41.5%. CONCLUSION: Despite the fact that Ahmed valve implant had suchlike results as other implants concerning the IOP control, complications rate due to hypotony or over filtration in the first days after the intervention are not that frequent as with other valve implants.