Aqueous flare and cells are inflammatory parameters of anterior chamber inflammation resulting from disruption of the blood-ocular barrier. The ocular inflammation related to anterior chamber cells and flare is assessed by conventional clinical grading systems through using the slit-lamp examination. However, a more quantitative and objective assessment is needed for more precise and reproducible inflammatory assessment in uveitis. Laser flare photometer (LFP) was introduced as a noninvasive, objective, and quantitative evaluation of aqueous flare intensity and number of cells in the anterior chamber with good accuracy and repeatability. The success of LFP allowed clinicians to further evaluate the pathophysiology of intra-ocular inflammation and to incorporate LFP measurements to their routine clinical practice for diagnosis, management, and treatment of uveitis cases. In this review, we will discuss the importance of clinical utilization of LFP and the correlation between LFP and clinical grading systems along with some technical aspects. Furthermore, we will give a literature summary on the current applications of LFP in clinical practice of cases which present with various types of uveitis and diverse ocular conditions with or without inflammation.

Posterior uveitis is sight-threatening disease entity that can be caused by infectious and non-infectious entities. Vision loss in posterior uveitis can be following complications such as cystoid macular edema, epiretinal membrane, artery and vein occlusions, vasculitis, papillitis, choroidal neovascular membrane, retinal neovascularization, tractional retinal detachment, vitreous hemorrhage, glaucoma, cataract, among others. Diagnosis of posterior uveitic entities have been revolutionized following introduction of choroidal imaging with techniques such as indocyanine green angiography (ICGA), optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA). Med Line search and PubMed search was performed pertaining to causes of posterior uveitis, ICGA in posterior uveitis, OCT in posterior uveitis, OCTA in posterior uveitis, retinal and choroidal vascular changes in posterior uveitis, quantification of choriocapillaris lesion area in posterior uveitis, subfoveal choroidal thickness in posterior uveitis, quantification of choriocapillaris in posterior uveitis, vascular indices for quantification of choriocapillaris. This review article highlights various changes in the choroid and the quantification of choroid using various parameters in ICGA, OCT and OCTA.

Anterior uveitis has various causes, but the majority of cases are viral induced. The most common viral anterior uveitis etiology includes double-stranded DNA viruses of the Herpesviridae family, including Alpha herpes virinae (herpes simplex 1 and 2 and varicella zoster virus), Beta herpesvirinae (cytomegalovirus), and less frequently, Gamma herpesvirinae (Epstein-Barr virus). In the last few decades, a growing body of evidence has correlated Fuchs uveitis etiology to the rubella virus from the Matonaviridae family, which has a single-stranded RNA genome. The clinical presentation of each of these uveitis is hypertensive granulomatous anterior uveitis; however, the very slight differences between them, which often overlap, make differential diagnosis sometimes difficult. Therefore, diagnostic laboratory tests such as polymerase chain reaction and antibody index or Goldmann-Witmer coefficient analyses on the aqueous humor help to identify the etiology in doubtful cases and thus to plan targeted treatment.

Till today, ocular tuberculosis (OTB) presents clinicians with significant challenges in diagnosis and management. There is no one-size-fits-all approach to a heterogeneous disease like OTB, and clinicians often have to consider a multitude of factors when initiating treatment, such as tuberculosis endemicity, the probability of a true OTB diagnosis in the setting of nonspecific ocular features, the effective duration of treatment, and the likelihood of vision-threatening complications in the patient. It is no wonder that treatment protocols are widely varied globally. There have been recent developments in the standardization of nomenclature and therapeutic strategies for OTB, as established by the Collaborative OTB Study Working Group. In this review, we referred to findings in retrospective studies, international clinical guidelines, and OTB consortiums, to explore the clinical presentations, investigations, and updated management principles for patients with presumed tubercular uveitis.

Rickettsioses are worldwide distributed infectious disease caused by intracellular small Gram-negative bacteria transmitted to humans by the bite of contaminated arthropods, such as ticks. Systemic disease typically consists of a triad of high fever, headache, and skin rash. It usually has a self-limited course, but severe, life-threatening complications can sometimes occur. It may be clinically difficult to differentiate rickettsial diseases from other febrile illnesses. Rickettsial infection has been largely underestimated as a cause of infectious uveitis for long decades in the past. Conversely, recent data show that ocular involvement is much more common than previously thought, with retinitis, retinal vasculitis, and neuroretinitis being the most typical and frequent findings. Early clinical diagnosis of rickettsial disease, while awaiting laboratory test results, is essential for prompt initiation of appropriate antibiotic treatment to prevent systemic and ocular morbidity. The prevention remains the mainstay of rickettsial infection control.

PURPOSE: We investigated the efficacy and safety of adalimumab (ADA) treatment for chronic recurrent Vogt-Koyanagi-Harada (VKH) patients with sunset glow fundus (SGF). METHODS: Medical records of 50 chronic recurrent VKH patients with SGF who received ADA treatment for more than 6 months were retrospectively reviewed. RESULTS: The mean age of chronic recurrent VKH patients with SGF was 55.9 ± 14.4 years, and the male/female ratio was 26/24. Before ADA treatment, the mean daily dose of systemic corticosteroids was 16.5 ± 12.7 mg, and 22 patients (44%) were under immunosuppressors. LogMAR visual acuity (VA), flare counts, subfoveal choroidal thickness (SFCT), indocyanine green angiography scores, and corticosteroid and cyclosporine doses were significantly reduced by ADA treatment at 6 months compared to baseline. Among all parameters, flare count was significantly related to LogMAR VA. LogMAR VA was significantly related to flare counts but not to SFCT nor to ICGA scores. ADA treatment was continued in 94%. CONCLUSION: ADA was shown to be effective in achieving remission of chronic recurrent VKH disease with SGF refractory to conventional treatments, and was generally well tolerated with few serious adverse events.

This case report describes the association between acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and Epstein–Barr virus (EBV) infection. A 26-year-old female presented with acute bilateral blurred vision and paracentral scotoma. The patient also had prodromal flu-like symptoms. Funduscopic examination showed bilateral yellow-white placoid lesions at the level of retinal pigment epithelium (RPE). Fluorescein Angiography showed characteristic early hypofluorescence and late hyperfluorescence of the lesions. The diagnosis of APMPPE was made based on these findings. Laboratory investigation showed a positive result for EBV serology test. Severe dry eye symptoms were presented at the end of 6-month follow-up. APMPPE may be associated with acute systemic EBV infection.

A 58-year-old male who underwent cataract extraction with combined intraocular lens and Hydrus^® Microstent (Ivantis Inc, Irvine, CA, US) implantation 2 years ago in the right eye (OD) due to advanced glaucoma presented with blurry vision in right eye (OD) for 3 months. The visual acuity was 20/60 and slit-lamp examination indicated mild anterior chamber inflammation with unexposed, functioning tube shunt superotemporally in OD. Optical coherence tomography demonstrated cystoid macular edema (CME) with subretinal fluid. Fluorescein angiography demonstrated petaloid pattern leakage of CME. Gonioscopy revealed a kinked appearance of a Hydrus^® Microstent protruding into the anterior chamber and causing iris chafing. Topical ketorolac tromethamine and prednisolone acetate were started. At the 2^nd month of follow-up, the anterior chamber was quiet, and the CME resolved completely. Protruded kinked Hydrus^® Microstent may lead to acute iridocyclitis and CME through iris chafing, which may be responsive to topical anti-inflammatory drops.

To describe two cases of Behçet's retinitis lesions in the macula causing sloughing of retinal tissue forming a full-thickness macular hole. This was a case series study. Case 1 was a 26-year-old presented, known case of Behçet's disease, presented with a large area of retinitis involving the center of the macula with overlying vitritis. One day after the initiation of treatment, vitritis improved, but the retinitis patch sloughed and created a full-thickness macular hole. Case 2 was a 31-year-old male, known case of Behçet's uveitis, who presented vitritis and multiple retinitis patches involving the macula of the left eye. Two weeks after infliximab infusion, the inflammation resolved with medical management, however, the retinitis patch was complicated by a full-thickness macular hole with an inferior rhegmatogenous retinal detachment. Retinitis at the macula can be complicated by a full-thickness macular hole.

A 20-year-old male Behçet uveitis (BU) patient presented with visual acuities (VAs) of hand movement in OD and counting fingers at 1 m in OS following treatment with corticosteroid monotherapy elsewhere. He had active intraocular inflammation OU along with macular hole and retinal detachment in OS. Infliximab (IFX) was started and vitreoretinal surgery was performed. He had infusion reaction with IFX, hepatotoxicity and depression with interferon, and resistance to adalimumab and tocilizumab therapies. Cytomegalovirus retinitis developed in OD following intravitreal dexamethasone implant and endophthalmitis developed in OS. At the 33^rd month of follow-up, the patient was in clinical remission; however, there was persistent angiographic inflammation under certolizumab pegol, cyclosporine, mycophenolate mofetil, and low-dose prednisolone treatment. The left eye was phthisical and VA was 0.4 in OD. Immunomodulatory treatment is given based on the severity of inflammation in BU and needs to be closely monitored for efficacy and adverse effects.