Eye pain is a common presentation in outpatient, urgent care, and emergency settings. Causes range from benign to vision-threatening. Family physicians should promptly identify red-flag features that require urgent or emergent ophthalmology referral. A painful eye with vision loss, severe photophobia, proptosis, hyphema, or corneal ulceration is a medical emergency. Patient history should include onset, associated vision changes, contact lens use, trauma, chemical exposure, systemic symptoms, and rheumatologic disease. Physical examination should include evaluation of visual acuity (eg, using a Snellen or Rosenbaum chart), pupillary reactions, and extraocular movements. The eyes should be inspected for redness, discharge, and corneal lesions with fluorescein, if available. Findings of significant photophobia, anisocoria, dendritic corneal lesions, or restricted eye movement should prompt immediate referral. Common emergent causes of eye pain include acute angle-closure glaucoma, orbital cellulitis, infectious keratitis, scleritis, and anterior uveitis. An algorithmic approach that distinguishes urgent vs nonurgent etiologies and ophthalmic vs nonophthalmic causes of eye pain can direct next steps.

Uveitis and scleritis are well-recognized extraintestinal manifestations of inflammatory bowel disease (IBD). Although ocular involvement typically follows IBD diagnosis, a meaningful subset of patients presents to ophthalmologists before intestinal disease is recognized, sometimes years earlier. Despite this, no standardized ophthalmologic screening protocols exist to guide early detection. We synthesized cohort studies, meta-analyses, and Mendelian randomization evidence on the ocular-intestinal temporal relationship in IBD. Patients with uveitis or scleritis have approximately double the risk of a subsequent IBD diagnosis (adjusted HR 1.44-2.25), with median diagnostic intervals exceeding two years and often longer in pediatric populations (>5 years). Mendelian randomization studies provide genetic evidence supporting a causal effect of IBD on uveitis. In a large pediatric cohort (n = 2,555), ocular manifestations preceded IBD in approximately 20% of cases. Uveitis occurs more frequently in Crohn's disease than in ulcerative colitis, and no ophthalmology guideline provides actionable screening criteria for IBD. We propose a tiered, risk-stratified framework to identify undiagnosed IBD in ophthalmology settings: (Tier 1) universal gastrointestinal symptom screening for non-infectious or recurrent uveitis and all scleritis; (Tier 2) targeted laboratory evaluation, including fecal calprotectin in high-risk patients; and (Tier 3) low-threshold gastroenterology referral for positive screens or persistent clinical concern. Lower referral thresholds are appropriate in pediatric populations. This framework is proposed to complement clinical judgment and requires prospective validation before adoption as standard practice. By recognizing ocular inflammation as an early systemic signal, ophthalmologists are uniquely positioned to reduce diagnostic delay and improve interdisciplinary care in IBD.

Psoriatic arthritis (PsA) is an immune-mediated inflammatory disease in which the IL-23/Th17/IL-17 axis contributes to musculoskeletal and extra-musculoskeletal inflammation. Ocular manifestations, particularly dry eye disease (DED), uveitis, and less frequently episcleritis and scleritis, are increasingly recognized across psoriatic disease, although their pathobiology and relationship to systemic inflammatory pathways remain incompletely defined.

This case report describes a case of Providencia stuartii panophthalmitis, a rare opportunistic ocular infection. A 58-year-old lady with diabetes mellitus presented with painful vision loss in the left eye for one day. Visual acuity was light perception with a relative afferent pupillary defect. Examination showed limitation of extra-ocular muscle movement in all gazes, proptosis, erythematous lid swelling, conjunctival injection, oedematous cornea, and hypopyon with fibrin in the anterior chamber. B-scan showed vitritis, loculations, and scleritis. Vitreous culture revealed P. stuartii. Concurrently,contrast-enhanced computed tomography (CECT) of the orbit demonstrated left eye proptosis, circumferential scleral thickening and enhancement, choroidal enhancement, and fat stranding across both the intraconal and extraconal spaces, highly suggestive of panophthalmitis. She was treated with intravitreal vancomycin and ceftazidime, topical ciprofloxacin and ceftazidime, and systemic ciprofloxacin and meropenem. Due to corneal perforation, evisceration was done. Vitreous, uveal, and conjunctival cultures grew P. stuartii. Chemosis and eye discharge were reduced with topical cefuroxime and chloramphenicol, but with residual necrotic tissue. P. stuartii infection is a rare and serious ocular infection with a poor visual outcome.

A 70-year-old male patient presented to Wuhan Aige Eye Hospital with a 1-month history of redness, pain, decreased vision in the right eye, and the pain was aggravated at night. Examination revealed multiple nodular scleral abscesses. After incision and drainage, nanopore targeted sequencing of the specimens identified Aspergillus flavus as the pathogen. The patient was diagnosed with fungal scleritis (scleral abscess) of the right eye. Susceptibility-guided systemic and topical antifungal therapy was administered for one month, leading to complete recovery. No recurrence was observed during the 5 months of follow-up.

Livedoid vasculopathy (LV) is a rare thrombo-occlusive disorder of the dermal microcirculation that may clinically resemble inflammatory vasculitis. In patients with rheumatoid arthritis (RA), the development of painful lower extremity ulcers often raises concern for rheumatoid vasculitis, making histopathological evaluation essential for accurate diagnosis and treatment selection. We present a case of a 45-year-old man with an eight-year history of seropositive RA receiving methotrexate, sulfasalazine, and baricitinib who developed painful lower extremity ulcers, edema, and episcleritis in the setting of high disease activity (Disease Activity Score 28 using C-reactive protein {DAS28-CRP} of 6.23). Given the suspicion of rheumatoid vasculitis, an extensive diagnostic workup was performed. Laboratory studies demonstrated elevated inflammatory markers and negative antineutrophil cytoplasmic antibodies. Skin biopsy revealed vascular wall hyalinization, luminal obliteration, and fibrin thrombi in the absence of inflammatory infiltrates or fibrinoid necrosis, establishing the diagnosis of livedoid vasculopathy. Treatment with systemic glucocorticoids and rituximab, administered according to the standard rheumatoid arthritis regimen, resulted in partial improvement in ocular inflammation, joint symptoms, and cutaneous ulceration. Anticoagulant therapy was not initiated because treatment escalation was primarily directed toward uncontrolled rheumatoid arthritis and severe extra-articular manifestations. Histopathological examination demonstrated vascular wall hyalinization, luminal obliteration, and fibrin thrombi in the absence of significant vascular inflammation or fibrinoid necrosis, establishing the diagnosis of livedoid vasculopathy and excluding rheumatoid vasculitis. Although initial clinical improvement was observed, recurrent ocular symptoms and persistent lower extremity ulceration developed following interruption of biologic therapy. Histopathological confirmation demonstrating thrombotic microvascular occlusion without vascular inflammation was essential for establishing the diagnosis and avoiding misclassification as rheumatoid vasculitis. This case highlights the importance of tissue diagnosis in patients with RA presenting with ulcerative cutaneous lesions and emphasizes the need to consider livedoid vasculopathy in the differential diagnosis of suspected rheumatoid vasculitis.

Janus kinases (JAKs) are a family of intracellular, non-receptor tyrosine kinases that play a crucial role in the JAK signaling pathway involved in the inflammatory process. Over the years, this pathway has garnered significant interest among researchers, leading to the development of various therapeutic agents aimed at blocking the pathway, thereby contributing to remarkable progress in the management of inflammatory diseases across multiple medical specialties. Although the use of JAK inhibitors in ophthalmology is still limited, evidence is gradually emerging on their role in managing uveitis and scleritis. One such agent is tofacitinib, a small-molecule pan-JAK inhibitor. Its therapeutic profile differs from that of biologics due to its partial and reversible inhibition of cytokines. Additionally, owing to its smaller molecular size, the drug is available in an oral formulation. In recent years, there has been a growing interest in JAK inhibitors, particularly tofacitinib, as a potential therapeutic option for refractory uveitis and scleritis in both adult and pediatric populations. Tofacitinib, either as monotherapy or in combination, has shown effectiveness in managing various uveitis cases that were unresponsive to conventional immunosuppressive therapies. It has also been explored in treatment-resistant scleritis. However, concerns persist regarding the potential adverse effects of tofacitinib, including cardiovascular events, thromboembolism, malignancies, and infections. This review aims to provide a comprehensive update on the role of tofacitinib in ocular inflammation, with particular emphasis on its clinical efficacy, safety profile, and the emerging literature surrounding its risks and side effects.