Superior limbic keratoconjunctivitis (SLK) is a chronic inflammatory disorder of the ocular surface, primarily affecting the superior bulbar and palpebral conjunctiva. It predominantly occurs in middle-aged women and is associated with conditions, such as dry eye disease, thyroid eye disease, and ocular graft-versus-host disease. Although its exact etiology remains unclear, mechanical microtrauma and tear film instability are key contributing factors. Given its relapsing-remitting nature, early diagnosis and appropriate management are essential to prevent chronic ocular discomfort and visual disturbances. To provide a comprehensive review of the pathophysiology, clinical presentation, diagnosis, and management strategies for SLK, emphasizing the latest advances in medical and surgical treatment. A literature review was conducted to analyze current evidence on the mechanisms, diagnosis, and treatment of SLK. The therapeutic approaches were categorized into medical, mechanical, and surgical interventions, highlighting their indications, efficacy, and limitations. Emerging treatments and their potential role in SLK management were also evaluated. SLK is an often underdiagnosed yet significant ocular surface disorder that requires a customized treatment approach. The management of SLK focuses on minimizing mechanical friction and controlling inflammation. In mild cases, patients typically respond well to ocular lubricants and mast cell stabilizers. For moderate cases, treatment may involve punctal occlusion and immunomodulatory therapy. Severe or refractory cases can benefit from supratarsal corticosteroid injections, scleral lenses, or surgical interventions such as conjunctival resection or thermal cauterization. While the overall prognosis is generally favorable, recurrence is common. Therefore, long-term follow-up is essential to optimize treatment outcomes and reduce the likelihood of relapses.

Superior limbic keratoconjunctivitis (SLK) and dry eye disease (DED) exhibit similar clinical manifestations, complicating diagnosis. We aimed to compare tear metabolomic profiles and secretory phospholipase A2 (sPLA2) levels in patients with SLK versus patients with DED. We established a cross-sectional study involving 56 subjects: 20 patients with SLK, 21 patients with DED, and 15 matched healthy controls (solely for measuring sPLA2). Tear fluids collected via Schirmer strips underwent liquid chromatography with tandem mass spectrometry metabolomic analysis. Metabolites were quantitatively analyzed and matched to metabolic pathways and biomarkers. Metabolic differences between patients with SLK and patients with DED were identified through multivariate statistical analysis. Western blot measured the content of sPLA2 in tears of the three groups. Tear analysis annotated 274 metabolites. Twenty-three metabolites showed significant differences (P < 0.05) between the 2 groups, comprising 20 increased and 3 decreased in SLK. Top differential metabolic pathways were glycerophospholipid, alpha-linolenic acid, and linoleic acid metabolism. Receiver operating characteristic (ROC) analysis showed that five metabolites could be considered as potential biomarkers for distinguishing SLK from DED. Tears PLA2 was significantly higher in SLK than healthy controls (p < 0.05), but without difference between SLK and DED. The study revealed distinct metabolomic profiles in SLK versus DED tears, with notable changes in glycerophospholipid metabolism and elevated sPLA2 levels in SLK. Tear metabolomics distinguishes SLK from DED at the molecular level through dysregulated glycerophospholipid metabolism. In SLK, compared with controls, this dysregulation coincides with elevated sPLA2, an enzyme hydrolyzing glycerophospholipids, indicating lipid-driven inflammation.

Ocular surface disease (OSD) encompasses a range of conditions that not only include the well-described dry eye disease (DED) components - such as hyperosmolarity, inflammation, ocular surface damage, and neurosensory compromise - but also eyelid-related disorders. These can stem from anatomical abnormalities or as consequences of DED, leading to various mechanical and inflammatory issues. These may include friction between the eyelids and the globe; irregular blink mechanics; and incomplete protection or even frank exposure of the ocular surface. Eyelid-associated ocular surface disease (EAOSD) includes conditions such as superior limbic keratoconjunctivitis, orbicularis oculi spasm (Jumping Orbicularis Sign), lid wiper epitheliopathy, and tight eyelid syndrome. Botulinum toxin, produced by the bacterium Clostridium botulinum, works by blocking the release of acetylcholine at the neuromuscular junction, leading to temporary muscle weakening. When mindfully injected into the orbicularis oculi, frontalis, or tarsal plate, botulinum toxin may reduce muscle tension around the eyelids, which improves eyelid tone and anatomic apposition between the eyelid and ocular surface tissues. Botulinum toxin can also be used to address abnormal blink patterns, incomplete blinking, nocturnal lid seal insufficiency, and lagophthalmos. Such interventions may alleviate symptoms associated with EAOSD. This paper examines the applications of botulinum toxin in the treatment of EAOSD. Other applications of botulinum toxin for addressing photophobia and excess trigeminal nerve tone are separately addressable topics.

Superior limbic keratoconjunctivitis (SLK) is a chronic inflammatory ocular surface disorder affecting the superior conjunctiva and limbus. Its pathogenesis entails a vicious cycle of microtrauma and inflammation. Besides its well-known association with thyroid disorders, SLK has also been associated with systemic conditions involving severe ocular surface disease. One condition that can secondarily develop SLK is ocular graft-versus-host disease (oGVHD). Ocular graft-versus-host disease, a complication of allogeneic hematopoietic stem-cell transplantation, is a pan-ocular surface disease that can lead to severe ocular complications and vision loss. Importantly, the occurrence of SLK in the setting of oGVHD is a marker of an augmented ocular surface distress that requires immediate aggressive management to prevent irreversible ocular surface damage, notably limbal stem-cell deficiency. Treatment of SLK in oGVHD includes aggressive lubrication, anti-inflammatory drops, serum/plasma drops, and large diameter contact lenses. In particular, scleral contact lenses are currently the most effective long-term treatment for SLK in oGVHD and can significantly reduce the risk of irreversible loss of vision. Of note, conjunctival resection or destruction (e.g., cauterization) is not recommended for treatment of SLK in ocular graft-versus-host disease. This review examines the pathophysiology and treatment modalities for SLK in oGVHD aimed at improving long-term outcomes.

To assess the fitting process and clinical feasibility of a novel large diameter rigid gas-permeable (RGP) corneal contact lens (CL) presenting regular or reverse geometry for managing keratoconus (KC). The lens was designed to rest on the peripheral cornea and vault over the cone, aiming to enhance visual quality, comfort, and corneal physiology. 32 KC patients across all severity stages, including central, paracentral and peripheral cones enrolled. Lens parameters were customized from corneal measurements obtained via Oculus Pentacam HR tomography, mainly based on sagittal height and accounting for adequate tear film clearance. Visual acuity (VA), contrast sensitivity (CS), ocular complications, and user satisfaction were evaluated at baseline, and at one week and three months of lens wear. Twenty-four patients (41 eyes) were fitted and completed the 3-month follow-up (median age of 28.5 years, 9 females). A median of 2 trial lenses per eye (interquartile range of 4.5) were needed during the fitting process. Significant improvements in median VA (baseline: 0.32 logMAR; three months: 0.01 logMAR; p = 0.002) and CS (p < 0.001 at all frequencies) were observed compared to baseline values. Ocular complications remained below clinical significance, with superior limbic keratoconjunctivitis showing significant reduction over time (p < 0.001). Patient satisfaction was high, with a median daily lens wear of 9.5 h. Most users (79.2%) reported consistent comfort with their CLs. The novel large diameter RGP corneal CL demonstrated comparable efficacy to existing RGP CL designs, offering high levels of comfort and improved vision with minimal ocular complications. The conjunctiva is a transparent, thin mucous membrane covering the sclera. This structure extends from the limbus, or the perimeter of the cornea, and covers both the sclera, where it is termed the "bulbar conjunctiva," and the posterior eyelid surfaces, where it is called the "palpebral conjunctiva." Keratoconjunctivitis is an inflammatory condition that affects both the superficial cornea and the conjunctiva. The term is derived from the words "keratitis," which refers to superficial corneal inflammation, and "conjunctivitis," which denotes conjunctival involvement. This ocular condition can arise from an expansive list of etiologies, including viral, bacterial, autoimmune, toxic, or allergic causes. Keratoconjunctivitis often results in significant discomfort and potential vision impairment. Viruses, particularly adenoviruses, are among the most common culprits, followed by bacterial and fungal pathogens in certain cases. Allergic keratoconjunctivitis, often associated with environmental allergens, as well as dry eye-related forms linked to tear film dysfunction, also contributes significantly to the condition. Autoimmune diseases such as Sjögren syndrome can further complicate the clinical spectrum of this disease by disrupting the ocular surface. Epidemiologically, keratoconjunctivitis is widespread, with varying prevalence depending on the subtype and geographic location. Viral keratoconjunctivitis, for instance, tends to occur in outbreaks, especially in crowded environments like schools or workplaces. Conversely, dry eye-related keratoconjunctivitis predominantly affects older populations, particularly postmenopausal women, due to hormonal changes affecting tear production. Patients with keratoconjunctivitis often present with a constellation of symptoms, including redness, photophobia, blurred vision, excessive tearing or dryness, and a gritty or foreign body sensation in the eye. In more severe cases, patients may report sharp pain, mucopurulent discharge, or difficulty keeping the eye open due to irritation. On examination, clinicians may note conjunctival hyperemia, corneal epithelial defects, lid swelling, or papillary reactions on the tarsal conjunctiva. These signs, combined with the patient's history, aid in differentiating the various subtypes of keratoconjunctivitis. A thorough investigation is essential to establish a definitive diagnosis. Evaluation typically includes a detailed clinical history, slit-lamp biomicroscopy, and, where indicated, laboratory tests such as viral cultures, polymerase chain reaction (PCR) testing for adenoviruses, or conjunctival scrapings for cytology and bacterial cultures. Tear film assessments, including the Schirmer test and tear break-up time (TBUT), are valuable in diagnosing dry eye-associated keratoconjunctivitis. Advanced imaging techniques, such as anterior segment optical coherence tomography (AS-OCT) and confocal microscopy, can provide further insights into the structural integrity of the cornea and conjunctiva. Management of keratoconjunctivitis highly depends on the underlying etiology. Viral keratoconjunctivitis typically requires supportive care, including artificial tears and cold compresses, as antiviral medications are rarely indicated. In contrast, bacterial keratoconjunctivitis demands prompt antibiotic therapy to prevent complications, such as corneal ulcers. Allergic keratoconjunctivitis often responds well to antihistamines, mast cell stabilizers, and allergen avoidance strategies. For dry eye-related cases, artificial tears, punctal plugs, and, in severe cases, immunomodulatory agents like cyclosporine can provide significant relief. Corticosteroids may be cautiously used in autoimmune-related keratoconjunctivitis, but their prolonged use must be carefully monitored due to the risk of cataracts and glaucoma. Looking to the future, advancements in the understanding of ocular surface inflammation and tear film dynamics are paving the way for more targeted therapies. Emerging treatments, such as biologic agents targeting specific inflammatory pathways, alongside gene therapies, hold promise in addressing refractory cases. Additionally, innovations in diagnostic tools, including point-of-care tests for tear biomarkers and artificial intelligence-driven imaging technologies, are expected to enhance early detection and personalized management of keratoconjunctivitis. Overall, keratoconjunctivitis is a complex and multifaceted condition requiring a nuanced approach to diagnosis and management. By integrating current evidence-based practices with emerging therapeutic and diagnostic advancements, healthcare providers can significantly improve outcomes for individuals affected by this debilitating condition. This activity will focus on more well-known entities causing combined keratoconjunctivitis. Specifically, this activity will discuss the entities known as epidemic keratoconjunctivitis (EKC), vernal keratoconjunctivitis (VKC), superior limbic keratoconjunctivitis (SLK), and keratoconjunctivitis sicca.