Review of ophthalmic emergencies in primary care: a comprehensive approach to red eye

Introduction

Up to 3 percent of visits to primary care doctors are related to eye issues (1). Red eye is among the most common presenting complaints in both primary and specialized healthcare (2). While many cases resolve spontaneously, some indicate serious or sight-threatening conditions that require prompt recognition. Early detection and treatment are essential for a favorable prognosis, supported by regular eye examinations and patient education. Red eye accounts for about 15% of ophthalmology consultations and 6% of visits to general practitioners in Eastern Europe (3). Causes range from mild to severe, making diagnosis challenging for non-ophthalmologists (4). Common causes include conjunctivitis, scleritis, episcleritis, uveitis, acute angle-closure glaucoma (AACG), and foreign bodies. Pain and/or photophobia help distinguish benign from serious conditions such as AACG, bacterial keratitis (BK), scleritis, or anterior uveitis (5). Recognizing clinical indicators like pupil changes, photophobia, and anterior chamber findings is necessary for differentiation (Table 1).

Rationale and knowledge gap

Despite the high prevalence of red eye in primary care and emergency settings, many frontline clinicians lack the specialized training to accurately differentiate benign cases from those requiring urgent ophthalmologic referral. Misdiagnosis or delayed recognition of vision-threatening conditions can lead to severe complications, including irreversible vision loss. There is a need for a structured, evidence-based approach to assist general practitioners and emergency physicians in efficiently evaluating and managing red eye presentations.

Objective

The objective of this review is to provide a comprehensive, clinically oriented framework for non-ophthalmologists to systematically assess and manage patients presenting with red eye (Figure 1). By consolidating updated diagnostic strategies and management options across a wide range of etiologies, this review aims to support timely recognition of vision-threatening conditions, guide appropriate referral decisions, and ultimately improve patient outcomes in primary care and emergency settings.

Figure 1 Algorithm for the diagnosis of red eye. This flowchart provides a structured approach to diagnosing red eye, guiding clinicians through a stepwise evaluation based on clinical findings. The red circles indicate findings that require urgent referral. CN, cranial nerve; HSV, herpes simplex virus; IOP, intraocular pressure; SLK, superior limbic keratoconjunctivitis; VZV, varicella zoster virus.

Infection and inflammation

Scleritis

Scleritis is a chronic inflammatory condition of the sclera that can be linked to systemic diseases or infections (6). It is more prevalent in females than males and typically affects middle-aged individuals (7). This condition may present with a gradual or acute onset, severe radiating pain exacerbated by ocular movement or touch, along with photophobia, tearing, and/or decreased visual acuity. Rarer subtypes of scleritis, such as scleromalacia perforans, demonstrate minimal symptomatology. A slit-lamp examination can evaluate for fixed, injected, and inflamed blood vessels and the extent of involvement (8). Providers should also assess for a violaceous hue to the sclera in natural light and a history of autoimmune symptoms such as rash or arthritis, which may point towards severe systemic illness (9). Scleritis is divided into anterior, which includes diffuse, nodular, and necrotizing subtypes, and posterior, which also features diffuse and nodular forms (10). The sclera’s anatomical structure comprises an extracellular matrix of collagen, elastin, and proteoglycans and the exact pathophysiology of scleritis remains a focus of ongoing research (10). Rao et al. examined tissue specimens from patients with end-stage scleritis and identified two histological patterns: rheumatoid arthritis-associated scleritis showed tissue necrosis with surrounding granulomatous inflammation, while idiopathic scleritis exhibited chronic inflammatory infiltrate without necrosis (11). Usui et al. (2008) further analyzed the inflammatory cells in necrotizing scleritis tissues using immunohistochemical staining, finding a dominance of B cells (CD20⁺) and macrophages (CD68⁺) in autoimmune-related cases, and macrophages followed by T cells (CD3⁺) in idiopathic cases (12). The diagnosis of scleritis is primarily based on clinical presentation and ocular examination (Table 1). However, several laboratory tests can help rule out coexisting diseases. These include antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), HLA-B27, fluorescent treponemal antibody absorption (FTA-ABS) test, and C-reactive protein (CRP). First-line treatments for scleritis include topical corticosteroid eye drops, such as prednisolone acetate or difluprednate, administered four times daily. Oral nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen 600 mg or naproxen 500 mg, may also be added to the treatment regimen if needed. Severe cases may require oral corticosteroids (e.g., prednisone at 1 mg/kg) or immunosuppressive agents like methotrexate or biologic agents such as infliximab, especially in conjunction with systemic corticosteroids (13). Patients without previously discovered systemic diseases should undergo further workup, as up to half of scleritis cases are associated with underlying conditions, like connective tissue disorders or vasculitis (8).

Episcleritis

Episcleritis is inflammation of superficial vessels in the episclera, between the conjunctiva and the sclera (14). It presents with sudden sectoral or diffuse redness, usually without pain, vision changes, or discharge, though tenderness may occur. Incidence is <1/1,000, more common in women aged 40–50 (15). Diffuse episcleritis typically resolves within three weeks but may recur, while nodular episcleritis causes longer and more painful episodes (16). It is usually unilateral but can be bilateral or alternating. Most cases are idiopathic, though up to one-third are linked to systemic autoimmune disease (17). Mild episcleritis, often associated with dry eye, may be conservatively managed with supportive measures of cool compresses and artificial tears four times daily (8). Treatment for moderate to severe episcleritis generally involves the use of oral NSAIDs as a first-line therapy, or mild topical corticosteroids (18). However, it is important to note that steroid use may lead to recurrence of episcleritis. Patients receiving this treatment should be monitored closely every 2–3 weeks until full resolution of symptoms, followed by a gradual steroid taper (8).

Keratitis

Keratitis is corneal inflammation with edema, inflammatory cell infiltration, and ciliary congestion. Causes may be infectious or non-infectious, systemic or localized. Microbial keratitis is the most common and a major concern in developing countries (19), caused by bacteria, fungi, viruses, or parasites (20). While the exact prevalence is unclear, corneal ulceration occurs at about 11 per 100,000 annually in the USA (21) and affects males more often (22). Diagnosis relies on slit-lamp exam with fluorescein to assess infiltrates and epithelial damage; corneal scrapings are recommended for infiltrates >1–2 mm to identify pathogens by staining or culture (8). Infectious keratitis may follow ocular procedures such as small incision lenticule extraction (SMILE), where the intrastromal junction favors pathogen invasion (23). These postoperative cases are difficult and require urgent management to prevent vision loss.

BK

BK is the most common microbial keratitis (24), presenting with painful epithelial and stromal ulceration, corneal opacity, melt, exudate, or hypopyon. Severe cases may progress to descemetocele, perforation, and blindness (25). Major pathogens include S. aureus, S. epidermidis, S. pneumoniae, and P. aeruginosa (26), which typically infect only when corneal barriers are disrupted by factors such as contact lens use, corticosteroids, ocular surgery, diabetes, or connective tissue disease (27). Topical antibiotics remain first-line therapy (28). Moxifloxacin and gatifloxacin are widely used off-label (29). Kowalski et al. reported moxifloxacin had comparable empirical coverage (92%) to cefazolin/tobramycin (93%) and cefuroxime/gentamicin (97%), supporting its use as monotherapy while awaiting culture results (30). Vancomycin remains essential for methicillin-resistant Staphylococcus aureus (MRSA), highlighting the need for early susceptibility testing given rising resistance (31). Corneal melt involves fibroblast and keratocyte activity; tetracyclines may help by inhibiting collagenase (32). The role of topical corticosteroids is debated (33). Some suggest benefit in reducing stromal melt, neovascularization, and scarring (34), while others warn of delayed healing and worsening infection (35). Urgent ophthalmology referrals are crucial to prevent vision loss.

Viral keratitis

Viral keratitis is another common form of infectious keratitis, frequently caused by herpes simplex virus (HSV), adenovirus, varicella zoster virus (VZV), Epstein-Barr virus (EBV), and cytomegalovirus (CMV) (36). Viral keratitis can become chronic and recurrent, posing a painful and sight-threatening challenge to clinicians. Among these, the herpes group of viruses dominates as the most prevalent cause of viral keratitis worldwide. A characteristic dendritic ulcer, visible under fluorescein slit lamp exam, typically aids in the clinical diagnosis of herpes simplex keratitis (HSK), the most common form of viral keratitis (37). Additional clinical signs of HSK include stromal opacity and neovascularization, often triggered by recurrent HSV-1 reactivation and subsequent viral shedding into deeper layers of the cornea (38). HSK is classified into four subtypes based on the affected corneal layer and whether the keratitis is due to primary or reactivated infection: (I) epithelial keratitis; (II) immune stromal keratitis; (III) stromal necrotic keratitis; and (IV) endotheliitis, with epithelial keratitis being the most common subtype (39). The virus’s direct effects include blood vessel ingrowth, leukocyte infiltration, and damage to the corneal stroma and endothelium. Notably, HSV keratitis has been shown to significantly impact quality of life (40), with repeated episodes resulting in corneal scarring and potentially blindness. Topical antiviral medication (acyclovir) is the primary treatment for epithelial HSK (41). Topical steroids are the mainstay of treatment for HSV stromal disease and endotheliitis and are used in conjunction with antiviral medication to prevent further recurrence of viral keratitis (42). In cases of recurrent HSV keratitis, a prophylactic course of oral antiviral medication (acyclovir) is administered for one year (43).

Fungal keratitis (FK)

FK is a severe infection of the cornea marked by complications such as corneal scarring, perforation, stromal destruction, and ulceration (44). Corneal ulcers are most commonly caused by the major fungal pathogens, molds (Fusarium and Aspergillus), and yeasts (Candida) (45). Geographically, filamentous fungi are more prevalent in tropical and subtropical regions, whereas yeast is more prevalent in temperate areas (46). FK occurs when fungal spores or hyphal fragments penetrate the protective epithelium and reach the stroma (47). Corneal infiltrates in FK typically appear dry with feathery edges and multiple satellite lesions (48). Clinical features of FK include mild pain, reflecting the slow progression of fungal pathogens deep into the cornea (49). Topical Natamycin is the preferred treatment for filamentous FK (50), with topical voriconazole added for Aspergillus keratitis that does not respond to natamycin alone. Despite natamycin being first-line, its effectiveness can be limited by emerging drug resistance among fungal species (51).

Conjunctivitis

Conjunctivitis, commonly known as pink eye, is the inflammation of the conjunctiva, the lubricating mucous membrane covering the eye’s outer surface. The conjunctiva is divided into two parts: the tarsal conjunctiva, which lines the inner eyelids, and the bulbar conjunctiva, which covers the eyeball up to the cornea (52). This condition affects millions of individuals annually and poses significant economic and social burdens (53). Conjunctivitis, or inflammation of the conjunctiva, can result from allergic or immunological reactions as well as infections, with viruses and bacteria being the most common infectious causes (54). Ocular allergy is the most prevalent form of non-infectious conjunctivitis and can significantly impact quality of life (55). Diagnosis is typically clinical; however, Gram stains, cultures, or polymerase chain reaction (PCR) can aid in cases of atypical conjunctivitis, neonatal conjunctivitis, or undetermined etiologies. While most cases are self-limiting and rarely lead to vision loss, conjunctivitis remains a frequent concern amongst patients seeking ophthalmic care due to its uncomfortable symptoms and potential for widespread transmission (56).

Bacterial conjunctivitis (BC)

BC is more common in children, usually caused by S. pneumoniae, H. influenzae, and M. catarrhalis; meningococcal cases may also occur (57). In adults, Staphylococcus predominates, while N. gonorrhoeae is a rare cause (57). BC arises from direct contact or overgrowth of native flora (56). It typically begins unilaterally with conjunctival hyperemia, foreign body sensation, and increased secretions (58), often leading to sticky eyelids and pruritus (59). Serious complications are uncommon (60), but keratitis risk increases in patients with corneal epithelial defects or dry eye. Contact lens wear should be avoided, as lenses may aggravate infection and harbor bacteria (61). Severe cases are best treated with the latest-generation fluoroquinolones; alternatives include polymyxin B/trimethoprim, ciprofloxacin, azithromycin solutions, or erythromycin and bacitracin ointments. In pediatrics, ciprofloxacin, ofloxacin, and tetracycline show the highest bactericidal activity, followed by gentamicin, tobramycin, and polymyxin combinations (62). Gonococcal conjunctivitis carries a high risk of perforation and blindness and requires immediate systemic ceftriaxone injection (63).

Viral conjunctivitis

Viral conjunctivitis is highly contagious and the most common form of conjunctivitis (64). It can be triggered by DNA viruses [e.g., adenovirus, HSV, and VZV], or RNA viruses (e.g., coxsackievirus, enterovirus, and picornavirus) (65). Among these, adenovirus is the most common cause (54). Infected individuals typically experience symptoms like watery discharge, ocular pruritus, tearing, and tender preauricular lymphadenopathy (66). Viral conjunctivitis is generally self-limiting and resolves within 2–4 weeks. In patients with current vesicular skin lesions or a history of perioral fever blisters, a fluorescein examination is recommended, as HSV can cause corneal dendritic lesions (67). The standard treatment for viral conjunctivitis caused by adenoviruses includes artificial tears and cold compresses. To reduce contagiousness, povidone-iodine (PVP-I) 0.8% can be used (68). It has been demonstrated that PVP-I 0.6%/DEX 0.1% significantly improves clinical resolution in patients with acute adenoviral conjunctivitis (69).

Allergic conjunctivitis

Allergic conjunctivitis is a type I hypersensitivity reaction triggered by allergens like dust and pollen, causing histamine release, mast cell degranulation, and activation of proinflammatory mediators (70). Mast cell activation induces vascular endothelial changes, adhesion molecule expression, and secretion of chemokines such as MIP-1 alpha and IL-8, contributing to the late-phase reaction (71). Clinically, it presents with chemosis, lid crusting, bilateral watery discharge, and symptoms like itching, sneezing, cough, and nasal congestion. Blurry vision, photophobia, or pain are uncommon and warrant ophthalmology referral (72). Treatment targets acute and chronic inflammation (73). Conservative measures include cold compresses and antihistamine/vasoconstrictor drops, which reduce chemosis and vascular permeability (74). Mast cell stabilizers are effective in moderate cases, especially seasonal allergic conjunctivitis with corneal involvement (75). NSAIDs such as ketorolac decrease prostaglandin E2 in tears, reducing itching (76).

Neonatal conjunctivitis

Ophthalmia neonatorum (ON), also known as neonatal conjunctivitis, is an inflammation of the conjunctiva occurring within the first 4 weeks of life. ON is typically transmitted to the infant from the mother’s birthing canal during delivery (77). Clinical signs include edema and erythema of the eyelids, purulent discharge, and inflammation of the palpebral conjunctivae (78). Many infectious cases are caused by sexually transmitted pathogens such as Chlamydia trachomatis and Neisseria gonorrhoeae, but ON can also result from HSV-2, Staphylococcus species, H. influenzae, and other gram-negative organisms (77,79). Among these, conjunctivitis caused by Neisseria gonorrhoeae is particularly severe and, if left untreated, can rapidly progress to corneal ulceration and cause permanent vision loss (80). For prophylaxis, topical erythromycin, or an aminoglycoside like tobramycin, has largely replaced silver nitrate and is utilized within 24 hours of birth (81). Treatment for gonococcal ON involves a one-time dose of ceftriaxone 125 mg intramuscular (IM) (82). For chlamydial ophthalmia or pneumonia, a two-week course of oral erythromycin is recommended (83).

Blepharitis

Blepharitis is a common inflammatory condition of the eyelids, characterized by a burning sensation, itching of the lid margins, flaking, and redness (72). Although rare, severe cases of blepharitis can lead to visual impairments secondary to keratopathy and corneal ulceration, as well as permanent alterations in eyelid morphology (84). Blepharitis is classified into two types based on location: anterior and posterior blepharitis (85). Anterior blepharitis affects the base of the eyelashes and their follicles, and is traditionally associated with staphylococcus, seborrheic dermatitis, and rosacea (86). Conversely, posterior blepharitis is primarily caused by underlying meibomian gland dysfunction (MGD), which is a condition marked by decreased glandular secretion and obstruction of the terminal ducts, reducing tear film stability and optical clarity (72,87). Marginal blepharitis refers to the combination of both anterior and posterior blepharitis, as there is frequently considerable overlap between the two types (88). Both posterior and anterior blepharitis can be caused by demodex mites, intracellular parasites that inhabit hair follicles and sebaceous glands (89). Maintaining proper eyelid hygiene is the cornerstone of treatment and is highly effective for managing blepharitis. Bacterial imbalance at the eyelid margin is believed to contribute to development of blepharitis, although the exact pathogenesis remains unclear. To date, bacitracin and erythromycin ointments are the most frequently used treatments (90).

Hordeolum

Hordeolum, or stye, is a purulent eyelid margin inflammation from sebaceous gland obstruction (91). External hordeolum affects the glands of Zeis, while internal hordeolum involves the meibomian glands (92). Staphylococcus species are the main cause and may occasionally cause cellulitis (93). Lesions often resolve spontaneously, but internal hordeola can become chronic or progress to chalazion if untreated (94). Standard care includes warm compresses and eyelid massage; topical antibiotics or mechanical drainage may be needed in refractory cases (95). Chronic conditions like diabetes or seborrheic dermatitis increase risk (96).

Endophthalmitis

Endophthalmitis is a severe form of ocular inflammation stemming from infection of the intraocular cavity and can lead to blindness if not treated promptly (97). The condition is classified as either “exogenous”; or “endogenous”; based on the source of the infection (98). Exogenous endophthalmitis arises when infecting agents penetrate the eye from outside the body, usually following penetrating trauma or intraocular surgery (99). Endogenous endophthalmitis originates from an internal source spreading through the bloodstream – this form is much less common (100). The condition usually presents suddenly with decreased visual acuity, pain, hypopyon, and eyelid edema (8). Most cases are caused by gram-positive bacteria (85.1%, mainly S. epidermidis), with gram-negative bacteria (10.3%) and fungi (Candida, Aspergillus, 4.6%) less common (101,102). Suspected cases require urgent ophthalmology referral. Diagnosis and treatment involve intraocular cultures, intravitreal antibiotics covering gram-positive and gram-negative bacteria, and sometimes systemic broad-spectrum antibiotics (103). Antifungals such as voriconazole, fluconazole, or amphotericin B are used when indicated (104). Severe cases may benefit from vitrectomy, which reduces infection and inflammation (105) and improves retinal oxygenation; vitrectomy is often more effective than intravitreal antibiotics alone in severe cases (106).

Orbital cellulitis (OC)

OC is a serious inflammatory condition, usually from an infectious source, affecting the contents of the globe and the surrounding soft tissues behind the orbital septum (107). While OC can occur at any age, it is more frequently observed in children (108). The most common causative microorganisms are S. pneumoniae, S. aureus, and S. pyogenes (109). Symptoms of orbital cellulitis include eyelid edema, conjunctival chemosis, proptosis, periorbital skin erythema, and decreased eye motility (110). The most common predisposing factor for orbital cellulitis across all age groups is secondary infection spreading from the paranasal sinuses (111). Other significant predisposing factors include intracranial infections, dental abscesses, and middle ear infections (112). On magnetic resonance imaging (MRI), orbital cellulitis is characterized by high signal intensity in T2-weighted fat-saturated sequences (113). Management of orbital cellulitis involves initiating intravenous broad-spectrum antibiotics and addressing any associated sinusitis. Surgical drainage may be performed when the infection does not resolve with antibiotics alone. While this approach effectively controls active infection, inflammation sequelae may persist for weeks to months (114). If not adequately treated, orbital cellulitis can lead to serious complications such as intracranial abscesses, vision loss, and meningitis (115).

Uveitis

Uveitis is inflammation of the uvea, affecting the iris, ciliary body, or choroid, and is classified as anterior, intermediate, posterior, or panuveitis (116). Incidence does not differ significantly between sexes (117). Risk factors include infections (CMV, tuberculosis, toxoplasmosis, HSV, syphilis) and systemic diseases like spondyloarthropathies (118), with toxoplasma gondii a leading cause globally (119). Clinically, patients present with photophobia, pain, ciliary flush, and tenderness (120). Slit-lamp examination reveals inflammatory cells in the anterior chamber and protein-induced flare (121). Uveitis arises from an imbalance between regulatory and inflammatory immune mechanisms, influenced by genetic and environmental factors (122). Treatment depends on type: anterior uveitis responds to topical corticosteroids (123), with cycloplegics (e.g., homatropine) preventing synechiae and alleviating pain (124,125). Intermediate uveitis with macular edema may require periocular corticosteroids (126) or intravitreal implants like Ozurdex and Retisert (127). Table 2 provides a comparative overview of symptoms, causes, and treatments for major red eye conditions.

Eye injury

Hyphema

Hyphema is blood in the anterior chamber, often caused by trauma, coagulopathies, uveitis, juvenile conditions, or intraocular surgery (128). Complications include corneal blood staining, elevated intraocular pressure (IOP), optic nerve atrophy, and permanent vision loss; trauma can also cause angle recession glaucoma (129). Patients with conditions like sickle cell disease have a higher risk, though most recover fully (130). Treatment includes elevating the head to 30°, topical analgesics (tetracaine or proparacaine), rigid eye shielding, bed rest, and avoiding antiplatelet/anticoagulants (131). Daily follow-ups monitor vision, IOP, and slit-lamp findings due to rebleeding risk in the first 10 days (8). Surgery is indicated for persistent high-grade hyphema, uncontrolled glaucoma, or elevated IOP (132).

Corneal abrasion

Corneal abrasion, also known as corneal epithelial defect, occurs when the top layer of the cornea, the corneal epithelium, is damaged or lost, typically due to non-penetrating trauma (133). Symptoms include reduced visual acuity, redness, excessive tearing, and photophobia, making corneal abrasions a common occurrence in emergency department settings (134,135). In addition to assessing for foreign bodies, a slit-lamp examination with fluorescein dye aids in the diagnosis and visualization of the abrasion’s location and size (8). Healing involves a complex process of cell migration, death, proliferation, differentiation, and extracellular matrix remodeling. Healing the corneal endothelium is particularly difficult as these cells do not regenerate. Rather, they rely on cell migration, spreading, and possible epithelial-mesenchymal transformation (136). Treatment typically involves aggressive lubrication, antibiotic drops or ointments with broad-spectrum coverage, and daily follow-up until recovery (133). Commonly used antibiotics include ofloxacin, ideal for its P. aeruginosa coverage in contact lens wearers, erythromycin, and polysporin (133,137). Although research regarding pain management continues to evolve, oral analgesics and a short course of dilute topical anesthetics such as tetracaine and proparacaine within the first 24 hours carries minimal risk and can minimize pain in patients (138,139). However, because not all ophthalmologists support routine outpatient use, this method is typically saved for minor, straightforward abrasions and is still debatable.

Subconjunctival hemorrhage (SCH)

SCH is a common cause of acute, painless red eye frequently seen in ophthalmology clinics (140). It occurs when blood from conjunctival or episcleral vessels leaks into the subconjunctival space (141). SCH can result from systemic diseases, trauma, or the rupture of fragile vessels after sudden pressure increases, such as vomiting or Valsalva maneuvers (142,143). Elderly patients with vascular conditions like arteriosclerosis, hypertension, and diabetes often have weakened conjunctival vessels prone to rupture. While trauma typically causes localized bleeding at the injury site, often in the temporal region, SCH tends to appear in the inferior and temporal areas of the conjunctiva (141). Treatment is generally not required, as the condition resolves on its own within 1–2 weeks, though recovery may extend up to 4 weeks in patients on anticoagulants (144).

Trichiasis

Trichiasis is a condition in which eyelashes grow abnormally towards the eye’s surface, causing discomfort. It can present as a few misdirected lashes in either a segmental or diffuse pattern (145). While trichiasis can occur at any age, it is more often seen in adults and presents with symptoms of pain, foreign body sensation, redness, and tearing in the affected eye (146). Major causes of trichiasis include chronic eyelid margin inflammation, skin disease, conjunctival disease, and scarring from surgery or trauma (147). If left untreated, trichiasis can lead to corneal ulceration, scarring, and ultimately, vision impairment (148). Treatment options vary from simple measures like epilating the misdirected lashes or using a bandage contact lens to more permanent solutions such as destroying the problematic lash roots with argon laser or electrolysis (149).

Pterygium

Pterygium is a benign fibrovascular growth extending toward the cornea, causing astigmatism, vision impairment, and recurrent inflammation (150). Risk factors include ultraviolet (UV) exposure, male sex, and age (151). It usually arises nasally in the interpalpebral zone, presenting with redness, dryness, irritation, and decreased vision, and is unique to humans (152). Vascular endothelial growth factor (VEGF) receptor 2 expression may predict recurrence (153), while matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) at the leading edge contribute to inflammation and corneal invasion (154). Redness and edema can be reduced with vasoconstrictors, and antihistamines prevent pruritus (155). Subconjunctival 5-fluorouracil halts progression in recurrent cases (156). Surgery is indicated if the visual axis is affected, astigmatism is significant, symptoms persist, or for cosmetic reasons (8).

Chemical injuries

Ocular chemical burns are an emergency that can severely impair vision and quality of life (157). Severity depends on exposure duration and chemical type (158). Tissue damage persists while chemicals remain in contact with the eye (159). Household disinfectants and cleaning agents are common pediatric causes (159). Alkalis cause more severe injury than acids, affecting both external and internal structures (160,161). Immediate treatment with thorough irrigation using clean water or isotonic solutions until surface pH reaches ~7 is critical (162). Irrigation should last at least 10 minutes, with a Morgan Lens allowing hands-free prolonged irrigation (163). Slit-lamp examination with fluorescein assesses corneal and conjunctival damage. Severe cases may require platelet-rich plasma drops or topical biologics to restore function (164).

Other

Glaucoma

Glaucoma is a progressive loss of retinal ganglion cells with optic nerve changes (165). It results from impaired aqueous humor outflow due to trabecular meshwork resistance or angle occlusion, causing elevated IOP (166,167). As the second leading cause of irreversible blindness in the USA, it is a major public health concern (168). Primary angle-closure glaucoma (PACG) occurs when the peripheral iris blocks aqueous flow, potentially progressing to AACG with sudden vision loss, severe eye pain, and headaches (169). IOP ≥30 mmHg warrants suspicion for AACG; IOP >40 mmHg with acute symptoms requires urgent ophthalmology referral. Workup includes visual fields, pupillary testing, slit-lamp exam, tonometry, gonioscopy, and optic nerve assessment (8). Treatment aims to lower IOP (170). Open-angle glaucoma is managed with medications like carbonic anhydrase inhibitors or trabeculoplasty (171,172). In PACG/AACG, urgent initiation of topical glaucoma medications (i.e., beta blockers, alpha-2 agonists, cholinergic agonists, and prostaglandin analogues), systemic carbonic anhydrase inhibitors, and mannitol is indicated. Definitive laser peripheral iridotomy relieves pupillary block, and severe or refractory cases may require drainage devices or trabeculectomy (8). Prophylactic laser peripheral iridotomy (LPI) is performed in the contralateral eye due to increased risk (173).

Dry eye syndrome (DES)

DES is a multifactorial disorder affecting tears and the ocular surface, impairing comfort and vision (174). The tear film has three layers: lipid (prevents evaporation), aqueous (moisturizes), and mucin (ensures even distribution) (175). It nourishes, lubricates, and removes debris from the eyes (176). Symptoms include blurred vision, burning, and pain, which can affect quality of life (177). If left untreated, DES can lead to persistent visual disturbance, discomfort, and potential damage to the eye’s surface. Both advancing age and female gender have been identified as significant risk factors for developing DES, though the exact pathogenesis remains unclear (178). Additionally, DES is often associated with systemic diseases, further complicating its management (179). Diagnosis involves tear-secretion tests, tear meniscus evaluation, and tear film break-up time (TBUT <5 sec indicates short TBUT-type DES) (180). Fluorescein staining may reveal punctate epithelial erosions in severe cases (181). Management includes tear retention drops, artificial tears, and gels (182).

Strengths and limitations

Strengths

This review provides a comprehensive, up-to-date synthesis of red eye presentations specifically aimed at primary care and frontline clinicians. By integrating recent advances in diagnosis and management with practical clinical frameworks, the article offers a valuable resource to improve the timely identification and treatment of serious ocular conditions. Unlike previous reviews, this article consolidates findings across a broad range of etiologies while maintaining an accessible, structured approach designed for non-ophthalmologists.

Limitations

As a review, this article may be subject to selection bias in the choice of referenced studies. While we aimed to include the most relevant and recent evidence, a systematic review methodology was not employed. Additionally, rapid advances in ophthalmic diagnostics and therapeutics mean that recommendations may require future updates as new technologies and treatment protocols emerge. Understanding the strengths and limitations of this review provides important context for applying its clinical recommendations and highlights areas for future investigation.

Use of topical steroids in ophthalmic emergencies

Although ocular inflammatory diseases such as scleritis, moderate to severe episcleritis, and uveitis can be effectively managed with topical corticosteroids, care must be taken when using them in emergency or primary care settings. An undiagnosed infectious etiology, such as bacterial, fungal, or herpetic keratitis, may exacerbate with steroid use, causing irreversible vision loss or delayed epithelial healing if the medication is administered improperly or too soon. Hence, unless there is a well-established follow-up and a clear, documented diagnosis, primary care physicians should refrain from starting topical steroids without first performing an ophthalmologic evaluation. The advantages and disadvantages of using steroids should be carefully considered when the inflammation is severe and threatening to the patient’s vision and an ophthalmology consultation is not possible right away. Steroids should, whenever feasible, be postponed until after corneal scraping and microbiological analysis, particularly in cases of suspected infectious keratitis.

Conclusions

Red eye is a common chief concern in both primary care and emergency settings, representing a broad spectrum of potential etiologies. It is important for healthcare providers to quickly and accurately distinguish benign causes from sight-threatening ones early on to initiate proper management. For example, allergic conjunctivitis is often self-limiting, while BK or uveitis requires prompt attention and targeted treatment. Differentiation can be best accomplished through thorough history-taking, detailed physical examination, and relevant diagnostic testing. Workup to rule out underlying systemic conditions, such as autoimmune diseases linked to scleritis, episcleritis, or uveitis, should also be considered when assessing for causes of red eye and the need for multidisciplinary involvement. Early detection and diagnosis can guide treatment options and mitigate the risk of complications. A basic examination of the pupils and their constriction response can effectively identify those needing urgent ophthalmologic referral. Immediate referral is also necessary for any patients experiencing visual blurring and significant eye pain, despite these symptoms not being systematically studied in all contexts. Management varies significantly based on underlying pathology but often includes antibiotics, steroids, anti-inflammatory drugs, anti-virals, antifungal agents, and supportive care such as lubricants and compresses. In addition to an individualized management approach, patient education plays a crucial role in further prevention of red eye and its course. To reduce disease burden, healthcare providers should encourage awareness of alarming symptoms while emphasizing regular eye examinations, hygiene, and proper contact lens usage. In this review, we highlighted effective examination and management strategies for 22 common causes of red eye, emphasizing practical clinical approaches that support accurate diagnosis, timely intervention, and appropriate referral. By providing a structured framework, this review aims to enhance clinician confidence, reduce misdiagnosis, and improve patient outcomes in the management of red eye presentations across diverse clinical environments.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://aes.amegroups.com/article/view/10.21037/aes-25-10/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aes.amegroups.com/article/view/10.21037/aes-25-10/coif). Mohammad Soleimani serves as an unpaid editorial board member of Annals of Eye Science from December 2024 to December 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Pflipsen M, Massaquoi M, Wolf S. Evaluation of the Painful Eye. Am Fam Physician 2016;93:991-8.
2. Pandey N, Srivastava RM, Kumar G, et al. Teleconsultation at a tertiary care government medical university during COVID-19 Lockdown in India - A pilot study. Indian J Ophthalmol 2020;68:1381-4. [Crossref] [PubMed]
3. Petricek I, Prost M, Popova A. The differential diagnosis of red eye: a survey of medical practitioners from Eastern Europe and the Middle East. Ophthalmologica 2006;220:229-37. [Crossref] [PubMed]
4. Lawan A. Causes of red eye in Aminu Kano Teaching Hospital, Kano-Nigeria. Niger J Med 2009;18:184-5. [Crossref] [PubMed]
5. Ahmed F, House RJ, Feldman BH. Corneal Abrasions and Corneal Foreign Bodies. Prim Care 2015;42:363-75. [Crossref] [PubMed]
6. Watson PG. Doyne Memorial Lecture, 1982. The nature and the treatment of scleral inflammation. Trans Ophthalmol Soc U K 1962;1982:257-81.
7. Homayounfar G, Nardone N, Borkar DS, et al. Incidence of scleritis and episcleritis: results from the Pacific Ocular Inflammation Study. Am J Ophthalmol 2013;156:752-8. [Crossref] [PubMed]
8. Gervasio K, Peck T. The Wills eye manual: office and emergency room diagnosis and treatment of eye disease. Lippincott Williams & Wilkins, 2021.
9. Allen R, Harper R. American Academy of Ophthalmology. Basic ophthalmology: essentials for medical students. 10th ed. San Francisco, CA: American Academy of Ophthalmology, 2016.
10. Okhravi N, Odufuwa B, McCluskey P, et al. Scleritis. Surv Ophthalmol 2005;50:351-63. [Crossref] [PubMed]
11. Rao NA, Marak GE, Hidayat AA. Necrotizing scleritis. A clinico-pathologic study of 41 cases. Ophthalmology 1985;92:1542-9.
12. Usui Y, Parikh J, Goto H, et al. Immunopathology of necrotising scleritis. Br J Ophthalmol 2008;92:417-9. [Crossref] [PubMed]
13. Sims J. Scleritis: presentations, disease associations and management. Postgrad Med J 2012;88:713-8. [Crossref] [PubMed]
14. Sainz de la Maza M, Molina N, Gonzalez-Gonzalez LA, et al. Clinical characteristics of a large cohort of patients with scleritis and episcleritis. Ophthalmology 2012;119:43-50. [Crossref] [PubMed]
15. McGavin DD, Williamson J, Forrester JV, et al. Episcleritis and scleritis. A study of their clinical manifestations and association with rheumatoid arthritis. Br J Ophthalmol 1976;60:192-226. [Crossref] [PubMed]
16. Daniel Diaz J, Sobol EK, Gritz DC. Treatment and management of scleral disorders. Surv Ophthalmol 2016;61:702-17. [Crossref] [PubMed]
17. Akpek EK, Uy HS, Christen W, et al. Severity of episcleritis and systemic disease association. Ophthalmology 1999;106:729-31. [Crossref] [PubMed]
18. Stone JH, Merkel PA, Spiera R, et al. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med 2010;363:221-32. [Crossref] [PubMed]
19. Tjia KF, van Putten JP, Pels E, et al. The interaction between Neisseria gonorrhoeae and the human cornea in organ culture. An electron microscopic study. Graefes Arch Clin Exp Ophthalmol 1988;226:341-5. [Crossref] [PubMed]
20. Keay L, Edwards K, Naduvilath T, et al. Microbial keratitis: predisposing factors and morbidity. Ophthalmology 2006;113:109-16. [Crossref] [PubMed]
21. Erie JC, Nevitt MP, Hodge DO, et al. Incidence of ulcerative keratitis in a defined population from 1950 through 1988. Arch Ophthalmol 1993;111:1665-71. [Crossref] [PubMed]
22. Titiyal JS, Negi S, Anand A, et al. Risk factors for perforation in microbial corneal ulcers in north India. Br J Ophthalmol 2006;90:686-9. [Crossref] [PubMed]
23. Soltani Shahgoli S, Cheraqpour K, Soleimani M, et al. Post-laser refractive surgery keratitis: A concise narrative review. J Int Med Res 2023;51:3000605231206054. [Crossref] [PubMed]
24. Durand ML, Barshak MB, Chodosh J. Infectious Keratitis in 2021. JAMA 2021;326:1319-20. [Crossref] [PubMed]
25. Butler TK, Spencer NA, Chan CC, et al. Infective keratitis in older patients: a 4 year review, 1998-2002. Br J Ophthalmol 2005;89:591-6. [Crossref] [PubMed]
26. Ung L, Bispo PJM, Shanbhag SS, et al. The persistent dilemma of microbial keratitis: Global burden, diagnosis, and antimicrobial resistance. Surv Ophthalmol 2019;64:255-71. [Crossref] [PubMed]
27. Tabbara KF, Chacra CTB. Infectious keratitis. In: Ocular Infections. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014:73-93.
28. Austin A, Schallhorn J, Geske M, et al. Empirical treatment of bacterial keratitis: an international survey of corneal specialists. BMJ Open Ophthalmol 2017;2:e000047. [Crossref] [PubMed]
29. Mather R, Karenchak LM, Romanowski EG, et al. Fourth generation fluoroquinolones: new weapons in the arsenal of ophthalmic antibiotics. Am J Ophthalmol 2002;133:463-6. [Crossref] [PubMed]
30. Kowalski RP, Kowalski TA, Shanks RM, et al. In vitro comparison of combination and monotherapy for the empiric and optimal coverage of bacterial keratitis based on incidence of infection. Cornea 2013;32:830-4. [Crossref] [PubMed]
31. Chang VS, Dhaliwal DK, Raju L, et al. Antibiotic Resistance in the Treatment of Staphylococcus aureus Keratitis: a 20-Year Review. Cornea 2015;34:698-703. [Crossref] [PubMed]
32. Burns FR, Stack MS, Gray RD, et al. Inhibition of purified collagenase from alkali-burned rabbit corneas. Invest Ophthalmol Vis Sci 1989;30:1569-75.
33. Cohen EJ. The case against the use of steroids in the treatment of bacterial keratitis. Arch Ophthalmol 2009;127:103-4. [Crossref] [PubMed]
34. Yi K, Chung TY, Hyon JY, et al. Combined treatment with antioxidants and immunosuppressants on cytokine release by human peripheral blood mononuclear cells - chemically injured keratocyte reaction. Mol Vis 2011;17:2665-71.
35. Tomas-Barberan S, Fagerholm P. Influence of topical treatment on epithelial wound healing and pain in the early postoperative period following photorefractive keratectomy. Acta Ophthalmol Scand 1999;77:135-8. [Crossref] [PubMed]
36. Koganti R, Yadavalli T, Naqvi RA, et al. Pathobiology and treatment of viral keratitis. Exp Eye Res 2021;205:108483. [Crossref] [PubMed]
37. Darougar S, Wishart MS, Viswalingam ND. Epidemiological and clinical features of primary herpes simplex virus ocular infection. Br J Ophthalmol 1985;69:2-6. [Crossref] [PubMed]
38. Kumaraguru U, Davis I, Rouse BT. Chemokines and ocular pathology caused by corneal infection with herpes simplex virus. J Neurovirol 1999;5:42-7. [Crossref] [PubMed]
39. Wang T, Dong M, Jiang Y, et al. Role of Dendritic Cells and Inflammatory Cells in Herpetic Endotheliitis: Analysis Using In Vivo Confocal Microscopy. Cornea 2018;37:748-54. [Crossref] [PubMed]
40. Reynaud C, Rousseau A, Kaswin G, et al. Persistent Impairment of Quality of Life in Patients with Herpes Simplex Keratitis. Ophthalmology 2017;124:160-9. [Crossref] [PubMed]
41. Wilhelmus KR. Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database Syst Rev 2015;1:CD002898. [Crossref] [PubMed]
42. Oral acyclovir for herpes simplex virus eye disease: effect on prevention of epithelial keratitis and stromal keratitis. Herpetic Eye Disease Study Group. Arch Ophthalmol 2000;118:1030-6.
43. Wu X, Chen X. Acyclovir for the treatment and prevention of recurrent infectious herpes simplex keratitis. Chin Med J (Engl) 2002;115:1569-72.
44. Cao J, Yang Y, Yang W, et al. Prevalence of infectious keratitis in Central China. BMC Ophthalmol 2014;14:43. [Crossref] [PubMed]
45. Ritterband DC, Seedor JA, Shah MK, et al. Fungal keratitis at the new york eye and ear infirmary. Cornea 2006;25:264-7. [Crossref] [PubMed]
46. Garg P, Roy A, Roy S. Update on fungal keratitis. Curr Opin Ophthalmol 2016;27:333-9. [Crossref] [PubMed]
47. Ansari Z, Miller D, Galor A. Current Thoughts in Fungal Keratitis: Diagnosis and Treatment. Curr Fungal Infect Rep 2013;7:209-18. [Crossref] [PubMed]
48. Wong TY, Ng TP, Fong KS, et al. Risk factors and clinical outcomes between fungal and bacterial keratitis: a comparative study. CLAO J 1997;23:275-81.
49. Dave TV, Dave VP, Sharma S, et al. Infectious endophthalmitis leading to evisceration: spectrum of bacterial and fungal pathogens and antibacterial susceptibility profile. J Ophthalmic Inflamm Infect 2019;9:9. [Crossref] [PubMed]
50. Prajna NV, Krishnan T, Mascarenhas J, et al. The mycotic ulcer treatment trial: a randomized trial comparing natamycin vs voriconazole. JAMA Ophthalmol 2013;131:422-9. [Crossref] [PubMed]
51. Mahmoudi S, Masoomi A, Ahmadikia K, et al. Fungal keratitis: An overview of clinical and laboratory aspects. Mycoses 2018;61:916-30. [Crossref] [PubMed]
52. Alfonso SA, Fawley JD, Alexa Lu X. Conjunctivitis. Prim Care 2015;42:325-45. [Crossref] [PubMed]
53. Ohnsman CM. Exclusion of students with conjunctivitis from school: policies of state departments of health. J Pediatr Ophthalmol Strabismus 2007;44:101-5. [Crossref] [PubMed]
54. Rapuano CJ. American Academy of Ophthalmology Cornea/External Disease Panel, Preferred practice pattern guidelines. Conjunctivitis, 2008.
55. Virchow JC, Kay S, Demoly P, et al. Impact of ocular symptoms on quality of life (QoL), work productivity and resource utilisation in allergic rhinitis patients--an observational, cross sectional study in four countries in Europe. J Med Econ 2011;14:305-14. [Crossref] [PubMed]
56. Shields T, Sloane PD. A comparison of eye problems in primary care and ophthalmology practices. Fam Med 1991;23:544-6.
57. Epling J. Bacterial conjunctivitis. BMJ Clin Evid 2012;2012:0704.
58. Mannis MJ. Bacterial conjunctivitis. The Cornea 1988;189-200.
59. Hørven I. Acute conjunctivitis: a comparison of fusidic acid viscous eye drops and chloramphenicol. Acta ophthalmologica 1993;71:165-8. [Crossref] [PubMed]
60. Sheikh A, Hurwitz B, van Schayck CP, et al. Antibiotics versus placebo for acute bacterial conjunctivitis. Cochrane Database Syst Rev 2012;CD001211. [Crossref] [PubMed]
61. Høvding G, Fagerholm P. Oftalmologi: nordisk lærebok og atlas. Studia 2004;
62. Block SL, Hedrick J, Tyler R, et al. Increasing bacterial resistance in pediatric acute conjunctivitis (1997-1998). Antimicrob Agents Chemother 2000;44:1650-4. [Crossref] [PubMed]
63. Mayor MT, Roett MA, Uduhiri KA. Diagnosis and management of gonococcal infections. Am Fam Physician 2012;86:931-8.
64. Sambursky RP, Fram N, Cohen EJ. The prevalence of adenoviral conjunctivitis at the Wills Eye Hospital Emergency Room. Optometry 2007;78:236-9. [Crossref] [PubMed]
65. Yoshida M, Hayasaka S, Yamada T, et al. Ocular findings in Japanese patients with varicella-zoster virus infection. Ophthalmologica 2005;219:272-5. [Crossref] [PubMed]
66. Puri LR, Shrestha GB, Shah DN, et al. Ocular manifestations in herpes zoster ophthalmicus. Nepal J Ophthalmol 2011;3:165-71. [Crossref] [PubMed]
67. Frary J, Petersen PT, Pareek M. Hutchinson's sign of ophthalmic zoster. Clin Case Rep 2019;8:219-20. [Crossref] [PubMed]
68. Monnerat N, Bossart W, Thiel MA. Povidoniod zur Behandlung von Adenoviruskonjunktivitis: eine In-vitro-Studie. Klin Monbl Augenheilkd 2006;223:349-52. [Crossref] [PubMed]
69. Pepose JS, Ahuja A, Liu W, et al. Randomized, Controlled, Phase 2 Trial of Povidone-Iodine/Dexamethasone Ophthalmic Suspension for Treatment of Adenoviral Conjunctivitis. Am J Ophthalmol 2018;194:7-15. [Crossref] [PubMed]
70. Bielory L, Delgado L, Katelaris CH, et al. ICON: Diagnosis and management of allergic conjunctivitis. Ann Allergy Asthma Immunol 2020;124:118-34. [Crossref] [PubMed]
71. Leonardi A, De Dominicis C, Motterle L. Immunopathogenesis of ocular allergy: a schematic approach to different clinical entities. Curr Opin Allergy Clin Immunol 2007;7:429-35. [Crossref] [PubMed]
72. Lindsley K, Matsumura S, Hatef E, et al. Interventions for chronic blepharitis. Cochrane Database Syst Rev 2012;2012:CD005556. [Crossref] [PubMed]
73. Bielory L. Allergic diseases of the eye. Med Clin North Am 2006;90:129-48. [Crossref] [PubMed]
74. La Rosa M, Lionetti E, Reibaldi M, et al. Allergic conjunctivitis: a comprehensive review of the literature. Ital J Pediatr 2013;39:18. [Crossref] [PubMed]
75. Bielory L, Friedlaender MH. Allergic conjunctivitis. Immunol Allergy Clin North Am 2008;28:43-58. vi. [Crossref] [PubMed]
76. Woodward DF, Nieves AL, Friedlaender MH. Characterization of receptor subtypes involved in prostanoid-induced conjunctival pruritus and their role in mediating allergic conjunctival itching. J Pharmacol Exp Ther 1996;279:137-42.
77. Makker K, Nassar GN, Kaufman EJ. Neonatal Conjunctivitis. 2025.
78. Fransen L, Klauss V. Neonatal ophthalmia in the developing world. Epidemiology, etiology, management and control. Int Ophthalmol 1988;11:189-96. [Crossref] [PubMed]
79. Akera C, Ro S. Medical concerns in the neonatal period. Clinics in Family Practice 2003;5:265-92.
80. Forbes GB, Forbes GM. Silver nitrate and the eyes of the newborn. Credé's contribution to preventive medicine. Am J Dis Child 1971;121:1-3. [Crossref] [PubMed]
81. Laga M, Plummer FA, Piot P, et al. Prophylaxis of gonococcal and chlamydial ophthalmia neonatorum. A comparison of silver nitrate and tetracycline. N Engl J Med 1988;318:653-7. [Crossref] [PubMed]
82. Fransen L, Nsanze H, Klauss V, et al. Ophthalmia neonatorum in Nairobi, Kenya: the roles of Neisseria gonorrhoeae and Chlamydia trachomatis. J Infect Dis 1986;153:862-9. [Crossref] [PubMed]
83. Zar HJ. Neonatal chlamydial infections: prevention and treatment. Paediatr Drugs 2005;7:103-10. [Crossref] [PubMed]
84. Lemp MA, Nichols KK. Blepharitis in the United States 2009: a survey-based perspective on prevalence and treatment. Ocul Surf 2009;7:S1-S14. [Crossref] [PubMed]
85. Huggins AB, Carrasco JR, Eagle RC Jr. MEN 2B masquerading as chronic blepharitis and euryblepharon. Orbit 2019;38:514-8. [Crossref] [PubMed]
86. Soh Qin R, Tong Hak Tien L. Healthcare delivery in meibomian gland dysfunction and blepharitis. Ocul Surf 2019;17:176-8. [Crossref] [PubMed]
87. Mathers WD. Ocular evaporation in meibomian gland dysfunction and dry eye. Ophthalmology 1993;100:347-51. [Crossref] [PubMed]
88. Zhao YE, Wu LP, Hu L, et al. Association of blepharitis with Demodex: a meta-analysis. Ophthalmic Epidemiol 2012;19:95-102. [Crossref] [PubMed]
89. Fromstein SR, Harthan JS, Patel J, et al. Demodex blepharitis: clinical perspectives. Clin Optom (Auckl) 2018;10:57-63. [Crossref] [PubMed]
90. Pflugfelder SC, Karpecki PM, Perez VL. Treatment of blepharitis: recent clinical trials. Ocul Surf 2014;12:273-84. [Crossref] [PubMed]
91. Cheng K, Law A, Guo M, et al. Acupuncture for acute hordeolum. Cochrane Database Syst Rev 2017;2:CD011075. [Crossref] [PubMed]
92. Gordon AA, Danek DJ, Phelps PO. Common inflammatory and infectious conditions of the eyelid. Dis Mon 2020;66:101042. [Crossref] [PubMed]
93. Mueller JB, McStay CM. Ocular infection and inflammation. Emerg Med Clin North Am 2008;26:57-72. vi. [Crossref] [PubMed]
94. Lindsley K, Nichols JJ, Dickersin K. Interventions for acute internal hordeolum. Cochrane Database Syst Rev 2010;CD007742. [Crossref] [PubMed]
95. Bragg KJ, Le PH, Le JK. Hordeolum (Archived). 2025.
96. Ansari AS, de Lusignan S, Hinton W, et al. The association between diabetes, level of glycaemic control and eye infection: Cohort database study. Prim Care Diabetes 2017;11:421-9. [Crossref] [PubMed]
97. Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina 2007;27:662-80. [Crossref] [PubMed]
98. Sunaric-Mégevand G, Pournaras CJ. Current approach to postoperative endophthalmitis. Br J Ophthalmol 1997;81:1006-15. [Crossref] [PubMed]
99. Doft B. Endophthalmitis management. Focal points: modules for clinicians. American Academy of Ophthalmology San Francisco, 1997.
100. Durand ML. Bacterial and Fungal Endophthalmitis. Clin Microbiol Rev 2017;30:597-613. [Crossref] [PubMed]
101. Gentile RC, Shukla S, Shah M, et al. Microbiological spectrum and antibiotic sensitivity in endophthalmitis: a 25-year review. Ophthalmology 2014;121:1634-42. [Crossref] [PubMed]
102. Ness T, Pelz K, Hansen LL. Endogenous endophthalmitis: microorganisms, disposition and prognosis. Acta Ophthalmol Scand 2007;85:852-6. [Crossref] [PubMed]
103. Seal D, Reischl U, Behr A, et al. Laboratory diagnosis of endophthalmitis: comparison of microbiology and molecular methods in the European Society of Cataract & Refractive Surgeons multicenter study and susceptibility testing. J Cataract Refract Surg 2008;34:1439-50. [Crossref] [PubMed]
104. Sadiq MA, Hassan M, Agarwal A, et al. Endogenous endophthalmitis: diagnosis, management, and prognosis. J Ophthalmic Inflamm Infect 2015;5:32. [Crossref] [PubMed]
105. Kuhn F, Gini G. Ten years after... are findings of the Endophthalmitis Vitrectomy Study still relevant today? Graefes Arch Clin Exp Ophthalmol 2005;243:1197-9. [Crossref] [PubMed]
106. Vitrectomy E. Results of the endophthalmitis vitrectomy study. Arch Ophthalmol 1995;113:1479-96.
107. Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of orbital complications in acute sinusitis. Laryngoscope 1970;80:1414-28. [Crossref] [PubMed]
108. Tsirouki T, Dastiridou AI, Ibánez Flores N, et al. Orbital cellulitis. Surv Ophthalmol 2018;63:534-53. [Crossref] [PubMed]
109. Kanski JJ, Bowling B. Clinical ophthalmology: a systematic approach. Elsevier Health Sciences, 2011.
110. Kyari F. Emergency management: orbital cellulitis. Community Eye Health 2018;31:60.
111. Chaudhry IA, Al-Rashed W, Arat YO. The hot orbit: orbital cellulitis. Middle East Afr J Ophthalmol 2012;19:34-42. [Crossref] [PubMed]
112. Janakarajah N, Sukumaran K. Orbital cellulitis of dental origin: case report and review of the literature. Br J Oral Maxillofac Surg 1985;23:140-5. [Crossref] [PubMed]
113. Rummeny E, Reimer P, Heindel W. MR imaging of the body. New York: Thieme, 2009.
114. Pushker N, Tejwani LK, Bajaj MS, et al. Role of oral corticosteroids in orbital cellulitis. Am J Ophthalmol 2013;156:178-183.e1. [Crossref] [PubMed]
115. Gupta S, Goyal R, Gupta RK. Clinical presentation and outcome of the orbital complications due to acute infective rhino sinusitis. Indian J Otolaryngol Head Neck Surg 2013;65:431-4. [Crossref] [PubMed]
116. Jabs DA, Nussenblatt RB, Rosenbaum JT, et al. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol 2005;140:509-16. [Crossref] [PubMed]
117. Chen SC, Chuang CT, Chu MY, et al. Patterns and Etiologies of Uveitis at a Tertiary Referral Center in Taiwan. Ocul Immunol Inflamm 2017;25:S31-8. [Crossref] [PubMed]
118. Gutteridge IF, Hall AJ. Acute anterior uveitis in primary care. Clin Exp Optom 2007;90:70-82. [Crossref] [PubMed]
119. Kijlstra A, Petersen E. Epidemiology, pathophysiology, and the future of ocular toxoplasmosis. Ocul Immunol Inflamm 2014;22:138-47. [Crossref] [PubMed]
120. Gilani CJ, Yang A, Yonkers M, et al. Differentiating Urgent and Emergent Causes of Acute Red Eye for the Emergency Physician. West J Emerg Med 2017;18:509-17. [Crossref] [PubMed]
121. Bal SK, Hollingworth GR. Red eye. BMJ 2005;331:438. [Crossref] [PubMed]
122. Lin P, Suhler EB, Rosenbaum JT. The future of uveitis treatment. Ophthalmology 2014;121:365-76. [Crossref] [PubMed]
123. Dodds EM. Treatment strategies in patients with anterior uveitis. Int Ophthalmol Clin 2000;40:55-68. [Crossref] [PubMed]
124. Dacey M. Ankylosing Spondylitis. In: Uveitis: A Practical Guide to the Diagnosis and Treatment of Intraocular Inflammation. Cham: Springer, 2017;135-41.
125. Babu K, Mahendradas P. Medical management of uveitis - current trends. Indian J Ophthalmol 2013;61:277-83. [Crossref] [PubMed]
126. Teo AYT, Betzler BK, Hua KLQ, et al. Intermediate Uveitis: A Review. Ocul Immunol Inflamm 2023;31:1041-60. [Crossref] [PubMed]
127. Arcinue CA, Cerón OM, Foster CS. A comparison between the fluocinolone acetonide (Retisert) and dexamethasone (Ozurdex) intravitreal implants in uveitis. J Ocul Pharmacol Ther 2013;29:501-7. [Crossref] [PubMed]
128. Zafar S, Canner JK, Mir T, et al. Epidemiology of Hyphema-Related Emergency Department Visits in The United States Between 2006 and 2015. Ophthalmic Epidemiol 2019;26:208-15. [Crossref] [PubMed]
129. Woreta FA, Lindsley KB, Gharaibeh A, et al. Medical interventions for traumatic hyphema. Cochrane Database Syst Rev 2023;3:CD005431. [Crossref] [PubMed]
130. Shiuey Y, Lucarelli MJ. Traumatic hyphema: outcomes of outpatient management. Ophthalmology 1998;105:851-5. [Crossref] [PubMed]
131. Brandt MT, Haug RH. Traumatic hyphema: a comprehensive review. J Oral Maxillofac Surg 2001;59:1462-70. [Crossref] [PubMed]
132. Wilson FM II. Traumatic hyphema: pathogenesis and management. Ophthalmology 1980;87:910-9. [Crossref] [PubMed]
133. Aalam W, Barry M, Alharbi M, et al. Diagnosis and Management of Corneal Abrasion Perception of (Primary Health Care Physicians and Emergency Physicians) and its Determinants in Saudi Arabia - A Survey. Middle East Afr J Ophthalmol 2021;28:151-8. [Crossref] [PubMed]
134. Hakimi AA, Carter S, Garg S. Detecting corneal injury with a selfie. Acad Emerg Med 2022;29:1403-4. [Crossref] [PubMed]
135. McGwin G Jr, Owsley C. Incidence of emergency department-treated eye injury in the United States. Arch Ophthalmol 2005;123:662-6. [Crossref] [PubMed]
136. Ljubimov AV, Saghizadeh M. Progress in corneal wound healing. Prog Retin Eye Res 2015;49:17-45. [Crossref] [PubMed]
137. Kaiser PKCorneal Abrasion Patching Study Group. A comparison of pressure patching versus no patching for corneal abrasions due to trauma or foreign body removal. Ophthalmology 1995;102:1936-42. [Crossref] [PubMed]
138. Swaminathan A, Otterness K, Milne K, et al. The Safety of Topical Anesthetics in the Treatment of Corneal Abrasions: A Review. J Emerg Med 2015;49:810-5. [Crossref] [PubMed]
139. Green SM, Tomaszewski C, Valente JH, et al. Use of Topical Anesthetics in the Management of Patients With Simple Corneal Abrasions: Consensus Guidelines From the American College of Emergency Physicians. Ann Emerg Med 2024;83:477-89. [Crossref] [PubMed]
140. Leibowitz HM. The red eye. N Engl J Med 2000;343:345-51. [Crossref] [PubMed]
141. Mimura T, Yamagami S, Usui T, et al. Location and extent of subconjunctival hemorrhage. Ophthalmologica 2010;224:90-5. [Crossref] [PubMed]
142. Duke ES. Conjunctival diseases. System of ophthalmology. 1st ed. London: Henry Kempton, 1965;461-75.
143. Levin AV, Morad Y. Ocular manifestations of child abuse. Ophthalmol Clin North Am 1990;3:249-64.
144. Tarlan B, Kiratli H. Subconjunctival hemorrhage: risk factors and potential indicators. Clin Ophthalmol 2013;7:1163-70. [Crossref] [PubMed]
145. Choo PH. Distichiasis, trichiasis, and entropion: advances in management. Int Ophthalmol Clin 2002;42:75-87. [Crossref] [PubMed]
146. Ferraz LC, Meneghim RL, Galindo-Ferreiro A, et al. Outcomes of two surgical techniques for major trichiasis treatment. Orbit 2018;37:36-40. [Crossref] [PubMed]
147. Ferreira IS, Bernardes TF, Bonfioli AA. Trichiasis. Semin Ophthalmol 2010;25:66-71. [Crossref] [PubMed]
148. Kormann RB, Moreira H. Treatment of trichiasis with high-frequency radio wave electrosurgery. Arquivos Brasileiros de Oftalmologia 2007;70:276-80. [Crossref] [PubMed]
149. Fea A, Turco D, Actis AG, et al. Ectropion, entropion, trichiasis. Minerva Chir 2013;68:27-35.
150. Liu T, Liu Y, Xie L, et al. Progress in the pathogenesis of pterygium. Curr Eye Res 2013;38:1191-7. [Crossref] [PubMed]
151. McCarty CA, Fu CL, Taylor HR. Epidemiology of pterygium in Victoria, Australia. Br J Ophthalmol 2000;84:289-92. [Crossref] [PubMed]
152. Di Girolamo N, Chui J, Coroneo MT, et al. Pathogenesis of pterygia: role of cytokines, growth factors, and matrix metalloproteinases. Prog Retin Eye Res 2004;23:195-228. [Crossref] [PubMed]
153. Gumus K, Karakucuk S, Mirza GE, et al. Overexpression of vascular endothelial growth factor receptor 2 in pterygia may have a predictive value for a higher postoperative recurrence rate. Br J Ophthalmol 2014;98:796-800. [Crossref] [PubMed]
154. Li DQ, Lee SB, Gunja-Smith Z, et al. Overexpression of collagenase (MMP-1) and stromelysin (MMP-3) by pterygium head fibroblasts. Arch Ophthalmol 2001;119:71-80.
155. Rong SS, Peng Y, Liang YB, et al. Does cigarette smoking alter the risk of pterygium? A systematic review and meta-analysis. Invest Ophthalmol Vis Sci 2014;55:6235-43. [Crossref] [PubMed]
156. Ghiasian L, Samavat B, Hadi Y, et al. Recurrent Pterygium: A Review. J Curr Ophthalmol 2021;33:367-78. [Crossref] [PubMed]
157. Trudo EW, Rimm W. Chemical injuries of the eye. Ophthalmic Care of the Combat Casualty 2003;41:115.
158. Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol 1997;41:275-313. [Crossref] [PubMed]
159. Beare JD. Eye injuries from assault with chemicals. Br J Ophthalmol 1990;74:514-8. [Crossref] [PubMed]
160. Haring RS, Sheffield ID, Channa R, et al. Epidemiologic Trends of Chemical Ocular Burns in the United States. JAMA Ophthalmol 2016;134:1119-24. [Crossref] [PubMed]
161. Le Q, Chen Y, Wang X, et al. Vision-related quality of life in patients with ocular chemical burns. Invest Ophthalmol Vis Sci 2011;52:8951-6. [Crossref] [PubMed]
162. Hemmati HD, Colby KA. Treating acute chemical injuries of the cornea. Am Acad Ophthalmol 2012. Available online: https://www.aao.org/eyenet/article/treating-acute-chemical-injuries-of-cornea
163. Ramponi DR. Chemical Burns of the Eye. Adv Emerg Nurs J 2017;39:193-8. [Crossref] [PubMed]
164. Soleimani M, Naderan M. Management Strategies of Ocular Chemical Burns: Current Perspectives. Clin Ophthalmol 2020;14:2687-99. [Crossref] [PubMed]
165. Shon K, Wollstein G, Schuman JS, et al. Prediction of glaucomatous visual field progression: pointwise analysis. Curr Eye Res 2014;39:705-10. [Crossref] [PubMed]
166. Sit AJ, Liu JH. Pathophysiology of glaucoma and continuous measurements of intraocular pressure. Mol Cell Biomech 2009;6:57-69.
167. Khazaeni B, Zeppieri M, Khazaeni L. Acute Angle-Closure Glaucoma. 2025.
168. Ezinne NE, Shittu O, Ekemiri KK, et al. Visual Impairment and Blindness among Patients at Nigeria Army Eye Centre, Bonny Cantonment Lagos, Nigeria. Healthcare (Basel) 2022;10:2312. [Crossref] [PubMed]
169. Uhm KB, Lee JM, Sung HK. Comparison of glaucomatous optic nerve damage in primary angle-closure glaucoma with and without acute attack. Korean J Ophthalmol 2005;19:201-7. [Crossref] [PubMed]
170. Heijl A, Leske MC, Bengtsson B, et al. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol 2002;120:1268-79. [Crossref] [PubMed]
171. Gulati V, Fan S, Gardner BJ, et al. Mechanism of Action of Selective Laser Trabeculoplasty and Predictors of Response. Invest Ophthalmol Vis Sci 2017;58:1462-8. [Crossref] [PubMed]
172. Li T, Lindsley K, Rouse B, et al. Comparative Effectiveness of First-Line Medications for Primary Open-Angle Glaucoma: A Systematic Review and Network Meta-analysis. Ophthalmology 2016;123:129-40. [Crossref] [PubMed]
173. Ang LP, Aung T, Chew PT. Acute primary angle closure in an Asian population: long-term outcome of the fellow eye after prophylactic laser peripheral iridotomy. Ophthalmology 2000;107:2092-6. [Crossref] [PubMed]
174. Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II Definition and Classification Report. Ocul Surf 2017;15:276-83. [Crossref] [PubMed]
175. Willcox MDP, Argüeso P, Georgiev GA, et al. TFOS DEWS II Tear Film Report. Ocul Surf 2017;15:366-403. [Crossref] [PubMed]
176. Javadi MA, Feizi S. Dry eye syndrome. J Ophthalmic Vis Res 2011;6:192-8.
177. Huang R, Su C, Fang L, et al. Dry eye syndrome: comprehensive etiologies and recent clinical trials. Int Ophthalmol 2022;42:3253-72. [Crossref] [PubMed]
178. Song P, Xia W, Wang M, et al. Variations of dry eye disease prevalence by age, sex and geographic characteristics in China: a systematic review and meta-analysis. J Glob Health 2018;8:020503. [Crossref] [PubMed]
179. Findlay Q, Reid K. Dry eye disease: when to treat and when to refer. Aust Prescr 2018;41:160-3. [Crossref] [PubMed]
180. Tsubota K. Short Tear Film Breakup Time-Type Dry Eye. Invest Ophthalmol Vis Sci 2018;59:DES64-70. [Crossref] [PubMed]
181. Messmer EM. The pathophysiology, diagnosis, and treatment of dry eye disease. Dtsch Arztebl Int 2015;112:71-81; quiz 82. [Crossref] [PubMed]
182. Hynnekleiv L, Magno M, Vernhardsdottir RR, et al. Hyaluronic acid in the treatment of dry eye disease. Acta Ophthalmol 2022;100:844-60. [Crossref] [PubMed]