Pediatric blepharokeratoconjunctivitis: a narrative review of the literature

Introduction

Background

Pediatric blepharokeratoconjunctivitis (PBKC), while carrying the risk of severe ocular morbidity, remains underdiagnosed and inadequately treated. This deficiency stems from a lack of understanding of the disease entity and that it is characterized by a constellation of symptoms and ocular surface pathology (1). In 2005, Hammersmith et al. reported the largest study at the time, including 29 children with PBKC (2). This study was one of the first to raise awareness of blepharokeratoconjunctivitis as common yet underrecognized in children. In the 20 years since, there have been concerted efforts to better understand the prevalence, pathophysiology, and clinical manifestations of PBKC as well as effective treatment of this potentially vision-threatening disease.

Rationale and knowledge gap

Historically, a variety of terms have been used to describe what we now understand as PBKC. These terms include staphylococcal blepharitis, childhood ocular rosacea, phylectenular keratoconjunctivits, and meibomitis-related keratoconjunctivitis (3-6). In 2024, Morales-Mancillas et al. proposed a standardized definition and diagnostic criteria for PBKC (5). A group of international expert panelists was selected to reach a consensus. The definition agreed upon is: “Pediatric Blepharokeratoconjunctivitis is a frequently under-diagnosed, sight-threatening, chronic and recurrent inflammatory eyelid margin disease associated with ocular surface involvement affecting children and adolescents. Its clinical spectrum includes chronic blepharitis, meibomitis, conjunctivitis, and corneal involvement ranging from superficial punctate keratitis and corneal infiltrates to vascularization and scarring.” (5).

Delayed diagnosis of PBKC stems from a lack of complete understanding of the disease process, in particular treating presentations such as recurrent chalazia, blepharitis, and phylectenular keratoconjunctivitis as isolated entities when oftentimes these clinical phenomena constitute the more complex clinical picture of PBKC (1,3,4). When treating each of these entities individually, treatment is often inadequate and results in incomplete response to treatment and recurrence of disease, resulting in severe complications and vision loss (1,4). The above standardized definition of PBKC is a major step forward in closing the PBKC knowledge gap.

Objective

This narrative review aims to provide a comprehensive overview of the epidemiology, pathophysiology, clinical characteristics, diagnostic criteria, complications, and treatment of PBKC that is understood to date with the ultimate goal of supporting healthcare providers in timely diagnosis and treatment of this challenging childhood ocular disease. Additionally, this review presents the use of imaging modalities in diagnosing PBKC and monitoring response to treatment, as well as the potential use of emerging therapies in treating PBKC. I present this article in accordance with the Narrative Review reporting checklist (available at https://aes.amegroups.com/article/view/10.21037/aes-25-49/rc).

Methods

A literature search was conducted utilizing the PubMed database. The search was conducted with the following terms: “pediatric blepharokeratoconjunctivitis”, “pediatric blepharitis”, and “pediatric blepharoconjunctivitis”. The search yielded articles published between 2005 and 2025. All studies included were written in English and included case reports, retrospective studies, and review articles. One randomized controlled trial was identified and included. Fifty-one articles were identified as relevant to the presented topic and independently reviewed by the author. All articles identified in the search process were included. There were no specific inclusion criteria. The only exclusion criterion was publication in a language other than English due to the inability to obtain a reliable translation. The search strategy is presented in Table 1.

Epidemiology

Prevalence

The global incidence and prevalence of PBKC remain undefined (4). In the United States, the estimated prevalence of PBKC was 0.59 cases per 10,000 children as reported by Fung et al. in 2024 (7). This estimate likely underestimates the true prevalence due to overlapping clinical features with other ocular diseases, leading to frequent misdiagnoses. PBKC accounts for a significant portion of referrals to tertiary care centers; Hammersmith et al. reported PBKC as the most common single diagnosis at referral to their institution, constituting 15–25% of the pediatric corneal referrals (3). A case series conducted in India reported a markedly higher incidence of PBKC at 12% of all pediatric cases seen in an ophthalmology clinic, whereas in a Hong Kong study, PBKC was the second most common diagnostic entity (8,9).

Age

PBKC may present from 5 months to teenage years, however, the mean age of onset for PBKC has been reported as ranging from 3 to 9 years, while mean age at diagnosis ranges from 6 to 10 years (3,6,10-12). The higher mean age at diagnosis is due to an often significant delay in diagnosis and referral to higher level care, sometimes delayed by as much as several years (3,13-15).

Sex

The sex distribution of PBKC varies across studies with some studies reporting a female predominance, with rates as high as 80–87% (1,4). In a South Korean study, 65.7% of PBKC patients were female; similarly, a Turkish study found 75% female predominance of PBKC (11,16). Other studies note an equal male-to-female ratio (7,15). An Indian study identified a male predominance (8).

Race and ethnicity

The prevalence and severity of PBKC vary across racial and ethnic groups. Asian and Hispanic children have shown higher rates of PBKC, with rates of diagnosis reported to be as high as twice the frequency of white children in the U.S. (7). Children of Indo-Pakistani, Middle Eastern, and Sri Lankan descent have been reported to show a higher incidence of severe complications compared to white children (17). A Singaporean study identified an overrepresentation of Indian children with PBKC compared to the general population, and a more severe clinical spectrum in the Asian population overall (18). In a Mexican study, Hispanic children with PBKC presented at an older mean age of diagnosis of 9.3 years compared to other reports with a tendency for higher risk of corneal involvement (15). Another study found that Hispanic patients had worse initial and final best-corrected visual acuity despite similar clinical presentation and prescribed treatments compared to non-Hispanic patients (19).

Pathophysiology

The pathophysiology of PBKC involves a complex interplay of multiple contributing factors, including meibomian gland dysfunction (MGD), bacterial colonization and infectious agents, a type IV hypersensitivity reaction, immune dysregulation and inflammation, Demodex mite infestation, genetic predisposition, and environmental influences (1,4,14).

MGD

MGD is a core feature of PBKC (1,3,5). MGD leads to tear film lipid deficiency and the activation of inflammatory pathways (10,20). Keratinization of epithelial cells can obstruct the gland’s opening, leading to intraglandular cystic dilation, gland atrophy, meibocyte loss, and altered meibum (1). Meibomian gland dropout, ductal dilation, and localized lid inflammation are distinctive signs of MGD in PBKC. Children with PBKC have shown higher rates of meibomian gland dropout compared to other groups (4).

Bacterial colonization

Bacterial colonization of the meibomian glands and ocular surface has been identified as a significant contributor to the pathophysiology of PBKC (1,4,10). Commonly implicated pathogens include Stalphylococcus aureus, Staphylococcus epidermidis, Propionibacterium acnes, and Corynebacteria (1,4,8,21). Inflammation results from the direct toxic action of staphylococcal exotoxins on the ocular surface (4,15,22).

Type IV hypersensitivity reaction

A type IV hypersensitivity reaction against bacterial cell wall antigens has also been implicated in the pathophysiology of PBKC (4,5,14,15). Children may be more susceptible to corneal damage due to an exaggerated, immature immune response to these bacterial antigens (4,13,15). Bacterial phospholipases disrupt the tear film and promote the release of inflammatory cytokines (21). Propionibacterium acnes, in particular, is hypothesized to play a pathogenic role by causing delayed-type hypersensitivity reactions that can lead to phylectenule formation (1,5). It may also promote a chronic inflammatory response leading to granuloma formation and recurrent chalazia (1).

Immune dysregulation

PBKC is characterized by persistent inflammation and immune system dysfunction. An excessive activation of the innate immune system, particularly toll-like receptors and the complement system, leads to an elevated production of proinflammatory cytokines and chemokines (1,6). These elevated levels of proinflammatory cytokines, such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and matrix metalloproteinases (MMPs) have been observed in the tears and conjunctival tissues of affected patients (1,6,23). These inflammatory mediators cause vascular changes, recruit immune cells, and compromise ocular surface integrity (6,23). T cells (CD4⁺, CD8⁺) contribute to the inflammatory response, with increased T helper (Th) 1 and Th17 pathways (24). Overexpression of the cathelicidin LL-37 (an antimicrobial peptide) and kallikrein (KLK5) is also thought to induce inflammation, angiogenesis, and neovascularization in PBKC, similar to what is observed in rosacea (6,23).

Demodex mite infestation

Ocular demodicosis has been reported as a potential cause of refractory PBKC (25). Both Demodex folliculorum and Demodex brevis mites have been implicated in the pathogenesis of PBKC (4,6). Wu et al. found that Demodex infestation was more frequent in individuals with blepharokeratoconjunctivitis compared to healthy subjects (56% vs 26%) and is associated with worse lid margin inflammation and MGD (13). Demodex mites can incite hypersensitivity reactions in younger people and may also act as vectors for bacteria (6,26). Demodex brevis, in particular, induces a granulomatous reaction by burrowing into the meibomian glands (4). The density of mites, rather than mere colonization, is correlated with pathogenic effect (1).

Genetic predisposition

A genetic predisposition is suspected to contribute to the disease process, possibly involving human leukocyte antigen (HLA)-B26 and HLA-B35 associations (18,19,27). Immunogenetic susceptibility factors play a role in how the host recognizes and responds to bacterial antigens (5,14,15,27).

Environmental factors

Environmental influences and hygiene have also been proposed as contributing factors in the pathogenesis of PBKC. Exposure to irritants and inadequate hygiene practices have been identified as risk factors for developing PBKC (4,6). The rise in severe PBKC during the coronavirus disease 2019 (COVID-19) pandemic suggested a link to increased bacterial load on face masks and potential microbial dysbiosis from increased periocular skin moisture (28). Socioeconomic factors, such as access to healthcare, transportation, and affordability of treatments may play a role in children presenting with worse disease (19).

Clinical features and diagnosis

PBKC has a prolonged course with exacerbations and recurrences and involves the eyelids, conjunctiva, and cornea (1,4-6,29). The differential diagnosis for PBKC includes vernal keratoconjunctivitis, atopic keratoconjunctivitis, viral conjunctivitis, and herpes simplex ocular disease (4,30).

Symptoms

Presenting symptoms include redness of the eyes, tearing, foreign body sensation, photophobia, ocular irritation or discomfort, burning, itching, and blurred vision (1,4-6,14,27). Symptoms are often more severe in the morning (17,29). Although PBKC is generally viewed as a bilateral condition, asymmetry can occur, where one eye has severe corneal involvement and the fellow eye has only mild eyelid symptoms (1,2,6,15). A high level of suspicion should be maintained in children with asymmetric presentation.

Eyelids

Recurrent chalazia is a major and highly suggestive feature, present in 5–75% of patients with PBKC. Chronic blepharitis is the most common palpebral manifestation. MGD is a core feature of PBKC, often presenting as inspissated glands, pouting, or capping of the glands. Lid margin telangiectasia, inflammation, and erythema are also common. Crusting, scaling, collarettes, and scurf may be present as well. Chronic cases can demonstrate ulceration of the lids, lid notching, madarosis, or trichiasis (1,3-5,8,11,13,15,27,29).

Conjunctiva

Conjunctival hyperemia is a consistent and frequently observed sign, particularly during active disease (1,6,8,13). Papillary and follicular reactions can also be present (1). Phylectenules may appear in the conjunctiva, limbus, or cornea. PBKC-related phylectenules can involve the paracentral and central cornea, leading to vascularization and visual impairment (1,6). One group reported a case series of three patients with PBKC who developed subconjunctival crystalline deposits (31). Another series reported a case of one patient with a Bitot-like spot thought to be associated with PBKC (32).

Cornea

Corneal involvement is a significant feature of PBKC, ranging from 5–81% of cases, and is often the latest stage of the disease (1,6,8,14,15,33,34). Superficial punctate keratitis (SPK) is the earliest and most common corneal sign; it is often focal but can be diffuse (1,6,14,15,18). Corneal vascularization is common and has been reported in up to 90.2% in some cohorts; it can involve significant clock hours and multiple quadrants (6,11,13,18,26,27,29). Corneal scarring and infiltrates occur frequently. Corneal thinning can also occur, and in severe cases, can lead to corneal ulceration and perforation (3,13,18,23,34,35). Corneal changes tend to be located inferiorly or inferotemporally and in peripheral/limbal areas (9,11,36).

Skin

Previously, skin manifestations such as flushing, facial erythema, and telangiectasia on the face, were thought to have a role in PBKC (6,13,27,29,37). In recent years, it has become understood and accepted that PBKC can occur in the complete absence of facial skin manifestations (1,5).

Diagnostic criteria

In 2024, The PBKC Study Group published diagnostic criteria for definitive PBKC and PBKC suspect in an effort to standardize diagnosis and subsequent appropriate treatment of PBKC. To make a proper diagnosis of PBKC, the patient must be <18 years of age and have one or more suggestive symptoms. Qualifying symptoms include recurrent chalazia, ocular irritation, burning, tearing, chronic discomfort, photophobia, foreign body sensation, and red eye. Additionally, the patient must present with one or more signs at each anatomical region of involvement: eyelid margin, conjunctiva, and cornea in order to be diagnosed definitively with PBKC. Eyelid margin signs include meibomitis, MGD, lid inflammation, lid erythema, chalazion, and hordeolum. Conjunctival signs include conjunctival hyperemia, conjunctivitis, and phylectenule. Corneal signs include infiltrates, vascularization, thinning, phylectenule, scarring, ulcer, pannus, and SPK. A diagnosis of PBKC suspect can be made when the lid margin and conjunctiva are involved but there is no corneal involvement (5).

Diagnostic technique

PBKC remains a clinical diagnosis, with slit-lamp biomicroscopy performed when possible. There have been several studies investigating the utility and efficacy of imaging tools in diagnosing and managing PBKC. Al-Hayouti et al. utilized color photography with and without instillation of topical fluorescein, keratograph meibography of the upper and lower eyelids, and anterior segment optical coherence tomography (AS-OCT) to grade clinical severity of PBKC; they found that the children in their cohort tolerated the imaging well and that they were able to achieve automated conjunctival hyperemia quantification (10). In another study, the same group evaluated non-contact infrared meibography and AS-OCT to detect meibomian gland and corneal changes in PBKC; again, they found that the children tolerated the imaging well and also found that these non-contact imaging technologies objectively demonstrated damage to meibomian glands and changes in corneal volume secondary to PBKC (38). Slit lamp photography may be useful in evaluating corneal neovascularization response to treatment (39). Plasencia et al. proposed a role for corneal topography in evaluating corneal involvement and understanding the reduced visual function resulting from refractive changes in moderate-to-severe cases of PBKC (36). Although PBKC has always been and remains a clinical diagnosis, the knowledge that certain imaging tools are well-tolerated by young children may allow for the adjunct usage of imaging in monitoring response to treatment in refractory cases.

Treatment

There is no definitive cure for PBKC. Treatment focuses on controlling inflammation, reducing bacterial load, improving meibomian gland function, and enhancing tear film quality. A multifaceted and individualized approach is necessary and often involves a step-wise progression of therapies (1,4,6,40).

Eyelid hygiene

Lid hygiene is the cornerstone of treatment for PBKC and consists of warm compresses to melt meibomian gland secretions and open gland orifices, gentle lid massage to assist secretion outflow, and eyelid cleansing with diluted baby shampoo or commercially available cleansers to help remove debris and reduce bacterial colonization along the lid margin. Compliance with sustained eyelid hygiene is critical in preventing recurrence of disease (1,4,8,40).

Topical medications

Topical antibiotics can be used in isolation or in combination with systemic antibiotics to treat mild cases of PBKC. Topical 0.5% erythromycin ointment can be safely used as monotherapy twice daily or at nighttime in children with mild PBKC for several weeks to months. When applied to a clean lid margin at bedtime, erythromycin ointment may decrease the bacterial load of staphylococcal species and other microflora (1). Azithromycin 1.5% eye drops have shown efficacy in controlling ocular redness, conjunctival phylectenules, corneal inflammation and blepharitis in PBKC cases unresponsive to lid hygiene and intermittent topical steroids (3,4,20).

Combination eye drops such as dexamethasone 0.1% with azithromycin 1.0% or dexamethasone 0.1% with moxifloxacin 0.5% can be effective in treating PBKC by reducing both bacterial load and inflammation (4). Tobramycin combinations with either dexamethasone or loteprednol etabonate offer similar safety and efficacy (41).

Topical corticosteroids are used to manage corneal inflammation and prevent neovascularization and scarring, especially during the acute phase of the disease (29). Lower potency steroids such as loteprednol 0.2–0.5% and fluorometholone 0.1% are preferred to reduce risks of ocular hypertension, secondary glaucoma, and cataract formation (2). Intraocular pressure must be closely monitored in children using topical corticosteroids due to the risk of ocular hypertensive response (1,42).

Calcineurin inhibitors such as cyclosporine A (CsA) and tacrolimus treat PBKC by inhibiting T-lymphocyte activation and calcineurin, thereby controlling lid, conjunctival, and corneal inflammation. CsA is often used as a steroid-sparing agent, with benefits typically starting after 4 weeks of treatment. CsA has been shown to reduce topical corticosteroid use in 99% of cases, with 90% discontinuing topical corticosteroid use entirely (1,24). Ocular stinging is a common side effect. Tacrolimus 0.3% ointment is reported to be 100 times more potent than CsA and may be considered a safer long-term alternative to steroids (4).

Systemic medications

Moderate to severe PBKC is often treated with systemic antibiotics as they possess both anti-inflammatory and antimicrobial properties (29,39,43). These can be used alone or in combination with topical treatments to augment treatment efficacy. Tetracyclines treat PBKC by inhibiting neutrophil chemotaxis and migration as well as lymphocyte proliferation (4). Doxycycline is the most commonly used tetracycline to treat PBKC; it is generally avoided in children under 8 years of age due to risk of teeth staining or enamel hypoplasia, although more recent data suggest that doxycycline is unlikely to cause these effects, even in younger children (1,44).

Macrolides are commonly used to treat PBKC (6). Erythromycin modulates proinflammatory cytokine production, prevents neutrophil adhesion, and alters sebum composition (4). Low-dose oral azithromycin inhibits leukocyte migration and decreases inflammatory mediators. Azithromycin is an attractive alternative due to its longer half-life, higher ocular penetration, lower gastrointestinal side effects, and anti-inflammatory properties (27).

Amoxicillin 400 mg with clavulanic acid 57 mg may be effective in treating PBKC. A small series of 7 patients treated with amoxicillin 400 mg/clavulanic acid 57 mg given twice daily for 1 month on average were effectively treated; there were no documented adverse or side effects, and 6 out of the 7 children had no recurrence of disease during a mean 6-month follow-up period (45).

Systemic immunosuppressants are reserved for severe, unresponsive, sight-threatening keratitis (1). These may include oral prednisone, followed by azathioprine, methotrexate or mycophenolate mofetil (3,4). These immunomodulatory agents typically require 3 months to achieve full effect (1).

Demodex treatment

Treatment of Demodex mite infestation targets reducing the mite population, as complete eradication is not feasible. Options include eyelid scrubs or massage with tea tree oil and oral ivermectin (25,26). 0.25% lotilaner ophthalmic solution has Food and Drug Administration (FDA) approval for Demodex blepharitis and has demonstrated safety and efficacy (4).

Dietary supplements

Omega-3 fatty acids compete with enzymes to decrease proinflammatory cytokine production, aiding in MGD and blepharitis-related ocular surface dryness (4). A daily dose of 2.5 mL of flaxseed oil prevented disease exacerbations in some patients whose disease recurred when systemic antibiotics were stopped (12). Further randomized controlled trials are needed to determine the efficacy of Omega-3 fatty acid and/or flaxseed supplementation in children with PBKC.

Emerging therapies

Intense pulsed light (IPL) therapy has been studied in adults for MGD and blepharitis to improve meibomian gland secretion, reduce telangiectasis, and eradicate Demodex (1). In 2022, Zhai et al. demonstrated safety and efficacy of low-fluence IPL therapy in improving symptoms and signs of moderate-to-severe blepharitis in 17 children. Most studies on this treatment have been conducted on adults, and more research is needed to determine the safety and efficacy in children (46).

Complications and visual outcomes

Vision loss in PBKC primarily stems from corneal involvement and its chronic, recurrent inflammatory nature, with the potential to cause irreversible visual impairment or even blindness.

Severe corneal disease can progress to ulceration, extensive scarring, significant vascularization, and even perforations, necessitating surgical intervention. Surgical repair of corneal perforations secondary to severe PBKC includes amniotic membrane transplantation, tectonic grafts, deep anterior lamellar keratoplasty (DALK) and penetrating keratoplasty (PKP) (23,34,35).

PBKC-induced inflammation and corneal changes frequently cause or exacerbate irregular astigmatism and higher order aberrations (HOAs) (14,36). The affected eyes carry a high risk of developing amblyopia that is either deprivational due to dense corneal opacities, refractive due to uncorrected astigmatism and/or anisometropia, or a combination of both. Scleral contact lenses may have a role in treating chronic PBKC (47). Refractive errors and amblyopia should be treated as early as possible with close follow-up to monitor response to treatment (12,48,49).

Strengths and limitations

The strengths of this review are its broad scope in representing the most relevant literature available on PBKC to date as well as the inclusion of the potential role for imaging tools in diagnosis/management and emerging therapies. International representation is present in the literature reviewed here.

There are several limitations to this review. The narrow search terms were a deliberate decision in efforts to capture the most relevant literature, especially with increasing knowledge and understanding of PBKC in recent years. Although the literature search captured publications with titles that did not include the search terms, such as ocular rosacea and ocular surface infections, other relevant publications may have been missed. In addition, the narrative nature of this literature review carries inherent limitations due to the less rigorous requirements as compared to a systematic review, which requires that included articles meet predetermined criteria. The only exclusion criterion was publication in a language other than English. Although this resulted in exclusion of only 3 articles identified during the search, exclusion of non-English studies may contribute to bias. Another limitation is the lack of randomized controlled trials available for inclusion; only 1 randomized controlled trial was identified in the literature search. Two Cochrane reviews on PBKC were published in 2016 and 2017: one on systemic treatments for PBKC and the other on topical treatments for PBKC (50,51). Both of these Cochrane reviews were unable to provide systematic recommendations due to the lack of studies meeting criteria for inclusion. This further emphasizes the need for additional research on PBKC. There is a need for well-designed randomized controlled trials investigating efficacy of the use of standardized diagnostic criteria as well as response to various treatment algorithms, both in the short-term as well as evaluating risk of recurrence in the long-term. Further investigation into the impact of imaging modalities in diagnosis and response to treatment may also enable earlier detection and intervention, mitigating severe disease and poor visual outcomes.

Conclusions

In recent years, PBKC has attracted significant attention within the ophthalmologic community in efforts to better understand the complex etiology, pathogenesis, and clinical picture so as to successfully treat this challenging and potentially vision-threatening childhood ocular disease. The standardized definition and diagnostic criteria proposed by the PBKC Study Group in 2024, once broadly adopted, will shorten the delay in diagnosis and hopefully reduce severity of disease with earlier interventions. Effective treatment and management remain a challenge. Imaging modalities such as color photography, meibography, AS-OCT, and topography may play a role in decreasing the delay in diagnosing PBKC and monitoring response to treatment. Further investigation is critical to advance care and improve visual outcomes in patients affected by PBKC.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editors (Roy S. Chuck & Joann J. Kang & Viral V. Juthani) for the series “Inflammatory Disorders of the Cornea and Ocular Surface” published in Annals of Eye Science. The article has undergone external peer review.

Reporting Checklist: The author has completed the Narrative Review reporting checklist. Available at https://aes.amegroups.com/article/view/10.21037/aes-25-49/rc

Peer Review File: Available at https://aes.amegroups.com/article/view/10.21037/aes-25-49/prf

Funding: None.

Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://aes.amegroups.com/article/view/10.21037/aes-25-49/coif). The series “Inflammatory Disorders of the Cornea and Ocular Surface” was commissioned by the editorial office without any funding or sponsorship. The author has no other conflicts of interest to declare.

Ethical Statement: The author is 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. Ortiz-Morales G, Ruiz-Lozano RE, Morales-Mancillas NR, et al. Pediatric blepharokeratoconjunctivitis: A challenging ocular surface disease. Surv Ophthalmol 2025;70:516-35. [Crossref] [PubMed]
2. Hammersmith KM, Cohen EJ, Blake TD, et al. Blepharokeratoconjunctivitis in children. Arch Ophthalmol 2005;123:1667-70. [Crossref] [PubMed]
3. Hammersmith KM. Blepharokeratoconjunctivitis in children. Curr Opin Ophthalmol 2015;26:301-5. [Crossref] [PubMed]
4. Awan R, Khan S, Khan WA. Pediatric blepharokeratoconjunctivitis: review of epidemiology, pathophysiology, and current treatments. Curr Opin Ophthalmol 2025;36:314-21. [Crossref] [PubMed]
5. Morales-Mancillas NR, Velazquez-Valenzuela F, Kinoshita S, et al. Definition and Diagnostic Criteria for Pediatric Blepharokeratoconjunctivitis. JAMA Ophthalmol 2024;142:39-47. [Crossref] [PubMed]
6. Mohamed-Noriega K, Loya-Garcia D, Vera-Duarte GR, et al. Ocular Rosacea: An Updated Review. Cornea 2025;44:525-37. [Crossref] [PubMed]
7. Fung SSM, Boghosian T, Perez C, et al. Epidemiology of Pediatric Ocular Surface Inflammatory Diseases in the United States Using the Optum Labs Data Warehouse. Ophthalmology 2024;131:568-76. [Crossref] [PubMed]
8. Gupta N, Dhawan A, Beri S, et al. Clinical spectrum of pediatric blepharokeratoconjunctivitis. J AAPOS 2010;14:527-9. [Crossref] [PubMed]
9. Wong VW, Lai TY, Chi SC, et al. Pediatric ocular surface infections: a 5-year review of demographics, clinical features, risk factors, microbiological results, and treatment. Cornea 2011;30:995-1002. [Crossref] [PubMed]
10. Al-Hayouti H, Daniel M, Hingorani M, et al. Automated Ocular Surface Image Analysis and Health-Related Quality of Life Utility Tool to Measure Blepharokeratoconjunctivitis Activity in Children. Cornea 2019;38:1418-23. [Crossref] [PubMed]
11. Moon J, Lee J, Kim MK, et al. Clinical Characteristics and Therapeutic Outcomes of Pediatric Blepharokeratoconjunctivitis. Cornea 2023;42:578-83. [Crossref] [PubMed]
12. Jones SM, Weinstein JM, Cumberland P, et al. Visual outcome and corneal changes in children with chronic blepharokeratoconjunctivitis. Ophthalmology 2007;114:2271-80. [Crossref] [PubMed]
13. Wu M, Wang X, Han J, et al. Evaluation of the ocular surface characteristics and Demodex infestation in paediatric and adult blepharokeratoconjunctivitis. BMC Ophthalmol 2019;19:67. [Crossref] [PubMed]
14. Mendoza-Zamora C, Gonzalez-Godinez S, Ortiz-Morales G, et al. The visual impact of higher-order aberrations in patients with pediatric blepharokeratoconjunctivitis. Int Ophthalmol 2024;44:60. [Crossref] [PubMed]
15. Rodríguez-García A, González-Godínez S, López-Rubio S. Blepharokeratoconjunctivitis in childhood: corneal involvement and visual outcome. Eye (Lond) 2016;30:438-46. [Crossref] [PubMed]
16. Barcsay-Veres A, Csorba A, Kovacs I, et al. Corticosteroid-sparing topical treatment with cyclosporin for juvenile keratoconjunctivitis. Sci Rep 2025;15:4671. [Crossref] [PubMed]
17. Viswalingam M, Rauz S, Morlet N, et al. Blepharokeratoconjunctivitis in children: diagnosis and treatment. Br J Ophthalmol 2005;89:400-3. [Crossref] [PubMed]
18. Teo L, Mehta JS, Htoon HM, et al. Severity of pediatric blepharokeratoconjunctivitis in Asian eyes. Am J Ophthalmol 2012;153:564-570.e1. [Crossref] [PubMed]
19. Wilberding M, Bolton EM, Bohnsack B, et al. Pediatric blepharokeratoconjunctivitis: findings and outcomes in Hispanic vs. Non-Hispanic patients. BMC Ophthalmol 2025;25:210. [Crossref] [PubMed]
20. Opitz DL, Harthan JS. Review of Azithromycin Ophthalmic 1% Solution (AzaSite(®)) for the Treatment of Ocular Infections. Ophthalmol Eye Dis 2012;4:1-14. [Crossref] [PubMed]
21. Çakır B, Sönmezoğlu BG, Şahin EÖ, et al. Evaluation of ocular surface microbiota in children with blepharoconjunctivitis. Graefes Arch Clin Exp Ophthalmol 2025;263:2359-67. [Crossref] [PubMed]
22. Hamada S, Khan I, Denniston AK, et al. Childhood blepharokeratoconjunctivitis: characterising a severe phenotype in white adolescents. Br J Ophthalmol 2012;96:949-55. [Crossref] [PubMed]
23. Nabih O, Hamdani H, El Maaloum L, et al. Spontaneous corneal perforation complicating ocular rosacea: Case report. Int J Surg Case Rep 2022;90:106597. [Crossref] [PubMed]
24. Dahlmann-Noor AH, Roberts C, Muthusamy K, et al. Cyclosporine A 1mg/ml in pediatric blepharokeratoconjunctivitis: Case series of 145 children and young people. Ocul Surf 2022;25:37-9. [Crossref] [PubMed]
25. Liang L, Safran S, Gao Y, et al. Ocular demodicosis as a potential cause of pediatric blepharoconjunctivitis. Cornea 2010;29:1386-91. [Crossref] [PubMed]
26. Patel NV, Mathur U, Gandhi A, et al. Demodex blepharokeratoconjunctivitis affecting young patients: A case series. Indian J Ophthalmol 2020;68:745-9. [Crossref] [PubMed]
27. Sari ES, Ozmen AT, Yildiz M, et al. Long-term, Low-Dose Oral Azithromycin Treatment for Chronic Severe Bilateral Blepharokeratoconjunctivitis in Pediatric Patients. J Pediatr Ophthalmol Strabismus 2024;61:358-64. [Crossref] [PubMed]
28. Barbara R, Khalili S, Maguire B, et al. Rise in the incidence of severe pediatric blepharokeratoconjunctivitis during the COVID-19 pandemic. J AAPOS 2023;27:216-9. [Crossref] [PubMed]
29. Rousta ST. Pediatric blepharokeratoconjunctivitis: is there a 'right' treatment?. Curr Opin Ophthalmol 2017;28:449-53. [Crossref] [PubMed]
30. Musa M, Bale BI, Suleman A, et al. Possible viral agents to consider in the differential diagnosis of blepharoconjunctivitis. World J Virol 2024;13:97867. [Crossref] [PubMed]
31. Mehta JS, Sagoo MS, Tuft SJ. Subconjunctival crystals in paediatric blepharokeratoconjunctivitis. Acta Ophthalmol Scand 2006;84:557-8. [Crossref] [PubMed]
32. Maudgil A, Rachdan D, Khan MS, et al. Bitot-like spots in children with normal vitamin A levels. Eye (Lond) 2022;36:1896-9. [Crossref] [PubMed]
33. Cetinkaya A, Akova YA. Pediatric ocular acne rosacea: long-term treatment with systemic antibiotics. Am J Ophthalmol 2006;142:816-21. [Crossref] [PubMed]
34. Fu L, Jones SM. Tectonic mini-Descemet stripping endothelial keratoplasty (mini-DSEK) in the management of corneal perforation secondary to pediatric blepharokerato conjunctivitis. J AAPOS 2023;27:45-7. [Crossref] [PubMed]
35. Pant OP, Hao JL, Zhou DD, et al. Tectonic keratoplasty using femtosecond laser lenticule in pediatric patients with corneal perforation secondary to blepharokeratoconjunctivitis: a case report and literature review. J Int Med Res 2019;47:2312-20. [Crossref] [PubMed]
36. Plasencia Salini R, Boghosian T, Khalili S, et al. Topographic corneal changes in children with moderate to severe blepharokeratoconjunctivitis. J AAPOS 2025;29:104108. [Crossref] [PubMed]
37. Donmez O, Akova YA. Pediatric Ocular Acne Rosacea: Clinical Features and Long Term Follow-Up of Sixteen Cases. Ocul Immunol Inflamm 2021;29:57-65. [Crossref] [PubMed]
38. Al-Hayouti H, Daniel M, Hingorani M, et al. Meibography and corneal volume optical coherence tomography to quantify damage to ocular structures in children with blepharokeratoconjunctivitis. Acta Ophthalmol 2019;97:e981-6. [Crossref] [PubMed]
39. Ceylan A, Onal I, Aydin FO, et al. Improvement of Clinical Findings, Meibography and Tear Film Parameters in Pediatric Ocular Rosacea Patients After a Standard Treatment Protocol. Ocul Immunol Inflamm 2024;32:2130-7. [Crossref] [PubMed]
40. Ortiz-Morales G, Morales-Mancillas NR, Paez-Garza JH, et al. Letter Regarding: Clinical Characteristics and Therapeutic Outcomes of Pediatric Blepharokeratoconjunctivitis. Cornea 2023;42:e10-1. [Crossref] [PubMed]
41. Comstock TL, Paterno MR, Bateman KM, et al. Safety and tolerability of loteprednol etabonate 0.5% and tobramycin 0.3% ophthalmic suspension in pediatric subjects. Paediatr Drugs 2012;14:119-30. [Crossref] [PubMed]
42. Mataftsi A, Narang A, Moore W, et al. Do reducing regimens of fluorometholone for paediatric ocular surface disease cause glaucoma? Br J Ophthalmol 2011;95:1531-3. [Crossref] [PubMed]
43. Gonser LI, Gonser CE, Deuter C, et al. Systemic therapy of ocular and cutaneous rosacea in children. J Eur Acad Dermatol Venereol 2017;31:1732-8. [Crossref] [PubMed]
44. Khaslavsky S, Starkey SY, Avraham S, et al. Treatment of pediatric ocular rosacea: A systematic review. Ann Dermatol Venereol 2023;150:199-201. [Crossref] [PubMed]
45. Cehajic-Kapetanovic J, Kwartz J. Augmentin duo™ in the treatment of childhood blepharokeratoconjunctivitis. J Pediatr Ophthalmol Strabismus 2010;47:356-60. [Crossref] [PubMed]
46. Zhai Z, Jiang H, Wu Y, et al. Safety and Feasibility of Low Fluence Intense Pulsed Light for Treating Pediatric Patients with Moderate-to-Severe Blepharitis. J Clin Med 2022;11:3080. [Crossref] [PubMed]
47. Severinsky B, Lenhart P. Scleral contact lenses in the pediatric population-Indications and outcomes. Cont Lens Anterior Eye 2022;45:101452. [Crossref] [PubMed]
48. Dionne E, Henick D, Rotruck J. Prevalence of Blepharokeratoconjunctivitis and Refractive Amblyopia Risk Factors in Children With Chalazia: Safety Considerations in Telehealth Management. J Pediatr Ophthalmol Strabismus 2025;62:278-85. [Crossref] [PubMed]
49. Valadez J, Arreguin AJ, Padovani-Claudio DA. Demographic disparities in the prevalence of pediatric corneal neovascularization cases at a tertiary care center. J AAPOS 2025;29:104224. [Crossref] [PubMed]
50. O'Gallagher M, Banteka M, Bunce C, et al. Systemic treatment for blepharokeratoconjunctivitis in children. Cochrane Database Syst Rev 2016;2016:CD011750. [Crossref] [PubMed]
51. O'Gallagher M, Bunce C, Hingorani M, et al. Topical treatments for blepharokeratoconjunctivitis in children. Cochrane Database Syst Rev 2017;2:CD011965. [Crossref] [PubMed]