Sie können Operatoren mit Ihrer Suchanfrage kombinieren, um diese noch präziser einzugrenzen. Klicken Sie auf den Suchoperator, um eine Erklärung seiner Funktionsweise anzuzeigen.
Findet Dokumente, in denen beide Begriffe in beliebiger Reihenfolge innerhalb von maximal n Worten zueinander stehen. Empfehlung: Wählen Sie zwischen 15 und 30 als maximale Wortanzahl (z.B. NEAR(hybrid, antrieb, 20)).
Findet Dokumente, in denen der Begriff in Wortvarianten vorkommt, wobei diese VOR, HINTER oder VOR und HINTER dem Suchbegriff anschließen können (z.B., leichtbau*, *leichtbau, *leichtbau*).
Dry eye disease (DED) poses a significant and escalating public health challenge. Effective diagnosis is crucial for optimal management. However, current practices are complicated and time-consuming. This paper proposes a revised framework for diagnosing and treating in Hong Kong, explicitly tailored to the local healthcare context and incorporating insights from global consensus guidelines. The framework emphasizes a streamlined assessment strategy and prioritizes direct symptom-based questioning alongside objective tests. It also includes a simplified corneal staining grading scheme to reduce complexity, considering the limited consultation time available in Hong Kong. Furthermore, the framework clearly outlines the appropriate treatment options based on the disease’s severity and etiological cause(s) and focuses on the need for long-term management through follow-up or referrals. By addressing the multifaceted nature of DED and considering local healthcare constraints, this framework seeks to enhance patient outcomes through timely diagnosis and accurate assessment and treatment of DED.
Prior Presentation: This manuscript has no history of prior presentation or publication.
Key Summary Points
Current practices in the management of dry eye disease (DED) are often complicated and time-consuming.
This paper introduces a clear and concise framework for diagnosing and managing DED tailored specifically to general ophthalmologists and eye care practitioners in Hong Kong, reflecting the nuances of the local healthcare system while incorporating global consensus guidelines.
The framework aims to provide a simple and practical tool by combining direct symptom-based questioning with objective tests, minimizing complexity in severity grading to streamline DED identification and assessment within the increasingly limited time frame available.
Additionally, it outlines potential treatment options based on the disease’s severity and etiological cause(s) and focuses on the need for long-term management through follow-up or referrals.
The proposed DED framework is customized to meet the unique needs of both patients and eye care practitioners within the Hong Kong context.
Introduction
Dry eye disease (DED) represents a significant and growing public health concern, particularly in aging populations [1‐3]. There is remarkable variability in the reported prevalence estimates in adult populations globally, ranging from 5 to 50% [4‐8]. In Asia, the estimated pooled prevalence of DED was 20.1% [9]. With increasing digital screen use and environmental stressors, the prevalence of DED is expected to rise, posing challenges to healthcare systems worldwide [10‐13].
Anzeige
According to the 2017 report of the Tear Film & Ocular Surface Society (TFOS) Dry Eye Workshop II (DEWS II), DED is characterized by the loss of homeostasis of the tear film, which includes tear hyperosmolarity, ocular surface inflammation and damage and neurosensory abnormalities [14].
Based on the DEWS II report, DED has been categorized into two main subtypes: aqueous-deficient dry eye (ADDE) and evaporative dry eye (EDE) [14]. ADDE occurs when there is insufficient tear production by the lacrimal glands, often associated with conditions such as Sjögren's syndrome [15, 16], while EDE is primarily due to excessive evaporation of the tear film, frequently linked to meibomian gland dysfunction (MGD) [17, 18]. Both forms of DED can overlap, and diagnosis is often complicated by the presence of multiple contributing factors, including environmental conditions and systemic diseases.
In recent years, the classification of DED has evolved with advancements in understanding its pathophysiology, particularly through the contributions of the Asian Dry Eye Society (ADES). The ADES proposed a more refined classification system that includes a third subtype known as "decreased wettability" dry eye (DWDE), which recognizes the role of membrane-associated mucin [19]. In this subtype, although tear production may be normal, the tears fail to adhere properly to the ocular surface because the membrane-associated mucin is deficient, resulting in an unstable tear film. This instability can contribute to symptoms of dryness and visual disturbance, despite the presence of an “apparently normal tear volume” [19].
The ADES classification system not only recognizes the conventional aqueous deficiency and evaporative mechanisms but also addresses the role of surface wettability in maintaining ocular hydration. This increased emphasis on wettability represents a shift from the traditional two-subtype model, acknowledging that the tear film’s interaction with the ocular surface is just as crucial as its production and evaporation [20]. This recognition has been supported by emerging evidence showing that even in patients without significant MGD or lacrimal gland insufficiency, an abnormal tear film can lead to significant discomfort and visual impairment due to poor surface spreading [21]. By including increased wettability as a distinct category, eye care practitioners can better tailor treatments to target specific mechanisms underlying the disease. For example, management strategies for DWDE may focus on improving the surface properties of the corneal epithelium or enhancing tear film spreading rather than merely addressing tear production or evaporation [19].
Anzeige
DED represents a significant burden on patients’ quality of life, particularly due to its chronic nature and the resultant visual disturbances that interfere with everyday activities including reading, prolonged use of digital devices and tasks requiring sustained visual focus [22‐24].
The most commonly reported symptoms include dryness, burning, itching, photophobia and the sensation of a foreign body in the eye. However, an important clinical paradox exists: the severity of patient-reported symptoms often does not correlate with clinical findings [25, 26]. This disparity between subjective symptoms and objective measures can complicate the diagnosis and management of DED, as patients may experience debilitating discomfort despite seemingly mild clinical signs. Conversely, some individuals present with significant ocular surface damage in the absence of severe symptoms, complicating timely diagnosis [27‐29].
DED’s impact on patients extends beyond ocular discomfort to influence psychosocial well-being and work productivity. Many patients experience a substantial decline in their ability to perform both professional and personal tasks, leading to frustration and social withdrawal [30]. Moreover, the chronic irritation and fluctuating vision associated with DED can cause fatigue and reduced concentration, particularly during prolonged screen use or reading, which is central to modern life [10]. In many cases, patients rely heavily on over-the-counter lubricants, opting for self-management rather than seeking ophthalmic care [31]. This reliance on lubricants, while offering temporary relief, often fails to address the underlying etiology of DED, leading to chronicity and exacerbation of symptoms [31]. Patients may also delay seeking professional care due to a lack of awareness about the multifactorial nature of DED, contributing to its underdiagnosis and suboptimal management in clinical practice [32, 33].
The pressure faced by healthcare systems, particularly in regions such as Hong Kong, where public and private clinics are often overwhelmed by high patient volumes, exacerbates the challenge of managing DED. The time constraints inherent in these fast-paced clinical environments make lengthy diagnostic protocols impractical, often leading to underdiagnosis or inadequate treatment. As a result, improving the efficiency of DED diagnosis and management is critical. Streamlined protocols that balance thoroughness with practicality could allow for earlier detection and tailored interventions, thus preventing the progression of DED and its long-term sequelae. Implementing such protocols could not only improve patient outcomes but also alleviate some of the burden on healthcare systems by reducing the incidence of severe, chronic DED that requires more intensive treatment [17, 34].
A Tailored Approach to the Diagnosis and Treatment of Dry Eye Disease
Environmental, demographic, and lifestyle factors are driving a reconsideration of current diagnostic and management guidelines for DED. In Singapore, the absence of clear and practical guidelines for the assessment, diagnosis, and management of DED has been recognized as a significant challenge for eye care practitioners, particularly due to the constraints posed by limited consultation times. To address these unmet needs, a new framework has been developed. Specifically, the Corneal Subspecialty Workgroup of the College of Ophthalmology, Academy of Medicine, Singapore, has created a national framework aimed at assisting eye care practitioners in managing DED [34]. This framework integrates recommendations from expert-endorsed groups, such as the TFOS DEWS II and the Asia Cornea Society Workgroup, in addition to evidence from the existing literature. Similarly, in Hong Kong, the Hong Kong DED Framework Working Group (“Working Group”), a panel of specialists in ophthalmology from private, public and academic institutions, has discussed and optimized a framework for diagnosing and managing DED tailored to Hong Kong’s specific healthcare environment. The foundations of the Hong Kong DED Framework (“Framework”, “DED Framework”) are based on evidence taken from the literature and Singapore framework, as well as opinions summarized from the discussion of the HK DED Framework Advisory Board Meeting held on March 23, 2024.
Recommendations
The Hong Kong DED Framework is outlined in Fig. 1. The framework consists of two pathways tailored for different clinical settings based on the consultation time available. The Streamlined Pathway facilitates consultation within 15 min, while the Optimal Pathway addresses various etiological causes of the disease when time permits. This framework aims to provide a clear and practical tool to diagnose, assess the severity, optimize the treatment regimens and discuss the systematic follow-up and referral based on clinical circumstances, availability of tools, and consultation time, allowing a personalized DED management for each patient and continuously advance the overall DED awareness and optimal patient care in Hong Kong community. It is proposed that the framework be used to triage patients with DED for specialist management across private, public or university healthcare settings. The framework can help identify moderate to severe cases and be used for referrals for DED specialist management. Implementing a system to direct these patients to specialists in DED management could benefit both patients and practitioners.
The Streamlined Pathway outlines a simple and concise assessment and management of DED, with minimal tests required when consultation time is limited.
Assessment of Patients’ Medical History and Risk Factors
The assessment of DED and the exclusion of other possible causes should start with evaluating the patient’s medical history; as shown in Fig. 1, a comprehensive patient history is paramount in identifying modifiable risk factors and underlying causes that could influence management [14].
Anzeige
Demographic factors play a significant role in the development of DED, with advancing age and female sex being among the most prominent. Additionally, environmental factors, such as a patient’s country of residence, climate or work environment, may exacerbate symptoms. Of note, working in dusty environments or in spaces with excessive air currents may exacerbate DED (Table 1).
Table 1
Risk factors for DED diagnosis
Demographic factors
Environmental factors
Induced factors
Systemic diseases
Medications
Advancing age
Country of residence
Excessive computer or screen use
Sjögren’s syndrome
Antihistamines
Female sex
Climate*
Contact lens wear
Rheumatoid arthritis
Tricyclic antidepressants
Refractive surgeries
Work environment**
Inadequate sleep
Ocular mucous membrane pemphigoid
Antiglaucoma medication containing preservatives
Previous ocular, facial, or intracranial surgeries
Low dietary intake of omega-3 fatty acids
Lupus
Graft-versus-host disease
*In general, the northern APAC regions (i.e., Japan, Korea) has drier climates than south APAC (i.e., Singapore, Philippines). In addition, East Asia has the highest prevalence while North America showed the lowest regional prevalence [90]. Also, patients from the semiarid and subtropical desert climates exhibited higher levels of fluorescein staining, while patients from the Mediterranean climates had milder corneal staining [91]
**Dusty, low humidity, air-conditioning, chemical environments, and spaces with excessive air currents are contributing factors to be considered. [92]
Induced factors are also important contributors to DED. Refractive surgeries, including LASIK and other procedures, are known to disrupt the ocular surface and contribute to the condition’s onset. The prolonged use of contact lenses can exacerbate ocular surface inflammation, and work environments that demand excessive screen time or exposure to air-conditioned settings further strain the tear film.
Systemic diseases, including autoimmune conditions, are frequently implicated in DED. Sjögren’s syndrome, rheumatoid arthritis and cicatricial pemphigoid are notable examples, as these disorders disrupt the normal functioning of the lacrimal and meibomian glands [35, 36]. Allergic conditions, such as atopy or allergic conjunctivitis, also play a role in exacerbating DED. Finally, the use of medications, such as antihistamines, antidepressants, anxiolytics, antiglaucomatous drugs and isotretinoin, may impact the risk of DED [37].
Symptom Assessment
DED symptoms include burning or itching of the eyes, a foreign body sensation, excessive tearing, pain, redness, and photophobia [38‐41]. The clinical picture may also be accompanied by dry or stringy discharge and fluctuating episodes of blurred vision [42, 43]. Symptoms worsen in dry conditions, particularly in low humidity and elevated temperatures [44, 45]. The framework emphasizes the prioritization of direct symptom-based questioning and proposes six key symptoms that resonate with patients suffering from DED in Hong Kong [46]: tearing, stinging/burning, redness, foreign body sensations/grittiness, visual fluctuations, and dryness. These symptoms are triaged via a simple yes/no response, and the presence of any of the six symptoms would trigger a targeted slit lamp examination to evaluate for the signs of DED.
Anzeige
Sign Assessment with Slit-Lamp Examination
Upon symptom assessment, the framework recommends slit-lamp examination for every patient with DED complaints, as it facilitates a detailed evaluation of the ocular surface and adnexa. The primary purpose of the slit-lamp examination is to document any physical signs of DED, assess the tear film's quality, quantity and stability, and investigate other potential sources of ocular irritation. Particular attention should be given to the skin for signs of acne, eczema, rosacea or other dermatological conditions that may impact ocular health. Examination of the eyelids is essential to detect conditions such as incomplete closure, erythema, or abnormal secretions, which can exacerbate dry eye symptoms. In addition, the adnexa should be checked for enlargement of the lacrimal glands, and the neck for signs of goiter. Proptosis, as well as the functionality of cranial nerves, especially the trigeminal and facial nerves, should be evaluated. Any evidence of systemic conditions, such as rheumatoid arthritis or Raynaud's phenomenon, should be noted, as they can have ocular manifestations, while reduced blinking in Parkinson’s disease should also be considered due to their role in increasing tear evaporation.
During the slit-lamp examination, a detailed analysis of the tear film, eyelids, conjunctiva and cornea should be conducted. Observing the tear film through the height of the meniscus, viscosity and debris helps in assessing its stability, while abnormalities in the lid margins and meibomian glands, such as blepharitis, abnormalities or blockage of meibomian gland orifices, character of meibomian gland secretions, keratinization, scarring, Demodex infestation and rosacea features provide insights into underlying causes of DED. Further assessment of the blinking patterns, puncta for blockages, and the cornea for epithelial defects or signs of prior surgery complete the ocular surface evaluation. Visual acuity in patients with DED typically remains stable, but any marked reduction should prompt an investigation for other ocular conditions.
Clinical Tests
When DED is suspected based on symptoms, patient history, comorbidities, and findings from a physical or slit-lamp examination, a targeted ocular evaluation is essential to verify the diagnosis. As outlined in Fig. 1, a systematic approach using a sequence of clinical tests should be followed to arrive at a definitive diagnosis.
The eye care practitioner should assess tear meniscus height, which provides an estimate of tear volume. A tear meniscus height of less than 0.25 mm [47, 48] observed during a slit-lamp examination strongly suggests dry eye.
Anzeige
Furthermore, the framework recommends that at least one positive result from homeostasis markers, such as fluorescein tear break-up time (F-TBUT) or ocular surface staining, in conjunction with symptoms, supports a definitive diagnosis of DED. This strategy allows eye care practitioners to assess and diagnose DED in a limited timeframe without needing access to the full range of recommended diagnostic tests.
The Fluorescein Tear Break-Up Time
The Fluorescein Tear Break-Up Time (F-TBUT) test is commonly used in clinical settings to assess tear film stability, an essential factor in DED diagnosis. The test involves the application of sodium fluorescein into the tear film, followed by observing the tear film under cobalt blue illumination. The patient is instructed to refrain from blinking during the procedure. The F-TBUT is defined as the interval, measured in seconds, from the patient's last blink to the appearance of the first dry spot on the tear film. According to the Asian Dry Eye Society (ADES), an F-TBUT of less than or equal to five seconds is considered abnormal, indicating potential tear film instability and an increased likelihood of DED [19]. However, it is important to note that this test is both invasive and subjective, which may impact the accuracy of dry eye diagnosis. Therefore, it is crucial to prioritize the use of objective and non-invasive diagnostic methods. Additionally, it is essential to perform the F-TBUT test in a consistent environment, ensuring that variables such as temperature and humidity are controlled. This consistency minimizes potential interference with test results and, consequently, with the diagnosis.
In addition to its utility in determining tear film stability, the tear film break-up pattern observed during the F-TBUT test may provide valuable information regarding the underlying cause of the patient’s dry eye condition. This diagnostic tool is particularly advantageous in low-resource settings, as it is inexpensive and requires minimal technology, making it suitable for widespread use across various regions in Asia. The pattern of tear film break-up can also assist clinicians in identifying the specific etiology of DED, aiding in more targeted treatment approaches for this multifactorial condition.
Ocular Surface Staining
Punctate staining of the ocular surface is a hallmark of numerous ocular conditions, and the use of instilled dyes plays a crucial role in the diagnosis and management of DED [45, 49]. Commonly used dyes include sodium fluorescein, rose bengal, and lissamine green. Fluorescein staining allows for the rapid evaluation of the ocular surface epithelium and tear film instability. While a combination of dyes (such as fluorescein and lissamine green) might enhance both comfort and staining efficacy, these combinations are not commercially available, limiting their routine use in practice [50].
The patterns and distribution of staining provide valuable insights into the nature of ocular irritation, aiding in the differentiation of DED from other conditions such as MGD, blepharitis, superior limbic keratoconjunctivitis (SLK), conjunctivochalasis (CCh), incomplete blinking and nocturnal lagophthalmos [35]. As outlined in Fig. 2, the pattern of ocular surface staining is instrumental in diagnosis [34]; for instance, predominant staining in the inferior cornea may prompt further investigation into the inferior lid margin for conditions such as blepharoconjunctivitis or trichiasis. Diffuse corneal staining accompanied by faint conjunctival involvement may suggest drug-induced keratopathy, which should be considered in the differential diagnosis. Accurate interpretation of the staining distribution is essential for DED identification and differential diagnosis from other underlying conditions, as indicated by tear film break-up patterns and other diagnostic features [34, 51].
The severity of DED can be assessed based on a combination of symptoms and clinical findings. The presence of a greater number of key symptoms, such as discomfort, visual disturbance and a burning sensation, often correlates with more severe DED [51]. Additionally, conjunctival hyperemia is frequently observed in moderate to severe cases [52, 53] and non-responsiveness to lubricant eye drops can indicate moderate to severe DED [54].
Moreover, various grading systems are employed to assess the severity of DED, with the Modified Oxford Scale [42] being the most commonly used due to its standardized approach and significant value in research contexts. However, the application of the Modified Oxford Scale may require high corneal and ocular surface specialty, potentially posing a barrier for eye care practitioners to adopt ocular staining for evaluating disease severity. To improve awareness among practitioners regarding staining grading classification, the DED Working Group proposes retaining the Modified Oxford Scale in the Optimal Pathway and employing a simplified staining grading scheme in the Streamlined Pathway.
As depicted in Table 2, the DED Working Group members have developed a local simplified grading scheme to objectively assess the ocular surface staining as a marker of DED severity. According to this scheme, mild DED is characterized by minimal ocular staining, while moderate DED involves positive corneal staining. Severe DED is diagnosed when both corneal and conjunctival staining are present. The proposed scheme emphasizes practical severity assessments, combining four indicators: lack of response to lubricants, number of symptoms presented, presence of conjunctival hyperemia, and objective evaluation of the ocular staining [55]. If any of these tests indicate moderate or severe DED, the patient should be considered a case of moderate-to-severe disease and treated accordingly.
Table 2
Proposed simplified DED severity grading scheme
Mild
Moderate
Severe
Conjunctival hyperemia
Negative
Positive
Positive
Non-responsiveness to lubricants
Negative
Positive
Positive
Cornea staining
None to minimal
Positive
Positive
Conjunctival staining
None to minimal
None to minimal
Positive
Medical Treatment Options for Dry Eye Disease
The treatment approach to DED should account for its multifactorial nature and be tailored based on the severity of the condition, and its underlying cause. Therapeutic options should also be aligned with local access to eye care and reimbursement constraints.
Ocular Lubricants
The first-line treatment for DED typically involves the use of over-the-counter artificial tears, which aim to replace or supplement the natural tear film. These ocular lubricants are widely available and vary in composition, with the choice often dictated by cost, availability, and patient preference. For mild or transient DED, options such as sodium hyaluronate, hydroxypropyl methylcellulose (HPMC), carboxymethylcellulose (CMC) and polyethylene glycol (PEG) are recommended, while more severe cases may benefit from a combination of agents, such as sodium hyaluronate with CMC. Trehalose, betaine, glycine, allantoin, ectoine, phospholipids and artificial tears are also beneficial to the ocular surface [56‐59]. The general principle is to select a more viscous lubricant for a more severe DED. It is essential for eye care practitioners to tailor the treatment regimen based on patient activities, such as increased frequency of drops during extended computer use or nighttime driving. Preservative-free formulations are particularly important in cases of frequent instillation or when the ocular surface epithelium is compromised, as preservatives like benzalkonium chloride (BAK) can exacerbate symptoms by causing ocular discomfort, punctate keratitis and reduced tear production [60]. In such cases, preservative-free eye drops are preferable, although they carry a risk of microbial contamination and should be used cautiously.
Lipid-containing eye drops or ointments have been developed to better mimic the combination of aqueous and lipid layers of the tear film lipid layer (TFLL). Evaporative dry eye (EDE), commonly caused by MGD, is attributed to a qualitative and/or quantitative defect of the lipid layer that leads to tear film instability [35]. Therefore, the lipid-based eye drops would be expected to benefit patients with EDE [53, 68]. For instance, a variety of oils, such as mineral oils, phospholipids, perfluorohexyloctane [61] and oil-in-water emulsions have been incorporated in formulations to help restore the lipid layer of the tear film by mimicking natural meibum. However, it is crucial to recognize that artificial tears do not address the underlying inflammatory or pathological mechanisms of DED and may be ineffective in providing long-term relief [62].
Topical Mucin Secretagogues
Based on the concept of tear film-oriented therapy as introduced in the ADES, topical mucin secretagogues can be considered an effective therapeutic approach for the decreased wettability DE, as they can replenish tear film layers and enhance tear film instability [19]. The availability of topical mucin secretagogues may vary across Asia, with diquafosol and rebamipide being the commercially available options. Although both drugs are known to increase the mucin levels of the ocular surface, their mechanisms of action are different.
Diquafosol binds to P2Y2 receptors, increasing intracellular calcium levels, which in turn stimulates the release of water and mucin secretion from conjunctival epithelial cells and goblet cells, respectively, into the mucosal layer of the tear film [63]. Moreover, an increase in lipid layer thickness has been reported after diquafosol instillation [64]. Rebamipide was originally used as a gastroprotective drug for treating peptic ulcer disease, and emerging studies show its ability to stimulate mucus glycoprotein synthesis and inhibit inflammatory cytokines and chemokines in various chemokines in various tissues, including the gastrointestinal tract and ocular surface [65, 66]. On the ocular surface, recent studies have shown that topical rebamipide increases the secretory and membrane-associated mucins by increasing the number of goblet cells [67].
Anti-inflammatory Therapy in DED
Inflammation is a core cause of the DED vicious cycle, and early initiation of anti-inflammatory therapies is recommended to break this cycle of pathophysiology and restore natural homeostasis at the ocular surface. However, there is limited guidance on when to initiate anti-inflammatory treatment in DED. The proposed Streamlined Pathway emphasizes identifying and managing inflammation as a central component, focusing on discerning the appropriate use of anti-inflammatory agents versus ocular lubricants based on patient presentation, the DED Working Group proposes initiating anti-inflammatory treatment for moderate-to-severe DED when conjunctival hyperemia and ocular staining (either corneal or conjunctival) are present. Clinical evidence supports the efficacy of anti-inflammatory eye drops in moderate-to-severe DED, showing significant improvements in both symptoms and corneal staining compared to lubricants alone [68].
Topical corticosteroids, such as loteprednol [69], prednisolone acetate [70, 71], and fluorometholone [72], are particularly effective due to their fast-acting anti-inflammatory effects. Steroids are commonly used in patients with DED presenting with redness, blepharitis, or ocular allergies. However, their long-term use must be approached cautiously due to risks such as elevated intraocular pressure, glaucoma, cataracts, and infections [73]. Typically, steroids are recommended for short-term use (2–4 weeks) with a tapering regimen, especially in conjunction with long-term therapies like cyclosporine A. The framework suggests the use of corticosteroids for short-term use (2–4 weeks), especially in conjunction with long-term therapies like cyclosporine A, for patients with recurrent inflammation.
Cyclosporine A, an immunomodulatory agent, offers a disease-modifying approach for DED [53]. Unlike corticosteroids, cyclosporine A is suitable for long-term use and does not carry the same risks of glaucoma or cataracts [74, 75]. Its anti-inflammatory properties have been shown to reduce hyperosmolarity, increase conjunctival goblet cell density, and decrease inflammatory markers [76]. Cyclosporine A alone is particularly useful for patients with chronic inflammation, though its effects tend to appear after several weeks due to its mechanism of action and T cell physiology, as it takes time to reduce T cell-mediated inflammation and achieve therapeutic levels within tissues. Therefore, for quick relief in signs and symptoms, combining short-term corticosteroids with cyclosporine A at the start of treatment can be considered to address the underlying inflammatory pathophysiology. Given the chronic nature of DED, long-term management with cyclosporine A is critical for preventing disease progression and maintaining ocular surface health.
Warm Compress Therapy for Meibomian Gland Dysfunction
Current treatments for MGD focus on improving meibum quality, relieving obstruction, and reducing associated inflammation. First-line therapies include warm compresses and eyelid hygiene, which aim to restore gland function and alleviate symptoms. Warm compresses, applied with a temperature of 40–45 °C for 5–10 min, effectively melt meibum and facilitate glandular drainage. Studies demonstrate their ability to improve tear film stability and reduce symptoms of dryness and irritation [77].
Patient Referral
As outlined in the framework, it is advised to refer the patient to a specialist or seek specialist advice without delay if they present with uncontrolled symptoms, require a specialist assessment for diagnosis, experience persistent or significant deterioration in vision or if ulcers or other indications of corneal damage necessitate further intervention. Additionally, a referral is recommended if an associated medical condition requires specialized attention. A same-day referral to a specialist is warranted if acute glaucoma, keratitis, or iritis is suspected. Alarm signals of a more serious underlying condition include a sudden onset of symptoms accompanied by systemic ill health, such as weight loss or fever.
Follow-Up in Dry Eye Disease Management
Follow-up evaluations in DED are critical for assessing the effectiveness of treatment, monitoring ocular health and providing patient reassurance. These evaluations help guide therapy adjustments, particularly when symptoms persist or ocular damage is detected. The frequency of follow-up depends on disease severity, the treatments used, and the patient’s response to those treatments. The DED Working Group recommends follow-up at least every 6 months. Regular monitoring is essential to prevent progression and to manage potential complications associated with DED, such as corneal damage and inflammation, which can lead to long-term visual impairment if untreated.
B. Optimal Pathway
DED Subtype Identification
DED subtype classification is essential for effective management and treatment strategies. When time and resources allow, incorporating additional tests into the diagnostic work-up can provide more insights into the condition and its underlying causes. Schirmer's test and tear osmolarity testing can confirm diagnoses, although their accuracy and availability may vary. In cases where these assessments yield inconclusive results, or if access to homeostasis markers is limited, it is advisable to refer patients to a specialist for a definitive diagnosis.
Corneal fluorescein staining is a critical tool for identifying punctate epithelial erosions, employing the Modified Oxford Scale for grading. However, this scale’s reliance on photographic references can complicate assessments for eye care practitioners who may not be familiar with these specialized tools. The classification of DED can be refined further through the examination of tear film break-up patterns [60].
As shown in Fig. 3, these patterns—area, spot, line, dimple, and random—provide crucial insights into the tear film’s stability [60]. Close observation of when tear film break-up occurs, whether immediately after eye opening, during fluorescein migration or following tear film stabilization, is essential. Additionally, assessing the break-up's distribution, shape and extent can guide the classification of DED into its subtypes.
Fig. 3
Representative fluorescein break-up patterns (FBUPs) (top left) area break; (top right) spot break; (middle left) line break; (middle right) dimple break; (bottom left) random break. FBUPs were classified by Yokoi et al. [60] with reference to (1) when fluorescein break-up occurs in relation to the upward movement of fluorescein-stained aqueous tear (UMF), which is observed after the subject’s eye was opened; (2) where fluorescein break-up occurs the interpalpebral zone of the cornea; and (3) the shape of the fluorescein break-up. Area breaks are diagnosed when UMF is not observed or is limitedly observed within the lower part of the cornea. Spot breaks are diagnosed as a spot-like shape immediately after eye opening and when at least one spot break is not erased during UMF. Line breaks are diagnosed as a vertical line–like shape during UMF at the lower part of the cornea, within which fluorescein intensity is decreased with time until the cessation of UMF. Dimple breaks are diagnosed as an irregular but vertical line–like shape during UMF within the zone closer to the central part of the cornea, within which fluorescein intensity increases with time until the cessation of UMF. Random breaks are diagnosed as an irregular and indefinite shape whose typical place for the break-up to occur differs with cases and with each blink. Random breaks must occur after the cessation of UMF
Aqueous-deficient dry eye (ADDE), characterized by line or area breaks, indicates decreased lacrimation. In contrast, mucin-deficient dry eye or decreased wettability DED presents with spot or dimple breaks, while evaporative dry eye (EDE) is associated with random tear film break-up patterns. This differentiation aids in tailoring treatment strategies according to the specific underlying pathology.
Furthermore, a systematic assessment of the primary etiological factors underlying DED is crucial (Table 3). In evaluating EDE, the focus should be on diagnosing and grading MGD through techniques such as meibography or interferometry. Particular attention should be paid to lid margin disease and the quality of the meibum, as well as measuring F-TBUT (≤ 5 s). The quality of expressed meibum will be graded using a four-point scale: Grade 0, clear fluid; Grade 1, slightly turbid; Grade 2, thick opaque; Grade 3, toothpaste-like; Grade 4, complete orifice blockage [78]. It is common to express the glands by applying digital pressure through the eyelids, but methods to standardize the application of force have also been developed. Tear film interferometer (LipiView II, TearScience, USA) can obtain a quantitative assessment of the lipid layer thickness (LLT). A 20-s video is captured to document the interference pattern of the tear film. LLT is derived from the reflected tear film interference pattern and is calculated as interferometric color units (ICUs), where 1 ICU represents approximately 1 nm. However, there is no standard cut-off of LLT as it is significantly affected by demographic factors such as age, sex, ocular surgical history and MGD type [79]. One study reported that an LLT of less than or equal to 75 nm could be used for the detection of obstructive MGD (sensitivity of 65.8% and specificity of 63.4%) [80]. Furthermore, tear film break-up patterns, particularly random break-ups and lid margin staining (≥ 2 mm length and ≥ 25% width), should be assessed.
Table 3
Criteria for DED diagnostic and subtype classification
DED diagnostic criteria
Presence of key subjective symptoms
+
Slit-lamp examination (tear meniscus height, lid margin, completeness of blinking)
+
F-TBUT \(\le \) 5 s
or
Ocular surface staining (> 5 corneal spots, > 9 conjunctival spots, or lid margin)
or
Distribution of staining for differential diagnosis
DED subtype classification
Evaporative dry eye
MGD diagnosis and severity (with meibography or interferometry: LLT \(\le \) 60 mm by LipiView interferometry)
Lid margin disease and quality of meibum: grade 0 (clear fluid), grade 1 (slightly turbid), grade 2 (thick opaque), grade 3 (toothpaste-like), grade 4 (complete orifice blockage)
F-TBUT \(\le \) 5 s
Tear break-up pattern: random break
CFS: lid margin staining (\(\ge \) 2 mm length and \(\ge \) 25% width)
Decreased wettability/mucin-deficient dry eye
Short BUT
F-TBUT \(\le \) 5 s*
Tear break up pattern: spot or dimple break, or rapid expansion
CFS: lid margin staining (\(\ge \) 2 mm length and \(\ge \) 25% width)
Aqueous-deficient dry eye
Tear meniscus height in slit-lamp examination: 0.2 mm (mild), 0.1 mm (moderate), 0.00 mm (severe)
Tear break-up pattern: area or line break
Optional Schirmer’s test (without anesthesia): ≤ 10 mm/5 min or
Strip meniscometry: < 4 mm
*In mucin-deficient dry eyes, the F-TBUT is ≤ 5 s [93]
For patients exhibiting decreased wettability DED, identifying rapid tear film expansion or specific patterns such as spot or dimple breaks can provide valuable diagnostic information. Significant lid margin staining, notably staining covering at least 2 mm in length and 25% of the lid margin width, is indicative of ocular surface involvement in increased wettability DED and warrants careful management.
Finally, in assessing ADDE, the height of the tear meniscus observed through slit-lamp examination serves as an essential indicator of disease severity. Measurements indicate mild dryness at 0.2 mm, moderate at 0.1 mm and severe at 0.0 mm. While not mandatory, additional tests such as the Schirmer’s test—performed without anesthesia—and strip meniscometry [81] can further evaluate tear production and stability. A Schirmer’s test score of ≤ 10 mm (without anesthesia) or ≤ 5 mm (with anesthesia), or a strip meniscometry of < 4 mm [82] can confirm the presence of ADDE. If time permits, meibomian gland expression may also provide insights into MGD, enhancing the comprehensive evaluation of DED.
Management Recommendation
For optimal management, it is generally recommended that patients with confirmed DED be reviewed at least every 6 months or sooner if symptoms are not well controlled. For those on topical corticosteroids, more frequent follow-up is advised to monitor for potential side effects, such as increased intraocular pressure or cataract formation. Additionally, when patients are not satisfied with the proposed medical treatments, additional interventions can be considered, including Lipiflow [83, 84], intense pulsed light [85, 86], low-level light therapy [87], microblepharoexfoliation [88], and quantum molecular resonance [89].
However, follow-up frequency may vary depending on the healthcare setting. In general practice or after discharge from specialist care, it may not always be feasible to maintain six-monthly reviews. In these cases, collaborative management between specialists and general practitioners, tailored to the local healthcare environment, is necessary to ensure that patients with DED receive appropriate long-term care.
Conclusions
DED is a significant and growing public health concern in Hong Kong, affecting a substantial portion of the population. Effective diagnosis and management are crucial for improving patient outcomes and alleviating the burden of this condition.
The proposed framework for diagnosing and treating DED in Hong Kong offers a comprehensive approach that addresses the multifaceted nature of the disease and considers the specific healthcare context in the region. By standardizing diagnostic practices and providing clear treatment guidelines, this framework aims to enhance the accuracy of DED diagnosis and facilitate timely intervention.
Implementing this framework has the potential to improve patient outcomes by enabling earlier detection, more effective treatment strategies, and reduced reliance on self-management. Additionally, it can alleviate the burden on healthcare systems by streamlining the diagnostic process and optimizing resource allocation.
Medical Writing/Editorial Assistance
The authors acknowledge the writing support and editorial assistance of Media MICE Pte. Ltd. (Singapore), funded by Santen Pharmaceutical (Hong Kong) Limited.
Author Contributions
Drs. Arthur Cheng, Douglas Lam, Kelvin Chong, Kendrick Shih, and Kelvin H. Wan contributed equally to this work.
Funding
This journal’s Rapid Service Fee were funded by Santen Pharmaceutical (Hong Kong) Limited.
Data Availability
The datasets generated, analyzed, and used in this manuscript are available from the corresponding author on reasonable request.
Declarations
Conflict of Interest
Drs. Arthur Cheng, Douglas Lam, Kelvin Chong, Kendrick Shih, and Kelvin H. Wan declare that they have received honorarium from Santen Pharmaceutical (Hong Kong) Limited for the advisory board meeting held to plan this manuscript. They have no other competing financial interests to disclose.
Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.
Schein OD, Tielsch JM, Munõz B, Bandeen-Roche K, West S. Relation between signs and symptoms of dry eye in the elderly. A population-based perspective. Ophthalmology. 1997;104(9):1395–401.PubMedCrossRef
2.
Schein OD, Muñoz B, Tielsch JM, Bandeen-Roche K, West S. Prevalence of dry eye among the elderly. Am J Ophthalmol. 1997;124(6):723–8.PubMedCrossRef
3.
[No Authors Listed] The epidemiology of dry eye disease: report of the Epidemiology Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):93–107.
4.
McCarty CA, Bansal AK, Livingston PM, Stanislavsky YL, Taylor HR. The epidemiology of dry eye in Melbourne, Australia. Ophthalmology. 1998;105(6):1114–9.PubMedCrossRef
5.
Viso E, Rodriguez-Ares MT, Gude F. Prevalence of and associated factors for dry eye in a Spanish adult population (the Salnes Eye Study). Ophthalmic Epidemiol. 2009;16(1):15–21.PubMedCrossRef
6.
Lekhanont K, Rojanaporn D, Chuck RS, Vongthongsri A. Prevalence of dry eye in Bangkok, Thailand. Cornea. 2006;25(10):1162–7.PubMedCrossRef
7.
Malet F, Le Goff M, Colin J, et al. Dry eye disease in French elderly subjects: the Alienor Study. Acta Ophthalmol. 2014;92(6):e429–36.PubMedCrossRef
8.
Vehof J, Kozareva D, Hysi PG, Hammond CJ. Prevalence and risk factors of dry eye disease in a British female cohort. Br J Ophthalmol. 2014;98(12):1712–7.PubMedCrossRef
9.
Moss SE, Klein R, Klein BE. Prevalence of and risk factors for dry eye syndrome. Arch Ophthalmol. 2000;118(9):1264–8.PubMedCrossRef
10.
Cai Y, Wei J, Zhou J, Zou W. Prevalence and incidence of dry eye disease in Asia: a systematic review and meta-analysis. Ophthalmic Res. 2022;65(6):647–58.PubMedCrossRef
11.
Schaumberg DA, Dana R, Buring JE, Sullivan DA. Prevalence of dry eye disease among US men: estimates from the Physicians’ Health Studies. Arch Ophthalmol. 2009;127(6):763–8.PubMedPubMedCentralCrossRef
12.
Dana R, Bradley JL, Guerin A, et al. Estimated prevalence and incidence of dry eye disease based on coding analysis of a large, all-age United States Health Care System. Am J Ophthalmol. 2019;202:47–54.PubMedCrossRef
13.
Fan Z, Du Y, Tang C, et al. Awareness, prevalence, and knowledge of dry eye among internet professionals: a cross-sectional study in China. Eye Contact Lens. 2023;49(3):92–7.PubMed
14.
Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II definition and classification report. Ocul Surf. 2017;15(3):276–83.PubMedCrossRef
15.
Zhao S, Le Q. Analysis of the first tear film break-up point in Sjögren’s syndrome and non-Sjögren’s syndrome dry eye patients. BMC Ophthalmol. 2022;22(1):1.PubMedPubMedCentralCrossRef
16.
Petroutsos G, Paschides CA, Karakostas KX, Psilas K. Diagnostic tests for dry eye disease in normals and dry eye patients with and without Sjögren’s syndrome. Ophthalmic Res. 1992;24(6):326–31.PubMedCrossRef
17.
Foulks GN, Nichols KK, Bron AJ, Holland EJ, McDonald MB, Nelson JD. Improving awareness, identification, and management of meibomian gland dysfunction. Ophthalmology. 2012;119(10 Suppl):S1-12.PubMedCrossRef
18.
Nichols KK, Foulks GN, Bron AJ, et al. The international workshop on meibomian gland dysfunction: executive summary. Investig Ophthalmol Vis Sci. 2011;52(4):1922–9.CrossRef
19.
Tsubota K, Yokoi N, Watanabe H, et al., Members of The Asia Dry Eye Society. A new perspective on dry eye classification: proposal by the Asia Dry Eye Society. Eye Contact Lens. 2020;46(Suppl 1(1)):S2–13 (Erratum in: Eye Contact Lens. 2020;46(5):e39).
20.
Yokoi N, Georgiev GA. Tear-film-oriented diagnosis for dry eye. Jpn J Ophthalmol. 2019;63(2):127–36.PubMedCrossRef
21.
Sullivan DA, Rocha EM, Aragona P, et al. TFOS DEWS II sex, gender, and hormones report. Ocul Surf. 2017;15(3):284–333.PubMedCrossRef
22.
Pouyeh B, Viteri E, Feuer W, et al. Impact of ocular surface symptoms on quality of life in a United States Veterans Affairs population. Am J Ophthalmol. 2012;153(6):1061-66.e3.PubMedCrossRef
23.
Miljanović B, Dana R, Sullivan DA, Schaumberg DA. Impact of dry eye syndrome on vision-related quality of life. Am J Ophthalmol. 2007;143(3):409–15.PubMedPubMedCentralCrossRef
24.
Uchino M, Schaumberg DA. Dry eye disease: impact on quality of life and vision. Curr Ophthalmol Rep. 2013;1(2):51–7.PubMedPubMedCentralCrossRef
25.
Wolffsohn JS, TravéHuarte S, Jones L, Craig JP, Wang MTM. Clinical practice patterns in the management of dry eye disease: a TFOS international survey. Ocul Surf. 2021;21:78–86.PubMedCrossRef
26.
Savini G, Prabhawasat P, Kojima T, Grueterich M, Espana E, Goto E. The challenge of dry eye diagnosis. Clin Ophthalmol. 2008;2(1):31–55.PubMedPubMedCentralCrossRef
27.
Sullivan BD, Crews LA, Messmer EM, et al. Correlations between commonly used objective signs and symptoms for the diagnosis of dry eye disease: clinical implications. Acta Ophthalmol. 2014;92(2):161–6.PubMedCrossRef
28.
McMonnies CW. Why the symptoms and objective signs of dry eye disease may not correlate. J Optom. 2021;14(1):3–10.PubMedCrossRef
29.
Hua R, Yao K, Hu Y, Chen L. Discrepancy between subjectively reported symptoms and objectively measured clinical findings in dry eye: a population-based analysis. BMJ Open. 2014;4(8): e005296.PubMedPubMedCentralCrossRef
30.
Uchino M, Uchino Y, Dogru M, et al. Dry eye disease and work productivity loss in visual display users: the Osaka study. Am J Ophthalmol. 2014;157(2):294–300.PubMedCrossRef
31.
Bilkhu P, Sivardeen Z, Chen C, et al. Patient-reported experience of dry eye management: an international multicentre survey. Cont Lens Anterior Eye. 2022;45(1): 101450.PubMedCrossRef
32.
Toth M, Jokić-Begić N. Psychological contribution to understanding the nature of dry eye disease: a cross-sectional study of anxiety sensitivity and dry eyes. Health Psychol Behav Med. 2020;8(1):202–19.PubMedPubMedCentralCrossRef
33.
Bron AJ, Tomlinson A, Foulks GN, et al. Rethinking dry eye disease: a perspective on clinical implications. Ocul Surf. 2014;12(2 Suppl):S1-31.PubMedCrossRef
34.
Tong L, Lim L, Tan D, Heng WJ, Lim J, Chan C, Arundhati A, Tan A, Corneal Subspecialty Workgroup, College of Ophthalmology, Academy of Medicine, Singapore. Assessment and management of dry eye disease and meibomian gland dysfunction: providing a Singapore framework. Asia Pac J Ophthalmol (Phila). 2021;10(6):530–41.
35.
Wolffsohn JS, Arita R, Chalmers R, et al. TFOS DEWS II diagnostic methodology report. Ocul Surf. 2017;15(3):539–74.PubMedCrossRef
36.
Henrich CF, Ramulu PY, Akpek EK. Association of dry eye and inflammatory systemic diseases in a tertiary care-based sample. Cornea. 2014;33(8):819–25.PubMedCrossRef
37.
Wong J, Lan W, Ong LM, Tong L. Non-hormonal systemic medications and dry eye. Ocul Surf. 2011;9(4):212–26.PubMedCrossRef
38.
Phadatare SP, Momin M, Nighojkar P, Askarkar S, Singh KK. A comprehensive review on dry eye disease: diagnosis, medical management, recent developments, and future challenges. Adv Pharm. 2015;1: 704946.
39.
Begley CG, Chalmers RL, Mitchell GL, et al. Characterization of ocular surface symptoms from optometric practices in North America. Cornea. 2001;20(6):610–8.PubMedCrossRef
40.
Lee AJ, Lee J, Saw SM, et al. Prevalence and risk factors associated with dry eye symptoms: a population-based study in Indonesia. Br J Ophthalmol. 2002;86(12):1347–51.PubMedPubMedCentralCrossRef
41.
Findlay Q, Reid K. Dry eye disease: when to treat and when to refer. Aust Prescr. 2018;41(5):160–3.PubMedPubMedCentralCrossRef
42.
Messmer EM. The pathophysiology, diagnosis, and treatment of dry eye disease. Dtsch Arztebl Int. 2015;112(5):71–81.PubMedPubMedCentral
43.
Muñoz-Villegas P, García-Sánchez G, Jauregui-Franco RO, Quirarte-Justo S, Sánchez-Ríos A, Olvera-Montaño O. Influence of environmental factors with clinical signs and symptoms in the management of dry eye disease. Clin Ophthalmol. 2024;18:2439–51.PubMedPubMedCentralCrossRef
44.
Song MS, Lee Y, Paik HJ, Kim DH. A Comprehensive analysis of the influence of temperature and humidity on dry eye disease. Korean J Ophthalmol. 2023;37(6):501–9.PubMedPubMedCentralCrossRef
45.
Bron AJ, Evans VE, Smith JA. Grading of corneal and conjunctival staining in the context of other dry eye tests. Cornea. 2003;22(7):640–50.PubMedCrossRef
46.
Guo B, Chan KY, Tse J, et al. Exploring the prevalence of dry eye disease in Hong Kong population. Investig Ophthalmol Vis Sci. 2024;65(7):2856.
47.
Mainstone JC, Bruce AS, Golding TR. Tear meniscus measurement in the diagnosis of dry eye. Curr Eye Res. 1996;15(6):653–61.PubMedCrossRef
Srinivas SP, Rao SK. Ocular surface staining: current concepts and techniques. Indian J Ophthalmol. 2023;71(4):1080–9.PubMedPubMedCentralCrossRef
50.
Jeng BH. 7—Diagnostic techniques in ocular surface disease. In: Ocular surface disease: cornea, conjunctiva and tear film. In: Holland EJ, Mannis MJ, Barry Lee W. W.B. Saunders; 2013. pp. 47–54.
51.
Baudouin C, Aragona P, Van Setten G, et al., ODISSEY European Consensus Group members. Diagnosing the severity of dry eye: a clear and practical algorithm. Br J Ophthalmol. 2014;98(9):1168–76.
52.
Rodriguez-Garcia A, Babayan-Sosa A, Ramirez-Miranda A, et al. A practical approach to severity classification and treatment of dry eye disease: a proposal from the Mexican Dry Eye Disease Expert Panel. Clin Ophthalmol. 2022;16:1331–55.PubMedPubMedCentralCrossRef
53.
Jones L, Downie LE, Korb D, et al. TFOS DEWS II management and therapy report. Ocul Surf. 2017;15(3):575–628.PubMedCrossRef
54.
Doughty MJ, Glavin S. Efficacy of different dry eye treatments with artificial tears or ocular lubricants: a systematic review. Ophthalmic Physiol Opt. 2009;29(6):573–83.PubMedCrossRef
55.
The definition and classification of dry eye disease: report of the definition and classification subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):75–92.
56.
Ballesteros-Sánchez A, Martinez-Perez C, Alvarez-Peregrina C, et al. Trehalose and dry eye disease: a comprehensive systematic review of randomized controlled trials. J Clin Med. 2023;12(23):7301.PubMedPubMedCentralCrossRef
57.
Abbate I, Zappulla C, Santonocito M, et al. Preclinical study of a new matrix to help the ocular surface in dry eye disease. Exp Eye Res. 2022;222: 109168.PubMedCrossRef
58.
Panchal H, Parihar L, Kumari T, Goswami M, Sharma K. Pharmacological actions and different mechanisms of allantoin. A review JETIR. 2024;12(11):b13–32.
59.
Chen X, Lin N, Li JM, et al. Ectoine, from a natural bacteria protectant to a new treatment of dry eye disease. Pharmaceutics. 2024;16(2):236.PubMedPubMedCentralCrossRef
60.
Yokoi N, Georgiev GA, Kato H, et al. Classification of fluorescein breakup patterns: a novel method of differential diagnosis for dry eye. Am J Ophthalmol. 2017;180:72–85.PubMedCrossRef
61.
Matossian C, Crowley M, Periman L, Sorkin S. Personalized management of dry eye disease: beyond artificial tears. Clin Ophthalmol. 2022;16:3911–8.PubMedPubMedCentralCrossRef
62.
Ballesteros-Sánchez A, De-Hita-Cantalejo C, Sánchez-González MC, et al. Perfluorohexyloctane in dry eye disease: a systematic review of its efficacy and safety as a novel therapeutic agent. Ocul Surf. 2023;30:254–62.PubMedCrossRef
Fukuoka S, Arita R. Increase in tear film lipid layer thickness after instillation of 3% diquafosol ophthalmic solution in healthy human eyes. Ocul Surf. 2017;15(4):730–5.PubMedCrossRef
65.
Eom Y, Chung SH, Chung TY, et al. Efficacy and safety of 1% and 2% rebamipide clear solution in dry eye disease: a multicenter randomized trial. BMC Ophthalmol. 2023;23(1):343.PubMedPubMedCentralCrossRef
66.
Ballesteros-Sánchez A, Sánchez-González MC, De-Hita-Cantalejo C, Gutiérrez-Sánchez E, Rocha-de-Lossada C, Sánchez-González JM. The efficacy and safety of rebamipide ophthalmic suspension (OPC-12759) in patients with dry eye disease: a systematic review of randomized controlled trials. J Clin Med. 2023;12(22):7155.PubMedPubMedCentralCrossRef
67.
Kase S, Shinohara T, Kase M. Effect of topical rebamipide on human conjunctival goblet cells. JAMA Ophthalmol. 2014;132(8):1021–2.PubMedCrossRef
68.
Maulvi FA, Desai DT, Kalaiselvan P, et al. Lipid-based eye drop formulations for the management of evaporative dry eyes. Cont Lens Anterior Eye. 2024;47(3): 102154.PubMedCrossRef
69.
Nguyen A, Kolluru A, Beglarian T. Dry eye disease: a review of anti-inflammatory therapies. Taiwan J Ophthalmol. 2023;13(1):3–12.PubMedPubMedCentralCrossRef
70.
Pflugfelder SC, Maskin SL, Anderson B, et al. A randomized, double-masked, placebo-controlled, multicenter comparison of loteprednol etabonate ophthalmic suspension, 0.5%, and placebo for treatment of keratoconjunctivitis sicca in patients with delayed tear clearance. Am J Ophthalmol. 2004;138(3):444–57.
71.
Liu SH, Saldanha IJ, Abraham AG, et al. Topical corticosteroids for dry eye. Cochrane Database Syst Rev. 2022;10(10):CD015070.
72.
Knopf MM. A double-blind study of fluorometholone. Am J Ophthalmol. 1970;70(5):739–40.PubMedCrossRef
73.
Perry HD, Solomon R, Donnenfeld ED, et al. Evaluation of topical cyclosporine for the treatment of dry eye disease. Arch Ophthalmol. 2008;126(8):1046–50.PubMedCrossRef
74.
Sall K, Stevenson OD, Mundorf TK, Reis BL. Two multicenter, randomized studies of the efficacy and safety of cyclosporine ophthalmic emulsion in moderate to severe dry eye disease. CsA Phase 3 Study Group. Ophthalmology. 2000;107(4):631–9 (Erratum in: Ophthalmology 2000 Jul;107(7):1220).
75.
Matsuda S, Koyasu S. Mechanisms of action of cyclosporine. Immunopharmacology. 2000;47(2–3):119–25.PubMedCrossRef
76.
Di Tommaso C, Valamanesh F, Miller F, et al. A novel cyclosporin a aqueous formulation for dry eye treatment: in vitro and in vivo evaluation. Investig Ophthalmol Vis Sci. 2012;53(4):2292–9.CrossRef
77.
Sabeti S, Kheirkhah A, Yin J, Dana R. Management of meibomian gland dysfunction: a review. Surv Ophthalmol. 2020;65(2):205–17.PubMedCrossRef
78.
Arita R, Minoura I, Morishige N, et al. Development of definitive and reliable grading scales for meibomian gland dysfunction. Am J Ophthalmol. 2016;169:125–37.PubMedCrossRef
79.
Jung JW, Park SY, Kim JS, Kim EK, Seo KY, Kim TI. Analysis of factors associated with the tear film lipid layer thickness in normal eyes and patients with dry eye syndrome. Investig Ophthalmol Vis Sci. 2016;57(10):4076–83.CrossRef
80.
Finis D, Pischel N, Schrader S, Geerling G. Evaluation of lipid layer thickness measurement of the tear film as a diagnostic tool for meibomian gland dysfunction. Cornea. 2013;32(12):1549–53.PubMedCrossRef
81.
Dogru M, Ishida K, Matsumoto Y, Goto E, Ishioka M, Kojima T, Goto T, Saeki M, Tsubota K. Strip meniscometry: a new and simple method of tear meniscus evaluation. Investig Ophthalmol Vis Sci. 2006;47(5):1895–901.CrossRef
82.
Blackie CA, Kowlitt MS, Akpek EK, Holland EJ, Donnenfield ED. Long-term (12-month) benefits of a single intense pulsed light (IPL) treatment followed by meibomian gland expression (MGX) for meibomian gland dysfunction. Ocul Surf. 2016;14(4):525–34.
83.
Blackie CA, Murakami D, Donnenfeld E, Oliff HS. Vectored thermal pulsation as a treatment for meibomian gland dysfunction: a review spanning 15 years. Ophthalmol Ther. 2024;13(8):2083–123.PubMedPubMedCentralCrossRef
84.
Giannaccare G, Taroni L, Senni C, Scorcia V. Intense pulsed light therapy in the treatment of meibomian gland dysfunction: current perspectives. Clin Optom (Auckl). 2019;11:113–26.PubMedCrossRef
85.
Ballesteros-Sánchez A, Gargallo-Martínez B, Sánchez-González MC, Sánchez-González JM. Intense pulse light combined with low-level light therapy in dry eye disease: a systematic review. Eye Contact Lens. 2023;49(1):8–13.PubMedCrossRef
86.
Glass GE. Photobiomodulation: the clinical applications of low-level light therapy. Aesthet Surg J. 2021;41(6):723–38.PubMedCrossRef
87.
Siddireddy JS, Tan J, Vijay AK, Willcox MDP. The effect of microblepharon exfoliation on clinical correlates of contact lens discomfort. Optom Vis Sci. 2019;96(3):187–99.PubMedCrossRef
88.
Ballesteros-Sánchez A, Gargallo-Martínez B, Gutiérrez-Ortega R, Sánchez-González JM. Eyelid exfoliation treatment efficacy and safety in dry eye disease, blepharitis, and contact lens discomfort patients: a systematic review. Asia Pac J Ophthalmol (Phila). 2023;12(3):315–25.PubMedCrossRef
89.
Ballesteros-Sánchez A, Sánchez-González JM, Tedesco GR, et al. Efficacy and safety of quantum molecular resonance electrotherapy in patients with aqueous-deficient, evaporative and mixed-type dry eye: a randomized interventional study. Ophthalmol Ther. 2024;13(2):495–507.PubMedCrossRef
90.
Papas EB. The global prevalence of dry eye disease: a Bayesian view. Ophthalmic Physiol Opt. 2021;41(6):1254–66.PubMedCrossRef
91.
Berg EJ, Ying GS, Maguire MG, et al., DREAM Study Research Group. Climatic and environmental correlates of dry eye disease severity: a report from the Dry Eye Assessment and Management (DREAM) Study. Transl Vis Sci Technol. 2020;9(5):25.
92.
Chlasta-Twardzik E, Górecka-Nitoń A, Nowińska A, Wylęgała E. The influence of work environment factors on the ocular surface in a one-year follow-up prospective clinical study. Diagnostics (Basel). 2021;11(3):392.PubMedCrossRef
93.
Lemp MA. The mucin-deficient dry eye. Int Ophthalmol Clin. 1973;13(1):185–189.
Bei der Festlegung der Intervalle für Kontrollkoloskopien nach einer Polypektomie sollten nicht ausschließlich polypenbezogene Merkmale berücksichtigt werden. Wie eine internationale Studie zeigt, beeinflussen auch individuelle demografische Faktoren, wie Geschlecht, Body-Mass-Index und Ethnie, das Rezidivrisiko.
In einer Kohortenstudie wurde ein Zusammenhang zwischen oralen Bakterien und Pilzen und dem Auftreten von Pankreaskarzinomen gesehen. Diese Assoziation könnte helfen, Patientinnen und Patienten für gezielte Vorsorgeuntersuchungen ausfindig zu machen.
Ein Team aus Frankreich hat Fälle von plötzlichem Herzstillstand während des Paris-Marathons ausgewertet. In fast 90% waren Männer betroffen, und zwar überwiegend auf dem letzten Kilometer vor dem Ziel.
Patienten mit Adipositas weisen erniedrigte Spiegel des N-terminalen pro-B-Typ-natriuretischen Peptids (NT-ProBNP) auf. Ob sich das auf die NT-proBNP-gestützte Diagnostik von Herzinsuffizienz auswirkt, haben britische Mediziner untersucht.
