Dry eye is a type of disease in which any cause of abnormal tear quality or quantity and kinetics leads to tear film instability and/or abnormalities on the ocular surface, accompanied by ocular discomfort. The main symptoms of dry eye include ocular dryness, foreign body sensation, visual fatigue, photophobia and vision loss, which can affect work and life in mild cases, and can lead to dryness, melting and perforation of the ocular surface, especially the corneal tissue in severe cases, which can seriously endanger visual function. At present, the number of dry eye patients is increasing, and the age distribution range is gradually widening, so it is extremely important to make a clear diagnosis and correct treatment for dry eye.
1.Diagnosis of dry eye.
1.1 Medical history.
Possible etiologies or triggers for the development of dry eye include.
(1) the patient’s work environment and nature: long-term work in an air-conditioned open, airless environment can cause dry eye symptoms, such as “ building disease syndrome ” (sick building syndrome, SBS), “ office eye syndrome ” (office eye syndrome, OES) (OES); often engaged in focused work or activities can also cause dry eye, such as prolonged use of computers, working in front of the fluorescent screen, reading can form “video display terminals syndrome” (video display terminals, VDT); in addition, watching movies in a dark room or driving for a long time to cause a reduction in transient eyes, can make the eye In addition, watching movies in a dark room or driving for a long time can increase the exposure of surface area and accelerate tear evaporation, which can also lead to dry eye.
(2) Local and systemic medications: long-term use of antihypertensive and antidepressant medications can reduce tear secretion; long-term use of topical antibiotic and antiviral eye medications can aggravate dry eye due to the toxicity of the medications themselves or preservatives.
(3) History of ocular trauma, surgery and past medical history: Ocular surface corneal rim stem cells are an important source of corneal epithelial renewal and are an important part of maintaining the health of the ocular surface epithelium. Ocular surface chemical injuries, thermal burns, long-term corneal contact lens wear, multiple surgeries or condensation of the corneal conjunctival rim, ocular aspergillosis and severe infections of the ocular surface can cause destruction or dysfunction of corneal rim stem cells. In addition, head radiation therapy and trigeminal nerve decompression may alter the corneal limbal stem cell stromal microenvironment.
(4) Patients with systemic immune diseases may have dry eye symptoms, such as rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus and Wegner’s granulomatosis, so inquiry into systemic conditions should not be ignored.
1.2 Symptoms.
The presence of dry eye symptoms is the most important and essential condition for the diagnosis of dry eye. The main symptoms include ocular dryness, foreign body sensation, burning sensation, visual fatigue, photophobia and varying degrees of visual acuity loss. Since the rate of positive clinical objective examinations is not parallel to the rate of dry eye symptoms, dry eye should be diagnosed when one or more of the above symptoms are frequently or persistently present. The inquiry of dry eye symptoms should be paid attention to, and for those with severe symptoms, the systemic medical history and concomitant symptoms such as the presence of dry mouth should be inquired in detail to determine whether there is a systemic disease, such as Sjogren’s syndrome (SS).
1.3 Clinical examination.
1.3.1 Slit lamp examination.
The following aspects should be noted.
(1) tear river width: normal ≥ 0.3 mm.
(2) Corneal changes: epithelial keratosis, blisters, ulcers, cloudiness, vascular opacities, etc.
(3) debris on the corneal surface and in the lower dome.
(4) Adhesions of the lid bulb.
(5) Conjunctival abnormalities: congestion, papillomatous hyperplasia, relaxation of the conjunctival bursa and accumulation of folds.
(6) Eyelid abnormalities: Meibomian gland dysfunction (MGD) with congestion, irregularity, thickening, blunting, and ectropion of the lid margin, obstruction of the gland orifice by yellow mucous secretions, and blurring of the gland ducts. Compression of the gland reveals either no lipid secretion or excessive discharge of abnormal lipid morphology.
1.3.2 Schirmer’s test.
Schirmer I test (SIt) checks the basic secretion of tears by taking 5mm×35mm of graduated test paper with one end reflexed by 5mm and gently placing it in the outer and outer 1/3 of the conjunctival sac under the tested eye, removing the filter paper after 5 minutes and measuring the wet length, generally ≥10mm/5min is normal. Schirmer II test (SIIt) Check the reflex secretion of tears by gently inserting a cotton swab (8mm long, 3.5mm wide at the tip) along the temporal wall of the nasal cavity parallel upwards to stimulate the nasal mucosa, then place the filter paper (same method as SIt test), remove the filter paper after five minutes and record the wet length, generally ≥10mm/5min is normal.
1.3.3 Tear film break-up time (TEAR break-up time, BUT).
Reflects the stability of the tear film. The method is to put a drop of 1% sodium fluorescein in the conjunctival sac of the subject, ask him to blink several times, and the time from opening the eye after the last transient to the appearance of the first black spot on the cornea is the BUT. non-contact BUT is to apply the tear film mirror to directly observe the break-up time of the tear film. Generally BUT>10s is normal.
1.3.4 Ocular surface staining in vivo.
Positive fluorescein staining reflects corneal epithelial cell defect, the scoring method divides the cornea into 4 quadrants, specifying no staining as 0 points, with staining divided into 3 levels: light, medium and heavy, 1 as staining less than 5 points, 3 as appearing lumpy staining or filaments, 2 points between the above two, with a total of 0 to 12 points. Positive tiger red and lisamine green staining reflects dry and necrotic corneal epithelial cells. Tiger red staining also shows epithelial cells without mucin coverage, dividing the ocular surface into 3 areas: nasal lid fissure bulbar conjunctiva, temporal lid fissure bulbar conjunctiva and cornea, with no staining as grade 0 and grade 3 as lamellar staining, with a total score of 0 to 9.
1.3.5 Tear clearance rate (TCR).
To understand whether there is a delay in tear clearance. Detected using fluorophotometric method, called fluorescein clearance test (FCT).
1.3.6 Tear osmolality.
This method is currently used for laboratory diagnosis, but there is no simple and practical method for clinical use.
1.3.7 Other tests.
Tear lactoferrin content measurement, tear fern-like change test, dry eye meter or tear film interferometry examination, conjunctival blot cytology examination, corneal topography and serological examination, etc.
1.4 Diagnostic criteria.
There are no unified international and domestic diagnostic criteria for dry eye. According to the latest research reports and our clinical studies, we suggest that the diagnosis can be made according to the following criteria.
(1) Subjective symptoms (positive for one or more of the first five of the following): dryness, foreign body sensation, burning sensation, visual fatigue, photophobia, pain, tearing, blurred vision, and eye redness.
(2) Tear film instability: BUT tear film rupture time: ≤10 seconds is abnormal.
(3) Tear reduction: Schirmer Test tear secretion test: ≤10mm/5min; lactoferrin content: ≤0.9ug/ml is abnormal.
(4) Ocular surface damage: fluorescein stain ≥3 and/or Tiger Red stain ≥3; blot cytology demonstrates decreased cuprocyte density, decreased nucleoplasmic ratio, presence of serpentine chromatin, and increased squamous epithelial hyperplasia.
(5) Increased tear osmolality: ≥312mOsm/L.
While excluding other causes, having 1+2 (≤5 sec) or 1+2 (≤10 sec) +3 can make the diagnosis of dry eye, and if 3 and 4 are present at the same time, the diagnosis can be strengthened.
2.Treatment of dry eye.
The etiology of dry eye is complex, and finding and treating the etiology is undoubtedly the key to dry eye treatment. We should actively search for the cause and combine multiple treatments according to symptoms and etiology, with the ultimate goal of improving ocular surface inflammation, restoring normal tear film structure and function, and maintaining the normal environment of the ocular surface.
2.1 Physical therapy.
Lipid deficient dry eyes are dry eyes caused by too little lipid secretion or abnormalities in lipids leading to rapid tear evaporation. The most common form is lid gland dysfunction (MGD), which is very common in oily skin and older individuals and has been increasing in recent years in women who have undergone cosmetic eyeliner surgery.
For this condition, lid cleansing is essential, including hot compresses, massage and scrubbing.
(1) First apply a hot compress to the eyelid for 5 to 10 minutes.
(2) Eyelid massage with rotating finger movements on the lid margin;
(3) scrubbing the lid margin with a milder cleansing solution.
2.2 Topical medication.
2.2.1 Replacement of tear components.
Aqueous-deficient dry eyes are caused by the lack of aqueous layer in the tear film due to various reasons, and such dry eyes are treated mainly with replacement of tear components, and the replacement needs to be close to the normal tear components, divided into two types of artificial tears and homologous serum.
(1) Artificial tears: There are many types of artificial tears available in China, and clinicians should be familiar with the advantages and disadvantages of each artificial tear component, viscosity, mechanism of action, type of preservative, etc., and make a corresponding choice according to the type and degree of dry eye, economic status of the patient and the patient’s response to treatment.
(2) Autologous serum: its composition is closest to normal tears, but due to its complicated preparation and restricted source, it is less commonly used and is generally applied only when severe dry eye will cause corneal complications.
2.2.2 Anti-inflammatory and immunosuppressive therapy.
Patients with dry eye often have a non-infectious immune-based inflammatory response on the ocular surface that may be associated with reduced sex hormone levels, reduced lymphocyte apoptosis, and an injury-healing response due to minor friction on the ocular surface. Many scholars have identified this inflammatory response as a common pathogenesis for all types of dry eyes. Therefore, anti-inflammatory and immunosuppressive treatment is an important measure in the treatment of dry eye.
(1) Corticosteroid eye drops: lower concentrations of hormone drops are effective in reducing dry eye symptoms and ocular surface inflammation, and the number of doses and duration of dosing are determined by the degree of dry eye, but should be minimized to avoid hormone-induced complications.
(2) Immunosuppressive eye drops: Local application of low concentration of immunosuppressive eye drops to suppress ocular surface inflammation. At present, the commonly used drugs in China are 0.05% cyclomycin A (CsA) ophthalmic solution and FK506 ophthalmic solution.
2.2.3 Lipid replacement therapy.
Lipid deficiency is commonly seen in patients with inadequate lipid secretion from the lid gland, and lipid replacement therapy may be effective in such patients, but no ideal drug is available.
2.3 Preservation of tears.
Tear replacement therapy may supplement some tears, but one should still try to preserve one’s own tears, prolong their stay on the ocular surface, and reduce the use of artificial tears.
2.3.1 Silicone eye shields and wet room lenses.
Provide an airtight environment to reduce air flow over the ocular surface and evaporation of tears for the purpose of preserving tears, very effective for patients with dry eyes and corneal exposure, and in some patients, artificial tears can even be discontinued.
2.3.2 Therapeutic corneal contact lenses.
For patients with mild dry eye, this type of treatment with artificial tears can receive better results, but the contact lens needs to be kept moist when used. In patients with moderate to severe dry eye, the lenses worn are prone to dryness and fall off, so they are less often used.
2.3.3 Tear punctal plugs and tear punctal closure.
Tear punctal plugs can temporarily block the tear ducts, prolong the residence time of the eye surface itself and reduce the frequency of artificial tears. Studies have shown that tear punctal plugs are more effective in patients with mild and moderate dry eyes, and the frequency of artificial tears is significantly reduced, even stopping the use of artificial tears. For patients with severe dry eye after the use of pessary ineffective can be considered to perform permanent tear punctal closure, including thermal cautery, surgical excision, etc.
2. 4 Surgical treatment.
For patients with severe dry eye, surgical treatment can be considered when the condition does not improve with any medication. Current surgical treatment includes autologous submandibular gland transplantation, but this procedure is only used to treat very severe dry eyes and may lead to severe corneal lesions.
2.5 Systemic drug therapy.
2.5.1 Sex hormone therapy.
The incidence of dry eye in postmenopausal women is significantly higher, suggesting that changes in sex hormone levels may be an important cause of dry eye. Some studies have found a decrease in both estrogen and androgen levels in menopausal women, and other studies have shown that reduced androgen levels are one of the main causes of reduced lacrimal gland function in SS patients. Therefore, topical androgens have been applied to improve the secretory function of the lacrimal and lid glands, with good results in some patients.
2.5.2 Oral antibiotics.
Tetracycline