NK is diagnosed on the basis of the patient's medical history and a careful examination of the eye and surrounding area.

With regard to the patient's medical history, special attention should be paid to any herpes virus infections and possible surgeries on the cornea, trauma, abuse of anaesthetics or chronic topical treatments, chemical burns or, use of contact lenses. It is also necessary to investigate the possible presence of diabetes or other systemic diseases such as multiple sclerosis.

The clinical examination is usually performed through a series of assessments and tools:

- General examination of cranial nerves, to determine the presence of nerve damage.

- Eye examinations:

1. Complete eye examination: examination of the eyelids, blink rate, presence of inflammatory reactions and secretions, corneal epithelial alterations.

2. Corneal sensitivity test: performed by placing a cotton wad or cotton thread in contact with the corneal surface: this only allows to determine whether corneal sensitivity is normal, reduced or absent; or using an esthesiometer that allows to assess corneal sensitivity.

3. Tear film function test, such as Schirmer's test, and tear film break-up time.

4. Fluorescein eye stain test, which shows any damage to the corneal and conjunctival epithelium

Conjunctival concretions can be seen easily by everting the eyelid. The projecting concretions should be removed. Removal is easily performed by a doctor. For example, using needles or sharp knife removes the concretion, under a local light anesthesia of the conjunctiva.

Diagnosis is done by direct observation under magnified view of slit lamp revealing the ulcer on the cornea. The use of fluorescein stain, which is taken up by exposed corneal stroma and appears green, helps in defining the margins of the corneal ulcer, and can reveal additional details of the surrounding epithelium. Herpes simplex ulcers show a typical dendritic pattern of staining. Rose-Bengal dye is also used for supra-vital staining purposes, but it may be very irritating to the eyes. In descemetoceles, the Descemet's membrane will bulge forward and after staining will appear as a dark circle with a green boundary, because it does not absorb the stain. Doing a corneal scraping and examining under the microscope with stains like Gram's and KOH preparation may reveal the bacteria and fungi respectively. Microbiological culture tests may be necessary to isolate the causative organisms for some cases. Other tests that may be necessary include a Schirmer's test for keratoconjunctivitis sicca and an analysis of facial nerve function for facial nerve paralysis.

According to Mackie's classification, neurotrophic keratitis can be divided into three stages based on severity:

1. "Stage I:" characterized by alterations of the corneal epithelium, which is dry and opaque, with superficial punctate keratopathy and corneal oedema. Long-lasting neurotrophic keratitis may also cause hyperplasia of the epithelium, stromal scarring and neovascularization of the cornea.

2. "Stage II:" characterized by development of epithelial defects, often in the area near the centre of the cornea.

3. "Stage III:" characterized by ulcers of the cornea accompanied by stromal oedema and/or melting that may result in corneal perforation.

Mild conjunctivochalasis can be asymptomatic and in such cases does not require treatment. Lubricating eye drops can be tried but do not often work.

If discomfort persists after standard dry eye treatment and anti-inflammatory therapy, surgery can be undertaken to remove the conjunctival folds and restore a smooth tear film. This conjunctivoplasty surgery to correct conjunctivochalasis typically involves resection of an ellipse-shaped segment of conjunctiva just inferior to the lower lid margin, and is usually followed either by suturing or amniotic membrane graft transplantation to close the wound.

Scleritis is best detected by examining the sclera in daylight; retracting the lids helps determine the extent of involvement. Other aspects of the eye exam (i.e. visual acuity testing, slit lamp examination, etc.) may be normal. Scleritis may be differentiated from episcleritis by using phenylephrine or neosynephrine eye drops, which causes blanching of the blood vessels in episcleritis, but not in scleritis.

Ancillary tests CT scans, MRIs, and ultrasonographies can be helpful, but do not replace the physical examination.

A pinguecula is one of the differential diagnoses for a limbal nodule. It may have an increased prevalence in Gaucher's disease.

The cornerstone of diagnosis is an accurate history, and a good clinical examination of the eye, to eliminate traumatic uveitis. Ultrasonography is a useful tool, as it can detect a thickened iris, but only in the hands of an expert.

Pingueculae may enlarge slowly over time, but are a benign condition, usually requiring no treatment. Artificial tears may help to relieve discomfort, if it occurs. If cosmesis is a concern, surgical excision is sometimes done. Occasionally, a pinguecula may become inflamed, a condition called pingueculitis. The cause of pingueculitis is unknown and there are no known infectious agents associated with it. If an inflamed pinguecula is causing discomfort or cosmetic concerns, it may be treated with an anti-inflammatory agent, such as prednisolone drops.

Because the disorder often occurs in people with typical dry eye symptoms, it can be difficult to distinguish readily the discomfort caused by the dry eye from that directly related to the redundant conjunctiva.

Scleritis can be classified as anterior scleritis and posterior scleritis. Anterior scleritis is the most common variety, accounting for about 98% of the cases. It is of two types : Non-necrotising and necrotising. Non-necrotising scleritis is the most common, and is further classified into diffuse and nodular type based on morphology. Necrotising scleritis accounts for 13% of the cases. It can occur with or without inflammation.

Prophylaxis consists of periodic administration of Vitamin A supplements. WHO recommended schedule, which is universally recommended is as follows:

- Infants 6–12 months old and any older children weighing less than 8 kg - 100,000 IU orally every 3–6 months

- Children over 1 year and under 6 years of age - 200,000 IU orally every 6 months

- Infants less than 6 months old, who are not being breastfed - 50,000 IU orally should be given before they attain the age of 6 months

Pterygium (conjunctiva) can be diagnosed without need for a specific exam, however corneal topography is a practical test (technique) as the condition worsens.

The diagnosis of Reis-Bücklers corneal dystrophy is based on the clinical presentation, rather than labs or imaging. Sometimes it is difficult to distinguish the disease from honeycomb dystrophy.

Treatment can occur in two ways: treating symptoms and treating the deficiency. Treatment of symptoms usually includes the use of artificial tears in the form of eye drops, increasing the humidity of the environment with humidifiers, and wearing wraparound glasses when outdoors. Treatment of the deficiency can be accomplished with a Vitamin A or multivitamin supplement or by eating foods rich in Vitamin A. Treatment with supplements and/or diet can be successful until the disease progresses as far as corneal ulceration, at which point only an extreme surgery can offer a chance of returning sight.

Topical antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye drops are applied to give rest to the eye. Pain medications are given as needed. Loose epithelium and ulcer base can be scraped off and sent for culture sensitivity studies to find out the pathogenic organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about a few weeks to several months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-healing ulcers, surgical intervention by an ophthalmologist with corneal transplantation may be required to save the eye. In all corneal ulcers it is important to rule out predisposing factors like diabetes mellitus and immunodeficiency.

As it is associated with excessive sun or wind exposure, wearing protective sunglasses with side shields and/or wide brimmed hats and using artificial tears throughout the day may help prevent their formation or stop further growth. Surfers and other water-sport athletes should wear eye protection that blocks 100% of the UV rays from the water, as is often used by snow-sport athletes. Many of those who are at greatest risk of pterygium from work or play sun exposure do not understand the importance of protection.

Some of the adverse outcomes associated with intra-operative injuries include:

- Increased length of stay. This is due to ophthalmology consults required, associated infections and treatment.

- Increased costs. This is due to increased length of stay, cost of treating the complications.

- Pain and discomfort for the patient. Corneal abrasions are extremely painful for the patient and the treatment consists of drops and ointments applied in the eye which may cause further discomfort for the patient.

Treatment is a relatively simple surgery in which excess skin of the outer lids is removed or tendons and muscles are shortened with one or two stitches. General anesthesia is sometimes used before local anesthetics are injected into the muscles around the eye. Prognosis is excellent if surgery is performed before the cornea is damaged.

@Congenital entropion:: may resolve with time ,or Hotz procedure

@Cicatricial entropion::

1 Anterior lamellar resection

2 Tarsal wedge resection

3 Transposition of tarso conjunctival wedge

4 Posterior lamellar graft

@Senile entropion::

1 Wies operation

2 Transverse everting suture

3 Quicker procedure

Classification can be either by cause or by extent of the inflamed area.

Diagnosis can be established on clinical grounds and this may be enhanced with studies on surgically excised corneal tissue and in some cases with molecular genetic analyses. As clinical manifestations widely vary with the different entities, corneal dystrophies should be suspected when corneal transparency is lost or corneal opacities occur spontaneously, particularly in both corneas, and especially in the presence of a positive family history or in the offspring of consanguineous parents.

Superficial corneal dystrophies - "Meesmann dystrophy" is characterized by distinct tiny bubble-like, punctate opacities that form in the central corneal epithelium and to a lesser extent in the peripheral cornea of both eyes during infancy that persists throughout life. Symmetrical reticular opacities form in the superficial central cornea of both eyes at about 4–5 years of age in "Reis-Bücklers corneal dystrophy". Patient remains asymptomatic until epithelial erosions precipitate acute episodes of ocular hyperemia, pain, and photophobia. Visual acuity eventually becomes reduced during the second and third decades of life following a progressive superficial haze and an irregular corneal surface. In "Thiel–Behnke dystrophy", sub-epithelial corneal opacities form a honeycomb-shaped pattern in the superficial cornea. Multiple prominent gelatinous mulberry-shaped nodules form beneath the corneal epithelium during the first decade of life in "Gelatinous drop-like corneal dystrophy" which cause photophobia, tearing, corneal foreign body sensation and severe progressive loss of vision. "Lisch epithelial corneal dystrophy" is characterized by feather shaped opacities and microcysts in the corneal epithelium that are arranged in a band-shaped and sometimes whorled pattern. Painless blurred vision sometimes begins after sixty years of life.

Corneal stromal dystrophies - "Macular corneal dystrophy" is manifested by a progressive dense cloudiness of the entire corneal stroma that usually first appears during adolescence and eventually causing severe visual impairment. In "Granular corneal dystrophy" multiple small white discrete irregular spots that resemble bread crumbs or snowflakes become apparent beneath Bowman zone in the superficial central corneal stroma. They initially appear within the first decade of life. Visual acuity is more or less normal. "Lattice dystrophy" starts as fine branching linear opacities in Bowman's layer in the central area and spreads to the preiphery. Recurrent corneal erosions may occur. The hallmark of "Schnyder corneal dystrophy" is the accumulation of crystals within the corneal stroma which cause corneal clouding typically in a ring-shaped fashion.

Posterior corneal dystrophies - "Fuchs corneal dystrophy" presents during the fifth or sixth decade of life. The characteristic clinical findings are excrescences on a thickened Descemet membrane (cornea guttae), generalized corneal edema and decreased visual acuity. In advanced cases, abnormalities are found in the all layers of the cornea. In "posterior polymorphous corneal dystrophy" small vesicles appear at the level of Descemet membrane. Most patients remain asymptomatic and corneal edema is usually absent. "Congenital hereditary endothelial corneal dystrophy" is characterized by a diffuse ground-glass appearance of both corneas and markedly thickened (2–3 times thicker than normal) corneas from birth or infancy.

Antibiotics are aimed at gram positive bacteria. Medical attention should be sought if symptoms persist beyond 2–3 days.

Cultures are not often taken or needed as most cases resolve either with time or typical antibiotics. Swabs for bacterial culture are necessary if the history and signs suggest bacterial conjunctivitis but there is no response to topical antibiotics. Viral culture may be appropriate in epidemic case clusters.

A patch test is used to identify the causative allergen in the case where conjunctivitis is caused by allergy.

Conjunctival scrapes for cytology can be useful in detecting chlamydial and fungal infections, allergy, and dysplasia, but are rarely done because of the cost and the general lack of laboratory staff experienced in handling ocular specimens. Conjunctival incisional biopsy is occasionally done when granulomatous diseases ("e.g.", sarcoidosis) or dysplasia are suspected.

Based on the presence of extraocular findings, such as neurological, auditory and integumentary manifestations, the "revised diagnostic criteria" of 2001 classify the disease as complete (eyes along with both neurological and skin), incomplete (eyes along with either neurological or skin) or probable (eyes without either neurological or skin) . By definition, for research homogeneity purposes, there are two exclusion criteria: previous ocular penetrating trauma or surgery, and other concomitant ocular disease similar to VKH disease.

A symblepharon is a partial or complete adhesion of the palpebral conjunctiva of the eyelid to the bulbar conjunctiva of the eyeball. It results either from disease (conjunctival sequelae of trachoma) or trauma. Cicatricial pemphigoid and, in severe cases, rosacea may cause symblepharon. It is rarely congenital. and its treament

1 ocular movements restricted

2 diplopia

3 lagophthalmos

4 cosmetic cause

types.

Anterior, adhesion in Anterior part

Posterior, adhesion in only fornices

total, adhesion involves whole lens

Complications.

prophylaxis, 1 sweeping a glass rod around fornices several times a day

2 therapeutic soft contact lens

curative treatment t, 1 mobilising surrounding cornea, 2 conjunctival or buccal mucosa graft, 3 amniotic membrane transplant