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

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.

There are a number of different treatments to deal with TSPK. Symptoms may disappear if untreated, but treatment may decrease both the healing time and the chances of remission.

- PRK laser eye surgery may cure this disease (NOTE: A full clinical study has not been done, but a case study of one person was reported in 2002 PRK-pTK as a treatment).

- Artificial tear eye-drops or ointments may be a suitable treatment for mild cases.

- Low-dosage steroidal eye-drops, such as prednisone, fluorometholone, loteprednol (Lotemax 0.5%) or rimexolone. Steroidal drops should be used with caution and the eye pressure should be regularly checked during treatment.

- Soft contact lenses.

- Ciclosporin is an experimental treatment for TSPK. It is usually used during transplants as it reduces the immune system response.

- Tacrolimus (Protopic 0.03% ointment) is also an experimental treatment.

- Laser eye treatment.

- Amniotic membrane (Case Study)

Diagnosis of PIC can be difficult because the appearance may be similar to other conditions and types of posterior uveitis, especially other forms of the so called white dot syndromes. The diagnosis is made by eliminating all the other possibilities by careful examination by an experienced ophthalmologist, aided with visual field testing and Fluorescein angiography (an intra-venous dye used to show the blood vessels at the back of the eye).

It is important that the correct diagnosis is made because treatment may be quite different for apparently similar conditions.

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.

Dry eyes can usually be diagnosed by the symptoms alone. Tests can determine both the quantity and the quality of the tears. A slit lamp examination can be performed to diagnose dry eyes and to document any damage to the eye.

A Schirmer's test can measure the amount of moisture bathing the eye. This test is useful for determining the severity of the condition. A five-minute Schirmer's test with and without anesthesia using a Whatman #41 filter paper 5 mm wide by 35 mm long is performed. For this test, wetting under 5 mm with or without anesthesia is considered diagnostic for dry eyes.

If the results for the Schirmer's test are abnormal, a Schirmer II test can be performed to measure reflex secretion. In this test, the nasal mucosa is irritated with a cotton-tipped applicator, after which tear production is measured with a Whatman #41 filter paper. For this test, wetting under 15 mm after five minutes is considered abnormal.

A tear breakup time (TBUT) test measures the time it takes for tears to break up in the eye. The tear breakup time can be determined after placing a drop of fluorescein in the cul-de-sac.

A tear protein analysis test measures the lysozyme contained within tears. In tears, lysozyme accounts for approximately 20 to 40 percent of total protein content.

A lactoferrin analysis test provides good correlation with other tests.

The presence of the recently described molecule Ap4A, naturally occurring in tears, is abnormally high in different states of ocular dryness. This molecule can be quantified biochemically simply by taking a tear sample with a plain Schirmer test. Utilizing this technique it is possible to determine the concentrations of Ap4A in the tears of patients and in such way diagnose objectively if the samples are indicative of dry eye.

The Tear Osmolarity Test has been proposed as a test for dry eye disease. Tear osmolarity may be a more sensitive method of diagnosing and grading the severity of dry eye compared to corneal and conjunctival staining, tear break-up time, Schirmer test, and meibomian gland grading. Others have recently questioned the utility of tear osmolarity in monitoring dry eye treatment.

In advanced stages, corneal neovascularization can threaten eyesight, which is why routine (annual) eye exams are recommended for contact lens patients.

Due to the different underlying causes, proper diagnosis, treatment, and prognosis can only be determined by an eye care professional. Punctate epithelial erosions may be treated with artificial tears. In some disorders, topical antibiotic is added to the treatment. Patients should discontinue contact lens wear until recovery.

There is no way to prevent keratoconjunctivitis sicca. Complications can be prevented by use of wetting and lubricating drops and ointments.

What happens with PIC depends a lot on the presence or absence of an important complication, Choroidal neovascularization (known as CNV).

Often, the inflammation in PIC is self limiting, not always requiring treatment.

However treatment is advised if there are many active or central lesions, or if there are signs of CNV.

Treatments for corneal neovascularization are predominately off-lab with a multitude of complications as a result. The desired results from medical therapy may not always occur, ergo an invasive procedure may be needed to prevent further decrease in corneal avascularity.

For contact lenses related hypoxia, ceasing the use of contact lenses is the first step until corneal neovascularization is addressed by a physician. Modern rigid gas permeable and silicon hydrogel contact lenses have a much higher level of oxygen transmissibility, making them effective alternatives to help prevent corneal neovascularization.

Topical administration of steroids and non-steroid anti-inflammatory drugs are first-line treatment for individuals with CNV. The administration of steroids can increase the risk of infection, glaucoma, cataracts, herpes simplex recurrence. The anti-inflammatory drugs, however, increase the risk of corneal ulceration and melting.

Since VEGF plays an important role in vasculogenesis and pathologic neovascularization associated with eye diseases, a potential treatment for CNV is to inhibit VEGF activity by competing the binding of VEGF with specific neutralizing anti-VEGF antibody. VEGF inhibitors include pegatanib sodium, ranibizumab, and off-label bevacizumab are currently used for treatment of various retinal disease. Anti-VEGF antibodies such as the application of ranibizumab or bevacizumab have has been shown to reduce corneal neovascularization. Both ranibizumab and bevacizumab uses the same mechanism and inhibits all iso-forms of VEGF. The significant reduction in invasion of in-growth blood vessels in terms of neovascular area and vessel caliber suggests that treatment with ranibizumab induces thinning of the blood vessels, however, there's no significant change of the blood vessel's length. Using anti-VEGF antibodies to treat CNV has some limitations such as it is not a cure and may require repeated treatments to maintain positive effects over time. Topical and/or subconjunctival administration of bevaicizumab or ranibizumab have demonstrated short-term safety and efficacy, however long term effects have not been documented. Anti-VEGF therapy is currently an experimental treatment.

If the cornea is inflamed via corneal neovascularization, the suppression of enzymes can block CNV by compromising with corneal structural integrity. Corneal neovascularization can be suppressed with a combination of orally administration of doxycycline and with topical corticosteroid.

Surgical Options

Invasive solutions for corneal neovascularization are reserved when the medical therapies do not provide the desired results.

Invading blood tissues and ablating tissues in the cornea can be obstructed by the use of laser treatments such as Argon and s. Irradiation and/or damages to adjacent tissues caused by the procedure can result in corneal hemorrhage and corneal thinning. Obstruction of the blood vessels can be unsuccessful due to the depth, size, and, high blood flow rate of the vessels. In conjunction, thermal damage from the lasers can trigger inflammatory response which can exaggerate the neovascularization.

An effective treatment is photodynamic therapy, however, this treatment has limited clinical acceptance due to high costs and many potential complications involved that are also related to laser ablation. Complications can include irradiation from previously injected photosensitive dye inducing apoptosis and necrosis of the endothelium and basement membrane.

Diathermy and cautery is a treatment where an electrolysis needle is inserted into the feeder vessels in the limbus. The vessels are obstructed by a coagulating current through the use of unipolar diathermy unit or by thermal cautery.

Treatment of herpes of the eye is different based on its presentation: epithelial keratitis is caused by live virus while stromal disease is an immune response and metaherpetic ulcer results from inability of the corneal epithelium to heal:

A specific clinical diagnosis of HSV as the cause of dendritic keratitis can usually be made by ophthalmologists and optometrists based on the presence of characteristic clinical features. Diagnostic testing is seldom needed because of its classic clinical features and is not useful in stromal keratitis as there is usually no live virus. Laboratory tests are indicated in complicated cases when the clinical diagnosis is uncertain and in all cases of suspected neonatal herpes infection:

- Corneal smears or impression cytology specimens can be analyzed by culture, antigen detection, or fluorescent antibody testing. Tzanck smear, i.e.Papanicolaou staining of corneal smears, show multinucleated giant cells and intranuclear inclusion bodies, however, the test is low in sensitivity and specificity.

- DNA testing is rapid, sensitive and specific. However, its high cost limits its use to research centers.

- Demonstration of HSV is possible with viral culture.

- Serologic tests may show a rising antibody titer during primary infection but are of no diagnostic assistance during recurrent episodes.

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.

Thygeson's superficial punctate keratopathy (TSPK; also "Thygeson Superficial Punctate Keratitis") is a disease of the eyes. The causes of TSPK are not currently known, but details of the disease were first published in the Journal of the American Medical Association in 1950 by the renowned American Ophthalmologist, Phillips Thygeson (1903–2002) - after whom it is named.

Photokeratitis can be prevented by using sunglasses or eye protection that transmits 5–10% of visible light and absorbs almost all UV rays. Additionally, these glasses should have large lenses and side shields to avoid incidental light exposure. Sunglasses should always be worn, even when the sky is overcast, as UV rays can pass through clouds.

The Inuit, Yupik, and other Arctic peoples carved snow goggles from materials such as driftwood or caribou antlers to help prevent snow blindness. Curved to fit the user's face with a large groove cut in the back to allow for the nose, the goggles allowed in a small amount of light through a long thin slit cut along their length. The goggles were held to the head by a cord made of caribou sinew.

In the event of missing sunglass lenses, emergency lenses can be made by cutting slits in dark fabric or tape folded back onto itself. The "SAS Survival Guide" recommends blackening the skin underneath the eyes with charcoal (as the ancient Egyptians did) to avoid any further reflection.

The pain may be temporarily alleviated with anaesthetic eye drops for the examination; however, they are not used for continued treatment, as anaesthesia of the eye interferes with corneal healing, and may lead to corneal ulceration and even loss of the eye. Cool, wet compresses over the eyes and artificial tears may help local symptoms when the feeling returns. Nonsteroidal anti-inflammatory drug (NSAID) eyedrops are widely used to lessen inflammation and eye pain, but have not been proven in rigorous trials. Systemic (oral) pain medication is given if discomfort is severe. Healing is usually rapid (24–72 hours) if the injury source is removed. Further injury should be avoided by isolation in a dark room, removing contact lenses, not rubbing the eyes, and wearing sunglasses until the symptoms improve.

Punctate epithelial erosions may be seen with different disorders:

- Rosacea

- Dry-eye syndrome

- Blepharitis

- Acute bacterial conjunctivitis

- Trauma

- Exposure keratopathy from poor eyelide closure

- Ultraviolet or chemical burn

- Contact lens-related disorder such as toxicity or tight lens syndrome

- Trichiasis

- Entropion or ectropion

- Floppy eyelid syndrome

- Chemotherapy i.e. cytosine arabinoside

- Thygeson's Superficial Punctate Keratopathy

Conjunctivitis is prevalent among children of the highlands of Ecuador. The finding supports the hypothesis that prolonged exposure to the sun at altitude—in the less dense atmosphere (with the resultant lower UV absorption)—is the main cause of the disease.

The symptoms of phlyctenular keratoconjunctivitis are primarily treated with application of an appropriate corticosteroid eye drop, such as prednisolone acetate (Pred Forte) or loteprednol (Lotemax). Loteprednol is increasingly preferred due to its lower risk of elevating intraocular pressure. The corticosteroid suppresses the immune response, reducing inflammation and improving most symptoms.

The causative agent (i.e. the source of the antigen that triggered the hypersensitive immune response) should also be identified. "Staphylococcus aureus" is usually the primary suspect, along with "Mycobacterium tuberculosis" in areas where TB is endemic, followed by "Chlamydia trachomatis". Active bacterial infections may be treated with a topical antibiotic or a combination antibiotic-steroid eye drop, such as tobramycin/dexamethasone (Tobradex). An oral tetracycline antibiotic (such as doxycycline) may be used in systemic or particularly severe/intractable infections. Erythromycin may be an effective alternative, especially in pediatric cases where the side effects of tetracyclines are unacceptable.

Artificial tears can reduce dryness and discomfort from corneal lesions. Photophobic discomfort can be mitigated with dark sunglasses.

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

Non-surgical treatments of FCED may be used to treat symptoms of early disease. Medical management includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. Hypertonic saline draws water out of the cornea through osmosis. When using a hairdryer, the patient is instructed to hold it at an arm's length or directed across the face on a cold setting, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation. The most common types of surgery for FCED are Descemet's stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK), which account for over half of corneal transplants in the United States.

More speculative future directions in the treatment of FED include in-vitro expansion of human corneal endothelial cells for transplantation, artificial corneas (keratoprosthesis) and genetic modification. Surgery where the central diseased endothelium is stripped off but not replaced with donor tissue, with subsequent Rho-Associated Kinase (ROCK) inhibition of endothelial cell division may offer a viable medical treatment.

A greater understanding of FED pathophysiology may assist in the future with the development of treatments to prevent progression of disease. Although much progress has been made in the research and treatment of FED, many questions remain to be answered. The exact causes of illness, the prediction of disease progression and delivery of an accurate prognosis, methods of prevention and effective nonsurgical treatment are all the subject of inquiries that necessitate an answer.

Increased attention must be given to research that can address the most basic questions of how the disease develops: what are the biomolecular pathways implicated in disease, and what genetic or environmental factors contribute to its progression? In addition to shaping our understanding of FED, identification of these factors would be essential for the prevention and management of this condition.

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.

The syndrome is marked by the appearance of characteristic lesions, known as phlyctenules, on the cornea and/or conjunctiva. These usually manifest as small (1 - 3 or 1 - 4 mm) raised nodules, pinkish-white or yellow in color, which may ulcerate (or, more rarely, necrose) and are often surrounded by dilated blood vessels. Corneal lesions are usually triangular in shape, with the base at the limbus and the apex pointing towards the center of the cornea.

Few studies have examined the prevalence of FCED on a large scale. First assessed in a clinical setting, Fuchs himself estimated the occurrence of dystrophia epithelialis corneae to be one in every 2000 patients; a rate that is likely reflective of those who progress to advanced disease. Cross-sectional studies suggest a relatively higher prevalence of disease in European countries relative to other areas of the world. Fuchs' dystrophy rarely affects individuals under 50 years of age.