Prior to any physical examination, the diagnosis of keratoconus frequently begins with an ophthalmologist's or optometrist's assessment of the person's medical history, particularly the chief complaint and other visual symptoms, the presence of any history of ocular disease or injury which might affect vision, and the presence of any family history of ocular disease. An eye chart, such as a standard Snellen chart of progressively smaller letters, is then used to determine the person's visual acuity. The eye examination may proceed to measurement of the localized curvature of the cornea with a manual keratometer, with detection of irregular astigmatism suggesting a possibility of keratoconus. Severe cases can exceed the instrument's measuring ability. A further indication can be provided by retinoscopy, in which a light beam is focused on the person's retina and the reflection, or reflex, observed as the examiner tilts the light source back and forth. Keratoconus is amongst the ophthalmic conditions that exhibit a scissor reflex action of two bands moving toward and away from each other like the blades of a pair of scissors.

If keratoconus is suspected, the ophthalmologist or optometrist will search for other characteristic findings of the disease by means of slit lamp examination of the cornea. An advanced case is usually readily apparent to the examiner, and can provide for an unambiguous diagnosis prior to more specialized testing. Under close examination, a ring of yellow-brown to olive-green pigmentation known as a Fleischer ring can be observed in around half of keratoconic eyes. The Fleischer ring, caused by deposition of the iron oxide hemosiderin within the corneal epithelium, is subtle and may not be readily detectable in all cases, but becomes more evident when viewed under a cobalt blue filter. Similarly, around 50% of subjects exhibit Vogt's striae, fine stress lines within the cornea caused by stretching and thinning. The striae temporarily disappear while slight pressure is applied to the eyeball. A highly pronounced cone can create a V-shaped indentation in the lower eyelid when the person's gaze is directed downwards, known as Munson's sign. Other clinical signs of keratoconus will normally have presented themselves long before Munson's sign becomes apparent, and so this finding, though a classic sign of the disease, tends not to be of primary diagnostic importance.

A handheld keratoscope, sometimes known as "Placido's disk", can provide a simple noninvasive visualization of the surface of the cornea by projecting a series of concentric rings of light onto the cornea. A more definitive diagnosis can be obtained using corneal topography, in which an automated instrument projects the illuminated pattern onto the cornea and determines its topography from analysis of the digital image. The topographical map indicates any distortions or scarring in the cornea, with keratoconus revealed by a characteristic steepening of curvature which is usually below the centreline of the eye. The technique can record a snapshot of the degree and extent of the deformation as a benchmark for assessing its rate of progression. It is of particular value in detecting the disorder in its early stages when other signs have not yet presented.

Once keratoconus has been diagnosed, its degree may be classified by several metrics:

- The steepness of greatest curvature from 'mild' ( 52 D);

- The morphology of the cone: 'nipple' (small: 5 mm and near-central), 'oval' (larger, below-center and often sagging), or 'globus' (more than 75% of cornea affected);

- The corneal thickness from mild (> 506 μm) to advanced (< 446 μm).

Increasing use of corneal topography has led to a decline in use of these terms.

Corneal perforation can be diagnosed by using the Seidel test. Any aqueous leakage is revealed during the Seidel test confirms corneal perforation. A fluorescence strip is wiped over the wound. If the clear aqueous humor from the eye runs through the yellow stain, the patient tests positive for corneal perforation.

Treatment options include contact lenses, intrastromal corneal ring segments, corneal collagen cross-linking, or corneal transplant.

When cross-linking is performed only after the cornea becomes distorted, vision remains blurry even though the disease is stabilised. As a result, combining corneal collagen cross-linking with LASIK ('LASIK Xtra') aims to strengthen the cornea at the point of surgery and may be useful in cases where a very thin cornea is expected after the LASIK procedure. This would include cases of high spectacle power and people with thin corneas before surgery. Definitive evidence that the procedure can reduce the risk of corneal ectasia will only become available a number of years later as corneal ectasia, if it happens, usually occurs in the late post-operative period. Some study show that combining LASIK with cross-linking adds refractive stability to hyperopic treatments and may also do the same for very high myopic treatments.

In 2016, the FDA approved the KXL system and two photoenhancers for the treatment of corneal ectasia following refractive surgery.

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.

The erosion may be seen by an eye doctor using the magnification of a biomicroscope or slit lamp. Usually fluorescein stain must be applied first and a cobalt blue-light used, but may not be necessary if the area of the epithelial defect is large. Optometrists and ophthalmologists have access to the slit lamp microscopes that allow for this more-thorough evaluation under the higher magnification. Mis-diagnosis of a scratched cornea is fairly common, especially in younger patients.

Some suggest that more time spent outdoors during childhood is effective for prevention.

Various methods have been employed in an attempt to decrease the progression of myopia, although studies show mixed results. Many myopia treatment studies have a number of design drawbacks: small numbers, lack of adequate control group, and failure to mask examiners from knowledge of treatments used.

Intraocular pressure should be measured as part of the routine eye examination.

It is usually only elevated by iridocyclitis or acute-closure glaucoma, but not by relatively benign conditions.

In iritis and traumatic perforating ocular injuries, the intraocular pressure is usually low.

The treatment of corneal perforation depends on the location, severity and the cause of damage

- Tissue adhesive can be used to seal small perforation, but this method cannot be used to treat perforations larger than 1 mm.

- Non infected corneal perforation generally heals when a pressure bandage is used.

- For certain types of corneal perforations, lamellar keratoplasty is used as treatment.

In an eye with iridocyclitis, (inflammation of both the iris and ciliary body), the involved pupil will be smaller than the uninvolved, due to reflex muscle spasm of the sphincter muscle of the iris.

Generally, conjunctivitis does not affect the pupils.

With acute angle-closure glaucoma, the pupil is generally fixed in mid-position, oval, and responds sluggishly to light, if at all.

Shallow anterior chamber depth may indicate a predisposition to one form of glaucoma (narrow angle) but requires slit-lamp examination or other special techniques to determine it.

In the presence of a "red eye", a shallow anterior chamber may indicate acute glaucoma, which requires immediate attention.

Although corneal abrasions may be seen with ophthalmoscopes, slit lamp microscopes provide higher magnification which allow for a more thorough evaluation. To aid in viewing, a fluorescein stain that fills in the corneal defect and glows with a cobalt blue-light is generally instilled first.

A careful search should be made for any foreign body, in particular looking under the eyelids. Injury following use of hammers or power-tools should always raise the possibility of a penetrating foreign body into the eye, for which urgent ophthalmology opinion should be sought.

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

The center of the cornea shows normal thickness, with an intact central epithelium, but the inferior cornea exhibits a peripheral band of thinning, to about 1–2 mm. The portion of the cornea that is immediately adjacent to the limbus is spared, usually a strip of about 1–2 mm. In PMD we can see high against the rule astigmatism along with horizontal bow ties. The inferior peripheral thinning is seen between the 4 o'clock and 8 o'clock positions.

PMD lacks apical corneal scarring, Rizutti's phenomenon, Munson's sign, and the central corneal thickness is usually normal.

The gold standard diagnostic test for PMD is corneal topography. However, it may not as specific as corneal pachymetry, because corneal topography only evaluates the degree and distribution of surface irregularities on the cornea, not the thickness of the cornea. Corneal topography may show a "crab claw-like" appearance, a finding that is seen in both keratoconus and in pellucid marginal degeneration. Thus, if corneal topography is used for diagnosis, it should be in conjunction with clinical findings of peripheral, inferior corneal thinning.

A diagnosis of myopia is typically made by an eye care professional, usually an optometrist or ophthalmologist. During a refraction, an autorefractor or retinoscope is used to give an initial objective assessment of the refractive status of each eye, then a phoropter is used to subjectively refine the patient's eyeglass prescription. Other types of refractive error are hyperopia, astigmatism, and presbyopia.

Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body be identified and removed, especially if containing iron as rusting will occur.

Occasionally the healed epithelium may be poorly adherent to the underlying basement membrane in which case it may detach at intervals giving rise to recurrent corneal erosions.

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

Given that episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches to be taken to help prevent episodes include:

- Environmental:

- ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.

- use of protective glasses especially when gardening or playing with children.

- General personal measures:

- maintaining general hydration levels with adequate fluid intake.

- not sleeping-in late as the cornea tends to dry out the longer the eyelids are closed.

- Pre-bed routine:

- routine use of long-lasting eye ointments applied before going to bed.

- occasional use of the anti-inflammatory eyedrop FML (prescribed by an ophthalmologist or optometrist) before going to bed if the affected eye feels inflamed, dry or gritty

- use of a hyperosmotic (hypertonic) ointment before bed reduces the amount of water in the epithelium, strengthening its structure

- use the pressure patch as mentioned above.

- use surgical tape to keep the eye closed (if Nocturnal Lagophthalmos is a factor)

- Waking options:

- learn to wake with eyes closed and still and keeping artificial tear drops within reach so that they may be squirted under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.

- It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fingers, before trying to open them, or keeping the affected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.

Quantitative comparisons between different eyes and conditions are usually made using RMS (root mean square). To measure RMS for each type of aberration involves squaring the difference between the aberration and mean value and averaging it across the pupil area. Different kinds of aberrations may have equal RMS across the pupil but have different effects on vision, therefore, RMS error is unrelated to visual performance. The majority of eyes have total RMS values less than 0.3 µm.

The most common method of classifying the shapes of aberration maps is to consider each map as the sum of fundamental shapes or basis functions. One popular set of basis functions are the Zernike polynomials. Each aberration may be positive or negative in value and induces predictable alterations in the image quality.

Because there is no limit to the number of terms that may be used by Zernike polynomials, vision scientists use the first 15 polynomials, based on the fact that they are enough to obtain a highly accurate description of the most common aberrations found in human eye. Among these the most important Zernike coefficients affecting visual quality are coma, spherical aberration, and trefoil.

Zernike polynomials are usually expressed in terms of polar coordinates (ρ,θ), where ρ is radial coordinate and θ is the angle. The advantage of expressing the aberrations in terms of these polynomials includes the fact that the polynomials are independent of one another. For each polynomial the mean value of the aberration across the pupil is zero and the value of the coefficient gives the RMS error for that particular aberration (i.e. the coefficients show the relative contribution of each Zernike mode to the total wavefront error in the eye). However these polynomials have the disadvantage that their coefficients are only valid for the particular pupil diameter they are determined for.

In each Zernike polynomial formula_1, the subscript n is the order of aberration, all the Zernike polynomials in which n=3 are called third-order aberrations and all the polynomials with n=4, fourth order aberrations and so on. formula_2 and formula_3 are usually called secondary Astigmatism and should not cause confusion. The superscript m is called the angular frequency and denotes the number of times the Wavefront pattern repeats itself.

List of Zernike modes and their common names:

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

Before LASIK surgery, people must be examined for possible risk factors such as keratoconus.

Abnormal corneal topography compromises of keratoconus, pellucid marginal degeneration, or forme fruste keratoconus with an I-S value of 1.4 or more is the most significant risk factor. Low age, low residual stromal bed (RSB) thickness, low preoperative corneal thickness, and high myopia are other important risk factors.

Most patients can be treated non-surgically with eyeglasses, or contact lenses.

The goal of investigation is the assessment of the severity of the ocular injury with an eye to implementing a management plan as soon as is required. The usual eye examination should be attempted, and may require a topical anesthetic in order to be tolerable. Many topical agents cause burning upon instillation. Proxymetacaine has been found to have the best tolerance.

Depending on the medical history and preliminary examination, the primary care physician should designate the eye injury as a "true emergency", "urgent" or "semi-urgent".

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.

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.

Depending on the type of ocular injury, either a "pressure patch" or "shield patch" should be applied. Up until circa 1987, pressure patches were the preferred method of treatment for corneal abrasions in non-contact lens wearers; Multiple controlled studies conducted by accredited organizations such as the American Academy of Ophthalmology have shown that pressure patching is of little or no value in healing corneal abrasions and is actually detrimental to healing in some cases. A Cochrane Review found that patching simple corneal abrasions may not improve healing or reduce pain. Pressure patching should never be used on an individual presenting with a corneal abrasion who has a history of contact lens wear. In this circumstance, a virulent infection caused by the bacterium Pseudomonas aeruginosa is at a clearly delineated increased risk for occurrence. These infections can cause blindness within 24 – 48 hours and there is a possibility that the infection can move into the peri-orbital socket, resulting in the need for evisceration of the eyeball. In rare cases, the infection can enter the brain and cause death to the patient.

In cases of globe penetration, pressure patches should never be applied, and instead a shield patch should be applied that protects the eye without applying any pressure. If a shield patch is applied to one eye, the other eye should also be patched due to eye movement. If the uninjured eye moves, the injured eye will also move involuntarily possibly causing more damage.