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)

Early diagnosis, targeted treatment according to the severity of the disease, and regular monitoring of patients with neurotrophic keratitis are critical to prevent damage progression and the occurrence of corneal ulcers, especially considering that the deterioration of the condition is often poorly symptomatic.

The purpose of treatment is to prevent the progression of corneal damage and promote healing of the corneal epithelium. The treatment should always be personalized according to the severity of the disease. Conservative treatment is typically the best option.

In stage I, the least serious, treatment consists of the administration of preservative-free artificial tears several times a day in order to lubricate and protect the ocular surface, improving the quality of the epithelium and preventing the possible loss of transparency of the cornea.

In stage II, treatment should be aimed at preventing the development of corneal ulcers and promoting the healing of epithelial lesions. In addition to artificial tears, topical antibiotics may also be prescribed to prevent possible infections. Patients should be monitored very carefully since, being the disease poorly symptomatic, the corneal damage may progress without the patient noticing any worsening of the symptoms. Corneal contact lenses can also be used in this stage of the disease, for their protective action to improve corneal healing.

In the most severe forms (stage III), it is necessary to stop the progression towards corneal perforation: in these cases, a possible surgical treatment option is tarsorrhaphy, i.e. the temporary or permanent closure of the eyelids by means of sutures or botulinum toxin injection. This protects the cornea, although the aesthetic result of these procedures may be difficult to accept for patients. Similarly, a procedure that entails the creation of a conjunctival flap has been shown to be effective in the treatment of chronic corneal ulcers with or without corneal perforation. In addition, another viable therapeutic option is amniotic membrane graft, which has recently been shown to play a role in stimulating corneal epithelium healing and in reducing vascularisation and inflammation of the ocular surface . Other approaches used in severe forms include the administration of autologous serum eye drops.

Research studies have focused on developing novel treatments for neurotrophic keratitis, and several polypeptides, growth factors and neuromediators have been proposed[25]. Studies were conducted on topical treatment with Substance P and IGF-1 (insulin-like growth factor-1), demonstrating an effect on epithelial healing[26]. Nerve Growth Factor (NGF) play a role in the epithelial proliferation and differentiation and in the survival of corneal sensory nerves. Topical treatment with murine NGF showed to promote recovery of epithelial integrity and corneal sensitivity in NK patients[27]. Recently, a recombinant human nerve growth factor eye drop formulation has been developed for clinical use[28].

Cenegermin, a recombinant form of human NGF, has recently been approved in Europe in an eye drop formulation for neurotrophic keratitis.

Depending on severity, therapies may range from topical or oral anti-inflammatories to irrigation and surgical repair.

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.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or as oral therapy. Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluoresence dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis increases T-regulatory cells in the eye, which likely contributes to disease regression.

In some cases an injection of posterior subtenon triamcinolone acetate may also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatments with Infliximab or other anti-TNF infusions may prove helpful.

The anti-diabetic drug metformin is reported to inhibit the process that causes the inflammation in uveitis.

In the case of herpetic uveitis, anti-viral medications, such as valaciclovir or aciclovir, may be administered to treat the causative viral infection.

Treatment options include contact lenses and intrastromal corneal ring segments for correcting refractive errors caused by irregular corneal surface, corneal collagen cross-linking to strengthen a weak and ectatic cornea, or corneal transplant for advanced cases.

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication including cataracts, glaucoma, band keratopathy, macular edema and permanent vision loss may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor into the outlook.

There is currently no defined treatment to ameliorate the muscle weakness of CPEO. Treatments used to treat other pathologies causing ophthalmoplegia has not been shown to be effective.

Experimental treatment with tetracycline has been used to improve ocular motility in one patient. Coenzyme Q has also been used to treat this condition. However, most neuro-ophthalmologists do not ascribe to any treatment.

Ptosis associated with CPEO may be corrected with surgery to raise the lids, however due to weakness of the orbicularis oculi muscles, care must be taken not to raise the lids in excess causing an inability to close the lids. This results in an exposure keratopathy. Therefore, rarely should lid surgery be performed and only by a neuro-ophthalmologist familiar with the disease.

The most common strabismus finding is large angle exotropia which can be treated by maximal bilateral eye surgery, but due to the progressive nature of the disease, strabismus may recur. Those that have diplopia as a result of asymmetric ophthalmoplegia may be corrected with prisms or with surgery to create a better alignment of the eyes.

Treatment of lagopthalmos can include both supportive care methods as well as surgical. If unable to receive surgery, artificial tears should be administered at least four times a day to the cornea to preserve the tear film. Leading up to a surgery, a patient can undergo a tarsorrhaphy which partially sews the eye shut temporarily to further protect the cornea as the patient waits for care. Multiple surgical treatments exist for Lagopthalmos but the most prevalent method includes weighing the upper eyelid down by surgically inserting a gold plate. Due to possible complications in conjunction with both the upper and lower eyelid, it might also be required to undergo a second surgery to tighten and elevate the lower eyelid to ensure both the upper and lower eyelids can fully close and protect the cornea.

Disease begins with vesicles that coalesce. There is severe progressing edema and rupture may occur in 24 hours or less.

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.

Keratopathy is common in older people. Keratopathy occurs after cataract surgery, its incidence has decreased since the advent of intraoperative viscoelastic agents that protect the endothelium.

Band keratopathy is a corneal disease derived from the appearance of calcium on the central cornea. This is an example of metastatic calcification, which by definition, occurs in the presence of hypercalcemia.

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.

Corneal ectatic disorders or corneal ectasia are a group of uncommon, noninflammatory, eye disorders characterised by bilateral thinning of the central, paracentral, or peripheral cornea.

- Keratoconus, a progressive, noninflammatory, bilateral, asymmetric disease, characterized by paraxial stromal thinning and weakening that leads to corneal surface distortion.

- Keratoglobus, a rare noninflammatory corneal thinning disorder, characterised by generalised thinning and globular protrusion of the cornea.

- Pellucid marginal degeneration, a bilateral, noninflammatory disorder, characterized by a peripheral band of thinning of the inferior cornea.

- Posterior keratoconus, a rare condition, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia, a complication of LASIK eye surgery.

- Terrien's marginal degeneration, a painless, noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.

The most commonly employed method is to use tape or a general purpose adhesive dressing. Unfortunately the adhesive used on the tape or dressing will generally be inappropriate for this use. The adhesive strength may change when reaching body temperature, or over time.

As the operation progresses this can cause the adhesive to stop working and become gooey, allowing the eyelids to move apart, and leaving behind a sticky residue. This leaves the cornea exposed to epithelial drying and/or abrasions, sometimes caused by the tape that was originally applied to protect the cornea. Alternatively, the adhesive strength may increase, which upon removal can result in eyelid bruising, tears, or eyelash removal.

Rolls of tapes are often “laying around” the operating theatre or kept in health care workers' pockets.

Therefore, they can be a source of hospital-acquired infections (HAI's) such as Methicillin-resistant Staphylococcus aureus (MRSA) & Vancomycin-resistant Enterococcus (VRE), with a 2010 study showing that 50% of partially used tape rolls tested positive for MRSA, VRE or both.

Most tapes and dressings are non-transparent and so it is not possible to see if the patient’s eyes are opened or closed throughout the case. It is not uncommon for the eyelids to move open as the case progresses, even with adhesive tapes stuck onto them. In a practical sense, these medical tapes/dressings may be difficult to remove from a patient because their ends can become stuck flush with the skin. The possibility of tape removal causing trauma is also significantly increased in older people, people with sensitive skin, dermatitis, dehydration or side effects of medications.

As noted above, there have been several studies looking at the efficacy and safety of eye ointments/lubricants as adjuncts with tape or as a stand-alone management for intra-operative eye closure. Unfortunately many in common use have problems. Petroleum gel is flammable and is best avoided when electrocautery and open oxygen are to be used around the face. Preservative-free eye ointment is preferred, as preservative can cause corneal epithelial sloughing and conjunctival hyperemia.

They have been implicated in blurred vision in up to 75% of patients and they do not protect from direct trauma.

Specially made eyelid occlusion dressings are available commercially, such as EyeGard (manufactured in the USA by KMI Surgical and marketed by Sharn Anesthesia), EyePro (Andsco Medical Pty Ltd, Australia) and Anesthesia-Aid (Sperian Protection). These dressings overcome most of the problems associated with tape or general purpose dressings.

Etiologies: Uveitis, interstitial keratitis, superficial keratitis, phthisis, sarcoidosis, trauma, intraocular silicone oil, systemic diseases (hypercalcemia, vitamin D intoxication, Fanconi's Syndrome, hypophosphatemia, gout, 'milk-alkali' syndrome, myotonic dystrophy, chronic mercury exposure).

Neurotrophic keratitis (NK) is a degenerative disease of the cornea caused by damage of the trigeminal nerve, which results in impairment of corneal sensitivity, spontaneous corneal epithelium breakdown, poor corneal healing and development of corneal ulceration, melting and perforation.

Neurotrophic keratitis is classified as a rare disease, with an estimated prevalence of less than 5 in 10,000 people in Europe. It has been recorded that on average, 6% of herpetic keratitis cases may evolve to this disease, with a peak of 12.8% of cases of keratitis due to herpes zoster virus.

The diagnosis, and particularly the treatment of neurotrophic keratitis are the most complex and challenging aspects of this disease, as a satisfactory therapeutic approach is not yet available.

The main treatment is symptomatic, since the underlying genetic defect cannot be corrected as of 2015. Symptomatic treatment is surgical.

Clinical signs include redness of the eye, pain, blurring of vision, photophobia and floaters.

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

There are 4 stages of disease, with stage 4 being the rarest and most severe.

- Stage 1 Cells infiltrate the periphery of the flap, without involving central cornea.

- Stage 2 Peripheral cells migrate to the center of the cornea, and impair vision; presentation is usually 2 to 3 days after surgery.

- Stage 3 Cells at the central cornea form clumps of dense cell aggregates.

- Stage 4 Otherwise known as central toxic keratopathy, stage 4 characteristically has no inflammatory cells at the anterior chamber or cornea, but there is central stromal necrosis, and the cornea becomes opacified; onset is usually 3 to 9 days after refractive surgery.

Cornea verticillata, also called Fleischer vortex, vortex keratopathy or whorl keratopathy, is a condition characterised by corneal deposits at the level of the basal epithelium forming a faint golden-brown whorl pattern. It is seen in Fabry disease or in case of prolonged amiodarone intake.

Florida keratopathy, also known as Florida spots, is an eye condition characterized by the presence of multiple spots within both corneas. It is most commonly seen in dogs and cats, but is also rarely seen in horses and birds. The disease is found in the southeastern parts of the United States. In other parts of the world it is confined to tropics and subtropics, and it is known as tropical keratopathy.

Florida keratopathy appears as multiple cloudy opacities in the stromal layer of the cornea. The spots appear concentrated at the center and become more diffuse at the periphery. They can range in size from one to eight millimeters. There are no other symptoms, and there is no response to treatment with either anti-inflammatory or antimicrobial drugs. Histological analysis of affected corneas has found acid-fast staining organisms, suggesting Florida keratopathy may be caused by a type of mycobacterium. The disease may be induced by repeated stings to the eyes by the little fire ant, "Wasmannia auropunctata".