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.

Because SO is so rarely encountered following eye injury, even when the injured eye is retained, the first choice of treatment may not be enucleation or evisceration, especially if there is a chance that the injured eye may regain some function. Additionally, with current advanced surgical techniques, many eyes once considered nonviable now have a fair prognosis.

However, only if the injured eye has completely lost its vision and has no potential for any visual recovery, prevention of SO is done by enucleation of the injured eye preferably within the first 2 weeks of injury. Evisceration—the removal of the contents of the globe while leaving the sclera and extraocular muscles intact—is easier to perform, offers long-term orbital stability, and is more aesthetically pleasing, i.e., a greater measure of movement of the prosthesis and thus a more natural appearance. There is concern, however, that evisceration may lead to a higher incidence of SO compared to enucleation. Several retrospective studies involving over 3000 eviscerations, however, have failed to identify a single case of SO.

Once SO is developed, Immunosuppressive therapy is the mainstay of treatment. When initiated promptly following injury, it is effective in controlling the inflammation and improving the prognosis. Mild cases may be treated with local application of corticosteroids and pupillary dilators. More severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc.), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.

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.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

The acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. However, ocular complications may require an subtenon or intravitreous injection of corticosteroids or bevacizumab. In refractory situations, other immunosuppressives such as cyclosporine, or tacrolimus, antimetabolites (azathioprine, mycophenolate mofetil or methotrexate), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed.

Horses that suffer from this disease can never be considered cured, although they can be managed by careful use of the therapy described above, and fast detection of new flare-ups. If the disease is not properly treated, it will eventually lead to blindness.

Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. Chronic eye effects such as cataracts, glaucoma, and optic atrophy can occur. Skin changes usually persist despite therapy.

The following may provide relief:

- Cold compresses

- Pad and bandage with antibiotics drops for 24 hours, heals most of the cases

- anaesthetic drops should not be used

- Oral analgesics if pain is intolerable

- Single dose of tranquilizers

Aponeurotic and congenital ptosis may require surgical correction if severe enough to interfere with vision or if cosmetics is a concern.

Treatment depends on the type of ptosis and is usually performed by an ophthalmic plastic and reconstructive surgeon, specializing in diseases and problems of the eyelid.

Surgical procedures include:

- Levator resection

- Müller muscle resection

- Frontalis sling operation (preferred option for oculopharyngeal muscular dystrophy)

Non-surgical modalities like the use of "crutch" glasses or Ptosis crutches or special scleral contact lenses to support the eyelid may also be used.

Ptosis that is caused by a disease may improve if the disease is treated successfully, although some related diseases, such as oculopharyngeal muscular dystrophy currently have no treatments or cures.

Sympathetic ophthalmia (SO) or Sympathetic uveitis is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

Ophthalmia (also called ophthalmitis) is inflammation of the eye. It is a medical sign which may be indicative of various conditions, including sympathetic ophthalmia (inflammation of both eyes following trauma to one eye), gonococcal ophthalmia, trachoma or "Egyptian" ophthalmia, ophthalmia neonatorum (a conjunctivitis of the newborn due to either of the two previous pathogens), photophthalmia and actinic conjunctivitis (inflammation resulting from prolonged exposure to ultraviolet rays), and others.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

Crooke’s glass is a prophylactic aid consisting of a spectacle lens combined with metallic oxides to absorb ultraviolet or infrared rays and should be used by those who are prone to exposure e.g. Welding workers, cinema operators.

Prophylaxis needs antenatal, natal, and post-natal care.

- Antenatal measures include thorough care of mother and treatment of genital infections when suspected.

- Natal measures are of utmost importance as mostly infection occurs during childbirth. Deliveries should be conducted under hygienic conditions taking all aseptic measures. The newborn baby's closed lids should be thoroughly cleansed and dried.

- If it is determined that the cause is due to a blocked tear duct, a gentle palpation between the eye and the nasal cavity may be used to clear the tear duct. If the tear duct is not cleared by the time the newborn is one year old, surgery may be required.

- Postnatal measures include:

- Chemical ophthalmia neonatorum is a self-limiting condition and does not require any treatment.

- Gonococcal ophthalmia neonatorum needs prompt treatment to prevent complications. Topical therapy should include

Systemic therapy: Newborns with gonococcal ophthalmia neonatorum should be treated for seven days with one of the following regimens ceftriaxone, cefotaxime, ciprofloxacin, crystalline benzyl penicillin

- Other bacterial ophthalmia neonatorum should be treated by broad spectrum antibiotics drops and ointment for two weeks.

- Neonatal inclusion conjunctivitis caused by Chlamydia trachomatis responds well to topical tetracycline 1% or erythromycin 0.5% eye ointment QID for three weeks. However systemic erythromycin should also be given since the presence of chlamydia agents in conjunctiva implies colonization of upper respiratory tract as well. Both parents should also be treated with systemic erythromycin.

- Herpes simplex conjunctivitis should be treated with intravenous acyclovir for a minimum of 14 days to prevent systemic infection.

Antibiotic ointment is typically applied to the newborn's eyes within 1 hour of birth as prevention against gonococcal ophthalmia. This maybe erythromycin, tetracycline, or silver nitrate.

The treatment of dysautonomia can be difficult; since it is made up of many different symptoms, a combination of drug therapies is often required to manage individual symptomatic complaints. Therefore, if an autoimmune neuropathy is the case, then treatment with immunomodulatory therapies is done, or if diabetes mellitus is the cause, control of blood glucose is important. Treatment can include proton-pump inhibitors and H2 receptor antagonists used for digestive symptoms such as acid reflux.

For the treatment of genitourinary autonomic neuropathy medications may include sildenafil (a guanine monophosphate type-5 phosphodiesterase inhibitor). For the treatment of hyperhidrosis, anticholinergic agents such as trihexyphenidyl or scopolamine can be used, also intracutaneous injection of botulinum toxin type A can be used for management in some cases.

Balloon angioplasty, a procedure referred to as transvascular autonomic modulation, is specifically not approved for the treatment of autonomic dysfunction.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Use of high doses of opioid drugs such as morphine, oxycodone, heroin, or hydrocodone can cause ptosis. Pregabalin (Lyrica), an anticonvulsant drug, has also been known to cause mild ptosis.

Ophthalmia nodosa is a cutaneous condition characterized by inflammation of the eye due to lodging of (for example) caterpillar hairs in the conjunctiva, cornea, or iris.

Post-operative care for patients with blast-related ocular trauma occurs in tertiary care facilities. Patients with closed globe injuries require observation and follow-up examination with an optometrist, including slit lamp microscope and dilated fundus inspection. Those who have been treated for open-globe repairs often experience a delay of post-operative treatment that ranges from 10–14 days after injury. This period is due to the treatment of other life-threatening injuries, as well as the necessity for accurate estimation of visual acuity outside of inflammation due to injury and surgical intervention.

In patients with facial burns, exposure keratopathy, or chronic epiphora, an ophthalmologist may suggest eyelid reconstruction surgery. Depending on the severity of physical trauma sustained, surgical realignment of the extraocular muscles may relieve strabismus. Realignment of the extraocular muscles is also indicated in chronic diplopia that occurs within 20-degrees of the visual field. All patients that have sustained a traumatic brain injury in the absence of ocular trauma are still recommended to obtain examination by an optometrist. Outside of the treatment facility, these patients must monitor any signs of late-onset ocular pathologies secondary to the bTBI, including decreased visual/reading ability and speed, photophobia, blurred vision, reduced accommodation abilities, and headaches.

Tropicamide is used as a mydriastic agent during cataract surgery. Anticholinergics such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. By blocking these receptors, the pupils are no longer capable of constriction and dilation results. Such alkaloids present in many plants of the family "Solanaceae" may also induce mydriasis when used

The neurotransmitter norepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals, resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place and the end result is dilation of the pupil. Cocaine itself is not typically used for this task, however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.

Opiates such as morphine and heroin do not cause pupil dilation. Instead they cause miosis (pupil contraction). Mydriasis occasionally occurs during opiate rebound and withdrawal.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.

The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.

Visual outcomes for patients with ocular trauma due to blast injuries vary, and prognoses depend upon the type of injury sustained. The majority of poor visual outcomes arise from perforating injuries: only 21% of patients with perforating injuries with pre-operative light perception had a final best-corrected visual acuity (BCVA) better than 20/200. Collectively, patients who experienced choroidal hemorrhage, perforated or penetrated globes, retinal detachment, traumatic optic neuropathy, and subretinal macular hemorrhage carried the highest incidence rates of BCVAs worse than 20/200. Reports from Operation Iraqi Freedom (OIF) indicate that 42% of soldiers with globe injuries of any kind had a BCVA greater than or equal to 20/40 six months after injury, and soldiers with intraocular foreign bodies (IOFBs) retained 20/40 or better vision in 52% of studied cases.

Globe perforation, oculoplastic intervention, and neuro-ophthalmic injuries contribute significantly to reported poor visual outcomes. 21% of tertiary centers treating patients exposed to blast trauma reported traumatic optic neuropathy (TON) in their patients, although avulsion of the optic nerve and TON were reported in only 3% of combat injuries. In the event that a victim of globe penetrating trauma cannot perceive any light within two weeks of surgical intervention, the ophthalmologist may choose to enucleate as a preventative measure against sympathetic ophthalmia. However, this procedure is extremely rare, and current reports indicate that only one soldier in OIF has undergone enucleation in a tertiary care facility to prevent sympathetic ophthalmia.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.