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.

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.

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.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

Mydriatic/cycloplegic agents, such as topical homatropine, which is similar in action to atropine, are useful in breaking and preventing the formation of posterior synechia by keeping the iris dilated and away from the crystalline lens. Dilation of the pupil in an eye with the synechia can cause the pupil to take an irregular, non-circular shape (Dyscoria) as shown in the photograph. If the pupil can be fully dilated during the treatment of iritis, the prognosis for recovery from synechia is good. This is a treatable status.

To subdue the inflammation, use topical corticosteroids. If the intra-ocular pressure is elevated then use a PGA such as Travatan Z.

Those with conjunctivitis may report mild irritation or scratchiness, but never extreme pain, which is an indicator of more serious disease such as keratitis, corneal ulceration, iridocyclitis, or acute glaucoma.

A red eye is an eye that appears red due to illness or injury. It is usually injection and prominence of the superficial blood vessels of the conjunctiva, or sclera, which may be caused by disorders of these or adjacent structures. Conjunctivitis and subconjunctival hemorrhage are two of the less serious but more common causes.

Management includes assessing whether emergency action (including referral) is needed, or whether treatment can be accomplished without additional resources.

Slit lamp examination is invaluable in diagnosis but initial assessment can be performed using a careful history, testing vision (visual acuity), and carrying out a penlight examination.

A synechia is an eye condition where the iris adheres to either the cornea (i.e. "anterior synechia") or lens (i.e. "posterior synechia"). Synechiae can be caused by ocular trauma, iritis or iridocyclitis and may lead to certain types of glaucoma. It is sometimes visible on careful examination but usually more easily through an ophthalmoscope or slit-lamp.

Anterior synechia causes closed angle glaucoma, which means that the iris closes the drainage way of aqueous humour which in turn raises the intraocular pressure. Posterior synechia also cause glaucoma, but with a different mechanism. In posterior synechia, the iris adheres to the lens, blocking the flow of aqueous humor from the posterior chamber to the anterior chamber. This blocked drainage raises the intraocular pressure.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

There are no prospective randomized controlled trials studying therapies for relapsing polychondritis. Evidence for efficacy of treatments is based on case reports and series of small groups of patients.

For mild cases limited to joint pain or arthritis, oral nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. Other treatments typically involve medications to suppress the immune system. Corticosteroids are frequently used for more serious disease. Steroid-sparing medications such as azathioprine or methotrexate may be used to minimize steroid doses and limit the side effects of steroids. For severe disease cyclophosphamide is often given in addition to high dose intravenous steroids.

Ophthalmic examination may reveal neovascularization (creation of new vessels in the retina), retinal vessel narrowing, retinal vessel cuffing, retinal hemorrhage, or possible vitritis (inflammation of the vitreous body) or choroiditis (inflammation of the choroid).

Retinal vasculitis presents as painless, decrease of visual acuity (blurry vision), visual floaters, scotomas (dark spot in vision), decreased ability to distinguish colors, and metamorphopsia (distortion of images such as linear images).

Many individuals have mild symptoms, which recur infrequently, while others may have persistent problems that become debilitating or life-threatening.

Herpes zoster ophthalmicus (HZO) and also known as ophthalmic zoster is a disease characterised by reactivation of dormant varicella zoster virus residing within the ophthalmic nerve (the first division of the trigeminal nerve). This condition is an important subtype of shingles, representing 15% of all cases.

Herpes zoster ophthalmicus is transmitted via direct contact or droplets. Varicella zoster virus is a DNA virus which produces acidophilic intranuclear inclusion bodies. The virus is neurotrophic in nature.

The frontal nerve is more commonly affected than the nasociliary nerve or lacrimal nerve.

Systemic corticosteroids such as (prednisone) can produce rapid improvement and are the “gold standard” for treatment. The temperature, white blood cell count, and eruption improve within 72 hours. The skin lesions clear within 3 to 9 days. Abnormal laboratory values rapidly return to normal. There are, however, frequent recurrences. Corticosteroids are tapered within 2 to 6 weeks to zero.

Resolution of the eruption is occasionally followed by milia and scarring. The disease clears spontaneously in some patients. Topical and/or intralesional corticosteroids may be effective as either monotherapy or adjuvant therapy.

Oral potassium iodide or colchicine may induce rapid resolution.

Patients who have a potential systemic infection or in whom corticosteroids are contraindicated can use these agents as a first-line therapy.

In one study, indomethacin, 150 mg per day, was given for the first week, and 100 mg per day was given for 2 additional weeks. Seventeen of 18 patients had a good initial response; fever and arthralgias were markedly attenuated within 48 hours, and eruptions cleared between 7 and 14 days.

Patients whose cutaneous lesions continued to develop were successfully treated with prednisone (1 mg/kg per day). No patient had a relapse after discontinuation of indomethacin.

Other alternatives to corticosteroid treatment include dapsone, doxycycline, clofazimine, and cyclosporine. All of these drugs influence migration and other functions of neutrophils.

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

JIA is best treated by a multidisciplinary team. The major emphasis of treatment for JIA is to help the child regain normal level of physical and social activities. This is accomplished with the use of physical therapy, pain management strategies, and social support. Another emphasis of treatment is to control inflammation and extra-articular symptoms quickly. Doing so should help to reduce joint damage and other symptoms, which will help reduce levels of permanent damage leading to disability.

Beneficial advances in drug treatment have been made over the last 20 years. Most children are treated with nonsteroidal anti-inflammatory drugs and intra-articular corticosteroid injections. Methotrexate, a disease-modifying antirheumatic drug (DMARD) is a powerful drug which helps suppress joint inflammation in the majority of JIA patients with polyarthritis (though less useful in systemic arthritis). Newer drugs have been developed recently, such as TNF alpha blockers, such as etanercept. No controlled evidence supports the use of alternative remedies such as specific dietary exclusions, homeopathic treatment, or acupuncture. However, an increased consumption of omega-3 fatty acids proved to be beneficial in two small studies.

Celecoxib has been found effective in one study.

Other aspects of managing JIA include physical and occupational therapy. Therapists can recommend the best exercise and also make protective equipment. Moreover, the child may require the use of special supports, ambulatory devices, or splints to help them ambulate and function normally.

Surgery is only used to treat the most severe cases of JIA. In all cases, surgery is used to remove scars and improve joint function.

Home remedies that may help JIA includes getting regular exercises to increase muscle strength and joint flexibility. Swimming is perhaps the best activity for all children with JIA. Stiffness and swelling can also be reduced with application of cold packs, but a warm bath or shower can also improve joint mobility.

In the future, genetic testing may be available allowing earlier detection of JIA. Early detection will help determine the severity of the disease in each child and help identify which therapies will be the most effective and beneficial treatment options.

Keratic precipitate (KP) is an inflammatory cellular deposit seen on corneal endothelium. Acute KPs are white and round in shape whereas old KPs are faded and irregular in shape. Mutton-fat KPs are large in shape and are greasy-white in color and are formed from macrophages and epithelioid cell. They are indicative of inflammatory disease. Mutton fat Kps are due to granulomatous iridocyclitis. Another variant called red KPs may be seen in hemorrhagic uveitis.

Children with Kawasaki disease should be hospitalized and cared for by a physician who has experience with this disease. When in an academic medical center, care is often shared between pediatric cardiology, pediatric rheumatology, and pediatric infectious disease specialists (although no specific infectious agent has been identified as yet). Treatment should be started as soon as the diagnosis is made to prevent damage to the coronary arteries.

Intravenous immunoglobulin (IVIG) is the standard treatment for Kawasaki disease and is administered in high doses with marked improvement usually noted within 24 hours. If the fever does not respond, an additional dose may have to be considered. In rare cases, a third dose may be given to the child. IVIG by itself is most useful within the first seven days of onset of fever, in terms of preventing coronary artery aneurysm.

Salicylate therapy, particularly aspirin, remains an important part of the treatment (though questioned by some) but salicylates alone are not as effective as IVIG. Aspirin therapy is started at high doses until the fever subsides, and then is continued at a low dose when the patient returns home, usually for two months to prevent blood clots from forming. Except for Kawasaki disease and a few other indications, aspirin is otherwise normally not recommended for children due to its association with Reye's syndrome. Because children with Kawasaki disease will be taking aspirin for up to several months, vaccination against varicella and influenza is required, as these infections are most likely to cause Reye's syndrome.

High-dose aspirin is associated with anemia and does not confer benefit to disease outcomes.

Corticosteroids have also been used, especially when other treatments fail or symptoms recur, but in a randomized controlled trial, the addition of corticosteroid to immune globulin and aspirin did not improve outcome. Additionally, corticosteroid use in the setting of Kawasaki disease is associated with increased risk of coronary artery aneurysm, so its use is generally contraindicated in this setting. In cases of Kawasaki disease refractory to IVIG, cyclophosphamide and plasma exchange have been investigated as possible treatments, with variable outcomes.

New research shows that identifying what type of JIA a child has can help target treatment and lead to more positive outcomes. Identifying the specific biomarkers related to each type of JIA can help form more personalized treatment plans and decrease remission rates.

Children with JIA are more susceptible to cardiovascular disease, depression, sleep disturbance, anxiety and fatigue than healthy individuals. There is also limited information that suggests that children with JIA are at increased risk for malignancies when being treated with TNF blockers.

Prognosis is more positive when gene testing is undergone to identify what subtype of JIA is present in the child. Standardized treatment protocols are in place specific to each subtype of JIA. Treatment is more successful when targeted to the specific subtype of JIA.

With early treatment, rapid recovery from the acute symptoms can be expected, and the risk of coronary artery aneurysms is greatly reduced. Untreated, the acute symptoms of Kawasaki disease are self-limited ("i.e." the patient will recover eventually), but the risk of coronary artery involvement is much greater. Overall, about 2% of patients die from complications of coronary vasculitis. Patients who have had Kawasaki disease should have an echocardiogram initially every few weeks, and then every one or two years to screen for progression of cardiac involvement.

Laboratory evidence of increased inflammation combined with demographic features (male sex, age less than six months or greater than eight years) and incomplete response to IVIG therapy create a profile of a high-risk patient with Kawasaki disease. The likelihood that an aneurysm will resolve appears to be determined in large measure by its initial size, in which the smaller aneurysms have a greater likelihood of regression. Other factors are positively associated with the regression of aneurysms, including being younger than a year old at the onset of Kawasaki disease, fusiform rather than saccular aneurysm morphology, and an aneurysm location in a distal coronary segment. The highest rate of progression to stenosis occurs among those who develop large aneurysms. The worst prognosis occurs in children with giant aneurysms. This severe outcome may require further treatment such as percutaneous transluminal angioplasty, coronary artery stenting, bypass grafting, and even cardiac transplantation.

A relapse of symptoms may occur soon after initial treatment with IVIG. This usually requires rehospitalization and retreatment. Treatment with IVIG can cause allergic and nonallergic acute reactions, aseptic meningitis, fluid overload and, rarely, other serious reactions. Overall, life-threatening complications resulting from therapy for Kawasaki disease are exceedingly rare, especially compared with the risk of nontreatment. Also, evidence indicates Kawasaki disease produces altered lipid metabolism that persists beyond the clinical resolution of the disease.

In mass drug administration (MDA) programmes, the treatment for onchocerciasis is ivermectin (trade name: Mectizan); infected people can be treated with two doses of ivermectin, six months apart, repeated every three years. The drug paralyses and kills the microfilariae causing fever, itching, and possibly oedema, arthritis and lymphadenopathy. Intense skin itching is eventually relieved, and the progression towards blindness is halted. In addition, while the drug does not kill the adult worms, it does prevent them for a limited time from producing additional offspring. The drug therefore prevents both morbidity and transmission for up to several months.

Ivermectin treatment is particularly effective because it only needs to be taken once or twice a year, needs no refrigeration, and has a wide margin of safety, with the result that it has been widely given by minimally trained community health workers.

For the treatment of individuals, doxycycline is used to kill the "Wolbachia" bacteria that live in adult worms. This adjunct therapy has been shown to significantly lower microfilarial loads in the host, and may kill the adult worms, due to the symbiotic relationship between "Wolbachia" and the worm. In four separate trials over 10 years with various dosing regimens of doxycycline for individualized treatment, doxycycline was found to be effective in sterilizing the female worms and reducing their numbers over a period of four to six weeks. Research on other antibiotics, such as rifampicin, has shown it to be effective in animal models at reducing "Wolbachia" both as an alternative and as an adjunct to doxycycline. However, doxycycline treatment requires daily dosing for at least four to six weeks, making it more difficult to administer in the affected areas.

Currently, no specific treatment for chikungunya is available. Supportive care is recommended, and symptomatic treatment of fever and joint swelling includes the use of nonsteroidal anti-inflammatory drugs such as naproxen, non-aspirin analgesics such as paracetamol (acetaminophen) and fluids. Aspirin is not recommended due to the increased risk of bleeding. Despite anti-inflammatory effects, corticosteroids are not recommended during the acute phase of disease, as they may cause immunosuppression and worsen infection.

Passive immunotherapy has potential benefit in treatment of chikungunya. Studies in animals using passive immunotherapy have been effective, and clinical studies using passive immunotherapy in those particularly vulnerable to severe infection are currently in progress. Passive immunotherapy involves administration of anti-CHIKV hyperimmune human intravenous antibodies (immunoglobulins) to those exposed to a high risk of chikungunya infection. No antiviral treatment for chikungunya virus is currently available, though testing has shown several medications to be effective "in vitro".