Ocular hypertension is treated with either medications or laser. Medications that lower intraocular pressure work by decreasing aqueous humor production and/or increasing aqueous humor outflow. Laser trabeculoplasty works by increasing outflow. The cannabinoids found in cannabis sativa and indica (marijuana) have been shown to reduce intraocular pressure, by up to 50% for approximately four to five hours. But due to the duration of effect, significant side-effect profile, and lack of research proving efficacy, the American Glaucoma Society issued a position statement in 2009 regarding the use of marijuana as a treatment for glaucoma.

Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.

- Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow.

- Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.

- Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

- Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).

- Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.

- Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an argon laser trabeculoplasty procedure.

A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm, frequency-doubled, Q-switched , which selectively targets melanin pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.

The preferred treatment of congenital glaucoma is surgical not medical. The initial procedures of choice are goniotomy or trabeculotomy if the cornea is clear, and trabeculectomy ab externo if the cornea is hazy. The success rates are similar for both procedures in patients with clear corneas. Trabeculectomy and shunt procedures should be reserved for those cases in which goniotomy or trabeculotomy has failed. Cyclophotocoagulation is necessary in some intractable cases but should be avoided whenever possible because of its potential adverse

effects on the lens and the retina.

Treatment is based on the cause of the retinopathy and may include laser therapy to the retina. Laser photocoagulation therapy has been the standard treatment for many types of retinopathy. Evidence show that laser therapy is generally safe and improves visual symptoms in sickle cell and diabetic retinopathy. In recent years targeting the pathway controlling vessel growth or angiogenesis has been promising. Vascular endothelial growth factor (VEGF) seems to play a vital role in promoting neovascularization. Using anti-VEGF drugs (antibodies to sequester the growth factor), research have shown significant reduction in the extent of vessel outgrowth. Evidence supports the use of anti-VEGF antibodies, such as bevacizumab or pegaptanib, seems to improve outcomes when used in conjunction with laser therapy to treat retinopathy of prematurity. The evidence is poorer for treatment of diabetic retinopathy. Use of anti-VEGF drugs did not appear to improve outcomes when compared to standard laser therapy for diabetic retinopathy.

Telemedicine programs are available that allow primary care clinics to take images using specially designed retinal imaging equipment which can then be shared electronically with specialists at other locations for review. In 2009, Community Health Center, Inc. implemented a telemedicine retinal screening program for low-income patients with diabetes as part of those patients annual visits at the Federally Qualified Health Center.

If the diagnostic workup reveals a systemic disease process, directed therapies to treat that underlying cause should be initiated. If the amaurosis fugax is caused by an atherosclerotic lesion, aspirin is indicated, and a carotid endarterectomy considered based on the location and grade of the stenosis. Generally, if the carotid artery is still patent, the greater the stenosis, the greater the indication for endarterectomy. "Amaurosis fugax appears to be a particularly favorable indication for carotid endarterectomy. Left untreated, this event carries a high risk of stroke; after carotid endarterectomy, which has a low operative risk, there is a very low postoperative stroke rate." However, the rate of subsequent stroke after amaurosis is significantly less than after a hemispheric TIA, therefore there remains debate as to the precise indications for which a carotid endarterectomy should be performed. If the full diagnostic workup is completely normal, patient observation is recommended.

Treatment requires careful consideration of angiographic findings when a choroidal neovascular membrane is suspected which is a condition that responds to treatment. A vitreo-retinal specialist (an ophthalmologist specialized in treatment of retinal diseases) should be consulted for proper management of the case.

Presumed ocular histoplasmosis syndrome and age-related macular degeneration (AMD) have been successfully treated with laser, anti-vascular endothelial growth factors and photodynamic therapy. Ophthalmologists are using anti-vascular endothelial growth factors to treat AMD and similar conditions since research indicates that vascular endothelial growth factor (VEGF) is one of the causes for the growth of the abnormal vessels that cause these conditions.

The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.

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.

Several treatments have been attempted for CRAS; however, none show definitive improvement in outcomes. The Undersea and Hyperbaric Medical Society lists Central Retinal Artery Occlusion (CRAO) as an approved indication for Hyperbaric Oxygen Therapy. This a treatment for CRAO that is covered by medical insurance in North America. Other treatments include ocular massage, anterior chamber paracentesis, and inhalation therapy of a mixture of 5% carbon dioxide and 95% oxygen.

Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients with atherosclerosis, deep venous thrombosis, atrial fibrillation, pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid artery embolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain. Hence, proper steps to prevent such an eventuality need to be taken.

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mg IV acetazolamide and 100 mg IV methylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. An ESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity, visual field testing, and by ophthalmoscopic examination.

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.

In 2009, the Undersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications for hyperbaric oxygen (HBO). When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatory cytokines may contribute to the improvement in vision. Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at the ophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.

The first line of management for chemical injuries is usually copious irrigation of the eye with an isotonic saline or sterile water. In the cases of chemical burns, one should not try to buffer the solution, but instead it with copious flushing.

Unless there is actual trauma to the eye itself (see below), extensive medical attention is generally not needed.

Applying an ice pack will keep down swelling and reduce internal bleeding by constricting the capillaries. Additionally, analgesic drugs (painkillers) can be administered to relieve pain.

An anecdotal remedy for a black eye involves the administering of raw meat to treat the condition - Research on this treatment has yet to find any evidence of this treatment being effective.

In cases of eyelid lace, sutures may be a part of appropriate management by the primary care physician so long as the laceration does not threaten the canaliculi, is not deep, and does not affect the lid margins.

Small extramacular lesions (lesions not threatening vision) may be observed without treatment. Sight-threatening lesions are treated for 4–6 weeks with triple therapy consisting of pyrimethamine, sulfadiazine, and folinic acid. During treatment with pyrimethamine, leukocyte and platelet counts should be monitored weekly. Folinic acid protects against the decrease in platelets and white blood cells induced by pyrimethamine.

Prednisone may be used for 3–6 weeks to reduce macular or optic nerve inflammation and can be started on day 3 of antibiotic therapy. Corticosteroids should not be used without concurrent antibiotic treatment or in immunocompromised patients due to the risk of exacerbation of the disease. Currently, there is no published evidence from randomized controlled trials demonstrating that corticosteroids would be an effective adjunct for treating ocular toxoplasmosis.

Trimethoprim-Sulfamethoxazole has been shown to be equivalent to triple therapy in the treatment of ocular toxoplasmosis and may be better tolerated. Clindamycin and azithromycin can also be considered as alternative therapies. Spiramycin may be used safely without undue risk of teratogenicity and may reduce the rate of transmission to the fetus.

AIDS patients require chronic maintenance treatment.

In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .

Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.

The development of accurate and reliable non-invasive ICP measurement methods for VIIP has the potential to benefit many patients on earth who need screening and/or diagnostic ICP measurements, including those with hydrocephalus, intracranial hypertension, intracranial hypotension, and patients with cerebrospinal fluid shunts. Current ICP measurement techniques are invasive and require either a lumbar puncture, insertion of a temporary spinal catheter, insertion of a cranial ICP monitor, or insertion of a needle into a shunt reservoir.

The prognosis tends to be good for patients with MG. It is often best not to treat mild cases of MG. Management necessitates avoidance of medications that can worsen neuromuscular transmission, such as aminoglycoside antibiotics, quinolone antibiotics, beta-blockers, chloroquine, anti-arrhythmics, calcium channel blockers, some anticonvulsants and intravenous iodinated contrast should be avoided.

MG is characteristically variable in course, with the frequency of diplopia and ptosis affected by environmental, emotional and physical factors such as bright sunlight, stress, viral illness, menstruation, pregnancy, etc. Spontaneous remission can occur in any patient and remain for years. In a study of the natural history of generalized MG among 168 patients (with an average follow-up of 12 years), 14% experienced complete remission.

Patients with mild-to-moderate ocular myasthenia are usually treated initially with oral anticholinesterase agents, Mestinon (pyridostigmine) being the most commonly employed. There have not been any randomized clinical trials conducted with these agents, and this treatment is often unsuccessful, particularly in resolving diplopia. Immunosuppressive therapy is then started and the agent of choice is usually prednisone. In a small controlled study this drug demonstrated greater efficacy than pyridostigmine. Steroid therapy is controversial, but in another study the results suggested that prednisone does decrease progression to generalized MG. There is no single recommended dosing regimen in light of the side effects commonly associated with chronic corticosteroid therapy, and the difficulty in weaning patients from steroids without exacerbation of symptoms. Response to prednisone therapy is variable.

Additionally, MG patients should be examined for thymomas, and if found, should undergo surgery to address this condition. A prophylactic thymectomy is controversial, but has been shown to be helpful in young MG patients with acute disease within 3 years of disease onset, in patients with enlarged thymus glands and for whom surgery is low-risk, and patients with generalized MG who are unresponsive to medical treatment.

The symptoms of ocular MG can also be addressed by non-medicinal means. Ptosis can be corrected with placement of crutches on eyeglasses and with ptosis tape to elevate eyelid droop. Diplopia can be addressed by occlusion with eye patching, frosted lens, occluding contact lens, or by simply placing opaque tape over a portion of eyeglasses. Also, plastic prisms (Fresnel prisms) can be attached to eyeglasses of a diplopic patient, allowing for alignment of vision from both eyes in the affected direction, but are often problematic if the degree of muscle weakness, and therefore ocular misalignment, fluctuates frequently.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development.

Thereafter, a period of observation of around 9 to 12 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

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.

This is most commonly achieved through the use of fresnel prisms. These slim flexible plastic prisms can be attached to the patient's glasses, or to plano glasses if the patient has no refractive error, and serve to compensate for the inward misalignment of the affected eye. Unfortunately, the prism only correct for a fixed degree of misalignment and, because the affected individual's degree of misalignment will vary depending upon their direction of gaze, they may still experience diplopia when looking to the affected side. The prisms are available in different strengths and the most appropriate one can be selected for each patient. However, in patients with large deviations, the thickness of the prism required may reduce vision so much that binocularity is not achievable. In such cases it may be more appropriate simply to occlude one eye temporarily. Occlusion would never be used in infants though both because of the risk of inducing stimulus deprivation amblyopia and because they do not experience diplopia.

Other management options at this initial stage include the use of botulinum toxin, which is injected into the ipsilateral medial rectus (botulinum toxin therapy of strabismus). The use of BT serves a number of purposes. Firstly, it helps to prevent the contracture of the medial rectus which might result from its acting unopposed for a long period. Secondly, by reducing the size of the deviation temporarily it might allow prismatic correction to be used where this was not previously possible, and, thirdly, by removing the pull of the medial rectus it may serve to reveal whether the palsy is partial or complete by allowing any residual movement capability of the lateral rectus to operate. Thus, the toxin works both therapeutically, by helping to reduce symptoms and enhancing the prospects for fuller ocular movements post-operatively, and diagnostically, by helping to determine the type of operation most appropriate for each patient.

A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.

Pseudomyopia refers to an intermittent and temporary shift in refractive error of the eye towards myopia, in which the focusing of light in front of the retina is due to a transient spasm of the ciliary muscle causing an increase in the refractive power of the eye. It may be either organic, through stimulation of the parasympathetic nervous system, or functional in origin, through eye strain or fatigue of ocular systems. It is common in young adults who have active accommodation, and classically occurs after a change in visual requirements, such as students preparing for an exam, or a change in occupation.

The major symptom is intermittent blurring of distance vision particularly noticeable after prolonged periods of near work, and symptoms of asthenopia. The vision may clear temporarily using concave (minus) lenses. The diagnosis is done by cycloplegic refraction using a strong cycloplegic like atropine or homatropine eye drops. Accommodative amplitude and facility may be reduced as a result of the ciliary muscle spasm.

Treatment is dependent on the underlying aetiology. Organic causes may include systemic or ocular medications, brain stem injury, or active ocular inflammation such as uveitis. Functional pseudomyopia is managed though modification of working conditions, an updated refraction, typically involving a reduction of a myopic prescription to some lower myopic prescription, or through appropriate ocular exercises.

The artery can re-canalize over time and the edema can clear. However, optic atrophy leads to permanent loss of vision. Irreversible damage to neural tissue occurs after only 90 minutes. Two thirds of patients experience 20/400 vision while only one in six will experience 20/40 vision or better.