It can be treated with laser coagulation, and more commonly with medication that stops and sometimes reverses the growth of blood vessels.

A randomized control trial found that bevacizumab and ranibizumab had similar efficacy, and reported no significant increase in adverse events with bevacizumab. A 2014 Cochrane review found that the systemic safety of bevacizumab and ranibizumab are similar when used to treat neovascular AMD, except for gastrointestinal disorders. Bevacizumab however is not FDA approved for treatment of macular degeneration. A controversy in the UK involved the off-label use of cheaper bevacizumab over the approved, but expensive, ranibizumab. Ranibizumab is a smaller fragment, Fab fragment, of the parent bevacizumab molecule specifically designed for eye injections. Other approved antiangiogenic drugs for the treatment of neo-vascular AMD include pegaptanib and aflibercept.

The American Academy of Ophthalmology practice guidelines do not recommend laser coagulation therapy for macular degeneration, but state that it may be useful in people with new blood vessels in the choroid outside of the fovea who don't respond to drug treatment. There is strong evidence that laser coagulation will result in the disappearance of drusen but does not affect choroidal neovascularisation. A 2007 Cochrane review on found that laser photocoagulation of new blood vessels in the choroid outside of the fovea is effective and economical method, but that the benefits are limited for vessels next to or below the fovea.

Photodynamic therapy has also been used to treat wet AMD. The drug verteporfin is administered intravenously; light of a certain wavelength is then applied to the abnormal blood vessels. This activates the verteporfin destroying the vessels.

Cataract surgery could possibly improve visual outcomes for people with AMD, though there have been concerns of surgery increasing the progression of AMD. A randomized controlled trial found that people who underwent immediate cataract surgery (within 2 weeks) had improved visual acuity and better quality of life outcomes than those who underwent delayed cataract surgery (6 months).

No medical or surgical treatment is available for this condition.

CNV is conventionally treated with intravitreal injections of angiogenesis inhibitors (also known as "anti-VEGF" drugs) to control neovascularization and reduce the area of fluid below the retinal pigment epithelium. Angiogenesis inhibitors include pegaptanib, ranibizumab and bevacizumab (known by a variety of trade names, such as Macugen, Avastin or Lucentis). These inhibitors slow or stop the formation of new blood vessels (angiogenesis), typically by binding to or deactivating the transmission of vascular endothelial growth factor ('VEGF'), a signal protein produced by cells to stimulate formation of new blood vessels. The effectiveness of angiogenesis inhibitors has been shown to significantly improve visual prognosis with CNV, the recurrence rate for these neovascular areas remains high.

CNV may also be treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin (Visudyne). The drug is given intravenously. It is then activated in the eye by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi.

To date, there is no known effective treatment for the non-proliferative form of macular telangiectasia type 2.

Treatment options are limited. No treatment has to date been shown to prevent progression. The variable course of progression of the disease makes it difficult to assess the efficacy of treatments. Retinal laser photocoagulation is not helpful. In fact, laser therapy may actually enhance vessel ectasia and promote intraretinal fibrosis in these individuals. It is hoped that a better understanding of the pathogenesis of the disease may lead to better treatments.

The use of vascular endothelial growth factor (VEGF) inhibitors, which have proven so successful in treating age-related macular degeneration, have not proven to be effective in non-proliferative MacTel type 2. Ranibizumab reduces the vascular leak seen on angiography, although microperimetry suggests that neural atrophy may still proceed in treated eyes.In proliferative stages (neovascularisation), treatment with Anti-VEGF can be helpful.

CNTF is believed to have neuroprotective properties and could thus be able to slow down the progression of MacTel type 2. It has been shown to be safe to use in MacTel patients in a phase 1 safety trial.

The most crucial aspect of managing patients with macular telangiectasia is recognition of the clinical signs. This condition is relatively uncommon: hence, many practitioners may not be familiar with or experienced in diagnosing the disorder. MacTel must be part of the differential in any case of idiopathic paramacular hemorrhage, vasculopathy, macular edema or focal pigment hypertrophy, especially in those patients without a history of retinopathy or contributory systemic disease.

Treatment options for macular telangiectasia type 1 include laser photocoagulation, intra-vitreal injections of steroids, or anti-vascular endothelial growth factor (anti-VEGF) agents. Photocoagulation was recommended by Gass and remains to date the mainstay of treatment. It seems to be successful in causing resolution of exudation and VA improvement or stabilization in selected patients. Photocoagulation should be used sparingly to reduce the chance of producing a symptomatic paracentral scotoma and metamorphopsia. Small burns (100–200 μm) of moderate intensity in a grid-pattern and on multiple occasions, if necessary, are recommended. It is unnecessary to destroy every dilated capillary, and, particularly during the initial session of photocoagulation, those on the edge of the capillary-free zone should be avoided.

Intravitreal injections of triamcinolone acetonide (IVTA) which have proved to be beneficial in the treatment of macular edema by their anti-inflammatory effect, their downregulation of VEGF production, and stabilization of the blood retinal barrier were reported anecdotally in the management of macular telangiectasia type 1. In two case reports, IVTA of 4 mg allowed a transitory reduction of retinal edema, with variable or no increase in VA. As expected with all IVTA injections, the edema recurred within 3–6 months, and no permanent improvement could be shown.14,15 In general, the effect of IVTA is short-lived and complications, mainly increased intraocular pressure and cataract, limit its use.

Indocyanine green angiography-guided laser photocoagulation directed at the leaky microaneurysms and vessels combined with sub-Tenon’s capsule injection of triamcinolone acetonide has also been reported in a limited number of patients with macular telangiectasia type 1 with improvement or stabilization of vision after a mean follow-up of 10 months.16 Further studies are needed to assess the efficacy of this treatment modality.

Recently, intravitreal injections of anti-VEGF agents, namely bevacizumab, a humanized monoclonal antibody targeted against pro-angiogenic, circulatory VEGF, and ranibizumab, a FDA-approved monoclonal antibody fragment that targets all VEGF-A isoforms, have shown improved visual outcome and reduced leakage in macular edema form diabetes and retinal venous occlusions. In one reported patient with macular telangiectasia type 1, a single intravitreal bevacizumab injection resulted in a marked increase in VA from 20/50 to 20/20, with significant and sustained decrease in both leakage on FA and cystoid macular edema on OCT up to 12 months. It is likely that patients with macular telangiectasia type 1 with pronounced macular edema from leaky telangiectasis may benefit functionally and morphologically from intravitreal anti-VEGF injections, but this warrants further studies.

Today, laser photocoagulation remains mostly effective, but the optimal treatment of macular telangiectasia type 1 is questioned, and larger series comparing different treatment modalities seem warranted. The rarity of the disease however, makes it difficult to assess in a controlled randomized manner.

However, these treatment modalities should be considered only in cases of marked and rapid vision loss secondary to macular edema or CNV. Otherwise, a conservative approach is recommended, since many of these patients will stabilize without intervention.

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.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity. The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect. Best results of intravitreal Triamcinolone have been found in eyes that have already undergone cataract surgery. Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis. A systematic review found evidence that eyes treated with the intravitreal injection of triamcinolone had better visual acuity outcomes compared to eyes treated with macular laser grid photocoagulation, or sham injections.

Associated visual loss rarely recovers and may even progress after the drug is discontinued.

Cessation of the drug at the first sign of toxicity is recommended. No treatment exists as yet for this disorder, so it is imperative that patients and their ophthalmologists be aware of the best practices for minimizing toxic damage.

Choroidal neovascularization (CNV) is the creation of new blood vessels in the choroid layer of the eye. Choroidal neovascularization is a common cause of neovascular degenerative maculopathy (i.e. 'wet' macular degeneration) commonly exacerbated by extreme myopia, malignant myopic degeneration, or age-related developments.

Presumed ocular histoplasmosis syndrome (POHS) is a syndrome affecting the eye, which is characterized by peripheral atrophic chorioretinal scars, atrophy or scarring adjacent to the optic disc and maculopathy.

The loss of vision in POHS is caused by choroidal neovascularization.

A maculopathy is any pathological condition of the macula, an area at the centre of the retina that is associated with highly sensitive, accurate vision.

Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm HO or else portal hypertension will ensue. Methods of shunt attenuation should aim to slowly occlude the vessel over several weeks to months in order to avoid complications associated with portal hypertension. These methods include ameroid ring constrictors, cellophane banding, intravascular or percutaneous silicone hydraulic occluders. The most common methods of attenuation used by veterinarians are ameroid ring constrictors and cellophane banding. Both methods have reportedly good outcomes in both cats and dogs, although the true composition of readily sourced cellophane has been found to be made from plastics (inert) and not cellulose (stimulates a fibrous reaction). Recently, a commercial supplier of regenerated cellulose based cellophane for veterinarians has been established for use of cellophane banding for portosystemic shunts in dogs and cats. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. When surgery is not an option, PSS is treated as are other forms of liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

The treatment options for asymptomatic AAA are management, surveillance with a view to eventual repair, and immediate repair. Two modes of repair are available for an AAA: open aneurysm repair, and endovascular aneurysm repair (EVAR). An intervention is often recommended if the aneurysm grows more than 1 cm per year or it is bigger than 5.5 cm. Repair is also indicated for symptomatic aneurysms.

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs. Blood pressure and lipids should, however, be treated per usual.