Clinical FeaturesOphthalmology

Management of Macular Oedema

Macular oedema is the end common pathway for many prevalent ophthalmic conditions. It is one of the leading causes of central visual loss.

Written by Dr Louise O’Toole, Consultant Medical Ophthalmologist, Bon Secours Hospital Glasnevin, Dublin – Mater Private Network, Dublin

The condition is characterized by the accumulation of fluid in the outer plexiform layer and the inner nuclear layer of the retina; it occurs secondary to the breakdown of the blood-retinal barrier. This causes an abnormal passage of proteins into retinal tissues resulting in osmotic water retention and consequent swelling.

When macular oedema occurs, patients may be aware of a fall in their central vision, they may also experience distortion and reduced colour vision.

Macular oedema can be diagnosed at the slit-lamp using high magnification; however Ocular Coherence Tomography (OCT) imaging facilitates both detection and quantification of the oedema. In recent times, the availability of OCT imaging has increased, allowing patients to access this investigation through both optometric as well as ophthalmic practitioners. Depending on the aetiology of the macular oedema, it has a different nomenclature.

A common cause of macular oedema is retinal vein occlusion (RVO). This may be secondary to a central, branch or hemiretinal vein occlusion. The prevalence of RVO increases with age. The most common association with RVO is undiagnosed hypertension. It is to be recommended that when patients are diagnosed with macular oedema secondary to RVO that they undergo 24- hour blood pressure monitoring. Open-angle glaucoma, diabetes mellitus, and hyperlipidemia have all been implicated as other primary risk factors for RVO. A hypercoagulable state also predisposes to the development of RVO. Conditions such as polycythemia, multiple myeloma, cryoglobulinemia, and Waldenstrom macroglobulinemia place patients at a higher risk of developing RVO. In a young patient who presents with a RVO a full systemic workup is mandated to detect such potential underlying causes.

The primary treatment of macular oedema secondary to RVO is to address the underlying cause. Macular oedema secondary to advanced hypertension can resolve following adequate hypertensive control. Otherwise, patients are treated with a course of intravitreal therapy. The agents used may either be steroids or more commonly an anti-Vascular endothelial growth factor (VEGF) agent. Such agents include ranibizumab (Lucentis), aflibercept (Eylea), and bevacizumab (Avastin). Intravitreal steroids have a longer duration of action but are associated with an increased risk of cataract formation and can cause raised intraocular pressure. When the macular oedema resolves, the patient’s visual acuity generally improves unless there is associated non perfusion of the macula. Patients may require ongoing treatment for several months to years to preserve their vision.

Patients with either Type 1 or Type 2 Diabetes Mellitus can develop diabetic macular oedema (DME). If the macular oedema does not involve the fovea, it can be treated by laser photocoagulation. However, laser scars can enlarge with time and encroach on the fovea leading to visual loss, so intravitreal therapy with either anti-VEGF agents or steroids is preferred by some for treating cases of DME with and without foveal involvement. Improving glycaemic control, regularising hypertension and treating hyperlipidaemia are known interventions to treat diabetic maculopathy. If DME has been present for some time, secondary structural changes can occur in the retina. These changes are termed disorganisation of retinal inner layers (DRIL). When these changes are seen, the visual prognosis for the patient is guarded.

Neovascular age related macular degeneration (nAMD) is associated with swelling of the central macula. Choroidal neovascularisation leads to both subretinal and intraretinal leakage of fluid as well as haemorrhage. The presence of chronic intraretinal fluid is associated with a poorer visual outcome. Treatment of nAMD is with sustained intravitreal anti-VEGF therapy to dry up the intraretinal fluid and prevent the development of fibrosis. Patients are monitored with serial OCT imaging and their intravitreal treatment frequency adjusted accordingly.

Cataract surgery is a recognised cause of macular oedema. When this occurs, it is termed pseudophakic cystoid macular oedema (CMO). The cataract surgery may have been either a complicated or an uncomplicated procedure. The patient may initially have good vision post cataract surgery which then falls in the following month, or else the vision may fail to improve vision at all post operatively. Many patients have subclinical CMO that is only detectable on OCT imaging and is self-limiting in nature. CMO is believed to be secondary to intraocular inflammation. The majority of patients with CMO will undergo resolution of their macular oedema following a course of combined topical NSAIDs and steroids. Sometimes intensive hourly treatment is required ab initio. A small subset of patients will require either a periocular or an intravitreal injection of steroid to settle this inflammatory condition. If cataract surgery is planned for their fellow eye, prophylactic anti-inflammatories are prescribed by many surgeons.

Macular oedema may also occur as a complication of other intraocular procedures. These procedures include panretinal photocoagulation and YAG laser. Cryotherapy is another procedure which is known to cause macular oedema.

Uveitis, no matter where it is located within the eye -anterior, intermediate, or posterior can result in macular oedema and consequently reduced vision.

The treatment of macular oedema secondary to uveitis is to treat the inflammatory cause with immunosuppressive agents. Chronic inflammatory changes at the macula can result in the development of choroidal neovascularisation.

Another cause of macular oedema is drug related. Fingolimid associated macular oedema (FAME) is well described. Fingolimid is an oral disease modifying therapy indicated for the treatment of multiple sclerosis. The risk of FAME is dose dependent. A baseline OCT is required before commencing Fingolimid and the patients should undergo regular monitoring while on treatment. Latanoprost is a topical therapy commonly used to treat primary open angle glaucoma and CMO is a recognised side effect. CMO has been reported following nicotinic acid and niacin supplementation with doses of greater than 1.5g/day.

Patients with retinitis pigmentosa have a reduced peripheral visual field. They may also develop CMO which will then further reduce their remaining central visual function. CMO in retinitis pigmentosa responds well to treatment with oral acetazolamide, topical dorzolamide or brinzolamide drops.

Macular oedema has a disparate range of causes and accordingly treatments. It can cause mild to profound visual loss, if left untreated as in the case of nAMD the visual loss can be irreversible. OCT imaging facilitates the early detection of macular oedema and with early intervention, patients’ sight can be preserved.

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