Cystoid macular oedema in uveitis: an unsolved problem.

Most papers on the subject of CMO associated with uveitis are retrospective, combine patients with different disease aetiologies, at different stages of evolution, and often describe patients who were previous treatment failures with other therapies besides the one under consideration. There are almost no prospective randomised double-masked controlled studies. This is perhaps in part due to the relative sparsity of uveitis patients seen by many uveitis centres. At the moment, treatment is largely empirical, based in large part on the studies, and others, quoted above. The need to regularly repeat courses of therapy, loss of efficacy of certain form of therapy after repeated use, and cumulative side-effects, all need to be taken into consideration when interpreting results and deciding upon the best approach to be adopted. The risks to the patient's well-being increase with the addition of systemic medication, and long-term steroid use can cause hypertension, induce or exacerbate diabetes, cause premature osteoporosis, cushingoid features, peptic ulceration and aseptic necrosis of the femoral head. Immunosuppressive drugs can be nephrotoxic, hepatotoxic, cause hypertension, gastric disturbances and excessive hair growth. The assessment of macular changes, both structurally and functionally, is the key aspect in understanding visual loss in CMO and also in predicting potential visualrecovery. The combined use of the various tools mentioned here, such as SLO, OCT and electrodiagnostic tests, may give us some of the necessary answers in this process. However, all these tests will need to be validated. A prospective analysis of CMO in cases of uveitis, especially if coupled with therapeutic intervention, will give us the opportunity to achieve this objective.