The main causes of visual loss are GON, cataract, and corneal endothelial damage. However, there are few systematic analyses of their prevalence, and the wide variations in the definition of outcomes and patients may have had previous glaucoma or cataract surgery. Hence, it is difficult to derive their true prevalence.

Glaucoma as defined by the presence of GON or need for glaucoma surgery is estimated to vary from 12 to 60 % [62, 71–73, 78–82, 87, 133] and the prevalence of cataract at 14 to 60 % [71, 78–80].

Some patients with CMV anterior segment infection present as a corneal endotheliitis with areas of stromal edema ranging from small localized lesions to diffuse edema (Fig. 10.4). Some of these patients were diagnosed during investigation for graft failure post-corneal transplant surgery, but some also had a history of previous hypertensive anterior uveitis. While small focal lesions may resolve with therapy, up to 63 % of eyes developed persistent diffuse edema causing visual loss despite medical therapy [75, 79, 87, 134–142]. Endothelial cell loss has been shown to occur in eyes with CMV anterior uveitis and is correlated with the viral load [81, 133]. Hence, the endothelial damage may be a consequence of repeated episodes of inflammation or related to the use of corticosteroids in some of these eyes [122, 123].

Although CMV predominantly affects the anterior segment in immunocompetent patients, there have been isolated case reports of retinitis. Although these patients were not HIV-positive nor transplant recipients, a significant number had received corticosteroids including periocular or intravitreal injections or corticosteroid implants or had associated systemic conditions which may impair the immune response such as diabetes mellitus. In contrast to HIV-infected patients with CMV retinitis, anterior chamber inflammation, vitritis, and vascular occlusion were common associated findings in the immunocompetent patients [114, 118–121].

Even more of an enigma was the development of an autoimmune retinopathy in a patient with recurrent CMV anterior uveitis. This otherwise healthy man had multiple relapses with oral valganciclovir and eventually required intravitreal ganciclovir implants for control. Although the anterior segment was quiet, he developed progressive retinal atrophy in the affected eye with constriction of visual fields and ablation of electroretinogram responses. Since the fellow eye was entirely normal, despite the presence of anti-retinal autoantibodies in his serum, a retinal dystrophy or paraneoplastic retinopathy was felt to be unlikely cause of the changes [143].

A small case series suggest that posterior segment changes in eyes with CMV anterior uveitis may be more common than what was previously thought. Although none of the 11 patients in this series had retinitis, nine (82 %) had some form of retinal abnormalities including prolonged arm retinal time (mean of 25 seconds) on fundus fluorescein angiography (FFA) in all nine (100 %), disc swelling in three patients of which two were only evident on FFA, and macula edema in four eyes. Only one of the 11 patients, who had macula edema, had atherosclerotic risk factors including diabetes mellitus, hypertension, and hyperlipidemia. Therefore, these changes may be secondary to a subclinical CMV vasculitis [144].

There are no clinical features that are pathognomic of CMV anterior uveitis, and the only diagnostic test available today that can distinguish it from an idiopathic hypertensive uveitis or that caused by other viruses is aqueous analysis using polymerase chain reaction (PCR) techniques for viral nucleic acid and/or intraocular antibody production as these patients are usually negative for sera CMV antigen and CMV IgM. Conventional stains or cytologic techniques require much larger volumes of fluid than what can be obtained via an aqueous tap, and the sensitivity of viral cultures is highly vulnerable to the condition of the specimen and contamination. Unfortunately even with PCR or intraocular antibody production techniques, a significant proportion of cases may be missed due to various reasons. Firstly, even with PCR, which enables the amplification of miniscule amounts of viral nucleic acid, the viral load in the limited volume of aqueous available may be below the detection limits of the test. Secondly, due to short-lived nature of the inflammation in eyes with acute recurrent disease, the detection of actively replicating virus may be subject to the timing of the tap. In addition, there is also data showing that there are differences in the load of viral antigen and viral antibody production between immunocompetent and immunocompromised patients [145–148]. Hence, these two tests complement each other and both should be done if available. In the series by Kongyai et al., the combination of antigen detection by PCR with the detection of a rise in the ratio of intraocular IgG to serum IgG of more than three (Goldmann-Witmer coefficient ) resulted in a higher sensitivity than if only either had been done alone. Only 60 % of the cases would have detected using PCR alone, and using GWC alone would have detected only 70 % of the cases [65].

Although an aqueous tap is a relatively safe procedure with only rare reports of introduction of air into the anterior chamber, transient hyphema, wound leak, and localized lens damage, these tests are costly and not readily accessible [59, 149, 150]. Therefore, other diagnostic techniques such as confocal microscopy have been assessed as for their potential in aiding diagnosis as it has been able to demonstrate the presence of an “owl’s eye sign,” which represents CMV inclusion bodies, in eyes with corneal endotheliitis [151]. It has not been proven though to be sufficiently sensitive nor specific in its ability to differentiate between infectious and noninfectious cases of anterior uveitis [152–156].

The visual outcome of CMV anterior uveitis is not well studied as most authors examine mainly recurrences with few reports of visual acuity. The prevalence of the main causes of visual loss is also not well documented with considerable variations in the definition of glaucoma as well as the population analyzed. However, the inflammation in acute recurrent anterior uveitis is short-lived, and the attacks may be few and far between. Although the IOP is more refractory in chronic uveitis, it is less elevated than in the acute form, and hence central vision may be preserved in these eyes. In most studies, at least 80 % of eyes have 20/40 or better vision at the last visit. In a series by Hwang et al., 13 of 20 eyes had a final vision worse than 20/40, four of which were possibly due to GON [71, 76, 78, 79, 82, 87, 133, 162].