Herein, we report a rare case of SO following uncomplicated SB surgery with cryoretinopexy and SRFD. SO should be kept in mind in any case of bilateral panuveitis associated with multiple serous RD with history of penetrating ocular surgery.
SO after vitreoretinal surgery has been reported in several studies2, 4-6.It is postulated that trauma to the uveal tract in the context of inadvertent perforation, SRFD or cryotherapy during SB surgery might be deliberate uveal antigens, melanin or outer photoreceptor antigens resulting access to the lymphatic systems of the conjunctival tissue exciting delayed hypersensitivity reaction inside the eye. 4-6The mechanism of hypersensitivity in the sympathizing eye may be due to the exposure of the uveal tissue to the conjunctival lymphatic system resulting in a cell-mediated immune response.6 This mechanism can explain the association of increase in the trend of the use of trans-conjunctival sutureless vitrectomy with increase in incidence of SO following vitreoretinal surgery because of more uveal incarceration6. In our case, SRFD perhaps increased the risk of uveal exposure to conjunctival lymphatic tissue. In one of the largest study of SO following surgery, Kilmartin et al. reported RD surgeries to be the most common procedure associated with development of SO, with the risk of SO after vitrectomy being twice of that external scleral buckling without any sex predilection.7
The onset of SO symptoms after operation usually occurs between 3 weeks and 6 months after surgery because of delayed hypersensitivity.8 In this case SO was developed 6 weeks later.
In a case series, Ozbek et al.9 reported three cases of SO following SB, however 2 cases had combined vitrectomy with SB and only in one case SO occurred following encircling buckle combined with 360 indirect retinal photocoagulations and SRFD in contrast to our case that had only one cryoretinopexy spots and one drainage site. In another similar case report by Parvaresh and Falavarjani, SO was found in a case with history of SB revision after 4 years, which the second surgery was combined with SRFD and cryoretinopexy.10 However, in our case, SO was happened in the first episode, without any surgical past history.
In a recent study by Tyagi et al, incidence of SO following vitreoretinal surgery was 0.038 % of all vitrectomy cases, and 9% of all cases of SO had vitreoretinal surgery.6 Seventy-five percent of cases underwent multiple ocular surgery before development of SO. 6 The most common anterior segment finding was non-granulomatous uveitis in 50 % in contrast to serous RD in 62.5 % of cases. 6 In our case we also found that anterior segment inflammation was less severe than posterior segment chorioretinal findings.
Most of the case presented in studies5-10 had simultaneous SB and vitrectomy or had previous trauma or multiple surgery, however our case had no extensive retinal or uveal tissue manipulation and had no combined surgery or previous surgery, so we assumed this would be of interesting. One of the plausible theory for this susceptibility might be Asian ethnicity and higher prevalence of VKH in our area.
One of the most important differential diagnoses of our case is VKH. It is well known that VKH is common uveitis etiology with similar clinical and imaging findings with SO1,11. Although sympathizing eye in SO presents initially with nongranulomatous uveitis clinically, it progresses to granulomatous uveitis8. VKH shows 3 successive stages: posterior uveitis, anterior segment involvement associated with posterior uveitis, and finally anterior granulomatous uveitis. Anterior uveitis and posterior uveitis both are present in SO patients seen within 2 weeks of disease onset8. In our case clinical features are more similar to SO than VKH, as our patient had no systemic sign or symptoms attributed to VKH or other systemic diseases causing choroiditis. The main differentiating clue between SO and VKH is the history of prior surgery or trauma in SO.
In terms of imaging findings in SO, on FAG, during the early phase of angiography multiple hyperfluorescent pinpoints leakages associated with late pooling resembling VKH and hypofluorescent foci were found. In the late phase of FAG, hyperfluorescence similar to acute posterior multifocal placoid pigment epitheliopathy (APMPPE) can be observed11. In our case it seems that because of FAG was performed after 4 days of steroid therapy, hyperfluorscence was less and hypofluorescent that is compatible with location of granuloma and cellular infiltration was more prominent. On ICGA the most common features are multiple hypocyanescent spots. In acute phase of SO, EDI-OCT discloses multiple serous retinal detachments associated with hyperreflective septa, massive choroidal thickening and loss of normal choroidal vascular architectures, irregular outer segments of photoreceptors similar to what are observed in acute phase of VKH. Visual outcome is worse in SO as compared with VKH disease8. Moreover, BCVA was improved in our case because of early diagnosis and prompt aggressive and adequate treatment.