We were able to evaluate the entire eyeball using the latest imaging equipment in a case of choroidal effusion induced by indapamide. The methods we used allowed an accurate diagnosis. In cases diagnosed as acute angle-closure glaucoma, characterized by elevated intraocular pressure and a narrow angle, the differential diagnosis is critical because cataract surgery is an invasive treatment. Uveal effusion syndrome is included in the differential diagnosis of choroidal effusion and is easily ruled out in this case because microphthalmia and scleral hypertrophy are detected by MRI and B mode ultrasound. Myopia, another condition that was present in this patient, is observed in most cases of drug-induced choroidal effusion . Multimodal imaging revealed that the entire eyeball was edematous in this case and helped us arrive at an accurate diagnosis.
However, the reasons for the extension of edema in the eye are still unclear. According to previous reports, it has been speculated that people who are sensitive to drugs may respond to them with vasodilation and increased vascular permeability due to increased synthesis of prostaglandin E2 [2, 4]. Prostaglandin E2 increases the protein content of the aqueous humor, leading to an increase in IOP . Since the cornea and lens are avascular tissues, they did not edema much even when exposed to prostaglandin E2, and the ciliary body and choroid are richly vascularized tissues and can easily become edematous. Thus, our case supports the mechanism by which ciliary edema causes the lens to move anteriorly, resulting in angle-closure glaucoma. Circulatory failure was suggested by the FA findings of vasodilation, leakage, and an area of nonperfusion corresponding to the choroidal effusion lesion, as well as the OCT finding of choroidal thickening . Choroidal effusion was caused by blood stasis.
The question that arises based on previous reports and this case is why drug-induced choroidal effusion tends to appear in the temporal region . We can speculate about a possible answer based on anatomical knowledge. Prostaglandin E2 production increases in response to indapamide [2, 4], and the venous drainage of arteries, especially long posterior ciliary arteries, is markedly congested , causing vasodilation and tissue edema. In the sclera and choroid, stagnant blood may cause choroidal effusion; myopia further increases their susceptibility to this effect because of the thinner sclera and choroid. Furthermore, in normal eyes, the choroidal vessels on the temporal side are coarser than those on the nasal side , and an inadequate temporal venous drain during circulatory failure results in choroidal effusion on the temporal side of the retina rather than on the nasal side. This is the difference between drug-induced choroidal effusion and circumferential choroidal effusion with hypotony because the eyeball cannot maintain its shape.
Multimodal imaging in this case gave us new information on pathology and was useful to confirm that the severity of edema differed depending on the parts of the eyeball and to reach the accurate diagnosis. MRI revealed that the entire eyeball was edematous in the case of indapamide-induced bilateral choroidal effusion. Based on the fact, a detailed history taken along with basic imaging investigations, such as OCT, B-mode and UBM, might be enough to diminish differential diagnosis and the management because all to do in daily practice is to confirm that the severity of edema differs depending on the parts of the eyeball. However, wider-view fundus photography and OCTs of both anterior and posterior segments are effective in detecting lesions in situations where mydriasis is difficult such as this case, acute angle-closure glaucoma or Vogt-Koyanagi-Harada disease which should be ruled out. On the other hand, UBM examination is quite invasive. Our patient actually refused it after treatment. It is difficult to use UBM for a follow-up examination. The OCT of the cornea/anterior segment gives us a lot of information non-invasively at once which is the condition of the ciliary body and anterior choroid, the corneal thickness, lens thickness, and anterior chamber depth. B-mode is also effective to detect choroidal detachment, but it is low resolution. The states of both retina and choroid can be investigated with high resolution posterior OCT. Thus, MRI is not mandatory every time, but OCTs of both anterior and posterior segments and wide-angle fundus photograph are able to show edema of the entire eyeball which indicates the pathology of indapamide-induced bilateral choroidal effusion. They enable to be an accurate diagnosis and a consecutive management.
In conclusion, we presented a case of acute angle-closure and choroidal effusion induced by indapamide intake; these conditions were accurately diagnosed using the latest equipment. The mechanisms are still unclear and need to be elucidated in future studies. Using multimodal imaging, however, we showed edema of the entire eyeball, which was useful for differential diagnosis, and we evaluated the ocular conditions before and after treatment.