Introduction

The choroid is attached to the sclera in the normal eye. It may be displaced by serous fluid or blood accumulating inside the potential space between the uvea and sclera, leading to choroidal detachment [1]. Serous choroidal detachments are typically associated with low intraocular pressure (IOP) or ocular hypotony, and most commonly occur after eye surgery. Inflammation, trauma, malignancy, and certain medications can also cause serous choroidal detachment [2,3,4,5,6,19, 20]. Our finding of concurrent ciliary body detachment in all cases of choroidal detachment sheds more light on the pathophysiology of the disease and the vicious cycle that transpires after choroidal detachment occurs. As the ciliary processes are the main site of aqueous humor production [13], ciliary body detachment may have an added detrimental effect on aqueous production and may thereby play an important role in postoperative hypotony.

A large persistent choroidal effusion may have immediate and long-lasting vision-threatening sequelae, particularly when it is associated with hypotony, maculopathy, or serous retinal detachment [2, 17]. However, most serous choroidal effusions follow a benign course as they may be asymptomatic and resolve spontaneously without treatment when the IOP gradually increases postoperatively [21]. If treatment is warranted, topical steroids are usually prescribed in an effort to increase IOP and reduce inflammation. Long-acting topical cycloplegics may be given to deepen the anterior chamber and prevent anterior synechiae and corneal endothelial cell loss [22]. When topical treatment is not sufficient, systemic steroids may be used [21, 23]. Surgical intervention is indicated when the choroidal detachment is longstanding or causes complications that can lead to loss of vision [24]. In our cohort, treatment was left to the treating physician’s discretion. All patients received topical steroids and cycloplegic agents, and some elected to add systemic steroids. Most maintained their visual acuity following resolution of the ciliary body detachment, even when it was longstanding. In the two patients who lost two or more Snellen lines of BCVA, a mature cataract and status post endophthalmitis were the presumed causes.

The major limitations of this study are the small number of patients examined and the heterogeneity of glaucoma types. Moreover, the various types of glaucoma surgeries performed in our cohort could have had different implications for the occurrence of ciliary body detachment. The strengths of the study are the prospective design and the long duration of follow-up.

To conclude, in this real-world prospective study, we found concurrent ciliary body detachment in all patients who presented with choroidal detachment following glaucoma surgery. This observation may deepen our understanding of the postoperative mechanism underlying hypotony. We found that all detachments resolved with no need for surgical intervention. Larger prospective studies are warranted.