ABSTRACT

Focal choroidal excavation is a choroidal pit that can be detected by optical coherence tomography. Central serous chorioretinopathy, choroidal neovascularization and polypoidal choroidal vasculopathy are pathologies associated with focal choroidal excavation. In this article, we present the follow-up and treatment outcomes of three eyes of two patients with focal choroidal excavation.

Introduction

Focal choroidal excavation is local idiopathic cupping of the choroid which is usually unilateral and not associated with any accompanying systemic disease.¹In 2006, Jampol et al.²first identified the lesion in an asymptomatic patient using optic coherence tomography (OCT). Margolis et al.³later used the term focal choroidal excavation for the areas of choroidal pitting observed near the macula on spectral domain (SD)-OCT in patients without posterior staphyloma or scleral ectasia. The condition causes symptoms like decreased vision and metamorphopsia, but its etiology is not fully understood. Studies have documented that focal choroidal excavation may be accompanied by choroidal vascular disorders including central serous chorioretinopathy (CSCR), choroidal neovascularization (CNV) and polypoidal choroidal vasculopathy (PCV), which are responsible for the visual symptoms.^4,5,6,7,8

In this report we present the treatment and follow-up results of three eyes of two patients with the rare condition of focal choroidal excavation.

Discussion

Focal choroidal excavation is a choroidal defect believed to be a congenital condition, though its etiology and pathogenesis are not yet fully understood, and is detectable on SD-OCT.¹This excavation has been termed ‘nonconforming’ if photoreceptors are detached from the RPE, or ‘conforming’ when the RPE follows the contours of the photoreceptor layer.³The nonconforming type exhibits a hyporeflective space on SD-OCT which does not appear in the conforming type.

Focal choroidal excavation is generally a stable, unchanging lesion.¹Our patient with bilateral involvement also had extrafoveal excavation in the fellow eye, but visual acuity was not affected and no complications resulted.

CSCR, CNV and PCV are all pathologies which may accompany focal choroidal excavation.^4,5,6,7,8It has not been determined whether CSCR leads to focal choroidal excavation or whether CSCR occurs as a complication of excavation. One of the proposed mechanisms is that excavation is mainly responsible for the pathology, causing atrophy of the overlying RPE and subsequent pump dysfunction, and CSCR occurs as a complication.⁷It has also been proposed that CNV and PCV are both the result of choroidal ischemia in areas of anatomic anomalies.¹

In a report from Margolis et al.³including 12 patients, CSCR was detected in 1 patient who later developed CNV during follow-up. Suzuki et al.⁷evaluated 7 eyes of 6 patients with CSCR and focal choroidal excavation. Although the subretinal fluid resolved in all cases, 3 patients later progressed to nonconforming excavation, which exhibits the same hyporeflectivity on OCT as subretinal fluid. The authors attributed this to persistent subretinal fluid around the lesion. In their series of 41 eyes, Lee et al.¹detected CSCR in 10 eyes, CNV in 9 eyes and PCV in 1 eye; 2 eyes with CSCR were treated with low-fluence PDT. Despite resolution of the subretinal fluid in these patients, they continued to exhibit separation of the RPE and photoreceptor layer (nonconforming type). The nonconforming type was shown to be significantly associated with visual symptoms and CSCR.¹This was also true in our two patients, who exhibited nonconforming excavation and experienced visual symptoms. They both reverted to the conforming type, after PDT in the first case and after intravitreal bevacizumab injection in the second case. The resolution of the hyporeflective area evident on OCT in both patients may be related to the decreased choroidal permeability following PDT in the first patient and resolution of the active focal exudation in the retina after intravitreal bevacizumab injection in the second patient. The fact that patients transition between types supports the idea that hyporeflective areas on OCT in the nonconforming type may be due to subretinal fluid. Neither of our patients fully regained their vision after treatment, which may be attributable to the presence of chronic CSCR and subsequent RPE dysfunction.

Conclusion

In one eye of our first case, focal choroidal excavation remained static over the course of follow-up and did not require treatment. The same patient’s other eye was treated with low-fluence PDT and the affected eye of our second case was treated with intravitreal bevacizumab; both eyes showed regression to conforming excavation after treatment. Studies with larger patient numbers and longer follow-up times are needed to better understand the etiology, course and treatment options of focal choroidal excavation.