There are many etiological factors that have led to the development of retinal pigment epithelial detachment (PED). In this paper, we have reported a patient with isolated multiple PEDs. Based on this fact, this paper aimed to give an overview of the causes of PEDs. 1. Introduction Retinal pigment epithelial detachment (PED) results in the separation between the retinal pigment epithelium (RPE) basement membrane and the inner collagenous layer of the Bruch’s membrane [1, 2]. It is not really an illness; however, it is an ocular finding which can be observed in several chorioretinal diseases such as central serous chorioretinopathy (CSC), age-related macular degeneration (AMD), and several inflammatory and ischemic chorioretinal diseases [3]. Several hypotheses have been proposed for the formation of pigment epithelium detachment (PED). In the past, PED was interpreted as a kind of fluid leakage from increased intravascular pressure of choroidal system [4]. The prevailing opinion was that, because of the debris collected in the inner layers of Bruch’s membrane, the physical relationship between Bruch’s membrane and the RPE may weaken, and thus choroidal fluid may passively accumulate under the retinal pigment epithelium (RPE). The filling pattern shown by fluorescein angiography (FA) and the impaired Bruch’s membrane structure supported this opinion [4]. However, Gass argued for a second opinion suggesting that PED may occur as a result of fluid leakage from the neovascular vessels proceeding in the inner layers of Bruch’s membrane, and this fluid may be an obstacle to display these vessels in angiography. According to the current hypothesis, the source of the fluid in PED, contrary to the prevailing opinion until the year 1986, can be the defect which occurred in elimination metabolism of RPE rather than choroid. It is hypothesized that the decrease in the hydraulic conductivity of Bruch’s membrane towards choroid can lead to accumulation of fluid in the subpigment epithelial field. At this stage, the hydrophobic character of Bruch’s membrane causes the development of resistance against fluid flow. This pathogenetic explanation for RPE detachment is found more challenging than previous concepts [4]. In this case, as a result of thickening of Bruch’s membrane and the hydrophobic character, active metabolic wastes, which originated from pigment cells, fail to reach choroidal circulation, and thus secondary choroidal neovascularization occurs. Today, in addition to these mechanisms, together with increased levels of “vascular endothelial growth factors,”
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