If there are defects in the retinal pigment epithelium without accumulation of fluid below the retina, a pachychoroid pigmentepitheliopathy (PPE) is present. Accumulation of fluid results in central serous chorioretinopathy (CSR). The development of secondary blood vessels, so-called choroidal neovascularization (CNV) leads to pachychoroid neovasculopathy (PNV). If parts of these new vessels bulge outward, so-called aneurysms develop within this CNV, defining pachychoroid aneurysmal type 1 CNV (or, still widely used, polypoidal choroidal vasculopathy (PCV)). Since the individual stages develop one after the other from the respective preliminary stage, pachychoroidal diseases of the macula are divided into 4 stages according to Siedlecki, Schworm and Priglinger:

Risk factors
CSR is sometimes called idiopathic CSR which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR. CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol. Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone), commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions, can trigger CSR, aggravate it and cause relapses. In a case report, a young male was using Prednisolone and began to display subretinal fluid indicative of CSR.
The build up of fluid in the lungs increases the pressure in the lungs leading to vasoconstriction. The coupled vasoconstriction and pulmonary hypertension causes the right side of the heart to fail which in turn, increases the venous hydrostatic pressure in the body. The summation of these effects ultimately leads to peripheral edema and ascites. All in all, the left side failure of the heart will lead to pulmonary edema whereas right side failure will lead to peripheral edema and ascites. The non-immune form of hydrops fetalis has many causes including:
Iron deficiency anemia
Paroxysmal supraventricular tachycardia resulting in heart failure
Deficiency of the enzyme beta-glucuronidase. This enzyme deficiency is the cause of the lysosomal storage disease called mucopolysaccharidosis type VII. Congenital disorders of glycosylation
Parvovirus B19 (fifth disease) infection of the pregnant woman (most common cause)
Cytomegalovirus in mother
Congenital pulmonary airway malformation (formerly called congenital cystic adenomatoid malformation)
Maternal syphilis and maternal diabetes mellitus
Alpha-thalassemia can also cause hydrops fetalis when all four of the genetic loci for α globin are deleted or affected by mutation. This is termed Hb Barts (consists of y-4 tetramers). Uncommonly, Niemann-Pick disease Type C (NPC) and Gaucher disease type 2 can present with hydrops fetalis. Turner syndrome
Tumors, the most common type of fetal tumor being teratoma, particularly a sacrococcygeal teratoma.