The suprachoroidal space is normally virtual because the choroid is in close apposition to the sclera. As fluid accumulates, this space becomes real, and the choroid is displaced from its normal position. Fluid accumulation, either serumlike or blood, also can occur within the choroid, which is a spongy tissue.
Serous choroidal detachment involves transudation of serum into the suprachoroidal space. This transudation may be due to increased transmural pressure, most frequently caused by globe hypotony of any etiology or trauma, or exudation of serum, most frequently caused by inflammation.
Hemorrhagic choroidal detachment is a hemorrhage in the suprachoroidal space or within the choroid caused by the rupture of choroidal vessels. This can occur spontaneously (rare), as a consequence of ocular trauma, during eye surgery, or after eye surgery. Except for posttraumatic cases, the clinical picture is very similar in most forms of hemorrhagic choroidal detachment, the only difference being the time of presentation. The outcome is generally worse for intraoperative hemorrhages, which often are accompanied by extrusion or loss of eye contents.
The exact triggering mechanism is unknown. An increase in transmural pressure in the choroidal vascular plexus can be caused by elevated blood pressure, low intraocular pressure (IOP), or a combination. An increase in vascular permeability is caused by inflammation. The consequence is passage of serum, with large protein molecules into the suprachoroidal space. Since the protein content of the fluid accumulating in the normally virtual suprachoroidal space is similar to plasma with an equal oncotic pressure, its spontaneous reabsorption is unlikely, unless the underlying cause (ie, inflammation, hypotony) is treated. A breakdown of the blood-aqueous barrier across the pigmented epithelium may cause a superimposed nonrhegmatogenous retinal detachment. As a sequela, linear areas of pigmented epithelium hypertrophy, called Verhoeff streaks, indicate the posterior limits of the retinal detachment after its reabsorption.
Serous choroidal detachments are recognized easily when large. More subtle, anterior, shallow ciliochoroidal detachments, although relatively common after glaucoma filtration surgery, are undetected or unreported. Suprachoroidal hemorrhage is a rare occurrence. Reported data vary between 0.05-6%, depending on the sample. [1, 2] See Causes for predisposing factors.
No mortality has been reported. Morbidity in serous choroidal detachment is significant. In phakic eyes, lens opacities can progress rapidly. Cyclitic pupillary membranes may develop. When a flat chamber is present, corneal endothelial damage and peripheral anterior synechiae can occur. Chronic choroidal detachment can lead to maculopathy and globe phthisis. In hemorrhagic detachment, morbidity is the same as for serous detachment, but the prognosis is worse. Loss of useful vision is reported in up to 40% of cases.
No racial predilection exists.
No sexual predilection exists.
Hemorrhagic detachments are seen more often in elderly patients.
During the postoperative period of any intraocular surgery, but especially after glaucoma surgery, increased venous pressure in the choroidal plexus may trigger choroidal hemorrhages. This risk can be increased in subjects under oral anticlotting treatment. Patients should be warned to avoid any effort likely to elicit a Valsalva effect, like lifting heavy objects, straining at stools, severe coughing.
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