Choroidal Detachment

Updated: Oct 04, 2021
  • Author: Huy D Nguyen, MD, MBA; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Suprachoroidal effusion, choroidal effusion, ciliochoroidal effusion, choroidal detachment, and ciliochoroidal detachment are commonly used terms describing a similar group of pathologies in which fluid collects in the potential space between the choroid and sclera. The suprachoroidal space is normally virtual, because the choroid closely opposes the overlying sclera. Traumatic and atraumatic factors alike may precipitate fluid accumulation in the potential space, separating the choroid from the sclera. Serum-like transudate or exudate or blood may accumulate in the space, thickening the originally vessel-rich 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), secondary to ocular trauma, secondary to eye surgery, or during the post-operative period. Hemorrhagic choroidal detachments can further be classified as expulsive or non-expulsive, with expulsive being a dreaded complication intraoperatively (or soon after surgery) or secondary to traumatic globe rupture.



Due to the highly vascular nature of the choriocapillaris in the choroid, and its dependency on equilibrium with other factors in the eye, nontraumatic conditions may contribute to the development of suprachoroidal effusion. Abrupt changes in intraocular pressure, serum osmotic and hydrostatic pressure, venous drainage, and uveoscleral outflow are commonly proposed etiologies.

Serous choroidal effusions more commonly result from atraumatic conditions, and are primarily a result of an imbalance in the pressure gradient between the choroidal capillary plexus and interstitial suprachoroidal space. The pressure in the suprachoroidal space is supplied by the intraocular pressure, whereas the low choroidal pressure is supplied by a functional aqueous and venous outflow, which is in part dependent upon systemic blood pressure. Therefore, a reduction in IOP — a common occurrence in many intraocular surgeries — would increase the pressure gradient and provide a favorable environment for driving serum out of the choroidal vasculature and into the suprachoroidal space.

On the other hand, an increase in hydrostatic pressure in the choroidal vasculature, as seen in hypertension, could result in the same process. Cytokines and other inflammatory molecules often make vasculature more permeable, so intraocular inflammatory states may increase the choroidal capillary permeability, driving serum into the suprachoroidal space. Altered oncotic pressures may also contribute to the development of choroidal effusions, as protein accumulation in the suprachoroidal space may attract serum and limit reabsorption. This occurs because the protein content of the fluid accumulating in the normally virtual suprachoroidal space is similar to plasma, with nearly equal oncotic pressures. [1, 2]  Treatment of the underlying cause is often necessary for reabsorption to ensue.

Hemorrhagic choroidal detachment is commonly associated with trauma, ocular surgery, and spontaneous rupture of ciliary arteries that may also be related to trauma. Intraoperative suprachoroidal hemorrhage is a dreaded complication as intraocular contents may expel from the incision site and usually results in loss of vision. [3]  Post-operative hemorrhagic choroidal effusion is usually the result of hypotony and inflammation, such as those following glaucoma filtering surgeries for once with high intraocular pressure. [4]  A breakdown of the blood-aqueous barrier across the pigmented epithelium may cause a superimposed non-rhegmatogenous 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, which are associated with after glaucoma filtration surgery, are often undetected or unreported. Suprachoroidal hemorrhage is a rare occurrence. Reported data vary between 0.05-6%, depending on the sample. [5, 6]  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 detachments, severe loss of vision to hand motion or worse is reported to be greater than 70%. [7, 8]


No racial predilection exists.


No sexual predilection exists.


Hemorrhagic detachments are seen more often in elderly patients.


Patient Education

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.