Choroidal Detachment 

Updated: Feb 10, 2017
Author: Carlo E Traverso, MD; Chief Editor: Andrew A Dahl, MD, FACS 



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.

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.




Rarely, choroidal detachments form spontaneously. Recent intraocular surgery is the most common association.[3, 4, 5, 6, 7] Eye trauma and corneal ulcers are frequent, and panretinal photocoagulation can also cause choroidal detachments.[8] The use of IOP-lowering medications has also reportedly been associated with serous choroidal detachments.[9, 10, 11, 12, 13, 14]

Serous detachment is typically painless, with a variable degree of vision loss.

Postoperative hemorrhagic choroidal detachments are characterized by sudden excruciating throbbing pain with an immediate loss of vision; both symptoms are almost pathognomonic.

Detachment can occur during or shortly after a Valsalva maneuver, straining at stools, coughing, or sneezing. Anticoagulants and aspirin may facilitate bleeding.

Intraoperative hemorrhage is characterized by the development of positive pressure, visualization of an enlarging dark mass obscuring the fundus reflex, and tendency to extrude eye contents through open surgical wounds.

Ciliochoroidal edema/detachment without evidence of intraocular surgery or trauma should be investigated for a neoplastic, vascular, or inflammatory cause.[15, 16]

Visual acuity usually is reduced, possibly as low as to light perception only, depending on the degree of interference with the visual axis.

Inflammation in the anterior and posterior segment varies.[17]

Intraocular pressure can be normal, low, or elevated; as a rule, low IOP accompanies serous detachments, and normal to high IOP accompanies hemorrhages.


The anterior chamber (AC) can be of normal depth, or it can be shallow or flat.

When no other causes for hypotony are evident after trauma or surgery, use gonioscopy to check for a cyclodialysis cleft.[18]

The fundus examination shows choroidal detachment, shown below.

Serous choroidal detachment. Two lobes (ie, supero Serous choroidal detachment. Two lobes (ie, superotemporal, supranasal) of fluid accumulation are visible. The choroidal folds seen at the posterior pole are due to concomitant hypotony.

Stage the detachment. The extent of detachment can be limited to one or more sectors, with the lobe(s) limited by the fibrous attachments corresponding to the vortex veins. Annular detachments involve the circumference for 360°. A large degree of fluid accumulation can cause contact between lobes on the visual axis, with retina-to-retina contact centrally (kissing choroidals), while little fluid accumulation can cause a flat and anterior detachment, visible only with ultrasound biomicroscopy (UBM). Kissing choroidal detachments are shown in the image below.

Kissing choroidal detachment. When the lobes of th Kissing choroidal detachment. When the lobes of the detachment are sufficiently large, retina-to-retina contact occurs. If this is extended centrally, the clinical picture is described as kissing choroidals. The extension of the lobes of detachment/edema is important for the decision-making process regarding the clinical management.

Suprachoroidal hemorrhages can be accompanied by vitreous hemorrhage, retinal detachment, and retinal breaks.[1] This is shown in the image below.

Postoperative suprachoroidal hemorrhage. In this b Postoperative suprachoroidal hemorrhage. In this buphthalmic aphakic eye, suprachoroidal hemorrhage resulted in vitreous hemorrhage, retinal detachment, and extrusion of retina and blood through the pupil into the anterior chamber.

Intraoperative hemorrhages can be complicated by loss of eye contents, resulting in vitreous, retina, or lens remnants incarcerated in the surgical incision or visible in the AC.

Retinal detachment on ophthalmoscopy

A nonrhegmatogenous retinal detachment can be superimposed to a choroidal detachment and characterized by shifting subretinal fluid.

Choroidal detachments are nontremulous.

Retinal vessels look normal.

Ora serrata may be visible without indentation.

B-scan ultrasonography

Retinal detachments are mobile and highly reflective.

Choroidal detachments are domed shaped and are serous or hemorrhagic.[19]

Chronic serous choroidal detachments

Solid intraocular tumors are identified by transillumination.

With serous detachments, transillumination reveals a bright reflex, which can be present in nonpigmented choroidal melanomas.


Serous detachments have no specific predisposing factors except nanophthalmos.[20]

Causes of serous detachments include globe hypotony, trauma, and inflammation.

Predisposing factors for choroidal hemorrhages are old age, diffuse arteriosclerosis, glaucoma, previous eye surgery, axial myopia, a choroidal hemorrhage in the fellow eye, sickle cell anemia, and very short axial length.

Postoperative hypotony is the most likely triggering factor.

Hemorrhage occurs when vessels rupture. Hemorrhage is more likely in patients with systemic hypertension, intraoperative tachycardia, or arteriosclerosis. Other predisposing factors include old age and previous eye surgery.

Sudden globe decompression during surgery, particularly if the eye is affected by glaucoma and surgery is initiated when the IOP is still elevated, also predisposes to choroidal detachment.[21]

The use of some medications has also reportedly been associated with serous choroidal detachments.[9, 10, 11, 12, 13, 14, 22]





Imaging Studies

B-scan ultrasonography can aid in differentiating between serum and blood collected under or within the choroid (shown in the image below). B-scan ultrasonography is also helpful to delimit and stage the extent of the detachment when media are not clear.

B-scan ultrasonography examination of choroidal de B-scan ultrasonography examination of choroidal detachment. Fluid appears to be serum on one side (upper) and blood on the other side (below). Retina-to-retina contact, or kissing choroidal detachment, is present.


Medical Care

As soon as the diagnosis is confirmed, topical corticosteroids, cycloplegics, and mydriatics should be prescribed for patients. Oral steroids can be used and are indicated when inflammation is a factor.[23] When the IOP is high, which can occur with hemorrhagic choroidal detachments, IOP-lowering drugs can be used. Osmotics and aqueous suppressants are recommended. Parasympathomimetics are contraindicated.

Surgical Care

If choroidal detachment persists longer than 1 week after the underlying cause has been identified and addressed, drainage of the suprachoroidal fluid should be considered. The 7-day limit is an indication only; individualized assessment is key. If an improvement is suspected, waiting longer and closely monitoring the patient may be warranted. Immediate action is indicated when lens-cornea touch or IOL-cornea touch exists. This condition causes endothelial corneal damage and acceleration of lens opacities.

AC Reformation

If the AC remains flat after the cause has been identified and addressed, injection of viscoelastics into the AC should be considered. If lens-cornea touch or IOL-cornea touch exists, the AC reformation should be performed immediately, at the slit lamp if possible, while waiting to assess the need for suprachoroidal fluid drainage.

The AC reformation at the slit lamp is best performed through a paracentesis tract in the peripheral cornea; paracentesis tracts usually are made at the time of cataract or glaucoma surgery.

If not present, a paracentesis should be made with extreme care because the eye is likely to be soft and sore with a peripherally flat chamber; otherwise, inadvertent iris and lens damage may result. Performing a small full-thickness corneal incision with a sharp 15° knife is safer.

A cooperative patient is mandatory if the procedure is to be performed safely at the slit lamp.

The AC reformation procedure requires preparation with topical anesthesia, povidone-iodine preparation, and assistants to hold the lids and head of the patient.

Suprachoroidal Fluid Drainage

The technique for suprachoroidal fluid drainage involves making a paracentesis in the peripheral cornea. A balanced salt solution (BSS) is injected to fill the AC. The paracentesis site made at the time of cataract or glaucoma surgery can be used.

Preoperatively, the sectors where the most fluid is accumulated should be identified by ophthalmoscopy or B-scan ultrasonography.

Beginning with the sector where the detachment is largest, posterior sclerostomy is performed at 4-5 mm from the limbus. Circumferential cuts are made, producing an incision of about 2 mm in length. This is shown in the illustration below.

Drainage of suprachoroidal space. After the poster Drainage of suprachoroidal space. After the posterior sclerostomies are performed, gentle infusion in the anterior chamber through a paracentesis tract helps the globe to maintain a tone while the fluid exit from the suprachoroidal space is facilitated.

As soon as the suprachoroidal space is reached, the fluid drains. Serous detachments drain clear yellow fluid. Hemorrhagic detachments drain dark red fluid, often particulated with blood clots, shown in the image below. Gentle poking with a blunt instrument a few millimeters around the sclerostomy helps drainage when spontaneous flow slows down.

Drainage of suprachoroidal space. The hemorrhagic Drainage of suprachoroidal space. The hemorrhagic fluid is darker than fresh blood. Mechanical gaping of the radial incisions facilitates the egress of fluid.

After one quadrant is drained, the AC is filled again with BSS, and the second quadrant receives a posterior sclerostomy in the same fashion. This procedure can be repeated for all 4 quadrants.

At the end, especially in highly myopic eyes without a lens, SF6 gas can be left in the vitreous cavity to tamponade. No agreement exists regarding the closure of sclerostomies, which some surgeons elect to leave unsutured to allow for more drainage.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Anticholinergic agents

Class Summary

Inhibit binding of acetylcholine to cholinergic receptor, which, in turn, produces cycloplegia and mydriasis.

Cyclopentolate hydrochloride 1% (AK-Pentolate, Cyclogyl, I-Pentolate)

Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia.

Induces mydriasis in 30-60 min and cycloplegia in 25-75 min. These effects last up to 24 h.

Atropine ophthalmic (Isopto, Atropair, Atropisol)

Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia.

Mydriatic agents

Class Summary

Instillation of a long-acting cycloplegic agent relaxes any ciliary muscle spasm that causes a deep aching pain and photophobia.

Tropicamide 1% (Mydriacyl, Tropicacyl)

Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulation.


Class Summary

Have both anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Orasone, Meticorten)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Prednisolone ophthalmic (AK-Pred, Econopred, Inflamase Forte)

Decreases inflammation and corneal neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability.

In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.



Further Outpatient Care

Monitor visual acuity, AC depth, IOP, and extension of the detachment.

After managing the underlying cause, a postoperative totally flat AC with corneal-lenticular touch should be managed surgically. A flat chamber with contact of the corneal endothelium with the lens or pseudophakos can lead to rapid corneal endothelial failure and decompensation, extensive anterior and posterior synechiae, and acceleration of cataract changes in phakic patients. It can also trigger aqueous misdirection.

Inpatient & Outpatient Medications

Prescribe topical steroids and cycloplegics. Oral steroids may be indicated.

Consider topical IOP-lowering agents, oral carbonic anhydrase inhibitors, and systemic osmotics in patients with significant IOP elevation.

Avoid anticoagulants or aspirin with suprachoroidal hemorrhage.[24]


In open globe surgery, particularly glaucoma surgery, hypotony must be avoided by careful suturing techniques.

During surgery, take care not to suddenly decompress the globe; use a paracentesis tract to slowly deflate it.

Preoperative osmotics or carbonic anhydrase inhibitors can be used to decrease the IOP to a safe level before surgery.

Whether or not to discontinue aspirin or anticoagulants in preparation for glaucoma surgery is not yet clear.

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.


Serous choroidal detachment or suprachoroidal hemorrhage can result in phthisis, retinal detachment, cataract formation, or intractable secondary glaucoma.[25]


The prognosis is guarded. In general, a correlation exists between the severity and extension of the detachment and the prognosis.

Preexisting eye conditions (eg, advanced glaucoma) influence the final functional outcome.

Even with treatment, loss of functional vision can occur in 10-80% of patients.[6]

In general, the prognosis for patients with choroidal hemorrhages is definitely worse than for those with serous choroidal detachments, especially when choroidal hemorrhages are intraoperative, where severe functional damage is frequent.

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.