Choroidal Detachment

Updated: Oct 04, 2021
Author: Huy D Nguyen, MD, MBA; Chief Editor: Andrew A Dahl, MD, FACS 



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.




Rarely, choroidal detachments form spontaneously. Recent intraocular surgery is the most common association.[7, 8, 9, 10, 11]  Eye trauma and corneal ulcers are frequent, and panretinal photocoagulation can also cause choroidal detachments.[12]  The use of IOP-lowering medications has also reportedly been associated with serous choroidal detachments.[13, 14, 15, 16, 17, 18]  

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.[19, 20]  

Visual acuity usually is often reduced, usually hand-motion or worse, depending on the degree of interference with the visual axis.

Inflammation in the anterior and posterior segment varies.[21]

Intraocular pressure can be normal, low, or elevated; as a general guide, 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.[22]

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 (appositional, kissing choroidals), best visualized with B-scan ultrasound. Minor fluid accumulation can cause a flat and anterior detachment, best visualized 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.[5]  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 (expulsion), resulting in vitreous, retina, or lens remnants incarcerated in the surgical incision or visible in the AC.

Retinal detachment on ophthalmoscopy

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

Choroidal detachments are nontremulous on B-scan ultrasound.

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 and often extend anteriorly toward the ciliary body, versus retinal detachments that are usually demarcated most anteriorly at the ora serrata.[23]

Chronic serous choroidal detachments

Solid intraocular tumors can be identified by transillumination.

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


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

Risk factors for serous detachments include intraocular inflammation, recent intraocular surgery, axial hyperopia, and nanophthalmos.[24]

Risk factors for hemorrhagic choroidal detachment

Systemic: hypertension, cardiovascular and cerebrovascular diseases, diabetes, atherosclerosis[25]

Ocular: high myopia, glaucoma, age-related macular degeneration, proliferative diabetic retinopathy[25]

Medications: anticoagulants, antiplatelets, and thrombolytic agents[25]

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.[13, 14, 15, 16, 17, 18, 26, 27]





Imaging Studies

B-scan ultrasonography can aid in differentiating between serum and blood collected under or within the choroid (shown in the image below) and can help delineate against a retinal detachment. 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.

Optical coherence tomography and wide field fundoscopy may also be used to discover and monitor choroidal detachment.[28, 29]



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.[30]  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. Topical corticosteroids are used to both reduce inflammation and increase IOP, and systemic corticosteroids usually are reserved for refractory cases unresponsive to topical therapy. Small postoperative suprachoroidal effusions usually heal spontaneously without intervention, but if a wound leak is identified, appropriate procedural intervention should be taken. 

Surgical Care

The time frame for surgical intervention is controversial, with many authors preferring to waiting 10 to 14 days to allow time for clot lysis, making drainage easier and more complete. 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.

Anterior chamber reformation

If the AC remains flat after the cause has been identified and addressed, consider injection of viscoelastics into the AC. If lens-cornea touch or IOL-cornea touch exists, the AC reformation should be performed immediately, at the slit lamp if the patient can tolerate, 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. 

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

Posterior draining sclerotomy

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 four 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.

Increasing IOP during draining will enable a more complete extrusion of suprachoroidal blood and may be accomplished with limbal infusion, an anterior chamber maintainer, or a long pars plana infusion.

Pars plana vitrectomy has also proven to be an efficacious surgical method and especially indicated for associated retinal detachment. A combined approach with previously mentioned sclerotomy and silicone oil instillation, to provide an internal tamponade and reduce the risk of rebleeding, has been reported to provide good outcomes.



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.[31]


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. Some surgeons propose prophylactic scleral windows in patients with prior choroidal detachments or those with high episcleral venous pressure risks such as in Sturge-Weber. 

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 intraocular content expulsion, phthisis, retinal detachment, cataract formation, or intractable secondary glaucoma.[32]


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.[10]

In general, the prognosis for patients with choroidal hemorrhages is 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 anticlotting or anticoagulation treatment. Patients should be warned to avoid any effort likely to elicit a Valsalva effect, like lifting heavy objects, straining at stools, severe coughing.