Retinal detachment

The entity retinal detachment (RD) was recognized early in 18th century by Saint-Yves who described the gross pathologic examination of detached retina. The first clinical description was provided by Beer in 1817, while Coccius was first to detect breaks in detached retina ophthalmoscopically (1851). Theories to explain the etiology of RD were proposed by Von Graefe, Girard-Teulon, Iwanoff, de Wecker at the end of the 19th century.

Retinal detachment (RD) occurs when the neurosensory retina separates from the underlying retinal pigment epithelium (RPE) and fluid accumulates within this potential space.

There are three categories of RD termed rhegmatogenous, exudative and tractional. Rhegmatogenous retinal detachment (RRD) is caused by a break in the retina (including round holes and tears), through which vitreous fluid passes from the vitreous cavity into the subretinal space, thus separating the sensory retina from the RPE. Exudative retinal detachment (ERD), also known as serous RD, occurs when subretinal fluid accumulates without a retinal break. This type of RD is often associated with choroidal tumors and posterior inflammatory diseases. The excessive accumulation of subretinal serous fluid in ERD may shift with changes in body position. Tractional retinal detachment (TRD) occurs when vitreoretinal adhesions or membranes mechanically pull the retina away from the RPE, without a retinal break (Fig. 1). This condition is most commonly associated with proliferative diabetic retinopathy, sickle cell disease, advanced retinopathy of prematurity. Vitreoretinal traction increases with age and frequently causes posterior vitreous detachments (detected in approximately two thirds of persons older than 70 years). Posterior vitreous detachments occur earlier in life in highly myopic eyes. In TRD, retinal breaks may develop secondarily. Combined retinal detachments with features of ERD and TRD may be associated with proliferative diabetic retinopathy or proliferative vitreoretinopathy and trauma.

RDD is also called “primary” detachment. Primary RD refers to i) rhegmatogenous detachment that occurs in a previously uninvolved phakic eye (an eye in which the crystalline lens is present) with no complicating factors such as underlying diabetic retinopathy or penetrating trauma or ii) detachment that occurs after cataract surgery. ERD and TRD are referred to as “secondary” or “non-rhegmatogenous” detachments.
The term “recurrent RD” is used to describe repeated occurrence of the primary detachment, occurrence of new or missed retinal breaks, or overgrowth of the retina by membranes and scar tissue.

Epidemilogy & risk factors

RD has an estimated incidence of 1:5,500-12,500 individuals per year. RRD is the most common cause of RD, with 0.01% annual risk and a lifetime risk (up to 60 years of age) of 0.6%. Acute RD occurs most commonly in the age group between 40 and 70 years.
Approximately 15% of individuals with RD in one eye develop detachment in the fellow eye. The risk for bilateral RRD ranges from 6–34% depending on the population studied and the associated risk factors. Bilateral RD is more common in aphakic eyes (in which the crystalline lens is absent) or pseudoaphakic eyes (in which the crystalline lens has been surgically removed and replaced by artificial lens).
Predisposition for RD is found in people of Jewish ethnicity, while low incidence is documented in African-Americans. Family predisposition is described in Jensen disease (retinochoroiditis juxtapapillaris). Men seem slightly more affected than women.

Risk Factors

Approximately 40-50% of RD are associated with high myopia, 30-40% with aphakia or pseudoaphakia, 10-20% with direct and/or severe ocular trauma. Due to liquefaction of the vitreous, the incidence of RD increases with age. Systemic disease (e.g. diabetes) can cause retinal pathology that may increase the risk of RD. Lattice degeneration, ocular infections and glaucoma are major risk factors for development of RRD. Specific sports (boxing, bungee jumping) may be associated with an increased risk of RD.

Clinical manifestations

Classic symptoms of all types RD are decreased vision and progressive monocular visual field loss. The latter is described by patients as “dark curtain ”, “cloud” or “web” over the field of vision and is due to mechanical disturbance of the retina by vitreoretinal traction. Patients frequently report history of light flashes or floaters that typically increase over a short period of time. Visual acuity may not be reduced if the detachment is peripherally located. Macular involvement leads to central vision loss. Vitreous hemorrhage may be present.

By definition, RRD, the most common type RD, is caused by one or more retinal breaks (full-thickness defects in the retina) (Fig. 2). Thus, on clinical examination, retinal break(s) must be present, although in some cases they may not be detected (e.g. in pseudoaphakic eyes). Pigmented cells described as “tobacco dust” are seen in the vitreous and occasionally in the anterior chamber. The underlying detached retina is opaque with a corrugated appearance and often undulates with eye movement. The subretinal fluid is usually clear. A major detachment shows an abnormal or diminished red reflex; however, this may not be present if the tear is in the periphery of the retina. Pupil examination is normal.

Retinal breaks and shifting fluid are characteristic for RRD, but not ERD and TRD. Secondary retinal breaks in TRD are possible. In some cases (trauma), pigment in the vitreous may be present also in TRD. Blocked transillumination and choroidal mass may be present in ERD. Intraocular pressure is usually normal in TRD, low in RRD and variable in ERD. RRD is an important cause of visual loss. If left untreated, symptomatic RRD invariably results in loss of vision.


RD occurs by the following principle mechanisms: a hole, tear or break in the neuronal layer allowing fluid from the vitreous cavity to separate sensory and RPE layers (i.e. RRD); traction from inflammatory or vascular fibrous membranes on the surface of the retina, which tether to the vitreous; exudation of material into the subretinal space from retinal vessels (such as in hypertension, central retinal venous occlusion, vasculitis, papilledema). Retinal detachments may be associated with congenital malformations, metabolic disorders, trauma, previous ocular surgery, vascular disease, choroidal tumors, high myopia, vitreous disease or degeneration.
Liquefaction of the vitreous is a major pre-requisite in the development of RRD. It occurs naturally with aging. This process is known as vitreous syneresis or synchysis senilis. It can also be associated with variety of congenital, inherited or acquired eye diseases and accelerated by high myopia, surgical and non-surgical trauma, and intraocular inflammation. Synchysis senilis is characterized by development of progressively enlarging pools (lacunae) of fluid within the vitreous gel. Significant liquefaction of the vitreous gel may lead to vitreous detachment (usually termed posterior vitreous detachment or PVD), which often precipitates RRD by producing tractional forces necessary to generate retinal breaks.

Posterior vitreous detachment (PVD) is typically an acute event that consists of partial or total (in majority of cases) separation of the posterior vitreous from the retina as a result of vitreous degeneration and shrinkage. Most persons develop PVD at some point in their lives. Less than 10% of patients with PVD are younger than 60 years of age, 30% of patients are in the seventh decade of life and more than 60% of patients are in the eighth decade of life. Patients with high myopia usually develop PVD earlier in life.

The most common symptoms of PVD are floaters of various types that may persist for months to years when uncomplicated, flashing lights, occasional vitreous hemorrhage and pigmentary debris. PVD may also be asymptomatic. In majority of cases, PVD is a benign condition that is not sight-threatening, does not require treatment and has no long-term complications. However, in the acute phase of PVD as the vitreous shrinks and detaches from the retina, tractional forces may be sufficient to cause a full-thickness tear in the retina. Such tears allow fluid to gain entry to the subretinal space. Due to rotational eye movements, gravitational and inertial forces or contracture of intraocular fibroproliferative tissue, vitreous currents force fluid through the retinal breaks and progressively extend the retinal detachment. A significant proportion of patients with acute PVD develop an associated retinal tear that can lead to RD and, if left untreated, permanent vision loss.

Retinal breaks may develop spontaneously in areas of strong vitreoretinal adhesion, typically along retinal vessels, or in patients with certain predisposing conditions, such as lattice retinal degeneration. In some cases patients describe a recent history of ocular trauma or surgery. Usually, the retinal breaks are located between the equator and ora serrata, or near the equator of the globe. Only 15% of retinal breaks develop posterior to the equator. Retinal breaks occur in about 6% of the general population, but most of them are benign atrophic holes that do not lead to RD.

There are several types of retinal breaks:

  • Flap tear (also known as “horseshoe” due to the U-shaped morphology) are usually located near the equator of the eye and are most common in middle age. They have an acute onset and frequently lead to detachment. As symptomatic flap tears are at high risk, they should be properly treated to prevent an RD (Fig. 3-4).
  • Atrophic retinal holes have round shape and gradual onset, are often within patches of lattice degeneration and are not associated vitreoretinal traction. Usually, they have low risk and do not require prophylactic treatment.
  • Ocular breaks are characterized by flap shape and acute onset. They consist of complete separation of a free-floating vitreous operculum from the underlying break. Ocular breaks tend to locate more posterior than the flap breaks. The risk of RD is intermediate. Decision for treatment should be taken case by case (Fig. 5).
  • Dialysis is a traumatic (or in some cases congenital) circumferential retinal tear by the ora serrata that has linear shape, acute onset and most commonly occurs in young individuals. Unlike the other breaks, vitreoretinal traction is on the posterior margin of the dialysis. The risk of RD is moderate (Fig. 6).


Lattice degeneration is one of the most important vitreoretinal abnormalities associated with an increased likelihood of retinal tears and RD. Approximately 30% of patients with RD also have lattice degeneration. Lattice degeneration is atrophic disease of the peripheral retina characterized by sharply demarcated round, oval or linear patches of retinal thinning that are circumferentially oriented and associated with liquefaction of the overlying vitreous gel (vitreoretinal degeneration). The disease occurs in 6 to 10% of the general population and is bilateral in approximately 50% of cases. Lattice degeneration can occur early in life and is usually diagnosed in the second decade of life. Lattice lesions are more common among patients with high myopia. Usually, the lesions are non-progressive or very slowly progressive. Lattice degeneration is typically asymptomatic unless associated with symptomatic retinal breaks. Thinning of the retinal surface of lattice degeneration may lead to formation of atrophic holes that occur in 20-35% of cases. Occasionally, they may encompass the entire lattice lesion. In this case, the overlying liquefied vitreous can pass through the hole into the subretinal space and predispose to retinal tears and retinal detachments. Longitudinal studies suggest that a new tear or detachment occurs in approximately 1% of patients with lattice retinal degeneration. No evidence of a benefit of prophylactic laser has been proven.

Retinal detachments after cataract surgery (pseudophakic RD) are probably due to vitreous changes (e.g. liquefaction and collapse of the vitreous secondary to diffusion of hyaluronic acid during surgery), disruption of the posterior capsule and vitreous loss at the time of surgery or following the surgical operation. The most important change in the vitreous after cataract surgery is the occurrence of PVD. Patients with pseudophakic RD, like those with other forms of RRD, usually present with symptoms of flashes of light, floaters, decreased visual acuity, or visual field defects. Over 50% of pseudophakic RD occur during the first year after cataract surgery. At 10 years, the risk of RD is 5 times higher in patients who had undergone cataract surgery than in those who did not have this surgical procedure. The overall risk of RRD after cataract surgery is approximately 1%. Post-cataract RRD tends to be more advanced, with total detachment (often involving the macula), multiple tiny breaks, fixed folds, and a higher incidence of proliferative vitreoretinopathy. Several risk factors for development of RD after cataract surgery have been suggested, e.g. high myopia and younger age. The occurrence of RD in the fellow eye increases the risk of RD in the eye undergoing cataract surgery.

Patients with high myopia (spherical equivalent of –6.0 diopters or more or an axial length of at least 26 mm) have 5- to 6-fold increased risk for developing RD. These patients represent only 10% of the general population but comprise 42% of the patients with RRD.

Blunt trauma is the leading cause of RD in children and adolescents. The vast majority of these patients are male. Boxers are at particularly high risk. Kickboxing and karate may also be associated with an increased risk of retinal tear. At the moment of impact, rapid compression and decompression of the globe may generate sufficient vitreoretinal traction to produce retinal tears. This type of tear can be detected and treated before it develops into RD. Individuals with high level of myopia should be advised to avoid activities carrying a risk of shock to the head or eye. Recommendations to avoid activities that may increase the intraocular pressure, such as diving and skydiving, in order to decrease the risk of RD have little supporting evidence.

Patients with congenital glaucoma and open-angle glaucoma are considered at increased risk for RRD.

Retinoschisis (splitting of the neurosensory retina into two layers) is responsible for about 2.5% of RRD cases. Most retinoschisis do not progress and do not require treatment. When both inner and outer layer holes develop, retinoschisis may convert into RRD, which will require a prompt treatment.

A cystic retinal tuft is a congenital abnormality that is characterized by a small, discreet, round or oval vitreoretinal lesion composed primarily of glial tissue. The lesion appears elevated, sharply circumscribed and chalky white. Vitreous condensations are attached to its surface, and its base may have pigmentary changes. It is estimated that the risk of RD in a patient with a cystic retinal tuft is only 0.3%.

In zonular traction tufts, thickened zonules are displaced posteriorly and attached to the anterior retina. This results in an abnormal tuft of tissue drawn from the surrounding retinal surface toward the ciliary body. RD due to development of retinal breaks in association with the zonular traction tuft occurs rarely.

Another condition that may lead to RD is a giant retinal tear, defined as a retinal tear that extends 3 clock hours (90 degrees) or more around the circumference of the globe. Individuals with high myopia and patients with Stickler’s syndrome have elevated risk of bilateral giant retinal tears. These cases are usually associated with a worse prognosis compared to breaks of other etiologies.

RRD is a common feature in several genetic syndromes. Stickler’s syndrome is the most common cause of RRD in young children, with most cases leading to total blindness if not diagnosed early. RRD develops in about 20% of individuals with Wagner syndrome and with patients with familial exudative vitreoretinopathy. Marshall syndrome, Knobloch syndrome, Marfan syndrome, Ehlers-Danlos syndrome are also at risk of development of RD.

Diagnosis & differential diagnosis

Patient history is essential in determining the diagnosis. Long standing floaters are often due to relatively benign conditions and do not represent an emergency. However, recent progressive onset of symptoms is highly suggestive of RD. Patients with sudden symptoms of new flashing lights, floaters or monocular loss of central or peripheral vision should be promptly evaluated by an ophthalmologist. If flashes or floaters are the only symptoms, the examination should urgently take place within a few days. However, in case of any visual loss, the examination should take place within 24 hours.

The eye examination should include check the vitreous for hemorrhage, detachment, and pigmented cells. Evaluation includes dilation of the pupil for indirect ophthalmoscopy combined with scleral depression to detect all retinal breaks. Slit-lamp biomicroscopy with a mirrored contact lens or a small indirect condensing lens may complement the examination. B-scan ultrasonography is useful to evaluate the peripheral retina and in case of vitreous hemorrhage.

Patients with subjective visual loss or vitreous pigment or hemorrhage on slit lamp examination should be considered at increased risk of retinal tear. Patients with uncomplicated PVD are at a small but significant continued risk (~3.5%) of subsequently developing retinal tear and detachment over the weeks after diagnosis. Fellow eye must always be carefully examined. If retinal breaks without detachment are detected, they may be treated on an outpatient basis with retinopexy (Fig. 4) (laser treatment applied to the retinal break and retinal pigment epithelium in order to induce the formation of a scar or, in some cases, cryotherapy). If a RD is detected, prompt surgical treatment is required.

Differential diagnosis

Differential diagnosis includes other peripheral retinal degenerations, such as lattice degeneration, retinal tufts, retinoschisis. Though these conditions may mimic RD, they have distinctive features that support the correct diagnosis. In case of uncertain diagnosis, additional examinations (e.g. laser spot test, B-scan ultrasonography) should be performed. Classic migraine with visual aura and occipital lobe disorders with migraine-like symptoms (ischemia, hemorrhage, arteriovenous malformation, epilepsy, neoplasms) should also be considered in the differential diagnosis. Postural hypotension can produce brief flashes or dimming of vision in all or part of the binocular visual field. Advanced proliferative diabetic retinopathy can lead to vitreous hemorrhage and mimic floaters associated with PVD.


Prophylactic treatment for conditions that may lead to RD is controversial. As a general rule, it should be undertaken only when the risk of complications from the treatment is lower than the risk of breaks leading to clinical RD. Prophylactic treatment may be suggestive in the following cases: symptomatic retinal breaks, large symptomatic operculated holes (Fig. 7), high-risk fellow eyes of nontraumatic giant retinal breaks, retinal breaks before cataract surgery, breaks and lattice degeneration in the fellow eye of RD, family history of RD, breaks due to trauma, breaks and lattice degeneration in highly myopic eyes. In all these conditions, close monitoring is advised. Current evidence supports prophylactic treatment only for symptomatic tractional tears. Patients undergoing prophylactic treatment should be warned about the possibility of developing a RD despite of the treatment and asked to seek immediate care if symptoms of RD are noted.

Asymptomatic retinal breaks in phakic eyes with lattice degeneration, high myopia, and fellow eye detachments show no significant benefit from prophylactic treatment. It is therefore recommended that patients with peripheral retinal degenerations that are at high risk for developing a RD, be properly educated and instructed to seek ophthalmologic care immediately if suggestive symptoms develop. Laser photocoagulation, cryotherapy and scleral buckling have been used in the prophylaxis of predisposing retinal lesions (in particular, in patients with RRD as a feature of genetic syndromes). The goal of treatment is to create a chorioretinal adhesion surrounding a break so that no communication exists between the vitreous cavity and the subretinal space.

Management for asymptomatic RD varies from conservative observation to surgery.
Symptomatic RD is an indication for surgery and requires immediate specialist referral. Prompt diagnosis and surgical treatment of RD can prevent impending vision loss or can restore vision. ERD usually does not require surgical intervention.

The three principal methods for reattachment of the retina include scleral buckling, vitrectomy (pars plana vitrectomy) and pneumatic retinopexy. In over 90% of cases, RD can be fixed successfully. In the best cases, more than one operation is needed in 10% of cases.

Scleral buckling surgery is the most common operation for RD and considered the “gold standard” for uncomplicated RRD. It aims at restoring the eye wall contact with the detached retina. Successful scleral buckling depends on accurate localization of the retinal breaks (by indirect ophthalmoscopy), induction of permanent chorioretinal adhesion (achieved by diathermy, cryotherapy or photocoagulation) and support of the retinal breaks on the buckle (accomplished with external scleral indentation with donor tissue or synthetic materials; solid silicone rubber or sponges are the most commonly employed buckling elements). A buckle may be affixed in an equatorial or radial orientation, may encircle the eye under the rectus muscles and be tightened like a belt, or may be arrayed in many combinations. The retina is reattached after the encircling scleral buckle has been secured and subretinal fluid has been drained.
In general, primary repair with scleral buckling lasts one to two hours. Repeat surgeries or more complex detachments may take longer. Scleral buckling results in high rates of stable and long-lasting successful reattachment (95% reattachment at 20 years reported). Vision is also preserved or substantially recovered (postoperative visual acuity of 20/50 or better).

Possible postoperative complications (lasting for several days or weeks) include prolonged recovery time, pain, swollen, red, or tender eye, infection, induced refractive error with increased myopia, floaters, strabismus, ocular motility disturbances. In less than 5% of cases, diplopia, cystoid macular edema, eyelid malpositions, retinal breaks, intraocular dislocation of an implanted lens, vitreous and choroidal hemorrhage, loss of vitreous during suturing or drainage, glaucoma, choroidal detachment, cataract formation, late extrusion or infection of the buckle may develop. Retinal vascular occlusion, anterior segment ischemia and endophthalmitis are extremely rare. Recurrent detachment is one of the most important complications after scleral buckling. Failure of reattachment is mainly due to development of proliferative vitreoretinopathy. In these cases, patients typically require further surgical intervention, including vitrectomy.

Vitrectomy is a surgical approach that relieves traction by removing the vitreous attached to the retinal breaks. Artificial vitreous substitutes are used to re-establish intraocular volume and mechanically flatten detached retina. They include gases (air and perfluorocarbon gases) and liquids (silicone oil and perfluorocarbon liquids). The gas gradually disappears during the postoperative period (within 1 to 4 weeks) and is replaced by fluid produced by the eye. Rarely in cases of primary detachment silicone oil is placed in the vitreous cavity and is usually removed from the eye if retina remains attached. With all of these procedures, either laser or cryopexy is used to "weld" the retina back in place. Sometimes a vitrectomy may be combined with a scleral buckle. Vitrectomy avoids some of the complications associated with scleral buckling (diplopia, choroidal detachment, perforation of the sclera, abnormalities in the eyelid, late extrusion and infection of the buckle), but carries higher risks of cataract formation in phakic eyes, glaucoma and new retinal breaks.

Pars plana vitrectomy is a surgical procedure that can be performed under local or general anesthesia in which the access into the eye is done through the pars plana, the section of the eye between the retina and the pars plicata. Pars plana vitrectomy was used in the past as primary surgical intervention only in complicated retinal detachments, such as very large tears, scar tissue on the retina, excessive blood in the vitreous, or detachments that failed by other methods. It is now an increasingly used as primary option for RRD repair and for removal of opacities and synechiae. The main advantage of this surgical procedure over scleral buckling alone is the ability to visualize all retinal breaks by using internal search with the indirect viewing systems and scleral indentation. If breaks are not identified, a higher failure rate may be expected. Using pars plana vitrectomy, high reattachment rates (more than 90% single-procedure attachment rate) and high rate of visual improvemet (visual acuity of 20/50 or better in up to 80% of cases) postoperatively are achieved in pseudophakic eyes, with low intraoperative complications. Most of the healing occurs during the first month, while full visual recovery may take a few months. Disadvantages of pars plana vitrectomy include the need for postoperative positioning, avoidance of airplane travel or traveling to altitude with a gas bubble in the eye, extended recovery time (depending on the type of gas placed). Other possible complications after include lens trauma (10%) and postoperative cataract (nuclear sclerosis) progression (80 to 98% of vitrectomized eyes).

Transconjunctival sutureless vitrectomy using a 25-gauge or 23-gauge incision has been introduced in recent years. This vitreoretinal surgery technique use a thin 25-gauge or 23-gauge, this the incisions left in the sclera after removal of the cannulas are so small that they seal without suturing, thereby minimizing surgically induced trauma, and decreasing the convalescence period, operating time, and postoperative inflammatory response.

Pneumatic retinopexy (an outpatient procedure performed under local anesthesia) is indicated for selected. These include a single retinal break and superior retinal breaks smaller than one clock hour. With this technique, the causative tear(s) are identified and treated via injection of a gas bubble (perfluoropropane or sulfur hexafluoride) into the vitreous space that pushes against the area of the retinal tear(s). Laser or cryo-surgery is used to secure the retina to the eye wall around the retinal tear. With appropriate positioning of the head, retinal breaks are closed by the bubble. Reattachment of the retina occurs through physiologic resorption of subretinal fluid. Gradual elution of gas from the eye leaves the retina reattached, with the retinal breaks permanently closed by the retinopexy scar.

The advantages of pneumatic retinopexy over the other procedures are reduced postoperative morbidity and recovery time. It is less invasive and less costly. However, it is not suitable as a treatment for every detachment owing to practical limitations in the ability to close breaks by head-positioning with an intraocular gas bubble. Contraindications may include inferior breaks, lattice degeneration, media opacities, uncontrolled glaucoma, pseudophakia or aphakia.

Disadvantages of the procedure include the necessity for correct postoperative positioning and close follow-up. In the postoperative period patients should avoid air travel. The most frequent postoperative complications include misplaced gas injection, persistent subretinal fluid or trapped gas, or inferior break that will need a new surgery. Endophthalmitis, macular folds, an increase in intraocular pressure, choroidal detachment, cataracts, epiretinal membranes, vitreous or subretinal hemorrhage are rare.

Despite the variety of surgical techniques, the management of RD remains a challenge. So far, only a few randomized controlled clinical trials compared directly different surgical techniques. Consequently, there are no results that consistently demonstrate the superiority of a single method. The use of combined surgical approaches is also an active area of clinical investigation. Data from case series suggest that primary detachments in phakic eyes with complexity exceeding the original indications for pneumatic retinopexy may be treated successfully with scleral buckling or vitrectomy, whereas vitrectomy appears to be preferable for corresponding detachments in pseudophakic eyes. Further prospective clinical trials are required to address the question as to which procedure is an appropriate therapeutic approach for RD.

Most retinal detachment surgery is successful, although a second operation is sometimes needed. The following factors may predict insufficient anatomical success after surgery: poor presenting vision, longer duration of symptoms before presentation, the presence of preoperative choroidal detachment, vitreous hemorrhage, large retinal breaks (≥ 1 clock hour), breaks located posterior to the equator (Fig. 8). The time between the occurrence of RD and the surgical repair appears to be of major importance for the functional results obtained after surgery.

Management of the fellow eye should take in consideration the data reporting prevalence of RD in the fellow eye at 4.5%, 16.4%, and 35.7% in phakic, pseudophakic, or aphakic eyes, respectively. Prophylactic treatment of retinal tears and lattice degeneration in fellow eyes does not always prevent the development of RD.


Spontaneous reattachment is extremely rare. With current therapeutic methods, over 90% of RD can be successfully treated, although in some cases a second treatment is needed. The visual outcome is not always predictable and, in general, better results correlate with a good initial visual acuity. About 40% of patients with successfully repaired detachment have excellent vision within 6 months of surgery. The other 60% of patients have various levels of reading and distance vision. Visual results are best if the RD is repaired before the macula detaches. If the macula was affected, only about 30% will get back reading vision. In general, the more severe the detachment and the longer it has been present, the less vision may be expected to return (the delay between the detachment and the surgery should be no longer than 7 days). Some patients, particularly those with chronic retinal detachment, do not recover vision. Treatment sometimes fails and vision may eventually be lost even under best circumstances and multiple attempts at repair.

RRD remains an important cause of preventable vision loss. Lattice degeneration, degenerative retinoschisis, cystic retinal tufts, and zonular traction tufts, have been identified as significant risk factors for RRD. Consequently, these lesions have been considered for close monitoring and/or prophylactic therapy. RRD is a significant post-surgical complication for patients who undergo cataract surgery, with 50% of detachments occurring within the first year following surgery. The risk is highest for patients who have intracapsular cataract extraction (ICCE). RD secondary to lattice degeneration tend to progress slowly, and are associated with surgical success rates of 98–100%. Patients with RD secondary to penetrating trauma have a poor prognosis.

Patient education

Patient education is of crucial importance to establish an early diagnosis and treatment of RD, and to preserve vision. All patients at risk should be instructed to notify their ophthalmologist promptly if the following warning signs of RD appear: sudden increase in floaters, a “showers” of floaters that look like spots, hairs or strings, sudden flashes of light in one or both eyes, a shadow or curtain over a portion of the visual field, a sudden blur in the vision. Patient education in RD and its symptoms is particularly important in highly myopic patients undergoing cataract surgery, patients following cataract surgery complicated with vitreous loss, and those undergoing YAG laser for secondary cataract.

References & disclaimer

Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages.Am J Ophthalmol. 2010 Mar;149(3):371-82.e1. Daniel A. Brinton and Charles P. Wilkinson. Retinal Detachment. Principles and Practice. Third edition. Oxfor University Press Inc., 2009.

D'Amico DJ. Primary Retinal Detachment. N Engl J Med. 2008 Nov 27;359(22):2346-54.

Sodhi A, Leung LS, Do DV, Gower EW, Schein OD, Handa JT. Recent Trends in the Management of Rhegmatogenous Retinal Detachment. Surv Ophthalmol. 2008 Jan-Feb;53(1):50-67.

Heimann H, Bartz-Schmidt KU, Bornfeld N, Weiss C, Hilgers RD, Foerster MH; Scleral Buckling versus Primary Vitrectomy in Rhegmatogenous Retinal Detachment Study Group. Scleral buckling versus primary vitrectomy in rhegmatogenous retinal detachment: a prospective randomized multicenter clinical study. Ophthalmology. 2007 Dec;114(12):2142-54.

Lois N, Wong D. Pseudophakic retinal detachment. Surv Ophthalmol. 2003 Sep-Oct;48(5):467-87.

Amar Agarwal. The Handbook of Ophthalmology. SLACK Inc., 2006.

Contributors: Katia Marazova, PhD, and Dr. Sarah Ayello-Scheer, MD, PhD (July 2011)

Disclaimer: This document contains information based on published scientific articles and is for educational purposes only. It is in no way intended as a substitute for qualified medical professional help, advice, diagnosis or treatment.