INTRODUCTION — Retinal detachment refers to the separation of the retina from the underlying retinal pigment epithelium and choroid. Without treatment, many peripheral retinal detachments progress to involve the central retina and lead to loss of vision.

This topic will address the pathophysiology, clinical presentation, treatment, and prevention of retinal detachment. Understanding the basic pathophysiology involved in the process of retinal tear formation and retinal detachment, and the symptoms and signs of the early stages of this process, are important in identifying high-risk patients and preventing loss of vision.

NORMAL ANATOMY — The retina is a multilayer of exquisitely organized neurons that line the back of the eye (picture 1 and picture 2). It is designed to convert photons (units of light energy) into neural impulses which travel along the visual pathways to the visual cortex. The retinal photoreceptors are some of the most metabolically active cells in the body. They line the outer portion of the neurosensory retina and their outer segments are in contact with the retinal pigment epithelium and underlying choroid. The choroidal circulation has the highest blood flow rate per cubic centimeter of tissue in the human body and provides a critical supply of oxygen to the outer third of the neurosensory retina and, in particular, to the retinal photoreceptors.

PATHOPHYSIOLOGY OF DETACHMENT — Retinal detachment occurs when the multilayer neurosensory retina separates from the underlying retinal pigment epithelium and choroid. This separation can occur either passively, as when a retinal hole or tear allows for an accumulation of fluid between the layers, or actively, as in the case of either vitreous traction or an exudative process (figure 1).

Regardless of etiology, separation of the retina from the underlying choroidal circulation results in outer retinal ischemia, with rapid and progressive photoreceptor degeneration [1]. The amount of photoreceptor degeneration and loss of vision can be minimized by rapid diagnosis and treatment [2-4]. Without treatment, most peripheral retinal detachments progress to involve the central retina and lead to loss of vision.

PRECURSOR CONDITIONS AND TYPES OF DETACHMENT — In most cases of rhegmatogenous retinal detachment, both posterior vitreous detachment (PVD) and retinal tears can be considered precursor conditions.

Posterior vitreous detachment — The vitreous is a clear gel-like structure in the back of the eye composed of collagen fibrils and hyaluronic acid that slowly liquefies and shrinks throughout life (vitreous liquefaction and degeneration). The shrinking vitreous exerts traction on the fibrils connecting the vitreous to the retina; breakage of these fibrils results in detachment of part of the vitreous from the retina. PVD is rare before the age of 40, but the prevalence increases to approximately 40 percent in the seventh decade and 86 percent by the ninth decade of life [5]. PVD can occur earlier in patients who are myopic, have had a history of ocular trauma, or have had ocular inflammation.

●Pathophysiology and relationship to detachment – In some cases, PVD causes a retinal hole or tear, which may then lead to detachment of the neurosensory retina from the retinal pigment epithelium as fluid from the vitreous cavity flows between the retina and the epithelium. This is termed a rhegmatogenous retinal detachment (see 'Rhegmatogenous retinal detachment' below) and is the most common cause of retinal detachment. Alternatively, when the vitreous has an abnormally strong attachment to the retina, traction from the shrinking vitreous can lead to separation of both the vitreous and neurosensory retina from the epithelium; this is a traction detachment, one form of nonrhegmatogenous retinal detachment. (See 'Nonrhegmatogenous retinal detachment' below.)

●Clinical course – PVD usually occurs over a period of one week but may take up to three months to completely develop [6,7]. Patients with a unilateral PVD are very likely to develop PVD in the other eye; in one series of 51 patients, 90 percent developed PVD in the contralateral eye within three years [8]. Patients diagnosed with PVD have a 3.4 percent chance of developing a retinal tear within six weeks [9]. The most common complications of PVD are retinal tears, vitreous hemorrhage, rhegmatogenous retinal detachment, and retinal or optic disc hemorrhage [10].

Retinal holes or tears — A discontinuity in the neurosensory retina can exist as a round retinal hole, or as a retinal tear. These are collectively referred to as retinal breaks. If a break then allows liquid vitreous fluid to pass through it into the subretinal space, a retinal detachment can occur. This process is analogous to a hole or tear in a piece of wallpaper in a room filled with water which then allows a large portion of wallpaper to be peel off of the wall as the water flows behind it (detachment) (picture 3). Holes and tears are diagnosed on ophthalmologic examination, often with the assistance of scleral indentation and depression.

Retinal holes are either atrophic or operculated. Atrophic holes are caused by lattice degeneration, not associated with vitreous traction, and are generally asymptomatic. If associated with subretinal fluid, these retinal detachments typically progress very slowly. This is a unique situation in which a rhegmatogenous retinal detachment can occur in the absence of a PVD. By contrast, operculated holes are generally round, associated with vitreous traction of PVD, and occur when the vitreous traction avulses a small piece of the retina into the vitreous cavity. They may be symptomatic or asymptomatic.

Retinal tears are breaks between the neurosensory retina and the underlying retinal epithelium, usually with persistent vitreous traction to one edge of the tear. Tears have a higher risk of progressing to retinal detachment than holes, as there is continued traction from the vitreous on the retina. A retinal tear is sometimes referred to as a horseshoe-shaped tear based on its shape, and if it is greater than three clock hours (90 degrees) in size it is referred to as a giant retinal tear. Tears are most commonly caused by PVD, but may also be caused by ocular trauma. PVD is more likely to result in retinal tears or holes if the patient has areas of abnormally strong vitreoretinal adhesion, such as areas of lattice degeneration. (See 'Epidemiology and risk factors' below.)

Retinal breaks can be symptomatic or asymptomatic. Asymptomatic retinal breaks have been reported in approximately 6 percent of eyes in clinical and autopsy studies [11] and are found on routine ophthalmologic examinations.

The incidence of subsequent retinal detachment among patients with untreated symptomatic retinal breaks is 35 to 47 percent, and 0 to 13.8 percent among those with asymptomatic retinal breaks [12].

Rhegmatogenous retinal detachment — Rhegmatogenous retinal detachments are the most common type of retinal detachment (figure 1). By definition, they are caused by retinal hole or tear (“rhegma” is Greek for tear). They are either nontraumatic (due to PVD) or, less commonly, traumatic (due to ocular injury) (picture 4) [13].

Nonrhegmatogenous retinal detachment — This type of detachment is either due to traction or an exudative process.

●Traction retinal detachment – Traction retinal detachments occur when the vitreous has an abnormally strong attachment to the retina. With vitreous liquefaction and subsequent contraction, the retina is pulled away from the retinal pigment epithelium (traction retinal detachment) without a retinal break or hole in the retina. Some examples of traction retinal detachments include vitreoretinal traction syndrome and diabetic traction retinal detachment.

●Exudative retinal detachment – Exudative retinal detachment occurs in patients who have an accumulation of fluid beneath the neurosensory retina and the retinal pigment epithelium without a retinal break. These types of retinal detachments are often associated with infectious or inflammatory conditions (eg, posterior scleritis due to sarcoidosis or syphilis) [14] but may occur either spontaneously, as with central serous chorioretinopathy, or in association with choroidal neoplasms/metastases.

EPIDEMIOLOGY AND RISK FACTORS — Nontraumatic rhegmatogenous retinal detachment (due to posterior vitreous detachment [PVD]) is the most common form of detachment and occurs in approximately 1 in 10,000 people per year [15,16]. Information on the prevalence of other forms is not available.

The risk of rhegmatogenous retinal detachment increases with age and is also higher among persons with myopia or a personal or family history of retinal detachment [5,17]. It can be a delayed complication of cataract surgery, other intraocular surgeries, or eye trauma. (See "Cataract in adults", section on 'Outcomes'.)

An association of retinal detachment (mostly rhegmatogenous) with use of fluoroquinolones has been reported; however, a meta-analysis of 10 studies did not confirm this association [18].

Risk factors for traction retinal detachment include conditions associated with neovascularization such as proliferative diabetic retinopathy, vitreomacular traction syndrome, retinopathy of prematurity, or sickle cell retinopathy. It can also occur in patients who have had perforating trauma and have developed a fibrotic transvitreal retinal band that contracts.

Lattice degeneration is considered to be an asymptomatic risk factor for the formation of retinal holes and potential detachment, although significant new tears or detachment occur in only 1 percent of patients with lattice degeneration [19]. This condition is present in 6 to 8 percent of the general population and in approximately 30 percent of patients with nontraumatic rhegmatogenous retinal detachment [20]. It is characterized histologically by localized retinal thinning in the periphery of the retina and is associated with overlying vitreous liquefaction, sclerotic lattice-like vessels, and abnormally strong areas of vitreoretinal adhesion.

CLINICAL PRESENTATION

Initial symptoms — Regardless of the cause, patients with retinal detachments present with painless loss of vision in the affected eye due to the separation of the retina from the underlying choroid. In most cases, the patient will experience symptoms of posterior vitreous detachment (PVD) as well, including floaters and flashes of light. However, retinal detachments can occasionally be asymptomatic.

Patients with the most common cause of retinal detachment, rhegmatogenous detachment following PVD, usually complain of an increasing number of floaters in the affected eye. The floaters may look like a cobweb or like one particularly large floater that appears to move in and out of central vision. The large floater represents the fibrous ring around the optic nerve and may have the appearance of "a large housefly."

Floaters are usually associated with acute PVD and result from the sudden separation of the vitreous gel from the surface of the retina. This sometimes dramatic presentation of vitreous floaters or debris can range from being an inconvenience or a nuisance to being visually disabling. The floaters usually resolve with time, settle down outside the visual axis, and/or become less noticeable.

Flashes of light called photopsias may also occur. As the posterior vitreous face separates from the underlying retinal surface, it may encounter areas of abnormally strong vitreoretinal adhesions. At these sites, the separating vitreous will tug on the surface of the retina and create a mechanical depolarization of the axons running through the nerve fiber layer of the retina. This is usually interpreted by the patient as a flash of light or photopsia that lasts less than one second and is sometimes associated with eye movement. These photopsias may be more easily seen in the dark or at night and are monocular. This appearance contrasts with the fortification spectra often described in patients with ocular migraines; this zigzagging light typically lasts 10 to 20 minutes, is seen in the peripheral visual field of both eyes, and is sometimes associated with blurry central vision. (See "Approach to the patient with visual hallucinations", section on 'Retinal pathology' and "Approach to the patient with visual hallucinations", section on 'Migraine aura'.)

Some patients complain of a shower of black spots, which is consistent with vitreous hemorrhage. Sometimes this shower of spots progresses, leaving the patient with a large vitreous hemorrhage and significantly impaired vision.

For patients who present with floaters, flashes, or black spots, a decrease in peripheral and then central vision is the most important symptom suggesting progression to rhegmatogenous retinal detachment [9].

Progression of symptoms — For patients with rhegmatogenous detachments, the rate of progression varies depending upon the size and location of the retinal break and movements of the eye. Detachments from large horseshoe retinal tears or giant retinal tears that have persistent vitreoretinal traction will usually progress over the period of days. By contrast, detachments from small horseshoe retinal tears progress more slowly over weeks to months [13].

As the retinal detachment progresses towards the macula, the size of the peripheral visual field defect will enlarge in a corresponding fashion. Patients will lose the ability to read once the retinal detachment involves the macula or the central area of the retina responsible for reading vision. Vision in patients with macula-off (involving the macula) rhegmatogenous retinal detachment usually ranges between 20/25 and ability to count fingers.

Nonrhegmatogenous detachments tend to progress over weeks to months.

DIAGNOSIS AND EVALUATION — The diagnosis of retinal detachment is based on history (eg, sudden onset of floaters, flashes of light [photopsias], and/or loss of vision) and ophthalmic examination. The examination requires slitlamp biomicroscopy and/or a dilated retinal examination, often with scleral depression.

Primary care evaluation — Patients presenting to primary care with a characteristic history should be initially evaluated by a test of visual acuity and confrontational evaluation of visual fields. Patients may also have their eyes dilated for a funduscopic examination; however, it is not practical for primary care providers to evaluate for retinal detachment, as the pathology is in the far periphery, and requires indirect ophthalmoscopy or wide-field retinal photography to visualize.

●Patients with high-risk features (visual field loss, subjective or objective decreased vision, or evidence of vitreous hemorrhage on funduscopic examination if this was performed) should be instructed to decrease eye movement (such as not reading or patching one eye with a black eye patch) and sent urgently to an ophthalmologist or retinal surgeon within one to two days [9].

●Patients without high-risk features may be referred to an ophthalmologist more electively (within one week).

Ophthalmologist evaluation — Patients who are referred to an ophthalmologist or retina specialist undergo a history and ophthalmic examination. All patients should be evaluated with slit lamp biomicroscopy and a dilated retinal examination. Anterior segment examination is performed looking for pigmented vitreous cells behind the lens of the eye. These cells are known as "tobacco dust" and represent liberated retinal pigment epithelial cells that have floated into the vitreous from under the neurosensory retina. Patients who have pigmented cells behind the lens have a very high probability of having a retinal tear. Funduscopic examination of these patients will usually reveal vitreous debris and often a white fibrous ring, called a Weiss ring, which corresponds to the area of contact between the posterior vitreous face and the round optic nerve.

A careful 360 degree peripheral retinal examination using an indirect ophthalmoscope also should be performed. Peripheral retina examination allows identification of vitreoretinal abnormalities, vitreoretinal areas of abnormal traction, round atrophic holes, operculated retinal breaks, or horseshoe retinal tears. Scleral depression during ophthalmoscopy is a very helpful technique for improving the view of the peripheral retina.

Patients should also undergo examination of the fellow eye as there is a relatively high rate of bilateral retinal tears or detachments (8 to 40 percent) [21] and an asymptomatic tear or detachment could otherwise be missed.

In patients with dense vitreous hemorrhage, an adequate ophthalmoscopic view of the retina may not be possible. No view of the posterior pole or peripheral retina will be obtained in cases where the vitreous cavity is filled with blood. In such cases, use of an ophthalmic B-scan ultrasound is needed to help identify large retinal breaks and/or retinal detachment (image 1). Ultrasound usually reveals the dense vitreous hemorrhage floating in the vitreous cavity as well as any retinal elevation. Since the resolution of ultrasonography is not as good as visual examination, patients with dense vitreous hemorrhages are often followed closely with sequential B-scan ultrasounds or they undergo surgical intervention with vitrectomy to allow careful examination of the retinal periphery [22]. (See 'Treatment of retinal detachments' below.)

Differential diagnosis — The following differential diagnosis applies to patients with floaters. Idiopathic vitreous floaters are the most common cause of floaters. In addition to PVD and retinal tears, other causes include:

●Vitreous hemorrhage (see "Overview of eye injuries in the emergency department", section on 'Vitreous hemorrhage')

●Vitreous inflammation (eg, toxoplasmic chorioretinitis)

●Ocular lymphoma

●Intraocular foreign body (see "Overview of eye injuries in the emergency department", section on 'Corneal abrasions and foreign bodies')

●Uveitis (see "Uveitis: Etiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations')

The differential diagnosis of acute vision loss is discussed elsewhere. (See "Approach to the adult with acute persistent visual loss".)

On examination, the retina occasionally appears to be detached but is actually not; this is termed pseudo retinal detachment. These cases need to be diagnosed by a retina specialist or ophthalmologist [23]. The appearance of retinal detachment may be due to:

●Peripheral senile retinoschisis, which is a splitting of the peripheral retina with an elevated retinal layer

●White without pressure, which is a white reflex at the vitreoretinal interface that is normally seen in some patients

●Choroidal lesions or infolding due to choroidal neoplasms, swelling, or hypotonia

MANAGEMENT OF PRECURSOR CONDITIONS

Posterior vitreous detachment — Patients who present with posterior vitreous detachment (PVD) and do not have any retinal breaks or tears, detachments, or vitreous hemorrhages on a 360 degree peripheral retina examination require only reassurance, education, and a plan for follow-up examination. They do not require any specific activity limitations. Patients can be informed that floaters should resolve over a period of 3 to 12 months as they settle down outside the visual axis.

Patients experiencing an episode of PVD are at increased risk of retinal tears and detachment, and they should be seen in follow-up in two to three months. However, the presence of any of the following should prompt sooner evaluation (within two to three weeks):

●Pigmented cells in the vitreous (retinal pigment epithelial cells that have migrated through the retinal break into the vitreous cavity), or evidence of vitreous hemorrhage on ophthalmologic examination

●Symptoms of flashes of light on a daily basis or with eye movement

●Personal of family history of retinal detachment

After two to three months, the risk of retinal tears or detachment typically returns to baseline. Studies have not successfully identified patients who require additional evaluation after the initial examination [24]. In a meta-analysis of retrospective studies that included 1600 patients with symptomatic PVD, delayed retinal tears (not seen on initial examination) were found in 1.8 percent; 83 percent of the patients with late tears had vitreous or retinal hemorrhage at initial examination of PVD or developed new symptoms [25].

Patients with PVD who have floaters that have become a permanent disabling symptom may require vitrectomy surgery. (See 'Procedures and outcomes' below.)

Retinal hole or tear — Patients who have a symptomatic retinal break (recent onset of flashing lights or hundreds of new floaters in affected eye) clearly benefit from laser retinopexy or cryoretinopexy to prevent retinal detachment [12,26]. (See 'Procedures and outcomes' below.)

For patients with asymptomatic retinal breaks, close follow-up or retinopexy treatment, with either laser or cryopexy, are both reasonable options. For patients who are extremely reliable and would prefer close observation, we see them at one month, three months, six months, and one year to assess for the development of retinal detachment. For patients who are not able to be seen in follow-up, or who have evidence of subretinal fluid associated with the retinal break, they are typically treated with laser or cryotherapy.

TREATMENT OF RETINAL DETACHMENTS — Treatment is dependent on many features including the type of detachment (rhegmatogenous versus nonrhegmatogenous, as determined by ophthalmologic examination), whether the patient is symptomatic or not, the extent of the detachment, and other patient and clinician factors [27].

Symptomatic rhegmatogenous retinal detachments — Treatment is indicated for nearly all patients with symptomatic detachments to prevent progression and loss of vision. If central visual acuity is still intact on initial patient presentation, treatment should be performed urgently (within one to two days) to prevent the detachment from spreading to the macula.

The choice of treatment depends of the type and size of the detachment:

●For small peripheral rhegmatogenous retinal detachments, the goal of treatment is to prevent the detachment from spreading posteriorly. This is achieved by forming adhesions between the retina and choroid in the area surrounding the tear using laser (photocoagulation) retinopexy or cryoretinopexy.

The chorioretinal scar created with these procedures may hold the retinal detachment in place and prevent it from spreading and threatening the macula. The choice between laser retinopexy or cryoretinopexy is based on the amount of subretinal fluid present and the preferences of the treating ophthalmologist. The procedures and associated outcomes are discussed below. (See 'Procedures and outcomes' below.)

●Large rhegmatogenous detachments require surgical treatment, with the goal of reattachment of the retina. Options include pneumatic retinopexy, permanent scleral buckle placement, and/or vitrectomy.

Few randomized trials are available to determine the optimal selection of one procedure over another, and the decision is often subjective [19]. Pneumatic retinopexy is an office procedure with lower costs and fewer complications and is appropriate as a first-line procedure for many non-complex cases. When not successful, more invasive procedures can be performed. The procedures and associated outcomes are discussed below. (See 'Procedures and outcomes' below.)

Asymptomatic rhegmatogenous retinal detachments — Asymptomatic retinal detachments appear to have a good prognosis without treatment. However, given the concern about potential loss of vision, we often treat patients with asymptomatic detachments with laser or cryoretinopexy, or scleral buckle or vitrectomy if larger, with the exception of those patients with small asymptomatic inferior rhegmatogenous detachments due to atrophic holes. These patients can be followed with close monitoring (at least every three months) or offered laser photocoagulation, discussed below. (See 'Procedures and outcomes' below.)

A case series of 16 patients with asymptomatic, untreated rhegmatogenous retinal detachments in 18 eyes found that none became symptomatic over a mean follow-up of 46 months [28]. It is uncertain whether these results are generalizable to all patients with asymptomatic retinal detachments, because the patients in this cohort were relatively young (mean age 56), none had a superior detachment, all had at least a partial demarcation line on presentation, all followed up reliably, and only 3 of the 18 detachments had retinal tears (many had atrophic holes).

Nonrhegmatogenous retinal detachments — Nonrhegmatogenous retinal detachments are primarily treated by addressing the underlying disease process.

However, patients who present with traction retinal detachments (due to severe diabetic retinopathy, penetrating ocular injury, or vitreomacular syndrome) may also benefit from retinal reattachment, in which case surgical intervention with a vitrectomy is required. During this surgery, extensive peeling of the traction-forming membranes is often required. Once the vitreoretinal traction is relieved, the retina will spontaneously reattach over a short period of time. (See 'Procedures and outcomes' below.)

In patients with exudative retinal detachment, diagnosing and treating the underlying etiology is critical to resolving the detachment and restoring vision [29]. Traditional retinal reattachment surgeries are not effective since exudative retinal detachments are not associated with a retinal break.

PROCEDURES AND OUTCOMES — The choice of procedure is dependent on many factors, including phakic status of the eye, family history of retinal detachment, location and chronicity of retinal detachment, overall health of the patient, and risk tolerance of the patient, and is beyond the scope of this topic.

The outcome of any procedure depends on the patient characteristics such as chronicity of detachment, the size of the retinal tears and detachments, presence of vitreous hemorrhage, whether the macula is involved, and the visual acuity on presentation. In the discussion below, the outcomes are for treatment of rhegmatogenous detachments; outcome data for nonrhegmatogenous detachments are not available as they vary based on the underlying disease process.

Retinal break or small rhegmatogenous retinal detachments

●Laser (photocoagulation) retinopexy – Patients who undergo laser (photocoagulation) retinopexy may be seated in front of a slit lamp after numbing the affected eye with topical drops. A contact lens is then placed on the surface of the eye in order to visualize the retinal break using the slit lamp biomicroscope. Once identified, the retinal break is surrounded by several rows of confluent 200 to 300 micron-size laser burns. The laser intensity necessary for these treatments can vary between 100 and 500 milliwatts depending upon the amount of cataract or vitreous hemorrhage present and fundus pigmentation. Patients may also be treated with a laser indirect ophthalmoscope that allows the clinician to examine, depress, and laser the retina at the same time. This delivery system allows for more peripheral treatment of the retina.

Laser treatment is associated with mild pain during the procedure. There is an extremely small risk of laser burn of the fovea. Once treatment is completed, it takes approximately one to two weeks for the body to form its maximal amount of chorioretinal adhesion. During this period, patients are usually advised to minimize eye movement (such as with reading). Sitting on a couch and watching TV is quite effective in minimizing head and eye movement.

•Outcome – Reported outcomes from laser retinopexy are limited to studies of treatment of retinal breaks not associated with detachment. Such treatment has been reported to be initially successful in approximately 80 percent of patients, with the remaining patients requiring further treatment due to inadequate closure of the break, new break formation, or subsequent retinal detachment [30,31]. In a systematic review of studies reporting outcomes among patients with symptomatic retinal breaks, the cumulated incidence of subsequent retinal detachment among those treated with laser photocoagulation or cryoretinopexy treatment was between 2.1 and 8.8 percent, compared with 35 to 47 percent among untreated patients [12].

●Cryoretinopexy – Patients who are treated with cryoretinopexy are usually given a subconjunctival injection of lidocaine over the area of the retinal break for anesthesia. Using the indirect ophthalmoscope, the cryotherapy probe is placed on the surface of the conjunctiva corresponding to the location of the retinal break. A freezing ball is created at the tip of this probe that freezes through the conjunctiva, sclera, choroid, and retina. A number of cryoretinopexy spots are created in order to contiguously surround the retinal break (figure 2).

The treatment typically requires a subconjunctival lidocaine injection and is associated with moderate levels of pain. Patients may experience periocular swelling and soreness for one to two days. Once treatment is completed, it takes approximately one to two weeks for the body to form its maximal amount of chorioretinal adhesion. During this period, patients are usually advised to minimize eye movement (such as with reading). Sitting on a couch and watching TV is quite effective in minimizing head and eye movement.

•Outcome – Data on outcomes after cryoretinopexy treatment are limited. In one study from the 1970s, 231 eyes with retinal breaks were treated successfully without subsequent retinal detachment or new break formation [32].

Large retinal detachments

●Pneumatic retinopexy – Pneumatic retinopexy is a procedure performed in the office and includes cryoretinopexy of the retinal break followed by injection of an intravitreal gas bubble (picture 5). With strict head positioning, retinal breaks that are in the superior, temporal, or nasal periphery of the retina can be tamponaded by the intravitreal gas bubble, closed, and sealed by the chorioretinal adhesion induced by cryoretinopexy. Once the retinal break is closed, the retinal epithelial cells quickly reabsorb the subretinal fluid, thereby reattaching the retina. This process of reabsorption usually takes about 24 to 48 hours [33,34].

It may also be possible to use pneumatic retinopexy in patients with retinal breaks that are in the inferior portion of the retina, using an inverted technique that requires patients to maintain a head-down position for six to eight hours per day [35].

•Outcome – Pneumatic retinopexy leads to successful retinal attachment in approximately 70 to 80 percent of patients after one procedure [33,34]. In a trial comparing pneumatic retinopexy with scleral buckling among patients with rhegmatogenous retinal detachment, the retina was successfully reattached with one or more procedures in 90 percent of those in the retinopexy group and in all of those in the scleral buckling group [36].

In cases of failure, most patients are treated with scleral buckle placement and/or vitrectomy.

●Scleral buckle – Scleral buckle is performed in the operating room. After a retrobulbar injection or infusion of lidocaine and bupivacaine, cryoretinopexy to the retinal breaks is performed, followed first by suturing of a silicone sponge or solid exoplant to the outside of the sclera that indents the wall of the eye and closes the retinal breaks, and then by drainage of subretinal fluid, if needed (figure 3). The scleral indentation created by the exoplant not only helps close the retinal break and allow the chorioretinal retinal adhesion to form but also helps reduce the vitreoretinal traction present.

A modification of the technique involves placing a small balloon catheter between the conjunctiva/Tenon capsule and the sclera underneath a retinal break to temporarily close it and allow sealing of the hole over a period of 12 to 24 hours. Once the retinal hole is sealed and closed and the subretinal fluid is reabsorbed, the balloon catheter can be safely removed.

•Outcome – A trial of 198 patients with rhegmatogenous retinal detachment compared outcomes between patients randomized to scleral buckling or pneumatic retinopexy [34]. The single-operation reattachment rate was higher for scleral buckling (82 versus 73 percent). However, visual acuity of 20/50 or better at six months was lower in the scleral buckling group (68 versus 87 percent). In another trial comparing pneumatic retinopexy with scleral buckling, the retina was successfully reattached with one of more procedures in 90 percent of those in the pneumatic retinopexy group, and all in the scleral buckling group [36].

In cases of failure, most patients are treated with vitrectomy.

●Vitrectomy – Patients who are pseudophakic or have more complicated retinal detachments, or those who have failed more conservative treatments, may require a vitrectomy (figure 4). With this procedure, three sclerotomies are made on the outside of the eye: one that allows fluid to infuse into the eye, and two others that are used to introduce instruments into the back part of the eye. Using a light pipe and a vitreous cutter, all of the central and peripheral vitreous is removed and all of the vitreoretinal traction on any of the breaks excised. The patient's retina can be flattened intraoperatively using an air bubble or heavier than water perfluorocarbon liquid. These patients are usually left with intravitreal air, a long-acting gas bubble (SF6 or C3F8), or silicone oil [37]. Those with an air or gas bubble are unable to travel on a plane until the bubble has been completely absorbed (one week for air and between three to eight weeks for gas, depending on the agent used).

•Outcome – Vitrectomy leads to successful retinal reattachment in approximately 80 to 90 percent of patients after one surgery in patients with rhegmatogenous retinal detachment [38]. In cases of failures, patients often require more extensive vitreoretinal procedures such as combined cataract extraction and intraocular lens placement, lensectomy, extensive epiretinal membrane peeling, subretinal fibrous band removal, relaxing retinotomies, and silicone oil tamponade. Virtually all patients over age 50 treated with vitrectomy will develop a visually significant cataract within 6 to 18 months.

PREVENTION AND REDUCTION OF CONSEQUENCES

Early diagnosis and treatment — The most important aspect of prevention is education of the patient about the symptoms of retinal detachment (see 'Clinical presentation' above). Early identification and treatment of retinal tears usually results in the prevention of a retinal detachment and significant loss of vision [12].

Prophylactic procedures — Prophylactic laser or cryoretinopexy has been suggested for patients with vitreoretinal abnormalities such as lattice degeneration with atrophic holes, vitreoretinal tags (congenital glial tags emanating from the retina into the vitreous), or small round retinal holes. However, a major limitation of prophylactic therapy is that most retinal detachments are due to retinal tears that develop in areas of the retina that appear normal prior to vitreous detachment [20]. Thus, treatment of peripheral retina vitreoretinal abnormalities may prevent a tear at those sites but not a tear in untreated normal-appearing retina.

The decision of whether to use prophylactic therapy is individualized based on clinical experience, expert opinion, and limited data [39]. There are some very high-risk patients, such as patients who have developed a giant retinal tear in the fellow eye, in whom prophylactic treatment may be reasonable; however, such a procedure may not be successful in preventing future tears or detachment [21].

Photoreceptor neuroprotection associated with surgery — Though not typical standard of care, some clinicians offer patients with macula-off (involving the macula) rhegmatogenous retinal detachment 5 L/minute of normobaric hyperoxia treatment prior to surgery to help reduce photoreceptor degeneration and potentially improve postoperative visual outcomes. Normobaric hyperoxia at 70 percent fraction of inspired oxygen (FIO₂) has been shown to reduce photoreceptor degeneration in a cat model of retinal detachment [40]. However, this treatment requires further study.

A number of potential neuroprotective agents are being tested clinically, which may prevent some of the retinal degeneration that occurs after detachment and potentially improve visual outcomes in patients with macula-off retinal detachment. These agents presumably would need to be injected into an eye with retinal detachment prior to surgical repair.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Detached retina (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Retinal detachment occurs when the multilayer neurosensory retina separates from the underlying retinal pigment epithelium and choroid. Without treatment, many symptomatic retinal detachments progress to involve the entire retina and lead to loss of vision. (See 'Pathophysiology of detachment' above.)

●Retinal detachments are classified as "rhegmatogenous" if they are the result of a retinal hole or retinal tear and as "nonrhegmatogenous" if due to traction or an exudative process. Rhegmatogenous detachments are most common, and they are often a consequence of posterior vitreous detachment (PVD), a normal event in people that often occurs between the ages of 50 and 75 (figure 1). (See 'Rhegmatogenous retinal detachment' above and 'Nonrhegmatogenous retinal detachment' above.)

●Risk factors for rhegmatogenous detachments include older age, myopia, focal thinning of the periphery of the retinal called lattice degeneration, and a personal or family history of retinal detachment. Retinal detachment can be a delayed complication of cataract surgery, other intraocular surgeries, or eye trauma. (See 'Epidemiology and risk factors' above.)

●Patients with retinal detachments present with painless loss of vision in the affected eye. Patients with retinal detachment will typically note a peripheral visual field defect, although involvement of the macula will result in a central defect

In most cases, the patient will experience symptoms of PVD as well, including floaters and flashes of light. However, retinal detachments can occasionally be asymptomatic. If a small retinal vessel is torn, the patient may note a shower of black spots (red blood cells) and/or a marked decrease in vision. (See 'Clinical presentation' above.)

●The diagnosis of retinal detachment is suspected based on history (eg, sudden onset of floaters, flashes of light [photopsias], and/or loss of vision) and confirmed by ophthalmologic examination. (See 'Clinical presentation' above and 'Diagnosis and evaluation' above.)

Patients with high-risk features (visual field loss, subjective or objective decreased vision, or evidence of vitreous hemorrhage on funduscopic examination) should be instructed to decrease eye movement (such as not reading or patching one eye with a black eye patch) and sent urgently to an ophthalmologist or retinal surgeon. Patients without high-risk features may be referred to an ophthalmologist more electively (within one week). (See 'Primary care evaluation' above.)

●Treatment of retinal detachment and precursor conditions dependent on many features including the type of detachment (rhegmatogenous versus nonrhegmatogenous), whether the patient is symptomatic, and the extent of the detachment:

•In the absence of retinal breaks or tears or vitreous pigmented cells, patients with PVD typically have a good prognosis and require no specific treatment, but they should have follow-up as described above. (See 'Management of precursor conditions' above.)

•For patients with a symptomatic retinal hole or tear, we suggest treatment with either laser photocoagulation or cryoretinopexy to prevent subsequent retinal detachment (Grade 2C). (See 'Management of precursor conditions' above and 'Retinal break or small rhegmatogenous retinal detachments' above.)

•For patients with asymptomatic retina hole or tear, close follow-up or laser treatment may be reasonable options as described above. (See 'Retinal hole or tear' above.)

•Patients with a symptomatic retinal detachment require treatment with one or more of the following procedures: laser or cryoretinopexy, pneumatic retinopexy, scleral buckle, or vitrectomy. Without treatment, there is a significant risk of permanent vision loss. (See 'Rhegmatogenous retinal detachment' above.)