Retinal Detachment

• Disruption of the internal limiting membrane and vitreoretinal adhesions: The vitreous normally exerts posteriorly directed pressure (approximately 15 mmHg) that maintains retinal apposition to the RPE. In rhegmatogenous detachment, the primary defect involves a full-thickness break in the neurosensory retina (either a horseshoe tear with flap elevation or a round hole). Vitreous liquefaction (synchesis) and tractional forces from vitreous detachment allow liquid vitreous to seep through this break into the subretinal space (between neurosensory retina and RPE), gradually elevating the retina away from its blood supply. The RPE normally maintains retinal apposition through active ion pumping (Na+/K+-ATPase) and tight junctional complexes; when breached, this hydraulic gradient is lost and gravitational forces extend the detachment progressively.

• Loss of photoreceptor–RPE metabolic coupling: Photoreceptors are metabolically dependent on diffusion of oxygen and nutrients (glucose, amino acids) from the choroidal circulation through the RPE, as the retina itself is avascular beyond the inner layers. Separation from the RPE disrupts this critical nutrient supply, particularly oxygen delivery, which is essential for maintaining the visual cycle (regeneration of 11-cis-retinol from all-trans-retinol by RPE65). Within hours of detachment, photoreceptors accumulate toxic metabolic byproducts, calcium influx increases through disrupted ion channels, and mitochondrial dysfunction initiates apoptotic cascades. Outer segment disorganization becomes apparent within 24–48 hours, and irreversible photoreceptor death progresses over days to weeks; macular involvement (central 6 mm) results in particularly rapid and severe vision loss. This explains the clinical urgency: timing to reattachment within 24–48 hours, particularly for macula-off detachments, is the strongest predictor of visual recovery.

• Tractional forces and vitreous traction in specialized contexts: In tractional retinal detachment, fibrovascular proliferation and scar formation (occurring in advanced diabetic retinopathy, proliferative vitreoretinopathy (PVR), and retinopathy of prematurity) create mechanical traction on the retina. These epiretinal and subretinal membranes contract over time, physically pulling the retina away from the wall of the eye without requiring a retinal break; the subretinal space fills not with liquid vitreous but with subretinal fluid from transudation. In exudative detachment, disruption of the blood–retinal barrier (outer barrier formed by tight junctions of RPE, inner barrier formed by endothelial tight junctions) results from inflammation (posterior uveitis, sympathetic ophthalmia), choroidal neovascularization, or choroidal thickening (Harada disease, nanophthalmos), allowing protein-rich fluid to accumulate in the subretinal space without retinal breaks or vitreous traction.

• Photoreceptor cell death mechanisms and electroretinographic changes: Following detachment, photoreceptors initially undergo functional suppression (detectable as reduced electroretinographic (ERG) amplitude within 24 hours) followed by structural degeneration. Apoptosis is initiated through multiple pathways: calcium overload activates calpains (calcium-dependent proteases), reactive oxygen species (ROS) overwhelm endogenous antioxidant systems (catalase, superoxide dismutase), and pro-apoptotic factors (Bad, caspase-3) are upregulated. Rod photoreceptors (responsible for peripheral and low-light vision) are more vulnerable than cone photoreceptors (responsible for central and color vision), explaining why peripheral detachments may initially preserve central vision. Müller glia and retinal pigment epithelial cells respond to detachment with glial activation and inflammatory cytokine production (TNF-α, IL-6), amplifying photoreceptor death. The critical window for reversibility is approximately 6–8 weeks for most detachments, though this varies with individual factors; macular detachments and those with associated proliferative vitreoretinopathy have shortened windows for recovery.

• Role of retinal breaks and vitreous traction in RRD propagation: The formation of retinal breaks is facilitated by posterior vitreous detachment (PVD), a normal age-related process where liquefied vitreous separates from the internal limiting membrane. In eyes with predisposing conditions (high myopia causing lattice degeneration and vitreous liquefaction, aphakia or pseudophakia altering vitreous architecture), vitreous traction at sites of retinal weakness creates horseshoe tears (elevation of a flap of retina with bleeding from retinal vessels at the apex) or atrophic holes (small, round, asymptomatic breaks in areas of retinal thinning). As the break persists, vitreous fluid enters the subretinal space; the density difference between vitreous and subretinal fluid creates ongoing gravitational effects and flow along planes of retinal weakness, extending the detachment centripetally. The rate of progression depends on break size (larger breaks allow faster fluid accumulation), location (superior breaks progress faster due to gravity), and vitreous liquidity (greater liquefaction accelerates progression).

• Rhegmatogenous retinal detachment (RRD)—primary mechanism is retinal breaks: RRD accounts for approximately 90% of all detachments and results from a break (tear or hole) in the neurosensory retina allowing vitreous fluid access to the subretinal space. Major risk factors include high myopia (refractive error >−6 diopters), which predisposes to lattice degeneration (areas of retinal thinning with vitreous liquefaction), and posterior vitreous detachment (PVD), a nearly universal age-related process where vitreous shrinkage and liquefaction create tractional stress on the vitreous base and equatorial retina. Prior intraocular surgery (particularly cataract extraction in the pre-phacoemulsification era and vitrectomy) increases risk by disrupting normal vitreous architecture and vitreoretinal adhesions; modern small-incision cataract surgery and premium intraocular lens implants have reduced but not eliminated this risk. Retinal tears and holes themselves are risk factors for future detachment; patients with detachment in one eye have approximately 10% risk of detachment in the fellow eye over 5–10 years, particularly if high myopia or lattice degeneration is present bilaterally. Acute PVD presents with classic symptoms of floaters and photopsia (flashing lights) and carries approximately 10–15% risk of associated retinal breaks and detachment. Family history of retinal detachment or myopia carries increased hereditary risk.

• Predisposing retinal and vitreous conditions for RRD: Lattice degeneration occurs in 6–8% of the general population and 20% of highly myopic eyes, consisting of thinned areas of retina (often at the equator) with liquefied vitreous overlying them; 1% of eyes with lattice degeneration develop retinal detachment. Vitreous liquefaction and synchesis are accelerated by high myopia (excessive axial length causes excessive vitreous volume and abnormal vitreous gel structure), trauma (blunt or penetrating ocular injury), and age. Retinal holes (small, round breaks in areas of retinal degeneration, typically in the equatorial region) are generally asymptomatic and carry lower detachment risk than tears, but symptomatic or large holes warrant prophylactic treatment. Retinal thinning and areas of vitreous base extension increase break risk. Aphakia (absence of natural lens, usually post-cataract extraction) and pseudophakia (artificial intraocular lens), particularly if lens implantation was performed decades ago with older techniques, increase detachment risk due to abnormal vitreous-zonular anatomy and vitreous liquefaction.

• Tractional retinal detachment—traction from proliferative membranes: Tractional detachment occurs when epiretinal (on retinal surface) and subretinal (beneath retina) fibrovascular membranes contract, mechanically pulling the retina centrally and off the eye wall. The most common cause is advanced diabetic retinopathy (PDR—proliferative diabetic retinopathy), where neovascularization of the disc or elsewhere on the retina triggers fibrovascular proliferation and progressive traction; tractional detachment occurs in approximately 5% of PDR cases. Proliferative vitreoretinopathy (PVR), a form of vitreous scarring that occurs in 5–10% of primary RRD cases and up to 50% of giant retinal tears, develops when retinal pigment epithelial cells migrate into vitreous and form contracting membranes; PVR is graded by severity (A, B, C1–C5) and represents a major challenge to successful primary retinal reattachment. Retinopathy of prematurity (ROP), a vasoproliferative disease occurring in premature infants with excessive oxygen exposure, can progress to tractional detachment of the temporal retina if untreated. Sickle cell retinopathy can lead to tractional changes and detachment. Ocular ischemic syndrome and central retinal artery occlusion can occasionally precipitate tractional detachment through neovascular proliferation. Severe penetrating trauma with vitreous hemorrhage and organization can lead to extensive tractional detachment.

• Exudative retinal detachment—accumulation of subretinal fluid without breaks or traction: Exudative detachment results from breakdown of the blood–retinal barrier (either outer barrier of RPE or inner barrier of choroidal vasculature) or from choroidal disease causing exudation. Posterior uveitis from various etiologies (sarcoidosis, toxoplasmosis, Vogt–Koyanagi–Harada (VKH) disease, syphilis, tuberculosis) causes inflammation of the choroid and RPE, increasing vascular permeability and leading to exudative detachment; VKH disease classically presents with bilateral exudative detachments. Acute retinal necrosis (ARN) from viral infection (HSV-1, HSV-2, VZV) presents with progressive outer retinal necrosis, hemorrhage, and exudative detachment. Nanophthalmos, a condition of abnormally small eye size with increased choroidal thickness and crowded intraocular anatomy, predisposes to exudative detachment through choroidal vascular congestion and increased permeability. Harada disease, an autoimmune condition causing choroidal inflammation, presents with exudative detachment, often bilateral and with characteristic "sunset" appearance of detachment (higher in superior periphery). Choroidal neovascularization (CNV) from age-related macular degeneration (AMD) or pathologic myopia can cause localized exudative detachment. Severe hypertension and preeclampsia/eclampsia can cause exudative detachment through choroidal ischemia and endothelial dysfunction. Orbital tumors (cavernous hemangioma, lymphoid tumors) compressing the eye can cause exudative detachment through impaired venous outflow. Hypotony (low intraocular pressure) from any cause (uveitis, post-operative leak, glaucoma valve malfunction) can lead to exudative detachment through choroidal swelling. Medications (notably topiramate and other carbonic anhydrase inhibitors, which cause angle closure and secondary effects) have been associated with exudative detachment.

• Floaters—sudden onset of new floaters or shadows: Patients with RRD typically present with sudden onset of multiple floaters (vitreous opacities appearing as spots, cobwebs, or shadows in the visual field), which reflect vitreous hemorrhage from torn retinal vessels, liquefied vitreous and RBC aggregates, or inflammatory exudates. Floaters are usually most apparent when looking at bright backgrounds. The sudden appearance of floaters, especially if accompanied by photopsia, is highly concerning for acute PVD with associated retinal break(s) and imminent detachment. In contrast, exudative detachment may develop more insidiously with gradual progressive visual symptoms; some patients may remain asymptomatic if peripheral retina is involved and macula is spared.

• Photopsia—flashing lights indicating vitreous traction on retina: Photopsia (flashing lights, lightning streaks, or brief visual phenomena) occurs when vitreous traction mechanically stimulates photoreceptors, depolarizing them and generating action potentials that are perceived as light in the absence of actual light stimuli. Photopsia is highly specific for acute PVD or active retinal traction and often precedes detachment by hours to days, making it a critical "red flag" symptom prompting urgent evaluation. Photopsia is typically peripheral (in the field where vitreous detachment is most active) and brief (lasting milliseconds to seconds), occurring in bursts particularly when eyes move rapidly or when head position changes. This symptom is often underappreciated by patients who may not immediately seek care, making provider education crucial.

• Visual field defect—shadow or curtain corresponding to location of detachment: As the detached retina physically lifts away from the eye wall, the corresponding area becomes functionally blind, producing a visual field defect that the patient perceives as a shadow, curtain, or "cobweb" in the peripheral vision (if peripheral retina is detached) or in the central field (if macula is involved). The defect is fixed (does not move with eye movements), unlike floaters which do move, and progresses as detachment extends. The location of the field defect corresponds to the anatomic location of detachment: a superior retinal detachment produces an inferior visual field defect (due to the inverted optical image on the retina), and a temporal detachment produces a nasal field defect. Macula-off detachment (detachment involving the central 6 mm of retina where central vision is mediated) causes dramatic, immediately noticed vision loss and represents an ophthalmologic emergency requiring same-day evaluation and treatment. Macula-sparing detachment may cause only peripheral field loss with preserved central vision initially, sometimes delaying patient presentation if the defect is in the peripheral field of the dominant eye or if the patient's attention is not drawn to it.

• Metamorphopsia and scotomas in macular involvement: When detachment approaches or involves the macula, patients experience metamorphopsia (distortion of straight lines into wavy or bent patterns) due to mechanical traction on photoreceptors causing displacement of the foveal center and irregular light refraction. Central scotomas (areas of absolute vision loss) or relative scotomas (areas of dimmed vision) may develop. These symptoms indicate imminent macular involvement and mandate emergent intervention.

• Decreased visual acuity and blurred vision: Visual acuity loss correlates with extent of retinal detachment and macula involvement. With macula-sparing RRD, visual acuity may remain 20/20 to 20/40, and some patients may not immediately notice vision changes if the detached area is nasal or temporal

Initial bedside assessment

• Visual acuity and confrontation fields: acuity is preserved in macula-on detachment and markedly reduced (often counting fingers or worse) once the fovea detaches. The field defect is fixed and lies opposite the detached quadrant (superior detachment → inferior field loss).
• Pupils: a relative afferent pupillary defect appears with large detachments and implies extensive neurosensory dysfunction, not media opacity.
• Slit lamp: Shafer's sign ("tobacco dust") — pigmented RPE cells liberated through a full-thickness break and suspended in the anterior vitreous — is highly predictive of a retinal tear. Intraocular pressure in the involved eye is typically lower than the fellow eye.

Confirmatory/gold-standard test

• Dilated indirect ophthalmoscopy with scleral depression: the standard of care for identifying and localizing every break. The detached retina appears elevated, corrugated, and undulating with eye movement; a horseshoe tear shows an elevated flap with its apex toward the posterior pole. Lincoff rules predict the location of the primary break from the configuration of subretinal fluid.
• B-scan ultrasonography: used when vitreous hemorrhage, dense cataract, or corneal opacity blocks the view. A detached retina is a highly reflective, mobile membrane tethered to the optic nerve head; a choroidal detachment is dome-shaped, extends anterior to the ora, and does not insert at the disc; a PVD membrane is thinner and not disc-tethered.
• OCT: settles the critical macula-on versus macula-off question and detects subclinical foveal fluid.

Subtype and severity classification

• Shifting subretinal fluid that pools dependently with position change, with no identifiable break, indicates exudative detachment; a taut, concave, immobile retina with fibrovascular membranes indicates tractional detachment.
• Proliferative vitreoretinopathy is staged by the Retina Society classification (grades A, B, C), which drives surgical planning and prognosis.

Immediate steps (any suspected RRD)

• Same-day referral to a vitreoretinal surgeon is the single most important action; the AAO Preferred Practice Pattern treats symptomatic detachment as an urgent condition because photoreceptor survival depends on time to reattachment.
• Activity restriction and positioning: bed rest with the head positioned so the detached quadrant is dependent limits fluid tracking toward the fovea while awaiting surgery. No topical or systemic drug reattaches a rhegmatogenous detachment — there is no medical first-line therapy.
• Timing: a macula-on detachment is the true emergency and is repaired without delay; a macula-off detachment is repaired promptly but the marginal benefit of operating within hours is smaller.

Break without detachment (prophylaxis)

• Laser photocoagulation or cryoretinopexy: creates a chorioretinal adhesion walling off a symptomatic horseshoe tear, preventing progression to detachment. Asymptomatic atrophic holes and most lattice degeneration are observed.

Definitive repair of RRD

• Pneumatic retinopexy: intravitreal expansile gas (SF6 or C3F8) plus retinopexy and strict head positioning; suited to a single superior break within the upper two-thirds of the retina. Contraindicated with inferior breaks, multiple breaks in different quadrants, significant PVR, media opacity, or an unreliable positioner.
• Scleral buckle: indents the sclera to relieve vitreous traction; favored in young phakic patients with formed vitreous.
• Pars plana vitrectomy (± gas or silicone oil tamponade): preferred with vitreous hemorrhage, pseudophakia, giant tears, or PVR.

Other subtypes

• Tractional: vitrectomy with membrane delamination; per AAO diabetic retinopathy guidance, panretinal photocoagulation and preoperative anti-VEGF (e.g., bevacizumab) reduce neovascular bleeding.
• Exudative: treat the cause — systemic corticosteroids for VKH or posterior uveitis, anti-VEGF for choroidal neovascularization, blood pressure control in preeclampsia. Surgery is generally inappropriate.

Contraindicated after gas tamponade

• Air travel or high-altitude ascent: the bubble expands, raising IOP and risking central retinal artery occlusion.
• Nitrous oxide anesthesia: diffuses into and expands the bubble; must be avoided until gas resorbs.

Complications of the disease

• Permanent central vision loss: photoreceptor apoptosis after foveal separation; signaled by macula-off status on OCT and by acuity that fails to recover despite anatomic reattachment.
• Proliferative vitreoretinopathy (PVR): RPE cells migrate through the break and form contractile membranes; the leading cause of surgical failure. Suspect when the retina becomes rigid with fixed folds and star-shaped puckering rather than undulating freely.
• Redetachment: new or reopened breaks under tractional membranes; recurrent field defect or fresh photopsia after surgery. Urgent re-referral.
• Fellow-eye detachment: the same predisposing myopia and lattice degeneration are usually bilateral; any new floaters in the other eye require dilated examination.
• Chronic detachment sequelae: demarcation lines, subretinal fibrosis, neovascular glaucoma, and ultimately phthisis bulbi.

Complications of treatment

• Endophthalmitis: intraocular bacterial inoculation after vitrectomy or intravitreal gas injection; pain, hypopyon, and worsening vision within days. Sight-threatening emergency — tap and inject intravitreal antibiotics.
• Acute IOP elevation: over-expansion of SF6/C3F8, especially with altitude or nitrous oxide; pain, corneal edema, and a non-perfused, pale disc if the central retinal artery closes. Emergency.
• Suprachoroidal hemorrhage: rupture of long posterior ciliary vessels during intraoperative hypotony; sudden pain and shallowing of the chamber. Emergency.
• Cataract: near-universal nuclear sclerosis after vitrectomy from altered lens oxygenation.
• Scleral buckle–specific: myopic refractive shift from axial elongation, diplopia from extraocular muscle disturbance, buckle extrusion or infection, and anterior segment ischemia when multiple rectus muscles or ciliary vessels are compromised.
• Silicone oil–specific: emulsification with secondary glaucoma and band keratopathy.
• Epiretinal membrane and cystoid macular edema: post-surgical inflammation; metamorphopsia with a thickened fovea on OCT.
• Sympathetic ophthalmia: rare autoimmune bilateral granulomatous uveitis after penetrating ocular surgery or trauma; blurred vision in the uninvolved eye demands urgent evaluation.

• The classic triad: sudden floaters + photopsia (flashes) + a curtain or shadow ascending or descending across the field, all painless and monocular. Painless monocular vision loss with flashes is retinal detachment until proven otherwise.
• Single best next step: urgent dilated fundoscopy by ophthalmology the same day — not CT, not MRI, not tonometry alone. If the fundus view is blocked by vitreous hemorrhage or cataract, the answer is B-scan ultrasonography.
• Buzzword to recognize: Shafer's sign / "tobacco dust" — pigmented cells in the anterior vitreous — means a full-thickness retinal break exists even if you cannot see it.
• Macula-on versus macula-off decides urgency: preserved central acuity with a peripheral field defect is the surgical emergency, because the fovea is still salvageable. Once acuity has dropped to counting fingers, the fovea is already off.
• The association examiners love: high myopia and lattice degeneration, plus the connective tissue disorders — Stickler syndrome (type II collagen: flat midface, cleft palate, sensorineural hearing loss, childhood detachment) and Marfan syndrome. Prior cataract surgery and blunt trauma are the acquired favorites.
• Distinguish the mimics: vitreous hemorrhage (diabetic, loss of red reflex, floaters without a fixed curtain), central retinal artery occlusion (instantaneous, complete, cherry-red spot, no flashes), amaurosis fugax (transient, resolves), and uncomplicated posterior vitreous detachment (flashes and floaters but a normal attached retina — still needs dilated exam).
• Shifting subretinal fluid with no visible break = exudative: think VKH, malignant hypertension/preeclampsia, or choroidal tumor. Treat the underlying disease; surgery is the distractor.
• After gas tamponade: no air travel, no mountain travel, and no nitrous oxide — bubble expansion can precipitate central retinal artery occlusion.