Retinopathy of prematurity
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Retinopathy of Prematurity (ROP)
Definition & Pathophysiology
ROP is a proliferative vasculopathy affecting the developing retina of premature, low-birthweight infants and is one of the leading causes of childhood blindness worldwide.
The retina has no blood vessels until the 4th month of gestation; vascular complexes then grow from optic disc hyaloid vessels toward the periphery. The nasal retina is fully vascularized by ~8 months gestation, but the temporal periphery vascularizes at or up to 1 month after term delivery. Prematurity interrupts this process in two phases:
- Hyperoxic phase (supplemental O₂ in NICU): Retinal vessels undergo vasoconstriction and obliteration — vascular growth is arrested.
- Hypoxic/vasoproliferative phase: The growing, metabolically active avascular retina becomes hypoxic, triggering VEGF-driven abnormal neovascularization at the vascular–avascular junction.
— Kanski's Clinical Ophthalmology, 10e; Harriet Lane Handbook, 23e
Risk Factors
| Major | Additional |
|---|---|
| Gestational age ≤30–32 weeks | Supplemental oxygen use |
| Birth weight <1,500 g | Neonatal sepsis |
| Prematurity (degree correlated to risk) | Hypoxemia / hypercarbia |
| — | Anaemia, low vitamin E |
| — | Failure to thrive |
| — | Caucasian race, male sex |
Risk factors are additive when concurrent. — Wills Eye Manual; Kanski's
Classification (ICROP 3rd Edition, 2021)
Zones (centred on the optic disc)
- Zone I: Posterior pole — radius = 2× the disc-to-fovea distance. Worst prognosis.
- Zone II: From zone I edge to the nasal ora serrata.
- Zone III: Residual temporal crescent anterior to zone II.
The zone of the most posterior ROP lesion defines the zone. An incursion 1–2 clock hours into a more posterior zone = a "notch."
Stages
| Stage | Description |
|---|---|
| 1 | Thin flat grey-white demarcation line at vascular–avascular junction |
| 2 | Ridge — elevated, has height and width; small neovascular tufts may appear posterior to it |
| 3 | Extraretinal fibrovascular proliferation extending into vitreous from ridge (mild/moderate/severe); peaks ~35 weeks post-conceptual age |
| 4A | Partial retinal detachment — extrafoveal |
| 4B | Partial retinal detachment — involving fovea |
| 5 | Total retinal detachment |
"Plus" Disease
At least 2 quadrants of posterior pole venous engorgement and arterial tortuosity. Denoted with "+", e.g., Stage 3+. Advanced plus disease also shows iris vascular engorgement, poor pupil dilation, and vitreous haze.
Pre-plus disease: Intermediate vascular changes insufficient to diagnose plus disease.
Aggressive posterior ROP (AP-ROP): Rapidly progressive zone I disease with extensive plus disease; may skip stages and progress directly to stage 5. Hemorrhages at the vascular–avascular junction may be present.
Type Classification (Treatment Guidance)
| Type | Criteria | Action |
|---|---|---|
| Type 1 (high-risk, treat) | Zone I, any stage with plus; Zone I, stage 3 without plus; Zone II, stage 2 or 3 with plus | Treat within 48–72 hours |
| Type 2 (watch closely) | Zone I, stage 1–2 without plus; Zone II, stage 3 without plus | Close follow-up |
— Wills Eye Manual; Kanski's Clinical Ophthalmology
Fundus Images
Staging Reference
Stage 3 ROP — Ridge with Extraretinal Proliferation
Progression Stages 1–3 and Laser Treatment
Screening
| Criterion | Detail |
|---|---|
| Indication | All infants with birth weight ≤1,500 g or gestational age ≤30 weeks |
| Also screen | Infants >30 wks with unstable clinical course / cardiorespiratory support |
| First exam timing (≤27 wks GA) | At 31 weeks postmenstrual age (PMA) |
| First exam timing (≥28 wks GA) | At 4 weeks chronologic age |
| <25 wks GA | Consider at 6 weeks chronologic age (earlier if severe comorbidities) — to detect AP-ROP |
Examination is by dilated indirect ophthalmoscopy.
— Harriet Lane Handbook, 23e; Wills Eye Manual
Treatment
Type 1 ROP / Threshold Disease
Laser photocoagulation (preferred over cryotherapy) — near-confluent ablation of the avascular peripheral retina. Must be done within 48–72 hours of diagnosis.
Anti-VEGF Therapy
Intravitreal bevacizumab (0.625 mg / 0.025 mL) is an emerging option, particularly for:
- Zone I cases (very posterior disease)
- When laser is not available
Long-term systemic effects in preterm infants are not yet fully established. If anti-VEGF is used, extended follow-up is mandatory due to risk of recurrence after 65–70 weeks PMA if retinal vascularization remains incomplete.
Stages 4–5 (Retinal Detachment)
Surgical repair by vitrectomy.
— Wills Eye Manual; Kanski's Clinical Ophthalmology
Cicatricial (Regressed) Disease
~20% of infants with active ROP develop cicatricial complications:
- Temporal vitreoretinal fibrosis
- Straightening of vascular arcades
- Macular dragging (disc and macula dragged temporally)
- Falciform retinal fold
- Retinal detachment / total detachment ("retrolental fibroplasia")
- Secondary angle-closure glaucoma (forward displacement of iris-lens diaphragm)
More posterior and more advanced active disease → worse cicatricial sequelae. — Kanski's Clinical Ophthalmology
Follow-Up Schedule
| Finding | Follow-up interval |
|---|---|
| Zone I, no ROP; zone I stage 1–2; zone II stage 3; AP-ROP concern | ≤1 week |
| Posterior zone II, immature; zone II stage 2; zone I regressing | 1–2 weeks |
| Zone II, no ROP; zone II stage 1; zone II regressing | 2 weeks |
| Zone III stage 1–2; zone III regressing | 2–3 weeks |
Discontinue acute screening when: Zone III vascularization attained without prior zone I/II ROP; PMA ≥50 weeks with no disease worse than zone II stage 3; or full vascularization to the ora serrata (for anti-VEGF–treated eyes).
Lifelong annual follow-up is indicated due to increased lifetime risk of myopia, strabismus, amblyopia, macular dragging, cataracts, glaucoma, and retinal detachment. — Wills Eye Manual
Differential Diagnosis
- FEVR (Familial Exudative Vitreoretinopathy): Hereditary, often asymmetric, no prematurity history
- Incontinentia pigmenti: X-linked dominant (girls); skin, CNS, dental anomalies
- Other causes of leukocoria (retinoblastoma, Coats disease, etc.)
Retinal detachment
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Retinal Detachment
Definition
Retinal detachment (RD) is separation of the neurosensory retina from the retinal pigment epithelium (RPE). It is broadly classified into rhegmatogenous (break-related) and non-rhegmatogenous (tractional and exudative) types based on the presence or absence of a retinal break.
— Robbins & Kumar Pathologic Basis of Disease
Types
1. Rhegmatogenous Retinal Detachment (RRD)
Most common type. Incidence ~1 in 10,000/year; both eyes eventually affected in ~10%.
Pathogenesis: A full-thickness retinal break (tear or hole) — in concert with vitreoretinal traction and at least partial vitreous liquefaction — allows liquefied vitreous to seep through the break into the subretinal space, separating the neurosensory retina from the RPE. Without liquefied vitreous and traction, RD almost never occurs even with a break present.
Causes of retinal breaks:
- Posterior vitreous detachment (PVD): vitreous collapses and exerts traction at points of strong retinal adhesion → horseshoe (flap) tears
- Lattice degeneration, snailtrack degeneration
- High myopia (>40% of RDs occur in myopic eyes): degeneration is more common; also at risk from macular holes
- Vitreous loss during cataract surgery or Nd:YAG laser capsulotomy
- Trauma
Distribution of breaks (~60% superotemporal, 15% superonasal, 15% inferotemporal, 10% inferonasal). ~50% of eyes with RD have more than one break, usually within 90° of each other.
2. Tractional Retinal Detachment (TRD)
Pathogenesis: Progressive contraction of fibrovascular membranes over large areas of vitreoretinal adhesion pulls the retina off the RPE — without a retinal break. PVD in these eyes is gradual and incomplete (unlike the acute PVD in RRD).
Causes:
- Proliferative diabetic retinopathy (most common)
- Retinopathy of prematurity (ROP)
- Sickle cell retinopathy
- Penetrating posterior trauma
- Proliferative vitreoretinopathy (PVR)
- Toxocariasis, FEVR
Types of traction:
- Tangential: epiretinal membrane contraction → retinal puckering
- Anteroposterior: fibrovascular membranes from posterior retina to vitreous base
- Bridging: membranes between different retinal areas, pulling them together
3. Exudative (Serous) Retinal Detachment
Pathogenesis: Subretinal fluid accumulates without a break or traction — leakage overwhelms the RPE pumping mechanism. Fluid accumulates under the retina from choroidal or retinal vascular sources.
Causes:
| Category | Examples |
|---|---|
| Neoplastic | Choroidal melanoma, metastases, choroidal hemangioma, retinoblastoma |
| Inflammatory | Vogt-Koyanagi-Harada (VKH) syndrome, posterior scleritis, sympathetic ophthalmia |
| Vascular | Coats disease, CNV, malignant hypertension, preeclampsia |
| Congenital | Optic pit, morning glory, choroidal coloboma |
| Iatrogenic | Post RD surgery, panretinal photocoagulation |
| Idiopathic | Uveal effusion syndrome, central serous chorioretinopathy (bullous) |
Key pearl: An intraocular tumour should be considered the cause of an exudative RD until proved otherwise. — Kanski's Clinical Ophthalmology
Clinical Features
Symptoms (RRD)
| Symptom | Explanation |
|---|---|
| Flashing lights (photopsia) | Vitreoretinal traction with acute PVD |
| Floaters (vitreous haemorrhage or pigment) | "Tobacco dust" = pigment in vitreous after RPE disruption |
| Curtain/shadow in visual field | Accumulating SRF detaching peripheral retina |
| Central vision loss | Macular involvement by SRF |
- ~60% of RRD patients report premonitory photopsia and floaters
- A lower field defect (superior break) is noticed more quickly than upper defect
- Field defect may partially resolve in the morning (spontaneous overnight reabsorption of SRF), then return during the day
Tractional RD: Photopsia and floaters are typically absent (no acute PVD); visual field loss progresses slowly and may be stable for months–years.
Exudative RD: Photopsia absent (no vitreoretinal traction); floaters if associated vitritis; both eyes may be involved simultaneously (e.g., VKH).
Signs
Rhegmatogenous RD
- Convex, corrugated, opaque retinal surface (retinal oedema)
- Mobile retina with shifting SRF
- Loss of choroidal pattern beneath elevated retina
- Retinal break(s) identifiable on indirect ophthalmoscopy
- Tobacco dust (Shafer sign) — pigmented cells in anterior vitreous (pathognomonic for break/RD)
- Vitreous haemorrhage in ~10%
Tractional RD
- Concave configuration, smooth surface (no break)
- Severely reduced retinal mobility; no shifting fluid
- Fibrovascular/vitreous membranes visible exerting traction
- Detachment rarely extends to ora serrata
- May become convex (combined TRD/RRD) if a new break develops in the tractional retina
Exudative RD
- Convex, smooth (not corrugated) surface
- Shifting subretinal fluid — hallmark: upright position → SRF collects inferiorly; supine → fluid shifts posteriorly detaching superior retina
- No retinal break
- Detachment typically does not extend to ora serrata
- Underlying tumour or choroidal pathology may be visible
- "Leopard spots" of RPE clumping after resolution
Fundus Images
Bullous exudative RD with subretinal fluid
RRD with PVR — pre and post vitrectomy/scleral buckle
Lincoff's Rules (SRF Distribution → Predict Break Location)
| SRF pattern | Likely break location |
|---|---|
| Shallow inferior RD, SRF higher on temporal side | Inferior temporal break |
| Inferior RD with equal fluid levels | Break at 6 o'clock |
| Bullous inferior RD | Break above the horizontal meridian |
| Subtotal RD with superior wedge of attached retina | Peripheral break nearest the highest border |
| SRF crosses vertical midline superiorly | Break near 12 o'clock |
The quadrant of the visual field defect is in the opposite quadrant to the primary break.
Longstanding RD Features
- Retinal thinning (atrophy) — do not misdiagnose as retinoschisis
- Intraretinal cysts (after ~1 year; usually resolve post-surgery)
- Subretinal demarcation lines ("high water marks") — RPE proliferation at flat–detached junction; appear after ~3 months
Proliferative Vitreoretinopathy (PVR) — Major Complication
PVR = epiretinal and subretinal membrane formation by RPE cells and retinal glial cells → tangential retinal traction → fixed folds → funnel-shaped detachment.
| Grade | Features |
|---|---|
| A (Minimal) | Diffuse vitreous haze, tobacco dust, pigmented clumps |
| B (Moderate) | Wrinkling of inner retinal surface, rolled break edges |
| C (Severe) | Fixed retinal star folds, full-thickness folds, funnel RD |
PVR most commonly follows surgery for RRD or penetrating injury.
Differential Diagnosis
| Condition | Key Distinguishing Feature |
|---|---|
| Degenerative retinoschisis | Bilateral, smooth, bullous, usually inferotemporal; no vitreous pigment or haemorrhage; inner/outer retinal holes may be present |
| X-linked retinoschisis | Stellate foveal petaloid changes; NFL separation; no RD initially |
| Choroidal detachment | Orange-brown, immobile, 4-lobed, extends anterior to ora serrata, low IOP, limited by vortex veins posteriorly |
| FEVR | Hereditary, asymmetric, no prematurity history |
Workup
- Dilated indirect ophthalmoscopy with scleral depression — both eyes (fellow eye ~10% risk)
- B-scan ultrasound — if media opacities prevent fundus view
- OCT — tractional membranes, macular involvement, retinoschisis vs RD
- IVFA — exudative RD: identify leakage source
- Systemic workup — if exudative RD (malignancy screen, inflammatory markers, BP)
Treatment
Rhegmatogenous RD
| Urgency | Situation | Action |
|---|---|---|
| Emergency | Macula-on (threatened) | Surgery ASAP |
| Urgent (within 72h) | Macula-off, recent onset | Better outcomes if within 72 hours |
| Semi-urgent (≤7 days) | Chronic macula-off | Within 1 week if possible |
Surgical options:
1. Pneumatic Retinopexy (outpatient, minimally invasive)
- Intravitreal gas bubble (SF₆ or longer-acting C₃F₈) + cryotherapy or laser
- Seals the break and tamponades the retina
- Reserved for uncomplicated RD with a small break or cluster of breaks <2 clock hours in the upper two-thirds of the peripheral retina
- Less invasive but lower success rates than scleral buckling
2. Scleral Buckling
- Silicone explant sutured to the sclera creates an inward indentation (buckle)
- Closes retinal breaks by apposing RPE to neurosensory retina and relieves vitreoretinal traction
- Configurations: radial, segmental, circumferential, or encircling
- Combined with cryotherapy to the break
- Preferred for post-traumatic dialysis detachments
3. Pars Plana Vitrectomy (PPV)
- Internal approach; removes vitreous, relieves traction
- Used for complex RRD, PVR, giant retinal tears, vitreous haemorrhage obscuring the break
- May use silicone oil or gas tamponade
- Also the primary approach for TRD (diabetic)
Tractional RD
- Depends on location (macular threat), etiology, and fellow eye status
- Surgical repair by vitrectomy with membrane peeling
Exudative RD
- Treat the underlying cause — detachment typically resolves
- Systemic corticosteroids for inflammatory causes (VKH, posterior scleritis)
- Anti-VEGF or laser for vascular causes (CNV, Coats)
- Radiation/surgical resection for choroidal tumours
Follow-Up
- All RRD patients require urgent referral to a retina specialist
- Post-op schedule: 1 day → 1 week → 1 month → 2–3 months → every 6–12 months
- Fellow eye must be examined and treated for predisposing lesions (lattice degeneration, tears)
- Serous and TRD follow-up depends on underlying etiology
— Kanski's Clinical Ophthalmology, 10e; Wills Eye Manual; Robbins & Kumar Pathologic Basis of Disease
Retinal detachment post graduate level
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Retinal Detachment — Postgraduate Level
1. Anatomy & Pathophysiological Basis
The neurosensory retina (NSR) and retinal pigment epithelium (RPE) are derived from the two layers of the optic cup and are not truly adherent — they are apposed within a potential subretinal space. Retinal attachment is maintained by:
- Active RPE fluid transport (pumping fluid from subretinal to choroidal space)
- Interdigitation of photoreceptor outer segments with RPE microvilli
- Interphotoreceptor matrix (IPCM) proteins
- Intraocular pressure maintaining apposition
- Vitreous face providing gentle support posteriorly
Any mechanism that overwhelms these forces — a retinal break + traction, fibrovascular traction, or RPE/choroidal fluid barrier failure — results in retinal detachment.
2. Classification
2.1 Rhegmatogenous Retinal Detachment (RRD)
Epidemiology: ~1 in 10,000/year. Fellow eye eventually affected in ~10%. >40% occur in myopic eyes.
Triad required for RRD:
- Full-thickness retinal break (tear or hole)
- Vitreous liquefaction (synchysis)
- Vitreoretinal traction
Without at least partial liquefaction and traction, a break almost never causes RD.
Types of Retinal Breaks
| Type | Mechanism | Risk of RD |
|---|---|---|
| Horseshoe (flap/U) tear | Acute PVD — vitreous traction avulses a flap | HIGH |
| Operculated hole | Flap fully avulsed; traction released | Moderate |
| Atrophic round hole | Focal retinal thinning; no acute PVD | Low (slow onset) |
| Dialysis | Circumferential tear at ora serrata; trauma or idiopathic | Variable |
| Giant retinal tear | Break ≥3 clock hours (90°); posterior flap inverts | Very high |
| Macular hole | Tangential traction on fovea; RD confined to posterior pole (especially high myopia) | Low except in myopia |
Predisposing Lesions
- Lattice degeneration — most important; peripheral atrophic thinning with overlying vitreous liquefaction and firm margin adhesion; atrophic holes within lattice + horseshoe tears at margin
- Snailtrack degeneration — silvery-white frost; atrophic holes more common than in lattice
- Retinoschisis — splitting within the retina; outer leaf holes + inner leaf holes → RD risk
- Pavingstone (cobblestone) degeneration — focal RPE/choroidal atrophy; very low RD risk
- Vitreous base avulsion — traumatic
- High myopia — thin retina, early PVD, large vitreous cavity
Subretinal Fluid (SRF) Dynamics — Modified Lincoff's Rules
SRF spread governed by: (a) gravity, (b) ora serrata/optic nerve as anatomical limits, (c) break location.
| SRF pattern | Predicted break location |
|---|---|
| Shallow inferior RD, SRF higher temporally | Inferior temporal break |
| Inferior RD, equal fluid levels | Break at 6 o'clock |
| Bullous inferior RD | Break above the horizontal meridian |
| Upper nasal break | SRF revolves around optic disc, rises temporally to the level of the break |
| Subtotal RD with superior wedge of attached retina | Break at periphery nearest the highest border |
| SRF crosses vertical midline superiorly | Break near 12 o'clock; lower RD edge = side of break |
The quadrant of the visual field defect is in the opposite quadrant to the primary break.
Break distribution in eyes with RRD: 60% superotemporal, 15% superonasal, 15% inferotemporal, 10% inferonasal. ~50% of eyes have >1 break, usually within 90° of each other.
2.2 Tractional Retinal Detachment (TRD)
Mechanism: Progressive contraction of fibrovascular epiretinal/subretinal membranes over large areas of vitreoretinal adhesion. PVD in TRD is gradual and incomplete (unlike the acute PVD of RRD) — plasma constituents leak from fibrovascular networks adherent to the posterior vitreous into the gel, which contracts.
Causes
- Proliferative diabetic retinopathy (PDR) — most common
- Retinopathy of prematurity (ROP)
- Sickle cell retinopathy
- Penetrating posterior trauma
- Proliferative vitreoretinopathy (PVR) post-surgery
- Toxocariasis, FEVR
Types of Traction in PDR
| Type | Description |
|---|---|
| Tangential | Epiretinal membrane contraction → retinal puckering, vessel distortion |
| Anteroposterior | Fibrovascular membranes from posterior retina to vitreous base |
| Bridging (trampoline) | Membranes between vascular arcades, pulling them together |
Key distinguishing signs
- Concave configuration (vs. convex in RRD/exudative)
- No retinal break
- Severely reduced retinal mobility; no shifting fluid
- Rarely extends to ora serrata
- If a tractional break develops → combined TRD/RRD (now convex, more urgent)
2.3 Exudative (Serous) Retinal Detachment
Mechanism: Fluid accumulates in the subretinal space without break or traction — RPE fluid transport overwhelmed by excess leakage from inflamed, neoplastic, or dysregulated choroidal/retinal vasculature.
Causes
| Category | Specific conditions |
|---|---|
| Neoplastic | Choroidal melanoma (commonest), metastases, choroidal hemangioma, retinoblastoma, multiple myeloma, retinal capillary hemangioblastoma |
| Inflammatory | Vogt-Koyanagi-Harada (VKH), posterior scleritis, sympathetic ophthalmia |
| Vascular | Coats disease, CNV, malignant hypertension, preeclampsia |
| Congenital | Optic pit, morning glory, choroidal coloboma |
| Iatrogenic | Post-RD surgery, panretinal photocoagulation |
| Idiopathic | Uveal effusion syndrome, bullous CSCR |
An intraocular tumour must be considered the cause of exudative RD until proved otherwise. — Kanski's Clinical Ophthalmology
Hallmark: Shifting subretinal fluid — SRF redistributes with gravity; inferior detachment in upright position, posterior/superior detachment in supine. Surface is smooth (not corrugated). Detachment does not extend to ora serrata.
3. Clinical Assessment
Symptoms
| Feature | RRD | TRD | Exudative |
|---|---|---|---|
| Photopsia | Present (~60%) | Absent | Absent |
| Floaters | Present | Absent | Present if vitritis |
| Curtain/field defect | Sudden onset, progresses | Slow, may be stable for months | Sudden to rapid |
| Morning improvement | Common (SRF reabsorbed overnight) | No | No |
| Bilateral | Rare | Uncommon | Common (VKH, hypertension) |
Signs
| Feature | RRD | TRD | Exudative |
|---|---|---|---|
| Retinal configuration | Convex, corrugated, opaque | Concave, smooth | Convex, smooth |
| Retinal mobility | Moderate | Severely reduced | Highly mobile |
| Shifting SRF | Present | Absent | Present (pathognomonic) |
| Retinal break | Present | Absent | Absent |
| Ora serrata extension | Extends to ora | Rarely reaches ora | Does not reach ora |
| Tobacco dust (Shafer sign) | Pathognomonic | Absent | Absent |
Fundus Images
Horseshoe retinal tear causing RRD
Macula-on RRD with superior horseshoe tear
Macula-off total RRD
4. Longstanding RD — Specific Features
- Retinal thinning (atrophy) — can mimic retinoschisis but has different mobility
- Intraretinal cysts — after ~1 year; tend to resolve post-surgery
- Demarcation lines ("high water marks") — RPE cell proliferation at junction of flat and detached retina; develop ~3 months after onset; represent increased adhesion but do not invariably limit SRF spread
- Macular pseudohole — impression of macular hole due to thin foveal retina when the posterior pole is detached; distinguish from true macular hole (important as macular holes cause RD in high myopia)
5. Proliferative Vitreoretinopathy (PVR) — The Major Complication
PVR is the principal cause of failed RD surgery and of late re-detachment. It results from epiretinal and subretinal membrane formation — by RPE cells, Müller cells, and fibrous astrocytes — that has migrated through retinal breaks and the vitreous, subsequently contracting to produce tangential retinal traction and fixed folds.
PVR Grading (Retina Society Classification)
| Grade | Features |
|---|---|
| A (Minimal) | Diffuse vitreous haze ("tobacco dust"), vitreous pigment clumps, pigmented clusters on inferior retina |
| B (Moderate) | Wrinkling of inner retinal surface; decreased vitreous gel mobility; rolled edges of retinal breaks; vascular tortuosity; retinal stiffness. Epiretinal membranes usually not clinically visible |
| C (Marked) | Rigid full-thickness retinal folds, often star-shaped; heavy vitreous condensation and strands. Divided into anterior (CA) and posterior (CP) based on equatorial location; extent expressed in clock hours |
| Advanced C | Gross reduction of retinal mobility; retinal shortening; funnel-shaped detachment |
PVR — Surgical Management
Goals: Release transvitreal traction (vitrectomy) + tangential surface traction (membrane dissection) → restore retinal mobility → allow break closure.
- Localized star folds: Remove central plaque of epiretinal membrane using picks or scissors; peel from retinal surface
- Internal limiting membrane (ILM) peeling in advanced PVR improves surgical success
- Relaxing retinotomy (peripheral or posterior) may be required for severe retinal shortening
- Perfluorocarbon liquid (PFCL) used intraoperatively to stabilize retina
- Replaced with long-acting gas (C₃F₈) or silicone oil for tamponade
PVR Fundus Images
6. Surgical Options for RRD
6.1 Pneumatic Retinopexy
Outpatient "office-based" procedure. Intravitreal gas bubble + cryotherapy or laser photocoagulation to seal the break.
Gases used:
- SF₆ (sulfur hexafluoride): doubles volume at 100%; lasts 10–14 days
- C₂F₆ (perfluoroethane): triples volume; lasts 30–35 days
- C₃F₈ (perfluoropropane): quadruples volume; lasts ~8 weeks (longest-acting)
Strict selection criteria:
- Single break or cluster of breaks spanning <2 clock hours
- Located in the upper two-thirds of the peripheral retina
- No significant PVR
Limitation: Lower anatomical success rates than scleral buckling.
Contraindication: Air travel until gas bubble fully absorbed (risk of acute IOP rise from gas expansion at altitude).
6.2 Scleral Buckling (External Surgery)
A silicone explant sutured to the external sclera creates an inward indentation (buckle) that:
- Closes retinal breaks by apposing RPE to NSR
- Reduces dynamic vitreoretinal traction at the break
- Relieves the vitreous base traction anteriorly
Explant types: Soft or hard silicone; sponge (segmental) or solid (encircling/circumferential)
Configuration choices: Radial, segmental, circumferential, or encircling — determined by break size, number, and configuration.
Technique steps: Peritomy → localization of breaks → cryoretinopexy → explant suturing → check buckle height → SRF drainage (if needed) → gas injection (if needed).
Always indicated for: Post-traumatic dialysis detachment.
Scleral buckling intraoperative photographs:
Common complications:
- Buckle infection/exposure/extrusion
- Diplopia (extraocular muscle tethering)
- Choroidal effusion
- Anterior segment ischaemia (encircling buckle)
- Induced myopia (encircling buckle increases axial length)
- Fish-mouthing of large U-tears after buckling
- Refractive change
Causes of failure:
- PVR — most common cause of late failure
- Failure to close all breaks
- Development of new breaks
6.3 Pars Plana Vitrectomy (PPV) — Internal Surgery
Modern gauge systems:
- 20-gauge (0.9 mm) — conventional
- 23-gauge, 25-gauge, 27-gauge — sutureless transconjunctival microincision vitrectomy (MIVS); now standard of care; shorter operative time, less trauma, faster rehabilitation
Basic PPV steps (for RD):
- Three-port entry: infusion cannula (IOP maintenance), light pipe (illumination), cutter
- Core vitrectomy → posterior vitreous detachment (PVD) induction
- Triamcinolone acetonide to stain vitreous for complete removal
- SRF drainage (internal via break or external via needle)
- Endolaser photocoagulation around all breaks
- Fluid–air exchange → gas or silicone oil tamponade
- Postoperative positioning to apply tamponade against breaks
Tamponading agents:
| Agent | Properties | Duration | Indications |
|---|---|---|---|
| Air | Non-expanding | Days | Short tamponade |
| SF₆ | 2× expansion at 100% | 10–14 days | Simple superior RD |
| C₂F₆ | 3× expansion | 30–35 days | Complex RD |
| C₃F₈ | 4× expansion | ~8 weeks | PVR, inferior breaks |
| Silicone oil | Non-expanding, permanent until removed | Months–years (then removed) | PVR, inferior RD, monocular patients, inability to posture |
| Heavy silicone oil | Higher specific gravity than water | Permanent until removed | Inferior breaks, PVR with inferior predominance |
| PFCL (perfluorocarbon liquid) | Intraoperative use only; heavier than water; flattens posterior retina | Intraoperative | Stabilization during membrane peeling, giant tears |
PPV indications over scleral buckle:
- PVR (any grade C or worse)
- Giant retinal tear (≥3 clock hours / 90°)
- Large posterior breaks
- Vitreous haemorrhage obscuring the break
- Diabetic TRD
- Post-traumatic RD
- Aphakic/pseudophakic RD with multiple/posterior breaks
- Previous failed scleral buckle
PPV-specific complications:
- Silicone oil glaucoma: Early → pupillary block (prevented by inferior Ando iridectomy in aphakic eyes); Late → emulsified oil in trabecular meshwork
- Cataract: Gas-induced (transient feathering of posterior subcapsular lens); silicone oil-induced (almost universal in phakic eyes — develop in virtually all cases)
- Gas-related IOP rise: Overfill or air travel
- Band keratopathy: With extended silicone oil
- Endophthalmitis: Rare but potential; slightly higher concern with small-gauge
- Intraocular gas expansion: Risk with nitrous oxide anaesthesia (must be avoided)
7. Specific Surgical Scenarios
Post-Cataract Surgery RRD
RRD after uncomplicated phacoemulsification is uncommon. Pre-operative risk factors: lattice degeneration, retinal breaks, high myopia. Key intraoperative risk: vitreous loss. PPV is usually employed.
Giant Retinal Tear (GRT)
Break ≥90° (3 clock hours). The posterior retinal flap tends to invert (fold posteriorly), preventing self-sealing. PFCL used intraoperatively to unfold and stabilize the flap, then endolaser followed by gas or silicone oil tamponade.
Macular Hole RD (High Myopia)
Posterior staphyloma + foveal thinning → macular hole → shallow RD confined to posterior pole. Initial SRF around hole. PPV + ILM peeling + gas (C₃F₈) face-down positioning.
8. Visual Prognosis
| Factor | Better prognosis | Worse prognosis |
|---|---|---|
| Macular status | Macula-on | Macula-off |
| Timing (macula-off) | Operated within 72 hours | Chronic, >7–10 days |
| Break location | Inferior, peripheral | Posterior, zone I |
| PVR | Absent | Grade C or higher |
| Duration of detachment | Short | Long (>1 year → photoreceptor atrophy) |
| Fellow eye | Good vision (motivates early treatment) | — |
Urgent surgery is needed in an acute progressive RD if the macula is threatened. Even if the macula is off, results are better if surgery is done within 72 hours. — Kanski's Clinical Ophthalmology
Visual outcomes for macula-off detachments do not change significantly if surgery is performed within 7–10 days of onset — beyond that, outcomes deteriorate. — Wills Eye Manual
9. Investigative Workup
| Investigation | Indication |
|---|---|
| Dilated indirect ophthalmoscopy + scleral depression | All cases; both eyes examined |
| B-scan ultrasound | Media opacity (VH, cataract, corneal scar) preventing fundal view |
| OCT | Macular status (on/off, pseudohole vs true hole); tractional membranes; subretinal fluid confirmation |
| IVFA | Exudative RD — identify leakage point; CNV characterisation |
| Fundus drawing / wide-field photography | Documentation, surgical planning |
| Systemic workup | Exudative RD → malignancy screen, autoimmune markers (ANA, chest XR for sarcoid/TB), BP |
10. Three Laws of Failed RD Surgery
The three commonest causes of failed retinal detachment surgery are: proliferative vitreoretinopathy, failure to close all breaks, and the development of new breaks. — Kanski's Clinical Ophthalmology, 10e
Sources: Kanski's Clinical Ophthalmology, 10e; Wills Eye Manual, 8e; Robbins & Kumar Pathologic Basis of Disease, 10e
Minimally invasive glaucoma surgeries
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