Iris Retraction Syndrome

Iris Retraction Syndrome (often shortened to IRS) is a rare eye condition. In plain terms, it means the colored part of the eye (the iris) bends backward toward the lens, making the front chamber of the eye look abnormally deep. This usually happens when fluid pressures inside the eye become unbalanced—most often because there’s a retinal detachment at the back of the eye and/or inflammation that lowers fluid production (hypotony). In many classic cases, the pupil is “sealed” to the lens by sticky adhesions (posterior synechiae), so fluid can’t pass forward normally; this “seal” contributes to the backward bowing of the iris. Breaking that seal or treating the inflammation can let the iris spring back to a normal shape. PubMedPubMed Central

Iris Retraction Syndrome means the iris bows backward in a concave shape and sits against the front of the lens. Because of this, the space in front of the iris (the anterior chamber) looks very deep. At the same time, the pupil is usually “sealed” all the way around by sticky scar tissue (posterior synechiae), so fluid cannot flow through the pupil normally—this is called complete pupillary block. Most reported patients also have retinal detachment and hypotony (abnormally low eye pressure). The low pressure, inflammation, and fluid shifts from the retinal detachment can create a suction-like pull behind the iris, while the scar tissue keeps the pupil closed. The result: the iris is dragged backward, the front chamber deepens, and the eye becomes inflamed and blurry. This pattern is the opposite of “iris bombé,” where the iris bows forward. EyeWikiPubMed Central

Doctors first pulled these ideas together in a landmark 1984 report that showed: (1) a stuck pupil (seclusion) is common, (2) the iris shape can flip back to normal when that seclusion is released, and (3) the configuration can toggle between “iris bombé” (bulging forward) and “iris retraction” (bending backward) when doctors start and stop drugs that reduce aqueous production (like carbonic anhydrase inhibitors). That work proposed a hydrodynamic explanation: more fluid is being removed behind the iris than the ciliary body is making, so pressure drops behind the iris and the iris bows backward. PubMed

Since then, case reports have broadened the picture. IRS still most often rides along with rhegmatogenous retinal detachment (RRD) and hypotony, but it can appear after eye surgery, alongside severe uveitis, or—rarely—even without hypotony when a contracting cyclitic membrane behind the iris pulls it backward. There are also modern reports of cancer immunotherapy (e.g., nivolumab) triggering uveitis, hypotony, and then IRS. PubMed CentralSpringerLink

Iris Retraction Syndrome is a shape problem of the iris caused by a pressure problem inside the eye.

  • In a healthy eye, fluid made by the ciliary body flows from the back chamber, through the pupil, into the front chamber, and drains away, keeping pressures balanced.

  • In IRS, something blocks or redirects that flow (often a stuck pupil and a leaky back of the eye from a retinal detachment). When more fluid leaves the back of the eye than the eye makes, the pressure behind the iris drops, the iris gets sucked backward against the lens, and the front chamber looks very deep.

  • Treating the cause (e.g., retinal detachment, severe inflammation) and releasing the stuck pupil often lets the iris move forward to its normal shape. PubMedPubMed Central

Key ideas to keep in mind (in plain words):

  • “Back-bowing” = iris curves backward toward the lens.

  • “Stuck pupil” (posterior synechiae) = iris glued to the lens; fluid can’t pass through the pupil normally.

  • “Hypotony” = eye pressure is too low; this is common in IRS and is a big clue.

  • “Toggle with drops” = when doctors suppress fluid production, some eyes flip from forward bulging to backward bowing—this supports the pressure-balance explanation. PubMed

It is not the same as the concave iris seen in pigment dispersion or some surgical flow problems, where pressure is usually normal or high and the problem is mechanical rubbing or reverse flow during procedures. In IRS, hypotony and retinal detachment/inflammation are the usual hallmarks, and pressure is often low. PubMed Central


Types

Because IRS is a final common iris shape that several problems can cause, it helps to group cases by the main driver:

  1. RRD-associated IRS (classic type)
    The most common pattern: a rhegmatogenous retinal detachment plus a stuck pupil and low pressure (hypotony) produce iris back-bowing. Often toggles with aqueous-suppressing drops. PubMed

  2. Non-rhegmatogenous detachment–associated IRS (exudative/serous RD)
    Less common. Some eyes with serous/exudative RD show iris retraction that can improve after dilation even before the retina is reattached, suggesting inflammation-mediated pressure changes, not only an open retinal break. Lippincott Journals

  3. Uveitis / cyclitic-membrane IRS
    Severe inflammation can shut down aqueous production (hypotony) or create a contracting membrane behind the iris that pulls it backward—even, rarely, without hypotony. SpringerLink

  4. Post-operative IRS
    Reported after cataract surgery or vitrectomy when a secluded pupil and an unrecognized RD are present. Treating the RD and releasing the pupil resolve the iris shape. PubMed

  5. Drug-associated IRS (via inflammation/hypotony)
    Immune-checkpoint inhibitors (e.g., nivolumab) can trigger uveitis, hypotony, and IRS; stopping the drug and fixing the pupil/retina can normalize the iris. PubMed Central

  6. With pupillary seclusion vs. without
    Most classic cases have 360° posterior synechiae (seclusion), but a minority lack seclusion and show other mechanisms on imaging. Lippincott Journals

  7. Unilateral vs. bilateral
    Usually one eye, but bilateral cases occur—especially when a systemic trigger (like immunotherapy-related uveitis) is involved. PubMed Central

  8. Acute vs. chronic
    Acute presentations may show quick toggling of iris shape; chronic ones often have choroidal detachment, PVR, and guarded prognosis. PubMed Central

  9. Hypotonous vs. normotensive (rare)
    Most are low-pressure eyes; normotensive cases suggest a tractional (cyclitic membrane) component. SpringerLink

  10. With choroidal detachment vs. without
    Choroidal detachment commonly travels with hypotony and chronic RD in IRS. PubMed Central


Causes

Think of these as situations that create the pressure imbalance, pupil seclusion, or traction that makes the iris bow backward:

  1. Rhegmatogenous retinal detachment (RRD) — the classic driver; fluid escapes through a retinal break faster than it’s made, dropping posterior pressure. PubMed

  2. Complete posterior synechiae (pupillary seclusion) — the pupil is sealed to the lens, trapping fluid compartments and setting up abnormal flow. PubMed

  3. Chronic uveitis — reduces aqueous production (hypotony), makes adhesions, and thickens fluids. PubMed Central

  4. Cyclitic membrane formation — a fibrous sheet behind the iris can physically pull the iris backward; sometimes present even when pressure isn’t low. SpringerLink

  5. Choroidal detachment/effusion with RD — deepens hypotony and adds to the pressure gradient. PubMed Central

  6. Proliferative vitreoretinopathy (PVR) — long-standing RD with cellular flow can support the hydrodynamic “suction” effect and inflammation. PubMed

  7. Over-suppression of aqueous (e.g., carbonic anhydrase inhibitors) in a detached eye — can flip eyes from bombé to retraction by pushing the balance toward posterior fluid egress. PubMed

  8. Post-cataract surgery with unrecognized RD and seclusion — the surgical history plus RD/seclusion reproduces the same setup. PubMed

  9. Post-vitrectomy in a secluded pupil — similar mechanism through altered flow and RD. PubMed Central

  10. Open-globe/posterior segment trauma — may lead to RD, hypotony, seclusion, and retraction. PubMed

  11. Exudative/serous retinal detachment — pressure dynamics shift without a retinal break; some cases improve after dilation before reattachment. Lippincott Journals

  12. Drug-induced uveitis (e.g., checkpoint inhibitors) — can cause hypotony and IRS. PubMed Central

  13. Severe inflammatory flares (e.g., HLA-B27 uveitis) — hypotony/seclusion from intense inflammation. (Mechanistic extension from uveitis literature.)

  14. Posterior scleritis with serous RD — can drive hypotony and posterior fluid shifts (rare but plausible inflammatory pathway).

  15. Chronic angle changes with very wide open angles in hypotony — a sign more than a cause; shows how pressure gradients reshape the anterior segment. PubMed Central

  16. Long-standing choroidal swelling (effusions) — worsens hypotony dynamics. PubMed Central

  17. Ciliary body shutdown (e.g., severe inflammation, ischemia) — directly lowers aqueous production. SpringerLink

  18. Cyclodialysis cleft — a detachment of the ciliary body that creates an abnormal outflow pathway and hypotony; UBM can reveal this. Lippincott Journals

  19. Secondary traction from posterior membranes (non-cyclitic) — tractional forces can contribute to posterior bowing in complex RD/PVR. PubMed Central

  20. Combined mechanisms — many eyes have more than one factor (RD + uveitis + seclusion), which is why imaging and stepwise management help. PubMed Central


Symptoms and signs

  1. Painless vision loss — often the main complaint when an RD is present. PubMed

  2. A noticeably deep front chamber — the eye can look unusually deep on slit lamp; clinicians see a wide-open angle on gonioscopy. PubMed Central

  3. Poorly reactive, often small pupil — because the iris is stuck to the lens around the entire edge. PubMed Central

  4. Photophobia (light sensitivity) — due to uveitis. PubMed Central

  5. Redness and tearing — from surface irritation and inflammation. PubMed Central

  6. Corneal edema / Descemet folds — hypotony and inflammation can make the cornea look steamy or wrinkled. PubMed Central

  7. Heterochromia (iris color change) — protein-rich fluid in the front can make the iris look different in color (often greenish). PubMed Central

  8. Very low eye pressure (hypotony) — a frequent finding that fits the mechanism. PubMed Central

  9. Signs of posterior synechiae — the iris edge is stuck 360° to the lens (seen at the slit lamp). PubMed Central

  10. Inflammatory “cell and flare” in the anterior chamber — tiny white cells/protein seen by the beam at slit lamp. PubMed Central

  11. Choroidal detachment on exam or ultrasound — common when hypotony is chronic. PubMed Central

  12. Retinal detachment — sometimes total; frequently present on dilated fundus exam or B-scan. PubMed Central

  13. Toggle phenomenon — shape may flip between bombé and retraction with aqueous-suppressing meds. PubMed

  14. Floaters or visual field defects — from the detachment itself.

  15. Later angle-closure attack (iris bombé) — if the configuration flips and blocks the angle, the eye can become painful and pressurized (a known complication). PubMed Central


Diagnostic tests

(Grouped the way a busy clinic thinks: simple bedside checks, hands-on maneuvers, labs for causes, electrical tests for retinal function, and imaging to map the anatomy.)

A) Physical exam tests (fast, non-invasive checks)

  1. Best-corrected visual acuity (BCVA)
    Tells you how much vision is lost and sets a baseline for later. In IRS with RD, vision is often markedly reduced.

  2. Pupil exam with light and near
    A small, poorly reactive pupil suggests posterior synechiae secluding the pupil. Observe the iris edge for a “stuck” look.

  3. Tonometry (Goldmann or handheld)
    Low pressure is a major clue in IRS. If pressure is normal, think about tractional mechanisms (e.g., cyclitic membrane). PubMed CentralSpringerLink

  4. Slit-lamp biomicroscopy
    Shows deep anterior chamber, cell/flare, corneal edema, and posterior synechiae—the core, front-of-the-eye signs. PubMed Central

  5. Gonioscopy
    Reveals a very wide open angle (peripheral iris pulled back) in IRS; helps distinguish from angle-closure causes. PubMed Central

  6. Dilated fundus exam (indirect ophthalmoscopy)
    Looks for retinal breaks, detachment, choroidal detachment, and PVR. If the view is hazy, proceed to B-scan. PubMed Central

B) Manual or office maneuvers (what you do to the eye to learn more)

  1. Pharmacologic dilation test
    If you can break posterior synechiae (using strong mydriatics/cycloplegics), the posterior chamber reforms and the iris may move forward, supporting an IRS mechanism with seclusion. PubMed Central

  2. Observing the “toggle” with aqueous-suppressant drops
    In classic reports, starting aqueous suppressants (e.g., acetazolamide) can flip bombé into retraction; stopping can flip it back—strong real-world evidence of the pressure-balance mechanism. PubMed

  3. Scleral depression during indirect exam
    Helps you find retinal breaks that explain the detachment and the pressure imbalance.

  4. Digital palpation (very gentle)
    A crude check reinforcing very soft globe (hypotony) when a tonometer isn’t available (not a replacement for tonometry).

  5. Response to cycloplegia
    Cycloplegic drops reduce ciliary spasm and open the pupil; improvement in iris contour supports a seclusion/inflammation component. PubMed Central

C) Lab and pathological tests (to uncover inflammatory/infectious drivers)

  1. Complete blood count (CBC) with differential
    Looks for leukocytosis/eosinophilia if infection/allergy contributes to the uveitis picture.

  2. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
    Gauge systemic inflammation that can match ocular uveitis.

  3. Syphilis serology (RPR/VDRL with confirmatory treponemal test)
    Always screen in unexplained uveitis; syphilis can mimic many eye diseases.

  4. Tuberculosis screening (IGRA, chest imaging as indicated)
    TB can drive uveitis and hypotony in certain settings.

  5. Sarcoidosis markers (ACE, lysozyme) ± chest imaging
    Sarcoid uveitis can lead to synechiae and hypotony.

  6. Autoimmune work-up (e.g., HLA-B27, ANA, RF, others as history suggests)
    Identifies systemic inflammatory disease linked to severe uveitis.

  7. Aqueous/vitreous sampling in atypical cases
    PCR or cytology when you suspect unusual infections or masquerade (e.g., lymphoma) alongside RD/uveitis patterns.

D) Electrodiagnostic tests (for retinal function when the view is poor or prognosis is unclear)

  1. Full-field electroretinogram (ffERG)
    Estimates global retinal function when media are cloudy or RD is present—useful for prognosis after repair.

  2. Multifocal ERG (mfERG)
    Samples macular function regionally; reduced signals suggest macular compromise in chronic RD.

  3. Electro-oculogram (EOG)
    Assesses RPE function, relevant in long-standing detachments where RPE “pump” behavior matters.

  4. Visual evoked potentials (VEP)
    Checks optic pathway integrity—useful if vision remains poor after reattachment and iris normalization.

E) Imaging tests (the heavy lifters for anatomy and mechanism)

  1. B-scan ultrasonography
    When the fundus view is blocked, B-scan shows retinal detachment, choroidal detachment, and membranes—cornerstones in IRS work-ups. PubMed Central

  2. Ultrasound biomicroscopy (UBM)
    High-resolution pictures of the iris–ciliary body region show posterior bowing, peripheral “step” or retraction, cyclodialysis clefts, and ciliary body detachment. It is one of the best tools to confirm the anterior-segment geometry in IRS. PubMed CentralLippincott Journals

  3. Anterior-segment OCT (AS-OCT)
    Non-contact confirmation of back-bowing and deep chamber, and documentation of change after dilation or synechiolysis. PubMed CentralLippincott Journals

  4. Macular OCT
    Shows hypotony maculopathy, subretinal fluid, and later tracks recovery after RD repair. PubMed Central

  5. Widefield color fundus photography
    Documents extent of detachment and PVR for surgical planning.

  6. Fluorescein angiography (FA)
    Highlights leakage from inflammation and optic disc edema in hypotony; helps separate inflammatory/exudative patterns. PubMed Central

  7. Indocyanine-green angiography (ICGA)
    Assesses choroidal circulation, helpful when exudative changes or posterior scleritis is suspected. PubMed Central

  8. Targeted MRI of the orbits (selected cases)
    Used when you suspect posterior scleritis, mass, or unusual inflammation that could explain the detachment/hypotony pattern.

  9. Post-dilation imaging “challenge” (repeat UBM/AS-OCT after mydriasis)
    If the iris shape normalizes after breaking synechiae, you’ve reinforced a seclusion-driven IRS mechanism. PubMed Central

  10. Follow-up imaging after treating uveitis or stopping a culprit drug
    Normalization of iris contour and pressure after anti-inflammatory therapy or cessation of nivolumab supports a drug-triggered uveitis → hypotony → IRS chain. PubMed Central

Non-pharmacological treatments

Important: The right plan depends on the cause. Many cases need retinal surgery to reattach the retina and restore normal pressure. Some steps below are office-based procedures or supportive care used before/around surgery.

  1. Urgent retina referral and close monitoring. Purpose: fast, coordinated care. Mechanism: speeds diagnosis and definitive repair. JAMA Network

  2. Protective eye shield & activity restriction if detachment/tear suspected. Purpose: reduce further damage; Mechanism: prevents external pressure/trauma.

  3. Patient positioning (guided by retina specialist). Purpose: helps tamponade work post-op; Mechanism: gravity positions gas/oil against retinal breaks.

  4. Laser peripheral iridotomy (LPI) when safe/appropriate. Purpose: create a new fluid path through the iris to break the pupillary block; Mechanism: laser makes a tiny hole so fluid equalizes and the iris relaxes forward. (Used selectively in IRS; not a stand-alone cure if a detachment is driving the process.) EyeWiki

  5. Laser synechiolysis in selected eyes. Purpose: break the iris–lens adhesions; Mechanism: frees the pupil to re-establish flow.

  6. Mechanical (surgical) synechiolysis at the slit lamp or in OR—see “Surgeries” below for the OR version. Purpose: physically release the pupil; Mechanism: restores front-to-back fluid communication.

  7. Anterior chamber viscoelastic reforming (office/OR). Purpose: temporarily push iris forward and open the pupil; Mechanism: restores chamber form while definitive treatment is planned.

  8. Periocular cold compresses for comfort if inflamed. Purpose: reduce surface irritation; Mechanism: counters hyperemia/edema.

  9. Lubrication (non-medicated tears/gel). Purpose: soothe corneal surface; Mechanism: stabilizes tear film when cornea is edematous/irritated.

  10. Avoidance of pressure-lowering drops in a hypotonic eye unless your specialist specifically instructs otherwise. Purpose: don’t worsen hypotony; Mechanism: avoids further lowering of pressure (some reports show acetazolamide can accentuate the concave iris). AAO

  11. Seal any wound leak (bandage contact lens, tissue adhesive) when present. Purpose: stop fluid loss; Mechanism: raises pressure toward normal.

  12. Drainage of large choroidal effusions (procedure). Purpose: relieve pressure behind the iris; Mechanism: lets the eye pressurize and the iris relax. PubMed Central

  13. Counseling about symptoms of detachment (flashes, floaters, curtain). Purpose: early detection; Mechanism: minimizes delay to repair. JAMA Network

  14. Medication review with oncologist if on immune checkpoint inhibitors. Purpose: manage rare medication-associated IRS; Mechanism: adjust systemic therapy if needed. PubMed

  15. Treat underlying uveitis triggers (non-drug measures)—sun/UV protection, rest, treat infections appropriately per physician guidance. Purpose: calm inflammation; Mechanism: reduces ciliary shutdown and synechiae formation.

  16. Nutritional support and hydration during recovery. Purpose: general healing; Mechanism: supports ocular tissues indirectly.

  17. Smoking cessation. Purpose: improved ocular vascular health; Mechanism: better perfusion and healing.

  18. Goggle/eye protection in sports/at-risk jobs. Purpose: prevent trauma that can lead to detachment.

  19. Glycemic and blood pressure control in diabetics/hypertensives. Purpose: protect retina; Mechanism: reduces microvascular stress.

  20. Follow-up schedule adherence. Purpose: detect recurrence or persistent block; Mechanism: timely adjustments in care.


Drug treatments

Doses are common starting points for adults; your eye specialist will individualize and taper. Always follow your doctor’s exact plan.

  1. Topical corticosteroid (e.g., prednisolone acetate 1% eye drops)

    • Dose/time: every 1–2 hours while awake for severe inflammation, then taper.

    • Purpose/mechanism: calms uveitis, reduces protein/cells that worsen block and hypotony.

    • Key side effects: steroid IOP rise (later), delayed healing, cataract with long use.

  2. Cycloplegic/mydriatic (e.g., atropine 1%)

    • Dose/time: 1 drop 1–2× daily.

    • Purpose/mechanism: relaxes ciliary spasm, pulls iris away from lens, helps break synechiae and relieve pupillary block.

    • Key side effects: light sensitivity, near-blur, rare systemic effects in children/elderly. PubMed Central

  3. Topical NSAID (e.g., ketorolac 0.5%)

    • Dose/time: 3–4× daily as adjunct.

    • Purpose/mechanism: additional anti-inflammatory support.

    • Side effects: stinging; rare corneal issues with prolonged use.

  4. Oral corticosteroid (e.g., prednisone)—selected cases with significant uveitis

    • Dose/time: e.g., 0.5–1 mg/kg/day short term with taper.

    • Purpose/mechanism: systemic inflammation control to restore ciliary function.

    • Side effects: glucose rise, mood/sleep changes, gastric upset—needs medical supervision.

  5. Topical hypertonic saline (5% drops/ointment) for corneal edema

    • Dose/time: drops QID or ointment HS.

    • Purpose/mechanism: draws fluid out of cornea to reduce halos.

    • Side effects: stinging.

  6. Cycloplegic alternative (e.g., homatropine 2–5%)

    • Dose/time: 2–3× daily.

    • Purpose/mechanism: similar to atropine with shorter effect.

    • Side effects: similar but milder than atropine.

  7. Aqueous suppressants (generally avoided in hypotony)

    • Note: Medications like beta-blockers or acetazolamide can worsen low pressure; they are not routine in IRS unless your surgeon has a special reason. AAO

  8. Antibiotic prophylaxis (topical) if epithelial defects or post-procedure

    • Dose/time: per surgeon.

    • Purpose/mechanism: prevents infection during healing.

    • Side effects: local irritation, allergy (rare).

  9. Antiglaucoma meds (short course) after retinal surgery if IOP spikes

    • Dose/time: individualized.

    • Purpose/mechanism: treat transient pressure rises from gas/oil or steroids after hypotony resolves.

    • Side effects: vary by class; used only when indicated.

  10. Pain control (oral acetaminophen)

  • Dose/time: as needed within safe limits.

  • Purpose/mechanism: comfort; does not treat IRS itself.

  • Side effects: liver limits if overdosed.

Clinical note: A published case showed that after starting atropine and steroid drops to open the pupil and calm inflammation, iris shape and pressure normalized before definitive retinal surgery—illustrating how breaking the block quickly helps. Definitive repair of the retinal detachment is still crucial.


Regenerative / stem-cell” drugs

There are no approved stem-cell or regenerative drugs specifically for IRS. However, when chronic uveitis drives the problem, specialists may use systemic immunomodulators to control inflammation and prevent synechiae and hypotony. These do not treat the retinal detachment itself; they support the eye by calming immune activity.

  • Methotrexate (weekly, oral or subcutaneous). Function: antimetabolite that dampens overactive immune cells; helps control uveitis. Mechanism: folate pathway inhibition reduces lymphocyte proliferation.

  • Mycophenolate mofetil (BID). Function: reduces lymphocyte DNA synthesis; mechanism: inosine monophosphate dehydrogenase inhibition.

  • Azathioprine (daily). Function: antimetabolite immunosuppression; mechanism: purine analogue reduces immune cell division.

  • Cyclosporine (BID). Function: T-cell suppression; mechanism: calcineurin inhibition reduces IL-2.

  • Adalimumab (every 2 weeks). Function: monoclonal antibody blocks TNF-α; FDA-approved for non-infectious uveitis.

  • Infliximab (IV at intervals). Function: TNF-α blocker used in refractory uveitis.

All of these require specialist oversight, screening, and lab monitoring. They are used for the underlying uveitis, not as a direct “IRS cure.”


Surgeries

  1. Pars plana vitrectomy (PPV) with retinal reattachment

    • Procedure: remove vitreous, find and treat breaks with endolaser, use gas or silicone oil tamponade.

    • Why: definitive repair for the most common driver (RRD), restores pressure balance so the iris returns to normal shape. JAMA Network

  2. Scleral buckle (sometimes combined with PPV)

    • Procedure: place a silicone band to support the retinal wall and close breaks from the outside.

    • Why: time-tested repair for selected detachments to stop fluid flow through breaks. JAMA Network

  3. Surgical synechiolysis ± peripheral iridectomy

    • Procedure: mechanically free the pupil from the lens; create a small surgical hole at the iris edge if needed.

    • Why: breaks the pupillary block, re-establishes fluid flow, lets the iris relax forward. EyeWiki

  4. Drainage of choroidal detachment/effusion

    • Procedure: controlled drainage in the OR.

    • Why: relieves posterior pressure, helps the eye re-pressurize and normalizes iris contour. PubMed Central

  5. Repair of postoperative problems (e.g., wound leak closure, IOL reposition/removal if causing inflammation/seclusion)

    • Procedure: tailored fix by the surgeon.

    • Why: removes the trigger (leak or mechanical irritation) so pressure and iris position normalize. AAO Journal


Prevention tips

  1. Seek urgent care for flashes, floaters, or a curtain of vision—early detachment repair prevents complications. JAMA Network

  2. Keep post-operative appointments and follow activity limits after any eye surgery.

  3. Use shields and avoid eye rubbing/trauma.

  4. Tell your eye surgeon about all medications, including cancer immunotherapies. PubMed

  5. Treat uveitis promptly as directed to avoid pupil seclusion. PubMed Central

  6. Don’t self-start pressure-lowering drops in a low-pressure eye. AAO

  7. Manage diabetes and blood pressure for retinal health.

  8. Stop smoking to improve ocular healing.

  9. Wear protective eyewear in sports/at work.

  10. Keep a symptom diary if inflammation recurs and bring it to visits.


When to see a doctor—right away

  • Sudden flashes, floaters, or a curtain/shadow in your vision. JAMA Network

  • Rapid drop in vision, especially after eye surgery. AAO Journal

  • A red, painful or very light-sensitive eye with blurred vision. PubMed Central

  • Any new symptoms after starting immune checkpoint inhibitors. PubMed


What to eat and what to avoid

What to favor:

  • Leafy greens (spinach, kale) for lutein/zeaxanthin—general retinal support.

  • Omega-3–rich fish (salmon, sardines) or plant sources (walnuts, flax) for anti-inflammatory benefits.

  • Colorful fruits/veg (berries, citrus, peppers) for antioxidants.

  • Lean proteins and adequate hydration to support healing.

  • Low-salt, balanced meals to avoid fluid swings and support blood pressure control.

What to limit/avoid:

  • Smoking and heavy alcohol—both slow repair.

  • Ultra-processed, high-sugar foods—may worsen systemic inflammation.

  • Excess salt if you have hypertension.

  • Supplements without medical advice, especially if you’re on steroids or immunomodulators (possible drug interactions).

(Diet helps overall eye health but doesn’t replace surgery or anti-inflammatory treatment when needed.)


FAQs

1) Is Iris Retraction Syndrome the same as iris bombé?
No. IRS bends the iris backward with a deep front chamber; iris bombé bends it forward with a shallow chamber.

2) Is IRS an emergency?
It’s urgent because it often means there’s a retinal detachment or severe inflammation. Quick evaluation can save vision. JAMA Network

3) Will eye pressure always be low?
Often yes, but not always. Some cases show normal pressure; a few even occur without measurable hypotony. EyeWikiPubMed Central

4) Can drops alone fix it?
Drops like steroids and atropine can break the pupil block and calm inflammation, but if a retinal detachment is the driver, surgery is usually needed.

5) Is a laser iridotomy enough?
Sometimes it helps, but it is not a cure-all if the retina is detached. The underlying cause still needs treatment. EyeWiki

6) Will my iris color change back?
If color change (heterochromia) came from inflammatory proteins, it can improve as inflammation settles. PubMed Central

7) Can IRS happen in both eyes?
It is usually one eye, but rare bilateral cases exist, including with immunotherapy. PubMed

8) Could my medicines cause it?
Very rarely. A few case reports link immune checkpoint inhibitors to IRS; your team will coordinate care if this applies. PubMed

9) What imaging will I need?
Most patients get B-scan ultrasound, sometimes UBM and OCT to map the front and back of the eye. EyeWiki

10) Can pressure-lowering drops help?
Not when pressure is already low—they can worsen hypotony. Your specialist will advise if and when pressure meds are appropriate. AAO

11) How fast does surgery happen?
Timing depends on the detachment type and inflammation level, but the retina team aims for prompt repair once the eye is optimized. JAMA Network

12) What is the outlook?
Outcome depends on how long the retina was detached and whether the macula was involved. Early repair usually means a better recovery. JAMA Network

13) Will I need more than one procedure?
Sometimes yes—especially with PVR or choroidal effusions. PubMed Central

14) Is IRS common after routine cataract surgery?
No—very rare. If it occurs, it’s often due to a secluded pupil or unrecognized detachment that needs attention. EyeWikiAAO Journal

15) Can lifestyle changes prevent IRS?
They can’t prevent all cases, but eye protection, quick attention to symptoms, and controlling systemic risks help reduce triggers and speed recovery. JAMA Network

Disclaimer: Each person’s journey is unique, treatment planlife stylefood habithormonal conditionimmune systemchronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 09, 2025.

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