Katarak Senilis
Published on May 12, 2026
Risk Factors
Advancing age, diabetes mellitus, smoking, UV-B exposure, hypertension, long-term corticosteroid use (systemic/inhaled/topical), ocular trauma, female sex (OR 1:8 vs. males), high myopia, exogenous estrogen (HRT), elevated BMI, excessive alcohol consumption, genetic predisposition (LIM2, EPHA2, TDRD7)
Etiology
Degenerative lens opacification (senile cataract is the most common); also secondary to metabolic disease, drug exposure, trauma, radiation, and congenital/genetic causes
Presentation
Progressive, painless decrease in visual acuity
Classic Exam
Lens opacity on slit lamp examination (dilated and undilated); absent or diminished red reflex on ophthalmoscopy; positive shadow test (immature cataract); negative shadow test (mature cataract)
Diagnostics
Visual acuity < 6/12 not correctable with pinhole; lens opacity graded by LOCS III; biometry for IOL power calculation; ocular USG if fundus cannot be visualized
Management
Surgery is the only definitive treatment. Phacoemulsification with foldable IOL implantation is the gold standard. Non-phacoemulsification techniques (SICS, ECCE, ICCE) reserved for resource-limited settings or complex cases.
Keywords
"Progressive painless vision loss," "lens opacity," "glare," "second sight," "myopic shift," "monocular diplopia," "shadow test positive/negative," "phacoemulsification," "IOL implantation"
01Pathophysiology
Cataract is defined as opacification of the crystalline lens that causes progressive decline in visual acuity. The lens is an avascular, biconvex structure composed of highly organized protein fibers (crystallins) enclosed within a capsule. Its transparency depends on the precise arrangement of these fibers and the maintenance of an appropriate intracellular environment.
The mechanism of cataract formation is multifactorial. Oxidation of membrane lipids, structural and enzymatic lens proteins, and DNA by peroxides and free radicals, particularly those generated by ultraviolet radiation, initiates the loss of transparency in the nucleus and cortex. This oxidative damage leads to protein aggregation, increasing molecular weight and optical density. As the refractive index of the nucleus changes, a progressive myopic shift occurs, which explains the clinical phenomenon of "second sight" in which a presbyopic patient temporarily regains near vision without reading glasses. Importantly, this myopic shift and second sight are characteristic of nuclear cataract and are not seen in posterior subcapsular or anterior cortical forms.
In cortical cataract, electrolyte imbalance leads to lens overhydration and liquefaction. Clinically this manifests as vacuoles, clefts, or lamellar separations visible on slit lamp. In nuclear cataract, protein denaturation from oxidation, proteolysis, and glycation causes the central lens to become opaque with a yellowish to brown discoloration visible on slit lamp.
The cataractous lens shows edema, protein alteration, proliferative changes, and disruption of lens fiber continuity. The degree of edema correlates with the stage of progression:
Immature (insipient): only partially opaque; lens still partially transparent
Mature: totally opaque with mild lens edema
Intumescent: maximal water content causing the lens to swell and the capsule to stretch, which can precipitate angle-closure (phacomorphic glaucoma)
Hypermature: relative dehydration with capsular wrinkling; liquefied cortex may leak proteins through the capsule, triggering phacolytic glaucoma
This pathophysiology directly explains why cataract causes glare: scattered light through irregular opacities reduces contrast sensitivity. It also explains monocular diplopia: a refractive gradient within a partially opaque nucleus creates a second focal point that cannot be corrected with glasses, prisms, or contact lenses.
02Classification and Clinical Manifestation
Classification by Anatomical Location
Nuclear
Location
Central nucleus of the lens
Key Clinical Features
Progressive yellowing/browning; myopic shift ("second sight"); worse distance vision initially; may improve near vision temporarily
Cortical
Location
Lens cortex (peripheral)
Key Clinical Features
Spoke-like opacities (water clefts, vacuoles); glare and light scatter; visual acuity may be preserved until opacities reach the visual axis
Posterior Subcapsular (PSC)
Location
Posterior lens surface, just inside the capsule
Key Clinical Features
Disproportionate glare and near-vision difficulty relative to mild opacity; strongly associated with corticosteroid use, diabetes, trauma, and radiation; rapid progression
Anterior Polar
Location
Central anterior capsule
Key Clinical Features
Usually small, non-progressive, and visually insignificant
Posterior Polar
Location
Central posterior capsule
Key Clinical Features
Congenital or developmental; risk of posterior capsule rupture during surgery due to capsule-cortex adhesion
Type | Location | Key Clinical Features |
|---|---|---|
Nuclear | Central nucleus of the lens | Progressive yellowing/browning; myopic shift ("second sight"); worse distance vision initially; may improve near vision temporarily |
Cortical | Lens cortex (peripheral) | Spoke-like opacities (water clefts, vacuoles); glare and light scatter; visual acuity may be preserved until opacities reach the visual axis |
Posterior Subcapsular (PSC) | Posterior lens surface, just inside the capsule | Disproportionate glare and near-vision difficulty relative to mild opacity; strongly associated with corticosteroid use, diabetes, trauma, and radiation; rapid progression |
Anterior Polar | Central anterior capsule | Usually small, non-progressive, and visually insignificant |
Posterior Polar | Central posterior capsule | Congenital or developmental; risk of posterior capsule rupture during surgery due to capsule-cortex adhesion |
Classification by Maturity
Immature (Insipient)
Description
Partially opaque; some lens fibers still clear
Shadow Test
Positive (shadow of iris visible on lens because opacification is incomplete)
Clinical Significance
Vision may still be correctable; not yet a surgical emergency
Mature
Description
Totally opaque; no light passes through
Shadow Test
Negative (no shadow because the entire lens is uniformly opaque)
Clinical Significance
Surgical indication; fundus cannot be evaluated
Intumescent
Description
Swollen lens with maximal hydration
Shadow Test
Variable
Clinical Significance
Urgent: risk of phacomorphic glaucoma (angle closure from lens swelling)
Hypermature (Morgagnian)
Description
Shrunken, wrinkled capsule; liquefied cortex
Shadow Test
Not applicable
Clinical Significance
Risk of phacolytic glaucoma (lens protein leakage inducing inflammatory open-angle glaucoma); dislocation risk
Stage | Description | Shadow Test | Clinical Significance |
|---|---|---|---|
Immature (Insipient) | Partially opaque; some lens fibers still clear | Positive (shadow of iris visible on lens because opacification is incomplete) | Vision may still be correctable; not yet a surgical emergency |
Mature | Totally opaque; no light passes through | Negative (no shadow because the entire lens is uniformly opaque) | Surgical indication; fundus cannot be evaluated |
Intumescent | Swollen lens with maximal hydration | Variable | Urgent: risk of phacomorphic glaucoma (angle closure from lens swelling) |
Hypermature (Morgagnian) | Shrunken, wrinkled capsule; liquefied cortex | Not applicable | Risk of phacolytic glaucoma (lens protein leakage inducing inflammatory open-angle glaucoma); dislocation risk |
Clinical Symptoms
Symptom | Explanation |
|---|---|
Decreased visual acuity | Most common complaint; progressive and painless |
Glare | Full spectrum: reduced contrast sensitivity, daytime sunlight glare, nighttime headlight glare |
Myopic shift / "Second sight" | Nuclear sclerosis increases lens refractive power, causing a temporary improvement in near vision in hyperopes/presbyopes; classic for nuclear cataract only |
Monocular diplopia | Nuclear irregularity creates dual refractive zones; NOT correctable with glasses/prisms/contact lenses |
Spots and haziness | Scattered opacities cause perceived floaters or foggy visual field |
03Diagnostic Workup
Snellen visual acuity + pinhole
Role
Best initial screening test
Key Findings
VA < 6/12 not improving with pinhole suggests a media opacity (not purely refractive error)
Shadow test (with penlight)
Role
Bedside screening tool at primary care
Key Findings
Positive = immature cataract; Negative = mature cataract
Direct ophthalmoscopy
Role
Screening; red reflex assessment
Key Findings
Diminished or absent red reflex indicates lens opacification
Slit lamp biomicroscopy (dilated and undilated)
Role
Gold standard for diagnosis
Key Findings
Allows direct visualization of lens opacity, grading by LOCS III, and identification of cataract type and complications
Intraocular pressure (IOP)
Role
Rule out concurrent glaucoma
Key Findings
Elevated IOP may indicate phacomorphic/phacolytic glaucoma
Fundoscopy / retinal evaluation
Role
Assess posterior segment integrity
Key Findings
Performed if media is clear enough; determines prognosis (e.g., diabetic retinopathy, macular degeneration)
Keratometry and biometry
Role
Routine preoperative for IOL power
Key Findings
Optical laser interferometry biometry (OLIB) preferred over A-scan USG (Recommendation Grade B, Level IIa)
Ocular USG (B-scan)
Role
When fundus cannot be visualized
Key Findings
Rules out retinal detachment, vitreous hemorrhage, posterior segment tumors behind a dense cataract
Specular microscopy
Role
Endothelial cell count
Key Findings
Not routine; performed when corneal endothelial pathology is suspected or in complicated cases
Blood tests (preoperative)
Role
Surgical clearance
Key Findings
Hemoglobin, WBC, platelets, random blood glucose
Test | Role | Key Findings |
|---|---|---|
Snellen visual acuity + pinhole | Best initial screening test | VA < 6/12 not improving with pinhole suggests a media opacity (not purely refractive error) |
Shadow test (with penlight) | Bedside screening tool at primary care | Positive = immature cataract; Negative = mature cataract |
Direct ophthalmoscopy | Screening; red reflex assessment | Diminished or absent red reflex indicates lens opacification |
Slit lamp biomicroscopy (dilated and undilated) | Gold standard for diagnosis | Allows direct visualization of lens opacity, grading by LOCS III, and identification of cataract type and complications |
Intraocular pressure (IOP) | Rule out concurrent glaucoma | Elevated IOP may indicate phacomorphic/phacolytic glaucoma |
Fundoscopy / retinal evaluation | Assess posterior segment integrity | Performed if media is clear enough; determines prognosis (e.g., diabetic retinopathy, macular degeneration) |
Keratometry and biometry | Routine preoperative for IOL power | Optical laser interferometry biometry (OLIB) preferred over A-scan USG (Recommendation Grade B, Level IIa) |
Ocular USG (B-scan) | When fundus cannot be visualized | Rules out retinal detachment, vitreous hemorrhage, posterior segment tumors behind a dense cataract |
Specular microscopy | Endothelial cell count | Not routine; performed when corneal endothelial pathology is suspected or in complicated cases |
Blood tests (preoperative) | Surgical clearance | Hemoglobin, WBC, platelets, random blood glucose |
The diagnostic workup for cataract begins at the primary care level (FPKTP) with three simple tools: visual acuity measurement using a Snellen chart with pinhole, a shadow test using a penlight, and direct ophthalmoscopy. A patient whose VA is less than 6/12 and does not improve with pinhole should raise suspicion for a media opacity rather than uncorrected refractive error. The shadow test helps stage the cataract at the bedside: a crescent-shaped shadow on the lens surface when light is directed from the side indicates an immature cataract, while the absence of a shadow indicates a mature cataract where the entire lens is opaque.
At the secondary/tertiary level (FPKTL), the definitive diagnostic tool is the slit lamp biomicroscope, which allows direct visualization and grading of the lens opacity. Slit lamp examination should be performed both before and after pupil dilation. The Lens Opacity Classification System III (LOCS III) is the most widely used grading criteria. While diagnosis can technically be made with a penlight and ophthalmoscope, the PNPK states that slit lamp examination (dilated and undilated) is the standard of care for cataract diagnosis.
Biometry is a routine preoperative study used to calculate the appropriate IOL power. The PNPK notes that optical biometry (e.g., OLIB) is superior to immersion A-scan ultrasound (Grade B, Level IIa). For patients with high myopia (axial length > 26 mm), swept-source OCT biometry and newer IOL formulas (Barrett Universal II, Olsen, Hill-RBF) are recommended for improved accuracy.
Ocular ultrasound (B-scan) is indicated when the fundus cannot be visualized due to dense media opacity. This is critical in mature/total monocular cataracts or cataracts suspected to result from posterior segment pathology or trauma, because the surgeon needs to know the status of the retina and vitreous before operating.
Specular microscopy for corneal endothelial cell count is reserved for patients with suspected corneal endothelial disease or complicated cases. If specular microscopy is unavailable, specular reflection using the slit lamp can provide a rough assessment of endothelial health.
04Management and Treatment
FPKTP
Visual Acuity
VA ≥ 6/12, stable
Management
Educate on risk factor avoidance; schedule follow-up if vision worsens
FPKTP
Visual Acuity
VA < 6/12 OR VA ≥ 6/12 but functionally dangerous
Management
Refer to FPKTL
FPKTL
Visual Acuity
VA ≥ 6/12, no functional impairment
Management
Best corrected spectacles; monitor
FPKTL
Visual Acuity
VA ≥ 6/12 but endangers safety of patient/others
Management
Cataract surgery
FPKTL
Visual Acuity
VA < 6/12
Management
Cataract surgery
Urgent surgical indication
Visual Acuity
Any
Management
Mature/intumescent cataract, phacomorphic glaucoma, phacolytic glaucoma, lens dislocation
Setting | Visual Acuity | Management |
|---|---|---|
FPKTP | VA ≥ 6/12, stable | Educate on risk factor avoidance; schedule follow-up if vision worsens |
FPKTP | VA < 6/12 OR VA ≥ 6/12 but functionally dangerous | Refer to FPKTL |
FPKTL | VA ≥ 6/12, no functional impairment | Best corrected spectacles; monitor |
FPKTL | VA ≥ 6/12 but endangers safety of patient/others | Cataract surgery |
FPKTL | VA < 6/12 | Cataract surgery |
Urgent surgical indication | Any | Mature/intumescent cataract, phacomorphic glaucoma, phacolytic glaucoma, lens dislocation |
Surgical Techniques
Phacoemulsification
Incision Size
2-3 mm
IOL
Foldable IOL (gold standard)
Indication
Standard of care; gold standard
FLACS (Femtosecond Laser Assisted)
Incision Size
Same as phaco
IOL
Foldable IOL
Indication
Low endothelial count, capsular fibrosis, white/hypermature cataract; comparable safety/efficacy to conventional phaco per ESCRS
SICS (Small Incision Cataract Surgery)
Incision Size
6-9 mm (scleral tunnel)
IOL
Rigid or foldable IOL
Indication
Resource-limited settings; very dense nucleus
ECCE (Extracapsular Cataract Extraction)
Incision Size
9-12 mm
IOL
Rigid IOL; 5-7 sutures required
Indication
Resource-limited settings; complex cases
ICCE (Intracapsular Cataract Extraction)
Incision Size
Large
IOL
IOL can be placed primarily or secondarily
Indication
Lens subluxation/luxation only
Technique | Incision Size | IOL | Indication |
|---|---|---|---|
Phacoemulsification | 2-3 mm | Foldable IOL (gold standard) | Standard of care; gold standard |
FLACS (Femtosecond Laser Assisted) | Same as phaco | Foldable IOL | Low endothelial count, capsular fibrosis, white/hypermature cataract; comparable safety/efficacy to conventional phaco per ESCRS |
SICS (Small Incision Cataract Surgery) | 6-9 mm (scleral tunnel) | Rigid or foldable IOL | Resource-limited settings; very dense nucleus |
ECCE (Extracapsular Cataract Extraction) | 9-12 mm | Rigid IOL; 5-7 sutures required | Resource-limited settings; complex cases |
ICCE (Intracapsular Cataract Extraction) | Large | IOL can be placed primarily or secondarily | Lens subluxation/luxation only |
The PNPK outlines the following operative sequence for phacoemulsification:
Corneal incision creation
Intracameral adrenaline injection followed by anterior capsule staining
Viscoelastic injection into the anterior chamber
Continuous curvilinear capsulorhexis (CCC)
Phacoemulsification and aspiration of lens material until clean
Intraocular lens implantation
Irrigation and aspiration of residual viscoelastic
Intracameral antibiotic injection and wound closure
IOL Selection
Foldable single-piece IOL placed within the capsular bag is the standard. The PNPK provides several important IOL pearls:
Silicone IOL is not recommended for patients with a history of posterior segment surgery or planned vitreoretinal surgery using silicone oil or gas tamponade, because silicone oil adherence to the IOL can impair visualization.
Single-piece foldable IOL should not be placed in the sulcus (only in the bag), as sulcus placement risks iris chafing, glaucoma, inflammation, hyphema, and macular edema.
Toric IOL should be considered when corneal astigmatism is ≥ 1.0 D, with greatest clinical benefit at ≥ 1.5 to 2.0 D (per ESCRS).
Multifocal IOL requires careful patient selection and counseling regarding possible reduced contrast sensitivity, glare, halo, and mildly hazy vision; patients may still need glasses for certain activities.
Non-foldable IOL is still acceptable when foldable IOL is unavailable, but requires suturing due to larger incision.
Indications for Secondary IOL Implantation
Secondary IOL is placed when the primary surgery could not include an IOL due to zonular or capsular bag inadequacy or elevated IOP during surgery. It is also indicated for aphakia, IOL subluxation/dislocation, IOL opacification, or refractive surprise. Secondary IOL implantation should only proceed once the eye is free of infection and inflammation.
Perioperative Protocol Highlights
Phase | Key Steps |
|---|---|
Preoperative | Verify patient identity, laterality, IOL type/power using WHO Surgical Safety Checklist with at least two team members; povidone-iodine antisepsis of periocular skin and conjunctiva (NICE, ESCRS); confirm biometry matches the correct eye; informed consent; preoperative systemic evaluation (BP, pulse, temperature, SpO2) |
Anesthesia | Topical (with or without intracameral), sub-Tenon, or peribulbar; chosen based on patient preference, anxiety level, expected duration, and risk factors (per NICE NG77, ESCRS) |
Intraoperative antibiotic | Intracameral antibiotic at end of surgery (levofloxacin, cefuroxime, or equivalent) to reduce endophthalmitis risk (ESCRS PREMED, NICE NG77) |
Wound closure | Seidel test if needed; confirm stable anterior chamber and acceptable IOP before ending |
Postoperative Management
Timing | Purpose |
|---|---|
Day 1-2 | Mandatory follow-up to detect early complications: wound leak, shallow anterior chamber, hypotony, elevated IOP, corneal edema, inflammation |
Day 4-7 | Detect endophthalmitis (highest incidence in first week); assess healing |
Day 21-30 | Evaluate for late complications; prescribe best corrected refraction; decide on contralateral eye surgery if bilateral cataract |
Postoperative medications (minimum 4 weeks unless otherwise indicated):
Combination antibiotic-steroid eye drops daily
Topical antibiotic alone for infection prevention
Topical steroid and/or NSAID for inflammation and CME prevention (combination steroid + NSAID strongly recommended for high-risk patients: diabetes, uveitis history, prior CME, complex surgery); duration approximately 3 to 4 weeks, adjusted by response
Oral analgesics, antiglaucoma agents, or corneal edema therapy as indicated
Eye shield/protector, especially during sleep in the first few days
Special Populations
Condition | Key Considerations |
|---|---|
Diabetes mellitus | Higher cataract risk and faster progression; control blood glucose to < 180 mg/dL preoperatively; fundus exam for diabetic retinopathy critical before surgery; prolong postoperative anti-inflammatory therapy to prevent macular edema; minimize intraoperative trauma |
Hypertension | Not a contraindication, but BP must be < 160/100 mmHg before surgery; risk of suprachoroidal or retrobulbar hemorrhage if uncontrolled |
Uveitis | Cataract often from chronic inflammation or steroid use; requires minimum 3 consecutive months of quiescence before surgery; preoperative and extended postoperative corticosteroid therapy; risk of posterior synechiae, early PCO, macular edema, phthisis bulbi |
High myopia (> -6 D or axial length > 26 mm) | Higher risk of zonular weakness, PCR, retinal detachment postoperatively; use swept-source OCT biometry; Barrett Universal II / Olsen / Hill-RBF formulas; target slight myopia (-0.5 D); consider capsular tension ring; preoperative retinal evaluation for lattice degeneration |
Bilateral cataract | Simultaneous bilateral surgery is NOT recommended per this guideline, due to the risk of bilateral endophthalmitis causing bilateral permanent blindness, despite the very low infection rate (0.02 to 0.05%) |
05Differential Diagnosis and Distractors
Uncorrected refractive error
Why It Looks Similar
Progressive blurry vision
Key Discriminator
Vision improves with pinhole or refraction in refractive error; does not improve (or improves minimally) in cataract
Open-angle glaucoma
Why It Looks Similar
Gradual vision loss in elderly
Key Discriminator
Glaucoma causes peripheral visual field loss first (tunnel vision); cataract causes central blurring and glare; glaucoma shows cupping of the optic disc, not lens opacity
Age-related macular degeneration (AMD)
Why It Looks Similar
Progressive central vision loss in elderly
Key Discriminator
AMD causes metamorphopsia (distortion) and central scotoma on Amsler grid; fundoscopy shows drusen or neovascularization; lens is clear
Diabetic retinopathy
Why It Looks Similar
Vision loss in a diabetic patient
Key Discriminator
Fundoscopy shows microaneurysms, hemorrhages, exudates, neovascularization; lens may be clear or coexist with cataract; test distinguishes source of vision loss
Acute angle-closure glaucoma
Why It Looks Similar
Sudden vision loss, red eye, elevated IOP
Key Discriminator
Presents with severe pain, nausea/vomiting, mid-dilated fixed pupil, corneal edema; cataract is painless; intumescent cataract may precipitate angle closure (phacomorphic), but the primary problem is the angle, not the lens
Posterior capsule opacification (PCO)
Why It Looks Similar
Decreased vision after cataract surgery
Key Discriminator
PCO occurs weeks to months after surgery; treated with Nd:YAG laser capsulotomy, not repeat surgery; the vignette will mention a history of previous cataract surgery
Retinal detachment
Why It Looks Similar
Sudden vision loss
Key Discriminator
Presents with flashes, floaters, and curtain-like visual field defect; painless but acute; fundoscopy or USG shows detached retina
Differential | Why It Looks Similar | Key Discriminator |
|---|---|---|
Uncorrected refractive error | Progressive blurry vision | Vision improves with pinhole or refraction in refractive error; does not improve (or improves minimally) in cataract |
Open-angle glaucoma | Gradual vision loss in elderly | Glaucoma causes peripheral visual field loss first (tunnel vision); cataract causes central blurring and glare; glaucoma shows cupping of the optic disc, not lens opacity |
Age-related macular degeneration (AMD) | Progressive central vision loss in elderly | AMD causes metamorphopsia (distortion) and central scotoma on Amsler grid; fundoscopy shows drusen or neovascularization; lens is clear |
Diabetic retinopathy | Vision loss in a diabetic patient | Fundoscopy shows microaneurysms, hemorrhages, exudates, neovascularization; lens may be clear or coexist with cataract; test distinguishes source of vision loss |
Acute angle-closure glaucoma | Sudden vision loss, red eye, elevated IOP | Presents with severe pain, nausea/vomiting, mid-dilated fixed pupil, corneal edema; cataract is painless; intumescent cataract may precipitate angle closure (phacomorphic), but the primary problem is the angle, not the lens |
Posterior capsule opacification (PCO) | Decreased vision after cataract surgery | PCO occurs weeks to months after surgery; treated with Nd:YAG laser capsulotomy, not repeat surgery; the vignette will mention a history of previous cataract surgery |
Retinal detachment | Sudden vision loss | Presents with flashes, floaters, and curtain-like visual field defect; painless but acute; fundoscopy or USG shows detached retina |
06Traps and High-Yield Pearls
The most common trap with cataract questions on licensing exams is confusing the indication for referral or surgery with the visual acuity threshold alone. The PNPK and international guidelines (NICE NG77, WHO 2030 Targets) clearly state that the decision to refer and operate should be based on functional impact on quality of life and daily activities, not solely on a visual acuity cutoff. A patient with VA of 6/12 or better who is a professional driver experiencing dangerous glare at night is a valid surgical candidate. Do not select "observe" just because the Snellen chart reads 6/12.
A second common trap involves the shadow test. Students often reverse the interpretation. Remember: a positive shadow test (shadow visible) means the lens is only partially opaque (immature), because the opacity acts as an obstacle casting a shadow from the translucent remainder. A negative shadow test (no shadow) means the lens is uniformly and totally opaque (mature), so there is no translucent region to create contrast.
Third, when a vignette describes a presbyopic patient who "no longer needs reading glasses," do not assume improvement. This is "second sight" from a nuclear cataract causing myopic shift. It signals worsening disease, not resolution.
Fourth, be careful with the intumescent cataract vignette. If a patient presents with acute eye pain, red eye, elevated IOP, and a swollen lens, the diagnosis is phacomorphic glaucoma (angle-closure secondary to lens swelling). The next step is to lower IOP medically first, then proceed with cataract extraction. Do not confuse this with primary angle-closure glaucoma, which is treated with laser peripheral iridotomy.
Fifth, for the endophthalmitis question: the PNPK and ESCRS recommend intracameral antibiotic (levofloxacin or cefuroxime) at the end of surgery as prophylaxis. If a vignette describes severe pain, vision loss, hypopion, and significant anterior chamber reaction within days of cataract surgery, the answer is endophthalmitis, and treatment per the Endophthalmitis Vitrectomy Study is intravitreal antibiotics (ceftazidime + vancomycin), with vitrectomy reserved for cases with vision of hand motion or worse (though ESCRS now recommends earlier vitrectomy regardless of presenting VA).
Finally, do not confuse TASS (Toxic Anterior Segment Syndrome) with infectious endophthalmitis. TASS occurs within 12 to 48 hours after surgery, is sterile (caused by contaminants on instruments or non-standard irrigating solutions), shows diffuse corneal edema with minimal pain, and responds to topical anti-inflammatory therapy. Endophthalmitis typically presents later (days to a week), with more severe pain and vitritis, and requires intravitreal antibiotics. When in doubt, the PNPK advises obtaining a specimen for microbiological culture before initiating treatment.
The core competency being tested across all cataract questions is the ability to (1) recognize the presentation and stage the disease accurately, (2) understand when to refer versus observe, (3) identify the gold-standard surgical approach and its alternatives, and (4) recognize and manage postoperative complications promptly.