Ophthalmology • Common eye conditions • Emergency medicine study note

Cataract: Types, Symptoms, Assessment, Treatment and Emergencies

Scope. A cataract is loss of transparency of the crystalline lens. It commonly develops gradually with age, but it can also be congenital, traumatic, metabolic, inflammatory, medication-related or secondary to another ocular disease. Most uncomplicated cataracts are painless and do not make the eye red; sudden visual loss, severe pain, a red eye or vomiting points to another urgent diagnosis or a cataract complication. This expanded lesson follows the supplied cataract slides and adds practical emergency assessment, safe referral, surgical principles, perioperative care and complications for medical students.

Emergency rule: a slowly progressive cloudy lens is not usually an emergency, but a painful red eye with sudden blur, halos, headache, nausea or vomiting may be lens-induced angle closure. Sudden loss of vision after cataract surgery may be endophthalmitis or another sight-threatening complication. Check visual acuity and pupils, avoid pressure if globe injury is possible, and arrange immediate/same-day ophthalmology for these presentations.

Learning objectives

Define cataract and relate normal lens anatomy and transparency to vision.
Recognise major age-related, secondary, traumatic, congenital and drug-related causes.
Distinguish nuclear, cortical and subcapsular morphologies and immature, mature and hypermature stages.
Describe typical symptoms and examine visual function and the lens systematically.
Identify lens-induced glaucoma, traumatic cataract, childhood leukocoria and postoperative emergencies.
Explain when glasses may help, when surgery is indicated, and the main surgical and intraocular lens options.
Plan safe perioperative teaching and recognise early and late complications.

1. Definition, anatomy and normal lens function

The crystalline lens is a transparent, biconvex structure behind the iris and pupil and in front of the vitreous. It is suspended from the ciliary body by zonular fibres and enclosed in a thin elastic capsule. The lens contributes to focusing light on the retina and changes shape during accommodation, allowing near vision. A cataract is any clinically significant opacity of this normally transparent lens or its capsule.

Lens component	Normal structure/function	Clinical importance
Lens capsule	Elastic basement membrane surrounding the lens.	Supports the lens and serves as a barrier during surgery; capsular rupture can allow vitreous loss or lens material to enter the eye.
Anterior lens epithelium	A single layer of cells under the anterior capsule; forms new lens fibres at the equator.	Metabolic injury or abnormal cell growth can produce focal or progressive opacities.
Lens cortex	Concentric layers of younger lens fibres around the nucleus.	Cortical opacities often appear as wedge-shaped spokes and scatter light, causing glare.
Lens nucleus	Central, older fibres compacted over time.	Age-related nuclear sclerosis can yellow or brown and shift refraction toward myopia.
Zonules and ciliary body	Zonules suspend the lens; ciliary muscle changes their tension during accommodation.	Weak or damaged zonules increase risk of lens subluxation and make surgery more complex.

The lens has no blood vessels. It depends on aqueous humour for nutrients and maintains clarity through highly ordered fibres, tightly controlled water and electrolyte balance, and soluble crystallin proteins. Light must pass through the cornea, aqueous, lens and vitreous without substantial scatter before reaching the retina. Lens opacity reduces transmission and scatters light, so patients may report glare and reduced contrast before a large change in chart acuity.

2. Epidemiology and public-health importance

Age-related cataract is common because lens proteins and fibres undergo cumulative biochemical change. Cataract is a major cause of avoidable vision impairment when access to assessment and surgery is limited. The World Health Organization continues to identify unoperated cataract among the leading causes of vision impairment globally. The supplied slide deck repeats an older estimate that age-related cataract accounted for 48% of world blindness, or about 18 million people. That is a historical estimate, not a current prevalence figure; current burden estimates depend on year, age group, definition and access to surgery. Do not quote an old slide statistic as a present-day Uganda rate.

In communities with limited access to eye care, late presentation may mean bilateral mature cataracts, falls, reduced independence and difficulty working or attending school. Cataract surgery can restore useful vision when retinal and optic-nerve function are adequate, but the outcome also depends on surgical quality, refractive correction, follow-up and treatment of coexisting ocular disease.

3. Causes and risk factors

Group	Examples	Clinical notes
Age-related	Progressive nuclear, cortical and posterior subcapsular opacities.	The commonest pattern in older adults; types can coexist in the same eye.
Metabolic/systemic disease	Diabetes mellitus, galactosaemia and selected metabolic or inherited disorders.	Diabetes increases cataract risk and can also cause retinopathy, so reduced vision should not automatically be attributed to lens opacity alone.
Ocular disease or surgery	Chronic uveitis, glaucoma treatment or surgery, retinal surgery, high myopia and previous intraocular procedures.	Inflammation and its treatment can both contribute. Uveitis should be well controlled before elective cataract surgery.
Medicines	Prolonged systemic or topical corticosteroids; selected phenothiazines and other drugs.	Posterior subcapsular opacity is a recognised association with corticosteroid exposure. Review all medicines; do not stop prescribed therapy abruptly without the prescriber.
Trauma	Blunt or penetrating injury, intraocular foreign body, electrical or chemical injury.	May cause rosette-shaped opacity, capsular disruption, inflammation or a rapidly progressive cataract. Always evaluate for associated globe, iris, retinal and optic-nerve injury.
Radiation/environment	Ionising radiation, ultraviolet exposure and occupational or therapeutic radiation.	Protective eyewear reduces avoidable exposure; avoid presenting any one exposure as the sole cause in an individual.
Congenital/inherited	Genetic lens-development disorders, rubella and other congenital infections, metabolic disease, syndromes such as myotonic dystrophy or Marfan syndrome.	Ask about family history, pregnancy/infection history, developmental concerns and systemic findings. A cataract in a baby may obstruct visual development.
Other modifiable associations	Smoking, excess alcohol, poor nutrition and chronic UV exposure are associated with increased risk.	Risk reduction supports general eye health but cannot reverse an established cataract.

The source slides also mention hypoglycaemia, high myopia, ocular foreign bodies and systemic illness. These are cues to ask about a broad history, rather than a checklist proving causation. Cataract may arise from more than one exposure and can coexist with glaucoma, diabetic retinopathy, macular disease or corneal opacity.

4. Pathophysiology: how a clear lens becomes opaque

Cataract formation reflects altered lens proteins, fibre-cell structure and water balance. Ageing, oxidative stress, ultraviolet or ionising radiation, raised glucose, inflammation, medicines or trauma can damage the proteins and membranes that keep lens fibres transparent. Proteins may aggregate or denature; fibre cells may swell, lose their orderly arrangement or become compacted; and water and ions may redistribute. These changes scatter or block light, producing focal or diffuse opacity.

The supplied slides describe hydration, lens-protein denaturation, sclerosis and epithelial injury. These are useful broad concepts, but the slide sequence is a simplified model rather than a single universal pathway. The term glaucomflecken refers more specifically to focal anterior subcapsular lens opacities that can appear after a severe episode of acute angle-closure glaucoma; it is not the expected mechanism of every cataract.

5. Classification by location and cause

5.1 Morphologic types

Type	Location/appearance	Typical functional effect or association
Nuclear sclerosis/cataract	Central nucleus becomes increasingly dense, yellow or brown.	Gradual distance blur, reduced contrast, altered colour perception and sometimes a temporary myopic shift (“second sight”).
Cortical cataract	Radial, wedge-shaped opacities in the outer cortex, often spoke-like.	Glare, halos and variable blur as spokes cross the visual axis; commonly age-related.
Posterior subcapsular cataract (PSC)	Granular or plaque-like opacity just in front of the posterior capsule, often near the visual axis.	Disproportionate glare and reading difficulty in bright light; may progress quickly and occur with steroids, diabetes or uveitis.
Anterior subcapsular cataract	Opacity immediately beneath the anterior capsule.	Can follow trauma, inflammation or abnormal lens epithelial response.
Congenital/paediatric cataract	Present at birth or developing in infancy or childhood; may be central, polar, lamellar, total or part of a syndrome.	Can deprive the developing visual system of a clear image and cause deprivation amblyopia or nystagmus.
Traumatic cataract	Opacity after blunt or penetrating injury; a classic rosette may follow blunt trauma.	May occur immediately or evolve later and is often accompanied by other serious ocular injuries.
Secondary/drug-induced cataract	Opacity associated with ocular disease, surgery, medication or systemic disorder.	Management includes attention to the underlying disease and medicine review as well as assessment of lens-related disability.

Nuclear, cortical and posterior subcapsular changes often occur together. The most visually important opacity is not always the largest: a small PSC near the visual axis may cause substantial glare and reading difficulty while a larger peripheral cortical spoke causes less trouble.

5.2 Maturity: immature, mature and hypermature

Stage	Clinical description	Important implications
Immature cataract	Part of the lens remains clear; lens opacity is incomplete and an iris shadow may still be visible on oblique illumination.	Visual effect varies with location and density; assess function and progression rather than relying on stage alone.
Mature cataract	The lens is densely or completely opaque; the red reflex is markedly reduced or absent and the pupil may appear white or pearly.	Fundus view may be obscured. The slide statement that vision is limited to perception of light is not universal; acuity depends on residual transparency, coexisting disease and testing conditions.
Hypermature cataract	Advanced lens degeneration with leakage and shrinkage of the cortex and a wrinkled anterior capsule. Longstanding cataracts may become liquefied or sclerotic.	Capsule and zonules may weaken; lens material can trigger inflammation or lens-induced glaucoma. A hypermature lens needs specialist assessment.

Two classic hypermature patterns are described in the slides. In a Morgagnian (liquefactive) cataract, the cortex liquefies and the dense nucleus settles inferiorly in milky fluid. In a sclerotic/shrunken cataract, cortex is resorbed and the lens shrinks; zonular weakness can cause subluxation, and a tremulous iris (iridodonesis) may be seen as the lens support changes. These are descriptive stages, not a substitute for assessing pain, pressure, vision and ocular anatomy.

6. Clinical features

6.1 Typical presentation

Gradual, painless blurring of vision over months or years, often in both eyes but not necessarily at the same rate.
Difficulty reading, recognising faces, seeing distant signs, working in dim light or performing familiar daily tasks.
Glare from sunlight or headlights, halos, reduced contrast and difficulty with night driving.
Colours may look faded, yellow or dull; bright light can worsen symptoms, particularly with PSC or cortical spokes.
Frequent change in spectacle prescription; nuclear sclerosis may cause a myopic shift so near vision temporarily seems better while distance vision worsens.
Monocular ghosting or doubling can occur from irregular lens opacity.
A white or grey pupillary reflex in advanced cataract; in a child, leukocoria always needs urgent assessment because retinoblastoma and other serious disorders must be excluded.

Uncomplicated cataract does not usually cause marked pain, acute redness, discharge, photophobia from surface irritation or sudden visual loss. Those symptoms should prompt a search for another diagnosis or an acute complication. Cataract also does not cause floaters or a curtain-like visual-field loss; these suggest vitreous or retinal disease.

7. Assessment and diagnosis

7.1 Focused history

Clarify onset, progression, laterality and functional effect. Ask about falls, school/work limitations, reading and independence.
Ask about glare, night vision, colour change, monocular doubling and whether glasses have helped.
Review diabetes, uveitis, glaucoma, prior trauma or surgery, high myopia, radiation exposure, steroid duration and family history.
Ask about pain, redness, headache, nausea, trauma, floaters, flashes, field loss, contact lenses and recent eye surgery—these are not routine cataract symptoms and may change the urgency.
For children, ask about age at onset, prematurity, infection or medicine exposure during pregnancy, family history, developmental milestones, strabismus and abnormal eye movements.

7.2 Examination

Visual acuity: measure each eye separately with habitual correction; use pinhole and refraction if available. Record near vision and functional limitations where relevant.
External eye and pupils: inspect for redness, corneal opacity, pupil abnormality, relative afferent pupillary defect, leukocoria and signs of trauma.
Red reflex: compare both eyes; a diminished or uneven reflex suggests media opacity but does not quantify retinal function.
Slit-lamp examination: assess the cornea, anterior chamber, iris, lens capsule and the location, density and maturity of opacity. Note inflammation, pseudoexfoliation, phacodonesis or zonular weakness.
Dilated fundus examination: assess retina, macula and optic nerve where the media allow. Look for diabetic retinopathy, age-related macular disease, optic-nerve damage or retinal pathology that may limit postoperative vision.
Glare testing: consider when reported glare is substantial despite relatively preserved standard chart acuity.
When the fundus cannot be seen: ocular ultrasonography may help detect retinal detachment or posterior-segment pathology. A dense cataract can hide coexisting disease, so explain uncertainty about final vision.

7.3 Tests for surgical planning

Keratometry measures corneal curvature, and ocular biometry measures axial length and other dimensions used to calculate intraocular lens power. Optical biometry is commonly used when possible; ultrasound A-scan biometry remains useful when optical measurement is not reliable or the cataract is very dense. These measurements are for surgical planning, not a general diagnostic requirement for every person with cataract. Additional corneal, retinal or optic-nerve tests are chosen according to the history and examination.

7.4 Differential diagnosis of gradual visual loss

Condition	Helpful clues	Assessment priority
Refractive error	Blur improves substantially with pinhole or updated prescription; clear lens.	Refraction and acuity with correction.
Corneal opacity or irregularity	Visible corneal scar, irregular surface, prior infection or trauma.	Fluorescein and slit-lamp examination.
Diabetic retinopathy/macular oedema	Diabetes, retinal haemorrhages or macular changes; may coexist with cataract.	Dilated fundus exam or retinal imaging.
Age-related macular disease	Central distortion, scotoma or reduced central vision disproportionate to lens opacity.	Macular examination and OCT when available.
Glaucoma/optic neuropathy	Peripheral field loss, optic-disc changes, colour deficit or relative afferent pupillary defect.	Pressure, optic nerve and field assessment.
Retinal detachment/vascular event	Sudden loss, flashes, floaters, curtain or field defect.	Same-day emergency retinal assessment; do not label as cataract.

A cataract seen on examination may not be the only cause of a patient’s visual impairment. In particular, treatable glaucoma, retinal detachment, macular disease, diabetic retinopathy or optic neuropathy must not be missed by assuming all blur is from the lens.

8. Cataract-related emergencies and urgent presentations

8.1 Lens-induced glaucoma

An enlarged intumescent cataract can crowd the anterior chamber and push the iris forward, precipitating pupillary block and angle closure (phacomorphic glaucoma). A hypermature lens can release proteins that obstruct aqueous outflow and provoke inflammation (phacolytic glaucoma). Either may present with a painful red eye, sudden blur, halos, headache, nausea or vomiting and elevated intraocular pressure. The pupil may be mid-dilated or poorly reactive and the cornea hazy. This is an ophthalmic emergency: urgently involve an eye clinician for pressure-lowering treatment and definitive management, often cataract extraction when safe. Do not manage a painful red eye as routine cataract or give unsupervised drops.

8.2 Traumatic cataract

After blunt or penetrating trauma, the lens may opacify immediately or later. First exclude open globe, intraocular foreign body, hyphema, iris or zonular injury, retinal tear/detachment and optic-nerve injury. If an open globe is possible, place a rigid shield, avoid tonometry and pressure, keep the patient fasting if surgery may be needed, provide analgesia and antiemetic treatment, and arrange emergency ophthalmology. Never delay globe-injury care to document or manage the cataract itself.

8.3 White pupil in an infant or child

Leukocoria can result from cataract, retinoblastoma, retinal disease or other serious disorders. An abnormal red reflex, new strabismus, nystagmus or unexplained poor vision requires urgent paediatric ophthalmology assessment. Congenital cataract can cause deprivation amblyopia because the visual pathways are developing; treatment timing is specialist-led and should not wait for routine adult cataract review.

8.4 Postoperative endophthalmitis

Same-day emergency: rapidly worsening vision, increasing pain, red eye, photophobia, hypopyon or marked inflammation after cataract surgery may indicate endophthalmitis. It is an intraocular infection and can permanently destroy sight. Contact ophthalmology immediately; surface antibiotic drops alone are inadequate and must not delay specialist examination and treatment.

Endophthalmitis often presents in the days after surgery but timing can vary. A patient may initially report that vision was improving and then becomes worse. Mild transient irritation is different from progressive pain, visual decline or marked inflammation, but any unexpected deterioration requires urgent review. Postoperative instructions should specify where the patient can obtain immediate help, including when traveling or outside clinic hours.

9. Management of uncomplicated cataract

9.1 Conservative support and visual aids

Update spectacles or near correction if refraction improves vision and symptoms remain acceptable.
Improve lighting and contrast for reading, reduce glare with hats or appropriate tinted/UV-protective eyewear and arrange practical support to reduce falls.
Optimise diabetes and other systemic disease and encourage smoking cessation and general eye-health measures.
Review medicines with the prescriber when steroid-associated cataract is suspected; do not stop needed steroids abruptly.
Explain that glasses and better lighting can help symptoms, but no eye drop or supplement has been proven to clear a clinically established cataract. Surgery is the definitive treatment when the visual effect warrants it.

9.2 When is surgery considered?

Cataract surgery is generally considered when the lens opacity is responsible for visual difficulty that matters to the patient’s daily activities, education, work, safety or quality of life, and the expected benefit outweighs the risks. There is no single visual-acuity number that automatically determines the need for surgery. A patient with relatively good chart acuity may be significantly disabled by glare, while another with worse acuity may function acceptably. Surgery may also be indicated to improve the view for treatment of retinal disease or to manage a cataract-related complication such as lens-induced glaucoma. The surgeon considers ocular co-disease, surgical complexity, patient goals, anaesthetic risk, access to follow-up and the likely visual potential.

9.3 Main surgical approaches

Technique	What happens	Present-day role
Phacoemulsification	A small incision is made; ultrasound energy breaks the nucleus into fragments that are aspirated while the posterior capsule is usually preserved. A foldable intraocular lens is placed in the capsular bag.	Common modern technique where equipment, training and case suitability permit; small wounds often allow faster recovery.
Extracapsular cataract extraction (ECCE)	The nucleus is removed through a larger incision while much of the capsule is retained; an intraocular lens is generally placed.	Useful in settings with limited phaco equipment, very dense lenses or particular surgical circumstances. Manual small-incision cataract surgery is an important extracapsular technique in many low-resource settings.
Intracapsular cataract extraction (ICCE)	The whole lens and its capsule are removed.	Now uncommon because it removes capsular support and increases aphakic and complication risks; may be considered for selected severely subluxated lenses or other special situations.
Intraocular lens (IOL) implantation	An artificial lens replaces the focusing power of the removed natural lens; type and position depend on capsular support and patient factors.	Usually performed during cataract surgery. If an IOL cannot safely be implanted, alternative optical rehabilitation is planned by the eye team.

The supplied slides list cryosurgery among cataract techniques. Cryoextraction was historically used to adhere to and remove the lens, but it is not a routine contemporary cataract operation; the relevant modern options are phacoemulsification and extracapsular techniques, with ICCE reserved for uncommon situations.

9.4 Intraocular lens choices and expectations

Monofocal IOLs provide focus at a chosen distance and many patients still need spectacles for near or distance tasks. Toric, multifocal or extended-depth-of-focus lenses may be offered to selected people after discussion of cost, visual trade-offs, glare, coexisting eye disease and local availability. The surgeon calculates the IOL power from biometry and discusses the intended refractive target. Surgery removes the cloudy lens but cannot reverse retinal or optic-nerve damage. Patients should understand the likely need for spectacles, possibility of residual refractive error, recovery time and warning symptoms.

10. Preoperative preparation: safe principles

Preoperative care begins with confirming the diagnosis, visual goals, laterality and surgical plan. It is not a fixed medication cocktail. The source slides mention non-steroidal anti-inflammatory drops, alpha-adrenergic agonists, anticholinergics, antibiotics and anxiolytics. These may be used selectively according to the surgeon’s protocol, pupil status, inflammation risk, anaesthetic plan, allergies and local guidance; they are not all routine for every patient.

Confirm the correct eye, procedure, consent, patient identity, medication/allergy history and documented surgical plan.
Review diabetes, blood pressure, heart/lung disease, anticoagulants, previous anaesthetic issues, drug allergies, steroid use and ability to lie still or communicate during surgery.
Assess ocular surface, cornea, anterior chamber, pupil dilation, zonules, pseudoexfoliation, glaucoma, uveitis, prior trauma/surgery and posterior-segment visual potential.
Measure corneal curvature and axial length, calculate IOL power and explain refractive goals and expected need for glasses.
Optimise active ocular infection or inflammation before elective surgery; complicated uveitis or a severely inflamed eye needs specialist planning.
Use infection-prevention, antisepsis, antibiotic prophylaxis and anaesthetic measures according to current local surgical protocol. Do not invent a universal drug dose from a classroom slide.
Arrange transportation or support where vision, sedation or anaesthesia makes travel unsafe, and provide understandable postoperative instructions before discharge.

11. Postoperative care and patient teaching

Postoperative treatment and review intervals are prescribed by the operating team and depend on technique, intraoperative events, inflammation and local service protocol. The slides list antibiotic and steroid drops, head elevation and avoiding exertion or trauma. Translate these into an individual written plan rather than giving a generic schedule that might conflict with the surgeon’s orders.

Use prescribed drops in the correct eye, at the correct intervals and for the planned duration. Wash hands, avoid touching the bottle tip to the eye and leave the interval advised between different drops.
Wear an eye shield while sleeping if advised; avoid rubbing, pressing or striking the operated eye and follow instructions about bathing, dust, swimming, heavy lifting and strenuous exercise.
Attend every follow-up visit even if vision is improving. Early checks assess wound integrity, inflammation, pressure, corneal clarity and IOL position; later review confirms refraction and retinal status.
Use a relative or caregiver to help with drops if vision, tremor, cognition or mobility makes self-administration unreliable.
Do not drive until the operating team confirms vision and safety meet local requirements.
Seek urgent help for worsening vision, increasing pain, redness, photophobia, discharge, flashes/floaters, a curtain or shadow, nausea/vomiting, sudden halos or a visibly displaced IOL.

Elevating the head briefly after surgery may be advised for comfort in some circumstances, but it is not a replacement for prescribed eye protection, drops or follow-up. Avoiding rubbing and trauma is important because an operated eye can be vulnerable while the incision heals.

12. Complications

12.1 Cataract-related complications before surgery

Functional blindness: severe lens opacity can prevent work, education, mobility and independent self-care.
Phacomorphic glaucoma: an enlarged lens crowds the anterior chamber and can close the drainage angle.
Phacolytic glaucoma: lens proteins from a hypermature cataract obstruct outflow and cause inflammation and raised pressure.
Lens-induced uveitis: exposed lens proteins after capsular disruption or advanced degeneration can provoke intraocular inflammation.
Lens subluxation/dislocation: zonular weakness may destabilise a hypermature or traumatic lens.
Paediatric amblyopia: an untreated congenital cataract blocks visual development and may cause permanent visual loss even when the lens is eventually removed.

12.2 Intraoperative complications

Posterior capsule rupture, vitreous loss, dropped lens material or difficulty placing the IOL.
Injury to the iris, cornea or wound; retained lens fragments; iris prolapse or poor pupil dilation.
Suprachoroidal haemorrhage, a rare but serious bleeding complication that may cause sudden pain, pressure rise and loss of the red reflex during surgery. This requires the surgical team to act immediately.

12.3 Early and late postoperative complications

Complication	Possible features/timing	Response
Endophthalmitis	Worsening vision, pain, red eye, photophobia, hypopyon or marked inflammation after surgery.	Immediate same-day ophthalmology; time-critical intraocular infection.
Ocular hypertension/glaucoma	Raised pressure, pain, halos, headache or blur; may follow retained viscoelastic, inflammation or steroid response.	Prompt pressure assessment by an eye clinician and treatment.
Corneal oedema or wound leak	Blur, discomfort, shallow chamber or wound abnormality.	Urgent surgical review when suspected.
Cystoid macular oedema	Central blur or distortion, often developing weeks after surgery.	Retinal/macular examination and OCT; treat according to surgeon/ophthalmologist.
Posterior capsule opacification (PCO)	Gradual blur or glare months to years later as cells cloud the retained capsule.	Can often be treated with Nd:YAG laser capsulotomy after specialist assessment; not a cataract returning.
IOL decentration or dislocation	Blur, glare, monocular diplopia or visible lens displacement.	Ophthalmic review; may need repositioning or exchange.
Retinal tear/detachment	New flashes, floaters, curtain or field loss.	Same-day retinal emergency assessment.
Ptosis, dysphotopsia or persistent inflammation	Drooping lid, unwanted arcs/halos, photophobia or lingering redness.	Report and review; rule out pressure rise, infection and macular disease.

13. Emergency-medicine and nursing responsibilities

Document onset, laterality, acuity in each eye, pupil findings, pain, pressure if safe, trauma, surgery date and key systemic risks.
Separate uncomplicated gradual cataract from acute red-eye, trauma, retinal or postoperative emergencies using the history and examination.
Shield a suspected open globe; avoid pressure, tonometry, topical manipulation or a pressure patch until globe integrity is established.
For painful red eye with suspected lens-induced glaucoma, keep the patient under urgent care, provide appropriate analgesia/antiemetic treatment and coordinate immediate ophthalmology. Definitive therapy is specialist-directed.
For postoperative visual decline or pain, contact the operating ophthalmologist or emergency eye service immediately and communicate the surgery date, symptoms and examination.
Check the patient’s understanding of drop administration, protect the eye from rubbing and identify barriers to follow-up, transport, affordability or caregiver support.
For children with leukocoria or abnormal red reflex, arrange urgent referral and avoid watchful waiting.

14. Applied cases

Case 1: Gradual blur and glare

A 68-year-old reports two years of slowly worsening distance vision and difficulty with night driving. There is no pain, redness or acute change. Visual acuity improves partially with pinhole; slit lamp shows nuclear sclerosis and cortical spokes. The next steps are refraction, assessment of daily-function impact, fundus examination for coexisting retinal disease and discussion of glasses or cataract surgery according to the patient’s goals.

Case 2: Painful red eye with an advanced cataract

A 76-year-old with a longstanding white lens develops severe eye pain, sudden blur, halos, headache and vomiting. The eye is injected, the cornea hazy and the pupil poorly reactive. Consider phacomorphic angle closure or another acute glaucoma. This needs immediate ophthalmology and pressure-lowering care; routine outpatient cataract booking is not enough.

Case 3: A baby with a white pupil

A caregiver notices a white reflex in photographs and the child has new strabismus. Congenital cataract is possible, but retinoblastoma and other sight-threatening conditions must also be excluded. Arrange urgent paediatric ophthalmology assessment; timely management protects visual development.

Case 4: Worsening sight after cataract surgery

Four days after surgery, a patient who initially saw better develops increasing pain, photophobia, redness and marked visual loss. Treat this as possible postoperative endophthalmitis until excluded. Contact ophthalmology immediately; do not reassure the patient or rely on routine drops alone.

15. Self-test

Where is the crystalline lens and what holds it in position?
What are the three main age-related cataract morphologies?
Which cataract type may cause marked glare and reading difficulty despite relatively preserved acuity?
What is the difference between immature, mature and hypermature cataract?
Why should reduced vision not automatically be attributed to an observed cataract?
Name two lens-induced glaucomas and the mechanism for each.
What must be excluded first after blunt or penetrating ocular trauma?
What postoperative symptoms require immediate same-day assessment?
What is posterior capsule opacification and how is it usually managed?
Why is congenital cataract time-sensitive in a child?

Answers

Behind the iris and pupil and in front of the vitreous; zonular fibres suspend it from the ciliary body.
Nuclear, cortical and posterior subcapsular cataract.
Posterior subcapsular cataract, particularly when near the visual axis.
Immature is partly opaque; mature is densely/fully opaque; hypermature shows advanced degeneration, cortical leakage/resorption and possible lens shrinkage or zonular weakness.
Retinal, macular, optic-nerve, corneal or refractive disorders may coexist and limit acuity even after surgery.
Phacomorphic glaucoma from lens enlargement and angle closure; phacolytic glaucoma from leakage of lens proteins obstructing outflow.
Open globe, intraocular foreign body and associated corneal, iris, retinal and optic-nerve damage.
Worsening vision, increasing pain, redness, photophobia, hypopyon, new flashes/floaters, curtain/field loss, halos with nausea or vomiting.
Clouding of the retained posterior capsule by lens epithelial cells after surgery; it is commonly treated with Nd:YAG laser capsulotomy when indicated.
The opacity can block the visual image during a critical period of visual development and cause deprivation amblyopia or nystagmus.

Key takeaways

Cataract causes usually gradual, painless blur and glare; pain, redness or sudden visual loss calls for another urgent diagnosis until proven otherwise.
Location matters: nuclear, cortical and posterior subcapsular cataracts affect vision differently, and morphology does not alone determine surgery.
Examine visual acuity, lens and posterior segment; coexisting glaucoma or retinal disease may limit visual recovery.
Glasses can help early symptoms. Surgery is considered when cataract-related impairment affects the patient’s life or when a complication/retinal treatment requires it.
Phacoemulsification and extracapsular approaches are current surgical options; ICCE and cryoextraction are historical or uncommon, selected techniques.
Phacomorphic/phacolytic glaucoma, traumatic cataract with possible globe injury, childhood leukocoria and postoperative endophthalmitis require urgent specialist care.