Refractive Errors: Myopia, Hypermetropia, and Astigmatism

1. Myopia (Nearsightedness)

• Axial myopia (most common): the eyeball is longer than normal. The axial length of a normal eye is 20-24 mm; in myopia it exceeds this range.
• Refractive (curvature) myopia: excessive curvature of the cornea or lens increases refractive power beyond what is needed.

• Usually discovered in childhood when children cannot see the blackboard at school.
• Progresses until approximately age 20-25 years.
• Pathologic (degenerative) myopia: a partly heritable condition with progressive posterior scleral weakening, increasing axial length (sometimes >40 mm), and formation of a posterior staphyloma. Complications include retinal holes, retinal detachment, choroidal neovascularization, and intraocular hemorrhage. Associated syndromes include Marfan, Stickler, and Cornelia de Lange.
• Rapidly progressing myopia after age 25 should prompt evaluation for diabetes mellitus or cataract development (nuclear sclerosis in high myopia can paradoxically increase myopic error).

2. Hypermetropia / Hyperopia (Farsightedness)

• Axial hypermetropia (most common): the eyeball is shorter than average axial length.
• Refractive hypermetropia: the cornea or lens has insufficient curvature (flatter than normal), reducing total refractive power.

• Near vision is typically more affected than distance vision, but in significant degrees both are blurred.
• Young patients can compensate with accommodation (the crystalline lens increases its curvature to add focusing power), masking the defect until their 40s when the lens loses pliability (presbyopia).
• When compensation fails, the first pair of glasses may need to correct for both distance and near (bifocals).
• Short axial length is anatomically associated with a narrow anterior chamber angle, predisposing to narrow-angle and acute angle-closure glaucoma.
• High bilateral hypermetropia is a common cause of ametropic amblyopia in children.

3. Astigmatism

• Regular astigmatism: the cornea has two principal meridians of maximal and minimal curvature that are perpendicular to each other. This is a variation in anatomy - most people have some degree of it - and it is not inherently pathological.
  • With-the-rule: vertical meridian is steepest (most common in young people).
  • Against-the-rule: horizontal meridian is steepest (more common in older patients).
• Irregular astigmatism: multiple irregular focal points, usually from corneal disease - scarring due to infection or trauma, pterygium, keratoconus, or post-surgical changes. Irregular astigmatism often cannot be corrected fully with spectacles and requires rigid contact lenses.

• Regular astigmatism: cylindrical (toric) lenses in spectacles or soft toric contact lenses.
• Laser ablation (PRK corrects up to ~3 D, LASIK up to ~5 D of astigmatism).
• Irregular astigmatism: rigid gas-permeable contact lenses; corneal procedures for the underlying cause.

Summary Comparison

Myopia

1. Definition

• Axial myopia (most common): the eyeball is longer than normal. The axial length of a normal eye is 20-24 mm; in myopia it exceeds this, and in pathologic myopia can reach 40 mm.
• Refractive (curvature) myopia: the cornea or lens has excessive curvature, increasing refractive power beyond what is needed for the axial length.

2. Classification

A. Simple (Physiological) Myopia

• The most common form; usually develops during school age.
• Typically stable by age 20-25 years.
• Fully correctable with glasses, contact lenses, or refractive surgery.
• Not associated with structural ocular disease.

B. Pathologic (Degenerative) Myopia

• Characterized by progressive anteroposterior elongation of the scleral envelope with secondary structural ocular changes due to mechanical stretching.
• A significant cause of legal blindness; maculopathy is the most common cause of visual loss in this group.
• Defined by: refractive correction > -6.00 D and/or axial length ≥ 26 mm.

C. Causes of Acquired / Accelerated Myopia

• Diabetes mellitus - reversible osmotic changes in the crystalline lens
• Nuclear cataract - increased refractive index of sclerosing lens nucleus
• Drug-induced - miotic drops (e.g., pilocarpine), sulfa drugs, tetracyclines
• Corneal ectasia - keratoconus or post-refractive surgery

3. Clinical Features

Symptoms

• Blurred distance vision - the cardinal symptom; near vision is relatively preserved
• Squinting to improve image clarity (reducing aperture narrows the circle of least confusion)
• Discovered during childhood school screening (inability to read the blackboard)
• Eyestrain and headaches from sustained near work in some cases
• In pathologic myopia: decreased central vision, often asymptomatic until middle adulthood when complications arise (macular hemorrhage, CNV)

Signs - External / Anterior

• Enlarged globe (buphthalmos-like appearance) in high myopia - pseudoproptosis can occur
• Deep anterior chamber (associated with increased axial length)
• High myopia can cause early-onset nuclear cataract and posterior subcapsular opacity

Signs - Fundus (Pathologic / High Myopia)

1. Tessellated (tigroid) fundus - diffuse attenuation of the RPE with visibility of large choroidal vessels, giving a tiled appearance
2. Anomalous optic disc - unusually small, large, or tilted; peripapillary chorioretinal atrophy (commonly as a temporal crescent)
3. Focal chorioretinal atrophy - patchy areas where choroidal vessels and even bare sclera are visible
4. Lacquer cracks - fine, irregular, yellow lines criss-crossing the posterior pole; ruptures in the RPE-Bruch membrane-choriocapillaris complex (in ~5% of highly myopic eyes); can be complicated by macular neovascularization (MNV)
5. Subretinal "coin" hemorrhages - develop from lacquer cracks in the absence of MNV
6. Fuchs spot - a pigmented macular scar representing a regressed area of MNV
7. Posterior staphyloma - focal ectasia of the posterior sclera (peripapillary or macular), present in approximately one-third of eyes with pathologic myopia; associated with macular hole formation and "dome-shaped macula"
8. Lattice degeneration - peripheral retinal thinning with risk of retinal breaks
9. Macular neovascularization (MNV) - occurs in ~10% of highly myopic eyes; presents as a grey/green subretinal lesion with subretinal blood or exudate; the prognosis for MNV in young myopic patients is better than in AMD

High myopia with macular hemorrhage (Wills Eye Manual)

Degenerative myopia - tessellated fundus with posterior changes (Kanski's)

Systemic Associations of High Myopia

• Marfan syndrome
• Stickler syndrome
• Down syndrome
• Ehlers-Danlos syndrome
• Noonan syndrome
• Pierre-Robin syndrome
• Prematurity
• Cornelia de Lange syndrome

4. Investigations

Refractive Assessment

1. Manifest refraction - subjective refraction without cycloplegia; establishes the working correction
2. Cycloplegic refraction - after instillation of a cycloplegic agent (e.g., cyclopentolate 1%); removes accommodative tone, giving the true refractive error; especially important in children and young adults
3. Autorefraction / retinoscopy - objective measures used to guide subjective refraction

Visual Acuity

• Snellen/LogMAR chart at 6 m (20 ft) for distance VA
• Pinhole test: improvement with pinhole confirms a refractive (not structural) cause of blurred vision

Biometry

• A-scan ultrasound or optical biometry (IOLMaster) to measure axial length - valuable in monitoring myopia progression and for surgical planning (phakic IOL, cataract)
• Keratometry - measures corneal curvature (K-readings); important before refractive surgery

Posterior Segment Investigations (for High/Pathologic Myopia)

1. Dilated fundus examination with indirect ophthalmoscopy - mandatory; search for retinal breaks, detachment, lattice degeneration. Scleral depression should be performed with care over a staphyloma
2. Slit lamp biomicroscopy with 60-D or 90-D lens - examine the macula, search for MNV (subretinal grey-green lesion, subretinal blood/fluid, exudate)
3. Optical Coherence Tomography (OCT) - the key imaging investigation:
   • Identifies MNV, foveal retinoschisis (a cause of vision loss in high myopia), macular holes, macular retinal detachment over a staphyloma, and intrachoroidal cavitation
   • OCT angiography (OCTA) can detect MNV without dye injection
4. Intravenous fluorescein angiography (IVFA) - for suspected MNV when OCT is equivocal
5. IOP measurement - by applanation tonometry (note: Schiotz or Tono-pen may underestimate IOP in highly myopic eyes due to altered scleral rigidity)
6. Visual fields - in suspected glaucoma; note that myopic visual field defects can mimic early glaucoma; progressive visual field loss in the absence of progressive myopia suggests true glaucoma

5. Management

A. Optical Correction (Non-Surgical)

• Concave (diverging, minus) lenses are the standard correction
• Fully correctable in simple myopia (20/40 or better in 95%+ of patients)
• In pathologic myopia, spectacles are palliative; correction is limited by the severity of the refractive error and posterior segment abnormalities

• Soft, rigid gas-permeable (RGP), or orthokeratology lenses
• RGP lenses are preferred for irregular corneas

B. Myopia Control (Slowing Progression in Children)

C. Refractive Surgery (Surgical Correction)

D. Management of Complications (Pathologic Myopia)

1. Retinal breaks - symptomatic breaks: laser photocoagulation, cryotherapy, or scleral buckling; asymptomatic breaks without surrounding pigmentation may also be treated
2. Rhegmatogenous retinal detachment (RRD) - vitreoretinal surgery (vitrectomy ± scleral buckle)
3. Macular neovascularization (MNV) - anti-VEGF therapy (intravitreal ranibizumab, bevacizumab, or aflibercept) is the treatment of choice; injection frequency is generally less than for AMD; laser photocoagulation may be considered for extrafoveal/juxtafoveal CNV but is seldom used
4. Macular retinoschisis / macular hole - vitrectomy; surgical outcomes are more unpredictable in myopic macular holes than idiopathic ones
5. Glaucoma - treated per standard glaucoma protocols; monitor for progression distinguishing myopic field loss from true glaucomatous damage
6. Cataract - standard phacoemulsification, but RD risk is higher post-operatively in high myopes; lens dislocation is a recognized rare risk

E. Protective Measures

• Polycarbonate safety goggles are recommended for sports in pathologic myopia - even minor trauma can cause choroidal rupture
• Scleral depression should be performed cautiously over a staphyloma (risk of choroidal damage)

Follow-up

• Simple myopia: routine refraction every 1-2 years; annually in children during progression phase
• Pathologic myopia (without complications): dilated examination every 6-12 months, watching for MNV, retinal breaks, and foveoschisis

Hypermetropia (Hyperopia / Farsightedness)

1. Definition

Optical correction of refractive errors - note hyperopia (Figure B) corrected with a convex (converging) lens (Figure C)

2. Classification

A. By Aetiology

B. By the Role of Accommodation (Donders' Classification)

C. By Degree

3. Clinical Features

Symptoms

• Small degrees of hypermetropia are asymptomatic and do not require correction
• High hypermetropia leads to constant accommodative effort - the child never relaxes their ciliary muscle
• May present with convergent squint (esotropia) - the link between accommodation and convergence causes the eyes to turn inward when the child accommodates to overcome hypermetropia
• Amblyopia - bilateral ametropic amblyopia from uncorrected high symmetrical hypermetropia; reduced VA in the absence of any organic lesion

• Asthenopia (eyestrain, headaches) - particularly with sustained near work such as reading; ciliary muscle fatigue
• Blurred near vision - particularly in absolute hypermetropia
• Distance vision initially preserved (corrected by accommodation)
• Difficulty concentrating; avoidance of reading tasks
• Photophobia and blepharospasm can occur in severe cases

• Accommodation starts failing (presbyopia); the previously compensated hypermetropia becomes manifest
• Blurred vision at all distances - both near and distance, since accommodation can no longer compensate even for distance
• The first pair of glasses may need to correct both distance and near tasks (bifocals)
• The onset of symptoms may be sudden and distressing because many patients were unaware of any refractive error

Signs

• High AC/A ratio accommodative effort apparent on slit lamp (miosis, convergence)
• Shallow anterior chamber - short axial length is anatomically associated with a narrow anterior chamber angle
• Small globe appearance
• In esotropia-associated cases: convergent squint manifest on cover test
• Hyperaemic optic disc appearance (pseudopapilloedema) can occasionally be seen in high hypermetropia - the small scleral canal is crowded, making the disc appear swollen

4. Investigations

Refraction

1. Manifest (non-cycloplegic) refraction - establishes the correction tolerated by the conscious patient; reveals only manifest hypermetropia; the patient's accommodation tends to reduce the measured error
2. Cycloplegic refraction - the definitive investigation; instillation of a cycloplegic agent paralyzes the ciliary muscle, revealing the total hypermetropia (latent + manifest):
   • Cyclopentolate 1% (0.5% in children <6 months) - standard agent; 1 drop repeated after 5 minutes; maximal cycloplegia in 30 minutes; recovery within 2-3 hours
   • Atropine 1% (stronger, longer duration) - used for high hypermetropia, heavily pigmented irides, or when cyclopentolate fails; instilled at home twice daily for 1-3 days before the appointment; visual effects last up to 2 weeks. Parents must stop if systemic toxicity (flushing, fever, restlessness) occurs
3. Retinoscopy - objective measurement; used alongside subjective refraction; dynamic retinoscopy confirms adequacy of cycloplegia
4. Autorefraction - quick objective screen; less reliable than retinoscopy in high hypermetropia

Ocular Investigations

1. Visual acuity - Snellen/LogMAR; in children, look for anisometropia (different refraction between eyes) and reduced BCVA suggesting amblyopia
2. Cover test and binocular vision assessment - to detect associated esotropia (latent or manifest); AC/A ratio measurement
3. Slit lamp examination - shallow anterior chamber depth (predicts angle-closure risk)
4. Gonioscopy - mandatory in all adult hypermetropic patients; up to one in six patients with hypermetropia of ≥1 D are primary angle closure suspects; routine gonioscopy should be considered in all adults with hypermetropia
5. IOP measurement - to screen for raised IOP and angle-closure glaucoma risk
6. Axial length (optical biometry / A-scan ultrasound) - documents short eye; important for IOL calculation if cataract surgery is planned
7. Corneal topography - before refractive surgery
8. Electrophysiology / neuroimaging - if amblyopia does not respond to treatment as expected, to exclude organic pathology

5. Management

A. Optical Correction

• These are the primary treatment and move the focal plane forward onto the retina
• In children without squint: In general, up to 4 D of hypermetropia should not be corrected if the child has no squint and no near vision difficulties (to avoid interfering with physiological emmetropization)
• In children with esotropia: The full cycloplegic correction must be prescribed even in children under 2 years of age - this is the key treatment for accommodative esotropia
• For children >8 years: prescribe the maximum 'plus' tolerated on non-cycloplegic refraction (manifest hypermetropia)

• Soft convex lenses; suitable for older children and adults
• Orthokeratology is not used for hypermetropia

• Indicated when there is convergence excess esotropia (high AC/A ratio): a reading addition reduces accommodative convergence at near, allowing bifoveal fixation
• Executive bifocals (upper-lower division at the pupillary lower border) are preferred in children
• The reading addition is gradually reduced and withdrawn through the early teenage years

B. Refractive Surgery

C. Management of Complications

• Refractive correction first - optical correction alone may improve VA significantly
• Occlusion (patching) of the better eye - the mainstay of amblyopia treatment; full-time or part-time depending on age and density of amblyopia; effective up to 7-8 years (strabismic) or into the teens (anisometropic)
• Atropine penalization of the normal eye - alternative when patch compliance is poor; particularly effective for mild-moderate anisometropic hypermetropic amblyopia
• Sensitive period closes at approximately 7-8 years; early detection and treatment is vital

• Full cycloplegic refractive correction is the first and definitive treatment
• Fully accommodative esotropia: glasses alone eliminate the deviation and restore binocular single vision (BSV)
• Partially accommodative esotropia: residual deviation requires surgery after full amblyopia treatment
• Bifocals for convergence excess

6. Complications

Astigmatism

1. Definition

• In myopia/hypermetropia, the entire system is uniformly under- or over-powered but optically spherical - a single point focus is formed (in front of or behind the retina).
• In astigmatism, no single focal point exists - the eye focuses different meridians at different distances.

2. Classification

A. By Regularity (most clinically important)

Regular Astigmatism

• The two principal meridians (of maximum and minimum curvature) are perpendicular to each other (90° apart).
• This is the most common type; most people have some degree of it.
• Not inherently pathological - it is a variation in anatomy.
• Fully correctable with cylindrical (toric) lenses.

Irregular Astigmatism

• The principal meridians are not perpendicular to each other, or there are multiple focal points scattered across the cornea.
• Usually caused by pathological changes in the corneal surface.
• Cannot be adequately corrected with spectacles or soft contact lenses.
• Requires rigid gas-permeable (RGP) contact lenses; in severe cases, corneal surgery.

• Keratoconus (most important - progressive corneal ectasia)
• Corneal scarring from infection (bacterial, herpetic, acanthamoeba keratitis) or trauma
• Pterygium - limbal growth that distorts the corneal curvature
• Pellucid marginal degeneration - inferior peripheral corneal thinning producing high ATR irregular astigmatism
• Post-surgical (penetrating keratoplasty, refractive surgery complications)
• Corneal dystrophies

B. By Aetiology

C. By Degree

3. Clinical Features

Symptoms

• Blurred vision at all distances - unlike myopia (blur at distance only) or hypermetropia (blur at near preferentially); astigmatism impairs both
• "Shadowing" or "ghosting" of images - objects appear to have a secondary faint shadow or double image
• Difficulty seeing fine detail - particularly affecting tasks like reading, recognizing faces, seeing lines precisely
• Asthenopia - eyestrain, fatigue, headaches after sustained visual tasks; more prominent in low-to-moderate astigmatism where the patient strains to compensate
• Tilting the head or squinting to find the axis of clearest vision
• In children: may present as frequent squinting, close viewing, or school difficulties
• Monocular diplopia - a single object appears doubled in one eye (pathognomonic of significant astigmatism or irregular astigmatism)
• In irregular astigmatism (e.g., keratoconus): progressive worsening of vision, frequent prescription changes, and ultimately poor corrected VA with spectacles

Signs

• Habitual head tilt or squinting
• In high astigmatism: reduced BCVA even with spectacle correction (if irregular)

• Keratoconus - hallmark signs:
  • Vogt striae - vertical tension lines in the posterior cornea (deep stroma)
  • Fleischer ring - iron deposits (haemosiderin) in the epithelium at the base of the cone; best seen with cobalt blue light
  • Munson sign - the lower lid bows outward (V-shape) when the patient looks down, due to the conical protrusion
  • Apical scarring - superficial stromal opacity at the cone apex
  • Acute corneal hydrops - sudden corneal oedema from rupture of Descemet membrane; presents as a white/grey corneal opacity with marked vision loss

• Egg-shaped or irregular mires (keratoscope rings) in keratoconus
• Scissor (waterdrop) reflex on retinoscopy in irregular astigmatism
• Oil droplet reflex on direct ophthalmoscopy at 0.5 m distance in keratoconus

Keratoconus - the most important cause of irregular astigmatism (Wills Eye Manual)

4. Investigations

Refractive Assessment

1. Subjective refraction - determines the full spectacle correction (sphere + cylinder + axis); the cylinder power and axis define the nature and severity of the astigmatism
2. Retinoscopy - objective measurement:
   • Regular astigmatism: the reflex moves differently in different meridians; neutralized with a cylindrical lens
   • Irregular astigmatism: a "scissor" or "waterdrop" reflex that cannot be neutralized with a simple cylinder
3. Cycloplegic refraction - important in children to reveal any latent hypermetropic component accompanying the astigmatism
4. Autorefractor - quick objective screen; less reliable for axis determination in irregular astigmatism

Keratometry

1. Manual or automated keratometry (ophthalmometry) - measures curvature of the central 3 mm of the cornea in two principal meridians; gives K-readings in dioptres or mm of radius:
   • Regular astigmatism: symmetric oval mires
   • Keratoconus: egg-shaped or irregular mires; steepened readings (often >47 D)
   • Essential before contact lens fitting and refractive surgery

Corneal Topography and Tomography

1. Videokeratography (corneal topography) - colour-coded map of the corneal surface:
   • Regular astigmatism: symmetric "bow-tie" pattern (equal opposite areas of steepening)
   • Keratoconus: inferior steepening, asymmetric bow-tie, progression from symmetric to inferotemporal displacement
   • Detects forme fruste (subclinical) keratoconus - a contraindication to LASIK
2. Scheimpflug tomography (Pentacam) - maps both anterior and posterior corneal surfaces plus pachymetry:
   • Shows posterior corneal elevation and thinning - more sensitive than topography for early keratoconus
   • Measures thinnest point location and corneal volume
3. Corneal OCT - produces epithelial map; useful for detecting subclinical keratoconus

Visual Acuity

1. Snellen / LogMAR VA - reduced BCVA despite optimal spectacle correction suggests irregular astigmatism
2. Hard (RGP) contact lens over-refraction - if VA improves with an RGP lens over the spectacle correction, this confirms irregular astigmatism as the cause of reduced BCVA

In Children

1. Prescribing threshold: A cylinder of 1.50 D or more should be prescribed in children, especially in anisometropia after age 18 months (to prevent meridional amblyopia)
2. Visual evoked potentials (VEPs) - used to assess amblyopia severity when behavioural testing is unreliable

5. Management

A. Optical Correction (Regular Astigmatism)

• The standard first-line treatment
• A cylindrical lens corrects by adding power only in the affected meridian
• Prescription written as: Sphere / Cylinder × Axis (e.g., +1.00 / -1.50 × 90)
• Children: prescribe cylinders of 1.50 D or more after age 18 months (especially with anisometropia) to prevent meridional amblyopia
• Full correction is generally well-tolerated

• Incorporate a cylindrical correction with orientation stabilization (ballasting, prism ballast, or truncation)
• Suitable for mild-moderate regular astigmatism
• Cannot correct irregular astigmatism

• The RGP lens vaults over the irregular corneal surface; the tear film between the lens and cornea fills in the irregularities, creating a smooth spherical refracting surface
• The treatment of choice for irregular astigmatism (keratoconus, post-graft astigmatism, corneal scarring)
• Also used when spectacles cause aniseikonia in high anisometropic astigmatism

• Scleral lenses vault the entire cornea; useful when standard RGPs cannot be tolerated
• Particularly valuable in advanced keratoconus and post-surgical irregular astigmatism

B. Refractive Surgery (Regular Astigmatism)

• Corneal topography to exclude irregular astigmatism and keratoconus
• Corneal pachymetry to ensure adequate residual stromal bed
• Corneal OCT for epithelial mapping

C. Management of Irregular Astigmatism (Keratoconus Pathway)

1. Advise cessation of eye rubbing - chronic eye rubbing is a major risk factor for progression
2. Glasses - for mild cases with low regular component
3. Soft contact lenses - mild keratoconus only
4. RGP or scleral contact lenses - the mainstay for moderate disease; corrects irregular astigmatism optically
5. Intracorneal ring segments (ICRS) - implanted within the corneal stroma; reshape the cornea and may allow return to contact lens wear in mild-moderate keratoconus
6. Corneal collagen cross-linking (CXL) - the only treatment that halts disease progression:
   • Creates new covalent bonds between collagen fibrils using riboflavin drops + UV-A light (365 nm)
   • FDA-approved protocol: 9 mm epithelial debridement; riboflavin for 30 minutes; UV-A for 30 minutes
   • Approved for age ≥14 years; can be used off-label for younger children
   • Should be offered for actively progressive keratoconus; does not improve BCVA
7. Penetrating keratoplasty (PK) or Deep Anterior Lamellar Keratoplasty (DALK) - for advanced disease with contact lens intolerance or unsatisfactory vision; DALK preserves the host endothelium; outcomes may be compromised by residual astigmatism requiring contact lenses post-graft
   • Post-keratoplasty astigmatism: RGP lenses; arcuate keratotomy ± compression sutures

6. Complications

Conjunctivitis

Definition

Diagnostic Algorithm: Follicles vs. Papillae

Diagnostic algorithm: follicles vs. papillae (Wills Eye Manual)

Causes and Clinical Features

1. BACTERIAL CONJUNCTIVITIS

A. Acute Bacterial Conjunctivitis (Non-Gonococcal)

• Staphylococcus aureus - most common in adults
• Streptococcus pneumoniae - common in children
• Haemophilus influenzae - common in children; risk of otitis and systemic spread
• Moraxella catarrhalis

• Usually bilateral (one eye 1-2 days before the other)
• Painless mucopurulent discharge
• Eyelids stuck together on waking - the classic complaint
• Gritty / foreign-body sensation
• Mild photophobia
• Vision usually normal

• Diffuse conjunctival injection (hyperaemia) involving tarsal and forniceal conjunctiva
• Discharge initially watery → rapidly becomes mucopurulent
• Eyelid oedema and erythema (more marked in severe cases)
• Papillary reaction on the tarsal conjunctiva
• Superficial corneal punctate epithelial erosions may occur
• Preauricular lymphadenopathy usually absent (except in gonococcal/meningococcal)
• About 60% are self-limiting within 1-2 weeks

B. Hyperacute (Gonococcal) Conjunctivitis

• Hyperacute onset (within 12-24 hours)
• Profuse purulent discharge (copious, cream-coloured pus)
• Marked conjunctival injection and severe chemosis
• Marked eyelid swelling and erythema
• Preauricular lymphadenopathy (present, unlike other bacterial)
• Corneal ulceration that can rapidly progress to perforation
• Systemic disseminated gonococcal infection may occur

C. Meningococcal Conjunctivitis

• Rare; usually affects children
• Hyperacute picture similar to gonococcal
• Life-threatening risk: up to 30% of cases develop systemic meningococcal disease without treatment
• Requires urgent systemic prophylaxis (IM benzylpenicillin or ceftriaxone)

2. VIRAL CONJUNCTIVITIS

A. Non-Specific Acute Follicular Conjunctivitis (most common form)

• Often preceded by upper respiratory tract infection (sore throat, coryzal symptoms)
• Unilateral onset then contralateral eye involved 1-2 days later (usually less severely)
• Watery (serous) discharge
• Redness, irritation, itching, mild photophobia
• Follicles on inferior palpebral conjunctiva - the hallmark
• Occasional small subconjunctival haemorrhages
• Preauricular lymphadenopathy - tender; the most useful distinguishing feature from bacterial
• Vision normal unless keratitis present

B. Pharyngoconjunctival Fever (PCF)

• Same ocular features as above plus prominent sore throat and fever
• Keratitis in ~30%
• Common in children; family clusters

C. Epidemic Keratoconjunctivitis (EKC)

• Severe follicular conjunctivitis
• Keratitis in ~80% - punctate corneal epithelial erosions staining with fluorescein; later subepithelial infiltrates (nummular keratitis) that cause prolonged visual blurring
• Marked photophobia
• Pseudomembranes on the tarsal conjunctiva in severe cases
• Large preauricular lymph node
• Can cause symblepharon and subconjunctival scarring in severe cases

D. Acute Haemorrhagic Conjunctivitis

• Rapid onset and resolution (1-2 weeks)
• Subconjunctival haemorrhages are the hallmark - often extensive
• Follicular conjunctivitis, watery discharge, eyelid swelling

E. Herpes Simplex Virus (HSV) Conjunctivitis

• Usually unilateral - important distinguishing feature
• Associated skin vesicles on lids or periorbital skin
• Follicular conjunctivitis
• Dendrites on cornea (pathognomonic) - detected with fluorescein staining
• Tender preauricular lymphadenopathy

F. Molluscum Contagiosum

• Caused by poxvirus; peak age 2-4 years
• Chronic follicular conjunctivitis from viral particle shedding by lid/lash margin lesions
• Examine the eyelash line carefully for the characteristic umbilicated, pearly-white lid nodule
• Conjunctivitis resolves after treatment of the skin lesion

G. Systemic Viral Infections

• Varicella, measles, mumps - associated follicular conjunctivitis
• Varicella-zoster (ophthalmic shingles) - conjunctivitis plus skin vesicles in V1 distribution
• COVID-19 (SARS-CoV-2) - conjunctivitis in a minority of cases; viral RNA can be isolated in tears

3. CHLAMYDIAL CONJUNCTIVITIS

A. Adult Inclusion Conjunctivitis

• Subacute onset of unilateral or bilateral redness, watering, and discharge
• Untreated, becomes chronic and may persist for several months
• Always ask about sexual exposure

• Watery or mucopurulent discharge
• Tender preauricular lymphadenopathy
• Large follicles most prominent in the inferior fornix and upper tarsal conjunctiva
• Superficial punctate keratitis (common)
• Peripheral corneal infiltrates after 2-3 weeks
• Chronic cases develop papillae (less follicles) with mild conjunctival scarring and superior corneal pannus

• Males: non-gonococcal urethritis (often asymptomatic), epididymitis, Reiter syndrome trigger
• Females: urethritis, dysuria, discharge; risk of PID and infertility; Fitz-Hugh-Curtis perihepatitis

B. Trachoma

• Mixed follicular and papillary conjunctivitis
• Mucopurulent discharge
• Follicles on the superior tarsal conjunctiva (WHO TF: ≥5 follicles on everted upper lid)
• Papillary hypertrophy (WHO TI: intense inflammation obscuring >half of deep tarsal vessels)
• Superior corneal pannus and punctate keratitis

• Conjunctival scarring - Herbert's pits (scarred limbal follicles), Arlt's line (linear tarsal scar)
• Trichiasis - eyelashes turn inward and scratch the cornea
• Entropion - eyelid margin turns inward
• Corneal scarring and blindness (from repeated abrasion + secondary bacterial infection)

4. ALLERGIC CONJUNCTIVITIS

A. Acute Allergic Conjunctivitis

• Cause: Acute exposure to environmental allergen (e.g., pollen)
• Typical in young children after playing outside in spring/summer
• Acute intense itching and watering
• Dramatic chemosis (conjunctival oedema) - alarming to parents
• Self-limiting within hours; cool compresses ± single drop of adrenaline 0.1% for severe chemosis

B. Seasonal Allergic Conjunctivitis ("Hay Fever Eyes")

• Allergens: Tree and grass pollens; worse in spring/summer
• Redness, watering, itching, sneezing, nasal discharge
• Mild papillary reaction, variable chemosis, lid oedema
• Normal vision

C. Perennial Allergic Conjunctivitis

• Allergens: House dust mites, animal dander, fungal spores; symptoms year-round, worse in autumn
• Milder and more chronic than seasonal form

D. Vernal Keratoconjunctivitis (VKC)

• Affects young males in hot/dry climates; seasonal (spring/summer) exacerbations
• Giant papillae on upper tarsal conjunctiva ("cobblestone" appearance)
• Limbal Horner-Trantas dots (white chalky deposits of eosinophil debris at the limbus)
• Intense itching, thick ropy mucous discharge, photophobia
• Shield ulcer on superior cornea - a serious complication

E. Atopic Keratoconjunctivitis (AKC)

• Occurs in older patients with atopic dermatitis
• Year-round, severe; may lead to conjunctival scarring, keratoconus, cataract, and corneal vascularization

5. NEONATAL CONJUNCTIVITIS (Ophthalmia Neonatorum)

• Hyperacute purulent discharge; risk of corneal perforation and blindness
• Treat systemically (ceftriaxone) + topical + co-treat for Chlamydia

• Also causes pneumonitis, rhinitis, otitis (systemic Chlamydia)
• Treat with oral erythromycin for 2 weeks

• May be associated with encephalitis (life-threatening)
• Treat with high-dose IV acyclovir

6. OTHER CAUSES

Summary: Key Distinguishing Features at a Glance