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PRIORITY 1 - FULL EXAM-DEPTH TEACHING NOTES

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1. STRABISMUS SENSORY PHYSIOLOGY

1.1 Suppression

• Confusion suppression - suppresses the different image from the deviating eye overlapping the fixation point of the fellow eye
• Diplopia suppression - suppresses the image of the fixation target falling on an eccentric retinal point in the deviating eye

• Worth 4-Dot (W4D): At near, targets are far apart - tests peripheral fusion. At distance, targets converge - tests central fusion. Suppression = sees only 2 (right eye dominant) or 3 (left eye dominant) lights
• Bagolini striated glasses: Most natural test. Sees full X = binocular, gap in one line = suppression scotoma
• 4-prism dioptre base-out test: No movement of deviating eye = deep central suppression (microtropia)

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1.2 Anomalous Retinal Correspondence (ARC)

• Small-angle (<10 PD) strabismus, usually esotropia
• Always associated with ARC and central suppression scotoma
• Amblyopia common
• 4 PD base-out test: no refixation movement (suppression)
• Bagolini: X seen but with small central gap (scotoma)

• Synoptophore (major amblyoscope): Compare objective vs subjective angle - difference = angle of anomaly
• Bagolini striated glasses: If strabismus but sees full X = harmonious ARC
• After-image test (Hering-Bielschowsky): After-images projected after fixing separately with each eye; if they do not cross at a common midpoint = ARC

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1.3 AC/A Ratio

• Calculated AC/A = IPD (cm) + (near deviation - distance deviation) / amplitude of accommodation stimulus
• Gradient AC/A = Change in deviation with +1.00 D or -1.00 D lenses (more clinically useful)

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1.4 Motor Fusion and Vergence

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1.5 Cyclodeviation and Double Maddox Rod Test

• One red, one white Maddox rod placed before each eye (rods oriented vertically, producing horizontal lines)
• If cyclodeviation present, the two lines are not parallel
• Degree of rotation measured by rotating one rod until lines are parallel - the angle rotated = the cyclodeviation in degrees
• Intorsion or extorsion >10 degrees suggests SO palsy

• Patient adopts an esotropia by converging the eyes to stimulate the near reflex, which dampens their congenital nystagmus
• Appears as esotropia but deviation reduces when one eye is covered (uncovering breaks the convergence and nystagmus returns)
• Treatment: surgery to correct the esotropia; may worsen nystagmus temporarily

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2. HORNER SYNDROME + ADIE'S TONIC PUPIL PHYSIOLOGY

2.1 Horner Syndrome - 3-Neuron Pathway

• Hypothalamus → descends ipsilaterally through brainstem → exits spinal cord at C8-T2 (ciliospinal centre of Budge)
• Causes: stroke, MS, syrinx, tumours of hypothalamus/brainstem

• Exits anterior horn at T1 → passes over lung apex → subclavian artery → up the neck along internal/external carotid bifurcation
• Synapse in the superior cervical ganglion (at level of C2/C3 vertebrae)
• Causes: Pancoast tumour (lung apex), cervical rib, thyroid surgery, carotid dissection, neck masses

• Travels with internal carotid artery into the cavernous sinus → joins the ophthalmic division of V1 → travels with the long ciliary nerves
• Innervates: dilator pupillae (pupil dilation) + Muller's muscle (upper lid elevation) + inferior tarsal muscle (lower lid retraction)
• Causes: carotid dissection (painful Horner), cavernous sinus lesion, cluster headache, middle ear pathology

• Miosis (loss of dilator pupillae)
• Ptosis 1-2 mm (loss of Muller's muscle)
• Lower lid elevation ("upside-down ptosis" or inverse ptosis - loss of inferior tarsal muscle)
• Anhidrosis of ipsilateral face (first/second order only - postganglionic fibres to sweat glands follow the external carotid artery, not the internal)
• Apparent enophthalmos (from the lid changes narrowing the palpebral aperture)

2.2 Pharmacological Testing for Horner

• Cocaine 4-10%: Blocks noradrenaline reuptake → normal pupil dilates; Horner pupil does NOT dilate (no NA available to be blocked because sympathetics not functioning). If anisocoria increases after cocaine = Horner confirmed.
• Apraclonidine 0.5-1% (now preferred, more accessible): Weak alpha-1 agonist, also alpha-2. In Horner syndrome, denervation hypersensitivity upregulates alpha-1 receptors on the pupil dilator. Apraclonidine therefore causes the Horner pupil to DILATE more than the normal pupil - reversal of anisocoria. Positive test = Horner confirmed.

• Releases stored NA from intact postganglionic nerve terminals
• First or second order lesion (preganglionic): Postganglionic neuron intact → still has NA stores → Horner pupil dilates with hydroxyamphetamine
• Third order lesion (postganglionic): No intact nerve terminals → no NA to release → Horner pupil does NOT dilate
• Wait 48 hours between cocaine and hydroxyamphetamine tests (cocaine depletes NA stores)

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2.3 Adie's Tonic Pupil

• Large, poorly reactive pupil (sphincter paresis)
• Poor accommodation (ciliary muscle paresis)
• Light-near dissociation (near response better preserved because more ciliary muscle fibres exist than sphincter fibres - aberrant reinnervation preferentially restores near response)
• Sector iris palsy on slit lamp (vermiform movements of the iris)

• Pupil becomes small (over months to years) due to aberrant reinnervation of the sphincter by originally-accommodative fibres
• The "old" tonic pupil is smaller than normal

• Supersensitivity of the denervated sphincter to cholinergic agents
• 0.1% (dilute) pilocarpine constricts the Adie's pupil but NOT a normal pupil (which requires 1% to constrict)
• This is the diagnostic test - standard 1% pilocarpine constricts both, so must use 0.1%

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3. CORNEAL TOPOGRAPHY AND TOMOGRAPHY

3.1 Placido Disc - Based Systems (Videokeratography)

• Anterior corneal curvature only - it uses reflected light from the tear film surface, so it cannot measure the posterior cornea
• Reflection-based, not transmission-based

• Axial (sagittal) curvature map: Averages curvature across the full meridian from the apex. Smooth, good for overall corneal power. May underestimate peripheral asphericities.
• Tangential (instantaneous) curvature map: Calculates point-by-point local curvature. More sensitive to local irregularities - better for detecting early keratoconus, contact lens-induced warpage, and peripheral disease. This is the map to use when you suspect pathology.

• Simulates what a manual keratometer would read from topography data
• Reports the two principal meridians and their axes
• Basis for toric IOL power selection

• Average of the 5 inferior paracentral points minus average of the 5 superior paracentral points at 3 mm zone
• Normal: <1.4 D. Suspicious: 1.4-1.8 D. Keratoconus: >1.8 D
• Keratoconus typically steepens inferiorly first

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3.2 Scheimpflug Tomography (Pentacam)

1. Anterior elevation map - anterior surface elevation relative to a best-fit sphere (BFS). Positive values = cornea is above the sphere (elevated). Expressed in microns.
2. Posterior elevation map - posterior surface elevation. This is the most sensitive marker for early keratoconus - the posterior surface bulges before the anterior surface or thinning becomes apparent.
3. Pachymetry map - full corneal thickness distribution. Thinnest point is displaced inferiorly/inferotemporally in keratoconus.
4. Anterior and posterior sagittal/tangential curvature maps

• Anterior elevation: +12 µm or more above BFS at thinnest point (suspicious)
• Posterior elevation: +16 µm or more above BFS = suspicious; >20 µm = high risk
• Minimum pachymetry: typically <500 µm; inferior thinning

• Combines multiple indices (anterior elevation, posterior elevation, pachymetry, pachymetric progression index, and the Ambrósio relational thickness)
• Expressed as deviation from a normal database in standard deviations
• BAD-D ≥1.6 = suspicious; ≥2.6 = keratoconus
• Designed to detect LASIK candidates at risk of post-LASIK ectasia - even forme fruste keratoconus (one eye of a KC pair, topographically normal)

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3.3 Keratoconus Indices and Grading

• Grades 1-2: Rigid contact lenses or crosslinking if progressive
• Grades 3-4: Intacs (intrastromal corneal ring segments), then keratoplasty if needed

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4. RETINOSCOPY + SUBJECTIVE REFRACTION PHYSICS

4.1 Retinoscopy (Skiascopy) - Core Physics

• With movement: The reflex moves in the same direction as the retinoscope streak/mirror tilt. Seen in hypermetropia, low myopia (less than 1/working distance D), or when using a plain mirror
• Against movement: Reflex moves opposite to the retinoscope. Seen in myopia greater than 1/working distance D (using a concave mirror or streak scope in minus cylinder mode)
• Neutralisation: At the far point conjugate - reflex fills the entire pupil, appears brightest and widest, with no movement. This is the endpoint.

• Gross finding: +2.00 DS at 1 m working distance
• Net: +2.00 - 1.00 = +1.00 DS

• Scissors reflex (split, irregular): Irregular astigmatism, keratoconus, corneal opacity. Cannot neutralise easily.
• Dull, small reflex: Dense media opacity (cataract, corneal scar)
• Bright, brisk reflex: Clear media, cooperative patient

• Age < 7 (high accommodative amplitude can mask hypermetropia)
• Accommodative esotropia (to reveal full latent hypermetropia driving the deviation)
• When manifest refraction differs significantly from subjective finding
• Atropine (1%) vs cyclopentolate (1%): Atropine has longer duration (2 weeks vs 24-48 hours), more complete cycloplegia, more useful in young children (< 5 years) and dark irides. Cyclopentolate is standard for most clinical uses. Atropine residual accommodation = ~0.5 D; cyclopentolate = ~1.5 D.

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4.2 Duochrome (Bichrome) Test

• Red filter: ~620 nm. Focused slightly behind the retina in the emmetropic eye.
• Green filter: ~535 nm. Focused slightly in front of the retina.
• In a correctly refracted eye: letters on red and green appear equally sharp (or red slightly clearer, acceptable endpoint)

• Not useful in patients with poor colour discrimination
• Only valid monocularly, under standard test conditions
• Should be done before or after cross-cylinder refinement of cylinder, not instead of it

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4.3 Irregular Reflex in Retinoscopy - Differential

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5. GLAUCOMA SURGERY PHYSIOLOGY

5.1 Trabeculectomy - Mechanism and Technique

1. Partial-thickness scleral flap (~50% depth): Acts as the guard. Tight sutures = high resistance = higher IOP (used in high-risk hypotony patients). Loose sutures = lower IOP. Releasable/laser-lysable sutures allow titration postoperatively.
2. Deep block excision (sclerostomy): Full-thickness opening into AC - this is the actual fistula. Punch (Kelly punch) creates the internal ostium.
3. Peripheral iridectomy (PI): Prevents iris plugging the internal ostium.
4. Bleb formation: Aqueous collects in the sub-Tenon space. Overlying conjunctiva becomes elevated = bleb. Bleb quality determines long-term success.

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5.2 Antimetabolites in Filtration Surgery

• Mechanism: Pyrimidine analogue - inhibits thymidylate synthase → blocks DNA synthesis → inhibits rapidly dividing fibroblasts
• Application: Subconjunctival injections (5 mg in 0.1 mL) postoperatively, up to 5 injections over 2 weeks if bleb failing
• Also used intraoperatively (soaked pledgets, 50 mg/mL, 5 minutes)
• Side effects: Corneal epithelial toxicity (filamentary keratitis, punctate erosions) - dose-limiting

• Mechanism: Alkylating agent - cross-links DNA → inhibits fibroblast proliferation more potently and durably than 5-FU
• Application: Intraoperative only (soaked sponge, 0.2-0.5 mg/mL, 1-5 minutes, titrated to risk). Applied under the scleral flap to the bare episclera before entering the AC.
• Superior to 5-FU for long-term bleb survival
• Risk: Hypotony maculopathy (too-thin bleb with over-drainage), avascular blebs with late infection risk, corneal endothelial toxicity
• Higher concentrations/longer time = thinner, more avascular bleb = better IOP but more risks

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5.3 Tube Shunts (Drainage Implants)

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5.4 MIGS (Minimally Invasive Glaucoma Surgery)

• iStent (inject): Titanium stent inserted through the trabecular meshwork (TM) into Schlemm's canal ab interno. Bypasses TM resistance (the site of ~75% of normal aqueous outflow resistance in POAG). Usually done at time of cataract surgery. IOP reduction ~3-5 mmHg.
• Hydrus: Intracanalicular scaffold spanning 3 clock hours of Schlemm's canal. Dilates canal, bypasses JCT, dilates collector channel ostia. More IOP reduction than single iStent.
• Both require a residual functional outflow system (episcleral venous pressure is the floor; cannot reduce IOP below ~8 mmHg).

• XEN gel stent (AqueSys/Allergan): Porcine gelatin crosslinked with glutaraldehyde. 45 µm inner lumen, 6 mm long. Drains from AC to sub-Tenon's space ab interno. Hagen-Poiseuille flow resistance is tuned to prevent hypotony. May still need antimetabolites. Bleb-dependent.
• Preserflo (InnFocus): PolyFEP (polyfluoroethylene) tube, 70 µm lumen, 8.5 mm length. Requires ab externo approach. No valve. Lower inflammatory response than XEN. Also bleb-dependent.

• CyPass (withdrawn): Ab interno into the suprachoroidal space. Withdrawn from market 2018 due to 5-year endothelial cell loss concerns.

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QUICK VIVA RECALL SUMMARY

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PRIORITY 2 - FULL EXAM-DEPTH TEACHING NOTES

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1. SWAP + FDT PERIMETRY PHYSIOLOGY

1.1 SWAP - Short Wavelength Automated Perimetry

• A given amount of RGC loss produces a larger proportional sensitivity loss on SWAP than on standard automated perimetry (SAP)
• Detects functional loss approximately 3-5 years before SAP

• More variable test-retest reliability than SAP (wider normal range, more scatter)
• Affected by media opacity and lens changes (yellowing lens absorbs blue light = false positives in older patients)
• Longer test time, more fatigue
• Now largely superseded by SITA-SWAP (shorter test algorithm using Swedish Interactive Threshold Algorithm) which reduces test time significantly
• FDT and OCT-based structural measures have reduced its clinical use

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1.2 FDT - Frequency Doubling Technology Perimetry

• The illusion is generated selectively by the My (parasol) ganglion cell subset - a subset of magnocellular pathway neurones with a specific non-linear spatial summation property (null zones in their receptive fields)
• These My cells constitute only ~3-5% of all RGCs but are disproportionately large, project to the magnocellular LGN layers, and are preferentially lost early in glaucoma
• By testing specifically the My pathway, FDT detects glaucomatous loss before SAP

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2. LOW VISION OPTICS - MAGNIFICATION FORMULAE

2.1 Definitions and Types of Magnification

1. Relative distance magnification
2. Relative size magnification
3. Angular magnification (telescopes)
4. Projection magnification (CCTV/electronic)

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2.2 Relative Distance Magnification

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2.3 Near Magnifiers - Standard Formula

• F = power of the magnifying lens in dioptres
• Reference distance used: 25 cm (the standard near point for a normal eye)
• Example: +20 D loupe → M = 20/4 = 5×

• EVD = 1/F (in metres) = focal length of the magnifier
• Smaller EVD = more magnification

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2.4 Telescopes

• Objective lens: Converging (positive)
• Eyepiece: Diverging (negative)
• Image: Upright, virtual
• Field of view: Narrow (limited by negative eyepiece)
• Length: Short (compact) - eyepiece is inside the focal length of objective
• Magnification: M = F_objective / |F_eyepiece|

• Objective lens: Converging (positive)
• Eyepiece: Converging (positive)
• Real intermediate image formed between the two lenses
• Image: Inverted, real intermediate image → requires erecting prism (Porro or roof prism) in binoculars to correct inversion
• Field of view: Wider than Galilean
• Length: Longer (objective focal length + eyepiece focal length between lenses)
• Better image quality and wider field - preferred for higher magnifications

• FOV decreases as magnification increases (trade-off)
• Depth of field also decreases with higher magnification (more critical focusing required)
• This is why very high magnification telescopes are difficult to use for dynamic tasks (walking, reading moving text)

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2.5 CCTV / Electronic Magnification

• Camera captures object and projects enlarged image onto a monitor
• Maximum magnification: up to 60× or more - far exceeds optical magnifiers
• Contrast enhancement and colour reversal possible (white text on black = high contrast)
• Not portable (traditionally desk-based), though modern portable e-magnifiers exist
• Best option for patients requiring very high magnification (severe central scotoma, VA < 3/60)

• Physiological basis of PRL: Cortical reorganisation - the cortical representation of the scotomatous fovea gradually comes to respond to the PRL region. V1 area 17 reorganises such that the peripheral retinal input takes over the cortical territory previously devoted to the damaged fovea.
• Eccentric viewing training: Teaches patients to deliberately use their PRL. They must re-learn reading direction and scanning patterns.
• The PRL most commonly develops inferiorly to the scotoma (placing text at the top of the scotoma, using the retina below the lesion).

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2.6 ETDRS Chart and logMAR Scoring

• 14 lines, 5 letters per line
• Each line = 0.1 logMAR change
• Each letter = 0.02 logMAR
• 5 letters = 0.1 logMAR = one line
• Scoring: start from 1.0 (6/60) and subtract 0.02 for each correct letter read above, or add 0.02 for each missed below
• More sensitive to small changes than Snellen (each letter scored individually, not all-or-nothing per line)

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3. SPECULAR MICROSCOPY - ENDOTHELIAL CELL ANALYSIS

3.1 Principle

• Contact (Haag-Streit): Higher magnification, better resolution, but requires topical anaesthetic
• Non-contact (Topcon SP3000, Konan): More commonly used clinically, no anaesthesia required

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3.2 Normal Endothelial Cell Parameters

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3.3 Polymegethism and Pleomorphism

1. Count: Is ECD adequate for planned surgery?
2. Mean cell area: Is it enlarged?
3. CV: Is polymegethism present?
4. % hexagonality: Is pleomorphism present?
5. Morphological abnormalities: Guttae (bright spots = endothelial excrescences into Descemet's membrane in Fuchs') visible as dark areas obscuring cell borders

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3.4 Pre-operative Assessment

• Autosomal dominant, chromosome 13 (TCF4 gene variant), late onset
• Guttae (collagen excrescences on Descemet's) appear first, centrally
• Leads to reduced ECD, then stromal and epithelial oedema
• Specular microscopy: dark areas (guttae) interspersed with bright cell outlines; reduced hexagonality and density

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4. ORBITAL PHYSIOLOGY

4.1 Orbital Venous Drainage - No Valves

1. Superior ophthalmic vein (SOV) → drains superiorly into the cavernous sinus. The SOV communicates with the angular vein (which connects to the facial vein), and with the inferior ophthalmic vein.
2. Inferior ophthalmic vein (IOV) → drains posteriorly into the cavernous sinus, or inferiorly through the inferior orbital fissure into the pterygoid venous plexus.

• Retrograde spread of infection: Facial/periorbital cellulitis can spread retrogradely via the angular vein → SOV → cavernous sinus → cavernous sinus thrombosis (CST). This is why periorbital/orbital cellulitis is a medical emergency.
• Carotid-cavernous fistula (CCF): Arterialisation of the cavernous sinus → retrograde flow into SOV → dilated, pulsatile SOV → proptosis, chemosis, elevated IOP, bruit. Dilated SOV on CT/MRI is a sign.
• Venous malformations: Orbital varices (distensible venous abnormalities) increase in size with Valsalva manoeuvre (↑ venous pressure) → intermittent proptosis.

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4.2 Orbital Fat and Proptosis

• Any space-occupying lesion (tumour, haematoma, abscess, vascular malformation, cyst) displaces the orbital fat and globe anteriorly
• Direction of displacement depends on the relationship of the lesion to the muscle cone:
  • Intraconal (within the muscle cone): Axial proptosis (straight forward)
  • Extraconal (outside the cone): Non-axial displacement away from the lesion

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4.3 Thyroid Eye Disease (TED) / Graves' Orbitopathy Physiology

1. TSH receptor antibodies (TRAb) cross-react with TSH receptors on orbital fibroblasts (and extraocular muscle fibroblasts). TSH-R are overexpressed on orbital fibroblasts in Graves' disease.
2. TRAb binding activates fibroblasts → proliferation and differentiation:
   • Some fibroblasts differentiate into adipocytes (fatty infiltration) → orbital fat expansion
   • Others become myofibroblasts → produce hyaluronic acid (glycosaminoglycans = GAGs) in the EOM and connective tissue → osmotic water retention → muscle swelling and fibrosis
3. IGF-1 receptor on orbital fibroblasts is also activated (IGF-1R signalling co-stimulated by TRAb) → additional fibroblast activation
4. T-cell infiltration and mast cells also contribute to the inflammatory cycle

• Proptosis: Enlarged EOM + increased orbital fat volume (rigid orbit cannot expand) → forward displacement
• Restrictive myopathy: Fibrosis of EOMs → diplopia (especially with the inferior rectus, most commonly affected first, then medial rectus)
• Compressive optic neuropathy (CON): Enlarged muscle bellies at orbital apex compress the optic nerve → reduced VA, RAPD, colour desaturation, visual field loss. This is the sight-threatening complication.
• Corneal exposure: Proptosis + lid retraction → lagophthalmos → exposure keratopathy

• Mild: Lid retraction <2 mm, proptosis <3 mm above normal, no corneal exposure, no optic nerve involvement
• Moderate-severe: Lid retraction ≥2 mm, proptosis ≥3 mm, intermittent or constant diplopia, no DON
• Sight-threatening: Dysthyroid optic neuropathy (DON) or corneal breakdown

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5. FFA PATTERNS - DR, CNV TYPES, CRVO/BRVO

5.1 FFA Physics Revision (from Kanski's)

• 70% of fluorescein is protein-bound (does not leak through intact vessel walls)
• 30% is free/unbound (leaks through fenestrated choriocapillaris; blocked by RPE tight junctions and inner BRB)

1. Choroidal flush (pre-arterial phase): 8-12 seconds. Patchy choriocapillaris filling (lobular pattern). Choroidal fluorescence seen through normal RPE as background haze.
2. Arterial phase: 10-15 seconds. Retinal arteries fill with fluorescein.
3. Arteriovenous (capillary) phase: Capillary bed fills; laminar flow seen in veins.
4. Venous phase: Full venous filling. Late venous = 1-2 min.
5. Late/recirculation phase: Dye washes out from normal vessels. Leakage persists and increases.

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5.2 Hyperfluorescence and Hypofluorescence

• Blockage (masking): Something blocks background/vessel fluorescence. Blood (preretinal/subretinal/sub-RPE), pigment, exudate, melanin.
• Vascular filling defect: Non-perfusion. Capillary non-perfusion in ischaemic DR, CRVO, BRVO, CRAO.

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5.3 FFA in Diabetic Retinopathy

• IRMA: within the retina, between existing blood vessel walls, no true leakage on FFA
• NVE: on the surface of or above the retina, new vessel growth, frank leakage

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5.4 FFA in CNV - Types 1, 2 and 3

• ICG (indocyanine green) is 98% protein-bound → does NOT leak through choriocapillaris fenestrations → better choroidal vessel visualisation
• Better for occult CNV (type 1) and polypoidal choroidal vasculopathy (PCV) - polyps are hyperfluorescent hot spots on late ICG
• Better for type 3 RAP lesions

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5.5 FFA in CRVO vs BRVO

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QUICK VIVA RECALL SUMMARY - PRIORITY 2

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PRIORITY 3 - FULL EXAM-DEPTH TEACHING NOTES

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1. ELECTRODIAGNOSIS ALGORITHM FOR UNEXPLAINED VISUAL LOSS

1.1 Why a Systematic Algorithm Matters

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1.2 The Algorithm - Step by Step

• If VA is reduced, first exclude optical causes (refraction, media opacity). Pinhole improvement suggests refractive cause.
• If pinhole does not improve VA, the loss is neural.

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• P50 reduced + N95 reduced → macular dysfunction (photoreceptor/bipolar level)
• P50 normal + N95 selectively reduced → RGC/optic nerve disease (retrograde atrophy or primary optic neuropathy)
• PERG normal overall → pathology is post-retinal (cortical or non-organic)

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• Reduced Arden ratio (<1.85) with normal ERG → Best's vitelliform macular dystrophy (RPE dysfunction without generalised retinal loss). This is the classic EOG-only pattern.
• Reduced EOG + reduced ERG → generalised retinal disease affecting both PR and RPE (advanced RP).

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• Pattern VEP using small check sizes (15') may detect early or subtle cortical dysfunction
• Non-organic visual loss (functional visual loss): All electrophysiological responses are normal. This is the objective confirmation that the visual system is intact. The pattern ERG and VEP require the patient to fixate but are otherwise relatively objective. If both are normal, non-organic cause is strongly supported.

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1.3 Ganglion Cell vs Optic Nerve - Distinction by Electrophysiology

• Demyelination = latency delay (the hallmark of myelin loss slowing conduction velocity)
• Axonal loss / compression = amplitude reduction without significant latency delay
• RGC selective = N95/P50 ratio reduced (N95 disproportionately affected)

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1.4 Complete Algorithm Summary Flowchart (Text Version)

Unexplained VA loss
        ↓
    PERG
   /      \
P50↓     P50 normal
(macular)  N95↓ selectively
   ↓          ↓
Flash ERG   Pattern VEP
   ↓             ↓
Normal ERG → mfERG  Delayed → demyelination
Reduced ERG → dystrophy/RP  Amplitude↓ → axonal/compressive
Electroneg → inner retina  Normal → early RGC (check mfERG)
                ↓
        ALL NORMAL
            ↓
    Non-organic / cortical
    (confirm with flash VEP)

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2. HRT + GDx IMAGING PHYSICS

2.1 Heidelberg Retina Tomograph (HRT) - Confocal Scanning Laser

• 3D topographic map of the optic disc and peripapillary retina
• Contour line is drawn manually around the disc margin (the only manual step)
• From this, the software computes: cup depth, cup area, rim area, cup-to-disc ratio, rim volume, mean retinal nerve fibre layer (RNFL) thickness around the disc

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2.2 HRT Analysis: MRA and GPS

• Compares rim area (in 6 sectors: superior, inferotemporal, inferonasal, nasal, superonasal, superotemporal) to a normative database of ~1200 healthy eyes
• For each sector and globally: classified as Normal / Borderline / Outside Normal Limits
• Takes into account disc size (larger discs have larger rims normally)
• MRA is the established HRT glaucoma classification tool

• Does not require manual disc margin contouring
• Uses 3D shape of the disc surface (a mathematical model of the optic disc shape - cup slope, cup depth, disc size, RNFL curve) to compute a probability of glaucoma
• Outputs a probability (0-1)

• Manual contour line introduces operator variability
• Reference plane affected by RNFL loss (thinning shifts the reference plane, introducing error)
• 3D topography reflects structural surface, not direct RNFL thickness measurement
• Poor reproducibility at the macula (not designed for macular analysis)

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2.3 GDx - Scanning Laser Polarimetry (SLP)

• RNFL thickness plotted around the optic disc in TSNIT order
• Normal RNFL has a characteristic double-hump pattern (superior and inferior peaks corresponding to the superior and inferior arcuate RNFL bundles) - the so-called "Batman" pattern
• Glaucomatous loss: loss of one or both humps, particularly the inferior peak
• The values should fall within the green shaded normative range

• The cornea itself is birefringent (especially the anterior corneal stroma), introducing background polarisation noise
• GDx VCC (Variable Corneal Compensation): measures and corrects corneal birefringence individually per patient
• GDx ECC: uses an enhanced algorithm for better corneal compensation

• Some patients show an atypical birefringence pattern (ATPB) from the macula (birefringence from Henle's fibre layer, the radiating axons around the fovea, is oriented differently)
• ATP appears as a temporal birefringence artefact that mimics RNFL thickening or causes erroneous inferior sector readings
• ATP is a pitfall: must be recognised as artefact, not pathology. It can make a glaucomatous eye look normal.

• A global summary parameter output by GDx
• NFI 0-30 = normal; 31-50 = borderline; >51 = outside normal limits
• Based on the TSNIT deviation pattern

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3. ULTRASONOGRAPHY PHYSICS (A-SCAN, B-SCAN, UBM)

3.1 Physics Principles

• Reflection (echo): Occurs at interfaces between tissues with different acoustic impedance (Z = density × velocity). Greater impedance mismatch = stronger echo.
• Attenuation: Absorption and scatter reduce beam intensity with depth. Higher frequency = more attenuation (less penetration). Lower frequency = less attenuation (deeper penetration) but less resolution.
• Resolution: Axial resolution = c / (2 × frequency), where c = speed of sound in tissue (~1540 m/s in soft tissue, ~1532 m/s in aqueous/vitreous). Higher frequency = better axial resolution.

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3.2 A-Scan (Amplitude Mode)

• X-axis = distance/depth (time of echo return)
• Y-axis = amplitude (strength of echo / reflectivity)
• Produces a 1D representation

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3.3 B-Scan (Brightness Mode)

• Transducer: 10 MHz for posterior segment/orbit
• Image: real-time grey-scale 2D
• Patient position: upright, probe on closed lid with gel

• Assess vitreous (PVD, vitreous haemorrhage, asteroid hyalosis, amyloid vitreous)
• Retinal detachment (smooth, mobile membrane; billowing on dynamic B-scan with eye movement)
• Choroidal detachment (bullous, peripheral, crosses ora serrata, does not cross disc - unlike RD)
• Optic disc drusen (hyperechoic plaque at disc, with acoustic shadowing)
• Staphyloma (posterior ectasia)
• Orbital masses (characterise size, location, reflectivity, vascularity with Doppler overlay)
• When media opacity prevents fundal view (dense cataract, corneal opacity, hyphaema, vitreous haemorrhage)

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3.4 UBM - Ultrasound Biomicroscopy

• Anterior chamber depth and angle (iridocorneal angle)
• Ciliary body: shape, position, cysts, tumours, cyclodialysis
• Zonules: visualised only with UBM (invisible to slit lamp or B-scan)
• Peripheral iris: plateau iris configuration, iris cysts
• Iridociliary sulcus: phakic IOL positioning
• Supraciliary space: cyclodialysis cleft, choroidal effusion anteriorly

• Angle closure mechanism: Distinguish pupil block (deep SC angle, forward iris bowing), plateau iris (normal AC depth but ciliary process anterior rotation pushing peripheral iris against TM), lens-related (large/anterior lens), aqueous misdirection (vitreous forward)
• Cyclodialysis cleft: Separation of ciliary body from scleral spur after trauma → hypotony. UBM shows the cleft directly.
• Plateau iris: Ciliary processes anteriorly rotated, mechanical obstruction of angle even after patent PI. Only diagnosable reliably by UBM.
• Phakic IOL vault: Distance between posterior IOL surface and anterior lens surface - must be >250 µm to avoid cataract

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3.5 Doppler Ultrasound (20 MHz)

• PSV (Peak Systolic Velocity) in cm/s
• EDV (End-Diastolic Velocity) in cm/s
• RI (Resistive Index) = (PSV - EDV) / PSV. Normal RI for ophthalmic artery ~0.72; CRA ~0.70.

• Ophthalmic artery (OA)
• Central retinal artery (CRA)
• Short posterior ciliary arteries (SPCA) - medial and lateral

• Raised RI in CRA/SPCA = increased vascular resistance (glaucoma, giant cell arteritis, ischaemic optic neuropathy, carotid artery disease)
• Reduced flow in giant cell arteritis (SPCA most affected - since GCA affects medium vessels, SPCA [medium calibre] are preferentially involved before CRA)
• Monitoring retrobulbar blood flow in NTG and POAG

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4. MULTIFOCAL ERG (mfERG) RING ANALYSIS

4.1 Principle

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4.2 Ring Analysis - Anatomy of the Rings

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4.3 Disease Patterns by Ring

• RNFL/GCC on OCT + 10-2 visual field + mfERG constitute the current AAO screening protocol
• mfERG Ring 2 reduction (paracentral scotoma) is an early sign before visible fundal changes or 10-2 field loss
• Ring 1 (fovea) is relatively spared early - this is the "bull's-eye" anatomical correlate

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4.4 mfERG Response Components

• P1 (first positive peak) - analogous to b-wave; reflects ON-bipolar + photoreceptor activity
• N1 (first negative trough) - analogous to a-wave; photoreceptor hyperpolarisation
• N2 (second negative trough) - inner retinal contribution

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5. CYCLODEVIATION PHYSIOLOGY - DOUBLE MADDOX ROD TEST (DEEPER DETAIL)

5.1 Torsional Anatomy - Which Muscle Does What

• Superior rectus (also elevates, adducts)
• Superior oblique (also depresses in adduction, abducts) - primary incyclotortor

• Inferior rectus (also depresses, adducts)
• Inferior oblique (also elevates in adduction, abducts) - primary excyclotortor

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5.2 Superior Oblique Palsy - Physiology of Cyclodeviation

• Tilting the head to the ipsilateral shoulder (same side as palsy) worsens the hypertropia
• Physiological basis: When head tilts right, the eyes counter-roll (ocular counter-rolling reflex, mediated by vestibulo-ocular reflex and utricular otolith input): right eye incyclotorts (needs SO + SR activation), left eye excyclotorts (IO + IR)
• In right SO palsy: tilting to the right forces the right eye to incyclotort, but SO is paralysed → SR acts alone → hypertropia increases
• Tilting to the contralateral shoulder (away from the palsy) decreases the hypertropia

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5.3 Double Maddox Rod Test - Full Physics

• Rods are placed in a trial frame with cylinders oriented vertically (so the generated light streaks are horizontal)
• Right eye: red Maddox rod; left eye: white Maddox rod
• Patient fixates a white point light in the dark
• Patient sees: one red horizontal line (right eye) and one white horizontal line (left eye)

• No cyclodeviation: Both lines are parallel and aligned horizontally
• Excyclotorsion of one eye: The line from that eye tilts (the line appears oblique, with the nasal end elevated - because the top of the eye is deviated outward, the horizontal streak tilts accordingly)
• Measurement: The rod in front of the affected eye is rotated until both lines are parallel. The angle of rotation = the degrees of cyclodeviation.
• Clinically significant SO palsy: usually >10° excyclotorsion

• The red/white line from the affected eye appears tilted
• The rod for that eye is rotated in the same direction as the tilt to neutralise it
• If the line tilts clockwise → rotate rod clockwise → degrees rotated = excyclotorsion amount

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5.4 Parks-Bielschowsky Three-Step Test (Context for SO Palsy Viva)

• Hypertropic eye: depressor palsy on that side, OR elevator palsy on opposite side (4 muscles possible)

• Eliminates 2 muscles (isolates which side - adducting or abducting depressor/elevator)

• Worse on ipsilateral tilt → SO palsy (incyclotortor required, SO paralysed)
• Worse on contralateral tilt → SR palsy

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QUICK VIVA RECALL SUMMARY - PRIORITY 3

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7-MONTH DNB/MS OPHTHALMOLOGY EXAM PREPARATION PLAN

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MASTER CURRICULUM MAP

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PART 1 — OCULAR EMBRYOLOGY

Overview: Why Embryology Matters in DNB Vivas

• Why congenital anomalies exist and what they look like
• The tissue of origin of every tumour
• Why certain structures are transparent, vascularised, or innervated the way they are
• Classic viva questions: "What is the embryological origin of...?" followed by "What congenital defect results from failure of...?"

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1. TIMELINE OF EYE DEVELOPMENT

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2. OPTIC VESICLE AND OPTIC CUP

2.1 Formation

• Neural plate folds to form the neural tube. Before closure, the optic sulci (paired grooves) appear in the forebrain (prosencephalon/diencephalon region) at ~22 days.
• As the neural tube closes, the optic sulci expand laterally → optic vesicles (hollow evaginations of the diencephalon wall), connected to the developing brain by the optic stalk.
• The optic vesicle makes contact with the overlying surface ectoderm and induces it to thicken → lens placode.

2.2 Invagination - Optic Cup Formation

• The optic vesicle and lens placode simultaneously invaginate:
  • Lens placode invaginates → lens pit → lens vesicle (pinches off from surface ectoderm by week 7)
  • Optic vesicle folds in on itself → optic cup (double-walled)

2.3 Optic Fissure (Choroidal Fissure / Embryonic Fissure)

• The invagination of the optic cup is not complete - a ventral groove remains = the optic fissure (also called choroidal fissure).
• The optic fissure allows the hyaloid artery (branch of ophthalmic artery) to enter the developing eye to supply the primary vitreous and lens.
• Fissure closes week 5-7, starting at the equatorial region and zipping anteriorly and posteriorly.

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3. LENS DEVELOPMENT

3.1 Induction

• Surface ectoderm is induced by the optic vesicle (without contact, no lens forms - the classic Spemann induction experiment)
• Surface ectoderm → lens placode → lens pit → lens vesicle (hollow sphere of epithelial cells, separates from surface ectoderm ~week 7)

3.2 Differentiation into Lens

• Anterior wall of lens vesicle = cuboidal epithelium → remains as the anterior lens epithelium (single layer under the anterior capsule; only mitotically active cells in the adult lens, at the germinative zone near the equator)
• Posterior wall of lens vesicle = elongates to fill the cavity → primary lens fibres = the embryonic nucleus of the adult lens

• Epithelial cells at the equatorial bow region continue to divide → migrate posteriorly → differentiate into secondary lens fibres
• New lens fibres are added in concentric shells throughout life - this is why the lens grows throughout life and older layers (embryonic nucleus) are never lost
• Lens fibres lose their nuclei and organelles → become transparent

3.3 Lens Sutures

• Secondary lens fibres from different directions meet at junction lines = lens sutures
• Embryonic nucleus: Y suture (upright anterior Y, inverted posterior Y) - visible on slit-lamp in children and some adults
• Adult nucleus: More complex star-shaped sutures with more branches as more fibres are added

3.4 Lens Capsule

• Formed by the lens epithelium (secretes type IV collagen and laminin)
• Thickest at the pre-equatorial anterior zone (~14 µm); thinnest at the posterior pole (~4 µm) - important in posterior capsule rupture during surgery

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4. VITREOUS DEVELOPMENT

4.1 Primary Vitreous

• Forms between the invaginating lens vesicle and the inner layer of the optic cup
• Composed of: ectodermal cells (from lens), mesodermal cells (from hyaloid vascular system), and primitive fibrillar material
• Contains the hyaloid vascular system:
  • Hyaloid artery (branch of ophthalmic artery) enters through the optic fissure → runs through vitreous → reaches posterior lens capsule → tunica vasculosa lentis (surrounds the lens) and pupillary membrane (anterior to lens)
  • This system is essential for lens nutrition during development when the lens is avascular

4.2 Secondary Vitreous

• Produced by the inner neuroblastic layer of the retina (~week 9 onwards)
• Avascular, clear gel - pushes primary vitreous centrally
• Primary vitreous is condensed into the Cloquet's canal (running from the optic disc to the posterior lens capsule - the path of the old hyaloid artery)

4.3 Tertiary Vitreous (Zonules)

• Formed by the non-pigmented epithelium of the ciliary body (pars plana and pars plicata)
• The zonular fibres (= tertiary vitreous) are fibrillin-containing microfibrils

4.4 Regression of the Hyaloid System

• Hyaloid artery regresses from ~month 4, completing regression by birth
• Failure of regression → persistent fetal vasculature (PFV) - previously called PHPV (persistent hyperplastic primary vitreous)
  • Unilateral dense white pupil (leukocoria) at birth
  • Microphthalmos, elongated ciliary processes visible
  • Fibrovascular plaque behind the lens
  • Can cause cataract, glaucoma, retinal detachment

• Mittendorf dot: Remnant of the hyaloid attachment on the posterior lens capsule (small white dot, inferior to the posterior pole of the lens)
• Bergmeister's papilla: Small tuft of glial tissue on the optic disc - remnant of hyaloid artery at the disc
• Cloquet's canal: The optically empty tunnel through the vitreous (path of the old hyaloid artery)

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5. RETINAL DEVELOPMENT

5.1 Layers from the Inner Layer of Optic Cup

5.2 Macular Development

• Macula develops late - the foveal pit begins to form around month 7 in utero as the inner retinal layers migrate away from the foveal centre (foveal depression = absence of inner nuclear and ganglion cell layers, with only cone photoreceptors and Muller cells at the centre)
• Foveal architecture is not complete until 4-6 months postnatal (this is why central fixation and high acuity develop progressively in infants)
• The critical period for amblyopia is related to this prolonged cortical and retinal maturation

5.3 Retinal Vascularisation

• Retinal vessels develop from the optic disc outward via two mechanisms:
  • Vasculogenesis: De novo formation from spindle cell precursors (astrocyte precursors migrating from the optic nerve ahead of the vessels guide vascular development)
  • Angiogenesis: Sprouting from existing vessels
• Reaches the nasal ora serrata at ~36 weeks gestation
• Reaches the temporal ora serrata at ~40 weeks (temporal retina is the last to vascularise)
• Relevance to ROP: Premature birth leaves peripheral temporal retina avascular. Oxygen suppresses vasoproliferative drive → on return to room air (relative hypoxia), VEGF spikes → neovascularisation (ROP). The junction between vascularised and avascular retina = ridge in ROP.

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6. CHOROID, SCLERA, IRIS AND CILIARY BODY DEVELOPMENT

6.1 Neural Crest Cells - The Key Player

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7. ANTERIOR SEGMENT DEVELOPMENT - NCC MIGRATION WAVES

• The TM differentiates from the 3rd wave NCC
• The angle recess forms by atrophy/remodelling of the anterior part of the NCC sheet, not by a "pulling back" - this is the current understanding
• Failure of normal NCC differentiation → Axenfeld-Rieger syndrome, Peters anomaly, aniridia (PAX6 gene)

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8. EYELID AND LACRIMAL DEVELOPMENT

8.1 Eyelids

• Eyelid folds appear at week 6 as surface ectodermal folds growing over the cornea
• Eyelids fuse at week 8-9
• Separate (reopens) at month 5 (weeks 20-24)
• Failure to separate → ankyloblepharon (persistent fusion of lid margins)
• Meibomian glands, cilia, and accessory glands develop from the ectodermal lid margin

8.2 Lacrimal Gland

• Develops from surface ectoderm of the superior conjunctival fornix (~week 6-7)
• Multiple cords of epithelium proliferate from the conjunctival fornix → canalise to form acini and ducts
• The accessory lacrimal glands (Krause and Wolfring) also derive from conjunctival epithelium

8.3 Lacrimal Drainage System

• Nasolacrimal duct develops from surface ectoderm buried between the lateral nasal process and the maxillary process
• Solid cord of ectoderm canalises from above (punctum) downward
• Last segment to canalise = the lower end (into the nose at the valve of Hasner) - hence congenital nasolacrimal duct obstruction (NLDO) is always at the lower end
• Full canalisation usually complete by birth; may be delayed up to 12 months in ~6% of infants → epiphora from birth (dacryostenosis)

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9. OPTIC NERVE AND VISUAL PATHWAY DEVELOPMENT

9.1 Optic Stalk → Optic Nerve

• The optic stalk connects the optic vesicle/cup to the diencephalon
• As RGC axons grow back from the retina, they fill the optic stalk → the stalk becomes the optic nerve
• The optic stalk has an inner and outer layer:
  • Inner layer: filled by RGC axons → becomes the nerve fibre bundles
  • Outer layer: becomes the glial support (astrocytes)
• Myelination: Begins at the lateral geniculate nucleus and proceeds toward the eye. Myelination reaches the optic disc at about birth (full-term). Normally stops at the lamina cribrosa. Myelination does NOT extend into the retinal nerve fibres (no oligodendrocytes past the lamina cribrosa). Myelinated nerve fibres in the retina = aberrant, white feathery patches around the disc.

9.2 Optic Chiasm

• RGC axons from the nasal hemiretina cross at the chiasm (contralateral pathway)
• RGC axons from the temporal hemiretina do NOT cross (ipsilateral pathway)
• The proportion of crossing fibres varies by species: in humans, ~53% of fibres cross (slightly more nasal retina than temporal due to the slight nasal dominance)

9.3 Visual Cortex

• The visual cortex (V1, striate cortex, area 17) develops its columnar organisation (ocular dominance columns) during the critical period
• Ocular dominance columns are present at birth in rudimentary form but require visual input to develop properly - this is the basis for the critical period and amblyopia

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10. CONGENITAL ANOMALY SUMMARY TABLE - HIGH YIELD EXAM POINTS

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QUICK VIVA RECALL - EMBRYOLOGY

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WHAT WAS COVERED ✓

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GAPS THAT COULD APPEAR IN A VIVA

• Exact timing of iris pigment development (pigment appears at ~6 months - explains why all babies have blue/grey eyes at birth)
• Ciliary body folding (pars plana vs pars plicata differentiation)
• Bruch's membrane composition from NCC + RPE

• Nuclear (embryonic nucleus affected = intrauterine insult in first trimester, e.g. rubella)
• Sutural (Y suture cataract - often stationary, benign)
• Posterior polar (posterior capsule weakness, surgical risk)
• Lamellar/zonular (peri-nuclear, metabolic cause, rickets, hypocalcaemia)
• Christmas tree cataract (myotonic dystrophy)

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EMBRYOLOGY GAP FILL 1 — CHOROID, UVEAL TRACT & IRIS PIGMENTATION

1.1 Choroid Development

• Vascular endothelium: Mesoderm (lateral plate) - forms the choriocapillaris, medium and large choroidal vessels
• Stromal cells, melanocytes, smooth muscle of vessel walls: Neural crest cells (NCC)

• Week 6-7: NCC migrate into the periocular mesenchyme between the optic cup and surface ectoderm → form the uveal stroma
• Week 7-8: Vascular channels (from mesoderm) organise into the three layers: choriocapillaris (innermost), Sattler's layer (medium vessels), Haller's layer (large vessels)
• Bruch's membrane forms between the choriocapillaris and RPE: composed of 5 layers (from inner to outer):
  1. RPE basement membrane (from RPE cells - neural ectoderm)
  2. Inner collagenous zone (from RPE and NCC)
  3. Elastin layer (from NCC)
  4. Outer collagenous zone (from NCC/choriocapillaris endothelium)
  5. Choriocapillaris basement membrane (from endothelial mesoderm)

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1.2 Ciliary Body Development

• Ciliary body epithelium (both pigmented and non-pigmented layers) = extension of the optic cup margin (neural ectoderm)
  • Outer pigmented layer = continuation of the RPE
  • Inner non-pigmented layer = continuation of the neurosensory retina
• Ciliary muscle (smooth) = NCC-derived (unique - most smooth muscle elsewhere is mesodermal)
• Pars plana vs pars plicata: The optic cup margin folds anteriorly at ~week 10. The folded anterior portion (70 ciliary processes) = pars plicata. The flat posterior portion = pars plana.
• Ciliary processes are vascularised by branches of the major arterial circle (formed by anastomosis of long posterior ciliary arteries + anterior ciliary arteries)

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1.3 Iris Development

• Iris pigment epithelium (both layers - anterior and posterior) = optic cup anterior extension (neural ectoderm)
• Iris stroma = NCC (3rd wave migration)
• Sphincter pupillae = neuroectoderm (optic cup - smooth muscle unique origin)
• Dilator pupillae = neuroectoderm (optic cup)
• Iris vessels = mesoderm endothelium

Iris Colour and Pigmentation - Development

• At birth, the iris stroma contains very little pigment (melanocytes from NCC are present but have not yet produced significant melanin)
• The blue-grey appearance is due to light scattering (Tyndall/Rayleigh effect) from the relatively unpigmented collagen stroma - short wavelengths (blue) scatter more than long wavelengths
• Over the first 6-12 months of life, melanocytes in the iris stroma become activated and produce melanin → iris colour deepens to its definitive adult colour
• Brown iris: Dense melanin in both the iris stroma AND the iris pigment epithelium
• Blue iris: Minimal stromal melanin; the Tyndall effect creates the blue appearance. The posterior IPE is always pigmented regardless of iris colour.
• Green/hazel: Intermediate amounts of stromal melanin

• Heterochromia iridis (different coloured irides): Can be congenital (Horner syndrome - sympathetic fibres trophic to melanocytes; Waardenburg syndrome - NCC melanocyte migration failure) or acquired (Fuchs' heterochromic iridocyclitis, haemosiderosis, siderosis)
• Horner syndrome in infancy → lighter iris on the affected side (sympathetic loss → reduced melanocyte stimulation → less melanin in developing stroma → permanent heterochromia if injury is before iris pigmentation is complete, i.e., before ~2 years)
• Albinism: Melanocytes present but non-functional (tyrosinase deficiency in OCA1) → no melanin in stroma OR IPE → translucent iris, marked photophobia, foveal hypoplasia (melanin required for normal foveal development), nystagmus

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1.4 Scleral Development

• Sclera = primarily NCC with contributions from mesoderm
• The episcleral and scleral proper layers form from NCC condensation around the optic cup
• Scleral thickness is greatest posteriorly near the optic nerve (1 mm) and thinnest just behind the rectus muscle insertions (0.3 mm) - the area of greatest surgical risk for globe perforation during retrobulbar injection

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EMBRYOLOGY GAP FILL 2 — CONGENITAL CATARACT: MORPHOLOGY, AETIOLOGY, SURGICAL SIGNIFICANCE

2.1 Epidemiology

• 3 in 10,000 live births
• 2/3 bilateral, 1/3 unilateral
• Aetiology breakdown:
  • 1/3 systemic association
  • 1/3 inherited (AD most common)
  • 1/3 unknown / sporadic
• Unilateral cataracts: usually sporadic, no family history, otherwise healthy infant - but carry a worse amblyopia prognosis (dense unilateral deprivation amblyopia)

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2.2 Morphology by Zone of Lens - Embryological Significance

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2.3 Aetiological Classification

Metabolic causes:

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Intrauterine infections (TORCH):

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Chromosomal and systemic associations:

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2.4 Posterior Polar Cataract - Why Surgically Critical

• The posterior capsule under the opacity is abnormally thin, brittle, and adherent to the opacity
• High incidence of posterior capsule rupture during hydrodissection (fluid wave reaches the adherent posterior pole and causes sudden rupture)
• Safe technique: Avoid aggressive hydrodissection; use hydrodelineation only; perform viscodissection gently; use low-flow phaco settings; anticipate and have vitrectomy prepared

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2.5 Anterior Polar Cataract

• Small, white dot at the anterior pole
• Usually stationary, visually insignificant
• If bilateral and central = may cause mild amblyopia - monitor refraction
• Cause: failure of lens vesicle to fully separate from surface ectoderm → small tag of ectoderm attached at anterior pole
• Pyramidal cataract: an anterior polar cataract where the opacity protrudes forward as a cone through the anterior capsule

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2.6 Management Principles of Congenital Cataract (Brief - Full detail in Paediatric Ophthalmology section)

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QUICK VIVA RECALL - GAP FILLS

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