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Ectropion

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Symptoms

• Epiphora (tear overflow / watering)
• Irritation, redness, mucous discharge
• May be asymptomatic in mild cases

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Types and Etiology

1. Involutional (Age-related) - Most Common

• Horizontal lid laxity - pulling the central lid 8 mm or more from the globe, with failure to snap back without blinking
• Lateral canthal tendon laxity - rounded lateral canthus; lower lid displaced >2 mm medially on traction
• Medial canthal tendon laxity - pulling the lid laterally; punctum displaced >1-2 mm (reaches limbus if mild, pupil if severe)

2. Cicatricial

• Burns, trauma, prior surgery
• Chronic dermatitis, ichthyosis, actinic damage
• Both lids may be involved; defect may be local or general

3. Paralytic

• Retraction of both upper and lower lids
• Brow ptosis (which may mimic narrowing of the palpebral aperture)
• Complications: Exposure keratopathy from lagophthalmos, epiphora from punctal malposition, failure of lacrimal pump, reflex hyperlacrimation from corneal exposure

4. Mechanical

5. Congenital

6. Allergic

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Signs

• Critical: Outward turning of the eyelid margin
• Superficial punctate keratopathy (SPK) from corneal exposure
• Conjunctival injection, thickening, and eventual keratinization from chronic dryness
• Eyelid scarring (cicatricial cases)
• Facial hemiparesis and lagophthalmos (paralytic cases)

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Workup

1. History: Prior surgery, trauma, chemical burn, CN VII palsy?
2. External examination:
   • Orbicularis oculi function
   • Horizontal eyelid laxity (snap-back test)
   • Punctal position
   • Eyelid tumor, scarring, herniated fat
   • If CN VII palsy + CN VIII deficit (hearing loss): CT/MRI brain to rule out acoustic neuroma
3. Slit lamp examination: Exposure keratopathy, conjunctival inflammation

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Treatment

Medical / Temporizing

1. Lubricating agents (artificial tears, ointment) for exposure keratopathy
2. Warm compresses + antibiotic ointment (bacitracin or erythromycin q.i.d.) for an inflamed, exposed eyelid margin; a short course of antibiotic-steroid ointment (neomycin/polymyxin B/dexamethasone) may help
3. Lid taping as a temporizing measure

Surgical - By Type

Note: In CN VII palsy, surgery is delayed 3-6 months as the ectropion may resolve spontaneously. Corneal exposure may make repair more urgent.

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Follow-Up

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Entropion

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Symptoms

• Irritation and foreign-body sensation (lashes rubbing cornea)
• Tearing
• Redness
• May be asymptomatic in very mild cases

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Signs

• Critical: Inward turning of the eyelid margin pushing otherwise normal lashes onto the globe
• Superficial punctate keratopathy (SPK) from lash-cornea contact
• Conjunctival injection
• In severe/long-standing cases: corneal epithelial defect, thinning, ulceration, pannus formation

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Types and Etiology

1. Involutional (Age-related) - Most Common

2. Cicatricial

• Cicatrizing conjunctivitis (mucous membrane pemphigoid, Stevens-Johnson syndrome)
• Trachoma
• Trauma and chemical burns
• Can affect upper or lower lid

3. Spastic

4. Congenital

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Workup

1. History: Previous surgery, trauma, chemical burn, or infection (trachoma, herpes simplex, varicella zoster)?
2. Slit lamp examination:
   • Corneal involvement (SPK, epithelial defect, ulceration)
   • Conjunctival or eyelid scarring (to identify cicatricial type)
3. External examination: Assess horizontal laxity, lower lid retractor function (excursion in downgaze), orbicularis function

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Treatment

Medical / Temporizing

1. Aggressive lubrication + antibiotic ointment (erythromycin or bacitracin q.i.d.) to protect the corneal surface
2. Everting the lid and taping with lateral traction - temporizing measure
3. Lubricants, soft bandage contact lenses, botulinum toxin into orbicularis - all short-term temporizing options
4. Quickert suture (at bedside or in-office) for spastic entropion - tightens lower lid retractors and rotates lid margin anteriorly

Surgical - By Type

Involutional Entropion

Cicatricial Entropion

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Comparison: Entropion vs. Ectropion

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Follow-Up

• If the cornea is uninvolved: no urgent attention required
• If corneal SPK or epithelial defect present: aggressive treatment and close follow-up (see Exposure Keratopathy management)

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Presbyopia

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Physiology of Accommodation (Normal)

• The lens is a biconvex, elastic structure suspended by zonular fibers (suspensory ligaments) attached to the ciliary body
• At rest, zonules are under tension, keeping the lens relatively flat (suited for distance vision)
• For near vision: parasympathetic stimulation (CN III) causes ciliary muscle contraction (both meridional and circular fibers), which releases zonular tension, allowing the lens to assume a more spherical, convex shape by its own elasticity - increasing refractive power
• In a child, the accommodative range is approximately 14 diopters

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Pathophysiology

1. Grows larger and thicker
2. Undergoes progressive denaturation of lens proteins - the lens becomes harder, less elastic, and less pliable
3. Loses the ability to change shape even when zonular tension is fully released by ciliary muscle contraction

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Epidemiology and Onset

• Typically presents in the 4th to 6th decade of life (symptoms usually noticed around age 40-45)
• Universal - affects all individuals regardless of prior refractive status
• Progressive and irreversible

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Symptoms

• Difficulty reading small print (most common presenting complaint)
• Need to hold reading material farther away ("short arm syndrome")
• Eyestrain and headaches after near work
• Blurred near vision, especially in dim light
• Fatigue with sustained reading

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Effect by Refractive Status

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Correction / Treatment

1. Spectacles (Glasses) - First-line

• Reading glasses - single-vision near correction for emmetropes
• Bifocals - distance correction above + near addition below; most common for existing glasses wearers
• Trifocals / Progressive addition lenses (PALs) - graduated correction for distance, intermediate, and near; no visible line

2. Contact Lenses

• Monovision contact lenses - dominant eye corrected for distance, non-dominant for near; relies on neuroadaptation and suppression of blur
• Multifocal contact lenses - simultaneous vision with distance and near zones

3. Surgical Options

Note on intracorneal inlay complications: decentration, dry eyes, keratolysis, corneal vascularization, and corneal haze requiring removal.

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Key Clinical Points

• The myopic patient is the exception - removing distance glasses may suffice for near vision despite presbyopia
• Pinhole testing improves acuity in refractive errors but does not restore accommodation lost in presbyopia
• Presbyopia is distinct from pathological causes of near vision loss (e.g., cataract, macular disease)
• New-onset presbyopia symptoms in a younger patient should prompt consideration of drug effects (e.g., anticholinergics) or systemic disease

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Keratoplasty (Corneal Transplantation / Corneal Grafting)

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General Indications

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Donor Tissue

• Removed within 12-24 hours of death
• Age-matching of donor and recipient is attempted
• Corneas from infants ≤3 years are rarely used even in paediatric transplants - associated with surgical, refractive, and rejection problems
• Stored at eye banks where pre-release evaluation includes:
  • Medical history and blood screening (to exclude contraindications)
  • Microscopic examination + endothelial cell count
• Storage methods:
  • Hypothermic storage: up to 7-10 days
  • Organ culture medium: up to 4 weeks (allows more time for evaluation)

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Types of Keratoplasty

1. Penetrating Keratoplasty (PK) - Full Thickness

• Common graft size: 7.5 mm
  • Small grafts → high astigmatism
  • Large grafts (>8 mm) → increased risk of peripheral anterior synechiae + raised IOP
• Donor button is ~0.25 mm larger than the host trephination site
• Preparation of donor cornea always precedes host excision (in case donor tissue is unsuitable)
• Trephination: mechanically guided manual or automated (including laser)
• Sutures: continuous, interrupted, or combination (Fig. 8.4)

• Topical steroids (prednisolone acetate 1% or dexamethasone 0.1%): initially every 2 hours, gradually tapered; long-term low-dose (once daily for a year or more) is usual
• Other immunosuppressants (oral azathioprine, topical/systemic ciclosporin): reserved for high-risk cases
• Cycloplegia (homatropine 2% b.d.): for 1-2 weeks
• Oral acyclovir: if pre-existing HSV keratitis, to minimize recurrence
• IOP monitoring: non-applanation method preferred (applanation unreliable over graft)
• Endothelial monitoring: central corneal thickness by pachymeter (indirect measure)
• Suture removal: typically at 12-18 months (longer in elderly); broken or loose sutures removed immediately to reduce vascularization and rejection risk

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2. Superficial Lamellar Keratoplasty (SLK)

• Opacification of superficial one-third of corneal stroma (not from recurrent disease)
• Marginal corneal thinning/infiltration (e.g., recurrent pterygium, Terrien marginal degeneration, limbal dermoid/tumour)
• Localized thinning or descemetocoele formation

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3. Deep Anterior Lamellar Keratoplasty (DALK)

• Anterior corneal disease with normal endothelium and no breaks/scars in Descemet membrane (e.g., keratoconus without history of acute hydrops, superficial trauma)
• Chronic inflammatory disease with high rejection risk (e.g., atopic keratoconjunctivitis)

• No risk of endothelial rejection (epithelial/subepithelial/stromal rejection can still occur)
• Less postoperative astigmatism
• Structurally stronger globe
• Increased availability of donor material (endothelial quality irrelevant)

• Technically difficult and time-consuming; high perforation risk
• Interface haze may limit final visual acuity
• Postoperative management similar to PK but lower-intensity steroids; sutures removable after ~6 months

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4. Endothelial Keratoplasty (EK)

Two Main Techniques:

• Minimal refractive change; structurally more intact globe
• Faster visual rehabilitation
• Minimal suturing required

• Significant learning curve; specialized equipment required
• Visual outcome often suboptimal due to: graft thickness differences, irregularities, high-order aberrations, donor-recipient interface fibrosis
• Endothelial rejection can still occur

Key Tip: DSAEK results in more rapid visual improvement and less risk of rejection than penetrating keratoplasty.

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5. Limbal Stem Cell Grafting

• Transplantation of a limited limbal area from the healthy fellow eye
• Complete limbal transplantation of a donor annulus
• Ex vivo expansion/culture of host or donor stem cells + transplantation

Important: In unilateral Stevens-Johnson syndrome or ocular cicatricial pemphigoid, donor tissue must not be taken from the unaffected fellow eye (use allograft, not autograft).

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Postoperative Complications

Early Complications (PK)

• Persistent epithelial defects
• Loose or protruding sutures (risk of infection, papillary hypertrophy)
• Wound leak (flat anterior chamber, iris prolapse)
• Uveitis, raised IOP
• Traumatic graft rupture
• Cystoid macular oedema
• Microbial keratitis, endophthalmitis
• Urrets-Zavalía syndrome (fixed dilated pupil) - rare
• Graft rejection

Late Complications

• Astigmatism
• Recurrence of underlying disease
• Late wound dehiscence
• Retrocorneal membrane formation
• Glaucoma
• Graft rejection / failure without rejection

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Corneal Graft Rejection

Immunological Privilege of the Cornea

• Absence of blood vessels and lymphatics
• Few antigen-presenting cells

Predisposing Factors

• Host stromal vascularization (most significant)
• Eccentric or large grafts (>8 mm diameter)
• Infection (especially herpetic)
• Glaucoma
• Previous keratoplasty
• HLA mismatch (HLA matching has small but beneficial effect on graft survival)
• Gender incompatibility: male donor cornea should NOT be given to a female recipient (recently identified as an important risk factor)

Symptoms

Signs by Rejection Layer

Management of Rejection

1. Preservative-free topical steroids hourly for 24 hours → gradual taper over weeks; steroid ointment at bedtime
2. Topical cycloplegia (homatropine 2% or atropine 1% once/twice daily)
3. Topical ciclosporin 0.05-2% (delayed onset)
4. Systemic steroids: oral prednisolone 1 mg/kg/day for 1-2 weeks OR IV methylprednisolone 500 mg/day for up to 3 days (if within 8 days of onset - particularly effective)
5. IOP monitoring throughout

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Blepharitis

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Classification

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Types, Aetiology and Pathophysiology

1. Anterior Blepharitis

a) Staphylococcal Blepharitis

• Causative agent: Staphylococcus aureus
• Mechanism: Abnormal cell-mediated immune response to components of S. aureus cell wall
• More common and severe in patients with atopic dermatitis
• Responsible for peripheral corneal infiltrates and red eyes in some patients
• More amenable to treatment and remission than posterior disease

b) Seborrhoeic Blepharitis

• Strongly associated with seborrhoeic dermatitis (scalp, nasolabial folds, skin behind ears, sternum)
• Characterized by greasy, waxy scales (scurf) clinging to lashes
• Less inflammatory than staphylococcal

2. Posterior Blepharitis (Meibomian Gland Dysfunction - MGD)

• Caused by dysfunction and altered secretions of meibomian glands
• Bacterial lipases → formation of free fatty acids → raises melting point of meibum → inspissation of glands → obstructed orifices
• Loss of tear film phospholipids (surfactants) → increased tear evaporation and osmolarity → unstable tear film
• Promotes growth of S. aureus
• More persistent and chronic than anterior blepharitis
• Strongly associated with acne rosacea

3. Demodex Blepharitis

• Caused by the hair follicle/sebaceous gland mite Demodex:
  • D. folliculorum longus → anterior blepharitis
  • D. folliculorum brevis → posterior blepharitis
• Collarettes (partially digested epithelial cells, keratin, waste, and mite eggs around lash bases) are considered pathognomonic
• Found normally in most older adults; symptomatic disease may relate to overpopulation or hypersensitivity to a commensal Bacillus carried by the mite
• Detection: under ×16 slit lamp magnification, rotating an epilated lash reveals mites (0.2-0.4 mm); slide microscopy for confirmation

4. Angular Blepharitis

• Inflammation localized to the medial and/or lateral canthal angles
• Associated with Moraxella spp.

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Symptoms

• Burning, grittiness, mild photophobia, crusting on waking
• Stinging - more common in posterior disease
• Itching, tearing, foreign body sensation
• Eyelid erythema
• Usually no visual disturbance
• Symptoms often worse in the morning (distinguishes from dry eye, where symptoms worsen later in the day)
• Bilateral and symmetrical involvement

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Signs

• Crusty, red, thickened eyelid margins with prominent blood vessels
• Inspissated (blocked) meibomian gland orifices
• Crusting and collarettes around lash bases (Demodex)
• Cylindrical sleeves on lashes (Demodex)

• Hard, fibrinous crusts adherent to lash bases (leave a bleeding ulcer when removed)
• Madarosis (lash loss), trichiasis, poliosis (whitening of lashes)

• Soft, greasy, easily removed scales (scurf)
• Oily lid margins; no ulceration

• Capping of meibomian orifices by oil globules
• Plugged, inspissated meibomian gland orifices
• Expressed toothpaste-like or frothy material at lid margin
• Froth on lid margin

• Conjunctival injection, mild mucous discharge, SPK
• Papillary conjunctivitis
• Inferior corneal punctate epithelial erosions
• Marginal keratitis, phlyctenules, corneal vascularization/scarring
• Rosacea (face/nose)

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Characteristics Comparison Table

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Secondary / Chronic Complications

• Papillary conjunctivitis
• Inferior corneal punctate erosions
• Corneal scarring and vascularization
• Salzmann nodular degeneration
• Stye (hordeolum) formation
• Marginal keratitis
• Bacterial keratitis (especially in contact lens wearers)
• Phlyctenular eye disease
• Blepharoconjunctivitis (if becomes chronic)

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Differential Diagnosis

• Pediculosis (eyelash lice)
• Demodicosis (cylindrical sleeves + microscopy)
• Sebaceous carcinoma - must be considered in intractable, unilateral, or asymmetric blepharitis (upper vs. lower lid asymmetry); warrants formal clinical workup

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Treatment

Step 1 - Lid Hygiene (All Types - First-line)

1. Warm compresses for 5-10 minutes b.i.d. to q.i.d. (softens crusts and meibum)
2. Lid margin scrubbing with wet cotton bud, clean wet face-cloth, or commercial soap/alcohol-impregnated eyelid scrub pads

   Note: Baby shampoo is NOT recommended - it destabilizes the tear film and is a common cause of contact dermatitis

3. For significant MGD: express accumulated meibum by rolling a finger anteriorly over the lid margin
4. Frequency: twice daily initially, reduce as symptoms improve; may need to be maintained indefinitely

Step 2 - Topical Antibiotics (Anterior Disease)

• Sodium fusidic acid, erythromycin, bacitracin, azithromycin, or chloramphenicol ointment
• Applied to anterior lid margin with cotton bud after lid hygiene, at bedtime (q.h.s.)

Step 3 - Dry Eye Management

• Preservative-free artificial tears 4-8 times per day if associated dry eyes

Step 4 - Oral Antibiotics (Moderate-Severe / Posterior Disease)

⚠️ Tetracyclines are contraindicated in pregnant women, nursing mothers, and children ≤8 years old. Use erythromycin 200 mg p.o. b.i.d. as an alternative.

Step 5 - Anti-inflammatory Agents

• Cyclosporine 0.05% or 0.09% eye drops b.i.d.
• Lifitegrast 5% drops b.i.d.
• Omega-3 fatty acid supplementation (oral)
• Topical antibiotic-steroid combinations (e.g., tobramycin/dexamethasone b.i.d.-t.i.d.) for unresponsive meibomitis
• Systemic steroids: for severe refractory cases

Step 6 - Demodex-Specific Treatment

• Tea-tree oil eyelid scrubs or hypochlorous acid eyelid cleansing agent once or twice daily for ≥6 weeks
• Mechanism: prevention of Demodex reproduction

Step 7 - Procedural (Refractory MGD)

• Thermal treatment to meibomian glands with expression
• Intense pulsed light (IPL) laser therapy
• Microblepharoexfoliation
• Probing of meibomian glands

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Follow-Up

• 2-4 weeks initially, depending on severity
• Eyelid scrubs and warm compresses may be reduced to once daily as the condition improves, but often need to be maintained indefinitely

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Blepharitis: Clinical Features, Management, and Squamous vs. Ulcerative Differences

Overview

• Squamous blepharitis = Seborrhoeic / non-ulcerative anterior blepharitis
• Ulcerative blepharitis = Staphylococcal / infective anterior blepharitis

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Squamous vs. Ulcerative Blepharitis - Detailed Comparison

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Full Clinical Features

Symptoms (Common to Both)

• Burning, grittiness, mild photophobia
• Crusting and redness of lid margins, worse on waking
• Itching, tearing, foreign body sensation
• Symptoms typically worse in the morning (contrast with dry eye: worse later in day)
• No visual disturbance
• Poor tolerance of contact lenses
• Stinging more prominent in posterior disease

Signs - Staphylococcal (Ulcerative)

• Hard, fibrinous crusts firmly adherent to lash bases
• Collarettes (cylindrical collections around individual lash bases)
• Small lid margin ulcers at lash bases when crusts are removed (hence "ulcerative")
• Madarosis (loss of lashes) - marked
• Trichiasis (misdirected lashes), poliosis (whitened lashes) in long-standing cases
• Notching and scarring of lid margin
• Papillary conjunctivitis, phlyctenules
• Marginal corneal infiltrates (peripheral)
• Inferior corneal punctate epithelial erosions
• Hordeolum (stye) formation

Signs - Seborrhoeic (Squamous)

• Soft, greasy, oily scales (scurf) on lid margins
• Hyperaemic, greasy anterior lid margins
• Lashes adherent to each other (not to lid margin)
• Mild papillary conjunctivitis
• Minimal lash loss; no true ulceration
• Associated generalized seborrhoeic dermatitis of scalp, face

Signs - Posterior (Meibomian Gland Dysfunction)

• Capping of meibomian orifices with oil globules
• Pouting, recession, or plugging of meibomian gland orifices
• Hyperaemia and telangiectasis of posterior lid margin
• Expressed meibum: turbid or toothpaste-like material; in severe cases, expression impossible
• Foamy, unstable tear film; froth at lid margins or inner canthi
• Lid transillumination: gland loss and cystic ductal dilation
• Associated with acne rosacea

Signs - Demodex

• Collarettes (pathognomonic) - partially digested epithelial cells + mite eggs around lash bases
• Cylindrical dandruff-like scaling
• Confirmed by epilating a lash and examining under slit lamp (mites 0.2-0.4 mm)

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Kanski's Summary Table (Table 2.4)

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Secondary Complications (All Types)

• Papillary conjunctivitis
• Inferior corneal punctate erosions → scarring and vascularization
• Salzmann nodular degeneration
• Stye (hordeolum) formation
• Marginal keratitis; bacterial keratitis (especially in contact lens wearers)
• Phlyctenular eye disease
• Blepharoconjunctivitis if chronic

⚠️ Red flag: Intractable, unilateral, or asymmetric blepharitis (particularly upper vs. lower lid asymmetry) is rarely a manifestation of sebaceous carcinoma of the eyelid and requires appropriate clinical workup.

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Management

Step 1 - Lid Hygiene (All Types - First-line, Indefinite)

1. Warm compresses for 5-10 minutes b.i.d. to q.i.d. - softens inspissated crusts and meibum
2. Lid margin scrubbing - using wet cotton bud, clean face-cloth, or commercial eyelid scrub pads
   • For MGD: add meibomian expression by rolling finger anteriorly over lid margin

   Note: Baby shampoo is NOT recommended - destabilizes the tear film and causes contact dermatitis

3. Perform twice daily initially; reduce frequency as condition improves but may need to be continued indefinitely

Step 2 - Topical Antibiotics (Anterior Disease)

• Sodium fusidic acid, erythromycin, bacitracin, azithromycin, or chloramphenicol ointment
• Applied to anterior lid margin after lid hygiene, at bedtime (q.h.s.)
• Used for active folliculitis; may be extended long-term

Step 3 - Artificial Tears

• Preservative-free artificial tears 4-8 times per day for associated dry eye and tear film instability

Step 4 - Oral Antibiotics (Moderate-Severe / Posterior / Refractory)

⚠️ Tetracyclines are contraindicated in pregnancy, nursing mothers, and children ≤8 years. Use erythromycin 200 mg p.o. b.i.d. as the alternative.

Step 5 - Anti-inflammatory / Immunomodulatory Agents

• Cyclosporine 0.05% or 0.09% eye drops b.i.d.
• Lifitegrast 5% drops b.i.d.
• Omega-3 fatty acid oral supplementation
• Topical antibiotic-steroid combinations (e.g., tobramycin 0.3%/dexamethasone 0.1% b.i.d.-t.i.d.) for unresponsive meibomitis

Step 6 - Demodex-Specific Treatment

• Tea-tree oil eyelid scrubs or hypochlorous acid eyelid cleansing once or twice daily for ≥6 weeks

Step 7 - Procedural (Refractory MGD)

• Thermal treatment to meibomian glands with expression
• Intense pulsed light (IPL) therapy
• Microblepharoexfoliation
• Meibomian gland probing

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Follow-Up

• Review at 2-4 weeks based on severity
• Lid hygiene may be reduced to once daily as condition improves but often needs indefinite maintenance

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Tear Film: Structure, Function, Secretion and Elimination

Overview

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Structure: The Three Layers

Layer 1 - Lipid Layer (Outermost) - 0.1 μm

• Outer non-polar phase: waxes, cholesterol esters, triglycerides
• Inner polar phase: phospholipids adjacent to the aqueous-mucin interface
• Polar lipids are bound to lipocalins within the aqueous layer - small proteins that bind hydrophobic molecules and contribute to tear viscosity

• Thickness increases with forced blinking; decreases with infrequent blinking
• Lid movement during blinking is important in releasing lipids from meibomian glands

1. Prevents evaporation of the aqueous layer - maintains tear film thickness
2. Acts as a surfactant allowing spread of the tear film over the ocular surface
3. Provides a smooth optical interface
4. Deficiency → evaporative dry eye (most common form of dry eye)

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Layer 2 - Aqueous Layer (Middle) - 7.0 μm (Thickest)

• Main lacrimal gland (orbital and palpebral lobes) - reflex tearing and emotional tearing
• Accessory lacrimal glands (Krause and Wolfring) - basal tear secretion; essential for maintaining the resting tear film

• Water (~98%)
• Electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻)
• Proteins: IgA (secretory), lysozyme, lactoferrin, lipocalin, albumin, growth factors
• Over 100 distinct proteins have been identified

1. Provides atmospheric oxygen to the avascular corneal epithelium
2. Antibacterial activity via IgA, lysozyme, lactoferrin
3. Washes away debris and noxious stimuli; transports leukocytes to injury sites
4. Optically enhances the corneal surface by abolishing minute surface irregularities
5. Maintains hydration of the ocular surface
6. Deficiency → aqueous-deficient dry eye (Sjögren and non-Sjögren types)

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Layer 3 - Mucous Layer (Innermost) - 0.2 μm

• Conjunctival goblet cells (principal source) - secretory mucins
• Accessory lacrimal glands (minor contribution)
• Surface epithelial cells of cornea and conjunctiva - produce transmembrane mucins that form the glycocalyx (extracellular cell coat)

1. Converts the hydrophobic corneal epithelium to a hydrophilic surface - essential for aqueous adherence (without mucin, aqueous tears cannot wet the corneal surface)
2. Lubrication - reduces friction during blinking
3. Traps and removes debris and microorganisms

• Rose Bengal staining of diseased epithelium indicates absence of transmembrane and gel mucous layers, leaving the cell surface exposed
• Goblet cell loss → mucin deficiency → tear film instability
• Causes of goblet cell loss: cicatrizing conjunctivitis, vitamin A deficiency, chemical burns, medication toxicity

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Spread of the Tear Film

1. Normal blink reflex
2. Contact between the external ocular surface and the eyelids
3. Normal corneal epithelium

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Secretion

Basal Tear Secretion

• Produced continuously by the accessory lacrimal glands of Krause and Wolfring
• Rate: approximately 1-2 μL/minute under normal resting conditions
• Maintains the resting tear film without reflex stimulation

Reflex Tear Secretion

• Produced by the main lacrimal gland in response to:
  • Corneal/conjunctival stimulation (noxious, tactile, chemical)
  • Emotional stimuli (crying)
  • Bright light

Neural Control of Secretion

• Preganglionic neurons arise from the lacrimal nucleus of the pons (nervus intermedius)
• Axons travel via CN VII (facial nerve) → greater superficial petrosal nerve → vidian nerve → sphenopalatine (pterygopalatine) ganglion (synapse)
• Postganglionic fibres travel via zygomatic branch of CN V₂ → anastomosis with lacrimal branch of CN V₁ → lacrimal gland
• Stimulation causes aqueous and mucus secretion

Hormonal Regulation

• Androgens - prime hormones responsible for regulating lipid (meibomian) production; androgen deficiency is implicated in dry eye
• Oestrogens and progesterone receptors in conjunctiva and lacrimal gland - essential for normal tissue function
• Strong association between dry eye and reduced systemic androsterone sulphate and epiandrosterone sulphate

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Elimination (Drainage)

Drainage Pathway

Tear lake (lacus lacrimalis) at medial canthus
        ↓
Upper and lower lacrimal puncta (on lid margins, ~6 mm from medial canthus)
        ↓
Upper and lower canaliculi
        ↓
Common canaliculus (present in ~90% of people)
        ↓
Valve of Rosenmuller (one-way valve - prevents reflux into canaliculi)
        ↓
Lacrimal sac (in lacrimal fossa, medial orbital wall)
        ↓
Nasolacrimal duct
        ↓
Valve of Hasner (inferior meatus of nasal cavity, last part to canalize)
        ↓
Inferior nasal meatus

Physiology of Drainage (Lacrimal Pump Mechanism)

1. Tears flow along the marginal tear strips medially, pooling in the lacus lacrimalis
2. With each blink (orbicularis oculi contraction): canaliculi and lacrimal sac are compressed → tears are forced down the nasolacrimal duct
3. When eyes open: canaliculus and sac expand → negative pressure (suction) draws tears from the conjunctival sac into the canaliculi

Causes of Drainage Failure (Epiphora)

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Tear Film Break-Up Time (BUT)

• Normal BUT: >10 seconds
• Abnormal (dry eye): ≤10 seconds
• Measured by instilling fluorescein and timing from a complete blink to the first random dry spot appearing in the tear film under cobalt blue slit lamp illumination

Marginal Tear Meniscus (Strip)

• A crude measure of aqueous tear volume
• Normal: 0.2-0.4 mm in height
• Dry eye: <0.25 mm or absent

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Tear Film Regulation Summary

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Mechanism of Dry Eye Disease (Integration)

1. Tear instability
2. Tear hyperosmolarity
3. Inflammation (present in 80% of KCS patients; both cause and consequence; rationale for steroid therapy)
4. Ocular surface damage

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Bell's Palsy

Definition

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Epidemiology

• Annual incidence: 23-40 per 100,000 (~1 in 60 persons in a lifetime)
• Affects men and women approximately equally
• Occurs at all ages and all times of the year
• Risk factors:
  • Pregnancy (particularly 3rd trimester and first 2 weeks postpartum; up to 3x increased risk cited)
  • Diabetes mellitus
  • Hypertension
• Recurrence reported in ~7% of cases

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Aetiology and Pathophysiology

• Herpes simplex virus type 1 (HSV-1): HSV-1 DNA has been identified in endoneurial fluid surrounding CN VII in surgical specimens from Bell's palsy patients; animal studies replicated facial paralysis by HSV inoculation. HSV-1 reactivation in the geniculate ganglion is the most widely accepted mechanism.
• Varicella-zoster virus (VZV): Implicated in up to one-third of cases and may be the second most common cause (when VZV is the cause with vesicular eruption, it becomes Ramsay Hunt syndrome, a separate diagnosis).
• Other viruses: HHV-6 (higher DNA copies in saliva of Bell's patients vs. controls), SARS-CoV-2, HIV seroconversion, and others have been implicated less commonly.
• Pathology: Inflammation and oedema → entrapment of the swollen nerve in the narrow labyrinthine segment of the facial canal → ischaemia and demyelination or axonal degeneration

Note: A recent Cochrane review showed antivirals against HSV are no more effective than placebo for complete recovery alone - this has cast some doubt on HSV as the sole causative agent.

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Anatomy Relevant to Bell's Palsy

• All muscles of facial expression
• Stapedius muscle (middle ear)
• Taste to anterior 2/3 of tongue (via chorda tympani)
• Secretomotor to lacrimal, submandibular, and sublingual glands
• Cutaneous sensation to small area behind the ear

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Clinical Features

Onset

• Acute - maximal weakness attained in 48 hours as a general rule; practically all cases reach maximum paralysis within 3-4 days

Symptoms

Signs

• Complete ipsilateral LMN facial palsy: weakness of upper and lower face (forehead involved - key distinction from UMN palsy)
• Inability to wrinkle forehead, raise eyebrow, close eye, show teeth, purse lips, inflate cheeks
• Loss of nasolabial fold; drooping of mouth corner
• Ectropion of lower lid, epiphora
• Normal otoscopy (essential - abnormal otoscopy = not Bell's palsy)
• Normal hearing (abnormal hearing = consider Ramsay Hunt or other cause)

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LMN vs. UMN Facial Palsy: Key Distinction

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Investigations

1. Typical acute presentation
2. No risk factors for other causes
3. No vesicular eruption in external ear canal (excludes Ramsay Hunt)
4. Normal neurological examination except facial nerve

• MRI with gadolinium: swelling and enhancement of the geniculate ganglion and facial nerve in the temporal bone (Fig. 452-4 Harrison's); enhancement in the labyrinthine, tympanic, and mastoid segments. Note: similar enhancement seen in Lyme disease, sarcoidosis, perineural malignancy
• ESR / CRP
• Fasting glucose / HbA1c (diabetes)
• Lyme serology (in endemic areas; Lyme may cause bilateral facial palsy)
• HIV serology
• ACE level + chest imaging (sarcoidosis)
• Lumbar puncture (Guillain-Barré consideration - may cause bilateral facial palsy)
• EMG/nerve conduction studies: useful prognostically after 10 days - evidence of denervation = axonal degeneration, indicates prolonged recovery

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Differential Diagnosis

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Prognosis

• 70% recover completely within 1-2 months
• 85% achieve near-normal function overall
• Incomplete paralysis in first 5-7 days = most favourable prognostic sign
• Return of taste within first week = good prognostic sign (recovery of taste precedes motor recovery)
• EMG after 10 days: evidence of denervation → axonal degeneration → delay of ~3 months before regeneration; may be incomplete
• MRI: pronounced contrast enhancement of facial nerve = worse prognosis
• Children: recovery rate ~90% regardless of treatment

• Synkinesis (aberrant nerve regeneration - eye blinks when mouth moves, "crocodile tears" on eating)
• Hemifacial spasm
• Persistent facial weakness and asymmetry

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Treatment

1. Eye Protection (Immediate - Prevent Corneal Damage)

• Paper tape to depress upper eyelid during sleep
• Lubricating eye drops (artificial tears) during the day
• Lubricating ointment at night
• Moisture chamber / eye patch if lagophthalmos is severe
• If Bell's phenomenon is absent (cornea not protected on attempted closure): more aggressive corneal protection required

2. Corticosteroids (Strong Evidence - First-line)

• Prednisone 60-80 mg daily for the first 5 days, then tapered over the next 5 days (total 10-day course)
• Start as early as possible (ideally within 72 hours of onset)
• Modestly shortens recovery and improves functional outcome
• Supported by large randomized controlled trials
• Children: recovery rate so high (90%) that steroids may not be necessary

3. Antiviral Therapy (Selective Use)

• Valacyclovir 1000 mg daily for 5-7 days OR acyclovir 400 mg five times daily for 10 days
• Large randomized trials found no added benefit of antivirals over steroids alone in typical Bell's palsy
• Use antivirals if: vesicular lesions in palate or external auditory canal (suggests VZV - Ramsay Hunt); severe/complete palsy; immunocompromised patient
• Cochrane review: antivirals alone no more effective than placebo

4. Physiotherapy

• Massage of weakened muscles
• Facial exercises

5. Surgical Decompression

• Controversial and rarely performed
• Transmastoid decompression considered in:
  • Severe complete palsy with EMG evidence of degeneration
  • No recovery by 3-4 months
  • Selected cases with complete denervation

6. Cosmetic / Rehabilitative Surgery (Permanent Paralysis)

• Various procedures to restore facial symmetry
• Gold weight implantation in upper lid for lagophthalmos
• Facial nerve grafting, muscle transfer

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Ophthalmic Complications and Management

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Proptosis

Definition

• The intraorbital optic nerve is 25 mm long vs. only 18 mm distance from the back of the globe to the optic canal - this slack allows significant forward globe displacement before the nerve is stretched

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Measurement

• Hertel exophthalmometer (most common) - uses the lateral orbital rim as a reference point; measures corneal apex protrusion
• Luedde exophthalmometer - simpler, single-eye measurement
• Normal value: ≤20 mm
• Proptosis: readings >20 mm OR ≥2-3 mm asymmetry between the two eyes (even if both values are within normal range)
• Measurements taken at rest and during Valsalva (to detect venous anomalies)

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Direction of Proptosis and Implied Pathology

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Pseudoproptosis (False Impression of Proptosis)

• Facial asymmetry
• Enlarged globe (high myopia, buphthalmos)
• Eyelid retraction (making eye appear to bulge)
• Contralateral enophthalmos (the normal eye appears proptotic by comparison)

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Causes of Proptosis

Classified by Aetiology

Key Clinical Mnemonics for Causes

• Sinusitis → orbital cellulitis
• Pseudotumour (idiopathic orbital inflammation)
• Infection (orbital cellulitis)
• Neoplasm
• Endocrine (thyroid eye disease)

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Clinical Assessment of Proptosis

Symptoms

• Protrusion of the eye
• Diplopia (double vision)
• Reduced vision (compressive optic neuropathy)
• Periorbital pain
• Exposure symptoms (dryness, grittiness)

Signs to Elicit

• Degree - Hertel exophthalmometer
• Direction - axial vs. dystopia
• Reducibility - retropulsion; non-reducible suggests fixed or rapidly expanding mass
• Pulsation + bruit (auscultate over closed lids) - AV fistula
• Positional change with Valsalva - venous lesion
• Lid retraction vs. true proptosis
• Ophthalmoplegia - restrictive vs. neurological (forced duction test; differential IOP test)
• Optic nerve function - VA, colour vision, RAPD, visual fields
• Fundus - disc swelling, optic atrophy, opticociliary collaterals, choroidal folds

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Investigations for Proptosis

• CT orbit - bone detail, sinuses, calcification (optic nerve meningioma - "tram-track" sign)
• MRI orbit - soft tissue definition, optic nerve
• Thyroid function tests (TFTs), thyroid antibodies
• CXR / chest CT - sarcoid, lymphoma
• Biopsy if neoplasm suspected

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Orbital Cellulitis

Definition

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Preseptal vs. Postseptal (Orbital) Cellulitis - Critical Distinction

The orbital septum is the critical anatomical barrier - a fibrous membrane extending from the orbital rim to the tarsal plates. Infection posterior to this = true orbital cellulitis.

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Epidemiology

• Can occur at any age but more common in children
• Most common source: paranasal sinusitis (especially ethmoid sinusitis)
• Perforation of the thin lamina papyracea (medial orbital wall) is the usual route from the ethmoid sinus

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Aetiology / Sources of Infection

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Causative Organisms

⚠️ Zygomycosis (Mucormycosis): Rapidly progressive, life-threatening sino-orbital infection in diabetics (especially ketoacidotic) or immunocompromised. Presents with severe pain, ophthalmoplegia, rapid visual loss, nasal eschar. Emergency surgical debridement + antifungals required.

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Clinical Features

Symptoms

• Rapid onset of periorbital pain, worsened by eye movement
• Swelling of the eye/lids
• Malaise, fever
• Visual impairment, double vision
• Recent history of nasal, sinus, or respiratory symptoms
• Headache (raised concern for intracranial extension)

Signs

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Investigations

1. CT orbits, sinuses, and brain with contrast - mandatory; confirms diagnosis; identifies:
   • Adjacent sinusitis (typically at least ethmoiditis)
   • Subperiosteal abscess (SPA) - most common on medial orbital wall
   • Orbital abscess (intraconal)
   • Intracranial extension
   • Retained foreign body
2. Full blood count (FBC/CBC) with differential
3. Blood cultures (before antibiotics)
4. Culture of nasal discharge
5. MRI - sometimes used additionally for soft tissue detail
6. Lumbar puncture if meningeal/cerebral signs
7. Tetanus immunization status (if traumatic)
8. Gram stain and culture of any wound drainage

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Complications

Ocular Complications

• Optic neuropathy (compressive - most feared vision-threatening complication)
• Exposure keratopathy
• Raised IOP / orbital compartment syndrome
• Central retinal artery or vein occlusion
• Endophthalmitis

Orbital Complications

• Subperiosteal abscess (SPA) - most commonly on medial orbital wall; requires drainage
• Orbital abscess - intraconal; requires urgent surgical drainage

Intracranial Complications (uncommon - 3-4% - but life-threatening)

• Cavernous sinus thrombosis (headache + CN III, IV, VI palsies → bilateral involvement)
• Meningitis
• Brain abscess
• Subdural empyema
• Epidural abscess
• Frontal bone osteomyelitis

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Differential Diagnosis of an Acutely Inflamed Orbit (Kanski Table 4.1)

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Treatment

1. Immediate Admission + Specialist Consultation (Mandatory)

• Hospital admission in all cases of true orbital cellulitis
• Urgent ophthalmology review (at minimum 4-hourly monitoring of optic nerve function)
• ENT/otolaryngology consultation (sinus disease management)
• Paediatric specialist input for children
• Infectious disease consultation in atypical, severe, or unresponsive cases
• Neurosurgery if meningeal signs or intracranial extension suspected
• Oral maxillofacial surgery if dental source (aggressive spread, cavernous sinus risk)

2. Optic Nerve Monitoring (Every 4 Hours Minimum)

• Visual acuity
• Colour vision
• Light brightness appreciation
• Pupillary reactions (RAPD)
• Deterioration → consider emergency surgical intervention

3. Intravenous Antibiotics (First-line)

• IV antibiotics until apyrexial for 4 days, then 1-3 weeks oral completion
• Mark extent of skin erythema with a surgical pen - to monitor progression or regression

4. Adjuvant Measures

• Topical nasal decongestant (e.g., oxymetazoline) for sinus drainage
• Nasal steroids (consider)

5. Surgery (Indications)

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Follow-Up

• Close review based on optic nerve monitoring every 4 hours initially
• Oral antibiotics continued for 1-3 weeks after discharge
• ENT follow-up for underlying sinus disease

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