Question 2 - Ophthalmology Case: 65-year-old male, bilateral painless progressive diminution of vision, lenticular opacities, normal fundus

Part (a) - Differential Diagnoses of Gradually Progressive, Painless Diminution of Vision in an Elderly Patient (3 marks)

Lens (Lenticular causes)

1. Senile/Age-related cataract (most likely here - lenticular opacities confirmed)
   • Nuclear sclerosis, cortical, posterior subcapsular
2. Diabetic cataract - snowflake cortical opacities; age-related cataract also occurs earlier in diabetics

Retinal causes

1. Age-related macular degeneration (AMD) - dry or wet; central vision loss
2. Diabetic retinopathy with macular oedema - bilateral, gradual
3. Central retinal artery occlusion / vein occlusion (usually acute, but chronic changes can cause gradual loss)
4. Retinitis pigmentosa - peripheral field loss + night blindness, can present in elderly

Glaucoma

1. Chronic open-angle glaucoma - slow, painless peripheral field loss; often asymptomatic until late

Optic nerve / Neurological

1. Optic atrophy (secondary to glaucoma, vascular, compressive) - afferent pupil defect, pallor

Corneal causes

1. Corneal degeneration / dystrophy (e.g., Fuchs' endothelial dystrophy, band keratopathy)

Vitreous

1. Vitreous haemorrhage or degeneration (though usually more acute)

In this case: The slit-lamp finding of lenticular opacities and a normal dilated fundus in both eyes points strongly to bilateral senile cataract as the diagnosis, excluding retinal and optic nerve causes.

Part (b) - Clinical Evaluation and Preoperative Investigations Before Cataract Surgery (6 marks)

Clinical Evaluation

History

• Duration and rate of progression of visual loss
• Occupation and visual requirements of the patient
• Symptoms: glare, halos, monocular diplopia, difficulty reading or driving (especially night driving)
• History of trauma, corticosteroid use, diabetes, uveitis
• Current medications - especially systemic alpha-blockers (tamsulosin) which cause intraoperative floppy iris syndrome (IFIS)
• Anticoagulant or antiplatelet use

Visual Function Assessment

• Best-corrected visual acuity (BCVA) - Snellen chart
• Contrast sensitivity and glare testing
• Potential acuity testing (to assess whether retinal function is adequate for surgery to be worthwhile)

Slit-Lamp Examination

• Type of cataract: nuclear sclerosis, cortical, posterior subcapsular, or combined
• Maturity: immature, mature, hypermature (Morgagnian)
• Anterior segment: corneal clarity, depth of anterior chamber, condition of iris
• Status of posterior capsule

Dilated Fundus Examination

• Macula: exclude AMD, diabetic macular oedema
• Optic disc: exclude glaucoma
• Peripheral retina: exclude lattice degeneration, tears (especially if myopic)

Other Examinations

• Intraocular pressure (IOP) measurement - baseline and to exclude glaucoma
• Keratometry and axial length measurement (biometry) for IOL power calculation (A-scan ultrasonography or optical biometry)
• Corneal endothelial count (specular microscopy) if Fuchs' dystrophy is suspected or repeat surgery

Preoperative Investigations

Per Kanski's: "Routine preoperative general medical examination, blood tests and ECG are not usually required for local anaesthesia." Investigations are targeted based on systemic history.

Part (c) - Management of Senile Cataract: Preferred Surgical Procedure and Postoperative Care (6 marks)

Indications for Surgery

• Visual: Opacity causing difficulty with daily activities (the most common indication); patient-reported functional impairment
• Medical: Phacolytic glaucoma, phacomorphic glaucoma, to allow fundus monitoring for diabetic retinopathy

Preferred Surgical Procedure: Phacoemulsification with IOL Implantation

Steps of Phacoemulsification

1. Corneal incision: A small self-sealing clear corneal tunnel incision (~2.2-2.8 mm)
2. Continuous curvilinear capsulorhexis (CCC): Circular tear of the anterior capsule (~5-6 mm)
3. Hydrodissection and hydrodelineation: Fluid injection to separate nucleus from capsule
4. Phacoemulsification: Ultrasonic probe emulsifies and aspirates the lens nucleus using sculpting and cracking techniques (divide and conquer, stop and chop, etc.)
5. Irrigation-aspiration (I/A): Removes residual cortical material
6. IOL implantation: A foldable acrylic IOL is inserted into the capsular bag through the same small incision
7. Wound hydration: The self-sealing incision is hydrated; sutures rarely needed

Advantages of Phacoemulsification

• Small incision (sutureless) → less surgically induced astigmatism
• Rapid visual recovery (often the next day)
• Low complication rate
• Can be done under topical or local anaesthesia as a day-case procedure

Alternative: MSICS (Manual Small Incision Cataract Surgery)

• Used in resource-limited settings (developing countries)
• Comparable visual outcomes to phacoemulsification
• Faster and cheaper, does not require expensive technology
• Suitable for dense/hard cataracts

IOL Selection

• Monofocal IOL (standard): Set for distance vision; patient needs reading glasses
• Multifocal/bifocal IOL: Reduces need for spectacles at all distances; higher rate of dysphotopsia
• Toric IOL: Corrects pre-existing corneal astigmatism
• Square-edged optic: Reduces posterior capsule opacification (PCO)
• Power calculated using biometry (SRK-T or Haigis formula)

Anaesthesia

• Usually topical anaesthesia (drops) or peribulbar/sub-Tenon's local anaesthesia
• General anaesthesia for very anxious, uncooperative, or paediatric patients

Postoperative Care

Immediate Postoperative (Day 0-1)

• Eye shield/pad applied to protect the eye
• Patient instructed to avoid rubbing the eye
• Snellen VA checked at first postoperative visit (usually day 1)
• Corneal clarity, IOP, and anterior chamber checked at slit lamp

Medications (typical regime)

• Topical antibiotic eye drops (e.g., moxifloxacin or chloramphenicol) - for 1-4 weeks to prevent endophthalmitis
• Topical corticosteroid (e.g., prednisolone acetate 1%) - to reduce postoperative inflammation; tapered over 4-6 weeks
• Topical NSAID (e.g., ketorolac or diclofenac) - reduces cystoid macular oedema (CMO)
• IOP-lowering drops if pressure elevated

Activity Restrictions

• No swimming, heavy lifting, or straining for 2-4 weeks
• Avoid rubbing the eye
• Night-time eye shield for 1 week

Follow-up Schedule

• Day 1, Week 1, Week 4-6 post-surgery
• Refraction and spectacle prescription at 4-6 weeks (when the eye has stabilized)

Complications to Watch For

• Posterior capsule opacification (PCO): Most common late complication; treated with Nd:YAG laser capsulotomy
• Cystoid macular oedema (CMO): Most common cause of reduced vision postoperatively
• Endophthalmitis: Rare but vision-threatening; presents with pain, hypopyon, reduced vision
• Corneal oedema (bullous keratopathy if endothelium damaged)
• Posterior capsule rupture with vitreous loss (intraoperative complication)
• IOL-related: Decentration, dysphotopsia
• Elevated IOP (steroid response or retained viscoelastic)

Summary Table

Mooren's Ulcer

Definition

Etiology and Pathogenesis

• Autoimmune mechanism: The leading theory is a host immune reaction against calgranulin C, a normally hidden antigen in corneal keratocytes, possibly unmasked by prior corneal insult (infection or surgery)
• Precipitating factors: Prior corneal surgery, infections (notably Hepatitis C virus - associated with Mooren-like ulcer)
• T-cell mediated stromal destruction with upregulation of matrix metalloproteinases (collagenases) leads to progressive corneal melting
• No infection is causative; it is sterile inflammation

Clinical Types

Clinical Features

Symptoms

• Severe, unrelenting pain - characteristic and often the dominant complaint
• Photophobia
• Lacrimation
• Blurred vision (due to corneal involvement)
• No systemic symptoms (distinguishes from systemic PUK)

Signs (Slit-Lamp)

Fig A: Mooren ulcer - peripheral ulceration with infiltrated leading edge

Fig B: Advanced Mooren ulcer with undermined, infiltrated central edge

1. Peripheral ulceration - starts nasally or temporally, involves the superficial one-third of the stroma, with variable epithelial loss
2. Undermined and infiltrated leading (central) edge - pathognomonic feature; the edge overhangs the bed of the ulcer
3. Circumferential spread - progresses along the limbus, then centrally
4. No clear zone between ulcer and limbus - the ulcer always involves the limbus (unlike marginal keratitis which has a lucid interval)
5. Vascularization - limbal vessels grow into the bed of the ulcer up to its leading edge but not beyond
6. Limbitis present; scleritis absent (key differentiating feature from systemic PUK)
7. Iritis may be present
8. Healing stage: thinning, vascularization, and scarring of the involved area

Differentials (Peripheral Corneal Ulcers)

Key rule: "Peripheral ulcerative keratitis is caused by infection until proven otherwise. In the absence of infection, investigate for systemic autoimmune disease." - Kanski's

Investigations

• Corneal scraping - Gram stain, KOH mount, culture (to exclude infection)
• Blood investigations: ANA, anti-dsDNA, ANCA (c-ANCA/p-ANCA), RF, anti-CCP (to exclude systemic autoimmune disease)
• Hepatitis B and C serology (Mooren-like ulcers associated with HCV)
• Chest X-ray (GPA/sarcoidosis)
• Syphilis serology (VDRL/TPHA)
• FBC, ESR, CRP

Complications

1. Severe irregular astigmatism (from corneal thinning and scarring)
2. Corneal perforation - particularly after minor trauma; spontaneous perforation is rare
3. Secondary bacterial infection
4. Cataract and glaucoma (secondary)
5. Corneal scarring with permanent visual loss

Treatment

Step 1 - Topical Medical Therapy (first line)

• Topical corticosteroids (e.g., prednisolone acetate 1%) - as frequently as hourly in active disease, then slowly tapered over several months
• Prophylactic topical antibiotic (low-frequency, to prevent secondary infection)
• Artificial tears (lubricants) - adjunctive, reduce desiccation
• Collagenase inhibitors - topical acetylcysteine 10-20% to inhibit stromal melting
• Topical ciclosporin (up to 2%) - takes weeks to act; used in resistant cases
• Tacrolimus 0.1% ointment - effective in refractory cases

Step 2 - Surgical (if no response to topical steroids)

• Conjunctival resection - excision of the perilimbal conjunctiva to remove the immune effector tissue driving corneal destruction
  • Excision extends 4 mm back from the limbus and 2 mm beyond the circumferential margins of the ulcer
  • May be combined with excision of necrotic tissue
  • Keratoepithelioplasty: suturing of a donor corneal lenticule onto the scleral bed to act as a physical barrier against conjunctival regrowth and further melting
  • Topical steroids continued postoperatively

Step 3 - Systemic Immunosuppression (bilateral/advanced/refractory disease)

• Systemic corticosteroids (prednisolone) - for rapid effect
• Methotrexate, azathioprine, mycophenolate - steroid-sparing agents
• Cyclophosphamide - for very severe cases
• Biological agents: Rituximab (anti-CD20) - shows promise in refractory cases
• Systemic doxycycline - acts as a systemic collagenase inhibitor

Step 4 - Management of Complications

• Lamellar keratectomy - in advanced disease with a "central island" of cornea; removes the inflammatory stimulus
• Corneal perforation: Tissue adhesive (cyanoacrylate glue), bandage contact lens, or penetrating keratoplasty (with immunosuppressive cover)
• Visual rehabilitation: Keratoplasty considered once inflammation has fully settled; systemic immunosuppression cover is required

Key Exam Points Summary

Orbital Cellulitis

Definition

Orbital Septum - Key Anatomical Landmark

• Preseptal cellulitis = infection anterior to septum (periorbital) - less dangerous
• Orbital cellulitis = infection posterior to septum - dangerous, requires hospitalization

Etiology and Sources of Infection

Causative Organisms

Note: Mucormycosis in diabetic or immunocompromised patients is rapidly progressive and life-threatening - always look for black eschar in nasal passages.

Clinical Features

Symptoms

• Rapid onset of periorbital pain, worsened by eye movement
• Swelling and redness of the eyelids
• Malaise, fever, headache
• Blurred vision and diplopia (double vision)
• Recent history of nasal congestion, sinusitis, or upper respiratory infection
• Tooth pain (if dental source)

Signs

Fig 7.3.1.1 - Orbital cellulitis: marked eyelid edema, erythema, and swelling (Wills Eye Manual)

1. Pyrexia - often marked
2. Eyelid signs: Tender, firm, warm, erythematous, edematous eyelids; periocular swelling
3. Conjunctival chemosis and injection, sometimes subconjunctival hemorrhage
4. Proptosis (exophthalmos) - may be non-axial (dystopia) if an abscess is present; may be obscured by lid swelling
5. Painful ophthalmoplegia - restricted, painful extraocular movements (hallmark distinguishing from preseptal)
6. Reduced visual acuity and dyschromatopsia (impaired color vision) - indicate optic nerve compression
7. Relative afferent pupillary defect (RAPD) - in severe cases; indicates optic neuropathy
8. Fundus: Choroidal folds, optic disc swelling, retinal venous congestion
9. Signs are usually unilateral, though edema may spread to the contralateral eyelid

Preseptal vs. Orbital Cellulitis - Key Differences

Investigations

Imaging (Most Important)

• CT scan of orbits, paranasal sinuses, and brain with contrast - investigation of choice
  • Confirms postseptal location of infection
  • Identifies sinusitis (typically ethmoiditis)
  • Detects subperiosteal abscess (most common along medial orbital wall)
  • Detects orbital abscess, intracranial extension
  • Excludes retained foreign body

CT scan: right orbital cellulitis showing fat stranding and right ethmoiditis (Wills Eye Manual)

• MRI - sometimes performed; better for intracranial complications (brain abscess, meningitis, cavernous sinus thrombosis)

Laboratory

• White cell count (WBC) with differential - leukocytosis
• Blood cultures - to identify bacteremia and guide antibiotic therapy
• Culture of nasal discharge
• Gram stain and culture of any wound discharge
• Lumbar puncture if meningeal/cerebral signs develop

Other

• Tetanus immunization status (in trauma cases)
• Blood glucose (to assess for diabetes/mucormycosis risk)
• Check nasal passages for black eschar in immunocompromised/diabetic patients (mucormycosis)

Complications

Ocular Complications

1. Optic neuropathy - from direct compression or ischemia; can lead to permanent blindness
2. Exposure keratopathy - from proptosis and chemosis
3. Raised intraocular pressure (IOP)
4. Endophthalmitis
5. Central retinal artery or vein occlusion

Orbital Complications

1. Subperiosteal abscess - most commonly along the medial orbital wall (adjacent to ethmoid sinuses)
2. Orbital abscess

Intracranial Complications (uncommon - 3-4% - but extremely serious)

1. Cavernous sinus thrombosis - suggested by CN III, IV, VI palsies + bilateral eye signs + high fever
2. Meningitis
3. Brain abscess
4. Subdural empyema, epidural abscess
5. Frontal bone osteomyelitis

Management

1. Immediate Steps

• Hospital admission is mandatory
• Urgent ophthalmology consultation
• Otorhinolaryngology (ENT) assessment for sinus disease
• Paediatric/Infectious disease specialist consultation (especially in children)
• Mark extent of periorbital erythema with a surgical marker to monitor progress
• Optic nerve function monitored at least every 4 hours (VA, color vision, light brightness appreciation, pupillary reactions)

2. Medical Treatment - IV Antibiotics (First Line)

• IV antibiotics continued until apyrexial for 4 days, then switched to oral antibiotics for 1-3 weeks
• Add nasal decongestant spray (e.g., oxymetazoline) for up to 3 days
• Nasal corticosteroid spray to aid resolution of sinusitis
• Lubricant eye ointment (erythromycin/bacitracin) for corneal exposure from chemosis

3. Surgical Treatment

• Presence of orbital abscess (requires drainage and debridement)
• No response to 48-72 hours of IV antibiotics
• Very severe sinus disease (sinus drainage by ENT)
• Rising IOP or worsening optic neuropathy despite antibiotics

• Drainage of subperiosteal or orbital abscess - surgical or endoscopic (transnasal endoscopic drainage preferred for medial subperiosteal abscess in children)
• Drainage of infected paranasal sinuses (functional endoscopic sinus surgery - FESS)
• Lateral canthotomy and cantholysis - emergency procedure for severely elevated IOP or acute optic nerve compression; decompresses the orbit by releasing the lateral canthal tendon
• Biopsy of inflammatory tissue in atypical presentations

Chandler Classification of Orbital Complications of Sinusitis

Key Exam Points Summary

Important note: A K Khurana's Comprehensive Ophthalmology is not available in the library. The answer below is compiled from Kanski's Clinical Ophthalmology (10th ed.) and the Wills Eye Manual - both are authoritative references covering the same content as Khurana. The structure, classification, tests, and management follow the standard Khurana syllabus closely.

Dry Eye Disease (Keratoconjunctivitis Sicca - KCS)

Definition

The Tear Film - Normal Structure

Etiology and Classification

A. Aqueous-Deficient Dry Eye (ADDE)

1. Sjögren Syndrome (SS) Dry Eye

• Primary SS: Dry eyes + dry mouth + parotid enlargement (sicca complex), without associated autoimmune disease
• Secondary SS: As above, associated with rheumatoid arthritis, SLE, or other connective tissue diseases
• Mechanism: Lymphocytic infiltration of lacrimal and salivary glands

2. Non-Sjögren Syndrome Dry Eye

• Lacrimal gland deficiency:
  • Primary: Age-related dry eye (most common), congenital alacrima, familial dysautonomia (Riley-Day syndrome)
  • Secondary: Lacrimal gland infiltration (sarcoidosis, lymphoma, AIDS), graft-versus-host disease, lacrimal gland ablation
• Lacrimal gland duct obstruction: Trachoma, cicatricial pemphigoid, chemical injuries, Stevens-Johnson syndrome
• Reflex hyposecretion:
  • Sensory block: contact lens wear, diabetes mellitus, refractive surgery (LASIK), neurotrophic keratitis
  • Motor block: VII cranial nerve palsy, systemic anticholinergic drugs

B. Evaporative Dry Eye (EDE) - More Common

Intrinsic causes

• Meibomian gland dysfunction (MGD) - most common cause overall; posterior blepharitis, rosacea
• Disorders of lid aperture: Lagophthalmos, lid retraction, proptosis (exposure keratopathy), facial nerve palsy
• Low blink rate: Parkinson's disease, prolonged computer/reading/television use
• Drug action: Antihistamines, beta-blockers, antispasmodics, diuretics

Extrinsic causes

• Vitamin A deficiency (goblet cell loss → mucin deficiency)
• Topical drugs and preservatives (BAK - benzalkonium chloride toxicity)
• Contact lens wear
• Ocular surface diseases: allergic conjunctivitis, trachoma

Key pathophysiologic mechanism: Four core inter-related mechanisms - tear instability → hyperosmolarity → inflammation → ocular surface damage - form a vicious cycle. Inflammation (present in 80% of patients) is both a cause and consequence of dry eye.

Symptoms

• Burning and stinging sensation
• Grittiness / foreign body sensation
• Dryness
• Excess reflex tearing (paradoxical - due to irritation)
• Blurred or fluctuating vision (clears transiently with blinking)
• Stringy or ropy mucous discharge
• Photophobia
• Redness
• Crusting of lids on waking

• Wind, air-conditioning, central heating, low humidity
• Smoke, dust, allergens
• Prolonged reading, computer use, television (reduce blink rate)
• Symptoms characteristically worsen over the course of the day (aqueous deficient) or may be worse in the morning (evaporative/MGD)

Note: "Symptoms are often out of proportion to clinical signs" - Wills Eye Manual

Clinical Signs

Eyelids

• Posterior (seborrhoeic) blepharitis with meibomian gland dysfunction - oil globules at gland orifices, inflamed gland margins
• Reduced blink rate; incomplete blink
• Lid margin irregularities

Tear Film

• Reduced or absent tear meniscus at inferior lid margin
  • Normal height: ≥0.5 mm, convex shape
  • Dry eye: Scanty, concave, or absent meniscus
• Excess debris or mucus in tear film
• Foam or froth at lid margins (MGD)

Conjunctiva

• Redness (injection)
• Rose Bengal staining - stains devitalized/dead epithelial cells (interpalpebral pattern)
• Lissamine green staining - similar to rose Bengal but better tolerated
• Conjunctivochalasis (redundant bulbar conjunctival folds)
• Keratinization (in severe/chronic disease)

Cornea

• Punctate epithelial erosions (PEE) - in the interpalpebral zone (inferior cornea), stained with fluorescein
• Mucous filaments (filamentary keratitis) - in severe cases
• Reduced corneal sensation (in severe/long-standing disease)

Investigations / Diagnostic Tests

1. Tear Film Break-Up Time (TBUT) - Most Important

• Fluorescein dye instilled; patient blinks, then keeps eyes open
• Time measured from last blink to first random dry spot appearing in the tear film
• Normal: >10 seconds
• Abnormal (dry eye): <10 seconds
• Non-invasive TBUT (NIBUT) can be measured with topographer or keratometer

2. Schirmer's Test - Measures Aqueous Secretion

Fig 5.8B: Schirmer's test strip placed at junction of medial two-thirds and lateral one-third of lower lid (Kanski's)

Single Schirmer test should not be the sole criterion; repeatedly abnormal results are highly supportive.

3. Ocular Surface Staining

Fig 5.8A: Tear film break-up - multiple dark dry spots in fluorescein-stained tear film (Kanski's)

• Fluorescein (blue light): Stains areas of epithelial loss (erosions); also used for TBUT
• Rose Bengal: Stains devitalized and dead epithelial cells and mucus strands; more irritating
• Lissamine green: Similar to rose Bengal, better tolerated, stains dead cells and mucus
• Distribution: Typically interpalpebral (exposed area between lids) and inferior cornea

4. Tear Film Osmolarity

• Measured with TearLab osmometer (point-of-care device)
• Normal: <308 mOsm/L
• Dry eye: ≥316 mOsm/L (hyperosmolarity is the core pathogenic mechanism)
• High specificity but variable between tests

5. Meibomian Gland Assessment

• Slit-lamp: Expressed secretions (clear/cloudy/solid), gland orifice obstruction
• Meibography: Infrared imaging of meibomian gland architecture (dropout/atrophy)

6. Conjunctival Impression Cytology

• Sample of conjunctival epithelium analyzed for:
  • Goblet cell density (reduced in dry eye)
  • Squamous metaplasia (keratinization)
  • Inflammatory cells

7. Tear Lysozyme / Lactoferrin Levels

• Reduced in aqueous-deficient dry eye
• Not routinely measured in clinical practice

8. Phenol Red Thread Test

• Thread impregnated with phenol red dye placed in lower fornix for 15 seconds
• Normal: >9 mm of wetting; Dry eye: <9 mm

Grading of Dry Eye Severity (DEWS 2007)

Treatment - Step-Ladder Approach (DEWS Levels)

Level 1 (Mild) - Education and Environment

• Patient education: reduce screen time, increase blink frequency
• Lifestyle modification: humidifiers, avoid smoke/wind/air-conditioning
• Artificial tears (preservative-free preferred) 4 times daily - first-line
  • Cellulose derivatives (hypromellose, methylcellulose) - mild cases
  • Carbomer gels - longer-lasting, slight blurring
  • Sodium hyaluronate, polyvinyl alcohol (PVA), propylene glycol
• Lid hygiene and warm compresses for MGD/blepharitis

Level 2 (Moderate) - Add Anti-inflammatory + Conserve Tears

• Increase artificial tears to every 1-2 hours (preservative-free only)
• Lubricating gel or ointment at bedtime
• Cyclosporine 0.05-0.09% eye drops b.i.d. (Restasis)
  • Immunomodulatory; reduces T-cell mediated inflammation
  • Takes 1-3 months for significant effect; often burns initially
  • A short course of mild topical steroid (loteprednol 0.5%, fluorometholone 0.1%) b.i.d.-q.i.d. for 1 month can be given concurrently to hasten effect
• Lifitegrast 5% eye drops b.i.d. (LFA-1 antagonist, blocks T-cell adhesion)
  • Symptomatic improvement within 2 weeks; full effect by 3 months
• Punctal occlusion (if above measures fail or impractical)
  • Collagen plugs (temporary, dissolve in 1-2 weeks)
  • Silicone/acrylic plugs (reversible, longer lasting)
  • Treat blepharitis/inflammation before occluding puncta
• Omega-3 fatty acid supplements (oral flaxseed oil)
• Topical short-term steroids (prednisolone, loteprednol) for acute exacerbations
• Moisture chamber spectacles / side shields

Level 3 (Severe) - Advanced Measures

• Autologous serum eye drops (contains growth factors, fibronectin, vitamins - approximates natural tears better than artificial tears)
• Umbilical cord serum drops
• All four puncta occluded (upper + lower)
• Bandage soft contact lens (for filamentary keratitis, corneal exposure)
• Scleral contact lenses (large PMMA/silicone lens that vaults the cornea; maintains fluid reservoir)
• Acetylcysteine 10% drops for filamentary keratitis (mucolytic)
• Manual debridement of corneal filaments

Level 4 (Very Severe) - Surgery

• Systemic anti-inflammatory agents (methotrexate, hydroxychloroquine for Sjögren's)
• Tarsorrhaphy (permanent or temporary) - reduces exposed ocular surface area and evaporation
• Salivary gland autotransplantation (parotid duct transposed to the temporal conjunctival fornix)
• Mucous membrane / amniotic membrane transplantation for corneal complications
• Conjunctival/limbal stem cell transplantation for severe surface disease

Special Conditions Associated with Dry Eye

Sjögren Syndrome

• Classic triad: Dry eyes + Dry mouth + Parotid gland enlargement
• Autoimmune: Anti-Ro (SSA) and Anti-La (SSB) antibodies
• Diagnosis: ACR criteria - anti-SSA/SSB positivity, ocular surface staining, labial salivary gland biopsy showing focal lymphocytic sialadenitis

Filamentary Keratitis

• Fine strands of mucus and desquamated epithelial cells anchored to the cornea
• Seen in severe dry eye, prolonged patching, keratoconus
• Treatment: Lubricants, acetylcysteine, bandage lens, manual debridement

Key Exam Points Summary