1. Chief complaints and HOPI
   Differentiate chronic painless visual-field loss from acute painful red-eye presentations.
2. Past, personal, family, and systemic history
   Identify risk factors for primary glaucoma and clues to secondary glaucoma.
3. General and ocular examination
   Include visual acuity, pupils, slit-lamp examination, IOP, gonioscopy, optic disc, retinal nerve fibre layer, and visual fields.
4. Provisional diagnosis and differential diagnoses
   Classify as open-angle, angle-closure, normal-tension, congenital/developmental, or secondary glaucoma.
5. Investigations and interpretation
   Goldmann applanation tonometry, pachymetry, gonioscopy, OCT RNFL/GCC, automated perimetry, optic-disc photography, and targeted tests for secondary causes.
6. Management protocol
   Urgency triage, target IOP, medical therapy, laser, surgery, follow-up, and counselling.

1. Long-case template - examination-ready, with headings and sample wording
2. POAG case - chronic open-angle glaucoma
3. Acute angle closure - emergency case and treatment protocol
4. All types comparison - POAG, PACG, normal-tension, and secondary glaucoma

Examination-Ready Glaucoma Case Template

1. Identification Data

• Name:
• Age / sex:
• Occupation:
• Address:
• Date of examination:
• Informant and reliability:
• Eye affected: right / left / both

2. Chief Complaints

Common glaucoma presentations

• Gradual, painless diminution of peripheral vision, often unnoticed, for ___ months/years
• Difficulty seeing at night or navigating stairs
• Frequent change of spectacles / blurred vision
• Headache may occur but is non-specific
• Usually no redness, pain, or discharge

• Intermittent episodes of blurred vision
• Halos around lights
• Brow ache/headache, often in dim illumination or evening
• Nausea or vomiting during acute attacks
• Painful red eye with sudden visual loss in acute angle closure

3. History of Present Illness

A. Characterize visual loss

• Onset: sudden or gradual?
• Course: progressive, stationary, episodic?
• Unilateral or bilateral?
• Central versus peripheral loss?
• Difficulty in low light or at night?
• Any problem with mobility, stairs, driving, or bumping into objects?

B. Ask for symptoms of raised IOP or angle closure

• Ocular pain or brow ache
• Redness
• Halos around lights
• Headache
• Nausea/vomiting
• Episodic blurring, especially in darkness, after dilatation, or after emotional stress

C. Screen for secondary glaucoma

• Previous ocular trauma, especially blunt trauma, hyphema, or angle recession
• Previous eye surgery, laser treatment, intravitreal injections
• Uveitis: pain, photophobia, redness, recurrent episodes
• Long-term steroid use: topical eye drops, oral tablets, inhalers, creams, injections
• Diabetes and proliferative diabetic retinopathy
• Retinal vein occlusion
• Ocular tumor, chronic retinal detachment
• Chemical injury
• High myopia
• Previous use of antiglaucoma drops, compliance, adverse effects, and last dose

D. Relevant medications

• Corticosteroids
• Topiramate or sulfonamide-related medicines, which can cause secondary angle closure
• Anticholinergics, sympathomimetics, antidepressants, or cold medications that may precipitate angle closure in predisposed eyes
• Systemic beta-blockers, antihypertensives, and vasodilators
• Previous glaucoma medications, duration, adherence, and side effects

4. Past Ocular History

• Previous eye examination and IOP readings
• Diagnosis of glaucoma, ocular hypertension, narrow angles, or optic-disc abnormality
• Prior laser peripheral iridotomy, SLT, trabeculectomy, tube shunt, MIGS, cataract surgery
• Trauma
• Uveitis
• Retinal disease or retinal laser
• Spectacle use and refractive error, especially high myopia or hypermetropia
• Previous steroid use
• History of amblyopia or poor vision since childhood

5. Past Medical History

• Diabetes mellitus
• Hypertension and antihypertensive treatment, particularly nocturnal hypotension
• Migraine, Raynaud phenomenon, sleep apnoea, or vascular disease, especially in normal-tension glaucoma
• Bronchial asthma/COPD, bradycardia, heart block, or heart failure, before prescribing topical beta-blockers
• Renal disease, liver disease, sulfonamide allergy, before systemic carbonic anhydrase inhibitors
• Thyroid disease
• Autoimmune disease/sarcoidosis/tuberculosis, if uveitis suspected

6. Personal History

• Diet and appetite
• Sleep pattern
• Bowel and bladder habits
• Smoking, alcohol, and substance use
• Occupation, driving, fall risk, and visual needs
• Drug allergy
• Long-term self-medication, especially steroids

7. Family History

• Glaucoma in parents, siblings, or children
• Blindness of unknown cause in relatives
• Early cataract surgery or laser iridotomy in relatives
• Diabetes and hypertension

8. General Physical Examination

• General condition and build
• Pulse and blood pressure
• Signs of diabetes, hypertension, or systemic steroid use
• Features suggesting connective-tissue or inflammatory disease, if relevant

9. Ocular Examination

A. Visual Acuity

• Refraction, if indicated
• Colour vision, particularly when another optic neuropathy is suspected
• Contrast sensitivity, if available

B. External Examination and Adnexa

• Lid abnormality, blepharitis
• Proptosis
• Facial asymmetry
• Signs of trauma
• Conjunctival congestion
• Corneal enlargement in congenital glaucoma

C. Pupillary Examination

• Size and shape
• Direct and consensual light reflexes
• Relative afferent pupillary defect (RAPD)
• Near response

D. Ocular Movements

• Extraocular movements
• Diplopia, if present

E. Slit-Lamp Examination

Conjunctiva and sclera

• Congestion
• Dilated episcleral vessels, suggesting raised episcleral venous pressure

Cornea

• Clear or oedematous cornea
• Microcystic epithelial oedema
• Pigment on endothelium, Krukenberg spindle in pigment dispersion
• Keratic precipitates in uveitis
• Haab striae in congenital glaucoma

Anterior chamber

• Depth: Van Herick grading at limbus
• Cells/flare
• Hyphema
• Peripheral anterior synechiae, if visible
• Shallow peripheral chamber suggests angle-closure risk

Iris

• Atrophy, transillumination defects
• Neovascularization of iris
• Pseudoexfoliative material at pupillary margin
• Posterior synechiae
• Iris bombe
• Sectoral iris atrophy

Lens

• Cataract and lens thickness
• Pseudoexfoliative material on anterior lens capsule
• Phacodonesis or lens subluxation
• Intumescent cataract in phacomorphic glaucoma

F. Intraocular Pressure

• Measure by Goldmann applanation tonometry whenever possible.
• Document time of measurement and current glaucoma medication.
• Measure both eyes.
• Consider repeat readings or diurnal IOP assessment if diagnosis or control is unclear.

• IOP alone does not diagnose glaucoma.
• Normal IOP does not exclude glaucoma.
• Thin corneas can cause underestimation of IOP and increase glaucoma risk.
• Record baseline untreated IOP if available.

G. Gonioscopy

• Angle open / narrow / closed
• Shaffer grade in all quadrants
• Pigmentation
• Peripheral anterior synechiae (PAS)
• Angle recession
• Neovascularization
• Sampaolesi line/pigment features
• Pseudoexfoliative material

• Open angle supports POAG, normal-tension glaucoma, pigmentary glaucoma, pseudoexfoliative glaucoma, or some secondary glaucomas.
• Narrow/occludable angle suggests primary angle-closure spectrum.
• PAS supports previous or chronic angle closure, uveitis, trauma, or neovascular glaucoma.
• Angle recession indicates traumatic glaucoma.

H. Fundus Examination

Optic nerve head

• Disc size
• Cup-disc ratio, vertical and horizontal
• Neuroretinal rim: thinning, notching, focal loss
• ISNT rule: normal rim thickness Inferior > Superior > Nasal > Temporal
• Cup asymmetry, especially difference >0.2
• Disc haemorrhage
• Laminar dot sign
• Baring of circumlinear vessels
• Bayonetting of vessels
• Peripapillary atrophy
• Pallor: pallor exceeding cupping suggests non-glaucomatous optic neuropathy

Retina

• RNFL defects, especially wedge-shaped superior or inferior defects
• Macula
• Diabetic retinopathy
• Retinal vein occlusion
• Neovascularization
• Other retinal causes of field loss

I. Visual Field Examination

• Reliability indices: fixation losses, false positives, false negatives
• Mean deviation (MD)
• Pattern standard deviation (PSD)
• Glaucoma hemifield test
• Pattern and location of defect
• Correlation with disc and OCT findings

Typical glaucomatous field defects

• Paracentral scotoma
• Nasal step
• Seidel scotoma

• Arcuate/Bjerrum scotoma
• Double arcuate scotoma

• Tunnel vision
• Temporal island
• Central island only

10. Investigations

Essential baseline tests

1. Goldmann applanation tonometry
   Record IOP, time, and medication status.
2. Central corneal thickness (pachymetry)
   Helps interpret IOP and risk.
3. Gonioscopy
   Classifies the glaucoma as open-angle or angle-closure and identifies secondary angle pathology.
4. Optic disc photography
   Provides objective baseline for future comparison.
5. OCT optic nerve head and RNFL analysis
   Include peripapillary RNFL and macular ganglion cell complex/inner plexiform layer analysis.
6. Standard automated perimetry
   Repeat unreliable fields and use serial tests to establish progression.
7. Dilated fundus examination
   To document disc, RNFL, macula, and retina.

Selective investigations

11. Diagnostic Reasoning and Classification

Primary open-angle glaucoma

• Open angle on gonioscopy
• Characteristic glaucomatous optic neuropathy
• Corresponding RNFL/GCC thinning and/or reproducible glaucomatous field defects
• No alternative ocular or neurological explanation
• IOP may be raised or within statistically normal range

Normal-tension glaucoma

• Open angle
• Typical disc and field damage
• Untreated IOP consistently in normal range
• Exclude mimics such as compressive optic neuropathy, ischemic optic neuropathy, and tilted disc

Primary angle-closure disease spectrum

• Primary angle-closure suspect: narrow/occludable angle without PAS, raised IOP, or glaucomatous neuropathy
• Primary angle closure: narrow angle with PAS and/or raised IOP, but no glaucomatous neuropathy
• Primary angle-closure glaucoma: angle closure with glaucomatous optic neuropathy and field loss

Secondary glaucoma

• Pseudoexfoliative
• Pigmentary
• Steroid-induced
• Traumatic/angle-recession
• Uveitic
• Neovascular
• Lens-induced: phacomorphic, phacolytic, lens-particle
• Post-surgical or aphakic/pseudophakic
• Raised episcleral venous pressure

12. Differential Diagnoses

A. Differential diagnosis of glaucomatous optic disc cupping

1. Physiological large cup
2. High myopic disc/tilted disc
3. Optic atrophy with pseudocupping
4. Compressive optic neuropathy
5. Ischemic optic neuropathy
6. Hereditary optic neuropathy
7. Previous optic neuritis
8. Congenital disc anomalies

Features favoring non-glaucomatous optic neuropathy

• Visual acuity or colour vision reduced out of proportion to cupping
• Pallor greater than cupping
• Marked RAPD
• Field defect respecting vertical meridian
• Young age or rapidly progressive asymmetric disease
• Neurological symptoms
• OCT/field pattern not matching disc findings

B. Differential diagnosis of a painful red eye with high IOP

1. Acute primary angle closure
2. Acute anterior uveitis with secondary glaucoma
3. Neovascular glaucoma
4. Lens-induced glaucoma
5. Phacolytic/phacomorphic glaucoma
6. Posner-Schlossman syndrome
7. Trauma-related glaucoma
8. Scleritis or keratitis, though these typically have different corneal/anterior chamber findings

13. Provisional Diagnosis Format

Example: POAG

Example: normal-tension glaucoma

Example: acute angle closure

14. Management Protocol

A. Immediate priorities

1. Establish whether this is an emergency:
   • Acute angle closure
   • Very high IOP with pain/corneal oedema
   • Neovascular glaucoma
   • Uveitic glaucoma with severe inflammation
   • Rapid visual deterioration
2. Identify glaucoma mechanism through gonioscopy and ocular examination.
3. Establish baseline:
   • IOP
   • CCT
   • Disc photos
   • OCT RNFL/GCC
   • Reliable visual field
   • Risk factors and expected lifetime risk

B. POAG and normal-tension glaucoma

Treatment goal

• Establish a target IOP based on baseline IOP, stage, rate of progression, life expectancy, fellow-eye status, and risk factors.
• A common initial goal for POAG is an IOP reduction of approximately 20% to 30% from baseline, then modify the target if progression occurs. AAO POAG guidance

First-line options

• Latanoprost
• Travoprost
• Bimatoprost
• Tafluprost

• Conjunctival hyperaemia
• Increased iris pigmentation
• Eyelash growth
• Periocular skin pigmentation/periorbitopathy
• Use caution in active uveitis or certain macular oedema risks

• Appropriate first-line or adjunctive option in open-angle glaucoma.
• Particularly useful when adherence, cost, medication intolerance, or drop burden is problematic.

Add-on topical medicines

• Beta-blocker: timolol
• Alpha-2 agonist: brimonidine
• Topical carbonic anhydrase inhibitor: dorzolamide/brinzolamide
• Fixed combinations to reduce drop burden
• Rho-kinase inhibitor where locally available

If IOP remains above target or progression continues

• Confirm adherence and correct drop instillation
• Review angle and secondary causes
• Escalate medication or perform/repeat SLT when appropriate
• Consider surgery:
  • Trabeculectomy with antimetabolite
  • Glaucoma drainage device/tube shunt
  • Selected MIGS procedures, usually with cataract surgery in appropriate mild-moderate open-angle disease
  • Cyclodestructive procedures in refractory cases/limited visual potential

C. Primary angle-closure disease

Primary angle-closure suspect

• Gonioscopy, risk assessment, patient education
• Consider prophylactic laser peripheral iridotomy (LPI) in high-risk occludable angles according to ophthalmology assessment
• Monitor angle, IOP, PAS, disc, and fields

Primary angle closure or angle-closure glaucoma

• LPI for pupillary-block mechanism
• Manage residual raised IOP with medication, laser, or surgery as needed
• Consider lens extraction when lens-related crowding/cataract materially contributes to angle closure
• Continue long-term monitoring because LPI does not eliminate all angle-closure mechanisms or glaucoma risk

D. Acute primary angle closure: emergency protocol

Initial emergency measures

• Topical aqueous suppressants:
  • Beta-blocker
  • Alpha-agonist
  • Topical carbonic anhydrase inhibitor
• Systemic carbonic anhydrase inhibitor, such as acetazolamide, if not contraindicated
• Hyperosmotic therapy, such as mannitol, in severe cases when required
• Topical steroid and analgesia/antiemetic as clinically needed
• Pilocarpine is generally considered after IOP begins to fall and iris perfusion improves, not as the sole initial treatment in a very high-pressure attack

Definitive management

• Laser peripheral iridotomy after corneal clarity and IOP permit
• Consider anterior-chamber paracentesis or laser iridoplasty in selected cases
• Assess the fellow eye urgently. A phakic fellow eye is commonly offered prompt prophylactic LPI because of high risk. AAO angle-closure guidance

E. Secondary Glaucoma: Treat the Cause

15. Follow-Up and Counselling

At every follow-up

• Symptoms and medication adherence
• Side effects and contraindications
• IOP, time, and treatment
• Visual acuity
• Optic disc/RNFL status
• Need for gonioscopy or repeat visual fields
• Assess progression, not only the absolute IOP

Patient counselling

• Glaucoma damage is irreversible, but progression is often preventable.
• Vision may feel normal until disease is advanced.
• Drops must be used regularly, even without symptoms.
• Demonstrate punctal occlusion: close eyelids gently and press the inner corner of the eye for 1-2 minutes after instillation to reduce systemic absorption.
• Do not stop drops without medical advice.
• Encourage screening of first-degree relatives.
• Give urgent return advice for sudden pain, redness, halos, marked blurring, headache, nausea, or vomiting.

16. Short Examination Presentation

Examination-Ready Uveitis Case Template

Definition: Uveitis is intraocular inflammation involving the uvea and may involve adjacent structures. By anatomical location, it is classified as anterior, intermediate, posterior, or panuveitis.

1. Identification Data

• Name:
• Age / sex:
• Occupation:
• Address:
• Date:
• Informant and reliability:
• Eye involved: right / left / both

2. Chief Complaints

Typical anterior uveitis

• Redness of eye for ___ days
• Ocular pain/brow ache for ___ days
• Photophobia for ___ days
• Blurred vision for ___ days
• Watering for ___ days

Intermediate uveitis

• Floaters for ___ weeks/months
• Painless diminution of vision for ___ weeks/months

Posterior uveitis / panuveitis

• Blurring of vision
• Floaters
• Metamorphopsia
• Scotoma
• Reduced night vision
• Usually minimal pain/redness unless anterior inflammation coexists

3. History of Present Illness

A. Characterize the presenting symptoms

Pain

• Onset, severity, continuous/intermittent
• Deep aching/brow ache?
• Pain on eye movement?
• Painful red eye suggests anterior uveitis, scleritis, keratitis, or acute angle closure.

Redness

• Sudden or gradual?
• Diffuse or circumcorneal/ciliary flush?
• Associated discharge? Purulent discharge suggests conjunctivitis rather than uveitis.

Photophobia

• Direct photophobia: discomfort when light enters the affected eye
• Consensual photophobia: pain in the affected eye when light is shone in the fellow eye, strongly supportive of anterior uveitis

Visual symptoms

• Blurring, floaters, flashes, scotoma, distortion, reduced night vision
• Sudden severe loss may suggest retinal detachment, occlusive vasculitis, endophthalmitis, or acute retinal necrosis.

B. Course and recurrence

• First episode or recurrent?
• Acute, chronic, or insidious onset?
• Unilateral, alternating, or bilateral?
• Any similar episodes in the past?
• Complete recovery between previous episodes?
• Previous treatment with topical/systemic steroids or immunosuppressants?

C. Ask for complications

• Halos, headache, nausea/vomiting: raised IOP/secondary glaucoma
• Progressive painless visual loss: cataract, cystoid macular oedema, vitritis
• Flashes, curtain-like visual loss: retinal tear/detachment
• Severe pain with marked reduction of vision after ocular surgery/injection: endophthalmitis

D. Infective exposure and risk history

• Previous tuberculosis or contact with TB
• Fever, weight loss, night sweats, chronic cough
• Sexually transmitted infection or past syphilis
• HIV risk or known immunosuppression
• Herpes simplex/zoster: unilateral facial rash, vesicles, previous cold sores
• Cat exposure or undercooked meat: toxoplasmosis risk
• Recent travel, tick exposure, and endemic infections based on local setting
• Recent COVID/viral illness, vaccination, or systemic infection if clinically relevant
• Recent ocular surgery, trauma, intravitreal procedure, or penetrating injury

E. Drug history

• Topical, oral, inhaled, injected, or dermatological corticosteroids
• Previous dilating drops/cycloplegics
• Anti-tubercular therapy, antivirals, antibiotics
• Immunosuppressive therapy or biologic medication
• Medication adherence and response
• Drug allergy

4. Past Ocular History

• Previous episode(s) of uveitis
• Laterality and frequency of attacks
• Prior diagnosis: anterior/intermediate/posterior/panuveitis
• Previous cataract, glaucoma, macular oedema, retinal detachment
• Ocular trauma or retained intraocular foreign body
• Eye surgery, including cataract surgery
• Laser procedures/intravitreal injections
• Contact-lens use
• Previous herpes zoster ophthalmicus
• Past use of topical steroids and steroid response
• Previous investigations and systemic diagnosis

5. Past Medical History

• HIV/AIDS and immunosuppressive therapy
• Malignancy, especially lymphoma
• Tuberculosis and syphilis testing/treatment history

6. Personal History

• Diet, appetite, sleep, bowel/bladder habits
• Smoking, alcohol, recreational drugs
• Sexual history only when relevant and sensitively obtained
• Occupation and exposure to animals, soil, chemicals, or travel
• Contact with tuberculosis
• Drug allergies
• Current medications, including steroids

7. Family History

• Ankylosing spondylitis/spondyloarthritis
• Psoriasis
• Inflammatory bowel disease
• Juvenile idiopathic arthritis
• Autoimmune disease
• Sarcoidosis
• Tuberculosis
• Blindness or recurrent red-eye disease in family

8. General Physical Examination

• General condition, nutrition, pallor, fever
• Pulse and blood pressure
• Lymphadenopathy
• Skin: psoriasis, erythema nodosum, vitiligo, vesicular rash, Behçet-like lesions
• Oral ulcers/genital ulcers where relevant
• Joints and spine: arthritis, sacroiliac tenderness, reduced spinal mobility
• Chest signs if TB/sarcoidosis suspected

9. Ocular Examination

A. Visual Acuity

• Refraction where needed
• Colour vision if optic nerve involvement is suspected
• Contrast sensitivity if available

B. External Examination

• Lid oedema
• Herpes zoster rash or scarring
• Ptosis
• Proptosis
• Facial skin lesions
• Lacrimal gland enlargement
• Conjunctival injection
• Pattern of redness: ciliary flush is common in anterior uveitis

C. Pupillary Examination

• Pupil size and shape
• Direct and consensual light reflex
• Relative afferent pupillary defect
• Irregular pupil due to posterior synechiae
• Miosis due to anterior uveitis
• Mid-dilated poorly reacting pupil suggests acute angle closure, not uncomplicated uveitis

D. Ocular Movements

• Full/restricted movements
• Pain on movement
• Diplopia
• Orbital signs if present

E. Slit-Lamp Examination

1. Conjunctiva and sclera

• Diffuse versus circumcorneal congestion
• Ciliary flush
• Nodules
• Scleritis/episcleritis signs
• Discharge, if any

2. Cornea

• Keratic precipitates (KPs)
• Fine/non-granulomatous KPs
• Large greasy “mutton-fat” KPs, suggesting granulomatous inflammation
• Arlt triangle: KPs distributed inferiorly in a triangular pattern
• Corneal oedema
• Band keratopathy in chronic uveitis/JIA
• Dendritic lesion or reduced corneal sensation, suggesting herpetic disease

3. Anterior chamber

• Depth: deep, normal, shallow
• Cells: grade using SUN grading if possible
• Flare: grade
• Fibrin
• Hypopyon
• Hyphema
• Pigment
• Anterior chamber reaction

SUN anterior chamber cell grading

Flare grading

• 0: none
• 1+: faint
• 2+: moderate, iris/lens details clear
• 3+: marked, iris/lens details hazy
• 4+: intense, fibrin/plastic aqueous

4. Iris

• Iris nodules: Koeppe nodules at pupillary margin, Busacca nodules on iris surface
• Posterior synechiae
• Iris bombe
• Sectoral iris atrophy, suggesting herpetic uveitis
• Diffuse iris atrophy
• Neovascularization of iris
• Heterochromia, as in Fuchs uveitis syndrome

5. Lens

• Complicated cataract, commonly posterior subcapsular
• Pigment on anterior lens capsule
• Posterior synechiae
• Pseudoexfoliative material if present

F. Intraocular Pressure

Interpretation

• IOP may be low in acute active anterior uveitis due to reduced aqueous production.
• IOP may rise due to trabeculitis, inflammatory debris, peripheral anterior synechiae, pupillary block, steroid response, or secondary glaucoma.
• Markedly raised IOP with unilateral recurrent anterior uveitis should raise suspicion of herpetic/CMV-associated disease, Posner-Schlossman syndrome, or uveitic glaucoma.

G. Gonioscopy

• Angle open/narrow/closed
• Peripheral anterior synechiae
• Angle neovascularization
• Increased pigmentation
• Angle recession
• Cyclitic membrane or inflammatory deposits

H. Posterior Segment Examination

Vitreous

• Vitreous cells
• Vitreous haze
• Snowballs
• Snowbanking
• Vitreous haemorrhage

Optic disc

• Hyperaemia
• Disc oedema
• Disc granuloma
• Optic atrophy
• Neovascularization

Retina and choroid

• Retinitis/chorioretinitis
• Choroidal granuloma
• Retinal vasculitis
• Perivascular sheathing
• Haemorrhages
• Exudates
• Macular oedema
• Serous retinal detachment
• Retinal necrosis
• Retinal detachment

10. Anatomical Classification

11. Investigations

A. Essential ocular investigations

1. Slit-lamp photography
   Documents KPs, synechiae, hypopyon, and anterior chamber inflammation.
2. IOP measurement
   At baseline and each follow-up to detect uveitic or steroid-induced glaucoma.
3. Dilated fundus examination and fundus photography
4. Optical coherence tomography (OCT) of macula
   Detects and monitors cystoid macular oedema, epiretinal membrane, and subretinal fluid.
5. Fluorescein angiography
   Useful for retinal vasculitis, optic-disc leakage, macular oedema, capillary non-perfusion, and choroidal inflammatory activity.
6. Indocyanine-green angiography
   Consider in selected choroidal disorders, such as VKH, birdshot chorioretinopathy, or multifocal choroiditis.
7. B-scan ultrasonography
   When media opacity prevents fundus view, to assess vitreous opacities, retinal detachment, choroidal thickening, mass, or posterior scleritis.
8. Ultrasound biomicroscopy/anterior-segment OCT
   When evaluating ciliary body lesions, plateau iris, cyclitic membrane, or occult anterior-segment pathology.

B. Targeted systemic work-up

Common baseline directed tests in recurrent, bilateral, granulomatous, intermediate, posterior, or panuveitis

12. Differential Diagnoses

A. Painful red eye with photophobia

1. Acute anterior uveitis
2. Infectious keratitis/corneal ulcer
3. Acute angle-closure glaucoma
4. Scleritis
5. Episcleritis
6. Conjunctivitis
7. Corneal abrasion/foreign body
8. Endophthalmitis

B. White cells/hypopyon in anterior chamber

1. Severe non-infectious anterior uveitis, including HLA-B27-associated disease
2. Behçet disease
3. Infectious endophthalmitis
4. Herpetic uveitis
5. Retinoblastoma in children
6. Intraocular lymphoma or other masquerade syndrome
7. Leukaemia-related ocular infiltration

C. Granulomatous uveitis

1. Sarcoidosis
2. Tuberculosis
3. Syphilis
4. Vogt-Koyanagi-Harada disease
5. Sympathetic ophthalmia
6. Herpetic disease
7. Lens-induced uveitis
8. Idiopathic granulomatous uveitis

D. Retinitis/chorioretinitis

1. Toxoplasmosis
2. CMV retinitis
3. Acute retinal necrosis due to HSV/VZV
4. Syphilitic uveitis
5. Tubercular choroiditis
6. Sarcoid choroiditis
7. Intraocular lymphoma

E. Masquerade syndromes

• Intraocular lymphoma
• Leukaemia
• Retinoblastoma in children
• Pigment dispersion
• Retinal detachment
• Ocular ischemic syndrome
• Intraocular foreign body

13. Provisional Diagnosis Format

Example 1: Acute anterior uveitis

Example 2: Chronic bilateral uveitis

Example 3: Herpetic disease

Example 4: Intermediate uveitis

14. Management Protocol

A. General principles

1. Confirm anatomical location and assess severity.
2. Exclude infectious uveitis and masquerade syndromes before escalating immunosuppression.
3. Identify and treat the underlying cause when possible.
4. Suppress inflammation promptly and adequately.
5. Prevent or treat complications: synechiae, cataract, glaucoma, macular oedema, band keratopathy, retinal detachment, and neovascularization.
6. Monitor visual acuity, anterior chamber activity, IOP, vitreous activity, retina, and OCT macula serially.
7. Coordinate care with rheumatology, infectious disease, paediatrics, or oncology when indicated.

B. Acute non-infectious anterior uveitis

1. Topical corticosteroid

• Prednisolone acetate 1%
• Dexamethasone ophthalmic preparations
• Difluprednate in selected severe cases

2. Cycloplegic/mydriatic

• Relieves ciliary spasm and pain
• Prevents or breaks posterior synechiae
• Stabilizes blood-aqueous barrier

• Cyclopentolate
• Homatropine
• Atropine for severe inflammation

3. Monitor IOP

• Treat elevated IOP with appropriate aqueous suppressants.
• Avoid miotics during active anterior uveitis because they may worsen inflammation and promote posterior synechiae.
• Be aware that topical/systemic steroid therapy may itself elevate IOP.

4. Treat the cause

• HLA-B27-associated disease: coordinate rheumatology review if systemic symptoms are present.
• Herpetic anterior uveitis: antiviral therapy plus carefully supervised anti-inflammatory therapy.
• Syphilis, TB, toxoplasmosis, CMV, or other infection: organism-specific therapy in collaboration with relevant specialists.

C. Intermediate, posterior, and panuveitis

Non-infectious disease

• Local corticosteroid therapy: periocular, intravitreal, or steroid implant in appropriate cases
• Systemic corticosteroids for bilateral, severe, posterior, or vision-threatening disease
• Steroid-sparing immunomodulatory therapy for chronic, recurrent, bilateral, or steroid-dependent disease:
  • Methotrexate
  • Mycophenolate mofetil
  • Azathioprine
  • Calcineurin inhibitors
  • Biologic therapy, such as adalimumab, for selected refractory non-infectious uveitis

Infectious disease

• Treat the infection first or concomitantly as indicated.
• Corticosteroids should not be given as unmonitored monotherapy when infectious uveitis is possible.
• Examples include antimicrobial treatment for toxoplasmosis, syphilis, TB, viral retinitis, or CMV, guided by ophthalmology and infectious-disease specialists.

D. Management of Complications

15. Follow-Up Plan

• Symptoms: pain, redness, photophobia, floaters, vision
• Visual acuity
• Anterior chamber cells/flare
• Corneal findings and KPs
• Posterior synechiae
• IOP
• Vitreous cells/haze
• Fundus findings
• OCT macula if posterior involvement or reduced vision
• Medication adherence and adverse effects

Typical follow-up

• Severe active anterior uveitis: early review, often within days
• Mild improving disease: review within 1-2 weeks as decided by ophthalmology
• Chronic/recurrent disease: individualized long-term surveillance
• Patients on systemic immunosuppression: coordinated ophthalmology and systemic monitoring

16. Counselling

• Uveitis is inflammation inside the eye and can threaten sight if untreated.
• The condition may recur, especially with HLA-B27 disease or chronic inflammatory disorders.
• Steroid drops must not be stopped abruptly without review.
• Regular follow-up is needed to detect cataract, glaucoma, and macular oedema.
• Seek urgent care for worsening pain, redness, sudden visual loss, flashes, floaters, or a curtain/shadow in vision.
• Systemic symptoms such as joint pain, back stiffness, skin rash, oral/genital ulcers, cough, breathlessness, fever, or weight loss should be reported.

17. Short Examination Presentation